Acrolein exposure is associated with increased cardiovascular disease risk

Natasha DeJarnett, Daniel J. Conklin, Daniel W. Riggs, John A. Myers, Timothy E. O'Toole, Ihab Hamzeh, Stephen Wagner, Atul Chugh, Kenneth Ramos, Sanjay Srivastava, Deirdre Higdon, David J. Tollerud, Andrew DeFilippis, Carrie Becher, Brad Wyatt, James McCracken, Wes Abplanalp, Shesh N. Rai, Tiffany Ciszewski, Zhengzhi XieRay Yeager, Sumanth D. Prabhu, Aruni Bhatnagar

Research output: Contribution to journalArticle

57 Citations (Scopus)

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<sup>+</sup>) and late (AC133<sup>-</sup>) 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.

Original languageEnglish (US)
Article numbere000934
JournalJournal of the American Heart Association
Volume3
Issue number4
DOIs
StatePublished - 2014
Externally publishedYes

Fingerprint

Acrolein
Cardiovascular Diseases
Cotinine
Coal
Platelet Activation
Aldehydes
Smoke
C-Reactive Protein
Fibrinogen
Lipid Peroxidation
Peroxidase
Tobacco
S-(3-hydroxypropyl)cysteine N-acetate
Linear Models
Atherosclerosis
Healthy Volunteers
Thrombosis
Leukocytes
Stem Cells
Blood Platelets

Keywords

  • Endothelium
  • Epidemiology
  • Inflammation
  • Risk factors
  • Smoking
  • Thrombosis
  • Tobacco

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

DeJarnett, N., Conklin, D. J., Riggs, D. W., Myers, J. A., O'Toole, T. E., Hamzeh, I., ... Bhatnagar, A. (2014). Acrolein exposure is associated with increased cardiovascular disease risk. Journal of the American Heart Association, 3(4), [e000934]. https://doi.org/10.1161/JAHA.114.000934

Acrolein exposure is associated with increased cardiovascular disease risk. / DeJarnett, Natasha; Conklin, Daniel J.; Riggs, Daniel W.; Myers, John A.; O'Toole, Timothy E.; Hamzeh, Ihab; Wagner, Stephen; Chugh, Atul; Ramos, Kenneth; Srivastava, Sanjay; Higdon, Deirdre; Tollerud, David J.; DeFilippis, Andrew; Becher, Carrie; Wyatt, Brad; McCracken, James; Abplanalp, Wes; Rai, Shesh N.; Ciszewski, Tiffany; Xie, Zhengzhi; Yeager, Ray; Prabhu, Sumanth D.; Bhatnagar, Aruni.

In: Journal of the American Heart Association, Vol. 3, No. 4, e000934, 2014.

Research output: Contribution to journalArticle

DeJarnett, N, Conklin, DJ, Riggs, DW, Myers, JA, O'Toole, TE, Hamzeh, I, Wagner, S, Chugh, A, Ramos, K, Srivastava, S, Higdon, D, Tollerud, DJ, DeFilippis, A, Becher, C, Wyatt, B, McCracken, J, Abplanalp, W, Rai, SN, Ciszewski, T, Xie, Z, Yeager, R, Prabhu, SD & Bhatnagar, A 2014, 'Acrolein exposure is associated with increased cardiovascular disease risk', Journal of the American Heart Association, vol. 3, no. 4, e000934. https://doi.org/10.1161/JAHA.114.000934
DeJarnett, Natasha ; Conklin, Daniel J. ; Riggs, Daniel W. ; Myers, John A. ; O'Toole, Timothy E. ; Hamzeh, Ihab ; Wagner, Stephen ; Chugh, Atul ; Ramos, Kenneth ; Srivastava, Sanjay ; Higdon, Deirdre ; Tollerud, David J. ; DeFilippis, Andrew ; Becher, Carrie ; Wyatt, Brad ; McCracken, James ; Abplanalp, Wes ; Rai, Shesh N. ; Ciszewski, Tiffany ; Xie, Zhengzhi ; Yeager, Ray ; Prabhu, Sumanth D. ; Bhatnagar, Aruni. / Acrolein exposure is associated with increased cardiovascular disease risk. In: Journal of the American Heart Association. 2014 ; Vol. 3, No. 4.
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T1 - Acrolein exposure is associated with increased cardiovascular disease risk

AU - DeJarnett, Natasha

AU - Conklin, Daniel J.

AU - Riggs, Daniel W.

AU - Myers, John A.

AU - O'Toole, Timothy E.

AU - Hamzeh, Ihab

AU - Wagner, Stephen

AU - Chugh, Atul

AU - Ramos, Kenneth

AU - Srivastava, Sanjay

AU - Higdon, Deirdre

AU - Tollerud, David J.

AU - DeFilippis, Andrew

AU - Becher, Carrie

AU - Wyatt, Brad

AU - McCracken, James

AU - Abplanalp, Wes

AU - Rai, Shesh N.

AU - Ciszewski, Tiffany

AU - Xie, Zhengzhi

AU - Yeager, Ray

AU - Prabhu, Sumanth D.

AU - Bhatnagar, Aruni

PY - 2014

Y1 - 2014

N2 - 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.

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KW - Endothelium

KW - Epidemiology

KW - Inflammation

KW - Risk factors

KW - Smoking

KW - Thrombosis

KW - Tobacco

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