Cap junction intercellular communication and cytotoxicity in normal human cells after exposure to smoke condensates from cigarettes that burn or primarily heat tobacco

Heating tobacco, rather than burning it, reduces tobacco combustion and pyr olysis products. This study tested the hypothesis that the simplified smoke chemistry of a cigarette which primarily heats tobacco (TOB-HT) significan tly reduces the potential to alter the structure or function of cellular pl asma membranes relative to low "tar" 1R4F and ultra low "tar" IR5F Kentucky reference cigarettes which burn tobacco, Gap junction intercellular commun ication (GJIC) and lactate dehydrogenase release (LDH) were used to quantif y functional and structural changes to the plasma membrane, respectively. C igarette smoke condensate (CSC) from the mainstream smoke of TOB-HT, IR4F a nd IR5F cigarettes ir ere compared in the GJIC and LDH release assays follo wing a l-hr exposure in vitro. Human bronchial/tracheal epithelial cells, c oronary artery endothelial cells, coronary artery smooth muscle cells, fore skin keratinocytes and the WB-344 rat liver epithelial cell line were studi ed. TOB-HT did not inhibit GJIC in any of the human cell types tested (P > 0.05) at concentrations where 1R4F and IR5F did inhibit GJIC (P < 0.05), TO B-HT did not elevate LDH release (P > 0.05) when tested at concentrations w here 1R4F and IR5F did elevate LDH release (P < 0.05), Our results suggest that CSC from TOB-HT cigarettes is less damaging to the structure or functi on of the cellular plasma membranes of a variety of human cell lines than C SC from 1R4F and 1R5F tobacco burning reference cigarettes. (C) 2000 Elsevi er Science Ltd. All rights reserved.