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24 Assuming a standard 25-year occupational exposure duration, well as use of a subchronic rather than a chronic study, an at 250 days/year (USEPA 2004c), this exposure level would cor- acceptable exposure concentration could be as much as 1000- respond to an average daily exposure of approximately 0.2 ppm fold lower than this value, or approximately 0.6 mg/m3. As EtO. Accounting for uncertainty regarding susceptibility of with ethene, it does not appear that hexene would be a greater potentially sensitive subpopulations, as well as relative potency health concern than the HAPs identified in Table 1. of EtO and ethene as assessed by Walker, Yuh et al. (2000),11 a comparable ethene concentration for the general population 4.2.2.4 Toxicity Criteria Based could be on the order of 1 ppm, or approximately 1 mg/m3.12 As on Surrogate Compounds with potential noncancer toxicity of ethene, it does not appear that potential carcinogenicity of ethene relative to emissions For several airport-related HAPs without existing toxicity would be greater than that for other carcinogenic HAPs. criteria we considered toxicity of surrogate compounds in the same class of compounds, assuming that toxicity would be comparable based on structural similarity. These HAPs 4.2.2.2 Glyoxal and Methylglyoxal included the aldehydes propanal (propionaldehyde) and Glyoxal and methylglyoxal are mutagenic aldehydes with butanal, for which we used acetaldehyde as a surrogate; the two carbonyl groups (IARC 1991; NEG 1995). There are no alkene 1-butene for which we used propene as a surrogate; toxicity studies available for deriving toxicity criteria for these and the 2-alkenal crotonaldehyde for which we used acrolein two compounds, but the available data suggest they could be as a surrogate. Compounds were selected as surrogates based carcinogenic. For example, in addition to being mutagenic, on having similar functional groups (i.e., an aldehyde, a carbon- glyoxal significantly increased the incidence of stomach carbon double bond, or both) and similar molecular weight. tumors in rats pretreated with an N-methyl-N-nitro-N- For all of these HAPs, we used surrogate compounds with nitrosoguanidine (MNNG), which is both mutagenic and lower molecular weight. Because toxicity tends to decrease carcinogenic (NEG 1995). In an in vitro study, levels of DNA with increasing molecular weight within a given class of adducts at equivalent molar concentrations were approxi- compounds (Segovia, Crovetto et al. 2002), use of toxicity mately 20-fold higher for methylglyoxal as compared with criteria for these surrogate compounds should be health- acetaldehyde (Vaca, Nilsson et al. 1998). Considering that protective. Table 7 shows the chemical structures for these these two aldehydes may be at least as potent as acetaldehyde, HAPs and their corresponding surrogate compounds. As- and are emitted in fairly large quantities, they may represent suming comparable toxicity for these HAPs and their corre- a health concern that is comparable if not greater than that sponding surrogate compounds, both propanal (propi- for the prioritized HAPs identified in Table 1. onaldehyde) and crotonaldehyde may be important HAPs to consider in terms of their potential health concern. Note that EPA Region 9 lists a preliminary remediation goal 4.2.2.3 1-Hexene for crotonaldehyde of 3.5 10-3 g/m3, based on an unpublished We identified a toxicity criterion for 1-hexene based on a oral cancer slope factor.14 Considering that crotonaldehyde is 13-week inhalation study in rats by Gingell, Bennick, and likely to be reactive, health effects associated with exposure to Malley (1999). Rats were exposed to hexene for 6 hr/day, crotonaldehyde are expected to be localized to the route of 5 days/week to concentrations of 0, 300, 1,000, and 3,000 ppm exposure (i.e., respiratory system for inhalation exposures, gas- (0, 1,033, 3,443 and 10,330 mg/m3) and evaluated for clinical trointestinal tract for oral exposures) rather than systemic. As signs of toxicity including effects on liver, kidney, and blood, such, it would not be appropriate to evaluate inhalation expo- and tissues were evaluated for histopathological signs of tox- sures using an oral toxicity criterion. In any case, the toxicity icity. The NOAEL from this study was 3,443 mg/m3, based on criterion used in this analysis provides a more conservative (i.e., decreased weight gain in female rats and slight organ weight more potent) estimate of toxicity for crotonaldehyde. changes in both male and female rats at 10,330 mg/m3. This NOAEL was adjusted as above for ethene yielding an adjusted 4.3 Calculation of Risk-Based NOAEL of 615 mg/m3.13 Accounting for uncertainty related Concentrations for Chronic to inter- and intraspecies variability, database deficiencies, as Health Effects 11 According to Walker, Yuh, et al. (2000), an EtO concentration of 1 ppm cor- Risk-based concentrations (RBCs) for cancer and non- responds with an ethene concentration of approximately 40 ppm. cancer health effects were calculated as follows: 28.0536( MW ) 12 1 ppm = 1mg / m 3 14The Region 9 PRG Table lists U.S. Environmental Protection Agency's Health 24.45 Effects Assessment Summary Tables (HEAST) as the source for the oral CSR. 5 days 6 hours However, the most recent (1997) HEAST Tables do not provide any toxicity in- 13 3443 mg / m 3 24 hours = 615 mg / m 3 7 days formation for crotonaldehyde.