Document N2QwZ1QmgEjE6yDBnmq3kRqMw

BENZENE IN FLORIDA GROUNDWATER AN ASSESSMENT OF THE SIGNIFICANCE TO HUMAN HEALTH )` FLORIDA PETROLEUM COUNCIL A DIVISION OF THE AMERICAN PETROLEUM INSTITUTE OCTOBER 1986 Florida Petroleum Council V1 325 John Knox Road Building F / Suite 210 Tallahassee, Florida 32303 American Petroleum Institute 1220 L Street, Northwest Washington, D.C. 20005 SAL 000000363 EXECUTIVE SUMMARY William D. Preston, Esq., Partner Hopping Boyd Green & Sams, P.A., Tallahassee, Florida r Introduction The purpose of the Benzene in Florida Groundwater Study (Study) is to produce, compile, and analyze all available information and thereby comprehensively characterize the probability of potential adverse health effects from human exposure to benzene via groundwater sources. The ultimate goal is to offer the private and public sectors in Florida a meaningful and well informed selection of potential actions to take regarding benzene in groundwater. Benzene is a known human carcinogen which has pro* duced an increased incidence of leukemia in highly *N exposed industrial workers. Carcinogenic effects also have been demonstrated to occur in experimental animals after lifetime exposure to high levels of atmospheric ben zene or to large doses given daily by the oral route. On the other hand, benzene is also a natural substance occurring in low concentrations (parts per million) in many plants and as normal metabolite in certain animals. It is present in higher concentrations in crude petroleum and is a component of motor fuels. Benzene is produced 1 by the combustion of most organic materials and is found in the exhaust of both gasoline and diesel powered vehi cles. As a pure raw material, benzene is used in the manu facture of detergents, pesticides, and many other chemical products. -N, At lower concentrations (parts per billion), benzene is ubiquitous in the environment. All humans have a body content, derived primarily from air and food, which exists in equilibrium with the environment. The regulation of benzene in groundwater at such low levels inevitably requires a consideration of its relationship to drinking water and, in turn, the potential impact of that drinking water on the population health risk from benzene from all environmental sources. The salient findings of the Study are as follows: Existing Regulations The Florida "maximum contaminant lever ("MCL") for benzene in both public drinking water systems and the most common class of groumdwater (Class G-II) is one Mg/1 (one part per billion). This health based standard, which is five times lower than the proposed U. S. Envi ronmental Protection Agency (EPA) MCL, is based, in part, upon risk analysis considerations and is expressly left subject to alteration in light of further Agency under standing of what potential risks exist. Current Florida regulations allow for at least some case-by-case flexibility in the application of this stringent one Mg/1 standard in J groundwater through the use of "exemptions" and "zones of discharge". Invoking these relief mechanisms essen tially requires a further assessment of potential health risks and other factors on a site specific basis. The State of Florida is expected soon to engage in further rulemaking that will determine what concentra" tions of benzene may be left in groundwater pursuant to the "State Underground Petroleum Environmental Re sponse Act of 1986"("SUPER Act"). Special care should be taken to insure that the regulations reflect the best scientific information available. Hazard Assessment Available literature on benzene toxicity to humans pri marily refers to instances involving high dose levels by inhalation. These observational cohort and epidemiolog ical studies demonstrate that acute and chronic toxicolog ical effects can occur as a result of high exposure to benzene in occupational settings. However, there are no reports of significant toxicological effects as a result of benzene ingestion via drinking water or food. Avenues of human exposure to benzene include food (beef, eggs, etc.) and ambient and indoor air (vehicular sources, cigarette smoke, etc.). Indoor air sources consti tute the most significant contributor ofhuman body con tent of benzene. Drinking water contributes less than 0.2 percent of the average human exposure to benzene. OIn summary, available scientific evidence and theory indicates that exposure to benzene through drinking water is unlikely to cause any significant adverse health effect in humans. Fate and Transport / Containment of Benzene in Groundwater Gasoline, which typically contains a small amount of benzene, may leak from underground tanks or pipes and thereby release this petroleum product to unsaturated soils above the water table or directly into groundwater. Gasoline is less dense than water, and the primary response to such releases should be to remove as rapidly as possible (by pumping) all of the "free product" that accumulates on top of the water table. This controls further lateral spreading of contamination and greatly reduces the source of gasoline components leaching as a soluble phase into the groundwater. Mathematical and computer models are available to predict and simulate the transportation and fate of ben zene in subsurface systems vulnerable to contamination in Florida. The models developed in this study demon strate that natural mitigation by volatilization and bio degradation are important factors in the total mitigation process. Field observations have confirmed predictions by the model for the time to reach low concentrations [i.e., 10-100 Mg/1 (ppb)] of benzene. The model indicates continuing reductions in benzene due to volatilization and biodegradation. However, field data indicate that a "leveling off" occurs within the 10-100 Mg/1 range. Con centrations of benzene below this amount are outside the verifiable range of the model due to the geohydrological 1 SAL 000000864 irregularities, sampling, analytical, and other uncertainties. Analytical uncertainty in the measurement of benzene below 10 Mg/1 is high, suggesting that practical demon stration of compliance at low concentrations would be severely complicated by analytical error. Risk Assessment The purpose ofestimating exposure-related human health risk is to assist in the establishment of regulations that best balance benefits and risks. In assessing risks associated with the presence of ben zene in underground sources of water, several factors weigh in favor of increased flexibility in the Florida ben zene groundwater standard because: Drinking water exposure to benzene constitutes such a small percentage of total exposure, the relative risk associated with the presence of benzene at concentra tions higher than the current Florida MCL is slight; Physiological pharmacokinetic considerations show that benzene exposure via water at 20 Mg/day (perhaps even higher) would not contribute measurably to the normal body content of benzene; and, Quantitative extrapolation of risk is overly conservative. All previous health risk studies have focused upon the concept of "dose". For an analysis to be truly meaningful, -however, it must account for biological processes (phar macokinetics): i.e., identification of how and at what rates benzene enters the body, is distributed within the body, changes within the body, and is excreted from the body. The primary factor regulating body content of benzene is average concentration of this constituent in the atmos phere. The body content is usually at an equilibrium with concentrations of benzene in the air due to a relatively quick exchange of benzene across the membranes of the lung, increments of benzene absorbed from the intestine are largely metabolized in the body with the remainder being excreted by exhalation. Benzene absorbed from the intestine produces only a transitory increase in body con tent that quickly reverts to a level of equilibrium with the atmosphere. The variability in an individual's total daily intake of benzene makes it difficult to observe any practical differ ences caused by changing the benzene intake from drink ing water by 20 Mg/ day (25 m|/ 1 at 0.8 1/day). Even in the statistical analysis of risk associated with benzene at 25 Mg/1 in drinking water, the upper bound estimate of increased carcinogenic response at that level among indi viduals in the exposedpopulation would be less than 10s or, with equal likelihood, it might be essentially zero. Conclusions Once detected on the groundwater, free phase petro leum hydrocarbons should be removed as quickly as possible to minimize the spread of the contaminant plume. Plume intercept technology is effective in cleaning up gasoline spill sites to low concentrations of benzene. Xrf Once benzene has reached about 100 Mg/1 in the groundwater, continued use of this cleanup action will not yield a substantial improvement over natural pro cesses. Trace residual hydrocarbons left in the subsur face at these concentrations will degrade in time through natural processes. Geohydrological models which predict the relation ship between sources of contamination and aquifers are useful tools as planning guides in projecting the extent of contamination and in evaluating cleanup strategies. The present Florida benzene water quality standard of one Mg/1 benzene is unnecessarily restrictive, both from a perspective of feasible site remedial action and from the standpoint of risk to public health and safety. In the 10-100 Mg/1 concentration range, the risk asso ciated with benzene in groundwater is exceedingly small. Ad linking water standard which limits intake of ben zene from this source to 20 Mg/day (25 Mg/1 at 0.8 1/day) is more than adequate to avoid any detectable risk of leukemia. Such standard should be applied only under circumstances where the groundwater will be used directly for human consumption. Should groundwater with traces of benzene be needed as a drinking watersource, it may be more economical to treat the water at the well outlet rather than in the aquifer. NOTE TO READER: Authors have been free to select data for their work. The American Petroleum Institute has not imposed a re quirement to use a given data set. This flexibility does not alter the overall conclusions but should be considered in comparing work by different authors. Although specific models have been used in this study, other models may be equally valid. 2 sal 000000865 PART TWO: HAZARD ASSESSMENT [ Forrest B. Thomas. Ph. D. Shell Development Company Houston. Texas ,v 2-1 TOXICOLOGICAL EFFECTS OF BENZENE 2-1.1 Introduction Several excellent reviews of the toxicological properties of benzene have been published recently: Fishbein (Ref. 2-1.9 [ 14]), Synder (Ref. 2-1.9 (32]), Aksoy (Ref. 2-1.9 [ I ]) and Mehlman(Ref. 2-1.9(22]). This section will therefore address only selected aspects of the extremely large toxi cological data base available for this compound in order to provide a perspective from which to evaluate other parts of this document. 2-1.2 Major Sources of Human Benzene Exposure It must be appreciated that benzene is ubiquitous. According to estimates from the National Research Council (Ref. 2-1.9 [24]), the dietary intake of benzene may be as high as 250 Mg daily, perhaps explaining ben zene concentrations of 8-20 ppb in the breath ofindividu als with no known exposure to this compound. The ben1 zene content ofspecific foods is reported to range from 2 ppb for canned beef to 2100 ppb for a boiled egg (Ref. 2-1.9 [23]). Recentresults from the National Toxicology Program (Ref. 2-1.9 [25]) indicate that virtually 100% of ^ benzene administered orally is absorbed into the body. Benzene concentrations in ambient air(urban and rural) have been estimated to range from 1-100 ppb (Ref. 2-1.9 [17]). Urban air is reported to contain higher levels than rural air, presumably due to the contribution of automo tive emissions of benzene (Ref. 2-1.9 [5]). After reviewing these data, the National Research Council (1980) calcu lated that an individual living in an urban environment containing a mean atmospheric benzene concentration of . 16 ppb (50 fig/m3) who breathes an average of 24 m3 of air ^ per day and absorbs approximately 50% of the dose (i.e., equilibrium state) will absorb approximately 600 pg of benzene daily. [16 ppb = 50 tigfm3 x 24 m3/day x 50% absorption = 600 Mg/day] ' ***"* Benzene is present in cigarette smoke at levels of 47-64 ppm, leading to estimates of the amount of benzene inhaled from a single cigarettes ranging from 10-31 fig. Using the upper estimate, a person smoking two packs (i.e., 40 cigarettes) per day will absorb up to 992 pg of benzene (assumes 80% of dose is absorbed; non-equili brium state). [Note: This discussion will not consider the contribution of secondary inhalation of cigarette smoke to the overall benzene exposure of a non-smoker.] [40 cigarettes/day x 31 Mg benzene/cigarette x 80% absorption = 992 Mg/day] The solubility of benzene in water is reported to be 1780 mg/1 at 25 C (Ref. 2-1.9 [2]). In a report issued by the EPA Office of Drinking Water (Ref. 2-1.9 [11]), it was estimated that 97.7% of the population served by public water systems is receiving water either free of benzene contamination or having levels less than 0.5 fig/1. Esti mates of daily human water consumption range from 0.8 to 2 1 / day. Assuming that the average adult consumes 2 liters of water daily, it can be calculated that drinking water with a benzene content of 0.5 pgf 1 would contrib ute 1 pg of benzene to the average daily dose (100% absorption assumed). [0.5 fig/1 x 2 I/day = 1.0 Mg/day] Summarizing the above calculations for what are consid ered major sources of human benzene exposure: Non-Smoker Smoker Food Air Cigarettes Water TOTAL 250 Mg/day 600 Mg/day LMg/day 851 Mg/day 250 Mg/day 600 Mg/day 992 Mg/ day 1 MR/day 1843 Mg/day 2-13 The Pharmacokinetics of Benzene The primary routes of benzene exposure are considered to be oral and inhalation. While there are data that benzene applied as a liquid or in solution to human skin can be absorbed fairly rapidly (Ref. 2-1.9 [4]), this route is gener ally discounted as being significant because of the rapid evaporation of benzene which effectively reduces the time of skin contact. Recent data from the National Toxicology Program (Ref. 2-1.9 [26]) indicates that virtually all of an oral dose of benzene dissolved in vegetable oil is absorbed in rats and mice. It is reasonable to assume that dietary fiber content may reduce both the rate and efficiency of ben zene absorption somewhat by complexing the hydrocar bon, but experimental evidence for this is unavailable. To be conservative, 100% absorption of benzene from food and water was assumed in the above calculations. The respiratory absorption of a hydrocarbon vapor such as benzene is a complex process which has only partially been characterized. Initially, when an animal (orman) is placed into an atmosphere containing benzene vapor, virtually ail of the hydrocarbon is absorbed into the blood stream and then distributed to the various tissues of the body. Each tissue will absorb some of the benzene from the blood with some tissues (e.g., those having a high 7 SAL 000000366 content of fat) absorbing relatively greater proportions of benzene compared to other tissues. The benzene absorbed by each tissue may be sequestered, released back to the blood unchanged, or processed by the specific metabolic enzymes which characterize the cells of that tissue. In time, a state ofdynamic equilibrium (often called "steady state") is established between the air, blood, and other body compartments. As more benzene is absorbed from the air, some of the previously absorbed benzene is exhaled unchanged from the body, some is metabolized to specific derivatives which may be further metabolized even in other distant tissues, and some is removed by the kidneys and excreted in the urine. As the animal approaches steady state, the apparent (i.e., net) absorp tion of the compound into the body can be seen to decrease substantially. As noted in Section 2-1.2 above, conservative estimates of 50-80% absorption have been assumed in calculating the contribution of ambient air and cigarette smoking to the total burden of benzene. Recent data from the NTP (1986) indicate that from a 6 hour exposure to 11 ppm of benzene vapor, the apparent absorption of benzene in mice is 50%, whereas at 1000 ppm, the apparent absorption is 9.7%. Values for sim ilarly exposed rats are 33% absorption at 13 ppm and 15% absorption at 870 ppm. Significant differences in the respiratory characteristics of commonly used laboratory animals exist and greatly influence the amount and rate at which a hydrocarbon vapor is absorbed into the body. Small animals, with their _ high metabolic rate, must have a relatively large supply of oxygen to the body (Ref. 2-1.9 [34]). While this could have been accomplished evoiutionarily by development of larger lungs relative to their body size, small animals such as mice and rats instead breathe more rapidly. It might be expected therefore that rodents should reach steady state more quickly than a man exposed to the same vapor concentration, but definitive experimental data in this regard have not been identified. 'The Lovelace Inhalation Toxicology Research Institute (ITRI), under contract with NTP, have characterized the respiratory parameters of the B6C3FI mouse and the F344 rat, (unpublished information from the butadiene research program). According to ITRI data, the average B6C3F1 mouse weighed 27.5 g and breathed 35 ml of air per minute (i.e., minute volume); the average F344 rat weighed 392 g and had a minute volume of 289.7 ml. Expressed on a kilogram body weight basis, the minute volume of the mouse is 127^ ml/kg and of the rat is 737 ml/kg. From this perspective, it is understandable why Sabourin et al. (1986) concluded that at similar exposure levels of benzene vapor, mice received 150-200% of the dose received by rats per kilogram body weight. Such differences in respiratory characteristics between species are especially important to exposures where the steady state condition has either not been reached or has been perturbed. Consideration of species differences must be incorporated in the quantitative modeling of animal inha lation data for estimation of human health risks. In par ticular, if one assumes a 70-kg man who breathes 7500 ml of air per minute, it can be calculated that the human minute volume/kg body weight is about one-seventh that of the rat and about one-twelfth that of the mouse. A similar picture of steady-state equilibrium can be developed for benzene absorbed from the gastrointestinal tract. As noted above, recent data from NTP (Sabourin et al., 1986) suggest that essentially all of a dose of benzene (dissolved in com oil) administered by gavage is absorbed by rats and mice. Two points should be emphasized with regard to oral exposures. First, the concentration of ben zene in the blood as a result of the administration of an oral bolus is seen to be a transient peak or spike. Dissolv ing benzene in a vehicle such as corn oil essentially results in a retardation in the absorption of benzene into the blood stream, suchthatall ofthe benzene is eventuallyabsorbed, but it requires a longer period of time. Benzene is metabolized via a number of possible path ways, summarized in Figure 2-1.8 [1]. Available informa tion indicates that benzene must be metabolized in order to exert its toxic effects. However, it is not clear at the present time which of the various metabolic pathways activates benzene to more toxic derivatives and which pathways result in detoxification. Various investigators have suggested that toxicity may be the result of covalent binding of benzene metabolites to cellular macromole cules such as DNA and protein, and a reactive benzene epoxide was postulated to be formed during the metabo lism of benzene by the cytochrome P-450 enzyme system (Ref. 2-1.9 [19]). Recent data, however, call into question whether benzene oxide is in fact formed to a significant degree during the metabolism of benzene (Ref. 2-1.9 [20]). Investigators at the Chemical Industry Institute of Toxi cology (Ref. 2-1.9 [16], [18]) suggest that polyphenol derivatives (e.g., hydroquinone and 1,2,4 -benzenetriol) may be responsible for the toxic effects of benzene, per haps via the autooxidative formation of highly reactive radicals which could bind to macromolecular targets. Goldstein et al. (Ref. 2-1.9 [15]) suggest that the benzene ring is cleaved metabolically forming muconaldehyde which is also capable of reacting with essential macro molecules. The role of various isomers of diphenol formed by cellular peroxidases, such as myeloperoxidase in the bone marrow in benzene toxicity remains to be evaluated (Ref. 2-1.9 [28]). See Figure 2-1.8 [I]. While it is not yet possible to identify which metabo lite^) of benzene is responsible for the profound cellular toxicity associated with this compound, quantitative risk modeling must recognize that significant qualitative and quantitative differences in the specific metabolic path ways for benzene are seen between species. The phenolic metabolites in the urine of benzene-treated mice, for example, have been found to comprise 50-65% glucurortide conjugates, 26-38% sulfate conjugates, and approximately 5% unconjugated phenol (Ref. 2-1.9 [33]). In contrast, Cornish and Ryan (Ref. 2-1.9 [6]) observed that approx imately 70% of the phenolic metabolites found in the urine of benzene-treated rats were sulfate conjugates. In man, virtually all of the phenolic compounds in the urine following benzene exposure exist as sulfate conjugates until the concentration of phenol in the urine reaches approximately 400 mg/1 when the sulfate pathway has apparently been saturated and products of glucuronide conjugation begin to appear (Ref. 2-1.9 [30]). Such data 8 SAL 000000867 2-J.9 REFERENCES: TOXICOLOGICAL EFFECTS OF BENZENE n [1] Aksoy. M. "Benzene as a Leukemogenic and Car cinogenic Agent", Amer. J. Indus. Med. 8:9-20, [18] Irons, R. D. "Quinones as Toxic Metabolites of Benzene", J. Toxicol. Environ. Health 16:673-678, 1985. [2] Andelman. J. B., Suess, M. J. "Polynuclear Aro 1985. [19] Jernina, D., Daly, J., Whitkop, B., Zaltzmari: matic Hydrocarbons in the Water Environment" Bull. WHO 43:479-508, 1970. [3] Battifora. H. A.. McCreary, P. A., Hahneman.B. M., Laing, G. H.. Hass, G. M. "Chronic Magne sium Deficiency in the Rat. Studies of Chronic Myelogenous Leukemia", Arch. Pathol. 86:610 ff., 1968. [4] Blank. 1. H.. McAuliffe, D. J. "Penetration of Ben zene through Human Skin", Invest. Dermatol. 85:522-526, 1985. [5] Brief, R. S., Lynch, J., Bernath, T., Scala, R. A., "Benzene in the Workplace", Amer. Ind. Hyg. Assn. J. 41:616-623, 1980. [6] Cornish, H., Ryan, R. "Metabolism of Benzene in Nonfasted, Fasted, and Aryl-hydroxylase Inhibited Rats." Toxicol. Appl. Pharmacol. 7:767-771, 1965. [7] Dameshek, W. "Some Speculations on the Myelo proliferative Syndrome", (editorial) Blood 6:372 ff., 1951. [8] Dameshek, W. "Certain Forms of Leukemia as Immunoproliferative Disorders." In Carcinogene sis: A Broad Critique. Williams and Wilkins Com pany, Baltimore, Maryland, pp 141 ff., 1970. [9] Delore, P., Bergamano, J. "Leucemie Aique en Cours d'Intoxication Bezenique" J. Med. Lyon 9:227-233, 1928. [10] Environmental Protection Agency, Ambient Water Quality Criteriafor Benzene. (PB81-117293), 1980. [ 11] Environmental Protection Agency, Benzene: Occur rence in Drinking Water, Food, and Air, (Prepared by JRB Associates), 1983. [12] Environmental Protection Agency, Carcinogen Assessment Group's Final Report on Population Risk to Ambient Benzene Exposures. (P83-0134), 1978. [13] Environmental Protection Agency, "Notice of Water Quality Criteria Documents", Federal Regis ter 45:79326, November 28, 1980. [14] Fishbein, L. "An Overview of Environmental and Toxicological Aspects of Aromatic Hydrocarbons. I. Benzene." Science Total Environ. 40:189-218, 1984. [15] Goldstein, B. D., Wilz, G., Javid, J., Amuroso, M. A., Rossman, T., Wolder, B. "Muconaldehyde, a Potential Toxic Intermediate of Benzene Metabo lism.", Adv. Exp. Biol. Med. 136A:331, 1981. [16] Greenlee, W. F., Sun, J. D., Bus, J. S. "A Proposed Mechanism of Benzene Toxicity: Formation of Reactive Intermediates from Polyphenol Metabo lites.", Toxicol. Appl. Pharmacol. 59:187-195, 1981. [17] International Agency for Research on Cancer (1ARC), IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans. Lyon, France, 29:93-148, May, 1982. Nirenberg, P., Udenfriend, S. "Role of Arene- Oxide-Oxepin System in the Metabolism of Aro matic Substrates. I. In Vitro Conversion of Benzene Oxide to a Premercapturic Acid and a Dihydro- diol", Arch. Biochem. Biophys. 128:176-183, 1968. [20] Johansson, I., Ingelman-Sundberg, M. "Hydroxyl Radical-Mediated, Cytochrome P-450-dependent Metabolic Activation of Benzene in Microsomes and Reconstituted Enzyme Systems from Rabbit Liver." J. Biol. Chem. 258:7311-7316,1983. [21] Maltoni, C., Conti, B., Cotti, G., Belpoggi, F. "Experimental Studies on Benzene Carcinogenicity at the Bologna Institute of Oncology: Current Results and Ongoing Research." Amer. J. Indus. Med. 7:415-446, 1985. [22] Mehlman, M. A., ed. Benzene: Scientific Debate. Proceedings of the International Conference on Benzene Sponsored by the Collegium Ramazzini, New York City, November 3-4, 1983. Alan R. Liss, New York, 1985. [23] National Research Council. Drinking Water and Health, Vol. 3, National Academy of Sciences, Washington, D.C., 1980. [24] National Research Council. Health Effects ofBe\ } zene: A Review, National Academy of Sciences,' Washington, D.C., 1976. [25] National Toxicology Program. Toxicology and Carcinogenesis Studies of Benzene (CAS No. 71- 43-2) in F344{N Rats and B6C3F1 Mice (Gavage Studies), Technical Report No. 289 (galley draft), National Toxicology Program, Washington, D.C., February, 1986. [26] Sabourin, P. J., Chen T-H, Lucicr, G., Bimbaum, L. S., Fisher,E., Henderson, R. F. "Effect of Dose on the Absorption and Excretion of 14C-Benzene Administered Orally or by Inhalation in Rats and Mice." Toxicol. Appl. Pharmacol. (Submitted for publication), 1986. [27] Santesson, C. G. "Uber Chronische Vergiftung mit Steinkohlentheerbenzin; vier Todefalle." Arch. Hyg. Berl. 31:336-376,1897. [28] Sawahata, T., Rickert, D.E., Greenlee, W. F. "Metabolism of Benzene and its Metabolites in Bone Marrow." In Toxicology of the Blood and Bone Marrow, Irons R. D., ed., Raven Press, New York, pp. 141-148, 1985. [29] Selling, L. "Benzol as a Leucotoxin. Studies on the Degeneration and Regeneration of the Blood and Haematopoietic Organs." Johns Hopkins Hosp. Reports 17:83-148, 1916. [30] Sherwood, R. J. "The Interpretation of Monitoring Results", Ann. Occup. Hyg. 15:409-421, 1972. _ [31] Sinkovics, J. G., Trujillo, J. M-, Pienta, R. J., Ahearn, M. J. "Leukemogenesis Stemming from Autoimmune Disease", In Genetic Concepts and 14 SAL 000000868 2-4 NONDRINICING-WATER EXPOSURE David H. Powell, Ph.D. William A. Tucker, Ph.D. Environmental Science and Engineering, Inc. Gainesville, Florida 2-4.1 Occurrence 2-4.1(1) Food h Data on the occurrence of benzene in food are limited. Mara and Lee (Ref. 2-4.4 [1!]) reported that benzene occurs naturally in fruits, fish, vegetables, nuts, dairy products, beverages, and eggs. These authors report con centrations ranging from 2 micrograms per kilogram (ng/kg) for canned beef to 2,100 Mg/kg for eggs. Cooked meats are reported to have higher benzene levels than raw meats, and it is postulated that the increased benzene levels observed after cooking meats is due to the break down of aromatic amino acids such and tyrosine (Ref. 2-4.4 [5]). / Low levels (< 10 Mg/ kg) of benzene in food could be due l to a partitioning from the ambient levels of atmospheric tenzene. The high levels observed in eggs indicate an intrinsic mechanism for the biochemical formation of benzene. Table 2-4.3 [1] summarizes the reported occur rence of benzene in foods. 2-4.1(2) Air The materials balance for benzene indicates that 95 per cent of environmental releases of benzene are to the atmosphere, and three-quarters of this release is asso ciated with fuel combustion (Ref. 2-4.4 [5]). As a result of these emissions, it is not surprising that ambient air levels of benzene have been correlated with traffic volumes (Ref. 2-4.4 [2]). Atmospheric benzene is ubiquitous; remote regions have measured concentrations usually ranging from 1 to 3.5 micrograms per cubic meter (Mg/m3). Higher levels are observed in urban and industrial environments. Table 2-4.3 [2] summarizes benzene concentration ranges and averages for various atmospheric environments. Indoor benzene levels have been studied in industrial settings. Inside chemical plants, reported concentrations range from 2,000 to 10,000 fig/mThe current Occupational Safety and Health Administration (OSH A) regula tion on workplace exposure is 32,000 Mg/ m3 (10 parts per million, ppm) for the time-weighted average (TWA) con centration for an 8 hour exposure with a peak maximum concentration of 160,000 Mg/m3 (50 ppm) for any 15 minute period during an 8 hour day (Ref.2-4.4 [I]). Indoor benzene levels in residences have been reported by Sample and Gilbert (Ref. 2-4.4 [14]) to have a median value of 15.0 mg/m3 and an arithmetic mean of 25.8 Mg/mJ foe 353 nighttime observations of benzene. There is a minimal correlation between indoor concentrations and outside ambient levels. The impact of smoking on indoor benzene concentrations appears to be important 60 in households containing one or more smokers. These households exhibit at least 50 percent greater concentra tions than households of nonsmokers. One cigarette can generate approximately 90 micrograms (Mg) of benzene (Ref. 2-4.4 [5]). The portion of the benzene in the main stream smoke is predominantly absorbed by the smoker and not exhaled. Mainstream smoke is that which the smoker inhales; however, the sidestream smoke which is released to the room often contains twice the quantity of some chemicals as the mainstream smoke (Ref.2-4.4 [6]). Therefore, of the 90 Mg of benzene released from each cigarette, possibly 60 Mg is released to the smoker's envi ronment through the sidestream smoke. 2-4.2 Exposure Reported benzene concentrations in foods do not involve all food groups, it is not known how representative these concentrations are of the concentrations in foods in general. Dietary intake of benzene has been estimated to be as high as 250 micrograms per day (Mg/ day) from beef, eggs, and rum alone (Ref. 2-4.4 [13]). Assuming that the average adult male weighs 70 kg, an intake of 250 Mg/day would be equivalent to 3.6 micrograms per kilogram per day (Mg/kg/day). In the absence of further data, Letkiewicz et al. (Ref. 2-4.4 [8]) assumed the dietary intake of benzene was at that level. Gilbert et al. (Ref. 2-4.4 [5]) estimated the ingestion due to only those foods with reported benzene concentrations (i.e., butter, cooked beef, eggs, and haddock), resulting in a daily ingestion intake of 31 to 108 Mg/day. Exposure to benzene in the atmosphere is highly varia ble; reported levels range between low parts-per-billion values in outside air to low parts-per-million in certain industrial settings. Median air concentrations of benzene have been calculated by Brodzinsky and Singh (Ref. 2-4.4 [3]) for rural/remote areas (4.5 Mg/m3), urban/suburban areas (8.9 Mg/m3), and source-dominated areas (9.6 Mg/m3). Thus, in urban/ suburban areas, people inhale approximately 180 Mg of benzene each day (at 20 cubic meters, m3, of air inhaled each day). As a comparison, a one-pack-per-day smoker inhales approximately 600 Mg/day of benzene from mainstream smoke. Exposure by these routes is substantial, but highly variable in the general population. Average annual atmospheric benzene concentrations and the size of exposed populations have been calculated by Mara and Lee (Ref. 2-2.4 [ 11]) based on air dispersion models. Approximately half of the population of the United States was estimated to be exposed to average atmospheric benzene concentrations between 3.5 and 13 Mg/m3. A newborn, formula-fed infant's respiratory intake of benzene can be expected to range from 1.0 to 2.2 Mg/kg/day, whereas the intake of a nonsm&king, 70kilogram (kg) adult male may vary between 1.5 to 360 Mg/kg/day, depending on ambient benzene concentra tions (Ref. 2-4.4 [8]). SAL 000000869 TABLE 2-4.3 [I] Foods Reported to Contain Benzene Fruits* Apple Citrus Fruit Cranberry and Bilberry Currants Guava Pineapple Strawberry Tomato Nuts* Filbert, roasted Peanut, roasted Macademia Nut Vegetables* Bean Leek Mushroom Onion, roasted Parsley Potato Soya Bean Trassi, cooked Dairy Products Butter (0.5 Mg/kg)b Blue Cheese* Cheddar Cheese* Other Cheese* / Meat, Fish, and Poultry Cooked beef (2 to 19 *tg/kg)` Chicken (<10 ^g/kg)d Egg, hard boiled (500 to 1,900 jig/kg)* Egg, uncooked (2100/ug/kg)h i>*ooG Haddock (100 to 200 jig/kg)f ' Lamb, heated (<10 pg/kg)3 Mutton, heated (<10 /^g/ kg)d Veal, heated (<10 Mg/kg)d Beverages Cocoa* Coffee* Jamaican Rum (120 #ig/kg)` Tea* Whiikey* Ref. 2-4.4 [16] h Ref. 2-4.4 [15] c Ref. 2-4.4 [13] * Ref. 2-4.4 [12] * Refs. 2-4.4 [9], [10] ' Irradiated and non-irradiated haddock, respectively. Ref. 2-4.4 [7] h Ref. 2-4.4 [11] Source: Ref. 2-4.4 [5] ) % TABLE 2-4.3 [2] Summary of Benzene Occurrence in Air Environment Benzene Concentration (^g/m1) Remote (Range) 1 Urban (Range) Residential -- Remote from Traffic (Average) Near Chemical Plant (Average) Near Refineries (Average) Gas Stations (Range) Sources: Refs. 2-4.4 [5], [8] 1 to 3.5 4 to 160 4.5 14 9 <1 to 32 .3^ /\n ` .'i'-L Al* K -r J 6oQ**-4 I./)^ *v J 'ft'"' ' ^l 0*0 61 SAL 000000870 2-4.4 REFERENCES: NONDRINKING-WATER EXPOSURE [!] American Conference of Governmental Industrial Hygienists (ACGIH), Threshold Limit Values for Chemical Substances and Physical Agents in the Work Room Environment, Cincinnati, Ohio, 1985. [2] Battelle, Environmental Monitoring -- Benzene, Battelle Columbus Laboratories, Columbus, Ohio, 1979. [3] Brodzinsky, R., Singh, H. B. Volatile Organic Chemicals in the Atmosphere: An Assessment of Available Data, prepared by SRI International, Menlo Park, California for Environmental Scien ces Research Laboratory, Office of Research and Development, U. S. Environmental Protection Agency, Research Triangle Park, No. Carolina, EPA-440/4-79-029b, 1982. [4] Drill, S., Thomas R. Environmental Sources of Benzene Exposure: Source Contribution Factors, Prepared by Mitre Corporation for the U. S. Envi ronmental Protection Agency, EPA-570/ 9-79-004, 1979. [5] Gilbert, D., Byrne, M., Harris, J., Steber, W., Woodruff, C. An Exposure and Risk Assessment for Benzene, Final Draft Report, Prepared by Arthur D. Little, Inc. for U. S. Environmental Pro tection Agency Office of Water and Waste Man agement, Washington, D. C. EPA Contract No. cinogenicity of Benzene, Summary Report, Wash ington, D. C., 1977. [14] Sample, C. J., Gilbert, D. Indoor Ambient Benzene Concentrations: An Assessment ofFactors Related to Indoor Air Quality. American Petroleum Insti tute, Washington, D. C., 1985. [15] Siek, T. J., Lindsey, R. C. "Semiquantitative Anal ysis of Fresh Sweet Cream Butter Volatiles", Jour nal of Dairy Sciences 53(6):700-703, 1970. [16] Van Stratten, S., Editor. Volatile Compounds in Food, 4th Edition, Supplement 1, Central Institute for Nutrition and Food Research TNO, Zeist, The Netherlands, 1977. Hale, R. W., Nedlock, J. W., Grubbs, H. J., and Powell, D. H. "The Distribution of Products between Mainstream and Sidestream Smoke", Tobacco Science 17:141-144, 1973. [7] Leibich, H. M., Koenig, W. A., Bayer, E. "Analysis of the Flavor of Rum by Gas-Liquid Chromato graphy and Mass Spectrometry",/. Chromato. Sci. 8:527-533, 1970. [8] Letkiewicz, F., Johnston, P., Macaluso, C., Elder, R., Yu,W., Bason, C. Occurrence of Benzene in Drinking Water, Food, and Air, Prepared by JRB Associates for U. S. Environmental Protection Agency Office of Drinking Water, Contract No. 68-01-6388, 1983. [9] MacLeod, A. J., Personal Communication to H. I. Chinn, (Cited in Drill, S., Thomas, R., Environmental Sources of Benzene Exposure: Source Con tribution Factors, 1979), 1977. [10] MacLeod, A. J., Cave, S. J. "Variations in the Volatile Flavour Components of Eggs", /. Sci. Food Agric. 27:799-806, 1976. [11] Mara, S. J., Lee, S. S. Assessment ofHuman Expo sure to Atmospheric Benzene, U. S. Environmental Protection Agency, Research Triangle Park, No. Carolina, EPA-450/3-78-031, 1978. Merritt, C. "Qualitative and Quantitative Aspects of Trace Volatile Components in Irradiated Foods J and Food Substances", Radiation Res. Rev. 3:353' 368, 1972. [13] National Cancer Institute (NCI). On Occurrence, Metabolism, and Toxicity including Reported Car- 62 SAL 000000871