Fall 2007by Peri Unligil, M.D. and David Eibling, M.D., GASP Board Members
The connection between air pollution and lung disease has been appreciated by the public for many years, facilitated no doubt by the images of lungs scarred by cigarette smoke and coal dust. However, the public and most physicians have only recently become more aware of the link between fine particulate air pollution and heart disease. This new awareness is undoubtedly due to the publication of an article strongly linking the two in the February 2007 issue of the New England Journal of Medicine, the most widely read and cited American medical journal. Publication of this article, “Long-Term Exposure to Air Pollution and Incidence of Cardiovascular Events in Women,” by Miller et al,1 triggered significant publicity as well as greater reflection on the topic by both the public and the medical profession. The authors examined the relationship between exposures to fine particulate mass in the <2.5 micrometer range, or PM 2.5, with cardiac risk in postmenopausal women without known coronary artery disease. Annual mean PM 2.5 exposures by zip code ranged from 3.4 ug/m3 to 28.3ug/m3, with a mean of 13.5ug/m3. They found that for every 10 ug/m3 rise in PM 2.5 in readings at air quality monitors in their zip code, the risk for suffering any type of cardiovascular event rose by 24%, and risk of death from cardiovascular disease rose by 76%. This increase in risk was present after controlling for other known cardiac risk factors and socioeconomic status. This study raised awareness that our cardiac risk is determined not only by our genes and factors which are under our control, such as cholesterol and smoking, but also by environmental exposures beyond individual control.
Research in the last few years has also given us insight into how this process occurs. A significant number of the particles in PM 2.5 pollution are ultrafine, i.e. between 10 and 100 nanometers (0.01 - 0.1 micrometers), and thus belong to the category of nanoparticles, which are defined as having at least one dimension less than 100 nm. In 2002, Nemmar et al demonstrated that radioactively labeled ultrafine particles easily crossed lung membranes to enter the bloodstream and thereby gain access to the entire vascular system.2 The small size of these nanoparticles also gives them unique properties (in this case, toxicities), due to their large surface area to size ratio.
The mechanism by which these ultrafine particles trigger heart disease once in the bloodstream is also being clarified. Mills et al demonstrated that both vascular dysfunction and impaired clot breakdown activity, i.e. fibrinolysis, could be measured in healthy men exposed to diluted diesel exhaust for one hour.3 A Finnish study by Pekkanen et al, done in adults with stable known coronary artery disease, revealed increased risk for ST segment depression during treadmill testing, (ST depression is a marker for coronary ischemia), when testing was done while ambient levels of ultrafine particulate pollution were increased.4 Most recently, Mills, Tornqvist et al demonstrated that men with stable coronary artery disease had a threefold increase in silent ischemia both at rest and with moderate exercise, measured by degree of ST depression, while breathing air containing dilute diesel exhaust controlled to reproduce typical traffic exposures, compared to filtered air. They also found that the subjects had a decrease in a marker for fibrinolysis six hours following the exposure to dilute exhaust. They thus conclude that increased ischemia and thrombosis are two mechanisms by which fine particulate exposure increases risk of cardiovascular events.5
Other studies before and after the NEJM article have corroborated its findings. A study in Germany, published in July 2007, found that the distance of a person’s home from a major road, ranging from >200 m to within 50 m, was associated with their risk for a high level of coronary artery calcification.6 This relationship was noted only in people who had not been working full time for at least 5 years, so one can assume the subjects spent more time at home, increasing the validity of the investigators’ study. Will a particular home zip code, city of residence, or distance of one’s home from a major street someday influence our recommendations to patients on an individual level, in the same manner as counseling regarding lifestyle changes for lipids and smoking? Probably not in the foreseeable future, since our home or city of residence is not easily changed. Rather, these findings must trigger a call for community-wide public health intervention. If awareness among the public increases to a level where pressure on both polluters and regulators is increased and measures are taken to improve a community’s exposure, this will benefit all who work and reside there. We can draw some local implications from these studies. While Pittsburghers are proud of the improvements they have seen in local air quality over the past few decades, a look at readings at Allegheny County monitors used in the landmark NEJM study gives us an idea of the work ahead. Data obtained in 2000 from 12 monitors in Allegheny County were used in the study. Readings from these same monitors in 2006 still ranged between 11.1 ug/m3 in South Fayette and 19.0 ug/m3 in Liberty.7 While only those monitors in Liberty and North Braddock exceeded the EPA standard of 15 ug/m3, the study shows us that significant cardiac effects from air pollution still exist for residents of Allegheny County. By working together to reduce these readings, we can reduce cardiac risk for all in Allegheny County. The significance of the NEJM article can thus be translated into action on a local level. GASP, through its educational outreach and efforts to monitor air quality regulators and local industry in Pittsburgh, plays a significant role in this endeavor.
1. Miller, K.A., et al., Long-term exposure to air pollution and incidence of cardiovascular events in women. N Engl J Med, 2007. 356(5): p. 447-58.
2. Nemmar, A., et al., Passage of inhaled particles into the blood circulation in humans. Circulation, 2002. 105(4): p. 411-4.
3. Mills, N.L., et al., Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation, 2005. 112(25): p. 3930-6.
4. Pekkanen, J., et al., Particulate air pollution and risk of STsegment depression during repeated su bmaximal exercise tests among subjects with coronary heart disease: the Exposure and Risk Assessment for Fine and Ultrafine Particles in Ambient Air (ULTRA) study. Circulation, 2002. 106(8): p. 933-8.
5. Mills, N.L. et al., Ischemic and Thrombotic Effects of Dilute Diesel-Exhaust Inhalation in Men with Coronary Heart Disease. N Eng J Med, 2007. 357(11): p. 1075-82.
6 .Hoffmann, B., et al., Residential exposure to traffic is associated with coronary atherosclerosis. Circulation, 2007. 116(5): p. 489-96.
7. AirData - Monitor Values Report - Criteria Air Pollutants 2007, US Environmental Protection Agency.
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