| 1. |
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| 2. |
- Arthur Hvidtfeldt, Ulla, et al.
(författare)
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Long-term exposure to fine particle elemental components and lung cancer incidence in the ELAPSE pooled cohort
- 2021
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Ingår i: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 193
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Tidskriftsartikel (refereegranskat)abstract
- Background: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the Effects of Low-level Air Pollution: A Study in Europe (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence.Methods: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants' baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status).Results: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m(3) PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m(3) PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m(3) PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative.Conclusions: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.
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| 3. |
- Calderón-Larrañaga, Amaia, et al.
(författare)
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COVID-19 : risk accumulation among biologically and socially vulnerable older populations
- 2020
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Ingår i: Ageing Research Reviews. - : Elsevier BV. - 1568-1637 .- 1872-9649. ; 63
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Forskningsöversikt (refereegranskat)abstract
- Emerging data show that the health and economic impacts of COVID-19 are being disproportionately borne by individuals who are not only biologically, but also socially vulnerable. Based on preliminary data from Sweden and other reports, in this paper we propose a conceptual framework whereby different factors related to bio-logical and social vulnerability may explain the specific COVID-19 burden among older people. There is already some evidence showing large social disparities in the prevention, treatment, prognosis and/or long-term consequences of COVID-19. The remaining question is to what extent these affect older adults specifically. We provide the rationale to address this question with scientific methods and proper study designs, where the interplay between individuals' biomedical status and their social environment is the focus. Only through interdisciplinary research integrating biological, clinical and social data will we be able to provide new insights into the SARS-CoV-2 pandemic and inform actions aimed at reducing older adults' vulnerability to COVID-19 or other similar pandemics in the future.
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| 4. |
- Chen, Jie, et al.
(författare)
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Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort : the ELAPSE project
- 2022
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 126:10, s. 1499-1507
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Tidskriftsartikel (refereegranskat)abstract
- Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed.Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders.Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3).Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.
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| 5. |
- Chen, Jie, et al.
(författare)
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Long-Term Exposure to Source-Specific Fine Particles and Mortality-A Pooled Analysis of 14 European Cohorts within the ELAPSE Project
- 2022
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Ingår i: Environmental Science and Technology. - : American Chemical Society (ACS). - 0013-936X .- 1520-5851. ; 56:13, s. 9277-9290
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Tidskriftsartikel (refereegranskat)abstract
- We assessed mortality risks associated with sourcespecific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 mu g/m(3) increase) across five identified sources. On a 1 mu g/m(3) basis, the residual oil-related PM2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5 mass, suggesting that past estimates using the generic PM2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.
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| 6. |
- Cole-Hunter, Thomas, et al.
(författare)
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Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort : An ELAPSE study
- 2023
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Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 171
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Tidskriftsartikel (refereegranskat)abstract
- Background: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson’s Disease (PD) remains limited.Objective: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts.Methods: Within the project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders.Results: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01–1.55), NO2 (1.13; 0.95–1.34 per 10 µg/m3), and BC (1.12; 0.94–1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58–0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95–1.62) or BC (1.28; 0.96–1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5.Conclusion: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality.
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| 7. |
- Ekström, Ingrid, 1988-, et al.
(författare)
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Environmental Air Pollution and Olfactory Decline in Aging
- 2022
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Ingår i: Journal of Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 130:2
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Olfactory impairment is increasingly common with older age, which may be in part explained by cumulative effects of exposure to inhaled toxins. However, population-based studies investigating the relationship between air pollution and olfactory ability are scarce.OBJECTIVES: We aimed to investigate associations between exposure to common air pollutants and longitudinal change in odor identification.METHODS: Our study of 2,468 participants (mean age = 72.3 y; 61.1% female), of which 1,774 participants (mean age = 70.5 y; 61.9% female) had at least two olfactory assessments over 12 y of follow-up from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), Stockholm, Sweden. Participants were free from cognitive impairment and neurodegenerative disease at baseline. Odor identification ability was assessed with Sniffin' Sticks. Change in olfactory performance was estimated with linear mixed models. Exposure to two major airborne pollutants [particulate matter with aerodynamic diameter <= 2.5 mu m (PM2.5) and nitrogen oxides (NOx)] for the 5 y preceding baseline was assessed using spatiotemporal dispersion models for outdoor levels at residential addresses.RESULTS: Participants showed significant decline in odor identification ability for each year in the study {f3 = - 0.20 [95% confidence interval (CI): -0.22, 0.18; p < 0.001]}. After adjustment for all covariates, residents of third [f3= - 0.09 (95% CI: -0.14, -0.04; p < 0.001)] and fourth [f3 = - 0.07 (95% CI: -0.12, -0.02; p = 0.005)] exposure quartiles of PM2.5 had faster rates of olfactory decline than residents from the first quartile. Similar results were observed for the third [f3= - 0.05 (95% CI: -0.10, -0.01; p = 0.029)] and fourth [f3= - 0.07 (95% CI: -0.11, -0.02; p = 0.006) quartiles of NOx].DISCUSSION: Our results suggest an association between air pollution exposure and subsequent olfactory decline. We speculate that cumulative effects of airborne pollutants on the olfactory system may be one underlying cause of olfactory impairment in aging.
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| 8. |
- Grande, Giulia, et al.
(författare)
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Association Between Cardiovascular Disease and Long-term Exposure to Air Pollution With the Risk of Dementia
- 2020
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Ingår i: JAMA Neurology. - : American Medical Association (AMA). - 2168-6149 .- 2168-6157. ; 77:7, s. 801-809
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Tidskriftsartikel (refereegranskat)abstract
- IMPORTANCE Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear.OBJECTIVE To investigate the association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association.DESIGN, SETTING, AND PARTICIPANTS Data for this cohort study were extracted from the ongoing Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study with baseline assessments from March 21, 2001, through August 30, 2004. Of the 5111 randomly selected residents in the Kungsholmen district of Stockholm 60 years or older and living at home or in institutions, 521 were not eligible (eg, due to death before the start of the study or no contact information). Among the remaining 4590 individuals, 3363 (73.3%) were assessed. For the current analysis, 2927 participants who did not have dementia at baseline were examined, with follow-up to 2013 (mean [SD] follow-up time, 6.01 [2.56] years). Follow-up was completed February 18, 2013, and data were analyzed from June 26, 2018, through June 20, 2019.EXPOSURES Two major air pollutants (particulate matter <= 2.5 mu m [PM2.5] and nitrogen oxide [NOx]) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses.MAIN OUTCOMES AND MEASURES The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling.RESULTS At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio [HR] for difference of 0.88 mu g/m(3)PM(2.5), 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 mu g/m(3)NO(x), 1.14 [95% CI, 1.01-1.29]). Heart failure (HR for PM2.5, 1.93 [95% CI, 1.54-2.43]; HR for NOx, 1.43 [95% CI, 1.17-1.75]) and ischemic heart disease (HR for PM2.5, 1.67 [95% CI, 1.32-2.12]; HR for NOx, 1.36 [95% CI, 1.07-1.71]) enhanced the dementia risk, whereas stroke appeared to be the most important intermediate condition, explaining 49.4% of air pollution-related dementia cases.CONCLUSIONS AND RELEVANCE This study found that long-term exposure to air pollution was associated with a higher risk of dementia. Heart failure and ischemic heart disease appeared to enhance the association between air pollution and dementia, whereas stroke seemed to be an important intermediate condition between the association of air pollution exposure with dementia.QUESTION Does cardiovascular disease play a role in the association between long-term exposure to air pollution and dementia?FINDINGS In this cohort study of 2927 participants in the Swedish National Study on Aging and Care in Kungsholmen, air pollution exposure was associated with dementia risk despite comparatively low exposure levels. Heart failure and ischemic heart disease enhanced this association, and the development of stroke seemed to be an important intermediate condition.MEANING In this study, virtually all of the association between air pollution and dementia seemed to occur through the presence or the development of cardiovascular disease, which suggests a need to optimize treatment of concurrent cardiovascular disease and risk factor control in older adults at higher risk for dementia and living in polluted urban areas. This cohort study investigates the association of long-term exposure to air pollution with dementia and evaluates the role of cardiovascular disease in the association among participants of the population-based Swedish National Study on Aging and Care in Kungsholmen.
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| 9. |
- Grande, Giulia, et al.
(författare)
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Long-Term Exposure to PM2.5 and Cognitive Decline : A Longitudinal Population-Based Study
- 2021
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Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 80:2, s. 591-599
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Tidskriftsartikel (refereegranskat)abstract
- Background: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear.Objectives: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association.Methods: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5μm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25%fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model.Results: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2–3.2) per interquartile range difference up to mean PM2.5 level (8.6μg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74–1.06). The presence of cerebrovascular diseases further increased such risk by 6%.Conclusion: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.
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| 10. |
- Gruzieva, Olena, et al.
(författare)
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Comparison of measured residential black carbon levels outdoors and indoors with fixed-site monitoring data and with dispersion modelling
- 2021
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Ingår i: Environmental Science and Pollution Research. - : Springer Science and Business Media LLC. - 0944-1344 .- 1614-7499. ; 28:13, s. 16264-16271
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Tidskriftsartikel (refereegranskat)abstract
- Epidemiologic studies on health effects of air pollution usually rely on time-series of ambient monitoring data or on spatially modelled levels. Little is known how well these estimate residential outdoor and indoor levels. We investigated the agreement of measured residential black carbon (BC) levels outdoors and indoors with fixed-site monitoring data and with levels calculated using a Gaussian dispersion model. One-week residential outdoor and indoor BC measurements were conducted for 15 families living in central Stockholm. Time-series from urban background and street-level monitors were compared to these measurements. The observed weekly concentrations were also standardized to reflect annual averages, using urban background levels, and compared spatially to long-term levels as estimated by dispersion modelling. Weekly average outdoor BC level was 472 ng/m3 (range 261-797 ng/m3). The corresponding fixed-site urban background and street levels were 313 and 1039 ng/m3, respectively. Urban background variation explained 50% of the temporal variation in residential outdoor levels averaged over 24 h. Modelled residential long-term outdoor levels were on average comparable with the standardized measured home outdoor levels, and explained 49% of the spatial variability. The median indoor/outdoor ratio across all addresses was 0.79, with no difference between day and night time. Common exposure estimation approaches in the epidemiology of health effects related to BC displayed high validity for residencies in central Stockholm. Urban background monitored levels explained half of the outdoor day-to-day variability at residential addresses. Long-term dispersion modelling explained half of the spatial differences in outdoor levels. Indoor BC concentrations tended to be somewhat lower than outdoor levels.
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| 11. |
- Gruzieva, Olena, et al.
(författare)
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Comparison of personal exposure to black carbon levels with fixed-site monitoring data and with dispersion modelling and the influence of activity patterns and environment
- 2024
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Ingår i: Journal of Exposure Science and Environmental Epidemiology. - 1559-0631 .- 1559-064X.
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Tidskriftsartikel (refereegranskat)abstract
- Background: Short-term studies of health effects from ambient air pollution usually rely on fixed site monitoring data or spatio-temporal models for exposure characterization, but the relation to personal exposure is often not known.Objective: We aimed to explore this relation for black carbon (BC) in central Stockholm.Methods: Families (n = 46) with an infant, one parent working and one parent on parental leave, carried battery-operated BC instruments for 7 days. Routine BC monitoring data were obtained from rural background (RB) and urban background (UB) sites. Outdoor levels of BC at home and work were estimated in 24 h periods by dispersion modelling based on hourly real-time meteorological data, and statistical meteorological data representing annual mean conditions. Global radiation, air pressure, precipitation, temperature, and wind speed data were obtained from the UB station. All families lived in the city centre, within 4 km of the UB station.Results: The average level of 24 h personal BC was 425 (s.d. 181) ng/m3 for parents on leave, and 394 (s.d. 143) ng/m3 for working parents. The corresponding fixed-site monitoring observations were 148 (s.d. 139) at RB and 317 (s.d. 149) ng/m3 at UB. Modelled BC levels at home and at work were 493 (s.d. 228) and 331 (s.d. 173) ng/m3, respectively. UB, RB and air pressure explained only 21% of personal 24 h BC variability for parents on leave and 25% for working parents. Modelled home BC and observed air pressure explained 23% of personal BC, and adding modelled BC at work increased the explanation to 34% for the working parents.Impact: Short-term studies of health effects from ambient air pollution usually rely on fixed site monitoring data or spatio-temporal models for exposure characterization, but the relation to actual personal exposure is often not known. In this study we showed that both routine monitoring and modelled data explained less than 35% of variability in personal black carbon exposure. Hence, short-term health effects studies based on fixed site monitoring or spatio-temporal modelling are likely to be underpowered and subject to bias.
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| 12. |
- Hedström, Anna Karin, et al.
(författare)
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Association between exposure to combustion-related air pollution and multiple sclerosis risk
- 2023
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 52:3, s. 703-714
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Tidskriftsartikel (refereegranskat)abstract
- Background: Smoking and occupational pulmonary irritants contribute to multiple sclerosis (MS) development. We aimed to study the association between ambient air pollution and MS risk and potential interaction with the human leukocyte antigen (HLA)-DRB1*15:01 allele.Methods: Exposure to combustion-related air pollution was estimated as outdoor levels of nitrogen oxides (NOx) at the participants’ residence locations, by spatially resolved dispersion modelling for the years 1990–18. Using two population-based case-control studies (6635 cases, 8880 controls), NOx levels were associated with MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Interaction between high NOx levels and the HLA-DRB1*15:01 allele regarding MS risk was calculated by the attributable proportion due to interaction (AP). In addition, a register study was performed comprising all MS cases in Sweden who had received their diagnosis between 1993 and 2018 (n = 22 173), with 10 controls per case randomly selected from the National Population register.Results: Residential air pollution was associated with MS risk. NOx levels (3-year average) exceeding the 90th percentile (24.6 µg/m3) were associated with an OR of 1.37 (95% CI 1.10–1.76) compared with levels below the 25th percentile (5.9 µg/m3), with a trend of increasing risk of MS with increasing levels of NOx (P <0.0001). A synergistic effect was observed between high NOx levels (exceeding the lower quartile among controls) and the HLA-DRB1*15:01 allele regarding MS risk (AP 0.26, 95% CI 0.13–0.29).Conclusions: Our findings indicate that moderate levels of combustion-related ambient air pollution may play a role in MS development.
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| 13. |
- Hvidtfeldt, Ulla Arthur, et al.
(författare)
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Long term exposure to air pollution and kidney parenchyma cancer – Effects of low-level air pollution : a Study in Europe (ELAPSE)
- 2022
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Ingår i: Environmental Research. - : Academic Press Inc.. - 0013-9351 .- 1096-0953. ; 215
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Particulate matter (PM) is classified as a group 1 human carcinogen. Previous experimental studies suggest that particles in diesel exhaust induce oxidative stress, inflammation and DNA damage in kidney cells, but the evidence from population studies linking air pollution to kidney cancer is limited.METHODS: We pooled six European cohorts (N = 302,493) to assess the association of residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) with cancer of the kidney parenchyma. The main exposure model was developed for year 2010. We defined kidney parenchyma cancer according to the International Classification of Diseases 9th and 10th Revision codes 189.0 and C64. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level.RESULTS: The participants were followed from baseline (1985–2005) to 2011–2015. A total of 847 cases occurred during 5,497,514 person-years of follow-up (average 18.2 years). Median (5–95%) exposure levels of NO2, PM2.5, BC and O3 were 24.1 μg/m3 (12.8–39.2), 15.3 μg/m3 (8.6–19.2), 1.6 10−5 m−1 (0.7–2.1), and 87.0 μg/m3 (70.3–97.4), respectively. The results of the fully adjusted linear analyses showed a hazard ratio (HR) of 1.03 (95% confidence interval [CI]: 0.92, 1.15) per 10 μg/m³ NO2, 1.04 (95% CI: 0.88, 1.21) per 5 μg/m³ PM2.5, 0.99 (95% CI: 0.89, 1.11) per 0.5 10−5 m−1 BCE, and 0.88 (95% CI: 0.76, 1.02) per 10 μg/m³ O3. We did not find associations between any of the elemental components of PM2.5 and cancer of the kidney parenchyma.CONCLUSION: We did not observe an association between long-term ambient air pollution exposure and incidence of kidney parenchyma cancer.
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| 14. |
- Hvidtfeldt, Ulla Arthur, et al.
(författare)
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Long-term low-level ambient air pollution exposure and risk of lung cancer - A pooled analysis of 7 European cohorts
- 2021
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Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 146
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Tidskriftsartikel (refereegranskat)abstract
- Background/aim: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence.Methods: The Effects of Low-level Air Pollution: a Study in Europe (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine particulate matter (PM2.5), black carbon (BC), and ozone (O-3) to assign exposure to cohort participants' residential addresses in 100 m by 100 m grids. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socioeconomic status). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines.Results: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO2, PM2.5, BC and O-3 (warm season) were 24.2 mu g/m(3) (19.5, 29.7), 15.4 mu g/m(3) (12.8, 17.3), 1.6 10(-5)m(-1) (1.3, 1.8), and 86.6 mu g/m(3) (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 mu g/m(3)). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 mu g/m(3). We did not observe associations between NO2, BC or O-3 and lung cancer incidence.Conclusions: Long-term ambient PM2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines.
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| 15. |
- Hvidtfeldt, Ulla Arthur, et al.
(författare)
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Multiple myeloma risk in relation to long-term air pollution exposure - A pooled analysis of four European cohorts
- 2023
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Ingår i: Environmental Research. - 0013-9351 .- 1096-0953. ; 239:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Air pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated. Methods: We pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. Results: During 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 mu g/m3 NO2, 1.04 (0.82, 1.33) per 5 mu g/m3 PM2.5, 0.99 (0.84, 1.18) per 0.5 10- 5 m-1 BCE, and 1.11 (0.87, 1.41) per 10 mu g/m3 O3. Conclusions: We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.
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| 16. |
- Liu, Shuo, et al.
(författare)
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Long-term exposure to low-level air pollution and incidence of asthma : the ELAPSE project
- 2021
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 57:6
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Tidskriftsartikel (refereegranskat)abstract
- Background: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 mu m (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults.Methods: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders.Results: Of 98326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 mu g.m(-3) for PM2.5, 1.17 (95% CI 1.10-1.25) per 10 mu g.m(-3) for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5 x 10(-5) m(-1) for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO 2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold.Conclusions: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.
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| 17. |
- Liu, Shuo, et al.
(författare)
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Long-term exposure to low-level air pollution and incidence of chronic obstructive pulmonary disease : The ELAPSE project
- 2021
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Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 146
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Tidskriftsartikel (refereegranskat)abstract
- Background: Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent.Objectives: We examined the association between long-term exposure to low-level air pollution and COPD incidence.Methods: Within the 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 mu m (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) in 2010 at participants' baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models.Results: Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 mu g/m(3) for PM2.5, 1.11 (1.06, 1.16) per 10 mu g/m(3) for NO2, and 1.11 (1.06, 1.15) per 0.5 10(-5) m(-1) for BC. Associations persisted in subset participants with PM2.5 or NO2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO2 and BC remained unchanged in two-pollutant models with PM2.5, whereas the HR for PM2.5 was attenuated to unity with NO2 or BC.Conclusions: Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO2 and BC may be the most relevant.
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| 18. |
- So, Rina, et al.
(författare)
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Long-term exposure to air pollution and liver cancer incidence in six European cohorts
- 2021
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 149:11, s. 1887-1897
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Tidskriftsartikel (refereegranskat)abstract
- Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the Effects of low-level air pollution: A study in Europe (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2), particulate matter with diameter <2.5 mu m (PM2.5), black carbon (BC), warm-season ozone (O-3), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 mu g/m(3)), PM2.5 (1.12, 0.92-1.36 per 5 mu g/m(3)), and BC (1.15, 1.00-1.33 per 0.5 10(-5)/m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5. Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2. Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.
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| 19. |
- Stafoggia, Massimo, et al.
(författare)
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A Random Forest Approach to Estimate Daily Particulate Matter, Nitrogen Dioxide, and Ozone at Fine Spatial Resolution in Sweden
- 2020
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Ingår i: Atmosphere. - : MDPI AG. - 2073-4433. ; 11:3
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Tidskriftsartikel (refereegranskat)abstract
- Air pollution is one of the leading causes of mortality worldwide. An accurate assessment of its spatial and temporal distribution is mandatory to conduct epidemiological studies able to estimate long-term (e.g., annual) and short-term (e.g., daily) health effects. While spatiotemporal models for particulate matter (PM) have been developed in several countries, estimates of daily nitrogen dioxide (NO2) and ozone (O-3) concentrations at high spatial resolution are lacking, and no such models have been developed in Sweden. We collected data on daily air pollutant concentrations from routine monitoring networks over the period 2005-2016 and matched them with satellite data, dispersion models, meteorological parameters, and land-use variables. We developed a machine-learning approach, the random forest (RF), to estimate daily concentrations of PM10 (PM<10 microns), PM2.5 (PM<2.5 microns), PM2.5-10 (PM between 2.5 and 10 microns), NO2, and O-3 for each squared kilometer of Sweden over the period 2005-2016. Our models were able to describe between 64% (PM10) and 78% (O-3) of air pollutant variability in held-out observations, and between 37% (NO2) and 61% (O-3) in held-out monitors, with no major differences across years and seasons and better performance in larger cities such as Stockholm. These estimates will allow to investigate air pollution effects across the whole of Sweden, including suburban and rural areas, previously neglected by epidemiological investigations.
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| 20. |
- Stafoggia, Massimo, et al.
(författare)
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Long-term exposure to low ambient air pollution concentrations and mortality among 28 million people : results from seven large European cohorts within the ELAPSE project
- 2022
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Ingår i: The Lancet Planetary Health. - : Elsevier B.V.. - 2542-5196. ; 6:1, s. e9-e18
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Tidskriftsartikel (refereegranskat)abstract
- Background Long-term exposure to ambient air pollution has been associated with premature mortality, but associations at concentrations lower than current annual limit values are uncertain. We analysed associations between low-level air pollution and mortality within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE).Methods In this multicentre longitudinal study, we analysed seven population-based cohorts of adults (age ≥30 years) within ELAPSE, from Belgium, Denmark, England, the Netherlands, Norway, Rome (Italy), and Switzerland (enrolled in 2000–11; follow-up until 2011–17). Mortality registries were used to extract the underlying cause of death for deceased individuals. Annual average concentrations of fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and tropospheric warm-season ozone (O3) from Europe-wide land use regression models at 100 m spatial resolution were assigned to baseline residential addresses. We applied cohort-specific Cox proportional hazard models with adjustment for area-level and individual-level covariates to evaluate associations with non-accidental mortality, as the main outcome, and with cardiovascular, non-malignant respiratory, and lung cancer mortality. Subset analyses of participants living at low pollutant concentrations (as per predefined values) and natural splines were used to investigate the concentration-response function. Cohort-specific effect estimates were pooled in a random-effects meta-analysis.Findings We analysed 28 153 138 participants contributing 257 859 621 person-years of observation, during which 3 593 741 deaths from non-accidental causes occurred. We found significant positive associations between non-accidental mortality and PM2·5, NO2, and black carbon, with a hazard ratio (HR) of 1·053 (95% CI 1·021–1·085) per 5 μg/m3 increment in PM2·5, 1·044 (1·019–1·069) per 10 μg/m3 NO2, and 1·039 (1·018–1·059) per 0·5 × 10−5/m black carbon. Associations with PM2·5, NO2, and black carbon were slightly weaker for cardiovascular mortality, similar for non-malignant respiratory mortality, and stronger for lung cancer mortality. Warm-season O3 was negatively associated with both non-accidental and cause-specific mortality. Associations were stronger at low concentrations: HRs for non-accidental mortality at concentrations lower than the WHO 2005 air quality guideline values for PM2·5 (10 μg/m3) and NO2 (40 μg/m3) were 1·078 (1·046–1·111) per 5 μg/m3 PM2·5 and 1·049 (1·024–1·075) per 10 μg/m3 NO2. Similarly, the association between black carbon and non-accidental mortality was highest at low concentrations, with a HR of 1·061 (1·032–1·092) for exposure lower than 1·5× 10−5/m, and 1·081 (0·966–1·210) for exposure lower than 1·0× 10−5/m.Interpretation Long-term exposure to concentrations of PM2·5 and NO2 lower than current annual limit values was associated with non-accidental, cardiovascular, non-malignant respiratory, and lung cancer mortality in seven large European cohorts. Continuing research on the effects of low concentrations of air pollutants is expected to further inform the process of setting air quality standards in Europe and other global regions.
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| 21. |
- Wu, Jing, et al.
(författare)
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Air pollution as a risk factor for Cognitive Impairment no Dementia (CIND) and its progression to dementia : A longitudinal study
- 2022
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Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 160
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Tidskriftsartikel (refereegranskat)abstract
- Background and aim: Accumulation of evidence has raised concern regarding the harmful effect of air pollution on cognitive function, but results are diverging. We aimed to investigate the longitudinal association of long-term exposure to air pollutants and cognitive impairment and its further progression to dementia in older adults residing in an urban area.Methods: Data were obtained from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K). Cognitive impairment, no dementia (CIND) was assessed by a comprehensive neuropsychological battery (scoring >= 1.5 standard deviations below age-specific means in >= 1 cognitive domain). We assessed long-term residential exposure to particulate matters (PM2.5 and PM10) and nitrogen oxides (NOx) with dispersion modeling. The association with CIND was estimated using Cox proportional hazards models with 3-year moving average air pollution exposure. We further estimated the effect of long-term air pollution exposure on the progression of CIND to dementia using Cox proportional hazards models.Results: Among 1987 cognitively intact participants, 301 individuals developed CIND during the 12-year followup. A 1-mu g/m(3) increment in PM2.5 exposure was associated with a 75% increased risk of incident CIND (HR = 1.75, 95 %CI: 1.54, 1.99). Weaker associations were found for PM10 (HR for 1-mu g/m(3) = 1.08, 95 %CI: 1.03-1.14) and NOx (HR for 10 mu g/m(3) = 1.18, 95 %CI: 1.04-1.33). Among those with CIND at baseline (n = 607), 118 participants developed dementia during follow-up. Results also show that exposure to air pollution was a risk factor for the conversion from CIND to dementia (PM2.5: HR for 1-mu g/m(3) = 1.90, 95 %CI: 1.48-2.43; PM10 : HR for 1-mu g/m(3) = 1.14, 95 %CI: 1.03-1.26; and NOR: HR for 10 mu g/m(3) = 1.34, 95 %CI: 1.07-1.69).Conclusion: We found evidence of an association between long-term exposure to ambient air pollutants and incidence of CIND. Of special interest is that air pollution also was a risk factor for the progression from CIND to dementia.
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| 22. |
- Wu, Jing, et al.
(författare)
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Air pollution, social engagement, and depression in older adults : Results from a Swedish population-based cohort study
- 2023
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Ingår i: Environmental Pollution. - 0269-7491 .- 1873-6424. ; 336
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Tidskriftsartikel (refereegranskat)abstract
- Although emerging research has investigated the relationship between outdoor air pollution and depression risk in older adults, the results remain inconclusive. We aimed to determine the relationship between long-term exposure to ambient air pollution and depression among older adults and explore whether active social engagement may modify this association. At baseline (2001–2004), 2812 depression-free older adults from Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) were included. SNAC-K is a longitudinal population-based cohort in Stockholm, Sweden. Incident depression cases occurred during 2004–2013 were ascertained using the Diagnostic and Statistical Manual of Mental Disorders 4th Edition. Air pollution [particulate matter (PM) and nitrogen oxides (NOx)] at the residency were estimated using dispersion models. Social engagement was measured as active participation in social activities (at least twice/week) or inactive (less than twice/week) in the last 12 months. The hazard ratios (HR) and 95% confidence intervals of depression from air pollution exposure of 3-year moving average before diagnosis (1-μg/m3 difference in PM2.5 and PM10, and 10-μg/m3 difference in NOx) were obtained from Cox models considering greenspace and noise. A product term of air pollutant and social activity was added to test the multiplicative interaction and attributable proportion due to interaction was calculated for assessing additive interaction. We identified 137 (4.9%) incident depression cases. Participants exposed to higher concentrations of PM2.5, NOx, and PM10 had 53% (HR:1.53 [1.22, 1.93]), 26% (HR:1.26 [1.01, 1.58]), and 7% (HR:1.07 [0.98, 1.18]) increased hazard of depression, respectively. These associations were largely attenuated in people with active social engagement (HR for PM2.5: 1.04 [0.70, 1.55]; HR for PM10: 0.98 [0.81, 1.18]; and HR for NOx: 1.09 [0.71, 1.66]). Our findings suggest long-term exposure to air pollution may be a risk factor for depression among older adults. An active social engagement might however decrease this risk.
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| 23. |
- Wu, Jing, et al.
(författare)
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Long-term exposure to transportation noise in relation to global cognitive decline and cognitive impairment : Results from a Swedish longitudinal cohort
- 2024
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Ingår i: Environment International. - 0160-4120 .- 1873-6750. ; 185
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Tidskriftsartikel (refereegranskat)abstract
- Background and aims: Transportation noise is an environmental exposure with mounting evidence of adverse health effects. Besides the increased risk of cardiovascular and metabolic diseases, recent studies suggest that long-term noise exposure might accelerate cognitive decline in older age. We examined the association between transportation noise and cognitive function in a cohort of older adults.Methods: The present study is based on 2594 dementia-free participants aged 60 + years from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). Global cognition score and CIND (cognitive impairment, no dementia) were assessed with a comprehensive neuropsychological battery at baseline and up to 16 years. Residential transportation noise resulting from road traffic, railway, and aircraft were estimated at the most exposed façade and the time-weighted average exposure was assessed. Linear mixed-effect models were used to assess the effect of long-term traffic noise exposure on the rate of change in global cognition score. Hazard ratios (HRs) and 95 % confidence intervals (CIs) of CIND by transportation noise exposure were obtained with Cox proportional hazard models.Results: Global cognition score decreased at an average rate of −0.041 (95 %CI −0.043, −0.039) per year. Aircraft noise was associated with a 0.007 (per 10 dB Lden; 95 %CI −0.012, −0.001) faster annual rate of decline. Global cognition score seems to be not affected by road traffic and railway noise. During the follow-up, 422 (21 %) participants developed CIND. A 10-dB Lden difference in exposure to aircraft and railway noise was associated with a 16 % (HR 1.16, 95 %CI 0.91, 1.49) and 26 % (HR 1.26, 95 %CI 1.01, 1.56) increased hazard of CIND in the multi-pollutant model, respectively. No association was found for road traffic (HR 1.00, 95 %CI 0.83, 1.21).Conclusions: Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.
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