Racial differences in exposure and glucuronidation of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)

✍ Scribed by Joshua E. Muscat; Mirjana V. Djordjevic; Stephen Colosimo; Steven D. Stellman; John P. Richie Jr

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: English
• Weight: 131 KB
• Volume: 103
• Category: Article
• ISSN: 0008-543X
• DOI: 10.1002/cncr.20953

✦ Synopsis

Abstract

BACKGROUND

In the United States, Blacks who smoke cigarettes have a higher mean blood concentration of the nicotine metabolite cotinine than White smokers. It has not been determined whether there are racial differences in the exposure to the cigarette smoke carcinogen 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) and in the detoxification of NNK metabolites.

METHODS

A community‐based cross‐sectional survey of 69 Black and 93 White smokers was conducted in lower Westchester County, New York. Information on smoking and lifestyle habits was collected and urinary concentrations of several tobacco smoke biomarkers were compared, including the NNK metabolite 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanol (NNAL) and its glucuronide (NNAL‐Gluc). A frequency histogram and probit plot of NNAL‐Gluc:NNAL ratios were constructed to determine slow and rapid glucuronidation phenotypes.

RESULTS

The mean concentrations of total NNAL, urinary cotinine, plasma cotinine, and thiocyanate were significantly higher in Black men than in White men for each cigarette smoked. In women, the only biomarker that was significantly elevated in Blacks was plasma cotinine. A higher proportion of White versus Black women was categorized as “rapid” glucuronidators (two‐tailed exact test, P = 0.03). In men, there were no significant differences in NNAL‐Gluc:NNAL phenotypes.

CONCLUSIONS

The higher rates of lung carcinoma in black men may be due in part to a higher level of exposure to tobacco smoke carcinogens. Cancer 2005. © 2005 American Cancer Society.