Drinking Water and Health, Volume 4 (1982) / Chapter Skim
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VII Toxicity of Selected Organic Contaminants in Drinking Water
VII Toxicity of Selected Organic Contaminants in Drinking Water
Pages 202-288
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From page 202... ...
Among them are nitrophenols, nitrobenzene, petroleum products, and polynuclear aromatic hydrocarbons, which are also evaluated in this chapter. Table VII-1 summarizes the acture and chronic SNARL's for the compounds reviewed in this chapter.
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In 1964 approximately 1,575 metric tons of acetonitrile were used in the United States (National Institute for Occupational Safety and Health, 1978a)
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. Observations in Humans Acute exposure of humans to acetonitrile by inhalation results in headache, dizziness, profuse sweating, vomiting, giddiness, hypernea, difficulty in breathing, palpitations, irregular pulse, convulsions, loss of consciousness, and death, usually resulting from respiratory arrest (Amdur, 1959; Grabois, 1955; National Institute for Occupational Safety and Health, 1978a)
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There are no studies dealing with subacute or chronic toxicity of acetonitrile administered orally to animals. Carcinogenicity, Mutagenicity, and Teratogenicity There are no reports indicating any possible carcinogenic, mutagenic, or teratogenic effects of acetonitrile (National Institute for Occupational Safety and Health, 1978a)
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2,3,7,8-Tetrachlorodibenzo-p-dioxin did not alter the acute toxicity of chloroform (Hook et al., 1978) , but Cornish et al.
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Carcinomas of the liver were observed most frequently in mice ingesting chloroform, among other organochlorine compounds. When administered orally in doses of 0.15 mg/kg/day in drinking water, chloroform did not enhance the growth or metastasis of Lewis lung carcinoma or increase the number of Ehrlich ascites tumor cells in mice inoculated with tumor cells (Caper and Williams, 1978~.
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Chloroform-treated rats of both sexes survived better than the controls, although both groups had a high incidence of nonneoplastic respiratory and renal diseases. There were consistent observations of decreases in plasma cholinesterase in female rats, which were shown to be related to activity against butyrylcholine but not to acetyl-,Bmethylcholine.
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, but it is miscible with aliphatic and aromatic hydrocarbons and other solvents and oils. Its molecular weight is 236.36.
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HEALTH ASPECTS Observations in Humans In August 1977, at the request of the Oil, Chemical, and Atomic Workers Union (OCAW) , the National Institute for Occupational Safety and Health (NIOSH)
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(1961) fed diets containing DBCP concentrations of 0, 5, 20, 150, 450, and 1,350 mg/kg to male and female rats for 90 days.
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They also observed that the use of S-9 activation in the mutagenesis assay eliminated the mutagenic activity of epichlorohydrin and produced a mutagenic effect from pure DBCP, suggesting the formation of a mutagenic metabolite. Allyl chloride, which is also an impurity in technical DBCP, was found to be mutagenic in these studies, but the mutagenic potency of this contaminant is less than that of either epichlorohydrin or technical DBCP.
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In previous NIOSH documents relating to epichlorohydrin (National Institute for Occupational Safety and Health, 1976, 1978b) , evidence has suggested that epichlorohydrin produces carcinogenic effects in both laboratory animals and in humans.
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Second, are the adverse effects of DBCP on the testes due to DBCP itself or to a contaminant such as epichlorohydrin, which is known to cause sterility as well as mutagenic and oncogenic effects (National Institute for Occupational Safety and Health, 1978b)
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is 10 ppm. IETAB OLISM During the 24 hours following oral administration of DMF to rats at 4 to 400 mg/kg, nonmetabolized DMF was detected in the blood at concentrations proportional to the dose given.
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An accumulation of N-methylformamide was detected in the blood and urine of dogs subjected to repeated inhalation exposures to DMF at 59 ppm. In rats exposed to substantially higher subacute concentrations of DMF (350 ppm)
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. Oral administration of ethanol to rats at 2.0 g/kg before inhalation exposures to DMF at 87, 104, or 209 ppm for 2 hours only or for 2 hours daily for S days was investigated by Eben and Kimmerle (1976~.
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(1978) exposed eight healthy men to DMF vapor at a concentration of 8.79 + 0.33 ppm for 6 hours daily for 5 consecutive days.
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When humans were exposed by inhalation to 10 ppm DMF vapor for 6 hours daily for 5 consecutive days, absorbed DM17 could be correlated with urinary N-methylformamide (Krivanek et al., 1977~. The rate of urinary excretion increased rapidly during the exposure period, peaked within 3 hours after the end of exposure, and was nearly zero by the beginning of the next exposure period.
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The greatest damage was found in the liver (Cruz and Corpino, 1978~. Subchronic and Chronic Effects Although the combined action of 5 mg/m3 inhaled DMF and a 30% aqueous solution of DMF cutaneously applied was negative, 10 mg/m3 inhaled DMF and a 60% aqueous solution of DMF disturbed phagocytosis and decreased glycogen content in neutrophils of rats in a chronic test (Medyankin, 1975~.
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reported that the combined action of DMF and 5-bromodeoxyuridine reversed the random, irregular growth pattern of cultured tumor cells to a regular pattern typical of nonmalignant cells. The effect was eliminated by removal of the DMP, which altered the components of the surface membrane glycoprotein whereas 5-bromodeoxyuridine did not.
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Chronic Exposure This SNARL cannot be calculated since there is a lack of adequate chronic exposure data. Nitrobenzene (C6H5NO2)
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(American Conference of Governmental Industrial Hygienists, 1980~. METABOLISM Nitrobenzene is a very lipid-soluble compound, having an oil to water partition coefficient of 800.
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reported a case of nitrobenzene poisoning in a child who was given `'oil of almonds" for relief of a cold. Acute nitrobenzene poisoning has also resulted from ingestion of denatured alcohol (Donovan, 1920; Wirtschafter and Wolpaw, 1944)
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Nitrobenzene is a powerful methemoglobin former, cyanosis appearing when methemoglobin levels reach 15~o. Blood methemoglobin levels from nitrobenzene have ranged from 0.6 g/lOO ml in industrial chronic exposures to l O g/ l OO ml in acute poisoning (Myslak
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1941; Wirtschafter and Wolpaw, 1944~. A minimum lethal dose of 4.0 ml has been reported by von Oettingen (1941~.
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Subchronic and Chronic Effects Levin (1927) demonstrated in-vivo production of methemoglobin by nitrobenzene in dogs, cats, and rats, but not in guinea pigs or rabbits.
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Using the acute 24-hour SNARL of 0.035 mg/liter and dividing by 7 days, one may derive the SNARL as: 0.035 m/liter 7 0.005 mg/liter. Chronic Exposure This SNARL cannot be calculated due to a lack of adequate chronic exposure data.
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4-Nitrophenol is probably the most important of the mononitrophenols in terms of quantities used and potential environmental contamination. Approximately 15,750 metric tons of 4-nitrophenol were used in 1976 (Chemical Marketing Reporter, 19761.
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The physical and chemical properties of the dinitrophenol isomers are summarized in Table VII-4. Six isomeric forms of trinitrophenol are possible, but significant commercial usage of these compounds is apparently limited to 2,4,6-trinitrophenol (picric acid)
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Excretion by mice, rats, rabbits, and guinea pigs is also rapid. Most doses were completely eliminated from the blood within 2 hours a*
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and ethereal sulfates (19%~; and 4-nitrophenol was excreted in the urine, 87~o as nitro compounds and 14~o as amino compounds, 65% of which occurred as glucuronic conjugates and 16~o as ethereal sulfates. Dinitrophenols Dinitrophenol isomers are readily absorbed from the gastrointestinal tract and through the skin and lungs (Gehring and Buerge, 1969b; Haney, 1959; von Oettingen, 1949~.
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(1954) also studied the phat~acokinetics of the other dinitrophenol isomers and showed that elimination from the blood of mice, rabbits, guinea pigs, rats, and monkeys was complete within 30 hours.
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Tr~nitrophenols Autopsy examination of dogs after lethal doses of picric acid (2,4,6-trinitrophenol) revealed yellow staining of the subcutaneous fat, lungs, intestines, and blood vessels (Dennie et al., 19291.
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Later, Gisclard and Woodward (1946) reported two fatal cases of dinitrophenol poisoning during manufacture of picric acid, when 2,4-dinitrophenol was produced as an intermediate.
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(1976) , ingestion or percutaneous absorption of picric acid may cause nausea, vomiting, diarrhea, abdominal pain, oliguria, anuria, yellow staining of the skin, pruritus, skin eruptions, stupor, convulsions, and death.
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Approximately 3 weeks prior to the outbreak, more than 90 metric tons of confiscated Japanese ammunition containing picric acid had been dumped in the immediate vicinity of the anchorage. The trichlorophenol was apparently carried over in the vapor phase into the freshwater supply upon distillation of the seawater.
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Guinea pigs develop allergic reactions following topical treatment with picric acid (Chase and Maguire, 1972; Landsteiner and DiSomma, 1940; Maguire, 1973; Maguire and Chase, 1972~.
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Cataracts developed in two of three guinea pigs on day 7 and 11 following daily intraperitoneal administration of 4-nitrophenol in doses of 8.3 to 12.5 mg/kg. Administration of 4-nitrophenol over a 20-day test period produced cataracts while similar dosing with 2- and 4-nitrophenol did not.
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Trinitrophenols No subchronic or chronic toxicity data in animals are available. Mutagenicity Szybalski ( 1958)
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rophenol. The committee found no data on carcinogenic effects of picric acid.
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observed the development of cataracts in guinea pigs given daily intraperitoneal doses of 4-nitrophenol at 8.3 to 12.5 mg/kg for 6 to 11 days. Despite the absence of control animals and other shortcomings of these data, they will still be used for the SNARL calculation.
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Using this value and an uncertainty factor of 1,000, and assuming a 20~o intake from water and a daily consumption of 2 liters by a 70-kg adult, one may calculate the chronic SNARL as: 10 mg/kg X 70 kg X 0 2 = 0.07 mg/liter 1,000 X 2 liters which is in good agreement with the chronic SNARL calculated from exposure data on humans. Tr~nitrophenol 24-Hour Exposure Only acute toxicity data on 2,4,6-trinitrophenol (picric acid)
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From page 247... ...
Navy personnel developed hematuria upon drinking water that contained picric acid in concentrations ranging from 2 to 20 mg/liter. Assuming that this exposure occurred over several days and that 2 mg/liter represents the minimum concentration in water, one may estimate a 7-day SNARL, using an uncertainty factor of 10, as: 2 mg/liter = 0 2 mg/liter.
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From page 248... ...
Refined petroleum solvents that may contaminate drinking water supplies may be classified according to the following major divisions: petroleum ether, rubber solvent, varnishmakers' or painters' naphtha, mineral spirits, Stoddard solvents, and kerosene (National Institute for Occupational Safety and Health, 1977a)
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Toxicity of Selected Organic Contaminants in Drinking Water 249 hydrocracked gasoline, and thermally cracked gasoline, reformats, and alkylate. Since the highest octane blending components in gasoline are aromatics and branched-chain alkanes, refineries attempt to produce a blending stream rich in these components.
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of Water-Soluble Fractions Equilibrated with Crude and Refined Oils Crude Oil Crude Oil No. 2 Fuel Water Solubility No.
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Recent toxicological and epidemiolog~cal evidence suggests that acute intoxication by these alkalies involves a transient depression of the central nervous system. Chronic intoxication with alkalies may lead to development of a more persistent polyneuropathy (National Institute for Occupational Safety and Health, 1977b)
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They are also the most soluble in water. The aromatic fraction contains benzene, alkyl derivatives of benzene, and small quantities of various polynuclear aromatic hydrocarbons.
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Chronic Effects In most of the studies on the chronic toxicity of benzene to animals, investigators used inhalation exposures. An exception was the study of Wolfe et al.
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This is illustrated by the recent, puzzling finding of a high frequency of brain tumors among workers in the petrochemical industry (Fox, 1980~. Other substantial limitations associated with the calculation of 24-hour and 7-day SNARL's for both benzene and toluene include the inadequacy of the oral toxicity data and the lack of data on synergistic interactions among petroleum constituents.
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Polynuclear Aromatic Hydrocarbons These compounds were reviewed previously by the Criteria and Standards Division, Office of Water Planning and Standards, U.S. Environmental Protection Agency (1979e)
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256 DRINKING WATER AND HEALTH contain substantial concentrations of PAM's (Andelman and Suess, 1970) , thereby contributing to the contamination of surface waters by these compounds.
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. The necessity for metabolic activation to express the carcinogenesis of PAH has prompted the investigation of PAH metabolism in numerous
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258 DRINKING WATER AND HEALTH animal models and human tissues. From these studies has emerged a general understanding of the mechanisms involved in the biotransformation of these compounds.
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Molecular orbital calculations can be used to predict the relative carcinogenic potential of a series of PAM's from their relative tendencies to form carbonium ion from their bay region dial epoxides. HEALTH ASPECTS Observations in Humans Although exposure to PAM's occurs predominantly by direct ingestion of the compounds in food and in drinking water, there are no studies to document the possible carcinogenic risk to humans by these routes of exposure.
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It has been reported that the acute oral LD50 for DMBA in mice is 350 mg/kg (National Institute for Occupational Safety and Health, 1978d)
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Mortality among female rats was approximately 65~o. Sixty-day-old adult rats that were given 20 mg of DMBA orally and 5 mg intravenously developed transient degenerative changes in the testes, which were most evident between 38 and 40 days after treatment.
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The use of S typhimur~um strains to detect chemically induced mutagens and microsomal preparations to provide metabolic activation has also made possible investigations of the mechanism of PAH-induced mutagenesis.
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in animals may not be valid given the diverse nature of PAH mixtures. · Few acute, subchronic, or chronic toxicity studies in animals have been conducted with oral exposure to defined PAH mixtures.
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In the absence of data for oral exposure to defined PAH mixtures, assessment of exposure to such mixtures must be based on or derived from exposure to a single PAH. However, it is not possible to determine 24-hour or 7-day SNARL's for this class of compounds because the acute toxicity data for pure PAM's and PAH mixtures are inadequate.
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Its vapor pressure is 1 mm Hg at 75°C (Weast and Astle, 1978~. METABOLISM As to be expected from its high octanol-water partition coefficient of 4898:1 (Roberts et al., 1977)
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Subchronic and Chronic Effects In preliminary subchronic feeding studies, diets containing 2,4,6-trichlorophenol were given ad libitum to groups of male and female F334 rats and B6C36~ mice for 7 weeks (National Cancer Institute, 1979~. The investigators continued to observe the animals for an additional week after the feeding was stopped.
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. In a more recent study, technical 2,4,6-trichlorophenol was administered in the diet of male and female F344 rats and male B6C3F~ mice at concentrations of 5,000 and 10,000 ~g/g for 105 to 107 weeks (National Cancer Institute, 1979~.
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Chronic Exposure No chronic SNARL can be calculated because tests with technical 2,4,6-trichlorophenol have yielded positive results in · · · · ~ aroma carcinogen City ~ Assays. REFERENCES Adler, B., R
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1975. Gas chromatographic determination of selected organic compounds added to wastewater.
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1972. Picric acid hypersensitivity: Cross-reactivity and cellular transfer.
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1929. Toxic reactions produced by the application of trinitrophenol (picric acid)
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1911. Picric acid and its surgical applications.
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1957. The enzymatic reduction of chloramphenicol, p-nitrobenzoic acid and other aromatic nitro compounds in mammals.
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1946. Hematuria due to picric acid poisoning at a naval anchorage in Japan.
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1973. IARC Monographs on the Evaluation of Carcinogenic Risk of the Chemical to Man: Certain Polycyclic Aromatic Hydrocarbons and Heterocyclic Compounds.
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VIII. Sensitization to picric acid; subsidia~y agents and mode of sensitization.
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Volume 3. Polynuclear Aromatic Hydrocarbons: Second International Symposium on Analysis, Chemistry, and Biology.
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XIII. Sensitization of guinea pigs with picric acid.
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National Institute for Occupational Safety and Health, Washington, D.C.
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78-212~1 National Institute for Occupational Safety and Health.
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U.S. Department of Health, Education, and Welfare, Public Health Se~vice, Center for Disease Control' National Institute for Occupational Safety and Health, Washington, D.C.
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From page 282... ...
on the semen of rabbits and the fertility of male and female rats. Toxicol.
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1970. Qualitative and quantitative studies on the metabolism of a series of aromatic hydrocarbons hy rat-li~er preparations.
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1980. A review of occurrences and treatment of polynuclear aromatic hydrocarbons.
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Leber, eds. Polynuclear Aromatic Hydrocarbons: Third International Symposium on Chemistry and Biology-Carcinogenesis and Mutagenesis.
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From page 286... ...
1979e. Polynuclear Aromatic Hydrocarbons: Ambient Water Quality Criteria.
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From page 287... ...
Leber, eds. Polynuclear Aromatic Hydrocarbons: Third lnternational Symposium on Chemistry and Biology-Carcinogenesis and Mutagenesis.
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1929. Aniline and nitrobenzene poisoning in infants.
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