Early BPA Exposure and Asthma Development
Terumi Midoro-Horiuti, M.D., Ph.D.
The University of Texas Medical Branch
NIEHS grants R21ES016428 and P30ES006676
An NIEHS-supported grantee and colleagues report that prenatal bisphenol A (BPA) exposure promotes the development of allergic asthma in a mouse model. They also provide evidence that one reason the mice are susceptible during the prenatal period might be because BPA-metabolizing enzymes have not yet developed.
The mice received BPA in their drinking water beginning at one week before pregnancy. To separate the effects from prenatal BPA exposure and early-postnatal exposure, the researchers transferred some pups after birth from their BPA-exposed mother to an unexposed mother or vice versa. Half of the pups were sensitized with an experimental allergen and then later challenged by inhalations of the allergen. The researchers found that the pups exposed to BPA prenatally only, or prenatally and through breast milk, developed asthma after the allergic challenge. Pups that received only postnatal exposure did not develop asthma.
To look for a possible mechanism for BPA’s enhancement of asthma development, the investigators assessed the expression of Ugt2b1, an enzyme that metabolizes BPA. They found that the enzyme was not detectable in mouse fetuses and newborn pups, but its levels increased by day five and approached adult levels by day 25. Whether this mechanism is at work in humans must still be studied.
Citation: Nakajima Y, Goldblum RM, Midoro-Horiuti T. 2012. Fetal exposure to bisphenol A as a risk factor for the development of childhood asthma: an animal model study. Environ Health 11:8.
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