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At least 19 recordsLinked to original sources
PubMedDate not supplied

Gasoline explosions, gasoline sniffing: an epidemic in young adolescents.

One hundred twenty-two patients between the ages of 10 and 15 were admitted to the Shriners Burns Institute between July 1981 and November 1984. Seventy-five of the 122 patients sustained burns as a direct result of liquid gasoline explosions. Thirty patients had thrown gasoline on a fire and 17 others admitted to having ignited gasoline with a match. During admission interviews, none of the patients admitted to gasoline sniffing; however, 19 patients were subsequently found to have been sniffing gasoline at the time of the accident. All of the patients with gasoline burns sustained much larger burns, had longer hospitalizations, and required more surgery than did patients burned by other means. Similarly, the 19 patients who had been sniffing gasoline had larger burns, had longer hospital stays, and required more surgery than did those injured by gasoline in other accidents. The most common cause of thermal injury in the ten-to-15 year age group is a gasoline-related accident. The histories of a large number of these adolescents may be compatible with explosions related to gasoline sniffing. Educational efforts relating to the explosive nature of the substance and the dangers of gasoline sniffing are warranted.

Adolescent↗
PubMed1975

The EPA National Fuels Surveillance Network. I. Trace constituents in gasoline and commercial gasoline fuel additives.

A National Fuels Surveillance Network has been established to collect gasoline and other fuels through the 10 regional offices of the Environmental Protection Agency. Physical, chemical, and trace element analytical determinations are made on the collected fuel samples to detect components which may present an air pollution hazard or poison exhaust catalytic control devices. A summary of trace elemental constituents in over 50 gasoline samples and 18 commercially marketed consumer purchased gasoline additives is presented. Quantities of Mn, Ni, Cr, Zn, Cu, Fe, Sb, B, Mg, Pb, and S were found in most regular and premium gasoline. Environmental implications of trace constituents in gasoline are discussed.

Air Pollutants↗
PubMed1992

A comparison of European High Test gasoline and PS-6 unleaded gasoline in their abilities to induce alpha 2u-globulin nephropathy and renal cell proliferation.

Male Fischer-344 rats were administered European High Test gasoline (EHT) (50-500 mg/kg), PS-6 unleaded gasoline (UG) (16-500 mg/kg) or 2,2,4-trimethylpentane (TMP) (0.95-30 mg/kg) by gavage for ten consecutive days. To measure cell replication, rats were exposed to [3H]thymidine continuously over the last 7 days of the exposure period. Twenty-four hours after the final dose, protein droplet (PD) accumulation, alpha 2u-globulin (alpha 2u) concentration and the nuclear labeling index (LI), as a measure of cell replication, were measured in the kidneys of control and treated rats. Dose-related increases in PD, alpha 2u and cell replication were detected in the kidneys of rats treated with either gasoline mixture or TMP. The accumulation of PD and the increase in alpha 2u was greater in the kidneys of UG- and TMP-treated rats than in the kidneys of rats treated with EHT. These differences were attributed to the higher composition of branched hydrocarbons in UG, which have been shown to be the biologically active components for these endpoints. The extent of renal cell proliferation was similar in both EHT-, UG- and TMP-treated rats. This suggests that other components besides the branched hydrocarbons are responsible for the increased renal cell replication in EHT-treated rats.

Administration, Oral↗
PubMed1986

Gas chromatographic and gas chromatographic-mass spectrometric determination of gasoline in a case of gasoline vapor and alcohol poisoning.

A case of fatal poisoning due to the combined effect of alcohol and gasoline following an automobile accident is described. Toxicological analyses by means of gas chromatography and gas chromatography-mass spectrometry permitted the identification and quantitation of alcohol and several hydrocarbons in the heart blood and in the gas in the lung. Great variation was found in the estimates of blood gasoline concentration, depending on which of six constituents of gasoline was chosen for quantitation. The cause of this variation is discussed, together with the possible mechanisms leading to death.

Adult↗
PubMed1992

The changes of gasoline compounds in blood in a case of gasoline intoxication.

A 44 year-old man, found in his gasoline vapor filled car, died of multiple organ failure on d 9. Blood samples from d 2-7 were analyzed by gas chromatography/mass spectrometry. The estimated half-lives of gasoline, toluene, ethylbenzene, m,p-xylene, and o-xylene were 16.9, 21.4, 27.5, 32.8, and 25.8 h respectively. The estimated initial gasoline concentration in blood was 247 micrograms/ml.

Acidosis↗
PubMed1985

Recreational gasoline sniffing: acute gasoline intoxication and latent organolead poisoning. Case reports and literature review.

Gasoline is a readily obtainable intoxicant that unfortunately lends itself to habitual abuse by sniffing, a practice found particularly among children and adolescents. The concerted effects of the multiple hydrocarbon and other constituents of gasoline result in a predictable acute toxic syndrome. Organoleads, primarily tetraethyl lead (TEL), cause a separate toxicologic symptom-sign complex that overlaps with the initial acute toxic syndrome. The different clinical symptomatology, effects on hemoglobin synthesis, and response to chelation therapy are all in keeping with the view that organolead poisoning is a separate and distinct toxicologic entity from that of classical elemental lead poisoning or "plumbism".

Adolescent↗
PubMed1993

Neurotoxic effects of gasoline and gasoline constituents.

This overview was developed as part of a symposium on noncancer end points of gasoline and key gasoline components. The specific components included are methyl tertiary butyl ether, ethyl tertiary butyl ether, tertiary amyl methyl ether, butadiene, benzene, xylene, toluene, methyl alcohol, and ethyl alcohol. The overview focuses on neurotoxic effects related to chronic low-level exposures. A few general conclusions and recommendations can be made based on the results of the studies to date. a) All the compounds reviewed are neuroactive and, as such, should be examined for their neurotoxicity. b) For most of the compounds, there is a substantial margin of safety between the current permissible exposure levels and levels that would be expected to cause overt signs of neurotoxicity in humans. This is not the case for xylene, toluene, and methanol, however, where neurologic effects are observed at or below the current Threshold Limit Value. c) For most of the compounds, the relationship between chronic low-level exposure and subtle neurotoxic effects has not been studied. Studies therefore should focus on examining the dose-response relationship between chronic low-level exposure and subtle changes in central nervous system function.

Environmental Exposure↗
PubMed1988

Rapid postexposure decay of alpha 2u-globulin and hyaline droplets in the kidneys of gasoline-treated male rats.

Unleaded gasoline induces nephropathy, characterized by rapid accumulation of hyaline (protein resorption) droplets in epithelial cells of the renal proximal convoluted tubules, only in male rats. The hepatic synthesis of the male rat-specific protein alpha 2u-globulin, a constituent of renal hyaline droplets, is unaltered by gasoline treatment (Olson et al., 1987). Renal alpha 2u-globulin content increased to 210% of control within 18 h of a single oral dose of gasoline (2.0 ml/kg); maximal levels (320% of control) were attained following gasoline administration for 3 d. Increases in renal alpha 2u-globulin caused by gasoline were accompanied by concurrent proliferation of hyaline droplets. However, within 3 d of terminating gasoline administration renal alpha 2u-globulin content decreased to the same level as that in unexposed rats, although renal hyaline droplet number returned to pretreatment levels somewhat more slowly. The conjoint effect of postexposure recovery and estradiol (an inhibitor of hepatic alpha 2u-globulin synthesis) administration was also determined in male rats. On postexposure d 3, 6, and 9, estradiol treatment (1 mg/kg, sc, 4 d, starting on d 9 of gasoline treatment) decreased renal alpha 2u-globulin content to 75%, 59%, and 48%, respectively, of that in rats allowed to recover from gasoline with no hormone treatment. Hepatic alpha 2u-globulin content in estradiol-treated rats was decreased by 74%, 97%, and 96% at the same intervals. Estradiol treatment during recovery from gasoline also appeared to increase the removal of accumulated hyaline droplets from the renal cortex. Thus, accumulation of alpha 2u-globulin-containing hyaline droplets after subacute exposure of male rats to gasoline is rapidly reversible, dependent on continuous exposure to gasoline and maintenance of the normal rate of hepatic alpha 2u-globulin synthesis. These results emphasize the dynamic state of renal cortical hyaline droplets and suggest strongly that gasoline hydrocarbons cause hyaline droplet accumulation by prolonging the half-time of degradation of alpha 2u-globulin.

Alpha-Globulins↗
PubMedDate not supplied

Individual and population exposures to gasoline.

Gasoline is a complex mixture of many constituents in varying proportions. Not only does the composition of whole gasoline vary from company to company and season to season, but it changes over time. The composition of gasoline vapors is dominated by volatile compounds, while "gasoline" in groundwater consists mainly of water-soluble constituents. Hydrocarbons, including alkanes, alkenes, and aromatics, make up the large majority of gasoline, but other substances, such as alcohols, ethers, and additives, may also be present. Given this inability to define "gasoline,h' exposures to individual chemicals or groups of chemicals must be defined in a meaningful exposure assessment. An estimated 111 million people are currently exposed to gasoline constituents in the course of refueling at self-service gasoline stations. Refueling requires only a few minutes per week, accruing to about 100 min per year. During that time, concentrations in air of total hydrocarbons typically fall in the range 20-200 parts per million by volume (ppmV). Concentrations of the aromatic compounds benzene, toluene, and xylene rarely exceed 1 ppmV. Some liquid gasoline is also released, generally as drops less than 0.1 g each, but with enough larger spills to raise the average loss per gallon dispensed to 0.23 g for stations with conventional nozzles and 0.14 g per refueling for stations with vapor recovery nozzles (Stage II controls). Some skin exposure may occur from these spills but the exposure has not been quantified. Two major types of vehicular emissions have been studied. Evaporative emissions include emissions while the vehicle is driven (running losses), emissions after the engine has been shut off but is still warm (hot soak), and emissions during other standing periods (diurnal) emissions. These evaporative emissions are dominated by the more volatile gasoline components. Tailpipe emissions include some unreacted gasoline constituents as well as products of combustion (including chemicals identical to some of the original constituents of the gasoline) and a variety of hydrocarbons and related compounds. Running losses are reported to fall in the range of 0.2 to 2.8 g of total hydrocarbons per mile driven, while benzene evaporative emissions range from 0.002 to 0.007 g/mile. Benzene levels inside travelling vehicles have been reported to average about 13 ppbV in Los Angeles. Tailpipe emissions amount to 0.3 to 1.0 g/mile of total hydrocarbons; emissions of benzene, polycylic aromatic hydrocarbons, and 1,3-butadiene have been reported to range from 0.015 to 0.04 g/mile, 0.00025 to 0.00046 g/mile, and 0.001 to 0.005 g/mile, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Environmental Exposure↗
PubMedDate not supplied

Short-term inhalation toxicity of methanol, gasoline, and methanol/gasoline in the rat.

Four- to five-week-old male and female Sprague Dawley rats were exposed to vapors of methanol (2500 ppm), gasoline (3200 ppm), and methanol/gasoline (2500/3200 ppm, 570/3200 ppm) six hours per day, five days per week for four weeks. Control animals were exposed to filtered room air only. Depression in body weight gain and reduced food consumption were observed in male rats, and increased relative liver weight was detected in rats of both sexes exposed to gasoline or methanol/gasoline mixtures. Rats of both sexes exposed to methanol/gasoline mixtures had increased relative kidney weight and females exposed to gasoline and methanol/gasoline mixtures had increased kidney weight. Decreased serum glucose and cholesterol were detected in male rats exposed to gasoline and methanol/gasoline mixtures. Decreased hemoglobin was observed in females inhaling vapors of gasoline and methanol/gasoline at 570/3200 ppm. Urine from rats inhaling gasoline or methanol/gasoline mixtures had up to a fourfold increase in hippuric acid, a biomarker of exposure to the toluene constituent of gasoline, and up to a sixfold elevation in ascorbic acid, a noninvasive biomarker of hepatic response. Hepatic mixed-function oxidase (aniline hydroxylase, aminopyrine N-demethylase and ethoxyresorufin O-deethylase) activities and UDP-glucuronosyltransferase activity were elevated in rats exposed to gasoline and methanol/gasoline mixtures. Histopathological changes were confined to very mild changes in the nasal passages and in the uterus, where decreased incidence or absence of mucosal and myometrial eosinophilia was observed in females inhaling gasoline and methanol/gasoline at 570/3200 ppm. It was concluded that gasoline was largely responsible for the adverse effects, the most significant of which included depression in weight gain in the males, increased liver weight and hepatic microsomal enzyme activities in both sexes, and suppression of uterine eosinophilia. No apparent interactive effects between methanol and gasoline were observed.

Animals↗
PubMed1989

Health effects of gasoline refueling vapors and measured exposures at service stations.

Liquid gasoline is a complex mixture of at least 150 hydrocarbons with about 60-70% alkanes (paraffins), 25-30% aromatics, and 6-9% alkenes. In order to evaluate the potential for health effects from inhaling gasoline vapors, it is essential to understand the major differences in the composition of vapors versus liquid gasoline. The small chain, low carbon-numbered components are more volatile and thus in higher percentages in the vapor phase than the larger and heavier molecules. It is noteworthy that the concentrations of aromatics (the more toxic of the gasoline components), are depleted to about 2% in the vapor phase, with the light paraffins (the less toxic) enriched to about 90%. Actual measurements of vapor exposure at service stations confirm that the vapor composition is primarily to low weight alkanes although benzene is also emitted and represents the chemical of greatest concern. A perceived health concern from inhaling gasoline vapors is the potential for carcinogenicity based on the induction of kidney tumors in male rats and liver tumors in female mice exposed to wholly-vaporized gasoline. However, the results of the animal studies are of questionable relevance for human risk assessment due to the unique mechanism operative only in the male rat and since the exposure was to wholly-vaporized gasoline rather than the gasoline vapor mixture to which humans are exposed. Recent research supports the hypothesis that branched-chain-alkanes bind to a globulin specific to make rats, alpha 2-u-globulin. The protein complex can not be degraded in the usual manner so that protein accumulation occurs in renal cells, leading to cytotoxicity, death, proliferation, and with prolonged exposure, kidney cancer. The results of epidemiology studies fail to link an increase in cancer to exposure to gasoline vapors.

Air Pollutants↗
PubMed1977

Response of microorganisms to an accidental gasoline spillage in an arctic freshwater ecosystem.

The response of microorganisms to an accidental spillage of 55,000 gallons of leaded gasoline into an Arctic freshwater lake was studied. Shifts in microbial populations were detected after the spillage, reflecting the migration pattern of the gasoline, enrichment for hydrocarbon utilizers, and selection for leaded-gasoline-tolerant microorganisms. Ratios of gasoline-tolerant/utilizing heterotrophs to "total" heterotrophs were found to be a sensitive indicator of the degree of hydrocarbon contamination. Respiration rates were elevated in the highly contaminated area, but did not reflect differences between moderately and lightly contaminated areas. Hydrocarbon biodegradation potential experiments showed that indigenous microorganisms could extensively convert hydrocarbons to CO(2). In situ measurement of gasoline degradation showed that, if untreated, sediment samples retained significant amounts of gasoline hydrocarbons including "volatile components" at the time the lake froze for the winter. Nutrient addition and bacterial inoculation resulted in enhanced biodegradative losses, significantly reducing the amount of residual hydrocarbons. Enhanced biodegradation, however, resulted in the appearance of compounds not detected in the gasoline. Since the contaminated lake serves as a drinking water supply, treatment to enhance microbial removal of much of the remaining gasoline still may be advisable.

Alaska↗
PubMed1993

State of the science on the carcinogenicity of gasoline with particular reference to cohort mortality study results.

As a result of the content of benzene in various streams of refinery products, including gasoline, it is not surprising that over the years studies and case reports have linked gasoline exposure to lymphopoietic cancers (LPC), particularly leukemia and multiple myeloma (MM). Of three recently conducted studies of gasoline-exposed workers, one shows strong associations with leukemia and MM, a second suggests some association with leukemia and did not analyze data for MM, and the third study is not possible to evaluate because of a major problem with study design. Other diseases of particular interest in relation to gasoline exposure are kidney cancer, malignant melanoma, and heart disease. One study suggests an association with kidney cancer, but the second study did not. There appears to be no association between employment in refineries or gasoline exposure and heart disease. However, evaluation of risk of kidney cancer and heart disease is somewhat difficult because investigators did not control for cigarette smoking, even though it is related to these diseases. This is of particular concern when studying gasoline-exposed workers, who because of the explosive nature of gasoline probably smoke less than the general population used for comparison of mortality. Some studies of refinery workers and gasoline-exposed workers in particular show an excess risk of death from malignant melanoma. Whether this latter association is the result of benzene/gasoline exposure, sunlight exposure, or a combination of the two cannot be determined with the data currently available.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinogens, Environmental↗
PubMed1993

Health effects of gasoline exposure. II. Mortality patterns of distribution workers in the United States.

In this study, the cohort consisted of 18,135 distribution employees with potential exposure to gasoline for at least one year at land-based terminals (n = 9,026) or on marine vessels (n = 9,109) between 1946 and 1985. The primary objective of the study was to determine the relationship, if any, between exposure to gasoline and mortality from kidney cancer or leukemia. In addition, other causes of death of secondary interest included multiple myeloma and heart diseases. The mortality of the cohort was observed through June 30, 1989. The results of this study indicated that there was no increased mortality from either kidney cancer or leukemia among marketing and marine distribution employees who were exposed to gasoline in the petroleum industry when compared to the general population. Among the land-based terminal employees, the kidney cancer standardized mortality ratio (SMR) was 65.4 (12 deaths) and leukemia SMR was 89.1 (27 deaths). For the marine cohort, the SMRs were 83.7 for kidney cancer (12 deaths) and 70.0 for leukemia (16 deaths), respectively. More importantly, based on internal comparisons, there was no association between mortality from kidney cancer or leukemia and various indices of gasoline exposure. In particular, neither duration of employment, duration of exposure, age at first exposure, year of first of exposure, job category, cumulative exposure, frequency of peak exposures, nor average intensity of exposure had any effect on kidney cancer or leukemia mortality. For acute myeloid leukemia, a nonsignificant mortality increase was found in land-based terminal employees (SMR = 150.5, 13 deaths), but no trend was detected when the data were analyzed by various gasoline exposure indices. This nonsignificant excess was limited to land-based terminal employees hired before 1948. On the other hand, a deficit of mortality from acute myeloid leukemia was observed among marine employees (SMR = 74.2, 5 deaths). For the two cohorts combined, SMR for acute myeloid leukemia was 117.1 based on 18 deaths. We did not find any relationship in our study between gasoline exposure and mortality from multiple myeloma or heart diseases. In general, we did not find any significantly increased mortality, either overall or from specific causes, associated with gasoline exposure in this study of marketing and marine distribution employees.

Cause of Death↗
PubMed1991

Benzene pollution from gasoline usage.

Local gasolines contain benzene ranging from 1.8 to 3.7% and their use can lead to significant exposure to benzene. Gasoline station attendants were found to be exposed to short-term exposure levels (STEL) of 0.064-179 ppm. Their 8-h time-weighted averaged (TWA) exposure ranged from 0.028 to 0.71 ppm. For motorcar service mechanics, TWA exposure levels ranged from 0.014 to 1.7 ppm. The exposure of drivers of gasoline delivery tankers ranged from 0.08 to 2.37 ppm for personal TWA exposure over the whole workshift. For local people not occupationally exposed to gasoline or other benzene-containing volatile chemicals, exposure from the ambient environment ranged from 0.0023 to 0.027 ppm. Gasoline usage also contributed to the contamination of surface water with benzene. Benzene levels in water samples taken from drains leading from gasoline stations were between 1.1 and 40.4 micrograms l-1.

Air Pollution↗
PubMed1989

Carcinogenic potential of gasoline and diesel engine oils.

Used gasoline engine oils are carcinogenic in mouse skin and mutagenic in Salmonella. The toxicity of fresh gasoline engine oils and that of fresh and used diesel engine oils are less well defined. The present studies examined the dermal carcinogenic potential of a series of fresh and used oils from both gasoline and diesel engines. The used oils represented a variety of operating conditions. The objective of the study was to assess the potential carcinogenic hazards associated with exposure to these materials. The majority of the used gasoline engine oils tested were carcinogenic although one oil, collected after a relatively short drainage interval, was inactive in the dermal carcinogenesis bioassay. Additionally, polycyclic aromatic hydrocarbon (PAH) concentrations were elevated in the used oils in comparison to the fresh oils. The fresh gasoline engine oils and both the fresh and used diesel engine oil samples were noncarcinogenic, and there was little evidence of elevated PAH levels in the used diesel engine oils. The carcinogenic potency of used oils from gasoline engines was related to drainage interval, but other factors such as contribution of the fuel due to blowby and driving cycle may also have been important. The used diesel engine oils were not carcinogenic even after extended use.

Animals↗