There is no carcinogenic or toxic effect of second-hand smoke.
However there are some people who have devoted their lives to smoking bans.
Guardian reports on the Junk Medical Journal Lancet report that says that smoking bans reduce premature labor but they also comment on asthma benefits. We all know that data dredging in observational epidemiology for small associations is the work of charlatans who have a political or, in this case, moral/aesthetic agenda.
A little cheating for a good cause? Easy? Tobacco haters unite under the banner of junk science for justice.
When presented with a contradiction, important to know the motives of the parties.
In this case the strategy of the anti smoking religionists is just like the climate campaigners, criminalize the opposition.
They wanna make smokers into criminal nuisances.
The National Bureau of Economic Research (NBER), which is objective and Boston-based, so inclined, if anything, to be lefty, did an objective, long-term study of impacts of smoking bans in America here:
and found no effects from smoking bans on deaths or hospitalizations, so what’s the disconnect?
Could all the positive association UK and American studies on smoking bans be cherry picking?
The most devastating evisceration of the EPA second-hand smoke junk science portfolio was done by a Federal Judge using the principles of Daubert V Merrill Dow (US Supreme Court 1993) jurisprudence.
The studies by Boffetta and 26 others in Europe for the WHO and James Enstrom and Goeffrey Kabat published in the British Medical Journal in 2005 both showed no cancer effect from second-hand smoke.
Second hand smoke studies invariably have been tortured analyses to show small associations that are less than proof of causation by a bunch.
A more recent study shows no cancer effect, and comments indicate the admissions by Medical people maybe they lied a little.
Here is the abstract and my comments on the WHO Boffetta study published in the Journal of the National Cancer Institute in 1998 and since ignored, as was Enstrom’s work published in the British Medical Journal except for the vitriol and vilification of Enstrom. Boffetta was too big a figure to attack, so the anti smoking fanatics just drove on.
Nothing like a moral/aesthetic campaign or ideology to kill science and suppress evidence.
You see is a study shows no toxic effect and is even just one study stacked up against small association studies, a pile of them–the no effect study wins. Read Einsteins quip about evidence deduced by one valid research project.
But if you hate smoke and tobacco–a little lying is ok.
Here’s a little from the Boffetta study linked above and published in 1998 before all this smoking ban hysteria started but it was warming up.
JNCI J Natl Cancer Inst
• Oxford Journals
• JNCI J Natl Cancer Inst
• Volume90, Issue19
• Pp. 1440-1450.
Multicenter Case-Control Study of Exposure to Environmental Tobacco Smoke and Lung Cancer in Europe
1. Paolo Boffetta, and 26 other authors.
1. Correspondence to Paolo Boffetta, M.D., M.P.H., International Agency for Research on Cancer, 150 cours Albert-Thomas, 69372 Lyon cedex 08, France (e-mail: firstname.lastname@example.org).
• Received February 27, 1998.
• Revision received July 15, 1998.
• Accepted July 29, 1998.
Background: An association between exposure to environmental tobacco smoke (ETS) and lung cancer risk has been suggested. To evaluate this possible association better, researchers need more precise estimates of risk, the relative contribution of different sources of ETS, and the effect of ETS exposure on different histologic types of lung cancer. To address these issues, we have conducted a case-control study of lung cancer and exposure to ETS in 12 centers from seven European countries. Methods: A total of 650 patients with lung cancer and 1542 control subjects up to 74 years of age were interviewed about exposure to ETS. Neither case subjects nor control subjects had smoked more than 400 cigarettes in their lifetime. Results: ETS exposure during childhood was not associated with an increased risk of lung cancer (odds ratio [OR] for ever exposure = 0.78; 95% confidence interval [CI] = 0.64-0.96). The OR for ever exposure to spousal ETS was 1.16 (95% CI = 0.93-1.44). No clear dose-response relationship could be demonstrated for cumulative spousal ETS exposure. The OR for ever exposure to workplace ETS was 1.17 (95% CI = 0.94-1.45), with possible evidence of increasing risk for increasing duration of exposure. No increase in risk was detected in subjects whose exposure to spousal or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to spousal and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant. Conclusions: Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure. [J Natl Cancer Inst 1998;90:1440-50]
As is usually the case, a read of the abstract will give one the essential information on the results. In this case cancer risks found by Boffetta’s group are:
1. RR of less than 1 with a confidence interval of 0.64-0.96 for non smoking children of smokers which means that children of smokers had less lung cancer than the general population.
2. Non smoking spouses risk of lung cancer 1.16 with a confidence interval of 0.93-1.44 and since the confidence interval (CI) includes 1.0, there is no risk found.
3. Workplace second hand smoke exposure for non smokers showed a lung cancer risk of 1.17 with a CI of 0.94-1.45 so, again, CI includes 1.0, and no evidence of risk of lung cancer.
4. The comment that weak evidence of dose response was found is nonsensical in the two populations cited, given 2 and 3 and they do qualify the dose response signal as “weak.”
The authors introduce their paper, its methodology and its context as a product of the International Cancer Studies group involved.
During the last 15 years, epidemiologic studies have been conducted on the association between exposure to environmental tobacco smoke (ETS) and lung cancer. Several authors and regulatory agencies have concluded that a causal link has been established [e.g., see (1–3)], whereas some authors consider that bias and confounding factors constitute a plausible explanation for the observed association [e.g., see (4)]. The available studies are-in most cases-too small to adequately assess the magnitude of the effect and to address specific aspects, such as the shape of the dose-response relationship, the effect of cessation of exposure, the importance of multiple sources of ETS exposure, and the interaction of ETS exposure with other risk factors of lung cancer. Furthermore, relatively few studies of such exposure are available from Europe (5–10). Characteristic of tobacco smoking in European countries are the mixed consumption of blond and black tobacco cigarettes (11) and the low prevalence-at least in the past-of smoking among women compared with men (12).
Since 1988, the International Agency for Research on Cancer (IARC) has coordinated an international, multicenter, case- control study of lung cancer in nonsmokers. The main objective of this study was to provide an estimate of the risk of lung cancer from exposure to ETS in western European populations that would be more precise than estimates available at that time. Secondary objectives of the study were to address more detailed aspects of the association between ETS and lung cancer and to study the role of factors other than ETS in lung carcinogenesis in nonsmokers. The study was designed originally to have a statistical power of 80% to detect a relative risk of 1.3 (at a 5% level of statistical significance) for an exposure with a prevalence of 40% and a control-to-case subject ratio of 2 (required number of case subjects, 572). Herein, we report the principal findings of this study. Results of a study from Sweden that partially overlaps with ours have been published recently (13). Detailed results of our multicenter study, stratified by sex, age, center, and histologic type, are available from IARC1.