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The European Union (EU) Ambient Air Quality Directive (AAQD) and Drinking Water Directive (DWD) are aimed at maintaining and improving air quality and ensuring high standards for potable water across the EU. Besides several other indicators, the AAQD and DWD consist of chemical parameters (substances or substance groups) that are regulated within this framework. All the substances are associated with various health outcomes, and many of them are classified as carcinogenic or probably/possibly carcinogenic with causal links. To quantify the health burden of the chemical substances included in the AAQD and DWD, we need information regarding population exposure, current baseline mortality/morbidity rates in the populations, and exposure-response functions (ERFs) or unit risks (URs) from previous epidemiological studies. During this study, we analyzed the availability of ERFs or URs and discussed their applicability in health impact assessments (HIAs). From the HIA perspective, ERFs─in terms of relative risk (RR), standardized mortality ratio (SMR), odds ratio (OR), or UR data─were available for many of the analyzed substances. However, for some substances such as acrylamide, antimony, boron, chlorate and chlorite, copper, microcystin-LR, and selenium, no risk measures could be identified. The aim of this study is to derive ERFs, which will allow HIAs for a larger number of chemicals when exposure data and baseline mortality/morbidity data are available. Currently, HIAs have largely focused only on main ambient pollutants such as particulate matter (PM10), fine particulate matter (PM2.5), nitrogen oxides (NOX), and ozone (O3). In contrast, health risks related to exposure to chemicals are much more diverse, and the health burdens should be quantified to a much greater extent.

Air pollution is increasingly discussed as a risk factor for dementia, but the biological mechanisms are not yet fully understood. Biological markers like telomere length are relevant to study with air pollution, as they are associated with aging and dementia. The study aimed to investigate the relationship between source-specific air pollution exposure and telomere length in a low-level air pollution area, and whether this potential relationship depended on future dementia status. The data originated from the Betula study in Northern Sweden, where 509 participants recruited between 1988 and 1995 were included to investigate the association between annual mean air pollution concentrations at the participants’ residences and relative leukocyte telomere length using a linear regression model. No association was observed between air pollution and telomere length, with regression slope estimates close to zero and p-values > 0.10 (e.g. PM2.5_total: β = 0.01 (-0.011, 0.025) and BC_total: β = 0.03 (95% CI: -0.046, 0.114). There were indications of a positive association between longer telomere length and higher exposure to air pollution among individuals later diagnosed with dementia (N = 74), but these findings were not conclusive (p-values > 0.10) (PM2.5_total: β = 0.03, p-value = 0.12; BC_total: β = 0.11, p-value = 0.17). Although not statistically significant, our findings contribute to the evidence from low-exposure settings, and it is important to report these types of findings for a balanced understanding of potential health effects.

Trafikverket har beviljat Institutionen för folkhälsa och klinisk medicin, Umeå universitet ett FOI-bidrag för projektet Reviderat underlag om hälsokonsekvenser av luftföroreningar, vilket ska komplettera underlagen om luftföroreningars hälsoeffekter till grund för rekommendationer i rapporten Analysmetod och samhällsekonomiska kalkylvärden för transportsektorn (ASEK-rapporten).

Projektets fyra delmoment syftar till

• att analysera hur morbiditetseffekter av kvävedioxid i sig kan uppskattas med direkta beräkningar
• att studera hur de i ASEK beräknade ohälsokostnaderna för slitageemissioner som PM10 påverkas av senare års resultat om sambanden mellan PM10, slitagepartiklar och mortalitet
• att bedöma vilka effekter av vägtrafikens föroreningar, specifikt kväveoxider och partiklar, på barns hälsa som det finns olika grad av evidens för och hur konsekvenserna kan uppskattas och värderas
• att föreslå en metod att uppskatta kostnader för emissioner genererande exponering för sekundärt bildade partiklar

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.

Introduction: Air pollution is a significant contributor to morbidity and mortality globally and has been linked to an increased risk of dementia. Previous studies within the Betula cohort in Northern Sweden have demonstrated associations between air pollution and dementia, as well as distinctive metabolomic profiles in dementia patients compared to controls. This study aimed to investigate whether air pollution is associated with quantitative changes in metabolite levels within this cohort, and whether future dementia status would modify this association.

Methods: Both short-term and long-term exposure to air pollution were evaluated using high spatial resolution models and measured data. Air pollution from vehicle exhaust and woodsmoke were analyzed separately. Metabolomic profiling was conducted on 321 participants, including 58 serum samples from dementia patients and a control group matched for age, sex, and education level, using nuclear magnetic resonance spectroscopy.

Results: No statistically significant associations were found between any metabolites and any measures of short-term or long-term exposure to air pollution. However, there were trends potentially suggesting associations between both long-term and short-term exposure to air pollution with lactate and glucose metabolites. Notably, these associations were observed despite the lack of correlation between long-term and short-term air pollution exposure in this cohort. There were also tendencies for associations between air pollution from woodsmoke to be more pronounced in participants that would later develop dementia, suggesting a potential effect depending on urban/rural factors.

Discussion: While no significant associations were found, the trends observed in the data suggest potential links between air pollution exposure and changes in lactate and glucose metabolites. These findings provide some new insights into the link between air pollution and metabolic markers in a low-exposure setting. However, addressing existing limitations is crucial to improve the robustness and applicability of future research in this area. The pronounced associations in participants who later developed dementia may indicate an influence of urban/rural factors, warranting further investigation.

OBJECTIVE: To assess a possible interaction effect between physical activity and air pollution on first incidence of ischaemic heart disease (IHD).

DESIGN: Prospective cohort study.

SETTING: Umeå, Northern Sweden.

PARTICIPANTS: We studied 34 748 adult participants of Västerbotten Intervention Programme cohort from 1990 to January 2014. Annual particulate matter concentrations (PM_2.5 and PM₁₀) at the participants' residential addresses were modelled and a questionnaire on frequency of exercise and active commuting was completed at baseline. Cox proportional hazards modelling was used to estimate (1) association with physical activity at different levels of air pollution and (2) the association with particulate matter at different levels of physical activity.

OUTCOME: First incidence of IHD.

RESULTS: Over a mean follow-up of 12.4 years, there were 1148 IHD cases. Overall, we observed an increased risk of IHD among individuals with higher concentrations of particles at their home address. Exercise at least twice a week was associated with a lower risk of IHD among participants with high residential PM_2.5 (hazard ratio (HR) 0.60; 95% CI: 0.44 to 0.82) and PM₁₀ (HR 0.55; 95% CI: 0.4 to 0.76). The same beneficial effect was not observed with low residential PM_2.5 (HR 0.94; 95% CI: 0.72 to 1.22) and PM₁₀ (HR 0.99; 95% CI: 0.76 to 1.29). An increased risk associated with higher long-term exposure to particles was only observed among participants that exercised in training clothes at most one a week and among those not performing any active commuting. However, only the interaction effect on HRs for exercise was statistically significant.

CONCLUSION: Exercise was associated with a lower risk of first incidence of IHD among individuals with higher residential particle concentrations. An air pollution-associated risk was only observed among those who exercised less. The findings support the promotion of physical activity and a mitigation of air pollution.

Background: There are increasing number of health impact assessment studies investigating the health effects by transferring trips made by motorised transport to active commuting; however, air pollution exposure during active commuting and its impact on health has been less thoroughly assessed. It is furthermore uncertain whether there is any interaction effect between air pollution and physical activity for the risk of cardiovascular diseases. The overall aim of the thesis was to improve the knowledge base for assessments of the total impact on health of a mode shift resulting in both increased physical activity and increased air pollution exposure, especially regarding combined effects on cardiovascular risks.

Methods: The thesis is based on four studies. In Study I, methodological issues related to the assessment of air pollution in previous studies on the health impact of changes in transport mode were critically reviewed. In Study II, the effect of leisure time and active commuting physical activity, on chronic diseases was quantified by conducting a random-effect meta-analysis. In two prospective cohort studies, participants of the Västerbotten Intervention Programme living in the Umeå region were studied to assess the impact as well as interaction effect of physical activity and air pollution on the incidence (Study III) and recurrence (Study IV) of cardiovascular diseases.

Results: In previous studies on the health impact of changes in transport mode, there was a large methodological discrepancy between studies due to different assumptions for air pollution exposure assessments in general populations and commuters as well as methods for estimation of impacts. Randomeffect meta-analyses showed a beneficial effect of leisure time physical activity and active commuting on morbidity among individuals performing these activities at the minimum level of physical activity recommended by WHO, equivalent to 11.25 MET-hours per week. Beneficial effects of exercise on firstincident ischemic heart disease (IHD) were observed among individuals with high residential PM10/PM2.5 concentrations, but not among individuals with low concentrations. Adverse effects associated with high residential PM10 and PM2.5 concentrations were only observed among the individuals whom less frequently exercised. A statistically significant interaction effect was found between air pollution and exercise in training clothes for first-incident IHD but not for recurrence of IHD/stroke.

Conclusions: The results in this thesis strengthen the public health message that physical activity is beneficial for cardiovascular health, even in areas with air pollution. Therefore, public health and transport policies should be designed to improve population health through promotion of active transport and mitigation of air pollution.

Introduction: A protective role of leisure time physical activity with regard to non-communicable chronic diseases (NCDs) is well established. However, shapes of dose-response relationships and the extent of BMI mediation between physical activity and disease risk are not well known. Furthermore, the knowledge about risk reductions from active commuting is limited. Methods: Meta-analyses of prospective cohort studies published from January 1990 to June 2019 were conducted, 1) to assess the effect of leisure time and commuting physical activity on cardiovascular disease (CVD), type 2 diabetes, breast cancer and colon cancer, and 2) to quantify the extent to which adjustment for BMI affect these relations. Results: Random effect meta-analyses of 59 prospective cohort studies estimated that individuals who engaged in 11.25 MET-hours/week of active commuting had a decreased risk of myocardial infarction (MI) by 18% (95% CI: 1-33%) and type 2 diabetes by 22% (95% CI: 4-37%) compared with non-commuters. Corresponding risk reductions for leisure-time physical activity (LTPA) were 22% for MI, 26% for CVD, 27% for heart failure, 23% for stroke, 22% for type 2 diabetes, 15% for colon cancer and 7% for breast cancer. Except for breast cancer, adjustment for BMI reduced the benefit of physical activity. Conclusion: Both active commuting and LTPA are associated with lower risk for NCD. Currently, available data is insufficient to establish detail and reliable dose-response curves.