(VCCEP) Tier 1 Pilot Submission for BENZENE - Tera

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Benzene epoxide Benzene P450 IIE1 Fe / OH• Phenol P450 IIE1 HO Source: Ross 2000. Benzene VCCEP Submission March 2006 O REARRANGEMENT P450 OH OH Figure 6.1: Major Metabolic Pathways for Benzene GSH Hydroquinone OH HO OH O EPOXIDE HYDROLASE P450 Benzene triol O trans,trans- Muconaldehyde OH PEROXIDASES / AUTOXIDATION Benzene dihydrodiol OH DIHYDRODIOL DEHYDROGENASE OH Catechol OH p-Benzoquinone O 95 S-Phenylmercapturic acid o-Benzoquinone O O S O O H C H NHCOCH 3 C COOH H O O NQO1 ? NQO1 4,4'-Diphenoquinone 4,4-Biphenol NQO1 O OH OH trans,trans- Muconic acid OH OH O Catechol OH OH Hydroquinone OH OH
7.0 Exposure Assessments This section summarizes the methodology, results and conclusions of the Tier I exposure assessment for benzene under VCCEP. As part of this pilot program, EPA has requested exposure information to be submitted to determine the extent of children's exposure to benzene. The types of exposure information needed for the Tier 1 assessment include the identification and characterization of the population groups exposed, and sources of the exposure, as well as frequencies, levels, and routes of exposure. The methodology employed in this assessment provides for both a thorough determination of childhood exposures to benzene and uses the available data to focus on those sources of exposure that are likely to have the most significant contribution to individuals’ total benzene exposures. In accordance with the numerous studies of personal benzene exposure, a child activity-based approach was used (Ott and Roberts, 1998; Wallace, 1996; Wallace et al., 1989a; Kinney et al., 2002; Philips et al., 2004; Adgate et al.; 2004a,b). 7.1 Methodology/Scope of the Assessment As suggested by EPA, exposure assessments for both children and prospective parents were conducted. Sources of exposure to benzene in the ambient environment can come from both chain-of-commerce and non-chain of commerce sources. In accordance with the notice of the program published in the Federal Register (2000), this assessment focused primarily on the evaluation of benzene exposures from chain of commerce sources (i.e., manufacturing, processing, and use of benzene). When relevant, exposures to benzene from non-chain of commerce sources were also quantified. For example, tobacco smoke was evaluated because it is a well documented source of personal benzene exposure (Wallace, 1988; Brunnemann, et al., 1990a, Daisey et al., 1994; and Darrall, et al., 1998). Additionally, the exposure assessments did not include exposures from intentional misuse scenarios. A child-centered approach has been used to define scenarios in which children may have exposure to benzene. Children may be exposed directly via personal proximity to benzene sources, or indirectly, during gestation or through human milk through their mothers. Women of childbearing age may be exposed via personal contact with benzene sources, and they may be exposed occupationally. Figure 7.1 graphically depicts the potential sources of benzene exposure for children and prospective parents. In defining these scenarios, chain-of-commerce information and data on naturally occurring levels have been used to determine the activities and settings that result in exposures. The prospective father has also been included in this exposure analysis due to potential reproductive effects that may result from the father’s exposure to benzene. Benzene VCCEP Submission March 2006 96
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Voluntary Children’s Chemical Eva
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6.1.2 Types of Adverse Health Effec
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Glossary of Terms μg Microgram AA
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STEL Short-Term Exposure Limit TEAM
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enzene induced pancytopenias can pr
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A fertility study in female rats ex
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estimate is very conservative both
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2.0 BASIS FOR INCLUSION OF BENZENE
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2.5 Air Monitoring Data Several of
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Table 3.1: Proposed Benzene AEGL Va
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4.0 Regulatory Overview This sectio
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passenger vehicles operated at cold
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Benzene has been designated a hazar
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products had ceased” [46 Fed. Reg
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5.0 CHEMICAL OVERVIEW This section
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Table 5.3: Environmental Fate and T
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general, the production rate is abo
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gasoline. Aromatic hydrocarbons, su
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The EPA Office of Air Quality Plann
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Benzene VCCEP Submission March 2006
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Table 5.11: Benzene Releases for Al
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6.1.2.2 Chronic Toxicity Toxicity a
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6.1.2.2e Other Hematopoietic Malign
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that transient, high peak exposures
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absorption compared to inhalation,
Page 51 and 52: increased risk of disease. It shoul
Page 53 and 54: The National Cancer Institute (NCI)
Page 55 and 56: exposure. This was also supported b
Page 57 and 58: follow-up of this same cohort, Wong
Page 59 and 60: development of MDS)and/or AML. It i
Page 61 and 62: quantification of benzene air conce
Page 63 and 64: 4.0, 95% CI = 1.8-9.3) but not ALL
Page 65 and 66: 6.2 Benzene Toxicology—Animal Haz
Page 67 and 68: eakage and loss was comparable whet
Page 69 and 70: Benzene VCCEP Submission March 2006
Page 71 and 72: Table 6.2: In Vivo Genotoxicity of
Page 73 and 74: Table 6.2 Continued: In Vivo Genoto
Page 75 and 76: 6.2.2.3 Transplacental Genotoxicity
Page 77 and 78: induce solid tumors in animals in t
Page 79 and 80: mice in the 300-ppm group had bilat
Page 81 and 82: decreases in maternal weight gain,
Page 87 and 88: increased resorptions. The effects
Page 89 and 90: proposed that transplacental effect
Page 91 and 92: glycerol lysis time, and incidence
Page 93 and 94: 6.2.5.2 Chronic Toxicity Repeat-dos
Page 95 and 96: LOAELs for carcinogenic effects in
Page 97 and 98: the measurements of doses are suspe
Page 99 and 100: intracellular pathogen, Listeria mo
Page 101: 2. Evidence indicates that myelotox
Page 105 and 106: throughout childhood, see Table 7.1
Page 107 and 108: 7.2 Sources of Benzene Exposure Chi
Page 109 and 110: Table 7.3: Outdoor Ambient Air Benz
Page 111 and 112: Table 7.5: County-Wide 24-hour Ambi
Page 113 and 114: Age-specific benzene intakes are pr
Page 115 and 116: Table 7.9: Total ADDs for Exposure
Page 117 and 118: Table 7.10 (cont.) Study Location a
Page 119 and 120: Table 7.11: Summary of Benzene Meas
Page 121 and 122: factor change attributable to benze
Page 123 and 124: where: ADD = average daily dose (mg
Page 125 and 126: Table 7.16: Total ADDS from In-Home
Page 127 and 128: Table 7.18: Summary of Age-Specific
Page 129 and 130: Table 7.20: Summary Statistics for
Page 135 and 136: In-Vehicle Exposures In-vehicle exp
Page 137 and 138: Table 7.30: Average of Mean In-Vehi
Page 139 and 140: e similar to those in other U.S. st
Page 141 and 142: vehicle); the total amount of time
Page 143 and 144: use of small non-road engine equipm
Page 145 and 146: Children may be exposed to benzene
Page 147 and 148: Table 7.36: Typical School Year Wee
Page 149 and 150: An addition of less than 1 µg/m 3
Page 151 and 152: In the mid-1990s, the American Petr
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Table 7.44: Dermal Benzene Absorpti
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Table 7.47: Product Names and Manuf
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Table 7.49: Summary of Age-Specific
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For children and non-smoking adults
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Benzene Exposure (mg/kg-day) Figure
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ackground pathways of exposure, inc
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8.1.3 EPA Default Risk Assessment N
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8.2.1 Potential for Increased Sensi
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These findings illustrate examples
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information associated with benzene
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species are more sensitive than oth
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8.2.3.1 Point of Departure for Non-
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Cancer risks were calculated using
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NONCANCER HAZARD QUOTIENT 1.00 0.09
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Table 8.1. Derivation of noncancer
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Table 8.3. Points of departure for
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Table 8.4. (cont.) Noncancer Hazard
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Table 8.5. Noncancer hazard quotien
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Table 8.6. Cancer risk estimates as
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Table 8.7. Indoor air comparison (i
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Table 8.9. Noncancer margins of saf
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Table 8.10. Noncancer margins of sa
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Table 8.11. Indoor air comparison (
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Table 8.13. (cont.) Notes: Cancer M
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the continental U.S. for each leuke
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in significant reductions in benzen
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Aksoy M (1977) Leukemia in workers
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Austin, C.C., Wang, D., Ecobichon,
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Buckley, J.D., Ribison, L.L., Swoti
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CONCAWE. 1996. Scientific basis for
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Ding, X-J, Li, Y., Ding, Y. el al.
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Forni, A. 1994. Comparison of chrom
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Goldwater LJ (1941) Disturbances in
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Hsieh, G.C., Parker, R.D., and Shar
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Jo, W.K. and Park, K.H. 1998. Expos
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Lange, A., Smolik, R., Zatonski, W.
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Lynge E, Andersen A, Nilsson R, Bar
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Meadows, A., Obringer, A. M. O., Ba
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Nedelcheva V, Gut I, Soucek P, Tich
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Picciani, D. 1979. Cytogenetic stud
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Ross D, Siegel D, Gibson NW, Pachec
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Sathiakumar, N., Delzell, E., Cole,
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Smith, M. T., Zhang, L. P., Wang, Y
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Thomas, K.W., Pellizzari, E.D., Cla
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United States Environmental Protect
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URS. 2002. Air Quality Trend in the
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Weisel, C.P. 2002. Assessing exposu
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Xing, S.G., Shi, X., Wu, Z.L., Chen
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(VCCEP) Tier 1 Pilot Submission for BENZENE - Tera

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