ObjectiveTo examine the effects of fish oil supplements on the clinical course of cardiovascular disease, from a healthy state to atrial fibrillation, major adverse cardiovascular events, and subsequently death.DesignProspective cohort study.SettingUK Biobank study, 1 January 2006 to 31 December 2010, with follow-up to 31 March 2021 (median follow-up 11.9 years).Participants415 737 participants, aged 40-69 years, enrolled in the UK Biobank study.Main outcome measuresIncident cases of atrial fibrillation, major adverse cardiovascular events, and death, identified by linkage to hospital inpatient records and death registries. Role of fish oil supplements in different progressive stages of cardiovascular diseases, from healthy status (primary stage), to atrial fibrillation (secondary stage), major adverse cardiovascular events (tertiary stage), and death (end stage).ResultsAmong 415 737 participants free of cardiovascular diseases, 18 367 patients with incident atrial fibrillation, 22 636 with major adverse cardiovascular events, and 22 140 deaths during follow-up were identified. Regular use of fish oil supplements had different roles in the transitions from healthy status to atrial fibrillation, to major adverse cardiovascular events, and then to death. For people without cardiovascular disease, hazard ratios were 1.13 (95% confidence interval 1.10 to 1.17) for the transition from healthy status to atrial fibrillation and 1.05 (1.00 to 1.11) from healthy status to stroke. For participants with a diagnosis of a known cardiovascular disease, regular use of fish oil supplements was beneficial for transitions from atrial fibrillation to major adverse cardiovascular events (hazard ratio 0.92, 0.87 to 0.98), atrial fibrillation to myocardial infarction (0.85, 0.76 to 0.96), and heart failure to death (0.91, 0.84 to 0.99).ConclusionsRegular use of fish oil supplements might be a risk factor for atrial fibrillation and stroke among the general population but could be beneficial for progression of cardiovascular disease from atrial fibrillation to major adverse cardiovascular events, and from atrial fibrillation to death. Further studies are needed to determine the precise mechanisms for the development and prognosis of cardiovascular disease events with regular use of fish oil supplements.

Background: Fine particulate matter (PM2.5), smoking, and genetic factors are associated with lung cancer. However, the relationship between PM2.5, smoking and subtypes of lung cancer remains unclear. Moreover, it is unclear whether genetic risk modifies the impact of PM2.5 and smoking on incident lung cancer.Methods: A total of 298,069 participants from the UK Biobank study without lung cancer at baseline were included in this study. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated using multivariable Cox proportional models for the association of lung cancer and its subtypes with PM2.5, smoking, and genetic risk. Potential gene-smoking or gene-PM2.5 interactions were also estimated. We further estimated population attributable fractions for incident lung cancer.Results: During 10.4 years of follow-up, 1683 incident lung cancer cases were identified. Our analysis found that genetic variants, smoking, and PM2.5 were significantly associated with incident lung cancer. For different histological types of lung cancer, the HRs for squamous cell lung carcinoma associated with PM2.5 (per 5 mu g/m(3) increment) andcurrent smoking were 2.76 (95 % CI: 1.72, 4.42, p < 0.001) and 48.64 (95 % CI: 27.96, 84.61, p < 0.001), while the HRs for lung adenocarcinoma were 1.59 (95 % CI: 1.13, 2.23, p < 0.001) and 9.89 (95 % CI: 7.91, 12.36, p < 0.001), respectively. We further found that participants with high levels of PM2.5 pollution and high genetic risk had the highest risk of incident lung cancer (HR = 1.81, 95 % CI: 1.39, 2.35, p < 0.001), while the interaction between PM2.5 and genetic risk was not statistically significant. We observed that the population attributable fractions of lung cancer attributable to current smoking and high PM2.5 exposure were estimated to be 67.45 % and 17.59 %.Conclusion: Genetic susceptibility, smoking, and PM2.5 are important risk factors for lung cancer. Both smoking and PM2.5 are more closely associated with an elevated risk of squamous cell lung cancer.

Much attention has been paid to the health effects of ambient particulate matter pollution; the effects of gaseous air pollutants have not been well studied. Emergency ambulance calls (EACs) may provide a better indicator of the acute health effects than the widely used health indicators, such as mortality and hospital admission. We estimated the short-term associations between gaseous air pollutants [nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3)] and EACs for all-cause, cardiovascular, and respiratory diseases in seven Chinese cities from 2014 to 2019. We used generalized additive models and random-effects meta-analysis to examine the city-specific and pooled associations. Stratified analyses were conducted by age, sex, and season. A total of 1,626,017 EACs were observed for all-cause EACs, including 230,537 from cardiovascular diseases, and 96,483 from respiratory diseases. Statistically significant associations were observed between NO2 and EACs for all-cause diseases, while the effects of SO2 were positive, but not statistically significant in most models. No significant relationship was found between O3 and EACs. Specifically, each 10 μg/m3 increase in the 2-day moving average concentration of NO2 was associated with a 1.07% [95% confidence interval (CI): 0.40%, 1.76%], 0.76% (95% CI: 0.19%, 1.34%) and 0.06% (95% CI: -1.57%, 1.73%) increase in EACs due to all-cause, cardiovascular and respiratory diseases, respectively. Stratified analysis showed a larger effect of NO2 on all-cause EACs in the cold season [excess relative risk (ERR): 0.33% (95% CI: 0.05%, 0.60%) for warm season, ERR: 0.77% (95% CI: 0.31%, 1.23%) for cold season]. Our study indicates that acute exposures to NO2 might be an important trigger of the emergent occurrence of all-cause, cardiovascular and respiratory diseases, and this effect should be of particular concern in the cold season. Further policy development for controlling gaseous air pollution is warranted to reduce the emergent occurrence of cardiopulmonary diseases.

Background: Evidence concerning the effects of different chemical components of particulate matter with an aerodynamic diameter of 2.5 mu m or less (PM2.5) on asthma is limited, and the methodology to compare the relative importance of different PM2.5 components is lacking. Objective: Our aim was to examine the associations between PM2.5 components and asthma and investigate which constituent of PM2.5 possessed the most harmful effect on asthma. Methods: A total of 45,690 subjects in 6 countries were surveyed from 2007 to 2010. We geocoded the residential community addresses of the participants and used satellite remote sensing and chemical transport modeling to estimate their annual average concentrations of PM2.5 constituents. Mixed-effects generalized additive models were utilized to examine the associations between PM2.5 constituents and prevalence of asthma. We further used counterfactual analyses to determine the potential number of asthma cases. Results: We identified 6178 patients with asthma among the participants, producing an asthma prevalence of 13.5%. The odds ratio for asthma associated with per-SD increment was 1.12 for PM2.5 mass, 1.12 for organic carbon, 1.18 for black carbon, 1.19 for sulfate, 1.28 for ammonium, and 1.21 for nitrate after controlling for potential confounders. Our counterfactual analyses suggested that ammonium was responsible for a substantial decline in asthma cases (by 1382 cases, corresponding to 22.37% of overall cases) if the concentration was reduced to the 5th percentile of the current level. Conclusions: Our study suggests that some chemical components of PM2.5 (including black carbon, organic carbon, sulfate, ammonium, and nitrate) might be hazardous constituents contributing to the prevalence of asthma; among them, ammonium might be responsible for a substantial proportion of asthma cases if reduced to a certain level.

Background Spontaneous abortion is one of the prevalent adverse reproductive outcomes, which seriously threatens maternal health around the world. Objective The current study is aimed to evaluate the association between maternal age and risk for spontaneous abortion among pregnant women in China. Methods This was a case-control study based on the China Birth Cohort, we compared 338 cases ending in spontaneous abortion with 1,352 controls resulting in normal live births. The main exposure indicator and outcome indicator were maternal age and spontaneous abortion, respectively. We used both a generalized additive model and a two-piece-wise linear model to determine the association. We further performed stratified analyses to test the robustness of the association between maternal age and spontaneous abortion in different subgroups. Results We observed a J-shaped relationship between maternal age and spontaneous abortion risk, after adjusting for multiple covariates. Further, we found that the optimal threshold age was 29.68 years old. The adjusted odds ratio (95% confidence interval) of spontaneous abortion per 1 year increase in maternal age were 0.97 (0.90–1.06) on the left side of the turning point and 1.25 (1.28–1.31) on the right side. Additionally, none of the covariates studied modified the association between maternal age and spontaneous abortion ( P > 0.05). Conclusions Advanced maternal age (>30 years old) was significantly associated with increased prevalence of spontaneous abortion, supporting a J-shaped association between maternal age and spontaneous abortion.

Introduction: Epidemiological evidence suggests associations between long-term exposure to air pollution and accelerated cognitive decline. China implemented a strict clean air action plan in 2013; however, it is unclear whether the improvement of air quality has alleviated cognitive impairment in the population. Methods: From the China Health and Retirement Longitudinal Study, 8536 Chinese adults were enrolled in 2011 and followed up in 2015. Satellite-based spatiotemporal models were used to estimate exposure to air pollutants (including particles with diameters <= 1.0 mu m [PM1], <= 2.5 mu m [PM2.5], <= 10 mu m [PM10], nitrogen dioxide [NO2], and ozone [O-3]). Cognitive function was evaluated using a structured questionnaire in three dimensions: episodic memory, orientation and attention, and visuoconstruction. The associations between changes in the levels of air pollutants and cognitive function were elucidated by a logistic model. The Bayesian Kernel Machine Regression (BKMR) model was applied to evaluate the cumulative effect of air pollutants. Results: The mean (standard deviation) age of all participants was 58.6 (8.7) years. The odds ratio (95% confi-dence interval) between the highest and the lowest quartile of PM1 exposure reduction for cognitive impairment was 0.46 (0.41, 0.53) after adjusting for confounders. Similar protective effects of cognitive function were observed with the decrease in the level of PM2.5 (0.34 [0.30, 0.39]), PM10 (0.54 [0.48, 0.62]), and NO2 (0.59 [0.51, 0.67]), while the reduction in O-3 appeared to be less related to changes in cognitive function (OR: 0.97 [0.85, 1.10]). The protective association of PM1 reduction was stronger in males than in females. Decreased in PM2.5 dominate the cognitive function benefit relative to PM1, PM10, NO2. Conclusions: The implementation of the clean air action plan led to a significant reduction in PM1, PM2.5, PM10, and NO2, which could slow the decline of cognitive function, while a reduction in O-3 may not.

BACKGROUND:To estimate the associations between ambient particulate matter (PM) pollution of different sizes (PM1, PM2.5, and PM10) and risk of rehospitalization among stroke patients, as well as the attributable burden in China. METHODS:We built a cohort of 1,066,752 participants with an index stroke hospitalization in Sichuan, China from 2017 to 2019. Seven-day and annual average exposures to PM pollution prior to the date of the index hospitalization were linked with residential address using a bilinear interpolation approach. Cox proportional hazard models were constructed to assess the association between ambient PM and the risk of rehospitalization. The burden of stroke rehospitalization was estimated using a counterfactual approach. RESULTS:245,457 (23.0 %) participants experienced rehospitalization during a mean of 1.15 years (SD: 0.90 years) of follow-up. Seven-day average concentrations of PM were associated with increased risk of rehospitalization: the hazard ratios (HRs) per 10 μg/m3 were 1.034 (95 % confidence interval [CI]: 1.029-1.038) for PM1, 1.033 (1.031-1.036) for PM2.5, and 1.030 (1.028-1.031) for PM10; the hazard ratios were larger for annual average concentrations: 1.082 (1.074-1.090) for PM1, 1.109 (1.104-1.114) for PM2.5, and 1.103 (1.099-1.106) for PM10. The associations were stronger in participants who were female, of minority ethnicity (non-Han Chinese), who suffered from an ischemic stroke, and those admitted under normal conditions. Population attributable fractions for stroke rehospitalization ranged from 4.66 % (95 % CI: 1.69 % to 7.63 %) for the 7-day average of PM1 to 17.05 % (14.27 % to 19.83 %) for the annual average of PM10; the reducible average cost of rehospitalization per participant attributable to PM ranged from 492.09 (178.19 to 806) RMB for the 7-day average of PM1 to 1801.65 (1507.89 to 2095.41) RMB for the annual average of PM10. CONCLUSIONS:Ambient PM pollution may increase the risk of rehospitalization in stroke patients and is responsible for a significant burden of stroke rehospitalization.

BACKGROUND:A national and comprehensive evaluation is lacking on the relationship between short-term exposure to submicron particulate matter (PM1) pollution and asthma mortality. METHODS:Data was obtained from 29,553 asthma deaths from the China National Mortality Surveillance System from 2015 to 2020. We used a bilinear interpolation approach to estimate each participant's daily ambient particulate matter pollution and meteorological variables exposure based on their geocoded residential address and a 10 km × 10 km grid from China High Air Pollutants and the fifth generation of European ReAnalysis-Land reanalysis data set. The associations were estimated using a time-stratified case-crossover design and conditional logistic regressions. RESULTS:Our results revealed significant associations between short-term exposure to various particulate matter and asthma mortality. The 5-day moving average of particulate matter exposure produced the most pronounced effect. Compared to fine particulate matter (PM2.5) and inhalable particulate matter (PM10), significantly stronger effects on asthma mortality related to PM1 pollution were noted. The ERs% for asthma mortality associated with each interquartile range (IQR) increase of exposures to PM1 (IQR: 19.2 μg/m3) was 5.59% (95% CI: 2.11-9.19), which is 14% and 22% higher than that for PM2.5 (IQR: 32.0 μg/m3, 4.82% (95% CI: 1.84-7.90)) and PM10 (IQR: 52.2 μg/m3, 4.37% (95% CI: 1.16-7.69)), respectively. The estimates remained consistent in various sensitivity analyses. CONCLUSIONS:Our study provided national evidence that acute exposures to various ambient particulate matter pollution can increase mortality due to asthma in China, highlighting stronger associations with ambient PM1 than PM2.5 and PM10. China needs to adjust the current ambient air quality standards urgently and pay greater attention to the adverse health effects of PM1.

Objective: To evaluate the associations between childhood, parental, and grandparental asthma.Methods: We studied 59,484 children randomly selected from 94 kindergartens, elementary, and middle schools in seven Chinese cities from 2012 to 2013, using a cross-sectional survey-based study design. Information on their and their family members' (parents, paternal grandparents, and maternal grandparents) asthma status were reported by children's parents or guardians. Mixed effects logistic regressions were used to assess hereditary patterns of asthma and mediation analysis was performed to estimate the potential mediation effect of parents on the association between grandparental asthma and childhood asthma.Results: The magnitude of ORs for childhood asthma increased as the number of family members affected by asthma increased. Among children who had one family member with asthma, childhood asthma was associated with asthma in maternal grandmothers (OR: 2.08, 95% CI: 1.67–2.59), maternal grandfathers (OR: 2.08, 95% CI: 1.71–2.53), paternal grandmothers (OR: 2.40, 95% CI: 1.93–2.99), and paternal grandfathers (OR: 2.59, 95% CI: 2.14–3.13). Among children who had two family members with asthma, the highest asthma risk was found when both parents had asthma (OR: 15.92, 95% CI: 4.66–54.45). Parents had a small proportion of mediation effect (9–12%) on the association between grandparental asthma and childhood asthma.Conclusions: Grandparents with asthma were associated with childhood asthma and parents with asthma partially mediated the association.