INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 140
POLYCHLORINATED BIPHENYLS AND TERPHENYLS
(SECOND EDITION)
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 draft prepared by Dr S. Dobson, Institute of Terrestrial
Ecology, United Kingdom, and Dr G.J. van Esch, Bilthoven, The
Netherlands
World Health Organization
Geneva, 1993
The International Programme on Chemical Safety (IPCS) is a joint
venture of the United Nations Environment Programme, the International
Labour Organization, and the World Health Organization. The main
objective of the IPCS is to carry out and disseminate evaluations of
the effects of chemicals on human health and the quality of the
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
Polychlorinated Biphenyls and Terphenyls. -- 2nd ed.
(Environmental health criteria; 140)
1.Environmental exposure 2.Environmental pollutants 3.Polychlorinated
biphenyls -- adverse effects 4.Polychlorinated biphenyls -- toxicity
5.Polychloroterphenyl compounds -- adverse effects
6.Polychloroterphenyl compounds -- toxicity I.Series
ISBN 92 4 157140 3 (NLM Classification: QV 633)
ISSN 0250-863X
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CONTENTS
INTRODUCTION
1. SUMMARY AND EVALUATION, CONCLUSIONS, RECOMMENDATIONS
1.1 Summary and evaluation
1.1.1 Introduction
1.1.2 Identity, physical, and chemical properties
1.1.3 Analytical methods
1.1.4 Production and uses
1.1.5 Environmental transport, distribution, and transformation
1.1.6 Environmental levels and human exposure
1.1.7 Kinetics and metabolism
1.1.8 Effects on organisms in the environment
1.1.8.1 Laboratory studies
1.1.8.2 Field studies
1.1.9 Effects on experimental animals and in vitro systems
1.1.9.1 Single exposure
1.1.9.2 Short-term exposure
1.1.10 Reproduction, embryotoxicity, and teratogenicity
1.1.11 Mutagenicity
1.1.12 Carcinogenicity
1.1.13 Special studies
1.1.14 Factors modifying toxicity, mode of action
1.1.15 Effects on humans
1.2 Conclusions
1.2.1 Distribution
1.2.2 Effects on experimental animals
1.2.3 Effects on humans
1.2.4 Effects on the environment
1.3 Recommendations
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1 Identity
2.1.1 Chemical formula and structure
2.1.2 Relative molecular mass
2.1.3 Common name
2.1.4 Chemical composition
2.1.5 Technical product
2.1.6 Purity and impurities
2.2 Physical and chemical properties
2.2.1 Log n-octanol/water partition coefficient
2.2.2 Conversion factors
2.3 Analytical methods
2.3.1 Sampling strategy and sampling methods
2.3.1.1 Extraction procedures
2.3.1.2 Sample clean-up
2.3.2 Separation and identification
2.3.2.1 Chromatographic separation
2.3.2.2 Gas-liquid chromatography
2.3.3 Quantification
2.3.4 Accuracy of PCB determinations
2.3.5 Confirmation
2.3.6 Detection limits
2.4 Codex questionnaire on analytical methods
2.4.1 Interpretation and comparability of data
2.5 Activities of the WHO Regional Office for Europe
2.6 Appraisal
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1 Natural occurrence
3.2 Man-made sources
3.2.1 Production levels and processes, uses
3.2.1.1 World production figures
3.2.1.2 Manufacturing processes
3.2.2 Uses
3.2.2.1 Completely closed systems
3.2.2.2 Nominally closed systems
3.2.2.3 Open-ended applications
3.2.2.4 Contamination of other compounds
3.2.3 Loss into the environment
3.2.3.1 Routes of environmental pollution
3.2.3.2 Release of PCBs into the atmosphere
3.2.3.3 Leakage and disposal of PCBs in industry
3.2.4 Thermal decomposition of PCBs
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION
4.1 Transport and distribution between media
4.1.1 Transport in air
4.1.1.1 Dry deposition
4.1.1.2 Precipitation deposition
4.1.2 Transport in soil
4.1.3 Transport in water
4.1.4 Transport between media
4.2 Biotransformation
4.2.1 Biodegradation
4.2.1.1 Bacteria
4.2.2 Biodegradation; individual congeners
4.2.2.1 Bacteria
4.2.2.2 Fungi
4.2.3 Photodegradation
4.2.4 Bioaccumulation, distribution in organisms, and elimination
4.2.4.1 Microorganisms
4.2.4.2 Plants
4.2.4.3 Aquatic invertebrates
4.2.4.4 Fish
4.2.4.5 Birds
4.2.4.6 Mammals
4.2.5 Appraisal
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1 Levels in the environment
5.1.1 Air
5.1.1.1 Rain and snow
5.1.1.2 Natural gas
5.1.2 Water
5.1.3 Soil
5.1.4 Aquatic and terrestrial organisms
5.1.4.1 Effect of dredging-contaminated sediment on organisms
5.1.4.2 Relationship to lipid content of organisms
5.1.4.3 Residues in different trophic levels and effects of diets
5.1.4.4 Effects of age, sex, and reproductive status on uptake and elimination
5.1.4.5 Time trends in residues
5.1.4.6 Seasonal patterns in residues
5.1.5 Appraisal
5.2 Levels in animal feed
5.3 Levels in human food
5.3.1 General
5.3.2 Drinking-water
5.3.3 Dairy products
5.3.4 Fish and shellfish
5.3.5 Influence of food processing
5.3.6 Food contamination by packaging materials
5.3.7 Appraisal
5.4 General population exposure
5.4.1 Air
5.4.2 Drinking-water
5.4.3 Intake by infants through mother's milk
5.4.4 Infant and toddler total diet
5.4.5 Total intake by adults via food
5.4.6 Total diet/market-basket studies
5.4.7 Total intake of major congeners by adults via food
5.4.8 Time trends in different matrices
5.5 Concentrations in the body tissues of the general population
5.5.1 Adipose tissue
5.5.1.1 PCBs in the fetus
5.5.1.2 Congeners in adipose tissue
5.5.2 Blood of the general population
5.5.3 Human milk
5.5.3.1 Major PCB congeners in human milk
5.5.3.2 Factors that influence the intake of PCBs with milk
5.5.4 Other tissues
5.6 Accidental exposures (Yusho and Yu-Cheng)
5.7 Occupational exposure
5.7.1 Accidental exposure
5.7.2 Occupational exposure during manufacture and use
5.7.2.1 Adipose tissue
5.7.2.2 Blood
6. KINETICS AND METABOLISM
6.1 Absorption
6.1.1 Inhalation
6.1.2 Dermal
6.1.3 Oral
6.2 Distribution
6.2.1 Inhalation (rat)
6.2.2 Oral (rat)
6.2.3 Oral (monkey)
6.2.4 Oral (humans)
6.2.5 Individual congeners of PCBs
6.2.6 Appraisal
6.3 Placental transport
6.3.1 Laboratory animals
6.3.2 Wildlife
6.3.3 Humans
6.4 Excretion and elimination
6.4.1 Following oral dosing
6.4.2 Following parenteral dosing
6.4.3 Humans
6.4.4 Elimination via milk (animals)
6.4.4.1 Elimination via breast milk
6.5 Metabolic transformation
6.5.1 PCBs
6.5.2 Dichlorobiphenyls
6.5.3 Tetrachlorobiphenyls
6.5.4 Hexachlorobiphenyls and higher chlorinated compounds
6.5.5 Retention and turnover
6.5.6 Appraisal
7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
7.1 Toxicity for microorganisms
7.1.1 Freshwater microorganisms
7.1.2 Marine and estuarine microorganisms
7.1.3 Soil microorganisms
7.1.4 Plankton communities
7.1.5 Interactions with other chemicals
7.1.6 Tolerance
7.2 Toxicity for aquatic organisms
7.2.1 Aquatic plants
7.2.2 Aquatic invertebrates
7.2.2.1 Short- and long-term toxicity
7.2.2.2 Response to temperature and salinity
7.2.2.3 Reproduction
7.2.2.4 Moulting
7.2.2.5 Behaviour
7.2.2.6 Population structure
7.2.2.7 Interactions with other chemicals
7.2.3 Fish
7.2.3.1 Short- and long-term toxicity
7.2.3.2 Carcinogenicity
7.2.3.3 Effects on developmental stages and reproduction
7.2.3.4 Physiological and biochemical effects
7.2.3.5 Behavioural effects
7.2.3.6 Interactions with other chemicals
7.2.4 Amphibians
7.2.5 Aquatic mammals
7.3 Toxicity for terrestrial organisms
7.3.1 Plants
7.3.2 Terrestrial invertebrates
7.3.3 Birds
7.3.3.1 Short-term toxicity
7.3.3.2 Egg production
7.3.3.3 Hatchability and embryotoxicity
7.3.3.4 Eggshell thinning
7.3.3.5 Effects on the male
7.3.3.6 The effects of stress
7.3.3.7 Physiological, biochemical, and behavioural effects
7.3.3.8 Interactive effects with other chemicals
7.3.4 Terrestrial mammals
7.3.4.1 Short-term toxicity
7.3.4.2 Reproductive effects
7.3.4.3 Physiological effects
7.4 Effects on organisms in the field
7.4.1 Plants
7.4.2 Fish
7.4.3 Birds
7.4.4 Mammals
7.4.4.1 Appraisal
8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS
8.1 Single exposures
8.1.1 Oral
8.1.2 Inhalation
8.1.3 Dermal
8.1.4 Other routes
8.2 Short-term exposures
8.2.1 Oral
8.2.1.1 Aroclors
8.2.1.2 Individual congeners
8.2.2 Intraperitoneal: reconstituted PCB mixtures
8.2.3 Dermal exposure
8.2.4 Appraisal
8.3 Skin and eye irritation, sensitization
8.4 Reproduction, embryotoxicity, and teratogenicity
8.4.1 Reproduction and embryotoxicity
8.4.1.1 Oral
8.4.2 Teratogenicity
8.4.2.1 Aroclors (oral)
8.4.2.2 Aroclors (subcutaneous)
8.4.2.3 Individual congeners (oral)
8.4.3 Appraisal
8.4.4 Mutagenicity and related end-points
8.4.4.1 DNA damage
8.4.4.2 Mutagenicity tests
8.4.4.3 Cell transformation
8.4.4.4 Cell to cell communication
8.4.4.5 Interaction
8.4.4.6 Cell division parameters
8.5 Carcinogenicity
8.5.1 Long-term toxicity/carcinogenicity
8.5.2 Tumour promotion/anticarcinogenic effects
8.5.3 Initiation, promotion, and other special studies on individual congeners
8.5.4 Skin carcinogenicity
8.5.5 Appraisal
8.6 Special studies: target-organ effects
8.6.1 Liver
8.6.1.1 PCB mixtures
8.6.1.2 Individual congeners
8.6.2 Enzyme induction
8.6.2.1 Effects on liver enzymes of PCBs
8.6.2.2 Effects on liver enzymes of "biologically filtered" PCB mixtures
8.6.2.3 Effects of individual congeners on liver enzymes
8.6.2.4 Appraisal
8.6.3 Effects on vitamins and mineral metabolism
8.6.3.1 Effects of PCB mixtures
8.6.3.2 Effects of individual congeners
8.6.4 Effects on the gastrointestinal tract
8.6.5 Effects on lipid metabolism
8.6.5.1 Effects of PCB mixtures
8.6.5.2 Effects of individual congeners
8.6.6 Effects on porphyrin metabolism
8.6.6.1 Effects of PCB mixtures
8.6.6.2 Effects of individual congeners
8.6.7 Effects on the endocrine system
8.6.7.1 Effects of PCB mixtures
8.6.7.2 Effects of individual congeners
8.6.8 Immunotoxicity
8.6.8.1 Effects of PCB mixtures
8.6.8.2 Effects of individual congeners
8.6.8.3 Appraisal
8.6.9 Neurotoxic effects
8.6.10 Skin effects
8.6.11 Effects on the lung
8.6.12 Miscellaneous
8.7 Factors modifying toxicity; mode of action
8.7.1 Factors modifying toxicity
8.7.2 Mechanisms of toxicity
8.7.3 Toxicity of impurities in commercial PCBs
9. EFFECTS ON HUMANS
9.1 General population exposure
9.1.1 Acute effects - poisoning incidents
9.1.2 Effects of short- and long-term exposure
9.1.2.1 Yusho and Yu-Cheng accidents
9.1.2.2 Effects of PCBs on babies and infants
9.1.3 Appraisal
9.2 Occupational exposure
9.2.1 Acute toxicity - poisoning incidents
9.2.1.1 Acute dermal effects
9.2.2 Effects of short- and long-term exposure
9.2.3 Appraisal
9.2.4 Special studies (target organ effects)
9.2.4.1 Effects on the liver
9.2.4.2 Immunotoxicity
9.2.4.3 Effects on the respiratory system
9.2.4.4 Neurotoxicity
9.2.4.5 Blood pressure
9.2.5 Mortality studies
9.2.6 Appraisal
10. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
POLYCHLORINATED TERPHENYLS
1. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
1.1 Identity
1.2 Physical and chemical properties
1.3 Analytical methods
2. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION
4. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
4.1 Residues in the environment
4.2 Residues in food
4.3 Concentrations in adipose tissue
4.4 Concentrations in blood
5. KINETICS AND METABOLISM
5.1 Absorption
5.2 Distribution
5.3 Biotransformation
6. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
6.1 Marine and estuarine organisms
6.2 Terrestrial invertebrates
6.3 Birds
7. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS
7.1 Single oral exposures
7.2 Short-term oral exposures
7.2.1 Rat
7.2.2 Monkey
7.3 Teratogenicity
7.4 Carcinogenicity
7.5 Miscellaneous effects
REFERENCES
ANNEX 1
RESUME
RESUMEN
WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR POLYCHLORINATED
BIPHENYLS (PCBs) AND POLYCHLORINATED TERPHENYLS (PCTs)
Members
Dr L.A. Albert, Consultores Ambientales Asociados, Xalapa, Veracruz,
Mexico
Professor U.G. Ahlborg, Institute of Environmental Medicine,
Karolinska Institute, Stockholm, Sweden
Dr V. Benes, Department of Toxicology and Reference Laboratory,
Institute of Hygiene and Epidemiology, Prague, Czechoslovakia
(Vice-Chairman)
Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
Experimental Station, Abbots Ripton, Huntingdon, United Kingdom
(Chairman)
Dr Yuzo Hayashi, Division of Pathology, National Institute of Hygienic
Sciences, Tokyo, Japan
Dr T. Lakhanisky, Division of Toxicology, Institute of Hygiene and
Epidemiology, Brussels, Belgium
Dr J. McKinney, US Environmental Protection Agency, Research Triangle
Park, North Carolina, USA
Dr Pang Ying Fa, Chinese Academy of Preventive Medicine, Beijing,
China
Dr T. Vermeire, National Institute of Public Health and Environmental
Protection, Bilthoven, Netherlands (Co-Rapporteur)
Dr E. Yrjänheikki, Regional Institute of Occupational Health, Oulu,
Finland
Observers
Dr M. Martens (Representative from ECETOC), Monsanto Services
International, Brussels, Belgium
Mrs H. B. Sundmark (Representative from ECETOC), Norsk Hydro a.s.
Porsgrunn, Research Centre, Porsgrunn, Norway
Secretariat:
Dr G.J. van Esch, Bilthoven, Netherlands (Co-Rapporteur and
Secretary)
Dr M. Kogevinas, Unit of Analytical Epidemiology, International Agency
for Research on Cancer (IARC), Lyon, France
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
publication. In the interest of all users of the environmental health
criteria monographs, readers are kindly requested to communicate any
errors that may have occurred to the Director of the International
Programme on Chemical Safety, World Health Organization, Geneva,
Switzerland, in order that they may be included in corrigenda, which
will appear in subsequent volumes.
* * *
A detailed data profile and a legal file can be obtained from the
International Register of Potentially Toxic Chemicals, Palais des
Nations, 1211 Geneva 10, Switzerland (Telephone no. 7988400/7985850).
ENVIRONMENTAL HEALTH CRITERIA FOR PCBs AND PCTs
A WHO Task Group on Environmental Health Criteria for PCBs and PCTs
met in Brussels from 28 May to 1 June 1990. The meeting was convened
in the Institute of Hygiene and Epidemiology in Brussels and sponsored
by the Belgian Ministry of Health. Mrs A.-M. Sacré-Bestin of the
Ministry opened the meeting and welcomed the participants on behalf of
the host country. Dr G.J. van Esch welcomed the participants on behalf
of the Heads of the three IPCS cooperating organizations
(UNEP/ILO/WHO). The Group reviewed and revised the draft Environmental
Health Criteria monograph and the companion Health and Safety Guide
and made an evaluation of the risks for human health and the
environment from exposure to PCBs and PCTs.
The first draft of the EHC monograph was prepared by Dr S. Dobson
(environmental aspects) and Dr G.J. van Esch (other sections) and was
based on contributions from several authors and countries. It was
prepared in close cooperation with the WHO Regional Office for Europe,
in Copenhagen.
The second draft was prepared by Dr G.J. van Esch, incorporating
comments received following the circulation of the first draft to the
IPCS contact points for Environmental Health Criteria monographs.
Dr K. Jager, Central Unit, IPCS, was responsible for the scientific
content of the final monograph and Mrs M.O. Head, Oxford, for the
editing.
The efforts of all who helped in the preparation and finalization of
the documents are gratefully acknowledged.
INTRODUCTION
The commercial production of the polychlorinated biphenyls (PCBs)
began in 1930, and, during the 1930s, cases of poisoning were reported
among men engaged in their manufacture. The nature of this
occupational disease was characterized by a skin affection with
acneiform eruptions; occasionally the liver was involved, in some
cases with fatal consequences. Subsequent safety precautions appear
largely to have prevented further outbreaks of this disease in
connection with the manufacture of PCBs, but, since 1953, cases have
been reported in Japanese factories manufacturing condensers.
The distribution of PCBs in the environment was not recognized until
Jensen started an investigation in 1964 to ascertain the origins of
unknown peaks, observed during the gas-liquid chromatographic
separation of organochlorine pesticides from wildlife samples. In
1966, he and his colleagues succeeded in attributing these to the
presence of PCBs. Since then, investigations in many parts of the
world have revealed the widespread distribution of PCBs in
environmental samples.
The serious outbreaks of poisoning in humans and in domestic animals
from the ingestion of food, accidentally contaminated with PCBs, have
stimulated investigations into the toxic effects of PCBs on animals
and on nutritional food chains. This has resulted in the limitation of
the commercial exploitation of PCBs and polychlorinated terphenyls
(PCTs), and in regulations to limit the residues in human and animal
food.
In recent years, many industrial nations have taken steps to control
the flow of PCBs into the environment. PCBs and PCB-containing
formulations are restricted (an exception is sometimes made for mono-
and dichloro-PCBs) for most uses. Now they are almost entirely
restricted to use in closed systems, such as isolating oils in
transformers, capacitors, and other electrical systems, and as a heat
transfer medium and hydraulic liquid. The most influential forces
leading to these restrictions have probably been the 1973 and 1987
decision-recommendations from the Organisation for Economic
Co-operation and Development (OECD).
The environmental impact of the PCBs and PCTs has been discussed at a
number of regional and international meetings and has been the subject
of several reviews, including: ATSDR (1989), DFG (1988), IARC (1978),
IRPTC (1988), Kimbrough (1987), Lorenz & Neumeier (1983a,b), NIOSH
(1987), NTIS (1972), OECD (1982), Slorach & Vaz (1983), WHO (1985a,b,
1986a,b) & WHO/EUR (1987).
In 1976, the World Health Organization published Environmental Health
Criteria 2: Polychlorinated biphenyls (PCBs) and terphenyls (PCTs)
(WHO, 1976), discussing and evaluating the data then available on
exposure levels and the effects of PCBs and PCTs on human beings, and,
to a lesser extent, on the environment.
Since then, a wealth of new information has become available.
The IPCS decided to update the above-mentioned EHC and also to produce
a Health and Safety Guide (HSG) and to do this in close coordination
with the WHO Regional Office for Europe, which prepared "PCBs, PCDDs
and PCDFs, prevention and control of accidental and environmental
exposures" as No. 23 of their Environmental Health Series (WHO/EURO,
1987). This publication includes a set of guidelines to assist Member
States in the development of strategies to reduce the probability of
accidents involving the environmental release of PCBs, PCDDS, and
PCDFs and also the severity of their hazardous effects, should such
accidents occur. In particular, it is intended to guide occupational
safety and health personnel and other staff, in workplaces and
environments where PCBs and/or PCB-containing equipment are in use, to
develop adequate safety measures, contingency planning, effective and
relevant accident response, and appropriate rehabilitation.
Within the scope of the present EHC on PCBs and PCTs, the PCDDs and
PCDFs have been mentioned where relevant. Full discussion of these
compounds and evaluation, however, can be found in the IPCS EHC 88:
Polychlorinated dibenzo- para-dioxins and dibenzofurans (WHO, 1989).
1. SUMMARY AND EVALUATION, CONCLUSIONS, RECOMMENDATIONS
1.1 Summary and evaluation
1.1.1 Introduction
Polychlorinated biphenyls (PCBs) were discovered before the turn of
the century and their usefulness for industry, because of their
physical properties, was recognized early. The PCBs have been used
commercially, since 1930, as dielectric and heat-exchange fluids and
in a variety of other applications. They have become widely
distributed in the environment throughout the world, and are
persistent and accumulate in food webs. Human exposure to PCBs has
resulted largely from the consumption of contaminated food, but also
from inhalation and skin absorption in work environments. PCBs
accumulate in the fatty tissues of humans and other animals and have
caused toxic effects in both, particularly if repeated exposure
occurs. The skin and liver are the major sites of pathology, but the
gastrointestinal tract, the immune system, and the nervous system are
also targets. Polychlorinated dibenzofurans (PCDFs), which are
contaminants in commercial PCB mixtures, contribute significantly to
their toxicity. The results of studies on rodents suggest that some
PCB congeners may be carcinogenic and that they can promote the
carcinogenicity of other chemicals.
It is clear from available data on polychlorinated biphenyls (PCBs)
and polychlorinated terphenyls (PCTs) that, in an ideal situation, it
would be preferable not to have these compounds in food at any level.
However, it is equally clear that the reduction of PCBs or PCTs
exposure from food sources to "zero" or to a level approaching zero,
would mean the elimination (prohibition of the consumption) of large
amounts of important food items, such as fish, but more importantly
breast milk. National and international scientific committees have to
decide where the proper balance lies between providing an adequate
degree of public health protection and avoiding excessive losses of
food.
No levels of PCBs or PCTs exposure that can provide an absolute
assurance of safety can be identified on the basis of the available
data.
1.1.2 Identity, physical, and chemical properties
PCBs are mixtures of aromatic chemicals, manufactured by the
chlorination of biphenyl in the presence of a suitable catalyst. The
chemical formula of PCBs can be presented as C12H10-nCln, where n is
a number of chlorine atoms within the range of 1-10.
Theoretically, 209 congeners are possible, but only about 130
congeners are likely to occur in commercial products. In addition,
PCBs may contain polychlorinated dibenzofurans (PCDFs) and chlorinated
quarterphenyls as impurities. These impurities are relatively stable
and resistant to chemical reactions, under normal conditions. All
congeners of PCBs are lipophilic and have a very low water solubility.
As a result, they easily enter the food chain and accumulate in fatty
tissues.
Commercial PCB mixtures contain PCDFs at levels ranging from a few
mg/kg up to 40 mg/kg. Polychlorinated dibenzo- p-dioxins (PCDDs), are
not found in commercial PCBs. However, when PCBs are mixed with other
chlorinated compounds, such as the chloro-benzenes used in
transformers, PCDDs can be found in the case of accidental fires and
during incineration.
Commercial PCB mixtures are light yellow or dark yellow in colour.
They do not crystallize, even at low temperatures, but turn into solid
resins. PCBs are, in practice, fire resistant, with rather high flash
points. They form vapours heavier than air, but they do not form any
explosive mixtures with air. They have very low electrical
conductivity, rather high thermal conductivity, and extremely high
resistance to thermal break-down. PCBs are chemically very stable
under normal conditions; however, when heated, other toxic compounds,
such as PCDFs, can be produced.
1.1.3 Analytical methods
In 1966, the discovery of PCBs in environmental samples raised
interest in the analysis of these compounds and their toxicity for
human beings and their environment.
Because of differences in the analytical methodology used, existing
data are not directly comparable; nevertheless, they can be used for
the establishment of control and preventive measures and for the
preliminary assessment of health and environmental risks associated
with these chemicals.
PCBs have been determined using gas chromatography (GC) techniques
with electron capture detection, often using packed columns, though
more sophisticated methods, such as capillary column and GC coupled
with mass-spectrometry (GC-MS), have been used in recent studies to
identify the individual congeners, to improve the comparability of the
analytical data from different sources, and to establish a basis for
toxicity assessment.
An extensive quality assurance programme is required for these
analyses and intercalibration studies have been implemented and
recommended. The quality and utility of the analytical data depend
critically on the validity of the sample and the adequacy of the
sampling. Furthermore, it is essential to have a planned and well
documented sampling programme; a detailed sampling procedure is
described in WHO/EURO (1987).
1.1.4 Production and uses
The commercial production of the PCBs began in 1930. They have been
widely used in electrical equipment, and smaller volumes of PCBs are
used as fire-resistant liquid in nominally closed systems.
By the end of 1980, the total world production of PCBs was in excess
of 1 million tonnes and, since then, production has continued in some
countries. Despite increasing withdrawal of the use, and restrictions
on the production, of PCBs, very large amounts of these compounds
continue to be present in the environment, either in use or as waste.
In recent years, many industrialized countries have taken steps to
control and restrict the flow of PCBs into the environment. The most
influential force leading to these restrictions has probably been a
1973 recommendation from the Organisation for Economic Co-operation
and Development (OECD) (WHO, 1976; IARC, 1978; OECD, 1982). Since
then, the 24 OECD member countries have restricted the manufacture,
sales, importation, exportation, and use of PCBs, as well as
establishing a labelling system for these compounds.
Current sources of PCB release include volatilization from landfills
containing transformer, capacitor, and other PCB-wastes, sewage
sludge, spills, and dredge spoils, and improper (or illegal) disposal
to open areas. Pollution may occur during the incineration of
industrial and municipal waste. Most municipal incinerators are not
effective in destroying PCBs. Explosions or overheating of
transformers and capacitors may release significant amounts of PCBs
into the local environment.
PCBs can be converted to PCDFs under pyrolytic conditions. The highest
yield of PCDFs under laboratory conditions was obtained at a
temperature between 550 and 700°C. Thus, the uncontrolled burning of
PCBs can be an important source of hazardous PCDFs. It is therefore
recommended that destruction of PCB-contaminated waste should be
carefully controlled, especially with regard to the burning
temperature (above 1000°C), residence time, and turbulence.
1.1.5 Environmental transport, distribution, and transformation
In the atmosphere, PCBs exist primarily in the vapour phase; the
tendency to adsorb on particulates increases with the degree of
chlorination. The virtually universal distribution of PCBs suggests
transport in air.
At present, the major source of PCB exposure in the general
environment appears to be the redistribution of PCBs, previously
introduced into the environment. This redistribution involves
volatilization from soil and water into the atmosphere with subsequent
transport in air and removal from the atmosphere via wet/dry
deposition (of PCBs bound to particulates) and then re-volatilization.
Concentrations of PCBs in precipitation range from 0.001 to
0.25 µg/litre. Since the volatilization and degradation rates of PCBs
vary between congeners, this redistribution leads to an alteration in
the composition of PCB mixtures in the environment.
In water, PCBs are adsorbed on sediments and other organic matter;
experimental and monitoring data have shown that PCB concentrations in
sediment and suspended matter are higher than those in associated
water columns. Strong adsorption on sediment, especially in the case
of the higher chlorinated PCBs, decreases the rate of volatilization.
On the basis of their water solubilities and n-octanol-water
partition coefficients, the lower chlorinated PCB congeners will sorb
less strongly than the higher chlorinated isomers. Although adsorption
can immobilize PCBs for relatively long periods in the aquatic
environment, desorption into the water column has been shown to occur
by both abiotic and biotic routes. The substantial quantities of PCBs
in aquatic sediments can therefore act as both an environmental sink
and a reservoir of PCBs for organisms. Most of the environmental load
of PCBs has been estimated to be in aquatic sediment.
The low solubility and the strong adsorption of PCBs on soil particles
limits leaching in soil; lower chlorinated PCBs will tend to leach
more than the highly chlorinated PCBs.
Degradation of PCBs in the environment is dependent on the degree of
chlorination of the biphenyl. In general, persistence of PCB congeners
increases as the degree of chlorination increases. In the atmosphere,
the vapour phase reaction of PCBs with hydroxyl radicals (which are
photochemically formed by sunlight) may be the dominant transformation
process. Estimated half-lives for this reaction in the atmosphere
range from about 10 days for a monochlorobiphenyl to 1.5 years for a
heptachlorobiphenyl.
In the aquatic environment, hydrolysis and oxidation do not
significantly degrade PCBs. Photolysis appears to be the only viable
abiotic degradation process in water; however, available experimental
data are not sufficient to determine its rate or importance in the
environment.
Microorganisms degrade mono-, di-, and trichlorinated biphenyls
relatively rapidly and tetrachlorobiphenyls slowly, whilst higher
chlorinated biphenyls are resistant to biodegradation. Chlorine
substitution positions on the biphenyl ring appear to be important in
determining the biodegradation rate. PCBs containing chlorine atoms in
the para positions are preferentially biodegraded. Higher
chlorinated congeners are biotransformed anaerobically, by a reductive
dechlorination, to lower chlorinated PCBs, which may then be
biodegradable by aerobic processes.
Several factors determine the degree of bioaccumulation in adipose
tissues: the duration and level of exposure, the chemical structure of
the compound, and the position and pattern of substitution. In
general, the higher chlorinated congeners are accumulated more
readily.
Experimentally determined bioconcentration factors of various PCBs in
aquatic species (fish, shrimp, oyster) range from 200 up to 70 000 or
more. In the open ocean, there is bioaccumulation of PCBs in higher
trophic levels with an increased proportion of higher chlorinated
biphenyls in higher ranking predators.
Transfer of PCBs from soil to vegetation takes place mainly by
adsorption on the external surfaces of terrestrial plants; little
translocation takes place.
1.1.6 Environmental levels and human exposure
Because of their high persistence, and their other physical and
chemical properties, PCBs are present in the environment all over the
world.
Globally, PCBs are found in air concentrations of 0.002 up to
15 ng/m3. In industrial areas, levels are higher (up to µg/m3). In
rain water and snow, PCBs are found in the range of nd (1 ng)-
250 ng/litre.
Under occupational conditions, the levels in the air may be much
higher. Under certain conditions, for instance, in the manufacturing
of transformers or capacitors, levels of up to 1000 µg/m3 have been
observed. In acute emergencies, concentrations of up to 16 mg/m3 have
been measured. In case of fires and/or explosions, soot may be
produced that contains high levels of PCBs. Levels of 8000 mg PCBs/kg
soot have been found. In the latter situation, PCDFs will also be
present. Polychlorinated dioxins (PCDDs) will be found in accidents
with transformers containing chlorinated benzenes, as well as PCBs.
In these emergency situations, ingestion, skin contamination, or
inhalation of soot particles may occur and result in serious exposure
of personnel. However, the exposure of the general population via air
will be very low.
Surface water may be contaminated by PCBs from atmospheric fallout,
from direct emissions from point sources, or from waste disposal.
Under certain conditions, levels of up to 100-500 ng/litre water have
been measured. In the oceans, levels of 0.05-0.6 ng/litre have been
found.
In non-contaminated areas, drinking-water contains less than 1 ng
PCBs/litre, but levels of up to 5 ng/litre have been reported. Soil
and sediments in different areas and depending on local conditions,
contain levels of PCBs ranging from <0.01 up to 2.0 mg/kg. In
polluted areas, the levels have been much higher, i.e., up to
500 mg/kg.
In past years, many thousands of samples of different foodstuffs have
been analysed in several countries for contaminants including PCBs.
Most samples have been taken from individual food items, especially
fish and other foods of animal origin, such as meat and milk. Human
food has become contaminated with PCBs by 3 main routes:
(a) uptake from the environment by fish, birds, livestock (via
food-chains), and crops;
(b) migration from packaging materials into food (mainly below
1 mg/kg, but, in some cases, up to 10 mg/kg);
(c) direct contamination of food or animal feed by an industrial
accident.
The levels for the most important PCB-containing food items were:
animal fat, 20-240 µg/kg; cow's milk, 5-200 µg/kg; butter,
30-80 µg/kg; fish, 10-500 µg/kg, on a fat basis. Certain fish species
(eel) or fish products (fish liver and fish oils) contain much higher
levels, up to 10 mg/kg. Vegetables, cereals, fruits, and a number of
other products contained levels of <10 µg/kg. The major foods in
which contamination with PCBs needs consideration are fish, shellfish,
meat, milk, and other dairy products. Median levels in fish, reported
in various countries, are of the order of 100 µg/kg (on a fat basis).
When comparisons have been made, it appears that the levels of PCBs in
fish are slowly decreasing.
PCBs concentrate in human adipose tissue and breast milk. The
concentrations of PCBs in the different organs and tissues depend on
their lipid contents, with the exception of the brain. PCB residues in
the adipose tissue of the general population in industrialized
countries range from less than 1 up to 5 mg/kg, on a fat basis.
The average concentrations of total PCBs in human milk fat are in the
range of 0.5-1.5 mg/kg fat, depending on the donor's residence,
life-style, and the analytical methods used. Women who live in
heavily-industrialized, urban areas, or who consume a lot of fish,
especially from heavily-contaminated waters, may have higher PCB
concentrations in their breast milk.
The composition of most PCB extracts from environmental samples does
not resemble that of the commercial PCB mixtures. It has also been
shown, using high-resolution gas chromatography analysis, that the
congener composition and the relative concentrations of the individual
components in adipose tissues and breast milk differ markedly from
those in the commercial PCBs. The GC patterns of PCBs in human adipose
tissue and breast milk contain relatively high concentrations of
mainly the higher chlorinated PCBs, such as: 2,4,5,3',4'-pentachloro
biphenyl; 2,4,5,2',4',5'-hexachlorobiphenyl, and 2,3,4,2',4',5'-
hexachlorobiphenyl; 2,3,4,5,2',4',5'-hepta- and 2,3,4,5,2',3',4'-
heptachlorobiphenyl. A few other PCB congeners are present in
much lower quantities, such as the most toxic, coplanar PCBs:
3,4,3',4'-tetra-, 3,4,5,3',4'-penta-, and 3,4,5,3',4',5'-
hexachlorobiphenyl.
It has been calculated that the daily intake of PCBs by infants from
breast milk, is of the order of 4.2 µg/kg body weight (5.2 µg/100 Kcal
consumed) (WHO/EURO, 1988). The average total of ingested PCBs from
breast milk, during the first 6 months of life, is 4.5 mg compared
with the calculated intake of 357 mg of PCBs over the subsequent
life-time (0.2 µg/kg per day from the diet of a 70-kg person over a
70-year life-time). Therefore, the nursing period contributes about
1.3% of the life-time intake, which is not large, in the light of the
benefits of breast-feeding (WHO/EURO, 1988).
On the basis of the evaluated background data, for adults the average
dietary intake of PCBs amounts to a maximum of 100 µg per week, or
approximately 14 µg/person per day. For a 70-kg person, this is an
intake equivalent to a maximum of 0.2 µg/kg body weight per day
(WHO/EURO, 1988).
1.1.7 Kinetics and metabolism
Animal studies have been reported involving mainly oral, inhalation,
and dermal exposures to both PCB mixtures and individual congeners. In
general, PCBs appear to be rapidly absorbed, particularly by the
gastrointestinal tract after oral exposure. It is clear that
absorption does occur in humans, but information on the rates of human
absorption of PCBs is limited.
From the available studies, the data on the distribution of PCBs,
suggest a biphasic kinetic process with rapid clearance from the blood
and accumulation in the liver and the adipose tissue of various
organs. There is also evidence of placental transport, fetal
accumulation, and distribution to milk. In some human studies, the
skin contained a high concentration of PCBs, but the concentration in
the brain was lower than that expected on the basis of the lipid
content.
Mobilization of PCBs from fat appears to depend largely on the rates
of metabolism of the individual PCB congeners. Excretion depends on
the metabolism of PCBs to more polar compounds, such as phenols,
conjugates of thiol compounds, and other water-soluble derivatives.
Metabolic pathways include hydroxylation, and conjugation with thiols
and other water-soluble derivatives, some of which can involve
reactive intermediates, such as the arene oxides. Rates of metabolism
have been shown to depend on the PCB structure and reflect both the
degree and position of chlorine substituents. The polar metabolites of
the more highly chlorinated PCBs appear to be eliminated primarily in
the faeces, but excretion in the urine can also be significant. An
important elimination route, is via (breast) milk. Certain PCB
congeners can also be eliminated via hair.
The available kinetic studies indicate that there is a wide divergence
in biological half-life among the individual congeners and this can
reflect differences in structure-dependent metabolism, tissue
affinities, and other factors affecting mobilization from storage
sites. Persistence in tissues is not always correlated with high
toxicity, and differences in toxicity between PCB congeners may be
associated with specific metabolites and/or their intermediates.
1.1.8 Effects on organisms in the environment
PCBs are universal, environmental contaminants and are present in most
environmental compartments, abiotic and biotic, throughout the world.
Since many countries have controlled both use and release, new input
into the environment is on a reduced scale compared with the past.
However, the available evidence suggests that the cycling of PCBs is
causing a gradual redistribution of some congeners towards the marine
environment. There is a trend for the highest chlorinated congeners to
accumulate preferentially. While much of the PCB is adsorbed on to
particulates in sediment, it is still bioavailable to organisms and
will continue to be accumulated in higher trophic levels.
1.1.8.1 Laboratory studies
Effects of PCB mixtures on microorganisms are highly variable with
some species adversely affected by a level of 0.1 mg/litre and others
unaffected by 100 mg/litre; effects on different species do not vary
consistently with the degree of chlorination of the mixtures. Almost
all of the studies of the effects of PCBs on aquatic organisms have
been concerned with Aroclor mixtures. Results have been extremely
variable with no consistent relationship between percentage
chlorination or environmental conditions and toxicity, even with
closely-related organisms. Over 96 h, under static conditions, LC50
values have ranged between 12 µg/litre and >10 mg/litre for various
aquatic invertebrate species and different Aroclor mixtures.
Flow-through conditions increased the toxicity of the PCBs. Generally,
the most toxic mixtures were Aroclors in the mid-range of
chlorination; low and high percentage chlorination mixtures were less
toxic. This was also true for sub-lethal effects, such as reproduction
effects in Daphnia. Crustaceans seem to be more susceptible to PCBs
during moult. In model populations, the community structure of
estuarine species changed on exposure to Aroclor 1254, with the
numbers of amphipods, bryozoans, crabs, and molluscs decreasing and
those of annelids, brachyopods, coelenterates, echinoderms, and
nemerines unaffected. Too few of the groups have been included in
acute tests to determine whether the results represent variation in
susceptibility to PCBs or differences in interaction between species.
There is a similar variation in the toxicity of PCB mixtures for fish,
with 96-h LC50s varying between 0.008 and >100 mg/litre. Long-term
tests have shown that acute exposure, particularly in static
conditions, considerably underestimates the toxicity of the PCB.
Rainbow trout was particularly susceptible, with embryo-larval stages
showing a 22-day LC50 of 0.32 µg/litre for Aroclor 1254 and a
no-observed-effect level (NOEL) over 22 days of 0.01 µg/litre for
Aroclors 1016, 1242, and 1254.
Freshwater fathead minnow showed NOELs of 5.4, 0.1, 1.8, and
1.3 µg/litre for Aroclors 1242, 1248, 1254, and 1260, respectively;
the estuarine sheephead minnow showed NOELs of 3.4 and 0.06 µg/litre
for Aroclors 1016 and 1254, respectively.
Experimental evidence has confirmed field observations demonstrating
reproductive impairment in seals fed on fish containing PCBs
accumulated in the wild. The effect occurs late in reproduction,
preventing implantation of the embryo in the uterine wall.
In short-term tests, the toxicity of Aroclor for birds increased with
increasing percentage chlorination; 5-day dietary LC50s ranged from
604 to >6000 mg/kg diet. The main reproductive effects of PCBs on
birds were reduced hatchability of eggs and embryotoxicity. These
effects continued after dosing ended, as the hens reduced their PCB
load via the eggs. There is no evidence that Aroclors cause egg-shell
thinning, directly; effects on the food consumption and body weight of
hens have an indirect effect on shell thickness. Sub-lethal effects on
behaviour and hormone secretion have been reported.
The acute toxicity of Aroclors for mink decreases with increasing
percentage chlorination, acute oral LD50s varying between >750 and
4000 mg/kg body weight; the ferret is less sensitive. Aroclor reduces
food consumption and, thus, the growth rate of young mink.
Reproduction of mink is reduced or eliminated by Aroclors, either
given directly or as natural contaminants in fish. Higher percentage
chlorinated Aroclors (notably 1254) have a greater effect. The
reproductive rate returns to normal after cessation of feeding with
Aroclor.
Bats are susceptible to Aroclor released from fat during migration.
Because the great majority of laboratory tests on aquatic and
terrestrial organisms were carried out using PCB mixtures, it is not
possible to identify which specific components of the mixtures were
responsible for effects. Similarly, because tests were conducted in
environmentally unrealistic conditions (e.g., beyond the solubility of
congeners and without sediment present in aquatic tests), it is
difficult to extrapolate from laboratory to field. However, it can
reasonably be assumed that any effects on populations of organisms,
likely to occur more generally in the environment in the future, will
already have been observed in local populations exposed to high PCB
levels in the past.
1.1.8.2 Field studies
Results suggesting effects of PCBs on fish populations in the field
are inconclusive. Interpretation of field data on birds is difficult,
since residues of many different organochlorines are also present.
Most authors have shown a correlation between effects (embryotoxicity)
and total organochlorine residues. Of the organochlorine compounds
present, PCB residues correlate best with the effects on embryos, but
the results cannot be regarded as proved field effects of the PCBs.
There is evidence (confirmed in laboratory studies) that PCBs reduce
the reproductive capacity of sea mammals. The effect is on the
implantation of the embryo, but there can also be physical changes in
the female reproductive tract.
Extrapolation from laboratory, acute and short-term tests to effects
at the population level in the field is not possible. Uncertainties
about which components of the PCB mixtures cause effects, the specific
congeners present in the environment, and the bioavailability of PCB
components to organisms, all combine to make estimates of likely
environmental exposures and effects difficult. The effects on sea
mammal populations can be regarded as proved, but the component(s) of
the PCB mixtures that are responsible are not yet known.
Given the trends towards increased contamination of the marine
environment, attention should be concentrated on the effects on marine
organisms. There is clear laboratory and field evidence of
reproductive effects on populations of sea mammals in heavily-polluted
areas. The residues and effects of PCBs on other populations of sea
mammals are likely to increase in the future. It is less clear whether
effects will be seen in other organisms, such as birds feeding on
marine prey.
Population and community effects on lower organisms, phytoplankton,
and zooplankton, would be expected to occur on the basis of laboratory
experiments. Both the extent and significance of such changes are
difficult to assess. From currently available information, effects on
fish populations would not be expected, though fish will act as a
route of exposure of fish-eating mammals and birds.
Previously reported effects on terrestrial species, fish-eating,
freshwater mammals and migratory bats, for example, should be less
evident as residues of PCBs are redistributed. Residues in terrestrial
biota currently show little decline overall, but information on
changes in congeners is scarce or absent. Declines in higher
chlorinated congeners would be expected to be slow.
1.1.9 Effects on experimental animals and in vitro systems
1.1.9.1 Single exposure
The acute toxicity of Aroclors, after a single oral exposure, is
generally low in rats. Young animals appear to be more sensitive
(LD50: 1.3-2.5 g/kg body weight) than adults (LD50: 4-11 g/kg body
weight). The lowest LD50 reported for Aroclor 1254 in adult rats was
1.0 g/kg body weight. No differences between the sexes were observed.
The dermal LD50 in rabbits ranged from >1.26 to <2 g/kg body weight
for Aroclor 1260 (in corn oil) and from 0.79 to <3.17 g/kg body
weight for some other undiluted PCB mixtures. With intravenous
application, an LD50 of 0.4 g/kg body weight for Aroclor 1254 was
shown in rats; the LD50 after intraperitoneal injection in the mouse
varied from 0.9 to 1.2 g/kg body weight.
1.1.9.2 Short-term exposure
The main targets in mammals, with short-term, oral exposure to PCB
mixtures or congeners, were the liver, the skin, the immune system,
and the reproductive system. The Rhesus monkey was the most sensitive
species tested, females being more sensitive than males. Adult female
Rhesus monkeys exposed to a diet containing Aroclor 1248 at a level of
2.5 mg/kg, or 0.09 mg/kg body weight per day, for 6 months, showed an
increased mortality rate, growth retardation, alopecia, acne, swelling
of the Meibomian glands, and possibly immunosuppression.
Microscopically, enlarged fatty liver with focal necrosis, and
epithelial hyperplasia, and keratinization of hair follicles were
found. At higher exposure levels, microscopic changes have also been
observed in other epithelial tissues, such as the sebaceous and
Meibomian glands, the gastric mucosa, gall bladder, bile duct, nail
beds, and the ameloblast. Serum levels of total lipid triglycerides
and cholesterol were decreased. Short-term exposure to commercial PCB
mixtures induced an increase in the concentrations of total lipids,
triglycerides, cholesterol, and/or phospholipids in the liver. Among
the PCB congeners, 3,4,3',4'-tetrachlorobiphenyl 3,4,5,3',4',5'-, and
2,4,6,2',4',6'-hexachlorobiphenyl were the most potent. Aroclor 1254,
at a dose level of 0.2 mg/kg body weight per day, also showed several
other effects, such as lymphoreticular lesions, fingernail detachment,
and gingival effects, but no acne and alopecia. A NOEL for the general
toxicity of Aroclor 1242 of 0.04 mg/kg body weight per day was
established in Rhesus monkeys. Relatively mild effects were shown in
suckling Rhesus monkeys, exposed to a much higher dose of Aroclor 1248
of 35 mg/kg body weight per day. Effects in the liver have been best
investigated in rats and include hypertrophy, fatty degeneration,
proliferation of the endoplasmic reticulum, porphyria, adenofibrosis,
bile-duct hyperplasia, cysts, and preneoplastic and neoplastic
changes. In studies on rats and mice, individual PCB congeners caused
effects in the liver, spleen, and thymus, the planar congeners being
most toxic. In monkeys, planar congeners, at doses of 1-3 mg/kg diet,
induced effects similar in character and severity to those produced by
Aroclor 1242, at a dose of 100 mg/kg diet, and Aroclor 1248, at a dose
of 25 mg/kg diet.
Following dermal exposure of rabbits and mice, PCB mixtures and some
congeners caused effects on the skin and liver, similar to those found
after oral exposure. In rabbits, thymic atrophy, a reduction of
germinal centres of the lymph nodes, and leukopenia were also
observed.
1.1.10 Reproduction, embryotoxicity, and teratogenicity
1.1.10.1 Reproduction and embryotoxicity
Comprehensive reproduction and teratogenicity studies have not been
conducted. In a 2-generation reproduction study on rats, a NOEL of
0.32 mg/kg body weight, based on reproductive parameters (Aroclor
1254) and a NOEL of 7.5 mg/kg body weight (Aroclor 1260) were
established. However, the lowest tested dose of 0.06 mg/kg body weight
resulted in increased relative liver weights in weanlings.
In Rhesus monkeys exposed to Aroclor 1016, a NOEL of 0.03 mg/kg body
weight was established, on the basis of reproductive parameters.
However, at this level, decreased birth weight was observed and the
lowest dose tested, of 0.01 mg/kg body weight, resulted in skin
hyperpigmentation.
For Aroclor 1248 (containing PCDFs), a NOEL of 0.09 mg/kg body weight
was established in Rhesus monkeys, 1 year after exposure ceased.
1.1.10.2 Teratogenicity
Available studies on rats and monkeys did not indicate any teratogenic
effects, when animals were dosed orally during organogenesis. A NOEL
of 50 mg/kg body weight for Aroclor 1254 was demonstrated in rats with
regard to pup weight, and a LOEL of 2.5 mg/kg body weight, on the
basis of fetotoxicity (lesion in thyroid follicular cells) could be
assumed.
In teratogenicity tests with individual congeners on mice, rats, and
Rhesus monkeys, no NOEL was demonstrated. In Rhesus monkeys a dose of
0.07 mg/kg body weight resulted in maternal toxic effects
(3,4,3',4'-tetrachlorobiphenyl).
1.1.11 Mutagenicity
PCB mixtures did not cause mutation or chromosomal damage in a variety
of test systems. Chromosome breakage was induced in human lymphocytes
in vitro by 3,4,3',4'-tetrachlorobiphenyl. High concentrations of
PCB mixtures may cause primary DNA damage, as evidenced by DNA single
strand breaks in alkaline elution assays.
1.1.12 Carcinogenicity
The interpretation of the available animal data involving commercial
PCB mixtures is often complicated by lack of information concerning
the presence, or contribution, of chlorinated dibenzofuran impurities
as well as variations in congener composition.
A number of long-term carcinogenicity studies have been carried out on
mice and rats. The PCB mixtures used were Kanechlors 300, 400, and
500, Aroclors 1254 and 1260, and Clophens A30 and A60. The Clophens
were reported to be free of PCDFs, but no data were provided on the
purity of the other PCB mixtures.
A significant increase in hepatocellular adenomas and/or carcinomas
was observed in mice fed a diet containing Kanechlor 500 and Aroclor
1254 at dose levels of approximately 15-25 mg/kg body weight. No
neoplasms could be detected in mice treated with Kanechlors 300 and
400.
In rats, an increase in hepatocellular adenomas and/or carcinomas was
noted in studies on Aroclors 1254 and 1260, and Clophen A30, with an
exposure period of more than one year. The increase in the incidence
of tumour-bearing animals in these studies was not considered to be
statistically significant, however, it was in the case of 2 other
studies. An increase in the incidence of hepatocellular (trabecular)
carcinomas and adenocarcinomas was demonstrated with Aroclor 1260 and
Clophen A60 administered at a dose level of approximately 5 mg/kg body
weight.
The liver tumours concerned were considered to be non-aggressive
(benign or of low malignancy, no metastasis) and not life shortening.
Adenofibrosis, a preneoplastic lesion and/or neoplastic nodules in the
liver were reported in some of the studies. In one test with Aroclor
1254, a dose-related increase in intestinal metaplasia and
adenocarcinomas of the glandular stomach was demonstrated in the rat.
There is a substantial body of evidence to support the enhancing
effects of PCBs on liver carcinogenesis in rodents pretreated with
hepatocarcinogens. There is weak evidence for the initiating activity
of PCB-mixtures in rodents. From the genotoxicity studies reported, it
can be concluded that PCB-mixtures can be regarded as non-genotoxic.
These results imply that the association of liver tumours with the
administration of PCBs in rodents is attributable to some epigenetic
mechanisms involving enforcement of cell proliferation in the liver
and other manifestations of liver toxicity, hence a threshold approach
can be followed in the evaluation of PCB toxicity. The possibility
that PCBs might enhance carcinogenesis in tissues other than the
liver, in animals pre-exposed to various tissue-specific carcinogens,
needs to be addressed. The anticarcinogenic activity of PCBs shown in
some studies, where PCBs were given to animals during, and prior to,
the administration of carcinogens, may be related to the microsomal,
enzyme-inducing properties of PCBs resulting in an increase in
detoxification.
Overall, there is reason to exercise caution in extrapolating the
available animal data on the carcinogenic potential of PCBs to humans.
1.1.13 Special studies
Lesions induced after exposure to PCB mixtures or individual congeners
concern the liver, skin, immune system, reproductive system, oedema
and disturbances of the gastrointestinal tract, and thyroid gland.
PCBs are able to induce various enzymes in the liver. This has been
demonstrated, in rats, mice, guinea-pigs, rabbits, dogs, and monkeys,
for Aroclors 1248, 1254, 1260, and Kanechlor 400 (induction of
cytochrome P450 and P448). The inducing ability increases with the
chlorine content in the molecule. It is also dependent on the congener
composition, congeners with chlorine in the para- and meta-
position inducing the P450 enzyme. For AHH induction, the position of
the chlorine seems to be more important than the degree of
chlorination. Congeners with both para- and at least two meta-
positions substituted by chlorine, are the most potent inducers of
AHH. Distinct inter-species variations have been demonstrated. The
lowest NOEL (0.025 mg/kg body weight) was found for Aroclor 1260 in
Osborn-Mendel rats.
Effects on the endocrine system are seen as alterations in hormonal
receptor binding and in steroid hormone balance. Direct and indirect
evidence for a weak estrogenic activity was observed for various
Aroclors. Decreased levels of gonadal hormones and increased relative
testes weight were found in rats exposed to 75 mg Aroclor 1242/kg diet
for 36 weeks. Decreased plasma corticosteroid levels without increased
adrenal weight, was found in female mice exposed to Aroclor 1254
(25 mg/kg diet) for 3 weeks. Increased adrenal weight was found in
another strain given a diet containing 200 mg/kg for 2 weeks.
PCB mixtures have shown an immunosuppressive effect in various animal
species, monkeys and rabbits being the most sensitive. The lowest NOEL
in monkeys was 0.1 mg/kg body weight, and, in rabbits, 0.18 mg/kg body
weight.
Depressed motor-activity was seen in mice administered a single oral
dose of 500 mg Aroclor 1254/kg body weight. This was probably in
relation to inhibition of the uptake and release of neurotransmitters.
PCB mixtures were found to decrease the levels of vitamins A and B1
in the blood and liver of rats. Decreased levels of vitamins A, B1,
B2, and B6 were seen in rats and mice exposed to PCB mixtures.
1.1.14 Factors modifying toxicity, mode of action
Commercial PCBs show a spectrum of toxic responses, partly resembling
that of PCDDs and PCDFs. In addition, the analogous structure-activity
relations of PCB congeners, with respect to most of their toxic
responses and to their potency in inducing P448-dependent AHH,
indicate that PCB congeners that are approximate stereoisomers of
2,3,7,8,-TCDD are the most active. These findings suggest a common
mechanism of action based on the affinity of these compounds for the
cytosolic AH-receptor protein. Toxic equivalence factors relating to
2,3,7,8-TCDD have been proposed for these coplanar PCB congeners. The
nature of the likely interactions between PCBs, PCDFs, and PCDDs has
not been adequately investigated. As PCBs can stimulate microsomal
enzyme activity, they can influence the action of other chemicals that
undergo microsomal metabolism. Other so-called, non-planar PCB
congeners may cause other more subtle toxicities. In addition, PCB
congeners, especially the lower chlorinated ones, may be metabolized
through arene oxide intermediates and methylsulfonyl metabolites.
1.1.15 Effects on humans
The toxicological evaluation of PCBs presents many problems. PCBs
usually occur as mixtures of many congeners, and many of the data on
the toxicity of the PCBs are based on the testing of these mixtures.
Some components of the mixtures are more easily degraded in the
environment than others. Thus, the general population may be exposed
to mixtures that are different from those to which workers, working
with PCBs, are exposed.
The general population is exposed to PCBs mainly through contaminated
food (aquatic organisms, meat and dairy products). The daily intake of
PCBs is of the order of some micrograms per person for most of the
industrialized countries. Such exposures have not been associated with
disease. The infant is exposed to PCBs through its mother's milk.
Daily intake of PCBs may be some micrograms/kg body weight.
There are great difficulties in assessing human health effects
separately for PCBs, PCDFs, or PCDDs, since, quite frequently, PCB
mixtures contain PCDFs. The presence of PCDDs has also been seen
occasionally, in accidents with certain mixtures. Commercial PCBs have
been shown to be contaminated with PCDFs and, therefore, in many
cases, it is not clear which effects are attributable to the PCBs
themselves and which to the much more toxic PCDFs. Thus, much of the
data that can be retrieved from large episodes of intoxication in
humans, e.g., the Yusho, Yu-Cheng, and other intoxications, probably
reflect effects of exposure to both PCDFs and PCBs.
The signs of intoxication in Yusho and Yu-Cheng patients were
hypersecretion of the Meibomian glands of the eyes, swelling of the
eyelids and pigmentation of the nails and mucous membranes,
occasionally associated with fatigue, nausea, and vomiting. This was
usually followed by hyperkeratosis and darkening of the skin with
follicular enlargement and acneiform eruptions. Furthermore, oedema of
the arms and legs, liver enlargement and liver disorders, central
nervous disturbances, respiratory problems e.g., bronchitis-like
disturbances, and changes in the immune status of the patients were
also observed. In children of Yusho- and Yu-Cheng patients, diminished
growth, dark pigmentation of the skin and mucous membranes, gingival
hyperplasia, xenophthalmic oedematous eyes, dentition at birth,
abnormal calcification of the skull, rocker bottom heel, and a high
incidence of low birth weight were observed. Whether or not a
correlation existed between the exposure and the occurrence of
malignant neoplasms in these patients could not be definitely
concluded, because the number of deaths was too small. However, a
statistically significant increase was observed in male patients, with
regard to mortality from all neoplasms, liver and lung cancer.
Under occupational conditions, skin rashes occurred a few hours after
acute exposure. Furthermore, itching, burning sensations, irritation
of the conjunctivae, pigmentation the fingers and nails, and chloracne
were found after exposure to high PCB concentrations. Chloracne is one
of the most prevalent findings among PCB-exposed workers. Besides
these dermal signs of intoxication, different authors have found liver
disturbances, immunosuppressive changes, transient irritation of the
mucous membranes of the respiratory tract, neurological and unspecific
psychological or psychosomatic effects, such as headache, dizziness,
depression, sleep and memory disturbances, nervousness, fatigue, and
impotence. The overall conclusion is that continuous occupational
exposure to high PCB and PCDF concentrations may result in effects on
the skin and liver.
Two large mortality studies were carried out on cohorts of workers.
When exposure to Aroclor 1254, 1242, and 1016 occurred, increased
mortality from cancer of the liver and gall bladder was observed in
one study and from neoplasms and cancer of the gastrointestinal tract
in the other. None of the available epidemiological studies provide
conclusive evidence of an association between PCB exposure and
increased cancer mortality, because of the small number of deaths in
exposed populations, the lack of dose-response relationships, and the
problem of contaminants in the PCB mixtures.
1.2 Conclusions
1.2.1 Distribution
Because of their physical and chemical properties, PCBs have become
dispersed globally, throughout the environment.
PCBs are almost universally present in organisms in the environment
and are readily bioaccumulated. Biomagnification in food chains has
also been demonstrated.
Higher chlorinated congeners accumulate preferentially.
1.2.2 Effects on experimental animals
The results of animal studies suggest that PCBs are immunosuppressive,
as assessed by alterations in gross measures of immune function
(spleen weight, thymus weight, and lymphocyte counts). NOELs in
monkeys have been estimated at 100 µg/kg for Aroclor 1248 and
<100 µg/kg body weight for Aroclor 1254. Immunosuppression appears to
be a congener-specific effect.
Reproductive toxicity is, in general, only seen at doses producing
systemic toxicity in the mother. Neonates feeding on contaminated
mother's milk (in monkeys and other animal species, used as models)
appear to be particularly sensitive to PCBs and show reduced growth
with other toxic symptoms. The NOEL for Aroclor 1016 on reproductive
effects is 30 µg/kg body weight for monkeys; no NOEL could be
established for the reproductive effects of Aroclor 1248.
PCBs are not genotoxic and there is inconclusive evidence for action
as tumour initiators. PCBs do act as tumour promoters. It can be
concluded that the toxicity of PCB mixtures can be evaluated on a
threshold basis.
1.2.3 Effects on humans
Exposure of the general population to PCBs will be principally through
food items. Babies will be exposed through the mother's milk.
Two large episodes of intoxication in humans have occurred in Japan
(Yusho) and Province of Taiwan (Yu-Cheng). The main symptoms in Yusho
and Yu-Cheng patients have frequently been attributed to contaminants
in the PCB mixtures, specifically, to PCDFs. The Task Group concluded
that symptoms may have been caused by the combined exposure to PCBs
and PCDFs. However, some of the symptoms, principally, the chronic
respiratory effects, may have been caused specifically by the
methylsulfone metabolites of certain PCB congeners.
1.2.4 Effects on the environment
While there have been reports of effects on local populations of
birds, the most important effect of PCBs on organisms in the
environment has been reproductive failure in sea mammals. This has
been observed principally in semi-enclosed seas and has led to
population declines, locally. The prediction that residues of PCBs in
the environment will gradually be redistributed towards the marine
environment indicates an increasing hazard for sea mammals in the
future.
1.3 Recommendations
* International agreement on analytical procedures to improve the
comparability of results of monitoring programmes is recommended.
Methodology for congener-specific analysis should continue to be
developed, though the value of analysis based on mixtures is
recognized.
* In order to ensure the reliability of analytical data,
inter-laboratory quality control studies are strongly recommended.
It is also recommended that an international network of technical
support and supervision is established, to allow developing
countries to participate in monitoring.
* Long-term studies using specific congeners, and studies on the
mechanism of action of constituents of PCBs mixtures, with special
regard to tumour promotion, are recommended to improve the
precision of the risk assessment of PCBs.
* Epidemiological studies to better assess the risk to neonates are
required, since new-born infants appear to be the most vulnerable
sector of the general population, because of high exposure through
milk.
* Sensitive and specific biomarkers for some of the more subtle
types of PCB toxicity (such as reproductive, immunological, and
neural toxicity) should be developed for use in future
epidemiological studies.
* Disposal of PCBs should be carried out by incineration in properly
designed and run facilities that can guarantee the constant high
temperatures (above 1000°C), residence time, and turbulence
necessary to ensure complete breakdown.
* Methods to remove PCBs already contained in landfills should be
investigated.
* Monitoring of PCBs in the environment and in wildlife should be
encouraged globally, to follow the expected redistribution of
residues already present.
* Marine mammals are susceptible to reproductive failure as a result
of PCB contamination. Studies on the population size and
reproductive success of cetaceans should be encouraged, together
with further research to establish which congeners are responsible
for the effects.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1 Identity
2.1.1 Chemical formula and structure
The chlorination of biphenyl can lead to the replacement of 1-10
hydrogen atoms by chlorine; the conventional numbering of substituent
positions is shown in the diagram:
The chemical formula can be presented as C12H10-nCln, where n, the
number of chlorine atoms in the molecule, can range from 1 to 10.
2.1.2 Relative molecular mass
The relative molecular mass depends on the degree of substitution.
Monochlorobiphenyl has a relative molecular mass of 188, while
completely chlorinated biphenyl (C12Cl10) has a relative molecular
mass of 494 (US EPA, 1980).
2.1.3 Common name
Common name: polychlorinated biphenyls (PCBs)
CAS Registry number: 1336-36-3
RTECS Registry number: TQ 1350000
2.1.4 Chemical composition
The PCBs are chlorinated hydrocarbons, manufactured commercially by
the progressive chlorination of biphenyl in the presence of a suitable
catalyst (e.g., iron chloride). Depending on the reaction conditions,
the degree of chlorination can vary between 21 and 68% (w/w). The
yield is always a mixture of different isomers and congeners. Thus, a
total of 209 theoretically different chemical components exist, but
only about 130 of these are likely to occur in commercial products or
mixtures of such compounds (Safe, 1990).
Seventy-eight out of the possible 209 PCB congeners can exist as
rotational isomers that are enantiomeric to each other. Nineteen PCBs,
of which 9 are components of commercial PCB formulations, have been
predicted to be stable at room temperature (Kaiser, 1974).
Puttmann et al. (1988) separated the atropisomers of
2,3,4,6,2',4'-hexachlorobiphenyl and demonstrated that they possess
different biological effects with regard to in vivo enzyme induction
(aminopyrine N-demethylase, aldrin epoxidase, cytochrome P-450
content, morphine UDP-glucuronosyl transferase) in Sprague-Dawley
rats.
Unlike the dioxins or dibenzofurans, the phenyl rings of a PCB are not
constrained through ring fusions and have relatively unconstrained
rotational freedom. Chlorines at the ortho (2,2', 6,6') positions
introduce constraints on rotational freedom that can hinder
coplanarity of the phenyl rings. X-ray crystallographic studies
(McKinney & Singh, 1981) indicate that the preferred conformation for
all PCBs, including those without ortho-substituents, is
noncoplanar. The proportion of molecules of a particular congener
assuming a coplanar configuration becomes increasingly small as the
degree of ortho-substitution and the energetic cost of conforming
increases. However, PCBs without ortho-substitution are often
referred to in the biological literature as the planar (or coplanar)
PCBs and all others as the nonplanar (or noncoplanar) PCBs. This
terminology, though somewhat misleading, is also used throughout this
publication for convenience and ease of referring back to the
published literature. It is widely recognized that certain biological
activities of the PCBs vary, at least quantitatively, with
stereochemical differences in the congeners.
Individual manufacturers have their own system of identification for
their products. In the Aroclor series, a 4-digit code is used;
biphenyls are generally indicated by 12 in the first 2 positions,
while the last 2 numbers indicate the percentage by weight of chlorine
in the mixture; thus, Aroclor 1260 is a polychlorinated-biphenyl
mixture containing 60% of chlorine. An exception to this
generalization is Aroclor 1016, which is a distillation product of
Aroclor 1242 containing only 1% of components with 5 or more chlorine
atoms (Burse et al., 1974). With other commercial products, the codes
may indicate the approximate mean number of chlorine atoms in the
components; thus Clophen A60, Phenochlor DP6, and Kanechlor 600 are
biphenyls with an average of about 6 chlorine atoms per molecule
(equivalent to 59% chlorine by weight).
Ballschmiter & Zell (1980) proposed a numbering system for the PCB
congeners, that was later adopted by the International Union of Pure
and Applied Chemists (IUPAC). The number, structure, and isomer group
are given for each congener in the paper of McFarland & Clarke (1989)
(see Appendix A). In the literature, the structure of a congener is
given in 2 ways; for example 2,2',5,5' or 2,5,2',5' (No 52).
Individual PCBs have been synthesized for use as reference samples in
the identification of gas-liquid chromatographic peaks, for
toxicological investigations, and for studying their metabolic fate in
living organisms, for which purpose they have been prepared labelled
with carbon-14 (Hutzinger et al., 1971; Jensen & Sundström, 1974a;
Sundström & Wachtmeister, 1975).
The proportions of PCBs with 1-9 chlorine substituents in the Aroclors
are shown in Table 1.
It is apparent, from gas chromatographic analyses of commercial
products, that PCB mixtures differ with respect to the individual
congeners present and their relative concentrations (Jensen &
Sundström, 1974a; Albro & Parker, 1979; Ballschmiter & Zell, 1980;
Albro et al., 1981; Mullin et al., 1984; Safe et al., 1985a;
Alford-Stevens, 1986).
There have been several investigations to identify individual PCBs in
commercial products. The components of the Aroclors were separated by
column and gas-liquid chromatography and many of the peaks
characterized by high-resolution mass spectrometry and nuclear
magnetic resonance, and also by comparison with synthesized PCBs
(Table 2) (see also DFG, 1988).
Jensen & Sundström (1974a) recognized that conventional gas-liquid
chromatography was not suitable for separating all the components, so
they devised a preliminary fractionation on a charcoal column, which
separated the component PCBs according to the number of chlorines in
the 2,6,2' or 6' positions in the molecule ( o-chlorines). They
compared the gas-liquid chromatographic peaks with those of 90
synthesized PCBs, and were able to characterize and quantify 60
components of Clophens A50 and A60.
Table 1. Approximate percentages (w/v) of Aroclors with different degrees of
chlorinationa
Number of Chlorine
chlorine weight Aroclor
atoms in (%)
molecule 1221 1232 1016 1242 1248 1254 1260
0 0 10 - -
1 18.8 50 26 2 3
2 31.8 35 29 19 13 2
3 41.3 4 24 57 28 18
4 48.6 1 15 22 30 40 11
5 54.4 22 36 49 12
6 59.0 4 4 34 38
7 62.8 6 41
8 66.0 8
9 68.8 1
a From: WHO/EURO (1987).
2.1.5 Technical product
Major trade names
The PCBs manufactured commercially are known by a variety of trade
names including: Aroclor, Pyranol, Pyroclor (USA), Phenoclor, Pyralene
(France), Clophen, Elaol (Germany), Kanechlor, Santotherm (Japan),
Fenchlor, Apirolio (Italy), and Sovol (USSR). Table 3 contains the
most common trade names for commercial products, some of which are not
in use any more (Brinkman & De Kok, 1980; WHO/EURO, 1987).
2.1.6 Purity and impurities
Commercial PCBs are not sold according to a composition specification,
but according to their physical properties. The composition of
Aroclors and Clophens has been presented in recent papers; the
composition of 5 Aroclors is shown in Tables 1 and 2. In Table 1, the
approximate composition is expressed as the percentage of chlorine
weight, and, in Table 2, the composition of the chlorine substitution
pattern is expressed in mol % (Albro & Parker, 1979; Albro et al.,
1981; Jones, 1988). The composition of the chlorine substitution
pattern for 4 Clophens is described by Duinker & Hillebrand (1983) and
Jones (1988). It should be kept in mind that nothing can be said about
the variations in the different lots of these mixtures. Impurities
known to be present in commercial PCBs are chlorinated dibenzofurans
and chlorinated naphthalenes (Vos et al., 1970; Bowes et al., 1975;
Albro & Parker, 1979; Albro et al., 1981; Duinker & Hillebrand, 1983;
Rappe et al., 1985a). The concentrations of PCDFs in Aroclor, Clophen,
Phenoclor, and Kanechlor are summarized in Tables 4 and 5.
Different authors have examined the presence of PCDFs in PCB mixtures.
Bowes et al. (1975) found 0.8-2.0 mg/kg in samples of Aroclor 1248 and
1260, but none in Aroclor 1016, 8.4 mg/kg in Clophen A60, and
13.6 mg/kg in Phenoclor DP-6. Rappe et al. (1985a) and Bentley (1983)
found levels of PCDFs up to 40 mg/kg in a number of commercial PCBs.
Recently, Wakimoto et al. (1988) found a number of extremely toxic
PCDFs in several Japanese and American commercial PCB preparations.
These isomer-specific analyses revealed the 2,3,7,8-tetra-,
1,2,4,7,8-penta-, 1,2,3,7,8-penta-, 2,3,4,7,8-penta-, and
1,2,3,6,7,8-hexachlorodibenzofurans. The concentrations in unused
Kanechlor 300, 400, 500, and 600, were 7.5, 26, 7.2, and 5.4 mg/kg,
respectively, and those in Aroclors 1242, 1248, 1254, and 1260, were
0.6, 3.7, 4.2, and 7.5 mg/kg, respectively. Brown et al. (1988) found
that the electrical use of PCB dielectric fluids in transformers and
capacitors did not increase the PCDFs content significantly.
More data about the occurrence of PCDFs in the different commercial
PCB mixtures are summarized in WHO/EURO (1987).
There are no reports on the presence of PCDDs in commercial mixtures
(Bowes et al., 1975). Wakimoto et al. (1988) could not find PCDDs in
the above samples of Kanechlors and Aroclors with a detection limit of
<2 µg/kg.
2.2 Physical and chemical properties
Individual pure PCB congeners are colourless, often crystalline
compounds, but commercial PCBs are mixtures of these congeners with a
clear, light yellow or dark colour. They do not crystallize at low
temperatures, but turn into solid resins. Because of the chlorine
atoms in the molecule, their density is rather high. PCBs are, in
practice, fire resistant with rather high flash-points (170-380°C).
They form vapours heavier than air, but do not form any explosive
mixtures with air. They possess very low electrical conductivity and
an extremely high resistance to thermal breakdown, and it is on the
basis of these properties that they are used as cooling liquids in
electrical equipment (US EPA, 1980; WHO/EURO, 1987; DFG, 1988).
Table 2. PCB compositions of aroclors in mol %a
IUPAC Chlorine Aroclor
No. substitution
pattern 1242 1016 1248 1254 1260
BP 0.01 0.50
1 2 0.68 0.80
2 3 0.04 0.10
3 4 0.22 1.00
4 2.2' 3.99 4.36 0.25
6 2.3' 1.24 1.37 0.69 0.07
7 2.4 1.04 1.16
8 2.4' 8.97 10.30 0.18
9 2.5 0.31 0.34 trace
10 2.6 0.13 0.20
12 3.4 0.09 0.11
13 3.4' 0.12 0.12
14 3.5 0.35 0.37
15 4.4' 0.99 1.07
16 2.3.2' 3.25 3.50 0.84
17 2.4.2' 2.92 3.14 0.19
18 2.5.2' 9.36 10.87 9.95 0.07
19 2.6.2' 0.97 1.08
20 2.3.3' 3.64 3.99
22 2.3.4' 2.64 2.80 1.24 trace trace
25 2.4.3' 1.68 1.79
26 2.5.3' 0.55 0.62 0.75
27 2.6.3' 0.54 0.58
28 2.4.4' 13.30 14.48 trace
31 2.5.4' 4.53 4.72 9.31 0.72
32 2.6.4' 2.15 2.31 1.46
33 3.4.2' 2.83 3.08
35 3.4.3' 0.66 0.38
37 3.4.4' 1.62 1.89 1.28 0.20 0.09
39 3.5.4' 1.03 1.08
40 2.3.2'.3' 0.15 0.18 1.12 0.26 0.04
41 2.3.4.2' 1.67 2.00
42 2.3.2'.4' 7.05 2.18 0.66
43 2.3.5.2' 0.44 0.47
44 2.3.2'.5' 1.06 1.14
45 2.3.6.2' 0.90 1.00 5.73 0.15
46 2.3.2'.6' 0.31 0.33
47 2.4.2'.4' 1.65 1.8 3.18 0.52 0.88
48 2.4.5.2' 1.33 1.41
Table 2. (cont'd).
IUPAC Chlorine Aroclor
No. substitution
pattern 1242 1016 1248 1254 1260
? 2.5.2'.4' - - 3.81 1.63 0.44
49 2.4.2'.5' 3.28 3.48
52 2.5.2'.5' 4.08 4.35 8.36 4.36 1.91
53 2.5.2'.6' 0.97 1.07 6.30 0.13
54 2.6.2'.6' 0.17 0.19
55 2.3.4.3' 0.11 0.43 0.12
56 2.3.3'.4' 0.60 trace 0.18 0.03
60 2.3.4.4' 0.21
66 2.4.3'.4' 0.81 0.14 4.95 2.24 0.22
70 2.5.3'.4' 1.11 6.38 4.75 0.85
71 2.6.3'.4' 0.65
72 2.5.3'.5' 0.33 2.10 1.01 0.28
74 2.4.5.4' 2.02 1.35 0.25 0.30 0.09
75 2.4.6.4' 2.18 2.40
76 3.4.5.2' trace trace 0.18 0.01
77 3.4.3'.4' 0.34 0.47 0.12 0.04
78 3.4.5.3' 0.52
79 3.4.3'.5' 0.24 trace 0.23 0.04
80 3.5.3'.5' trace trace trace
81 3.4.5.4' 0.28
83 2.3.5.2'.3' trace 0.32 0.09
84 2.3.6.2'.3' 0.38 0.01 0.71 1.72 0.69
85 2.3.4.2'.4' 0.40 0.55 2.15 0.31
? 2.3.4.3'.5' 0.02 0.55 0.14
87 2.3.4.2'.5' 0.09 1.05 3.81 1.10
91 2.3.6.2'.4' trace 1.78 5.00 3.22
92 2.3.5.2'.5' 0.12 0.20 0.63 0.21
95 2.3.6.2'.5' 0.53 0.18
97 2.4.5.2'.3' 0.78 2.59 0.63
98 2.4.6.2'.3' 0.13 0.04
99 2.4.5.2'.4' 0.55 2.52 6.10 0.82
101 2.4.5.2'.5' 0.27 1.50 6.98 5.04
102 2.4.5.2'.6' trace trace trace
105 2.3.4.3'.4' 0.25
106 2.3.4.5.3' 0.40 0.06
108 2.3.4.3'.5' 0.46 0.16
110 2.3.6.3'.4' 1.69 8.51 3.57
113 2.3.6.3'.5' 0.39 0.01 3.10 trace 0.01
114 2.3.4.5.4' 0.25 0.03
118 2.4.5.3'.4' 8.09 2.00
120 2.4.5.3'.5' 0.31 trace 0.15 3.01
121 2.4.6.3'.5' 0.92 4.32 3.51 0.57
Table 2. (cont'd).
IUPAC Chlorine Aroclor
No. substitution
pattern 1242 1016 1248 1254 1260
123 3.4.5.2'.4' 0.36
? 3.4.5.2'.3' trace 0.76 1.88
126 3.4.5.3'.4' 0.03 0.16 1.59
127 3.4.5.3'.5' 0.05
128 2.3.4.2'.3'.4' 1.31 0.47
131 2.3.4.6.2'.3' 0.14 0.01
132 2.3.4.2'.3'.6' trace 2.00 2.77
133 2.3.5.2'.3'.5' 1.13 0.03 0.06
134 2.3.5.6.2'.3' 0.11 0.38 1.01
135 2.3.5.2'.3'.6' 0.20 0.29
136 2.3.6.2'.3'.6' 0.20 0.34 1.12
138 2.3.4.2'.4'.5' 0.08 0.19 4.17 5.01
143 2.3.4.5.2'.6' 0.07
148 2.3.5.2'.4'.6' 0.12 0.07 0.06
149 2.4.5.2'.3'.6' 0.77 3.59 9.52
151 2.3.5.6.2'.5' trace 0.33 0.06
153 2.4.5.2'.4'.5' 0.02 0.13 3.32 8.22
154 2.4.5.4'.6' 0.14
156 2.3.4.5.3'.4' 0.41
157 2.3.4.3'.4'.5' 0.18 0.03
158 2.3.4.6.3'.4' 0.46 0.18
159 2.4.5.2'.3'.5' 0.75 1.48
163 2.3.5.6.3'.4' trace
167 2.4.5.3'.4'.5' 0.21 0.17
168 2.4.6.3'.4'.5' 0.56 4.23 0.59
170 2.3.4.5.2'.3'.4' 0.43 0.62
171 2.3.4.6.2'.3'.4' 0.30 4.31
174 2.3.4.5.2'.3'.6' trace 0.09
176 2.3.4.6.2'.3'.6' 0.09 trace 0.57
177 2.3.5.6.2'.3'.4' trace
179 2.3.5.6.2'.3'.6' 0.56 0.83
180 2.3.4.5.2'.4'.5' 0.76 7.20
181 2.3.4.5.6.2'.4' 0.28 2.72
182 2.3.4.5.2'.4'.6' trace 0.47
183 2.3.4.6.2'.4'.5' 1.16 2.58
185 2.3.4.5.6.2'.5' 1.11 5.65
186 2.3.4.5.6.2'.6' trace trace 0.37
187 2.3.5.6.2'.4'.5' 0.48 1.12
189 2.3.4.5.3'.4'.5' 0.13
190 2.3.4.5.6.3'.4' 0.02
192 2.3.4.5.6.3'.5' 0.20 0.97
Table 2. (cont'd).
IUPAC Chlorine Aroclor
No. substitution
pattern 1242 1016 1248 1254 1260
193 2.3.5.6.3'.4'.5' 2.30
194 2.3.4.5.2'.3'.4'.5' 2.21
195 2.3.4.5.6.2'.3'.4' trace
196 2.3.4.5.2'.3'.4'.6' 0.79
197 2.3.4.6.2'.3'.4'.6' 0.30
198 2.3.4.5.6.2'.3'.5' 1.00 0.15
199 2.3.4.5.6.2'.3'.6' 0.38
200 2.3.4.6.2'.3'.5'.6' trace 0.15
202 2.3.5.6.2'.3'.5'.6' trace 0.31
203 2.3.4.5.6.2'.4'.5' 0.08
204 2.3.4.5.6.2'.4'.6' trace 0.13
205 2.3.4.5.6.3'.4'.5' 0.01
206 2.3.4.5.6.2'.3'.4'.5' 0.51
207 2.3.4.5.6.2'3'.4'.6' 1.15
208 2.3.4.5.6.2'.3'.5'.6' 1.64
? 2.3.4.5.6.2'.3'.5'.6' 0.18
a From: Albro & Parker (1979); Albro et el. (1981).
Table 3. The trade marks of PCB products and mixtures containing PCBsa
Aceclor (t) Disconon (c) PCBs
Apirolio (t,c) Dk (t,c) Phenoclor (t,c)
Aroclor (t,c) Duconol (c) Polychlorinated biphenyl
Arubren Dykanol (t,c) Polychlorobiphenyl
Asbestol (t,c) EEC-18 Pydraulc
Askarel Elemex (t,c) Pyralene (t,c)
Bakola 131 (t,c) Eucarel Pyranol (t,c)
Biclor (c) Fenchlor (t,c) Pyroclor (t)
Chlorextol (t) Hivar (c) Saf-T-Kuhl (t,c)
Chlorinated Biphenyl Hydol (t,c) Santotherm FRb
Chlorinated Diphenyl Inclor Santovac 1 and 2
Chlorinol Inerteen (t,c) Siclonyl (c)
Chlorobiphenyl Kanechlor (t,c) Solvol (t,c)
Clophen (t,c) Kennechlor Sovol
Clorphen (t) Montar Therminol FRb
Delor Nepolin
Diaclor (t,c) No-Flamol (t,c)
Dialor (c) PCB
a From: WHO/EURO (1987).
b Previous products (FR-series) used as pressure oil contained PCBs, but current
products are a different series and do not contain PCBs.
c Previous products (A-series) e.g., PYDRAUL A-200 contained PCBs, but current
commercial products are B, C, or D-series and do not contain any chlorinated
compounds.
(t) Used in transformers.
(c) Used in capacitors.
Table 4. Concentrations of chlorinated dibenzofuransa in Aroclor, Clophen, and
Phenoclorb
PCB 4-Cl 5-Cl 6-Cl Total
Aroclor 1248 (1969) 0.5 (25) 1.2 (60) 0.3 (15) 2.0
Aroclor 1254 (1969) 0.1 (6) 0.2 (12) 1.4 (82) 1.7
Aroclor 1254 (1970) 0.2 (13) 0.4 (27) 0.9 (60) 1.5
Aroclor 1260 (1969) 0.1 (10) 0.4 (40) 0.5 (50) 1.0
Aroclor 1260 (lot AK3) 0.2 (25) 0.3 (38) 0.3 (38) 0.8
Aroclor 1016 (1972) ND ND ND
Clophen A-60 1.4 (17) 5.0 (59) 2.2 (26) 8.4
Phenoclor DP-6 0.7 (5) 10.0 (74) 2.9 (21) 13.6
a Expressed as mg PCB/kg. Values in parentheses represent quantity as percentage
of total dibenzofurans.
b From: Bowes et al. (1975).
ND = not detected (0.001 mg/kg).
Table 5. Concentrations of chlorinated dibenzofurans in Kanechlorsa
Kanechlor Chlorodibenzofurans Concentration
(mg/kg)
Di- Tri- Tetra- Penta- Hexa- Hepta- b c
300 + + 1 1.5
400 + + + + 18 17
500 + + + + 4 2.5
600 + + + + 5 3
a From: Nagayama et al. (1975).
b Calculated from peak heights.
c Calculated by perchlorination method.
PCBs have a high degree of chemical stability under normal conditions.
They are very resistant to a range of different oxidants and other
chemicals. According to laboratory tests, they stay chemically
unchanged, even in the presence of oxygen or some active metals at
high temperatures (up to 170°C) and for protracted periods (WHO/EURO,
1987).
PCBs are practically insoluble in water, whereas they dissolve easily
in hydrocarbons, fats, and other organic compounds and they are
readily absorbed by fatty tissues (WHO/EURO, 1987).
Some physical and chemical data for a number of Aroclors are presented
in Table 6.
Foreman & Bidleman (1985) estimated the liquid phase vapour pressures,
at 25°C, of 134 PCB congeners found in 5 Aroclor fluids, using a
capillary gas chromatographic method in conjunction with published
retention indices of PCBs.
Burkhard et al. (1985) predicted Henry's Law Constants from the ratio
of the liquid (or subcooled liquid) vapour pressure and aqueous
solubility for PCB congeners. The predicted values were in fair
agreement with experimental values and the error for these constants
was estimated to be a factor of 5 in the temperature range of 0-40°C.
For the PCB congeners, Henry's Law Constants were independent of the
relative molecular mass and increased approximately an order of
magnitude with a 25°C increase in temperature.
Aqueous solubility is considered an essential parameter for predicting
the fate and transport of organic chemicals in the environment. As
already stated, some physical and chemical data are given for 6
Aroclor mixtures in Table 6 (Alford-Stevens, 1986). However, during
the last 5 years, much more information on aqueous solubility, melting
points, entropies of melting, Henry's law constants, and vapour
pressures has become available. This information concerns not only PCB
mixtures but also individual congeners.
Opperhuizen et al. (1988) studied the aqueous solubilities of 45
chlorinated biphenyls and the relationships between activity
coefficient and chemical structure parameters (total surface area
(TSA) and total molecular volume (TMV)) of hydrophobic chemicals, to
understand the nature of hydrophobicity. The aqueous solubilities of
PCBs showed a linear relationship between logarithms of aqueous
activity coefficients or TSA and TMV.
Table 6. Physical and chemical properties of a number of Aroclorsa
Substance Water Vapour Density Appearance Henry's Law Refractive index Boiling point
Aroclor solubility pressure (g/cm3) constant (distillation
(mg/litre) (torr) 25°C 25°C (atm-m3/mol range) (750
25°C at 25°C)b torr, °C)
1016 0.42 4.0 × 10-4 1.33 Clear, mobile oil 2.9 × 10-4 1.6215-1.6235 325-356
(at 25°C)
1221 0.59c 6.7 × 10-3 1.15 Clear, mobile oil 3.5 × 10-3 1.617-1.618 (at 20°C) 275-320
1232 0.45 4.1 × 10-3 1.24 Clear, mobile oil unknown unknown 290-325
1242 0.24 4.1 × 10-3 1.35 Clear, mobile oil 5.2 × 10-4 1.627-1.629 (at 20°C) 325-366
1248 0.054 4.9 × 10-4 1.41 Clear, mobile oil 2.8 × 10-3 unknown 340-375
1254 0.021 7.7 × 10-5 1.50 Light yellow 2.0 × 10-3 1.6375-1.6415 365-390
viscous oil (at 25°C)
1260 0.0027 4.0 × 10-5 1.58 Light yellow 4.6 × 10-3 unknown 385-420
sticky resin
a From: IARC (1978); WHO/EURO (1987); ATSDR (1989).
b These Henry's Law Constants were estimated by dividing the vapour pressure by the water solubility. The first water solubility
given in this table was used for the calculation. The resulting estimated Henry's law constant is only an average for the
entire mixture; the individual chlorobiphenyl isomers may vary significantly from the average. Burkhard et al. (1985)
estimated the following Henry's Law Constants (atm-m3/mol) for various Aroclors at 25°C: 1221 (2.28 × 10-4), 1242 (3.43 × 10-4),
1248 (4.4 × 10-4), 1254 (2.83 × 10-4), 1260 (4.15 × 10-4).
c At 24°C.
Dickhut et al. (1986) studied the solubilities of 6 higher chlorinated
biphenyl congeners at different temperatures and found that the
solubility increased exponentially with temperature in the range of
0.4-80°C. From the temperature dependence of solubility, enthalpies of
solution were calculated. The same r