UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 171
DIESEL FUEL AND EXHAUST EMISSIONS
This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.
Environmental Health Criteria 171
DIESEL FUEL AND EXHAUST EMISSIONS
First draft prepared by the staff members of the Fraunhofer Institute
of Toxicology and Aerosol Research, Germany, under the coordination of
Dr. G. Rosner
Published under the joint sponsorship of the United Nations
Environment Programme, the International Labour Organisation, and the
World Health Organization, and produced within the framework if the
Inter-Organization Programme for the Sound Management of Chemicals.
World Health Organization
Geneva, 1996
The International Programme on Chemical Safety (IPCS) is a joint
venture of the United Nations Environment Programme, the International
Labour Organisation, and the World Health Organization. The main
objective of the IPCS is to carry out and disseminate evaluations of
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environment. Supporting activities include the development of
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that could produce internationally comparable results, and the
development of manpower in the field of toxicology. Other activities
carried out by the IPCS include the development of know-how for coping
with chemical accidents, coordination of laboratory testing and
epidemiological studies, and promotion of research on the mechanisms
of the biological action of chemicals.
WHO Library Cataloguing in Publication Data
Diesel Fuel and exhaust emission
(Environmental health criteria ; 171)
1.Air pollutants, Enviromental 2.Air pollution 3.Fueloils
I.International Programme on Chemical Safety II.Series
ISBN 92 4 157171 3 (NLM Classification: WA 754)
ISSN 0250-863X
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CONTENTS
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
PREAMBLE
ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL AND EXHAUST EMISSIONS
WHO DRAFTING GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL
AND EXHAUST EMISSIONS
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL AND
EXHAUST EMISSIONS
PART A: DIESEL FUEL
A1. SUMMARY
A1.1 Identity, physical and chemical properties, and
analytical methods
A1.2 Sources of human and environmental exposure
A1.3 Environmental transport, distribution, and
transformation
A1.4 Environmental levels and human exposure
A1.5 Effects on laboratory mammals and in vitro test
systems
A1.6 Effects on humans
A1.7 Effects on other organisms in the laboratory and the
field
A1.8 Evaluation of human health risks
A1.9 Evaluation of effects on the environment
A2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS
A2.1 Identity
A2.1.1 Fuel components
A2.1.1.1 Alkanes
A2.1.1.2 Alkenes
A2.1.1.3 Aromatic compounds
A2.1.1.4 Sulfur
A2.1.2 Fuel additives
A2.1.2.1 Cetane number improvers
A2.1.2.2 Smoke suppressors
A2.1.2.3 Flow improvers
A2.1.2.4 Cloud-point depressors
A2.1.2.5 Wax anti-settling additives
A2.1.2.6 Other additives
A2.1.3 Quality aspects of diesel fuels
A2.1.3.1 Ignition performance and cetane
number
A2.1.3.2 Density
A2.1.3.3 Sulfur content
A2.1.3.4 Viscosity
A2.1.3.5 Cold-flow properties
A2.2 Physical and chemical properties
A2.3 Analytical methods
A2.4 Conversion factors
A3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
A3.1 Natural occurrence
A3.2 Anthropogenic sources
A3.2.1 Production and use
A3.2.1.1 Production process
A3.2.1.2 Use
A3.2.1.3 Production and consumption
levels
A3.2.2 Emissions during production and use
A3.2.2.1 Air
A3.2.2.2 Water
A3.2.2.3 Soil
A3.2.3 Accidental releases to the environment
A4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
A4.1 Transport and distribution between media
A4.1.1 Evaporation from and dissolution in the
aqueous phase
A4.1.2 Transport in and adsorption onto soil and
sediment
A4.1.2.1 Soil
A4.1.2.2 Sediment
A4.2 Transformation and removal
A4.2.1 Photooxidation
A4.2.2 Biodegradation
A4.2.2.1 Microbial degradation
A4.2.2.2 Phytoplankton and marine algae
A4.2.2.3 Invertebrates and vertebrates
A4.2.3 Bioaccumulation
A4.2.4 Tainting
A4.2.5 Entry into the food chain
A4.3 Ultimate fate after use
A4.3.1 Use in motor vehicles
A4.3.2 Spills
A4.3.3 Disposal
A5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
A5.1 Environmental levels
A5.2 Exposure of the general population
A5.3 Occupational exposure during manufacture,
formulation, or use
A6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
A7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
A7.1 Single exposure
A7.2 Short-term exposure
A7.2.1 Subacute exposure
A7.2.1.1 Dermal exposure
A7.2.1.2 Inhalation
A7.2.2 Subchronic exposure
A7.2.2.1 Dermal exposure
A7.2.2.2 Inhalation
A7.3 Long-term exposure
A7.3.1 Dermal exposure
A7.3.2 Inhalation
A7.4 Dermal and ocular irritation; dermal sensitization
A7.4.1 Dermal irritation
A7.4.2 Ocular irritation
A7.4.3 Sensitization
A7.5 Reproductive toxicity, embryotoxicity, and
teratogenicity
A7.6 Mutagenicity and related end-points
A7.6.1 In vitro
A7.6.2 In vivo
A7.7 Carcinogenicity
A7.7.1 Dermal exposure
A7.7.2 Inhalation
A8. EFFECTS ON HUMANS
A8.1 Exposure of the general population
A8.2 Occupational exposure
A9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD
A9.1 Laboratory experiments
A9.1.1 Microorganisms
A9.1.1.1 Water
A9.1.1.2 Soil
A9.1.2 Aquatic organisms
A9.1.2.1 Plants (phytoplankton)
A9.1.2.2 Invertebrates
A9.1.3 Terrestrial organisms
A9.1.3.1 Plants
A9.1.3.2 Invertebrates
A9.1.3.3 Vertebrates
A9.2 Field observations
A9.2.1 Microorganisms.
A9.2.1.1 Water
A9.2.1.2 Soil
A9.2.2 Aquatic organism
A9.2.3 Terrestrial organisms
A9.2.3.1 Plants
A9.2.3.2 Invertebrates
A9.2.3.3 Vertebrates
A10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE
ENVIRONMENT
A10.1 Evaluation of human health risks
A10.1.1 Exposure of the general population
A10.1.2 Occupational exposure
A10.1.3 Non-neoplastic effects
A10.1.4 Neoplastic effects
A10.2 Evaluation of effects on the environment
A11. RECOMMENDATIONS
A11.1 Recommendations for the protection of human health
A11.2 Recommendation for the protection of the environment
A11.3 Recommendations for further research
A12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
PART B: DIESEL EXHAUST EMISSIONS
B1. SUMMARY
B1.1 Identity, physical and chemical properties, and
analytical methods
B1.2 Sources of human and environmental exposure
B1.3 Environmental transport, distribution, and
transformation
B1.4 Environmental levels and human exposure
B1.5 Kinetics and metabolism in laboratory animals and
humans
B1.5.1 Deposition
B1.5.2 Retention and clearance of particles
B1.5.3 Retention and clearance of polycyclic
aromatic hydrocarbons adsorbed onto diesel
soot
B1.5.4 Metabolism
B1.6 Effects on laboratory mammals and in vitro test
systems
B1.7 Effects on humans
B1.8 Effects on other organisms in the laboratory and the
field
B1.9 Evaluation of human health risks
B1.9.1 Non-neoplastic effects
B1.9.2 Neoplastic effects
B1.10 Evaluation of effects on the environment
B2. IDENTITY AND ANALYTICAL METHODS
B2.1 Identity
B2.1.1 Chemical composition of diesel exhaust
gases
B2.1.2 Type and composition of emitted particulate
matter
B2.2 Analytical methods
B2.2.1 Sampling
B2.2.1.1 Sampling from undiluted exhaust
gas (raw gas sampling)
B2.2.1.2 Sampling from diluted exhaust
(dilution tube sampling)
B2.2.2 Extraction from particles
B2.2.3 Clean-up and fractionation
B2.2.4 Chemical analysis
B2.3 Conversion factors
B3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
B3.1 Anthropogenic sources
B3.1.1 Diesel exhaust emissions
B3.1.1.1 Emission of chemical
constituents with the gaseous
portion of diesel exhaust
B3.1.1.2 Emission of particulate matter
and adsorbed components in
diesel exhaust gases
B3.1.2 Parameters that influence diesel exhaust
emissions
B3.1.2.1 Engine conditions
B3.1.2.2 Fuel specification
B3.1.2.3 Malfunction
B3.1.3 Total emissions by diesel engines
B3.1.4 Control of emissions
B3.1.4.1 Particle traps
B3.1.4.2 Catalytic converters
B3.2 Regulatory approaches
B4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
B4.1 Transport and distribution between media
B4.2 Transformation and removal
B5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
B5.1 Exposure of the general population
B5.2 Occupational exposure
B5.2.1 Truck drivers and mechanics
B5.2.2 Bus garage and other bus workers
B5.2.3 Fork-lift truck operators
B5.2.4 Railroad workers
B5.2.5 Mine workers
B5.2.6 Fire fighters
B5.3 Biomonitoring
B5.3.1 Urinary mutagenicity
B5.3.2 Other analyses
B6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
B6.1 Deposition
B6.2 Retention and clearance of particles
B6.3 Retention and clearance of polycyclic aromatic
hydrocarbons adsorbed onto diesel soot
B6.4 Metabolism
B7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
B7.1 Single exposure
B7.2 Short-term exposure
B7.3 Long-term exposure and studies of carcinogenicity
B7.3.1 Non-neoplastic effects
B7.3.2 Carcinogenicity
B7.3.2.1 Inhalation
B7.3.2.2 Other routes of exposure
B7.4 Dermal and ocular irritation; dermal sensitization
B7.5 Reproductive toxicity, embryotoxicity, and
teratogenicity
B7.5.1 Reproductive toxicity
B7.5.2 Embryotoxicity
B7.5.3 Teratogenicity
B7.6 Mutagenicity and related end-points
B7.6.1 In vitro
B7.6.2 In vivo
B7.6.3 DNA adduct formation
B7.7 Special studies
B7.7.1 Immunotoxicity
B7.7.2 Behavioural effects
B7.8 Factors that modify toxicity; toxicity of
metabolites
B7.9 Mechanisms of toxicity; mode of action
B7.9.1 Carcinogenic effects
B7.9.1.1 DNA-reactive mechanisms
B7.9.1.2 Cytotoxicity with regenerative
cell proliferation
B7.9.1.3 Effects of particles
B7.9.1.4 Effects of polycyclic aromatic
hydrocarbons
B7.9.2 Noncarcinogenic effects
B8. EFFECTS ON HUMANS
B8.1 General population
B8.1.1 Acute exposure: olfactory, nasal, and
ocular irritation
B8.1.2 Air pollution
B8.2 Occupational exposure
B8.2.1 Effects on the respiratory system
B8.2.1.1 Symptoms
B8.2.1.2 Acute changes in pulmonary
function
B8.2.1.3 Pulmonary effects
B8.2.2 Epidemiological studies (noncarcinogenic
effects)
B8.2.2.1 Effects on the respiratory
system
B8.2.2.2 Effects on the circulatory
system
B8.2.3 Epidemiological studies (carcinogenic
effects)
B8.2.3.1 Lung cancer
B8.2.3.2 Urinary bladder cancer
B9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD
B10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE
ENVIRONMENT
B10.1 Exposure of the general population
B10.2 Occupational exposure
B10.3 Non-neoplastic effects
B10.3.1 Hazard identification
B10.3.1.1 Humans
B10.3.1.1 Experimental animals
B10.3.2 Dose-response assessment
B10.3.2.1 Epidemiological studies
B10.3.2.2 Studies in experimental animals
B10.3.3 Exposure assessment
B10.3.4 Risk characterization
B10.3.4.1 Humans
B10.3.4.2 Experimental animals
B10.4 Neoplastic effects
B10.4.1 Hazard identification
B10.4.1.1 Lung cancer: occupational
exposure
B10.4.1.2 Urinary bladder cancer:
occupational exposure
B10.4.2 Dose-response assessment
B10.4.2.1 Lung cancer
B10.4.2.2 Urinary bladder cancer
B10.4.3 Exposure assessment
B10.4.4 Risk characterization
B10.4.4.1 Human lung cancer
B10.4.4.2 Human urinary bladder cancer
B10.4.4.3 Risk characterization based on
studies in experimental animals
Appendix B10.1 Construction of a biologically
based (alternative) model
Appendix B10.2 E-M algorithm
Appendix B10.3 A tumour growth model
B11. RECOMMENDATIONS
B11.1 Recommendations for the protection of human health
B11.2 Recommendation for the protection of the environment
B11.3 Recommendations for further research
B12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
REFERENCES
RESUMÉ
RESUMEN
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
Every effort has been made to present information in the Criteria
monographs as accurately as possible without unduly delaying their
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International Register of Potentially Toxic Chemicals, Case postale
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This publication was made possible by grant number 5 U01
ES02617-15 from the National Institute of Environmental Health
Sciences, National Institutes of Health, USA, and by financial support
from the European Commission.
Environmental Health Criteria
PREAMBLE
Objectives
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WHO DRAFTING GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL
AND EXHAUST EMISSIONS
WHO, Geneva, 6-9 December 1993
Members
Dr J.A. Bond, Chemical Industry Institute of Toxicology, Research
Triangle Park, NC, United State
Dr R.P. Bos, University of Nijmegen, Nijmegen, Netherlands
Dr R. Brown, Medical Research Council Toxicology Unit, University of
Leicester, Leicester, United Kingdom (Joint Rapporteur)
Dr Chao Chen, Human Health Assessment Group, United States
Environmental Protection Agency, Washington DC, United States
Dr I. Farkas, National Institute of Hygiene, Budapest, Hungary
Dr E. Garshick, Pulmonary Section, Brockton/West Roxbury VA Medical
Center, West Roxbury, MA, United States
Dr P. Gustavsson, North Western Health Board, Stockholm, Sweden
Dr D. Guth, United States Environmental Protection Agency, Research
Triangle Park, NC, United States
Dr U. Heinrich, Department of Experimental Hygiene, Fraunhofer
Institute of Toxicology and Aerosol Research, Hanover, Germany
Dr R.F. Hertel, Federal Health Office, Bundesgesundheitsamt, Berlin,
Germany
Professor G. Oberdörster, Department of Environmental Medicine,
University of Rochester Medical Center, Rochester, NY, United States
Dr W. Pepelko, United States Environmental Protection Agency,
Washington DC, United States
Dr P.J.A. Rombout, Laboratory of Toxicology, National Institute of
Public Health and Environmental Protection, Bilthoven, Netherlands
(Vice-Chairman)
Dr G. Rosner, Hazardous Substances Documentation Group, Fraunhofer
Institute of Toxicology and Aerosol Research, Hanover, Germany
Dr J. Roycroft, National Institute of Environmental Health Sciences,
Research Triangle Park, NC, United States
Dr A. Sivak, Environmental Health Sciences, Saint Augustine, FL,
United States (Chairman)
Dr B.H. Thomas, Environmental Health Directorate, Ottawa, Canada
Dr L. Turrio, Istituto Superiore di Sanita, Laboratorio Tossicologia
Comparata e Ecotossicologia, Rome, Italy
Mr. R. Waller, Department of Health, London, United Kingdom
Secretariat
Dr P. Boffetta, International Agency for Research on Cancer, Lyon,
France (6-7 December 1993)
Dr E. Smith, International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland
Representatives/Observers
CONCAWE
Dr R.H. McKee, Exxon Biomedical Sciences, East Millstone, NJ,
United States
UNITED KINGDOM DEPARTMENT OF THE ENVIRONMENT
Dr P.T.C. Harrison, MRC Institute of Environment & Health,
Leicester, United Kingdom
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL AND
EXHAUST EMISSIONS
Fraunhofer Institute of Toxicology & Aerosol Research, Hanover
27 June-1 July 1994
Members
Dr J.A. Bond, Chemical Industry Institute of Toxicology, Research
Triangle Park, NC, United States
Dr R. Brown, Medical Research Council Toxicology Unit, University of
Leicester, Leicester, United Kingdom
Dr Chao Chen, Human Health Assessment Group, United States
Environmental Protection Agency, Washington DC, United States
Dr E. Garshick, Pulmonary Section, Brockton/West Roxbury VA Medical
Center, West Roxbury, MA, United States
Dr U. Heinrich, Department of Experimental Hygiene, Fraunhofer
Institute of Toxicology and Aerosol Research, Hanover, Germany
Dr R.F. Hertel, Federal Health Office, Bundesgesundheitsamt, Berlin,
Germany
Dr Jun Kagawa, Tokyo Women's Medical College, Tokyo, Japan
Professor G. Oberdörster, Department of Environmental Medicine,
University of Rochester Medical Center, Rochester, NY, United States
Dr P.J.A. Rombout, Laboratory of Toxicology, National Institute of
Public Health and Environmental Protection, Bilthoven, Netherlands
Dr M. Roller, Medizinishes Institut für Umwelthyglene an der
Universität Düsseldorf, Düsseldorf, Germany Dr G. Rosner, Hazardous
Substances Documentation Group, Fraunhofer Institute of Toxicology and
Aerosol Research, Hanover, Germany
Dr A. Sivak, Environmental Health Sciences, Saint Augustine, FL,
United States
Dr L. Turrio, Istituto Superiore di Sanita, Laboratorio Tossicologia
Comparata e Ecotossicologia, Rome, Italy
Mr R. Waller, Department of Health, London, United Kingdom
Secretariat
Dr H. Moller, International Agency for Research on Cancer, Lyon,
France
Dr E. Smith, International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland
Dr M. Younes, European Centre for Environment and Health, Bilthoven,
Netherlands
Representatives/Observers
Dr Lutz Von Meyerinck, BP Oil Europe, Brussels, Belgium
GERMAN AUTOMOBILE ASSOCIATION
Dr N. Pelz, Mercedes-Benz AG, Stuttgart, Germany
ILSI
Dr I.T. Salmeen, Chemistry Department, Ford Motor Company,
Dearborn, MI, United States
IUTOX
Dr P. Montuschi, Department of Pharmacology, School of Medicine,
Catholic University of the Sacred Heart, Rome, Italy
ENVIRONMENTAL HEALTH CRIETERIA FOR DIESEL FUEL AND EXHAUST EMISSIONS
A WHO Task Group on Environmental Health Criteria for Diesel Fuel
and Exhaust Emissions met at the Fraunhofer Institute of Toxicology
and Aerosol Research, Hanover, Germany from 27 June to 1 July 1994.
Dr G. Rosner, Fraunhofer Institute, welcomed the participants on
behalf of the Institute and its Director, Professor U. Mohr, and
Dr E.M. Smith, IPCS, welcomed the participants on behalf of
Dr M. Mercier, Director of the IPCS, and on behalf of the heads of the
three IPCS cooperating organizations (UNEP, ILO, and WHO). The Task
Group reviewed and revised the draft and evaluated the risks for human
health and the environment from exposure to diesel fuel and exhaust
emissions.
The first draft of the monograph was prepared at the Fraunhofer
Institute. After international circulation for comment, this draft was
extensively revised by a Working/Drafting Group, convened at WHO,
Geneva, from 6 to 9 December 1993, and a second draft was prepared for
further international circulation for comment. The membership of the
drafting group is shown previously. A final draft, incorporating
comments received from the IPCS contact points for Environmental
Health Criteria monographs and new material, was completed at the
Fraunhofer Institute under the coordination of Dr G. Rosner, with
important contributions to the text from the following Institute staff
members:
Dr B. Bellman
Dr A. Boehnke
Dr O. Creutzenberg
Dr J. Kielhorn
Dr E.M. Smith of the IPCS Central Unit was responsible for the
scientific content of the monograph and Mrs E. Heseltine, Lajarthe,
France, for the editing.
The efforts of all who helped in the preparation and finalization
of the monograph are gratefully acknowledged.
PART A DIESEL FUEL
A1. SUMMARY
A1.1 Identity, physical and chemical properties, and analytical
methods
Diesel fuel is a complex mixture of normal, branched, and cyclic
alkanes (60 to > 90% by volume; hydrocarbon chain length, usually
between C9 and C30); aromatic compounds, especially alkylbenzenes
(5-40% by volume); and small amounts of alkenes (0-10% by volume)
obtained from the middle-distillate, gas-oil fraction during petroleum
separation. Benzene, toluene, ethylbenzene, and xylenes and polycyclic
aromatic hydrocarbons (PAHs), especially naphthalene and its
methyl-substituted derivatives, may be present at levels of parts per
million in diesel fuel. The sulfur content of diesel fuels depends on
the source of crude oil and the refinery process. It is regulated by
law in a number of countries and is usually between 0.05 and 0.5
weight percent. Additives are used to influence the flow, storage, and
combustion of diesel fuel, to differentiate products, and to meet
trademark specifications. At room temperature, diesel fuels are
generally moderately volatile, slightly viscous, flammable, brown
liquids with a kerosene-like odour. The boiling ranges are usually
between 140 and 385°C (> 588°C for marine diesel fuel); at 20°C, the
density is 0.87-1.0 g/cm3 and the water solubility is
0.2-5 mg/litre. The quality and composition of diesel fuel influence
the emissions of pollutants from diesel engines considerably.
Important variables are ignition behaviour (expressed in terms of
cetane number), density, viscosity, and sulfur content. The
specifications of commercial diesel fuel differ considerably in
different countries.
Heating fuels and some kerosene jet fuels produced during the
refining process may have a composition similar to that of diesel
fuel, although with different additives. Biological data on these
mixtures have therefore also been taken into account in the
assessments of toxicity and ecotoxicity.
Owing to the complexity of the diesel fuel mixture, there is no
specific analytical method, and the analytical techniques used in most
environmental assessments are suitable only for measuring the total
petroleum hydrocarbon mixture. The methods consist of preliminary
solvent extraction, a clean-up procedure to remove naturally occurring
hydrocarbons, and subsequent detection by gravimetry, infrared
spectroscopy or gas chromatography. Neither the gravimetric nor the
infrared technique provides useful qualitative or quantitative
information on contaminants and can thus be used only for screening.
Gas chromatography combined with detection techniques such as flame
ionization and mass spectrometry is the standard procedure for
analysing environmental samples. Many other methods are available for
the analysis of individual hydrocarbons in diesel fuels.
A1.2 Sources of human and environmental exposure
Diesel fuels are produced by refining crude oils. In order to
meet technical specifications for performance, diesel fuels are
generally blended; further formulation with additives improves their
properties for specific uses. Diesel fuels are widely used as
transportation fuels. The more volatile fuels, with low viscosity, are
required for high-speed engines and the heavier grades for railroad
and ship diesel engines. Much heavy-duty road transport is powered by
diesel engines. Passenger cars powered by diesel engines are becoming
increasingly more common in Europe and Japan (10-25%), whereas in
North America the percentage of diesel-fuelled passenger cars is about
1-2%, with a slightly decreasing tendency. Diesel fuel is used in
stationary engines and in boilers, e.g. reciprocating engines, gas
turbines, pipeline pumps, gas compressors, steam processing units in
electric power plants, burner installations, and industrial space and
water heating facilities.
Over the last five years, the worldwide demand for diesel fuels
has increased steadily. In 1985, the following amounts of diesel fuel
were consumed: about 170 000 kt per year in North America; about
160 000 kt per year, including gas oils, in the European Union; and
about 46 000 kt per year in Australia, Japan, and New Zealand,
equivalent to a total of 1062 kt per day. In 1990, world demand was
reported to be about 1110 kt per day.
No information is available on emissions during the production of
diesel fuels; however, this source would seem to be of minor
importance, because the refining process is carried out in closed
systems. Emissions may occur principally during storage and
transportation. Diesel fuels are released as a result of spills and at
filling stations during the refuelling of vehicles. The atmosphere and
the hydrosphere are the most heavily affected environmental
compartments. Soil contamination with diesel fuels may occur during
accidents and is also a problem in railroad yards. The numerous
techniques for cleaning soils contaminated with diesel fuel include
excavation, biological methods, and containment.
A1.3 Environmental transport, distribution, and transformation
Very few data are avilable on the environmental fate of diesel
fuels, but the mechanisms of their distribution and transformation are
considered to be comparable to those of heating fuels, such as No. 2
fuel oil, which have been well studied. Spills of diesel fuel on water
spread almost immediately to form a 'slick'. The polar and
low-relative-molecular-mass components dissolve and leach out of the
slick, and the volatile components evaporate from the surface;
microbial degradation also begins. Chemical and biological weathering
alter the composition of the spill. These processes are dependent on
temperature; spills that occur in Arctic conditions are more
persistent than those that occur in temperate climates. In marine
environments, most of the low-relative-molecular-mass aromatic species
are dissolved into the water phase, but the primary branched alkanes,
cycloalkanes, and remaining aromatic compounds may remain in sediments
for more than a year.
Although no information is available on the photooxidation of
diesel fuels in water and air, evaporated oil components are degraded
photochemically. No. 2 fuel oil has been shown to be photooxidized
rapidly in water under environmental conditions.
The individual constituents of diesel fuel are inherently
biodegradable, to varying degrees and at different rates. The
n-alkane, n-alkylaromatic, and simple aromatic molecules in the C10-C22
range are the most readily degradable. Smaller molecules are generally
rapidly metabolized. Long-chain n-alkanes are more slowly degraded,
owing to their hydrophobicity and because they are viscous or solid at
ambient temperatures. Branched alkanes and cycloalkanes are relatively
resistant to biological breakdown, and PAHs are resistant. The overall
rates of degradation of hydrocarbons are limited by temperature, water
content, oxygen, pH, inorganic nutrients, and microbial metabolic
versatility.
Unicellular algae can take up and metabolize both aliphatic and
aromatic hydrocarbons, but the extent to which this actually occurs in
nature is poorly understood. Unlike microorganisms that use petroleum
carbons as a carbon source, animals generally oxidize and conjugate
products, rendering end-products that are more soluble and therefore
easier to excrete. All animal species tested can take up petroleum
hydrocarbons. PAHs, crude oil, and refined petroleum products are
known to induce cytochrome P450 enzymes and to increase the levels of
hydrocarbon metabolism in numerous marine and freshwater fish species.
Few data are available on the bioaccumulation of diesel fuel in
the laboratory, but there is plentiful evidence from studies of spills
and laboratory studies on other oils, particularly No. 2 fuel oil,
that aquatic organisms bioconcentrate hydrocarbons. The
n-octanol-water partition coefficient for diesel fuel is 3.3-7.06,
which suggests high potential bioaccumulation; however, many of the
lower-relative-molecular-mass compounds are readily metabolized, and
the actual bioaccumulation of higher-relative-molecular-mass compounds
is limited by their low water solubility and large molecular size.
Thus, actual bioaccumulation may be low.
Fish have been tainted by diesel fuel after spills. No data are
available on the biomagnification of diesel fuel.
No experimental data are available on the movement of diesel fuel
through the soil, although a direct correlation between the movement
and kinematic viscosity has been proposed. The movement of kerosene
through soil depends on the moisture content and nature of the soil.
A1.4 Environmental levels and human exposure
As diesel fuels are complex mixtures, the environmental levels
have not been measured. The individual constituents of diesel fuels
can be detected in almost all compartments of the environment,
although their source cannot be verified. The general population may
be exposed to diesel fuel at filling stations and as a result of
spills.
Occupational exposure to diesel fuel occurs in a large number of
activities. Because of their low volatility, diesel fuels should
generate only low concentrations of vapours at normal temperatures,
but high operating temperatures can result in significant
concentrations.
A1.5 Effects on laboratory mammals and in-vitro test systems
The acute toxicity of diesel fuels is low after oral or dermal
exposure or after inhalation. The oral LD50 value was > 5000 mg/kg
body weight in all species tested (mouse, rabbit, rat, guinea-pig).
Dermal application resulted in an LD50 value of > 5000 mg/kg body
weight in mice and rabbits, although values of > 2000 mg/kg body
weight were reported for some kerosenes and middle distillates, with
different protocols and lower limit doses. The LC0 value in rats
exposed by inhalation was about 5 mg/litre, except for one
straight-run middle distillate for which a value of 1.8 mg/litre was
seen.
In rabbits treated dermally with up to 8000 µl/kg body weight per
day and mice with up to 40 000 mg/kg body weight per day, acanthosis
and hyperkeratosis due to severe irritation were seen. Rabbits were
more sensitive than mice. Inhalation of diesel fuel was neuro-
depressive in mice at concentrations up to 0.2 mg/litre but not
in rats exposed to up to 6 mg/litre. Body and liver weights were
reduced in rats.
Mice, rats, and dogs did not show significant cumulative toxicity
after inhalation of up to 1.5 mg/litre subchronically. The specific
nephropathy syndrome seen in male rats is linked to an inherent
accumulation of hyalin droplets in the renal tubules.
The only effects of long-term exposures were ulceration after
dermal application to mice (250 or 500 mg/kg body weight per day) and
significant alterations in organ weight after inhalation of 1 or
5 mg/litre by rats. In both studies the mean body weights were
reduced.
Various types of diesel fuels were slightly to severely
irritating to the skin of rabbits. Diesel fuels do not irritate the
eye, but some kerosenes have been reported to have a slight irritating
effect. Diesel fuels do not cause skin sensitization.
Diesel and jet fuels (kerosene) were neither embryotoxic nor
teratogenic in two studies in rats exposed by inhalation to 100 or
400 ppm and in one study in which rats were given up to 2000 mg/kg
body weight per day by gavage. In the last study, reduced fetal weight
was observed.
Tests in Salmonella typhimurium did not provide clear evidence
of mutagenicity. Some positive findings in S. typhimurium and in
mouse lymphoma cells were considered to be equivocal owing to the
inconsistency of the results. Tests for genotoxicity in mice in vivo
(induction of micronuclei or chromosomal aberrations) also gave
equivocal or negative responses.
Diesel fuels induced a low level of dermal carcinogenicity. In
the present state of research, it cannot be concluded whether the
carcinogenic potency of diesel fuels is mediated by a genotoxic
mechanism or by chronic dermal damage.
A1.6 Effects on humans
Non-occupational exposure to diesel fuel can occur during manual
filling of fuel tanks. The primary source of dermal exposure is
accidental spills, which result in immediate high levels of exposure
but are of short duration.
After accidental dermal contact, anuria, renal failure, gastro-
intestinal symptoms, and cutaneous hyperkeratosis have been reported.
Toxic lung disease has been observed after accidental ingestion of
diesel fuel and subsequent aspiration. Persistent productive cough has
been reported after inhalation. In a case-control study of men exposed
to diesel fuel, an increased risk for cancer of the lung other than
adenocarcinoma was found; a positive association was also seen with
prostatic cancer, although a higher risk was noted for the group with
'nonsubstantial' exposure than for that with 'substantial' exposure.
In a cross-sectional study of factory workers exposed to kerosene jet
fuels, dizziness, headache, nausea, palpitation, pressure in the
chest, and eye irritation were found to be more prevalent than in
unexposed controls. The time-weighted average concentration of
vapour from the fuel in the breathing zone was estimated to be
128-423 mg/m3.
A1.7 Effects on other organisms in the laboratory and the field
Diesel fuel is more toxic than crude oil to aquatic organisms and
plants. The ecotoxicity of diesel fuel is generally attributed to
soluble aromatic compounds, but insoluble aliphatic hydrocarbons may
also be implicated. Of the aromatic compounds, monoaromatics are the
least toxic, their acute toxicity increasing with molecular mass up to
the four- to five-ring compounds, although these are poorly soluble in
seawater. In some animals, e.g. fish and birds, physical coating of
the body surface by the fuel can produce toxicity and mortality.
Laboratory experiments have been carried out on diesel fuel,
water-soluble fractions, oil-water dispersions, and microencapsulated
oil. Diesel fuel did not significantly reduce the growth in culture of
the green alga Euglena gracilis, whereas a low concentration (0.1%)
almost completely inhibited the growth of Scenedesmus quadricauda.
Light diesel fuel (0.05%) stimulated the growth, photosynthesis, and
chlorophyll asynthesis of Chlorella salina but slightly inhibited
respiration; at higher concentrations, the growth rate and
photosynthesis were greatly reduced. Long-term exposure inhibited the
growth of the benthic algae Ascophyllum nodosum and Laminaria
digitata. In blue-green algae, photosynthesis was reduced by the
aromatic and asphaltic fractions but not by the aliphatic fraction.
Diesel fuel was acutely toxic to Daphnia spp., chironomid
larvae, and the mollusc Viviparus bengalensis (Gastropoda). A
concentration of 0.1 ml/litre caused the death of tidepool copepods,
Tigriopus californicus, within five days.
Mytilus edulismussels accumulate diesel fuel, have markedly
reduced feeding and growth rates, and show reproductive toxicity after
chronic exposure to diesel fuel. The EC50 for spawning in mussels
exposed for 30 days was about 800 µg/litre. The LC50 of micro-
encapsulated diesel oil after exposure of maturing mussels for
30 days was about 5000 µg/litre. Diesel oil was more toxic to larvae
than to juveniles: 10 µg/litre had adverse effects on the growth of
larvae.
Freshwater crabs (Barytelphusa cunicularis) exposed to sublethal
concentrations of diesel fuel for up to 96 h generally reduced their
oxygen consumption, particularly at lower exposures up to 8 h. With
longer exposures, the oxygen consumption was equal to or higher than
that of the controls.
In 96-h tests of acute toxicity in juvenile salmonids under
static conditions, diesel fuel was more toxic to pink salmon,
Onchorhychus gorbuscha (LC50: 32-123 mg/litre), than to cohosalmon,
O. kisutch (LC50: 2186-3017 mg/litre), or rainbow trout,
O. mykiss (LC50: 3333-33 216 mg/litre), irrespective of water type.
The threshold for detection of behavioural responses of cod
( Gadus morhua L.) exposed to diesel fuel in seawater was within
100-400 ng/litre. The Antarctic fish Pagothenia borchgrevinki
withstood an undiluted water-soluble fraction of diesel fuel oil for
up to 72 h but showed signs of stress.
Birds are affected externally and internally by oil
contamination. Diesel fuel destroys the waterproof nature of the
birds' plumage and is ingested during preening. Diesel and fuel oil
fed by gavage at 2 ml/kg body weight to ducks caused lipid pneumonia,
extreme inflammation of the lungs, fatty infiltration of the liver,
and hepatic degeneration after 24 h. Administration of diesel or fuel
oil at 1 ml/kg caused severe irritation of the digestive tract and
toxic nephrosis. Higher doses resulted in adrenal enlargement (mainly
due to hyperplasia of cortical tissue), depression of plasma
cholinesterase levels, ataxia, and tremors. Doses up to 20 ml/kg body
weight were not fatal to healthy birds, but the LD50 for diesel and
fuel oil administered to birds under stress was 3-4 ml/kg body weight.
After spills of diesel fuel, zooplankton appear to be highly
vulnerable to dispersed and dissolved petroleum constituents but less
so to floating oils. Aquatic organisms may be affected in a number of
ways, including direct mortality (fish eggs, copepods, and mixed
plankton), external contamination by oil (chorions of fish eggs and
cuticles and feeding appendages of crustaceans), tissue contamination
by aromatic constituents, abnormal development of fish embryos, and
altered metabolic rates.
A1.8 Evaluation of human health risks
The general population can be exposed to diesel fuel and other
middle distillates at filling stations, as a result of accidental
spills, during the handling of such fuels, and during use of kerosene
for domestic cooking or heating. Workers can be exposed to diesel fuel
and other middle distillates while handling and discharging the fuel
at terminals, storage tanks, and filling stations; during the
manufacture, repair, maintenance, and testing of diesel engines and
other equipment; during use of diesel fuel as a cleaning agent or
solvent; and in handling and routine sampling of diesel fuel in the
laboratory. Owing to the low volatility of diesel fuel, only low
concentrations of vapour are likely to occur at room temperature,
although in confined spaces at high temperatures significant levels
may be found.
Exposure to vapour is minimal during the normal handling of
diesel fuel. The most likely effect on human health is dermatitis
after skin contact. Diesel fuel is a skin irritant but does not appear
to irritate the eye. Acute toxic effects on the kidney can occur after
dermal exposure, but the effects of long-term dermal absorption of low
concentrations are unknown.
Diesel fuels are toxic when ingested, sometimes resulting in
regurgitation and aspiration, which can cause chemical pneumonia; the
same is true for any hydrocarbon in a particular range of viscosity.
In rodents exposed by inhalation to diesel fuel at concentrations
up to 0.2 mg/litre, a neurodepressive effect was seen in mice but not
in rats at the higher concentrations. Subchronic exposure by
inhalation to various distillate fuels induced specific
alpha2-microglobulin nephropathy in male rats; this effect is
considered irrelevant for humans.
Diesel fuels were neither embryotoxic nor teratogenic in animals
exposed orally or by inhalation.
There is no clear evidence of mutagenic activity in bacteria, and
the results of other tests for genotoxicity in vitro and in vivo were
equivocal.
A case-control study of workers exposed to diesel fuel suggested
an increased risk for cancer of the lung other than adenocarcinoma and
for prostatic cancer. In neither case was there an exposure-response
relationship. In view of the small number of studies available, the
small number of cases, and the correspondingly wide confidence
intervals, no conclusion can be drawn about the carcinogenicity to
humans of diesel fuel.
In mice, dermally administered diesel fuels had weak carcinogenic
potential. In view of the absence of clear genotoxicity, cancer could
be induced by nongenotoxic mechanisms, e.g. by chronic dermal
irritation characterized by repeated cycles of skin lesions, causing
epidermal hyperplasia.
A1.9 Evaluation of effects on the environment
The environment can be polluted by accidental release of diesel
fuel on a large scale, such as during tanker disasters and pipeline
leaks, or on a smaller scale from contamination of soil around
factories or garages. In water, diesel fuel spreads almost
immediately, polar and low-relative-molecular-mass components dissolve
and leach out, volatile components evaporate from the water surface,
and microbial degradation begins. The extent to which 'weathering'
takes place depends on the temperature and on climatic conditions. The
chemical composition of spills changes with time: after spillage on
water, some fractions evaporate, and the evaporated diesel components
are degraded photochemically; in sediment, diesel fuel appears
generally to be delivered to bottom sediments by settling particles;
in soil, the components of diesel fuel migrate at different rates,
depending on the soil type.
The individual constituents of diesel fuel are inherently
biodegradable, but the rates of biodegradation depend heavily on
physical and climatic conditions and on microbial composition.
Aquatic organisms, in particular molluscs, bioaccumulate
hydro-carbons to varying extents, but the hydrocarbons are depurated
on transfer to clean water. Diesel fuel may be bioaccumulated; no data
are available about biomagnification.
Spills of diesel fuel have an immediate detrimental effect on the
environment, causing substantial mortality of biota. Recolonization
may occur after about one year, depending on the animal or plant
species and the chemical and physical content of the spill residues.
Aquatic organisms that survive diesel fuel spills can be affected by
external oil contamination and tissue accumulation: abnormal
development and altered metabolic rates are signs of the resulting
stress.
A2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS
A2.1 Identity
Diesel fuels are a gas-oil fraction occurring during petroleum
separation and commonly known as middle distillates (International
Agency for Research on Cancer, 1989a). Gas oils are generally blended
materials formulated to meet technical specifications (CONCAWE, in
press). Commercial diesel fuels contain aliphatic, olefinic,
cycloparaffinic, and aromatic hydrocarbons (see section A2.1.1), and
additives (see section A2.1.2) to improve their fuelling properties
(Sandmeyer, 1981).
Four qualities of diesel fuel are available commercially: diesel
fuel (general), diesel fuel No. 1, diesel fuel No. 2, and diesel fuel
No. 4 (see Table 1). The composition of diesel fuels is comparable to
that of heating oils (e.g. No. 1 and No. 2 fuel oils), except for the
additives (International Agency for Research on Cancer, 1989a; Agency
for Toxic Substances and Disease Registry, 1995).
Diesel fuel No. 2 is used mainly as automobile fuel and
corresponds to diesel fuel (general). In Europe (countries of the
European Union (EU) and European Free Trade Area (EFTA)), the
specifications for diesel fuel for transportation purposes are given
in European standard EN 590 (European Committee for Standardization,
1993), which also provides for changes in the specifications to meet
the requirements of different climatic conditions. In Sweden, two
further qualities of on-road diesel fuel are available: environmental
class 1 and class 2 (city diesel), with sulfur contents of 0.05% and
0.001%, respectively (Standardization Board in Sweden, 1991). The
sulfur content of city diesel corresponds to that of kerosene. Diesel
fuel for ship engines is covered by the International Standards
Organization (ISO) standard 8217 (International Standards
Organization, 1987). In the United States of America, three grades of
diesel fuel are available: diesel fuel No. 1 (relatively high
volatility) for road vehicle engines subject to frequent speed and
load changes; diesel fuel No. 2 (lower volatility) for industrial or
heavy-duty, high-load engines running at uniform speed; and diesel
fuel No. 4 (viscous) for low- and medium-speed engines such as those
used in ships (American Society for Testing and Materials, 1988,
1992).
Several types of kerosene, also derived from the gas-oil fraction
of petroleum separation, are used as aviation turbine fuels (JP fuels,
jet fuels). Their hydrocarbon composition is comparable to that of
diesel fuels.
A2.1.1 Fuel components
A2.1.1.1 Alkanes
Normal, branched, and cyclic alkanes (paraffins) are the most
abundant components (about 65-85%) of diesel fuels. Pristane
(2,6,10,14-tetramethylpentadecane) and phytane (2,6,10,14-
tetramethyl-hexadecane) are of particular interest environmentally, as
the ratios of pristane to heptadecane and of phytane to octadecane
make it possible to identify the source of a fuel spill; furthermore,
as these ratios increase during biological degradation, they can be
used to estimate the age of an environmental contamination and the
degree of elimination. Cycloalkanes and bicycloalkanes constitute a
significant portion of the mixture, but individual compounds are
present only at low levels and are difficult to analyse. Alkyl
derivatives of cyclopentane, cyclohexane, and cycloheptane are common
components (Block et al., 1991; Table 2).
A2.1.1.2 Alkenes
Alkenes are not common components of crude oil but may be
present in diesel fuel if converted products are added after cracking.
These alkenes have predominantly branched and cyclic structures (Block
et al., 1991). The total alkene content of diesel fuels is up to 10%
(CONCAWE, 1985) (see also Table 2).
A2.1.1.3 Aromatic compounds
Aromatic compounds constitute 5-30% of automotive diesel fuel,
5-40% of marine diesel fuel (CONCAWE, 1985), and 10-30% of diesel
fuel No. 2 (Block et al., 1991). Table 2 shows the specifications of
commercial diesel fuels in this regard.
Table 1. Synonyms and trade names of commercial diesel fuels
Name CAS CAS Registry Range of Synonyms
name number carbon
numbers
Diesel fuel Diesel oil 68334-30-5 C9-C20a Auto diesel, automotive
(general) C10-C28b diesel oil, DERV, diesel,
diesel fuel oil, diesel
oil, gas oil
Diesel fuel Not assigned C9-C16c Diesel fuel oil No. 1,
No. 1 (essentially C4-C16 (for diesel oil No. 1, No. 1
equivalent to wide-cut dieseld
kerosene, aviation)c
8008-20-6)
Diesel fuel No. 2 68476-34-6 Diesel fuel, diesel fuel
No. 2 diesel (applicable for oil No. 2, diesel oil
fuel specific No. 2, No. 2 diesele
viscosity
limits)
Diesel fuel 68476-31-3 C10-C30f Marine diesel fuel,
No. 4 distillate marine diesel
fuel
Adapted from International Agency for Research on Cancer (1989a) and supplemented
a From CONCAWE (in press)
b From CONCAWE (1985); automotive gas oil (automotive diesel fuel, DERV)
c From CONCAWE (1985, 1995)
d In Europe, fuels similar to US diesel No. 1 are commonly referred to as
'kerosene' or 'Arctic diesel'
e Term uncommon in Europe. In the United Kingdom, distillate fuels are frequently
categorized as Class A1 (road diesel) and A2 (off-highway diesel)
f From CONCAWE (1985); distillate marine diesel
Only trace quantities of toxicologically relevant benzene,
toluene, ethyl benzene, and xylene compounds (for physicochemical
properties, see Table 6) are present in diesel fuel No. 2, but
significant levels are found in diesel fuel No. 1 (Arctic diesel),
which has lower flash-point specifications (Block et al., 1991); the
International Agency for Research on Cancer (1989a) cites a
flash-point of 0.25-0.5%. The concentration of benzene in kerosenes is
< 0.01% by volume; wide-cut aviation kerosenes may have higher
levels, but they are usually < 1% by volume (IPCS, 1986; CONCAWE,
1995; IPCS, 1993).
Table 2. Hydrocarbon specifications of some commercial diesel fuel oils
Specification Diesel Keroseneb Distillate Diesel
fuela marine fueld
dieselc
Paraffins/naphthenes 65-95e 78-96 60-90
(volume %) (wide-cut
aviation, < 1)
n-Hexane (volume %) < 0.01
(wide-cut
aviation, < 1)
Saturates (volume %) 59.4-76.6
Olefins (volume %) 0-10 0-5 0-10 0.0-1.0
Aromatics (volume %) 5-30 4-25 5-40 23.4-39.6
(wide-cut
aviation,
6-25)
Aromaticity (weight %) 11-15
See also Table 1
a From CONCAWE (1985, in press); fuel oil similar to diesel fuel (general)
b From CONCAWE (1985, 1995); fuel oil similar to diesel fuel No. 1
c From CONCAWE (1985, in press); fuel oil similar to diesel fuel No. 4
d From German Scientific Association for Petroleum, Natural Gas, and Coal (1991);
three samples of diesel fuel (general)
e Depending on origin of crude oil
Alkyl benzenes (particularly C3 and C4) are common components of
diesel fuel. Polycyclic aromatic hydrocarbons (PAHs), e.g.
naphthalene, phenanthrene, acenaphthene, acenaphthylene, fluorene,
fluoranthene, and pyrene, are also present, as are alkyl- and
cycloalkyl-substituted homologues of these substances, the predominant
ones being naphthalene and its methyl-substituted derivatives (see
Table 6 for physicochemical properties) (Block et al., 1991).
As some PAHs and the benzene, toluene, ethyl benzene, and xylene
components have been shown to be toxic and ecotoxic, these classes of
compounds are usually included in analytical procedures for
environmental contamination by diesel fuel. The PAH content of diesel
fuels varies widely, the highest levels being found in low-quality
fuel blended for large users (frequently railroad companies). The
mid-range aromatic (and PAH) content of diesel blends is limited by
the cetane number specification (Block et al., 1991) (see section
A2.1.3).
The concentrations of total PAHs in diesel fuel are < 5% by
volume, although some marine diesel fuels may contain > 10% by volume
(CONCAWE, 1985; International Agency for Research on Cancer, 1989a).
In straight-run gas-oil components, which are the major blending
material of diesel fuel (see section A3.2.1.1), three-ring PAHs
predominate; use of heavier atmospheric vacuum or cracker gas oils in
a diesel-fuel mixture leads to an increasing content of four- to
six-ring PAHs (CONCAWE, in press).
The concentrations of these constituents in a commercial diesel
fuel (unspecified) and, for comparison, in No. 2 fuel oil are shown in
Table 3. It should be noted that the PAH content of No. 2 fuel oil is
not limited by cetane number specification, so that it may include a
larger proportion of these hydrocarbons (Block et al., 1991). Table 3
also gives the composition of the water-soluble fractions of diesel
and No. 2 fuel oils and indicates how the solubility of a compound
affects the composition of the fraction and of the whole oil.
A2.1.1.4 Sulfur
The sulfur content of middle distillates depends on the source of
crude oil (Booth & Reglitzky, 1991; CONCAWE, 1995). The sulfur content
of most diesel fuels is 0.1-0.5% by weight; it is higher than that of
gasoline, which is about 0.02% by weight (Scheepers & Bos, 1992a).
Only diesel fuel No. 4 (distillate marine diesel) has a sulfur level
> 1% by weight (CONCAWE, 1985, in press). ISO standard 8217
(International Standards Organization, 1987) specifies a sulfur
content of marine diesel fuel of 1.0-2.0% by weight.
The sulfur content of some diesel fuels ranges from 0.01 to > 3%
by weight. In Europe (countries of EU and EFTA), the sulfur content is
restricted to a maximum of 0.2-0.3% by weight, and, as of 1996, it
will be further reduced to 0.05% by weight (European Commission,
1993). In the United States in 1988, the maximal sulfur content
permitted was 0.5% by weight for diesel fuels No. 1 and 2 and 2.0% by
weight for diesel fuel No. 4 (American Society for Testing and
Table 3. Concentrations of toxicologically relevant aromatic hydrocarbons in diesel fuel and No. 2 fuel oil and in 10% water-soluble
fractions prepared from them
Compound Diesel fuela Diesel fuelb No. 2 fuelc No. 2 fueld Water-soluble fractions (µg/litre)
(% by wt) (% by wt) (% by wt) (% by wt)
No. 2 Diesel
fueld fuela
Benzene 0.1 > 0.02 0.006-0.008 NR 550 344
Toluene 0.7 0.25-0.5 0.01-0.08 NR 1040 777
Alkylbenzenese 970
Ethylbenzene 0.2 0.25-0.5 0.01-0.08 NR 139
Xylene 0.5 0.25-0.5 0.01-0.08 NR 875
Polycyclic aromatic hydrocarbons
Naphthalene 0.4 0.273 0.4 840 6.6
1-Methylnaphthalene NR NR 0.82 340 66.2
2-Methylnaphthalene NR 0.67 1.89 480 108
Dimethylnaphalenese NR NR 3.11 240 NR
Trimethylnaphthalenese NR NR 1.84 30 NR
Fluorenese NR NR 0.36 20 NR
Phenanthrenese NR 0.15 0.53 20 NR
NR, not reported
a From Dunlap & Beckmann (1988); the analytical method is not described in detail; the concentration of benzene seems to be
unusually high.
b From International Agency for Research on Cancer (1989a); according to CONCAWE (1985), some marine diesel fuels may contain
more than 10% polycyclic aromatic hydrocarbons.
c From Stone (1991); summary of several reports
d From Anderson et al. (1974); US National Research Council (1985)
e Total of several isomers
Materials, 1988); in October 1993, the maximum was reduced to 0.05% by
weight (US Environmental Protection Agency, 1992a; American Society
for Testing and Materials, 1992). The permitted sulfur level in Brazil
is > 3% by weight (A. Sivak, personal communication, 1993). In Japan,
the sulfur content of diesel fuels was reduced to 0.2% by weight in
1994, and a further reduction, to 0.05% by weight, is under discussion
(CONCAWE, 1990a). Blended marine diesel fuel may also contain up to
about 15% residual components, i.e. material with an initial
boiling-point above about 350°C (CONCAWE, in press).
A2.1.2 Fuel additives
Only agents that are added to fuels at a concentration < 1% are
described as 'additives'. A more appropriate term for substances
present at higher concentrations is 'fuel components'. Fuels are
treated with additives for a number of reasons (see Table 4 and
below); they also differentiate products and determine the trademark
quality of commercial fuels (Fabri et al., 1990).
A2.1.2.1 Cetane number improvers
Cetane number improvers upgrade the ignition characteristics of a
base fuel more economically than refinery processes (Fabri et al.,
1990) (see section A2.1.3). Primary alkyl nitrates (e.g. isooctyl
nitrate) are often used to improve cetane number. Polyethyleneglycol
dinitrates, although effective at much lower concentrations, have a
number of disadvantages, including their price and the fact that they
may not improve the performance of fuel in low-compression engines
(Russell, 1989).
A2.1.2.2 Smoke suppressors
Organometallic compounds containing barium, calcium, manganese,
or iron have been used to reduce diesel smoke. With barium-based
products, 85-95% of the metal is emitted as particulates in the
exhaust (Russell, 1989); however, barium and calcium compounds are no
longer used.
A2.1.2.3 Flow improvers
Cold-flow improvers increase the fluidity of the fuel by
modifying the growth of wax crystals formed by higher homologues of
paraffins at low temperatures. The wax content of diesel fuels is
influenced by the origin of the crude oil, the distillation range of
the fuel, and the source of blend components (Coley, 1989).
Table 4. Diesel fuel additives
Additive Material Concentration Effect
(ppm)
Ignition improvers, Organic nitratesa Enhancement of self-ignition qualitiesa
cetane enhancersa
Smoke suppressors, Organic compounds of Ca, Ba, Reduction of soot; increase in metal
combustion enhancersa or (sometimes)Mga sulfate emissionsa
Detergentsa Amines, imidazolines, Prevention and removal of coke deposits
succinimides, etc.b on fuel injector tips, etc.a
Flow improvers Olefin-ester copolymers 50-500 Interaction with wax crystals and
modification of their growth; prevention
of formation of agglomerates
Cloud-point depressors Olefin-ester copolymers About 1000 Depression of cloud-point; prevention of
formation of agglomerates
Wax anti-settlers Modified ethylene-vinyl 100-500c Reduction of crystal size and rate of
acetate copolymersc settling; prevention of formation of agglomerates
Anti-static agents Not reported Not reported Reduction of building up of charges of
static electricity
Anti-corrosion chemicals Alkenyl succinic acids and 5-50 Prevention of corrosion or rusting of
esters, dimer acids, amine storage tanks, pipelines, and metal fuel
salts system components
Table 4 (contd)
Additive Material Concentration Effect
(ppm)
Antioxidants Hindered phenols or amines 25-200 Prevention of aging processes
Anti-foam agents Silicones Up to 20 Reduction of foaming tendency; reduction
of risk of ground pollution from oil spills
Dehazers Quaternary amine salts 5-50 Reduction of formation of hazes;
acceleration of haze clearance
Biocides Imines, amines, About 200 Prevention of growth of bacteria and
imidazolines, etc. fungi in storage tank bottoms
Lubricants Surface-active agents such 50-500 Compensation of lower viscosity of fuels
as polyfunctional acids and in low-temperature regions
derivatives
Odour maskers Natural, identical substances, 10-100 Reduction or elimination of smell
such as vanillin and terpenesc
From Coley (1989), except as noted
a From Organisation for Economic Co-operation and Development (1993)
b From Russell (1989)
c From Fabri et al. (1990)
A2.1.2.4 Cloud-point depressors
Diesel fuels must be easily filterable, as wax crystals formed at
low temperatures can clog fuel filters. Cloud-point depressors are
therefore added (Fabri et al., 1990) which consist of substances with
lower cloud-points, e.g. kerosene. Addition of 10% kerosene lowers the
cloud-point of diesel fuel by about 2°C. Olefin-ester copolymers
depress the cloud-point by 3-4°C but are not currently in commercial
use (Coley, 1989).
A2.1.2.5 Wax anti-settling additives
These additives inhibit the tendency of wax to settle by reducing
the crystal size and slowing the settling rate. A five-fold reduction
in wax crystal size slows the settling rate by one-twenty-fifth. With
increasing temperature, small dispersed crystals redissolve more
readily than settled wax (Coley, 1989).
A2.1.2.6 Other additives
Detergents, including amines, amides, imidazolines, and
succinates, are used to reduce injector nozzle fouling. Detergents
such as polyalkenyl succinimides also improve fuel stability,
resistance to corrosion, and combustion efficiency (Russell, 1989).
Antistatic agents lower the risk of building up a charge of static
electricity during pumping at high rates at bulk terminals or in
large-capacity truck fuel tanks.
Other additives used are anti-oxidants (phenols, amines),
anti-corrosion chemicals (alkenyl succinic acids, esters, dimer acids,
amine salts), anti-foam agents (silicones), dehazers (anti-emulsion
agents) (quaternary ammonium salts), biocides, lubricants for cold
regions (surface-active polyfunctional acid derivatives), and odour
maskers (vanillin, terpenes) (Coley, 1989; Fabri et al., 1990).
A2.1.3 Quality of diesel fuels
A2.1.3.1 Ignition performance and cetane number
The cetane number determines the ignition performance of
transport fuels relative to a scale on which methyl naphthalene
corresponds to a combustion rate of 0 and cetane to one of 100
(Scheepers & Bos, 1992a). The cetane number is calculated by comparing
the ignition quality of a fuel with that of two reference fuel blends
of known cetane numbers under standard operating conditions (American
Society for Testing and Materials method D 613 CFR). A high cetane
number improves cold starting and engine durability and reduces noise,
fuel consumption, smoke emissions during warm-up, and exhaust
emissions (Russell, 1989). In Europe (countries of the EU and EFTA),
the minimal cetane number must be in the range 45-49, depending on the
climatic conditions (European Committee for Standardization, 1993);
cetane numbers are usually 49-53 (CONCAWE, 1987). In the United
States, the cetane number must be at least 30 for diesel fuel No. 4
and 40 for diesel fuels No. 1 and 2 (American Society for Testing and
Materials, 1988, 1992).
A2.1.3.2 Density
The density of diesel fuel influences engine performance: higher
density leads to enrichment of the fuel:air mixture, which results in
greater engine power output. Enrichment may, however, increase the
particulate content of exhaust gas emissions (Fabri et al., 1990) (see
section B3.1.2.2). A density range is specified in fuel standards in
some countries (American Society for Testing and Materials, 1992;
European Committee for Standardization, 1993).
A2.1.3.3 Sulfur content
Gas and particle emissions in diesel engine exhaust are
influenced by the sulfur content of the fuel; there is a direct
relationship between particle production and sulfur content (Hare,
1986) (see section B3.1.2.2).
A2.1.3.4 Viscosity
Too low a viscosity can lead to wear in the injection pump; too
high a viscosity impairs fuel injection and mixture formation (Fabri
et al., 1990). In Europe (countries of the EU and EFTA), the viscosity
of commercial diesel fuels at a temperature of 40°C must be
1.5-4.5 mm2/s (European Committee for Standardization, 1993). In the
United States, the permitted ranges of viscosity at 40°C are
1.3-2.4 mm2/s for diesel fuel No. 1, 1.9-4.1 mm2/s for diesel fuel
No. 2, and 5.5-45.0 mm2/s for diesel fuel No. 4 (American Society
for Testing and Materials, 1988, 1992).
A2.1.3.5 Cold-flow properties
Cloud-point and cold filter plugging point characterize the
behaviour of diesel fuels at low temperatures (Fabri et al., 1990).
These points are lowered by the addition of cloud-point depressors and
by special blending techniques, e.g. increasing the kerosene content
of the fuel (see section A2.1.2).
Changes in diesel fuel quality have been assessed. Wade & Jones
(1984) reported a deterioration in fuel quality with decreasing cetane
number and found that a 90% increase in boiling-point led to greater
emissions of particulates, nitrogen oxides and PAHs. A decline in
diesel fuel quality on the European market was predicted, as the
rising demand would lead to greater use of fuels from catalytic or
thermal cracking processes (CONCAWE, 1987) (see section A3.2.1.1). A
study by the Organisation for Economic Co-operation and Development
(1993) indicated an improvement in the quality of diesel fuel in the
United States due to a decline in aromaticity.
A2.2 Physical and chemical properties
Diesel fuel is a brown, slightly viscous, flammable liquid at
room temperature (Sandmeyer, 1981). It generally has a kerosene-like
odour (Agency for Toxic Substances and Disease Registry, 1995). Its
physical and chemical properties are listed in Table 5.
The water solubility of diesel fuels varies. The aqueous
solubility of crude and fuel oils in the environment is clearly
dependent on the salinity of the water and the age of the oil slick
(see section A4.1.1) and is of the same order of magnitude as the
solubility of fuel oils: at room temperature, 0.37-0.53 mg/litre in
sea water (Boehm & Quinn, 1974) and 0.7-11 mg/litre in tap water
(Lysyj & Russell, 1974). The solubility of a fuel slick decreases with
its age as the concentration of long-chain hydrocarbons increases; the
solubility of fresh crude oil is 29.3-32.3 mg/litre, whereas that of
weathered crude oil is 0.06-23.2 mg/litre at 25°C (Mackay & Shiu,
1976).
The physicochemical properties of the toxicologically relevant
benzene, toluene, ethyl benzene, xylene and PAH components are given
in Table 6.
A2.3 Analytical methods
Exhaustive identification and quantification of the individual
constituents of commercial diesel fuel (see section A2.1) is almost
impossible owing to their number and complexity. In most environmental
assessments, therefore, the mixture is analysed as total petroleum
hydrocarbon (Block et al., 1991). All such methods involve preliminary
solvent extraction of the matrix, with e.g. trichlorotrifluoroethane.
This step may also extract naturally occurring hydrocarbons, which
interfere with the analysis; however, some of these compounds are
polar and can be removed on silica gel. Three analytical methods are
available:
Table 5. Physicochemical properties of diesel fuels
Property Diesel fuel Diesel fuel Diesel fuel Diesel fuel
(general) No. 1 No. 2 No. 4
Melting-point (°C) - 34a 18a - 29-9a
Boiling range (°C) 160-190b 145-300 (wide-cut 282-338a 170-420d
143-384e aviation, 45-280)c 101- > 588a
193-293a
Flash-point (°C) > 56b > 21 - < 55 52 (closed cup)a > 56d
58-66e (wide-cut aviation, > 54 (closed cup)a
(Pensky-Martens) < 21)c
38 (closed cup)a
Autoignition temperature (°C) 177-329a 254-285a 263a
Density (g/cm3) 0.81-0.90 (15°C)b 0.805 (wide-cut 0.87-0.95 0.87-0.92 (15°C)d
0.82-0.84 (15°C)e aviation, 0.75-0.801) (20°C) 0.81-0.94 (15°C)
(15°C)c 0.81-0.94 1 (20°C)
(15°C)
Kinematic viscosity (mm2/s) 2-7.4 (40°C)b 1.5-2.5 (wide-cut 2-7.4 (40°C)d
2.20-3.25 (40°C)e aviation, about 1.1
(20°C)c
Vapour pressure (kPa) About 40 (40°C)b About 10 (wide-cut 2.83-35.2 2.83-35.2 (21°C)a
0.04f aviation, 140-210) (21°C)a
(Reid, 37.8°C)c
2.83-35.2 (21°C)a
Table 5 (contd)
Prpoerty Diesel fuel Diesel fuel Diesel fuel Diesel fuel
(general) No. 1 No. 2 No. 4
Water solubility (mg/litre) 1f About 5 (20°C)a About 5 (20°C)a About 5 (20°C)a
0.2f
Henry's law constant 4.3 × 103f 6.03-7.5 × 105a 6.03-7.5 × 105a 6.03-7.5 × 105a
(Pa × m3/mol) (20°C)
n-Octanol-water partition 3.3-7.06a 3.3-7.06a 3.3-7.06a
coefficient (log Kow)
Soil sorption coefficient 3.04f 3.0-6.7a 3.0-6.7a 3.0-6.7a
(log Koc)
Diffusion coefficient in air 4.63 × 10-2f
(cm2/s)
Odour threshold (ppm) 0.7a 0.5g
a From Agency for Toxic Substances and Disease Registry (1995)
b From CONCAWE (in press); automotive gas oil
c From CONCAWE (1985, 1995); kerosenes
d From CONCAWE (in press); distillate marine diesel
e From German Scientific Association for Petroleum, Natural Gas, and Coal (1991); average of three samples
f From Custance et al. (1993); water solubility measured, other data from literature; no further details
g From Fraser Williams (Scientific Systems) Ltd (1985)
-- Gravimetric detection: determination of the weight of residue
remaining after solvent evaporation. Although this method is
useful for measuring gross contamination, it cannot be used in
trace analysis.
-- Infrared detection: the absorbance of petroleum hydrocarbons is
detected in a solvent matrix at the maximal value, near
2930 cm-1. This carbon-hydrogen bond stretching absorbance is
directly related to the hydrocarbon concentration in the extract.
The results are dependent on the hydrocarbon standard used for
quantification.
-- Gas chromatographic detection: capillary gas chromatography
combined with flame ionization or mass spectrometric detection.
The gravimetric and infrared techniques are fast, relatively
simple and widely accepted by regulatory authorities; however, they do
not provide sufficient qualitative and quantitative information on
composition. Gas chromatography is therefore the standard procedure
used to identify and quantify fuel constituents in environmental
samples. Different distribution and degradation processes in
environmental compartments (see section A4) mean that the composition
of petroleum hydrocarbons in air, water, soil, and biota may differ
considerably from that of the original fuel. Newton et al. (1991)
developed an analytical method for identifying and quantifying traces
of diesel contamination in tinned fish products on the basis of the
n-alkane pattern.
Because of the suspected toxicity of aromatic components in
diesel fuel, a detailed analysis is often necessary. Two groups of
compounds are detected:
-- volatile aromatic compounds: Analysis of these minor components
of diesel fuel requires special enrichment techniques, such as
purge-trap gas chromatography, and methods of detection including
flame ionization and mass spectrometry.
-- PAHs: Gas chromatography with flame ionization or mass
spectrometric detection, or liquid chromatography, is used after
solvent extraction. As PAHs are poorly resolved from the diesel
fuel matrix, gas chromatography-mass spectrometry is necessary in
most cases to quantify the components. The target analytes of
commonly used analytical methods do not, however, include C3
and C4 alkyl-substituted benzenes or most alkyl-substituted
PAHs in diesel fuels.
Table 6. Physicochemical properties of aromatic components of diesel fuel
Aromatic compound Water solubility Henry's law constant Diffusion coefficient (cm2/s) Octanol-water partition
(mg/litre) (Pa × m3/mol) In air In water coefficient (log Pow)
Benzene 1791 550 0.087 9.8 × 10-6 1.99
Toluene 534.8 602 0.083 8.6 × 10-6 2.52
Ethylbenzene 161.0 855 0.076 7.8 × 10-6 2.94
Xylene 156.0 778 0.076 1 × 10-5 2.94
Polycyclic aromatic 0.067 0.007 0.067 2.12 × 10-6 5.30
hydrocarbons
Adapted from Custance et al. (1993)
A2.4 Conversion factors
As diesel fuel vapour is a complex mixture of gases, it is
impossible to give a conversion factor for converting parts per
million in the gaseous phase to SI units.
A3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
A3.1 Natural occurrence
Diesel fuels are derived from crude oil, which can be considered
a 'natural product'. Nevertheless, human and environmental exposure
results almost exclusively from anthropogenic activities.
A3.2 Anthropogenic sources
A3.2.1 Production and use
A3.2.1.1 Production process
Diesel fuel is produced during the refining of crude oils but is
generally blended to meet the specifications for technical
performance. The blending components may be produced by atmospheric
distillation of crude oil (straight-run atmospheric gas oil), vacuum
distillation of atmospheric residue (vacuum gas oil), thermal cracking
(thermally cracked gas oil), or catalytic cracking processes (e.g.
light catalytically cracked gas oil; cycle oil). The main components
are straight-run gas oils: 80% of European automotive diesel fuel is
made up of these components (Booth & Reglitzky, 1991). Secondary
processing of heavier fractions is increasingly necessary in order to
meet product demand (CONCAWE, in press).
Diesel fuel No. 1 is manufactured by a straight-run distillate
process (Agency for Toxic Substances and Disease Registry, 1995);
diesel fuel No. 2 is generally made by mixing straight-run and
catalytically cracked distillates; and diesel fuel No. 4 is produced
by adding blending stocks to distillation residues in order to meet
viscosity specifications (International Agency for Research on Cancer,
1989a). Further variations are introduced by formulation with
additives to improve fuel properties (see section A2.1.2).
A3.2.1.2 Use
Diesel fuel is widely used as a transport fuel for light- and
heavy-duty vehicles; the Organisation for Economic Co-operation and
Development (1993) classifies vehicles weighing < 3.5 t as light-duty
and those weighing > 3.5 or, occasionally, > 5 t as heavy-duty.
Diesel fuel No. 1 is suitable for engines that undergo frequent
changes in speed and load (Agency for Toxic Substances and Disease
Registry, 1995). Heavier grades (diesel fuels No. 2 and 4) are used
for trucks, railroad and marine diesel engines, and stationary engines
in continuous high-load service (Sandmeyer, 1981; International Agency
for Research on Cancer, 1989a). Diesel fuels are also used in
stationary gas turbines, e.g. to generate electric power during
peak-load periods. Residual fuel oils, such as diesel fuel No. 4, are
used to generate steam in electric power plants (International Agency
for Research on Cancer, 1989a), in commercial and industrial burner
installations without preheating facilities, in plants and factories
for space and water heating, for pipeline pumping, and in gas
compression; they are also sprayed on unmade roads to compact the
surface and are used in the manufacture of asphalt cement (Agency for
Toxic Substances and Disease Registry, 1995).
A3.2.1.3 Production and consumption levels
The demand for diesel fuel has increased worldwide over time. In
1990, world demand was about 1100 kt/day (Booth & Reglitzky, 1991).
The production and consumption of diesel fuel in different regions
over time are shown in Table 7.
Diesel-fuelled passenger cars are relatively common in western
Europe. The percentages of passenger cars with diesel engines in
various European countries over time are shown in Table 8. In many
European countries, taxi-cabs are equipped almost exclusively with
diesel engines. In 1985, diesel-fuelled heavy-duty trucks comprised
about 86% of the fleet in Norway, 89% in Denmark, 95% in Sweden, and
100% in the former Federal Republic of Germany. In some countries of
Europe, diesel fuel consumption has increased steadily over the last
decade, and consumption for heavy-duty vehicles is predicted to more
than double between 1980 and 2005 (Organisation for Economic
Co-operation and Development, 1993). In western Germany, diesel fuel
consumption was almost 60% higher in 1990 (about 5100 kt) than in 1984
(about 3200 kt) (Federal Ministry for Transport, 1992).
Diesel-fuelled passenger cars are less common in North America.
In the United States in 1986, about 1.6% of passenger cars were
diesel-fuelled, and the tendency was predicted to decrease slightly
(US Department of Energy, 1988). In contrast, 82% of heavy-duty trucks
were diesel-fuelled in 1985 (Organisation for Economic Co-operation
and Development, 1993), and 59300 kt of diesel fuel were consumed by
highway traffic in 1986, representing 14.8% of all the highway fuel
used and about one-half of United States diesel fuel consumption.
On-road use of diesel fuel was predicted to increase to 15.5% of all
highway fuel (66600 kt) in 1995. A difference in fuel use patterns is
seen between light- and heavy-duty vehicles. In 1986, about 4000 kt
were used by passenger cars and light trucks, with an estimate of
about 2300 kt for 1995, whereas in 1986 about 55300 kt were used by
heavy-duty trucks, with an estimate of 64300 kt for 1995 (US
Department of Energy, 1988). In Canada, only about 1% of passenger
cars are equipped with diesel engines. In 1992, 14126 kt of diesel
fuel were produced; 13508 kt were sold for domestic purposes (heating)
and about 10849 kt for on-road use (Thomas, personal communication,
1994).
The percentage of diesel-fuelled vehicles is increasing in Japan
(Table 9).
Table 7. Production and use of diesel fuel (including gas oils in
Europe) in different regions, and development over time
Region Production/ 1975 (kt) 1980 (kt) 1985 (kt)
Use
United States Production 134 967 138 323 135 181
Use 133 300 136 161 130 297
Canada Production 19 187
Use 19 130
OECD (all 24 Production 370 240 408 848 372 728
countries) Use 380 181 403 642 386 081
OECD (Europe) Production 173 474
Use 190 960
European Union Production 152 091
Use 163 132
Australia, Japan, Production 44 886
New Zealand Use 45 694
Adapted from International Agency for Research on Cancer (1989a);
OECD, Organisation for Economic Co-operation and Development
A3.2.2 Emissions during production and use
A3.2.2.1 Air
No data are available on emissions during the production and use
of diesel fuel. Release to the atmosphere during production in the
refining process is unlikely, as closed systems are used, but
volatilization may occur during storage and transport. Diesel fuel may
be released into the atmosphere as a result of spills during storage
and transport and at filling stations during bulk storage and vehicle
tank filling. The low-relative-molecular-mass constituents
(short-chain alkanes, benzene, toluene, ethyl benzene, and xylene
compounds) are the most likely to evaporate under environmental
conditions.
Table 8. Percentage of diesel passenger cars in western Europe, and
development over time
Country Diesel passenger cars (%)
1984 1988 1991 1992a
France 15.8 21.1 25.5 38
Germany (without former 16.9 15.1 15.3 14.9
German Democratic Republic) (1993)b
Germany (without former About 8 13.6 13
German Democratic Republic)c
Italy 18.7 11.9 7.4 NR
Spain (without station wagons) 15.3 10.5 14.6 NR
United Kingdom 1.1 4.5 11.3 12.5
United Kingdomd NR 5 9 19 (1993)
Adapted from American Automobile Manufacturers Association (1993),
unless otherwise stated; NR, not reported
a From Menne et al. (1994)
b With the former German Democratic Republic
c From German Institute for Scientific Research (1993)
d From Quality of Urban Air Review Group (1993)
Table 9. Percentage of diesel-fuelled vehicles in Japan and
development over time
Year Passenger cars (%) Trucks (%) Buses (%)
1984 3.8 23.7 49.5
1988 5.8 28.5 63.2
1991 8.3 40.7 81.7
Adapted from American Automobile Manufacturers Association (1993)
A3.2.2.2 Water
No data are available on effluents and emissions during diesel
fuel production. Diesel fuel oils may be released to surface waters as
a result of leakage from storage tanks or tankers (see section
A3.2.3). In the United States, the total volumes of spills of diesel
fuel oils in 1991 were (Agency for Toxic Substances and Disease
Registry, 1993): diesel fuel No. 1, 10.6 t (20 notations); diesel fuel
No. 2, 8.9 t (28 notations); and diesel fuel No. 4, 39.3 t (35
notations).
Groundwater can be contaminated with diesel fuel constituents by
leakage from underground bulk storage tanks, but quantitative data are
lacking. In the Province of New Brunswick, Canada (Thomas, personal
communication, 1993), of a total of 671 gasoline, diesel, and fuel oil
tanks examined in 1987, 11% leaked diesel or fuel oil; in 1989, 6% of
1085 tanks had leaks; and in 1991, 13% of 539 tanks leaked fuel. No
data were available about the amounts leaked, and diesel contamination
was determined on the basis of a cluster of 'middle-range peaks'
detected by gas chromatography.
On the basis of chronic petroleum inputs to sediments of
Narragansett Bay and Rhode Island Sound, United States, Van Vleet &
Quinn (1978) estimated that about 200 kt of petroleum hydrocarbons may
be released to surface waters worldwide from municipal treatment
plants. The precise source of the inputs cannot be verified in most
cases, but they are due, for example, to accidental discharge to sewer
systems, disposal of used crankcase and lubricating oils, oil washed
from roads, and atmospheric deposition of hydrocarbons.
No data were available from other countries.
A3.2.2.3 Soil
Diesel fuels may be released to soil as a result of accidental
spills (see section A3.2.3) and leakage from storage tanks or
pipelines. Diesel-contaminated soil is a major problem in railroad
yards, where diesel fuel is used in locomotives and as a solvent to
clean moving metal parts (the remaining paraffins give a waxy
anti-corrosive coat). Spillage during refuelling, engine maintenance,
and steam cleaning, leakage from fuel storage tanks, and absorption of
diesel fuel on sand used for traction are other possible sources of
soil contamination (Dineen, 1991); however, no quantitative data are
available.
A3.2.3 Accidental releases to the environment
Data on the accidental release of diesel fuels are summarized in
Table 10. The effects on the environment depend on both the amount and
environmental conditions.
Table 10. Diesel fuel spills and their effects on the environment (see also section A9.2)
Year Place Amount (t); type Effects Reference
of diesel fuela
Aquatic environment
1972 North of Puget Sound, > 600; diesel fuel Substantial mortality of some intertidal taxa; Woodin et al. (1972)
Washington State, USA No. 2 larval recruitment within six months
1973 East Lamma Channel 2000-3000; Almost total kill of meiofauna within four days; Wormald (1976);
near Hong Kong diesel fuel No. 4 heavy mortality among bivalves and molluscs, Stirling (1977)
Nerita albicilla and Monodonta labio, and in
marine fish farms; almost no effect on
Clypeomorus humilis or Planaxis sulcatus
1978 Svea, Mijenfjord, Norway 111 Most fuel trapped in ice; transport out of fjord Carstens &
during break-up; heavy mortality among shoreline Sendstad (1979)
invertebrates in some regions of fjord
1983 Yaquina Bay, Oregon, About 240 (with Decline in population of Rhepoxynius abronius Kemp et al. (1986)
USA Bunker C oil) by 75%; influence of spill not clear
1984 Queen Charlotte 130 (plus 30 t Low fuel levels in water during flood tide, high McLaren (1985)
Islands, Canada gasoline) levels during ebb as diesel was retained in
sediment; high mortality among barnacles
Table 10 (contd)
Year Place Amount (t); type Effects Reference
of diesel fuela
1987 Macquarie Island, 230; diesel fuel High mortality among one species of holothuroid, Pople et al. (1990)
Australia No. 4 one of isopod, one of limpet, and one of chiton;
decreased populations of crab, two species of
starfish, and gastropod; small number of dead
algae; slow recovery of organisms
1989 Arthur Harbor, 510; diesel fuel High mortality among limpets; partial recovery one Kennicutt et al.
Antarctica No. 1 year after spill; small effect on macroalgae (1991a,b,1992a,b)
Terrestrial environment
1983 San Bernadino County, 3 Hydrocarbon contamination up to 1500 mg/kg; Frankenberger et al.
CA, USA plume migrating towards surface water; in-situ (1989)
bioremediation (see also section A3.2.4)
NR Califonia, USA 193; diesel fuel Contamination at 6-34 m below surface; Peters et al. (1992)
No. 2 hydrocarbon levels at 18.3, about 1500 mg/kg;
remediation by flooding with surfactants
(see also section A3.2.4)
aWhen available
A4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
Few data are available on the environmental fate of diesel
fuels, but there are adequate data on the environmental behaviour of
individual hydrocarbon components. The transport, distribution, and
transformation of crude oils and some fuel oils (e.g. heating oils
No. 1 and 2) have been studied, and the mechanisms of distribution and
transformation are considered to be comparable to those of diesel
fuel.
The calculated half-lives for the toxicologically relevant PAH
components are listed in Table 11.
A4.1 Transport and distribution between media
Diesel fuels are released into the environment mainly during
storage, transport, and use (see section A3.2.3). The hydrosphere and
geosphere are the affected compartments.
A4.1.1 Evaporation from and dissolution in the aqueous phase
Oils and fuels spilled on water spread out almost immediately;
polar and low-relative-molecular-mass components dissolve and leach
out of the slick; and volatile components evaporate from the water
surface. With the start of microbial degradation the pattern of
substances changes, as was observed, for example, after a major oil
spill off the French coast (Atlas et al., 1981). The sum of these
processes is known as chemical and biological 'weathering'. At the
same time, the oil is emulsified to oil-in-water and water-in-oil
('mousse') emulsions (Atlas & Bartha, 1973). In laboratory experiments
with several diesel fuels, however, stable mousses were not formed at
any temperature (US National Research Council, 1985). Experiments
with South Louisiana crude oil showed that the evaporation rate was
more than twice the dissolution rate (Harrison et al., 1975). The loss
by evaporation of oil spread on water, which in oil spills amounts to
about 25% of the total released mass, is generally dependent on the
following factors (US National Research Council, 1985):
-- the exposed area, which increases with time as the film spreads;
-- the oil-phase vapour pressures, which decrease with time as the
low-relative-molecular-mass components evaporate. Components
with vapour pressures higher than that of n-octane evaporate
rapidly from the surface of spilled fuel oil, while those with
vapour pressures lower than that of n-octadecane persist and
form a viscous residue that retards the volatilization of other
constituents (Regnier & Scott, 1975);
-- the oil-air mass transfer coefficient, which depends on wind
speed and hydrocarbon diffusivity (for the diffusion coefficient
in air, see section A2.2, Table 5);
-- diffusion barriers, such as emulsions, or formation of a 'skin'
on the surface. Many surface waters have a thin layer of organic
material of natural origin on the surface, and these films may
reduce spread and volatilization, altering the persistence and
concentration of the oil in water (Edgerton et al., 1987).
Table 11. Calculated half-lives of polycyclic aromatic hydrocarbon
components in environmental compartments
Component Air Water Soil Sediment
Naphthalene 1 day 1 week 2 months 8 months
Acenaphthalene 2 days 3 weeks 8 months 2 years
Fluorene 2 days 3 weeks 8 months 2 years
Phenanthrene 2 days 3 weeks 8 months 2 years
Anthracene 2 days 3 weeks 8 months 2 years
Pyrene 1 week 2 months 2 years 6 years
Fluoranthene 1 week 2 months 2 years 6 years
Chrysene 1 week 2 months 2 years 6 years
Benz[a]anthracene 1 week 2 months 2 years 6 years
Benzo[a]fluoranthene 1 week 2 months 2 years 6 years
Benzo[a]pyrene 1 week 2 months 2 years 6 years
Perylene 1 week 2 months 2 years 6 years
Dibenz[a,h]anthracene 1 week 2 months 2 years 6 years
Adapted from Mackay et al. (1992)
On the basis of the constant of Henry's law (see section A2.2,
Table 5) and the classification of Thomas (1990), diesel fuels can be
considered to volatilize significantly from the aqueous phase. The
constant may change during volatilization, as the composition of the
mixture changes with time. Lockhart et al. (1987) observed a clear
decrease in the hydrocarbon composition of the 50% water-soluble
fraction of diesel fuel in open-aerated test cylinders. Within 48 h,
the concentration of hydrocarbons with a very low boiling-point
(< 115°C) decreased from 0.73 to 0.04 mg/litre and that of
hydrocarbons with a low boiling-point (115-270°C) from 3.2 to
0.17 mg/litre. Under sealed or open non-aerated conditions, there were
only minor changes. Regnier & Scott (1975) showed that n-decane
volatilizes from diesel fuel with a half-life of 1.65 h at 30°C,
whereas the half-life was 9.67 h at 5°C in a darkened chamber with a
constant wind speed of 21 km/h. Edgerton et al. (1987) reported that
diesel fuel spilled on ice had lost only 2-4% of its lightest fraction
after 10 days.
Dissolution of spilled oils and fuels in water is less important
from the viewpoint of mass loss than the ecotoxic effects of the
mixture. Lysyj & Russell (1974) conducted long-term experiments (42
days) on the dissolution of different fuel oils and gasoline in water.
After a period of stable concentration, during which physical
dissolution was probably the main mechanism for oil-to-water transfer,
the dissolution of organic compounds accelerated, probably because of
chemical modification by oxidation or microbial action of the
water-insoluble petroleum fraction.
Under equilibrium mass-transfer conditions, the levels of PAHs
(naphthalene and its methyl derivatives, acenaphthene, fluorene,
phenanthrene, anthracene, and fluoranthene) in the water phase in
contact with commercial automobile diesel fuel were about four to six
orders of magnitude lower than those in the diesel fuel itself, i.e.
in the low microgram per litre range. The concentrations of these
constituents were likely to be smaller under non-equilibrium
conditions but might be higher in the presence of surfactants,
emulsifiers, or co-solvents (Lee et al., 1992). When No. 2 fuel oil
and kerosene were placed in contact with drinking-water for 17 h,
although each fuel contained about 50% by weight of aliphatic
hydrocarbons, the water-soluble fractions contained primarily aromatic
compounds: total, > 93% by weight; proportion of benzene and
substituted derivatives, 19.4% by weight in No. 2 fuel oil and 53.2%
by weight in kerosene (Coleman et al., 1984). The chemical composition
of the water-soluble fractions of No. 2 fuel oil is compared with that
of the whole oil in Table 3.
During chemical weathering, other changes in composition (e.g.
autoxidation of n-alkanes) may occur that are not necessarily
associated with a net mass loss (Davis & Gibbs, 1975).
A4.1.2 Transport in and adsorption onto soil and sediment
A4.1.2.1 Soil
The movement of diesel fuel through soil is directly correlated
with its kinematic viscosity (see section A2.2, Table 5). As the
viscosity is about one-half that of water and about one-fourth to
one-fifth that of gasoline, the rate of percolation of water into soil
is about twice and that of gasoline about four to five times that of
diesel fuel (Stone, 1991). The retardation coefficient (Rd) is an
indicator of the migration of substances into groundwater. In the
aqueous phase, the maximal rate of movement of dissolved compounds is
that of groundwater, which is represented by an Rd of 1. Stone (1991)
calculated the Rd from the adsorption isotherms of individual diesel
constituents, and derived the following classification:
-- low mobility (Rd > 100): fluorene, phenanthrene, pyrene,
benzanthracene, benzo[ a]pyrene, fluoranthene;
-- medium mobility (100 > Rd > 10): naphthalene, dimethylbenzenes,
ethylbenzene, toluene;
-- high mobility (Rd < 10): benzene, quinoline, cresols, phenol.
In effect, soil contaminated with diesel fuel acts like a
chromatographic column, separating individual constituents by their
adsorption. Experimental data on the adsorption of diesel fuels on
soils and their transport are not available; however, the movement of
a synthetic kerosene through a clay-sand soil was dependent on the
moisture content. With increasing moisture content, the penetration
rate of nonvolatile components through the soil increased and the
adsorption of more volatile components decreased. In contrast, upward
mobility of the individual constituents (both volatile and
nonvolatile) of the fuel decreased with increasing moisture content.
In fully water-saturated soil, upward transport of kerosene was
completely inhibited (Acher et al., 1989). Desorption of a simulated
kerosene applied to three types of soil with the same moisture content
but different contents of organic matter was found to be complete
after 30 days under environmental conditions. The slowest desorption
was from the soil with the highest level of organic matter (Yaron et
al., 1989). Transport of kerosene through three types of sand was
influenced mainly by volatilization of C9-C13 hydrocarbon
constituents; the increase in the viscosity of the kerosene residue
was followed by a decrease in the infiltration rate (Galin et al.,
1990).
A4.1.2.2 Sediment
In marine environments, oils and fuels are generally delivered to
bottom sediments on settling particles. In areas with low
concentrations of suspended material (i.e. terrigenous minerals,
plankton, detrital particles, resuspended bottom sediments), the rates
of hydrocarbon sedimentation would be low (US National Research
Council, 1985).
No experimental data are available on diesel fuels in sediments.
In laboratory experiments with fuel oil, binding of the hydrocarbon
components to clay minerals of marine sediments was shown to be due to
physical adsorption of the van der Waals type. The compounds are
associated firmly because, once they are incorporated into sediments,
desorption to the overlying water is slow. Saturated hydrocarbon
constituents of fuel oils were transported slowly to the sediment
(Meyers & Quinn, 1973). In studies of a laboratory marine ecosystem to
which No. 2 fuel oil was added for 24 weeks, the concentrations in the
sediment remained low until 135 days after the start of the
experiment. Then, a steep increase was seen, leading to a level of 9%
by weight of the total fuel added (i.e. 12% by weight of the total
saturated hydrocarbons). The highest concentrations of saturated
hydrocarbons were found in the surface flocculent layer; 2-3 cm below
the sediment surface, the levels were below the detection limit. The
smaller particles (< 45 µm) of water-suspended material seemed to
adsorb about twice as much fuel oil as larger particles (> 45 µm)
(Wade & Quinn, 1980). In a comparable study in a model marine
ecosystem with No. 2 fuel oil, the particulate matter contained 40-50%
of the total amount of aliphatic hydrocarbons added and only 3-21% of
the aromatic fraction, indicating that most of the aromatic
hydrocarbons were dissolved in the water phase (see section A4.1.1)
(Gearing et al., 1980). Although biodegradation may remove many of the
soluble aromatic hydrocarbons (see section A4.2.2), 10-20% by weight
of the fuel oil, consisting primarily of branched alkanes,
cycloalkanes, and aromatics, may remain in the upper 2 cm of sediment
for over a year (Gearing et al., 1980; Oviatt et al., 1982).
A4.2 Transformation and removal
A4.2.1 Photooxidation
No data were available on the photooxidation of diesel fuel in
air or water. In the atmosphere, all evaporated oil components are
degraded photochemically by hydroxy radicals and other species within
hours or days to carbon monoxide, carbon dioxide, and oxygenated
compounds (US National Research Council, 1985; IPCS, 1986, 1993).
Under laboratory conditions, No. 2 fuel oil was rapidly photo-oxidized
in water. Two photooxidant pools were identified: hydrogen peroxide
and a mixture of indane and tetralin hydrogen peroxides, the first
being the faster acting (Herbes & Whitley, 1983). Peroxides are formed
by two mechanisms: the first is the reaction of free radicals with
triplet oxygen to produce peroxy radicals and hydroperoxides, which
continue the chain reaction; the second is addition of excited singlet
oxygen to reactive acceptors such as olefins. The photodegradation
products of fuel oils are phenols, naphthols, and carboxylic acids
(Larson et al., 1977, 1979).
A4.2.2 Biodegradation
A4.2.2.1 Microbial degradation
The individual constituents of spilled oil are inherently
degradable to varying degrees and at different rates. The n-alkane,
n-alkylaromatic, and simple aromatic molecules in the C10-C22
and the most readily degradable. Smaller molecules are generally range
are the least toxic rapidly metabolized, although they tend to be more
toxic. Long-chain n-alkanes are more slowly degraded because of
their hydrophobicity and also because they are viscous or solid at
ambient temperatures. Branched alkanes and cycloalkanes are relatively
resistant to attack. PAHs are the compounds most recalcitrant to
microbial degradation (Morgan & Watkinson, 1988).
A study of the breakdown of heating oils and diesel fuels in a
sub-soil demonstrated breakdown rates of 0.014-0.022 g/kg per day,
which were slower than the rates of topsoil degradation (Flowers et
al., 1984). The mineralization rates for heavy oils, sludges, and
crude oils were 0.02-0.6 gram of hydrocarbon per kilogram of soil per
day. Under Arctic conditions, the rates were considerably slower.
The relative contribution of bacteria and fungi to hydrocarbon
degradation is unclear. At acid pH, fungi are clearly more important,
but closer to neutrality hydrocarbon contamination tends to enhance
bacterial growth.
The overall rates of hydrocarbon degradation are limited by:
-- temperature (optimal temperature for biodegradation, 30-40°C);
-- water content (in soils, water contents of 50-80% capacity are
optimal for microbial activity);
-- oxygen (the metabolism of both aliphatic and aromatic
hydro-carbons normally requires oxygen);
-- pH (hydrocarbons are mineralized most rapidly at 6.5-8.0);
-- inorganic nutrients (as petroleum contaminants are extremely
deficient in nitrogen and phosphorus, a large quantity of carbon
sources tends to result in rapid depletion of the available pools
of major nutrients, i.e. enhancement of degradation in fertilized
soils);
-- microbial metabolic versatility (topsoils generally contain many
hydrogen-degrading bacteria, typically 105 - 106 per gram, but the
content of subsoils is unclear) (Morgan & Watkinson, 1988).
A remedial treatment consisting of liming, fertilization, and
tilling was evaluated on a laboratory scale for its effectiveness in
cleaning up a sand, a loam, and a clay-loam soil contaminated at
50-135 mg/g of soil by diesel and other oils. The disappearance of
hydrocarbons was maximal at 27°C (Song et al., 1990).
In sandy soils, 50-85% of the hydrocarbons were degraded within a
few weeks, depending on the experimental conditions. Degradation
efficiency increased with additional soil inoculation (Grundmann &
Rehm, 1991).
Frehland et al. (1992) examined the substrate specificity and
growth conditions of nine bacterial strains on samples of
diesel-contaminated soil under different conditions. The
biodegradative properties of Pseudomonas spp. were superior (59, 60,
and 80% in three samples) than those of Micrococcus, Bacillus,
Acinetobacter, and other species tested.
A4.2.2.2 Phytoplankton and marine algae
Unicellular algae can take up and metabolize both aliphatic and
aromatic hydrocarbons, but the extent to which this occurs in nature
is poorly understood. The ability to metabolize naphthalene is
widespread (US National Research Council, 1985).
A4.2.2.3 Invertebrates and vertebrates
Unlike microorganisms, which use petroleum as a source of carbon,
animals generally oxidize and conjugate products to render them more
soluble and therefore easier to excrete. All animal groups tested can
take up petroleum hydrocarbons, either through the body surface,
across respiratory surfaces, or via the gut, the route varying with
the organism and its feeding habits. In copepods (Calanus
helgolandicus), dietary uptake was more important than that from
water (Corner et al., 1976), but aromatic hydrocarbons accumulated by
the polychaete Neanthes arenaceodentata were derived from water and
not from sediment (Rossi, 1977). Hydrocarbons are stored in lipid-rich
tissues. The principal route of metabolism of hydrocarbons by
metazoans is conversion of lipophilic compounds by cytochrome
P450-dependent monooxygenases or mixed-function oxidases to
derivatives that are more water-soluble. Mixed-function oxygenase
activity has been found in all fish species studied. Lee (1981)
reported 18 marine invertebrate species belonging to four phyla
(Annelida, Arthropoda, Echinodermata, and Mollusca) that are known to
contain mixed-function oxidase activity in the hepatopancreas,
digestive gland, and other tissues. Sea birds and some other waterfowl
also have cytochrome P450 systems, but few estimates have been made of
their capacity for hydrocarbon metabolism. Some crude oils, PAHs, and
refined petroleum products are known to induce cytochrome P450 enzymes
and to increase the levels of hydrocarbon metabolism in marine and
freshwater fish, including embryonic and larval forms and polychaetes
(US National Research Council, 1985). Induction is usually described
in terms of the rate of metabolism of benzo[a]pyrene in vitro.
A4.2.3 Bioaccumulation
Few data are available on the bioaccumulation of diesel fuel
itself, although there is adequate evidence from studies on other oils
that aquatic organisms bioconcentrate hydrocarbons. The
n-octanol-water partition coefficient (log Pow) for diesel fuel is
3.3-7.1 (see section A2.2, Table 5). Although a higher bioaccumulation
potential might be expected from these log Pow values, the measured
bioconcentration factors are lower than predicted because many
compounds of low relative molecular mass, such as substituted
benzenes, are readily metabolized, and the actual bioaccumulation of
compounds of higher relative molecular mass is limited by their low
water solubility and large molecular size.
In a continuous-flow system, diesel fuel was taken up by
Mytilus edulis mussels exposed for 41 days to a concentration of
200-400 µg/litre. The hydrocarbon levels in tissue were about 1000
times higher after exposure than before. Depuration was rapid during
the first 15-20 days and then decreased rapidly to a minimum (Fossato
& Canzonier, 1976).
The accumulation of No. 2 fuel oil has been studied in a number
of organisms (Lee, 1977). When No. 2 fuel oil (38% aromatics) was
added to a commercial shrimp pond, the concentration of naphthalenes
in shrimps, clams, and oysters exceeded the level in ambient water
after 38 days. Depuration in clean water was complete after 10 days
for shrimps and after 47-96 days for oysters (Cox et al., 1975). In a
flow-through system to study accumulation of a No. 2 fuel oil-water
dispersion, aromatic petroleum hydrocarbons were accumulated at a rate
of 89.6 mg/kg tissue by Rangia cuneata (clams) and 311.7 mg/kg by
Crassostrea virginica (oysters) during 8 h of exposure. The
bioaccumulation factor for methyl naphthalenes in clams was 2.3-26.7
and increased with increasing alkylation of the naphthalene ring.
Depuration in clean water was complete after 28 days (Neff et al.,
1976a). The fuel components of a small spill of No. 2 fuel oil had the
following biological half-lives in mussels (Mytilus edulis): aliphatic
hydrocarbons (C16 and C23), 0.2 and 0.8 days; alkyl naphthalenes
(C2 and C3), 0.9 and 1.5 days; phenanthrene, 2.1 days (Farrington
et al., 1982). Lobsters exposed to a simulated small spill of No. 2.
fuel oil bioconcentrated PAH constituents in the hepato-pancreas and
muscle within three to four days after exposure. The levels remained
elevated for up to 10-11 days, and depuration was complete after 20-21
days.
The polychaetous annelid Neanthes arenaceodentata rapidly
accumulated 14C-naphthalene (to a biomagnification of 40 times) from
solution during exposure for 24 h and slowly released the accumulated
hydrocarbons within 300 h after return to clean sea water (Rossi,
1977).
Oral administration of South Louisiana crude oil to mallard ducks
(Anas platyrhynchus) at a dose of 5 ml daily led to detectable
aromatic petroleum hydrocarbon levels in each of the tissues examined:
liver, breast muscle, heart muscle, skin, brain, uropygial gland, and
blood. The skin and the underlying adipose tissue had accumulated far
more aromatic hydrocarbons than other tissues. The individual
components did not accumulate in the same relative concentrations as
in the crude oil, suggesting different uptake and/or metabolism; two-
and three-membered, condensed ring aromatic compounds were accumulated
to a greater extent than alkylbenzenes (Lawler et al., 1978).
A4.2.4 Tainting
Tainting (unpleasant off-flavours) of various aquatic organisms
by petroleum hydrocarbons has been reported, and diesel fuel has been
suspected of tainting fish in freshwater rivers. Mackie et al. (1972)
reported tainted rainbow trout up to at least nine days after a spill
of diesel fuel into water (Six Mile Water, Ireland). Ackman & Noble
(1973) described tainting of whitefish in the Athabaska River, Canada,
which was attributed to diesel fuel from a railroad yard.
A4.2.5 Entry into the food chain
No data are available on the effect of diesel fuel on the food
chain. The effects of petroleum compounds on the marine food web have
been studied, e.g. on zooplankton Calanus helgolandicus (Corner et
al., 1976), on phytoplankton (Mahoney & Haskin, 1980), and on
freshwater crayfish, one of the primary foods of waterfowl (Tarshis,
1981). In a study in situ on the distribution, biotransformation, and
flux of PAHs in the aquatic food chain (seston --> mussel [ Mytilus
edulis] --> eider duck [ Somateria molissima]), the PAH composition
changed significantly (Broman et al., 1990). The theoretical
inhalation of atmospheric PAHs was insignificant in comparison with
exposure from food. PAHs were biotransformed relatively rapidly. Their
concentrations did not increase with increasing trophic level.
A4.3 Ultimate fate after use
A4.3.1 Use in motor vehicles
Diesel fuel is combusted in motor vehicles and stationary engines
(see section A3.2.1.2). The resulting exhaust is discussed in Part B.
A4.3.2 Spills
The fate of diesel fuel after accidental spills is eventual
degradation by abiotic and biotic processes (see section A3.2.3)
A4.3.3 Disposal
In general, incineration is recommended for fuel oils (Fraser
Williams (Scientific Systems) Ltd, 1985). This procedure is also
useful for disposing of fuel production wastes.
Because diesel fuel is released during use, mainly accidentally
into water or onto soil (see sections A3.2.2.2, A3.2.2.3, and A3.2.3),
the affected compartments may have to be remediated. In general, oil
spills on beaches and into surface waters can be treated by burning
off; absorption onto straw, polyurethane foam, activated carbon, or
peat; or addition of sinking agents, gelling agents, or dispersants.
Mechanical systems can also be used (Fraser Williams (Scientific
Systems) Ltd, 1985). Various operations for treating soil affected by
diesel fuel have been reviewed (Dineen, 1991) and are as follows:
-- Disposal: excavation of contaminated soil and disposal at a
regulated landfill; the treatment used most commonly during the
last decade; advantageous for small volumes.
-- Biodegradation: The natural process of soil microorganisms,
which is stopped by a spill as a result of depletion of oxygen or
nutrients (mostly nitrogen and phosphorus), is restored by
providing sufficient amounts of the depleted substances. The
process can be carried out in situ (Frankenberger et al., 1989)
(see section A3.2.3, Table 10) or after excavation.
Biodegradation is the most widely applicable alternative to
landfill disposal, although its duration is uncertain and may be
relatively long and a large space is required (see sections
A9.1.1.2 and A9.1.3.1).
-- Thermal treatment: incineration of contaminated soil e.g. in
cement kilns or in specially designed thermal units, where the
soil is baked to remove the fuel, which is subsequently oxidized
(thermal desorption). The thermal desorption process is also
feasible in situ. In cement kilns, the desorbed diesel fuel is
used for heating the kiln, and the soil is incorporated into the
cement mixture.
-- Road base: The contaminated soil is spread on roads under
construction and is compacted and oiled before paving. If the
affected soil has a high proportion of expandable clays, it may
not be suitable as a road base.
-- Asphalt batching: The contaminated soil replaces part of the
sand and gravel component of asphalt; this is possible only if
the content of expandable clays is not too high.
-- Chemical oxidation: A strong oxidant, usually hydrogen
peroxide, in combination with a silica polymer stabilizer to
control the reaction is used to oxidize diesel hydrocarbons to
carbon dioxide and water. The reaction is highly exothermic, and
uncontrolled volatilization and leaching of some constituents may
occur.
-- Fixation: addition of a strong base to convert diesel
hydrocarbons to organic acids and subsequent treatment with a
dissolved silica polymer to effectively encapsulate the acids in
amorphous silica; immobilizes diesel fuel in situ and prevents
migration into surface or groundwater. The long-term stability of
the immobilized chemicals is, however, unknown.
-- Soil washing: Diesel fuel is washed out of soil by a
biodegradable, non-toxic surfactant (Peters et al., 1992). The
operation is feasible in situ and after excavation and is
particularly effective on materials with a low surface:volume
ratio (e.g. gravels and coarse sands). The major disadvantage is
the need to collect and treat or dispose of the
surfactant-diesel mixture after washing.
-- Containment: construction of a low-permeability surface
structure ('cap') that prevents infiltration of rain, snow, and
other moisture that could lead to leaching of diesel constituents
into groundwater. Long-term monitoring of the area of the spill
is necessary.
A5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
A5.1 Environmental levels
As diesel fuels are complex mixtures of a great variety of
hydrocarbons (see section A2.1), general 'environmental levels' cannot
be described. The individual constituents of diesel fuels should be
detectable in almost all compartments of the environment, but the
sources cannot be verified.
A5.2 Exposure of the general population
Nonoccupational exposure to diesel fuel occurs when fuel tanks
are filled manually. The primary source of dermal exposure is
accidental spills, although these exposures to high levels are of
short duration. Drinking-water can be contaminated by components of
petroleum products, including diesel fuel, after leakage into
groundwater from underground storage tanks. Specific data are not
available on the contribution of diesel fuel components to groundwater
contamination. Owing to the low volatility of diesel fuels at normal
temperatures, there is little exposure to vapours (International
Agency for Research on Cancer, 1989a).
A5.3 Occupational exposure during manufacture, formulation, or use
Workers are exposed to diesel fuel in a number of occupations,
including manual handling and discharge of fuels; loading and
unloading of diesel fuel; retailing at filling stations; manufacture,
repair, maintenance, and testing of diesel engines and other
equipment; use of diesel fuel as a cleaning agent or solvent; and
laboratory handling and routine sampling of diesel fuel (CONCAWE,
1985).
At normal temperatures, low concentrations of vapours are likely
to be generated from diesel fuels, owing to their low volatility. Only
in confined spaces or at high operating temperatures do significant
levels of vapour occur. Hydrogen sulfide gas may evolve from residual
fuel oils (CONCAWE, 1985).
A6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
No quantitative data are available; however, the systemic and
local effects observed after exposure to diesel fuels by various
routes indicate that they are absorbed dermally, orally, and by
inhalation.
A7. EFFECTS ON LABORATORY MAMMALS AND IN-VITRO TEST SYSTEMS
A7.1 Single exposure
Diesel fuels have a low order of acute toxicity after
administration orally, dermally, or by inhalation. Acute LD50 Table
12. In rats and mice, the values after oral or dermal exposure were
values are summarized in generally > 5000 mg/kg body weight, and the
values in rabbits after dermal exposure were > 2000 mg/kg body
weight. Since the physicochemical properties of kerosenes are similar
to those of diesel fuels (see also section A2.1), the LD50 values
for various types of kerosene are included.
Beck et al. (1984) reported an oral LD50 value of 7500 mg/kg
body weight (9 ml/kg body weight) for a market-place sample of diesel
fuel in male and female rats. Gross necropsy of animals that died
during the test showed haemorrhagic gastroenteritis, gastrointestinal
tympani, and pneumonia with abscess formation. No deaths were seen
among rabbits treated dermally with 5000 mg/kg body weight under an
occlusive covering for 24 h.
After oral administration of 12 000 mg/kg body weight kerosene to
rats, no change was seen in heart weight or in the relative weights of
lung, spleen, and kidney. There were no histopathological changes
(Muralidhara et al., 1982). Exposure of rats for 8 h by inhalation to
about 0.1 mg/litre deodorized kerosene did not induce adverse effects.
Four male cats that inhaled 6.4 mg/litre for 6 h showed no toxic
effects on the central nervous system or body weight during the
exposure or during a subsequent 14-day observation period (Carpenter
et al., 1976).
Male Sprague-Dawley rats given JP-5 jet fuel at a dose of
18 912 mg/kg body weight (24 ml/kg body weight) orally had
vacuolization of periportal hepatocytes and serum enzyme alterations,
indicating hepatic damage, within two days (Parker et al., 1981). All
male and female B6C3F1 mice treated dermally with 5000-40000 mg/kg
body weight marine diesel fuel survived a 14-day observation period
(US National Toxicology Program, 1986).
Table 12. Acute toxicity (LD50 and LC50 values) of diesel and other fuels
Fuel Species Route LD50 or Dose Reference
LC50
Diesel fuels
Diesel fuel (market-place sample) Rat Oral LD50 7500 mg/kg bw Beck et al. (1984)
Diesel fuel (market-place sample) Rabbit Dermal LD50 > 5000 mg/kg bw Beck et al. (1984)
Home heating oil No. 2a Rat Oral LD50 14 500-21 100 µg/kg bw American Petroleum
Institute (1980a,b,c)
Home heating oil No. 2a Rabbit Dermal LD50 > 5000 µg/kg bw American Petroleum
Institute (1980a,b,c)
Marine diesel fuel, JP-5, JP-8 Mouse Oral LD50 > 16 000 mg/kg bw Schultz et al. (1981)
shale, or petroleum oila
Marine diesel fuel, shale, or Mouse Dermal LD50 > 16 000 mg/kg bw Schultz et al. (1981)
petroleum oila
Other fuels
Straight-run middle distillateb Rat Oral LD50 > 5000 mg/kg bw American Petroleum
Institute (1985a)
Hydrodesulfurized middle distillateb Rat Oral LD50 > 5000 mg/kg bw American Petroleum
Institute (1982a,b)
Straight-run middle distillateb Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum
Institute (1985a)
Hydrodesulfurized middle distillateb Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum
Institute (1982a,b)
Straight-run middle distillateb Rat Inhalation LC50 1.8 mg/litre American Petroleum
Institute (1987a)
Table 12 (contd)
Fuel Species Route LD50 or Dose Reference
LC50
Hydrodesulfurized middle distillateb Rat Inhalation LC50 4.6 mg/litre American Petroleum
Institute (1983a)
Light catalytically cracked distillatec Rat Oral LD50 4660 mg/kg bw (m) American Petroleum
3200 mg/kg bw (f) Institute (1985b)
Light catalytically cracked distillatec Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum
Institute (1985b)
Light catalytically cracked distillatec Rat Inhalation LC50 4.7-5.4 mg/litre American Petroleum
Institute (1986a,b)
Jet fuel Aa Rat Oral LD50 > 25 000 µl/kg bw American Petroleum
Institute (1980d)
JP-5 shale oild Mouse Dermal LD50 8000 mg/kg bw Schultz et al. (1981)
JP-5 petroleum oild Mouse Dermal LD50 11 200 mg/kg bw Schultz et al. (1981)
JP-8 shale oila Mouse Dermal LD50 6400 mg/kg bw Schultz et al. (1981)
JP-8 petroleum oila Mouse Dermal LD50 8000 mg/kg bw Schultz et al. (1981)
Jet fuel Aa Rabbit Dermal LD50 > 5000 µl/kg bw American Petroleum
Institute (1980d)
Kerosenea Rat Oral LD50 50 000 mg/kg bw Parker et al. (1981)
Kerosenea Guinea-pig Oral LD50 16 320 mg/kg bw Deichmann et al. (1944)
Kerosenea Rabbit Oral LD50 22 720 mg/kg bw Deichmann et al. (1944)
Straight-run kerosenea Rat Oral LD50 > 5000 mg/kg bw American Petroleum
Institute (1985c)
Hydrodesulfurized kerosenea Rat Oral LD50 > 5000 mg/kg bw American Petroleum
Institute (1982b)
Table 12 (contd)
Fuel Species Route LD50 or Dose Reference
LC50
Straight-run kerosenea Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum
Institute (1985c)
Hydrodesulfurized kerosenea Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum
Institute (1982c)
Petroleum-derived hydrocarbona Rat Inhalation LC50 > 5.3 mg/litre American Petroleum
Institute (1987b)
Petroleum-derived hydrocarbona Rat Inhalation LC50 > 5.2 mg/litre American Petroleum
Institute (1983c)
Deodorized kerosenee Rat Inhalation LC50 > 0.1 mg/litre Carpenter et al. (1976)
(saturation)
a Hydrocarbon fraction similar to that of diesel fuel (see section A2.1)
b Hydrocarbon fractions from which also diesel fuels are gained during petroleum separation (see section A3.2.1.1)
c Blending component of diesel fuel
d Narrow boiling range
e Used as a solvent, not a fuel; very low aromaticity
Exposure of Sprague-Dawley rats to an aerosol of diesel fuel at a
concentration × time product of 8 mg.h/litre caused less than 1%
mortality and was estimated to represent the maximal tolerated
exposure. On this basis, 12 mg.h/litre was chosen as the highest
concentration in a study of repeated exposure (see section A7.2).
After exposure to 0.5 mg/litre for 2 h, a transient depression of the
startle reflex was observed. Further findings were a dose-related
decrease in respiratory frequency and influx of polymorphonuclear
cells into the lungs for several days. In a 6-h inhalation test, the
no-observed-adverse-effect level (NOAEL) was 2.7 mg/litre (Dalbey et
al., 1982, 1987).
A7.2 Short-term exposure
A7.2.1 Subacute exposure
A7.2.1.1 Dermal exposure
Dermal exposure to 0.1 ml/kg body weight per day kerosene for one
week was not lethal to male mice. Significant decreases in the
relative weights of thymus, spleen, adrenals, and abdominal lymph
nodes were observed (Upreti et al., 1989).
Eight rabbits (weighing 2.5-3.5 kg) were exposed dermally
(occlusive covering, 24 h/day, five days per week, two weeks) to 4 or
8 ml/kg body weight per day of a market-place sample of diesel fuel.
None of the animals given the low dose died, although there was a
weight loss of 0.3 kg, while five animals given the high dose died
with a weight loss of 0.5 kg; the control group had a weight gain of
0.2 kg. Severe chronic dermal irritation and anorexia were seen, which
were followed by cachexia and death (Beck et al., 1984).
Three doses between 1 and 10 ml/kg body weight per day of 10, 30,
or 50% fuel oil No. 2 were applied to the skin of New Zealand white
rabbits. After a 12-day treatment including a two-day rest, acute
dermal corrosion was seen in all animals treated with the 10% oil and
in animals given 10 ml/kg body weight per day of the 30 or 50% oil.
There was histopathological evidence of dermal toxicity in all treated
groups (American Petroleum Institute, 1980a,b,c).
Application of 8000 µl/kg body weight per day of jet fuel A to
four male and four female New Zealand white rabbits for 12 days,
including a two-day rest, induced acute dermal corrosion.
Histopathological evidence of dermal and hepatic toxicity and
hyperplastic changes in the urinary bladder transitional epithelium
were seen (American Petroleum Institute, 1980d).
Groups of five male and five female New Zealand white rabbits
were treated with 200, 1000, or 2000 mg/kg body weight per day of a
straight-run distillate, a light catalytically cracked distillate, or
two hydrodesulfurized distillates, three times per week for four
weeks. Moderate to severe irritation was seen, the degree of skin
irritation being directly related to the number of doses applied.
Microscopic examination of the skin at the application sites revealed
the presence of acanthosis and hyperkeratosis (American Petroleum
Institute, 1983a, 1984, 1985a,b).
In a study of marine diesel fuel containing 12.7% paraffins,
43.7% naphthalenes, and 43.6% aromatic compounds, groups of male and
female B6C3F1 mice received dermal applications (with an occlusive
covering) of 2000, 8000, 20000, or 40000 mg/kg body weight per day for
14 consecutive days. None of the animals at 20000 or 40000 mg/kg body
weight per day survived. Skin lesions were observed in all treated
groups, which consisted of moderate acanthosis, parakeratosis, and
hyperkeratosis. These findings were accompanied by a mixed cellular
inflammatory infiltrate in the upper dermis. The NOAEL was 8000 mg/kg
body weight per day. In the same study, JP-5 navy fuel containing
52.8% cycloparaffins, 30.8% paraffins, 15.9% aromatics, and 0.5%
olefins (see also Table 2) was applied at doses of 5000-40000 mg/kg
body weight per day for 14 days. All animals at 40000 mg/kg body
weight per day and females at 30000 mg/kg body weight per day group
died before the end of the study. Body weight loss was observed at
doses > 10 000 mg/kg body weight per day. The dermal findings were
similar to those in the study of marine diesel fuel. The NOAEL was
5000 mg/kg body weight per day (US National Toxicology Program, 1986).
A7.2.1.2 Inhalation
Rats (strain, age, and sex not specified) were exposed for
6 h/day to a droplet aerosol of deodorized kerosene at a mean
concentration of 7.7 mg/litre for four days. After a day with no
treatment, the skin of the extremities was dry and flakes had formed.
The body weight remained unchanged (Carpenter et al., 1976).
CD-1 mice were exposed for 8 h/day for five days to uncombusted
diesel vapour at concentrations of 0.065, 0.135, or 0.204 mg/litre.
The dose-response for neurotoxicity (measured by square-box activity)
was 50% of the control level at the high dose, 100% at the medium
dose, and 150% at the low dose. A drastic deterioration of motor
coordination was seen at the high dose in the rotarod test. In the hot
plate test, increased sensitivity followed by tolerance was seen at
the high dose, a slight increase at the medium dose, and a substantial
increase at the low dose; normalization occurred in all groups within
24 h. No effects were seen in the inclined plane test or the corneal
reflex test. Vasodilatation, poor grooming, and tremors were
described. In general, the most obvious effects were on the nervous
system, diesel fuel acting as a neurodepressant (Kainz & White, 1982,
1984).
Dalbey et al. (1982, 1987) investigated the toxic effects of
diesel fuel aerosols to assess the health risks of their military use
as smoke screens. Groups of male and female Sprague-Dawley rats were
exposed to concentrations of 1.3-6 mg/litre for 2 or 6 h, one or three
times per week, for a total of nine exposures; 12 mg.h/litre was
chosen as the highest concentration-time product that caused 6.25%
mortality. A significant depression of body weight and a slower growth
rate were seen initially, and liver weights were significantly
decreased. No neurotoxicity was seen. Histologically, there was focal
accumulation of free pulmonary cells and increased numbers of
leukocytes in bronchial lavage fluid. In pulmonary function tests, a
non-dose-dependent change in lung volume was seen, involving a
decrease in total and vital capacity and increases in functional
residual capacity and residual volume. No other organs were affected.
Groups of 20 male and 20 female Sprague-Dawley rats exposed by
inhalation to 0.025 mg/litre of one of three hydrodesulfurized middle
distillates for 6 h/day on five days per week for four weeks showed no
treatment-related changes. Mild subacute inflammatory changes were
observed in the nasal respiratory mucosa of the animals in one group
that had been exposed to distillate API 81-09 (American Petroleum
Institute, 1986c).
A7.2.2 Subchronic exposure
A7.2.2.1 Dermal exposure
Groups of 10 male and 10 female B6C3F1 mice received dermal
applications under an occlusive covering of 250 or 4000 mg/kg body
weight per day marine diesel fuel or 500-8000 mg/kg body weight per
day JP-5 navy fuel for five days per week for 13 weeks. The marine
diesel fuel caused no treatment-related deaths. Males had reduced body
weight gain; mild chronic active dermatitis at the site of application
was observed at the highest dose. At 1000 mg/kg body weight per day,
all animals survived and had weight gains similar to those of the
controls. Exposure to JP-5 navy fuel killed five males at the
high-dose group and caused dermatosis, splenic extramedullary
haematopoiesis, and liver karyomegaly in all groups (US National
Toxicology Program, 1986).
A7.2.2.2 Inhalation
The results of studies of subchronic inhalation of various
distillate fuels are summarized in Table 13.
Table 13. Studies of subchronic exposure to distillate fuels by inhalation
Fuel Species Exposure (high dose) Results Reference
Diesel fuels
Diesel fuel Rat 4 h/d, 2 d/week, 13 weeks + Reversible loss of body weight; Lock et al. (1984)
8 weeks' recovery (1.5 mg/litre) no other apparent effect
Marine diesel fuela Mouse, rat 90 d, continuous (0.05 and Nephrotoxic effects specific to Bruner (1984)
0.3 mg/litre) male rats
Other fuels
JP-8 jet fuelb Mouse, rat 24 h/d, 7 d/week,90 d + 24 Nephrotoxic effects specific to Mattie et al. (1991)
months' recovery (1 mg/litre) male rats
JP-5 jet fuelb Rat, dog 24 h/d, 7 d/week,90 d Nephrotoxic effects specific to Gaworski et al. (1984)
(0.75 mg/litre) male rats
JP-4 jet fuelb Mouse, rat 6 h/d, 5 d/week,12 months Nephrotoxic effects specific to Bruner et al. (1993)
(5 mg/litre) male rats; increased incidence
of hepatocellular adenomas in
female mice
Deodorized Rat, dog 6 h/d, 5 d/week,13 weeks No apparent effects Carpenter et al. (1976)
kerosenec (0.1 mg/litre)
a Hydrocarbon fraction similar to that of diesel fuel
b Narrow boiling range
c Not a fuel; very low aromaticity
Groups of 25 male rats and four male dogs were exposed to
deodorized kerosene at concentrations up to 0.1 mg/litre,
approximately the saturation limit at 25°C, for 6 h/day on five days
per week for about 13 weeks. Although dose-related changes were
observed in survival, body weight gain, organ weights, and
haematological and clinical chemical parameters, none of the findings
was statistically significantly different from those in controls. No
pathological change was seen in any of the organs examined (Carpenter
et al., 1976).
Groups of 12 male and 12 female Sprague-Dawley rats were exposed
in whole-body chambers for 4 h/day on two days per week for 13 weeks
to 0.25, 0.75, or 1.5 mg/litre aerosolized diesel fuel, followed by an
eight-week recovery period. There were no deaths. All treated animals
lost weight, indicating slight toxicity, during the first four weeks
of exposure, but the effect was reversed during the recovery period in
most cases. A slight depression of the startle reflex was seen at the
start of the study, and the number of macrophages in bronchial lavage
fluid was slightly elevated in all treated animals immediately after
cessation of exposure. Further tests of pulmonary function, gas
exchange, and dynamic lung function did not reveal any significant,
dose-related change. Overall, no significant cumulative toxicity was
seen (Lock et al., 1984).
A specific effect of diesel fuel in male rats, the hyaline
droplet nephropathy syndrome, was seen in several studies. Gaworski et
al. (1984) studied the effects of a 90-day exposure to 0.15 or
0.75 mg/litre JP-5 jet fuel derived from either petroleum or shale oil
for 24 h/day, in groups of three male and three female beagle dogs, 75
male and 75 female Fischer 344 rats, and 111-150 female C57Bl/6 mice.
The toxicity of the two types of fuel was not significantly different.
The only substantial effect at both concentrations was a renal tubular
lesion in male rats, probably caused by hyaline droplet accumulation
and unique to male rats. Other signs of toxicity were mild liver-cell
changes and mild nasal inflammation in rats. Cowan & Jenkins (1980)
studied petroleum and shale-oil marine diesel fuel using an identical
study design. Reduced body weight gain and hyaline droplet nephropathy
were reported in male rats. In another study, groups of 95 male and 75
female Fischer 344 rats and 100 male and 100 female C57Bl/6 mice were
exposed for 24 h/day on seven days per week to JP-8 jet fuel at
concentrations up to 1 mg/litre for 90 days, and then held for 20-21
months in order to assess the long-term consequences of exposure. The
main finding was accumulation of hyaline droplets in the kidneys of
male rats (Mattie et al., 1991). In a 90-day study, groups of 75 male
and 75 female Fischer 344 rats were exposed continuously to 0.05 or
0.3 mg/litre of marine diesel fuel. The main finding was again hyaline
droplet nephropathy in males at both levels (Bruner, 1984). In a study
of the carcinogenicity of JP-4 jet fuel vapour, hyaline droplet
nephropathy was observed in groups of 100 male Fischer 344 rats
exposed for 6 h/day, five days per week for 12 months to
concentrations up to 5 mg/litre (Bruner et al., 1993) (see also
section A7.7).
The hyaline droplet nephropathy syndrome is not considered to be
relevant for humans. It is linked to an inherent peculiarity of renal
protein. The histopathological sequence is: accumulation in the renal
proximal tubules of an excessive amount of hyaline droplets containing
alpha2-microglobulin, a special protein of male rats which is
synthesized in the liver; cytotoxicity and single-cell necrosis of the
tubular epithelium; sustained regenerative tubule-cell proliferation;
development of intraluminar granular casts from sloughed cell debris;
tubular dilatation and papillary mineralization; foci of tubule
hyperplasia; and renal tubule tumours (US Environmental Protection
Agency, 1991). Mechanistically, a globulin-substance complex that is
resistant to hydrolytic degradation is responsible for the protein
overload in kidneys.
A7.3 Long-term exposure
A7.3.1 Dermal exposure
Groups of 50 male and 50 female B6C3F1 mice received dermal
administrations of 250 or 500 mg/kg body weight per day marine diesel
fuel or JP-5 navy fuel on the clipped dorsal interscapular region on
five days per week for 103 weeks. (The doses were derived from studies
reported in section A7.2.) The high dose of marine diesel fuel caused
a dose- and time-dependent reduction in mean body weight in animals of
each sex, by up to 23% after week 40 in males and up to 20% after week
72 in females. Survival of treated females was decreased, and exposure
to the high dose was stopped at week 84 owing to severe ulceration.
Application of 500 mg/kg body weight per day JP-5 navy fuel resulted
in a time-dependent reduction in mean body weight in animals of each
sex: by up to 22% after week 76 in males and up to 25% after week 60
in females. Treatment of females with the high dose had to be
terminated at week 90. Overall, JP-5 navy fuel caused a lesser chronic
inflammatory response than marine diesel fuel (US National Toxicology
Program, 1986).
A7.3.2 Inhalation
Groups of 100 male and 100 female Fischer 344 rats and C57Bl/6
mice were exposed to JP-4 jet fuel vapour for 6 h/day on five days per
week for 12 months at concentrations of 1 or 5 mg/litre (see section
A7.7). The sex-specific alpha2-microglobulin nephropathy syndrome was
observed in 21% of male controls and in 20% of males at the low dose,
and 77% at the high dose (see also section A7.2). No significant,
dose-related alteration was seen in clinical findings, mortality,
haematological parameters, or clinical chemistry. All treated male
rats had a significant reduction in mean body weight. At the high
dose, male rats had significantly increased relative liver and kidney
weights and females had a significant decrease in relative spleen
weight. These alterations were not significant in comparison with
absolute organ weights (Bruner et al., 1993).
A7.4 Dermal and ocular irritation; dermal sensitization
A7.4.1 Dermal irritation
The results of studies of dermal irritation (Table 14) must be
interpreted critically, as different protocols were used, e.g. in
Europe and the United States. The main difference is in exposure time:
24 h in the American protocols and 4 h in those of the European Union
and the Organisation for Economic Co-operation and Development, which
may pose a problem when only mild irritation is observed, leading to a
classification of 'non-irritant' according to protocols of the latter
organizations.
A market-place sample of diesel fuel, tested at a dose of 0.5 ml
for 24 h in rabbits, was assessed as 'extremely irritating',
corresponding to a Draize score of 6.81 (Beck et al., 1984).
Topical applications three times a week to mice of various types
of kerosene and gas oil with boiling ranges similar to that of diesel
fuel produced degenerative changes in the skin surface, including
necrosis and hyperplasia (CONCAWE, 1991).
Four types of American military fuels were investigated:
petroleum JP-5 fuel, shale JP-5 fuel, petroleum marine diesel fuel,
and shale marine diesel fuel. None was active in the Draize test, in
which six female New Zealand white rabbits received 0.5 ml of
undiluted fuel on intact and abraded skin under an occlusive covering
for 24 h (Cowan & Jenkins, 1980). Applications to rabbit skin of
0.5 ml of various shale oil- and petroleum-derived fuels under
occlusive dressings for 4 h were not irritating (Schultz et al.,
1981).
Various modifications of fuel oil No. 2 (10, 30, and 50%) were
found to be moderately irritating to rabbit skin (American Petroleum
Institute, 1980a,b,c), and two hydrodesulfurized middle distillates
resulted in primary irritation indices of 4.3 and 5.9 (American
Petroleum Institute, 1982a,b). A straight-run middle distillate had a
moderately irritating effect, with an irritation index of 3.2
(American Petroleum Institute, 1985d). Jet fuel A was classified as
mildly irritating, with an irritation score of 1.96 (American
Petroleum Institute, 1980d). A hydrosulfurized kerosene was moderately
irritating, with an index of 4 (American Petroleum Institute, 1982c).
A light catalytically cracked distillate (American Petroleum
Institute, 1985d) and a straight-run kerosene (American Petroleum
Institute, 1985e) had severely irritating effects, with irritation
indexes of 5.5 and 5.6.
Table 14. Studies of dermal irritation in rabbits exposed for 24 h to various fuels
Fuel Classification of Reference
irritationa
Diesel fuel Extremely irritating Beck et al.
(1984)
Marine diesel fuel or marine Not irritating Cowan & Jenkins
shale fuel (1980)
Hydrodesulfurized middle Moderately irritating American Petroleum
distillate Institute (1982a,b)
Straight-run middle distillate Moderately irritating American Petroleum
Institute (1985d)
Light catalytically cracked Severely irritating American Petroleum
distillate Institute (1985d)
Heating oil No. 2 Moderately irritating American Petroleum
Institute (1980a,b,c)
Jet fuel A Mildly irritating American Petroleum
Institute (1980d)
Various kerosenes Slightly to severely CONCAWE (1995)
irritating
Shale oil- and Not irritating Schultz et al. (1981)
petroleum-derived fuels
Hydrodesulfurized kerosene Moderately irritating American Petroleum
Institute (1982c)
Straight-run kerosene Severely irritating American Petroleum
Institute (1985e)
a Note differences in protocols between regulations of the United States and
the Organisation for Economic Co-operation and Development (see section A7.4.1)
A7.4.2 Ocular irritation
All of the available reports indicate no or, at the most, a
slight irritating effect of diesel fuels and kerosenes on the rabbit
eye.
Four types of American military fuels (petroleum JP-5 fuel, shale
JP-5 fuel, petroleum marine diesel fuel, and shale marine diesel fuel)
gave generally negative responses in the Draize test, in which nine
female New Zealand white rabbits were given 0.1 ml of undiluted
substance (Cowan & Jenkins, 1980). A market-place sample of diesel
fuel (0.1 ml, undiluted) was also not irritating in the Draize test
(Beck et al., 1984). None of several kerosenes tested was more than
slightly irritating to the eye (CONCAWE, 1995), and none of the shale
oil- and petroleum-derived fuels tested caused visible irritation in
the rabbit eye (0.1 ml, undiluted) (Schultz et al., 1981).
Three modifications of fuel oil No. 2 (10, 30, and 50%) were
classified as mildly irritating in rabbits (American Petroleum
Institute, 1980a,b,c). Two hydrodesulfurized middle distillates did
not cause primary irritation in the Draize test (American Petroleum
Institute, 1982a,b); a straight-run middle distillate (American
Petroleum Institute, 1985d) and a straight-run kerosene also gave
negative results (American Petroleum Institute, 1985e). Jet fuel A was
classified as mildly irritating, with an average score of 2.67 after
one day and 0 after seven days (American Petroleum Institute, 1980d).
A hydrodesulfurized kerosene was not irritating (American Petroleum
Institute, 1982c).
A7.4.3 Sensitization
Three modifications of fuel oil No. 2 (10, 30, and 50%) were were
classified as non-sensitizing for the skin of guinea-pigs (American
Petroleum Institute, 1980a,b,c). A straight-run middle distillate
(American Petroleum Institute, 1985d), a straight-run kerosene
(American Petroleum Institute, 1985e), jet fuel A (American Petroleum
Institute, 1980d), a hydrodesulfurized middle distillate (American
Petroleum Institute, 1984), and a light catalytically cracked
distillate (American Petroleum Institute, 1985c) were also not
sensitizing.
Four types of fuels used in the United States Army, petroleum
JP-5 fuel, shale JP-5c fuel, petroleum marine diesel fuel, and shale
marine diesel fuel, were not sensitizing in a modified Landsteiner
test in groups of 24 guinea-pigs (Cowan & Jenkins, 1980). A
straight-run kerosene, hydrosulfurized kerosene, jet fuel A (CONCAWE,
1995), and shale oil- and petroleum-derived jet and diesel fuels
(Schultz et al., 1981) were also not sensitizing.
A7.5 Reproductive toxicity, embryotoxicity, and teratogenicity
Groups of 20 pregnant CRL:COBS rats were exposed by inhalation on
days 6-15 of gestation to 100 or 400 ppm of diesel fuel for 6 h/day
(American Petroleum Institute, 1979). A significant reduction in
maternal food consumption was seen at the high concentration, and
maternal body weight gain and fetal weights were reduced, although not
statistically significantly. Overall, no significant, dose-related
effects were observed in dams, and the compound had no teratogenic or
embryotoxic effect and no effect on fetal growth or development.
No signs of developmental or maternal toxicity were seen when
groups of 20 pregnant rats were exposed to jet fuel A or fuel oil for
6 h/day on days 6-15 of gestation (Beliles & Mecler, 1982).
Sprague-Dawley rats were fed 500, 1000, 1500, or 2000 mg/kg body
weight per day of JP-8 aviation fuel by gavage on days 6-15 of
gestation, and fetuses were examined on day 20. Significantly reduced
body weights were seen in dams at the two higher doses and in fetuses
at 1000-2000 mg/kg body weight per day, but the number of
malformations was not altered. The investigators concluded that JP-8
aviation fuel is a developmental toxin at doses > 1000 mg/kg body
weight per day but is not teratogenic (Cooper & Mattie, 1993).
A7.6 Mutagenicity and related end-points
A7.6.1 In vitro
Various samples of diesel and related fuels have been tested for
mutagenicity in Salmonella typhimurium (Henderson et al., 1981;
Conaway et al., 1984; Vandermeulen et al., 1985; US National
Toxicology Program, 1986; McKee et al., 1994). Negative results were
obtained in direct, unmodified Ames' assays (Conaway et al., 1984;
Vandermeulen et al., 1985; US National Toxicology Program, 1986). In
one study, refined shale oil, jet fuel, and shale oil- and
petroleum-derived marine diesel fuel were not mutagenic (Schultz et
al., 1981). Negative results were also found in studies of aliphatic
and aromatic fractions of diesel fuel in S. typhimurium TA98, TA100,
and TA1535 in the presence of an exogenous metabolic system (Henderson
et al., 1981).
The number of revertants of TA98 increased to 2.3-2.5 times the
background levels in a suspension assay (Conaway et al., 1984), but
increases were found at a limited number of doses. In a modified
Salmonella assay with an extraction step to concentrate the
mutagenic aromatic compounds, addition of an exogenous metabolic
system from Aroclor-induced hamster liver, and use of TA98 as the most
responsive strain, increased numbers of revertants were seen (McKee et
al., 1994); but the number never exceeded twice the background
response, and the results were considered to be equivocal.
A dimethyl sulfoxide extract of an intermediate, catalytically
cracked distillate (CAS No. 644741-60-2) was mutagenic in
S. typhimurium TA98 with an increased concentration of exogenous
metabolic system to optimize detection. Of two dimethyl sulfoxide
extracts of light hydrocracked distillate (CAS-No. 64741-77-7) tested
in the same system, one induced a weak, non-dose-dependent response,
while the other induced a clear dose-dependent positive response
(Blackburn et al., 1984). Under the same assay conditions, five
samples of cracked middle distillates also gave positive results
(German Scientific Association for Petroleum, Natural Gas, and Coal,
1991). These results in a series of assays in Salmonella with a number
of variations provide no clear evidence of mutagenic activity. In the
unicellular alga Chlamydomonas reinhardtii (streptomycin resistant)
tested in a natural aquatic environment, water-soluble fractions of
two crude and two refined oils did not induce forward mutations
(Vandermeulen & Lee, 1986). Neither aliphatic nor aromatic dimethyl
sulfoxide fractions of diesel fuel No. 7911 induced mutation in
S. typhimurium. After reaction with nitrogen dioxide, which may
activate the mutagenicity of diesel exhaust, it was mutagenic in
strain TA100, the aromatic fraction being 40-fold more active than the
aliphatic fraction (Henderson et al., 1981).
A market-place sample of diesel fuel did not induce mutation in
L5178Y tk+/- mouse lymphoma cells with or without metabolic
activation (Conaway et al., 1984). A hydrodesulfurized middle
distillate (CAS 64742-80-9) was active in the presence of metabolic
activation, but the concentrations were cytotoxic (American Petroleum
Institute, 1987c).
A7.6.2 In vivo
Undiluted diesel fuel No. 2 increased the frequency of
chromosomal aberrations in the bone marrow of Sprague-Dawley rats
given single or repeated (five days; 125, 417, or 1250 mg/kg body
weight) oral doses. Diesel fuel given intraperitoneally for one or
five days at 0.6, 2, or 6ml/kg body weight significantly increased the
number of aberrant cells at the highest dose (Conaway et al., 1984).
In order to assess these findings further, McKee et al. (1994)
evaluated micronucleus induction by diesel fuel No. 2 and related
materials in male and female CD-1 mice treated by gavage at up to
5 g/kg body weight. No effect was seen.
No effect was seen on the frequency of dominant lethal mutations
in male CD-1 mice exposed to 100 or 400 ppm of either diesel fuel or
jet fuel A for 6 h/day, five days per week for eight weeks (American
Petroleum Institute, 1980e, 1981).
A7.7 Carcinogenicity
A7.7.1 Dermal exposure
Diesel fuel has been shown to have at least weak carcinogenic
potency after dermal administration in a number of studies. As some of
the test samples contained low concentrations of carcinogenic PAHs, it
has been suggested (Biles et al., 1988) that the tumours induced may
have been a consequence of the dermal damage produced by repeated
treatment with these materials. The available studies are summarized
in Table 15.
Doses of 25 mg per animal of petroleum and shale fuels were
applied to groups of 25 male and 25 female C3H/HeN mice three times a
week, for 62 weeks for jet fuel A with subsequent observation up to
105 weeks, and for 104 weeks for JP-4 fuel. Controls received mineral
oil. The shale and petroleum diesel fuels were characterized for
boiling range (jet A, 171-271°C; JP-4, 60-249°C) and sulfur content
(jet A: petroleum, 3510 ppm; shale, 89 ppm; JP-4: petroleum, 1830 ppm;
shale, 199 ppm). After 60 weeks, increased incidences of squamous-cell
carcinomas and fibrosarcomas were reported (jet A: petroleum, 26%;
shale, 28%; JP-4: petroleum, 26%; shale, 50%; controls, 0-2%), but no
statistical analysis was reported (Clark et al., 1988).
Groups of 50 male and 50 female B6C3F1 mice were given 250 or
500 mg/kg body weight per day marine diesel fuel dermally, on five
days per week for 103 or 84 weeks (see section A7.3.). A control group
received the vehicle, acetone, only. The survival rates were 26/50
males and 29/50 females at the high dose at 84 weeks, 20/49 males and
12/50 females at the low dose at 104 weeks, and 30/50 male and 40/50
female controls. Males at the high dose had a significantly increased
number of hepatocellular adenomas or carcinomas (29%; control, 18%).
The total incidences of squamous-cell papillomas and carcinomas at the
application site and the adjacent inguinal site were: control, 1/50;
low dose, 2/49; high dose, 3/50 in males; and control, 0/50; low dose,
1/45; and high dose, 2/48 in females. No information was available on
historical frequencies in acetone-treated mice; the incidence of
papillomas and carcinomas in 3500 observations in untreated mice was
0.3-0.4%. In a parallel study with JP-5 navy fuel, 1/50 papillomas
were seen at the low dose and 4/49 carcinomas at the high dose in
males, and 0/49 carcinomas were seen at the low dose and 1/47 at the
high dose in females. The investigators concluded that there was
equivocal evidence for the carcinogenicity of marine diesel fuel and
no evidence for the carcinogenicity of JP-5 navy fuel (US National
Toxicology Program, 1986).
Two middle-distillate fractions of each of two crude oils
(boiling range, 170-370°C) were painted at a dose of 50 mg onto the
skin of male C3H mice twice a week for 18 months. The yield of benign
and malignant tumours (details not specified) was 2-19 % (Lewis,
1983).
Table 15. Studies of chronic dermal exposure of mice (usually 50 mice/group) to distillate fuels
Fuel Exposure Results Reference
Marine diesel fuel 0, 250, and 500 mg/kg bw, 1/50, 2/49, and 3/50 (m) and 0/50, 1/45, and 2/48 (f) US National Toxicology
5 d/week, 103 weeks with squamous-cell papillomas and carcinomas after Program (1986)
104 weeks
Straight-run gas oil 25 mg/animal, twice/week, Occasional ulcerations, scarring, epidermal dysplasia; American Petroleum
(laboratory sample)a up to 2 years after 2 years, 17/50 with tumours; controls, 0% Institute (1985c)
Straight-run middle 50 µl/animal, twice/week, Mild to moderate irritation (mild desquamation, American Petroleum
distillatea up to 2 years occasional scabbing); after 2 years, 10/50 with Institute (1989a)
squamous-cell carcinomas or fibrosarcomas;
controls, 0%
Straight-run 50 µl/animal, twice/week, 29/50 with malignant and 1/50 with benign tumours; American Petroleum
keroseneb > 2 years latency, 76 weeks; controls, 0% Institute (1989a)
Two cracked 50 µl/animal, twice/week, Mild to moderate irritation; after 24 months, 39/50 American Petroleum
distillatesc up to 2 years and 26/50 with tumours Institute (1989a)
Intermediate 50 mg/animal, twice/week, 42/43 with tumours; mean latency, 17 weeks; Blackburn et al. (1984)
catalytically cracked 80 weeks controls, 0/50
distillatec
Two hydrodesulfurized 50 µl/animal, twice/week, Acanthosis, fibrosis, hyperkeratosis, crusting; at end American Petroleum
middle distillatesa lifetime of study, 24/50 and 27/50 with tumours (no controls Institute (1989b)
reported)
Table 15 (contd)
Fuel Exposure Results Reference
Hydrodesulfurized 50 µl/animal, twice/week, 26 malignant and 1 benign tumours; latency, 77 American Petroleum
keroseneb > 2 years weeks (no controls reported) Institute (1989b)
Jet A and JP-4 fuels 25 mg/animal, three After 60 weeks, increased skin tumour rate; jet A, Clark et al. (1988)
from shale or times/ week, 62 weeks 26% petroleum, 28% shale; JP-4, 26% petroleum,
petroleum oilsb + observation (jet A) 50% shale
or 104 weeks (JP-4)
Two middle-distillate 50 mg/animal, twice/week, 2-19% tumour rate (no further information) Lewis (1983)
fractions 18 months
No. 2 fuel oilb 12, 25, or 50 µl/animal, Overall tumour rate, 10%; control, 0% Witschi et al. (1987)
three times/week, up to
100 weeks
Two heating oilsa 25 µl/animal, three 7/50 and 9/50 with tumours; control, 0/50 Biles et al. (1988)
times/week, lifetime
a Hydrocarbon fractions similar to that of diesel fuel (see section A2.1)
b Hydrocarbon fractions from which also diesel fuels are gained during petroleum separation (see section A3.2.1.1)
c Blending component of diesel fuel
Application of American Petroleum Institute No. 2 fuel oil
dermally to C3H mice at 12, 25, or 50 µl per animal, three times
weekly for up to 100 weeks induced an overall tumour incidence (type
not specified) of 10% (15/150 in the three treatment groups; controls,
0/100) (Witschi et al., 1987).
Ten samples of middle-distillate fuels were applied dermally to
C3H/HeJ mice at a dose of 25 µl, three times a week for life. A virgin
heating oil blending base (142-307°C) and a commercial No. 2 heating
oil (156-352°C) had aromatic contents closest to that of diesel fuel.
The blending base induced five skin carcinomas and two papillomas in
50 animals, and the commercial heating oil produced eight skin
carcinomas and one papilloma in 50 animals. There were no tumours in
the respective control groups (Biles et al., 1988).
A7.7.2 Inhalation
Fischer 344 rats and C57Bl/6 mice were exposed for 6 h/day on
five days per week for 12 months to 1 or 5 mg/litre of fuel vapours
(see section A7.3), followed by a 12-month recovery period. No
significant pulmonary neoplastic changes were seen. Female mice at the
high dose had a slightly but significantly increased incidence of
benign hepatocellular adenomas (10%; controls, 2%); however, the trend
was reversed in male mice. No conclusions about carcinogenic potency
were drawn from this study (Bruner et al., 1993).
A8. EFFECTS ON HUMANS
A8.1 Exposure of the general population
Like similar petroleum distillates, such as kerosene, diesel fuel
can cause dermal irritation and defatting after dermal exposure
(Sandmeyer, 1981). Considerable exposure and subsequent absorption may
also result in acute renal failure secondary to acute renal tubular
necrosis. A 28-year-old man developed progressive oliguria one day
after washing his hair with diesel fuel and had acute tubular necrosis
on renal biopsy (Barrientos et al., 1977). A 47-year-old man developed
acute tubular necrosis after cleaning his arms and hands with diesel
oil for several weeks (Crisp et al., 1979). Both recovered renal
function.
Accidental aspiration of diesel fuel resulted in immediate
coughing, followed by dyspnoea, cyanosis, and loss of consciousness
(Perez Rodriguez et al., 1976). X-Ray examination revealed diffuse
alveolar infiltrates. Mildly elevated levels of alkaline phosphatase,
serum glutamic-oxaloacetic transaminase, and serum glutamic-pyruvic
transaminase were also seen. After 37 days, residual infiltrates
remained, but the patient had improved. In another case, abdominal
pain and vomiting followed ingestion of a reported 1.5 litres of
diesel fuel. Pulmonary infiltrates were noted, presumably from
subsequent aspiration of diesel fuel (Boudet et al., 1983).
A8.2 Occupational exposure
The odour threshold values for diesel fuels No. 1 and 4 are
reported to be 0.7 and 0.5 ppm, respectively (see section A2.2, Table
5). Six volunteers exposed to 140 mg/m3 of deodorized kerosene for
15 min did not experience throat irritation. Olfactory fatigue was
induced in three subjects, and one reported taste sensation. The
investigators suggested that this concentration was the sensory
threshold for kerosene and estimated the odour threshold at
0.6 mg/m3 (Carpenter et al., 1976).
Acne and folliculitis developed on the arms and thighs of a man
who had worked in various automobile workshops for 15 years. He had
handled diesel oil with his bare hands and then wiped them on his
trousers (Das & Misra, 1988). Hyperkeratosis was noted in 320 drivers
working in Russian oil fields with regular dermal contact with diesel
fuel (Gusein-Zade, 1974). A 33-year-old man was exposed to diesel fuel
vapour (concentration not reported) for 10 days while driving a truck
with a fuel injector leak. He developed abdominal cramps, nausea,
vomiting, and then acute renal failure with anaemia and
thrombocytopenia (Reidenberg et al., 1964). Two aviators who were
exposed to JP-5 fuel vapour for 1 h while flying a small airplane
experienced eye irritation, difficulties in coordination and
concentration, and fatigue (Porter, 1990).
Siemiatycki et al. (1987) conducted a case-control study in
Montreal, Canada, and found an increased risk for squamous-cell
carcinoma of the lung in men exposed to diesel fuel. When all types of
lung cancer except adenocarcinoma were combined, an odds ratio
(adjusted for smoking) of 1.6 (90% confidence interval (CI), 1.0-2.4;
n = 39) was found for 'any' exposure. In four subcategories, the odds
ratios were 1.9 (short-low), 2.0 (short-high), 1.1 (long-low), and 2.0
(long-high). The possible effects of exposure to combustion products
were not taken into consideration. An association with prostatic
cancer was also observed, although there was no dose-response
relationship, with odds ratios of 2.3 (CI, 1.3-4.0; n = 17) for the
subgroup with nonsubstantial exposure and 1.4 (0.7-2.9; n = 8) in
the subgroup with substantial exposure.
In another case-control study, no association was found between
the occurrence of renal-cell cancer and occupational exposure to fuel
oils, including diesel fuel (levels and duration not quantified)
(Partanen et al., 1991).
In a cross-sectional epidemiological study, the effects of
long-term exposure of factory workers to jet fuels (not specified) was
investigated. Dizziness, headache, nausea, palpitation, pressure in
the chest, and eye irritation were found to be more prevalent than in
unexposed controls. The time-weighted average concentration of jet
fuel vapour in the breathing zone was estimated to be 128-423 mg/m3
(Knave et al., 1978).
A9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD
Comparison and evaluation of studies of the ecotoxicological
effects of diesel fuel are complicated by a number of factors:
(1) There are comparatively few ecotoxicological studies on
diesel fuel, and most work in the 1970s was concentrated on the
effects of No.2 fuel oil, which has a similar but not identical
chemical composition to diesel fuel No. 2 (see section A2). The
composition of marine diesel fuel differs greatly from both (see
Table 1). As described in the same section, diesel fuel itself has
various specifications in different countries; in particular, the
composition of non-hydrocarbon compounds from e.g. catalytic processes
or additives may vary widely. There may also be differences between
batches of the same oil (Hedtke & Puglisi, 1982) (see Table 20). The
amount of the chemical actually in solution is also pertinent to
ecotoxicological studies. Table 3 gives the concentration ranges of
toxicologically relevant constituents of diesel and No. 2 fuel oil as
a whole and as 10% water-soluble fractions.
(2) The chemical composition of fuel oils and, as a consequence,
their toxicity change with time, as oil can be modified by
biodegradation, photooxidation, and volatilization (see section A4).
Their toxicity also depends on whether they are mixed with water (sea
water or freshwater), sediment, or soil, the temperature (tropical or
Arctic), and physical conditions (e.g. storm conditions with continual
mixing and breaking up of oil). Oil modified by these processes is
usually less toxic than fresh oil (Baker, 1970; Morrow, 1973).
(3) A variety of methods have been used in ecotoxicological
studies on fuel oils. There is an obvious difference between
conditions in the laboratory and the field. Most of the field studies
that have been reported are related to fuel spills. In laboratory
studies, either water-soluble fractions (see below) or oil-water
dispersions have been used, and the methods of preparing them vary
among laboratories. Oil films and, more recently, microencapsulated
diesel oil have also been tested. In none of the laboratory studies
reported were test media prepared with 'water accommodated fractions',
as described and recommended by CONCAWE (1993) in laboratory protocols
for petroleum products. Thus, the amount of product that must be added
to a given volume of medium to produce the effects reported cannot be
derived from the results of these studies, making comparison of data
on ecotoxicity from different studies practically impossible.
Hedtke & Puglisi (1982) tested the lethality of No. 2 fuel oil in
two species of freshwater fish and two species of amphibians and found
variable LC50 values (see Table 20). Oil-water dispersions were very
toxic to fish. It is thought that these tiny oil droplets make contact
with the gills and directly damage the respiratory epithelium
(Engelhardt et al., 1981; Poirier et al., 1986). With floating oils,
the relationship between toxicity and oil-water contact is a function
of the equilibrium time for the soluble components of the oil and
water, death occurring more rapidly when the oil is added 96 h before
the organisms are exposed. Flow-through tests were more sensitive than
static tests, as, in the latter, the chemical nature and toxicity of
the oil change with time (Hedtke & Puglisi, 1982). Lockhart et al.
(1987) showed that the results of static tests in fish varied
considerably with aeration of test containers. Although flow-through
techniques give a better estimate of real exposure conditions, many of
the results reported in the literature are of static tests.
(4) The susceptibility of organisms to fuel oils and their
components depends not only on the species and strain but also on the
biological stage and the time of development within stages (Kühnhold,
1977; Winters et al., 1977). As the effects of No. 2 fuel oil and
diesel oil have been tested in a wide variety of organisms and life
stages under various conditions, direct comparison is difficult.
In spite of these difficulties, it can be concluded that diesel
oil is generally more toxic than crude oil, as seen, for example, in
barnacle nauplii (Winters et al., 1977), Daphnia (Cladocera),
chironomid larvae, and the mollusc Viviparus bengalensis (Gastropoda)
(Das & Konar, 1988). Crude oils themselves differ in toxicity,
depending on their source (Anderson, 1977a; Winters et al., 1977), as
do their corresponding products.
Rice et al. (1977a) concluded that the toxicity of fuel oil is
due to the chemical toxicity of soluble aromatic compounds rather than
to the physical toxicity of dispersed oil droplets. Physical coating
by oil of the gills of fish and the feathers of birds is also a cause
of toxicity. Monoaromatic compounds seem to be the least toxic, their
acute toxicity increasing with molecular size up to the four- to
five-ring compounds (e.g. chrysene and benzo[ a]pyrene) (Neff et al.,
1976b; Rice et al., 1977a), but they are not very soluble in sea water
(see Table 6). The toxicity of one-, two-, and three-ring compounds
(benzenes, naphthalenes, and phenanthrenes, respectively), seemed to
increase with increasing degrees of alkylation of the aromatic
nucleus. Neff et al. (1976b) reported 96-h LC50 values of 0.3-0.6 ppm
for 1-methylphenanthrene, fluoranthrene, and phenanthrene, indicating
the high toxicity of these polynuclear aromatic compounds for the
polychaete, Neanthes arenaceodentata. Of the pure compounds tested
by Winters et al. (1977), the most toxic to barnacle nauplii were
indan, naphthalene, xylene, and substituted benzenes and naphthalenes.
In four freshwater species, the water-soluble fraction was again
associated with the substituted benzenes, and naphthalenes were found
to be associated with the observed toxicity (Lockhart et al., 1987).
The concentrations of naphthalenes, methylnaphthalenes, and
dimethylnaphthalenes are particularly high in fuel oils (see Table 3),
and these compounds have been used as analytical markers in several
studies.
Experiments involving microencapsulated oil fractions have shown
that insoluble fractions also inhibit growth, e.g. of juvenile mussels
(Stromgren & Nielsen, 1991). Anderson (1979) indicated that the larval
stage might be the most sensitive to No. 2 fuel oil. Eggs of fish and
invertebrates were often tolerant, and adults were sometimes more
sensitive than juveniles.
Extensive studies have been carried out on lethal toxicity to
marine organisms under the same conditions. The 96-h LC50 values for
a wide range of invertebrates in static exposure conditions
(temperature, 18-22°C) were 1-20 ppm for crude oil in water and
0.4-6 ppm for No. 2 fuel oil (Anderson et al., 1974; Neff et al.,
1976b; Rossi et al., 1976). At 4-10°C, the 96-h LC50 values appeared
to be lower (Rice et al., 1976, 1977a). Table 16 gives the results of
lethality studies reported from several laboratories.
Table 16. Lethality (median lethal concentrations) to marine
zooplankton of physically dispersed and water-soluble
fractions of No. 2 fuel oil
Zooplankton Oil-water dispersions Water-soluble
(mg/litre) fractions (mg/litre)
Ctenophora 0.59 (1 day)
Mollusca
Clams
Embryos 0.43 (2 days)
Larvae 1.3 (2 days)
Larvae 0.53 (10 days)
Pteropods < 0.2 (2 days)
Crustacea
Barnacles 2.6 (1-h LC50)
Copepods 1.0 (3 days)
Amphipods 0.3 (2 days) 2.5 (3 days)
Decapods
Shrimp post-larvae 1.7; 9.4
Lobsters 1.2-6.6
Teleosts 1.5
Adapted from US National Research Council (1985). Values are for total
measured (extractable) hydrocarbons, calculated from initial
concentrations measured by spectroscopy and chromatography
No. 2 fuel oil (mostly the water-soluble fraction) has been found
to have sublethal effects in all phyla examined (Anderson, 1977a,b,
1979; US National Research Council, 1985). With increasing
concentrations, alterations were seen in the respiratory rate of the
fish Cyprinodon variegatus (Anderson et al., 1974) and Oncorhynchusm
gorbuscha (pink salmon) (Rice et al., 1977b), the crustaceans
Mysidopsis almyra and Penaeus aztecus, and the glass shrimp
Palaemoetes pugio (Anderson, 1979); and changes were found in the
pulse rate in embryonic estuarine fish, C. variegatus and Fundulus
heteroclitus (Anderson, 1977a) These effects have been used as a
measure of stress caused by exposure. Dysregulation of the ability to
regulate internal concentrations of solutes (osmotic and ionic
regulation) was demonstrated in the brown shrimp Penaeus aztecus
(Anderson et al., 1974; Cox, 1974; Anderson, 1979). The behaviour of
F. similus exposed to a 100% water-soluble fraction of No. 2 fuel
oil was correlated with the content of naphthalene in four organs
(Dixit & Anderson, 1977). Sublethal studies on No. 2. fuel oil showed
reduced growth rates, survival, and reproduction in a range of
organisms (Anderson, 1979; Table 17), including the annelid Neanthes
arenaceodentata (Rossi & Anderson, 1978) and the estuarine fish
F. grandis (Ernst et al., 1977).
A9.1 Laboratory experiments
Diesel fuel is a complex mixture of substances with a range of
solubilities in water (see section A2.2). In testing for aquatic
toxicity, it is important that the constituents in the medium be
characterized (Bennett et al., 1990), but these are seldom reported.
The results described in this section refer to diesel fuel, unless
otherwise stated.
As the solubility of diesel fuel in sea and freshwater is low,
investigations of the effects of diesel fuel on organisms in the
laboratory often involve preparation of a water-soluble fraction or an
oil-water dispersion. Water-soluble fractions can be prepared by
stirring one part of diesel fuel into nine parts of (sea) water for
20 h (Anderson et al., 1974) or one part of diesel fuel into eight
parts of sea water for 24 h (Pulich et al., 1974), and then extracting
the water phase. The resulting water phases contain 6-20 µg/ml of
total hydrocarbons; the 100% water-soluble fraction of No. 2 fuel oil
contains about 7 µg/ml of total hydrocarbons. Results are expressed as
the concentration (percent dilution of the water-soluble fraction)
and/or as the measured hydrocarbon concentration that causes the
specified level of effect. The results cannot, however, be correlated
with the original amount of fuel oil that was added to produce the
water-soluble fraction or oil-water dispersion (CONCAWE, 1993).
Table 17. Effects of No. 2 fuel oil on the growth and reproduction of marine animals
Species Exposure Concentration (ppm) Growth or reproduction Reference
(days)
TH TN TA
Fish
Cyprinodon variegatus 7 2.0 0.6 1.7 0% of eggs hatched Anderson et al. (1976)
Decapods
Rithropanopeus harrasii 27 1.0 0.3 0.9 Reduced survival and Neff et al. (1976b)
extended development to
megalopa
Palaemonetes pugio 12 0.9 0.3 0.8 Reduced growth rate of Tatem (1977)
larvae
3 1.4 0.6 Reduced viability of eggs
from exposed gravid females
Polychaetes
Neanthes arenaceodentata 22 1.0 0.3 0.9 Reduced growth of larvae Rossi & Anderson (1976)
28 0.3 0.1 Reduced growth of Anderson (1977a)
juveniles by 30%
Ctenodrilus serratus 28 2.2 0.5 1.4 Reduced survival and Carr & Reish (1977)
reproduction
Ophryotrocha sp. 28 1.3 0.3 0.9 Reduced survival and Carr & Reish (1977)
reproduction
From Anderson (1977b)
TH, total hydrocarbons; TN, total naphthalenes; TA, total aromatic compounds
Oil-water dispersions are produced by shaking a measured quantity
of oil in water for 5 min (Anderson et al., 1974) or 30 min (Pulich et
al., 1974). In some cases, the oil-water dispersion is maintained by
continuous mixing, but more usually it is allowed to settle, and the
aquatic organisms are exposed to the material in the water and to a
surface film. The effects seen in such tests can be due to both
physical action and toxicity, especially in small invertebrates such
as Daphnia.
Insoluble fractions of crude oil and other hydrocarbon
formulations strongly inhibited growth when they were
microencapsulated and ingested by juvenile mussels (Stromgren et al.,
1986; Stromgren & Reiersen, 1988) and larvae (Stromgren & Nielsen,
1991). In microcapsules with a thin acacia-gelatine structure, the
total oil is dispersed into particles of 1-10 µm, which are suitable
for ingestion by Mytilus larvae. The water-soluble components leak
through the wall, providing a low concentration, and are ingested by
the molluscs.
None of the studies involved use of the 'water accommodated
fractions' recommended by CONCAWE (1993), which allows the results to
be expressed as 'loading rate', defined as the amount of product that
must be equilibrated with the aqueous test medium in order to produce
a specified level of effect.
A9.1.1 Microorganisms
A9.1.1.1 Water
Marcus & Scott (1989) tested the effects of 0, 10, 20, and 40%
water-soluble fractions of a shale-diesel fuel mixture and a
petroleum-diesel fuel mixture on the growth of faecal coliform
bacteria. The 20 and 40% fractions of the petroleum-diesel fuel
mixture resulted in significantly lower bacterial densities than the
shale-diesel fuel mixture. The latter appeared to biostimulate or
mediate against toxicity, suggesting a difference in the chemical
characteristics of the two fuels.
The effects of diesel and furnace oils, petrol, kerosene, and
Assam crude oil and their paraffinic, aromatic, and asphaltic
fractions (higher relative molecular mass, poorly defined) on the
photosynthesis and respiration of blue-green algae (Cyanobacteria), in
particular Anabaena doliolum were investigated by Singh & Gaur (1990).
The chemical composition of the diesel and furnace oils was almost
identical, with 37 and 36% paraffins, 51 and 54% aromatic compounds,
and 6 and 0.6% asphaltic compounds, respectively. The aromatic
fractions of these oils were the most toxic, followed by the asphaltic
fractions; photosynthesis was reduced to 40% by the aromatic fractions
and to 50% by the asphaltic fractions of both oils at a concentration
of 5.0 mg/litre. The effects were dependent on concentration up to
10 mg/litre. Photosynthesis was stimulated 160% by 5 mg/litre of the
paraffinic fractions of crude oil , but only 100% by those of diesel
oil and 110% by those of furnace oil. In general, crude oil inhibited
photosynthesis and respiration by A. doliolum least and diesel and
furnace oils the most.
A9.1.1.2 Soil
In outdoor lysimeters, the toxicity of spills of 2.3 ml/cm2
diesel and heating fuels was investigated in soil microbes, using
Microtox(R) measurements (Wang & Bartha, 1990). (For parallel assays
of seed germination and plant growth, see section A9.1.3.1.) At time
0, both fuels were moderately toxic (EC50 = 80-90 mg of contaminated
soil); this was followed by a period of increased toxicity, which
started to decrease after 6-12 weeks. The values in soils treated by
biodegradation returned to background within 20 weeks, although diesel
fuel had significant residual toxicity in untreated soil. Seed
germination and plant growth were inhibited in a similar manner, and
diesel oil was more toxic and persistent than heating oil (section
A9.1.3.1). Biodegradation treatment, in which the conditions for
hydrocarbon degradation by microbes were optimized by mixing,
aeration, pH control, and addition of mineral nutrients (fertilizers),
strongly decreased fuel persistence and toxicity.
A9.1.2 Aquatic organisms
A9.1.2.1 Plants (phytoplankton)
Experiments in both the laboratory and the field have shown that
hydrocarbons can inhibit algal growth, although enhancement is
occasionally noted at lower concentrations of oil (US National
Research Council, 1985).
After 12 days of exposure to 10% diesel oil, the growth of cells
of Euglena gracilis was not significantly reduced, whereas a
concentration of 0.1% almost completely inhibited the growth of
Scenedesmus quadricauda. Cells of S. quadricauda grown in culture
media containing diesel fuel (concentration not given) became
chlorotic, suggesting damage to the photosynthesizing system
(Dennington et al., 1975).
A concentration of 0.05% light diesel fuel was found to stimulate
growth rate, growth yield, photosynthesis, and chlorophyll a
synthesis, while at the same time slightly inhibiting the respiration
of Chlorella salina CU-1 (Chan & Chiu, 1985). At higher
concentrations (0.5 or 5%), the growth rate, growth yield, and
photosynthesis were greatly reduced (to 50, 50, and 62% and 43, 32,
and 41% of the control levels, respectively), but the effect on algal
respiration was less severe (81% with 0.5% diesel and 86% with 5%).
Diesel fuel containing dispersants caused greater inhibition than did
the compounds separately.
The lengthwise growth of the benthic algae Ascophyllum nodosum
and Laminaria digitata and other rocky-shore communities was
measured while they were kept in 50-m3 concrete basins and exposed
continuously to diesel fuel for two years (Bokn, 1987). An average
hydrocarbon concentration of 130 µg/litre continuously inhibited
growth in both species, while a concentration of 30 µg/litre caused
periodic inhibition. Under oil-free conditions during the subsequent
season, the plants recovered completely.
Boiler fuel was more toxic than diesel fuel to the kelp
Macrocystis; both fuels reduced photosynthesis (Baker, 1970).
A9.1.2.2 Invertebrates
(a) Several species
The acute toxicity of diesel fuel to Daphnia (Cladocera),
chironomid (insect) larvae, and the mollusc Viviparus bengalensis
(Gastropoda) was tested after the organisms were acclimatized to
laboratory conditions for four, two, and four days, respectively. The
bioassays were conducted at 28 ± 2°C with unchlorinated borehole water
(pH 7.0 ± 0.2; oxygen, 8 mg/litre; free carbon dioxide, 1.2 mg/litre;
total alkalinity as calcium carbonate, 240 mg/litre; hardness,
260 mg/litre). The results are shown in Table 18. Plankton and insect
larvae exhibited erratic, uncoordinated movements before becoming
lethargic. In the mollusc, active avoidance and heavy secretion of
mucus were observed. The concentrations at which these behavioural
changes occurred were not specified (Das & Konar, 1988).
Fourteen species of five phyla (Echinodermeta, Mollusca,
Annelida, Arthropoda, and Urochordata) were exposed to 0.5% No. 2
diesel fuel in sea water. Only the larvae of the echinoderm
Crossaster, which were also the largest, survived up to eight days;
all of the other larvae died 3-72 h after being placed in the
fuel-water mixture (Chia, 1973).
The periwinkles Pachymelania aurita (Muller) and Tympanotonus
fuscatus (Linne) were exposed to refined diesel fuel films for 24
and 48h at concentrations of 2.5, 5.0, 7.0, or 10.0% and to emulsions
for 24 h at concentrations of 0.5, 1.5, 2.5, or 3.5%; they were then
shaken for 2 min with brackish water. After exposure to the emulsion,
the periwinkles were washed and reintroduced into oil-free, brackish
water for 24 h and their activity recorded. Both surface films and
emulsions were harmful to both gastropods, the emulsions being the
more toxic. T. fuscatus was less susceptible than P. aurita,
possibly because the former can retract further into its shell. The
mean percentage survival in the presence of oil film (7.5% diesel
fuel) was 100% at 24 h and 80% at 48 h for T. fuscatus and 80% at 24 h
and 50% at 48 h for P. aurita. The mean percentage survival in the
presence of 3.5% diesel fuel-water emulsion was 90% for T. fuscatus
and 80% for P. aurita (Dambo, 1993).
Table 18. Acute toxicity of diesel fuel to Daphnia (Cladocera),
chironomid larvae (insects), and the mollusc Viviparus
bengalensis (Gastropoda)
Species LC5 (mg/litre) LC50 (mg/litre) LC95 (mg/litre)
Daphnia magna 1.5 (0.8-2.5) 20 (19.2-21.0) 38.5 (37.5-39.5)
Chironomid 5.0 346.0 (238-455) 865.0 (750-1018)
larvae
Viviparus 2.0 254.0 (185-320) 637.0 (575-700)
bengalensis
From Das & Konar (1988)
(b) Molluscs
The feeding rate and growth of mussels ( Mytilus edilus L.) was
markedly reduced when they were exposed to 30 or 130 µg/litre diesel
fuel for eight months (Widdows et al., 1985). Recovery of
physiological responses (clearance rate, respiration, food absorption
efficiency, and ammonia excretion) after transfer to unpolluted water
was concomitant with the depuration of hydrocarbons from the tissues.
Mussels exposed to either dose recovered completely within about 55
days.
The effects on the nutrient storage system and reproductive
cell systems of the mussel M. edilus of exposure to a diesel
hydrocarbon-sea water emulsion and subsequent depuration were studied
in order to assess the capacity of these systems to recover after
discontinuation of exposure to the oil. After 144 days of exposure to
hydrocarbon concentrations of 27 and 128 units, the volume of storage
cell types was significantly reduced and there was a reduction in the
volume of ripe gametes. After 53 days of depuration, the volume of the
storage cells and of developing gametes increased. Exposure to either
concentration also increased the volume of atretic (degenerating)
gametes, but depuration allowed a return to normal (Lowe & Pipe,
1986). The authors suggested that exposure to the hydrocarbons reduced
the storage reserves and increased gamete atresia and resorption, so
that the storage pool was partially replenished, enabling the organism
to tolerate better the hydrocarbon insult.
The sensitivity of M. edulis to pollution with diesel fuel
depends on the salinity of the water (Tedengren & Kautsky, 1987). Low
salinity and diesel fuel acted synergistically to a greater degree in
Baltic than in North Sea mussels.
Adults and larvae of M. edulis were exposed to microencapsulated
diesel fuel at concentrations of 200, 600, 1000, 1300, or
5000 µg/litre and the effects on mortality, larval growth, and
spawning frequency were recorded (Stromgren & Nielsen, 1991). The EC50
for spawning in mussels exposed for 30 days was about 800 µg/litre,
and the LC50 (30days) for maturing mussels was about 5000 µg/litre.
The longitudinal growth of larvae was significantly reduced at
10 µg/litre; the EC50 for growth (10 days) corresponded to about
25-30 µg/litre (Stromgren & Nielsen, 1991), which is lower than the
EC50 of about 1000 µg/litre for growth of juvenile mussels reported
by Stromgren & Reiersen (1988).
Diesel fuel is therefore more toxic to mussel larvae than to
juveniles.
The EC50 values (10 days) for growth of larvae of the Quahog
clam, Mercenaria spp., exposed to water-soluble fractions of various
crude and refined fuels were 220-4200 µg/litre, indicating that the
insoluble fractions of hydrocarbons, ingested as microcapsules, are
far more toxic than the water-soluble fractions alone (Byrne & Calder,
1977). Stromgren et al. (1986) drew the same conclusion from their
results for the growth of juvenile mussels. Larval mortality during
exposure to diesel fuel increased steeply up to 50 µg/litre, at which
dose only 20-30% survived 10 days of exposure. At 500 µg/litre, there
was 100% mortality. Byrne & Calder (1977) reported LC50 values (10
days) of 50-2100 µg/litre for larvae of Mercenaria spp.
(c) Crustaceans
Freshwater crabs (Barytelphusa cunicularis) were exposed to
sublethal concentrations of diesel fuel (4.5, 3.7, 3.2, and 2.6 ppm)
for 24, 48, 72, and 96 h, respectively (Sarojini et al., 1989). The
oxygen consumption of the crabs was measured as an index of stress
caused by the fuel and compared with that of normal controls. The
crabs responded in general by lowering their oxygen consumption up to
8 h (down to 50% at 4 h), particularly at the lower doses; with longer
exposures, the oxygen consumption was higher than (approx. 120% at
24 h) or equal to (at 96 h) that of the controls.
Gammarus spp. (Crustacea, Amphipoda) were obtained from marine
and brackish water in the North and Baltic Seas and tested in two
laboratories for their sensitivity to diesel-fuel pollution (Tedengren
et al., 1988). G. oceanicus was obtained from the Fucus belt at a
depth of 1-3 m and G. duebeni from rock pools of various salinities.
The respiration, excretion, and atomic O:N and O:P ratios of the two
species were compared after a 6-h exposure to 10 mg/litre diesel fuel
emulsified in a syringe and injected into experimental aquaria; the
resulting hydrocarbons were not measured. Exposure to diesel fuel
generally resulted in decreased oxygen consumption and a rise in
nutrient excretion, leading to lowered O:N and O:P ratios.
G. oceanicus was the most sensitive, and the response was aggravated
by simultaneous lowering or raising of the salinity. No signs of
impaired swimming or other physical or mechanical effects were
detected in either species. The investigators concluded that
G. duebenihas a greater tolerance to pollutants and changes in
salinity, probably because it has broad physiological niches and has
evolved in and become adapted to more variable environments.
In a comparison of the effects of an oil-water dispersion of
diesel fuel, kerosene, gasoline, and benzene on the tidepool copepod
Tigriopus californicus, diesel fuel was the most detrimental: a
concentration of 0.10 ml/litre sea water caused 100% mortality within
five days (Barnett & Kontogiannis, 1975).
(d) Fish
Freshwater
Table 19 shows the results of a series of 96-h static tests for
acute toxicity with diesel fuel in freshwater on several species of
juvenile salmonids, Oncorhynchus kisutch (coho), O. gorbuscha
(pink), and O. mykiss (rainbow trout), exposed at 14°C in 16 h of
light and 8 h of darkness (Wan et al., 1990). The average loading
density was 250 mg/litre (range, 100-420 mg/litre) of Canadian diesel
fuel with a pour-point of -17.8°C. Three types of water were used for
dilution: soft acid city tapwater, hard alkaline lakewater, and
intermediate reconstituted deionized city tapwater. The LC50 values
varied between the species from 32 to 33216 mg/litre. Diesel fuel was
more toxic to pink salmon than to coho salmon or rainbow trout,
irrespective of the water type.
The LC values for diesel fuel in golden orfe (Leuciscus idus
melanotus) in a static test were: LC0 = 40-120 mg/litre; LC50 =
120-160 mg/litre; LC100 = 160-205 mg/litre (Juhnke & Lüdemann,
1978).
Various freshwater fish (Fundulus diaphanus, Roccus saxatilis,
Lepomis gibbosus, Roccus americanus, Anguilla rostrata, and Cyrinus
carpio) were exposed to No. 2 or No. 4 fuel oil (both dispersed) in
a static test at 19°C, pH 7.1, and 60 mg/litre hardness (Rehwoldt et
al., 1974). The 96-h LC50 values for No. 2 fuel oil ranged from
22.2 mg/litre for striped bass (Roccus saxatilis) to 49.1 mg/litre
for carp (Cyrinus carpio); those for No.4 fuel oil ranged from
21 mg/litre for banded killifish (Fundulus diaphanus) to 48.1 mg/litre
for carp. These concentrations represent total oil added and not the
oil dissolved in the water column.
Table 19. Acute toxicity of diesel fuel to juvenile Pacific salmonids in different
types of freshwater
Water type Salmonid LC50 (mg/litre
24-h 48-h 72-h 96-h
Soft Coho 28 972 28 972 12 345 10 299
Pink 1 972 276 84 74
Rainbow > 32 000 5 525 4 600 3 017
Intermediate Coho > 55 560 > 55 560 33 216 33 216
(reconstituted) Pink 1 829 376 133 123
Rainbow 168 363 168 363 28 787 2 186
Hard (lake) Coho > 26 743 26 743 4 845 3 333
Pink 1 404 302 48 32
Rainbow > 23 108 23 108 5 102 2 447
From Wan et al. (1990). Coho, Oncorhynchus kisutch; pink, O. gorbuscha; rainbow
trout, O. mykiss
The LC50 values of water-soluble fractions and emulsions and
the floating layer of No. 2 fuel oil for four freshwater species under
static and flow-through conditions are shown in Table 20 (Hedtke &
Puglisi, 1982).
Marine
In an investigation of the threshold doses at which cod (Gadus
morhua L.) detected samples of Ekofisk diesel fuel, sea water was
allowed to gravitate through the diesel fuel. The total content of
dissolved materials, estimated by gas chromatography, were 15%
benzenes, 2% toluenes, 6% xylenes, 15% naphthalenes, 3% phenols, 42%
n-alkanes (C10-C25), and 17% unidentified compounds. There were
no visible surface films or microdroplets in the samples, although the
authors suspected the presence of undissolved microdroplets. Behaviour
was observed with a sea-water olfactometer, and reaction patterns
after injection of samples (snapping, increased activity, coughing,
darting, backing) were noted. The most frequent reaction was snapping
of jaws followed by a short period of activity. None of the doses
produced alarm reactions. The mean activity scores increased with
increasing doses of oil compounds. In a set of four experiments, the
threshold for detection of diesel oil compounds was 100-400 ng/litre,
showing that cod detect fuel compounds at doses lower than those
hitherto observed (Hellstrom & Doving, 1983).
The effect of acute exposure to the water-soluble fraction of
Arctic diesel fuel (1:9 with sea water) on survival and metabolic rate
was studied in an Antarctic fish (Pagothenia borchgrevinki). The
fish proved to be extremely tolerant and withstood an undiluted
water-soluble fraction for at least 72 h. None died as a direct
consequence of contact with the water-soluble fraction, but they
showed signs of stress. In unpolluted water, little spontaneous
swimming activity was seen, but on transfer into water containing
diesel fuel they became agitated and increased their swimming activity
for a short time. Their ventilation rates increased but later
decreased; the depth of each ventilation increased considerably.
Coughing became apparent shortly after transfer and persisted for up
to 72 h. The haematocrit increased and remained elevated throughout
the experiment. Oxygen consumption was increased to about twice that
of the controls (Davison et al., 1992).
In further studies on P. borchgrevinki (Davison et al., 1993),
a water-soluble fraction was prepared (1:2 with sea water) and then
diluted to 33%; the fish were kept for seven days. On initial
placement, behaviour similar to that with the higher concentration in
the previous experiment was noted. After seven days, the only
noticeable differences between exposed and control fish of similar
weight and length were large amounts of mucus streaming from opercula,
increased coughing, and slightly deeper ventilation. Plasma chloride
and osmolarity were similar in the two groups. Haematocrit and
haemoglobin concentration were significantly higher in the treated
fish; spleen weights and oxygen consumption were similar. This
Antarctic fish can thus survive prolonged periods of exposure to low
levels of water-soluble hydrocarbons.
Table 20. 96-h LC50 values for No. 2 fuel oil on freshwater organisms under various conditions
Species Life stage Test conditions Effect Concentration
(µl/litre water)
Jordanella floridae (flagfish) Adult Water-soluble fraction of 10% No mortality No dilution
oil-water mixture; static
Emulsion; flow-through LC50 60.5
Pimephales promelas (fathead minnow) Adult Emulsion; flow-through LC50 38.6
Water-soluble fraction of 10% No mortality No dilution
oil-water mixture; static
Floating layer; static LC50 > 160 000
48 300 (2nd
sample)
Rana sylvatica (frog) Larvae Water-soluble fraction of LC50 413 000
10% oil-water mixture; static
Emulsion; static LC50 26.4
Emulsion; flow-through LC50 4.9
Floating layer; static LC50 < 5000
Ambystoma maculatum (salamander) Larvae Emulsion; flow-through LC50 86.4
From Hedtke & Puglisi (1982)
(e) Amphibians
Larvae of the frog Rana sylvatica were tested in 96-h static and
flow-through tests with No. 2 fuel oil as a water-soluble fraction, an
emulsion, or a floating layer (Hedtke & Puglisi, 1982) (Table 20).
Flow-through exposure to the emulsion was the most toxic (LC50 =
4.9 µl/litre), and static exposure to the water-soluble fraction was
the least toxic (LC50 = 413 000 µl/litre). The LC50 of No. 2 fuel
oil emulsion in larvae of the salamander Ambystoma maculatum in a
flow-through test was 86.4 µl/litre).
A9.1.3 Terrestrial organisms
A9.1.3.1 Plants
Seed germination and growth of soya beans and ryegrass were
inhibited by a diesel fuel spill of 2.3 ml/m2 (Wang & Bartha, 1990;
see sections A3.2.4 and A9.1.1.2). Four weeks after the spill,
biodegradation had at least partially restored the ability of the soil
to support seed germination and plant growth. Morphological effects,
such as reverse geotropism, were noted on some partially emerged
seedlings. In untreated diesel-contaminated soil, there was no
evidence of seed germination or plant growth. Parallel experiments
showed that heating oil was less toxic.
A9.1.3.2 Invertebrates
No data were available.
A9.1.3.3 Vertebrates
Birds are affected externally and internally by oil
contamination. The fuel rapidly destroys the waterproofing of the
birds' plumage, and as the birds attempt to preen the contaminant off
their feathers they ingest fuel. When No. 1 fuel oil was administered
by gavage at doses of 1-4 ml/kg body weight to ducks, a dose of
2 ml/kg caused lipid pneumonia, extreme inflammation of the lungs, and
fatty infiltration and degeneration of the liver after 24 h (Croxall,
1977). Administration of 1 ml of diesel or No. 1 fuel oil/kg produced
severe irritation of the digestive tract (enteritis), with diarrhoea
and bile pigments in faeces. Signs of toxic nephrosis were also noted.
Adrenal enlargement (mainly hyperplasia of cortical tissue),
depression of plasma cholinesterase levels, and incoordination,
ataxia, and tremors were reported at higher doses. The treatment was
not fatal to healthy birds, even at doses up to 20 ml/kg body weight;
however, when No. 1 fuel and diesel fuel were administered to birds
under stress, the LD50 was 3-4 ml/kg body weight (Hartung & Hunt,
1966).
A9.2 Field observations
The following information is derived mostly from observations
made after diesel spills (see Table 10).
A9.2.1 Microorganisms
A9.2.1.1 Water
No data were available.
A9.2.1.2 Soil
Six weeks after the ship Bahia Paraiso spilled Arctic diesel
fuel into the Antarctic Sea, the impact of the spill on microbial
ecology was investigated (Karl, 1992). The acute effects on the
metabolic activities of sedimentary microorganisms appeared to be
negligible, even in saturated sea water.
A9.2.2 Aquatic organisms
In field studies conducted after fuel spills to investigate the
effects on populations and ecosystems, zooplankton appeared to be
highly vulnerable to dispersed and dissolved petroleum constituents
but less so to floating oils. Field observations on oil spills in
general showed that individual organisms were affected in many ways,
including direct mortality (fish eggs, copepods, mixed plankton),
external contamination by fuel (chorion of fish eggs, cuticles, and
feeding appendages of crustacea), tissue contamination by aromatic
constituents, abnormal development of fish embryos, and altered
metabolic rates (US National Research Council, 1985). A spill of
No. 2 diesel fuel was extremely toxic: faunal repopulation of the
affected areas did not occur during the subsequent eight months
(Blumer et al., 1970). A spill of 750000 litres of No. 2 diesel fuel
caused substantial mortality in some taxa of the intertidal
population, whereas others showed little or no effect. There was
substantial recovery within six months, and there was no observable
mortality among the subtidal fauna or flora (Woodin et al., 1972).
After a spill of marine diesel fuel (2000-3000 t) off Hong Kong, much
of the oil was carried to land by onshore winds. Wormald (1976)
described the effects of the oil spill on intertidal meiofauna. Within
four days of the spill, there was almost total mortality: nematodes
and harpacticoid copepods were observed in an advanced state of decay,
and other meiofauna were not detected. The aromatic fractions probably
evaporated within four to six weeks but persisted longer in deeper
sediment. Harpacticoids and nematodes did not recolonize the beach
until nearly eight months after the spill. The density of meiofauna at
all stations observed reached a maximum 10 months after the spill and
subsequently showed large fluctuations, which were probably the result
of ecological successions during recovery of the beach fauna. One year
later, an increase in the number of macrofauna, especially polychaete
worms, was noted, which may have been responsible for the decrease in
meiofaunal populations. High rainfall 11 months after the spill may
have brought the soluble aromatic compounds nearer to the surface and
decreased the harpacticoids and nematode populations. After 15 months,
the meiofauna were again well established. Recovery at high shore
stations began only when the oil content of the sediment had decreased
by at least 50%, primarily through physical dispersion. Recolonization
of the lower shore had occurred earlier. Stirling (1977) studied the
effects of this spill on rocky shore fauna (see also Table 10),
concentrating on large, common species of gastropods (Monodonta labio,
Thais clavigera, Nerita albicilla, N. polita, Lunella coronata,
Clypeomorus humilis, and Planaxis sulcatus), bivalve molluscs (Donax
semignosus, Atactodea striata, Tapes philippinarum, and Circe
stutzeri), and crustaceans (shore and hermit crabs). Acute mortality
of gastropods was greatest at moderately contaminated sites where
oil-dispersing chemicals had been applied to floating oil slicks.
Long-term disturbances were most significant at the heavily polluted
sites where dispersants had not been used. Recovery of animals taken
from the oiled beaches was studied in clean salt water in the
laboratory. Bivalve molluscs and the gastropods Monodonta labioand
Thais clavigera were the most sensitive and Clypeomorus humilisand
Planaxis sulcatus the least sensitive. Field observations of acute
mortality were consistent with this order of sensitivity. Population
studies showed the greatest reductions in Monodonta labio and Nerita
albicilla, which were eliminated for at least 13 months from the
site of greatest oil pollution.
The release of 600 000 litres of Arctic diesel fuel from the
Bahia Paraiso in 1989 coated intertidal macroalgae, limpets, and
birds as well as sediments and shores (Kennicutt et al., 1991b).
Macroalgae (Leptosomia simplex and Monostroma spp.) were only
moderately affected. Intertidal limpet (Nacella concinna) populations
were reduced by 50% within the first few weeks after the spill
(Kennicutt et al., 1990), and a year later had still not fully
recovered (Kennicutt & Sweet, 1992). Bottom-feeding organisms, such as
clams (Laternula elliptica) and fish (Harpagifer anarcticus and
Notothenia coriiceps neglecta) were found to have PAHs in their gut
contents and muscle tissues (Kennicutt et al., 1991b). After the
spill, all of the chicks of the local population of South Polar skuas
(Catharacta maccormicki) died, although few of the adults or the
chicks died from direct contact with oil (Eppley, 1992). Within less
than two years, and at many locations within a few weeks, the PAH
content of sediment and intertidal organisms returned to background
levels (Kennicutt & Sweet, 1992), owing partly to the high volatility
of the spilled fluid and the high energy environment. Sampling of
intertidal limpets showed that the tissue contaminants were primarily
naphthalenes, but fluorenes and phenanthrenes were often the most
abundant aromatic contaminants in tissues with higher concentrations
of PAHs (Kennicutt & Sweet, 1992; Kennicutt et al., 1992b) After a
spill of 8000 litres of diesel fuel into an unspoiled freshwater
stream in California, United States, most animals were affected within
one to four days. Thousands of aquatic insects perished; some
crayfish, aquatic leeches, and freshwater planarians were killed; and
over 2500 fish, tadpoles (but no frogs), snakes, a turtle, and common
merganser (Mergus merganser) were found dead (Bury, 1972).
A9.2.3 Terrestrial organisms
A9.2.3.1 Plants
Diesel fuel was applied at 10 litres/m2 to the soil of five
common plant communities in north-east Greenland, comprising wet
marsh, grassland, and three types of dwarf-shrub heath. The plant
species were observed for up to three years after the application.
Within a few days, most species had lost chlorophyll or had abscissing
leaves. Species with xeromorphic leaf characteristics reacted more
slowly than species with orthophyllous leaves. During three successive
growing seasons, shrubs and forbs showed no signs of recovery.
Graminoids showed slight resistance and recovered in all mesic and wet
plots but were killed in dry plots. Three species of sedge (Carex
bigelowii, C. saxatilis, and C. stans) and mosses recovered to some
extent in all plots. Recovery of mosses was excellent in the wet
plots, good in the mesic plots, and poor in the dry plots. In general,
the phytotoxic effects of diesel fuel were much more pronounced than
those of crude oil in similar plots (Holt, 1987).
A9.2.3.2 Invertebrates
No data were available.
A9.2.3.3 Vertebrates
No data were available.
A10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
A10.1 Evaluation of human health risks
Diesel fuel is produced commercially in various qualities with
regard to volatility, aromaticity, cetane number, and sulfur content.
The composition of diesel fuel, which influences the type and amount
of compounds emitted in the exhaust, has not changed greatly during
the last few decades, although the cetane number has been slightly
increased, resulting in better ignition, and the sulfur content, which
influences the release of particulate matter, has been reduced in some
countries. Owing to the lack of data on diesel fuel, some data on
heating oils and kerosenes (jet fuels) with compositions similar to
that of diesel fuel are included in the evaluations of toxicological
and environmental effects.
A10.1.1 Exposure of the general population
The general population can be exposed to diesel fuel and other
middle distillates at filling stations, as a result of accidental
spills, when handling such fuels, or when using kerosene for domestic
cooking or heating. No data on exposure were available.
A10.1.2 Occupational exposure
Workers can be exposed to diesel fuel and other middle
distillates during manual handling and discharge of the fuel, i.e.
during retailing at filling stations; manufacture, repair,
maintenance, and testing of diesel engines and other equipment; in
jobs where diesel fuel is used as a cleaning agent or solvent; and in
the handling and routine sampling of diesel fuel in the laboratory. At
room temperature, very low concentrations of vapours are likely to be
generated from diesel fuel because of its low volatility; significant
levels of vapour are likely to occur only in confined spaces and at
high temperatures.
A10.1.3 Non-neoplastic effects
Diesel fuels are toxic when ingested, usually accidentally.
Ingestion may result in regurgitation and aspiration, which can cause
chemically induced pneumonia. The latter effect is, however, not
specific for diesel fuel and can occur with all hydrocarbons of a
particular viscosity range.
Exposure to vapours is minimal during normal handling of diesel
fuel. The most likely effect on human health is dermatitis as a result
of skin contact. Dermal absorption takes place and can result in acute
toxic effects on the kidney. The health effects of long-term
absorption of low levels are unknown, but the available data on acute
human toxicity indicate that practices such as washing hands in diesel
fuel should be avoided. Although groundwater contamination and entry
into drinking-water are potential sources of adverse health effects,
such contamination would be noticeable and affect palatability so that
inadvertent ingestion of contaminated drinking-water is unlikely.
In experimental animals, diesel fuel has little acute toxicity after
exposure orally, dermally, or by inhalation. The oral LD50 values in
rats were > 5000 mg/kg body weight and those in mice, rabbits, and
guinea-pigs even higher. After short-term dermal exposure of mice for
14 consecutive days, the NOAEL for two middle distillates (marine
diesel and JP-5 navy fuel) was 5000-8000 mg/kg body weight per day.
Inhalation of up to 0.2 mg/litre had a neurodepressive effect in mice
but not in rats. Subchronic exposure to various distillate fuels
induced mainly alpha2-microglobulin nephropathy in male rats, which is
not considered relevant for humans.
Female mice that received dermal applications of 250 or 500 mg/kg
body weight per day of marine diesel fuel or JP-5 navy fuel on five
days per week for 103 weeks showed decreased survival due to severe
ulceration. Rats and mice exposed by inhalation to 1 or 5 mg/litre had
significant alterations in organ weight.
Diesel fuel irritates the skin but not the eye.
Exposure to diesel or jet fuels orally or by inhalation was
neither embryotoxic nor teratogenic in rats; although doses toxic to
the dams reduced fetal weight, no effects on viability were seen.
No clear evidence of mutagenic activity was seen in a series of tests
in Salmonella typhimurium. A positive response achieved only under
special conditions appeared to be equivocal. Other tests for
genotoxicity in vitro or in vivo did not show clearly positive
responses.
Owing to lack of data, a quantitative risk assessment is not
possible.
A10.1.4 Neoplastic effects
A case-control study of cancers at several sites in relation to
exposure to diesel fuel suggested an increased risk for lung cancer
other than adenocarcinoma and for prostatic cancer. In neither case
was there an exposure-response relationship. As few studies were
available, the number of cases was small, and the confidence intervals
were correspondingly wide, no conclusion can be drawn at present about
the carcinogenicity to humans of diesel fuel.
Twelve studies of dermal carcinogenicity in animals demonstrated
that diesel fuels have weak carcinogenic potency in mice. As no clear
genotoxicity is seen, cancer may be induced by nongenotoxic
mechanisms, such as chronic dermal irritation characterized by
repeated cycles of skin lesions and epidermal hyperplasia.
A10.2 Evaluation of effects on the environment
Although there are numerous data on the environmental behaviour
of the individual components of diesel fuel, few data are available
on diesel fuel as a whole. The environment can be polluted by
accidental release of diesel fuel on a large scale, such as during
tanker disasters and pipeline leaks, or on a smaller scale, from
contamination of soil around factories and garages.
In water, diesel fuel spreads out almost immediately, polar and
low-relative-molecular-mass components dissolve and leach out of the
slick, volatile components evaporate from the water surface, and
microbial degradation begins. The extent to which such 'weathering'
takes place depends on the temperature and climatic conditions, and
the chemical composition of spills changes with time. After spillage
on water, some fractions evaporate, and the evaporated diesel
components are degraded photochemically. In sediment, diesel fuel is
generally delivered to bottom sediments by settling particles. In
soil, the various components of diesel fuel migrate at different
rates, depending on the soil type.
The individual constituents of diesel fuel are inherently
biodegradable, but the rates depend greatly on the physical and
climatic conditions and microbial composition. PAHs are the most
recalcitrant molecules.
Aquatic organisms, in particular molluscs, bioaccumulate
hydrocarbons to various extents, but the hydrocarbons are depurated on
transfer to clean water. Bioaccumulation of diesel fuel may occur, but
there are few data to indicate biomagnification.
Although there have been a number of spills of diesel fuel, few
reports are available on their environmental effects. Generally,
diesel fuel is more toxic than crude oil to aquatic and plant species.
Spills of diesel fuel have an immediate detrimental effect on the
environment, causing substantial mortality of biota; recolonization
occurs after about one year, depending on the animal and plant species
involved and the chemical and physical content of the spill residues.
Aquatic organisms that survive diesel fuel spills can still be
affected by external contamination and tissue accumulation; abnormal
development and altered metabolic rates are signs of such stress.
There are few data on the effects of diesel fuel on aquatic and
terrestrial organisms in experimental situations. In studies of
water-soluble fractions and emulsions of diesel fuel, the actual
chemical composition has rarely been analysed, although this is
crucial to an understanding of the toxicity of diesel fuel. No data
are available about flow-through conditions or mesocosms, which better
reflect environmental conditions
A11. RECOMMENDATIONS
A11.1 Recommendations for the protection of human health
Exposure to diesel fuel may cause irritation and dermatitis;
therefore, skin contact should be avoided, and diesel fuel should not
be used for cleaning purposes.
A11.2 Recommendation for the protection of the environment
As for all petroleum products, accidental releases to the
environment should be avoided and should be cleaned up as soon as
possible if they occur.
A11.3 Recommendations for further research
A basic data set on the aquatic toxicity of diesel fuels,
including complete analysis of test substances, should be generated.
The fate and environmental impact of diesel fuel spills and leakages
should be investigated in laboratory and controlled field studies.
The exposure of humans to diesel fuel in various situations should be
quantified.
The mechanism of the carcinogenic action of diesel fuel on the
skin of experimental animals should be clarified.
A12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
The carcinogenic risks of diesel fuels for human beings were
evaluated by a working group convened by the International Agency for
Research on Cancer in 1988 (International Agency for Research on
Cancer, 1989a). It concluded that there was inadequate evidence for
the carcinogenicity of diesel fuels in humans, and there was limited
evidence for the carcinogenicity of marine diesel fuel in experimental
animals.
PART B
B1. SUMMARY
B1.1 Identity, physical and chemical properties, and analytical
methods
Diesel engine exhaust emissions contain hundreds of chemical
compounds, which are emitted partly in the gaseous phase and partly in
the particulate phase of the exhaust. The major gaseous products of
combustion are carbon dioxide, oxygen, nitrogen, and water vapour;
carbon monoxide, sulfur dioxide, nitrogen oxides, and hydrocarbons and
their derivatives are also present. Benzene and toluene are present in
the lower weight percent range in the gaseous part of the hydrocarbon
fraction. Other gaseous exhaust components are low-relative-molecular-
mass polycyclic aromatic hydrocarbons (PAHs).
A main characteristic of diesel exhaust is the release of
particles at a rate about 20 times greater than that from
gasoline-fuelled vehicles. The particles are composed of elemental
carbon, organic compounds adsorbed from fuel and lubricating oil,
sulfates from fuel sulfur, and traces of metallic components. Most of
the total particulate matter appears to occur in the submicrometre
range, between 0.02 and 0.5 µm. Agglomeration may occur during aging,
up to a maximal diameter of 30 µm. The emitted particles have a large
surface area. Organic compounds generally contribute 10-30% of the
total particulate matter, but poorly designed and maintained engines
may result in as much as 90%. Higher-relative-molecular-mass,
oxygenated and nitro-PAHs occur at concentrations of parts per million
in this fraction.
Specific transient or steady-state driving cycles are used in
measuring vehicle emissions. The exhaust can be sampled from undiluted
or diluted exhaust gas. It is difficult to obtain artefact-free
samples, as exhaust constituents can undergo chemical reactions,
adsorption and desorption processes, and condensation and diffusion.
The toxicologically relevant PAHs in diesel particulate matter are
usually determined by Soxhlet extraction, clean-up, and fractionation,
with subsequent analysis by high-performance liquid chromatography or
gas chromatography coupled with mass spectrometry.
B1.2 Sources of human and environmental exposure
Diesel engine exhausts are emitted mainly from motor vehicles;
other sources are stationary, railway locomotive, and ship diesel
engines. The emissions from diesel motor vehicles have been well
described, but the individual results are often not comparable owing
to differences in parameters such as driving cycle, engine type, and
fuel composition. The individual components are emitted in the
following quantities: carbon dioxide, about 1 kg/km; carbon monoxide,
nitrogen oxides, total gaseous hydrocarbons, and particulate matter,
0.1-20 g/km; and aliphatic compounds, alcohols, aldehydes, light
aromatics, and PAHs, micrograms per kilometer. The emissions of carbon
monoxide, nitrogen oxides, total gaseous hydrocarbons, and particulate
matter are regulated by law in a number of countries.
In principle, there is no difference between the quality and
quantity of exhaust emissions from light- and heavy-duty engines,
although heavy-duty vehicles release larger relative amounts of
particulate matter. Exhaust emissions depend on driving cycle
(transient or steady state), engine conditions (injection and
aspiration techniques, maintenance, total mileage), and fuel
composition (sulfur content, aromaticity, volatility); adjustment of
the engine plays a major role.
The release of particulate matter increases with decreasing
air:fuel ratio, increasing load, and increasing temperature. More
particulate is released from older, intensively used engines than from
new, low-mileage engines, probably because of a greater consumption of
lubricating oil. The emission of particles from light-duty diesel
vehicles is also correlated with the sulfur content of the fuel, as
the formation of metal sulfates increases the particle mass; particle
emissions from heavy-duty vehicles have not yet been established.
Increasing fuel aromaticity also increases particle emissions.
PAHs and oxygenated PAHs from diesel and spark-ignition engines
are qualitatively similar. Oxygenated and nitrated PAHs are emitted in
the low microgram per kilometer range, but the actual concentrations
of these compounds are uncertain, as decomposition and formation can
occur during sampling. PAH emissions increase with increasing load and
temperature and with the age of the engine, probably owing to
increased consumption of lubricating oil. PAH emissions also depend on
the injection technique of the engine: they increase with increasing
air:fuel ratio in engines with direct injection, whereas they decrease
in engines with indirect injection. The aromaticity and volatility of
the fuel are directly correlated with the emission of PAHs.
Malfunction of engine devices, especially the fuel injection system,
increases the emission of the main exhaust components. There are few
data on the contribution of diesel motor emissions to the total
man-made release of combustion products.
Diesel exhaust emissions can be reduced by improving engine
design and by use of particle traps (trap oxidizers) and catalytic
converters. While particle traps remove both the soot and soluble
organic compounds adsorbed onto the particles, catalytic converters
reduce the levels mainly of carbon monoxide and gaseous hydrocarbons.
In practice, it is dificult to regenerate particulate traps. Catalytic
converters require fuels with a low sulfur content, as sulfur poisons
the active centres of the catalyst.
B1.3 Environmental transport, distribution, and transformation
The compartment first affected by diesel exhaust emissions is the
atmosphere. The hydrosphere and geosphere are contaminated indirectly
by dry and wet deposition. The environmental fate of the individual
constituents of diesel exhaust is generally well known: Particles
behave like (non-reacting) gas molecules with regard to their
mechanical transport in the atmosphere; they may be transported over
long distances and even penetrate the stratosphere. The overall
removal rate of diesel particles is estimated to be low, resulting in
an atmospheric lifetime of several days. During aging, particles may
coagulate, with higher fall-out rates, thus reducing the total
airborne level. The elemental carbon of diesel particulates may act as
a catalyst in the formation of sulfuric acid by oxidation of sulfuric
dioxide. The organic components adsorbed on elemental carbon may
undergo a number of physical and chemical reactions with other
atmospheric compounds and during exposure to sunlight.
B1.4 Environmental levels and human exposure
As diesel exhaust is a complex mixture of a great variety of
compounds, general 'environmental levels' cannot be given. The
individual components of diesel exhaust should be detectable in all
compartments of the environment, although their source cannot usually
be verified. The environmental levels of most of the individual
constituents are known.
The general population is most likely to be exposed to diesel
exhaust in busy streets or parking areas, particularly underground.
The identification of sources is difficult, and the contribution of
diesel exhaust to total pollution by traffic combustion products is
generally calculated on the basis of emission factors and the
percentage of diesel-fuelled vehicles. The levels of exposure of the
general population and workers to diesel particulate matter are
toxicologically relevant. The daily average ambient concentrations of
diesel particulates near roads are 8-42 µg/m3. The estimated annual
average concentrations were 5-10 µg/m3 in urban areas and
< 1.5 µg/m3 in rural areas in Germany and 1-2 µg/m3 in urban
areas and 0.6-1 µg/m3 in rural areas in the United States of America.
The concentrations are directly correlated with traffic density and
decrease with increasing distance from roads. Identification of
sources may also be difficult in work-places, especially in mines,
where the total dust burden is high. Carbon core analysis has been
used to determine specific exposure to diesel exhaust in the
work-place, and the levels of particulate matter to which workers are
exposed have been reported to be 0.04-0.134 mg/m3 for truck drivers
and 0.004-0.192 mg/m3 for railroad workers. Total respirable
particles and total suspended particles have also been used as
measures of occupational exposure.
B1.5 Kinetics and metabolism in laboratory animals and humans
B1.5.1 Deposition
Diesel exhaust particles, with a mass median aerodynamic diameter
of about 0.2 µm, undergo some filtration in the nose, and the
deposition efficiency in the lung is only slightly greater than the
minimal value found for particles with a mass median aerodynamic
diameter of about 0.5 µm. Thus, 10-15% of inhaled diesel soot
particles are deposited in the alveolar region of the lung of rats and
guinea-pigs; in humans, about 10% is deposited in the alveolar region.
B1.5.2 Retention and clearance of particles
Mucociliary clearance of particles from ciliated airways is
almost complete within 24 h. The long-term clearance of diesel
particles from the alveolar region was measured in several studies in
rats exposed by inhalation to labelled diesel or test particles.
Half-times of 60-100 days were reported for controls with low lung
burdens (< 1 mg/lung), whereas the half-times increased to 100-600
days in rats with lung burdens increasing from 1 to 60 mg/lung. In
several studies, effects were seen to be caused by particle overload,
which has been described in a variety of species and with a number of
particulate materials. The phenomenon is generally observed when the
deposition rate of particles of low solubility and low acute toxicity
exceeds their clearance rate for a considerable time. The half-time of
unimpaired alveolar clearance in humans is several hundred days, which
is longer than that in rats.
A dosimetric lung model was developed on the basis of data on the
deposition and retention of diesel particles in rats after long-term
inhalation and of data on particle deposition and retention in humans.
The model can be used to predict retention of diesel particles and
adsorbed organic material in the lungs of people of different ages. No
data are available on changes in the retention of individual compounds
after prolonged exposure to diesel exhaust.
B1.5.2 Retention and clearance of polycyclic aromatic hydrocarbons
adsorbed onto diesel soot
PAHs in diesel soot adhere strongly to the surface of particles.
About 50% of the PAHs adsorbed onto diesel particles is cleared from
the lung within one day, but the retention half-times for the
remaining PAHs were 18-36 days. Studies with 3 H-benzo[ a]pyrene and
14C-nitropyrene show that when PAHs are associated with particulate
matter, their clearance from the lungs is significantly delayed in
comparison with the clearance of inhaled PAHs not associated with
particulate matter.
B1.5.4 Metabolism
Benzo[ a]pyrene coated on diesel exhaust particles was metabolized
by oxidation to benzo[ a]pyrene phenols, diols, and quinones in the
lung and in cell cultures of pulmonary macrophages. Nitropyrene
adsorbed to diesel particles was metabolized to acetylaminopyrene-
phenol after inhalation. More DNA adducts were found in the lungs and
type II cells of rats exposed to diesel exhaust than in controls. The
oxidative metabolism of some organic compounds to epoxides may be
responsible for the formation of these adducts, but adducts were found
only after exposure to particles. Certain organic substances in diesel
exhaust have been shown to be responsible for the formation of DNA
adducts; however, the carbonaceous core itself (without extractable
organic material) can also induce adducts, by chronic damage of
epithelial cells.
B1.6 Effects on laboratory mammals and in vitro test systems
The few data available suggest that diesel exhaust has little
acute toxicity. Mice treated intratracheally with diesel exhaust
particles died due to lung oedema; the LD50 was about 20 mg/kg body
weight. Methanol-extracted diesel exhaust particles were not lethal a
concentrations up to about 33 mg/kg body weight. In hamsters, the LD50
after intraperitoneal administration was 1280 mg/kg body weight. No
data are available for exposure by inhalation.
Exposure of rats, guinea-pigs, and cats to diesel exhaust with a
particle content of 6 mg/m3 for about four weeks altered lung
function, including a 35% increase in pulmonary flow resistance in
guinea-pigs and a 10% decrease in vital capacity (expiratory flow) in
cats. Histopathologically, focal thickening of alveolar walls, a
significantly increased type-II cell labelling index, and
accumulations of particleladen macrophages were found. The
accumulations were located near the terminal bronchioles and became
larger, due to macrophage attachment (sequestration), during a
subsequent recovery period.
Mice, rats, hamsters, cats, and monkeys did not have drastic
decreases in body weight or reduced survival times after long-term
inhalation of up to 4 mg/m3 . Dose-related toxic effects seen in all
species after long-term inhalation of diesel exhaust were: increases
up to 400% in lung weight; pulmonary inflammation measurable by
biochemical (cytoplasmic marker enzymes, collagen) and cytological
(increase in polymorphonuclear neutrophils) parameters; impairment of
lung mechanics; increasing numbers of particle-laden macrophages with
focal accumulations (sequestration) under overload conditions; and
subsequent proliferative alterations of epithelial cells and onset of
fibrosis.
Limited information on reproductive and developmental toxicity
suggests that inhalation of diesel exhaust is not critical. In most
experiments, no effects were seen in mice, rats, hamsters, rabbits, or
monkeys; however, after intraperitoneal injection, sperm abnormalities
were seen in mice given diesel exhaust particles and embryotoxicity
occurred in hamsters given diesel exhaust extract.
Most tests for genotoxicity in vitro have been performed with
diesel exhaust extracts rather than with total exhaust; positive
responses were found in the absence of metabolic activation, i.e. the
genotoxic effects appeared to be PAH-independent. About one-half of
investigations in vivo gave negative responses; the only positive
responses were sister chromatid exchange induction with total diesel
exhaust and with organic extracts and micronucleus induction with
organic extracts.
Immunotoxic effects were generally not seen after inhalation of
diesel exhaust; however, an enhanced anti-ovalbumin immunoglobulin E
antibody titre was seen in one study and an increased susceptibility
to infections in mice in two experiments. Studies in rats suggested
that inhalation of diesel exhaust affects behavioural and
neurophysiological status.
In studies of the carcinogenicity of diesel exhaust administered
by inhalation to rats, the gaseous phase (without the particulate
fraction) was not carcinogenic. In all valid studies in rats, diesel
exhaust was found to be carcinogenic at particle concentrations of >
2 mg/m3, corresponding to an equivalent continuous exposure of about
1mg/m3. No effect was seen in hamsters or mice. In studies by
intratracheal instillation, both diesel exhaust particles and carbon
black induced tumours, and the surface area of the carbonaceous
particles appeared to be correlated with the tumorigenic potency.
Long-term inhalation of carbon black virtually devoid of PAHs at
similar concentrations also resulted in lung tumours in rats.
It is not clear whether the carcinogenicity of diesel exhaust
involves DNA-reactive or non-DNA-reactive mechanisms (or a
combination). Various models have been used to elucidate the
carcinogenicity of diesel exhaust.
B1.7 Effects on humans
Diesel exhaust contributes to air pollution in general. Although
the role of diesel particles cannot be singled out in acute or chronic
studies, they may be partly responsible for the range of health
effects found to be associated with air pollution.
Typical diesel exhaust has a characteristic odour, which some
people find offensive, particularly at high concentrations. The
symptoms seen after acute and chronic exposure to diesel exhaust have
been described in studies and anecdotal reports of occupationally
exposed subjects. Acute exposure to diesel exhaust has been associated
with irritation of the ocular and nasal mucous membranes, and an
increased frequency of respiratory symptoms has been observed in
occupational cohorts; however, the contribution of diesel particulates
is not known. No consistent short-term effect on pulmonary functions
has been found, but asthma attacks have been reported.
In a controlled study in which eight healthy non-smoking
volunteers were exposed to diluted diesel exhaust in a chamber for
60 min, the phagocytosis rate of alveolar macrophages in broncho-
alveolar lavage fluid was reduced.
Some cross-sectional and longitudinal studies on workers with
long-term occupational exposure to diesel exhaust show decrements in
lung function and an increased prevalence of respiratory symptoms, but
these studies are limited by short exposure. Cohort studies in which
deaths from cardiovascular and/or cerebrovascular disease due to
diesel emissions were investigated did not show a significant excess.
The relationships between cancers of the lung and of the urinary
bladder and occupational exposure to diesel exhaust have been
evaluated in a number of epidemiological studies. Only those studies
that were considered relevant for evaluating the carcinogenic effects
of diesel exhaust are included in this monograph. The most relevant
studies with regard to lung cancer are those of railroad workers, bus
garage workers, and stevedores, who have definite exposure to diesel
exhaust. The four most informative studies all reported an increased
risk for lung cancer, with relative risks ranging from 1.4 for
railroad workers and 1.3-2.4 for bus garage workers (depending on
exposure category), to a three- to sixfold increase in risk for
stevedores (depending on the exposure assessment used, but with wide
confidence intervals). Adjustment for smoking was possible in one
case-control study of railroad workers and in the study of stevedores,
and in both cases, the effect of diesel exposure was not materially
influenced. In the three studies in which smoking could not be
adjusted for, the analysis was based on comparisons of subgroups of
the cohorts, so that confounding by tobacco smoking was less likely
than when external comparison groups were used.
Several case-control studies have been conducted to examine the
relationship between urinary bladder cancer and presumed exposure to
diesel exhaust. An increased risk was found, especially for truck
drivers; however, all of these studies are limited by poor
characterization of exposure. Hence, a causative association between
exposure to diesel exhaust and an increased risk for urinary bladder
cancer cannot be established.
B1.8 Effects on other organisms in the laboratory and the field
The effect of diesel emissions as such have been addressed in
only one study, of green algae.
B1.9 Evaluation of human health risks
The risk assessment paradigm of the United States National
Academy of Sciences (US National Research Council, 1983) was used to
assess the risks for both cancer and non-cancer end-points. The four
steps in this process comprise: (1) hazard identification, (2)
dose-response assessment, (3) exposure assessment, and (4) risk
characterization.
Epidemiological studies of long duration with well-defined
exposure and follow-up (> 20 years) are considered to be the most
informative. Four studies of lung cancer in occupationally exposed
individuals met these criteria. The relative risks for lung cancer
associated with exposure to diesel exhaust were generally low and were
susceptible to chance, to the effects of unmeasured confounding
factours, and to the difficulty in accurately adjusting for known
confounding factors. Studies with less precise definitions of exposure
support the conclusions of these studies. Overall, it is considered
that diesel exhaust is probably carcinogenic to humans; however, no
quantitative data are available for estimating human risk.
B1.9.1 Non-neoplastic effects
Two general approaches were used for risk characterization: a
no-observed-adverse effect level (NOAEL) divided by an uncertainty
factor; and a benchmark concentration. In both approaches, a
sophisticated dosimetric model was used which decreases any
uncertainty in interspecies extrapolation of dose.
The no-effect level of diesel exhaust particles in humans was
calculated to be 0.139 mg/m3. The guidance value for the general
population calculated from the dosimetric model was 5.6 µg/m3, and
that calculated without the model was 2.3 µg/m3.
The benchmark concentration approach takes into account the
entire exposure-response relationship rather than relying on a single
data point from studies by inhalation, as in the NOAEL approach. Three
sensitive end-points were identified: chronic alveolar inflammation,
impaired lung clearance, and hyperplastic lung lesions. The benchmark
concentrations, calculated from the same dosimetric model used in the
NOAEL approach, were 0.9-2 µg/m3for inflammation, 1.2-3 µg/m3 for
impaired lung clearance, and 6.3-14 µg/m3 for hyperplastic lesions.
B1.9.2 Neoplastic effects
A linearized multistage model was used to estimate unit risks due
to exposure to diesel exhaust. Because the results of the available
epidemiological studies were considered inadequate for a quantitative
estimate of unit risk, data from several studies of long-term
inhalation in rats were used in which carcinogenesis occurred at
concentrations >2 mg/m3. A unit risk of 3.4 × 10-5 µg/m3 (geometric
mean of four risk estimates) diesel exhaust particles was calculated.
An alternative biologically based model yielded a similar unit risk,
under the assumption that diesel particles affect cell initiation
and/or proliferation at low concentrations.
B1.10 Evaluation of effects on the environment
Insufficient information was available to evaluate the specific
effects of diesel exhaust emissions. The effects of combusted diesel
fuel should be similar to those of other fossil fuels and are related
to the consumption of diesel fuel.
B2. IDENTITY AND ANALYTICAL METHODS
B2.1 Identity
Diesel engine emissions contain hundreds of chemical compounds,
which are emitted partly in the gaseous phase and partly in the
particulate phase of the exhaust. These substances form particles or
contribute to the gaseous phase of the emissions, depending on vapour
pressure, temperature, and the concentration of individual species.
The amount and composition of diesel exhaust are related to engine
conditions and fuel specifications (see sections B3.1.2.1 and
B3.1.2.2). A total of 445 compounds has been identified or tentatively
identified as constituents of diesel exhaust emissions (Westerholm,
1987).
Diesel exhaust has an offensive odour (odour threshold, 320 ppm).
Compounds with a relative molecular mass > 80 mainly determine the
odour (Scheepers & Bos, 1992b). Partridge et al. (1987) concluded that
benzaldehyde and a methylbenzaldehyde isomer are the major substances
responsible; unburnt aromatic hydrocarbons may also contribute.
Aldehyde levels and odour emissions are directly correlated with the
total hydrocarbon content of the exhaust; decreased hydrocarbon levels
lead to diesel exhaust with less odour (Organisation for Economic
Co-operation and Development, 1993).
B2.1.1 Chemical composition of diesel exhaust gases
The main gaseous products of diesel exhaust are carbon dioxide,
oxygen, nitrogen, and water vapour; carbon monoxide, sulfur dioxide,
nitrogen oxides, and hydrocarbons and their derivatives are also
present. A representative composition of diesel exhaust gas
(light-duty engine) is shown in Table 21.
The levels of carbon monoxide, nitrogen oxides, total
hydrocarbons, and particulates emitted by diesel engines are regulated
by law in a number of countries (see section B3.2). The composition of
diesel exhaust gases is similar to that of gasoline engine gases, but
because of the relatively higher fuel:air ratio, carbon monoxide and
hydrocarbons occur in lower concentrations in diesel exhaust, and the
emission of nitrogen oxides, particulate matter, and sulfur compounds
is higher (the latter being due mainly to the higher sulfur content of
diesel fuels). The relative concentrations in the aldehyde fraction
are as follows: about 45% by weight formaldehyde, 17% by weight
acetaldehyde, 14% by weight acetone and acrolein, < 10% by weight
crotonaldehyde, propionaldehyde, isobutyraldehyde, benzaldehyde, and
hexanaldehyde; methylethylketone is also present (Volkswagen AG,
1989).
Table 21. Composition of light-duty diesel engine exhaust
Component Concentration
(% by weight)
Carbon dioxide 7.1
Water vapour 2.6
Oxygen 15.0
Nitrogen 75.2
Carbon monoxide 0.03
Hydrocarbons 0.0007
Nitrogen oxides 0.03
Hydrogen 0.002
Sulfur dioxide 0.01
Sulfates 0.00016
Aldehydes 0.0014
Ammonia 0.00005
Particulates 0.006
Adapted from Volkswagen AG (1989)
Diesel exhaust contains toxicologically relevant compounds such
as benzene, toluene, ethylbenzene, xylene, and PAHs. In the
hydrocarbon fraction, benzene and toluene are present in relative
concentrations of 11 and 4% by weight, respectively (Volkswagen AG,
1989).
Possible sources of PAHs in diesel exhaust are unburnt PAHs from
the fuel, pyrosynthesis of PAHs during combustion, crankcase oils, and
engine and/or exhaust system deposits (Scheepers & Bos, 1992a). These
constituents occur partly in the gaseous fraction of total
hydrocarbons (benzene, toluene, ethylbenzene, and xylene components,
PAHs of lower relative molecular mass) and partly in the particulate
fraction due to adsorption (PAHs of higher relative molecular mass).
The partitioning of constituents between the particulate and gas
phases has been measured by several investigators (Hampton et al.,
1983; Schuetzle, 1983; Schuetzle & Frazier, 1986). Most PAHs with five
or more rings and aliphatic hydrocarbons with more than 18 carbon
atoms are expected to be primarily adsorbed onto particles (Schuetzle,
1983). There is a direct relationship between adsorption behaviour and
vapour pressure (Hampton et al., 1983); compounds with vapour
pressures < 10-5 mbar (7.5 × 10-6 mm Hg; 2.09 kPa) at room
temperature occur predominantly in the particulate phase. An empirical
relationship between boiling-point and particle- to gas-phase
partition coefficients has been derived for PAHs and aliphatic
hydrocarbons in order to estimate gas-phase emission rates (Schuetzle
& Frazier, 1986). According to this equation, the concentration of
e.g. anthracene in the gaseous phase is about 20 times higher than
that in the particle phase, whereas the levels of e.g. pyrene and
fluoranthene are nearly equal in the two phases. Oxygenated PAHs are
found in diesel engine exhaust at concentrations as high (Volkswagen
AG, 1989) or twice as high (Jensen & Hites, 1983) as those of their
parent PAHs, perhaps because these engines have a larger air:fuel
ratio than gasoline motors (Scheepers & Bos, 1992a). 9-Fluorenone and
9,10-anthracenequinone are especially abundant in diesel exhaust
(Schuetzle & Frazier, 1986). In tests of diesel passenger cars by
Volkswagen AG (1989), phenalene-1-one, naphthalene dicarboxylic acid
anhydride, cyclopenta[ def]phenanthrene-4-one, monoaldehydes of
phenanthrene and anthracene, mono- and diketones of benzanthracenes
and benzo[cd]pyrene, and benzofluorenones were also found (for
artefact formation during sampling, see section B2.2.1; for emission
factors, see section B3.1.1.1).
Nitrogen-substituted PAHs are formed during combustion as a
result of either nitration of PAHs by nitric acid or addition of
nitrogen monoxide or dioxide to PAH free radicals generated during
combustion (Schuetzle, 1983). In the exhaust of a four-cylinder diesel
engine, nitrofluorene, dinitrofluorenone, nitroanthracene,
nitrofluoranthene, mono- and dinitropyrenes, and nitrobenzo[ a]pyrene
were detected at concentrations about one order of magnitude lower
than those of oxygenated PAHs (Volkswagen AG, 1989).
A number of investigators have found nitrated PAHs in extracts of
diesel engine exhaust particles (Handa et al., 1983; Hartung et al.
1984). Many three-, four-, and five-ring structures are involved
(Schuetzle et al., 1982). The concentration of 1-nitropyrene, one of
the prevalent species, has been reported to be 15-25 mg/kg particulate
matter, whereas benzo[ a]pyrene has been found at concentrations up
to 50 mg/kg. The nitrated PAHs are important in determining the health
effects of exposure to diesel exhaust, since they are effective
mutagens in microbial and human cell systems (Pederson & Siak, 1981;
Pitts et al., 1982; Patton et al., 1986). Some nitrated PAHs are
carcinogenic to animals (Ohgaki et al., 1985; Imaida et al., 1991).
Combustion products originating from fuel and lubricating oil
additives or from corrosion may also occur. For example, nitrate-based
cetane improvers (see also section A2.1.2) are assumed to form nitro-
PAHs (Organisation for Economic Co-operation and Development, 1993).
B2.1.2 Type and composition of emitted particulate matter
Diesel exhaust is characterized by a higher content (10-20-fold)
of particulate matter than that of gasoline-fuelled passenger cars
(Egebäck & Bertilsson, 1983; Volkswagen AG, 1989; Williams et al.,
1989; CONCAWE, 1990b; Hammerle et al., 1994a). How soot particles are
formed is still under discussion, but the precursor is probably
acetylene generated during combustion. As a result of the numerous
cracking, dehydration, and polymerization processes, quite large
amounts of carbon, hydrogen, hydroxyl, and oxygen radicals are
available in the combustion chamber, which can produce cyclic and
polycyclic aromatic hydrocarbons from acetylene by polymerization and
ring closure. With increasing polymerization, the carbon content of
the macromolecule increases, finally generating graphite-like soot
particles (Klingenberg et al., 1991).
Investigations of two four-cylinder engines with direct and
indirect injection (see also section B3.1.2.1) showed that the emitted
particles range in shape and size from spherical particles of
< 0.01 µm to cluster and chain agglomerates with maximal dimensions
of 30 µm (Dolan et al., 1980; Amann & Siegla, 1982; Klingenberg et
al., 1991). The formation of agglomerates (coagulation, 'aging') is
dependent not only on engine and exhaust conditions but also on
environmental factors, such as photochemical processes and humidity.
Between 50 and 80% of the total particulate emission occurs in the
range of 0.02-0.5 µm (Israel et al., 1982). According to Amann &
Siegla (1982), the emitted particles have a concentric, lamellar
structure arranged around the centre, similar to the structure of
carbon black.
Emitted soot particles are composed of elemental carbon, adsorbed
organic compounds (soluble organic fraction) from fuel and lubricating
oil, traces of metallic compounds (iron, calcium, and zinc at < 0.6%
by weight; Volkswagen AG, 1989), and sulfates. The organic components
of emitted particles are distributed over the surface. Numerous data
on the relative proportions of organic compounds are available
(Horvath et al., 1987; Williams et al., 1987; Volkswagen AG, 1989;
Williams et al., 1989; CONCAWE, 1992). Depending on the engine
conditions and testing cycle, the organic compounds comprise 10-90% of
the total particulate mass. The ranges of various constituents of
particulate matter in nine light-duty and four heavy-duty vehicles
(see also section B3.1.2.1) are shown in Table 22. The driving cycles
used were combined European Union tests (ECE-15 and 'high speed'
extra-urban driving cycle [EUDC]) for the light-duty vehicles and
modified ECE-R49 tests for the heavy-duty engines (see also section
B2.2.1); four fuels with different sulfur contents and an aromatic
content of about 25% by volume were used (CONCAWE, 1992). (For a
description of the influence of fuel composition on exhaust emissions,
see section B3.1.2.2.)
This study showed considerable variation, and no obvious
influence of fuel composition or engine conditions was discernible,
although a difference was seen between fuel and lubricating oil
hydrocarbons derived from light- and heavy-duty vehicles,
respectively. This is probably due to the different driving cycles:
transient in the case of light vehicles, steady state in the case of
heavy-duty engines. In the individual data, adjustment of the engine
appeared to play a major role. In the same study, PAHs were determined
in the soluble organic fraction of the exhausts of three light-duty
vehicles representing different engine conditions and of the four
heavy-duty engines. The data are shown in Table 23. The constituents
of the particulate matter of the exhaust are clearly dependent on the
driving cycle used. Under steady-state conditions (heavy-duty
engines), the PAH content is about one order of magnitude lower than
that under transient conditions (light-duty vehicles). In addition,
transient conditions lead to considerable variations in levels. In the
study of Volkswagen AG (1989) on a four-cylinder diesel engine in the
US-72-test, a hot start was used, and higher levels of fluoranthene,
pyrene, benzo[ ghi]fluoranthene and benzo[ c]phenanthrene were
found, perhaps due to either engine condition or driving cycle.
According to Volkswagen AG (1989), some of the PAHs, and especially
pyrene, benz[ a]anthracene and benzo[ a]pyrene, seemed to decompose
during sampling (see section B2.2.1).
Table 22. Particulate matter content of exhausts from light- and heavy-duty vehicles
Constitutent Particulate matter (% by weight) Reference
Light-duty vehiclesa Heavy-duty vehiclesa
Carbon 32.6-85.1 39.7-81.7 CONCAWE (1992)
82-88 (passenger 68-89 Williams et al.
cars) (1989)b
76-83 (light vans)
60-75 Hammerle et al.
(1994a)c
Fuel-derived 1.1-55.0 9.8-32.5 CONCAWE (1992)
hydrocarbons 6.0-18 Hammerle et al.
(1994a)c
Lubricating 4.2-54.4 4.0-25.9 CONCAWE (1992)
oil-derived 5.7-15 Hammerle et al.
hydrocarbons (1994a)c
Soluble organic 10.2-64.7 14.0-58.4 CONCAWE (1992)
fraction 14-26 (passenger 22-90 Williams et al.
cars) (1989)b
36-48 (light vans)
Sulfate (excluding 0.6-12.2 1.4-7.5 CONCAWE (1992)
bound water) 3.3 (passenger 0.3-6.9 Williams et al.
cars) (1989)b
2.5 (light vans) 1.5-2.0 Hammerle et al.
(1994a)c
a According to the Organisation for Economic Co-operation and Development (1993),
light-duty vehicles are generally classified as vehicles with a weight < 3.5 t,
occasionally < 5 t; heavy-duty vehicles are those weighing > 5 t.
b Measurements for four passenger cars and 15 light vans in different Australian
driving cycles corresponding roughly to US-FTP-72 and -75 tests for heavy-duty
vehicles, and 10 trucks and two buses in one Australian urban traffic driving cycle
c Five passenger cars and light vans in European Motor Vehicle Emissions group cycle
and US-FTP-75 test
Table 23. Polycyclic aromatic hydrocarbon content of the soluble organic fraction of
particulate matter in diesel exhaust
Constituent Soluble organic fraction Referenceb
(mg/kg particulate matter
Light-duty Heavy-duty
vehiclesa vehicles
Fluoranthene 8-238 4-52 CONCAWE (1992)
553-560 Volkswagen AG (1989)
Pyrene 11-287 7-90 CONCAWE (1992)
579-668 Volkswagen AG (1989)
Benzo[ghi]fluoranthene 36-61 3-6 CONCAWE (1992)
+ benzo[c]phenanthrene 163-179 Volkswagen AG (1989)
Benz[a]anthracene 9-285 1-16 CONCAWE (1992)
61-82 Volkswagen AG (1989)
Triphenylene and 14-138 4-13 CONCAWE (1992)
chrysene 117-138 Volkswagen AG (1989)
Benzo[b,j]fluoranthene 4-87 1-10 CONCAWE (1992)
180-193c Volkswagen AG (1989)
Benzo[a]fluoranthen 6-69 CONCAWE (1992)
Benzo[e]pyrene 8-40 1-2 CONCAWE (1992)
85-90 Volkswagen AG (1989)
Benzo[a]pyrene 2-48 1-3 CONCAWE (1992)
38-54 Volkswagen AG (1989)
Perylene 5-32 2 CONCAWE (1992)
4-8 Volkswagen AG (1989)
Dibenz[a,j]anthracene 10-78 CONCAWE (1992)
Indeno[123-cd]pyrene 6-54 CONCAWE (1992)
55-73 Volkswagen AG (1989)
Dinbenz[a,h]- or 3-40 CONCAWE (1992)
-[a,c]anthracene
Benzo[ghi]perylene 25-65 1-5 CONCAWE (1992)
75-82 Volkswagen AG (1989)
Anthracene 3-7 CONCAWE (1992)
Dibenz[a,i]pyrene 8-31 CONCAWE (1992)
Coronene and 9-52 CONCAWE (1992)
dibenzo[a,e]pyrene 33-48d Volkswagen AG (1989)
a According to the Organisation for Economic Co-operation and Development (1993),
light-duty vehicles are generally classified as vehicles with a weight < 3.5 t,
occasionally < 5 t; heavy-duty vehicles are those weighing > 5 t.
b From Volkswagen AG (1989): US-72 tests with one four-cylinder engine
c Including benzo[k]fluoranthene
d Excluding dibenz[a,e]pyrene
B2.2 Analytical methods
B2.2.1 Sampling
Driving cycles are specified to simulate on-road conditions for
measuring vehicle emissions (Grimmer et al., 1988). The test
procedures can be divided in two basic types: steady-state and
transient cycle tests. In the European Union and Japan, mainly
steady-state tests are used, in which emissions from engines are
measured at specified combinations of speed and load. The most widely
used official tests for light- and heavy-duty vehicles are as follows:
Light-duty vehicles:
* US FTP-75: transient cycle; cold start; driving distance, 17.8
km; 10-min break after 28.7 min (United States) (Volkswagen AG,
1989)
* US SET: transient cycle; 'sulfate emission test'; hot start;
simulating rush-hour freeway driving; driving distance, 21.7 km
(United States) (Volkswagen AG, 1989)
* ECE 15: transient cycle; cold start; simulating city-centre
driving; driving distance, 4.052 km (European Union) (CONCAWE,
1990a)
* US HDC: steady-state cycle; 'highway driving cycle'; hot start;
driving distance, 16.5 km; maximal speed, 96.4 km/h (United
States) (Volkswagen AG, 1989)
* EUDC: steady-state cycle; 'extra-urban driving cycle'; hot start
(after ECE 15); driving distance, 6.755 km; maximal speed,
120km/h (European Union) (CONCAWE, 1990a)
Heavy-duty vehicles:
* HD-FTP: transient cycle; 'heavy-duty federal test procedure';
simulating metropolitan driving (United States) (Organisation for
Economic Co-operation and Development, 1993);
* ECE 13: steady-state cycle at 13 different modes; identical to
ECE R49 (European Union) (Organisation for Economic Co-operation
and Development, 1993). Various bus cycles are also used to test
heavy-duty vehicles that are characterized by frequent
stop-and-go driving (Westerholm & Egebäck, 1991; Prakash et al.,
1992).
It is difficult to avoid artefacts in sampling. Exhaust gas
constituents can undergo chemical reactions, adsorption and desorption
processes, and condensation or diffusion. For example, oxygenated and
nitrated PAHs are chemically unstable, and artefacts may form on the
sampling device, especially if large sampling volumes are needed (Lee
& Schuetzle, 1983). Both decreases and increases in the concentrations
of PAHs and oxy-PAHs were observed during sampling in a study by
Volkswagen AG (1989); in particular, degradation of pyrene and
nitropyrene and formation of naphthalene dicarboxylic acid anhydride
on the filter occurred. PAHs can be converted into nitroarenes (Pitts
et al., 1978; Lee et al., 1980; Gibson et al., 1981; Lee & Schuetzle,
1983; Schuetzle & Perez, 1983; Gaddo et al., 1984; Levsen et al.,
1988).
The sampling techniques used for the collection of the gaseous
and particulate phases of diesel exhaust comprise dilution tube
sampling and raw gas sampling.
B2.2.1.1 Sampling from undiluted exhaust gas (raw gas sampling)
The device for sampling motor vehicle exhaust (total flow method;
Kraft & Lies, 1981; Grimmer et al., 1973) consists of a glass cooler,
a condensate separator, and a special micron filter of
paraffin-impregnated glass-fibre material providing separation of
> 99.9% of particles of 0.3-0.5 µm. The cooler is fed with cold tap
water, and the filter is placed on top of the cooler to remove any
uncondensed liquid or solid exhaust gas constituents that may pass
through the cooler coil. The particulate filter retains undissolved
particles of the exhaust gas, while the condensate consists of the
dissolved components (Volkswagen AG, 1989).
The US Environmental Protection Agency (Lies et al., 1986)
defines the 'particulate phase' as all materials (with the exception
of condensed water) which, at a temperature of < 51.7°C, are retained
on a special filter after dilution with air. Large volumes are
collected with this type of sampling, making analysis of trace
components difficult. The sample volumes are reduced by diverting the
exhaust emission flow and sampling only a part. It is difficult to
ensure a representative partial flow, as the amount of exhaust gas
produced varies considerably over time (Volkswagen AG, 1989).
B2.2.1.2 Sampling from diluted exhaust (dilution tube sampling)
The exhaust is mixed with ambient air in a dilution tunnel in a
constant volume sampler method (Behn et al., 1985). The total flow of
air and exhaust is kept constant with a suitable fan in a constant
volume sampler unit. This sampling technique more realistically
reflects the immediate dilution of exhaust leaving the tailpipe of
vehicles on the road. The concentrations of exhaust components are,
however, reduced in accordance with the degree of dilution (magnitude,
1:10), and components that are present only at low concentrations
cannot be determined.
There are various techniques for sampling gaseous constituents.
Substances present at sufficiently high concentrations are commonly
sampled in a plastic bag; adsorption onto solid materials, consisting
of extremely porous, tiny plastic pellets (e.g. Tenax; diameter,
0.1-0.2 mm; specific surface area, 20-50 m2/g), or absorption in
liquids are also used. Particulate constituents are sampled by
filtration (Lee & Schuetzle, 1983; Volkswagen AG, 1989).
B2.2.2 Extraction from particles
PAHs adsorbed onto diesel exhaust particles are of toxicological
relevance, and there are numerous methods for extracting these
constituents. The most frequently used method is Soxhlet extraction,
which permits extraction of 99% of the soluble organic fraction within
8 h; an additional 16 h are necessary to extract the remaining 1%.
Extraction is frequently carried out by sequentially changing the
solvents, from polar to nonpolar, e.g. toluene, toluene or n-propanol,
dichloromethane, and acetonitrile. PAHs may be further extracted by
refluxing the exhaust particulates in solvent for 1 h. Sublimation and
extraction by ultrasonic agitation are also used (Lee & Schuetzle,
1983; Levsen, 1988), and supercritical fluids such as carbon dioxide
are effective (Hawthorne & Miller, 1986). The extraction efficiency of
various solvents is still under discussion (Köhler & Eichhoff, 1967;
Swarin & Williams, 1980; Schuetzle & Perez, 1981; Grimmer et al.,
1982; Lee & Schuetzle, 1983; Schuetzle et al., 1985; Levsen, 1988).
Aromatic solvents and their combinations seem to be best suited for
extracting PAHs from diesel particulates (Levsen, 1988).
B2.2.3 Clean-up and fractionation
Complex fractionation schemes for separating the exhaust extract
into aliphatic compounds, aromatic compounds, and moderately and
highly polar fractions after the removal of acidic and basic fractions
have been described by Petersen & Chuang (1982) and Levsen (1992).
During fractionation, further artefacts may be produced by the
components of a complex sampling mixture like diesel exhaust,
especially with acidic and basic extraction and aggressive column
separation procedures.
B2.2.4 Chemical analysis
Chemical analysis of separated, cleaned compounds of diesel
exhaust involves numerous techniques, including thin-layer
chromatography, gas chromatography, gas chromatography with mass
spectrometric detection, and high-performance liquid chromatography
(US National Institute for Occupational Safety and Health, 1991).
Jinno et al. (1986) determined PAHs by supercritical fluid
chromatography with a photodiode array detector.
The detection methods vary widely and include ultra-violet,
visible, and fluorescence spectrophotometry, mass spectrometry, and
more or less specific devices, such as flame ionization, nitrogen
flame ionization, and sulfur-specific and electron-capture detectors
(US National Institute for Occupational Safety and Health, 1991). A
thermal optical method for determining elemental carbon is currently
being used as a surrogate for measurement of worker exposure in almost
all internal investigations at the US National Institute for
Occupational Safety and Health (Niemeier, personal communication,
1994).
Analytical methods are available for determining the organic
constituents of diesel particulate matter, with special emphasis on
the determination of PAHs and their nitrated and oxygenated
derivatives (Levsen, 1988).
B2.3 Conversion factors
Because diesel exhaust emissions are complex mixtures of
different gases and particles, it is impossible to give a conversion
factor for converting parts per million to SI units.
B3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
B3.1 Anthropogenic sources
Diesel exhaust emissions are exclusively man-made and are
distributed primarily in the atmosphere. The hydrosphere and geosphere
may also be affected owing to dry and wet deposition of the exhaust
constituents; however, determination of the source of deposited
compounds is difficult. No data are available on the individual
components of diesel exhaust and their deposition.
B3.1.1 Diesel exhaust emissions
Diesel fuels are widely used as transport fuels, and exhaust
emissions are released mainly by road traffic. Although many
investigations of these emissions have been reported, the individual
results are frequently not comparable because the experimental
parameters, e.g. driving cycles, are different, or different
dimensions were chosen. For example, the results of tests on emissions
from light-duty vehicles refer mainly to kilometres driven, whereas
those for heavy-duty vehicles are related to the engine power in
kilowatt-hours. Furthermore, the statistical power of studies of
emission factors is often limited by the small number of vehicles or
engines examined. Some investigators change more than one parameter
(e.g. sulfur content or aromaticity of the fuel) during their studies,
so that the specific cause of changes in exhaust composition is
difficult to assess. Adjustment of individual engine and fuel
parameters plays a major role in determining the quality and quantity
of exhaust emissions (see sections B3.1.2.1 and B3.1.2.2).
Further sources of diesel exhaust emissions include off-road and
stationary engines (reciprocating or gas turbine), electricity
generating plants, pipeline pumping, gas compression, commercial and
industrial furnace installations, and space and water heaters in
plants and factories (see section A3.2.1.2). Diesel exhaust is also
emitted from marine and inland ships' engines; residual fuels and
other heavy grades (for example Bunker C) are used in ocean shipping
(von Meyerinck, personal communication, 1994).
B3.1.1.1 Emission of chemical constituents with the gaseous portion
of diesel exhaust
The exhaust emissions from diesel-fuelled vehicles are generally
given as milligrams of component emitted per kilometre of driving
distance (Egebäck & Bertilsson, 1983; Westerholm et al., 1986;
Westerholm, 1987; Volkswagen AG, 1989; CONCAWE, 1990b; Westerholm &
Egebäck, 1991; Prakash et al., 1992; Scheepers & Bos, 1992a). Data for
verifying tests are issued by national regulatory bodies, e.g. the
German Federal Office for Motor Vehicles (1993, 1994). Depending on
the testing cycle, diesel engine, and fuel (see sections B3.1.1.1 and
B3.1.1.2), the data show considerable differences even though the
values are of the same order of magnitude. Emission factors used in
different regions to estimate the effects of regulated chemical
constituents (carbon monoxide, nitrogen oxides, and hydrocarbons) in
air are shown in Table 24.
Like all hydrocarbon fuel-burning engines, diesel engines release
significant amounts of carbon dioxide. Westerholm & Egebäck (1991)
measured emission factors of about 1 kg/km from a bus and a truck in
the US transient cycle and the bus cycle. In measurements of emissions
from six buses in four driving cycles (US transient cycle and three
bus cycles), Prakash et al. (1992) found emission factors up to about
4 kg/km, especially in the bus cycles. For five European diesel
passenger cars and one light van, Hammerle et al. (1994a) determined
emission factors of 162-252 g/km carbon dioxide in the European Motor
Vehicle Emissions cycle and the US FTP-75 test. Diesel engines are the
most efficient of all common types of combustion engines, with peak
thermal efficiencies typically > 40%, owing to the relatively large
air:fuel ratio during combustion (see section B3.1.2.1) (Organisation
for Economic Co-operation and Development, 1993).
Table 24. Emission factors for diesel vehicles in 1985 used as standards for estimating total impact
Region Passenger cars Commercial vehicles
g/km g/kg Average < 5 t > 5 t
g/km g/kg g/km g/kg g/km g/kg
Carbon monoxide
Denmark 1.0 2.0
Germanya 1.5 20 16
Netherlands 2.7 35 3.9 14 2.0 20 4.6 14
European Union 19 19 16
Austria 22.8 22.8 20
Sweden 10.5
Switzerland 4.0
United Statesb 3.1-6.2
Nitrogen oxides
Germanya 1.0 14 58
Netherlands 0.8 10 18.3 66 0.6 6 22.8 69
European Union 14 18 62
Sweden 39
Switzerland 14.0
United Statesb 3.1
Hydrocarbons
Germanya 0.5 7 12
Netherlands 0.6 10 4.6 17 0.9 9 6.3 19
Table 24 (contd)
Region Passenger cars Commercial vehicles
g/km g/kg Average < 5 t > 5 t
g/km g/kg g/km g/kg g/km g/kg
Hydrocarbons (contd)
European Union 10 13 9
Sweden 3.9
Switzerland 3.0
United Statesb 1.2
Adapted from Organisation for Economic Co-operation and Development (1993)
a Excluding former German Democratic Republic
b 1975-83, trucks tested in the US transient cycle
Cyanides, ammonia, and sulfur dioxide are detectable in the
gaseous portion of diesel exhaust. The average emission factors given
by Volkswagen AG (1989) for seven passenger diesel cars with four- and
five-cylinder engines in three driving cycles (US 75 test with cold
start, US sulfate emission test, US highway driving test) were
0.6 mg/km cyanides, 1.1 mg/km ammonia, and 233.0 mg/km sulfur dioxide.
The emission of individual organic components and classes of
compounds, summarized as total hydrocarbons, are shown in Table 25,
which provides an overview of the quantities of individual substances
emitted in diesel exhausts. Heavy-duty vehicles release more
low-boiling hydrocarbons than passenger cars; however, the difference
could be due to the driving cycle used, which involves frequent
changes of speed and load (see section B2.2.1). The emissions of
adsorbed organic components, such as PAHs (see section B3.1.1.2), are
correlated with the release of particulate matter.
B3.1.1.2 Emission of particulate matter and adsorbed components in
diesel exhaust gases
The emission of total particulate matter from diesel exhaust is
shown in Table 26. Analysis of the particulate matter released from
heavy-duty vehicles gave the following emission factors (Westerholm &
Egebäck, 1991): 170-370 mg/km carbon, 8-71 mg/km soluble organic
compounds derived from fuel, 56-167 mg/km soluble organic compounds
derived from lubricating oil, 1.4-37 mg/km soluble sulfates, and
0.6-3.7 mg/km nitrate. Comparable values were not available for
light-duty vehicles.
As PAHs and oxygenated PAHs from diesel and spark-ignition
engines are qualitatively similar, their differentiation in the
environment is difficult (Behymer & Hites, 1984); however,
benzo[ b]naphtho-[2,1-d]thiophene is specific for diesel exhaust and
can therefore be used as a marker (Grimmer et al., 1979). Emissions of
PAH components are shown in Table 27.
In experiments with one bus and one truck, Westerholm & Egebäck
(1991) detected 30-220 µg/km of particulate-associated PAHs. The
compounds measured included dibenzothiophene and its 4- and 3-methyl
derivatives, 2-methylfluorene, phenanthrene and its methylated
derivatives, anthracene and its 2-methyl derivative, fluoranthene,
pyrene and its 1- and 2-methyl derivatives, retene, benzo[ a]fluorene,
benzo[ ghi]fluoranthene, cyclopenta[ cd]pyrene, benzo[ a]anthracene,
chrysene or triphenylene, benzo[ b,k]fluoranthene, benzo[ e]pyrene,
benzo[ a]pyrene, perylene, indeno[1,2,3-cd]fluoranthene,
indeno[1,2,3-cd]pyrene, picene, benzo[ ghi]perylene, and coronene.
The emission factors for 1-nitropyrene were 0.13-7.3 µg/km.
Table 25. Emission factors for individual organic constituents and
classes of compounds in the gaseous portion of diesel
exhaust
Class of compound Emission factor (mg/km)
or constituent
Light-duty vehiclesa Heavy-duty vehiclesa
Straight-chain aliphatic hydrocarbons
Sum of C1-C4 5.3-6.6 (C1 + C2)b
< 1 - < 143c
Sum of > C4 < 1-5c
Olefins
Ethylene 25.6-90.7d 32-135e
13.5-16.9b 19.0-82.9f
< 1-31c
Propylene 7.3-22e
8.1-44.0f
1,3-Butadiene 0.2g
Acetylene 5.7-7.4b 27.9-106.9 (+ ethane)f
Alcohols Methanol 1.6d
Ethanol < 1.2-22.2d
Aldehydes
Formaldehyde 8.1b 60-255e
7.9-20.7d 140-150h
4.2-9.1g 19.0-207.4 f*
Acetaldehyde 3.1b 18-137e
< 22-36d 40-50h
2.0-4.4g
Crotonaldehyde 1.2b
Acrolein < 1-1.8d 8.5-36e
4h
Benzaldehyde 0.6b 10-14h
Light aromatic compounds
Benzene 2.6-4.3b 4.5-13.1e
ND-6c 6.9-30.5f
9.5-18.1d
0.15-3.47g
Table 25. (cont'd)
Class of compound Emission factor (mg/km)
or constituent
Light-duty vehiclesa Heavy-duty vehiclesa
Toluene 1.1-1.9b 2-13.7e
ND-2c 7.4-32.5f
< 1.0d
Ethylbenzene NDc
Xylenes NDc 7.8-41.7f
Phenols 0.7-1.5b
ND, not determined
a According to the Organisation for Economic Co-operation and
Development (1993), light-duty vehicles are generally classified as
vehicles with a weight < 3.5 t, occasionally < 5 t; heavy-duty
vehicles are those weighing > 5 t.
b From Volkswagen AG (1989): various numbers of diesel passenger cars
in three driving cycles (US-75 test with cold start, US sulfate
emission test, US highway driving test); determination of aldehydes
only in the US-75 test
c From Scheepers & Bos (1992a): two diesel passenger cars (< 50 000 and
> 100 000 km on odometer) in ECE test, 15 min at 90 km/h and 15 min
at 120 km/h
d From Egebäck & Bertilsson (1983): two passenger cars in US-78 test
e From Westerholm & Egebäck (1991): a bus and a truck in bus cycle with
different diesel fuels
f From Prakash et al. (1992): one bus in four driving cycles (US
transient cycle, three bus cycles) with the exception (*) of eight
buses in the same driving cycles
g From Hammerle et al. (1994a): five passenger cars and one light van
in European Motor Vehicle Emissions Group cycle
h From Westerholm et al. (1986): one heavy-duty vehicle on a chassis
dynamometer with two diesel fuels
i Mainly phenols, cresols and xylenols
Table 26. Emission factors for total particulate matter from diesel exhaust
Measurement conditions Emission factor (mg/km) Reference
Light-duty vehiclesa
Seven passenger cars in three driving cycles 166.4-238.7 Volkswagen AG (1989)
(US-FTP-75 test with cold start; US sulfate emission
test; US highway driving test)
Four passenger cars, 15 light vans in three 180-250 (passenger cars) Williams et al. (1989)
Australian driving cycles (corresponding roughly to 360-440 (light vans)
US-72 and US-75 tests)
Seven passenger cars, two light vans in combined 70-365 (passenger cars) CONCAWE (1990b)
ECE 15/EUDC test with four diesel fuels 233-609 (light vans)
Various Germanyb, 300 Organisation for Economic
Netherlands, 600 Co-operation and Development
Sweden, 400 (1993)
61 passenger cars and 30 light vans without catalyst 39-188 (mean, 104) Federal Office for Motor Vehicles
(optimally tuned) incombined ECE 15/EUDC test (1993)
73 passenger cars and 45 light vans with catalyst 48-127 (mean, 90) Federal Office for Motor Vehicles
(optimally tuned) in combined ECE 15/EUDC test (1993)
Table 26 (contd)
Measurement conditions Emission factor (mg/km) Reference
44 passenger cars and 8 light vans without catalyst 52-117 (mean, 95) Federal Office for Motor Vehicles
(optimally tuned) inUS FTP-75 test (1993)
118 passenger cars and 34 light vans with catalyst 50-118 (mean, 71) Federal Office for Motor Vehicles
(optimally tuned) inUS FTP-75 test (1993)
Five passenger cars and 1 light van in European Motor 52-117 Hammerle et al. (1994a)
Vehicle Emissions Group cycle and US FTP-75 test
Heavy-duty vehiclesa
One vehicle on chassis dynamometer (bus cycle); 680-1000 Westerholm et al. (1986)
two diesel fuels with different contents of sulfur and
aromatic compounds
10 trucks, 2 buses in one Australian driving cycle 800-7150 Williams et al. (1989)
simulating urban traffic
One bus, one truck in two driving cycles (bus cycle; 230-600 Westerholm & Egebäck (1991)
US transient cycle) with two diesel fuels
106 trucks and buses in ECE-R49 driving cycle 0.056-0.606 g/kWh Federal Office for Motor Vehicles
(1994)
Table 26 (contd)
Measurement conditions Emission factor (mg/km) Reference
Various Netherlands, 800 (< 5 t) Organisation for Economic
3300 (> 5 t) Co-operation and Development
Sweden, 400 (< 5 t) (1993)
1700 (> 5 t)
13 trucks and buses (three with particulate trap, 584-804 (without trap) Lowenthal et al. (1994)
10 without) in bus cycle with two diesel fuels 67-206 (with trap)
a According to the Organisation for Economic Co-operation and Development (1993), light-duty vehicles are generally classified as
vehicles with a weight < 3.5 t, occasionally < 5 t; heavy-duty vehicles are those weighing > 5 t.
b Without the former German Democratic Republic
Table 27. Emission factors for polycyclic aromatic hydrocarbons in
diesel exhaust
Constituent Emission factor (µg/km)
Light-duty vehiclesa Heavy-duty vehiclesa
Anthracene 17-63b 0.9-3.2c; 9-26d;
3-14d+; 1.6e
Phenanthrene 140f 4.2-25c
295-524b 163-308d; 79-186d+;
12.2e
Fluoranthene 172f 10-39c
58-200g 27-34d; 14-17d+
60.4-79.7g 13.0e
Pyrene 186 15-102c
< 0.9-22 28-31d; 9-21d+
66.6-87.1 22.6e
Chrysene 40 9.5-26c
14-67 8-32d; 4-12d+
10.7-22.3 Not measurede
Benzo[b,k]fluoranthene 40 1.6-8.4c
2.6-47 9-12d,h; 2-8d,h+
10.3-15.2 5.6e
Benzo[ghi]fluoranthene 40f 1.4-13c; 6.9e
Cyclopenta[cd]pyrene 2f 2.5-11c
0.81ag* 1.4e
Benzo[e]pyrene 3-38b 1.6-23c
13.8-16.9 5-9d; 1-7d+; 2.6e
Benzo[a]pyrene 10 0.8-12c
< 1-19 2-3d; 0.4-2d+
4.0-5.3 1.3e
Benzo[a]anthracene 25 3.0-12c
8-43 5-12d; 1-4d+
2.7-3.9 3.6e
Indeno[123-cd]pyrene 15f 0.7-15c
3.5-4.4g
Benzo[ghi]perylene 20 0.6-30c
< 1-18 2-4d; 0.5-1d+
8.7-11.7 Not detected
(detection limit
not given)e
Table 27 (contd)
Constituent Emission factor (µg/km)
Light-duty vehiclesa Heavy-duty vehiclesa
Perylene < 1-2b Not measuredc
0.5-0.6g 1.0e
Coronene 10f < 0.1-12c
5.43g* Not detected
(detection limit
not given)e
a According to the Organisation for Economic Co-operation and
Development (1993), light-duty vehicles are generally classified as
vehicles with a weight < 3.5 t, occasionally < 5 t; heavy-duty
vehicles are those weighing > 5 t.
b From Scheepers & Bos (1992a): two diesel passenger cars (< 50 000
and > 100 000 km on odometer) in ECE test
c From Westerholm et al. (1986): one heavy-duty vehicle on a chassis
dynamometer (bus cycle)
d From Lowenthal et al. (1994): 13 trucks and buses (three with
particulate trap [d+], 10 without) in bus cycle
e From Rogge et al. (1993): two heavy-duty vehicles in special
driving cycle
f From Egebäck & Bertilsson (1983): average of two passenger cars in
US-78 test
g From Volkswagen AG (1989): seven passenger cars in three driving
cycles (US-75 test with cold start, US sulfate emission test, US
highway driving test) with the exception (*) of one four-cylinder
engine, US-72 test with hot start
h Isomers not specified
The emission of oxygenated PAHs by two diesel passenger cars (one
four-cylinder and one five-cylinder engine, US 72 test with hot start)
was 4-40 µg/km. In a comparable test (one four-cylinder engine, same
driving cycle), the emission of nitro-PAHs was 0.1-3.5 µg/km. As a
result of possible artefact formation during sampling (see section
B2.2.1), these measurements are uncertain (Volkswagen AG, 1989). It is
suspected that nitrate-based cetane improvers (see section A2.1.2)
could increase nitro-PAH emissions in exhaust (Organisation for
Economic Co-operation and Development, 1993).
There are no significant differences in the emissions of adsorbed
single substances between light- and heavy-duty vehicles, although
heavy-duty vehicles release larger relative amounts of particulate
matter (Salmeen et al., 1985).
The chlorine content of diesel fuel is typically < 1 ppm
(Oehme et al., 1991). Thus, no dioxins were found in the exhaust of
heavy vehicles, at a detection limit of 100 pg/litre of fuel (Marklund
et al., 1990). The dioxin emissions from one light-duty (indirect
injection) and one heavy-duty (direct injection) diesel engine under
different load conditions on a chassis dynamometer were 0.009-0.141 ng
of toxicity equivalents per litre of fuel consumed. The highest value
was reported in emissions from the light-duty engine at full load.
Overall, the emissions were of the same order of magnitude as the
dioxin emissions from a petrol-fuelled engine with a catalytic
converter (Schwind et al., 1991).
B3.1.2 Parameters that influence diesel exhaust emissions
B3.1.2.1 Engine conditions
In general, diesel engines are operated with excess air; the
air:fuel ratio is about 1.5, and at lower air:fuel ratios, much more
smoke is emitted (Organisation for Economic Co-operation and
Development, 1993). Wide local variations in the equivalence ratio and
the temperature of the mixture are caused by the heterogeneous nature
of the combustion process. To avoid over-rich mixtures and to improve
the air:fuel mixing processes, wall wetting and delay of fuel
injection are used (CONCAWE, 1986). In naturally aspirated engines,
the amount of air in the cylinder is independent of the power output.
For these engines, the maximal power output is limited by the amount
of fuel that can be injected without smoke formation. In turbocharged
engines, however, increasing the amount of fuel injected increases the
energy in the exhaust gas, and the turbocharger pumps more air into
the combustion chamber. For this reason, the power output of
turbocharged engines is not, in general, limited by smoke. Low
air:fuel ratios can occur only during transient acceleration. Most
turbocharged engines are further equipped with a cooling system
(intercooler) in which compressed air reduces adverse thermal effects.
In both types of engines, fuel is injected either directly into the
combustion chamber or indirectly into a separate pre-chamber where it
is mixed and partly burnt before reaching the main combustion chamber
(Organisation for Economic Co-operation and Development, 1993).
Scheepers & Bos (1992a) reported that most heavy-duty vehicles have
direct injection motors, and indirect injection is used for light-duty
vehicles.
The most important influences of engine conditions on diesel
exhaust emissions are summarized in Table 28. Contrasting results are
sometimes obtained with regard to the effect of engine conditions on
diesel exhaust emissions. Adjustment of the engine plays a major role
(CONCAWE, 1990b), which was slightly less in the US FTP-75 test cycle
than in the European cycle.
Table 28. Influence of engine conditions on diesel exhaust emissions
Condition Change Influence on exhaust emissions Reference
Air:fuel ratio Increase Increased emissions of hydrocarbons and particulate soluble Organisation for Economic
fraction; decreased particulate and nitrogen oxide emissions Co-operation and
from turbocharged and intercooled engines Development (1993)
Increased PAH emissions, decreased particulate emissions from Barbella et al. (1988)
direct injection engines; decreased PAH and particulate emissions
from indirect injection engines
Increased nitrogen oxide emissions, decreased particulate Iida et al. (1986)
emissions from direct injection engines
Injection timing Advance Increased particulate emissions from indirect injection engines Du et al. (1984); Williams et
al. (1989)
Decreased particulate and hydrocarbon emissions; increased Organisation for Economic
nitrogen oxide emissions Co-operation and Development (1993)
No influence on concentrations of PAHs and oxy-PAHs adsorbed Jensen & Hites (1983)
on particulate matter
Delay Decreased nitrogen oxide emissions, increased volumetric fuel Organisation for Economic
consumption Co-operation and Development (1993)
Table 28. Influence of engine conditions on diesel exhaust emissions
Condition Change Influence on exhaust emissions Reference
Injection timing Delay Decreased particulate emissions from indirect injection engines; Williams et al. (1989)
(contd) increased particulate emissions from direct injection engines
Small effect on PAH emissions from indirect injection engines Schuetzle & Frazier (1986)
Small effect on particulate emissions from direct injection engines Campbell et al. (1981a)
No influence on concentrations of PAHs and oxy-PAHs adsorbed Jensen & Hites (1983)
on particulate matter
Load and Increase Increased particulate and PAH emissions at high loads; decreased Pipho et al. (1986)
temperature particulate emissions at very high load from indirect injection
engines
Decreased concentrations of PAHs and oxy-PAHs adsorbed on Jensen & Hites (1983)
particulate matter
Decrease Decreased particulate and nitrogen oxide emissions; extremely Organisation for Economic
cold charge air may increase hydrocarbon emissions Co-operation and
Development (1993)
Lowest PAH emissions at medium load; enrichment of three- Pipho et al. (1986)
and four-ring PAHs during idling (indirect injection engines)
PAH, polycyclic aromatic hydrocarbons
(a) Engine aging
Increased emissions of hydrocarbons, particulates, and PAHs have
been reported from older, more intensively used light- and heavy-duty
vehicle engines in comparison with newer ones (Stenberg et al., 1983;
Braddock & Perry, 1986; Scheepers & Bos, 1992a). Stenberg et al.
(1983) proposed that the combustion of more lubricating oil in older
vehicles contributes to the enhanced emissions. Prakash et al. (1992)
measured the emission characteristics of several buses and reported
that a properly maintained engine would not emit significantly more
hydrocarbons and nitrogen oxides during its lifetime, whereas carbon
monoxide and particulate emissions could increase with age. These
findings are similar to those of Volkswagen AG (1989) on the influence
of distance travelled on exhaust emissions from one diesel passenger
car over a total distance of about 30 000 km in three driving cycles
(US FTP test, US sulfate emission test, US highway driving test). The
average deterioration factors, relative to the emissions at about
2500 km, were carbon monoxide, 0.97; nitrogen oxides, 0.96;
hydrocarbons, 0.91; particulates, 1.07; fluoranthene, 0.96; pyrene,
1.06; chrysene, 0.62; benzo[ b,k]fluoranthene, 1.11; benzo[ e]pyrene,
1.51; benzo[ a]pyrene, 0.68; perylene, 0.96; indeno[1,2,3-cd]pyrene,
2.91; and benzo[ ghi]perylene, 3.43.
(b) Lubricating oil
As a result of emission control techniques such as turbocharging,
intercooling, and injection timing, the relative importance of
emissions caused by lubricating oils has increased (Organisation for
Economic Co-operation and Development, 1993). Lubricating oils have
been hypothesized to be a sink for incomplete combustion products such
as PAHs and their derivatives, which are scrubbed from the exhaust
gas. When this 'enriched' lubricating oil leaks into the combustion
chamber, the constituents may be emitted in the exhaust (Scheepers &
Bos, 1992a; see section B2.1.1). McKee & Plutnick (1989) found,
however, that carcinogenic PAHs accumulate in gasoline- but not in
diesel-fuelled engine oils.
Oil consumption can be reduced by improving engine manufacturing
specifications and engine seals (Organisation for Economic
Co-operation and Development, 1993). The particle-bound hydrocarbons
derived from lubricating oil contribute up to about 50% by weight in
light-duty vehicles and to a maximum of about 26% by weight of the
total emitted particulate matter (see section B2.1.2, Table 22).
Experiments with 13C radiolabelled lubricating oil in three
light-duty vehicles showed that addition of up to 3% lubricating oil
increases the emitted particulate matter by about 50%, and the
particulates consist mainly of the soluble organic fraction adsorbed
onto the particles (Williams et al., 1989).
B3.1.2.2 Fuel specification
Fuel parameters influence the particulate emissions of diesel
engines but seem to be less important than other parameters like
engine adjustment, load, and maintenance (Weidmann et al., 1988).
The actual trend in legislation of the quality of diesel fuel, i.e. to
a lower sulfur and aromatic content, will improve emissions,
especially of particles. In addition, the more stringent emission
standards in many countries will decrease diesel-related emissions.
(a) Sulfur content
There have been numerous investigations on the influence of
sulfur content in diesel fuel on the release of particulate matter
(CONCAWE, 1990b; Van Beckhoven, 1991; Westerholm & Egebäck, 1991;
Scheepers & Bos, 1992a). The sulfur content is presumed to be directly
correlated with the release of particulate matter. About 3-5% of the
fuel sulfur in light-duty vehicles and 2-3% of that in heavy-duty
vehicles reacts with metal sulfates which are adsorbed onto the
particulate matter, increasing its mass and its hygroscopic
properties, as metal sulfates tend to absorb significant amounts of
water from the atmosphere (Organisation for Economic Co-operation and
Development, 1993).
A reduced sulfur content leads to decreased levels of
particulates in the exhaust of light-duty vehicles. For example,
investigations on seven passenger cars and two light vans in a
combined ECE 15/EUDC testing cycle with four diesel fuels of different
sulfur contents (0.055, 0.12, 0.22, and 0.31% by weight) showed a
statistically significant reduction in the emission of particulates up
to a maximum of 7.4%. The investigators noted variations in
particulate levels between the different vehicles, however, that were
about two orders of magnitude higher than could be attributed directly
to the influence of the sulfur content (CONCAWE, 1990b).
Reduction of the emission rates of heavy-duty vehicles by
lowering the fuel sulfur content is still under discussion. In a study
of four heavy-duty engines in the ECE R49-13 mode driving cycle with
the same four fuels as described above, no statistically significant
reduction in emitted particulate matte was seen (CONCAWE, 1990b). In
experiments with one heavy-duty vehicle on a chassis dynamometer bus
cycle with two different fuels, however, a considerable reduction in
the release of particles was found (Westerholm et al., 1986). This
result was confirmed by Westerholm & Egebäck (1991) who investigated
one bus and one truck in three driving cycles (ECE 13 test, bus cycle,
US transient test) with eight diesel fuels of different sulfur and
aromatic contents. Comparable results were found by Gairing et al.
(1994) in tests with one heavy-duty engine (direct injection) in ECE
R49 with 12 different fuels. Adjustment of the engines again appeared
to be a decisive factor.
(b) Aromaticity (density)
Aromaticity can be directly associated with density, as a higher
density is frequently achieved by a larger content of aromatic
compounds. Obviously, increasing the aromaticity leads to increased
emissions of particulate matter, although volumetric fuel consumption
is decreased (CONCAWE, 1986). This finding was confirmed by Hare
(1986) for light- and heavy-duty vehicles on the basis of data from
the automobile industry. The presumed increase in the release of
particulates is 0.5-1.9% for a 1% by volume change in aromatic
content. In a study of four light-duty vehicles in three Australian
driving cycles (resembling roughly the US 72 and 75 tests), Williams
et al. (1989) found reductions in particulate emissions of 22-27% at a
10% difference in fuel aromaticity. Unfortunately, the two fuels also
differed in sulfur content and volatility. Van Beckhoven (1991)
achieved comparable results with passenger cars with indirect
injection but found no significant influence for heavy-duty direct
injection engines. Experiments by Westerholm & Egebäck (1991) on one
bus and one truck showed a reduction in the emission of particulates
when fuel with low levels of sulfur and aromatics was used. The
increased aromatic content is probably also the source of higher
levels of PAHs and nitro-PAHs in the exhaust (Schuetzle & Frazier,
1986; Westerholm, 1987; Westerholm & Egebäck, 1991; Organisation for
Economic Co-operation and Development, 1993).
(c) Volatility
The volatility of diesel fuels is described by the boiling range,
and especially by the 10% boiling-point (low boiling end fraction) and
the 90% boiling-point (high boiling end fraction) of the mixture. The
influence of the boiling range, particularly the 90% boiling-point, on
the release of particulate matter is still under discussion. While
some investigators (Hare, 1986; Williams et al., 1989) assume that
emissions of particulate matter increase with an increased 90%
boiling-point, others have not been able to confirm this effect,
suggesting that other parameters, such as sulfur content and
aromaticity, are responsible for the increase (Westerholm & Egebäck,
1991; Organisation for Economic Co-operation and Development, 1993).
(d) Cetane number
An increase in cetane number lowers the emission of diesel
particulate matter. A slight decrease in cetane number, combined with
a small increase in the density of diesel fuels (see section A2.1.3),
was predicted in 1987 to result in an increase in emissions from 3 to
12% for carbon monoxide, and to maxima of 2% for nitrogen oxides, 7%
for hydrocarbons, and 6% for particles (CONCAWE, 1987).
B3.1.2.3 Malfunction
Malfunctions or defective components of the engine or exhaust gas
system may result in considerably higher emissions than those from a
properly maintained engine. Up to twofold increases in emissions of
carbon monoxide, hydrocarbons, and particulate matter have been
measured even in the absence of a significant effect on power or fuel
consumption (Ullman et al., 1984). Malfunction of the fuel injection
system may contributed markedly to higher emissions (Organisation for
Economic Co-operation and Development, 1993). Volkswagen AG (1989)
tested a diesel passenger car with defective injection nozzles in
three driving cycles (US FTP test, US sulfate emission test, US
highway driving cycle) and found statistically significant increases
in the emissions of carbon monoxide (up to about 25%), hydrocarbons
(up to about 45%), and particulate matter (up to about 15%), whereas
the release of nitrogen oxides was almost unaffected. The amounts of
benzene and PAHs emitted were slightly increased. Comparable results
were obtained by Williams et al. (1989) for the release of particles
by several light-duty vehicles equipped with defective injectors.
Malfunction of US medium- to heavy-duty vehicle diesel engines
increased the amount of nitrogen oxide emitted to about 4%, that of
hydrocarbons to about 75%, and that of particulates to about 140%
(Organisation for Economic Co-operation and Development, 1993).
B3.1.3 Total emissions by diesel engines
Few data are available on the emissions of different constituents
of diesel exhaust into the atmosphere and their contribution to the
total release by traffic and industry. The contribution of heavy-duty
vehicles seems to be much greater than that of passenger cars, despite
lower percent kilometres. For example, in westen Germany, only 8% of
the total annual urban mileage was attributable to heavy-duty vehicles
(Fromme, 1990). In contrast, in 1987, power plants contributed 15.3%
(85 000 t), industry 63.5% (360 000 t), domestic and minor consumers
8.1% (44 000 t), and total traffic 13% (72 000 t) to the particles
released (Metz, 1989). The contribution of diesel particulate matter
to the total particle burden of the atmosphere is highly dependent on
local conditions (Table 29).
Diesel vehicles, particularly in the light-duty category,
represent a smaller proportion of motor traffic in the United States
than in most European countries. Measurements from two heavy-duty
vehicles in 1982 indicated that light- and heavy-duty diesel vehicles
contributed about 6% to the total fine aerosol, organic carbon
emissions in the Los Angeles basin, about 1200 kg/day being emitted by
heavy-duty vehicles and 600-870 kg/day by light-duty vehicles
(Hildemann et al., 1991; Rogge et al., 1993).
B3.1.4 Control of emissions
The automotive industry has made efforts to reduce diesel exhaust
emissions (Obländer, 1991; Fortnagel, 1992; Hammerle et al., 1994b),
and technology is advancing.
B3.1.4.1 Particle traps
Particle traps are placed in the exhaust system to collect
particulate matter and to clean the filter by burning the trapped
particles (trap oxidizers). Most traps are based on cellular ceramic
monolith material or ceramic silica fibre coils. Many regeneration
techniques have been developed for trap oxidizers (Organisation for
Economic Co-operation and Development, 1993), including thermal
regeneration, which is the burning of collected particulate matter,
and catalytic regeneration, in which fuel catalysts, e.g. iron and
copper, containing organic compounds form finely dispersed metal
particles during combustion to reduce the burning temperature of the
diesel particles so that there is more efficient regeneration
(Volkswagen AG, 1989; Hammerle et al., 1994b). Traps remove the
soluble organic fraction adsorbed onto particles and the dry
carbonaceous soot, while catalysts can remove substances only from the
soluble organic fraction. In catalytic regeneration, over 95% of the
metal used as fuel catalyst is retained in the trap (Hammerle et al.,
1994b).
Studies of the emissions of one light-duty diesel passenger car
by Volkswagen AG (1989) showed that the release of particulates was
reduced by a thermal trap by at least 80% during the collection phase
and by about 60% during the regeneration phase; the reduction was 80%
for the whole cycle. Sulfate emissions decreased to about 50%;
however, emission of carbon monoxide increased by about 10%, probably
due to additional burning and/or incomplete oxidation of particulate
matter on the trap. Comparable experiments with a catalytically
regenerated trap, with addition of a manganese compound, also showed a
trap efficiency of about 80% for particulate matter. Hydrocarbon and
carbon monoxide emissions were slightly increased, probably due to
incomplete oxidation on the trap. Sulfate emissions were reduced to
less than half, emissions of PAHs were reduced to about 25%, and those
of phenol and aldehydes to about 25-33%. About 10% of the manganese
catalyst was detected in the exhaust.
Measurements with a heavy-duty vehicle on a chassis dynamometer
to test two particle traps showed decreases of 79 and 86% in the
release of particles, depending on the trap and fuel characteristics.
The emissions of hydrocarbon, carbon monoxide, aldehydes, and PAHs
were slightly reduced (Westerholm et al., 1986).
Table 29. Diesel exhaust emissions and their contribution to total anthropogenic emissions
Region Year Annual emissions (kt/year) Reference
NOx CO HC PM SO2
Light-duty vehicles
Germanya 1986 52 (3.3)b 76 (1.2)b 23 (2.2)b 15 (26.3)b NR Fromme (1990)
1987 NR NR NR 12 (2.2)c NR Metz (1989)
United Kingdom 1991 (0.7)c (0.4)c (1.1)c (2)c,d (0.2)c Quality of Urban Air Review
Group (1993)
Light- and heavy-duty vehicles
Europe NR NR NR NR NR (1.6)c OECD (1993)
United States 1984 NR NR NR NR 620 (3)c OECD (1993)
1986 NR NR NR 54.8 (20)b NR Carey (1987)
(4)c
Germanya 1989 640 240 150 55 NR Federal Environment
Agency(1991)
Heavy-duty vehicles
OECD (Europe) 1980 1548 (13)c NR 393 (4)c NR 361 (2)c OECD (1993)
Germanya 1986 502 (32.2)b 130 (2.1)b 104 (10.0)b 37 (64.7)b 35 (2)c OECD (1993); Fromme (1990)
(17)c (2)c (4)c (7)c
1987 NR NR NR 32.5 (5.9)c NR Metz (1989)
Table 29 (cont'd).
Region Year Annual emissions (kt/year) Reference
NOx CO HC PM SO2
Heavy-duty vehicles (contd)
Germany 1988 614 351 1.31 NR 38 Federal Environment Agency
(1992)
United Kingdom 1991 (19.9)c (1.9)c (5.4)c (14)c,d (1.0)c Quality of Urban Air
Review Group (1993)
Canadae 1985 265 104 37 20 21 Environment Canada
(1990)
NOx, nitrogen oxides; CO, carbon monoxide; HC, hydrocarbons; PM, particulate matter; SO2, sulfur dioxide; NR, not reported; OECD,
Organsiation for Economic Co-operation and Development
a Excluding the former German Democratic Republic
b Percentage of total traffic emissions
c Percentage of total man-made emissions
d PM10
e Sum of light- and heavy-duty trucks
The effect of a ceramic wall-flow monolith particulate trap was
studied on the emissions of a 1979 heavy-duty diesel engine with
direct injection in two steady-state modes. Reductions of 70% (50% at
full load) and 86% (75% at full load) in particle release were found.
There was also a decrease in the soluble organic fraction, whereas the
emitted portion of volatile organic carbons was only slightly reduced.
The trap had almost no effect on the release of nitrogen oxides (Dorie
et al., 1987).
The measurements of Lowenthal et al. (1994) on 13 trucks and
buses (three with particulate traps, 10 without) in a bus cycle showed
a similar reduction in the release of particles (Table 26). There was
a significant decrease in the emission of particle-bound PAHs.
B3.1.4.2 Catalytic converters
Diesel catalytic converters reduce gaseous and particle-bound
hydrocarbon constituents of the exhaust, e.g. aldehydes, PAHs, nitro-
PAHs, and carbon monoxide. Regeneration systems are not needed, as
particulate matter is not collected by common flow-through catalytic
converters. The efficiency in controlling particulates is, however,
much lower than that of traps. Disadvantages of catalytic converters
are further conversion of nitrogen monoxide to the more toxic nitrogen
dioxide and of sulfur dioxide to particulate sulfates (Organisation
for Economic Co-operation and Development, 1993). Catalysts that
selectively oxidize organic compounds and oxidize almost no sulfur
dioxide are currently in use. Removal of sulfur from diesel fuels
would allow the use of more active catalysts; use of catalysts in
diesel vehicles run on sulfur-containing fuel is limited because the
strong adsorbing tendency of sulfur partly inactivates the catalyst
(Hammerle et al., 1994b; see section A2.1.1).
B3.2 Regulatory approaches
The levels of carbon monoxide, nitrogen oxides, total
hydrocarbons, and particulates emitted by diesel engines are regulated
by law in a number of countries (Table 30). Most other industrialized
countries have adapted United States or European regulations (for
details, see CONCAWE, 1990a and Mercedes-Benz AG, 1994a).
B4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
Few data are available on the fate of diesel exhaust in the
atmosphere, which is the first environmental compartment affected. In
general, the effects on the overall environment of diesel fuel
combustion are typical of those of fossil fuel burning. The
contribution of diesel fuel emissions is proportional to diesel fuel
consumption both locally and globally.
Table 30. Limit values for components of diesel exhaust
Region Carbon Nitrogen Hydrocarbons Particulates Comments
monoxide oxides
Light-duty vehicles (g/km)
Austria 2.1 0.62 0.25 0.124 < 3.5 t; since 1991; from 1995,
adoption of European Union
standards planned
Canada 2.1 0.62 0.25 0.12 Since 1987
European Union 2.72 0.97 (with 0.14 Since 1992
hydrocarbons)
1.0 0.7 0.08 From 1996
Finland Since 1993
Japan 2.1 0.7 0.62 None Since 1986
2.1 0.5 0.4 0.2 Since 1994
Sweden, Norway 2.1 0.62 (city) 0.25 0.124 < 3.5 t; from motor year 1992
0.76 (highway)
Switzerland 2.1 0.62 (city) 0.25 0.124 < 3.5 t; since 1988; from 1995,
0.76 (highway) adoption of European Union
standards planned
USA (California) 2.1-5.2 0.2-0.6 0.2-0.3 (except 0.05 (up to Depending on mileage
methane) 31 000 km)
US Environmental 2.1-2.6 0.6-0.8 0.2 0.05-0.12 Depending on mileage
Protection Agency
Table 30 (contd)
Region Carbon Nitrogen Hydrocarbons Particulates Comments
monoxide oxides
Heavy-duty vehicles (g/kWh)
Austria 4.9 9.0 1.23 0.4
Canada 15.5 5.0 1.3 0.25 g/bhp-h
15.5 5.0 1.3 0.1 g/bhp-h; from 1995-97
European Union 4.5 8.0 1.1 0.36 Since 1992
4.0 7.0 1.1 0.15 From 1995-96
Japan 7.4 5.0 2.9 0.7 Indirect injection engines
7.4 6.0 2.9 0.7 Direct injection engines
Sweden 4.9 9.0 1.23 0.4
USA 15.5 5.0 1.3 0.07 g/bhp-h; bus
15.5 4.0 1.3 0.1 g/bhp-h; truck
15.5 5.0 1.3 0.05 g/bhp-h; bus; from 1998
15.5 4.0 1.3 0.1 g/bhp-h; truck; from 1998
Adapted from Mercedes-Benz AG (1994b); reference year, 1994, unless otherwise stated; bhp-h, brake horsepower-hour
Thus, the major components of diesel exhaust contribute to acid
deposition (nitrogen and sulfur oxides), tropospheric ozone formation
(carbon monoxide, nitrogen oxides, and hydrocarbons), and global
warming (carbon dioxide and particulates; carbon monoxide, nitrogen
oxides and hydrocarbons by ozone formation).
The environmental fate of released particulate matter and of
organic compounds, particularly the PAHs, is important environmentally.
The mechanisms of the distribution and transformation of individual
hydrocarbons in diesel exhaust have been well described (IPCS, 1986,
1993).
B4.1 Transport and distribution between media
The major fraction (50-80%) of the particulate emissions of
diesel engines is in the submicron size, ranging from 0.02 to 0.5 µm
(see section B2.1.2). Once particles have been emitted, their
mechanical transport in the atmosphere is like that of gas molecules
(nonreactive). Together with carbon particles from other combustion
processes, they may be transported over long distances and even
penetrate the stratosphere (Muhlbaier Dasch & Cadle, 1989).
Only one study was available on the agglomeration behaviour of
the particles in the atmosphere. Albrechcinski et al. (1985) measured
the aging behaviour of particulate matter from a 1978 diesel passenger
car in a 600-m3 model chamber with a nominal exhaust gas dilution of
150:1 and found peak mean aerosol diameters, based on volume size
distributions, of 0.1-0.18 µm for 'fresh' aerosol. The concentrations
of total particulate decreased during aging of the aerosol due to
coagulation, fall-out, and perhaps losses to the walls of the chamber.
The average decrease was 20% after 8 h and 60% after 24 h. Excess
nitrogen dioxide seemed to inhibit particle growth. Particles with an
average diameter of 1-10 µm constituted approximately 10% of the fresh
aerosol, but this percentage decreased during aging as a result of
apparently rapid fall-out of larger particles. It is not clear whether
these results are also representative of the particle emission pattern
of modern diesel passenger cars.
Model experiments of the gas-phase chemistry of nitrogen oxides,
total hydrocarbons, and sulfur dioxide from diesel exhaust were
performed by varying parameters such as irradiation, nitrogen dioxide
concentration, and ozone concentration (Albrechcinski et al., 1985).
Irradiation alone had only a minimal effect, but excess nitrogen
dioxide led to higher rates of decay of nitrogen monoxide in the dark
than under irradiation, probably because of photodissociation of
nitrogen dioxide to nitrogen monoxide. As nitrogen monoxide is rapidly
converted to nitrogen dioxide in the presence of excess ozone, the
nitrogen oxide concentration decreased as the ozone concentration
reached a maximum, presumably partly because of the formation of
nitric acid which was deposited onto the chamber walls. Since reactive
organic compounds were not added, the authors considered that the
experiments were not representative of urban atmospheres.
The hydrosphere and geosphere may be affected indirectly by
diesel exhaust emissions after dry or wet deposition of particulate
matter or individual constituents (see section B4.2). In experiments
with dysprosium-traced diesel fuel, Horvath et al. (1988) (see section
B5.1) found 0.012-0.07 g diesel particulate matter per gram of road
dust.
B4.2 Transformation and removal
Atmospheric removal of airborne carbon particles consists mainly
of dry deposition and scavenging by precipitation (wet deposition).
The rate of wet removal is directly correlated to the ratio of organic
to elemental carbon and is low for small ratios (Muhlbaier Dasch &
Cadle, 1989). As the overall removal rate of diesel particulates is
estimated to be low, the atmospheric life-time is several days
(Jaenicke, 1986).
The elemental carbon of diesel particulates may act as a catalyst
in the formation of sulfuric acid by oxidation of sulfur dioxide. The
oxidation reaction is assumed to occur on the surface of solid soot
particles or in liquid drops containing soot particles (Novakov, 1984;
Mészįros & Mészįros, 1989). Furthermore, diesel particles themselves
contain sulfate, adsorbed in the form of metal sulfates, at a
concentration of about 1-12% by weight, depending on the sulfur
content of the fuel (see section B2.1.2), which may be washed off if
the particles come into contact with precipitation. The organic
compounds adsorbed on the emitted particulate matter may undergo a
number of physical and chemical reactions (volatilization of
low-relative-molecular-mass compounds, formation of secondary
aerosols, oxidation, nitration) with other atmospheric compounds or
during exposure to sunlight (Pitts et al., 1985). The estimated
half-lives for unbound PAHs in the atmosphere range from one day
(naphthalene) to one week (e.g. pyrene, chrysene, benzofluoranthenes,
benzo[a]pyrene) (Mackay et al., 1992; see Table 11); however, PAHs
adsorbed onto particles may be more stable to nitrogen dioxide and
ozone than airborne PAHs (Gibson et al., 1981).
B5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
Because diesel exhaust is a complex mixture of a great variety of
compounds (see also section B2.1), general 'environmental levels'
cannot be described. The individual constituents of diesel exhaust
should be detectable in all compartments of the environment. Since
diesel exhaust is only one of numerous other sources, the levels of
individual compounds cannot be correlated directly to diesel exhaust.
Particulate matter appears to be the most relevant fraction of
diesel exhaust for the general population and workers exposed to
diesel exhaust emissions from a toxicological point of view. The
concentration of particles is about 10- to 20-fold higher in diesel
exhaust than in the exhaust from gasoline-fuelled vehicles, and the
particle diameters are in the respirable range.
B5.1 Exposure of the general population
The general population is exposed to high levels of diesel
exhaust in certain microenvironments, such as busy streets and parking
areas. Exposure to the main gaseous components of diesel exhaust --
carbon dioxide, carbon monoxide, nitrogen oxides, and total
hydrocarbons -- can be estimated from the emission factors given in
section B3, the kilometrage of diesel vehicles in relation to total
traffic, and atmospheric dispersion models (Cuddihy et al., 1984;
Volkswagen AG, 1989). In view of the fact that measured emission
factors vary widely (see section B3.1.1) and are mainly dependent on
adjustment of individual engines, the validity of these estimations is
limited.
On a global basis, there are wide variations in the contribution
of diesel emissions to total airborne particulate matter, which
depends on the following factors: percentage of diesel vehicles in the
total volume of traffic; type, age, and maintenance of individual
engines (see section B3.1.2.1); fuel quality (e.g. sulfur content and
aromaticity; see section B3.1.2.2); and emission control techniques.
Particle concentrations in environmental air samples are usually given
as total particle concentrations, with no differentiation by source.
The contribution of diesel particulate matter is then estimated on the
basis of the percentage of diesel vehicle emissions in the total
emissions from traffic or total man-made emissions. Emissions from
running stationary diesel engines have up to now not been taken into
account. Data on emissions from light- and heavy-duty vehicles in some
industrialized countries are shown in Table 30 (section B3.1.3). The
proportion of the concentrations to which people are exposed that is
attributable to diesel vehicles varies widely, depending on traffic
flow and composition in the vicinity and the magnitude of background
pollution from other sources.
In a study in the United Kingdom (Waller et al., 1965),
measurements were made at a sampling site at the centre of a busy
street canyon, where traffic flows were typically 1200 gasoline and
600 diesel vehicles per hour, in order to assess the maximal
concentrations of traffic pollutants in urban areas. The contributions
of airborne particulate matter, expressed as seasonal means for
daytime working hours, were 200-421 µg/m3, after allowance for the
urban background measured at nearby control sites. The additional
particulate matter was attributed primarily to the diesel vehicles,
while the corresponding contribution to carbon monoxide, averaging
15 ppm (17 mg/m3), was associated mainly with the gasoline vehicles.
In France, Joumard & Perrin (1988) measured atmospheric
particulate matter (diameter, 0.01-25 µm) in a 30-40-m wide street
open to pedestrians, with two central lanes reserved for use by bus
services involving weekday traffic of more than 1000 vehicles per day
in each direction. The measurement point was in the immediate vicinity
of two bus stops, 3 m from the edge of the pavement and at a height of
2.5 m. The particle concentrations, determined by measuring ß
radiation, were 34 µg/m3 during the period 23.00-05.00 h and
67 µg/m3 during 07.00-19.30 h.
Airborne particle concentrations were calculated for an
eight-lane American freeway and for four- and six-lane European
autoroutes. The one-dimensional Gaussian model used neglects chemical
reactions during transport and possible deposition on the ground and
assumes turbulent mixing in the air. The calculated maximal
concentrations were 7-13 µg/m3 close to the road, and these
decreased with distance from the measuring point. About 100 m away,
the estimated particle concentration at a height of 1.5 m was three to
four times lower than that next to the motorway (Volkswagen AG, 1989).
Particle emissions, especially from diesel vehicles, were
estimated roughly for various locations by the lead surrogate method,
in which historical ambient lead concentrations in urban areas are
used as indices of mobile source pollutant levels. Particle emission
factors for light- and heavy-duty vehicles and the distribution
characteristics of lead and diesel particulate are also taken into
consideration (Rykowski & Brochu, 1986). The results are shown in
Table 31.
Concentrations of particles from diesel engines in the
environment were determined in Vienna, Austria, at several measuring
points during a four-week period. As there was only one distributor of
diesel fuel for the whole network of service stations in Vienna, the
rare earth element dysprosium was added as an indicator to the fuel at
this central point, which was distributed to diesel vehicles at
service stations and then emitted with the exhaust. Dust samples
collected from the air were subjected to neutron activation analysis
and the level of dysprosium was determined. The proportion of
dysprosium in diesel soot was calculated on the basis of emission
factors for diesel engines in the literature and from laboratory
experiments, assuming that the marker is totally transferred from fuel
to exhaust during combustion. At seven of the 11 measuring points for
different traffic densities, the concentrations were almost linearly
correlated to traffic density. Ambient particulate levels increased by
5.5 µg/m3 per 500 diesel vehicles per hour, from 10.3 in a residential
area to 23.6 µg/m3 near an urban freeway; the mean value was
14.4 µg/m3. The diesel particulate concentration in the centre of
Vienna was calculated to be 11 µg/m3 by correlating the measured
values and traffic density. At four measuring stations, significant
deviations from linearity were found which were due to local
conditions. The concentration of the marker was below the detection
limit before the testing period and one year later (Horvath et al.,
1988). A deficiency of the study is that the dysprosium concentrations
of diesel fuel before the addition were not taken into account, so
that the emission factors used may not reflect the true situation
(Holländer, personal communication, 1994). Nevertheless, the measured
ambient particle concentrations fit well with estimated data for
diesel exhaust emissions by other investigators.
Table 31. Estimated particle concentrations emitted from diesel
engine exhaust
Location and year Concentration
(µg/m3)
United Statesa, cities with > 1 million 1.3-3
residents (1984)
United Statesa, cities with 100 000-250 000 residents 0.7-1.7
Naples, Italy, urban area (1982) 7.2-35.1
Birmingham, United Kingdom, urban area (1982) 3.2-20.3
Birmingham, United Kingdom, university area (1982) 0.8-5.5
Stockholm, Sweden, inner city (1982) 2.5-16.4
From Rykowski & Brochu (1986)
a According to Cuddihy et al. (1984), the proportion of
diesel-fuelled light-duty vehicles in the United States was
about 2%.
In a programme to measure airborne diesel soot levels in
Düsseldorf, Germany, the total carbon content of fine dust (particle
diameter, < 7µm) at a busy crossing was 8-42 µm3 as a daily
average, 18 µg/m3 as an annual average, 21 µg/m3 on workdays, and
14 µg/m3 on weekends. The carbon content after solvent extraction
(elemental carbon) was 6-32 µg/m3 as a daily average, 16 µg/m3 on
workdays, and 10 µg/m3 on weekends. In a residential area in
Duisburg, Germany, the concentration of elemental carbon was 3 µg/m3.
The method of determination was as follows: a defined volume of air
was sucked through a fibreglass filter, and the respirable particle
fraction was separated. This fine dust was further separated into an
incinerable portion (according to German standard method TRGS 900),
total carbon, and the carbon content after liquid extraction
(elemental carbon). Total and elemental carbon were determined by
coulometry. By correlation with diurnal changes in carbon and nitrogen
monoxide concentrations, the main particle source was shown to be
automobile traffic at the sampling location. Correlation of a traffic
census with working day and weekend particle levels showed that the
airborne particulate matter was due primarily to diesel vehicles
(Elbers & Muratyan (1991). Further measurements at the same place in
1991 and 1992 confirmed the results (Elbers & Richter, 1994).
Validation of the analytical method gave detection limits of 0.39 for
elemental carbon (relative standard deviation, 14% or 4.4 µg/m3) and
0.65 µg/m3 for total carbon (relative standard deviation, 13% or
7.8 µg/m3).
The weekly average ambient concentrations of diesel particulate
in Germany were estimated to be 5-10 µg/m3 in urban areas, 15-25 µg/m3
in urban areas close to busy streets, and < 1.5 µg/m3 in rural
areas; however, the method used for the estimations was not reported
(State Committee for Immission Protection, 1992).
Estimates of the US Environmental Protection Agency for 1986 gave
annual mean ambient concentrations of diesel particle in the United
States of 2.6 µg/m3 in urban areas and 2.4 µg/m3 in rural areas. A
prediction for 1995 gave values of 1.5 µg/m3 for urban and 1.2 µg/m3
for rural areas (Mauderly, 1992). Higher concentrations were estimated
by the Motor Vehicles Manufacturing Association (Sienicki & Mago,
1992), which predicted a mean value of 2.7 µg/m3 for the city of Los
Angeles in 1995. Lower levels were estimated in a study by the US
Environmental Protection Agency (1993) in which national average
emission factors for diesel vehicles for 1988 were multiplied by urban
and rural mileage. For 1990 and 1995, the annual exposure levels were
estimated to be 2.0 and 1.2 µg/m3 in urban air and 1.1 and 0.6 µg/m3
in rural air, respectively. These estimates were confirmed by ambient
monitoring. Using data from the early 1980s, when the proportion of
diesel vehicles, the number of kilometres travelled, and emission
standards differed from present characteristics, McClellan (1986)
derived ambient diesel particulate concentrations of 10-30 µg/m3 on
American urban freeways and in urban street canyons.
B5.2 Occupational exposure
The levels of particulate matter to which workers are exposed
when their predominant exposure to exhaust is that from diesel engines
are described in this section. It is difficult to determine the
contribution of diesel exhaust to respirable particles, as they
include not only those from diesel engines but also others generated
in the worker's environment, such as sand, dirt, coal dust, and
cigarette smoke particles. Thus, the levels of total and respirable
particulates reported in jobs with potential exposure to diesel
exhaust may be significant overestimates of the actual exposure. Only
two occupational groups have been studied in this regard: railroad
workers (Woskie et al., 1988a,b) and mechanics and drivers in the
trucking industry (Zaebst et al., 1991). The specific exposures of
these groups to diesel particles range from 0.026 to 0.192 mg/m3. In
the railroad workers, cigarette smoke was found to account for a
substantial proportion of total respirable particulate matter, and the
geometric mean exposure to respirable particulates of workers not
exposed to diesel exhaust was reduced by over 80% when the
contribution of cigarette particulate was considered (Woskie et al.,
1988a).
The principal marker chosen to measure exposure of workers in the
trucking industry (including road drivers, local drivers, stevedores,
and mechanics) to diesel exhaust was elemental carbon, which is
derived from the core of the diesel exhaust particle and represents
about 20% of respirable particulate; cigarette smoke does not
contribute appreciable amounts of elemental carbon. Mechanics and
stevedores had the highest exposure to diesel exhaust, and truck
drivers had lower levels (Zaebst et al., 1991). The degree to which a
marker of diesel exhaust exposure actually represents true exposure
depends on the nature of all sources of respirable particles in the
work-place. Occupational exposure to particulates is summarized in
Table 32.
Table 32. Reported occupational exposure to particulates among
workers exposed to diesel exhaust
Occupational group Particles (mg/m3)
Total Respirable Diesel
Railroad workers 0.01-1.99 0.06-0.41 0.051-0.192a
Mine workers 0-23.0 0-16.1
Truck drivers 0.1-1.0 0.13-1.2 0.025b
Bus garage and bus 0.15-1.2 0.01-0.61
workers
Stevedores 0.157b
Truck mechanics 0.133b
a Estimated using nicotine to account for exposure to cigarette smoke
b Based on carbon core analysis, with an estimated 20% of respirable
particulate due to carbon (Steenland et al., 1992)
Because 1-nitropyrene is associated with the particle fraction of
diesel exhaust, this compound was used as an indicator of the
particulate fraction of diesel exhaust derived from various sources
(e.g. ships, railroad engines, heavy-duty road vehicles, fork-lift
trucks) (Scheepers et al., 1994a,b). The 1-nitropyrene content of
fresh and aged diesel exhaust was measured in small air samples
extracted with acetone by sonication and detected by gas
chromatography-mass spectrometry. The following concentrations of
respirable diesel exhaust were determined: 0.044-0.33 mg/m3 in
various work-places with fork-lift trucks, 0.10-0.37 mg/m3 in
railroad engine repair shops, 0.080mg/m3 in a river vessel, and 0.67
or 3.33 mg/m3 in the breathing zone of railroad workers.
B5.2.1 Truck drivers and mechanics
In a study of 15 truck drivers in Geneva, Switzerland, exposure
to particulate matter was measured during one working day with a
direct-reading instrument and by sampling beside the drivers in the
truck cabin (Guillemin et al., 1992). Local drivers had greater
exposure to particulate matter (0.3 mg/m3) than long-distance
drivers (0.1 mg/m3) and spent more time in polluted areas, such as
streets with heavy traffic and construction sites. Smoking did not
influence the exposure of professional truck drivers to particulate
matter, probably because the ventilation rate of the truck cabins was
relatively high, even on cold days.
Industrial hygiene surveys were conducted during warm and cold
weather at eight terminals and truck repair shops to determine
exposure to submicrometre particles of elemental carbon among American
workers in one of four jobs -- road drivers, local drivers, stevedores,
and mechanics -- all of whom were exposed mainly to diesel aerosol
(Zaebst et al., 1991). The overall arithmetic mean exposure was
5.1 µg/m3 for 72 long-distance road drivers, 5.4 µg/m3 for 66
local drivers, 26.6 µg/m3 for 80 mechanics, and 31.3 µg/m3 for 54
stevedores exposed to diesel fork-lift trucks. The background
concentrations in the same cities were 3.4 µg/m3 on 21 major
highways and 1.4 µg/m3 in 23 residential areas. The exposures of the
truck drivers were significantly higher than the background
concentrations in residential areas but could not be distinguished
from the background highway concentrations.
Area air sampling in an American truck repair shop in 1987 gave
the following results, depending on the sampling location: 0.225 and
0.32 µg/m3 submicrometre particles, 0.26 and 0.51 µg/m3 respirable
particles, and 0.63 and 0.66 µg/m3 total particulate matter. The
values for elemental carbon were 86-118 µg/m3 submicrometre
particles and 159-214 µg/m3 total carbon. In personal samples from
four mechanics, 79-193 µg/m3 submicrometre elemental carbon were
found (US National Institute for Occupational Safety and Health,
1990a).
The concentrations of particles collected on fibreglass filters
at 25 work-places in Germany where mainly fork-lift trucks and trucks
were used were 0.02-0.8 mg/m3 in area samples and 0.13-1.2 mg/m3
in personal samples (Lehmann et al., 1990). Area measurements in two
German truck repair garages (five samples from each) showed
concentrations of incinerable fine dust (according to German standard
method TRGS 900) of 0.11-0.40 mg/m3 (Blome et al., 1990).
Personal samples from truck drivers who loaded diesel-engined
trucks onto car ferries in Sweden showed particle concentrations of
0.1-1.0 mg/m3 (Ulfvarson et al., 1987). The drivers may also have
been exposed to diesel exhaust from the ferries.
B5.2.2 Bus garage and other bus workers
In area samples taken in an American bus garage in 1989, the
concentrations of particles were 0-0.1 mg/m3 submicrometre
particles, 0-0.3 mg/m3 respirable particles, 0-0.22 mg/m3 total
particulate matter, and 0.014-0.326 mg/m3 elemental carbon (US
National Institute for Occupational Safety and Health, 1990b).
The concentrations of smoke were measured in two diesel bus
garages in London, United Kingdom, from high-volume samplers for
successive periods through the day and night, which were linked to bus
movements and the exposure of the maintenance staff. The contribution
from the buses was assessed by subtracting the background values at
control sites outside the garages. In the most polluted garage,
0.3-1.2mg/m3 of smoke were measured during working periods (Waller
et al., 1985).
In Sweden, a particle concentration of 0.46 mg/m3 was found
during personal sampling in periods of high activity (arrival and
departure of buses) (Ulfvarson et al., 1987).
Area air sampling of the concentrations of incinerable fine dust
(according to German standard method TRGS 900) in two bus depots (six
samples in each) and one bus garage (three samples) in Germany showed
concentrations of 0.22-0.37 mg/m3 (Blome et al., 1990).
The respirable dust levels in bus garages in Italy and the United
States ranged from <0.01 to 0.73 mg/m3 (Gamble et al., 1987a). The
total dust levels in bus garages in Denver, Colorado, United States,
were 0.01-0.81 mg/m3 (Apol, 1983; Pryor, 1983).
B5.2.3 Fork-lift truck operators
Area samples taken in one American trucking terminal where
diesel-powered fork-lift trucks were used in 1987 contained
48-62 µg/m3 submicrometre particles, 34-57 µg/m3 respirable
particles, and 62-97 µg/m3 total particles (US National Institute
for Occupational Safety and Health, 1989a). The concentrations of
elemental carbon in area samples from another American trucking
terminal in 1988 were 40-44 µg/m3, and those in personal samples
from fork-lift operators were 33-77 µg/m3 (US National Institute for
Occupational Safety and Health, 1989b). Area samples taken in an
American freight dock contained concentrations of <12 and 294 µg/m3
respirable dust. The levels were significantly higher in areas where
unfiltered rather than filtered diesel motors were used (US National
Institute for Occupational Safety and Health, 1990c).
A mean concentration of 31.3 µg/m3 of submicrometre elemental
carbon was found in personal samples from stevedores operating
diesel-powered fork-lift trucks. About 10 times less was found for
operators of gasoline- or propane-powered trucks (Zaebst et al.,
1991).
The concentrations of particles in the breathing zone during use
of diesel-powered fork-lift trucks for loading, unloading, and
warehousing operations in American ammunition storage magazines were
< 0.01 to1.3 mg/m3 (Ungers, 1984) and 0.5-5.0 mg/m3 (Ungers, 1985).
B5.2.4 Railroad workers
The mean levels of total particulate matter were 0.38 mg/m3
(range, 0.1-0.8) in Finnish locomotive cabs and 1.99 mg/m3 (range,
0.07-8.7) in roundhouses (Heino et al., 1978). In three German engine
sheds, the ambient concentrations of incinerable fine dust were
0.1-0.41mg/m3 (Blome et al., 1990).
A summary of American literature showed time-weighted average
levels of 0.05-0.07 mg/m3 (8-h) in tunnels, 0.16 mg/m3 (7.5-h)
during freighting, 0.01 mg/m3 (5-h) in switchyards, and 0.27 mg/m3
(8-h) in cabooses (Hobbs et al., 1977). The arithmetic mean
concentrations of total respirable particles in personal samples from
shop workers, engineers, brakemen, conductors, and farmers in the
American railroad industry (after correction for the estimated
contribution of cigarette smoke particulates) were 51-192 µg/m3
(Woskie et al., 1988a).
B5.2.5 Mine workers
Diesel vehicles and machines have been used in nearly all
American mines since the 1960s (Wichmann & Brüske-Hohlfeld, 1991). The
mean concentration of diesel particulate matter in personal and area
samples in mines where diesel equipment was used was 4.6 mg/m3
(range, 0.2-14) (Holland, 1978). Total respirable dust levels of
0.6-1.7 mg/m3 were found by personal sampling (Wheeler et al.,
1981); average concentrations of 0.9-2.7 mg/m3 were found in
full-shift personal samples, and the range for full-shift area samples
was 0-16.1 mg/m3 (Reger et al., 1982). The 8-h time-weighted average
level of respirable particulate matter in personal samples taken in an
American molybdenum mine was 0.2-1.9 mg/m3 (Cornwell, 1982). Total
respirable dust concentrations of 1.1-4.4 mg/m3 were reported in an
American gold mine (Daniel, 1984). The US Mine Safety and Health
Administration reported that the concentrations of diesel particulate
matter in American mines other than coal mines were 0.3-1.5 mg/m3
(Mauderly, 1992).
Data from a salt mine in Canada showed a diesel particulate level
of about 0.5 mg/m3 (Johnson & Carlson, 1986).
In area samples from different work-places in eight German coal
mines, the levels of airborne diesel particulate matter (incinerable
fine dust) were 0.19-0.70 mg/m3 (Blome et al., 1990). In German
potash-salt mines, depending on the district, 0.2-0.4 mg/m3 of
diesel particles were measured (Bauer et al., 1990).
B5.2.6 Fire fighters
The average concentration of total particulate matter in personal
samples from fire-fighters in Boston, New York City, and Los Angeles,
United States, in 1985 was between < 0.1 and 0.48 mg/m3. On a typical
day in Boston or New York City, exposure to diesel exhaust particles
was estimated to be about 0.225 mg/m3 after correction for the
contributions of background and smoking. Simulation of 'worst-case'
exposures in Los Angeles fire stations gave a maximal concentration of
0.748 mg/m3 total particles (Froines et al., 1987).
B5.3 Biomonitoring
B5.3.1 Urinary mutagenicity
The occurrence of mutagens, measured by the Ames test, in the
urine and faeces of eight car mechanics occupationally exposed to
diesel exhaust was compared with that of a reference group of nine
office workers. The samples were collected over 48 h; information was
also gathered on dietary intake, smoking habits, and medication. No
enhancement of the incidence or degree of faecal or urinary
mutagenicity was seen (Willems et al., 1989).
Post-shift urinary mutagenicity was measured by the Ames test in
306 samples from 87 railroad workers with a range of exposures to
diesel exhaust (Schenker et al., 1992). Exposure was measured
throughout the work shift by constant-flow personal sampling pumps. In
separate analyses of smokers and nonsmokers, no independent
association was seen with exposure to diesel exhaust. The workers with
the highest median exposure to respirable particles attributable to
diesel exhaust (113 µg/m3) were railroad engineering shop workers.
In studies of the effect of diesel exhaust on stevedores on
'roll-on-roll-off' ships (Ulfvarson et al., 1987), no difference in
mutagenicity to Salmonella typhimurium TA98 or Escherichia coli WP
2 uvr A was seen in urine collected during periods of exposure and
of no exposure. Similarly, no increase in urinary mutagenicity was
found in samples from six volunteers before and after exposure to
diesel exhaust collected from an experimental automobile run for 3.7 h
at 60 km/h and 2580 rpm.
B5.3.2 Other analyses
Samples of total suspended particulate matter were collected in a
repair shop for train engines, and the diesel exhaust concentrations
were determined using 1-nitropyrene as a biomarker (see section B5.2).
Urinary metabolites and the corresponding nitro-substituted
derivatives were detected by immunoassay in the urine of three
diesel-engine mechanics. They had a significantly increased excretion
of metabolites in comparison with two office clerks (Scheepers et al.,
1994b).
B6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS
B6.1 Deposition
The mass median aerodynamic diameter of diesel exhaust particles
in long-term studies in animals exposed by inhalation was 0.17-0.25 µm
(Lewis et al., 1986; Lee et al., 1987; Wolff et al., 1987;
Creutzenberg et al., 1990). The deposition efficiency of particles of
this size range is lower than that of smaller particles, for which the
deposition by diffusion increases with decreasing diameter. The
deposition efficiency of particles with a diameter > 0.5 µm increases
with the aerodynamic diameter, owing to sedimentation and impaction.
The nose has hardly any filter effect for diesel particles because the
fraction of particles < 0.4 µm deposited in the nose is very low
(Heyder et al., 1986).
After short-term inhalation by rats of 0.29-µm fused
aluminosilicate particles, 8% was deposited in the bronchi and 13% in
the lungs (Raabe et al., 1988). A total of 10-20% diesel exhaust
particles was deposited in rats and guinea-pigs (Chan et al., 1981;
Lee et al., 1983; Dutcher et al., 1984). In humans, the alveolar
deposition efficiency of 0.2-µm particles was 10-20%, and no bronchial
deposition was detected (Heyder et al., 1986).
These experimental results agree well with those of a predictive
model for deposition of inhaled diesel exhaust particles in laboratory
animals and humans (Yu & Xu, 1987). In humans, the deposition
efficiency was about 7% in the alveolar region and 4% in the
tracheobronchial region. The model can also predict the fractions that
will be deposited in different airway generations; maximal deposition
occurs in the alveolar region (twentieth generation) of adults and of
children over two years of age.
The length and concentration of exposure had no significant
effect on deposition in rats exposed to 0, 0.4, 3.5, or 7.1 mg/m3
diesel exhaust particles for 6, 12, 18, or 24 months, when deposition
of 0.1-µm gallium oxide particles was used as the indicator (Wolff et
al., 1987).
B6.2 Retention and clearance of particles
The kinetics of inhaled substances are conveniently described by
their pulmonary clearance and retention. These terms are often used
interchangeably, but it should be kept in mind that the fraction
cleared from the lung plus the fraction retained in the lung account
for the total deposited amount (retention = deposition - clearance).
Thus, in the following paragraphs, the term 'clearance' refers to a
clearance rate ( r, per unit of time) and the term 'retention' to a
biological half-time ( t “), provided there is a constant rate of
exponential clearance (ln2/ t “).
Clearance of diesel particles from the alveolar region is
important in the long-term effects of particles on cells, as it is
more than two orders of magnitude slower than mucociliary clearance,
measured in several studies in rats administered labelled diesel or
surrogate particles by inhalation. The pulmonary retention half-times
in studies in which the lung burden of diesel soot was also reported
are summarized in Table 33. The equivalent continuous exposure
concentration is calculated by multiplying the actual concentration by
the number of hours of weekly exposure divided by 168 h. This figure
allows a comparison of exposure levels in studies with different
exposure protocols. The assumption is that Habers' law ( c × t =
constant) is applicable. This is probably valid until a certain burden
of particulate is reached in the lung; however, when that level is
exceeded (particle overload), the calculation is increasingly invalid.
The retention half-time in these studies was 60-100 days in
control rats with low lung burdens and up to 600 days in animals with
high lung burdens. In a double logarithmic plot of retention
half-times and lung burden, a linear relationship can be seen for lung
burdens of diesel particles above 1mg per lung (Figure 1).
The gaseous phase of diesel exhaust appears to have no effect on
alveolar clearance in rats or hamsters (Heinrich et al., 1986a).
The retardation of lung clearance is not specific to diesel
exhaust but is known as 'lung overloading by particles'. This effect
is characterized by (i) an overwhelming of normal alveolar
macrophage-mediated clearance processes under certain conditions of
exposure, (ii) resulting in lung burdens greater than predicted from
deposition kinetics at low concentrations, (iii) with associated
pathophysiological changes including altered macrophage function,
inflammation, and pulmonary fibrosis, and (iv) an uncertain
association with an increased incidence of lung tumours in rats
(McClellan, 1990).
The effect of overloading lung clearance mechanisms was
investigated in NMRI and C57Bl mice, Wistar and Fischer 344 rats, and
Syrian golden hamsters exposed to particulates, including test toner
(polymer pigmented with carbon black), polyvinyl chloride, carbon
black, diesel exhaust, and two crystalline forms of titanium dioxide
(anatase and rutile), at concentrations of 0.8-64 mg/m3 for up to
two years. In rats, lung overloading generally occurred after exposure
to 0.5-1.5 mg per lung or about 1 mg of material per gram of lung
tissue. A two- to 10-fold decrease in the clearance rate was seen
after heavy particulate loading in all of these rodent species (Muhle
et al., 1990).
In comparisons of the effects of particles of different
densities, the retained volume of particles appears to be a more
useful parameter than the retained mass, as alveolar macrophages have
an upper volumetric uptake limit. The particulate overload effect
appears to be initiated in rats when the average particle volume per
alveolar macrophage exceeds about 60m3, and alveolar
macrophage-mediated particle clearance virtually ceases when the
phagacytosed particulate volume exceeds an average of 600m3 (Morrow,
1988).
At a lung burden above threshold, signs of lung overloading in
Fischer 344 rats persisted for 15 months after cessation of exposure
(Bellmann et al., 1992). Retardation of alveolar clearance was also
observed in hamsters and mice at a lung burden above about 1 mg per
lung. For mice, no data were available with regard to lung burdens
below 1 mg per lung, but retardation of alveolar clearance is probably
already present at lower lung burdens. Lung overloading is thus seen
in a variety of species with various materials. It is generally
observed after the threshold lung burden of particles of low
solubility and low acute toxicity is exceeded for a considerable time
(Muhle et al., 1990). The effects of overloading should be considered
in extrapolating the health effects seen at high concentrations in
experiental animals to the low concentrations occurring in the
environment or the work-place.
The alveolar clearance rates of highly insoluble particles differ
among species, with retention half-times ranging from 50 to 100 days
in rodents to several hundred days in dogs and man (Figure 2). In
human lung, the retention half-time of insoluble, nontoxic particles
may be >500 days (Bailey et al., 1985a,b).
Table 33. Pulmonary retention of insoluble particles in rats after exposure to diesel exhaust, and lung burden of diesel soot
Strain and sex No./group Duration of Exposure Pulmonary retention Reference
exposure
(h/week)
Concentration (mg/m3) Duration Lung burden Material Half-time
(weeks) (mg/lung) studied (days)
Actual Equivalent
continuous
Fischer 344, 4 140 0 0 0 0 14C-Diesel 77 Chan et al.
male 0.25 0.21 7 0.2 exhaust 90 (1984)
0.25 0.21 16 0.5 92
6.00 5.00 1 0.7 166
6.00 5.00 9 6.5 562
6.00 5.00 16 11.8 (> 1000)
Wistar, female 5-7 90 0 0 13 0 59Fe2O3 61 Creutzenberg
0.84 0.45 0.63 (0.3 µm) 94 et al. (1990);
2.5 1.34 2.5 119 Heinrich et
6.98 3.74 8.2 330 al. (1995)
0 0 52 0 72
0.84 0.45 2.8 121
2.5 1.34 10.7 254
6.98 3.74 35.7 541
0 0 78 0 96
0.84 0.45 5.5a 221
2.5 1.34 12.2 272
6.98 3.74 58.8 687
Table 33 (contd)
Strain and sex No./group Duration of Exposure Pulmonary retention Reference
exposure
(h/week)
Concentration (mg/m3) Duration Lung burden Material Half-time
(weeks) (mg/lung) studied (days)
Actual Equivalent
continuous
Fischer 344, 8 35 0.15 0.03 18 0.035 Diesel 87 Griffis et al.
male and 0.94 0.20 0.22 exhaust 99 (1983)
female 4.10 0.85 1.89 165
Fischer 344, 4 140 6.00 5.00 1 1.7 14C-Diesel 61 Lee et al.
male 6.00 5.00 3 4.4 exhaust 124 (1987)
6.00 5.00 6 10.4 192
Fischer 344, 15-16 (lung 35 0 0 104 0 134Cs-Fused 79 Wolff et al.
male and burden) 0.35 0.07 0.6 aluminosilicate 81 (1987)
female 10 3.50 0.73 11.5 particles 264
(retention) 7.00 1.46 20.5 (2 µm) 240
a Measured; value derived by interpolation from data at 52 and 104 weeks
Retention of diesel particles in the lungs and lymph nodes has
been reported in Fischer 344 and Wistar rats after long-term
inhalation (Brightwell et al., 1986; Ishinishi et al., 1986; Mauderly
et al., 1987; Strom et al., 1988; Creutzenberg et al., 1990; Strom et
al., 1990). Some results with regard to lung burden are included in
Table 33. Because clearance of lung burdens above about 1 mg per lung
was impaired after long-term, continuous inhalation of a concentration
equivalent to about 0.5mg/m3, no steady-state lung burden was found
at serial sacrifice at up to two years. About 20% of the lung burden
of diesel particles was found in lung-associated lymph nodes at that
time.
Mathematical models have been developed to calculate the
retention of diesel particles in rats. Yu & Yoon (1990) and Yu et al.
(1991) developed a dosimetry model to predict the retention of diesel
particles and associated organic compounds in rats and humans of
different ages. The model indicates that lung clearance would not be
impaired in humans exposed to a concentration < 0.05 mg/m3 for
24 h/day. The highest lung burden per unit of lung weight was
calculated for five-year-old children. This model was used to assess
the risk of inhaling diesel particles (Pepelko & Chen, 1993).
B6.3 Retention and clearance of polycyclic aromatic hydrocarbons
adsorbed onto diesel soot
The clearance of particles from ciliated airways by the
mucociliary escalator after bronchial deposition is virtually complete
within 24 h. For soluble organic material like PAHs on the surface of
carbon particles, diffusion-limited clearance through the airway
epithelium to capillary blood was found to be slower in the bronchial
region than in the alveoli (Gerde et al., 1991a, 1993a,b).
PAHs in diesel soot adhere strongly to the surface of the
particles. Several studies have shown that the association of PAHs
with particles significantly slows the clearance of the PAHs from
lungs in comparison with the clearance of inhaled PAHs unassociated
with particulate matter.
After inhalation by Fischer 344 rats of 3H-benzo[ a]pyrene
adsorbed onto diesel soot (0.1% by mass) for 30 min, biphasic lung
clearance was noted. In a first, fast phase, about 50% of the inhaled
compound was cleared with a half-time of about 1 h, predominantly by
mucociliary clearance. At the end of exposure, about 15% of the 3H
label was found in blood, liver, and kidney, indicating rapid, direct
absorption of this fraction of 3H-benzo[ a]pyrene and its metabolites
into blood. The remaining 50% was retained in the lung, with a
half-time of 18 days; this is one-third of the retention half-time of
diesel particles. Thus, removal of benzo[ a]pyrene and its metabolites
from the particle carrier may be the rate-limiting step of this
clearance process (Sun et al., 1984). In contrast, more than 95% of
pure 3H-benzo[a]pyrene was cleared from the lung within 12 h after
inhalation (Sun et al., 1982).
These results were confirmed and extended to another PAH,
1-nitropyrene (Bond et al., 1986a,b), when the clearance of
14C-labelled compound adsorbed to diesel soot was determined by the
same method in Fischer 344 rats. After exposure to 490 ng/litre of
pure labelled compound, about 90% was cleared in the first, fast
clearance phase, with a retention half-time of 1 h; after exposure to
650 ng/litre of 14C-1-nitropyrene adsorbed onto diesel particles,
45% of the labelled compound was cleared from the lungs in the first
phase, with a half-time of about 2 h. The remaining 55% was retained
with a half-time of 36 days, which was twice the corresponding value
for 3H-benzo[ a]pyrene in the study of Sun et al. (1984).
On the basis of their data on the clearance of 3H-benzo[ a]pyrene
and 14C-1-nitropyrene, Bond et al. (1986b) predicted equilibrium
lung burdens in humans after long-term inhalation. Assuming inhalation
of 3.5 g/m3 of particles containing 0.1% benzo[ a]pyrene and
1-nitropyrene over an 8-h working day, they predicted equilibria of
160 ng benzo[ a]pyrene and 31 ng 1-nitropyrene per lung. No data are
available on changes in the retention of individual compounds after
prolonged exposure to diesel exhaust.
The clearance of a very low concentration (2.6 g/g particles) of
3H-benzo[ a]pyrene adsorbed onto diesel particles was measured in
Sprague-Dawley rats after intratracheal instillation (Bevan & Ruggio,
1991). Only 25% was cleared in the early, fast phase; a long-term
retention half-time of eight days was calculated for the remainder
during a three-day follow-up, which was similar to the clearance in
that period in the study of Sun et al. (1984).
B6.4 Metabolism
In the studies of Sun et al. (1984) and Bond et al. (1986a,b),
the levels of 3H-benzo[ a]pyrene and 14C-1-nitropyrene and their
metabolites in extracts of lung homogenates after inhalation of diesel
exhaust particles were measured by high-performance liquid
chromatography. Sun et al. detected oxidized metabolites 30 min after
inhalation: 35% of the 3H-benzo[ a]pyrene had been metabolized in
equal amounts to phenols (3-hydroxy- and 9-hydroxybenzo[ a]pyrene)
and quinones (1,6 and 3,6 isomers). Twenty days later, only 13%
phenols and 5% quinones were detected. In the study of Bond et al.
(1986b), about 30% of the 3H-1-nitro-pyrene had been metabolized to
acetylaminopyrenephenol (6 and 8 isomers) and about 40% remained
unmetabolized 1 h after inhalation. Oxidative metabolism of
14C-benzo[ a]pyrene, in solution or adsorbed onto diesel particles
at a concentration of 500 pmol/106 cells, was also detected in cell
cultures of pulmonary macrophages obtained from beagle dogs. The
quantity of metabolites increased with incubation time up to 45 and
125 pmol/106 cells in extracts and in the media, respectively, after
48 h of incubation. After incubation for 6 h, the major metabolites
found in extracts of cells were benzo[ a]pyrene-7,8-diol (0.5pmol/106
cells) and benzo[a]pyrene-4,5-diol (0.2 pmol/106 cells); those in
extracts of culture medium were benzo[ a]pyrene-7,8-diol (1.7 pmol/106
cells) and benzo[ a]pyrene-9,10-diol (1.4 pmol/106 cells), in
comparison with a total concentration of metabolites of 2.5 pmol/106
cells in the extracts and 6 pmol/10 6 cells in the medium. Minor
metabolites were benzo[ a]pyrene phenols (3-hydroxy- and
9-hydroxy-benzo[ a]pyrene) and benzo[ a]pyrene quinones (6,12, 1,5,
and 3,5 isomers). The quantities of metabolite were similar when
macrophages were incubated with benzo[ a]pyrene in solution or
adsorbed onto diesel particles (Bond et al., 1984).
Using the 32P-postlabelling technique, Wong et al. (1986) found
increased DNA adduct formation in the lungs of Fischer 344 rats after
exposure for 31 months to diesel exhaust containing 7.1 mg/m3
particles. After exposure of Fischer 344 rats and Syrian golden
hamsters to dilutions of diesel engine exhaust for six months to two
years, the level of haemoglobin adducts (2-hydroxyethylvaline and
2-hydroxypropylvaline), corresponding to the metabolic conversion of
5-10% of inhaled ethylene and propylene to its oxides, increased
dose-dependently (Törnqvist et al., 1988). An adduct of
benzo[ a]pyrenediol epoxide with deoxyguanosine was identified after
inhalation of benzo[a]pyrene adsorbed onto carbon black (20 mg/g)
(Wolff et al., 1989), demonstrating the production of epoxides of PAHs
by oxidative metabolism.
Methods for extracting diesel soot before testing for
genotoxicity in vitro have been discussed. As dichloromethane and
dimethyl sulfoxide do not correspond to leaching conditions in the
lung, it can be assumed that the bioavailability of genotoxic
materials is lower in lungs than in vitro. An investigation of
dipalmitoyl phosphatidylcholine, the primary component of
physiological surfactant, demonstrated that the genotoxicity
associated with diesel particles inhaled into the lung can be
activated by the solubilization and dispersion properties of pulmonary
surfactants. This finding was confirmed in mammalian cells for sister
chromatid induction (Keane et al., 1991) and for chromosomal
aberrations and micronucleus formation (Gu et al., 1991, 1992).
B7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO SYSTEMS
B7.1 Single exposure
Data on the acute toxicity of diesel exhaust are very limited;
the two available studies suggest that diesel exhaust particles and
their extracts have little acute toxicity.
Male ICR mice were administered diesel exhaust particles by
intratracheal instillation, and mortality due to lung oedema was
assessed for up to 24 h. At a dose of 0.9 mg per animal, all animals
died within 24 h. The LD50 value was 0.6 mg per animal, equivalent
to about 20 mg/kg body weight. Diesel exhaust particles washed three
times with methanol did not cause death at a dose of 1 mg per mouse,
suggesting that the primary source of toxicity is the extractable
organic compounds rather than the particles themselves. These
compounds may produce superoxide radicals that damage endothelial
cells (Sagai et al., 1993).
The LD50 value for diesel exhaust extract in adult Syrian
golden hamsters after intraperitoneal injection was 1280 mg/kg body
weight (Pereira et al., 1982).
B7.2 Short-term exposure
Tracer-monitored DNA synthesis, indicating a proliferative
response, was observed in whole lung tissue of groups of 3-10 Fischer
344 rats exposed to diesel exhaust by inhalation at 6 mg/m3 for
20h/day on seven days per week for periods of 1-14 days. The response
was maximal after two days of exposure, showing a fourfold increase.
The type II cell labelling index was significantly higher (fourfold)
than that in controls after two and three days of exposure to diesel
exhaust. Both values returned to control levels after a one-week
recovery period. Experiments involving incorporation of 14C-palmitic
acid revealed transient changes in lipid metabolism after one day of
exposure, with a threefold increase in the amount of phosphatidyl-
choline in lung tissue (Wright, 1986).
Exposure of various species by inhalation to 6 mg/m3 resulted
in slight alterations in lung function and histopathological changes.
Groups of 10 male Chinese hamsters were exposed for 8 h/day on
seven days per week for six months to particle concentrations of
either 6 or 12 mg/m3 diesel exhaust.
Measurements of pulmonary function indicated dose-related
increases in lung weight and dose-related decreases in vital and
diffusion capacity. Pathological evaluation revealed oedema,
thickening of the alveolar lining, a possible increase in collagen,
and the presence of numerous particle-laden macrophages, which almost
filled the alveolar spaces (Vinegar et al., 1981).
Groups of 41-51 male and female Hartley guinea-pigs were exposed
for 20 h/day on seven days per week to exhaust from a light-duty
diesel engine diluted to attain a concentration of 6 mg/m3
particulate matter. Separate groups were exposed to raw exhaust and
exhaust that had been irradiated with ultra-violet light for an
average of about 1 h. Pulmonary function was measured, and
electrocardiography was conducted on animals exposed for four weeks;
those examined for histological changes were exposed for eight weeks.
The only changes noted after four weeks were a 35% increase in
pulmonary flow resistance and a small, but significant decrease in
heart rate in animals exposed to irradiated exhaust. No changes in the
electrocardiogram were noted. The pathological changes were limited to
hyperplasia of alveolar lining cells and slight focal thickening of
the interstitium in occasional alveoli with accumulation of
particle-laden macrophages. Growth rates were unaffected (Wiester et
al., 1980).
As part of the same study, cats (Pepelko et al., 1981) and male
rats (15 per group) (Pepelko, 1982) were exposed for four weeks to
unirradiated exhaust under identical conditions. The pulmonary
function of rats was unchanged; the only changes were significant
increases in vital and total lung capacity, but these differences were
quite small and of questionable significance. The only functional
change noted in the cats was a decrease in maximal expiratory flow
rate at 10% of vital capacity. The pathological changes were again
limited to focal thickening of the alveolar walls near accumulations
of particle-laden macrophages. In general, the functional and
pathological changes were limited under these experimental conditions.
Kaplan et al. (1982) exposed male Fischer 344 rats (168 per
group), A/J mice (672 per group), and male Syrian golden hamsters (236
per group) to 1.5 mg/m3 of diesel exhaust particles for 20 h/day on
seven days per week for three months or to clean air. Animals were
killed at the end of exposure and after an additional six-month
recovery period. Mortality was not increased during the observation
period, and body weight was not significantly altered in any species.
At the end of exposure, the relative weight of the lung was
significantly increased in rats. In mice, the pulmonary adenoma
response was increased but not significantly. In all three species,
grey to black discolouration of the lungs and lung-associated lymph
nodes were observed. Microscopically, most of the particulate was
found in macrophages, but some was free. After six months' exposure to
clean air, the lungs of all species had considerably less pigment
accumulated in foci.
Sixteen male Fischer 344 rats were exposed to 6 mg/m3 diesel
exhaust for periods ranging from 6 h to 63 days, with subsequent
histological examination of the lungs. The numbers of diesel
particulate-containing alveolar macrophages, type II alveolar cells,
and inflammatory cells were found to be increased over those in eight
controls. After a nine-week exposure, accumulation of macrophages was
observed near the terminal bronchioles (White & Garg, 1981). In rats
that inhaled 6 mg/m3 diesel exhaust for two weeks and were either
killed immediately or allowed to recover for six weeks before
sacrifice, there was no statistical difference in the number of
macrophage aggregates (240 000 and 220 000 per lung); however, the
aggregates in the recovery group had significantly higher average
diameter and volume, demonstrating macrophage attachment after the end
of exposure (Garg, 1983).
The observations of Wiester et al. (1980) and Garg (1983)
demonstrate the importance of alveolar macrophages in the clearance of
particles of low solubility. These are engulfed by alveolar
macrophages and eliminated via the mucociliary escalator and
gastrointestinal tract, or, in the case of lung particle overloading,
increasing fractions are sequestered in focal areas of the lung tissue
and transferred to the lymph nodes (Muhle et al., 1990).
B7.3 Long-term exposure and studies of carcinogenicity
B7.3.1 Non-neoplastic effects
No obvious signs of toxicity were observed in groups of 183 male
and 183 female Fischer 344 rats exposed by inhalation to diesel
exhaust at 0.35, 3.5, or 7.1 mg/m3 for 7 h/day on five days per week
for up to 30 months (Mauderly et al., 1987). The body weights did not
differ significantly from those of controls, and the exposures did not
affect the life span of animals of either sex. Focal fibrotic and
proliferative lung disease was observed in parallel with progressive
accumulation of diesel soot in the lung. Henderson et al. (1988)
reported the results of biochemical and cytological analyses of lung
lavage fluid and lung tissue from rats and mice exposed in the same
study, including determinations of lactic dehydrogenase, glutathione
reductase, ß-glucuronidase, glutathione, and hydroxyproline, and the
numbers of macrophages and neutrophils. No changes were seen in rats
or mice exposed to 0.35 mg/m3 , but at higher concentrations dose-
and duration-dependent increases in biochemical parameters and cell
numbers in lavage fluid were observed, indicating a chronic
inflammatory response. Lung weights were also increased in male and
female mice exposed to the two higher levels for any length of time,
in rats exposed to 7.0 mg/m3 for 12 months or longer, in female rats
exposed to 3.5 mg/m3 for 18 months, and in males exposed to
3.5 mg/m3 for 24 months. Tissue enzyme levels, measured in lung
lavage fluid as an indicator of damage, were consistently raised in
rats and mice at the two higher exposure levels and in lung tissue of
rats and mice at various times (most pronounced at 7 mg/m3). These
changes probably indicate an increase in lung tissue due to increased
inflammatory cells and epithelial cell proliferation.
In the same study, Mauderly et al. (1988) described focal
proliferative, fibrotic, and emphysematous changes in the lungs of
animals at the higher doses. Measurements in vivo revealed a
reduction in lung volume and compliance.
In a follow-up study, Mauderly et al. (1990) exposed male Fischer
344 rats that were either normal or had pre-existing pulmonary
emphysema (elastase-treated) to diesel soot at 3.5 mg/m3 for 7 h/day
on five days per week for 24 months, to determine whether
emphysematous rats were more susceptible to diesel exhaust. No
increase in susceptibility was seen. The emphysematous lungs had a
lower accumulation of particles than the normal lungs, which prevented
an overproportional response of the compromised animals.
Male and female Fischer 344 rats exposed to diesel exhaust
particles at 0.7, 2.2, or 6.6 mg/m3 for 16 h/day on five days per
week for two years or to filtered diesel exhaust showed an
exposure-related reduction in the rate of weight gain throughout the
study at the highest dose and an increase in absolute lung weight at
the two higher doses (Brightwell et al., 1986, 1989).
Groups of 72 male and 72 female Fischer 344 rats exposed to
diesel exhaust particles at 2 mg/m3 for 7 h/day on five days per
week for 24 months showed alveolar type II cell hyperplasia,
inhibition of long-term clearance of particles and pulmonary
lipidosis. No immunological abnormalities, no induction of pulmonary
or hepatic xenobiotic metabolizing enzymes, and no effects on
mortality, body weight gain, organ:body weight ratios or clinical
chemical parameters were seen (Lewis et al., 1986, 1989). In the same
study, a dose-related depression in phagocytic activity was seen in
alveolar macrophages (Castranova et al., 1985), and a trend to
increased pulmonary arterial wall thickness was observed in comparison
with controls (Vallyathan et al., 1986).
In groups of 15 male monkeys, exposure to diesel exhaust (as
described above) resulted in mild obstructive airway disease, but
there was no evidence of restrictive lung disease. The effects were
observed throughout the exposure period, after 6, 12, 18, and 24
months (Lewis et al., 1989).
Reduced body weight, significantly increased lung:body weight
ratios, and type II cell proliferation were seen in female Fischer 344
rats exposed to whole-fraction diesel exhaust at 5 mg/m3 for 8 h/day
on seven days per week for 24 months (Iwai et al., 1986).
Groups of 96 male and 96 female Syrian golden hamsters, female
NMRI mice, and female Wistar rats were exposed to diesel engine
emissions at 4.4 mg/m3 for 19 h/day on five days per week for
120-140 weeks (Heinrich et al., 1986a; Stöber, 1986). The body weights
of mice were significantly reduced, by about 12%. Lung weights were
increased after two years of exposure, by two- to threefold in rats
and mice and by 50-70% in hamsters. Different levels of histological
response were seen in the three species. Hamsters had thickened
alveolar septa and bronchioalveolar hyperplasia. Of the mice, 64% had
bronchioalveolar hyperplasia (controls, 5%), 71% had multifocal
alveolar lipoproteinosis, and 43% had multifocal interstitial fibrosis
(controls, 4%). The nose, larynx, and trachea were not affected.
Treated rats showed severe inflammatory changes in the lungs,
thickened septa, foci of macrophages, and hyperplastic and metaplastic
lesions, but no significant changes in respiratory rate, minute
volume, compliance, or resistance were seen in 14 exposed rats.
Significantly increased airway resistance and a significant decrease
in dynamic lung compliance were observed in rats after two years of
exposure. The hamsters had a significant increase in airway resistance
and a nonsignificant reduction in lung compliance at termination of a
one-year exposure; these changes persisted during the second year of
exposure. In the same experiments, filtered diesel exhaust did not
have the same effects as total exhaust in any of the three species
(Heinrich et al., 1986a).
Groups of 27 female Fischer 344 rats and about 50 male and 50
female C57Bl/6N and ICR mice were exposed to particle concentrations
of 2-4 mg/m3 for 4 h/day on four days per week for up to 24 months.
After 12 months, the incidence of alveolar hyperplasia was increased
in all animals. Exposed rats had more severe inflammation than
controls, with inflammatory exudate into the nose, and bronchitis and
pneumonia, but this effect was ascribed to the housing, which was not
specific pathogen-free (Takemoto et al., 1986).
Groups of nine male Hartley guinea-pigs were exposed at
concentrations of 0.25, 0.75, or 1.5 mg/m3 for 20 h/day on 5.5 days
per week for up to two years. An analysis of the alveolar capillary
membrane by quantitative morphometry showed that it was thickened as a
result of an increase in the absolute tissue volume of interstitium
and type II cells. Exposure to 0.75 mg/m3 for six months caused
fibrosis in regions of macrophage clusters and focal type II cell
proliferation, as observed under the light microscope. No appreciable
change in morphometric parameters was seen after exposure to the
lowest dose, but the higher doses increased the thickness of alveolar
septa and the numbers of various types of alveolar cells (Barnhart et
al., 1981, 1982).
As part of this investigation, Fischer 344 rats were exposed by
inhalation to 0.25 or 1.5 mg/m3 diesel exhaust particles, and
various biochemical and cytological studies were conducted up to 36
weeks (Misiorowski et al., 1980). At the high dose, normalized lung
weight, the rate of collagen synthesis, and the cellular and lipid
content of lung tissue were significantly increased after six months.
It was concluded that the reactivity of fibrogenic cells had been
enhanced. In a long-term study of respiratory end-points in male
guinea-pigs, including light and electron microscopy, lavage cytology,
and lung tissue biochemistry, the lowest-observable-adverse-effect
level (LOAEL) was 0.796 and the no-observable-adverse-effect level
(NOAEL) was 0.258 mg/m3 (US Environmental Protection Agency, 1992b).
Groups of 120 male Fischer 344 rats, 450 male A/J mice, and 120
male Syrian hamsters were exposed to 0.25, 0.75, or 1.5 mg/m3 diesel
exhaust particles for 20 h/day on seven days per week for 15 months.
Mortality was not increased in any species. A dose-related deposition
of pigment was observed histopathologically in alveolar macrophages
and regional lymph nodes. Accumulation of alveolar macrophages was
associated with an increase in connective tissue in alveolar walls,
with mild fibrosis and proliferation of type II pneumocytes; these
effects were termed pneumoconiosis. No treatment-related responses
were found in organs other than the respiratory tract. The LOAEL was
0.735 and the NOAEL, 0.242 mg/m3 (Kaplan et al., 1983).
Groups of 120 male and 95 female Fischer 344/Jcl rats were
exposed to light-duty diesel engine exhaust particulates at 0, 0.1,
0.4, 1.1, or 2.3 mg/m3 or heavy-duty diesel engine exhaust
particulates at 0, 0.5, 1.0, 1.8, or 3.7 mg/m3 for 16 h/day on six
days per week for up to 30 months (Ishinishi et al., 1986, 1988;
Suzuki et al., 1990). The body weights of females exposed to the
highest dose of heavy-duty engine exhaust were decreased throughout
the study by 15-20% in comparison with controls. No changes were
observed histopathologically in the lungs at any concentration.
Accumulation of particle-laden macrophages was observed at levels
> 0.4 mg/m3. In areas of macrophage accumulation, bronchiolar
epithelium replaced alveolar epithelium in the ducts. Proliferation of
bronchiolar epithelium and type II cells and oedematous thickening and
fibrosis of the alveolar septum were observed, which developed into
small fibrotic lesions classified as hyperplastic. The incidences of
hyperplastic lesions were 4, 4, 6, 12, and 87 per 124 rats exposed to
light-duty engine exhaust and 1, 3, 7, 14, and 25 per 124 rats in
those exposed to heavy-duty engine exhaust. The LOAELs were
1.2 mg/m3 for light-duty and 1.0 mg/m3 for heavy-duty exhaust, and
the NOAELs were 0.4 and 0.5 mg/m3, respectively (US Environmental
Protection Agency, 1992b).
In the same experimental series, Kato et al. (1992) studied
non-neoplastic lesions in the respiratory organs of the rats every six
months. The marked changes consisted of intake of diesel particles by
type I epithelium, hypertrophy, and glandular proliferation of type II
epithelium, with many extended microvilli and increased numbers and
size of lamellar inclusion bodies, focal increase of collagen fibres
in the interstitium, and infiltration of particle-laden macrophages,
neutrophils, mast cells, and plasma cells into the interstitium of
alveolar septa. The most marked changes in the airway were focal
shortening of cilia and protrusions of nonciliated cells. These
morphological changes appeared in all groups exposed to particle
concentrations > 1 mg/m3 after six months of exposure and were more
marked with increasing particle concentration and with time.
Exposure of Syrian golden hamsters to 4 or 11 mg/m3 diesel
exhaust for 7 h/day on five days per week for five months resulted in
enlargement of liver sinusoids and loss of cristae in mitochondria
(Meiss et al., 1981).
The induction of pulmonary adenomas and carcinomas in rats after
long-term inhalation of carbon black is proposed to be due partly to
inflammatory cells and their mediators (Driscoll et al., 1995;
Oberdörster et al., 1995; Driscoll et al., in press). After exposure
of rats to carbon black at 1, 7, or 50 mg/m3 for 6 h/day on five
days per week for 13 weeks, 353, 1923, and 7112 µg of carbon,
respectively, were deposited per lung. After exposure to air or to
1 mg/m3 of carbon black, no macrophage inflammatory protein-2
(MIP-2) mRNA expression and no increase in inflammatory cells was
observed; with 7 or 50mg/m3, both MIP-2 mRNA and the number of
neutrophils in bronchoalveolar lavage fluid were increased, and the
hprt frequencies were 3.2 and 4.2 times greater than in controls.
Groups of 25 cats were exposed to either clean air or diesel
exhaust for 8 h/day on seven days per week for two years at a
concentration of 6 mg/m3 through week 62 and to 12 mg/m3 for weeks
62-124. Some of the cats were then held in clean air for an additional
six months. No response was seen after 61 weeks, but after 123 weeks
signs of restrictive lung disease were observed. Total lung capacity,
forced vital capacity, functional residual capacity, peak expiratory
flow rates, and diffusion capacity were significantly decreased
(Moorman et al., 1985). Morphological evaluation revealed
exposure-related lesions in the centriacinar region of the lungs,
bronchiolar epithelial metaplasia associated with the presence of
ciliated and basal cells, and alveolar macrophages containing diesel
particle-like inclusions. After six months' recovery in clean air, the
metaplasia had disappeared but the fibrosis had progressed (Hyde et
al., 1985). In exposed cats, the epithelium of the terminal and
respiratory bronchioles consisted of ciliated, basal, and Clara cells,
whereas controls had only Clara cells (Plopper et al., 1983). These
observations indicate that the foci of the lesions were the
epithelium, the interstitial compartments, and the centriacinar region
of the lung. The metaplastic changes suggest that cancer may be
induced by continuous exposure, while the other major effect is
pulmonary fibrosis resulting in restrictive disease which is not
ameliorated and in fact progresses after removal from exposure.
Progression of effects is probably due to continued lung overloading
with particulate matter, despite cessation of exposure.
The dose-dependent effects on lung morphology, histopathology,
biochemistry, and cytology after long-term exposure to diesel exhaust
described above are reflected in the following findings seen in rats
at a lung burden of about 0.5 mg/lung (Henderson et al., 1988; Muhle
et al., 1990):
-- The wet and dry weights of lungs increase by up to fourfold in
comparison with those of concurrent controls. This is due to
severe functional overloading in the lung, resulting in enhanced
leukocyte influx and tissue proliferation.
-- Pulmonary inflammation is manifested by cytological (increased
numbers of polymorphonuclear neutrophils) and biochemical (lactic
dehydrogenase, collagen in lung lavage fluid) parameters.
-- The retention of material is characterized by an increasing
number of particle-laden macrophages and by black discolouration
of lungs due to sequestration of accumulated particles.
Additionally, increased transfer of material to the
lung-associated lymph nodes is observed.
-- Later findings during inhalation are proliferative alterations of
the epithelial cells and onset of fibrosis.
B7.3.2 Carcinogenicity
B7.3.2.1 Inhalation
Rats were exposed in several studies to diesel emissions
containing > 2 mg/m3 of particles for more than two years,
resulting in the induction of pulmonary tumours (Table 34). Many
organic and inorganic gaseous components were also present in the test
atmospheres, and the relatively high concentration of some pulmonary
irritants like nitrogen dioxide, aldehydes, and sulfur dioxide may
have contributed to the inflammatory response and to epithelial cell
damage and subsequent cell proliferation. Exposure to gaseous PAHs,
like naphthalene which is toxic to Clara cells, may influence the
metabolic state of pulmonary cells. It is not clear however, whether
the combined exposure to particles and gases in these experiments
favoured tumour induction. It should be noted that Brightwell et al.
(1986), Heinrich et al. (1986a), Iwai et al. (1986), Ishinishi et al.
(1986), and Takaki et al. (1989) have reported that the gaseous phase,
i.e. the proportion of exhaust without particles, does not induce
pulmonary tumours.
Table 34. Carcinogenicity of diesel engine exhaust in rats
Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference
sex (mg/m3)a (observation burden of error (%)b
period) (mg/lung) No. % Mean
Actual Continuous (f+m) (%)
Wistar 40 m 8.3 1.5 6 h/d, 5 d/week, up NR 1 17c NR Karagianes
40 m Clean air to 20 months 0 et al.
(20 months) (1981)
Fischer 72 f 6.6 3.1 16 h/d, 5 d/week, 24 NR 39 54 38.5 < 0.1 Brightwell
344 71 m months (30 months) 16 23 et al.
72 f 2.2 1.1 11 15 9.7 < 0.1 (1986, 1989)
72 m 3 4
71 f 0.7 0.4 0 0.7
72 m 1 1
Filtered exhaust 0
0
142 f Clean air 1 1 1.4
140 m 3 2
Wistar 95 f 4.4 2.5 19 h/d, 5 d/week, 32 NR 17 18 < 0.1 Heinrich et
92 f Filtered exhaust months (up to death) 0 al. (1986a)
96 f Clean air 0
Table 34 (contd)
Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference
sex (mg/m3)a (observation burden of error (%)b
period) (mg/lung) No. % Mean
Actual Continuous (f+m) (%)
Fischer
344/Jcl
Light-duty 60 f 2 1.1 16 h/d, 6 d/week, 30 NR 1 2 2.4 NR Ishinishi
engine 64 m months (30 months) 2 3 et al.
59 f 1 0.6 2 3 4.1 (1986,1988;
64 m 3 5 Takaki et al.
61 f 0.4 0.2 0 0.8 (1989)
64 m 1 2
59 f 0.1 0.06 2 3 1.6
64 m 0
59 f Clean air 2 3 3.3
64 m 2 3
Heavy-duty 60 f 4 2.3 3 5 6.5 1.8
engine 64 m 5 8
59 f 2 1.1 1 2 3.3
64 m 3 5
61 f 1 0.6 0 0
64 m 0
59 f 0.4 0.2 1 2 0.8
64 m 0
59 f Clean air 1 2 0.8
64 m 0
16 m Filtered exhaust 0
Table 34 (contd)
Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference
sex (mg/m3)a (observation burden of error (%)b
period) (mg/lung) No. % Mean
Actual Continuous (f+m) (%)
Fischer 19 f 4.9 1.6 8 h/d, 7 d/week, 24 NR 8 42 < 1d Iwai et al.
344 16 f Filtered exhaust months (24 or 30 0 (1986)
22 f Clean air months) 1 5
Fischer 15 f 2.0-4.0 0.2-0.4 4 h/d, 4 d/week, 24 NR 0 NR Takemoto
344 15 f Clean air months (24 months) 0 et al.
(1986)
Fischer 69 f 7 1.5 7 h/d, 5 d/week, 30 NR 13 19 16.1 < 0.1 (f) Mauderly et
344/Crl 74 m months (up to death) 10 14 1.7 (m) al. (1986)
68 f 3.5 0.7 2 3 4.6
63 m 4 6
68 f 0.35 0.07 0 0.7
70 m 1 1
68 f Clean air 0 1.4
73 m 2 3
Fischer 227 f+m 7 1.5 7 h/d, 5 d/week, 30 20.8 12.8 < 0.1 Mauderly et
344/N Crl 221 f+m 3.5 0.7 months (up to death) 11.5 3.6 4.8 al. (1987)
223 f+m 0.35 0.07 0.6 1.3
230 f+m Clean air (24 months) 0.9
Table 34 (contd)
Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference
sex (mg/m3)a (observation burden of error (%)b
period) (mg/lung) No. % Mean
Actual Continuous (f+m) (%)
Wistar 100 f 7.0 3.8 18 h/d, 5 d/week, 24 63.9 22 22.0 < 0.1 Heinrich et
200 f 2.5 1.3 months (30 months) 23.7 11 5.5 < 1 al. (1992,
198 f 0.8 0.5 6.3 0 1995);
217 f Clean air (24 months) NR 1 0.5 Heinrich
(1994)
Fischer 212 f+m 6.3 3.0 16 h/d, 5 d/week, 24 85.4 38 17.9 17.9 NR Nikula et al.
344/N 210 f+m 2.4 1.1 months (24 months) 40.7 13 6.2 6.2 (1994)
214 f+m Clean air (23 months) 3 1.4 1.4
Fischer 49 f 4.7 1.3 15 h/d, 3 d/week, 24, NR 6 12.2 NR Kawabata
344/N 42 f 4.7 1.3 12, or 6 months 8 19.0 et al.
45 f 4.7 1.3 1 2.2 (1993)
48 f Clean air 5 10.4
Fischer 183 f+m 2.0 0.4 7 h/d, 5 d/week, 24 NR 8 4.4 4.4 NR Lewis et al.
344/N 180 f+m Clean air months 6 3.3 3.3 (1989)
From Pott & Heinrich (1987) and supplemented; NR, not reported
a Mass median aerodynamic diameter, 0.17-0.25 µm; 'Continuous', equivalent continuous value
b Unilateral Fisher's exact test
c Only six animals investigated
d With Yates' correction
No difference in lung tumour incidence was seen in groups of male
and female rats exposed for 7 h/day on five days per week for 24
months either to diesel exhaust particulates at 2 mg/m3 or to
filtered air (Lewis et al., 1989).
Exposure of six male Wistar rats to diesel exhaust soot at
8.3 mg/m3 and coal dust for up to 20 months gave inconclusive
results (Karagianes et al., 1981). The study had little statistical
power owing to the small group size, and the insufficient duration of
exposure may have prevented detection of tumours, although one mammary
fibroadenoma and one lung bronchiolar adenoma were detected. One
subcutal fibrosarcoma and one renal lymphoma were seen in controls.
Eight bronchioalveolar adenomas and nine squamous-cell tumours
were seen in 95 rats (18%) that had inhaled 4.4 mg/m3 diesel exhaust
for 19 h/day on five days per week for 32 months. No tumours were
observed in controls (Heinrich et al., 1986a). The dose-dependent
carcinogenic potency of diesel exhaust was confirmed in a study in
which rats were exposed to diesel exhaust at concentrations of 0.8,
2.5, or 7.0 mg/m3 for 18 h/day on five days per week for 24 months
(Heinrich et al., 1992; Heinrich, 1994; Heinrich et al., 1995).
In male and female rats exposed to diesel exhaust at 6.6 mg/m3,
a high incidence of lung tumours was observed in animals dying or
sacrificed after 24 months (24/25 females, 12/27 males). The incidence
of lung tumours (Table 34) was derived by pooling pulmonary adenomas;
squamous-cell carcinomas; adenocarcinomas; mixed ademomas,
adenocarcinomas, and squamous-cell carcinomas; and mesotheliomas.
Non-neoplastic pulmonary lesions were not described (Brightwell et
al., 1986, 1989).
Groups of 24 female Fischer 344 rats were exposed to clean air,
to whole-fraction (4.9 mg/m3 particulates) fuel, or to filtered
diesel exhaust for 8 h/day on seven days per week for 24 months. After
six months of exposure, the rats exposed to whole exhaust had lower
body weights than those in the other two groups; after 18 months, both
exposed groups showed body weight reduction. The relative lung weight
was increased after 12 months' exposure to whole exhaust, and
epithelial proliferation and significantly elevated numbers of lung
tumours were seen in animals exposed to the whole fraction after six
months. Increased incidences of leukaemia and mammary gland tumours
were also reported in animals exposed to whole or filtered exhaust;
however, because of the small numbers of animals, the significance of
the results cannot be determined (Iwai et al., 1986).
A total of 140 female and 140 male Fischer 344/N rats (in groups
of three males and three females, five males and five females, or
eight males and eight females, depending on the end-point) were
exposed for 16 h/day on five days per week for up to 24 months,
beginning at eight weeks of age, to particles of diesel exhaust or
carbon black at 2.5 or 6.5 mg/m3 of air, or to clean air (Mauderly
et al., 1994). Rats were killed after 3, 6, 12, 18, or 23 months of
exposure for histopathological assessment and measurement of lung and
lung-associated lymph node burdens of particles, lung weight,
bronchoalveolar lavage indicators of inflammation, DNA adducts in
whole lung and alveolar type II cells, and chromosomal anomalies in
circulating lymphocytes. Diesel exhaust and carbon black had nearly
identical effects, with a similar relation to exposure. There was a
dose-related slowing of particle clearance after three months, with
progressive accumulation of particles in lungs and lymph nodes.
Inflammation, epithelial proliferation, and fibrosis were progressive
and related to dose. Diesel exhaust slightly increased the number of
lung DNA adducts, and the numbers of DNA adducts in type II cells were
increased by both diesel exhaust and carbon black. No exposure-related
chromosomal damage was found in circulating lymphocytes. The incidence
of primary lung neoplasms was increased significantly and was related
to the doses of both diesel exhaust and carbon black. The types of
neoplasms were identical and included benign adenomas, malignant
adenocarcinomas, squamous-cell carcinomas, and adenosquamous
carcinomas; squamous cysts were also seen. The neoplasms had similar
growth characteristics when transplanted; 50-67% of the transplanted
squamous-cell carcinomas and 25-40% of the transplanted
adenocarcinomas grew after injection into athymic mice (Table 35),
whereas the squamous cysts did not.
Fischer 344/Jcl rats were exposed to a range of concentrations of
exhaust emission particulates from light-duty (up to 2 mg/m3) or
heavy-duty diesel engines (up to 4 mg/m3) for 16 h/day on six days
per week for up to 30 months. After 18 months, marked hyperplasia of
type II cells was noted in the groups at higher exposures. After 30
months, treatment-related pulmonary hyperplastic lesions were
detected, and a dose-response relationship was seen for tumours in the
groups exposed to heavy-duty but not light-duty diesel exhaust. The
lung tumours were diagnosed as adenocarcinomas, squamous-cell
carcinomas, or adenosquamous carcinomas. A significant correlation was
observed between the incidence of anthracosis and areas with
hyperplastic lesions; furthermore, anthracosis and hyperplastic
lesions did not appear in lungs exposed to particle-free exhaust. The
authors concluded that the occurrence of hyperplastic lesions was
dependent on the presence of carbon particles (Ishinishi et al., 1986,
1988; Takaki et al., 1989).
Table 35. Growth in athymic mice of lung tumours from rats exposed to
diesel exhaust and carbon black
Type of tumour Carbon black Diesel exhaust
Number Growing Number Growing
implanted No. % implanted No. %
Adenocarcinom 8 2 25 10 4 40
Squamous-cell 2 1 50 3 2 67
carcinoma
Squamous cyst 19 0 0 7 0 0
From Mauderly et al. (1994)
In a large-scale study of unfiltered diesel exhaust, 1097 Fischer
344 rats were exposed for up to 30 months to 0.35, 3.5, or 7.0 mg/m3
of diesel soot. A group of 365 rats exposed to clean air served as
controls. Exposure to exhaust did not cause overt signs of toxicity,
and no significant, exposure-related alterations in body weight were
observed. Rats were killed at six-month intervals, examined for their
lung burdens of diesel soot, and subjected to complete necropsy.
Diesel soot accumulated at all doses but minimally in the low-dose
group. An increased incidence of tumours was observed in the groups at
the medium and high doses; most (81%) of the tumours were observed
after two years of exposure. The inhaled soot concentration and the
lung burden of diesel soot were highly significantly related to tumour
incidence ( P < 0.001) (Mauderly et al., 1987). In a follow-up study
with longer daily exposure (16 h/day), the dose-dependency of the
tumour incidence was reproduced (Nikula et al., 1994). In this study,
the carcinogenicity of diesel exhaust soot (8% extractable organic
material; 2.5 mg/m3) was compared with that of carbon black (0.12%
extractable organic material; 6.5 mg/m3 ) in 1152 male and female
Fischer 344 rats exposed for 16 h/day on five days per week for up to
24 months and examined histopathologically. The lung burden of
particles was greater after exposure to diesel exhaust than to carbon
black, but the neoplastic response in the lung was similar and usually
occurred late in the study. When the lung burden of particles was used
as the dose parameter, the carcinogenicity of carbon black was
greater than that of diesel exhaust soot.
Groups of 50 four-week-old female Fischer 344 rats were exposed
to diesel soot at a mean concentration of 4.73 mg/m3 for 15 h/day
three times per week for 6, 12, or 24 months, and animals that died
after 18-30 months were evaluated for tumours. After 30 months, all
animals, including controls, were sacrificed and examined for lung
tumours. The incidences of lung tumours were 10.4% in controls and
2.2% after six months' exposure to diesel exhaust, 19.0% after 12
months, and 12.2% after 24 months. No statistical analysis was
presented, but it seems unlikely that there was a significant effect
(Kawabata et al., 1993).
Concurrent administration of known carcinogens with diesel
exhaust has also been studied. Exposure of rats to diesel exhaust
given an intraperitoneal injection of N-nitrosodiisopropylamine or
N-nitrosodiethylamine did not influence the rates of tumours induced
by the nitrosamines (Takemoto et al., 1986). The effects of treatment
of hamsters with N-nitrosodiethylamine or benzo[ a]pyrene were not
influenced by subsequent administration of diesel exhaust, whereas
pretreatment of mice with benzo[ a]pyrene or dibenzanthracene followed
by diesel exhaust gave inconsistent results. Exposure to diesel
exhaust did not affect the total tumour rates in rats pretreated with
6.25 or 12.5 g/kg body weight of N-nitrosodipentylamine; however,
the incidence of squamous-cell tumours was increased in both
pretreated groups (Heinrich et al., 1986a).
Hamsters were exposed for two years to unfiltered diesel exhaust
at 0, 0.7, 2.2, or 6.6 mg/m3 or to filtered diesel exhaust, and
groups of control and treated hamsters were administered
N-nitrosodiethylamine subcutaneously before the beginning of
exposure. The rate of pulmonary tumours was not increased by diesel
exhaust, with or without pretreatment with the nitrosamine. Several
hamsters that developed 'wet tail' infection after six months on test,
resulting in significant mortality (46%), were treated with
oxytetracycline, chloramphenicol, and dimetridazole (Brightwell et
al., 1986, 1989).
Overall, the only clear effect in these studies of
co-carcinogenicity in rats was an increase in the percentage of
malignant tumours in animals treated with diesel exhaust plus
carcinogens in comparison with the carcinogen alone (Heinrich et al.,
1986a).
The results of studies in other species (mice, hamsters, and
monkeys) treated by inhalation are given in Table 36. Heinrich et al.
(1982) found significant increases in lung tumour incidence in mice,
but this result could not be repeated in later studies (Heinrich et
al., 1986a, 1992, 1995). Small but statistically significant increases
in lung tumour incidence were reported in ICR and C57Bl mice (Takemoto
et al., 1986) and in female Sencar mice (Pepelko & Peirano, 1983);
however, because only small increases in non-malignant tumours were
seen only in females in the study of Pepelko & Peirano (1983), the
results must be considered to be weakly positive or equivocal.
Hamsters showed no response to diesel exhaust.
Table 36. Long-term studies of diesel exhaust by inhalation in species other than rats
Strain, species No. and sex Exposure Results Reference
Material Particles Duration
(mg/m3)
NMRI mouse 2 × 96 f (a) Exhaust 4 19 h/d, 5 d/week, Lung tumours (adenomas and Heinrich et al.
(b) Filtered 27-28 months adenocarcinomas) (a) 24/76 (32%), (1986a)
(c) Clean air including 13 (17%) adenocarcinomas;
(b) 29/93 (31%), including 18 (19%)
adenocarcinomas; (c) 11/84 (13%),
including 2 (2.4%) adenocarcinomas
Incidence in historical controls,
< 32%
ICR and 315 ICR, Exhaust or 2.0-4.0 4 h/d, 4 d/week, Lung tumours (adenomas and Takemoto et al.
C57Bl/6N 297 C57Bl/6N clean air 13-28 months adenocarcinomas). ICR: 14/56; (1986)
mice, newborn (sex 7/60 in controls; C57Bl/6N:
unspecified) 17/150; 1/51 in controls
Sencar mouse 2 × 130 f (a) Exhaust 12 8 h/d, 7 d/week, Adenomas and carcinomas Pepelko &
2 × 130 m (b) Clean air to 15 months of (a) m: 5.9%; f: 16.3% Peirano (1983)
age (from (b) m: 3.8%; f: 7.2%
conception to
sacrifice)
NMRI mouse 2 × 80 f (a) Exhaust 7.5 18 h/d, 5 d/week, Lung tumours Heinrich et al.
(b) Clean air 13.5 months, 9.5 (a) 32.1% (1992, 1995)
months' recovery (b) 30%
Table 36 (contd)
Strain, species No. and sex Exposure Results Reference
Material Particles Duration
(mg/m3)
NMRI and 3 × 120 f (a) Exhaust 4.5 18 h/d, 5 d/week; Lung tumours Heinrich et al.
C57Bl/6N mice 3 × 120 f (b) Filtered NMRI, 23 months; NMRI: (a) 23.3% (1992, 1995)
(c) Clean air C57Bl, 24 months (b) 46.7%
+ 6 months' (c) 30%
recovery C57Bl: (a) 8.5%
(b) 3.6%
(c) 5.1%
Syrian golden 3 × 48 f (a) Exhaust 3.9 ± 0.5 7-8 h/d, 5 d/week, No effect on survival, no lung Heinrich et al.
hamster (b) Filtered up to 30 months tumours (1982)
(c) Clean air
Syrian golden 3 × 48 f (a) Exhaust 4 19 h/d, 5 d/week, Normal life span, no lung tumours Heinrich et al.
hamster 3 × 48 m (b) Filtered 27-28 months (1986a)
(c) Clean air
Syrian golden 52 f + 52 m (a) Exhaust 0.7, 2.2, 16 h/d, 5 d/week, No significant increase in