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. 2015 Dec;123(12):1302-8.
doi: 10.1289/ehp.1409251. Epub 2015 May 29.

Acrolein Exposure in U.S. Tobacco Smokers and Non-Tobacco Users: NHANES 2005-2006

Affiliations

Acrolein Exposure in U.S. Tobacco Smokers and Non-Tobacco Users: NHANES 2005-2006

K Udeni Alwis et al. Environ Health Perspect. 2015 Dec.

Abstract

Background: Acrolein is a highly reactive α,β unsaturated aldehyde and respiratory irritant. Acrolein is formed during combustion (e.g., burning tobacco or biomass), during high-temperature cooking of foods, and in vivo as a product of oxidative stress and polyamine metabolism. No biomonitoring reference data have been reported to characterize acrolein exposure for the U.S.

Objectives: Our goals were to a) evaluate two acrolein metabolites in urine--N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3HPMA) and N-acetyl-S-(2-carboxyethyl)-L-cysteine (CEMA)--as biomarkers of exposure to acrolein for the U.S. population by age, sex, race, and smoking status; and b) assess tobacco smoke as a predictor of acrolein exposure.

Methods: We analyzed urine from National Health and Nutrition Examination Survey (NHANES 2005-2006) participants ≥ 12 years old (n = 2,866) for 3HPMA and CEMA using ultra-high-performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry (UPLC/ESI-MSMS). Sample-weighted linear regression models stratified for non-tobacco users versus tobacco smokers (as defined by serum cotinine and self-report) characterized the association of urinary 3HPMA and CEMA with tobacco smoke exposure, adjusting for urinary creatinine, sex, age, and race/ethnicity.

Results: 3HPMA and CEMA levels were higher among tobacco smokers (cigarettes, cigars, and pipe users) than among non-tobacco users. The median 3HPMA levels for tobacco smokers and non-tobacco users were 1,089 and 219 μg/g creatinine, respectively. Similarly, median CEMA levels were 203 μg/g creatinine for tobacco smokers and 78.8 μg/g creatinine for non-tobacco users. Regression analysis showed that serum cotinine was a significant positive predictor (p < 0.0001) of both 3HPMA and CEMA among tobacco smokers.

Conclusions: Tobacco smoke was a significant predictor of acrolein exposure in the U.S. population.

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Conflict of interest statement

The authors declare they have no actual or potential competing financial interests.

Figures

Figure 1
Figure 1
N-Acetyl-S-(3-hydroxypropyl)-l-cysteine (3HPMA) and N-acetyl-S-(2-carboxyethyl)-l-cysteine (CEMA) are urinary biomarkers of acrolein exposure.
Figure 2
Figure 2
Least-square mean (95% confidence intervals) for each cigarette smoked per day (CPD) category of urinary 3HPMA (A) and CEMA (B) concentrations among exclusive cigarette smokers with serum cotinine > 10 ng/mL, adjusted for sex, age, race/ethnicity, and urinary creatinine.
Figure 3
Figure 3
Percent distribution of urinary 3HPMA and CEMA (μg/g creatinine) among tobacco smokers and non-tobacco users: NHANES 2005–2006 (percentages not sample weighted).

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