UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 195
Hexachlorobenzene
This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.
Environmental Health Criteria 195
First draft prepared by Mr R. Newhook and Ms W. Dormer,
Health Criteria, Canada
Published under the joint sponsorship of the United Nations
Environment Programme, the International Labour Organisation, and the
World Health Organization, and produced within the framework of the
Inter-Organization Programme for the Sound Management of Chemicals.
World Health Organization
Geneva, 1997
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WHO Library Cataloguing in Publication Data
Hexachlorobenzene.
(Environmental health criteria ; 195)
1. Hexachlorobenzene - toxicity 2.Hexachlorobenzene - adverse effects
3. Environmental exposure I. Series
ISBN 92 4 157195 0 (NLM Classification: QV 633)
ISSN 0250-863X
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CONTENTS
ENVIRONMENTAL HEALTH CRITERIA FOR HEXACHLOROBENZENE
PREAMBLE
ABBREVIATIONS
PREFACE
1. SUMMARY AND CONCLUSIONS
1.1. Identity, physical and chemical properties,
and analytical methods
1.2. Sources of human and environmental exposure
1.3. Environmental transport, distribution and
transformation
1.4. Environmental levels and human exposure
1.5. Kinetics and metabolism in laboratory
animals and humans
1.6. Effects on laboratory animals and in vitro tests
1.7. Effects on humans
1.8. Effects on other organisms in the
laboratory and field
1.9. Evaluation of human health risks and
effects on the environment
1.9.1. Health effects
1.9.2. Environmental effects
1.10. Conclusions
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL
METHODS
2.1. Identity
2.2. Physical and chemical properties
2.3. Analytical methods
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1. Sources, uses and production processes
3.2. World production levels
3.3. Entry into the environment
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION
4.1. Environmental transport and degradation
4.2. Bioaccumulation and biomagnification
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1. Environmental levels
5.1.1. Air
5.1.2. Water
5.1.3. Soil
5.1.4. Sediment
5.1.5. Biota
5.1.6. Food and drinking-water
5.2. General population exposure
5.2.1. Human tissues and fluids
5.2.2. Intake from ambient air
5.2.3. Intake from drinking-water
5.2.4. Intake from foods
5.2.5. Apportionment of intakes
5.2.6. Trends in exposure of the general
population over time
5.2.7. Occupational exposure during
manufacture, formulation or use
6. KINETICS AND METABOLISM
6.1. Aquatic and terrestrial biota
6.2. Mammals
7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS
7.1. Single exposure
7.2. Short-term and subchronic exposure
7.3. Long-term toxicity and carcinogenicity
7.4. Mutagenicity and related end-points
7.5. Reproductive and developmental toxicity
7.6. Immunotoxicity
8. EFFECTS ON HUMANS
8.1. General population exposure
8.2. Occupational exposure
9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD
9.1. Short-term exposure
9.1.1. Aquatic biota
9.1.2. Terrestrial biota
9.2. Long-term exposure
9.2.1. Aquatic biota
9.2.2. Terrestrial biota
10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT
10.1. Evaluation of human health risks
10.1.1. Exposure
10.1.2. Health effects
10.1.3. Approaches to risk assessment
10.1.3.1 Non-neoplastic effects
10.1.3.2 Neoplastic effects
10.2. Evaluation of effects on the environment
11. RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH AND
THE ENVIRONMENT
12. FURTHER RESEARCH
12.1. Environment
12.2. Human health
13. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
REFERENCES
RÉSUMÉ ET CONCLUSIONS
RÉSUMEN Y CONCLUSIONES
NOTE TO READERS OF THE CRITERIA MONOGRAPHS
Every effort has been made to present information in the criteria
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A detailed data profile and a legal file can be obtained from the
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This publication was made possible by grant number 5 U01 ES02617-
15 from the National Institute of Environmental Health Sciences,
National Institutes of Health, USA, and by financial support from the
European Commission and the Federal Ministry for the Environment,
Nature Conservation and Nuclear Safety, Germany.
Environmental Health Criteria
PREAMBLE
Objectives
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The original impetus for the Programme came from World Health
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* Identity - physical and chemical properties, analytical methods
* Sources of exposure
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* Environmental levels and human exposure
* Kinetics and metabolism in laboratory animals and humans
* Effects on laboratory mammals and in vitro test systems
* Effects on humans
* Effects on other organisms in the laboratory and field
* Evaluation of human health risks and effects on the environment
* Conclusions and recommendations for protection of human health
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* Previous evaluations by international bodies, e.g., IARC, JECFA,
JMPR
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WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR HEXACHLOROBENZENE
Members
Dr D. Arnold, Health Canada, Tunney's Pasture, Ottawa, Ontario Canada
Dr A. Göcmen, Department of Pediatrics, Faculty of Medicine,
Hacettepe University, Hacettepe, Ankara, Turkey
Professor B. Jansson, Institute of Applied Environmental Research,
ITM-Solna, Stockholm University, Stockholm, Sweden
Dr J. Jarrell, Foothills Hospital, Calgary Regional Health
Authority, Calgary, Alberta, Canada
Dr A. Langley, South Australian Health Commission, Rundle Mall,
Australia ( Chairman)
Mr R. Newhook, Bureau of Chemical Hazards, Environmental
Substances Division, Health Canada, Tunney's Pasture, Ottawa,
Ontario, Canada ( Rapporteur)
Dr D. Peakall, Wimbledon, London, United Kingdom
( Vice-chairman)
Dr A.G. Smith, Medical Research Council Toxicology Unit,
Hodgkin Building, University of Leicester, Leicester,
United Kingdom
Dr J. Sunyer, Department of Epidemiology and Public Health,
Institut Municipal d'Investigacio Medica, Barcelona, Spain
Dr A. van Birgelen, National Health and Environmental Effects
Research Laboratory, Pharmacokinetics Branch, US Environmental
Protection Agency, Research Triangle Park, North Carolina, USAa
Dr J. Vos, National Institute of Public Health and the Environment
(RIVM), Hygiene, Bilthoven, The Netherlands
a Dr A. Van Birgelen's present address: National Institute of
Environmental Health Sciences, Research Triangle Park, North
Carolina, USA
Observers
Dr J. de Gerlache, Solvay SA, Department of Chemical Safety and
Toxicology, Brussels, Belgium (Representing EURO CHLOR)
Dr Roger Drew, Toxicology Information Section, Safety, Health &
Environment Division, ICI Australia Operations Pty Ltd., ICI
House, Melbourne, Victoria, Australia (Representing European
Centre for Ecotoxicology and Toxicology of Chemicals)
Secretariat
Dr G.C. Becking, Interregional Research Unit, International
Programme on Chemical Safety, Research Triangle Park, North
Carolina USA ( Secretary)
Ms W. Dormer, Bureau of Chemical Hazards, Environmental
Substances Division, Health Canada, Tunney's Pasture, Ottawa,
Ontario, Canada ( Temporary Adviser to Secretariat)
Dr J. Wilbourn, Unit of Carcinogen Identification and Evaluation,
International Agency for Research on Cancer, Lyon, France
IPCS TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR HEXACHLOROBENZENE
A WHO Task Group on Environmental Health Criteria for
Hexachlorobenzene met in Geneva from 26 February to 1 March 1996.
Dr G.C. Becking, IPCS, welcomed the participants on behalf of Dr M.
Mercier, Director of the IPCS, and the three cooperating organizations
(UNEP/ILO/WHO). The group reviewed and revised the draft and made an
evaluation of the risks for human health and the environment from
exposure to hexachlorobenzene.
The first draft was prepared by Mr R. Newhook and Ms W. Dormer,
Health Canada, Ottawa, Canada. These authors also prepared the draft
reviewed by the Task Group, which incorporated the comments received
following circulation of the first draft to IPCS Contact Points for
Environmental Health Criteria monographs.
The IPCS gratefully acknowledges the financial and other support
of the Health Protection Branch, Health Canada. This support was
indispensable for the completion of this monograph.
Dr G.C. Becking (IPCS, Central Unit, Inter-regional Research
Unit) and Dr P.G. Jenkins (IPCS, Central Unit, Geneva) were
responsible for the overall scientific content and the technical
editing, respectively, of this monograph.
The efforts of all who helped in the preparation and finalization
of this publication are gratefully acknowledged.
ABBREVIATIONS
BCF bioconcentration factor
BMF biomagnification factor
DL detection limit
HCB hexachlorobenzene
i.p. intraperitoneal
ND not detectable
PCT porphyria cutanea tarda
p,p'DDE 1,1'-(2,2-dichloroethylidene)-bis[4-chlorobenzene]
SER smooth endoplasmic reticulum
T3 triiodothyronine
T4 thyroxine
PREFACE
The preparation of comprehensive Environmental Health Criteria
(EHC), as outlined in the Preamble of this monograph, is an extremely
time-consuming and resource-intensive procedure. Often countries have
prepared recent comprehensive reviews on chemicals as required by
their national legislation, and the International Programme on
Chemical Safety (IPCS) has been asked by Member States to determine
how best to utilize such national reviews during the preparation of
international EHC. Utilizing such national documents should avoid
duplication of effort and result in the more rapid production of more
concise IPCS EHC monographs.
This monograph on hexachlorobenzene has been prepared using as
background document the review (Supporting Document) prepared under
the Canadian Environmental Protection Act (CEPA), dated June 1993.
From this document, staff of Health Canada have chosen only the most
relevant studies for assessing the human and environmental risks from
exposure to hexachlorobenzene. These have been described from the
original references and supplemented by additional information
published more recently. This has resulted in a concise monograph,
yet one that supplies sufficient information for the reader to
understand the basis for the conclusions reached by the Task Group.
Readers who wish to consult the text of the Canadian Supporting
Document can obtain a copy from the Director, IPCS, World Health
Organization, Geneva, Switzerland.
1. SUMMARY AND CONCLUSIONS
1.1 Identity, physical and chemical properties, and
analytical methods
Hexachlorobenzene (HCB) is a chlorinated organic compound with
moderate volatility. It is practically insoluble in water, but is
highly lipid-soluble and bioaccumulative. Technical grade HCB contains
up to 2% impurities, most of which is pentachlorobenzene. The
remainder includes the higher chlorinated dibenzo- p-dioxins,
dibenzofurans and biphenyls. Analysis of HCB in environmental media
and biological materials generally involves extraction of the sample
into organic solvents, often followed by a clean-up step, to produce
organic extracts for gas chromatography/mass spectrometry (GC/MS) or
gas chromatography with electron capture detection (GC/ECD).
1.2 Sources of human and environmental exposure
HCB was at one time used extensively as a seed dressing to
prevent fungal disease on grains, but this use was discontinued in
most countries in the 1970s. HCB continues to be released to the
environment from a number of sources, including the use of some
chlorinated pesticides, incomplete combustion, old dump sites and
inappropriate manufacture and disposal of wastes from the manufacture
of chlorinated solvents, chlorinated aromatics and chlorinated
pesticides.
1.3 Environmental transport, distribution and transformation
HCB is distributed throughout the environment because it is
mobile and persistent, although slow photodegradation in air and
microbial degradation in soil do occur. In the troposphere, HCB is
transported long distances and removed from the air phase through
deposition to soil and water. Significant biomagnification of HCB
through the food chain has been reported.
1.4 Environmental levels and human exposure
Low concentrations of HCB are present in ambient air (a few
ng/m3 or less) and in drinking-water and surface water (a few
ng/litre or less) in areas that are distant from point sources around
the world. However, higher levels have been measured near point
sources. HCB is bioaccumulative and has been detected in
invertebrates, fish, reptiles, birds and mammals (including humans)
distant from point sources, particularly in fatty tissues of organisms
at higher trophic levels. Mean levels in adipose tissue of the human
general population in various countries range from tens to hundreds of
ng/g wet weight. Based on representative levels of HCB in air, water
and food, the total intake of HCB by adults in the general population
is estimated to be between 0.0004 and 0.003 µg/kg body weight per day.
This intake is predominantly from the diet. Owing to the presence of
HCB in breast milk, mean intakes by nursing infants have been
estimated to range from < 0.018 to 5.1 µg/kg body weight per day in
various countries. The results of most studies on the levels of HCB in
foods and human tissues over time indicate that exposure of the
general population to HCB declined from the 1970s to the mid-1990s in
many locations. However, this trend has not been evident during the
last decade in some other locations.
1.5 Kinetics and metabolism in laboratory animals and humans
There is a lack of toxicokinetic information for humans. HCB is
readily absorbed by the oral route in experimental animals and poorly
via the skin (there are no data concerning inhalation). In animals and
humans, HCB accumulates in lipid-rich tissues, such as adipose tissue,
adrenal cortex, bone marrow, skin and some endocrine tissues, and can
be transferred to offspring both across the placenta and via mothers'
milk. HCB undergoes limited metabolism, yielding pentachlorophenol,
tetrachlorohydroquinone and pentachlorothiophenol as the major
metabolites in urine. Elimination half-lives for HCB range from
approximately one month in rats and rabbits to 2 or 3 years in
monkeys.
1.6 Effects on laboratory animals and in vitro tests
The acute toxicity of HCB to experimental animals is low (1000 to
10 000 mg/kg body weight). In animal studies, HCB is not a skin or eye
irritant and does not sensitize the guinea-pig.
The available data on the systemic toxicity of HCB indicate that
the pathway for the biosynthesis of haem is a major target of
hexachlorobenzene toxicity. Elevated levels of porphyrins and/or
porphyrin precursors have been found in the liver, other tissues and
excreta of several species of laboratory mammals exposed to HCB.
Porphyria has been reported in a number of studies in rats with
subchronic or chronic oral exposure to between 2.5 and 15 mg HCB/kg
body weight per day. Excretion of coproporphyrins was increased in
pigs ingesting 0.5 mg HCB/kg body weight per day or more (no effects
were observed at 0.05 mg HCB/kg body weight per day in the latter
study). Repeated exposure to HCB has also been shown to affect a wide
range of organ systems (including the liver, lungs, kidneys, thyroid,
skin, and nervous and immune systems), although these have been
reported less frequently than porphyria.
HCB is a mixed-type cytochrome-P-450-inducing compound, with
phenobarbital-inducible and 3-methylcholanthrene-inducible properties.
It is known to bind to the Ah receptor.
In chronic studies, mild effects on the liver (histopathological
changes, enzyme induction) occurred in several studies of rats exposed
to between 0.25 and 0.6 mg HCB/kg body weight per day; the NOELs in
these studies were 0.05 to 0.07 mg HCB/kg body weight per day.
Concentrations of neurotransmitters in the hypothalamus were altered
in mink dams with chronic dietary exposure to 0.16 mg HCB/kg body
weight per day, and in their offspring exposed throughout gestation
and nursing. Calcium homoeostasis and bone morphometry were affected
in subchronic studies on rats at 0.7 mg HCB/kg body weight per day,
but not at 0.07 mg/kg body weight per day.
The carcinogenicity of HCB has been assessed in several adequate
bioassays on rodents. In hamsters fed diets yielding average doses of
4, 8 or 16 mg/kg body weight per day for life, there were increases in
the incidence of liver cell tumours (hepatomas) in both sexes at all
doses, haemangioendotheliomas of the liver at 8-16 mg/kg body weight
per day, and adenomas of the thyroid in males at the highest dose.
Dietary exposure of mice to 6, 12 and 24 mg/kg body weight per day for
120 weeks resulted in an increase in the incidence of liver cell
tumours (hepatomas) in both sexes at the two higher doses (not
significant, except for females at the highest dose). In utero,
lactational and oral exposure of rats to HCB in diets yielding average
lifetime doses ranging from 0.01 to 1.5 mg/kg body weight per day
(males) or 1.9 mg/kg body weight per day (females) for up to 130 weeks
post utero produced increased incidences, at the highest dose, of
neoplastic liver nodules and adrenal phaeochromocytomas in females and
of parathyroid adenomas in males. In another long-term study on rats,
exposure for up to 2 years to diets yielding average HCB doses of 4-5
and 8-9 mg/kg body weight per day induced increases in the incidences
of hepatomas and of renal cell adenomas at both doses in both sexes,
and of hepatocellular carcinomas, bile duct adenomas/ carcinomas and
adrenal phaeochromocytomas and adrenal cortical adenomas in females.
High incidences of liver tumours have also been reported in some more
limited studies in which single dietary concentrations were
administered to small groups of female rats. In addition, it has been
reported that, following subchronic dietary exposure to HCB, mice,
hamsters and rats developed tumours in the liver, bile duct, kidney,
thymus, spleen and lymph nodes. Dietary exposure to HCB promoted the
induction of liver tumours by polychlorinated terphenyl in mice and by
diethylnitrosamine in rats.
Except in the case of renal tumours in male rats (which appear at
least in part to be the result of hyaline droplet nephropathy) and
hepatomas in rats (which may result from hyperplastic responses to
hepatocellular necrosis), mechanistic studies that address the
relevance to humans of the tumour types induced by HCB have not been
identified.
HCB has little capability to induce directly gene mutation,
chromosomal damage and DNA repair. It exhibited weak mutagenic
activity in a small number of the available studies on bacteria and
yeast, although it should be noted that each of these studies has
limitations. There is also some evidence of low-level binding to DNA
in vitro and in vivo, but at levels well below those expected for
genotoxic carcinogens.
In studies of reproduction, oral exposure of monkeys to as little
as 0.1 mg HCB/kg body weight per day for 90 days affected the light
microscopic structure and ultrastructure of the surface germinal
epithelium, an unusual target for ovarian toxins. This dose also
caused ultrastructural injury to the primordial germ cells. These
specific target sites, which are damaged further at higher doses, were
associated with otherwise normal follicular, oocyte and embryo
development, suggesting specificity of HCB action within the site of
the ovary. Male reproduction was only affected at much higher doses
(between 30 and 221 mg/kg body weight per day) in studies on several
non-primate species.
Transplacental or lactational exposure of rats and cats to
maternal doses of between 3 and 4 mg/kg body weight per day was found
to be hepatotoxic and/or affected the survival or growth of nursing
offspring. In some cases, these or higher doses reduced litter sizes
and/or increased the number of stillbirths. (Adverse effects on
suckling infants have generally been observed more frequently, and at
lower doses, than embryotoxic or fetotoxic effects). The offspring of
mink with chronic exposure to as little as 1 mg HCB/kg diet
(approximately 0.16 mg/kg body weight per day) had reduced birth
weight and increased mortality to weaning. Although skeletal and renal
abnormalities have been observed in fetuses in some studies of rats
and mice exposed to HCB during gestation, these were either not
clearly related to treatment or occurred at doses that were also
maternally toxic. In two studies, one of which included lactational
and postnatal exposure, neurobehavioural development of rat pups was
affected by in utero exposure to HCB at oral maternal doses of 0.64
to 2.5 mg HCB/kg body weight per day.
The results of a number of studies have indicated that HCB
affects the immune system. Rats or monkeys exposed to between 3 and
120 mg HCB/kg body weight per day had histopathological alterations in
the thymus, spleen, lymph nodes and/or lymphoid tissues of the lung.
Chronic exposure of beagle dogs to 0.12 mg/kg body weight per day
caused nodular hyperplasia of the gastric lymphoid tissue. In a number
of studies on rats, humoral immunity and, to a lesser extent, cell-
mediated immunity were enhanced by several weeks exposure to HCB in
the diet, while macrophage function was unaltered. As little as 4 mg
HCB/kg diet (approximately 0.2 mg/kg body weight per day) during
gestation, through nursing and to 5 weeks of age increased humoral and
cell-mediated immune responses and caused accumulation of macrophages
in the lung tissue of rat pups. In contrast, HCB has been found to be
immunosuppressive in most studies with mice; doses of as little as
0.5-0.6 mg/kg body weight per day for several weeks depressed
resistance to infection by Leishmania or to a challenge with tumour
cells, decreased cytotoxic macrophage activity of the spleen, and
reduced the delayed-type hypersensitivity response in offspring
exposed in utero and through nursing. In a number of studies on
various strains of rats, short-term or subchronic exposure to HCB
affected thyroid function, as indicated by decreased serum levels of
total and free thyroxine (T4) and often, to a lesser extent,
triiodothyronine (T3).
1.7 Effects on humans
Most data on the effects of HCB on humans originate from
accidental poisonings that took place in Turkey in 1955-1959, in which
more than 600 cases of porphyria cutanea tarda (PCT) were identified.
In this incident, disturbances in porphyrin metabolism, dermatological
lesions, hyperpigmentation, hypertrichosis, enlarged liver,
enlargement of the thyroid gland and lymph nodes, and (in roughly half
the cases) osteoporosis or arthritis were observed, primarily in
children. Breast-fed infants of mothers exposed to HCB in this
incident developed a disorder called pembe yara (pink sore), and most
died within a year. There is also limited evidence that PCT occurs in
humans with relatively high exposure to HCB in the workplace or in the
general environment.
The few available epidemiological studies of cancer are limited
by small size, poorly characterized exposures to HCB and exposure to
numerous other agents, and are insufficient to assess the
carcinogenicity of HCB to humans.
1.8 Effects on other organisms in the laboratory and field
In studies of the acute toxicity of HCB to aquatic organisms,
exposure to concentrations in the range of 1 to 17 µg/litre reduced
production of chlorophyll in algae and reproduction in ciliate
protozoa, and caused mortality in pink shrimp and grass shrimp, but
did not cause mortality in freshwater or marine fish. In longer-term
studies, the growth of sensitive freshwater algae and protozoa was
affected by a concentration of 1 µg/litre, while concentrations of
approximately 3 µg/litre caused mortality in amphipods and liver
necrosis in large-mouth bass.
1.9 Evaluation of human health risks and effects on the environment
1.9.1 Health effects
The Task Group concluded that the available data are sufficient
to develop guidance values for non-neoplastic and neoplastic effects
of HCB.
For non-neoplastic effects, based on the lowest reported NOEL
(0.05 mg HCB/kg body weight per day), for primarily hepatic effects
observed at higher doses in studies on pigs and rats exposed by the
oral route, and incorporating an uncertainty factor of 300 (× 10 for
interspecies variation, × 10 for intraspecies variation, and × 3 for
severity of effect), a TDI of 0.17 µg/kg body weight per day has been
derived.
The approach for neoplastic effects is based on the tumorigenic
dose TD5 i.e., the intake associated with a 5% excess incidence of
tumours in experimental studies in animals. Based on the results of
the two-generation carcinogenicity bioassay in rats and using the
multi-stage model, the TD5 value is 0.81 mg/kg body weight per day
for neoplastic nodules of the liver in females. Based on consideration
of the insufficient mechanistic data, an uncertainty factor of 5000
was used to develop a health-based guidance value of 0.16 µg/kg body
weight per day.
1.9.2 Environmental effects
The Task Group pointed out that there are very few experimental
studies on which an environmental risk assessment can be made. Levels
of HCB in surface water are generally several orders lower than those
expected to present a hazard to aquatic organisms, except in a few
extremely contaminated locations. However, HCB concentrations in the
eggs of sea birds and raptors from a number of locations from around
the world approach those associated with reduced embryo weights in
herring gulls (1500 µg/kg), suggesting that HCB has the potential to
harm embryos of sensitive bird species. Similarly, levels of HCB in
fish at a number of sites worldwide are within an order of magnitude
of the dietary level of 1000 µg/kg associated with reduced birth
weight and increased mortality of offspring in mink. This suggests
that HCB has the potential to cause adverse effects in mink and
perhaps other fish-eating mammals.
1.10 Conclusions
a) HCB is a persistent chemical that bioaccumulates owing to its
lipid solubility and resistance to breakdown.
b) Animal studies have shown that HCB causes cancer and affects a
wide range of organ systems including the liver, lungs, kidneys,
thyroid, reproductive tissues and nervous and immune systems.
c) Clinical toxicity, including porphyria cutanea tarda in children
and adults, and mortality in nursing infants, has been observed
in humans with high accidental exposure.
d) Various measures are warranted to reduce the environmental burden
of HCB.
e) The following health-based guidance values for the total daily
intake (TDI) of HCB in humans have been suggested: for non-cancer
effects, 0.17 µg/kg body weight/day; for neoplastic effects,
0.16 µg/kg body weight/day.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS
2.1 Identity
Hexachlorobenzene (HCB) is a chlorinated aromatic hydrocarbon
with the chemical formula C6Cl6. Its CAS registry number is 118-74-1.
Synonyms: perchlorobenzene, pentachlorophenyl chloride, phenyl
perchloryl
Trade names: Amatin, Anticarie, Bunt Cure, Bunt-No-More, Co-op Hexa,
Granox NM, Julin's Carbon Chloride, No Bunt, No Bunt
40, No Bunt 80, No Bunt Liquid, Sanocide, Smut-Go,
Snieciotox, HexaCB
2.2 Physical and chemical properties
Some physical and chemical properties of HCB are listed in
Table 1. At ambient temperature, HCB is a white crystalline that is
virtually insoluble in water, but is soluble in ether, benzene and
chloroform (NTP, 1994). It has a high octanol/water partition
coefficient, low vapour pressure, moderate Henry's Law constant and
low flammability. Technical grade HCB is available as a wettable
powder, liquid and dust (NTP, 1994). Technical grade HCB contains
about 98% HCB, 1.8% pentachlorobenzene and 0.2% 1,2,4,5-
tetrachlorobenzene (IARC, 1979), and it is known to contain a variety
of impurities, including hepta- and octachlorodibenzofurans,
octachlorodibenzo- p-dioxin and decachlorobiphenyl (Villanueva et
al., 1974; Goldstein et al., 1978).
Table 1. Physical and chemical properties of hexachlorobenzenea
Property Value
Relative molecular mass 284.79
Melting point (°C) 230
Boiling point (°C) 322 (sublimates)
Density (g/cm3 at 20°C 1.5691
Vapour pressure 0.0023
(Pa at 25°C)
Log octanol/water partition coefficient 5.5
Water solubility 0.005
(mg/litre at 25°C)
Henry's Law Constant (caluclated)b 131
(Pa/mol per m3)
Conversion factors 1 ppm = 11.8 mg/m3
1 mg/m3 = 0.08 ppm
a From ATSDR (1990); Mackay et al. (1992)
b The Henry's Law Constant has been calculated using the
tabled values for aqueous solubility and vapour pressure
2.3 Analytical methods
Analytical methods for the determination of HCB in environmental
samples and biological tissues vary depending upon the matrix and
representative methods for various matrices, and are summarized in
Tables 2 and 3.
Table 2. Analytical methods for determining hexachlorobenzene in environmental samplesa
Sample Sample preparation Analytical Sample Recovery Reference
matrix methodb detection
limit
Water Extract with dichloromethane, GC/ECD 0.05 mg/kg 95 ± 10-20% US EPA (1982)
exchange to hexane,
concentrate; Florisil column
chromatography as a clean-up
Water Extract with dichloromethane GC/MS 1.9 mg/kg No data US EPA (1982)
at pH 11 and 2, concentrate
Air Glass fibre filter and XAD2 HRGC/ 0.18 pg/m3 >99% Hippelein et al. (1993)
traps separated by a PUF LRMS
disk; extraction with toluene
Air Polyurethane foam (PUF) GC/ECD <0.1 µg/m3 94.5±8% Lewis & MacLeod (1982)
sampling cartridge, extraction
with diethyl ether in hexane
Air Polyurethane foam (PUF) GC/ECD low pg/m3 93±1.1% Oehme & Stray (1982)
plugs, extraction with hexane, range (not
fractionation by HPLC specified)
Air Porous polyurethane foam GC/ECD No data Tenax more Billings &
(PUF), or Tenax-GC resin; effective Bidleman (1980)
filters refluxed with than PUF in
dichloromethane and retaining HCB
chlorinated solvents removed
and refluxed with hexane;
clean-up by alumina
chromatography
Table 2 contd.
Sample Sample preparation Analytical Sample Recovery Reference
matrix methodb detection
limit
Air Adsorb on Amberlite XAD-2 GC/PID 0.014 mg/m3 approx Langhorst &
resin separated by a silanized 95 ± 12% Nestrick (1979)
glass wool plug, desorption
with carbon tetrachloride.
Air Trace Atmospheric Gas Analyser approx No data Thomson et al. (1980)
using negative atmospheric 0.35 µg/m3
pressure chemical ionization
for trace gas analysis;
collection from ambient air and
transfer into a carrier of CO2
for analysis
Soil, Hexane extraction GC/ECD 10 mg/kg 78±2.6% to DeLeon et al. (1980)
chemical 96.5±3.6%
waste
disposal
site samples
Soil Extract with dichloromethane GC/MS 18 mg/kg No data US EPA (1986b)
5 mg/kg
Sediment Solvent extraction subjected GC/MS 46% Lopez-Avila et al.
to acid-base fractionation; (1983)
base/neutral fraction subjected
to silica gel chromatography
Table 2 contd.
Sample Sample preparation Analytical Sample Recovery Reference
matrix methodb detection
limit
Wastes, Extract with dichloromethane GC/MS 190 mg/kg No data US EPA (1986b)
non-water 50 mg/kg
miscible
Wastes, soil Extract with dichloromethane GC/MS 20 µg/litrec No data US EPA (1986b)
a Portions of the table were taken from ATSDR (1990)
b GC = gas chromatography; ECD = electron capture detector; MS = mass spectrometry; PID = photoionization detector;
HRGC = high-resolution gas chromatography; LRMS = low-resolution mass spectrometry
c Identification limit; detection limits for actual samples are several orders of magnitude higher depending upon the
sample matrix and extraction procedure employed.
Table 3. Analytical methods for determining hexachlorobenzene in biological materials
Sample Sample preparation Analytical Sample Recovery Reference
matrix method detection
limit
Fish tissue Grind with sodium sulfate, extract GC/ECD approx No data Oliver & Nicol (1982)
with hexane/acetone, clean-up by 0.05 µg/kg
Na2SO4/Alumina/silica gel/Florisil
column followed by a H2SO4 column
on silica gel
Fish tissue Extraction with hexane/isopropanol, GC/ECD No data No data Lunde & Ofstad (1976)
solvent and sulfuric acid
partitioning
Fish tissue Sulfuric acid digestion, silica gel GC/ECD 10-15 µg/kg 93% Lamparski et al. (1980)
column chromatography, methylation,
alumina column chromatography
Oyster Extraction with acetone/acetonitrile, GC/ECD No data No data Murray et al. (1980)
tissue partitioning into petroleum ether,
silica gel chromatography
Adipose Extraction with hexane, subjected GC/ECD No data 87.4-92.6% Watts et al. (1980)
tissue to Florisil clean-up and one-fraction
(chicken) elution
Adipose Extraction (solvent not specified), HRGC/MS 12 µg/kg No data Stanley (1986)
tissue bulk lipid removal, Florisil
fractionation
Adipose Extraction with benzene/acetone, GC/ECD 0.12 µg/kg 79-95% Mes (1992)
tissue Florisil fractionation
Table 3 contd.
Sample Sample preparation Analytical Sample Recovery Reference
matrix method detection
limit
Blood/urine Extraction with carbon tetrachloride, GC/PID 4.1 µg/kg 83% Langhorst &
silica gel column chromatography, (urine) Nestrick (1979)
concentrate 16 µg/kg
(blood)
Blood Extraction with hexane, concentrate GC/ECD No data No data US EPA (1980)
Blood Extraction with hexane/isopropanol GC/ECD No data No data Lunde & Bjorseth (1977)
Breast milk Extraction with acetone/benzene, GC/ECD 33 µg/kg 70-82% Mes et al. (1993)
Florisil fractionation
GC = gas chromatography; ECD = electron capture detector; PID = photoionization detector; HRGC = high-resolution gas
chromatography; MS = mass spectrometry
3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE
3.1 Sources, uses and production processes
Industrial synthesis of HCB may be achieved through the
chlorination of benzene at 150-200°C using a ferric chloride catalyst
or from the distillation of residues from the production of
tetrachloroethylene (US EPA, 1985a). HCB may also be synthesized by
refluxing hexachlorocyclohexane isomers with sulfuryl chloride or
chlorosulfonic acid in the presence of a ferric chloride or aluminum
catalyst (Brooks & Hunt, 1984).
Historically, HCB had many uses in industry and agriculture. The
major agricultural application for HCB used to be as a seed dressing
for crops such as wheat, barley, oats and rye to prevent growth of
fungi. The use of HCB in such applications was discontinued in many
countries in the 1970s owing to concerns about adverse effects on the
environment and human health. HCB may continue to be used for this
purpose in some countries; for example, HCB was still used in 1986 as
a fungicide, seed-dressing and scabicide in sheep in Tunisia (Jemaa et
al., 1986). However, it is uncertain as to whether HCB is still used
for this purpose.
In industry, HCB has been used directly in the manufacture of
pyrotechnics, tracer bullets and as a fluxing agent in the manufacture
of aluminum. HCB has also been used as a wood-preserving agent, a
porosity-control agent in the manufacture of graphite anodes, and as a
peptizing agent in the production of nitroso and styrene rubber for
tyres (Mumma & Lawless, 1975). It is likely that some of these
applications have been discontinued, although no information is
available.
Although HCB production has ceased in most countries, it is still
being generated inadvertently as a by-product and/or impurity in
several chemical processes. HCB is formed as a reaction by-product of
thermal chlorination, oxychlorination, and pyrolysis operations in the
manufacture of chlorinated solvents (mainly carbon tetrachloride,
trichloroethylene and tetrachloroethylene) (Government of Canada,
1993). The concentrations of HCB in distillation bottoms was estimated
to be 25%, 15% and 5%, respectively, for tetrachloroethylene, carbon
tetrachloride and trichloroethylene (Jacoff et al., 1986). While HCB
could potentially also be a contaminant in the final product, it was
not detected (detection limit 5 mg/litre) in carbon tetrachloride and
tetrachloroethylene in an investigation in Canada (personal
communication to Health Canada by Mr John Schultiess, Dow Chemical
Canada Inc., 1991). Analysis of production lots of tri- and
tetrachloroethylene produced in Europe in 1996 failed to detect HCB at
a detection limit of 2 µg/litre solvent (personal communication to the
IPCS by Mr C. de Rooij, Solvay Corporation Europe, 1996).
HCB is also generated as a waste by-product during the
manufacture of chlorinated solvents, chlorinated aromatics and
pesticides (Jacoff et al., 1986). The waste streams from the
production of pentachloronitrobenzene (PCNB), chlorothalonil and
dacthal are expected to contribute the bulk of HCB released from the
pesticide industry (Brooks & Hunt, 1984), although HCB can also be
generated as a waste by-product from the production of
pentachlorophenol, atrazine, simazine, propazine and maleic hydrazide
(Quinlivan et al., 1975; Mumma & Lawless, 1975). These pesticides are
also known to contain HCB as an impurity in the final product, usually
at levels of less than 1% HCB when appropriate procedures are used for
the synthesis and purification stages (Tobin, 1986). When such
procedures are not met, the level of HCB could be much higher (e.g.,
pentachloronitrobenzene has been reported to contain 1.8-11% HCB
(Tobin, 1986)). However, owing to many voluntary and regulatory
pressures, it is unlikely that such high levels of HCB are present in
today's pesticide formulations, but no information is available to
substantiate this point.
The chlor-alkali industry produces chlorine (Cl2), hydrogen and
caustic soda (NaOH) by electrolysis of purified and concentrated
sodium chloride (NaCl). Processes using graphite anodes are known to
produce HCB as a by-product (Quinlivan et al., 1975; Mumma & Lawless,
1975; Alves & Chevalier, 1980) owing to the reaction of chlorine with
graphite anode materials such as carbon and oils. Depending on the
purification procedures, the final products might also be contaminated
with HCB. In some countries, graphite anodes have been replaced by
dimensionally stabilized anodes (DSA), which do not generate HCB
(Government of Canada, 1993).
Incineration is an important source of HCB in the environment.
Emission levels from incinerators are very site-specific, and
therefore generic levels are difficult to estimate. Earlier
information yielded a crude estimate of the total HCB released from
all municipal incinerators in the USA to be 57-454 kg/year (US EPA,
1986a), but levels currently emitted are not known.
3.2 World production levels
Few recent data on the quantities of HCB produced are available.
Worldwide production of pure HCB was estimated to be 10 000
tonnes/year for the years 1978-1981 (Rippen & Frank, 1986). An
estimated 300 tonnes was produced by three manufacturers in the USA in
1973 (IARC, 1979). HCB was produced/imported in the European Community
at 8000 tonnes/year in 1978 (Rippen & Frank, 1986), and a company in
Spain used to produce an estimated 150 tonnes of HCB annually (IARC,
1979). Approximately 1500 tonnes of HCB were manufactured annually in
Germany for the production of the rubber auxiliary PCTP (BUA, 1994),
but this production was discontinued in 1993. No further centres of
HCB manufacture in Europe or North America have been identified.
Production of HCB has declined as a result of restrictions on its use
starting in the 1970s.
Considerable amounts of HCB are inadvertently produced as a by-
product in the manufacture of chlorinated solvents, chlorinated
aromatics and chlorinated pesticides. Jacoff et al. (1986) estimated
that approximately 4130 tonnes of HCB are generated annually as a
waste product in the USA and that nearly 77% of this is produced from
the manufacture of three chlorinated solvents: carbon tetrachloride,
trichloroethylene and tetrachloroethylene. The remainder is produced
by the chlorinated pesticide industry. In 1977, about 300 tonnes of
HCB were generated in Japan as a waste by-product in the production of
tetrachloroethylene, almost all of which was incinerated (IARC, 1979).
It was estimated that >5000 tonnes HCB/year were produced as a by-
product during tetrachloroethylene production in the Federal Republic
of Germany in 1980 (Rippen & Frank, 1986). However, recent estimates
for Europe from ECSA (European Chlorinated Solvent Association; P.G.
Johnson (1996) personal communication to IPCS) indicate that up to
4000 tonnes/year of HCB are produced as a by-product during certain
tetrachloroethylene production processes and that over 99% of this by-
product was incinerated at high temperatures.
3.3 Entry into the environment
Currently, the principal sources of HCB in the environment are
estimated to be the manufacture of chlorinated solvents, the
manufacture and application of HCB-contaminated pesticides, and
inadequate incineration of chlorine-containing wastes. It should be
noted that only a small fraction of the HCB generated as a by-product
may be released, depending on the process technology and waste-
disposal practices employed. For example, according to the US Toxic
Chemical Release Inventory (TRI), releases of HCB from the ten largest
processing facilities were 460 kg, most of this to air, compared with
almost 542 000 kg transferred offsite as waste. The TRI data are not
comprehensive, since only certain types of facilities are required to
report (ATSDR, 1994). ECSA (P.G. Johnson, personal communication to
IPCS) estimated that European emissions of HCB were about 200 kg/year
in 1993.
As discussed in the previous section, HCB is a contaminant of a
number of chlorinated pesticides. Since most current applications for
these products are dispersive, most HCB from this source will be
released to the environment.
Substantial quantities of HCB are also contained in the wastes
generated through the manufacture of chlorinated solvents and
pesticides. In the mid-1980s in the USA, 81% of these HCB-containing
wastes were disposed of by incineration, compared to 19% via
landfilling (Jacoff et al., 1986). It is likely that the amount of HCB
wastes disposed of by incineration has since increased, although
information has not been found to confirm this point. HCB can be
emitted from incinerators as a result of incomplete thermal
decomposition of these wastes and as a product of incomplete
combustion (PIC) from the thermal decomposition of a variety of
chlorinated organics such as Kepone, mirex, chlorobenzenes,
polychlorinated biphenyls, pentachlorophenol, polyvinyl chloride and
mixtures of chlorinated solvents (Ahling et al., 1978; Dellinger et
al., 1991).
Although only a small proportion of the HCB-containing waste
generated in the USA is landfilled, HCB may continue to leach to
groundwater from previously landfilled HCB waste sites. The
contribution of this route is uncertain, although HCB is not easily
leached, and landfills containing HCB are now designed to prevent
leachate losses into adjacent water systems (Brooks & Hunt, 1984). HCB
emission into the atmosphere from landfills containing HCB wastes
occurs from slow volatilization and from displacement of the
contaminated soil (Brooks & Hunt, 1984).
HCB has been detected in emissions from a number of industries,
including paint manufacturers, coal and steel producers, pulp and
paper mills, textile mills, pyrotechnics producers, aluminum smelters,
soap producers and wood-preservation facilities (Quinlivan et al.,
1975; Gilbertson, 1979; Alves & Chevalier, 1980), probably reflecting
the use of products contaminated with HCB. Municipal and industrial
wastewater facilities may also discharge HCB-contaminated effluents
(Environment Canada/Ontario Ministry of the Environment, 1986; King &
Sherbin, 1986), probably owing to inputs from industrial sources.
Long-range transport plays a significant role as a means of
redistribution of HCB throughout the environment. Wet deposition
(deposition via rain or snowfall) is the primary mechanism for
transport of HCB from the atmosphere to aquatic and terrestrial
systems in Canada (Eisenreich & Strachan, 1992). For example, it is
estimated that long-range transport and total deposition to the
Canadian environment is approximately 510 kg/year, an amount that is
similar to that from all other sources combined (Government of Canada,
1993).
4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION
4.1 Environmental transport and degradation
HCB is distributed throughout the environment because it is
mobile and resistant to degradation. Volatilization from water to air
and sedimentation following adsorption to suspended particulates are
the major removal processes from water (Oliver, 1984a; Oliver &
Charlton, 1984). Once in the sediments, HCB will tend to accumulate
and become trapped by overlying sediments (Oliver & Nicol, 1982).
Although HCB is not readily leached from soils and sediments, some
desorption does occur and may be a continuous source of HCB to the
environment, even if inputs to the system cease (Oliver, 1984a; Oliver
et al., 1989). Chemical or biological degradation is not considered to
be important for the removal of HCB from water or sediments (Callahan
et al., 1979; Mansour et al., 1986; Mill & Haag, 1986; Oliver & Carey,
1986). In the troposphere, HCB is transported over long distances by
virtue of its persistence, but does undergo slow photolytic
degradation (the half-life is approximately 80 days; Mill & Haag,
1986), or is removed from the air phase via atmospheric deposition to
water and soil (Bidleman et al., 1986; Ballschmiter & Wittlinger,
1991; Lane et al., 1992a, 1992b). In soil, volatilization is the major
removal process at the surface (Kilzer et al., 1979; Griffin & Chou,
1981; Schwarzenbach et al., 1983; Nash & Gish, 1989), while slow
aerobic (half-life of 2.7-5.7 years) and anaerobic biodegradation
(half-life of 10.6-22.9 years) are the major removal processes at
lower depths (Beck & Hansen, 1974; Howard et al., 1991).
4.2 Bioaccumulation and biomagnification
The bioaccumulative properties of HCB result from the combination
of its physicochemical properties (high octanol/water partition
coefficient) and its slow elimination due to limited metabolism
related to its high chemical stability. Organisms generally accumulate
HCB from water and from food, although benthic organisms may also
accumulate HCB directly from sediment (Oliver, 1984b; Knezovich &
Harrison, 1988; Gobas et al., 1989). The uptake of HCB in benthic
invertebrates has been investigated in a number of laboratory and
field studies. The results demonstrated that some HCB in sediments is
available to infaunal species. Reported bioaccumulation factorsa
(BAF) for invertebrates in HCB-containing sediments range from 0.04 to
0.58 in high-organic-content sediment to 1.95 in low-organic-content
a Defined as tissue concentration (wet weight) divided by sediment
concentration (dry weight). BAFs from Oliver (1984b) were divided
by 6.67 to convert tissue dry weight to wet weight.
sediment (Oliver, 1984b; Knezovich & Harrison, 1988; Gobas et al.,
1989). The bioavailability of sediment-bound HCB is inversely related
to sediment organic carbon content (Knezovich & Harrison, 1988), and
varies with the type and size of the organisms and their feeding
habits (Boese et al., 1990), the extent of contact with sediment pore
and interstitial waters (Landrum, 1989), and the surface area of the
substrate (Swindoll & Applehans, 1987). Landrum (1989) suggested that
the bioavailability of sediment-sorbed chemicals declines as the
contact time between the sediment and a contaminant increases. For
example, Schuytema et al., (1990) observed that addition of HCB-spiked
sediments did not result in a significant increase in the uptake of
HCB by the worm ( Lumbriculus variegatus), amphipods ( Hyalella
azteca and Gammarus lacustris), and fathead minnows ( Pimephales
promelas) in a laboratory recirculating water/sediment system.
However, there was a substantial increase of HCB levels in bed
sediment, suggesting that sediment served as a more effective sink for
HCB than the organisms.
The biomagnification factor (BMF) for HCB in the earthworm
Eisenia andrei after exposure via food was 0.068 on a wet weight
basis (0.071 on a lipid basis) (Belfroid et al., 1994a), the biota
lipid-to-soil accumulation factor, defined as the ratio of the
concentration in the animal to that on the soil, was 215 g soil dry
weight/g lipid (Belfroid et al., 1994b), and the bioconcentration
factors (BCFs) for earthworms kept in water were found to be between
48 × 104 and 62 × 104 ml water/g lipid (Belfroid et al., 1993).
Field studies indicate that exposure via food is important for
organisms at higher trophic levels, as significant biomagnification
has been observed in several studies in natural aquatic ecosystems. In
Lake Ontario, Oliver & Niimi (1988) observed that tissue residue
concentrations increased from plankton (mean = 1.6 ng/g wet weight) to
mysids (mean = 4.0 ng/g wet weight) to alewives (mean = 20 ng/g wet
weight) to salmonids (mean = 38 ng/g wet weight). Braune & Norstrom
(1989) used field data on body burdens of HCB in the herring gull
( Larus argentatus) and one of its principal food items, the alewife
( Alosa pseudoharengus) in a Great Lakes food chain to calculate a
biomagnification factor (whole body, wet weight basis) of 31.
5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
5.1 Environmental levels
HCB has been detected in air, water, sediment, soil and biota.
Representative levels reported in various environmental media in many
countries are presented in Tables 4, 5 and 6.
5.1.1 Air
HCB is widely dispersed in ambient air, and is generally present
at low concentrations. Mean concentrations of HCB in air removed from
point sources in Canada, Norway, Sweden, Germany, the USA, the Arctic
and the Antarctic range from 0.04 to 0.6 ng/m3 (Table 4). Levels of
HCB in air are generally similar between urban, rural and remote
sites, reflecting the persistence and long-range transport of this
substance.
Airborne concentrations of HCB measured in the USA near nine
chlorinated solvent and pesticide plants in 1973 and 1976 were much
higher than background levels (Spigarelli et al., 1986).
Concentrations as high as 24 µg/m3 were detected in the immediate
vicinity of one plant, while the maximum concentration of HCB distant
from the site was 0.36 µg/m3. The highest levels were associated with
the production of perchloroethylene, trichloroethylene and carbon
tetrachloride, and with plants where onsite landfill and open pit
waste disposal were practiced. More recently, Grimalt et al. (1994)
reported that airborne concentrations of HCB in a community in the
vicinity of a organochlorine factory built in 1898 in Catalonia,
Spain, averaged 35 ng/m3, compared with 0.3 ng/m3 in Barcelona, the
reference community for this study. It is not known how representative
the data from these studies are, as HCB releases are expected to be
minimized from industries using appropriate modern technology and
waste management practices.
No data are available on the levels of HCB in indoor air.
Table 4. Levels of hexachlorobenzene in ambient air (ng/m3)
Location Year Detection Mean Rangea Reference
limit
Canada (Windsor, Ontario) 1987-1990 0.03 0.13 ND-0.44 Environment Canada (1992)
Canada (Ontario)
- industrial/urban areas 1985-1989 0.007 0.167 0.07-0.31 Lane et al. (1992b)
- rural areas 0.094 0.02-0.31
Canada (Egbert, Ontario) 1988-1989 - >0.054 0.00004-0.64 Hoff et al. (1992)
Canada (Walpole Island) 1988-1989 0.02 0.15 ND-0.34 Environment Canada (1992)
Canadian High Arctic 1987 0.15 ND-0.154 Patton et al. (1989)
(Beaufort Sea)
Bear Island (Arctic)
- summer
- winter 0.001 0.04 0.029-0.045 Oehme & Stray (1982)
0.001 0.111 0.059-0.188
Southern Ocean and 1990 0.06 0.04-0.078 Bidleman et al. (1993)
Antarctica
Enewetak Atoll 1979 0.10 0.095-0.13 Atlas & Giam (1981)
(Pacific Ocean)
Spitzbergen
- summer 0.001 0.071 0.05-0.085 Oehme & Stray (1982)
- winter 0.001 0.086 0.071-0.095
Table 4 contd.
Location Year Detection Mean Rangea Reference
limit
Germany (Hamburg - 1986-1987 0.6 0.3-2.5 Bruckmann et al. (1988)
residential, suburban
and industrial sites)
South Germany 1986-1990 0.21 0.058-0.52 Morosini et al. (1993)
Norway (Lillestrom) 0.001 0.162 0.055-0.234 Oehme & Stray (1982)
Sweden (Aspvreten) 1984 0.067 0.054->0.165 Bidleman et al. (1987)
Sweden (Stockholm) 1983-1985 0.07 0.054->0.130 Bidleman et al. (1987)
Spain
- (near organochlorine 1989 & 1992 - 35 11-44 Grimalt et al. (1994)
compounds factory)
- hospital in Barcelona - 0.3 0.25-0.4
USA (Portland, Oregon) 1984 0.075 0.05-0.11 Ligocki et al. (1985)
USA - chemical production ND-24000 Spigarelli et al. (1986)
plants
USA - urban areas 1975-1979 0.1 0.5 ND-4.4 Carey et al. (1985)
a ND = not detected
5.1.2 Water
Levels of HCB in freshwater in Europe and North America are
generally below 1 ng/litre (Table 5), although higher values have been
reported in aquatic systems that receive industrial discharges and
surface run-off. In the connecting channels to the Great Lakes in
Canada, HCB levels were often found to exceed 1.0 ng/litre,
particularly near point sources. Levels in the St. Clair River near
the Dow Chemical outfall were as high as 87 ng/litre in 1985 and
75 ng/litre in 1986 (Oliver & Kaiser, 1986).
Mean concentrations of HCB in seawater rarely exceed 1 ng/litre
(Table 5) (Ernst, 1986; Burton & Bennett, 1987). In the Nueces Estuary
in Texas, USA, the highest level (0.61 ng/litre) was found near
sewage outfalls (Ray et al., 1983a). Higher concentrations (up to
196 ng/litre) were observed in the Forth Estuary in Scotland, near
domestic and chemical industry discharges (Rogers et al., 1989).
5.1.3 Soil
Data identified on levels of HCB in soil are quite limited and
are summarized in Table 6. The most extensive data are from the 1972
US National Soils Monitoring Program, in which the concentrations of a
variety of pesticides were determined at 1483 sites from 37 states
(Carey et al., 1979). HCB was detected at 11 sites, with a range of
concentrations in positive samples from 10 to 440 µg/kg dry weight. Of
24 samples of agricultural soil in British Columbia, Canada, where HCB
had last been applied as a seed treatment 10-15 years prior to the
survey, 6 had detectable HCB residues of between 1.3 and 2.2 ng/g dry
weight (Wilson & Wan, 1982).
Mean concentrations of HCB reported from uncontaminated soil in
Europe were found to range from 0.3 ng/g in Switzerland (Müller, 1982)
to 5.1 ng/g in a Swedish rural heathland soil (Thomas et al., 1985)
(it was not indicated whether concentrations were on a dry or wet
weight basis). Soil from a farming area in Italy contained 40 ng/g
(dry or wet weight basis not indicated) (Leoni & D'Arca, 1976). HCB
levels were not markedly increased by long-term application of sludge
to land in Germany at a rate of 50 to 500 tons per ha and averaged
2.8 ng/g (dry or wet weight basis not indicated) (Witte et al.,
1988a,b). Monitoring programmes in Germany yielded average levels of
HCB contamination of soil ranging from approximately 1 ng/g dry weight
in the North Rhine-Westphalia (1990) to approximately 6 ng/g dry
weight in Baden-Württemberg (1988) (BUA, 1994).
Table 5. Concentrations of hexachlorobenzene (ng/litre) in drinking-water and surface water
Location Year Detection Mean Rangea Reference
limit
Drinking-water
Canada (Ontario) 1980 0.01 0.1 0.06-0.2 Oliver & Nicol (1982)
Canada (Maritime Provinces) 1985-1988 2.0 ND Environment Canada (1989)
Croatia
- Sisak 1988-1989 0.5 1.0a <1-4 Fingler et al. (1992)
- Zagreb 2.0a 1-3
USA 1977-1981 100 ND US EPA (1985b)
Surface water
Canada
- Lake Superior 1986 0.007 0.026 0.018-0.040 Stevens & Neilson
- Lake Huron 0.033 0.018-0.073 (1989)
- Georgian Bay 0.041 0.032-0.054
- Lake Erie 0.078 0.025-0.260
- Lake Ontario 0.063 0.020-0.113
Canada-St. Clair River 1985 0.30-87 Oliver & Kaiser (1986)
- tributaries to 0.08-0.79
St. Clair R.
Table 5 contd.
Location Year Detection Mean Rangea Reference
limit
Canada (Atlantic Region); 1979-1989 2.0 ND-2.2 Leger 1991
lakes, streams, reservoirs,
estuaries, coastal waters
Germany (Elbe) 1990 - 12 3-62 BUA (1994)
Greece (Strimon River) 1985-1986 - 1.52 0.5-2.8 Kilikidis et al. (1992)
Italy (tributaries to
Adriatic Sea) 1977-1978 1.0 ND Galassi & Provini (1981)
Mediterranean Sea 1982-1983 0.1 2.13 ND-12.6 El-Dib & Badawy (1985)
Netherlands/Belgium 1993 10 <10 <10 RIWA (1993)
Netherlands 1987 - <10 ND-100 De Walle et al. (1995)
North Sea (coastal waters
and estuaries) 1979-1980 2.7 0.03-15 Ernst (1986)
Scotland (Forth Estuary) 1987 0.01 <0.01-196 Rogers et al. (1989)
Scotland (Forth Estuary) 1990 0.7-8.0 Harper et al. (1992)
Spain (Ebre Delta) 1985-1986 0.0005 0.041 ND-1.0 Grimalt et al. (1988)
USA (Texas-estuary) 1980 0.24 <0.01-0.61 Ray et al. (1983a)
USA (coastal, surface <0.1 <0.1-26 Cross et al. (1987)
microlayer)
a median value
Table 6. Levels of hexachlorobenzene in soil (ng/g dry weight)
Source Year Detection Mean Rangea Reference
limit
Canada (British Columbia) 1.0 Wilson & Wan (1982)
- agricultural soils <1.0-2.2
- near a former grain 260 ng/g
treatment plant
Czech/Polish Border - - 3.25 0.47-4.8 Holoubek et al. (1994)
(Giant Mountains)
Germany (contaminated soil) 1989 0.3-339 Hagenmaier et al. (1992)
India 1987 24a 0-165 Nair & Pillai (1989)
Italy (farming area) 1971-1972 40 Leoni & D'Arca (1976)
Netherlands - Ochten 1993 - 18 5.1-66 Hendriks et al. (1995)
- Gelderse Poort 80 73-89
Netherlands 1987 - <10 <80 De Walle et al. (1995)
Sweden 5.1 Thomas et al. (1985)
USA 1968-1973 10-440 Carey et al. (1979)
USA (chemical plants) 0.002 ND-5 700 000 Spigarelli et al. (1986)
USA (hazardous waste sites) 1977-1978 20 000-400 000 Davis & Morgan (1986)
USA (5 locations near Love 0.1 1.04-5.6 0.15-26.3 Ding et al. (1992)
Canal)
a ng/g wet weight
Levels in soil are highest near industrial sources of HCB. Levels
as high as 12 600 ng/g dry weight were reported at one landfill site
in Canada (Wilson & Wan, 1982), and 570 µg/g (dry or wet weight not
indicated) on the grounds of a chlorinated solvent and pesticide
production plant in the USA (Spigarelli et al., 1986). Soils near a
former grain treatment plant in Canada contained 260 ng/g dry weight
of HCB (Wilson & Wan, 1982). Levels of HCB in soils from contaminated
floodplains in the Netherlands ranged from 5.1 to 89 ng/g dry weight
(Hendriks et al., 1995).
5.1.4 Sediment
HCB strongly sorbs to sediment and suspended matter, and
differences in the concentrations in the water as well as in the
composition of the sediments and suspended matter result in a wide
range of concentrations in this medium.
In sediment samples collected from 1979 to 1989 in the Atlantic
provinces of Canada, HCB was reported to be below the limit of
detection of 0.2 ng/g dry weight in 140 of 152 samples (Leger, 1991).
In surveys conducted from 1980 to 1983, HCB levels in sediments from
the Great Lakes ranged from 0.02 to 840 ng/g dry weight (Oliver &
Nicol, 1982; Fox et al., 1983; Kaminsky et al., 1983; Oliver &
Bourbonniere, 1985; Bourbonniere et al., 1986; Oliver et al., 1989;
IJC, 1989). Analyses of sediment cores from Lake Ontario indicated
that levels of HCB have declined from the 1960s to the early 1980s but
more recent data are not available to determine if this downward trend
has continued (Oliver & Nicol, 1982; Oliver et al., 1989). HCB levels
in sediment sampled from eight lakes in northern remote Canada (date
of sampling not specified) ranged from 0.09 to 1.80 ng/g dry weight
(Muir et al., 1995).
Levels as high as 5100 ng/g dry weight were detected in the Rhine
River in Baden-Württemberg, Germany, in 1986 (BUA, 1994). The majority
of sediment samples taken from the rivers Rhine and Elbe between 1980
and 1990 contained levels of HCB between 10 and 500 ng/g dry weight,
although levels below 1 ng/g dry weight were determined in some other
locations (BUA, 1994). A Nordic study on chlorinated compounds in the
Baltic, Kattegat and Skagerrak (œstfeldt et al., 1994) found HCB
concentrations in sediment ranging from 1 to 20 ng/g loi (loss on
ignition), the higher values occurring mainly in the Bothnian Bay. An
extreme value of 63 ng/g loi was found in Öresund between Denmark and
Sweden. Levels of HCB in sediment samples collected near effluent
discharges along a stream in Pakistan ranged from <0.05 to 94.5 ng/g
wet weight (Tehseen et al., 1994).
Higher levels of HCB in sediments were reported in studies
conducted near point sources. As much as 280 000 ng HCB/g dry weight
was detected in 1985 downstream of the Dow Chemical sewer discharges
in the St. Clair River, USA (Oliver & Pugsley, 1986).
5.1.5 Biota
HCB has been detected in invertebrates, fish, reptiles, birds and
mammals from around the world. Following the detection of HCB in
tissues of wild birds by De Vos in 1967, high residues were often
found in predatory birds, whereas minor quantities were detected in
fish, mussels and birds of the aquatic environment (Vos et al., 1968;
Koeman et al., 1969). Based on Canadian data from monitoring studies
in birds, HCB levels declined sharply from the mid-1970s (the earliest
data available) and into the early 1980s, after which they levelled
off (Noble & Elliott, 1986; Environment Canada/Department of Fisheries
and Oceans/Health and Welfare Canada, 1991).
Levels of HCB in freshwater mussels in the Great Lakes and
connecting channels have been found to range from 0.1 ng/g wet weight
to 24 ng/g wet weight (Kauss & Hamdy, 1985; Innes et al., 1988;
Muncaster et al., 1989). A similar range (4.4-26 ng/g wet weight) was
observed in benthic amphipods, the pelagic amphipod Pseudalibrotus
litoralis and brittle stars from the Beaufort Sea (Hargrave et al.,
1989). Lower levels (0.1-1.8 ng/g wet weight) were observed in mussels
( Mytilus galloprovincialis) from the Ebro Delta in the Western
Mediterranean, and these levels were observed to decline from 1980 to
1992 (Solé et al., 1994). Levels in marine species of clams and
oysters from the USA were reported in several studies to be < 1 ng/g
wet weight (Phelps et al., 1986; Eisenberg & Topping, 1984; Ray et
al., 1983b). Similarly, levels in invertebrates, including mussels
( Mytilus edulis), soft clams ( Mya arenaria), lugworms ( Arenicola
marina), and polychaetes ( Nereis diversicolor), were <1 ng/g
fresh weight in the German Wadden Sea (Ernst, 1986). Bjerk & Brevik
(1980) reported higher levels (50-350 ng/g wet weight) of HCB in crabs
( Carcinus maenas, Pagurus sp.), snails ( Littorina littorea),
brittle stars ( Ophiura albida) and sea stars ( Asteroidea) from the
contaminated Frierfjord in Norway, which receives discharge from
various industries located in the region, and HCB and related
compounds were reported to originate from one main source
(unspecified) in the area. œstfeldt et al. (1994) found that mussels
( Mytilus edulis) from the Baltic contain higher levels of HCB
(200-800 ng/g lipid weight) than mussels from Kattegat (11-20 ng/g
lipid weight).
In a 1981-1982 survey of HCB levels in fish from watersheds in
Eastern Canada, whole body concentrations in brook trout ( Salvelinus
fontinalis) and yellow perch ( Perca flavescens) ranged from below
the limit of detection (4.2 ng/g in 1981; 0.2 ng/g in 1982) to 54 ng/g
for trout and 15 ng/g wet weight for perch (Peterson & Ray, 1987).
Relatively high body burdens of HCB have been observed in fish in Lake
Ontario and connecting channels. HCB was not detected (ND) in juvenile
spottail shiners ( Notropis hudsonius) from Lakes Superior and Erie
(detection level = 1 ng/g wet weight) (Suns et al., 1983; Environment
Canada/Department of Fisheries and Oceans/Health and Welfare Canada,
1991), while mean body burdens in shiners in Lake Ontario ranged from
ND to 13 ng/g wet weight, and those in the Detroit, Niagara, and
St Clair rivers averaged 5 ng/g wet weight, ND to 8 ng/g wet weight,
and 231 ng/g wet weight, respectively (Suns et al., 1985). Mean
concentrations of HCB in the muscle tissue of various species of
salmonids from Lake Ontario ranged from 5 to 37 ng/g wet weight (Niimi
& Oliver, 1989).
Levels of HCB measured in whole fish species taken from major
rivers and lakes in the USA (including known contaminated areas)
ranged from <2 to 913 ng/g wet weight (Kuehl et al., 1983; DeVault,
1985; Schmitt et al., 1990; Kuehl & Butterworth, 1994). Levels in
roach ( Rutilus rutilus L.) and perch ( Perca fluviatilis L.) from
the "moderately polluted" Lahn River in Germany ranged from ND to
233 ng/g wet weight, with a mean of 1 ng/g (Schuler et al., 1985).
Concentrations of HCB in the whole bodies of carp ( Cyprinus carpio)
from the mouth of tributaries to Lake Ontario and the Niagara River
ranged from 52 to 1600 ng/g on a lipid basis (6.7 to 205 ng/g on a
fresh weight basis). The highest values were measured near hazardous
waste dumps and industrial facilities (as high as 1600 ng/g fat)
(Jaffe & Hites, 1986). Brunn & Manz (1982) reported a mean whole-body
concentration of HCB in fish (mainly trout) from inland rivers,
streams, and ponds in Germany of 5 ng/g wet weight. The highest levels
were recorded from fish caught in rivers.
HCB levels in seawater are generally lower than those in
freshwater, resulting in lower levels in edible parts of marine fish.
In fish taken from the North Sea (species not reported), HCB levels in
fish muscle tissues averaged 0.3-0.4 ng/g wet weight, with a maximum
of 0.8 ng/g (Ernst, 1986). HCB concentrations in livers averaged
42 ng/g wet weight for cod ( Gadus morhua) and 4 ng/g (range of
0.2-14 ng/g) for flounder ( Platichthis flesus). These levels were
comparable to levels measured in fish near the coast of southwest
Greenland and in the North Atlantic Ocean. Livers of cod from the
coast of southwest Greenland contained 32.4 ng/g on average, and those
of hake ( Merluccius merluccius) from the North Atlantic Ocean
averaged 40.5 ng/g) (Ernst, 1986). Levels of HCB were below the
determination limit (DL) in cod liver (DL = 5 ng/g) and herring muscle
(DL = 1 ng/g) of fish from the Clyde Sea near Scotland (Kelly &
Campbell, 1994). Cod from the Firth of Forth had mean liver levels of
38.7 ng/g wet weight, and levels in herring muscle of 2.0 and 2.3 ng/g
wet weight were observed in fish from the Firth of Forth and North
Sea, respectively (Kelly & Campbell, 1994). In surveillance monitoring
of contaminants in fish from coastal waters near England and Wales,
concentrations of HCB in livers of cod ( Gadus morhua), whiting
( Merlangius merlangus), dab ( Limanda limanda) and flounder
( Platichthys flesus) were 2-290, 5-230, 3-55 and 1-52 ng/g,
respectively (all results on a wet tissue weight basis) (MAFF/HSE,
1994). Levels of HCB in muscle tissues of herring ( Clupea harengus)
from the Baltic Sea ranged from <1 to 39 ng/g (Hansen et al., 1985);
concentrations in whitefish ( Coregonus lavaretus) and trout ( Salmo
trutta) ranged from <1 to 9 ng/g fresh weight in a 1992 survey
(Atuma et al., 1993).
Fish taken from the contaminated waters of the Frierfjord in
Norway contained mean concentrations of HCB in liver of 11 600 ng/g
for saithe ( Pollachius virens), and 16 800 ng/g for cod ( Gadus
morhua) (Bjerk & Brevik, 1980). Levels of HCB from fish taken from
the uncontaminated Sogndalfjord were much lower, averaging 18 ng/g wet
weight in livers of cod ( Gadus morhua), 8 ng/g in haddock
( Melanogrammus aeglefinus) and 1 ng/g in lemon sole ( Microstomus
kitt) and flounder ( Platichthys flesus) (Skåre et al., 1985).
Flounder ( Platichthis flesus) taken from the Elbe Estuary in
Germany, downstream from Hamburg (a highly industrialized area),
contained mean levels of HCB in muscle of 688 ng/g (range 84-1907 ng/g
wet weight). Further downstream, towards the mouth of the river,
levels were lower, averaging 12.5 ng/g (range 2-32 ng/g) (Kohler et
al., 1986).
The mean level of HCB in 15 snapping turtle eggs from Ontario,
Canada was 27.1 ng/g wet weight (Bishop et al., 1995).
The levels of HCB in birds have been similar across the various
regions of Canada since the 1980s, probably as a combined result of
emission reductions and the long-range transport of HCB to remote
locations. Mean concentrations of HCB in herring gull eggs ( Larus
argentatus) in 1991 ranged from 16 to 71 ng/g wet weight at various
colonies in the Great Lakes, and were relatively uniform across lakes
(Environment Canada/Department of Fisheries and Oceans/Health and
Welfare Canada, 1991). These levels were approximately an order of
magnitude lower than in 1974. The mean level of HCB in herring gull
eggs from Norwegian coastal waters in 1981 was 120 ng/g wet weight
(Moksnes & Norheim, 1986). In a study from the Netherlands, mean
levels in eggs of common terns collected in 1987 were 0.03 µg/g wet
weight and in those of black-headed gulls collected in 1988 were
93 µg/g fat (Stronkhorst et al., 1993). Levels of HCB found in eggs of
sea-bird species ( Haematopus ostralegus, Larus ridibundus, Larus
argentatus and Sterna hirundo) from the banks of a river near an
organochlorine chemical plant in Germany were < 500 ng/g wet weight
(Heidmann, 1986); mean levels of less than 15 ng/g wet weight were
found in eggs of several species of land birds, including rooks
( Corvus frugilerus) and sparrow hawks ( Accipiter nisus) from
agricultural, industrial and rural sites. Recent surveys have
indicated similar levels of HCB in the eggs of five other predatory
bird species across Canada (means ranged from 10 to 53 ng/g wet
weight) (Noble & Elliott, 1986; Pearce et al., 1989; Noble et al.,
1992). However, the mean level of HCB in peregrine falcon ( Falco
peregrinus) eggs collected across Canada from 1980 to 1987 was
279 ng/g wet weight, and concentrations ranged as high as 1060 ng/g
wet weight (Peakall et al., 1990).
HCB has been found to accumulate in lipids of the common
goldeneye duck ( Bucephala clangula) that overwinter in the Niagara
River (mean of 150 ng/g) (Foley & Batcheller, 1988) and the Detroit
River (mean of 1700 ng/g) (Smith et al., 1985a) in the USA. Goldeneye
wintering in the Baltic Sea contained average levels of 250 ng/g lipid
(Falandysz & Szefer, 1982). Levels of HCB in the livers of silver
seagulls taken from estuaries in Germany were lower in 1988 than 1989
(approximately 80 and 150 ng/g fat, respectively, in samples from the
River Ems estuary). Higher levels were observed for both years in
liver samples of birds taken from the River Elbe estuary (>250 ng/g
fat) (BUA 1994).
In breast muscle tissue samples from various species of birds,
HCB concentrations tend to be progressively greater at higher trophic
levels (i.e., piscivores > molluscivores > omnivores > grazers)
(Environment Canada/Department of Fisheries and Oceans/Health and
Welfare Canada, 1991).
In the blubber of marine mammals in the Canadian Arctic, mean
levels of HCB were 19 ng/g wet weight for ringed seals ( Phoca
hispida) and 491 ng/g wet weight for beluga whales ( Delphinapterus
leucas) (Norstrom et al., 1990), while male belugas sampled in the
Gulf of St. Lawrence contained up to 1340 ng/g (Béland et al., 1991).
Blubber from male and female white-beaked dolphins ( Lagerorhunchus
albirostris) collected near the Newfoundland coast averaged
1110 ng/g and 880 ng/g wet weight, respectively. Lower levels
(290 ng/g and 100 ng/g wet weight) were observed in blubber from male
and female pilot whales ( Globicephala meleana), also collected near
the Newfoundland coast (Muir et al., 1988). The higher levels observed
in the dolphins may reflect greater exposure to HCB because of
overwintering and feeding in the Gulf of St. Lawrence. Blubber of
harbour porpoises ( Phocoena phocoena) collected in Poland between
1989 and 1990 contained an average of 573 ng/g wet weight (Kannan et
al., 1993), and those collected around the coast of Scotland between
1989 and 1991 contained an average of 263 ng/g (Wells et al., 1994).
Levels of HCB in the blubber of bottlenosed dolphins also collected
off the coast of Scotland contained an average of 276 ng/g (Wells et
al., 1994). Levels in the blubber of three species of dolphins from
the Bay of Bengal, southern India, were low, ranging from 1.1 to
13 ng/g wet weight (Tanabe et al., 1993). Harbour seals ( Phoca
vitulina) found sick or dead in Norwegian waters due to a disease
outbreak caused by a morbilli virus had a mean HCB level in the
blubber of 27 ng/g wet weight (range of 5-94 ng/g) (Skaare et al.,
1990).
Limited data were found on levels of HCB in terrestrial mammals.
In a 1973-1974 survey of HCB in the adipose tissue of fox ( Vulpes
vulpes), doe ( Capreolus capreolus) and wild boar ( Sus scrofa) in
Germany, HCB concentrations ranged from <10 to 3110 ng/g. The lowest
levels were observed in the does, presumably because they are
herbivorous, whereas foxes and wild boar feed on small animals and are
therefore more affected by biomagnification of HCB (Koss & Manz,
1976). Similar patterns were evident in a study from Sweden, in which
rabbits ( Oryctolagus cuniculus, muscle), moose ( Alcaes alcaes,
muscle), reindeer ( Rangifer tarandus, suet) and osprey ( Pandion
haliaetus, muscle) were found to contain 9, 15, 51 and 330 ng HCB/g
lipid weight, respectively (Jansson et al., 1993). The mean
concentration in 66 serum samples taken in muskoxen in the Canadian
Northwest Territories in 1989 was 2.8 ng/g (range of 1.1-7.5 ng/g)
(Salisbury et al., 1992). The mean concentration of HCB in fat samples
from 58 caribou from the same region ranged from 32.93 to 129.4 ng/g
(lipid corrected) (Elkin & Bethke, 1995). The mean concentration of
HCB in the livers and lipids of adult river otters ( Lutra
canadensis) in western Canada were 3 ng/g and 30 ng/g wet weight,
respectively, for females and 4 ng/g and 25 ng/g wet weight,
respectively, for males (Somers et al., 1987). Concentrations of HCB
in mink carcasses collected in Ontario in the late 1970s and early
1980s ranged from < 0.5 to 10 ng/g wet weight (Proulx et al., 1987).
In the Canadian north, the mean level of HCB in the fat of polar bears
( Ursus maritimus) hunted between 1982 and 1984 was 296 ng/g wet
weight (Norstrom et al., 1990).
5.1.6 Food and drinking-water
HCB is commonly detected, at low levels, in food (Table 7).
Levels of HCB tend to be highest in fatty foods and/or those that have
been treated with HCB-contaminated pesticides. The most extensive data
identified have been collected through the United States Food and Drug
Administration (US FDA) Total Diet Study. The results of the surveys
from 1982 to 1991 indicate that HCB is detectable (DL = 0.1 ng/g) in a
small fraction of food items, most often dairy products, meats, and
peanuts/peanut butter (KAN-DO Office and Pesticides Team, 1995). In
the most recent surveys, conducted during 1990-1991, mean levels were
less than 1 ng/g for all products.
Table 7. Concentration (µg/kg wet weight unless otherwise specified) of hexachlorobenzene in various foods
Country Food Mean contenta Range Reference
Australia cereals 0.01 < 0.01-0.01 Kannan et al. (1994)
pulses 0.02 0.01-0.05
oils 0.07 0.02-0.11
beverages 0.03 0.02-0.04
vegetables 0.01 < 0.01-0.02
fruits 0.01 < 0.01-0.02
dairy products 0.55 0.14-1.6
meat and fat 0.46 0.01-3.0
fishes 4.2 < 0.01-60
Canada fresh meat & eggs 0.17 Davies (1988)b
root vegetables & potato 0.04
fresh fruit ND(<0.01)
leafy/other above-ground vegetables 0.02
2% milk 0.16
Canada apples ND(<0.2)-2.6 OMAF/OME (1988)
peaches ND(<0.2)
tomatoes ND(<0.2)
potatoes ND(<0.2)
wheat ND(<0.2)
eggs ND(<0.2)
hamburger 0.39 0.2-0.57
prime beef ND(<0.2)-0.21
pork ND(<0.2)
chicken ND(<0.2)
Table 7 contd.
Country Food Mean contenta Range Reference
Germany milk 0.22d 0.088-0.45d Fürst et al. (1992)
cream 0.98d 0.31-1.30d
butter 4.86d 2.32-6.88d
cheese 2.72d 2.16-3.70d
India cereals 0.03 0.01-0.04 Kannan et al. (1992a)
pulses (edible seeds of legumes) 0.07 0.02-0.16
spices 0.22 <0.01-0.54
oils 1.5 0.09-2.8
milk 0.03 0.01-0.10
butter 1.7 0.86-2.4
fishes & prawn 0.07 <0.01-0.55
meat & animal fat 0.61 0.02-4.8
Mexico cheese 16.67d 1 Albert et al. (1990)
Morocco eggs 20.9 0.09-300 Kessabi et al. (1990)
poultry liver 5.1 trace-30.0
bovine liver 21.9 1.2-119.8
bovine kidney 15.1 trace-133.0
Papua New cheese 0.43 Kannan et al. (1994)
Guinea pork fat 0.40
chicken 0.20
striped mullet 0.04
tilapia 0.01 0.02-0.05
mud crab 0.03 < 0.01-0.02
oyster 0.02 < 0.01-0.05
Table 7 contd.
Country Food Mean contenta Range Reference
Solomon Islands pork 0.14
chicken 0.06
greenspotted kingfish 0.03 0.01-0.06 Kannan et al. (1994)
indian mackerel 0.01 0.01
paddletail snapper 0.01 0.01
Southern Baltic canned cod-livers 60 ± 6 50-76 Falandysz et al. (1993)
Spain bologna - fresh 2.57d Ariño et al. (1992)
- cooked 2.48d
Spain pork sausage Ariño et al. (1992)
- before curing 6.63d
- after 30 days curing 6.0d
Spain ham - fresh 3.46d Ariño et al. (1992)
- cured 1.29d
Spain pork 2.86-3.9d Ariño et al. (1993)
Spain lamb - chop, raw 14.67d Conchello et al. (1993)
- chop, grilled 12.06d
- leg, raw 8.53d
- leg, roasted 7.02d
Spain chicken 120 ± 10 To-Figueras et al. (1986)
calf 249 ± 37
rabbit 860 ± 159
pork 169 ± 20
sheep 225 ± 35
butter 315 ± 18
Table 7 contd.
Country Food Mean contenta Range Reference
United Kingdom bread ND (10) MAFF/HSE (1994)
milk 0.6
butter ND(10)
cheese 3.33d
ewes' cheese ND(10)
pasta ND(10)
beef burgers ND(10)
canned meat 10d
cooked meats 10d
lamb ND(10)
rabbit ND(10)
salami ND(10)
United Kingdom sausages ND(10) MAFF/HSE (1994)
pies and pasties ND(10)
salmon (tinned) 2.0
breaded cod ND(2.0)
fish cakes 2.0
mackerel 20
plaice ND(2.0)
prawn products ND(2.0)
sardines (tinned) ND(2.0)
Table 7 contd.
Country Food Mean contenta Range Reference
United Kingdom carrot 0.0317 Wang & Jones (1994)
potato 3.35
cabbage 0.0418
cauliflower 0.0729
lettuce 0.108
onion 0.0014
bean 0.0101
pea 0.0039
tomato 0.0139
USA cheese, processed 0.2 ND-0.5 US FDA
cheese, cheddar 0.1 ND-0.5 (unpublished)c
beef, ground (regular) 0.1 ND-0.4
beef, chuck roast 0.3 ND-1.0
beef, round steak 0.2 ND-1.0
beef, loin/sirloin steak 0.2 ND-1.0
USA lamb chop 0.3 ND-1.0 US FDA
frankfurters 0.1 ND-0.6 (unpublished)c
cod/haddock fillet ND(0.1) ND-0.2
eggs, scrambled 0.1 ND-0.3
eggs, fried 0.2 ND-0.7
peanut butter 0.2 ND-0.4
peanuts, dry roasted 0.3 ND-1.0
watermelon 0.1 ND-0.5
butter 0.6 ND-1.0
cream 0.1 ND-0.4
Table 7 contd.
Country Food Mean contenta Range Reference
Viet Nam rice 0.03 <0.01-0.05 Kannan et al. (1992b)
pulses 0.04 <0.01-0.18
oil 1.2
butter 5.0
animal fat 0.41 0.29-0.65
meat 0.11 0.03-0.18
fish 0.05 0.01-0.31
prawn 0.03
shellfish 0.04
crab 0.17
caviar 3.8 1.9-7.2