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Published on: October 22, 2020
Inflammatory markers and secondhand tobacco smoke exposure among U.S. workers
John D Clark1, James D Wilkinson, William G LeBlanc
1Department of Epidemiology and Public Health, University of Miami Miller School of Medicine, Miami, Florida 33101, USA.
Background:
Self-reported exposure to secondhand smoke (SHS) has been associated with elevated inflammatory markers in adults. The association between SHS indicated by serum cotinine and markers of inflammation has not been investigated in adult workers.
Methods:
Using the subpopulation of employed participants (20 years and older) who were non-smokers and denied home SHS exposure from the National Health and Nutrition Examination Survey (NHANES) 1999-2002, the association between serum cotinine and inflammatory markers (C-reactive protein, fibrinogen, homocysteine, and white blood cells) was analyzed. Inflammatory marker values were log-transformed and expressed as geometric means with 95% confidence intervals (CI). Serum cotinine was categorized as either no cotinine (below the detection limit), low cotinine (above the detection limit and <0.2 ng/ml), or high cotinine (>or=0.2 and <15.0 ng/ml). The association between serum cotinine and inflammatory markers was analyzed using univariate and multivariate-adjusted linear regression.
Results:
Geometric mean serum cotinine was significantly higher among non-smokers reporting SHS exposure in the workplace (0.17 vs. 0.10 ng/ml, P < 0.01). Workers exposed to low and high levels of cotinine had significantly higher homocysteine levels relative to non-exposed workers; mean homocysteine differences remained significant in the multivariable model (i.e., 0.363 and 0.491 mg/dl increase, respectively).
Conclusion:
Exposure to SHS as measured by serum cotinine may result in increased homocysteine levels among adult workers. These results provide further evidence in support of universal workplace smoking restrictions in order to protect worker health. Further research is required to determine the adverse effects of workplace SHS exposure on cardiovascular risk.
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