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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
ASD was, on average, 47% as long as AGD, and these two measurements were correlated (R = 0.47, p < 0.0001). However, the model predicting ASD as a function of baby's age and weight fit poorly (adjusted [R.sup.2] = 0.10). The fit for the model using ASD/weight as a function of age and age squared was better (adjusted [R.sup.2] = 0.47) but did not fit as well as the model using AGI ([R.sup.2] = 0.61). ASD/weight was associated with MEP concentration (regression coefficient = -0.429; 95% CI, -0.722 to -0.137). For the other phthalate metabolites, regression coefficients were less significant (all p-values between 0.11 and 0.97).
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Summary phthalate score. We used the summary phthalate score as defined in "Materials and Methods" to study the effect of joint exposure to more than one AGI-associated phthalate. The summary phthalate score was directly related to the proportion of boys with short AGI (p = 0.001). Of the 10 boys whose phthalate scores were high (score = 11-12), all but one had a short AGI. Conversely, of the 11 boys whose scores were low (score = 0 or 1), only one had a short AGI. The ORs for having a short AGI for high summary phthalate score compared with low (OR = 90.0; 95% CI, 4.88 to 1,659), and high compared with medium (29.4; 95% CI, 3.4 to 251) were large and significant, although the confidence intervals were very wide. These data are shown graphically in Figure 1.
Discussion
In the recent National Health and Nutrition Examination Survey (NHANES 1999-2000), most of the general population in the United States had measurable exposure to multiple phthalates (CDC 2003; Silva et al. 2004a). The samples in the present study and in NHANES were both analyzed using comparable methods and standards by the same laboratory, although the specific metabolites that were measured in the two studies differed somewhat. We compared the medians and 75th percentiles of the AGI-associated phthalate metabolite concentrations among two groups of mothers in our study (those whose boys fell in the short AGI group and all others) with those of females in the NHANES sample (Table 7). In the analysis of the NHANES samples, monoburyl phthalate includes both MBP and MiBP, which were measured separately in our study. Metabolite concentrations for mothers of boys with short AGI were consistently higher than those of other mothers. Compared with women in the NHANES sample, metabolite concentrations for our population were somewhat lower. However, our population cannot be directly compared with NHANES: the proportion of pregnant women in the NHANES sample is unknown, and age distributions differ. Nonetheless, these data demonstrate that the four AGI-associated phthalate metabolites are prevalent in the U.S. female population, and levels were not unusually high among mothers whose sons had a short AGI.
Although not identical, AGD in pups is most similar to AGD as we defined it in this study. In rodents, AGD has been shown to be one of the most sensitive end points for phthalates such as DBP (Mylchreest et al. 2000) and other antiandrogens such as flutamide (Barlow and Foster 2003; McIntyre et al. 2001) and finasteride (Bowman et al. 2003). It is difficult to compare the dose to humans from low-level, ongoing, environmental exposure with that delivered to rodents experimentally in a narrow window of gestation. Nonetheless, it is likely that the doses to which our participants were exposed are lower than those used in toxicologic settings, suggesting that humans may be more sensitive to prenatal phthalate exposure than rodents. This greater sensitivity in humans has been observed for other toxicants. For example, humans are more sensitive to trenbolone by an order of magnitude (Neumann 1976). This greater sensitivity is thought to be a result of rodents' higher metabolic rate and more rapid inactivation of toxicants, both of which have been shown to be inversely related to body size (White and Seymour 2005).
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