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y UIOMOTI4E GA.S0LTXE 65-26 n .` cancer hypothesis in mind and Little data are available on duration of exposure or r-=e since first exposure in relation to kidney cancer (2281) . f t.J A _atrospective case-control study (2276) :gas conducted to ' examine increased risk of renal cell carcinoma. Only 4 of the 92 cancer cases and 122 of the i,558 non-neoplastic control patients had any occupational exposure to gasoline. This finding suggests that there is no independent effect of occupational gasoline exposure on risk for renal cell carcinoma. Thus the epidemiologic Literature provides no consistent evidence for a relationship between gasoline exposure and kidney cancer in man. A small epidemiology study recently reported to EPA found leukemia deaths in auto mechanics and gas station attendants to be in excess of standard mortality ratios; however. more definitive studies are necessary to determine if the leukemia excess is associated with gasoline, benzene or other chemicals in their work environment (2285) . 65.3.3 Toxicology of Gasoline Components A brief overview of the toxicology of the major hydrocarbon r components of automotive gasoline (see Table 65-3) are summarized �+ below. The acute toxicity values for these components are presented in Table 65-4. n-Hexane Hexane may be the most highly toxic member of the alkanes. When ingested, it causes nausea. vertigo, bronchial and general intestinal , irritation and CNS effects. It also presents an acute aspiration hazard. Acute exposure occurs primarily through inhalation. Non-specific symptoms :such as vertigo, headache, nausea and vomiting are the first to be manifested. At high concentrations, a narcosis-like state appears as a result of CNS depression. Pre-narcotic symptoms occur at vapor concentrations ranging from 1500-2500 ppm. n-Hexane irritates the eyes and mucous membranes. These effects can be seen after an exposure of 880 ppm for 15 minutes. Skin contact primarily causes fat removal and cutaneous irritation. Chronic exposure ca n-hexane vapors causes peripheral neuropathy. The first clinical sign of neural damage is a feeling of numbness in the toes and fingers. Progression leads to further symmetrical sensory impairment in the distal portions of the extremities and to loss of J muscular stretching reflexes. Ultimately. symmetrical muscular weakness develops. chiefly in the distal portion of the extremities. Paralysis develops with varying degrees of impaired grasping and walking. This may include muscular atrophy (sensorimocor poly- neuropathy) . The development of electrophysiological changes parallels the severity of the clinical picture. In the most severe cases, nerve conductivity is neutralized. In some cases, cranial, nerve involvement is also observed. After exposure ceases, recovery begins within 6 to 6/87 �i �