The most important anthropogenic sources of primary particulate matter (PM) in ambient air in Europe are exhaust and non-exhaust emissions from road traffic and combustion of solid biomass. There is convincing evidence that PM, almost regardless of source, has detrimental health effects. An important issue in health impact assessments is what metric, indicator and exposure-response function to use for different types of PM. The aim of this study is to describe sectorial contributions to PM exposure and related premature mortality for three Swedish cities: Gothenburg, Stockholm and Umea. Exposure is calculated with high spatial resolution using atmospheric dispersion models. Attributed premature mortality is calculated separately for the main local sources and the contribution from long-range transport (LRT), applying different relative risks. In general, the main part of the exposure is due to LRT, while for black carbon, the local sources are equally or more important. The major part of the premature deaths is in our assessment related to local emissions, with road traffic and residential wood combustion having the largest impact. This emphasizes the importance to resolve within-city concentration gradients when assessing exposure. It also implies that control actions on local PM emissions have a strong potential in abatement strategies.

Residential wood combustion (RWC) is an important contributor to air quality in numerous regions worldwide. This study is the first extensive evaluation of the influence of RWC on ambient air quality in several Nordic cities. We have analysed the emissions and concentrations of PM_2.5 in cities within four Nordic countries: in the metropolitan areas of Copenhagen, Oslo, and Helsinki and in the city of Umeå. We have evaluated the emissions for the relevant urban source categories and modelled atmospheric dispersion on regional and urban scales. The emission inventories for RWC were based on local surveys, the amount of wood combusted, combustion technologies and other relevant factors. The accuracy of the predicted concentrations was evaluated based on urban concentration measurements. The predicted annual average concentrations ranged spatially from 4 to 7 µg m⁻³ (2011), from 6 to 10 µg m⁻³ (2013), from 4 to more than 13 µg m⁻³ (2013) and from 9 to more than 13 µg m⁻³ (2014), in Umeå, Helsinki, Oslo and Copenhagen, respectively. The higher concentrations in Copenhagen were mainly caused by the relatively high regionally and continentally transported background contributions. The annual average fractions of PM_2.5 concentrations attributed to RWC within the considered urban regions ranged spatially from 0 % to 15 %, from 0 % to 20 %, from 8 % to 22 % and from 0 % to 60 % in Helsinki, Copenhagen, Umeå and Oslo, respectively. In particular, the contributions of RWC in central Oslo were larger than 40 % as annual averages. In Oslo, wood combustion was used mainly for the heating of larger blocks of flats. In contrast, in Helsinki, RWC was solely used in smaller detached houses. In Copenhagen and Helsinki, the highest fractions occurred outside the city centre in the suburban areas. In Umeå, the highest fractions occurred both in the city centre and its surroundings.

Background: Residential wood combustion (RWC) is one of the largest sources of fine particles (PM_2.5) in the Nordic cities. The current study aims to calculate the related health effects in four studied city areas in Sweden, Finland, Norway, and Denmark. Methods: Health impact assessment (HIA) was employed as the methodology to quantify the health burden. Firstly, the RWC induced annual average PM_2.5 concentrations from local sources were estimated with air pollution dispersion modelling. Secondly, the baseline mortality rates were retrieved from the national health registers. Thirdly, the concentration-response function from a previous epidemiological study was applied. For the health impact calculations, the WHO-developed tool AirQ + was used. Results: Amongst the studied city areas, the local RWC induced PM_2.5 concentration was lowest in the Helsinki Metropolitan Area (population-weighted annual average concentration 0.46 µg m^− 3) and highest in Oslo (2.77 µg m^− 3). Each year, particulate matter attributed to RWC caused around 19 premature deaths in Umeå (95% CI: 8–29), 85 in the Helsinki Metropolitan Area (95% CI: 35–129), 78 in Copenhagen (95% CI: 33–118), and 232 premature deaths in Oslo (95% CI: 97–346). The average loss of life years per premature death case was approximately ten years; however, in the whole population, this reflects on average a decrease in life expectancy by 0.25 (0.10–0.36) years. In terms of the relative contributions in cities, life expectancy will be decreased by 0.10 (95% CI: 0.05–0.16), 0.18 (95% CI: 0.07–0.28), 0.22 (95% CI: 0.09–0.33) and 0.63 (95% CI: 0.26–0.96) years in the Helsinki Metropolitan Area, Umeå, Copenhagen and Oslo respectively. The number of years of life lost was lowest in Umeå (172, 95% CI: 71–260) and highest in Oslo (2458, 95% CI: 1033–3669). Conclusions: All four Nordic city areas have a substantial amount of domestic heating, and RWC is one of the most significant sources of PM_2.5. This implicates a substantial predicted impact on public health in terms of premature mortality. Thus, several public health measures are needed to reduce the RWC emissions.

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/m³ 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.

Long-term exposure to air pollution is associated with cardiovascular events. A main suggested mechanism is that air pollution accelerates the progression of atherosclerosis, yet current evidence is inconsistent regarding the association between air pollution and coronary artery and carotid artery atherosclerosis, which are well-established causes of myocardial infarction and stroke. We studied associations between low levels of long-term air pollution, coronary artery calcium (CAC) score, and the prevalence and area of carotid artery plaques, in a middle-aged population-based cohort. The Swedish CArdioPulmonary bioImage Study (SCAPIS) Gothenburg cohort was recruited during 2013-2017 and thoroughly examined for cardiovascular risk factors, including computed tomography of the heart and ultrasonography of the carotid arteries. In 5070 participants (age 50-64 years), yearly residential exposures to air pollution (PM_2.5, PM₁₀, PM_coarse, NO_x, and exhaust-specific PM_2.5 1990-2015) were estimated using high-resolution dispersion models. We used Poisson regression to examine associations between long-term (26 years' mean) exposure to air pollutants and CAC score, and prevalence of carotid artery plaques, adjusted for potential confounders. Among participants with carotid artery plaques, we also examined the association with plaque area using linear regression. Mean exposure to PM_2.5 was low by international standards (8.5 μg/m³). There were no consistent associations between long-term total PM_2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM_2.5 and larger plaque area in participants with carotid plaques. Associations with traffic-related air pollutants were consistently positive for both a high CAC score and bilateral carotid artery plaques. These associations were independent of road traffic noise. We found stronger associations among men and participants with cardiovascular risk factors. The results lend some support to atherosclerosis as a main modifiable pathway between low levels of traffic-related ambient air pollution and cardiovascular disease, especially in vulnerable individuals.