Military Jet Fuel (JP-4)
Its Possible Implication on Public Health
Copyright 2000 David J. Miller
At this time I know of no other paper that has drawn a broad review regarding benzene, toluene, xylene, hexane and their metabolites with regard to petroleum products like (military) JP-4 jet fuel and the implication to public health now and in the future.
If one reviews the literature on benzene it goes back to the beginning of the 20th century and continues today, however for those parties benzene affected the most, they have little or no idea of its danger or its causation. Their life and quality of health being affected the most.
Some may view this presentation with a meta analysis argument, however my fundamental motive is edification, bringing about dialogue even debate, illuminating issues, establishing proper measures appropriate for a remedy.
Physicians acknowledge benzene's effect on bone marrow immune system and the CNS, however by taking an analytical approach one could ignore the synergism of the exposure due to a lack of proficiency in occupational and environmental medicine.
To assist in achieving that goal I choose military (JP-4) jet fuel due to its composition and wide use during the 1950's, 60's, 70's and part of the 1980's.
"During the distillation of crude oil to make JP-3 and JP-4 a wide cut is take of the distillate so as to include both the naptha (gasoline) and kerosene fraction, JP-4 is typically composed of about 50-60% gasoline and the remainder is kerosene1. Now with almost fifty years since JP-4 being standardized under MIL-F-5624A1." It's clear (with the body of information presented in (ATSDR) Agency for Toxic Substances and Disease Registry Publication Toxicological Profile for JP-4 and JP-7 June 1995, henceforth to be referred to as the profile) a serious balance review must be initiated due to JP-4's composition of hydro-carbons to include (additives) itemized with generic identification, Page 70. Note aromatic hydro-carbons are concentrations in weight percent, Page 72, 73, 74.
CONCERNS: (THE PROFILE)2
Page 3 1.3 (How might one be exposed to jet fuel JP-4 and JP-7?) "Workers involved in making or transporting or in refueling military aircraft that use JP-4 might breath air containing it."
Page 38 2.4 Relevance to public health "thus apart from those individuals involved in the manufacturing process, persons living or working near or on a military base would constitute the greatest population at risk for JP-4 and JP-7 exposure."
To digress, if those concerns apply to JP-4 and JP-7 then similar situations would warrant the same attention due to possible evaporation from petroleum storage tank farms and emissions due to transfer of product JP-4 etc. from point of transport truck, rail or barge without vapor recovery systems.
Although vapor recovery systems are being installed, the question of (past exposure) and those most likely at risk identified in the profile need to be addressed more fully to expand those factors for occupational and residential exposure. Example Machle3 writes in (Chronic Intoxication), "This term is applied to poisoning which results from exposure to low concentrations of gasoline vapor for long periods of time; severe acute symptoms do not appear, but minor symptoms of a general nature are manifested a few weeks or months after the exposure has started and become progressively worse, the patient may become disabled in a month or in several years." The implications are profound if the exposure is compounded, Goldstein4. As Toranosuke Ishimaru5 articulates here, "the six occupations noted at a higher frequency among the index cases than in the controls in Table 4 were selected for an examination in more detail of the relation of occupational exposure and A-BOMB exposure (Table 7) note relationship between occupational exposure to benzene or medical x-ray occupations and atomic bomb exposure status; frequency of history of 6 selected occupations. Continuing - in general, the risk was approximately 5 times higher among those with a history of any of these six occupations in comparison with those without. The relative risks in the proximal group and in the distal and non-exposed group were 6.0 and 4.5, respectively."
Continuing with the profiles concern of risk to handlers we then can review Lindquist, R.6 "Our results indicate a three-fold increase risk of developing leukemia for professional drivers who are exposed to petroleum products, i.e., gasoline or diesel and their motor exhausts, our findings support previous work suggesting an increased risk of acute non-lymphocytic leukemia after occupational exposure to petroleum products (3)". From a public health perspective we can no longer ignore past exposure only because of present and future implication and that impact on society.
To reinforce those concerns of previous risk, Pier Alberto Bertazzi7 reports, "the most distinctive pattern of increased cancer mortality seemed to be the one observed in association with moving operations. Significant excess mortality from all cancers, lung cancer and brain tumors was noted." (Continuing further) "The greatest opportunity for exposure to volatile hydrocarbons occurred during the loading operation, which required the manual connection of all filler pipes to the trucks and train tanks and manual measurements of product levels in tanks."
"In addition, workers were exposed while staying at the filling platform especially during the hot season, to volatiles coming from open tanks of standing trucks, and trains."
Now there's an obligation to ask at what levels do these hydrocarbons have a genotoxic effect on those exposed? Ralph I. Nilsson8 established these thoughts. "The results at different exposure levels indicate that even a low level exposure to benzene possibly in combination with other compounds in gasoline, may cause a genotoxic effect (Table 111, V.) as both tests measure damage to DNA. Our findings indicate a genotoxic effect at benzene exposure levels of around 0.1 ppm."
The before mentioned citations demonstrate the danger to individual workers; however we must readdress (the profile's) community concerns with more clarity. This can be accomplished by reviewing E.G. Knox9. "The apparent hazards included oil refineries oil storage and distribution depots, railway lines, and other industrial sites. Effective ranges extended as far as 5km from the sources. This suggested a hazard related to large scale uses of fossil fuels, especially petroleum, operating through leakage or evaporation or combustion, perhaps all three."
Benzene, toluene, hexane, xylene and lead have been identified in (the Profile)2 on Page 3, Paragraph 2. "When they enter the environment as part of jet fuel they may behave the same way as when they are released alone." That being the case, one is compelled to at least review some of those complications associated with those chemicals and their metabolites.
In the formulation of this review I've adhered to scientific discipline, balanced with objectivity. That mosaic, if you will, began to focus on a perspective that was more widespread than I had anticipated regarding occupation, exposure and illness. This all crescendoed while doing a literature search that directed this author to a paper which Lesley Rushton11 had written and made reference to "a proportional mortality study of all deaths over a 10 year period in New Hampshire found high proportional mortality ratios (PMR's) for service station workers for leukemia, suicide, emphysema and mental conditions."
Once again this odyssey has been punctuated with an intriguing citation. This was of great interest only because I had to travel to Britain by paper to learn what had transpired in my own back yard. The excitement was soon tempered by the sheer dynamics of the report! Eugene Schwartz10, M.D. MPH states in the report, "Further the finding of an excess proportion of deaths from suicide in both groups is consistent with the known neurotoxic potential of solvent exposure. Acute exposure to solvents may produce transient and reversible central nervous system symptoms including headache, dizziness, and incoordination. At higher concentrations convulsions, loss of consciousness, and death may result. Long-term exposure to solvents can result in memory impairment and behavioral changes, including irritability, depressive symptoms, and emotional stability. Gasoline is a complex mixture of hydrocarbons blended with a combination of additives including antiknock agents, inhibitors, and dyes, of the more than 40 components, most are paraffins, naphthenes, aromatics, and olefins. The benzene content of gasoline is between 1% and 3% by volume and is higher in unleaded than in leaded fuels (McDermott and Voss, 1979)". Further on, "recent data indicate that gasoline vapor may be carcinogenic apart from its benzene component." (Note: JP-4 is 50 to 60% gasoline).
Individuals subjected to benzene and other compounds should be instructed of the quantitative risk associated with the nature of their exposure in order that appropriate medical protocol may be established for present and future assessment and care. Once those parties are instructed of the dangers of exposure, they can immediately take steps needed to lessen the burden on the already stressed (MFO) mixed functioned oxidases process.
"Benzene is converted to toxic metabolites mostly mixed function oxidases MFO in the liver and bone marrow. MFO-inducing drugs (e.g., phenobarbital, alcohol) and certain chemicals (e.g., chlordane, parathion) may increase the rate at which toxic metabolites of benzene are formed. Theoretically persons with rapid synthesizing marrows, the fetus, infants and children, persons with hemolytic anemia or with agranulocytosis are at increased risk12. The Environmental Protection Agency (EPA) classifies benzene as a Group A carcinogen and has estimated that a lifetime exposure to 0.004 PPM benzene in air will result in, at most, 1 additional case of leukemia in 10,000 people exposed. (EPA risk estimates assume there is no threshold for benzene's carcinogenic effects.)"
An interesting characteristic of petroleum hydrocarbons, (in relationship to the MFO process) is a seemingly kindling effect to addiction. Yasuhiro Takeuchi13 writes, "Lasarew (1929) reported that the narcotic effect of petroleum hydrocarbons became stronger as the number of carbon atoms became larger, and that aromatic hydrocarbons had stronger narcotic effects than paraffins."
Harrington14 says, "The well-recognized acute narcotic effect of organic solvents has recently led various researchers to suggest that a chronic neuroasthenic syndrome can follow repeated low doses. Some workers, mainly in Scandinavia, postulated that organic psychoses can ensue from such exposure." (Axelson et al, 1980).
To expand on these two points of view, its clear a demonstration would be needed to indicate tissue reaction. That evidence was articulated by J.M. de Gandarias.15 "A dense accumulation of enkephalin immunoreactive fibers was seen in the basal portion of the lateral septal nucleus and the densest accumulation of enkephalin-containing processes was observed in the globus pallidus, ansa lenticularis and amygdaloid complex, forming a continuous field extending over these areas. This enkephalinergic distribution is coincident with previous reports (Akil et al, 1984; Zamir et al, 1985). (Continuing further) "The limbic systems is usually affected by organic solvents exposure and it has been demonstrated that aromatic hydrocarbons can cause behavioral changes in mood and even (addiction). This is the case for the largely studied "glue sniffers" (Schikler et al, 1982; Lazar et al, 1983).
The hypothesis I bring forth now is, could benzene be the underlying catalyst that stimulates addiction on most levels, drug and alcohol, and if so an uncorrected condition would create a cycle difficult to break. Could elevated ambient air levels of benzene be a new facet of concern, ever stressing the MFO process in relationship to addiction?
REFERENCE: BENZENE, TOLUENE, HEXANE, XYLENE and LEAD
I have (emphasis, real concern) with past exposure to JP-4 and those particular chemicals incorporated into the formula only because of existing documentation and possible public health consequences.
Example: Benzene: and Breast Tumor Tissue
Gregory G. Oakley16 writes , "In addition, studies have demonstrated the copper-dependent oxidation of chemically similar structures, e.g., hydroquinone and 3-hydroxyestradiol, metabolites of benzene and 17B-Estradiol, respectively, to reactive intermediates that induce oxidative DNA damage (19, 20). This pattern of genotoxicity is similar to that reported in the DNA of human breast tumor tissue 21)."
It would seem the point of concern here could be either primary (occupational) or secondary exposure expressed as ambient air concentrations from automobiles, trucks, buses, trains, and domestic exposure, for example, gasoline powered lawn or recreational equipment, combined with alcohol or another substance that would place extra burden on the MFO process.
N-Hexane, Xylene and Toluene and Occupational Exposure
Katsuyuki Murata17 examines workers exposed to n-hexane, xylene and toluene and writes, "The C-CV rsa reflects the activity in the parasympathetic nervous system (Pagani et al, 1986, Hayano et al, 1990a, 1991, Ewing, 1992). Organic solvents, therefore, may affect the CV rr through depression of parasympathetic activity."
OLFACTORY AND CAUSATION
At this juncture it would be appropriate to explore a (reactive route) of toxic exposure, the olfactory pathway and its implication on health. Robert Ader18 states, "Even before sympathetic innervation of lymphoid tissues was recognized, it was known that lesions of the brain, especially the hypothalamus and limbic systems, had immunological consequences"18, (further on), "Medical or posterior hypothalamic lesions are associated with reduced numbers T and B cells and enhanced allograft rejection."
Claudia Miller19, M.D., M.S. has presented these thoughts, "The olfactory nerves provide the most direct link between the outside chemical environment and the brain. There is no blood-brain barrier where these nerves enter the brain as there is for other portions of the brain. The olfactory nerves communicate directly with the limbic portion of the brain, the so-called "primitive smell brain." This brain area is essential for laying down new memories (hippocampus) and regulates mood (amygdala). In addition, it supplies much of the input to the hypothalamus, which in turn regulates autonomic nervous system and endocrine function. Temperature regulation, smooth muscle tone and appetitive behaviors are influenced by hypothalamic output. For many chemically sensitive patients and Gulf Veterans, mood and memory difficulties are their most disabling symptoms. The possibility exists that such symptoms could be triggered by extraordinarily low level chemical exposures and that sensitivity could spread to chemically unrelated substances as a consequence of limbic sensitization or partial kindling."
EXAMPLES OF ASSOCIATED TOXIC EXPOSURE
As the profile2 previously indicated, handlers and persons living in proximity of operational activity are of concern; page 3 addresses those chemical elements and their behavior. "We have some information on several chemicals found in jet fuel (for example, benzene, toluene, hexane, xylene and lead). We know more about what happens to them when they enter the environment as individual chemicals. When they enter the environment as part of jet fuel, they may behave the same way as when they are released alone."
These chemicals, being heavier than air, are capable of having an intrusive effect on workers or populations via ambient inhalation. Remembering Knox9, "Effective ranges are extended as far as 5KM from the sources. This suggested a hazard related to large scale uses of fossil fuels, especially petroleum, operating through leakage or evaporation or combustion , perhaps all three." James W. Tetrud, M.D.20 narrates a case study of an individual and petroleum ingestion. He states, "There is little doubt that the relatively small quantity of ingested petroleum waste caused this individual's Parkinsonism. The temporal relationship between ingestion of the substance and subsequent emergence of parkinsonism is clear-cut." (Further on), "In another report, Pezzoli et all described a case of Parkinsonism in a leather worker chronically exposed to n-hexane." Pezzoli's21 report states, "Since n-hexane is the substance to which the patient had been mostly exposed, a possible toxic action of this volatile hydrocarbon, alone or associated with the other glue compounds and capable of inducing signs of Parkinsonism has to be considered."
There seems to be sufficient documentation that suggest petroleum produces causation, however that's little solace to anyone at risk and develops symptoms.
Without doubt the many sequels following petroleum exposure can have an exhausting effect on both patient, (family), and physician, due to the many symptoms and changing protocols. A team strategy with expanded expertise would benefit not only the patient directly, but also reassure family members that appropriate clinical direction had been taken.