Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear.
To investigate the ...association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association.
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.
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.
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.
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.
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.
•This study investigated air pollution exposure and Atrial Fibrillation episodes.•Participants were 75-year-old equipped with hand-held ECG recorders in Stockholm.•Short-term PM10 levels were ...associated with increased risk of atrial fibrillation.•More pronounced associations for participants with hypertension, diabetes or overweight.
Atrial fibrillation (AF), prevalent in approximately 1–3% of the population, is associated with a higher risk of stroke, dementia, mortality, and a reduced quality of life. Air pollution may be associated with heart rhythm disturbances, but there is limited evidence regarding whether short-term changes in air pollution levels are associated with acute onset of AF episodes.
We screened 8,899 randomly selected 75-yearolds living in Stockholm without previously known AF for AF using home-based short-term ambulatory 1-lead ECG-measurements 2–4 times a day for 14 days. Screenings were carried out in 2012–2013 and 2016–2018. We used generalized estimating equations to quantify the association between PM2.5, PM10, NO2 and O3 obtained from a fixed monitoring station and risk of AF onset among participants with AF observed during the screening period, adjusting for temperature, relative humidity and temporal factors. We explored potential susceptible subgroups.
Among 218 participants with 469 AF episodes we observed higher odds of AF following higher 24-hour mean levels of PM10 and O3, reaching statistical significance for PM10 levels averaged over the previous 12–24-hours OR 1.10 (95%CI 1.01–1.19) per IQR of PM10 (7.8 µg/m3). In subgroup analyses, PM2.5 was more strongly associated with AF among participants with hypertension and PM10 and O3 were more strongly associated with AF among participants with diabetes and overweight.
These results suggest that in an urban setting with relatively low levels of ambient air pollution, hourly changes in pollutant levels may increase the risk of acute episodes of both asymptomatic and symptomatic AF, especially among people with diabetes, hypertension or overweight.
The COVID-19 pandemic has impacted on public health in several ways. The aim of the study was to investigate changes in lifestyle, adiposity, and cardiometabolic markers among young adults in Sweden ...during the COVID-19 pandemic and their determinants.
The study included 1 004 participants from the population-based birth cohort BAMSE. Anthropometrics, body composition (bioelectric impedance analyses), pulse, and blood pressure were measured before (December 2016-May 2019; mean age 22.6 years) and during (October 2020-June 2021; mean age 25.7 years) the COVID-19 pandemic. Lifestyle changes during the pandemic were assessed through a questionnaire.
All measures of adiposity (weight, BMI, body fat percentage, trunk fat percentage) and cardiometabolic markers (blood pressure, pulse) increased during the study period (e.g., body fat percentage by a median of + 0.8% in females, p < 0.001, and + 1.5% in males, p < 0.001). Male sex, non-Scandinavian ethnicity, BMI status (underweight and obesity), and changes in lifestyle factors, e.g., decreased physical activity during the pandemic, were associated with higher increase in BMI and/or adiposity.
Lifestyle factors, adiposity and cardiometabolic markers may have been adversely affected among young adults in Sweden during the COVID-19 pandemic compared with the preceding years. Targeted public health measures to reduce obesity and improve healthy lifestyle are important to prevent future non-communicable diseases.
Ozone (O
) 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 O
and cardiovascular (CV) and respiratory mortality.
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 O
and hourly values for PM
, PM
, NO
, and NO
from a fixed monitor.
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/m
higher 2-day and 7-day average O
respectively. Individuals previously hospitalized for myocardial infarction demonstrated 1.8% (95% CI: 0.4%, 3.4%) higher risk of CV death per 10 μg/m
higher 2-day average O
and similar associations were observed in individuals with no previous hospitalization for any cause. Individuals with previous hospitalizations did not show susceptibility towards O
-related risk of respiratory mortality. We observed no associations for other pollutants.
Short-term ozone exposure is associated with CV and respiratory mortality and our results may suggest higher susceptibility to CV mortality following O
exposure in individuals previously hospitalized for myocardial infarction. Higher risks were also observed in individuals with cardiovascular death as their first presentation of disease.
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.
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.
Based on detailed emission databases, monitoring data, and high-resolution dispersion models, we calculated source contributions to PM with aerodynamic diameter
(
), PM with aerodynamic diameter
(
), 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.
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:
) were associated with a 4.0% higher risk of incident stroke per interquartile range (IQR),
95% confidence interval (CI): 0.04, 7.8. This association was primarily related to BC from traffic exhaust.
(range:
) and
(range:
) were not associated with stroke. Associations with incident IHD were observed only for
exposure from residential heating.
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.
Few studies have examined associations between long-term exposure to fine particulate matter (PM2.5) and lung function decline in adults.
To determine if exposure to traffic and PM2.5 is associated ...with longitudinal changes in lung function in a population-based cohort in the Northeastern United States, where pollution levels are relatively low.
FEV1 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 PM2.5 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.
Living less than 100 m from a major roadway was associated with a 23.2 ml (95% confidence interval CI, -44.4 to -1.9) lower FEV1 and a 5.0 ml/yr (95% CI, -9.0 to -0.9) faster decline in FEV1 compared with more than 400 m. Each 2 μg/m(3) increase in average of PM2.5 was associated with a 13.5 ml (95% CI, -26.6 to -0.3) lower FEV1 and a 2.1 ml/yr (95% CI, -4.1 to -0.2) faster decline in FEV1. There were similar associations with FVC. Associations with FEV1/FVC ratio were weak or absent.
Long-term exposure to traffic and PM2.5, at relatively low levels, was associated with lower FEV1 and FVC and an accelerated rate of lung function decline.
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.
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.
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.
We examined 5842 participants (mean age 51 ± 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.
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.
•Living nearby a major road was associated with higher arterial stiffness.•Particle matter measured by satellite was not associated with arterial stiffness.•No associations were observed for short-term exposure to air pollution.
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 µm 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.
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.
To examine exposure to ambient air pollutants within EPA standards and lung function in a large cohort study.
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, 1995-2011) who were not current smokers, with previous-day pollutant levels in compliance with EPA standards. We compared lung function (FEV1 and FVC) after previous-day exposure to particulate matter less than 2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) 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.
Exposure to pollutant concentrations in the "moderate" range of the EPA Air Quality Index was associated with a 20.1-ml lower FEV1 for PM2.5 (95% confidence interval CI, -33.4, -6.9), a 30.6-ml lower FEV1 for NO2 (95% CI, -60.9, -0.2), and a 55.7-ml lower FEV1 for O3 (95% CI, -100.7, -10.8) compared with the "good" range. The 1- and 2-day moving averages of PM2.5, NO2, and O3 before testing were negatively associated with FEV1 and FVC.
Short-term exposure to PM2.5, NO2, and O3 within current EPA standards was associated with lower lung function in this cohort of adults.
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