PUBLIC HEALTH ASSESSMENT
NAVAL AIR STATION FALLON
(a/k/a FALLON NAVAL AIR STATION)
FALLON, CHURCHILL COUNTY, NEVADA
Jet fuels are one of the primary fuels for turbine engines worldwide and are the most widelyavailable aviation fuels. Commercial illuminating kerosene was the fuel chosen for early jetengines because of its availability compared to gasoline during wartime. As a result, thedevelopment of commercial jet aircraft following WWII centered primarily on the use ofkerosene-type fuels. Thus, many commercial jet fuels today have basically the same compositionas kerosene, but are under more stringent specifications than those for kerosene (Irwin 1997). JetPropulsion 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 ofsome North Atlantic Treaty Organization (NATO) countries since 1972 and since 1992-1996 bythe 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 jetequivalents Jet A (domestic flights) and Jet A-1 (international flights) are used internationally onan 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 beingkerosene (>98%). Most petroleum products are made from crude oil. Crude oil containsprimarily hydrocarbon compounds linked in chains of different carbon lengths. Gasoline is ablend of compounds with shorter carbon chains. Kerosene is a blend of the middle distillate ormedium carbon chain compounds. Diesel fuel and home heating fuel contain longer carbonchain compounds. Gasoline typically contains more benzene and benzene-containingcompounds than kerosene and diesel fuel.
Kerosene normally has a boiling range well above the boiling-point of benzene; accordingly, thebenzene content of JP-8 is usually below 0.02%. In the United States, gasoline typically containsless than 1% benzene by volume, but in other countries the benzene concentration may be as highas 5% (ATSDR 2000).
Human Health Considerations:
This section of the document describes the health effects, both non-cancer and cancer, in animalsand humans (where available) following exposure to raw fuel and emission via different routes of exposure.
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 inhalingliquid droplets or indirectly as a result of inhaling vomit containing JP-8. can be aspirated in tothe lungs (directly or indirectly via vomiting).
JP-8 can cause irritation, redness, skin rash, and the perception of skin heat or burning when incontact with the skin, usually as a result of prolonged contact. Due to the physical and chemicalcharacteristics of JP-8, it does not easily wash off the skin. Repeated and/or long-term skinexposure can result in defatting of the skin and dermatitis. Ullrich (1999) reported that dermalexposure (uncovered multiple or single large dose) to JP-8 in female mice resulted in immunesuppression. The immunosuppressive effects occurred 24-48 hours post-exposure.Immunosupressive effects have not been reported in military personnel workingacutely/chronically with JP-8. Wolfe et al. (1997) reported on the health effects associated withshort-term exposure to JP-8 in animals. In rabbits, 4 hour dermal exposure resulted in slighterythema. In rats, inhalation exposure to concentrations greater than 3,000 mg/m3 resulted ineye and upper respiratory irritation.
There are two reported human neurotoxicity studies regarding chronic effects of repeatedexposure to JP-4/JP-8. Smith et al. (1997) reported that military workers exposed to JP-4/JP-8for nine months exhibited significantly increased postural sway patterns, but only under the mostdifficult testing condition. McInturf et al. (2001) reported that USAF personnel exposed to JP-8for at least 4 months, showed a significant deficit in two parameters of eye blink response. Thereare multiple animal studies regarding the neurotoxicity of JP-8. Ritchie et al. (2001b) provides areview of the neurotoxicity of selected hydrocarbon fuels.
Several animal studies have reported immunosupression following dermal exposure to raw JP-8or by inhalation to JP-8 aerosol (Harris et al. 1997a,b and 2000; Ullrich, 1999; and Ullrich andLyons 2000). The animals were exposed to JP-8 at concentrations and via routes that wouldrepresent exposures seen in military personnel working directly with JP-8. Based on modelingresults and distance from the potential source, offsite residents are not expected to have JP-8exposure at levels resulting in immunosuppression. We do not know if JP-8 jet fuel isimmunosuppressive 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 higherconcentrations on a more frequent basis than the general population with reports of limited healtheffects. Pleil et al. (2000) reported that military fuel system maintenance personnel had thehighest overall exposure to JP-8 compounds. Whereas, military personnel exposed to aircraftexhaust in typical outdoor settings have measurable exposure at least 10 times less than the fuelsystem maintenance workers. Also, there was a slight measurable elevation in JP-8 compoundsin personnel at air force bases without direct aircraft or jet fuel contact as compared to thegeneral public. The mean level of benzene in breath of nonsmoking personnel was 1.92 ug/m3for controls and 5.43 ug/m3 for the exposed workers, with smoking providing an additional400% 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 andchronic effects (see Table 5 of Appendix C). Therefore, it is not expected that lower levels ofexposure to jet fuel vapors and emissions typically seen in the general population would result inadverse health effects.
Human or other animal cancer studies regarding JP-8 exposure could not be located. TheInternational Agency for Research on Cancer (IARC) has concluded that there is insufficientinformation available to determine if jet fuels cause cancer.
There are limited epidemiological data regarding cancer in humans following chronic inhalationexposure to kerosene. Studies have shown that no association, between the use of kerosenestoves 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 5of Appendix C) or expected from exposure to gasoline, jet fuel, and/or jet exhaust emissions hasbeen 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 thatbenzene 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 humancarcinogen and formaldehyde is a probable human carcinogen. Studies in animals, as low as 6.25ppm, have shown that 1,3-butadiene is carcinogenic in mice and rats at multiple organ sites (EPA1998). Human epidemiologic studies have reported an association between 1,3-butadieneexposure and lymphatic leukemia in styrene-butadiene rubber workers. It's important to note thatthere is a lack of quantitative exposure data in the monomer plant workers and the polymer plantworkers exposure data is limited but suggest that concentrations greater than 1 ppm for years arenecessary to increase the risk of cancer in workers. Ambient air levels of 1,3-butadiene in urbanand suburban locations ranged from 0.10 to 0.46 ppb while levels in smoke-filled bars rangedfrom 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 (seeTable 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 industrialworkers, 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 aromatichydrocarbons (PAHs) and nitro-PAHs. The addition of performance additives to vehicle fuel canincrease PAH emissions (Mi et al. 1998). The DHHS and IARC have determined that certainPAHs are probable human carcinogens.
There are several types of leukemia. They are grouped two ways: (1) by how quickly the diseasedevelops 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 ormyeloid cells.
Acute myelogenous leukemia (AML), also referred to as Acute Non-Lymphocytic Leukemia isthe most common tumor associated with benzene exposure. Some scientists believe the evidencedemonstrates 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 responsebetween benzene exposure and leukemia mortality in the Pliofilm cohort was due to AMLs andconsideration of other types of leukemia diluted the dose response. Epidemiologic data havesuggested that a threshold of at least 200 ppm-years of benzene exposure in air is necessary toincrease the risk of AML (Raabe and Wong, 1996; Crump, 1994).
EPA (1997) states that the primary type of lymphohematopoietic cancer induced by chemicalsand radiation in humans is myeloid leukemia, that administration of human leukemia-inducingagents in mice results in more lymphohematopoietic tumors, and that mice are more responsivethan rats to the induction of lymphohematopoietic neoplasia following administration of humanleukemogens. Additionally, the origin of the resulting neoplasms in mice and rats are primarilylymphoid.
Acute lymphocytic leukemia (ALL) is the most common type (approximately 75%) of leukemiain young children. It can also affect adults, especially those age 65 and older. Malignancies inthis disease can arise from either T-cell or B-cell lymphocytes. The majority (~80%) of ALLcases arise from the B-cell lymphocytes. The causes of ALL are not known, but experts believethat a combination of genetic and environmental factors are instrumental.
The ALL incidence rate peaks in children between the ages of two and three. Caucasian childrenare more likely to get ALL than African American children. Several genetic mutationsassociated with ALL have been identified. The majority of leukemias have geneticrearrangements, called translocations. A translocation occurs when some genetic material(genes) on a chromosome is altered, or moved, between a pair of chromosomes. The mostcommon translocation in ALL is t(12;21), which represents a genetic shift between chromosome12 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 syndromehave 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. Forexample, Kinlen and Balkwill (2001) compared childhood leukemia mortality in wartime andpostwar cohorts of Orkney and Shetland children. In Orkney and Shetland (the UK'snorthernmost islands), during World War II, local people were outnumbered by servicemenstationed 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. Overallthere was not a significant seasonal variation for all childhood cancers combined. However fordiagnosis-specific malignancies, there was a significant seasonal variation for ALL (peak insummer), 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, NVare between 39 and 40 degrees north.
Some viruses called retroviruses cause leukemia in animals. One virus associated with humanleukemia is human T-cell lymphtrophic virus type-1 (HTLV-1), which may cause some cases ofadult acute T-cell leukemia. A virus causing ALL has not been found.
The general population can be exposed to jet fuel (JP-8 and Jet A) vapors and emissions in theair. 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 volatileorganic compounds (1,3-butadiene, formaldehyde, and benzene) and polycyclic organiccompounds/particulate matter.
People living near airports or military air bases may also be exposed to higher levels of jet fuelvapors than the general population. People are exposed to many of the same jet fuel chemicals atgasoline 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 coldweather 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 fuelsare 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 higherbenzene content (see C-1). Additionally, the difference between military and commercial jet fuelis in the performance enhancing additives. Some of the additives are formulated withhydrocarbons found in fuel (e.g., ethylbenzene and xylene), but none of the additives areconsidered 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.
|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)
(combined typically <0.2% by volume)
fuel system icing inhibitors,
detergents & dispersants
fuel system icing inhibitors,
detergents & dispersants
Exposure to benzene occurs during vehicle refueling. However, the exposure level can varygreatly depending on the environmental conditions and filling procedure. Exposureconcentrations for benzene during vehicle refueling ranged from approximately 1.5 ppb to 1.3ppm (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 andadjacent to major roadways (Egeghy, 2000). Egeghy et al. (2000) indicated that benzeneconcentrations can be 3-8 times higher inside vehicles than in ambient air and that the meanconcentration of benzene in breath before refueling was 8.6 ug/m3. The mean level of benzenein breath immediately after refueling was 160 ug/m3. Interestingly, the reported backgroundlevels 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 takeoffcycle (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, andclimbout (EPA, 1999). Generally, volatile organic compound emissions rates are highest whenengines are operating at low power, such as when idling or taxiing. Taxi/idle time depends onairport 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 formedduring the idle mode. Interestingly, the idle mode only represented approximately 10% of thetotal fuel used during the engine test.
|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 reportedthat Chicago's Midway Airport (approximately 300,000 LTO/year) was in the top five pollutantsource contributors. Road vehicle emissions were the number one contributor, with emissionsfrom 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 (approximately25% of the estimated cancer risk). Chicago's Midway Airport represented approximately 10% ofthe estimated cancer risk with road vehicles representing 25% (EPA, 1993). Table D-2 provides acomparison of the relative volume of traffic at Chicago O'Hare, NASF and Reno/TahoeInternational Airport.
The Illinois EPA (IEPA) recently reported that emissions from Chicago O'Hare InternationalAirport (one of the world's busiest airports) have an impact on air quality in adjacentcommunities, but that the impact did not result in levels higher than those found in a typicalurban environment (IEPA, 2002).
Cancer Incidence near airports:
Most of the published hypothetical cancer risks associated with airports have been based onextrapolated probabilities to known carcinogens emitted (measured or estimated) from airplanes. Two studies investigated the cancer incidence of communities near airports. The IllinoisDepartment of Pubic Health (2001) examined actual cancer incidence observed in communitiesnear 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 tosubstantiate a clear and observable elevation of cancer cases among communities residing closeto airports.
One would expect air concentrations of airplane and vehicle emissions to be greater near theseairports as compared to the Fallon, NV area. The results of these epidemiologic studies suggestthat cancer and leukemia rates associated with airplane emissions would not be elevated in theareas 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.
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 tobenzene, since benzene related leukemia is predominantly of the AML type. A review of thechemical composition of jet fuel (JP-8 and Jet A) found no other compounds, includingadditives, 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. Anassociation 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 onseveral air toxic compound investigations surrounding airports, more benzene, 1,3-butadiene, andformaldehyde are produced from vehicles than airplanes. Based on ATSDR's review, it appearsthat exposure to emissions from airplanes (commercial and military) in the Fallon, NV area is notresponsible for the ALL reported in the community.
ATSDR: Case Studies in Environmental Medicine - Benzene Toxicity. April 2000. ATSDRPublication 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 ofHealth and Human Services; August 1996.
Berman E, House DE, Allis JW, et al. 1992. Hepatotoxic interactions of ethanol with allylalcohol 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 itsinteraction with pentobarbital and strychnine. Toxicol Lett 17:145-149.
Childers JW, Witherspoon CL, Smith LB, and Pleil JD. 2000. Real-time and integratedmeasurement 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 piloformcohort 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 biologicalmonitoring 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 SouthwestChicago. Final Summary Report. Submitted to: U.S.EPA Region 5 Air and Radiation Divisionby ViGYAN. EPA Contract No. 68-D0-0018. April 1993.
EPA. 1997. Chemical and Radiation Leukemogenesis in Humans and Rodents and the Value ofRodent Models for Assessing Risks of Lymphohematopoietic Cancers. National Center forEnvironmental 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 EnvironmentalAssessment. 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). Toxicitystudies in rats of simple mixtures of chemicals with the same or different target organs. ToxicolLett, 82-83, 505-512.
Gough M. 2002. Antagonism-no synergism-in pairwise tests of carcinogens in rats. RegulatoryToxicology and Pharmacology, 35, 383-392.
Groten JP, Schoen ED, van Bladeren PJ, Kuper CF, van Zorge JA, Feron VJ. (1997). Subacutetoxicity of a mixture of nine chemicals in rats: detecting interactive effects with a fractionatedtwo-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. FoodChem Toxicol, 29(4), 249-258.
Harper CC, Faroon O, and Mehlman MA. 1993. Carcinogenic effects of benzene as a majorcomponent of gasoline and jet fuels. In E.J. Calabrese and P.T. Kostecki, eds., HydrocarbonContaminated Soils: Volume III. Lewis Publishers. 215-241.
Harris LW, Lennox WJ, Talbot BG, et al. 1984. Toxicity of anticholinesterases: Interactions ofpyridostigmine 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 jetfuel exposure. Toxicol Ind Health. 13(1): 43-55.
Harris DT, Sakiestewa D, Robledo RF, and Witten M. 1997b. Short-term exposure to JP-8 jetfuel 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-termJP-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 10heterocyclic 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 NearChicago 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. EnvironmentalContaminants Encyclopedia: Jet Fuel 8. National Park Service, Water Resources Division, FortCollins, Colorado.
Jonker D, Woutersen RA, van Bladeren PJ, Til HP, Feron VJ. (1993). Subacute (4-wk) oraltoxicity of a combination of four nephrotoxins in rats: comparison with the toxicity of theindividual compounds. Food Chem Toxicol, 31(2), 125-136.
Jonker D, Woutersen RA, van Bladeren PJ, Til HP, Feron VJ. (1990). 4-week oral toxicity studyof a combination of eight chemicals in rats: comparison with the toxicity of the individualcompounds. Food Chem Toxicol, 28(9), 623-631.
Kinlen LJ, Balkwill A. 2001. Infective cause of childhood leukaemia and wartime populationmixing in Orkney and Shetland, UK. The Lancet: Volume 357: 858.
McInturf SM, Bekkedal MY, Ritchie GD, Nordholm AF and Rossi J. 2001. Effects of repeatedJP-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 onPAH emission. Chemosphere. 36(9): 2031-2041.
Pleil JD, Smith LB, Zelnick SD. 2000. Personal exposure to JP-8 jet fuel vapors and exhaust atair force bases. Environ Health Perspect. 108(3):183-192.
Raabe GK, and Wong O. 1996. Leukemia mortality by cell type in petroleum workers withpotential 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 reviewof 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) andMary Ann Simmons (Navy Environmental Health Center). August 5, 2002.
Seed J, Brown RP, Olin SS, and Foran JA. (1995). Chemical mixtures: Current risk assessmentmethodologies 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. April1999.
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. JOccup Environ Med. Jul;39(7): 623-632.
Takayama S, Hasegawa H, Ohgaki H. (1989). Combination effects of forty carcinogensadministered 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. ToxicolSci. 52(1): 61-67.
Ullrich SE and Lyons HJ. 2000. Mechanisms involved in the immunotoxicity induced bydermal 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 TestCells: Best Estimates. Aircraft Environmental Support Office, Naval Aviation Depot-NorthIsland, San Diego, CA. AESO Report No. 2001-7. December 2000.
Wallace L. 1996. Environmental exposure to benzene: An update. Environ Health Perspect104(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 March2000. <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 toxicityevaluation of JP-8 jet fuel and JP-8 jet fuel containing additives. Govt. Reports Announcements & Index (GRA&I), Issue 09.
The Agency for Toxic Substances and Disease Registry (ATSDR) received two sets of commentsduring the public comment period (February 12, 2003 to March 17, 2003) for the NASF PublicHealth 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 statementsmade in the PHA. These clarifications or corrections related to the following topics: descriptionsof 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 contaminationwithin 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 inthat no data exist regarding communication between the intermediate and shallow alluvial aquifersystems in this area. Hydraulic gradients generally are believed to be upward from theintermediate aquifer into the shallow aquifer in this area, but no detailed studies have been doneto quantify this relation in the areas east of NASF."
Response: Studies at hydrogeological investigations at NASF have shown that there is anupward hydraulic gradient from the intermediate aquifer to the shallow aquifer, thus preventingthe downward migration of contaminants into the intermediate aquifer (Battelle 2001 - seereferences in main document). Although it is true that studies have not been conducted toconfirm this relationship in the areas east of NASF, monitoring wells in the shallow aquifer nearthe station boundary have detected mostly very low concentrations of PAHs. ATSDR isconfident that site-related contaminants in the shallow aquifer have not migrated off site at levelsthat would pose a health hazard.
Comment: "Page 3 Air paragraph. I believe this is misleading. While winds are predominantlyfrom the north, west and south, occasionally the winds do blow to the north or northwest towardstown. Releases during periods when the winds are in this minority direction would still distributecontaminants towards town. Also, several case locations were indeed downwind from NASFwhen considering only the predominant wind directions. This comment also applies to the secondparagraph on page 10."
Response: The comment addresses ATSDR's presentation of prevailing wind patterns. Theprevailing wind pattern is important to note in any evaluation of air exposures, because thispattern will determine the direction in which contaminants will blow most frequently. Ourdescription of prevailing wind patterns is consistent with more than 5 years of meteorologicaldata that have been collected in the area. Therefore, no changes have been made in the publichealth 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.