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    IPCS INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
    Health and Safety Guide No. 83

    POLYBROMINATED BIPHENYLS  (PBBs)
    HEALTH AND SAFETY GUIDE






    UNITED NATIONS INTERNATIONAL

    ENVIRONMENT PROGRAMME LABOUR ORGANISATION

    WORLD HEALTH ORGANIZATION




    WORLD HEALTH ORGANIZATION, GENEVA 1993

    This is a companion volume to Environmental Health Criteria 152:
    Polybrominated biphenyls (PBBs)

    Published by the World Health Organization for the International
    Programme on Chemical Safety (a collaborative programme of the United
    Nations Environment Programme, the International Labour Organisation,
    and the World Health Organization)

    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

    WHO Library Cataloguing in Publication Data

    Polybrominated biphenyls : health and safety guide.

    (Health and safety guide ; no. 83)

    1.Biphenyl compounds - standards  I.Series

    ISBN 92 4 151083 8          (NLM Classification: WA 240)
    ISSN 0259-7268

    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
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    (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
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    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. PRODUCT IDENTITY AND USES
         1.1. Identity
         1.2. Physical and chemical properties
         1.3. Analysis
         1.4. Production and uses
         1.5. Thermal decomposition

    2. SUMMARY AND EVALUATION
         2.1. Sources of human and environmental exposure
         2.2. Environmental transport, distribution, and transformation
         2.3. Environmental levels and human exposure
         2.4. Kinetics and metabolism
         2.5. Effects on organisms in the environment
         2.6. Effects on experimental animals and  in vitro test systems
         2.7. Effects on humans
         2.8. Overall evaluation of the toxicity

    3. CONCLUSIONS AND RECOMMENDATIONS
         3.1. Conclusions
         3.2. Recommendations

    4. HUMAN HEALTH HAZARDS, PREVENTION AND PROTECTION, EMERGENCY ACTION
         4.1. Human health hazards, prevention and protection, first aid
              4.1.1. Advice to physicians
                     4.1.1.1  Symptoms of poisoning30
                     4.1.1.2  Medical advice
              4.1.2. Health surveillance advice
         4.2. Explosion and fire hazards
              4.2.1. Explosion hazards
              4.2.2. Fire hazards
         4.3. Storage
         4.4. Transport
         4.5. Spillage
         4.6. Disposal

    5. HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION

    6. CURRENT REGULATIONS, GUIDELINES, AND STANDARDS
         6.1. Previous evaluation by international bodies
         6.2. Exposure limit values
         6.3. Specific restrictions
         6.4. Labelling, packaging, and transport
         6.5. Waste disposal

    BIBLIOGRAPHY
    

    INTRODUCTION

    The Environmental Health Criteria (EHC) monographs produced by the
    International Programme on Chemical Safety include an assessment of
    the effects on the environment and on human health of exposure to a
    chemical or combination of chemicals, or physical or biological
    agents.  They also provide guidelines for setting exposure limits.

    The purpose of a Health and Safety Guide is to facilitate the
    application of these guidelines in national chemical safety
    programmes. The first three sections of a Health and Safety Guide
    highlight the relevant technical information in the corresponding EHC. 
    Section 4 includes advice on preventive and protective measures and
    emergency action; health workers should be thoroughly  familiar with
    the medical information to ensure that they can act efficiently in an
    emergency.  The section on regulatory information has been extracted
    from the legal file of the International Register of Potentially Toxic
    Chemicals (IRPTC) and from other United Nations sources.

    The target readership includes occupational health services, those in
    ministries, governmental agencies, industry, and trade unions who are
    involved in the safe use of chemicals and the avoidance of
    environmental health hazards, and those wanting more information on
    this topic.  An attempt has been made to use only terms that will be
    familiar to the intended user.  However, sections 1 and 2 inevitably
    contain some technical terms.  A bibliography has been included for
    readers who require further background information.

    Revision of the information in this Guide will take place in due
    course, and the eventual aim is to use standardized terminology. 
    Comments on any difficulties encountered in using the Guide would be
    very helpful and should be addressed to:

    The Director
    International Programme on Chemical Safety
    World Health Organization
    1211 Geneva 27
    Switzerland

    THE INFORMATION IN THIS GUIDE SHOULD BE CONSIDERED AS A STARTING POINT
    TO A COMPREHENSIVE HEALTH AND SAFETY PROGRAMME

    1.  PRODUCT IDENTITY AND USES

    1.1  Identity

    Chemical formula:             C12 H(10-x-y)Brx+y

                                  (both x and y = 1 to 5)

    Chemical structure:

    CHEMICAL STRUCTURE 1

    Molecular weight:             154.21 + 78.90 (x+y)

    Common trade names:           Adine 0102; Berkflam B10; Bromkal 80-9D;
                                  FireMaster BP-6; FireMaster FF-1;
                                  Flammex B10; HFO 101; Octabromobiphenyl
                                  FR 250 BA; Octabromobiphenyl XN-1902.

     Composition of technical products

    PBBs synthesized for commercial use as fire retardants contain a
    mixture of various brominated biphenyls, chiefly the hexa-, octa-,
    nona-, and decabromobiphenyls, as well as small amounts of related
    brominated substances.

    1.2  Physical and Chemical Properties

    PBBs are solids with a low volatility that decreases with an increase
    in the number of bromine atoms. PBBs are virtually insoluble in water,
    soluble in fat and slightly to highly soluble in various organic
    solvents, the solubility also decreasing with an increase in the
    number of bromine atoms.   These compounds are relatively stable and
    chemically unreactive, though highly brominated PBB mixtures degrade
    rather rapidly on exposure to ultraviolet radiation.

    The technical mixtures are typically white, off-white, or beige
    powders.

    1.3  Analysis

    Gas chromatography with electron-capture or mass-spectrometric
    detection are useful techniques for determining PBB levels. 
    High-resolution gas chromatography is preferred as this makes it
    possible to determine specific congeners, but reference compounds are
    available for only a few of the 209 possible PBB congeners.

    1.4  Production and Uses

    The commercial production of PBBs (as FireMaster(R)) was started in
    the USA in 1970.  After the production of about 6000 tonnes, further
    production was virtually discontinued in 1974 after the inadvertent
    addition of PBBs to animal feed. This resulted in the contamination of
    farm animals and their subsequent massive destruction. Approximately
    400 tonnes of octa- and decabromobiphenyl were produced in the USA
    until 1979. Bromkal 80-9D was produced in Germany until 1985; a few
    hundred tonnes per year of Adine 0102 are currently being produced in
    France; in 1977, production of decabromobiphenyl ceased in the United
    Kingdom.

    PBBs are mainly used as flame retardants in moulded thermoplastics,
    mostly in small appliances and automotive applications.  Earlier
    applications in synthetic fibres have been discontinued.

    1.5  Thermal Decomposition

    The products of the thermal decomposition of PBBs depend on the
    temperature, the amount of oxygen present, and a number of other
    factors.  Investigations into the pyrolysis of FireMaster BP-6 in the
    absence of oxygen (600-900 C) have shown that bromobenzenes and lower
    brominated biphenyls are formed, but no polybrominated furans.  In
    contrast, pyrolysis in the presence of oxygen (700-900 C) yielded
    some di- to heptabromodibenzofurans.  In the presence of polystyrene
    and polyethylene, higher levels were found. Pyrolysis of FireMaster
    BP-6 with PVC at 800 C yielded mixed bromochlorobiphenyls.  There is
    no information on the nature of the products of incineration of
    PBB-containing compounds.  Little is known about the toxicity of
    brominated and brominated/chlorinated dioxins and furans, but their
    toxicity is estimated to be of about the same order as that of
    chlorinated dioxins and furans.

    2.  SUMMARY AND EVALUATION

    2.1  Sources of Human and Environmental Exposure

    PBBs were introduced as flame retardants in the early 1970s. Prior to
    November 1974, hexabromobiphenyl was the most commercially significant
    PBB in the USA and was incorporated into ABS (acrylonitrile-butadiene-
    styrene) plastics (PBB content 10% - mainly small appliance and
    automotive applications), coatings and lacquers, and polyurethane
    foam. The other PBB flame retardants have similar uses.

    Losses of PBB into the environment during normal production can occur
    through emission into the air and waste waters, and through losses
    into the soil and into landfills, but these quantities have been found
    to be generally low.  These chemicals can also enter the environment
    during shipping and handling, and following accidents, as occurred in
    Michigan, USA, in 1973.

    PBBs can also enter the environment as a result of the incineration of
    materials containing PBB, as well as during accidental fires, with the
    formation of other toxic chemicals, such as polybromodibenzofurans or
    mixed bromochloro derivatives.

    Most of the total production of these compounds will ultimately enter
    the environment, either unchanged or as breakdown products.

    2.2  Environmental Transport, Distribution, and Transformation

    Long-range transport of PBB in the atmosphere has not been proven, but
    the presence of these compounds in Arctic seal samples indicates a
    wide geographical distribution.

    The main route by which PBBs enter the aquatic environment is in
    industrial waste discharges and leachates from industrial dumping
    sites, as well as by erosion of polluted soils.  PBBs are almost
    insoluble in water and are primarily found in the sediments of
    polluted lakes and rivers.

    Pollution of the soil can originate from point sources such as a PBB
    production plant or a waste dump. Once introduced into the soil, PBBs
    do not appear to be translocated readily. PBBs have been found to be
    200 times more soluble in a landfill leachate than in distilled water;
    this may result in a wider distribution in the environment.  The
    hydrophobic properties of PBBs make them easily adsorbed, from aqueous
    solutions, on to soil particles.  Preferential adsorption of PBB
    congeners has been noted depending on the characteristics of the soil
    (e.g., organic matter content) as well as on the degree and position
    of the bromine substitution.

    PBBs are stable and persistent, lipophilic, and only slightly soluble
    in water; some of the congeners are poorly metabolized and therefore
    accumulate in the lipid compartments of biota. Once they have been
    released into the environment, they can reach the food chain, where
    they are accumulated.

    PBBs have been detected in fish from several regions.  The ingestion
    of fish is a means of PBB transfer to mammals and birds. PBBs have
    also been detected in ducks, a turtle, in the eggs of water birds, as
    well as in the fat of deer, rabbits, coyote, ravens, reindeer, seals,
    and osprey.

    The degradation of PBBs by purely abiotic chemical reactions
    (excluding photochemical reactions) is considered unlikely.  PBBs have
    been reported to be persistent under field conditions.  Soil samples
    from a former PBB manufacturing site, analysed several years after the
    Michigan incident, still contained PBBs, though the congener
    composition was different, indicating partial degradation of the PBB
    residue in the soil sample.

    Under laboratory conditions, PBBs are easily degraded by ultraviolet
    radiation. Photodegradation of the commercial FireMaster(R) mixture
    led to decreased concentrations of the more highly substituted PBB
    congeners. The rates and extent of the photolytic reactions of PBBs in
    the environment have not been determined in detail, though field
    observations indicate high persistence of the original PBBs or partial
    degradation to less brominated compounds.

    In laboratory investigations, mixtures of PBB appear to be fairly
    resistant to microbial degradation.

    No uptake or degradation of PBBs by plants has been recorded. In
    contrast, PBBs are easily absorbed by animals, and although they were
    found to be very persistent in animals, small amounts of PBB
    metabolites have been detected. The main metabolic products were
    hydroxy-derivatives and, in some cases, there was evidence of
    partially debrominated PBBs.  No investigations of sulfur-containing
    metabolites analogous to those of PCBs have been reported.

    The bioaccumulation of PBBs in fish has been investigated.
    Bioaccumulation of PBBs in terrestrial animals has been investigated
    for avian and mammalian species.  Data were obtained through field
    observations, evaluation of the Michigan disaster, and through
    controlled feeding studies. Generally, the accumulation of PBBs in
    body fat depended on dosage and duration of exposure.

    For the individual congeners of PBB, bioaccumulation has been found to
    increase with degree of bromination, up to at least the
    tetrabromobiphenyls.  Higher brominated congeners can be expected to
    accumulate to an even higher degree.  However, no such information is
    available for decabromobiphenyl (DeBB).  It is possible that DeBB is
    poorly absorbed.

    2.3  Environmental Levels and Human Exposure

    There is only one report on PBB levels in air, the concentrations
    being measured in the vicinity of three PBB-manufacturing or
    PBB-processing plants in the USA.

    PBB levels in surface waters were monitored in the same vicinity, as
    well in the area of the Gratiot County landfill (Michigan, USA), which
    received more than 100 tonnes of waste between 1971 and 1973,
    containing 60-70% PBB.

    Groundwater monitoring data from Gratiot County have shown trace
    levels of PBBs even outside the landfill area; however, PBBs were not
    detected in drinking-water wells in the area.

    Data on soil pollution by PBBs are available for areas of manufacture,
    use, or disposal, and for soils from fields of the PBB-contaminated
    Michigan farms. 

    In the Michigan disaster, FireMaster(R) was inadvertently added to
    animal feed. It was almost a year later that the mixing error was
    discovered and the analyses indicated that PBBs were responsible.
    During this time (summer 1973-May 1974), contaminated animals and
    their produce entered the human food supply, and the environment of
    the State of Michigan. Hundreds of farms were affected and thousands
    of animals had to be slaughtered and buried, as well as thousands of
    tonnes of farm produce.

    Most data available on the PBB contamination of wildlife refer to fish
    and birds, primarily water-fowl, in the vicinity of industrial sites,
    and to marine mammals.

    Recent reports on the PBB contamination of fish, terrestrial and
    marine mammals, and birds in Europe and USA indicate a wide
    distribution of these compounds.  The congener pattern found in fish
    samples is quite different from that found in commercial products. 
    Many of the main compounds found could well be the result of
    photochemical debromination of decabromobiphenyl (BB 209), but this
    has not been confirmed.

    Occupational exposure has been found in employees of US chemical
    plants, and in farm workers, as a result of the Michigan PBB incident. 
    Median levels of PBB in serum and adipose tissue were higher among
    chemical workers.  Information is not available on occupational
    exposure associated with manufacturing, formulation, and commercial
    uses from other companies or countries.

    For most human populations, the exposure to PBBs from various sources
    has not been measured directly.  Widespread human exposure has been
    reported from Michigan, USA, as a result of direct contact with
    contaminated feed, but mainly from consumption of PBBs in meat, eggs,
    and dairy products.  At least 2000 families (mainly farmers and their
    neighbours) were exposed to high levels of PBBs.  Recently, PBBs have
    been detected in cow's and human milk in Germany.

    The congener patterns in these human samples were different from those
    found in fish.  The concentration of BB 153 was higher in the human
    milk than in fish.

    The routes by which the general population is exposed to PBBs are not
    well known.  Present knowledge indicates that the ambient air and
    water do not contain high levels.  Lipid-rich food, especially from
    contaminated waters, is probably of great importance.  There is no
    information on the level of exposure from indoor air or on dermal
    exposure from materials containing PBB flame retardants.

    The PBB congener pattern found in human milk samples collected in
    Germany resembles that found in cow's milk from the same region, but
    the levels in the human samples were substantially higher.

    An estimate of daily intake of PBB for the general population from
    food has to be based on very few data.  If fish is assumed to contain
    20 g PBB/kg lipid and 5% lipid and that a 60-kg person eats 100 g
    fish/day, the intake will be 0.002 g/kg body weight per day.  A
    PBB concentration of 0.05 g/kg lipid in milk and a milk consumption
    of 500 ml/day will give the same person a PBB intake of about
    0.00002 g/kg body weight per day.

    An infant of 6 kg body weight consuming 800 ml breast milk (3.5%
    lipid) per day will ingest 0.01 g PBB/kg body weight per day, if the
    milk contains 2 g PBB/kg lipid.

    2.4  Kinetics and Metabolism

    Gastrointestinal absorption of PBBs varies according to the degree of
    bromination, the lower brominated compounds being more easily
    absorbed.  There is inadequate information concerning the absorption
    of DeBB and OcBB.

    PBBs are distributed throughout the entire body of animal species and
    human beings, with highest equilibrium concentrations being found in
    the adipose tissues. Relatively high levels are also found in the
    liver; in particular, the more toxic congeners appear to be
    concentrated in the liver. The partitioning of the various PBB
    congeners appears to differ in different tissues. Generally, there is
    a marked tendency for bioaccumulation. In mammals, transfer of PBBs to
    offspring occurs through the transplacental and milk routes. Human
    breast milk was found to have levels of 2,2',4,4',5,5'-
    hexabromobiphenyl, more than 100 times higher than the maternal serum.

    During a multigeneration study on rats, administration of PBBs to one
    generation resulted in detectable residues in more than two subsequent
    generations. Eggs of avian species are also affected by the maternal
    PBB body burden.

    Many PBB congeners are persistent in biological systems.  There was no
    evidence of significant metabolism or excretion of the more abundant
    components of the FireMaster(R) mixture, or of octa- or
    decabromobiphenyl.  In vitro studies showed that the metabolism of
    PBBs is affected by the structure-activity relationship. PBBs were
    metabolized by phenobarbital-induced microsomes only if they possessed
    adjacent non-brominated carbons meta and para to the biphenyl bridge
    on at least one ring. Metabolism by 3-methylcholanthrene-induced
    microsomes required adjacent non-brominated ortho and meta positions
    on at least one ring of lower substituted congeners; a higher degree
    of bromination appeared to prevent metabolism.  Hydroxylated
    derivatives have been identified in vertebrates as major  in vitro
    and  in vivo metabolism products of lower brominated biphenyls. The
    metabolic yield was relatively low. The hydroxylation reaction
    probably proceeds via both arene oxide intermediates and by direct
    hydroxylation.

    Humans, rats, rhesus monkeys, pigs, cows, and chickens eliminate PBBs
    mainly in the faeces.  In most cases, elimination rates seem to be
    slow. Concentrations of 2,2',4,4',5,5'-hexabromobiphenyl observed in
    the bile and faeces of humans were about 1/2 to 7/10 of the serum
    levels, or approximately 0.5% of the adipose levels. Treatment to
    increase elimination of PBB in animals or humans was usually
    unsuccessful.  Another pathway of elimination could be excretion in
    milk.

    Complex and varied relationships were found among PBB tissue
    concentrations with time after PBB administration to rats or other
    animals. They are described by several compartmental models. A
    half-life of approximately 69 weeks was calculated for the elimination
    of 2,2',4,4',5,5'-hexabromobiphenyl from body fat of the rats; this
    period increased to more than 4 years for rhesus monkeys.  The average
    half-life of 2,2',4,4',5,5'-hexabromobiphenyl in humans has been
    estimated to be between 7.8 and 12 years; periods ranging from 4.6 to
    94.7 years have been suggested in the literature.  Some differences in
    retention and turnover have been demonstrated between individual PBB
    congeners. The results of analyses of serum from farmers and chemical
    workers for 2,3',4,4',5-pentabromobiphenyl have been inconsistent. 
    This inconsistency is probably due to the different sources of
    exposure.  The workers were exposed to all compounds of FireMaster(R),
    while the Michigan population was exposed to contaminated meat and
    milk containing a different mixture of PBBs as a result of metabolic
    processes in farm animals. Bromine levels did not decrease in the
    adipose tissue of rats when they were given technical grade
    octabromobiphenyl.  No information is available on the retention of
    decabromobiphenyl.

    Humans may have a greater tendency to retain certain PBB congeners
    than experimental animals. This factor should be taken into
    consideration in evaluating the human health hazards associated with
    these chemicals.

    In conclusion, all the available data indicate that PBBs have a marked
    tendency to bioaccumulate and persist.  Metabolism is poor and the
    half-life in man is in the order of 8-12 years, or longer.

    2.5  Effects on Organisms in the Environment

    Only few data are available on the effects of PBBs on organisms in the
    environment. They refer to microorganisms, water fleas, water birds,
    and farm animals.

    Water birds nesting on islands in northwestern Lake Michigan were
    studied to determine whether environmental contaminants were affecting
    their reproduction.  Seventeen contaminants, including PBB, were
    measured, but none seemed to have a pronounced effect on reproduction.

    Farm animals that ingested feed inadvertently containing Firemaster(R)
    FF-1, in place of magnesium oxide, became sick. The estimated average
    exposure of cows on the first identified, highly contaminated farm was
    250 mg/kg body weight. The clinical signs of toxicity were a 50%
    reduction in feed consumption (anorexia) and a 40% decrease in milk
    production a few weeks after ingestion of the contaminated feed.
    Although the supplemented feed was discontinued within 16 days, milk
    production did not recover. Some animals showed an increased frequency
    of urination and increased lacrimation, and developed haematomas,
    abscesses, abnormal hoof growth, lameness, alopecia, hyperkeratosis,
    and cachexia, and several died within 6 months of exposure.
    Altogether, the death rate on this farm was 24 out of 400. The death
    rate of 6-18-month-old calves was much higher. About 50% died within 6
    weeks, only 2 out of 12 surviving after 5 months. They developed
    hyperkeratosis over their entire bodies. There were also a variety of
    reproductive problems.

    Necropsy findings have been reported for some of the mature cows that
    died in the 6 months after exposure. Histopathological studies
    revealed variable liver and kidney changes.

    The clinical signs and pathological changes noted above were later
    confirmed in controlled feeding studies (anorexia, dehydration,
    excessive lacrimation, emaciation, hyperkeratosis, reproductive
    difficulties, some clinical chemistry changes, and renal damage).

    A drop in production and sterility were reported from herds with a low
    level of contamination.  This was in contrast to the results from
    controlled studies which did not show significant differences between
    herds with low-level contamination and control herds.

    Although it was cattle feed that was originally contaminated, other
    animal feeds became involved by cross-contamination, e.g., in the
    machinery used to prepare other feeds. It is likely that the exposure
    from these sources was not as high as that of the cattle.  Although
    other animals (poultry, pigs, horses, rabbits, goats, and sheep) were
    reported as being exposed and were killed, details of ill effects were
    not recorded.

    No information is available on the effect of PBBs on ecosystems.

    2.6  Effects on Experimental Animals and In Vitro Test Systems

    Commercial mixtures show relatively low acute toxicity (LD50
    >1 g/kg body weight) in rats, rabbits, and quails following oral or
    dermal administration.  Deaths and acute manifestations of toxicity
    are delayed after administration of PBB.  The total dose administered
    determines the degree of toxicity, whether given as a single dose or
    as repeated doses over short periods (up to 50 days).  The toxicity of
    PBBs is higher with multiple-dose rather than with single-dose
    administration. 

    The few studies performed with commercial mixtures of octa- and
    decabromobiphenyl resulted in no mortality of rats or fish. Of the
    individual PBB congeners, only 3 hexa isomers have been tested,
    3,3',4,4',5,5'-HxBB and 2,3',4,4',5,5'-HxBB being more toxic to rats
    than 2,2',4,4',5,5'-HxBB.  On the basis of limited data, OcBB and DeBB
    appear to be less toxic than the PBB mixtures, and less well absorbed.

    In many acute and short-term studies, signs of PBB (mostly FireMaster)
    toxicity include reductions in feed consumption.  At lethal doses, the
    cause of death cannot be ascribed to pathology in a particular organ,
    but rather the animals develop a "wasting syndrome" as the first
    indication of toxicity.  At death, the loss in body weight can be as
    great as 30-40%.  The few studies with technical OcBB and DeBB show no
    such effects.

    The morphological and histopathological changes due to PBB are most
    prominent in the liver. Enlargement of the liver frequently occurs at
    doses lower than those required to produce body weight changes. The
    principal histopathological alterations in rodent species may consist
    of extensive swelling and vacuolation of hepatocytes, proliferation of
    the smooth endoplasmic reticulum, and single-cell necrosis.  The
    severity of the lesions depends on the dose and composition of the PBB
    material given.

    Decreases in thymus weights were observed in rats, mice, and cattle
    after doses of FireMaster(R), but not after OcBB or DeBB.

    After exposure of rats to low concentrations of PBBs, there have been
    some reports of increase in thyroid weight and histological changes in
    the thyroid.

    It is evident that individual PBB congeners differ in their pattern of
    toxicity. The more toxic isomers and congeners cause a decrease in
    thymus and/or body weight and produce pronounced histological changes
    in the liver and thymus. The halogenated biphenyls have been
    categorized on the basis of structure. Category 1 comprises isomers
    and congeners lacking orthosubstituents (coplanar PBBs).
    Mono-ortho-substituted derivatives constitute the second category.
    Other PBBs (mainly those with two or more orthobromines) form the
    third category. The congeners in the first category tend to elicit the
    most severe effects, those in the second and third categories showing
    less severe toxicological effects. Within the category, the degree of
    bromination may also influence toxicity. 

    Of all the combinations tested, 3,3',4,4',5,5'-HxBB was found to be
    the most toxic PBB.  This congener is present in low concentrations as
    a constituent of FireMaster(R).  Of the major FireMaster(R)
    constituents, 2,3,3',4,4',5-HxBB appeared to be the most toxic,
    followed by 2,3',4,4',5,5'-HxBB and 2,3',4,4',5-PeBB.  The main
    component of the FireMaster(R) mixture, 2,2',4,4',5,5'-HxBB was
    relatively non-toxic, as was 2,2',3,4,4',5,5'-HpBB, the second most
    abundant constituent.

    Technical OcBB and DeBB contain various amounts of other brominated
    biphenyls.  Information on other contaminants is lacking.

    The common skin and eye irritation tests, as well as sensitization
    tests, resulted in no, or only mild, reactions to the technical PBB
    mixtures tested (OcBB and DeBB). However, hyperkeratosis and hair loss
    were seen in cattle, and lesions resembling chloracne were seen in
    rhesus monkeys following the ingestion of a FireMaster(R) mixture. 
    Hyperkeratosis of the inner surface of the rabbit ear was produced by
    FireMaster, but not by its main components (2,2',4,4',5,5'-HxBB and
    2,2',3,4,4',5,5'-HpBB). Fractionation of FireMaster(R) revealed that
    most activity was associated with the more polar fractions containing
    minor components.  Treatment with sunlight-irradiated HxBB caused
    severe hyperkeratosis in rabbit ears.

    In rats, low-dose, long-term feeding of technical OcBB did not affect
    food consumption and body weight, but an increase in the relative
    liver weights of exposed rats was found at 2.5 mg/kg body weight for
    7 months.  Long-term feeding of FireMaster(R) to rats at doses of
    10 mg/kg body weight for 6 months did not affect food consumption. 
    Doses of 1 mg/kg body weight for a 6-month period affected liver
    weight.  The thymus weight was decreased by a dose of 0.3 mg/kg body
    weight in female rats.  Histopathological changes were also noted.
    Controlled long-term feeding studies in cattle exposed to low doses of
    FireMaster(R) showed no adverse effects, as indicated by food intake,
    clinical signs, clinicopathological changes, or performance.  Minks,
    guinea-pigs, and monkeys appeared to be more susceptible to PBB
    toxicity. 

    Long-term effects have been recorded in rats related to pronounced
    retention of the administered PBBs following pre- or perinatal
    exposure to high doses of FireMaster(R).

    The most common adverse effects on reproduction were fetal wastage and
    a decrease in viability of the offspring.  Some effects were still
    noted in mink at concentrations of 1 mg/kg diet.  Following a
    12.5-month exposure to FireMaster(R) (0.3 mg/kg diet), a minor
    decrease was observed in the viability of the offspring of rhesus
    monkeys.  The monkeys received a daily dose of 0.01 mg/kg body weight
    and a total dose of 3.8 mg/kg body weight.  Reproduction and
    neurobehavioural studies in monkeys and rats with a low level of
    exposure could not be appropriately evaluated since insufficient
    information was given in the published papers on the experimental
    design of the study.  A weak teratogenic potential was seen in rodents
    at high doses that may have caused some maternal toxicity.

    PBBs interact with the endocrine system. Rats and pigs were found to
    have dose-related decreases in serum thyroxine and triiodothyronine.
    PBBs have also been reported to affect the levels of steroid hormones;
    the extent depends on the species as well as the dose and the period
    of administration. 

    PBBs produce porphyria in rats and male mice at doses as low as
    0.3 mg/kg body weight per day; the no-effect level was 0.1 mg/kg per
    day.  PBBs had a pronounced influence on vitamin A storage, as well as
    effects on the intermediary metabolism.

    Atrophy of the thymus was a frequent observation following PBB
    exposure. Other lymphoid tissues have also been affected.
    FireMaster(R) also induced further indications of a suppressed immune
    function.  Data is not available concerning the effects of OcBB, DeBB,
    or individual PBB congeners.

    One of the most intensively studied effects of PBBs is their induction
    of mixed function oxidase (MFO) enzymes. Consistently, FireMaster(R)
    was found to be a mixed-type inducer of hepatic microsomal enzymes in
    rats, as well as in all other animal species tested. Induction was
    also found to a lesser extent in other tissues. The ability to induce
    hepatic microsomal enzymes differed for individual PBB congeners. 
    Correlations between structure and microsomal enzyme-inducing activity
    have been demonstrated.

    Several studies have shown that PBBs are able to alter the biological
    activity of a variety of drugs and toxicants. This may be due partly
    to the ability of PBBs to induce the microsomal enzymes involved in
    activation or deactivation of xenobiotics.

    The FireMaster(R) mixture, and some of its major components, were
    found to be capable of inhibiting intercellular communication  in
     vitro. This inhibition occurs at non-cytotoxic concentrations.  Both
    the cytotoxicity and the metabolic cooperation-inhibiting properties
    of PBB congeners seem to be related to their structure, i.e., presence
    or lack of ortho-substitution.  In vitro and  in vivo assays
    (microbial and mammalian cell mutagenesis, mammalian cell chromosomal
    damage, mammalian cell transformation, and DNA damage and repair
    (UDS)) have failed to indicate any mutagenicity or genotoxicity of
    individual PBB congeners or commercial mixtures.

    Long-term carcinogenicity studies with PBBs have shown that the
    principal site of tumours is the liver. The incidences of
    hepatocellular carcinoma were significantly increased in both sexes of
    mice and rats receiving oral doses of the FireMaster(R) mixture. 
    Bromkal 80-9 (technical nonabromobiphenyl) induced carcinogenic
    effects in the liver in mice receiving diets containing 100 mg/kg diet
    (5 mg/kg per day), or more, for 18 months.  The lowest dose of PBB
    that produced tumours (mostly adenomas) in rodents was 0.5 mg/kg body
    weight per day for 2 years.  The rats receiving 0.15 mg/kg in addition
    to pre- and perinatal exposure did not show any adverse effects. The
    carcinogenicity of technical octabromobiphenyl and decabromobiphenyl
    has not been studied.

    Neither FireMaster BP-6 nor 2,2',4,4',5,5'-hexabromobiphenyl showed
    tumour-initiating (using TPA as promoter) or tumour-promoting (using
    DMBA as initiator) activity in a mouse skin bioassay. However, in
    other mouse skin models (using DMBA or MNNG as initiators), both
    FireMaster FF-1 and 3,3',4,4',5,5'-hexabromobiphenyl, but not
    2,2',4,4',5,5'-hexabromobiphenyl, showed tumour-promoting activity. 
    In a two-stage rat liver bioassay using phenobarbital as promoter,
    3,3',4,4'-tetrabromobiphenyl showed a weak initiating activity.  In
    the two-stage rat liver model, using diethylnitrosamine and partial
    hepatectomy, FireMaster, 3,3',4,4'-tetrabromobiphenyl, and
    2,2',4,4',5,5'-hexabromobiphenyl showed tumour-promoting activity, but
    3,3,',4,4',5,5'-hexabromobiphenyl did not.

    The results of the studies on cell communication, the negative results
    on genotoxicity and mutagenicity, and the results of tumour-promotion
    assays indicate that the mixtures and congeners studied cause cancer
    by epigenetic mechanisms.  No information is available on technical
    octa-, nona-, or decabromobiphenyl.

    The mechanisms of action underlying the many manifestations of the
    toxicity of PBBs and related compounds are not known. However, some of
    the effects, such as the wasting syndrome, thymus atrophy,
    hepatotoxicity, skin disorders, and the reproductive toxicity, may be
    related to interaction with the so-called Ah- or TCDD-receptors
    causing alteration in the expression of a number of genes.  Different
    PBB congeners vary in their interaction with the receptor, the
    coplanar congeners being more active.

    Many of the PBB effects are seen after long-lasting exposure.  The
    reason for this observation may be the pronounced accumulation of some
    PBB congeners and the poor ability of the body to metabolize and
    eliminate them.  This results in a build-up of the chemical in the
    body which overcomes the compensatory mechanisms and leads to adverse
    effects.

    Some polybrominated naphthalenes (PBNs), known contaminants of the
    FireMaster(R) mixture, are potent toxicants and teratogens. Although
    PBNs are only present at low levels in the FireMaster(R) mixture, it
    is possible they may contribute to its toxicity.

    Studies of the FireMaster(R) mixture and its main component,
    2,2',4,4',5,5'-HxBB, showed that the photolysis products were more
    toxic than the original PBB. Under some conditions of pyrolysis of
    FireMaster(R), polybrominated dibenzofurans are formed. The pyrolysis
    products of technical OcBB caused liver enlargement.

    2.7  Effects on Humans

    There have been no examples of acute PBB toxicosis in humans with
    which to compare the potential effects at lower exposures following
    the poisoning incident in Michigan, USA, in 1973. The main
    epidemiological studies were conducted by the Michigan Department of
    Public Health (MDPH) and the Environmental Science Laboratory, Mount
    Sinai School of Medicine, New York (ESL). 

    It was estimated that the most highly exposed people consumed 5-15 g
    PBB in milk over a 230-day period.  Some additional exposure may have
    occurred by consuming meat.  The exposure in some of the farmers, and
    most of the general population, in Michigan was much lower.  For them
    the total exposure was 9-10 mg.  However, some people in this group
    may have received a total exposure of about 800-900 mg.  A total dose
    of 9 mg corresponds to 0.15 mg/kg body weight, and 900 mg to 15 mg/kg
    body weight for a 60-kg average adult; the dose/kg body weight will be
    higher for children.

    In 1974, the first MDPH study compared the health status of people on
    quarantined farms with people on non-quarantined farms in the same
    area. Although a variety of symptoms were reported by both groups,
    there was no pattern to the differences between the groups.  The
    heart, liver, spleen, nervous system, urinalysis, blood counts, and
    all other medical conditions examined were found to be normal. In a
    later, comprehensive, MDPH study including groups with different
    levels of exposure, there was no positive association between serum
    concentrations of PBB and reported symptoms or disease frequencies.
    The ESL studies involved about 990 farm residents, 55 chemical
    workers, and a group of Wisconsin dairy farmers who were used as a
    control group. The prevalence of symptoms in Michigan farmers was
    greater than the prevalence in Wisconsin farmers. The greatest
    differences were in the broad classification of neurological and
    musculoskeletal symptoms. Elevated serum concentrations of some liver
    enzymes and carcinoembryonic antigen were more prevalent in Michigan
    farmers than in Wisconsin farmers. Chemical workers had a higher
    prevalence of chest and skin symptoms and a lower prevalence of
    musculoskeletal symptoms than farmers. Although the results of the ESL
    studies were at times interpreted differently from the results of
    comparable studies, there was one area of consistent agreement. None
    of the sets of studies demonstrated a positive dose-response
    relationship between PBB levels in serum or in adipose tissue and the
    prevalence of symptoms or abnormal clinical measurements. Several
    clinical areas were investigated by more intensive special studies.
    Examination of the neurological aspects by means of objective
    performance tests revealed, in one study, a negative correlation
    between serum PBB levels and performance test scores, particularly in
    males in the older age groups. The other studies showed no association
    between the concentration of PBB in serum or fat and performance in a
    battery of tests measuring memory, motor strength, coordination,
    cortical-sensory perception, personality, higher cognitive
    functioning, and other functions. The paediatric aspects of PBB
    exposure were examined in the families in the ESL studies. Although
    many symptoms were reported, physical examination failed to reveal any
    objective alteration that could be attributed to PBB. There were
    different views about the more subtle neuropsychological effects in
    the offspring, and the results of investigations of developmental
    abilities also remain controversial. The same is true for the
    investigation of lymphocyte and immune function. One set of authors
    found no differences in lymphocyte count or functions between groups
    with high and low serum PBB levels, the other found a significant
    decrease in T and B lymphocyte subpopulations in about 40% of an
    exposed Michigan group compared with unexposed groups, and also
    impaired lymphocyte function, i.e., decreased response to mitogens.

    The epidemiological studies reviewed were planned to evaluate the
    relationship between PBB exposure and a large number of adverse
    effects, including behavioural effects and subjective complaints. 
    However, most of the studies suffer from major faults in design that
    introduced confounders which make it difficult or impossible to draw
    valid conclusions.  The follow-up time has not been long enough to
    evaluate a possible carcinogenic effect.

    Two small groups of workers were identified with occupational exposure
    to a mixture of PBBs, or to DeBB and DBBO.  Lesions resembling
    chloracne were found in 13% of the workers exposed to the PBB mixture,
    but such lesions were not seen in the workers exposed to DeBB. 
    However, a significantly higher prevalence of hypothyroidism was seen
    in the latter group.

    2.8  Overall Evaluation of the Toxicity

    The only lifetime and carcinogenicity study with a PBB mixture was
    conducted in rats and mice in a recent NTP bioassay.  The lowest dose
    tested that still produced carcinogenic effects was 0.5 mg/kg body
    weight per day (liver tumours in rodents).  In other carcinogenicity
    studies, 3 mg/kg body weight given for 6 months resulted in a
    carcinogenic response.  The 6-month study demonstrates that a less
    than lifetime exposure at similar doses will also result in similar
    adverse effects.  Effects on reproduction in subhuman primates and
    mink may occur at somewhat lower doses.

    In addition, in the 2-year NTP study, a daily dose of 0.15 mg/kg body
    weight per day and prenatal and perinatal exposure of the dam to
    0.05 mg/kg body weight per day did not result in any adverse effects. 
    Thus, the total daily intake from food, water, air, and soil should be
    less than 0.15 g/kg body weight per day, extrapolating from the NOAEL
    (no-observed-adverse-effect level) of a positive carcinogenicity
    study, using an uncertainty (and safety) factor of 1000, since these
    compounds probably induce cancer by an epigenetic mechanism.

    The total dose received by the subpopulation in Michigan was estimated
    to have ranged from 0.15 to 15 mg/kg body weight over a 230-day
    period.  For this population, dividing the doses over a lifetime for
    the average human being would be equivalent to a daily dose ranging
    from 6 ng to 0.6 g/kg body weight per day.

    Estimates for the general population indicate a total intake by adults
    of 2 ng PBB/kg body weight per day from known sources, and an intake
    of 10 ng/kg body weight per day for infants receiving breast milk.  It
    should be kept in mind that these estimates are based on a very
    limited and regional data base.

    These calculations assume that a steady state for PBBs would not be
    reached over a lifetime, and that short-term, higher exposures can be
    substituted for long-term, lower exposures, since these compounds are
    extremely poorly metabolized and excreted.

    Insufficient information is available for OcBB, NoBB, and DeBB to
    calculate a total daily intake that would not result in adverse
    effects.

    3.  CONCLUSIONS AND RECOMMENDATIONS

    3.1  Conclusions

    Most of the PBB congeners found in commercial flame retardants are
    lipophilic, persistent, and bioaccumulating.  These compounds are
    biomagnified in environmental food-webs and pose a particular threat
    to organisms in the higher levels of these webs.  Furthermore, some
    PBB products form toxic polybrominated dibenzofurans during combustion
    processes.

    In addition to emissions during manufacture and use, PBB will enter
    the environment from the widespread use of flame-retarded products.  A
    considerable part of the PBB produced will probably reach the
    environment sooner or later because of the high stability of these
    compounds.

    PBBs are also found in environmental and human samples also from
    places far from known point sources.  The congener patterns in the
    environmental samples do not match those found in the technical
    products indicating environmental alteration, possibly photochemical
    debromination.

    Very little information is currently available on the degree of
    exposure of the general population to PBBs.  However, in the few
    instances where measurements have been made, trace amounts of PBBs
    were identified.  At present, this exposure does not give rise to
    concern but further build-up should be avoided.  Human data from the
    Michigan episode (see sections 2.3 and 2.7) suggest that exposures in
    Michigan were several orders of magnitude greater than the exposure of
    the general population.  No definitive health effects could be
    correlated with PBB exposure in the Michigan population, though the
    follow-up period has not been long enough for the occurrence of cancer
    to be evaluated.  Since the PBB levels remain high in adipose tissue
    and serum in the Michigan population, their internal exposure
    continues.  In contrast, in Michigan cattle toxic effects were
    observed.  This discrepancy is explained by differences in the degree
    of exposure of the cattle.

    Occupational exposure has been examined in only two plants in the USA. 
    It appears that chloracne-like lesions may develop in workers
    producing PBB, and hypothyroidism in workers exposed to DBB.  No
    studies have been conducted in workers incorporating deca-, octa-, or
    nonabromobiphenyl into commercial products.

    PBBs are extremely persistent in living organisms and have been shown
    to produce chronic toxic effects and cancer in animals.  Though the
    acute toxicity was low, cancer was induced at a dose of 0.5 mg/kg body
    weight per day and the no-observed-effect level was 0.15 mg/kg body
    weight per day.  A number of chronic toxic effects have been observed
    in experimental animals at doses around 1 mg/kg body weight per day
    following long-term exposure.

    3.2  Recommendations

     General

    *    The Task Group is of the opinion that human beings and the
         environment should not be exposed to PBBs, in view of their high
         persistency and bioaccumulation and the potential adverse effects
         at very low levels after long-term exposure.  Therefore, PBBs
         should no longer be used commercially.

    *    Because of the limited data on the toxicity of DeBB and OcBB,
         their extreme persistence, and their potential for breakdown in
         the environment and through combustion to more toxic persistent
         compounds, they should also not be used commercially unless their
         safety has been demonstrated.

     Future work

    *    It is known that observations on the Michigan cohort are still
         continuing.  Publication of these data is required.

    *    Future human and environmental PBB monitoring should be expanded
         and be congener specific, and include the OcBB, NoBB, and DeBB. 
         These compounds should be included in monitoring programmes for
         other halogenated compounds.

    *    The time trends and geographical distribution of PBB levels in
         the environment should continue to be monitored.  The release of
         PBBs into the environment from waste disposal sites should be
         surveyed.

    *    Thermolysis experiments should be conducted to simulate the
         conditions in accidental fires and municipal incinerators.

    *    Research should be continued on the mechanisms of toxicity and
         carcinogenicity of PBBs and related compounds.  PBBs may serve as
         model compounds for mechanistic research. Purified congeners
         should be used in these studies.

    *    The effects on reproduction have not been not well elucidated. 
         Therefore, well designed long-term reproductive studies should be
         performed, at low doses, using a sensitive species.

    *    There is also a need for more information on the bioavailability
         and toxicokinetics of OcBB/NoBB, DeBB and selected congeners. 

    4.  HUMAN HEALTH HAZARDS, PREVENTION AND PROTECTION, EMERGENCY ACTION

    4.1  Human Health Hazards, Prevention and Protection, First Aid

    PBBs are highly brominated organic substances.  They are very
    persistent and can be hazardous for human beings if incorrectly or
    carelessly handled.  It is therefore essential that the correct
    precautions are observed during handling and use.

    4.1.1  Advice to physicians

    4.1.1.1  Symptoms of poisoning

    The acute oral and dermal toxicity is low.  In occupational
    conditions, skin itching, peeling, scaling and (halo) acne are found
    after exposure to PBBs.  Besides these dermal signs of intoxication,
    liver disturbances, chest irritation, and neurological and unspecific
    effects, such as depression, memory disturbances and nervousness, have
    been reported, but not confirmed.

    4.1.1.2  Medical advice

    Medical treatment is symptomatic and supportive.

    4.1.2  Health surveillance advice

    A complete medical history of regularly exposed workers should be
    taken, and physical examination made, on an annual basis, and
    monitoring of PBB levels in blood serum should be done (frequency
    depending on the results).

    4.2  Explosion and Fire Hazards

    4.2.1  Explosion hazards

    PBBs are not flammable; on the contrary, they are flame retardants. 
    However, on heating, toxic fumes, such as hydrogen bromide and
    brominated dibenzofurans may be formed.

    4.2.2  Fire hazards

    Extinguish fires with alcohol-resistant foam, carbon dioxide, or
    powder.  Fire-fighters should be equipped with self-contained
    breathing apparatus, eye protection, and full protective clothing.

    The use of water spray should be confined to the cooling of unaffected
    stock, thus avoiding the accumulation of polluted run-off from the
    site.

    4.3  Storage

    Products should be stored in locked buildings, out of reach of
    animals, children, and unauthorized personnel.  Do not store near
    foodstuffs or animal feed.

    4.4  Transport

    Comply with any local requirements regarding movements of hazardous
    goods.  Do not transport in the same compartment as foodstuffs.  Check
    that containers are sound and labels undamaged before despatch.

    4.5  Spillage

    Before dealing with any spillage, precautions should be taken as
    required, and appropriate personal protection should be used. Prevent
    material from spreading or contaminating other cargo, vegetation, or
    waterways, by making a barrier of the most suitable available
    material, e.g., earth or sand.

    Empty any product remaining in damaged/leaking containers into a clean
    empty drum, which should then be tightly closed and suitably labelled.

    Sweep up spillage with sawdust, sand, or earth (moisten for powders),
    and dispose of safely.

    Absorb spilled liquid with sawdust, sand, or earth, sweep up and place
    the sweepings in a closeable container for later transfer to a safe
    place for disposal.

    As soon as possible after the spillage and before reuse, cover all
    contaminated areas with damp sawdust, sand, or earth.  Sweep up and
    place the sweepings in a closeable container for later transfer to a
    safe place for disposal.  Care should be taken to avoid run-off into
    watercourses.

    4.6  Disposal

    Any surplus product, contaminated absorbents, and containers should be
    disposed of in an appropriate way.  Waste material should be burned in
    a proper incinerator designed for organohalogen waste disposal with
    effluent-gas scrubbing.  For PBB wastes, incineration must be for more
    than 2 seconds at 1200 C or higher.  Combustion of PBBs at lower
    temperatures can produce brominated dibenzofurans.  If high
    temperature incineration is not possible, bury waste in an approved
    dump or landfill where there is no risk of contamination of surface or
    groundwater.  Decomposition of PBBs will be extremely slow.

    Comply with any local legislation regarding disposal of toxic wastes. 
    Puncture container to prevent reuse.

    5.  HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION

    PBBs are very resistant to degradation and very persistent in the
    environment.  Because of their high solubility in fat, they
    bioaccumulate, especially in the fatty tissues of all living
    organisms, and biomagnify in the higher trophic levels of the food
    chain.  Although their acute toxicity is relatively low, this
    bioaccumulation and biomagnification may lead to toxic effects.

    Industrial discharges occurring during manufacture, formulation, or
    technical applications should be treated properly and should not be
    allowed to pollute the environment.  Any spillage or unused product
    should be treated and disposed of properly (see section 4.5 and 4.6)
    and should be prevented from spreading to the environment.

    6.  CURRENT REGULATIONS, GUIDELINES, AND STANDARDS

    The information given in this section has been extracted from the
    International Register of Potentially Toxic Chemicals (IRPTC) legal
    file and other United Nations sources.  A full reference to the
    original national document from which the information was extracted
    can be obtained from IRPTC.

    The reader should be aware that regulatory decisions about chemicals
    taken in a certain country can only be fully understood in the
    framework of the legislation of that country.  Furthermore, the
    regulations and guidelines of all countries are subject to change and
    should always be verified with the appropriate regulatory authorities
    before application.

    6.1  Previous Evaluation by International Bodies

    The International Agency for Research on Cancer (IARC) evaluated
    polybrominated biphenyls in 1986 and 1987 and concluded that there was
    inadequate evidence of their carcinogenicity in humans, but sufficient
    evidence of their carcinogenicity in experimental animals (Group 2B).

    6.2  Exposure Limit Values

    No exposure limit values for PBBs were found.

    6.3  Specific Restrictions

    In the USA, all use of hexabromobiphenyls, the main PBB isomer used in
    industrial processes, was discontinued in 1974, because of the hazard
    to human health discovered after its accidental misuse in Michigan in
    1973.  The US Environmental Protection Agency has since required
    notification regarding any manufacture or importation of PBBs.  The
    purpose of this requirement is to confirm that there are no
    significant sources of these substances and to ensure that EPA has the
    opportunity to investigate the circumstances of any resumption of
    production.

    In Canada, all commercial, manufacturing, and processing uses are
    banned.

    In the countries of the EEC, PBBs may not be used in textile articles,
    such as garments, undergarments and linen intended to come into
    contact with the skin.

    6.4  Labelling, Packaging, and Transport

    The United Nations Committee of Experts on the Transportation of
    Dangerous Goods classifies PBBs in:

         Hazard Class 9:     miscellaneous dangerous substance

         Packing Group II:   substances presenting medium danger

    The European Community legislation requires the labelling of PBBs as
    harmful substances using the symbol.

    FIGURE 1

    The label must read:

          Danger of cumulative effects.  This material and its container
          must be disposed of in a safe way.  It should be stated on the
          label whether the substance is a specific isomer or a mixture of
          isomers.

    6.5  Waste Disposal

    No waste disposal regulations for PBBs were found.

    BIBLIOGRAPHY

    GOSSELIN, R.E., SMITH, R.P., HODGE, H.C., & BRADDOCK, J.E.  (1984) 
     Clinical toxicology of commercial products. 5th ed. Baltimore,
    Maryland, Williams and Wilkins Company.

    IARC  (1972-present)  IARC Monographs on the evaluation of
     carcinogenic risk of chemicals to man, Lyon, International Agency
    for Research on Cancer.

    IRPTC  (1987)   IRPTC legal file 1986. Geneva, International Register
    of Potentially Toxic Chemicals, United Nations Environment Programme.

    IRPTC  (1985)   IRPTC file on treatment and disposal methods for waste
     chemicals. Geneva, International Register of Potentially Toxic
    Chemicals, United Nations Environment Programme.

    IRPTC   Data profile on individual chemical substances (unpublished
    file).  Geneva, International Register of Potentially Toxic Chemicals,
    United Nations Environment Programme.

    SAX, N.I.  (1984)   Dangerous properties of industrial materials. New
    York, van Nostrand Reinhold Company, Inc.

    UNITED NATIONS  (1991)   Consolidated list of products whose
     consumption and/or sale have been banned, withdrawn, severely
     restricted or not approved by Governments. 4th Ed. New York, United
    Nations.

    UNITED NATIONS  (1986)   Recommendations on the transport of dangerous
     goods. 4th ed. New York, United Nations.

    WHO (In Press, 1993)   Environmental health criteria 152.
     Polybrominated biphenyls (PBBs). Geneva, World Health Organization. 

    


    See Also:
       Toxicological Abbreviations