RE: Dioxin and diabetes

["Henshel, Diane S." <dhenshel@indiana.edu>]

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

-----Original Message-----
From: david bell
To: Multiple recipients of list DIOXIN-L
Sent: 10/30/99 5:59 PM
Subject: Dioxin and diabetes

I have seen the assertion that dioxin causes diabetes in humans, based
on 
small-scale epidemiology. To my understanding, the reference below
(1999) is 
the largest scale epidemiology study of dioxin, and it finds that
exposure 
to dioxin does not cause diabetes.

The difficulty in interpreting whether dioxin causes cancer in humans
comes 
from two perspectives. 1. The workers were also known to be exposed to
known 
human carcinogens (other chemicals). Therefore it is not possible to
ascribe 
any increase in cancer solely to dioxin. 2. The increase in cancer is
not 
one specific cancer, but all cancers. Since chemicals normally induce
cancer 
in one, or a few organs, this finding actually increases the difficulty
of 
asserting that dioxin is responsible (see 1 above).

******************************************


TI:  Cancer, heart disease, and diabetes in workers exposed to 
2,3,7,8-tetrachlorodibenzo-p-dioxin
AU:  Steenland_K, Piacitelli_L, Deddens_J, Fingerhut_M, Chang_LI
NA:  INT AGCY RES CANC,150 COURS ALBERT THOMAS,F-69372 LYON,FRANCE 
NIOSH,CINCINNATI,OH,45226
JN:  JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1999, Vol.91, No.9, 
pp.779-786
IS:  0027-8874
DT:  Article
AB:  Background: In 1997, the International Agency for Research on
Cancer 
classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a group 1 human

carcinogen, based largely on four highly exposed industrial cohorts that

showed an excess of all cancers combined. In this study, we extended the

follow-up period for the largest of these cohorts By 6 years and
developed a 
job-exposure matrix. Methods: We did cohort mortality analyses involving

5132 chemical workers at 12 U.S. plants by use of life table techniques 
(U.S. population referent) and Cox regression (internal referent). We 
conducted exposure-response analyses for 69% of the cohort with adequate

work history data and adequate plant data on TCDD contamination, All P 
values are two-sided. Results: The standardized mortality ratio (SMR)
for 
all cancers combined was 1.13 (95% confidence interval = 1.02- 1.25). We

found statistically significant positive linear trends in SMRs with 
increasing exposure for all cancers combined and for lung cancer. The
SMR 
for all cancers combined for the highest exposure group was 1.60 (95% 
confidence interval = 1.15-1.82). SMRs for heart disease showed a weak 
increasing trend with higher exposure (P = .14). Diabetes (any mention
on 
the death certificate) showed a negative exposure-response trend.
Internal 
analyses with Cox regression found statistically significant trends for 
cancer (15-year lag time) and heart disease (no lag). Conclusions: Our 
analyses suggest that high TCDD exposure results in an excess of all
cancers 
combined, without any marked specificity, However, excess cancer was
limited 
to the highest exposed workers, with exposures that were likely to have
been 
100-1000 times higher than those experienced by the general population
and 
similar to the TCDD levels used in animal studies.

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