BackgroundNumerous studies have found that ambient air pollution has been associated with cardiovascular disease exacerbation.ObjectivesGiven previous findings, we hypothesized that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, contributing to an increased vulnerability to elevated concentrations of ambient particles.MethodsA prospective longitudinal study of 1,003 MI survivors was performed in six European cities between May 2003 and July 2004. We compared repeated measurements of interleukin 6 (IL-6), fibrinogen, and C-reactive protein (CRP) with concurrent levels of air pollution. We collected hourly data on particle number concentrations (PNC), mass concentrations of particulate matter (PM) < 10 μm (PM10) and < 2.5 μm (PM2.5), gaseous pollutants, and meteorologic data at central monitoring sites in each city. City-specific confounder models were built for each blood marker separately, adjusting for meteorology and time-varying and time-invariant covariates. Data were analyzed with mixed-effects models.ResultsPooled results show an increase in IL-6 when concentrations of PNC were elevated 12–17 hr before blood withdrawal [percent change of geometric mean, 2.7; 95% confidence interval (CI), 1.0–4.6]. Five day cumulative exposure to PM10 was associated with increased fibrinogen concentrations (percent change of arithmetic mean, 0.6; 95% CI, 0.1–1.1). Results remained stable for smokers, diabetics, and patients with heart failure. No consistent associations were found for CRP.ConclusionsResults indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins, as seen in increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events.

Rationale: Few studies have examined associations between longterm exposure to fine particulate matter (PM 2.5 ) and lung function decline in adults.Objectives: To determine if exposure to traffic and PM 2.5 is associated with longitudinal changes in lung function in a population-based cohort in the Northeastern United States, where pollution levels are relatively low.Methods: FEV 1 and FVC were measured up to two times between 1995 and 2011 among 6,339 participants of the Framingham Offspring or Third Generation studies. We tested associations between residential proximity to a major roadway and PM 2.5 exposure in 2001 (estimated by a land-use model using satellite measurements of aerosol optical thickness) and lung function. We examined differences in average lung function using mixed-effects models and differences in lung function decline using linear regression models. Current smokers were excluded. Models were adjusted for age, sex, height, weight, pack-years, socioeconomic status indicators, cohort, time, season, and weather.Measurements and Main Results: Living less than 100 m from a major roadway was associated with a 23.2 ml (95% confidence interval [CI], 244.4 to 21.9) lower FEV 1 and a 5.0 ml/yr (95% CI, 29.0 to 20.9) faster decline in FEV 1 compared with more than 400 m. Each 2 mg/m 3 increase in average of PM 2.5 was associated with a 13.5 ml (95% CI, 226.6 to 20.3) lower FEV 1 and a 2.1 ml/yr (95% CI, 24.1 to 20.2) faster decline in FEV 1 . There were similar associations with FVC. Associations with FEV 1 /FVC ratio were weak or absent.Conclusions: Long-term exposure to traffic and PM 2.5 , at relatively low levels, was associated with lower FEV 1 and FVC and an accelerated rate of lung function decline.

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

Our results suggest that exposure to moderate levels of air pollution may influence serum levels of inflammatory markers.

Rationale: Short-term exposure to ambient air pollution has been associated with lower lung function. Few studies have examined whether these associations are detectable at relatively low levels of pollution within current U.S. Environmental Protection Agency (EPA) standards. Objectives: To examine exposure to ambient air pollutants within EPA standards and lung function in a large cohort study. Methods: We included 3,262 participants of the Framingham Offspring and Third Generation cohorts living within 40 km of the Harvard Supersite monitor in Boston, Massachusetts (5,358 examinations, 1995Massachusetts (5,358 examinations, -2011) who were not current smokers, with previousday pollutant levels in compliance with EPA standards. We compared lung function (FEV 1 and FVC) after previous-day exposure to particulate matter less than 2.5 mm in diameter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) in the "moderate" range of the EPA Air Quality Index to exposure in the "good" range. We also examined linear relationships between moving averages of pollutant concentrations 1, 2, 3, 5, and 7 days before spirometry and lung function. Measurements and Main Results: Exposure to pollutant concentrations in the "moderate" range of the EPA Air Quality Index was associated with a 20.1-ml lower FEV 1 for PM 2.5 (95% confidence interval [CI], 233.4, 26.9), a 30.6-ml lower FEV 1 for NO 2 (95% CI, 260.9, 20.2), and a 55.7-ml lower FEV 1 for O 3 (95% CI, 2100.7, 210.8) compared with the "good" range. The 1-and 2-day moving averages of PM 2.5 , NO 2 , and O 3 before testing were negatively associated with FEV 1 and FVC.Conclusions: Short-term exposure to PM 2.5 , NO 2 , and O 3 within current EPA standards was associated with lower lung function in this cohort of adults.Keywords: chronic obstructive pulmonary disease; asthma; air pollutants; U.S. Environmental Protection Agency A substantial body of evidence has shown that modest shortterm increases in ambient air pollution, especially PM 2.5 (particles with an aerodynamic diameter < 2.5 mm) and ground level ozone (O 3 ), but also nitrogen dioxide (NO 2 ), increase risk of hospitalization for chronic obstructive pulmonary disease (COPD) and respiratory mortality (1-4). Several studies have found that short-term (1-3 d) increases in PM 2.5 , NO 2 , and O 3 are associated with decreases in FEV 1 , FVC, and/or peak expiratory flow rate in healthy subjects (5-11) and in those with preexisting COPD or asthma (12)(13)(14)(15).Air quality has improved substantially since the 1980s and 1990s, when many epidemiologic investigations of lung function and air pollution were completed (16). To protect public health and in accordance with its mandate, the EPA has continued to review the latest evidence and reevaluate air quality standards. Recently, the EPA lowered the annual standard for PM 2.5 from 15 to 12 mg/m 3 and reduced the daily Air Quality Index (AQI) cut-off for "moderate" PM 2.5 from 15.4 to 12 mg/m 3 . It remains unclear whether acute effects of criteria air pollutants (inclu...

ObjectiveTo examine the association of atrial fibrillation (AF) with cognitive decline and dementia in old age, and to explore the cognitive benefit of antithrombotic treatment in patients with AF.MethodsThis population-based cohort study included 2,685 dementia-free participants from the Swedish National Study on Aging and Care in Kungsholmen, who were regularly examined from 2001–2004 to 2010–2013. AF was ascertained from clinical examination, ECG, and patient registry. Global cognitive function was assessed using the Mini-Mental State Examination. We followed the DSM-IV criteria for the diagnosis of dementia, the NINDS-AIREN (National Institute of Neurological Disorders and Stroke and Association Internationale pour la Recherché et l'Enseignement en Neurosciences) criteria for vascular dementia, and the NINCDS-ADRDA (National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association) criteria for Alzheimer disease. Data were analyzed using multiple linear mixed-effects and Cox regression models.ResultsWe identified 243 participants (9.1%) with AF at baseline. During the 9-year follow-up period, 279 participants (11.4%) developed AF and 399 (14.9%) developed dementia. As a time-varying variable, AF was significantly associated with a faster annual Mini-Mental State Examination decline (β coefficient = −0.24, 95% confidence interval [CI]: −0.31 to −0.16) and an increased hazard ratio (HR) of all-cause dementia (HR = 1.40, 95% CI: 1.11–1.77) and vascular and mixed dementia (HR = 1.88, 95% CI: 1.09–3.23), but not Alzheimer disease (HR = 1.33, 95% CI: 0.92–1.94). Among people with either prevalent or incident AF, use of anticoagulant drugs, but not antiplatelet treatment, was associated with a 60% decreased risk of dementia (HR = 0.40, 95% CI: 0.18–0.92).ConclusionAF is associated with a faster global cognitive decline and an increased risk of dementia in older people. Use of anticoagulant drugs may reduce dementia risk in patients with AF.

Objective To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. Design Pooled analysis of eight cohorts. Setting Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. Participants 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM 2.5 ), nitrogen dioxide, ozone, and black carbon. Main outcome measures Deaths due to natural causes and cause specific mortality. Results Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM 2.5 , nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m 3 in PM 2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m 3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM 2.5 , nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m 3 an increase of 5 µg/m 3 in PM 2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. Conclusions Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.

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