Interquartile Range Increase In PM2 Research Articles

Associations of Ambient Particulate Matter with Maternal Thyroid Autoimmunity and Thyroid Function in Early Pregnancy.

This prospective birth cohort study evaluated the association of exposure to PM2.5 (diameter ≤2.5 μm), PM1-2.5 (1-2.5 μm), and PM1 (≤1 μm) with maternal thyroid autoimmunity and function during early pregnancy. A total of 15,664 pregnant women were included at 6 to 13+6 gestation weeks in China from 2018 to 2020. Single-pollutant models using generalized linear models (GLMs) showed that each 10 μg/m3 increase in PM2.5 and PM1-2.5 was related with 6% (odds ratio [OR] = 1.06, 95% confidence interval [CI]: 1.01, 1.12) and 15% (OR = 1.15, 95% CI: 1.08, 1.22) increases in the risk of thyroid autoimmunity, respectively. The odds of thyroid autoimmunity significantly increased with each interquartile range increase in PM2.5 and PM1-2.5 exposure (P for trend <0.001). PM1 exposure was not significantly associated with thyroid autoimmunity. GLM with natural cubic splines demonstrated that increases in PM2.5 and PM1-2.5 exposure were associated with lower maternal FT4 levels, while a negative association between PM1 and FT4 levels was found when exposure exceeded 32.13 μg/m3. Only PM2.5 exposure was positively associated with thyrotropin (TSH) levels. Our findings suggest that high PM exposure is associated with maternal thyroid disruption during the early pregnancy.

Ambient air pollution, lifestyle, and genetic predisposition on all-cause and cause-specific mortality: A prospective cohort study

BackgroundAlthough it is widely acknowledged that long-term exposure to ambient air pollution is closely related to the risk of mortality, there were inconsistencies in terms of cause-specific mortality and it is still unknown whether lifestyle and genetic susceptibility could modify the association. MethodsThis population-based prospective cohort study involved 461,112 participants from the UK Biobank. The land-use regression model was used to estimate the concentrations of particulate matter (PM2.5, PMcoarse, PM10), and nitrogen oxides (NO2 and NOx). The association between air pollution and mortality was evaluated using Cox proportional hazard models. Furthermore, a lifestyle score incorporated with smoking status, physical activity, alcohol consumption, and diet behaviors, and polygenic risk score using 12 genetic variants, were developed to assess the modifying effect of air pollution on mortality outcomes. ResultsDuring a median follow-up of 14.0 years, 33,903 deaths were recorded, including 17,083 (2835; 14,248), 6970, 2429, and 1287 deaths due to cancer (lung cancer, non-lung cancer), cardiovascular disease (CVD), respiratory and digestive disease, respectively. Each interquartile range (IQR) increase in PM2.5, NO2 and NOx was associated with 7 %, 6 % and 5 % higher risk of all-cause mortality, respectively. Specifically, for cause-specific mortality, each IQR increase in PM2.5, NO2 and NOx was also linked to mortality due to cancer (lung cancer and non-lung cancer), CVD, respiratory and digestive disease. Furthermore, additive and multiplicative interactions were identified between high ambient air pollution and unhealthy lifestyle on mortality. In addition, associations between air pollution and mortality were modified by lifestyle behaviors. ConclusionLong-term exposure to air pollutants increased the risk of all-cause and cause-specific mortality, which was modified by lifestyle behaviors. In addition, we also revealed a synergistically detrimental effect between air pollution and an unhealthy lifestyle, suggesting the significance of joint air pollution management and adherence to a healthy lifestyle on public health.

Air pollutants, genetic susceptibility, and incident schizophrenia in later life: A prospective study in the UK Biobank

ObjectiveAir pollution has been linked to multiple psychiatric disorders, but little is known on its long-term association with schizophrenia. The interaction between air pollution and genetic susceptibility on incident schizophrenia has never been reported. We aimed to explore the associations between long-term air pollution exposure and late-onset schizophrenia and evaluate whether genetic susceptibility could modify the association. MethodsThis population-based prospective cohort study included 437,802 middle-aged and elderly individuals free of schizophrenia at baseline in the UK Biobank. Land use regression models were applied in the estimation of the annual average concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter (PM2.5), and inhalable particulate matter (PM10) at residence. The associations between air pollutants and schizophrenia were evaluated by using Cox proportional hazard models. A polygenic risk score of schizophrenia was constructed for exploring potential interaction of air pollutants with genetic susceptibility. ResultsAn interquartile range increase in PM2.5, PM10, NO2, and NOx was associated with the hazard ratios (HR) for incident schizophrenia at 1.19, 1.16, 1.22, and 1.09, respectively. The exposure-response curves for the association of air pollution with incident schizophrenia were approximately linear. There are additive interactions of air pollution score (APS), PM10, NO2, and NOx with genetic risk. Specifically, compared with participants with low genetic susceptibility and low APS, the HR was 3.23 for individuals with high genetic risk and high APS, among which 0.49 excess risk could be attributed to the additive interaction, accounting for 15 % of the schizophrenia risk. ConclusionThis large-scale, prospective cohort study conveys the first-hand evidence that long-term air pollution exposure could elevate schizophrenia incidence in later life, especially for individuals with higher genetic risks. The findings highlight the importance of improving air quality for preventing the late-onset schizophrenia in an aging era, especially among those with high genetic risks.

Prenatal exposure to air pollutant mixtures and birthweight in the upstate KIDS cohort

BackgroundSingle-pollutant models have linked prenatal PM2.5 exposure to lower birthweight. However, analyzing air pollutant mixtures better captures pollutant interactions and total effects. Unfortunately, strong correlations between pollutants restrict traditional methods. ObjectivesWe explored the association between exposure to a mixture of air pollutants during different gestational age windows of pregnancy and birthweight. MethodsWe included 4,635 mother-infant dyads from a New York State birth cohort born 2008–2010. Air pollution data were sourced from the EPA’s Community Multiscale Air Quality model and matched to the census tract centroid of each maternal home address. Birthweight and gestational age were extracted from vital records. We applied linear regression to study the association between prenatal exposure to PM2.5, PM10, NOX, SO2, and CO and birthweight during six sensitive windows. We then utilized Bayesian kernel machine regression to examine the non-linear effects and interactions within this five-pollutant mixture. Final models adjusted for maternal socio-demographics, infant characteristics, and seasonality. ResultsSingle-pollutant linear regression models indicated that most pollutants were associated with a decrement in birthweight, specifically during the two-week window before birth. An interquartile range increase in PM2.5 exposure (IQR: 3.3 µg/m3) from the median during this window correlated with a 34 g decrement in birthweight (95 % CI: −54, −14), followed by SO2 (IQR: 2.0 ppb; β: −31), PM10 (IQR: 4.6 µg/m3; β: −29), CO (IQR: 60.8 ppb; β: −27), and NOX (IQR: 7.9 ppb; β: −26). Multi-pollutant BKMR models revealed that PM2.5, NOX, and CO exposure were negatively and non-linearly linked with birthweight. As the five-pollutant mixture increased, birthweight decreased until the median level of exposure. DiscussionPrenatal exposure to air pollutants, notably PM2.5, during the final two weeks of pregnancy may negatively impact birthweight. The non-linear relationships between air pollution and birthweight highlight the importance of studying pollutant mixtures and their interactions.

Long-term exposure to ambient air pollution and risk of microvascular complications among patients with type 2 diabetes: a prospective study.

Patients with type 2 diabetes (T2D) may disproportionately suffer the adverse cardiovascular effects of air pollution, but relevant evidence on microvascular outcome is lacking. We aimed to examine the association between air pollution exposure and the risk of microvascular complications among patients with T2D. This prospective study included 17 995 participants with T2D who were free of macro- and micro-vascular complications at baseline from the UK Biobank. Annual average concentrations of particulate matter (PM) with diameters <2.5 μm (PM2.5), <10 μm (PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOx) were assessed using land use regression models. Cox proportional hazards regression was used to estimate the associations of air pollution exposure with incident diabetic microvascular complications. The joint effects of the air pollutant mixture were examined using quantile-based g-computation in a survival setting. In single-pollutant models, the adjusted hazard ratios (95% confidence intervals) for composite diabetic microvascular complications per interquartile range increase in PM2.5, PM10, NO2 and NOx were 1.09 (1.04-1.14), 1.06 (1.01-1.11), 1.07 (1.02-1.12) and 1.04 (1.00-1.08), respectively. Similar significant results were found for diabetic nephropathy and diabetic neuropathy, but not for diabetic retinopathy. The associations of certain air pollutants with composite microvascular complications and diabetic nephropathy were present even at concentrations below the World Health Organization limit values. Multi-pollutant analyses demonstrated that PM2.5 contributed most to the elevated risk associated with the air pollutant mixture. In addition, we found no interactions between air pollution and metabolic risk factor control on the risk of diabetic microvascular complications. Long-term individual and joint exposure to PM2.5, PM10, NO2 and NOx, even at low levels, was associated with an increased risk of diabetic microvascular complications, with PM2.5 potentially being the main contributor.

Co-exposure to multiple air pollutants, genetic susceptibility, and the risk of myocardial infarction onset: a cohort analysis of the UK Biobank participants.

The relationship between the long-term joint exposure to ambient air pollution and incidence of myocardial infarction (MI) and modification by genetic susceptibility remain inconclusive. We analysed 329 189 UK Biobank participants without MI at baseline. Exposure concentrations to particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx) were obtained. Air pollution score assessing the joint exposure was calculated, and its association with MI was evaluated via Cox model under the P value aggregation framework. Genetic susceptibility to MI was evaluated by incorporating polygenic risk score (PRS) into models. Risk prediction models were also established. During a median follow-up of 13.4 years, 9993 participants developed MI. Per interquartile range increase of PM2.5, PM10, NO2, and NOx resulted in 74% [95% confidence intervals (CIs) 69%-79%], 67% (63%-72%), 46% (42%-49%), and 38% (35%-41%) higher risk of MI. Compared with the lowest quartile (Q1) of air pollution score, the multivariable adjusted hazard ratio (HR) (95%CIs) of Q4 (the highest cumulative air pollution) was 3.50 (3.29-3.72) for MI. Participants with the highest PRS and air pollution score possessed the highest risk of incident MI (HR = 4.88, 95%CIs 4.35-5.47). Integrating PRS, air pollution exposure, and traditional factors substantially improved risk prediction of MI. Long-term joint exposure to air pollutants including PM2.5, PM10, NO2, and NOx is substantially associated with increased risk of MI. Genetic susceptibility to MI strengthens such adverse joint association. Air pollutions together with genetic and traditional factors enhance the accuracy of MI risk prediction.

Ambient traffic related air pollution in relation to ovarian reserve and oocyte quality in young, healthy oocyte donors

Studies in mice and older, subfertile women have found that air pollution exposure may compromise female reproduction. Our objective was to evaluate the effects of air pollution on ovarian reserve and outcomes of ovarian stimulation among young, healthy females. We included 472 oocyte donors who underwent 781 ovarian stimulation cycles at a fertility clinic in Atlanta, Georgia, USA (2008–2019). Antral follicle count (AFC) was assessed with transvaginal ultrasonography and total and mature oocyte count was assessed following oocyte retrieval. Ovarian sensitivity index (OSI) was calculated as the total number of oocytes divided by total gonadotrophin dose × 1000. Daily ambient exposure to nitric oxide (NOx), carbon monoxide (CO), and particulate matter ≤ 2.5 (PM2.5) was estimated using a fused regional + line-source model for near-surface releases at a 250 m resolution based on residential address. Generalized estimating equations were used to evaluate the associations of an interquartile range (IQR) increase in pollutant exposure with outcomes adjusted for donor characteristics, census-level poverty, and meteorological factors. The median (IQR) age among oocyte donors was 25.0 (5.0) years, and 31% of the donors were racial/ethnic minorities. The median (IQR) exposure to NOx, CO, and PM2.5 in the 3 months prior to stimulation was 37.7 (32.0) ppb, 612 (317) ppb, and 9.8 (2.9) µg/m3, respectively. Ambient air pollution exposure in the 3 months before AFC was not associated with AFC. An IQR increase in PM2.5 in the 3 months before AFC and during stimulation was associated with −7.5% (95% CI −14.1, −0.4) and −6.4% (95% CI −11.0, −1.6) fewer mature oocytes, and a −1.9 (95% CI −3.2, −0.5) and −1.0 (95% CI −1.8, −0.2) lower OSI, respectively. Our results suggest that lowering the current 24-h PM2.5 standard in the US to 25 µg/m3 may still not adequately protect against the reprotoxic effects of short-term PM2.5 exposure.

Joint association of air pollution exposure and inflammation-related proteins in relation to infant lung function

Background and aimSystemic inflammation is one potential mechanism underlying negative impact of air pollution on lung function. Levels of inflammation-related proteins have the potential to characterize infants’ susceptibility to air pollution induced lung function impairment. This study aimed to examine the interplay between air pollution exposure and inflammation-related proteins on lung function in 6-months-old infants. MethodsIn the EMIL birth cohort from Stockholm (n = 82), dynamic spirometry, along with measurement of plasma levels of 92 systemic inflammation-related proteins (Olink Proseek Multiplex Inflammation panel) have been carried out in infants aged six months. Time-weighted average exposure to particles with an aerodynamic diameter of <10 μm (PM10), <2.5 μm (PM2.5), and nitrogen dioxide (NO2) at residential addresses from birth and onwards was estimated via validated dispersion models. To characterize the abnormality of inflammation-related protein profile, for each protein in each infant, we calculated the relative deviance of the protein level from age- and sex-specific median in terms of its age- and sex-specific interquartile range (IQR), followed by computing the absolute value of the smallest relative deviance, “minimum absolute deviance”. Using linear regression models, interaction of air pollution and the abnormal inflammatory profile on lung function was estimated on the additive scale. ResultsWe found joint association of PM exposure and an abnormal inflammatory protein profile in relation to FEV0.5 and FVC. For 0.1 unit increase in minimum absolute deviance, one IQR increase in PM10 was associated with 85.9 ml (95% CI: −122.9, −48.9) additional decrease in FEV0.5, and 72.3 ml (95% CI: −121.5, −23.2) additional decrease in FVC. Similar results were obtained with PM2.5 exposure, while less apparent for NO2. ConclusionsEarly life air pollution exposure and abnormal inflammation-related protein profiles may interact synergistically towards lower lung function in infants.

Association of PM2.5 mass and its components with ovarian reserve in a northern peninsular province, China: The critical exposure period and components

BackgroundA possible role of PM2.5 components on ovarian reserve has not been adequately unexplored. ObjectiveTo evaluate the association between PM2.5 components and women’ ovarian reserve over critical exposure periods in northern China, where the level of air pollution is among the nation’s highest. MethodsWe included 15,102 women with serum anti-Müllerian hormone (AMH) measurements from the Center for Reproductive Medicine of Shandong University during 2015–2019. Concentrations of PM2.5 and its five major components (0.1° × 0.1°), including sulfate, nitrate, ammonium, organic matter, and black carbon, were assigned to each residential address. Multivariable linear mixed effect models combined with constituent-residual models were performed to estimate the effect sizes of essential components over six short- to long-term exposure periods. ResultsThe strength of association was stronger during the process from primary to small antral follicle compared with other longer windows. For every interquartile range increase in PM2.5 mass was associated with − 8.7% (95%CI: −12.3%, −4.9%) change in AMH and the effect size was greatest for sulfate. Women with the lower level of attained education and those living inland were more susceptible compared with other population subgroups. ConclusionExposure to specific components of air pollution during critical exposure windows is associated with a decline in ovarian reserve. These data add to the growing body of evidence that environmental factors have adverse effects on reproductive health, particularly for vulnerable population subgroups.

Associations between residential greenness and air pollution and the incident metabolic syndrome in a Thai worker cohort.

Increasing air pollution and decreasing exposure to greenness may contribute to the metabolic syndrome (MetS). We examined associations between long-term exposure to residential greenness and air pollution and MetS incidence in the Bangkok Metropolitan Region, Thailand. Data from 1369 employees (aged 52-71years) from the Electricity Generating Authority of Thailand cohort from 2002 to 2017 were analyzed. The greenness level within 500m of each participant's residence was measured using the satellite-derived Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI). The kriging approach was used to generate the average concentration of each air pollutant (PM10, CO, SO2, NO2, and O3) at the sub-district level. The average long-term exposure to air pollution and greenness for each participant was calculated over the same period of person-time. Cox proportional hazards models were used to analyze the greenness-air pollution-MetS associations. The adjusted hazard ratio of MetS was 1.42 (95% confidence interval (CI): 1.32, 1.53), 1.22 (95% CI: 1.15, 1.30), and 2.0 (95% CI: 1.82, 2.20), per interquartile range increase in PM10 (9.5μg/m3), SO2 (0.9ppb), and CO (0.3ppm), respectively. We found no clear association between NDVI or EVI and the incidence of MetS. On the contrary, the incident MetS was positively associated with NDVI and EVI for participants exposed to PM10 at concentrations more than 50μg/m3. In summary, the incidence of MetS was positively associated with long-term exposure to air pollution. In areas with high levels of air pollution, green spaces may not benefit health outcomes.

Ambient air pollution associated with incident asthma, subsequent cardiovascular disease and death: A trajectory analysis of a national cohort

No previous study has examined the impact of air pollution on the cardiovascular disease (CVD) trajectory, especially among asthmatic subjects. Based on the UK Biobank cohort, we retrieved 292,227 adults free of asthma and CVD aged 37–73 years at recruitment (2006–2010). Annual mean concentrations of particulate matter (PM10 and PM2.5) and nitrogen oxides (NO2 and NOx) were assessed at each individual’s addresses. We used multi-state models to estimate the associations of air pollution with the trajectory from healthy to incident asthma, subsequent CVD, and death. During a median follow-up of 11.7 years, a total of 6338 (2.2%) participants developed asthma, among which, 638 (10.1%) subsequently proceeded to CVD. We observed significant impacts of various air pollutants on the CVD dynamic transitions, with a more substantial effect of particulate matter pollutants than gaseous air pollutants. For example, the hazard ratios (95% confidence intervals) for per interquartile range increase in PM2.5 and PM10 were 1.28 (1.13, 1.44) and 1.27 (1.13, 1.43) for transitions from incident asthma to subsequent CVD. In conclusion, long-term air pollution exposure could affect the CVD trajectory. Distinguishing the effect of air pollutants on CVD transition stages has great significance for CVD health management and clinical prevention, especially among asthma patients.

The Association of Air Pollution Exposure With Glucose and Lipid Levels: The Role of an Extreme Air Pollution Event Alongside 2 Decades of Moderate Exposure.

Extreme air pollution events and moderate exposure to fine particulate matter (PM2.5) are associated with increased cardiometabolic risk. The World Trade Center (WTC) Health Program general responder cohort includes responders to the WTC disaster. We investigated whether their exposure to this extreme air pollution event (2001) was associated with long-term metabolic outcomes, independently from the associations of intermediate-term PM2.5 exposure later in life (2004-2019). We included 22,447 cohort members with cholesterol (n= 96,155) and glucose (n= 81,599) laboratory results. Self-reported WTC exposure was derived from a questionnaire. PM2.5 exposure was derived from a satellite-based model. We observed an increase of 0.78 mg/dL (95% confidence interval (CI): 0.30, 1.26) in glucose and 0.67 mg/dL (95% CI: 1.00, 2.35) in cholesterol levels associated with an interquartile range increase in PM2.5 averaged 6 months before the study visit. Higher WTC-exposure categories were also associated with higher cholesterol (0.99 mg/dL, 95% CI: 0.30, 1.67, for intermediate exposure) and glucose (0.82 mg/dL, 95% CI: 0.22, 1.43, for high exposure) levels. Most associations were larger among people with diabetes. Extreme air pollution events and intermediate PM2.5 exposure have independent metabolic consequences. These exposures contributed to higher glucose and lipids levels among WTC responders, which may be translated into increased cardiovascular risk.

Long-term exposure to ambient air pollution, genetic susceptibility, and the incidence of bipolar disorder: A prospective cohort study

There is mounting recent evidence showing that air pollution exposure may be related to the risk of mental health, yet the association between long-term exposure to air pollution and the risk of incident bipolar disorder (BD) remains unclear. Thus we aim to identify associations between air pollution and the incidence of BD in a prospective population-based cohort. In total, 482,726 participants who were free of BD from the UK Biobank were included in this prospective study. We applied time-varying Cox proportional hazards models, accounting for relevant confounders, and used annual-year moving averages of air pollution as time-varying exposures. The genetic risk for BD was categorized into three categories (low, intermediate, and high) according to the tertiles of polygenic risk score. During a median of 10.79-year follow-up, 923 incident BD events were recorded. Long-term exposures to PM2.5, PM10, NO2, and NOx were associated with increased BD risk. Estimated HRs (95% CIs) for each interquartile range increase in PM2.5, PM10, NO2, and NOx concentrations were 1.31 (1.18–1.45), 1.19 (1.09–1.31), 1.19 (1.08–1.30), and 1.16 (1.07–1.26), respectively. Associations were still observed and even stronger at pollutant concentrations lower than WHO air quality guideline. In subgroup analysis stratified by genetic risk, we observed consistent associations between all pollutants and BD risk in intermediate and high genetic risk groups, but not in low genetic risk group. For example, the HRs (95% CIs) for PM2.5 were 1.00 (0.94–1.53), 1.30 (1.06–1.59), and 1.34 (1.16–1.54) in low, intermediate, and high genetic groups, respectively. In conclusion, long-term exposure to air pollution was significantly associated with an elevated risk of BD. Associations of air pollution with BD occurred only within intermediate and high genetic risk categories and were even stronger at the pollutants levels below WHO air quality guidelines. These findings could help inform policy makers regarding ambient air quality standards and BD management.

Long non-coding RNAs mediate the association between short-term PM2.5 exposure and circulating biomarkers of systemic inflammation

Although short-term fine particulate matter (PM2.5) exposure is associated with systemic inflammation, the effect of lncRNA on these association remains unknown. This study aims to investigate whether the plasma lncRNA mediate the effect of short-term PM2.5 exposure on systemic inflammation. In this cross-sectional study, plasma Clara cell protein 16 (CC16), interleukin 6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α) and lncRNA expression levels were measured in 161 adults between March and April in 2018 in Shijiazhuang, China. PM2.5 concentrations were estimated 0–3 days prior to the examination date and the moving averages were calculated. Multiple linear regressions were used to evaluate the associations between PM2.5, the four biomarkers and lncRNA expression levels. Mediation analyses were performed to explore the potential roles of lncRNA expression in these associations. The median concentration of PM2.5 ranged from 39.65 to 60.91 mg/m3 across different lag days. The most significant effects on IL-6 and TNF-α per interquartile range increase in PM2.5 were observed at lag 0–3 days, with increases of 0.70 pg/mL (95% CI: 0.33, 1.07) and 0.21 pg/mL (95% CI: 0.06, 0.36), respectively. While the associations between PM2.5 and IL-8 (0.68 pg/mL, 95% CI: 0.34, 1.02) and CC16 (3.86 ng/mL, 95% CI: 1.60, 6.13) were stronger at lag 0 day. Interestingly, a negative association between PM2.5 and the expression of four novel lncRNAs (lnc-ACAD11–1:1, lnc-PRICKLE1-4:1, lnc-GPR39–7:2, and lnc-MTRNR2L12–3:6) were observed at each lag days. Furthermore, these lncRNAs mediated the effects of PM2.5 on the four biomarkers, with proportions of mediation ranged from 2.27% (95% CI: 1.19%, 9.82%) for CC16 to 35.60% (95% CI: 17.16%, 175.45%) for IL-6. Our findings suggested that plasma lncRNA expression mediat the acute effects of PM2.5 exposure on systematic inflammation. These highlight a need to consider circulating lncRNA expression as biomarkers to reduce health risks associated with PM2.5.

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.

Association Between Long-Term Exposure to Fine Particulate Matter Constituents and Progression of Cerebral Blood Flow Velocity in Beijing: Modifying Effect of Greenness.

Few studies have explored the effects of fine particulate matter (PM2.5) and its constituents on the progression of cerebral blood flow velocity (BFV) and the potential modifying role of greenness. In this study, we investigated the association of PM2.5 and its constituents, including sulfate (SO4 2-), nitrate (NO3 -), ammonium (NH4 +), organic matter (OM), and black carbon (BC), with the progression of BFV in the middle cerebral artery. Participants from the Beijing Health Management Cohort who underwent at least two transcranial Doppler sonography examinations during 2015-2020 were recruited. BFV change and BFV change rate were used to define the progression of cerebral BFV. Linear mixed effects models were employed to analyze the data, and the weighted quantile sum regression assessed the contribution of PM2.5 constituents. Additionally, greenness was examined as a modifier. Among the examined constituents, OM exhibited the strongest association with BFV progression. An interquartile range increase in PM2.5 and OM exposure concentrations was associated with a decrease of -16.519cm/s (95% CI: -17.837, -15.201) and -15.403cm/s (95% CI: -16.681, -14.126) in BFV change, and -10.369cm/s/year (95% CI: -11.387, -9.352) and -9.615cm/s/year (95% CI: -10.599, -8.632) in BFV change rate, respectively. Furthermore, stronger associations between PM2.5 and BFV progression were observed in individuals working in areas with lower greenness, those aged under 45years, and females. In conclusion, reducing PM2.5 levels in the air, particularly the OM constituent, and enhancing greenness could potentially contribute to the protection of cerebrovascular health.

Association between Air Pollution and Short-Term Outcome of ST-Segment Elevation Myocardial Infarction in a Tropical City, Kaohsiung, Taiwan

ST-segment elevation myocardial infarction (STEMI), one of the primary factors leading to global mortality, has been shown through epidemiological studies to have a relationship with short-term exposure to air pollutants; however, the association between air pollutants and the outcome of STEMI has not been well studied. The aim of this study was to estimate the impact of air pollutants on the outcomes of STEMI. Data on particulate matter &lt;2.5 μm (PM2.5), &lt;10 μm (PM10), nitrogen dioxide (NO2), and ozone (O3) at each of the 11 air monitoring stations in Kaohsiung City were collected between 1 January 2012 and 31 December 2017. Medical records of non-trauma patients aged &gt; 20 years who had presented to the Emergency Department (ED) with a principal diagnosis of STEMI were extracted. The primary outcome measure was in-hospital mortality. After adjusting for potential confounders and meteorological variables, we found that an increase in the interquartile range (IQR) in NO2 was associated with an elevated risk of in-hospital mortality in patients with STEMI. Moreover, there was an observed higher risk of in-hospital mortality associated with an increase in the IQR of NO2 during the warm season, specifically in lag 3 (3 days prior to the onset, OR = 3.266; 95%CI: 1.203–8.864, p = 0.02). Conversely, an IQR increase in PM10 was associated with an increased risk of in-hospital mortality in patients with STEMI in lag 3 (OR = 2.792; 95%CI: 1.115–6.993, p = 0.028) during the cold season. Our study suggests that exposure to NO2 (during the warm season) and PM10 (during the cold season) may contribute to a higher risk of poor prognosis in patients with STEMI.

Exposure to ambient air pollution with depressive symptoms and anxiety symptoms among adolescents: A national population-based study in China

BackgroundAir pollution threatens adolescents' physical health and adversely affects adolescents' mental health. Previous studies mostly focused on the effects of air pollution on physical health, but there were few studies on the effects of air pollution on mental health. MethodsWe collected scores of depressive symptoms and anxiety symptoms from 15,331 adolescents from 43 schools in eleven provinces in September and November 2017. The data on air pollution comes from the China High Air Pollutants dataset, which included concentrations of particulate matter with diameters of ≤1.0 μm (PM1), diameters of ≤2.5 μm (PM2.5), and diameters of ≤10 μm (PM10), as well as nitrogen dioxide (NO2). The associations between air pollution and depressive and anxiety symptoms among adolescents were estimated using generalized linear mixed models. ResultsDepressive and anxiety symptoms among Chinese adolescents were 16% and 32%, respectively. In the adjusted model, an interquartile range (IQR) increase from PM2.5 was associated with the odds of anxiety symptoms [odds ratio (OR) = 1.01; 95% confidence interval (CI): 1.00, 1.01, P = 0.002]. Also, an IQR increase in PM10 was significantly associated with the odds of anxiety symptoms (OR = 1.01; 95% CI: 1.00, 1.01, P = 0.029). Compared with the lowest quartile, the adjusted OR of anxiety symptoms for the highest quartile of PM2.5 and PM10 were 1.29 (1.15, 1.44) and 1.23 (1.06, 1.42), respectively. In addition, the association between PM2.5 and depressive symptoms was significant. The robustness of the results was also confirmed by stratification and sensitivity analyses. ConclusionsExposure values for airborne particulate matter were associated with depressive symptoms and anxiety symptoms in adolescents, particularly for PM2.5 and PM10 with anxiety symptoms among adolescents.

Fine and coarse particulate air pollution and hospital admissions for a wide range of respiratory diseases: a nationwide case-crossover study.

The associations between fine and coarse particulate matter (PM2.5 and PM2.5-10) air pollution and hospital admissions for full-spectrum respiratory diseases were rarely investigated, especially for age-specific associations. We aim to estimate the age-specific associations of short-term exposures to PM2.5 and PM2.5-10 with hospital admissions for full-spectrum respiratory diseases in China. We conducted an individual-level case-crossover study based on a nationwide hospital-based registry including 153 hospitals across 20 provincial regions in China in 2013-20. We applied conditional logistic regression models and distributed lag models to estimate the exposure- and lag-response associations. A total of 1 399 955 hospital admission records for various respiratory diseases were identified. The associations of PM2.5 and PM2.5-10 with total respiratory hospitalizations lasted for 4 days, and an interquartile range increase in PM2.5 (34.5 μg/m3) and PM2.5-10 (26.0 μg/m3) was associated with 1.73% [95% confidence interval (95% CI): 1.34%, 2.12%)] and 1.70% (95% CI: 1.31%, 2.10%) increases, respectively, in total respiratory hospitalizations over lag 0-4 days. Acute respiratory infections (i.e. pneumonia, bronchitis and bronchiolitis) were consistently associated with PM2.5 or PM2.5-10 exposure across different age groups. We found the disease spectrum varied by age, including rarely reported findings (i.e. acute laryngitis and tracheitis, and influenza) among children and well-established associations (i.e. chronic obstructive pulmonary disease, asthma, acute bronchitis and emphysema) among older populations. Besides, the associations were stronger in females, children and older populations. This nationwide case-crossover study provides robust evidence that short-term exposure to both PM2.5 and PM2.5-10 was associated with increased hospital admissions for a wide range of respiratory diseases, and the spectra of respiratory diseases varied by age. Females, children and older populations were more susceptible.

Associations of long-term exposure to air pollution, physical activity with blood pressure and prevalence of hypertension: the China Health and Retirement Longitudinal Study.

Long-term exposure to air pollution and physical activity (PA) are linked to blood pressure and hypertension. However, the joint effect of air pollution and PA on blood pressure and hypertension are still unknown in Chinese middle-aged and older adults. A total of 14,622 middle-aged and older adults from the China Health and Retirement Longitudinal Study wave 3 were included in this study. Ambient air pollution [particulate matter with diameter ≤ 2.5 μm (PM2.5), or ≤10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbonic oxide (CO)] were estimated using satellite-based spatiotemporal models. PA was investigated using International Physical Activity Questionnaire. Generalized linear models were used to examine the associations of air pollution, PA score with blood pressure [systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP)], and the prevalence of hypertension. Subgroup analysis was conducted to investigate the effects of air pollution on blood pressure and the prevalence of hypertension in different PA groups. The results showed that for each inter-quartile range (IQR) increase in PM2.5 (25.45 μg/m3), PM10 (40.56 μg/m3), SO2 (18.61 μg/m3), NO2 (11.16 μg/m3), CO (0.42 mg/m3) and PA score (161.3 MET/h-week), the adjusted odd ratio (OR) of hypertension was 1.207 (95% confidence interval (CI): 1.137, 1.281), 1.189 (95%CI: 1.122, 1.260), 1.186 (95%CI: 1.112, 1.266), 1.186 (95%CI: 1.116, 1.260), 1.288 (95%CI: 1.223, 1.357), 0.948 (95%CI: 0.899, 0.999), respectively. Long-term exposure to PM2.5, PM10, SO2, NO2, and CO was associated with increased SBP, DBP, and MAP levels. For example, each IQR increase in PM2.5 was associated with 1.20 mmHg (95%CI: 0.69, 1.72) change in SBP, 0.66 mmHg (95%CI: 0.36, 0.97) change in DBP, and 0.84 mmHg (95%CI: 0.49, 1.19) change in MAP levels, respectively. Each IQR increase in PA score was associated with -0.56 mmHg (95%CI: -1.03, -0.09) change in SBP, -0.32 mmHg (95%CI: -0.59, -0.05) change in DBP, and -0.33 mmHg (95%CI: -0.64, -0.02) change in MAP levels, respectively. Subgroup analysis found that the estimated effects in the sufficient PA group were lower than that in the insufficient PA group. Long-term exposure to air pollutants is associated with increased blood pressure and hypertension risk, while high-level PA is associated with decreased blood pressure and hypertension risk. Strengthening PA might attenuate the adverse effects of air pollution on blood pressure and hypertension risk.