Long-term exposure to ambient ozone at workplace is positively and non-linearly associated with incident hypertension and blood pressure: longitudinal evidence from the Beijing-Tianjin-Hebei medical examination cohort.

BACKGROUND: There is limited longitudinal evidence on the hypertensive effects of long-term exposure to ambient O3. We investigated the association between long-term O3 exposure at workplace and incident hypertension, diastolic blood pressure (DBP), systolic blood pressure (SBP), pulse pressure (PP), and mean arterial pressure (MAP) in general working adults. METHODS: We conducted a cohort study by recruiting over 30,000 medical examination attendees through multistage stratified cluster sampling. Participants completed a standard questionnaire and comprehensive medical examination. Three-year ambient O3 concentrations at each employed participant's workplace were estimated using a two-stage machine learning model. Mixed-effects Cox proportional hazards models and linear mixed-effects models were used to examine the effect of O3 concentrations on incident hypertension and blood pressure parameters, respectively. Generalized additive mixed models were used to explore non-linear concentration-response relationships. RESULTS: A total of 16,630 hypertension-free working participants at baseline finished the follow-up. The mean (SD) O3 exposure was 45.26 (2.70) ppb. The cumulative incidence of hypertension was 7.11 (95% CI: 6.76, 7.47) per 100 person-years. Long-term O3 exposure was independently, positively and non-linearly associated with incident hypertension (Hazard ratios (95% CI) for Q2, Q3, and Q4 were 1.77 (1.34, 2.36), 2.06 (1.42, 3.00) and 3.43 (2.46, 4.79), respectively, as compared with the first quartile (Q1)), DBP (ß (95% CI) was 0.65 (0.01, 1.30) for Q2, as compared to Q1), SBP (ß (95% CI) was 2.88 (2.00, 3.77), 2.49 (1.36, 3.61) and 2.61 (1.64, 3.58) for Q2, Q3, and Q4, respectively), PP (ß (95% CI) was 2.12 (1.36, 2.87), 2.03 (1.18, 2.87) and 2.14 (1.38, 2.90) for Q2, Q3, and Q4, respectively), and MAP (ß (95% CI) was 1.39 (0.76, 2.02), 1.04 (0.24, 1.84) and 1.12 (0.43, 1.82) for Q2, Q3, and Q4, respectively). The associations were robust across sex, age, BMI, and when considering PM2.5 and NO2. CONCLUSIONS: To our knowledge, this is the first cohort study in the general population that demonstrates the non-linear hypertensive effects of long-term O3 exposure. The findings are particularly relevant for policymakers and researchers involved in ambient pollution and public health, supporting the integration of reduction of ambient O3 into public health interventions.

Prevalence of hyperuricemia and the population attributable fraction of modifiable risk factors: Evidence from a general population cohort in China.

Data on updated hyperuricemia prevalence in Beijing-Tianjin-Hebei (BTH) region in China, which is one of the world-class urban agglomerations, is sparse. Overweight/obesity, alcohol consumption, smoking and sedentary behavior are modifiable risk factors (MRFs) for elevated serum uric acid (SUA), but their population attributable fractions (PAFs) for hyperuricemia is still unclear. Using baseline data from the BTH Physical Examination General Population Cohort, we calculated the crude- and adjusted-prevalence of hyperuricemia based on the 30,158 participants aged 18-80 years. Hyperuricemia was defined as SUA >420 µmol/L in men and >360 µmol/L in women, or currently use of uric acid lowering drugs. Overweight/obesity, alcohol consumption, smoking and sedentary behavior were considered as MRFs and their adjusted PAFs were estimated. The prevalence of hyperuricemia was 19.37%, 27.72% in men and 10.69% in women. The PAFs and 95% confidence intervals for overweight, obesity were 16.25% (14.26-18.25%) and 12.08% (11.40-12.77%) in men, 13.95% (12.31-15.59%) and 6.35% (5.97-6.74%) in women, respectively. Alcohol consumption can explain 4.64% (2.72-6.56%) hyperuricemia cases in men, but with no statistical significance in women. Cigarette smoking contributed to 3.15% (1.09-5.21%) cases in men, but a much lower fraction in women (0.85%, 0.49-1.22%). Compared with sedentary time <2 h per day, the PAFs of 2-4 h, 4-6 h, and more than 6 h per day were 3.14% (1.34-4.93%), 6.72% (4.44-8.99%) and 8.04% (4.95-11.13%) in men, respectively. Sedentary time was not found to be associated with hyperuricemia in women. These findings concluded that hyperuricemia is prevalent in this representative Chinese adult general population with substantial sex difference. Four MRFs (overweight/obesity, alcohol consumption, cigarette smoking and sedentary behavior) accounted for a notable proportion of hyperuricemia cases. The PAF estimations enable the exploration of the expected proportion of hyperuricemia cases that could be prevented if the MRFs were removed, which warrants the public health significance of life-style intervention.

Associations between night-time sleep duration and fasting glucose and ratio of triglyceride to high-density lipoprotein cholesterol among adults free of type 2 diabetes or without diagnosed type 2 diabetes: a multicentre, cross-sectional study in China.

OBJECTIVES: We aimed to assess the associations between night-time sleep duration and fasting glucose (FG), triglyceride (TG) to high-density lipoprotein cholesterol (HDL-C) ratio and body mass index (BMI) among adults free of type 2 diabetes (T2D) or without diagnosed T2D. DESIGN: Cross-sectional study. SETTING: Medical examination centres at six hospitals in Beijing-Tianjin-Hebei region, China. PARTICIPANTS: Participants were recruited via multistage, stratified cluster sampling. We included adults free of T2D or without diagnosed T2D who attended for physical examination and completed the validated questionnaire. 32 497 participants were included in the study, of whom 52.50% were men. PRIMARY AND SECONDARY OUTCOME MEASURES: FG, TG, HDL-C, height and weight were measured. RESULTS: Overall, 12.80% and 9.67% reported night sleep duration <7 hours and ≥9 hours, respectively; 6.91% had elevated FG and 3.57% had undiagnosed T2D. Sleep duration had an independent, U-shaped associated with FG (ß1 (linear term)=-0.111, p=0.047; ß2 (quadratic term)=0.008, p=0.026) with 6.9 hours of sleep associated with the lowest FG and a negative association with BMI (ß=-0.154, p<0.001). BMI mediated a U-shaped association of sleep duration with TG/HDL-C (ß1=-0.040, p=0.017; ß2=0.003, p=0.023). CONCLUSIONS: Both short and long night-time sleep was associated with elevated FG, and short sleep duration was associated with increased BMI. BMI mediated a U-shaped association between sleep duration and TG/HDL-C.

Association of long-term exposure to PM2.5 in workplace with fasting plasma glucose among asymptomatic adults: A multicenter study in North China.

BACKGROUND: The impacts of long-term high exposure to PM2.5 in workplace on glucose metabolism in asymptomatic working adults (AWAs) have rarely been explored. OBJECTIVES: To assess the relationship between long-term exposure to workplace PM2.5 and glucose metabolism in asymptomatic general working adults in heavily polluted regions. METHODS: We used the baseline data of the asymptomatic working participants from the Beijing-Tianjin-Hebei Medical Examination Cohort, which recruited adults undergoing medical examinations. A machine learning-based spatial-temporal model was used to estimate daily average PM2.5 concentrations in the participants' workplaces. We assessed the association of long-term PM2.5 concentrations (three years prior to the interview) and fasting plasma glucose (FPG) using generalized linear mixed-effects models (GLMM) with inclusion of potential confounders. Stratified analyses by sex, age, BMI and smoking status, and two pollutant models were further performed. RESULTS: A total of 37,619 individuals were interviewed and 28,865 were included in the analyses. The mean FPG was 5.20 (0.96) mmol/L, and the estimated three-year average concentration of PM2.5 exposure was 69.51 (6.92) µg/m3. We detected a significant association of long-term exposure to workplace PM2.5 and FPG, a 10 µg/m3 increase in the long-term workplace PM2.5 exposure was associated with 0.075 (95%CI: 0.050-0.100) mmol/L elevated FPG and 25% (OR = 1.25, 95%CI: 1.05-1.50) elevated odds of abnormal fasting glucose metabolism with control of the potential confounding. The detected association between workplace PM2.5 and FPG metabolism remained significant in males, individuals aged > 44 years, overweight and/or obese people, both smokers and non-smokers, and when NO2, SO2, O3, and CO were included in the model. CONCLUSIONS: Long-term exposure to workplace PM2.5 was associated with elevated FPG and/or odds of abnormal glucose metabolism among AWAs. Male, middle-aged, overweight and/or obese AWAs were more susceptible to workplace PM2.5 regardless of smoking status.

Association Between Habitual Night Sleep Duration and Predicted 10-Year Cardiovascular Risk by Sex Among Young and Middle-Aged Adults.

Purpose: We hypothesize the association between sleep duration and cardiovascular disease (CVD) risk varies with age category; however, evidence for the relationship between sleep duration and CVD risk among young and middle-aged adults remains scarce. This research aims to assess the association between night sleep duration and cardiovascular risk by sex among young and middle-aged Chinese adults. Patients and Methods: We used the baseline data of a cohort of adults for physical examination by stratified cluster sampling. The Framingham risk score and the Pittsburgh Sleep Quality Index were used to measure CVD risk and sleep duration, respectively. Demographic characteristics, lifestyle factors, height, weight, total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C) were collected. We performed multiple logistic regressions to examine the association between night sleep duration and the predicted cardiovascular risk. Results: We included 27,547 participants aged 18-64 years free of CVD, cerebral stroke, and not taking lipid-lowering agents. Overall, 12.7%, and 20.4% were at medium and high predicted CVD risk, respectively; 11.9% and 12.3% reported short and long sleep, respectively. Short sleep was independently associated with 23% (95% CI: 1.08-1.40) increased odds of medium-to-high CVD risk and 26% (95% CI: 1.11-1.45) increased odds of high CVD risk among females. Whereas long sleep was independently associated with 17% (95% CI: 0.71-0.98) decreased odds of medium-to-high CVD risk among males. Conclusion: Among young and middle-aged adults, long sleep was associated with decreased odds of CVD risk in males, whereas short sleep was associated with increased odds of cardiovascular risk in females.

Abnormal fasting blood glucose enhances the risk of long-term exposure to air pollution on dyslipidemia: A cross-sectional study.

Both long-term exposure to air pollution and abnormal fasting blood glucose (FBG) are linked to dyslipidemia prevalence. However, the joint role of air pollution and FBG on dyslipidemia remains unknown clearly. In this study, we aimed to test whether abnormal FBG could enhance the risks of long-term exposure to air pollutants on dyslipidemia in general Chinese adult population. The present study recruited 8917 participants from 4 cities in Hebei province, China. Participants' individual exposure to air pollutants was evaluated by the Empirical Bayesian Kriging statistical model in ArcGIS10.2 geographic information system. Dyslipidemia was defined according to Guidelines for the Prevention and Treatment of Dyslipidemia in Chinese Adults. Subjects were grouped into normal, prediabetes, diabetes according to FBG level. Generalized linear models were applied to analyze the interaction of air pollutants and FBG on dyslipidemia prevalence. The prevalence of dyslipidemia was 43.83% in our investigation. After adjusting all covariates, we found the risk of four air pollutants (PM2.5, PM10, NO2, SO2) on dyslipidemia prevalence was stronger as higher FBG level, and the adjusted odd ratio of interaction (ORinter (95% CI)) between PM2.5, PM10, NO2, SO2 and FBG levels on dyslipidemia was 1.171 (1.162, 1.189), 1.119 (1.111, 1.127), 1.124 (1.115, 1.130), 1.107 (1.098, 1.115), respectively. Stratified analyses indicated the modifying effects of FBG on the association of air pollution with dyslipidemia were stronger among male, less than 65 years old, overweight/obesity (all Pinter<0.1). Our study concluded that high FBG levels strengthened the risk of long-term exposure to air pollution on dyslipidemia, especially more noticeable in male, less than 65 years old, overweight.

Association between ambient particulate matter exposure and metabolic syndrome risk: A systematic review and meta-analysis.

Although the association between ambient particulate matter and metabolic syndrome (MetS) has been investigated, the effect of particulate matter (PM) on MetS is inconclusive. We conducted a systematic review and meta-analysis to study the association between long-term ambient PM exposure and MetS risk. The data from five databases were extracted to analyze the association between ambient PM exposure and MetS risk. A random-effects model was performed to estimate the overall risk effect. The present systematic review and meta-analysis illustrated that an increase of 5 µg/m3 in annual PM2.5 or PM10 concentration was associated with 14% or 9% increases of MetS risk, respectively (PM2.5, RR = 1.14, 95%CI [1.03, 1.25]; PM10, RR = 1.09, 95%CI [1.00, 1.19]). The population-attributable risk (PAR) was 12.28% for PM2.5 exposure or 8.26% for PM10 exposure, respectively. There was statistical association between PM2.5 exposure and risk of MetS in male proportion ≥50%, Asia, related disease or medication non-adjustment subgroup as well as cohort study subgroups, respectively. The significant association between PM10 exposure and risk of MetS was observed in male proportion ≥50% and calories intake adjustment subgroups, respectively. Sensitivity analyses showed the robustness of our results. No publication bias was detected. In conclusion, there was positive association between long-term PM exposure and MetS risk. 12.28% of MetS risk could be attributable to PM2.5 exposure.

Associations of long-term exposure to traffic-related air pollution with risk of valvular heart disease based on a cross-sectional study.

Emerging evidence demonstrated that traffic-related air pollution induced adverse effects on cardiovascular system. We designed a population-based cross-sectional study to explore the association between residential proximity to major roadways, traffic density and the prevalence of valvular heart disease (VHD). A total of 34040 subjects from a Rural Health Project between 2013 and 2018 were collected. According to the inclusion and exclusion criteria, 4158 participants were enrolled in the final analysis. And we calculated the subjects' proximity to major roadways and collected the traffic density on the major roadways. Transthoracic echocardiography (TTE) was performed to diagnose the VHD, according to the current AHA/ACC (the American Heart Association and the American College of Cardiology) guidelines. Differences between groups were examined by the one-way ANOVAs for continuous variables and the chi-square tests for categorical variables. A logistic regression models were used to assess the associations. The stratified analysis by age and sex were conducted to further analyze the association. The restricted cubic spline analysis was performed to further evaluate the association between road way distance and VHD. Bonferroni test was used to adjust the significance level. The subjects closer to the major roads had the higher risk of tricuspid regurgitation (TR) (odds risk, OR = 1.519, 95% confidence intervals, 95%CI: 1.058-2.181), especially in female. The risk of VHD was positive (high traffic density VS low traffic density, OR = 1.799, 95%CI: 1.221-2.651), especially in female. In addition, the high traffic density was associated with the risk of mitral regurgitation (MR) (OR = 1.758, 95%CI: 1.085-2.848). The restricted cubic spline analysis found a threshold distance of about 300 m, where had the lowest risk of VHD, aortic regurgitation (AR), MR, TR. Our results found a positive association between traffic-related air pollution and VHD especially in female.

Sperm mtDNA copy number, telomere length, and seminal spermatogenic cells in relation to ambient air pollution: Results of a cross-sectional study in Jing-Jin-Ji region of China.

Evidences on the association of air pollutants and semen quality were limited and mechanism-based biomarkers were sparse. We enrolled 423 men at a fertility clinic in Shijiazhuang, China to evaluate associations between air pollutants and semen quality parameters including the conventional ones, sperm mitochondrial DNA copy number (mtDNAcn), sperm telomere length (STL) and seminal spermatogenic cells. PM2.5, PM10, CO, SO2, NO2 and O3 exposure during lag0-90, lag0-9, lag10-14 and lag70-90 days were evaluated with ordinary Kringing model. The exposure-response correlations were analyzed with multiple linear regression models. CO, PM2.5 and PM10 were adversely associated with conventional semen parameters including sperm count, motility and morphology. Besides, CO was positively associated with seminal primary spermatocyte (lag70-90, 0.49; 0.14, 0.85) and mtDNAcn (lag0-90, 0.37; 0.12, 0.62, lag10-14, 0.31; 0.12, 0.49), negatively associated with STL (lag0-9, -0.30; -0.57, -0.03). PM2.5 was positively associated with mtDNAcn (0.50; 0.24, 0.75 and 0.38; 0.02, 0.75 for lag0-90 and lag70-90) while negatively associated with STL (lag70-90, -0.49; -0.96, -0.01). PM10 and NO2 were positively associated with mtDNAcn. Our findings indicate CO and PM might impair semen quality testicularly and post-testicularly while seminal spermatogenic cell, STL and mtDNAcn change indicate necessity for more attention on these mechanisms.

Carbon black nanoparticles induce pulmonary fibrosis through NLRP3 inflammasome pathway modulated by miR-96 targeted FOXO3a.

Carbon black nanoparticle (CBNP) is a core constituent of air pollutants like fine particulate matter (PM2.5) as well as a common manufactural material. It was proved to pose adverse effects on lung function and even provoke pulmonary fibrosis. However, the underlying mechanisms of CBNPs-induced pulmonary fibrosis remain unclear. The present study aimed to investigate the mechanism of fibrotic effects caused by CBNPs in rat lung and human bronchial epithelial (16HBE) cells. Forty-nine male rats were randomly subjected to 7 groups, means the 14-day exposure group (30 mg/m3), the 28-day exposure groups (5 mg/m3 and 30 mg/m3), the 90-day exposure group (30 mg/m3) and their respective controls. Rats were nose-only-inhaled CBNPs. 16HBE cells were treated with 0, 50, 100 and 200 µg/mL CBNPs respectively for 24 h. Besides, Forkhead transcription factor class O (FOXO)3a and miR-96 overexpression or suppression 16HBE cells were established to reveal relative mechanisms. Our results suggested CBNPs induced pulmonary fibrosis in time- and dose-dependent manners. CBNPs induced persisting inflammation in rat lung as observed by histopathology and cytology analyses in whole lung lavage fluid (WLL). Both in vivo and in vitro, CBNPs exposure significantly increased the expression of NLRP3 inflammasome, accompanied by the increased reactive oxygen species (ROS), decreased miR-96 and increased FOXO3a expressions dose -and time-dependently. MiR-96 overexpression or FOXO3a suppression could partially rescue the fibrotic effects through inhibiting NLRP3 inflammasome. Conclusively, our research show that CBNPs-induced pulmonary fibrosis was at least partially depended on activation of NLRP3 inflammasome which modulated by miR-96 targeting FOXO3a.

Increased risk of carotid atherosclerosis for long-term exposure to indoor coal-burning pollution in rural area, Hebei Province, China.

Smoky coal burning is a predominant manner for heating and cooking in most rural areas, China. Air pollution is associated with the risk of atherosclerosis, however, the link between indoor air pollution induced by smoky coal burning and atherosclerosis is not very clear. Therefore, we designed a cross-sectional study to evaluate the association of long-term exposure to smoky coal burning pollutants with the risk of atherosclerosis. 426 and 326 participants were recruited from Nangong, China and assigned as the coal exposure and control group according to their heating and cooking way, respectively. The indoor air quality (PM2.5, CO, SO2) was monitored. The association between coal burning exposure and the prevalence of atherosclerosis was evaluated by unconditional logistic regression analysis, adjusted for confounding factors. The inflammatory cytokines mRNAs (IL-8, SAA1, TNF-α, CRP) expression in whole blood were examined by qPCR. People in the coal exposure group had a higher risk of carotid atherosclerosis compared with the control (risk ratio [RR], 1.434; 95% confidence interval [95%CI], 1.063 to 1.934; P = 0.018). The association was stronger in smokers, drinkers and younger (<45 years old) individuals. The elevation of IL-8 (0.24, 95%CI, 0.06-0.58; P < 0.05), CRP (0.37, 95%CI, 0.05-0.70; P < 0.05), TNF-α (0.41, 95%CI, 0.14-0.67; P < 0.01) mRNAs expression in whole blood were positively related to coal exposure. Our results suggested long-term exposure to smoky coal burning emissions could increase the risk of carotid atherosclerosis. The potential mechanism might relate that coal burning emissions exposure induced inflammatory cytokines elevation which had adverse effects on atherosclerotic plaque, and then promoted the development of atherosclerosis.