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There is highly suggestive evidence for an effect of air pollution exposure on dementia-related outcomes, but evidence is not yet present to clearly pinpoint which pollutants are the probable causal agents. The aims of this study was to assess the longitudinal association between exposures of fine ambient particulate matter (PM2.5) from residential wood burning, and vehicle exhaust, with dementia. We used data from the Betula study, a longitudinal study of dementia in Umeå, Northern Sweden. The study size was 1 806 and the participants were followed from study entry (1993-1995) to 2010. Modelled levels of source-specific fine particulate matter at the residential address were combined with information on wood stoves or wood boilers, and with validated data on dementia diagnosis and individual-level characteristics from the Betula study. Cox proportional hazards models were used to estimate Hazard Ratios (HRs) and their 95% CIs for dementia incidence (vascular dementia and Alzheimer's disease), adjusted for individual-level characteristics. The emission of PM2.5 from local residential wood burning was associated with dementia incidence with a hazard ratio of 1.55 for a 1 μg/m3 increase in PM2.5 (95% Confidence Interval (CI): 1.00-2.41, p-value 0.05). Study participants with an address in an area with the highest quartile of PM2.5 from residential wood burning and who also had a wood-burning stove were more likely to develop dementia than those in the lower three quartiles without a wood-burning stove with hazard ratios of 1.74 (CI: 1.10-2.75, p-value 0.018). Particulate matter from traffic exhaust seemed to be associated with dementia incidence with hazard ratios of 1.66, (CI: 1.16-2.39), p-value 0.006, and 1.41 (CI: 0.97-2.23), p-value 0.07, in the third and fourth quartiles, respectively. If the associations we observed are causal, then air pollution from residential wood burning, and air pollution from traffic, might be independent important risk factors for dementia.

Evidence of air pollution exposure, namely, ambient particulate matter (PM), during pregnancy and an increased risk of autism in children is growing; however, the unique PM sources that contribute to this association are currently unknown. The aim of the present study was to investigate local, source-specific ambient PM exposure during pregnancy and its associations with childhood autism, specifically, and autism spectrum disorders (ASD) as a group. A cohort of 40,245 singleton births from 2000 to 2009 in Scania, Sweden, was combined with data on locally emitted PM with an aerodynamic diameter < 2.5 µm (PM 2.5 ). A flat, two-dimensional dispersion model was used to assess local PM 2.5 concentrations (all-source PM 2.5 , small-scale residential heating- mainly wood burning, tailpipe exhaust, and vehicle wear-and-tear) at the mother’s residential address during pregnancy. Associations were analyzed using binary logistic regression. Exposure to local PM 2.5 during pregnancy from each of the investigated sources was associated with childhood autism in the fully adjusted models. For ASD, similar, but less pronounced, associations were found. The results add to existing evidence that exposure to air pollution during pregnancy may be associated with an increased risk of childhood autism. Further, these findings suggest that locally produced emissions from both residential wood burning and road traffic-related sources (tailpipe exhaust and vehicle wear-and-tear) contribute to this association.

Background Air pollution is one of the leading causes of mortality and morbidity worldwide. Experimental studies, and a few epidemiological studies, suggest that air pollution may cause acute exacerbation of psychiatric disorders, and even increase the rate of suicide attempts, but epidemiological studies on air pollution in association with psychiatric disorders are still few. Our aim was to investigate associations between daily fluctuations in air pollution concentrations and the daily number of visits to a psychiatric emergency unit. Methods Data from Sahlgrenska University Hospital, Gothenburg, Sweden, on the daily number of visits to the Psychiatric emergency unit were combined with daily data on monitored concentrations of respirable particulate matter(PM 10 ), ozone(O 3 ), nitrogen dioxides(NO 2 ) and temperature between 1st July 2012 and 31st December 2016. We used a case-crossover design to analyze data with conditional Poisson regression models allowing for over-dispersion. We stratified data on season. Results Visits increased with increasing PM 10 levels during the warmer season (April to September) in both single-pollutant and two-pollutant models. For example, an increase of 3.6% (95% Confidence Interval, CI, 0.4–7.0%) was observed with a 10 μg/m3 increase in PM 10 adjusted for NO 2 . In the three-pollutant models (adjusting for NO 2 and O 3 simultaneously) the increase was 3.3% (95% CI, −0.2-6.9). There were no clear associations between the outcome and NO 2 , O 3 , or PM 10 during the colder season (October to March). Conclusions Ambient air particle concentrations were associated with the number of visits to the Psychiatric emergency unit in the warm season. The results were only borderline statistically significant in the fully adjusted (three-pollutant) models in this small study. The observation could be interpreted as indicative of air pollution as either exacerbating an underlying psychiatric disorder, or increasing mental distress, even in areas with comparatively low levels of air pollution. In combination with the severe impact of psychiatric disorders and mental distress on society and individuals, our results are a strong warrant for future research in this area.

Background Alzheimer’s disease (AD) and other dementias currently represent the fifth most common cause of death in the world, according to the World Health Organization, with a projected future increase as the proportion of the elderly in the population is growing. Air pollution has emerged as a plausible risk factor for AD, but studies estimating dementia cases attributable to exposure to fine particulate matter (PM 2.5 ) air pollution and resulting monetary estimates are lacking. Methods We used data on average population-weighted exposure to ambient PM 2.5 for the entire population of Sweden above 30 years of age. To estimate the annual number of dementia cases attributable to air pollution in the Swedish population above 60 years of age, we used the latest concentration response functions (CRF) between PM 2.5 exposure and dementia incidence, based on ten longitudinal cohort studies, for the population above 60 years of age. To estimate the monetary burden of attributable cases, we calculated total costs related to dementia, including direct and indirect lifetime costs and intangible costs by including quality-adjusted life years (QALYs) lost. Two different monetary valuations of QALYs in Sweden were used to estimate the monetary value of reduced quality-of-life from two different payer perspectives. Results The annual number of dementia cases attributable to PM 2.5 exposure was estimated to be 820, which represents 5% of the annual dementia cases in Sweden. Direct and indirect lifetime average cost per dementia case was estimated to correspond € 213,000. A reduction of PM 2.5 by 1 μg/m 3 was estimated to yield 101 fewer cases of dementia incidences annually, resulting in an estimated monetary benefit ranging up to 0.01% of the Swedish GDP in 2019. Conclusion This study estimated that 5% of annual dementia cases could be attributed to PM 2.5 exposure, and that the resulting monetary burden is substantial. These findings suggest the need to consider airborne toxic pollutants associated with dementia incidence in public health policy decisions.

Background Air pollution has been linked to breast cancer risk, but previous studies have seldom considered specific exposure windows, like pregnancy. During pregnancy the breast undergoes substantial changes and exposures may have a stronger impact than if they occurred during other time periods. This study aims to identify associations between ambient air pollution exposure during pregnancy and risk of early-onset breast cancer. Methods Using nationwide data from Swedish registers, we constructed a cohort consisting of all cancer-free women in Sweden giving birth to their first child between 1991 and 2015. Residential exposure to nitrogen dioxide (NO 2 ), particulate matter < 10 μm (PM 10 ) and < 2.5 μm (PM 2.5 ) were modelled based on air pollution concentrations from 2019. Particulate matter between 2.5 and 10 μm (PM coarse ) was calculated separately. Detailed data on residential addresses (including exact moving dates) were available for the entire study period, allowing for spatial variation in the exposure dataset. Mean air pollution levels were assessed at first pregnancy, last pregnancy, 35 years of age, and 2 years after the last delivery. Associations were evaluated using Cox proportional hazards regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Results Among 1,019,076 women, 12,085 (1.2%) were diagnosed with breast cancer and 65.2% moved at least once between their first pregnancy and two years after their last delivery. All exposures during pregnancy periods were positively associated with breast cancer, with the highest HR observed for exposure to PM coarse during the last pregnancy (HR PMcoarse  = 1.12 (95% CI = 1.04, 1.20) per 5 μg/m 3 increase). The lowest HR were for NO 2 levels estimated at 35 years of age, regardless of pregnancy status (HR NO2  = 1.03 (95% CI = 0.99, 1.06) per 10 μg/m 3 increase). In analyses differentiating between invasive breast cancer and ductal carcinoma in situ, only invasive breast cancer was associated with air pollution exposure. Conclusions In this cohort study, air pollution exposure was consistently associated with increased risk of early-onset breast cancer.

Black carbon (BC) is an air pollutant of growing concern due to its adverse impacts on health and climate. Growing evidence suggests that BC could have a number of negative impacts on morbidity and mortality, but more evidence is needed. The objectives of this study are to quantify any associations between BC exposure and cause-specific (cardiovascular and cancer) mortality outcomes. Using the Malmö Diet and Cancer Cohort linked with a high-resolution dispersion model, we examined the association between long-term exposure to locally emitted BC, nitrogen oxides (NO ) and fine particulate matter (PM ) with cardiovascular and cancer mortality. In fully adjusted models, BC exposure was consistently associated with cardiovascular mortality (HR 1.15 [1.06-1.26] per IQR increase), an association that was stronger and more robust than for PM2.5 or NO . This association was present across all models, all time periods and both sets of exposure intervals. This association was stronger than with the other pollutants. Less clear association was found between any pollutant and cancer mortality. This study shows associations between BC exposure and especially cardiovascular mortality, consistent with international evidence showing similar impacts. For cancer mortality, there were tendencies of an association with BC but less clear than for cardiovascular mortality. These findings suggest a unique role of BC in air pollution-related cardiovascular mortality and support the need for action on mitigation of air pollution in general and BC in particular.

Introduction Air pollution is associated with increased risk of cardiovascular disease, possibly through chronic systemic inflammation that promotes the progression of atherosclerosis and the risk of cardiovascular events. This study aimed to investigate the associations between air pollution and established biomarkers of inflammation and cardiovascular disease. Methods The Cardiovascular Subcohort of the Malmö Diet and Cancer cohort includes 6103 participants from the general population of Malmö, Sweden. The participants were recruited 1991–1994. Annual mean residential exposure to particulate matter < 2.5 and < 10 μm (PM 2.5 and PM 10 ), and nitrogen oxides (NO x ) at year of recruitment were assigned from dispersion models. Blood samples collected at recruitment, including blood cell counts, and biomarkers (lymphocyte- and neutrophil counts, C-reactive protein (CRP), soluble urokinase-type plasminogen activator receptor (suPAR), lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ), ceruloplasmin, orosomucoid, haptoglobin, complement-C3, and alpha-1-antitrypsin) were analyzed. Multiple linear regression models were used to investigate the cross-sectional associations between air pollutants and biomarkers. Results The mean annual exposure levels in the cohort were only slightly or moderately above the new WHO guidelines of 5 μg/m 3 PM 2.5 (10.5 μg/m 3 PM 2.5 ). Residential PM 2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA 2 and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with PM 10 . There were no associations between air pollutants and suPAR, leukocyte counts or CRP. The associations between particles and biomarkers were still significant after removing outliers and adjustment for CRP levels. The associations were more prominent in smokers. Conclusion Long-term residential exposure to moderate levels of particulate air pollution was associated with several biomarkers of inflammation and cardiovascular disease. This supports inflammation as a mechanism behind the association between air pollution and cardiovascular disease.

Background Few studies have assessed the mental health of principals, or studied associations with both organizational and social work environment factors and occupational balance. The purpose of the present study was therefore to investigate associations between supporting and demanding organizational and social work environment factors, occupational balance and stress symptoms in principals. Methods A total of 4309 surveys (2316 from the first round, 1992 from the second round), representing 2781 Swedish principals who had responded to at least one of two surveys, were included in the present study. The surveys include questions about socio-demographic factors, occupational balance, overtime work, and supporting and demanding organizational and social work environment factors, as well as questions about personal stress and exhaustion. Generalized Estimating Equations (GEE) models were used to specify a repeated measures model with a dichotomous outcome (binary logistic regression) and multiple independent factors. Data from two surveys were combined, taking into account dependent observations due to the fact that many study subjects had participated in both surveys. Results Associations were found between occupational balance (Q1: OR 2.52, 95% CI 2.03–3.15; Q2: OR 4.95, 95% CI 3.86–6.35; Q3: OR 9.29, 95% CI 6.99–12.34), overtime work (Once a week: OR 1.51, 95% CI 1.10–2.08; Sometimes a week: OR 1.31, 95% CI 1.03–1.66), supportive private life (OR 1.50, 95% CI 1.36–1.66), supportive colleagues at the leadership level (OR 1.24, 95% CI 1.14–1.36), supportive management (OR 1.17, 95% CI 1.07–1.28) and no or negligible stress symptoms. In addition, role demands (OR 0.72, 95% CI 0.63–0.83), having a container function (OR 0.72, 95% CI 0.64–0.82), collaboration with employees (OR 0.77, 95% CI 0.66–0.89), role conflicts (OR 0.75, 95% CI 0.66–0.89) and having a buffer function (OR 0.86, 95% CI 0.77–0.97) were associated with lower likelihood to rate no or negligible stress symptoms. Conclusions The occupational balance of principals is strongly associated with no or negligible stress symptoms, and thus is a promising venue for promoting well-being. Improvements should be made to several factors in the organizational and social work environments to improve principals’ chances of having occupational balance, and therefore better mental health.

Air pollution is increasingly discussed as a risk factor for dementia, but the biological mechanisms are not yet fully understood. Biological markers like telomere length are relevant to study with air pollution, as they are associated with aging and dementia. The study aimed to investigate the relationship between source-specific air pollution exposure and telomere length in a low-level air pollution area, and whether this potential relationship depended on future dementia status. The data originated from the Betula study in Northern Sweden, where 509 participants recruited between 1988 and 1995 were included to investigate the association between annual mean air pollution concentrations at the participants’ residences and relative leukocyte telomere length using a linear regression model. No association was observed between air pollution and telomere length, with regression slope estimates close to zero and p-values > 0.10 (e.g. PM 2.5 _total: β = 0.01 (-0.011, 0.025) and BC_total: β = 0.03 (95% CI: -0.046, 0.114). There were indications of a positive association between longer telomere length and higher exposure to air pollution among individuals later diagnosed with dementia ( N  = 74), but these findings were not conclusive (p-values > 0.10) (PM2.5_total: β = 0.03, p-value = 0.12; BC_total: β = 0.11, p-value = 0.17). Although not statistically significant, our findings contribute to the evidence from low-exposure settings, and it is important to report these types of findings for a balanced understanding of potential health effects.

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 PM 10 and PM 2.5 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 PM 10 and PM 2.5 lag 1–5 years was 9.50 µg/m 3 and 5.61 µg/m 3 , respectively. Increased risks were identified for PM 10 -Traffic (35% [95% CI 0–82%]) and PM 2.5 -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 PM 2.5 -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 PM 10 -Traffic and PM 2.5 -Exhaust, and conversely, a negative association for PM 2.5 -Wood burning, no clear exposure–response relationships were evident.