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BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent.

OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women.

METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2.5μm, ≤10μm, and 2.5–10μm in diameter (PM2.5, PM10, and PMcoarse, respectively); PM2.5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.

RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2.5 {hazard ratio (HR)=1.08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m(3)}, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m(3)], PMcoarse[1.20 (95% CI: 0.96, 1.49 per 5 μg/m(3)], and NO(2) [1.02 (95% CI: 0.98, 1.07 per 10 μg/m(3)], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m(3), p=0.04].

CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women.

Growing evidence indicates that air pollution can negatively impact cognitive functions. The olfactory system is interesting in this context as it is directly exposed to pollutants and also associated with cognitive functions. The aim of this study was to investigate long- and short-term PM_2.5 exposure in association with olfactory functions. Scores from odor tests were obtained from the Betula project - a longitudinal cohort study. Estimates of annual mean PM_2.5 concentrations at the participants' residential address were obtained from a dispersion-model. Daily mean PM_2.5 concentrations were obtained from a measuring station close to the test location. We found a positive association between long-term PM_2.5 exposure and odor identification, i.e. exposure was associated with a better ability to identify odors. We also found an interaction effect between PM_2.5 and age on odor identification. We found no associations between any PM_2.5 exposure and odor detection or between short-term PM_2.5 exposure and olfactory functions.

Background: There is growing evidence for a negative impact of traffic-related air pollution on risk of dementia. However, the contribution of noise exposure to this association has been rarely examined.

Objective: We aimed to investigate the individual and combined effect of noise and air pollution on risk of dementia.

Methods: Data on dementia incidence over a 15 year period was obtained from the Betula project, a longitudinal study on health and ageing. Estimates of annual mean levels of nitrogen oxides (NOx) at the participants’ residential address were obtained using a land-use regression model. Modelled data provided road traffic noise levels (Leq. 24 h) at the participants’ residential address at baseline. Cox proportional hazard regression was used to calculate hazard ratios (HR).

Results: Of 1721 participants at baseline, 302 developed dementia during the follow up period. Exposure to noise levels (Leq. 24 h) > 55 dB had no significant effect on dementia risk (HR 0.95; CI: 0.57, 1.57). Residing in the two highest quartiles of NOx exposure was associated with an increased risk of dementia. The risk associated with NOx was not modified by adjusting for noise. Moreover, we found no significant interaction effects between NOx and road traffic noise on dementia risk.

Conclusion: We found no evidence that exposure to road traffic noise, either independently or in combination with traffic air pollution, was associated with risk of dementia in our study area. Our results suggest that pollution should be considered the main component in the association between traffic related exposures and dementia.

Background: Growing evidence show that long term exposure to air pollution increases the risk of dementia.

Objective: The aim of this study was to investigate associations between PM_2.5 exposure and dementia in a low exposure area, and to investigate the role of olfaction and the APOE ε4 allele in these associations.

Methods: Data were drawn from the Betula project, a longitudinal study on aging, memory, and dementia in Sweden. Odor identification ability was assessed using the Scandinavian Odor Identification Test (SOIT). Annual mean PM_2.5 concentrations were obtained from a dispersion-model and matched at the participants’ residential address. Proportional hazard regression was used to calculate hazard ratios.

Results: Of 1,846 participants, 348 developed dementia during the 21-year follow-up period. The average annual mean PM2.5 exposure at baseline was 6.77 µg/m³, which is 1.77 µg/m³ above the WHO definition of clean air. In a fully adjusted model (adjusted for age, sex, APOE, SOIT, cardiovascular diseases and risk factors, and education) each 1 µg/m³ difference in annual mean PM_2.5-concentration was associated with a hazard ratio of 1.23 for dementia (95% CI: 1.01–1.50). Analyses stratified by APOE status (ε4 carriers versus non-carriers), and odor identification ability (high versus low), showed associations only for ε4 carriers, and for low performance on odor identification ability.

Conclusion: PM_2.5 was associated with an increased risk of dementia in this low pollution setting. The associations between PM_2.5 and dementia seemed stronger in APOE carriers and those with below average odor identification ability.

A high turnover among principals may disrupt the continuity of leadership and negatively affect teachers and, by extension, the students. The aim was to investigate to what extent various work environment factors and signs of exhaustion were associated with reported intentions to change workplace among principals working in compulsory schools. A web-based questionnaire was administered twice, in 2018 and in 2019. Part I of the study involved cross-sectional analyses of the associations 2018 (n = 984) and 2019 (n = 884) between occupational factors, signs of exhaustion, and the intention to change workplace, using Generalized Estimating Equations models. Part II involved 631 principals who participated in both surveys. The patterns of intended and actual changes of workplace across two years were described, together with associated changes of occupational factors and signs of exhaustion. Supportive management was associated with an intention to stay, while demanding role conflicts and the feeling of being squeezed between management and co-workers (buffer-function) were associated with the intention to change workplace. The principals who intended to change their workplace reported more signs of exhaustion. To increase retention among principals, systematic efforts are probably needed at the national, municipal, and local level, in order to improve their working conditions.

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 PM₁₀), 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 A2 (Lp-PLA₂), 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/m³ PM_2.5 (10.5 μg/m³ PM_2.5). Residential PM_2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA₂ and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with PM₁₀. 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.

Air pollution is a major contributor to the global burden of disease and has been linked to several diseases and conditions, including cardiovascular disease. The biological mechanisms are related to inflammation and increased coagulability, factors that play an important role in the pathogenesis of venous thromboembolism (VTE, i.e., deep vein thrombosis or pulmonary embolism). This study investigates if long-term exposure to air pollution is associated with increased VTE incidence. The study followed 29 408 participants from the Malmö Diet and Cancer (MDC) cohort, which consists of adults aged 44–74 recruited in Malmö, Sweden between 1991 and 1996. For each participant, annual mean residential exposures to particulate matter <2.5 μg (PM_2.5) and <10 μg (PM₁₀), nitrogen oxides (NO_x) and black carbon (BC) from 1990 up to 2016 were calculated. Associations with VTE were analysed using Cox proportional hazard models for air pollution in the year of the VTE event (lag0) and the mean of the prior 1–10 years (lag1-10). Annual air pollution exposures for the full follow-up period had the following means: 10.8 μg/m³ for PM_2.5, 15.8 μg/m³ for PM₁₀, 27.7 μg/m³ for NO_x, and 0.96 μg/m³ for BC. The mean follow-up period was 19.5 years, with 1418 incident VTE events recorded during this period. Exposure to lag1-10 PM_2.5 was associated with an increased risk of VTE (HR 1.17 (95%CI 1.01–1.37)) per interquartile range (IQR) of 1.2 μg/m³ increase in PM_2.5 exposure. No significant associations were found between other pollutants or lag0 PM_2.5 and incident VTE. When VTE was divided into specific diagnoses, associations with lag1-10 PM_2.5 exposure were similarly positive for deep vein thrombosis but not for pulmonary embolism. Results persisted in sensitivity analyses and in multi-pollutant models. Long-term exposure to moderate concentrations of ambient PM_2.5 was associated with increased risks of VTE in the general population in Sweden.

While prenatal exposure to ambient air pollution has been shown to be associated with reduced birth weight, there is substantial heterogeneity across studies, and few epidemiological studies have utilized source-specific exposure data. The aim of the present study was, therefore, to investigate the associations between local, source-specific exposure to fine particulate matter (PM2.5) during pregnancy and birth weight. An administrative cohort comprising 40,245 singleton births from 2000 to 2009 in Scania, Sweden, was combined with data on relevant covariates. Investigated sources of PM2.5 included all local sources together as well as tailpipe exhaust, vehicle wear-and-tear, and small-scale residential heating separately. The relationships between these exposures, rep-resented as interquartile range (IQR) increases, and birth weight (continuous) and low birth weight (LBW; <2500 g) were analyzed in crude and adjusted models. Each local PM2.5 source investigated was associated with reduced birth weight; average decreases varied by source (12–34 g). Only small-scale residential heating was clearly associated with LBW (adjusted odds ratio: 1.14 (95% confidence interval: 1.04–1.26) per IQR increase). These results add to existing evidence that prenatal exposure to ambient air pollution disrupts fetal growth and suggest that PM2.5 from both vehicles and small-scale residential heating may reduce birth weight.

BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants.

METHODS: We used data from 22 European cohort studies, which created a total study population of 367 251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2·5 μm (PM2·5), less than 10 μm (PM10), and between 10 μm and 2·5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis.

FINDINGS: The total study population consisted of 367 251 participants who contributed 5 118 039 person-years at risk (average follow-up 13·9 years), of whom 29 076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2·5 of 1·07 (95% CI 1·02-1·13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0·95). HRs for PM2·5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1·06, 95% CI 1·00-1·12) or below 20 μg/m(3) (1·07, 1·01-1·13).

INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value.

FUNDING: European Community's Seventh Framework Program (FP7/2007-2011).

BACKGROUND: Air pollution has been associated with cardiovascular mortality, but it remains unclear as to whether specific pollutants are related to specific cardiovascular causes of death. Within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE), we investigated the associations of long-term exposure to several air pollutants with all cardiovascular disease (CVD) mortality, as well as with specific cardiovascular causes of death.

METHODS: Data from 22 European cohort studies were used. Using a standardized protocol, study area-specific air pollution exposure at the residential address was characterized as annual average concentrations of the following: nitrogen oxides (NO2 and NOx); particles with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and 10 μm to 2.5 μm (PMcoarse); PM2.5 absorbance estimated by land-use regression models; and traffic indicators. We applied cohort-specific Cox proportional hazards models using a standardized protocol. Random-effects meta-analysis was used to obtain pooled effect estimates.

RESULTS: The total study population consisted of 367,383 participants, with 9994 deaths from CVD (including 4,992 from ischemic heart disease, 2264 from myocardial infarction, and 2484 from cerebrovascular disease). All hazard ratios were approximately 1.0, except for particle mass and cerebrovascular disease mortality; for PM2.5, the hazard ratio was 1.21 (95% confidence interval = 0.87-1.69) per 5 μg/m and for PM10, 1.22 (0.91-1.63) per 10 μg/m.

CONCLUSION: In a joint analysis of data from 22 European cohorts, most hazard ratios for the association of air pollutants with mortality from overall CVD and with specific CVDs were approximately 1.0, with the exception of particulate mass and cerebrovascular disease mortality for which there was suggestive evidence for an association.

PURPOSE Digoxin resembles estrogen chemically and may have estrogenic effect. We hypothesized that digoxin use might increase breast cancer incidence and examined if use might be associated with risk of breast cancer, categorized by estrogen receptor (ER) status. To determine if being under care for heart disease biased the findings, rate ratios in users of angina drugs were similarly evaluated as a control exposure group.

PATIENTS AND METHODS Women using digoxin and angina drugs were identified in the nationwide Danish Prescription Database, available between 1995 and 2008. Incident breast cancers were identified in the Danish Cancer Registry and further classifying by ER status. Relative risks (RR) were compared to nonusers using age- and period-adjusted incidence rate ratios.

RESULTS Two thousand one hundred forty-four of 104,648 women using digoxin developed breast cancer. Current digoxin users were at increased risk of breast cancer (RR, 1.39; 95% CI, 1.32 to 1.46), but risk was not increased in former users (RR, 0.91; 95% CI, 0.83 to 1.00). The increased risks in digoxin users were marginally higher for ER-positive breast cancers (RR, 1.35; 95% CI, 1.26 to 1.45) and ER unknown breast cancers (RR, 1.51; 95% CI, 1.38 to 1.64) than for ER-negative breast cancers (RR, 1.20; 95% CI, 1.03 to 1.40). Among 137,493 women exposed to angina drugs only (a comparison group with cardiovascular disease; n = 2,658 breast cancers), incidence was not increased in current or former users.

CONCLUSION Women currently using digoxin had a significantly increased risk of breast cancer. Risk normalized when digoxin was stopped. No risk increases were observed in women using angina drugs only. The higher risk of developing ER-positive breast cancers supports an estrogen-mimicking mechanism.

OBJECTIVES: Acute type A aortic dissection (ATAAD) is a rare but severe condition, routinely treated with emergent cardiac surgery. Many surgeons have the notion that patients with ATAAD tend to come in clusters, but no studies have examined these observations. This investigation was undertaken to study the potential association between the lunar cycle and the incidence of ATAAD.

METHODS: We collected information on 2995 patients who underwent ATAAD surgery at centres from the Nordic Consortium for Acute Type A Aortic Dissection collaboration. We cross-referenced the time of surgery with lunar phase using a case-crossover design with 2 different definitions of full moon (>99% illumination and the 7-day full moon period).

RESULTS: The period when the moon was illuminated the most (99% definition) did not show any significant increase in incidence for ATAAD surgery. However, when the full moon period was compared with all other moon phases, it yielded a relative risk of 1.08 [95% confidence interval (CI) 1.00-1.17, P = 0.057] and, compared to waxing moon, only the relative risk was 1.11 (95% CI 1.01-1.23, P = 0.027). The peak incidence came 4-6 days after the moon was fully illuminated.

CONCLUSIONS: This study found an overrepresentation of surgery for ATAAD during the full moon phase. The explanation for this is not known, but we speculate that sleep deprivation during full moon leads to a temporary increase in blood pressure, which in turn could trigger rupture of the aortic wall. While this finding is interesting, it needs to be corroborated and the clinical implications are debateable.

BACKGROUND: Air pollution is associated with cardiovascular morbidity and mortality, but its role in the development of congestive heart failure (CHF) and the role of different pollution sources in cardiovascular disease remain uncertain.

METHODS: Participants were enrolled in the Malmö Diet and Cancer cohort in 1991-1996 with information on lifestyle and clinical indicators of cardiovascular disease. The cohort participants were followed through registers until 2016. Annual total and local source-specific concentrations of particulate matter less than 10 μm and 2.5 μm (PM₁₀ and PM_2.5), black carbon (BC), and nitrogen oxides (NO_x) from traffic, residential heating, and industry were assigned to each participant's address throughout the study period. Cox proportional hazards models adjusted for possible confounders was used to estimate associations between air pollution 1-5 years prior to outcomes of incident CHF, fatal myocardial infarction (MI), major adverse coronary events (MACE), and ischemic stroke.

RESULTS: Air pollution exposure levels (mean annual exposures to PM_2.5 of 11 μg/m³ and NO_x of 26 μg/m³) within the cohort were moderate in terms of environmental standards. After adjusting for confounders, we observed statistically significant associations between NO_x and CHF (hazard ratio [HR] 1.11, 95% confidence interval [CI] 1.01-1.22) and NO_x and fatal MI (HR 1.10, 95%CI 1.01-1.20) per interquartile range (IQR) of 9.6 μg/m³. In fully adjusted models, the estimates were similar, but the precision worse. In stratified analyses, the associations were stronger in males, ever-smokers, older participants, and those with baseline carotid artery plaques. Locally emitted and traffic-related air pollutants generally showed positive associations with CHF and fatal MI. There were no associations between air pollution and MACE or stroke.

DISCUSSION/CONCLUSION: In an area with low to moderate air pollution exposure, we observed significant associations of long-term residential NO_x with increased risk of incident CHF and fatal MI, but not with coronary events and stroke.

BACKGROUND: Air pollution exposure is associated with hospital admissions and emergency room visits for cardiopulmonary disease and stroke. Iceland's capital area, Reykjavik, has generally low air pollution levels, but traffic and natural sources contribute to pollution levels. The objective of this study was to investigate temporal associations between emergency hospital visits and air pollutants ozone (O3), nitrogen dioxide (NO2), and particulate matter (PM10) in the Icelandic capital area.

METHODS: We constructed a time series of the daily number of adults who visited the emergency room, or were acutely admitted for stroke or cardiorespiratory causes to Landspitali University Hospital 1 January 2003 -- 31 December 2009 from the hospital in-patient register. We used generalized additive models assuming Poisson distribution, to analyze the daily emergency hospital visits as a function of the pollutant levels, and adjusted for meteorological variables, day of week, and time trend with splines.

RESULTS: Daily emergency hospital visits increased 3.9% (95% confidence interval (CI) 1.7-6.1%) per interquartile (IQR) change in average O3 the same and two previous days. For females, the increase was 7.8% (95% CI 3.6-12.1) for elderly (70+), the increase was 3.9% (95% CI 0.6-7.3%) per IQR increase of NO2. There were no associations with PM10.

CONCLUSIONS: We found an increase in daily emergency hospital visits associated with O3, indicating that low-level exposure may trigger cardiopulmonary events or stroke.

Volcanic ash contributed significantly to particulate matter (PM) in Iceland following the eruptions in Eyjafjallajökull 2010 and Grímsvötn 2011. This study aimed to investigate the association between different PM sources and emergency hospital visits for cardiorespiratory causes from 2007 to 2012. Indicators of PM₁₀ sources; “volcanic ash”, “dust storms”, or “other sources” (traffic, fireworks, and re-suspension) on days when PM₁₀ exceeded the daily air quality guideline value of 50 µg/m³ were entered into generalized additive models, adjusted for weather, time trend and co-pollutants. The average number of daily emergency hospital visits was 10.5. PM₁₀ exceeded the air quality guideline value 115 out of 2191 days; 20 days due to volcanic ash, 14 due to dust storms (two days had both dust storm and ash contribution) and 83 due to other sources. High PM₁₀ levels from volcanic ash tended to be significantly associated with the emergency hospital visits; estimates ranged from 4.8% (95% Confidence Interval (CI): 0.6, 9.2%) per day of exposure in unadjusted models to 7.3% (95% CI: −0.4, 15.5%) in adjusted models. Dust storms were not consistently associated with daily emergency hospital visits and other sources tended to show a negative association. We found some evidence indicating that volcanic ash particles were more harmful than particles from other sources, but the results were inconclusive and should be interpreted with caution.

High or low ambient temperatures pose a risk factor for the worsening or onset of psychiatric disorders. The aim of this study was to investigate the association between ambient temperature and psychiatric emergency visits in an urban region in a temperate climate. The daily number of visits to a psychiatric emergency room (PEVs) at Sahlgrenska University Hospital, Gothenburg, Sweden and the daily mean temperature were extracted for the study period 1 July 2012 to 31 December 2017. Case-crossover analysis with distributed lag non-linear models was used to analyse the data by season. The warm season was defined as May to August and the cold season as November to February. Shorter lags periods were used for the warm season than the cold season. In the analysis, temperatures at the 95th percentile was associated with 14% (95% confidence interval (CI): 2%, 28%) increase in PEVs at lag 0⁻3 and 22% (95%CI: 6%, 40%) for lags 0⁻14 during the warm season, relative to the seasonal minimum effect temperature (MET). During the cold season temperatures at the 5th percentile were associated with 25% (95% CI: -8%, 13%) and 18% (95% CI: -30%, 98%) increase in PEVs at lags 0⁻14 and 0⁻21 respectively. We observed an increased number of PEVs at high and low temperatures; however, not to a statistically significant extent for low temperatures. Our findings are similar to what has been found for somatic diseases and in studies of other mental health outcomes in regions with more extreme climates. This merits the inclusion of individuals with psychiatric disorders in awareness planning for climate warning systems.

Cognitive function is a crucial determinant of human capital. The Lancet Commission (2020) has recognized air pollution as a risk factor for dementia. However, the scientific evidence on the impact of air pollution on cognitive outcomes across the life course and across different income settings, with varying levels of air pollution, needs further exploration. A systematic review was conducted, using Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) Guidelines to assess the association between air pollution and cognitive outcomes across the life course with a plan to analyze findings as per the income status of the study population. The PubMed search included keywords related to cognition and to pollution (in their titles) to identify studies on human participants published in English until 10 July 2020. The search yielded 84 relevant studies that described associations between exposure to air pollutants and an increased risk of lower cognitive function among children and adolescents, cognitive impairment and decline among adults, and dementia among older adults with supportive evidence of neuroimaging and inflammatory biomarkers. No study from low-and middle-income countries (LMICs)was identified despite high levels of air pollutants and high rates of dementia. To conclude, air pollution may impair cognitive function across the life-course, but a paucity of studies from reLMICs is a major lacuna in research.

BACKGROUND: Exposure to air pollution has been suggested to increase the risk of dementia, but studies on this link often lack a detailed screening for dementia and data on important confounders.

OBJECTIVE: To determine the association of exposure to air pollution with the risk of dementia and cognitive decline in the population-based Rotterdam Study.

METHODS: Between 2009 and 2010, we determined air pollutant concentrations at participants residential addresses using land use regression models. Determined air pollutants include particulate matter <10μm (PM10) and <2.5μm (PM2.5), a proxy of elemental carbon (PM2.5 absorbance), nitrogen oxide (NOx), and nitrogen dioxide (NO2). As the individual air pollutant levels were highly correlated (r = 0.71-0.98), we computed a general marker covering all air pollutants based on a principal component analysis. We followed participants up for dementia until 2018 and determined cognitive performance during two subsequent examination rounds. Using Cox and linear mixed models, we related air pollution to dementia and cognitive decline.

RESULTS: Of the 7,511 non-demented participants at baseline, 545 developed dementia during a median follow-up of 7 years. The general marker of all air pollutants was not associated with the risk of dementia (hazard ratio [95% confidence interval]: 1.04 [0.95-1.15]), neither were the individual air pollutants. Also, the general marker of all air pollutants or the individual air pollutant levels were not associated with cognitive decline.

CONCLUSION: In this study, we found no clear evidence for an association between exposure to air pollution and the risk of dementia or cognitive decline.

Rationale: Prospective cohort studies have shown that chronic exposure to particulate matter and traffic related air pollution is associated with reduced survival. However, the effects on non-malignant respiratory mortality are less studied and those reported are less consistent.

Objectives: We have investigated the relationship of long-term exposure to air pollution and non-malignant respiratory mortality in 16 cohorts with individual level data within the multi center European Study of Cohorts for Air Pollution Effects (ESCAPE).

Methods: Data from 16 ongoing cohort studies from Europe were used. The total number of subjects was 307,553. There were 1,559 respiratory deaths during follow-up.

Measurements: Air pollution exposure was estimated by land use regression models at the baseline residential addresses of study participants and traffic-proximity variables were derived from geographical databases, following a standardized procedure within ESCAPE study. Cohort-specific hazard ratios obtained by Cox proportional hazard models from standardized individual cohort analyses were combined using meta-analyses. Main Results: We found no significant associations between air pollution exposure and non-malignant respiratory mortality. Most hazard ratios were slightly below unity, with the exception of the traffic-proximity indicators.

Conclusions: In this study of 16 cohorts there was no association between air pollution exposure and non malignant respiratory mortality.

Background: Breathlessness is a major cause of suffering and disability globally. The symptom relates to multiple factors including asthma and lung function, which are influenced by hereditary factors. No study has evaluated potential inheritance of breathlessness itself across generations.

Methods: We analysed the association between breathlessness in parents and their offspring in the Respiratory Health in Northern Europe, Spain and Australia generation study. Data on parents and offspring aged ≥18 years across 10 study centres in seven countries included demographics, self-reported breathlessness, asthma, depression, smoking, physical activity level, measured Body Mass Index and spirometry. Data were analysed using multivariable logistic regression accounting for clustering within centres and between siblings.

Results: A total of 1720 parents (mean age at assessment 36 years, 55% mothers) and 2476 offspring (mean 30 years, 55% daughters) were included. Breathlessness was reported by 809 (32.7%) parents and 363 (14.7%) offspring. Factors independently associated with breathlessness in parents and offspring included obesity, current smoking, asthma, depression, lower lung function and female sex. After adjusting for potential confounders, parents with breathlessness were more likely to have offspring with breathlessness, adjusted OR 1.8 (95% CI 1.1 to 2.9). The association was not modified by sex of the parent or offspring.

Conclusion: Parents with breathlessness were more likely to have children who developed breathlessness, after adjusting for asthma, lung function, obesity, smoking, depression and female sex in both generations. The hereditary components of breathlessness need to be further explored.

Aim: Heritability of cough has not yet been studied. We aimed to evaluate if individuals with cough are more likely to have offspring who develop cough, and if these associations differ by type of cough (productive/nonproductive).

Methods: The RHINESSA Generation Study (Respiratory Health In Northern Europe, Spain and Australia) includes 7155 parents (initially aged 30–54) answering detailed questionnaires in 2000 and 2010, and 8176 offspring ⩾20 years answering similar questionnaires in 2012–2019. Chronic cough was categorised as productive or nonproductive (dry) cough. Associations between parental and offspring cough were analysed using mixed-effects logistic regression, adjusting for offspring age, sex, body mass index, smoking history, education level, current asthma, rhinitis, nocturnal gastroesophageal reflux; parent sex and smoking history; centre and family.

Results: Among parents with nonproductive cough, 11% of their offspring reported nonproductive cough, compared with 7% of offspring to parents without nonproductive cough, adjusted odds ratio (aOR) 1.59 (95% confidence interval 1.20–2.10). Among parents with productive cough, 14% of their offspring reported productive cough, compared with 11% of offspring to parents without productive cough, aOR 1.34 (1.07–1.67). No associations were found between parent productive cough–offspring nonproductive cough, nor between parent nonproductive cough–offspring productive cough.

Conclusions: Parents with chronic cough are more likely to have offspring with chronic cough independent of parental asthma, suggesting cough to be a separate heritable trait. The type of cough is important, as the nonproductive cough in parent associates only with nonproductive cough in offspring, and the same applied for productive cough.

BACKGROUND: The adverse health effects of high concentrations of hydrogen sulfide (H2S) exposure are well known, though the possible effects of low concentrations have not been thoroughly studied. The aim was to study short-term associations between modelled ambient low-level concentrations of intermittent hydrogen sulfide (H2S) and emergency hospital visits with heart diseases (HD), respiratory diseases, and stroke as primary diagnosis.

METHODS: The study is population-based, using data from patient-, and population-registers from the only acute care institution in the Reykjavik capital area, between 1 January, 2007 and 30 June, 2014. The study population was individuals (≥18yr) living in the Reykjavik capital area. The H2S emission originates from a geothermal power plant in the vicinity. A model was used to estimate H2S exposure in different sections of the area. A generalized linear model assuming Poisson distribution was used to investigate the association between emergency hospital visits and H2S exposure. Distributed lag models were adjusted for seasonality, gender, age, traffic zones, and other relevant factors. Lag days from 0 to 4 were considered.

RESULTS: The total number of emergency hospital visits was 32961 with a mean age of 70 years. In fully adjusted un-stratified models, H2S concentrations exceeding 7.00μg/m3 were associated with increases in emergency hospital visits with HD as primary diagnosis at lag 0 risk ratio (RR): 1.067; 95% confidence interval (CI): 1.024-1.111, lag 2 RR: 1.049; 95%CI: 1.005-1.095, and lag 4 RR: 1.046; 95%CI: 1.004-1.089. Among males an association was found between H2S concentrations exceeding 7.00μg/m3, and HD at lag 0 RR: 1.087; 95%CI: 1.032-1.146 and lag 4 RR: 1080; 95%CI: 1.025-1.138; and among those 73 years and older at lag 0 RR: 1.075; 95%CI: 1.014-1.140 and lag 3 RR: 1.072; 95%CI: 1.009-1.139. No associations were found with other diseases.

CONCLUSIONS: The study showed an association between emergency hospital visits with HD as primary diagnosis and same day H2S concentrations exceeding 7.00μg/m3, more pronounced among males and those 73 years and older than among females and younger individuals.

OBJECTIVES: To study the association between daily mortality and short-term increases in air pollutants, both traffic-related and the geothermal source-specific hydrogen sulfide (H2S).

DESIGN: Population-based, time stratified case-crossover. A lag time to 4 days was considered. Seasonal, gender and age stratification were calculated. Also, the best-fit lag when introducing H2S >7 µg/m(3) was selected by the Akaike Information Criterion (AIC).

SETTING: The population of the greater Reykjavik area (n=181 558) during 2003-2009.

PARTICIPANTS: Cases were defined as individuals living in the Reykjavik capital area, 18 years or older (N=138 657), who died due to all natural causes (ICD-10 codes A00-R99) other than injury, poisoning and certain other consequences of external causes, or cardiovascular disease (ICD-10 codes I00-I99) during the study period.

MAIN OUTCOME MEASURE: Percentage increases in risk of death (IR%) following an interquartile range increase in pollutants.

RESULTS: The total number of deaths due to all natural causes was 7679 and due to cardiovascular diseases was 3033. The interquartile range increased concentrations of H2S (2.6 µg/m(3)) were associated with daily all natural cause mortality in the Reykjavik capital area. The IR% was statistically significant during the summer season (lag 1: IR%=5.05, 95% CI 0.61 to 9.68; lag 2: IR%=5.09, 95% CI 0.44 to 9.97), among males (lag 0: IR%=2.26, 95% CI 0.23 to 4.44), and among the elderly (lag 0: IR%=1.94, 95% CI 0.12 to 1.04; lag 1: IR%=1.99, 95% CI 0.21 to 1.04), when adjusted for traffic-related pollutants and meteorological variables. The traffic-related pollutants were generally not associated with statistical significant IR%s.

CONCLUSIONS: The results suggest that ambient H2S air pollution may increase mortality in Reykjavik, Iceland. To the best of our knowledge, ambient H2S exposure has not previously been associated with increased mortality in population-based studies and therefore the results should be interpreted with caution. Further studies are warranted to confirm or refute whether H2S exposure induces premature deaths.

Air pollution is one of the leading causes of morbidity and mortality worldwide. Low-emission zones (LEZ) have been increasingly implemented in cities throughout Europe as a measure to reduce the adverse health effects and premature deaths associated with traffic-related air pollution. In the present study, a health impact analysis was conducted to estimate the effect of a hypothetical LEZ on mortality and morbidity in Malmö, Sweden. Baseline health statistics were gathered from health registers and applied to each resident according to individual-level data on age and/or sex. Concentration-response parameters were derived from current epidemiological literature, specifically meta-analyses. A Gaussian dispersion model (AERMOD) combined with a detailed emission database was used to calculate NO₂ emissions from traffic, which could be applied on an individual-level using data on each person's residential coordinates. The adjusted exposure scenario replaced all vehicles on municipal roads having Euro 5 or lower emission standards with Euro 6 equivalents. This LEZ would, on average, decrease NO₂ concentrations by 13.4%, preventing an estimated 9-26 deaths in Malmö each year. Additionally, 12 respiratory disease hospitalizations, 8 childhood asthma cases, and 9 cases of hypertensive disorders of pregnancy were estimated to be avoided annually. These results suggest that LEZs can effectively improve air quality, reduce greenhouse gas emissions, and safeguard public health.

Environmental injustice, characterized by lower socioeconomic status (SES) persons being subjected to higher air pollution concentrations, was explored among pregnant women in Scania, Sweden. Understanding if the general reduction of air pollution recorded is enjoyed by all SES groups could illuminate existing inequalities and inform policy development. "Maternal Air Pollution in Southern Sweden", an epidemiological database, contains data for 48,777 pregnancies in Scanian hospital catchment areas and includes births from 1999-2009. SES predictors considered included education level, household disposable income, and birth country. A Gaussian dispersion model was used to model women's average NOX and PM2.5 exposure at home residence over the pregnancy period. Total concentrations were dichotomized into emission levels below/above respective Swedish Environmental Protection Agency (EPA) Clean Air objectives. The data were analyzed using binary logistic regression. A sensitivity analysis facilitated the investigation of associations' variation over time. Lower-SES women born outside Sweden were disproportionately exposed to higher pollutant concentrations. Odds of exposure to NOX above Swedish EPA objectives reduced over time, especially for low-SES persons. Environmental injustice exists in Scania, but it lessened with declining overall air pollution levels, implying that continued air quality improvement could help protect vulnerable populations and further reduce environmental inequalities.

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.

PURPOSE: To determine the long-term risk of retinal detachment following pediatric cataract surgery and to identify risk factors for retinal detachment.

METHODS: We included all children (aged 0 to 17 years) who during the time period of 1977 to 2005 underwent pediatric cataract surgery in Denmark, excluding cataract cases caused by trauma, or acquired systemic or acquired ocular pathology, and cases with ocular anomalies associated with the development of retinal detachment. Cases of cataract were ascertained from the mandatory Danish National Patient Register, and information on retinal detachment was based on medical chart review.

RESULTS: Among 1043 eyes of 656 children undergoing surgery for pediatric cataract, 25 eyes (23 children) developed retinal detachment at a median time of 9.1 years after surgery. The overall 20-year risk of retinal detachment was 7% (95% confidence interval [CI]: 3%-11%) among cataract patients. In otherwise normal children having isolated cataract, the risk was 3% (95% CI: 0%-7%). A significantly higher risk of developing retinal detachment was found in children with mental retardation (23% [95% CI: 9%-35%]) or in cataract cases with other ocular or systemic anomalies (16% [95% CI: 6%-24%]).

CONCLUSIONS: The estimated overall risk of retinal detachment 20 years after pediatric cataract surgery was 7%, but only 3% for isolated cataract. Particularly high risks of retinal detachment after cataract surgery were associated with mental retardation and having other ocular or systemic diseases.

Using publicly available data, we identified areas likely to be underreporting snakebites and highlighted these areas instead of leaving them "white" on the incidence map. The effects of the case detection bias on the distribution of resources against snakebites could decrease. Although not yet verified empirically, our study provides an example of how snake bite epidemiology may be investigated in similar settings worldwide at a low cost.

Vetenskapsrådets SIMSAM initiativ syftar till att stärka multidisciplinär registerforskning i Sverige. Inom SIMSAM-nätverket i Umeå arbetar vi tvärvetenskapligt med sikte på att utvecklas till ett center med excellens kring mikrodataforskning som knyter samman barndomen med livslång hälsa och välfärd. Just nu fokuserar vi på att få tillgång till sammanlänkade data från ett flertal nationella och regionala register för att komma vidare med vår planerade forskning. Dessutom har Umeå-nätverket nyligen fått i uppdrag att leda den nationella samordningen av SIMSAM initiativet.

The app-based COVID Symptom Study was launched in Sweden in April 2020 to contribute to real-time COVID-19 surveillance. We enrolled 143,531 study participants (≥18 years) who contributed 10.6 million daily symptom reports between April 29, 2020 and February 10, 2021. Here, we include data from 19,161 self-reported PCR tests to create a symptom-based model to estimate the individual probability of symptomatic COVID-19, with an AUC of 0.78 (95% CI 0.74–0.83) in an external dataset. These individual probabilities are employed to estimate daily regional COVID-19 prevalence, which are in turn used together with current hospital data to predict next week COVID-19 hospital admissions. We show that this hospital prediction model demonstrates a lower median absolute percentage error (MdAPE: 25.9%) across the five most populated regions in Sweden during the first pandemic wave than a model based on case notifications (MdAPE: 30.3%). During the second wave, the error rates are similar. When we apply the same model to an English dataset, not including local COVID-19 test data, we observe MdAPEs of 22.3% and 19.0% during the first and second pandemic waves, respectively, highlighting the transferability of the prediction model.

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

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

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

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

Background: Despite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers.

Methods: We performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM2.5), inhalable particulate matter (PM10), and nitrogen oxides (NOx) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders.

Results: Median long-term PM2.5 exposure was 6.2 µg/m3. Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m2. PM2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m3 (interquartile range, IQR). PM2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m3. There was a tendency towards an association between PM10 and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent.

Conclusion: In this large general population sample at low exposure levels, we found a surprising association between PM2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology.

Background: Experimental studies suggest that exposures may impact respiratory health across generations via epigenetic changes transmitted specifically through male germ cells. Studies in humans are, however, limited. We aim to identify epigenetic marks in offspring associated with father’s preconception smoking.

Methods: We conducted epigenome-wide association studies (EWAS) in the RHINESSA cohort (7–50 years) on father’s any preconception smoking (n = 875 offspring) and father’s pubertal onset smoking < 15 years (n = 304), using Infinium MethylationEPIC Beadchip arrays, adjusting for offspring age, own smoking and maternal smoking. EWAS of maternal and offspring personal smoking were performed for comparison. Father’s smoking-associated dmCpGs were checked in subpopulations of offspring who reported no personal smoking and no maternal smoking exposure.

Results: Father’s smoking commencing preconception was associated with methylation of blood DNA in offspring at two cytosine-phosphate-guanine sites (CpGs) (false discovery rate (FDR) < 0.05) in PRR5 and CENPP. Father’s pubertal onset smoking was associated with 19 CpGs (FDR < 0.05) mapped to 14 genes (TLR9, DNTT, FAM53B, NCAPG2, PSTPIP2, MBIP, C2orf39, NTRK2, DNAJC14, CDO1, PRAP1, TPCN1, IRS1 and CSF1R). These differentially methylated sites were hypermethylated and associated with promoter regions capable of gene silencing. Some of these sites were associated with offspring outcomes in this cohort including ever-asthma (NTRK2), ever-wheezing (DNAJC14, TPCN1), weight (FAM53B, NTRK2) and BMI (FAM53B, NTRK2) (p < 0.05). Pathway analysis showed enrichment for gene ontology pathways including regulation of gene expression, inflammation and innate immune responses. Father’s smoking-associated sites did not overlap with dmCpGs identified in EWAS of personal and maternal smoking (FDR < 0.05), and all sites remained significant (p < 0.05) in analyses of offspring with no personal smoking and no maternal smoking exposure. Conclusion: Father’s preconception smoking, particularly in puberty, is associated with offspring DNA methylation, providing evidence that epigenetic mechanisms may underlie epidemiological observations that pubertal paternal smoking increases risk of offspring asthma, low lung function and obesity.

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/m³ 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: Little is known on childhood exposure to air pollution and adult chronic respiratory outcomes.

Aim: To investigate associations between air pollution and greenness in childhood and adult lung health.

Methods: In selected centres of the RHINESSA study (age 18-52) we analysed the outcomes respiratory symptoms (≥3 symptoms), severe wheeze (wheeze last year with breathlessness, no cold) and late onset asthma (>10 years). We calculated mean annual exposures of PM2.5, PM10, NO2 (µg/m³) and greenness (Normalized Difference Vegetation Index, 100m buffer) from offspring's birth till age 18, categorised into mean exposure <10 years and 11-18 years. We performed multilevel logistic regression clustered by family, stratified by centre and adjusted for childhood passive smoke and parental asthma.

Results: 12% had ≥3 respiratory symptoms, 7.7% severe wheeze, and 9.4% late onset asthma. Overall estimates: greenness was associated with less respiratory symptoms, PM2.5 and NO2 with more late onset asthma. Exposure <10 years: Greenness was associated with less wheeze in Tartu (OR 0.29, 95%CI 0.11-0.73). PM2.5 (OR 1.22, 95%CI 1.00-1.48) and NO2 (OR 1.06, 95%CI 1.01-1.11) were risk factors for late onset asthma in Bergen. PM10 was a risk factor for respiratory symptoms (OR 1.21, 95%CI 1.04-1.41) in Uppsala and late onset asthma (OR 1.23, 95%CI 1.02-1.45) in Bergen. Exposure 11-18 years: Greenness was protective for respiratory symptoms (OR 0.29, 95%CI 0.10-0.86) and wheeze (OR 0.39, 95%CI 0.19-0.80) in Tartu.

Conclusions: Childhood exposure to greenness was associated with less respiratory symptoms, while air pollutants were associated with more respiratory symptoms (some centres) and late onset asthma.

Psychological factors such as anxiety and depression are prevalent in patients with asthma. The purpose of this study was to investigate the relationship between respiratory symptoms and psychological status and to estimate the importance of psychological status in comparison with other factors that are known to be associated with respiratory symptoms. This study included 2270 subjects aged 20-44 (52% female) from Sweden, Iceland, and Norway. Each participant underwent a clinical interview including questions on respiratory symptoms. Spirometry and methacholine challenge were performed. Symptoms of depression and anxiety were measured using the Hospital Anxiety and Depression Scale (HADS). Eighty-two percent of the subjects reported no anxiety or depression whatsoever, 11% reported anxiety, 2.5% depression and 4% reported both anxiety and depression. All respiratory symptoms, such as wheezing, breathlessness and nightly symptoms, were more common, at a statistically significant level, in participants who had depression and anxiety, even after adjusting for confounders (ORs 1.33-1.94). The HADS score was the most important determinant for nightly symptoms and attacks of breathlessness when at rest whereas bronchial responsiveness was the most important determinant for wheezing, and breathlessness when wheezing. The probability of respiratory symptoms related to HADS score increased with increasing HADS score for all respiratory symptoms. In conclusion, there is a strong association between respiratory symptoms and psychological status. There is therefore a need for interventional studies designed to improve depression and anxiety in patients with respiratory symptoms.

Recent studies indicate that monitoring only fine particulate matter (PM2.5) may not be enough to understand and tackle the health risk caused by particulate pollution. Health effects per unit PM2.5 seem to increase in countries with low PM2.5, but also near local pollution sources (e.g., traffic) within cities. The aim of this study is to understand the differences in the characteristics of lung-depositing particles in different geographical regions and urban environments. Particle lung deposited surface area (LDSAal) concentrations and size distributions, along with PM2.5, were compared with ambient measurement data from Finland, Germany, Czechia, Chile, and India, covering traffic sites, residential areas, airports, shipping, and industrial sites. In Finland (low PM2.5), LDSAal size distributions depended significantly on the urban environment and were mainly attributable to ultrafine particles (<100 nm). In Central Europe (moderate PM2.5), LDSAal was also dependent on the urban environment, but furthermore heavily influenced by the regional aerosol. In Chile and India (high PM2.5), LDSAal was mostly contributed by the regional aerosol despite that the measurements were done at busy traffic sites. The results indicate that the characteristics of lung-depositing particles vary significantly both within cities and between geographical regions. In addition, ratio between LDSAal and PM2.5 depended notably on the environment and the country, suggesting that LDSAal exposure per unit PM2.5 may be multiple times higher in areas having low PM2.5 compared to areas with continuously high PM2.5. These findings may partly explain why PM2.5 seems more toxic near local pollution sources and in areas with low PM2.5. Furthermore, performance of a typical sensor based LDSAal measurement is discussed and a new LDSAal2.5 notation indicating deposition region and particle size range is introduced. Overall, the study emphasizes the need for country-specific emission mitigation strategies, and the potential of LDSAal concentration as a health-relevant pollution metric.

Air pollution is estimated to cause more than 7000 deaths annually in Sweden alone. To reduce the impact of air pollution and to plan and build sustainable cities, it is vital that research is translated into efficient decisions and practice. However, how do civil servants in a municipality access research results? How do they normally find relevant information, and what obstacles are there to accessing and applying research results? As part of the collaborative and transdisciplinary research project Air Pollution Research in Local Environmental Planning (ARIEL), these questions were explored through interviews and seminars with civil servants within the Malmö Municipality Environmental Office. We found that the civil servants generally have proficiency in processing research results, but often do not use such results as part of their everyday decision making and practices. Instead, the data and measurements used are mostly produced case-by-case within the municipal sector itself. Information about best practices is also collected via a number of knowledge access practices, involving the Internet or social networks within other municipalities. Lack of time, paywalls, and the insufficient applicability of research hinder the dissemination of up-to-date results. This slows down the process whereby research, funded by tax-money, can be put to best practice in the effort to create healthy and sustainable cities.

OBJECTIVES: To investigate the association of early snus use initiation (≤15 years of age) with asthma and asthma symptoms.

DESIGN: Cross-sectional analysis of a population-based cohort.

SETTING: Study centres in Norway, Sweden, Iceland, Denmark and Estonia, from 2016 to 2019.

PARTICIPANTS: 9002 male and female participants above 15 years of age of the Respiratory Health in Northern Europe, Spain and Australia study.

MAIN OUTCOME MEASURES: Current asthma and asthma symptoms.

RESULTS: The median age of study participants was 28 years (range 15-53) and 58% were women. 20% had used snus, 29% men and 14% women. Overall, 26% of males and 14% of females using snus started ≤15 years of age. Early snus use initiation was associated with having three or more asthma symptoms (OR 2.70; 95% CI 1.46 to 5.00) and a higher asthma symptom score (β-coefficient (β) 0.35; 95% CI 0.07 to 0.63) in women. These associations were weak in men (OR 1.23; 95% CI 0.78 to 1.94; β 0.16; 95% CI -0.06 to 0.38, respectively). There was evidence for an association of early snus initiation with current asthma (OR 1.72; 95% CI 0.88 to 3.37 in women; OR 1.31; 95% CI 0.84 to 2.06 in men). A sensitivity analysis among participants without smoking history showed stronger estimates for all three outcomes, in both men and women, statistically significant for three or more asthma symptoms in women (OR 3.28; 95% CI 1.18 to 9.10). Finally, no consistent associations with asthma outcomes were found for starting snus after age 15 years.

CONCLUSIONS: Snus initiation in puberty was associated with higher likelihood of asthma and asthma symptoms, with the highest estimates in females and those without smoking history. These results raise concerns about the health adversities of early snus initiation and emphasise the need for public health initiatives to protect young people from this tobacco product.

The increasing prevalence of asthma is linked to westernization and urbanization. Farm environments have been associated with a lower risk of asthma development. However, this may not be universal, as the association differs across birth cohorts and farming methods. The aim of this study was to investigate the associations of farm upbringing with asthma in different generations and at different times in history. The study population consisted of three generations: 13,868 subjects participating in the ECRHS in 2010, their 9,638 parents, and their 8,885 offspring participating in RHINESSA in 2013. Information on place of upbringing and self-reported ever asthma was provided via questionnaires. Logistic regression was performed including subgroup analysis stratified by generation and birthyear into ten-year-intervals. The prevalence of asthma increased from 8% among grandparents to 13% among parents and to 18% among offspring. An overall analysis showed an inverse association of farm upbringing on the risk of asthma (OR = 0.64; 95%CI 0.55-0.74). Subgroup analysis stratified into ten-year-intervals showed a tendency towards a more pronounced inverse association between growing up on a farm and asthma among subjects born in the 1940s (0.74; 0.48-1.12), 1950s (0.70; 0.54-0.90) and 1960s (0.70; 0.52-0.93). For subjects born in 1970 and thereafter this association appeared less consistent. While growing up on a farm was associated with a reduced risk of developing asthma in participants born between 1945-1999, this was mainly driven by generations born from 1945 to 1973.

Air pollution is responsible for one in eight premature deaths worldwide, and thereby a major threat to human health. Health impact assessments of hypothetic changes in air pollution concentrations can be used as a mean of assessing the health impacts of policy, plans and projects, and support decision-makers in choices to prevent disease.

The aim of this study was to estimate health impacts attributable to a hypothetical decrease in air pollution concentrations in the city of Malmö in Southern Sweden corresponding to a policy on-road transportations without tail-pipe emissions in the municipality. We used air pollution data modelled for each of the 326,092 inhabitants in Malmö by a Gaussian dispersion model combined with an emission database with >40,000 sources. The dispersion model calculates Nitrogen Oxides (NO_x) (later transformed into Nitrogen Dioxide (NO₂)) and particulate matter with an aerodynamic diameter < 2.5 μg/m³ (PM_2.5) with high spatial and temporal resolution (85 m and 1 h, respectively).

The average individual reduction was 5.1 (ranging from 0.6 to 11.8) μg/m³ in NO_2, which would prevent 55 (2% of all deaths) to 93 (4%) deaths annually, depending on dose-response function used. Furthermore, we estimate that the NO₂ reduction would result in 21 (6%) fewer cases of incident asthma in children, 95 (10%) fewer children with bronchitis every year, 30 (1%) fewer hospital admissions for respiratory disease, 87(4%) fewer dementia cases, and 11(11%) fewer cases of preeclampsia every year. The average reduction in PM_2.5 of 0.6 (ranging from 0.1 till 1.7) μg/m³ would mean that 2729 (0.3%) work days would not be lost due to sick-days and that there would be 16,472 fewer restricted activity days (0.3%) that year had all on-road transportations been without tail-pipe emissions.

Even though the estimates are sensitive to the dose-response functions used and to exposure misclassification errors, even the most conservative estimate of the number of prevented deaths is 7 times larger than the annual traffic fatalities in Malmö, indicating a substantial possibility to reduce the health burden attributed to tail-pipe emissions in the study area.

Planetary health is being or should be added to medical training curricula in accordance with association consensus. Several articles published in recent years have addressed concern on the implementation, and the challenges that can occur if not addressed properly. This scoping narrative literature review focuses on planetary health as a concept, as well as challenges and suggested solutions to address these challenges. Planetary health is an important concept and needs to be addressed in all medical training. We found that one main challenge is implementation without ensuring the right competences and resources. Medically trained teachers set out to understand and teach complex natural and social systems. At some institutions the time allocated to teach planetary health is limited or non-existent. Case studies and student led teaching are solutions suggested, while other argue that true interdisciplinarity by inviting experts are more in line with what we expect from other subjects. In conclusion, the roots of planetary health, the enormous health risks at stake and nature of the subject requires medical training to adopt a true inter/trans-disciplinary approach to succeed. It might not be expected for all students to become planetary health experts, but all need a general understanding of the most important aspects and values.

PURPOSE OF REVIEW: The aim of this review is to identify the key contextual and methodological differences in health impact assessments (HIA) of ambient air pollution performed for Europe. We limited our review to multi-country reviews. An additional aim is to quantify some of these differences by applying them in a HIA template in three European cities.

RECENT FINDINGS: Several HIAs of ambient air pollution have been performed for Europe, and their key results have been largely disseminated. Different studies have, however, come up with substantial differences in attributed health effects. It is of importance to review the background contributing to these differences and to quantify their importance for decision makers who will use them. We identified several methodological differences that could explain the discrepancy behind the number of attributable deaths or years of life lost. The main differences are due to the exposure-response functions chosen, the ways of assessing air pollution levels, the air pollution scenarios and the study population. In the quantification part, we found that using risk estimates from the European Study of Cohorts for Air Pollution Effects (ESCAPE) instead of the American Cancer Society (ACS) study could nearly double the attributable burden of ambient air pollution. This study provides some insights into the differential results in previously published HIAs on air pollution in Europe. These results are important for stakeholders in order to make informed decisions.

Background: Studies have shown that ambient air pollution is linked to preeclampsia (PE), possibly via generation of oxidative stress in the placenta. Telomere length and mitochondrial DNA copy number (mtDNAcn) are sensitive to oxidative stress damage. Objective: To study the association between prenatal exposure to ambient nitrogen oxides (NO_x, a marker for traffic-related air pollution), and PE, as well as potential mediation effects by placental telomere length and mtDNAcn.

Methods: This is a cross-sectional study of 42 preeclamptic and 95 arbitrarily selected normotensive pregnant women with gestational ambient NO_x exposure assessment in southern Scania, Sweden. Hourly concentrations of NO_x were estimated at the residential addresses by a Gaussian-plume dispersion model with 100 × 100 m spatial resolutions and aggregated into trimester-specific mean concentrations. Placental relative mtDNAcn and telomere length were measured using qPCR. Linear and logistic regression models were used to investigate associations, adjusted for perinatal and seasonal characteristics.

Results: Exposure was categorized into low and high exposures by median cut-offs during first [11.9 μg/m³; interquartile range (IQR) 7.9, 17.9], second (11.6 μg/m³; IQR: 7.1, 21.1), third trimesters (11.9 μg/m³; IQR: 7.7, 19.5) and entire pregnancy (12.0 μg/m³; IQR: 7.6, 20.1). Increased risk of PE was found for high prenatal NO_x exposure during the first trimester (OR 4.0; 95% CI: 1.4, 11.1; p = 0.008), and entire pregnancy (OR 3.7; 95% CI: 1.3, 10.4; p = 0.012). High exposed group during the first trimester had lower placental relative mtDNAcn compared with low exposed group (−0.20; 95% CI: −0.36, −0.04; p = 0.01). Changes in relative mtDNAcn did not mediate the association between prenatal NO_x exposure and PE. No statistically significant association was found between placental relative telomere length, prenatal NO_x exposure and PE.

Conclusion: In this region with relatively low levels of air pollution, ambient NO_x exposure during the first trimester was associated with reduced placental relative mtDNAcn and an increased risk of PE. However, we did not find any evidence that mtDNAcn or TL mediated the association between air pollution and PE. Future research should further investigate the role of mtDNAcn for pregnancy complications in relation to exposure to ambient air pollution during pregnancy.

The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.

Background: Ambient particulate matter is a leading risk factor for disease globally. Particulate matter 10 (PM10) and particulate matter 2.5 (PM2.5) are derived from different sources, including operating motor vehicles as well as from industrial activities. In this study we investigate the association between increased concentrations of PM and total daily visits to the psychiatric emergency unit (PEV). Further, the aim is to identify specific risk groups who are more susceptible to the effects of air pollution exposure by studying sex, age, ongoing psychiatric follow-up and diagnoses of depression/anxiety or substance use.

Material and methods: The sample was comprised of data from 2740 days to 81 548 PEVs at Sahlgrenska University Hospital in Gothenburg and daily mean concentrations of PM10 and PM2.5. A time-stratified case-crossover design was used to analyse associations between air pollution and PEVs.

Results: Mean number of daily PEVs were 35 and sex distribution was even. PM exposure was associated with total PEV at lag 0 (the same day), by RR 1.016 (95% confidence interval [CI] 1.004–1.028) and RR 1.020 (95%CI 1.003–1.038) per 10 μg/m3 increase in PM10 and PM2.5, respectively. In females, PEV were increased at lag 0 and lag 1, and in males at lag 1 and lag 2. In the age-stratified analysis, PEVs significantly increased following PM exposure amongst individuals aged 35–65 years by lag 0–2 and in individuals who had contact with outpatient care at lag 0 to lag 1. There were no associations between air pollution and PEVs for any specific diagnostic group evaluated (amongst depression, anxiety and substance use disorder).

Conclusions: The results indicate that acute exposure to PM10 and PM2.5 may trigger acute worsening in mental health in both males and females, especially among 35–65 year old individuals. However, in subgroups of the most common psychiatric diagnoses, we did not observe statistically significant associations with PM exposure.

The objective of this study is to increase the knowledge regarding school principals' work situations by examining the associations between various factors and the school principals' assessments of their ability or wish to work until 65 years of age or longer. The 1356 participating school principals in this study were aged between 50 and 64 years of age. Individual and work factors were evaluated in relation to two dichotomized outcomes: i.e., can work and want to work beyond 65 years of age, respectively. Generalized Estimating Equations (GEE) models were used to specify bivariate and multivariate cross-sectional logistic regression models that accounted for repeated measurements. The results showed that, both in 2018 and 2019, about 83% of the school principals stated that they could work and about 50% stated that they wanted to work until 65 years of age and beyond. School principals' exhaustion symptoms and experiences of an excessive burden were statistically significantly associated with whether they both could not and did not want to work beyond 65 years of age. Additionally, the school principals' experiences of support from the executive management in the performance of their managerial duties was of primary importance for whether the school principals wanted to work until 65 years of age and beyond. To conclude, it is important that school principals receive sufficient support from the management to cope with their often very stressful leadership tasks so that they have the opportunity to be able and willing to continue working their entire working life. The study strengthens the robustness of the theoretical SwAge model regarding the investigated factors related to determinant factors for a sustainable working life and as a basis for developing practical tools for increased employability for people of older ages.

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.

Individual differences in cognitive performance increase with advancing age, reflecting marked cognitive changes in some individuals along with little or no change in others. Genetic and lifestyle factors are assumed to influence cognitive performance in ageing by affecting the magnitude and extent of age-related brain changes (i.e., brain maintenance or atrophy), as well as the ability to recruit compensatory processes. The purpose of this review is to present findings from the Betula study and other longitudinal studies, with a focus on clarifying the role of key biological and environmental factors assumed to underlie individual differences in brain and cognitive ageing. We discuss the vital importance of sampling, analytic methods, consideration of non-ignorable dropout, and related issues for valid conclusions on factors that influence healthy neurocognitive ageing.