Second Hand Smoking Myths

Don't Let Real Science Get In The Way!

Dr. Bernard M. Wagner, the editor of Modern Pathology, recently wrote, "Are there 450,000 smoking-related deaths per year in America? Maybe...but no human beings are ever studied to find out". Wagner went on to say the biggest obstacle to knowing what is actually going on is the low autopsy rate in this country, about 10%.

Perhaps the best (or maybe the worst) example of the LaLonde effect is the recent report of the Environmental Protection Agency on the "dangers" of second-hand smoke (ETS).

In an article published in the Winter 93-94 issue of Bostonia, a magazine published by Boston University, the EPA Report was vigorously attacked by Dr. John C. Luik, a non-smoker, and a senior associate of the Niagara Institute, Ontario, Canada. As Luik showed, the EPA study was based on some 30 studies from several different countries. These studies dealt, essentially, with the effect of smoking by a smoking husband or wife on a non-smoking spouse. Of the thirty studies, 24 showed no statistically significant connection between ETS (environmental tobacco smoke) and lung cancer. However, while the EPA saw fit to discuss and refer to all 30 studies, it made a statistical analysis of only 11 U.S. studies. EPA conceded that ten of these studies also showed no statistically significant increase in lung cancer risk. One study alone showed such a risk, but to show such a risk, the EPA was obliged to reduce the statistical "confidence factor" which it normally uses in such analyses from 95% to 90%!

The EPA then went on to merge all of the eleven studies together (a statistically invalid procedure since the studies were not all structured the same way), and to reanalyze the results, using the newly reduced "confidence factor". By folding, mutilating and stapling the data, the EPA decided that the spouses of smokers had a risk of developing 119 lung cancers, as opposed to a risk of 100 such cancers in the spouses of non-smokers. Without the reduction in the "confidence factor", no statistically significant risk could have been shown. None-the-less, the EPA branded ETS a "carcinogen".
Writing in Toxological Pathology, Alvan Feinstein, a Yale University epidemiologist quotes another prominent epidemiologist as saying this about the EPA report: "Yes, it's rotten science, but it's in a worthy cause. It will help us to get rid of cigarettes and become a smoke-free society". The "LaLonde Effect" is alive and well!

Check This Out!

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Lung Cancer & Heavy Smoking:
Nearly 90 percent of people who develop lung cancer are smokers, yet only about 10 percent of lifetime smokers will develop the disease.

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Second Hand Smoke - Biggest Hoax Of the 20th Century!

It is barely an exaggeration to say that the prohibitionists invented secondhand tobacco smoke (and rechristened it “environmental tobacco smoke”) because it is (still) difficult to justify prohibition for the smoker’s own good. Anti-tobacco activist Stanton Glantz wrote in 1986: “The issue should be framed in the rhetoric of the environment, toxic chemicals, and public health rather than the rhetoric of saving smokers from themselves or the cigarette companies” (p. 150).

“[It] is safe,” writes Sullum, “to say that the hazards of secondhand smoke have been grossly exaggerated” (p. 159). As the evidence reviewed by Sullum himself suggests (see chapter 5), this conclusion may well be an understatement. The health hazards of secondhand smoke may be the hoax of the twentieth century. The strand of junk science underlying this hoax owes much to the 1992 EPA report that classified secondhand tobacco smoke as a “Group A carcinogen.” It may be useful to quote a source that was not available to Sullum at the time of his writing, namely, the recent judgment of U.S. District Judge William Osteen: “The court is faced with the ugly possibility that EPA adopted a methodology for each chapter, without explanation, based on the outcome sought in that chapter. . . . The record and EPA’s explanations to the court make it clear that using standard methodology, EPA could not produce statistically significant results with its selected studies” (Flue-Cured Tobacco Cooperative v. EPA, No. 6:93CV00370 at 60, 77, M.D.N.C., July 17, 1998).
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Most Smoking Studies = JUNK!

ALL Epidemiologic Studies are Junk Science
and the worst threat to humanity ever 'invented'.
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All the anti-smoking studies are Epidemiologic Studies
Of the 80 'spousal' studies most referred to by anti-smokers,the 31 'workplace' studies most referred to by anti-smokers,and the 36 'childhood' studies most referred to by anti-smokers,
for each category
over 80 % are NOT Statistically Significant

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Risk of Lung Cancer:
A relative risk of 1.19, even if the data were not manipulated, is extremely weak. It is of the same general magnitude as the risk that an American citizen faces of dying in a bicycling accident over the course of a lifetime. It is a risk that is less than that associated with developing colon cancer by drinking chlorinated water, which is in most U.S. cities' water supplies. It is generally accepted in the medical literature that any time a relative risk is less than 2.0, the distinct possibility exists that the finding is artifactual and a consequence of the influence of confounding factors.
For instance, many studies indicate that dietary factors alone can influence the rate of development of lung cancer, both in smokers and in nonsmokers, through a relative risk in the range of 20 to 30 percent or so, the same relative magnitude of risk attributed to ETS by the EPA. Multiple reports from the National Cancer Institute and others demonstrate that, because of their lifestyles, the diets of smokers tend to be deficient in beta carotene, vitamins A, C, and E, folate, selenium, and other nutrients known to be anti-carcinogenic. In addition, smokers have lower blood levels of beta carotene and other nutrients than can be explained by diet alone. Characteristically, smokers exhibit other high-risk behaviors that reflect an unhealthy lifestyle. Although the degree to which nonsmoking spouses share such high-risk behaviors has not been extensively quantified and is currently under study, it is only common sense that many of the various risks, especially the dietary ones, might be shared.
As individuals grow older, they have an increased risk for the development of lung cancer, as well as other cancers. Age, then, becomes a very important confounding variable in any study that evaluates the effect of an environmental agent on the development of lung cancer. The EPA analysis, as well as some of the original reports, did not control for this important variable.
There are more than 20 other confounding factors that have been identified as important to assessing risk for lung cancer. When the suggested relative risk is very low, as it is in passive smoking, a single uncontrolled or unaccounted variable can cause a totally spurious interpretation. The EPA's risk assessment acknowledged that confounders are important to any evaluation of ETS as a potential carcinogen. Its concern for confounders was extremely limited, however, and their influence was evaluated by employing a modeling of data by a method as yet untested and unproved by conventional peer review. The EPA, in essence, ignored its own guidelines and established requirements to rule out confounding as an alternative explanation for an association before basing causal inference on epidemiologic results. Until studies take these variables into consideration, we will never know the true risks of ETS exposure.



British Medical Journal report:

Most recently of all, an explosive new study that seriously questions the impact of environmental tobacco smoke on health was published by the British Medical Journal (16 May 2003). According to the study, one of the largest of its kind, the link between environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.

Are non-smokers at risk from ETS?This is what everyone wants to know. The truth is that the scientific establishment has found it impossible to reach agreement on the issue. Interviewed on Radio 4's Desert Island Discs (23 February 2001), Professor Sir Richard Doll, the first scientist to publish research that suggested a correlation between lung cancer and primary smoking, commented: 'The effects of other people smoking in my presence is so small it doesn't worry me.'
Professor Doll's comments may surprise some people but not those who have analysed the argument about passive smoking in detail. In 1992, for example, the American Environmental Protection Agency published a report that was said to demonstrate the link between passive smoking and ill health in non-smokers. In 1996 however a US federal court ruled that the EPA had completely failed to prove its case. It was found not only to have abandoned recognised statistical practice, but to have excluded studies which did not support its pre-determined conclusion, and to have been inconsistent in its classification of ETS compared with other substances.
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All (EVERY ONE) Smoking Studies Are Listed HERE .
See for yourself what they prove!

Smoking & Pregnancy Myths:

Sudden Infant Death Syndrome is not even a specific disease, but just an unexplained death. The risk factors (other than sleeping position) are identical with socioeconomic disadvantage. In The Netherlands, SIDS deaths increased by 10 times between 1971 and 1985, despite declines in maternal smoking during this period, because of a switch in the customary sleeping position (AC Engelberts, GA de Jonge. Choice of sleeping position for infants: possible association with cot death. Arch Dis Childhood 1990;65:462-467.) After publicity against the prone sleeping position, death rates fell 37% in just one year.

So-called maternal smoking harms are really medical deficiencies that are maliciously being blamed on the victims themselves.
Courtesy of Carol Thompson 08/23/93 Smokers' Rights Action Group P.O. Box 259575 Madison, WI 53725-9575 Phone: 608-249-4568

Anti-smokers also falsely blame other poor birth outcomes on maternal smoking. Respiratory Distress Syndrome should not be attributed to smoking because most studies find less RDS among smokers' babies (E Lieberman, J Torday et al. Association of intrauterine cigarette smoke exposure with indices of fetal lung maturation. Obstet Gynecol 1992;79:564-570).

In more rational times, before the anti-tobacco hysteria began in earnest, women who smoked continued to smoke and enjoy other normal pleasures of life without guilt during their pregnancies. Many even smoked during labor to help them relax and take the edge off their pain. If their doctors mentioned smoking at all, it would be to advise them to perhaps cut down if they were heavy smokers, something which most did intuitively because they didn’t “feel” like smoking as much.

But pity the poor North American smoker today who becomes pregnant, because she will be told that if she continues to smoke at all (or have any alcohol or caffeine) during her pregnancy, she is putting her developing fetus at high risk of death or disability.

Nothing could be further from the truth, as the following annotated bibliographies and tables will show.

Though there is considerable evidence showing that on average the babies of women who smoke during pregnancy weigh on average a few ounces less than babies of women who do not smoke and that the rate of low birthweight babies is somewhat higher for smokers, there is no credible evidence for the hyperbolic claims that the babies of smokers have a higher mobidity and mortality rate. Quite the contrary, the babies of women who smoke during pregnancy have a better survival rate ounce for ounce, a somewhat lower rate of congenital defects, a lower rate of Down’s syndrome, a lower rate of infant respiratory distress syndrome and a somewhat lower rate of childhood cancer than do the babies of non-smokers.

Dr. Richard L. Naeye, a leading obstetrical researcher who studied more than 58,000 pregnancies, states unequivocally:

“We recently found no significant association between maternal smoking and either stillbirths or neonatal deaths when information about the underlying disorders, obtained from placental examinations, was incorporated into the analyses. Similar analyses found no correlation between maternal smoking and preterm birth. The most frequent initiating causes of preterm birth, stillbirth, and neonatal death are acute chorioamnionitis, disorders that produce chronic low blood flow from the uterus to the placenta, and major congenital malformations. There is no credible evidence that cigarette smoking has a role in the genesis of any of these disorders.”

[“Cognitive and Behavioral Abnormalities in Children Whose Mothers Smoked Cigarettes during Pregnancy,” Developmental and Behavioral Pediatrics, Dec l992: 13(6); p. 425, emphasis added].

Here.
The Study focused on more than 35,500 people who had never smoked but who had spouses who did. The researchers found that exposure to passive smoking was not associated with deaths from heart disease or lung cancer.