Cigarette smoking continues to be the most preventable cause of illness and death and has been linked to the development and prognosis of cancer. Current smokers have higher levels of inflammation than nonsmokers, and inflammation can remain elevated in former smokers even years following cessation. Inflammation can also be enhanced by stress. This study examined cortisol and inflammatory responses to a laboratory stressor in breast cancer survivors who formerly smoked compared to their counterparts who had never smoked. Participants included 89 women (age=51.6±8.9 years) who had completed treatment for stage 0-IIIA breast cancer within the past three years and were at least two months post surgery, radiation or chemotherapy, whichever occurred last. Cortisol and interleukin-6 (IL-6) were evaluated in response to a standardized laboratory speech and mental arithmetic stressor. Former (n=25) and never (n=64) smokers did not differ by cancer stage, cancer treatment, comorbidities, time since cancer treatment, depression, or stress. Despite having similar cortisol responses to the stressor, former smokers had exaggerated IL-6 responses two hours post-stressor compared to never smokers. This effect persisted after controlling for age, BMI, time since treatment, education, and antidepressant use. An exaggerated and prolonged inflammatory response to stress could be one mechanism underlying the persistent inflammation observed in former smokers.
Copyright © 2012 Elsevier Ltd. All rights reserved.