A case-control study comprising 224 male and 92 female incident lung cancer cases and the same number of individually matched hospital controls was conducted from June 1983 to June 1984 in Guangzhou, People's Republic of China, to evaluate the association between indoor air pollution and lung cancer risk. Guangzhou residents were exposed to several sources of pollution in their homes, most importantly to cooking fumes. Increased risks were found among subjects living in a house without a separate kitchen (the exposure odds ratio was 2.4 (95% confidence interval (CI) 1.4-4.2) for men and 5.9 (95% CI 2.1-16.0) for women). Similarly, living in a house with poor air circulation was associated with an exposure odds ratio of 2.1 (95% CI 1.2-3.8) for men and 3.6 (95% CI 1.4-9.3) for women. A trend in the association between lung cancer risk and factors pertaining to house and kitchen ventilation was observed, and a decreasing risk of lung cancer was observed for several variables indicating better ventilation, even after adjustment for potential confounders such as education, occupation, living area, smoking, and history of chronic respiratory diseases. No statistically significant differences were found between cases and controls for frequency of cooking at home, presence of a chimney in the kitchen, or type of cooking fuel. Smoking was clearly related to risk of lung cancer in both men and women, and among nonsmoking women, exposure to tobacco smoke from their spouses was also associated with an increased risk. These results suggest that, in addition to smoking, indoor air pollution may be a risk factor for lung cancer.

The COVID-19 virus outbreak has been declared a “global pandemic”. Therefore, “lockdown” was issued in affected countries to control the spread of the virus. To assess air pollution during and after lockdowns, this study selected pandemic hotspots in China (Wuhan), Japan (Tokyo), Korea (Daegu), and India (Mumbai) and compared the Air Quality Index (AQI) in these areas for the past three years. The results indicated that air pollution levels were positively correlated with a reduction in pollutant levels during and after lockdowns in these cities. In Tokyo, low levels of air pollution, no significant change in the distribution of “good” and “moderate” days was observed during lockdown. In Daegu, mid-level air pollution, the percentage of “unhealthy” days (AQI>100) markedly reduced during lockdown; however, this reverted after lockdown was lifted. In Wuhan and Mumbai, high air pollution levels, the percentage of unhealthy days remarkably decreased during lockdown and continued to reduce after lockdown. It was found that PM 2.5 was the critical pollutant for all cities because its sub-AQI was the largest of the six pollutant species for the majority of days. In addition, PM 10 dominated the overall AQI for 2.2–9.6% of the period in Wuhan and Mumbai, and its sub-AQI reduced during lockdown. The mean sub-AQI for NO 2 , SO 2 , CO, and O 3 was within the “good” category for all cities. In conclusion, the lockdown policy reduced air pollution in general and this reduction was more significant for regions with high air pollution levels.

Lung development continues from the embryonic period to adulthood. Previous epidemiological studies have noted that maternal exposure of atmospheric pollutants during the sensitive windows disturbed the lung development and increased the risk of lung diseases after birth, but the experimental evidence was insufficient. In the present study, we exposed plug-positive mice to PM2.5 (3 mg/kg b.w.) by oropharyngeal aspiration every other day, and intended to test whether maternal PM2.5 exposure affected prenatal lung development in the offspring. First, maternal PM2.5 exposure decreased embryo weight and crown-rump length at E18.5 but not in earlier developmental stages (E0–E16.5). Second, maternal PM2.5 exposure did not prevent lung-bud and tracheal specification, and did not cause abnormalities in branching morphogenesis, distal lung epithelium, and mesenchyme differentiation in earlier stages of lung development (E0–E16.5). However, the exposure significantly disturbed the distal lung epithelium and mesenchyme differentiation of lung, led to reduced intact rings of trachea, and suppressed the expression of lung development-related genes (Nkx2.1, Tbx4, Tbx5, and Sox9) at E18.5. Finally, we found that the exposure not only increased PM2.5-bound metal content (Pb and Cu) but also caused inflammatory response in the placenta, which transmitted from the mother to the fetus and contributed to the developmental abnormalities.

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