In a large population-based study of 454,921 adults aged 37 to 73 years, a higher level of air pollution was associated with higher odds of asthma. Moreover, a higher level of air pollution increased the odds of current wheezing and asthma-related hospitalization. Furthermore, an increase in air pollution was correlated with decrease lung function among individuals with asthma.
The adverse effects of air pollutants on the lungs may be explained by autophagy, dysregulated cell immunity, epigenetic modifications, impaired of phagocytosis, inflammatory cell infiltration, disruption of cellular signaling pathways and the airway epithelial barrier, oxidative stress, and parenchymal destruction4. However, previous studies have yielded inconsistent results regarding the impact of air pollution on asthma prevalence and lung function. To our knowledge, most studies have focused on young people, resulting in a limited understanding of adults. Children may be more susceptible to detrimental respiratory ambient air pollution than adults are, particularly through its effect on lung development15. Asthma in adults is characterized as less atopic and more complex than asthma in children16, suggesting a difference between children and adults with asthma and that asthma in adults is more likely to be influenced by factors other than atopy-related factors, such as air pollution17. Therefore, the analysis of associations between air pollution and asthma in adults is warranted.
Different studies of different air pollutants have yielded inconsistent results regarding the association between air pollution and asthma prevalence. A retrospective cross-sectional study with 11,585 individuals found that exposure to higher ambient NO2 but not PM2.5, PM10, or SO2 was associated with increased asthma prevalence among Taiwanese adults17. Furthermore, data from three European cohort studies found that PM10 and NO2 was associated with the prevalence of asthma among adults18. In the present study, exposure to air pollutants, including PM2.5, PM10, NO2, and NOx, but not PMcoarse significantly increased the prevalence of asthma with greater impacts on older participants, females, obese individuals, and current smokers. The explanations for the sex differences may include the higher prevalence of asthma in females, the influence of female hormones, and anatomical differences between males and females, which may strengthen the association between air pollution and asthma prevalence in women19. As individuals age, the natural decrease in lung function and the weakening of the immune system may increase the vulnerability of the respiratory system to air pollution, resulting in a more pronounced effect in older populations20. Moreover, a large 16-year follow-up cohort showed that exposure to smoking increased the risk of asthma for both active smokers and passive smokers21, which helped explain the results observed in the smoking subgroups. Moreover, it is generally accepted that obesity is also a risk factor for asthma in adults22, which may make the effects of air pollution on asthma prevalence more pronounced in obese individuals. Owing to the variability of this association among populations, additional research is necessary to confirm the disparities in this relationship and clarify the potential underlying causes.
Air pollution may also affect asthma outcomes, such as current wheezing, asthma-related hospitalization. A systematic review that encompassed 22 studies and utilized a case-crossover design concluded that PM2.5, NO2, CO, and O3 but not SO2 or PM10 were significantly linked with asthma exacerbation including visits to emergency departments and hospitalizations11. Another systematic review of 67 studies observed that short-term exposure to O3, NO2, and SO2 was related to increased odds of asthma exacerbations including hospital admissions and asthma-associated emergency room visits23. Similarly, our results revealed that exposure to air pollutants, especially PM2.5, NO2 and NOx was associated with increased odds of current wheezing and asthma hospitalization, indicating that air pollution may increase the risk of asthma exacerbation.
The associations between air pollution and lung function have also been assessed in previous studies with different conclusions. Some studies have shown that air pollution consisting of PM2.5, PM10, and NO2 was linked to a decrease in lung function24,25,26. However, a Tasmanian Longitudinal Health Study revealed no significant interactions between NO2 and asthma prevalence and subsequent changes in lung function27. In addition, a prospective single-center panel study did not find significant evidence that exposure to air pollution (NO2/O3) affects clinical control including lung function among individuals with asthma, however, the sample size was small, with only 32 participants included8. Our results found that exposure to PM2.5, PMcoarse, PM10, NO2 and NOx was significantly associated with a decrease in FEV1, FVC, and FEV1/FVC. Moreover, the associations between air pollution and asthma prevalence, current wheezing, hospitalization, and lung function exhibited partial inconsistencies across multiple studies, possibly due to differing measures of air pollutants, diverse populations, or varying definitions of outcomes. Further research, as well as longitudinal studies, is needed to explore the relationships among these factors to investigate whether there is a causal association.
The major strength of this study is that the well-organized and rigorously defined large population-based analysis provided adequate statistical power to evaluate impacts of air pollution on asthma and lung function in adults. Nevertheless, there are several limitations to this study. First, the cross-sectional design limits the value of the results in establishing causal associations. Second, the definition of asthma outcomes was not strict enough due to the form of the subjective questionnaire. Third, estimation of the effects of air pollution focused on individual pollutants, which may not accurately reflect the real-world presence of air pollution mixtures. Fourth, owing to data limitations, postbronchodilator lung function data are not available. Finally, our findings were analyzed among individuals aged 37 to 73 years; therefore, the conclusions may not be generalizable to children and adolescents.
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