820K87013 March 31, 1987 ETHYLBENZENE Health Advisory Office of Drinking Water U.S. Environmental Protection Agency I. INTRODUCTION The Health Advisory (HA) Program, sponsored by the Office of Drinking Water (ODW), provides information on the health effects, analytical method- ology and treatment technology that would be useful in dealing with the contamination of drinking water. Health Advisories describe nonregulatory concentrations of drinking water contaminants at which adverse health effects would not be anticipated to occur over specific exposure durations. Health Advisories contain a margin of safety to protect sensitive members of the population. Health Advisories serve as informal technical guidance to assist Federal, State and local officials responsible for protecting public health when emergency spills or contamination situations occur. They are not to be construed as legally enforceable Federal standards. The HAs are subject to change as new information becomes available. Health Advisories are developed for One-day, Ten-day, Longer-term (approximately 7 years, or 10% of an individual's lifetime) and Lifetime exposures based on data describing noncarcinogenic end points of toxicity. Health Advisories do not quantitatively incorporate any potential carcinogenic risk from such exposure. For those substances that are known or probable human carcinogens, according to the Agency classification scheme (Group A or B), Lifetime HAs are not recommended. The chemical concentration valuas for Group A or B carcinogens are correlated with carcinogenic risk estimates by employing a cancer potency (unit risk) value together with assumptions for lifetime exposure and the consumption of drinking water. The cancer anit risk is usually derived from the linear multistage model with 95% upper confidence limits. This provides a low-dose estimate of cancer risk to hunans that is considered unlikely to pose a carcinogenic risk in excess of the stated values. Excess cancer risk estimates may also be calculated using the One-hit, Weibull, Logit or Probit models. There is no current understanding of the biological mechanisms involved in cancer to suggest that any one of these models is able to predict risk more accurately than another. Because each model is based on differing assumptions, the estimates tnat are derived can differ by several orders of magnitude. ------- Ethylbenzene March 31, 1987 -2- This Health Advisory is based on information presented in the Office of Drinking Water's Health Effects Criteria Document (CD) for Sthylbenzene (U.S. EPA, 1985a). The HA and CD formats are similar for easy reference. Individuals desiring further information on the toxicological data base or rationale for risk characterization should consult the CD. The CD is available for review at each EPA Regional Office of Drinking Water counterpart (e.g., Water Supply Branch or Drinking Water Branch), or for a fee from the National Technical Information Service, U.S. Department of Commerce, 5235 Port Royal Rd., Springfield, VA 22161, PB # 86-117835/AS. The toll-free number is (800) 336-4700; in the Washington, D.C. area: (703) 487-4650. II. GENERAL INFORMATION AND PROPERTIES (Verschueren, 1983; Amoore and Hautala, 1983) Chemical Name Ethylbenzene Cas No. 100-41-4 Chemical Structure Synonyms Phenyl ethane, ethylbenzol, EB Uses Styrene manufacture Acetophenone manufacture Solvent Asphalt constituent Naptha constituent Properties Chemical Formula C8H1 0 Molecular Weight 106.18 Physical State (25°C) Colorless liquid Boiling Point 136.2°C Melting Point -94.97°C Density Vapor Pressure 7 mm at 20°C Water Solubility 152 mg/L (at 20°C) Log Octanol/Water Partition 3.15 Coefficient Taste Threshold (water) 0.029 mg/L Odor Threshold (water) 0.029 mg/L Odor Threshold (air) 0.062 mg/L Conversion Factor — ------- Ethylbenzene March 31, 1987 -3- Occurrence Ethylbenzene, a clear, flammable liquid found in gasoline, is produced commercially by the alkylation of benzene with ethylene. In 1982, the U.S. production of ethylbenzene totaled 3.3 million tons. Very little information is available on the occurrence of ethylbenzene in 12,000 drinking water supplies in the U.S. drawing water from surface rivers and streams. However, the testing of 945 ground water supplies has revealed that approximately 0.6 % contain ethylbenzene. The median concentration detected in "non random" segment of the study was 0.87 ug/L (Westrick et al., 1983). III. PHARMACOKINETICS Absorption Data regarding the absorption of ethylbenzene from the gastrointestinal tract of humans following oral ingestion could not be located. Since approximately 90% of an oral dose of ethylbenzene (1.78 g/rabbit) is excreted as metabolites (SI Masry et al., 1956), the chemical is readily absorbed in rabbits. For human volunteers exposed by inhalation to ethylbenzene for 8 hours at 100, 187, 200 or 370 mg/m-^, the average percent of vapor absorbed (measured spectrophotometrically) through the respiratory tract was 64% (Bardodej and Bardodejova, 1970). Absorption of an aqueous solution of ethylbenzene through human hand skin (109.3 to 113.9 mg/L for 1 to 2 hours) was equivalent to 118 ug/cm2/hour (Dutkiewicz and Tyras, 1967). Distribution Following a 6-hour inhalation exposure at 1 mg/m3, absorbed ethylbenzene is distributed throughout the body in rats. However, the highest levels were detected in the kidney, lung, adipose tissue, digestive tract and liver (Chin et al., 1980). Metabolism After inhalation exposure, ethylbenzene undergoes rapid metabolism in humans, primarily to form mandelic acid and phenylglyoxylic acid. These two metabolites accounted for 64% and 25%, respectively, of the absorbed dose in humans (Bardodej and Bardodejova, 1970). Formation of minor metabolites including methylphenyl carbinol and 2-ethylphenol accounted for approximately 5% and 1%, respectively, in humans (Bardodej and Bardodejova, 1970; Angerer and Lehnert, 1979). The major metabolites formed in humans and rats are not the same. Mandelic acid and phenylglyoxylic acid constitute 64 and 25% of the metabolites in humans (Bardodej and Bardodejova, 1970), while in ------- Ethylbenzene March 31, 1987 -4- rats, 1-phenylethanol (25%), benzole acid (27%) and mandelic acid (25%) are the main metabolites (Engstrom, 1985). Excretion Urinary excretion of metabolites by rabbits was reported to be complete within 24 hours after oral dosing with 1.78 grams/rabbit (El Masry et al., 1956). In humans, most of the inhaled dose was eliminated in the urine within 24 hours after exposure was terminated (Engstrom and Bjarstrom, 1978; Hagemann and Angerer, 1979). IV. HEALTH EFFECTS Humans 0 In experiments with human volunteers, an 8-hour inhalation exposure to ethylbenzene at a concentration of 100 ppm (435 mg/m3) did not result in adverse health effects (Bardodej and Bardodejova, 1970). Increasing this level (increase not specified) resulted in sleepiness, fatigue, headache and mild eye and respiratory irritation. Animals Short-term Exposure 0 Estimated acute LD^Q values of 3.5 g/kg to 5.46 g/kg were reported in rats (Wolf et al., 1956; Smyth et al., 1962). 0 An acute dermal LD50 value of 17.8 ml/kg (approximately 15,400 nig/kg) was reported in rabbits (Smyth et al., 1962). 0 An inhalation exposure of 4,000 ppm (approximately 17,400 rtig/Ti3) for four hours was lethal to 3 of 6 rats (Smyth et al., 1962). 0 During LD50 studies systemic toxic effects were observed predominantly in the liver and kidney (Wolf et al., 1956) and central nervous system (Faustov, 1958). 0 Other acute effects include irritation of the conjunctiva (Wolf et al., 1956) and slight necrosis of the cornea (Smyth et al., 1962). Long-term Exposure 0 Liver and kidney effects were observed in rats (10 females/dose) exposed orally to ethylbenzene in olive oil for six months (Wolf et al., 1956). Doses of 408 and 680 mg/kg/day caused increases in liver and kidney weights, and cloudiness and swelling of hepatocytes and renal tubular epithelium. No effects were observed in rats exposed to 13.6 and 136 mg/kg/day. 0 No chronic exposure studies were identified in the available literature. ------- Ethylbenzene March 31, 1987 -5- Reproductive Effects 0 No studies on the effects of ethylbenzene on reproduction were located in the available literature. Developmental Effects 0 Ethylbenzene did not elicit embryotoxicity, fetotoxicity or terato- genicity in inhalation studies at concentrations up to 1,000 ppm (4,348 mg/ra3) in rats and rabbits for 6 to 7 hours/day on days 1 to 19 and 1 to 24 of gestation, respectively (Hardin et al., 1981). 0 Female rats exposed at 1,000 ppm had increased liver, kidney and spleen weights suggestive of maternal toxicity. There was no maternal toxicity observed when the rats were exposed to 100 ppm of ethylbenzene. {Hardin et al., 1981). Mutagenicity 0 No mutagenic activity was detected in S_._ typhimurium strains TA98, TA100, TA1535, TA1537 following ethylbenzene exposure both with and without metabolic activation in plate assays at concentrations up to 3 mg/plate (Florin et al., 1980; Nestmann et al., 1980). 0 Dean et al. (1985) reported that ethylbenzene (0.2 to 2,000 ug/plate) did not induce mutations in bacteria, gene conversion in yeast or chromosome damage in rat liver (RL4) epithelial cells. 0 In the Drosophila recessive lethal test, ethylbenzene did not increase the frequency of recessive lethals (Donner et al., 1979). Carcinogenicity 0 Pertinent data on the carcinogenic potential of ethylbenzene were not identified in the available literature. An NCI bioassay is in the planning stage. V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS Health Advisories (HAs) are generally determined for One-day, Ten-day, Longer-term (approximately 7 years) and Lifetime exposures if adequate data are available that identify a sensitive noncarcinogenic end point of toxicity. The HAs for noncarcinogenic toxicants are derived using the following formula: HA = (NOAEL or LOAEL) x (BW) = /L ( /L} (UF) x ( L/day) where: NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level in mgAg bw/day. ------- Ethylbenzene March 31, 1987 -6- BW = assumed body weight of a. child (10 kg) or an adult (70 kg). UF = uncertainty factor (10, 100 or 1,000), in accordance with NAS/ODW guidelines. L/day = assumed daily water consumption of a child (1 L/day) or an adult (2 L/day). One-day Health Advisory No adequate dose-response data exist using the oral route of exposure from which to calculate a One-day Health Advisory. Therefore, the derivation of the one-day level is based upon a 100 ppm (435 mg/m3) NOAEL identified in 18 human male volunteers following a single 8-hour inhalation exposure as conducted by Bardodej and Bardodejova (1970). An inhalation absorption efficiency of 64% is used, based on data from that study (Bardodej and Bariodejova, 1970). The total absorbed dose and the One-day HA for a 10 kg child are calculated as follows: Step 1: Determination of Total Absorbed Dose (TAD) TAD = (435 mg/m3) (8 m3/day) (0.64) = 3UQ mg/kg/day Step 2: Determination of One-day HA One-day HA = (_31 .8 mg/kg/day) (10 kg) = 32 mg/L (32000 ug/L) (10) (1 L/day) where: 435 mg/m3 = NOAEL based on absence of effects in humans following inhalation exposure. 8 m3/day = assumed volume of air inhaled per daily 8-hour exposure. 0.64 = absorption efficiency reported by Bardodej and Bardodejova (1970). 70 kg = assumed body weight of an adult. 10 kg = assumed body weight of a child. 2 L/day = assumed daily water consumption of an adult. 1 L/day = assumed daily water consumption of a child. 10 = uncertainty factor, chosen in accordance with NAS/ODW guidelines for use with a NOAEL from a human study. ------- Ethylbenzene March 31, 1987 -7- Ten-day Health Advisory Because of the lack of appropriate exposure duration data, the ten-day HA will be calculated from the One-day HA. The One-day HA will be divided by 10 to give estimated Ten-day HA values. The resulting Ten-day HA for a child is as follows: Ten-day HA = 32 m/L = 3.2 mg/L (3,200 ug/L) Longer-term Health Advisory; There are insufficient data to calculate a Longer-term HA. It is recommended that the DWEL, adjusted for 10 kg, be used as a conservative estimate for a longer-term exposure. Lifetime Health Advisory The Lifetime HA represents that portion of an individual's total exposure that is attributed to drinking water and is considered protective of noncar- cinogenic adverse health effects over a lifetime exposure. The Lifetime HA is derived in a three step process. Step 1 determines the Reference Dose (RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti- mate of a daily exposure to the human population that is likely to be without appreciable risk of deleterious effects over a lifetime, and is derived from the NOAEL (or LOAEL), identified from a chronic (or suJbchronic) study, divided by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level (DWEL) can be determined (Step 2)-. A DWEL is a medium-specific (i.e., drinking water) lifetime exposure level, assuming 100% exposure from that medium, at which adverse, noncarcinogenic health effects would not be expected to occur. The DWEL is derived from the multiplication of the RfD by the assumed body weight of an adult and divided by the assumed daily water consumption of an adult. The Lifetime HA is determined in Step 3 by factoring in other sources of exposure, the relative source contribution (RSC). The RSC from drinking water is based on actual exposure data or, if data are not available, a value of 20% is assumed for synthetic organic chemicals and a value of 10% is assumed for inorganic chemicals. If the contaminant is classified as a Group A or B carcinogen, according to the Agency's classification scheme of carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in assessing the risks associated with lifetime exposure to this chemical. The study by Wolf et al. (1956) has been determined to be the most appropriate for derivation of the Lifetime Health Advisory. Rats were administered oral gavage doses of 13.6, 136, 408 or 680 mg/kg/day ethylbenzene in olive oil for 130 days of the 182-day test period. A vehicle control of olive oil (2.5 ml) was run concurrently. No effects were noted in groups of rats exposed at 13.6 and 136 mg/kg/day. Increases in liver and kidney weights were reported following oral administration of 408 or 680 mg/kg/day. There were also slight histopathological changes at these dose levels. These included cloudiness and swelling of hepatocytes and renal tubular epithelium. From these results, a NOAEL of 136 mg/kg/day was identified. A Drinking Water Equivalent Level (DWEL) and Lifetime Health Advisory are calculated as follows: ------- Ethylbenzene March 31, 1987 -8- Step 1: Determination of the Reference Dose (RfD) RfD = (136 mg/kg/day) (5 ) ,= 0>097 mg/kg/day (1,000) (7) where: 136 mg/kg/day = NOAEL for absence of renal and hepatic effects in rats exposed for 130 days. 5/7 = conversion of 5 days/week dosing regimen to continuous 7 days/week exposure pattern. 1,000 = uncertainty factor, chosen in accordance with NAS/ODW guidelines for use with a NOAEL from an animal study of less-than-lifetime duration. Step 2: Determination of the Drinking Water Equivalent Level (DWEL) DWEL = (0.097 mg/kg/day)(70 kg) = 3.4 mg/L (3,400 ug/L) (2 L/day) where: 0.097 mgA9/<3ay = RfD. 70 kg = assumed body weight of an adult. 2 L/day = assumed daily water consumption of an adult. Step 3: Determination of the Lifetime Health Advisory Lifetime HA = (3.4 mg/L) (20%) =0.68 mg/L where: 3.4 mg/L = DWEL. 20% = assumed relative source contribution from water. Evaluation of Carcinogenic Potential 0 Because of the lack of data, an assessment of the carcinogenic risk of ethylbenzene is not possible at this time. ° The International Agency for Research on Cancer has not classified ethylbenzene in any of its categories of carcinogenic potential. 0 Applying the criteria described in EPA's guidelines for assessment of carcinogen .risk (U.S. EPA, 1986), ethylbenzene is classified in Group D: not classified. This category is for agents with inadequate animal evidence of carcinogenicity. ------- Ethylbenzene March 31, 1987 -9- VI. OTHER CRITERIA, GUIDANCE AND STANDARDS 0 The American Conference of Government Industrial Hygienists has recommended an occupational standard (TWA) in air and TLV of 100 ppm (435 mg/m3; ACGIH, 1980). 0 EPA/ODW has proposed a RMCL of 0.68 mg/L (U.S. EPA, 1985e). VII. ANALYTICAL METHODS 0 Analysis of ethylbenzene is by a purge-and-trap gas chromatographic procedure used for the determination of volatile aromatic organic compounds in water (U.S. EPA, 1985b). This method calls for the bubbling of an inert gas through the sample and trapping ethylbenzene on an adsorbant material. The adsorbant material is heated to drive off ethylbenzene onto a gas chromatographic column. The gas chromato- graph is temperature programmed to separate the method analytas which are then detected by the photoionization detector. This method is applicable to the measurement of ethylbenzene over a concentration range of 0.02 to 1500 ug/L. Confirmatory analysis for benzene is by mass spectrometry (U.S. EPA, 1985c). The detection limit for confirmation by mass spectrometry is 0.2 ug/L. VIII. TREATMENT TECHNOLOGIES 0 Aeration appears to offer the best potential for removing ethylbenzene from contaminated water. Ethylbenzene has a high Henry's Law Constant of 35 atm (U.S. EPA, 1985d). 0 In an actual packed aeration column (PAC) pilot testing program, ethylbenzene removal efficiencies ranged from 71.8 to >99.8% (U.S. EPA, 1985d). The column used had a one foot diameter and was packed with Tripack packing material (#2). Influent concentrations of ethylbenzene ranged from <1 to 200 ug/L. Air-to-water ratios varied from 10:1 to 126:1. Liquid loading rates varied from 12.7 to 50.9 gpm/ft2. Ambient water temperature was 70°F. Removal efficiencies were >90% for all test runs but one. In this single exception, an efficiency of 71.8% was obtained. In this test run the ethylbenzene concentration was high (200 ppb) and the air-to-water ratio low - 10:1 (U.S. EPA, 1985d). 0 A field test of PAC also was conducted on water contaminated by a gasoline spill (Cummins, 1985). Several benzene derivatives including ethylbenzene were found in this water. The aeration column was 7.3 x 0.6 m and was packed to 5.5 m with 1 inch plastic saddles. Air-to-water ratios of from 8:1 to 88:1 were used. Ethylbenzene was decreased to below detection (<0.5 ug/L) whenever the air-to-water ratios were 20:1 or greater. Ethylbenzene was detected if lower air-to-water ratios were used. A total of 75 samples were tested. ------- Ethylbenzene March 31, 1987 -10- 0 Decarbonators, which can be considered as modified aerators, were used to remove synthetic organic contaminants including ethylbenzene at Water Factory 21 (U.S. EPA, 1985d). The air-to-water ratio was 22:1. Levels of influent ethylbenzene contamination were 0.067 and 0.23 ug/L. The decarbonators removed 39.8 and 56.51% of the ethylbenzene, respectively. 0 Granular activated carbon (GAG) also is at least partially effective in the removal of ethylbenzene from solution by adsorption. Over two separate trial periods, GAC was found to remove some of the ethylbenzene from contaminated drinking water. At an influent concentration of 0.06 ug/L, 45% of the ethylbenzene was removed. When the influent was 0.07 ug/L, 17% was removed (McCarty et al., 1979). 0 Application of PAC for ethylbenzene removal was tested at the Sunny Isles Water Treatment Plant (Florida) (U.S. EPA, 1985d). For a 14-month period, 7.1 mg/L PAC was added to the water at the wellfield. For 3 of 5 samples analyzed, >99% of the ethylbenzene was removed; for 2 samples, the removal rate was only 33%. 0 In one study, conventional treatment was found to reduce the ethyl- benzene in water containing 0.7 ug/L by 43% (U.S. EPA, 1985d). ------- Ethylbenzene March 31, 1987 -1 1- IX. REFERENCES ACGIH. 198.0. American Conference of Industrial Government Hygienists. Ethylbenzene. Documentation of the Threshold Limit Values. 4th ed., p. 176. Amoore, J.E., and E. Hautala. 1983. Odor as an aid to chemical safety; odor threshold compared with Threshold Limit Values and volatilities for 214 industrial chemicals in air and water dilution. J. Appl. Toxicol. 3:272-290. Angerer, J., and G. Lehnert. 1979. Occupational chronic exposure to solvents. VIII. Phenolic compounds: Metabolites of alkylbenzenes in man: Simultaneous exposure to ethylbenzene and xylenes. Int. Arch. Occup. Environ. Health. 43:145-150. Bardodej, Z., and E. Bardodejova. 1970. Biotransformation of ethylbenzene, styrene and alpha-methylstyrene in man. Am. Ind. Hyg. Assoc. J. 31:206-209. Chin, B.H., J.A. McKelvey, T.R. Tyler, L.J. Calisti, S.J. Kozbelt and L.J. Sullivan. 1980. Absorption, distribution and excretion of ethylbenzene, ethylcyclohexane and methylethylbenzene isomers in rats. Bull. Environ. Contain. Toxicol. 24:477-483. Cummins, M.D. 1985. Field evaluation of packed column stripping, Pastrap, LA. U.S. Environmental Protection Agency, Office of Drinking Water. Dean, B.J., T.M. Brooks, G. Hodson-Walker and D.H. Hutson. 1985. Genetic toxicology testing of 41 industrial chemicals. Mutat. Res. 153:57-77. Donner, M., J. Maki-Paakkanen, N. Norppa, M. Sorsa and H. Vaino. 1979. Genetic toxicology of xylenes. Mutat. Res. 74:171-172. Dutkiewicz, T., and H. Tyras. 1967. Study of the skin absorption of ethyl- benzene in man. Br. J. Ind. Med. 24:330-332. El Masry, A.M., J.N. Smith and R.T. Williams. 1956. The metabolism of alkylbenzenes: n-Propylbenzene and n-butylbenzene with further obser- vations on ethylbenzene. Biochem. J. 64:50-56. Engstrom, J., and R. Bjurstrom. 1978. Exposure to xylene and ethylbenzene. II. Concentration in subcutaneous adipose tissue. Scand. J. Work Environ. Health. 4:195-203. Engstrom, K.L. 1984. Metabolism of inhaled ethylbenzene in rats. Scand. J. Work Environ. Hlth. 10:83-87. Faustov, A.S. 1958. Toxicity of aromatic hydrocarbons. I. Comparative toxicity of some aromatic hydrocarbons. II. Some problems of the toxic- hygiene properties of aromatic hydrocarbons. Tr. Voronezh. Gos. Med. Inst. 35:247-255; 257-262. (Chem. Abstr. 54:25279d) ------- Ethylbenzene March 31, 1987 -12- Florin, I., L. Rutberg, M. Curvall and C.R. Enzell. 1980. Screening of tobacco smoke constituents for mutagenicity using the Ames test. Toxi- cology. 18:219-232. Hagemann, J., and J. Angerer. 1979. Biological monitoring in occupational ethylbenzene loading. Kolloq., Ber. Jahrestag. Dtsch. Ges. Arbeitsmed., 19th. pp. 421-425. (Chem. Abstr. 94:196880) Hardin, B.D.., G.P. Bond, M.R. Sikov, F.D. Andrew, R.P. Beliles and R.W. Niemeier< 1981. Testing of selected workplace chemicals for teratogenic potential. Scand. J. Work Environ. Health. 7{Suppl. 4):66-75. Kiese, M., and W. Lenk. 1973. w- and (w-1)-Hydroxylation of 4-chloropro- pionanilide by rabbits and rabbit liver microsomes. Biochem. Pharmacol. 22:2565-2574. McCarty, P.L., D. Argo and M. Reinhard. 1979. Operational experiences with activated carbon adsorbers at Water Factory 21. JAWWA. 11:683-689. Mihail, G., A. Zlavog, V. Anghelache and J. Bodnar. 1972. Serum ornithine carbamoyltransferase, test for evaluating hepatic alterations caused by some industrial toxic substances. Igiena. 21:267-276. (Chem. Abstr. 79:1036) NCI. 1983. National Cancer Institute. National Toxicology Program — Toxicology Testing Program. Chemicals on Standard Protocol: Management Status. June 15, 1983. Nestmann, E.R., E.G-H. Lee, T.I. Matula, G.R. Douglas and J.C. Mueller. 1980. Mutagenicity of constituents identified in pulp and paper mill effluents using the Salmonella/mammalian-microsome assay. Mutat. Res. 79:203-212. Smyth, H.F., C.P. Carpenter, C.S. Weil, U.C. Pozzani and J.A. Stregel. 1962. Range-finding toxicity data. List VI. Am. Ind. Hyg. Assoc. J. 23:95-107. U.S. EPA. 1985a. U.S. Environmental Protection Agency. Draft. Drinking water criteria document for ethylbenzene. Office of Drinking Water. U.S. EPA. 1985b. U.S. Environmental Protection Agency. Method 503.1. Volatile aromatic organic compounds in water by purge and trap gas chromatography. Environmental Monitoring and Support Laboratory, Cincinnati, Ohio 45268. U.S. EPA. 1985c. U.S. Environmental Protection Agency. Method 524.1. Volatile organic compounds in water by purge and trap gas chromatography/mass spectrometry. Environmental Monitoring and Support Laboratory, Cincinnati, Ohio 45268. U.S. EPA. 1985d. U.S. Environmental Protection Agency. (Draft) Technologies and costs for the removal of synthetic organic chemicals from potable water supplies. Science and Technology Branch, CSD, ODW, Washington, D.C. ------- Ethylbenzene March 31, 1987 -13- U.S. EPA. 1985e. U.S. Environmental Protection Agency. Proposed RMCL for SOCs, IOCS and Microbials. Federal Register. 50(219):46936-47023. November 13. U.S. EPA. 1986. U.S. Environmental Protection Agency. Guidelines for carcinogen risk assesment. Federal Register. 51 {185) .-33992-34003. September 24. Verschueren, K. 1983. Handbook of Environmental Data on Organic Chemicals. 2nd ed. Van Nostrand Reinhold Company, NY. pp. 628-630. Vinokurova, M.I. 1970, Combined effect of styrene, butadiene and ethylbenzene on the functional indexes of the cardiovascular system. Tr. Azerb. Nauchno.-Issled. Inst. Gig. Tr. Prof. Zabol. 4:21-26. (Chem. Abstr. 81:140347) Westrick, J.J., J.W. Mello and R.F. Thomas. 1983. The ground water supply survey: Summary of volatile organic contaminant occurrence data. EPA-ODW/TSD, Cincinnati, Ohio. Wolf, M.A., V.K. Rowe, D.D. McCollister, R.L. Hollingsworth and F. Oyen. 1956. lexicological studies of certain alkylated benzenes and benzene. Arch. Ind. Health. 14:387-398. ------- |