Imperial Tobacco Canada Ltd

Montréal, Canada

Imperial Tobacco Canada Ltd

Montréal, Canada
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Cote F.,Imperial Tobacco Canada Ltd. | Letourneau C.,Imperial Tobacco Canada Ltd. | Mullard G.,British American Tobacco | Voisine R.,Imperial Tobacco Canada Ltd.
Regulatory Toxicology and Pharmacology | Year: 2011

In 2005, Human-Smoked (HS) tar and nicotine yields from commercial Canadian cigarettes were determined using a part filter analysis method to obtain estimates representative of human smoking behavior. In 2006, new cigarette designs were introduced to ensure compliance with the Canadian Low Ignition Propensity (LIP) regulations. It was not known how the changes in product design would affect HS yields. To assess the impact of the cigarette design modifications on HS yields, a further group of Canadian smokers was recruited for smoking the modified version of 10 products previously assessed. No differences in estimated HS tar yields were found between products following product modification. The HS nicotine yield was different for one product. In general, HS yields were higher than ISO machine yields while Canadian intense machine yields were more representative of the maximum HS yields. The same product ranking order was obtained for HS yields and the two machine yields but differences between the mean HS yields and ISO yields were smaller as the product ISO yields increased. Higher HS yields were measured when products were smoked by male smokers. The methodology used in this study showed the wide range of HS yields obtained by smokers as well as a good degree of stability in average HS yields just before and after the introduction of LIP regulations. © 2010 Elsevier Inc.


Liu C.,British American Tobacco | DeGrandpre Y.,Imperial Tobacco Canada Ltd. | Porter A.,3515 Connaught | Griffiths A.,British American Tobacco | And 4 more authors.
Food and Chemical Toxicology | Year: 2011

The US Institute of Medicine has encouraged the pursuit and development of potential reduced-exposure products (PREPs) - tobacco products that substantially reduce exposure to one or more tobacco toxicants and can reasonably be expected to reduce the risk of one or more specific diseases or other adverse health effects. One potential approach is to reduce levels of some smoke toxicant precursors, such as proteins and polyphenols, in tobacco. We describe a treatment process involving aqueous tobacco extraction and treatment with protease; filtration of the extract to remove peptides, amino acids and polyphenols, and recombination of extract and treated tobacco. The process reduced levels of protein nitrogen (59%), polyphenols (33-78%) and nicotine (12%) while sugars increased 16%. ISO mainstream smoke yields of 43 toxicants were measured from cigarettes containing treated tobaccos; lower yields of tar, nicotine, carbon monoxide (16-20%), acrylonitrile, ammonia, aromatic amines, pyridine, quinolene and hydrogen cyanide (33-51%), tobacco specific nitrosamines (25-32%); phenolics (24-56%), benzene (16%), toluene (25%) and cadmium (34%) were obtained. There were significantly increased yields of formaldehyde (49%) and isoprene (17%). Reductions in sidestream yields of nitrogenous smoke toxicants and increases in sidestream yields of several carbonyls, benzo(a)pyrene and isoprene were also observed. © 2011 Elsevier Ltd.


Morin A.,Imperial Tobacco Canada Ltd | Shepperd C.J.,British American Tobacco | Eldridge A.C.,British American Tobacco | Poirier N.,Imperial Tobacco Canada Ltd | Voisine R.,Imperial Tobacco Canada Ltd
Regulatory Toxicology and Pharmacology | Year: 2011

A clinical study conducted in Canada compared two methods of estimating exposure to cigarette smoke in 192 volunteer subjects: 43 smokers of 4-6. mg, 49 of 8-12. mg and 50 of 14-15. mg ISO tar yield cigarettes and 50 non-smokers. Estimates of mouth level exposure (MLE) to nicotine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), pyrene and acrolein were obtained by chemical analysis of spent cigarette filters. Estimates of smoke constituent uptake were achieved by analysis of urinary biomarkers for total nicotine equivalents (nicotine, cotinine, trans-3'-hydroxycotinine plus their glucuronide conjugates), NNK (total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) plus glucuronide), pyrene (1-hydroxy pyrene plus glucuronide) and acrolein (3-hydroxylpropyl-mercapturic acid) plus the nicotine metabolite cotinine in plasma and saliva. The objective of our study was to confirm the correlations between measures of human exposure obtained by filter analysis and biomarkers. Significant correlations (. p<. 0.001) were found between MLE and the relevant biomarker for each smoke constituent. The adjusted values of the Pearson correlation coefficients (. r) were 0.80 (nicotine), 0.77 (acrolein) and 0.44 (pyrene). NNK correlations could not be obtained because of the low NNK yield of Canadian cigarettes. Unexpectedly high levels of acrolein biomarker found in non-smokers urine on one of the two days sampled emphasised the need for more than one sampling occasion per period and an awareness of non-tobacco sources of smoke constituents under investigation. No consistent dose response, in line with ISO tar yield smoked, of MLE estimates was found for nicotine, pyrene and acrolein and respective biomarkers. The influence of demographics on our results has also been examined. © 2010 Elsevier Inc.


Morin A.,Imperial Tobacco Canada Ltd | Poirier N.,Imperial Tobacco Canada Ltd | Prefontaine D.,Imperial Tobacco Canada Ltd | Lacasse M.,Imperial Tobacco Canada Ltd
Beitrage zur Tabakforschung International/ Contributions to Tobacco Research | Year: 2010

Flue-curing is a post harvest conditioning process which strongly affects the tobacco leaf chemistry, and consequently the chemical properties of tobacco smoke. Several studies identified the major changes in tobacco chemistry occurring during flue-curing. It is not known how flue-curing contributes to changes in bioactivity of cigarette smoke condensate (CSC). In this study, tobacco leaves collected throughout the twelve days of flue-curing were used to prepare cigarettes that were smoked to generate CSC samples. The assessment of mutagenicity was performed using the Bacterial Reverse Mutation/Ames test with Salmonella typhimurium TA98 in the presence of S9 metabolic activation. CSC from cured leaves were significantly more mutagenic than CSC from uncured leaves. The number of revertants was positively influenced by the duration of the curing. The effect of the duration of curing on the number of revertants was more pronounced with increasing CSC concentration.


Talbot S.,University of Montréal | Lin J.C.-J.,Imperial Tobacco Canada Ltd. | Lahjouji K.,University of Montréal | Roy J.-P.,Imperial Tobacco Canada Ltd. | And 3 more authors.
Peptides | Year: 2011

Pulmonary inflammation is an important pathological feature of tobacco smoke-related lung diseases. Kinin B1 receptor (B1R) is up-regulated in the rat trachea chronically exposed to cigarette-smoke. This study aimed at determining (1) whether exposure to total particulate matter of the cigarette smoke (TPM) can induce B1R in human alveolar epithelial A549 cells, (2) the mechanism of B1R induction, (3) the functionality of de novo synthesized B1R, and (4) the role of B1R in TPM-induced increase of superoxide anion (O2 -) level. Results show that A549 cells exposed to 10 μg/ml TPM increased O 2 - level along with B1R (protein and mRNA) and IL-1β mRNA. In contrast, B2R and TNF-α mRNA were not affected by TPM. The increasing effect of TPM on O2 - level was not significantly affected by the B1R antagonist SSR240612. TPM-increased B1R mRNA was prevented by co-treatments with N-acetyl-l-cysteine (potent antioxidant), diphenyleneiodonium (NADPH oxidase inhibitor), IL-1Ra (interleukin-1R antagonist) and SN-50 (specific inhibitor of NF-kB activation) but not by pentoxifylline (TNF-α release inhibitor), indomethacin and niflumic acid (COX-1 and -2 inhibitors). Stimulation of B1R with a selective agonist (des-Arg9-BK, 10 μM; 30 min) increased O2 -production which was prevented by apocynin and diphenyleneiodonium (NADPH oxidase inhibitors). Data suggest that the increased expression of B1R by TPM in A549 cells is mediated by oxidative stress, IL-1β and NF-kB but not by cyclooxygenases or TNF-α. The amplification of O2 - levels via the activation of B1R-NADPH oxidase may exacerbate pulmonary inflammation and contribute to the chronicity of tobacco smoke-related lung diseases. © 2011 Elsevier Inc. All rights reserved.


Kaur N.,University of Montréal | Lacasse M.,Imperial Tobacco Canada Ltd. | Roy J.-P.,Imperial Tobacco Canada Ltd. | Cabral J.-L.,Imperial Tobacco Canada Ltd. | And 5 more authors.
Inhalation Toxicology | Year: 2010

The Borgwaldt RM20S® smoking machine enables the generation, dilution, and transfer of fresh cigarette smoke to cell exposure chambers, for in vitro analyses. We present a study confirming the precision (repeatability r, reproducibility R) and accuracy of smoke dose generated by the Borgwaldt RM20S® system and delivery to exposure chambers. Due to the aerosol nature of cigarette smoke, the repeatability of the dilution of the vapor phase in air was assessed by quantifying two reference standard gases: methane (CH 4, r between 29.0 and 37.0 and RSD between 2.2% and 4.5%) and carbon monoxide (CO, r between 166.8 and 235.8 and RSD between 0.7% and 3.7%). The accuracy of dilution (percent error) for CH4 and CO was between 6.4% and 19.5% and between 5.8% and 6.4%, respectively, over a 10-1000-fold dilution range. To corroborate our findings, a small inter-laboratory study was carried out for CH4 measurements. The combined dilution repeatability had an r between 21.3 and 46.4, R between 52.9 and 88.4, RSD between 6.3% and 17.3%, and error between 4.3% and 13.1%. Based on the particulate component of cigarette smoke (3R4F), the repeatability (RSD=12%) of the undiluted smoke generated by the Borgwaldt RM20S® was assessed by quantifying solanesol using high-performance liquid chromatography with ultraviolet detection (HPLC/UV). Finally, the repeatability (r between 0.98 and 4.53 and RSD between 8.8% and 12%) of the dilution of generated smoke particulate phase was assessed by quantifying solanesol following various dilutions of cigarette smoke. The findings in this study suggest the Borgwaldt RM20S® smoking machine is a reliable tool to generate and deliver repeatable and reproducible doses of whole smoke to in vitro cultures. © 2010 Informa Healthcare USA, Inc.


Kaur N.,University of Montréal | Cabral J.-L.,Imperial Tobacco Canada Ltd. | Morin A.,Imperial Tobacco Canada Ltd. | Waldron K.C.,University of Montréal
Journal of Chromatography A | Year: 2011

Advanced smoke generation systems, such as the Borgwaldt RM20S® smoking machine used in combination with the BAT exposure chamber, allow for the generation, dilution and delivery of fresh cigarette smoke to cell or tissue cultures for in vitro cell culture analyses. Recently, our group confirmed that the Borgwaldt RM20S® is a reliable tool to generate and deliver repeatable and reproducible exposure concentrations of whole smoke to in vitro cultures [1]. However, the relationship between dose and diluted smoke components found within the exposure chamber has not been characterized. The current study focused on the development of a headspace stir bar sorptive extraction (HSSE) method to chemically characterize some of the vapor phase components of cigarette smoke generated by the Borgwaldt RM20S® and collected within a cell culture exposure chamber. The method was based on passive sampling within the chamber by HSSE using a Twister™ stir bar. Following exposure, sorbed analytes were recovered using a thermal desorption unit and a cooled injection system coupled to gas chromatograph/mass spectrometry for identification and quantification. Using the HSSE method, sixteen compounds were identified. The desorption parameters were assessed using ten reference compounds and the following conditions led to the maximal response: desorption temperature of 200°C for 2min with cryofocussing temperature of -75°C. During transfer of the stir bars to the thermal desorption system, significant losses of analytes were observed as a function of time; therefore, the exposure-to-desorption time interval was kept at the minimum of 10±0.5min. Repeatability of the HSSE method was assessed by monitoring five reference compounds present in the vapor phase (10.1-12.9% RSD) and n-butyl acetate, the internal standard (18.5% RSD). The smoke dilution precision was found to be 17.2, 6.2 and 11.7% RSD for exposure concentrations of 1, 2 and 5% (v/v) cigarette vapor phase in air, respectively. A linear response of analyte abundance was observed as a function of dilution. Extrapolation to 100% (v/v) cigarette vapor phase, i.e., undiluted smoke, gave yields for the five compounds ranging from 6 to 450ng for 10min exposure. © 2010 Elsevier B.V.


Lin J.C.-J.,Imperial Tobacco Canada Ltd | Talbot S.,University of Montréal | Lahjouji K.,University of Montréal | Roy J.-P.,Imperial Tobacco Canada Ltd | And 3 more authors.
Peptides | Year: 2010

Pulmonary inflammation is an important pathological feature of tobacco smoke related lung diseases such as chronic obstructive pulmonary disease (COPD). Kinin type 1 and type 2 receptors (B1R, B2R) are known to be associated with inflammatory responses of the lungs and other organs. In this study, we investigated whether cigarette smoke-induced airway inflammation could up-regulate B1R and B2R in correlation with IL-1β and TNF-α. Rat lung slices treated with 5 μg/ml total particulate matter (TPM) of cigarette smoke for 24 h showed an enhanced expression of B1R and IL-1β by 5-fold and 30-fold, respectively, in comparison to vehicle treatment (dimethyl sulfoxide). However, higher concentrations of TPM failed to induce B1R. No significant increase of B2R or TNF-α gene induction was observed. IL-1 receptor antagonist (IL-1Ra, 2 ng/ml) significantly blocked B1R gene induction by TPM, while 500 μM pentoxifylline, TNF-α inhibitor, reduced it partially. Western blot analysis showed a 2-fold enhanced expression of B 1R in rat lung slices treated with 5 μg/ml TPM for 24 h and such protein expression was totally blocked by a co-treatment with IL-1Ra but not with pentoxifylline. In addition to the lower airways, rat trachea subchronically exposed to cigarette whole smoke exhibited 11-fold B1R gene induction in comparison with those exposed only to air. Our results demonstrate the involvement of B1R in cigarette smoke-induced airway inflammation through a mechanism which is mediated by the pro-inflammatory cytokine IL-1β. © 2010 Elsevier Inc. All rights reserved.


Patent
IMPERIAL TOBACCO CANADA Ltd | Date: 2010-10-14

The present invention pertains to hinge lid packages, for example cigarette packages, with features that reduce the force required to open and close the package, keep the lid tightly closed when not in use and/or improve the luxurious feel of the package during opening and closing, in comparison to similar packages that do not include these features.


PubMed | Imperial Tobacco Canada Ltd
Type: Journal Article | Journal: Peptides | Year: 2010

Pulmonary inflammation is an important pathological feature of tobacco smoke related lung diseases such as chronic obstructive pulmonary disease (COPD). Kinin type 1 and type 2 receptors (B(1)R, B(2)R) are known to be associated with inflammatory responses of the lungs and other organs. In this study, we investigated whether cigarette smoke-induced airway inflammation could up-regulate B(1)R and B(2)R in correlation with IL-1 and TNF-. Rat lung slices treated with 5 g/ml total particulate matter (TPM) of cigarette smoke for 24 h showed an enhanced expression of B(1)R and IL-1 by 5-fold and 30-fold, respectively, in comparison to vehicle treatment (dimethyl sulfoxide). However, higher concentrations of TPM failed to induce B(1)R. No significant increase of B(2)R or TNF- gene induction was observed. IL-1 receptor antagonist (IL-1Ra, 2 ng/ml) significantly blocked B(1)R gene induction by TPM, while 500 M pentoxifylline, TNF- inhibitor, reduced it partially. Western blot analysis showed a 2-fold enhanced expression of B(1)R in rat lung slices treated with 5 g/ml TPM for 24 h and such protein expression was totally blocked by a co-treatment with IL-1Ra but not with pentoxifylline. In addition to the lower airways, rat trachea subchronically exposed to cigarette whole smoke exhibited 11-fold B(1)R gene induction in comparison with those exposed only to air. Our results demonstrate the involvement of B(1)R in cigarette smoke-induced airway inflammation through a mechanism which is mediated by the pro-inflammatory cytokine IL-1.

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