Long-term Air Pollution Exposure Research Articles

An assessment of the mediating role of hypertension in the effect of long-term air pollution exposure on dementia

Background: Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect. Methods: We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000–2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM2.5, PM10, and NO2. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders. Results: Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer’s disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes. Conclusions: The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.

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 measures of central hemodynamics and arterial stiffness among multiethnic Chicago residents

ObjectivesTo examine whether long-term air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters.MethodsWe assessed central hemodynamic parameters including central blood pressure, cardiac parameters, systemic vascular compliance and resistance, and brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes.ResultsThe cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013–2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-µg/m3 increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01).ConclusionThis population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans.

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.

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.

Air pollution, cardiorespiratory fitness and biomarkers of oxidative status and inflammation in the 4HAIE study

The aim of this study was to investigate the associations between cardiorespiratory fitness (CRF), long-term air pollution exposure and biochemical markers of oxidative status and inflammation. This is a cross-sectional investigation focusing on biochemical markers of oxidative status and inflammation. Participants were Caucasian (N = 1188; age 18–65 years) who lived for at least 5 years in a high air-polluted (Moravian-Silesian; MS) or low air-polluted (South Bohemia; SB) region of the Czech Republic. Healthy runners and inactive individuals were recruited. A multiple regression analysis was used to explain the relationship between multiple independent variables (CRF, trunk fat mass, sex, socioeconomic status, and region (MS region vs. SB region) and dependent variables (oxidative status, inflammation). CRF, trunk fat mass, age and sex significantly predicted almost all selected markers of oxidative status and inflammation (except GSSG, GSH/GSSG and BDNF). Participants living in the MS region presented significantly higher GPx (by 3.1%) and lower BDNF values (by 4.5%). All other investigated biochemical markers were not significantly influenced by region. We did not find meaningful interactions between long-term air-pollution exposure versus markers of oxidative status and inflammation. However, we showed various significant interactions with sex, age, CRF and body composition. The significant association of living in the high air polluted MS region with the BDNF level warrants further attention.

Air Pollution and Cardiac Arrest: A More Significant Intermediate Role of COPD than Cardiac Events.

No prior studies have linked long-term air pollution exposure to incident sudden cardiac arrest (SCA) or its possible development trajectories. We aimed to investigate the association between long-term exposure to air pollution and SCA, as well as possible intermediate diseases. Based on the UK Biobank cohort, Cox proportional hazard model was applied to explore associations between air pollutants and SCA. Chronic obstructive pulmonary disease (COPD) and major adverse cardiovascular events (MACE) were selected as intermediate conditions, and multistate model was fitted for trajectory analysis. During a median follow-up of 13.7 years, 2884 participants developed SCA among 458 237 individuals. The hazard ratios (HRs) for SCA were 1.04-1.12 per interquartile range increment in concentrations of fine particulate matter, inhalable particulate matter, nitrogen dioxide, and nitrogen oxides. Most prominently, air pollutants could induce SCA through promoting transitions from baseline health to COPD (HRs: 1.06-1.24) and then to SCA (HRs: 1.16-1.27). Less importantly, SCA could be developed through transitions from baseline health to MACE (HRs: 1.02-1.07) and further to SCA (HRs: 1.12-1.16). This study provides novel and compelling evidence that long-term exposure to air pollution could promote the development of SCA, with COPD serving as a more important intermediate condition than MACE.

Effects of short- and long-term exposures to multiple air pollutants on depression among the labor force: A nationwide longitudinal study in China

BackgroundDepression prevalence has surged within the labor force population in recent years. While links between air pollutants and depression were explored, there was a notable scarcity of research focusing on the workforce. MethodsThis nationwide longitudinal study analyzed 27,457 workers aged 15–64. We estimated monthly mean concentrations of fine particulate matter (PM2.5), its primary components, and Ozone (O3) at participants' residences using spatiotemporal models. To assess the relationship between short- (1 to 3 months) and long-term (1 to 2 years) exposure to various air pollutants and depressive levels and occurrences, we employed linear mixed–effects models and mixed–effects logistic regression. We considered potential occupational moderators, such as labor contracts, overtime compensation, and total annual income. ResultsWe found significant increases in depression risks within the workforce linked to both short- and long-term air pollution exposure. A 10 μg/m3 rise in 2-year average PM2.5, black carbon (BC), and O3 concentrations correlated with increments in depressive scores of 0.009, 0.173, and 0.010, and a higher likelihood of depression prevalence by 0.5 %, 12.6 %, and 0.7 %. The impacts of air pollutants and depression were more prominent in people without labor contracts, overtime compensation, and lower total incomes. ConclusionExposures to air pollutants could increase the risk of depression in the labor force population. The mitigating effects of higher income, benefits, and job security against depression underscore the need for focused mental health interventions.

Long-term exposure to air pollution and precocious puberty in South Korea

Background and aimThe increasing prevalence of precocious puberty (PP) has emerged as a significant medical and social problem worldwide. However, research on the relationship between long-term air pollution exposure and PP has been relatively limited. We thus investigated the association between long-term air pollution exposure and the onset of PP in South Korea. MethodsWe investigated a retrospective cohort using the Korea National Health Insurance Database. Six-year-old children born from 2007 to 2009 were examined (2013–2015). We included boys ≤10 years and girls aged ≤9 years who visited hospitals for early pubertal development, were diagnosed with PP per the ICD-10 (E228, E301, and E309), and received gonadotropin-releasing hormone agonist treatment. We analyzed data for boys up until 10 years old (60-month follow-up) and for girls up to 9 years old (48-month follow-up). We assessed the association between long-term air pollution exposure and the onset of PP using a Cox proportional hazard model. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) per 1 μg/m3 increase in fine particulate matter (PM2.5) and particulate matter (PM10) and per 1 ppb increase in sulfur dioxide (SO2), nitrogen dioxide (NO2), and ozone (O3). ResultsThis study included 1,205,784 children aged six years old between 2013 and 2015. A positive association was found between the 48-month moving average PM2.5 (HR: 1.019; 95% CI: 1.012, 1.027), PM10 (HR: 1.009; 95% CI: 1.006, 1.013), SO2 (HR: 1.037; 95% CI: 1.018, 1.055), and O3 (HR: 1.006; 95% CI: 1.001, 1.010) exposure and PP in girls but not boys. ConclusionsThis study provides valuable insights into the harmful effects of air pollution during childhood and adolescence, emphasizing that air pollution is a risk factor that should be managed and reduced.

Exposure to ambient air pollution and cognitive function: an analysis of the English Longitudinal Study of Ageing cohort

BackgroundAn increasing number of studies suggest adverse effects of exposure to ambient air pollution on cognitive function, but the evidence is still limited. We investigated the associations between long-term exposure to air pollutants and cognitive function in the English Longitudinal Study of Ageing (ELSA) cohort of older adults.MethodsOur sample included 8,883 individuals from ELSA, based on a nationally representative study of people aged ≥ 50 years, followed-up from 2002 until 2017. Exposure to air pollutants was modelled by the CMAQ-urban dispersion model and assigned to the participants’ residential postcodes. Cognitive test scores of memory and executive function were collected biennially. The associations between these cognitive measures and exposure to ambient concentrations of NO2, PM10, PM2.5 and ozone were investigated using mixed-effects models adjusted for time-varying age, physical activity and smoking status, as well as baseline gender and level of education.ResultsIncreasing long-term exposure per interquartile range (IQR) of NO2 (IQR: 13.05 μg/m3), PM10 (IQR: 3.35 μg/m3) and PM2.5 (IQR: 2.7 μg/m3) were associated with decreases in test scores of composite memory by -0.10 (95% confidence interval [CI]: -0.14, -0.07), -0.02 [-0.04, -0.01] and -0.08 [-0.11, -0.05], respectively. The same increases in NO2, PM10 and PM2.5 were associated with decreases in executive function score of -0.31 [-0.38, -0.23], -0.05 [-0.08, -0.02] and -0.16 [-0.22, -0.10], respectively. The association with ozone was inverse across both tests. Similar results were reported for the London-dwelling sub-sample of participants.ConclusionsThe present study was based on a long follow-up with several repeated measurements per cohort participant and long-term air pollution exposure assessment at a fine spatial scale. Increasing long-term exposure to NO2, PM10 and PM2.5 was associated with a decrease in cognitive function in older adults in England. This evidence can inform policies related to modifiable environmental exposures linked to cognitive decline.

Multiple dietary patterns and the association between long-term air pollution exposure with type 2 diabetes risk: Findings from UK Biobank cohort study

BackgroundEvidence of modifying effect of various dietary patterns (DPs) on risk of type 2 diabetes (T2D) induced by long-term exposure to air pollution (AP) is still rather lacking, which therefore we aimed to explore in this study. MethodsWe included 78,230 UK Biobank participants aged 40–70 years with at least 2 typical 24-hour dietary assessments and without baseline diabetes. The annual average concentration of particulate matter with diameter micrometers ≤2.5 (PM2.5) and ≤10 (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) estimated by land use regression model was the alternative proxy of long-term AP exposure. Three well-known prior DPs such as Mediterranean diet (MED), dietary approaches to stop hypertension diet (DASH), and empirical dietary inflammatory pattern (EDIP), as well as three posterior DPs derived by the rank reduced regression model were used to capture participants’ dietary habits. Cox regression models were used to estimate AP-T2D and DP-T2D associations. Modifying effect of DPs on AP-T2D association was assessed using stratified analysis and heterogeneity test. ResultsDuring a median follow-up 12.19 years, 1,693 participants developed T2D. PM2.5, PM10, NO2, and NOX significantly increased the T2D risk (P <0.05), with hazard ratio (HR) and 95% confidence interval (95% CI) for per interquartile range increase being 1.09 (1.02,1.15), 1.04 (1.00, 1.09), 1.11 (1.04, 1.18), and 1.08 (1.03, 1.14), respectively. Comparing high with low adherence, healthy DPs were associated with a 14–41% lower T2D risk. Participants with high adherence to MED, DASH, and anti-EDIP, alongside the posterior anti-oxidative dietary pattern (AODP) had attenuated and statistically non-significant NO2-T2D and NOX-T2D associations (Pmodify <0.05). ConclusionsMultiple forms of healthy DPs help reduce the T2D risk associated with long-term exposure to NO2 and NOX. Our findings indicate that adherence to healthy DPs is a feasible T2D prevention strategy for people long-term suffering from NO2 and NOX pollution.

The role of lifestyle in the association between long-term ambient air pollution exposure and cardiovascular disease: a national cohort study in China

BackgroundCardiovascular disease (CVD) caused by air pollution poses a considerable burden on public health. We aim to examine whether lifestyle factors mediate the associations of air pollutant exposure with the risk of CVD and the extent of the interaction between lifestyles and air pollutant exposure regarding CVD outcomes.MethodsWe included 7000 participants in 2011–2012 and followed up until 2018. The lifestyle evaluation consists of six factors as proxies, including blood pressure, blood glucose, blood lipids, body mass index, tobacco exposure, and physical activity, and the participants were categorized into three lifestyle groups according to the number of ideal factors (unfavorable, 0–1; intermediate, 2–4; and favorable, 5–6). Satellite-based spatiotemporal models were used to estimate exposure to ambient air pollutants (including particles with diameters ≤ 1.0 μm [PM1], ≤ 2.5 μm [PM2.5], ≤ 10 μm [PM10], nitrogen dioxide [NO2], and ozone [O3]). Cox regression models were used to examine the associations between air pollutant exposure, lifestyles and the risk of CVD. The mediation and modification effects of lifestyle categories on the association between air pollutant exposure and CVD were analyzed.ResultsAfter adjusting for covariates, per 10 μg/m3 increase in exposure to PM1 (HR: 1.09, 95% CI: 1.05–1.14), PM2.5 (HR: 1.04, 95% CI: 1.00–1.08), PM10 (HR: 1.05, 95% CI: 1.03–1.08), and NO2 (HR: 1.11, 95% CI: 1.05–1.18) was associated with an increased risk of CVD. Adherence to a healthy lifestyle was associated with a reduced risk of CVD compared to an unfavorable lifestyle (HR: 0.65, 95% CI: 0.56–0.76 for intermediate lifestyle and HR: 0.41, 95% CI: 0.32–0.53 for favorable lifestyle). Lifestyle played a significant partial mediating role in the contribution of air pollutant exposure to CVD, with the mediation proportion ranging from 7.4% for PM10 to 14.3% for PM2.5. Compared to an unfavorable lifestyle, the relative excess risk due to interaction for a healthier lifestyle to reduce the effect on CVD risk was − 0.98 (− 1.52 to − 0.44) for PM1, − 0.60 (− 1.05 to − 0.14) for PM2.5, − 1.84 (− 2.59 to − 1.09) for PM10, − 1.44 (− 2.10 to − 0.79) for NO2, and − 0.60 (− 1.08, − 0.12) for O3.ConclusionsLifestyle partially mediated the association of air pollution with CVD, and adherence to a healthy lifestyle could protect middle-aged and elderly people from the adverse effects of air pollution regarding CVD.

Causal association between long-term exposure to air pollution and incident Parkinson’s disease

Epidemiological evidence for long-term air pollution exposure and Parkinson’s disease (PD) is controversial, and analysis of causality is limited. We identified 293,888 participants who were free of PD at baseline in the UK Biobank (2006–2010). Time-varying air pollution [fine particulate (PM2.5) and ozone (O3)] exposures were estimated using spatio-temporal models. Incident cases of PD were identified using validated algorithms. Four methods were used to investigate the associations between air pollution and PD, including (1) standard time-varying Cox proportional-hazard model; (2) Cox models weighted by generalized propensity score (GPS) and inverse-probability weights (IPW); (3) instrumental variable (IV) analysis; and (4) negative control outcome analysis. During a median of 11.6 years of follow-up, 1822 incident PD cases were identified. Based on standard Cox regression, the hazard ratios (95% confidence interval) for a 1 µg/m3 or ppb increase in PM2.5 and O3 were 1.23 (1.17, 1.30) and 1.02 (0.98, 1.05), respectively. Consistent results were found in models weighted by GPS and IPW, and in IV analysis. There were no significant associations between air pollution and negative control outcomes. This study provides evidence to support a causal association between PM2.5 exposure and PD. Mitigation of air pollution could be a protective measure against PD.

Long-term air pollution exposure is associated with higher incidence of ST-elevation myocardial infarction and in-hospital cardiogenic shock

Previous studies have reported the association between myocardial infarction (MI) and air pollution (AP). However, limited information is available regarding the long-term effects of AP on the relative incidence rates of ST-elevation MI (STEMI) and Non-ST-elevation MI (NSTEMI). We investigated the association between long-term exposure to AP and the incidence of STEMI. Between January 2006 and December 2015, a total of 45,619 eligible patients with Acute Myocardial Infarction (AMI) were enrolled in the Korea Acute MI Registry (KAMIR) and KAMIR-National Institutes of Health. Mixed-effect regression models were used to examine the association between the annual average ambient AP before MI onset and the incidence of STEMI, and to evaluate the association of AP with the incidence of in-hospital cardiogenic shock. After mixed-effect regression model analysis, particulate matter (PM) 10 µm or less in diameter (PM10) was associated with increased incidence of STEMI compared with NSTEMI (odds ratio [OR] 1.009, 95% Confidence Interval [CI] 1.002–1.016; p = 0.012). For in-hospital cardiogenic shock complication, PM10 and SO2 were associated with increased risk, PM10 (OR 1.033, 95% CI 1.018–1.050; p < 0.001), SO2 (OR 1.104, 95% CI 1.006–1.212; p = 0.037), respectively. Policy-level strategies and clinical efforts to reduce AP exposure are necessary to prevent the incidence of STEMI and severe cardiovascular complications.

Long-term air pollution exposure and risk of SARS-CoV-2 infection: A UK-wide cohort study

BackgroundThe association between air quality and risk of SARS-CoV-2 infection is poorly understood. We investigated this association using serological individual-level data adjusting for a wide range of confounders, in a large population-based cohort (COVIDENCE UK). MethodsWe assessed the associations between long-term (2015–19) nitrogen dioxide (NO2) and fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5), exposures with SARS-CoV-2 infection, level of antibody response among those infected, and COVID-19 disease severity. We used serological data from 10,489 participants in the COVIDENCE UK cohort, and estimated annual average air pollution exposure at each participant's home postcode. ResultsAfter controlling for potential confounders, we found a positive association between 5-year NO2 and PM2.5 exposures and the risk of seropositivity: 10 unit increase in NO2 (μg/m3) was associated with an increasing risk of seropositivity by 1.092 (95% CI 1.02 to 1.17; p-for-trend 0.012). For PM2.5, 10 unit increase (μg/m3) was associated with an increasing risk of seropositivity by 1.65 (95% CI 1.015–2.68; p-for-trend 0·049). In addition, we found that NO2 was positively associated with higher antibody titres (p-for-trend 0·013) among seropositive participants, with no evidence of an association for PM2.5. ConclusionOur findings suggest that the long-term burden of air pollution increased the risks of SARS-CoV-2 infection and has important implications for future pandemic preparedness. This evidence strengthens the case for reducing long-term air pollution exposures to reduce the vulnerability of individuals to respiratory viruses.

The Role of Neighborhood Air Pollution in Disparate Racial and Ethnic Asthma Acute Care Use.

The share of Black or Latinx residents in a census tract remains associated with asthma-related Emergency Department visit rates after controlling for socioeconomic factors. The extent to which evident disparities relate to within-city heterogeneity of long-term air pollution exposure remains unclear. To investigate the role of intraurban spatial variability of air pollution in asthma acute care use disparity. An administrative database was used to define census tract population-based incidence rates of asthma-related Emergency Department visits. We estimate the association between census tract incidence rates and (a) average fine and coarse particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), and sulfur dioxide (SO2); and (b) racial/ethnic composition using generalized linear models controlling for socioeconomic and housing covariates. We additionally examine for attenuation of incidence risk ratios (IRR) associated with race/ethnicity when controlling for air pollution exposure. PM2.5, PM10, and SO2 are each associated with census tract-level incidence rates of asthma-related ED visits and multipollutant models show evidence of independent risk associated with PM10 and SO2. Association between census tract incidence rates and Black resident share (IRR [CI] = 1.51 [1.48-1.54]) is attenuated by 24% when accounting for air pollution (1.39 [1.35-1.42]), and the association with Latinx resident share (1.11 [1.09-1.13]) is attenuated by 32% (1.08 [1.06-1.10]). Neighborhood-level rates of asthma acute care use are associated with local air pollution. Controlling for air pollution attenuates associations with census tract racial/ethnic composition, suggesting that intracity variability in air pollution could contribute to neighborhood-to-neighborhood asthma morbidity disparities.

Long-term exposure to air pollution and incidence of gastric and the upper aerodigestive tract cancers in a pooled European cohort: The ELAPSE project.

Air pollution has been shown to significantly impact human health including cancer. Gastric and upper aerodigestive tract (UADT) cancers are common and increased risk has been associated with smoking and occupational exposures. However, the association with air pollution remains unclear. We pooled European subcohorts (N = 287,576 participants for gastric and N = 297,406 for UADT analyses) and investigated the association between residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone in the warm season (O3w) with gastric and UADT cancer. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,305,133 and 5,434,843 person-years, 872 gastric and 1139 UADT incident cancer cases were observed, respectively. For gastric cancer, we found no association with PM2.5, NO2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 μg/m3 increase in PM2.5, 1.19 (1.08-1.30) per 10 μg/m3 increase in NO2, 1.14 (1.04-1.26) per 0.5 × 10-5 m-1 increase in BC and 0.81 (0.72-0.92) per 10 μg/m3 increase in O3w. We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM2.5, NO2 and BC increased incidence of UADT cancer was observed.

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.

Genetic susceptibility modifies the association of long-term air pollution exposure on Parkinson’s disease

Inconsistent findings exist regarding the potential association between polluted air and Parkinson’s disease (PD), with unclear insights into the role of inherited sensitivity. This study sought to explore the potential link between various air pollutants and PD risk, investigating whether genetic susceptibility modulates these associations. The population-based study involved 312,009 initially PD-free participants with complete genotyping data. Annual mean concentrations of PM2.5, PM10, NO2, and NOx were estimated, and a polygenic risk score (PRS) was computed to assess individual genetic risks for PD. Cox proportional risk models were employed to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the associations between ambient air pollutants, genetic risk, and incident PD. Over a median 12.07-year follow-up, 2356 PD cases (0.76%) were observed. Compared to the lowest quartile of air pollution, the highest quartiles of NO2 and PM10 pollution showed HRs and 95% CIs of 1.247 (1.089–1.427) and 1.201 (1.052–1.373) for PD incidence, respectively. Each 10 μg/m3 increase in NO2 and PM10 yielded elevated HRs and 95% CIs for PD of 1.089 (1.026–1.155) and 1.363 (1.043–1.782), respectively. Individuals with significant genetic and PM10 exposure risks had the highest PD development risk (HR: 2.748, 95% CI: 2.145–3.520). Similarly, those with substantial genetic and NO2 exposure risks were over twice as likely to develop PD compared to minimal-risk counterparts (HR: 2.414, 95% CI: 1.912–3.048). Findings suggest that exposure to air contaminants heightens PD risk, particularly in individuals genetically predisposed to high susceptibility.

Effects of Residential Proximity to Industrial Zone on Respiratory Symptoms among Residents in Parit Raja, Batu Pahat

Introduction: The industrial park in the district of Parit Raja, Batu Pahat resulted in rapid growth of the town during the last 20 years and has been a reason of concern that this park also has contributed greatly to the problem of air pollution. The aim of this study was to evaluate the association between industrial air pollution and respiratory symptoms in adults living in the Parit Raja. Methods: A comparative cross-sectional study was undertaken among residents in the district of Parit Raja, Batu Pahat, Johor, Malaysia. A total of 110 residents aged between 19 and 65 years were randomly selected and information on personal characteristics and respiratory symptoms was obtained through a validated questionnaire. The prevalence of respiratory symptoms was compared between residents recruited from the areas situated about 5km radius of the industrial park (exposed) and &gt;5km radius from the industrial park (comparative). Results: A total of 34.5% and 25.5% of adults from the exposed group reported experiencing coughing for the last 3 months and chest tightness for the last 3 years. The logistic regression models showed that symptoms of coughing was associated with the exposed group (aOR=6.34, 95% CI=2.08-19.35), male respondents (aOR=3.18, 95% CI=1.10-9.16) and who stay in Part Raja for more than 14 years (aOR=3.16, 95% CI=1.14-8.79). Conclusion: This study demonstrated that long-term air pollution exposures are consistently associated with respiratory symptoms in residents living in the proximity of industrial parks. Therefore, public health initiatives that aim to provide more conducive environment are needed, especially for residents living near industrial parks.