In our study, a population-based time-series model was used to investigate the association between short-term air pollutants (PM2.5, PM10, SO2, NO2 and O3) exposure and COPD mortality in Wuhan, China, during January 1, 2014 to December 31, 2019. The results showed that the concentrations of PM10, SO2, and NO2 were significantly positively associated with COPD mortality. As far as we know, this was the first time-series study assessed the adverse effects of air pollutants on COPD mortality in China.
During 2014 to 2019, the levels of ambient air pollution were relatively high in Wuhan, China. The daily mean concentrations of PM2.5 (59.03 µg/m3), PM10 (90.48 µg/m3) and NO2 (48.84 µg/m3) exceeded the values of WHO Air Quality Guidelines (10, 20, 40 µg/m3 respectively). And the daily mean concentrations of SO2 and O3 were 12.91 and 91.77 µg/m3, which were within the Air Quality Guidelines values (20, 100 µg/m3 respectively). The concentrations of air pollutants showed relatively stable trends. PM2.5, PM10, SO2 and NO2 peaked in winter. It was probable that coal-burning was still the important source of heat and energy in China. Furthermore, in winter, the dispersion of pollutants was poor. However, O3 was mostly formed by the conversion of nitrogen oxides and volatile organic compounds under high temperature, sufficient sunshine and low humidity, which finally led to the peak values of O3 in summer. By the end of 2019, the number of motor vehicles exceed 3.3 million in Wuhan, and vehicle emission also became one of the major sources of environmental air pollution.
Our results showed that ambient air pollutants were positively associated with COPD mortality in single pollutant models. The effects on COPD mortality peaked within 4 day (lag03) and the strongest association estimated were observed for SO2. An increase of 10 µg/m3 of PM10 was associated with a 0.581%(95%CI:0.054%-1.111%) increase in COPD mortality. Moogavkar et.al reported a significantly positive association between PM10 and the risk of COPD mortality with a increase of 2.66% (95%CI:0.12%-5.20%) in COPD mortality per 25 µg/m3 increase in PM10 . And a meta-analysis by Zhu et al. also concluded that a 10 µg/m3 increase in PM10 was associated with a 1.1% (95%CI:0.8%-1.4%) increase in COPD mortality . While, a case-crossover study in Cook city showed a lack of association between PM10 and the risk of mortality for COPD . We did not found significantly association between the concentrations of PM2.5 and COPD mortality, consistent with the results of a large population-based cohort study in Metropolitan Vancouver, Canada . But a meta-analysis concluded that a 10 µg/m3 increase in daily PM2.5 was associated with a 2.5%(95%CI:1.5%-3.5%) increase in COPD mortality. And in a COPD cohort, Faustini et al found that effects on respiratory mortality among COPD subjects were particularly elevated 11.6%(95%CI:2.0%-22.2%) from PM2.5 per 11 µg/m3 increase.
Interestingly, our findings demonstrated that gaseous pollutants had stronger effects on COPD mortality than particulate matter. Similarly, other studies also suggested that compared to particulate matter, gaseous pollutant had stronger effects on COPD exacerbation and daily outpatient visits of respiratory diseases[24, 25]. Our estimates showed that a 10 µg/m3 of NO2 was significantly associated with a 1.815%(95%CI:0.523%-3.125%) increase in COPD mortality. In a 6-year cohort study including all residents aged 51–90 years in Oslo, Norway, the results found that the concentrations of NO2 on COPD mortality appeared to have significantly linear effects. While Hart et al found positive but nonsignificant associations of COPD mortality with NO2, PM2.5 and SO2 exposure in industry workers.
SO2 mainly came from burning of fossil fuels, with the promotion of clean fuels in Wuhan recently, the concentration of SO2 gradually decreased. The mean concentrations of SO2 in Wuhan was 12.91 µg/m3, which could be considered as low-level compared with many other Chinese cities[5, 28, 29]. But our results showed that every increase of 10 µg/m3 of SO2 was associated with 4.316%(95%CI:1.002%-7.738%) increase in COPD mortality, which was higher than the estimated reported in several previous studies. And Zhang et al also demonstrated that SO2 had a stronger effect on cardiovascular mortality in Hefei, China. The reason for this phenomenon was still unclear, but Samoli et al found that when the concentration of SO2 at a lower level, the impact of SO2 to mortality is greater than the high concentration, which might partially explain the effects of SO2 in our study. Furthermore, similar with the results of a meta-analysis, we did not find significant association between the concentrations of O3 and COPD mortality. To sum up, the inconformity with our findings might due to the different chemical compositions of PM10 or PM2.5 in different areas, which could result in different effects on COPD mortality. In addition, the meteorological factors might influent the effects of air pollutants, but the compositions of air pollutants and meteorological conditions varied in different regions. Moreover, the age, socioeconomic status and education level and so on were able to modify the effects of air pollutants.
Although the mechanical explanation of adverse effects of ambient air pollution on COPD mortality remains unclear, identifying the associations of ambient air pollution in different exposure windows is of great importance in the estimation of health risk. In our study, we found that exposure to air pollutants at lag03 yielded the strongest estimates on COPD mortality. Another time-series study in Hefei, China also found the similar phenomenon in the associations between ambient air pollution and cardiovascular mortality.
Subgroup analysis showed that females seemed to suffer more risk of COPD mortality from ambient air pollution. In addition, the results showed that the air pollution estimates of < 65 year group were higher than those for older adults, though the estimates were almost nonsignificant. Only 7.2% in our study were < 65 year group, the sample size might be a strong confounder. A population based cohort study also showed that the relative risks for COPD mortality associated with a 0.78 µg/m3 elevation in black carbon concentrations were 1.06 (95%CI:0.97–1.15) and 1.08 (95%CI:0.97–1.20) for males and females, and 1.31 (95%CI:1.07–1.60) and 1.04 (95%CI:0.97–1.12) for < 65 and ≥ 65 year groups .Similar with the results from a population based UK Biobank study, it concluded that the adverse effects of PM2.5 and NO2 on COPD prevalence were stronger in females. However, Naess et al documented that males were more susceptible to air pollution (PM10, PM2.5, SO2) than females. The reasons for our gender-specific findings were still unclear and needed further investigation. Furthermore, the concentrations of PM10, SO2 and NO2 were significantly associated with COPD mortality for older adults, effective public health prevention policies specified for older adults should be made to reduce the burden of COPD.
Two-pollutant models were implemented in our study to explore the possible role of single pollutants. We concluded that the estimates of PM2.5, PM10 and O3 decreased after the inclusion of SO2 or NO2, consistent with the previous studies[29, 34]. These results revealed the relatively independent associations of SO2 and NO2. The associations of SO2 and NO2 on COPD mortality might better reflect the associations between air pollution and COPD mortality in Wuhan compared with other pollutants.
Though this study was a population-based time-series study which covered all population in Wuhan, there were some limitations. Firstly, the average of ten fixed sited monitoring data of air pollutant concentrations were used to infer exposures of individuals, which might lead to potential misclassification exposure and ignore the spatial impact of air pollution on COPD. Secondly, due to data unavailability, some factors including personal social information (such as tobacco use, body mass index and so on) that could affect the effects were not controlled. Thirdly, we could not rule out the non-relevant death records due to obesity or other reasons than air pollution.