Arterial Disease

Some Topics

  • Air Pollution

    Exhaust from all combustion engines combine to produce local adverse effects on the health of car users and all innocent bystanders. Cities have become islands of toxic chemicals from the unrestrained use of vehicles burning fossil fuels.

    Driving a car is the most polluting act an average citizen commits. Cars have two opposite personalities. One is friendly and attractive the other is destructive and can be lethal. Emissions from passenger vehicles are going up in Canada and the US despite attempts to make engines more fuel efficient and despite the addition of antipollution devices. The main reason is that cars are getting bigger and pick-up trucks and sports vehicles are often replacing smaller, lighter passenger cars. The average new vehicle in 2001 consumed more fuel that its counterpart in 1988. In the USA in 1987 cars averaged 25.9 miles to the gallon. Fuel efficiency dropped to 24.6 miles/gallon by 1998 and is dropping further as larger vehicles replace smaller ones.

    Air pollution is associated with increased hospital admissions for cardiovascular diseases with increases in acute morbidity and mortality. D'Ippoliti et al studied 6531 patients in Rome who were hospitalized for acute myocardial infarction from January 1995 to June 1997. Air pollution data were taken from 5 city monitors. Positive associations were found for total suspended particulates, NO2 and CO. The strongest and most consistent effect was found for total suspended particulates.

    Increases in fine particulate matter air pollution increase the risk for myocardial infarctions, strokes, and heart failure. For example, particle deposition in the lungs activates the sympathetic nervous system and triggers the release of systemic pro-inflammatory responses. Brook and Rajagopalanb stated: "Higher circulating levels of inflammatory cytokines cause vascular endothelial dysfunction and activation of vasoconstrictive pathways while blunting vasodilator capacity. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common mechanism of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, airborne fine particles may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.

    vovKlot et al conducted a multicenter study involving 22,006 survivors of a first myocardial infarction in European cities. Air concentrations of nitrogen dioxide, carbon monoxide, ozone, and particles (PM10) were measured: 6655 cardiac readmissions were observed. Cardiac readmissions increased in association with same-day concentrations of PM10. Effects of similar strength were observed for carbon monoxide, nitrogen dioxide and ozone, They concluded that air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infarction survivors in 5 European cities.

    Simkhovich et et al confirmed that epidemiologic studies show that increased levels of air pollutants are positively associated with cardiovascular morbidity and mortality. They stated:`Inhalation of air pollutants affects heart rate, heart rate variability, blood pressure, vascular tone, blood coagulability, and the progression of atherosclerosis. Major mechanisms of inhalation-mediated cardiovascular toxicity include activation of pro-inflammatory pathways and generation of reactive oxygen species. Although most studies focus on the influence of systemic effects, recent studies indicate that ultrafine particles may be translocated into the circulation and directly transported to the vasculature and heart where they can induce cardiac arrhythmias and decrease cardiac contractility and coronary flow.`

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