Jump to full article: SourceWatch (Center for Media & Democracy), 2009-09-01
Intro: This article is part of the Tobacco portal on Sourcewatch, sponsored by the American Legacy Foundation. Help expose the truth about the tobacco industry.
Secondhand smoke, "also known as environmental tobacco smoke (ETS) or passive smoke, is a mixture of two forms of smoke from burning tobacco products," according to the American Cancer Society: Sidestream smoke, which is smoke that comes from a lighted cigarette, pipe, or cigar, and "mainstream smoke," the smoke the smoker himself inhales and exhales.[1]
Video on secondhand smoke produced by the U.S. Surgeon General
Contents
* 1 Secondhand smoke and human health
* 2 Cardiac effects
* 3 Tobacco industry toxicity testing not revealed to public
* 4 The "Biological Plausibility" Argument
* 5 Tobacco industry documents
* 5.1 R.J. Reynolds
* 5.2 Philip Morris
* 6 SourceWatch Resources
* 7 External links
* 7.1 General Information
* 8 References
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Secondhand smoke and human health
According to the U.S. Surgeon General, secondhand smoke contains a number of poisonous gases and chemicals, including hydrogen cyanide (used in chemical weapons), carbon monoxide (an odorless, colorless gas found in car exhaust), butane (used in lighter fluid), ammonia (used in household cleaners), and toluene (found in paint thinners). Eleven compounds in tobacco smoke have been identified by the International Agency for Research on Cancer as Group 1 Human Carcinogens. They are: 2-naphthylamine, 4-aminobiphenyl, benzene, vinyl chloride, ethylene oxide, arsenic, beryllium, nickel compounds, chromium, cadmium and polonium-210.[2]
In December 1992 the U.S. Environmental Protection Agency (EPA) issued a risk assessment titled "The Respiratory Health Effects of Passive Smoking," that concluded that secondhand smoke is a known human carcinogen which kills about 3,000 nonsmokers each year and is responsible for up 300,000 cases of bronchitis and pneumonia in children annually. The EPA's study stated that secondhand tobacco smoke is associated with increased risk of lower respiratory tract infections such as bronchitis and pneumonia. EPA estimated that 150,000 to 300,000 respiratory infections annually in infants and young children up to 18 months are attributable to secondhand smoke. EPA also concluded that secondhand smoke was associated middle ear effusions, upper respiratory tract irritation, and small reductions in lung function, and that it increased severity of asthma symptoms in children. EPA estimated that up to one million asthmatic children have their condition worsened by exposure to secondhand smoke and that tobacco smoke exposure may also be a risk factor for the development of new cases of asthma.[3]
"The U.S. Environmental Protection Agency (EPA) has classified secondhand smoke as a Group A Human carcinogen, which means that there is sufficient evidence to conclude that it causes cancer in humans. Environmental tobacco smoke has also been classified as a "known human carcinogen" by the U.S. National Toxicology Program.
"Secondhand tobacco smoke contains over 4,000 chemical compounds. More than 60 of these are known or suspected to cause cancer." [1]
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Cardiac effects
A 2001 study published in the Journal of the American Medical Association (JAMA) showed that inhaling secondhand smoke substantially reduced coronary flow velocity reserve in healthy nonsmokers. Coronary flow velocity reserve is a measure of the ability of the coronary arteries to dilate in order to increase blood flow in response to a stimulus or stressor. The cells that line blood vessels are called "endothelial cells," and a decline in coronary flow velocity reserve indicates "endothelial dysfunction," an impairment of the ability of the coronary arteries to dilate in response to a variety of stimuli. The 2001 study's authors conclude that this finding provides direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.[4]
A 2004 study published in the British Medical Journal (BMJ) revealed that people exposed to high levels of secondhand tobacco smoke (also known as "passive smoking") are more likely to develop coronary artery disease. Cotinine is a breakdown product of nicotine. The study found that people with higher concentrations of serum cotinine were 50-60% more likely to have coronary artery disease, but their risk of stroke was not increased. [5]
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Tobacco industry toxicity testing not revealed to public
In 2005, researchers and the University of California, San Francisco reviewed unpublished in vivo research on secondhand cigarette smoke performed by scientists at the Philip Morris Tobacco Company during the 1980s at its overseas biological lab Institut f�r Biologische Forschung, or INBIFO. Between 1981 and 1989 PM performed at least 115 studies at INBIFO on the toxicity of secondhand tobacco smoke. The existence of these studies on secondhand smoke was unknown until the tobacco industry's internal documents were made public on the Internet in 1998. The studies revealed that inhaled fresh secondhand smoke is approximately four times more toxic per gram in its total particulate matter than mainstream cigarette smoke (the smoke the smoker himself inhales). The condensate (commonly known as "tar") derived from secondhand smoke is approximately three times more toxic per gram and two to six times more tumorigenic per gram than the condensate produced by mainstream smoke when applied to skin. Philip Morris never revealed the results of these studies to the public or any government.[6]
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The "Biological Plausibility" Argument
Public acceptance of the scientific link between tobacco smoke and disease resulted in increasing public concern about the health effects of chronically inhalation of secondhand smoke in public places and on the job. The argument linking secondhand smoke with disease was known inside the industry as the "biological plausibility argument," and it goes like this:
1) Mainstream and secondhand smoke are chemically similar, 2) Mainstream and secondhand smoke both contain carcinogens, 3) Secondhand smoke consists of the same carcinogens, 4) Therefore it is biologically plausible that secondhand smoke causes lung cancer in nonsmokers.[7]
R.J. Reynolds chemist David J. Doolittle wrote in 1990:
When considering the biological plausibility model we must recognize two well-documented observations regarding ETS [environmental tobacco smoke]:
1) Some non-smokers are exposed to ETS as evidenced by subjective impressions (annoyance), and nicotine and cotinine in urine samples. 2) Even though present at very low concentrations, ETS does contain IARC [International Agency for Research on Cancer] human carcinogens, as well as mutagens and cytotoxins. Thus, we cannot disprove the notion that some non-smokers are exposed to carcinogens, mutagens, and cytotoxins in ETS. Also, even though the level of exposure to these chemicals is extraordinarily small, it is extremely difficult to absolutely prove that these exposures will never adversely affect any individual. This, in effect, forms the basis for the biological plausibility model.[8]
A 1999 Philip Morris report argues against the "Biological Plausibility" argument, saying "ETS [environmental tobacco smoke] has never been shown to be carcinogenic in any animal species." PM did not publicly reveal the results of over 100 in-house experiments it performed on ETS at INBIFO during the 1980s that concluded ETS was more toxic and carcinogenic than mainstream smoke.[9] . . .
R.J. Reynolds
In a 1994 brainstorming document, R. J. Reynolds sought to determine strategies the company could use to fight the emerging information that secondhand smoke is hazardous to health. In response to the question, "What is the most important strategy we [RJR] could take?" respondents answered,
* "We must incite smokers to rebel and spread that rebellion to nonsmokers now! We must be repetitious and persistent. All media, all intellectual levels. What do we have to lose?"
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