Early-Life Bisphenol A Exposure and Child Body Mass Index
Early-Life Bisphenol A Exposure and Child Body Mass Index
Background Early-life exposure to bisphenol A (BPA) may increase childhood obesity risk, but few prospective epidemiological studies have investigated this relationship.
Objective We sought to determine whether early-life exposure to BPA was associated with increased body mass index (BMI) at 2–5 years of age in 297 mother–child pairs from Cincinnati, Ohio (HOME Study).
Methods Urinary BPA concentrations were measured in samples collected from pregnant women during the second and third trimesters and their children at 1 and 2 years of age. BMI z-scores were calculated from weight/height measures conducted annually from 2 through 5 years of age. We used linear mixed models to estimate BMI differences or trajectories with increasing creatinine-normalized BPA concentrations.
Results After confounder adjustment, each 10-fold increase in prenatal (β = –0.1; 95% CI: –0.5, 0.3) or early-childhood (β = –0.2; 95% CI: –0.6, 0.1) BPA concentrations was associated with a modest and nonsignificant reduction in child BMI. These inverse associations were suggestively stronger in girls than in boys [prenatal effect measure modification (EMM) p-value = 0.30, early-childhood EMM p-value = 0.05], but sex-specific associations were imprecise. Children in the highest early-childhood BPA tercile had lower BMI at 2 years (difference = –0.3; 95% CI: –0.6, 0.0) and larger increases in their BMI slope from 2 through 5 years (BMI increase per year = 0.12; 95% CI: 0.07, 0.18) than children in the lowest tercile (BMI increase per year = 0.07; 95% CI: 0.01, 0.13). All associations were attenuated without creatinine normalization.
Conclusions Prenatal and early-childhood BPA exposures were not associated with increased BMI at 2–5 years of age, but higher early-childhood BPA exposures were associated with accelerated growth during this period.
Child obesity is one of the greatest public health challenges worldwide (World Health Organization 2010). Excess food consumption and inadequate physical activity are major risk factors for obesity, but emerging evidence suggests that exposure to obesogens—chemicals that alter adipogenesis or metabolism—might play a role in increasing obesity risk beyond these traditional risk factors (Janesick and Blumberg 2012; Romano et al. 2014; Tang-Peronard et al. 2011). The developing fetus and infant may be especially sensitive to obesogens because of their immature detoxification pathways and sensitivity to environment inputs. Most epidemiological studies of environmental chemical obesogens have been limited to organochlorine compounds; few have examined contemporary chemicals, such as bisphenol A (BPA) (Tang-Peronard et al. 2011).
BPA is a high-production-volume chemical used to produce polycarbonate plastics and resins, and there is ubiquitous exposure among persons in industrialized countries (Braun et al. 2012; Lee et al. 2014; Quirós-Alcalá et al. 2013; Valvi et al. 2013). BPA is a suspected endocrine disruptor and may affect the metabolism or action of hormones or receptors involved in the etiology of obesity, including glucocorticoids, gonadal hormones, and peroxisome proliferator activated receptors (Janesick and Blumberg 2012; Ross and Desai 2013). One animal study suggests that the obesogenic effect of BPA may by modified by the availability of methyl donors (e.g., folate) for DNA methylation, thus permanently altering the programming of adipogenesis, appetite, or energy metabolism, and increasing later-life obesity risk (Dolinoy et al. 2007).
Although some animal studies suggest that BPA is a candidate obesogen, others do not (reviewed by Harley et al. 2013). Cross-sectional human studies suggest that urinary BPA concentrations are associated with increased body mass index (BMI) or obesity in adults and children, but these findings could result from confounding or reverse causation because diet is an important source of BPA exposure and obesity is linked to certain dietary patterns (Carwile and Michels 2011; Sharpe and Drake 2013; Trasande et al. 2012; Wang et al. 2012). Two prospective cohort studies examining early-life BPA exposure report contradictory findings: One found higher BMI among children with higher prenatal BPA exposure (Valvi et al. 2013), and another reported lower BMI with higher prenatal exposure (Harley et al. 2013). These studies suggest that girls, as well as children born to women who smoke during pregnancy, may be more susceptible to prenatal BPA exposure.
We investigated whether prenatal or early-childhood BPA exposure was associated with BMI or waist circumference in children 2–5 years of age from a population-based, prospective cohort study conducted in Cincinnati, Ohio. We also determined whether the association between prenatal BPA exposure and child BMI was modified by maternal folate levels, child sex, or prenatal tobacco smoke exposure.
Abstract and Introduction
Abstract
Background Early-life exposure to bisphenol A (BPA) may increase childhood obesity risk, but few prospective epidemiological studies have investigated this relationship.
Objective We sought to determine whether early-life exposure to BPA was associated with increased body mass index (BMI) at 2–5 years of age in 297 mother–child pairs from Cincinnati, Ohio (HOME Study).
Methods Urinary BPA concentrations were measured in samples collected from pregnant women during the second and third trimesters and their children at 1 and 2 years of age. BMI z-scores were calculated from weight/height measures conducted annually from 2 through 5 years of age. We used linear mixed models to estimate BMI differences or trajectories with increasing creatinine-normalized BPA concentrations.
Results After confounder adjustment, each 10-fold increase in prenatal (β = –0.1; 95% CI: –0.5, 0.3) or early-childhood (β = –0.2; 95% CI: –0.6, 0.1) BPA concentrations was associated with a modest and nonsignificant reduction in child BMI. These inverse associations were suggestively stronger in girls than in boys [prenatal effect measure modification (EMM) p-value = 0.30, early-childhood EMM p-value = 0.05], but sex-specific associations were imprecise. Children in the highest early-childhood BPA tercile had lower BMI at 2 years (difference = –0.3; 95% CI: –0.6, 0.0) and larger increases in their BMI slope from 2 through 5 years (BMI increase per year = 0.12; 95% CI: 0.07, 0.18) than children in the lowest tercile (BMI increase per year = 0.07; 95% CI: 0.01, 0.13). All associations were attenuated without creatinine normalization.
Conclusions Prenatal and early-childhood BPA exposures were not associated with increased BMI at 2–5 years of age, but higher early-childhood BPA exposures were associated with accelerated growth during this period.
Introduction
Child obesity is one of the greatest public health challenges worldwide (World Health Organization 2010). Excess food consumption and inadequate physical activity are major risk factors for obesity, but emerging evidence suggests that exposure to obesogens—chemicals that alter adipogenesis or metabolism—might play a role in increasing obesity risk beyond these traditional risk factors (Janesick and Blumberg 2012; Romano et al. 2014; Tang-Peronard et al. 2011). The developing fetus and infant may be especially sensitive to obesogens because of their immature detoxification pathways and sensitivity to environment inputs. Most epidemiological studies of environmental chemical obesogens have been limited to organochlorine compounds; few have examined contemporary chemicals, such as bisphenol A (BPA) (Tang-Peronard et al. 2011).
BPA is a high-production-volume chemical used to produce polycarbonate plastics and resins, and there is ubiquitous exposure among persons in industrialized countries (Braun et al. 2012; Lee et al. 2014; Quirós-Alcalá et al. 2013; Valvi et al. 2013). BPA is a suspected endocrine disruptor and may affect the metabolism or action of hormones or receptors involved in the etiology of obesity, including glucocorticoids, gonadal hormones, and peroxisome proliferator activated receptors (Janesick and Blumberg 2012; Ross and Desai 2013). One animal study suggests that the obesogenic effect of BPA may by modified by the availability of methyl donors (e.g., folate) for DNA methylation, thus permanently altering the programming of adipogenesis, appetite, or energy metabolism, and increasing later-life obesity risk (Dolinoy et al. 2007).
Although some animal studies suggest that BPA is a candidate obesogen, others do not (reviewed by Harley et al. 2013). Cross-sectional human studies suggest that urinary BPA concentrations are associated with increased body mass index (BMI) or obesity in adults and children, but these findings could result from confounding or reverse causation because diet is an important source of BPA exposure and obesity is linked to certain dietary patterns (Carwile and Michels 2011; Sharpe and Drake 2013; Trasande et al. 2012; Wang et al. 2012). Two prospective cohort studies examining early-life BPA exposure report contradictory findings: One found higher BMI among children with higher prenatal BPA exposure (Valvi et al. 2013), and another reported lower BMI with higher prenatal exposure (Harley et al. 2013). These studies suggest that girls, as well as children born to women who smoke during pregnancy, may be more susceptible to prenatal BPA exposure.
We investigated whether prenatal or early-childhood BPA exposure was associated with BMI or waist circumference in children 2–5 years of age from a population-based, prospective cohort study conducted in Cincinnati, Ohio. We also determined whether the association between prenatal BPA exposure and child BMI was modified by maternal folate levels, child sex, or prenatal tobacco smoke exposure.
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