HormonesSarah H Chung1, Kepher H Makambi2 and Offie P Soldin3*
3Departments of Oncology, Medicine, Physiology and Biophysics, Obstetrics and Gynecology, Pharmacology and Medicine, Bioanalytical Core Laboratory, Georgetown University Medical Center; Lombardi Comprehensive Cancer Center, Washington, DC, USA
- *Corresponding Author:
- Dr. Offie P. Soldin
Lombardi Comprehensive Cancer Center, NRB E207
Georgetown University Medical Center, 3970 Reservoir Road
N.W., Washington D.C. 20057, USA
E-mail: [email protected]
Received February 05, 2014; Accepted October 31, 2014; Published November 04, 2014
Citation: Chung SH, Makambi KH, Soldin OP (2014) Tobacco Smoke Exposure, C-reactive Protein and Steroid Hormones Measured by Tandem Mass Spectrometry in Healthy Women. J Steroids Horm Sci 5:147. doi:10.4172/2157-7536.1000147
Copyright: © 2014 Chung SH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Introduction: High sensitivity C-reactive protein (hsCRP) is a reliable biomarker of inflammation. Plasma CRP increases dramatically after severe trauma, bacterial infection and inflammation. The hsCRP accurately and sensitively measures basal levels of CRP, including in the areas of increased risk of developing myocardial infarction. Tobacco smoking has also been indicated to influence pregnancy outcomes and infertility. Methods: We examined the associations between smoking, circulating hsCRP, and steroid hormone levels in healthy, non-pregnant women of reproductive age. Serum hsCRP concentrations were analyzed using immunoturbidimetry. Based on cotinine levels and self-questionnairres, the women were divided into three separate groups of smokers, nonsmokers
and passive smokers (secondhand exposure). Steroids and cotinine levels were measured by isotope dilution tandem mass spectrometry. Results: A significant, positive correlation was observed between hsCRP and cotinine levels indicating an association between cigarette smoking and inflammation. However, no association was found between hsCRP and cotinine levels in both the non-smoker and passive smoker group. Also, hsCRP levels were significantly associated with increased BMI scores.
Conclusions: Combined factors of increased smoke exposure and obesity were significantly correlated with increased hsCRP levels, suggesting that multiple conditions confer additive risk to an inflammatory state. To determine the role of inflammation in women’s health, further studies are essential to determine the interacting relationship between hsCRP and sex hormone levels in women with disease.