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- Stockfelt, Leo, 1981, et al.
(author)
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Long-Term Exposure to Particulate Air Pollution, Black Carbon, and Their Source Components in Relation to Ischemic Heart Disease and Stroke
- 2019
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In: Journal of Environmental Health Perspectives. - Durham : National Institute of Environmental Health Sciences. - 0091-6765 .- 1552-9924. ; 127:10
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Journal article (peer-reviewed)abstract
- BACKGROUND: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources.OBJECTIVES: We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities.METHODS: ), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models.RESULTS: exposure from residential heating.DISCUSSION: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations.
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- Frostad, J. J., et al.
(author)
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Mapping development and health effects of cooking with solid fuels in low-income and middle-income countries, 2000-18: a geospatial modelling study
- 2022
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In: Lancet Global Health. - 2214-109X. ; 10:10
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Journal article (peer-reviewed)abstract
- Background More than 3 billion people do not have access to clean energy and primarily use solid fuels to cook. Use of solid fuels generates household air pollution, which was associated with more than 2 million deaths in 2019. Although local patterns in cooking vary systematically, subnational trends in use of solid fuels have yet to be comprehensively analysed. We estimated the prevalence of solid-fuel use with high spatial resolution to explore subnational inequalities, assess local progress, and assess the effects on health in low-income and middle-income countries (LMICs) without universal access to clean fuels. Methods We did a geospatial modelling study to map the prevalence of solid-fuel use for cooking at a 5 km x 5 km resolution in 98 LMICs based on 2.1 million household observations of the primary cooking fuel used from 663 population-based household surveys over the years 2000 to 2018. We use observed temporal patterns to forecast household air pollution in 2030 and to assess the probability of attaining the Sustainable Development Goal (SDG) target indicator for clean cooking. We aligned our estimates of household air pollution to geospatial estimates of ambient air pollution to establish the risk transition occurring in LMICs. Finally, we quantified the effect of residual primary solid-fuel use for cooking on child health by doing a counterfactual risk assessment to estimate the proportion of deaths from lower respiratory tract infections in children younger than 5 years that could be associated with household air pollution. Findings Although primary reliance on solid-fuel use for cooking has declined globally, it remains widespread. 593 million people live in districts where the prevalence of solid-fuel use for cooking exceeds 95%. 66% of people in LMICs live in districts that are not on track to meet the SDG target for universal access to clean energy by 2030. Household air pollution continues to be a major contributor to particulate exposure in LMICs, and rising ambient air pollution is undermining potential gains from reductions in the prevalence of solid-fuel use for cooking in many countries. We estimated that, in 2018, 205000 (95% uncertainty interval 147000-257000) children younger than 5 years died from lower respiratory tract infections that could be attributed to household air pollution. Interpretation Efforts to accelerate the adoption of clean cooking fuels need to be substantially increased and recalibrated to account for subnational inequalities, because there are substantial opportunities to improve air quality and avert child mortality associated with household air pollution. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd.
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- Aasvang, Gunn Marit, et al.
(author)
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Burden of disease due to transportation noise in the Nordic countries.
- 2023
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In: Environmental research. - 1096-0953. ; 231:Pt 1
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Journal article (peer-reviewed)abstract
- Environmental noise is of increasing concern for public health. Quantification of associated health impacts is important for regulation and preventive strategies.To estimate the burden of disease (BoD) due to road traffic and railway noise in four Nordic countries and their capitals, in terms of DALYs (Disability-Adjusted Life Years), using comparable input data across countries.Road traffic and railway noise exposure was obtained from the noise mapping conducted according to the Environmental Noise Directive (END) as well as nationwide noise exposure assessments for Denmark and Norway. Noise annoyance, sleep disturbance and ischaemic heart disease were included as the main health outcomes, using exposure-response functions from the WHO, 2018 systematic reviews. Additional analyses included stroke and type 2 diabetes. Country-specific DALY rates from the Global Burden of Disease (GBD) study were used as health input data.Comparable exposure data were not available on a national level for the Nordic countries, only for capital cities. The DALY rates for the capitals ranged from 329 to 485 DALYs/100,000 for road traffic noise and 44 to 146 DALY/100,000 for railway noise. Moreover, the DALY estimates for road traffic noise increased with up to 17% upon inclusion of stroke and diabetes. DALY estimates based on nationwide noise data were 51 and 133% higher than the END-based estimates, for Norway and Denmark, respectively.Further harmonization of noise exposure data is required for between-country comparisons. Moreover, nationwide noise models indicate that DALY estimates based on END considerably underestimate national BoD due to transportation noise. The health-related burden of traffic noise was comparable to that of air pollution, an established risk factor for disease in the GBD framework. Inclusion of environmental noise as a risk factor in the GBD is strongly encouraged.
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7. |
- Andersson, Eva M., 1968, et al.
(author)
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Road traffic noise, air pollution and cardiovascular events in a Swedish cohort
- 2020
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In: Environmental Research. - : Elsevier BV. - 0013-9351. ; 185
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Journal article (peer-reviewed)abstract
- Urbanization and increasing road traffic cause exposure to both noise and air pollution. While the levels of air pollutants such as nitrogen oxides (NOx) have decreased in Sweden during the past decades, exposure to traffic noise has increased. The association with cardiovascular morbidity is less well established for noise than for air pollution, and most studies have only studied one of the two highly spatially correlated exposures. The Swedish Primary Prevention Study cohort consists of men aged 47 to 55 when first examined in 1970-1973. The cohort members were linked to the Swedish patient registry through their personal identity number and followed until first cardiovascular event 1970-2011. The address history during the entire study period was used to assign annual modelled residential exposure to road traffic noise and NOx. The Cox proportional hazards model with age on the time axis and time-varying exposures were used in the analysis. The results for 6304 men showed a non-significant increased risk of cardiovascular disease for long-term road traffic noise at the home address, after adjusting for air pollution. The hazard ratios were 1.08 (95% CI 0.90-1.28) for cardiovascular mortality, 1.14 (95% CI 0.96-1.36) for ischemic heart disease incidence and 1.07 (95% CI 0.85-1.36) for stroke incidence, for noise above 60 dB, compared to below 50 dB. This study found some support for cardiovascular health effects of long-term exposure to road traffic noise above 60 dB, after having accounted for exposure to air pollution.
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8. |
- Andersson, L., et al.
(author)
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Inflammatory and coagulatory markers and exposure to different size fractions of particle mass, number and surface area air concentrations in the Swedish hard metal industry, in particular to cobalt
- 2021
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In: Biomarkers. - : Informa UK Limited. - 1354-750X .- 1366-5804. ; 26:6
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Journal article (peer-reviewed)abstract
- Purpose To study the relationship between inhalation of airborne particles and cobalt in the Swedish hard metal industry and markers of inflammation and coagulation in blood. Methods Personal sampling of inhalable cobalt and dust were performed for subjects in two Swedish hard metal plants. Stationary measurements were used to study concentrations of inhalable, respirable, and total dust and cobalt, PM10 and PM2.5, the particle surface area and the particle number concentrations. The inflammatory markers CC16, TNF, IL-6, IL-8, IL-10, SAA and CRP, and the coagulatory markers FVIII, vWF, fibrinogen, PAI-1 and D-dimer were measured. A complete sampling was performed on the second or third day of a working week following a work-free weekend, and additional sampling was taken on the fourth or fifth day. The mixed model analysis was used, including covariates. Results The average air concentrations of inhalable dust and cobalt were 0.11 mg/m(3) and 0.003 mg/m(3), respectively. For some mass-based exposure measures of cobalt and total dust, statistically significant increased levels of FVIII, vWF and CC16 were found. Conclusions The observed relationships between particle exposure and coagulatory biomarkers may indicate an increased risk of cardiovascular disease.
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9. |
- Andersson, Lena, 1965-, et al.
(author)
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Respiratory health and inflammatory markers : Exposure to respirable dust and quartz and chemical binders in Swedish iron foundries
- 2019
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In: PLOS ONE. - : PLOS. - 1932-6203. ; 14:11
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Journal article (peer-reviewed)abstract
- PURPOSE: To study the relationship between respirable dust, quartz and chemical binders in Swedish iron foundries and respiratory symptoms, lung function (as forced expiratory volume FEV1 and vital capacity FVC), fraction of exhaled nitric oxide (FENO) and levels of club cell secretory protein 16 (CC16) and CRP.METHODS: Personal sampling of respirable dust and quartz was performed for 85 subjects in three Swedish iron foundries. Full shift sampling and examination were performed on the second or third day of a working week after a work free weekend, with additional sampling on the fourth or fifth day. Logistic, linear and mixed model analyses were performed including, gender, age, smoking, infections, sampling day, body mass index (BMI) and chemical binders as covariates.RESULTS: The adjusted average respirable quartz and dust concentrations were 0.038 and 0.66 mg/m3, respectively. Statistically significant increases in levels of CC16 were associated with exposure to chemical binders (p = 0.05; p = 0.01) in the regression analysis of quartz and respirable dust, respectively. Non-significant exposure-responses were identified for cumulative quartz and the symptoms asthma and breathlessness. For cumulative chemical years, non-significant exposure-response were observed for all but two symptoms. FENO also exhibited a non significant exposure-response for both quartz and respirable dust. No exposure-response was determined for FEV1 or FVC, CRP and respirable dust and quartz.CONCLUSIONS: Our findings suggest that early markers of pulmonary effect, such as increased levels of CC16 and FENO, are more strongly associated with chemical binder exposure than respirable quartz and dust in foundry environments.
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10. |
- Andersson, Lena, 1965-, et al.
(author)
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Respiratory Health and Inflammatory Markers : Exposure to Cobalt in the Swedish Hard Metal Industry
- 2020
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In: Journal of Occupational and Environmental Medicine. - : Lippincott Williams & Wilkins. - 1076-2752 .- 1536-5948. ; 62:10, s. 820-829
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Journal article (peer-reviewed)abstract
- OBJECTIVE: To study the relationship between inhalable dust and cobalt and respiratory symptoms, lung function, exhaled nitric oxide in expired air and CC16 in the Swedish hard metal industry.METHODS: Personal sampling of inhalable dust and cobalt, medical examination including blood sampling was performed for 72 workers. Exposure-response relationships was determined using logistic, linear and mixed model analysis.RESULTS: The average inhalable dust and cobalt concentrations were 0.079 and 0.0017 mg/m, respectively. Statistically significant increased serum levels of CC16 were determined when the high and low cumulative exposures for cobalt were compared. Non-significant exposure-response relationships was observed between cross-shift inhalable dust or cobalt exposures and asthma, nose dripping and bronchitis.CONCLUSIONS: Our findings suggest an exposure-response relationship between inhalable cumulative cobalt exposure and CC16 levels in blood, which may reflect an injury or a reparation process in the lungs.
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11. |
- Axelsson, Gösta, 1950, et al.
(author)
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Annoyance and worry in a petrochemical industrial area - prevalence, time trends and risk indicators
- 2013
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In: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1660-4601. ; 10:4, s. 1418-1438
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Journal article (peer-reviewed)abstract
- Abstract: In 1992, 1998, and 2006, questionnaires were sent to stratified samples of residents aged 18–75 years living near petrochemical industries (n = 600–800 people on each occasion) and in a control area (n = 200–1,000). The aims were to estimate the long-term prevalence and change over time of annoyance caused by industrial odour, industrial noise, and worries about possible health effects, and to identify risk indicators. In 2006, 20% were annoyed by industrial odour, 27% by industrial noise (1–4% in the control area), and 40–50% were worried about health effects or industrial accidents (10–20% in the control area). Multiple logistic regression analyses revealed significantly lower prevalence of odour annoyance in 1998 and 2006 than in 1992, while industrial noise annoyance increased significantly over time. The prevalence of worry remained constant. Risk of odour annoyance increased with female sex, worry of health effects, annoyance by motor vehicle exhausts and industrial noise. Industrial noise annoyance was associated with traffic noise annoyance and worry of health effects of traffic. Health-risk worry due to industrial air pollution was associated with female sex, having children, annoyance due to dust/soot in the air, and worry of traffic air pollution.
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12. |
- Azzouz, Mehjar, 1999, et al.
(author)
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Air pollution and biomarkers of cardiovascular disease and inflammation in the Malmo Diet and Cancer cohort
- 2022
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In: Environmental Health. - : Springer Science and Business Media LLC. - 1476-069X. ; 21:1
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Journal article (peer-reviewed)abstract
- 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 Malmo Diet and Cancer cohort includes 6103 participants from the general population of Malmo, Sweden. The participants were recruited 1991-1994. Annual mean residential exposure to particulate matter < 2.5 and < 10 mu m (PM2.5 and PM10), and nitrogen oxides (NOx) at year of recruitment were assigned from dispersion models. Blood samples collected at recruitment, including blood cell counts, and biomarkers (lymphocyte- and neutrophil counts, C-reactive protein (CRP), soluble urokinase-type plasminogen activator receptor (suPAR), lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), ceruloplasmin, orosomucoid, haptoglobin, complement-C3, and alpha-1-antitrypsin) were analyzed. Multiple linear regression models were used to investigate the cross-sectional associations between air pollutants and biomarkers. Results The mean annual exposure levels in the cohort were only slightly or moderately above the new WHO guidelines of 5 mu g/m(3) PM2.5 (10.5 mu g/m(3) PM2.5). Residential PM2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA(2) and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with 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.
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13. |
- Azzouz, Mehjar, 1999, et al.
(author)
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Does socioeconomic and environmental burden affect vulnerability to extreme air pollution and heat? A case-crossover study of mortality in California.
- 2024
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In: Journal of exposure science & environmental epidemiology. - 1559-064X.
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Journal article (peer-reviewed)abstract
- Extreme heat and air pollution is associated with increased mortality. Recent evidence suggests the combined effects of both is greater than the effects of each individual exposure. Low neighborhood socioeconomic status ("socioeconomic burden") has also been associated with increased exposure and vulnerability to both heat and air pollution. We investigated if neighborhood socioeconomic burden or the combination of socioeconomic and environmental exposures ("socioenvironmental burden") modified the effect of combined exposure to extreme heat and particulate air pollution on mortality in California.We used a time-stratified case-crossover design to assess the impact of daily exposure to extreme particulate matter <2.5μm (PM2.5) and heat on cardiovascular, respiratory, and all-cause mortality in California 2014-2019. Daily average PM2.5 and maximum temperatures based on decedent's residential census tract were dichotomized as extreme or not. Census tract-level socioenvironmental and socioeconomic burden was assessed with the CalEnviroScreen (CES) score and a social deprivation index (SDI), and individual educational attainment was derived from death certificates. Conditional logistic regression was used to estimate associations of heat and PM2.5 with mortality with a product term used to evaluate effect measure modification.During the study period 1,514,292 all-cause deaths could be assigned residential exposures. Extreme heat and air pollution alone and combined were associated with increased mortality, matching prior reports. Decedents in census tracts with higher socioenvironmental and socioeconomic burden experienced more days with extreme PM2.5 exposure. However, we found no consistent effect measure modification by CES or SDI on combined or separate extreme heat and PM2.5 exposure on odds of total, cardiovascular or respiratory mortality. No effect measure modification was observed for individual education attainment.We did not find evidence that neighborhood socioenvironmental- or socioeconomic burden significantly influenced the individual or combined impact of extreme exposures to heat and PM2.5 on mortality in California.We investigated the effect measure modification by socioeconomic and socioenvironmental of the co-occurrence of heat and PM2.5, which adds support to the limited previous literature on effect measure modification by socioeconomic and socioenvironmental burden of heat alone and PM2.5 alone. We found no consistent effect measure modification by neighborhood socioenvironmental and socioeconomic burden or individual level SES of the mortality association with extreme heat and PM2.5 co-exposure. However, we did find increased number of days with extreme PM2.5 exposure in neighborhoods with high socioenvironmental and socioeconomic burden. We evaluated multiple area-level and an individual-level SES and socioenvironmental burden metrics, each estimating socioenvironmental factors differently, making our conclusion more robust.
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14. |
- Azzouz, Mehjar, 1999, et al.
(author)
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Long-term ambient air pollution and venous thromboembolism in a population-based Swedish cohort.
- 2023
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In: Environmental pollution (Barking, Essex : 1987). - : Elsevier. - 1873-6424 .- 0269-7491. ; 331:Pt 1
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Journal article (peer-reviewed)abstract
- 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 29408 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 <2.5μg (PM2.5) and <10μg (PM10), nitrogen oxides (NOx) 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: 10.8μg/m3 for PM2.5, 15.8μg/m3 for PM10, 27.7μg/m3 for NOx, and 0.96μg/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 PM2.5 was associated with an increased risk of VTE (HR 1.17 (95%CI 1.01-1.37)) per interquartile range (IQR) of 1.2μg/m3 increase in PM2.5 exposure. No significant associations were found between other pollutants or lag0 PM2.5 and incident VTE. When VTE was divided into specific diagnoses, associations with lag1-10 PM2.5 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 PM2.5 was associated with increased risks of VTE in the general population in Sweden.
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15. |
- Barregård, Lars, 1948, et al.
(author)
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Impact on Population Health of Baltic Shipping Emissions
- 2019
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In: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1660-4601. ; 16:11
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Journal article (peer-reviewed)abstract
- Emission of pollutants from shipping contributes to ambient air pollution. Our aim was to estimate exposure to particulate air pollution (PM2.5) and health effects from shipping in countries around the Baltic Sea, as well as effects of the sulfur regulations for fuels enforced in 2015 by the Baltic Sulfur Emission Control Area (SECA). Yearly PM2.5 emissions, from ship activity data and emission inventories in 2014 and 2016, were estimated. Concentrations and population exposure (0.1 degrees x 0.1 degrees) of PM2.5 were estimated from a chemical transport mode, meteorology, and population density. Excess mortality and morbidity were estimated using established exposure-response (ER) functions. Estimated mean PM2.5 per inhabitant from Baltic shipping was 0.22 mu g/m(3) in 2014 in ten countries, highest in Denmark (0.57 mu g/m(3)). For the ER function with the steepest slope, the number of estimated extra premature deaths was 3413 in total, highest in Germany and lowest in Norway. It decreased by about 35% in 2016 (after SECA), a reduction of >1000 cases. In addition, 1500 non-fatal cases of ischemic heart disease and 1500 non-fatal cases of stroke in 2014 caused by Baltic shipping emissions were reduced by the same extent in 2016. In conclusion, PM2.5 emissions from Baltic shipping, and resulting health impacts decreased substantially after the SECA regulations in 2015.
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16. |
- Bugge, M. D., et al.
(author)
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Reactive hyperemia and baseline pulse amplitude among smelter workers exposed to fine and ultrafine particles
- 2020
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In: International Archives of Occupational and Environmental Health. - : Springer Science and Business Media LLC. - 0340-0131 .- 1432-1246. ; 93, s. 399-407
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Journal article (peer-reviewed)abstract
- Objective: Ambient exposure to fine particles is associated with increased cardiovascular morbidity and mortality. Associations between occupational particulate matter (PM) exposure and cardiovascular disease have been studied less. The objective of this study was to examine associations between PM exposure and endothelial function among workers in Norwegian smelters. Methods: We examined endothelial function with Endo-PAT equipment after a working day (WD) and on a day off (DO) in 59 furnace workers recruited from three metal smelters in Norway. The difference in baseline pulse amplitude (BPA) and reactive hyperemia index (RHI) between the 2days was analysed in relation to individual exposure to PM < 250nm (PM250) or the respirable aerosol fraction of particles, and adjusted for relevant covariates. Results: The exposure to PM250 ranged from 0.004 to 5.7mg/m3. The mean BPA was significantly higher on WD relative to DO (772 vs. 535, p = 0.001). This difference was associated with PM concentrations among participants ≥ 34years, but not among the younger workers. Reactive hyperemia was significantly lower on workdays relative to days off (1.70 vs. 1.84, p = 0.05). This difference was observed only among participants above the age 34. No associations with PM exposure were observed. Conclusions: PM exposure was associated with higher BPA among participants older than 34years. BPA reflects microvessel pulsatility. Our results may indicate an age-dependent cardiovascular susceptibility to PM exposure. Endothelial function measured by RHI was reduced on WD among participants 34years and older, but we found no associations between PM exposure and RHI. © 2019, The Author(s).
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17. |
- Carlsen, Hanne Krage, et al.
(author)
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Incident cardiovascular disease and long-term exposure to source-specific air pollutants in a Swedish cohort
- 2022
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In: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 209
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Journal article (peer-reviewed)abstract
- 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 PM2.5), black carbon (BC), and nitrogen oxides (NOx) 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 PM2.5 of 11 μg/m3 and NOx of 26 μg/m3) within the cohort were moderate in terms of environmental standards. After adjusting for confounders, we observed statistically significant associations between NOx and CHF (hazard ratio [HR] 1.11, 95% confidence interval [CI] 1.01–1.22) and NOx 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 NOx with increased risk of incident CHF and fatal MI, but not with coronary events and stroke. © 2022
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18. |
- Collaboration Global Burden of Disease,, et al.
(author)
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Measuring progress from 1990 to 2017 and projecting attainment to 2030 of the health-related Sustainable Development Goals for 195 countries and territories: a systematic analysis for the Global Burden of Disease Study 2017
- 2018
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In: Lancet. - : Elsevier BV. - 0140-6736. ; 392:10159, s. 2091-2138
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Journal article (peer-reviewed)abstract
- BACKGROUND: Efforts to establish the 2015 baseline and monitor early implementation of the UN Sustainable Development Goals (SDGs) highlight both great potential for and threats to improving health by 2030. To fully deliver on the SDG aim of "leaving no one behind", it is increasingly important to examine the health-related SDGs beyond national-level estimates. As part of the Global Burden of Diseases, Injuries, and Risk Factors Study 2017 (GBD 2017), we measured progress on 41 of 52 health-related SDG indicators and estimated the health-related SDG index for 195 countries and territories for the period 1990-2017, projected indicators to 2030, and analysed global attainment. METHODS: We measured progress on 41 health-related SDG indicators from 1990 to 2017, an increase of four indicators since GBD 2016 (new indicators were health worker density, sexual violence by non-intimate partners, population census status, and prevalence of physical and sexual violence [reported separately]). We also improved the measurement of several previously reported indicators. We constructed national-level estimates and, for a subset of health-related SDGs, examined indicator-level differences by sex and Socio-demographic Index (SDI) quintile. We also did subnational assessments of performance for selected countries. To construct the health-related SDG index, we transformed the value for each indicator on a scale of 0-100, with 0 as the 2.5th percentile and 100 as the 97.5th percentile of 1000 draws calculated from 1990 to 2030, and took the geometric mean of the scaled indicators by target. To generate projections through 2030, we used a forecasting framework that drew estimates from the broader GBD study and used weighted averages of indicator-specific and country-specific annualised rates of change from 1990 to 2017 to inform future estimates. We assessed attainment of indicators with defined targets in two ways: first, using mean values projected for 2030, and then using the probability of attainment in 2030 calculated from 1000 draws. We also did a global attainment analysis of the feasibility of attaining SDG targets on the basis of past trends. Using 2015 global averages of indicators with defined SDG targets, we calculated the global annualised rates of change required from 2015 to 2030 to meet these targets, and then identified in what percentiles the required global annualised rates of change fell in the distribution of country-level rates of change from 1990 to 2015. We took the mean of these global percentile values across indicators and applied the past rate of change at this mean global percentile to all health-related SDG indicators, irrespective of target definition, to estimate the equivalent 2030 global average value and percentage change from 2015 to 2030 for each indicator. FINDINGS: The global median health-related SDG index in 2017 was 59.4 (IQR 35.4-67.3), ranging from a low of 11.6 (95% uncertainty interval 9.6-14.0) to a high of 84.9 (83.1-86.7). SDG index values in countries assessed at the subnational level varied substantially, particularly in China and India, although scores in Japan and the UK were more homogeneous. Indicators also varied by SDI quintile and sex, with males having worse outcomes than females for non-communicable disease (NCD) mortality, alcohol use, and smoking, among others. Most countries were projected to have a higher health-related SDG index in 2030 than in 2017, while country-level probabilities of attainment by 2030 varied widely by indicator. Under-5 mortality, neonatal mortality, maternal mortality ratio, and malaria indicators had the most countries with at least 95% probability of target attainment. Other indicators, including NCD mortality and suicide mortality, had no countries projected to meet corresponding SDG targets on the basis of projected mean values for 2030 but showed some probability of attainment by 2030. For some indicators, including child malnutrition, several infectious diseases, and most violence measures, the annualised rates of change required to meet SDG targets far exceeded the pace of progress achieved by any country in the recent past. We found that applying the mean global annualised rate of change to indicators without defined targets would equate to about 19% and 22% reductions in global smoking and alcohol consumption, respectively; a 47% decline in adolescent birth rates; and a more than 85% increase in health worker density per 1000 population by 2030. INTERPRETATION: The GBD study offers a unique, robust platform for monitoring the health-related SDGs across demographic and geographic dimensions. Our findings underscore the importance of increased collection and analysis of disaggregated data and highlight where more deliberate design or targeting of interventions could accelerate progress in attaining the SDGs. Current projections show that many health-related SDG indicators, NCDs, NCD-related risks, and violence-related indicators will require a concerted shift away from what might have driven past gains-curative interventions in the case of NCDs-towards multisectoral, prevention-oriented policy action and investments to achieve SDG aims. Notably, several targets, if they are to be met by 2030, demand a pace of progress that no country has achieved in the recent past. The future is fundamentally uncertain, and no model can fully predict what breakthroughs or events might alter the course of the SDGs. What is clear is that our actions-or inaction-today will ultimately dictate how close the world, collectively, can get to leaving no one behind by 2030. FUNDING: Bill & Melinda Gates Foundation.
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19. |
- Dierschke, Katrin, et al.
(author)
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Acute respiratory effects and biomarkers of inflammation due to welding-derived nanoparticle aggregates
- 2017
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In: International Archives of Occupational and Environmental Health. - : Springer Science and Business Media LLC. - 0340-0131 .- 1432-1246. ; 90:5, s. 451-463
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Journal article (peer-reviewed)abstract
- Welders are exposed to airborne particles from the welding environment and often develop symptoms work-related from the airways. A large fraction of the particles from welding are in the nano-size range. In this study we investigate if the welders' airways are affected by exposure to particles derived from gas metal arc welding in mild steel in levels corresponding to a normal welding day. In an exposure chamber, 11 welders with and 10 welders without work-related symptoms from the lower airways and 11 non-welders without symptoms, were exposed to welding fumes (1 mg/m(3)) and to filtered air, respectively, in a double-blind manner. Symptoms from eyes and upper and lower airways and lung function were registered. Blood and nasal lavage (NL) were sampled before, immediately after and the morning after exposure for analysis of markers of oxidative stress. Exhaled breath condensate (EBC) for analysis of leukotriene B4 (LT-B4) was sampled before, during and immediately after exposure. No adverse effects of welding exposure were found regarding symptoms and lung function. However, EBC LT-B4 decreased significantly in all participants after welding exposure compared to filtered air. NL IL-6 increased immediately after exposure in the two non-symptomatic groups and blood neutrophils tended to increase in the symptomatic welder group. The morning after, neutrophils and serum IL-8 had decreased in all three groups after welding exposure. Remarkably, the symptomatic welder group had a tenfold higher level of EBC LT-B4 compared to the two groups without symptoms. Despite no clinical adverse effects at welding, changes in inflammatory markers may indicate subclinical effects even at exposure below the present Swedish threshold limit (8 h TWA respirable dust).
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20. |
- Ellingsen, D. G., et al.
(author)
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A study of atherothrombotic biomarkers in welders
- 2019
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In: International Archives of Occupational and Environmental Health. - : Springer Science and Business Media LLC. - 0340-0131 .- 1432-1246. ; 92:7, s. 1023-1031
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Journal article (peer-reviewed)abstract
- Introduction: Studies have shown that welders have increased cardiovascular mortality. This may be due to airborne particulate matter (PM) exposure. Elevated levels of PM in polluted urban air have been associated with increased cardiovascular mortality and morbidity. This study seeks to explore potential mechanisms for the increased cardiovascular mortality in welders. Methods: Seventy welders were compared to 74 referents. Exposure to PM was assessed by personal full-shift sampling of work room air the last 2days before collection of blood samples. Selected biomarkers of pro-coagulant activity, endothelial/platelet activation and systemic inflammation were determined in the samples. Results: The welders had been occupationally exposed to PM for 15years on average. The geometric mean current exposure to PM was 8.1mg/m3. They had statistically significantly higher concentrations of TNF-α, P-selectin, CD40L, prothrombin fragment 1 + 2 and d-dimer than the referents. Increasing concentrations of d-dimer and CD40L were observed by increasing current exposure to PM. Discussion: The study shows that welders highly exposed to welding PM were in a pro-thrombotic state with increased thrombin generation and consequently higher d-dimer concentrations. The welders had also increased endothelial/platelet activation as compared to the referents. These alterations are compatible with increased cardiovascular mortality as previously reported among welders. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.
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21. |
- García-Trabanino, Ramón, et al.
(author)
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Heat stress, dehydration, and kidney function in sugarcane cutters in El Salvador - A cross-shift study of workers at risk of Mesoamerican nephropathy.
- 2015
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In: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 142, s. 746-755
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Journal article (peer-reviewed)abstract
- An epidemic of progressive kidney failure afflicts sugarcane workers in Central America. Repeated high-intensity work in hot environments is a possible cause. To assess heat stress, dehydration, biomarkers of renal function and their possible associations. A secondary aim was to evaluate the prevalence of pre-shift renal damage and possible causal factors. Sugarcane cutters (N=189, aged 18–49 years, 168 of them male) from three regions in El Salvador were examined before and after shift. Cross-shift changes in markers of dehydration and renal function were examined and associations with temperature, work time, region, and fluid intake were assessed. Pre-shift glomerular filtration rate was estimated (eGFR) from serum creatinine. The mean work-time was 4 (1.4–11) hours. Mean workday temperature was 34–36 °C before noon, and 39–42 °C at noon. The mean liquid intake during work was 0.8 L per hour. There were statistically significant changes across shift. The mean urine specific gravity, urine osmolality and creatinine increased, and urinary pH decreased. Serum creatinine, uric acid and urea nitrogen increased, while chloride and potassium decreased. Pre-shift serum uric acid levels were remarkably high and pre-shift eGFR was reduced (<60 mL/min) in 23 male workers (14%). The high prevalence of reduced eGFR, and the cross-shift changes are consistent with recurrent dehydration from strenuous work in a hot and humid environment as an important causal factor. The pathophysiology may include decreased renal blood flow, high demands on tubular reabsorption, and increased levels of uric acid.
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22. |
- Global Burden of Disease, Collaboration, et al.
(author)
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Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017
- 2018
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In: Lancet. - : Elsevier BV. - 0140-6736. ; 392:10159, s. 1923-1994
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Journal article (peer-reviewed)abstract
- BACKGROUND: The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk-outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk-outcome pairs, and new data on risk exposure levels and risk-outcome associations. METHODS: We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk-outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017. FINDINGS: In 2017, 34.1 million (95% uncertainty interval [UI] 33.3-35.0) deaths and 1.21 billion (1.14-1.28) DALYs were attributable to GBD risk factors. Globally, 61.0% (59.6-62.4) of deaths and 48.3% (46.3-50.2) of DALYs were attributed to the GBD 2017 risk factors. When ranked by risk-attributable DALYs, high systolic blood pressure (SBP) was the leading risk factor, accounting for 10.4 million (9.39-11.5) deaths and 218 million (198-237) DALYs, followed by smoking (7.10 million [6.83-7.37] deaths and 182 million [173-193] DALYs), high fasting plasma glucose (6.53 million [5.23-8.23] deaths and 171 million [144-201] DALYs), high body-mass index (BMI; 4.72 million [2.99-6.70] deaths and 148 million [98.6-202] DALYs), and short gestation for birthweight (1.43 million [1.36-1.51] deaths and 139 million [131-147] DALYs). In total, risk-attributable DALYs declined by 4.9% (3.3-6.5) between 2007 and 2017. In the absence of demographic changes (ie, population growth and ageing), changes in risk exposure and risk-deleted DALYs would have led to a 23.5% decline in DALYs during that period. Conversely, in the absence of changes in risk exposure and risk-deleted DALYs, demographic changes would have led to an 18.6% increase in DALYs during that period. The ratios of observed risk exposure levels to exposure levels expected based on SDI (O/E ratios) increased globally for unsafe drinking water and household air pollution between 1990 and 2017. This result suggests that development is occurring more rapidly than are changes in the underlying risk structure in a population. Conversely, nearly universal declines in O/E ratios for smoking and alcohol use indicate that, for a given SDI, exposure to these risks is declining. In 2017, the leading Level 4 risk factor for age-standardised DALY rates was high SBP in four super-regions: central Europe, eastern Europe, and central Asia; north Africa and Middle East; south Asia; and southeast Asia, east Asia, and Oceania. The leading risk factor in the high-income super-region was smoking, in Latin America and Caribbean was high BMI, and in sub-Saharan Africa was unsafe sex. O/E ratios for unsafe sex in sub-Saharan Africa were notably high, and those for alcohol use in north Africa and the Middle East were notably low. INTERPRETATION: By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning. FUNDING: Bill & Melinda Gates Foundation.
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23. |
- Hansson, Marit, et al.
(author)
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HIV/AIDS awareness and risk behavior among students in Semey, Kazakhstan: a cross-sectional survey.
- 2008
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In: BMC international health and human rights. - 1472-698X. ; 8
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Journal article (peer-reviewed)abstract
- BACKGROUND: Until recently, young people in Kazakhstan have been only moderately affected by the global HIV epidemic. Today, however, the HIV epidemic in Central Asia is one of the most rapidly increasing epidemics in the world. It is mainly concentrated to vulnerable groups such as intravenous drug users, sex workers, the purchasers of sexual services and the financially marginalized. Young, sexually active people may however be the gateway for the epidemic to the general population, and knowledge about their attitudes and behavior is therefore important in planning preventive measures. METHODS: To gather information about young students and their attitudes and knowledge about HIV/AIDS, we collected 600 structured questionnaires and made 23 semi-structured interviews among three groups of students. Response rate was 99%. RESULTS: Almost 99% of the respondents had heard of HIV/AIDS, and 89% could identify ways to protect oneself against sexually transmitted HIV/AIDS. The main routes of transmission, sexual contact without condom and intravenous drug use, were both identified by 97% of the students. Twenty-five percent of the female students and 75% of the male students had had one or more sexual partners. More than 30% of the young men had purchased sex, and homosexuality was widely stigmatized. CONCLUSION: Risks for the spread of HIV/AIDS among young people in Kazakhstan include prostitution as well as stigmatization of the HIV positive and of homosexuals. Protective factors are good knowledge about risks and protection, and opportunities to talk and gather information about sexuality and HIV/AIDS.
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24. |
- Hasslöf, Helena, et al.
(author)
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Long-term exposure to air pollution and atherosclerosis in the carotid arteries in the Malmö diet and cancer cohort.
- 2020
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In: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 191
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Journal article (peer-reviewed)abstract
- Long-term exposure to air pollution increases the risk of cardiovascular morbidity and mortality, but the mechanisms are not fully known. Current evidence suggests that air pollution exposure contributes to the development of atherosclerosis. There are few studies investigating associations between air pollution and carotid plaques, a well-known precursor of cardiovascular disease.A Swedish population-based cohort (aged 45-64yearsat recruitment) was randomly selected from the Malmö Diet and Cancer study between 1991 and 1994, of which 6103 participants underwent ultrasound examination of the right carotid artery to determine carotid plaque presence and carotid intima media thickness (CIMT). Participants were assigned individual residential air pollution exposure (source-specific PM2.5, PM10, NOx, BC) at recruitment from Gaussian dispersion models. Logistic and linear regression models, adjusted for potential confounders and cardiovascular risk factors, were used to investigate associations between air pollutants and prevalence of carotid plaques, and CIMT, respectively.The prevalence of carotid plaques was 35%. The mean levels of PM2.5 and PM10 at recruitment were 11 and 14μg/m3, most of which was due to long range transport. The exposure contrast within the cohort was relatively low. PM2.5 exposure was associated with carotid plaques in a model including age and sex only (OR 1.10 (95% CI 1.01-1.20) per 1μg/m3), but after adjustment for cardiovascular risk factors and socioeconomic status (SES) the association was weak and not significant (OR 1.05 (95% CI 0.96-1.16) per 1μg/m3). The pattern was similar for PM10 and NOx exposure. Associations between air pollutants and plaques were slightly stronger for long-term residents and in younger participants with hypertension. There was no clear linear trend between air pollution exposure and plaque prevalence. Non-significant slightly positive associations were seen between air pollution exposures and CIMT.In this large, well-controlled cross-sectional study at low exposure levels we found no significant associations between air pollution exposures and subclinical atherosclerosis in the carotid arteries, after adjusting for cardiovascular risk factors and SES. Further epidemiological studies of air pollution and intermediate outcomes are needed to explain the link between air pollution and cardiovascular events.
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25. |
- Johannesson, Sandra, 1975, et al.
(author)
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Urban air pollution and effects on biomarkers of systemic inflammation and coagulation: a panel study in healthy adults
- 2014
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In: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 26:2, s. 84-94
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Journal article (peer-reviewed)abstract
- Context: Urban particulate air pollution is associated with cardiovascular diseases and mortality, possibly mediated through systemic inflammation and increased blood viscosity. Objectives: To examine short-term effects of exposure to urban air pollution on blood biomarkers for systemic inflammation and coagulation in a panel of healthy adults living in Gothenburg, Sweden. Materials and methods: The 16 volunteers, all non-smokers, median age 35 years, were called for blood sampling the morning after a day with high levels of urban particulate matter (PM10>30 mu g/m(3)) or a day with low levels (PM10<15 mu g/m(3) and NO2 <35 mu g/m(3)). Associations between exposure to air pollution and each biomarker (C-reactive protein, fibrinogen, serum amyloid A, coagulation factor VIII, plasminogen activator inhibitor-1, p-selectin, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, Clara cell protein 16 and surfactant protein D) were examined using a linear mixed-effects model. Results: In total, 12 sampling sessions were performed, six after high-pollution and six after low-pollution days, over 21 months. The ratio of air pollution levels between high-and low-pollution days was five for PM10 (median: 49 and 10 mg/m(3)) and two for NO2 (median: 47 and 24 mg/m(3)). No significant increase in blood levels of any of the biomarkers were seen after days with high air pollution levels compared with low levels. Conclusion: Biomarkers of inflammation and coagulation were not found to be significantly increased in the mornings after days with elevated levels of urban air pollution compared with low levels when performing repeated blood samplings in healthy volunteers.
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26. |
- Kilbo Edlund, Karl, et al.
(author)
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Health Risk Assessment of PM2.5 and PM2.5-Bound Trace Elements in Thohoyandou, South Africa
- 2021
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In: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1660-4601. ; 18:3
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Journal article (peer-reviewed)abstract
- We assessed the health risks of fine particulate matter (PM2.5) ambient air pollution and its trace elemental components in a rural South African community. Air pollution is the largest environmental cause of disease and disproportionately affects low- and middle-income countries. PM2.5 samples were previously collected, April 2017 to April 2018, and PM2.5 mass determined. The filters were analyzed for chemical composition. The United States Environmental Protection Agency's (US EPA) health risk assessment method was applied. Reference doses were calculated from the World Health Organization (WHO) guidelines, South African National Ambient Air Quality Standards (NAAQS), and US EPA reference concentrations. Despite relatively moderate levels of PM2.5 the health risks were substantial, especially for infants and children. The average annual PM2.5 concentration was 11 mu g/m(3), which is above WHO guidelines, but below South African NAAQS. Adults were exposed to health risks from PM2.5 during May to October, whereas infants and children were exposed to risk throughout the year. Particle-bound nickel posed both non-cancer and cancer risks. We conclude that PM2.5 poses health risks in Thohoyandou, despite levels being compliant with yearly South African NAAQS. The results indicate that air quality standards need to be tightened and PM2.5 levels lowered in South Africa.
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27. |
- Kilbo Edlund, Karl, et al.
(author)
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High-resolution dispersion modelling of PM2.5, PM10, NOx and NO2 exposure in metropolitan areas in Sweden 2000‒2018 – large health gains due to decreased population exposure
- 2024
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In: Air Quality, Atmosphere and Health. - 1873-9318 .- 1873-9326.
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Journal article (peer-reviewed)abstract
- Ambient air pollution remains the major environmental cause of disease. Accurate assessment of population exposure and small-scale spatial exposure variations over long time periods is essential for epidemiological studies. We estimated annual exposure to fine and coarse particulate matter (PM2.5, PM10), and nitrogen oxides (NOx, NO2) with high spatial resolution to examine time trends 2000‒2018, compliance with the WHO Air Quality Guidelines, and assess the health impact. The modelling area covered six metropolitan areas in Sweden with a combined population of 5.5 million. Long-range transported air pollutants were modelled using a chemical transport model with bias correction, and locally emitted air pollutants using source-specific Gaussian-type dispersion models at resolutions up to 50 × 50m. The modelled concentrations were validated using quality-controlled monitoring data. Lastly, we estimated the reduction in mortality associated with the decrease in population exposure. The validity of modelled air pollutant concentrations was good (R2 for PM2.5 0.84, PM10 0.61, and NOx 0.87). Air pollution exposure decreased substantially, from a population weighted mean exposure to PM2.5 of 12.2µgm−3 in 2000 to 5.4µgm−3 in 2018. We estimated that the decreased exposure was associated with a reduction of 2719 (95% CI 2046–3055) premature deaths annually. However, in 2018, 65%, 8%, and 42% of residents in the modelled areas were still exposed to PM2.5, PM10, or NO2 levels, respectively, that exceeded the current WHO Air Quality Guidelines for annual average exposure. This emphasises the potential public health benefits of reductions in air pollution emissions.
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28. |
- Kilbo Edlund, Karl, et al.
(author)
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Long-term ambient air pollution and coronary atherosclerosis : results from the Swedish SCAPIS study
- 2024
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In: Atherosclerosis. - : Elsevier. - 0021-9150 .- 1879-1484.
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Journal article (peer-reviewed)abstract
- 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 (PM2.5), <10 μm (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 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 PM2.5 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, 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.
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29. |
- Kilbo Edlund, Karl, et al.
(author)
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Long-term ambient air pollution and coronary atherosclerosis: Results from the Swedish SCAPIS study.
- 2024
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In: Atherosclerosis. - 1879-1484.
-
Journal article (peer-reviewed)abstract
- 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.We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n=30154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5μm (PM2.5), <10μm (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.Median 10-year average PM2.5 exposure was 6.2μg/m3 (range 3.5-13.4μg/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 PM2.5 was associated with NCP (adjusted OR 1.34, 95% CI 1.13, 1.58, per 2.05μg/m3). Associations with significant stenoses were inconsistent.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.
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30. |
- Kilbo Edlund, Karl, et al.
(author)
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Long-term exposure to air pollution, coronary artery calcification, and carotid artery plaques in the population-based Swedish SCAPIS Gothenburg cohort.
- 2022
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In: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 214:Pt 2
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Journal article (peer-reviewed)abstract
- 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 (8.5μg/m3). 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.
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31. |
- Kilbo Edlund, Karl, et al.
(author)
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Occupational particle exposure and chronic kidney disease: a cohort study in Swedish construction workers.
- 2024
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In: Journal of Occupational and Environmental Medicine. - : BMJ Publishing Group Ltd. - 1351-0711 .- 1470-7926. ; 81:5, s. 238-243
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Journal article (peer-reviewed)abstract
- Increasing epidemiological and experimental evidence suggests that particle exposure is an environmental risk factor for chronic kidney disease (CKD). However, only a few case-control studies have investigated this association in an occupational setting. Hence, our objective was to investigate associations between particle exposure and CKD in a large cohort of Swedish construction workers.We performed a retrospective cohort study in the Swedish Construction Workers' Cohort, recruited 1971-1993 (n=286089). A job-exposure matrix was used to identify workers exposed to nine different particulate exposures, which were combined into three main categories (inorganic dust and fumes, wood dust and fibres). Incident CKD and start of renal replacement therapy (RRT) were obtained from validated national registries until 2021 and analysed using adjusted Cox proportional hazards models.Exposure to inorganic dust and fumes was associated with an increased risk of CKD and RRT during working age (adjusted HR for CKD at age <65 years 1.15, 95%CI 1.05 to 1.26). The elevated risk did not persist after retirement age. Exposure to cement dust, concrete dust and diesel exhaust was associated with CKD. Elevated HRs were also found for quartz dust and welding fumes.Workers exposed to inorganic particles seem to be at elevated risk of CKD and RRT. Our results are in line with previous evidence of renal effects of ambient air pollution and warrant further efforts to reduce occupational and ambient particle exposure.
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32. |
- Koranyi, Isa, et al.
(author)
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Precarious employment and occupational accidents and injuries - a systematic review
- 2018
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In: Scandinavian Journal of Work Environment & Health. - : Scandinavian Journal of Work, Environment and Health. - 0355-3140 .- 1795-990X. ; 44:4, s. 341-350
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Journal article (peer-reviewed)abstract
- Objectives Precarious employment conditions have become more common in many countries over the last decades, and have been linked to various adverse health outcomes. The objective of this review was to collect and summarize existing scientific research of the relationship between dimensions of precarious employment and the rate of occupational injuries. Methods A protocol was developed in accordance with the PRISMA-P checklist for systematic literature reviews. We searched PubMed, Web of Science and Scopus for articles on observational studies from North America, Europe, Australia and New Zealand published in peer-reviewed journals 1990-2017. A minimum of two independent reviewers assessed each article with respect to quality and eligibility criteria. Articles of high/moderate quality meeting all specified inclusion criteria were included in the review. Results The literature search resulted in 471 original titles, of which 17 articles met all the inclusion criteria. The most common exposures were in descending order; temporary employment, multiple jobs, working for a subcontractor at the same worksite/temp agency, part-time, self-employment, hourly pay, union membership, insurance benefits, flexible versus fixed work schedule, wages, job insecurity, work-time control and precarious career trajectories. Ten studies reported a positive association between precarious employment and occupational injuries. Four studies reported a negative association, and three studies did not show any significant association. Conclusions This review supports an association between some of the dimensions of precarious employment and occupational injuries; most notably for multiple jobholders and employees of temp agencies or subcontractors at the same worksite. However, results for temporary employment are inconclusive. There is a need for more prospective studies of high quality, designed to measure effect sizes as well as causality.
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33. |
- Kriit, Hedi Katre, et al.
(author)
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Using Distributed Lag Non-Linear Models to Estimate Exposure Lag-Response Associations between Long-Term Air Pollution Exposure and Incidence of Cardiovascular Disease
- 2022
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In: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1661-7827 .- 1660-4601. ; 19:5
-
Journal article (peer-reviewed)abstract
- Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM2.5 ) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1–10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1–5-and 6–10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM2.5 total, BC, and IHD. However, for PM2.5 from local sources, a 20% risk increase per 1 µg/m3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2–4-year PM2.5 and BC, and also lags 8–9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1–5-and 6–10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.
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34. |
- Li, Huiqi, et al.
(author)
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A Cross-Sectional Study of the Cardiovascular Effects of Welding Fumes.
- 2015
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In: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 10:7
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Journal article (peer-reviewed)abstract
- OBJECTIVES: Occupational exposure to particulate air pollution has been associated with an increased risk of cardiovascular disease. However, the risk to welders working today remains unclear. We aimed to elucidate the cardiovascular effects of exposure to welding fumes. METHODS: In a cross-sectional study, structured interviews and biological sampling were conducted for 101 welders and 127 controls (all non-smoking males) from southern Sweden. Personal breathing zone sampling of respirable dust was performed. Blood pressure (BP) and endothelial function (using peripheral arterial tonometry) were measured. Plasma and serum samples were collected from peripheral blood for measurement of C-reactive protein, low-density lipoprotein, homocysteine, serum amyloid A, and cytokines. RESULTS: Welders were exposed to 10-fold higher levels of particles than controls. Welders had significantly higher BP compared to controls, an average of 5 mm Hg higher systolic and diastolic BP (P≤0.001). IL-8 was 3.4 ng/L higher in welders (P=0.010). Years working as a welder were significantly associated with increased BP (β=0.35, 95%CI 0.13 - 0.58, P=0.0024 for systolic BP; β=0.32, 95%CI 0.16 - 0.48, P<0.001 for diastolic BP, adjusted for BMI) but exposure to respirable dust was not associated with BP. No clear associations occurred between welding and endothelial function, or other effect markers. CONCLUSIONS: A modest increase in BP was found among welders compared to controls suggesting that low-to-moderate exposure to welding fumes remains a risk factor for cardiovascular disease.
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35. |
- Molnár, Peter, 1967, et al.
(author)
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Residential NOx exposure in a 35-year cohort study. Changes of exposure, and comparison with back extrapolation for historical exposure assessment
- 2015
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In: Atmospheric Environment. - : Elsevier BV. - 1352-2310 .- 1873-2844. ; 115, s. 62-69
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Journal article (peer-reviewed)abstract
- In this study we aimed to investigate the effects on historical NOx estimates on time trends, spatial distributions, exposure contrasts, the effect of relocation patterns and the effects of back extrapolation. Historical levels of nitrogen oxides (NOx) from 1975 to 2009 were modeled with high resolution in Gothenburg, Sweden, using historical emission databases and Gaussian models. Yearly historical addresses were collected and geocoded from a population-based cohort of Swedish men from 1973 to 2007, with a total of 160,568 address years. Of these addresses, 146,675 (91%) were within our modeled area and assigned a NOx level. NOx levels decreased substantially from a maximum median level of 43.9μg/m3 in 1983 to 16.6μg/m3 in 2007, mainly due to lower emissions per vehicle km. There was a considerable variability in concentrations within the cohort, with a ratio of 3.5 between the means in the highest and lowest quartile. About 50% of the participants changed residential address during the study, but the mean NOx exposure was not affected. About half of these moves resulted in a positive or negative change in NOx exposure of >10μg/m3, and thus changed the exposure substantially. Back extrapolation of NOx levels using the time trend of a background monitoring station worked well for 5-7 years back in time, but extrapolation more than ten years back in time resulted in substantial scattering compared to the "true" dispersion models for the corresponding years. These findings are important to take into account since accurate exposure estimates are essential in long term epidemiological studies of health effects of air pollution.
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36. |
- Mwase, Nandi S, et al.
(author)
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Health Impact of Air Pollution from Shipping in the Baltic Sea: Effects of Different Spatial Resolutions in Sweden.
- 2020
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In: International journal of environmental research and public health. - : MDPI AG. - 1660-4601. ; 17:21
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Journal article (peer-reviewed)abstract
- In 2015, stricter regulations to reduce sulfur dioxide emissions and particulate air pollution from shipping were implemented in the Baltic Sea. We investigated the effects on population exposure to particles <2.5 µm (PM2.5) from shipping and estimated related morbidity and mortality in Sweden's 21 counties at different spatial resolutions. We used a regional model to estimate exposure in Sweden and a city-scale model for Gothenburg. Effects of PM2.5 exposure on total mortality, ischemic heart disease, and stroke were estimated using exposure-response functions from the literature and combining them into disability-adjusted life years (DALYS). PM2.5 exposure from shipping in Gothenburg decreased by 7% (1.6 to 1.5 µg/m3) using the city-scale model, and 35% (0.5 to 0.3 µg/m3) using the regional model. Different population resolutions had no effects on population exposures. In the city-scale model, annual premature deaths due to shipping PM2.5 dropped from 97 with the high-sulfur scenario to 90 in the low-sulfur scenario, and in the regional model from 32 to 21. In Sweden, DALYs lost due to PM2.5 from Baltic Sea shipping decreased from approximately 5700 to 4200. In conclusion, sulfur emission restrictions for shipping had positive effects on health, but the model resolution affects estimations.
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37. |
- Nilsson Sommar, Johan, et al.
(author)
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Long-term exposure to particulate air pollution and black carbon in relation to natural and cause-specific mortality: a multicohort study in Sweden
- 2021
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In: Bmj Open. - : BMJ. - 2044-6055. ; 11:9
-
Journal article (peer-reviewed)abstract
- Objectives To estimate concentration-response relationships for particulate matter (PM) and black carbon (BC) in relation to mortality in cohorts from three Swedish cities with comparatively low pollutant levels. Setting Cohorts from Gothenburg, Stockholm and Umea, Sweden. Design High-resolution dispersion models were used to estimate annual mean concentrations of PM with aerodynamic diameter <= 10 mu m (PM10) and <= 2.5 mu m (PM2.5), and BC, at individual addresses during each year of follow-up, 1990-2011. Moving averages were calculated for the time windows 1-5 years (lag1-5) and 6-10 years (lag6-10) preceding the outcome. Cause-specific mortality data were obtained from the national cause of death registry. Cohort-specific HRs were estimated using Cox regression models and then meta-analysed including a random effect of cohort. Participants During the study period, 7 340 cases of natural mortality, 2 755 cases of cardiovascular disease (CVD) mortality and 817 cases of respiratory and lung cancer mortality were observed among in total 68 679 individuals and 689 813 person-years of follow-up. Results Both PM10 (range: 6.3-41.9 mu g/m(3)) and BC (range: 0.2-6.8 mu g/m(3)) were associated with natural mortality showing 17% (95% CI 6% to 31%) and 9% (95% CI 0% to 18%) increased risks per 10 mu g/m(3) and 1 mu g/m(3) of lag1-5 exposure, respectively. For PM2.5 (range: 4.0-22.4 mu g/m(3)), the estimated increase was 13% per 5 mu g/m(3), but less precise (95% CI -9% to 40%). Estimates for CVD mortality appeared higher for both PM10 and PM2.5. No association was observed with respiratory mortality. Conclusion The results support an effect of long-term air pollution on natural mortality and mortality in CVD with high relative risks also at low exposure levels. These findings are relevant for future decisions concerning air quality policies.
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38. |
- Olstrup, Henrik, et al.
(author)
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The Long-Term Mortality Effects Associated with Exposure to Particles and NOx in the Malmö Diet and Cancer Cohort
- 2023
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In: Toxics. - : MDPI. - 2305-6304. ; 11:11
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Journal article (peer-reviewed)abstract
- In this study, the long-term mortality effects associated with exposure to PM10 (particles with an aerodynamic diameter smaller than or equal to 10 µm), PM2.5 (particles with an aerodynamic diameter smaller than or equal to 2.5 µm), BC (black carbon), and NOx (nitrogen oxides) were analyzed in a cohort in southern Sweden during the period from 1991 to 2016. Participants (those residing in Malmö, Sweden, born between 1923 and 1950) were randomly recruited from 1991 to 1996. At enrollment, 30,438 participants underwent a health screening, which consisted of questionnaires about lifestyle and diet, a clinical examination, and blood sampling. Mortality data were retrieved from the Swedish National Cause of Death Register. The modeled concentrations of PM10, PM2.5, BC, and NOx at the cohort participants’ home addresses were used to assess air pollution exposure. Cox proportional hazard models were used to estimate the associations between long-term exposure to PM10, PM2.5, BC, and NOx and the time until death among the participants during the period from 1991 to 2016. The hazard ratios (HRs) associated with an interquartile range (IQR) increase in each air pollutant were calculated based on the exposure lag windows of the same year (lag0), 1–5 years (lag1–5), and 6–10 years (lag6–10). Three models were used with varying adjustments for possible confounders including both single-pollutant estimates and two-pollutant estimates. With adjustments for all covariates, the HRs for PM10, PM2.5, BC, and NOx in the single-pollutant models at lag1–5 were 1.06 (95% CI: 1.02–1.11), 1.01 (95% CI: 0.95–1.08), 1.07 (95% CI: 1.04–1.11), and 1.11 (95% CI: 1.07–1.16) per IQR increase, respectively. The HRs, in most cases, decreased with the inclusion of a larger number of covariates in the models. The most robust associations were shown for NOx, with statistically significant positive HRs in all the models. An overall conclusion is that road traffic-related pollutants had a significant association with mortality in the cohort.
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39. |
- Pyko, Andrei, et al.
(author)
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Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts.
- 2023
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In: Environmental health perspectives. - : Environmental Health Perspectives. - 1552-9924 .- 0091-6765. ; 131:1
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Journal article (peer-reviewed)abstract
- Transportation noise may induce cardiovascular disease, but the public health implications are unclear.The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes.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.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.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.
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40. |
- Ronnblad, T., et al.
(author)
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Precarious employment and mental health: a systematic review and meta-analysis of longitudinal studies
- 2019
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In: Scandinavian Journal of Work Environment & Health. - : Scandinavian Journal of Work, Environment and Health. - 0355-3140 .- 1795-990X. ; 45:5, s. 429-443
-
Research review (peer-reviewed)abstract
- Objectives Precarious employment (PE) is a term used to describe non-standard employment forms characterized by low security that may have negative effects on mental health. The objective of this review was to systematically review the evidence for effects of PE on mental health and identify important areas for further research. Methods A protocol was developed following PRISMA-P guidelines. Web of Science, PubMed and PsycINFO were searched up to 4 September 2017. All unique records were assessed for eligibility and quality by at least two reviewers. Data from included studies were summarized in forest plots and meta-analyses using a random-effects model. Evidence quality was rated using the GRADE method. Results We obtained 3328 unique records, of which 16 studies of sufficient quality met the inclusion criteria. Moderate quality evidence (GRADE score 3 of 4) was found for an adverse effect of job insecurity on mental health; summary odds ratio (OR) 1.52 [95% confidence interval (CI) 1.35-1.70]. There was very low quality (GRADE 1 of 4) evidence for effects of temporary employment or unpredictable work hours on mental health. Five studies on multidimensional exposures all showed adverse effects, weighted average OR 2.01 (95% CI 1.60-2.53). Conclusions Research on PE and mental health is growing, but high-quality prospective studies are still scarce. Job insecurity likely has an adverse effect on mental health. A clear multi-dimensional definition of PE is lacking, and harmonization efforts are needed. Further single-variable observational studies on job insecurity or temporary employment should not be prioritized.
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41. |
- Roswall, N., et al.
(author)
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Long-Term Exposure to Transportation Noise and Risk of Incident Stroke: A Pooled Study of Nine Scandinavian Cohorts
- 2021
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In: Environmental Health Perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 129:10
-
Journal article (peer-reviewed)abstract
- BACKGROUND: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. OBJECTIVE: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. METHODS: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution. RESULTS: During follow-up (median = 19.5 y), 11,056 stroke cases were identified. Road traffic noise (Lden) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of <= 2.5 mu m (PM2.5) and NO2]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. <= 40 dB) (HR = 1.12; 95% CI: 0.99, 1.27), but not with higher exposure (>= 50 dB, HR = 0.94; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke. DISCUSSION: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise.
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42. |
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43. |
- Stockfelt, Leo, 1981, et al.
(author)
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A controlled chamber study of effects of exposure to diesel exhaust particles and noise on heart rate variability and endothelial function
- 2022
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In: Inhalation Toxicology. - : Taylor and Francis Ltd.. - 0895-8378 .- 1091-7691. ; 34:5-6, s. 159-170
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Journal article (peer-reviewed)abstract
- Background: Adverse cardiovascular effects are associated with both diesel exhaust and road traffic noise, but these exposures are hard to disentangle epidemiologically. We used an experimental setup to evaluate the impact of diesel exhaust particles and traffic noise, alone and combined, on intermediary outcomes related to the autonomic nervous system and increased cardiovascular risk. Methods: In a controlled chamber 18 healthy adults were exposed to four scenarios in a randomized cross-over fashion. Each exposure scenario consisted of either filtered (clean) air or diesel engine exhaust (particle mass concentrations around 300 µg/m3), and either low (46 dB(A)) or high (75 dB(A)) levels of traffic noise for 3 h at rest. ECG was recorded for 10-min periods before and during each exposure type, and frequency-domain heart rate variability (HRV) computed. Endothelial dysfunction and arterial stiffness were assessed after each exposure using EndoPAT 2000. Results: Compared to control exposure, HRV in the high frequency band decreased during exposure to diesel exhaust, both alone and combined with noise, but not during noise exposure only. These differences were more pronounced in women. We observed no synergistic effects of combined exposure, and no significant differences between exposure scenarios for other HRV indices, endothelial function or arterial stiffness. Conclusion: Three-hour exposure to diesel exhaust, but not noise, was associated with decreased HRV in the high frequency band. This indicates activation of irritant receptor-mediated autonomic reflexes, a possible mechanism for the cardiovascular risks of diesel exposure. There was no effect on endothelial dysfunction or arterial stiffness after exposure. © 2022 The Author(s).
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44. |
- Stockfelt, Leo, 1981, et al.
(author)
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[Air pollution may exacerbate covid-19]. : Luftföroreningar kan förvärra covid-19-sjukdom.
- 2020
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In: Lakartidningen. - 1652-7518. ; 117
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Research review (peer-reviewed)abstract
- Several published and pre-print studies report associations between exposure to air pollution and COVID-19 mortality. While further epidemiological and experimental studies are still needed to prove causality, the association is plausible and consistent with the literature: Air pollution is associated with inferior outcomes in other respiratory infections, may act as carrier for the virus, exerts negative effects on the airways and is associated with cardiopulmonary comorbidities that lead to a poorer prognosis in COVID-19 patients. The lockdown to inhibit the spread of COVID-19 has led to substantial decreases in air pollution levels in many countries.
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45. |
- Stockfelt, Leo, 1981
(author)
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Cardiovascular and pulmonary health effects of air pollution - long term effects in Sweden and effects of wood smoke
- 2016
-
Doctoral thesis (other academic/artistic)abstract
- Exposure to air pollution is associated with increased morbidity and mortality in cardiovascular and pulmonary diseases. Main suggested mechanisms are airway and systemic inflammation, affecting hemostasis in the short term and atherosclerosis in the long term. Few studies have investigated the effects over decades, or which time-windows of exposure are the most relevant. In Sweden and many other countries wood burning is one of the largest sources of air pollution. The main aims of this thesis are to increase the knowledge of the mechanisms through which wood smoke causes respiratory and cardiovascular diseases, and the effects of long-term exposure to air pollution in a Swedish cohort. In an experimental chamber study in healthy adults, short-term exposure to two types of wood smoke was associated with symptoms and biomarkers of airway effects, but not with biomarkers of systemic inflammation or coagulation. This indicated that relatively low doses of wood smoke induce effects on airway epithelial permeability and possibly airway inflammation. In a long-term cohort study of residential exposure to nitric oxides (NOx) in Gothenburg, we observed a time trend of decreasing exposure. Back extrapolation of exposure was fairly correct for 5-7 years but not for longer time spans, showing that historical dispersion models and residential history are important for accurate long-term exposure estimations. Total nonaccidental mortality was associated with residential NOx exposure. The effect estimates were similar for NOx exposure the last year, the mean NOx exposure the last 5 years, and the mean NOx exposure since enrolment. The effect estimates for cause-specific cardiovascular mortality were similar to those for total mortality. The effect was near linear with no evidence of any threshold, and only marginally affected by confounders and effect modifiers.
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46. |
- Stockfelt, Leo, 1981, et al.
(author)
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Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans.
- 2012
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In: Inhalation toxicology. - : Informa UK Limited. - 1091-7691 .- 0895-8378. ; 24:1, s. 47-59
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Journal article (peer-reviewed)abstract
- Introduction: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. Materials and Methods: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM(2.5) were 295 µg/m(3) and 146 µg/m(3), number concentrations 140 000/cm(3) and 100 000/cm(3). Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. Results: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. Conclusions: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.
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47. |
- Stockfelt, Leo, 1981, et al.
(author)
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Long term effects of residential NOx exposure on total and cause-specific mortality and incidence of myocardial infarction in a Swedish cohort.
- 2015
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In: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 142, s. 197-206
-
Journal article (peer-reviewed)abstract
- BACKGROUND AND AIMS: Exposure to air pollution has been linked to total and cardiopulmonary mortality. However, few studies have examined the effects of exposure over decades, or which time windows of long term exposure are most relevant. We investigated the long term effects of residential air pollution on total and cause-specific mortality and incidence of myocardial infarction in a well-characterized cohort of men in Sweden. METHODS: A cohort of 7494 men in Gothenburg was examined in 1970-1973 and followed subsequently to determine predictors of cardiovascular disease. We collected data on residential address and cause-specific mortality for the years 1973-2007. Each individual was assigned yearly nitrogen oxides (NOx) exposure based on dispersion models. Using multivariable Cox regression and generalized additive models with time-dependent exposure, we studied the association between three different time windows of residential NOx exposure, and selected outcomes. RESULTS: In the years 1973-2007, a total of 5669 deaths, almost half of which were due to cardiovascular diseases, occurred in the cohort. Levels of NOx exposure decreased during the study period, from a median of 38µg/m3 in 1973 to 17µg/m3 in 2007. Total non-accidental mortality was associated with participants' NOx exposure in the last year (the year of outcome) (HR 1.03, 95% CI 1.01-1.05, per 10µg/m3), with the mean NOx exposure during the last 5 years, and with the mean NOx exposure since enrolment (HR 1.02, 95% CI 1.01-1.04 for both). The associations were similar (HR 1.01-1.03), but generally not statistically significant, for cardiovascular, ischemic heart disease, and acute myocardial infarction mortality, and weaker for cerebrovascular and respiratory mortality. There was no association between NOx exposure and incident myocardial infarction. DISCUSSION AND CONCLUSIONS: Long term residential exposure to NOx at these relatively low exposure levels in Gothenburg was associated with total non-accidental mortality. The association was as strong for NOx exposure in the last year as for longer exposure windows. The effect was near linear, and only marginally affected by confounders and effect modifiers. The improved air quality in Gothenburg has by these estimates led to a 6% decrease in excess non-accidental mortality during the study period.
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48. |
- Stockfelt, Leo, 1981, et al.
(author)
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Long-term effects of total and source-specific particulate air pollution on incident cardiovascular disease in Gothenburg, Sweden
- 2017
-
In: Environmental Research. - : Elsevier BV. - 0013-9351. ; 158, s. 61-71
-
Journal article (peer-reviewed)abstract
- Background and aims: Long-term exposure to air pollution increases cardiopulmonary morbidity and mortality, but it is not clear which components of air pollution are the most harmful, nor which time window of exposure is most relevant. Further studies at low exposure levels have also been called for. We analyzed two Swedish cohorts to investigate the effects of total and source-specific particulate matter (PM) on incident cardiovascular disease for different time windows of exposure. Methods: Two cohorts initially recruited to study predictors of cardiovascular disease (the PPS cohort and the GOT-MONICA cohort) were followed from 1990 to 2011. We collected data on residential addresses and assigned each individual yearly total and source-specific PM and Nitrogen Oxides (NO) exposures based on dispersion models. Using multivariable Cox regression models with time-dependent exposure, we studied the association between three different time windows (lag 0, lag 1-5, and exposure at study start) of residential PM and NO exposure, and incidence of ischemic heart disease, stroke, heart failure and atrial fibrillation. Results and discussion: During the study period, there were 2266 new-onset cases of ischemic heart disease, 1391 of stroke, 925 of heart failure and 1712 of atrial fibrillation. The majority of cases were in the PPS cohort, where participants were older. Exposure levels during the study period were moderate (median: 13 mu g/m(3) for PM10 and 9 mu g/m(3) for PM2.5), and similar in both cohorts. Road traffic and residential heating were the largest local sources of PM air pollution, and long distance transportation the largest PM source in total. In the PPS cohort, there were positive associations between PM in the last five years and both ischemic heart disease (HR: 1.24 [95% CI: 0.98-1.59] per 10 mu g/m(3) of PM10, and HR: 1.38 [95% CI: 1.08-1.77] per 5 mu g/m(3) of PM2.5) and heart failure. In the GOT-MONICA cohort, there were positive but generally non-significant associations between PM and stroke (HR: 1.48 [95% CI: 0.88-2.49] per 10 mu g/m(3) of PM10, and HR: 1.50 [95% CI: 0.90-2.51] per 5 mu g/m(3) of PM2.5, in the last five years). Effect estimates were stronger for women, non-smokers, and higher socioeconomic classes. Exposure in the last five years seemed to be more strongly associated with outcomes than other exposure time windows. Associations between source-specific PM air pollution and outcomes were mixed and generally weak. High correlations between the main pollutants limited the use of multi-pollutant models. Conclusions: The main PM air pollutants were associated with ischemic heart disease and stroke (in women) at the relatively low exposure levels in Gothenburg, Sweden. The associations tended to be stronger for women than for men, for non-smokers than for smokers, and for higher socioeconomic classes than for lower. The associations could not be attributed to a specific PM source or type, and differed somewhat between the two cohorts. The results of this study confirm that further efforts to reduce air pollution exposure should be undertaken in Sweden to reduce the negative health effects in the general population.
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49. |
- Stockfelt, Leo, 1981, et al.
(author)
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Short-term chamber exposure to low doses of two kinds of wood smoke does not induce systemic inflammation, coagulation or oxidative stress in healthy humans
- 2013
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In: Inhalation Toxicology. - : Informa UK Limited. - 0895-8378 .- 1091-7691. ; 25:8, s. 417-425
-
Journal article (peer-reviewed)abstract
- Introduction: Air pollution increases the risk of cardiovascular diseases. A proposed mechanism is that local airway inflammation leads to systemic inflammation, affecting coagulation and the long-term risk of atherosclerosis. One major source of air pollution is wood burning. Here we investigate whether exposure to two kinds of wood smoke, previously shown to cause airway effects, affects biomarkers of systemic inflammation, coagulation and lipid peroxidation. Methods: Thirteen healthy adults were exposed to filtered air followed by two sessions of wood smoke for three hours, one week apart. One session used smoke from the start-up phase of the wood-burning cycle, and the other smoke from the burn-out phase. Mean particle mass concentrations were 295 mu g/m(3) and 146 mu g/m(3), and number concentrations were 140 000/cm(3) and 100 000/cm(3), respectively. Biomarkers were analyzed in samples of blood and urine taken before and several times after exposure. Results after wood smoke exposure were adjusted for exposure to filtered air. Results: Markers of systemic inflammation and soluble adhesion molecules did not increase after wood smoke exposure. Effects on markers of coagulation were ambiguous, with minor decreases in fibrinogen and platelet counts and mixed results concerning the coagulation factors VII and VIII. Urinary F-2-isoprostane, a consistent marker of in vivo lipid peroxidation, unexpectedly decreased after wood smoke exposure. Conclusions: The effects on biomarkers of inflammation, coagulation and lipid peroxidation do not indicate an increased risk of cardiovascular diseases in healthy adults by short-term exposure to wood smoke at these moderate doses, previously shown to cause airway effects.
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50. |
- Thacher, Jesse D., et al.
(author)
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Exposure to long-term source-specific transportation noise and incident breast cancer : A pooled study of eight Nordic cohorts
- 2023
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In: Environment International. - : Elsevier. - 0160-4120 .- 1873-6750. ; 178
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Journal article (peer-reviewed)abstract
- Background: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence.Methods: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution.Results: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th–95th percentile) 5-year residential road traffic noise was 54.8 (40.0–67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2–65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99–1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96–1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99–1.18) for road traffic and 1.19 (0.95–1.49) for railway noise.Conclusions: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.
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