The effect of sidestream tobacco smoke combined with other pollutants is largely unknown. Previously, we found that distal airway epithelial repair was inhibited in mice exposed to sidestream tobacco smoke (TS) for 5 days followed by single exposure to naphthalene (NA), a common polycyclic aromatic hydrocarbon found in cigarette smoke, diesel exhaust, and pesticide formulations. The main injury target of NA is the nonciliated (Clara) bronchiolar cell. NA injury normally resolves in two weeks. Repair in mice exposed to TS and NA was unresolved in the distal bronchioles 14 days post-NA injury. We hypothesized that repair inhibition persisted as a first step towards long-term airway remodeling and expanded the previous study by evaluating repair 21 days after acute NA injury. Repair was evaluated using high resolution histopathology, TEM, and quantitative morphometry. In animals exposed to TS and NA, repair was still impaired; re-differentiation of Clara cells at the bronchoalveolar duct junction was incomplete, indicating repair was continuing. Compared to 14 days post-NA-injury, repair at 21 days post-NA treatment was more extensive. Animals exposed only to TS had epithelium similar to controls. While TS exposure impairs bronchiolar epithelial repair after NA exposure, this effect appears to be slowly resolving over time.
- Bronchiolar injury and repair
- Environmental tobacco smoke
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