Ecotoxicology and environmental safety · 2025
Maternal diesel exhaust exposure exacerbates neonatal hyperoxia-induced lung injury in rats.
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Chang Yu-Shan, Ho Sheng-Yuan, Chou Hsiu-Chu, Chen Chung-Ming
Аннотация
OBJECTIVES: Prenatal exposure to air pollution is associated with an increased risk of lung disease in offspring. However, animal studies on the effects of intrauterine exposure on fetal lung development are limited and yield inconsistent results. This study aimed to investigate the effects of maternal exposure to diesel exhaust particles (DEP) during pregnancy on offspring lung development and whether it would exacerbate neonatal hyperoxia-induced lung injury.
STUDY DESIGN: Pregnant Sprague-Dawley rats were administered a daily intranasal dose of 500 µg of DEP or phosphate-buffered saline (PBS) from gestational days 16-21. After birth, pups were assigned to room air (RA) or hyperoxia (85 % O2). Four groups were established: PBS + RA, PBS + O2, DEP + RA, and DEP + O2. Pups were sacrificed on postnatal day 14 for lung examination.
RESULTS: Offspring born to DEP-exposed dams had lower birth weights. Hyperoxia disrupted alveolarization, with effects further amplified in pups born to DEP-exposed dams. Maternal DEP exposure increased oxidative stress, inflammation, and NF-κB activation compared to controls, and these effects were worsened by hyperoxia. Metabolomic analysis revealed significant metabolic changes, including disruptions in galactose, starch, and amino sugar metabolism.
CONCLUSIONS: Maternal DEP exposure disrupts offspring lung development, increases oxidative stress and inflammation, and exacerbates the effects of postnatal hyperoxia.
STUDY DESIGN: Pregnant Sprague-Dawley rats were administered a daily intranasal dose of 500 µg of DEP or phosphate-buffered saline (PBS) from gestational days 16-21. After birth, pups were assigned to room air (RA) or hyperoxia (85 % O2). Four groups were established: PBS + RA, PBS + O2, DEP + RA, and DEP + O2. Pups were sacrificed on postnatal day 14 for lung examination.
RESULTS: Offspring born to DEP-exposed dams had lower birth weights. Hyperoxia disrupted alveolarization, with effects further amplified in pups born to DEP-exposed dams. Maternal DEP exposure increased oxidative stress, inflammation, and NF-κB activation compared to controls, and these effects were worsened by hyperoxia. Metabolomic analysis revealed significant metabolic changes, including disruptions in galactose, starch, and amino sugar metabolism.
CONCLUSIONS: Maternal DEP exposure disrupts offspring lung development, increases oxidative stress and inflammation, and exacerbates the effects of postnatal hyperoxia.