Search

Background: Fine particulate matter (PM 2.5 ) is noxious to female reproductive development and facilitates the occurrence of subsequent diseases. Early menopause is initiative factor of female aging. But due to the lack of historical exposure of PM 2.5 , we could not gain insight into the linkage between ambient PM 2.5 exposure and early menopause., Methods: We conducted a community-based retrospective cross-sectional study and pooled 1173 postmenopausal women. The machine learning algorithm of LightGBM was processed to derive the historical concentrations of PM 2.5 based on aerography of 1956-2022. The quantile g-computation and binary logistic regression were employed to estimate the mixed and single associations between PM 2.5 and early menopause., Results: The visibility topped the most important feature for derivations of historical PM 2.5 concentrations. The R 2 of 10-fold cross-validation and predictive capability during processing were all above 0.8. The prevalence of early menopause was 7.3 %. Each 10 µg/m 3 PM 2.5 increased the prevalence of early menopause during prior 2 years exposure (OR: 1.49, 95 %CI: 1.03-2.16) and spring and autumn (OR: 1.28, 95 %CI: 1.07-1.54). After adjusting the reverse effects of temperature, the prior 2 years exposure of PM 2.5 remained positively associated with early menopause in the fourth quantile vs the first quantile (OR: 3.36, 95 %CI: 1.53-7.36) in the spring and autumn. The higher BMI (OR: 1.40, 95 %CI: 1.14-1.72), waistline (OR: 1.42, 95 %CI: 1.09-1.85) and unfavourable dietary habits of less meat (OR: 1.72, 95 %CI: 1.11-2.68), more fried food (OR: 2.39, 95 %CI: 1.15-4.99) elevated the prevalence of early menopause., Conclusions: The accurate environmental exposure assessment of historical PM 2.5 vigorously promoted the researches on the relationship between PM 2.5 and early menopause. It sounds the alarm on female infertility menace associated with particulate matter especially during the turbulent 2 years before menopause., 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 Authors. Published by Elsevier Inc. All rights reserved.)

Epidemiological findings have determined the linkage of fine particulate matter (PM 2.5 ) and the morbidity of hypertension. However, the mode of action and specific contribution of PM 2.5 component in the blood pressure elevation remain unclear. Platelets are critical for vascular homeostasis and thrombosis, which may be involved in the increase of blood pressure. Among 240 high-PM 2.5 exposed, 318 low-PM 2.5 exposed workers in a coking plant and 210 workers in the oxygen plant and cold-rolling mill enrolled in present study, both internal and external exposure characteristics were obtained, and we performed linear regression, adaptive elastic net regression, quantile g-computation and mediation analyses to analyze the relationship between urine metabolites of polycyclic aromatic hydrocarbons (PAHs) and metals fractions with platelets indices and blood pressure indicators. We found that PM 2.5 exposure leads to increased systolic blood pressure (SBP) and pulse pressure (PP). Specifically, for every 10 μg/m 3 increase in PM 2.5 , there was a 0.09 mmHg rise in PP. Additionally, one IQR increase in urinary 1-hydroxypyrene (1.06 μmol/mol creatinine) was associated with a 3.43 % elevation in PP. Similarly, an IQR increment of urine cobalt (2.31 μmol/mol creatinine) was associated with a separate 1.77 % and 4.71 % elevation of SBP and PP. Notably, platelet-to-lymphocyte ratio (PLR) played a mediating role in the elevation of SBP and PP induced by cobalt. Our multi-pollutants results showed that PAHs and cobalt were deleterious contributors to the elevated blood pressure. These findings deepen our understanding of the cardiovascular effects associated with PM 2.5 constituents, highlighting the importance of increased vigilance in monitoring and controlling the harmful components in PM 2.5 ., 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. Published by Elsevier B.V.)

Air pollution has been recognized as a contributing factor to sleep disorders (SD), which have been correlated with an elevated susceptibility to a variety of human diseases. Nevertheless, research has not definitively established a connection between SD and interior decorative volatile organic compounds (ID-VOCs), a significant indoor air pollutant. In this study, we employed a mouse model exposed to ID-VOCs to explore the impacts of ID-VOCs exposure on sleep patterns and the potential underlying mechanism. Of the 23 key compositions of ID-VOCs identified, aromatic hydrocarbons were found to be the most prevalent. Exposure to ID-VOCs in mice resulted in SD, characterized by prolonged wake fullness and decreased sleep during the light period. ID-VOCs exposure triggered neuroinflammatory responses in the suprachiasmatic nucleus (SCN), with microglia activation leading to the overproduction of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α), and complement component 1q (C1q), ultimately inducing A1 astrocytes. Consequently, the upregulation of branched chain amino acid transaminase 2 (BCAT2) in A1 astrocytes resulted in elevated extracellular glutamate and disruption of the wake-sleep transition mechanism, which might be the toxicological mechanism of SD caused by ID-VOCs., 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 Elsevier B.V. All rights reserved.)

Background: Ultrafine particle (UFP) has been linked with higher risks of cardiovascular diseases; however, the biological mechanisms remain to be fully elucidated., Objectives: This study aims to investigate the cardiovascular responses to short-term UFP exposure and the biological pathways involved., Methods: A longitudinal panel study was conducted among 32 healthy, non-smoking young adults in Shanghai, China, who were engaged in five rounds of follow-ups between December 2020 and November 2021. Individual exposures were calculated based on the indoor and outdoor real-time measurements. Blood pressure, arterial stiffness, targeted biomarkers, and untargeted proteomics and metabolomics were examined during each follow-up. Linear mixed-effect models were applied to analyze the exposure and health data. The differential proteins and metabolites were used for pathway enrichment analyses., Results: Short-term UFP exposure was associated with significant increases in blood pressure and arterial stiffness. For example, systolic blood pressure increased by 2.10 % (95 % confidence interval: 0.63 %, 3.59 %) corresponding to each interquartile increase in UFP concentrations at lag 0-3 h, while pulse wave velocity increased by 2.26 % (95 % confidence interval: 0.52 %, 4.04 %) at lag 7-12 h. In addition, dozens of molecular biomarkers altered significantly. These effects were generally present within 24 h after UFP exposure, and were robust to the adjustment of co-pollutants. Molecular changes detected in proteomics and metabolomics analyses were mainly involved in systemic inflammation, oxidative stress, endothelial dysfunction, coagulation, and disturbance in lipid transport and metabolism., Discussion: This study provides novel and compelling evidence on the detrimental subclinical cardiovascular effects in response to short-term UFP exposure. The multi-omics profiling further offers holistic insights into the underlying biological pathways., 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 Authors. Published by Elsevier Ltd.. All rights reserved.)

Ground-level ozone (O 3 ) is one of the major air pollutants. A large body of literature has linked O 3 air pollution to various adverse human health effects. The objective of this study is to attain a comprehensive and in-depth understanding of the progress and frontiers of research on O 3 and human health. We used bibliometric methods to summarize publications on O 3 air pollution and public health between 1990 and 2022 obtained from the Web of Science Core Collection database. VOSviewer and R software were used for bibliometric analysis and visualization. A total of 4501 relevant papers were included in the analysis. There has been a significant increase in the number of publications since 2013, with the USA being the major contributor, followed by China and England. Harvard University was the most prolific research institution, followed by the US Environmental Protection Agency and the University of North Carolina System. Professor Joel Schwartz was the most published author and has established a complex network of national and international collaborations. Co-occurrence analysis of keywords suggested evolving research hotspots, from toxicological studies to population-based epidemiological studies and from the respiratory system to the extra-pulmonary system. Research on O 3 and its human health effects has progressed rapidly over the past few decades, but academic disparities still persist between developed and developing countries. There is an urgent need to strengthen international cooperation to address the public health challenges posed by rising O 3 air pollution in the future., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Kawasaki disease (KD) is an acute, systemic vasculitis that primarily affects children aged under the age of 5. While environmental factors have been linked to the development of KD, the specific role of ozone (O 3 ) pollution in triggering the disease onset remains uncertain. This study aimed to examine the associations between short-term O 3 exposure and KD onset in children. Utilizing a satellite-based model with a spatial resolution of 1 × 1 km, we matched 1808 KD patients (out of a total of 6115 eligible individuals) to pre-onset ozone exposures based on their home addresses in East China between 2013 and 2020. Our findings revealed a significant association of O 3 exposure with KD onset on the day of onset (lag 0 day). However, this association attenuated and became statistically insignificant on lag 1 and lag 2 days. Each interquartile range (52.32 μg/m 3 ) increase in O 3 concentration at lag 0 day was associated with a 16.2% (95% CI: 3.6%, 30.3%) increased risk of KD onset. The E-R curve for O 3 exhibited a plateau at low concentrations and then increased rapidly at concentrations ≥75 μg/m 3 . Notably, these associations were stronger in male children, younger children (<2 years of age) and patients experiencing KD onset during the warm season. This study provides novel epidemiological evidence indicating that short-term O 3 exposure is associated with an increased risk of childhood KD onset. These findings emphasized the importance of considering this environmental risk factor in KD prevention strategies., 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.)

Numerous epidemiological studies have demonstrated links between short-term ozone exposure to various adverse health outcomes, but some ozone-induced pathological mechanisms remain unclear. To fill this knowledge gap, we enrolled 36 healthy young adults living in high-ozone areas and performed an untargeted metabolomic analysis in serum collected before, during, and after their travel to a low-ozone scenic area. Reviewing the literature, we found 16 metabolites significantly associated with ozone, pointing to neurological health, type 2 diabetes (T2D) risk, and cardiovascular health. Notably, we observed significant changes in these 16 metabolites from the ozone reduction when participants traveled from the campus to the scenic area (adjusted p-value < 0.05). However, when ozone increased after participants returned to campus from the scenic area, we observed that T2D risk and cardiovascular health-related metabolites returned to their original state (adjusted p-value < 0.05), but neurological health-related metabolites did not change significantly with ozone exposure. Our study showed that ozone exposure was linked to prompt alterations in serum metabolites related to cardiovascular health and T2D risk but less sensitive changes in neurological health-related metabolites. Among many lipids, free fatty acids and acylcarnitines were the most sensitive compounds positively associated with changes in ozone 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 B.V. All rights reserved.)

Background: There is limited longitudinal evidence on the hypertensive effects of long-term exposure to ambient O 3 . We investigated the association between long-term O 3 exposure at workplace and incident hypertension, diastolic blood pressure (DBP), systolic blood pressure (SBP), pulse pressure (PP), and mean arterial pressure (MAP) in general working adults., Methods: We conducted a cohort study by recruiting over 30,000 medical examination attendees through multistage stratified cluster sampling. Participants completed a standard questionnaire and comprehensive medical examination. Three-year ambient O 3 concentrations at each employed participant's workplace were estimated using a two-stage machine learning model. Mixed-effects Cox proportional hazards models and linear mixed-effects models were used to examine the effect of O 3 concentrations on incident hypertension and blood pressure parameters, respectively. Generalized additive mixed models were used to explore non-linear concentration-response relationships., Results: A total of 16,630 hypertension-free working participants at baseline finished the follow-up. The mean (SD) O 3 exposure was 45.26 (2.70) ppb. The cumulative incidence of hypertension was 7.11 (95% CI: 6.76, 7.47) per 100 person-years. Long-term O 3 exposure was independently, positively and non-linearly associated with incident hypertension (Hazard ratios (95% CI) for Q2, Q3, and Q4 were 1.77 (1.34, 2.36), 2.06 (1.42, 3.00) and 3.43 (2.46, 4.79), respectively, as compared with the first quartile (Q1)), DBP (β (95% CI) was 0.65 (0.01, 1.30) for Q2, as compared to Q1), SBP (β (95% CI) was 2.88 (2.00, 3.77), 2.49 (1.36, 3.61) and 2.61 (1.64, 3.58) for Q2, Q3, and Q4, respectively), PP (β (95% CI) was 2.12 (1.36, 2.87), 2.03 (1.18, 2.87) and 2.14 (1.38, 2.90) for Q2, Q3, and Q4, respectively), and MAP (β (95% CI) was 1.39 (0.76, 2.02), 1.04 (0.24, 1.84) and 1.12 (0.43, 1.82) for Q2, Q3, and Q4, respectively). The associations were robust across sex, age, BMI, and when considering PM 2.5 and NO 2 ., Conclusions: To our knowledge, this is the first cohort study in the general population that demonstrates the non-linear hypertensive effects of long-term O 3 exposure. The findings are particularly relevant for policymakers and researchers involved in ambient pollution and public health, supporting the integration of reduction of ambient O 3 into public health interventions., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Due to a combination of lifestyle risk factors, the burden of cardiovascular disease (CVD) has been increasing in China, affecting an estimated 330 million people. Environmental risk factors can exacerbate these risks or independently contribute to CVD. Ozone is an overlooked and invisible risk factor, and it plays a significant role in the development of CVD. Our study provides a novel quantification of the ozone-attributable CVD mortality burden based on daily maximum 8-h average ozone concentration during May to October (6mDMA8) in Chinese adults in 2050, projected under Shared Socioeconomic Pathways 585 and 126, and using the updated WHO air quality guideline level. The study also considers the contributions made by changes in ozone exposure, population aging, population size, and baseline death rates of CVD between 2019 and 2050. While adopting a sustainable and green pathway (SSP 126) can reduce the projected magnitude of premature CVD deaths to 359,200 in 2050, it may not be sufficient to reduce the CVD mortality burden significantly. Therefore, it is crucial to implement strategies for stricter ozone control and reducing the baseline death rate of CVD to mitigate the impacts of ozone on Chinese adults.

Background: Exposure to traffic-related air pollution (TRAP) has been associated with increased risks of respiratory diseases, but the biological mechanisms are not yet fully elucidated., Objectives: Our aim was to evaluate the respiratory responses and explore potential biological mechanisms of TRAP exposure in a randomized crossover trial., Methods: We conducted a randomized crossover trial in 56 healthy adults. Each participant was exposed to high- and low-TRAP exposure sessions by walking in a park and down a road with high traffic volume for 4 h in random order. Respiratory symptoms and lung function, including forced expiratory volume in the first second ( FEV 1 ), forced vital capacity (FVC), the ratio of FEV 1 to FVC, and maximal mid-expiratory flow (MMEF), were measured before and after each exposure session. Markers of 8-isoprostane, tumor necrosis factor- α ( TNF- α ), and ezrin in exhaled breath condensate (EBC), and surfactant proteins D (SP-D) in serum were also measured. We used linear mixed-effects models to estimate the associations, adjusted for age, sex, body mass index, meteorological condition, and batch (only for biomarkers). Liquid chromatography-mass spectrometry was used to profile the EBC metabolome. Untargeted metabolome-wide association study (MWAS) analysis and pathway enrichment analysis using mummichog were performed to identify critical metabolomic features and pathways associated with TRAP exposure., Results: Participants had two to three times higher exposure to traffic-related air pollutants except for fine particulate matter while walking along the road compared with in the park. Compared with the low-TRAP exposure at the park, high-TRAP exposure at the road was associated with a higher score of respiratory symptoms [2.615 (95% CI: 0.605, 4.626), p = 1.2 × 10 - 2 ] and relatively lower lung function indicators [ - 0.075 L (95% CI: - 0.138 , - 0.012 ), p = 2.1 × 10 - 2 ] for FEV 1 and - 0.190 L / s (95% CI: - 0.351 , - 0.029 ; p = 2.4 × 10 - 2 ) for MMEF]. Exposure to TRAP was significantly associated with changes in some, but not all, biomarkers, particularly with a 0.494 -ng / mL (95% CI: 0.297, 0.691; p = 9.5 × 10 - 6 ) increase for serum SP-D and a 0.123 -ng / mL (95% CI: - 0.208 , - 0.037 ; p = 7.2 × 10 - 3 ) decrease for EBC ezrin. Untargeted MWAS analysis revealed that elevated TRAP exposure was significantly associated with perturbations in 23 and 32 metabolic pathways under positive- and negative-ion modes, respectively. These pathways were most related to inflammatory response, oxidative stress, and energy use metabolism., Conclusions: This study suggests that TRAP exposure might lead to lung function impairment and respiratory symptoms. Possible underlying mechanisms include lung epithelial injury, inflammation, oxidative stress, and energy metabolism disorders. https://doi.org/10.1289/EHP11139.

Hourly observations in northern China city of Taiyuan were performed to compare secondary inorganic aerosol (SIA) reaction mechanisms, and emission effects on SIA during the pre-lock and COVID-19 lock days. Emission control implemented and meteorological conditions during lock days both caused beneficial impact on air quality. NO 2 showed the highest decrease ratio of -49.5%, while the relative fraction of NO 3 - in PM 2.5 increased the most (2.7%). Source apportionment revealed the top three contributors to PM 2.5 were secondary formation (SF), coal combustion (CC), and vehicle exhaust (VE) during both pre-lock and lock days. EC lock/pre were all lower than 1, suggesting the overall reduction of primary emissions during lock days, while the higher ratio of (SIA/EC) lock/pre (1.01-1.36) indicated the enhanced secondary formation in lock days. The ratio of SIA of pollution to clean days during lock periods considerably higher by 23.7% compared with that in pre-lock periods, which was indicated SIA secondary formation was more pronounced and contributed great to pollution days in lock periods though secondary formation existed in pre-lock and lock periods. Enhanced secondary formation of NO 3 - and SO 4 2- during lock days might be mainly due to the increased in aqueous and gas-phase reactions, respectively. Except for SF, high contribution of VE and CC were also important for high SIA concentration in pre-lock and lock days, respectively. The decreased contribution of VE weakens its contribution to SIA formation, indicating the effectiveness of VE emission control, as confirmed during the COVID-19 pandemic. This study highlights the aqueous and gas-phase reactions for nitrate and sulfate, respectively, which contributed to heavy pollution, as well as indicated the important role of VE on SIA formation, suggesting the urgent need to further strengthen controls on vehicle emissions., 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.)

Rationale: Air pollution has been linked with sleep disturbance in adults, but the association in children remains unclear. Objectives: To examine the associations of prenatal and postnatal exposure to fine particulate matter (particulate matter ⩽2.5 μm in aerodynamic diameter; PM 2.5 ) with sleep quality and sleep disturbances among children in 551 Chinese cities. Methods: A total of 1,15,023 children aged 3-7 years from the Chinese National Cohort of Motor Development were included. Sleep quality was measured using the Children's Sleep Habits Questionnaire (CSHQ). PM 2.5 exposure was estimated using a satellite-based model. Generalized additive mixed models with Gaussian and binomial distributions were used to examine the associations of PM 2.5 exposure with CSHQ scores and risk of sleep disturbance, respectively, adjusting for demographic characteristics and temporal trends. Measurements and Main Results: Early-life PM 2.5 exposure was associated with higher total CSHQ score, and the association was stronger for exposure at age 0-3 years (change of CSHQ score per interquartile range increase of PM 2.5  = 0.46; 95% confidence interval [CI], 0.29-0.63) than during pregnancy (0.22; 95% CI, 0.12-0.32). The associations were more evident in sleep-disordered breathing and daytime sleepiness. Postnatal PM 2.5 exposure was associated with increased risk of sleep disturbance (adjusted odds ratio for per-interquartile range increase of PM 2.5 exposure at age 0-3 years, 1.10; 95% CI, 1.04-1.15), but no associations were found for prenatal exposure. Children who were exclusively breastfed for <6 months and had neonatal ICU admission may be more vulnerable to sleep disturbance related to PM 2.5 exposure. Conclusions: PM 2.5 exposure can impair sleep quality in preschool children.

Changes in human genome-wide long noncoding RNAs (lncRNAs) associated with air pollution are unknown. This study aimed to investigate the effect of air pollution on human exosomal lncRNAs. A randomized, crossover trial was conducted among 35 healthy adults. Participants were allocated to 4 h exposure in road (high air pollution) and park (low air pollution) sessions in random order with a 2 week washout period. RNA sequencing was performed to measure lncRNAs. Differential lncRNAs were identified using a linear mixed-effect model. Mean concentrations of air pollutants such as ultrafine particles (UFP), black carbon (BC), carbon monoxide (CO), and nitrogen dioxide (NO 2 ) were 2-3 times higher in the road than those in the park. Fifty-five lncRNAs [false discovery rate (FDR) < 0.05] including lncRNA NORAD, MALAT1, and H19 were changed in response to air pollution exposure. We found that 54 lncRNAs were associated with CO, 49 lncRNAs with UFP, 49 lncRNAs with BC, 48 lncRNAs with NO 2 , and 4 lncRNAs with PM 2.5 (FDR < 0.05). These differential lncRNAs participated in dozens of pathways including cardiovascular signaling, epithelial cell proliferation, inflammation, and transforming growth factor. This trial for the first time profiled changes of human exosomal lncRNAs following air pollution. Our findings revealed multiple biological processes moderated by lncRNAs and provided epigenetic insights into cardiovascular effects of air pollution.

Background: The relationships between short-term ozone exposure and the acute exacerbations of asthma in adults have not been fully studied. Existing studies commonly ignored the effects of ozone on mild or early asthma exacerbations., Objective: To investigate the associations between short-term ozone exposure and asthma exacerbations in Chinese adults., Methods: We administered health management for adult asthma patients through the Respiratory Home Platform and required them to monitor their lung function every morning and evening by themselves. Finally, a total of 4,467 patients in 18 Chinese cities were included in the current analyses, with 79,217 pairs of lung function records. The maximum daily 8-h average ozone concentrations were collected from fixed-site air quality monitoring stations. We calculated diurnal peak expiratory flow (PEF) variation using morning and evening measurements of PEF and then defined different severity of asthma exacerbations with diurnal PEF variations >10, 15, and 20%, respectively. A binomial distributed generalized additive mixture model combined with distribution non-linear models was applied to examine the association of ozone with asthma exacerbations. We further conducted stratified analyses by sex, age, season of lung function tests, and region., Measurements and Results: We found that short-term ozone exposure was independently associated with an elevated risk of asthma exacerbations defined by lung function and the effects could last for about 2 days. At lag 0-2 days, each 10 μg/m 3 increment in ozone concentration was associated with odds ratios of 1.010 [95% confidence interval (CI): 1.003, 1.017], 1.014 (95% CI: 1.005, 1.023), and 1.017 (95% CI: 1.006, 1.028) for asthma exacerbations that were defined by diurnal PEF variation over 10, 15, and 20%, respectively. The associations remained significant after adjusting for other pollutants, and became unstable when using 24-h average ozone concentration. We also found that the associations were relatively stronger in males, those aged 45 years and older, and in the warm season., Conclusions: Our results suggest that short-term ozone exposure can increase the risk of asthma exacerbations, even in the early stage of exacerbation. Male and older asthma patients may be more vulnerable to ozone air pollution, especially in the warm season., Competing Interests: SH was employed by Guangzhou Homesun Medical Technology Co. Ltd. The remaining 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 Fang, Huang, Zhu, Lei, Xu, Niu and Chen.)

Exposure to PM 2.5 increases blood pressure (BP) and cardiovascular morbidity and mortality. We conducted a randomized controlled panel study in Shijiazhuang, China among 55 healthy college students randomly assigned to either the control (CON) or SPORTS group with intervention of 2000 m jogging in 20 min for 3 times in 4 days, and 3-round health examinations from November 15, 2020 to December 6, 2020. We aimed to evaluate whether moderate physical activity (PA) protected BP health against PM 2.5 exposure and explore potential mechanisms through myokines and inflammation. Individual PM 2.5 exposure was calculated based on outdoor and indoor PM 2.5 concentration monitoring data as well as time-activity diary of each subject. In the CON group, the exposure-response curve for SBP was linear with a threshold concentration of approximately 31 μg/m 3 , while an increment of SBP level was 4.38 mm Hg (95%CI: 0.17 mm Hg, 8.59 mm Hg) at lag03 for each 10-μg/m 3 increase in PM 2.5 , using linear mixed-effect models. For inflammatory indicators, PM 2.5 exposure was associated with significant increases in eosinophil counts and proportion in CON group, but decreases in MCP-1 and TNF-α in SPORTS group. Meanwhile, higher myokines including CLU and IL-6 were observed in SPORTS group compared to the CON group. Further mediation analyses revealed that eosinophil counts mediated the elevated BP in CON group, whereas MCP-1 and TNF-α were also crucial mediating cytokines for the SPORTS group, as well as CLU and IL-6 acted as mediators on BP and inflammation indicators in SPORTS group. This study suggests that moderate PA could counteract the elevated BP induced by PM 2.5 exposure via myokines-suppressed inflammation pathways., 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.)

This review aimed to systematically summarize the epidemiological literature on the cardiorespiratory effects of PM 2.5 published during the 13 th Five-Year Plan period (2016-2020) in China. Original articles published between January 1, 2016 and June 30, 2021 were searched in PubMed, Web of Science, the China National Knowledge Internet Database and Wanfang Database. Random- or fixed-effects models were used to pool effect estimates where appropriate. Of 8558 records identified, 145 met the full eligibility criteria. A 10 µg/m³ increase in short-term PM 2.5 exposure was significantly associated with increases of 0.70%, 0.86%, 0.38% and 0.96% in cardiovascular mortality, respiratory mortality, cardiovascular morbidity, and respiratory morbidity, respectively. The specific diseases with significant associations included stroke, ischemic heart disease, heart failure, arrhythmia, chronic obstructive pulmonary disease, pneumonia and allergic rhinitis. The pooled estimates per 10 µg/m³ increase in long-term PM 2.5 exposure were 15.1%, 11.9% and 21.0% increases in cardiovascular, stroke and lung cancer mortality, and 17.4%, 11.0% and 4.88% increases in cardiovascular, hypertension and lung cancer incidence respectively. Adverse changes in blood pressure, heart rate variability, systemic inflammation, blood lipids, lung function and airway inflammation were observed for either short-term or long-term PM 2.5 exposure, or both. Collectively, we summarized representative exposure-response relationships between short- and long-term PM 2.5 exposure and a wide range of cardiorespiratory outcomes applicable to China. The magnitudes of estimates were generally smaller in short-term associations and comparable in long-term associations compared with those in developed countries. Our findings are helpful for future standard revisions and policy formulation. There are still some notable gaps that merit further investigation in China., 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. Published by Elsevier B.V.)

Background: Traffic-related air pollution (TRAP) has been associated with changes in gene-specific DNA methylation. However, few studies have investigated impact of TRAP exposure on genome-wide DNA methylation in circulating blood of human., Objective: To explore the association between TRAP exposure and genome-wide DNA methylation., Methods: We conducted a randomized, crossover exposure trial among 35 healthy adults in Shanghai, China. All subjects were randomly allocated to a traffic-free park or a main road for consecutive 4 h, respectively. Blood genome-wide DNA methylation after each exposure session was measured by the Infinium Methylation EPIC BeadChip (850K). The differentially methylated CpGs loci associated with TRAP exposure were identified using linear mixed-effect model., Results: The average concentrations of traffic-related air pollutants including black carbon, ultrafine particles, carbon dioxide, and nitrogen dioxide were 2-3 times higher in the road compared to those in the park. Methylation levels of 68 CpG loci were significantly changed (false discovery rate < 0.05) following TRAP exposure, among which 49 were hypermethylated and 19 were hypomethylated. The annotated genes based on the differential CpGs loci were related to pathways in cardiovascular signaling, cytokine signaling, immune response, nervous system signaling, and metabolism., Conclusions: We found that TRAP exposure was associated with DNA methylation in dozens of genes concerning cardiometabolic health. This trial for the first-time profiled genome-wide methylation changes induced by TRAP exposure using the 850K assay, providing epigenetic insights in understanding the cardiometabolic effects of TRAP exposure., Competing Interests: Declaration of competing interest The authors declared no conflicts of interest., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Despite the adoption of air quality control measures, the influence of regional transport on volatile organic compounds (VOCs) pollution has gradually increased in Beijing. In this study, the whole observation period (September 24 to December 12, 2020) was divided into heating period and non-heating period to explore the impact of changing VOCs sources in different observation periods, and also classified into "Type-N" and "Type-S" periods both in non-heating period and heating period to explore the impact of regional transport from the northern and southern regions of sampling site, respectively. The average VOCs concentrations in northern Beijing during observation period were 22.6 ± 12.6 ppbv, which showed a decrease trend in recent years compared with other studies. And higher VOCs concentrations were observed in Type-S than in Type-N period. The positive matrix factorization results showed that vehicular exhaust dominated VOCs (26.1%-33.7%), but coal combustion could not be ignored in heating period, when it was twice that in non-heating period. In particular, coal combustion dominated VOCs in southern trajectories (30.9%) in heating period. The analysis of concentration weighted trajectory showed that coal combustion was affected by regional transport from the southeast regions of Beijing, while vehicular exhaust was affected by urban and the southeast regions of Beijing. Regarding human health risks, the carcinogenic risks of benzene and ethylbenzene exceeded the acceptable cancer risk value (1 × 10 -6 ), and were higher in Type-S than in Type-N period. The results indicated that regional transport from urban areas and the areas south of Beijing had a significant impact on VOCs in northern Beijing. Thus, targeted control measures for different potential pollution regions are important for controlling VOCs pollution in Beijing., 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.)

A system-wide cardiovascular response to traffic-related air pollution (TRAP) has been rarely described. To systemically understand the mechanisms underlying cardiovascular effects of TRAP, we conducted a randomized, crossover trial in 56 young adults, who engaged in two 4-hour exposure sessions on a main road and in a park, alternately. We measured personal exposures to traffic-related air pollutants (TRAPs), including fine and ultrafine particulate matter, black carbon, nitrogen dioxide, and carbon monoxide. Lipidomics, targeted proteomics, urine metabolomics, targeted biomarkers, ambulatory blood pressure and electrocardiogram were measured. We used linear mixed-effects models to estimate the associations. The exposures to TRAPs except for fine particulate matter in the road session were 2-3 times higher. We observed elevated blood pressure and decreased heart rate variability (HRV) after TRAP exposure, accompanied by dozens of molecular alterations involving systemic inflammation, oxidative stress, endothelial dysfunction, coagulation, and lipid metabolism. Pathways like vascular smooth muscle cell proliferation and biomarkers like trimethylamine N-Oxide might also be disturbed. Some of these TRAP-related molecular biomarkers were also associated with changes of blood pressure or HRV. Our results provided systematical mechanistic profiling for the cardiovascular effects of TRAP using multi omics, which may have implications in TRAP control., (Copyright © 2022 Elsevier B.V. All rights reserved.)

The Diverse Life-Course Cohort (DLCC) is a large-scale prospective study including around 130,000 participants in mainland China. The primary aims of DLCC include contributing to knowledge on noncommunicable chronic disease determinants, particularly cardiometabolic diseases, and exploring the long-term effect of ambient air pollutants or other environmental risk factors on health among all-age populations. The cohort consists of several sub-populations that cover the whole life-course and diverse resources: from premarital to adolescents, adults from workplace and communities ranged from 18 to 93 years old. Baseline assessment (2017-2021) included face-to-face standardized questionnaire interview and measurements to assess social and biological factors of health. Blood samples were collected from each participant (except for children younger than 6) to establish the biobank. DLCC consists of two visits. Visit 1 was conducted from 2017, and 114850 individuals from one of the world-class urban agglomerations: Beijing, Tianjin, and Hebei area were recruited. By the end of 2021, at least one follow-up was carried out, with an overall follow-up rate of 92.33%. In 2021, we initiated Visit 2, newly recruited 9,866 adults from Guangdong province (South China) and Hebei province (Central China), with research focuses on the comparations on ambient pollution hazards and other unique dietary or environmental risks for health. The baseline survey of Visit 2 was finished in July 2021. DLCC is still ongoing with a long-term follow-up design, and not limited by the current funding period. With reliable data and the well-established biobank which consists of over 120,000 individuals' blood samples, DLCC will provide invaluable resources for scientific research., (© 2022. The Author(s).)

Both long-term exposure to air pollution and abnormal fasting blood glucose (FBG) are linked to dyslipidemia prevalence. However, the joint role of air pollution and FBG on dyslipidemia remains unknown clearly. In this study, we aimed to test whether abnormal FBG could enhance the risks of long-term exposure to air pollutants on dyslipidemia in general Chinese adult population. The present study recruited 8917 participants from 4 cities in Hebei province, China. Participants' individual exposure to air pollutants was evaluated by the Empirical Bayesian Kriging statistical model in ArcGIS10.2 geographic information system. Dyslipidemia was defined according to Guidelines for the Prevention and Treatment of Dyslipidemia in Chinese Adults. Subjects were grouped into normal, prediabetes, diabetes according to FBG level. Generalized linear models were applied to analyze the interaction of air pollutants and FBG on dyslipidemia prevalence. The prevalence of dyslipidemia was 43.83% in our investigation. After adjusting all covariates, we found the risk of four air pollutants (PM 2.5 , PM 10 , NO 2 , SO 2 ) on dyslipidemia prevalence was stronger as higher FBG level, and the adjusted odd ratio of interaction (OR inter (95% CI)) between PM 2.5 , PM 10 , NO 2 , SO 2 and FBG levels on dyslipidemia was 1.171 (1.162, 1.189), 1.119 (1.111, 1.127), 1.124 (1.115, 1.130), 1.107 (1.098, 1.115), respectively. Stratified analyses indicated the modifying effects of FBG on the association of air pollution with dyslipidemia were stronger among male, less than 65 years old, overweight/obesity (all P inter <0.1). Our study concluded that high FBG levels strengthened the risk of long-term exposure to air pollution on dyslipidemia, especially more noticeable in male, less than 65 years old, overweight., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Epidemiological studies have associated ozone exposure with cardiovascular diseases, but the molecular mechanisms were not elucidated. We performed an untargeted serum proteomic analysis in a randomized, crossover, controlled exposure trial. We recruited 32 healthy young adults and asked them to receive filtered air and 200-ppb ozone exposures for 2 h in a random order before serum collection. Linear mixed-effect models were used to identify differentially expressed proteins (DEPs) between the two exposures and Gene Ontology enrichment and ingenuity pathway analysis were performed to determine their biological function. A total of 56 DEPs were identified. For example, acute ozone exposure increased coagulation factor X and factor VII-activating protease by 20.96% and 28.35%, respectively. Whereas, protein Z, protein Z-dependent protease inhibitor, and plasminogen decreased by 13.62%, 33.54%, and 10.47%, respectively. We also observed a 42.32% decrease in paraoxonase 3 and evident changes in four apolipoproteins. Additionally, we found 18.21% and 95.82% increases in L-selectin and β2-microglobulin, respectively, and significant changes in three complements. DEPs and enriched pathways suggest that short-term ozone exposure may promote coagulation, suppress fibrinolysis, disrupt lipoprotein metabolism, activate immune responses, and affect the complement system. These findings provide additional insights into the mechanisms linking acute ozone exposure to thrombosis., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Aims: Although previous studies have linked short-term exposure to fine particulate matter (PM 2.5 ) air pollution with various molecular biomarkers of cardiovascular system, limited evidence is available for indicators at clinical or subclinical levels. We examined the associations between short-term PM 2.5 exposure and a range of clinical or subclinical indicators of cardiovascular health in general population., Methods and Results: A longitudinal repeated-measure study was conducted among 247,640 participants who repeatedly visited health examination centers in 15 typical cities across China from 2013 to 2020. A total of 19 well-established indicators of cardiovascular risk or injury were evaluated and air quality data at nearest fixed-site monitors were collected. Linear mixed-effects models with distributed lag models were used to analyze the potentially lagged effects of PM 2.5 . The average daily PM 2.5 concentration was 48 μg/m 3 during the study period. PM 2.5 exposure was associated with significant changes of 16 indicators with the effects generally peaked on lag 0 to 3 day. For an interquartile range (IQR) elevation (37 μg/m 3 ) in PM 2.5 concentrations over lag 0-7 day, the cumulative percentage changes were 0.50% to 1.27% in heart rates and blood pressure, 0.10% to 5.04% in inflammatory markers, -0.29% to 1.39% in blood viscosity parameters, -0.67% to 3.45% in blood lipids, 0.89% in blood homocysteine, 0.13% to 0.78% in myocardial enzymes, and 3.03% in pulse wave velocity. These associations were not substantially changed after adjusting concomitant exposures to gaseous pollutants., Conclusion: Short-term exposure to PM 2.5 may induce early cardiovascular effects in general population, including acute inflammation, myocardial injury, increased blood viscosity, vascular stiffness and hyperlipidemia., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Rationale: Transcriptome-wide analysis is powerful in studying systemic RNA changes following environmental exposures. However, impacts of ozone inhalation on circulating transcriptome have not yet been examined., Objectives: To explore the impact of acute ozone exposure on circulating transcriptome using RNA sequencing (RNA-seq)., Methods: We recruited 32 healthy young adults in a randomized, crossover, controlled exposure trial. Each participant completed two 2-h exposure sessions of ozone (200 ppb) and clean air, respectively. Blood samples were collected at the end of each session and were used for RNA-seq. The differentially expressed genes associated with ozone exposure were assessed using Bayesian adjusted statistics from linear models in the limma R package., Results: A total of 29 participants finished this trial and donated their blood samples for transcriptome analysis. The average concentration of ozone was 7.8 ± 2.6 ppb under clean air and 201.1 ± 1.7 ppb under ozone exposure session. A total of 1899 genes were significantly changed (1067 up-regulated and 832 down-regulated) by ozone exposure at a false discovery rate < 0.05, in which 403 genes had a fold change of > 1.2 or < 0.8. The top 10 terms of biological processes showed that most of the differentially expressed genes were related to various functions, such as neutrophil degranulation, immune response, and neutrophil activation. Pathway enrichment analysis showed dozens of pathways were dysregulated after ozone exposure, including mitochondrial dysfunction, and glucocorticoid receptor signaling., Conclusion: For the first time this trial characterized the genome-wide changes of mRNA in response to ozone exposure. We identified a range of differentially expressed genes that were involved in dozens of biological processes and pathways, providing novel biological insights into the systemic health effects of ozone., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Congenital anomalies (CAs) are the leading causes for children's disabilities and mortalities worldwide. The associations between air pollution and CAs are not fully characterized in fetuses born by in vitro fertilization (IVF) who are at high risk of congenital anomalies., Methods: We conducted a cross-sectional study including 16,971 IVF cycles from three hospitals in Hebei Province, China, 2014-2019. Air quality data was obtained from 149 air monitoring stations. Individual average daily concentrations of PM 2.5 , PM 10 , NO 2 , SO 2 , CO, and O 3 were estimated by spatiotemporal kriging method. Exposure windows were divided into 5: preantral follicle period, antral follicle period, germinal period, embryonic period and early fetal period. Logistic generalized estimating equations were used to estimate the associations between air pollutants and overall or organ-system specific congenital anomalies. Negative control exposure method was used to detect and reduce bias of estimation., Results: We found increasing levels of PM 2.5 and PM 10 were associated with higher risk of overall congenital anomalies during early fetal period, equating gestation 10-12 weeks (OR: 1.05, 95% CI: 1.02-1.09, p = 0.013 for a 10 μg/m 3 increase of PM 2.5 ; OR: 1.03, 95% CI: 1.01-1.06, p = 0.021 for a 10 μg/m 3 increase of PM 10 ). Cleft lip and cleft palate were associated with PM 10 in germinal period and early fetal period. The CAs of eye, ear, face and neck were related to CO in preantral follicle stage. We did not find an association between chromosome abnormalities and air pollution exposure., Conclusions: We concluded that ambient air pollution was a risk factor for congenital anomalies in the fetuses conceived through IVF, especially exposure in early fetal period., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Government management is the main tool to solve environmental pollution. Considering the unique fiscal decentralization institution in China, this paper investigates the effect of foreign direct investment (FDI) on urban haze pollution in China from the perspective of spatial econometrics. The Generalized Spatial Two Stage Least Squares (GS2SLS) method is employed to treat the spatial correlation of air pollution. Based on a panel dataset comprising 276 Chinese cities during 2004-2018, we find a positive effect of FDI on urban haze pollution. For one standard deviation increase in FDI, the average annual PM2.5 concentration increase by 1.5%, ceteris paribus. Evidence also suggests that this effect varies across regions with different levels of fiscal decentralization. Through the test of the moderating effect and the threshold effect, we found that the higher of the fiscal decentralization, the weaker of the impact of FDI on haze pollution. This study proposes a new solution for sustainable development: increasing the financial autonomy of local governments to restrain the attraction of non-cleaner investment., (Copyright © 2021. Published by Elsevier Ltd.)

Rationale: It remains unknown whether long-term ozone exposure can impair lung function. Objectives: To investigate the associations between long-term ozone exposure and adult lung function in China. Methods: Lung function results and diagnosis of small airway dysfunction (SAD) were collected from a cross-sectional study, the China Pulmonary Health Study ( N  = 50,991). We used multivariable linear and logistic regression models to examine the associations of long-term ozone exposure with lung function parameters and SAD, respectively, adjusting for demographic characteristics, individual risk factors, and longitudinal trends. We then performed a stratification analysis by chronic obstructive pulmonary disease (COPD). Measurements and Main Results: We observed that each 1 SD (4.9 ppb) increase in warm-season ozone concentrations was associated with a 14.2 ml/s (95% confidence interval [CI], 8.8-19.6 ml/s] decrease in forced expiratory flow at the 75th percentile of vital capacity and a 29.5 ml/s (95% CI, 19.6-39.5 ml/s) decrease in mean forced expiratory flow between the 25th and 75th percentile of vital capacity. The odds ratio of SAD was 1.09 (95% CI, 1.06-1.11) for a 1 SD increase in warm-season ozone concentrations. Meanwhile, we observed a significant association with decreased FEV 1 /FVC but not with FEV 1 or FVC. The association estimates were greater in the COPD group than in the non-COPD group. Conclusions: We found independent associations of long-term ozone exposure with impaired small airway function and higher SAD risks, while the associations with airflow obstruction were weak. Patients with COPD appear to be more vulnerable.

The biological mechanism of adverse health outcomes related to exposure to traffic-related air pollution (TRAP) needs elucidation. We conducted a randomized, crossover trial among healthy young students in Shanghai, China. Participants wore earplugs and were randomly assigned to a 4-hour walking treatment either along a traffic-polluted road or through a traffic-free park. We conducted untargeted analyses of plasma exosome transcriptomics, serum mass spectrometry-based proteomics, and serum metabolomics to evaluate changes in genome-wide transcription, protein, and metabolite profiles in 35 randomly selected participants. Mean personal exposure levels of ultrafine particles, black carbon, nitrogen dioxide, and carbon monoxide in the road were 2-3 times higher than that in the park. We observed 3449 exosome mRNAs, 58 serum proteins, and 128 serum metabolites that were significantly associated with TRAP. The multi-omics analysis showed dozens of regulatory pathways altered in response to TRAP, such as inflammation, oxidative stress, coagulation, endothelin-1 signaling, and renin-angiotensin signaling. We found that several novel pathways activated in response to TRAP exposure: growth hormone signaling, adrenomedullin signaling, and arachidonic acid metabolism. Our study served as a demonstration and proof of concept on the evidence that associated TRAP exposure with global molecular changes based on the multi-omics level., (Copyright © 2021 Elsevier B.V. All rights reserved.)

The biological mechanisms underlying the associations between atmospheric ozone exposure and adverse cardiometabolic outcomes are yet to be identified. Imbalanced autonomic nervous system (ANS) as well as activations of the sympatho-adrenomedullary (SAM) and hypothalamic-pituitary-adrenal (HPA) axes are among possible early biological responses triggered by ozone, and may eventually lead to cardiometabolic abnormalities. To determine whether acute ozone exposure causes ANS imbalance and increases the secretion of neuroendocrine stress hormones, we conducted a randomized, double-blind, crossover trial, under controlled 2-hour exposure to either ozone (200 ppb) or clean air with intermittent exercise among 22 healthy young adults. Here we found that, compared to clean air exposure, acute ozone exposure significantly decreased the high-frequency band of heart rate variability, even after adjusting for heart rate and pre-exposure to ambient air pollutants and meteorological factors. Ozone exposure also significantly increased the serum levels of stress hormones, including corticotrophin-releasing factor, adrenocorticotropic hormone, adrenaline, and noradrenaline. Metabolomics analysis showed that acute ozone exposure led to alterations in stress hormones, systemic inflammation, oxidative stress, and energy metabolism. Our results suggest that acute ozone exposure may trigger ANS imbalance and activate the HPA and SAM axes, offering potential biological explanations for the adverse cardiometabolic effects following acute ozone exposure., (Copyright © 2021 Elsevier B.V. All rights reserved.)

A few studies on volatile organic compound (VOC) emission inventories in coal resource-based cities have been reported, and previous emission inventories lacked verification. Herein, using Yangquan as a case study, emission factor (EF) method and "(tracer ratio) TR - positive matrix factorization (PMF)" combined method based on atmospheric data were used to establish and verify the VOC emission inventory in coal resource-based cities, respectively. The total VOC emissions in Yangquan were 9283.2 t [-40.0%, 62.1%] in 2018, with industrial processes being the major contributors. Alkanes (35.8%), aromatics (25.0%), and alkenes (19.8%) were the main compounds in the emission inventory. The verification results for both species emission and source structure were in agreement, indicating the accuracy of VOC emission inventory based on EF method to a certain extent. However, for some species (ethane, propane, benzene, and acetylene), the EF method indicated emissions lower than those obtained from the TR results. Furthermore, the summer-time emission contribution from fossil fuel combustion indicated by the EF method (23.4%) was lower than that obtained from the PMF results (38.4%). Overall, these discrepancies could be attributed to the absence of a coal gangue source in the EF method. The verification results determined the accuracy of the VOC emission inventory and identified existing problems in the estimation of the VOC emission inventory in coal resource-based cities. In particular, not accounting for the coal gangue emissions may result in an underestimation of VOC emissions in coal resource-based cities. Thus, coal gangue emissions should be considered in future research., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

It remains unclear whether carbon content in airway macrophages (AM) can predict personal short-term exposure to fine particulate matter (PM 2.5 ) air pollution and its respiratory health effects. We aimed to evaluate the pathway from personal PM 2.5 exposure to adverse respiratory outcomes through AM carbon content. We designed a longitudinal panel study with 3 scheduled follow-ups among 113 non-smoking patients of chronic obstructive pulmonary disease in Shanghai, China, from April 2017 to January 2019. We quantified AM carbon content from induced sputum by image analysis, tested lung function and measured sputum levels of 4 pro-inflammatory cytokines and 2 anti-inflammatory cytokines. We applied the "meet in the middle" approach incorporating linear mixed-effect models to evaluate the associations from external PM 2.5 exposure to respiratory outcomes through AM carbon content. Our results indicated that personal exposure to PM 2.5 within 24 h was significantly associated with decreased forced expiratory volume in 1s and anti-inflammatory cytokines, as well as increased macrophages and pro-inflammatory cytokines. These changes were accompanied by increased areas of AM carbon and higher percentage of AM area occupied by carbon, both of which were associated with increased levels of pro-inflammatory cytokines and decreased levels of anti-inflammatory cytokines. Exposure to ambient black carbon and organic carbon in PM 2.5 within 2 days was significantly associated with increased AM carbon area and percentage of AM area occupied by carbon. Our findings reinforced the causality in respiratory health effects of PM 2.5 in which increased AM carbon content might serve as a valid exposure biomarker., (Copyright © 2021. Published by Elsevier Ltd.)

Although the association between ambient particulate matter and metabolic syndrome (MetS) has been investigated, the effect of particulate matter (PM) on MetS is inconclusive. We conducted a systematic review and meta-analysis to study the association between long-term ambient PM exposure and MetS risk. The data from five databases were extracted to analyze the association between ambient PM exposure and MetS risk. A random-effects model was performed to estimate the overall risk effect. The present systematic review and meta-analysis illustrated that an increase of 5 μg/m 3 in annual PM 2.5 or PM 10 concentration was associated with 14% or 9% increases of MetS risk, respectively (PM 2.5 , RR = 1.14, 95%CI [1.03, 1.25]; PM 10 , RR = 1.09, 95%CI [1.00, 1.19]). The population-attributable risk (PAR) was 12.28% for PM 2.5 exposure or 8.26% for PM 10 exposure, respectively. There was statistical association between PM 2.5 exposure and risk of MetS in male proportion ≥50%, Asia, related disease or medication non-adjustment subgroup as well as cohort study subgroups, respectively. The significant association between PM 10 exposure and risk of MetS was observed in male proportion ≥50% and calories intake adjustment subgroups, respectively. Sensitivity analyses showed the robustness of our results. No publication bias was detected. In conclusion, there was positive association between long-term PM exposure and MetS risk. 12.28% of MetS risk could be attributable to 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 © 2021 Elsevier B.V. All rights reserved.)

Background: Previous studies have suggested acute effects of ambient fine particulate matter (PM 2.5 ) air pollution on respiratory health among children, but evidence for PM 2.5 constituents and respiratory health were still limited., Objectives: To investigate associations of short-term exposure to PM 2.5 and its constituents with airway inflammation, lung function, and airway microbiota in children., Methods: We conducted a longitudinal panel study with 3 repeated health measurements among 62 children in Shanghai, China from November 2018 to June 2019. Respiratory health was measured by fractional exhaled nitric oxide (FeNO), saliva tumor necrosis factor-α (TNF-α), lung function (forced vital capacity and forced exhaled volume in 1 s), and microbiota diversity in buccal mucosa samples. Based on the linear mixed-effect models, we applied the single-constituent models and the constituent-PM 2.5 adjustment models to examine the associations between PM 2.5 constituents and health outcomes., Result: Short-term exposure to PM 2.5 was associated with higher TNF-α, FeNO levels and reduced lung function. Among all constituents, organic carbon, elemental carbon, NO 3 - and NH 4 + had the consistent and strongest associations with airway inflammation biomarkers and lung function parameters, followed by metallic elements. We also found short-term PM 2.5 exposure was associated with decreased diversity in buccal mucosa bacterial community and two bacterial phyla, Fusobacteria and Proteobacteria, were identified as differential microbes with PM 2.5 exposure., Conclusion: Short-term exposure to PM 2.5 may impair children's respiratory health represented by higher airway inflammation, lower lung function and altered buccal mucosa microbial colonization. Organic carbon, elemental carbon, NO 3 - and NH 4 + may dominate these effects., Competing Interests: Declaration of competing interest The authors declared no conflicts of interests., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: Exposure to fine particulate matter (PM 2.5 ) has been linked with adverse cardiorespiratory health conditions. However, evidence for PM 2.5 constituents is still scarce, especially among patients with chronic obstructive pulmonary disease (COPD)., Objective: To investigate the associations of short-term exposure to different chemical constituents of PM 2.5 with measures of cardiac and lung function in COPD patients., Methods: We conducted a retrospective panel study among 100 COPD patients who received repeated measures of left ventricular ejection fraction (LVEF), forced expiratory volume in 1 s (FEV 1 ), forced vital capacity (FVC) and peak expiratory flow (PEF) in Shanghai, China from August 2014 to September 2019. Daily PM 2.5 and PM 2.5 constituents were obtained from fixed-site monitoring station. Linear mixed-effects models were used to estimate the associations of PM 2.5 ., Results: We found water-soluble ions of PM 2.5 , mainly NO 3 - , SO 4 2- , and NH 4 + were robustly associated with reduced LVEF, and the reductions in LVEF associated with an IQR increase of them ranged from 1.8% to 2.0% (lag 1 d). Metal constituents such as Cu and As were associated with FEV 1 , FVC and PEF. The corresponding reductions in lung function parameters for an IQR increase of them ranged from 1.4% to 2.3% (lag 0 or 1 d). These associations remained relatively robust after adjusting for total PM 2.5 mass and gaseous pollutants., Conclusions: Our results suggest that water-soluble ions and several metal/metalloid elements might be important constituents in PM 2.5 that were associated with reduced cardiorespiratory function among COPD patients., 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 © 2021 Elsevier B.V. All rights reserved.)

Evidences on the association of air pollutants and semen quality were limited and mechanism-based biomarkers were sparse. We enrolled 423 men at a fertility clinic in Shijiazhuang, China to evaluate associations between air pollutants and semen quality parameters including the conventional ones, sperm mitochondrial DNA copy number (mtDNAcn), sperm telomere length (STL) and seminal spermatogenic cells. PM 2.5 , PM 10 , CO, SO 2 , NO 2 and O 3 exposure during lag0-90, lag0-9, lag10-14 and lag70-90 days were evaluated with ordinary Kringing model. The exposure-response correlations were analyzed with multiple linear regression models. CO, PM 2.5 and PM 10 were adversely associated with conventional semen parameters including sperm count, motility and morphology. Besides, CO was positively associated with seminal primary spermatocyte (lag70-90, 0.49; 0.14, 0.85) and mtDNAcn (lag0-90, 0.37; 0.12, 0.62, lag10-14, 0.31; 0.12, 0.49), negatively associated with STL (lag0-9, -0.30; -0.57, -0.03). PM 2.5 was positively associated with mtDNAcn (0.50; 0.24, 0.75 and 0.38; 0.02, 0.75 for lag0-90 and lag70-90) while negatively associated with STL (lag70-90, -0.49; -0.96, -0.01). PM 10 and NO 2 were positively associated with mtDNAcn. Our findings indicate CO and PM might impair semen quality testicularly and post-testicularly while seminal spermatogenic cell, STL and mtDNAcn change indicate necessity for more attention on these mechanisms., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background: Exposure to fine particulate matter (with an aerodynamic diameter ≤ 2·5 μm, PM 2·5 ) air pollution has been associated with skin-related diseases or disorders., Objectives: To evaluate the potential skin-protective effects of fish-oil supplementation against PM 2·5 exposure., Materials and Methods: This is an exploratory analysis based on a pilot randomized, double-blind, placebo-controlled trial among 65 healthy young adults between September 2017 and January 2018 in Shanghai, China. We randomly assigned participants to take either fish oil or placebo 2·5 g daily for four consecutive months. Four rounds of skin D-Squame ® tape samples were collected in the last 2 months, and five secondary biomarkers of skin inflammation and oxidative stress were measured. Fixed-site PM 2·5 concentrations on campus were measured in real time. We used linear mixed-effect models to analyse the associations between short-term PM 2·5 exposure and biomarkers in each group., Results: The 24-h average PM 2·5 concentration was 34·68 ± 15·83 μg m -3 . There were generally weaker associations between PM 2·5 and biomarkers in the fish-oil group than in the placebo group, but the associations and the between-group differences varied by biomarkers and lag periods. Compared with the placebo group, for a 10-μg m -3 increase in PM 2·5 concentration, the increments of interleukin-1α and carbonyl protein in the fish-oil group were 41·55% smaller [95% confidence interval (CI) 4·61-78·48%] at lag 0-48 h and 22·01% smaller (95% CI 11·25-32·77%) at lag 0-24 h, respectively. No significant between-group differences were observed for other biomarkers., Conclusions: This study suggested that dietary fish-oil supplementation may improve biomarkers of skin inflammation and oxidative-stress response to short-term PM 2·5 exposure., (© 2020 British Association of Dermatologists.)

Maternal exposure to air pollution is associated with poor reproductive outcomes in in vitro fertilization (IVF). However, the susceptible time windows are still not been known clearly. In the present study, we linked the air pollution data with the information of 9001 women receiving 10,467 transfer cycles from August 2014 to August 2019 in The Second Hospital of Hebei Medical University, Shijiazhuang City, China. Maternal exposure was presented as individual average daily concentrations of PM 2.5 , PM 10 , NO 2 , SO 2 , CO, and O 3, which were predicted by spatiotemporal kriging model based on residential addresses. Exposure windows were divided to five periods according to the process of follicular and embryonic development in IVF. Generalized estimating equation model was used to evaluate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for association between clinical pregnancy and interquartile range increased average daily concentrations of pollutants during each exposure period. The increased PM 2.5 (adjusted OR = 0.95, 95% CI: 0.90, 0.99), PM 10 (adjusted OR = 0.93, 95% CI: 0.89, 0.98), NO 2 (adjusted OR = 0.89, 95% CI: 0.85, 0.94), SO 2 (OR = 0.94, 95% CI: 0.90, 0.98), CO (adjusted OR = 0.93, 95% CI: 0.89, 0.97) whereas decreased O 3 (OR = 1.08, 95% CI: 1.02, 1.14) during the duration from preantral follicles to antral follicles were the strongest association with decreased probability of clinical pregnancy among the five periods. Especially, women aged 20-29 years old were more susceptible in preantral-antral follicle transition stage. Women aged 36-47 years old were more vulnerable during post-oocyte retrieve period. Our results suggested air pollution exposure during preantral-antral follicle transition stage was a note-worthy challenge to conceive among females receiving IVF., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Sulfur dioxide (SO 2 ) is a common exogenous atmospheric pollutant. Studies have shown that SO 2 can cause vasodilation as a gas signaling molecule, but the specific signaling pathways are not well understood. This study aimed to explore the underlying mechanism behind the effects of SO 2 on vasodilation of isolated rat aorta. The results showed that when the dose of SO 2 was 30 μM, the vasodilation of endothelium-intact rings was partially suppressed by LY294002 and N G -nitro-l-arginine methyl ester, and the protein levels of phosphoinositide 3-kinase (PI3K), p-Akt, and p -endothelial nitric oxide synthase ( p -eNOS) were significantly increased. When the dose of SO 2 was 300 μM or 1500 μM, the vasodilation of endothelium-denuded rings did not change after application of the inhibitor, but the protein levels of PI3K, p-Akt, and p-eNOS were significantly decreased, and the activity of NOS and the level of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) were significantly increased. We speculate that the mechanism of SO 2 -induced vasodilatation likely involved the endothelial PI3K/Akt/eNOS and NO/cGMP signal pathways. In addition, at the concentration of 1500 μM, SO 2 markedly increased the level of caspase-3 and caspase-9. The results suggest that high concentrations of SO 2 may cause damage to blood vessels. This study will help to further inform the etiologies of SO 2 -related cardiovascular disease.

Limited studies have been conducted to evaluate the short-term relationships between exposure to coarse particulate matter (PM 2.5-10 ) and outpatient visits in China. We designed this time-series analysis in a Chinese city Yancheng, to explore the relationship of PM 2.5-10 with outpatient visits for cardiopulmonary diseases. The study period was from 2013 to 2015. A typical generalized additive model was used. We explored the lag patterns by building a series of lag of exposure. We also built two-pollutant models to ascertain the independence of PM 2.5-10 . Stratified analyses were applied to compare the season-specific associations. Finally, we pooled the concentration-response (C-R) curves for PM 2.5-10 and outpatient visits. We recorded a daily average of 85 and 43 outpatient visits for cardiovascular and respiratory causes, respectively. PM 2.5-10 exposures of lag 05 day yielded the best estimates for both outcomes. Per 10-μg/m 3 increase in PM 2.5-10 , there was a 1.69% (95% confidence interval [CI]: 0.68%-2.72%) increase in outpatient visits for respiratory causes, and a 0.85% (95% CI: 0.13%-1.57%) increase for cardiovascular causes. The association kept robust after adjusting for PM 2.5 and O 3 , and there were larger associations in warm seasons. The C-R curves had a larger slope for respiratory diseases in relatively lower concentrations (<30 μg/m 3 ), and PM 2.5-10 was positively associated with cardiovascular diseases in higher concentrations (>30 μg/m 3 ). This study indicated significant associations of PM 2.5-10 with cardiopulmonary outpatient visit. Such results may be used for health risk assessment and policy making for particulate air pollution control., 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 Inc. All rights reserved.)

Background: Caloric restriction (CR) is known to improve health and extend lifespan in human beings. The effects of CR on adverse health outcomes in response to particulate matter (PM) exposure and the underlying mechanisms have yet to be defined., Results: Male C57BL/6 J mice were fed with a CR diet or ad libitum (AL) and exposed to PM for 4 weeks in a real-ambient PM exposure system located at Shijiazhuang, China, with a daily mean concentration (95.77 μg/m 3 ) of PM 2.5 . Compared to AL-fed mice, CR-fed mice showed attenuated PM-induced pulmonary injury and extra-pulmonary toxicity characterized by reduction in oxidative stress, DNA damage and inflammation. RNA sequence analysis revealed that several pulmonary pathways that were involved in production of reactive oxygen species (ROS), cytokine production, and inflammatory cell activation were inactivated, while those mediating antioxidant generation and DNA repair were activated in CR-fed mice upon PM exposure. In addition, transcriptome analysis of murine livers revealed that CR led to induction of xenobiotic metabolism and detoxification pathways, corroborated by increased levels of urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and decreased cytotoxicity measured in an ex vivo assay., Conclusion: These novel results demonstrate, for the first time, that CR in mice confers resistance against pulmonary injuries and extra-pulmonary toxicity induced by PM exposure. CR led to activation of xenobiotic metabolism and enhanced detoxification of PM-bound chemicals. These findings provide evidence that dietary intervention may afford therapeutic means to reduce the health risk associated with PM exposure.

Background: Pregnancy complications, such as gestational diabetes mellitus (GDM) and hypertensive disorders of pregnancy (HDP), have a great impact on public health. Exposure to ambient air pollution during pregnancy may cause pregnancy complications. The aim of our study is to explore the risk of trimester-specific maternal exposure to air pollutants on complications of pregnancy., Methods: PubMed, EMBASE, Web of Science, and Cochrane were systematically searched for cohort studies published before October 27, 2019 which reported the association between ambient air pollutants (PM 2.5 , PM 10 , CO, NO, NO 2 , NO x , O 3 , and SO 2 ) and pregnancy complications (GDM, HDP, preeclampsia, and gestational hypertension) during different exposure windows. A meta-analysis was applied to combine relative risks (RRs) and their confidence intervals (CIs) from eligible studies. Quality assessment was conducted and Egger test was used to evaluate the publication bias. All statistical analyses were performed by STATA software (Version 15, StataCorp, College Station, Texas, USA)., Results: This meta-analysis consisted of 33 cohort studies conducted on 22,253,277 pregnant women. Meta-analyses showed during the first trimester, there were significant associations of PM 10 with gestational hypertension (RR = 1.07, 95% CI: 1.02-1.12 per 10 μg/m 3 , I 2  = 0.0%), of SO 2 with GDM (RR = 1.04, 95% CI: 1.00-1.08 per 1 ppb increment, I 2  = 54.1%), of PM 2.5 with preeclampsia (RR = 0.97, 95% CI: 0.95-1.00 per 5 μg/m 3 , I 2  = 4.1%). During the entire pregnancy, PM 2.5 significantly increased the risk of hypertensive disorders of pregnancy (RR = 1.18, 95% CI: 1.02-1.34 per 5 μg/m 3 , I 2  = 85.1%). Egger test indicated that wide-scale publication bias was unlikely., Conclusion: Maternal exposure to ambient air pollutants is associated with pregnancy complications especially during the first trimester. Further large multicenter cohort studies considering different constituents of pollutants, levels of disease severity, sensitive populations, and various exposure windows are warranted in the future research., Competing Interests: Declaration of competing interest We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted., (Copyright © 2020 Elsevier Inc. All rights reserved.)

The determination of PM 2.5 -induced biological response is essential for understanding the adverse health risk associated with PM 2.5 exposure. In this study, we conducted cell-based bioassays to measure the toxic effects of PM 2.5 exposure, including cytotoxicity, oxidative stress, genotoxicity and inflammatory response. The concentration-response relationship was analyzed by benchmark dose (BMD) modeling and the BMDL 10 was used to estimate the biological potency of PM 2.5 exposure. PM 2.5 samples were collected from three typical megacities of China (Beijing, BJ; Wuhan, WH; Guangzhou, GZ) in typical seasons (winter and summer). The total PM, water-soluble fractions (WSF), and organic extracts (OE) were prepared and subjected to examination of toxic effects. The biological potencies for cytotoxicity, oxidative stress and genotoxicity were generally higher in winter samples, while the inflammatory potency of PM 2.5 was higher in summer samples. The relative health risk (RHR) was determined by integration of the biological potencies and the cumulative exposure level, and the ranks of RHR were BJ-W > WH-W > BJ-S > WH-S > GZ-W > GZ-S. Notably, we note that different PM 2.5 compositions were associated with distinct biological effects, and the health effects distribution of PM 2.5 varied in regions and seasons. These findings demonstrate that the approach of integrated cell-based bioassays could be used for the evaluation of health effects of 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 © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Many studies have reported that air pollution, especially fine particulate matter (PM 2.5 ), has a significant impact on health and causes economic loss. Gansu Province is in the northwest of China, which is a typical economically underdeveloped area. However, few studies have evaluated the economic loss of PM 2.5 related to health effects in this province. In this study, a log-linear exposure-response function was used to estimate the health impact of PM 2.5 in 14 cities in Gansu Province from 2015 to 2017, and the amended human capital (AHC) and cost of illness (COI) method were used to evaluate the related economic loss caused by the health impact from PM 2.5 . The results show that the estimated total number of health endpoints attributed to PM 2.5 pollution were 1,644,870 (95%CI: 978,484-2,215,921), 1,551,447 (95%CI: 917,025-2,099,182) and 1,531,372 (95%CI: 899,769-2,077,772) in Gansu Province from 2015 to 2017, respectively. Correspondingly, the economic losses related to health damage caused by PM 2.5 pollution were 42,699 (95%CI: 32,380-50,768) million Chinese Yuan (CNY), 43,982 (95%CI: 33,305-52,386) million CNY and 44,261 (95%CI: 33,306-52,954) million CNY, which were equivalent to 6.45% (95%CI: 4.89%-7.67%), 6.28% (95%CI: 4.75%-7.48%), and 5.93% (95%CI: 4.64%-7.10%) of the region Gross Domestic Product (GDP) from 2015 to 2017, respectively. It could be seen that the proportions of health economic loss to GDP were generally high, although the proportion had a slight downward trend. The economic loss from chronic bronchitis and all-cause mortality accounted for more than 94% of the total economic loss. The health impact, economic loss and per capita economic loss in Lanzhou, the provincial capital city of Gansu, were obviously higher than other cities from the same province. The economic loss in Linxia accounted for the highest proportion of GDP. The health impacts in the Hexi region, including the cities of Jiuquan, Jiayuguan, Zhangye, Jinchang and Wuwei, were generally lower, but the economic loss and per capita economic loss were still higher. We also found that urbanization and industrialization were highly correlated with health economic loss caused by PM 2.5 pollution. In conclusion, the PM 2.5 -related health economic burden in Gansu Province was serious. As an economically underdeveloped region, it was very important to further adopt rigid and effective pollution control policies.

Based on ground-based lidar and microwave radiometer observations in Hangzhou from 1 January 2013 to 31 December 2015, the monthly characteristics of diurnal extinction as well as atmospheric boundary layer (ABL) were studied. The interactions between temperature (T), humidity fields including relative humidity (RH) and specific humidity (SH) and atmospheric stratification (AS) were analyzed to discuss the meteorological factors in the Yangtze River Delta region during the study period. The top of ABL MPL varied from 0.8 km to 1.0 km throughout in January with higher extinction intensity close to the surface combined to the largest PM 2.5 about 100-120 μg/m 3 . Then the ABL MPL could develop up to 1.5 km in the spring due to the weaker extinction during the daytime. The RH in the whole column in January and December was lower than the mean value (ranging from 5% to 20%) distributed from the ground to 3 km. From May to September, the RH anomaly profiles became positive contributed to larger extinction by strengthened the particle scattering ability. In January and December, the AS was stable from the surface to 3 km coincided with the extinction distribution; while in July and August, the gradient of Δθ se decreased which favored the diffusion of particle in the air. Moreover, April and October presented turning points in the variation of θ se . The humidity field reveals a stable condition in January and December which favored particles suppressed from the near surface to 3 km; the temperature field has tended towards a neutral state in most months except for February. The first change-point of the meteorological fields was found in April possibly attributable to the abnormal abrupt in the subtropical high. This study could have important reference for understanding regional air quality and governing air control., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Plenty of epidemiological evidences have shown that ambient particulate matter (PM2.5) exposure increased the prevalence of cardiovascular disease, but the potential mechanism has not been known clearly. We established mice models by ambient PM2.5 exposure system to explore the adverse effects of PM2.5 on cardiac function in mice. Forty-eight C57BL/6 mice were randomly divided into 3 groups and exposed to filtered air (FA), unfiltered air (UA) and concentrated PM2.5 air (CA) for 8 or 16 weeks, 6 hours per day, 7 days per week, respectively. The changes of cardiac structure and function, histological analysis and related mechanism were investigated. The main manifestations of cardiac structure were cardiac hypertrophy and fibrosis in a dose- and time-dependent manner after PM2.5 exposure, which led to the decrease of cardiac systolic function. Cardiac hypertrophy in mice might be regulated by PI3K/Akt/FoxO1 signal. Cardiac fibrosis might be attributed to inflammatory infiltration caused by macrophage activation. Consequently, our data indicated that cardiac hypertrophy and fibrosis might be important factors of PM2.5-induced cardiac dysfunction in mice., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Background: A new Air Quality Health Index (AQHI) was developed in Canada or several single cities as a promising health risk communication tool., Objectives: To construct a national AQHI in China and compare its validity in predicting daily mortality risk with the existing Air Quality Index (AQI)., Methods: We established the AQHI as the sum of excess total mortality risks associated with multiple air pollutants in 272 representative Chinese cities from 2013 to 2015 (termed as "total AQHI"). The mortality risks per unit change of air pollutant concentrations were determined according to a time-series analysis in each city. Separate AQHIs were established for subgroups classified by age and sex and for main cardiopulmonary diseases (termed as "specific AQHIs"). For validation, AQHIs and AQI were established using the data of 2015 (N = 272) and compared their associations with daily mortality using the data of 2013-2014 (N = 144)., Results: The concentration-response coefficients of fine particulate matter, nitrogen dioxide and ozone were adopted in constructing AQHI. There were almost linear exposure-response relationships between AQHIs and daily mortality. The total AQHI and specific AQHIs had very similar associations with daily mortality. AQHI and AQI showed similar associations with daily cause-specific mortality in terms of average magnitude, numbers of cities of positive associations and model fit statistics., Conclusions: AQHI may have comparable performance with AQI in communicating acute health risks of air pollution in China. There seems no need to establish specific AQHIs for different age groups, gender and causes of deaths., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Combined atmospheric oxidant capacity (O x ), represented by the sum of nitrogen dioxide (NO 2 ) and ozone (O 3 ), is an important hazardous property of outdoor air pollution mixture. It remains unknown whether its adverse effects can be ameliorated by dietary fish-oil supplementation., Objective: To assess the effects of fish-oil supplementation against oxidative stress induced by acute O x exposure., Methods: We conducted a randomized, double-blinded and placebo-controlled study among 65 young adults in Shanghai, China between September 2017 and January 2018. We randomly assigned participants to receive either 2.5 g/day of fish oil or placebo, and conducted four repeated physical examinations during the last two months of treatments. O x concentrations were calculated as the sum of hourly measurements of NO 2 and O 3 . We measured six biomarkers on systemic oxidative stress and antioxidant activity. Linear mixed-effect models were used to assess the short-term effects of O x on biomarkers in each group., Results: During our study period, the 72-h average O x concentration was 93.6 μg/m 3 . Short-term exposure to O x led to weaker changes in all biomarkers in the fish oil group than in the placebo group. Compared with the placebo group, for a 10-μg/m 3 increase in O x , there were smaller decrements in myeloperoxidase (MPO, difference = 5.92%, lag = 0-2 d, p = 0.03) and malondialdehyde (MDA, difference = 5.00%, lag = 1 d, p = 0.04) in the fish-oil group; there were also larger increments in total antioxidant capacity (TAC, difference = 16.33%, lag = 2 d, p = 0.02) and in glutathione peroxidase (GSH-Px, difference = 8.89%, lag = 0-2 d, p = 0.03) in the fish-oil group. The estimated differences for MPO were robust to adjustment for all co-pollutants and the differences for other biomarkers remained for some co-pollutants., Conclusions: This trial provides first-hand evidence that dietary fish-oil supplementation may alleviate the systemic oxidative stress induced by O x ., (Copyright © 2019 Elsevier Inc. All rights reserved.)

To assess the carcinogenic potential of PM2.5 exposure, we developed a cell-based experimental protocol to examine the cell transformation activity of PM2.5 samples from different regions in China. The seasonal ambient PM2.5 samples were collected from three megacities, Beijing (BJ), Wuhan (WH), and Guangzhou (GZ), from November 2016 to October 2017. The mean concentrations of PM2.5 were much higher in the winter season (BJ: 109.64 μg/m 3 , WH: 79.99 μg/m 3 , GZ: 49.99 μg/m 3 ) than that in summer season (BJ: 42.40 μg/m 3 , WH: 25.82 μg/m 3 , GZ: 19.82 μg/m 3 ). The organic extracts (OE) of PM2.5 samples from combined summer (S) (June, July, August) or winter (W) (November, December, January) seasons were subjected to characterization of chemical components. We treated human bronchial epithelial (HBE) cells expressing CYP1A1 (HBE-1A1) with PM2.5 samples at doses ranging from 0 to 100 μg/mL (0, 1.563, 3.125, 6.25, 12.5, 25, 50, 100 μg/mL) and determined the phenotype of malignant cell transformation. A dose-response relationship was analyzed by benchmark dose (BMD) modeling, and the potential were indicated by BMDL 10 . The order of the carcinogenic risk of seasonal PM2.5 samples from high to low was BJ-W, WH-W, GZ-W, WH-S, BJ-S, and GZ-S. Notably, we found that the alteration in the lung cancer-related biomarkers, KRAS, PTEN, p53, c-Myc, PCNA, pAKT/AKT, and pERK/ERK was congruent with the activity of cell transformation and the content of specific components of polycyclic aromatic hydrocarbon (PAHs) bound to PM2.5. Taken together, we have successfully developed a cell-based alternative model for the evaluation of potent carcinogenicity upon long-term PM2.5 exposure., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Few epidemiological studies have evaluated the respiratory effects of personal exposure to nitrogen dioxide (NO 2 ), a major traffic-related air pollutant. The biological pathway for these effects remains unknown., Objectives: To evaluate the short-term effects of personal NO 2 exposure on lung function, fractional exhaled nitric oxide (FeNO) and DNA methylation of genes involved., Methods: We conducted a longitudinal panel study among 40 college students with four repeated measurements in Shanghai from May to October in 2016. We measured DNA methylation of the key encoding genes of inducible nitric oxide synthase (NOS2A) and arginase (ARG2). We applied linear mixed-effect models to assess the effects of NO 2 on respiratory outcomes., Results: Personal exposure to NO 2 was 27.39 ± 23.20 ppb on average. In response to a 10-ppb increase in NO 2 exposure, NOS2A methylation (%5 mC) decreased 0.19 at lag 0 d, ARG2 methylation (%5 mC) increased 0.21 and FeNO levels increased 2.82% at lag 1 d; and at lag 2 d the percentage of forced vital capacity, forced expiratory volume in 1 s and peak expiratory flow in predicted values decreased 0.12, 0.37 and 0.67, respectively. The model performance was better compared with those estimated using fixed-site measurements. These effects were robust to the adjustment for co-pollutants and weather conditions., Conclusions: Our study suggests that short-term personal exposure to NO 2 is associated with NOS2A hypomethylation, ARG2 hypermethylation, respiratory inflammation and lung function impairment. The use of personal measurements may better predict the respiratory effects of NO 2 ., (Copyright © 2019 Elsevier Inc. All rights reserved.)