Evidence on the associations between long-term exposure to multiple air pollutants and cardiopulmonary mortality is limited, especially for developing regions with higher pollutant levels. We aimed to characterise the individual and joint (multi-pollutant) associations of long-term exposure to air pollutants with cardiopulmonary mortality, and to identify air pollutant that primarily contributes to the mortality risk. We followed 37,442 participants with a mean age of 43.5 years in four cities in northern China (Tianjin, Shenyang, Taiyuan, and Rizhao) from January 1998 to December 2019. Annual particulate matter (PM) with diameters ≤2.5 μm (PM_2.5), ≤10 μm (PM₁₀), sulfur dioxide (SO₂) and nitrogen dioxide (NO₂) were estimated using daily average values from satellite-derived machine learning models and monitoring stations. Time-varying Cox proportional hazards model was used to evaluate the individual association between air pollutants and mortality from non-accidental causes, cardiovascular diseases (CVDs), non-malignant respiratory diseases (RDs) and lung cancer, accounting for demographic and socioeconomic factors. Effect modifications by age, sex, income and education level were also examined. Quantile-based g-Computation integrated with time-to-event data was additionally applied to evaluate the co-effects and the relative weight of contributions for air pollutants. During 785,807 person-years of follow-up, 5812 (15.5%) died from non-accidental causes, among which 2932 (7.8%) were from all CVDs, 479 (1.3%) from non-malignant RDs, and 552 (1.4%) from lung cancer. Long-term exposure to PM₁₀ (mean [baseline]: 136.5 μg/m³), PM_2.5 (mean [baseline]: 70.2 μg/m³), SO₂ (mean [baseline]: 113.0 μg/m³) and NO₂ (mean [baseline]: 39.2 μg/m³) were adversely and consistently associated with all mortality outcomes. A 10 μg/m³ increase in PM_2.5 was associated with higher mortality from non-accidental causes (hazard ratio 1.20; 95% confidence interval 1.17–1.23), CVDs (1.23; 1.19–1.28), non-malignant RDs (1.37; 1.25–1.49) and lung cancer (1.14; 1.05–1.23). A monotonically increasing curve with linear or supra-linear shape with no evidence of a threshold was observed for the exposure-response relationship of mortality with individual or joint exposure to air pollutants. PM_2.5 consistently contributed most to the elevated mortality risks related to air pollutant mixture, followed by SO₂ or PM₁₀. There was a strong and positive association of long-term individual and joint exposure to PM₁₀, PM_2.5, SO₂, and NO₂ with mortalities from non-accidental causes, CVDs, non-malignant RDs and lung cancer in high-exposure settings, with PM_2.5 potentially being the main contributor. The shapes of associations were consistent with a linear or supra-linear exposure-response relationship, with no lower threshold observed within the range of concentrations in this study. 10.13039/501100012166 National Key Research and Development Program of China , the 10.13039/501100004543 China Scholarship Council , the 10.13039/501100001809 National Natural Science Foundation of China , 10.13039/501100003453 Natural Science Foundation of Guangdong Province .

Numerous studies have demonstrated that exposure to ambient ozone (O₃) could have adverse effects on children’s respiratory health. However, previous studies mainly focused on asthma and wheezing. Evidence for allergic rhinitis and bronchitic symptoms (e.g., persistent cough and phlegm) associated with O₃ is limited, and results from existing studies are inconsistent. This study included a total of 59,754 children from the seven northeastern cities study (SNEC), who were aged 2 to 17 years and from 94 kindergarten, elementary and middle schools. Information on doctor-diagnosed allergic rhinitis (AR), persistent cough, and persistent phlegm was collected during 2012–2013 using a standardized questionnaire developed by the American Thoracic Society (ATS). Information for potential confounders was also collected via questionnaire. Individuals’ exposure to ambient ozone (O₃) during the four years before the investigation was estimated using a satellite-based random forest model. A higher level of O₃ was significantly associated with increased risk of AR and bronchitic symptoms. After controlling for potential confounders, the OR (95% CI) were 1.13 (1.07–1.18), 1.10 (1.06–1.16), and 1.12 (1.05–1.20) for AR, persistent cough, and persistent phlegm, respectively, associated with each interquartile range (IQR) rise in O₃ concentration. Interaction analyses showed stronger adverse effects of O₃ on AR in children aged 7–17 years than those aged 2–6 years, while the adverse association of O₃ with cough was more prominent in females and children aged 7–12 years than in males and children aged 2–6 and 13–17 years. This study showed that long-term exposure to ambient O₃ was significantly associated with higher risk of AR and bronchitic symptoms in children, and the association varies across age and gender. Our findings contribute additional evidence for the importance of controlling O₃ pollution and protecting children from O₃ exposure.