Exposure to particulate air pollution increases total natural and cardiovascular mortality. However, it is less clear which types and sources of particles are the most harmful. We analyzed associations between long-term exposure to source-specific locally emitted particles and total natural and cardiovascular mortality in Swedish cohorts. Using high-resolution dispersion models of particles from different sources, and address registries, we assigned annual individual residential mean concentrations to population-based cohorts in Gothenburg, Stockholm and Umeå 1990-2011. Time and cause of death were assigned from registries. Associations between long-term mean lagged exposures and mortality were estimated using Cox regression models adjusted for possible confounders, and meta-analyzed. 7344 natural deaths, including 2755 cardiovascular deaths, occurred among the 68,679 participants. Exposure levels were moderate but generally above the WHO 2021 guidelines. We observed positive associations with natural mortality for the last five years of exposure to road traffic exhaust particles (HR 1.02, 95% CI 1.00-1.04, per IQR, and 1.10, 95% CI 1.00-1.22, per 1 µg/m3), and road wear particles (HR 1.02, 95% CI 1.00-1.04, per IQR, and HR 1.02, 95% CI 1.00-1.03, per 1 µg/m3), but not for particles from residential heating. Adjustment for road traffic noise, or particles from residential heating, did not substantially affect the results for traffic-related particles. For cardiovascular mortality, associations with particles from both sources were positive but not statistically significant. Natural mortality was associated with local emissions of traffic-related particles in a multi-cohort study at moderate exposure-levels, lending some support for further efforts to reduce traffic emissions.

Supplementary Table S1 shows Spearman correlations per (sub) cohort between NO2, PM2.5, BC, and O3 (warm season) among participants with full information in the main model

Supplementary Figure S1 shows box plots of exposures by individual (sub-) cohort study.

The mechanisms by which temperature exposure affects health outcomes remain unclear. In this study, we conducted three repeated measurements (2020-2022) by collecting self-sampled volumetric dry blood spots (DBSs) from 807 participants from the Swedish BAMSE cohort (mean age 25.9 years). By estimating individual-address level daily temperature using a high-resolution spatiotemporal model, we found that 58 (16%) of the 365 studied inflammation-related proteins were significantly associated with short-term exposure to ambient temperatures. The impact of temperature exposure was modified by sex, smoking, asthma, and concurrent exposure to air pollution. The temperature-associated proteins were linked to lung function, blood pressure, and HbA1c with validations in the UK Biobank. Furthermore, peak temperature exposure (both cold and heat) was associated with significantly increased proteomic age acceleration. Our findings suggest that ambient temperature exposure may cause adverse health effects through perturbating inflammation-related proteins.

Supplementary Figure S4 shows the natural cubic splines for air pollutants and breast cancer incidence

Supplementary Figure S3 shows the results from single- and multi-pollutant models and the cumulative risk index for breast cancer

BACKGROUND:Accumulating evidence links air pollution exposure to late-life cognitive deterioration. Whether air pollution alters brain structure remains poorly understood. Thus, we aimed to quantify the association between long-term exposure to particulate matter ≤2.5 µm and ≤10 µm (PM2.5 and PM10, respectively) and late-life brain structural changes. METHODS:In the Swedish National Study on Aging and Care in Kungsholmen, Stockholm, 555 participants free from dementia underwent brain magnetic resonance imaging (MRI) scans at baseline and after 6 years (cohorts <78 years) or after 3 and 6 years (cohorts aged ≥78 years). After the exclusion of participants with neurological conditions (including previous stroke) and suboptimal MRI quality, we had 457 participants with available repeated MRI examinations, where total brain tissue volume, ventricles, hippocampus, and white matter hyperintensities volumes were assessed. PM2.5 and PM10 have been assessed since 1990 using dispersion models at residential addresses. Brain volumes have been standardized using baseline mean and SD. Long-term exposure to PM2.5 and PM10 in relation to the baseline and longitudinal brain MRI volumes were tested through multiadjusted (age, sex, educational level, smoking, socioeconomic status, and neighborhood household mean income) linear regression models. RESULTS:At study entry, the mean (SD) age of the participants was 70 (SD, 8.9) years and 41% were males. Individuals who before baseline had been exposed to levels of PM2.5 or PM10 above the median (8.5 and 14.9 μg/m3, respectively) had smaller total brain tissue volume (β, -0.20 [95% CI, -0.33 to -0.06] and β, -0.14 [95% CI, -0.28 to -0.01], respectively) at baseline than those with lower PM2.5 and PM10 levels. Participants exposed during the follow-up to PM2.5>8.7 μg/m3 had on average an annual shrinkage of total brain tissue volume of 0.22 (95% CI, -0.43 to -0.01) and an annual increase of 0.25 (95% CI, 0.07-0.43) of the white matter hyperintensities as compared with participants exposed to PM2.5<8.7 μg/m3. No association was detected between PM10 and an annual rate of change in brain MRI volumes. CONCLUSIONS:Long-term exposure to comparatively low levels of PM2.5 was associated with a greater load of structural brain changes, encompassing brain atrophy and vascular pathology. These findings, in a dementia- and cerebrovascular disease-free sample, underscore the importance of addressing air pollution as a modifiable risk factor for late-life cognitive decline, and highlight the need for targeted interventions to prevent its detrimental effects on brain integrity.

ABSTRACT Background Emerging evidence suggests that air quality may impact muscle health. However, most studies are limited by cross‐sectional designs or short follow‐ups. We assessed the association of long‐term exposure to ambient air pollutants with changes in muscle mass and strength in older adults. Methods We included 3249 participants from the SNAC‐K longitudinal study (mean age 74.3 years; 35.8% males). Muscle strength (measured through handgrip and chair stand tests), muscle mass (derived from calf circumference) and physical performance (assessed through walking speed at a usual pace) were assessed over a 12‐year period. Probable sarcopenia was defined as reduced muscle strength as per the EWGSOP2 criteria. Residential exposure to PM2.5, PM10 and nitrogen oxide (NOx) was estimated for the 5 years preceding baseline. Cox regressions and linear mixed models examined the association of air pollutant exposure with, respectively, probable sarcopenia and longitudinal changes in muscle parameters. Results Over 12 years, the cumulative incidence of probable sarcopenia increased with higher exposure (above vs. below the median values) to NOx (36% vs. 28%), PM2.5 (35% vs. 28%) and PM10 (35% vs. 28%). The association between air pollutant levels and the risk of probable sarcopenia was nonlinear (pnonlinearity = 0.002 for NOx, 0.001 for PM2.5 and 0.003 for PM10), with an increased risk showing a plateau at very high levels. Higher exposures were associated with an increased risk of developing probable sarcopenia, by 25% for NOx and PM2.5 (HR 95% CI: 1.07–1.47 for both) to 33% (HR 95% CI: 1.14–1.56) for PM10. Elevated pollutant exposure was associated with significantly greater annual declines in lower‐limb strength (chair stand test: 0.40–0.48 s) and walking speed (0.004 m/s). Conclusions Long‐term exposure to moderate levels of ambient air pollutants may increase the risk of probable sarcopenia and accelerate declines in lower‐limb strength and physical performance in older adults.

Supplementary Figure S5 shows the results for air pollutants and breast cancer of models including confounders violating the assumption of proportional hazards as strata

Supplementary Figure S2 shows the results of the two-pollutant models of single and co-pollutants and breast cancer

Supplementary Table S3 shows air pollution exposure extrapolated back to the time of enrolment and time-varying exposure analysis using residential history between enrolment and end-of follow-up based on the Danish Eulerian Hemispheric Model (DEHM). Extrapolation was performed using the absolute difference and the ratio between the baseline and 2010 periods.

Supplementary Table S2 shows sensitivity analyses including additional confounders in the subset of the pooled cohort with the available information according to age

BACKGROUND:We investigated the association of peak expiratory flow (PEF) with dementia; cognitive impairment, no dementia (CIND); and transition from CIND to dementia, and possible underlying neuropathological mechanisms. METHODS:A population-based cohort of adults aged 60+ was followed over 15 years to detect dementia (Diagnostic and Statistical Manual of Mental Disorders, 4th edition criteria), CIND (assessed through a cognitive battery), and progression from CIND to dementia, in relation to baseline PEF observations. A subsample (n = 462) had 6-year follow-up data on brain magnetic resonance imaging markers of neurodegeneration and small vessel disease. RESULTS:In fully adjusted models, poor PEF performance (< 10th vs. ≥ 80th percentile) was associated with increased hazards for dementia (hazard ratio [HR] = 1.89; 95% confidence interval [CI] = 1.23-2.92) and CIND (HR = 1.55; 95% CI = 1.01-2.38) and CIND progression to dementia, although not statistically significantly (HR = 2.44; 95% CI = 0.78-6.88). People with poor PEF also experienced the fastest ventricular enlargement (β coefficient = 0.67 mL/year; 95% CI = 0.13-1.21) and had the highest likelihood of developing lacunes (odds ratio = 5.05; 95% CI = 1.01-25.23). DISCUSSION:Poor lung function contributes to cognitive deterioration possibly through accelerated brain atrophy and microvascular damage. HIGHLIGHTS:Poor lung function increased the risk of dementia and mild cognitive impairment (MCI). Poor lung function accelerated the progression from MCI to dementia. Poor lung function was linked to brain microvascular damage and global brain atrophy.

Rationale: The benefits of improved air quality on asthma remain understudied. Objectives: Our aim was to investigate associations of changes in ambient air pollution with incident asthma from school age until young adulthood in an area with mostly low air pollution levels. Methods: Participants in the BAMSE (Swedish abbreviation for Children, Allergy, Environment, Stockholm, Epidemiology) birth cohort from Stockholm without asthma before the 8-year follow-up were included (N = 2,371). We estimated the association of change in individual-level air pollutant exposure (particulate matter with an aerodynamic diameter ≤ 2.5 μm [PM2.5] and ≤ 10 μm [PM10], black carbon [BC], and nitrogen oxides [NOx]) from the first year of life to the 8-year follow-up with asthma incidence from the 8-year until the 24-year follow-up. Multipollutant trajectories were identified using the group-based multivariate trajectory model. We also used parametric G-computation to quantify the asthma incidence under different hypothetical interventions regarding air pollution levels. Results: Air pollution levels at residency decreased during the period, with median reductions of 5.6% for PM2.5, 3.1% for PM10, 5.9% for BC, and 26.8% for NOx. A total of 395 incident asthma cases were identified from the 8-year until the 24-year follow-up. The odds ratio for asthma was 0.89 (95% confidence interval [CI], 0.80-0.99) for each interquartile range reduction in PM2.5 (equal to 8.1% reduction). Associations appeared less clear for PM10, BC, and NOx. Five multipollutant trajectories were identified; the largest reduction trajectory displayed the lowest odds of asthma (odds ratio, 0.55; 95% CI, 0.31-0.98) compared with the lowest reduction trajectory. If the PM2.5 exposure had not declined up to the 8-year follow-up, the hypothetical asthma incidence was estimated to have been 10.9% higher (95% CI, 0.8-20.8%). Conclusions: A decrease in PM2.5 levels during childhood was associated with a lower risk of incident asthma from school age to young adulthood in an area with relatively low air pollution levels, suggesting broad respiratory health benefits from improved air quality.

Background Short-term studies of health effects from ambient air pollution usually rely on fixed site monitoring data or spatio-temporal models for exposure characterization, but the relation to personal exposure is often not known. Objective We aimed to explore this relation for black carbon (BC) in central Stockholm. Methods Families ( n = 46) with an infant, one parent working and one parent on parental leave, carried battery-operated BC instruments for 7 days. Routine BC monitoring data were obtained from rural background (RB) and urban background (UB) sites. Outdoor levels of BC at home and work were estimated in 24 h periods by dispersion modelling based on hourly real-time meteorological data, and statistical meteorological data representing annual mean conditions. Global radiation, air pressure, precipitation, temperature, and wind speed data were obtained from the UB station. All families lived in the city centre, within 4 km of the UB station. Results The average level of 24 h personal BC was 425 (s.d. 181) ng/m 3 for parents on leave, and 394 (s.d. 143) ng/m 3 for working parents. The corresponding fixed-site monitoring observations were 148 (s.d. 139) at RB and 317 (s.d. 149) ng/m 3 at UB. Modelled BC levels at home and at work were 493 (s.d. 228) and 331 (s.d. 173) ng/m 3 , respectively. UB, RB and air pressure explained only 21% of personal 24 h BC variability for parents on leave and 25% for working parents. Modelled home BC and observed air pressure explained 23% of personal BC, and adding modelled BC at work increased the explanation to 34% for the working parents. Impact Short-term studies of health effects from ambient air pollution usually rely on fixed site monitoring data or spatio-temporal models for exposure characterization, but the relation to actual personal exposure is often not known. In this study we showed that both routine monitoring and modelled data explained less than 35% of variability in personal black carbon exposure. Hence, short-term health effects studies based on fixed site monitoring or spatio-temporal modelling are likely to be underpowered and subject to bias.

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.

Despite the known link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality is understudied. Therefore, we investigated the association between long-term exposure to air pollution and CKD-related mortality in a large multicentre population-based European cohort. Cohort data were linked to local mortality registry data. CKD-death was defined as ICD10 codes N18-N19 or corresponding ICD9 codes. Mean annual exposure at participant's home address was determined with fine spatial resolution exposure models for nitrogen dioxide (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 μm (PM2.5) and several elemental constituents of PM2.5. Cox regression models were adjusted for age, sex, cohort, calendar year of recruitment, smoking status, marital status, employment status and neighbourhood mean income. Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 μg/m3, BC (1.26 (1.03-1.53) per 0.5 × 10- 5/m), NO2 (1.13 (0.93-1.38) per 10 μg/m3) and inverse for O3 (0.71 (0.54-0.93) per 10 μg/m3). Results were robust to further covariate adjustment. Exclusion of the largest sub-cohort contributing 226 cases, led to null associations. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality. In conclusion, our results suggest an association between air pollution from different sources and CKD-related mortality.

BACKGROUND AND AIMS:Transportation noise is an environmental exposure with mounting evidence of adverse health effects. Besides the increased risk of cardiovascular and metabolic diseases, recent studies suggest that long-term noise exposure might accelerate cognitive decline in older age. We examined the association between transportation noise and cognitive function in a cohort of older adults. METHODS:The present study is based on 2594 dementia-free participants aged 60 + years from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). Global cognition score and CIND (cognitive impairment, no dementia) were assessed with a comprehensive neuropsychological battery at baseline and up to 16 years. Residential transportation noise resulting from road traffic, railway, and aircraft were estimated at the most exposed façade and the time-weighted average exposure was assessed. Linear mixed-effect models were used to assess the effect of long-term traffic noise exposure on the rate of change in global cognition score. Hazard ratios (HRs) and 95 % confidence intervals (CIs) of CIND by transportation noise exposure were obtained with Cox proportional hazard models. RESULTS:Global cognition score decreased at an average rate of -0.041 (95 %CI -0.043, -0.039) per year. Aircraft noise was associated with a 0.007 (per 10 dB Lden; 95 %CI -0.012, -0.001) faster annual rate of decline. Global cognition score seems to be not affected by road traffic and railway noise. During the follow-up, 422 (21 %) participants developed CIND. A 10-dB Lden difference in exposure to aircraft and railway noise was associated with a 16 % (HR 1.16, 95 %CI 0.91, 1.49) and 26 % (HR 1.26, 95 %CI 1.01, 1.56) increased hazard of CIND in the multi-pollutant model, respectively. No association was found for road traffic (HR 1.00, 95 %CI 0.83, 1.21). CONCLUSIONS:Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.

It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO2, only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion.

Background Post COVID-19 conditions, also known as long COVID, are of public health concern, but little is known about their underlying risk factors. We aimed to investigate associations of air pollution exposure with long COVID among Swedish young adults. Methods We used data from the BAMSE (Children, Allergy, Environment, Stockholm, Epidemiology [in Swedish]) cohort. From October 2021 to February 2022 participants answered a web-questionnaire focusing on persistent symptoms following acute SARS-CoV-2 infection. Long COVID was defined as symptoms after confirmed infection with SARS-CoV-2 lasting for two months or longer. Ambient air pollution levels (particulate matter <2.5 mu m [PM2.5], <10 mu m [PM10], black carbon [BC] and nitrogen oxides [NOx]) at individual-level addresses were estimated using dispersion modelling.Findings A total of 753 participants with SARS-CoV-2 infection were included of whom 116 (15.4%) reported having long COVID. The most common symptoms were altered smell/taste (n = 80, 10.6%), dyspnea (n = 36, 4.8%) and fatigue (n = 34, 4.5%). Median annual PM2.5 exposure in 2019 (pre-pandemic) was 6.39 (interquartile range [IQR] 6.06-6.71) mu g/m3. Adjusted Odds Ratios (95% confidence intervals) of PM2.5 per IQR increase were 1.28 (1.02-1.60) for long COVID, 1.65 (1.09-2.50) for dyspnea symptoms and 1.29 (0.97-1.70) for altered smell/taste. Positive associations were found for the other air pollutants and remained consistent across sensitivity analyses. Associations tended to be stronger among participants with asthma, and those having had COVID during 2020 (versus 2021).Interpretation Ambient long-term PM2.5 exposure may affect the risk of long COVID in young adults, supporting efforts for continuously improving air quality. Copyright (c) 2023 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).