Effect of ambient O3 on respiratory mortality and synergies with meteorological factors in Shenyang, China
Results in the current study demonstrated a significant positive correlation between daily ambient O3 exposure and respiratory mortality in Shenyang, Northeast China. For a 10 µg/m3 increase in O3 concentration, respiratory mortality for the total, females, and males increased by 0.85% (95% CI 0.18%, 1.52%), 1.26% (95% CI 0.24%, 2.28%), and 0.62% (95% CI − 0.27%, 1.51%), respectively.
Multiple global studies have verified that O3 exposure is linked with a higher risk of death9,23. However, the specific figures differ depending on the geographical area. In the current study, we observed that the impact of O3 and respiratory mortality was more pronounced under warm weather conditions, aligning with prior research findings5,24. Several global studies have unambiguously established that O3 is associated with a higher likelihood of death; however, the specific figures differ depending on the geographical area. Pattenden et al. assessed the acute effects of O3 in summer on respiratory mortality by analyzing data from 15 urban areas in England and Wales25. They reported that per 10 µg/m3 of 8-hour O3 exposure, there was a mean rate ratio of 1.003 (0.996–1.011) for respiratory mortality. Vicedo-Cabrera et al. showed that per 10 µg/m3 increase in O3 concentration resulted in a RR of 1.001 (1.000-1.003) across 406 locations in 20 countries26. Previous investigations done in other Chinese cities yielded similar results. In Guangzhou, a 10-µg/m3 rise in O3 (lag 0–3) raised the mortality of respiratory disease by 0.78% (0.33–1.24%)4.
We investigated various lag structures in light of the potential longer-term impacts of pollution on health. The findings revealed that the deleterious effects of O3 persisted many days, with respiratory mortality having the highest estimated risk with a one-day lag, suggesting an acute effect of O3 on respiratory exacerbation and associated healthcare burden. Acute effects of O3 have also been found in previous studies. Previous investigations have also revealed the immediate and short-lag impacts of O3 on mortality outcomes5,27. In this study, RRs were higher on the moving average lag days, which is in agreement with earlier studies suggesting that cumulative exposure to air pollutants would increase the risk of mortality28,29,30.
Stratified studies indicated that the impact of O3 on respiratory mortality was more pronounced during the warm season, aligning with findings from China31,32,33. Regional variances partially could explain this result. Climatic variations result in lower winter temperatures in northern China compared to the south. People in northern regions tend to engage in outdoor activities less frequently and typically keep their windows closed to maintain warmth, which leads to a reduction in O3 exposure. On the other hand, during the warm season, people tend to spend more time outdoors and typically leave the windows open. Elevated O3 concentrations and conducive exposure conditions are likely to enhance exposure levels for individuals in the northern regions. Individuals in the southern region experience reduced levels of O3 as a result of heightened precipitation events and the prevalent use of air conditioning.
Subgroup analysis indicated that gender influenced the impact of O3. The results show that women had a higher risk of O3 mortality during both single and multi-day delays. This is in line with earlier studies that found a higher risk for women13,34. This may pertain to the physiological distinctions between males and females. Anatomical variations among them encompass airway diameter, distribution of red blood cell count, and hemoglobin levels. Females possess smaller airways and a reduced number of red blood cells, which increases their likelihood of developing airway reactivity and heightens their susceptibility to the adverse effects of pollutants. Nevertheless, certain studies have indicated contrary findings, implying inconsistent effects based on gender4,35,36. Factors such as a history of smoking, increased external occupational exposures, and reduced awareness of health care services challenge the assertion that males are more susceptible to O3. Future research is necessary to examine gender differences in the health effects of O3.
We conducted a multi-pollutant model to evaluate the robustness of the results. After accounting for co-pollutants, the impact estimates of O3 significantly decrease. This finding suggests that additional pollutants influence the health impacts of O3. Given the significant covariance among pollutants, further research is necessary to elucidate the potential mechanisms underlying these interactions37. Across the entire datasets and during both warm and cold periods, effect estimates for O3 showed minimal variation and were not statistically significant, indicating stability in the primary outcome.
Previous research on animals has shown that O3 exposure can raise Th2 cytokine levels, eosinophilic airway inflammation, and IL-33 airway hyper-responsiveness in a way that depends on the dose. Inhaling O3 generates reactive oxygen species (ROS), leading to oxidative damage and heightened mitochondrial oxidative stress22. O3 stimulates adrenergic and glucocorticoid receptors, leading to the release of adrenaline and cortisol into the bloodstream, which exacerbates O3-induced lung damage and inflammation38. Moreover, numerous epidemiological studies indicate that extended exposure to ambient O3 significantly contributes to respiratory mortality, especially in areas with elevated O3 levels.
This study presents several limitations. Initially, despite adjusting for long-term trends and eliminating confounding variables, we could not completely exclude the influence of individual variations, including exercise, diet, and other lifestyle factors. These characteristics can influence individual responses to pollutants, leading to differing effects of O3. The effect estimates in this study are not universally applicable to all individuals in the city. We obtain air pollution statistics from fixed monitoring sites, which may not accurately represent individual exposure levels. The exposure measurement error resulting from individual variations in exposure relative to monitoring station data will lead to overestimation or underestimation of impact estimates for each individual. Third, we exclusively collected mortality data from three hospitals in Shenyang, potentially leading to an insufficient sample size to accurately represent the population of the research area. Furthermore, because of data limitations, we were unable to investigate the impacts of socioeconomic and demographic characteristics on O3, which requires additional knowledge in the future.
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