Acrolein Exposure in U.S. Tobacco Smokers and Non-Tobacco Users: NHANES 2005-2006.
Acrolein Exposure in U.S. Tobacco Smokers and Non-Tobacco Users: NHANES 2005-2006.
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DOI：
10.1289/ehp.1409251
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发表时间：
2015-12
影响因子：
10.4
通讯作者：
Blount BC
中科院分区：
文献类型：
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作者：
Alwis KU;deCastro BR;Morrow JC;Blount BC
丙烯醛是一种高度反应性的α，β不饱和醛和呼吸道刺激物。丙烯醛在燃烧过程中形成（例如，燃烧烟草或生物质），在食物的高温烹饪过程中，以及在体内作为氧化应激和多胺代谢的产物。没有报告生物监测参考数据来描述美国人群的丙烯醛暴露。我们的目标是a）评估尿中的两种丙烯醛代谢物-N-乙酰基-S-（3-羟丙基）-l-半胱氨酸（3 HPMA）和N-乙酰基-S-（2-羧乙基）-l-半胱氨酸（CEMA）-作为美国人群按年龄、性别、种族和吸烟状况暴露于丙烯醛的生物标志物;和B）评估烟草烟雾作为丙烯醛暴露的预测因子。我们使用超高效液相色谱-电喷雾串联质谱法（UPLC/ESI-MSMS）分析了国家健康与营养调查（NHANES 2005-2006）≥ 12岁参与者（n = 2，866）尿液中的3 HPMA和CEMA。非烟草使用者与烟草吸烟者（根据血清可替宁和自我报告定义）分层的样本加权线性回归模型表征了尿3 HPMA和CEMA与烟草烟雾暴露的相关性，调整了尿肌酐、性别、年龄和种族/民族。吸烟者（香烟、雪茄和烟斗使用者）的HPMA和CEMA水平高于非吸烟者。吸烟者和非吸烟者的中位3 HPMA水平分别为1，089和219 μg/g肌酐。同样，吸烟者的CEMA水平中位数为203 μg/g肌酐，非吸烟者为78.8 μg/g肌酐。回归分析表明，血清可替宁是吸烟者中3 HPMA和CEMA的显著正预测因子（p < 0.0001）。吸烟是美国人群丙烯醛暴露的重要预测因素。Alwis KU，deCastro BR，Morrow JC，Blount BC. 2015.美国吸烟者和非吸烟者的丙烯醛暴露：NHANES 2005-2006。环境健康展望123：1302-1308; http：dx.doi.org/10.1289/ehp.1409251
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. population. 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. 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. 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. Tobacco smoke was a significant predictor of acrolein exposure in the U.S. population. Alwis KU, deCastro BR, Morrow JC, Blount BC. 2015. Acrolein exposure in U.S. tobacco smokers and non-tobacco users: NHANES 2005–2006. Environ Health Perspect 123:1302–1308; http://dx.doi.org/10.1289/ehp.1409251