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At least 19 recordsLinked to original sources
PubMed2004

The levels of kerosene components in biological samples after repeated dermal exposure to kerosene in rats.

The current study was experimentally investigated using rats whether or not kerosene components are accumulated from daily repeated dermal exposure. Rats received daily 1h-exposure to kerosene for 5 days (5K), daily 1h-exposure for 4 days and left for 1 day (4KL), a single 1h-exposure (1K), a single 1h-exposure and left for 1 day (1KL), or a single 1h-exposure, sacrificed and left dead for 1 day (1KLD). Kerosene components, trimethylbenzenes (TMBs) and aliphatic hydrocarbons (AHCs) in blood and tissues were determined by GC-MS. In blood, almost the same concentrations of TMBs were detected in the rats sacrificed immediately after exposure (5K, 1K and 1KLD), and only trace levels were detected in the rats sacrificed 1 day after exposure (4 and 1KL). Almost the same levels of AHCs in blood were detected among groups except for the rats sacrificed 1 day after a single exposure (1KL), in which AHCs were slightly lower. These results suggest that (1) AHCs tend to be accumulated from daily exposure, while TMBs do not, (2) the proportions of detected kerosene components in blood can be an indicator of whether the last exposure occurred just before death or not, (3) the kerosene levels last at least 1 day without blood circulation.

Adipose Tissue↗
PubMed1982

[Comparative studies on the toxicity of various dieelectrics, kerosene derivatives, used in the electroerosion technic. I. Morphological, cytoenzymatic and biochemical changes in the liver of rats chronically exposed to kerosene hydrocarbons].

Rats exposed to cosmetic kerosene mists (odourless kerosene), concentration of 75 and 300 mg/m3 for 14 days, underwent morphological and cytoenzymatic liver tests and biochemical tests of lipids composition in this organ. In addition, lipids concentration and activity of test--enzymes in blood serum were determined. The findings were: passive congestion, fine--droplet fatty degeneration in I zones of clusters and increased number of Browicz--Kupffer's phagocytes near liver triads. Those changes were accompanied by: decreased activity of succinic dehydrogenese (SDH), tetrazolic NADPH--reductase (NADPH-r.t.) and glucose-6-phosphatase (G-6-P-ase) and increased activity of adenosine triphosphatase (Mg++-ATP-ase) and acid phosphatase (AcP). In blood serum medium increase of base phosphatase (AP), 5-nucleotidase (5-Nt) and leucyloaminepeptidase (LAP) and decreased activity of prothrombin (Pt) were found. In addition, it was demonstrated that liver steatosis was characterized by cumulation of free fatty acids, phospholipids and cholesterol esters with simultaneous decrease in triglycerides content in this organ. The obtained results indicate that changes induced by kerosene hydrocarbons in liver are focal and cumulate in I zones of liver clusters. The degree of lesion varies with the extent of exposure, and results from toxic effects of this preparation on hepatic cells lypoproteid membranes.

Alanine Transaminase↗
PubMed1989

Alveolar liquid pressures in nonedematous and kerosene-washed rabbit lung by micropuncture.

We studied the relationship between alveolar interfacial pressure and lung volume in kerosene-filled lungs, nonedematous air-filled lungs on lung deflation and inflation, and air-filled lungs after washing with kerosene or the Dow Corning oil, 0.65 cs dimethyl siloxane (DC200). We used the micropipet-servonulling technique to measure alveolar liquid pressure (Pliq) in the alveolar liquid layer of isolated rabbit lungs at different airway pressures (Palv). It was not possible to measure pressure in kerosene or in DC200 by micropuncture because of its low electrical conductivity. We used the Laplace law for a spherical membrane to estimate alveolar surface tension (T). In the kerosene-filled lung, the pressure drop (delta P = Pliq - Palv) across the alveolar surfactant-kerosene interface was 1.1 cm H2O at TLC and decreased to 0.5 cm H2O at 71% TLC. These values corresponded to T values of 2.2 and 0.9 dyne/cm at TLC and 71% TLC, which were in agreement with in vitro measurements using the captive bubble technique. In the air-filled lung on inflation, delta P values were 12.7 and 15.7 cm H2O at 48% and 76% TLC. Corresponding T values were 14 and 21 dyne/cm. Thus, alveolar surface tension on lung inflation is surface area dependent. In the kerosene-washed and DC200-washed lungs, delta P values were 16 and 14.5 cm H2O at TLC and decreased to 9 and 8 cm H2O at 50-56% TLC. These values indicated a reduction of 40-60% in alveolar surface tension with lung deflation from TLC to 50% TLC. The results indicate that alveolar surface tension in both kerosene-filled and kerosene-washed air-filled lungs is surface area dependent. This is due to a surfactant-kerosene interface in the kerosene-filled lung and a surfactant-kerosene-air interface in the kerosene-washed lung.

Air↗
PubMed2003

Dermal absorption of kerosene components in rats and the influence of its amount and area of exposure.

The influences of amount and area of dermal exposure to kerosene upon the levels of kerosene components in biological samples were examined in vivo and in vitro. Thirty-two rats were randomly divided into four groups and exposed to kerosene through the abdominal skin for 2h. The amounts (soaked in cotton) and area of kerosene exposed were 1 ml/4 cm(2) in Group I, 4 ml/4 cm(2) in Group II, 4 ml/16 cm(2) in Group III and 16 ml/64 cm(2) in Group IV. Before, then 5, 10, 20, 30, 45, 60, 90 and 120 min after exposure, 0.5 ml of blood was collected. Solid tissue samples, including the exposed skin area, were harvested at 120 min. Kerosene components were analyzed by gas chromatography/mass spectrometry. Trimethylbenzens (TMBs) that are easily absorbed kerosene components, appeared at 5-20 min. The time course changes in TMB levels in blood were significantly different between Groups I and II or Groups I and III, and almost identical between Groups II and III. Similar trends were observed in tissue samples at 120 min. High concentrations of aliphatic hydrocarbons (AHCs) were detected in the exposed skin and the AHC levels were dependent on the amount of kerosene exposed per unit area. These results suggest that (1) dermal absorption of kerosene occurs soon after dermal exposure started, (2) absorption of TMBs is influenced by the total amount of kerosene rather than area of exposure, and (3) AHCs remaining in the skin at significant levels are influenced by the amount of kerosene per unit area exposed.

Administration, Cutaneous↗
PubMed1982

Effect of interstitial fluid (kerosene) on pressure-volume characteristics of rat lung.

Although pulmonary interstitial edema has been estimated to decrease pulmonary compliance (CL), it has been experimentally difficult to demonstrate whether the observed changes in CL are directly due to the presence of interstitial fluid or if they result instead from concomitant pulmonary vascular engorgement and/or alveolar edema. Since kerosene-inflated lungs do not leak, we were able to use kerosene to measure the effect on CL of the accumulation of interstitial fluid (kerosene) in the postmortem rat lung. Pressure-volume (PV) studies of the lung were done during the progressive increase in interstitial fluid (kerosene). Analysis of the deflation limbs of the quasistatic PV curves obtained following serial inflations with kerosene indicated that the maximal volume of kerosene [MV35, equal to the maximum tissue plus airway volume at a transpulmonary pressure (Ptp) of 35 cmH2O] was 3.8 +/- 1.2 ml (31.0 +/- 11.8%) greater than TLC35 [air volume at Ptp of 35 cmH2O prior to kerosene inflation]. The increases in interstitial kerosene volume had no effect on kerosene PV characteristics, as was demonstrated by superimposing lung PV curves obtained at various states of interstitial filling. We conclude that the interstitial compartment is large and very compliant and that the presence of even great amounts of fluid limited to this compartment does not restrict lung expansion.

Animals↗
PubMed2002

Distribution of kerosene components in rats following dermal exposure.

The systemic distribution of kerosene components in blood and tissues was analysed in rats following dermal exposure. Four types of trimethylbenzenes (TMBs) and aliphatic hydrocarbons (AHCs) with carbon numbers 9-16 (C(9)-C(16)) were analysed as major kerosene components by capillary gas chromatography/mass spectrometry (GC/MS). The kerosene components were detected in blood and all tissues after a small piece of cotton soaked with kerosene was applied to the abdominal skin. The amounts of TMBs detected were higher than those of AHCs. Greater increases in TMB levels were found in adipose tissue in an exposure duration-dependent manner. The amounts of TMBs detected were only at trace levels following post-mortem dermal exposure to kerosene. These findings suggest that kerosene components were absorbed percutaneously and distributed to various organs via the blood circulation. Post-mortem or ante-mortem exposure to kerosene could be distinguished when the exposure duration was relatively long. Adipose tissue would seem to be the most useful for estimating the degree of kerosene exposure.

Animals↗
PubMed2003

Skin analysis following dermal exposure to kerosene in rats: the effects of postmortem exposure and fire.

To evaluate the usefulness of skin analysis for the forensic examination of cases involving postmortem dermal exposure to kerosene and/or fire, an experimental study using rats was performed. Rats received dermal exposure to kerosene before or after death, and the effect of fire was determined by burning an area of exposed skin after death. Kerosene concentrations in skin and blood were determined by gas chromatography-mass spectrometry and microscopic observation was performed for skin samples. No differences were observed in skin kerosene levels between antemortem and postmortem exposure. Kerosene concentrations in mildly burned skin where the stratum corneum (SC) was retained were approximately 84% compared to those in non-burned exposed skin, whereas concentrations in severely burned skin where the SC was almost completely burned off were 28% of non-burned skin. Even in non-exposed control skin 14% of the original kerosene concentrations could be detected, which was considered to be caused by contamination during the experimental protocol combined with kerosene's property of a high affinity for the SC. These results suggest that (1) skin analysis is useful in estimating the type of petroleum product involved in crimes or accidents even for postmortem exposure, (2) whether the SC is retained or not primarily determined the kerosene levels in burned skin, and (3) attention must be paid to evaluate the results obtained from skin samples in the light of the circumstances surrounding the case.

Abdomen↗
PubMed2000

Kerosene soot genotoxicity: enhanced effect upon co-exposure with chrysotile asbestos in Syrian hamster embryo fibroblasts.

Epidemiological and experimental studies have suggested an enhancement of asbestos-induced bronchogenic carcinoma by cigarette smoke. Further, our recent experimental and epidemiological studies have indicated that besides smoking, several other compounds including kerosene soot may accelerate disease processes in asbestos-exposed animals as well as in the humans. Incomplete combustion of kerosene oil generates large volumes of soot, which contains various polycyclic aromatic hydrocarbons and aliphatic compounds. As reported earlier, exposure to kerosene soot is known to cause biochemical and pathological changes in the pulmonary tissue, which may cause cardiopulmonary disorders. In this study we investigated genotoxic effects caused by kerosene soot and chrysotile asbestos as well as co-exposure of kerosene soot and chrysotile using Syrian hamster embryo fibroblasts (SHE). The micronucleus assay revealed a significant increase of induced micronuclei (MN), (P</=0.05) in SHE cells after treatment with kerosene soot (0.5-1.0 microg/cm(2)) for 66 h (36 MN/1000 cells). Combined treatment with chrysotile and soot induced up to 110 MN/1000 cells (chrysotile alone: 80 MN/1000 cells; concentrations: 1 microg/cm(2), exposure times: 66 h). Kinetochore staining revealed mainly clastogenic effects in all cases (soot: 21.3% CRMN(+); chrysotile: 27%; soot+chrysotile: 27.6%; control: 20.8%). This is the first study showing that kerosene soot is not only genotoxic but it can also elevate the genotoxic potential of chrysotile asbestos. This information may be of importance for workers occupationally exposed to asbestos and domestically exposed to kerosene soot.

Animals↗
PubMedDate not supplied

Role of chemical mediators in bronchoconstriction induced by kerosene.

Kerosene is a by product of petroleum used in some countries for cleaning, lighting and cooking purposes. Rodriguez de la Vega et al (1981) have presented evidences of the relation between bronchial asthma and the manipulation of kerosene. Since the experiments performed by our group showed that the acute inhalation of the aerosol of kerosene induces bronchoconstriction in rabbits (Casacó et al 1982), we investigated its effect on guinea pig respiratory physiology. In order to elucidate the implication of histamine and arachidonic acid metabolites in kerosene induced bronchoconstriction, we investigated the influence of the administration to guinea pig of a single dose of the histamine H1 antagonist mepyramine (0.1 mg/kg i.v.) 10 minutes before the aerosol and also the effect of the steroidal antinflammatory drug triamcinolone in rabbits (5 mg/kg i.m.) daily during 4 days before the inhalation of kerosene. The histamine concentrations in guinea pig blood before and after the aerosol were also compared. The inhalation of kerosene during 5 min. (20.4 mg/L) by guinea pigs resulted in an increase of airway resistance without increase of blood histamine concentration. On the other hand, the bronchoconstrictive effect of kerosene in guinea pigs and rabbits was not modified by the previous treatment with mepyramine or triamcinolone respectively. The results suggest that the acute bronchoconstriction induced by kerosene is mediated neither by stimulation of histamine H1 receptors nor by the release of chemical mediators.

Airway Resistance↗
PubMed1976

Kerosene intoxication: an experimental approach to the etiology of the CNS manifestations in primates.

Baboons were utilized to investigate the clinicopathologic effects of kerosene, given via various routes, on the primate brain. The animals were divided into five groups: Group 1 - normal controls; Group II - kerosene administered intratracheally; Group III - kersoene injected into the left cardiac ventricle; Group IV - kerosene injected into right carotid artery; Group V - kerosene injected into portal vein. Results indicate that the primate brain is resistent to the direct toxic effects of kerosene. Even when the dose is very large, the microcirculation of the liver and lung filter out sufficient amounts of kerosene to protect the brain from damage. It is assumed that the CNS manifestations following ingestion of kerosene are due to hypoxia secondary to aspiration pneumonia.

Animals↗
PubMed1982

Pulmonary toxicity following gastrointestinal ingestion of kerosene.

The continuous controversy concerning the treatment for acute hydrocarbon ingestions led to a study of the pulmonary effects of kerosene absorption from the gastrointestinal tract in dogs. Gastrostomies and cervical esophageal transections with a proximal esophageal fistula were performed on 11 dogs under general anesthesia. Following a return of normal bowel function each animal was given 20 cc/kg of a commercial-grade kerosene by gastrostomy tube. The dogs were randomly divided into two groups for necropsy at 24 and at 72 hours, and each dog had chest radiographs prior to instillation of the kerosene and at 6, 24, 48, and 72 hours, depending on their group. The dogs were given an overdose of barbiturate for euthanasia. Tissue was randomly selected from the lungs and examined using standard microscopic and histologic techniques. No clinical complications were observed in any of the animals following the kerosene instillation. No radiologic or histologic evidence of pulmonary changes due to kerosene was found. The lack of pulmonary pathologic changes following kerosene ingestion in dogs protected from aspiration suggests that the treatment for kerosene poisoning should be confined to supportive measures. Induction of emesis is contraindicated in the management of hydrocarbon ingestion.

Animals↗
PubMed1994

[Case of death by fire with kerosene--analysis of contents of trachea and stomach].

UNLABELLED: In death caused by fuel oil burning, it's difficult to examine the vital reaction in the burning skin surface. In these cases, in stead of skin examination, we've been determining the fuel oil in blood. In this case, besides this method, we tried to examine the contents of the trachea of a person who died of kerosene oil burns. CASE: A 49-year-old female was found dead in a cabin. Burns on her body ranged from first to fourth-degree, and 91% of the body was charred. Carbon particles were detected within the trachea and the bronchus, and were slightly detected in the gastric contents and the esophagus. Carboxyhemoglobin concentration was found to be 21% in the right heart blood and 22% in the left heart blood. The level of cyanide detected was 4.3 microM in the right heart blood and 1.7 microM in the left heart blood. Ethanol was not detected in either sample. Kerosene components were detected in each sample (blood, trachea content, gastric content and body surface). According to the formulation of kerosene components, results of contents of the trachea were most likely from a kerosene on the market. In the blood, many volatile paraffin hydrocarbons were found, and, on the body surface, many high boiling-point paraffin hydrocarbons were detected. The means that values of detected kerosene formulation from the blood and trachea contents were similar to types of kerosene on the market. From these results, we concluded that the victim inhaled kerosene vapor.(ABSTRACT TRUNCATED AT 250 WORDS)

Burns↗
PubMed2000

Skin cleaning with kerosene facilitates passage of carcinogens to the lungs of animals treated with used gasoline engine oil.

Solvents such as kerosene or gasoline may be used by workers to clean their skin following contact with oily materials. This practice is not recommended, as it is well known that the solvent will defat the skin. Many also suspect that solvent washing may increase exposure by carrying materials through the skin; however, there is little documentation of this. Auto mechanics may be exposed to used gasoline engine oil (UGEO), an animal carcinogen which forms carcinogen-DNA adducts in skin and lung following topical application. This study was designed to determine if cleaning with kerosene following exposure to UGEO altered absorption of carcinogens from this material. UGEO or new oil (NO) was applied to the shaved skins of groups of HSD-ICR mice for five days. At 1 or 8 hours after application, the treated skins were cleaned with either kerosene or a commercial cleaner, or were not cleaned. Animals were sacrificed 24 hours after the last application, skins and lungs harvested, and DNA analyzed for carcinogen-DNA adducts by 32P-postlabeling. Five applications of UGEO significantly increased carcinogen-DNA adduct levels in both lungs and skin compared to animals treated with NO. DNA adduct levels in the skin were reduced significantly in groups washed with kerosene or commercial cleaner. Washing at one as opposed to eight hours after UGEO application resulted in lower adduct levels regardless of cleaner. DNA adduct levels in the lung were reduced when the commercial cleaner was used, again in a time-related fashion. However, cleaning with kerosene resulted in mean carcinogen-DNA adduct levels in the lung which were significantly higher than even the positive controls, regardless of cleaning time. This is the first demonstration that kerosene cleaning facilitates passage of carcinogens through the skin, resulting in higher levels of genetic damage in a critical internal organ.

Administration, Cutaneous↗
PubMed1992

Diminution in kerosene-mediated induction of drug metabolizing enzymes by asbestos in rat lungs.

In order to determine the pulmonary toxicity of kerosene and its ignition product (soot) in asbestos exposed subjects, the activities of phase I and phase II drug metabolizing enzymes in rat lungs after single intratracheal co-exposure to Indian chrysotile asbestos and kerosene or its soot and Indian chrysotile were assayed. Exposure to kerosene or its soot resulted in a significant increase in the level of microsomal cytochrome P-450 and the activity of P-450 dependent monooxygenase, benzo(a)pyrene hydroxylase, as well as in the activities of microsomal epoxide hydrase and cytosolic glutathione-S-transferase (GST). However, in chrysotile exposed animals a reverse pattern in these parameters was recorded. The co-exposure to chrysotile and kerosene or chrysotile and soot led to a significant depletion in cytochrome P-450 level and a decrease in the activities of benzo(a)pyrene hydroxylase, epoxide hydrase and GST when compared to kerosene and soot controls, respectively. These results suggest that asbestos by altering the pulmonary drug metabolizing enzyme system may increase the toxic potential of kerosene and its ignition product in the respiratory system.

Animals↗
PubMed1989

Dermal exposure to kerosene.

Young healthy albino male mice were subjected to repeated exposure to kerosene by wrapping each of their hind feet with a muslin cloth (1 x 10 cm) wetted with kerosene (0.1 ml). Exposure varied from 15 to 60 min/day for 7 consecutive days. Repeated exposure to kerosene produced histologic changes in the foot pad skin and popliteal lymph nodes of mice and systemic toxic manifestations such as variation in hematologic profile, significant decreases in relative weight of thymus, spleen and abdominal lymph nodes and altered histology. Three weeks of non-exposure rest indicated the reversible nature of kerosene-induced toxicity. Furthermore, observations made in 24 human subjects chronically exposed to kerosene in an automobile workshop revealed high incidence of oil acne and dermatitis of varying degrees. The study demonstrates a need for caution where ever prolonged dermal exposure to kerosene in occupational situations obtains.

Adult↗
PubMedDate not supplied

Tracheal ultrastructure in kerosene treated guinea pigs. A preliminary report.

p6high correlation between the usage of kerosene and the appearance of asthmatic crises has been demonstrated. The ultrastructure of the upper respiratory tract of animals treated with kerosene has not been previously reported. Kerosene aerosol was administered for 15 minutes daily during 21 days to adult male guinea pigs with fragments of trachea being processed for ultrathin electron microscopical studies. Controls did not receive any treatment. Trachea of guinea pigs submitted to kerosene aerosols showed swelling, ruffling and breakdown of the ciliary membrane. The regularly arranged ciliary border was disturbed to a certain degree in some areas by the development of cytoplasmatic protrusions at the apical part of the ciliated cells. An eosinophilic infiltrate was observed deep inside the epithelium and into the lamina propria. Therefore, these ciliary alterations can be considered as one of the most important changes induced by kerosene in tracheal epithelial cells. The protrusions may represent a sign of cell alteration produced by kerosene aerosol inhalation in the guinea pig.

Aerosols↗
PubMed2002

Emission of polycyclic aromatic hydrocarbons, toxicity, and mutagenicity from domestic cooking using sawdust briquettes, wood, and kerosene.

Smoke samples, in both gas and particulate matter (PM) phases, of the three domestic stoves were collected using U.S. EPA modified method 5 and were analyzed for 17 PAH (HPLC-UV), acute toxicity (Microtox test), and mutagenicity (Amestest). The gas phase of smoke contributed > or = 95% of 17 PAH, > or = 96% of toxicity, and > or = 60% of mutagenicity. The highest emission factor of 17 PAH was from sawdust briquettes (260 mg/kg), but the highest emission of 11 genotoxic PAH was from kerosene (28 mg/kg). PM samples of kerosene smoke were not toxic. The total toxicity emission factor was the highest from sawdust, followed by kerosene and wood fuel. Smoke samples from the kerosene stove were not mutagenic. TA98 indicated the presence of both direct and indirect mutagenic activities in PM samples of sawdust and wood fuel but only direct mutagenic activities in the gas phase. TA100 detected only direct mutagenic activities in both PM and gas-phase samples. The higher mutagenicity emission factor was from wood fuel, 12 x 10(6) revertants/kg (TA100-S9) and 3.5 x 10(6) (TA98-S9), and lower from sawdust, 2.9 x 10(6) (TA100-S9) and 2.8 x 10(6) (TA98-S9). The low burning rate and high efficiency of a kerosene stove have resulted in the lowest PAH, toxicity, and mutagenicity emissions from daily cooking activities. The bioassays produced toxicity and mutagenicity results in correspondence with the PAH content of samples. The tests could be used for a quick assessment of potential health risks.

Cooking↗
PubMedDate not supplied

Biological and health effects of exposure to kerosene-based jet fuels and performance additives.

Over 2 million military and civilian personnel per year (over 1 million in the United States) are occupationally exposed, respectively, to jet propulsion fuel-8 (JP-8), JP-8 +100 or JP-5, or to the civil aviation equivalents Jet A or Jet A-1. Approximately 60 billion gallon of these kerosene-based jet fuels are annually consumed worldwide (26 billion gallon in the United States), including over 5 billion gallon of JP-8 by the militaries of the United States and other NATO countries. JP-8, for example, represents the largest single chemical exposure in the U.S. military (2.53 billion gallon in 2000), while Jet A and A-1 are among the most common sources of nonmilitary occupational chemical exposure. Although more recent figures were not available, approximately 4.06 billion gallon of kerosene per se were consumed in the United States in 1990 (IARC, 1992). These exposures may occur repeatedly to raw fuel, vapor phase, aerosol phase, or fuel combustion exhaust by dermal absorption, pulmonary inhalation, or oral ingestion routes. Additionally, the public may be repeatedly exposed to lower levels of jet fuel vapor/aerosol or to fuel combustion products through atmospheric contamination, or to raw fuel constituents by contact with contaminated groundwater or soil. Kerosene-based hydrocarbon fuels are complex mixtures of up to 260+ aliphatic and aromatic hydrocarbon compounds (C(6) -C(17+); possibly 2000+ isomeric forms), including varying concentrations of potential toxicants such as benzene, n-hexane, toluene, xylenes, trimethylpentane, methoxyethanol, naphthalenes (including polycyclic aromatic hydrocarbons [PAHs], and certain other C(9)-C(12) fractions (i.e., n-propylbenzene, trimethylbenzene isomers). While hydrocarbon fuel exposures occur typically at concentrations below current permissible exposure limits (PELs) for the parent fuel or its constituent chemicals, it is unknown whether additive or synergistic interactions among hydrocarbon constituents, up to six performance additives, and other environmental exposure factors may result in unpredicted toxicity. While there is little epidemiological evidence for fuel-induced death, cancer, or other serious organic disease in fuel-exposed workers, large numbers of self-reported health complaints in this cohort appear to justify study of more subtle health consequences. A number of recently published studies reported acute or persisting biological or health effects from acute, subchronic, or chronic exposure of humans or animals to kerosene-based hydrocarbon fuels, to constituent chemicals of these fuels, or to fuel combustion products. This review provides an in-depth summary of human, animal, and in vitro studies of biological or health effects from exposure to JP-8, JP-8 +100, JP-5, Jet A, Jet A-1, or kerosene.

Aircraft↗