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Latini, G, C de Felice, G Presta, A del Vecchio, I Paris, F Ruggieri and P Mazzeo. 2003. In utero exposure to di-(2-ethylhexyl)-phthalate and human pregnancy duration. Environmental Health Perspectives, on line 19 August 2003. Latini et al. confirm significant and widespread presence of the phthalate DEHP and its metabolite, MEHP, in the blood of newborn infants in an Italian hospital. 88% of cord blood samples had DEHP and/or MEHP. They also report a small but statistically significant increase in risk of preterm birth associated with exposure to MEHP. The link between MEHP and preterm birth is important. Premature birth has risen 23% in the US since the 1980s. Infants born prematurely are more at risk to infant mortality and then, if they survive, to a pattern of health problems throughout life. No consensus has been reached about why preterm birth is increasing, although contamination in the womb has been identified as a potential factor. A recent study, for example, showed an increased risk of preterm birth associated with DDE levels. DDE exposures, however, have dropped over the past 20 years since DDT was banned. Hence DDE cannot be causing the current rise. Thus this new link to a ubiquitous contaminant identifies a new avenue of research for understanding preterm birth's causes. What did they do? Latini et al. took cord blood from babies at birth in a hospital in Brindisi, Italy. They then analyzed the blood for the phthalate di-(2-ethylhexyl)-phthalate (DEHP) and its metabolite mono-ethylhexyl-phthalate (MEHP). In a statistical analysis, they then examined the relationships between several aspects of the infants' health at birth and exposure to DEHP and MEHP What did they find? The study focused on babies born in 84 consecutive births in the Brindisi hospital. Of them, 39 were male, 45 female. Eleven out of the 84 were preterm, with only 3 very low birth weight infants. Four of them were considered "small for gestational age." None were the result of in vitro fertilization. They found DEHP and/or MEHP present in 88% of the cord serum samples they measured. Both were present in 77%. The concentrations averaged 1.19±1.15 µg/ml DEHP and 0.52±0.61 µg/ml MEHP.
Several other infant characteristics, including sex, birth weight and neonatal jaundice showed no association with phthalate exposure. What does it mean? These results open up new chapters in (1) the search for why preterm birth rates are increasing in the US, and (2) the possible health consequences of exposure to the phthalate DEHP. Given the relatively small sample size, this work bears repeating before firm conclusions can be reached. But the striking difference it reveals in the distribution of gestational ages of babies with MEHP exposure vs. those without (figure above) should command the attention of medical researchers trying to explain the pre-term birth epidemic. As the US Centers for Disease has established, phthalate exposure is widespread in American women. Now this study reveals a link between one phthalate, DEHP, and preterm birth. It is worth noting that DEHP, like DDE (discussed above), is an anti-androgen (it interferes with the ability of androgen to bind with the androgen receptor and turn on the suite of genes that androgen normally activates). Whether this common mode of action is a clue to the causation of preterm birth remains to be established. Until they resolve whether these results are real or artifactual, it would be sensible to avoid DEHP/MEHP exposures during pregnancy.
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