Rationale: Short-term exposure to air pollution has been associated with asthma exacerbation and increased healthcare use caused by asthma, but its effect on asthma mortality remains largely unknown. Objectives: To quantitatively assess the association between short-term exposure to air pollution and asthma mortality. Methods: We investigated 4,454 individuals who lived in Hubei province, China, and died from asthma between 2013 and 2018. A case-crossover design and conditional logistic regression models were applied for data analyses. Exposures to particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5), particulate matter ≤10 μm in aerodynamic diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) were estimated by inverse distance weighted averages of all monitoring stations within 50 km from each case’s home address. Measurements and Main Results: Each interquartile range (IQR) increase of PM2.5 (lag 3; IQR, 47.1 μg/m3), NO2 (lag 03; IQR, 26.3 μg/m3), and O3 (lag 3; IQR, 52.9 μg/m3) were positively associated with asthma mortality, with odds ratios of 1.07 (95% confidence interval, 1.01–1.12), 1.11 (95% confidence interval, 1.01–1.22), and 1.09 (95% confidence interval, 1.01–1.18), respectively. There was no evidence of departure from linearity for these associations. Further adjustment for other pollutants did not change the associations materially. We did not observe significant associations between PM10, SO2, and CO exposures and asthma mortality. Overall, the estimates remained consistent in various sensitivity analyses. Conclusions: Our results provide new evidence that short-term exposures to PM2.5, NO2, and O3 may increase asthma mortality risk. Further studies are needed to confirm our findings in other populations.

Rationale: Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with adverse effects on the respiratory system. However, the association between internal levels of PAH metabolites and lung function levels remains unclear. Objectives: We investigated the relationships between urinary PAH metabolite concentrations and lung function levels in a general Chinese population. Methods: Lung function and 12 urinary PAH metabolites were measured in 2,747 participants from the Wuhan-Zhuhai cohort in China. Associations between urinary PAH metabolites and lung function were analyzed by linear mixed models. We also investigated associations among urinary PAH metabolite concentrations, traffic exposure time, and dietary PAH exposure. Measurements and Main Results: We found significant associations between increased levels of urinary PAH metabolites and reduced lung function. Each 1-U increase in log-transformed levels of 2-hydroxynaphthalene, 9-hydroxyfluorene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, 3-hydroxyphenanthrene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 1-hydroxypyrene, or total urinary PAH metabolites was associated with a 23.79-, 19.36-, 41.76-, 36.87-, 33.47-, 27.37-, 39.53-, 34.35-, 25.03-, or 37.13-ml reduction in FEV₁, respectively (all P < 0.05). Each 1-U increase in 2-hydroxynaphthalene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, or total urinary PAH metabolites was associated with a 24.39-, 33.90-, 27.15-, 28.56-, 27.46-, or 27.99-ml reduction in FVC, respectively (all P < 0.05). The total urinary PAH metabolites concentration was positively associated with both traffic exposure time and dietary PAH exposure among nonsmokers. Conclusions: Total and specific urinary PAH metabolites were associated with lung function reduction in a general Chinese population. Further studies are needed to investigate the potential mechanism by which PAHs induces lung function reduction.

Microplastics (MPs) have received a lot of attention and have been detected in multiple environmental matrices as a new environmental hazard, but studies on human internal exposure to MPs are limited. Here, we collected lung tissue samples from 12 nonsmoking patients to evaluate the characteristics of MPs in human lung tissues using an Agilent 8700 laser infrared imaging spectrometer and scanning electron microscopy. We detected 108 MPs covering 12 types in the lung tissue samples, with a median concentration of 2.19 particles/g. Most of the MPs (88.89%) were sized between 20 to 100 μm. Polypropylene accounts for 34.26% of the MPs in the lung tissues, followed by polyethylene terephthalate (21.30%) and polystyrene (8.33%). Compared with males and those living far from a major road (≥300 m), females and those living near the main road (<300 m) had higher levels of MPs in lung tissues, which positively correlated with platelet (PLT), thrombocytocrit, fibrinogen (FIB), and negatively related with direct bilirubin (DB). These findings help confirm the presence in the respiratory system and suggest the potential sources and health effects of inhaled MPs.