Characterization of acrylonitrile exposure in the United States based on urinary n-acetyl-S-(2-cyanoethyl)-l-cysteine (2CYEMA): NHANES 2011–2016

Abstract

Background: Acrylonitrile is a possible human carcinogen that is used in polymers and formed in tobacco smoke. We assessed acrylonitrile exposure in the US population by measuring its urinary metabolites N-acetyl-S-(4-hydroxy-2-methyl-2-buten-1-yl)-L-cysteine (2CYEMA) and N-acetyl-S-(1-cyano-2-hydroxyethyl)-L-cysteine (1CYHEMA) in participants from the 2011–2016 National Health and Nutrition Examination Survey. Objective: To assessed acrylonitrile exposure using population-based biomonitoring data of the US civilian, non-institutionalized population. Methods: Laboratory data for 8,057 participants were reported for 2CYEMA and 1CYHEMA using ultrahigh-performance liquid chromatography / tandem mass spectrometry. Exclusive tobacco smokers were distinguished from non-users using a combination of self-reporting and serum cotinine data. We used multiple linear regression models to fit 2CYEMA concentrations with sex, age, race/Hispanic origin, and tobacco user group as predictor variables. Results: The median 2CYEMA level was higher for exclusive cigarette smokers (145 μg/g creatinine) than for non-users (1.38 μg/g creatinine). Compared to unexposed individuals (serum cotinine ≤ 0.015 ng/ml) and controlling for confounders, presumptive second-hand tobacco smoke exposure (serum cotinine > 0.015 – ≤ 10 ng/ml and 0 cigarettes per day, CPD) was significantly associated with 36% higher 2CYEMA levels ( p <0.0001). Smoking 1–10 CPD was significantly associated with 6,720% higher 2CYEMA levels ( p <0.0001). Significance: We show that tobacco smoke is an important source of acrylonitrile exposure in the US population and provide important biomonitoring data on acrylonitrile exposure.

Comparison of urinary mercapturic acid excretions in users of various tobacco/nicotine products

“…Possible reasons for falsely elevated levels in these groups were discussed in the review 26 . Recently published CEMA results from the NHANES study 68 confirm the significantly higher levels in smokers (median: 145 μg/g crea) compared with nonsmokers (1.38 μg/g crea) and a clear, consumption (CPD)‐based dose–response relationship. The latter finding is also in agreement with results from our study (Table S4) and reports from the literature 23,31,46 For HTP users, a significant dose–response relationship for two dose markers was found (Table S4).…”

“…Possible reasons for falsely elevated levels in these groups were discussed in the review. 26 Recently published CEMA results from the NHANES study 68 confirm the significantly higher levels in smokers (median: 145 μg/g crea) compared with nonsmokers (1.38 μg/g crea) and a clear, consumption (CPD)-based dose-response relationship.…”

“…Urinary CEMA is a well‐established biomarker of exposure to acrylonitrile, a possible human carcinogen (IARC Group 2B). Apart from occupational exposure, tobacco smoke is the main source for exposure to acrylonitrile for non‐occupationally exposed indviduals 67,68 . Product‐related average releases of acrylonitrile from a literature evaluation amounted to 15.8–24.5 μg/cig (CC), 0.13–0.38 μg/10 puffs (EC), and 0.16–0.26 μg/stick (HTP), resulting in median daily intakes of 208.5 (CC), 2.2 (EC), and 2.4 (HTP) μg/day for common users of these products 26 .…”

The exposure to volatile organic chemicals associates positively with rheumatoid arthritis: a cross-sectional study from the NHANES program

“…Acrylonitrile has been extensively applied as raw materials to manufacture acrylic fibers, plastics, synthetic rubbers, and acrylamide ( 41 ). It was pointed out that smoking were important sources of acrylonitrile exposure in the US population ( 42 ). The exposure to acrylonitrile at concentrations 20 ppm would result in headaches, nausea and dizziness ( 43 ), and acrylonitrile was identified as possibly carcinogenic to humans (Group 2B) ( 44 ).…”

Biomarkers of Electronic Nicotine Delivery Systems (ENDS) use

“…ENDS users) [ 65 , 66 ]. A potential limitation of using VOC metabolites as indicators of smoking reduction in dual users is their relatively short physiological half-time (few hours) [ 67 ]. VOCs may not be sensitive enough to detect the non-daily use of combustible products in clinical trials with ENDS products.…”