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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.
Int J Cancer ; 149(11): 1887-1897, 2021 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-34278567

RESUMO

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 µm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), 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 µg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5 µg/m3 ), 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.


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Neoplasias Hepáticas/etiologia , Adulto , Poluentes Atmosféricos/toxicidade , Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Europa (Continente)/epidemiologia , Feminino , Humanos , Incidência , Neoplasias Hepáticas/epidemiologia , Masculino , Pessoa de Meia-Idade , Tamanho da Partícula , Material Particulado/toxicidade , Modelos de Riscos Proporcionais
3.
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
4.
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
5.
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
6.
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.

7.
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
8.
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
9.
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.

10.
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
11.
Environ Res ; 171: 36-43, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30654247

RESUMO

BACKGROUND: Short-term exposure to air pollution has been associated with cardiovascular events, potentially by promoting endothelial cell activation and inflammation. A few large-scale studies have examined the associations and have had mixed results. METHODS: We included 3820 non-current smoking participants (mean age 56 years, 54% women) from the Framingham Offspring cohort examinations 7 (1998-2001) and 8 (2005-2008), and Third Generation cohort examination 1 (2002-2005), who lived within 50 km of a central monitoring station. We calculated the 1- to 7-day moving averages of fine particulate matter (PM2.5), black carbon (BC), sulfate (SO42-), nitrogen oxides (NOx), and ozone before examination visits. We used linear mixed effect models for P-selectin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1, lipoprotein-associated phospholipase A2 activity and mass, and osteoprotegerin that were measured up to twice, and linear regression models for CD40 ligand and interleukin-18 that were measured once, adjusting for demographics, life style and clinical factors, socioeconomic position, time, and meteorology. RESULTS: We found negative associations of PM2.5 and BC with P-selectin, of ozone with MCP-1, and of SO42- and NOx with osteoprotegerin. At the 5-day moving average, a 5 µg/m3 higher PM2.5 was associated with 1.6% (95% CI: - 2.8, - 0.3) lower levels of P-selectin; a 10 ppb higher ozone was associated with 1.7% (95% CI: - 3.2, - 0.1) lower levels of MCP-1; and a 20 ppb higher NOx was associated with 2.0% (95% CI: - 3.6, - 0.4) lower levels of osteoprotegerin. CONCLUSIONS: We did not find evidence of positive associations between short-term air pollution exposure and endothelial cell activation. On the contrary, short-term exposure to higher levels of ambient pollutants were associated with lower levels of P-selectin, MCP-1, and osteoprotegerin in the Framingham Heart Study.


Assuntos
Poluição do Ar/estatística & dados numéricos , Biomarcadores/metabolismo , Células Endoteliais/fisiologia , Exposição Ambiental/estatística & dados numéricos , Poluentes Atmosféricos , Feminino , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Material Particulado
12.
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
13.
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
14.
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
15.
Arterioscler Thromb Vasc Biol ; 37(9): 1793-1800, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-28751572

RESUMO

OBJECTIVE: The objective of this study is to examine associations between short-term exposure to ambient air pollution and circulating biomarkers of systemic inflammation in participants from the Framingham Offspring and Third Generation cohorts in the greater Boston area. APPROACH AND RESULTS: We included 3996 noncurrent smoking participants (mean age, 53.6 years; 54% women) who lived within 50 km from a central air pollution monitoring site in Boston, MA, and calculated the 1- to 7-day moving averages of fine particulate matter (diameter<2.5 µm), black carbon, sulfate, nitrogen oxides, and ozone before the examination visits. We used linear mixed effects models for C-reactive protein and tumor necrosis factor receptor 2, which were measured up to twice for each participant; we used linear regression models for interleukin-6, fibrinogen, and tumor necrosis factor α, which were measured once. We adjusted for demographics, socioeconomic position, lifestyle, time, and weather. The 3- to 7-day moving averages of fine particulate matter (diameter<2.5 µm) and sulfate were positively associated with C-reactive protein concentrations. A 5 µg/m3 higher 5-day moving average fine particulate matter (diameter<2.5 µm) was associated with 4.2% (95% confidence interval: 0.8, 7.6) higher circulating C-reactive protein. Positive associations were also observed for nitrogen oxides with interleukin-6 and for black carbon, sulfate, and ozone with tumor necrosis factor receptor 2. However, black carbon, sulfate, and nitrogen oxides were negatively associated with fibrinogen, and sulfate was negatively associated with tumor necrosis factor α. CONCLUSIONS: Higher short-term exposure to relatively low levels of ambient air pollution was associated with higher levels of C-reactive protein, interleukin-6, and tumor necrosis factor receptor 2 but not fibrinogen or tumor necrosis factor α in individuals residing in the greater Boston area.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Mediadores da Inflamação/sangue , Inflamação/induzido quimicamente , Exposição por Inalação/efeitos adversos , Material Particulado/efeitos adversos , Adulto , Idoso , Biomarcadores/sangue , Boston , Proteína C-Reativa/metabolismo , Monitoramento Ambiental , Feminino , Humanos , Inflamação/sangue , Inflamação/diagnóstico , Interleucina-6/sangue , Masculino , Pessoa de Meia-Idade , Tamanho da Partícula , Receptores Tipo II do Fator de Necrose Tumoral/sangue , Medição de Risco , Fatores de Risco , Fatores de Tempo , Regulação para Cima , Saúde da População Urbana
16.
BMJ Open ; 7(3): e013455, 2017 03 16.
Artigo em Inglês | MEDLINE | ID: mdl-28302634

RESUMO

OBJECTIVES: Traffic and ambient air pollution exposure are positively associated with cardiovascular disease, potentially through atherosclerosis promotion. Few studies have assessed associations of these exposures with thoracic aortic calcium Agatston score (TAC) or abdominal aortic calcium Agatston score (AAC), systemic atherosclerosis correlates. We assessed whether living close to a major road and residential fine particulate matter (PM2.5) exposure were associated with TAC and AAC in a Northeastern US cohort. DESIGN: Cohort study. SETTING: Framingham Offspring and Third Generation participants residing in the Northeastern USA. PARTICIPANTS AND OUTCOME MEASURES: Among 3506 participants, mean age was 55.8 years; 50% female. TAC was measured from 2002 to 2005 and AAC up to two times (2002-2005; 2008-2011) among participants from the Framingham Offspring or Third Generation cohorts. We first assessed associations with detectable TAC (logistic regression) and AAC (generalised estimating equation regression, logit link). As aortic calcium scores were right skewed, we used linear regression models and mixed-effects models to assess associations with natural log-transformed TAC and AAC, respectively, among participants with detectable aortic calcium. We also assessed associations with AAC progression. Models were adjusted for demographic variables, socioeconomic position indicators and time. RESULTS: There were no consistent associations of major roadway proximity or PM2.5 with the presence or extent of TAC or AAC, or with AAC progression. Some estimates were in the opposite direction than expected. CONCLUSIONS: In this cohort from a region with relatively low levels of and variation in PM2.5, there were no strong associations of proximity to a major road or PM2.5 with the presence or extent of aortic calcification, or with AAC progression.


Assuntos
Poluição do Ar/estatística & dados numéricos , Aorta/diagnóstico por imagem , Calcinose/diagnóstico por imagem , Material Particulado/efeitos adversos , Características de Residência/estatística & dados numéricos , Emissões de Veículos , Poluentes Atmosféricos/efeitos adversos , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada Multidetectores , Fatores de Risco
17.
Arterioscler Thromb Vasc Biol ; 36(8): 1679-85, 2016 08.
Artigo em Inglês | MEDLINE | ID: mdl-27312220

RESUMO

OBJECTIVE: Long-term exposure to traffic and particulate matter air pollution is associated with a higher risk of cardiovascular disease, potentially via atherosclerosis promotion. Prior research on associations of traffic and particulate matter with coronary artery calcium Agatston score (CAC), an atherosclerosis correlate, has yielded inconsistent findings. Given this background, we assessed whether residential proximity to major roadway or fine particulate matter were associated with CAC in a Northeastern US study. APPROACH AND RESULTS: We measured CAC ≤2 times from 2002 to 2005 and 2008 to 2011 among Framingham Offspring or Third-Generation Cohort participants. We assessed associations of residential distance to major roadway and residential fine particulate matter (2003 average; spatiotemporal model) with detectable CAC, using generalized estimating equation regression. We used linear mixed effects models to assess associations with loge(CAC). We also assessed associations with CAC progression. Models were adjusted for demographic variables, socioeconomic position markers, and time. Among 3399 participants, 51% had CAC measured twice. CAC was detectable in 47% of observations. At first scan, mean age was 52.2 years (standard deviation 11.7); 51% male. There were no consistent associations with detectable CAC, continuous CAC, or CAC progression. We observed heterogeneous associations of distance to major roadway with odds of detectable CAC by hypertensive status; interpretation of these findings is questionable. CONCLUSIONS: Our findings add to prior work and support evidence against strong associations of traffic or fine particulate matter with the presence, extent, or progression of CAC in a region with relatively low levels of and little variation in fine particulate matter.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Automóveis , Doença da Artéria Coronariana/epidemiologia , Exposição Ambiental/efeitos adversos , Habitação , Material Particulado/efeitos adversos , Calcificação Vascular/epidemiologia , Emissões de Veículos , Idoso , Angiografia Coronária/métodos , Doença da Artéria Coronariana/diagnóstico , Monitoramento Ambiental/métodos , Feminino , Humanos , Modelos Lineares , Modelos Logísticos , Masculino , Massachusetts , Pessoa de Meia-Idade , Tomografia Computadorizada Multidetectores , Razão de Chances , Valor Preditivo dos Testes , Medição de Risco , Fatores de Risco , Fatores de Tempo , Calcificação Vascular/diagnóstico
18.
Int J Hyg Environ Health ; 219(4-5): 389-97, 2016 07.
Artigo em Inglês | MEDLINE | ID: mdl-27053353

RESUMO

BACKGROUND: Associations have been reported between daily ambient temperature and all-cause and cardiovascular mortality. However, the potential harmful effect of temperature on out-of-hospital cardiac arrest (OHCA) is insufficiently studied. OBJECTIVES: The objective of this study was to investigate the short-term association between ambient temperature and the occurrence of OHCA. METHODS: In 5961 cases of OHCAs treated by Emergency Medical Service occurring in Stockholm County we investigated the association between the preceding 24-h and 1h mean ambient temperature, obtained from a fixed monitoring station, and OHCA using a time-stratified case-crossover design. RESULTS: We observed a V-shaped relationship between preceding mean 24-h and 1-h ambient temperature and the occurrence of OHCAs. For mean 24-h temperature we observed an odds ratio (OR) of 1.05 (1.00-1.11) for each 5°C below the optimum temperature and 1.05 (0.96-1.18) for each 5°C above the optimum. We observed similar results for 1-h mean temperature exposure. Results for temperatures above the optimum temperature showed evidence of confounding by ozone. CONCLUSION: Ambient temperature below an optimum temperature was associated with increased risk of OHCA in Stockholm. Temperature above an optimum temperature was not significantly associated with OHCA.


Assuntos
Parada Cardíaca Extra-Hospitalar/epidemiologia , Temperatura , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Monitoramento Ambiental , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Ozônio/análise , Material Particulado/análise , Risco , Suécia/epidemiologia
19.
Am J Epidemiol ; 183(7): 680-8, 2016 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-26968943

RESUMO

Straight metalworking fluids have been linked to cardiovascular mortality in analyses using binary exposure metrics, accounting for healthy worker survivor bias by using g-estimation of accelerated failure time models. A cohort of 38,666 Michigan autoworkers was followed (1941-1994) for mortality from all causes and ischemic heart disease. The structural model chosen here, using continuous exposure, assumes that increasing exposure from 0 to 1 mg/m(3) in any single year would decrease survival time by a fixed amount. Under that assumption, banning the fluids would have saved an estimated total of 8,468 (slope-based 95% confidence interval: 2,262, 28,563) person-years of life in this cohort. On average, 3.04 (slope-based 95% confidence interval: 0.02, 25.98) years of life could have been saved for each exposed worker who died from ischemic heart disease. Estimates were sensitive to both model specification for predicting exposure (multinomial or logistic regression) and characterization of exposure as binary or continuous in the structural model. Our results provide evidence supporting the hypothesis of a detrimental relationship between straight metalworking fluids and mortality, particularly from ischemic heart disease, as well as an instructive example of the challenges in obtaining and interpreting results from accelerated failure time models using a continuous exposure in the presence of competing risks.


Assuntos
Doenças Cardiovasculares/mortalidade , Exposição Ocupacional/estatística & dados numéricos , Feminino , Humanos , Masculino , Indústria Manufatureira/estatística & dados numéricos , Michigan/epidemiologia , Modelos Teóricos , Fatores de Tempo
20.
Epidemiology ; 27(2): 194-201, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26562062

RESUMO

BACKGROUND: Prior studies including the Framingham Heart Study have suggested associations between single components of air pollution and vascular function; however, underlying mixtures of air pollution may have distinct associations with vascular function. METHODS: We used a k-means approach to construct five distinct pollution mixtures from elemental analyses of particle filters, air pollution monitoring data, and meteorology. Exposure was modeled as an interaction between fine particle mass (PM2.5), and concurrent pollution cluster. Outcome variables were two measures of microvascular function in the fingertip in the Framingham Offspring and Third Generation cohorts from 2003 to 2008. RESULTS: In 1,720 participants, associations between PM2.5 and baseline pulse amplitude tonometry differed by air pollution cluster (interaction P value 0.009). Higher PM2.5 on days with low mass concentrations but high proportion of ultrafine particles from traffic was associated with 18% (95% confidence interval: 4.6%, 33%) higher baseline pulse amplitude per 5 µg/m and days with high contributions of oil and wood combustion with 16% (95% confidence interval: 0.2%, 34%) higher baseline pulse amplitude. We observed no variation in associations of PM2.5 with hyperemic response to ischemia observed across air pollution clusters. CONCLUSIONS: PM2.5 exposure from air pollution mixtures with large contributions of local ultrafine particles from traffic, heating oil, and wood combustion was associated with higher baseline pulse amplitude but not hyperemic response. Our findings suggest little association between acute exposure to air pollution clusters reflective of select sources and hyperemic response to ischemia, but possible associations with excessive small artery pulsatility with potentially deleterious microvascular consequences.


Assuntos
Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/estatística & dados numéricos , Dedos/irrigação sanguínea , Hiperemia/epidemiologia , Microvasos/fisiopatologia , Material Particulado/análise , Doença Arterial Periférica/epidemiologia , Fluxo Pulsátil , Adulto , Idoso , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/análise , Feminino , Humanos , Isquemia , Modelos Lineares , Masculino , Manometria , Pessoa de Meia-Idade , Análise Multivariada , Tempo (Meteorologia)
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