health and safety plan solid waste management unit assessment

METHYiL ETHYL KETONE 41-14
axons in the peripheral and central nemous system, as well as severe
potentiation of hexane neurotoxicity and shortened onset of
morphological and clinical signs developed in animals exposed to the
methyl ethyl ketone/hexane mixture. Motor impairment of the methyl
ethyl ketone/hexane treated rats varied from a waddling gait and
eversion of hind limbs to quadriplegia. Methyl ethyl ketone alone did
not produce neuropathy. Rats exposed to extremely high concentrations
of pure methyl ethyl ketone (6000-10,000 ppm), however, developed
severe bronchopneumonia and died.
The potentiation effect of methyl ethyl ketone on hexane-induced
neuropathy has also been observed with methyl butyl ketone (1029,103O).
Hats intoxicated by continuous exposure to air containing methyl ethyl
ketone and methyl butyl ketone vapor in a ratio of 1125:225 ppm
developed clinical evidence of neuropathy after 25 days; rats inhaling
225 ppm methyl butyl ketone alone exhibited neuropathy after 66 days.
Methyl ethyl ketone potentiates the neurotoxic effects of methyl
butyl ketone and hexane presumably by stimulating their metabolism to
neurotoxic metabolites (1015). Both hexane and methyl butyl ketone
share common products in their metabolic pathways, i.e., 2,5-hexanediol
and 2,5-hexanedione. Hexanedione is believed to be the neurotoxic
agent (1030,1014). Administration of hexane and methyl ethyl ketone
together results in a significant increase in the activity of
mixed-function oxygenase enzymes in rats (1004) and the urinary
excretion of 2,S-hexanedione is increased after administration of the
methyl ethyl ketone/methyl butyl ketone mixture to rats (1002).
Furthermore, administration of 2,5-hexanedione produced effects
indistinguishable from hexane or methyl butyl ketone neurotoxicity
(1014).
41.3.2 Human and Epidemiologic Studies
41.3.2.1 Short-term Toxicologic Effects
Berg & A. (1016) reported a case of retrobular neuritis in an
U-year-old male exposed to methyl ethyl ketone while removing paint in
an enclosed area. Symptoms included a dull headache, mild vertigo and
diminished vision in both eyes. Ophthalmic examination and testing 2
hours later revealed marked enlargment of the blind spot and superior
arcuate-type defects in both eyes. Blood analysis showed the presence
of methanol and formaldehyde. Thirty-six hours after exposure, vision
returned to normal. Berg postulated that the patient had suffered
optic nerve toxicity induced by methanol formed from the metabolism of
methyl ethyl ketone.
Munies and Wurster (1031) demonstrated that methyl ethyl ketone in
contact with the skin resulted in a partial dehydration of the Stratum
corneum. Wehlberg (1009) showed that the spontaneoy transient
whitening of the skin caused by excessive exposure to methyl ethyl
ketone is due to a change in structure and the removal of the skin
lipids rather than by vasoconstriction.
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