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BACKGROUND: An association between dampness at home and respiratory conditions has been convincingly demonstrated in children. Fewer studies have been performed in adults, and data are lacking for chronic rhinosinusitis (CRS). With a prevalence of 10.9% in Europe, CRS imposes a significant burden on quality of life, as well as economy.

OBJECTIVE: Our aim was to study CRS and other respiratory conditions in relation to dampness at home in a representative sample of adults.

METHODS: The Swedish GA(2) LEN questionnaire was answered by 26 577 adults (16-75 years) and included questions on respiratory symptoms, smoking, education and environmental exposure. CRS was defined according to the EP(3) OS criteria. Dampness was defined as reporting water damage, floor dampness or visible moulds in the home during the last 12 months. The dampness score was ranked from 0 to 3, counting the number of signs of dampness reported.

RESULTS: Dampness at home was reported by 11.3% and was independently related to respiratory conditions after adjustment for demographic and socio-economic factors and smoking: CRS odds ratio (OR) 1.71; allergic rhinitis OR 1.24; current asthma OR 1.21; wheeze OR 1.37; nocturnal dyspnoea OR 1.80; nocturnal coughing OR 1.34; and chronic bronchitis OR 1.64. The risk of CRS and most of the other respiratory conditions was further elevated in subjects reporting multiple signs of dampness.

CONCLUSIONS AND CLINICAL RELEVANCE: This study demonstrated an independent association between dampness at home and CRS in adults. The high burden of this and the other respiratory conditions studied is a strong argument in favour of countering indoor dampness by improving building standards.

Aim: There has been a lack of population‐based longitudinal data on serum ferritin in very low birth weight (VLBW) infants during hospitalisation. Our aim was to fill this gap in the knowledge and investigate risk factors for elevated serum ferritin and associations between erythrocyte transfusions and longitudinal growth.

Methods: We retrospectively reviewed longitudinal data on 126 VLBW infants treated at Umeå University Hospital, Sweden, between 2010‐2013.

Results: The infants’ mean gestational age and birth weight were 26.9 weeks and 899 grams. Most (91%) received erythrocyte transfusions and the majority had multiple erythrocyte transfusions. There was a significant correlation between serum ferritin and the volume of transfusions. Almost two‐thirds had at least one serum ferritin measurement of more than 350 µg/L, indicating iron overload. In those with complete anthropometric data (n=78) there was no significant effect of serum ferritin concentrations in relation to longitudinal growth, but there was a positive association between the erythrocyte transfusion dose and longitudinal growth in VLBW infants born before 25 weeks.

Conclusion: This is the first population‐based study to investigate longitudinal data on serum ferritin in VLBW infants during hospitalisation. The unexpected positive finding in the subgroup born at less than 25 weeks needs further research with a larger cohort.

BACKGROUND: Exhaled nitric oxide (FeNO) has a potential clinical role in asthma management. Constitutive factors such as age, height and male gender, as well as individual characteristics, as IgE sensitisation and smoking, affect levels of FeNO in population-based studies. However their effect on FeNO in subjects with asthma has been scarcely studied.

OBJECTIVE: To study the effects on FeNO of these commonly regarded determinants, as demonstrated in healthy subjects, as well as menarche age and parental smoking, in a population of asthmatics.

MATERIAL AND METHODS: FeNO was measured in 557 subjects with asthma from the Swedish GA2LEN study. Allergic sensitisation was assessed by skin prick tests to most common aeroallergens. Upper airway comorbidities, smoking habits, smoking exposure during childhood, hormonal status (for women) were questionnaire-assessed.

RESULTS: Male gender (p<0.001), greater height (p<0.001) and sensitisation to both perennial allergens and pollen (p<0.001) related to higher FeNO levels. Current smoking (p<0.001) and having both parents smoking during childhood, vs having neither (p<0.001) or only one parent smoking (p=0.002), related to lower FeNO. Women with menarche between 9-11 years of age had lower FeNO than those with menarche between 12-14 years of age (p = 0.03) or 15-17 years of age (p=0.003).

CONCLUSIONS AND CLINICAL RELEVANCE: Interpreting FeNO levels in clinical practice is complex and constitutional determinants, as well as smoking and IgE sensitization, are of importance in asthmatic subjects and should be accounted for when interpreting FeNO levels. Furthermore, menarche age and parental smoking during childhood and their effects on lowering FeNO deserve further studies.

Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.

Methods: In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5–10 μm in diameter (PM_2.5, PM₁₀, and PM_coarse), PM_2.5 absorbance, nitrogen oxides (NO₂ and NO_x) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.

Results: Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM_2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89–3.14 per 10^–5/m³), and weak positive or null associations with the other pollutants. Hazard ratio for PM_2.5 absorbance (1.01; 0.38–2.71 per 10^–5/m³) and all other pollutants were lower for nonmalignant than for malignant brain tumors.

Conclusion: We found suggestive evidence of an association between long-term exposure to PM_2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.

OBJECTIVE: Previous studies have found that excessive daytime sleepiness (EDS) is a more common problem in asthmatic subjects than in the general population. The aim of this study was to investigate whether the prevalence of EDS is increased in asthmatic subjects and, if so, to analyse the occurrence of potential risk factors for EDS in asthmatics.

METHODS: Cross-sectional epidemiological study. In 2008, a postal questionnaire was sent out to a random sample of 45,000 individuals aged 16-75 years in four Swedish cities.

RESULTS: Of the 25,160 persons who participated, 7.3% were defined as having asthma. The prevalence of EDS was significantly higher in asthmatic subjects (42.1% vs 28.5%, p<0.001) compared with non-asthmatic subjects. Asthma was an independent risk factor for EDS (adjusted OR 1.29) and the risk of having EDS increased with asthma severity. Risk factors for EDS in subjects with asthma included insomnia (OR, 3.87; 95% CI, 3.10-4.84), chronic rhinosinusitis (OR, 2.00; 95% CI, 1.53-2.62), current smoking (OR, 1.60; 95% CI, 1.15-2.22) and obesity (OR, 1.53; 95% CI, 1.09-2.13).

CONCLUSIONS: EDS is a common problem among subjects with asthma. Asthma is an independent risk factor for having EDS. Furthermore, subjects with asthma often have other risk factors for EDS, many of them potentially modifiable.

The aim of this study was to investigate if there are differences in symptom ratings and plasma concentrations of oxylipins as a measure of acute inflammation between individuals with building-related symptoms (BRS) and referents during exposure to rooms where people experienced BRS and rooms where they did not experience BRS. Medically examined individuals with BRS and healthy, age and sex matched referents working in the same building were exposed for 60 min. Ratings of symptoms and collection of blood to measure oxylipins in plasma were performed before and after each exposure. Individuals with BRS reported more symptoms (mostly mucosal) than the referents in the problem rooms and there was a tendency towards a difference between the groups in concentration of metabolites from the cyclooxygenase pathway (COX). The mean reported intensity of symptoms among all participants was also found to be positively correlated with both COX and lipoxygenase (LOX-15) oxylipins in problem rooms.

Background: Perfluoroalkyl substances (PFAS) are persistent synthetic chemicals that may affect components of metabolic risk through the peroxisome proliferator-activated receptor but epidemiological data remain scarce and inconsistent.

Objective: To estimate associations between repeated measurements of the main PFAS in plasma and total cholesterol, triglycerides and hypertension among the control subjects from a population-based nested case-control study on diabetes type 2 in middle-aged women and men.

Methods: Participants (n = 187) were free of diabetes at both baseline and follow-up visits to the Västerbotten Intervention Programme, 10 years apart: during 1990 to 2003 (baseline) and 2001 to 2013 (follow-up). Participants left blood samples, completed questionnaires on diet and lifestyle factors, and underwent medical examinations, including measurement of blood pressure. PFAS and lipids were later determined in stored plasma samples. Associations for the repeated measurements were assessed using generalized estimating equations.

Results: Six PFAS exceeded the limit of quantitation. Repeated measures of PFAS in plasma, cardiometabolic risk factors and confounders, showed an average decrease of triglycerides from −0.16 mmol/l (95% confidence interval [CI]: −0.33, 0.02 for PFOA) to −0.26 mmol/l (95% CI: −0.50, −0.08 for PFOS), when comparing the highest tertile of PFAS plasma levels with the lowest. Associations based on average PFAS measurements and follow-up triglycerides revealed similar inverse associations, although attenuated. The estimates for cholesterol and hypertension were inconsistent and with few exception non-significant.

Conclusions: This study found inverse associations between PFAS and triglycerides, but did not support any clear link with either cholesterol or hypertension.

Background: Perfluoroalkyl substances (PFAS) have drawn much attention due to bioaccumulation potential and their current omnipresence in human blood. We assessed whether plasma PFAS, suspected to induce endocrine-disrupting effects, were prospectively associated with clinical type 2 diabetes (T2D) risk.

Methods: We established a nested case-control study within the Swedish prospective population-based Västerbotten Intervention Programme cohort. Several PFAS were measured in plasma from a subset of 124 case-control pairs at baseline (during 1990–2003) and at 10-year follow-up. T2D cases were matched (1:1) according to gender, age and sample date with participants without T2D (controls).

Conditional logistic regressions were used to prospectively assess risk of T2D by baseline PFAS plasma concentrations. Associations between long-term PFAS plasma levels (mean of baseline and follow-up) and insulin resistance (HOMA2-IR) and beta-cell function (HOMA2-B%) at follow-up were prospectively explored among 178 and 181 controls, respectively, by multivariable linear regressions.

Results: After adjusting for gender, age, sample year, diet and body mass index, the odds ratio of T2D for the sum of PFAS (Σ z-score PFAS) was 0.52 (95% confidence interval, CI: 0.20, 1.36), comparing third with first tertile; and 0.92 (95% CI: 0.84, 1.00) per one standard deviation increment of sum of log-transformed PFAS. Among the controls, the adjusted β of HOMA2-IR and HOMA-B% for the sum of PFAS were −0.26 (95% CI: −0.52, −0.01) and −9.61 (95% CI: −22.60, 3.39) respectively comparing third with first tertile.

Conclusions: This prospective nested case-control study yielded overall inverse associations between individual PFAS and risk of T2D, although mostly non-significant. Among participants without T2D, long-term PFAS exposure was prospectively associated with lower insulin resistance.

Persistent organochlorine pollutants (POPs) have shown to be involved in the atherosclerotic process and to cause endothelial cell dysfunction. To assess longitudinally whether plasma concentrations of different POPs were associated with blood pressure and risk of hypertension in middle-aged women and men. Study subjects were 850 participants in the VIP (Västerbotten Intervention Programme) with 2 blood samples and blood pressure measurements, 10 years apart, during 1990 to 2003 (baseline) and during 2000 to 2013 (follow-up). Dioxin-like and nondioxin-like polychlorinated biphenyls (DL-PCBs, NDL-PCBs) and p,p'-dichlorodiphenyldichloroethylene (DDE) were measured. Associations were assessed using generalized estimating equations. At baseline sampling 49% and at follow-up 64% had hypertension. DL-PCBs and DDE, but not NDL-PCBs or hexachlorobenzene, were associated with hypertension. Only the association for DL-PCBs remained statistically significant after lipid-standardization and adjustment for body mass index and total serum lipids. The multivariable-adjusted odds ratio of hypertension based on repeated measurements were 1.52 (95% confidence interval, 1.08-2.13) for DL-PCBs (third versus first tertile of lipid-standardized POPs). In stratified adjusted analyses, odds ratio for those born after 1950 increased to 3.99 (95% confidence interval, 2.15-7.43), whereas no association was observed among those born earlier. Based on repeated measurements, the accumulated exposure to DL-PCBs and DDE, although less clear for the latter, may disrupt the normal blood pressure levels and increase the odds of hypertension. Moreover, individuals experiencing early-life POP exposure may be at elevated risk of vascular POP effects.

Nuts are rich in nutrients and mounting evidence shows that consumption reduces cardiovascular disease (CVD) incidence. Nuts may also be a major source of aflatoxin B₁, a potent liver carcinogen and the risk/benefit balance is unknown. Based on national statistics and data from the PREDIMED intervention trial, we estimated the potential CVD-reduction if Swedes aged 55-79 consumed 30 g nuts/day, instead of the current national average of five grams per day. We also assessed the reduction in disability-adjusted life years (DALYs) due to myocardial infarction (MI) and stroke. We estimated the aflatoxin B₁ exposure from nuts and calculated the margin of exposure. The approximation that one nanogram aflatoxin B₁/kg body weight/day results in one additional liver cancer case/10 million person-years was used to estimate the number of liver cancer cases. The increased nut consumption scenario prevented more than 7000 CVDs in 2013 (306/100,000 person-years) and contributed to about 55,000 saved DALYs for stroke and 22,000 for MI. The concomitant increase in aflatoxin B₁ exposure caused an estimated zero to three additional cases of liver cancer, corresponding to 159 DALYs spent, emphasizing the associated risks. Increased nut consumption, as part of a varied healthy diet, is warranted even when aflatoxin B₁ exposure is taken into account. However, efforts to reduce aflatoxin exposure from food are essential.

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.

Summary: In a population-based case-control study, we demonstrate that middle-aged women who were active with walking or in different physical spare time activities were at lower risk of later sustaining a hip fracture compared to more sedentary women.

Introduction: In middle-aged women participating in the Umeå Fracture and Osteoporosis (UFO) study, we investigated whether physical activity is associated with a subsequent decreased risk of sustaining a hip fracture.

Methods: The UFO study is a nested case-control study investigating associations between bone markers, lifestyle, and osteoporotic fractures. We identified 81 female hip fracture cases that had reported lifestyle data before they sustained their fracture. Each case was compared with two female controls who were identified from the same cohort and matched for age and week of reporting data, yielding a total cohort of 237 subjects. Mean age at baseline was 57.2 ± 5.0 years, and mean age at fracture was 65.4 ± 6.4 years.

Results: Conditional logistic regression analysis with adjustments for height, weight, smoking, and menopausal status showed that subjects who were regularly active with walking or had a moderate or high frequency of physical spare time activities (i.e. berry/mushroom picking and snow shovelling) were at reduced risk of sustaining a hip fracture (OR 0.14; 95% CI; 0.05–0.53 for walking and OR 0.19; 95% CI; 0.08–0.46, OR 0.17, 95% CI; 0.05–0.64 for moderate and high frequency of spare time activities, respectively) compared to more sedentary women.

Conclusion: An active lifestyle in middle age seems to reduce the risk of future hip fracture. Possible mechanisms may include improved muscle strength, coordination, and balance resulting in a decreased risk of falling and perhaps also direct skeletal benefits.

Middle-aged women with active commuting had significantly lower risk for wrist fracture than women commuting by car/bus.

INTRODUCTION: Our purpose was to investigate whether a physically active lifestyle in middle-aged women was associated with a reduced risk of later sustaining a low-trauma wrist fracture.

METHODS: The Umeå Fracture and Osteoporosis (UFO) study is a population-based nested case-control study investigating associations between lifestyle and fragility fractures. From a cohort of ~35,000 subjects, we identified 376 female wrist fracture cases who had reported data regarding their commuting habits, occupational, and leisure physical activity, before they sustained their fracture. Each fracture case was compared with at least one control drawn from the same cohort and matched for age and week of reporting data, yielding a total of 778 subjects. Mean age at baseline was 54.3 ± 5.8 years, and mean age at fracture was 60.3 ± 5.8 years.

RESULTS: Conditional logistic regression analysis with adjustments for height, body mass index, smoking, and menopausal status showed that subjects with active commuting (especially walking) were at significantly lower risk of sustaining a wrist fracture (OR 0.48; 95 % CI 0.27-0.88) compared with those who commuted by car or bus. Leisure time activities such as dancing and snow shoveling were also associated with a lower fracture risk, whereas occupational activity, training, and leisure walking or cycling were unrelated to fracture risk.

CONCLUSION: This study suggests that active commuting is associated with a lower wrist fracture risk, in middle-aged women.

BACKGROUND: Very few studies have examined whether a long-term beneficial effect of physical activity on lung function can be influenced by living in polluted urban areas.

OBJECTIVE: We assessed whether annual average residential concentrations of nitrogen dioxide (NO₂) and particulate matter with aerodynamic diameters < 2.5 μm (PM_2.5) and <10 μm (PM₁₀) modify the effect of physical activity on lung function among never- (N = 2801) and current (N = 1719) smokers in the multi-center European Community Respiratory Health Survey.

METHODS: Associations between repeated assessments (at 27-57 and 39-67 years) of being physically active (physical activity: ≥2 times and ≥1 h per week) and forced expiratory volume in 1 s (FEV₁) and forced vital capacity (FVC) were evaluated using adjusted mixed linear regression models. Models were conducted separately for never- and current smokers and stratified by residential long-term NO₂, PM_2.5 mass and PM₁₀ mass concentrations (≤75th percentile (low/medium) versus >75th percentile (high)).

RESULTS: Among current smokers, physical activity and lung function were positively associated regardless of air pollution levels. Among never-smokers, physical activity was associated with lung function in areas with low/medium NO₂, PM_2.5 mass and PM₁₀ mass concentrations (e.g. mean difference in FVC between active and non-active subjects was 43.0 mL (13.6, 72.5), 49.5 mL (20.1, 78.8) and 49.7 mL (18.6, 80.7), respectively), but these associations were attenuated in high air pollution areas. Only the interaction term of physical activity and PM₁₀ mass for FEV₁ among never-smokers was significant (p-value = 0.03).

CONCLUSIONS: Physical activity has beneficial effects on adult lung function in current smokers, irrespective of residential air pollution levels in Western Europe. Trends among never-smokers living in high air pollution areas are less clear.

BACKGROUND: Long-term exposure to air pollution is hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country-specific. OBJECTIVES: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations. METHODS: Fifteen population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE), were analysed. Residential exposure to particulate matter and nitrogen oxides was modelled with land use regression using a uniform protocol. Traffic exposure was assessed with traffic indicator variables. We analysed systolic and diastolic BP in participants medicated and non-medicated with BP lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis. RESULTS: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in non-medicated participants (0.35 mmHg [95% CI: 0.02-0.68] and 0.22 mmHg [95% CI: 0.04-0.40] per 4,000,000 vehicles × m/day, respectively). The estimated odds ratio for prevalent hypertension was 1.05 [95% CI: 0.99-1.11] per 4,000,000 vehicles × m/day. Modelled air pollutants and BP were not clearly associated. CONCLUSIONS: In this first comprehensive meta-analysis of European population-based cohorts we observed a weak positive association of high residential traffic exposure with BP in non-medicated participants, and an elevated OR for prevalent hypertension. The relationship of modelled air pollutants with BP was inconsistent.

Ozone and nitrogen oxides (NO x ) are air pollutants with known associations to adverse health effects on humans. Few studies have simultaneously measured ozone and nitrogen oxides with high spatial resolution. The main aim of this paper was to assess the levels and variation of ground-level ozone, NO2 and NO x in two Swedish cities. An additional aim was to describe the levels of these pollutants within and between three different types of measurement sites (regional background, urban background and traffic sites) and within and between different measurement periods of the year. Three weekly sampling campaigns of NO x and ozone were conducted simultaneously at 20 sites in two Swedish regions using Ogawa badges. Ozone was measured at 20 additional sites in each area. The median ozone concentration for all measurements was statistically significantly higher in Malmö (67 μg/m(3)) compared to Umeå (56 μg/m(3)), and in both cities, ozone levels were highest in April. Measurement period was a more important factor for describing the variation in ozone concentrations than the type of measurement site. The levels of NO2 and NO x were statistically significantly higher in the Malmö area (8.1 and 12 μg/m(3)) compared to the Umeå area (4.5 and 8.9 μg/m(3)). The levels were generally highest at the sites categorized as traffic, while the variability between different seasons was sparse.

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.

Our study is based on individual data on people's home and work addresses, as well as their age, sex and physical capacity, in order to establish realistic bicycle-travel distances. A transport model is used to single out data on commuting preferences in the County Stockholm. Our analysis shows there is a very large potential for reducing emissions and exposure if all car drivers living within a distance corresponding to a maximum of a 30 min bicycle ride to work would change to commuting by bicycle. It would result in > 111,000 new cyclists, corresponding to an increase of 209% compared to the current situation.

Mean population exposure would be reduced by about 7% for both NO_x and black carbon (BC) in the most densely populated area of the inner city of Stockholm. Applying a relative risk for NO_x of 8% decrease in all-cause mortality associated with a 10 μg m^− 3decrease in NO_x, this corresponds to > 449 (95% CI: 340–558) years of life saved annually for the Stockholm county area with 2.1 million inhabitants. This is more than double the effect of the reduced mortality estimated for the introduction of congestion charge in Stockholm in 2006. Using NO₂ or BC as indicator of health impacts, we obtain 395 (95% CI: 172–617) and 185 (95% CI: 158–209) years of life saved for the population, respectively. The calculated exposure of BC and its corresponding impacts on mortality are likely underestimated. With this in mind the estimates using NO_x, NO₂ and BC show quite similar health impacts considering the 95% confidence intervals.

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.

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.

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 (PM2.5 ) 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 PM2.5 total, BC, and IHD. However, for PM2.5 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 PM2.5 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.

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.

Introduction: Electric vehicles (EVs) are heavily promoted as beneficial for climate and health. In most studies, it is assumed that EVs contribution to urban air pollution is zero due to no tailpipe emissions, ignoring the contribution of non-exhaust particles (brake, tire and road wear), which are unregulated in EU. This study of Stockholm, Sweden, aims to 1) assess how a future vehicle fleet impacts concentrations of particles of size less than 2.5 μm (PM2.5) and evaluate the expected health outcomes economically and 2) compare this with CO2 savings.

Methods: Source specific dispersion models of exhaust and non-exhaust PM2.5 was used to estimate the population weighted concentrations. Thereafter exposure differences within a business as usual (BAU2035) and a fossil free fuel (FFF2035) scenario were used to assess expected health and economic impacts. The assessment considered both exhaust and non-exhaust emissions, considering the vehicle weight and the proportion of vehicles using studded winter tires. Health economic costs were retrieved from the literature and societal willingness to pay was used to value quality-adjusted life-years lost due to morbidity and mortality.

Results: The mean population weighted exhaust PM2.5 concentration decreased 0.012 μg/m3 (39%) in FFF2035 as compared to BAU2035. Assuming 50% higher road and tire wear PM2.5 emission because of higher weight among EVs and 30% less brake wear emissions, the estimated decrease in wear particle exposures were 0.152 (22%) and 0.014 μg/m3 (1.9%) for 0 and 30% use on studded winter tires, respectively. The resulting health economic costs were estimated to €217M and €32M, respectively. An increase by 0.079 μg/m3 (11%) was however estimated for 50% use of studded winter tires, corresponding to an €89M increase in health costs.

Conclusion: Considering both exhaust and wear generated particles, it is not straight forward that an increase of EVs will decrease the negative health impacts.

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.

OBJECTIVES: To conduct a health economic evaluation of a proposed investment in urban bicycle infrastructure in Stockholm County, Sweden.

DESIGN: A cost-effectiveness analysis is undertaken from a healthcare perspective. Investment costs over a 50-year life cycle are offset by averted healthcare costs and compared with estimated long-term impacts on morbidity, quantified in disability-adjusted life years (DALYs). The results are re-calculated under different assumptions to model the effects of uncertainty.

SETTING: The Municipality of Stockholm (population 2.27 million) committed funds for bicycle path infrastructure with the aim of achieving a 15% increase in the number of bicycle commuters by 2030. This work is based on a previously constructed scenario, in which individual registry data on home and work address and a transport model allocation to different modes of transport identified 111 487 individuals with the physical capacity to bicycle to work within 30 min but that currently drive a car to work.

RESULTS: Morbidity impacts and healthcare costs attributed to increased physical activity, change in air pollution exposure and accident risk are quantified under the scenario. The largest reduction in healthcare costs is attributed to increased physical activity and the second largest to reduced air pollution exposure among the population of Greater Stockholm. The expected net benefit from the investment is 8.7% of the 2017 Stockholm County healthcare budget, and 3.7% after discounting. The economic evaluation estimates that the intervention is cost-effective and each DALY averted gives a surplus of €9933. The results remained robust under varied assumptions pertaining to reduced numbers of additional bicycle commuters.

CONCLUSION: Investing in urban infrastructure to increase bicycling as active transport is cost-effective from a healthcare sector perspective.

Background and objective: Long-term exposure to cadmium (Cd) causes renal dysfunction, but its change with exposure is unknown. We aimed at assessing the evolution of Cd-induced renal effects after a reduction in dietary exposure to Cd in rice.

Methods: 412 residents in previously Cd-polluted and non-polluted areas were examined twice: in 1998 and 2006. Changes in blood Cd, urinary Cd, and kidney function (N-acetyl-β-D-glucosaminidase = NAG, β2-microglobulin, and albumin in urine) were measured. Results: In the most polluted area, mean blood Cd was 8.9 μg/L in 1998 and 3.3 μg/L in 2006, and urinary Cd was 11.6 and 9.0 μg/g creatinine in 1998 and 2006, respectively. Urinary albumin in 1998 increased with urinary Cd but no such exposure-response appeared for 2006 albumin versus urinary Cd 1998, indicating recovery. Other biomarkers of kidney function were also elevated in 1998. Partial recovery was observed for NAG, among women, and suggested for β2-microglobulin, among young individuals. The probability of having a β2-microglobulin above the 95th percentile in 2006 was high in those with an elevated β2-microglobulin in 1998 (odds ratio: 24.8, 95% CI: 11.2-55.3), whereas corresponding estimates for albumin and NAG were 3.0 (1.2-7.5) and 2.6 (1.6-4.4), respectively.

Conclusions: Results suggest that a Cd-mediated increase in urinary albumin excretion is reversible upon substantial reduction of exposure. For the markers of tubular effects, a tendency towards improvement, but not complete recovery, was observed. Data from repeated observations suggests that β2-microglobulin may be more informative than NAG as an indicator for the individual's future tubular function.

Background: Despite decreasing mortality from cardiovascular disease (CVD), there are persistent inequities in mortality between socioeconomic groups. Primary preventative medications reduce mortality in CVD; thus, inequitable treatments will contribute to unequal outcomes. Physicians might contribute to inequality by prescribing preventative medication for CVD to themselves in a biased manner.

Aim: To determine whether primary medications for preventing CVD were prescribed inequitably between physicians and non-physicians.

Design and setting: This retrospective study retrieved registry data on prescribed medications for all physicians in Sweden aged 45–74 years, during 2013, and for reference non-physician individuals, matched by sex, age, residence, and level of education. The outcome was any medication for preventing CVD, received at least once during 2013.

Method: Age and the sex-specific prevalence of myocardial infarction (MI) among physicians and non-physicians were used as a proxy for the need for medication. Thereafter, to limit the analysis to preventative medication, we excluded individuals that were diagnosed with CVD or diabetes. To analyse differences in medication usage between physicians and matched non-physicians, we estimated odds ratios (ORs) with conditional logistic regression and adjusted for need and household income.

Results: MI prevalences were 5.7% for men and 2.3% for women, among physicians, and 5.4% for men and 1.8% for women, among non-physicians. We included 25,105 physicians and 44,366 non-physicians. The OR for physicians receiving any CVD preventative medication, compared to non-physicians, was 1.65 (95% confidence interval 1.59–1.72).

Conclusion: We found an inequity in prescribed preventative CVD medications, which favoured physicians over non-physicians.

BACKGROUND: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources.

OBJECTIVES: We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities.

METHODS: ), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models.

RESULTS: exposure from residential heating.

DISCUSSION: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations.

Background: Despite global achievements in reducing early childhood mortality, disparities remain. There have been empirical studies of inequalities conducted in low- and middle-income countries. However, there have been no epidemiological studies on socioeconomic inequalities and early childhood survival in Myanmar.

Objective: To estimate associations between two measures of parental socioeconomic status - household wealth and education - and age-specific early childhood mortality in Myanmar.

Methods: Using cross-sectional data obtained from the Myanmar Demographic Health Survey (2015-2016), univariate and multiple logistic regressions were performed to investigate associations between household wealth and highest attained parental education, and under-5, neonatal, post-neonatal and child mortality. Data for 10,081 children born to 5,932 married women (aged 15-49 years) 10 years prior to the survey, were analysed.

Results: Mortality during the first five years was associated with household wealth. In multiple logistic models, wealth was protective for post-neonatal mortality. After adjusting for individual proximate determinants, the odds of post-neonatal mortality in the richest households were 85% lower (95% CI: 50-96%) than in the poorest households. However, significant association was not found between wealth and neonatal mortality. Parental education was important for early childhood mortality; the highest benefit from parental education was for child mortality in the one- to five-year age bracket. After adjusting for proximate determinants, children with a higher educated parent had 95% (95% CI 77-99%) lower odds of death in this age group compared with children whose parents' highest educational attainment was at primary level. The association between parental education and neonatal mortality was not significant.

Conclusions: In Myanmar, household wealth and parental education are important for childhood survival before five years of age. This study identified nuanced age-related differences in associations. Health policy must take socioeconomic determinants into account in order to address unfair inequalities in early childhood mortality.

BACKGROUND: We have reported that increased fraction of exhaled nitric oxide (FeNO), a measure of TH2 -driven airway inflammation, and blood eosinophil count, a marker of systemic eosinophil inflammation, correlated with asthma attacks in a population-based study.

OBJECTIVE: To investigate the relation between simultaneously elevated FeNO and serum eosinophil cationic protein (S-ECP) levels and asthma events among asthmatics.

METHODS: Measurements of FeNO (elevated ≥ 25 ppb) and S-ECP (elevated ≥ 20 ng/mL) were done in 339 adult asthmatics. Asthma events (attacks and symptoms) were self-reported.

RESULTS: Simultaneously normal S-ECP and FeNO levels were found in 48% of the subjects. Subjects with simultaneously elevated S-ECP and FeNO (13% of the population) had a higher prevalence of asthma attacks in the preceding 3 months than subjects with normal S-ECP and FeNO (51% vs. 25%, p = 0.001). This was not found for subjects with singly elevated S-ECP (p = 0.14) or FeNO (p = 0.34) levels. Elevated S-ECP and FeNO levels was independently associated to asthma attacks in the preceding 3 months after adjusting for potential confounders (OR (95% CI) 4.2 (2.0-8.8).

CONCLUSIONS: Simultaneous elevated FeNO and S-ECP related to a higher likelihood of asthma attacks in the preceding 3 months. This indicates that there is a value in measuring both FeNO and systemic eosinophilic inflammation in patients with asthma in order to identify individuals at high risk of exacerbations.

Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancersof the stomach and upper aerodigestive tract (UADT). We investigated the association of long-term exposure to ambient airpollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land-useregression models for particulate matter (PM) below 10mm (PM10), below 2.5mm (PM2.5), between 2.5 and 10mm (PMcoarse),PM2.5absorbance and nitrogen oxides (NO2and NOX) as well as approximated by traffic indicators. Cox regression modelswith adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined withrandom effects meta-analyses. During average follow-up of 14.1 years of 305,551 individuals, 744 incident cases of gastriccancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5mg/m3of PM2.5was 1.38 (95% CI 0.99; 1.92)for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures consid-ered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influencemarkedly the effect estimate for PM2.5and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5wasfound in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study showsan association between long-term exposure to PM2.5and gastric cancer, but not UADT cancers, suggesting that air pollutionmay contribute to gastric cancer risk.

Cadmium and lead accumulate in humans and can have toxic effects. Exposure to cadmium is well known to cause kidney damage. Cadmium binds to metallothioneins, proteins that play a role in cadmium transport. Lead exposure’s main effect is on the central nervous system, but associations with kidney disease have also been found, although it is unknown if the latter is a causal association. The main source of both metals within the non-smoking population is from the diet.

This thesis aims to 1) compare the biomarkers lead and cadmium concentration in whole-blood, plasma and urine with regard to their ability to discriminate between individuals with different mean concentrations, and to describe the effect of urinary dilution, 2) estimate the association between end-stage renal disease and blood concentrations of cadmium, lead and mercury, using prospectively collected samples for exposure evaluation, 3) use longitudinal data on kidney function makers to evaluate kidney recovery after a substantial decrease in cadmium exposure, and 4) assess the influence of metallothionein polymorphisms (MT1A rs11076161, MT2A rs10636 and MT2A rs28366003) on cadmium-associated kidney toxicity and recovery due to a reduction in Cd exposure.

Repeated sampling of whole-blood, plasma and urine was conducted on 48 occupationally lead-exposed men and 20 individuals under normal environmental lead exposure, for estimation of the day-to-day and between individual-variation. Prospective samples were obtained for 118 cases that later in life developed end-stage renal disease, and 378 matched controls. Erythrocyte cadmium, lead, and mercury concentrations were determined and the risk of developing end-stage renal disease associated with metal concentrations was estimated. For evaluation of kidney recovery after a reduction in cadmium exposure and to test for gene-environment interactions, follow-up data on N-acetyl-β‑d-glucosaminidase, β₂‑microglobulin, albumin, and gene polymorphisms were obtained for 412 individuals within the Chinese population and the relation to blood and urinary cadmium was assessed.

The concentration of lead in blood was found to be the biomarker with the largest fraction of the total variance attributable to between-individual variation, and was therefore the biomarker with the best ability to discriminate between individuals with different mean concentrations, both for individuals under occupational and normal environmental exposure (91 and 95%, respectively). Adjusting for urinary dilution had a great effect on the fraction of the total variance attributable to between-individual variation among individuals with normal lead exposure but only a minor effect among those who were occupationally exposed. Variance analysis showed that blood concentrations were also the best discriminating biomarker for cadmium.

Erythrocyte lead was, in a univariate model, associated with an increased risk of developing end-stage renal disease [odds ratio (OR) = 1.54 for an interquartile range increase, with a 95% confidence interval (CI) = 1.18-2.00], while erythrocyte mercury was negatively associated (OR = 0.75 for an interquartile range increase, with a 95% CI = 0.56-0.99). For erythrocyte cadmium, the OR was 1.15 with a 95% CI of 0.99-1.34. Associations with lead and cadmium were only seen among men. In the study on kidney recovery, the proportion of individuals with albumin level above the 95th percentile decreased between baseline and follow up, but no decrease was found for the tubular markers N-acetyl-β‑d-glucosaminidase and β₂-microglobulin. Metallothionein polymorphisms modified cadmium-associated effects on N-acetyl-β‑d-glucosaminidase and β₂-microglobulin levels but did not modify cadmium-associated change in any of the kidney function markers between baseline and follow up after a substantial decrease in exposure.

Blood concentrations of lead and cadmium are the biomarkers with the best ability to discriminate between individuals with different mean concentrations. Adjustment for urinary dilution has great influence on the fraction of the total variance attributed to between individual variation among urine samples with low lead concentrations, but only a small influence on samples with high lead concentrations. This suggests a difference in excretion. The association between end-stage renal disease and low-level lead exposure, as assessed through prospective erythrocyte samples, gives reason for concern, although further studies are needed to determine causality. A cadmium-associated increase in albumin is reversible after a substantial reduction in exposure, but this is not the case for the observed tubular effects. The tubular kidney effects of cadmium might be modified by the MT1A rs11076161 polymorphism.

Objectives: To estimate concentration-response relationships for particulate matter (PM) and black carbon (BC) in relation to mortality in cohorts from three Swedish cities with comparatively low pollutant levels.

Setting: Cohorts from Gothenburg, Stockholm and Umeå, Sweden.

Design: High-resolution dispersion models were used to estimate annual mean concentrations of PM with aerodynamic diameter ≤10 μm (PM10) and ≤2.5 μm (PM2.5), and BC, at individual addresses during each year of follow-up, 1990-2011. Moving averages were calculated for the time windows 1-5 years (lag1-5) and 6-10 years (lag6-10) preceding the outcome. Cause-specific mortality data were obtained from the national cause of death registry. Cohort-specific HRs were estimated using Cox regression models and then meta-analysed including a random effect of cohort.

Participants: During the study period, 7 340 cases of natural mortality, 2 755 cases of cardiovascular disease (CVD) mortality and 817 cases of respiratory and lung cancer mortality were observed among in total 68 679 individuals and 689 813 person-years of follow-up.

Results: Both PM10 (range: 6.3-41.9 μg/m 3) and BC (range: 0.2-6.8 μg/m 3) were associated with natural mortality showing 17% (95% CI 6% to 31%) and 9% (95% CI 0% to 18%) increased risks per 10 μg/m 3 and 1 μg/m 3 of lag1-5 exposure, respectively. For PM2.5 (range: 4.0-22.4 μg/m 3), the estimated increase was 13% per 5 μg/m 3, but less precise (95% CI -9% to 40%). Estimates for CVD mortality appeared higher for both PM10 and PM2.5. No association was observed with respiratory mortality.

Conclusion: The results support an effect of long-term air pollution on natural mortality and mortality in CVD with high relative risks also at low exposure levels. These findings are relevant for future decisions concerning air quality policies.

This study aims to estimate the mortality risk associated with air pollution in a Swedish cohort with relatively low exposure. Air pollution models were used to estimate annual mean concentrations of particulate matter with aerodynamic diameter ≤ 2.5 µm (PM2.5 ), primary emitted car-bonaceous particles (BC/pOC), sea salt, chemically formed particles grouped as secondary inorganic and organic aerosols (SIA and SOA) as well as ozone (O3 ) and nitrogen dioxide (NO2 ). The exposure, as a moving average was calculated based on home address for the time windows 1 year (lag 1), 1–5 years (lag 1–5) and 1–10 years (lag 1–10) preceding the death. During the study period, 1151 cases of natural mortality, 253 cases of cardiovascular disease (CVD) mortality and 113 cases of respiratory and lung cancer mortality were observed during 369,394 person-years of follow-up. Increased natural mortality was observed in association with NO2 (3% [95% CI −8–14%] per IQR) and PM2.5 (2% [95% CI −5–9%] for an IQR increase) and its components, except for SOA where a decreased risk was observed. Higher risk increases were observed for CVD mortality (e.g., 18% [95% CI 1–39%] per IQR for NO2 ). These findings at low exposure levels are relevant for future decisions concerning air quality policies.

This study aims to use dispersion-modeled concentrations of nitrogen oxides (NOx) and black carbon (BC) to estimate bicyclist exposures along a network of roads and bicycle paths. Such modeling was also performed in a scenario with increased bicycling. Accumulated concentrations between home and work were thereafter calculated for both bicyclists and drivers of cars. A transport model was used to estimate traffic volumes and current commuting preferences in Stockholm County. The study used individuals' home and work addresses, their age, sex, and an empirical model estimate of their expected physical capacity in order to establish realistic bicycle travel distances. If car commuters with estimated physical capacity to bicycle to their workplace within 30 min changed their mode of transport to bicycle, >110,000 additional bicyclists would be achieved. Time-weighted mean concentrations along paths were, among current bicyclists, reduced from 25.8 to 24.2 mu g/m(3) for NOx and 1.14 to 1.08 mu g/m(3) for BC. Among the additional bicyclists, the yearly mean NOx dose from commuting increased from 0.08 to 1.03 mu g/m(3). This would be expected to yearly cause 0.10 fewer deaths for current bicycling levels and 1.7 more deaths for additional bicycling. This increased air pollution impact is much smaller than the decrease in the total population.

AIMS: To estimate the overall health impact of transferring commuting trips from car to bicycle.

METHODS: In this study registry information on the location of home and work for residents in Stockholm County was used to obtain the shortest travel route on a network of bicycle paths and roads. Current modes of travel to work were based on travel survey data. The relation between duration of cycling and distance cycled was established as a basis for selecting the number of individuals that normally would drive a car to work, but have a distance to work that they could bicycle within 30 minutes. The change in traffic flows was estimated by a transport model (LuTrans) and effects on road traffic injuries and fatalities were estimated by using national hospital injury data. Effects on air pollution concentrations were modelled using dispersion models.

RESULTS: Within the scenario, 111,000 commuters would shift from car to bicycle. On average the increased physical activity reduced the one-year mortality risk by 12% among the additional bicyclists. Including the number of years lost due to morbidity, the total number of disability adjusted life-years gained was 696. The amount of disability adjusted life-years gained in the general population due to reduced air pollution exposure was 471. The number of disability adjusted life-years lost by traffic injuries was 176. Also including air pollution effects among bicyclists, the net benefit was 939 disability adjusted life-years per year.

CONCLUSIONS: Large health benefits were estimated by transferring commuting by car to bicycle.

AIMS: To estimate the association between long-term exposure to particulate air pollution and sub-clinical atherosclerosis based on the existence of plaque and the carotid intima-media thickness (cIMT).

METHODS: Visualization of asymptomatic atherosclerotic disease for optimum cardiovascular prevention (VIPVIZA) is a randomised controlled trial integrated within the Västerbotten Intervention Programme, an ongoing population-based cardiovascular disease (CVD) prevention programme in northern Sweden. Individuals aged 40, 50, or 60 years with one or more conventional CVD risk factors in Umeå municipality were eligible to participate. The 1425 participants underwent an ultrasound assessment of cIMT and plaque formation during the period 2013-2016 and at 3-year follow-up. Source-specific annual mean concentrations of particulate matter with aerodynamic diameter ≤10 μm (PM10) and ≤2.5 μm (PM2.5), and black carbon (BC) at the individual's residential address were modelled for the calendar years 1990, 2001 and 2011. Poisson regression was used to estimate prevalence ratios for presence of carotid artery plaques, and linear regression for cIMT.

RESULTS: The plaque prevalence was 43% at baseline and 47% at follow-up. An interquartile range (IQR) increase in PM10 (range in year 2011: 7.1-13.5 μg/m³) was associated with a prevalence ratio at baseline ultrasound of 1.11 (95% CI 0.99-1.25), 1.08 (95% CI 0.99-1.17), and 1.00 (95% CI 0.93-1.08) for lag 23, 12 and 2 years, and at follow-up 1.04 (95% CI 0.95-1.14), 1.08 (95% CI 1.00-1.16), and 1.01 (95% CI 0.95-1.08). Similar prevalence ratios per IQR were found for PM2.5 and BC, but with somewhat lower precision for the later. Particle concentrations were however not associated with the progression of plaque. No cross-sectional or longitudinal associations of change were found for cIMT.

CONCLUSIONS: This study of individuals with low/moderate risk for CVD give some additional support for an effect of long-term air pollution in early subclinical atherosclerosis.

Several studies have investigated the relation between bone mass density and cadmium exposure, but only few studies have been performed on fractures and biomarkers of cadmium. This study analyzed the association between hip fracture risk and cadmium in erythrocytes (Ery-Cd). Prospective samples from the Northern Sweden Health and Disease Study's biobank were used for 109 individuals who later in life had sustained a low-trauma hip fracture, matched with two controls of the same age and gender. The mean concentration of Ery-Cd (±SD) in case samples was 1.3 ± 1.4 versus 0.9 ± 1.0 μg/L in controls. The odds ratio (OR) was 1.63 [95 % confidence interval (CI) 1.10-2.42] for suffering a hip fracture for each microgram per liter increase in Ery-Cd. However, when taking smoking into consideration (never, former, or current), neither Ery-Cd nor smoking showed a statistically significant increase in fracture risk. Using multiple conditional logistic regression with BMI, height, and smoking, the estimated OR for a 1-μg/L increase in Ery-Cd was 1.52 (95 % CI 0.77-2.97). Subgroup analysis showed an increased fracture risk among women (OR = 1.94, 95 % CI 1.18-3.20, for a 1 μg/L increase), which also remained in the multiple analysis (OR = 3.33, 95 % CI 1.29-8.56). This study shows that fracture risk is associated with Ery-Cd. It is, however, not possible to draw firm conclusions on whether cadmium is the causal factor or whether other smoking-related factors cause this association. Subgroup analysis shows that cadmium is a risk factor for hip fracture among women.

Objectives: The study aims to make use of individual data to estimate the impact on premature mortality due to both existing commuter bicycling and the potential impact due to increased physical activity through shifting transport mode from car commuting to bicycling.

Methods: Using registry data on home and work addresses for the population of Stockholm County the shortest bicycling route on a network of bicycle paths and roads was retrieved. Travel survey data were used to establish current modes of commuting. The relation between duration of bicycling and distance bicycled within the general population in 2015 was established as a basis for identifying individuals that currently drive a car to work but were estimated to have the physical capacity to bicycle to work within 30 min. Within this mode-shift scenario from car-to-bike the duration of bicycling per week was estimated, both among current and potential bicycle commuters. The health impact assessment (HIA) on mortality due to bicycle commuting physical activity was estimated using the same relative risk as within the WHO Health Economic Assessment Tool.

Results: The current number of bicycle commuters were 53 000, and the scenario estimated an additional 111 000. Their mean bicycle distances were 4.5 and 3.4 km, respectively. On average these respective amounts of physical activity reduced the yearly mortality by 16% and 12%, resulting in 11.3 and 16.2 fewer preterm deaths per year.

Conclusion: The HIA of transferring commuting by car to bicycle estimated large health benefits due to increased physical activity.

Diabetes mellitus (DM) incidence have been assessed in connection with air pollution exposure in several studies; however, few have investigated associations with source-specific local emissions. This study aims to estimate the risk of DM incidence associated with source-specific air pollution in a Swedish cohort with relatively low exposure. Individuals in the Västerbotten intervention programme cohort were followed until either a DM diagnosis or initiation of treatment with glucose-lowering medication occurred. Dispersion models with high spatial resolution were used to estimate annual mean concentrations of particulate matter (PM) with aerodynamic diameter ≤10 μm (PM₁₀) and ≤2.5 μm (PM_2.5) at individual addresses. Hazard ratios were estimated using Cox regression models in relation to moving averages 1-5 years preceding the outcome. During the study period, 1479 incident cases of DM were observed during 261,703 person-years of follow-up. Increased incidence of DM was observed in association with PM₁₀ (4% [95% CI: -54-137%] per 10 μg/m³), PM₁₀-traffic (2% [95% CI: -6-11%] per 1 μg/m³) and PM_2.5-exhaust (11% [95% CI: -39-103%] per 1 μg/m³). A negative association was found for both PM_2.5 (-18% [95% CI: -99-66%] per 5 μg/m³), but only in the 2nd exposure tertile (-10% [95% CI: -25-9%] compared to the first tertile), and PM_2.5-woodburning (-30% [95% CI: -49-4%] per 1 μg/m³). In two-pollutant models including PM_2.5-woodburning, there was an 11% [95% CI: -11-38%], 6% [95% CI: -16-34%], 13% [95% CI: -7-36%] and 17% [95% CI: 4-41%] higher risk in the 3rd tertile of PM₁₀, PM_2.5, PM₁₀-traffic and PM_2.5-exhaust, respectively, compared to the 1st. Although the results lacked in precision they are generally in line with the current evidence detailing particulate matter air pollution from traffic as an environmental risk factor for DM.

BACKGROUND: Cadmium (Cd), lead (Pb), and mercury (Hg) cause toxicological renal effects, but the clinical relevance at low-level exposures in general populations is unclear. The objective of this study is to assess the risk of developing end-stage renal disease in relation to Cd, Pb, and Hg exposure.

METHODS: A total of 118 cases who later in life developed end-stage renal disease, and 378 matched (sex, age, area, and time of blood sampling) referents were identified among participants in two population-based prospective cohorts (130,000 individuals). Cd, Pb, and Hg concentrations were determined in prospectively collected samples.

RESULTS: Erythrocyte lead was associated with an increased risk of developing end-stage renal disease (mean in cases 76 μg/L; odds ratio (OR) 1.54 for an interquartile range increase, 95% confidence interval (CI) 1.18-2.00), while erythrocyte mercury was negatively associated (2.4 μg/L; OR 0.75 for an interquartile range increase, CI 0.56-0.99). For erythrocyte cadmium, the OR of developing end-stage renal disease was 1.15 for an interquartile range increase (CI 0.99-1.34; mean Ery-Cd among cases: 1.3 μg/L). The associations for erythrocyte lead and erythrocyte mercury, but not for erythrocyte cadmium, remained after adjusting for the other two metals, smoking, BMI, diabetes, and hypertension. Gender-specific analyses showed that men carried almost all of the erythrocyte lead and erythrocyte cadmium associated risks.

CONCLUSIONS: Erythrocyte lead is associated with end-stage renal disease but further studies are needed to evaluate causality. Gender-specific analyses suggest potential differences in susceptibility or in exposure biomarker reliability.

OBJECTIVES: Exposure to trichloramine (NCl(3)) in indoor swimming-pool environments is known to cause mucous membrane irritation, but if it gives rise to changes in lung function or asthma in adults is not known. (1) We determined lung function in volunteers before and after exposure to indoor pool environments. (2) We studied the occurrence of respiratory symptoms and asthma in a cohort of pool workers.

DESIGN/METHODS/PARTICIPANTS: (1) We studied two groups of volunteers, 37 previously non-exposed healthy persons and 14 pool workers, who performed exercise for 2 h in an indoor pool environment. NCl(3) in air was measured during pool exposures and in 10 other pool environments. Filtered air exposures were used as controls. Lung function and biomarkers of pulmonary epithelial integrity were measured before and after exposure. (2) We mailed a questionnaire to 1741 persons who indicated in the Swedish census 1990 that they worked at indoor swimming-pools.

RESULTS: (1) In previously non-exposed volunteers, statistically significant decreases in FEV(1) (forced expiratory volume) and FEV(%) (p=0.01 and 0.05, respectively) were found after exposure to pool air (0.23 mg/m(3) of NCl(3)). In pool workers, a statistically significant decrease in FEV(%) (p=0.003) was seen (but no significant change of FEV(1))(.) In the 10 other pool environments the median NCl(3) concentration was 0.18 mg/m(3). (2) Our nested case/control study in pool workers found an OR for asthma of 2.31 (95% CI 0.79 to 6.74) among those with the highest exposure. Exposure-related acute mucous membrane and respiratory symptoms were also found.

CONCLUSIONS: This is the first study in adults showing statistically significant decreases in lung function after exposure to NCl(3). An increased OR for asthma among highly exposed pool workers did not reach statistical significance, but the combined evidence supports the notion that current workroom exposures may contribute to asthma development. Further research on sensitive groups is warranted.

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: Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer (BC). Little is known about whether exposure to air pollution influences BC in the general population.

OBJECTIVE: To evaluate the association between long-term exposure to ambient air pollution and BC incidence.

DESIGN, SETTING, AND PARTICIPANTS: We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO2 and NOx), particulate matter (PM) with diameter <10μm (PM10), <2.5μm (PM2.5), between 2.5 and 10μm (PM2.5-10), PM2.5absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the European Study of Cohorts for Air Pollution Effects project.

OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for BC incidence.

RESULTS AND LIMITATIONS: During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC risk. The summary HRs associated with a 10-μg/m(3) increase in NO2 and 5-μg/m(3) increase in PM2.5 were 0.98 (95% confidence interval [CI] 0.89-1.08) and 0.86 (95% CI 0.63-1.18), respectively. Limitations include the lack of information about lifetime exposure.

CONCLUSIONS: There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC.

PATIENT SUMMARY: We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at place of residence and bladder cancer risk.

BACKGROUND: Ambient air pollution is suspected to cause lung cancer. We aimed to assess the association between long-term exposure to ambient air pollution and lung cancer incidence in European populations.

METHODS: This prospective analysis of data obtained by the European Study of Cohorts for Air Pollution Effects used data from 17 cohort studies based in nine European countries. Baseline addresses were geocoded and we assessed air pollution by land-use regression models for particulate matter (PM) with diameter of less than 10 μm (PM10), less than 2·5 μm (PM2·5), and between 2·5 and 10 μm (PMcoarse), soot (PM2·5absorbance), nitrogen oxides, and two traffic indicators. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses.

FINDINGS: The 312 944 cohort members contributed 4 013 131 person-years at risk. During follow-up (mean 12·8 years), 2095 incident lung cancer cases were diagnosed. The meta-analyses showed a statistically significant association between risk for lung cancer and PM10 (hazard ratio [HR] 1·22 [95% CI 1·03-1·45] per 10 μg/m(3)). For PM2·5 the HR was 1·18 (0·96-1·46) per 5 μg/m(3). The same increments of PM10 and PM2·5 were associated with HRs for adenocarcinomas of the lung of 1·51 (1·10-2·08) and 1·55 (1·05-2·29), respectively. An increase in road traffic of 4000 vehicle-km per day within 100 m of the residence was associated with an HR for lung cancer of 1·09 (0·99-1·21). The results showed no association between lung cancer and nitrogen oxides concentration (HR 1·01 [0·95-1·07] per 20 μg/m(3)) or traffic intensity on the nearest street (HR 1·00 [0·97-1·04] per 5000 vehicles per day).

INTERPRETATION: Particulate matter air pollution contributes to lung cancer incidence in Europe.

FUNDING: European Community's Seventh Framework Programme.

Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutants, although not consistently. It was the aim to investigate possible associations between outdoor air pollution at the residence and the incidence of kidney parenchyma cancer in the general population. We used data from 14 European cohorts from the ESCAPE study. We geocoded and assessed air pollution concentrations at baseline addresses by land-use regression models for particulate matter (PM10 , PM2.5 , PMcoarse , PM2.5 absorbance (soot)) and nitrogen oxides (NO2 , NOx ), and collected data on traffic. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses to calculate summary hazard ratios (HRs). The 289,002 cohort members contributed 4,111,908 person-years at risk. During follow-up (mean 14.2 years) 697 incident cancers of the kidney parenchyma were diagnosed. The meta-analyses showed higher HRs in association with higher PM concentration, e.g. HR=1.57 (95%CI: 0.81-3.01) per 5μg/m(3) PM2.5 and HR=1.36 (95%CI: 0.84-2.19) per 10(-5) m(-1) PM2.5 absorbance, albeit never statistically significant. The HRs in association with nitrogen oxides and traffic density on the nearest street were slightly above one. Sensitivity analyses among participants who did not change residence during follow-up showed stronger associations, but none were statistically significant. This study provides suggestive evidence that exposure to outdoor PM at the residence may be associated with higher risk for kidney parenchyma cancer; the results should be interpreted cautiously as associations may be due to chance.

BACKGROUND: Promotion of active commuting provides substantial health and environmental benefits by influencing air pollution, physical activity, accidents, and noise. However, studies evaluating intervention and policies on a mode shift from motorized transport to cycling have estimated health impacts with varying validity and precision.

OBJECTIVE: To review and discuss the estimation of air pollution exposure and its impacts in health impact assessment studies of a shift in transport from cars to bicycles in order to guide future assessments.

METHODS: A systematic database search of PubMed was done primarily for articles published from January 2000 to May 2016 according to PRISMA guidelines.

RESULTS: We identified 18 studies of health impact assessment of change in transport mode. Most studies investigated future hypothetical scenarios of increased cycling. The impact on the general population was estimated using a comparative risk assessment approach in the majority of these studies, whereas some used previously published cost estimates. Air pollution exposure during cycling was estimated based on the ventilation rate, the pollutant concentration, and the trip duration. Most studies employed exposure-response functions from studies comparing background levels of fine particles between cities to estimate the health impacts of local traffic emissions. The effect of air pollution associated with increased cycling contributed small health benefits for the general population, and also only slightly increased risks associated with fine particle exposure among those who shifted to cycling. However, studies calculating health impacts based on exposure-response functions for ozone, black carbon or nitrogen oxides found larger effects attributed to changes in air pollution exposure.

CONCLUSION: A large discrepancy between studies was observed due to different health impact assessment approaches, different assumptions for calculation of inhaled dose and different selection of dose-response functions. This kind of assessments would improve from more holistic approaches using more specific exposure-response functions.

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.