PUBLIC HEALTH ASSESSMENT
NAVAL AIR STATION FALLON
(a/k/a FALLON NAVAL AIR STATION)
FALLON, CHURCHILL COUNTY, NEVADA
APPENDIX D: KEROSENE-BASED JET FUEL: JET PROPULSION FUEL-8 (JP-8) AND COMMERCIAL JET FUEL (JET A)
Background:
Jet fuels are one of the primary fuels for turbine engines worldwide and are the most widely available aviation fuels. Commercial illuminating kerosene was the fuel chosen for early jet engines because of its availability compared to gasoline during wartime. As a result, the development of commercial jet aircraft following WWII centered primarily on the use of kerosene-type fuels. Thus, many commercial jet fuels today have basically the same composition as kerosene, but are under more stringent specifications than those for kerosene (Irwin 1997). Jet Propulsion Fuel (JP-8) is basically the same as jet fuel used by the commercial airline industry (i.e. Jet A), except for performance enhancing additives. JP-8 has been used by the militaries of some North Atlantic Treaty Organization (NATO) countries since 1972 and since 1992-1996 by the US Air Force, the US Army and the Japanese Self-Defense Forces.
Approximately 60 billion gallons of JP-8 (F-34 international designation) and the commercial jet equivalents Jet A (domestic flights) and Jet A-1 (international flights) are used internationally on an annual basis, with approximately half being used in the US (Ritchie et al. 2001a).
Jet fuel (JP-8 and Jet A) is mixture of many chemicals, with the primary component being kerosene (>98%). Most petroleum products are made from crude oil. Crude oil contains primarily hydrocarbon compounds linked in chains of different carbon lengths. Gasoline is a blend of compounds with shorter carbon chains. Kerosene is a blend of the middle distillate or medium carbon chain compounds. Diesel fuel and home heating fuel contain longer carbon chain compounds. Gasoline typically contains more benzene and benzene-containing compounds than kerosene and diesel fuel.
Kerosene normally has a boiling range well above the boiling-point of benzene; accordingly, the benzene content of JP-8 is usually below 0.02%. In the United States, gasoline typically contains less than 1% benzene by volume, but in other countries the benzene concentration may be as high as 5% (ATSDR 2000).
Human Health Considerations:
This section of the document describes the health effects, both non-cancer and cancer, in animals and humans (where available) following exposure to raw fuel and emission via different routes of exposure.
Non-cancer:
The main acute health hazard associated with JP-8 is aspiration in to the lungs, of liquid JP-8, such as might occur if the fuel is accidentally swallowed. This can occur by directly inhaling liquid droplets or indirectly as a result of inhaling vomit containing JP-8. can be aspirated in to the lungs (directly or indirectly via vomiting).
JP-8 can cause irritation, redness, skin rash, and the perception of skin heat or burning when in contact with the skin, usually as a result of prolonged contact. Due to the physical and chemical characteristics of JP-8, it does not easily wash off the skin. Repeated and/or long-term skin exposure can result in defatting of the skin and dermatitis. Ullrich (1999) reported that dermal exposure (uncovered multiple or single large dose) to JP-8 in female mice resulted in immune suppression. The immunosuppressive effects occurred 24-48 hours post-exposure. Immunosupressive effects have not been reported in military personnel working acutely/chronically with JP-8. Wolfe et al. (1997) reported on the health effects associated with short-term exposure to JP-8 in animals. In rabbits, 4 hour dermal exposure resulted in slight erythema. In rats, inhalation exposure to concentrations greater than 3,000 mg/m3 resulted in eye and upper respiratory irritation.
There are two reported human neurotoxicity studies regarding chronic effects of repeated exposure to JP-4/JP-8. Smith et al. (1997) reported that military workers exposed to JP-4/JP-8 for nine months exhibited significantly increased postural sway patterns, but only under the most difficult testing condition. McInturf et al. (2001) reported that USAF personnel exposed to JP-8 for at least 4 months, showed a significant deficit in two parameters of eye blink response. There are multiple animal studies regarding the neurotoxicity of JP-8. Ritchie et al. (2001b) provides a review of the neurotoxicity of selected hydrocarbon fuels.
Several animal studies have reported immunosupression following dermal exposure to raw JP-8 or by inhalation to JP-8 aerosol (Harris et al. 1997a,b and 2000; Ullrich, 1999; and Ullrich and Lyons 2000). The animals were exposed to JP-8 at concentrations and via routes that would represent exposures seen in military personnel working directly with JP-8. Based on modeling results and distance from the potential source, offsite residents are not expected to have JP-8 exposure at levels resulting in immunosuppression. We do not know if JP-8 jet fuel is immunosuppressive in humans, but it appears that the mouse is more sensitive.
It should be noted that, in general, military personnel working with jet fuel are exposed to higher concentrations on a more frequent basis than the general population with reports of limited health effects. Pleil et al. (2000) reported that military fuel system maintenance personnel had the highest overall exposure to JP-8 compounds. Whereas, military personnel exposed to aircraft exhaust in typical outdoor settings have measurable exposure at least 10 times less than the fuel system maintenance workers. Also, there was a slight measurable elevation in JP-8 compounds in personnel at air force bases without direct aircraft or jet fuel contact as compared to the general public. The mean level of benzene in breath of nonsmoking personnel was 1.92 ug/m3 for controls and 5.43 ug/m3 for the exposed workers, with smoking providing an additional 400% incremental mean body burden of benzene. Additionally, air modeling indicates that off-site concentrations of benzene (0.222 ug/m3) are below levels of health concern for acute and chronic effects (see Table 5 of Appendix C). Therefore, it is not expected that lower levels of exposure to jet fuel vapors and emissions typically seen in the general population would result in adverse health effects.
Cancer:
Human or other animal cancer studies regarding JP-8 exposure could not be located. The International Agency for Research on Cancer (IARC) has concluded that there is insufficient information available to determine if jet fuels cause cancer.
There are limited epidemiological data regarding cancer in humans following chronic inhalation exposure to kerosene. Studies have shown that no association, between the use of kerosene stoves for cooking and bronchial cancer, was found among nonsmoking females (ATSDR 1996).
Long term exposure to levels of benzene much higher than that modeled for Fallon (see Table 5 of Appendix C) or expected from exposure to gasoline, jet fuel, and/or jet exhaust emissions has been shown to cause cancer in humans and animals (see leukemia discussion in next section). The Department of Health and Human Services (DHHS) and IARC have determined that benzene is a human carcinogen.
Emissions from vehicles and airplanes contain volatile organic compounds, including 1,3-butadiene and formaldehyde. The DHHS has determined that 1,3-butadiene is a human carcinogen and formaldehyde is a probable human carcinogen. Studies in animals, as low as 6.25 ppm, have shown that 1,3-butadiene is carcinogenic in mice and rats at multiple organ sites (EPA 1998). Human epidemiologic studies have reported an association between 1,3-butadiene exposure and lymphatic leukemia in styrene-butadiene rubber workers. It's important to note that there is a lack of quantitative exposure data in the monomer plant workers and the polymer plant workers exposure data is limited but suggest that concentrations greater than 1 ppm for years are necessary to increase the risk of cancer in workers. Ambient air levels of 1,3-butadiene in urban and suburban locations ranged from 0.10 to 0.46 ppb while levels in smoke-filled bars ranged from 1.2 to 8.4 ppb (EPA 1998). The modeled annual average air concentration for 1,3-butadiene from aircraft emissions at Naval Air Station Fallon was estimated to be 0.3 ppb (see Table 5 of Appendix C). Formaldehyde has been shown to cause nasal cancer in animals. Excess mortality from leukemia and brain cancer was generally not seen among industrial workers, which suggests that the excess for these cancers among workers is due to something other than formaldehyde.
JP-8, gasoline and emissions from airplanes and vehicles contain polycyclic aromatic hydrocarbons (PAHs) and nitro-PAHs. The addition of performance additives to vehicle fuel can increase PAH emissions (Mi et al. 1998). The DHHS and IARC have determined that certain PAHs are probable human carcinogens.
Leukemia:
There are several types of leukemia. They are grouped two ways: (1) by how quickly the disease develops and (2) by the type of blood cell affected. Leukemia is either acute or chronic. Leukemia can appear in either of two major types of white blood cells - lymphoid cells or myeloid cells.
Acute myelogenous leukemia (AML), also referred to as Acute Non-Lymphocytic Leukemia is the most common tumor associated with benzene exposure. Some scientists believe the evidence demonstrates that benzene-induced leukemia is only of the AML type (Snyder and Kalf 1994; Crump 1994; and Irons and Stillman 1996). Crump (1994) reported that the dose response between benzene exposure and leukemia mortality in the Pliofilm cohort was due to AMLs and consideration of other types of leukemia diluted the dose response. Epidemiologic data have suggested that a threshold of at least 200 ppm-years of benzene exposure in air is necessary to increase the risk of AML (Raabe and Wong, 1996; Crump, 1994).
EPA (1997) states that the primary type of lymphohematopoietic cancer induced by chemicals and radiation in humans is myeloid leukemia, that administration of human leukemia-inducing agents in mice results in more lymphohematopoietic tumors, and that mice are more responsive than rats to the induction of lymphohematopoietic neoplasia following administration of human leukemogens. Additionally, the origin of the resulting neoplasms in mice and rats are primarily lymphoid.
Acute lymphocytic leukemia (ALL) is the most common type (approximately 75%) of leukemia in young children. It can also affect adults, especially those age 65 and older. Malignancies in this disease can arise from either T-cell or B-cell lymphocytes. The majority (~80%) of ALL cases arise from the B-cell lymphocytes. The causes of ALL are not known, but experts believe that a combination of genetic and environmental factors are instrumental.
The ALL incidence rate peaks in children between the ages of two and three. Caucasian children are more likely to get ALL than African American children. Several genetic mutations associated with ALL have been identified. The majority of leukemias have genetic rearrangements, called translocations. A translocation occurs when some genetic material (genes) on a chromosome is altered, or moved, between a pair of chromosomes. The most common translocation in ALL is t(12;21), which represents a genetic shift between chromosome 12 and 21. It (t(12;21)) occurs in approximately 20-25% of ALL patients. Approximately 20% of adults and 5% of children with ALL have a genetic shift called Philadelphia (Ph) chromosome (t(9;22)).
Certain inherited diseases can increase the risk for leukemia. Children with Down's syndrome have a 20-fold increased risk of developing acute leukemia versus the general population.
Scientists are studying viruses and other infectious agents that may cause leukemia. For example, Kinlen and Balkwill (2001) compared childhood leukemia mortality in wartime and postwar cohorts of Orkney and Shetland children. In Orkney and Shetland (the UK's northernmost islands), during World War II, local people were outnumbered by servicemen stationed there in case of a northern invasion. Childhood leukemia increased 3.6-fold, (p=0.001) in the wartime, but not in the postwar, cohort compared with national Scottish rates. Ross et al. (1999) investigated seasonal variations in the diagnosis of childhood cancer in the US. Overall there was not a significant seasonal variation for all childhood cancers combined. However for diagnosis-specific malignancies, there was a significant seasonal variation for ALL (peak in summer), rhabdomyosarcoma (peak in spring/summer), and hepatoblastoma (peak in summer). Additionally, when cancer cases were evaluated for latitudes greater than 40 degrees north, seasonal patterns were apparent only for ALL and hepatoblastoma. Reno, NV and Fallon, NV are between 39 and 40 degrees north.
Some viruses called retroviruses cause leukemia in animals. One virus associated with human leukemia is human T-cell lymphtrophic virus type-1 (HTLV-1), which may cause some cases of adult acute T-cell leukemia. A virus causing ALL has not been found.
Exposure Considerations:
The general population can be exposed to jet fuel (JP-8 and Jet A) vapors and emissions in the air. EPA has conducted air quality studies near several commercial airports and in certain cities. The EPA (1993) reported that aircraft engines are major source contributors for several volatile organic compounds (1,3-butadiene, formaldehyde, and benzene) and polycyclic organic compounds/particulate matter.
People living near airports or military air bases may also be exposed to higher levels of jet fuel vapors than the general population. People are exposed to many of the same jet fuel chemicals at gasoline stations, in their garage, while using lawn mowers and other gasoline-powered tools, and near areas with vehicle traffic. Additionally, some people use kerosene heaters during cold weather seasons, which would also result in exposure to jet fuel chemicals (JP-8 and Jet A are >98% kerosene). People working in military and commercial jet fuel industries, where jet fuels are used, may be exposed to higher levels than the general population.
A chemical comparison of jet fuels and gasoline indicates that gasoline has a much higher benzene content (see C-1). Additionally, the difference between military and commercial jet fuel is in the performance enhancing additives. Some of the additives are formulated with hydrocarbons found in fuel (e.g., ethylbenzene and xylene), but none of the additives are considered leukemogenic. In general, it appears that as a source of air pollution in urban areas, motor vehicle emissions contribute more volatile organic compounds (including benzene, 1,3-butadiene and formaldehyde) than jet engine emissions.
Table D-1: General Chemical Comparison between JP-8, Jet A and Unleaded Gasoline
| Chemicals | JP-8 | Jet A | Unleaded Gasoline |
| Benzene | > 0.02% | >0.02% | > 1.0% |
| Primary constituents | >98% kerosene (C7 through C18 range) |
>98% kerosene (C7 through C18 range) |
>98% refined hydrocarbons (C4 through C12 range) |
| Additives (combined typically <0.2% by volume) |
antioxidants, metal deactivators, static dissipator, corrosion inhibitors, fuel system icing inhibitors, octane enhancers, ignition controllers, detergents & dispersants |
antioxidants, |
antioxidants, metal deactivators, static dissipator, corrosion inhibitors, fuel system icing inhibitors, octane enhancers, ignition controllers, detergents & dispersants |
Exposure to benzene occurs during vehicle refueling. However, the exposure level can vary greatly depending on the environmental conditions and filling procedure. Exposure concentrations for benzene during vehicle refueling ranged from approximately 1.5 ppb to 1.3 ppm (Smith, 1999).
Ambient concentrations of benzene range from 2-19 ug/m3, with higher levels in urban areas (Wallace, 1996). Because approximately 85% of atmospheric benzene is from mobile sources (motor vehicles, airplanes,...), higher concentrations are often detected inside motor vehicles and adjacent to major roadways (Egeghy, 2000). Egeghy et al. (2000) indicated that benzene concentrations can be 3-8 times higher inside vehicles than in ambient air and that the mean concentration of benzene in breath before refueling was 8.6 ug/m3. The mean level of benzene in breath immediately after refueling was 160 ug/m3. Interestingly, the reported background levels of benzene in breath of nonsmokers ranged from 0.8 to 5.3 ug/m3.
Aircraft activity considerations:
Aircraft activity and the resulting ground level emissions are defined by the landing and takeoff cycle (LTO). The LTO cycle operation modes are defined by standard power settings for aircraft. An LTO cycle is comprised of five components: approach, taxi/idle-in, taxi/idle-out, takeoff, and climbout (EPA, 1999). Generally, volatile organic compound emissions rates are highest when engines are operating at low power, such as when idling or taxiing. Taxi/idle time depends on airport specific operational procedures, and would generally be less at a military airbase.
In a U.S. Navy report (2000), hazardous pollutants from aircraft engine test cells were estimated. It was reported that approximately 94% of the total hazardous air pollutants emitted were formed during the idle mode. Interestingly, the idle mode only represented approximately 10% of the total fuel used during the engine test.
Table D-2: Comparison of aircraft activity (landing and take off cycle (LTO/year)) at three airports in the United States
| Fallon Naval Air Station | Reno/Tahoe International Airport | Chicago Midway Airport | Chicago O'Hare International Airport* |
| <50,000 LTO/year** | >130,000 LTO/year | >300,000 LTO/year | >800,000 LTO/year |
*Chicago O'Hare International Airport the one of the busiest
airports in the world.
**This does not include "touch and go" operations.
A 1993 EPA study of the cancer risks attributed to air pollution in Southwest Chicago reported that Chicago's Midway Airport (approximately 300,000 LTO/year) was in the top five pollutant source contributors. Road vehicle emissions were the number one contributor, with emissions from Chicago's Midway Airport ranking number five. In general this means that cars, trucks, buses and trains are the major contributors of carcinogens in Southwest Chicago (approximately 25% of the estimated cancer risk). Chicago's Midway Airport represented approximately 10% of the estimated cancer risk with road vehicles representing 25% (EPA, 1993). Table D-2 provides a comparison of the relative volume of traffic at Chicago O'Hare, NASF and Reno/Tahoe International Airport.
The Illinois EPA (IEPA) recently reported that emissions from Chicago O'Hare International Airport (one of the world's busiest airports) have an impact on air quality in adjacent communities, but that the impact did not result in levels higher than those found in a typical urban environment (IEPA, 2002).
Cancer Incidence near airports:
Most of the published hypothetical cancer risks associated with airports have been based on extrapolated probabilities to known carcinogens emitted (measured or estimated) from airplanes. Two studies investigated the cancer incidence of communities near airports. The Illinois Department of Pubic Health (2001) examined actual cancer incidence observed in communities near Chicago's O'Hare and Midway airports and the Washington State Department of Health (1999) similarly investigated Seattle's SeaTac airport. Both studies found no evidence to substantiate a clear and observable elevation of cancer cases among communities residing close to airports.
One would expect air concentrations of airplane and vehicle emissions to be greater near these airports as compared to the Fallon, NV area. The results of these epidemiologic studies suggest that cancer and leukemia rates associated with airplane emissions would not be elevated in the areas adjacent to the Fallon Naval Training Station.
Exposure to Chemical Mixtures:
ATSDR considered interactive effects (cumulative, additive, synergistic, and antagonistic) of chemicals following exposure to multiple chemicals to the extent of the scientific knowledge in this area. ATSDR has reviewed the scientific literature surrounding chemical interactions and noted that if the estimated exposure doses for individual contaminants detected at the site are below doses shown to cause adverse effects, then ATSDR considers that the combined effect of multiple chemicals is not expected to result in adverse health effects. Several animal and human studies (Berman et al. 1992; Caprino et al. 1983; Drott et al. 1993; Harris et al. 1984) have reported thresholds for interactions. Studies have shown that exposure to a mixture of chemicals is unlikely to produce adverse health effects as long as components of that mixture are detected at levels below the NOAEL for individual compounds (Seed et al. 1995; Feron et al. 1995). Additionally the absence of interactions at doses 10-fold or more below effect thresholds have been demonstrated by Jonker et al. (1990) and Groten et al. (1991). Specifically, in two separate subacute toxicity studies in rats (Groten et al. 1997; Jonker et al. 1993), adverse effects disappeared altogether as the dose was decreased to below the threshold level. Specific to fuel related exposures, ATSDR's review of physiologically based pharmacokinetic model predictions indicate that toluene, ethylbenzene, and xylene are not expected to influence (no interaction) the hematotoxic and carcinogenic effects of benzene at exposure concentrations below approximately 20 ppm of each component (ATSDR, 2002). For carcinogens, the interactions are more difficult to quantify at environmental doses because at the lower doses observed from environmental exposure a large study group (humans or animals) is needed for statistical significance. In an animal study, Takayama et al. (1989) reported that 40 substances tested in combination at 1/50 of their cancer effect level (CEL) resulted in an increase in cancer. However, Hasegawa et al. (1994) reported no increase in cancer when dosing animals at 1/100 of the CEL for 10 compounds. It should be noted that typical environmental exposures to chemicals (non-carcinogens and carcinogens) are greater than 1000 times below laboratory-induced health effect thresholds. In a review of a recently released 1970s study on binary mixtures of carcinogens in rats, Gough (2002) reported that testing chemicals in pairwise combinations produced no convincing evidence for synergistic carcinogenic interactions and by contrast, the same tests produced several examples of antagonism.
Summary:
The majority of leukemia cases (15/16) in Fallon, NV are the acute lymphocytic leukemia (ALL) type. This would suggest that these leukemias resulted from something other than exposure to benzene, since benzene related leukemia is predominantly of the AML type. A review of the chemical composition of jet fuel (JP-8 and Jet A) found no other compounds, including additives, that are considered to cause leukemia. Incomplete combustion of a variety of fuels, including wood, gasoline, tobacco, gasoline, diesel fuel and jet fuel produces 1,3-butadiene. An association between 1,3-butadiene and lymphatic leukemia has been reported in styrene-butadiene workers at levels higher than that found in ambient air adjacent to an airport. Based on several air toxic compound investigations surrounding airports, more benzene, 1,3-butadiene, and formaldehyde are produced from vehicles than airplanes. Based on ATSDR's review, it appears that exposure to emissions from airplanes (commercial and military) in the Fallon, NV area is not responsible for the ALL reported in the community.
References:
ATSDR: Case Studies in Environmental Medicine - Benzene Toxicity. April 2000. ATSDR Publication Number: ATSDR-HE-CS-2001-0003.
ATSDR: Interaction Profile for: benzene, toluene, ethylbenzene, and xylenes (BTEX). Atlanta, GA: US Department of Health and Human Services; DRAFT for Public Comment, May 2002.
ATSDR: Toxicological Profile for Jet Fuels (JP-5 and JP-8). Atlanta, GA: US Department of Health and Human Services; August 1996.
Berman E, House DE, Allis JW, et al. 1992. Hepatotoxic interactions of ethanol with allyl alcohol or carbon tetrachloride in rats. J Toxicol Environ Health 37(1): 161-176.
Caprino L, Borrelli F, Anonetti, et al. 1983. Sex-related toxicity of somatostatin and its interaction with pentobarbital and strychnine. Toxicol Lett 17:145-149.
Childers JW, Witherspoon CL, Smith LB, and Pleil JD. 2000. Real-time and integrated measurement of potential exposure to particle-bound polycyclic aromatic hydrocarbons (PAHs) from aircraft exhaust. Environ Health Perspect. 108(9):853-862.
Crump KS. 1994. Risk of benzene-induced leukemia: a sensitivity analysis of the piloform cohort with additional follow-up and new exposure estimates. J Toxicol Environ Health 42:219-242.
Drott P, Meurling S, Gebre-Medhin M. 1993. Interactions of vitamins A and E and retinol-binding protein to healthy Swedish children---evidence of thresholds of essentiality and toxicity. Scand J Clin Lab Invest 53:275-280.
Egeghy PP, Tornero-Velez R, and Rappaport SM. 2000. Environmental and biological monitoring of benzene during self-service automobile refueling. Environ Health Perspect. 108(12):1195-1202.
EPA. 1993. Estimation and Evaluation of Cancer Risks Attributed to Air Pollution in Southwest Chicago. Final Summary Report. Submitted to: U.S.EPA Region 5 Air and Radiation Division by ViGYAN. EPA Contract No. 68-D0-0018. April 1993.
EPA. 1997. Chemical and Radiation Leukemogenesis in Humans and Rodents and the Value of Rodent Models for Assessing Risks of Lymphohematopoietic Cancers. National Center for Environmental Assessment-Washington Office. Office of Research and Development. EPA/600/R-97/090. May 1997.
EPA. 1998. Health risk assessment of 1,3-butadiene. National Center for Environmental Assessment. Office of Research and Development. NCEA-W-0267. January 1998.
EPA. 1999. Evaluation of Air Pollutant Emissions from Subsonic Commercial Jet Aircraft. EPA420-R-99-013. April 1999.
Feron VJ, Groten JP, van Zorge JA, Cassee FR, Jonker D, van Bladeren PJ. (1995). Toxicity studies in rats of simple mixtures of chemicals with the same or different target organs. Toxicol Lett, 82-83, 505-512.
Gough M. 2002. Antagonism-no synergism-in pairwise tests of carcinogens in rats. Regulatory Toxicology and Pharmacology, 35, 383-392.
Groten JP, Schoen ED, van Bladeren PJ, Kuper CF, van Zorge JA, Feron VJ. (1997). Subacute toxicity of a mixture of nine chemicals in rats: detecting interactive effects with a fractionated two-level factorial design. Fundam Appl Toxicol, 36(1), 15-29.
Groten JP, Sinkeldam EJ, Muys T, Luten JB, van Bladeren PJ. (1991). Interaction of dietary Ca, P, Mg, Mn, Cu, Fe, Zn and Se with the accumulation and oral toxicity of cadmium in rats. Food Chem Toxicol, 29(4), 249-258.
Harper CC, Faroon O, and Mehlman MA. 1993. Carcinogenic effects of benzene as a major component of gasoline and jet fuels. In E.J. Calabrese and P.T. Kostecki, eds., Hydrocarbon Contaminated Soils: Volume III. Lewis Publishers. 215-241.
Harris LW, Lennox WJ, Talbot BG, et al. 1984. Toxicity of anticholinesterases: Interactions of pyridostigmine and physostigmine with soman. Drug Chem Toxicol 7:507-526.
Harris DT, Sakiestewa D, Robledo RF, and Witten M. 1997a. Immunological effects of JP-8 jet fuel exposure. Toxicol Ind Health. 13(1): 43-55.
Harris DT, Sakiestewa D, Robledo RF, and Witten M. 1997b. Short-term exposure to JP-8 jet fuel results in long-term immunotoxicity. Toxicol Ind Health. 13(5): 559-570.
Harris DT, Sakiestewa D, Robledo RF, Young RS, and Witten M. 2000. Effects of short-term JP-8 jet fuel exposure on cell-mediated immunity. Toxicol Ind Health. 16(2): 78-84.
Hasegawa R, Miyata E, Futakuchi M, Hagiwara A, Nagao M, Sugimura T, et al. (1994). Synergistic enhancement of hepatic foci development by combined treatment of rats with 10 heterocyclic amines at low doses. Carcinogenesis, 15(5), 1037-1041.
IEPA. 2002. Final Report: Chicago O'Hare Airport Air Toxic Monitoring Program June-December, 2000. Illinois Environmental Protection Agency, Bureau of Air. May 2002.
Illinois Department of Public Health. 2001. Cancer Incidence in Populations Living Near
Chicago O'Hare and Midway Airports, Illinois 1987-1997. November 2001.
<http://www.idph.state.il.us/about/pdf/O'Harereportpdf.pdf 
> (As of 6/24/2002).
Irwin RJ, VanMouwerik M, Stevens L, Seese MD, and Basham W. 1997. Environmental Contaminants Encyclopedia: Jet Fuel 8. National Park Service, Water Resources Division, Fort Collins, Colorado.
Jonker D, Woutersen RA, van Bladeren PJ, Til HP, Feron VJ. (1993). Subacute (4-wk) oral toxicity of a combination of four nephrotoxins in rats: comparison with the toxicity of the individual compounds. Food Chem Toxicol, 31(2), 125-136.
Jonker D, Woutersen RA, van Bladeren PJ, Til HP, Feron VJ. (1990). 4-week oral toxicity study of a combination of eight chemicals in rats: comparison with the toxicity of the individual compounds. Food Chem Toxicol, 28(9), 623-631.
Kinlen LJ, Balkwill A. 2001. Infective cause of childhood leukaemia and wartime population mixing in Orkney and Shetland, UK. The Lancet: Volume 357: 858.
McInturf SM, Bekkedal MY, Ritchie GD, Nordholm AF and Rossi J. 2001. Effects of repeated JP-8 jet fuel exposure on eyeblink conditioning in humans. Abstract. The Toxicologist. 60(1): 555.
Mi HH, Lee WJ, Chen SJ, Lin TC, Wu TL, and Hu JC. 1998. Effect of gasoline additives on PAH emission. Chemosphere. 36(9): 2031-2041.
Pleil JD, Smith LB, Zelnick SD. 2000. Personal exposure to JP-8 jet fuel vapors and exhaust at air force bases. Environ Health Perspect. 108(3):183-192.
Raabe GK, and Wong O. 1996. Leukemia mortality by cell type in petroleum workers with potential exposure to benzene. Environ Health Perspect 104(6):1381-1392.
Ritchie GD, Bekkedal MY, Bobb AJ, and Still KR. 2001a. Biological and Health Effects of JP-8 Exposure. Report No. TOXDET 01-01. Naval Health Research Center Detachment (Toxicology), Wright-Patterson Air Force Base, Ohio.
Ritchie GD, Still KR, Alexander WK, Nordholm AF, Rossi J, and Mattie DR. 2001b. A review of the neurotoxicity risk of selected hydrocarbon fuels. J Toxicol Environ Health, B 4: 101-191.
Rogers, D. 2001. Electronic mail correspondence between Captain Roy Rogers (NASF) and Mary Ann Simmons (Navy Environmental Health Center). August 5, 2002.
Seed J, Brown RP, Olin SS, and Foran JA. (1995). Chemical mixtures: Current risk assessment methodologies and future directions. Regul. Toxicol. Pharmacol, 22, 76-94.
Smith RG. 1999. A study on benzene exposure during vehicle refueling. Maxxam Report#: 9900387 for the Health Protection Branch, Health Canada. Contract #: CCME#: 989-040. April 1999.
Smith LB, Bhattacharya A, Lemasters G, Succop P, Puhala E, Medvedovic M, and Joyce J. 1997. Effect of low-level exposure to jet fuel on postural balance of US Air Force personnel. J Occup Environ Med. Jul;39(7): 623-632.
Takayama S, Hasegawa H, Ohgaki H. (1989). Combination effects of forty carcinogens administered at low doses to male rats. Jpn J Cancer Res, 80(8), 732-736.
Ullrich SE. 1999. Dermal application of JP-8 jet fuel induces immune suppression. Toxicol Sci. 52(1): 61-67.
Ullrich SE and Lyons HJ. 2000. Mechanisms involved in the immunotoxicity induced by dermal application of JP-8 jet fuel. Toxicol Sci. 58(2): 290-298.
U.S. Navy. 2000. Hazardous Air Pollutants from Department of Defense Aircraft Engine Test Cells: Best Estimates. Aircraft Environmental Support Office, Naval Aviation Depot-North Island, San Diego, CA. AESO Report No. 2001-7. December 2000.
Wallace L. 1996. Environmental exposure to benzene: An update. Environ Health Perspect 104(Suppl 6):1129-1136.
Washington State Department of Health. 1999. Progress Report: Cancer Cluster Investigation,
SeaTac International Airport. Updated February 1999, Updated December 1999, Updated March
2000. <http://www.metrokc.gov/health/seatac/index.htm > (as of 6/26/02).
Wolfe RE, Kinead ER, Feldmann ML, Leahy HF, and Jederberg WW. 1997. Acute toxicity evaluation of JP-8 jet fuel and JP-8 jet fuel containing additives. Govt. Reports Announcements & Index (GRA&I), Issue 09.
APPENDIX E: RESPONSE TO PUBLIC COMMENTS
The Agency for Toxic Substances and Disease Registry (ATSDR) received two sets of comments during the public comment period (February 12, 2003 to March 17, 2003) for the NASF Public Health Assessment. Comments questioning the validity of statements made in the PHA, or comments correcting word spelling or sentence syntax, ATSDR reviewed the information, verified any inaccuracies, and made the necessary changes.
Comments generally consisted of a request for clarification or correction of technical statements made in the PHA. These clarifications or corrections related to the following topics: descriptions of the hydrology (e.g., aquifers, surface water, and drinking water wells) in the vicinity of NASF; and technical updates or clarifications on the programs to monitor and remediate contamination within NASF. Corrections or modifications were made in the document as appropriate.
The following comments required responses not readily incorporated into the text of the PHA.
Comment: "Page 2 Private Drinking Water Paragraph: There is no basis for the conclusion in that no data exist regarding communication between the intermediate and shallow alluvial aquifer systems in this area. Hydraulic gradients generally are believed to be upward from the intermediate aquifer into the shallow aquifer in this area, but no detailed studies have been done to quantify this relation in the areas east of NASF."
Response: Studies at hydrogeological investigations at NASF have shown that there is an upward hydraulic gradient from the intermediate aquifer to the shallow aquifer, thus preventing the downward migration of contaminants into the intermediate aquifer (Battelle 2001 - see references in main document). Although it is true that studies have not been conducted to confirm this relationship in the areas east of NASF, monitoring wells in the shallow aquifer near the station boundary have detected mostly very low concentrations of PAHs. ATSDR is confident that site-related contaminants in the shallow aquifer have not migrated off site at levels that would pose a health hazard.
Comment: "Page 3 Air paragraph. I believe this is misleading. While winds are predominantly from the north, west and south, occasionally the winds do blow to the north or northwest towards town. Releases during periods when the winds are in this minority direction would still distribute contaminants towards town. Also, several case locations were indeed downwind from NASF when considering only the predominant wind directions. This comment also applies to the second paragraph on page 10."
Response: The comment addresses ATSDR's presentation of prevailing wind patterns. The prevailing wind pattern is important to note in any evaluation of air exposures, because this pattern will determine the direction in which contaminants will blow most frequently. Our description of prevailing wind patterns is consistent with more than 5 years of meteorological data that have been collected in the area. Therefore, no changes have been made in the public health assessment in response to this comment.
More importantly, ATSDR emphasizes that the conclusions for air exposures are based on multiple lines of evidence, and not simply on the prevailing wind patterns. For instance, our conclusion regarding inhalation exposures to pollutants found in aircraft emissions is based on four different observations: (1) the results of our modeling analysis, which showed no evidence of elevated contamination; (2) the results of CDCs environmental and biological sampling, which did not find elevated levels of any chemicals in jet fuel and engine exhaust; (3) our review of epidemiological studies conducted at commercial airports having far greater landing and takeoff activity than NASF; and (4) the prevailing wind direction.
