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[Discussion]
A genital tubercle, which is to develop into the penis, in a
male fetus is formed in the early fourth week of pregnancy. A
urogenital fold is also formed in the same period, of which
midline fusion from the proximal to distal region forms the
urethra by 15th-16th week of pregnancy. This process is thought
to depend on androgen from the fetal testicles, and hypospadias
appears if endocrine secretion in this period is insufficient or
disturbed by external effects.
Some organochlorine compounds act as estrogen receptor agonists
and affect hormone levels. Epidemiologic studies had found
before Dec. 31, 2000, odds rate increase for mothers handling
pesticides (Kristensen 1997, Weidner 1998) and for residents
near industrial waste treatment plants (Dolk 1998). Survey of
more recent studies found reports on effects of DES exposure,
higher prevalence in agricultural and industrial cities, and
association with fathers' occupations. However, quantitative
analysis of exposure of victims to endocrine disruptors using
biological samples did not find significant correlation. Studies
are thus too few to for definite conclusion on the association
of endocrine disruptors and hypospadias. Experimental designs
with high reliability are needed for future studies on this
problem.
[Conclusions]
Literature survey concerning epidemiology of endocrine
disruptors and hypospadias was performed for a period up to Oct.
31, 2004. A cohort study reported a risk increase due to DES
exposure in utero. Another study found no association of
hypospadias with mother's serum DDE level. Hypospadias is thus
scarcely studied in relation to organochlorine compounds.
Experimental designs with high reliability are needed for future
studies on this problem.
[Literature]
Table 2.8 1: Cohort
studies on the relationship of endocrine disruptors with
hypospadias
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