Tobacco Smoke Is a Major Source of Aromatic Amine Exposure in U.S. Adults: 2013–2014 National Health and Nutrition Examination Survey (NHANES)

Author:

Seyler Tiffany1ORCID,Mazumder Shrila1ORCID,Ahamed Rayaj1ORCID,Zhu Wanzhe1ORCID,Blount Benjamin C.1ORCID,Apelberg Benjamin J.2ORCID,Wang Lanqing1ORCID

Affiliation:

1. 1Tobacco and Volatiles Branch, Division of Laboratory Sciences, National Center for Environmental Health, U.S. Centers for Disease Control and Prevention, Atlanta, Georgia.

2. 2Center of Tobacco Products, U.S. Food and Drug Administration, Silver Spring, Maryland.

Abstract

Abstract Background: Cigarette smoking increases the risk of cancer, cardiovascular diseases, and premature death. Aromatic amines (AA) are found in cigarette smoke and are well-established human bladder carcinogens. Methods: We measured and compared total urinary levels of 1-aminonaphthalene (1AMN), 2-aminonaphthalene (2AMN), and 4-aminobiphenyl (4ABP) in adults who smoked cigarettes exclusively and in adult nonusers of tobacco products from a nationally representative sample of non-institutionalized U.S. population in the 2013–2014 National Health and Nutrition Examination Survey. Results: Sample-weighted geometric mean concentrations of AAs in adults who smoked cigarettes exclusively compared with adult nonusers were 30 times higher for 1AMN and 4 to 6 times higher for 2AMN and 4ABP. We evaluated the association of tobacco-smoke exposure with urinary AAs using sample-weighted multiple linear regression models to control for age, sex, race/ethnicity, diet, and urinary creatinine. Secondhand smoke exposure status was categorized using serum cotinine (SCOT) among adult nonusers (SCOT ≤ 10 ng/mL). The exposure for adults who smoked cigarettes exclusively (SCOT > 10 ng/mL) was categorized on the basis of the average number of self-reported cigarettes smoked per day (CPD) in the five days prior to urine collection. The regression models show AAs concentration increased with increasing CPD (P < 0.001). Dietary-intake variables derived from the 24-hours recall questionnaire were not consistently significant predictors of urinary AAs. Conclusions: This is the first characterized total urinary AA concentrations of the U.S. adult non-institutionalized population. Our analyses show that smoking status is a major contributor to AA exposures. Impact: These data provide a crucial baseline for exposure to three AAs in U.S. non-institutionalized adults.

Funder

Centers for Disease Control and Prevention

U.S. Food and Drug Administration

Publisher

American Association for Cancer Research (AACR)

Subject

Oncology,Epidemiology

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