Over the past three or four decades, there have been important advances in the understanding of the actions, exposure-response characteristics, and mechanisms of action of many common air pollutant

https://www.jstor.org/stable/pdfplus/3431520.pdf

Human Health Effects of Air Pollution

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(13)60898-3.pdf

Global association of air pollution and heart failure: a systematic review and meta-analysis

Cardiovascular Toxicity of Nicotine: Implications for Nicotine Replacement Therapy

Background Transdermal nicotine therapy is widely used to aid smoking cessation, but there is uncertainty about its safety in patients with cardiac disease. Methods In a randomized, double-blind, placebo-controlled trial at 10 Veterans Affairs medical centers, we randomly assigned 584 outpatients (of whom 576 were men) with at least one diagnosis of cardiovascular disease to a 10-week course of transdermal nicotine or placebo as an aid to smoking cessation. The subjects were monitored for a total of 14 weeks for the primary end points of the study (death, myocardial infarction, cardiac arrest, and admission to the hospital due to increased severity of angina, arrhythmia, or congestive heart failure); the secondary end points (admission to the hospital for other reasons and outpatient visits necessitated by increased severity of heart disease); any side effects of therapy; and abstinence from smoking. Results There were 48 primary and 78 secondary end points noted in a total of 95 subjects. At least one of...

https://www.nejm.org/doi/pdf/10.1056/NEJM199612123352402

The Safety of Transdermal Nicotine as an Aid to Smoking Cessation in Patients with Cardiac Disease

In the December 1952 smog disaster in London, a substantial increase in mortality was closely associated with the increase in air pollution. Deaths from cardiovascular causes were elevated as well as respiratory deaths. The increase was greatest in the elderly. Hospital admissions were increased for both respiratory and cardiovascular diseases. Since then, many studies have reported associations between lower concentrations of air pollution and daily mortality. Little attention has been paid to the question of hospital admissions for cardiovascular illness, however. This study examined the association between air pollution and cardiovascular hospital admissions for persons aged 65 years and older in the Detroit, Michigan, metropolitan area during the years 1986-1989. After controlling for seasonal and other long-term temporal trends, temperature, and dew point temperature, the particulate matter with an aerodiameter of < or = 10 microns (PM10) was associated with daily admissions for ischemic heart disease (relative risk (RR) = 1.018, 95% confidence interval (CI) 1.005-1.032 for an interquartile range (32 micrograms/m3) increase in pollution). SO2, CO, and ozone made no independent contribution to ischemic heart disease admissions. Both PM10 (RR = 1.024, 95% CI 1.004-1.044) and CO (RR = 1.022, 95% CI 1.010-1.034 for an interquartile range (1.28 ppm) increase in pollution) showed independent associations with heart failure admissions. These results were robust to alternate methods of estimation and weather control.

Air Pollution and Hospital Admissions for Cardiovascular Disease in Detroit, Michigan

Patients with atherosclerotic cardiovascular disease may be adversely affected by the presence of carboxyhemoglobin, even at low concentrations. We investigated the effects of carbon monoxide exposure on myocardial ischemia during exercise in 63 men with documented coronary artery disease. On each test day, subjects performed two symptom-limited incremental exercise tests on a treadmill; the tests were separated by a recovery period and 50 to 70 minutes of exposure to either room air or air containing one of two concentrations of carbon monoxide (117 +/- 4.4 ppm or 253 +/- 6.1 ppm). The order of exposure was assigned randomly. On each occasion, neither the subjects nor the study personnel knew whether the subjects had been exposed to room air or to one of the concentrations of carbon monoxide. Exposure to room air resulted in a mean carboxyhemoglobin level of 0.6 percent, exposure to the lower level of carbon monoxide resulted in a carboxyhemoglobin level of 2.0 percent, and exposure to the higher level of carbon monoxide resulted in a level of 3.9 percent. An effect of carbon monoxide on myocardial ischemia was demonstrated objectively by electrocardiographic changes during exercise. We observed a decrease of 5.1 percent (90 percent confidence interval, 1.5 to 8.7 percent; P = 0.02) and a decrease of 12.1 percent (90 percent confidence interval, 9.0 to 15.3 percent; P less than or equal to 0.0001) in the length of time to a threshold ischemic ST-segment change (ST end point) after carbon monoxide exposures that produced carboxyhemoglobin levels of 2.0 percent and 3.9 percent, respectively. The length of time to the onset of angina decreased by 4.2 percent (90 percent confidence interval, 0.7 to 7.9 percent; P = 0.054) at the 2.0 percent carboxyhemoglobin level and by 7.1 percent (90 percent confidence interval, 3.1 to 10.9 percent; P = 0.004) at the 3.9 percent carboxyhemoglobin level. Significant dose-response relations were found in both the change in the length of time to the ST end point (P less than or equal to 0.0001) and the change in the length of time to the onset of angina (P = 0.02). We conclude that low levels of carboxyhemoglobin exacerbate myocardial ischemia during graded exercise in subjects with coronary artery disease.

Short-Term Effects of Carbon Monoxide Exposure on the Exercise Performance of Subjects with Coronary Artery Disease

The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with well-documented coronary artery disease, who had exertional angina pectoris and ischemic ST-segment changes in their electrocardiograms, were studied. Results from three randomized, double-blind test visits (room air, low and high CO) were compared. The effect of CO exposure was determined from the percent difference in the end points obtained on exercise tests performed before and after a 1-hr exposure to room air or CO. The exposures resulted in postexercise carboxyhemoglobin (COHb) levels of 0.6% +/- 0.3%, 2.0% +/- 0.1%, and 3.9% +/- 0.1%. The results obtained on the 2%-COHb day and 3.9%-COHb day were compared to those on the room air day. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) decreases in the time to development of ischemic ST-segment changes after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. In addition, there were 4.2% (p = 0.027) and 7.1% (p = 0.002) decreases in time to the onset of angina after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. A significant dose-response relationship was found for the individual differences in the time to ST end point and angina for the pre- versus postexposure exercise tests at the three carboxyhemoglobin levels. These findings demonstrate that low doses of CO produce significant effects on cardiac function during exercise in subjects with coronary artery disease.

Effects of carbon monoxide on myocardial ischemia.

source toxic air pollutants specified in the Clean Air Act [formaldehyde, benzene, butadiene, and polycyclic organic matter (POM)], as well as for methanol, an important alternative fuel. HEI planned the workshop in collaboration with repre? sentatives of the U.S. EPA, California EPA, California Air Resources Board, and the automotive and petroleum industries. Scientists from academia, industry, and government participated in working groups on specific compounds. Although cancer was the primary health effect for most compounds, there was also much dis? cussion of noncancer endpoints. HEI's report focuses on research needs related to understanding the effects of these agents at concentrations in the ambient air. Section 202(1)(2) ofthe 1990 Clean Air Act Amendments deals with regulation of mobile-source air toxics. It specifies that within 54 months after the date of the enactment ofthe amendments of 1990, the EPA

HEI's mobile air toxics project.

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Short-Term Effects of Carbon Monoxide Exposure on the Exercise Performance of Subjects with Coronary Artery Disease

Effects of carbon monoxide on myocardial ischemia.

HEI's mobile air toxics project.