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Long-term exposure to ambient particulate pollutants (PM2.5 and PM10) may increase the risk of chronic kidney disease (CKD), but the results of previous research were limited and inconsistent. The purpose of this study was to assess the relationships of PM2.5 and PM10 with CKD. This study was a cohort study based on the physical examination data of 2082 Beijing residents from 2013 to 2018 in the Beijing Health Management Cohort (BHMC). A land-use regression model was used to estimate the individual exposure concentration of air pollution based on the address provided by each participant. CKD events were identified based on self-report or medical evaluation (estimated glomerular filtration rate, eGFR less than 60 ml/min/1.73 m2). Finally, the associations of PM2.5 and PM10 with CKD were calculated using univariate and multivariate logistic regression models. During the research period, we collected potentially confounding information. After adjusting for confounders, each 10 μg/m3 increase in PM2.5 and PM10 exposure was associated with an 84% (OR: 1.84; 95% CI: 1.45, 2.33) and 37% (OR: 1.37; 95% CI: 1.15, 1.63) increased risk of CKD. Adjusting for the four common gaseous air pollutants (CO, NO2, SO2, O3), the effect of PM2.5 and PM10 on CKD was significantly enhanced, but the effect of PM10 was no longer significant in the multi-pollutant model. The results of the stratified analysis showed that PM2.5 and PM10 were more significant in males, middle-aged and elderly people over 45 years old, smokers, drinkers, BMI ≥ 24 kg/m2, and abnormal metabolic components. In conclusion, long-term exposure to ambient PM2.5 and PM10 was associated with an increased risk of CKD. [ABSTRACT FROM AUTHOR]

Air pollution and ischemic stroke (IS) are both vital factors affecting the health of Beijing citizens. This study aims at exploring the associations between air pollution, meteorology, and the hospital admission of IS (IS HA). Information on 476,659 IS inpatients in secondary and higher hospitals in Beijing from 2013 to 2018 were collected. A time-stratified case-crossover design with the generalized additive model and the distributed lag nonlinear model were used. In the single-pollutant models, an inter-quartile range increase in O3, SO2, CO, and NO2 resulted in a significant highest increase in IS HA by 2.23% (95% CI: 1.56%, 2.90%), 1.53% (95% CI: 1.12%, 1.95%), 1.05% (95% CI: 0.70%, 1.40%), and 0.51% (95% CI: 0.24%, 0.79%) on the day of pollution, so did PM2.5 and PM10 by 1.13% (95% CI: 0.68%, 1.59%) and 1.19% (95% CI: 0.74%, 1.64%) at a lag of 0–5 days. There was a nonlinear relationship between meteorology and IS HA. In the multivariate model, the cumulative relative risks with a maximum lag time of 21 days of PM2.5 and NO2 were 1.11 (95% CI: 1.04, 1.19) and 0.88 (95% CI: 0.82, 0.94), while the effects of SO2, O3, and meteorology were insignificant. The findings suggested that particulate pollutants could increase the risk of IS, and the elderly were more sensitive to it, while the results of gaseous pollutants are still discordant. The control of air pollution and the protection of susceptible populations should receive higher attention from policymakers. [ABSTRACT FROM AUTHOR]

Air pollutants' effect on ischemic stroke (IS) has been widely reported. But the effect of high-level concentrations during people's outdoor periods among hypertension patients was unknown. Peak-hour concentrations were defined considering air pollutants' high concentrations as well as people's outdoor periods. We conducted a time-series study and used the generalized additive model to analyze peak-hour concentrations' acute effect. A total of 315,499 IS patients comorbid with hypertension were admitted to secondary and above hospitals in Beijing from 2014 to 2018. A 10 µg/m3 (CO: 1 mg/m3) increase of the peak-hour concentrations was positively associated with IS hospital admissions among hypertension patients. The maximum effect sizes were as follows: for PM2.5, 0.17% (95% confidence interval [CI]: 0.10–0.24%) at Lag0 and 0.22% (95% CI: 0.12–0.33%) at Lag0–5; for PM10, 0.09% (95% CI: 0.05–0.13%) at Lag5 and 0.17% (95% CI: 0.09–0.26%) at Lag0–5; for SO2, 0.87% (95% CI: 0.46–1.29%) at Lag5; for NO2, 0.83% (95% CI: 0.62–1.04%) at Lag0 and 0.86% (95% CI: 0.59–1.13%) at Lag0–1; for CO 1.23% (95% CI: 0.66–1.80%) at Lag0 and 1.33% (95% CI: 0.33–2.35%) at Lag0–5; for O3 0.23% (95% CI: 0.12–0.35%) at Lag0 and 0.20% (95% CI: 0.05–0.34%) at Lag0–1. The effect sizes of PM2.5, NO2, and O3 remained significant after adjusting daily mean. Larger effect sizes were observed for PM2.5 and PM10 in cool season and for O3 in warm season. As significant exposure indicators of air pollution, peak-hour concentrations exposure increased the risk of IS hospital admissions among hypertension patients and it is worthy of consideration in relative environmental standard. It is suggested for hypertension patients to avoid outdoor activity during peak hours. More relevant searches are required to further illustrate air pollutant's effect on chronic disease population. [ABSTRACT FROM AUTHOR]

Exposure to ambient particulate matter with a diameter of <2.5 μm (PM 2.5) has been linked to increases in blood pressure. The aim of this study was to assess the effects of short-term exposure to PM 2.5 on blood pressure in office workers in Beijing, China. A total of 4801 individuals aged 18–60 years underwent an annual medical examination between 2013 and 2017. Levels of air pollutants were obtained from 35 fixed monitoring stations and correlated with the employment location of each participant to predict personal exposure via kriging interpolation. Linear mixed-effects models were used to estimate the changes in blood pressure associated with PM 2.5 exposure at various lag times. After adjusting for personal characteristics and other potential confounders, each interquartile range increase in PM 2.5 was associated with a 0.413-mmHg (95% confidence interval [CI]: 0.252–0.573), 0.171-mmHg (95% CI: 0.053–0.288), 0.278-mmHg (95% CI: 0.152–0.404), and 0.241-mmHg (95% CI: 0.120–0.362) increase in systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial pressure, respectively (p < 0.05). Men, individuals previously diagnosed with hypertension, and subjects working in the northern districts of Beijing had larger changes in blood pressure, and the effect sizes were 0.477-mmHg (95% CI: 0.286–0.669), 0.851-mmHg (95% CI: 0.306–1.397, and 0.672-mmHg (95% CI: 0.405–0.940). The findings suggested that exposure to PM 2.5 had adverse effects on blood pressure, especially among males and hypertensive patients. Image 1 • Individual PM 2.5 exposure was measured by Kriging interpolation method. • Blood pressure increased significantly with elevations in PM 2.5 for lag 4–6 days. • Stronger effects were found among males and hypertensive patients. [ABSTRACT FROM AUTHOR]