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Environment

Primary Care Corner with Geoffrey Modest MD: Air Pollution and Heart Disease

6 Jul, 16 | by EBM

By Dr. Geoffrey Modest

Yet another study found an increase in heart disease in people exposed to air pollution/fine-particulate matter exposure (see doi.org/10.1016/ S0140-6736(16)00378-0).

Details:

  • 6795 participants. Aged 45-84, enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) from 6 different US cities (Baltimore, Chicago, LA County, New York City, St Paul, Winston-Salem)
  • Median age 62, 53% women, 39% white, 12% Chinese, 27% black, 22% Hispanic), 50-80% with at least some post-high school education, 15% smokers, BMI 28, 45% with hypertension and SBP 128 mmHg, 12% diabetic, 15% on statins and cholesterol/HDL/LDL=190/50/115
  • Followed 10 years with repeated measurements of coronary artery calcium by CT (CAC score) as well as carotid artery intima-media thickness (CIMT); concentrations of fine particulate matter (PM5, which reflects particulate matter <2.5 mm in diameter) and nitrogen oxides (NOx) were estimated based on residence-specific spatio-temporal pollution concentration models, which include community-specific measurements, monitoring data and geographical predictors.
  • Baseline CAC was 145 Agatston units, which is already pretty elevated, but not so surprising for the demographics of the study (see https://www.mesa-nhlbi.org/Calcium/input.aspxfor the MESA CAC score: input age, sex, race/ethnicity and CAC score to get a sense of the meaning of the score)

Results:

  • Overall, CAC increased on average by 24 Agatston units/yrand CIMT 12mm/yr.
  • Participant-specific air pollutant concentrations averaged over the years 2000-2010 ranged: for PM5from 9.2-22.6 mg PM2.5/m3 and for NOx from 7.2-139.2 parts/billion (ppb) [PM2.5 highest in LA County, NOx highest in New York City]
  • For each 5 mg PM5/m3 increase, CAC progressed by 4.1 Agatston units/yr (CI 1.4-6.8), controlling for the usual suspects (age, sex, ethnicity, BMI, physical activity, smoking/second-hand smoke, employment, total and HDL cholesterol, triglycerides, statin use, neighborhood socioeconomic index, level of education, income)
  • For each 40 ppb increase in NOx, CAC progressed by 4.8 Agatston units/yr (0.9-8.7). This relationship was stronger in hypertensive, non-obese individuals and in those >65 yo.
    • No clear association with CIMT

Commentary:

  • There have been many studies over the past 1-2 decades finding a relationship between particulate exposure or air pollution with atherosclerotic disease (MI, strokes). The current study was a prospective long-term one which looked at the process of atherosclerosis itself. My reading of the literature is that CIMT is a much less accurate predictor of atherosclerotic events than the CAC (CIMT really measures arterial injury more than atherosclerosis itself). And CAC has really good sensitivity and specificity for clinical atherosclerotic events over an array of clinical settings (it’s the best of the nontraditional cardiac risk factors).
  • This study provides strong evidence that the relationship between particulate exposure/air pollution and heart disease is mediated through atherosclerosis (vs simply being from endothelial dysfunction, arrhythmias, ), that the process is dose-related and progressive, and that there would be a reasonable expectation that improving air quality would lead to improvements in atherosclerosis-related outcomes. Though I should add that there are also data from the MESA study that endothelial dysfunction may also play a role: see Krishnam RM. J Am Coll Cardiol 2012; 60:2158; and there was a small study at our health center in Boston finding an association between particulate exposure and cardiac autonomic function within hours of the exposure: see Lee M. Am J Cardiol 2016; 117:151)
  • Though I think this study is quite impressive regarding the relationship between air pollution and atherosclerosis, it would be interesting to see more granular data: was this as true for those with no underlying atherosclerosis by CAC at baseline? Also, was there a difference in actual clinical events (vs just changes in the surrogate marker of CAC; though as a perspective, there are a slew of other studies finding increased strokes/MIs)?
  • So, again, on an individual level, it is useful to incorporate air quality as one of our many risk factors for clinical atherosclerotic disease both in terms of nonpharmacologic therapies (weight, diet, exercise, stress reduction, etc.), perhaps with further education around minimizing exposure to air pollution on particularly bad days, and for use of meds (statins, ). And, on a society level, and especially with increasing pollution in many countries associated with “modernization” and perhaps exacerbated further by climate change, this study reinforces the importance of public health initiatives to decrease air pollution/particulate exposures.

http://blogs.bmj.com/ebm/2015/08/05/primary-care-corner-with-geoffrey-modest-md-comparison-of-the-2013-accaha-lipid-guidelines-to-atpiii/

http://blogs.bmj.com/ebm/2016/04/13/primary-care-corner-with-geoffrey-modest-md-coronary-artery-calcium-scores-from-regular-chest-cts/

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