Low-level Air Research Articles

Exposure to Low-Level Air Pollution and Hyperglycemia Markers during Pregnancy: A Repeated Measure Analysis.

Epidemiologic evidence has emerged showing an association between exposure to air pollution and increased risks of gestational diabetes mellitus (GDM). This study examines the effect of low-level air pollution exposure on a subclinical biomarker of hyperglycemia (i.e., HbA1c) in pregnant people without diabetes before conception. We measured HbA1c in 577 samples repeatedly collected from 224 pregnant people in Rochester, NY, and estimated residential concentrations of PM2.5 and NO2 using high-resolution spatiotemporal models. We observed a U-shaped trajectory of HbA1c during pregnancy with average HbA1c levels of 5.13 (±0.52), 4.97 (±0.54), and 5.43 (±0.40)% in early-, mid-, and late pregnancy, respectively. After adjustment for the U-shaped trajectory and classic GDM risk factors, each interquartile range increase in 10 week NO2 concentration (8.0 ppb) was associated with 0.09% (95% CI: 0.02 to 0.16%) and 0.18% (95% CI: 0.08 to 0.28%) increases in HbA1c over the entire pregnancy and in late pregnancy, respectively. These associations remained robust among participants without GDM. Using separate distributed lag models, we identified a period between 8th and 14th gestational weeks as critical windows responsible for increased levels of HbA1c measured at 14th, 22nd, and 30th gestational weeks. Our results suggest that low-level air pollution contributes to hyperglycemia in medically low-risk pregnant people.

Long-term exposures to low concentrations of source-specific air pollution, road-traffic noise, and systemic inflammation and cardiovascular disease biomarkers

ObjectivesAir pollution and traffic noise are detrimental to cardiovascular health. However, the effects of different sources of these exposures on cardiovascular biomarkers remain unclear. We explored the associations of long-term exposure to source-specific air pollution (vehicular exhausts and residential woodsmoke) at low concentrations and road-traffic noise with systemic inflammation and cardiovascular disease biomarkers. Material and methodsModeled outdoor exposure to fine particulate matter (aerodynamic diameter ≤2.5 μm; PM2.5) from vehicular exhausts and residential woodsmoke, nitrogen dioxide (NO2) from road traffic, and road-traffic noise were linked to the home addresses of the participants (Finnish residents aged 25–74) in the FINRISK study 1997–2012. The participants were located in the cities of Helsinki, Vantaa, and the region of Turku, Finland. The outcomes were high-sensitivity C-reactive protein (CRP), a biomarker for systemic inflammation, and cardiovascular disease biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin I. We performed cross-sectional analyses with linear and additive models and adjusted for potential confounders. ResultsWe found no association between PM2.5 from vehicular exhausts (% CRP difference for 1 μg/m3 increase in PM2.5: −0.9, 95% confidence interval, CI: −7.2, 5.8), or from residential woodsmoke (% difference: −8.1, 95% CI: −21.7, 7.9) and CRP (N = 4147). Road-traffic noise >70 dB tended to be positively associated with CRP (% CRP difference versus noise reference category of ≤45 dB: 18.3, 95% CI: −0.5, 40.6), but the association lacked significance and robustness (N = 7142). Otherwise, we found no association between road-traffic noise and CRP, nor between NO2 from road traffic and NT-proBNP (N = 1907) or troponin I (N = 1951). ConclusionLong-term exposures to source-specific, fairly low-level air pollution from vehicular exhausts and residential woodsmoke, or road-traffic noise were not associated with systemic inflammation and cardiovascular disease biomarkers in this urban area.

The effect of low-level air pollution exposure on weight at birth

The effect of low-level air pollution exposure on weight at birth

Systemic oxidative stress levels during the course of pregnancy: Associations with exposure to air pollutants

Increased systemic oxidative stress, implicated in adverse pregnancy outcomes for both mothers and fetuses, has been associated with gestational exposure to air pollutants such as polycyclic aromatic hydrocarbons (PAHs), fine particulate matter (PM2.5), and nitrogen dioxide (NO2). However, it is unclear whether exposure to pollutants at levels below the current air quality standards can increase oxidative stress in pregnant women. In a cohort of 305 pregnant persons residing in western New York, we examined the association between exposure to PM2.5, NO2, and PAHs (measured as urinary 1-hydroxypyrene) and urinary biomarkers of oxidative stress (malondialdehyde [MDA] and 8-hydroxy-2′-deoxyguanosine [8-OHdG]) measured in each trimester. After controlling for gestational stage, maternal age, lifestyles, and socioeconomic factors, each interquartile range (IQR) increase in 1-hydroxypyrene concentration (65.8 pg/ml) was associated with a 7.73% (95%CI: 3.18%,12.3%) higher in MDA levels throughout the pregnancy and in the first and second trimester. An IQR increase in PM2.5 concentration (3.20 μg/m3) was associated with increased MDA levels in the first trimester (8.19%, 95%CI: 0.28%,16.1%), but not the 2nd (−7.99%, 95% CI: 13.8%, −2.23%) or 3rd trimester (−2.81%, 95% CI: 10.0%, 4.38%). The average cumulative PM2.5 exposures in the 3–7 days before urine collection were associated with increased 8-OHdG levels during the second trimester, with the largest difference (22.6%; 95% CI: 3.46%, 41.7%) observed in relation to a one IQR increase in PM2.5 concentration in the previous 7 days. In contrast, neither oxidative stress biomarker was associated with NO2 exposure. Observed in pregnant women exposed to low-level air pollution, these findings expanded previously reported associations between systemic oxidative stress and high-level PM2.5 and PAH concentrations. Further, the first and second trimesters may be a susceptible window during pregnancy for oxidative stress responses to air pollution exposure.

Joint associations of air pollutants during pregnancy, infancy, and childhood with childhood persistent asthma: Nationwide database study in Japan

The joint effect of air pollutants at relatively low levels requires further investigation. Here, a database study was performed to evaluate the effects of exposure to mixtures of air pollutants during pregnancy, infancy, and childhood on childhood persistent asthma. We used the Japan Medical Data Center database, which provides access to family linkages and healthcare provider addresses, and included child-mother dyads in which the child was born between January 2010 and January 2017. The exposure of interest was ground-level air pollutants, and the primary outcome was childhood persistent asthma at 45 years of age, as defined based on outpatient and inpatient asthma disease codes and/or asthma medication dispensing claims. The weighted quantile sum (WQS) regression was used to evaluate the effects of air pollutant mixtures on 52,526 child-mother dyads from 1149 of 1907 municipalities (60.3 %) in Japan. The WQS regression models showed that with every 10th percentile increase in the WQS index, ground-level air pollutants during pregnancy, infancy, and childhood increased the risk of childhood persistent asthma by an odds ratio of 1.04 (95 % CI: 1.02–1.05; p<0.001), 1.02 (95 % CI: 1.01–1.03; p<0.001), and 1.03 (95 % CI: 1.01–1.04; p<0.001), respectively. Moreover, particulate matter with an aerodynamic diameter ≤ 2.5 µm was assigned the highest weight across all three exposure periods. Relatively high weights were assigned to suspended particulate matter and photochemical oxidants during pregnancy, carbon monoxide during infancy, and photochemical oxidants during childhood. Our study showed that a mixture of low-level air pollutants has a detrimental association with childhood persistent asthma.

#506 Long-term exposure to air pollution and CKD-associated mortality: results from the pooled cohort of the European multicentre ELAPSE-study

Abstract Background and Aims Air pollution has been shown to be associated with cause-specific mortality. However, mortality due to chronic kidney disease (CKD) is understudied in this context, with no European data available so far. We investigated the relation between long-term exposure to air pollution and CKD-associated mortality in the Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE). Method Data of five population-based cohorts from four European countries from the pooled ELAPSE cohort were linked to data from local mortality registries. CKD-associated mortality was defined using ICD10 codes N18-N19 or corresponding ICD9 codes. Mean annual exposure at home address was determined with Europe-wide hybrid land use regression models for nitrogen dioxide (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 µm (PM2.5) and several elemental constituents of PM2.5 with a spatial resolution of 100 m x 100 m. Cox regression models were adjusted for age (time-axis), cohort and sex (both as strata), calendar year of recruitment, smoking status, marital status, employment status and neighborhood mean income. Results Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were observed for all pollutants, positive for PM2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 µg/m3 increase), BC (1.26 (1.03-1.53) per 0.5 × 10− 5/m), NO2 (1.13 (0.93-1.38) per 10 µg/m3) and negative for O3 (0.71 (0.54-0.93) per 10 µg/m3). Results were robust when additionally adjusting for smoking intensity and duration, BMI, education or residential greenness, but susceptible to cohort selection. Findings are mainly based on the large Austrian cohort, that contributed 226 cases. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different PM2.5 sources including traffic, industry, biomass and oil burning and long-range transport, were associated with CKD-related mortality. Conclusion In conclusion, our results suggest a possible association between air pollution from different sources with CKD-related mortality. Our results indicate that measures to improve air quality and decrease air pollution might also be beneficial from a renal perspective.

Long-term ambient air pollution and coronary atherosclerosis: Results from the Swedish SCAPIS study

Background and aimsDespite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis. MethodsWe performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM2.5), <10 μm (PM10), and nitrogen oxides (NOx) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders. ResultsMedian 10-year average PM2.5 exposure was 6.2 μg/m3 (range 3.5–13.4 μg/m3). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m3). Associations with significant stenoses were inconsistent. ConclusionsIn this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.

Interaction of physical activity and low-level air pollution on cardiovascular disease: a prospective cohort study in UK Biobank.

To investigate theassociations of physical activity (PA), low-level air pollution, and interaction on cardiovascular diseases (CVD) incidence based on the UK Biobank. PA was measured by the International Physical Activity Questionnaire and five air pollutants were estimated using Land Use Regression. All association estimates were based on Cox regression. Dose-response relationship was explored by restricted cubic spline, while multiplicative and additive interaction were examined by Pinteraction and relative excess risk due to interaction (RERI). As deviating proportional hazards assumption, we analyzed data as follow-up < 4years and ≥ 4years, separately. PA with 1000-4000 Metabolic Equivalent Task (MET) min/week showed the strongest protective impact on CVD incidence, while only low-level nitrogen dioxides (NO2) showed negative impact among five air pollutants and was considered for further analysis. Multiplicative interaction between PA and NO2 was observed during ≥ 4years follow-up (Pinteraction = 0.049) while not during < 4years (Pinteraction = 0.290). Positive additive interactions were found for high PA and low NO2 (< 20 μg/m3) group (RERI: 0.07, 95% confidence intervals: 0.02-0.11) during < 4years, and for moderate PA with NO2 at 40- μg/m3 (0.07, 0.02-0.13) and < 20 μg/m3 (0.07, 0.02-0.12), while high PA showed similar results with NO2 at 40-, 20- and < 20 μg/m3 during ≥ 4years. PA about 1000-4000 METs min/week showed the lowest CVD risk. Possibility of interaction with PA and NO2 is more likely to present with the increase in follow-up duration. We call for the optimal thresholds of PA, and exploring interaction thoroughly by considering types of PA.

Long-term exposure to ambient air pollution and risk of leukemia and lymphoma in a pooled European cohort

Leukemia and lymphoma are the two most common forms of hematologic malignancy, and their etiology is largely unknown. Pathophysiological mechanisms suggest a possible association with air pollution, but little empirical evidence is available. We aimed to investigate the association between long-term residential exposure to outdoor air pollution and risk of leukemia and lymphoma. We pooled data from four cohorts from three European countries as part of the “Effects of Low-level Air Pollution: a Study in Europe” (ELAPSE) collaboration. We used Europe-wide land use regression models to assess annual mean concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) at residences. We also estimated concentrations of PM2.5 elemental components: copper (Cu), iron (Fe), zinc (Zn); sulfur (S); nickel (Ni), vanadium (V), silicon (Si) and potassium (K). We applied Cox proportional hazards models to investigate the associations. Among the study population of 247,436 individuals, 760 leukemia and 1122 lymphoma cases were diagnosed during 4,656,140 person-years of follow-up. The results showed a leukemia hazard ratio (HR) of 1.13 (95% confidence intervals [CI]: 1.01–1.26) per 10 μg/m3 NO2, which was robust in two-pollutant models and consistent across the four cohorts and according to smoking status. Sex-specific analyses suggested that this association was confined to the male population. Further, the results showed increased lymphoma HRs for PM2.5 (HR = 1.16; 95% CI: 1.02–1.34) and potassium content of PM2.5, which were consistent in two-pollutant models and according to sex. Our results suggest that air pollution at the residence may be associated with adult leukemia and lymphoma.

Diverging Behaviors of Simulated Tropical Cyclones in Moderate Vertical Wind Shear

Abstract As a follow-on to a previous study that examined the tilt and precession evolution of tropical cyclones (TCs) in a critical shear regime, this study examines the processes leading to the subsequent divergent evolutions in tilt and intensity. The control experiment fails to resume its precession and reintensify, while the perturbed experiments with enhanced upper-level inner-core vorticity resume the precession after a precession hiatus period. In the control experiment, a mesoscale negative absolute vorticity region forms at the upper levels due to tilting in strong downtilt convection. This upper-level, negative-vorticity region is inertially unstable, causing the inward acceleration of upper-level radial inflow. This upper-level inflow subsequently becomes negatively buoyant due to diabatic cooling and descends, bringing midlevel, low equivalent potential temperature (θE) air into the inner-core TC boundary layer, significantly disrupting the low-level TC circulation. Consequently, the disrupted TC vortex in the control is unable to recover. The upper-level negative vorticity region is absent in the perturbed experiments due to weaker downtilt convection, preventing the emergence of the disruptive inner-core downdraft. The weaker downtilt convection is caused by several factors. First, a stronger circulation aloft advects hydrometeors farther downwind, resulting in greater separation of the cooling-driven downdraft from the convective updraft region, and thus weaker dynamically forced lifting at low levels. Second, the mean θE of the low-level air feeding downtilt convection is smaller. Third, there is stronger and deeper adiabatic descent uptilt, causing more low-θE air diluting the downtilt updraft region. These results show how the full vortex structure is important to diverging TC evolutions in moderately sheared environments.

Long-Term Exposure to Low-Level and Mortality: Investigation of Heterogeneity by Harmonizing Analyses in Large Cohort Studies in Canada, United States, and Europe.

Studies across the globe generally reported increased mortality risks associated with particulate matter with aerodynamic diameter () exposure with large heterogeneity in the magnitude of reported associations and the shape of concentration-response functions (CRFs). We aimed to evaluate the impact of key study design factors (including confounders, applied exposure model, population age, and outcome definition) on effect estimates by harmonizing analyses on three previously published large studies in Canada [Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE), 1991-2016], the United States (Medicare, 2000-2016), and Europe [Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), 2000-2016] as much as possible. We harmonized the study populations to individuals years of age, applied the same satellite-derived exposure estimates, and selected the same sets of potential confounders and the same outcome. We evaluated whether differences in previously published effect estimates across cohorts were reduced after harmonization among these factors. Additional analyses were conducted to assess the influence of key design features on estimated risks, including adjusted covariates and exposure assessment method. A combined CRF was assessed with meta-analysis based on the extended shape-constrained health impact function (eSCHIF). More than 81 million participants were included, contributing 692 million person-years of follow-up. Hazard ratios and 95% confidence intervals (CIs) for all-cause mortality associated with a increase in were 1.039 (1.032, 1.046) in MAPLE, 1.025 (1.021, 1.029) in Medicare, and 1.041 (1.014, 1.069) in ELAPSE. Applying a harmonized analytical approach marginally reduced difference in the observed associations across the three studies. Magnitude of the association was affected by the adjusted covariates, exposure assessment methodology, age of the population, and marginally by outcome definition. Shape of the CRFs differed across cohorts but generally showed associations down to the lowest observed levels. A common CRF suggested a monotonically increased risk down to the lowest exposure level. https://doi.org/10.1289/EHP12141.

Long-term exposure to low-level air pollution and greenness and mortality in Northern Europe. The Life-GAP project

BackgroundAir pollution has been linked to mortality, but there are few studies examining the association with different exposure time windows spanning across several decades. The evidence for the effects of green space and mortality is contradictory. ObjectiveWe investigated all-cause mortality in relation to exposure to particulate matter (PM2.5 and PM10), black carbon (BC), nitrogen dioxide (NO2), ozone (O3) and greenness (normalized difference vegetation index - NDVI) across different exposure time windows. MethodsThe exposure assessment was based on a combination of the Danish Eulerian Hemispheric Model and the Urban Background Model for the years 1990, 2000 and 2010. The analysis included a complete case dataset with 9,135 participants from the third Respiratory Health in Northern Europe study (RHINE III), aged 40–65 years in 2010, with mortality follow-up to 2021. We performed Cox proportional hazard models, adjusting for potential confounders. ResultsAltogether, 327 (3.6 %) persons died in the period 2010–2021. Increased exposures in 1990 of PM2.5, PM10, BC and NO2 were associated with increased all-cause mortality hazard ratios of 1.40 (95 % CI1.04–1.87 per 5 μg/m3), 1.33 (95 % CI: 1.02–1.74 per 10 μg/m3), 1.16 (95 % CI: 0.98–1.38 per 0.4 μg/m3) and 1.17 (95 % CI: 0.92–1.50 per 10 μg/m3), respectively. No statistically significant associations were observed between air pollution and mortality in other time windows. O3 showed an inverse association with mortality, while no association was observed between greenness and mortality. Adjusting for NDVI increased the hazard ratios for PM2.5, PM10, BC and NO2 exposures in 1990. We did not find significant interactions between greenness and air pollution metrics. ConclusionLong term exposure to even low levels of air pollution is associated with mortality. Opening up for a long latency period, our findings indicate that air pollution exposures over time may be even more harmful than anticipated.

Fanning the Flames: Low-Level Air Pollution and Risk of Surgery or Mortality for Persons with IBD.

Fanning the Flames: Low-Level Air Pollution and Risk of Surgery or Mortality for Persons with IBD.

Deck level air extraction and its impact on trichloramine concentrations in an indoor swimming pool: A numerical study

Trichloramine (NCl3) is a disinfection by-product (DBP) that forms in swimming pool water due to water chlorination. It easily becomes airborne when water is agitated and can impair lung functions and cause illnesses such as asthma and bronchitis in workers and bathers, when inhaled. In indoor swimming pools, NCl3 must be removed from the breathing zones with mechanical ventilation. Since it tends to accumulate at the water surface, ASHRAE's recommendations are to add lower extraction vents to capture DBP. However, no guideline is found in literature on the number of vents, their position in the enclosure or their minimum airflow rate. This paper presents a numerical investigation of the impacts on NCl3 concentrations when adding extraction vents at deck level in a swimming pool hall in Montreal (Canada). The efficiency of four ventilation scenarios that include low extraction vents was determined numerically and compared to the reference case which does not have lower-level exhaust vents. Results show that the position of these vents affects the air movement above the water surface, causing either unwanted accumulation or reduction of NCl3. The most significant reduction was obtained when placing these vents on the side of the enclosure where low level air supplied grills are located. Finally, the NCl3 that is not extracted is sent upwards and diluted thanks to the nearby air delivery grills. The results demonstrate the importance of a numerical assessment of the airflow patterns in a pool enclosure and especially above the water and deck before planning the position of these deck level extraction vents.

Mechanical and Thermal Forcings of Asian Large-Scale Orography on Spring Cloud Amount and Atmospheric Radiation Budget over East Asia

Abstract Asian large-scale orography profoundly influences circulation in the North Hemisphere. Considerable spring top-of-the-atmosphere (TOA) radiative cooling over Southeast China (SEC) is very likely related to upstream orography forcing. Here we investigate the mechanical and thermal forcings of Asian large-scale orography, particularly the Tibetan Plateau (TP), on downstream East Asian cloud amount and atmospheric radiation budget during March–April using the Global Monsoons Model Intercomparison Project simulations. The thermal forcing drives significant surface heating and a low-level cyclone over the TP, pumping low-level air to the middle troposphere. Ascent and water vapor convergence triggered by the thermal forcing favor air condensation, low–middle clouds, and resultant strong spring cloud radiative cooling over SEC. Moreover, the thermal forcing moves the position of cloud radiative cooling westward toward the TP. The TP’s blocking role weakens low-level westerlies over SEC, but its deflecting role increases downstream high-level westerlies, dynamically favoring cloud formation over SEC and the eastward ocean. In addition, the TP can force ascent and increase cloud amounts over the western and central TP. The thermal forcing contributes to 57.1% of total cloud amount and 47.6% of TOA cloud radiative cooling induced by the combined orography forcing over SEC while the mechanical one accounts for 79.4% and 95.8% of the counterparts over the ocean to the east of SEC. Our results indicate that Asian large-scale orography shapes the contemporary geographical distribution of spring East Asian cloud amount and atmospheric radiation budget to a large extent. Significance Statement Clouds tied to large-scale topography and circulation exhibit some remarkable geographical distributions. The global strongest cloud radiative cooling, with an intensity of up to −90 W m−2, occurs over Southeast China (SEC) during March–April. The primary purpose of this study is to understand the influences of Asian large-scale orography, particularly the Tibetan Plateau (TP), on this unique climatic phenomenon using the latest climate model simulations. Our results show that Asian large-scale orography forcing significantly increases ascent, low–middle cloud formation, and resultant strong spring cloud radiative cooling over SEC and downstream ocean. The sensible-heat-driven air pump induced by the TP’s thermal forcing maintains strong cloud radiative cooling over SEC. This study provides valuable insights that link Asian large-scale orography forcing to downstream cloud–radiation characteristics.

Association between long-term exposure to low level air pollutants and incident end-stage kidney disease in the UK Biobank: A prospective cohort

BackgroundPrevious studies suggest that air pollution can increase the risk of incident chronic kidney disease (CKD). However, the association between end-stage kidney disease (ESKD) and co-exposure to relatively low-level air pollutants remains unclear. MethodsA prospective cohort was designed based on UK Biobank. From 1 January 2010 to 12 November 2021, 453,347 participants were followed up over a median of 11.87 years. Principal component analysis was used to identify major patterns of five air pollutants, including PM2.5, PM2.5-10, PM10, NO2, and NOx. Sub-distribution hazards models were used to estimate the associations between air pollution, individually or jointly, and incident ESKD, CKD, and all-cause death, respectively. ResultsPrincipal component analysis identified two principal components, namely RC1 (PM2.5, NO2, and NOx) and RC2 (PM2.5-10 and PM10). An elevated risk of incident ESKD was associated with an interquartile range (IQR) increase in PM2.5 (hazard ratio: 1.11, 95% confidence interval: 1.02–1.22), NO2 (1.16, 1.04–1.30), NOx (1.08, 1.00–1.17), and RC1 (1.12, 1.02–1.23). An elevated risk of incident CKD was associated with an IQR increase in PM2.5 (1.05, 1.03–1.07), NO2 (1.04, 1.02–1.06), NOx (1.03, 1.02–1.05), and RC1 (1.04, 1.02–1.06). An increased risk of all-cause mortality was associated with an IQR increase in PM2.5 (1.02, 1.00–1.04). Restricted cubic spline analyses indicated a monotonic elevating association of PM2.5, NO2, NOx, and RC1 with ESKD incidence. ConclusionsLong-term exposure to PM2.5, NO2, NOx, and their complex was associated with elevated ESKD incidence, even at relatively lower levels of air pollution.

Air pollution, alcohol consumption, and the risk of elevated liver enzyme levels: a cross-sectional study in the UK Biobank.

Evidences on the association between exposure to air pollution and liver enzymes was scarce in low pollution area. We aimed to investigate the association between air pollution and liver enzyme levels and further explore whether alcohol intake influence this association. This cross-sectional study included 425,773 participants aged 37 to 73years from the UK Biobank. Land Use Regression was applied to assess levels of PM2.5, PM10, NO2, and NOx. Levels of liver enzymes including AST, ALT, GGT, and ALP were determined by enzymatic rate method. Long-term low-level exposure to PM2.5 (per 5-μg/m3 increase) was significantly associated with AST (0.596% increase, 95% CI, 0.414 to 0.778%), ALT (0.311% increase, 0.031 to 0.593%), and GGT (1.552% increase, 1.172 to 1.933%); The results were similar for PM10; NOX and NO2 were only significantly correlated with AST and GGT Significant modification effects by alcohol consumption were found (P-interaction < 0.05). The effects of pollutants on AST, ALT, and GGT levels gradually increased along with the weekly alcohol drinking frequency. In conclusion, long-term low-level air pollutants exposure was associated with elevated liver enzyme levels. And alcohol intake may exacerbate the effect of air pollution on liver enzymes.

Medium term moderate to low-level air pollution exposure is associated with higher C-reactive protein among healthy Danish blood donors

Air pollution is a significant contributor to the global burden of disease with a plethora of associated health effects such as pulmonary and systemic inflammation. C-reactive protein (CRP) is associated with a wide range of diseases and is associated with several exposures. Studies on the effect of air pollution exposure on CRP levels in low to moderate pollution settings have shown inconsistent results.In this cross-sectional study high sensitivity CRP measurements on 18,463 Danish blood donors were linked to modelled air pollution data for NOx, NO2, O3, CO, SO2, NH3, mineral dust, black carbon, organic carbon, sea salt, secondary inorganic aerosols and its components, primary PM2.5, secondary organic aerosols, total PM2.5, and total PM10 at their residential address over the previous month. Associations were analysed using ordered logistic regression with CRP quartile as individuals outcome and air pollution exposure as scaled deciles. Analyses were adjusted for health related and socioeconomic covariates using health questionnaires and Danish register data.Exposure to different air pollution components was generally associated with higher CRP (odds ratio estimates ranging from 1.11 to 1.67), while exposure to a few air pollution components was associated with lower CRP. For example, exposure to NO2 increased the odds of high CRP 1.32-fold (95%CI 1.16–1.49), while exposure to NH3 decreased the odds of high CRP 0.81-fold (95%CI 0.73–0.89).This large study among healthy individuals found air pollution exposure to be associated with increased levels of CRP even in a setting with low to moderate air pollution levels.

Effects of low-level air pollution exposures on hospital admission for myocardial infarction using multiple causal models

Myocardial infarctions have been associated with PM2.5, and more recently with NO2 and O3, however counterfactual designs have been lacking and argument continues over the extent of confounding control. Here we introduce a doubly robust, counterfactual-based approach that deals with nonlinearity and interactions in associations between confounders and both outcome and exposure, as well as a double negative controls approach that capture omitted confounders.We used data from over 4 million admissions for myocardial infarction in the US Medicare population between 2000 and 2016 and linked them by ZIP code of residence to high resolution predictions of annual PM2.5, NO2, and O3. We computed the counts of admissions for each ZIP code-year. In the doubly robust approach, we divided each pollutant into deciles, and for each decile, we fitted a gradient boosting machine model to estimate the effects of covariates, including the co-pollutants, on the counts. We used these models to predict, for all ZIP code-years, the expected counts had everyone be exposed in that decile. We also estimated the probability of being in that decile given all covariates, again with a gradient boosting machine, and used inverse probability weights to compute the weighted average rate of MI admission in each decile. In the negative control approach, for each pollutant, we fitted a quasi-Poisson model to estimate the exposure effect, adjusting for covariates including the co-pollutants, and negative exposure and outcome controls to control for unmeasured confounding.Each 1-μg/m3 increase in annual PM2.5 increased the admission for MI by 1.37 cases per 10,000 person-years (95% CI: 1.20, 1.54) in the doubly robust approach, and by 0.69 cases (95% CI 0.60, 0.78) using the negative control approach. Elevated risks were seen even below annual PM2.5 level of 8 μg/m3. Results for NO2 and O3 were inconsistent.

Land–Atmosphere Interactions Partially Offset the Accelerated Tibetan Plateau Water Cycle through Dynamical Processes

Abstract The Tibetan Plateau (TP) has become wetter and warmer during the past four decades, which leads to an adjustment in the surface energy budget, characterized by enhanced surface latent heat and weakened surface sensible heat. However, the impacts of these surface energy changes on climate are unclear. In this study, we investigate the atmospheric response to the altered surface energy budget in the monsoon season over the TP using regional climate simulations. The inhibited surface sensible heating weakens the thermal effect of the TP, which further suppresses low-level convergence and upper-level divergence, thereby weakening the water vapor flux convergence over the plateau. The weakening of low-level air humidity by this dynamical response exceeds the supply from the enhanced surface evaporation, causing decreased precipitation (decreasing more in the wet eastern plateau and less in the dry west). Further analyses show that the precipitation frequency increases mainly for light precipitation while decreasing for heavy precipitation. It is thus demonstrated that on the TP, land surface energy–atmosphere interactions can mitigate the rate of precipitation increase, suppress the increase in frequency of heavy precipitation, and weaken the east–west contrast in precipitation amount, through a dynamical mechanism. Overall, land–atmosphere interactions on the TP exert negative feedback to partially offset the accelerated plateau water cycle under a changing climate.