RE: Dioxin and diabetes

["david bell" <burnt_paper@hotmail.com>]

>  Please realize that death certificates do not always include mentions of
>diabetes if the diabetes was not implicated in the cause of death.
>Therefore, the results of the study are interesting, but not definitive 
>with
>regard to dioxin "causing" diabetes.

Agreed; nonetheless, this is the largest and most thorough study of dioxin 
exposure in humans, and it finds a negative correlation between dioxin 
exposure and mention of diabetes on the death certificate. Therefore, the 
balance of evidence from human studies is that dioxin causes does not cause 
diabetes in humans.

While I can accept that this is not proof, it is a long way from the 
unqualified assertion that dioxin causes diabetes.

>  Further, it does not include
>developmental exposure to dioxin, which may induce effects not seen only 
>due
>to mature adult exposures.
>Diane Henshel
>

agreed. I believe that the epidemiology of the Seveso incident shows that 
dioxin exposure is associated with a decreased risk of breast cancer- a 
finding which is also seen in the rat bioassay. In contrast, there has been 
some work recently which shows that prenatal dioxin can enhance sensitivity 
to breast carcinogenesis in adult life (see ref below).

cheers
david bell

          Prenatal TCDD and predisposition to mammary cancer in the rat
          Brown_NM, Manzolillo_PA, Zhang_JX, Wang_J, Lamartiniere_CA
       JN:
          CARCINOGENESIS, 1998, Vol.19, No.9, pp.1623-1629
      AB:           Prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin 
(TCDD) was investigated for its potential
          to predispose to breast cancer. Analysis of mammary gland 
differentiation and cell proliferation were
          used as biomarkers. Timed pregnant Sprague-Dawley CD rats were 
gavaged with 1 mu g TCDD/kg on
          day 15 post-conception. Control animals were treated with the same 
volume of vehicle (sesame oil)
          on the same schedule. Mammary gland differentiation studies 
revealed that prenatal TCDD treatment,
          as compared with sesame oil treatment, resulted in significantly 
more terminal end buds and fewer
          lobules II in 50-day-old offspring, but no significant alterations 
to mammary gland differentiation in
          21-day-old offspring. Terminal end buds are the most susceptible 
terminal ductal structures and
          lobules the least susceptible to carcinogenesis. Prenatal TCDD 
treatment did not alter labeling index
          in the mammary terminal ductal structures of 21- and 50-day-old 
rats, but the total proliferative
          compartment in terminal end buds of 50-day-old rats was larger 
Prenatal TCDD treatment resulted in
          an increased number of chemically induced mammary adenocarcinomas 
in rats. TCDD delayed time
          of vaginal opening and caused disruption to the estrous cycle. 
Alteration to mammary gland
          differentiation (increased number of terminal end buds) is 
correlated with increased susceptibility to
          mammary cancer from prenatal exposure to TCDD.

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