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BackgroundPolybrominated diphenyl ethers (PBDEs) are widely used in Western countries.ObjectivesBecause the prevalence of cryptorchidism appears to be increasing, we investigated whether exposure to PBDEs was associated with testicular maldescent.MethodsIn a prospective Danish–Finnish study, 1997–2001, all boys were examined for cryptorchidism. We analyzed whole placentas (for 95 cryptorchid/185 healthy boys) and individual breast milk samples (62/68) for 14 PBDEs and infant serum samples for gonadotropins, sex-hormone binding globulin, testosterone, and inhibin B.ResultsIn 86 placenta–milk pairs, placenta PBDE concentrations in fat were lower than in breast milk, and a larger number of congeners were nondetectable. There was no significant difference between boys with and without cryptorchidism for individual congeners, the sum of 5 most prevalent, or all 14 congeners. The concentration of PBDEs in breast milk was significantly higher in boys with cryptorchidism than in controls (sum of BDEs 47, 153, 99, 100, 28, 66, and 154: median, 4.16 vs. 3.16 ng/g fat; p < 0.007). There was a positive correlation between the sum of PBDEs and serum luteinizing hormone (p < 0.033). The sum of PBDEs in breast milk did not differ between Denmark and Finland (median, 3.52 vs. 3.44 ng/g fat), but significant differences in some individual congeners were found.ConclusionsTwo different proxies were used for prenatal PBDE exposure, and levels in breast milk, but not in placenta, showed an association with congenital cryptorchidism. Other environmental factors may contribute to cryptorchidism. Our observations are of concern because human exposure to PBDEs is high in some geographic areas.

In support of an assessment of the mortality impacts of the Kuwait Oil Fires we interviewed six European experts in epidemiology and toxicology using formal procedures for elicitation of expert judgment. While the primary focus of the elicitations was to characterize the public health impacts of the fires, the experts provided quantitative estimates of the mortality impacts of hypothetical changes in the levels of ambient fine particulate matter (PM2.5) in both the United States and Europe. Uncertainty was assessed by asking each expert to provide the 5th, 25th, 50th, 75th, and 90th percentiles of their subjective cumulative probability density function for each quantity of interest. The results suggest that many regulatory risk assessments underestimate the impacts of PM2.5 mortality; confirm that only a small fraction of the mortality impact occurs within the first few months after exposure; and indicate that it may be important to better address the differential toxicities of particles from various source classes. By providing quantitative estimates of the uncertainty in current estimates of PM2.5 mortality risks, the study facilitates structured analysis of the value of further research on PM2.5 and its impacts.

for providing useful comments to help frame our analysis. We performed this research as consultants to Exxon Chemical Americas. The opinions are those of the authors and should not be attributed to Exxon or Harvard.

Polychlorinated dibenzo-p-dioxins (PCDDs) are highly toxic environmental contaminants, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent dioxin. Here, we studied the effects of TCDD on bone. Two rat strains, Han/Wistar (H/W) and Long-Evans (L-E), were used because they exhibit a 1000-fold sensitivity difference in acute lethality of TCDD, which difference is related to the aryl hydrocarbon receptor (AHR). TCDD inhibited the tibial growth dose dependently, the effect being manifested at lower doses in the more sensitive L-E strain. In H/W rats the effect of TCDD was seen only at the high dose of 170 microg/kg (p < 0.05), whereas in the sensitive L-E rats a significant reduction of bone growth was already seen at 1.7 microg/kg (p < 0.01). This reduction was caused by the smaller tibial size because the diaphyseal bone mineral density (BMD) did not change. The three-point bending breaking force of the tibia was significantly reduced in H/W rats at 170 microg/kg (p < 0.05), but tibial stiffness was lower already at the dose of 17 microg/kg (p < 0.05). In the sensitive L-E strain, both breaking force and stiffness were reduced at the dose of 17 microg/kg (p < 0.001). These results indicate that TCDD dose-dependently interferes with bone growth, modeling, and mechanical strength. The altered transactivation domain of AHR is associated with a lower sensitivity of bone to TCDD in H/W rats, suggesting that AHR plays a role in modulating the effects of dioxins on bone.

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