Time filter

Source Type

Montréal, Canada

Imasco Minerals Inc., IMPERIAL TOBACCO CANADA Ltd, IMASCO Ltd and INTERNATIONAL MARBLE & STONE Co. | Date: 1999-10-19

pigment colorants. argillite, granite and quartzite sand-blast sand, poultry grit and aggregate; [siliceous black stag for aggregates and sands;] carbonate, granite and quartzite sands and aggregate for stucco, terrazzo, architectural precast, masonry, and decorative purposes; ground dolomite and calcium carbonate (limestone) for fine industrial filters; soil conditioners; formulated (premixed) stucco products; namely, finish coat and fogcoat; formulated (premix) stucco products; namely, basecoat.

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.

Kaur N.,University of Montreal | Cabral J.-L.,Imperial Tobacco Canada Ltd | Morin A.,Imperial Tobacco Canada Ltd | Waldron K.C.,University of Montreal
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.

Cote F.,Imperial Tobacco Canada Ltd | Letourneau C.,Imperial Tobacco Canada Ltd | Mullard G.,Group Research and Development | 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.

Talbot S.,University of Montreal | Lin J.C.-J.,Imperial Tobacco Canada Ltd | Lahjouji K.,University of Montreal | 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.

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