
2011 Study Abstract
Prospective clinical studies have suggested that the rate of congenital cryptorchidism has increased since the 1950s. It has been hypothesized that this may be related to environmental factors. Testicular descent occurs in two phases controlled by Leydig cell-derived hormones insulin-like peptide 3 (INSL3) and testosterone. Disorders in fetal androgen production/action or suppression of Insl3 are mechanisms causing cryptorchidism in rodents. In humans, prenatal exposure to potent estrogen Diethylstilbestrol (DES) has been associated with increased risk of cryptorchidism. In addition, epidemiological studies have suggested that exposure to pesticides may also be associated with cryptorchidism. Some case–control studies analyzing environmental chemical levels in maternal breast milk samples have reported associations between cryptorchidism and chemical levels. Furthermore, it has been suggested that exposure levels of some chemicals may be associated with infant reproductive hormone levels.
- Background
- Testicular descent
- Animal studies
- Human studies
- Exposure to estrogens/estrogenic agents
- Pesticides
- PCBs
- Dioxins
- Flame retardants
- Phthalates
2011 Study Conclusion
Various xenobiotics have been found to disrupt the endocrine system in animals. Reduction in the dominance of androgens to estrogens, and interference with androgen or Insl3 production or action during fetal life, are apparent mechanisms causing cryptorchidism in animals. When evaluating associations between fetal exposure to estrogenic agents and cryptorchidism in humans, exposure to DES was associated with an increased risk of cryptorchidism. Studies evaluating pesticide use in a geographical area or parental possible occupational exposure to pesticides, have suggested that also exposure to them may be associated with an increased risk of cryptorchidism in boys. Some case–control studies evaluating maternal breast milk levels of chemicals have reported associations between congenital cryptorchidism and the levels of environmental chemicals with possible endocrine disrupting activities. No clear positive association was reported in studies evaluating levels of endocrine disrupting chemicals in placenta, cord serum or maternal serum. Maternal breast milk phthalate and PBDE levels have shown anti-androgen-like associations with infant reproductive hormone levels. More studies are needed to confirm the observed associations and to evaluate associations between cryptorchidism and combined exposures.
Sources and more information
- Cryptorchidism and endocrine disrupting chemicals, sciencedirect pii/S0303720711006782, doi:10.1016/j.mce, 2011.11.
More DES DiEthylStilbestrol Resources
- DES studies on cancers and screening.
- DES studies on epigenetics and transgenerational effects.
- DES studies on fertility and pregnancy.
- DES studies on gender identity and psychological health.
- DES studies on in-utero exposure to DES and side-effects.
- DES studies on the genital tract.
- Papers on DES lawsuits.
- DES videos and posts tagged DES, the DES-exposed, DES victims.
I too was born with one I descended fetal ovarian tissue instead of a testis. My other testis did drop normally but never matures to normal adult size. Unfortunately the ovarian tissue became malignant. In addition I’ve had life long gender issues. We have suspected some EDC as to the cause
Thanks for your comment and for contributing to showing the true picture of the devastating impacts of endocrine disrupting chemicals.
Reblogged this on Milieunet.
thanks Erik