BACKGROUND:Several studies from different countries have shown that merchant seafarers have an increased cancer risk compared to the general population. The aim of this study was to provide updated information on cancer incidence in a cohort of Swedish seafarers. METHODS:A cohort consisting of all Swedish seafarers from the Swedish Seafarers' Register 1985-2013 was linked to the Swedish Cancer Register 1985-2020. Seafarers with at least 5 years of sea service (N = 38,030; 76% men and 24% women) were included in the analyses. Standardized incidence ratios (SIR) were calculated for cancer by specific site, period of first signing, job category, type of vessel, and gender, using cancer incidence in the general population as reference. RESULTS:In seafarers who had worked on different types of vessels (not solely passenger ferries), there were 5076 cases of cancer during the follow-up period, and total cancer risk was increased (SIR 1.14; 95% confidence interval [CI] 1.11-1.17). Most cases occurred in seafarers who had their first signing before 1985. The risk of lung cancer was increased in all job categories, especially in engine room crew members (SIR 1.98; 95% CI 1.53-2.57). There were 16 mesothelioma cases in engine officers (SIR 3.75; 95% CI 2.30-6.12). CONCLUSIONS:This cohort study of seafarers in Sweden confirms that Swedish seafarers had an increased overall cancer risk compared with the general population, particularly those signing before 1985 and working on different types of vessels.

INTRODUCTION:Ambient air pollution and road traffic noise are stroke risk factors, but evidence on their potential joint effects remains limited. This study investigated the independent and joint associations of air pollution and road traffic noise on stroke incidence using both multiplicative and additive scales. METHODS:We followed stroke incidence in ten cohorts in Sweden, Denmark, and Finland. We modelled annual average levels of outdoor particulate matter < 2.5 µm (PM2.5), nitrogen dioxide (NO2) and road traffic noise at residential addresses. We applied Cox proportional hazards regression to evaluate their single association. We assessed multiplicative interaction with interaction terms in Cox models and additive interaction using the Relative Excess Risk due to Interaction method. RESULTS:We followed 136,897 adults for 20 years, and 8.0 % experienced stroke incidence. PM2.5, NO2 and road traffic noise were associated with higher stroke risk in single-exposure models. Multiplicative models showed higher HRs between PM2.5 and stroke at higher levels of noise and vice versa: HRs per 5 μg/m3 of PM2.5 were 1.06 (95 % CI:0.94-1.21) at 40 dB and 1.11 (95 % CI:0.85-1.44) at 80 dB of road traffic noise; HRs per 12 dB of road traffic noise were 1.06 (95 % CI:1.01-1.11) at 4 μg/m3 and 1.17 (95 % CI:0.82-1.68) at 48 μg/m3 of PM2.5. Additive models showed that the combined association of PM2.5 and road traffic noise was 4 % (RERI = 0.04 (95 % CI:-0.05;1.12)) higher than the sum of their individual association. CONCLUSION:PM2.5 and road traffic noise showed a non-significant synergistic association on stroke incidence.

OBJECTIVE:The aim of the study was to investigate the risk for disability pension in overweight and obese employees with or without metabolic syndrome. METHODS:In a cohort based on occupational health data 1992-2009, the risk for any type of disability pension was analyzed with adjusted hazard ratios and 95% confidence intervals (CIs) both in normal weight, overweight, and obese employees and if the risk from metabolic syndrome was influenced by age and gender. RESULTS:Both overweight and obese employees had an increased risk for disability pension. Among employees with metabolic syndrome, hazard ratio was 1.89 (95% CI = 1.28-2.78) for young overweight men, 1.95 (95% CI = 1.03-3.69) for young obese men, and 2.26 (95% CI = 0.98-5.29) for young obese women. CONCLUSIONS:Metabolic syndrome increased the risk for disability pension in young male employees with overweight and obesity.

Background The association between socioeconomic status (SES) and environmental burden is context-dependent. Those with low SES may be more likely to live near major roads and industries where environmental exposures are high but may also be more likely to live further away from city centers. The aim of this study was to investigate the association between SES and environmental burden in Sweden. Methods The Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort recruited participants from six Swedish cities during 2013-2018. Residential environmental exposures (particulate matter <2.5 m [PM2.5], road traffic noise, and lack of greenspace) and neighborhood-level SES factors (proportions with low-income, low education, unemployment, rental units, foreign born) were assessed from participants' addresses in 2018. Individual-level SES factors (financial buffer, education, occupation, type of living, foreign born) were obtained from a questionnaire and neighborhood data from Statistics Sweden. Linear regression models were used to analyze the link between environmental exposures and SES factors. Correlations between SES factors were analyzed using Cram & eacute;r's V and Spearman rank correlations. Results The study included 23 320 SCAPIS participants in 1939 neighborhoods. The explanatory power of SES factors differed substantially between factors and cities. A model with all ten SES factors could account for 25-88 %, 36-60 %, and 49-81 % of the spatial variance in PM2.5, noise, and lack of greenspace respectively. Neighborhoods with more low-income earners, rental units and foreign born had more environmental burden. Neighborhoods with more inhabitants with low education and unemployment had less environmental burden. Associations were generally non-linear. Individual-level SES factors were not associated with environmental burdens after adjusting for neighborhood SES factors. Individual and neighborhood SES were weakly correlated. Conclusion Neighborhood SES factors accounted for a large proportion of the variance in environmental burdens, whereas individual SES factors did not. The relationship between SES and environmental burden differed greatly between indicators and cities.

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 mu m (PM2.5), <10 mu m (PM10), and nitrogen oxides (NOx) 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 PM2.5 exposure was 6.2 mu g/m(3) (range 3.5-13.4 mu g/m(3)). 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 PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 mu g/m(3)). 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, PM2.5 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.

[This corrects the article DOI: 10.1016/j.lanepe.2024.101091.].

Background:Available evidence suggests a link between exposure to transportation noise and an increased risk of obesity. We aimed to assess exposure-response functions for long-term residential exposure to road traffic, railway and aircraft noise, and markers of obesity.Methods:Our cross-sectional study is based on pooled data from 11 Nordic cohorts, including up to 162,639 individuals with either measured (69.2%) or self-reported obesity data. Residential exposure to transportation noise was estimated as a time-weighted average Lden 5 years before recruitment. Adjusted linear and logistic regression models were fitted to assess beta coefficients and odds ratios (OR) with 95% confidence intervals (CI) for body mass index, overweight, and obesity, as well as for waist circumference and central obesity. Furthermore, natural splines were fitted to assess the shape of the exposure-response functions.Results:For road traffic noise, the OR for obesity was 1.06 (95% CI = 1.03, 1.08) and for central obesity 1.03 (95% CI = 1.01, 1.05) per 10 dB Lden. Thresholds were observed at around 50-55 and 55-60 dB Lden, respectively, above which there was an approximate 10% risk increase per 10 dB Lden increment for both outcomes. However, linear associations only occurred in participants with measured obesity markers and were strongly influenced by the largest cohort. Similar risk estimates as for road traffic noise were found for railway noise, with no clear thresholds. For aircraft noise, results were uncertain due to the low number of exposed participants.Conclusion:Our results support an association between road traffic and railway noise and obesity.

Background:Transportation noise has been linked with cardiometabolic outcomes, yet whether it is a risk factor for atrial fibrillation (AF) remains inconclusive. We aimed to assess whether transportation noise was associated with AF in a large, pooled Nordic cohort. Methods:We pooled data from 11 Nordic cohorts, totaling 161,115 participants. Based on address history from five years before baseline until end of follow-up, road, railway, and aircraft noise was estimated at a residential level. Incident AF was ascertained via linkage to nationwide patient registries. Cox proportional hazards models were utilized to estimate associations between running 5-year time-weighted mean transportation noise (Lden) and AF after adjusting for sociodemographics, lifestyle, and air pollution. Findings:We identified 18,939 incident AF cases over a median follow-up of 19.6 years. Road traffic noise was associated with AF, with a hazard ratio (HR) and 95% confidence interval (CI) of 1.02 (1.00-1.04) per 10-dB of 5-year mean time-weighted exposure, which changed to 1.03 (1.01-1.06) when implementing a 53-dB cut-off. In effect modification analyses, the association for road traffic noise and AF appeared strongest in women and overweight and obese participants. Compared to exposures ≤40 dB, aircraft noise of 40.1-50 and > 50 dB were associated with HRs of 1.04 (0.93-1.16) and 1.12 (0.98-1.27), respectively. Railway noise was not associated with AF. We found a HR of 1.19 (1.02-1.40) among people exposed to noise from road (≥45 dB), railway (>40 dB), and aircraft (>40 dB) combined. Interpretation:Road traffic noise, and possibly aircraft noise, may be associated with elevated risk of AF. Funding:NordForsk.

Introduction: Perfluoroalkyl substances (PFAS) are persisting chemicals with endocrine disruptive and carcinogenic properties. Previous studies involving cohorts with high PFAS exposure have not shown an increased risk of breast cancer. Research on PFAS and breast cancer according to hormone receptor status is limited. This study aims to investigate the association between PFAS exposure and hormone receptor-positive breast cancer. Materials and Methods: In 2013, high levels of PFAS (sum of PFAS >10,000 ng/L), dominated by perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS) were found in the drinking water from one of the two waterworks in Ronneby, Sweden. Breast cancer diagnoses and information of adjuvant endocrine therapy were retrieved from the Swedish Cancer Register and The Prescribed Drug Register 2006-2016 for a cohort of women residing in the municipality between 1985 and 2013 (n=24,509). Individual exposure was assessed based on municipality waterworks distribution data linked to annual residential addresses. Cox proportional hazards models were used in the analysis. The highest achieved educational level was used as an indicator of socioeconomic position. Sensitivity and subgroup analysis were performed for prepubertal exposure and diagnosis before or after age 50 (assumed menopause). Results: There were 313 cases of malignant breast cancer among women <= 85 years between 2006 and 2016. Of these, 224 cases (72%) were considered hormone receptor-positive based on the first prescription of adjuvant endocrine therapy, antiestrogens (40%) or aromatase inhibitor (60%). Among women ever living at a residential address with high PFAS exposure, the hazard ratio (HR) for breast cancer classified as hormone receptor-positive was 0.84; 95% confidence interval (CI) 0.61, 1.14. Findings were similar before and after menopause. Conclusion: High PFAS exposure from drinking water, dominated by PFOS and PFHxS, was not associated with an elevated risk of hormone receptor-positive breast cancer.

AimThe aim was to investigate mortality among Swedish seafarers compared to the general population, and differences in mortality between occupational categories and differences over time.MethodsLongitudinal register-based cohort study of 85,169 Swedish seafarers registered in the Swedish Transport Agency's Seafarers' Registry (SR) 1985-2013. The cohort was matched with the Swedish Cause of Death Register. Standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) were calculated stratified by gender, job category, start of sea service, and time registered in the SR. Seafarers were followed until 66 years of age. Mortality by diseases was analyzed for seafarers with at least 5 years of sea service and mortality due to external causes was analyzed for all seafarers.ResultsTotal mortality was increased among men who started to work before 1985 (SMR: 1.27, 95% CI: 1.21-1.32) and borderline significantly increased among women (SMR: 1.14, 95% CI: 0.99-1.32). Mortality ratios due to lung cancer, accidents, suicides, and mental disorders including substance abuse, were increased among seafarers who started to work before 1985. Mortality risks were particularly increased among the crew. SMRs tended to decrease over time, but mortality due to accidents was still increased among the crew who started to work 1985 or later (SMR: 1.64, 95% CI: 1.02-2.63).ConclusionSwedish seafarers had an increased mortality compared to the general population in 1985-2013, particularly the crew. There is still an increased mortality in accidents among crew who started to work 1985 or later.

Abstract 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 AND AIM: Despite firm evidence for an association between long-term air pollution exposure and cardiovascular events also at low exposure levels, previous epidemiological studies on the association with atherosclerosis have been inconsistent. The aim of this study was to investigate associations between long-term low-level air pollutant exposure and coronary atherosclerosis. METHOD: We performed a cross-sectional analysis in the large Swedish CardioPulmonary bioImaging Study (SCAPIS, n = 30 154). Men and women 50–64 years old were recruited from the general population of six Swedish cities 2013–2018. Outcomes were coronary atherosclerosis (segment involvement score, SIS), coronary artery calcium score (CACS), and non-calcified coronary plaque (NCP) prevalence. Hourly total and source-specific residential PM2.5, PM10, and NOx were modelled in dispersion models with high spatial resolution and averaged over 10 years before recruitment. Prevalence odds ratios (POR) were estimated with ordinal logistic regression models adjusted for site and known risk factors, based on a directed acyclical graph. RESULTS: Median PM2.5 exposure was 6.2 µg/m3; 44% of participants had detectable coronary atherosclerosis. PM2.5 was not associated with SIS or CACS, but with a higher NCP prevalence (POR 1.65, 95% CI 1.18, 2.31, per interquartile range [2.05 µg/m3] higher PM2.5) with a dose-response pattern (p = 0.034 for linear trend). Other pollutants and source-specific exposures did not demonstrate consistent positive associations with any of the outcomes. CONCLUSIONS: In this large, middle-aged general population sample at low exposure levels, PM2.5 exposure was not associated with estimates of general coronary atherosclerosis or calcification, yet appeared to be associated with non-calcified plaques, which may reflect an association with the early phase of atherosclerosis or more vulnerable forms of atherosclerosis. The main funder of SCAPIS is the Swedish Heart and Lung Foundation. Funding for this study was provided by the Swedish Research Council for Health, Working Life and Welfare (FORTE).

OBJECTIVES:To elucidate whether occupational exposure to soft paper dust increases the incidence of cancer.METHODS:We studied 7988 workers in Swedish soft paper mills from 1960 to 2008, of whom 3233 (2 187 men and 1046 women) had more than 10 years of employment. They were divided into high exposure (>5 mg/m3 for >1 year) or lower exposure to soft paper dust based on a validated job-exposure matrix. They were followed from 1960 to 2019, and person-years at risk were stratified according to gender, age, and calendar-year. The expected numbers of incident tumors were calculated using the Swedish population as the reference, and standardized incidence ratios (SIR) with 95% confidence intervals (95% CI) were assessed.RESULTS:Among high-exposure workers with more than 10 years of employment, there was an increased incidence of colon cancer (SIR 1.66, 95% CI 1.20-2.31), small intestine cancer (SIR 3.27, 95% CI 1.36-7.86), and thyroid gland cancer (SIR 2.68, 95% CI 1.11-6.43), as well as lung cancer (SIR 1.56, 95% CI 1.12-2.19). Among the lower-exposed workers there was an increased incidence of connective tissue tumors (sarcomas) (SIR 2.26, 95% CI 1.13-4.51) and pleural mesothelioma (SIR 3.29, 95% CI 1.37-7.91).CONCLUSION:Workers in soft paper mills with high exposure to soft paper dust have an increased incidence of large and small intestine tumors. Whether the increased risk is caused by paper dust exposure or some unknown associated factors is unclear. The increased incidence of pleural mesothelioma is probably linked to asbestos exposure. The reason for increased incidence of sarcomas is unknown.

Background: Epidemiological studies linking type 2 diabetes (T2D) and exposure to per-and polyfluoroalkyl substances (PFAS), are limited and have yielded conflicting results. This register-based study aimed to investigate the risk of T2D among Swedish adults who had been exposed to PFAS from highly contaminated drinking water for decades.Methods: The study included 55,032 adults (aged >= 18 years) from the Ronneby Register Cohort, who ever lived in Ronneby during 1985-2013. Exposure was assessed using the yearly residential address and the absence ("never-high") or presence ("ever-high") of high PFAS contamination in the municipal drinking water supply; the latter was subdivided into "early-high" and "late-high" exposure with cut-off at 2005. Incident T2D cases were retrieved from the National Patient Register and the Prescription Register. Cox proportional hazard models with time-varying exposure were used to estimate hazard ratios (HRs). Stratified analyses were performed based on age (18-45 vs > 45).Results: Elevated HRs for T2D were observed when comparing "ever-high" to "never-high" exposure (HR 1.18, 95% CI 1.03-1.35), as well as when comparing "early-high" (HR 1.12, 95% CI 0.98-1.50) or "late-high" (HR 1.17, 95% CI 1.00-1.37) to "never-high", after adjusting for age and sex. Individuals aged 18-45 years had even higher HRs. Adjusting for the highest-achieved education level attenuated the estimates, but the directions of associations remained. Elevated HRs were also found among those who had lived in areas with a heavily contaminated water supply for 1-5 years (HR 1.26, 95% CI 0.97-1.63) and 6-10 years (HR 1.25, 95% CI 0.80-1.94).Conclusion: This study suggests an increased risk of T2D after long-term high PFAS exposure through drinking water. In particular, a higher risk of early onset diabetes was found, indicating increased susceptibility to PFAS-related health effects at younger ages.

Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.

OBJECTIVE:To elucidate whether occupational noise exposure increases the mortality from ischemic heart disease (IHD) and stroke, and if exposure to paper dust modified the risks. METHODS:We studied 6686 workers from soft paper mills, with occupational noise exposure, < 85 dBA, 85-90 dBA and > 90 dBA, and high (> 5 mg/m3) exposure to paper dust. Person-years 1960-2019 were stratified according to gender, age, and calendar-year. Expected numbers of deaths were calculated using the Swedish population as the reference and standardized mortality ratios (SMR) with 95% confidence intervals (95% CI) were assessed. RESULTS:SMR for IHD was 1.12 (95% CI 0.88-1.41) for noise < 85 dBA, 1.18 (95% CI 0.90-1.55) for 85-90 dBA, and 1.27 (95% CI 1.10-1.47) among workers exposed > 90 dBA. Joint exposure to high noise exposure and high exposure to paper dust resulted in slightly higher IHD mortality (SMR 1.39, 95% CI 1.15-1.67). SMR for ischemic stroke was 0.90 (95% CI 0.37-2.15) for noise < 85 dBA, 1.08 (95% CI 0.45-2.59) for 85-90 dBA, and 1.48 (95% CI 0.99-2.00) among workers exposed > 90 dBA. High noise exposure and high exposure to paper dust resulted in higher ischemic stroke mortality (SMR 1.83, 95% CI 1.12-2.98). CONCLUSION:Noise levels > 90 dBA was associated with increased IHD mortality. Combined exposures of noise and paper dust may further increase the risks. Our results do not provide support for a causal relationship for ischemic stroke. Residual confounding from smoking has to be considered. Workers need to be protected from occupational noise levels exceeding 90 dBA.

Environmental noise is the second largest environmental risk factor in disease burden estimates for Europe. While socioeconomic inequalities in noise exposure have been reported, the impact of socioeconomic status (SES) on the disease burden attributable to noise exposure has to our knowledge not been reported previously. The aim of this study is to assess the impact of SES on traffic noise exposure and the associated disease burden in selected Nordic populations. We employed nationwide data on road traffic noise exposure and SES from Danish and Norwegian Nationwide Models. The impact of household income and education on traffic noise exposure was assessed using linear regression analyses. Burden of disease estimates were calculated for populations stratified according to their level of income and education in terms of Disability-Adjusted Life Years (DALY) for high degree of noise annoyance, high degree of sleep disturbance and ischaemic heart disease. The most consistent finding observed for the Danish population was that, compared to medium and low household income, high household income was associated with lower noise exposure. Moreover, the burden of disease estimates for high noise annoyance were up to 20% lower in the high compared to the lower household income groups.

Background: Transportation noise may induce cardiovascular disease, but the public health implications are unclear. Objectives: The study aimed to assess exposure–response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes. Methods: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors. Results: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB Lden for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB Lden for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure–response relations. A threshold at around 55 dB Lden was suggested in the exposure–response relation for road traffic noise and IHD. Discussion: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745

Background: Several studies have shown associations between cadmium (Cd) exposure and an increased risk of fractures. However, the size of the risk is still unclear and proper adjustment for smoking is a challenge. The aim of this study was to quantify the association between dietary cadmium measured in blood and fracture risk in the general Swedish population through a large population-based case-control study in never-smokers.Methods: The study included 2113 incident cases with osteoporosis-related fractures and the same number of age- and sex-matched controls in never-smokers from the Swedish population-based Malm & ouml; Diet and Cancer study cohort. Cd in blood (B-Cd) was analyzed at baseline (1991-1996). Incident osteoporosis-related fractures (of the hip, distal radius, and proximal humerus) up to the year 2014 were identified using the National Patient Register. Associations between B-Cd and fractures were analyzed using logistic regression.Results: Median B-Cd was 0.22 mu g/L (P25 = 0.16, P75 = 0.31) among 2103 cases and 0.21 (P25 = 0.15, P75 = 0.30) among 2105 controls. The risk of fracture was significantly increased (OR 1.58; 95 % confidence interval 1.08-2.31, per mu g/L of B-Cd), after adjustment for age, sex, BMI, physical activity, and fiber consumption. In analyses by cadmium quartiles, the OR increased monotonically and was significant in the highest quartile of B-Cd (for B-Cd > 0.31 versus B-Cd < 0.15 mu g/L; OR 1.21; 95 % confidence interval 1.01-1.45).Conclusion: Even modestly increased blood cadmium in never-smokers is associated with increased risk of incident osteoporosis-related fractures.

Long-term exposure to air pollution is associated with cardiovascular events. A main suggested mechanism is that air pollution accelerates the progression of atherosclerosis, yet current evidence is inconsistent regarding the association between air pollution and coronary artery and carotid artery atherosclerosis, which are well-established causes of myocardial infarction and stroke. We studied associations between low levels of long-term air pollution, coronary artery calcium (CAC) score, and the prevalence and area of carotid artery plaques, in a middle-aged population-based cohort. The Swedish CArdioPulmonary bioImage Study (SCAPIS) Gothenburg cohort was recruited during 2013-2017 and thoroughly examined for cardiovascular risk factors, including computed tomography of the heart and ultrasonography of the carotid arteries. In 5070 participants (age 50-64 years), yearly residential exposures to air pollution (PM2.5, PM10, PMcoarse, NOx, and exhaust-specific PM2.5 1990-2015) were estimated using high-resolution dispersion models. We used Poisson regression to examine associations between long-term (26 years' mean) exposure to air pollutants and CAC score, and prevalence of carotid artery plaques, adjusted for potential confounders. Among participants with carotid artery plaques, we also examined the association with plaque area using linear regression. Mean exposure to PM2.5 was low by international standards (8.5 mu g/m(3)). There were no consistent associations between long-term total PM2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM2.5 and larger plaque area in participants with carotid plaques. Associations with traffic-related air pollutants were consistently positive for both a high CAC score and bilateral carotid artery plaques. These associations were independent of road traffic noise. We found stronger associations among men and participants with cardiovascular risk factors. The results lend some support to atherosclerosis as a main modifiable pathway between low levels of traffic-related ambient air pollution and cardiovascular disease, especially in vulnerable individuals.