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Background: Air pollution is a large environmental health hazard whose exposure and health effects are unequally distributed among individuals. This is, at least in part, due to gene-environment interactions, but few studies exist. Thus, the current study aimed to explore genetic susceptibility to airway inflammation from short-term air pollution exposure through mechanisms of gene-environment interaction involving the SFTPA, GST and NOS genes., Methods: Five thousand seven hundred two adults were included. The outcome measure was fraction of exhaled nitric oxide (FeNO), at 50 and 270 ml/s. Exposures were ozone (O 3 ), particulate matter < 10 µm (PM 10 ), and nitrogen dioxide (NO 2 ) 3, 24, or 120-h prior to FeNO measurement. In the SFTPA, GST and NOS genes, 24 single nucleotide polymorphisms (SNPs) were analyzed for interaction effects. The data were analyzed using quantile regression in both single-and multipollutant models., Results: Significant interactions between SNPs and air pollution were found for six SNPs (p < 0.05): rs4253527 (SFTPA1) with O 3 and NO x , rs2266637 (GSTT1) with NO 2 , rs4795051 (NOS2) with PM 10 , NO 2 and NO x , rs4796017 (NOS2) with PM 10 , rs2248814 (NOS2) with PM 10 and rs7830 (NOS3) with NO 2 . The marginal effects on FeNO for three of these SNPs were significant (per increase of 10 µg/m 3 ):rs4253527 (SFTPA1) with O 3 (β: 0.155, 95%CI: 0.013-0.297), rs4795051 (NOS2) with PM 10 (β: 0.073, 95%CI: 0.00-0.147 (single pollutant), β: 0.081, 95%CI: 0.004-0.159 (multipollutant)) and NO 2 (β: -0.084, 95%CI: -0.147; -0.020 (3 h), β: -0.188, 95%CI: -0.359; -0.018 (120 h)) and rs4796017 (NOS2) with PM 10 (β: 0.396, 95%CI: 0.003-0.790)., Conclusions: Increased inflammatory response from air pollution exposure was observed among subjects with polymorphisms in SFTPA1, GSTT1, and NOS genes, where O 3 interacted with SFTPA1 and PM10 and NO 2 /NO x with the GSTT1 and NOS genes. This provides a basis for the further exploration of biological mechanisms as well as the identification of individuals susceptible to the effects of outdoor air pollution., (© 2023. The Author(s).)

Background: The developing lung is highly susceptible to environmental toxicants, with both short- and long-term exposure to ambient air pollutants linked to early childhood effects. This study assessed the short-term exposure effects of nitrogen dioxide (NO 2 ) and particulate matter (PM 10 ) on lung function in infants aged 6 weeks, 6, 12 and 24 months, the early developmental phase of child growth., Methods: Lung function was determined by multiple breath washout and tidal breathing measurement in non-sedated infants. Individual exposure to NO 2 and PM 10 was determined by hybrid land use regression and dispersion modelling, with two-week average estimates (preceding the test date). Linear mixed models were used to adjust for the repeated measures design and an age*exposure interaction was introduced to obtain effect estimates for each age group., Results: There were 165 infants that had lung function testing, with 82 of them having more than one test occasion. Exposure to PM 10 (μg/m 3 ) resulted in a decline in tidal volume at 6 weeks [-0.4 ml (-0.9; 0.0), p = 0.065], 6 months [-0.5 ml (-1.0; 0.0), p = 0.046] and 12 months [-0.3 ml (-0.7; 0.0), p = 0.045]. PM 10 was related to an increase in respiratory rate and minute ventilation, while a decline was observed for functional residual capacity for the same age groups, though not statistically significant for these outcomes. Such associations were however less evident for exposure to NO 2 , with inconsistent changes observed across measurement parameters and age groups., Conclusion: Our study suggests that PM 10 results in acute lung function impairments among infants from a low-socioeconomic setting, while the association with NO 2 is less convincing., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Evidence of the role of interactions between air pollution and pollen exposure in subjects with allergic asthma is limited and need further exploration to promote adequate preventive measures. The objective of this study was to assess effects of exposure to ambient air pollution and birch pollen on exacerbation of respiratory symptoms in subjects with asthma and allergy to birch., Methods: Thirty-seven subjects from two Swedish cities (Gothenburg and Umeå) with large variation in exposure to both birch-pollen and air pollutants, participated in the study. All subjects had confirmed allergy to birch and self-reported physician-diagnosed asthma. The subjects recorded respiratory symptoms such as rhinitis or eye irritation, dry cough, dyspnoea, the use of any asthma or allergy medication and peak respiratory flow (PEF), daily for five consecutive weeks during two separate pollen seasons and a control season without pollen. Nitrogen oxides (NO x ), ozone (O 3 ), particulate matter (PM 2.5 ), birch pollen counts, and meteorological data were obtained from an urban background monitoring stations in the study city centres. The data were analysed using linear mixed effects models., Results: During pollen seasons all symptoms and medication use were higher, and PEF was reduced in the subjects. In regression analysis, exposure to pollen at lags 0 to 2 days, and lags 0 to 6 days was associated with increased ORs of symptoms and decreased RRs for PEF. Pollen and air pollution interacted in some cases; during low pollen exposure, there were no associations between air pollution and symptoms, but during high pollen exposure, O 3 concentrations were associated with increased OR of rhinitis or eye irritation, and PM 2.5 concentrations were associated with increased ORs of rhinitis or eye irritation, dyspnea and increased use of allergy medication., Conclusions: Pollen and air pollutants interacted to increase the effect of air pollution on respiratory symptoms in allergic asthma. Implementing the results from this study, advisories for individuals with allergic asthma could be improved, minimizing the morbidities associated with the condition., (© 2022. The Author(s).)

Background: Air pollution is associated with cardiovascular morbidity and mortality, but its role in the development of congestive heart failure (CHF) and the role of different pollution sources in cardiovascular disease remain uncertain., Methods: Participants were enrolled in the Malmö Diet and Cancer cohort in 1991-1996 with information on lifestyle and clinical indicators of cardiovascular disease. The cohort participants were followed through registers until 2016. Annual total and local source-specific concentrations of particulate matter less than 10 μm and 2.5 μm (PM 10 and PM 2.5 ), black carbon (BC), and nitrogen oxides (NO x ) from traffic, residential heating, and industry were assigned to each participant's address throughout the study period. Cox proportional hazards models adjusted for possible confounders was used to estimate associations between air pollution 1-5 years prior to outcomes of incident CHF, fatal myocardial infarction (MI), major adverse coronary events (MACE), and ischemic stroke., Results: Air pollution exposure levels (mean annual exposures to PM 2.5 of 11 μg/m 3 and NO x of 26 μg/m 3 ) within the cohort were moderate in terms of environmental standards. After adjusting for confounders, we observed statistically significant associations between NO x and CHF (hazard ratio [HR] 1.11, 95% confidence interval [CI] 1.01-1.22) and NO x and fatal MI (HR 1.10, 95%CI 1.01-1.20) per interquartile range (IQR) of 9.6 μg/m 3 . In fully adjusted models, the estimates were similar, but the precision worse. In stratified analyses, the associations were stronger in males, ever-smokers, older participants, and those with baseline carotid artery plaques. Locally emitted and traffic-related air pollutants generally showed positive associations with CHF and fatal MI. There were no associations between air pollution and MACE or stroke., Discussion/conclusion: In an area with low to moderate air pollution exposure, we observed significant associations of long-term residential NO x with increased risk of incident CHF and fatal MI, but not with coronary events and stroke., (Copyright © 2022. Published by Elsevier Inc.)

Background: Ambient particulate matter is a leading risk factor for disease globally. Particulate matter 10 (PM 10 ) and particulate matter 2.5 (PM 2.5 ) are derived from different sources, including operating motor vehicles as well as from industrial activities. In this study we investigate the association between increased concentrations of PM and total daily visits to the psychiatric emergency unit (PEV). Further, the aim is to identify specific risk groups who are more susceptible to the effects of air pollution exposure by studying sex, age, ongoing psychiatric follow-up and diagnoses of depression/anxiety or substance use., Material and Methods: The sample was comprised of data from 2740 days to 81 548 PEVs at Sahlgrenska University Hospital in Gothenburg and daily mean concentrations of PM 10 and PM 2.5 . A time-stratified case-crossover design was used to analyse associations between air pollution and PEVs., Results: Mean number of daily PEVs were 35 and sex distribution was even. PM exposure was associated with total PEV at lag 0 (the same day), by RR 1.016 (95% confidence interval [CI] 1.004-1.028) and RR 1.020 (95%CI 1.003-1.038) per 10 μg/m 3 increase in PM 10 and PM 2.5 , respectively. In females, PEV were increased at lag 0 and lag 1, and in males at lag 1 and lag 2. In the age-stratified analysis, PEVs significantly increased following PM exposure amongst individuals aged 35-65 years by lag 0-2 and in individuals who had contact with outpatient care at lag 0 to lag 1. There were no associations between air pollution and PEVs for any specific diagnostic group evaluated (amongst depression, anxiety and substance use disorder)., Conclusions: The results indicate that acute exposure to PM 10 and PM 2.5 may trigger acute worsening in mental health in both males and females, especially among 35-65 year old individuals. However, in subgroups of the most common psychiatric diagnoses, we did not observe statistically significant associations with PM exposure., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM 2.5 ) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1-10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1-5- and 6-10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM 2.5 total, BC, and IHD. However, for PM 2.5 from local sources, a 20% risk increase per 1 µg/m 3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2-4-year PM 2.5 and BC, and also lags 8-9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1-5- and 6-10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke.

Exposure to air pollution is of great concern for public health although studies on the associations between exposure estimates and personal exposure are limited and somewhat inconsistent. The aim of this study was to quantify the associations between personal nitrogen oxides (NO x ), ozone (O 3 ) and particulate matter (PM 10 ) exposure levels and ambient levels, and the impact of climate and time spent outdoors in two cities in Sweden. Subjects (n = 65) from two Swedish cities participated in the study. The study protocol included personal exposure measurements at three occasions, or waves. Personal exposure measurements were performed for NO x and O 3 for 24 h and PM 10 for 24 h, and the participants kept an activity diary. Stationary monitoring stations provided hourly data of NO x , O 3 and PM, as well as data on air temperature and relative humidity. Data were analysed using mixed linear models with the subject-id as a random effect and stationary exposure and covariates as fixed effects. Personal exposure levels of NO x , O 3 and PM 10 were significantly associated with levels measured at air pollution monitoring stations. The associations persisted after adjusting for temperature, relative humidity, city and wave, but the modelled estimates were slightly attenuated from 2.4% (95% CI 1.8-2.9) to 2.0% (0.97-2.94%) for NO x , from 3.7% (95% CI 3.1-4.4) to 2.1% (95% CI 1.1-2.9%) for O 3 and from 2.6% (95% 0.9-4.2%) to 1.3% (95% CI - 1.5-4.0) for PM 10 . After adding covariates, the degree of explanation offered by the model (coefficient of determination, or R 2 ) did not change for NO x (0.64 to 0.63) but increased from 0.46 to 0.63 for O 3 , and from 0.38 to 0.43 for PM 10 . Personal exposure to NO x , O 3 and PM has moderate to good association with levels measured at urban background sites. The results indicate that stationary measurements are valid as measure of exposure in environmental health risk assessments, especially if they can be refined using activity diaries and meteorological data. Approximately 50-70% of the variation of the personal exposure was explained by the stationary measurement, implying occurrence of misclassification in studies using more crude exposure metrics, potentially leading to underestimates of the effects of exposure to ambient air pollution., (© 2021. The Author(s).)

Background: Air pollution is one of the leading causes of mortality and morbidity worldwide. Experimental studies, and a few epidemiological studies, suggest that air pollution may cause acute exacerbation of psychiatric disorders, and even increase the rate of suicide attempts, but epidemiological studies on air pollution in association with psychiatric disorders are still few. Our aim was to investigate associations between daily fluctuations in air pollution concentrations and the daily number of visits to a psychiatric emergency unit., Methods: Data from Sahlgrenska University Hospital, Gothenburg, Sweden, on the daily number of visits to the Psychiatric emergency unit were combined with daily data on monitored concentrations of respirable particulate matter(PM 10 ), ozone(O 3 ), nitrogen dioxides(NO 2 ) and temperature between 1st July 2012 and 31st December 2016. We used a case-crossover design to analyze data with conditional Poisson regression models allowing for over-dispersion. We stratified data on season., Results: Visits increased with increasing PM 10 levels during the warmer season (April to September) in both single-pollutant and two-pollutant models. For example, an increase of 3.6% (95% Confidence Interval, CI, 0.4-7.0%) was observed with a 10 μg/m3 increase in PM 10 adjusted for NO 2 . In the three-pollutant models (adjusting for NO 2 and O 3 simultaneously) the increase was 3.3% (95% CI, -0.2-6.9). There were no clear associations between the outcome and NO 2 , O 3 , or PM 10 during the colder season (October to March)., Conclusions: Ambient air particle concentrations were associated with the number of visits to the Psychiatric emergency unit in the warm season. The results were only borderline statistically significant in the fully adjusted (three-pollutant) models in this small study. The observation could be interpreted as indicative of air pollution as either exacerbating an underlying psychiatric disorder, or increasing mental distress, even in areas with comparatively low levels of air pollution. In combination with the severe impact of psychiatric disorders and mental distress on society and individuals, our results are a strong warrant for future research in this area.