Following is the abstract of a scientific study showing that exposure to
tetrachlorodioxin, the most dangerous chemical in Agent Orange, results in a
depletion of vitamin A levels in exposed animals. This may be a very
important paper for understanding Gulf War Illness. At time of the Viet Nam
war, no one knew that such exposures affected vitamin A levels and no one
knew that vitamin A was critical to normal functioning of the immune system.
This knowledge is only being put together now.

It is probable that health problems associated with Agent Orange exposure
in Viet Nam and chemical exposures in the Persian Gulf are essentially the
same in that both are results of effects on the immune system. What this
means is that tests have to be done to see if Gulf War era chemicals affect
the immune system as does Agent Orange and if these effects result in Gulf
War Illness.

It may be that those responsible for using chemicals in the Persian Gulf
didn’t know about the problem. Obtaining this information may be critical to
understanding what caused Gulf War Illness after 1991 and what may cause
similar illnesses this time.

Bill Plapp, retired insecticide toxicologist

1: Toxicol Sci 2001 Jul;62(1):166-75 Related Articles, Links
 
Hepatic vitamin a depletion is a sensitive marker of
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in four rodent species.

Fletcher N, Hanberg A, Hakansson H.

Institute of Environmental Medicine, Karolinska Institutet, PO Box 210, S-171
77 Stockholm, Sweden.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-treated animals show altered
retinoid homeostasis and exhibit signs of toxicity similar to those of
vitamin A-deficient animals. In this study we established dose-response
curves for sublethal oral doses of TCDD and hepatic vitamin A gain in four
rodent species. This was done to evaluate any potential correlation between
decreased hepatic vitamin A gain and other TCDD-induced effects, particularly
depressed body weight gain and hepatic CYP1A induction. Young Hartley guinea
pigs, Sprague-Dawley rats, C57BL/6 mice, and Golden Syrian hamsters were
given single oral doses of TCDD at up to 2.5, 100, 1000, and 1000 microg/kg
bw, respectively, and killed 28 days after treatment. Hepatic vitamin A gain
was decreased 25% compared to controls at estimated doses of 0.1, 0.9, 1.1
and 3.6 microg/kg bw in guinea pigs, hamsters, rats, and mice, respectively.
CYP1A induction and hepatic vitamin A gain were affected at similar dose
levels and showed similar, but inverse dose-response curves in each of the
four species, consistent with the hypothesis that altered vitamin A
homeostasis is Ah-receptor mediated. In addition, there was an apparent
correlation between the dose-response curves for decreased hepatic vitamin A
gain and decreased body weight gain in all species. Taken together with the
known importance of vitamin A in body weight regulation, this result was
consistent with a contributing role for altered retinoid homeostasis in the
wasting syndrome induced by TCDD.

PMID: 11399804 [PubMed - indexed for MEDLINE]

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