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ProMED: MeOH toxic outbreak, Kenya

Gary Greenberg Gary.Greenberg at Duke.Edu
Sat Nov 18 15:00:07 EST 2000


Date: 17 Nov 2000 
From: Charlene Repique <repique at cber.fda.gov> 
Source: Reuters via CNN.com, 17 Nov 2000 [edited]
<http://www.cnn.com/2000/WORLD/africa/11/17/kenya.brew.reut/index.html>


Death toll from fatal Kenyan brew rises to nearly 100 -
-----------------------------------------------------

Nearly 100 people have died in Kenya after drinking a fatally
contaminated illegal brew, and another 400 people are hospitalized, some
suffering from blindness, Kenyan police said on Friday. 

- -- ProMED-mail <http://www.promedmail.org>

[Methanol (wood alcohol) is produced from the destructive distillation
of wood. Epidemics of methanol toxicity have resulted from the
consumption of methanol-contaminated whiskey. The formation of 2 toxic
metabolites, formaldehyde and formic acid, causes methanol poisoning.
The elimination rate depends upon the the folate pool. In primates it is
generally small and consequently primates (including humans) are more
sensitive to methanol toxicity than other animals.

Methanol is widely available in formulations including antifreeze,
windshield washer fluid, Sterno canned heat, shellacs, various paints,
paint removers, varnishes, duplicating fluids, and gasoline additives.

Fatalities have been reported after ingestion of 15 ml or 3 teaspoons of
a 40 percent solution, although 30 ml is generally considered a minimal
lethal dose. With aggressive medical care it is possible to survive the
ingestion of 500-600 ml.  However, consumption of as little as 10 ml may
cause blindness, with the amount varying with the individual.

Methanol is well absorbed from the gastrointestinal tract and peak
levels occur generally within 30-90 minutes. It is distributed into
tissues, so concentrations in the vitreous humor and optic nerve are
high. The highest concentrations are found in the kidney, liver and
gastrointestinal tract, with smaller concentrations in the brain, muscle
and adipose tissues.

Methanol is oxidized 10 times more slowly than ethanol. Consequently
there is a longer elimination half-life.

Onset of symptoms varies between 40 minutes and 72 hours
post-ingestion.  Co-ingestion with alcohol will delay the appearance of
symptoms, but the absence of symptoms does not exclude serious toxicity.
The usual latent period is 12-24 hours.

Clinical signs may include headache, vertigo, lethargy and confusion,
which are common in mild to moderate ethanol intoxications. Coma and
convulsions appear in severe cases, probably as a result of cerebral
edema.  Methanol produces little to no euphoria, unlike ethanol.

Blurred vision, decreased visual acuity, and photophobia (sensitivity to
light) are common complaints. Constricted visual fields, fixed and
dilated pupils, retinal edema and hyperemia of the optic disk are common
clinical findings. Prompt initial therapy is necessary to reverse
symptoms, though visual defects have persisted in up to 25 percent of
severe cases.

Methanol is a mucosal irritant and may produce nausea, vomiting and
abdominal pain, not unlike large doses of ethanol.

Early in the clinical course, gut decontamination with ipecac or lavage
may be indicated.  However, if the methanol is mixed with ethanol, these
patients may not realize something is out of the ordinary until it is
too late for this type of treatment to be helpful.

Intravenous administration of ethanol in a 10 percent dextrose solution
may be helpful. As ethanol prolongs the elimination half-life of
methanol, the treatment may take several days and the patient should be
hospitalized. Dialysis may be necessary to prevent kidney failure as
well. - Mod.TG]

..............................tg/pg/es
-- 
Gary N. Greenberg, MD MPH    Sysop / Moderator Occ-Env-Med-L MailList
gary.greenberg at duke.edu     Duke Occupat, Environ, Int & Fam Medicine
OEM-L Maillist Website:                      http://occhealthnews.com


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