Biomedical Engineering Reference
In-Depth Information
vanilla extract, and perfumes. In 1904, nearly 2 million workers used
methanol in some form. This additional exposure resulted in the
increase in the ingestion of methanol in place of ethanol. In a review,
Wood and Buller (1904) reported 54 cases of blindness and death
because of drinking or inhalation exposure and an additional 84 cases of
death, but no blindness. In addition, 90 cases of blindness, followed by
death because of drinking of methylated spirits were reported in this
review (Wood and Buller, 1904). By 1913, hundreds of cases of
methanol poisoning from ingestion or inhalation exposure had been
reported in a review by Baskerville (1913).
Early industrial cases of acute methanol poisoning, via both the
dermal and inhalation routes, were reported when methanol was used as
a solvent, but reports of oral methanol poisoning rarely occurred in the
literature until after 1890 when pure methanol was produced at a low
cost. In 1910, some cheap wines, brandies, and whiskey were reported
to contained 24-43% methanol as a substitute for the more expensive
ethanol (Ziegler, 1921).
It was not until 1923 the poisoning of a group of dockworkers in
Hamburg following the ingestion of methanol, that the role of methanol
ingestion was first accepted as the casual agent in a mass poisonings
(Reif, 1923).
Woods (1912) postulated that on the basis of his experience with
methanol poisoning patents, if 10 people drank 4 ounces (
100 grams)
of Colombia sprits four would die, two out of the four would develop
blindness before they die. Six would live, but two would develop
blindness over time (Wood, 1912). On the basis of this postulation,
the dose that is lethal to about half of the exposed individuals is about
1.4 g/kg. This value is in line with other estimates that 0.3-1.0 g/kg is a
minimal lethal in humans (Kavet and Nauss, 1990). It is difficult to get
better or more accurate values based on the actual amount of methanol
ingestion, because the value is subjective in most cases. There also
appears to a variable susceptibility in the human population (Kavet and
Nauss, 1990). The ingestion of ethanol with methanol, which slows
methanol metabolism and the hepatic folate status, which is important
in the metabolism of formate, both can affect the methanol susceptibil-
ity in humans (Anonymous, 1997).
