Effect of endosulfan on male reproductive development - Children's Health

Environmental Health Perspectives, Dec, 2003 by Habibullah Saiyed, Aruna Dewan, Vijay Bhatnagar, Udyavar Shenoy, Rathika Shenoy, Hirehall Rajmohan, Kumud Patel, Rekha Kashyap, Pradip Kulkarni, Bagalur Rajan, Bhadabhai Lakkad

In Figure 6, serum testosterone levels are plotted against age for study and control individuals. Regression lines drawn for the study and control individuals indicate that the average serum testosterone levels for the study group are lower for the same age. Similarly, in Figure 7, serum LH levels are plotted against age in study and control individuals. The regression lines indicate that average serum levels for the same age are higher in the study group.

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Endosulfan exposure. Endosulfan was detected in serum samples of 78% of the children in the study group and 29% of the children in the control group. Table 4 shows the serum endosulfan levels in the study and control groups. The levels of endosulfan in the study group children are significantly higher (p < 0.001).

Discussion

Our study results, after controlling for age, showed significantly lower SMR scores and serum testosterone levels and higher levels of serum LH in the study group compared with controls. To link these changes with endosulfan exposure, we should look at two issues: biologic plausibility of the cause-effect relationship and pathways of endosulfan exposure.

Biologic plausibility. There are reports of testicular toxicity of endosulfan manifested as decreased spermatogenesis and testicular hormone synthesis (steroidogenesis), as evidenced by a decrease in spermatid count in testes and in sperm count in the cauda epididymis and by changes in marker enzymes for testicular steroidogenesis in adult animals (Chitra et al. 1999; Singh and Pandey 1989, 1990; Sinha et al. 1995). These effects were seen at much lower dosages and shorter durations if exposures occurred during the prenatal or prepubertal periods (Dalsenter et al. 1999; Sinha et al. 1995, 1997, 2001). Singh and Pandey (1990) also reported profound decreases in the levels of plasma LH, FSH, and testosterone associated with decrease in testicular testosterone in pubertal rats exposed to endosulfan for 30 days. Thus, our observations of low testosterone levels in male children conform with the animal studies. Lower SMR scores appear to reflect lower serum testosterone levels for age. In our study, it is not possible to confirm disturbed spermatogenesis observed in animal studies.

The higher prevalence of congenital abnormalities related to testicular descent observed in the study group should not be overlooked simply because it failed to achieve statistical significance (which may be due to small sample size), because there is indirect evidence of endosulfan exposure associated with undescended testes in a human population from Spain. Garcia-Rodriguez et al. (1996) reported a higher incidence of hospital admissions to University of Granada Hospital for cryptorchidism from districts near the Mediterranean coast, where there is intensive use of pesticides. A subsequent study reported endosulfan isomers and/or metabolites in adipose tissue of 40% of children who were admitted to the same hospital for a variety of reasons (Olea et al. 1999), indicating that significant endosulfan exposures occurred in the region. In the present study, there is a definite history of endosulfan exposure that is likely to have occurred during the prenatal period.