The Lie That Secondhand Smoke Causes Heart Disease

How the anti-smokers take indecent liberties with the evidence to deceive the public

The Montana Smoking Ban Heart Attack Study

This study was recycled from over a year before, and it is garbage because they don't even know if patients were exposed to secondhand smoke, nor whether they even spent any appreciable time in a smoke-free workplace (most heart attack victims are over 65 years of age)

Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. Richard P. Sargent, Robert M. Shepard, Stanton A. Glantz. BMJ 2004 Apr 24;328:977-980. Glantz's two co-authors were attending physicians at St Peter's Community Hospital in Helena, Montana, "a geographically isolated community with one hospital serving a population of 68 140." "The attending physician made the diagnosis at the time of discharge, and the hospital billing staff assigned the codes. (Two of the authors (RPS and RMS) were attending physicians for 18 of the 304 admissions included in this study and so assigned the diagnosis." [So, two of the authors were in a position to directly influence the admission rates. And the isolation they cite as a study strength makes collusion with others likely -cast] They admit that "We did not make any direct observations to measure how much exposure to secondhand smoke was reduced during the months when the law was in force. We do not know the prevalence of smoking in venues covered by ban, though the city-county health department reported that all but two businesses complied."

(Mont. Smoking Ban Cuts Heart Attacks. By Daniel Q. Haney, AP Medical Editor aka corrupt anti-smokers' whore. DATE: APRIL 1, 2003. [<= HINT: April Fool's Day.]) "Sargent, who with co-author Dr. Robert Shepard encouraged passage of the ordinance, presented the data Tuesday to applause at the annual scientific meeting in Chicago of the American College of Cardiology." They were presumably applauded for their willingness to commit fraud.

Even veteran anti-smokers such as G.C. Kabat reject this study. (Effect of Public Smoking Ban in Helena, Montana. Geoffrey C. Kabat. BMJ 2004 Jun 5;328(7452):1379.) "Firstly, the researchers had no information on whether exposure to second hand smoke changed as a result of the ban. They also did not present any information on whether smoking habits were affected by the ban. If the study was concerned to isolate an effect of second hand tobacco smoke, it should have been restricted to the 33% of the study population who were never smokers.... Finally, the "immediate effect" should make anyone stop and question the connection the authors are asserting. There are few interventions in public health that have such an immediate impact. Even if all active smokers in Helena had quit smoking for at least a year, one would not expect to see such a dramatic effect. The attempt to make claims about the effects of smoking bans based on this very weak ecological study raises disturbing questions about our ability to distinguish between sound science and wishful thinking." [This last is an understatement. The publication of a study such as this actually answers any questions about the willingness of anti-smokers in general and the British Medical Journal in particular to indulge in scientific fraud and misrepresentation, in order to push their political agenda -cast]

The alcohol hangover. JG Wiese, MG Shlipak, WS Browner. Ann Intern Med 2000 Jun 6;132(11):897-902. Hangover "may also be an independent risk factor for cardiac death" - considering its marked physical effects, this is a no-brainer.

The Pueblo, Colorado Smoking Ban Heart Attack Study - ditto

They don't even know if patients were exposed to either active or secondhand smoke, nor whether they even went to a bar. Furthermore:

"A critical piece of information is omitted from both the Pueblo Health Department press release and from the Campaign for Tobacco-Free Kids press release: that the expected number of heart attacks during the six-month period preceding the Pueblo smoking ban is substantially higher than the expected number of heart attacks during the six-month period after the Pueblo smoking ban. The reason for this is that the six-month period preceding the Pueblo smoking ban includes the winter months, while the six-month period following the Pueblo ban includes the summer months, and heart attack admissions during the winter have been shown to be substantially higher than during the summer. Since there were two winters and only one summer in the 18-month baseline period (before the smoking ban in Pueblo) and only one winter but two summers in the follow-up period (after the smoking ban), one would expect to see a decrease in the number of reported heart attacks, even in the absence of a smoking ban. In fact, there are 53% more cases of acute myocardial infarction (heart attacks) during the winter compared to the summer (see: Spencer FA, Goldberg RJ, Becker RC. Seasonal distribution of acute myocardial infarction in the Second National Registry of Myocardial Infarction. Journal of the American College of Cardiology 1998; 31:1226-1233). In the Mountain region of the country (which includes Colorado), there are 50.3% more heart attacks during the winter than the summer." (New Study Links Smoke-Free Ordinances to Fewer Heart Attacks. The Pueblo City-County Health Department. PR Newswire, Nov. 14, 2005; Premature Conclusions from Pueblo: More Information and More Research Needed Before Taking this to the Public. By Michael Siegel. Nov. 19, 2005.) The lie-spewing filth released this fraudulent "study" via press release, without access to original material, so we are forced to link to the anti-smokers' anointed "friend" of smokers, whose job is to sugar-coat their poison with fake sympathy. This is not merely "weak science," as he pretends; it is deliberate FRAUD.

See how the mass media misrepresented this flagrant fraud as a legitimate study, and handed the anti-smoking vermin a platform to spout their lies: "Dr. Donald Lavan, a cardiologist at the University of Pennsylvania and a heart association spokesman, called the study preliminary but important. 'We know that when people stop smoking, we start to see improvements in six months for the individual,' but this study shows the benefit to the community as well, he said. 'It reaffirms the fact that secondhand smoke is deleterious to all people,' Lavan said." (Study: Heart Attacks Drop With Smoking Ban. Nov. 14, 2005 (AP).

The Irish Smoking Ban

(Impact of a national smoking ban on the rate of admissions to hospital with acute coronary syndromes. E Cronin, P Kearney, P Sullivan. Presented at the annual scientific symposium of the European Society of Cardiology, 2007. Citation: European Heart Journal 2007;28(Abstract Supplement):585.)

Purpose: A ban on smoking in public places was introduced in Ireland on the 29th of March 2004. As both active and passive smoking are risk factors for coronary atherosclerosis, this might be expected to lead to a decrease in the number of patients presenting with acute coronary syndromes (ACS).

Methods: We analysed data collected in a continuous registry of all patients admitted to hospital with ACS in the south-western region, catchment population 620,525, to ascertain whether the ban has led to a decrease in the number of presentations to hospital with ACS.

Results: In the year ending 28th March 2004, there were 1277 admissions with ACS. In the year 29/03/2004 to 28/03/2005 there were 1092 admissions with ACS. This represents an absolute decline of 185, or 14.5%. The absolute decline was similar in males and females (15.6% and 12.0% respectively), but greater in smokers than in non-smokers (22.8% vs. 10.46%). The results are not accounted for by trends in hospital admissions with ACS in the preceding nine months.

Conclusions: A national ban on smoking in public places resulted in a decrease in admissions for ACS, especially in smokers. Our study provides evidence of the rapid effect of banning smoking in public places on decreasing the burden of ACS."

The lie-spewing media breathlessly proclaimed that "More than 17,000 heart attacks could be prevented in the UK after smoking in public places was banned, a conference heard yesterday. It could mean one in seven of the 123,000 heart attacks annually across the UK could be prevented if the results were replicated." Dr Edmond Cronin, of Cork University Hospital in Ireland, lied outright: "A national ban on smoking in public places resulted in a decrease in admissions for heart attack, especially in smokers. Our study provides evidence of the rapid effect of banning smoking in public places on decreasing the burden of heart attacks." (Smoking ban 'reduces heart attack rate'. By Rebecca Smith. The Telegraph, Sep. 5, 2007.)

These claims are a lie, because they used the admission rates of only nine months before as their baseline, and disregard the fact that a strong decline in heart disease deaths was already occurring, which began long before the smoking ban began on on March 29, 2004!

(Deaths from principal causes registered in the years 1998 to 2006. Central Statistics Office Ireland, accessed 9-5-07.)

The Reuters writer used the story as a pretext for a general spew-fest, but admitted that, "There was no significant change in heart attacks in the second year after the ban, indicating a possible step change in medical outcomes." (Heart attacks tumble after Irish smoking ban. By Ben Hirschler. Reuters, Sep 4, 2007.) Because actual heart disease deaths continued to decline during this period, the drop in admissions most likely reflects a "step change" in the admission policy, not the outcome! (For example, British doctors were historically less likely to admit patients for a heart attack than doctors in the U.S., with no difference in outcome.)

The Truth

Heart disease death rates have fallen steadily since 1961 to levels below those of the year 1900. (Fig. 1. In: Achievements in Public Health, 1900-1999: Decline in Deaths from Heart Disease and Stroke -- United States, 1900-1999. MMWR 1999 Aug 6;48(30):649-656.)

The decline in death rates since 1970 has been as large among smokers as among non-smokers: When the sharp decline in heart disease death rates began in the United States in the 1960s, it was the same in smokers as in non-smokers: "Nonsudden CHD death decreased by 64% (95% CI 50% to 74%, Ptrend<0.001), and SCD rates decreased by 49% (95% CI 28% to 64%, Ptrend<0.001). These trends were seen in men and women, in subjects with and without a prior history of CHD, and in smokers and nonsmokers." (Temporal trends in coronary heart disease mortality and sudden cardiac death from 1950 to 1999: the Framingham Heart Study. CS Fox, JC Evans, MG Larson, WB Kannel, D Levy. Circulation 2004 Aug 3;110(5):522-527.) The decline in cigarette smoking has been much greater in middle-aged men than in middle-aged women, which is not at all in accord with the equivalence in the decline in mortality for the sexes. And the decline began before any significant number of smoking bans.

For socioeconomic reasons, smokers and passive smokers are more likely to have been exposed to infectious causes of heart disease, such as cytomegalovirus. The anti-smokers' studies deliberately ignore the role of infection, in order to falsely blame active smoking and secondhand smoke for the excess. This is the reason that the pretended effects of secondhand smoke are so similar to the pretended effects of active smoking.

The "Heart Rate Variabilty" Scam

Effects of passive smoking on heart rate variability, heart rate and blood pressure: an observational study. D Felber Dietrich, J Schwartz, C Schindler, JM Gaspoz, JC Barthélémy, JM Tschopp, F Roche, A von Eckardstein, O Brändli, P Leuenberger, DR Gold, U Ackermann-Liebrich. Int J of Epidemiol 2007;36(4):834-840. [This is a Joel Schwartz/Harvard School of Public Health study, which means that they grind an ax promoting hysteria about particulates, and always ignore infection.] This study claimed to find lower LF power (~199 vs. ~234 ms²), higher heart rate (~75.3 vs. ~73.4 bpm), and higher diastolic blood pressure (~83.3 vs. ~81.8 mmHg) in ETS-exposed >2h/d vs. nonexposed subjects (estimated from Fig. 2). However, these are not the direct measurements of those values, they have all been jiggered by being "adjusted for study site, sex, age, education, BMI, diabetes and beta-blocker intake."

They claim that "Our study provides further evidence that ETS exposure is associated with cardiac autonomic dysregulation, which may be an intermediate step in the pathway to cardiac instability;" and that "LF, which is considered to represent both sympathetic and parasympathetic activities, was lower in subjects with higher ETS exposure. We also observed ETS-associated increases in heart rate and, more weakly, in DBP, consistent with increases in sympathetic stimulation." [Except that this claim that LF is associated with cardiac sympathetic innervation and function is bogus: "Several previous investigations have cast doubt on the validity of LF power as a measure of sympathetic activity, because of dissociations between LF power and cardiac norepinephrine spillover, directly recorded sympathetic nerve traffic, and plasma norepinephrine levels (4,6,23). Such dissociations are especially glaring in patients with congestive heart failure, which is characterized by decreased LF power (11) despite marked cardiac sympathetic activation." Moak, 2007].

This study admits that the small differences between ETS-exposed and non-exposed subjects were present 24 hours a day (i.e., when no exposure to ETS occurred): "Since few people are exposed to ETS during sleep, we restricted analyses to the sleep period, when acute exposure can be excluded and found results similar to those of the 24-h measures. Therefore, we think that our findings do not reflect acute responses." But, when the same differences are present during non-exposure as during acute exposure, the only conclusion that could legitimately be drawn is that ETS exposure does not produce those differences in the first place. However, rather than making the valid deduction that those differences were probably due to small pre-existing differences in health conditions between the exposed and the non-exposed subjects which were not accounted for in their analysis, these charlatans spout pseudo-scientific mumbo-jumbo:

"ETS may affect autonomic control of the heart through activation of neural receptors of the respiratory tract. On the other hand, gaseous components, soluble fractions of the particulate component and ultrafine particle components of ETS may be absorbed in the lung and have additional systemic effects. In the experimental setting, chronic ETS exposure has been shown to increase proinflammatory cytokines and arterial resistance, to decrease concentrations of antioxidants and to increase lipid peroxidation. We found no evidence of ETS-associated increases in inflammation as measured by CRP and other causal mechanisms may predominate with low-grade chronic exposure. Recent work by Bartoli and colleagues suggests that particle exposures alter barometric reflexes, a pathway through which ETS exposure might also influence HRV. Ultrafine particles are associated with oxidative stress, as well as with reduced HRV." This is nothing but a snow job! They are trying to make people believe in an effect which they could not demonstrate exists in the first place!

Eating Causes Heart Rate Changes

Periprandial changes of the sympathetic-parasympathetic balance related to perceived satiety in humans. LF Harthoorn, E Dransfield. Eur J Appl Physiol 2008 Mar;102(5):601-608. "Subjects were exposed to a lunch-inducedhunger-satiety shift, while profiling diverse sensory, physiological, and biochemical characteristics at 15 min intervals.... Finally, neither chewing nor swallowing contributed to a heart rate increase at food consumption, but orosensory stimulation, as tested with modified sham feeding, caused a partial increase of heart rate."

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cast 02-02-08