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Objectives: Socioeconomic status (SES) is in many cases related to air pollution exposure, but less is known about its effects on susceptibility to air pollution. The main aim of this study was to analyse the impact of SES on health effects associated with exposure to fine particles (PM_2.5).

Methods: Firstly, a systematic literature review of studies analysing the impacts of SES on health effects related to air pollution exposure was carried out. Secondly, a meta-analysis was performed by analysing studies on long-term mortality associated with exposure to PM_2.5 divided into different SES groups.

Results: The meta-analysis showed that the relative risk (RR) for all-cause mortality associated with PM_2.5 did not depend on individual education or income. It also revealed that adjustment for individual lifestyle factors (such as smoking, alcohol intake, physical activity, eating behaviours, and body mass index), in addition to adjustment for SES, did not significantly change the RR.

Conclusion: The association between all-cause mortality and PM_2.5 did not depend on education or individual income. Due to the high heterogeneity observed, further studies are required to draw firm conclusions.

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population’s average exposure to annual mean total PM10 and PM2.5 lag 1–5 years was 9.50 µg/m3 and 5.61 µg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0–82%]) and PM2.5-Exhaust (33% [95% CI − 2 to 79%]) in the second exposure tertile for lag 1–5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure–response relationships were evident.

Background: Many studies reported associations between long-term exposure to environmental factors and mortality; however, little is known on the combined effects of these factors and health. We aimed to evaluate the association between external exposome and all-cause mortality in large administrative and traditional adult cohorts in Europe.

Methods: Data from six administrative cohorts (Catalonia, Greece, Rome, Sweden, Switzerland and the Netherlands, totaling 27,913,545 subjects) and three traditional adult cohorts (CEANS-Sweden, EPIC-NL-the Netherlands, KORA–Germany, totaling 57,653 participants) were included. Multiple exposures were assigned at the residential addresses, and were divided into three a priori defined domains: (1) air pollution [fine particulate matter (PM2.5), nitrogen dioxide (NO₂), black carbon (BC) and warm-season Ozone (warm-O3)]; (2) land/built environment (Normalized Difference Vegetation Index—NDVI, impervious surfaces, and distance to water); (3) air temperature (cold- and warm-season mean and standard deviation). Each domain was synthesized through Principal Component Analysis (PCA), with the aim of explaining at least 80% of its variability. Cox proportional-hazards regression models were applied and the total risk of the external exposome was estimated through the Cumulative Risk Index (CRI). The estimates were adjusted for individual- and area-level covariates.

Results: More than 205 million person-years at risk and more than 3.2 million deaths were analyzed. In single-component models, IQR increases of the first principal component of the air pollution domain were associated with higher mortality [HRs ranging from 1.011 (95% CI: 1.005–1.018) for the Rome cohort to 1.076 (1.071–1.081) for the Swedish cohort]. In contrast, lower levels of the first principal component of the land/built environment domain, pointing to reduced vegetation and higher percentage of impervious surfaces, were associated with higher risks. Finally, the CRI of external exposome increased mortality for almost all cohorts. The associations found in the traditional adult cohorts were generally consistent with the results from the administrative ones, albeit without reaching statistical significance.

Discussion: Various components of the external exposome, analyzed individually or in combination, were associated with increased mortality across European cohorts. This sets the stage for future research on the connections between various exposure patterns and human health, aiding in the planning of healthier cities.

Air pollution's short-term effects on a wide range of health outcomes have been studied extensively, primarily focused on vulnerable groups (e.g., children and the elderly). However, the air pollution effects on the adult working population through sick leave have received little attention. This study aims to 1) estimate the associations between particulate matter ≤2.5 μm³ (PM_2.5) and sick leave episodes and 2) calculate the attributable number of sick leave days and the consequential productivity loss in the City of Stockholm, Sweden. Individual level daily sick leave data was obtained from Statistics Sweden for the years 2011–2019. Daily average concentrations of PM_2.5 were obtained from the main urban background monitoring station in Stockholm. A case-crossover study design was applied to estimate the association between short-term PM_2.5 and onset of sick leave episodes. Conditional logistic regression was used to estimate the relative increase in odds of onset per 10 μg/m³ of PM_2.5, adjusting for temperature, season, and pollen. A human capital method was applied to estimate the PM2.5 attributable productivity loss. In total, 1.5 million (M) individual sick leave occurrences were studied. The measured daily mean PM_2.5 concentration was 4.2 μg/m³ (IQR 3.7 μg/m³). The odds of a sick leave episode was estimated to increase by 8.5% (95% CI: 7.8–9.3) per 10 μg/m³ average exposure 2–4 days before. Sub-group analysis showed that private sector and individuals 15–24 years old had a lower increase in odds of sick leave episodes in relation to PM_2.5 exposure. In Stockholm, 4% of the sick leave episodes were attributable to PM_2.5 exposure, corresponding to €17 M per year in productivity loss. Our study suggests a positive association between PM_2.5 and sick leave episodes in a low exposure area.

Aims: Patient characteristics and treatment setting are potential predictors of premature dropout from lifestyle interventions, but their relative importance is unknown.

Methods: From the quality registry of the unit for behavioral medicine, Umeå University hospital, we identified 2589 patients who had been enrolled in a multimodal lifestyle intervention for cardiometabolic risk reduction between 2006 and 2015. Baseline characteristics predicting dropout before 1-year follow-up were selected by a stepwise logistic regression algorithm.

Results: Better physical health and older age predicted full participation, with odds ratios for premature dropout (ORs) of.44 (95% confidence interval (CI).31-.63), and.47 (95% CI.34-.65) in the highest compared to the lowest quartile, respectively. Odds of premature dropout were also lower among female participants,.71 (95% CI.58-.89). Premature dropout was predicted by higher BMI, snuffing tobacco, and smoking, with ORs of 1.53 (95% CI 1.13-2.08) in the highest compared to the lowest quartile of BMI, 1.37 (95% CI 1.03-1.81) comparing snuff user with non-users and 2.53 (95% CI 1.79-3.61) comparing smokers with non-smokers. Odds ratio for premature dropout among inpatients compared with outpatients was.84 (95% CI.68-1.04).

Conclusion: Higher risk at baseline predicts premature dropout.

Background and aims: Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis.

Methods: We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM_2.5), <10 μm (PM₁₀), and nitrogen oxides (NO_x) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders.

Results: Median 10-year average PM_2.5 exposure was 6.2 μg/m³ (range 3.5–13.4 μg/m³). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM_2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m³). Associations with significant stenoses were inconsistent.

Conclusions: In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM_2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.

Background: Road-traffic noise may influence the development of cardiovascular events such as stroke and myocardial infarction, but etiological mechanisms remain unclear. This study aimed to assess the relationship between long-term road-traffic noise exposure and coronary atherosclerosis in Sweden.

Methods: In the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort, including 30,154 subjects aged 50-65 years, recruited between 2013 and 2018, coronary atherosclerosis was measured based on computer tomography (CT) scans as coronary artery calcium score, segment involvement score (SIS), and non-calcified plaques (NCP) at enrollment. Based on modified Nordic model, road-traffic noise exposure was modeled for 2000, 2013, and 2018 with interpolation for intermediate years. We investigated the association between time-weighted long-term exposure to road-traffic noise (Lden) and the prevalence of atherosclerosis using ordinal logistic regression models adjusting for potential socioeconomic, behavioral, and environmental confounders, including air pollution.

Results: No clear associations were found between road-traffic noise and coronary atherosclerosis. The odds ratio for coronary artery calcium score was 1.00 (95% confidence interval [CI] = 0.96, 1.04), SIS 0.99 (0.96, 1.03), and NCP 0.98 (0.90, 1.03) per interquartile range (9.4 dB Lden) for road-traffic noise exposure during 10 years before enrollment. No consistent associations were observed in site-specific analyses or using shorter exposure periods. Furthermore, exposure-response analyses revealed no clear trends, and there were no strong interactions between road-traffic noise and cardiovascular risk factors in relation to the atherosclerosis markers.

Conclusions: Long-term exposure to road-traffic noise was not linked to coronary atherosclerosis or calcification in relatively healthy, middle-aged populations in Sweden.

BACKGROUND: Incident cases of stroke, myocardial infarction, and preterm birth have established exposure-response functions associated with air pollution. However, there are no studies reporting detailed costs per case for these health outcomes that are adapted to the cost-benefit tools that guide the regulation of air pollution.

OBJECTIVES: The primary objective was to establish non-fatal per-case monetary estimates for stroke, myocardial infarction, and preterm birth attributable to air pollution in Sweden, and the secondary objective was to ease the economic evaluation process of air pollution morbidity effects and their inclusion in cost-benefit assessments.

METHODS: Based on recommendations from the literature, the case-cost analysis considered direct and indirect medical costs, as well as production losses and informal costs relevant for the calculation of the net present value. A literature search was conducted to estimate the costs of each category for each incident case in Sweden. Informal costs were estimated using the quality-adjusted life-years approach and the corresponding willingness-to-pay in the Swedish population. The total average per-case cost was estimated based on specific health outcome durations and severity and was discounted by 3.5% per year. Sensitivity analysis included varying discount rates, severity of health outcome, and the range of societal willingness to pay for quality-adjusted life years.

RESULTS: The average net present value cost estimate was €2016 460k (185k-1M) for non-fatal stroke, €2016 24k (16k-38k) for myocardial infarction, and €2016 34k (19k-57k) for late preterm birth. The main drivers of the per-case total cost estimates were health outcome severity and societal willingness to pay for risk reduction. Varying the discount rate had the largest effect on preterm birth, with costs changing by ±30% for the discount rates analysed.

RECOMMENDATION: Because stroke, myocardial infarction, and preterm birth have established exposure-response functions linking these to air pollution, cost-benefit analyses should include the costs for these health outcomes in order to adequately guide future air pollution and climate change policies.

Introduction: The behaviour change technique taxonomy version 1 was developed to identify the smallest active ingredients of a lifestyle intervention, that is, behaviour change techniques (BCTs) based on a written description. By participation and direct observation of an intervention, we intend to not only identify BCTs but also assess exposure time for each BCT. Adding the dimension of exposure time should enable us to make quantitative comparisons between the different BCTs employed. We intend to demonstrate this by studying the hypotheses that exposure to information-related BCTs is similar for all targeted lifestyle modalities but decreases in the course of the intervention.

Methods: During 5-week intensive multimodal lifestyle interventions at a Swedish clinic for lifestyle medicine, we identified BCTs according to behaviour change technique taxonomy version 1 and noted exposure times to BCTs in all mandatory parts of the behaviour change intervention.

Results: Two hundred thirty-one independent intervention components were evaluated. BCTs 8.1 Behavioural practice/rehearsal (126 h), 4.1 Instruction on how to perform the behaviour (98 h) and 6.1 Demonstration of the behaviour (65 h) were the most common in terms of exposure time. Relative exposure to BCTs with an informative nature was similar for the different treatment phases (33%−37%−28%; p = 0.09) but higher for physical activity compared to food habits, stress management and unspecific lifestyle medicine (63%−25%−22%−25%; p < 0.001).

Conclusions: The behaviour change technique taxonomy version 1 can be extended by adding exposure time for different BCTs. The resulting BCT–exposure profile can be used for assessing the relative importance of different behaviour change strategies.

OBJECTIVES: The authors aimed to evaluate whether blood cadmium (B-Cd), lead (B-Pb) and mercury (B-Hg) in children differ regionally in 9 countries, and to identify factors correlating with exposure.

MATERIAL AND METHODS: The authors performed a cross-sectional study of children aged 7-14 years, living in 2007-2008 in urban, rural, or potentially polluted ("hot spot") areas (ca. 50 children from each area, in total 1363 children) in 6 European and 3 non-European countries. The authors analyzed Cd, Pb, and total Hg in blood and collected information on potential determinants of exposure through questionnaires. Regional differences in exposure levels were assessed within each country.

RESULTS: Children living near industrial "hot-spots" had B-Cd 1.6 (95% CI: 1.4-1.9) times higher in the Czech Republic and 2.1 (95% CI:1.6-2.8) times higher in Poland, as compared to urban children in the same countries (geometric means [GM]: 0.13 μg/l and 0.15 μg/l, respectively). Correspondingly, B-Pb in the "hot spot" areas was 1.8 (95% CI: 1.6-2.1) times higher than in urban areas in Slovakia and 2.3 (95% CI: 1.9-2.7) times higher in Poland (urban GM: 19.4 μg/l and 16.3 μg/l, respectively). In China and Morocco, rural children had significantly lower B-Pb than urban ones (urban GM: 64 μg/l and 71 μg/l, respectively), suggesting urban exposure from leaded petrol, water pipes and/or coal-burning. Hg "hot spot" areas in China had B-Hg 3.1 (95% CI: 2.7-3.5) times higher, and Ecuador 1.5 (95% CI: 1.2-1.9) times higher, as compared to urban areas (urban GM: 2.45 μg/l and 3.23 μg/l, respectively). Besides industrial exposure, traffic correlated with B-Cd; male sex, environmental tobacco smoke, and offal consumption with B-Pb; and fish consumption and amalgam fillings with B-Hg. However, these correlations could only marginally explain regional differences.

CONCLUSIONS: These mainly European results indicate that some children experience about doubled exposures to toxic elements just because of where they live. These exposures are unsafe, identifiable, and preventable and therefore call for preventive actions.