14 research outputs found
Bisphenol A Exposure and Asthma Development in School-Age Children: A Longitudinal Study
<div><p>Background</p><p>Although the effect of bisphenol A on various health outcomes has been extensively examined, few studies have investigated its effect on asthma.</p><p>Objective</p><p>We hypothesized that exposure to bisphenol A in school-age children was associated with wheezing and asthma.</p><p>Methods</p><p>Participants included 127 children aged 7–8 years without a previous asthma diagnosis in an elementary school in Seoul, Korea. Three surveys were conducted, each 2 years apart. Bisphenol A concentration was measured at the baseline survey, and PC<sub>20</sub>, which is defined as the methacholine concentration that induces a decrease in FEV<sub>1</sub> of 20% from baseline, was measured at every survey. Associations between bisphenol A concentration at 7–8 years of age and wheezing, asthma, and PC<sub>20</sub> at ages up to 11–12 years were examined using generalized estimating equations, a marginal Cox regression model, and a linear mixed model.</p><p>Results</p><p>The log-transformed creatinine-adjusted urinary bisphenol A concentration at 7–8 years was positively associated with wheezing (odds ratio, 2.48; 95% confidence interval, 1.15–5.31; <i>P</i> = .02) and asthma (hazard ratio, 2.13; 95% confidence interval, 1.51–3.00; <i>P</i><.001) at ages up to 11–12 years. Bisphenol A was also negatively associated with PC<sub>20</sub> (ß = −2.33; <i>P</i> = .02). When stratified by sex, the association between bisphenol A and asthma remained significant only in girls (hazard ratio, 2.45; 95% confidence interval, 2.18–2.76; <i>P</i><.001).</p><p>Conclusion</p><p>Increased urinary bisphenol A concentrations at 7–8 years old were positively associated with wheezing and asthma and negatively associated with PC<sub>20</sub> at ages up to 11–12 years.</p></div
Association of urinary BPA concentrations (log transformed, µg/g creatinine) at 7–8 years with wheezing and asthma over 11–12 years of age, by longitudinal analyses.
<p>HR, hazard ratio.</p><p>* Number with outcome/total number for analysis.</p>†<p>Generalized estimating equation with a logit link model adjusted for gender, parental asthma history, fetal and environmental tobacco smoke exposure, pet ownership, and grade at enrollment.</p>‡<p>Marginal Cox model considering grade-at-enrollment clustering adjusted for gender, parental asthma history, fetal and environmental tobacco smoke exposure, and pet ownership.</p><p>Association of urinary BPA concentrations (log transformed, µg/g creatinine) at 7–8 years with wheezing and asthma over 11–12 years of age, by longitudinal analyses.</p
Overview of study population sampling and follow-up.
<p>Overview of study population sampling and follow-up.</p
Association of urinary BPA concentrations (log transformed, µg BPA/g creatinine) at 7–8 years with wheezing, PC<sub>20</sub>, and current asthma at 7–8, 9–10, and 11–12 years of age.
<p>*Logistic regression model adjusted for gender, parental asthma history, fetal and environmental tobacco smoke exposure, pet ownership, and grade at enrollment.</p>†<p>Linear regression model adjusted for gender, parental asthma history, fetal and environmental tobacco smoke exposure, pet ownership, and grade at enrollment.</p>‡<p>Number with outcome/total number for analysis.</p>§<p>Total number for analysis.</p><p>Association of urinary BPA concentrations (log transformed, µg BPA/g creatinine) at 7–8 years with wheezing, PC<sub>20</sub>, and current asthma at 7–8, 9–10, and 11–12 years of age.</p
Relationship between urinary BPA concentration and PC<sub>20</sub>.
<p>Penalized regression spline of log-transformed urinary BPA concentrations at 7–8 years on PC<sub>20</sub> at ages up to 11–12 years. Solid lines, spline curve; shaded area, 95% confidence intervals. The model is adjusted for gender, parental asthma history, fetal and environmental tobacco smoke exposure, and pet ownership.</p
Additive Effect between IL-13 Polymorphism and Cesarean Section Delivery/Prenatal Antibiotics Use on Atopic Dermatitis: A Birth Cohort Study (COCOA)
<div><p>Background</p><p>Although cesarean delivery and prenatal exposure to antibiotics are likely to affect the gut microbiome in infancy, their effect on the development of atopic dermatitis (AD) in infancy is unclear. The influence of individual genotypes on these relationships is also unclear. To evaluate with a prospective birth cohort study whether cesarean section, prenatal exposure to antibiotics, and susceptible genotypes act additively to promote the development of AD in infancy.</p><p>Methods</p><p>The Cohort for Childhood of Asthma and Allergic Diseases (COCOA) was selected from the general Korean population. A pediatric allergist assessed 412 infants for the presence of AD at 1 year of age. Their cord blood DNA was subjected to interleukin (IL)-13 (rs20541) and cluster-of-differentiation (CD)14 (rs2569190) genotype analysis.</p><p>Results</p><p>The combination of cesarean delivery and prenatal exposure to antibiotics associated significantly and positively with AD (adjusted odds ratio, 5.70; 95% CI, 1.19–27.3). The association between cesarean delivery and AD was significantly modified by parental history of allergic diseases or risk-associated IL-13 (rs20541) and CD14 (rs2569190) genotypes. There was a trend of interaction between IL-13 (rs20541) and delivery mode with respect to the subsequent risk of AD. (<i>P</i> for interaction = 0.039) Infants who were exposed prenatally to antibiotics and were born by cesarean delivery had a lower total microbiota diversity in stool samples at 6 months of age than the control group. As the number of these risk factors increased, the AD risk rose (trend p<0.05).</p><p>Conclusion</p><p>Cesarean delivery and prenatal antibiotic exposure may affect the gut microbiota, which may in turn influence the risk of AD in infants. These relationships may be shaped by the genetic predisposition.</p></div
Comparison of indoor environmental factors between the16 children with children’s interstitial lung diseases and their 47 matched control.
a<p>Variables in the previous 1 year.</p>*<p><i>P</i><0.05.</p
Additive effects of mode of delivery, prenatal antibiotic exposure, and parental history of allergic diseases on the development of atopic dermatitis (AD) at 1 year of age.
<p>*Adjusted for gestational age at birth, sex, pre-pregnancy maternal body-mass index, maternal age at delivery, maternal education level, prenatal exposure to smoke, prenatal exposure to pets, and presence of older sibling(s).</p>†<p>Risk factors were: parental history of allergic diseases, prenatal use of antibiotics, and cesarean delivery.</p
Case ascertainment criteria.
<p>(A) Chest radiography showing diffuse, ill-defined ground-glass opacities and several ill-defined small nodular opacities in both lungs (in the 4 weeks after respiratory symptoms started). (B) Chest computed tomography showing diffuse centrilobular nodules in both lungs, with ground-glass opacities suggestive of peribronchiolar fibrosis (in the 4 weeks after respiratory symptoms started). (C) The most striking histological feature, interstitial thickening and fibrosis with a centrilobular distribution and relative sparing of the subpleural parenchyma (upper one-third). Original magnification ×40. (D) Interstitial fibroblasts proliferating in a pale myxoid stroma (arrows) and collapsed alveolar spaces lined by activated pneumocytes (arrowhead). Original magnification ×200.</p
Characteristics of the participating infants.
<p>*n, number of children with each characteristic; d, the total number of children with information available on this characteristic.</p>†<p>graduated from graduate school.</p