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Ambient Air Pollution Is Associated With the Severity of Coronary Atherosclerosis and Incident Myocardial Infarction in Patients Undergoing Elective Cardiac Evaluation

View Article: PubMed Central - PubMed

ABSTRACT

Background: The effect of air pollution exposure on atherosclerosis severity or incident clinical events in patients with coronary artery disease is not known.

Methods and results: We conducted a prospective longitudinal cohort study of 6575 Ohio residents undergoing elective diagnostic coronary angiography. Multinomial regression and Cox proportional hazards models were used to assess the relationship between exposure to fine particulate matter <2.5 μm in diameter (PM2.5) and nitrogen dioxide on coronary artery disease severity at baseline and risk of myocardial infarction, stroke, or all‐cause mortality over 3 years of follow‐up. Among participants with coronary artery disease, exposure to PM2.5 levels was associated with increased likelihood of having coronary atherosclerosis that was mild (odds ratio 1.43, 95% CI 1.11–1.83, P=0.005) and severe (odds ratio 1.63, 95% CI 1.26–2.11, P<0.0001), with the effect on severe coronary artery disease being significantly increased compared with mild disease (Ptrend=0.03). Exposure to higher PM2.5 levels was also significantly associated with increased risk of incident myocardial infarction (hazard ratio 1.33, 95% CI 1.02–1.73, P=0.03) but not stroke or all‐cause mortality. The association of PM2.5 with incident myocardial infarction was not affected after adjustment for Framingham Adult Treatment Panel III (ATP III) risk score or statin therapy. In comparison, there were no significant associations between nitrogen dioxide levels and all‐cause mortality or risk of stroke after adjustment for Framingham ATP III risk score.

Conclusions: Exposure to PM2.5 increased the likelihood of having severe coronary artery disease and the risk of incident myocardial infarction among patients undergoing elective cardiac evaluation. These results suggest that ambient air pollution exposure may be a modifiable risk factor for risk of myocardial infarction in a highly susceptible patient population.

No MeSH data available.


Distribution of residential ZIP codes in the GeneBank cohort. The geographic locations of the residential ZIP codes reported by GeneBank participants residing in Ohio are denoted by red dots. Most participants were clustered in metropolitan regions, particularly the surrounding Cleveland area, although there are also relatively high‐density clusters in the northeast, central, and southwest regions of Ohio.
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jah31671-fig-0001: Distribution of residential ZIP codes in the GeneBank cohort. The geographic locations of the residential ZIP codes reported by GeneBank participants residing in Ohio are denoted by red dots. Most participants were clustered in metropolitan regions, particularly the surrounding Cleveland area, although there are also relatively high‐density clusters in the northeast, central, and southwest regions of Ohio.

Mentions: Air pollution variables included average estimated daily exposure levels of PM2.5 and NO2 during the 36 months prior to enrollment and the 36 months after enrollment for cross‐sectional and prospective analyses, respectively. As shown in Figure 1, GeneBank participants who reported their residential ZIP codes as being located in Ohio were clustered in metropolitan regions, particularly in the area surrounding Cleveland. Estimated exposure levels for PM2.5 in the 36 months before and after enrollment were available for ≈6100 Ohio residents and ranged from 10 to 21 μg/m3, whereas NO2 levels were available for ≈4600 participants and ranged from 5 to 23 parts per billion (Figure 2). Exposure levels of each pollutant during the 36 months before and after enrollment were strongly correlated with each other, with comparable means, whereas PM2.5 and NO2 levels were only weakly correlated with each other regardless of exposure period (Figure S1). Based on data from the EPA, PM2.5 levels in Ohio during the pre‐ and postenrollment periods (1998–2010) were comparable to US national and regional trends, whereas NO2 levels were lower. This may have been caused by the small number of monitoring sites for NO2, which led to fewer participants receiving assignments for this pollutant compared with PM2.5 and limiting exposure contrast.


Ambient Air Pollution Is Associated With the Severity of Coronary Atherosclerosis and Incident Myocardial Infarction in Patients Undergoing Elective Cardiac Evaluation
Distribution of residential ZIP codes in the GeneBank cohort. The geographic locations of the residential ZIP codes reported by GeneBank participants residing in Ohio are denoted by red dots. Most participants were clustered in metropolitan regions, particularly the surrounding Cleveland area, although there are also relatively high‐density clusters in the northeast, central, and southwest regions of Ohio.
© Copyright Policy - creativeCommonsBy-nc
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5015312&req=5

jah31671-fig-0001: Distribution of residential ZIP codes in the GeneBank cohort. The geographic locations of the residential ZIP codes reported by GeneBank participants residing in Ohio are denoted by red dots. Most participants were clustered in metropolitan regions, particularly the surrounding Cleveland area, although there are also relatively high‐density clusters in the northeast, central, and southwest regions of Ohio.
Mentions: Air pollution variables included average estimated daily exposure levels of PM2.5 and NO2 during the 36 months prior to enrollment and the 36 months after enrollment for cross‐sectional and prospective analyses, respectively. As shown in Figure 1, GeneBank participants who reported their residential ZIP codes as being located in Ohio were clustered in metropolitan regions, particularly in the area surrounding Cleveland. Estimated exposure levels for PM2.5 in the 36 months before and after enrollment were available for ≈6100 Ohio residents and ranged from 10 to 21 μg/m3, whereas NO2 levels were available for ≈4600 participants and ranged from 5 to 23 parts per billion (Figure 2). Exposure levels of each pollutant during the 36 months before and after enrollment were strongly correlated with each other, with comparable means, whereas PM2.5 and NO2 levels were only weakly correlated with each other regardless of exposure period (Figure S1). Based on data from the EPA, PM2.5 levels in Ohio during the pre‐ and postenrollment periods (1998–2010) were comparable to US national and regional trends, whereas NO2 levels were lower. This may have been caused by the small number of monitoring sites for NO2, which led to fewer participants receiving assignments for this pollutant compared with PM2.5 and limiting exposure contrast.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The effect of air pollution exposure on atherosclerosis severity or incident clinical events in patients with coronary artery disease is not known.

Methods and results: We conducted a prospective longitudinal cohort study of 6575 Ohio residents undergoing elective diagnostic coronary angiography. Multinomial regression and Cox proportional hazards models were used to assess the relationship between exposure to fine particulate matter <2.5 μm in diameter (PM2.5) and nitrogen dioxide on coronary artery disease severity at baseline and risk of myocardial infarction, stroke, or all‐cause mortality over 3 years of follow‐up. Among participants with coronary artery disease, exposure to PM2.5 levels was associated with increased likelihood of having coronary atherosclerosis that was mild (odds ratio 1.43, 95% CI 1.11–1.83, P=0.005) and severe (odds ratio 1.63, 95% CI 1.26–2.11, P<0.0001), with the effect on severe coronary artery disease being significantly increased compared with mild disease (Ptrend=0.03). Exposure to higher PM2.5 levels was also significantly associated with increased risk of incident myocardial infarction (hazard ratio 1.33, 95% CI 1.02–1.73, P=0.03) but not stroke or all‐cause mortality. The association of PM2.5 with incident myocardial infarction was not affected after adjustment for Framingham Adult Treatment Panel III (ATP III) risk score or statin therapy. In comparison, there were no significant associations between nitrogen dioxide levels and all‐cause mortality or risk of stroke after adjustment for Framingham ATP III risk score.

Conclusions: Exposure to PM2.5 increased the likelihood of having severe coronary artery disease and the risk of incident myocardial infarction among patients undergoing elective cardiac evaluation. These results suggest that ambient air pollution exposure may be a modifiable risk factor for risk of myocardial infarction in a highly susceptible patient population.

No MeSH data available.