Biomedical Engineering Reference
In-Depth Information
study, the LOEL was 2000 ppm (
1600mg/kg) (Rogers et al., 1993)
and in the developmental rats study the LOAEL was 10,000 ppm
(
3700mg/kg) (Nelson et al., 1985). In these developmental studies,
oxidative damage would have been present at the LOEL/LOAEL doses
and higher.
It has been shown that methanol causes oxidative stress in rats.
Methanol, which is water soluble, is widely distributed throughout the
body. High doses of methanol saturated the catalase enzyme in rodents
(600-1000mg/kg); the blood methanol level increases dramatically and
there is a likely increase in ROS and oxidative damage throughout the
various organ and tissues in the body.
While oxidative DNA damage, based on an increase in 8-oxodG,
does not result in mice, rabbits, and primates given a high dose of
methanol, one could draw the conclusion that methanol-induced DNA
damage would not be observed in rats given a similar dose. MDA, a
product of lipid peroxidation, showed clear evidence of carcinogenicity
in rats (NTP, 1988). HNE, another product of lipid peroxidation was
increased in bone marrow of mice given methanol. One therefore could
conclude that products of lipid peroxidation may be a potential mecha-
nism for cancer in rodents.
8.4 HUMAN CANCER DATA
There are no epidemiological studies of cancer in humans exposed
primarily to methanol. In other epidemiological studies where methanol
may be present with other chemicals, no evidence suggests that
methanol is a human cancer risk.
8.5 CONCLUSION
Is methanol a carcinogen in animals or humans? There have been no
“gold standard” bioassays of methanol in animals. Methanol is not
considered mutagenic and the limited animals studies do not clearly
support that methanol is a cancer producing agent in rodents. The doses
