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Background: The effect of non-optimal ambient temperatures (low and high temperatures) on lung function and the underlying mechanisms remains unclear., Methods: Forty-three (20 males, 23 females) healthy non-obese volunteers with an average of 23.9 years participated in the controlled temperature study. All volunteers underwent three temperature exposures in a sequence (moderate [18 °C], low [6 °C], and high [30 °C] temperatures) lasting 12 h with air pollutants controlled. lung function parameters (forced vital capacity [FVC], forced expiratory volume in 1 s [FEV 1 ], and peak expiratory flow [PEF]) were determined in each exposure. Blood and urine samples were collected after each exposure and assayed for inflammatory markers [C-reactive protein (CRP), procalcitonin (PCT), platelet-lymphocyte ratio (PLR), and neutrophil-lymphocyte ratio (NLR)] and oxidative damage markers [protein carbonylation (PCO), 4-hydroxy-2-nominal-mercapturic acid (HNE-MA), 8-iso-prostaglandin-F 2α (8-isoPGF 2α ), and 8-hydroxy-2-deoxyguanosine (8-OHdG)]. Mixed-effects models were constructed to assess the changes of the above indexes under low or high temperatures relative to moderate temperature, and then the repeated measures correlation analyses were performed., Results: Compared with moderate temperature, a 2.20% and 2.59% net decrease in FVC, FEV 1 , and a 5.68% net increase for PEF were observed under low-temperature exposure, while a 1.59% net decrease in FVC and a 7.29% net increase in PEF under high-temperature exposure were found (all P < 0.05). In addition, low temperature elevated inflammatory markers (PCT, PLR, and NLR) and oxidative damage markers (8-isoPGF 2α , 8-OHdG), and high temperature elevated HNE-MA. Repeated measures correlation analyses revealed that PCT (r = -0.33) and NLR (r = -0.31) were negatively correlated with FVC and HNE-MA (r = -0.35) and 8-OHdG (r = -0.31) were negatively correlated with the FEV 1 under low-temperature exposure (all P < 0.05)., Conclusion: Non-optimal ambient temperatures exposure alters lung function, inflammation, and oxidative damage. Inflammation and oxidative damage might be involved in low temperature-related lung function reduction., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

The effect of PM 2.5 exposure on lung function reduction has been well-documented, but the underlying mechanism remains unclear. MiR-4301 may be involved in regulating pathways related to lung injury/repairment, and this study aimed to explore the potential role of miR-4301 in PM 2.5 exposure-associated lung function reduction. A total of 167 Wuhan community nonsmokers were included in this study. Lung function was measured and personal PM 2.5 exposure moving averages were evaluated for each participant. Plasma miRNA was determined by real-time polymerase chain reaction. A generalized linear model was conducted to assess the relationships among personal PM 2.5 moving average concentrations, lung function, and plasma miRNA. The mediation effect of miRNA on the association of personal PM 2.5 exposure with lung function reduction was estimated. Finally, we performed pathway enrichment analysis to predict the underlying pathways of miRNA in lung function reduction from PM 2.5 exposure. We found that each 10 μg/m 3 increase in the 7-day personal PM 2.5 moving average concentration (Lag0-7) was related to a 46.71 mL, 1.15%, 157.06 mL/s, and 188.13 mL/s reductions in FEV 1 , FEV 1 /FVC, PEF, and MMF, respectively. PM 2.5 exposure was negatively associated with plasma miR-4301 expression levels in a dose‒response manner. Additionally, each 1% increase in miR-4301 expression level was significantly associated with a 0.36 mL, 0.01%, 1.14 mL/s, and 1.28 mL/s increases in FEV 1 , FEV 1 /FVC, MMF, and PEF, respectively. Mediation analysis further revealed that decreased miR-4301 mediated 15.6% and 16.8% of PM 2.5 exposure-associated reductions in FEV 1 /FVC and MMF, respectively. Pathway enrichment analyses suggested that the wingless related-integration site (Wnt) signaling pathway might be one of the pathways regulated by miR-4301 in the reduction of lung function from PM 2.5 exposure. In brief, personal PM 2.5 exposure was negatively associated with plasma miR-4301 or lung function in a dose‒response manner. Moreover, miR-4301 partially mediated the lung function reduction associated with PM 2.5 exposure., 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 Elsevier Ltd. All rights reserved.)

Adverse health effects of ambient ozone are getting widespread attention, but the evidence on the relationship between ozone levels and circulatory system diseases are limited and inconsistent. Daily data for ambient ozone levels and hospitalizations for total circulatory diseases and five subtypes in Ganzhou, China from January 1, 2016 to December 31, 2020 were collected. We constructed a generalized additive model with quasi-Poisson regression accounting for lag effects to estimate the associations between ambient ozone levels and the number of hospitalized cases of total circulatory diseases and five subtypes. The differences among gender, age, and season subgroups were furtherly assessed through stratified analysis. A total of 201,799 hospitalized cases of total circulatory diseases were included in the present study, including 94,844 hypertension (HBP), 28,597 coronary heart disease (CHD), 42,120 cerebrovascular disease (CEVD), 21,636 heart failure (HF), and 14,602 arrhythmia. Significantly positive associations were observed between ambient ozone levels and daily hospitalizations for total circulatory diseases and all subtypes except arrhythmia. Each 10 μg/m 3 increase in ozone concentration, the risk of hospitalizations for total circulatory diseases, HBP, CHD, CEVD, and HF increased by 0.718% (95% confidence interval, 0.156%-1.284%), 0.956% (0.346%-1.570%), 0.499% (0.057%-0.943%), 0.386% (0.025%-0.748%), and 0.907% (0.118%-1.702%), respectively. The above associations remained significant after adjusting for other air pollutants. The risk of hospitalization for circulatory diseases was higher in warm season (May to October) and varied in gender and age subgroups. This study suggested that short-term exposure to ambient ozone may increase the risk of hospitalizations for circulatory diseases. Our findings reinforce the importance of reducing ambient ozone pollution levels for protecting public health., 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 Elsevier Ltd. All rights reserved.)

Objective: Previous epidemiological studies have shown that both long-term and short-term exposure to fine particulate matters (PM 2.5 ) were associated with the morbidity and mortality of circulatory system diseases (CSD). However, the impact of PM 2.5 on CSD remains inconclusive. This study aimed to investigate the associations between PM 2.5 and circulatory system diseases in Ganzhou., Methods: We conducted this time series study to explore the association between ambient PM 2.5 exposure and daily hospital admissions for CSD from 2016 to 2020 in Ganzhou by using generalized additive models (GAMs). Stratified analyses were also performed by gender, age, and season., Results: Based on 201,799 hospitalized cases, significant and positive associations were found between short-term PM2.5 exposure and hospital admissions for CSD, including total CSD, hypertension, coronary heart disease (CHD), cerebrovascular disease (CEVD), heart failure (HF), and arrhythmia. Each 10 μg/m 3 increase in PM 2.5 concentrations was associated with a 2.588% (95% confidence interval [CI], 1.161%-4.035%), 2.773% (95% CI, 1.246%-4.324%), 2.865% (95% CI, 0.786%-4.893%), 1.691% (95% CI, 0.239%-3.165%), 4.173% (95% CI, 1.988%-6.404%) and 1.496% (95% CI, 0.030%-2.983%) increment in hospitalizations for total CSD, hypertension, CHD, CEVD, HF, and arrhythmia, respectively. As PM 2.5 concentrations rise, the hospitalizations for arrhythmia showed a slow upward trend, while other CSD increased sharply at high PM 2.5 levels. In subgroup analyses, the impacts of PM 2.5 on hospitalizations for CSD were not materially changed, although the females had higher risks of hypertension, HF, and arrhythmia. The relationships between PM 2.5 exposure and hospitalizations for CSD were more significant among individuals aged ≤65 years, except for arrhythmia. PM 2.5 had stronger effects on total CSD, hypertension, CEVD, HF, and arrhythmia during cold seasons., Conclusion: PM 2.5 exposure was positively associated with daily hospital admissions for CSD, which might provide informative insight on adverse effects of PM 2.5 ., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 You, Cao, Guo, Wang, Qiu, Zhou, Zhou, Chen and Zhang.)

The short-term impacts of urban air pollution on the platelet-lymphocyte ratio (PLR) and neutrophil-lymphocyte ratio (NLR) remain obscure. In this study, we included 3487 urban adults from the Wuhan-Zhuhai cohort. Individual inhalation exposure to air pollutants was estimated by combining participants' daily breath volume and ambient concentrations of six air pollutants (including fine particulate matter (PM 2.5 ), inhalable particulate matter (PM 10 ), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), carbon monoxide (CO) and ozone (O 3 )). The cumulative impacts were assessed by applying lag structures of up to 7 days before the survey date. Associations of air pollutants with PLR and NLR were assessed using a linear mixed model and Bayesian kernel machine regression (BKMR) model. We found that PLR was negatively related to PM 2.5 (lag02-lag06), PM 10 (lag02-lag07), NO 2 (lag02-lag07), and SO 2 (lag03-lag05) and NLR was negatively related to PM 10 (lag05 and lag07). In the BKMR model, a negative joint association between the six-air-pollutant mixture and PLR and NLR was observed, whereas PM 10 and NO 2 appeared to be more important than the other pollutants in the mixture. The negative impact of air pollutants was stronger in males, participants with lower body mass index (< 24 kg/m 2 ), those cooking meals at home, drinkers, and non-exercisers. In conclusion, short-term exposure to air pollutants is significantly related to PLR and NLR in peripheral blood. PLR and NLR may provide new insight into the molecular mechanism underlying the adverse health impact of air pollutants., (Copyright © 2021. Published by Elsevier B.V.)

PM 2.5 exposure leads to lung function alteration. The potential pathway underlying above association, especially the role of DNA methylation is unclear. The objectives of this study are to evaluate the associations of personal PM 2.5 concentrations with DNA methylation at the epigenome-wide level, and investigate how PM 2.5 -related DNA methylation affects lung function. A total of 402 observations of non-smokers were selected from the Wuhan-Zhuhai cohort. PM 2.5 exposure was estimated through a model established in the same population. Blood DNA methylation levels were determined through Illumina Infinium MethylationEPIC BeadChips. Lung function was tested through spirometry on the day of blood sampling. The associations of PM 2.5 exposure with DNA methylation and DNA methylation with lung function were determined through linear mixed models. Ten PM 2.5 -related CpG sites (mapped to 7 different genes) were observed with false discovery rate <0.05. Methylation levels of cg24821877, cg24862131, cg23530876, cg11149743 and cg10781276 were positively associated with PM 2.5 concentrations. While methylation levels of cg10314909, cg08968107, cg18362281, cg24663971 and cg17834632 were negatively associated with PM 2.5 concentrations. The top CpG was cg24663971 (P = 1.51✕10 -9 ). Among the above 10 sites, significantly positive associations of methylation levels of cg24663971 with FVC%pred and FEV 1 %pred, and cg10314909 with FVC, FVC%pred, and FEV 1 %pred were observed. Age had modification effect on the associations between cg24663971 methylation and FVC%pred, and the associations were more obvious among participants with age ≥58 years. In conclusion, PM 2.5 exposure was associated with DNA methylation, and PM 2.5 -related DNA methylation was associated with lung function among Wuhan urban non-smokers., 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 Ltd. All rights reserved.)

1-bromopropane is a US Environmental Protection Agency-identified significant hazardous air pollutant with concerned adverse respiratory effect. We aimed to investigate the relationship between 1-bromopropane exposure and pulmonary function and the underlying role of oxidative damage, which all remain unknown. Pulmonary function and urinary biomarkers of 1-bromopropane exposure (N-Acetyl-S-(n-propyl)-L-cysteine, BPMA) and oxidative damage to DNA (8-hydroxy-deoxyguanosine, 8-OHdG) and lipid (8-iso-prostaglandin-F2α, 8-iso-PGF2α) were measured for 3259 Chinese urban adults from the Wuhan-Zhuhai cohort. The cross-sectional relationship of BPMA with pulmonary function and the joint relationship of BPMA and 8-OHdG or 8-iso-PGF2α with pulmonary function were investigated by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α were evaluated by mediation analysis. Additionally, a panel of 138 subjects was randomly convened from the same cohort to evaluate the stability of BPMA repeatedly measured in urine samples collected over consecutive three days and intervals of one, two, and three years, and to estimate the longitudinal relationship of BPMA with pulmonary function change in three years. We found each 3-fold increase in BPMA was cross-sectionally related to FVC and FEV 1 reductions by 29.88-mL and 25.67-mL, respectively (all P < 0.05). Joint relationship of BPMA and 8-OHdG rather than 8-iso-PGF2α with reduced pulmonary function was observed. Moreover, 8-OHdG significantly mediated 9.44% of the BPMA-related FVC reduction. Findings from the panel revealed a fair to excellent stability (intraclass correlation coefficient: 0.43-0.79) of BPMA in repeated urines collected over a period of three years. Besides, BPMA was longitudinally related to pulmonary function reduction in three years: compared with subjects with persistently low BPMA level, those with persistently high BPMA level had 79.08-mL/year and 49.80-mL/year declines in FVC and FEV 1 , respectively (all P < 0.05). Conclusively, 1-bromopropane exposure might impair pulmonary function of urban adult population, and oxidative DNA damage might be a potential mechanism underlying 1-bromopropane impairing pulmonary function especially FVC., 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 Ltd. All rights reserved.)

Background: The effect of long-term PM 2.5 exposure on lung function has not been well established., Objectives: To investigate the effects of long-term personal PM 2.5 exposure on lung function decline, obstructive, and restrictive ventilatory disorders., Method: Personal PM 2.5 concentrations were evaluated using an estimation model. Lung function parameters including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV 1 ) and peak expiratory flow (PEF) were measured in 3053 Wuhan participants from the Wuhan-Zhuhai cohort and were repeated every 3 years. Participants were classified into persistently high exposure group, persistently low exposure group and inconsistent exposure group according to the median of PM 2.5 concentration of each visit. Mixed linear models with subject-specific random intercept were used to assess the association of 3-year change of lung function with personal PM 2.5 exposure, and generalized linear models were used to assess the association of 6-year change of lung function with personal PM 2.5 exposure. Cox regression models were applied to assess the associations of PM 2.5 with obstructive and restrictive ventilatory disorders., Results: The medians of personal PM 2.5 concentrations at baseline and two follow-ups were 153.18, 209.57 and 83.78 μg/m 3 , respectively. Compared with participants in the persistently low exposure group, participants in the persistently high exposure group showed a 2.99 % (95 % CI: 0.91, 5.08), a 380.15 mL/s (95 % CI: 32.82, 727.48) and a 5.98 % (95 % CI: 0.84, 11.11) additional decline in FEV 1 /FVC, PEF and PEFpred after 6 years, respectively. Stratified analyses showed that age, gender, body mass index, smoking status and drinking status had no significant modification effect on the associations. The associations of PM 2.5 exposure with obstructive and restrictive ventilatory disorders were not significant, except for a positive association between persistently high PM 2.5 exposure and restrictive ventilatory disorder among ever drinkers., Conclusion: Long-term high PM 2.5 exposure was associated with FEV 1 /FVC, PEF and PEFpred declines., 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 B.V. All rights reserved.)

Background: Sulfur dioxide (SO 2 ) has been reported to be related to the mortality of respiratory diseases, but the relationship between SO 2 and hospital inpatient visits with respiratory diseases and the potential impact of different seasons on this relationship is still unclear., Methods: The daily average concentrations of air pollutants, including SO 2 and meteorological data in Ganzhou, China, from 2017 to 2019 were collected. The data on daily hospitalization for respiratory diseases from the biggest hospital in the city were extracted. The generalized additive models (GAM) and the distributed lag non-linear model (DLNM) were employed to evaluate the association between ambient SO 2 and daily inpatient visits for respiratory diseases. Stratified analyses by gender, age, and season were performed to find their potential effects on this association., Results: There is a positive exposure-response relationship between SO 2 concentration and relative risk of respiratory inpatient visits. Every 10 μg/m 3 increase in SO 2 was related to a 3.2% (95% CI: 0.6-6.7%) exaltation in daily respiratory inpatient visits at lag3. In addition, SO 2 had a stronger association with respiratory inpatient visits in women, older adults (≥65 years), and warmer season (May-Oct) subgroups. The relationship between SO 2 and inpatient visits for respiratory diseases was robust after adjusting for other air pollutants, including PM 10 , NO 2 , O 3 , and CO., Conclusion: This time-series study showed that there is a positive association between short-term SO 2 exposure and daily respiratory inpatient visits. These results are important for local administrators to formulate environmental public health policies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Zhou, Gao, Wang, Chen and Zhang.)

Fine particulate matter (PM 2.5 ) is still the primary air pollutant in most Chinese cities and its adverse effects on lung function have been widely reported. However, short-term effects of individual exposure to PM 2.5 on pulmonary expiration flow indices remain largely unknown. In this study, we examined the short-term effects of real-time individual exposure to PM 2.5 on lung function in a panel of 115 healthy adults. We measured individual real-time PM 2.5 exposure and lung function. Environmental PM 2.5 concentrations in the same period were collected from the nearest monitoring station. Generalized linear model was used to assess the effects of individual PM 2.5 exposure on lung function after adjusting for potential confounders. Individual PM 2.5 exposure ranged from 18.5 to 42.4 μg/m 3 with fluctuations over time and ambient PM 2.5 concentrations presented a moderate trend of fluctuation at the same day. Except forced expiratory volume in 1 s (FEV 1 ) decline related to 2-h moving average PM 2.5 exposure, no significant associations between individual PM 2.5 exposure and other volume indices including forced vital capacity (FVC) and FEV 1 /FVC ratio were observed. The adverse effects of individual PM 2.5 exposure on pulmonary expiration flow indices including peak expiratory flow (PEF), maximal mid-expiratory flow (MMF) and forced expiratory flow at 50%, and 75% of vital capacity (FEF 50% and FEF 75% ) were observed to be strongest at 2 moving average hours and could last for 24 h. Stratified analysis showed greater and longer effects among participants who were aged over 40 years, males, or smokers. These findings suggested that individual PM 2.5 exposure was significantly associated with altered lung function, especially with pulmonary expiration flow indices decline, which was strongest at 2 moving average hours and could last for 24 h., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Atmospheric PM 2.5 -bound metals have been widely addressed, but research on the exposure levels and sources of personal PM 2.5 -bound metals among urban community residents is limited. The aim of this study is to explore the exposure levels and sources of 24-h personal PM 2.5 -bound metals among community inhabitants in Wuhan, China. We conducted a penal study of 216 observations with measurements of 16 metals bounded to 24-h personal PM 2.5 samples in April-May, 2014, 2017. Analyses of covariance were used to compare PM 2.5 -bound metal levels across different living habits and ambient conditions. Principal component analysis (PCA) with varimax rotation was performed to explore PM 2.5 -bound metal sources. Personal PM 2.5 -bound aluminum (Al) (113.41 ng/m 3 ) showed the highest geometric mean (GM) concentration, followed by lead (Pb) (90.89 ng/m 3 ), zinc (Zn) (67.71 ng/m 3 ), and iron (Fe) (51.85 ng/m 3 ). The elevated levels of PM 2.5 -bound Al, vanadium (V), manganese (Mn), arsenic (As), rubidium (Rb), cadmium (Cd), and thallium (Tl) were found in participants with cigarette smoke exposure, compared with those without. The concentrations of Rb and strontium (Sr) were positively associated with the time spent outdoors. The increased concentration of nickel (Ni) was found in individuals who spent > 30 min/day in traffic. The elevated levels of V, Mn, and cobalt (Co) were associated with a short distance from dwellings to the main road. The results of PCA showed that PM 2.5 -bound metals might come from five sources: As, selenium (Se), Rb, Cd, Tl, and Pb from cigarette smoke exposure; Al, V, Mn, Fe, and Sr from crustal dust; copper (Cu) and antimony (Sb) from industrial activities; Ni and Co from traffic emission; and Zn from coal combustion. The concentrations of PM 2.5 -bound metals in this study were at moderate levels. Cigarette smoke exposure, industrial activities, traffic emission, and coal combustion might be major anthropogenic sources of personal PM 2.5 -bound metal exposures in Wuhan, China.

Background: Short-term effects of fine particulate matter (PM 2.5 ) exposure on lung function have been reported. However, few studies have assessed PM 2.5 exposure on the personal level, and the mechanism underlying the effects of PM 2.5 exposure on lung function remains less clear., Objectives: To evaluate the association between personal PM 2.5 exposure and lung function alteration in general population and to explore the roles of systematic inflammation and oxidative damage in this association., Methods: A total of 7685 lung function tests were completed among 4697 urban adults in Wuhan, China. Plasma C-reactive protein (CRP), urinary 8-iso-prostaglandin-F 2α (8-iso-PGF 2α ) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were measured. Personal PM 2.5 exposure levels were estimated using an estimation model from the actual measurements of individual PM 2.5 levels in 191 participants. Mixed linear models were used to evaluate the association between personal PM 2.5 exposure and lung function. Mediation analyses were conducted to investigate the roles of CRP, 8-iso-PGF 2α and 8-OHdG in above associations., Results: After adjusting for confounders, each 10 μg/m 3 increase in the previous-day personal PM 2.5 exposure was associated with 2.94 mL, 2.02 mL and 16.14 mL/s decreases in forced vital capacity (FVC), forced expiration volume in 1 s (FEV 1 ) and peak expiratory flow, respectively. The associations were more obvious among never smokers compared with current smokers. Cumulative 7-day exposure to PM 2.5 led to the strongest adverse effects on lung function. Among never smokers with high PM 2.5 exposure levels, a positive relationship was observed between personal PM 2.5 level and urinary 8-iso-PGF 2α , and 8-iso-PGF 2α meditated 4.69% and 12.30% of the association between the 7-day moving PM 2.5 concentration and FVC and FEV 1 , respectively. We did not observe a significant positive association between PM 2.5 exposure and plasma CRP or urinary 8-OHdG., Conclusion: Short-term personal exposure to PM 2.5 is associated with reduced pulmonary ventilation function. Urinary 8-iso-PGF 2α partly mediates these associations., 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 © 2020 Elsevier B.V. All rights reserved.)

Exposure to fine particulate matter (PM 2.5 ) have been associated with adverse respiratory outcomes, but long-term effect of personal exposure on lung function remains largely unknown. We conducted a panel study of 158 adult residents with 394 measurements of personal PM 2.5 concentration and lung function within six years to investigate the long-term association. Linear mixed models were used to identify the associations between lung function changes in relation to different levels of persistent personal PM 2.5 exposure in three or six years. We further attempted to validate resident areas (city) and smoking status as potential predictors of the long-term PM 2.5 exposure levels (persistently high/ persistently low) by generating ROC curves. Compared with subjects who had persistently low exposure level, those with persistently high levels of personal PM 2.5 exposure had an additional 3.63 % decline in FEV 1 /FVC in three years (-3.63 [-7.25, -0.02]), while 7.15 % decline in six years (-7.15 [-14.27, -0.03]). BMI can modify the association. The AUCs were 0.68 (95 %CI: 0.54, 0.82), 0.75 (0.64, 0.86), and 0.82 (0.71, 0.93) for models including smoking status, resident areas, and smoking status combining resident areas respectively. These findings provide new evidence for the long-term effect of personal PM 2.5 exposure on lung function decline., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Fine particulate matter (PM 2.5 ) exposure has been associated with lung function decline, but impact of PM 2.5 constituents especially for polycyclic aromatic hydrocarbons (PAHs) on lung function is unclear among community population. We enrolled 224 Chinese participants who participated in two study periods (2014-2015 and 2017-2018) of the Wuhan-Zhuhai cohort as a panel, and quantified the associations of personal PM 2.5 and sixteen PM 2.5 -bound PAHs with lung function levels as well as lung function change in three years by linear mixed models. Diagnostic ratios were calculated to identify potential sources of PM 2.5 -bound PAHs in Wuhan and Zhuhai separately. In single-constituent models, we found that each one interquartile-range increase of naphthalene, acenaphthene, fluoranthene and pyrene were associated with 26.82, 60.99, 45.25 and 23.37 mL decline in FVC respectively; while fluoranthene and pyrene were associated with 27.43 and 15.49 mL decline in FEV 1 respectively. Similar results were observed in consitituent-PM 2.5 joint models and single-constituent residual models. Persistently long-term high levels of three HMW-PAHs (benzo[a]anthracene, dibenzo[a,h]anthracene, and benzo[ghi]perylene) were associated with 214.65, 226.13, and 265.00 mL decline in FVC decline in three years, compared with persistently low exposure level groups. The associations were different between Wuhan and Zhuhai. The results of diagnostic ratios suggested the differences in PAH emissions between two cities. Our findings provide evidence that both short- and long-term PM 2.5 -bound PAH exposures might affect lung function., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Few studies have compared the biological effects of PM 2.5 from coal combustion, gasoline exhaust and urban ambient air, and the roles of polycyclic aromatic hydrocarbons (PAHs) and metals playing in the process remain unclear. In this study, PM 2.5 samples from coal combustion, gasoline exhaust and urban ambient air were analyzed for 16 PAHs and 23 metals. Cytotoxic and inflammatory effects of different PM 2.5 were evaluated on differentiated THP-1 and A549 cells, respectively. We found that the coal combustion PM 2.5 samples induced stronger cytotoxic and inflammatory effects (p < 0.05). Pearson's correlation and principal component analysis showed that the PAHs containing four or more benzenoid rings and specific metals of cadmium, thallium, zinc and lead were positively related to the biological effects. Our results suggested that coal combustion PM 2.5 might be a more serious health hazard. Specific PAHs and metals might be account for the PM 2.5 induced biological effects., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Fine particle (PM 2.5 )-related lung damage has been reported in most studies regarding environmental or personal PM 2.5 concentrations. To assess effects of personal PM 2.5 exposures on lung function, we recruited 20 postgraduate students and estimated the individual doses of inhaled PM 2.5 based on their microenvironmetal PM 2.5 concentrations, time-activity patterns and refereed inhalation rates. During the period of seven consecutive days in each of the four seasons, we repeatedly measured the daily lung function parameters and airway inflammation makers such as fractional exhaled nitric oxide (FeNO) as well as systemic inflammation markers including interleukin-1β on the final day. The high individual dose (median (IQR)) of inhaled PM 2.5 was 957 (948) μg/day. We observed a maximum FeNO increase (9.1% (95%CI: 2.2-15.5)) at lag 0 day, a maximum decrease of maximum voluntary ventilation (11.8% (95% CI: 4.6-19.0)) at lag 5 day and a maximum interleukin-1β increase (103% (95% CI: 47-159)) at lag 2 day for an interquartile range increase in the individual dose of inhaled PM 2.5 during the four seasons. Short-term exposure to PM 2.5 assessed by the individual dose of inhaled PM 2.5 was associated with higher airway and systemic inflammation and reduced lung function. Further studies are needed to understand better underlying mechanisms of lung damage following acute exposure to PM 2.5., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Some studies have shown an association between obesity or exposure to polycyclic aromatic hydrocarbons (PAHs) and the risk of diabetes. This study aimed to investigate the interaction of obesity and urinary monohydroxy-PAHs (OH-PAHs) on diabetes. Individuals (n = 2716) were drawn from the baseline survey of the Wuhan-Zhuhai Cohort Study. They completed the physical examination, measurements of lung function, biochemical indices and urinary OH-PAHs levels. Additive effect of obesity and urinary ΣOH-PAHs levels on diabetes was assessed by calculating the relative excess risk due to interaction (RERI) and the attributable proportion (AP) due to interaction. Several urinary OH-PAHs were positively associated with diabetes in individuals with central obesity or normal weight (p < 0.05 for all). Among individuals with poor lung function, the RERI between urinary ΣOH-PAHs and waist circumstance (WC, RERI: 0.866, 95% CI: -0.431, 2.164, p = 0.192) or waist-to-height ratio (WHtR, RERI: 1.091, 95% CI: -0.124, 2.305, p = 0.078) was found; the AP due to the interaction between urinary ΣOH-PAHs and WC or WHtR was 0.383 (95% CI: -0.07, 0.80, p = 0.086) or 0.465 (95% CI: 0.019, 0.912, p = 0.04). The results indicated that central obesity may enhance the effect of exposure to background PAHs on diabetes in individuals with poor lung function., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Previous studies have suggested that short-term exposure to ambient air pollution was associated with pediatric hospital admissions and emergency room visits for certain respiratory diseases; however, there is limited evidence on the association between short-term air pollution exposure and pediatric outpatient visits. Our aim was to quantitatively assess the short-term effects of ambient air pollution on pediatric outpatient visits for respiratory diseases. We conducted a time-series study in Yichang city, China between Jan 1, 2014 and Dec 31, 2015. Daily counts of pediatric respiratory outpatient visits were collected from 3 large hospitals, and then linked with air pollution data from 5 air quality monitoring stations by date. We used generalized additive Poisson models to conduct linear and nonlinear exposure-response analyses between air pollutant exposures and pediatric respiratory outpatient visits, adjusting for seasonality, day of week, public holiday, temperature, and relative humidity. Each interquartile range (IQR) increase in PM 2.5 (lag 0), PM 10 (lag 0), NO 2 (lag 0), CO (lag 0), and O 3 (lag 4) concentrations was significantly associated with a 1.91% (95% CI: 0.60%, 3.23%), 2.46% (1.09%, 3.85%), 1.88% (0.49%, 3.29%), 2.00% (0.43%, 3.59%), and 1.91% (0.45%, 3.39%) increase of pediatric respiratory outpatient visits, respectively. Similarly, the nonlinear exposure-response analyses showed monotonic increases of pediatric respiratory outpatient visits by increasing air pollutant exposures, though the associations for NO 2 and CO attenuated at higher concentrations. These associations were unlikely modified by season. We did not observe significant association for SO 2 exposure. Our results suggest that short-term exposures to PM 2.5 , PM 10 , NO 2 , CO, and O 3 may account for increased risk of pediatric outpatient visits for respiratory diseases, and emphasize the needs for reduction of air pollutant exposures for children., (Copyright © 2017. Published by Elsevier Ltd.)

Short-term exposures to outdoor air pollutants have been associated with lower lung function, but the results are inconsistence. The effects of different pollutant levels on lung function changes are still unclear. We quantified the effects of outdoor air pollution exposure (NO 2 , PM 10 , O 3 , and PM 2.5 ) on lung function among 1,694 female non-smokers from the Wuhan-Zhuhai Cohort in China by using linear mixed model. We further investigated the associations in the two cities with different air quality levels separately to quantify the effects of different pollutant level exposure on lung function. We found the moving averages of NO 2 , PM 10 , and PM 2.5 concentrations were significantly associated with reduced FVC. In city at high pollutant level, the moving average of NO 2 , PM 10 , O 3 , and PM 2.5 exposures were significantly associated with both FVC and FEV 1 reductions. In the low-level air pollution city, PM 10 (Lag03-Lag05) and O 3 concentrations (Lag01-Lag03) were significantly associated with reduced FVC, while PM 10 (Lag03-Lag05), O 3 (Lag0-Lag03), and PM 2.5 (Lag04-Lag06) exposure were significantly associated with reduced FEV 1 . Our results suggest that outdoor air pollution is associated with short-term adverse effects on lung function among female non-smokers. The adverse effects may persist for longer durations within 7 days at higher air pollutant levels.

Health conditions may greatly modify the association between particulate matter (PM) and heart rate variability (HRV), but whether the modification of PM effect by coronary artery disease (CAD) risk status depends on the PM levels remains unknown. We investigated the associations between personal exposures to PM with aerodynamic diameter of ≤10μm (PM10) and ≤2.5μm (PM2.5) and concurrent HRV, and whether the effect of PM on HRV was modified by Framingham risk score (FRS) in healthy subjects with different PM exposure levels. Personal exposures to PM10 and PM2.5 were measured for 24h in 152 volunteers of community residents who were free of cardiovascular disease in two cities (Zhuhai and Wuhan) that differ in air quality. Simultaneously, 24h HRV indices were obtained from 3-channel Holter monitor. FRS was calculated based on age, sex, lipid profiles, blood pressure, diabetes, and smoking status. Linear regression models were constructed after adjusting for potential confounders. We found significant decrease in total power (TP) and low power (LF) with increased PM10 concentrations (P for trend<0.05) in the high PM levels city (Wuhan) and total population, but not in the low PM levels city (Zhuhai). We also observed significant modification of FRS on PM10 effect in Wuhan. Interestingly, elevated PM10 was associated in a greater decreased HRV in the low FRS subgroup, but not in the high FRS subgroup. However, we did not find any significant main effects of PM2.5 or PM2.5-FRS interactions on HRV in city-specified or city-combined analyses. Overall, the findings indicate that individual coronary risk profiles may modulate the association between particulate air pollution and HRV in high PM exposure levels., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Background: Many studies have linked ambient fine particulate matter (PM2.5) air pollution to different cardiopulmonary diseases in the general population. However the complex mechanisms underlying PM2.5-induced adverse health effects are not yet to be fully elucidated., Method: In this study, we aimed to identify genes and pathways that may contribute to PM2.5-induced lung toxicity in humans through genome-wide approaches. Human bronchial epithelial (HBE) cells, exposed to various concentrations of PM2.5 collected from Wuhan, China, showed decreased cell viability in a dose-dependent manner. HBE cells were exposed to 200 μg/ml and 500 μg/ml PM2.5 and microarrays were used to obtain a global view of the transcriptomic responses., Results: A total of 970 and 492 genes were identified that significantly changed after 200 μg/ml and 500 μg/ml PM2.5 exposures, respectively. PM2.5 induced a large number of genes involved in inflammatory and immune response, response to oxidative stress, and response to DNA damage stimulus, which might contribute to PM2.5 related cardiopulmonary diseases. Pathway analysis revealed that different dose of PM2.5 triggered partially common disturbed pathways. Flow cytometry assay evidenced that there were statistically significant differences in the G1 phase of cell cycle after low or high-dose PM2.5 exposure when compared to the unexposed controls. Only high-dose PM2.5 significantly increased the proportion of cells in the S phase of cell cycle., Conclusion: We identified many genes and pathways that altered significantly in HBE cells after PM2.5 exposures. These findings are important in providing further understanding of the mechanisms underlying PM2.5-induced adverse health effects., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Objectives: To investigate the effects of the urinary metabolite profiles of background exposure to the atmospheric pollutants polycyclic aromatic hydrocarbon (PAH) and Framingham risk score (FRS), which assesses an individual's cardiovascular disease risk, on heart rate variability (HRV)., Methods: The study conducted from April to May 2011 in Wuhan, China, included 1978 adult residents with completed questionnaires, physical examinations, blood and urine samples, and 5-min HRV indices (including SD of all normal to normal intervals (SDNN), root mean square successive difference (rMSSD), low frequency (LF), high frequency (HF) and their ratio (LF/HF), and total power) obtained from 3-channel Holter monitor. 12 urinary PAH metabolites were measured by gas chromatography-mass spectrometry. FRS was calculated by age, sex, lipid profiles, blood pressure, diabetes and smoking status. Linear regression models were constructed after adjusting for potential confounders., Results: Elevated total concentration of hydroxynaphthalene (ΣOHNa) was significantly associated, in a dose-responsive manner, with decreased SDNN and LF/HF (ptrend=0.014 and 0.007, respectively); elevated total concentration of hydroxyfluorene (ΣOHFlu) was significantly associated with reduced SDNN, LF and LF/HF (ptrend=0.027, 0.003, and <0.0001, respectively); and elevated total concentration of all PAH metabolites (ΣOH-PAHs) was associated with decreased LF and LF/HF (ptrend=0.005 and <0.0001, respectively). Moreover, increasing quartiles of FRS were significantly associated with decreased HRV indices, except LF/HF (all ptrend<0.0001). Interestingly, individuals in low-risk subgroups had greater decreases in SDNN, LF and LF/HF in relation to ΣOH-PAHs, ΣOHNa and ΣOHFlu than those in high-risk subgroups (all p<0.05)., Conclusions: Environmental PAH exposure may differentially affect HRV based on individual coronary risk profiles.

Background: Millions of people rely on N95 filtering facepiece respirators to reduce the risk of airborne particles and prevent them from respiratory infections. However, there are no respirator fit testing and training regulations in China. Meanwhile, no study has been conducted to investigate the fit of various respirators. The objective of this study was to investigate whether people obtained adequate fit when wearing N95 filtering facepiece respirators (FFRs) used widely in China., Methods: Fifty adult participants selected using the Chinese respirator fit test panel donned 10 common models of N95 FFRs. Fit factors (FF) and inward leakage were measured using the TSI PortaCount Plus. Each subject was tested with three replications for each model. A subject was considered to pass the fit test when at least two of the three FFs were greater than 100. Two models were conducted fit tests before and after training to assess the role of training., Results: The geometric mean FFs for each model and trained subjects ranged from <10 to 74.0. The fifth percentile FFs for only two individual respirator models were greater than 10 which is the expected level of performance for FFRs. The passing rates for these two models of FFRs were 44.7% and 20.0%. The passing rates were less than 10.0% for the other eight models. There were 27 (54%) participants who passed none of the 10 FFRs. The geometric mean FFs for both models when the subjects received training (49.7 and 74.0) were significantly larger than those when the same group of subjects did not receive any training (29.0 and 30.9) (P<0.05)., Conclusions: FFRs used widely in China should be improved according to Chinese facial dimensions. Respirator users could benefit from respirator training and fit testing before using respirators.

Background: Human exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations., Methods and Findings: We studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job-exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure-response relationships between CDE (measured in milligrams/cubic meter-years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023-1.029), respiratory diseases (1.069, 1.064-1.074), respiratory tuberculosis (1.065, 1.059-1.071), and cardiovascular disease (1.031, 1.025-1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01-1.11), ischemic heart disease (1.65, 1.35-1.99), and pneumoconiosis (11.01, 7.67-14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m(3). After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives., Conclusions: Long-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease. Please see later in the article for the Editors' Summary.

The increase in air pollution has posed numerous new challenges for human society, making the exploration of an effective method for predicting air pollutant concentrations highly significant. The current research faces several primary challenges: the neglect of non-Euclidean characteristics of site distribution on data and the strong spatiotemporal dependencies in the dispersion process of pollutants. To address these issues, this paper constructs a spatiotemporal hybrid prediction model – the MGAtt-LSTM method – for predicting PM 2.5 concentrations, which employs the dynamic multi-graph attention module (MGAtt) to tackle spatial dependencies and Long Short-Term Memory networks (LSTM) to address temporal dependencies. Additionally, extensive experiments are conducted by using historical air pollutant monitoring data and meteorological data from the Beijing-Tianjin-Hebei region. The results demonstrate that the proposed MGAtt-LSTM model achieved superior performance in concentration prediction compared to existing benchmark models. • The neural network consists of multi-graph attention network and LSTM network. • Air pollution data in North China and meteorological data are used to forecast. • The uneven distribution of pollutant sites is considered to predict PM 2.5 concentrations precisely. • The use of multi-graph attention networks addresses the issue of traditional GCN methods relying on fixed graph structures. [ABSTRACT FROM AUTHOR]

The article presents the study conducted on interaction of RARB variant with polycyclic aromatic hydrocarbon exposure on lung function. Topics of discussion includes studies suggest that genetic variants may imapct the association of air pollutants with respiratory results. Epidemiological studies also presents the relation between polycyclic aromatic hydrocarbon in air pollution on the altered lung function.

[Display omitted] • Urinary acrolein metabolites (UAMs) were repeatedly measured over a period of 3 years. • UAMs were cross-sectionally associated with pulmonary function (PF) reduction. • UAMs were longitudinally associated with PF decline in 3 years. • 8-OHdG, CRP, and CC16 aggravated and/or mediated acrolein-associated PF reduction. • This is the first study to report the associations of UAMs with PF. Acrolein is a significant high priority hazardous air pollutant with pulmonary toxicity and the leading cause of most noncancer adverse respiratory effects among air toxics that draws great attention. Whether and how acrolein exposure impacts pulmonary function remain inconclusive. To assess the association of acrolein exposure with pulmonary function and the underlying roles of oxidative DNA damage, inflammation, and pulmonary epithelium integrity. Among 3,279 Chinese adults from the Wuhan-Zhuhai cohort, associations of urinary acrolein metabolites (N-Acetyl-S-(2-carboxyethyl)-L-cysteine, CEMA; N-Acetyl-S-(3-hydroxypropyl)-L-cysteine, 3HPMA) as credible biomarkers of acrolein exposure with pulmonary function were analyzed by linear mixed models. Joint effects of biomarkers of oxidative DNA damage (8-hydroxy-deoxyguanosine), inflammation (C-reactive protein, CRP), and pulmonary epithelium integrity (Club cell secretory protein, CC16) with acrolein metabolites on pulmonary function and the mediating roles of these biomarkers were assessed. Besides, a subgroup (N = 138) was randomly recruited from the cohort to assess the stabilities of acrolein metabolites and their longitudinal associations with pulmonary function change in three years. Significant inverse dose–response relationships between acrolein metabolites and pulmonary function were found. Each 10-fold increment in CEMA, 3HPMA, or ΣUACLM (CEMA + 3HPMA) was cross-sectionally related to a 68.56-, 40.98-, or 46.02-ml reduction in FVC and a 61.54-, 43.10-, or 50.14-ml reduction in FEV 1 , respectively (P < 0.05). Furthermore, acrolein metabolites with fair to excellent stabilities were found to be longitudinally associated with pulmonary function decline in three years. Joint effects of acrolein metabolites with 8-hydroxy-deoxyguanosine, CRP, and CC16 on pulmonary function were identified. CRP significantly mediated 5.97% and 5.51% of CEMA-associated FVC and FEV 1 reductions, respectively. 8-hydroxy-deoxyguanosine significantly mediated 6.78%, 6.88%, and 7.61% of CEMA-, 3HPMA-, and ΣUACLM-associated FVC reductions, respectively. Acrolein exposure of general adults was cross-sectionally and longitudinally related to pulmonary function decline, which was aggravated and/or partly mediated by oxidative DNA damage, inflammation, and pulmonary epithelium injury. [ABSTRACT FROM AUTHOR]

Urban environmental air pollution has become a serious public issue in China. However, the potential adverse effects of different air pollutants on liver function are still unclear. We aimed to explore the associations of air pollutants exposure with liver function, and analyzed short-term impact in two cities with different levels of air pollution. We included 3892 residents from the Wuhan (high-pollution area)-Zhuhai (low-pollution area) cohort. Liver enzymes including alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in fasting peripheral blood were determined by a fully automatic biochemical analyzer. Individual air pollutants inhalation exposure was estimated by combining his/her daily breathing volume and the concentrations of six air pollutants, including particulate matter (PM 2.5), inhalable particulate matter (PM 10), nitrogen dioxide (NO 2), sulfur dioxide (SO 2), carbon monoxide (CO) and ozone (O 3), from local ambient air monitoring stations. The associations of air pollutants with ALT and AST were evaluated using linear mixed models. We found positive associations of PM 2.5 (lag01-lag07), PM 10 (lag01-lag07), NO 2 (lag01-lag07), SO 2 (lag01-lag07), CO (lag01-lag06) and O 3 (lag01-lag02) with ALT and PM 10 (lag04-lag07) with AST. In Wuhan, exposure to PM 2.5 (lag01-lag07), PM 10 (lag01-lag07), NO 2 (lag01-lag07) and SO 2 (lag01-lag07) was associated with increased ALT, and PM 10 (lag04-lag07) and NO 2 (lag01-lag03) exposure was significantly associated with increased AST. While in Zhuhai, although all six air pollutants (PM 2.5 [lag01-lag07], PM 10 [lag01-lag02], NO 2 [lag01-lag04], SO 2 [lag01-lag03], CO [lag01-lag07] and O 3 [lag01-lag03]) were significantly associated with increased ALT, no pollutant was significantly associated with increased AST. Our results suggest that short-term exposure to air pollutants has adverse effects on liver function among urban adults. Such adverse effects last longer in high-pollution area than that in low-pollution area. Image 1 • We explored adverse effect of air pollutants with higher levels on liver function. • The short-term impact in different air pollution area was analyzed in this study. • A method was adopted to assess personal air pollutants inhalation exposure. • Short-term exposure to air pollutants can affect serum ALT and AST levels. [ABSTRACT FROM AUTHOR]