Scientific analysis of second-hand smoke by the tobacco industry, 1929-1972.
ABSTRACT The 1972 U.S. surgeon general's report The Health Consequences of Smoking was the first to include a warning about exposure to second-hand smoke. Because the tobacco industry has a record of withholding the results of their research from the public, we searched the internal tobacco industry documents and compared internal industry research on second-hand smoke to what the industry published in the open scientific literature through 1972. We found chemical analyses, sensory evaluations, and discussions of sidestream cigarette smoke (the smoke emitted by the cigarette between puffs, the main component of second-hand smoke), beginning in 1929. American Tobacco Company research in the 1930s indicated that, compared with mainstream smoke, sidestream smoke was produced in larger quantities and contained, per cigarette, 2 times more nicotine and 12 times more ammonia. Research funded by the Tobacco Industry Research Committee in the 1950s revealed that sidestream smoke contained, per unit cigarette, higher concentrations of carcinogenic polycyclic aromatic hydrocarbons, per unit mass, including four times more 3,4 benzopyrene. In 1956 and 1957, respectively, Philip Morris and R. J. Reynolds also began to research sidestream smoke. In 1961, Philip Morris began to do sensory evaluation and modification of sidestream odor during product development. This sensory evaluation of sidestream smoke was the first biological testing of sidestream smoke by a tobacco company. Prior to the release of the 1972 U.S. surgeon general's report, the tobacco industry published the majority of its findings in the open scientific literature and does not appear to have perceived second-hand smoke as a threat to human health.
SourceAvailable from: Jose Luiz Figueiredo[Show abstract] [Hide abstract]
ABSTRACT: This experimental study aimed to evaluate the effects of central catalase inhibition on cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS) for 3 weeks. A total of 20 males Wistar rats (320-370g) were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4(th)V). Femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. Rats were exposed to SSCS for three weeks, 180 minutes per day, 5 days/week [carbon monoxide (CO): 100-300 ppm)]. Baroreflex was tested with one pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and one depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Cardiovascular responses were evaluated before and 15 minutes after 3-amino-1, 2, 4-triazole (ATZ, catalase inhibitor, 0.001g/100μL) injection into the 4(th) V. Vehicle treatment into the 4(th) V did not change cardiovascular responses. Central catalase inhibition increased tachycardic peak, attenuated bradycardic peak and reduced HR range at 15 minutes, increased MAP at 5, 15 and 30 min and increased HR at 5 and 15 min. In rats exposed to SSCS, central ATZ increased basal MAP after 5 min and increased HR at 5, 15 and 30 minutes, respectively, and attenuated bradycardic peak at 15 minutes. This study suggests that brain oxidative stress caused by SSCS influences autonomic regulation of the cardiovascular system.06/2013; 7(2):200-7. DOI:10.12816/0006043
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ABSTRACT: Objectifs Le patient tabagique bénéficiant d’une intervention de chirurgie plastique est exposé à un risque majoré de complications péri- et postopératoires. Il nous semblait utile d’établir une mise au point sur le retentissement négatif, en particulier cicatriciel, du tabagisme et sur les bénéfices incontestables du sevrage. Nous souhaitons proposer un délai minimal de sevrage pré- et postopératoire en vue de réduire les risques et d’optimiser les résultats de l’intervention. Méthodes Une revue de la littérature a été réalisée sur la période 1972–2014 en interrogeant cinq bases de données (Medline, PubMed Central, Cochrane library, Pascal et Web of Science). Résultats La fumée de cigarette agit de manière diffuse et multifactorielle dans l’organisme. L’hypoxie et l’ischémie tissulaire ainsi que les désordres immunitaires induits par le tabac sont responsables de l’altération du processus cicatriciel. Une partie de ces effets est réversible au sevrage. Les données de la littérature conseillent un délai d’arrêt du tabagisme préopératoire situé entre 3 et 8 semaines et allant jusqu’à 4 semaines postopératoires. L’utilisation de traitements substitutifs nicotiniques double le taux d’abstinence à court terme. Le chirurgien doit s’aider d’un tabacologue en cas de dépendance importante de son patient. Conclusions Un sevrage tabagique total de 4 semaines préopératoires et jusqu’à la cicatrisation primaire du site opératoire, soit 2 semaines postopératoires, semble optimiser les conditions chirurgicales sans majorer le risque anesthésique. Un accompagnement du sevrage aussi bien humain que médicamenteux est recommandé.Annales de Chirurgie Plastique Esthétique 10/2014; 60(1). DOI:10.1016/j.anplas.2014.06.011 · 0.59 Impact Factor
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ABSTRACT: Purpose: Environmental tobacco smoke (ETS) is widely regarded as a major modifiable risk factor for age-related macular degeneration (AMD). Yet, precisely how it exerts its pathological effects is poorly understood. Since early-stage AMD is characterized by choroidal capillary loss, this study examined the effect of sidestream smoke (SS), the major component of ETS, on the viability of choroidal endothelial cells (EC), with an emphasis on the role of aberrant cell and basement membrane (BM) architecture in mediating SS-induced response. Methods: Chorioretinal ECs (RF/6A) were treated with SS and cell viability and architecture were analyzed by colorimetric assay and actin cytoskeletal organization, respectively. The structure of RF/6A EC-secreted BM was examined by immunofluorescence for collagen IV and immunoblotting for lysyl oxidase (LOX), a collagen-crosslinking enzyme. Finally, fresh RF/6A ECs were cultured on decellularized SS-treated BM to evaluate its active role in EC dysfunction. Results: RF/6A EC viability decreased progressively with increasing SS dose, which correlated strongly with a significant decline in actin cytoskeleton-dependent EC spreading. SS also caused marked disruption of the RF/6A EC-secreted BM that was accompanied by suppression of LOX expression. Further, fresh, non SS-treated RF/6A ECs exhibited a significant loss in viability and actin cytoskeletal organization when cultured on SS-treated corrupt BM. Conclusions: These findings indicate that aberrant physical cues in the form of EC and BM architecture likely play an important role in choriocapillaris dysfunction seen in SS-associated early AMD and implicate choroidal BM as a potential target for AMD management strategies.Investigative ophthalmology & visual science 04/2014; 55(5). DOI:10.1167/iovs.13-13659 · 3.66 Impact Factor