Pesticide exposure during pregnancy increases chances of reproductive disorders in sons.

Oct 04, 2008

Andersen HR, IM Schmidt, P Grandjean, TK Jensen, E Budtz-Joergensen, MB Kjaerstad, J Baelum, JB Nielsen, NE Skakkebaek and KM Main. 2008. Impaired reproductive development in sons of women occupationally exposed to pesticides during pregnancy. Environmental Health Perspectives 116:566–572.


Sons of pregnant women who worked at a greenhouse in Denmark while pregnant had a higher incident of undescended testicles than previously reported and blood hormone levels that differed significantly from normal. Development was affected by the exposure, lending more support that women of child bearing age should reduce contact with pesticides. The exact cause-effect relationship between pesticides and testes effects needs to be re-evaluated using a larger population.


in the past several decades, male reproductive disorders have been increasing. One theory why is that the group of disorders, collectively termed testicular dysgenesis syndrome (TDS), is caused by environmental factors that influence the hormone balance of the fetus.

Hormone levels that differ from normal can change how male reproductive organs form and develop. An imbalance can cause diseases and disorders such as genital malformations, testicular cancer and reduced semen count.

Industrialized countries have the highest prevalence of male reproductive problems, presumably due to the abundance of synthetic compounds with hormone-like properties in the environment. Studies with laboratory animals consistently show a strong association between prebirth or early life exposure to compounds with estrogenic or anti-androgenic properties and increased abnormalities of the male reproductive system.

What did they do?

Pregnant women working at greenhouses in Funen, Denmark, were recruited for this study. The women were interviewed about their pesticide exposure, reproductive history and lifestyle.

A total of 197 pregnancies were studied. These pregnancies resulted in 113 boys and 90 girls.

The 113 mother and son pairs were categorized in the occupationally ‘exposed’ (91 pairs) or ‘non-exposed’ (22 pairs) group. The exposed group consisted of women who directly worked with pesticides, handled plants within a week after treatment and/or worked in an area where pesticides were used more than once a month. Female workers who did not fit in any of these criteria were considered unexposed, or the control, group. Most control group women worked in greenhouses where chemical pesticides were not used or had been replaced by biological forms of pest control.

The male infants were examined at 3 months by a single pediatrician following the standardized procedure used by the Nordic Cryptorchidism Study Group. Some of the measured parameters included testicular position and size and penile length. Blood samples were obtained from 85 boys and assayed for level of various reproductive hormones.

What did they find?

Seven out of the 113 boys examined in the study had undescended testicles. All of them were born to exposed mothers.

Due to the small sample size of the control group, the prevalence of undescended testicles between exposed and non-exposed groups was not statistically significant. However, the prevalence of undescended testicles in these boys (6.2%) was significantly higher than previously reported among Danish boys born in the Copenhagen area (1.9%) and examined by the same study team, using the same procedure, and largely the same examining physician.

Boys born to exposed mothers also had significantly shorter penises than those born to controls. Further, the study also suggested that sons of exposed mothers had smaller testicles, reduced levels of testosterone and inhibin B, and elevated levels of sex hormone binding globin (SHBG), follicle-stimulating hormone (FSH) and luteinizing hormone (LH)/testosterone ratio.

What does it mean?

Pregnant women exposed to pesticides have an increased risk of delivering sons with smaller penises and testicles and with altered levels of reproductive hormones. Additionally, the Danish greenhouse workers in this study had a three-fold increased risk of delivering a son with undescended testicles compared to pregnant women in Copenhagen.

These findings suggest that pesticide exposure during fetal testicular development may adversely affect both testosterone-producing and sperm-producing cells. Most of the pregnant greenhouse workers in the exposed group were removed from pesticide-related jobs as their pregnancies progressed, suggesting that critical period of exposure in this study was the first weeks of pregnancy.

Limitations of this study include the small number of subjects, which restricted the power to test for differences between the exposed and unexposed groups. However, statistically significant differences in penile length and in overall hormonal changes were seen, despite the small sample size.

The authors classified women as exposed or unexposed to pesticides based on their work activities, not according to pesticide levels in maternal blood. Therefore, some women in the control group may be incorrectly classified as unexposed.

Another limitation was that factors such as maternal smoking or alcohol consumption that might explain the differences in infants’ reproductive development were not included in the study. Although the prevalence of smoking and alcohol intake among greenhouse workers was reported to be similar to or lower than in Copenhagen, larger sample size is needed to control these additional maternal factors.

This study has several strengths. All boys in the study (and most of the boys in the comparison study in Copenhagen) were examined by the same physician who was unaware of the infants’ pesticide exposure status. Further, standardized methods were used to look at a variety of measurements of reproductive development, including penile length, testicular size, sex hormone levels and other hormone levels. Taken together, these measurements give an overall assessment of male reproductive function.

In summary, these findings support the hypothesis that fetal exposure to man-made compounds disrupts human male reproductive health. Further, these results are consistent with similar strong associations found in wildlife and laboratory animals.


Boisen, KA, M Kaleva, KM Main, HE Virtanen, AM Haavisto, IM SchmidtI, M Chellakooty, IN Damgaard, C Mau, M Reunanen, NE Skakkebaek and J Toppari.  2004.  Difference in prevalence of congenital cryptorchidism in infants between two Nordic countriesLancet 363:1264-1269.

Mayo Clinic. Undescended testicles (chryptorchidism).

Our Stolen Future. Male reproductive disorders.

Our Stolen Future. Pesticides and male infertility.

Skakkebaek, NE, E Rajpert-De Meyts and KM Main. 2001. Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects. Human Reproduction 16:972-978.

Pesticide risks and pregancy



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