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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Prenatal exposure to bisphenol A and child wheeze from birth to 3 years of age
Adam J Spanier1, Robert S Kahn, Allen R Kunselman
1Department of Pediatrics, Penn State University Hershey Medical Center, Hershey, Pennsylvania 17033-0850, USA. aspanier@hmc.psu.edu
Insights
Prenatal exposure to Bisphenol A (BPA), an endocrine disruptor, was linked to increased wheeze in infants. This association diminished over time, with early gestation exposure being most significant.
Area of Science:
- Environmental Health
- Pediatric Respiratory Health
- Endocrinology
Background:
- Bisphenol A (BPA) is an endocrine-disrupting chemical prevalent in the environment.
- BPA exposure is known to promote asthma in experimental models.
- The link between prenatal BPA exposure and wheeze in human infants remains understudied.
Purpose of the Study:
- To investigate the relationship between prenatal Bisphenol A (BPA) exposure and the occurrence of wheeze in early childhood.
- To determine if BPA exposure during pregnancy is associated with wheezing illnesses in infants.
Main Methods:
- A prospective birth cohort study involving 398 mother-infant pairs.
- Measurement of BPA concentrations in serial maternal urine samples throughout pregnancy.
- Assessment of parent-reported child wheeze every six months for three years using generalized estimating equations.
Main Results:
- Bisphenol A (BPA) was detected in 99% of maternal urine samples.
- Higher mean prenatal BPA levels were associated with increased odds of wheeze at 6 months of age (AOR=2.3).
- Urinary BPA concentrations at 16 weeks gestation were associated with wheeze up to 3 years (AOR=1.2), but not at later time points.
Conclusions:
- Mean prenatal Bisphenol A (BPA) exposure is associated with a higher likelihood of wheeze in early infancy.
- The impact of BPA on wheeze risk decreases as the child ages.
- Exposure timing is critical, with BPA levels at 16 weeks gestation showing a significant association with wheeze development.
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 creatinine-standardized 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.
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