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vll Toxicity of Selectecl Organic Contaminants in Drinking Water The compounds evaluated in this chapter were selected for essentially the same reasons as those enumerated at the beginning of Chapter VI. Chloroform is included because new information has become available since it was evaluated in the first volume of Drinking Water and Health (National Academy of Sciences, 1977~. Dibromochloropropane appears for the first time in this report because of its occurrence in drinking water resulting from its use in agriculture. Toxicological information is required for a large number of solvents that are appearing with greater frequency in wastewater, thereby posing a real or potential hazard for contamination of drinking water. Among them are nitrophenols, nitrobenzene, petroleum products, and polynuclear aromatic hydrocarbons, which are also evaluated in this chapter. Table VII-1 sum- marizes the acture and chronic SNARL's for the compounds reviewed in this chapter. Acetonitrile (CH3CN) Nitriles characteristically contain a cyano group, C-N. Acetonitrile a mononitrile having the formula CH3CN-is also known as methylcyanide, cyanomethane, or ethanenitrile (National Institute for Occupational Safety and Health, 1978a). A colorless liquid, acetonitrile is infinitely soluble in water and has a molecular weight of 41.1. Because of their versatile chemical reactivity, nitrites have many industrial uses, such as in the manufacture of plastics, synthetic fibers, and elastomers, and as a solvent 202

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Toxicity of Selected Organic Contaminants in Drinking Water 203 TABLE VII-1 Summation of Acute and Chronic Exposure Levels for Organic Chemicals Reviewed in this Chapter Suggested No-Adverse-Response Level (SNARL), mg/liter, by Exposure Perioda Chemical 24-Hour 7-Day Chronic Nitrobenzene 0.035 0.005 Mononitrophenol 0.29 Dinitrophenol 0.11 b Tr~nitrophenol 4.9 0.2 Benzene 0.25 2,4,6-Tr~chlorophenol 17.5 2.5 aSee text for details on individual compounds. bThis is the average from two calculated SNARL's; see text for details. in the extractive distillation that separates olefins from diolefins, butadiene from butylene, and isoprene from isopentene (Merck Index, 1976; National Institute for Occupational Safety and Health, 1978a; Pozzani et al., 1959~. In 1964 approximately 1,575 metric tons of acetonitrile were used in the United States (National Institute for Occupational Safety and Health, 1978a). The major occupational exposures to nitrites occur primarily by the der- mal and inhalation routes. Depending upon the amount absorbed, nitrites may cause hepatic, renal, cardiovascular, gastrointestinal, and central nervous system disorders, regardless of the route of administration. Although these effects are usually attributed to the metabolic release of cyanide, they may also be partly due to the intact molecule (National In- stitute for Occupational Safety and Health, 1978a). The time-weighted average (TWA) standard for nitrites published by the National Institute for Occupational Safety and Health (NIOSH) is based on reports indicating that certain nitrites are sources of cyanide ions. The TWA for acetonitrile is 20 ppm for up to a 10-hour workshi* in a 40-hour work week (National Institute for Occupational Safety and Health, 1978a). METABOLISM There has been little work concerned with the metabolism and disposition of acetonitrile. In studies by Dequidt and Haguenoer (1972) and Hague- noer and Dequidt (1975a), rats received intraperitoneal injections of

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204 DRINKING WATER AND HEALTH acetonitrile in doses ranging from 600 to 2,340 mg/kg. The tissues were analyzed for acetonitrile and both free and combined hydrogen cyanide content. In general, acetonitrile was found to be rather evenly distributed among the various organs, and hydrogen cyanide was found in nearly all organs in varying concentrations. In subsequent studies, Haguenoer and Dequidt (1975b) obtained similar results following the administration of acetonitrile to rats via the inhalation route. A series of studies have shown that humans absorb nitrites through the skin (Sunderman and Kincaid, 1953; Wolfsie, 1960) and through the res- piratory tract (Amdur, 1959; Dalhamn et al., 1968; McKee et al., 1962; Pozzani et al., 19591. After absorption, nitrites may be metabolized to an alpha-cyanohydrin or to inorganic cyanide, which is oxidized to thio- cyanate and excreted in the urine. Nitriles also undergo other types of reactions depending on the moiety to which the cyano group is attached. The cyano group may be converted to a carboxylic acid derivative and am- monia or may be incorporated into cyanocobalamin (National Institute for Occupational Safety and Health? 1978a). HEALTH ASPECTS In general, adverse effects resulting from exposure to the nitrites' in- cluding acetonitrile, occur primarily by the dermal and inhalation routes. Depending on the amount absorbed, nitrites may cause toxic effects in- volving the hepatic, renal, cardiovascular, gastrointestinal, and central nervous systems. These effects may be due in part to the intact molecules, but are also attributed to the metabolic release of cyanide. There are substantial differences among the various nitrites with regard to the amounts necessary to cause poisoning, the durations of exposure' and the time intervals between exposure and manifestation of the adverse effects. These differences are associated with the rate and extent of the release of cyanide ion (Amdur, 1959; National Institute for Occupational Safety and Health, 1978a). Observations in Humans Acute exposure of humans to acetonitrile by inhalation results in head- ache, dizziness, profuse sweating, vomiting, giddiness, hypernea, difficul- ty in breathing, palpitations, irregular pulse, convulsions, loss of con- sciousness, and death, usually resulting from respiratory arrest (Amdur, 1959; Grabois, 1955; National Institute for Occupational Safety and Health, 1978a). Most deaths have followed industrial exposures, and ef

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Toxicity of Selected Organic Contaminants in Drinking Water 205 fects have generally been observed anywhere from 3 to 12 hours after ex- posure (National Institute for Occupational Safety and Health, 1978a). This delayed onset of effects has been explained by Amdur (1959) as a slow release of cyanide and its metabolism to thiocyanate. There are ap- parently no reports of toxicity in humans following ingestion of acetonitrile. Observations in Other Species Acute toxic effects observed in animals include labored breathing, anuria, ataxia, cyanosis, coma, and death. Tissue distribution studies indicate that mononitriles are distributed uniformly in the various organs and that cyanide metabolites are found in the spleen, stomach, and skin, smaller amounts being present in the liver, lungs, kidneys, heart, brain, muscle, intestines, and testes (Dequidt and Haguenoer, 1972; Pozzani et al., 1959). Most studies conducted in animals have been concerned with toxicity following inhalation. Studies of orally adminstered acetonitrile have shown LDso's in various species as follows: Sherman rats, 3.8 g/kg (Smyth and Carpenter, 19481; rats, 1.34-6.68 g/kg (Pozzani et al., 1959~; and guinea pigs, 0.14 g/kg (Pozzani et al., 1959~. Kimura et al. (1971) found that the oral toxicity of acetonitrile varied according to the age of the rat. The acute oral LD50's for 14-day-old, young adult, and adult rats were 0.16 g/kg, 3.1 g/kg, and 3.5 g/kg, respectively. Acetonitrile was significantly more toxic in the 14-day-old rat than in the adult. 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 ef- fects of acetonitrile (National Institute for Occupational Safety and Health, 1978a). Acrylonitrile (vinyl cyanide) is suspected of inducing cancer in both animals and humans (National Institute for Occupational Safety and Health, 1978c). CONCLUSIONS AND RECOMMENDATIONS Suggested No-Adverse-Response Level {SNARLJ 24-Hour Exposure There are no adequate data from which to calculate a 24-hour or 7-day SNARL.

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206 DRINKING WATER AND HEALTH Chronic Exposure There are no adequate data from which to calculate a chronic exposure SNARL. Chloroform (CHCI3) Chloroform was evaluated in the first and third volumes of Drinking Water and Health (National Academy of Sciences, 1977, pp. 713-717; 1980a, pp. 203-204~. The following material, which became available after these volumes were published, updates and, in some instances, reevaluates the information in the earlier reports. Also included are some references that were not assessed id the original report. HEALTH EFFECTS Observations in Humans No new data. Observations in Other Species Hewitt et al. (1979) observed an increased uptake of glutamate-pyruvate transaminase (GPl) and decreased uptake of indicator organic anions and cations in kidney slices from male Swiss-Webster mice exposed to chloroform. Pretreatment of the animals with mirex did not markedly alter either the hepatotoxic or nephrotoxic effects of chloroform. However, pretreatment with kepone potentiated chloroform hepatotoxic- ity and may have increased chloroform-induced kidney damage. The authors concluded that ingestion of kepone may increase the sensitivity of the liver and kidneys to chloroform toxicity. The toxicity of chloroform was more pronounced in males than in fe- males of the following barrier-reared strains of mice: Tif:MAGf, Tif:MF2f, C3H/TifBomf, DBA/JBomf, C57BL/6J/Bomf, and A/JBomf strains. The C3H/TifBomf strain proved to be the most sensitive of the several strains tested (Pericin and Thomann, 1979~. 2,3,7,8-Tetrachloro- dibenzo-p-dioxin did not alter the acute toxicity of chloroform (Hook et al., 1978), but Cornish et al. (1977) showed that the toxicity of chloroform can be markedly potentiated by prior treatment with ethanol or phenobar- bital. Mutagenicity In studies by Agustin and Lim-Sylianco (1978), chloroform showed DNA-damaging and chromosome-breaking (clasto- genic) activity; however, it had no direct effect on base-pair and frame

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Toxicity of Selected Organic Contaminants in Drinking Water 207 shift mutations. Chloroform also caused frame shift mutations in male mice after metabolic activation. Vitamin E treatment decreased the mutagenicity and clastogenicity of chloroform. Clemens et al. (1979) reported genotypic differences in responses to the toxic effects of chloroform that were manifestations of differences in renal rather than hepatic responses or the ability to repair renal damage. In these studies, the authors showed that DBA/2J male mice were more sen- sitive to the 10-day lethal effect of chloroform than were C57BL/6J males, whereas the sensitivity of B6D2F~ (C57BL/6J X DBA/2J) mice was in- termediate. This relative order of sensitivity was preserved following sublethal doses of labelled chloroform with respect to accumulation in subcellular fractions and renal (but not hepatic) dysfunction. Kidneys from mice of the three genotypes were able to repair tubular damage from chloroform. Prior to toxic exposure to chloroform, covalent binding of labeled chloroform to renal microsomes was greater in DBA than in C57BL mice. Pretreatment with phenobarbital enhanced covalent bind- ing by renal microsomes from DBA, but not from C57BL mice. Testoster- one propionate and medroxyprogesterone acetate sensitized the kidneys of both sexes in DBA/2J and C57BL/6J mice. Progesterone and hydrocorti- sone sodium phosphate sensitized the kidneys to chloroform in DBA/2J males but not in DBA/2J females or in C57BL/6J mice of either sex. In the presence of metabolically active mouse liver microsomes and bacteria, chloroform was not activated to mutagenic species (Greim et al., 1977~. It also gave negative results in the Ames test and failed to increase the frequency of sister chromatic exchange (SCE) in fibroblasts of Chinese hamsters (Li et al., 1979~. Results from a study by White et al. (1979) also indicated that chloroform did not increase SCE values. Simmon (1977) reported that bromoform, dibromochloromethane, and bromodichloro- methane are mutagenic whereas chloroform is not mutagenic in Salmo- nella typhimurium strains TA1535 and TA100. Carcinogenicity Reuber (1979) recently reviewed the literature con- cerning the carcinogenicity of 14 organochlorine pesticides in mice. Car- cinomas of the liver were observed most frequently in mice ingesting chloroform, among other organochlorine compounds. When ad- ministered orally in doses of 0.15 mg/kg/day in drinking water, chloroform did not enhance the growth or metastasis of Lewis lung car- cinoma or increase the number of Ehrlich ascites tumor cells in mice in- oculated with tumor cells (Caper and Williams, 1978~. However, when ad- ministered at 15 mg/kg/day in similar experiments it caused increases in pulmonary tumor foci after inoculation with Lewis lung carcinoma cells and in the number of Ehrlich ascites tumor cells. At both doses, it led to

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208 DRINKING WATER AND HEALTH more organ invasions by B16 melanoma after inoculation with the tumor cells. When administered by oral intubation, it produced kidney tumors in male Osborne-Mendel rats (Weisburger, 1977~. A series of studies was conducted at the Huntington Research Center in England, using beagle dogs, specific pathogen-free Sprague-Dawley rats, and three stocks (C57BL, CBA, and CSI) of mice, which were given chloroform in a toothpaste base (Heywood et al., 1979; Palmer e! al., 1979; Roe et al., 1979~. The beagle dogs were given the mixture orally in gelatin capsules 6 days/week for 7.5 years, followed by a 20- to 24-week recovery period (Heywood et al., 1979~. Groups of males and females received 0.5 ml/kg/day of the vehicle (toothpaste without chloroform), and eight dogs of each sex remained untreated. The treated groups were composed of eight dogs of both sexes, each receiving chloroform in doses equivalent to 15 and 30 mg/kg/day in the toothpaste vehicle. Another group of the same size received an equivalent amount of toothpaste (0.5 ml/kg/day) without chloroform. At the end of the exposure, a small number of macroscopic and microscopic neoplasms were observed. One dog in each chloroform-treated group had a malignant tumor, but there were no tumors in the livers or kidneys of any dog. Overall, exposure to chloroform in a toothpaste base was not associated with any effects on the incidence of any kind of neoplasia. Groups of 50 cesarean-derived specific pathogen-free male and female Sprague-Dawley rats received either chloroform in doses equivalent to 60 mg/kg/day in a toothpaste base or the vehicle only by gavage 6 days/week for 80 weeks. They were then observed for as long as 15 weeks more (Palmer et al., 19791. Chloroform-treated rats of both sexes survived bet- ter than the controls, although both groups had a high incidence of non- neoplastic respiratory and renal diseases. There were consistent observa- tions of decreases in plasma cholinesterase in female rats, which were shown to be related to activity against butyrylcholine but not to acetyl-,B- methylcholine. Tumors of various sites were observed in 39~o of chloro- form-treated rats of both sexes examined histologically, compared with 38~o of the vehicle controls. There were no treatment-related effects on the incidence of liver or kidney tumors. However, histological observations of malignant mammary tumors were reported in more treated than con- trol rats, but these differences were not statistically different. In another study, mice were given chloroform in a toothpaste base by gavage or in arachis oil in doses up to 60 mg/kg/day, 6 days/week for 8 weeks (Roe et al., 1979~. Control groups were left untreated or given the vehicle only. In general, there were more survivors in the chloroform- treated groups than in the control group. Treatment was not associated with any type of neoplasia. In male, but not female, ICI mice receiving

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Toxicity of Selected Organic Contaminants in Drinking Water -209 doses of 60 mg/kg/day, but not in those given 17 mg/kg/day, chloroform in a toothpaste base was associated with an increased incidence of epi- thelial tumors of the kidney. A more pronounced effect of the same kind was observed in mice given chloroform at 60 mg/kg/day in an arachis oil vehicle. This treatment was also associated with a higher incidence and severity of nonneoplastic renal disease. At the dose levels tested, namely 113 and 400 times greater than the average human exposure resulting from the use of toothpaste containing 3.5% chloroform, no adverse effects were seen in the liver and there was no increased incidence of liver tumors, even in the CBA strain with the greatest susceptibility to liver tumor for- mation. At the 17 mg/kg/day level, which is 113 times greater than the average exposure of humans from toothpaste, no excess of renal tumors was observed in males of the particularly susceptible ICI strain. Teratogenicity No new data. CONCLUSIONS AND RECOMMENDATIONS Suggested No-Adverse-Response Level (SNARLJ The following calculations are for noncarcinogenic effects only. 24-Hour Exposure A SNARL of 22 mg/liter was calculated in Drink- ing Water and Health, Volume 2 (National Academy of Sciences, 1980a). Details of the calculation are contained in that volume. 7-Day Exposure This was calculated to be one-seventh (3.2 mg/liter) of the 24-hour SNARL. Chronic Exposure form is a carcinogen in animals. This value cannot be calculated because chloro 1,2-Dibrom~3-chloropropane (C3H5Br2CI) 1,2-Dibromo-3-chloropropane (DBCP) is an amber-brown liquid with a low vapor pressure and solubility (O.l~o w/w), but it is miscible with aliphatic and aromatic hydrocarbons and other solvents and oils. Its molecular weight is 236.36. Since the 1950's, DBCP has been used as a soil fumigant and nemato- cide in emulsifiable concentrates, liquid concentrates. powders, granules, and other formulations. It has been marketed under such trade names as Negmagon, Fumazone, Nemaset, Nematox, and Nemafume.

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210 DRINKING WATER AND HEALTH DBCP is produced primarily by the bromination of allyl chloride at room temperature. Technical grade DBCP has been shown to contain up to loo impurities, including epichlorohydrin and allyl chloride. The levels of these compounds and 14 other identified impurities may vary among batches. In contrast to the other impurities' epichlorohydrin is added intentionally as a stabilizer. 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) inspected manufacturing facilities in California. In September of that year. an emergency temporal standard for exposure to DBCP was issued by the Occupational Safety and Health Administration (OSHA). A permanent standard for DBCP exposure, which was established on March 17, 1978, limits employee exposure to 1 ppb as an 8-hour time- weighted average concentration. This OSHA standard also prohibited eye and skin contact and provided for monitoring of employee exposure, engineering controls, safe work practices, and various other regulatory re- quirements. A rebuttable presumption against registration (RPAR) and continued registration of pesticide products containing DBCP was issued by the U.S. Environmental Protection Agency (EPA) on September 22, 1977 (U.S. Environmental Protection Agency, 1977~. Both the OSHA standard and the EPA RPAR were based primarily on toxicological findings in animals, suggesting that DBCP causes sterility and is carcinogenic. The NIOSH recommendation for an occupational exposure standard for DBCP was based not only on its carcinogenic and sterilizing potential, but also on its ability to cause diminished renal func- tion, degeneration and cirrhosis of the liver, and mutagenesis in chroni- cally exposed employees. Observations in Other Species Acute Effects Studies by Torkelson et al. ( 1961 ) and by Rakh- matullaev (1971) indicate that the acute oral LDso for DBCP in rats and other animals such as guinea pigs, mice, rabbits, and chickens ranges from 170 to 350 mg/kg. Mice and rabbits appear to be somewhat less sen- sitive than chickens. Effects preceding death following lethal exposures to DBCP included depression, analgesia, skeletal muscle incoordination, and paralysis. DBCP produced slight irritation when applied to the eye,

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Toxicity of Selected Organic Contaminants in Drinking Water 211 but corneal irritation was not noted. Dermal application of DBCP produced only transient erythema in rabbits, but both single and repeated dermal exposure produced subcutaneous necrosis with polymorphonuclear leucocyte infiltration. Using a modified Draize technique, Torkelson et al. (1961) reported a dermal LDso of 1,400 mg/kg in rabbits exposed for 24 hours to undiluted DBCP at 60 ppm. Inhalation exposure to vaporized DBCP produced respiratory irritation, apathy, and ataxia. Clouding of the lens and cornea and mortality occurred at higher concentrations. A 1-hour LC50 of 368 ppm was observed in rats, but delayed deaths and kidney pathology were noted following inhalation exposures to concentra- tions as low as 50 ppm. Subchronic Effects Torkelson et al. (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. Female rats exhibited increased kidney weights at )() _ , . , ~ . . . . . . . . . 111~/~g alla a~ ~llg~ler aoses, retarded welgnt gain at doses of 150 mg/kg and higher, and increased liver weight at 450 mg/kg. There were no Growth effects in male rats fed diets oontninina lo then An m~r/lrn ~, ~^-~ 4 ~ ~A A-459 / ~,5~ ~ ~ ~ ~ ~ _ ~ ~ ~ . . . .. . ~ ulstologlca1 effects were minimal at all dosage levels in both sexes. In contrast to the diet exposure studies, repeated inhalation exposure produced poor growth, increased susceptibility to secondary infection, and both gross and histological changes in the testes of male rats at the lowest exposure rate tested (50 exposures of 7 hours daily, 5 days a week to DBCP at 5 ppm). Hicher concentrations of DBCP produced mortality _ ~ _ ~ ,,, . . ^. . and similar findings were observed in monkeys, guinea pigs, and rabbits. Intramuscular injection of testosterone, cortisone, and ACTH (adrenocor- ticotropic hormone) failed to protect male rats against the testicular ef- fects of exposure to DBCP (Torkelson et al., 19611. Mutagenicity DBCP was shown to be directly mutagenic to Salmo- nella typhimurium TA1530 and Escherichia cold Poll A by Rosenkrantz (1975~. Prival et al. (1977) reported that the compound is a direct weak mutagen in Salmonella TA1535. Blum and Ames (1977) reported mutagenic effects with DBCP in Salmonella TA100 with metabolic activa- tion. The observation of Vogel and Chandler (1974) that 1,2-dibromo- propane was also mutagenic in Drosophila could have been due to the ability of vicinal 1,2-dibromides to rearrange in solution to fo'-',, reactive bromonium ion. The substitution of a chlorine atom on the third carbon of propane would probably not alter this property significantly. Thus, DBCP would be expected to be mutagenic on the basis of its 1,2-dibro- mide configuration. However, Biles et al. (1978), in a more recent reeval- uation of the mutagenicity of DBCP, suggest that most, if not all, of the

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212 DRINKING WATER AND HEALTH mutagenic effects attributed to the technical grade of DBCP used in previous mutagenesis assays is due to epichlorohydrin or to other highly mutagenic contaminants in the technical product. Using Salmonella typhimurium TA1535 with and without S-9 activation, these investigators demonstrated mutagenic effects (increased revertants at doses ranging from 0 to 1,600 ~g/plate) with technical DBCP, pure epichlorohydrin, and distillates from the technical product. Pure (redistilled) DBCP did not produce mutagenic effects even at high dosage levels. On the basis of the mutagenesis assay data, these authors calculated that the mutagenic ef- fect of technical DBCP can be attributed almost entirely to the presence of the stabilizer epichlorohydrin in the technical product. 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 contami- nant is less than that of either epichlorohydrin or technical DBCP. Carcinogenicity The EPA RPAR Final Position Document for DBCP (U.S. Environmental Protection Agency, 1978) describes four studies that attribute carcinogenic effects to DBCP in laboratory animals. The first of these is the National Cancer Institute (NCI) (1978) bioassay of DBCP for possible carcinogenicity. Partial results of this study have also been published by Weisburger (1977), and preliminary observations on the car- cinogenicity of DBCP were reported by Olson et al. (1973~. Two additional studies, which were sponsored by Dow Chemical, were conducted at the Hazelton Laboratories. The fourth study was a skin bioassay study con- ducted by Van Duuren at the New York Medical Center. An earlier report by Van Duuren (1977) describes the carcinogenicity of epichlorohydrin, allyl chloride, and other DBCP-related halohydrocarbons. When the NCI carcinogenicity bioassay was initiated in 1972, DBCP was only one of several halohydrocarbons under test. It was administered by gavage 5 days a week to male and female Osborne-Mendel rats at dosage levels of 12 and 24 mg/kg for 14 weeks' after which the dosages were increased to 15 and 30 mg/kg for a period of 73 or 64 weeks, respec- tively. Similar studies with male and female B6C3F~ mice were also con- ducted at higher concentrations of DBCP. The major conclusions of this study were that, "In rats and mice of both sexes, statistically significant incidences of squamous-cell carcinomas of the forestomach occurred in each dosed group with a positive association between dose level and tumour incidence." The NCI also concluded that DBCP is carcinogenic to the mammary gland of female rats. Toxic nephropathy was observed in

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278 DRINKING WATER AND HEALTH Lyle, W. H., T.W.M. Spence, W.M. McKinneley, and K. Duckers. 1979. Dimethylfor- mamide and alcohol intolerance. Br. J. Ind. Med. 36:63-66. MacMath, I.F., and J. Apley. 1954. Cyanosis from absorption of marking-ink in newborn babies. Lancet 2:895-896. Maguire, H.C., Jr. 1973. The bioassay of contact allergens in the guinea pig. J. Soc. Cosmet. Chem. 24:151-162. Maguire, H.C., Jr., and M.W. Chase. 1972. Studies on the sensitization of animals with sim- ple chemical compounds. XIII. Sensitization of guinea pigs with picric acid. J. Exp. Med. 135:357-375. Makhinya, A.P. 1964. Effect of certain nitrophenols on the organoleptic qualities of water and the sanitary conditions of water basins. Vopr. Gigieny Nasalen. Mest, Kiev, Sb. 5:43-46. [Chem. Absts. 64: 15580c, 1966.] Makhinya, A. P. 1969. Comparative hygienic and sanita~y-toxicological studies of nitrophenol isomers in relation to their normalization in river waters. Prom. Zagryazeniya Vodoemov (9):84-95. [Chem. Absts. 72:047231c. 1970.] Makotchenko, V.M, and Zh.B. Akhmetov. 1972. [in English summary] Adrenal cortex function in chronic nitrobenzene poisoning of guinea pigs and the effect of hydrocortisone on the course of poisoning. Farmakol. Toksikol. 35:247-249. Malmgren, R.A., B.E. Bennison, and T.W. McKinley, Jr. 1952. Reduced antibody titers in mice treated with carcinogenic and cancer chemotherapeutic agents. Proc. Soc. Exp. Biol. Med. 79:484-4~. Marshall, S., M.D. Whorton, R.M. Krauss, and W. Palmer. 1977. The effects of pesticides on testicular function. J. Urol. 11 :257-259. Matsuguma, H.J. 1967. Nitrophenols. Pp. 888-894 in R. E. Kirk and D . F. Othmer. eds. Kirk-Othmer Encyclopedia of Chemical Toxicology. Vol. 13. Second edition. Wiley- Interscience, New York. Maxfield, M.E., J.R. Barnes, A. Azar, and H.T. Trochimowicz. 1975. Urinary excretion of metabolite following experimental human exposures to DMF or to DMAC. J. Occup. Med. 17:506-511. Mazumdar, S., C. Redmond, W. Sollecito, and N. Sussman. 1975. An epidemiological study of exposure to coal tar pitch volatiles among coke oven workers. J. Air Pollut. Con- trol. Assoc. 25:382-389. McAuliffe, C. 1966. Solubility in water of paraffin, cycJoparaffin, olefin, acetylene, cycloolefin, and aromatic hydrocarbons. J. Phys. Chem. 70:1267-1275. MaAuliffe, C.D. 1977. Evaporation and solution of C2 to C'0 hydrocarbons from crude oils on the sea surface. Pp. 363-372 in D.A. Wolfe, J.W. Anderson, D.K. Button, D.C. Malins, T. Roubal, and U. Varanasi, eds. Fate and Effects of Petroleum Hydrocarbons in Marine Organisms and Ecosystems. Pergamon Press, New York. McCann, J., and B.N. Ames. 1976. Detection of carcinogens as mutagens in the Salmonella/microsome test: Assay of 300 chemicals: Discussion. Proc. Natl. Acad. Sci. USA 73:950-954. McCann, J., E. Choi, E. Yamasaki, and B.N. Ames. 1975. Detection of carcino?gens as mutagens in the Salmonella/microsome test: Assay of 300 chemicals. Proc. Natl. Acad. Sci. USA 72:5135-5139. McKee, H.C., J.W. Rhoades, J. Campbell. and A.L. Gross. 1962. Acetonitrile in body fluids related to smoking. Public Health Rep. 77:553-554. Medyankin, A.V. 1975. Complex action of dimethyl formamide under conditions of a Jong- term experiment. Gig. Sanit. (USSR) No. 9:39-42. [Chem. Absts. 83:202471d, 1975.] Miller, E.C. 1978. Some current perspectives on chemical carcinogenesis in humans and ex- perimental animals: Presidential address. Cancer Res. 38:1479-1496.

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