TOXIC FREE ASIA TOUR

TOXICOLOGICAL PROFILES FOR KEY POLLUTANTS IN BHOPAL

This is a detailed outline intended to profide scientific background on certain organic pollutants.

  All information is from Appendix 3 of the Bhopal Report

Carbon tetrachloride

Carbon tetrachloride is a manufactured compound that does not occur naturally (US EPA
1988). It is a clear, colourless, non-flammable liquid, which is heavier than water, and it
is moderately soluble in water. Carbon tetrachloride itself does not burn but poisonous
gases are produced in fire, including phosgene and hydrogen chloride. It uses as solvent
for oils, fats, lacquers, varnishes, rubber waxes and resins. Carbon tetrachloride was
formerly used as dry cleaning agent and fire extinguisher. Because of its harmful and
ozone depleting effects, these uses are now banned and it is only used in some industrial
applications. Principally it was used in the production of chlorofluorocarbon (CFC)
refrigerants (Budavari et al 1986; WHO 1993) but this use of carbon tetrachloride was
stopped in 1996 when CFC-11 and CFC-12 have been banned (UNEP 1997).
Carbon tetrachloride is a substance which can cause cancer in animals and humans (US
EPA 1997) and has been classified as Group 2B carcinogen (possibly carcinogenic to
humans) by International Agency for Research on Cancer (IARC 1999). Carbon
tetrachloride induces hepatic cell prolifiration and DNA synthesis. It also has a mutagenic
effect and induces aneuploidy in several in-vitro systems (IARC 1999). High exposure to
carbon tetrachloride can cause liver, kidney, and central nervous system damage. Liver
swells and cells are damaged or destroyed. Kidneys are also damaged, causing a build-up
of wastes in the blood. If exposure is low and then stops, the liver and kidneys can repair
the damaged cells and function normally again (ATSDR 1997). If exposure is very high,
the nervous system, including the brain, is affected. People may feel intoxicated and
experience headaches, dizziness, sleepiness, and nausea and vomiting. These effects may
subside if exposure is stopped, but in severe cases, coma and even death can occur
(ATSDR 1997).
Carbon tetrachloride may enter the environment from industrial effluents, municipal
treatment plant discharges, or spills (Menzer et al. 1986; US EPA 1988). It has been
found in the river waters in the areas influenced by the chlorinated organic solvent plant
(Amaral et al. 1996). Carbon tetrachloride is relatively stable in the environment. If
carbon tetrachloride released to land, it does not sorb onto soil, but migrates readily to
ground water and is believed to remain in ground water for several years (US EPA 1988).
Under anaerobic conditions carbon tetrachloride can be biotransformed producing
hazardous intermediates such as chloroform and methylene chloride (Hashsham et al.
1995) and carbon disulphide under sulphate reducing conditions (Delvin & Muller 1999;
Hashsham et al. 1995).
Carbon tetrachloride has been detected in drinking water (Abernathy 1994). In the EPA
Ground Water Supply Survey on drinking water supplies that used groundwater as a
source (Cotruvo et al. 1986) carbon tetrachloride was among six most frequently
occuring in the samples analysed with the maximum concentration of 16ug/l. In the study
carried out in different cities in Galicia, Spain (Freiria-Gandara et al. 1992) it was found
that concentration of carbon tetrachloride in treated drinking water (if detected) was in
the range between 39.5 and 1.5ug/l. In the similar investigation of drinking water in
Barcelona, Spain (Amaral et al. 1996) the levels of carbon tetrachloride were less than
0.1ug/l.
The maximum level of this compound in drinking water stipulated by the World Health
Organization is 2ug/l (WHO 1993). The Environmental Protection Agency (US EPA
1998) has set a limit for carbon tetrachloride of 5ug/l. The EPA recommends that
drinking water levels which are “safe” for short-term exposures for a 10kg child
consuming 1 litre of water per day: a one-day exposure of 4mg/l; a ten day exposure to
0.2mg/l; up to 7 year exposure to 0.07mg/l (US EPA 1998).
Carbon tetrachloride belongs to the organohalogen compounds whose presence in
groundwater are controlled by the European Community Environmental Legislation.
Article 3 of EC Council Directive 80/68/EEC of 17 December 1979 on the protection of
groundwater against pollution caused by certain dangerous substances (EEC 1979) and
amended later (EEC 1991) says that Member States shall take necessary steps to prevent
the introduction into groundwater of substances in List I and organohalogen compounds
are among the groups of the compounds listed there.
The quality objective of 12ug/l for the aquatic environment (including inland surface
waters, estuary waters, internal coastal waters other than estuary waters, and territorial
waters) is set for carbon tetrachloride by the EC Council Directive 86/280/EEC (EEC
1986) and amended in 1988 (EEC 1988).
The EC Council Directive 76/769/EEC (EEC 1976) which last was amended in 1996
(EEC 1996) restricts marketing and use of carbon tetrachloride. Carbon tetrachloride may
not be used in concentrations equal to or greater than 0.1% by weight in substances and
preparation placed on the market for sale to the general public and/or in diffusive
applications such as in surface cleaning and cleaning of fabrics.
Carbon tetrachloride is included in Group II of Annex B of controlled substances of the
Montreal Protocol (UNEP 1997) as an ozone depleting compound. Article 2D on carbon
tetrachloride says that level of consumption and production of this substance, calculated
using a complex formula, should not exceed zero from 1 January 1996. However, the
developing countries are entitled to delay implementation for ten years in order to meet
their basic domestic needs, as specified in the Article 5.

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References
Abernathy, C.O. (1994) A retrospective on drinking water. In: Water contamination and health. Wang,
R.G.M. [Ed], Marcel Dekker, Inc., New York: 1-14
Amaral, O.C., Otero, R., Grimalt, J.O. & Albaiges, J. (1996) Volatile and semi-volatile organochlorine
compounds in tap and riverine waters in the area of influence of a chlorinated organic solvent factory.
Water Resources. 30(8): 1876-1884
ATSDR (1997) ARSDR’s Toxicological profiles on CD ROM. Agency for Toxic Substances and Disease
Registry, U.S. Public Health Service. CRC Publishers
Budavari, S.M., O’Neil, J., Smith A. and Heckleman P.E. [Eds] (1986) The Merck index: an encyclopaedia
of chemicals, drugs and biologicals. 11th Edn Merck and Co, Inc., New Jersey, USA
Cotruvo, J., Goldhaber, S. & Vogt, C. (1986) Regulatory significance of organic contamination in the
decade of the 1980s. In: Organic carcinogens in drinking water. Ram, N.M., Calabrese, E.J. &
Christman, R.F. [Ed]. John Wiley and Sons, New York: 511-530
Delvin, J.F. & Muller, D. (1999) Field and laboratory studies of carbon tetrachloride transformation in
sandy aquifer under sulfate reducing conditions. Environmental Science and Technology 33(7): 1021-
1027
EEC (1976) Council Directive 76/769/EEC of 27 July 1976 on the approximation of lows, regulations and
administrative provisions of the Member States relating to restrictions on the marketing and use of
certain dangerous substances and preparations. OJ L 262: 201-203
EEC (1979) Council Directive 80/68/EEC of 17 December 1979 on the protection of groundwater against
pollution caused by certain dangerous substances. OJ L 020: 43-48
EEC (1986) Council Directive 86/280/EEC of 12 June 1986 on limit values and quality objectives for
discharges of certain dangerous substances included in List I of the Annex to Directive 76/464/EEC.
OJ L 181: 16-27
EEC (1988) Council Directive 88/347/EEC of 16 June 1988 on limit values and quality objectives for
discharges of certain dangerous substances included in List I of the Annex to Directive 76/464/EEC.
OJ L 158: 35-41
EEC (1991) Council Directive 91/692/EEC of 23 December 1991 standardizing and rationalizing reports
on the implementation of certain Directives relating to the environment. OJ L 377: 48-54
EEC (1996) Commission Directive 96/55/EC of 4 September 1996 adapting to technical progress for the
2 nd time Annex I to Council Directive 76/769/EEC of 27 July 1976 on the approximation of lows,
regulations and administrative provisions of the Member States relating to restrictions on the
marketing and use of certain dangerous substances and preparations (chlorinated solvents). OJ L 231:
20-21
Freiria-Gandara, M.J., Lorenzo-Ferreira, R.A., Alvarez-Devesa, A. & Bermejo, F. (1992) Occurance of
halogenated hydrocarbons in the water supply of different cities of Galicia (Spain). Environmental
Technology 13:437-447
Hashsham, S.A., Scholze, R. & freedman, D.L (1995) Cobalamin-enhanced anaerobic biotransformation of
carbon tetrachloride. Environmental Science and Technology 29(11): 2856-2863
IARC (1999) Carbon tetrachloride. IARC Monographs Vol.71, p.401
Menzer, R.E. & Nelson, J.O (1986) Water and soil pollutants. In: Casarett and Doull’s Toxicology: The
Basic Science of Poisons. Third Edition. Klaasen, C.D, Emdur, M.O. & Doll, J. [Ed]. Macmillan
Publishing Company. ISBN 0-02-364650-0, pp.825-856
UNEP (1997) The 1987 Montreal Protocol on Substances that Deplete the Ozone Layer, as adjusted and
amended by the second Meeting of the Parties (London, 27-29 June, 1990), and by the fourth Meeting
of the parties (Copenhagen, 23-25 November 1992), and further adjusted by the seventh Meeting of the
Parties (Vienna, 5-7 December 1995), and further adjusted and amended by the ninth Meeting of the
Parties (Montreal, 15-17 September 1997)
US EPA (1988) Reviews of environmental contamination and toxicology. Vol. 106, Environmental
Protection Agency, Office of Drinking Water Health Advisories, Springer-Verlag New York Inc. ISSN
0179-5953: 21-35
US EPA (1997) Chemicals known to the state to cause cancer or reproductive toxicity.
Environmental Protection Agency, Office Of Environmental Health Hazard Assessment Safe Drinking
Water And Toxic Enforcement Act Of 1986
US EPA (1998) National Primary Drinking Water Regulations. Technical Factsheet on Carbon
tetrachloride. Environmental Protection Agency, Office of Groundwater and Drinking Water
WHO (1993) Guidelines for drinking-water quality. Vol.1: Recommendations. Second Edition, ISBN 92 4
154460 0, 188p.

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Chloroform

Chloroform is a heavy, colourless, non-flammable liquid. It has a characteristic pleasant,
sweet, ethereal odour and a sweetish burning taste. The odour is non-irritant (CEC 1986).
It has been extensively used in the past as an anaesthetic (Snyder & Andews 1996).
Currently the largest use of chloroform is to make HCFC-22, an ozone-depleting
refrigerant (Holbrook 1993). The Montreal Protocol, the international legislation which
protects the ozone layer, has set targets for reducing the use of HCFC-22, but it will not
be totally phased out until 2030 (UNEP 1997).
Chloroform is the most abundant of the trihalomethanes (THMs) which are generated as
by-products during water disinfection using chlorine-containing compounds (Oxenford
1996; ATSDR 1997; Health Canada 1996). Additionally it can be formed in washing
machines into which chlorinated bleach has been added (Shepherd & Corsi 1996), in the
natural waters where chlorine-containing effluents have been discharged (Mills et al.
1998). Exposure to chloroform may occur when breathing contaminated air, drinking
contaminated water or through skin contact (Weisel & Chen 1994; Weisel & Jo 1996).
Water is possibly now the major source of environmental exposure to chloroform.
Chloroform has been specified by the International Agency for Research on Cancer in the
Group 2B as possibly carcinogenic to humans (IARC 1998). Investigation on animals
have shown that the main target organs for carcinogenicity from chloroform are liver,
kidney, and/or intestine (Dunnick & Melnik 1993; Snyder & Andews 1996; Chiu et al.
1996). A guideline value of 200ug/l was calculated to correspond to an excess lifetime
cancer risk of 10 -5 by the World Health Organisation (WHO 1993). The Maximum
Contaminant Level (MCL) of 100ug/l in drinking water which is delivered to any user of
a public water system is set by EPA for the total THMs (US EPA 1999). There are four
contaminants included in this group: chloroform, bromodichloromethane,
dibromochloromethane and bromoform (Oxenford 1996).
It is not known whether chloroform causes reproductive effects or birth defects in people,
but animal studies have shown that miscarriages occurred in rats and mice that breathed
air containing 30–300 ppm chloroform during pregnancy and also in rats that ate
chloroform during pregnancy. Offspring of rats and mice that breathed chloroform during
pregnancy had birth defects. Abnormal sperm were found in mice that breathed air
containing 400 ppm chloroform for a few days (ATSDR 1997).
The levels of chloroform found in treated drinking water depend upon water treatment
practice, age of the water, water temperature (Health Canada 1996) and can vary in the
range from less than 1ug/l to 200ug/l (Wallace 1997; Health Canada 1996). Levels less
than 10ug/l have been found in the US rural ground water (Wallace 1997), mean value of
84ug/l has been reported for the surface waters (if detected) in the same survey.
Chloroform evaporates easily into the air. Most of the chloroform in air breaks down
eventually, but it is a slow process. The breakdown products in air include phosgene and
hydrogen chloride, which are both toxic (ATSDR 1997). It is poorly absorbed to soil and
can travel through soil to groundwater where it can persist for years. Chloroform
dissolves easily in water and some of it may break down to other chemicals (ATSDR
1997).
The presence of chloroform (as organohalogen compound) in groundwater is controlled
by European Community Environmental Legislation. Article 3 of EC Council Directive
80/68/EEC of 17 December 1979 on the protection of groundwater against pollution
caused by certain dangerous substances (EEC 1979) and amended later (EEC 1991) says
that Member States shall take necessary steps to prevent the introduction into
groundwater of substances in List I and organohalogen compounds are among the groups
of the compounds listed there.
The quality objective of 12ug/l for the aquatic environment (including inland surface
waters, estuary waters, internal coastal waters other than estuary waters, and territorial
waters) is set for chloroform by the EC Council Directive 86/280/EEC (EEC 1986) and
amended in 1988 (EEC 1988).
The EC Council Directive 76/769/EEC (EEC 1976) which last was amended in 1996
(EEC 1996) restricts marketing and use of chloroform. Chloroform may not be used in
concentrations equal to or greater than 0.1% by weight in substances and preparation
placed on the market for sale to the general public and/or in diffusive applications such as
in surface cleaning and cleaning of fabrics.

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References
ATSDR (1997) ATSDR’s Toxicological profiles on CD ROM. Agency for Toxic Substances and Disease
Registry, U.S. Public Health Service. CRC Publishers
CEC (1986) Chloroform. In: Organochlorine solvents: health risk to workers. Publ: Commission of the
European Communities, ISBN 0-85186-078-8: 17-53
Chiu, N., Orme-Zavaleta, J., Chiu, A., Chen, C., DeAngelo, A., Brattin, W. & Blancato, J. (1996)
Characterization of cancer risk associated with exposure to chloroform. Environmental Carcinogenesis
& Ecotoxicology Reviews. Journal of Environmental Science and Health C14(2): 81-104
Dunnick, J.K & Melnik, R.L. (1993) Assessment of the carcinogenic potential of chlorinated water:
experimental studies of chlorine, chloramine and trihalomethanes. Journal of the National Cancer
Institute 85(10): 818-823
EEC (1976) Council Directive 76/769/EEC of 27 July 1976 on the approximation of laws, regulations and
administrative provisions of the Member States relating to restrictions on the marketing and use of
certain dangerous substances and preparations. OJ L 262: 201-203
EEC (1979) Council Directive 80/68/EEC of 17 December 1979 on the protection of groundwater against
pollution caused by certain dangerous substances. OJ L 020: 43-48
EEC (1986) Council Directive 86/280/EEC of 12 June 1986 on limit values and quality objectives for
discharges of certain dangerous substances included in List I of the Annex to Directive 76/464/EEC.
OJ L 181: 16-27
EEC (1988) Council Directive 88/347/EEC of 16 June 1988 on limit values and quality objectives for
discharges of certain dangerous substances included in List I of the Annex to Directive 76/464/EEC.
OJ L 158: 35-41
EEC (1991) Council Directive 91/692/EEC of 23 December 1991 standardizing and rationalizing reports
on the implementation of certain Directives relating to the environment. OJ L 377: 48-54
EEC (1996) Commission Directive 96/55/EEC of 4 September 1996 adapting to technical progress for the
2 nd time Annex I to Council directive 76/769/EEC of 27 July 1976 on the approximation of lows,
regulations and administrative provisions of the Member States relating to restrictions on the
marketing and use of certain dangerous substances and preparations (chlorinated solvents). OJ L 231:
20-21
Health Canada (1996) A one-year survey of halogenated disinfection by-products in the distribution system
of treatment plant using three different disinfection processes. Published by authority of the Minister of
Health, Canada. ISBN 0-662-25172-5, 59p.
Holbrook, M.T. (1993) Chloroform. IN: Kroschwitz, J.I. & Howe-Grant, (Eds). The Kirk-Othmer
Encyclopedia of Chemical Technology, Fourth Edition .Publ. Wiley-Interscience, N.Y. Volume 5, pp
1051-1062
IARC (1998) Overall evaluation of carcinogenicity: an updating of IARC Monographs Volumes 1 to 42.
Chloroform. Supplement 7, p.152
Mills, W.B., Lew, C.S. & Loh, J.Y. (1998) Predictions of potential human health and ecological risks from
power plant discharges of total residual chlorine and chloroform into rivers. Environmental Science
and Technology 32(14): 2162-2171
Oxenford, J.L. (1996) Disinfection by-products: current practices and future directions. In: Disinfection by-products
in water treatment: the chemistry of their formation and control. Minear, R.A. & Amy G.A.
[Ed] CRC Press, Inc. ISBN 1-56670-136-8: 3-16
Shepherd, J.L. & Corsi, R.L. (1996) Chloroform in indoor air and wastewater: the role of residential
washing machines. Journal of Air and Waste Management Association 46: 631-642
Snyder, R. & Andews, L.S. (1996) Toxic effects of solvents and vapours. In: Casarett and Doull’s
Toxicology: The Basic Science of Poisons. Fifth Edition. Klaasen, C.D, Amdur, M.O. & Doull, J. [Ed].
Mc-Graw-Hill, ISBN 0-07-105476-6, pp.737-772
UNEP (1997) The 1987 Montreal Protocol on Substances that Deplete the Ozone Layer, as adjusted and
amended by the second Meeting of the Parties (London, 27-29 June, 1990), and by the fourth Meeting
of the parties (Copenhagen, 23-25 November 1992), and further adjusted by the seventh Meeting of the
Parties (Vienna, 5-7 December 1995), and further adjusted and amended by the ninth Meeting of the
Parties (Montreal, 15-17 September 1997)
Wallace, L.A. (1997) Human exposure and body burden for chloroform and other trihalomethanes. Critical
Reviews in Environmental Science and Technology 27(2): 113-194
Weisel, C.P. & Chen, W.J. (1994) Exposure to chlorination by-products from hot water uses. Risk Analysis
14(1): 101-107
Weisel, C.P. & Jo W-K. (1996) Ingestion, inhalation, and dermal exposures to chloroform and
trichloroethene from tap water. Environmental Health Perspectives 104(1): 48-51
WHO (1993) Guidelines for drinking-water quality. Vol.1: Recommendations. Second Edition, ISBN 92 4
154460 0, 188p.

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Trichloroethene

Trichloroethene is a clear, colourless, heavy liquid with a pleasant, sweetish, chloroform-like
odour, and a sweet burning taste. It easily evaporates at room temperature.
Trichloroethene is non-flammable substance but it can decompose at high temperature in
the air producing hydrochloric acid, phosgene and other compounds (CEC 1986). Other
names of trichloroethene are trichloroethylene and ethylene trichloride.
Trichloroethene is a chlorinated solvent which was produced since the 1920s in many
countries by chlorination of ethylene or acetylene (IARC 1995). Another method of
producing trichloroethylene is by direct chlorination of ethylene dichloride to form
trichloroethylene and tetrachloroethylene (ATSDR 1997). Oxychlorination of chlorinated
wastes from PVC manufacturing (EDC tars) can be used to make chlorinated solvents
including trichloroethene, but this method also results in the generation of large quantities
of dioxins (EA 1997, ICI 1994). It has been used in vapour degreasing in 1920s, later it
was introduced for use in dry cleaning but its use in this industry has declined sharplysince the 1950s.
In the 1990s, 80-90% of trichloroethene worldwide was used for
degreasing metals (IARC 1995). Use for all applications in Western Europe, Japan and
the United States in 1990 was about 225 thousand tonnes. Other uses include processes
requiring strong solvent action to dissolve rubbers and resins and in the manufacture of
paints, lacquers and adhesives and oils from animal and vegetable matter. The textile
industry also uses trichloroethylene as a solvent in waterless dying and finishing
operations (ASTDR 1997). It is also used as a chain terminator in the production of
polyvinyl chloride, has also been used in fire extinguishing and fire retarding applications
(CEC 1986).
Trichloroethene is photochemically reactive compound and it can decompose in the
presence of free radicals. Stabilisers such as epoxides (including the carcinogen
epichlorohydrin) or combinations of epoxides, esters and amines are added to commercial
trichloroethene to prevent it becoming acidic towards equipment and degreased materials
(CEC 1986).
Trichloroethylene is not thought to occur naturally in the environment. However, it is
present in most underground water sources and many surface waters as a result of the
manufacture, use, and disposal of the chemical (Hughes et al. 1994, WHO 1993, ATSDR
1997).
Trichloroethene was found at different levels in drinking water supplies: in Galicia
(Spain) in range of concentrations between 1 and 11.6ug/l (Freiria-Gandara et al. 1992),
in drinking water samples from Zagreb, Croatia, contained 0.69 to 35.90 ug/l (ATSDR
1997), and up to 212 ug/l in the drinking water from two villages in Finland (Vartiainen
et al 1993). It was also detected in the breath of people after inhalation and dermal
exposure to tap water contaminated with trichloroethene (Weisel & Jo 1996). The World
Health Organisation guideline value for trichloroethene in drinking water is 70ug/l,
assuming that this route provides 10% of exposure (WHO 1993). The maximum
contaminant level (MCL) for trichloroethylene in drinking water set by US
Environmental Protection Agency is 5 ug/l (US EPA 1999). Some surface waters have
been found to contain more than 400ug/l of this contaminant (CEC 1986).
Trichloroethylene easily dissolves in water, and it remains there for a long time. Under
anaerobic conditions (for example in ground water) trichloroethene may degrade to more
toxic compounds including vinyl chloride (Klier et al. 1999, Su & Puls 1999, WHO
1993). Trichloroethene itself could be formed as a degradation product of another
chlorinated volatile compound – 1,1,2,2-tetrachloroethane (Loran & Olsen 1999).
Trichloroethylene may absorb to particles in water, which will cause it to eventually
settle to the bottom sediment (ATSDR 1997). Soil contamination by trichloroethene has
been reported with concentration ranging from below 1mg/kg to approximately
1500mg/kg (Ho et al. 1999). Trichloroethylene evaporates less easily from the soil than
from water and may remain in soil for a long time.Among the most heavily trichloroethene
-exposed people are those working in the degreasing of metals, who are exposed by inhalation.
Breathing large amounts of trichloroethylene may cause impaired heart function, coma, and death.
Breathing it for long periods may cause nerve, lung, kidney, and liver damage. Inhaling small amounts
for short periods of time may cause headaches, lung irritation, dizziness, poor co-ordination,
and difficulty concentrating. Drinking large amounts of trichloroethylene may
cause nausea, liver and kidney damage, convulsions, impaired heart function, coma, or
death. Drinking small amounts of trichloroethylene for long periods may cause liver and
kidney damage, nervous system effects, impaired immune system function and impaired
foetal development in pregnant women, although the extent of some of these effects is
not yet clear. Skin contact with trichloroethylene for short periods may cause skin rashes
(ATSDR 1997).
Trichloroethene has been classified by International Agency for Research on Cancer in
Group 2A (probably carcinogenic to humans) (IARC 1995). The most important
observations are the elevated risk for cancer of the liver and biliary tract and the modestly
elevated risk for non-Hodgkin's lymphoma. Trichloroethylene-contaminated groundwater
may marginally increase a risk for non-Hodgkin's lymphoma. It has been shown to
induce lung and liver tumours in various strains of mice (Fisher & Allen 1993, WHO
1993). It is also a weakly active mutagen in bacteria and yeast (WHO 1993).
Trichloroethene is in the first list of priority substances of the Commission Regulation
(EC) No 1179/94 (EC1994) which is a part of the Council Regulation (EEC) No 793/93
on the evaluation and control of the risks of existing substances (EEC 1993).
Discharges of trichloroethene during several industrial processes (including production of
tetrachloroethene and trichloroethene) and usage of trichloroethene for degreasing of
metals are controlled by the European Community Legislation and special provisions are
set relating to trichloroethene in the Council Directive 90/415/EEC (EEC 1990). The
quality objective of 10ug/l for the aquatic environment (including inland surface waters,
estuary waters, internal coastal waters other than estuary waters, and territorial waters) is
set for trichloroethene in the same Directive.
Article 5(6) of the recent document (EC 1999) concerning limitation of emissions of
volatile organic compounds due to the use of organic solvents in certain activities and
installations says that substances or preparations which, because of their content of
volatile organic compounds classified as carcinogens, mutagens, or toxic to reproduction,
shall be replaced as far as possible by less harmful substances or preparations within the
shortest possible time.

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References
ATSDR (1997) ATSDR’s Toxicological profiles on CD ROM. Agency for Toxic Substances and Disease
Registry, U.S. Public Health Service. CRC Publishers
CEC (1986) Trichloroethylene. In: Organochlorine solvents: health risk to workers. Publ: Commission of
the European Communities. ISBN 0-85186-078-8: 93-130EA (1997) Regulation of dioxin releases
from the Runcorn operations of ICI and EVC. Information Report.
Environmental Agency Licence GD03177G0003. Pub. By Crown. 36pp.
EC (1994) Commission Regulation (EC) No 1179/94 of 25 May 1994 concerning the first list of priority
substances as foreseen under Council Regulation (EEC) No 793/93. OJ L 131: 3-4
EC (1999) Council Directive 1999/13/EC of 11 March 1999 on the limitation of emission of volatile
organic compounds due to the use of organic solvents in certain activities and installations. OJ L 85: 1-
22
EEC (1990) Council Directive of 27 July 1990 amending Annex II to Directive 86/280/EEC on limit values
and quality objectives for discharges of certain dangerous substances included in list I of the Annex to
Directive 76/464/EEC. OJ L 219:49-57
EEC (1991) Council Directive 91/692/EEC of 23 December 1991 standardizing and rationalizing reports
on the implementation of certain Directives relating to the environment. OJ L 377: 48-54
EEC (1993) Council Regulation (EEC) No 793/93 of 23 March 1993 on the evaluation and control of the
risks of existing substances. OJ L 84: 1-75
Fisher, J.W. & Allen, B.C. (1993) Evaluating the risk of liver cancer in humans exposed to
trichloroethylene using physiological models. Risk Analysis 13(1): 87-95
Freiria-Gandara, M.J., Lorenzo-Ferreira, R.A., Alvarez-Devesa, A. & Bermejo, F. (1992) Occurance of
halogenated hydrocarbons in the water supply of different cities of Galicia (Spain). Environmental
Technology 13: 437-447
Ho, S.V., Athmer, C., Sheridan, P.W., Hughes, B.M., Orth, R., McKenzie, D., Brodsky, P.H., Shapiro,
A.M., Sivavec, T.M., Salvo, J., Schultz, D., Landis, R., Griffith, R. & Shoemaker, S. (1999) The
Lasagna technology for in situ soil remediation. 2. Large field test. Environmental Science and
Technology 33(7): 1092-1099
Hughes, K., Meek, M.E. & Windle, W. (1994) Trichloroethylene: Evaluation of risks to health from
environmental exposure in Canada. Environmental Carcinogenesis and Ecotoxicology Reviews.
Journal of Environmental Science and Health 12(2): 527-543
IARC (1995) Trichloroethylene. IARC Monographs Vol.63, p.75
ICI (1994) Report of the Chief Inspector HMIP authorisation AK6039 Improvement Condition part 8, table
8.1, item 2: Formation of dioxines in oxychlorination, significance for human health and monitoring
proposals. ICI Chemicals and Polymers report NWJP/BMTD, 27 th April, 1994, 16pp.
Loran, M.M. & Olsen, L. (1999) Degradation of 1,1,2,2-tetrachloroethane in a freshwater tidal wetland:
field and laboratory evidence. Environmental Science and Technology 33(2): 227-234
Su, C. & Puls, R.W. (1999) Kinetics of trichloroethene reduction by zerovalent iron and tin: pretreatment
effect, apparent activation energy, and intermediate products. Environmental Science and Technology
33(1): 163-168
Vartiainen, T., Pukkala, E., Rienoja, T., Strandman, T., Kaksonen, K. (1993) Population exposure to
trichloroethene and tetrachloroethene and cancer risk - 2 cases of drinking-water pollution.
Chemosphere 27(7): 1171-1181
Weisel, C.P. & Jo, W-K (1996) Ingestin, inhalation, and dermal exposures to chloroform and
trichloroethene from tap water. Environmental Health Perspectives 104(1): 48-51
WHO (1993) Guidelines for drinking-water quality. Vol.1: Recommendations. Second Edition, ISBN 92 4
154460 0, 188p.

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Tetrachloroethene

Tetrachloroethene is a clear liquid, which is heavier than water, with a sweet chloroform-like
odour. Tetrachloroethene itself does not burn but it can produce poisonous gases in
fire including hydrogen chloride and phosgene (US EPA 1989). Other names for
tetrachloroethene include perchloroethylene and tetrachloroethylene.
Tetrachloroethene was first prepared in 1821 by Faraday by thermal decomposition of
hexachloroethane (Hickman 1993). Tetrachloroethene is one of the most important
chlorinated solvents worldwide and it has been produced commercially since the early1900s.
About 513 thousand tonnes were used in all applications in Western Europe,
Japan and the United States in 1990 (IARC 1995). Tetrachloroethene is typically
produced as a co-product with either trichloroethene or carbon tetrachloride from from
hydrocarbons, partially chlorinated hydrocarbons, and chlorine (Hickman 1993).
Oxychlorination of chlorinated wastes from PVC manufacturing (EDC tars) can be used
to make chlorinated solvents including tetrachloroethene, but this method also results in
the generation of large quantities of dioxins (EA 1997, ICI 1994). Most of the
tetrachloroethene produced was used for the dry cleaning garments and smaller amounts
were used for degreasing and in the production of chlorofluorocarbons (CFCs) (IARC
1995). However, this latter application will have been reduced since the Montreal
Protocol banned CFC-11 and CFC-12 over most of the world (UNEP 1997).
Tetrachloroethene was used in the textile industry for processing, finishing and sizing
(US EPA 1998). Other uses include: insulating/cooling fluid in electric transformers; in
typewriter correction fluids, as veterinary medication against worms, and it was once
used as grain fumigant (US EPA 1998).
Tetrachloroethene is well known environmental contaminant. It has been detected in air,
lakes, rainwater, seawater, rivers, soil, food and human tissues (ATSDR 1997; Bauer
1990; CEC 1986). It has also been found in drinking water at concentration in the range
from 10ug/l to 180 ug/l (Bauer 1990; Freiria-Gandara et al. 1992; Vartiainen et al. 1993;
CEC 1986). Contamination of well water with the concentration of 375ug/l was recorded
at a waste disposal site due to tetrachloroethene leaching through soil (CEC 1986). The
World Health Organisation guideline value for tetrachloroethene in drinking water is
40ug/l assuming that 10% of exposure comes from this source (WHO 1993). The
maximum contaminant level (MCL) for tetrachloroethene in drinking water set by US
Environmental Protection Agency is 5 ug/L (US EPA 1999). Tetrachloroethene has also
been detected in the effluents from industrial plants and refineries and in sewage
treatment plant effluents before and after chlorination (Santillo et al. 1997; US EPA
1989; CEC 1986).
The majority of the produced tetrachloroethene (80-85%) is lost in the atmosphere as a
result of evaporation during production, storage and use (US EPA 1994; CEC 1986) and
only 1% is released to water. Releases of tetrachloroethene to the environment are
primarily from alkali and chlorine industries (US EPA 1998). In 1992, more than 12.3
million pounds (5584.2 tonnes) of perchloroethylene were released to the atmosphere, 10
thousand pounds (4.54 tonnes) to surface water, 13 thousand pounds (5.9 tonnes) to
underground injection sites, and 9 thousand pounds (4.07 tonnes) to land from U.S.
facilities (US EPA 1994). Once released into environment tetrachloroethene can undergo
transformation. The degradation of tetrachloroethene through biotic mechanism includes
the formation of lesser chlorinated compounds including trichloroethene, cis- and trans-1,2-
dichloroethene, and vinyl chloride (Klier et al. 1999). In the air a photochemical
degradation occurs with trichloroacethyl chloride as a major degradation product and
phosgene a lesser one (CEC 1986).
The major route of human exposure to tetrachloroethene is from inhalation of
contaminated urban air, especially near point sources such as dry cleaners, drinking
contaminated water from contaminated aquifers (US EPA 1998), drinking water
distributed in pipelines with vinyl liners (Webler & Brown 1993), and inhalation of
contaminated occupational atmospheres in metal degreasing and dry cleaning industries
(US EPA 1998).
Exposure to very high concentrations of tetrachloroethene can cause dizziness,
headaches, sleepiness, confusion, nausea, difficulty in speaking and walking, and
unconsciousness (ATSDR 1997). Prolonged and frequently repeated dermal exposure
can cause irritation, dryness, and dermatitis due to defatting (US EPA 1994).
Tetrachloroethene is classified as Group 2A carcinogen (probably carcinogenic to
humans) by the International Agency for Research on Cancer (IARC 1995). This
compound induces leukemia in rats and increases risk for oesophageal cancer, non-Hodgkin’s
lymphoma and cervical cancer (IARC 1995). Tetrachloroethene has been
shown to cause liver tumours in mice and kidney tumours in male rats (ASTDR 1997). It
has been found that exposure to tetrachloroethene-contaminated drinking water was
associated with an increased risk of leukemia and bladder cancer and that the risk was
dose related (Aschengrau et al. 1993).
Specific provisions are set by the European Community Legislation relating to
tetrachloroethene in the Council Directive 90/415/EEC (EEC 1990) which controls
discharges of tetrachloroethene during several industrial processes (including production
of tetrachloroethene, trichloroethene, carbon tetrachloride and chlorofluorocarbons) and
usage of tetrachloroethene for degreasing of metals. The quality objective of 10ug/l for
the aquatic environment (including inland surface waters, estuary waters, internal coastal
waters other than estuary waters, and territorial waters) is set for tetrachloroethene in the
same Directive.
Article 5(6) of the recent document (EC 1999) concerning limitation of emissions of
volatile organic compounds due to the use of organic solvents in certain activities and
installations says that substances or preparations which, because of their content of
volatile organic compounds classified as carcinogens, mutagens, or toxic to reproduction,
shall be replaced as far as possible by less harmful substances or preparations within the
shortest possible time.
Tetrachloroethene is in the first list of priority substances of the Commission Regulation
(EC) No 1179/94 (EC1994) which is a part of the Council Regulation (EEC) No 793/93
on the evaluation and control of the risks of existing substances (EEC 1993).

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References
Aschengrau, A., Ozonoff, D., Paulu, C., Coogan, P., Vezina, R., Heeren, T. & Zhang, Y. (1993) Cancer
risk and tetrachloroethylene-contaminated drinking water in Massachusetts. Archives of
Environmental Health 48(5): 284-292
Bauer, U. (1990) Occurrence of tetrachloroethylene in the FRG. In: Organohalogen compounds. Vol.2:
Dioxin’90 – EPRI-Seminar. Hutzinger, O. & Fiedler, H. [Ed] published by Ecoinforma Press,
Bayreuth, FRG. pp385-388
CEC (1986) Perchloroethylene. In: Organochlorine solvents: health risk to workers. Publ: Commission of
the European Communities, ISBN 0-85186-078-8: 191-224EA (1997) Regulation of dioxin releases
from the Runcorn operations of ICI and EVC. Information Report.
Environmental Agency Licence GD03177G0003. Pub. By Crown. 36pp.
EC (1994) Commission Regulation (EC) No 1179/94 of 25 May 1994 concerning the first list of priority
substances as foreseen under Council Regulation (EEC) No 793/93. OJ L 131: 3-4
EC (1999) Council Directive 1999/13/EC of 11 March 1999 on the limitation of emission of volatile
organic comp[ouinds due to the use of organic solvents in certain activities and installations. OJ L 85:
1-22
EEC (1990) Council Directive of 27 July 1990 amending Annex II to Directive 86/280/EEC on limit values
and quality objectives for discharges of certain dangerous substances included in list I of the Annex to
Directive 76/464/EEC. OJ L 219: 49-57
EEC (1991) Council Directive 91/692/EEC of 23 December 1991 standardizing and rationalizing reports
on the implementation of certain Directives relating to the environment. OJ L 377: 48-54
EEC (1993) Council Regulation (EEC) No 793/93 of 23 March 1993 on the evaluation and control of the
risks of existing substances. OJ L 84: 1-75
Freiria-Gandara, M.J., Lorenzo-Ferreira, R.A., Alvarez-Devesa, A. & Bermejo, F. (1992) Occurrence of
halogenated hydrocarbons in the water supply of different cities of Galicia (Spain). Environmental
Technology, 13: 437-447
Hickman, J.C. (1993) Tetrachloroehylene. Chlorocarbons, -hydrocarbons (CHCl=CCl2). In: Kirk-Othmer
Encyclopedia of Chemical Technology. [Eds] Jacqueline I. Kroschwits; Mary Howe-Grant. Fourth
edition, Vol. 6. John Wiley & Sons, Inc. pp.50-59
IARC (1995) Tetrachloroethylene. IARC Monographs Vol.63, p.159
ICI (1994) Report of the Chief Inspector HMIP authorisation AK6039 Improvement Condition part 8, table
8.1, item 2: Formation of dioxines in oxychlorination, significance for human health and monitoring
proposals. ICI Chemicals and Polymers report NWJP/BMTD, 27 th April, 1994, 16pp.
Klier, N.J., West, R.J. & Donberg, P.A. (1999) Aerobic biodegradation of dichloroethylenes in surface and
subsurface soils. Chemosphere 38(5): 1175-1188
Santillo, D., Labounskaia, I., Stringer, R.L. & Johnston, P. A. (1997) Report on the analysis of industrial
wastewaters from the Frutarom VCM/PVC plant near Haifa, Israel and adjacent shoreline sediments
for organic contaminants. Greenpeace Research Laboratories Technical Note 03/97
UNEP (1997) The 1987 Montreal Protocol on Substances that Deplete the Ozone Layer, as adjusted and
amended by the second Meeting of the Parties (London, 27-29 June, 1990), and by the fourth Meeting
of the parties (Copenhagen, 23-25 November 1992), and further adjusted by the seventh Meeting of the
Parties (Vienna, 5-7 December 1995), and further adjusted and amended by the ninth Meeting of the
Parties (Montreal, 15-17 September 1997)
US EPA (1989) Tetrachloroethylene. US Environmental Protection Agency factsheets for regulated
chemicals. Aquire Database, ERL-Duluth, US Environmental Protection Agency
US EPA (1994) Chemical summary for perchloroethylene. Office of Pollution Prevention and Toxics. US
Environmental Agency
US EPA (1998) Technical factsheet on: Tetrachloroethylene. National primary drinking water regulations.
Drinking water and health. Office of Ground Water and Drinking Water, US Environmental Protection
Agency
US EPA (1999) Current drinking water standards. National primary and secondary drinking water
regulations. Office of Ground Water and Drinking Water. US Environmental Protection Agency
Vartiainen, T., Pukkala, E., Rienoja, T., Strandman, T., Kaksonen, K. (1993) Population exposure to
trichloroethene and tetrachloroethene and cancer risk - 2 cases of drinking-water pollution.
Chemosphere 27(7): 1171-1181
Webler, T. & Brown, H.S. (1993) Exposure to tetrachloroethylene via contaminated drinking pipes in
Massachusetts: a predictive model. Archives of Environmental Health 48(5): 293-297
WHO (1993) Guidelines for drinking-water quality. Vol.1: Recommendations. Second Edition, ISBN 92 4
154460 0, 188p.

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Hexachloroethane

Hexachloroethane is a white crystalline solid with a camphor-like odour. It is non-flammable
compound but it can decompose at high temperature (400-500 0 C) to give
tetrachloroethylene, carbon tetrachloride and chlorine (Snedecor 1993).
Hexachloroethane is formed as a by-product in many industrial chlorination processes
designed to produce lower chlorinated hydrocarbons. Commercially it is produced by
chlorination or oxychlorination of tetrachloroethene either in the presence of catalysts or
under especial conditions (photochemical chlorination) (Snedecor 1993). Chlorination of
hexachlorobutadiene has also been used to produce hexachloroethane. Additionally,
hexachloroethane can be formed as a pyrolisis product during decomposition of
trichloroethene and tetrachloroethene (Yasuhara & Morita 1990; Yasuhara 1993). It is
also formed during incineration of materials containing chlorinated hydrocarbons
(ATSDR 1996).
Historically hexachloroethane had wide and quite extensive applications. It was used in
the past by the military in the production of pyrotechnic devices and screening smoke
(DHHS 1998, Snedecor 1993). Hexachloroethane has been used in metal and alloy
production, mainly in refining aluminium alloys. It was also used for removing impurities
from molten metals, recovering metals from ores or smelting products, and improving the
quality of various metals and alloys. Hexachloroethane has been used as a degassing
agent for magnesium. Hexachloroethane has also been used as an additive in combustible
liquids (ignition suppressant) and fire extinguishing fluids (smoke generated by
hexachloroethane is used as a flame retardant). Hexachloroethane has had a variety of
applications as a polymer additive. It has flame-proofing qualities, increases sensitivity to
radiation cross-linking, and it is used as a vulcanising agent. Added to polymer fibres,
hexachloroethane acts as a swelling agent and increases affinity for dyes.
Hexachloroethane has also served as a fixer for some types of experimental photography
and xerography (DHHS 1998, Snedecor 1993). At present hexachloroethane is not
manufactured as an end-use product in the United, but it is formed as a by-product in the
production of some chemicals (DHHS 1998, ATSDR 1996).
Hexachloroethane is not produced naturally in the environment. This compound is one of
the most common environmental pollutants which was detected in air, surface water,
drinking water and soil around chemical dump sites in the USA (DHHS 1998). Potential
sources of hexachloroethane release to the environment include: formation during
combustion and incineration of chlorinated wastes, release to air due to volatility and
inefficient solvent recovery (hexachloroethane is an impurity in some chlorinated
solvents), and formation during chlorination of sewage effluent prior to discharge (DHHS
1998). Hexachloroethane is also reported produced in small quantities from chlorination
of raw water during drinking water treatment (IARC 1991).
If released to soil, this compound may persist for one year and could potentially
contaminate groundwater where it can persist for up to 2 years (Howard et al. 1991).
Hexachloroethane volatilises slowly from dry soil surfaces.
When hexachloroethane enters water, volatilisation appears to be the dominant removal
mechanism (half-life in the surface water is up to 6 month). Moderate to slight adsorption
to suspended solids and sediments may occur. Biodegradation is not expected to occur at
a rate which would make this an important fate process in natural water systems.
However, under certain conditions (in the presence of sulphides) hexachloroethane can
undergo reductive dehalogenation producing lower chlorinated compounds such as
tetrachloroethylene, pentachloroethane and trichloroethylene (Miller et al. 1998; Butler &
Hayes 1998). Bioconcentration of hexachloroethane in aquatic species has been
demonstrated. It was shown that absorption of selected waterborne chloroethanes
including hexachloroethane occurs in large adult fish and results in distribution kinetics
similar to those observed in inhalation exposures (McKim et al. 1996).
If released to air, hexachloroethane exists almost entirely in the vapour phase. This
compound is not expected to degrade in the troposphere. Half-life of hexachloroethane in
the air is about 73 years (Howard et al. 1991). As a result of its persistence in the
troposphere, long range transport is expected to occur.
The most probable routes of human exposure to hexachloroethane are dermal contact and
ingestion of contaminated drinking water and, to a lesser extent inhalation (DHHS 1998).
It has been listed among 148 hazardous air pollutants highlighted in the comprehensive
evaluation of the potential public health implication of outdoor air toxic compounds
concentrations across the United States (Woodruff et al. 1998).
Hexachloroethane has been reported to adversely affect the central nervous system and
the eye (ATSDR 1996). The neurologic effects are mild, generally reported as an
inability to close the eyelid, irritated, inflamed and watering eyes. Hexachloroethane is
moderately irritating to the skin, mucous membranes, and liver in humans. Liver and
kidney effects have been observed in animals acutely exposed to hexachloroethane by
ingestion (ATSDR 1996; Bucher 1996). The US Department of Health and Human
Services has determined that hexachloroethane may reasonably be anticipated to be a
carcinogen (DHHS 1998). The International Agency for Research on Cancer classified
hexachloroethane in Group 2B (possibly carcinogenic to humans).
The use and marketing of hexachloroethane is regulated by the European Community
Legislation. EC directive 97/16/EC (EC 1997) added hexachloroethane to Annex I of
Council Directive 76/769/EEC (EEC 1976) and banned most its uses in the non-ferrous
metal industry. The only exceptions made were for some non-integrated foundries casting
aluminium and for certain magnesium alloys.

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References
ATSDR (1996) Toxicological profile for hexachloroethane (update). Atlanta, GA. US Department of
Health and Human Services. Public Health Service
Bucher, J.R. (1996) NTR Technical Report on renal toxicity studies of selected halogenated ethanes
administrated by gavage to F344/N rats. US Department of Health and Human Services. NIH
Publication 96-3935, February 1996. 52pp.
Butler, E.C. & Hayes, K.F (1998) Effects of solution composition and pH on the reductive dechlorination
of hexachloroethane by iron sulfide. Environmental Science and Technology 32(9): 1276-1284
DHHS (1998) Report on carcinogens. Summary. 8 th Edition. US Department of Health and Human
Services, 1998, 252pp.EC (1997) Directive 97/16/EC of the European Parliament and of the Council of
10 April 1997 amending
for the 15 th time Directive 76/769/EEC on restrictions on the marketing and use of certain dangerous
substances and preparations. OJ L 116: 31-32
EEC (1976) Council Directive 76/769/EEC of 27 July 1976 on approximation of the laws, regulations and
administrative provisions of the Member States relating to restrictions on the marketing and use of
certain dangerous substances and preparations. OJ L 262: 201-203
Howard, P.H., Boethling, R.S., Jarvis, W.F., Meylan, W.M. & Michalenko, E.M. (1991) Handbook of
environmental degradation rates. Pub. By Lewis Publishers, Inc. ISBN 0 87371 358 3, 725pp.
IARC (1991) Chlorinated drinking water. IARC Monographs on the evaluation of carcinogenic risks to
humans. Vol. 52. ISBN 92 832 1252 5, pp.45-128
McKim, J.M., Nichols, J.W., Lien, G.J., Hoffman, A.D., Galliant, C.A. & Stokes, G.N. (1996) Dermal
absorption of three waterborne chloroethanes in rainbow trout (Oncorhynchus mykiss) and channel
catfish (Ictalurus punctatus). Fundamental and Applied Toxicology 31: 218-228
Miller, P.L., Vasudevan, D., Gschwend, P.M. & Roberts, A.L. (1998) Transformation of hexachloroethane
in sulfidic natural water. Environmental Science and Technology 32(9): 1269-1275
Snedecor, G (1993) Hexachloroethane. Chlorocarbons, -hydrocarbons (CHCl=CCl2). In: Kirk-Othmer
Encyclopedia of Chemical Technology. [Eds] Jacqueline I. Kroschwits; Mary Howe-Grant. Fourth
edition, Vol. 6. John Wiley & Sons, Inc. pp.29-31
Woodruff, T.J., Axelrad, D.A., Caldwell, J., Morello-Frosch, R. & Rosenbaum, A. (1998) Public health
implication of 1990 air toxics concentrations across the United Staes. Environmental Health
Perspectives 106(5): 245-251
Yasuhara, A. & Morita, M. (1990) Formation of chlorinated compounds in pyrolisis of trichloroethylene.
Chemosphere 21(4-5): 479-486
Yasuhara, A. (1993) Thermal decomposition of tetrachloroethylene. Chemosphere 26(8): 1507-1512

Return to Index

Chlorinated benzenes

The production of chlorinated benzenes is a multiple product operation achieved by direct
chlorination of benzene in the liquid phase using a ferric chloride catalyst. Only limited
control can be exerted over the final product mix. The distillation train used for
separating the mixture has a limited resolving power and the distillates are always
mixtures of close boiling isomers which can be further separated by crystallisation (see
eg Bryant 1993). Distillation also gives rise to chlorinated tars.
12 chlorinated benzenes are possible, with substitution patterns as follows:
1 chlorine monchlorobenzene,
2 chlorines 1,2-di-, 1,3-di- and 1,4-dichlorobenzenes
3 chlorines 1,2,3-tri-, 1,2,4-tri- and 1,3,5-trichlorobenzenes
4 chlorines 1,2,3,4-tetra-, 1,2,3,5,-tetra- and 1,2,4,5-tetrachlorobenzenes
5 chlorines Pentachlorobenzene
6 chlorines hexachlorobenzene.
Both technological changes and environmental concerns have severely affected the
production of chlorobenzenes; today only monochlorobenzene and 1,2- and 1,4-
dichlorobenzenes are manufactured in large quantities. These are often produced
together, with the economically optimised reaction yielding approximately 85%
monochlorobenzene, 10% 1,4-dichlorobenzene and 5% 1,2-dichlorobenzene.
Monochlorobenzene yield can be increased to 90% by careful monitoring of the reaction
mix density and recycling of unreacted benzene, but total elimination of dichlorobenzene
formation is not economical. Should the primary interest be in the para- isomer, yield
may be increased by use of a selective catalyst, or the mix can be further chlorinated to
produce a mixture of 1,4-dichlorobenzene and 1,2,4-trichlorobenzene. These two
products can easily be separated by distillation (Bryant 1993, CEC 1986).

1.Mono- and di-chlorobenzenes.
Chlorobenzene, 1,2-dichlorobenzene and 1,3-dichlorobenzene are colourless liquids; 1,4-
dichlorobenzene forms colourless crystals at room temperature (Ware 1988a & b).
One of the earliest uses of chlorobenzene was as an intermediate for the explosive picric
acid during the first World War (CEC 1986). It is used as a solvent and as an
intermediate in chemical synthesis. In the US in the 1980s, the predominant use was for
the production of ortho- and para-chlorobenzenes. Theses are used as intermediates for
rubber chemicals, antioxidants, dyes and pigments, pharmaceuticals and agricultural
chemicals. The fungicide benomyl, and carbofuran and the parathion group of
insecticides are all derived from chlorobenzene. One previously important use was in the
manufacture of DDT. Chlorobenzene production has fallen due to the development of
other routes to aniline and phenol and the restriction of DDT use. By various routes,
chlorobenzene is also used for the manufacture of specialty silicones, Grignard reagents
and catalysts (Bryant 1993). Release to the environment is expected to derive from its
use as a solvent, either through fugitive emissions or volatilisation from pesticides for
which it used as a carrier. Thus, inhalation is thought to be a major route of exposure for
humans since it is rarely if ever found in food. It bioaccumulates in algae, fish and
aquatic invertebrates. Mammalian metabolites are reported to be p-chlorophenol, p-chlorocatechol
and p-chlorophenyl mercapturic acid. Human exposure causes CNS
depression and respiratory tract irritation and animal studies have reported liver necrosis,
renal toxicity and effects on the pancreas, blood and lymph and adrenal glands (Ware
1988a, Meek et al. 1994a). Canada has derived a TDI of 8.1ug/kg body weight/day;
estimated exposures (0.05-0.14ug/kg/day) are considerably lower than this (Meek et al.
1994a).
Ware (1988b) reports human symptoms after exposure to DCBs, but does not distinguish
between isomers. Effects reported are anaemia, skin lesions, vomiting, headaches, eye
and respiratory tract irritation, anorexia, weight loss, yellow atrophy of the liver, blood
dyscrasias, porphyria, and chromosomal breaks in blood samples. Animal experiments
recorded liver and kidney damage to be the most frequent effects, though high doses
caused CNS perturbation and death through respiratory depression. The
dichlorobenzenes are bioaccumulative in algae, aquatic invertebrates and fish (Ware
1988b). All three have also been reportedly found in blood (Ware 1988b).
1,2-Dichlorobenzene is produced unavoidably in the production of monochlorobenzene,
but it is also possible to maximise dichlorobenzene production to 98% of the reaction
mixture using suitable catalysts or alternative production methods leading to specific
isomers. It is used mainly in the production of dyes and pesticides after conversion to
1,2-dichloro- 4-nitrobenzene or dichloroaniline. Other uses include the solvent phase in
the production of toluene di-isocyantes, production of deodorants and disinfectants and
on a small scale as a heat transfer fluid. According to Meek et al. (1994b), the largest use
is in degreasing for the metal and automotive industries.
Exposed laboratory animals exhibited hepatic, renal and haematological effects as well as
lymphoid depletion of the thymus and spleen and multifocal mineralisation of both
muscular and heart muscles (Ware 1988b, Meek et al. 1994b). Developmental toxicity
was only observed at concentrations which were overtly toxic to the mother. Human
toxicity data are sparse, but chromosomal aberrations, anaemia and leukemia have been
reported (Meek et al. 1994b). Mammals metabolise 1,2-dichlorobenzene to phenols,
catechols, most of which are excreted after conjugation with glucoronic or sulphuric
acids. Mercapturic acids may also be produced. The primary metabolites in humans are
conjugated phenols (Ware 1988b). 1,2-dichlorobenzene is found in air, food, breast milk
and drinking water (Meek et al. 1994b). It is also toxic to higher plants, inducing
abnormal mitosis (cell division) in onions (Ware 1988b).
1,3-Dichlorobenzene is growing in importance as a starting product in the manufacture of
dyes, pesticides and pharmaceuticals. However, this has not yet reached commercial
importance. There are some other small, specialised uses, but larger markets have not
been developed, mainly because 1,3-dichlorobenzene only occurs as a minor constituent
(approx 1%) of the technical dichlorobenzene reaction mix, and to produce it by other
routes is expensive (Bryant 1993). Mammalian (and human) metabolism is as for 1,2-
dichorobenzene above, but generally little is known about this 1,3-dichlorobenzene in
comparison to the more commercially important dichlorobenzenes.
1,4-Dichlorobenzene (p-dichlorobenzene) is used largely in the production of deodorant
blocks and room deodorants. It is also used as a moth control agent, as an insecticide and
an intermediate for production of insecticides and dyes. An emerging market is in the
manufacture of poly(phenylene sulphide) resin (PPS), and minor uses are as a germicide,
fungicideand extreme pressure lubricant (Bryant 1993, CEC 1986). 1,4-dichlorobenzene
is not spontaneously combustible and does not assist fire, but it is flammable
nevertheless. It may be absorbed both through the inhalation of vapours, through the skin
and though consumption of contaminated food. Human symptoms include damage to the
liver, kidneys and lungs. Accidental poisoning of children, presumably who have eaten
moth repellant was widespread in the 1970s (CEC 1986). Once absorbed, 1,4-
dichlorobenzene is stored in the adipose tissue, and has been detected in human samples
(CEC 1986, Ware 1988b). The metabolism of 1,4-dichlorobenzene by mammals varies
from that of the other two isomers in that mercapturic acids are not formed. 1,4-
dichlorobenzene causes abnormal mitosis in higher plants. 1,4-Dichlorobenzene has been
reported in human adipose tissue, as well as in blood (Ware 1988b).

2.Trichlorobenzenes
1,2,3- and 1,2,4-trichlorobenzene have been produced from the dehydrohalogenation of
the unwanted isomers of the production of the pesticide 1,2,3,4,5,6-
hexachlorocyclohexane. This is of limited application.Environmental regulations have
curbed the use and discharge of trichlorobenzenes to the
environment, as least in Europe and the USA (Harper et al. 1992, Bryant 1993). Not
surprisingly, therefore, little research appears to have been carried out in comparison with
some other chlorobenzenes.
The general human population would probably receive their greatest exposure to
trichlorobenzenes through inhalation. The toxicity of all three appear similar; they
damage the liver, kidney and thyroid. There is some indication of slight fetotoxicity at
high doses. There is little evidence of mutagenicity and too few data are available for the
trichlorobenzenes to given a carcinogenicity classification (Giddings et al. 1994a). All
three isomers are toxic to phytoplankton (Sicko-Goad et al. 1989a-d, Sicko-Goad &
Andresen 1993a & b).
1,2,3-trichlorobenzene has been detected in air, drinking water, food and breast milk
(Giddings et al. 1994a) as well as industrially polluted surface waters (Harper et al. 1992)
and sediment (Labunska et al. 1998), though it was not found in human adipose tissue
from Canada (Hermanson et al. 1997). Little is known about its toxicity other than its
ability to damage the liver, kidney and thyroid (Giddings et al. 1994a).
More information is available about 1,2,4-trichlorobenzene. According to Giddings et al.
(1994a), only 1,2,4-trichlorobenzene has industrial application in Canada. It is imported
for solvent and intermediate use. Environmental releases come from industrial
discharges and from spillage of dielectric fluids. As mentioned above, it is toxic to the
liver, thyroid and kidney. Liver and kidney weights and porphyrin excretion increase. In
some studies, more severe liver damage has occurred, including necrotic and non-necrotic
degeneration. 1,2,4-trichlorobenzene may be found in all environmental media,
though there is insufficient analytical data to tell how widespread contamination is and it
was not found in human adipose tissue from Canada (Hermanson et al. 1997).
Giddings et al. (1994a) report 1,3,5-trichlorobenzene air, drinking water, food, breast
milk, though it was not found in human adipose tissue from Canada (Hermanson et al.
1997). It can be found in association with industrial operations (Harper et al. 1992).



3.Tetrachlorobenzenes

Giddings et al. (1994b) reviewed toxicity and exposure data for the tetrachlorobenzenes.
They are no longer used or produced in Canada and releases come only from dielectric
fluid spills and long-range transport. 1,2,4,5-Tetrachlorobenzene used to be used in the
production of 2,4,5-trichlorophenol on a large scale, but this use has now been largely
discontinued. There are not expected to be large differences between the behaviour of
the isomers. Uptake of 1,2,4,5-tetrachlorobenzene was studied in rainbow trout. It is not
volatile enough to evaporate from water easily, and is accumulated by the fish, through
its gills. Bioaccumulation depended upon the rate of activity and oxygen uptake of the
fish, and only the low water solubility prevented significant toxicity occurring (Brauner
et al. 1994).
The greatest exposure of the general population is probably through food. All isomers
were found to affect the liver, kidney, thyroid and lungs, with 1,2,4,5-tatrachlorobenzene
being the most toxic. Not enough information was available to classify
tetrachlorobenzenes as to carcinogenicity.
In addition to the effects noted above, 1,2,4,5-tetrachlorobenzene has also caused changes
in the spleen, thymus, lymph nodes and haematological parameters in animals (Giddings
et al. 1994b). An increase in chromosomal aberrations was seen in workers exposed to
1,2,4,5-tetrachlorphenol at a pesticide manufacturing complex (Giddings et al. 1994b).
In rats, 1,2,3,4- and 1,2,3,5-tetrachlorobenzene caused reduction in the number of live
offspring at concentrations too low to adversely affect the mother (Giddings et al. 1994b).
All isomers have been detected in ambient air, drinking water and food and 1,2,3,4- and
1,2,3,5-tetrachlorobenzene have been identified in breast milk (Giddings et al 1994b),
though none of the isomers were detected in Canadian human adipose tissue (Hermanson
et al. 1997).

4.Pentachlorobenzene
Giddings et al. (1994c) found that though no longer manufactured or used in Canada,
pentachlorobenzene could still enter the environment through spillage of dielectric fluids
or atmospheric transport. Animal studies demonstrate weight loss and effects on the
liver, thymus, kidney, adrenal glands and digestive tract. Anaemia and malformation of
sperm also occurred. There is some indication of fetotoxicity and developmental toxicity.
The thyroid was impacted, with and thyroid hormone (free and total thyroxin)
concentrations reduced. Pentachlorobenzene cannot be assigned a carcinogenicity
classification because of lack of data. Pentachlorbenzene accumulates in, and is toxic to
algae (Sicko-Goad et al. 1989d).
Pentachlorobenzene has been detected in air, drinking water, food and breast milk
(Giddings et al. 1994b), though according to Hermanson et al. (1997) it was found in less
than 15% of human adipose samples collected in Ontario, Canada.

5.Hexachlorobenzene
Hexachlorobenzene (HCB) is a manufactured chemical, which was used as a wood
preservative, as a fungicide for treating seeds, and as an intermediate in organic syntheses
(Budavari et al. 1989). Additionally, hexachlorobenzene may be formed as an unwanted
by-product in the synthesis of other organochlorine compounds high-temperature sources
(Newhook & Meek 1994, Sala et al. 1999). The UNECE (1998) lists HCB alongside
PCDD/Fs and PAHs as being the most important POPs emitted from stationary sources.
HCB emissions from waste incineration, metallurgical industries and burning of
chlorinated fuels are highlighted (UNECE 1998)(Annex V).
HCB is toxic to aquatic life, land plants, land animals, and humans. It is listed by the
IARC as a Group 2B carcinogen, i.e. possible carcinogen to humans and also appears to
be a tumour promoter. Hexachlorobenzene may damage the developing foetus, liver,
immune system, thyroid and kidneys and CNS. The liver and nervous system are the
most sensitive to its effects. Porphyria is a common symptom of HCB toxicity. High or
repeated exposure may damage the nervous system, and can cause irritability, difficulty
with walking and co-ordination, muscle weakness, tremor and/or a feeling of pins and
needles on the skin. Repeated exposure, especially when skin effects occur, can lead to
permanent skin changes, such as changes in pigmentation, tight, thickened skin, easy
wrinkling, skin scarring, fragile skin, and increased hair growth, especially on the face
and forearms (ATSDR 1997, Newhook & Meek 1994). Recent research (van Birgelen
1998) suggests that HCB has dioxin-like toxicity and more epidemiological studies
should be undertaken especially concerning infants fed breast milk in countries with HCB
exposure levels.
With the exception of occupational settings, almost all human exposure occurs via food.
The greatest body of information on HCB toxicity to humans derives from an incident in
Turkey between 1955 and 1959, when HCB-treated grain was made into bread. More
than 600 people experienced porphyria cutanea tarda. Children of exposed women had
skin lesions and 95% of them died at less than one year old. In the long term (20-30
years), some people continued to have abnormal porphyrin biochemistry and
neurological, orthopaedic and dermatological symptoms persisted. Hexachlorobenzene is
also thought to have caused porphyria cutanea tarda in populations exposed industrially
and through food (Newhook & Meek 1994). High concentrations of HCB were found
both in workers at an electrochemical plant at Flix in Spain and the local residents. The
authors of the study stated that HCB exposure was associated with specific health effects
in the most highly exposed subjects (Sala et al. 1999).
Once introduced into environment, HCB strongly absorb to soil materials and almost no
desorption take place (Bahnick & Doucette 1988). It is bioaccumulative and
biomagnifies. It can be measured in ambient air, drinking water, soil, food and breast
milk (Newhook and Meek 1994).
HCB is one of twelve priority POPs intended for global action by the UN Environment
Programme (UNEP) Governing Council. It is intended that HCB will be phased out
worldwide under a convention currently being drawn up (UNEP 1995, 1997).
Furthermore, HCB is included on Annex I of the Draft UNECE POPs Protocol under the
Convention on Long-Range Transboundary Air Pollution (LRTAP)(UNECE 1998).
Within the EC, discharges of HCB are controlled as stipulated by EC Council Directive
86/280/EEC, which amends Directive 76/464/EEC, regarding pollution caused by certain
dangerous substances discharged into the aquatic environment (EC 1986, 1976).
HCB is also included in the list of priority hazardous substances agreed by the Third and
Fourth North Sea Conferences (MINDEC 1990, 1995), where continuous reduction of all
hazardous substances was agreed with the ultimate aim of reducing environmental
concentrations of hazardous substances to near background levels (synthetic substances
to zero) within the next 25 years. The 1998 Ministerial Meeting of the OSPAR
Commission (OSPAR 1998a) further reinforced these objectives. HCB is included on the
OSPAR 1998 List of Candidate Substances, Annex 3 of the OSPAR Strategy with regard
to Hazardous Substances (OSPAR 1998b).

Return to Index

References
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Bahnick, D.A. & Doucette, W.J. (1988) Use of molecular connectivity indices to estimate soil sorption
coefficients for organic chemicals. Chemosphere 17: 1703-1715 .
Brauner, C.J., Randall, D.J., Neuman, J.F. & Thurston, R.V. (1994) The effect of exposure to 1,2,4,5-
tetrachlorobenzene and the relationship between toxicant and oxygen uptake in rainbow trout
(Oncorhynchus mykiss) during exercise. Environ. Toxic. and Chem. 13(11): 1813-1820
Bryant, J.G. (1993) Chlorinated benzenes. IN: Kroschwitz, J.I. & Howe-Grant, (Eds). The Kirk-Othmer
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Budavari, S.M., O’Neil, J., Smith A. and Heckleman P.E. [Eds] (1989) The Merck index: an encyclopaedia
of chemicals, drugs and biologicals. 11th Edn Merck and Co, Inc., New Jersey, USA
CEC (1986) p-dichlorobenzene. IN: Organo-chlorine solvents: Health risks to workers. Publ:
Commission of the European Communities, ISBN 0-85186-078-8, pp1-16
EEC (1976) Council Directive 76/464/EEC of 4 May 1976 on pollution caused by certain dangerous
substances discharged into the aquatic environment of the Community. OJ L 129: 23-29 as amended.
European Community Environmental Legislation Volume 7: Water.
EEC (1986) Council Directive 86/280/EEC of 12 June 1986 on limit values and quality objectives for
discharges of certain dangerous substances included in List 1 of the Annex to Directive 76/464/EEC.
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environment exposure in Canada. Environ. Carcino. & Ecotox. Revs., C12(2): 517-525
Giddings, M., Meek, M.E. & Gomes, R. (1994b) Tetrachlorobenzenes: Evaluation of risks to health from
environment exposure in Canada. Environ. Carcino. & Ecotox. Revs., C12(2): 473-481
Giddings, M., Meek, M.E. & Gomes, R. (1994c) Pentachlorobenzene: Evaluation of risks to health from
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Harper, D.J., Ridgeway, I.M. & Leatherland, T.M. (1992) Concentrations of hexachlorobenzene,
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Hermanson, M.H., Monosmith, C.L. & Donnelly-Kelleher, M.T. (1997) Seasonal and spatial trends of
certain chlorobenzene isomers in the Michigan atmosphere. Atmosph. Environ. 31(4): 567-573
Labunska, I., Stringer, R., Santillo, D. & Stephenson, A. (1998) Identification and environmental
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environmental exposure in Canada. Environ. Carcin. Ecotox. Revs. 12(2): 409-415
Meek, M.E., Giddings, M. & Gomes, R. (1994b) 1,2-Dichlorobenzene: evaluation of risks to health from
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Newhook, R. & Mek, M.E. (1994) Hexachlorobenzene: Evaluation of risks to health from Environmental
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fatty acid composition and quantitative morphology. II. 1,3,5-Trichlorobenzene. Arch. Environ.
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fatty acid composition and quantitative morphology. I. 1,2,4-Trichlorobenzene. Arch. Environ.
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eliminate emissions and discharges of persistent organic pollutatns, including the development of an
international legally binding instrument. UNEP Governing Council, 7 th February 1997.
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human milk. Environ. Health Persp. 106(11): 683-688
Ware, G.W. (Ed.)(1988a) Chlorobenzene. Rev. Environ. Contam.Toxicol. 106: 37-49
Ware, G.W. (Ed.)(1988b) Ortho-, meta- and para- dichlorobenzene. Rev. Environ. Contam.Toxicol. 106:
51-6

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Alkylbenzenes

Alkylbenzenes are single-ring aromatic compounds containing one or more aliphatic side
chains. While there are theoretically thousands of alkylbenzenes, the major products of
commence and, therefore, those to which humans are most likely to be exposed included
toluene (methylbenzene), ethylbenzene, cumene (isopropylbenzene), and three xylenes
(1,2-, 1,3-, and 1,4-dimethylbenzene).
The occurrence of these compounds in the environment is due to their presence in crude
oil and petroleum products. Alkylbenzenes are also produced following the degradation
of the linear alkylbenzene sulphonate (LAS) detergents. The alkylbenzenes are highly
resistant to degradation and may accumulate in sediments (Preston & Raymundo 1993).
Alkylbenzenes are useful sewage markers (Chalaux et al. 1995) and due to their stability
in sediments, they are very useful in tracing the transport of contaminants from their
point sources. Monoaromatic (benzene derivatives) and polyaromatic hydrocarbons
(PAHs) are considered to be the most toxic, and are known to be present at the highest
concentrations during the initial phase of a crude oil spill (Overton 1994).
The acute toxicity of inhaled alkylbenzenes is best described as central nervous system
(CNS) depression (Andrews & Snyder, 1986). Acute toxicity does not vary very much
within the group. In animal models, relatively similar concentrations of inhaled
alkylbenzene vapours were found to be lethal. Impaired reaction times and impaired
speech are the two most commonly noted CNS effects (Klaassen et al. 1996). All
alkylbenzenes mention above are irritating to the eyes and mucous membranes, can cause
irritation and burning of the skin, and all are narcotics at high concentrations. Benzene
itself is a known carcinogen. Chronic exposure can lead to bone marrow depression,
which in a few cases, can progress to leukemia (Budavari et al. 1989).

References
Andrews, L.S. & Snyder, R. (1986) Toxic effects of solvents and vapors. In Toxicology: the basic science
of poisons. Klaasen C.D., Ambur M.O. and Doull J. [Eds], MacMillan Publishing Co., New York:
636-668
Budavari, S.M., O’Neil, J., Smith A., and Heckleman P.E. [Eds] (1989) The Merck index: an
encyclopaedia of chemicals, drugs and biologicals. 11th Edn Merck and Co, Inc., New Jersey, USA
Chalaux N., Takada H., Bayona J.M. (1995) Molecular markers in Tokyo Bay sediments – sources and
distribution. Marine Environmental Research, Vol., 40, No.1, pp.77-92
Klaassen, C.D, Amur, M.O. & Doull, J. [Eds] (1996) Toxicology: The basic science of poisons. 5 th Edition,
McGraw-Hill Companies Inc. IBSN 0-07-105476-6
Overton, E.B. (1994). Toxicity of petroleum. In: Basic Environmental Toxicology. Cockerham & Shane
[Eds], Chapter 5: 133-156
Preston, M.R. & Raymundo, C.C. (1993) The associations of linear alkyl benzenes with the bulk properties
of sediments from the River Mersey estuary. Environmental Pollution, Vol.81, pp. 7-13.

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DDT and metabolites

Technical DDT is made by condensing chloral hydrate with chlorobenzene in
concentrated sulfuric acid. It was first synthesized in 1874, but only in 1939 Mueller and
his coworkers discovered its insecticidal properties (ATSDR 1997). DDT is one of the
most notorious environmental pollutants and has been banned or restricted in most
western countries. Few DDT manufacturers are left. Hindustan Insecticides Ltd (India)
currently manufactures DDT and is cited by several sources (Dinham 1993; FAO/UNEP
1991; RSC 1991). EniChem Synthesis S.p.A. (Italy) are listed by some sources (Dinham
1993; FAO/UNEP 1991), though production is believed to have ceased. Other
manufacturers, for whom the current status is not certain are: P.T. Montrose Pesticido
Nusantara (Indonesia) (Dinham 1993; FAO/UNEP 1991), and All-India Medical (RSC
1991). Unnamed producers are thought also to be operating in China, Mexico, Russia,
South Korea and former Soviet Union States (WWF 1998).
DDT is an insecticide, which was first widely used during the Second World War to
control disease-carrying insects. Such insects are known as vectors, and thus DDT is
often described as being used for “vector control”. For a time it was also used in
agriculture (see eg Carson 1962; Cooper 1991), but because of its environmental impact
this has been almost universally banned. Consequently, today it is again licensed almost
exclusively for vector control. However, it is thought that some of DDT manufactured for
vector control is on fact illegally used in agriculture.
The term “DDT” refers to technical DDT, which is a mixture of several compounds and
may not always have the same composition. The main component is p,p’DDT, though it
also contains a variable mix of other compounds. These are reported by different sources
to include 15-20% of o,p’-DDT (ATSDR 1997; DHHS 1998), 4% p,p’-DDE (Smith
1991; DHHS 1998) and traces of other compounds (ATSDR 1997; DHHS 1998).
DDT is poorly absorbed through the skin, with powder forms being far less easily taken
up than oil-based formulations. DDT is readily absorbed through the gastrointestinal
tract, with increased absorption in the presence of fats (ASTDR 1997). Inhalation
exposure of powders may also take place though the may in fact be trapped in the upper
reaches of the respiratory tract and be ingested rather than through the lungs (ATSDR
1997; Smith 1991). In people who not work with DDT, food is the greatest source of
exposure.
DDT is bioaccumulative. The main ingredient, p,p’-DDT, is broken down in the
environment or in the body to p,p’-DDE and smaller quantities of other chemicals. p,p’-DDE
is more persistent both in the body and the environment than p,p-DDT (Smith
1991) and responsible for most of the observed toxic effects, unless there has been recent
exposure to technical DDT.
DDT is moderately to slightly toxic to studied mammalian species via the oral route
(RSC 1991; Meister 1992; ASTDR 1997). The primary target of DDT is the nervous
system and high doses can cause trembling, increased susceptibility to cold and fear, with
convulsions happening at the highest doses. Death can occur through respiratory arrest,
though animals that survive a day or more after the last dose usually recover completely
(Smith 1991). It has caused chronic effects on the nervous system, liver, kidneys, and
immune systems in experimental animals (ASTDR 1997; WHO 1979). There is evidence
that DDT causes reproductive effects in test animals, including reduced fertility (ASTDR
1997).
Dose levels at which effects were observed in test animals are very much higher than
those that may be typically encountered by humans (WHO 1979; Smith 1991). Human
occupational and dietary exposure to DDT may differ both in dose and in chemical
nature. Occupational exposure would be to technical DDT (predominantly p,p-DDT)
whereas dietary exposure, especially in those countries where DDT is no longer used,
would be predominantly to p,p-DDE, although there are several breakdown products to
which individuals would also be exposed (Longnecker et al. 1997; ATSDR 1997).
Several of the DDT group are endocrine disruptors, exhibiting different modes of action.
Several are weakly oestrogenic. Of these, o,p’-DDT is the most active. p,p’-DDE, the
compound likely to be present at highest concentrations in most humans, is an
antiandrogen (Longnecker et al. 1997).
Acute effects likely in humans due to low to moderate exposure may include nausea,
diarrhea, increased liver enzyme activity, irritation (of the eyes, nose or throat), disturbed
gait, malaise and excitability; at higher doses, tremors and convulsions are possible
(ASTDR 1997).
The IARC classified p,p’-DDT as possbly carcinogenic to humans (group 2B) and the US
Department of Health and Human Services regards it as being “reasonably anticipated to
be a human carcinogen” (DHHS 1998).
However, DDT’s most severe impacts are on the environment. DDT, or rather, its
metabolite, p,p’-DDE, causes the thinning of bird’s eggshells through perturbation of
calcium metabolism. Eggshell thinning caused by p,p’-DDE results in crushed eggs, or,
if the egg is not crushed, the embryo can die of dehydration as too much water is lost
through the thinned shell (Hickey & Anderson 1968; Newton 1995; Provini & Galassi
1999). Tests on 15 different toxic pollutants found that only p,p’-DDE has the ability to
thin shells over an extended period (Haegele & Tucker 1974; Peakall & Lincer 1996).
Although DDT primarily causes population decline through reproductive failure, though
it may also kill highly exposed birds directly (Carson 1962; Fry 1995; Cooper 1995;
Newton et al. 1982; Garcelon & Thomas 1997). Analysis of kestrels and sparrowhawks
in the 1960s and 1970s suggest that some were being killed directly by p,p’-DDE
exposure (Newton et al. 1982).
Some bird populations which previously suffered from p,p’-DDE impacts of egg-shell
thinning and egg breakage are no longer at such risk. Studies in the UK on the grey
heron, Ardea cinerea L., (Newton et al. 1993) show that levels of DDE in herons or their
eggs have significantly declined. A study on grey herons in France noted that levels of
p,p’-DDE in eggs were lower than levels associated with reproductive effects reported in
the wild or in laboratory studies (de Cruz et al.1997).
However, some effects of organochlorines in seabirds have been observed recently
despite the general downward trend in many organochlorines. In the Arctic, present p,p’-DDE
levels in Canadian tundra peregrines, Fennoscandian merlin and white-tailed sea
eagle are still causing significant egg shell thinning (de Wit et al. 1997).
DDT is controlled under numerous international legal instruments - notably the PIC
Convention, the LRTAP POPs protocol, the Barcelona Convention, the Helsinki
Convention, the IJC and the draft UNEP POPs Convention. It is also, of course, included
under wider groupings of organochlorine pesticides or organohalogens under the various
waste trade Conventions and the OSPAR Convention. Agricultural use of DDT is almost
totally banned, but its use is frequently retained for public health purposes. According to
FAO/UNEP (1991) DDT is banned in Chile, Cuba, the EC, Liechtenstein, Mexico,
Panama, Republic of Korea, Singapore, Sri Lanka, Sweden, Togo and the USSR and has
been withdrawn from sale in Canada and Poland. It is severely restricted in Argentina,
Belize, China, Colombia, Dominica, Ecuador, Japan, Kenya, Mauritius, the USA,
Venezuela, and Yugoslavia. In many of these countries, use is only permitted for control
of critical disease vectors and would be carried out only at the behest of the government
health department. In addition, DDT is banned (except for drug use) in the countries
which are party to the 1992 Helsinki Convention. Unfortunately, DDT is still diverted
illegally from government health programmes to agricultural use on a regular basis. This
is known or suspected to have happened in Bangladesh, Belize, Ecuador, India, Kenya,
Madagascar, Mexico and Tanzania (WWF 1998).

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129
Provini, A.& Glassi S. (1999) Polychlorinated Biphenyls and Chlorinated Pesticides in Bird Eggs from
Calabria (Southern Italy). Ecotoxicology and Enviromental Safety 43:91-97
RSC (1991) The Agrochemicals Handbook, 3rd Edition. Publ: Royal Society of Chemistry Information
Services, Cambridge, UK.
Smith, A. G. (1991) Chlorinated hydrocarbon insecticides IN: Handbook of Pesticide Toxicology, Volume
2, Classes of Pesticides, Hayes, W.J.Jr. & Laws, E.R.Jr. (Eds.), Publ: Academic Press, Inc, pp731-915
WHO (1979) DDT and its derivatives. Environmental Health Criteria 9. World Health Organizations,
Geneva, 1979, 194pp.
WWF (1998) Resolving the DDT dilemma. Publ: WWF US & WWF Canada, Washington & Toronto,
52pp.

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Hexachloro-1,3-butadiene

Hexachloro-1,3-butadiene (HCBD) is a colourless liquid with a turpentine-like odour.
This compound is not found naturally in the environment. HCBD either commercially
manufactured or is known to be a by-product of the manufacture of chlorinated
hydrocarbons such as tetrachloroethene, trichloroethene, and carbon tetrachloride
(ATSDR 1997; US EPA, 1986, Johnston et al. 1994; Botta et al. 1996). It is always
present in relatively small quantities (up to 5% and more of hexachlorobutadiene in the
chlorolysis process of 1,2-dichloroethane for the production of carbon tetrachloride and
tetrachloroethene), but, because of the huge production of volatile chlorinated solvents,
the amounts of hexachlorobutadiene from the different processes are relevant (Botta et al.
1996). It is also reported as a contaminant in technical formulations of
pentachlorophenol, used widely as a wood preservative (Goodrichmahoney et al. 1993).
Hexachlorobutadiene was first prepared in 1877 by the chlorination of hexyl oxide
(ATSDR 1997).
Hexachlorobutadiene is used as a chemical intermediate in the manufacture of rubber
compounds (ATSDR 1997). Lesser quantities of hexachlorobutadiene are used as a
solvent, a fluid for gyroscopes, a heat transfer liquid, hydraulic fluid, and as a chemical
intermediate in the production of chlorofluorocarbons and lubricants. Small quantities are
also used as a laboratory reagent. In the international market, Russia is reported to be one
of the major users of hexachlorobutadiene, where it is used as a fumigant on grape crops
(ATSDR 1997).
Hexachlorobutadiene is a wide spread environmental contaminant. It can exist in the
atmosphere as a vapour or adsorbed to airborne particulate matter. HCBD and it has been
found in wastewater from chlorine industry, leachate from landfills and hazardous waste
sites, and also in air, soils, surface water and sediments (ATSDR 1997; Santillo &
Labounskaia 1997 a & b; Choudhary 1995). It has also been detected in fly ash from the
inceniration of HCBD-containing hazardous wastes (Choudhary 1995).
Hexachlorobutadiene is toxic compound. Acute toxic effects may include the death of
animals, birds, or fish, and death or low growth rate in plants. Acute effects are seen two
to four days after animals or plants come in contact with a toxic chemical substance (US
EPA, 1986; Choudhary 1995). Chronic toxic effects may include shortened lifespan,
reproductive problems, lower fertility, and changes in appearance or behaviour.
Hexachlorobutadiene has high acute and chronic toxicity to aquatic life (US EPA, 1986).
Kidney was found to be a main target organ for HCBD (Jonker et al. 1996; Choudhary
1995). If ingested, HCBD concentrates in the kidney, interferes with fundamental
processes of cell respiration and can, as a result of conjugation with other compounds in
the body, react with DNA resulting in cell death or the development of tumours
(Choudhary 1995; ATSDR 1997). Short and longer-term exposure to very low doses via
food, induced kidney and liver damage in laboratory animals, with juveniles more at risk
than adults. It was shown that human exposures to HCBD were associated with highly
significant increases in a number of individual and summed bile acid measures in the
study of the possible hepatic effects of different chlorinated compounds including HCBD
(Driscoll et al. 1992)
The International Agency for Research on Cancer concluded that there was limited
evidence of HCBD carcinogenicity in rats and classified HCBD as compound not
classifiable as to human carcinogenicity (Group 3) (IARC 1999). The US
Environmental Protection Agency considers HCBD to be a possible human carcinogen
and has classified it as a Group C carcinogen (IRIS 1993).

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References
ATSDR (1997) ARSDR’s Toxicological profiles on CD ROM. Agency for Toxic Substances and Disease
Registry, U.S. Public Health Service. CRC Publishers
Botta, D. Dancelli, E. & Mantica, E. (1996) A case history of contamination by polychloro-1,3-butadiene.
Environmental Science and Technology 30(2): 453-462
Choudhary, G. (1995) Human health perspecives on environmental exposure to hexachlorobutadiene: a
review. Environ. Carcino. & Ecotox. Revs. C13(2): 179-203
Driscoll, T.R., Hamdam, H.H., Wang, G., Wright, P.F.A. & Stacey, N.H. (1992) Concentrations of
individual serum or plasma bile acids in workers exposed to chlorinated aliphatic hydrocarbons. British
Journal of Industrial Medicine 49: 700-705
Goodrichmahoney, J.W., I.P. Murarka, L.J. Hocombe and M.E. Horn (1993). Pentachlorophenol-treated
wood poles and crossarms - toxicity characteristic leaching procedure (tclp) results. Environment
International 19(6): 535-542.
IARC (1999). 1,1,2,3,4,4-Hexachlorobutadiene. IARC Monographs. International Agency for Research on
Cancer. Geneva. Vol. 73, p. 277
IRIS (1993) Hexachlorobutadiene. Integrated Risk Information System. US EPA, Washington, DC. May
14, 1993
Johnston, P.A., R.L. Stringer, R. Clayton and R.J. Swindlehurst (1994). Regulation of toxic chemicals in
the North Sea: The need for an adequate control strategy. North Sea Monitor June 1994: 9-16.
Jonker, D., Woutersen, R.A. & Feron, V.J. (1996) Toxicity of mixutes of nephrotoxicants with similar or
dissimilar mode of action. Food and Chemical Toxicology 34: 1075-1082
Santillo, D. & Labounskaia, I. (1997a) Petkim: Organic Analytical report 1: Analysis of marine sediments
and seawater from locations adjacent to the main wastewater discharges of the Petkim chemical
complex, Aliaga, Turkey. Greenpeace Research Laboratories Technical note 08/97
Santillo, D. & Labounskaia, I. (1997b) Petkim: Organic analytical report 2: Analysis of wastes generated
by integrated chemical production processes, including the manufacture of VCM and chlorinated
organic solvents, at the Petkim chemical complex, Aliaga, Turkey. Greenpeace Research Laboratories
Technical Note 09/97
US EPA (1986). Factsheets for regulated chemicals: Hexachlorobutadiene. Office of Environmental Health
Hazard Assessment.

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Hexachlorocyclohexane

A mixture of hexachlorocyclohexanes is produced by the photochemical reaction between
chlorine and benzene (Safe 1993). Technical grade hexachlorocyclohexane (HCH)
comprised of different isomeric forms. The approximate isomer content is alpha-HCH
(60-70%), beta-HCH (7-10%), gamma-HCH (14-15%), delta-HCH (7%), and epsilon-HCH
(1-2%). Lindane is the gamma isomer of hexachlorocyclohexane and it is
commercially produced by purification of the technical HCH (Safe 1993). This
compound has been produced worldwide for use as an insecticide to control
grasshoppers, cotton and rice pests, wireworms, and other soil pests. Lindane has been
used for protection of seeds, for treatment of poultry and livestock, and for control of
household insects. It is also still used as a scabicide and pediculocide, usually as lotions,
creams, and shampoos.
Alpha-, beta-, and gamma-HCH are the most important isomers in terms of
environmental impact. The relatively high stability and lipophilicity of HCH and its
global use pattern has resulted in significant environmental contamination by this
chlorinated hydrocarbon. Once introduced into environment HCH may persist for many
years (Martijn & Schreuder 1993). The beta-isomer is more persistent than others
(ATSDR 1997).
Human intake of HCH compounds is largely through food consumption (Toppari et al.
1995). Alpha-, beta- and gamma-HCH have been recorded in human breast-milk with the
beta-isomer being the most ubiquitous (Waliszewski et al. 1996; Safe 1993). The
generally less widespread nature of the alpha- and gamma-isomers in comparison to beta-HCH
is due to the more rapid clearance of these isomers from the body. Like many
persistent organochlorines, HCH levels in the body have been found to increase with age
(ASTDR 1997).
Hexachlorocyclohexane isomers have been detected in air, surface and ground water, soil
and sediments (El-Gendy et al. 1991; Safe 1993; Xu 1994; Tan & Vijayaletchumy 1994;
Skark & Zullei-Seibert 1995; Ramesh et al. 1991), plants (Xu 1994), birds, fish and
mammals (Smith 1991; Xu 1994; Abd-Allah 1994; Norstrom & Muir 1994). In humans
lindane mostly concentrates in adipose tissue (Safe 1993). It has been reported that
lindane and other organochlorine compounds can be transferred through the pathway
soil®earthworm®bird/mammal (Hernandez, et al. 1992; Romijn et al. 1994) thereby
causing secondary poisoning.
Lindane, the gamma-isomer of hexachlorocyclohexane, is toxic to animals, humans, and
aquatic species. Acute animal poisoning by lindane causes increased respiratory rate,
restlessness accompanied by increased frequency of urination, intermittent muscular
spasms of the whole body, salivation, grinding of teeth and consequent bleeding from the
mouth, backward movement with loss of balance and somersaulting, retraction of the
head, convulsions, gasping and biting, and collapse and death usually within a day (Smith
1991).
Chronic health effects can occur at some time after exposure to lindane and can last for
months or years. Lindane has been shown to cause liver, lung, endocrine gland and
certain other types of cancer in animals (Smith 1991). Repeated overexposure may
damage the liver. Chronic toxic effects may also include shortened lifespan, reproductive
problems, lower fertility, and changes in appearance or behaviour. The differential
actions of hexachlorocyclohexane isomers may produce variable effects on different
regions of the nervous systems and in different species of animals (Nagata et al. 1996).
Hexachlorocyclohexane may be introduced to the environment from industrial
discharges, insecticide applications or spills, and may can cause significant damage.
Acute toxic effects may include the death of animals, birds, or fish, and death or low
growth rate in plants (Bunton 1996, Smith 1991). The insecticide load in surface waters
does not ordinarily reach concentrations acutely toxic to aquatic fauna. However, lindane
has high chronic toxicity to aquatic life. The effects of the low insecticide concentrations
often appear only after relatively long exposure times. Chronic exposure to insecticides,
such as lindane, (Schulz et al. 1995) can be hazardous to freshwater macroinvertebrates
even at unexpectedly low concentrations. The low-concentration effects may depend on
both species and substance and therefore cannot be predicted from toxicity data at higher
concentrations.
Hexachlorocyclohexane, as a toxic, persistent and bioaccumulative chemical, is a subject
to the European Community legislation. The limit values and quality objectives for
discharges of hexachlorocyclohexane are set by the Council Directive 84/491/EEC (EEC
1984) as amended. The uses of hexachlorocyclohexane (including lindane) were severely
restricted under the Persistent Organic Pollutants (POPs) Protocol, which was adopted in
1998 and has 36 contracting parties encompassing not only Europe but also Canada and
the United States of America (UNECE 1998). The POPs Protocol is part of the 1979
Convention on Long-Range Transboudary Air Pollution (LRTAP), which is under the
auspices of the United Nations Economic Council for Europe. Lindane is also included in
the Annex III of the 1998 Rotterdam Convention on the Prior Informed Consent
procedure (PIC procedure) among 27 other chemicals (FAO/UNEP 1998). Under the PIC
procedure countries should not export any chemical to any other country without first
receiving explicit permission. In order to avoid unfair trade barriers arising through the
implementation of the Convention, any country that has denied import of any chemical
must also stop producing it domestically and may not import it from any country that is
not a Party to the Convention.

References
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EEC (1984) Council Directive 84/491/EEC of 9 October 1984 on limit values and quality objectives for
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FAO/UNEP (1998) Rotterdam Convention on the prior informed consent procedure for certain hazardous
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Nagata K., Huang C.S., Hamilton B.J., Carter D.B., Narahashi T. (1996). Differential-effects of
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