US EPA

1104484 

Journal Article 

[RETRACTED] Maternal diesel inhalation increases airway hyperreactivity in ozone-exposed offspring 

Auten, RL; Gilmour, MI; Krantz, QT; Potts, EN; Mason, SN; Foster, WM 

2012 

Yes 

American Journal of Respiratory Cell and Molecular Biology
ISSN: 1044-1549
EISSN: 1535-4989 

46 

4 

454-460 

English 

22052876 

10.1165/rcmb.2011-0256OC 

WOS:000302691900006 

https://www.atsjournals.org/doi/10.1165/rcmb.2011-0256OC
Exit
 

has retraction 3075617 Retraction: Maternal diesel inhalation increases airway hyperreactivity in ozone-exposed offspring

Air pollutant exposure is linked with childhood asthma incidence and exacerbations, and maternal exposure to airborne pollutants during pregnancy increases airway hyperreactivity (AHR) in offspring. To determine if exposure to diesel exhaust (DE) during pregnancy worsened postnatal ozone-induced AHR, timed pregnant C57BL/6 mice were exposed to DE (0.5 or 2.0 mg/m(3)) 4 hours daily from Gestation Day 9-17, or received twice-weekly oropharyngeal aspirations of the collected DE particles (DEPs). Placentas and fetal lungs were harvested on Gestation Day 18 for cytokine analysis. In other litters, pups born to dams exposed to air or DE, or to dams treated with aspirated diesel particles, were exposed to filtered air or 1 ppm ozone beginning the day after birth, for 3 hours per day, 3 days per week for 4 weeks. Additional pups were monitored after a 4-week recovery period. Diesel inhalation or aspiration during pregnancy increased levels of placental and fetal lung cytokines. There were no significant effects on airway leukocytes, but prenatal diesel augmented ozone-induced elevations of bronchoalveolar lavage cytokines at 4 weeks. Mice born to the high-concentration diesel-exposed dams had worse ozone-induced AHR, 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 DE in pregnancy provokes a fetal inflammatory response that, combined with postnatal ozone exposure, impairs alveolar development, and causes a more severe and long-lasting AHR to ozone exposure. 

diesel; fetal inflammation; ozone; airway hyperreactivity