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[Discussion]
Recent prospective studies have found no significant increase of
testicular cancer risk by exposure to DES. The results of
case-control studies are indeterminate. DES cannot therefore be
established as a risk factor for testicular cancer.
The correlation of cancer risk with the exposure of the case's
mother reported in a case-control study indicates the necessity
of studying effects of prenatal exposure.
Prospective cohort studies on farm workers and pesticide
spraying operators found relative risks within a range of
1.1-1.6, which were not statistically significant. Reports on
the relationship of cancer incidence and occupation in general
may be numerous, but actually only few were retrieved in the
present survey, presumably because the results were negative as
far as testicular cancer was concerned, and consequently,
pesticide exposure is not highly correlated with the disease. On
the other hand, major persistent organochlorine compounds, such
as PCB, DDT, HCH and HCB, have not yet specifically been
studied.
Substances other than organochlorine compounds have scarcely
been studied in this context, although such substances include
compounds with androgen-like activities such as bisphenol A.
They also must be studied in relation to testicular cancer.
Few epidemiologic findings are available, which do not permit
evaluation of the causality. Relationships of chemical agents
and testicular cancer have yet to be elucidated.
[Conclusions]
Literature concerning epidemiology of endocrine disruptors and
testicular cancer was surveyed. Prenatal exposure to
organochlorine compounds was reported to be significant in a
study. No report concluded that DES significantly increases
testicular cancer risk. Substances other than DES have scarcely
been studied in this context and evaluation of the causality is
impossible. Experimental designs with high reliability are
needed for future studies on this problem.
[Literature]
Table 2.5 1: Cohort studies on the relationship of endocrine disruptors with testicular cancer
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