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Menthol Cigarette Smoking & Neuroinflammation

Institution: Brentwood Biomedical Research Institute
Investigator(s): Arthur Brody, M.D.
Award Cycle: 2014 (Cycle 23) Grant #: 23XT-0002 Award: $100,979
Subject Area: Disparities /Prevention/ Cessation/ Nicotine Dependence
Award Type: Exploratory/Developmental Award

Initial Award Abstract

California has a large population of racial and ethnic groups that have high rates of smoking menthol cigarettes. In Los Angeles, 58.1% of the population classifies themselves as either African-American or Hispanic/Latino compared to 29.8% of the general U.S. population. African-American and Hispanic/Latino smokers are considerably more likely to use menthol cigarettes (70-80% and 32-66%, respectively) than White (non-Hispanic) (23-30%) smokers, and a central issue with these cigarettes is that smokers who use them have lower cessation rates in standardized treatment programs than smokers who use non-menthol cigarettes. Though many factors have been implicated in the initiation and continued usage of menthol cigarettes, studies of smoking-related biological markers demonstrate that menthol itself may increase nicotine blood levels and increase other measures of cigarette smoke exposure. These elevated levels could potentially contribute to the greater severity of Tobacco Dependence found in menthol cigarette smokers.

For this Exploratory/Developmental study, we will examine the effects of menthol (and non-menthol) cigarette smoking on brain inflammation (or neuroinflammation) in humans, based on several lines of research indirectly indicating this effect from smoking. Using positron emission tomography (PET) scanning and a recently developed tracer for examining brain inflammation, we will determine if menthol (and non-menthol) cigarette smoking affects brain inflammation. To do this, menthol and non-menthol cigarette smokers will undergo PET scanning of the brain in the satiated state (smoking per their usual habit on the day of scanning and smoking to satiety immediately prior to scanning). Nonsmoking control participants will undergo the same PET procedure with no smoking, and these scans will be compared between groups.

We hypothesize that, during PET scanning, cigarette smokers as a group will have higher binding of the tracer that is a marker for brain inflammation than non-smokers, indicating that cigarette smoking is associated with brain inflammation. We further hypothesize that menthol cigarette smokers will have higher binding of the tracer on PET scanning than non-menthol cigarette smokers, indicating that menthol cigarette smoking results in greater brain inflammation than non-menthol cigarette smoking. We also anticipate that higher blood nicotine levels will be associated with more binding of the tracer during PET scanning, indicating that higher levels of nicotine exposure will be associated with greater brain inflammation. Study findings may demonstrate a mechanism by which menthol and non-menthol cigarette smoking affect brain function.