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43 8.1.7 Uncertainties Persist in the health risk of various exposure groups the most, given the Measurement of Reactive Aldehydes variation in the spatial and temporal relationship between the multiple airport emission sources (aircraft, GSE, termi- Despite the apparent importance of acrolein, its quantita- nal traffic, etc.) and potential exposure groups (e.g., nearby tive detection remains elusive. This is true for glyoxal, residents, airport-based workers, passengers). Identification methylglyoxal, and crotonaldehyde as well. of the emission sources that most greatly impact the health risk of various exposure groups has not been thoroughly 8.2 Dispersion Models and the examined. Atmospheric Evolution of Hazardous Air Pollutants 8.3 Health Effects of Specific The following knowledge gaps affect the airport commu- Hazardous Air Pollutants nity's ability to predict accurately HAP concentrations near In this section we discuss critical data gaps for HAPs with airports, to discern the impact of airports on local air quality, potentially significant exposures. Specifically, for several of and to identify which airport sources are most important for the HAPs there are no currently established toxicity criteria, determining health risks. including for many of the low-molecular weight aldehydes, the alkenes 1-pentene and 1-hexene, and the petroleum 8.2.1 Measurements of Ambient HAP hydrocarbon 2,2,4-trimethylpentane (2,2,4-TMP). Concentrations Near Airports Even though numerous studies have focused on ambient 8.3.1 Glyoxal and Methylglyoxal HAP measurements near airports, the challenge of unam- biguously assigning an airport contribution and quantifying There is very little information regarding the toxicity of source apportionment remains largely unmet. Few studies the aldehydes glyoxal and methylglyoxal. As discussed above, have been able to distinguish airport versus urban sources or these aldehydes are mutagenic and may also be carcinogenic aircraft versus non-aircraft sources, as they have mostly relied (IARC 1991; NEG 1995; Vaca, Nilsson et al. 1998). Glyoxal on VOC sampling with low temporal resolution (canister also has immunologic properties, can cause contact der- sampling with subsequent GC analysis). Furthermore, these matitis, and is considered a strong human contact sensitizer studies have been limited in duration. Comparison with (NEG 1995). There are no studies available, however, to eval- dispersion/chemistry models would be beneficial to both uate effects of long-term exposure to either of these reactive model validation and source apportionment. aldehydes. 8.2.2 Validation of Dispersion Models 8.3.2 Low-Molecular Weight Aldehydes The model currently required by the FAA for airport air There are very little data to evaluate the potential effects of quality assessments, EDMS, is inadequate for predicting at- long-term inhalation exposure to some of the low-molecular mospheric concentrations of HAPs since it does not possess weight aldehydes that also have potentially significant expo- any chemical transformation mechanisms. Without these sures. These include the straight chain aldehydes propanal mechanisms, concentrations of HAPs can only be predicted (propionaldehyde), butanal, and hexanal; and the 2-alkenal as if they were stable gases (similar to carbon monoxide). This crotonaldehyde (butenal). Based on structural similarity to is inappropriate and does not allow realistic assessments of formaldehyde and acetaldehyde, the straight chain aldehydes exposure. The ability of any dispersion model, whether it could have carcinogenic potential, although this potential is incorporates such mechanisms or not, to predict accurately expected to decrease with increasing molecular weight. In one absolute concentrations of both criteria pollutants and HAPs study, crotonaldehyde induced liver tumors in rats exposed at various locations near an airport must be validated with via drinking water (Chung, Tanaka, and Hecht 1986). The concerted measurements of pollutant concentrations. effect was not dose-related, however, which complicates interpretation of this observation. 8.2.3 Identification of the Emission Sources Most Important to On-Airport 8.3.3 Alkenes and Off-Airport Exposure There is very little toxicity information for several of the Although aircraft are generally the largest emission source alkenes that also have potentially significant exposures, of HAPs at an airport, they do not necessarily impact the including for ethene, 1-butene, 1-pentene, and 1-hexene. For

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44 this analysis the researchers identified only one chronic study of 2,2,4-TMP at only one exposure concentration (Short et al. for evaluating toxicity of ethene (Hamm, Guest, and Gent 1984) 1989, as cited in U.S. EPA 2006). Short et al. found that 2,2,4- and one subchronic study for evaluating inhalation toxicity of TMP promoted development of neoplastic lesions in the kid- 1-hexene (Gingell, Bennick, and Malley 1999). Additional neys of male but not female rats. Results from other studies chronic studies with ethene and 1-hexene in a different species indicate that the ability of 2,2,4-TMP to induce kidney would reduce uncertainty associated with potential toxicity of nephropathy is due to binding of 2,2,4-TMP to the protein these two alkenes. We did not identify any studies for evaluat- alpha-2-globulin (e.g., Dietrich and Swenberg 1991), and ing inhalation toxicity of 1-butene or 1-pentene. EPA has concluded that kidney nephropathy associated with the alpha-2-globulin protein is relevant to humans (USEPA 1991d). Nonetheless, toxicity of 2,2,4-TMP should be evalu- 8.3.4 2,2,4-Trimethylpentane ated in a subchronic or chronic inhalation concentration- The research team only identified one study involving in- response study, to determine whether there are effects in halation exposure to 2,2,4-TMP; it evaluated kidney toxicity other tissues besides the kidney.