Environmental Pollution and Cardiovascular Disease : Part 1 of 2: Air Pollution
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ABSTRACT:
SUBMITTER: Sagheer U
PROVIDER: S-EPMC11198409 | biostudies-literature | 2023 Dec
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC11198458 | biostudies-literature
Project description:Air pollution exposure is a well-established risk factor for several adverse respiratory outcomes, including airways diseases and lung cancer. Few studies have investigated the relationship between air pollution and interstitial lung disease (ILD) despite many forms of ILD arising from environmental exposures. There are potential mechanisms by which air pollution could cause, exacerbate, or accelerate the progression of certain forms of ILD via pulmonary and systemic inflammation as well as oxidative stress. This article will review the current epidemiologic and translational data supporting the plausibility of this relationship and propose a new conceptual framework for characterizing novel environmental risk factors for these forms of lung disease.
| S-EPMC4388120 | biostudies-other
Project description:BackgroundAmbient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.MethodsWe investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).ResultsEach increase of 10 μg/m3 PM2.5 (overall range, 2.9-28.0 μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure <8 μg/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8-12 μg/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12-20 μg/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ μg/m3 (CVD: HR 1.19; 95% CI 1.10-1.28). Results were robust to alternative approaches to PM2.5 exposure assessment and statistical analysis.ConclusionsLong-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12 µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.
| S-EPMC7124502 | biostudies-literature
Project description:Genetic susceptibility is likely to play a role in response to air pollution. Hence, gene-environment interaction studies can be a tool for exploring the mechanisms and the importance of the pathway in the association between air pollution and a cardiovascular outcome. In this article, we present a systematic review of the studies that have examined gene-environment interactions in relation to the cardiovascular health effects of air pollutants. We identified 16 articles meeting our search criteria. Of these studies, most have focused on individual functional polymorphisms or individual candidate genes. Moreover, they were all based on 3 study populations that have been extensively investigated in relation to air pollution effects: the Normative Aging Study, Air Pollution and Inflammatory Response in Myocardial Infarction Survivors: Gene-Environment Interaction in a High Risk Group, and Multiethnic Study of Atherosclerosis. In conclusions, the studies differed substantially in both the cardiovascular outcomes examined and the polymorphisms examined, so there is little confirmation of results across cohorts. Gene-environment interaction studies can help explore the mechanisms and the potential pathway in the association between air pollution and a cardiovascular outcome; replication of findings and studies involving multiple cohorts would be needed to draw stronger conclusions.
| S-EPMC3073822 | biostudies-literature
Project description:BACKGROUND:Long-term exposure to ambient particulate matter (PM) air pollution is associated with increased cardiovascular disease (CVD); however, the impact of PM on clinical risk factors for CVD in healthy subjects is unclear. We examined the relationship of PM with levels of circulating lipids and blood pressure in the Third National Health and Nutrition Examination Survey (NHANES III), a large nationally representative US survey. METHODS:This study was based on 11,623 adult participants of NHANES III (1988-1994; median age 41.0). Serum lipids and blood pressure were measured during the NHANES III examination. Average exposure for 1988-1994 to particulate matter <10 ?m in aerodynamic diameter (PM10) at the residences of participants was estimated based on measurements from US Environmental Protection Agency monitors. Multivariate linear regression was used to estimate the associations of PM10 with lipids and blood pressure. RESULTS:An interquartile range width increase in PM10 exposure (11.1 ?g/m) in the study population was associated with 2.42% greater serum triglycerides (95% confidence interval: 1.09, 3.76); multivariate adjusted means of triglycerides according to increasing quartiles of PM10 were 137.6, 142.5, 142.6, and 148.9 mg/dl, respectively. An interquartile range width increase in PM10 was associated with 1.43% greater total cholesterol (95% confidence interval: 1.21, 1.66). These relationships with triglycerides and total cholesterol did not differ by age or region. Associations of PM10 with blood pressure were modest. CONCLUSIONS:Findings from this large, diverse study indicate that greater long-term PM10 exposure is associated with elevated serum triglycerides and total cholesterol, potentially mediating air pollution-related effects on CVD.
| S-EPMC4959464 | biostudies-literature
Project description:Psychosocial and environmental stress exposures across the life course have been shown to be relevant in the development of cardiovascular disease (CVD). Assessing more than one stressor from different domains (e.g., individual and neighborhood) and across the life course moves us towards a more integrated picture of how stress affects health and well-being. Furthermore, these individual and neighborhood psychosocial stressors act on biologic pathways, including immune function and inflammatory response, which are also impacted by ubiquitous environmental exposures such as air pollution. The objective of this study is to evaluate the interaction between psychosocial stressors, at both the individual and neighborhood level, and air pollution on CVD. This study used data from the 2009-2011 Behavioral Risk Factor Surveillance System (BRFSS) from Washington State. Adverse childhood experiences (ACEs) measured at the individual level, and neighborhood deprivation index (NDI) measured at the zip code level, were the psychosocial stressors of interest. Exposures to three air pollutants-particulate matter (both PM2.5 and PM10) and nitrogen dioxide (NO₂)-were also calculated at the zip code level. Outcome measures included several self-reported CVD-related health conditions. Both multiplicative and additive interaction quantified using the relative excess risk due to interaction (RERI), were evaluated. This study included 32,151 participants in 502 unique zip codes. Multiplicative and positive additive interactions were observed between ACEs and PM10 for diabetes, in models adjusted for NDI. The prevalence of diabetes was 1.58 (95% CI: 1.40, 1.79) times higher among those with both high ACEs and high PM10 compared to those with low ACEs and low PM10 (p-value = 0.04 for interaction on the multiplicative scale). Interaction was also observed between neighborhood-level stressors (NDI) and air pollution (NO₂) for the stroke and diabetes outcomes on both multiplicative and additive scales. Modest interaction was observed between NDI and air pollution, supporting prior literature on the importance of neighborhood-level stressors in cardiovascular health and reinforcing the importance of NDI on air pollution health effects. ACEs may exert health effects through selection into disadvantaged neighborhoods and more work is needed to understand the accumulation of risk in multiple domains across the life course.
| S-EPMC5877017 | biostudies-literature
Project description:ObjectiveWe aimed to assess racial differences in air pollution exposures to ambient fine particulate matter (particles with median aerodynamic diameter <2.5 µm [PM2.5]) and black carbon (BC) and their association with cardiovascular disease (CVD) risk factors, arterial endothelial function, incident CVD events, and all-cause mortality.Approach and resultsData from the HeartSCORE study (Heart Strategies Concentrating on Risk Evaluation) were used to estimate 1-year average air pollution exposure to PM2.5 and BC using land use regression models. Correlates of PM2.5 and BC were assessed using linear regression models. Associations with clinical outcomes were determined using Cox proportional hazards models, adjusting for traditional CVD risk factors. Data were available on 1717 participants (66% women; 45% blacks; 59±8 years). Blacks had significantly higher exposure to PM2.5 (mean 16.1±0.75 versus 15.7±0.73µg/m3; P=0.001) and BC (1.19±0.11 versus 1.16±0.13abs; P=0.001) compared with whites. Exposure to PM2.5, but not BC, was independently associated with higher blood glucose and worse arterial endothelial function. PM2.5 was associated with a higher risk of incident CVD events and all-cause mortality combined for median follow-up of 8.3 years. Blacks had 1.45 (95% CI, 1.00-2.09) higher risk of combined CVD events and all-cause mortality than whites in models adjusted for relevant covariates. This association was modestly attenuated with adjustment for PM2.5.ConclusionsPM2.5 exposure was associated with elevated blood glucose, worse endothelial function, and incident CVD events and all-cause mortality. Blacks had a higher rate of incident CVD events and all-cause mortality than whites that was only partly explained by higher exposure to PM2.5.
| S-EPMC5864550 | biostudies-literature
Project description:Research to date demonstrates a relationship between exposure to ambient air pollutants and cardiovascular disease (CVD). Many studies have shown associations between short-term exposures to elevated levels of air pollutants and CVD events, and several cohort studies suggest effects of long-term exposure on cardiovascular mortality, coronary heart disease events, and stroke. The biologic mechanisms underlying this long-term exposure relationship are not entirely clear but are hypothesized to include systemic inflammation, autonomic nervous system imbalance, changes in vascular compliance, altered cardiac structure, and development of atherosclerosis. The Multi-Ethnic Study of Atherosclerosis provides an especially well-characterized population in which to investigate the relationship between air pollution and CVD and to explore these biologic pathways. This article reviews findings reported to date within this cohort and summarizes the aims and anticipated contributions of a major ancillary study, the Multi-Ethnic Study of Atherosclerosis and Air Pollution.
| S-EPMC4016948 | biostudies-literature
Project description:Objective: The purpose of this study was to investigate the sex correlations of particulate matters (PM2.5, PM10, PM2.5-10), NO2 and NOx with ASCVD risk in the UK Biobank population. Methods: Among 285,045 participants, pollutants were assessed and correlations between ASCVD risk were stratified by sex and estimated using multiple linear and logistic regressions adjusted for length of time at residence, education, income, physical activity, Townsend deprivation, alcohol, smocking pack years, BMI and rural/urban zone. Results: Males presented higher ASCVD risk than females (8.63% vs. 2.65%, p < 0.001). In males PM2.5, PM10, NO2, and NOx each were associated with an increased ASCVD risk >7.5% in the adjusted logistic models, with ORs [95% CI] for a 10 μg/m3 increase were 2.17 [1.87-2.52], 1.15 [1.06-1.24], 1.06 [1.04-1.08] and 1.05 [1.04-1.06], respectively. In females, the ORs for a 10 μg/m3 increase were 1.55 [1.19-2.05], 1.22 [1.06-1.42], 1.07 [1.03-1.10], and 1.04 [1.02-1.05], respectively. No association was observed in both sexes between ASCVD risk and PM2.5-10. Conclusion: Our findings may suggest the possible actions of air pollutants on ASCVD risk.
| S-EPMC10569126 | biostudies-literature
Project description:Environmental health studies relate how exposures (eg, chemicals) affect human health and disease; however, in most cases, the molecular and biological mechanisms connecting an exposure with a disease remain unknown. To help fill in these knowledge gaps, we sought to leverage content from the public Comparative Toxicogenomics Database (CTD) to identify potential intermediary steps. In a proof-of-concept study, we systematically compute the genes, molecular mechanisms, and biological events for the environmental health association linking air pollution toxicants with 2 cardiovascular diseases (myocardial infarction and hypertension) as a test case. Our approach integrates 5 types of curated interactions in CTD to build sets of "CGPD-tetramers," computationally constructed information blocks relating a Chemical- Gene interaction with a Phenotype and Disease. This bioinformatics strategy generates 653 CGPD-tetramers for air pollution-associated myocardial infarction (involving 5 pollutants, 58 genes, and 117 phenotypes) and 701 CGPD-tetramers for air pollution-associated hypertension (involving 3 pollutants, 96 genes, and 142 phenotypes). Collectively, we identify 19 genes and 96 phenotypes shared between these 2 air pollutant-induced outcomes, and suggest important roles for oxidative stress, inflammation, immune responses, cell death, and circulatory system processes. Moreover, CGPD-tetramers can be assembled into extensive chemical-induced disease pathways involving multiple gene products and sequential biological events, and many of these computed intermediary steps are validated in the literature. Our method does not require a priori knowledge of the toxicant, interacting gene, or biological system, and can be used to analyze any environmental chemical-induced disease curated within the public CTD framework. This bioinformatics strategy links and interrelates chemicals, genes, phenotypes, and diseases to fill in knowledge gaps for environmental health studies, as demonstrated for air pollution-associated cardiovascular disease, but can be adapted by researchers for any environmentally influenced disease-of-interest.
| S-EPMC7548289 | biostudies-literature