Biomedical Engineering Reference
In-Depth Information
3
Human Toxicity
JOHN J. CLARY
Bio Risk, Midland, MI, USA
3.1
INTRODUCTION
The information on human toxicity is primarily from accidentrial or
deliberate ingestion of methanol as a substitute for ethanol. The early
human data also contains information about occupational over exposure
both from the inhalation and dermal routes. Most of the data are a result
of a single overexposure. There are a very few reports of methanol
toxicity due to repeat sublethal exposure. The difference in the human
response to methanol when compared to most of the animal data is due
to the difference in metabolism between rodents and humans. In
humans, the rate-limiting step in the metabolism of methanol is the
buildup of formic acid in the blood due to the saturation of the enzyme,
formic dehydrogenase. In rodents, the problem appears to be related to
the build up of blood methanol as a result to the saturation of the enzyme
catalase, the enzyme, that is, primarily responsible for the breakdown of
methanol to formaldehyde (Kavet and Nauss, 1990). In humans, a
different enzyme (alcohol dehydrogenase, ADH) carries out the break-
down of methanol to formaldehyde (Kavet and Nauss, 1990).
Humans are more sensitive to the toxic action of methanol than
animal species. In the rat, for instance, the acute lethal dose is about
6-10 times higher than the dose, that is, required to produce death in
humans (Gilger and Potts, 1955).
This chapter examines dietary exposure to methanol and normal
blood levels of methanol and formic acid in humans. The result of
