La exposición prenatal al Bisfenol A es un factor de riesgo para la sibilancia.


El Bisfenol A, comunmente abreviado como BPA, es un compuesto orgánico con dos grupos funcionales fenol. Es un bloque disfuncional de muchos importantes plásticos y aditivos plásticos (utilizado en mamaderas). Sumándose a la retahíla de estudios que ponen en tela de juicio la seguridad de este producto, usado para fabricar plásticos de uso cotidiano, un nuevo estudio afirma que las mujeres embarazadas corren más riesgo de que el niño tenga sibilancias. Difundido en la reunión anual de la Pediatric Academic Societies, celebrada esta semana, el hallazgo supone hace luz sobre la potencial peligrosidad de este producto químico en el desarrollo de los fetos durante los primeros meses de embarazo. Así, la investigación encontró que la exposición a altos niveles de BPA durante los tres primeros meses de gestación hace más probable que su recién nacido experimente sibilancias (un sonido silbante y chillón durante la respiración) durante los primeros tres años de vida.

A los seis meses, los niños tenían dos veces más probabilidades de padecer sibilancias, prolongándose hasta los tres años, pero en las futuras madres expuestas al BPA después del primero trimestre de embarazo, los investigadores no observaron el mismo efecto.

Los niveles de este químico considerados altos en este estudio corresponden a cifras de BPA que van desde 0,4 hasta 37,5 microgramos por litro. En concreto, el 99% de las madres analizadas tenían niveles detectables de BPA urinaria en algún momento durante el estudio, y los factores asociados con el aumento de sus niveles estaban relacionados con trabajar como cajera, comer hortalizas en conserva y la exposición al humo de tabaco.Vía: http://es.sott.net/articles/show/6117-La-exposicion-prenatal-al-Bisfenol-A-BPA-dobla-el-riesgo-de-sibilancias-en-los-ninos

Prenatal Bisphenol A Is a Risk Factor for Early Transient Wheeze

Adam J. Spanier, Robert S. Kahn, Allen Kunselman, Richard Hornung, Bruce P. Lanphear. Pediatrics, Penn State University Hershey Medical Center, Hershey, PA; Public Health Sciences, Penn State University Hershey Medical Center, Hershey, PA; Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH; Child & Family Research Institute, BC Children's Hospital, Faculty of Health Sciences, Simon Fraser University, Vancouver, BC, Canada.

BACKGROUND: Bisphenol A (BPA), a chemical used in the production of plastics and epoxy resins for many consumer products, is routinely detectable in over 90% of the US population. There is preliminary evidence for a range of human health consequences. Perinatal BPA exposure has been reported to promote experimental asthma in mice, but there are no human data.
OBJECTIVE: To examine the relationship between prenatal BPA exposure and wheeze in early childhood.
DESIGN/METHODS: We examined a birth cohort study of 398 mother-infant dyads, enrolled in early pregnancy. Maternal urine was collected at 16 weeks and 26 weeks gestation, as well as birth, for measurement of urinary BPA levels. The mean of maternal urinary BPA concentrations over the three collection points was the primary exposure measure. Child wheeze (yes/ no) was assessed via parent report every six months for three years. A repeated measures logistic regression model was used for analysis.
RESULTS: Of 367 children with respiratory outcome data available, 99% were born to a mother with detectable urinary BPA at some point during pregnancy. The geometric mean urinary BPA was 2.4 µg/g of creatinine (95% CI 2.3, 2.6). In multivariable analysis, mean prenatal BPA (dichotomized at the median) was not associated with wheeze (p= 0.47), but there was an interaction of BPA with time (p=0.003). At six months of age, the odds of wheeze for the high BPA group compared to the low BPA group was 2.22 (95% confidence interval: 1.24, 3.97), but by three years, there was no association of mean prenatal BPA with wheeze (adjusted odds ratio 0.57, 95% CI: 0.29, 1.11). We also examined effects the timing of prenatal BPA exposure by replacing mean BPA with each of the three prenatal BPA measures in separate models. Maternal urinary BPA concentration at 16 weeks gestation was associated with wheeze (AOR 1.24, 95% CI 1.0, 1.52), but the 26 week gestation and birth maternal urinary BPA were not (AOR 1.14, 95% CI 0.90, 1.44 and AOR 0.90, 95% CI 0.71, 1.13). There was no interaction of BPA with time in these prenatal BPA exposure timing models.
CONCLUSIONS: Prenatal BPA exposure, especially during early pregnancy, was associated with increased odds of transient wheeze in children. If other studies confirm these findings, policies should be implemented to minimize exposure to BPA for women of childbearing age.


E-PAS20112805.2

Session: Platform Session: Environmental / International Epidemiology (3:30 PM - 5:30 PM)
Date/Time: Sunday, May 1, 2011 - 3:45 PM
Room: Korbel 3C - Colorado Convention Center
Course Code: 2805

vía: http://www.abstracts2view.com/pas/view.php?nu=PAS11L1_2398

Enlaces externos relacionados: Documental Varones en desaparición.