Polycyclic aromatic hydrocarbons, selected non-heterocyclic (EHC 202, 1998)

UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 202

SELECTED NON-HETEROCYCLIC
POLICYCLIC AROMATIC HYDROCARBONS

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.

First and second drafts prepared by staff members at the Fraunhofer
Institute of Toxicology and Aerosol Research, Hanover, Germany, under
the coordination of Dr R.F. Hertel, Dr G. Rosner, and Dr J. Kielhorn,
in cooperation with Dr E. Menichini, Italy, Dr P.L. Grover, United
Kingdom, and Dr J. Blok, Netherlands. Dr P. Muller, Canada, and Dr R.
Schoeny and Dr T.L. Mumford, USA, prepared and revised the drafts of
Appendix I.

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 of the
Inter-Organization Programme for the Sound Management of Chemicals

World Health Organization
Geneva, 1998

The International Programme on Chemical Safety (IPCS),
established in 1980, is a joint venture of the United Nations
Environment Programme (UNEP), the International Labour Organisation
(ILO), and the World Health Organization (WHO). The overall objectives
of the IPCS are to establish the scientific basis for assessment of
the risk to human health and the environment from exposure to
chemicals, through international peer-review processes, as a
prerequisite for the promotion of chemical safety, and to provide
technical assistance in strengthening national capacities for the
sound management of chemicals.

The Inter-Organization Programme for the Sound Management of
Chemicals (IOMC) was established in 1995 by UNEP, ILO, the Food and
Agriculture Organization of the United Nations, WHO, the United
Nations Industrial Development Organization, and the Organisation for
Economic Co-operation and Development (Participating Organizations),
following recommendations made by the 1992 United Nations Conference
on Environment and Development, to strengthen cooperation and increase
coordination in the field of chemical safety. The purpose of the IOMC
is to promote coordination of the policies and activities pursued by
the Participating Organizations, jointly or separately, to achieve the
sound management of chemicals in relation to human health and the
environment.

WHO Library Cataloguing in Publication Data

Selected non-heterocyclic polycyclic aromatic hydrocarbons.

(Environmental health criteria ; 202)
1. Polycyclic hydrocarbons, Aromatic 2.Environmental exposure
3.Occupational exposure 4.Risk assessment - methods
I.INternational Programme on Chemical Safety II.Series

ISBN 92 4 157202 7 (NLM Classification: QD 341.H9)
ISSN 0250-863X

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CONTENTS

NOTE TO READERS OF THE CRITERIA MONOGRAPHS

PREAMBLE

WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA
FOR SELECTED NON-HETEROCYCLIC POLYCYCLIC AROMATIC HYDROCARBONS

ENVIRONMENTAL HEALTH CRITERIA FOR SELECTED NON-HETEROCYCLIC POLYCYCLIC
AROMATIC HYDROCARBONS

1. SUMMARY
1.1. Selection of compounds for this monograph
1.2. Identity, physical and chemical properties, and analytical
methods
1.3. Sources of human and environmental exposure
1.4. Environmental transport, distribution, and transformation
1.5. Environmental levels and human exposure
1.5.1. Air
1.5.2. Surface water and precipitation
1.5.3. Sediment
1.5.4. Soil
1.5.5. Food
1.5.6. Aquatic organisms
1.5.7. Terrestrial organisms
1.5.8. General population
1.5.9. Occupational exposure
1.6. Kinetics and metabolism
1.7. Effects on laboratory mammals and in vitro
1.8. Effects on humans
1.9. Effects on other organisms in the laboratory and the field

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS
2.1. Identity
2.1.1. Technical products
2.2. Physical and chemical properties
2.3. Conversion factors
2.4. Analytical methods
2.4.1. Sampling
2.4.1.1 Ambient air
2.4.1.2 Workplace air
2.4.1.3 Combustion effluents
2.4.1.4 Water
2.4.1.5 Solid samples
2.4.2. Preparation

2.4.3. Analysis
2.4.3.1 Gas chromatography
2.4.3.2 High-performance liquid chromatography
2.4.3.3 Thin-layer chromatography
2.4.3.4 Other techniques
2.4.4. Choice of PAH to be quantified

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1. Natural occurrence
3.2. Anthropogenic sources
3.2.1. PAH in coal and petroleum products
3.2.2. Production levels and processes
3.2.3. Uses of individual PAH
3.2.4. Emissions during production and processing of PAH
3.2.4.1 Emissions to the atmosphere
3.2.4.2 Emissions to the hydrosphere
3.2.5. Emissions during use of individual PAH
3.2.6. Emissions of PAH during processing and use
of coal and petroleum products
3.2.6.1 Emissions to the atmosphere
3.2.6.2 Emissions to the hydrosphere
3.2.6.3 Emissions to the geosphere
3.2.6.4 Emissions to the biosphere
3.2.7. Emissions of PAH caused by incomplete combustion
3.2.7.1 Industrial point sources
3.2.7.2 Other diffuse sources

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
4.1. Transport and distribution between media
4.1.1. Physicochemical parameters that dtermine
environmental transport and distribution
4.1.2. Distribution and transport in the gaseous phase
4.1.3. Volatilization
4.1.4. Adsorption onto soils and sediments
4.1.5. Bioaccumulation
4.1.5.1 Aquatic organisms
4.1.5.2 Terrestrial organisms
4.1.6. Biomagnification
4.2. Transformation
4.2.1. Biotic transformation
4.2.1.1 Biodegradation
4.2.1.2 Biotransformation
4.2.2. Abiotic degradation
4.2.2.1 Photodegradation in the environment
4.2.2.2 Hydrolysis
4.2.3. Ultimate fate after use

5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.1. Atmosphere
5.1.1.1 Source identification
5.1.1.2 Background and rural levels

5.1.1.3 Industrial sources
5.1.1.4 Diffuse sources
5.1.2. Hydrosphere
5.1.2.1 Surface and coastal waters
5.1.2.2 Groundwater
5.1.2.3 Drinking-water and water supplies
5.1.2.4 Precipitation
5.1.3. Sediment
5.1.3.1 River sediment
5.1.3.2 Lake sediment
5.1.3.3 Marine sediment
5.1.3.4 Estuarine sediment
5.1.3.5 Harbour sediment
5.1.3.6 Time trends of PAH in sediment
5.1.4. Soil
5.1.4.1 Background values
5.1.4.2 Industrial sources
5.1.4.3 Diffuse sources
5.1.4.4 Time trends of PAH in soil
5.1.5. Food
5.1.5.1 Meat and meat products
5.1.5.2 Fish and marine foods
5.1.5.3 Dairy products: cheese, butter, cream
milk, and related products
5.1.5.4 Vegetables
5.1.5.5 Fruits and confectionery
5.1.5.6 Cereals and dried food products
5.1.5.7 Beverages
5.1.5.8 Vegetable and animal fats and oils
5.1.6. Biota
5.1.7. Animals
5.1.7.1 Aquatic organisms
5.1.7.2 Terrestrial organisms
5.2. Exposure of the general population
5.2.1. Indoor air
5.2.2. Food
5.2.3. Other sources
5.2.4. Intake of PAH by inhalation
5.2.5. Intake of PAH from food and drinking-water
5.3. Occupational exposure
5.3.1. Occupational exposure during processing and use
of coal and petroleum products
5.3.1.1 Coal coking
5.3.1.2 Coal gasification and coal liquefaction
5.3.1.3 Pteroleum refining
5.3.1.4 Road paving
5.3.1.5 Roofing
5.3.1.6 Impregnation of wood with creosotes
5.3.1.7 Other exposures

5.3.2. Occupational exposure resulting from incomplete
combustion of mineral oil, coal, and their products
5.3.2.1 Aluminium production
5.3.2.2 Foundries
5.3.2.3 Other workplaces

6. KINETICS AND METABOLISM IN LABORATORY MAMMALS AND HUMANS
6.1. Absorption
6.1.1. Absorption by inhalation
6.1.2. Absorption in the gastrointestinal tract
6.1.3. Absorption through the skin
6.2. Distribution
6.3. Metabolic transformation
6.3.1. Cytochromes P450 and PAH metabolism
6.3.1.1 Individual cytochrome P450 enzymes
that metabolize PAH
6.3.1.2 Regulation of cytochrome P450 enzymes
that metabolize PAH
6.3.2. Metabolism of benzo [a]pyrene
6.4. Elimination and excretion
6.5. Retention and turnover
6.5.1. Human body burdens of PAH
6.6. Reactions with tissue components
6.6.1. Reactions with proteins
6.6.2. Reactions with nucleic acids
6.7. Analytical methods
7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO
7.1. Toxicity after a single exposure
7.1.1. Benzo [a]pyrene
7.1.2. Chrysene
7.1.3. Dibenz [a,h]anthracene
7.1.4. Fluoranthene
7.1.5. Naphthalene
7.1.6. Phenanthrene
7.1.7. Pyrene
7.2. Short-term toxicity
7.2.1. Subacute toxicity
7.2.1.1 Acenaphthene
7.2.1.2 Acenaphthylene
7.2.1.3 Anthracene
7.2.1.4 Benzo [a]pyrene
7.2.1.5 Benz [a]anthracene
7.2.1.6 Dibenz [a,h]anthracene
7.2.1.7 Fluoranthene
7.2.1.8 Naphthalene
7.2.1.9 Phenanthrene
7.2.1.10 Pyrene
7.2.2. Subchronic toxicity
7.2.2.1 Acenaphthene
7.2.2.2 Anthracene
7.2.2.3 Benzo [a]pyrene
7.2.2.4 Fluorene

7.2.2.5 Fluoranthene
7.2.2.6 Naphthalene
7.2.2.7 Pyrene
7.3. Long-term toxicity
7.3.1. Anthracene
7.3.2. Benz [a]anthracene
7.3.3. Dibenz [a,h]anthracene
7.4. Dermal and ocular irritation and dermal sensitization
7.4.1. Anthracene
7.4.2. Benzo [a]pyrene
7.4.3. Naphthalene
7.4.4. Phenanthrene
7.5. Reproductive effects, embryotoxicity, and teratogenicity
7.5.1. Benzo [a]pyrene
7.5.1.1 Teratogenicity in mice of different
genotypes
7.5.1.2 Reproductive toxicity
7.5.1.3 Effects on postnatal development
7.5.1.4 Immunological effects in pregnant
rats and mice
7.5.2. Naphthalene
7.5.2.1 Embryotoxicity
7.5.2.2 Toxicity in cultured embryos
7.6. Mutagenicity and related end-points
7.7. Carcinogenicity
7.7.1. Single substances
7.7.1.1 Benzo [a]pyrene
7.7.1.2 Benzo [e]pyrene
7.7.2. Comparative studies
7.7.2.1 Carcinogenicity
7.7.2.2 Further evidence
7.7.3. PAH in complex mixtures
7.7.4. Transplacental carcinogenicity
7.7.4.1 Benzo [a]pyrene
7.7.4.2 Pyrene
7.8. Special studies
7.8.1. Phototoxicity
7.8.1.1 Anthracene
7.8.1.2 Benzo [a]pyrene
7.8.1.3 Pyrene
7.8.1.4 Comparisons of individual PAH
7.8.2. Immunotoxicity
7.8.2.1 Benzo [a]pyrene
7.8.2.2 Dibenz [a,h]anthracene
7.8.2.3 Fluoranthene
7.8.2.4 Naphthalene
7.8.2.5 Comparisons of individual PAH
7.8.2.6 Exposure in utero
7.8.2.7 Mechanisms of the immunotoxicity of PAH
7.8.3. Hepatotoxicity
7.8.3.1 Benzo [a]pyrene
7.8.3.2 Comparisons of individual PAH

7.8.4. Renal toxicity
7.8.5. Ocular toxicity of naphthalene
7.8.6. Percutaneous absorption
7.8.7. Other studies
7.8.7.1 Benzo [k]fluoranthene
7.8.7.2 Benzo [a]pyrene
7.8.7.3 Phenanthrene
7.8.7.4 Comparisons of individual PAH
7.9. Toxicity of metabolites
7.9.1. Benzo [a]pyrene
7.9.2. 5-Methylchrysene
7.9.3. 1-Methylphenanthrene
7.10. Mechanisms of carcinogenicity
7.10.1. History
7.10.2. Current theories
7.10.3. Theories under discussion
7.10.3.1 Acenaphthene and acenaphthylene
7.10.3.2 Anthracene
7.10.3.3 Benzo [a]pyrene
7.10.3.4 Benz [a]anthracene
7.10.3.5 Benzo [c]phenanthrene
7.10.3.6 Chrysene
7.10.3.7 Cyclopenta [c,d]pyrene
7.10.3.8 Fluorene
7.10.3.9 Indeno[1,2,3- cd]pyrene
7.10.3.10 5-Methylchrysene
7.10.3.11 1-Methylphenanthrene
7.10.3.12 Naphthalene
7.10.3.13 Phenanthrene
7.10.3.14 Investigations of groups of PAH

8. EFFECTS ON HUMANS
8.1. Exposure of the general population
8.1.1. Naphthalene
8.1.1.1 Poisoning incidents
8.1.1.2 Controlled studies
8.1.2. Mixtures of PAH
8.1.2.1 PAH in unvented coal combustion
in homes
8.1.2.2 PAH in cigarette smoke
8.1.2.3 PAH in coal-tar shampoo
8.2. Occupational exposure
8.3. Biomarkers of exposure to PAH
8.3.1. Urinary metabolites in general
8.3.2. 1-Hydroxypyrene
8.3.2.1 Method of determination
8.3.2.2 Concentrations
8.3.2.3 Time course of elimination
8.3.2.4 Suitability as a biomarker
8.3.3. Mutagenicity in urine
8.3.4. Genotoxicity in lymphocytes

8.3.5. DNA adducts
8.3.5.1 Method of determination
8.3.5.2 Concentrations
8.3.5.3 Suitability as a biomarker
8.3.6. Antibodies to DNA adducts
8.3.7. Protein adducts
8.3.8. Activity of cytochrome P450
8.3.9. Cell surface differentiation antigens in lung cancer
8.3.10. Oncogene proteins

9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD
9.1. Laboratory experiments
9.1.1. Microorganisms
9.1.1.1 Water
9.1.1.2 Soil
9.1.2. Aquatic organisms
9.1.2.1 Plants
9.1.2.2 Invertebrates
9.1.2.3 Vertebrates
9.1.2.4 Sediment-dwelling organisms
9.1.2.5 Toxicity of combinations of PAH
9.1.3. Terrestrial organisms
9.1.3.1 Plants
9.1.3.2 Invertebrates
9.1.3.3 Vertebrates
9.2. Field observations
9.2.1. Microorganisms
9.2.1.1 Water
9.2.1.2 Soil
9.2.2. Aquatic organisms
9.2.2.1 Plants
9.2.2.2 Invertebrates
9.2.2.3 Vertebrates
9.2.3. Terrestrial organisms
9.2.3.1 Plants
9.2.3.2 Invertebrates
9.2.3.3 Vertebrates

10 EVALUATION OF RISKS TO HUMAN HEALTH AND EFFECTS ON THE
ENVIRONMENT
10.1. Human health
10.1.1. Exposure
10.1.1.1 General population
10.1.1.2 Occupational exposure
10.1..2 Toxic effects
10.1.2.1 Bioavailability
10.1.2.2 Acute toxicity
10.1.2.3 Irritation and allergic sensitization
10.1.2.4 Medium-term toxicity
10.1.2.5 Carcinogenicity
10.1.2.6 Reproductive toxicity
10.1.2.7 Immunotoxicity
10.1.2.8 Genotoxicity

10.2. Environment
10.2.1. Environmental levels and fate
10.2.2. Ecotoxic effects
10.2.2.1 Terrestrial organisms
10.2.2.2 Aquatic organisms

11 RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH AND THE
ENVIRONMENT
11.1. General recommendations
11.2. Protection of human health
11.3. Recommendations for further research
11.3.1. General
11.3.2. Protection of human health
11.3.3. Environmental protection
11.3.4. Risk assessment

12 PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
12.1. International Agency for Research on Cancer
12.2. WHO Water Quality Guidelines
12.3. FAO/WHO Joint Expert Committee on Food Additives
12.4. WHO Regional Office for Europe Air Quality Guidelines

APPENDIX I. SOME APPROACHES TO RISK ASSESSMENT FOR POLYCYCLIC AROMATIC
HYDROCARBONS
I.1 Introduction
I.2 Approaches to risk assessment
I.2.1 Toxicity equivalence factors and related approaches
I.2.1.1 Principle
I.2.1.2 Development and validation
I.2.1.2.1 Derivation of the potency of
benzo [a]pyrene
I2.1.2.2 Derivation of the relative potency of
PAH other than benzo [a]pyrene
I.2.1.3 Application
I.2.2 Comparative potency approach
I.2.2.1 Principle
I.2.2.2 Development and validation
I.2.2.3 Key implicit and explicit assumptions
I.2.2.4 Application
I.2.3 Benzo [a]pyrene as a surrogate for the PAH fraction
of complex mixtures
I.2.3.1 Principle
I.2.3.2 Development and validation
I.2.3.3 PAH profiles of complex mixtures
I.2.3.4 Potency of complex mixtures
I.2.3.5 Key implicit and explicit assumptions
I.2.3.6 Application
I.3 Comparison of the three procedures
I.3.1 Individual PAH approach
I.3.2 Comparative potency approach
I.3.3 Benzo [a]pyrene surrogate approach

APPENDIX II; SOME LIMIT VALUES
II.1 Exposure of the consumer
II.2 Occupational exposure
II.3 Classification
II.3.1 European Union
II.3.2 USA

REFERENCES

RESUME

RESUMEN

Environmental Health Criteria

PREAMBLE

Objectives

The WHO Environmental Health Criteria Programme was initiated in
1973, with the following objectives:

(i) to assess information on the relationship between exposure to
environmental pollutants and human health and to provide
guidelines for setting exposure limits;

(ii) to identify new or potential pollutants;

(iii) to identify gaps in knowledge concerning the health effects of
pollutants;
(iv) to promote the harmonization of toxicological and
epidemiological methods in order to have internationally
comparable results.

The first Environmental Health Criteria (EHC) monograph, on
mercury, was published in 1976; numerous assessments of chemicals and
of physical effects have since been produced. Many EHC monographs have
been devoted to toxicological methods, e.g. for genetic, neurotoxic,
teratogenic, and nephrotoxic effects. Other publications have been
concerned with e.g. epidemiological guidelines, evaluation of
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elderly.

Since the time of its inauguration, the EHC Programme has widened
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addition to their health effects.

The original impetus for the Programme came from resolutions of
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The EHC monographs have become widely established, used, and
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The recommendations of the 1992 United Nations Conference on
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Content

The layout of EHC monographs for chemicals is outlined below.

* Summary: a review of the salient facts and the risk evaluation of
the chemical
* Identity: physical and chemical properties, analytical methods
* Sources of exposure
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* Kinetics and metabolism in laboratory animals and humans
* Effects on laboratory mammals and in-vitro test systems
* Effects on humans
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* Previous evaluations by international bodies, e.g. the
International Agency for Research on Cancer, the Joint FAO/WHO
Expert Committee on Food Additives, and the Joint FAO/WHO
Meeting on Pesticide Residues

Selection of chemicals

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Chairperson and Rapporteur of the Task Group to check for any errors.

It is accepted that the following criteria should initiate the
updating of an EHC monograph: new data are available that would
substantially change the evaluation; there is public concern about
health or environmental effects of the agent because of greater
exposure; an appreciable time has elapsed since the last evaluation.

All participating institutions are informed, through the EHC
progress report, of the authors and institutions proposed for the
drafting of the documents. A comprehensive file of all comments
received on drafts of each EHC monograph is maintained and is
available on request. The chairpersons of task groups are briefed
before each meeting on their role and responsibility in ensuring that
these rules are followed.

WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR SELECTED
NON-HETEROCYCLIC POLYCYCLIC AROMATIC HYDROCARBONS
Hanover, Germany, 25-29 September 1995

Members

Dr P.E.T. Douben, Her Majesty's Inspectorate of Pollution, London,
United Kingdom (Chairman)

Dr P.L. Grover, Institute for Cancer Research, Sutton, United Kingdom

Dr R.F. Hertel, Bundesgesinstitut für gesundheitlichen
Verbraucherschutz und Veterinarmedizin, Berlin, Germany

Professor J. Jacob, Biochemisches Institut für Umweltcarcinogene,
Grosshausdorf, Germany

Dr J Kielhorn, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany

Dr R.W. Luebke, National Health and Ecology Effects Laboratory, US
Environmental Protection Agency, Research Triangle Park, NC, USA
(Joint Rapporteur)

Mr H. Malcolm, Institute of Terrestrial Ecology, Monks Wood,
Huntingdon, Cambridgeshire, United Kingdom (Joint Rapporteur)

Dr I. Mangelsdorf, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany

Dr E. Menichini, Istituto Superiore di Sanita, Rome, Italy

Dr P. Muller, Ministry of Environment and Energy, Toronto, Ontario,
Canada

Dr J.L. Mumford, National Health and Environmental Effects Research
Laboratory, US Environmental Protection Agency, Research Triangle
Park, NC, USA

Dr G. Rosner, Freiburg, Germany

Dr R. Schoeny, National Center for Environmental Assessment, US
Environmental Protection Agency, Cincinnati, OH, USA
Dr T. Sorahan, Institute of Occupational Health, University of
Birmingham, Birmingham, United Kingdom

Dr Kimber L. White, Jr, Medical College of Virginia, Virginia
Commonwealth University, Richmond, VA, USA (Vice-Chairman)

Secretariat

Dr E. Smith, International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland

Dr. M. Castegnaro, International Agency for Research on Cancer, Lyon,
France

Assisting the Secretariat

Dr S. Artelt, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany

Dr A. Boehncke, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany

Dr O. Creutzenburg, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Germany

1. SUMMARY

1.1 Selection of compounds for this monograph

Polycyclic aromatic hydrocarbons (PAH) constitute a large class
of compounds, and hundreds of individual substances may be released
during incomplete combustion or pyrolysis of organic matter, an
important source of human exposure. Studies of various environmentally
relevant matrices, such as coal combustion effluents, motor vehicle
exhaust, used motor lubricating oil, and tobacco smoke, have shown
that the PAH in these mixtures are mainly responsible for their
carcinogenic potential.

PAH occur almost always in mixtures. Because the composition of
such mixtures is complex and varies with the generating process, all
mixtures containing PAH could not possible be covered in detail in
this monograph. Thus, 33 individual compounds (31 parent PAH and two
alkyl derivatives) were selected for evaluation on the basis of the
availability of relevant data on toxicological end-points and/or
exposure (Table 1). Since epidemiological studies, which are essential
for risk assessment, were available only for mixtures, however,
Sections 8 and 10 present the results of studies of mixtures of PAH,
in contrast to the rest of the monograph.

Numerous papers and reviews have been published on the
occurrence, distribution, and transformation of PAH in the environment
and on their ecotoxicological and toxicological effects. Only
references from the last 10-15 years are cited in this monograph,
unless no other information was available; reviews are cited for older
studies and for further information.

1.2 Identity, physical and chemical properties, and analytical
methods

The term 'polycyclic aromatic hydrocarbons' commonly refers to a
large class of organic compounds containing two or more fused aromatic
rings made up of carbon and hydrogen atoms. At ambient temperatures,
PAH are solids. The general characteristics common to the class are
high melting- and boiling-points, low vapour pressure, and very low
water solubility which tends to decrease with increasing molecular
mass. PAH are soluble in many organic solvents and are highly
lipophilic. They are chemically rather inert. Reactions that are of
interest with respect to their environmental fate and possible sources
of loss during atmospheric sampling are photodecomposition and
reactions with nitrogen oxides, nitric acid, sulfur oxides, sulfuric
acid, ozone, and hydroxyl radicals.

Ambient air is sampled by collecting suspended particulate matter
on glass-fibre, polytetrafluoroethylene, or quartz-fibre filters by
means of high-volume or passive samplers. Vapour-phase PAH, which
might volatilize from filters during sampling, are commonly trapped by
adsorption on polyurethane foam. The sampling step is by far the most
important source of variability in results.

Table 1. Polycyclic aromatic hydrocarbons evaluated in this monograph

Common name CAS name Synonym^a CAS Registry No.

Acenaphthylene Acenaphthylene 91-20-3
Acenaphthene Acenaphthylene, 1,2-dihydro- 208-96-8
Anthanthrene Dibenzo[def,mno]chrysene 191-26-4
Anthracene Anthracene 120-12-7
Benz[a]anthracene Benz[a]anthracene 1,2-Benzanthracene, 56-55-3
tetraphene
Benzo[a]fluorene 11 H-Benzo[a]fluorene 1,2-Benzofluorene 238-84-6
Benzo[b]fluorene 11 H-Benzo[b]fluorene 2,3-Benzofluorene 243-17-4
Benzo[b]fluoranthene Benz[e]acephenanthrylene 3,4-Benzofluoranthene 205-99-2
Benzo[ghi]fluoranthene Benzo[ghi]fluoranthene 2,13-Benzofluoranthene 203-12-3
Benzo[j]fluoranthene Benzo[j]fluoranthene 10,11-Benzofluoranthene 205-82-3
Benzo[k]fluoranthene Benzo[k]fluoranthene 11,12-Benzofluoranthene 207-08-9
Benzo[ghi]perylene Benzo[ghi]perylene 1,12-Benzoperylene 191-24-2
Benzo[c]phenanthrene Benzo[c]phenanthrene 3,4-Benzophenanthrene 195-19-7
Benzo[a]pyrene Benzo[a]pyrene 3,4-Benzopyrene^b 50-32-8
Benzo[e]pyrene Benzo[e]pyrene 1,2-Benzopyrene 192-97-2
Chrysene Chrysene 1,2-Benzophenanthrene 218-01-9
Coronene Coronene Hexabenzobenzene 191-07-1
Cyclopenta[cd]pyrene Cyclopenta[cd]pyrene Cyclopenteno[cd]pyrene 27208-37-3
Dibenz[a,h]anthracene Dibenz[a,h]anthracene 1,2:5,6-Dibenzanthracene 53-70-3
Dibenzo[a,e]pyrene Naphtho[1,2,3,4-def]chrysene 1,2:4,5-Dibenzopyrene 192-65-4
Dibenzo[a,h]pyrene Dibenzo[b,def]chrysene 3,4:8,9-Dibenzopyrene 189-64-0
Dibenzo[a,i]pyrene Benzo[rst]pentaphene 3,4:9,10-Dibenzopyrene 189-55-9
Dibenzo[a,l]pyrene Dibenzo[def,p]chrysene 1,2:3,4-Dibenzopyrene 191-30-0
Fluoranthene Fluoranthene 206-44-0
Fluorene 9H-Fluorene 86-73-7
Indeno[1,2,3-cd]pyrene Indeno[1,2,3-cd]-pyrene 2,3-o-Phenylenpyrene 193-39-5
5-Methylchrysene Chrysene, 5-methyl- 3697-24-3
1-Methylphenanthrene Phenanthrene, 1-methyl- 832-69-9

Table 1. (continued)

Common name CAS name Synonym^a CAS Registry No.

Naphthalene Naphthalene 91-20-3
Perylene Perylene peri-Dinaphthalene 198-55-0
Phenanthrene Phenanthrene 85-01-8
Pyrene Pyrene Benzo[def]phenanthrene 129-00-0
Triphenylene Triphenylene 9,10-Benzophenanthrene 217-59-4

Extensive lists of synonyms have been imported by the IARC (1983) and Loening & Merritt (1990).
^a Common synonym appearing in the literature
^b Also reported as benzo[def]chrysene

Air is sampled at the workplace at low flow rates; particles are
collected on glass-fibre or polytetrafluoroethylene filters and
vapours on Amberlite XAD-2 resin. Devices for sampling stack gases are
composed of a glass-fibre or quartz-fibre filter in front of a cooler
to collect condensable matter and an adsorbent (generally XAD-2)
cartridge. Vehicle exhausts are sampled under laboratory conditions,
with standard driving cycles simulating on-road conditions. Emissions
are collected either undiluted or after dilution with filtered cold
air.

Many extraction and purification techniques have been described.
Depending on the matrix, PAH are extracted from samples with a Soxhlet
apparatus, ultrasonically, by liquid-liquid partition, or, after
sample dissolution or alkaline digestion, with a selective solvent.
Supercritical fluid extraction from various environmental solids has
also been used. The efficiency of extraction depends heavily on the
solvent used, and many of the solvents commonly used in the past were
not appropriate. Extracted samples are usually purified by column
chromatography, particularly on alumina, silica gel, or Sephadex LH-20
but also by thin-layer chromatography.

Identification and quantification are routinely performed by gas
chromatography with flame ionization detection or by high-performance
liquid chromatography (HPLC) with ultraviolet and fluorescence
detection, generally in series. In gas chromatography, fused silica
capillary columns are used, with polysiloxanes (SE-54 and SE-52) as
stationary phases; silica-C18 columns are commonly used in HPLC. A
mass spectrometric detector is often coupled to a gas chromatograph in
order to confirm the identity of peaks.

The choice of PAH to be determined depends on the purpose of the
measurement, e.g. for health-orientated or ecotoxicological studies or
to investigate sources. Testing for different sets of compounds may be
required or recommended at national and international levels.

1.3 Sources of human and environmental exposure

Little information is available on the production and processing
of PAH, but it is probable that only small amounts of PAH are released
as a direct result of these activities. The PAH found principally are
used as intermediates in the production of polyvinylchloride and
plasticizers (naphthalene), pigments (acenaphthene, pyrene), dyes
(anthracene, fluoranthene), and pesticides (phenanthrene).

The largest emissions of PAH result from incomplete combustion of
organic materials during industrial processes and other human
activities, including:

- processing of coal, crude oil, and natural gas, including coal
coking, coal conversion, petroleum refining, and production of
carbon blacks, creosote, coal-tar, and bitumen;
- aluminium, iron and steel production in plants and foundries;
- heating in power plants and residences and cooking;
- combustion of refuse;
- motor vehicle traffic; and
- environmental tobacco smoke.

PAH, especially these of higher molecular mass, entering the
environment via the atmosphere are adsorbed onto particulate matter.
The hydrosphere and geosphere are affected secondarily by wet and dry
deposition. Creosote-preserved wood is another source of release of
PAH into the hydrosphere, and deposition of contaminated refuse, like
sewage sludge and fly ash, contributes to emissions of PAH into the
geosphere. Little information is available about the passage of PAH
into the biosphere. PAH occur naturally in peat, lignite, coal, and
crude oil. Most of the PAH in hard coals are tightly bound within the
coal structure and cannot be leached out.

The release of PAH into the environment has been determined by
identification of a characteristic PAH concentration profile, but this
has been possible in only a few cases. Benzo [a]pyrene has frequently
been used as an indicator of PAH, especially in older studies.
Generally, emissions of PAH are only estimates based on more or less
reliable data and give only a rough idea of exposure.

The most important sources of PAH are as follows:

Coal coking: Airborne emissions of PAH from coal coking in
Germany have decreased significantly over the last 10 years as a
result of technical improvements to existing plants, closure of old
plants, and reduced coke production. Similar situations are assumed to
exist in western Europe, Japan, and the USA, but no data were
available.

Production of aluminium (mainly special coal anodes), iron,
and steel and the binding agents used in moulding sand in foundries:
Little information is available.

Domestic and residential heating: Phenanthrene, fluoranthene,
pyrene, and chrysene are emitted as major components. The emissions
from wood stoves are 25-1000 times higher than those from
charcoal-fired stoves, and in areas where wood burning predominates
for domestic heating the major portion of airborne PAH may be derived
from this source, especially in winter. The release of PAH during
residential heating is thus assumed to be an important source in
developing countries where biomass is often burnt in relatively simple
stoves.

Cooking: PAH may be emitted during incomplete combustion of
fuels, from cooking oil, and from food being cooked.

Motor vehicle traffic: The main compounds released from
petrol-fuelled vehicles are fluoranthene and pyrene, while naphthalene
and acenaphthene are abundant in the exhaust of diesel-fuelled
vehicles. Although cyclopenta [cd]-pyrene is emitted at a high rate
from petrol-fuelled engines, its concentration in diesel exhaust is
only just above the limit of detection. The emission rates, which
depend on the substance, the type of vehicle, its engine conditions,
and the test conditions, range from a few nanograms per kilometre to
> 1000 mg/km. PAH emissions from vehicle engines are dramatically
reduced by fitting catalytic converter devices.

Forest fires: In countries with large forest areas, fires can
make an imprtant contribution to PAH emissions.

Coal-fired power plants: PAH released into the atmosphere from
such plants consist mainly of two- and three-ring compounds. In
contaminated areas, the PAH levels in ambient air may be higher than
those in the stack gases.

Incineration of refuse: The PAH emissions in stack gases from
this souce in a number of countries were < 10 mg/m³.

1.4 Environmental transport, distribution, and transformation

Several distribution and transformation processes determine the
fate of both individual PAH and mixtures. Partitioning between water
and air, between water and sediment, and between water and biota are
the most important of the distribution processes.

As PAH are hydrophobic with low solubility in water, their
affinity for the aquatic phase is very low; however, in spite of the
fact that most PAH are released into the environment via the
atmosphere, considerable concentrations are also found in the
hydrosphere because of their low Henry's law constants. As the
affinity of PAH for organic phases is greater than that for water,
their partition coefficients between organic solvents, such as
octanol, and water are high. Their affinity for organic fractions in
sediment, soil, and biota is also high, and PAH thus accumulate in
organisms in water and sediments and in their food. The relative
importance of uptake from food and from water is not clear. In
Daphnia and molluscs, accumulation of PAH from water is positively
correlated with the octanol:water partition coefficient ( K_ow). In
fish and algae that can metabolize PAH, however, the internal
concentrations of different PAH are not correlated with the K_ow.

Biomagnification - the increase in the concentration of a
substance in animals in successive trophic levels of food chains - of
PAH has not been observed in aquatic systems and would not be expected
to occur, because most organisms have a high biotransformation
potential for PAH. Organisms at higher trophic levels in food chains
show the highest potential biotransformation.

PAH are degraded by photodegradation, biodegradation by
microorganisms, and metabolism in higher biota. Although the last
route of transformation is of minor importance for the overall fate of
PAH in the environment, it is an important pathway for the biota,
since carcinogenic metabolites may be formed. As PAH are chemically
stable, with no reactive groups, hydrolysis plays no role in their
degradation. Few standard tests for the biodegradation of PAH are
available In general, they are biodegraded under aerobic conditions,
the biodegradation rate decreasing drastically with the number of
aromatic rings. Under anaerobic conditions, degradation is much
slower.

PAH are photooxidized in air and water in the presence of
sensitizing radicals like OH, NO₃, and O₃. Under laboratory
conditions, the half-life of the reaction with airborne OH radicals is
about one day, whereas reactions with NO₃ and O₃ usually have much
lower velocity constants. The adsorption of high-molecular-mass PAH
onto carbonaceous particles in the environment should stabilize the
reaction with OH radicals. The reaction of two- to four-ring PAH,
which occur mainly in the vapour phase, with NO₃ leads to nitro-PAH,
which are known mutagens. The photooxidation of some PAH in water
seems to be more rapid than in air. Calculations based on
physicochemical and degradation parameters indicate that PAH with four
or more aromatic rings persist in the environment.

1.5 Environmental levels and human exposure

PAH are ubiquitous in the environment, and various individual PAH
have been detected in different compartments in numerous studies.

1.5.1 Air

The levels of individual PAH tend to be higher in winter than in
summer by at least one order of magnitude. The predominant source
during winter is residential heating, while that during summer is
urban motor vehicle traffic. Average concentrations of 1-30 ng/m³ of
individual PAH were detected in the ambient air of various urban
areas. In large cities with heavy motor vehicle traffic and extensive
use of biomass fuel, such as Calcutta, levels of up to 200 ng/m³ of
individual PAH were found. Concentrations of 1-50 ng/m³ were detected
in road tunnels. Cyclopenta [cd]pyrene and pyrene were present at
concentrations up to 100 ng/m³. In a subway station, PAH
concentrations of up to 20 ng/m³ were measured. Near industrial
sources, the average concentrations of individual PAH ranged from 1 to
10 ng/m³. Phenanthrene was present at up to a maximum of about 310
ng/m³.

The background values of PAH are at least one or two orders of
magnitude lower than those near sources like motor vehicle traffic.
For example, the levels at 1100 m ranged from 0.004 to 0.03 ng/m³.

1.5.2 Surface water and precipitation

Most of the PAH in water are believed to result from urban
runoff, from atmospheric fallout (smaller particles), and from asphalt
abrasion (larger particles). The major source of PAH varies, however,
in a given body of water. In general, most samples of surface water
contain individual PAH at levels of up to 50 ng/litre, but highly
polluted rivers had concentrations of up to 6000 ng/litre. The PAH
levels in groundwater are within the range 0.02-1.8 ng/litre, and
drinking-water samples contain concentrations of the same order of
magnitude. Major sources of PAH in drinking-water are asphalt-lined
storage tanks and delivery pipes.

The levels of individual PAH in rainwater ranged from 10 to 200
ng/litre, whereas levels of up to 1000 ng/litre have been detected in
snow and fog.

1.5.3 Sediment

The concentrations of individual PAH in sediment were generally
one order of magnitude higher than those in precipitation.

1.5.4 Soil

The main sources of PAH in soil are atmospheric deposition,
carbonization of plant material, and deposition from sewage and
particulate waste. The extent of pollution of soil depends on factors
such as its cultivation, its porosity, and its content of humic
substances.

Near industrial sources, individual PAH levels of up to 1 g/kg
soil have been found. The concentrations in soil from other sources,
such as automobile exhaust, are in the range 2-5 mg/kg. In unpolluted
areas, the PAH levels were 5-100 µg/kg soil.

1.5.5 Food

Raw food does not normally contain high levels of PAH, but they
are formed by processing, roasting, baking, or frying. Vegetables may
be contaminated by the deposition of airborne particles or by growth
in contaminated soil. The levels of individual PAH in meat, fish,
dairy products, vegetables and fruits, cereals and their products,
sweets, beverages, and animal and vegetable fats and oils were within
the range 0.01-10 µg/kg. Concentrations of over 100 µg/kg have been
detected in smoked meat and up to 86 µg/kg in smoked fish; smoked
cereals contained up to 160 µg/kg. Coconut oil contained up to 460
µg/kg. The levels in human breast milk were 0.003-0.03 µg/kg.

1.5.6 Aquatic organisms

Marine organisms are known to adsorb and accumulate PAH from
water. The degree of contamination is related to the extent of
industrial and urban development and shipping movements. PAH
concentrations of up to 7 mg/kg have been detected in aquatic
organisms living near industrial effluents, and the average levels of
PAH in aquatic animals sampled at contaminated sites were 10-500
µg/kg, although levels of up to 5 mg/kg were also detected.

The average levels of PAH in aquatic animals sampled at various
sites with unspecified sources of PAH were 1-100 µg/kg, but
concentrations of up to 1 mg/kg were found, for example, in lobsters
in Canada.

1.5.7 Terrestrial organisms

The concentrations of PAH in insects ranged from 730 to 5500
µg/kg. The PAH content of earthworm faeces depends significantly on
the location: those in a highly industrialized region in eastern
Germany contained benzo [a]pyrene at concentrations up to 2 mg/kg.

1.5.8 General population

The main sources of nonoccupational exposure are: polluted
ambient air, smoke from open fireplaces and cooking, environmental
tobacco smoke, contaminated food and drinking-water, and the use of
PAH-contaminated products. PAH can be found in indoor air as a result
of residential heating and environmental tobacco smoke at average
concentrations of 1-100 ng/m³, with a maximum of 2300 ng/m³.

The intake of individual PAH from food has been estimated to be
0.10-10 µg/day per person. The total daily intake of benzo [a]pyrene
from drinking-water was estimated to be 0.0002 µg/person. Cereals and
cereal products are the main contributors to the intake of PAH from
food because they are a major component of the total diet.

1.5.9 Occupational exposure

Near a coke-oven battery, the levels of benzo [a]pyrene ranged
from < 0.1 to 100-200 µg/m³, with a maximum of about 400 µg/m³. In
modern coal gasification systems, the concentration of PAH is usually
< 1 µg/m³ with a maximum of 30 µg/m³. Personal samples taken from
operators of petroleum refinery equipment showed exposure to 2.6-470
µg/m³. In samples of air taken near bitumen processing plants at
refineries, the total PAH levels were 0.004-50 µg/m³. Near road
paving operations, the total PAH concentrations in personal air
samples were up to 190 µg/m³, and the mean value in area air samples
was 0.13 µg/m³. The PAH levels in personal air samples taken at an
aluminium smelter were 0.05-9.6 µg/m³, but urine samples of workers
at an aluminium plant contained very low levels. Area air samples
contained PAH concentrations of up to 5 µg/m³ in one German foundry,

3-40 µg/m³ at iron mines and 4-530 µg/m³ at copper mines. The
concentrations of PAH in cooking fumes in a food factory ranged from
0.07 to 26 µg/m³.

1.6 Kinetics and metabolism

PAH are absorbed through the pulmonary tract, the
gastrointestinal tract, and the skin. The rate of absorption from the
lungs depends on the type of PAH, the size of the particles on which
they are absorbed, and the composition of the adsorbent. PAH adsorbed
onto particulate matter are cleared from the lungs more slowly than
free hydrocarbons. Absorption from the gastrointestinal tract occurs
rapidly in rodents, but metabolites return to the intestine via
biliary excretion. Studies with ³²P-postlabelling of percutaneous
absorption of mixtures of PAH in rodents showed that components of the
mixtures reach the lungs, where they become bound to DNA. The rate of
percutaneous absorption in mice according to the compound.

PAH are widely distributed throughout the organism after
administration by any route and are found in almost all internal
organs, but particularly those rich in lipids. Intravenously injected
PAH are cleared rapidly from the bloodstream of rodents but can cross
the placental barrier and have been detected in fetal tissues.

The metabolism of PAH is complex. In general, parent compounds
are converted via intermediate epoxides to phenols, diols, and
tetrols, which can themselves be conjugated with sulfuric or
glucuronic acids or with glutathione. Most metabolism results in
detoxification, but some PAH are activated to DNA-binding species,
principally diol epoxides, which can initiate tumours.

PAH metabolites and their conjugates are excreted via the urine
and faeces, but conjugates excreted in the bile can be hydrolysed by
enzymes of the gut flora and reabsorbed. It can be inferred from the
available information on the total human body burden that PAH do not
persist in the body and that turnover is rapid. This inference
excludes those PAH moieties that become covalently bound to tissue
constituents, in particular nucleic acids, and are not removed by
repair.

1.7 Effects on laboratory mammals and in vitro

The acute toxicity of PAH appears to be moderate to low. The
well-characterized PAH, naphthalene, showed oral and intravenous LD₅₀
values of 100-500 mg/kg body weight (bw) in mice and a mean oral LD₅₀
of 2700 mg/kg bw in rats. The values for other PAH are similar. Single
high doses of naphthalene induced bronchiolar necrosis in mice, rats,
and hamsters.

Short-term studies showed adverse haematological effects,
expressed as myelotoxicity with benzo [a]pyrene, haemolymphatic
changes with dibenz [a,h]-anthracene, and anaemia with naphthalene;
however, in a seven-day study by oral and intraperitoneal
administration in mice, tolerance to the effect of naphthalene was
observed.

Systemic effects caused by long-term treatment with PAH have been
described only rarely, because the end-point of most studies has been
carcinogenicity. Significant toxic effects are manifested at doses at
which carcinogenic responses are also triggered.

In studies of adverse effects on the skin after dermal
application, non- or weakly carcinogenic PAH such as perylene,
benzo [e]pyrene, phenanthrene, pyrene, anthracene, acenaphthalene,
fluorene, and fluoranthene were inactive, whereas carcinogenic
compounds such as benz [a]anthracene, dibenz [a,h]-anthracene, and
benzo [a]pyrene caused hyperkeratosis. Anthracene and naphthalene
vapours caused mild eye irritation. Benzo [a]pyrene induced contact
hypersensitivity in guinea-pigs and mice.

Benz [a]anthracene, benzo [a]pyrene, dibenz [a,h]anthracene,
and naphthalene were embrotoxic to mice and rats. Benzo [a]pyrene
also had teratogenic and reproductive effects. Intensive efforts have
been made to elucidate the genetic basis of the embryotoxic effect of
benzo [a]pyrene. Fetal death and malformations are observed only if
the cytochrome P450 monooxy-genase system is inducible, either in the
mother (with placental permigration) or in the embryo. Not all of the
effects observed can be explained by genetic predisposition, however:
in mice and rabbits, benzo [a]pyrene had transplacental carcinogenic
activity, resulting in pulmonary adenomas and skin papillomas in the
progeny. Reduced fertility and oocyte destruction were also observed.

PAH have also been studied extensively in assays for genotoxicity
and cell transformation; most of the 33 PAH covered in this monograph
are genotoxic or probably genotoxic. The only compounds for which
negative results were found in all assays were anthracene, fluorene,
and naphthalene. Owing to inconsistent results, phenanthrene and
pyrene could not be reliably classified for genotoxicity.

Comprehensive work on the carcinogenicity of PAH shows that 17 of
the 33 studied are, or are suspected of being, carcinogenic (Table 2).
The best-characterized PAH is benzo [a]pyrene, which has been studied
by all current methods in seven species. PAH that have been the
subject of 12 or more studies are anthanthrene, anthracene,
benz [a]anthracene, chrysene, dibenz [a,h]-anthracene,
dibenzo [a,i]pyrene, 5-methylchrysene, phenanthrene, and pyrene.

Special studies of the phototoxicity, immunotoxicity, and
hepatotoxicity of PAH are supplemented by reports on the ocular
toxicity of naphthalene. Anthracene, benzo [a]pyrene, and some other
PAH were phototoxic to mammalian skin and in cell cultures in vitro
when applied with ultraviolet radiation. PAH have generally been

reported to have immunosuppressive effects. After intraperitoneal
treatment of mice with benzo [a]pyrene, immunological parameters were
strongly suppressed in the progeny for up to 18 months. Increased
liver regeneration and an increase in liver weight have also been
observed. The effect of naphthalene in inducing formation of cataracts
in the rodent eye has been attributed to the inducibility of the
cytochrome P450 system in studies in which genetically different mouse
strains were used.

Theoretical models to predict the carcinogenic potency of PAH
from their structures, based on a large amount of experimental work,
were presented as early as the 1930s. The first model was based on the
high chemical reactivity of certain double bonds (the K-region
theory). A later systematic approach was based on the chemical
synthesis of possible metabolites and their mutagenic activity. This
'bay region' theory proposes that epoxides adjacent to a bay region
yield highly stabilized carbonium ions. Other theoretical approaches
are the 'di-region theory' and the 'radical cation potential theory'.

Many individual PAH are carcinogenic to animals and may be
carcinogenic to humans, and exposure to several PAH-containing
mixtures has been shown to increase the incidence of cancer in human
populations. There is concern that those PAH found to be carcinogenic
in experimental animals are likely to be carcinogenic in humans. PAH
produce tumours both at the site of contact and at distant sites. The
carcinogenic potency of PAH may vary with the route of exposure.
Various approaches to assessing the risk associated with exposure to
PAH, singly and in mixtures, have been proposed. No one approach is
endorsed in this monograph; however, the data requirements,
assumptions, applicability, and other features of three quantitative
risk assessment processes that have been validated to some degree are
described.

1.8 Effects on humans

Because of the complex profile of PAH in the environment and in
workplaces, human exposure to pure, individual PAH has been limited to
scientific experiments with volunteers, except in the case of
naphthalene which is used as a moth-repellant for clothing.

After dermal application, anthracene, fluoranthene, and
phenanthrene induced specific skin reactions, and benzo [a]pyrene
induced reversible, regressive verrucae which were classified as
neoplastic proliferations. The systemic effects of naphthalene are
known from numerous cases of accidental intake, particularly by
children. The lethal oral dose is 5000-15 000 mg for adults and 2000
mg taken over two days for a child. The typical effect after dermal or
oral exposure is acute haemolytic anaemia, which can also affect
fetuses transplacentally.

Table 2. Summary of results of tests for genotoxicity and
carcinogenicity for the 33 polycyclic aromatic hydrocarbons studies

Compound Genotoxicity Carcinogenicity

Acenaphthene (?) (?)
Acenaphthylene (?) No studies
Anthanthrene (+) +
Anthracene - -
Benz[a]anthracene + +
Benzo[b]fluoranthene + +
Benzo[j]fluoranthene + +
Benzo[ghi]fluoranthene (+) (-)
Benzo[k]fluoranthene + +
Benzo[a]fluorene (?) (?)
Benzo[b]fluorene (?) (?)
Benzo[ghi]perylene + -
Benzo[c]phenanthrene (+) +
Benzo[a]pyrene + +
Benzo[e]pyrene + ?
Chrysene + +
Coronene (+) (?)
Cyclopenta[cd]pyrene + +
Dibenz[a,h]anthracene + +
Dibenzo[a,e]pyrene + +
Dibenzo[a,h]pyrene (+) +
Dibenzo[a,i]pyrene + +
Dibenzo[a,l]pyrene (+) +
Fluoranthene + (+)
Fluorene - -
Indeno[1,2,3-cd]pyrene + +
5-Methylchrysene + +
1-Methylphenanthrene + (-)
Naphthalene - (?)
Perylene + (-)
Phenanthrene (?) (?)
Pyrene (?) (?)
Triphenylene + (-)

+, positive; -, negative; ?, questionable
Parentheses, result derived from small database

Tobacco smoking is the most important single factor in the
induction of lung tumours and also for increased incidences of tumours
of the urinary bladder, renal pelvis, mouth, pharynx, larynx, and
oesophagus. The contribution of PAH in the diet to the development of
human cancer is not considered to be high. In highly industrialized
areas, increased body burdens of PAH due to polluted ambient air were
detected. Psoriasis patients treated with coal-tar are also exposed to
PAH.

Occupational exposure to soot as a cause of scrotal cancer was
noted for the first time in 1775. Later, occupational exposure to tars
and paraffins was reported to induce skin cancer. The lung is now the
main site of PAH-induced cancer, whereas skin tumours have become more
rare because of better personal hygiene.

Epidemiological studies have been conducted of workers exposed at
coke ovens during coal coking and coal gasification, at asphalt works,
foundries, and aluminium smelters, and to diesel exhaust. Increased
lung tumour rates due to exposure to PAH have been found in coke-oven
workers, asphalt workers, and workers in Söderberg potrooms of
aluminium reduction plants. The highest risk was found for coke-oven
workers, with a standardized mortality ratio of 195. Dose-response
relationships were found in several studies. In aluminium plants, not
only urinary bladder cancer but also asthma-like symptoms, lung
function abnormalities, and chronic bronchitis have been observed.
Coke-oven workers were found to have decreased serum immunoglobulin
levels and decreased immune function. Occupational exposure to
naphthalene for five years was reported to have caused cataract.

Several methods have been developed to assess internal exposure
to PAH. In most of the studies, PAH metabolites such as urinary
thioethers, 1-naphthol, b-naphthylamine, hydroxyphenanthrenes, and
1-hydroxypyrene were measured in urine. The latter has been used
widely as a biological index of exposure.

The genotoxic effects of PAH have been determined by testing for
mutagenicity in urine and faeces and for the presence of micronuclei,
chromosomal aberrations, and sister chromatid exchange in peripheral
blood lymphocytes. In addition, adducts of benzo [a]pyrene with DNA
in peripheral lymphocytes and other tissues and with proteins like
albumin as well as antibodies to DNA adducts have been measured.

1-Hydroxypyrene in urine and DNA adducts in lymphocytes have been
investigated as markers in several studies. 1-Hydroxpyrene can be
measured more easily than DNA adducts, there is less variation between
individuals, and lower levels of exposure can be detected. Both
markers have been used to assess human exposure in various
environments. Increased 1-hydroxpyrene excretion or DNA adducts were
found at various workplaces in coke plants, aluminum manufacturing,
wood impregnation plants, foundries, and asphalt works. The highest
exposures were those of coke-oven workers and workers impregnating
wood with creosote, who took up 95% of total of PAH through the skin,
in contrast to the general population in whom uptake via food and
tobacco smoking predominate.

Estimates of the risk associated with exposure to PAH and PAH
mixtures are based on estimates of exposure and the results of
epidemiological studies. Data for coke-oven workers resulted in a
relative risk for lung cancer of 15.7. On this basis, the risk of the
general population for developing lung cancer over a lifetime has been
calculated to be 10^-4 to 10^-5 per ng of benzo [a]pyrene per m³ air.

In other words, about one person in 10 000 or 100 000 would be
expected to develop lung cancer in his or her lifetime as a result of
exposure to benzo [a]pyrene in air.

1.9 Effects on other organisms in the laboratory and the field

PAH are acutely toxic to fish and Daphnia magna in combination
with absorption of ultraviolet radiation and visible light. Metabolism
and degradation alter the toxicity of PAH. At low concentrations, PAH
can stimulate the growth of microorganisms and algae. The most toxic
PAH for algae are benz [a]anthracene (four-ring), the concentration
at which given life parameters are reduced by 50% (EC₅₀) being 1-29
µg/litre, and benzo [a]pyrene (five-ring), with an EC₅₀ of 5-15
µg/litre. The EC₅₀ values for algae for most three-ring PAH are
240-940 µg/litre. Naphthalene (two-ring) is the least toxic, with
EC₅₀ values of 2800-34 000 µg/litre.

No clear difference in sensitivity was found between different
taxonomic groups of invertebrates like crustaceans, insects, molluscs,
polychaetes, and echinoderms. Naphthalene is the least toxic, with
96-h LC₅₀ values of 100-2300 µg/litre. The 96-h LC₅₀ values for
three-ring PAH range between < 1 and 3000 µg/litre. Anthracene may be
more toxic than the other three-ring PAH, with 24-h LC₅₀ values
between < 1 and 260 µg/litre. The 96-h LC₅₀ values for four-, five-,
and six-ring PAH are 0.2-1200 µg/litre. Acute toxicity (LC₅₀) in fish
was seen at concentrations of 110 to > 10 000 µg/litre of
naphthalene, 30-4000 µg/litre of three-ring PAH (anthracene, 2.8-360
µg/litre), and 0.7-26 µg/litre for four- or five-ring PAH.

Contamination of sediments with PAH at concentrations of 250
mg/kg was associated with hepatic tumours in free-living fish. Tumours
have also been induced in fish exposed in the laboratory. Exposure of
fish to certain PAH can also cause physiological changes and affect
their growth, reproduction, swimming performance, and respiration.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS

2.1 Identity

The name 'polycyclic aromatic hydrocarbons' (PAH) commonly refers
to a large class of organic compounds containing two or more fused
aromatic rings, even though in a broad sense non-fused ring systems
should be included. In particular, the term 'PAH' refers to compounds
containing only carbon and hydrogen atoms (i.e. unsubstituted parent
PAH and their alkyl-substituted derivatives), whereas the more general
term 'polycyclic aromatic compounds' also includes the functional
derivatives (e.g. nitro- and hydroxy-PAH) and the heterocyclic
analogues, which contain one or more hetero atoms in the aromatic
structure (aza-, oxa-, and thia-arenes). Some authors refer to
polycyclic aromatic compounds as 'polycyclic organic matter', and the
term 'polynuclear' is frequently used for 'polycyclic', as in
'polynuclear aromatic compounds'.

More than 100 PAH have been identified in atmospheric particulate
matter (Lao et al., 1973; Lee et al., 1976a) and in emissions from
coal-fired residential furnaces (Grimmer et al., 1985), and about 200
have been found in tobacco smoke (Lee et al., 1976b, 1981).

The selection of PAH evaluated in this monograph is discussed in
Section 1. The nomenclature, common names, synonyms, and abbreviations
used are given in Table 1 in that section. The structural formulae are
shown in Figure 1. Molecular formulae, relative molecular masses, and
CAS Registry numbers are given in Table 3.

2.1.1 Technical products

Technical-grade naphthalene, also known as naphthalin and tar
camphor, has a minimum purity of 95%. The impurities reported are
benzo [b]thiophene (thianaphthene) when naphthalene is obtained from
coal-tar and methylindenes when it is derived from petroleum (Society
of German Chemists, 1989).

Commercially available anthracene, also known by the trade name
Tetra Olive N2G (IARC, 1983), has a purity of 90-95% (Hawley, 1987).
The impurities reported are phenanthrene, chrysene, carbazole (Hawley,
1987), tetracene, naphthacene (Budavari et al., 1989), and pyridine at
a maximum of 0.2% (IARC, 1983). The following purities were reported
for other technical-grade products: acenaphthene, 95-99%;
fluoranthene, > 95% (Griesbaum et al., 1989); fluorene, about 95%;
phenanthrene, 90%; and pyrene, about 95% (Franck & Stadelhofer, 1987).

The other compounds are generally produced as chemical
intermediates and for research purposes (see also sections 3.2.2 and
3.2.3). Reference materials certified to be of geater than 99% purity
are available for 22 of the PAH considered (Community Bureau of
Reference, 1992); the remaining compounds are commercially available
as chemical standards, with a purity of 99% or more.

Table 3. Identity of polycyclic aromatic hydrocarbons covered in this
volume ranked according to molecular mass

Compound Molecular Relative CAS
formula molecular Registry
mass No.

Naphthalene C₁₀H₈ 128.2 91-20-3
Acenaphthylene C₁₂H₈ 152.2 208-96-8
Acenaphthene C₁₂H₁₀ 154.2 83-32-9
Fluorene C₁₃H₁₀ 166.2 86-73-7
Anthracene C₁₄H₁₀ 178.2 120-12-7
Phenanthrene C₁₄H₁₀ 178.2 85-01-8
1-Methylphenanthrene C₁₅H₁₂ 192.3 832-69-9
Fluoranthene C₁₆H₁₀ 202.3 206-44-0
Pyrene C₁₆H₁₀ 202.3 129-00-0
Benzo[a]fluorene C₁₇H₁₂ 216.3 238-84-6
Benzo[b]fluorene C₁₇H₁₂ 216.3 243-17-4
Benzo[ghi]fluoranthene C₁₈H₁₀ 226.3 203-12-3
Cyclopenta[cd]pyrene C₁₈H₁₀ 226.3 2720837-3
Benz[a]anthracene C₁₈H₁₂ 228.3 56-55-3
Benzo[c]phenanthrene C₁₈H₁₂ 228.3 195-19-7
Chrysene C₁₈H₁₂ 228.3 218-01-9
Triiphenylene C₁₈H₁₂ 228.3 217-59-4
5-Methylchrysene C₁₉H₁₄ 242.3 3697-24-3
Benzo[b]fluoranthene C₂₀H₁₂ 252.3 205-99-2
Benzo[j]fluoranthene C₂₀H₁₂ 252.3 205-82-3
Benzo[k]fluoranthene C₂₀H₁₂ 252.3 207-08-9
Benzo[a]pyrene C₂₀H₁₂ 252.3 50-32-8
Benzo[e]pyrene C₂₀H₁₂ 252.3 192-97-2
Perylene C₂₀H₁₂ 252.3 198-55-0
Anthanthrene C₂₂H₁₂ 276.3 191-26-4
Benzo[ghi]perylene C₂₂H₁₂ 276.3 191-24-2
Indeno[1,2,3-cd]pyrene C₂₂H₁₂ 276.3 193-39-5
Dibenz[a,h]anthracene C₂₂H₁₄ 278.4 53-70-3
Coronene C₂₄H₁₄ 300.4 191-07-1
Dibenzo[a,e]pyrene C₂₄H₁₄ 302.4 192-65-4
Dibenzo[a,h]pyrene C₂₄H₁₄ 302.4 189-64-0
Dibenzo[a,i]pyrene C₂₄H₁₄ 302.4 189-55-9
Dibenzo[a,l]pyrene C₂₄H₁₄ 302.4 191-30-0

PAH considered (Community Bureau of Reference, 1992); the remaining
compounds are commercially available as chemical standards, with a purity of
99% or more.

2.2 Physical and chemical properties

Physical and chemical properties relevant to the toxicological
and ecotoxicological evaluation of the PAH are summarized in Table 4.
It should be kept in mind that the values for any one parameter may be
derived from different sources, with different methods of measurement
or calculation, so that individual values cannot be compared directly
unless the original sources are consulted. In particular, the vapour
pressures reported in the literature for the same PAH vary by up to
several orders of magnitude (Mackay & Shiu, 1981; Lane, 1989).
Variations are also seen in the reported solubility in water of
various PAH, although the values are generally within one order of
magnitude (National Research Council Canada, 1983). Flash-points were
available only for three compounds with high molecular mass (for
naphthalene, 78.9°C by the open-cup method and 87.8°C by the closed-cup
method; anthracene, 121°C by the closed-cup method; and phenanthrene,
171°C by the open-cup method). Explosion limits were available only
for naphthalene (0.9-5.9 vol %) and ananthrene (0.6 vol %) (Lewis,
1992). Vapour density (air = 1) was 4.42 for naphthalene (IARC,
1973), 5.32 for acenaphthene, 6.15 for anthracene (Lewis, 1992), 6.15
for phenanthrene, and 8.7 for benzo[a]pyrene (National Institute for
Occupational Safety and Health and Occupational Safety and Health
Administration, 1981).

The physical and chemical properties are largely determined by
the conjugated alpha-electron systems, which vary fairly regularly
with the number of rings and molecular mass, giving rise to a more or
less wide range of values for each parameter within the whole class.
At room temperature, all PAH are solids. The general characteristics
common to the class are high melting- and boiling-points, low vapour
pressure, and very low solubility in water. PAH are soluble in many
organic solvents (IARC, 1983; Agency for Toxic Substances and Disease
Registry, 1990; Lide, 1991) and are highly lipophilic.

Vapour pressure tends to decrease with increasing molecular mass,
varying by more than 10 orders of magnitude. This characteristic
affects the adsorption of individual PAH onto particulate matter in
the atmosphere and their retention on particulate matter during
sampling on filters (Thrane & Mikalsen, 1981). Vapour pressure
increases markedly with ambient temperature (Murray et al., 1974),
which additionally affects the distribution coefficients between
gaseous and particulate phases (Lane, 1989). Solubility in water tends
to decreases with increasing molecular mass. For additional
information, refer to section 4.1.

PAH are chemically inert compounds (see also section 4.4). When
they react, they undergo two types of reaction: electrophilic
substitution and addition. As the latter destroys the aromatic
character of the benzene ring that is affected, PAH tend to form
derivatives by the former reaction; addition is often followed by
elimination, resulting in net substitution. The chemical and
photochemical reactions of PAH in the atmosphere have been reviewed

Table 4. Physical and chemical properties of polycyclic aromatic compounds covered in this monograph, ranked by molecular mass

Compound Colour Melting- Boiling- Vapour Density^c n-Octanol: Solubility in Henry's law
point^a point pressure water water at 25°C constant at
(°C) (°C) (Pa at 25°C) partition (µg/litre)^d 25°C (kPa)
coefficient
(log K_ow)

Naphthalene White^b 81 217.9^c 10.4^g 1.154^{25 h} 3.4^j 3.17 x 10⁴ 4.89 x 10^{-2 k}

Acenaphthylene 92-93 8.9 x 10^{-1 g} 0.899^{16/2 h} 4.07^f 114 x 10^{-3 l}
Acenaphthene White^b 95 279^h 2.9 x 10^{-1 g} 1.024^{90/4 h} 3.92^f 3.93 x 10³ 1.48 x 10^{-2 k}
Fluorene White^e 115-116 295^e 9.0 x 10^{-2 g} 1.203^{0/4 h} 4.18^m 1.98 x 10³ 1.01 x 10^{-2 n}
Anthracene Colourless^o 216.4 342^e 8.0 x 10^{-4 g} 1.283^{25/4 h} 4.5^j 73 7.3 x 10^{-2 n}
Phenanthrene Colourless^p 100.5 340^h 1.6 x 10^{-2 g} 0.980^{4 h} 4.6^j 1.29 x 10³ 3.98 x 10^{-3 k}
1-Methylphenanthrene 123 354-355^y 5.07^s 255 (24°C)^t
Fluoranthene Pale yellow^h 108.8 375^h 1.2 x 10^{-3 g} 1.252^{0/4 h} 5.22^u 260 6.5 x 10^-4
(20 °C)^w
Pyrene Colourless^e 150.4 393^h 6.0 x 10^{-4 g} 1.271^{23/4 h} 5.18^j 135 1.1 x 10^{-3 n}
Benzo[a]fluorene Colourless^x 189-190^h 399-400^y 5.32^z 45
Benzo[b]fluorene Colourless^x 213.5 401-402^y 1.226^aa 5.75^z 2.0
Benzo[ghi]fluoranthene Yellow^bb 128.4 432^cc 1.345^{23 dd}
Cyclopenta[cd]pyrene Orange^x 170 439^ee
Benz[a]anthracene Colourless^b 160.7 400^b 2.8 x 10^{-5 g} 1.226^aa 5.61^f 14
Benzo[c]phenanthrene Colourless^x 66.1 1.265^ff
Chrysene Colourless 253.8 448^h 8.4 x 10^-5 1.274^{20/4 e} 5.91^u 2.0
with blue (20°C)^gg
fluoresence^b
Triphenylene Colourless^x 199 425^bb 1.3^p 5.45^hh 43
5-Methylchrysene Colourless^x 117.1 458ⁱⁱ 62 (27°C)^jj
Benzo[b]fluoranthene Colourlessⁱ 168.3 481^kk 6.7 x 10^-5 6.12^f 1.2^ll 5.1 x 10^-5
(20°C)^gg (20°C)^w
Benzo[j]fluoranthene Yellow^b 165.4 480^ee 2.0 x 10^{-6 l} 6.12^mm 2.5ⁿⁿ

Table 4. (continued)

Renzo[k]fluoranthene Pale yellow^h 215.7 480^h 1.3 x 10^-8 6.84^m 0.76^f 4.4 x 10^-5
(20°C)^oo (20°C)^w
Benzo[a]pyrene Yellowish^e 178.1 496^kk 7.3 x 10^-7oo 1.351^pp 6.50^u 3.8 3.4 x 10^-5
(20°C)
Benzo[e]pyrene Pale yellow^x 178.7 493^kk 7.4 x 10^-7qq 6.44^rr 5.07 (23°C)^tt
Perylene Yellow to 277.5 503^ss 1.35^v 5.3^uu 0.4
colourless^c
Anthanthrene Golden yellow^bb 264 547^yy 1.39^v
Benzo[ghi]perylene Pale yellow- 278.3 545ⁱⁱ 1.4 x 10^{-8 ww} 1.329^{20 xx} 7.10^u 0.26 2.7 x 10^-5
green^bb (20°C)^w
Indeno[1,2,3-cd]pyrene Yellowⁱ 163.6 536^yy 1.3 x 10^-8 6.58^f 62^f 2.9 x 10^-5
(20°C)^gg (20°C)^w
Dibenz[a,h]anthracene Colourlessⁱ 266.6 524^yy 1.3 x 10^-8 1.282ⁱ 6.50^zz 0.5 (27°C)^jj 7 x 10^{-6 l}
(20°C)
Coronene Yellow^h 439 525^aaa 2.0 x 10^{-10 qq} 1.37^b 5.4^uu 0.14
Dibenzo[a,e]pyrene Pale yellow^h 244.4 592^vv
Dibenzo[a,h]pyrene Golden yellowⁱ 317 596^vv
Dibenzo[a,i]pyrene Greenish-yellowishⁱ 282 594^vv 3.2 x 10^{-10 mm} 7.30^hh 0.17^l 4.31 x 10^{-6 l}
Dibenzo[a,l]pyrene Pale yellowⁱ 162.4 595^vv

^a From Karcheret al. (1985); Karcher (1988)
^b From Lewis (1992)
^c When two temperatures are given as superscripts, they indicate the specific gravity, i.e. the density of the substance at the first
reported temperature relative to the density of water at the second reported temperature. When there is no value, or only one, for
temperature, the datum is in grains per millilitre, at the indicated temperature, if any.

Table 4 (continued)

^d From Mackay & Shiu (1977), except where noted
^e From Budavari (1989)
^f From National Toxicology Program (1993)
^g From Sonnefeld et al. (1983)
^h From Lide (1991)
ⁱ From IARC (1977)
^j From Karickhoff et al. (1979)
^k From Mackay et al. (1979)
^l Calculated by Syracuse Research Center; from National Toxicology Program (1993)
^m Calculated as per Leo et al. (1971); from US Environmental Protection Agency (1980)
ⁿ From Mackay & Shiu (1981)
^o When pure, colourless with violet fluorescence; from Budavari (1989)
^p From Hawley (1987)
^q From National Institute for Occupational Safety and Health and Occupational Safety and Health Administration (1981)
^r From Kruber & Marx (1938)
^s Calculated by Karcher et al. (1991)
^t From May et al. (1978)
^u From Bruggeman et al. (1982)
^v At ambient temperature; from Inokuchi & Nakagaki (1959)
^w From Ten Hulscher et al. (1992)
^x Personal observation by J. Jacob, Germany, on high-purity, certified reference materials
^y From Kruber (1937)
^z Calculated by Miller et al. (1985)
^aa From Schuyer et al. (1953)
^bb From IARC (983)
^cc From Kruber & Grigoleit (1954)
^dd From Ehrlich & Beevers (1956)
^ee Reported by Grimmer (1983a)
^ff From Beilstein Institute for Organic Chemistry (1993)
^gg Reported by Sims & Overcash (1983)
^hh Calculated by Yalkowsky & Valvani (1979)
ⁱⁱ Calculated by White (1986)
^jj From Davis et al. (1942)
^kk From review by Bjorseth (1983); original references cited by White (1986)
^ll Temperature not given; reported by Sims & Overcash (1983)
^mm Calculated by National Toxicology Program (1993)
ⁿⁿ Temperature not given; unpublished result cited by Wise et al. (1981)
^oo From US Environmental Protection Agency (1980)

Table 4 (continued)

^pp From Kronberger & Weiss (1944)
^qq From review of Santodonato et al. (1981)
^rr Calculated by Ruepert et al. (1985)
^ss From Verschueren (1983)
^tt From Schwarz (1977)
^uu From Brooke et al. (1986)
^vv From Agency for Toxic Substances and Disease Registry (1990)
^xx From White (1948)
^yy Estimated from gas chromatographis retention time; from Grimmer (1983a)
^zz From Means et al. (1980)
^aaa From Von Boente (1955)

(Valerio et al., 1984; Lane, 1989). After photodecomposition in the
presence of air and sunlight, a number of oxidative products are
formed, including quinones and endoperoxides. PAH have been shown
experimentally to react with nitrogen oxides and nitric acid to form
the nitro derivatives of PAH, and to react with sulfur oxides and
sulfuric acid (in solution) to form sulfinic and sulfonic acids. PAH
may also be attacked by ozone and hydroxyl radicals present in the
atmosphere. The formation of nitro-PAH is particularly important owing
to their biological impact and mutagenic activity (IARC, 1984a,
1989a). In general, the above reactions are of interest with regard to
the environmental fate of PAH, but the results of experimental studies
are difficult to interpret because of the complexity of interactions
occurring in environmental mixtures and the difficulty in eliminating
artefacts during analytical determinations. These reactions are also
considered to be responsible for possible losses of PAH during ambient
atmospheric sampling (see section 2.4.1.1).

2.3 Conversion factors

Atmospheric concentrations of PAH are usually expressed as
micrograms or nanograms per cubic meter. At 25°C and 101.3 kPa, the
conversion factors for a compound of given relative molecular mass are
obtained as follows:

ppb = µg/m³ × 24.45/relative molecular mass

µg/m³ = ppb × relative molecular mass/24.45.

For example, for benzo [a]pyrene, 1 ppb = 10.3 µg/m³ and
1 µg/m³ = 0.0969 ppb.

2.4 Analytical methods

Tables 5 and 6 present as examples a limited number of methods
that are applied to 'real' samples of different matrices. The methods
and sources were selected, as far as possible, according to the
following criteria: accessibility of the bibliographic source,
completeness of the description of the procedure, practicability with
common equipment for this type of analysis (even if experienced
personnel are required), recency, and whether it is an official,
validated, or recommended method.

2.4.1 Sampling

2.4.1.1 Ambient air

The physical state of PAH in the atmosphere must be considered
when selecting the sampling apparatus. Compounds with five or more
rings are almost exclusively adsorbed on suspended particulate matter,
whereas lower-molecular-mass PAH are partially or totally present in
the vapour phase (Coutant et al., 1988). When ambient air is
monitored, it is common practice to monitor only particle-bound PAH

Table 5. Analytical methods for polycyclic aromatic hydrocarbons in air

Matrix Sampling, extraction Clean-up Analysis Limit of Reference
detection^a

Ambient air Sampling on GF+PUF, at 45 m³/h; Liquid-liquid partition GC/MS Yamasaki et al.
Soxhlet extraction with cyclohexane with cyclohexane: (1982)
H₂O:DMSO, then CC
with SiO₂
Sampling on GF+PUF, at 30 m³/h; CC with Al₂O₃ + HPLC/FL 0.01-0.7 Keller &
Soxhlet extraction with petroleum ether SiO₂ ng/m³ Bidleman (1984)
(GF) and DCM (PUF)
Sampling on GF (particle diameter TLC with SiO₂ HPLC/UV 0.01-0.3 Greenberg et al.
< 15 µm), at 68 m³/h; Soxhlet extraction + FL ng/m³ (1985)
with cyclohexane, DCM, and acetone
Sampling on GF at 83 m³/h; sonication TLC with SiO₂ GC/FID Valerio et al.
(cyclohexane) (1992)

Emissions Sampling by glass wool, condenser, Liquid-liquid partition GC/FID 10 ng/m³ Colmsjo et al.
(municipal and XAD-2; extraction with acetone with DMF (1986a)
incinerator) (glass-wool and XAD-2, by Soxhlet)

Vehicle Sampling by GF and condenser; liquid- CC with SiO₂ and GC/FID 2.5-20 ng Grimmer et al.
exhaust liquid partition with acetone:H₂O: Selphadex LH-20 per test (1979)
cyclohexane and DMF:H,O:cyclohexane
Sampling in dilution tunnel by Liquid-liquid partition GC/FID or Westerholm et
PTFE-coated GF and condenser; Soxhlet with cyclohexane: GC/MS al. (1988)
extraction of filter (DCM) and H₂O:DMF
condensate (acetone); remaining
aqueous phase extracted with DCM

Table 5. (continued)

Matrix Sampling, extraction Clean-up Analysis Limit of Reference
detection^a

Indoor air Sampling on GF (particle diameter TLC with acetyloxylated Spectrofluorescence Lioy at al. (1988)
< 10 µm) at 10 l/min; sonication cellulose (benzo[a]pyrene only)
(cyclohexane)
Sampling on quartz-fibre filtre and GC/MS Chuang at al.
XAD-4 at 226 l/min; Soxhlet extraction (1991)
with DCM
Sampling on PTFE-coated GF at filtration; then CC HPLC/FL 0.02-0.12 Daisey & Gundel
20 l/minfor 24 h; Soxhlet extraction SiO₂ cartridge), ng/m^{3 b} (1993)
with DCM optional
Sampling on GF and PUF, at 20 litres/min GC/FID, GC/MS US Environmental
for 24 h; Soxhlet extraction (10% ether: or HPLC/UV + FL Protection Agency
n-hexane) (1990)

Workplace air Sampling on PTFE filter and XAD-2 GC/FID 0.3-0.5 µg NIOSH (1994a,b)
at 2 l/min; sonication or Soxhlet per sample
extraction of filter^c, extraction of HPLC/UV 0.05-0.8 µg
XAD-2 with toluene (for GC) or + FL per sample
acetonitrile (for HPLC)

Workplace air Sampling on filter (GF, quartz fibre, CC (XAD-2) GC/FID approx 0.5 German
PTFE or silver membrane) at 2 litres/min; µg/m³ Research
sonication or Soxhlet extraction with Commission
cyclohexane or toluene (1991)

Tobacco Sampling by acetone trap; solvent CC (SiO₂ + Sephadex GC/MS + ng/cigarette Lee at al. (1976b)
smoke partition scheme (acids/bases/neutral LH-20); then NMR
compounds/PAH) HPLC/UV

Table 5 (continued)

GC glass fibre; PUF, polyurethane foam; DMSO, dimethyl sulfoxide; CC, column chromatography; GC, gas chromatography;
MS, mass spectrometry; DCM, dichloromethane; HPLC, high-performance liquid chromatography; FL, fluorescence detection;
TLC, thin-layer chromatography; UV, ultraviolet detection; FID, flame-ionization detection; DMF, N-dimethylformamide;
PTFE, polytetrafluoroethylene; NMR, nuclear magnetic resonance
^a Various PAH
^b The following PAH can be determined: fluoranthene, pyrene, chrysene, benzo[e]pyrene, benzo[b]fluoranthene,
benzo[k]fluoranthene, benzo[a]pyrene, benzo[ghi]perylene, indeno[1,2,3-cd]pyrene.
^c Appropriate solvent must be determined by recovery tests on specific samples.

Table 6. Analytical methods for polycyclic aromatic hydrocarbons in matrices other than air

Matrix Extraction Clean-up Analysis Limit of Reference
detection^a

Tap-water Preconcentration on PUF; Liquid-liquid partition GC/FID or TLC 0.1 ng/litre Basu & Saxena
extraction (with acetone and with cyclohexane: (Al₂O₃: acetyl (1978a)
cyclohexane) H₂O:methanol and celluose) with FL
cyclohexane: H₂O: detector
DMSO; then CC
OWN)

Groundwater Liquid-liquid partition with CC (SiO₂), if needed GC/FID µg/litre level US Environmental
DCM GC/MS 10 µg/litre Protection Agency
HPLC/UV + FL 0-01-2 µg/litre (1986a)

Wastewater Liquid-liquid partition with CC (SiO₂), if needed GC/FID or 0.01 -0.2 µg/litre US Environmental
DCM HPLC/UV+FL (by HPLC) Protection Agency
(1984a)

Seawater Liquid-liquid partition with CC (SiO₂ + Al₂O₂) GC/FID or Desideri at al.
n-hexane or CCl4 HPLC/UV (1984)

Soil Sonication with DCM CC (Al2O2); then GC/MS 1 µg/kg Vogt at
liquid-liquid partition al. (1987)
(n-hexane:H₂O:DMSO)
Soxhlet extraction with DCM CC (Florisil cartridge) HPLC/UV + FL 1 µg/kg Jones et a[.
(1989a)

Sediment Soxhlet extraction with DCM CC (SiO₂ + Sephadex HPLC/DAD/MS Quilliam & Sim
LH20) (1988)

Sonication with acetone: CC (Florisil) HPLC/UV + FL 1-160 µg/kg Marcus et al.
n-hexane (1988)

Table 6. (continued)

Matrix Extraction Clean-up Analysis Limit of Reference
detection^a

Meat and fish (I) digestion (alcoholic KOH), Liquid-liquid partition GC/FID 2.5-20 ng/ Grimmer &
products (I), then liquid-liquid partition with cyclohexane: sample Bohnke (1979b)
vegetable oils (methanol: H₂O:cyclohexane) H₂O:DMF); then CC
(II), and sewage (II) dissolution in cyclohexane (SiO₂ + Sephadex
sludge (III) (III) refluxing with acetone LH20)

Food (total Refluxing with alcoholic KOH, Liquid-liquid partition HPLC/FL 0.002-0.7 µg/kg Dennis et al.
diet) extraction with isooctane (isooctane:H₂O:DMF); (1983)
then CC (SiO₂ cartridge)
Saponification with alcoholic CC (SiO₂) HPLC/FL 0.03-2 µg/kg de Vos et al.