Elderly chronic obstructive pulmonary disease (COPD) patients often face long-term adverse health issues post-COVID-19, but longitudinal and comprehensive assessments are limited. The study aimed to assess 2-year trajectories of both self-reported symptoms and lung function in elderly COPD patients after SARS-CoV-2 infection and to explore potential molecular mechanisms underlying long COVID progression through serum proteomic analysis. This longitudinal cohort study followed up elderly COPD patients at 1, 1.5, and 2 years post-COVID-19. Patients were assigned to the Control or Long-COVID group based on the presence of new-onset and significant fatigue. They completed questionnaires, pulmonary function tests, routine laboratory tests, and serum proteomic analysis. Patients in the Long-COVID group consistently experienced a heavier symptom burden throughout the follow-up period, including lower EQ-VAS scores, higher mMRC and CAT scores, and experienced more frequent adverse events. Several parameters of both pulmonary ventilation function and small airway function were lower in the Long-COVID group at 1-year and 1.5-year follow-ups. Although not statistically significant, the Long-COVID group showed slightly poorer diffusion capacity at all three follow-up visits. The phenomenon of lung function improvement at the 1.5-year follow-up, which was conducted in summer, was not observed in the Long-COVID group. Additionally, at the 2-year follow-up, serum proteomic analysis revealed upregulation of blood coagulation and platelet activation, as well as complement system dysregulation in patients with long COVID. Proteins associated with coagulation and thrombosis (FLNA, FN1, ITGA2B, FGB, and ITGB3) and complement system (C8A, C8B, VTN, C3, and CFH) were identified as hub differentially expressed proteins (DEPs). Elderly COPD patients with long COVID showed a persistently greater symptom burden and more frequent adverse outcomes, even up to two years post-infection. These individuals exhibited worse pulmonary ventilation function, particularly at the first and second follow-up visits, along with slightly lower diffusion capacity throughout all three follow-up visits. Disordered coagulation, platelet activation, and complement system may be the underlying molecular mechanisms and therapeutic targets.

Mounting evidence indicates that global warming leads to frequent, intense, and prolonged heatwaves, significantly increasing the risk of preterm birth (PTB). It is therefore necessary to work out the extent of the disease burden caused by heatwaves and the effects of the climate adaptation measures in the future. This study aims to evaluate the heatwave-attributable PTB across 367 Chinese cities from 2025 to 2100 under different climate scenarios based on shared socioeconomic pathways (SSP1-2.6, SSP2-4.5, and SSP5-8.5), and explore the potential effects of climate adaptation measures in terms of landscape interventions (cool roofs, green roofs, and urban trees). We found that high-emission climate scenarios will significantly increase the number of heatwave days, leading to a high incidence rate of PTB. The number of heatwave days will increase from 9.96 in 2025 to 127.70 in 2100 and the attributed PTB rate increases from 24.58 to 206.76 per million births under the highest emission scenario (SSP5-8.5), which is 2.6 times higher than that under the low-emission climate scenario SSP1-2.6. Landscape intervention strategies exhibit considerable effectiveness in mitigating heatwave-attributable PTB, but their effectiveness will be offset as the number of heatwave days increases, especially in high-emission climate scenarios. Our findings indicate that as global warming continues, future generations will face an increasing risk of PTB, and therefore mitigating global warming is imperative to ensure the birth outcomes and lifelong development of future generations.

As global warming intensifies, the rising temperature is posing a great threat to human health, particularly among vulnerable population groups such as the elderly, young children, and pregnant women. Fetal development is highly vulnerable to the ambient environment, and exposure to high temperatures may contribute to adverse birth outcomes, which can significantly impact the postnatal growth and development of children, and cause significant socioeconomic burdens. Nevertheless, how high temperature influences the risk of adverse birth outcomes and how to mitigate these effects remain unclear. This article systematically reviews epidemiological evidence about the impact of high-temperature exposure on adverse birth outcomes, summarizes the underlying biological mechanisms, and proposes coping strategies. An increasing amount of evidence indicates that high-temperature exposure could contribute to a spectrum of adverse birth outcomes, including spontaneous abortion, stillbirth, preterm birth, low birth weight, and congenital anomalies. The underlying mechanisms involve increased maternal core temperature and dehydration, disruptions in placental function, alterations in hormonal profiles, augmented oxidative stress, and inflammatory responses. Accordingly, appropriate measures can be taken to mitigate the adverse effects of high temperature on birth outcomes, such as maintaining appropriate body temperature and sufficient water intake, inhibiting uterine contractions, regulating hormones, and suppressing oxidative stress and inflammation. Previous research has shed partial light on this significant scientific issue. However, ongoing studies still face some challenges: Firstly, the lack of a standardized definition for high-temperature exposure complicates the identification and categorization. Variations in the definition of high-temperature exposure, encompassing different intensities and durations, can lead to disparate conclusions. Secondly, discrepancies between pregnant women's actual high-temperature exposure and outdoor conditions impact the accuracy of analysis results. The actual duration of high-temperature exposure should exclude the period spent in air-conditioned indoor environments, yet obtaining this information is challenging. Thirdly, critical exposure windows and sensitive populations remain undefined. Moreover, the underlying mechanisms are not yet fully understood. The associations between specific indicators and adverse birth outcomes are relatively straightforward to identify, but establishing causality is complex. Overall, these factors impede the development of further prevention and control measures. Future research should pay more attention to the following aspects: (1) Standardizing the definition of high-temperature exposure, which may involve different regional, demographic, and other characteristic factors; (2) gathering precise epidemiological and specific subject information. Based on the large-scale datasets, more detailed stratified studies should be conducted to identify these critical parameters, including threshold temperatures and exposure windows. Additionally, a more comprehensive exploration of the molecular mechanism is essential to provide precise scientific support for the development of targeted prevention and treatment strategies. To fulfill these objectives, it is essential to integrate expertise from multidisciplinary fields, including epidemiology, biomedicine, meteorology, and other relevant disciplines. Through collaborative endeavors, more efficacious strategies can be identified to mitigate the adverse impact of high-temperature exposure on maternal and child health in the foreseeable future, ensuring an improved start for every new life.

Background:Elderly patients with chronic obstructive pulmonary disease (COPD) face a heightened risk of developing long coronavirus disease (COVID); however the exact clinical characteristics and underlying mechanisms remain unclear. Methods:We enrolled 85 elderly COPD patients, of whom 43 reported newly onset persistent fatigue (the most dominant complaint of long COVID) within 1 year after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and they were allocated to the Long-COVID group. The remaining 42 patients were assigned to the Control group. Patients completed questionnaires, pulmonary function tests, chest CT, routine laboratory tests, and blood proteomic analysis. Results:Long-COVID patients had a longer course of COPD (> 5 years, 76.8% vs 52.4%) and duration of SARS-CoV-2 infection (10.0 days vs 7.0 days) (All P < 0.05), higher symptom burden, worse pulmonary ventilation function and a more rapid decrease in DLCO (All P < 0.05). Proteomic analysis indicated disruptions in inflammation and energy metabolism, potentially underlying long COVID in these patients. The machine learning model identified wheezing, the duration of SARS-CoV-2 infection, EIF2S3 (eukaryotic translation initiation factor 2 subunit gamma), current FEV1/FVC (%), and the course of COPD as key features distinguishing Long-COVID patients, and exhibited excellent performance. Conclusion:Elderly COPD patients with a longer COPD course and duration of COVID-19 are more prone to develop long COVID, with decreased pulmonary ventilation and diffusion ability. Disordered inflammation regulation and energy metabolism may be the potential mechanisms, highlighting the importance of monitoring inflammation and metabolic dysregulation in elderly COPD patients after recovery from COVID-19.

ObjectivesAir pollution has been suggested as an important risk factor for chronic obstructive pulmonary disease (COPD); however, evidence of interactive effects on COPD between different factors was sparse, especially for young adults. We aimed to assess the combined effects of ambient ozone (O3) and household air pollution on COPD in young individuals.MethodsWe conducted a population-based study of residents aged 15–50 years in the low-income and middle-income regions of western China. We used multivariable logistic regression models to examine the associations between long-term ozone exposure and COPD in young individuals.ResultsA total of 6537 young cases were identified among the participants, with a COPD prevalence rate of 7.8 (95% CI 7.2% to 8.5%), and most young COPD individuals were asymptomatic. Exposure to household air pollution was associated with COPD in young patients after adjustment for other confounding factors (OR 1.82, 95% CI 1.41 to 2.37). We also found positive associations of COPD with O3per IQR increase of 20 ppb (OR 1.92, 95% CI 1.59 to 2.32). The individual effects of household air pollution and O3were 1.68 (95% CI 1.18 to 2.46) and 1.55 (95% CI 0.99 to 2.43), respectively, while their joint effect was 3.28 (95% CI 2.35 to 4.69) with the relative excess risk due to interaction of 1.05 (95% CI 0.33 to 1.78).ConclusionsThis study concludes that exposure to ambient O3and household air pollution might be important risk factors for COPD among young adults, and simultaneous exposure to high levels of the two pollutants may intensify their individual effects.

Background: Exposure to particulate matter (PM) has been a major public health threat, but the potentially differential effects on asthma of PM remain largely unknown in high altitude settings. We evaluated the effects of ambient PM on asthma in high altitude settings. Methods: The study recruited a representative sample from high altitude settings using a multistage stratified sampling procedure. Asthma was defined by a self-reported history of diagnosis by a physician or by wheezing symptoms in the preceding 12 months. The annual mean PM2.5 and PM10 concentrations were calculated for each grid cell at 1-km spatial resolution based on the geographical coordinates. Results: We analyzed data for participants (mean age 39.1 years, 51.4% female) and 183 (3.7%, 95% confidence interval (CI): 3.2-4.2) of the participants had asthma. Prevalence was higher in women (4.3%, 95% CI 3.5-5.1) than in men (3.1%, 2.4-3.8) and increasing with higher concentration of PM exposures. For an interquartile range (IQR) difference (8.77 mg/m3) in PM2.5 exposure, the adjusted odds ratio (OR) was 1.64 (95% CI 1.46-1.83, P < 0.001) for risk of asthma. For PM10, there was evidence for an association with risk of asthma (OR 2.34, 95% CI: 1.75-3.15, P < 0.001 per IQR of 43.26 mg/m3). Further analyses showed that household mold or damp exposure may aggravate PM exposure associated risks of asthma. Conclusions: This study identified that PM exposure could be a dominate environmental risk factor for asthma but largely unconsidered in the high-altitude areas. The association between PM exposure and asthma should be of interest for planners of national policies and encourage programs for prevention of asthma in residents living at high altitudes.

Background Multimorbidity causes substantial disease and economic burdens on individuals and the health care system. Objective This study aimed to explore the disease burden of multimorbidity and the potential correlations among chronic noncommunicable diseases (NCDs) in a rural population in Henan, China. Methods A cross-sectional analysis was performed using the baseline survey of the Henan Rural Cohort Study. Multimorbidity was defined as the simultaneous occurrence of at least two NCDs in a participant. This study examined the multimorbidity pattern of 6 NCDs, including hypertension, dyslipidemia, type 2 diabetes mellitus, coronary heart disease, stroke, and hyperuricemia. Results From July 2015 to September 2017, a total of 38,807 participants (aged 18-79 years; 15,354 men and 23,453 women) were included in this study. The overall population prevalence of multimorbidity was 28.1% (10,899/38,807), and the multimorbidity of hypertension and dyslipidemia was the most common (8.1%, 3153/38,807). Aging, higher BMI, and unfavorable lifestyles were significantly associated with a higher risk of multimorbidity (multinomial logistic regression, all P<.05). The analysis of the mean age at diagnosis suggested a cascade of interrelated NCDs and their accumulation over time. Compared with participants without 2 conditional NCDs, participants with 1 conditional NCD would have higher odds of another NCD (1.2-2.5; all P<.05), and those with 2 conditional NCDs would elevate the odds of the third NCD to 1.4-3.5 (binary logistic regression, all P<.05). Conclusions Our findings indicate a plausible tendency for the coexistence and accumulation of NCDs in a rural population in Henan, China. Early prevention of multimorbidity is essential to reduce the NCD burden in the rural population.

BACKGROUND:Both ambient ozone exposure and residential greenness are linked to the aging process. However, their interactive effect on molecular biomarkers of aging (telomere length (TL) and mitochondrial DNA copy number (mtDNA-CN)) remains unclear.METHODS:This study was conducted among 6418 rural Chinese adults. The concentration of ambient ozone was assessed using a random forest model. Residential greenness was represented by the normalized difference vegetation index (NDVI). Molecular biomarkers of aging (relative TL and relative mtDNA-CN) were determined by quantitative real-time polymerase chain reaction. Generalized linear regression models were applied to investigate the independent and combined effects of ambient ozone and residential greenness on relative TL and relative mtDNA-CN.RESULTS:The estimated percent changes and 95 % confidence intervals (CIs) of relative TL in response to per-unit increase in ambient ozone were -22.43 % (-23.74 %, -21.18 %), -14.19 % (-15.63 %, -12.72 %) and -4.50 % (-6.57 %, -2.27 %) for participants with low (NDVI ≤ 0.53), moderate (0.54-0.55) and high (≥0.56) residential greenness exposure, respectively, while the corresponding figures of relative mtDNA-CN were -12.63 % (-13.84 %, -11.31 %), -9.52 % (-10.60 %, -8.33 %) and 2.12 % (0.20 %, 4.19 %). Furthermore, negative interactive effects between ambient ozone and residential greenness exposure on molecular biomarkers of aging were observed (Pfor interaction < 0.001 for relative TL, and 0.098 for relative mtDNA-CN).CONCLUSIONS:Long-term exposure to high concentrations of ambient ozone and low residential greenness was associated with decreased mtDNA-CN and shortened TL. The adverse effect of ambient ozone exposure on molecular biomarkers of aging may be attenuated by increased residential greenness.

Long-term exposure to ambient ozone links to aging biomarkers and increased risk for atherosclerotic cardiovascular diseases (ASCVD). However, the roles of aging biomarkers in the association of long-term exposure to ambient ozone with ASCVD are unclear. A total of 5298 participants completed the questionnaire and physical examination and provided biological specimens. Aging biomarkers (telomere length [TL] and mitochondrial copy number [mtDNA-CN]) were measured by using a real-time polymerase chain reaction method. The concentration of ambient ozone was assessed using a random forest model. Associations of ambient ozone or aging biomarkers with 10-year ASCVD risk were analyzed using logistic regression models. The roles of aging biomarkers in the association of ambient ozone exposure with 10-year ASCVD risk were explored by mediation analysis. The adjusted odds ratios and 95% confidence interval of high 10-year ASCVD risk were 1.16 (1.08, 1.25), 0.71 (0.60, 0.85), and 0.78 (0.64, 0.96) in association with each 1-unit increment in ambient ozone (1 μg/m 3 ) concentration, relative TL, and mtDNA-CN, respectively. The mediated proportion of the association between ambient ozone exposure and high 10-year ASCVD risk by TL or mtDNA-CN was 21.13% or 7.75%, respectively. The total proportion of association between ambient ozone exposure and high 10-year ASCVD risk mediated by TL plus mtDNA-CN was 21.02%. Long-term exposure to ambient ozone was associated with increased 10-year ASCVD risk, and the association was partially mediated by aging biomarkers (shortened TL and decreased mtDNA-CN). This study indicated that ambient ozone pollution–related ASCVD risk might be partially explained by the telomere–mitochondrial axis of aging.

Background: To assess the associations of platelet traits and obesity indices with aging biomarkers (telomere length (TL) and mitochondrial DNA copy number (mtDNA-CN)). Methods: A cross-sectional study was performed among 5091 rural Chinese adults. Obesity indices (waist circumference (WC), waist-to-hip ratio (WHR) and waist-to-height ratio (WHtR)) and platelet traits (plateletcrit (PCT), platelet large cell ratio (P-LCR), mean platelet volume (MPV) and platelet distribution width (PDW)) were collected by physical examination. The aging biomarkers were determined by quantitative real-time polymerase chain reaction. Generalized linear regression models and mediation analysis were applied to explore the relationships between platelet traits, obesity indices, and aging biomarkers. Results: The mean age of the participants was 56 years (range: 18–79). Each one-unit increment in WC, WHR and WHtR were related to a 0.316 (95% confidence interval (CI): −0.437, −0.196), 0.323 (95% CI: −0.513, −0.134) and 0.277 (95% CI: −0.400, −0.153) decrease in relative TL; or a 0.102 (95% CI: −0.197, −0.007), 0.109 (95% CI: −0.258, −0.041) and 0.101 (95% CI: −0.199, −0.004) decrease in relative mtDNA-CN. The proportions of obesity indices with aging biomarkers mediated by platelet indices ranged from 2.85% to 10.10%. Conclusions: Increased central obesity indices in relation to shortened relative TL or decreased mtDNA-CN were mediated by platelet traits, indicating that obesity in association with the accelerated aging process may be partially attributable to abnormal platelet activity.

To the Editor: Chronic airflow obstruction (CAO) is a characteristic feature of chronic obstructive pulmonary disease (COPD) and occurs due to airway and/or alveolar abnormalities typically associated with exposure to noxious particles or gases. The major risk factor for CAO is cigarette smoking, but exposure to solid fuel likely influences CAO development. Studies have found that solid fuel exposure is associated with a high prevalence of CAO, particularly among women. Comparing COPD caused by either solid fuel or tobacco smoke exposure is very significant because about 3 billion people are exposed to solid fuel smoke, and 1.01 billion people smoke tobacco, globally. This study aimed to investigate and compare the clinical and functional characteristics of CAO patients exposed to solid fuel and tobacco smoke using propensity score matching (PSM) in western China.

Objectives Pulmonary function impairment and chronic respiratory symptoms after tuberculosis are relatively common in low-income and middle-income countries. We aimed to estimate the impact of post-tuberculosis (post-TB) on pulmonary function. Methods This large cross-sectional, population-based study included subjects aged 15 years or older with technically acceptable postbronchodilator spirometry measurements. Post-TB was diagnosed on the basis of radiological evidence and/or medical history. Airflow obstruction was defined as a postbronchodilator forced expiratory volume in 1 s/forced vital capacity ratio below the lower limit of normal of Global Lung Function Initiative (GLI) lung function equations. Small airway dysfunction was diagnosed if at least two of the following indicators were less than 65% of predicted: maximal mid-expiratory flow, forced expiratory flow (FEF) 50% or FEF 75%. Results In this population sample (N=8680, mean age: 40.1 years), 610 (7.0% (95% CI 6.5 to 7.6) participants were post-TB. Post-TB subjects had more frequent respiratory symptoms (46.8% vs 28.3%). Among post-TB subjects, 130 (21.3% (95% CI 18.1 to 24.8)) had airflow obstruction; OR of airflow obstruction was significantly associated with post-TB after adjustment for other confounding factors (OR 1.31, 95% CI 1.05 to 1.62). Post-TB was also associated with small airway dysfunction (OR 1.28, 95% CI1.07 to 1.53), which was present in 297 (48.9% (95% CI 33.9 to 53.0)) post-TB subjects. Conclusions Our findings support existing knowledge that post-TB is positively associated with pulmonary function impairment and make for frequent respiratory symptoms. Post-TB should be considered as a potentially important cause of airflow obstruction and respiratory symptoms in patients originating from countries with a high burden of tuberculosis.

BACKGROUND:Obesity and ambient air pollution are independent risk factors of type 2 diabetes mellitus (T2DM), however, the evidence regarding their joint associations on T2DM was sparsely studied in low-middle income countries.METHODS:A total of 38,841 participants were selected from Henan Rural Cohort study which was carried out during 2015-2017. Obesity was identified by body mass index (BMI), WC (waist circumstance), WHR (waist-to-hip ratio), WHtR (waist-to-height ratio), BFP (body fat percent), and VFI (visceral fat index). Three-year averaged-concentrations of NO2, PM1, PM2.5, and PM10 were assessed by using the method of spatiotemporal model incorporated into the satellites data. The independent associations of obesity indicators and exposure to air pollutants on fasting blood glucose (FBG) and T2DM were assessed by generalized linear and logistic regression model, respectively, and their interaction associations on T2DM were quantified by using relative excess risk due to interaction (RERI), attributable proportion due to interaction (AP), and synergy index (S).RESULTS:Positive associations of six obesity measures and four air pollutants with FBG levels and prevalent T2DM were observed. Obese participants measured by BMI plus high exposure to NO2, PM1, PM2.5 and PM10 were related to a 2.96-fold (2.66-3.29), 2.87-fold (2.58-3.20), 2.98-fold (2.67-3.32) and 3.01-fold (2.70-3.35) increased risk for prevalent T2DM, respectively; similarity of joint associations of the other obesity measures and air pollutants on T2DM were observed. The additive associations of different obesity measures and air pollutants with prevalent T2DM were further found.CONCLUSIONS:The synergistic associations of obesity and air pollutants on FBG levels and prevalent T2DM were observed, indicating that obese participants were at high risk for prevalent T2DM in highly polluted rural regions.

Background Long-term exposure to ambient ozone links to aging biomarkers and increased risk for atherosclerotic cardiovascular diseases (ASCVD). However, the roles of aging biomarkers in the association of long-term exposure to ambient ozone with ASCVD are unclear. Methods A total of 5298 participants completed the questionnaire and physical examination and provided biological specimens. Aging biomarkers (telomere length [TL] and mitochondrial copy number [mtDNA-CN]) were measured by using a real-time polymerase chain reaction method. The concentration of ambient ozone was assessed using a random forest model. Associations of ambient ozone or aging biomarkers with 10-year ASCVD risk were analyzed using logistic regression models. The roles of aging biomarkers in the association of ambient ozone exposure with 10-year ASCVD risk were explored by mediation analysis. Results The adjusted odds ratios and 95% confidence interval of high 10-year ASCVD risk were 1.16 (1.08, 1.25), 0.71 (0.60, 0.85), and 0.78 (0.64, 0.96) in association with each 1-unit increment in ambient ozone (1 mu g/m(3)) concentration, relative TL, and mtDNA-CN, respectively. The mediated proportion of the association between ambient ozone exposure and high 10-year ASCVD risk by TL or mtDNA-CN was 21.13% or 7.75%, respectively. The total proportion of association between ambient ozone exposure and high 10-year ASCVD risk mediated by TL plus mtDNA-CN was 21.02%. Conclusions Long-term exposure to ambient ozone was associated with increased 10-year ASCVD risk, and the association was partially mediated by aging biomarkers (shortened TL and decreased mtDNA-CN). This study indicated that ambient ozone pollution-related ASCVD risk might be partially explained by the telomere-mitochondrial axis of aging.

Background: Although independent association of socioeconomic status (SES) or physical activity (PA) with obesity has been well-documented in urban settings, their independent and joint associations on obesity measures are limited in rural regions. Methods: Almost 38,000 ( n = 37,922) individuals were included from the Henan Rural Cohort Study. The International Physical Activity Questionnaire (IPAQ) was used to evaluate PA. Obesity was reflected by body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), body fat percentage (BFP), and visceral fat index (VFI). The independent and interactive effects of SES and PA on obesity were analyzed by logistic regression models and generalized linear regression models, respectively. Results: Compared with high education level, the OR (95%CI) of obesity defined by BMI with low education level was 1.466 (1.337, 1.608), 1.064 (0.924, 1.225), and 1.853 (1.625, 2.114) in total population, men and women, respectively. Besides, the OR (95%CI) of obesity defined by BMI associated with per capita monthly income were 1.089 (1.015, 1.170), 1.192 (1.055, 1.347), 1.038 (0.951, 1.133) in total population, men and women, respectively. Similar results had been observed in other obesity measures. Negative interactive association of low education level and PA on obesity measures were observed only in women (all P < 0.05). Conclusions: This study suggests that women are more susceptible to obesity concerning low SES and that adequate PA may be a potential target for mitigating the negative effect of low SES on obesity in women. Clinical Trial Registration: The Henan Rural Cohort Study has been registered at Chinese Clinical Trial Register (Registration number: ChiCTR-OOC-15006699) http://www.chictr.org.cn/showproj.aspx?proj=11375 .

Background: Although long-term exposure to higher air pollutants and lower residing greenness related to disorders of glucose homeostasis have been reported, their interaction effects on glucose homeostasis in developing countries remained unclear. Methods: A total of 35, 482 participants were obtained from the Henan Rural Cohort (n = 39, 259). Exposure to air pollutants (PM1, PM2.5, PM10 and NO2) were predicted by using a spatiotemporal model-based on satellites data. Residing greenness was reflected by Enhanced Vegetation Index (EVI) and Normalized Difference Vegetation Index (NDVI) which were derived from satellites data. Independent associations of single or mixture of air pollutant or residing greenness with glucose homeostasis markers were analyzed by quantile regression models and quantile g (qg)-computation method, respectively. Furthermore, interaction effects of residing greenness and air pollution on glucose homeostasis markers were analyzed by generalized additive models. Results: Positive associations of single or mixture of air pollutants (PM1, PM2.5, PM10 or NO2) with fasting plasma glucose (FPG) were observed, while negative associations of single or mixture of air pollutants with insulin or HOMA-? were observed. Residing greenness was negatively associated with FPG but positively related to insulin or HOMA-?. Quantile regression revealed the heterogeneity were observed in the associations the residing greenness or air pollutants with glucose homeostasis markers (insulin or HOMA-beta) across deciles of the glucose homeostasis markers distributions. Furthermore, joint associations of single air pollutant and residing greenness on glucose homeostasis markers were found. Conclusions: The results indicated that exposure to air pollution had negative effect on glucose homeostasis markers and these effects may be modified by living in higher green space. These findings suggest that increased residing greenness and air pollution control may have joint effect on decreased the risk of diabetes. Clinical trial registration: The Henan Rural Cohort study has been registered at Chinese Clinical Trial Register (Registration number: ChiCTR-OOC-15006699, http://www.chictr.org.cn/showproj.aspx?proj=11375). (c) 2021 Elsevier B.V. All rights reserved.

BACKGROUND:Exposure to single air pollutant and physical activity (PA) were associated with an altered mitochondrial DNA copy number (mtDNA-CN). However, studies on the interactive effects of single or a mixture of air pollutants and PA on mtDNA-CN were limited. METHODS:A total of 2707 Chinese adults were obtained from the Henan Rural Cohort Study. Spatiotemporal models were used to estimate particulate matter (PMs) (PM with an aerodynamic diameter ≤ 1.0 μm (PM1), ≤2.5 μm (PM2.5) or ≤ 10 μm (PM10)) and nitrogen dioxide (NO2) concentrations. Relative mtDNA-CN was measured by quantitative real-time polymerase chain reaction. Linear regression and quantile g-computation models were applied to examine associations of single or mixture of air pollutants with relative mtDNA-CN. The interactive effects of single or mixture of air pollutants and PA on relative mtDNA-CN were visualized by using Interaction plots. RESULTS:Each 1 μg/m3 increment in PM1, PM2.5, PM10 or NO2 was associated with a 5.11% (95% confidence interval: 3.71%, 6.53%), 6.77% (4.81%, 8.76%), 3.05% (2.22%, 3.87%) or 4.99% (3.45%, 6.55%) increase in relative mtDNA-CN. Each one-quartile increment in mixture of the four air pollutants was related to a 0.053 (0.032, 0.075) increase in relative mtDNA-CN. Negative interaction effects of single or mixture of air pollutants and PA on relative mtDNA-CN were observed. CONCLUSIONS:The positive associations of single or mixture of air pollutants with relative mtDNA-CN were counteracted by PA at certain levels, implying that PA may be a costless and effective approach to decrease negative effects of air pollution on mtDNA-CN.

Background: Chronic obstructive pulmonary disease (COPD) is a public health challenge globally. The burden of COPD is high in never-smokers but little is known about its causes. We aimed to find the prevalence and correlates of COPD in never-smokers, with a special focus on solid fuel exposure.Methods: We conducted a cross-sectional study in Western China. COPD was defined by FEV1/FVC < lower limits of normal (LLN). Descriptive statistics and multivariable logistic regression were used for analyses.Results: Six thousand two hundred and seventy one patients were enrolled between June 2015 and August 2016. The prevalence of COPD in never-smokers was 15.0% (95% confidence interval 14.1–15.9). The common independent predictors of COPD in never-smokers included age ≥60 years, exposure to solid fuel, living in a rural area and a history of tuberculosis. Participants with solid fuel exposure were 69% more likely to have COPD (adjusted odds ratio 1.69, 95% CI 1.41–2.04) than those without such exposure. In addition, we found a positive association between small airway dysfunction and solid fuel exposure (OR 1.35, 95% CI 1.18–1.53).Conclusions: This study confirmed the substantial burden of COPD among never-smokers and also defined the risk factors for COPD in never-smokers. Furthermore, we found a positive association between solid fuel exposure and COPD or small airway dysfunction.

Objectives: The study aimed to explore the association between Ideal cardiovascular health (ICH) and health-related quality of life (HRQoL) using the European Quality of Life Five Dimension Five Level Scale (EQ-5D-5L) among rural population.Methods: This study included 20,683 participants aged 18–79 years from “the Henan Rural Cohort study”. Generalized linear and Tobit regression models were employed to explore the associations of ICH with EQ-5D-5L utility scores and visual analogue scale (VAS) scores, respectively.Results: The mean EQ-5D-5L utility scores and VAS scores were 0.962 ± 0.095 and 79.52 ± 14.02, respectively. Comparing with poor CVH participants (EQ-5D-5L utility scores and VAS scores: 0.954 ± 0.111 and 78.44 ± 14.29), people with intermediate and ideal CVH had higher EQ-5D-5L utility scores (0.969 ± 0.079 and 0.959 ± 0.099) and VAS scores (80.43 ± 13.65 and 79.28 ± 14.14). ICH scores were positively correlated with EQ-5D-5L utility scores (0.007 (0.004, 0.009)) and VAS scores (0.295 (0.143, 0.446)), respectively.Conclusions: Higher ICH scores is positive associated with better HRQoL in rural population, which suggests that improvement of cardiovascular health may help to enhance HRQoL among rural population.

Background: Low socio-economic status (SES) and exposure to single-air pollutant relate to increased prevalent atherosclerotic cardiovascular diseases (ASCVD), however, interactive effect between SES and exposure to singleor multiple-air pollutants on high 10-year ASCVD risk remains unclear. Methods: A total of 31,162 individuals were derived from the Henan Rural Cohort Study. Concentrations of air pollutants (particulate matter with an aerodynamic diameter < 1.0 pm (PM1), <2.5 pm (PM2.5) or <10 pm (PM10), nitrogen dioxide (NO2)) were assessed using a spatiotemporal model based on satellites data. Independent and joint associations of SES, single- and multiple- air pollutants with high 10-year ASCVD risk were evaluated using logistic regression models, quantile g-computation and structural equation models. The interactive effects of SES and exposure to single- or multiple air pollutants on high 10-year ASCVD risk were visualized by using Interaction plots. Results: Exposure to single air pollutant (PM1, PM2.5, PM10 or NO2) related to increased high 10-year ASCVD risk among individuals with low education level or personal average monthly income, compared to the ones with high education level or personal average monthly income. Furthermore, similar results of exposure to mixture of air pollutants with high 10-year ASCVD risk were observed. Positive interactive effects between low SES and exposure to high single air pollutant or the mixture of air pollutants on high 10-year ASCVD risk were observed. Conclusion: Positive association of low SES with high 10-year ASCVD risk was amplified by exposure to high levels of single air pollutant or a mixture of air pollutants, implying that individuals with low SES may more susceptible to air pollution-related adverse health effect. (C) 2021 Elsevier B.V. All rights reserved.