Academic journal article Environmental Health Perspectives

Organochlorine Pesticides and Male Genital Anomalies in the Child Health and Development Studies

Academic journal article Environmental Health Perspectives

Organochlorine Pesticides and Male Genital Anomalies in the Child Health and Development Studies

Article excerpt

Increasing rates of cryptorchidism and hypospadias in human populations may be caused by exogenous environmental agents. We conducted a case-control study of serum levels of p,p'-dichlorodiphenyltrichloroethane (DDT) and its major metabolite, p,p'-dichlorodiphenyldichloroethylene (DDE), and cryptorchidism and hypospadias in the Child Health and Development Study, a longitudinal cohort of pregnancies that occurred between 1959 and 1967, a period when DDT was produced and used in the United States. Serum was available from the mothers of 75 male children born with cryptorchidism, 66 with hypospadias, and 4 with both conditions. We randomly selected 283 controls from the cohort of women whose male babies were born without either of these conditions. Overall, we observed no statistically significant relationships or trends between outcomes and serum measures. After adjusting for maternal race, triglyceride level, and cholesterol level, compared with boys whose mothers had serum DDE levels < 27.0 ng/mL, boys whose mothers had serum DDE levels [greater than or equal to] 61.0 ng/mL had odds ratios of 1.34 [95% confidence interval (CI), 0.51-3.48] for cryptorchidism and 1.18 (95% CI, 0.46-3.02) for hypospadias. For DDT, compared with boys whose mothers had serum DDT levels < 10.0 ng/mL, boys whose mothers had serum DDT levels [greater than or equal to] 20.0 ng/mL had adjusted odds ratios of 1.01 (95% CI, 0.44-2.28) for cryptorchidism and 0.79 (95% CI, 0.33-1.89) for hypospadias. This study does not support an association of DDT or DDE and hypospadias or cryptorchidism. Key words: cryptorchidism, DDE, DDT, hypospadias, insecticides, male genital anomalies, organochlorine, pregnancy. doi: 10.1289/ehp.7382 available via http://dx.doi.org/[Online 4 November 2004]

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Hypospadias (an abnormal opening of the urethra) and cryptorchidism (a failure of one or both testides to descend) are two relatively common male genital congenital anomalies, occurring in 35 of 10,000 and 40 of 10,000 births, respectively (Paulozzi 1999). Recent evidence has suggested that hypospadias and cryptorchidism have increased in frequency in some populations (Paulozzi 1999). This is of public health significance, particularly because of the well-known association between cryptorchidism and testicular cancer (Wilson and Foster 1985; Toppari et al. 1996), which also appears to be on the increase (Toppari et al. 1996).

In mammals, cryptorchidism depends on mullerian-inhibiting hormone, androgens, and intra-abdominal pressure (Wilson and Foster 1985). The formation of the male external genitalia in utero also occurs under the influence of androgens (Baskin et al. 2001). There is suggestion that increasing rates of hypospadias and cryptorchidism may be caused partly by early exposure to endocrine-disrupting chemicals in the environment (Beard et al. 1984; Berkowitz et al. 1995; Depue 1984; Hjertkvist et al. 1989; Jackson 1988; Landrigan et al. 2003; McBride et al. 1991; Sharpe and Skakkebaek 1993; Sweet et al. 1974; Swerdlow et al. 1983; Toppari et al. 1996). This hypothesis is supported by the higher rates of urogenital anomalies, including cryptorchidism, in studies of sons exposed in utero to diethylstilbestrol, a potent estrogen (Cosgrove et al. 1977; Gill et al. 1979).

Although the use of one potent environmental endocrine disruptor, dichlorodiphenyl-trichloroethane (DDT), has been banned in the United States since 1972, concerns about its potential health effects continue because of its worldwide use in the eradication of malaria, its accumulation in the human food chain, and its long half-life in human tissues due to its lipophilicity (Clarkson 1995). DDT functions as an exogenous estrogen (Bulger and Kupfer 1983) and, in animal studies, has been shown to suppress Leydig cell development, alter secretion of mullerian-inhibiting substance by the Sertoli cells, and cause negative feedback inhibition at the fetal pituitary gland (Sharpe and Skakkebaek 1993). …

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