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1.
Lancet Planet Health ; 5(9): e620-e632, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34508683

RESUMO

BACKGROUND: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. METHODS: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. FINDINGS: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 µg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 µg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 µg/m3 for PM2·5 and 40 µg/m3 for NO2. INTERPRETATION: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. FUNDING: Health Effects Institute.


Assuntos
Poluição do Ar , Doença das Coronárias , Acidente Vascular Cerebral , Adulto , Poluição do Ar/efeitos adversos , Doença das Coronárias/induzido quimicamente , Doença das Coronárias/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Incidência , Estudos Multicêntricos como Assunto , Acidente Vascular Cerebral/epidemiologia
2.
J Alzheimers Dis ; 80(2): 591-599, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33579834

RESUMO

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.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Disfunção Cognitiva/etiologia , Material Particulado/efeitos adversos , Idoso , Poluição do Ar , Transtornos Cerebrovasculares/epidemiologia , Disfunção Cognitiva/epidemiologia , Exposição Ambiental , Feminino , Humanos , Estudos Longitudinais , Masculino , Testes de Estado Mental e Demência , Pessoa de Meia-Idade , Tamanho da Partícula , Fatores Socioeconômicos , Suécia/epidemiologia
3.
Environ Int ; 146: 106249, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33197787

RESUMO

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 (O3) 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 socio-economic 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 O3 (warm season) were 24.2 µg/m3 (19.5, 29.7), 15.4 µg/m3 (12.8, 17.3), 1.6 10-5m-1 (1.3, 1.8), and 86.6 µg/m3 (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 µg/m3). 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 µg/m3. We did not observe associations between NO2, BC or O3 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
4.
Environ Res ; 193: 110568, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33278469

RESUMO

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/m3 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/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Incidência , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
5.
Environ Epidemiol ; 4(5): e117, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-33134770

RESUMO

Air pollution represents a major public health threat in India affecting 19% of the world's population at extreme levels. Despite this, research in India lags behind in large part due to a lack of comprehensive air pollution exposure assessment that can be used in conjunction with health data to investigate health effects. Our vision is to provide a consortium to rapidly expand the evidence base of the multiple effects of ambient air pollution. We intend to leapfrog current limitations of exposure assessment by developing a machine-learned satellite-informed spatiotemporal model to estimate daily levels of ambient fine particulate matter measuring less than 2.5 µm (PM2.5) at a fine spatial scale across all of India. To catalyze health effects research on an unprecedented scale, we will make the output from this model publicly available. In addition, we will also apply these PM2.5 estimates to study the health outcomes of greatest public health importance in India, including cardiovascular diseases, chronic obstructive pulmonary disease, pregnancy (and birth) outcomes, and cognitive development and/or decline. Thus, our efforts will directly generate actionable new evidence on the myriad effects of air pollution on health that can inform policy decisions, while providing a comprehensive and publicly available resource for future studies on both exposure and health effects. In this commentary, we discuss the motivation, rationale, and vision for our consortium and a path forward for reducing the enormous burden of disease from air pollution in India.

6.
JAMA Neurol ; 77(7): 801-809, 2020 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-32227140

RESUMO

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 µm [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 µg/m3 PM2.5, 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 µg/m3 NOx, 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.


Assuntos
Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/epidemiologia , Demência/epidemiologia , Exposição Ambiental/efeitos adversos , Idoso , Poluentes Atmosféricos/efeitos adversos , Estudos de Coortes , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Suécia/epidemiologia
7.
Ann Emerg Med ; 76(2): 179-190, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-31983500

RESUMO

STUDY OBJECTIVE: We evaluate the importance of hospital bed occupancy for 30-day mortality, inhospital mortality, readmission for inpatient care within 30 days, and revisits to the emergency department (ED) within 7 days among all adult patients visiting the ED. METHODS: This was an observational cohort study including all adult patients visiting 6 EDs in Stockholm Region, Sweden. ED visits from 2012 to 2016 were categorized into groups by hospital bed occupancy in 5% intervals between 85% and 105%. A proportional hazards model was used to estimate adjusted hazard ratios with 95% confidence intervals (CIs). The model was stratified by hospital and adjusted for age, sex, comorbidities, hospital stays in the year preceding the index visit, marital status, length of education, and weekday/weekend timing of visit. RESULTS: A total of 816,832 patients with 2,084,554 visits were included. Mean hospital bed occupancy was 93.3% (SD 3.3%). In total, 28,112 patients died within 30 days, and 17,966 patients died inhospital. Hospital bed occupancy was not associated with 30-day mortality (hazard ratio for highest category of occupancy ≥105% was 1.10; 95% CI 0.96 to 1.27) or inhospital mortality. Patients discharged from the ED at occupancy levels greater than 89% had a 2% to 4% higher risk of revisits to the ED within 7 days. A 10% increase in hospital bed occupancy was associated with a 16-minute increase (95% CI 16 to 17 minutes) in ED length of stay and 1.9-percentage-point decrease (95% CI 1.7 to 2.0 percentage points) in admission rate. CONCLUSION: We did not find an association between increasing hospital bed occupancy and mortality in our sample of 6 EDs in Stockholm Region, Sweden, despite increased length of stay in the ED and a decline in admissions for inpatient care.


Assuntos
Ocupação de Leitos/estatística & dados numéricos , Serviço Hospitalar de Emergência , Mortalidade Hospitalar , Hospitalização/estatística & dados numéricos , Hospitais de Ensino/estatística & dados numéricos , Readmissão do Paciente/estatística & dados numéricos , Adulto , Idoso , Estudos de Coortes , Feminino , Hospitais Universitários/estatística & dados numéricos , Humanos , Masculino , Pessoa de Meia-Idade , Mortalidade , Avaliação de Resultados em Cuidados de Saúde , Suécia
8.
J Am Coll Emerg Physicians Open ; 1(6): 1312-1319, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33392538

RESUMO

Objectives: Emergency department (ED) crowding is a major problem across the world. Studies investigating the association between crowding and mortality are many, but the quality is inconsistent and there are very few large, high-quality multicenter studies that are properly designed to deal with confounding due to case mix. The aim of this study is to investigate the association between ED crowding and 30-day mortality. Methods: We conducted an observational cohort study at all 7 EDs in Stockholm Region, Sweden 2012-2016. The crowding exposure was defined as the mean hourly ED census during the shift that the exposed patient arrived, divided with the expected ED census for this shift. The expected ED census was estimated using a separate linear model for each hospital with year and shift as predictors. The exposure was categorized in 3 groups: reference (lowest 75% of observations), moderate (75%-95% of observations), and high (highest 5% of observations). Hazard ratios (HR) for all-cause mortality within 30 days were estimated with a Cox proportional hazards model. The model was adjusted for age, sex, triage priority, arrival hour, weekend, arrival mode, chief complaint, number of prior hospital admissions, and comorbidities. Results: 884,228 patients who visited the ED 2,252,656 times were included in the analysis. The estimated HR (95% confidence interval) for death within 30-days was 1.00 (0.97-1.03) in crowding category 75%-95% and 1.08 (1.03-1.14) in the 95%-100% category. Conclusions: In a large cohort study including 7 EDs in Stockholm Region, Sweden we identified a significant association between high levels of ED crowding and increased 30-day mortality.

9.
Environ Health Perspect ; 127(10): 107012, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31663781

RESUMO

BACKGROUND: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources. OBJECTIVES: We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities. METHODS: Based on detailed emission databases, monitoring data, and high-resolution dispersion models, we calculated source contributions to PM with aerodynamic diameter ≤10µm (PM10), PM with aerodynamic diameter ≤2.5µm (PM2.5), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models. RESULTS: We observed 5,166 and 3,119 incident IHD and stroke cases, respectively, in 114,758 participants. Overall, few consistent associations were observed between the different air pollution measures and IHD or stroke incidence. However, same-year levels of ambient locally emitted BC (range: 0.01-4.6 µg/m3) were associated with a 4.0% higher risk of incident stroke per interquartile range (IQR), 0.30 µg/m3 [95% confidence interval (CI): 0.04, 7.8]. This association was primarily related to BC from traffic exhaust. PM10 (range: 4.4-52 µg/m3) and PM2.5 (range: 2.9-22 µg/m3) were not associated with stroke. Associations with incident IHD were observed only for PM2.5 exposure from residential heating. DISCUSSION: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations. https://doi.org/10.1289/EHP4757.


Assuntos
Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Isquemia Miocárdica/epidemiologia , Material Particulado , Acidente Vascular Cerebral/epidemiologia , Poluentes Atmosféricos , Carbono , Doenças Cardiovasculares/epidemiologia , Estudos de Coortes , Feminino , Hospitalização , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Suécia/epidemiologia , Emissões de Veículos
10.
Environ Pollut ; 245: 1-8, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30399483

RESUMO

BACKGROUND: Several studies have reported associations between exposure to particulate matter and incidence of out-of-hospital cardiac arrest (OHCA) and some have observed associations with ozone (O3). There are no studies investigating susceptibility based on previous disease history to short-term O3 exposure and the risk of OHCA. AIM: To investigate the role of previous cardiovascular-related hospitalizations in modifying the associations between the risk of OHCA and short-term increase in O3 concentrations. METHODS: A time-stratified case-crossover analysis of 11,923 OHCA registered in the Swedish Register for Cardiopulmonary Resuscitation from 2006 to 2014 was performed. Using personal identification numbers, OHCA were linked to all previous hospitalizations in Sweden since 1987 to create susceptible groups based on the principal diagnosis code at discharge. Susceptibility was based on hospitalization for i) acute myocardial infarction; ii) heart failure; iii) arrhythmias; iv) diabetes; v) hypertension; and vi) stroke. Moving 2 and 24-h averages for O3, PM2.5, PM10, and NO2 were constructed from hourly averages. RESULTS: A 10 µg/m3 higher 2-h average O3 concentration was associated with a 2% higher risk of OHCA (95% CI, 0% 3%). Associations were similar for 24-h average O3 and in individuals with or without hospitalizations for AMI, heart failure, diabetes, hypertension or stroke. Individuals with previous hospitalizations for arrhythmias had a lower risk of OHCA with higher O3. No associations were observed for other pollutants. CONCLUSIONS: Short-term exposure to O3 was associated with an elevated risk of OHCA, however, previous hospitalizations for cardiovascular diseases were not associated with additionally augmented risks.


Assuntos
Poluentes Atmosféricos/toxicidade , Exposição Ambiental , Hospitalização , Parada Cardíaca Extra-Hospitalar/etiologia , Ozônio/toxicidade , Idoso , Poluentes Atmosféricos/análise , Exposição Ambiental/análise , Feminino , Humanos , Incidência , Masculino , Parada Cardíaca Extra-Hospitalar/epidemiologia , Ozônio/análise , Material Particulado/análise , Material Particulado/toxicidade , Readmissão do Paciente , Medição de Risco , Acidente Vascular Cerebral , Suécia/epidemiologia
11.
Environ Int ; 121(Pt 1): 139-147, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30205320

RESUMO

BACKGROUND: Studies of air pollution exposure and arterial stiffness have reported inconsistent results and large studies employing the reference standard of arterial stiffness, carotid-femoral pulse-wave velocity (CFPWV), have not been conducted. AIM: To study long-term exposure to ambient fine particles (PM2.5), proximity to roadway, and short-term air pollution exposures in relation to multiple measures of arterial stiffness in the Framingham Heart Study. METHODS: We assessed central arterial stiffness using CFPWV, forward pressure wave amplitude, mean arterial pressure and augmentation index. We investigated long-and short-term air pollution exposure associations with arterial stiffness with linear regressions using long-term residential PM2.5 (2003 average from a spatiotemporal model using satellite data) and proximity to roadway in addition to short-term averages of PM2.5, black carbon, particle number, sulfate, nitrogen oxides, and ozone from stationary monitors. RESULTS: We examined 5842 participants (mean age 51 ±â€¯16, 54% women). Living closer to a major roadway was associated with higher arterial stiffness (0.11 m/s higher CFPWV [95% CI: 0.01, 0.22] living <50 m vs 400 ≤ 1000 m). We did not observe association between arterial stiffness measures and long-term PM2.5 or short-term levels of PM2.5, particle number, sulfate or ozone. Higher levels of black carbon and nitrogen oxides in the previous days were unexpectedly associated with lower arterial stiffness. CONCLUSIONS: Long-term exposure to PM2.5 was not associated with arterial stiffness but positive associations with living close to a major road may suggest that pollutant mixtures very nearby major roads, rather than PM2.5, may affect arterial stiffness. Furthermore, short-term air pollution exposures were not associated with higher arterial stiffness.


Assuntos
Poluentes Atmosféricos/análise , Exposição Ambiental , Material Particulado/análise , Rigidez Vascular , Emissões de Veículos/análise , Adulto , Idoso , Poluição do Ar/análise , Boston , Feminino , Humanos , Modelos Lineares , Estudos Longitudinais , Masculino , Massachusetts , Pessoa de Meia-Idade , Análise de Onda de Pulso
12.
Environ Health ; 17(1): 37, 2018 04 13.
Artigo em Inglês | MEDLINE | ID: mdl-29653570

RESUMO

BACKGROUND: Ozone (O3) has been associated with cardiorespiratory mortality although few studies have explored susceptible populations based on prior disease. We aimed to investigate the role of previous hospitalization on the association between short-term exposure to O3 and cardiovascular (CV) and respiratory mortality. METHODS: We performed time series analyses using generalized additive models and case-crossover on 136,624 CV and 23,281 respiratory deaths in Stockholm County (1990-2010). Deaths were linked to hospital admissions data. We constructed 2-day and 7-day averages using daily 8-h maximum for O3 and hourly values for PM2.5, PM10, NO2, and NOx from a fixed monitor. RESULTS: We observed a 0.7% (95% CI: 0.1%, 1.3%) and 2.7% (95% CI: 0.8%, 4.6%) higher risk of CV and respiratory death per 10 µg/m3 higher 2-day and 7-day average O3 respectively. Individuals previously hospitalized for myocardial infarction demonstrated 1.8% (95% CI: 0.4%, 3.4%) higher risk of CV death per 10 µg/m3 higher 2-day average O3 and similar associations were observed in individuals with no previous hospitalization for any cause. Individuals with previous hospitalizations did not show susceptibility towards O3-related risk of respiratory mortality. We observed no associations for other pollutants. CONCLUSION: Short-term ozone exposure is associated with CV and respiratory mortality and our results may suggest higher susceptibility to CV mortality following O3 exposure in individuals previously hospitalized for myocardial infarction. Higher risks were also observed in individuals with cardiovascular death as their first presentation of disease.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Doenças Cardiovasculares/mortalidade , Exposição Ambiental/análise , Hospitalização/estatística & dados numéricos , Ozônio/efeitos adversos , Doenças Respiratórias/mortalidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Doenças Cardiovasculares/induzido quimicamente , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/epidemiologia , Doenças Respiratórias/induzido quimicamente , Suécia/epidemiologia
13.
Eur Heart J ; 35(13): 861-8, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24302272

RESUMO

BACKGROUND: Although ozone (O3) and other pollutants have been associated with cardiovascular morbidity and mortality, the effects of O3 on out-of-hospital cardiac arrest (OHCA) have rarely been addressed and existing studies have presented inconsistent findings. The objective of this study was to determine the effects of short-term exposure to air pollution including O3 on the occurrence of OHCA, and assess effect modification by season, age, and gender. METHODS AND RESULTS: A total of 5973 Emergency Medical Service-assessed OHCA cases in Stockholm County 2000-10 were obtained from the Swedish cardiac arrest register. A time-stratified case-crossover design was used to analyse exposure to air pollution and the risk of OHCA. Exposure to O3, PM2.5, PM10, NO2, and NOx was defined as the mean urban background level during 0-2, 0-24, and 0-72 h before the event and control time points. We adjusted for temperature and relative humidity. Ozone in urban background was associated with an increased risk of OHCA for all time windows. The respective odds ratio (confidence interval) for a 10 µg/m(3) increase was 1.02 (1.01-1.05) for a 2-h window, 1.04 (1.01-1.07) for 24-h, and 1.05 (1.01-1.09) for 3 day. The association with 2-h O3 was stronger for events that occurred outdoors: 1.13 (1.06-1.21). We observed no effects for other pollutants and no effect modification by age, gender, or season. CONCLUSION: Short-term exposure to moderate levels of O3 is associated with an increased risk of OHCA.


Assuntos
Poluição do Ar/efeitos adversos , Parada Cardíaca Extra-Hospitalar/induzido quimicamente , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/toxicidade , Estudos de Casos e Controles , Criança , Pré-Escolar , Estudos Cross-Over , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Pessoa de Meia-Idade , Óxido Nítrico/toxicidade , Parada Cardíaca Extra-Hospitalar/epidemiologia , Ozônio/toxicidade , Material Particulado/toxicidade , Suécia/epidemiologia , Fatores de Tempo , Adulto Jovem
14.
Eur Heart J ; 29(23): 2894-901, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19004842

RESUMO

AIMS: Air pollution has been associated with ventricular arrhythmias in patients with implantable cardioverter defibrillators (ICDs) for exposure periods of 24-48 h. Only two studies have investigated exposure periods <24 h. We aimed to explore such effects during the 2 and 24 preceding hours as well as in relation to distance from the place of the event to the air pollution monitor. METHODS AND RESULTS: We used a case-crossover design to investigate the effects of particulate matter <10 microm in diameter (PM10) and nitrogen dioxide (NO2) in 211 patients with ICD devices in Gothenburg and Stockholm, Sweden. Events interpreted as ventricular arrhythmias were downloaded from the ICDs, and air pollution data were collected from urban background monitors. We found an association between 2 h moving averages of PM10 and ventricular arrhythmia [odds ratio (OR) 1.31, 95% confidence interval (CI) 1.00-1.72], whereas the OR for 24 h moving averages was 1.24 (95% CI 0.87-1.76). Corresponding ORs for events occurring closest to the air pollution monitor were 1.76 (95% CI 1.18-2.61) and 1.74 (95% CI 1.07-2.84), respectively. Events occurring in Gothenburg showed stronger associations than in Stockholm. CONCLUSION: Moderate increases in air pollution appear to be associated with ventricular arrhythmias in ICD patients already after 2 h, although future studies including larger numbers of events are required to confirm these findings. Representative geographical exposure classification seems important in studies of these effects.


Assuntos
Arritmias Cardíacas/induzido quimicamente , Morte Súbita Cardíaca/etiologia , Desfibriladores Implantáveis/efeitos adversos , Exposição Ambiental/efeitos adversos , Dióxido de Nitrogênio/toxicidade , Oxidantes Fotoquímicos/toxicidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluição do Ar/efeitos adversos , Estudos Cross-Over , Monitoramento Ambiental , Feminino , Parada Cardíaca/induzido quimicamente , Humanos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Material Particulado/toxicidade , Suécia , Fatores de Tempo
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