Prenatal Pesticide Exposure Linked to Early Breast Growth

Emma Hitt, PhD

March 15, 2012

March 15, 2012 — Prenatal exposure to currently approved pesticides in greenhouse workers appears to be linked to earlier breast development in their daughters as measured 10 years later, according to a new report by Christine Wohlfahrt-Veje, MD, from the University Department of Growth and Reproduction, Rigshospitalet, Copenhagen, Denmark, and colleagues. The authors report their findings in an article published online March 9 in the International Journal of Andrology.

According to the researchers, several factors may influence the timing of puberty, including endocrine-disrupting chemicals, which may also influence other aspects of ovarian development and female reproductive health.

The authors sought to evaluate girls whose mothers were exposed to nonpersistent contemporary pesticides in early pregnancy through their work in greenhouses. Age of onset of breast development and level of reproductive hormone levels were assessed in a follow-up study of the daughters of these workers.

A total of 90 (77 exposed, 13 unexposed) infant girls were evaluated at 3 months. Because of loss of study participants, additional girls with comparable demographic backgrounds were added to the unexposed group (53 exposed, 30 unexposed) and evaluated at age 6 to 11 years.

In prenatally exposed girls, mean onset of breast budding was 8.9 years (95% confidence interval [CI], 8.2 - 9.7 years) compared with 10.4 years (95% CI, 9.3 - 17.6 years) in the unexposed girls (P = .05) and 10.0 years (95% CI, 9.7 - 10.3 years) in a Danish reference population.

Exposed girls had higher serum androstenedione levels (mean, 0.79 vs 0.58 nmol ⁄ L; P = .046) and lower anti-Müllerian hormone compared with the unexposed girls (mean, 16.4 vs 21.3 pmol ⁄ L; P > .05) and the girls in the reference group (20.2 pmol ⁄ L; P = .012).

"[O]ur findings suggest that prenatal exposure to currently approved pesticides may cause earlier breast development in girls," Dr. Wohlfahrt-Veje and colleagues note. "This association appeared not to be because of changes in gonadotropins, but rather to higher androgen levels, which indirectly may increase oestrogens through aromatization," they add.

According to the researchers, androgen concentrations may disturb the development of (pre)antral follicles if hyperandrogenism occurs prenatally or postnatally.

The authors add that "altered prenatal programming of steroidogenic enzymes may be responsible for the associations found at school age. However, pesticides with many possible ways of action were used in the greenhouses, and we cannot exclude that the combined exposure may be responsible for our observations."

The authors conclude that the "long-term consequences of our worrying findings with regard to adult reproductive functions still remain unknown."

The authors have disclosed no relevant financial relationships.

Int J Androl. Published online March 9, 2012. Abstract

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