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ARCHIVED - 1,4-Dichlorobenzene - PSL1

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Environment Canada
Health Canada
1993
ISBN: 0-662-21061-1
Cat. No.: En40-215/23E

(ARCHIVED - PDF Version - 168 K)

Canadian Environmental Protection Act

Table of Contents

List of Tables

  • Table 1. Estimated Total Daily Intake of a Piscivorous Mammal Exposed to 1,4-Dichlorobenzene under "Worst-case" Conditions
  • Table 2. Estimated Daily Intake of 1,4-Dichlorobenzene from Various Sources by Canadians

Synopsis

1,4-Dichlorobenzene is produced in and imported into Canada. Approximately 3 500 tonnes per year are currently used in Canada as an air freshener, as a deodorizer in urinals, and as a moth and bird repellent. In Canada 1,4-dichlorobenzene is present at measurable concentrations in municipal and industrial effluents, ambient and indoor air, ground and surface water, sediment, and biota. 1,4-Dichlorobenzene is not persistent in air or surface water but persists and accumulates in sediment under anaerobic conditions.

The maximum concentration of 1,4-dichlorobenzene in surface waters in Canada was approximately 300 times less than the effects threshold estimated for the most sensitive aquatic species identified. 1,4-Dichlorobenzene is volatile but the highest mean level of 1,4-dichlorobenzene in Canadian air was approximately 12 700 times less than the effects threshold estimated for wild mammals in studies in which inhalation was the principal route of exposure. No data on the toxicological effects of 1,4-dichlorobenzene to benthic organisms were identified. Therefore, it was not possible to determine whether 1,4-dichlorobenzene concentrations found in sediments could result in harmful effects to these biota.

1,4-Dichlorobenzene is present in low concentrations and has a short half-life in the atmosphere. As such, it is not expected to contribute significantly to the formation of ground-level ozone, global warming, or depletion of stratospheric ozone.

Based on limited available data on concentrations in ambient and indoor air, drinking water and food, the average total daily intakes of 1,4-dichlorobenzene for various age groups in the general population have been estimated. These average daily intakes are less (by approximately 40 to 780 times) than the tolerable daily intake derived on the basis of studies in laboratory animals. The tolerable daily intake is the intake to which it is believed that a person can be exposed over a lifetime without harmful effect.

Based on these considerations, it has been determined that there is insufficient information to conclude whether 1,4-dichlorobenzene is entering the environment in quantities or under conditions that may be harmful to the environment. It has, however, been concluded that 1,4-dichlorobenzene is not entering the environment in quantities or under conditions that may constitute a danger to the environment on which human life depends, or to human life or health.

1.0 Introduction

The Canadian Environmental Protection Act (CEPA) requires the federal Ministers of the Environment and of Health to prepare and publish a Priority Substances List that identifies substances, including chemicals, groups of chemicals, effluents, and wastes that may be harmful to the environment or constitute a danger to human health. The Act also requires both Ministers to assess these substances and determine whether they are "toxic" as defined in section 11 of the Act which states:

"...a substance is toxic if it is entering or may enter the environment in a quantity or concentration or under conditions

  1. having or that may have an immediate or long-term harmful effect on the environment;
  2. constituting or that may constitute a danger to the environment on which human life depends; or
  3. constituting or that may constitute a danger in Canada to human life or health."

Substances that are assessed as "toxic" according to section 11 may be placed on Schedule I of the Act, and considered for possible development of regulations, guidelines or codes of practice to control any aspect of their life cycle, from the research and development stage through manufacture, use, storage, transport and ultimate disposal.

The assessment of whether 1,4-dichlorobenzene is "toxic", as defined under CEPA, was based on the determination of whether it enters or is likely to enter the Canadian environment in a concentration or quantities or under conditions that could lead to exposure of humans or other biota to levels that could cause adverse effects.

The assessment of whether the 1,4-dichlorobenzene is "toxic" to human health under CEPA, is based principally on documentation prepared by staff of Health Canada for the International Programme on Chemical Safety (IPCS). Between 1984 and 1987, original data relevant to the assessment of risks to health associated with exposure to the chlorinated benzenes (excluding hexachlorobenzene) were reviewed by Health Canada staff in the preparation of a draft IPCS Environmental Health Criteria Document (EHC). The current assessment has been updated and expanded to emphasize data most relevant to the assessment of the risks associated with exposure to 1,4-dichlorobenzene in the general environment in Canada.

In preparation of the IPCS document, a wide variety of scientific databases were searched to update information provided in earlier contractors' reports. These earlier reports included an annotated bibliography on the chlorobenzenes (excluding hexachlorobenzene) by Peter Strahlendorf (1978), and a criteria document on chlorobenzenes (including hexachlorobenzene) by Michael Holliday and Associates (1984a, 1984b). Additional information was identified during peer review of the draft Environmental Health Criteria Document by IPCS focal points and a Task Group of Experts who met in June 1990. In February 1991, a search of ENVIROLINE, Chemical Abstracts, Pollution Abstracts, Environmental Bibliography, IRIS, MEDLINE, and BIOSIS databases was conducted to identify recent data relevant to assessment, in particular, of the risks to Canadians. Data relevant to assessment of whether 1,4-dichlorobenzene is "toxic" to human health obtained after completion of these sections of this report (i.e., May 1992), were not considered for inclusion.

Data relevant to the assessment of whether 1,4-dichlorobenzene is "toxic" to the environment were identified from existing review documents, published reference texts and on-line searches completed in November 1990 of the following commercial databases: ASFA, BIOSIS, CAB Abstracts, Chemical Abstracts, Chemical Evaluation Search and Retrieval System (CESARS), CIS, ENVIROLINE, Hazardous Substances Database, International Register of Potentially Toxic Chemicals (IRPTC), National Technical Information Service (NTIS), TOXLINE, and the Toxic Release Inventory Data Base. Studies published after November 1990 were identified by a review of relevant journals as well as Current Contents (agriculture, biology, and environmental sciences). Information received after December 1992 was not included in the environmental sections of this report. Although much of the research on 1,4-dichlorobenzene has been conducted outside of Canada, where possible, Canadian data on sources, use patterns, fate, and effects of this substance on the environment were emphasized.

Although review articles were consulted where considered appropriate, original studies that form the basis for the determination of "toxic" under CEPA were critically evaluated by staff of Health Canada (human exposure and effects on human health) and Environment Canada (entry and environmental exposure and effects). The following officials contributed to preparation of the report:

B. Elliott (Environment Canada)
C. Fortin (Environment Canada)
M. Giddings (Health Canada)
R.G. Liteplo (Health Canada)
K. Lloyd (Environment Canada)
M.E. Meek (Health Canada)

R. Gomes of Health Canada also contributed to the consolidation of the Assessment Report.

In this report, a synopsis is presented that will appear in the Canada Gazette. Section 2.0 presents a summary of the technical information critical to the assessment, which is presented in greater detail in unpublished supporting documentation. The assessment of whether 1,4-dichlorobenzene is "toxic", as defined under CEPA, is presented in Section 3.0.

As part of the review and approvals process established by Environment Canada, the environmental sections of this Assessment Report were reviewed by Dr. Brett Betts (Washington State Department of Ecology, Seattle, Washington), Dr. Peter Chapman (EVS Consultants, Vancouver, British Columbia), Dr. Arthur Niimi (Department of Fisheries and Oceans, Burlington, Ontario), and Dr. Barry Oliver (Zenon Environmental Laboratories, Burnaby, British Columbia). Sections related to the effects on human health were approved by the Standards and Guidelines Rulings Committee of the Bureau of Chemical Hazards of Health Canada. The entire Assessment Report was reviewed and approved by the CEPA Management Committee of Environment Canada and Health Canada.

Copies of this Assessment Report and the unpublished supporting documentation are available upon request from the following:

Environmental Health Centre
Room 104
Health Canada
Tunney's Pasture
Ottawa, Ontario,
Canada
K1A 0L2

Commercial Chemicals Branch
Environment Canada
14th Floor, Place Vincent Massey
351 Saint-Joseph Boulevard
Hull, Quebec,
Canada
KIA 0H3

2.0 Summary of Information Critical to Assessment of "Toxic"

2.1 Identity, Properties, Production, and Uses

1,4-Dichlorobenzene, also known as para-dichlorobenzene or p-dichlorobenzene, is a neutral, colourless, flammable solid (U.S. EPA, 1986) with a molecular weight of 147.01 and the empirical formula C6H4Cl2. 1,4-Dichlorobenzene has a moderate vapour pressure (90 Pa @ 25°C), a low water solubility (79 mg/L @ 25°C), and a moderate octanol/water partition coefficient (log Kow = 3.4) [Mackay et al., 1992]. Its organic carbon partition coefficient, calculated from the log Kow value suggested by Mackay et al. (1992), is 1 030. 1,4-Dichlorobenzene absorbs infrared radiation, including wavelengths in the 7-13 mm region (Sadtler Research Laboratories, 1982).

1,4-Dichlorobenzene is produced by chlorination of benzene in the liquid phase with a catalyst. This substance typically contains less than 0.1% monochlorobenzene and trichlorobenzenes, and less than 0.5% each of 1,2- and 1,3-dichlorobenzene (Kao and Poffenberger, 1979). The analytical methods by which 1,4-dichlorobenzene is quantified in environmental media include gas chromatography with flame ionization or electron capture detection and gas chromatography/mass spectrometry (Oliver and Nicol, 1982; Oliver and Bothen, 1982).

1,4-Dichlorobenzene is produced in and imported into Canada (Camford Information Services, 1991). In the past few years, the amount imported into Canada has increased while domestic production has declined. Overall, the Canadian demand for 1,4-dichlorobenzene has remained steady at approximately 3 500 tonnes per year over the past 5 years. This number is not expected to change during the next 5 years (Camford Information Services, 1991). The amount of 1,4-dichlorobenzene produced in the United States in 1990 was 62.6 kilotonnes (Chemical Marketing Reporter, 1990).

In Canada, 1,4-dichlorobenzene is used as an air freshener, a urinal deodorizer, and in moth and bird repellents (Camford Information Services, 1991). Quantitative data on use patterns for this substance were only identified for the period 1977 to 1979, when 9.3% of the annual demand was used in the production of deodorant blocks, and 0.7% was used in the production of moth crystals (Environment Canada, 1983, unpublished). In the United States, 1,4-dichlorobenzene has a wider variety of applications, including use in the synthesis of polyphenylene sulfide (PPS) resin and 1,2,4-trichlorobenzene (Chemical Marketing Reporter, 1990).

2.2 Entry into the Environment

There are no known natural sources of 1,4-dichlorobenzene, and quantitative information on its release into the Canadian environment from anthropogenic sources is limited. On the basis of its volatility and the dispersive nature of its uses, it is expected that all of the 3 500 tonnes of 1,4-dichlorobenzene used annually in Canada are released into the environment. It has also been suggested that 1,4-dichlorobenzene may be produced from the dehalogenation of more highly chlorinated chlorobenzenes (Bosma et al., 1988; Holliger et al., 1992; Fathepure et al., 1988).

Data concerning the release of 1,4-dichlorobenzene into the atmosphere from industrial and municipal facilities in Canada were not identified. However, releases of the substance in liquid effluents from these facilities have been reported. Under the Ontario Municipal/Industrial Strategy for Abatement (MISA) program, 1,4-dichlorobenzene was detected in effluents discharged from organic chemical manufacturing plants into the St. Clair River at Sarnia, and Corunna, Ontario, between October 1, 1989 and January 31, 1991. The amounts released were estimated to range between 0.002 and 0.365 kg/day. Also under the MISA program, loading values ranging between 0.001 and 0.055 kg/day were reported for the St. Lawrence, Welland, and Mary's Rivers (OME, 1992, unpublished; OME, 1992a, 1992b).

1,4-Dichlorobenzene was detected (mean mass loading value of 143 g/day) in waste water treatment plant effluents discharged into the Strait of Georgia in the Vancouver area between March and December 1987 (Fanning et al., 1989). Based on the results of a study conducted between 1985 and 1986, 1,4-dichlorobenzene was also present in effluent from 5 of 10 textile mills located in Ontario and Quebec (Environment Canada, 1989a) where concentrations as high as 71.1 mg/L were reported.

1,4-Dichlorobenzene was detected at concentrations up to 9.6 mg/L in process effluents from pulp and paper mills in Ontario (OME, 1991a, 1991b). Mean concentrations ranging from 900 to 1 400 ng/L 1,4-dichlorobenzene were detected in effluents from water pollution control plants at Galt, Waterloo, and Welland, Ontario (Melcer et al., 1988). 1,4-Dichlorobenzene was also detected in one third of the samples of digested sludge collected between 1980 and 1985 from 15 Canadian municipal treatment facilities where the maximum concentration was 1 500 ng/g (Webber and Lesage, 1989). The highest concentration of 1,4-dichlorobenzene (detection limit = 220 ng/g; 4% detection frequency), in treated sludge obtained from 2 of 37 municipal water pollution control plants in Ontario in 1987 was 2 644 ng/g (OME, 1988).

2.3 Exposure-related Information

2.3.1 Fate

There are a number of processes that affect the distribution and transformation of 1,4-dichlorobenzene in the environment, including the following: atmospheric photo-oxidation; volatilization; partitioning to soil, sediment and biota; and aerobic degradation (Howard et al., 1989; Howard, 1991; Mackay et al., 1992; Garrison and Hill, 1972, Wakeham et al., 1983; Callahan et al., 1979; Ellington et al., 1988). 1,4-Dichlorobenzene that is not removed from the environment by degradative processes, ultimately accumulates in anaerobic sediments and possibly groundwater.

1,4-Dichlorobenzene absorbs radiation weakly at wavelengths greater than 300 nm, and therefore, direct photolysis of this substance in the atmosphere is not likely (Bunce et al., 1987). However, 1,4-dichlorobenzene will react with photochemically produced hydroxyl radicals in the atmosphere with an estimated half-life of 31 days (Howard, 1989). Mackay et al., (1992) estimated a mean half-life in the atmosphere of approximately 3 weeks for 1,4-dichlorobenzene on the basis of photo-oxidation and advection processes. The presence of 1,4-dichlorobenzene in rainwater indicates that it persists long enough to be returned to the earth's surface by atmospheric wash out (Ligocki et al., 1985).

Volatilization is the predominant mechanism for the removal of 1,4-dichlorobenzene from surface water and soil (Mackay et al., 1992; Callahan et al., 1979; Garrison and Hill, 1972; Wakeham et al., 1983; Howard, 1991). Volatilization half-lives ranging between < 1 day and 31 days have been reported (Wakeham et al., 1983; Howard et al., 1989).

1,4-Dichlorobenzene is slowly biodegraded in soil under aerobic conditions (Bouwer et al., 1981; Haider et al., 1981; van der Meer et al., 1987). Mackay et al. (1992) selected a half-life of approximately 8 months for 1,4-dichlorobenzene in soil, while Howard (1991) reported a half-life ranging from 4 weeks to 6 months. Based on its estimated organic carbon sorption coefficient (Koc) of 1 030, the soil mobility potential of 1,4-dichlorobenzene was classified as low, according to the scale presented by McCall et al. (1981). However, evidence for leaching of 1,4-dichlorobenzene through soil has been reported by Elder et al., (1981), Zoeteman et al., (1980), and Wilson et al. (1981). The presence of 1,4-dichlorobenzene in a plume of contaminated groundwater a distance of 3 500 metres from sewage disposal beds confirms the persistence of this substance under anaerobic conditions (Barber, 1988).

1,4-Dichlorobenzene that partitions to sediment, particularly the organic fraction of bottom sediments, can persist for long periods of time with little likelihood of anaerobic degradation (Oliver and Nicol, 1982). On the basis of an analysis of core sediment samples obtained from Lake Ontario, it has been reported that 1,4-dichloro-benzene has been accumulating over a period of 60 years, with the highest concentrations correlating with peak production of chlorobenzenes in North America during the 1960s (Oliver and Nicol, 1984; Durham and Oliver, 1983). Based on review of the literature, Mackay et al. (1992) selected a mean half-life of approximately 2 years for 1,4-dichlorobenzene in the first 1 cm of sediment. Within sediments, 1,4-dichloro-benzene is expected to equilibrate between the pore water and the organic phase (Di Toro et al., 1991).

Oliver and Nimii (1983) reported bioconcentration factors ranging from 370 to 720 (whole fish) for the rainbow trout (Oncorhynchus mykiss) exposed to 1,4-dichlorobenzene under laboratory conditions. Bioconcentration factors ranged from 100 to 450 and increased to 1 400 at day 23 of a 60-day early life stage (egg to 2-week alevin stage) study of the rainbow trout, in a continuous flow system (Calamari et al., 1982). Biological half-lives of less than 1 day and less than 5 days were reported for the bluegill sunfish (Lepomis macrochirus) [Barrows et al., 1980] and the oligochaete worms (Tubifex tubifex and Limnodrilus hoffmeisteri) [Oliver, 1987], respectively.

2.3.2 Concentrations

1,4-Dichlorobenzene has been detected in air, surface water, groundwater, drinking water, sediments, biota, and food in Canada.

The mean concentration of 1,4-dichlorobenzene in ambient air sampled between October 1988 and December 1990 at 23 sites across Canada was 0.92 mg/m3 (Environment Canada, 1991). 1,4-Dichlorobenzene was measured above the detection limit (0.1 mg/m3) in 99% of the samples, and the mean levels of 1,4-dichlorobenzene ranged from 0.22 to 2.94 mg/m3 (Environment Canada, 1991). The maximum (24-hour) concentrations were highest in industrial sections of Vancouver (4.82 mg/m3), Toronto (15.7 mg/m3), and Windsor (14.6 mg/m3). The mean concentration of 1,4-dichlorobenzene in air sampled between February 1989 and November 1990 at a rural site (Walpole Island) in Ontario was 1.37 mg/m3; the maximum level was 3.53 mg/m3 (Environment Canada, 1991).

Concentrations of 1,4-dichlorobenzene in indoor air are often higher than those in ambient air because of its presence in consumer products (e.g., moth repellents and space deodorants). In a 1984 study of 188 homes in Los Angeles and Contra Costa, California, the ratios of median overnight concentrations of 1,4-dichlorobenzene in indoor/outdoor air in a sub-sample of 57 homes ranged from 1.4 to 1.8 (Wallace et al., 1988). It is possible that ratios may be higher in colder climates, because of better insulation and less ventilation in winter, although reliable relevant data on ratios of concentrations in indoor/outdoor air in Canada were not identified.

Mean and median concentrations of 1,3- and 1,4-dichlorobenzene (combined) in indoor air in the U.S. Total Exposure Assessment Methodology (TEAM) study ranged from 0.44 to 71 mg/m3 (Wallace et al., 1985, 1986; Wallace, 1986; Pellizzari et al., 1982). In the only report of the TEAM study in which 1,4-dichlorobenzene was measured separately, median overnight concentrations in indoor air in 57 homes in California ranged from 0.4 to 2.8 mg/m3 (Wallace et al., 1988). The range of individual measured concentrations is often very broad, with maximum values sometimes exceeding 1 000 mg/m3 (1,3- and 1,4-dichlorobenzene combined) [Pellizari et al., 1982]. Information on concentrations of 1,4-dichlorobenzene in indoor air in Canada, available at the time of completion of the health-related sections of this assessment, was restricted to a limited and probably unrepresentative number of homes (Chan et al., 1990). The average concentration of 1,4-dichlorobenzene (detection limit = 6.0 ng/tube) in 12 homes sampled in November and December, 1986 was 15.0 mg/m3 (range 1 to 107 mg/m3) [Chan et al., 1990]. The average concentration in ambient air outside these homes was 0.3 mg/m3. In repeat sampling of 6 of these homes in February and March 1987, 1,4-dichlorobenzene was not detected in 3 (detection limit = 6 ng/tube), while the reported mean concentration in ambient air was 10.2 mg/m3.

For samples of surface water collected between 1986 and 1989, the mean annual concentrations of 1,4-dichlorobenzene in the Niagara River were reported to range between 0.82 ng/L at Fort Erie and 2.47 ng/L at Niagara-on-the-Lake (NRDIG, 1988, 1990). Based on a monitoring program of surface and raw drinking water supplies in six provinces (Alberta, Quebec, New Brunswick, Nova Scotia, Newfoundland, and Prince Edward Island) conducted from February 1987 to May 1989, the levels of 1,4-dichlorobenzene in surface water ranged between 0.57 to 130 ng/L in the provinces where it was detected (Environment Canada, 1992).

1,4-Dichlorobenzene was detected in groundwater adjacent to landfill sites in North Bay, and Burlington, Ontario, and at an industrial waste site near Ville Mercier, Quebec. Concentrations ranged from 2 000 to 40 000 ng/L (Reinhard et al., 1984; Pankow et al., 1984 and 1985; Martel and Ayotte, 1989). A maximum concentration of 19 000 ng/L was reported for untreated leachate obtained from a chemical manufacturing plant landfill in Sarnia, Ontario in 1985 (King and Sherbin, 1986).

Information on concentrations of 1,4-dichlorobenzene in Canadian drinking water supplies is limited. 1,4-Dichlorobenzene was detected in 6 of 90 potable water samples taken at 30 water treatment facilities across Canada between August and December 1979 (Otson et al., 1982a, 1982b). Mean and maximum concentrations were less than 1 mg/L (the limit of detection for 1,4-dichlorobenzene was not specified, however, for 1,2-dichlorobenzene and 1,2,4-trichlorobenzene, the quantitation limit was 1 mg/L). Based on analysis of dichlorobenzenes in the water supplies of three cities in Ontario, Oliver and Nicol (1982) concluded that most of the dichlorobenzene present in drinking water occurs as the 1,4-isomer, due probably to its release into surface water from urinal deodorant blocks. Concentrations in this study ranged from 8 to 20 ppt with a mean of 13 ppt (0.013 mg/L) [detection limit ~ 1 ppt (0.001 mg/L)]. The 1,4-isomer of dichlorobenzene was detected in 4 of 143 samples of raw and treated water collected in Quebec in May 1985, and February and July 1986 at concentrations below 1 mg/L (detection limit = 0.1 mg/L) [Vachon, 1986]. Traces of 1,4-dichlorobenzene were detected (detection limit < 1 mg/L) in 3 of 29 treated municipal water supplies in Alberta during 1980 to 1985 (Alberta Environment, 1985). In a survey of drinking water from 139 locations in the 4 Atlantic provinces between 1985 and 1988, the dichlorobenzenes were not detected in 1 210 samples analyzed (detection limit = 0.02 mg/L). However, it should be noted that 23% and 77% of the samples taken for analysis of 1,2- and 1,4-dichlorobenzene isomers, respectively, were contaminated and therefore not analyzed or included (Environment Canada, 1989b, 1989c, 1989d, 1989e).

Recent data on the concentrations of 1,4-dichlorobenzene in sediments in Canada are limited to one investigation of the effects of municipal sewage outfalls from Victoria, British Columbia, on sea bottom sediments. 1,4-Dichlorobenzene was consistently detected in sediments at the Macaulay Point outfall at concentrations ranging from 1 to 1 710 ng/g (mean 141 ng/g) [dry weight] (EVS Consultants, 1992). All other identified data on the levels in Canadian sediment are from the late 1970s to early 1980s. Durham and Oliver (1983) examined the vertical distribution of 1,4-dichlorobenzene in bottom sediments in Lake Ontario near the mouth of the Niagara River in 1981, and reported that the maximum concentration of 1,4-dichlorobenzene was 1 100 ng/g (dry weight) at a depth from 8 to 9 cm. Concentrations of total dichlorobenzene isomers have also been measured in sediments collected during 1984 and 1985 from the St. Clair River near petrochemical plants near Sarnia (Oliver and Pugsley, 1986). The average concentration was 5 500 ng/g, while the maximum concentration was 34 000 ng/g (43 samples were analyzed). Based on data for the ratio of isomers (Oliver, 1992, personal communication), the corresponding average concentration of 1,4-dichlorobenzene in these sediments was approximately 524 ng/g.

No data on the concentrations of 1,4-dichlorobenzene in wild mammals or birds, and few data on levels in other environmental biota in Canada were identified. The level of 1,4-dichlorobenzene in tissue from mussels (Modiolus sp.), collected at the outfall of a municipal sewage effluent at Clover Point near Victoria, British Columbia, was below the detection limit (5 mg/kg) [EVS Consultants, 1992]. Levels of 1,4-dichlorobenzene in lake trout (Salvelinus namaycush), collected from Lake Ontario in 1980 and 1981, ranged up to 4 ng/g (wet weight) [Oliver and Nicol, 1982; Fox et al., 1983]. Concentrations in this species were lower elsewhere in the Great Lakes (Oliver and Nicol, 1982). Concentrations of 1,4-dichlorobenzene in amphipods and oligochaetes collected in Lake Ontario in 1981 were reported to be 370 and 630 ng/g (dry weight), respectively (Fox et al., 1983). MacLaren Marex Ltd. (1979) reported concentrations up to 590 ng/g (dry weight) for total 1,3- and 1,4-dichlorobenzenes in clams (blue mussels) taken from estuarine sediment contaminated by industrial discharge from a chemical manufacturing plant in the East River of Pictou Harbour at Pictou, Nova Scotia.

Information on concentrations of 1,4-dichlorobenzene in Canadian food supplies is limited. In a limited study of fresh food composites from Ontario, 1,4-dichlorobenzene was detected only in the milk (2% fat content) composite at a concentration of 0.00055 µg/g (Davies, 1988). Other composites analyzed included the following: leafy vegetables; fruits; root vegetables, including potatoes; and eggs and meat. The composites were prepared from samples obtained in 4 retail grocery stores; the detection limit for all composite samples was 0.0001 µg/g.

1,4-Dichlorobenzene has been detected in breast milk. The mean concentration of the 1,3- and 1,4-isomers combined (calculated as 1,3-dichlorobenzene) was 6.1 ng/g with a maximum of 75 ng/g in breast milk of Canadian women taken 3 to 4 weeks after parturition (detected in 86% of the 210 samples, though the limit of detection was not specified) [Mes et al., 1986].

2.4 Effects-related Information

2.4.1 Experimental Animals and In Vitro

Following oral administration of 1,4-dichlorobenzene, Hollingsworth et al. (1956) reported that 2 800 mg/kg bw and 4 000 mg/kg bw were lethal to 100% of guinea pigs and rats, respectively. There were no deaths in guinea pigs and rats exposed to 1 600 mg/kg bw and 1 000 mg/kg bw, respectively.

The only sub-chronic study in which 1,4-dichlorobenzene has been administered by inhalation is that conducted in rats, guinea pigs, rabbits and monkeys by Hollingsworth et al. (1956). Following exposure to 950 mg/m3 7 hours per day, 5 days per week in this study, there was a decrease in body weight gain (> 10%) in guinea pigs and in rats, an increase in liver and kidney weights, and cloudy swelling and granular degeneration in the liver of rats. The no-observed-effect-level (NOEL) for rats and guinea pigs was 580 mg/m3; for monkeys, mice and rabbits, it was 950 mg/m3.

Increased incidence and severity of kidney cortical tubular degeneration in male Fischer 344/N rats (600 mg/kg bw/day) and mild to moderate centrilobular hepatocytomegaly (900 mg/kg bw/day) and minimal to mild hepatocytomegaly (675 mg/kg bw/day) in B6C3F1 mice have been observed following oral administration of 1,4-dichlorobenzene for 13 weeks (NTP, 1987). The NOELs in these studies were 337.5 mg/kg bw in mice and 300 to 600 mg/kg bw in male and female rats, respectively (NTP, 1987).

The chronic toxicity and carcinogenicity of 1,4-dichlorobenzene have been examined in rats and mice following both inhalation (Loeser and Litchfield, 1983) and ingestion (NTP, 1987). Loeser and Litchfield (1983) reported increases in liver and kidney weights, urinary protein, and coproporphyrin in the high dose group of rats administered 0, 450 or 3 000 mg/m3 1,4-dichlorobenzene 5 hrs per day, 5 days per week for 76 weeks followed by 36 weeks without exposure. There was no evidence of toxicity in mice following exposure to the same concentrations for a shorter period, 57 weeks followed by 19 weeks without exposure. There were no treatment-related effects on the incidence of tumours observed in either species, though the relatively short exposure period (76 weeks in rats, 57 weeks in mice) and the high early mortality in mice may have decreased the sensitivity of this bioassay for carcinogenicity. The NOELs in rats and mice were 450 and 3000 mg/m3, respectively.

In the U.S. NTP (1987) study, female F344 rats and male and female B6C3F1 mice ingested 0, 300 or 600 mg/kg bw/day while male rats received 0, 150 or 300 mg/kg bw/day by gavage in corn oil 5 days per week for 103 weeks. In both sexes of mice, there was an increased incidence of non-neoplastic liver lesions, including cytomegaly and karyomegaly, hepatocellular degeneration, and individual cell necrosis at both doses. There was also an increased incidence of nephropathy in male mice and renal tubular regeneration in female mice at both doses. Positive trends in the incidence of hepatocellular adenomas, hepatocellular carcinomas, and hepatocellular adenomas and carcinomas (combined), were observed in both sexes of mice exposed to 1,4-dichlorobenzene with the incidences in the high dose groups all being significantly greater than those in vehicle controls. There was also a significantly increased incidence of hepatocellular adenomas and adenomas or carcinomas (combined) in low dose male mice. Rare tumours called hepatoblastomas were also observed in 4 male mice in the high dose group, each of which also had a hepatocellular carcinoma. Marginal increases in the incidences of pheochromocytomas (all types) of the adrenal gland in male mice (statistically significant only in the high dose group), and in the incidence of follicular cell adenomas of the thyroid gland in female mice were observed.

In male rats exposed to 1,4-dichlorobenzene in the NTP study, increased incidence of the following were observed: nephropathy; epithelial hyperplasia of the renal pelvis; mineralization of the collecting tubules in the renal medulla; and focal hyperplasia of the renal tubular epithelium. The incidence of nephropathy in low and high dose females was also increased in comparison with vehicle controls. Neoplastic lesions in rats in the U.S. NTP bioassay included a dose-related increase in the incidence of tubular cell adenocarcinomas in the kidney of male rats. One high dose male also had a tubular cell adenoma. These tumours were not observed in exposed or vehicle control female rats. A marginal increase in the incidence of mononuclear cell leukaemia in exposed male rats was observed when compared to controls.

On the basis of these results, it was concluded that there was clear evidence of carcinogenicity in male F344/N rats and both male and female B6C3F1 mice. There was, however, no evidence of carcinogenicity in female F344/N rats (NTP, 1987).

The induction by 1,4-dichlorobenzene of kidney tumours in the male rat is believed to be associated with hyaline droplet formation resulting in a characteristic alpha-2-microglobulin nephropathy (hyaline droplet nephropathy). The mechanism of induction of such tumours in the male rat by several chemicals including 1,4-dichlorobenzene, is well established (Short et al., 1987; Goldsworthy et al., 1988; Murty et al., 1988; Charbonneau et al., 1989). It involves increased formation of protein droplets in kidney tubules associated with reabsorption of low molecular weight proteins (the P-2 segment). The reabsorbed protein is taken up by lysozymes and accumulates, due to a defect in protein metabolism by the renal tissue. The hyaline droplets characteristic of this effect have been shown to be composed of lysosomes overloaded with alpha-2-microglobulin. Excessive lysosomal activity is associated with increased cell proliferation leading ultimately, in a few cases, to renal tubular adenocarcinomas in the male rat. The protein involved, alpha-2-microglobulin, occurs in large amounts in the male Fischer 344 rat, but amounts are not significant in the female rat, mice or humans (Olson et al., 1990).

For 1,4-dichlorobenzene, there is much evidence to support the involvement of hyaline droplet accumulation in the induction of the tubular cell adenocarcinomas in the male rat. Bomhard et al. (1988) demonstrated hyaline droplet accumulation in male rats following exposure to 1,4-dichlorobenzene with no indication of any such effects in female rats. Charbonneau et al. (1989) reported that 1,4-dichlorobenzene (single exposure in F344 rats to 300 or 500 mg/kg bw in corn oil) increased protein droplet formation and cell proliferation in male but not female rat kidneys, whereas equimolar doses of 1,2-dichlorobenzene had no effect. The maximum amount of radioactivity reversibly bound to alpha-2-microglobulin by 1,4-[14C]dichlorobenzene was also 2 times that of an equimolar dose of 1,2-[14C]dichlorobenzene.

The weight of evidence indicates that 1,4-dichlorobenzene is not genotoxic in either in vivo or in vitro assays (see Supporting Documentation). Negative results were obtained in an assay of DNA damage (unscheduled DNA synthesis) in the liver of mice following oral exposure to up to 1 000 mg/kg bw 1,4-dichlorobenzene (Steinmetz and Spanggord, 1987), though there was a small statistically significant increase in S-phase DNA replication (indicative of proliferation) seen in males only.

Available studies concerning the embryotoxicity, foetotoxicity, and teratogenicity of 1,4-dichlorobenzene include two studies following inhalation in rabbits (Hayes et al., 1985) and rats (Loeser and Litchfield, 1983) and one study following ingestion in rats (Giavini et al., 1986). No investigations on the reproductive effects of 1,4-dichlorobenzene were identified. In several of these studies, relatively minor embryotoxic and foetotoxic effects have been observed, but only at doses of 1,4-dichlorobenzene which were toxic to the mother.

2.4.2 Humans

Available data on the effects of exposure to 1,4-dichlorobenzene in humans are restricted to one epidemiological study and to case reports concerning mainly accidental exposure to or misuse of moth crystals and space deodorants. No clinical investigations on the effects of exposure in human volunteers were identified. In the only identified cross-sectional epidemiological study of workers exposed to 1,4-dichlorobenzene, there was no evidence of "organic injury or untoward haematological effects" reported during periodic medical examinations in 58 workers exposed to various concentrations of 1,4-dichlorobenzene, although levels between 50 and 80 ppm were irritating to the eyes and nose; irritation was severe at 160 ppm (Hollingsworth et al., 1956). However, little information on study design was presented in the published account of this investigation.

2.4.3 Ecotoxicology

The information that was identified on the toxicity of 1,4-dichlorobenzene to aquatic biota includes data on acute and chronic effects in bacteria, algae, invertebrates, and fish. Studies that are cited below were conducted under closed, static or continuous flow conditions and were considered reliable for a volatile compound such as 1,4-dichlorobenzene. No suitable data on toxicity to sediment-dwelling biota or terrestrial biota including wild mammals, birds, and vascular plants were identified. Similarly, no empirical data regarding adverse effects of 1,4-dichlorobenzene on wildlife due to decreased availability or quality of prey were identified.

The lowest LC50 (48 hour) reported for acute toxicity was 1.18 mg/L for rainbow trout (Oncorhynchus mykiss) [Calamari et al., 1983]. For the water flea (Daphnia magna), Canton et al. (1985) reported a 48-h LC50 of 2.2 mg/L, while Calamari et al. (1983) reported a 24-h IC50 (for immobilization) of 1.6 mg/L. Inhibition of growth (96-h EC50 ) and photosynthesis (3-h EC50 ) in the freshwater algae (Selenastrum capricornutum) were reported at concentrations of 1.6 mg/L and 5.2 mg/L 1,4-dichlorobenzene, respectively (Calamari et al., 1982, 1983).

Impairment of reproduction was the most sensitive endpoint identified, related to the toxicity of 1,4-dichlorobenzene to aquatic organisms. Calamari et al. (1982) reported a 28-d no-observed-effect-concentration (NOEC) and lowest-observed-effect-concentration (LOEC) [for effects on reproduction] of 0.22 and 0.40 mg/L, respectively, for Daphnia magna. In a similar study, the authors reported a 14-d EC50 (for effects on reproduction) of 0.93 mg/L (Calamari et al., 1983). For fish, Carlson and Kosian (1987) reported a NOEC of 0.57 mg/L and a LOEC (for effects on growth) of 1.0 mg/L, for the fathead minnow (Pimephales promelas), continuously exposed to 1,4-dichlorobenzene for 32 days during the embryo and early larval stages.

3.0 Assessment of "Toxic" Under CEPA

3.1 CEPA 11(a) Environment

1,4-Dichlorobenzene is produced in and imported into Canada and is released into the Canadian environment. Few data were identified concerning the amounts entering the environment. Due to its volatility and the dispersive nature of its uses, most of the 3 500 tonnes of 1,4-dichlorobenzene used in Canada is estimated to be released into the environment. 1,4-Dichlorobenzene has been measured in municipal and industrial effluents, air, ground and surface waters, sediment, and biota in Canada. While 1,4-dichlorobenzene does not persist in ambient air and surface water, it can persist and accumulate in sediment under anaerobic conditions.

Exposure of benthic organisms to 1,4-dichlorobenzene is known to occur in sediments in Lake Ontario, the St. Clair River, and Macaulay Point, Victoria, British Columbia. However, no toxicological data were identified that would enable a conclusion to be reached on the possible biological effects resulting from this exposure.

Daphnia magna was identified as the most sensitive aquatic organism to 1,4-dichlorobenzene. The 28-day LOEC for reduced fertility was 400 µg/L. Dividing this value by a factor of 10 (to account for inter-species differences in sensitivity as well as extrapolation from laboratory to field conditions) results in an estimated effects threshold of 40 µg/L. The highest concentration of 1,4-dichlorobenzene in Canadian surface waters (0.130 µg/L, measured in the early 1980s in the Niagara River) is approximately 300 times less than the estimated effects threshold. Therefore, no adverse effects are expected to result from exposure of pelagic organisms to 1,4-dichlorobenzene in Canadian surface waters.

A worst-case exposure scenario was developed for a representative fish-eating mammal, mink (Mustela vison) in southern Ontario to ascertain the most significant route of exposure. Mink are opportunistic carnivores with aquatic organisms comprising up to 100% of their diet. The total daily intake of 1,4-dichlorobenzene estimated for mink (Table 1) was 2 096 ng/kg bw, with inhalation being the major route of exposure.

Table 1 Estimated Total Daily Intake of a Piscivorous Mammal Exposed to 1,4-Dichlorobenzene under "Worst-case" Conditions
Exposure Route Environmental Levelsa Daily Rate of Consumption (per kg bw)b Daily Intake (ng/kg bw)
air 3.53 mg/m3 0.55 m3/d 1 941
surface water 1.6 ng/L 0.1 L/d 0.16
biota (fish) 1.0 ng/g 155 g/d 155
Total 2 096
  1. The level in air is the maximum level measured in a rural environment (Walpole Island, Ontario); the level in surface water is the mean level measured in Lake Ontario, and comparable to that in the St. Clair River in 1985 and Niagara-on-the-Lake in 1988; the level in biota is that measured in predatory fish in Lake Ontario in the early 1980s and is comparable to the maximum level predicted based on a BCF of 720.
  2. Inhalation rate from Stahl (1967); drinking rate from Calder and Braun (1983); and ingestion rate from Nagy (1987), assuming a diet of 75% fish.

In the absence of studies on wildlife, the effects threshold for mink was estimated on the basis of results of a chronic inhalation study in rats. In this study, no treatment-related effects were observed at a concentration of 450 mg/m3 (Loeser and Litchfield, 1983). Using a factor of 10 to account for variability in extrapolating from a laboratory to a field situation, the effects threshold was estimated to be 45 mg/m3. The highest concentration of 1,4-dichlorobenzene reported for ambient rural air in Canada is approximately 12 700 times less than this effects threshold. Data on the toxicological effects of 1,4-dichlorobenzene on birds and terrestrial plants were not identified.

Although, on the basis of available data, the levels of 1,4-dichlorobenzene present in air and surface water are not expected to cause adverse effects in aquatic biota or wildlife, there were no data upon which to evaluate the significance of concentrations in sediment to benthic biota. Therefore, the available information is insufficient to conclude whether 1,4-dichlorobenzene is entering the environment in quantities or under conditions that may be harmful to the environment.

3.2 CEPA 11(b): Environment on Which Human Health Depends

Although 1,4-dichlorobenzene is volatile at tropospheric temperatures and absorbs infrared radiation in wavelengths ranging from 7 to 13 mm, this substance is removed from the atmosphere by photo-oxidation (mean half-life of approximately 3 weeks) resulting in low, steady-state concentrations in the atmosphere (< 1 mg/m3). As such, 1,4-dichlorobenzene is not expected to contribute significantly to formation of ground-level ozone, global warming or depletion of stratospheric ozone.

On the basis of available data, it has been concluded that 1,4-dichlorobenzene is not entering the environment in quantities or under conditions that may constitute a danger to the environment on which human life depends.

3.3 CEPA 11(c): Human Life or Health

Population Exposure

On the basis of the available data, it is likely that the general population is exposed to 1,4-dichlorobenzene principally in air, particularly indoor air (Table 2). However, it should be noted that reliable data on concentrations of 1,4-dichlorobenzene in indoor air in Canada were not identified and, as a result, it was necessary to calculate intake from this source on the basis of data collected in the United States. For suckling infants, breast milk is a more important source (estimated daily intake from this source, 0.7 mg/kg bw) than food for other age groups (estimated daily intake from this source, 0.0005 to 0.008 mg/kg bw) though it appears still to contribute less to total intake for this age group than indoor air (estimated daily intake for infants aged 0 to 6 months from indoor air, 0.1 to 1.3 mg/kg bw). The total daily intake of 1,4-dichlorobenzene for various age groups in the Canadian population is estimated to range from 0.1 to 2.1 mg/kg bw.

Table 2 Estimated Daily Intake of 1,4-Dichlorobenzene from Various Sources by Canadians
Medium1 Estimated Intake (mg/kg bw/day)
0-6 moa 7 mo-4 yrb 5-11 yrc 12-19 yrd 20-70 yre
Ambient Airf 0.01-0.1 0.01-0.2 0.02-0.2 0.01-0.2 0.01-0.2
Indoor Airg 0.1-1.3 0.1-1.7 0.1-1.9 0.1-1.5 0.1-1.5
Drinking Waterh - 0.0008- 0.0004- 0.0003- 0.0003-
  < 0.06 < 0.03 < 0.02 < 0.02
Foodi 0.7j 0.008 0.004 0.002 0.0005
Total Intake 0.8-2.1 0.1-2.0 0.1-2.1 0.1-1.7 0.1-1.7

mo = months

1. Data were insufficient to estimate intake from soil.

  1. Assumed to weigh 7 kg, breathe 2 m3 of air per day, and drink 750 ml of breast milk (as food) per day (Environmental Health Directorate, 1991).
  2. Assumed to weigh 13 kg, breathe 5 m3 of air per day, drink 0.8 L of water per day, and consume 194.5 g per day of 2% cow's milk (Environmental Health Directorate, 1991).
  3. Assumed to weigh 27 kg, breathe 12 m3 of air per day, drink 0.9 L of water per day, and consume 185.61 g per day of 2% cow's milk (Environmental Health Directorate, 1991).
  4. Assumed to weigh 57 kg, breathe 19 m3 of air per day, drink 1.3 L of water per day, and consume 196.2 g per day of 2% cow's milk (Environmental Health Directorate, 1991).
  5. Assumed to weigh 69 kg, breathe 23 m3 of air per day, drink 1.5 L of water per day, and consume 60.64 g per day of 2% cow's milk (Environmental Health Directorate, 1991).
  6. Based on range of mean concentrations of 1,4-dichlorobenzene reported in a survey of ambient air from 23 sites across Canada (0.22 to 2.94 mg/m3) [Environment Canada, 1991], assuming 4 of 24 hours are spent outdoors daily (Environmental Health Directorate, 1991).
  7. Based on maximum ratio of median overnight concentrations in indoor versus outdoor air in 57 homes in Los Angeles and Contra Costa (1.8) [Wallace et al., 1988] times mean concentrations reported in a survey of ambient air from 23 sites across Canada (0.22 to 2.94 mg/m3), assuming 20 of 24 hours are spent indoors daily (Environmental Health Directorate, 1991).
  8. Based on a range of mean concentrations of 1,4-dichlorobenzene in Canadian drinking water of 0.013 µg/L (Oliver and Nicol, 1982) to < 1 µg/L (Otson et al., 1982a, 1982b).
  9. Based on a concentration of 0.00055 mg/g 1,4-dichlorobenzene detected in a 2% cow's milk composite from Ontario (Davies, 1988).
  10. Based on a mean concentration of 1,3-dichlorobenzene and 1,4-dichlorobenzene (combined) detected in breast milk (6.1 ng/g) from the Canadian National Survey (Mes et al., 1986) and assuming the density of breast milk is equal to 1.0.

Effects

Available data are inadequate to assess the carcinogenicity of 1,4-dichlorobenzene in humans. An increased incidence of renal tubular cell adenocarcinomas in male rats and hepatocellular adenomas and carcinomas in male and female mice has been observed in an NTP carcinogenesis bioassay (NTP, 1987); only marginal increases of other tumours, restricted to single sexes, were observed. On the basis of these results, it was concluded that there was clear evidence of carcinogenicity in male F344/N rats and both male and female B6C3F1 mice.

In general, a compound for which there is adequate evidence of carcinogenicity in two species would be classified in Group II (probably carcinogenic to humans) of the classification scheme developed for use in the derivation of the Guidelines for Canadian Drinking Water Quality (Environmental Health Directorate, 1989).

However, available data indicate that the observed increase in renal tumours in F344 rats caused by 1,4-dichlorobenzene is a species and sex specific response which is unlikely to be relevant to humans exposed to this substance in the general environment (see Section 2.4.1). The weight of the available data indicate that 1,4-dichlorobenzene is not genotoxic in either in vitro or in vivo assays. Based on these results and the additional observation of an increase in DNA replication but no evidence of DNA damage in the liver of B6C3F1 mice following exposure to 1,4-dichlorobenzene (Steinmetz and Spanggord, 1987), this substance may act as a non-genotoxic, hepatic carcinogen in this species. Therefore, 1,4-dichlorobenzene has been classified in Group III (possibly carcinogenic to humans) of the classification scheme developed for use in the derivation of the Guidelines for Canadian Drinking Water Quality (Environmental Health Directorate, 1989).

For compounds classified in Group III, a tolerable daily intake (TDI) is derived on the basis of a no- or lowest-observed-(adverse)-effect-level (NO[A]EL or LO[A]EL) in a study conducted by the most relevant route of exposure, divided by an uncertainty factor, which when considered appropriate, takes into account the limited evidence of carcinogenicity.

The TDI has been derived, on the basis of the results of studies conducted by the route of exposure which is most important for the general population (i.e., inhalation). This value is also more conservative than a TDI which would be derived on the basis of results of studies in which 1,4-dichlorobenzene was administered orally.

The TDI has been derived on the basis of the results of the longest-term inhalation study, as follows:

Scientific formula

where:

  • 450 mg/m3 is the NOEL based on increased liver and kidney weights, urinary protein, and coproporphyrin observed at higher concentrations in rats in the longest-term inhalation study (Loeser and Litchfield, 1983);
  • 5/24 and 5/7 is the conversion of 5 hours per day, 5 days per week of administration to continuous exposure;
  • 0.144 m3 is the assumed inhaled air volume of rats (NIOSH, 1985);
  • 0.25 kg is the assumed body weight of adult rats (NIOSH, 1985);
  • 500 is the uncertainty factor (× 10 for inter-species variation; × 10 for intra-species variation; × 5 for evidence of carcinogenicity, though not observed in this study).

The total daily intake of 1,4-dichlorobenzene for various age groups in the Canadian population is estimated to range from 0.1 to 2.1 mg/kg bw. These estimated average daily intakes are less (by 37 to 780 times) than the TDI derived above.

On the basis of available data, it has been concluded that 1,4-dichlorobenzene is not entering the environment in quantities or under conditions that may constitute a danger in Canada to human life or health.

3.4 Conclusion

Based upon available data, it has been determined that there is insufficient information to conclude whether 1,4-dichlorobenzene is entering the environment in quantities or under conditions that may be harmful to the environment. It has, however, been concluded that 1,4-dichlorobenzene is not entering the environment in quantities or under conditions that may constitute a danger to the environment on which human life depends, or to human life or health.

4.0 Recommendations

  1. Since 1,4-dichlorobenzene is manufactured in Canada and no data concerning emissions to the atmosphere from point sources were identified, it is recommended that additional data on quantities released to the atmosphere and resulting atmospheric concentrations be acquired.
  2. Reliable data on concentrations of 1,4-dichlorobenzene in indoor air of homes and buildings in Canada have not been identified. Consequently, it is recommended that such data be acquired.
  3. Since virtually all available data concerning concentrations of 1,4-dichloro-benzene in sediment are outdated, it is recommended that concentrations of this substance in sediment near effluent outfalls from municipal waste treatment plants, textile plants and chemical manufacturing plants be determined.
  4. It is recommended that the toxicity of 1,4-dichlorobenzene in benthic organisms present in the Canadian environment be determined.

5.0 References

Alberta Environment. 1985. Drinking water survey. Municipal Engineering Branch, Pollution Control Division.

Barber, L.B. 1988. Dichlorobenzene in ground water: evidence for long-term persistence. Ground Water 26(6): 696-702.

Barrows, M.E., S.R. Petrocelli, and K.J. Macek. 1980. Bioconcentration and elimination by bluegill sunfish (Lepomis macrochirus). In: R. Haque, ed., Dynamics, Exposure and Hazard Assessment of Toxic Chemicals. Ann Arbor Science, Michigan. 379-392.

Bomhard, E., G. Luckhaus, W.-H. Voight, and E. Loeser. 1988. Induction of light hydrocarbon-nephropathy by p-dichlorobenzene. Arch. Toxicol., 61: 433-439.

Bosma, T.N.P., J.R. van der Meer, G. Schraa, M. E. Tros, and A.J.B. Zehnder. 1988. Reductive dechlorination of all trichloro- and dichlorobenzene isomers. FEMS Microbiolog. Ecol. 53: 223-229.

Bouwer, E.J., P.L. McCarty, and J.C. Lance. 1981. Trace organic behavior in soil columns during rapid infiltration of secondary wastewater. Water Res. 15: 151-159.

Bunce, N.J., J.P. Landers, J. Langshaw, and J.S. Nakai. 1987. Laboratory experiments to assess the importance of photochemical transformation during the atmospheric transport of chlorinated aromatic pollutants. 80th Annual meeting of APCA (Air Pollution Control Association), June 21-26, 1987. New York.

Calamari, D., S. Galassi, and F. Setti. 1982. Evaluating the hazard of organic substances on aquatic life: the para-dichlorobenzene example. Ecotoxic. Environ. Saf. 6: 369-378.

Calamari, D., S. Galassi, F. Setti, and M. Vighi. 1983. Toxicity of selected chlorobenzenes to aquatic organisms. Chemosphere 12(2): 253-262.

Calder, W.A., and E.J. Braun. 1983. Scaling of osmotic regulation in mammals and birds. Am. J. Physiol. 244: R601-R606.

Callahan, M., M. Slimak, N. Gabel, I. May, C. Fowler, R. Freed, P. Jennings, R. Durfee, F. Whitmore, B. Maestri, W. Mabey, B. Holt, and C. Gould. 1979. Water-related environmental fate of 129 priority pollutants. Volume II. Office of Water Planning and Standards/Office of Water and Waste Management, U.S. Environmental Protection Agency, Section V. (EPA 440/4-79-029b).

Camford Information Services Inc. 1991. Chlorobenzene CPI Product Profile. Don Mills, Ontario. 4 pp.

Canton, J.H., W. Sloof, H.J. Kool, J. Struys, Th. J.M. Pouw, R.C.C. Wegman, and G.J. Piet. 1985. Toxicity, biodegradability, and accumulation of a number of Cl/N-containing compounds for classification and establishing water quality criteria. Reg. Toxicol. Pharm. 5: 123-131.

Carlson, A.R., and P.A. Kosian. 1987. Toxicity of chlorinated benzenes to fathead minnows (Pimephales promelas). Arch. Environ. Contam. Toxicol. 16: 129-135.

Chan, C.C., L. Vainer, J.W. Martin, and D.T. Williams. 1990. Determination of organic contaminants in residential indoor air using an adsorption-thermal desorption technique. J. Air Waste Manage. Assoc. 40(1): 62-67.

Charbonneau, M., J. Strasser, E.A. Lock, M.J. Turner, and J.A. Swenberg. 1989. Involvement of reversible binding to a-2µ-globulin in 1,4-dichlorobenzene-induced nephrotoxicity. Toxicol. Appl. Pharmacol., 99: 122-132.

Chemical Marketing Reporter. 1990. Chemical profile. p-dichlorobenzene. July 16, 1990.

Davies, K. 1988. Concentrations and dietary intake of selected organochlorines, including PCBs, CDDs and PCDFs in fresh food composites grown in Ontario, Canada. Chemosphere 17(2): 263-276.

Di Toro, D.M., C.S. Zarba, D.J. Hansen, W.J. Berry, R.C. Swartz, C.E. Cowan, S.P. Pavlou, H.E. Allen, N.A. Thomas, and P.R. Paquin. 1991. Technical basis for establishing sediment quality criteria for nonionic organic chemicals using equilibrium partitioning. Environ. Toxicol. Chem. 10: 1541-1583.

Durham, R.W., and B.G. Oliver. 1983. History of Lake Ontario contamination from the Niagara River by sediment radiodating and chlorinated hydrocarbon analysis. J. Great Lakes Res. 9(2): 160-168.

Elder, V.A., B.L. Proctor, and R.A. Hites. 1981. Organic compounds found near dump sites in Niagara Falls, New York. Environ. Sci. Technol. 15(10): 1237-1243.

Ellington, J.J., F.E. Stancil, W.D. Payne, and D.C. Trusty. 1988. Measurement of hydrolysis rate constants for evaluation of hazardous waste land disposal. Volume 3. Data on 70 chemicals. Environmental Research Laboratory, U.S. Environmental Protection Agency. EPA/600/3-88/-28.

Environmental Health Directorate. 1989. Derivation of maximum acceptable concentrations and esthetic objectives for chemicals in drinking water. Guidelines for Canadian Drinking Water Quality-Supporting Documentation. Bureau of Chemical Hazards, Health and Welfare Canada.

Environmental Health Directorate. 1991. Draft internal report on recommended approach and reference values for exposure assessments for CEPA Priority Substances (September 18, 1991). Unpublished. Bureau of Chemical Hazards, Health and Welfare Canada.

Environment Canada. 1983. Chlorobenzene use patterns. Unpublished. Use Patterns Division, Commercial Chemicals Branch, Environment Canada. 5 pp.

Environment Canada. 1989a. Environmental assessment of the Canadian textile industry. Chemical Industries Division, Industrial Programs Branch, Environment Canada. Report EPS 5/TX/1.

Environment Canada. 1989b. Atlantic Region Federal-Provincial toxic chemical survey of municipal drinking water sources. Data Summary Report, Province of New Brunswick, 1985-1988. Inland Waters Directorate, Water Quality Branch. IWD-AR-WQB-89-155.

Environment Canada. 1989c. Atlantic Region Federal-Provincial toxic chemical survey of municipal drinking water sources. Data Summary Report, Province of Prince Edward Island, 1985-1988. Inland Waters Directorate, Water Quality Branch. IWD-AR-WQB-89-156.

Environment Canada. 1989d. Atlantic Region Federal-Provincial toxic chemical survey of municipal drinking water sources. Data Summary Report, Province of Newfoundland, 1985-1988. Inland Waters Directorate, Water Quality Branch. IWD-AR-WQB-89-157.

Environment Canada. 1989e. Atlantic Region Federal-Provincial toxic chemical survey of municipal drinking water sources. Data Summary Report, Province of Nova Scotia, 1985-1988. Inland Waters Directorate, Water Quality Branch. IWD-AR-WQB-89-154.

Environment Canada. 1991. Update and summary report. Measurement program for toxic contaminants in Canadian urban air. Unpublished. River Road Environmental Technology Centre. PMD 91-2.

Environment Canada. 1992. National Water Quality Data Bank (NAQUADAT). Database for 1,4-dichlorobenzene. Water Quality Branch, Environment Canada.

EVS Consultants. 1992. Sediment and related investigations off the Macaulay and Clover Point sewage outfall. Final report to the Capital Regional District, Victoria, British Columbia. 193 pp.

Fanning, M.L., D.J. Jones, D.W. Larson, and R.G. Hunter. 1989. Environmental Monitoring 1987 Iona Deep Sea Outfall Project. Beak Associates Consulting (B.C.) Ltd., Vancouver, British Columbia.

Fathepure, B.Z., J.M. Tiedje, and S.A. Boyd. 1988. Reductive dechlorination of hexachlorobenzene to tri-and dichlorobenzenes in anaerobic sewage sludge. Appl. Environ. Microbiol. 54(2): 327-330.

Fox, M.E., J.H. Carey, and B.G. Oliver. 1983. Compartmental distribution of organochlorine contaminants in the Niagara River and the Western Basin of Lake Ontario. J. Great Lakes Res. 9(2): 287-294.

Garrison, A.W., and D.W. Hill. 1972. Organic pollutants from mill persist in downstream waters. American Dyestuff Reporter 21-25.

Giavini, E., M.L. Boccia, M. Prati, and C. Vismara. 1986. Teratologic evaluation of p-dichlorobenzene in the rat. Bull. Environ. Contam. Toxicol. 37: 164-168.

Goldsworthy, T.L., O. Lyght, V.L. Burnett, and J.A. Popp. 1988. Potential role of 2µ-globulin, protein droplet accumulation, and cell replication in the renal carcinogenicity of rats exposed to trichloroethylene, perchloroethylene, and pentachloroethane. Toxicol. Appl. Toxicol. 96: 367-379.

Haider, K., G. Jagnow, R. Kohnen, and S.U. Lim. 1981. Degradation of chlorinated benzenes, phenols and cyclohexane derivatives by benzene- and phenol-utilizing soil bacteria under aerobic conditions. In: M.R. Overcash, ed. Decomposition of Toxic and Nontoxic Organic Compounds in Soil. Ann Arbor Science, Ann Arbor, Michigan.

Hayes, W.C., T.R. Hanley, T.S. Gushow, K.A. Johnson, and J.A. John. 1985. Teratogenic potential of inhaled dichlorobenzenes in rats and rabbits. Fundam. Appl. Toxicol. 5(1): 190-202.

Holliday, M.G., and F.R. Engelhardt. 1984a. Chlorinated benzenes. A criteria review. Prepared for Monitoring and Criteria Division, Bureau of Chemical Hazards, Health and Welfare Canada, Ottawa.

Holliday, M.G., F.R. Engelhardt, and I. Maclachlan. 1984b. Chlorobenzenes: an environmental health perspective. Prepared for Health and Welfare Canada, Ottawa.

Holliger, C., G. Schraa, A.J.M. Stams, and A.J.B. Zehnder. 1992. Enrichment and properties of an anaerobic mixed culture reductively dechlorinating 1,2,3-trichloro-benzene to 1,3-dichlorobenzene. Appl. Environ. Microbiol. 58(5): 1636-1644.

Hollingsworth, R.L., V.K. Rowe, F. Oyen, H.R. Hoyle, and H. Spencer. 1956. Toxicity of para-dichlorobenzene; determinants on experimental animals and human subjects. Arch. Ind. Health 14: 138-147.

Howard, P.H. 1991. Handbook of environmental degradation rates. Lewis Publishers, Inc., Chelsea, Michigan.

Howard, P.H., G.W. Sage, W.F. Jarvis, and D.A. Gray. 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Volume II. Solvents. Lewis Publishers, Inc., Chelsea, Michigan.

Kao, C., and N. Poffenberger. 1979. Chlorinated benzenes. In: M. Grayson and D. Eckroth, eds. Kirk Othmer. Encyclopedia of Chemical Technology. 3rd Edition. Volume 5. John Wiley & Sons, Toronto, Ontario. 797-808 pp.

King, L., and G. Sherbin. 1986. Point sources of toxic organics to the upper St. Clair River. Water Pollut. Res. J. Canada 21(3): 433-443.

Ligocki, M.P., C. Leuenberger, and J.F. Pankow. 1985. Trace organic compounds in rain-II. Gas scavenging of neutral organic compounds. Atmos. Environ. 19(10): 1609-1617.

Loeser, E., and M.H. Litchfield. 1983. Review of recent toxicology studies on p-dichlorobenzene. Fd. Chem. Toxicol. 21(6): 825-832.

Mackay, D., W.Y. Shiu, and K.C. Ma. 1992. The Illustrated Handbook of Physical-Chemical Properties and Environmental Fate for Organic Chemicals. Volume I. Monoaromatic Hydrocarbons, Chlorobenzenes, and PCBs. Lewis Publishers, Inc. Michigan. 697 pp.

MacLaren Marex Inc. 1979. Report on an environmental survey for chlorobenzenes at four coastal sites in Nova Scotia. 18 pp. Report prepared for Environmental Protection Service, Halifax, Nova Scotia. 33 pp.

Martel, R., and P. Ayotte. 1989. État de la situation sur la contamination de la nappe souterraine dans la région de la ville de Mercier. Ministère de l'Environnement du Québec.

McCall, J.P., D.A. Laskowski, R.L. Swann, and H.J. Dishburger. 1981. Measurement of sorption coefficients of organic chemicals and their use in environmental fate analysis. In: Test protocols for environmental fate and movement of toxicants. Proceedings of a symposium, Association of Official Analytical Chemists, 94th Annual Meeting, October 21-22, 1980. Washington.

Melcer, H., H. Monteith, and S.G. Nutt. 1988. Variability of toxic trace contaminants in municipal sewage treatment plants. Wat. Sci. Tech. 20(4/5): 275-284.

Mes, J., D.J. Davies, D. Turton, and W.-F. Sun. 1986. Levels and trends of chlorinated hydrocarbon contaminants in the breast milk of Canadian women. Food Additives and Contaminants 3(4): 313-322.

Murty, C.V.R., M.J. Olson, B.D. Garg, and A.K. Ray. 1988. Hydrocarbon induced hyaline droplet ephropathy in male rats during senescence. Toxicol. Appl. Toxicol. 96: 380-392.

Nagy, K.A. 1987. Field metabolic rate and food requirement scaling in mammals and birds. Ecol. Mono. 57: 111-128.

NIOSH (National Institute for Occupational Safety and Health). 1985. Registry of Toxic Effects of Chemical Substances. 1983-1984 Cumulative supplement to the 1981-1982 edition. U.S. Department of Health and Human Services.

NRDIG (Niagara River Data Interpretation Group). 1988. Joint evaluation of upstream/downstream Niagara River monitoring data. 1986-1987. 37 pp.

NRDIG (Niagara River Data Interpretation Group). 1990. Joint evaluation of upstream/downstream Niagara River monitoring data. 1988-1989. 72 pp.

NTP (National Toxicology Program). 1987. NTP Technical Report on the toxicology and carcinogenicity studies of 1,4-dichlorobenzene (CAS No. 106-46-7) in F344/N rats and B6C3F1 mice (gavage studies). U.S. Dept. of Health and Human Services, Research Triangle Park, North Carolina. NTP TR 319. p. 198.

Oliver, B.G. 1987. Biouptake of chlorinated hydrocarbons from laboratory-spiked and field sediments by oligochaete worms. Environ. Sci. Technol. 21(8): 785-790.

Oliver, B.G. 1992, personal communication. Zenon Laboratories, Burnaby, British Columbia.

Oliver, B.G., and K.D. Bothen. 1982. Extraction and clean-up procedures for measuring chlorobenzenes in sediments and fish by capillary gas chromatography. Intern. J. Environ. Anal. Chem. 12: 131-139.

Oliver, B.G., and K.D. Nicol. 1982. Chlorobenzenes in sediments, water, and selected fish from Lakes Superior, Huron, Erie, and Ontario. Environ. Sci. Technol. 16(8): 532-536.

Oliver B.G., and K.D. Nicol. 1984. Chlorinated contaminants in the Niagara River, 1981-1983. Sci. Total Environ. 39: 57-70.

Oliver, B.G., and A.J. Niimi. 1983. Bioconcentration of chlorobenzenes from water by rainbow trout: correlations with partition coefficients and environmental residues. Environ. Sci. Technol. 17: 287-291.

Oliver, B.G., and C.W. Pugsley. 1986. Chlorinated contaminants in St. Clair River sediments. Water Poll. Res. J. Canada. 21(3): 368-379.

Olson, M.J., J.T. Johnson, and C.A. Reidy. 1990. A comparison of male rat and human urinary proteins: implications for human resistance to hyaline droplet nephropathy. Toxicol. Appli. Pharmacol. 102: 524-536.

OME (Ontario Ministry of the Environment). 1988. Thirty-seven municipal water pollution control plants. Volume 1. Municipal/Industrial Strategy for Abatement (MISA). Interim Report. 97 pp.

OME (Ontario Ministry of the Environment). 1991a. Preliminary report on the first six months of process effluent monitoring in the MISA pulp and paper sector (January 1, 1990 to June 30, 1990). Municipal/Industrial Strategy for Abatement (MISA), Water Resources Branch, Ontario Ministry of the Environment. 176 pp.

OME (Ontario Ministry of the Environment). 1991b. Preliminary report on the second six months of process effluent monitoring in the MISA pulp and paper sector (July 1, 1990 to December 31, 1990). Municipal/Industrial Strategy for Abatement (MISA), Water Resources Branch, Ontario Ministry of the Environment. 159 pp.

OME (Ontario Ministry of the Environment). 1992. Twelve month report. Unpublished. Organic manufacturing sector. Municipal Strategy for Abatement (MISA), Municipal/Industrial Strategy for Abatement (MISA), Water Resources Branch, Ontario Ministry of the Environment. 81 pp.

OME (Ontario Ministry of the Environment). 1992a. Six month monitoring data report organic chemical manufacturing sector (October 1, 1989 to March 31, 1990). Municipal/Industrial Strategy for Abatement (MISA), MISA Industrial Section, Water Resources Branch, Ontario Ministry of the Environment. 123 pp.

OME (Ontario Ministry of the Environment). 1992b. Twelve month monitoring data report. Inorganic chemical sector. (December 1, 1989 to November 30, 1990; February 1, 1990 to January 31, 1991). Municipal/Industrial Strategy for Abatement (MISA), MISA Industrial Section, Water Resources Branch, Ontario Ministry of the Environment. 81 pp.

Otson, R., D.T. Williams, and D.C. Biggs. 1982a. Relationship between raw water quality, treatment, and occurrence of organics in Canadian potable water. Bull. Environ. Contam. Toxicol. 28: 396-403.

Otson, R., D.T. Williams, and P.D. Bothwell. 1982b. Volatile organic compounds in water at thirty Canadian potable water treatment facilities. J. Assoc. Off. Anal. Chem. 65(6): 1370-1374.

Pankow, J.F., L.M. Isabelle, J.P. Hewetson, and J.A. Cherry. 1984. A syringe and cartridge method for down-hole sampling for trace organics in ground water. Ground Water 22(3): 330-339.

Pankow, J.F., L.M. Isabelle, J.P. Hewetson, and J.A. Cherry. 1985. A tube and cartridge method for down-hole sampling for trace organic compounds in ground water. Ground Water 23(6): 775-782.

Pellizzari, E.D., T.D. Harthwell, B.S.H. Harris, R.D. Waddell, D.A. Whitaker, and M.D. Erikson. 1982. Purgeable organic compounds in mothers' milk. Bull. Environ. Contam. Toxicol. 28: 322-328.

Reinhard, M., N.L. Goodman, and J.F. Barker. 1984. Occurrence and distribution of organic chemicals in two landfill leachate plumes. Environ. Sci. Technol. 18(12): 953-961.

Sadtler Research Laboratories. 1982. 1,4-Dichlorobenzene. Sadtler Research Laboratories, Division of Bio-Rad Laboratories, Inc.

Short, B.G., V.L. Burnett, M.G. Cox, J.S. Bus, and J.A. Swenberg. 1987. Site-specific renal toxicity and cell proliferation in male rats exposed to petroleum hydrocarbons. Lab. Invest. 57(5): 564-577.

Stahl, W.R. 1967. Scaling of respiratory variables in mammals. J. Appl. Physiol. 22: 453-460.

Steinmetz, K.L., and R.J. Spanggord. 1987. Examination of the potential of p-dichlorobenzene to induce unscheduled DNA synthesis or DNA replication in the in vivo-in vitro mouse hepatocyte DNA repair assay. (Task 1). Unpublished. Report prepared by SRI International, U.S.A., for U.S. Chemical Manufacturers Association and submitted to WHO by ICI, Central Toxicology Laboratory.

Strahlendorf, P.W. 1978. Chorinated benzenes as potential environmental health hazards: a review. Prepared for Monitoring and Criteria Section, Health Protection Branch, Health and Welfare Canada, Ottawa.

U.S. EPA (Environmental Protection Agency). 1986. Locating and estimating air emissions from sources of chlorobenzenes. U.S. Environmental Protection Agency, Office of Air Quality. EPA-450/4-84-007m. 135 pp.

Vachon, J. 1986, personal communication. Direction de l'eau souterraine et potable, Ministère de l'environnement, Québec.

van der Meer, J.R., W. Roelofsen, G. Schraa, and A.J.B. Zehnder. 1987. Degradation of low concentrations of dichlorobenzenes and 1,2,4-trichlorobenzene by Pseudomonas sp. strain P51 in nonsterile soil columns. FEMS Microbiol. Ecology 45: 333-341.

Wakeham, S.G., A.C. Davis, and J.L. Karas. 1983. Mesocosm experiments to determine the fate and persistence of volatile organic compounds in coastal seawater. Environ. Sci. Technol. 17: 611-617.

Wallace, L.A. 1986. Personal exposures, indoor and outdoor air concentrations and exhaled breath concentrations of selected volatile organic compounds measured for 600 residents of New Jersey, North Dakota, North Carolina, and California. Toxicol. Environ. Chem. 12: 215-236.

Wallace, L.A., E.D. Pellizzari, T.D. Hartwell, C.M. Sparacino, L.S. Sheldon, and H. Zelon. 1985. Personal exposures, indoor-outdoor relationships, and breath levels of toxic air pollutants measured for 355 persons in New Jersey. Atmosp. Environ. 19(10): 1651-1661.

Wallace, L.A., E.D. Pellizzari, T.D. Hartwell, H. Zelon, C. Sparacino, R. Perritt, and R. Whitmore. 1986. Concentrations of 20 volatile organic compounds in the air and drinking water of 350 residents of New Jersey compared with concentrations in their exhaled breath. J. Occup. Med. 28(8): 603-608.

Wallace, L.A., E.D. Pellizzari, T.D. Hartwell, R. Whitmore, H. Zelon, R. Perritt, and L. Sheldon. 1988. The California TEAM study: breath concentrations and personal exposures to 26 volatile compounds in air and drinking water of 188 residents of Los Angeles, Antioch, and Pittsburg, California. Atmospheric Environment 22(10): 2141-2163.

Webber, M.D., and S. Lesage. 1989. Organic contaminants in Canadian municipal sludges. Waste Management & Research 7: 63-82.

Wilson, J.T., C.G. Enfield, W.J. Dunlap, R.L. Cosby, D.A. Foster, and L.B. Baskin. 1981. Transport and fate of selected organic pollutants in a sandy soil. J. Environ. Qual. 10(4): 501-506.

Zoeteman, B.C.J., K. Harmsen, J.B.H.J. Linders, C.F.H. Morra, and W. Slooff. 1980. Persistent organic pollutants in river water and ground water of the Netherlands. Chemosphere 9: 231-249.

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