Article Text
Abstract
Background Waterpipe tobacco (WPT) smoking is associated with deleterious effects on cardio-pulmonary systems which may have adverse repercussions in pathophysiology and progression of chronic lung and cardiovascular diseases. We compared the biomarkers of systemic inflammation, lipid mediators, injury/repair and oxidative stress between groups of non-smokers (NS), exclusive WPT smokers (WPS), exclusive cigarette smokers (CS) and dual WPS and CS (DS).
Methods Two cohorts were recruited. Cohort I consisted of WPS (n=12), CS (n=26), DS (n=10) and NS (n=25). Cohort II consisted of WPS (n=33) and NS (n=24). Plasma and urine samples were collected and analysed for various systemic biomarkers.
Results Compared with NS, plasma levels of inflammatory mediators (interleukin (IL)-6, IL-8, IL1β and tumor necrosis factor-α) were significantly higher in WPS and CS, and were further augmented in DS. Endothelial biomarkers (intracellular adhesion molecule-1, prostaglandin E-2 and metalloproteinase-9) were significantly higher in CS. Most notably, pro-resolving lipid mediator (resolvin E1) and biomarkers of immunity, tissue injury, and repair were significantly lower in WPS and CS. Urinary levels of 8-isoprostane were significantly higher in all smoking groups in cohort I, while 8-isoprostane, myeloperoxidase, receptor for advanced glycation end products (RAGE), En-RAGE and matrix metalloproteinase-9 were significantly higher in all smoking groups in cohort II.
Conclusions Biomarkers of inflammation, oxidative stress, immunity, tissue injury and repair were elevated in WPS and CS groups. Furthermore, concurrent use of WPT and cigarettes is more harmful than cigarette or WPT smoking alone. These data may help inform the public and policy-makers about the dangers of WPT smoking and dual use of tobacco products.
- biomarkers
- waterpipe
- hookah
- cigarette smokers
- inflammation
- oxidative stress
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Footnotes
NAK and GL contributed equally.
Contributors NAK, NOFK, IR conceived and designed the experiments, wrote and edited the manuscript. KPS did data analysis, wrote and edited the manuscript. IR and NOFK obtained research funding and study design and experimental plans/assays. NAK, GL, NOK, FKP recruited the volunteers. NAK, GL, QW, DY, SRM, NOK, FKP performed the experiments. All authors contributed to manuscript preparation and approved the final version prior to submission.
Funding This work was supported in part by a National Institutes of Health (NIH) Grants, NIH 1R01HL135613, NIH 1R01HL085613 and the Food and Drug Administration (FDA) Center for Tobacco Products (CTP) via the National Institute on Drug Abuse (NIDA) of the NIH, NIHFDACTP grant# 1R01DA042470 (to Irfan Rahman) and R01DA042471 (to Nada O.F. Kassem). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the FDA.
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval Cohort I: approved by the General Clinical Research Center of the University of Rochester Research Subjects Review Board (IRB#RSRB00063526). Cohort II: Study procedures were approved by the San Diego State University Institutional Review Board (IRB# 2445100).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement All data relevant to the study are included in the article or uploaded as supplementary information.