Prenatal Di(2-ethylhexyl)Phthalate Exposure and Length of Gestation Among an Inner-City Cohort

Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY 10032, USA.
PEDIATRICS (Impact Factor: 5.47). 12/2009; 124(6):e1213-20. DOI: 10.1542/peds.2009-0325
Source: PubMed


Our objective was to assess the relationship between di(2-ethylhexyl)phthalate (DEHP) exposure during pregnancy and gestational age at delivery among 311 African American or Dominican women from New York City.
Forty-eight-hour personal air and/or spot urine samples were collected during the third trimester. DEHP levels were measured in air samples and 4 DEHP metabolite levels were measured in urine. Specific gravity was used to adjust for urinary dilution. Gestational age was abstracted from newborn medical records (n = 289) or calculated from the expected date of delivery (n = 42). Multivariate linear regression models controlled for potential confounders.
DEHP was detected in 100% of personal air samples (geometric mean: 0.20 microg/m(3) [95% confidence interval [CI]: 0.18-0.21 microg/m(3)]); natural logarithms of air concentrations were inversely but not significantly associated with gestational age. Two or more of the DEHP metabolites were detected in 100% of urine samples (geometric mean: 4.8-38.9 ng/mL [95% CI: 4.1-44.3 ng/mL]). Controlling for potential confounders, gestational age was shorter by 1.1 days (95% CI: 0.2-1.8 days) for each 1-logarithmic unit increase in specific gravity-adjusted mono(2-ethylhexyl)phthalate concentrations (P = .01) and averaged 5.0 days (95% CI: 2.1-8.0 days) less among subjects with the highest versus lowest quartile concentrations (P = .001). Results were similar and statistically significant for the other DEHP metabolites.
Prenatal DEHP exposure was associated with shorter gestation but, given inconsistencies with previous findings for other study populations, results should be interpreted with caution, and additional research is warranted.

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Available from: Lori Hoepner, Sep 24, 2014
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    • "Thus, phthalates have become a ubiquitous environmental contaminant and as a result, general population is continuously exposed to them. Some human exposure studies during last decade have shown effects on reproduction, DNA damage to sperm (Pant et al., 2010; Rozati et al., 2002), early onset of puberty in females (Wolff et al., 2010), anomalies of reproductive tract (Desdoits-Lethimonier et al., 2012), infertility (Rozati et al., 2002; Tranfo et al., 2012) and adverse outcomes of phthalate exposure during pregnancy including fetal development (Latini et al., 2006; Whyatt et al., 2009). Although far less investigated, there are reports suggesting that phthalates may adversely affect other functions and systems such as thyroid signalling (Meeker et al., 2007), neuro-development (Miodovnik et al., 2011) asthma and allergies (Jaakkola and Knight, 2008), and insulin resistance (Stahlhut et al., 2007). "
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    • "), decreased sperm quality (Duty et al., 2004; Hauser et al., 2007), and length of gestation (Adibi et al., 2009; Whyatt et al., 2009) although conflicting reports are also available (Duty et al., 2005a; Jonsson et al., 2005; Rais-Bahrami et al., 2004). "
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    • "Outcomes of interest included pre-pregnancy weight, BMI, and weight gain during pregnancy, all measured using self-reports. The statistical analyses assessing the relation between urinary phthalate metabolites and anthropometric measures were not described, but the qualitative results were presented in the text (Whyatt et al., 2009). A study conducted in Denmark (Boas et al., 2010) evaluated 845 children 4–9 years of age who were previously enrolled in a birth cohort. "
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