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. 2014 Aug 6;3(4):e000934.
doi: 10.1161/JAHA.114.000934.

Acrolein Exposure Is Associated With Increased Cardiovascular Disease Risk

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Free PMC article

Acrolein Exposure Is Associated With Increased Cardiovascular Disease Risk

Natasha DeJarnett et al. J Am Heart Assoc. .
Free PMC article

Abstract

Background: Acrolein is a reactive aldehyde present in high amounts in coal, wood, paper, and tobacco smoke. It is also generated endogenously by lipid peroxidation and the oxidation of amino acids by myeloperoxidase. In animals, acrolein exposure is associated with the suppression of circulating progenitor cells and increases in thrombosis and atherogenesis. The purpose of this study was to determine whether acrolein exposure in humans is also associated with increased cardiovascular disease (CVD) risk.

Methods and results: Acrolein exposure was assessed in 211 participants of the Louisville Healthy Heart Study with moderate to high (CVD) risk by measuring the urinary levels of the major acrolein metabolite-3-hydroxypropylmercapturic acid (3-HPMA). Generalized linear models were used to assess the association between acrolein exposure and parameters of CVD risk, and adjusted for potential demographic confounders. Urinary 3-HPMA levels were higher in smokers than nonsmokers and were positively correlated with urinary cotinine levels. Urinary 3-HPMA levels were inversely related to levels of both early (AC133(+)) and late (AC133(-)) circulating angiogenic cells. In smokers as well as nonsmokers, 3-HPMA levels were positively associated with both increased levels of platelet-leukocyte aggregates and the Framingham Risk Score. No association was observed between 3-HPMA and plasma fibrinogen. Levels of C-reactive protein were associated with 3-HPMA levels in nonsmokers only.

Conclusions: Regardless of its source, acrolein exposure is associated with platelet activation and suppression of circulating angiogenic cell levels, as well as increased CVD risk.

Keywords: endothelium; epidemiology; inflammation; risk factors; smoking; thrombosis; tobacco.

Figures

Figure 1.
Figure 1.
Association between smoking and 3‐hydroxypropylmercapturic acid (3‐HPMA) levels. A, Mean urine cotinine levels in self‐reported non‐smokers and smokers. B, Mean 3‐HPMA (μg/g creatinine) levels for low (<200 μg/g creatinine) and high (≥200 μg/g creatinine) cotinine strata. C and D, 3‐HPMA and cotinine regression in non‐smokers and smokers.
Figure 2.
Figure 2.
Adjusted association between platelet–leukocyte aggregates and 3‐hydroxypropylmercapturic acid (3‐HPMA) and cotinine. A, Scatterplot of the predicted mean of platelet–leukocyte aggregate levels and mean 3‐HPMA levels (log‐transformed μg/g creatinine). The model was adjusted for ethnicity, BMI, hypertension, diabetes, diuretics, CABG/PCI/stents, angiotensin‐receptor blockers, and smoking status. Non‐smokers (solid black line): β=0.010, R2=0.004, P=0.497. Smokers (solid red line): β=0.035, R2=0.055, P=0.035. B, Scatterplot of the predicted mean of platelet–leukocyte aggregate levels regressed against cotinine (log‐transformed μg/g creatinine) levels. The model was adjusted for ethnicity, BMI, hypertension, diabetes, diuretics, CABG/PCI/stents, and angiotensin‐receptor blockers. Non‐smokers (solid black line): β=0.007, R2=0.011, P=0.244. Smokers (solid red line): β=0.023, R2=0.048, P=0.049. BMI indicates body mass index; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention.
Figure 3.
Figure 3.
Association between CVD risk and 3‐hydroxypropylmercapturic acid (3‐HPMA). A, Mean 3‐HPMA levels for low risk (Framingham Risk Score [FRS]<20) and high risk (FRS≥20 or experienced a cardiovascular event) CVD risk categories. B, Mean 3‐HPMA levels for low and high CVD risk categories in self‐reported non‐smokers. C, Mean 3‐HPMA levels for low (FRS<20) and high (FRS≥20) FRS in patients without clinical manifestation of CVD. CVD indicates cardiovascular disease.

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References

    1. Bhatnagar A. Environmental cardiology: studying mechanistic links between pollution and heart disease. Circ Res. 2006; 99:692-705. - PubMed
    1. Brook RD, Rajagopalan S, Pope CA, III, Brook JR, Bhatnagar A, Diez‐Roux AV, Holguin F, Hong Y, Luepker RV, Mittleman MA, Peters A, Siscovick D, Smith SC, Jr, Whitsel L, Kaufman JD. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation. 2010; 121:2331-2378. - PubMed
    1. Ezzati M, Lopez AD. Estimates of global mortality attributable to smoking in 2000. Lancet. 2003; 362:847-852. - PubMed
    1. Haussmann HJ. Use of hazard indices for a theoretical evaluation of cigarette smoke composition. Chem Res Toxicol. 2012; 25:794-810. - PubMed
    1. Ghilarducci DP, Tjeerdema RS. Fate and effects of acrolein. Rev Environ Contam Toxicol. 1995; 144:95-146. - PubMed

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