Pesquisa sugere que exposição de gestantes ao bisfenol-A(BPA) aumenta o risco de asma nas crianças, por Henrique Cortez

Efeitos do BPA no organismo. Imagem: Environmental Working Group

[Ecodebate] A longo dos últimos anos crescem as evidências dos riscos à saúde decorrentes da exposição ao bisfenol-A(BPA), já associado a desordens reprodutivas, desordens hormonais, obesidade, problemas no desenvolvimento cerebral, câncer de mama e próstata. O assunto tomou tal proporção que, em uma mudança de posição, a Food and Drug Administration (FDA), agência que controla alimentos e remédios nos Estados Unidos, está manifestando preocupações sobre possíveis riscos à saúde provocados pelo BPA, um componente de garrafas e embalagens de alimentos de plástico amplamente usado no mercado. Na análise anterior, feita em 2008, a agência havia considerado o uso da substância seguro.

Em 15/01/2010, a agência disse que tinha “algumas preocupações sobre os efeitos potenciais do BPA no cérebro, no comportamento e na próstata de fetos, bebês e crianças”. Informou que se uniria a outras agências federais de saúde para estudar o produto químico em animais e humanos.

Agora, em novo estudo [Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups], pesquisadores expuseram ratas prenhas ao BPA, em dosagens proporcionais a uma mulher grávida, ao longo da gestação e do período de amamentação, identificando que a exposição aumentou o risco do desenvolvimeto de asma. A pesquisa foi publicada na edição de fevereiro da revista Environmental Health Perspectives.

Além aumento do risco em si, pesquisadores também identificaram o aumento da sensibilidade aos diferentes fatores desencadeantes, potencializando o riscos de crises de asma.

O estudo foi financiado pelo The National Institute for Environmental Health Sciences e pelo National Institute for Allergy and Infectious Disease

O artigo ” Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups“, de Terumi Midoro-Horiuti, Ruby Tiwari, Cheryl S. Watson, Randall M. Goldblum, Environmental Health Perspectives, Research Article, published 05 Out 2009 | doi:10.1289/ehp.0901259, está disponível para acesso integral, nos formatos HTML e PDF. Para acessar no formato HTML clique aqui e em formato PDF clique aqui.

Para maiores informações transcrevemos, abaixo, o abstract:

Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups
Terumi Midoro-Horiuti1,2, Ruby Tiwari1, Cheryl S. Watson2, Randall M. Goldblum1,2
1 Department of Pediatrics, Child Health Research Center, and, 2 Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, USA

Abstract

Background: We recently reported that various environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators in vitro.

Objectives: We hypothesized that environmental estrogens would enhance allergic sensitization as well as bronchial inflammation and responsiveness. To test this hypothesis, we exposed fetal and neonatal mice to the common environmental estrogen bisphenol A (BPA) via maternal loading and assessed the pups’ response to allergic sensitization and bronchial challenge.

Methods: Female BALB/c mice received 10 µg/mL BPA in their drinking water from 1 week before impregnation to the end of the study. Neonatal mice were given a single 5 µg intraperitoneal dose of ovalbumin (OVA) with aluminum hydroxide on postnatal day 4 and 3% OVA by nebulization for 10 min on days 13, 14, and 15. Forty-eight hours after the last nebulization, we assessed serum IgE antibodies to OVA by enzyme-linked immunosorbent assay (ELISA) and airway inflammation and hyperresponsiveness by enumerating eosinophils in bronchoalveolar lavage fluid, whole-body barometric plethysmography, and a forced oscillation technique.

Results: Neonates from BPA-exposed mothers responded to this “suboptimal” sensitization with higher serum IgE anti-OVA concentrations compared with those from unexposed mothers (p < 0.05), and eosinophilic inflammation in their airways was significantly greater. Airway responsiveness of the OVA-sensitized neonates from BPA-treated mothers was enhanced compared with those from unexposed mothers (p < 0.05).

Conclusions: Perinatal exposure to BPA enhances allergic sensitization and bronchial inflammation and responsiveness in a susceptible animal model of asthma.

Editor’s Summary

Different forms of mercury (Hg) vary with regard to uptake, metabolism, and neurotoxic effects. Humans are primarily exposed to organic methylmercury (MeHg) in seafood but are also exposed to inorganic Hg vapor released from dental amalgams; effects of joint exposures to MeHg and inorganic Hg vapor have not been studied extensively. Ishitobi et al. (p. 242) measured Hg levels in the brains of offspring of Long-Evans hooded rats exposed to MeHg (0, 3, 6, or 9 ppm as drinking solution), Hg vapor (0, 300, or 1,000 µg/m3 for 2 hr/day), or MeHg and Hg vapor beginning 30 days before breeding and ending on gestation day 18. The authors report that increasing levels of MeHg in the absence of Hg vapor predicted total Hg, inorganic Hg, and organic Hg levels in the brains of neonatal pups, but exposure to Hg vapor in the absence of MeHg was not a consistent predictor of brain Hg levels. The authors also report evidence of complex interactions between MeHg and Hg-vapor exposures that they conclude suggests an increase in brain Hg levels (and a potential increase in neurotoxicity) with combined exposure to MeHg and Hg vapor at levels relevant to human exposures.
Keywords: airway hyperresponsiveness, asthma, bisphenol A, environmental estrogen, eosinophilia, experimental asthma, IgE, maternal exposure, perinatal sensitization.

Citation: Midoro-Horiuti T, Tiwari R, Watson CS, Goldblum RM 2009. Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups. Environ Health Perspect 118:273-277. doi:10.1289/ehp.0901259

Received: 27 July 2009; Accepted: 05 October 2009; Published: 05 October 2009

Address correspondence to T. Midoro-Horiuti, Child Health Research Center, Children’s Hospital Room 2.300, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0366 USA. Telephone: (409) 772-3832. Fax: (409) 772-1761. E-mail: tmidoro@utmb.edu

We thank R.A. Johnston for technical assistance in using the forced oscillation technique.

This project was supported by grant R21 ES016428 from the National Institute of Environmental Health Sciences (T.M.H.) and by grants K08 AI1055792 (T.M.H.) and R01 AI1052428 (R.M.G.) from the National Institute of Allergy and Infectious Diseases.

The authors declare they have no competing financial interests.

Por Henrique Cortez, do EcoDebate, 05/02/2010

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