Enhancement between environmental tobacco smoke and arsenic on emphysema-like lesions in mice.

Chronic obstructive pulmonary diseases (COPD) have been the major cause of mortality worldwide. Early identification of populations at risk allows us to prevent the occurrence and to reduce the cost of health care. In human studies, exposure to environmental tobacco smoke (ETS) and arsenic respectively increased the risk of chronic lung diseases, including COPD. We suspected that ETS and arsenic might enhance the risk of COPD. In our present study, we evaluated this hypothesis in mice and tried to identify early biomarkers for chemicals-induced lung lesions. Mice inhaled ETS and/or administrated arsenite via gavage for 4 weeks. At the end of experiment, exposure to ETS or arsenite alone failed to cause lung lesions or inflammation. However, co-exposure to ETS and arsenite significantly induced emphysema-like lesions, characterized with enlarged alveolar spaces and destruction of alveolar structure, although inflammation was not observed. Furthermore, co-exposure to ETS and arsenite significantly increased plasma 8-oxodeoxyguanosine (8-OHdG) levels. Our results indicated that co-exposure to ETS and arsenite induced emphysematous lesions, and plasma 8-OHdG might serve as an early biomarker for co-exposure of ETS and arsenite. With information about ETS and arsenic exposure in human populations, plasma 8-OHdG will help us to identify individuals at risk.