Authors
Elisabete Weiderpass et al
Title
Organochlorines and Endometrial Cancer
Journal
Cancer Epidemiology Biomarkers & Prevention Vol. 9,487-493, 2000
Summary
There is widespread concern that environmental pollutants such as dichlorodiphenyltrichloroethane
(DDT) and polychlorinated biphenyls (PCBs) may cause or contribute to
the development of cancer in humans. It is thought that, although weakly
estrogenic, organochlorines may increase overall estrogen exposure and
thus increase the risk of developing breast cancer. The authors of the
present paper propose that because the endometrium is more sensitive
to estrogenic stimulation than the breast, the adverse effects of estrogenic
organochlorines should be more easily detected in the endometrium. Therefore
the goal of this study was to test the hypothesis that elevated blood
concentrations of specific organochlorines is associated with an increased
risk of endometrial cancer. To test this hypothesis the authors carried
out a population-based case-control study of organochlorine pesticides
and PCB congeners in 154 endometrial cancer cases and 205 population
controls in Sweden. Women 50-74 years of age, resident between February
1996 and November 1997 in 12 Swedish counties on the largest Swedish
lakes were recruited into the study. It was assumed that the intake
of organochlorine compounds through ingestion of contaminated fish would
be higher in these counties than elsewhere in Sweden. Since hormone
replacement therapy or prior hysterectomy are recognized risk factors
for endometrial cancer, women reporting these were excluded from this
study. Subsequently, 134 women with endometrial cancer were excluded
because they had used hormone replacement therapy, leaving 154 cases
in the study. The lipid portion of serum samples was analyzed for 10
organchlorine pesticides and 10 PCB congeners. Samples from cases were
collected immediately after diagnosis and before surgery or any other
cancer therapy. There was no difference between cases and controls regarding
fish consumption patterns, but women in the control group reported more
breast-feeding than cases (a major excretory route for organochlorine
compounds).
Among DDT metabolites, the concentration of p, p'-DDE (the principal
metabolite of p, p'-DDT) was highest (600-700ng/g lipid) and the average
concentrations of other pesticides were usually lower by a factor of
10 or more. For all compounds, the range of exposure was substantial
both among cases and controls. In unadjusted analyses, median concentrations
of p,p'-DDT, p,p'-DDE, ß-HCH, and oxychlordane were higher among
cases than controls. However, after adjustment for age and BMI in logistic
regression, ORs were close to unity and there was no evidence of exposure-risk
relationships across quartiles of contaminant concentrations. In the
analyses of organochlorines as continuous variables, no associations
were found between risk for endometrial cancer and any of the 10 pesticides
evaluated. Among the 10 PCB congeners, CB153 had the highest concentration
(mean ~ 236ng/g lipid), whereas CB28, CB52, and CB102 often had concentrations
below the limit of quantification (2ng/g lipid). Unadjusted mean concentrations
of CB28 and CB118 were higher among cases than controls. However, after
adjustment there was no significant trend in risk. Finally, in the analysis
of the 10 different PCB measurements in continuous form, there was no
significant association between any of the congeners and endometrial
cancer risk. On the other hand, after standardizing for lipid content
in different tissues, the mean concentration of organochlorines in this
study were in the lower range compared to those reported previously
for controls in North American and European breast cancer studies, where
sampling occurred in the late 1980s and early 1990s and average concentrations
were 1,020-2,200 ng/g lipid for p,p'-DDE and 350-1,300 ng/g lipid for
total PCBs. The somewhat lower average exposure in this study (sampling
1996-1997) at least partially reflects the continuous decline in Europe
and North America after banning of these compounds. The data do not
support the hypothesis that, in this population, organochlorine exposure
increases the risk for endometrial cancer.