Academic journal article Environmental Health Perspectives

Prenatal Exposure to Bisphenol A and Child Wheeze from Birth to 3 Years of Age

Academic journal article Environmental Health Perspectives

Prenatal Exposure to Bisphenol A and Child Wheeze from Birth to 3 Years of Age

Article excerpt

BACKGROUND: Bisphenol A (BPA), an endocrine-disrupting chemical that is routinely detected in > 90% of Americans, promotes experimental asthma in mice. The association of prenatal BPA exposure and wheeze has not been evaluated in humans.

OBJECTIVE: We examined the relationship between prenatal BPA exposure and wheeze in early childhood.

METHODS: We measured BPA concentrations in serial maternal urine samples from a prospective birth cohort of 398 mother--infant pairs and assessed parent-reported child wheeze every 6 months for 3 years. We used generalized estimating equations with a logit link to evaluate the association of prenatal urinary BPA concentration with the dichotomous outcome wheeze (wheeze over the previous 6 months).

RESULTS: Data were available for 365 children; BPA was detected in 99% of maternal urine samples during pregnancy. In multivariable analysis, a one-unit increase in log-transformed creatininestandardized mean prenatal urinary BPA concentration was not significantly associated with child wheeze from birth to 3 years of age, but there was an interaction of BPA concentration with time (p = 0.003). Mean prenatal BPA above versus below the median was positively associated with wheeze at 6 months of age [adjusted odds ratio (AOR) = 2.3; 95% confidence interval (CI): 1.3, 4.1] but not at 3 years (AOR = 0.6; 95% CI: 0.3, 1.1). In secondary analyses evaluating associations of each prenatal BPA concentration separately, urinary BPA concentrations measured at 16 weeks gestation were associated with wheeze (AOR = 1.2; 95% CI: 1.0, 1.5), but BPA concentrations at 26 weeks of gestation or at birth were not.

CONCLUSIONS: Mean prenatal BPA was associated with increased odds of wheeze in early life, and the effect diminished over time. Evaluating exposure at each prenatal time point demonstrated an association between wheeze from 6 months to 3 years and log-transformed BPA concentration at 16 weeks gestation only.

KEY WORDS: bisphenol A, BPA, child, cotinine, prenatal, tobacco, wheeze. Environ Health Perspect 120:916-920 (2012). http://dx.doi.org/10.1289/ehp.1104175 [Online 14 February 2012]

Asthma is one of the most common chronic and disabling conditions of childhood (Bloom et al. 2010). The prevalence of asthma in children has risen in the last few decades, currently affecting 1 in 10 children (Akinbami et al. 2011; Bloom et al, 2010). Several environmental risk factors for asthma have been identified, such as tobacco smoke and airborne pollutants (McConnell et al. 2010; Oberg et al. 2011). The reasons for the increase in childhood asthma are largely unknown, but other environmental exposures may play a role.

Recent studies have implicated exposure to plastic products in the development of childhood respiratory problems. Investigators have found an association of exposure to plastic wall materials (any plastic wall surfaces) with the development of bronchial obstruction, persistent wheeze, cough, and phlegm in children (Jaakkola et al. 1999, 2000). Jaakkola et al. (2006) found that exposure to plastic wall materials also was associated with more than two times the odds of asthma in adults. Indoor concentrations of common organic plasticizers (2,2,4-trimethy1-1,3-pentanediol monoisobutyrate and 2,2,4-trimethy1-1,3-pentanediol diisobutyrate) in schools also have been associated with increased prevalence of asthmatic symptoms in students (Kim et al. 2007). Thus, the evidence for an association between plastic exposures and wheeze is growing, but it is unclear whether specific plastic constituents, such as bisphenol A (BPA) or phthalates, act as risk factors for childhood respiratory problems.

BPA is a high-production-volume chemical used in the manufacture of some plastics and epoxy resins that are found in many consumer products. The primary route of human exposure to BPA is through dietary ingestion Wilson ec al. 2007). Unfortunately, there is little information about the variability and routes of BPA exposure in pregnant women (Braun et al. …

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