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Background: Epidemiological evidence on the association of PM 2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) and its specific components with hypertension and blood pressure is limited., Methods: We applied information of participants from the World Health Organization's (WHO) Study on Global Ageing and Adult Health (SAGE) to estimate the associations of long-term PM 2.5 mass and its chemical components exposure with blood pressure (BP) and hypertension incidence in Chinese adults ≥ 50 years during 2007-2018. Generalized linear mixed model and Cox proportional hazard model were applied to investigate the effects of PM 2.5 mass and its chemical components on the incidence of hypertension and BP, respectively., Results: Each interquartile range (IQR = 16.80 μg/m 3 ) increase in the one-year average of PM 2.5 mass concentration was associated with a 17 % increase in the risk of hypertension (HR = 1.17, 95 % CI: 1.10, 1.24), and the population attributable fraction (PAF) was 23.44 % (95 % CI: 14.69 %, 31.55 %). Each IQR μg/m 3 increase in PM 2.5 exposure was also related to increases of systolic blood pressure (SBP) by 2.54 mmHg (95 % CI:1.99, 3.10), and of diastolic blood pressure (DBP) by 1.36 mmHg (95 % CI: 1.04, 1.68). Additionally, the chemical components of SO 4 2- , NO 3 - , NH 4 + , OM, and BC were also positively associated with an increased risk of hypertension incidence and elevated blood pressure., Conclusions: These results indicate that long-term exposure to PM 2.5 mass and its specific components may be major drivers of escalation in hypertension diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Evidence on the associations of fine particulate matter (PM 2.5 ) with cardiopulmonary mortality in the oldest-old (aged 80+ years) people remains limited., Methods: We conducted a time-stratified case-crossover study of 1,475,459 deaths from cardiopulmonary diseases in China to estimate the associations between short-term exposure to ambient PM 2.5 and cardiopulmonary mortality among the oldest-old people., Findings: Each 10 μg/m 3 increase in PM 2.5 concentration (6-day moving average [lag05]) was associated with higher mortality from cardiopulmonary diseases (excess risks [ERs] = 1.69%, 95% confidence interval [CI]: 1.54%, 1.84%), cardiovascular diseases (ER = 1.72%, 95% CI: 1.54%, 1.90%), and respiratory diseases (ER = 1.62%, 95% CI: 1.33%, 1.91%). Compared to the other groups, females (ER = 1.94%, 95% CI: 1.73%, 2.15%) (p for difference test = 0.043) and those aged 95-99 years (ER = 2.31%, 95% CI: 1.61%, 3.02%) (aged 80-85 years old was the reference, p for difference test = 0.770) presented greater mortality risks. We found 14 specific cardiopulmonary causes associated with PM 2.5 , out of which emphysema (ER = 3.20%, 95% CI: 1.57%, 4.86%) had the largest association. Out of the total deaths, 6.27% (attributable fraction [AF], 95% CI: 5.72%, 6.82%) were ascribed to short-term PM 2.5 exposure., Conclusions: This study provides evidence of PM 2.5 -induced cardiopulmonary mortality and calls for targeted prevention actions for the oldest-old people., Funding: This work was supported by the National Key Research and Development Program of China, the National Natural Science Foundation of China, the Foreign Expert Program of the Ministry of Science and Technology, the Natural Science Foundation of Guangdong, China, and the Science and Technology Program of Guangzhou., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Although studies have estimated the associations of PM 2.5 with total mortality or cardiopulmonary mortality, few have comprehensively examined cause-specific mortality risk and burden caused by ambient PM 2.5 . Thus, this study investigated the association of short-term exposure to PM 2.5 with cause-specific mortality using a death-spectrum wide association study (DWAS). Individual information of 5,450,764 deaths during 2013-2018 were collected from six provinces in China. Daily PM 2.5 concentration in the case and control days were estimated by a random forest model. A time-stratified case-crossover study design was applied to estimate the associations (access risk, ER) of PM 2.5 with cause-specific mortality, which was then used to calculate the population-attributable fraction (PAF) of mortality and the corresponding mortality burden caused by PM 2.5 . Each 10 μg/m 3 increase in PM 2.5 concentration (lag03) was associated with a 0.80 % [95 % confidence interval (CI): 0.73 %, 0.86 %] rise in total mortality. We found greater mortality effect at PM 2.5 concentrations < 50 μg/m 3 . Stratified analyses showed greater ERs in females (1.01 %, 95 %CI: 0.91 %, 1.11 %), children ≤ 5 years (2.17 %, 95 %CI: 0.85 %, 3.51 %), and old people ≥ 70 years. We identified 33 specific causes (level 2) of death which had significant associations with PM 2.5 , including 16 circulatory diseases, 9 respiratory diseases, and 8 other causes. The PAF estimated based on the overall association between PM 2.5 and total mortality was 3.16 % (95 %CI: 2.89 %, 3.40 %). However, the PAF was reduced to 2.88 % (95 %CI: 1.88 %, 3.81 %) using the associations of PM 2.5 with 33 level 2 causes of death, based on which 250.15 (95 %CI: 163.29, 330.93) thousand deaths were attributable to short-term PM 2.5 exposure across China in 2019. Overall, this study provided a comprehensive picture on the death-spectrum wide association between PM 2.5 and morality in China. We observed robust positive cause-specific associations of PM 2.5 with mortality risk, which may provide more precise basis in assessing the mortality burden of air pollution., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: It remains unclear whether type 2 diabetes and the complication of arthritis are causally related to the PM 2.5 pollutant. Therefore, we aimed to investigate the associations of long-term PM 2.5 exposure with type 2 diabetes and with arthritis in type 2 diabetes patients., Materials and Methods: This study used data from the China Health and Retirement Longitudinal Survey (CHARLS) implemented during 2011-2018. The associations were analyzed by Cox proportional hazards regression models, and the population-attributable fraction (PAF) was calculated to assess the burden of type 2 diabetes and arthritis-attributable to PM 2.5 ., Results: A total of 21,075 participants were finally included, with 19,121 analyzed for PM 2.5 and type 2 diabetes risk and 12,427 analyzed for PM 2.5 and arthritis risk, of which 1,382 with newly-diagnosed type 2 diabetes and 1,328 with arthritis during the follow-up. Overall, each 10 μg/m 3 increment in PM 2.5 concentration was significantly associated with an increase in the risk of type 2 diabetes (HR = 1.26, 95 %CI1.22 to 1.31), and the PAF of type 2 diabetes attributable to PM 2.5 was 13.54 %. In type 2 diabetes patients, each 10 μg/m 3 increment in PM 2.5 exposure was associated with an increase in arthritis (HR = 1.42, 95 %CI: 1.28 to 1.57), and the association was significantly greater than that (H = 1.23, 95 %CI: 1.19 to 1.28) in adults without type 2 diabetes. The PAFs of arthritis-attributable to PM 2.5 in participants with and without type 2 diabetes were 18.54 % and 10.69 %, respectively., Conclusion: Long-term exposure to PM 2.5 may increase the risk of type 2 diabetes and make type 2 diabetes patients susceptible to arthritis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Previous studies have attempted to clarify the relationship between the occurrence of pulmonary tuberculosis (PTB) and exposure to air pollutants. However, evidence from multi-centres, particularly at the national level, is scarce, and no study has examined the modifying effect of greenness on air pollution-TB associations. In this study, we examined the association between long-term exposure to ambient air pollutants (PM 10 p.m. 2.5 , and O 3 ) and monthly PTB or smear-positive pulmonary tuberculosis (SPPTB) incidence to further evaluate whether these associations were affected by greenness in mainland China using a two-stage analytic procedure. PM 2.5 was positively associated with both PTB and SPPTB incidence, with relative risk (RR) of 1.12 (95% confidence interval [CI]: 1.03, 1.22) and 1.08 (95% CI: 1.02, 1.10) per 10 μg/m 3 increase, respectively. Furthermore, PM 10 was positively associated with PTB incidence, with RR of 1.07 (95% CI: 1.01, 1.13). However, O 3 was not associated with the monthly incidence of PTB or SPPTB. The normalized difference vegetation index (NDVI) exhibited a modifying effect on the association between PM 2.5 exposure and SPPTB incidence in northern areas, with RR of 1.16 (95% CI: 1.03, 1.31) in lower mean annual NDVI areas than in the higher areas (RR = 0.98, 95% CI: 0.87, 1.09). This nationwide analysis indicated that NDVI could reduce the effect of air pollutants on TB incidence particularly in the northern areas. Long-term exposure to particulate matter (PM) may increase the occurrence of PTB or SPPTB in China, and further studies involving larger numbers of SPPTB cases are required to confirm the effects of PM exposure on SPPTB incidence in the future., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Ozone (O 3 ) exposure may lead to the development and exacerbation of asthma or wheezing in postnatal children; however, it has rarely been studied before and during pregnancy. Wheezing is one of the most common symptoms when diagnosing of asthma; thus, we investigated the associations of O 3 exposure before and during pregnancy with wheezing in preschool children and the potential susceptible exposure windows from a heavily polluted city in China. This population-based birth cohort study, which included 3725 mother-child pairs from Guangzhou, began in 2016, and the follow-up period ended on July 31, 2020. We used a spatiotemporal land-use-regression model combined with activity patterns to estimate the daily O 3 exposure levels during the pre-pregnancy period and each trimester, and wheezing was recorded by reviewing medical records. We used the Cox proportional hazard model to quantify the effects of O 3 exposure on childhood wheezing adjusted for potential confounders. No significant association was detected between pre-pregnancy exposure to O 3 and childhood wheezing. However, increased ambient O 3 exposures throughout pregnancy and in the second trimester were positively associated with the risk of childhood wheezing, with hazard ratios (HRs) and 95% confident intervals (CIs) per interquartile range (IQR) increment of 1.22 (95% CI: 1.04-1.44) and 1.31 (95% CI: 1.09-1.58), respectively. The effects of maternal O 3 exposure on childhood wheezing risk was stronger when the exposure occurred in the warm conception season (P < 0.05). Significant childhood wheezing risk could be attributable to maternal O 3 exposure, especially during the second trimester and with warm-season conception in Guangzhou. Further cohorts of children, particularly school age children who have more robust asthma diagnoses, should be investigated in the future., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Although studies have investigated the association between early-life exposure to fine particulate matter (PM 2.5 ) and childhood asthma/wheezing, results are inconsistent and the susceptible exposure window remains largely unknown., Methods: A prospective birth cohort study was conducted to recruit pregnant women during their early pregnancy, and to follow up them and their children up to 3-4 years old. Diagnosis of asthma/wheezing was extracted from children's medical records. A spatiotemporal land-use regression (ST-LUR) model was used to assess maternal exposure to PM 2.5 during pregnancy and their children's exposure after birth. The Cox proportional hazards model and accelerated failure time model (for violation of proportional hazards assumption) were applied to estimate the effects of prenatal and postnatal exposures to PM 2.5 on the risk of childhood asthma/wheezing., Results: A total of 3725 children were included, and 392 children (10.52%) were diagnosed with asthma/wheezing. Both prenatal and postnatal exposures to PM 2.5 were positively associated with the risk of asthma/wheezing. Each interquartile range (IQR) increment in PM 2.5 exposure during the entire pregnancy (4.8 μg/m 3 ) and the period from birth to the end of follow-up (1.5 μg/m 3 ) was associated with adjusted hazard ratios (HRs) of 1.44 [95% confidence interval (CI): 1.13, 1.85] and 2.74 (95% CI: 2.59, 2.91), respectively. Subgroup analyses showed greater HRs for PM 2.5 exposures during the pseudoglandular stage (6-16 gestational weeks [GWs]: IQR = 4.8 μg/m 3 , HR = 1.10, 95% CI: 1.02, 1.18) and canalicular stage (16-24 GWs: IQR = 4.8 μg/m 3 , HR = 1.13, 95% CI:1.03, 1.23) than other stages, and also showed significant effects in the first three-year period after birth (IQR = 1.5 μg/m 3 , HR = 2.37, 95% CI: =2.24, 2.51)., Conclusion: Higher prenatal and postnatal PM 2.5 exposures may increase the risk of childhood asthma/wheezing. The pseudoglandular stage, canalicular stage, and the first three years after birth may be key susceptible to exposure windows., (© 2022 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.)

(1) Background: As the most common eye disease diagnosed in emergency departments, conjunctivitis has caused serious health and economic burdens worldwide. However, whether air pollution may be a risk factor for conjunctivitis is still inconsistent among current evidence. (2) Methods: We searched the literature on the relationship between air pollution and conjunctivitis in multiple English databases before 18 March 2019. Meta-analysis, meta-regression, and funnel plots were used to integrate the data, identify the sources of bias, and determine the publication bias, respectively. (3) Results: A total of 2450 papers were found, 12 of which were finally included. The pooled relative risk for each 10 μg/m 3 increase of air pollution on conjunctivitis was 1.0006 (95%CI: 0.9993-1.0019) for CO, 1.0287 (1.0120-1.0457) for NO 2 , 1.0089 (1.0030-1.0149) for O 3 , 1.0004 (0.9976-1.0032) for PM 2.5 , 1.0033 (0.9982-1.0083) for PM 10 , and 1.0045 (0.9908-1.0185) for SO 2 . In the subgroup, PM 2.5 and O 3 had a greater impact on conjunctivitis risk in women than in men, and people <18 years old than those ≥18 years old. Relative humidity significantly modified the risk of O 3 on conjunctivitis ( p = 0.023), explaining 45% of the between-study heterogeneity. (4) Conclusion: Globally, air pollution has considerable health risks for conjunctivitis. Females and the youth were more vulnerable to PM 2.5 , NO 2 , and O 3 . Reductions of air pollution levels are still warranted to protect the vulnerable populations.

Although a few studies have analyzed the associations between ambient air pollutants and the development of tuberculosis (TB), most have been conducted in the core countries with inconsistent results. In this study, we used a distributed lag non-linear model to investigate the associations between the newly diagnosed TB cases and daily exposure to particulate matter with an aerodynamic diameter of <10μm (PM 10 ), nitrogen dioxide (NO 2 ), and sulfur dioxide (SO 2 ) in Chengdu, a severely polluted city. There were 36,108 newly diagnosed active TB cases from January 1, 2010 to December 31, 2015 in Chengdu. In a single-pollutant model, the cumulative relative risk of active TB cases was 1.06 [lag of 0 to 21days, 95% confidence interval (CI): 1.01-1.11] for each 10μg/m 3 increase in PM 10 above the threshold of 70μg/m 3 ; 1.06 (lag of 0 to 2days, 95% CI: 1.03-1.09) for each 10μg/m 3 increase in NO 2 above the threshold of 40μg/m 3 ; and 1.07 (lag of 0 to 2days, 95% CI: 1.02-1.12) for each 10μg/m 3 increase in SO 2 above the threshold of 60μg/m 3 . Meanwhile, we found a positive association in males after exposure to a 10μg/m 3 increase in SO 2 above the threshold of 60μg/m 3 at a lag of 0 to 2days. Exposure to PM 10 , NO 2 , and SO 2 was associated with an increment in the incidence of active TB cases., (Copyright © 2018. Published by Elsevier B.V.)

Background: Although studies have investigated the association between early‐life exposure to fine particulate matter (PM2.5) and childhood asthma/wheezing, results are inconsistent and the susceptible exposure window remains largely unknown. Methods: A prospective birth cohort study was conducted to recruit pregnant women during their early pregnancy, and to follow up them and their children up to 3–4 years old. Diagnosis of asthma/wheezing was extracted from children's medical records. A spatiotemporal land‐use regression (ST‐LUR) model was used to assess maternal exposure to PM2.5 during pregnancy and their children's exposure after birth. The Cox proportional hazards model and accelerated failure time model (for violation of proportional hazards assumption) were applied to estimate the effects of prenatal and postnatal exposures to PM2.5 on the risk of childhood asthma/wheezing. Results: A total of 3725 children were included, and 392 children (10.52%) were diagnosed with asthma/wheezing. Both prenatal and postnatal exposures to PM2.5 were positively associated with the risk of asthma/wheezing. Each interquartile range (IQR) increment in PM2.5 exposure during the entire pregnancy (4.8 μg/m3) and the period from birth to the end of follow‐up (1.5 μg/m3) was associated with adjusted hazard ratios (HRs) of 1.44 [95% confidence interval (CI): 1.13, 1.85] and 2.74 (95% CI: 2.59, 2.91), respectively. Subgroup analyses showed greater HRs for PM2.5 exposures during the pseudoglandular stage (6–16 gestational weeks [GWs]: IQR = 4.8 μg/m3, HR = 1.10, 95% CI: 1.02, 1.18) and canalicular stage (16–24 GWs: IQR = 4.8 μg/m3, HR = 1.13, 95% CI:1.03, 1.23) than other stages, and also showed significant effects in the first three‐year period after birth (IQR = 1.5 μg/m3, HR = 2.37, 95% CI: =2.24, 2.51). Conclusion: Higher prenatal and postnatal PM2.5 exposures may increase the risk of childhood asthma/wheezing. The pseudoglandular stage, canalicular stage, and the first three years after birth may be key susceptible to exposure windows. [ABSTRACT FROM AUTHOR]