Perinatal bisphenol A exposure beginning before gestation enhances allergen sensitization, but not pulmonary inflammation, in adult mice.
Bisphenol A (BPA), a monomer of polycarbonate plastics and epoxide resin, is a high-production-volume chemical implicated in asthma pathogenesis when exposure occurs to the developing fetus. However, few studies have directly examined the effect of in utero and early-life BPA exposure on the pathogenesis of asthma in adulthood. This study examines the influence of perinatal BPA exposure through maternal diet on allergen sensitization and pulmonary inflammation in adult offspring. Two weeks before mating, BALB/c dams were randomly assigned to a control diet or diets containing 50 ng, 50 μg or 50 mg BPA/kg of rodent chow. Dams remained on the assigned diet throughout gestation and lactation until postnatal day (PND) 21 when offspring were weaned onto the control diet. Twelve-week-old offspring were sensitized to ovalbumin (OVA) and subsequently challenged with aerosolized OVA. Sera, splenocytes, bronchoalveolar lavage fluid and whole lungs were harvested to assess allergen sensitization and pulmonary inflammation after OVA challenge. Serum anti-OVA IgE levels were increased two-fold in offspring exposed to 50 μg and 50 mg BPA/kg diet, compared with control animals. In addition, production of interleukin-13 and interferon-γ were increased in OVA-stimulated splenocytes recovered from BPA-exposed mice. Pulmonary inflammation, as indicated by total and differential leukocyte counts, cytokines, chemokines and pulmonary histopathology inflammatory scores, however, was either not different or was reduced in offspring exposed to BPA. Although these data suggest that perinatal BPA exposure beginning before gestation enhances allergen sensitization by increasing serum IgE and splenocyte cytokine production, a substantial impact of BPA on OVA-induced pulmonary inflammation in adulthood was not observed.
1 Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
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O'Brien
2 Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, MI, USA.
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IL
Bergin
1 Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
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DC
Dolinoy
3 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, School of Medicine, University of Michigan, Ann Arbor, MI, USA.
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Zaslona
4 Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
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RJ
Little
4 Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
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Y
Tao
3 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, School of Medicine, University of Michigan, Ann Arbor, MI, USA.
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M
Peters-Golden
1 Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
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Mancuso
D000818:Animals; D001559:Benzhydryl Compounds / Q000633:toxicity*; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D006967:Hypersensitivity / Q000209:etiology*; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008807:Mice, Inbred BALB C; D010636:Phenols / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D018675:Toxicity Tests; D000098826:Bisphenol A Compounds
D001559:Benzhydryl Compounds; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds