Methanol Toxicity

a slidecast by Dane Whitman

BackgroundConventional Uses

Chemical Feedstock(formaldehyde, acetic acid, chloromethane, and methyl ter-butyl ether)

Chemical Solvent(paints, carburetor cleaners, plastics, plywood, and automobile windshield washer solutions)

Fuel

Additive for HydraulicFracturing

Estimated 1992

Release (US)

Reported Release to:

(million lbs/year)

Atmosphere 195

Underground Injection

27

Land 3.3

Water

Total

16.4

251.7

Adapted from Malcolm Pirnie (1999)

Biochemical Mechanisms

●Study by Liesivuori & Savolainen (1991)

Looked to understand effects of methanol toxicity.

Monitored occupational methanol exposure

Looked to understand toxicity through chemical mechanisms.

Exposure

Inhalation and Skin Absorption.

58% Retention Rate in Humans.

Potentially damages eyes, heart, brain, kidneys.

Metabolization

●Methanol→Formaldehyde→Formic Acid

Performed by Alcohol Dehydrogenase and Formaldehyde Dehydrogenase in Liver.

Inhibition of Cytochrome c- Oxidase

Last Enzyme in Electron Transport Chain

Metabolic Acidosis

●“Circulus Hypoxicus”

Formic Acid poisoning more severe with drop in pH.

Formic Acid is itself acidic. (who knew?...)

Formic Acid causes Lactic Acid production

Excretion

●Formic Acid half life?

20 hours.

Methanol exposure results in higher urinary levels of calcium, ammonia, and formic acid.

Conclusions

●Urine tests of workers exposed to methanol showed formic acid levels up to six times higher than that in the control.

While methanol is a potentially severe health hazard, very few reports are made of methanol poisoning.

References

Liesivuori and Savolainen (1991) Methanol and Formic Acid Toxicity: Biochemical Mechanisms, Pharmacology and Toxicology.

Malcolm Pirnie (1999) Evaluation of the Fate and Transport of Methanol in the Environment.

Wikipedia, (2013) Cytochrome c Oxidase,http://en.wikipedia.org/wiki/Cytochrome_oxidase