Particulate Air Pollution Exposure Research Articles

Lung function benefits of traditional Chinese medicine Qiju granules against fine particulate air pollution exposure: a randomized controlled trial.

Multiple targets are considered as the causes of ambient fine particulate matter [aerodynamic diameters of < 2.5 μm (PM2.5)] induced lung function injury. Qiju granules are derived from the traditional Chinese medicine (TCM) formula known as Qi-Ju-Di-Huang-Wan (Lycium, Chrysanthemum, and Rehmannia Formula, QJDHW), which has been traditionally used to treat symptoms such as cough with phlegm, dry mouth and throat, and liver heat. This treatment approach involves attenuating inflammation, oxidative stress, and fibrosis response. This study investigated the effects of Qiju granules on protecting lung function against PM2.5 exposure in a clinical trial. A randomized, double-blinded, and placebo-controlled trial was performed among 47 healthy college students in Hangzhou, Zhejiang Province in China. The participants were randomly assigned to the Qiju granules group or the control group based on gender. Clinical follow-ups were conducted once every 2 weeks during a total of 4 weeks of intervention. Real-time monitoring of PM2.5 concentrations in the individually exposed participants was carried out. Data on individual characteristics, heart rate (HR), blood pressure (BP), and lung function at baseline and during the follow-ups were collected. The effects of PM2.5 exposure on lung function were assessed within each group using linear mixed-effect models. In total, 40 eligible participants completed the scheduled follow-ups. The average PM2.5 level was found to be 64.72 μg/m3 during the study period. A significant negative correlation of lung function with PM2.5 exposure concentrations was observed, and a 1-week lag effect was observed. Forced expiratory volume in one second (FEV1), peak expiratory flow (PEF), maximal mid-expiratory flow (MMEF), forced expiratory flow at 75% of forced vital capacity (FVC) (FEF75), forced expiratory flow at 50% of FVC (FEF50), and forced expiratory flow at 25% of FVC (FEF25) were significantly decreased due to PM2.5 exposure in the control group. Small airway function was impaired more seriously than large airway function when PM2.5 exposure concentrations were increased. In the Qiju granules group, the associations between lung function and PM2.5 exposure were much weaker, and no statistical significance was observed. The results of the study showed that PM2.5 exposure was associated with reduced lung function. Qiju granules could potentially be effective in protecting lung functions from the adverse effects of PM2.5 exposure. identifier: ChiCTR1900021235.

Personal Strategies to Reduce the Cardiovascular Impacts of Environmental Exposures.

Ubiquitous environmental exposures increase cardiovascular disease risk via diverse mechanisms. This review examines personal strategies to minimize this risk. With regard to fine particulate air pollution exposure, evidence exists to recommend the use of portable air cleaners and avoidance of outdoor activity during periods of poor air quality. Other evidence may support physical activity, dietary modification, omega-3 fatty acid supplementation, and indoor and in-vehicle air conditioning as viable strategies to minimize adverse health effects. There is currently insufficient data to recommend specific personal approaches to reduce the adverse cardiovascular effects of noise pollution. Public health advisories for periods of extreme heat or cold should be observed, with limited evidence supporting a warm ambient home temperature and physical activity as strategies to limit the cardiovascular harms of temperature extremes. Perfluoroalkyl and polyfluoroalkyl substance exposure can be reduced by avoiding contact with perfluoroalkyl and polyfluoroalkyl substance-containing materials; blood or plasma donation and cholestyramine may reduce total body stores of perfluoroalkyl and polyfluoroalkyl substances. However, the cardiovascular impact of these interventions has not been examined. Limited utilization of pesticides and safe handling during use should be encouraged. Finally, vasculotoxic metal exposure can be decreased by using portable air cleaners, home water filtration, and awareness of potential contaminants in ground spices. Chelation therapy reduces physiological stores of vasculotoxic metals and may be effective for the secondary prevention of cardiovascular disease.

Individual Risk Factors of PM2.5 Associated With Wintertime Mortality in Urban Patients With COPD

Air pollution contributes to premature mortality, but potential impacts differ in populations with existing disease, particularly for individuals with multiple risk factors. Although COPD increases vulnerability to air pollution, individuals with COPD and other individual risk factors are at the intersection of multiple risks and may be especially susceptible to the effect of acute outdoor air pollution. What is the association between wintertime air pollution and mortality in patients with COPD and the modifying role of individual risk factors? This study evaluated 19,243 deceased veterans with prior COPD diagnosis who had resided in 25 US metropolitan regions (2016-2019). Electronic health records included patient demographic characteristics; smoking status; and comorbidities such as asthma, coronary artery disease (CAD), obesity, and diabetes. Using geocoded addresses, individuals were assigned wintertime fine particulate matter (particulate matter smaller than 2.5 μg in diameter [PM2.5]) and nitrogen dioxide air pollution exposures. Associations between acute air pollution and mortality were estimated by using a time-stratified case-crossover design with a conditional logistic model, and individual risk differences were assessed according to stratified analysis. A 1.05 (95%CI, 1.02-1.09) mortality risk was estimated for each 10 μg/m3 increase in daily wintertime PM2.5). Older patients and Black individuals displayed elevated risk. Obesity was a substantial air pollution-related mortality risk factor (OR, 1.11; 95%CI, 1.01-1.23), and the estimated risk for individuals with obesity plus CAD or obesity plus diabetes was 16%higher. Wintertime PM2.5 exposure was associated with elevated mortality risk in people with COPD, but individuals with multiple comorbidities, notably obesity, had high vulnerability. Our study suggests that obesity, CAD, and diabetes are understudied modifiers of air pollution-related risks for people with existing COPD.

Ambient particulate matter air pollution exposure and ovarian cancer incidence in the USA: An ecological study.

To investigate associations between air particulate matter of ≤2.5 μm in diameter (PM2.5 ) and ovarian cancer. County-level ecological study. Surveillance, epidemiology, and end results from a collection of state-level cancer registries across 744 counties. Data from the Environmental Protection Agency's network for PM2.5 monitoring was used to calculate trailing 5- and 10-year PM2.5 county-level values. County-level data on demographic characteristics were obtained from the American Community Survey. A total of 98 751 patients with histologically confirmed ovarian cancer as a primary malignancy from 2000 to 2016. Generalised linear regression models were developed to estimate the association between PM2.5 and PM10 levels, over 5- and 10-year periods of exposure, and ovarian cancer risk, after accounting for county-level covariates. Risk ratios for associations between ovarian cancer (both overall and specifically epithelial ovarian cancer) and PM2.5 levels. For the 744 counties included, the average PM2.5 level from 1990 through 2018 was 11.75 μg/m3 (SD = 3.7) and the average PM10 level was 22.7 μg/m3 (SD = 5.7). After adjusting for county-level covariates, the overall annualised ovarian cancer incidence was significantly associated with increases in 5-year PM2.5 (RR = 1.11 per 10 units (μg/m3 ) increase, 95% CI 1.06-1.16). Similarly, when the analysis was limited to epithelial cell tumours and adjusted for county-level covariates there was a significant association with trailing 5-year PM2.5 exposure models (RR = 1.12 per 10 units increase, 95% CI 1.08-1.17). Likewise, 10-year PM2.5 exposure was associated with ovarian cancer overall and with epithelial ovarian cancer. Higher county-level ambient PM2.5 levels are associated with 5- and 10-year incidences of ovarian cancer, as measurable in an ecological study.

Particulate Air Pollution Exposure and Stroke among Adults in Israel.

Stroke is the second most common cause of death and disability in the world. Many studies have found fine particulate matter (PM2.5) exposure to be associated with an increased risk of atherosclerotic cardiovascular disease, mostly focusing on ischemic heart disease and acute myocardial infarction. In a national analysis conducted in Israel-an area with unique climate conditions and high air pollution levels, we estimated the association between short-term PM2.5 exposure and ischemic stroke, intracerebral hemorrhage (ICH), or transient ischemic attacks (TIA). Using the Israeli National Stroke Registry, we obtained information on all stroke cases across Israel in 2014-2018. We obtained daily PM2.5 exposures from spatiotemporally resolved exposure models. We restricted the analytical data to days in which PM2.5 levels did not exceed the Israeli 24 h standard (37.5 µg/m3). We repeated the analysis with a stratification by sociodemographic characteristics and comorbidities. For all outcomes, the exposure-response curves were nonlinear. PM2.5 exposure was associated with a higher ischemic stroke risk, with larger effect estimates at higher exposure levels. Although nonsignificant, the exposure-response curve for TIA was similar. The associations with ICH were nonsignificant throughout the PM2.5 exposure distribution. The associations with ischemic stroke/TIA were larger among women, non-Jewish individuals, older adults, and individuals with diabetes, hypertension, and ischemic heart disease. In conclusion, short-term PM2.5 exposure is associated with a higher risk for ischemic stroke and possibly TIA, even when PM2.5 concentrations do not exceed the Israeli air quality guideline threshold. Vulnerability to the air pollution effects differed by age, sex, ethnicity, and comorbidities.

COPD with Eosinophilic Inflammation is Susceptible to Particulate Air Pollution Exposure

COPD with Eosinophilic Inflammation is Susceptible to Particulate Air Pollution Exposure

Aerosol Oxidative Potential in the Greater Los Angeles Area: Source Apportionment and Associations with Socioeconomic Position.

Oxidative potential (OP) has been proposed as a possible integrated metric for particles smaller than 2.5 μm in diameter (PM2.5) to evaluate adverse health outcomes associated with particulate air pollution exposure. Here, we investigate how OP depends on sources and chemical composition and how OP varies by land use type and neighborhood socioeconomic position in the Los Angeles area. We measured OH formation (OPOH), dithiothreitol loss (OPDTT), black carbon, and 52 metals and elements for 54 total PM2.5 samples collected in September 2019 and February 2020. The Positive Matrix Factorization source apportionment model identified four sources contributing to volume-normalized OPOH: vehicular exhaust, brake and tire wear, soil and road dust, and mixed secondary and marine. Exhaust emissions contributed 42% of OPOH, followed by 21% from brake and tire wear. Similar results were observed for the OPDTT source apportionment. Furthermore, by linking measured PM2.5 and OP with census tract level socioeconomic and health outcome data provided by CalEnviroScreen, we found that the most disadvantaged neighborhoods were exposed to both the most toxic particles and the highest particle concentrations. OPOH exhibited the largest inverse social gradients, followed by OPDTT and PM2.5 mass. Finally, OPOH was the metric most strongly correlated with adverse health outcome indicators.

Long-term exposure to particulate matter was associated with increased dementia risk using both traditional approaches and novel machine learning methods

Air pollution exposure has been linked to various diseases, including dementia. However, a novel method for investigating the associations between air pollution exposure and disease is lacking. The objective of this study was to investigate whether long-term exposure to ambient particulate air pollution increases dementia risk using both the traditional Cox model approach and a novel machine learning (ML) with random forest (RF) method. We used health data from a national population-based cohort in Taiwan from 2000 to 2017. We collected the following ambient air pollution data from the Taiwan Environmental Protection Administration (EPA): fine particulate matter (PM2.5) and gaseous pollutants, including sulfur dioxide (SO2), carbon monoxide (CO), ozone (O3), nitrogen oxide (NOx), nitric oxide (NO), and nitrogen dioxide (NO2). Spatiotemporal-estimated air quality data calculated based on a geostatistical approach, namely, the Bayesian maximum entropy method, were collected. Each subject's residential county and township were reviewed monthly and linked to air quality data based on the corresponding township and month of the year for each subject. The Cox model approach and the ML with RF method were used. Increasing the concentration of PM2.5 by one interquartile range (IQR) increased the risk of dementia by approximately 5% (HR = 1.05 with 95% CI = 1.04–1.05). The comparison of the performance of the extended Cox model approach with the RF method showed that the prediction accuracy was approximately 0.7 by the RF method, but the AUC was lower than that of the Cox model approach. This national cohort study over an 18-year period provides supporting evidence that long-term particulate air pollution exposure is associated with increased dementia risk in Taiwan. The ML with RF method appears to be an acceptable approach for exploring associations between air pollutant exposure and disease.

Source-Apportioned Particulate Air Pollution and 30-day Readmissions Among Heart Failure Patients

BACKGROUND AND AIM: Fine particulate air pollution (PM2.5) exposure is associated with increased risk of hospital readmissions. This study aims to determine if this association differs according to the attributable source of the PM2.5. METHODS: We used zero-inflated poisson mixed-effects models to associate source-apportioned PM2.5 with the number of 30-day readmissions after HF diagnosis. The study cohort included patients diagnosed with HF who had a hospital visit at a University of North Carolina Healthcare System facility between July 5, 2004, and December 31, 2010. The exposure was the annual average source-apportioned PM2.5 at the date of HF diagnosis. Patient zip code was included as a random effect and models were adjusted for year of diagnosis, sex, race, age, smoking status and 2010 census block group measures of urbanicity, percent receiving public assistance, median income, and median house value. PM2.5 was apportioned into the sources using a Chemical Mass Balance Gas Constrained-Iteration model. Results are presented as the percent change in number of expected readmissions per interquartile range increase in source-apportioned PM2.5 and the associated 95% confidence interval (CI). RESULTS: We observed associations with 30-day readmissions for gasoline (16.89%; 95% CI = 4.82-30.36), diesel (9.87%; 95% CI = 1.72-18.69), and secondary organic carbon (SOC; 20.44%; 95% CI = 8.29-33.95) PM2.5. Associations were greater for study participants in a census block group with an income below the median value. Associations were also greater for Black HF patients compared to white HF patients. CONCLUSIONS: Associations between 30-day readmissions and PM2.5 appear greatest for traffic and SOC-related sources which may be due to a combination of differential toxicity as well as the distribution of these sources amongst HF patients. This abstract does not necessarily represent the views or policies of the US Environmental Protection Agency. KEYWORDS: Heart failure, hospital utilization, particulate matter, air pollution

The potential involvement of inhaled iron (Fe) in the neurotoxic effects of ultrafine particulate matter air pollution exposure on brain development in mice

BackgroundAir pollution has been associated with neurodevelopmental disorders in epidemiological studies. In our studies in mice, developmental exposures to ambient ultrafine particulate (UFP) matter either postnatally or gestationally results in neurotoxic consequences that include brain metal dyshomeostasis, including significant increases in brain Fe. Since Fe is redox active and neurotoxic to brain in excess, this study examined the extent to which postnatal Fe inhalation exposure, might contribute to the observed neurotoxicity of UFPs. Mice were exposed to 1 µg/m3 Fe oxide nanoparticles alone, or in conjunction with sulfur dioxide (Fe (1 µg/m3) + SO2 (SO2 at 1.31 mg/m3, 500 ppb) from postnatal days 4–7 and 10–13 for 4 h/day.ResultsOverarching results included the observations that Fe + SO2 produced greater neurotoxicity than did Fe alone, that females appeared to show greater vulnerability to these exposures than did males, and that profiles of effects differed by sex. Consistent with metal dyshomeostasis, both Fe only and Fe + SO2 exposures altered correlations of Fe and of sulfur (S) with other metals in a sex and tissue-specific manner. Specifically, altered metal levels in lung, but particularly in frontal cortex were found, with reductions produced by Fe in females, but increases produced by Fe + SO2 in males. At PND14, marked changes in brain frontal cortex and striatal neurotransmitter systems were observed, particularly in response to combined Fe + SO2 as compared to Fe only, in glutamatergic and dopaminergic functions that were of opposite directions by sex. Changes in markers of trans-sulfuration in frontal cortex likewise differed in females as compared to males. Residual neurotransmitter changes were limited at PND60. Increases in serum glutathione and Il-1a were female-specific effects of combined Fe + SO2.ConclusionsCollectively, these findings suggest a role for the Fe contamination in air pollution in the observed neurotoxicity of ambient UFPs and that such involvement may be different by chemical mixture. Translation of such results to humans requires verification, and, if found, would suggest a need for regulation of Fe in air for public health protection.

Particulate matter air pollution exposure disrupts the Nrf2 pathway in sinonasal epithelium via epigenetic alterations in a murine model.

Particulate matter air pollution exposure disrupts the Nrf2 pathway in sinonasal epithelium via epigenetic alterations in a murine model.

Association of Exposure to Particulate Matter Air Pollution With Semen Quality Among Men in China

The health effects of exposure to particulate matter (PM) on male fertility remain unclear. Although PM exposure has been linked with semen quality, the results were inconsistent. To examine the association of different size fractions of PM (<2.5 μm [PM2.5], 2.5-10 μm [PM2.5-10], and ≤10 μm [PM10]) exposure with semen quality in China. This retrospective cohort study was conducted using data on men whose wives underwent assisted reproductive technology procedures in a tertiary hospital in Shanghai, China, from January 1, 2013, to December 31, 2019. Participants were from 340 prefecture-level cities of China and were followed up from the date of their first visit until December 31, 2019. Data were analyzed from December 1, 2020, to May 15, 2021. Exposure to PM2.5, PM2.5-10, and PM10 during the entire period (0-90 days before semen ejaculation) and key periods of sperm development (0-9, 10-14, and 70-90 days before semen ejaculation). Semen quality, including sperm count, concentration, and motility. A total of 33 876 men were included in the final analysis, with a mean (SD) age of 34.1 (5.7) years and large variation of PM exposure. For example, the median exposure to PM2.5 during the entire period of sperm development was 46.05 (IQR, 34.38-61.65) μg/m3. During the entire period of sperm development, exposures to higher levels of PM were significantly associated with lower total and progressive sperm motility. For total sperm motility, an IQR increase in PM2.5 exposure was associated with an estimated effect decrease of -3.60% (95% CI, -3.93% to -3.26%); an increase in PM2.5-10 exposure, with an estimated effect decrease of -0.45% (95% CI, -0.76% to -0.14%); and an increase in PM10 exposure, with an estimated effect decrease of -2.44% (95% CI, -2.91% to -1.96%). Similar results were observed for progressive motility. An IQR increase in PM2.5 or PM10 exposures was associated with an estimated effect decrease on sperm progressive motility of -1.87% (95% CI, -2.37% to -1.36%) and -1.05% (95% CI, -1.45% to -0.64%), respectively. However, no significant associations were observed between PM exposure during the entire period of sperm development and sperm count or concentration. These findings suggest that PM exposure may adversely affect sperm motility and highlight the need to reduce ambient particulate air pollution exposure for reproductive-aged men.

Dynamics of skin microvascular blood flow in 4-6-year-old children in association with pre- and postnatal black carbon and particulate air pollution exposure.

A growing body of evidence indicates that cardiovascular health in adulthood, particularly that of the microcirculation, could find its roots during prenatal development. In this study, we investigated the association between pre- and postnatal air pollution exposure on heat-induced skin hyperemia as a dynamic marker of the microvasculature. In 139 children between the ages of 4 and 6 who are followed longitudinally within the ENVIRONAGE birth cohort, we measured skin perfusion by Laser Doppler probes using the Periflux6000. Residential black carbon (BC), particulate (PM10 and PM2.5) air pollution, and nitrogen dioxide (NO2) levels were modelled for each participant's home address using a high-resolution spatiotemporal model for multiple time windows. We assessed the association between skin hyperemia and pre- and postnatal air pollution using multiple regression models while adjusting for relevant covariates. Residential BC exposure during the whole pregnancy averaged (IQR) 1.42 (1.22-1.58) µg/m3, PM10 18.88 (16.64 - 21.13) µg/m3, PM2.5 13.67 (11.5 - 15.56) µg/m3 and NO2 18.39 (15.52 - 20.31) µg/m3. An IQR increment in BC exposure during the third trimester of pregnancy was associated with an 11.5 % (95% CI: -20.1 to -1.9; p=0.020) lower skin hyperemia. Similar effect estimates were retrieved for PM10, PM2.5 and NO2 (respectively 13.9 % [95% CI: -21.9 to -3.0; p=0.003], 17.0 % [95% CI: -26.7 to -6.1; p=0.004] and 12.7% [95 % CI: -22.2 to -1.9; p=0.023] lower skin hyperemia). In multipollutant models, PM2.5 showed the strongest inverse association with skin hyperemia. Postnatal exposure to BC, PM10, PM2.5 or NO2, was not associated with skin hyperemia at the age of 4 to 6, and did not alter the previous reported prenatal associations when taken into account. Our findings support that BC, particulate air pollution, and NO2 exposure, even at low concentrations, during prenatal life, can have long-lasting consequences for the microvasculature. This proposes a role of prenatal air pollution exposures over and beyond postnatal exposure in the microvascular alterations which were persistent into childhood.

Abstract 11282: Meta-Analysis of Residential Portable Air Cleaner Use and Circulating Inflammatory Biomarkers

Introduction: Fine particulate matter air pollution (PM 2.5 ) exposure is associated with elevated circulating inflammatory biomarkers implicated in cardiovascular disease (CVD). Portable Air Cleaners (PAC)s reduce PM 2.5 exposure and may lower concentrations of inflammatory biomarkers. Methods: We performed a systematic review and meta-analysis of randomized crossover trials of in-home high efficiency particulate air (HEPA) PACs vs. sham control on changes in CRP, IL-6, and/or TNFα among adults with no smoking exposure using Medline, Embase, and Cochrane Central Register of Controlled Trials with the Ovid Platform, Inspec, Compendix, and Web of Science Core Collection. Two investigators (S.W, D.W.) independently screened and reviewed the studies. We used RevMan 5.3 to perform the meta-analysis. Results: Search results included 459 articles screened, 26 selected for full review, and 14 that met inclusion criteria, representing N=724 participants included in the meta-analysis. Ten studies reported CRP, 9 reported IL-6, and 5 reported TNFα. Based on WHO guidelines, 5 studies were in regions of extreme PM 2.5 exposure (&gt;35 μg/m 3 ), 3 were high (10-35 μg/m 3 ), 3 were low (&lt;10 μg/m 3 ), and 2 lacked baseline PM 2.5 . Median (± S.D.) duration of HEPA/sham use was 9 ± 6.6 days. Reductions in PM 2.5 ranged from 2.6 to 54.9 μg/m 3 (35-82%) and varied by baseline PM 2.5 , although reporting of baseline PM 2.5 was incomplete across trials. Compared to sham PAC use, active PACs were associated with a 7% lower CRP (95% CI -13%, 0%) and 12% lower IL-6 (-22%, -2%), P&lt;0.05 for both (Figure). Subgroup analyses demonstrated consistency of effect of PACs across levels of baseline PM 2.5 . Conclusions: Our data demonstrate that PAC use is associated with significant reductions in circulating CRP and IL-6, with a magnitude of effect similar to clinical trials of statins and IL-1β inhibition. Given the role of inflammation in CVD, PACs may be useful to reduce systemic inflammation and cardiovascular risk.

Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway

Urban fine particulate matter (PM2.5) is a deleterious risk factor in the ambient air and is recognized to exacerbate atherosclerosis. Perivascular adipose tissue (PVAT) secretes a large number of inflammatory cytokines and plays a crucial role in the pathogenic microenvironment of atherogenesis. However, there is a lack of knowledge about the role of PVAT inflammation in the genesis of PM2.5-related atherosclerosis. The aim of this research was to probe the latent links between PM2.5 exposure and PVAT inflammation and further discovered the underlying mechanisms of PM2.5-triggered atherosclerosis pathogenesis. Apolipoprotein E-deficient (ApoE−/−) mice were exposed to real-world atmospheric PM2.5 or filtered clean air for three months, the Wnt5a inhibitor Box5 and the Ror2 inhibitor β-Arrestin2 were applied to verify the possible mechanisms. We noticed that the average daily PM2.5 mass concentration was 84.27 ± 28.84 μg/m3. PM2.5 inhalation might significantly expedite the deterioration of atherosclerosis, increase the protein and mRNA expressions of MCP-1, IL-6, TNF-α, Wnt5a, and Ror2 in PVAT tissues, upregulate the distributions of IL-6, TNF-α, MCP-1, and leptin in the histological sections of PVAT, promote lipid deposition in the aorta, elevate the plasma levels of leptin, MCP-1, IL-6, TNF-α, LDL-C, TC, and TG, however, decrease the plasma levels of adiponectin and HDL-C, downregulate the distribution of adiponectin. Nevertheless, these effects caused by PM2.5 exposure were dramatically diminished after the administration of Box5 or β-Arrestin2. This research illuminated that PVAT inflammation was involved in the PM2.5-induced atherosclerosis process, as well as lipid deposition, which was closely associated with the activation of the Wnt5a/Ror2 signaling pathway.

Association between eye-level greenness and lung function in urban Chinese children

BackgroundHealth effects of greenness perceived by residents at eye level has received increasing attention. However, the associations between eye-level greenness and respiratory health are unknown. The aim of the study was to investigate the associations between exposure to eye-level greenness and lung function in children. MethodsFrom 2012 to 2013, a total of 6740 school children in seven cities in northeast China were recruited into this cross-sectional study. Forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), peak expiratory flow rate (PEF), and maximum mid expiratory flow rate (MMEF) were measured to evaluate lung function and to define lung impairment. Eye-level greenness was extracted from segmented Tencent Map street view images, and a corresponding green view index (GVI) was calculated. Higher GVIs mean more greenness coverage. Mixed-effects logistic regressions were used to estimate the health effects on lung impairment per interquartile range (IQR) increase in GVI. Linear regressions were used to estimate the associations between GVI and lung function. The health effects of ambient air pollutants were also assessed, including particulate matter with an aerodynamic diameter <1.0 μm (PM1), <2.5 μm (PM2.5), <10 μm (PM10) as well as nitrogen dioxide (NO2). ResultsAn increase of GVI800m was associated with lung impairment in FEV1, FVC, PEF and MMEF, with ORs ranging from 0.68 (95% CI: 0.59, 0.79) to 0.83 (95% CI: 0.74, 0.93). The associations between an IQR increase of GVI800m and FEV1 (48.15 ml, 95% CI: 30.33–65.97 ml), FVC (50.57 ml, 95% CI: 30.65–70.48 ml), PEF (149.59 ml/s, 95% CI: 109.79–189.38 ml/s), and MMEF (61.18 ml/s, 95% CI: 31.07–91.29 ml/s) were significant, and PM1, PM2.5, and PM10 were found to be mediators of this relationship. ConclusionMore eye-level greenness was associated with better lung function and reduced impairment. However, eye-level greenness associations with lung function became non-significant once lower particulate matter air pollution exposures were considered.

Differential impacts of particulate air pollution exposure on early and late stages of spermatogenesis

BackgroundDespite increasing evidence that particulate air pollution has adverse effects on human semen quality, few studies examine the impact of air pollution on clinically relevant thresholds used to diagnose male fertility problems. Furthermore, exposure is often assessed using average air pollution levels in a geographic area rather than individualized estimates. Finally, physiologically-informed exposure windows are inconsistent. ObjectivesWe sought to test the hypothesis that airborne particulate exposures during early-phase spermatogenesis will have a differential impact on spermatogenic formation compared to late-phase exposures, using an individualized model of exposure to particulate matter ≤ 2.5 µm and ≤ 10 µm (PM2.5 and PM10, respectively). MethodsFrom an original cohort of 183 couples, we conducted a retrospective analysis of 130 healthy males seeking to become parents, using spermatogenesis-relevant exposure windows of 77–34 days and 37–0 days prior to semen collection to encompass sperm development stages of mitosis/meiosis and spermiogenesis, respectively. Individualized residential exposure to PM2.5 and PM10 was estimated by selecting multiple air pollution sensors within the same geographic air basin as participants and employing inverse distance weighting to calculate mean daily exposure levels. We used multiple logistic regression to assess the association between pollution, temperature, and dichotomized World Health Organization semen parameters. ResultsDuring the early phase of spermatogenesis, air pollution exposure is associated with 1.52 (95% CI: 1.04–2.32) times greater odds of < 30% normal heads per 1-unit increase in IQR for PM2.5. In the late phase of spermatogenesis, air pollution exposure is associated with 0.35 (95% CI: 0.10–0.74) times greater odds of semen concentration < 15 million/mL per 1-unit increase in IQR for PM2.5, and 0.28 (95% CI: 0.07–0.72) for PM10. ConclusionParticulate exposure has a differential and more deleterious impact on sperm during early-phase spermatogenesis than late-phase.

Abstract MP70: Short-term Fine Particulate Air Pollution Is Associated With Shorter Sleep Duration And Higher Sleep Variability In Adolescents

Introduction: Sleep deprivation and large sleep variability are potential risk factors for obesity and cardiovascular diseases. While it is plausible that particulate air pollution may contribute to these unfavorable sleep patterns, very few studies have been conducted to assess the association between fine particulate (PM 2.5 ) air pollution and objectively measured sleep duration and its variability in an adolescent U.S. population. Hypothesis: We tested the hypothesis that higher individual-level short-term PM 2.5 exposure is associated with shorter sleep duration and higher sleep variability among adolescents. Methods: We analyzed the available data collected from 421 adolescents who participated in the follow-up examination of the population-based Penn State Child Cohort (PSCC) study. To estimate individual-level short-term PM 2.5 exposure, a personal nephelometer (Thermo pDR-1200) was used to measure real-time PM 2.5 concentration for 24 hours from the study participants. The 24-hour mean PM 2.5 concentration was used to quantify the short-term PM 2.5 exposure. To obtain objectively-measured habitual sleep duration (HSD) and habitual sleep variability (HSV), an actigraphy (GT3X+) was used to collect sleep data for 7 consecutive nights, including 1 night in parallel with the PM 2.5 monitoring and 6 nights thereafter. HSD and HSV were calculated as the intra-individual mean and standard deviation (SD) of the 7-night sleep duration, respectively. Participants with &lt; 5 nights (70% of 7 nights) of data were excluded from the analyses. The associations between the individual-level PM 2.5 exposure and HSD/HSV were evaluated by using multi-variable adjusted linear regression models, controlling for age, race, sex, BMI percentile, environmental temperature, and relative humidity. Results: The mean (SD) age of the study population was 16.9 (2.2) years. The study sample consisted of 54% males and 78% whites. The 24-hour mean (SD) of PM 2.5 concentration was 16.9 (26.8) μg/m 3 , while the average HSD and HSV were 7.0 (0.9) hours and 1.2 (0.6) hours, respectively. We observed that a 10 μg/m 3 increase in the 24-hour mean PM 2.5 was associated with significantly lower HSD [β (SE): -0.06 (0.03) hours, p=0.02] and larger HSV [β (SE): 0.04 (0.02) hours, p=0.04]. The effect sizes were approximately 7% of their respective SDs. Conclusion: Individual-level short-term PM 2.5 exposure is associated with objective-measured shorter sleep duration and higher night-to-night sleep variability among U.S. adolescents. These observed associations suggest that particulate air pollution exposure in early life may impact habitual sleep pattern, which may in turn be associated with the risks of obesity and cardiovascular diseases in later life.

Does Physical Activity Modify the Association between Air Pollution and Recurrence of Cardiovascular Disease?

We aimed to assess a possible interaction effect between physical activity and particulate air pollution exposure on recurrence of ischemic heart disease (IHD) and stroke. We followed 2221 adult participants comprising first time IHD (1403) and stroke (818) cases from the Västerbotten Intervention Program between 1 January 1990 to 31 December 2013. During mean follow-up times of 5.5 years, 428 and 156 participants developed IHD and stroke recurrence, respectively. PM2.5 concentrations above the median (5.48 µg/m3) were associated with increased risk of IHD and stroke recurrence by 13% (95% CI −17–45%) and 21% (95% CI −19–80%), respectively. These risk increases were however only observed among those that exercised at most once a week at 21% (95% CI −5–50%) and 25% (95% CI −19–90%) for IHD and stroke recurrence, respectively. Higher frequency of exercise at recruitment was positively associated with IHD and stroke recurrence but only the association with IHD recurrence among participants with low residential PM2.5 was statistically significant (96% increased risk (95%-CI 22–215%)). However, no interaction effect between physical activity and PM2.5 exposure was found. Our findings suggest that physical activity may reduce the air pollution exposure associated risk for recurrent cardiovascular disease, likely by reducing the inflammatory response.

Early-life exposure to submicron particulate air pollution in relation to asthma development in Chinese preschool children

Emerging research suggested an association of early-life particulate air pollution exposure with development of asthma in childhood. However, the potentially differential effects of submicron particulate matter (PM; PM with aerodynamic diameter ≤1 μm [PM1]) remain largely unknown. This study primarily aimed to investigate associations of childhood asthma and wheezing with in utero and first-year exposures to size-specific particles. We conducted a large cross-sectional survey among 5788 preschool children aged 3 to 5 years in central China. Inutero and first-year exposures to ambient PM1, PM with aerodynamic diameter less than or equal to 2.5 μm, and PM with aerodynamic diameter less than or equal to 10 μm at 1×1-km resolution were assessed using machine learning-based spatiotemporal models. Atime-to-event analysis was performed to examine associations between residential PM exposures and childhood onset of asthma and wheezing. Early-life size-specific PM exposures, particularly during pregnancy, were significantly associated with increased risk of asthma, whereas no evident PM-wheezing associations were observed. Each 10-μg/m3 increase in in utero and first-year PM1 exposure was accordingly associated with an asthma's hazard ratio in childhood of 1.618 (95% CI, 1.159-2.258; P= .005) and 1.543 (0.822-2.896; P= .177). Subgroup analyses suggest that short breast-feeding duration may aggravate PM-associated risk of childhood asthma. Each 10-μg/m3 increase in in utero exposure to PM1, for instance, was associated with a hazard ratio of 2.260 (1.393-3.666) among children with 0 to 5 months' breast-feeding and 1.156 (0.721-1.853) among those longer breast-fed. Our study added comparative evidence for increased risk of childhood asthma in relation to early-life PM exposures, highlighting stronger associations with ambient PM1 than with PM with aerodynamic diameter less than or equal to 2.5 μm and PM with aerodynamic diameter less than or equal to 10 μm.