Long-term exposure to outdoor air pollution and risk factors for cardiovascular disease within a cohort of older men in Perth.
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ABSTRACT:
SUBMITTER: Vander Hoorn S
PROVIDER: S-EPMC8006998 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:Mosaic loss of chromosome Y (mLOY) can occur in a fraction of cells as men age, which is potentially linked to increased mortality risk. Smoking is related to mLOY; however, the contribution of air pollution is unclear. OBJECTIVE:We investigated whether exposure to outdoor air pollution, age, and smoking were associated with mLOY. METHODS:We analyzed baseline (1989-1993) blood samples from 933 men ?65?years of age from the prospective Cardiovascular Health Study. Particulate matter ?10??m (PM10), carbon monoxide, nitrogen dioxide, sulfur dioxide, and ozone data were obtained from the U.S. EPA Aerometric Information Retrieval System for the year prior to baseline. Inverse-distance weighted air monitor data were used to estimate each participants' monthly residential exposure. mLOY was detected with standard methods using signal intensity (median log-R ratio (mLRR)) of the male-specific chromosome Y regions from Illumina array data. Linear regression models were used to evaluate relations between mean exposure in the prior year, age, smoking and continuous mLRR. RESULTS:Increased PM10 was associated with mLOY, namely decreased mLRR (p-trend?=?0.03). Compared with the lowest tertile (?28.5??g/m3), the middle (28.5-31.0??g/m3; ??=?-0.0044, p?=?0.09) and highest (?31??g/m3; ??=?-0.0054, p?=?0.04) tertiles had decreased mLRR, adjusted for age, clinic, race/cohort, smoking status and pack-years. Additionally, increasing age (??=?-0.00035, p?=?0.06) and smoking pack-years (??=?-0.00011, p?=?1.4E-3) were associated with decreased mLRR, adjusted for each other and race/cohort. No significant associations were found for other pollutants. CONCLUSIONS:PM10 may increase leukocyte mLOY, a marker of genomic instability. The sample size was modest and replication is warranted.
| S-EPMC5971001 | biostudies-literature
Project description:BackgroundAir pollution is a large environmental health hazard whose exposure and health effects are unequally distributed among individuals. This is, at least in part, due to gene-environment interactions, but few studies exist. Thus, the current study aimed to explore genetic susceptibility to airway inflammation from short-term air pollution exposure through mechanisms of gene-environment interaction involving the SFTPA, GST and NOS genes.MethodsFive thousand seven hundred two adults were included. The outcome measure was fraction of exhaled nitric oxide (FeNO), at 50 and 270 ml/s. Exposures were ozone (O3), particulate matter < 10 µm (PM10), and nitrogen dioxide (NO2) 3, 24, or 120-h prior to FeNO measurement. In the SFTPA, GST and NOS genes, 24 single nucleotide polymorphisms (SNPs) were analyzed for interaction effects. The data were analyzed using quantile regression in both single-and multipollutant models.ResultsSignificant interactions between SNPs and air pollution were found for six SNPs (p < 0.05): rs4253527 (SFTPA1) with O3 and NOx, rs2266637 (GSTT1) with NO2, rs4795051 (NOS2) with PM10, NO2 and NOx, rs4796017 (NOS2) with PM10, rs2248814 (NOS2) with PM10 and rs7830 (NOS3) with NO2. The marginal effects on FeNO for three of these SNPs were significant (per increase of 10 µg/m3):rs4253527 (SFTPA1) with O3 (β: 0.155, 95%CI: 0.013-0.297), rs4795051 (NOS2) with PM10 (β: 0.073, 95%CI: 0.00-0.147 (single pollutant), β: 0.081, 95%CI: 0.004-0.159 (multipollutant)) and NO2 (β: -0.084, 95%CI: -0.147; -0.020 (3 h), β: -0.188, 95%CI: -0.359; -0.018 (120 h)) and rs4796017 (NOS2) with PM10 (β: 0.396, 95%CI: 0.003-0.790).ConclusionsIncreased inflammatory response from air pollution exposure was observed among subjects with polymorphisms in SFTPA1, GSTT1, and NOS genes, where O3 interacted with SFTPA1 and PM10 and NO2/NOx with the GSTT1 and NOS genes. This provides a basis for the further exploration of biological mechanisms as well as the identification of individuals susceptible to the effects of outdoor air pollution.
| S-EPMC10308777 | biostudies-literature
Project description:The US Environmental Protection Agency is required to reexamine its National Ambient Air Quality Standards (NAAQS) every 5 years, but evidence of mortality risk is lacking at air pollution levels below the current daily NAAQS in unmonitored areas and for sensitive subgroups.To estimate the association between short-term exposures to ambient fine particulate matter (PM2.5) and ozone, and at levels below the current daily NAAQS, and mortality in the continental United States.Case-crossover design and conditional logistic regression to estimate the association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day of death and 1 day prior) and mortality in 2-pollutant models. The study included the entire Medicare population from January 1, 2000, to December 31, 2012, residing in 39?182 zip codes.Daily PM2.5 and ozone levels in a 1-km × 1-km grid were estimated using published and validated air pollution prediction models based on land use, chemical transport modeling, and satellite remote sensing data. From these gridded exposures, daily exposures were calculated for every zip code in the United States. Warm-season ozone was defined as ozone levels for the months April to September of each year.All-cause mortality in the entire Medicare population from 2000 to 2012.During the study period, there were 22?433?862 million case days and 76?143?209 control days. Of all case and control days, 93.6% had PM2.5 levels below 25 ?g/m3, during which 95.2% of deaths occurred (21?353?817 of 22?433?862), and 91.1% of days had ozone levels below 60 parts per billion, during which 93.4% of deaths occurred (20?955?387 of 22?433?862). The baseline daily mortality rates were 137.33 and 129.44 (per 1 million persons at risk per day) for the entire year and for the warm season, respectively. Each short-term increase of 10 ?g/m3 in PM2.5 (adjusted by ozone) and 10 parts per billion (10-9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with a relative increase of 1.05% (95% CI, 0.95%-1.15%) and 0.51% (95% CI, 0.41%-0.61%) in daily mortality rate, respectively. Absolute risk differences in daily mortality rate were 1.42 (95% CI, 1.29-1.56) and 0.66 (95% CI, 0.53-0.78) per 1 million persons at risk per day. There was no evidence of a threshold in the exposure-response relationship.In the US Medicare population from 2000 to 2012, short-term exposures to PM2.5 and warm-season ozone were significantly associated with increased risk of mortality. This risk occurred at levels below current national air quality standards, suggesting that these standards may need to be reevaluated.
| S-EPMC5783186 | biostudies-literature
Project description:BackgroundHigher exposure to outdoor air pollution is associated with increased cardiopulmonary deaths, but there is limited evidence about the association between outdoor air pollution and diagnosed cardiovascular disease. Our study aimed to estimate the size of the association between long term exposure to outdoor air pollution and prevalent cardiovascular disease.MethodsWe carried out a cross-sectional analysis of data on more than 19,000 white adults aged 45 and older who participated in three representative surveys of the English population in 1994, 1998 and 2003, examining the relationship between self-reported doctor-diagnosed cardiovascular disease and exposure to outdoor air pollutants using multilevel regression techniques and meta-analysis.ResultsThe combined estimates suggested that an increase of 1 microg m-3 in concentration of particulate matter less than 10 microns in diameter was associated with an increase of 2.9% (95% CI -0.6% to 6.5%) in prevalence of cardiovascular disease in men, and an increase of 1.6% (95%CI -2.1% to 5.5%) in women. The year-specific analyses showed strongly positive associations in 2003 between odds of cardiovascular disease in both men and women and exposure to particulate matter but not in 1994 or 1998. We found no consistent associations between exposure to gaseous air pollutants and doctor-diagnosed cardiovascular disease.ConclusionThe associations of prevalent cardiovascular disease with concentration of particulate matter less than 10 microns in diameter, while only weakly positive, were consistent with the effects reported in cohort studies. The results provide evidence of the size of the association between particulate air pollution and the prevalence of cardiovascular disease but no evidence for an association with gaseous pollutants. We found strongly positive associations between particulate matter and cardiovascular disease in 2003 only, which highlights the importance of replicating findings in more than one population.
| S-EPMC2716315 | biostudies-literature
Project description:BackgroundRecent studies have indicated long-term effects on mortality of particulate and sulphur dioxide (SO(2)) pollution, but uncertainties remain over the size of any effects, potential latency and generalisability.MethodsA small area study was performed across electoral wards in Great Britain of mean annual black smoke (BS) and SO(2) concentrations (from 1966) and subsequent all-cause and cause-specific mortality using random effect models within a Bayesian framework adjusted for social deprivation and urban/rural classification. Different latencies and changes in associations over time were assessed.ResultsSignificant associations were found between BS and SO(2) concentrations and mortality. The effects were stronger for respiratory illness than other causes of mortality for the most recent exposure periods (shorter latency times) and most recent mortality period (lower pollutant concentrations). In pooled analysis across four sequential 4 year mortality periods (1982-98), adjusted excess relative risk for respiratory mortality was 3.6% (95% CI 2.6% to 4.5%) per 10 microg/m(3) BS and 13.2% (95% CI 11.5% to 14.9%) per 10 ppb SO(2), and in the most recent period (1994-8) it was 19.3% (95% CI 5.1% to 35.7%) and 21.7% (95% CI 2.9% to 38.5%), respectively.ConclusionsThese findings add to the evidence that air pollution has long-term effects on mortality and point to continuing public health risks even at the relatively lower levels of BS and SO(2) that now occur. They therefore have importance for policies on public health protection through regulation and control of air pollution.
| S-EPMC2094283 | biostudies-literature
Project description:To help understand the pathophysiologic mechanisms linking air pollutants and cardiovascular disease (CVD), we employed a repeated measures design to investigate the associations of four short-term air pollution exposures - particulate matter less than 2.5 μm in diameter (PM2.5), nitrogen dioxide (NO2), ozone (O3) and sulfur dioxide (SO2), with two blood markers involved in vascular effects of oxidative stress, soluble lectin-like oxidized LDL receptor-1 (sLOX-1) and nitrite, using data from the Multi-Ethnic Study of Atherosclerosis (MESA). Seven hundred and forty participants with plasma sLOX-1 and nitrite measurements at three exams between 2002 and 2007 were included. Daily PM2.5, NO2, O3 and SO2 zero to seven days prior to blood draw were estimated from central monitors in six MESA regions, pre-adjusted using site-specific splines of meteorology and temporal trends, and an indicator for day of the week. Unconstrained distributed lag generalized estimating equations were used to estimate net effects over eight days with adjustment for sociodemographic and behavioral factors. The results showed that higher short-term concentrations of PM2.5, but not other pollutants, were associated with increased sLOX-1 analyzed both as a continuous outcome (percent change per interquartile increase: 16.36%, 95%CI: 0.1-35.26%) and dichotomized at the median (odds ratio per interquartile increase: 1.21, 95%CI: 1.01-1.44). The findings were not meaningfully changed after adjustment for additional covariates or in several sensitivity analyses. Pollutant concentrations were not associated with nitrite levels. This study extends earlier experimental findings of increased sLOX-1 levels following PM inhalation to a much larger population and at ambient concentrations. In light of its known mechanistic role in promoting vascular disease, sLOX-1 may be a suitable translational biomarker linking air pollutant exposures and cardiovascular outcomes.
| S-EPMC8087633 | biostudies-literature
Project description:Cardiovascular disease is the number one cause of death globally and air pollution can be a contributing cause. Acute myocardial infarction and cardiac arrest are frequent manifestations of coronary heart disease. The objectives of the study were to investigate the association between 4 657 out-of-hospital cardiac arrests (OHCA) and hourly and daily outdoor levels of PM(10), PM(2.5), coarse fraction of PM (PM(10-2.5)), ultrafine particle proxies, NO(x), NO(2), O(3) and CO in Copenhagen, Denmark, for the period 2000-2010. Susceptible groups by age and sex was also investigated. A case-crossover design was applied. None of the hourly lags of any of the pollutants were significantly associated with OHCA events. The strongest association with OHCA events was observed for the daily lag4 of PM(2.5), lag3 of PM(10), lag3 of PM(10-2.5), lag3 of NO(x) and lag4 of CO. An IQR increase of PM(2.5) and PM(10) was associated with a significant increase of 4% (95% CI: 0%; 9%) and 5% (95% CI: 1%; 9%) in OHCA events with 3 days lag, respectively. None of the other daily lags or other pollutants was significantly associated with OHCA events. Adjustment for O(3) slightly increased the association between OHCA and PM(2.5) and PM(10). No susceptible groups were identified.
| S-EPMC3544842 | biostudies-literature
Project description:Despite considerable air pollution prevention and control measures that have been put into practice in recent years, outdoor air pollution remains one of the most important risk factors for health outcomes. To identify the potential research gaps, we conducted a scoping review focused on health outcomes affected by outdoor air pollution across the broad research area. Of the 5759 potentially relevant studies, 799 were included in the final analysis. The included studies showed an increasing publication trend from 1992 to 2008, and most of the studies were conducted in Asia, Europe, and North America. Among the eight categorized health outcomes, asthma (category: respiratory diseases) and mortality (category: health records) were the most common ones. Adverse health outcomes involving respiratory diseases among children accounted for the largest group. Out of the total included studies, 95.2% reported at least one statistically positive result, and only 0.4% showed ambiguous results. Based on our study, we suggest that the time frame of the included studies, their disease definitions, and the measurement of personal exposure to outdoor air pollution should be taken into consideration in any future research. The main limitation of this study is its potential language bias, since only English publications were included. In conclusion, this scoping review provides researchers and policy decision makers with evidence taken from multiple disciplines to show the increasing prevalence of outdoor air pollution and its adverse effects on health outcomes.
| S-EPMC6522200 | biostudies-literature
Project description:ObjectivesThe role of outdoor air pollution in the incidence of chronic obstructive pulmonary disease (COPD) remains unclear. We investigated this question using a large, nationally representative cohort based on primary care records linked to hospital admissions.MethodsA cohort of 812?063 patients aged 40-89?years registered with 205 English general practices in 2002 without a COPD diagnosis was followed from 2003 to 2007. First COPD diagnoses recorded either by a general practitioner (GP) or on admission to hospital were identified. Annual average concentrations in 2002 for particulate matter with an aerodynamic diameter <10?µm (PM10) and <2.5?µm (PM2.5), nitrogen dioxide (NO2), ozone and sulfur dioxide (SO2) at 1?km(2) resolution were estimated from emission-based dispersion models. Hazard ratios (HRs) per interquartile range change were estimated from Cox models adjusting for age, sex, smoking, body mass index and area-level deprivation.Results16?034 participants (1.92%) received a COPD diagnosis from their GP and 2910 participants (0.35%) were admitted to hospital for COPD. After adjustment, HRs for GP recorded COPD and PM10, PM2.5 and NO2 were close to unity, positive for SO2 (HR=1.07 (95% CI 1.03 to 1.11) per 2.2?µg/m(3)) and negative for ozone (HR=0.94 (0.89 to 1.00) per 3?µg/m(3)). For admissions HRs for PM2.5 and NO2 remained positive (HRs=1.05 (0.98 to 1.13) and 1.06 (0.98 to 1.15) per 1.9?µg/m(3) and 10.7?µg/m(3), respectively).ConclusionsThis large population-based cohort study found limited, inconclusive evidence for associations between air pollution and COPD incidence. Further work, utilising improved estimates of air pollution over time and enhanced socioeconomic indicators, is required to clarify the association between air pollution and COPD incidence.
| S-EPMC4283678 | biostudies-literature
Project description: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 ?m [PM2.5] and nitrogen oxide [NOx]) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. Main Outcomes and Measures:The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling. Results:At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio [HR] for difference of 0.88 ?g/m3 PM2.5, 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 ?g/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.
| S-EPMC7105952 | biostudies-literature