You are here:
Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone Exposed Offspring
Citation:
Auten, R. L., M. I. GILMOUR, Q. T. KRANTZ, E. N. Potts, N. S. Mason, AND M. W. Foster. Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone Exposed Offspring. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY. American Thoracic Society, New York, NY, 46(4):454-60, (2012).
Impact/Purpose:
Maternal diesel exposure followed by exposure of newborn rat pups to ozone causes enhanced, persistent, airway hyperreactivity to methacholine challenge and worsened alveolar development
Description:
Air pollutant exposure is linked with childhood asthma incidence and exacerbations, and maternal exposure to airborne pollutants during pregnancy increases airway hyperreactivity (ARR) in offspring. To determine if exposure to diesel exhaust during pregnancy worsened postnatal ozone-induced ARR, timed pregnant C57BL/6 mice were exposed to diesel exhaust (0.5 or 2.0 mg/m3) 4 h daily from gestation day (GD) 7 to 17, or received twice weekly oropharyngeal aspirations of the collected diesel exhaust particles (DEPs). Placentas and fetal lungs were harvested on gestation day 18 for cytokine analysis. In other litters, pups born to air, diesel exhaust or diesel particle exposed dams were exposed to filtered air or 1 ppm ozone beginning the day after birth, for 3h/day, 3d/week for 4 weeks. Additional pups were monitored following a 4 week recovery period. Diesel inhalation or aspiration during pregnancy increased levels of placental and fetal lung cytokines IL-Iß, TNFα, IL-6, KC, RANTES, and eotaxin. There were no significant effects on airway inflammation after 4 weeks, however mice born to the high-concentration diesel exposed dams had worse ozone-induced airway hyperreactivity which persisted in the 4 week recovery animals. Prenatal diesel exposure combined with postnatal ozone exposure also worsened secondary alveolar crest development. We conclude that maternal inhalation of diesel exhaust in pregnancy provokes a fetal inflammatory response that, combined with postnatal ozone exposure, impairs alveolar development, and causes a more severe and long-lasting airway hyperresponsiveness to ozone exposure.
