Low Levels Of Air Pollution Research Articles

Do air pollution levels influence enforcement by regulators? Evidence from China

This paper examines the relationship between air pollution levels and regulators’ enforcement levels and observes that air pollution levels in firms’ locations reduce enforcement from regulators. Moreover, regulators are more likely to suffer from type II errors when air pollution levels in firms’ locations are higher, verifying the effect of regulators’ unwillingness to travel due to air pollution. The cross-sectional analysis suggests that enforcement from regulatory authorities in areas with lower air pollution levels than in firms’ locations, positioned at great distances from firms’ locations, and with greater workloads is less strict when air pollution levels in firms’ locations are higher. We further test whether air pollution levels reduce the efficiency of regulators and find that firms with lower earnings quality and weaker corporate governance are less likely to be subjected to enforcement by regulators when air pollution levels in the firms’ locations are higher.

Perceived air pollution reduces consumers' self‐disclosure: The role of tense arousal

AbstractConsumers are often reluctant to disclose their personal information to retailers. How to promote consumers' self‐disclosure has been a focal point of interest for marketers and researchers. Using a total of eight multimethod studies (N = 5281) which composite a study with secondary data, a field study, a natural experiment, and five lab experiments, we show that a perception of high (vs. low) levels of air pollution decreases consumers' self‐disclosure willingness and behavior. This effect is mediated by tense arousal and moderated by (1) whether consumers are aware of the impact of perceived air pollution levels on tense arousal and (2) under which environment consumers disclose their personal information (an environment playing low‐paced soothing background music vs. a one playing high‐paced rock background music). We also rule out regulatory focus and mood valence as alternative process variables. Our findings extend past literature on perceived air pollution, tense arousal, and self‐disclosure. The results also suggest marketers, retailers, and service providers mitigate the negative impact of air pollution perception on consumers' self‐disclosure by playing low‐paced soothing background music in retailing contexts.

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

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

Association of household solid fuel use and long-term exposure to ambient air pollution with estimated 10-year high cardiovascular disease risk among postmenopausal women

This study aimed to explore the separate and joint effects of long-term ambient air pollution and household air pollution exposure on 10-year high cardiovascular disease (CVD) risk among postmenopausal women. A total of 4679 postmenopausal women from the China Health and Retirement Longitudinal Study (CHARLS) were included in this study. Information of fuel type was collected by standard questionnaires and use of solid fuel was considered as a proxy for household air pollution. Data of ambient air pollutants (PM1, PM2.5, PM10, SO2, NO2, CO, O3) were obtained from the ChinaHighAirPollutants (CHAP) datasets. Logistic regression models were performed to assess the separate and joint effects of long-term exposure to ambient air pollution and use of solid fuel on 10-year high CVD risk. We found use of solid fuel and its duration and ambient air pollutants (PM1, PM2.5, PM10, SO2, NO2) were all positively associated with 10-year high CVD risk among postmenopausal women (P < 0.05). Compared to those used clean fuel and exposed to low ambient air pollution levels, odds ratios (ORs) and 95% confidence intervals (CIs) for participants using solid fuels and exposed to high ambient air pollution levels (PM1, PM2.5, PM10, SO2, NO2, CO, O3) were 1.66 (1.35, 2.05), 1.66 (1.35, 2.04), 1.49 (1.22, 1.83), 1.28 (1.05, 1.57), 1.67 (1.34, 2.07), 1.28 (1.04, 1.57), 1.46 (1.18, 1.80), respectively. Moreover, significant additive interactions of solid fuel use with PM1 and PM2.5 on 10-year high CVD risk were observed, with approximately 18% and 23% of 10-year high risk of CVD attributable to the interaction. Overall, indoor and outdoor air pollution had separate and joint effects on 10-year high CVD risk among postmenopausal women. Therefore, simultaneously improving indoor and outdoor air quality are of great importance and could have a joint impact on prevention of CVD and improved health among postmenopausal women.

Sex differential effects on the joint contribution of air pollution and biological aging on cognitive performance in individuals at risk of Alzheimer’s disease

AbstractBackgroundAir pollution is associated with cognitive performance, risk for AD and may accelerate biological aging. Biological aging due to telomere shortening has been associated with cognitive impairment. However, few studies have looked at the link between air pollution, telomere length, and cognitive performance among sexes. In this study, we investigated the joint effect of sex, air pollution, and leukocyte telomere length (LTL), on cognitive performance in cognitively unimpaired (CU) individuals at risk of AD.MethodThe study included 1,472 middle‐aged CU adults with increased risk of AD from the ALFA study [Table 1]. Residential exposure to air pollutants including nitrogen dioxide (NO2) and particulate matter (PM2.5, PM10) was estimated by land use regression models. LTL was determined by qPCR from DNA extracted from peripheral blood leukocytes. LTL was residualized against chronological age and sex (rLTL). A cognitive battery was administered to assess verbal memory, psychomotor speed, visual processing and executive function. Further, episodic memory (EM), executive function and Preclinical Alzheimer Cognitive Composite (PACC) composites were calculated by averaging normalized raw scores of the subtests. Models were corrected by chronological age, years of education and APOE‐ε4 status. Sex‐specific effects were investigated by adjusting interaction models.ResultThere was no overall effect of neither rLTL nor air pollution on cognitive performance, but crossover interactions with sex were found. Exposure to higher levels of NO2 and PM2.5 were associated with worse EM only in men [Figure 1]. Three‐way interaction models revealed longer rLTL and lower levels of air pollution were associated with better performance on PACC (for PM2.5, PM10 and NO2) and EM (for PM10 and NO2) among men. In women, these associations were only observed at higher exposure levels of air pollution [Figure 2].ConclusionThe results show that lower levels of air pollution allow for the protective effect of rLTL on cognitive performance only in men for whom air pollution had a stronger negative impact. In women, the results show different mechanisms through which air pollution and rLTL affect cognitive performance. Further analyses will be conducted to gain insight into the observed effects.

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

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

Associations of low levels of air pollution with cardiometabolic outcomes and the role of diet quality in individuals with obesity

BackgroundExposure to air pollution is associated with adverse cardiometabolic health effects and increased mortality, even at low concentrations. Some of the biological mechanisms through which air pollution can affect cardiometabolic health overlap with health outcomes associated with diet quality and changes in diet. ObjectiveThe objective of this study is to investigate associations of air pollutants at average concentrations below the World Health Organization, 2021 air quality guidelines with cardiometabolic outcomes. Furthermore, potential interaction between air pollutants and diet quality will be assessed. Methods82 individuals with obesity participated in a combined weight loss and weight loss maintenance study for a total of 33 weeks. A secondary analysis was conducted incorporating air pollution measurements. Data were analysed with linear mixed-effects models. ResultsA total of 17 significant associations were observed for single pollutants with 10 cardiometabolic outcomes, predominantly related to blood lipids, hormones, and glucose regulation. Diet quality, as measured by the Baltic Sea Diet score, did not appear to mediate the association of air pollution with cardiometabolic outcomes, however, diet quality was observed to significantly modify the association of PM2.5 with total cholesterol, and the associations of NO and O3 with ghrelin. DiscussionThese findings suggest that exposure to ambient air pollutants, especially particulate matter, at levels below World Health Organization, 2021 air quality guidelines, were associated with changes in cardiometabolic risk factors. Diet may be a personal-level approach for individuals to modify the impact of exposure to air pollution on cardiometabolic health.

Abstract 14863: Omega-3 Fatty Acids Intake and Oxylipins Production in Response to Short-Term Ambient Air Pollution Exposure in Healthy Adults

Rationale: Exposure to air pollution is associated with adverse health effects through systemic inflammation and oxidative stress. One mechanism of beneficial effects of omega-3 polyunsaturated fatty acids (n-3 FA) is mediated via their inflammation resolution process by generating bioactive lipid mediators known as oxylipins. Objective: This study examined the association between n-3 FA-derived bioactive oxylipins and short-term exposure to ambient air pollution in healthy adults. Methods: Fifteen healthy adults were enrolled into either high or low n-3 groups based on n-3 FA intake and the participants underwent 4-5 blood collections for lipidomic profile of 55 oxylipins. Associations between ambient ozone, nitrogen dioxide (NO 2 ), and fine particulate matter (PM 2.5 ) levels and plasma oxylipins were assessed using mixed-effects models stratified by fatty acids levels. Results: Average concentrations of ozone (40.8±11.1 ppb), NO 2 (5.3±3.8 ppb), and PM 2.5 (10.2±4.1 μg/m 3 ) were below national ambient air quality standards during the study period. Compared to the low n-3 group exposed to ozone and PM 2.5 , high n-3 group had significant reduction in arachidonic acids (AA) derived pro-inflammatory oxylipins produced by lipoxygenase (LOX). For instance, 12 HETE was negatively associated with ozone levels [for an IQR increase in ozone, -58.1% (95% CI:-96.8, -19.4) vs. 14.5% (95% CI:-33, 62)] and PM 2.5 concentrations [for an IQR increase in PM 2.5 , -29.6% (95% CI:-49.1, -10.1) vs. 28.5% (95% CI:-3.8, 60.9)] at lag4 in the high n-3 group while the association was null in the low n-3 group. In contrast, high n-3 group exposed to ozone and PM 2.5 had significant increases in EPA and DHA derived pro-resolving oxylipins produced by LOX and cytochrome p450 (CYP) and soluble epoxide hydrolase (sEH) compared to the low n-3 group. Conclusions: We observed negative associations between short-term ambient air pollutants and pro-inflammatory oxylipins in the high n-3 groups, while the associations between short-term ambient air pollutants and pro-resolving oxylipins were positive in the high n-3 groups, suggesting that n-3 derived lipid mediators may mediate the inflammation resolution process in response to low levels of ambient air pollution in healthy adults.

Short-Term Ambient Air Pollution Exposure and Risk of Out-of-Hospital Cardiac Arrest in Sweden: A Nationwide Case-Crossover Study.

Background Air pollution is one of the main risk factors for cardiovascular disease globally, but its association with out-of-hospital cardiac arrest at low air pollution levels is unclear. This nationwide study in Sweden aims to investigate if air pollution is associated with a higher risk of out-of-hospital cardiac arrest in an area with relatively low air pollution levels. Methods and Results This study was a nationwide time-stratified case-crossover study investigating the association between short-term air pollution exposures and out-of-hospital cardiac arrest using data from the SRCR (Swedish Registry for Cardiopulmonary Resuscitation) between 2009 and 2019. Daily air pollution levels were estimated in 1×1-km grids for all of Sweden using a satellite-based machine learning model. The association between daily air pollutant levels and out-of-hospital cardiac arrest was quantified using conditional logistic regression adjusted for daily air temperature. Particulate matter <2.5 μm exposure was associated with a higher risk of out-of-hospital cardiac arrest among a total of 29 604 cases. In a multipollutant model, the association was most pronounced for intermediate daily lags, with an increased relative risk of 6.2% (95% CI, 1.0-11.8) per 10 μg/m3 increase of particulate matter <2.5 μm 4 days before the event. A similar pattern of association was observed for particulate matter <10 μm. No clear association was observed for O3 and NO2. Conclusions Short-term exposure to air pollution was associated with higher risk of out-of-hospital cardiac arrest. The findings add to the evidence of an adverse effect of particulate matter on out-of-hospital cardiac arrest, even at very low levels below current regulatory standards.

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

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

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

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

Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Air Pollution: What’s Next?

Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Air Pollution: What’s Next?

Effect of short-term exposure to air pollution on daily cardio- and cerebrovascular hospitalisations in areas with a low level of air pollution.

Exposure to air pollution is associated with increased cardio- and cerebrovascular diseases. However, the evidence regarding the short-term effect of air pollution on cardio- and cerebrovascular hospitalisations in areas with relatively low air pollution levels is limited. This study aims to examine the effect of short-term exposure to different air pollutants on hospital admissions due to cardio- and cerebrovascular diseases in rural and regional Australia with low air pollution. The study was conducted in five local Government areas of Hunter New England Local Health District (HNE-LHD). Hospitalisation data from January 2018 to February 2020 (820 days) were accessed from the HNE-LHD admitted patients' dataset. Poisson regression model was used to examine the association between the exposure (air pollutants) and outcome variables (hospitalisation due to cardio- and cerebrovascular disease). The concentrations of gaseous air pollutants, Sulphur Dioxide (SO2), Nitrogen Dioxide (NO2), Ozone (O3), Carbon Monoxide (CO), and Ammonia (NH3) were below national benchmark concentrations for every day of the study period. In single pollutant models, SO2 and NO2 significantly increased the daily number of cardio- and cerebrovascular hospitalisations. The highest cumulative effect for SO2 was observed across lag 0-3 days (Incidence Rate Ratio, IRR: 1.77; 95% Confidence Interval, CI: 1.18-2.65; p-value: 0.01), and for NO2, it was across lag 0-2 days (IRR: 1.13; 95% CI: 1.02-1.25; p-value: 0.02). In contrast, higher O3 was associated with decreased cardio- and cerebrovascular hospitalisations, with the largest effect observed at lag 0 (IRR: 0.94; 95% CI: 0.89-0.98; p-value: 0.02). In the multi-pollutant model, the effect of NO2 remained significant at lag 0 and corresponded to a 21% increase in cardio- and cerebrovascular hospitalisation (95% CI: 1-44%; p-value = 0.04). Thus, the study revealed that gaseous air pollutants, specifically NO2, were positively related to increased cardio- and cerebrovascular hospitalisations, even at concentrations below the national standards.

Multiphase Kinetic Modeling of Air Pollutant Effects on Protein Modification and Nitrotyrosine Formation in Epithelial Lining Fluid.

Exposure to ambient air pollution is a major risk factor for human health. Inhalation of air pollutants can enhance the formation of reactive species in the epithelial lining fluid (ELF) of the respiratory tract and can lead to oxidative stress and oxidative damage. Here, we investigate the chemical modification of proteins by reactive species from air pollution and endogenous biological sources using an extended version of the multiphase chemical kinetic model KM-SUB-ELF 2.0 with a detailed mechanism of protein modification. Fine particulate matter (PM2.5) and nitrogen dioxide (•NO2) act synergistically and increase the formation of nitrotyrosine (Ntyr), a common biomarker of oxidative stress. Ozone (O3) is found to be a burden on the antioxidant defense system but without substantial influence on the Ntyr concentration. In simulations with low levels of air pollution, the Ntyr concentration in the ELF is consistent with the range of literature values for bronchoalveolar lavage fluid from healthy individuals. With high levels of air pollution, however, we obtain strongly elevated Ntyr concentrations. Our model analysis shows how chemical reactions of air pollutants can modify proteins and thus their functionality in the human body, elucidating a molecular pathway that may explain air pollutant effects on human health.

Impact of meteorological parameters and air pollutants on airborne concentration of Betula pollen and Bet v 1 allergen

The intensity of birch pollen season is expressed by seasonal pollen integral (SPIn, the sum of the mean daily pollen concentration during the birch pollination period) and the amount of Bet v 1 allergen released per birch pollen grain expressed by pollen allergen potency (PAP). Betula pollen and Bet v 1 allergen were simultaneously measured in the air of Bratislava from 2019 to 2022 by using two Burkard traps (Hirst-type and cyclone) in order to evaluate the causes of the seasonal variation in the SPIn and PAP levels. The highest SPIn (19,975 pollen/m3) was observed in 2022 and the lowest one (1484 pollen/m3) in 2021. The average daily PAP level (4.0 pg Bet v 1/pollen) was highest in 2019 and lowest (2.5 pg Bet v 1/pollen) in 2020. We found that seasonal variation in SPIn was associated mainly with the changes in environmental conditions during the pre-season period, whereas the year-to-year variation in PAP levels was attributed to environmental conditions during both pre- and in-season periods. Our results indicate that rainy weather in June 2020 and cold overcast weather in January‒February 2021 resulted in low SPIn in 2021. On the other hand, dry weather in June 2021 and warm weather in January‒February 2022 resulted in high SPIn in 2022. The low average daily PAP level in 2020 was associated with (1) low levels of gaseous air pollutants in March, when the ripening of pollen takes place; (2) an earlier start of the birch main pollen season (MPS); and (3) dry weather during the MPS. On the other hand, high PAP level in 2019 was associated with higher levels of air pollutants in March and during the MPS.

Association of air pollution and green space with all-cause general practitioner and emergency room visits: A cross-sectional study of young people and adults living in Belgium

BackgroundResiding in areas with lower levels of air pollution and higher green space is beneficial to physical and mental health. We investigated associations of PM2.5, tree cover and grass cover with in-hours and out-of-hours GP visits and ER visits, for young people and adults. We estimated potential cost savings of GP visits attributable to high PM2.5. MethodsWe linked individual-level health insurance claims data of 315,123 young people (10–24 years) and 885,988 adults (25–64 years) with census tract-level PM2.5, tree cover and grass cover. Deploying negative binomial generalized linear mixed models, we estimated associations between quartile exposures and the three outcome measures. ResultsFor in-hours and out-of-hours GP visits, among young people as well as adults, statistically significant pairwise differences between quartiles suggested increasing beneficial effects with lower PM2.5. The same outcomes were statistically significantly less frequent in quartiles with highest tree cover (>30.00%) compared to quartiles with lower tree cover, but otherwise pairwise differences were not statistically significant. These associations largely persisted in rural and urban areas. Among adults living in urban areas lower grass cover was associated with increased in-hours GP visits and ER visits. Assuming causality, reducing PM2.5 levels to the lowest quartile (4.91–7.49 μg/m³), among adults, 195,964 in-hours and 74,042 out-of-hours GP visits could be avoided annually. Among young people, 27,457 in-hours and 22,423 out-of-hours GP visits could be avoided annually. Nationally, this amounts to an annual potential cost saving of €43 million (€5.7 million in out-of-pocket payments and €37.2 million in compulsory health insurance). ConclusionHigher ambient PM2.5 and lower tree cover show associations with higher non-urgent and urgent medical care utilization. These findings confirm the importance of reducing air pollution and fostering green zones, and that such policies may contribute positively to economic growth.

Prevalence of small airway dysfunction in the Swiss PneumoLaus Cohort.

Recent evidence identified exposure to particulate matter of size ≤2.5 µm (PM2.5) as a risk factor for high prevalence of small airway dysfunction (SAD). We assessed the prevalence of SAD in a European region with low air pollution levels. SAD was defined as a maximum mid-expiratory flow (MMEF) <65% of predicted value (PV) or MMEF <lower limit of normal (LLN) measured by spirometry in the Swiss PneumoLaus cohort. We performed bivariate and multivariable analysis with MMEF criteria, age, sex, body mass index, respiratory symptoms and smoking status. Mean PM2.5 values were obtained from a Swiss national database. Among 3351 participants (97.6% Caucasian, 55.7% female sex, mean age 62.7 years), we observed MMEF <65% PV in 425 (12.7%) and MMEF <LLN in 167 (5.0%) individuals. None of the participants had both MMEF <LLN and ≥65% PV. MMEF <65% PV and MMEF <LLN were significantly associated with age, smoking status, cough, sputum and dyspnoea, whereas a positive association with MMEF <65% PV was observed for individuals aged >65 years only. In an area where ambient PM2.5 concentration was <15 µg·m-3 during the observation period (2010 and 2020), ≥72% of participants with SAD were ever-smokers. The observed low prevalence of SAD of 5.0-12.7% depending on criteria employed may be related to lower PM2.5 exposure. Smoking was the main factor associated with SAD in an area with low PM2.5 exposure. Employing a MMEF threshold <65% PV carries a risk of SAD overdiagnosis in elderly individuals.

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

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

Low-level ambient sulfur dioxide exposure and genetic susceptibility associated with incidence of idiopathic pulmonary fibrosis: A national prospective cohort study

BackgroundThe association between long-term air pollution exposure and the development of idiopathic pulmonary fibrosis (IPF) has been established, but the evidence regarding the effect of low levels of air pollution, especially ambient sulfur dioxide (SO2), is limited. Besides, the combined effect and interaction between genetic susceptibility and ambient SO2 on IPF remain uncertain. MethodsThis study retrieved data from 402,042 participants who were free of IPF at baseline in the UK Biobank. The annual mean concentration of ambient SO2 was estimated for each participant based on their residential addresses using a bilinear interpolation method. Cox proportional hazard models were used to examine the relationship between ambient SO2 and incident IPF. We further generated a polygenic risk score (PRS) for IPF and estimated the combined effects of genetic susceptibility and ambient SO2 on incident IPF. ResultsAfter a median follow-up of 11.78 years, 2562 cases of IPF were identified. The results indicated that each 1 μg/m3 increase in ambient SO2 was associated with a hazard ratio (HR) (95% confidence interval [CI]) of 1.67 (1.58, 1.76) for incident IPF. The study found statistically significant synergistic additive interaction between genetic susceptibility and ambient SO2. Individuals with high genetic risk and high ambient SO2 exposure had a higher risk of developing IPF (HR = 7.48, 95% CI:5.66, 9.90). ConclusionThe study suggests that long-term exposure to ambient SO2, even at concentrations lower than current air quality guidelines set by the Word Health Organization and European Union, may be an important risk factor for IPF. This risk is more pronounced among people with a high genetic risk. Therefore, these findings emphasize the need to consider the potential health effects of SO2 exposure and the necessity for stricter air quality standards.

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

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