health and safety plan solid waste management unit assessment

AUTOMOTIVE GASOLINE 65-26
cancer hypothesis in mind and little data are available on duration of
exposure or time since first exposure in relation to kidney cancer
(2281).
A retrospective case-control study (2276) was conducted to
examine increased risk of renal cell carcinoma. Only 4 of the 92
cancer cases and 122 of the 1,558 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
components of automotive gasoline (see Table 65-3) are summarized
below. The acute toxicity values for these components are presented in
Table 65-4.
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 to 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
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 (sensorimotor polyneuropathy).
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
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