Ozone pollution and hospital admissions for cardiovascular events.

AIMS: The available literature on morbidity risk of cardiovascular diseases associated with ambient ozone pollution is still limited. This study examined the potential acute effects of exposure to ambient ozone pollution on hospital admissions of cardiovascular events in China. METHODS AND RESULTS: A two-stage multi-city time-series study approach was used to explore the associations of exposure to ambient ozone with daily hospital admissions (n = 6 444 441) for cardiovascular events in 70 Chinese cities of prefecture-level or above during 2015-17. A 10 µg/m3 increment in 2-day average daily 8 h maximum ozone concentrations was associated with admission risk increases of 0.46% [95% confidence interval (CI): 0.28%, 0.64%] in coronary heart disease, 0.45% (95% CI: 0.13%, 0.77%) in angina pectoris, 0.75% (95% CI: 0.38%, 1.13%) in acute myocardial infarction (AMI), 0.70% (95% CI: 0.41%, 1.00%) in acute coronary syndrome, 0.50% (95% CI: 0.24%, 0.77%) in heart failure, 0.40% (95% CI: 0.23%, 0.58%) in stroke and 0.41% (95% CI: 0.22%, 0.60%) in ischemic stroke, respectively. The excess admission risks for these cardiovascular events associated with high ozone pollution days (with 2-day average 8-h maximum concentrations ≥100 µg/m3 vs. < 70 µg/m3) ranged from 3.38% (95% CI: 1.73%, 5.06%) for stroke to 6.52% (95% CI: 2.92%, 10.24%) for AMI. CONCLUSION: Ambient ozone was associated with increased hospital admission risk for cardiovascular events. Greater admission risks for cardiovascular events were observed under high ozone pollution days. These results provide evidence for the harmful cardiovascular effects of ambient ozone and call for special attention on the control of high ozone pollution.

Short-Term Exposure of PM2.5 and Epigenetic Aging: A Quasi-Experimental Study.

Epigenetic age (EA) is an emerging DNA methylation-based biomarker of biological aging, but whether EA is causally associated with short-term PM2.5 exposure remains unknown. We conducted a quasi-experimental study of 26 healthy adults to test whether short-term PM2.5 exposure accelerates seven EAs with three health examinations performed before, during, and after multiple PM2.5 pollution waves. Seven EAs were derived from the DNA methylation profiles of the Illumina HumanMethylationEPIC BeadChip from CD4+ T-helper cells. We found that an increase of 10 µg/m3 in the 0-24 h personal PM2.5 exposure prior to health examinations was associated with a 0.035, 0.035, 0.050, 0.055, 0.052, and 0.037-unit increase in the changes of z-scored DNA methylation age acceleration (AA,Horvath), AA (Hannum), AA (GrimAge), DunedinPoAm, mortality risk score (MS), and epiTOC, respectively (p-values < 0.05). The same increase in the 24-48 h average personal PM2.5 exposure yielded smaller effects but was still robustly associated with the changes in AA (GrimAge), DunedinPoAm, and MS. Such acute aging effects of PM2.5 were mediated by the changes in several circulating biomarkers, including EC-SOD and sCD40L, with up to ∼28% mediated proportions. Our findings demonstrated that short-term PM2.5 exposure could accelerate aging reflected by DNA methylation profiles via blood coagulation, oxidative stress, and systematic inflammation.

Association of exposure to fine particulate matter wave over the preconception and pregnancy periods with adverse birth outcomes: Results from the project ELEFANT.

BACKGROUND: No study has explored the effects of sustained maternal exposure to high-level ambient fine particulate matter (PM2.5) within a short period, i.e., PM2.5 wave, on adverse birth outcomes, though increasing epidemiological studies demonstrated that exposure to single days of high ambient PM2.5 could increase risks of adverse birth outcomes. In this study, we aim to evaluate associations of maternal PM2.5 wave exposure around pregnancy with preterm birth (PTB), small for gestational age (SGA), and large for gestational age (LGA). METHODS: Totally 10,916 singleton pregnant women from all 16 districts in Tianjin, China, and their followed-up birth outcomes were included in this study. We defined PM2.5 wave as at least 2 consecutive days with daily average PM2.5 concentration exceeding 75 µg/m3, and 90th, 92.5th, 95th, 97.5th, 99th percentiles of PM2.5 distribution during the study period in Tianjin, respectively. Cox proportional hazard model was applied to evaluate the durational effects of PM2.5 wave during each exposure window on PTB, SGA, and LGA after adjusting for potential confounders. RESULTS: Exposure to PM2.5 wave over the preconception and pregnancy periods was associated with increased risks of adverse birth outcomes. For PTB, the strongest association was found during the first trimester when PM2.5 wave was defined as at least 4 consecutive days with daily average PM2.5 concentration >90th (HR, 10.46; 95% CI, 6.23-17.54); and for SGA (HR, 6.23; 95% CI, 3.34-11.64) and LGA (HR, 4.70; 95% CI, 3.35-6.59), the strongest associations both were found when PM2.5 wave was defined as at least 2 consecutive days with daily average PM2.5 concentration >99th. Additionally, the risks of adverse birth outcomes generally increased at higher PM2.5 thresholds or longer durations of PM2.5 wave. CONCLUSION: Prolonged exposure to high-level PM2.5 over preconception and pregnancy periods was associated with increasing risks of PTB, SGA and LGA.

Co-exposure to multiple air pollutants and sleep disordered breathing in patients with or without obstructive sleep apnea: A cross-sectional study.

BACKGROUND: Air pollution may be a contributing risk factor for obstructive sleep apnea (OSA). However, the health effects of co-exposure to multiple air pollutants on OSA patients remain unclear. OBJECTIVES: To assess the joint effect of multi-pollutant on sleep disordered breathing (SDB) parameters in patients with or without OSA and identify the dominant pollutants. METHODS: A total of 2524 outpatients from April 2020 to May 2021 were recruited in this cross-sectional study. Ambient air pollutant data were obtained from the nearest central monitoring stations to participants' residential address. SDB parameters were measured by the ApneaLink devices, including apnea-hypopnea index (AHI), hypopnea index (HI), oxygen desaturation index (ODI), average oxygen saturation (SpO2), percentage sleep time with <90% saturation (T90), and desaturation. Bayesian kernel machine regression (BKMR) was applied to evaluate the effects of multiple pollutants. RESULTS: Significant associations were observed between air pollutants and SDB parameters (including increases in AHI, HI, ODI, and desaturation) among patients with OSA. Co-exposure to air pollutants was positively correlated with AHI, HI, and ODI. PM10 and O3 dominated the effects of pollutant mixtures on OSA, with the highest posterior inclusion probability (PIP) values of 0.592 and 0.640, respectively. Stratified analysis showed that, compared to male patients with OSA, stronger effects on the SDB parameters were observed in female patients. Stronger associations were also found in the warm season than those in the cold season. CONCLUSION: Co-exposure to air pollutants was associated with SDB parameters among patients with OSA, PM10 and O3 might play the dominant roles.

Associations between personal noise exposure and heart rate variability were modified by obesity and PM2.5: The study among obese and normal-weight adults (SONA).

Noise pollution has been documented to increase the risks of cardiovascular disorders, which can be predicted by heart rate variability (HRV), nevertheless, there has been limited evidence on the modifiers of noise pollution. Environmental fine particulate matter (PM2.5) and obesity status are both growing major concerns of cardiovascular disease burden. Our study aims to investigate whether these two factors may modify the associations between noise exposure and HRV indices. An investigation was performed on 97 (53 normal-weight and 44 obese) participants aged 18-26 years, with continuous 5-min personal exposure assessment and ambulatory electrocardiogram monitoring for 24 h. This study found that personal exposure to noise was associated with decreased HRV level and imbalanced cardiac autonomic function, as indicated by decreases in standard deviation of normal-to-normal intervals (SDNN), square root of the mean squared differences of successive intervals (rMSSD), the percentage of R-R intervals that differ from each other by more than 50 ms (pNN50), low-frequency (LF) power, high-frequency (HF) power, and increases in LF-HF-Ratio. Stronger associations between personal noise exposure and HRV indices were observed among obese participants and participants with higher PM2.5 exposure levels compared to their counterparts. For SDNN, a 1 dB(A) increment in personal noise exposure at 3h-average was associated with a 1.25% (95%CI: -1.64%, -0.86%) decrease among obese participants, and a 0.11% (95%CI: -0.38%, 0.16%) decrease among normal-weight participants (P for subgroup difference<0.001); and a 0.87% (95%CI: -1.20%, -0.54%) decrease among participants with higher PM2.5 exposure levels, and a 0.22% (95%CI: -0.58%, 0.14%) decrease among participants with lower PM2.5 exposure levels (P for subgroup difference = 0.008). Obesity and PM2.5 may aggravate the adverse effects of noise on HRV, which has implications for targeted prevention of cardiovascular disease burden associated with noise pollution.

Ambient particulate air pollution, blood cell parameters, and effect modification by psychosocial stress: Findings from two studies in three major Chinese cities.

The associations between particulate matter (PM) exposure, psychosocial stress and blood cell parameters are bringing novel insights to characterize the early damage of multiple diseases. Based on two studies conducted in three Chinses cities using cross-sectional (Beijing, 425 participants) and panel study (Tianjin and Shanghai, 92 participants with 361 repeated measurements) designs, this study explored the associations between short-term exposure to ambient PM and blood cell parameters, and the effect modification by psychosocial stress. Increasing PM2.5 exposure was significantly associated with decreases in red blood cell (RBC) count and mean corpuscular hemoglobin concentration (MCHC), and increases in mean corpuscular volume (MCV), platelets count (PLT) and platelet hematocrit (PCT) in both studies. For instance, a 10 µg/m3 increment in PM2.5 concentration was associated with a 1.04% (95%CI: 0.16%, 1.92%) increase in PLT (4-d) and a 1.09% (95%CI: 0.31%, 1.87%) increase in PCT (4-d) in the cross-sectional study, and a 0.64% (95%CI: 0.06%, 1.22%) increase in PLT (1-d) and a 0.72% (95%CI: 0.33%, 1.11%) increase in PCT (1-d) in the panel study, respectively. In addition, stronger increases in MCV, PLT, and PCT associated with PM2.5 exposure were found in higher psychosocial stress group compared to lower psychosocial stress group (p for interaction <0.10), indicating that blood cell parameters of individuals with higher psychosocial stress might be more susceptible to the early damages of PM2.5 exposure.

Association of DNA methylation in circulating CD4+T cells with short-term PM2.5 pollution waves: A quasi-experimental study of healthy young adults.

BACKGROUND: Fine particulate matter (PM2.5) is a modifiable environmental risk factor with established adverse effects on human health. However, associations between acute PM2.5 fluctuation and DNA methylation remain unknown. METHODS: A quasi-experimental study utilizing naturally occurring PM2.5 pollution waves (PPWs) was conducted on 32 healthy young adults. Repeated follow-up measurements were performed and participants served as their own controls before, during, and after PPWs. Exposure measurements including indoor and ambient PM2.5 levels, and equivalent personal PM2.5 exposure were further estimated based on the time-location information. DNA methylation profiles of circulating CD4+T cells were obtained using Illumina HumanMethylationEPIC BeadChip. Linear mixed-effect models were applied to estimate the associations between two scenarios (during-PPWs vs. pre-PPWs periods and during-PPWs vs. post-PPWs periods) and methylation level of each CpG site. We further validated their associations with the personal PM2.5 exposure, and GO and KEGG analyses and mediation analysis were conducted accordingly. RESULTS: Data from 26 participants were included in final analysis after quality control. Short-term high PM2.5 exposure was associated with DNA methylation changes of participants. Nine differently methylated CpG sites were not only significantly associated with PPWs periods but also with personal PM2.5 exposure in 24-h prior to the health examinations (p < 0.01). Gene ontology analysis found that five sites were associated with two pathways relating to membrane protein synthesis. PM2.5-related changes in CpG sites were mediated by sP-selectin, 8-isoPGF2α, EGF, GRO, IL-15, and IFN-α2, with mediated proportions ranging from 9.65% to 23.40%. CONCLUSIONS: This is the first quasi-experimental study showing that short-term high PM2.5 exposure could alter the DNA methylation of CD4+T cells, which provided valuable information for further exploring underlying biological mechanisms and epigenetic biomarkers for PM2.5-related acute health effects.

Long-Term Exposure to Ambient PM2.5 and Increased Risk of CKD Prevalence in China.

BACKGROUND: Fine particulate matter (PM2.5) is an important environmental risk factor for cardiopulmonary diseases. However, the association between PM2.5 and risk of CKD remains under-recognized, especially in regions with high levels of PM2.5, such as China. METHODS: To explore the association between long-term exposure to ambient PM2.5 and CKD prevalence in China, we used data from the China National Survey of CKD, which included a representative sample of 47,204 adults. We estimated annual exposure to PM2.5 before the survey date at each participant's address, using a validated, satellite-based, spatiotemporal model with a 10 km×10 km resolution. Participants with eGFR <60 ml/min per 1.73 m2 or albuminuria were defined as having CKD. We used a logistic regression model to estimate the association and analyzed the influence of potential modifiers. RESULTS: The 2-year mean PM2.5 concentration was 57.4 µg/m3, with a range from 31.3 to 87.5 µg/m3. An increase of 10 µg/m3 in PM2.5 was positively associated with CKD prevalence (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.22 to 1.35) and albuminuria (OR, 1.39; 95% CI, 1.32 to 1.47). Effect modification indicated these associations were significantly stronger in urban areas compared with rural areas, in males compared with females, in participants aged <65 years compared with participants aged ≥65 years, and in participants without comorbid diseases compared with those with comorbidities. CONCLUSIONS: These findings regarding the relationship between long-term exposure to high ambient PM2.5 levels and CKD in the general Chinese population provide important evidence for policy makers and public health practices to reduce the CKD risk posed by this pollutant.

Short-term exposure to ambient nitrogen dioxide and increased hospitalization burden for depression in China: a multicity analysis.

Evidence for the increased hospitalization burden, including admissions, expenditures and length of hospital stay (LOS) for depression attributable to ambient nitrogen dioxide (NO2) is lacking. We investigated the associations between short-term exposure to ambient NO2 and attributable admissions, hospitalization expenditures and LOS for depression in 57 Chinese cities during 2013-2017 using a well-established two-stage time-series study approach. Short-term exposure to ambient NO2 was associated with significantly increased admissions, hospitalization expenditures and LOS for depression, and the attributable fractions were 6.87% (95% CI: 2.90%, 10.65%), 7.12% (3.01%, 11.04%) and 6.12% (2.59%, 9.50%) at lag02, respectively. The projected total attributable admissions, hospitalization expenditures and LOS for depression related to ambient NO2 at the national level were 23,335 (9,863, 36,181) admissions, 318.70 (134.43, 492.21) million CNY and 539.55 (227.99, 836.99) thousand days during the study period, respectively. Short-term exposure to ambient NO2 is associated with increased hospitalization burden for depression.

Chemical constituents and sources of indoor PM2.5 and cardiopulmonary function in patients with chronic obstructive pulmonary disease: Estimation of individual and joint effects.

BACKGROUND: The cardiopulmonary effects of chemical constituents and sources of indoor fine particulate matter (PM2.5) remain unclear. OBJECTIVES: To examine the individual and joint effects of constituents of indoor PM2.5 on cardiopulmonary function of patients with chronic obstructive pulmonary disease (COPD) and the role of identified sources. METHODS: This panel study recruited 43 stable COPD patients from November 2015 to May 2016 in Beijing, China. Daily indoor and outdoor PM2.5 were collected for five consecutive days simultaneously. Twenty-four elements were measured and principal component analysis was used for source appointment. Pulmonary function and blood pressure (BP) were also measured at daily visit. The linear mixed-effect models were used to estimate the effect of each constituent and source. Bayesian kernel machine regression (BKMR) models were used to estimate the overall effect of all measured constituents. RESULTS: The combustion, indoor soil/dust and road dust sources were identified as the main sources of indoor PM2.5 and combustion sources contributed over 40% during the heating season. Most constituents were significantly associated with elevated BP of COPD patients and the joint effects of mixed exposures were also significant especially during the heating season. Most associations of chemical constituents with pulmonary function were negative but not statistically significant during the heating season, as was the joint effect. Few associations were observed during the non-heating season. Further, we observed combustion sources throughout the study period and road dust sources during the heating season were significantly associated with increased BP but not decreased pulmonary function. CONCLUSION: The combustion and road dust sources and their related constituents of indoor PM2.5 could cause adverse effects on cardiovascular function of COPD patients especially during the heating season, but the effect on pulmonary function still needs to be further studied.

Associations of long-term exposure to air pollution with blood pressure and homocysteine among adults in Beijing, China: A cross-sectional study.

BACKGROUND: Studies on the hypertensive effect of long-term exposure to air pollution are mixed, and sparse evidence exists regarding its effects on homocysteine (Hcy), another crucial risk factor for cardiovascular disease (CVD). METHODS: We collected data from 23,256 participants aged 18-74 years at baseline (years 2017-2018) from a community-based cohort in China. A linear combination of concentrations from monitoring stations at the participants' home and work addresses, weighted by the time, was used to estimate two-year exposures to particulate matter with fine particles≤2.5 µm (PM2.5), aerodynamic diameter≤10 µm (PM10), nitrogen dioxide (NO2) and sulfur dioxide (SO2). Generalized linear regressions and logistic regressions were conducted to examine the associations between air pollution and systolic blood pressure (SBP), diastolic blood pressure (DBP), Hcy, hypertension and co-occurrence of hypertension and hyperhomocysteinemia (HHcy). RESULTS: The results showed that each interquartile range (IQR) increase in PM2.5 (16.1 µg/m3), PM10 (19.3 µg/m3) and SO2 (3.9 µg/m3) was significantly associated with SBP (changes: 0.64-1.86 mmHg), DBP (changes: 0.35-0.70 mmHg) and Hcy (changes: 0.77-1.04 µmol/L) in the fully adjusted model. These air pollutants were also statistically associated with the prevalence of co-occurrence of hypertension and HHcy (ORs: 1.22-1.32), which were stronger than associations with the prevalence of hypertension (ORs: 1.09-1.19). The hypertensive effects of exposure to PM2.5, PM10 and SO2 were more pronounced among elder participants, obese participants, those with established CVD or a high 10-year CVD risk and those with a family history of hypertension. However, interaction analyses of Hcy showed different patterns. Additionally, moderate level of physical activity and active travel mode benefited individuals in resisting the health impacts of air pollution on both blood pressure (BP) and Hcy. CONCLUSIONS: Our study supports a positive relationship between air pollution and BP and Hcy among adults in Beijing, and close attention to vulnerable populations and healthy lifestyles could effectively benefit further cardiovascular health.

Effect of short-term exposure to particulate air pollution on heart rate variability in normal-weight and obese adults.

BACKGROUND: The adverse effects of particulate air pollution on heart rate variability (HRV) have been reported. However, it remains unclear whether they differ by the weight status as well as between wake and sleep. METHODS: A repeated-measure study was conducted in 97 young adults in Beijing, China, and they were classified by body mass index (BMI) as normal-weight (BMI, 18.5-24.0 kg/m2) and obese (BMI ≥ 28.0 kg/m2) groups. Personal exposures to fine particulate matter (PM2.5) and black carbon (BC) were measured with portable exposure monitors, and the ambient PM2.5/BC concentrations were obtained from the fixed monitoring sites near the subjects' residences. HRV and heart rate (HR) were monitored by 24-h Holter electrocardiography. The study period was divided into waking and sleeping hours according to time-activity diaries. Linear mixed-effects models were used to investigate the effects of PM2.5/BC on HRV and HR in both groups during wake and sleep. RESULTS: The effects of short-term exposure to PM2.5/BC on HRV were more pronounced among obese participants. In the normal-weight group, the positive association between personal PM2.5/BC exposure and high-frequency power (HF) as well as the ratio of low-frequency power to high-frequency power (LF/HF) was observed during wakefulness. In the obese group, personal PM2.5/BC exposure was negatively associated with HF but positively associated with LF/HF during wakefulness, whereas it was negatively correlated to total power and standard deviation of all NN intervals (SDNN) during sleep. An interquartile range (IQR) increase in BC at 2-h moving average was associated with 37.64% (95% confidence interval [CI]: 25.03, 51.51%) increases in LF/HF during wakefulness and associated with 6.28% (95% CI: - 17.26, 6.15%) decreases in SDNN during sleep in obese individuals, and the interaction terms between BC and obesity in LF/HF and SDNN were both statistically significant (p <  0.05). The results also suggested that the effects of PM2.5/BC exposure on several HRV indices and HR differed in magnitude or direction between wake and sleep. CONCLUSIONS: Short-term exposure to PM2.5/BC is associated with HRV and HR, especially in obese individuals. The circadian rhythm of HRV should be considered in future studies when HRV is applied.

Effects of air purification of indoor PM2.5 on the cardiorespiratory biomarkers in young healthy adults.

Ambient fine particulate matter (PM2.5 ), as one of the predominant air pollutants, has achieved effective control in recent years in China. Whether the use of indoor air purifiers is still necessary needs further exploration. A randomized crossover trial was conducted in 54 healthy students in Beijing, China. Participants were randomized assigned to the use of real or sham high-efficiency particulate air filter (HEPA) for a week and changed the status after a washout period. Health measurements of cardiorespiratory biomarkers were performed at the end of each period. Linear mixed-effects models were used to evaluate the association between PM2.5 exposure and cardiorespiratory biomarkers. Compared with sham air purification, average diastolic blood pressure (DBP), fractional exhaled nitric oxide (FeNO), and 8-isoprostane (8-isoPGF2α) levels decreased significantly in the real purification. The effects of indoor air purification on lung function indicators including forced expiratory volume in one second (FEV1 ), peak expiratory flow (PEF), and forced expiratory flow between the 25th and 75th percentile of forced vital capacity (FEF25%-75% ) were also significant. Our findings showed a protective effect of indoor HEPA air purifiers on cardiorespiratory health of young healthy adults reflected by the decreased blood pressure, respiratory inflammation, and systematic oxidative stress and improved lung function.

Negative ions offset cardiorespiratory benefits of PM2.5 reduction from residential use of negative ion air purifiers.

Negative ion air purifiers (NIAPs), as a less costly alternative to the HEPA filtration, have been increasingly deployed in China and potentially elsewhere. While reducing indoor concentrations of fine particulate matter (PM2.5 ), NIAPs generate massive amounts of negative ions that may be of health concern. We performed week-long interventions with NIAPs in the dormitories of 56 healthy college students living in Beijing. In a randomized order, each student underwent a true and a sham NIAP session. Cardiorespiratory outcomes were measured before and after each session. The use of true NIAPs reduced indoor PM2.5 concentrations significantly, while notably increased negative ion levels. Increases in PM2.5 and negative ion (NI) exposure were independently associated with increased urinary concentration of malondialdehyde, a biomarker of systemic oxidative stress, resulting in a null net effect of NIAP on malondialdehyde. Likewise, no significant net effects of NIAPs were observed for other outcomes indicative of lung function, vascular tone, arterial stiffness, and inflammation. Our findings suggest that negative ions, possibly along with their reaction products with the room air constituents, adversely affect health. The downsides do not support the use of NIAPs as a health-based mitigation strategy to reduce PM2.5 exposure, especially in residences with PM2.5 concentrations that are not extremely high.

Association between short-term exposure to ambient particulate air pollution and biomarkers of oxidative stress: A meta-analysis.

BACKGROUND: Exposure to ambient particulate air pollution contributes substantially to the mortality and morbidity due to cardiovascular diseases (CVD), respiratory diseases and neurodegenerative diseases. Several hypothetical mechanisms have been proposed to explain these associations, particularly oxidative stress. Malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and Superoxide Dismutase (SOD) are typical biomarkers of oxidative stress and have been frequently investigated. However, the association between exposure to ambient particulate matter (PM) and these biomarkers has not been well established. OBJECTIVES: Evaluate the association between ambient particulate air pollution and biomarkers of oxidative stress based on existing epidemiological studies. METHODS: A systematic literature search was conducted in databases of Science Direct, PubMed, Web of Science, and Scopus up to April 24, 2020 to summarize epidemiological studies reporting the association between exposure to ambient PM (PM2.5, PM10, or both) and biomarkers of oxidative stress, and a meta-analysis was performed for the associations reported in individual studies using a random-effect model. RESULTS: This meta-analysis included 23 epidemiological studies (13 identified for 8-OHdG, 11 identified for MDA and 5 identified for SOD). A 10 µg/m3 increase in short-term exposure to ambient PM2.5 was associated with pooled percent changes of 2.10% (95% CIs: -0.13%, 4.38%), 1.60% (95% CIs: 0.21%, 3.01%) and -0.61% (95% CIs: -1.92%, 0.72%) in 8-OHdG, MDA and SOD, respectively. CONCLUSION: Short-term exposure to ambient PM2.5 was associated with a significantly increased level of MDA, indicating that ambient particulate air pollution may contribute to increased oxidative stress.

Identification of potential markers for internal exposure to ambient ozone in oral cavity of healthy adults.

BACKGROUND: Ozone is a highly oxidative gaseous pollutant associated with adverse health outcomes, but markers for internal exposure to ambient ozone are not well-established. METHODS: We aimed to evaluate the feasibility and suitability of the markers in oral microbiome for ambient ozone exposure. Between March and May in 2018, 97 healthy adults were examined on 2 or 3 occasions for oral swab sampling. Hourly concentrations of ambient ozone 1-7 days preceding sampling were collected. Mixed-effect models were fitted to examine the associations between ambient ozone and the diversity and taxon abundances of oral microbiome. Receiver operating characteristic (ROC) curves estimated the accuracies of markers to delineate between samples exposed to different concentrations of ambient ozone. The associations between the makers and lung function were further examined by linear mixed effect models. RESULTS: The averages of daily mean concentrations of ambient ozone (O3-daily), maximum 8-h means (O3-8hmax) and 1-h maximums (O3-1hmax) were respectively 72 µg/m³, 123 µg/m³ and 144 µg/m³. O3-daily was positively associated with α-diversity of oral microbiome, but the exposure-response curves only yielded positive associations in the range of O3-daily from 60 µg/m³ to 75 µg/m³. Results of O3-8hmax and O3-1hmax were consistent with these of O3-daily. With an interquartile range increase in O3-daily at lag04, the abundance of Proteobacteria decreased by 3.1% (95% CI: -4.0%, -2.2%) and Firmicutes increased by 3.3% (95% CI: 2.3%, 4.3%), whilst the Proteobacteria:Firmicutes ratio (P/F) decreased by 0.9 (95% CI: -1.5, -0.4). The areas under ROC curves for Proteobacteria, Firmicutes and P/F were 0.8535, 0.7569 and 0.8929, respectively. Proteobacteria and P/F were associated with forced expiratory volume in the first second and fractional exhaled nitric oxide significantly. CONCLUSION: Ambient ozone disturbs oral microbial homeostasis. Proteobacteria, Firmicutes and their ratio may be potential markers for short-term ambient ozone exposure, and indicators of airway inflammation or lung function decline.

Association between particulate matter air pollution and risk of depression and suicide: systematic review and meta-analysis.

BACKGROUND: Some recent studies examined the effect of ambient particulate matter (PM) pollution on depression and suicide. However, the results have been inconclusive.AimsTo determine the overall relationship between PM exposure and depression/suicide in the general population. METHOD: We conducted a systematic review and meta-analysis of case-crossover and cohort studies to assess the association between PM2.5 (particles with an aerodynamic diameter of 2.5 µm or less) or PM10 (particles with an aerodynamic diameter between 2.5 and 10 µm) exposure and depression/suicide. RESULTS: A total of 14 articles (7 for depression and 7 for suicide) with data from 684 859 participants were included in the meta-analysis. With a 10 µg/m3 increase in PM2.5 we found a 19% (odds ratio [95% CI] 1.19 [1.07, 1.33]) increased risk of depression and a marginally increased risk of suicide (odds ratio [95% CI] 1.05 [0.99, 1.11]) in the general population. We did not observe any significant associations between increasing exposure to PM10 and depression/suicide. Sensitivity and subgroup analyses were used to determine the robustness of results. The strongest estimated effect of depression associated with PM2.5 appeared in a long-term lag pattern (odds ratio [95% CI] 1.25 [1.07, 1.45], P < 0.01) and cumulative lag pattern (odds ratio [95% CI] 1.26 [1.07, 1.48], P < 0.01). CONCLUSIONS: The meta-analysis suggested that an increase in ambient PM2.5 concentration was strongly associated with increased depression risk in the general population, and the association appeared stronger at long-term lag and cumulative lag patterns, suggesting a potential cumulative exposure effect over time.Declaration of interestNone.

Different health effects of indoor- and outdoor-originated PM2.5 on cardiopulmonary function in COPD patients and healthy elderly adults.

Numerous research has explored the associations of outdoor or indoor fine particulate matter (PM2.5 ) and health effects; however, few studies compared the effects of indoor PM2.5 originated from outdoor (PM2.5,os ) and indoor sources (PM2.5,is ). To assess the associations of PM2.5,os and PM2.5,is with cardiopulmonary function in patients with chronic obstructive pulmonary disease (COPD) and healthy elderly adults, blood pressure (BP) and pulmonary function were repeatedly examined in 43 COPD patients and their 32 healthy spouses in Beijing, China. Iron was used as tracer element to separate PM2.5,os and PM2.5,is . Mixed-effects models were applied to assess the associations of PM2.5,os or PM2.5,is and health effects after controlling for potential confounders. There was a reduction in forced expiratory volume in first second (FEV1 ) in COPD patients associated with PM2.5,is during the heating season. PM2.5,os was positively associated with diastolic BP (DBP) in healthy elderly adults during the heating season. There was a reduction in peak expiratory flow (PEF) in healthy elderly adults associated with PM2.5,os during the non-heating season. Exposure to indoor- and outdoor-originated PM2.5 had different health effects on cardiopulmonary function in different populations. The results provide supporting evidence for improving indoor air quality to promote public health among susceptible population.

Projections of the effects of global warming on the disease burden of ischemic heart disease in the elderly in Tianjin, China.

BACKGROUND: Ischemic heart disease (IHD) is one of the leading causes of deaths worldwide and causes a tremendous disease burden. Temperature is an important environmental determinant among the many risk factors for IHD. However, the emerging temperature-related health risks of IHD in the elderly is limited because of the lack of estimates that integrate global warming and demographic change. METHODS: Data on daily IHD deaths in the elderly aged ≥65 years and meteorological conditions were collected in Tianjin, a megacity of China, from 2006 to 2011. First, the baseline relationship between the temperature and years of life lost (YLL) from IHD was established. Then, future assessments were performed in combination with temperature projections for 19 global-scale climate models (GCMs) under 3 representative concentration pathways (RCPs) for the 2050s and 2070s. RESULTS: Increased YLL from IHD in the elderly was found to be associated with future ambient temperatures. The annual temperature-related YLL from IHD in the 2050s and 2070s were higher than the baseline. For instance, increases of 4.5, 14.9 and 38.3% were found under the RCP2.6, RCP4.5 and RCP8.5 scenarios, respectively, in the 2070s. The most significant increases occurred in warm season months. The increase in heat-related YLL will not be completely offset, even with the 25% adaptation assumed. When considering demographic change, the temperature-related disease burden of IHD in the elderly will be exacerbated by 158.4 to 196.6% under 3 RCPs in the 2050s and 2070s relative to the baseline. CONCLUSIONS: These findings have significant meaning for environmental and public health policy making and interventions towards the important issue of the health impacts of global warming on the elderly.

Association of emergency room visits for respiratory diseases with sources of ambient PM2.5.

Previous studies have reported associations of short-term exposure to different sources of ambient fine particulate matter (PM2.5) and increased mortality or hospitalizations for respiratory diseases. Few studies, however, have focused on the short-term effects of source-specific PM2.5 on emergency room visits (ERVs) of respiratory diseases. Source apportionment for PM2.5 was performed with Positive Matrix Factorization (PMF) and generalized additive model was applied to estimate associations between source-specific PM2.5 and respiratory disease ERVs. The association of PM2.5 and total respiratory ERVs was found on lag4 (RR = 1.011, 95%CI: 1.002, 1.020) per interquartile range (76 µg/m3) increase. We found PM2.5 to be significantly associated with asthma, bronchitis and chronic obstructive pulmonary disease (COPD) ERVs, with the strongest effects on lag5 (RR = 1.072, 95%CI: 1.024, 1.119), lag4 (RR = 1.104, 95%CI: 1.032, 1.176) and lag3 (RR = 1.091, 95%CI: 1.047, 1.135), respectively. The estimated effects of PM2.5 changed little after adjusting for different air pollutants. Six primary PM2.5 sources were identified using PMF analysis, including dust/soil (6.7%), industry emission (4.5%), secondary aerosols (30.3%), metal processing (3.2%), coal combustion (37.5%) and traffic-related source (17.8%). Some of the sources were identified to have effects on ERVs of total respiratory diseases (dust/soil, secondary aerosols, metal processing, coal combustion and traffic-related source), bronchitis ERVs (dust/soil) and COPD ERVs (traffic-related source, industry emission and secondary aerosols). Different sources of PM2.5 contribute to increased risk of respiratory ERVs to different extents, which may provide potential implications for the decision making of air quality related policies, rational emission control and public health welfare.