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FUEL OILS 66-23<br />

observed in the lung, nasal cavity <strong>and</strong> sinuses, digestive system,<br />

brain, skin, pancreas <strong>and</strong> kidney. Leukemias <strong>and</strong> lymphomas have also<br />

been reported (1817).<br />

66.3.3 Toxicology of Fuel Oil Components<br />

A brief overview of the toxicology of the major hydrocarbon<br />

components of fuel oils are summarized below (see Table 66-5).<br />

n-Hew<br />

Hexane may be the most highly toxic member of the alkanes. When<br />

ingested, it causes nausea, vertigo, bronchial <strong>and</strong> general intestinal<br />

irritation <strong>and</strong> CNS effects. It also presents an acute aspiration<br />

hazard. Acute exposure occurs primarily through inhalation.<br />

Non-specific symptoms such as vertigo, headache, nausea <strong>and</strong> vomiting<br />

are the first to be manifested. At high concentrations, a<br />

narcosis-like state appears as a result of CNS depression.<br />

Pre-narcotic symptoms occur at vapor concentrations ranging from<br />

1500-2500 ppm. n-Hexane irritates the eyes <strong>and</strong> mucous membranes.<br />

These effects can be seen after an exposure of 880 ppm for 15 minutes.<br />

Skin contact primarily causes fat removal an@ cutaneous irritation.<br />

Chronic exposure to n-hexane vapors causes peripheral neuropathy.<br />

The first clinical sign of neural damage is a feeling of numbness in<br />

the toes <strong>and</strong> fingers. Progression leads to further symmetrical sensory<br />

impairment<br />

muscular<br />

in the<br />

stretching<br />

distal portions<br />

reflexes.<br />

of the extremities <strong>and</strong> to loss of<br />

Ultimately, symmetrical muscular<br />

weakness<br />

Paralysis<br />

develops,<br />

develops<br />

chiefly<br />

with<br />

in the<br />

varying<br />

distal<br />

degrees<br />

portion of the extremities.<br />

of impaired grasping <strong>and</strong><br />

walking; This may include muscular atrophy (sensorimotor<br />

polyneuropathy). The development of electrophysiological changes<br />

parallels the severity of the clinical. picture. In the most severe<br />

cases, neme conductivity is neutralized. In some cases, cranial nerve<br />

involvement is also observed. After exposure ceases, recovery begins<br />

within 6 to 10 months in mild to moderate cases, but may take up to 3<br />

years in serious cases. The threshold level at which neuropathy occurs<br />

has not been<br />

people exposed<br />

firmly established<br />

to concentrations<br />

but symptoms have<br />

ranging from 10 to<br />

been observed in<br />

200 ppm for 9-12<br />

months.<br />

In animals, signs of narcosis are seen after mice are exposed to<br />

vapor levels of 16,000 ppm for 5 minutes. Death generally occurred at<br />

concentrations between 43,800 <strong>and</strong> 52,000 ppm after 9-119 minutes. The<br />

oral ID,, is cited as 24 mL/kg for 14.day-old rats <strong>and</strong> 49 mL/kg for<br />

young adult rats.<br />

Long-term inhalation experiments in rats suggest that the first<br />

signs of neurotoxicity appear after they are exposed to levels of 200<br />

ppm for 24 weeks. This higher threshold to induce neurotoxicity in<br />

animals may be due to differences in metabolism. Specifically,<br />

2-heexanol is the chief metabolite in animals, while 2,5-hexanedione<br />

6/87<br />

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