The Toxicity of Diesel Exhaust: Implications for Primary Care

Irina N. Krivoshto, BA; John R. Richards, MD; Timothy E. Albertson, MD, MPH, PhD; Robert W. Derlet, MD

Disclosures

J Am Board Fam Med. 2008;21(1):55-62. 

In This Article

Cardiac Effects

Acute coronary syndrome (ACS) and other thrombotic effects have been associated with acute exposure to diesel exhaust.[9,10] A recent study by Mills and associates evaluated men with previous myocardial infarction who were exposed to diesel exhaust during moderate exercise. Significant ST-segment depression was noted, as well as diminished release of endothelial tissue plasminogen activator.[11] Possible mechanisms to explain these results include diesel exhaust-induced coronary vasoconstriction, transient thrombus formation, carbon monoxide exposure, and altered myocardial energetics.[12] Another recent study of 1816 postmenopausal women with long-term exposure to air pollution, of which diesel exhaust represented a significant proportion, concluded there was an increased risk of cardiovascular disease and death proportional to the level of exposure.[13] One European study group examined the association between exposure to diesel exhaust and hospital admission for ischemic heart disease in 8 cities and found that patients 65 years and older had a significantly increased risk of ACS after exposure to diesel pollution.[14] In a study performed in a major European city, Peters et al determined that exposure to traffic, with its high levels of diesel exhaust, was associated with the onset of myocardial infarction within 1 hour. They concluded the time spent in traffic was consistently linked with an increased risk of myocardial infarction.[15]

Diesel exhaust particles (DEPs) have been shown to be cardiotoxic in animal studies. Minami and colleagues demonstrated in a guinea pig model that DEPs had a negative inotropic effect, induced arrhythmias, and caused sudden cardiac death.[16] Another animal study by Sakakibara et al determined that DEP-induced cardiotoxicity could not be prevented with propranolol, atropine, verapamil, diltiazem, diphenhydramine, indomethacin, superoxide dismutase, or catalase.[17] Diesel exhaust induces heart rate variability, ventricular arrhythmia, a significant decrease in left-ventricular systolic pressure, and an increase in left-ventricular end-diastolic pressure in animal models.[18,19] It is postulated that DEP produces superoxide radicals, which cause irreversible myocardial damage leading to cardiac arrest.[20]

DEPs also have been shown to induce immunoglobulin E synthesis and cause histamine release.[21] Histamine is a potent coronary vasoconstrictor and platelet and thrombin activator, and it up-regulates P-selectin on endothelial cell surfaces.[22] A high incidence of serious cardiac arrhythmias was noted in patients with implanted cardioverter defibrillators who had significant exposure to air pollution.[23] Zanobetti and Schwartz reported that diabetics have twice the risk of ACS-related admission because of particulate air pollution exposure.[24] Another study from Finland found that patients undergoing serial cardiac exercise testing had a higher incidence of ST-segment depression during days of high particulate air pollution.[25] Progression of atherosclerosis has also been linked to air pollution exposure.[26]

Occupational hazards may also be a factor in development of coronary artery disease. Finkelstein et al, after controlling for smoking, reported higher incidence of ischemic heart disease in heavy equipment operators chronically exposed to DEPs.[27] It may then be important for primary care physicians to inquire about occupational or environmental exposure to diesel exhaust from patients presenting with chest pain and dyspnea. For patients whose ACS was indeed precipitated by acute exposure to diesel exhaust, it will be important to counsel them about avoiding diesel fumes in the future.

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