Abstract-In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM Ͻ2.5 m in diameter (PM 2.5 ) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM 2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM 2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality. (Circulation. 2010;121:2331-2378.)

Background-Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown. Methods and Results-We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass Ͻ2.5 m (PM 2.5 ), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 g/m 3 PM 2.5 during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 g/m 3 PM 2.5 in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively). Conclusions-The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.

Abstract-Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short-and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions. Key Words: AHA Scientific Statements Ⅲ air pollution Ⅲ cardiovascular diseases Ⅲ respiration R ecently, the American Heart Association (AHA) published "Guidelines for Primary Prevention of Cardiovascular Disease and Stroke" as an aid to healthcare professionals and their patients without established coronary artery disease or other atherosclerotic diseases. 1 The statement was intended to complement the AHA/American College of Cardiology (ACC) "Guidelines for Preventing Heart Attack and Death in Patients with Atherosclerotic Cardiovascular Disease." 2 Both sets of recommendations emphasized multifactorial interventions, especially more intensive measures/ goals to modify individual cardiovascular risk factors with diet, drugs, exercise, weight management, complete smoking cessation, and avoidance of secondhand smoke (SHS), or combinations thereof.Over the last decade, however, a growing body of epidemiological and clinical evidence has led to a heightened concern about the potential deleterious effects of ambient air pollution on health and its relation to heart disease and stroke. Of special interest are several environmental air pollutants that include carbon monoxide, oxides of nitrogen, sulfur dioxide, ozone, lead, and particulate matter ("thoracic particles" [PM 10 ] Ͻ10 m in aerodynamic diameter, "fine particles" [PM 2.5 ] Ͻ2.5 m, and "coarse particles" [PM 10 to 2.5 ]). These pollutants are associated with increased hospitalization 3 and mortality due to cardiovascular disease, 4 -6 especially in persons with congestive heart failure, frequent arrhythmias, or both. 7 The well-established causal associations between active and passive smoking with heart disease and stroke support the plausibility of an adverse effect of PM on the cardiovascular system.The most recent analysis of the National Mortality and Morbidity Air Pollution Study (NMMAPS), based on data from 90 of the largest cities in the United States, estimated that daily total and cardiopulmonary mortality incr...

Heavy physical exertion can trigger the onset of acute myocardial infarction, particularly in people who are habitually sedentary. Improved understanding of the mechanisms by which heavy physical exertion triggers the onset of myocardial infarction and the manner in which regular exertion protects against it would facilitate the design of new preventive approaches.

The first decade of experience with case-crossover studies has shown that the design applies best if the exposure is intermittent, the effect on risk is immediate and transient, and the outcome is abrupt. However, this design has been used to study single changes in exposure level, gradual effects on risk, and outcomes with insidious onsets. To estimate relative risk, the exposure frequency during a window just before outcome onset is compared with exposure frequencies during control times rather than in control persons. One or more control times are supplied by each of the cases themselves, to control for confounding by constant characteristics and self-confounding between the trigger's acute and chronic effects. This review of published case-crossover studies is designed to help the reader prepare a better research proposal by understanding triggers and deterrents, target person times, alternative study bases, crossover cohorts, induction times, effect and hazard periods, exposure windows, the exposure opportunity fallacy, a general likelihood formula, and control crossover analysis. INTRODUCTIONA case-crossover study (18, 26) is a scientific method to answer the question, "Was this event triggered by something unusual that happened just before?" The simple part of the question is "What happened just before?" The challenging part is to quantify "How unusual was that?" The latter question must be answered for all people in the study who experience the outcome event (disease onset, injury, or behavioral change), not just the people who had the hypothesized triggers just before.We started developing the design in 1988 to avoid control selection bias in the Myocardial Infarction (MI) Onset Study (29). The original study aim was to use a case-control approach to investigate why the incidence of MI peaks in the morning. Who should be the controls? We were concerned that noncases drawn from the general population would be a biased sample not only because of healthyvolunteer bias, but also healthy-day bias. These subjects would be more likely to decline to be interviewed on stressful days. We also ruled out patients hospitalized for other emergencies, because they would be biased by whatever triggered their Next we realized that we could make the opposite comparison by also asking morning cases about their afternoon exposures on the previous day. Finally, it dawned on us that we could compare each patient's experience on their MI day with their experience on the day before. This would give us a perfectly matching control for each patient-the same patient at the same time on the day before.Eventually we saw how we could have multiple control days for each patient by asking about exposure frequency during the entire week, month, or year before. When we applied epidemiologic theory to this approach, we realized it was like a nonexperimental crossover experiment observed retrospectively. We are often asked whether a case-crossover design would be appropriate to study a given hypothesis. This review is intended to...

Several modifiable health behaviors were associated with maintenance of good erectile function, even after comorbid conditions were considered. Lifestyle factors most strongly associated with erectile dysfunction were physical activity and leanness.

Background-Marijuana use in the age group prone to coronary artery disease is higher than it was in the past. Smoking marijuana is known to have hemodynamic consequences, including a dose-dependent increase in heart rate, supine hypertension, and postural hypotension; however, whether it can trigger the onset of myocardial infarction is unknown. Methods and Results-In the Determinants of Myocardial Infarction Onset Study, we interviewed 3882 patients (1258 women) with acute myocardial infarction an average of 4 days after infarction onset. We used the case-crossover study design to compare the reported use of marijuana in the hour preceding symptoms of myocardial infarction onset to its expected frequency using self-matched control data. Of the 3882 patients, 124 (3.2%) reported smoking marijuana in the prior year, 37 within 24 hours and 9 within 1 hour of myocardial infarction symptoms. Compared with nonusers, marijuana users were more likely to be men (94% versus 67%, PϽ0.001), current cigarette smokers (68% versus 32%, PϽ0.001), and obese (43% versus 32%, Pϭ0.008). They were less likely to have a history of angina (12% versus 25%, PϽ0.001) or hypertension (30% versus 44%, Pϭ0.002). The risk of myocardial infarction onset was elevated 4.8 times over baseline (95% confidence interval, 2.4 to 9.5) in the 60 minutes after marijuana use. The elevated risk rapidly decreased thereafter. Conclusions-Smoking marijuana is a rare trigger of acute myocardial infarction. Understanding the mechanism through which marijuana causes infarction may provide insight into the triggering of myocardial infarction by this and other, more common stressors.

These prospective data from a study of U.S. male physicians suggest that habitual vigorous exercise diminishes the risk of sudden death during vigorous exertion.