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IV Toxicity of Selected Drinking Water Contaminants CHEMICALS EVALUATED the health effects of a large number of contaminants found in drinking water were evaluated in Drinking Water and Health (National Academy of Sciences, 19771. The compounds evaluated in this chapter were selected for the following reasons: 1. Sufficient new data have become available to justify further attention to several chemicals examined in the first study. 2. New contaminants have been identified in drinking water subse- quent to the first study. 3. Several compounds were judged to be of concern because of potential spill situations. 4. The chlorination of drinking water or the use of other disinfectants yields compounds that require toxicological evaluation. A list of such compounds was prepared by the Safe Drinking Water Subcommittee on Chemistry of Disinfectants and Products. They are evaluated in this chapter by the Subcommittee on Toxicology. The 1977 study (National Academy of Sciences, 1977) examined the radioactive, particulate, and chemical contaminants found in drinking 67

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68 DRINKING WATER AND H"LTH water. Radioactive contaminants are not considered in this study. Asbestos was one of the particulates examined in the first study. A reevaluation of this contaminant will be justified when the several studies now underway are completed. The number of volatile organic com- pounds identified in drinking water supplies has increased from approximately 300 at the time of the first study to 700 at the present time and will continue to grow. Limitations of time, manpower, and scientific information have not permitted an in-depth evaluation of most of the compounds recently found in drinking water. It was the belief of this subcommittee that it could perform a more valuable service to the Environmental Protection Agency (EPA) in the future if it evaluated criteria documents that were prepared by the EPA or other groups contracted to conduct these tasks. It will be necessary for the EPA to develop a mechanism for a comprehensive search and review of the literature in order to make in-depth hazard assessments for these chemicals. It is the consensus of this subcommittee that this cannot be done appropriately by the National Academy of Sciences because time and staff requirements far exceed those available. Neither can it be expected that the scientists who donate their services on these subcom- mittees will have the resources or time to carry out the routine aspects of this task. ACUTE EXPOSURES In addition to providing information on chronic toxicity, the subcommit- tee has evaluated the potential acute toxicity insofar as justified by the available data. These data will provide a basis for making judgments of possible health erects resulting from accidental spills of chemicals into drinking water supplies. To this end the subcommittee has provided a suggested no-adverse-response level (SNARL) for acute exposures of 24 hr or 7 days. These values are calculated based on the assumption that 100% of the exposure to the chemical was supplied by drinking water during either the 24-hr or 7-day period. In those few cases where the chemical is a known or suspected carcinogen' the potential for carcinogenicity after an acute exposure has not been considered These acute SNARL's were calculated only when there was human exposure data or sublethal animal data. LD50's were not used as a basis for calculation. Some 7-day values were derived by dividing the 2=hr SNARL by 7, but only when the data were very good. The converse was

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Toxicity of Selected Drinking Water Contaminants 69 not done nor were data obtained from studies of lifetime exposures used to establish acute SNARL's. In some cases in which data from inhalation exposures were used there was information on absorption/retention. The details concerning retention and absorption are given in the monographs for each chemical. It must be emphasized that these calculated acute SNARL's should not be used to estimate hazard from exposures exceeding 7 days. They are not a guarantee of absolute safety. Furthermore, SNARL's are based on exposure to a single agent and do not take into account possible interactions with other contaminants. In all cases the safety or uncertainty factor used in the calculations of the SNARL's reflect the degree of confidence regarding the data as well as the combined judgment of the subcommittee members. As in the previous report, the following assumptions were used when assigning an uncertainty factor to calculate either the acute or chronic SNARL's: An uncertainty (safety) factor of 10 was used when good chronic or acute human exposure data were available and supported by chronic or acute data in other species. A factor of 100 was used when good chronic or acute toxicity data were available for one or more species. A factor of 1,000 was used when the acute or chronic toxicity data were limited or incomplete. CHRONIC EXPOSURES When the chemical of concern was not a known or suspected carcinogen, the subcommittee calculated a SNARL for chronic exposure. In most cases, whenever chronic SNARLS's were estimated, data were available from studies lasting a major portion of the lifetime of the experimental animal. For these SNARL's an arbitrary assumption was made that 20~o of the intake of the chemical of concern was from drinking water. Because of this assumption it would be inappropriate to use these values as though they were maximum contaminant intakes. A risk estimate rather than a chronic exposure SNARL was provided in those cases in which there was adequate evidence of carcinogenicity [see Drinking Water and Health (National Academy of Sciences, 1977) for details]. Table IV-1 summarizes the acute and chronic SNARL's as well as the carcinogenic risk estimates for the chemicals reviewed in this report.

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70 DRINKING WATER AND H"LTH TABLE IV- ~ Summation of Acute and Chronic Exposure Levels and Carcinogenic Risk Estimates for Chemicals Reviewed Suggested No-Adverse-Response Upper 95% Level (SNARL), mg/liter, Confidence by Exposure Perioda Estimate of Lifetime Cancer Chemical24-hour 7-day Chronic Risk per,ug/literb Acrylonitrile1.3 x 10-6 Benzene 1 2.6 Benzene hexachloride3.5 0.5 Cadmium 0~08 0.005 Carbon tetrachloride14 2.0 Dichloro difluoromethane350 5.6 1,2-Dichloroethane7.0 x 10-7 Epichlorohydrin0.84 0.53 Ethylene dibromide9.1 x 10-6 Methylene chloride35 5.0 Polychlorinated biphenyl0.35 0.05 Tetrachloroethylene172 24.5 1.4 x 10-7 1, 1,1-Trichloroethane490 70 3.8 Trichloroethylene TrichloroQuoromethane Toluene Uranium Xylenes Bromide Catechol Chlorine dioxide Chlorite Chloroform Oi bromochloromet inane 2,4-Dichlorophenol Hexachlorobenzene Iodide Resorcinol 105 15 88 8 420 35 0.34 3.5 0.21 21 11.2 1,400 224 2.3 2.2 22 18 115.5 11.7 0.38 0.21 3.2 0.03 16.5 0.5 0.7 1.19 2.9 x 10-5 a See text for details on individual compounds. b See Drinking Water and Health (National Academy of Sciences, 1977) for details.

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Toxicity of Selected Drinking Water Contaminants 71 CHEMICALS SELECTED BY EPA Acrylonitrile (CH2=CHCN) Acrylonitrile is an unsaturated synthetic organic compound that has a variety of applications. Primarily it is used in the production of acrylic and modacrylic fibers, nitrite rubber, and plastics. As a pot nt, highly effective fumigant it is used most often to protect grain, dried fruit, walnuts, and tobacco against insect pests. Annual production totals approximately 682 million kg (U.S. Environmental Protection Agency, 1 978a). Acrylonitrile, also known as 2-propenenitrile, vinyl cyanide, and cyanoethylene, is a colorless, highly flammable liquid with a mild, pungent odor resembling that of peach pits. It is manufactured by the reaction of propylene with ammonia in air. Its boiling point is 77.3C. At 20C its solubility in water is 7.35 g/100 ml, and the specific gravity of the liquid is 0.811 (Manufacturing Chemists Association, 19741. The principal exposure of humans to acrylonitrile is likely to occur through atmospheric contamination. Patterson et al. (1976) estimated that the total emission from manufacturing processes in 1974 was 14 million kg. There is relatively little information on the movement, fate, and persistence of acrylonitrile in water. Zabezhinskaya et al. (1962) reported that at an initial concentration of 10 mg/liter, only 46% remained after 24 hr. 19% after 48 hr. and 537O after 96 hr. Under some conditions, the relatively high vapor pressure of acrylonitrile would probably promote the escape of the compound to the atmosphere. METABOLISM The metabolism of acrylonitrile has not been studied systematically with radio-labeled material. Investigators studying the metabolism of acrylo- nitrile have concentrated on ascertaining the fate of the cyano group of the molecule. Brieger et al. (1952) reported that inhaled acrylonitrile is metabolized first to the free cyano group, and then to thiocyanate. They found high cyanate levels and high thiocyanate levels in the blood of rats, dogs, and monkeys that had been treated with acrylonitrile. In a study with both oral and intraperitoneal administration of acrylonitrile in rats, mice, and Chinese hamsters, Gut et al. (1975) observed that thiocyanate was eliminated in the urine and that acrylonitrile was bound strongly to components of the blood. There appeared to be an interspecific difference in the metabolic pattern: less cyanide formed in rats than in mice. Earlier studies (Dudley and Neal, 1942; Lawton et al.,

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72 DRINKING WATER AND H"LTH 1943; Paulet et al., 1966) indicated the same lack of agreement on the principal metabolic product of acrylonitrile. Some of the studies reported cyanide, and others, thiocyanate, as the principal breakdown product. The fate of the remainder of the molecule has not been established. The possibility of conjugation has been raised by Hashimoto and Kanai (1972) who reported binding of acrylonitrile with cysteine and gluta- thione with a concomitant decrease in sulfhydryl (SH) groups. Earlier work by these investigators indicated that a large amount of injected acrylonitrile was unchanged after treatment of rabbits, guinea pigs, and rats. HEALTH ASPECTS Observations in Humans A recent report by the DuPont Corporation to government regulatory agencies stated that acrylonitrile may be a carcinogen (Anonymous, 1977~. It also stated that preliminary results of an epidemiological study of workers in a polymerization operation with potential for exposure to acrylonitrile indicated excess cancer incidence and cancer mortality as compared with company and national experi- ence. This study included about 470 males who began working in the polymerization area of the plant between 1950 and 1955 and who are still actively employed or have been retired from the company (Anonymous, 19771. The DuPont report emphasizes that the data are preliminary and that more exhaustive studies are under way. A number of incidents of illnesses and fatalities have been caused by the industrial and structural pest control uses of acrylonitrile. The compound is an acute poison and a severe skin and eye irritant. It may be toxic when inhaled, ingested, or absorbed through intact skin. Symptoms of exposure include nasal and respiratory oppression, vomiting, nausea, weakness, fatigue, headache, and diarrhea (Patterson en al., 19761. The symptoms of poisoning from acrylonitrile are very similar to those from cyanide. Such poisoning generally results from inhalation by workers of vapor in industrial settings where the concen- tration of acrylonitrile varies from 16 to 100 ppm. No fatalities have been reported under these conditions. In contrast to the safety record of acrylonitrile in the chemical industry, the use of the compound in structural pest control has resulted in a number of fatalities (Davis, 1967; Davis e! al., 1973; Patterson et al., 1976; Radimer et al., 1974; Sartorelli, 1966). The reported fatalities generally resulted from direct exposure to acrylonitrile or from too rapid a return to a building that had been fumigated with the compound.

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Toxicity of Selected Drinking Water Contaminants 73 Death resulted following symptoms that are similar to those of cyanide poisoning. However, death has also occurred as the result of toxic epidermal necrolysis (Radimer et al., 1974~. Acrylonitnle, when used for fumigation, is generally combined with other materials such as meth- ylene chloride and carbon tetrachlonde. Consequently, it is somewhat difficult to disassociate the symptoms of one compound from another. Observations in Other Species Acute Elects Investigating acute poisoning after intravenous injec- tion of acrylonitrile in dogs and rabbits, Paulet et al. (1961) absented considerable differences in interspecific response to cyanide intoxication. Symptoms of nervous disorders dominated the picture. Electroencepha- lographic records show that the higher nervous centers were affected. The investigators also found hyperglycemia and a decrease in the concentration of plasma inorganic phosphate. Acute oral toxicity values (LDso's) for acrylonitrile range from 27 to 128 mg/kg for mice (Benes and Cerna, 1959; Zell!e,r et al., 1969) and from 78 to 93 mg/kg for rats (Benes and Cerna, 1959; Smyth and Carpenter, 1948~. Acrylonitrile has also been characterized as a serious hazard in inhalation studies conducted by the Union Carbide Corporation in rats (Union Carbide Corporation, 1970~. After breathing saturated air for 5 min. all exposed animals died. After breathing 100 ppm for 4 hr. all of six rats died; for 2 hr. one of six; and for 1 hr. none of six. After breathing 500 ppm for 4 hr. none of six died, and for 8 hr. one of six died (Union Carbide Corporation, 19701. Roudabush et al. (1965) reported that acute dermal LDso values from acrylonitrile were 0.28 mg/kg when applied to the abraded skin of rabbits, 0.46 mg/kg on the intact skin of guinea pigs, and 0.84 mg/kg on the abraded skin of guinea pigs. Subchronic and Chronic Effects There are surprisingly few long-term studies on the toxicity of acrylonitrile in laboratory animals. None of the few studies in the literature was designed to establish a no-adverse-e~ect or minimal-effect dosage level. Dudley et al. (1942) conducted a three-part study of the inhalation toxicity of acrylonitrile. In a preliminary series, they exposed four rhesus monkeys and two dogs for 4 hr/day, 5 days/week for 4 weeks to an average concentration of 0.12 mg/liter (56 ppm) of acrylonitrile in air. These experiments indicated that dogs are more susceptible to acryloni- trile than are monkeys and that repeated exposure to concentrations of 0.12 mg/liter produces no signs of cumulative action. In the second part of their study, they exposed 16 rats, 16 guinea pigs, 3 rabbits, and 4 cats

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74 DRINKING WATER AND H"LTH in the same manner for 8 weeks to an average concentration of 0.22 mg/liter (100 ppm) of acrylonitrile in air. These experiments show that rats, guinea pigs, and rabbits tolerate repeated exposures to 0.22 mg/liter acrylonitrile in air over a period of 8 weeks; that cats are definitely more sensitive to acrylonitrile than are rodents; and that there is no evidence of cumulative action of acrylonitrile. In the third part of the study, they exposed 16 rats (8 adult, 8 young animals), 16 guinea pigs, 4 rabbits, 4 cats, and 2 rhesus monkeys in the same way to an average concentration of 0.33 mg/liter (153 ppm) acrylonitrile in air. These experiments showed that repeated exposures to 153 ppm were definitely toxic to guinea pigs, rats, and rabbits and were much more toxic to monkeys and cats. The exposures produced irritation of eyes and nose, loss of appetite, gastrointestinal disturbances, and incapacitating weakness of hind legs from which the animals recovered relatively rapidly. Even after exposure to such high concentrations no definite evidence of cumulative action was observed. In a study on the ejects of acrylonitrile on rats Barnes (1970) noted no adverse ejects. Six rats were given 15 successive oral doses of 30 mg/kg, followed by seven doses of 50 mg/kg, and then 13 doses of 75 mg/kg over a period of 7 weeks. The investigators supplied no details on the types of observations that were made to assess toxicity. Studies have also been conducted on the toxicity of acrylonitrile to adult rats following daily intraperitoneal administration of the com- pound (Knobloch et al., 19711. Daily injection of 50 mg/kg for 3 weeks produced a statistically significant loss of body weight; leucocytosis; signs of damage and functional disturbances of liver and kidneys; increase in the weight of liver, kidneys, and heart; and histological damage. Microscopic examination of the organs of these animals showed slight damage of neuronal cells of the cortex and brain stem and parenchymal degeneration of liver and kidneys. Unfortunately, no other dosage rates were included in this study. Following the reports of epidemiological evidence of the carcinogeni- city of acrylonitrile, Norris ( 1977) initiated a 2-year feeding and inhalation study in rats. In the ingestion study, acrylonitrile was incorporated into the drinking water of laboratory rats at concentrations of 0, 35, 100, and 300 mg/liter (corresponding to 0, 4, 10, and 30 mg/kg/day). In the inhalation study, male and female rats were exposed to 0, 20, and 80 ppm acrylonitrile for 6 hr/day' 5 days/week. In April 1977, interim results of the 2-year studies were reported (National Institute for Occupational Safety and Health, 1977; Norris, 1977~. Rats ingesting 35 mg/liter acrylonitrile exhibited mild signs of toxicity while

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Toxicity of Selected Drinking Water Contaminants 75 those ingesting lOO and 300 mg/liter showed marked signs of toxicity. Norris (1977) reported that both male and female rats that ingested lOO or 300 mg/liter acrylonitrile for 12 months developed stomach papillo- mas (1 of 20 rats at lOO mg/liter and 12 of 20 at 300 mg/liter); central nervous system tumors (2 of 20 at 35 mg/liter, 2 of 20 at 100 mg/liter, and 3 of 20 at 300 mg/liter); and Zymbal gland carcinoma (2 of 20 at lOO mg/liter, and 2 of 20 at 300 mg/liter). No such tumors were seen in control animals. In the inhalation study, after 1 year of exposure to 80 ppm acrylonitrile. 26 rats died and three developed central nervous system tumors that were comparable to those reported in the ingestion study. Gross examination of other rats in this study, who were also exposed to 80 ppm acrylonitrile by inhalation, revealed an increased incidence of ear canal tumors and mammary region masses. In animals exposed to 20 ppm, there was an apparent increase in subcutaneous masses of the mammary region, although no ear canal or central nervous _ 1 ~.1 ~1 system tumors were observed. (other than neoplasms, signs of toXlClty were limited to decreased water and food consumption and decreased body weight gain. Mutagenicity The mutagenicity of acrylonitrile has been demon- strated in the Salmonella typhimurium test (Milvy and Wolff, 1977) and in E. cold WP2 strains (Venitt and Bushell, 1977~. In the Ames (Salmonella) assay, acrylonitrile was active in the presence of a mouse liver homogenate, producing mutations in three tester strains. Bacteria were exposed by spotting the acrylonitrile on a lawn of Salmonella; by shaking a reaction mixture consisting of bacteria, liver homogenate, and acrylonitrile; and by exposing the homogenate and bacteria to an atmosphere containing acrylonitrile. By the latter method mutagenicity was observed at exposures as low as 57 mg/liter. Acrylonitrile was also mutagenic in various DNA-repair strains of E. cold WP-2. The effects were weak in plate incorporation tests, but assays using a simplified fluctuation test showed acrylonitrile to be significantly mutagenic at doses that were 20 to 40 times lower than those giving significant results in the plate test. Use of the different DNA-repair strains indicated that acrylonitrile causes DNA damage of the type that is exemplified by methyl methanesulfonate. Carcinogenicity Acrylonitrile has given positive results in a rat feeding study. Epidemiological evidence also contributes strong evidence to implicate acrylonitrile as a carcinogen. These studies are discussed above.

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76 DRINKING WATER AND H"LTH Reproduction The subcommittee found no studies on reproductive effects of acrylonitrile. Teralogenicity The subcommittee noted no studies reporting the teratogenicity of acrylonitrile. Carcinogenic Risk Estimate The interim results of a 2-year ingestion study with acrylonitrile in the drinking water of rats give evidence of what appears to be an increase in cancer at several sites (Norris, 1977~. Dose-response data (Norris, 1977) were used to estimate both the lifetime risk and an upper 957 confidence bound on the lifetime risk at the low dose level. These are estimates of lifetime human risks which have been corrected for species conversion on a dose/surface area basis. The risk estimates are expressed as a probability of cancer after a lifetime consumption of 1 liter/day of water containing 1 ~g/liter of the compound under study. For example, a risk of 1 x 10-6 implies a lifetime probability of 2 x 10-5 of cancer if 2 liters/day were consumed and the concentration of the carcinogen was 10 ,ug/liter. This means that at a concentration of 10 ~g/liter during a lifetime exposure this compound would be expected to produce one excess case of cancer for every 50,000 persons exposed. If the population of the United States is taken to be 220 million people this translates into 4,400 excess lifetime deaths from cancer or 62.8 per year. For acrylonitrile at a concentration of I ~g/liter, the estimated lifetime risk for humans is 6.7 x 10-7. The upper 95% confidence estimate is 1.3 x 10-6. Both of these estimates are the averaged risks calculated from the male and female rats. They are based on preliminary data of Norris (1977) and are subject to change when the study is completed. CONCLUSIONS AND RECOMMENDATIONS Based on toxicological investigations, the Food and Agriculture Organi- zation/World Health Organization (FAD/WHO, 1965) concluded that an acceptable daily intake of acrylonitrile for humans could not be determined. Both epidemiological and controlled feeding and inhalation studies since 1965 indicate that acrylonitrile is a carcinogen. Therefore, it would not seem possible to establish a long-te~ acceptable level for this compound in drinking water. Unfortunately, since LD50 studies indicate only the level of short-term toxicity, short-te~ exposure limits cannot be calculated.

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Toxicity of Selected Drinking Water Contaminants 77 Antimony (Sb) Antimony is a metal that is chiefly a by-product of base metal and silver ores. It has oxidation states of + 3 (trivalent) and + 5 (pentavalent) and forms compounds with halides, oxygen, sulfur, and organic anions such as tartrate, thioglycollate, and thioglycollamide. It is used industrially in flameproofing textiles, in vulcanizing of rubber, and in the manufacture of paint pigments, electronic semiconductors, thermoelectric devices, and fireworks (National Institute for Occupational Safety and Health, 1978; Robert and Boston, 1974~. Antimony compounds also have medical application (Gross, 1974; Harvey, 1975~. Organic antimonial compounds are used as parasiticides to treat different forms of schistosomiasis, bilharziasis, and leishmaniasis. Most exposure of humans to antimony compounds occurs in industrial settings. Schroeder (1970) has estimated the human daily intake from all sources to be about 100 ,ug. METABOLISM Trivalent and pentavalent antimony are differently distributed and excreted. Trivalent compounds have a great affinity for erythrocytes and, therefore, give low plasma concentrations. Pentavalent compounds tend to remain in the plasma. The trivalent form is excreted at a much slower rate in the urine than pentavalent antimony probably because it collects at much lower levels in plasma (National Institute for Occupational Safety and Health, 1978; Robert and Boston, 1974~. After administration of a single therapeutic dose of trivalent antimony only logo was recovered in 24 hr. whereas 5097O of the pentavalent form was recovered in 24 hr (Harvey, 19751. Most trivalent antimony (tartar emetic) is excreted in the feces, whereas the pentavalent forms are excreted mainly in the urine. The distribution of antimony to the tissues has not been thoroughly studied. However, in guinea pigs the trivalent compounds are found in high concentration in the thyroid and liver while the pentavalent forms are found in the liver and spleen after oral dosing. Abdallah and Saif (1962), in their studies of humans, showed that the highest concentrations of antimony occur in the liver, followed by the thyroid and heart. They administered sodium antimony dimercaptosuccinate (~24Sb) intra- venously. The liver, heart, and thyroid retained antimony for 20 days. When three 100-mg doses of antimony were administered intramuscular- ly over 9 days there was still considerable antimony in these tissues 53 days later.

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254 DRINKING WATER AND HEALTH Pomerantz, I., J. Burke, D. Firestone, J. McKinney, J. Roach, and W. Troffcr. 1978. Chemistry of PCBs and PBBs. Environ. Health Perspect. 24:1333-1346. Potts, C. L. 1965. Cadmium proteinuna-the health of battery workers exposed to cadmium oxide dust. Ann. Occup. Hyg. 8:55~1. Prendergast, J. A., R. A. Jones, L. J. Jenkins, Jr.? and J. Siegel. 1967. Effects on experimental animals of long-term inhalation of tnchloroethylene, carbon tetrachlonde, 1, 1,1-trichloroethane, dichlorodifluoromethane, and I,1-dichloroethylene. Toxicol. Appl. Phannacol. 10:27~289. Pnezdzialc, J., and S. Bakula. 1975. Acute poisoning with 1,2-dichloroethane. Wiad. Lek. 28:983-987. (In Russian.) Pyykko, K., H. Tahti, and H. Vapaatalo. 1977. Toluene concentrations in various tissues of rats after inhalation and oral administration. Arch. Toxicol. 38:169-176. Radimer, G. F., J. H. Davis, and A. B. Ackerman. 1974. Fumigant-induced toxic cpidermal necrolysis. Arch. Dermatol. 1 10:13~104. Raff, R., and B. V. Ettling. 1966. Hydroquinone, resorcinol and pyrocatechol. Pp. 462~92 in R. E. Kirk, and D. F. Othmer, eds., Encyclopedia of Chemical Technology, 2nd. ed. Vol. 11. John Wiley and Sons, New York. Raipta, C., K. Husman, and A. Tossavainen. 1976. Lens changes in car painters exposed to a m~xture of organic solvents. Albrecht von Graefes Arch. Klin. Exp. Ophthalmol. 200: 149-156. Rajamanickam, C., J. Amrutavalli, M. R. S. Rao, and G. Padmanaban. 1972. Effect of hexachlorobenzene on haem synthesis. Biochem. J. 129:381-387. Raleigh, R. L. 1974. Conversation and memorandum to Dr. Stanley C. Mazaleski. Rannug, U., and C. Ramel. 1977. Mutagenicity of waste products from vinyl chloride industries. J. Toxicol. Environ. Health 2:1019~1029. Rannug, U., R. Gothe, and C. A. Wachtmeister. 1976. The mutagenicity of chloroethylene oxide, chloroacetaldehyde, 2-cholorethanol and chloroacetic acid, conceivable metabo lites of vinyl chlonde. Chem. Biol. Interact. 12:2S 1-263. Rapoport, I. A. 1948. [Effect of ethylene oxide, glycidol and glycols on gene mutations.] Dokl. Akad. Nauk SSSR 60(3):469-472. (Russian) Rauws, A. G., and M. J. Van Logten. 1975. The influence of dietary chloride on bromide excretion in the rat. Toxicology 3:29-32. Reinhardt, C. F., L. S. Mullin, and M. E. Maxfield. 1973. Epinephrine-induced cardiac arrhythmia potential of some common industrial solvents. J. C)ccup. Med. 15:953-955. Renner, G., and K. P. Schuster. 1977. 2,4,5-Tnchlorophenol, a new urinary metabolitc of hexachlorobenzene. Toxicol. Appl. Pharmacol. 39:355-356. Rennick, B., and A. Quebbemann, 1970. Site of excretion of catechols and catcchola mine: Renal metabolism of catechol. Am. J. Physiol. 2 1 8 :1307-13 12. Rhudy, R. L., D. C. Lindberg, J. W. Goode, D. J. Sullivan, and E. J. Gralla. 1978. Ninety- day subacute inhalation study with toluene in albino rats. Abstr. 150. Toxicol. Appl. Pharmacol. 45:28~285. Richardson, A. P. 1937. Toxic potentialities of continued administration of chlorate for blood and tissues. J. Pharmacol. Exp. Ther. 59:101-113. Richardson, K. E. 1973. The effect of partial hepatectomy on the toxicity of ethylene glycol, glycolic acid, glyoxylic acid and glycine. Toxicol. Appl. Pharmacol. 24:53~538. Ringer, R. K., R. J. Aulerich, and M. Zabik. 1972. Effect of dieta~y polychIorinated biphenyls on growth and reproduction of mink. Pp. 149-154 in Proceedings of the American Chemical Society Meetir~g, August 28, 1972 (164th A. C. S. National Meeting, New York).Vol. 12,No.2.

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Toxicity of Selected Drinking Water Contaminants 255 Robert, K. H., and P. Boston. 1974. Preliminary Review on Antimony. EPA Contract 68- 02-1210. Roberts, C. J. C., and F. P. F. Marshall. 1976. Recovery after "lethal" quantity of paint remover. Br. Med. J. 4:2~21. Rodkey, F. L., and H. A. Collison. 1977. Effect of dihalogenated methanes on the in viva production of carbon monoxide and methane by rats. Toxicol. Appl. Pharmacol. 40:3 47. Rosenblatt, D. H., T. A. Miller, J. C. Dacre, I. Muul, and D. R. Cogley, eds. 1975. Preliminary assessment of ecological hazards and toxicology of environmental pollu- tants at Rocky Mountain Arsenal. Pp. F-1-F-18 in Appendix F. Chlorate Salts. U.S. Anny Medical Bioengineering Research and Development Laboratory, Fod Detrick, Frederick, Md. Rosenblum, I. 1958. Bromide intoxication: I. Production of experimental intoxication in dogs. J. Pharmacol. Exp. Ther. 122:379-385. Rosensteel, R. E., and T. W. Thoburn. 1975. Health Hazard Evaluation/Toxicity Determination. Report 744-175. Prepared by Olin Corporation, Pisgah Forest, N.C., for National Institute for Occupational Safety and Health. NIOSH TR-HHE-747-175. Available from National Technical Information Service, Springfield, Va., as Report No. 246/481. 12 pp. Ross, V. 1925. Potassium chlorate: its influence on the blood oxygen-binding capacity (hemoglobin concentration), its rate of excretion and quantities found in the blood after feeding. J. Pharmacol. 25:47-52. Roth, R. P., R. T. Drew, R. J. Lo, and J. R. Fouts. 1975. Dichloromethane inhalation, carboxyhemoglobin concentrations, and drug metabolizing enzymes in rabbits. Toxicol. Appl. Pharrnacol. 33:427~37. Roudabush, 11. L., C. J. Terhaar, D. W. Fassett, and S. P. Dziuba. 1965. Comparative acute eKects of some cherrucals on the skin of rabbits and guinea pigs. Toxicol. Appl. Pharmacol. 7: 559-565. Ro~ve V. K., D. O. McCoilister, H. C. Spencer, E. M. Adams, and D. D. Irish. 1952a. l'apor toxicity of tetrachloroethylene for laboratory animals and hun~.an subjects. AMA Arch. Ind. Hyg. Occup. Med. 5:56~579. Rowe, V. K. H. C. Spencer' D. D. 1McCollister, R. L. Hollingsworth, and E. M. Adams. 1952b. Toxicity of ethylene dibromide determined on expenmental animals. AMA Arch. Ind. Hyg. Occup. Med. 6:158-173. Rowe, V. K.? T. Wujkowski, M. A. Wolf, S. E. Sadek, and R. D. Stewart. 1963. Toxicity of a solvent mixture of l,l,l-trichloroethane and tetrachloroethylene as determined by experiments on laboratory animals and human subjects. Am. Ind. Hyg. Assoc. J. 24:541-554. Sakamoto, N. 1976. Metabolism of tetrachloroethylene in guinea pigs. Jpn. J. Ind. Health 18: 1 1-16. [English summary] Saland, G. 1967. Accidental exposure to perchloroethylene. N. Y. State J. Med. 67:235 236 1. Salvini, M., S. Binaschi, and M. Rival 1971a. Evaluation of the psychophysiological functions in humans exposed to the "threshold limit value" of 1, 1,1-trichloroethane. Br. J. Ind. Med. 28:28~292. Salvini, M., S. Binaschi, and M. Rival 1971b. Evaluation of the psychophysiological functions in humans exposed to tachloroethylene. Br. ]. Ind. Med. 28:293-295. San Martin de Viale, L. C.. A. A. Viale, S. Nacht, and M. Grinstein. 1970. Experimental porphyria induced in rats by hexachlorobenzene. A study of the porphyrins excreted by urine. Clin. China. Acta 28:1~23.

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