Cardiovascular Effects Of Air Pollution Research Articles

Nutritional Solutions to Reduce Risks of Negative Health Impacts of Air Pollution.

Air pollution worldwide has been associated with cardiovascular and respiratory morbidity and mortality, particularly in urban settings with elevated concentrations of primary pollutants. Air pollution is a very complex mixture of primary and secondary gases and particles, and its potential to cause harm can depend on multiple factors—including physical and chemical characteristics of pollutants, which varies with fine-scale location (e.g., by proximity to local emission sources)—as well as local meteorology, topography, and population susceptibility. It has been hypothesized that the intake of anti-oxidant and anti-inflammatory nutrients may ameliorate various respiratory and cardiovascular effects of air pollution through reductions in oxidative stress and inflammation. To date, several studies have suggested that some harmful effects of air pollution may be modified by intake of essential micronutrients (such as B vitamins, and vitamins C, D, and E) and long-chain polyunsaturated fatty acids. Here, we review the existing literature related to the potential for nutrition to modify the health impacts of air pollution, and offer a framework for examining these interactions.

The role of oxidative stress in the cardiovascular actions of particulate air pollution.

Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.

Altered Nitric Oxide Bioavailability Contributes to Diesel Exhaust Inhalation‐Induced Cardiovascular Dysfunction in Man

BackgroundDiesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. We investigated the role of nitric oxide (NO) bioavailability in mediating these effects.Methods and ResultsIn 2 randomized double‐blind crossover studies, healthy nonsmokers were exposed to diesel exhaust or filtered air. Study 1: Bilateral forearm blood flow was measured during intrabrachial infusions of acetylcholine (ACh; 5 to 20 μg/min) and sodium nitroprusside (SNP; 2 to 8 μg/min) in the presence of the NO clamp (NO synthase inhibitor NG‐monomethyl‐l‐arginine (l‐NMMA) 8 μg/min coinfused with the NO donor SNP at 90 to 540 ng/min to restore basal blood flow). Study 2: Blood pressure, arterial stiffness, and cardiac output were measured during systemic NO synthase inhibition with intravenous l‐NMMA (3 mg/kg). Following diesel exhaust inhalation, plasma nitrite concentrations were increased (68±48 versus 41±32 nmol/L; P=0.006) despite similar l‐NMMA–induced reductions in basal blood flow (−20.6±14.7% versus −21.1±14.6%; P=0.559) compared to air. In the presence of the NO clamp, ACh and SNP caused dose‐dependent vasodilatation that was not affected by diesel exhaust inhalation (P>0.05 for both). Following exposure to diesel exhaust, l‐NMMA caused a greater increase in blood pressure (P=0.048) and central arterial stiffness (P=0.007), but reductions in cardiac output and increases in systemic vascular resistance (P>0.05 for both) were similar to those seen with filtered air.ConclusionsDiesel exhaust inhalation disturbs normal vascular homeostasis with enhanced NO generation unable to compensate for excess consumption. We suggest the adverse cardiovascular effects of air pollution are, in part, mediated through reduced NO bioavailability.Clinical Trial RegistrationURL: http://www.ClinicalTrials.gov. Unique identifiers: NCT00845767 and NCT01060930.

From Particles to Patients: Oxidative Stress and the Cardiovascular Effects of Air Pollution

Air pollution, especially airborne particulate matter (PM), is associated with an increase in both morbidity and mortality from cardiovascular disease, although the underlying mechanisms remain incompletely established. The one consistent observation that links the pulmonary and cardiovascular effects of inhaled PM is oxidative stress. This article examines the evidence for the role of oxidative stress in the cardiovascular effects of air pollution, beginning with observations from epidemiological and controlled exposure studies and then exploring potential mechanistic pathways involving free radical generation from PM itself, to effects of PM on cell cultures, isolated organs, healthy animals and animal models of disease. Particular emphasis is placed on the vascular and atherosclerotic effects of urban air pollution and diesel exhaust emissions as rich sources of environmental ultrafine particles.

Smouldering hearts: A Mills and Boon classic

Air pollution is an important modifiable risk factor for cardiovascular disease. Acute exposure has been linked to a range of cardiovascular events including acute myocardial infarction and death. We have demonstrated that exposure to dilute diesel exhaust causes detrimental vascular and thrombotic effects that promote atherogenesis and myocardial ischaemia. These effects appear to be mediated through adverse effects on nitric oxide bioavailability. The epidemiology, pathophysiology and potential aetiology of the adverse cardiovascular effects of air pollution on the nitric oxide system will be discussed.

Order out of Chaos: Elucidating the Opposing Effects of Air Pollutants and Heat on Blood Pressure

Vol. 120, No. 2 News | Science SelectionsOpen AccessOrder out of Chaos: Elucidating the Opposing Effects of Air Pollutants and Heat on Blood Pressureis accompanied byOpposing Effects of Particle Pollution, Ozone, and Ambient Temperature on Arterial Blood Pressure Bob Weinhold Bob Weinhold Search for more papers by this author Published:1 February 2012https://doi.org/10.1289/ehp.120-a76aCited by:2AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit A body of research suggests that people with diabetes may be especially vulnerable to adverse cardiovascular effects of air pollution and heat, although the combined effects of these factors are not clear. Now an international team of researchers sheds light on potential impacts of this dual exposure [EHP 120(2):241–246; Hoffmann et al.]. In a study of the short-term effects of ambient air pollutants and temperature on arterial blood pressure in 70 people with type 2 diabetes mellitus, they found opposing effects—fine particulate matter (PM2.5) and black carbon in particular, were associated with increases in systolic blood pressure (SBP), whereas ozone and higher temperature were associated with decreases.The study subjects, from the Boston, Massachusetts, area, ranged in age from 45 to 86 and were evaluated between September 2006 and August 2010. Each participant lived within 25 km of a central air pollution monitor. At each of 5 clinic visits spaced 2 weeks apart, participants answered questions and underwent blood and urinary analyses and clinical examinations. Mixed models that accounted for repeated measures in individual participants were used to estimate associations between air pollutants and temperature and blood pressure.The researchers estimated that each interquartile increase in PM2.5 or black carbon in the 5 days prior to a clinical examination was linked with an average increase in SBP of 1.4 mmHg and 2.2 mmHg, respectively. In contrast, an interquartile increase in ozone was associated with a 5.2-mmHg decrease in SBP. Each increase of 11.5°C in mean temperature was associated with a 3.2-mmHg decrease in SBP before adjusting for ozone exposure. Estimated increases in blood pressure with PM2.5 exposure were greater in people with elevated baseline blood pressure, whereas associations with ozone exposure and temperature were greater in people with lower to normal blood pressure. Estimated differences in blood pressure tended to be progressively greater for each of up to 5 additional days of exposure prior to each clinical exam.The researchers accounted for possible confounding factors such as sociodemographic variables, lifestyle indicators, prescription drug use, tobacco smoke, health history, and season. However, they were not able to estimate personal levels of exposure using the local and area monitoring stations, and factors such as physical activity were not addressed.The authors note that the opposing effects may not cancel each other out and could plausibly act negatively in independent ways. Decreased SBP can be good in moderation, but it could be dangerous if lowered suddenly and significantly, especially in subjects with compromised vascular compensation mechanisms, which is common in diabetic patients.FiguresReferencesRelatedDetailsCited by Dong G, Wang J, Zeng X, Chen L, Qin X, Zhou Y, Li M, Yang M, Zhao Y, Ren W and Hu Q (2015) Interactions Between Air Pollution and Obesity on Blood Pressure and Hypertension in Chinese Children, Epidemiology, 10.1097/EDE.0000000000000336, 26:5, (740-747), Online publication date: 1-Sep-2015. Dong G, Qian Z, Xaverius P, Trevathan E, Maalouf S, Parker J, Yang L, Liu M, Wang D, Ren W, Ma W, Wang J, Zelicoff A, Fu Q and Simckes M (2013) Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China, Hypertension, 10.1161/HYPERTENSIONAHA.111.00003, 61:3, (578-584), Online publication date: 1-Mar-2013. Related articlesOpposing Effects of Particle Pollution, Ozone, and Ambient Temperature on Arterial Blood Pressure21 October 2011Environmental Health Perspectives Vol. 120, No. 2 February 2012Metrics About Article Metrics Publication History Originally published1 February 2012Published in print1 February 2012 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Cardiovascular effects of air pollution

Cardiovascular effects of air pollution

Exposure to nitrogen dioxide is not associated with vascular dysfunction in man

Background: Exposure to air pollution is associated with increased cardiorespiratory morbidity and mortality. It is unclear whether these effects are mediated through combustion-derived particulate matter or gaseous components, such as nitrogen dioxide.Objectives: To investigate the effect of nitrogen dioxide exposure on vascular vasomotor and six fibrinolytic functions.Methods: Ten healthy male volunteers were exposed to nitrogen dioxide at 4 ppm or filtered air for 1 h during intermittent exercise in a randomized double-blind crossover study. Bilateral forearm blood flow and fibrinolytic markers were measured before and during unilateral intrabrachial infusion of bradykinin (100–1000 pmol/min), acetylcholine (5–20 μg/min), sodium nitroprusside (2–8 μg/min), and verapamil (10–100 μg/min) 4 h after the exposure. Lung function was determined before and after the exposure, and exhaled nitric oxide at baseline and 1 and 4 h after the exposure.Results: There were no differences in resting forearm blood flow after either exposure. There was a dose-dependent increase in forearm blood flow with all vasodilators but this was similar after either exposure for all vasodilators (p > .05 for all). Bradykinin caused a dose-dependent increase in plasma tissue-plasminogen activator, but again there was no difference between the exposures. There were no changes in lung function or exhaled nitric oxide following either exposure.Conclusion: Inhalation of nitrogen dioxide does not impair vascular vasomotor or fibrinolytic function. Nitrogen dioxide does not appear to be a major arbiter of the adverse cardiovascular effects of air pollution.

Particulate air pollution and coronary heart disease

Air pollution poses a significant health risk. The article focuses on the adverse effects of air pollution on the cardiovascular system. Short-term and long-term studies clearly indicate that relatively modest exposures to particulate matter in the ambient air are associated with increased morbidity and mortality due to coronary heart disease. In humans, inhalational exposure to particulate air pollutants decreases heart rate variability, causes ST-segment depression and endothelial dysfunction, increases blood pressure and blood coagulability, and accelerates the progression of atherosclerosis. Mechanisms of air pollution-induced cardiotoxicity include increased generation of reactive oxygen species followed by activation of proinflammatory and prothrombotic pathways. In experimental settings, ultrafine air pollutants instilled directly into the cardiac vasculature depress cardiac contractility and decrease coronary flow. Both effects are attenuated by the use of a free radical scavenger. Reactive oxygen species-related mechanisms of air pollution cardiotoxicity might become a valid target in developing new pharmacological strategies aimed at decreasing adverse effects of air pollution during extreme episodes (fires, earthquakes, industrial accidents, acts of terrorism). Educating patients and the general population on the negative cardiovascular effects of air pollution might be helpful in decreasing the risk of developing air pollution-related coronary heart disease.

Air Quality and Cardiovascular Health

Ambient particulate matter has been associated consistently with an increased risk for mortality largely due to cardiovascular diseases.1 Although the relative risk estimates from epidemiological studies are small, they apply to almost the entire population of the United States. Consequently, exposure to ambient particles produces considerable burden of disease, and its mitigation offers the benefit of improving life expectancy.2 Articles see pp 941 and 949 Over the past decade, research has substantiated the understanding of the pathophysiological mechanisms linking ambient particles to the cardiovascular system3,4 once it was noted that ambient air pollution elicits systemic inflammatory responses in the general population.5 An update of the American Heart Association statement on air pollution and cardiovascular disease3 is under way. Mechanisms considered for active and secondhand smoke as well as ambient air pollution are strikingly similar.4,6,7 They include progression of atherosclerotic plaques to vulnerable forms, prothrombotic states, endothelial dysfunction, and altered autonomic nervous system control (Figure). Increased systemic oxidative stress is considered the key mechanism responsible for most of these pathophysiological changes. Increased risks for cardiovascular disease in general and coronary artery disease in particular have been documented for active and secondhand smoke as well as ambient particulate matter. Deep venous thrombosis has been added to this list recently.8 Figure. Overview on pathomechanism linking ambient air pollution,4 secondhand smoke,7 and active smoking to acute coronary syndromes. Nevertheless, the public health relevance of particulate matter in the light of the smoking literature remains hotly debated. Smokers are exposed to considerably higher cumulative doses of particulate matter than the general nonsmoking population. Mortality due to low doses of ambient particles may be considered counterintuitive compared with doses of particles tolerated by smoking individuals. A systematic assessment of the exposure-response function ranging from low doses of inhaled particles …

Modification of the Interleukin-6 Response to Air Pollution by Interleukin-6 and Fibrinogen Polymorphisms

BackgroundEvidence suggests that cardiovascular effects of air pollution are mediated by inflammation and that air pollution can induce genetic expression of the interleukin-6 gene (IL6).ObjectivesWe investigated whether IL6 and fibrinogen gene variants can affect plasma IL-6 responses to air pollution in patients with cardiovascular disease.MethodsWe repeatedly determined plasma IL-6 in 955 myocardial infarction survivors from six European cities (n = 5,539). We conducted city-specific analyses using additive mixed models adjusting for patient characteristics, time trend, and weather to assess the impact of air pollutants on plasma IL-6. We pooled city-specific estimates using meta-analysis methodology. We selected three IL6 single-nucleotide polymorphisms (SNPs) and one SNP each from the fibrinogen α-chain gene (FGA) and β-chain gene (FGB) for gene–environment analyses.ResultsWe found the most consistent modifications for variants in IL6 rs2069832 and FBG rs1800790 after exposure to carbon monoxide (CO; 24-hr average; p-values for interaction, 0.034 and 0.019, respectively). Nitrogen dioxide effects were consistently modified, but p-values for interaction were larger (0.09 and 0.19, respectively). The strongest effects were seen 6–11 hr after exposure, when, for example, the overall effect of a 2.2% increase in IL-6 per 0.64 mg/m3 CO was modified to a 10% (95% confidence interval, 4.6–16%) increase in IL-6 (p-value for interaction = 0.002) for minor homozygotes of FGB rs1800790.ConclusionsThe effect of gaseous traffic-related air pollution on inflammation may be stronger in genetic subpopulations with ischemic heart disease. This information could offer an opportunity to identify postinfarction patients who would benefit more than others from a cleaner environment and antiinflammatory treatment.

Adverse cardiovascular effects of air pollution

Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular disease in urban communities. Acute exposure has been linked to a range of adverse cardiovascular events including hospital admissions with angina, myocardial infarction, and heart failure. Long-term exposure increases an individual's lifetime risk of death from coronary heart disease. The main arbiter of these adverse health effects seems to be combustion-derived nanoparticles that incorporate reactive organic and transition metal components. Inhalation of this particulate matter leads to pulmonary inflammation with secondary systemic effects or, after translocation from the lung into the circulation, to direct toxic cardiovascular effects. Through the induction of cellular oxidative stress and proinflammatory pathways, particulate matter augments the development and progression of atherosclerosis via detrimental effects on platelets, vascular tissue, and the myocardium. These effects seem to underpin the atherothrombotic consequences of acute and chronic exposure to air pollution. An increased understanding of the mediators and mechanisms of these processes is necessary if we are to develop strategies to protect individuals at risk and reduce the effect of air pollution on cardiovascular disease.

Vulnerability to cardiovascular effects of air pollution in people with diabetes

Vulnerability to cardiovascular effects of air pollution in people with diabetes

Cardiovascular effects of air pollution

Air pollution is a heterogeneous mixture of gases, liquids and PM (particulate matter). In the modern urban world, PM is principally derived from fossil fuel combustion with individual constituents varying in size from a few nanometres to 10 microm in diameter. In addition to the ambient concentration, the pollution source and chemical composition may play roles in determining the biological toxicity and subsequent health effects. Nevertheless, studies from across the world have consistently shown that both short- and long-term exposures to PM are associated with a host of cardiovascular diseases, including myocardial ischaemia and infarctions, heart failure, arrhythmias, strokes and increased cardiovascular mortality. Evidence from cellular/toxicological experiments, controlled animal and human exposures and human panel studies have demonstrated several mechanisms by which particle exposure may both trigger acute events as well as prompt the chronic development of cardiovascular diseases. PM inhaled into the pulmonary tree may instigate remote cardiovascular health effects via three general pathways: instigation of systemic inflammation and/or oxidative stress, alterations in autonomic balance, and potentially by direct actions upon the vasculature of particle constituents capable of reaching the systemic circulation. In turn, these responses have been shown to trigger acute arterial vasoconstriction, endothelial dysfunction, arrhythmias and pro-coagulant/thrombotic actions. Finally, long-term exposure has been shown to enhance the chronic genesis of atherosclerosis. Although the risk to one individual at any single time point is small, given the prodigious number of people continuously exposed, PM air pollution imparts a tremendous burden to the global public health, ranking it as the 13th leading cause of morality (approx. 800,000 annual deaths).

Short term effects of air pollution on hospitalizations for cardiovascular diseases in eight French cities: The PSAS program

Short term associations between air pollution indicators and hospitalizations for cardiovascular diseases have been suggested by epidemiological and clinical studies. The present study aims at estimating the association between particles with diameter <10 microm (PM(10)), nitrogen dioxide (NO(2)) and ozone and hospitalizations for cardiovascular diseases in eight French cities during the 1998-2003 period. The daily number of hospitalizations in each city was extracted from the French hospital information system (PMSI) for cardiovascular diseases, cardiac diseases, ischemic heart diseases and stroke. Excess relative risks (ERRs) of hospitalization associated with a 10 microg/m(3) increase in pollutant levels were estimated in each city by fitting a Poisson regression model, controlling for well-known confounding factors and temporal trends. City-specific results were then combined by inverse variance weighting. Daily number of hospitalizations for cardiovascular diseases was associated with PM(10) levels (for a 10 microg/m(3) increase, ERR=0.8%, 95% CI: [0.2, 1.5]), with NO(2) (1.1%, [0.6, 1.6]) but not with ozone (0.1% [-0.2%, 0.5%]). Associations were stronger in people aged 65 years and over, and when only hospitalizations for ischemic heart diseases were considered. No association was found between strokes and air pollution levels. Our study suggests that the ambient levels of air pollutants currently experienced in the eight French cities, which are close to European air quality guidelines, are yet linked to a short term increase of hospitalizations for cardiovascular diseases. These results are consistent with epidemiological and toxicological data on the cardiovascular effects of air pollution.

Diabetes and Cardiovascular Effects of Air Pollution

P-050 Introduction: the effects of air pollution and cardiovascular diseases (CVD) have been studied in several cities. Previous studies have reported the risk increase in diabetics when compared to non-diabetic groups. This study was conducted to estimate the effect modification of air pollution effects on CVD induced by diabetes. Methods: This study carried out from 2001 to 2004 and we adopted generalized linear Poisson regression models to assess the effects of PM10, CO, NO2, SO2, and O3 on CVD on diabetic and non-diabetic groups controlling for seasonality (long and short-term trends) and weather variables using a semi-parametric smoother (spline). The 2 days cumulative effects of air pollutants were assessed using 2 day moving average. Results: PM10 was not associated with cardiovascular diseases in any group. An interquartile range increase on SO2 concentration (8.0 μg/m3) was associated with increases of 6.0% (95% CI: 4.0–8.0) and 17.0% (95% CI: −1.0–34.0) on CVD admissions for non-diabetic and diabetic groups, respectively. Conclusion: This study showed that air pollution has a remarkable impact on cardiovascular morbidity, mainly in a high susceptible group like the diabetic population, reinforcing the necessity of additional studies to confirm these finds. This study was funded by: UNISANTOS, and CEACL-UNIFESP.

Air Pollution: The Plaque of the Matter

Vol. 114, No. 4 EnvironewsOpen AccessAir Pollution: The Plaque of the Matter Rebecca Clay Haynes Rebecca Clay Haynes Search for more papers by this author Published:1 April 2006https://doi.org/10.1289/ehp.114-a218aAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Particulate matter measuring less than 2.5 microns (PM2.5) has been widely linked to heart disease. These tiny particles of dust, soot, and smoke accompany emissions from power plants and vehicle exhaust, and lead to an estimated 60,000 premature deaths per year in the United States. EPA standards limit average human exposure of PM2.5 to a maximum of 15 micrograms per cubic meter. Now a study published in the 21 December 2005 issue of JAMA shows that long-term exposure to PM2.5 even at levels within federal standards accelerates the development of atherosclerosis in laboratory mice by increasing plaque development, especially when the mice are also fed a high-fat diet.Mice do not naturally develop plaque, a fatty deposit on the inner lining of arteries; the 28 mice used in the study were genetically modified to do so. The animals were divided into two subgroups, one fed a normal diet, the other a high-fat diet. Those subgroups were then divided again, with half breathing air containing concentrated PM2.5 at levels equivalent to 15.2 micrograms per cubic meter and the other half breathing particle-free filtered air. The air pollution group was exposed for six hours per day, five days per week, for six months.Researchers found measurable changes in the extent and severity of plaque formation in the aorta as well as artery inflammation and reduced function of the arterial lining. In animals that breathed polluted air and ate a high-fat diet, 41.5% of the arterial interior measured was filled with plaque, compared to 13.2% in animals that breathed filtered air and ate a normal diet.In humans, high plaque levels can lead to heart attacks and strokes. “These results can be very applicable to the human population, especially in urban environments,” says coauthor Lung Chi Chen, an associate professor of environmental medicine at the New York University School of Medicine. “We found that the combination of air pollution and diet had a dramatic effect on plaque formation, leading to inflammation and heart disease.”“It was surprising in this study to see the impact of exposure to a relatively low PM concentration on plaque development,” says Kevin Dreher, a principal investigator studying the cardiovascular effects of air pollution within the EPA’s National Health and Environmental Effects Research Laboratory. “While both dietary groups developed plaque when exposed to polluted air, the high-fat diet led to more consistent and statistically significant increase alterations of plaque development. Fat in the diet appears to be an important effect modifier when coupled with exposure to air particulate pollution.”Chen and his group are now gathering results on heart rate and blood pressure changes in these same mice. In ongoing studies, they are also examining specific mechanisms that could link air pollution, diet, and heart disease. In particular, they are trying to better define which components in PM2.5 most likely promote plaque formation and atherosclerosis.FiguresReferencesRelatedDetails Vol. 114, No. 4 April 2006Metrics About Article Metrics Publication History Originally published1 April 2006Published in print1 April 2006 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Air pollution and the heart

Despite legislation, leading to dramatic decreases in levels of air pollution since the time of the great smogs, a large body of epidemiological evidence has demonstrated that pollution continues to have adverse effects on human health. One striking finding from the epidemiological data is that patients with cardiovascular disease are susceptible to acute rises in ambient pollutants. Mortality and hospital admissions for myocardial infarction, congestive cardiac failure and cardiac arrhythmia all increase with a rise in the concentration of both particulate and gaseous pollutants. Before concluding that this association is a causal one, plausible pathophysiological mechanisms are required. Evidence is accumulating in support of two mechanistic hypotheses: inhalation of pollutants might provoke a local inflammatory response with the consequent release into the circulation of pro-thrombotic and inflammatory cytokines. A systemic response of this nature would put individuals with coronary atheroma at increased risk of cardiac events; exposure to pollutants may have an adverse effect on cardiac autonomic control, leading to an increased risk of arrhythmia in susceptible patients. Clarification of the pollutants involved and the precise mechanisms of action is essential in designing measures by which susceptible individuals might be protected from the adverse cardiovascular effects of air pollution.

Cardiovascular implications of exposure to traffic air pollution during exercise.

Regular aerobic exercise is recommended by physicians to improve health and longevity. However, individuals exercising in urban regions are often in contact with air pollution, which includes particles and gases associated with respiratory disease and cancer. We describe the recent evidence on the cardiovascular effects of air pollution, and the implications of exercising in polluted environments, with a view to informing clinicians and other health professionals. There is now strong evidence that fine and ultra fine particulate matter present in air pollution increases cardiovascular morbidity and mortality. The main mechanisms of disease appear to be related to an increase in the pathogenic processes associated with atherosclerosis. People exercising in environments pervaded by air contaminants are probably at increased risk, due to an exercise-induced amplification in respiratory uptake, lung deposition and toxicity of inhaled pollutants. We make evidence-based recommendations for minimizing exposure to air-borne toxins while exercising, and suggest that this advice be passed on to patients where appropriate.

CARDIOVASCULAR EFFECTS ASSOCIATED WITH AIR POLLUTION: POTENTIAL MECHANISMS AND METHODS OF TESTING

A recent series of epidemiologic reports have shown associations between fine particulate matter (PM) levels and increased cardiovascular morbidity and mortality. Elevated PM levels have been linked with cardiac events, including serious ventricular arrhythmias and myocardial infarction. A workshop brought together epidemiologists, cardiologists, and toxicologists from academia, government, and industry to examine plausible mechanisms that could be responsible for such effects, and to consider the armamentarium of noninvasive tests available to examine these relationships. Possible mechanisms considered by the participants include: (a) effects on the autonomic nervous system; (b) alterations on ion channel function in myocardial cells; (c) ischemic responses in the myocardium; and (d) inflammatory responses triggering endothelial dysfunction, atherosclerosis, and thrombosis. A large number of tests were identified to assess specific mechanistic pathways underlying the cardiovascular effects of air pollution and include: (a) autonomic control of the cardiovascular system assessed primarily by heart-rate variability; (b) myocardial substrate and vulnerability assessed by the electrocardiogram and estimations of ejection fraction and wall motion abnormalities in imaging studies; and (c) endothelial function, atherosclerosis, and thrombosis assessed by clotting parameters, cytokines, lipid profiles, and forearm blood flow. A variety of approaches ranging from molecular and genetic investigations to human clinical studies were recommended to further investigate the important epidemiologic associations.