Long-term Air Pollution Exposure Research Articles

Long-Term Air Pollution Exposure and Severity of Idiopathic Pulmonary Fibrosis: Data from the IPF-PRO Registry.

While exposure to air pollution is a known risk factor for adverse pulmonary outcomes, its impact in individuals with idiopathic pulmonary fibrosis (IPF) is less well understood. To investigate the effects of long-term exposure to air pollution on disease severity and progression in patients with IPF and to determine whether genomic factors, such as MUC5B promoter polymorphism or telomere length, modify these associations. We performed analyses at enrollment and after one year of follow-up in the IPF-PRO Registry, a prospective observational registry that enrolled individuals with IPF at 46 US sites from June 2014 to October 2018. Five-year average pollution exposures (PM2.5, NO2, O3) prior to enrollment date were estimated at participants' residential addresses with validated national spatio-temporal models. Multivariable regression models estimated associations between pollution exposure and physiologic measurements (FVC, DLCO, supplemental oxygen use at rest) and quality of life measurements (St. George's Respiratory Questionnaire [SGRQ], EuroQoL, Cough and Sputum Assessment Questionnaire) at enrollment. Cox proportional hazard models estimated associations between pollutants and a composite outcome of death, lung transplant, or >10% absolute decline in FVC % predicted in the year after enrollment. Models were adjusted for individual-level and spatial confounders, including proxies for disease onset. Gene-environment interactions with MUC5B and telomere length were assessed. Of 835 participants, 94% were non-Hispanic Whites, 76% were male, mean (SD) age was 70 (7.7) years. In fully adjusted analyses, higher PM2.5 exposure was associated with worse quality of life per SGRQ activity score (3.48 [95% confidence interval (CI) 0.64, 6.32] per 2µg/m3 PM2.5) and EuroQoL scores (-0.04 [95%CI -0.06, -0.01] per 2µg/m3 PM2.5), and lower FVC % predicted and lower DLCO% predicted at enrollment. Each 3 parts per billion difference in O3 exposure was associated with a 1.57% [95% CI 0.15, 2.98] higher FVC % predicted at enrollment, although this effect was attenuated in multi-pollutant models. There was no association between NO2 and enrollment measures, between pollution exposure and one-year outcomes, or evidence for gene-environment interactions. In the IPF-PRO Registry, long-term exposure to PM2.5 was associated with worse quality of life and lung function at enrollment, but not with short-term disease progression or mortality. There was no evidence of effect modification by interaction of genomic factors with pollution. The reason for the unexpected relationship between O3 exposure and higher FVC is unclear.

Benefits of hypothetical air pollution reduction interventions on NCDs in Belgium

Abstract Background The adverse health impact of air pollution on non-communicable diseases (NCDs) is well documented, yet methodological tools for assessing the potential health benefits of interventions are lacking. This study uses a parametric g-computation approach to evaluate the impact of hypothetical interventions targeting long-term air pollution exposure on reducing NCDs prevalence in Belgium, using data from three national Health Interview Surveys (BHIS 2008-2013-2018). Methods BHIS data (n = 27,536) were linked to environmental data at participants’ residential addresses. A g-computation approach was used to calculate the potential impact fractions of air quality interventions on several NCDs. Regression models were adjusted for socio-economic, environmental and lifestyle factors. The scenarios involved reducing individual long-term air pollution exposure to WHO air quality guideline levels, followed by investigating dose-response functions through various percentage reductions in air pollution exposure. Results Significant associations were found between air pollution and asthma, stroke, and multimorbidity. Adhering to WHO air quality guidelines would substantially reduce stroke risk in Belgium by 0.87% (95% CI:0.38; 1.35) for PM2.5 and 0.32% (95% CI:-0.05; 0.70) for NO2, preventing 63% and 22% of cases, respectively. For asthma, risk reduction was 1.43% (95% CI:-0.53; 3.4) for PM2.5 and 0.83% (95% CI: 0.01; 1.63) for NO2, preventing 27% and 16% of cases, respectively. For multimorbidity, risk reduction was 3.20 % (95% CI: -1.75; 8.16) for PM2.5 and 0.43% (95% CI:-2.03; 2.90) for NO2, preventing 7% and 0.4% of cases, respectively. Results revealed a clear dose-response association between air pollution reduction and the prevalence of stroke, asthma, and multimorbidity in Belgium. Conclusions This study demonstrates that air pollution reduction interventions could effectively decrease the prevalence of asthma, stroke, and multimorbidity in Belgium. Key messages • Air pollution reduction interventions could effectively decrease the prevalence of asthma, stroke, and multimorbidity in Belgium. • The g-computation approach to assess PIF of interventions represents a straightforward approach for drawing causal inferences from observational data.

Ambient air pollution exposure is associated with liver fat and stiffness in Latino youth with a more pronounced effect in those with PNPLA3 genotype and more advanced liver disease

BackgroundExposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD). ObjectivesWe sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity. MethodsData was analyzed from 113 Latino youth (age 11–19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM2.5), ≤ 10μm (PM10), nitrogen dioxide (NO2), 8-hour maximum ozone (8hrMax-O3), 24-hr O3, and redox-weighted oxidative capacity (Oxwt) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined. ResultsShort-term exposure to 8hrMax-O3 was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O3 and Oxwt were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM10, 8hrMax-O3, 24-hr O3, and Oxwt and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO2 and liver stiffness were stronger in those with severe liver disease. DiscussionAir pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage.

Childhood Air Pollution Exposure Associated with Self-reported Bronchitic Symptoms in Adulthood.

Rationale: Few studies have examined the effects of long-term childhood air pollution exposure on adult respiratory health, including whether childhood respiratory effects underlie this relation. Objectives: To evaluate associations between childhood air pollution exposure and self-reported adult bronchitic symptoms while considering child respiratory health in the Southern California Children's Health Study. Methods: Exposures to nitrogen dioxide (NO2), ozone, and particulate matter <2.5 μm and <10 μm in diameter (PM10) assessed using inverse-distance-squared spatial interpolation based on childhood (birth to age 17 yr) residential histories. Bronchitic symptoms (bronchitis, cough, or phlegm in the past 12 mo) were ascertained via a questionnaire in adulthood. Associations between mean air pollution exposure across childhood and self-reported adult bronchitic symptoms were estimated using logistic regression. We further adjusted for childhood bronchitic symptoms and asthma to understand whether associations operated beyond childhood respiratory health impacts. Effect modification was assessed for family history of asthma, childhood asthma, and adult allergies. Measurements and Main Results: A total of 1,308 participants were included (mostly non-Hispanic White [56%] or Hispanic [32%]). At adult assessment (mean age, 32.0 yr; standard deviation [SD], 4.7), 25% reported bronchitic symptoms. Adult bronchitic symptoms were associated with NO2 and PM10 childhood exposures. Odds ratios per 1-SD increase were 1.69 (95% confidence interval, 1.14-2.49) for NO2 (SD, 11.1 ppb) and 1.51 (95% confidence interval, 1.00-2.27) for PM10 (SD, 14.2 μg/m3). Adjusting for childhood bronchitic symptoms or asthma produced similar results. NO2 and PM10 associations were modified by childhood asthma, with greater associations among asthmatic individuals. Conclusions: Childhood NO2 and PM10 exposures were associated with adult bronchitic symptoms. Associations were not explained by childhood respiratory health impacts; however, participants with childhood asthma had stronger associations.

Air Pollution and Breast Cancer Incidence in the Multiethnic Cohort Study.

Recent studies suggested fine particulate matter (PM2.5) exposure increases the risk of breast cancer, but evidence among racially and ethnically diverse populations remains sparse. Among 58,358 California female participants of the Multiethnic Cohort (MEC) Study followed for an average of 19.3 years (1993-2018), we used Cox proportional hazards regression to examine associations of time-varying PM with invasive breast cancer risk (n = 3,524 cases; 70% African American and Latino females), adjusting for sociodemographics and lifestyle factors. Subgroup analyses were conducted for race and ethnicity, hormone receptor status, and breast cancer risk factors. Satellite-based PM2.5 was associated with a statistically significant increased incidence of breast cancer (hazard ratio [HR] per 10 μg/m3, 1.28 [95% CI, 1.08 to 1.51]). We found no evidence of heterogeneity in associations by race and ethnicity and hormone receptor status. Family history of breast cancer showed evidence of heterogeneity in PM2.5-associations (Pheterogeneity = .046). In a meta-analysis of the MEC and 10 other prospective cohorts, breast cancer incidence increased in association with exposure to PM2.5 (HR per 10 μg/m3 increase, 1.05 [95% CI, 1.00 to 1.10]; P = .064). Findings from this large multiethnic cohort with long-term air pollutant exposure and published prospective cohort studies support PM2.5 as a risk factor for breast cancer. As about half of breast cancer cannot be explained by established breast cancer risk factors and incidence is continuing to increase, particularly in low- and middle-income countries, our results highlight that breast cancer prevention should include not only individual-level behavior-centered approaches but also population-wide policies and regulations to curb PM2.5 exposure.

7115 Long-Term Exposure To Air Pollution And Precocious Puberty In Korea

Abstract Disclosure: J. Choi: None. J. Oh: None. R. Lee: None. E. Mun: None. K. Kim: None. E. Ha: None. H. Kim: None. Backgrounds and Aims The increasing prevalence of precocious puberty is emerging as a significant medical and social problem worldwide. However, limited research has investigated the relationship between long-term air pollution exposure and precocious puberty. We aimed to investigate the association between long-term air pollution exposure and first onset of precocious puberty in South Korea, nationwide. Methods: We investiagted a retrospective cohort using Korea National Health Insurance Database. Children born from 2007 to 2009 were followed-up from the age of six (2013 to 2015). We included boys aged ≤10 years and girls aged ≤ 9 years who visited hospitals for early pubertal development and were diagnosed with precocious puberty according to the ICD-10 (E228, E301,and E309) and gonadotropin-releasing hormone agonist (GnRHa) treatment. We conducted the association between long-term air pollution exposure and first onset of precocious puberty using a Cox proportional hazard model. We estimated the hazard ratios (HR) and 95% confidence intervals (CI) per 1 μg/m3 increase for fine particulate matter (PM2.5) and particulate matter (PM10) and per 1 ppb increase for sulfur dioxide (SO2), nitrogen dioxide (NO2), and ozone (O3). Results: A total of 1,205,784 childrens aged six years old were included during 2013­-2015. A positive association was found that the association between 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), O3 (HR: 1.006, 95% CI: 1.001, 1.010) exposure and precocious puberty in girls. In contrast, no association was found in boys. Conclusions Our findings supported that long-term exposure to air pollution is associated with an increased risk of precocious puberty. The study provides valuable insights into the harmful effects of air pollution during childhood and adolescence, emphasizing that air pollution is a modifiable risk factor that can be managed and improved. Presentation: 6/1/2024

Long-term exposure to ambient air pollution and risk of lung cancer – A comparative analysis of incidence and mortality in four administrative cohorts in the ELAPSE study

BackgroundStudies have linked air pollution to lung cancer incidence and mortality, but few have compared these associations, which may differ due to cancer survival variations. We aimed to evaluate the association between long-term air pollution exposure and lung cancer incidence and compare findings with previous lung cancer mortality analyses within the same cohorts. MethodsWe analyzed four population-based administrative cohorts in Denmark (2000–2015), England (2011–2017), Norway (2001–2016) and Rome (2001–2015). We assessed residential exposure to annual average fine particulate matter (PM2.5), nitrogen dioxide (NO₂), black carbon (BC), and warm-season ozone (O3) using Europe-wide land use regression models. We used Cox proportional hazard models to evaluate cohort-specific hazard ratios (HRs) and 95% confidence intervals (CIs) for lung cancer incidence identified using hospital admission records (English and Roman cohorts) or cancer registries (Danish and Norwegian cohorts). We evaluated the associations at low exposure levels using subset analyses and natural cubic splines. Cohort-specific HRs were pooled using random-effects meta-analyses, separately for incidence and mortality. ResultsOver 93,733,929 person-years of follow-up, 111,949 incident lung cancer cases occurred. Incident lung cancer was positively associated with PM2.5, NO2 and BC, and negatively associated with O3. The negative O3 association became positive after adjustment for NO2. Associations were almost identical or slightly stronger for lung cancer incidence than mortality in the same cohorts, with respective meta-analytic HRs (95% CIs) of 1.14 (1.06, 1.22) and 1.12 (1.02, 1.22) per 5 μg/m3 increase in PM2.5, and 1.10 (1.04, 1.16) and 1.09 (1.02, 1.16) per 10 μg/m3 increase in NO2. Positive associations persisted for both incidence and mortality at low pollution levels with similar magnitude. ConclusionsWe found similarly elevated risks of lung cancer incidence and mortality in association with residential exposure to PM2.5, NO2 and BC in meta-analyses of four European administrative cohorts, which persisted at low pollution levels.

Air pollution and perk consumption

This study examines the relationship between air pollution and perk consumption and finds strong evidence that firms headquartered in areas with severe air pollution have higher levels of perk consumption. Two plausible mechanisms are executives' higher physiological needs for clean air and stronger bargaining power. We also find that the positive relationship between air pollution and perk consumption strengthens when it is difficult to compensate executives for their long-term air pollution exposure through monetary salaries. Additional analysis indicates that increased perk consumption may mitigate the harm of air pollution on firms' performance, supporting the incentive view of perk consumption from a new perspective of air pollution.

Air pollution below US regulatory standards and cardiovascular diseases using a double negative control approach

Growing evidence suggests that long-term air pollution exposure is a risk factor for cardiovascular mortality and morbidity. However, few studies have investigated air pollution below current regulatory limits, and causal evidence is limited. We use a double negative control approach to examine the association between long-term exposure to air pollution at low concentration and cardiovascular hospitalizations among US Medicare beneficiaries aged ≥65 years between 2000 and 2016. The expected values of the negative outcome control (preceding-year hospitalizations) regressed on exposure and negative exposure control (subsequent-year exposure) are treated as a surrogate for omitted confounders. With analyses separately restricted to low-pollution areas (PM2.5 < 9 μg/m³, NO2 < 75.2 µg/m3 [40 ppb], warm-season O3 < 88.2 μg/m3 [45 ppb]), we observed positive associations of the three pollutants with hospitalization rates of stroke, heart failure, and atrial fibrillation and flutter. The associations generally persisted in demographic subgroups. Stricter national air quality standards should be considered.

Long-term exposure to air pollution at residential and workplace addresses and breast cancer risk: A case-control study nested in the French E3N-Générations cohort from 1990 to 2011

BackgroundAn increasing evidence links air pollution to breast cancer (BC) risk. Yet, pollutant exposure estimates at the workplace location in pollution exposure assessment have not been considered. ObjectivesThis study investigates the association between particulate matters (PM2·5, PM10) and nitrogen dioxide (NO2) atmospheric concentrations (1990–2011), at the women’s residential and workplace locations, and BC risk. MethodsThis case-control study of 2419 BC cases and 2984 controls, was nested in the French prospective E3N cohort. The annual mean PM2·5, PM10 and NO2 concentrations were estimated using a Land Use Regression model (50 m x 50 m resolution) and assigned to the women’s geocoded residential and workplace locations, from cohort recruitment to their index date (date of case diagnosis). Odds ratios (OR) and 95 % confidence intervals (CI) were estimated using multivariate logistic regression models. ResultsAn increased BC risk was observed for a 10 µg/m3 increase of the 1990–2011 average PM2·5 concentration estimates (OR=1·28; CI 1·00, 1·63). An increased risk was suggested for a 10 µg/m3 increase for PM10 (OR=1·09; CI 0·92, 1·30) and NO2 (OR=1·05; CI 0·97, 1·13). No effect modification by menopausal status, nor difference by hormone receptor status were observed. DiscussionThis study is the first to estimate BC risk and long-term air pollutant exposure from both, residential and workplace location histories. Results suggest that residential PM2·5, PM10 and NO2 concentrations are strongly correlated with workplace ones, indicating that residential data may serve as proxy for overall exposure. Future studies should consider exposure during commuting.

Association between long-term air pollution exposure and risk of autoimmune diseases in South Korea

Association between long-term air pollution exposure and risk of autoimmune diseases in South Korea

Association of Long-Term Air Pollution Exposure with Cerebrovascular and Other Dementia-Related Neuropathologies at Autopsy in a Community-Based Cohort

Association of Long-Term Air Pollution Exposure with Cerebrovascular and Other Dementia-Related Neuropathologies at Autopsy in a Community-Based Cohort

Reduced odor identification linked to long-term air pollution exposure: findings from the KORA FIT study in Augsburg, Germany

Reduced odor identification linked to long-term air pollution exposure: findings from the KORA FIT study in Augsburg, Germany

Air pollutants, genetic susceptibility and the risk of schizophrenia: large prospective study.

Evidence linking air pollutants and the risk of schizophrenia remains limited and inconsistent, and no studies have investigated the joint effect of air pollutant exposure and genetic factors on schizophrenia risk. To investigate how exposure to air pollution affects schizophrenia risk and the potential effect modification of genetic susceptibility. Our study was conducted using data on 485 288 participants from the UK Biobank. Cox proportional hazards models were used to estimate the schizophrenia risk as a function of long-term air pollution exposure presented as a time-varying variable. We also derived the schizophrenia polygenic risk score (PRS) utilising data provided by the UK Biobank, and investigated the modification effect of genetic susceptibility. During a median follow-up period of 11.9 years, 417 individuals developed schizophrenia (mean age 55.57 years, s.d. = 8.68; 45.6% female). Significant correlations were observed between long-term exposure to four air pollutants (PM2.5; PM10; nitrogen oxides, NOx; nitrogen dioxide, NO2) and the schizophrenia risk in each genetic risk group. Interactions between genetic factors and the pollutants NO2 and NOx had an effect on schizophrenia events. Compared with those with low PRS and low air pollution, participants with high PRS and high air pollution had the highest risk of incident schizophrenia (PM2.5: hazard ratio = 6.25 (95% CI 5.03-7.76); PM10: hazard ratio = 7.38 (95% CI 5.86-9.29); NO2: hazard ratio = 6.31 (95% CI 5.02-7.93); NOx: hazard ratio = 6.62 (95% CI 5.24-8.37)). Long-term exposure to air pollutants was positively related to the schizophrenia risk. Furthermore, high genetic susceptibility could increase the effect of NO2 and NOx on schizophrenia risk.

Multiple air pollutant exposure is associated with higher risk of all-cause mortality in dialysis patients: a French registry-based nationwide study.

Little is known about the effect of combined exposure to different air pollutants on mortality in dialysis patients. This study aimed to investigate the association of multiple exposures to air pollutants with all-cause and cause-specific death in dialysis patients. This registry-based nationwide cohort study included 90,373 adult kidney failure patients initiating maintenance dialysis between 2012 and 2020 identified from the French REIN registry. Estimated mean annual municipality levels of PM2.5, PM10, and NO2 between 2009 and 2020 were combined in different composite air pollution scores to estimate each participant's exposure at the residential place one to 3 years before dialysis initiation. Adjusted cause-specific Cox proportional hazard models were used to estimate hazard ratios (HRs) per interquartile range (IQR) greater air pollution score. Effect measure modification was assessed for age, sex, dialysis care model, and baseline comorbidities. Higher levels of the main air pollution score were associated with a greater rate of all-cause deaths (HR, 1.082 [95% confidence interval (CI), 1.057-1.104] per IQR increase), regardless of the exposure lag. This association was also confirmed in cause-specific analyses, most markedly for infectious mortality (HR, 1.686 [95% CI, 1.470-1.933]). Sensitivity analyses with alternative composite air pollution scores showed consistent findings. Subgroup analyses revealed a significantly stronger association among women and fewer comorbid patients. Long-term multiple air pollutant exposure is associated with all-cause and cause-specific mortality among patients receiving maintenance dialysis, suggesting that air pollution may be a significant contributor to the increasing trend of CKD-attributable mortality worldwide.

Statistical Analysis Plan for the AIRCARD Study: Individual Long-Term Air and Noise Pollution Exposure and Cardiovascular Disease Incidence and Mortality - A Prospective Cohort Study Utilizing DANCAVAS and VIVA Screening Trials.

The AIRCARD study is designed to investigate the relationship between long-term exposure to air and noise pollution and cardiovascular disease incidence and mortality. We aim to conduct a robust prospective cohort analysis assessing the cumulative and differential impacts of air and noise pollution exposure on cardiovascular disease and mortality. This study will adjust for relevant confounders, including traditional cardiovascular risk factors, socioeconomic indicators, and lipid-lowering agents. This prospective cohort study will include 27,022 male participants aged 65-74, recruited from the two large Danish DANCAVAS and VIVA trials, both population-based randomized, multicentered, clinically controlled studies. We will assess long-term exposure to air pollutants using the state-of-the-art DEHM/UBM/AirGIS modeling system and noise pollution through the Nord2000 and SoundPLAN models, covering data from 1979 to 2019. This statistical analysis plan is strictly formulated to predefine the analytical approach for all outcomes and key study variables before data access. The primary analysis will utilize Cox proportional hazards models, adjusted for confounders identified in our cohort (age, body mass index, hypertension, diabetes, smoking status, family history of heart disease, socioeconomic factors, and lipid-lowering agents). This statistical analysis plan further includes Spearman rank correlation to explore inter-pollutant associations. The AIRCARD study addresses global concerns about the impact of air and noise pollution on cardiovascular disease. This research is important for understanding how the pollutants contribute to cardiovascular disease. We aim to provide insights into this area, emphasizing the need for public health measures to mitigate pollution exposure. Our goal is to provide policymakers and healthcare professionals with information on the role of environmental factors in cardiovascular health that could influence global strategies to reduce the cardiovascular disease burden associated with pollution. The design of this SAP ensures transparency and verifiability, considering the complexities of evaluating environmental health impacts over an extended period.

Exposure to Air Pollution, Genetic Susceptibility, and Psoriasis Risk in the UK

Psoriasis is a common autoinflammatory disease influenced by complex interactions between environmental and genetic factors. The influence of long-term air pollution exposure on psoriasis remains underexplored. To examine the association between long-term exposure to air pollution and psoriasis and the interaction between air pollution and genetic susceptibility for incident psoriasis. This prospective cohort study used data from the UK Biobank. The analysis sample included individuals who were psoriasis free at baseline and had available data on air pollution exposure. Genetic analyses were restricted to White participants. Data were analyzed between November 1 and December 10, 2023. Exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter with a diameter less than 2.5 µm (PM2.5), and particulate matter with a diameter less than 10 µm (PM10) and genetic susceptibility for psoriasis. To ascertain the association of long-term exposure to NO2, NOx, PM2.5, and PM10 with the risk of psoriasis, a Cox proportional hazards model with time-varying air pollution exposure was used. Cox models were also used to explore the potential interplay between air pollutant exposure and genetic susceptibility for the risk of psoriasis incidence. A total of 474 055 individuals were included, with a mean (SD) age of 56.54 (8.09) years and 257 686 (54.36%) female participants. There were 9186 participants (1.94%) identified as Asian or Asian British, 7542 (1.59%) as Black or Black British, and 446 637 (94.22%) as White European. During a median (IQR) follow-up of 11.91 (11.21-12.59) years, 4031 incident psoriasis events were recorded. There was a positive association between the risk of psoriasis and air pollutant exposure. For every IQR increase in PM2.5, PM10, NO2, and NOx, the hazard ratios (HRs) were 1.41 (95% CI, 1.35-1.46), 1.47 (95% CI, 1.41-1.52), 1.28 (95% CI, 1.23-1.33), and 1.19 (95% CI, 1.14-1.24), respectively. When comparing individuals in the lowest exposure quartile (Q1) with those in the highest exposure quartile (Q4), the multivariate-adjusted HRs were 2.01 (95% CI, 1.83-2.20) for PM2.5, 2.21 (95% CI, 2.02-2.43) for PM10, 1.64 (95% CI, 1.49-1.80) for NO2, and 1.34 (95% CI, 1.22-1.47) for NOx. Moreover, significant interactions between air pollution and genetic predisposition for incident psoriasis were observed. In the subset of 446 637 White individuals, the findings indicated a substantial risk of psoriasis development in participants exposed to the highest quartile of air pollution levels concomitant with high genetic risk compared with those in the lowest quartile of air pollution levels with low genetic risk (PM2.5: HR, 4.11; 95% CI, 3.46-4.90; PM10: HR, 4.29; 95% CI, 3.61-5.08; NO2: HR, 2.95; 95% CI, 2.49-3.50; NOx: HR, 2.44; 95% CI, 2.08-2.87). In this prospective cohort study of the association between air pollution and psoriasis, long-term exposure to air pollution was associated with increased psoriasis risk. There was an interaction between air pollution and genetic susceptibility on psoriasis risk.

Air pollution exposure and mortality from neurodegenerative diseases in the Netherlands: A population-based cohort study

BackgroundLong-term exposure to ambient air pollution has been linked with all-cause mortality and cardiovascular and respiratory diseases. Suggestive associations between ambient air pollutants and neurodegeneration have also been reported, but due to the small effect and relatively rare outcomes evidence is yet inconclusive. Our aim was to investigate the associations between long-term air pollution exposure and mortality from neurodegenerative diseases. MethodsA Dutch national cohort of 10.8 million adults aged ≥30 years was followed from 2013 until 2019. Annual average concentrations of air pollutants (ultra-fine particles (UFP), nitrogen dioxide (NO2), fine particles (PM2.5 and PM10) and elemental carbon (EC)) were estimated at the home address at baseline, using land-use regression models. The outcome variables were mortality due to amyotrophic lateral sclerosis (ALS), Parkinson's disease, non-vascular dementia, Alzheimer's disease, and multiple sclerosis (MS). Hazard ratios (HR) were estimated using Cox models, adjusting for individual and area-level socio-economic status covariates. ResultsWe had a follow-up of 71 million person-years. The adjusted HRs for non-vascular dementia were significantly increased for NO2 (1.03; 95% confidence interval (CI) 1.02–1.05) and PM2.5 (1.02; 95%CI 1.01–1.03) per interquartile range (IQR; 6.52 and 1.47 μg/m3, respectively). The association with PM2.5 was also positive for ALS (1.02; 95%CI 0.97–1.07). These associations remained positive in sensitivity analyses and two-pollutant models. UFP was not associated with any outcome. No association with air pollution was found for Parkinson's disease and MS. Inverse associations were found for Alzheimer's disease. ConclusionOur findings, using a cohort of more than 10 million people, provide further support for associations between long-term exposure to air pollutants (PM2.5 and particularly NO2) and mortality of non-vascular dementia. No associations were found for Parkinson and MS and an inverse association was observed for Alzheimer's disease.

Long-term air pollution exposure and the risk of primary graft dysfunction after lung transplantation

Background: Primary graft dysfunction (PGD) contributes substantially to both short and long-term mortality after lung transplantation but the mechanisms that lead to PGD are not well understood. Exposure to ambient air pollutants is associated with adverse events during waitlisting for lung transplantation, and chronic lung allograft dysfunction but its association with PGD has not been studied. We hypothesized that long-term exposure of the lung donor and recipient to high levels of ambient air pollutants would increase the risk of PGD in lung transplant recipients. Methods: Using data from 1428 lung transplant recipients and their donors enrolled in the Lung Transplant Outcomes Group (LTOG) observational cohort study, we evaluated the association between the development of PGD and zip-code based estimates of long-term exposure to six major air pollutants (ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, PM2.5 and PM10) in both the lung donor and the lung recipient. Exposure estimates used daily EPA air pollutant monitoring data and were based on the geographic centroid of the each subject’s residential zip code. Associations were tested in both univariable and multivariable models controlling for known PGD risk factors. Results: We did not find strong associations between air pollutant exposures in either the donor or the recipient and PGD. Conclusions: Exposure to ambient air pollutants, at the levels observed in this study, may not be sufficiently harmful to prime the donor lung or the recipient to develop PGD particularly when considering the robust associations with other established PGD risk factors.

Comparing traditional and causal inference methodologies for evaluating impacts of long-term air pollution exposure on hospitalization with Alzheimer's disease and related dementias.

Alzheimer's disease and related dementias (ADRD) present a growing public health burden in the United States. One actionable risk factor for ADRD is air pollution: multiple studies have found associations between air pollution and exacerbation of ADRD. Our study builds on previous studies by applying modern statistical causal inference methodologies-generalized propensity score (GPS) weighting and matching-on a large, longitudinal dataset. We follow 50 million Medicare enrollees to investigate impacts of three air pollutants-fine particular matter (PM${}_{2.5}$), nitrogen dioxide (NO${}_2$), and summer ozone (O${}_3$)-on elderly patients' rate of first hospitalization with ADRD diagnosis. Similar to previous studies using traditional statistical models, our results found increased hospitalization risks due to increased PM${}_{2.5}$ and NO${}_2$ exposure, with less conclusive results for O${}_3$. In particular, our GPS weighting analysis finds IQR increases in PM${}_{2.5}$, NO${}_2$, or O${}_3$ exposure results in hazard ratios of 1.108 (95% CI: 1.097-1.119), 1.058 (1.049-1.067), or 1.045 (1.036-1.054), respectively. GPS matching results are similar for PM${}_{2.5}$ and NO${}_2$ with attenuated effects for O${}_3$. Our results strengthen arguments that long-term PM${}_{2.5}$ and NO${}_2$ exposure increases risk of hospitalization with ADRD diagnosis. Additionally, we highlight strengths and limitations of causal inference methodologies in observational studies with continuous treatments. Keywords: Alzheimer's disease and related dementias, air pollution, Medicare, causal inference, generalized propensity score.