Background
Endocrine disrupting chemicals are suspected of contributing to the high prevalence of genital malformations and low testicular volumes in Danish boys and the low semen quality in Danish men.
Many pesticides are known to have endocrine disrupting abilities. Modern non-persistent insecticides have been shown to exhibit oestrogenic and anti-androgen activities and disturb steroidogenic enzymes in vitro.
In a previous study, sons of women who were occupationally exposed to non-persistent pesticides in early pregnancy showed signs of impaired reproductive function (reduced genital size and altered serum hormone concentrations) at three months of age.
Aim
To assess the possible long-term effects of prenatal pesticide exposure on boys at age 6-11 years.
Methods
Pregnant women working in greenhouses in Denmark were enrolled into a cohort study and their sons followed up first at 3 months of age. Exposure levels were assessed at enrolment into the study.
The boys who participated in the 3-month examination were re-examined at 6–11 years of age.
Ninety-four boys (59 exposed, 35 unexposed) underwent genital examinations including ultrasound of testicular volumes, puberty staging (Tanner), anthropometry, and blood sampling.
Results
Only a few of the boys had reached puberty (n = 3). Among prepubescent boys, testicular volume and penile length (age- and weight-adjusted) were reduced if mothers were exposed to pesticides.
The effects were associated with the maternal exposure levels, so that high exposed boys had smaller genitals than medium-exposed boys, who had smaller genitals than those who were unexposed.
Boys of mothers in the high exposure group (n = 23) had 24.7% smaller testes (95% CI: -62.2; -10.1) and 9.4% shorter penile length (95% CI: -16.8; -1.1) compared with the unexposed.
The testicular volume and penile length at school age could be tracked to measures from the same boys made at 3 months, e.g. those that had small testes at school age also had small testes at 3 months.
Pituitary and testicular hormone serum concentrations did not differ between exposed and unexposed boys. Eight prenatally exposed boys had genital malformations (no unexposed).
These boys had smaller testis, shorter penile length and lower inhibin-B concentrations than prepubertal boys without genital malformations.
Conclusion
The findings support the results obtained at three months of age and indicate that prenatal pesticide exposure has long-term effects on reproductive function in boys.
