Association Of Air Pollution Exposure Research Articles

Residential ambient air pollution exposure and the development of white matter microstructure throughout adolescence

BackgroundRecent evidence suggests an association of air pollution exposure with brain development, but evidence on white matter microstructure in children is scarce. We investigated how air pollution exposure during pregnancy and childhood impacts longitudinal development of white matter microstructure throughout adolescence. MethodsOur study population consisted of 4108 participants of Generation R, a large population-based birth cohort from Rotterdam, the Netherlands. Residential air pollution exposure to 14 air pollutants during pregnancy and childhood was estimated with land-use regression models. Diffusion tensor images were obtained around age 10 and 14, resulting in a total of 5422 useable scans (n = 3082 for wave 1 and n = 2340 for wave 2; n = 1314 for participants with data on both waves). We calculated whole-brain fractional anisotropy (FA) and mean diffusivity (MD) and performed single- and multi-pollutant analyses using mixed effects models adjusted for life-style and socioeconomic status variables. ResultsHigher exposure to PM2.5 during pregnancy, and PM10, PM2.5, PM2.5-10, and NOX during childhood was associated with a consistently lower whole-brain FA throughout adolescence (e.g. – 0.07 × 10−2 FA [95%CI -0.12; −0.02] per 1 standard deviation higher PM2.5 exposure during pregnancy). Higher exposure to silicon (Si) in PM2.5 and oxidative potential of PM2.5 during pregnancy, and PM2.5 during childhood was associated with an initial higher MD followed by a faster decrease in MD throughout adolescence (e.g. – 0.02 × 10−5 mm2/s MD [95%CI -0.03; −0.00] per year of age per 1 standard deviation higher Si exposure during pregnancy). Results were comparable when performing the analysis in children with complete data on the outcome for both neuroimaging assessments. ConclusionsExposure to several pollutants was associated with a consistently lower whole-brain FA throughout adolescence. The association of few pollutants with whole-brain MD at baseline attenuated throughout adolescence. These findings suggest both persistent and age-limited associations of air pollution exposure with white matter microstructure.

Association between exposure to air pollution and arterial stiffness in participants with and without atherosclerotic cardiovascular disease.

To assess the association of air pollution exposure at different time scales with arterial stiffness in participants with and without atherosclerotic cardiovascular disease (ASCVD). We measured participants' arterial stiffness with brachial-ankle pulse wave velocity (baPWV) from October 2016 to January 2020. Concentrations of air pollutants including fine particles < 2.5μm aerodynamic diameter (PM2.5), inhalable particles < 10μm aerodynamic diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) measured by fixed ambient air monitoring stations were collected for short- (7-day) and long-term (365-day) exposure assessment. We used generalized estimating equations (GEEs) to analyze and further explored the modification effects between ASCVD and air pollutants. Seven hundred sixty-five participants were finally included and four hunderd sixty (60.1%) participants had a history of ASCVD. Based on the partial regression coefficients (β) and 95% confidence intervals (95% CI) calculated from GEEs using linear regression, each 10μg/m3 increase in long-term exposure to PM2.5 and PM10 was associated with 31.85cm/s (95% CI, 17.97 to 45.73) and 35.93cm/s (95% CI, 21.01to50.84) increase in baPWV. There was no association between short-term exposure to air pollution and arterial stiffness. Although no significant interaction effect was observed between air pollution and ASCVD, baPWV showed a greater increment in the subgroup without ASCVD. Long-term exposure to air pollution is closely associated with higher arterial stiffness in participants with and without ASCVD. Reducing air pollution exposure is essential in the primary and secondary prevention of ASCVD.

Associations of air pollution exposures in preconception and pregnancy with birth outcomes and infant neurocognitive development: analysis of the Complex Lipids in Mothers and Babies (CLIMB) prospective cohort in Chongqing, China

ObjectivesTo investigate the associations of traffic-related air pollution exposures in early pregnancy with birth outcomes and infant neurocognitive development.DesignCohort study.SettingEligible women attended six visits in the maternity clinics of two...

Risk/benefit trade-off of habitual physical activity and air pollution on mortality: A large-scale prospective analysis in the UK Biobank

BackgroundPrevious observational studies have indicated associations of physical activity (PA) and air pollution with mortality. A few studies have evaluated air pollution and PA interactions for health. Still, the trade-off between the harmful effects of air pollution exposure and the protective effects of PA remains controversial and unclear. ObjectiveThis study aimed to investigate the joint association of air pollution and PA with mortality risks. MethodsThis prospective cohort study included 322,092 participants from 2006 to 2010 and followed up to 2021 in the UK Biobank study. The concentrations of air pollutants (2006–2010), including particulate matter (PM) with diameters <=2.5 mm (PM2.5), <=10 mm (PM10), and between 2.5 and 10 mm (PM2.5–10), and nitrogen oxides (NO2 and NOx) were obtained. Information on PA measured by the International Physical Activity Questionnaire short form (2006–2010) and wrist-worn accelerometer (2013–2015) were collected. All-cause and cause-specific mortalities were recorded. Cox proportional hazard models were used to investigate the associations of air pollution exposure and PA with mortality risks. The additive and multiplicative interactions were also examined. ResultsDuring a mean follow-up of 11.83 years, 16629 deaths were recorded. Compared with participants reporting low PA, higher PA was negatively associated with all-cause [hazard ratio (HR), 0.74; 95% CI, 0.71–0.78], cancer (HR, 0.85; 95% CI, 0.80–0.90), CVD (HR, 0.79; 95% CI, 0.71–0.87), and respiratory disease-specific mortality (HR, 0.51; 95% CI, 0.44–0.60). Exposure to PM2.5 (HR, 1.05; 95% CI, 1.00–1.09) and NOx (HR, 1.06; 95% CI, 1.02–1.10) was connected with increased all-cause mortality risk, and significant PM2.5-associated elevated risks for CVD mortality and NOx-associated elevated risks for respiratory disease mortality were observed. No obvious interaction between PA and PM2.5 or NOx exposure was detected. ConclusionsOur study provides additional evidence that higher PA and lower air pollutant levels are independently connected with reduced mortality risk. The benefits of PA are not significantly affected by long-term air pollution exposure, indicating PA can be recommended to prevent mortality regardless of air pollution levels. Our findings highlight the importance of public health policies and interventions facilitating PA and reducing air pollution in reducing mortality risks and maximizing health benefits. Future investigation is urgently needed to identify these findings in areas with severe air pollution conditions.

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.

DNA methylation mediates the effects of PM2.5 and O3 on ceramide metabolism: A novel mechanistic link between air pollution and insulin resistance

Insulin resistance (IR), linked to air pollution, is an initial stage of early-onset Type 2 diabetes mellitus (T2DM). While ceramide metabolism plays an important role in IR pathogenesis, the effects of air pollution on this process and its mechanisms remain unclear. We recruited young adults aged 18–30 years to a panel study in Wuhan, China. Using personal portable devices and stationary monitoring stations, we tracked particulate matter with aerodynamic diameters≤ 2.5 µm (PM2.5) and Ozone (O3) levels. Liquid chromatography/mass spectrometry (LC-MS) based metabolomics quantified ceramide metabolism, and Illumina Infinium Human Methylation 850 kBeadChip assay measured deoxyribonucleic acid (DNA) methylation. Linear mixed-effects models assessed relationships of air pollution with i) IR indexes, ii) ceramide metabolism, and iii) DNA methylation. Mediation analysis was subsequently performed to evaluate the potential mediating effect of DNA methylation in the association between air pollution and ceramide metabolism. PM2.5 and O3 were associated with elevated IR. Specifically, each 10 μg/m3 increase in PM2.5 and O3 at lag0–12 h significantly increased triglyceride‑glucose index (TyG index) and TyG-BMI (TyG - Body mass index) by 0.88%, 0.89% and 0.26%, 0.26%, respectively. Furthermore, levels of eight ceramides were altered by air pollution exposure, and nine methylated CpG sites in inflammation genes mediated the effects of air pollution on ceramide metabolism. Our findings imply the existence of a novel mechanism connecting air pollution to IR.

Long-term PM2.5 exposure is associated with asthma prevalence and exhaled nitric oxide levels in children.

Exhaled nitric oxide concentration (FENO) is a marker of airway inflammation. This study aimed to evaluate the association of air pollution exposure with FENO levels and asthma prevalence with respiratory symptoms in school children. We analyzed 4736 school children who reside in six townships near industrial areas in central Taiwan. We evaluated asthmatic symptoms, FENO, and conducted the environmental questionnaire. The personal exposure of PM2.5, NO, and SO2 was estimated using land-use regression models data on children's school and home addresses. Annual exposure to PM2.5 was associated with increased odds of physician-diagnosed asthma (OR = 1.595), exercise-induced wheezing (OR = 1.726), itchy eyes (OR = 1.417), and current nasal problems (OR = 1.334) (P < 0.05). FENO levels in the absence of infection were positively correlated with age, previous wheezing, allergic rhinitis, atopic eczema, near the road, and for children with high exposure to PM2.5 (P < 0.05). An increase of 1 μg/m3 PM2.5 exposure was significantly associated with a 1.0% increase in FENO levels for children after adjusting for potential confounding variables, including exposures to NO and SO2. Long-term exposures to PM2.5 posed a significant risk of asthma prevalence and airway inflammation in a community-based population of children. Annual exposure to PM2.5 was associated with increased odds of physician-diagnosed asthma and nasal problems and itchy eyes. Long-term exposures to PM2.5 were significantly associated with FENO levels after adjusting for potential confounding variables. This is first study to assess the association between FENO levels and long-term air pollution exposures in children near coal-based power plants. An increase of 1 μg/m3 annual PM2.5 exposure was significantly associated with a 1.0% increase in FENO levels. Long-term exposures to PM2.5 posed a significant risk of asthma prevalence and airway inflammation in a community-based population of children.

Association of air pollution exposure and increased coronary artery disease risk: the modifying effect of genetic susceptibility

BackgroundBoth genetic factors and air pollution are risk factors for coronary artery disease (CAD), but their combined effects on CAD are uncertain. The study aimed to comprehensively investigate their separate, combined and interaction effects on the onset of CAD.MethodsWe utilized data from the UK Biobank with a recruitment of 487,507 participants who were free of CAD at baseline from 2006 to 2010. We explored the separate, combined effect or interaction association among genetic factors, air pollution and CAD with the polygenic risk score (PRS) and Cox proportional hazard models.ResultsThe hazard ratios (HRs) [95% confidence interval (CI)] of CAD for 10-µg/m3 increases in PM2.5, NO2 and NOx concentrations were 1.25 (1.09, 1.44), 1.03 (1.01, 1.05) and 1.01 (1.00, 1.02), respectively. Participants with high PRS and air pollution exposure had a higher risk of CAD than those with the low genetic risk and low air pollution exposure, and the HRs (95% CI) of CAD in the PM2.5, PM10, NO2 and NOx high joint exposure groups were 1.56 (1.48, 1.64), 1.55(1.48, 1.63), 1.57 (1.49, 1.65), and 1.57 (1.49, 1.65), respectively. Air pollution and genetic factors exerted significant additive effects on the development of CAD (relative excess risk due to the interaction [RERI]: 0.12 (0.05, 0.19) for PM2.5, 0.17 (0.10, 0.24) for PM10, 0.14 (0.07, 0.21) for NO2, and 0.17 (0.10, 0.24) for NOx; attributable proportion due to the interaction [AP]: 0.09 (0.04, 0.14) for PM2.5, 0.12 (0.07, 0.18) for PM10, 0.11 (0.06, 0.16) for NO2, and 0.13 (0.08, 0.18) for NOx).ConclusionExposure to air pollution was significantly related to an increased CAD risk, which could be further strengthened by CAD gene susceptibility. Additionally, there were positive additive interactions between genetic factors and air pollution on the onset of CAD. This can provide a more comprehensive, precise and individualized scientific basis for the risk assessment, prevention and control of CAD.

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.

Identifying critical windows of air pollution exposure during preconception and gestational period on birthweight: a prospective cohort study

BackgroundFew studies have assessed air pollution exposure association with birthweight during both preconception and gestational periods.MethodsLeveraging a preconception cohort consisting of 14220 pregnant women and newborn children in Shanghai, China during 2016–2018, we aim to assess associations of NO2 and PM2.5 exposure, derived from high-resolution spatial-temporal models, during preconception and gestational periods with outcomes including term birthweight, birthweight Z-score, small-for-gestational age (SGA) and large-for-gestational age (LGA). Linear and logistic regressions were used to estimate 3-month preconception and trimester-averaged air pollution exposure associations; and distributed lag models (DLM) were used to identify critical exposure windows at the weekly resolution from preconception to delivery. Two-pollutant models and children’s sex-specific associations were explored.ResultsAfter controlling for covariates, one standard deviation (SD) (11.5 μg/m3, equivalent to 6.1 ppb) increase in NO2 exposure during the second and the third trimester was associated with 13% (95% confidence interval: 2 – 26%) and 14% (95% CI: 1 – 29%) increase in SGA, respectively; and one SD (9.6 μg/m3) increase in PM2.5 exposure during the third trimester was associated with 15% (95% CI: 1 – 31%) increase in SGA. No association have been found for outcomes of birthweight, birthweight Z-score and LGA. DLM found that gestational weeks 22–32 were a critical window, when NO2 exposure had strongest associations with SGA. The associations of air pollution exposure tended to be stronger in female newborns than in male newborns. However, no significant associations of air pollution exposure during preconception period on birthweight outcomes were found.ConclusionConsistent with previous studies, we found that air pollution exposure during mid-to-late pregnancy was associated with adverse birthweight outcomes.

Associations of Air Pollution Exposure and COVID-19 Vaccinations with the Risk of COVID-19 Hospitalizations in Southern California

Associations of Air Pollution Exposure and COVID-19 Vaccinations with the Risk of COVID-19 Hospitalizations in Southern California

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.

Association of air pollution exposure during pregnancy and early childhood with children's cognitive performance and behavior at age six

BackgroundThe impact of air pollution on neurodevelopment in children has attracted much attention in recent times. We aim to clarify the association between prenatal and postnatal air pollutant exposure and children's cognitive performance and behavior at age six. MethodsThis study was conducted based on a birth cohort study in Japan. Children's intelligence quotient (IQ) was assessed using the Wechsler Intelligence Scale for Children and a score <85 was deemed as low intelligence. A score ≥60 on the Child Behavior Checklist indicated behavioral problems. Exposure to outdoor fine particulate matter (PM2.5) during pregnancy and early childhood was estimated using a spatiotemporal model, while indoor concentrations of air pollutants inside subjects' homes were measured for a week when the child was of ages 1.5 and 3. The associations of exposure to air pollution during pregnancy and after childbirth with cognitive performance and behavior were analyzed using logistic regression models. ResultsThe estimated exposure to outdoor PM2.5 during pregnancy and early childhood was not associated with decreased cognitive performance. However, exposure during the first trimester, 0–1 and 3–5 years of age was associated with children's externalizing problems (odds ratios (ORs) were 2.77 [95% confidence interval (CI): 1.05–7.29], 1.66 [95%CI: 1.05–2.62], and 1.80 [95%CI: 1.19–2.74] per interquartile range (IQR) increase, respectively). Exposure to indoor PM2.5 and coarse particles after childbirth was associated with lower full scale IQ (ORs were 1.46 [95%CI: 1.03–2.08] and 1.85 [95%CI: 1.12–3.07] per IQR increase, respectively). However, some inverse associations were also observed. ConclusionsThese results suggest associations between prenatal and postnatal exposure to outdoor air pollution and behavioral problems, and between indoor air pollution after childbirth and cognitive performance at age six. However, the effects of exposure to outdoor PM2.5 during pregnancy on cognitive performance were not observed.

Association of long-term exposure to ambient air pollution with retinal neurodegeneration: the prospective Alienor study

Chronic exposure to air pollution may have adverse effects on neurodegenerative diseases. Glaucoma, the second leading cause of blindness worldwide, is a neurodegenerative disease of the optic nerve, characterized by progressive thinning of the retinal nerve fiber layer (RNFL). We investigated the relationship of air pollution exposure with longitudinal changes of RNFL thickness in the Alienor study, a population-based cohort of residents of Bordeaux, France, aged 75 years or more. Peripapillary RNFL thickness was measured using optical coherence tomography imaging every 2 years from 2009 to 2020. Measurements were acquired and reviewed by specially trained technicians to control quality. Air pollution exposure (particulate matter ≤2.5 μm (PM2.5), black carbon (BC), nitrogen dioxide (NO2)) was estimated at the participants’ geocoded residential address using land-use regression models. For each pollutant, the 10-year average of past exposure at first RNFL thickness measurement was estimated. Associations of air pollution exposure with RNFL thickness longitudinal changes were assessed using linear mixed models adjusted for potential confounders, allowing for intra-eye and intra-individual correlation (repeated measurements).The study included 683 participants with at least one RNFL thickness measurement (62% female, mean age 82 years). The average RNFL was 90 μm (SD:14.4) at baseline. Exposure to higher levels of PM2.5 and BC in the previous 10 years was significantly associated with a faster RNFL thinning during the 11-year follow-up (−0.28 μm/year (95% confidence interval (CI) [-0.44;-0.13]) and −0.26 μm/year (95% CI [-0.40;-0.12]) per interquartile range increment; p < 0.001 for both). The size of the effect was similar to one year of age in the fitted model (−0.36 μm/year). No statistically significant associations were found with NO2 in the main models.This study evidenced a strong association of chronic exposure to fine particulate matter with retinal neurodegeneration, at air pollution levels below the current recommended thresholds in Europe.

The association between air pollution and the severity at diagnosis and progression of systemic sclerosis-associated interstitial lung disease: results from the retrospective ScleroPol study

ObjectiveTo investigate the association of air pollution exposure with the severity of interstitial lung disease (ILD) at diagnosis and ILD progression among patients with systemic sclerosis (SSc)-associated ILD.MethodsWe conducted a retrospective two-center study of patients with SSc-associated ILD diagnosed between 2006 and 2019. Exposure to the air pollutants particulate matter of up to 10 and 2.5 µm in diameter (PM10, PM2.5), nitrogen dioxide (NO2), and ozone (O3) was assessed at the geolocalization coordinates of the patients’ residential address. Logistic regression models were used to evaluate the association between air pollution and severity at diagnosis according to the Goh staging algorithm, and progression at 12 and 24 months.ResultsWe included 181 patients, 80% of whom were women; 44% had diffuse cutaneous scleroderma, and 56% had anti-topoisomerase I antibodies. ILD was extensive, according to the Goh staging algorithm, in 29% of patients. O3 exposure was associated with the presence of extensive ILD at diagnosis (adjusted OR: 1.12, 95% CI 1.05–1.21; p value = 0.002). At 12 and 24 months, progression was noted in 27/105 (26%) and 48/113 (43%) patients, respectively. O3 exposure was associated with progression at 24 months (adjusted OR: 1.10, 95% CI 1.02–1.19; p value = 0.02). We found no association between exposure to other air pollutants and severity at diagnosis and progression.ConclusionOur findings suggest that high levels of O3 exposure are associated with more severe SSc-associated ILD at diagnosis, and progression at 24 months.

Association between Residential Exposure to Air Pollution and Incident Coronary Heart Disease Is Not Mediated by Leukocyte Telomere Length: A UK Biobank Study.

Higher air pollution exposure and shorter leukocyte telomere length (LTL) are both associated with increased risk of coronary heart disease (CHD), and share plausible mechanisms, including inflammation. LTL may serve as a biomarker of air pollution exposure and may be intervened with to reduce the risk of CHD. To the best of our knowledge, we are the first to test the mediation effect of LTL in the relationship between air pollution exposure and incident CHD. Using the UK Biobank (UKB) data (n = 317,601), we conducted a prospective study linking residential air pollution exposure (PM2.5, PM10, NO2, NOx) and LTL to incident CHD during a mean follow-up of 12.6 years. Cox proportional hazards models and generalized additive models with penalized spline functions were used to model the associations of pollutant concentrations and LTL with incident CHD. We found non-linear associations of air pollution exposure with LTL and CHD. Pollutant concentrations in the lower range were decreasingly associated with longer LTL and reduced risk of CHD. The associations between lower pollutant concentrations and reduced risk of CHD, however, were minimally mediated by LTL (<3%). Our findings suggest that air pollution influences CHD through pathways that do not involve LTL. Replication is needed with improved measurements of air pollution that more accurately assesses personal exposure.

Ambient air pollution exposure linked to long COVID among young adults: a nested survey in a population-based cohort inSweden.

Post COVID-19 conditions, also known as long COVID, are of public health concern, but little is known about their underlying risk factors. We aimed to investigate associations of air pollution exposure with long COVID among Swedish young adults. We used data from the BAMSE (Children, Allergy, Environment, Stockholm, Epidemiology [in Swedish]) cohort. From October 2021 to February 2022 participants answered a web-questionnaire focusing on persistent symptoms following acute SARS-CoV-2 infection. Long COVID was defined as symptoms after confirmed infection with SARS-CoV-2 lasting for two months or longer. Ambient air pollution levels (particulate matter ≤2.5μm [PM2.5], ≤10μm [PM10], black carbon [BC] and nitrogen oxides [NOx]) at individual-level addresses were estimated using dispersion modelling. A total of 753 participants with SARS-CoV-2 infection were included of whom 116 (15.4%) reported having long COVID. The most common symptoms were altered smell/taste (n=80, 10.6%), dyspnea (n=36, 4.8%) and fatigue (n=34, 4.5%). Median annual PM2.5 exposure in 2019 (pre-pandemic) was 6.39 (interquartile range [IQR] 6.06-6.71) μg/m3. Adjusted Odds Ratios (95% confidence intervals) of PM2.5 per IQR increase were 1.28 (1.02-1.60) for long COVID, 1.65 (1.09-2.50) for dyspnea symptoms and 1.29 (0.97-1.70) for altered smell/taste. Positive associations were found for the other air pollutants and remained consistent across sensitivity analyses. Associations tended to be stronger among participants with asthma, and those having had COVID during 2020 (versus 2021). Ambient long-term PM2.5 exposure may affect the risk of long COVID in young adults, supporting efforts for continuously improving air quality. The study received funding from the Swedish Research Council (grant no. 2020-01886, 2022-06340), the Swedish Research Council for Health, Working life and Welfare (FORTE grant no. 2017-01146), the Swedish Heart-Lung Foundation, Karolinska Institute (no. 2022-01807) and Region Stockholm (ALF project for cohort and database maintenance).

Long-term associations of air pollution exposure with liver enzymes among adult employees of the Electricity Generating Authority of Thailand: A longitudinal cohort study

Exposure to particulate air pollution may induce hepatotoxic effects via low-grade inflammation. However, only a few longitudinal epidemiological studies have investigated the long-term effects of air pollution on liver enzyme levels. The present study examined associations between long-term air pollution exposure and serum liver enzymes [alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT)] in employees of the Electricity Generating Authority of Thailand (EGAT) in Thailand's Bangkok Metropolitan Region (BMR). We conducted secondary analyses using the data obtained from 2022 subjects (mean age, 41.2 years as of 2009) of the EGAT3 cohort study (2009–2019). The daily mean concentration of each air pollutant (PM10, O3, NO2, SO2, and CO) was estimated at the sub-district level in BMR from 2008 to 2019 using the Kriging approach. Long-term exposure for each subject was defined as the 1-year average concentrations before the date of the physical examination in 2009, 2014, and 2019. We used linear mixed effects models to assess associations between air pollution and serum liver enzymes. Interquartile range increases in PM10 and O3 were related to decreased ALP [-2.4% (95%CI: -3.0, −1.9) and −6.6% (−7.3, −5.9), respectively] after potential confounders were adjusted. Positive associations between NO2, SO2, and CO with ALP were found [5.7% (4.8, 6.5), 4.5% (4.0, 5.0), and 0.8 (0.3, 1.4), respectively]. Elevated AST was also associated with higher PM10 [1.7% (0.8, 2.5)] and O3 [5.7% (4.5, 6.9)]. However, AST was negatively associated with NO2 [-2.9% (−4.0, −1.8)] and SO2 [-1.7% (−2.3, −1.1)]. In contrast to other air pollutants, we only observed a positive association between O3 and ALT [3.4% (1.5, 5.3)]. The alteration in liver enzyme levels was significantly associated with long-term exposure to air pollution, which may raise the possibility of hepatocellular damage.

Genetic risk modifies the effect of long-term fine particulate matter exposure on coronary artery disease

BackgroundAlthough both environmental and genetic factors were linked to coronary artery disease (CAD), the extent to which the association of air pollution exposure with CAD can be influenced by genetic risk was not well understood. MethodsA total of 41,149 participants recruited from the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) were included. Genetic risk scores of CAD were constructed based on 540 genetic variants. Long-term PM2.5 exposures were assessed by adopting satellite-based PM2.5 estimations at 1-km resolution. We used stratified Cox proportional hazards regression model to examine the impact of PM2.5 exposure and genetic risk on CAD risk, and further analyzed modification effect of genetic predisposition on association between PM2.5 exposure and CAD risk. ResultsDuring a median of 13.01 years of follow-up, 1,373 incident CAD events were observed. Long-term PM2.5 exposure significantly increased CAD risk, and the hazard ratios (HRs) [95% confidence intervals (CIs)] were 1.27 (1.05–1.54) and 1.95 (1.57–2.42) among intermediate and high PM2.5 exposure groups compared to low PM2.5 exposure group. The relative risks of CAD were 40% (HR: 1.40, 95%CI: 1.18–1.66) and 133% (HR: 2.33, 95%CI: 1.94–2.79) higher among individuals at intermediate and high genetic risk than those at low genetic risk. Compared with individuals with both low genetic risk and low PM2.5 exposure, those with high genetic risk and high PM2.5 exposure had highest CAD risk, with HR of 4.37 (95%CI: 3.13–6.11). We observed significant multiplicative (P < 0.001) and additive interaction [relative excess risk due to interaction (95%CI): 2.75 (1.32–4.20); attributable proportion due to interaction (95%CI): 0.56 (0.42–0.70)] between genetic risk and PM2.5 exposure on CAD. ConclusionThis study provided evidence that long-term PM2.5 exposure might increase CAD risk, especially among people at high genetic risk. Our findings highlighted the importance of taking strategies on air quality improvement to cardiovascular disease prevention.

Outdoor residential air pollution exposure and the development of brain morphology across childhood: a longitudinal study

Background and aim: Emerging evidence suggests a relationship between exposure to air pollution and brain morphology in children, but little is known about how air pollution exposure influences the development of brain structures throughout childhood. We aim to study the association of air pollution exposure during pregnancy and childhood with the development of brain morphology from age 6-16 years. Methods: We used data from 4,243 children of the Generation R study, a birth cohort in Rotterdam, the Netherlands. We estimated the concentrations of fourteen air pollutants at participant´s home addresses during pregnancy and childhood, using land use regression models. We included structural brain images at three time points, namely at age 6-10 years, 9-12 years, and 13-16 years. We assessed the association between the air pollutants and brain volumes with linear mixed models, fitting an interaction term for age and each pollutant. Models were adjusted for socioeconomic status and lifestyle characteristics. Results: Higher air pollution exposure during pregnancy was associated with a slower decrease of cortical grey matter volume starting at around age 10 and a slower increase of corpus callosum volume (e.g. -12.7 mm3 increase in corpus callosum volume [95%CI -22.0; -3.3] with each year of age per 10 &amp;#x3bc;g/m3 increase in nitrogen dioxide exposure). Childhood exposure was associated with a faster decrease of putamen and caudate nucleus volume, and a slower increase of hippocampus volume. Higher exposure to air pollution during pregnancy and childhood was associated with a slower increase of thalamus volume. Air pollution exposure was not associated with cerebellum, amygdala, nucleus accumbens or globus pallidus volume. Conclusions: Air pollution exposure was associated with region-specific differences in age-related growth trajectories. Air pollution exposure during childhood might affect different brain regions than exposure during pregnancy. Keywords: air pollution, neurodevelopment, children, traffic