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.
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ABSTRACT: The experiments described in this thesis were designed to shed some more light on the mechanisms underlying cigarette smoke-induced lung emphysema. We used elastase instillation to induce lung emphysema, and subsequently perfused the lungs ex-vivo with buffer at a range of flows to measure changes in the resulting pressure. Unfortunately there was no clear relation between morphometric measures of lung damage and the flow/pressure profiles. We investigated whether exposure of mice to cigarette smoke in our experimental set-up led to the predisposition of emphysematous lesions towards the upper parts of the lungs that is seen in smoking humans. We showed that this was indeed the case, and, therefore, concluded that exposure of mice in our experimental set-up could serve as a valid model for cigarette smoke-induced emphysema in humans, at least with regard to the distribution of damage throughout the lungs. After having shown this, we applied the model to investigate the effects of one of the less well studied components of cigarette smoke: humic acid (HA). We hypothesised that deposition of HA would potentiate smoke-induced damage to the lungs, and thus the development of emphysema. Indeed, when mice were exposed to cigarette smoke for 2 months, after HA instillation in to the lungs, they had developed emphysematous lesions, whereas this was not the case in the mice that had been exposed to smoke or HA only. Our observation that HA potentiated the lung-damaging effects of smoking provides an explanation for the fact that many pack-years of smoking are generally required for symptoms to become clearly manifest, supposedly the time needed to get sufficient HA accumulation in the airways in order to catalyse the cytotoxic effects of smoking. Based on findings that cigarette smoke acts as a double-edged sword in the lungs, both inflicting tissue damage and depleting acid retinoids (molecules implied in tissue regeneration), the following hypothesis was formulated: a low vitamin A status can increase the susceptibility to cigarette smoke-induced lung emphysema. We exposed mice with a normal and a low, but not deficient, vitamin A status to cigarette smoke to test this, and found the hypothesis to be true. Unexpectedly, levels of acid retinoids remained normal in the lungs of the smoke-exposed animals, irrespective of their vitamin A status. Levels of retinol and retinyl palmitate were decreased in the lungs of animals with the low status. This could provide a possible explanation for the increased susceptibility, given their potent anti-oxidant activity, which could protect against cigarette smoke-induced damage. Involuntarily exposure to cigarette smoke in a nose-only system causes stress in experimental animals, through a combination of factors. We speculated that stress-induced hyperthermia might explain the high levels of mortality we experienced in both controls and smoke-exposed animals during our nose-only exposure experiments. Surprisingly, we found that mice instead showed a pronounced hypothermia during their stay in the nose-only exposure tubes, which we could attribute to the massive metal nosepieces. Unfortunately, preventing hypothermia by heating the nosepieces did not decrease parameters of stress, nor did it reduce mortality.
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ABSTRACT: To examine the tactics the tobacco industry in Germany used to avoid regulation of secondhand smoke exposure and to maintain the acceptance of public smoking. Systematic search of tobacco industry documents available on the internet between June 2003 and August 2004. In West Germany, policymakers were, as early as the mid 1970s, well aware of the fact that secondhand smoke endangers non-smokers. One might have assumed that Germany, an international leader in environmental protection, would have led in protecting her citizens against secondhand smoke pollution. The tobacco manufacturers in Germany, however, represented by the national manufacturing organisation "Verband" (Verband der Cigarettenindustrie), contained and neutralised the early debate about the danger of secondhand smoke. This success was achieved by carefully planned collaboration with selected scientists, health professionals and policymakers, along with a sophisticated public relations programme. The strategies of the tobacco industry have been largely successful in inhibiting the regulation of secondhand smoke in Germany. Policymakers, health professionals, the media and the general public should be aware of this industry involvement and should take appropriate steps to close the gap between what is known and what is done about the health effects of secondhand smoke.Tobacco control 05/2006; 15(2):e1. DOI:10.1136/tc.2005.012336 · 5.15 Impact Factor