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Andreoli C.,British American Tobacco Italia SpA | Gregg E.O.,ENI S.p.A | Puntoni R.,British American Tobacco GRandD | Gobbi V.,British American Tobacco Italia SpA | And 2 more authors.
Clinical Chemistry and Laboratory Medicine | Year: 2011

Background: The aim of this study was to investigate the possible correlation between smoking status and biomarkers of exposure (BoE) and biological effect (BoBE) in monozygotic twins discordant for smoking status (smoker and non-smoker pairs). By eliminating potential genetic variability in this manner, a clearer pattern of the effects of lifestyle and environmental exposures should become apparent. Methods: This was a cross-sectional study on monozygotic healthy twins (44 subjects, 26 males and 18 females) with a mean age 31.5 years. BoE to cigarette smoke and BoBE were measured in body fluids (24 h urine and blood) after medical pre-screening. Results: All BoE were significantly higher in the smoker twins. Among BoBE, 11-dehydrothromboxane B2 (11-dehydro TBX), 2,3-dinorthromboxane B2 (2,3-dinor TBX), 8-epi-prostaglandin F2α (8-epiPGF), hydroxyproline (OHP), fibrinogen, white blood cell (WBC), neutrophil and lymphocyte counts and heart rate were statistically significantly increased in the smoker compared to the non-smoker twins. Moreover, statistically significant correlations between neutrophil count and 11-dehydro TBX (r=0.32), WBC and 8- epiPGF (r=0.33), OH-P and 8-epiPGF (r=0.49) and heart rate and fibrinogen (r=0.46) were observed. Conclusions: The study results confirmed the reliability of the BoE for the evaluation of smoking status. Moreover, a subset of the BoBE, reported as being associated with inflammatory conditions and early stages of vascular disorders, has emerged as showing a consistent relationship with smoking status from the present and the previous studies. By using monozygotic twin pairs, genetic variability has been excluded as a possible source of variability in this study. These results should assist in the interpretation of other population studies using these biomarkers. © 2011 by Walter de Gruyter.

Andreoli C.,British American Tobacco Italia SpA | Bassi A.,British American Tobacco Italia SpA | Gregg E.O.,ENI S.p.A | Nunziata A.,British American Tobacco Italia SpA | And 2 more authors.
Clinical Chemistry and Laboratory Medicine | Year: 2015

Background: Despite the well-documented role of cigarette smoke in the development of chronic obstructive pulmonary disease (COPD), lung cancer and cardiovascular disease, biomarkers for screening or monitoring disease progression and outcome remain elusive, particularly for COPD and lung cancer. Inflammatory cells and mediators are likely to be involved in the disease processes, but their importance is still poorly understood. The purpose of this study was to investigate early changes in immunological markers associated with smoking in healthy monozygotic twins without a detectable disease discordant for smoking, thereby minimising data variability due to genetic background. Methods: Twenty-two monozygotic twin pairs, aged 31.5±6.3 years, entered the study. One of each twin pair was a smoker and the other a non-smoker. None of the subjects reported any diseases or clinically defined respiratory symptoms or airflow limitation. Each subject donated blood samples for determination of total leukocytes and subpopulations, lymphocyte subpopulation plus pro-inflammatory mediators (interleukin-8, tumour necrosis factor-α, soluble tumour necrosis factor-α receptors and C-reactive protein). Results: We observed a significant increase in the number of circulating leukocytes and neutrophils in smokers compared to non-smokers. Smokers also had significantly higher numbers of B cells and CD4+ T cells, plus an increased CD4/CD8 ratio. The numbers of NK cells were statistically significant lower in smokers compared to non-smokers. Conclusions: While the prognostic significance of these changes is uncertain, results suggest that smoking is associated with immune changes, independent of genetic background and environmental conditions. © 2015, British American Tobacco, published by De Gruyter 2015.

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