IPCS INCHEM Home
    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
    epidemiological, experimental laboratory, and risk-assessment methods
    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

        The World Health Organization welcomes requests for permission to
    reproduce or translate its publications, in part or in full.
    Applications and enquiries should be addressed to the Office of
    Publications, World Health Organization, Geneva, Switzerland, which
    will be glad to provide the latest information on any changes made to
    the text, plans for new editions, and reprints and translations
    already available.

    (c) World Health Organization 1993

        Publications of the World Health Organization enjoy copyright
    protection in accordance with the provisions of Protocol 2 of the
    Universal Copyright Convention. All rights reserved.

        The designations employed and the presentation of the material in
    this publication do not imply the expression of any opinion whatsoever
    on the part of the Secretariat of the World Health Organization
    concerning the legal status of any country, territory, city or area or
    of its authorities, or concerning the delimitation of its frontiers or
    boundaries.

        The mention of specific companies or of certain manufacturers'
    products does not imply that they are endorsed or recommended by the
    World Health Organization in preference to others of a similar nature
    that are not mentioned. Errors and omissions excepted, the names of
    proprietary products are distinguished by initial capital letters.


    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:

    CHEMICAL STRUCTURE

    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