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42 Information gaps identified in this report are described in the following sections. 8.1 Emissions-Related Knowledge Gaps These information gaps affect the accuracy of emission inventories (and any related health risk assessments). 8.1.1 Effect of Temperature on Aircraft HAP Emissions Near Idle HAP emission rates can vary by well over a factor of 3 within the range of conditions encountered by many airports. There are no measurements at subfreezing temperatures, even though a significant portion of annual aviation activity occurs during such conditions. 8.1.2 Characterization of True Idle Levels and Times-in-Mode Since the gas-phase HAP emissions are dominated by the idle phase, knowledge of actual idle times is necessary. Addi- tionally, since the emission factor is a strong function of throttle setting, knowledge of the real-world power levels used are necessary. Emission indices for true ground idle (sometimes labeled 4%) can be a factor of 2+ greater than the 7% ICAO certification point. The likely distribution of throt- tle settings used as the aircraft progresses from the terminal to the runway (or the taxi-phase of an LTO) is unknown. This time-in-mode problem is probably highly variable and dependent on the frequency of flights. This problem does not lend itself to a simple relationship expressed as total emis- sions per LTO. Since most emission inventories (i.e., those made under NEPA requirements) are required to consider average condi- tions and not worst-case scenarios, day-to-day variability or the impact of severe delays are not captured, nor is plane-to- plane variability. Any attempt to quantify the health risk posed by acute effects of HAPs must accurately account for situations in which emissions and concentrations are highest (e.g., long delays, low mixing heights, etc). 8.1.3 Full Characterization of HAP Emissions Near Idle Thrust Measurements of HAP emissions indices have been per- formed at a limited number of power levels near idle (e.g., at APEX1,2,3 the common engine thrust settings were 4%, 7%, and 15%). A significant amount of interpolation is required to portray the effect of engine power on emission indices. 8.1.4 Single-Engine Taxiing As discussed in Section 5.1.3, the prevalence of single- engine taxiing is unclear, though anecdotally is thought to be rare. If actually prevalent, this could have a large impact on emission inventories. 8.1.5 General Aviation Emissions Characterization With the exception of lead emissions, which are well char- acterized, emissions from the general aviation category of piston engines are largely unknown. 8.1.6 Breadth of Measurements Across Engine Types The APEX campaigns increased the total number of com- mercial turbofan engines characterized to more than 10. This is not necessarily a representative sample of aircraft engines. There are scant data on the variation of hydrocarbon emis- sions with engine age and maintenance history. S E C T I O N 8 Crucial Knowledge Gaps
8.1.7 Uncertainties Persist in the Measurement of Reactive Aldehydes Despite the apparent importance of acrolein, its quantita- tive detection remains elusive. This is true for glyoxal, methylglyoxal, and crotonaldehyde as well. 8.2 Dispersion Models and the Atmospheric Evolution of Hazardous Air Pollutants The following knowledge gaps affect the airport commu- nityâs ability to predict accurately HAP concentrations near airports, to discern the impact of airports on local air quality, and to identify which airport sources are most important for determining health risks. 8.2.1 Measurements of Ambient HAP Concentrations Near Airports Even though numerous studies have focused on ambient HAP measurements near airports, the challenge of unam- biguously assigning an airport contribution and quantifying source apportionment remains largely unmet. Few studies have been able to distinguish airport versus urban sources or aircraft versus non-aircraft sources, as they have mostly relied on VOC sampling with low temporal resolution (canister sampling with subsequent GC analysis). Furthermore, these studies have been limited in duration. Comparison with dispersion/chemistry models would be beneficial to both model validation and source apportionment. 8.2.2 Validation of Dispersion Models The model currently required by the FAA for airport air quality assessments, EDMS, is inadequate for predicting at- mospheric concentrations of HAPs since it does not possess any chemical transformation mechanisms. Without these mechanisms, concentrations of HAPs can only be predicted as if they were stable gases (similar to carbon monoxide). This is inappropriate and does not allow realistic assessments of exposure. The ability of any dispersion model, whether it incorporates such mechanisms or not, to predict accurately absolute concentrations of both criteria pollutants and HAPs at various locations near an airport must be validated with concerted measurements of pollutant concentrations. 8.2.3 Identification of the Emission Sources Most Important to On-Airport and Off-Airport Exposure Although aircraft are generally the largest emission source of HAPs at an airport, they do not necessarily impact the health risk of various exposure groups the most, given the variation in the spatial and temporal relationship between the multiple airport emission sources (aircraft, GSE, termi- nal traffic, etc.) and potential exposure groups (e.g., nearby residents, airport-based workers, passengers). Identification of the emission sources that most greatly impact the health risk of various exposure groups has not been thoroughly examined. 8.3 Health Effects of Specific Hazardous Air Pollutants In this section we discuss critical data gaps for HAPs with potentially significant exposures. Specifically, for several of the HAPs there are no currently established toxicity criteria, including for many of the low-molecular weight aldehydes, the alkenes 1-pentene and 1-hexene, and the petroleum hydrocarbon 2,2,4-trimethylpentane (2,2,4-TMP). 8.3.1 Glyoxal and Methylglyoxal There is very little information regarding the toxicity of the aldehydes glyoxal and methylglyoxal. As discussed above, these aldehydes are mutagenic and may also be carcinogenic (IARC 1991; NEG 1995; Vaca, Nilsson et al. 1998). Glyoxal also has immunologic properties, can cause contact der- matitis, and is considered a strong human contact sensitizer (NEG 1995). There are no studies available, however, to eval- uate effects of long-term exposure to either of these reactive aldehydes. 8.3.2 Low-Molecular Weight Aldehydes There are very little data to evaluate the potential effects of long-term inhalation exposure to some of the low-molecular weight aldehydes that also have potentially significant expo- sures. These include the straight chain aldehydes propanal (propionaldehyde), butanal, and hexanal; and the 2-alkenal crotonaldehyde (butenal). Based on structural similarity to formaldehyde and acetaldehyde, the straight chain aldehydes could have carcinogenic potential, although this potential is expected to decrease with increasing molecular weight. In one study, crotonaldehyde induced liver tumors in rats exposed via drinking water (Chung, Tanaka, and Hecht 1986). The effect was not dose-related, however, which complicates interpretation of this observation. 8.3.3 Alkenes There is very little toxicity information for several of the alkenes that also have potentially significant exposures, including for ethene, 1-butene, 1-pentene, and 1-hexene. For 43
this analysis the researchers identified only one chronic study for evaluating toxicity of ethene (Hamm, Guest, and Gent 1984) and one subchronic study for evaluating inhalation toxicity of 1-hexene (Gingell, Bennick, and Malley 1999). Additional chronic studies with ethene and 1-hexene in a different species would reduce uncertainty associated with potential toxicity of these two alkenes. We did not identify any studies for evaluat- ing inhalation toxicity of 1-butene or 1-pentene. 8.3.4 2,2,4-Trimethylpentane The research team only identified one study involving in- halation exposure to 2,2,4-TMP; it evaluated kidney toxicity of 2,2,4-TMP at only one exposure concentration (Short et al. 1989, as cited in U.S. EPA 2006). Short et al. found that 2,2,4- TMP promoted development of neoplastic lesions in the kid- neys of male but not female rats. Results from other studies indicate that the ability of 2,2,4-TMP to induce kidney nephropathy is due to binding of 2,2,4-TMP to the protein alpha-2µ-globulin (e.g., Dietrich and Swenberg 1991), and EPA has concluded that kidney nephropathy associated with the alpha-2µ-globulin protein is relevant to humans (USEPA 1991d). Nonetheless, toxicity of 2,2,4-TMP should be evalu- ated in a subchronic or chronic inhalation concentration- response study, to determine whether there are effects in other tissues besides the kidney. 44
