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_ -� CrLS 66.23 <br /> 061er4ed in the lung, nasal cavirir - and sinuses. digestive s ~ <br /> 'stain. ystam, <br /> skin_ pancreas and kidney. Leukemias and lymphomas have also <br /> been reported (1$17) . <br /> 66.3.3 Toxicalo¢y 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 /> Hexane may be the most highly toxic member of the alkanes. then <br /> ittgesced, iz causes nausea, vertigo, bronchial and general intestinal 3 <br /> irritation and CNS effects. It also presents an acute aspiratson <br /> hazard. Acute exposura occurs pri zr ly through inhalation. F <br /> Yon specific svmpccros such as vertigo, headache. nausea and vomiti <br /> are the first co be manifestng <br /> ed_ at high concencratxons, s <br /> narcosis-like scat& appears as a resulr- of CVS depression. <br /> P=e-narcotic svmpcams. occur at vapor concentrations ranging from <br /> 1500.2500 ppm- n•Hexane irritates the eyes and mucous membrineS_ <br /> These effects can be seen after an exposure of 880 ppm for 15 minutes. <br /> Skin contact primarily causes fat removal and cutaneous irritation. <br /> chronic exposure cc n-hexane vapors causes <br /> The first clinical sign of neural damage is a feeling peripheral <br /> of numbnesstn <br /> the toes and fingers. Progression leads co further symmetrical sensory <br /> impairment in the distal portions of the extremities and to loss of <br /> =scular stretching reflexes. Ultimately, symmetrical muscular <br /> Paralysi ddevel s, chiefly in the distal portion of the extremieies. <br /> Paralysis develops with varying degrees of impaired grasping and <br /> talking. This may include muscular acro is { <br /> palvneuropachv) . The development of electrophysiological(sensorimocnr <br /> parallels the severity of the clinical uchanges <br /> a l In most <br /> cases. nerve coaductivicy is ne+scraliaed. In same cases. ecranialsnerve <br /> ittvalvemen= is also observed. After exposure ceases. :ecovery begins �. <br /> tichin 6 to l0 months in mild to moderate cases. but may cake uo cm 3 <br /> Dears in serious cases. The threshold level ac which neuroaachv occurs <br /> aas not been firmly established bur svmpcoms have been observed in <br /> :eo4Le exposed to concancracions rangin <br /> .oncns. g r-nm 10 to 200 ppm --:or 9-12 <br /> In animals, sighs of narcosis are seen after mice are exposed to <br /> tapor levels of 16.000 ppm for 5 minutes . Deach generally occurred at p, <br /> concentrations between 43.800 and 52.000 <br /> oral ppm after 9-t19 minutes. The <br /> LD is cited as 24 mL/kg for 14-dav-old rats and '_4 mL,'�;g for <br /> ?oung adult rats. <br /> Long-term inhalation experiments in rats suggest that the first y' <br /> Signs of neurotoxicity appear after they are exposed to levels of 200 <br /> ppm for 24 weeks. This higher chreshold co induce neurotoxicity in <br /> animals may be nue <br /> to differences in metabolism. Specxfically, <br /> 2.hexanol is the chief metabolite in animals . : Rile- 2.5-hexanecione <br /> u <br /> 6/87 , <br />