| 1. |
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| 2. |
- Arthur Hvidtfeldt, Ulla, et al.
(author)
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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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In: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 193
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Journal article (peer-reviewed)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. |
- Beelen, Rob, et al.
(author)
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Development of NO2 and NOx land use regression models for estimating air pollution exposure in 36 study areas in Europe : the ESCAPE project
- 2013
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In: Atmospheric Environment. - : Elsevier. - 1352-2310 .- 1873-2844. ; 72, s. 10-23
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Journal article (peer-reviewed)abstract
- Estimating within-city variability in air pollution concentrations is important. Land use regression (LUR) models are able to explain such small-scale within-city variations. Transparency in LUR model development methods is important to facilitate comparison of methods between different studies. We therefore developed LUR models in a standardized way in 36 study areas in Europe for the ESCAPE (European Study of Cohorts for Air Pollution Effects) project.Nitrogen dioxide (NO2) and nitrogen oxides (NOx) were measured with Ogawa passive samplers at 40 or 80 sites in each of the 36 study areas. The spatial variation in each area was explained by LUR modeling. Centrally and locally available Geographic Information System (GIS) variables were used as potential predictors. A leave-one out cross-validation procedure was used to evaluate the model performance.There was substantial contrast in annual average NO2 and NOx concentrations within the study areas. The model explained variances (R2) of the LUR models ranged from 55% to 92% (median 82%) for NO2 and from 49% to 91% (median 78%) for NOx. For most areas the cross-validation R2 was less than 10% lower than the model R2. Small-scale traffic and population/household density were the most common predictors. The magnitude of the explained variance depended on the contrast in measured concentrations as well as availability of GIS predictors, especially traffic intensity data were important. In an additional evaluation, models in which local traffic intensity was not offered had 10% lower R2 compared to models in the same areas in which these variables were offered.Within the ESCAPE project it was possible to develop LUR models that explained a large fraction of the spatial variance in measured annual average NO2 and NOx concentrations. These LUR models are being used to estimate outdoor concentrations at the home addresses of participants in over 30 cohort studies.
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| 4. |
- Berglind, Niklas, et al.
(author)
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Air Pollution Exposure : A Trigger for Myocardial Infarction?
- 2010
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In: International Journal of Environmental Research and Public Health. - : MDPI AG. - 1661-7827 .- 1660-4601. ; 7:4, s. 1486-1499
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Journal article (peer-reviewed)abstract
- The association between ambient air pollution exposure and hospitalization for cardiovascular events has been reported in several studies with conflicting results. A case-crossover design was used to investigate the effects of air pollution in 660 first-time myocardial infarction cases in Stockholm in 1993-1994, interviewed shortly after diagnosis using a standard protocol. Air pollution data came from central urban background monitors. No associations were observed between the risk for onset of myocardial infarction and two-hour or 24-hour air pollution exposure. No evidence of susceptible subgroups was found. This study provides no support that moderately elevated air pollution levels trigger first-time myocardial infarction.
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| 5. |
- Bero Bedada, Getahun, et al.
(author)
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Short-term Exposure to Ozone and Mortality in Subjects With and Without Previous Cardiovascular Disease
- 2016
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In: Epidemiology. - 1044-3983 .- 1531-5487. ; 27:5, s. 663-669
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Journal article (peer-reviewed)abstract
- BACKGROUND: Exposure to ground level ozone (O3) is a public health problem associated with a range of risks across population subgroups. Our aim was to investigate the role of previous cardiovascular diseases (CVDs) in mortality related to short-term O3 exposure.METHODS: Deaths between 1990 and 2010 in Stockholm County were matched with previous hospitalizations in Swedish registries. An urban background monitoring station provided hourly values of air quality data, from which we calculated 8-hour running averages and daily 8-hour maximum. We analyzed associations between daily O3 concentrations and mortality among persons with and without previous CVD hospitalization with a generalized additive model adjusted for time trend, influenza, and weather. We also performed two-pollutant models.RESULTS: There were 302,283 nontrauma-related deaths, out of which 196,916 had previous CVD hospitalization. The mean concentration of daily maximum 8-hour O3 was 62.9 μg/m. An average 10 μg/m increase in the same and preceding day was associated with an increased mortality of 1.72% (95% confidence interval: 0.44%, 3.02%) in those with prior admission for acute myocardial infarction (AMI), which was more than three times higher than for those with no previous AMI (0.50, 95% confidence interval: 0.10%, 0.89%, P value for interaction 0.098). The association between O3 and mortality remained essentially unchanged in two-pollutant models with NO2, NOx, and PM10.CONCLUSIONS: Our study indicates that short-term exposure to O3 is associated with increased mortality in those with a previous hospitalization for AMI.
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| 6. |
- Calderón-Larrañaga, Amaia, et al.
(author)
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COVID-19 : risk accumulation among biologically and socially vulnerable older populations
- 2020
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In: Ageing Research Reviews. - : Elsevier BV. - 1568-1637 .- 1872-9649. ; 63
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Research review (peer-reviewed)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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| 7. |
- Chen, Jie, et al.
(author)
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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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In: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 126:10, s. 1499-1507
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Journal article (peer-reviewed)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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| 8. |
- Chen, Jie, et al.
(author)
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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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In: Environmental Science and Technology. - : American Chemical Society (ACS). - 0013-936X .- 1520-5851. ; 56:13, s. 9277-9290
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Journal article (peer-reviewed)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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| 9. |
- Cole-Hunter, Thomas, et al.
(author)
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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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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 171
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Journal article (peer-reviewed)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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| 10. |
- Cyrys, Josef, et al.
(author)
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Variation of NO2 and NOx concentrations between and within 36 European study areas : Results from the ESCAPE study
- 2012
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In: Atmospheric Environment. - : Elsevier BV. - 1352-2310 .- 1873-2844. ; 62, s. 374-390
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Journal article (peer-reviewed)abstract
- The ESCAPE study (European Study of Cohorts for Air Pollution Effects) investigates long-term effects of exposure to air pollution on human health in Europe. This paper documents the spatial variation of measured NO2 and NOx concentrations between and within 36 ESCAPE study areas across Europe.In all study areas NO2 and NOx were measured using standardized methods between October 2008 and April 2011. On average, 41 sites were selected per study area, including regional and urban background as well as street sites. The measurements were conducted in three different seasons, using Ogawa badges. Average concentrations for each site were calculated after adjustment for temporal variation using data obtained from a routine monitor background site.Substantial spatial variability was found in NO2 and NOx concentrations between and within study areas; 40% of the overall NO2 variance was attributable to the variability between study areas and 60% to variability within study areas. The corresponding values for NOx were 30% and 70%. The within-area spatial variability was mostly determined by differences between street and urban background concentrations. The street/urban background concentration ratio for NO2 varied between 1.09 and 3.16 across areas. The highest median concentrations were observed in Southern Europe, the lowest in Northern Europe.In conclusion, we found significant contrasts in annual average NO2 and NOx concentrations between and especially within 36 study areas across Europe. Epidemiological long-term studies should therefore consider different approaches for better characterization of the intra-urban contrasts, either by increasing of the number of monitors or by modelling.
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| 11. |
- de Hoogh, Kees, et al.
(author)
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Comparing land use regression and dispersion modelling to assess residential exposure to ambient air pollution for epidemiological studies
- 2014
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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 73, s. 382-392
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Journal article (peer-reviewed)abstract
- Background: Land-use regression (LUR) and dispersion models (DM) are commonly used for estimating individual air pollution exposure in population studies. Few comparisons have however been made of the performance of these methods. Objectives: Within the European Study of Cohorts for Air Pollution Effects (ESCAPE) we explored the differences between LUR and DM estimates for NO2, PM10 and PM2.5. Methods: The ESCAPE study developed LUR models for outdoor air pollution levels based on a harmonised monitoring campaign. In thirteen ESCAPE study areas we further applied dispersion models. We compared LUR and DM estimates at the residential addresses of participants in 13 cohorts for NO2; 7 for PM10 and 4 for PM2.5. Additionally, we compared the DM estimates with measured concentrations at the 20-40 ESCAPE monitoring sites in each area. Results: The median Pearson R (range) correlation coefficients between LUR and DM estimates for the annual average concentrations of NO2, PM10 and PM2.5 were 0.75 (0.19-0.89), 0.39 (0.23-0.66) and 0.29 (0.22-0.81) for 112,971 (13 study areas), 69,591 (7) and 28,519(4) addresses respectively. The median Pearson R correlation coefficients (range) between DM estimates and ESCAPE measurements were of 0.74(0.09-0.86) for NO2; 0.58 (0.36-0.88) for PM10 and 0.58 (0.39-0.66) for PM2.5. Conclusions: LUR and dispersion model estimates correlated on average well for NO2 but only moderately for PM10 and PM2.5, with large variability across areas. DM predicted a moderate to large proportion of the measured variation for NO2 but less for PM10 and PM2.5.
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| 12. |
- Ekström, Ingrid, 1988-, et al.
(author)
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Environmental Air Pollution and Olfactory Decline in Aging
- 2022
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In: Journal of Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 130:2
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Journal article (peer-reviewed)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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| 13. |
- Eriksson, Charlotta, et al.
(author)
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Residential traffic noise exposure assessment : application and evaluation of European Environmental Noise Directive maps
- 2013
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In: Journal of Exposure Science and Environmental Epidemiology. - : Springer Science and Business Media LLC. - 1559-0631 .- 1559-064X. ; 23:5, s. 531-538
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Journal article (peer-reviewed)abstract
- Digital noise maps produced according to the European Environmental Noise Directive (END) could provide valuable exposure information in noise and health research. However, their usefulness in epidemiological studies has not been evaluated. The objective of this study was to apply and evaluate Swedish END maps for assessments of residential traffic noise exposure. END maps from three Swedish cities were used to assess residential traffic noise exposure for a population sample of 2496 men and women included in a national Environmental Health Survey. For each subject, we assessed noise levels manually and automatically at three geographical points, using survey data to locate dwellings within buildings. Cohen's kappa coefficient (kappa) was used to assess agreement between the noise estimates. To evaluate the maps, we compared the observed and predicted proportions of annoyed residents as a function of noise exposure using survey data and already established exposure-response relationships. The root mean square deviation (r.m.s.) was used to assess the precision of observed estimates. The agreement between the noise estimates ranged from kappa = 0.4 to 0.8. Generally, there was a high correspondence between observed and predicted exposure-response relationships for noise annoyance, regardless of method and if data on dwelling location within building were used. The best precision was, however, found when we manually corrected the noise level according to the location of the dwelling within buildings (r.m.s. = 0.029). Noise maps based on the END appear useful for assessing residential traffic noise exposure, particularly if combined with survey data on dwelling location.
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| 14. |
- Eriksson, Charlotta, et al.
(author)
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Traffic noise and cardiovascular health in Sweden : the roadside study
- 2012
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In: Noise & Health. - : Medknow. - 1463-1741 .- 1998-4030. ; 14:59, s. 140-147
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Journal article (peer-reviewed)abstract
- Long-term exposure to traffic noise has been suggested to increase the risk of cardiovascular diseases (CVD). However, few studies have been performed in the general population and on railway noise. This study aimed to investigate the cardiovascular effects of living near noisy roads and railways. This cross-sectional study comprised 25,851 men and women, aged 18-80 years, who had resided in Sweden for at least 5 years. All subjects participated in a National Environmental Health Survey, performed in 2007, in which they reported on health, annoyance reactions and environmental factors. Questionnaire data on self-reported doctors diagnosis of hypertension and/or CVD were used as outcomes. Exposure was assessed as Traffic Load (millions of vehicle kilometres per year) within 500 m around each participants residential address. For a sub-population (n = 2498), we also assessed road traffic and railway noise in L den at the dwelling facade. Multiple logistic regression models were used to assess Prevalence Odds Ratios (POR) and 95 Confidence Intervals (CI). No statistically significant associations were found between Traffic Load and self-reported hypertension or CVD. In the sub-population, there was no association between road traffic noise and the outcomes; however, an increased risk of CVD was suggested among subjects exposed to railway noise >= 50 dB(A); POR 1.55 (95 CI 1.00-2.40). Neither Traffic Load nor road traffic noise was, in this study, associated with self-reported cardiovascular outcomes. However, there was a borderline-significant association between railway noise and CVD. The lack of association for road traffic may be due to methodological limitations.
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| 15. |
- Grande, Giulia, et al.
(author)
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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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In: JAMA Neurology. - : American Medical Association (AMA). - 2168-6149 .- 2168-6157. ; 77:7, s. 801-809
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Journal article (peer-reviewed)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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| 16. |
- Grande, Giulia, et al.
(author)
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Long-Term Exposure to PM2.5 and Cognitive Decline : A Longitudinal Population-Based Study
- 2021
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In: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 80:2, s. 591-599
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Journal article (peer-reviewed)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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| 17. |
- Gruzieva, Olena, et al.
(author)
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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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In: Environmental Science and Pollution Research. - : Springer Science and Business Media LLC. - 0944-1344 .- 1614-7499. ; 28:13, s. 16264-16271
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Journal article (peer-reviewed)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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| 18. |
- Gruzieva, Olena, et al.
(author)
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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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In: Journal of Exposure Science and Environmental Epidemiology. - 1559-0631 .- 1559-064X.
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Journal article (peer-reviewed)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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| 19. |
- Hagenbjörk-Gustafsson, Annika, et al.
(author)
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Determinants of personal exposure to some carcinogenic substances and nitrogen dioxide among the general population in five Swedish cities
- 2014
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In: Journal of Exposure Science and Environmental Epidemiology. - : Springer Science and Business Media LLC. - 1559-0631 .- 1559-064X. ; 24:4, s. 437-443
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Journal article (peer-reviewed)abstract
- Environmental levels of airborne carcinogenic and related substances are comparatively better known than individual exposure and its determinants. We report on a personal monitoring program involving five Swedish urban populations. The aim of the program was to investigate personal exposure to benzene, 1,3-butadiene, formaldehyde, and nitrogen dioxide (NO2). The measurements were performed among 40 inhabitants during seven consecutive days, in one urban area each year, during 2000-2008. The estimated population exposure levels were 1.95 mu g/m(3) for benzene, 0.56 mu g/m(3) for 1,3-butadiene, 19.4 mu g/m(3) for formaldehyde, and 14.1,mu g/m(3) for NO2. Statistical analysis using a mixed-effects model revealed that time spent in traffic and time outdoors contributed to benzene and 1,3- butadiene exposure. For benzene, refueling a car was an additional determinant influencing the exposure level. Smoking or environmental tobacco smoke were significant determinants of exposure to NO2, benzene, and 1, 3-butadiene. Those with a gas stove had higher NO2 exposure. Living in a single-family house increased the exposure to formaldehyde significantly. In a variance component model, the between-subject variance dominated for 1,3-butadiene and formaldehyde, whereas the between-city variance dominated for NO2. For benzene, the between-subject and between-cities variances were similar.
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| 20. |
- Hedström, Anna Karin, et al.
(author)
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Association between exposure to combustion-related air pollution and multiple sclerosis risk
- 2023
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In: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 52:3, s. 703-714
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Journal article (peer-reviewed)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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| 21. |
- Hvidtfeldt, Ulla Arthur, et al.
(author)
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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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In: Environmental Research. - : Academic Press Inc.. - 0013-9351 .- 1096-0953. ; 215
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Journal article (peer-reviewed)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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| 22. |
- Hvidtfeldt, Ulla Arthur, et al.
(author)
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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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In: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 146
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Journal article (peer-reviewed)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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| 23. |
- Hvidtfeldt, Ulla Arthur, et al.
(author)
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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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In: Environmental Research. - 0013-9351 .- 1096-0953. ; 239:1
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Journal article (peer-reviewed)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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| 24. |
- Hänninen, Otto, et al.
(author)
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Seasonal patterns of outdoor PM infiltration into indoor environments: review and meta-analysis of available studies from different climatological zones in Europe
- 2011
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In: Air Quality, Atmosphere & Health. - : Springer Science and Business Media LLC. - 1873-9318 .- 1873-9326. ; 4:3-4, s. 221-233
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Journal article (peer-reviewed)abstract
- Epidemiologists have observed higher risks for exposure to ambient particulate matter (PM) in the summer than in other seasons. This increased risk may be partly due to seasonal behaviour and higher exposures to indoor PM in the summer in relation to outdoor pollutant levels during winter when windows are kept closed and less time is spent outdoors. In this report, we analyse data from six European studies, based on three different methods of estimating outdoor to indoor infiltration factors, with the aim of characterizing the geographical and seasonal patterns of PM infiltration. The highest infiltration levels were observed for the summer in both a European combined dataset consisting of 382 observations of the average PM2.5 infiltration factor for 1 day to 2weeks in regional data sets for Northern, Central and Southern Europe as well as for all ten cities individually. Th lowest values were observed for the winter, with spring and autumn displaying intermediate values. In all datasets and cities, the variability between residences and days within each season was much higher than the seasonal trend. PM10 data were available from two studies, revealing that the PM10 infiltration factors ranged from 70 to 92% of the corresponding PM2.5 values. Some differences between the studies may be associated with the study designs and applied methods of determining the infiltration factor. The ratio of summer to winter PM2.5 infiltration ranged from 1.3 in Rome to 2.3 in Helsinki, and the corresponding regional ratio ranged from 1.5 in Central Europe to 1.8 in Northern and Southern Europe. It is suggested that similar differences can be expected in epidemiological concentration–response relationships due to the modification in seasonal exposure associated with buildings and time spent indoors.
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| 25. |
- Korek, Michal, et al.
(author)
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Can dispersion modeling of air pollution be improved by land-use regression? An example from Stockholm, Sweden
- 2017
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In: Journal of Exposure Science and Environmental Epidemiology. - : Springer Science and Business Media LLC. - 1559-0631 .- 1559-064X. ; 27:6, s. 575-581
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Journal article (peer-reviewed)abstract
- Both dispersion modeling (DM) and land-use regression modeling (LUR) are often used for assessment of long-term air pollution exposure in epidemiological studies, but seldom in combination. We developed a hybrid DM-LUR model using 93 biweekly observations of NOx at 31 sites in greater Stockholm (Sweden). The DM was based on spatially resolved topographic, physiographic and emission data, and hourly meteorological data from a diagnostic wind model. Other data were from land use, meteorology and routine monitoring of NOx. We built a linear regression model for NOx, using a stepwise forward selection of covariates. The resulting model predicted observed NOx (R-2 = 0.89) better than the DM without covariates (R-2 = 0.68, P-interaction < 0.001) and with minimal apparent bias. The model included (in descending order of importance) DM, traffic intensity on the nearest street, population (number of inhabitants) within 100 m radius, global radiation (direct sunlight plus diffuse or scattered light) and urban contribution to NOx levels (routine urban NOx, less routine rural NOx). Our results indicate that there is a potential for improving estimates of air pollutant concentrations based on DM, by incorporating further spatial characteristics of the immediate surroundings, possibly accounting for imperfections in the emission data.
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