Guidance

Petrol: toxicological overview

Updated 29 October 2024

Main points

Kinetics and metabolism

As petrol is a mixture of chemicals, there is no definitive ADME (absorption, distribution, metabolism, and excretion) data.

Health effects of acute exposure

Exposure to petrol vapour in confined or poorly ventilated areas may cause rapid onset of unconsciousness.

The main hazard associated with petrol is chemical pneumonitis that may arise following aspiration of vomitus (secondary to ingestion) or inhalation of aerosol (or aspiration of liquid) during manual siphoning.

Inhalation may cause dizziness, excitement, and incoordination.

Ingestion may cause nausea, vomiting and diarrhoea.

Petrol vapour may be irritating to the eyes and respiratory system.

Health effects of chronic exposure

Prolonged skin exposure to petrol may cause a variety of dermatotic conditions and is generally a result of inadequate or inappropriate use of personal protective equipment.

Chronic exposure to high levels (particularly arising from recreational inhalation) is associated with a range of neurological disorders.

Petrol does not have a measurable effect on human reproduction or development.

There is currently no unequivocal evidence to link petrol with the incidence of cancer in humans but there is limited evidence for carcinogenicity in animals.

Kinetics and metabolism

Absorption

Petrol is a complex mixture of hydrocarbons and so there is no definitive ADME data available for animals or humans. The onset of local or systemic effects following dermal, oral and inhalation exposure indicates that these are all potential routes of entry for petrol vapour or liquid.

Dermal exposure to petrol can be retrospectively identified following solvent extraction of hydrocarbons from the skin surface. However, the profile of hydrocarbons found in the systemic circulation after cutaneous exposure is markedly different to that extracted from the skin (8), indicating selective uptake and distribution of individual hydrocarbon components.

Excretion

The predominant route of elimination for volatile components of petrol is considered to be via expired air. This assumption is based on clinical observation; there are no experimental studies to confirm this route of elimination in humans.

Sources and Route of Human Exposure

Petrol is a complex mixture of aliphatic and aromatic hydrocarbons derived from blending fractions of crude oil with brand-specific additives. The actual composition of petrol will vary according to the source of crude oil, the manufacturing process and between batches.

Unless otherwise stated, this document pertains to unleaded petrol and not products of combustion or individual chemical components (benzene, toluene, xylene, butadiene, etc). Vapour concentrations are expressed as ppm and refer to total hydrocarbon present. However, it should be noted that this conventional measure of concentration introduces a source of error and should be considered at best an approximation, as the average molecular weight (on which the calculation of ppm is based) may vary according to temperature, brand, or batch of technical product.

Petrol contains mixture of volatile hydrocarbons and so inhalation is the most common form of exposure (11). Petrol vapour can reach supra-lethal concentrations in confined or poorly ventilated areas, although such exposures are rare (12-14). A representative sample of petrol vapour concentrations under different exposure scenarios are summarised in Table 1. It should be noted that the chemical composition (hydrocarbon profile) of petrol vapour differs substantially from the corresponding liquid. Petrol vapour is predominantly (>70%) composed of light (C₄ & C₅) hydrocarbons (15) whereas liquid petrol contains mainly (>80%) C₆ to C₁₂ compounds (16). The intentional inhalation of vapour (‘sniffing’ or ‘huffing’) has been extensively documented (17-22).

Table 1: Representative vapour concentrations, expressed in parts per million (ppm) or mass of total hydrocarbons per unit volume (mg m^-3) under different conditions.

Vapour concentration (ppm)	Scenario	Notes	Ref.
25,000	Air above open barrel in unventilated out-house on ‘hot’ day	(Note 1)	(12)
5-320	Air around tanker during bulk-loading	(Note 1)	(23)
2-100	Air around petrol pump in service station	(Note 1)	(24)
1-5	Air within petrol service station	(Note 2)	(25)
174	Worker at bulk loading facility	(Note 3)	(16)
13	Road tanker driver	(Note 3)	(16)
4	Service station worker	(Note 3)	(16)

Note 1: Environmental conditions not reported

Note 2: Temperature varied from 4.5 to 25°C. Recovered petrol components were predominantly (72%) C₄ and C₅ aliphatic hydrocarbons.

Note 3: Average exposure values. Environmental conditions not reported. Vapour concentration reported as the sum of all detected hydrocarbon constituents.

It is generally considered that dermal absorption of petrol does not contribute significantly to systemic signs of toxicity.

Accidental ingestion of petrol by adults is often the result of siphoning petrol tanks whereas the incidence of petrol ingestion in children is relatively low (7, 12).

Health effects of acute or single exposure

Human data

General toxicity

The acute health risks involved in handling and using petrol are minimal, provided that the product(s) are used in accordance with appropriate health and safety practices (26).

The main health effect associated with petrol exposure is chemical pneumonitis, resulting from pulmonary aspiration of vomitus following ingestion (27). A rare complication of petrol intoxication may be cardiac arrhythmia and ventricular fibrillation, attributed to increased myocardial sensitivity to endogenous catecholamines (28).

Vascular endothelial damage of the lung, liver, kidney, and spleen has been described following severe intoxication with associated renal lipid degeneration confined mainly to the proximal tubules (1, 6).

Inhalation

Petrol vapour is readily detectable by most individuals at concentrations below 1 to 2ppm (29) (as reviewed by (7)) although prior exposure within 24 hours or chronic, occupational exposure may increase the olfactory threshold (30).

It has been suggested that the concentration of petrol vapour is the primary determinant of acute toxicity rather than duration of exposure (31). This assumption is based on exposures of less than 30 minutes and relates to one study of three dogs dosed with different petrol products (32).

The minimum concentration of petrol vapour required to elicit a mild response (cough) is probably less than 140ppm (Table 2), although there are no human studies which have determined the exact threshold for this effect.

Following inhalation, effects on the CNS are readily apparent above 900ppm within a few minutes, the morbidity of which resembles alcohol intoxication (dizziness, excitement, incoordination, etc.).

In sufficient concentration (>10,000ppm), petrol may act as an anaesthetic, sometimes resulting in immediate loss of consciousness (1). Indeed, the rapidity of this effect has been implicated as a significant factor in fatal incidents (12-14, 31).

Ingestion

Ingestion of petrol may cause acute, generalised signs of GI tract irritation, including nausea, vomiting, colic and diarrhoea (7). The relatively low oral toxicity of petrol is comparable to that of other petrochemical products such as kerosene (2 to 17g kg^-1) (33) and ingestion of 7.5g kg^-1 has been reported to be the lethal dose in adult humans in the absence of pulmonary effects caused by aspiration of ingested petrol or vomitus (1).

Table 2: Summary of the human inhalation toxicity of petrol vapour in human volunteer studies.

Concentration (ppm)	Duration	Temperature	Effect(s)	Ref
140-270	8h	23 °C	Mild irritation (cough, sore throat), conjunctival hyperaemia.	(30)
200	0.5h	n/s	Threshold level for eye irritation.	(35)
900	8h	22 °C	Mild CNS effects (dizziness). Tolerable.	(30)
2600	1h	n/s	Onset of neuromuscular effects (incoordination.	(30)
> 10,700	< 5 min	n/s	Rapid onset of dizziness and ‘drunkenness’ (ataxia, confusion). Threshold level for onset of anaesthetic effects.	(30)

Table 3: Summary of the human inhalation toxicity of petrol vapour in case studies. *Refers to estimated concentrations based on post-incident measurements

Concentration (ppm)	Duration	Temperature	Effect(s)	Ref
8000 – 35,000*	Minutes	‘hot’	Death occurred sometime within 45 minutes of initial exposure	(12)
5000 – 16,000*	Minutes	n/s	Death occurred sometime within 5 minutes of exposure	(31)

Dermal or ocular exposure

Mild ocular irritation may follow prolonged (8h) exposure to low concentrations (140ppm) of petrol vapour (30) or shorter (30 minute) exposure to vapours above 200ppm (35). More pronounced signs of ocular toxicity (lacrimation) occur above concentrations of 1000ppm (35). One study attributed ocular irritation to the presence of hydrocarbon component(s) present in the most volatile fraction of petrol: “The substance causing eye irritation was distilled from gasoline at extremely low temperatures and in very small amounts” (30).

Skin lesions resulting from acute exposure to liquid petrol are rare and generally result only from prolonged contact (hours) with undiluted product (5). Thus, the extent of skin injury is primarily related to the duration of the exposure rather than concentration. Petrol ‘burns’ resemble scalding, with an initial erythema leading to blister formation (5). Prolonged dermal exposure (45 minutes to 12 hours) may lead to partial or full thickness burns with associated loss of epidermis and coagulation necrosis (3, 6). Discolouration of the skin (brown/yellow/gold) has been observed and attributed to dye additives.

Dermal exposure to petrol is not considered to be a major factor in systemic toxicity (1): this is based upon the assumption that skin contamination will occur concomitantly to inhalation of petrol vapour (which is considered the predominant route of entry). However, several clinical reports have suggested that dermal exposure may substantially contribute to systemic toxicity (2, 6) and it has been recommended that debridement of contaminated skin may limit continued systemic absorption in cases where prolonged dermal exposure has occurred (2). Systemic toxicity resulting from dermal exposure has been noted with other hydrocarbon mixtures such as diesel (36).

Neurotoxicity

As with other hydrocarbon solvents, petrol has anaesthetic (narcotic) properties (Table 2). Petrol also contains a number of potentially neurotoxic chemicals including n-hexane, benzene, butadiene, toluene, ethylbenzene, xylene and trimethyl pentane (37). The approximate concentration of each constituent in liquid petrol and vapour are given in Table 4.

Table 4: Average concentration of potentially neurotoxic constituents of liquid petrol and vapour (11, 38). Numbers in brackets refer to range of values. Vapour values expressed as percentage of total hydrocarbons recovered from air samples obtained during the manual filling of cars (conditions and duration not reported).

Chemical	Liquid Concentration (%w/w)	Vapour Concentration (%w/w)
Benzene	2.5 (0.2 – 4.7)	1.7 (0 – 5.4)
1,3-Butadiene	< 0.1	0.65 (0 – 4.6)
Ethylbenzene	2.6 (1.0 – 5.4)	.009 (0 – 0.1)
n-Hexane	2.5 (0.8 – 5)	1.37 (0 – 6.5)
Toluene	11.4 (2.7 – 21.0)	1.63 (0 – 7.1)
Xylene	10.6 (5.8 – 15.8)	0.48 (0 – 2.1)

Historically, lead (as tetraethyl lead; TEL) has been identified as the principal component of petrol responsible for neurological deficits following intentional (recreational) inhalation or massive acute exposure. However, European legislation has prohibited the use of TEL in petrol since January 2000 (39). Therefore, there is currently a paucity of human data pertaining to the acute neurological effects of current (unleaded) petrol products other than narcosis.

Delayed effects following acute exposure

A variety of delayed, neurological deficits have historically been associated with the acute inhalation of petrol vapour, including peripheral neuritis, impairment of memory, paresthesia, ataxis, and epilepsy (1). A late-onset autoimmune glomerulonephritus has also been observed following acute exposure (4). There is limited evidence to suggest that long-term pulmonary residual effects may occur following chemical pneumonitis (as a result of aspiration-induced pneumonitis) (27, 40), the effects of which are of unknown clinical relevance (41).

Animal data and in-vitro data

The acute toxicity of petrol in a variety of animal species is broadly consistent with that reported in humans, being predominantly associated with CNS, pulmonary and renal effects (42). Data on LD₅₀ and skin and eye irritation are shown in Table 5.

Table 5: Acute toxicity data for petrol [43].

Test	Species	Result
Acute oral (LD50)	Rat	13.6g kg-1
Sensitisation	Guinea pig	Not sensitising
Primary dermal irritancy	Rabbit	Slight
Acute dermal	Rabbit	No mortalities
Primary eye	Rabbit	Non irritating

Health effects following chronic or repeated exposure

Human data

General toxicity

Dysfunction of the central nervous system is the predominant pathological condition associated with chronic exposure to high levels and such effects arising from frequent, recreational exposure (‘sniffing’ or ‘huffing’) have been extensively documented (17-22, 44-49). There is currently insufficient evidence to unequivocally link chronic (occupational) exposure to petrol with other pathological conditions (50). This may be because petrochemical workers are potentially exposed to a wide range of chemicals in addition to other confounding factors (42).

Historically, lead has been identified as the principal component of petrol responsible for neurotoxicity (51) and studies have demonstrated a link between lead body burden and neurological deficits as a result of petrol abuse (‘sniffing’ or ‘huffing’) (52). However, it should be noted that the volatility of tetraethyl lead (TEL) is relatively low (0.4mm Hg at 25ºC) and so prolonged dermal exposure associated with the practice of petrol sniffing is likely to be the predominant route of entry for TEL rather than inhalation (7). Since 2000, petrol has only been commercially available in ‘unleaded’ form within the UK and most of Europe. This policy limits the concentration of lead in marketable petrol to less than 0.005g L^-1 as defined at Annex I of the 1998 EU Directive (39).

Whilst there is a known association between chronic petrol exposure and renal cancer in male rats (53-55), there is currently no evidence to link petrol exposure and renal cancer in humans (56, 57). It is generally accepted that the susceptibility of male rats is mediated via a specific protein (α-2-microglobin) which is absent in other mammals (54, 58).

Genotoxicity

At relatively high concentrations (1000 to 2500ppm) in cell culture medium, petrol was mutagenic in drosophila melanogaster (59).

Negative results have been reported when petrol was investigated for its ability to induce gene mutations in bacteria (Salmonella assay) and mammalian cells using the mouse lymphoma assay (60). Negative results were also obtained in another mammalian cell assay for gene mutation using a human lymphoblastoid cell line (61). Negative results were reported in an in vivo bone marrow assay for clastinogenicity in the rat (60).

There is a report of positive results being obtained using the UDS (unscheduled DNA synthesis) assay: limited studies in vitro (essentially only one dose level used) gave a positive result using rat hepatocytes and marginal effect in human and mouse hepatocytes. In the same report, negative results were obtained from in vivo UDS assays in the rat, but a slight increase in UDS was observed in mice (62).

Overall, it can be concluded that petrol does not have significant mutagenic activity.

Carcinogenicity

Epidemiological studies have not demonstrated a statistically significant link between cancer and occupational exposure to petrol (63-71). However, the IARC has classified petrol as “possibly carcinogenic to humans” (Group 2B) mainly on the basis that there was inadequate evidence for the carcinogenicity in humans but there was limited evidence for the carcinogenicity in experimental animals. It was also noted that certain components of petrol are known or possible human carcinogens such as benzene and 1,3-butadiene. (57).

Petrol is assigned the Risk Phrase R45 (“may cause cancer”) under the Chemical Hazard Information and Packaging for Supply (CHIPS) Regulations.

Reproductive and developmental toxicity

No reports specifically pertaining to the human reproductive or developmental toxicity of petrol were identified. The NOAEL for reproductive toxicity in a two-generation rat study was reported to be 20,000mg m^-3 (72).

Petrol is not classified under CHIPS (Chemical Hazards Information and Packaging Supply) regulations as a reproductive or developmental hazard.

References 

[1] Machle W (1941). ‘gasoline intoxication’ Journal of the American Medical Association 117, 1965-1971.

[2] Hansbrough JF, Zapata-Sirvent R, Dominic W, Sullivan J, Boswick J and Wang XW (1985). ‘Hydrocarbon contact injuries’ Journal of Trauma - Injury, Infection and Critical Care 25, 250-2.

[3] Schneider MS, Mani, MM and Masters FW (1991). ‘Gasoline-induced contact burns’ Journal of Burn Care & Rehabilitation 12, 140-3.

[4] Simpson LA and Cruse CW (1981). ‘Gasoline immersion injury’ Plastic and Reconstructive Surgery 67, 54-7.

[5] Binns H, Gursel E and Wilson N. (1978). ‘Gasoline contact burns’ Journal of the American College of Emergency Physicians 7, 404-5.

[6] Walsh WA, Scarpa FJ, Brown RS, Ashcraft KW, Green VA, Holder TM and Amoury RA (1974). ‘Gasoline immersion burn’ New England Journal of Medicine 291, 830.

[7] ‘Toxicology update. Gasoline’ (1989). Journal of Applied Toxicology 9, 203-10.

[8] Hieda Y, Tsujino Y and Takeshita H (2005). ‘Skin analysis to determine causative agent in dermal exposure to petroleum products’ Journal of Chromatography B 823, 53-9.

[9] Harman AW, Frewin DB and Priestly BG (1981). ‘Induction of microsomal drug metabolism in man and in the rat by exposure to petroleum’ Occupational and Environmental Medicine 38, 91-7.

[10] Rao GS and Pandya KP (1980). ‘Hepatic metabolism of heme in rats after exposure to benzene, gasoline and kerosene’ Archives of Toxicology 46, 313-7.

[11] Cecil R, Ellison RJ, Larnimaa K, Margary SA, Mata JM, Morcillo L, Muller JM, Peterson DR and Short D. (1997). ‘exposure profile: gasoline’ CONCAWE Report 97/52.

[12] Aiden R (1958). ‘petrol-vapour poisoning’ British Medical Journal ii, 369-370.

[13] Ainsworth R (1960). ‘petrol-vapour poisoning’ British Medical Journal 1, 1547-1548.

[14] Takamiya M, Niitsu H, Saigusa K, Kanetake J. and Aoki Y. (2003). ‘A case of acute gasoline intoxication at the scene of washing a petrol tank’ Legal Medicine (Tokyo) 5, 165-9.

[15] Halder CA, Van Gorp GS, Hatoum NS and Warne TM (1986). ‘Gasoline vapor exposures. Part II. Evaluation of the nephrotoxicity of the major C4/C5 hydrocarbon components’ American Industrial Hygiene Association Journal 47, 173-5.

[16] Carter M, Claydon M, Giacopetti D, Money C, Pizzella G, Margary A. and Viinanen R. (2002). ‘A survey of european gasoline exposures for the period’ 1999 to 2001. CONCAWE Report 9/02.

[17] Edminster SC and Bayer MJ (1985). ‘Recreational gasoline sniffing: acute gasoline intoxication and latent organolead poisoning. Case reports and literature review’ Journal of Emergency Medicine 3, 365-70

[18] Cairney S, Maruff P, Burns C and Currie B (2002). ‘The neurobehavioural consequences of petrol (gasoline) sniffing’ Neuroscience & Behavioral Reviews 26, 81-9.

[19] Flanagan RJ and Ives RJ (1994). ‘Volatile substance abuse’ Bulletin on Narcotics 46, 49-78.

[20] Fortenberry JD (1985). ‘Gasoline sniffing’ American Journal of Medicine 79, 740-4.

[21] Remington G and Hoffman BF (1984). ‘Gas sniffing as a form of substance abuse’ Canadian Journal of Psychiatry 29, 31-5.

[22] Poklis A and Burkett CD (1977). ‘Gasoline sniffing: a review’ Clinical Toxicology 11, 35- 41.

[23] Periago JF and Prado C (2005). ‘Evolution of occupational exposure to environmental levels of aromatic hydrocarbons in service stations’ Annals of Occupational Hygiene 49, 233-40.

[24] McDermott HJ and Vos GA (1979). ‘Service station attendants’ exposure to benzene and gasoline vapors’ American Industrial Hygiene Association Journal 40, 315-21.

[25] Kearney CA and Dunham DB (1986). ‘Gasoline vapor exposures at a high volume service station’ American Industrial Hygiene Association Journal 47, 535-9.

[26] Henry JA (1998). ‘Composition and toxicity of petroleum products and their additives’ Human & Experimental Toxicology 17, 111-23.

[27] Litovitz T and Greene AE (1988). ‘Health implications of petroleum distillate ingestion’ Occupational Medicine 3, 555-68.

[28] Litovitz T (1988). ‘Myocardial sensitization following inhalation abuse of hydrocarbons’ Occupational Medicine 3, 567-568.

[29] Amoore J, Von Burg R and Whittemore I (1983). ‘Detectibility of Gasoline by its Odor’ The Toxicologist. 22nd Annual Meeting of the Society of Toxicologists. March 6-11.

[30] Drinker P, Yaglou CP and Warren MF (1943). ‘The threshold toxicity of gasoline vapour’ Journal of Industrial Hygiene & Toxicology 25, 225-232.

[31] Wang CC and Irons GV Jr (1961). ‘Acute gasoline intoxication’ Archives of Environmental Health 2, 714-6.

[32] Haggard HW (1920). ‘the anaesthetic and convulsant effects of gasoline vapour’ Journal of Pharmacology & Experimental Therapeutics 16, 401-404.

[33] Chilcott RP (2006). ‘Kerosene: toxicological overview’ Health Protection Agency Compendium of Chemical Hazards.

[34] Banner W Jr and Walson PD (1983). ‘Systemic toxicity following gasoline aspiration’ American Journal of Emergency Medicine 1, 292-4.

[35] Davis A, Schafer LJ and Bell ZG (1960). ‘The effects on human volunteers of exposure to air containing gasoline vapor’ Archives of Environmetal Health 1, 548-54.

[36] Barrientos A, Ortuno MT, Morales JM, Tello FM and Rodicio JL (1977). ‘Acute renal failure after use of diesel fuel as shampoo’ Archives of Internal Medicine 137, 1217.

[37] Ritchie GD, Still KR, Alexander WK, Nordholm AF, Wilson CL, Rossi J, 3rd and Mattie DR (2001). ‘A review of the neurotoxicity risk of selected hydrocarbon fuels’ Journal of Toxicology and Environmental Health, Part B, 223-312.

[38] Coker DT, Christian F, Claydon MF, Irvine D, Portail C, Tindle P, Webb CLF and Eyres AR (1987). ‘A Survery of exposures to gasoline vapour’ CONCAWE Report 4/87.

[39] European Union (1998). Directive 98/70/EC of the European parliament and of the Council: Amendment to Coucnil Directive 93/12/EEC. Official Journal of the European Communities 350/59.

[40] Eade NR, Taussig LM and Marks MI (1974). ‘Hydrocarbon pneumonitis’ Pediatrics 54, 351-7.

[41] Seymour FK and Henry JA (2001). ‘Assessment and management of acute poisoning by petroleum products’ Human & Experimental Toxicology 20, 551-62.

[42] International Agency for the Research on Cancer (IARC) (1989). ‘Occupational exposures in petroleum refining: Crude oil and major petroleum fuels’ IARC Monographs on the evaluation of carcinogenic risks to humans. Volume 45. Lyon.

[43] Beck LS, Hepler DI and Hansen KL (1984) ‘The acute toxicity of selected hydrocarbons’ Princeton Scientific Publishers, Inc.,

[44] Cairney S, Maruff P, Burns CB, Currie J and Currie BJ (2004). ‘Neurological and cognitive impairment associated with leaded gasoline encephalopathy’ Drug Alcohol Dependance 73, 183-8.

[45] Cairney S, Maruff P, Burns CB, Currie J. and Currie BJ (2005). ‘Neurological and cognitive recovery following abstinence from petrol sniffing’ Neuropsychopharmacology 30, 1019-27.

[46] Goodheart RS and Dunne JW (1994). ‘Petrol sniffer’s encephalopathy. A study of 25 patients’ Medical Journal of Australia 160, 178-81.

[47] Maruff P, Burns CB, Tyler P, Currie BJ and Currie J (1998). ‘Neurological and cognitive abnormalities associated with chronic petrol sniffing’ Brain 121 (Pt 10), 1903-17.

[48] Poklis A (1976). ‘Death resulting from gasoline “sniffing”: a case report’ Journal of Forensic Science Society 16, 43-6.

[49] Valpey R, Sumi SM, Copass MK and Goble GJ (1978). ‘Acute and chronic progressive encephalopathy due to gasoline sniffing’ Neurology 28, 507-10.

[50] Harrington JM (1987). ‘The health experience of workers in the petroleum manufacturing and distribution industry’ CONCAWE report number 2/87.

[51] Kovarik W (2005). ‘Ethyl-leaded gasoline: how a classic occupational disease became an international public health disaster’ International Journal of Occupational and Environmental Health 11, 384- 97.

[52] Seshia SS, Rjani KR, Boeckx RL and Chow PN (1978). ‘The neurological manifestations of chronic inhalation of leaded gasoline’ Developmental Medicine & Child Neurology 20, 323-34.

[53] Halder CA, Holdsworth CE, Cockrell BY and Piccirillo VJ (1985). ‘Hydrocarbon nephropathy in male rats: identification of the nephrotoxic components of unleaded gasoline’ Toxicology and Industrial Health 1, 67-87.

[54] Olson MJ, Garg BD, Murty CV and Roy AK (1987). ‘Accumulation of alpha 2u-globulin in the renal proximal tubules of male rats exposed to unleaded gasoline’ Toxicology and Applied Pharmacology 90, 43-51.

[55] Short BG, Burnett VL, Cox MG, Bus JS and Swenberg JA (1987). ‘Site-specific renal cytotoxicity and cell proliferation in male rats exposed to petroleum hydrocarbons’ Laboratory Investigation 57, 564-77.

[56] Trump BF, Lipsky MM, Jones TW, Heatfield BM, Higginson J, Endicott K and Hess HB (1984) ‘An Evaluation of the significance of experimental hydrocarbon toxicity in man’ Princeton Scientific Publishers Inc., New Jersey

[57] IARC (1989). ‘Occupational Exposure in Petroleum Refining; Crude Oil and Major Petroleum Fuels’ IARC Monographs on the Evaluation of Carcinogenic Risks to Humans 45.

[58] Olson MJ, Johnson JT and Reidy CA (1990). ‘A comparison of male rat and human urinary proteins: implications for human resistance to hyaline droplet nephropathy’ Toxicology and Applied Pharmacology 102, 524-36.

[59] Nylander PO, Olofsson H, Rasmuson B and Svahlin H (1978). ‘Mutagenic effects of petrol in Drosophila melanogaster I. Effects of benzene and 1,2- dichloroethane’ Mutation Research 57, 163-7.

[60] Conaway CC, Schreiner CA and Cragg ST (1984) ‘Mutagenicity evaluation of petroleum hydrocarbons’ Princeton Scientific Publishers Inc, New Jersey

[61] Richardson KA, Wilmer JL, Smith-Simpson D and Skopek TR (1986). ‘Assessment of the genotoxic potential of unleaded gasoline and 2,2,4- trimethylpentane in human lymphoblasts in vitro’ Toxicology and Applied Pharmacology 82, 316-22.

[62] Loury DJ, Smith-Oliver T, Strom S, Jirtle R, Michalopoulos G and Butterworth BE (1986). ‘Assessment of unscheduled and replicative DNA synthesis in hepatocytes treated in vivo and in vitro with unleaded gasoline or 2,2,4- trimethylpentane’ Toxicology and Applied Pharmacology 85, 11-23.

[63] Dement JM, Hensley L and Gitelman A (1997). ‘Carcinogenicity of gasoline: a review of epidemiological evidence’ Annals of the New York Academy of Sciences 837, 53-76.

[64] Enterline PE (1993). ‘Review of new evidence regarding the relationship of gasoline exposure to kidney cancer and leukemia’ Environmental Health Perspectives 101 Suppl 6, 101- 3.

[65] Enterline PE and Viren J (1985). ‘Epidemiologic evidence for an association between gasoline and kidney cancer’ Environmental Health Perspectives 62, 303-12.

[66] McLaughlin JK (1993). ‘Renal cell cancer and exposure to gasoline: a review’ Environmental Health Perspectives 101 Suppl 6, 111-4.

[67] McLaughlin JK, Blot WJ, Mandel JS, Schuman LM, Mehl ES and Fraumeni JF Jr (1983). ‘Etiology of cancer of the renal pelvis’ Journal of the National Cancer Institute 71, 287-91.

[68] McLaughlin JK, Blot WJ, Mehl ES, Stewart PA, Venable FS and Fraumeni JF Jr (1985). ‘Petroleum-related employment and renal cell cancer’ Journal of Occupational Medicine 27, 672-4.

[69] McLaughlin JK, Mandel JS, Blot WJ, Schuman LM, Mehl ES and Fraumeni JF Jr (1984). ‘A population–based case–control study of renal cell carcinoma’ Journal of the National Cancer Institute 72, 275-84.

[70] Norell S, Ahlbom A, Olin R, Erwald R, Jacobson G, Lindberg-Navier I and Wiechel KL (1986). ‘Occupational factors and pancreatic cancer’ British Journal of Industrial Medicine 43, 775-8.

[71] Rushton L and Alderson MR (1983). ‘Epidemiological survey of oil distribution centres in Britain’ British Journal of Industrial Medicine 40, 330-9.

[72] McKee RH, Dally S, Dmytrasz BA, Gonnet J F, Hagemann RE, Mackerer CR, Nessel CS, Priston RA and Riley AJ (2000). ‘An assessment of the reproductive toxicity of gasoline vapour’ CONCAWE Report number 00/53. Brussels.

Email chemcompendium@ukhsa.gov.uk if you have any questions about this guidance or enquiries@ukhsa.gov.uk if you have any other questions.

Feedback survey

Help us improve the compendium of chemical hazards by taking our short survey.