scholarly journals Ten Years and More of ‘Biosciences’ in CORESTA - A Brief Historic Overview

Author(s):  
W Röper

AbstractIn June 2001, the CORESTA2 Board formally decided to broaden the scope of CORESTA by engaging in biosciences (other than tobacco agronomy and phytopathology), starting with in vitro toxicity testing and biomarkers of tobacco (smoke) exposure. Until then, work addressing biological aspects of smoking had only been done since 1996 by a special committee within CORESTA, reporting directly to the Scientific Commission, the Smoking Behaviour Committee. Membership of that committee was - similar to ACAC3 - by invitation only. The broadened scope consequently led to the re-shaping of the then Study Groups ‘Smoke’ and ‘Technology’ into ‘Smoke Science’ (SS) and ‘Product Technology’ (PT).Subsequently, three Sub-Groups (SG) and Task Forces (TF) were set up, reflecting this change: i) SG Smoking Behaviour (name change of former Committee in 2001), ii) TF ‘Nicotine Intake’ (2001, later on named ‘Nicotine Uptake’, disbanded in 2009) and iii) TF ‘In vitro Toxicity Testing of Tobacco Smoke’ (2002). Finally, a new SG ‘Biomarkers’ was launched in 2009 with a wider scope than its predecessor TF ‘Nicotine Uptake’. The work of these groups has had and still has significant impact on the scientific work within CORESTA, leading to numerous presentations at CORESTA meetings and publications in peer-reviewed journals.This paper provides a brief analysis of some 270 presentations and posters addressing tobacco smoke toxicity, human smoking behaviour or biomarkers, delivered at CORESTA Congresses and SSPT Joint Meetings between 1993 and 2011. More than 50% of these papers covered different aspects of toxicology, mainly in vitro toxicity testing methodologies, smoke exposure systems and other equipments. Other papers described the influence of cigarette design parameters on smoke toxicity. Approaches to human risk assessment were presented, including the search for suitable in vitro models of the major smoking related human diseases.CORESTA began discussing smoking behaviour topics at their Vienna meeting in 1995 and received five respective presentations there; indeed, the issue has various aspects, from smoking topography and human smoke yield to smoke uptake, deposition and retention, and… Why do people smoke at all?As early as 1996, a presentation was given on the determination of urinary mutagenicity in volunteers exposed to ETS (environmental tobacco smoke), apparently indicating a need for CORESTA to engage in this field and to face new challenges. Indeed, our knowledge of biomarkers and how to measure them has increased considerably over the years, and there is a clear trend towards using this knowledge for conducting clinical studies into the assessment of ‘modified risk tobacco products’.

2012 ◽  
Vol 147 (5) ◽  
pp. 876-884 ◽  
Author(s):  
Marcelo B. Antunes ◽  
John J. Chi ◽  
Zhi Liu ◽  
Natalia Goldstein-Daruech ◽  
James N. Palmer ◽  
...  

Objective To evaluate changes in the expression of biofilm-related genes when exposed to tobacco smoke and oxidative stress. Study Design Experimental, in vitro. Setting Laboratories of Rhinology and Microbiology, University of Pennsylvania. Subjects and Methods Bacterial biofilm mass was measured using crystal violet staining and measurement of the optical density. Biofilm-related genes of the Pseudomonas aeruginosa PAO1 strain ( pilF, flgK, lasI, lasB, rhlA, and algC) were studied following repetitive exposure to exogenous tobacco smoke and hydrogen peroxide. This was done using a reporter plasmid. Results After 1 exposure to smoke, there was no change in biofilm formation. However, after 2 and 3 exposures, the biofilm formed had an increased mass ( P < .05). With respect to oxidative stress in the form of H2O2, bacterial cultures demonstrated a dose- and time-dependent induction of biofilm formation compared with control conditions. Gene expression following repetitive smoke exposure demonstrated an increase in expression of pilF, flgK, algC, and lasI genes ( P < .05); a decrease in rhlA ( P < .05); and no significant change in the lasB gene ( P = 0.1). Gene expression following H2O2 exposure demonstrated an increase in pilF ( P < .05), whereas the other genes failed to demonstrate a statistical change. Conclusions Repetitive tobacco smoke exposure leads to molecular changes in biofilm-related genes, and exposure to oxidative stress in the form of H2O2 induces biofilm growth in PAO1. This could represent adaptative changes due to oxidative stress or chemically mediated through any of the several chemicals encountered in tobacco smoke and may explain increased biofilm formation in microbes isolated from smokers.


Author(s):  
E Gregg ◽  
T Bachmann ◽  
R Bito ◽  
X Cahours ◽  
M McEwan ◽  
...  

AbstractIn recent years, the increased availability of tobacco products other than conventional cigarettes, the use of puffing topography devices for smoking behaviour studies and the use of biomarkers to study smoke constituents exposure have generated the need for a more comprehensive set of definitions concerning smoking behaviour and exposure to smoke. The definitions offered in this paper are based on many years of practical experience and on consensus within a broad group of scientists working in these areas. It is intended that, with wider and more consistent usage, these definitions should reduce any misunderstandings and facilitate interpretation of future studies.


Sign in / Sign up

Export Citation Format

Share Document