Man-made chemicals in our environment may be harmful, in particular for the developing child with potential irreversible effects into adulthood. Considering the rapid increase in use and distribution of such chemicals over the past decades, it is tempting to speculate whether these changes contribute to the increase in some health problems.
The prevalence of hypospadias and cryptorchidism in boys has increased in some countries, parallel to adult testicular cancer and impaired semen quality. Many countries report an earlier onset of puberty, in particular in girls. In addition, there is evidence that some environmental chemicals contribute to postnatal obesity.
Our data from prospective cohort studies show associations of early pre- and perinatal chemical exposure with reproductive outcomes in both sexes, body composition and puberty.
Exposure to persistent chemicals such as polybrominated diphenyl ethers (flame retardants) and polychlorinated pesticides increased the risk of giving birth to a son with cryptorchidism. Exposure to phthalate monoesters (plastic emollients) was negatively correlated with infant serum testosterone levels and anogenital distance (AGD). AGD is a measure of androgen effect in the newborn, which is positively associated with semen quality in adulthood. Childhood exposure to phthalates additionally lowered thyroid hormone and IGF1 levels and affected growth patterns.
Early prenatal exposure to modern pesticides was associated with earlier onset of breast development in girls, smaller genital size in boys and an increase in body fat percentage. The latter effect was enhanced if the mother also smoked during pregnancy and the child was carrier of a specific genetic polymorphism, underlining the importance of interaction between life style, genetic susceptibility and exposure scenarios.
Thus, current evidence suggests that growth and reproductive development in both sexes may be susceptible to endocrine disrupting chemicals.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details are unavailable.
05 - 09 May 2012
European Society of Endocrinology