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Decrease in anogenital distance among male infants with prenatal phthalate exposure
Environmental Health Perspectives, August, 2005 by Shanna H. Swan, Katharina M. Main, Fan Liu, Sara L. Stewart, Robin L. Kruse, Antonia M. Calafat, Catherine S. Mao, J. Bruce Redmon, Christine L. Ternand, Shannon Sullivan, J. Lynn Teague
In light of the toxicologic literature for MBP, MBzP, and MiBP (Ema et al. 2003; Foster et al. 1980, 1981; Gray et al. 2000; Nakahara et al. 2003), our data suggest that the end points affected by these phthalates are quite consistent across species. A boy with short AGI has, on average, an AGI that is 18% shorter than expected based on his age and weight as well as an increased likelihood of testicular maldescent, small and indistinct scrotum, and smaller penile size. These changes in AGD and testicular descent are consistent with those reported in rodent studies after high-dose phthalate exposure (Ema et al. 2003; Gray et al. 2000; Mylchreest et al. 2000). The lack of association for MCPP and MMP, which have not been widely studied, is not inconsistent with the toxicologic literature.
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With respect to DEP and its metabolite MEP, we note that there are three other human studies suggesting reproductive toxicity (Colon et al. 2000; Duty et al. 2003b; Main KM, unpublished data). It is therefore uncertain whether the absence of data in rodents showing reproductive toxicity is the result of failure to detect it, unmeasured confounding in human studies, or interspecies differences in response to these compounds.
DEHP has been shown to shorten AGD (Gray et al. 2000) and reduce testosterone (Parks et al. 2000). Although MEHP was not associated with AGD in our data, the associations for the oxidative metabolites of DEHP (MEOHP and MEHHP) were of comparable magnitude with those for metabolites of DBP and BzBP, although not statistically significant. Thus, it is unclear whether MEOHP and MEHHP are (inversely) associated with AGI, although associations are of borderline statistical significance because of our sample size, or whether human and rodent responses to this phthalate and its metabolites differ.
Masculinization of external male genitalia, represented by longer AGD, is controlled by dihydrotestosterone (Clark et al. 1990). Ema and Miyawaki (2001) demonstrated that this metabolite of testosterone is markedly decreased by prenatal administration of MBP, suggesting that MBP acts as an antiandrogen. AGD in male rodents is associated with other adverse developmental effects (Foster and Mclntyre 2002) and some phthalate-induced changes have been shown to be permanent. For example, Barlow et al. (2004) report that prenatal exposure to 500 mg/kg/day DBP resulted in permanently decreased AGD and testicular dysgenesis. They also report that in utero DBP exposure induced proliferative Leydig cell lesions. Follow-up of exposed children until adulthood will be required to determine whether long-term effects, including testicular dysgenesis, are seen in humans after prenatal phthalate exposure.
Several recent studies of the variability of phthalate monoester concentration in human samples suggest that phthalate concentration in humans is fairly stable, perhaps reflecting habitual use of phthalate-containing household and consumer products (Colon et al. 2000; Hauser et al. 2004; Hoppin et al. 2002). These studies lend support to the use of a single sample for exposure assessment. We obtained only a single prenatal urine sample from each woman, and most samples were obtained quite late in pregnancy (mean = 28.3 weeks). Therefore, the measured phthalate metabolite levels may not reflect exposure during the most sensitive developmental window, resulting in some degree of exposure misclassiflcation. However, unless this misclassification varied systematically with outcome, such errors would bias the effect estimate toward the null. In fact, the categorical analysis, which should be less sensitive to such misclassification, showed stronger associations than did the continuous analysis.
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