First, we shall present the article and/or study that has been submitted which fosters self-serving jubilation in the anti-smoking community. 

Following this we will proceed to shed light on the inaccuracies and meaningless results of the studies.

"Secondhand smoke kills, according to a new study!," is frantically shouted from the bold type headlines of newspapers and magazine articles. Mostly it is uneducated and/or issue biased newspaper reporters who add the hype to the already deceitful study. Either they don't bother to read the study for themselves (or they do and don't understand the scientific implications), relying on misleading statements from the researchers themselves, or they are far more interested in the fear mongering factor that makes for good reading and do not bother to check with anyone how accurate or reliable a study is. Not to mention it is more politically correct to nod their head yes and insert their own views and conclusions based on the scary sounding research title and bits of information that they have heard. 

Whether it is a reporter with no concept of what it is they are actually reporting, simply relaying the study du jour, or a health organization or researcher submitting a report, none of what they say can be taken at face value.  News reports are manipulated and then hyped, as are practically all of the studies on secondhand smoke. Smokers or non-smokers who want to see accurate scientific data on the issue of tobacco smoke are not going to get it from the media, politicians or public health officials. 

Here we will look at the current secondhand smoke releases and discuss the junk science, the media lies and omissions and the research manipulation and press releases intended to attain more support for their smoke-free agenda.  


Globe and Mail Article, July 12, 2001 - Secondhand smoke can triple risk of  
    lung cancer 

The Centers for Disease Control, March 21, 2001 - National Report on Human 
    Exposure to Environmental Chemicals 

Associated Press, July 24, 2001 - Study Finds Even Limited Exposure to 
    Secondhand Smoke Can Harm Arteries 

National Post OnLine, February 21, 2002 - Second-hand smoke linked to crib 
   death, report shows 

PRNewswire, June 19, 2002 - IARC Monographs Programme Declares 
    Second-Hand Tobacco Smoke Carcinogenic To Humans 

Associated Press, July 31, 2002 - Researcher hoping for big changes from  
    study tying second-hand smoke to feline lymphoma 

United Press International, March 11, 2003 - Smoking linked to cavities in 

WebMD, April 1, 2003 - Smoking Ban Saves Lives in Montana Town 

BBC News, February 11, 2004 - Smoking 'a blight on fertility' 

Circulation, May 2005 - Cardiovascular Effects of Secondhand Smoke  
Nearly as Large as Smoking 



Secondhand smoke can triple risk of lung cancer


Secondhand smoke can triple risk of lung cancer 
 Source: Globe and Mail, July 12, 2001 Region: CANADA
People who are routinely exposed to a lot of secondhand smoke, such as workers in bars and restaurants, can see their risk of lung cancer triple, a new study says. The Canadian study provides some of the most compelling scientific evidence yet for a total ban on workplace smoking, including bars and restaurants.
The research, published in the International Journal of Cancer, found that the greater the amount of smoke in a workplace, the greater the risks. "These data absolutely back a smoking ban in all workplaces, including bars," said Dr. Kenneth Johnson, senior epidemiologist at the surveillance and risk-assessment division of Health Canada and the lead researcher. 

Dr. Roberta Ferrence, director of the Ontario Tobacco Research Unit, said, "What's important about this research is it demonstrates a dose-response: The more exposure you have, the higher your risk. "While this may seem obvious, it has long been contested by the tobacco industry." Dr. Ferrence said she hopes that this "strong new evidence will prompt strong new action" to expand smokefree workplace laws.

"There's an underlying [belief] that secondhand smoke increases your risk of developing lung cancer by 20-25 per cent, and maybe that can be explained away by publication bias," Dr. Johnson said. "But when you see the risk rising by 75 per cent right up to a tripling of the risk, it's hard to argue that nothing is going on."
The new research found that when the number of "occupational smoker years" (the number of smokers in the workplace multiplied by the worker's years of service) reaches 26, the risk of lung cancer has doubled. (That could mean two smoking co-workers over 13 years or five smoking co-workers over five years. It could also mean 26 customers daily for a year in a bar.) When researchers looked at the upper third of workers -- those exposed to the most secondhand smoke -- they found the lung cancer risk was more than tripled.
Since the early 1980s, more than three dozen studies have examined the impact of secondhand smoke on non-smokers, but the Health Canada research is the first original Canadian data.
In the International Journal of Cancer, Dr. Johnson wrote that it is not surprising to see higher risks associated with workplace exposure because studies have consistently demonstrated that the intensity of exposure is higher on the job than at home. The level of nicotine in the air of bars is up to 15 times higher than in the home of a smoker.
Discussion on this article to be followed by the actual study abstract:

The author of this article, Mr. Picard, seems to have missed or intentionally has failed to include the following statement from the study:

"Although more years of and more intense residential passive smoke exposure tended to be associated with higher risk estimates, no clear dose-response relationship was evident."

Mr. Picard, supposedly a qualified Health Reporter, added, "[the study] provides some of the most compelling scientific evidence yet for a total ban on workplace smoking, including bars and restaurants.”

It does?  THE most compelling evidence? On the contrary, not one of the findings presented in this study reached statistical significance. Including the “dose-response” findings (increased risk with increased exposure). In fact, one of the tables shows that the risk DECREASED with increased exposure.

How would Picard explain that?

For further discussion pertaining to this article, Martha Perske, known for her meticulous and exacting work uncovering the corruption of scientific and statistical data by anti-smoking funds-motivated scientists and institutions, adds her astonishment and keen-eyed observations in the SpeakEasyForum.
She continues to take another reporter to task for his rendition of this study in the Chattanooga (TN) Times & Free Press: 

Dear Edward Colby: 

Lesson No. 1 in reporting on a study is that you give all relevant data, which you failed do in the case of the Canadian study.  I refer to your article, “Study finds more evidence of secondhand smoke harm,” published in the Chattanooga (TN) Times & Free Press, July 18, 2001.  

Your alarmist claim that the lung cancer risk for nonsmokers working with smokers “climbs steadily over time and increases based on the number of smokers in the workplace” is not supported by some of the results in Table III of the Canadian study.  Contrary to your claim, results presented in Table III show that the risk for those exposed to the MOST secondhand smoke in the workplace (64 or more smoker years) is LESS than for those exposed to 26-64 smoker years.  The odds ratio for exposure to 26-64 smoker years is 1.98 – but for 64 or more smoker years it drops to 1.58. 

Why did you not mention that? 

Again, contrary to your claim that the risk increases with increased exposure, this study shows a consistent DECREASE in risk with increased exposure for nonsmokers living and working with smokers.  It’s right there, plain as day, if you had bothered to look.   The odds ratios for nonsmokers living and working with smokers for 1-24 years, 25-45 years, and 46 or more years are, respectively, 1.46, 1.40, and 1.35. 

Surely, such a decreased risk with increased exposure is newsworthy, but not one word from you about it. 

Likewise, not one word from you about the study authors’ cautionary statement that the small number of cases in this study “precludes drawing strong conclusions.” 

In fact, Mr. Colby, not one of the findings reported in this study is statistically significant. 

The fact that you did not report all relevant data from this study is being widely circulated via the Internet.  It falls under the category of biased and sloppy reporting and does not speak well for you or your newspaper. 


It's time now to take a look at the actual abstract of the study which either Picard did not do or simply decided to pull a fast one on the public:

Epidemiology and Cancer Prevention 
Lifetime residential and workplace exposure to environmental tobacco smoke and lung cancer in never-smoking women, Canada 1994-97  


Although the risk of lung cancer among never-smokers living with a spouse who smokes has been extensively studied, the impact of lifetime residential and workplace environmental tobacco smoke has received less attention. As part of a large population-based case-control study of lung cancer, we collected lifetime residential and occupational passive smoking information from 71 women with lung cancer and 761 healthy control subjects, all of whom reported being lifetime 
nonsmokers. The adjusted odds ratio (OR) for lung cancer associated with residential passive exposure only was 1.21 (95% confidence interval [CI] 0.5-2.8). Although more years of and more intense residential passive smoke exposure tended to be associated with higher risk estimates, no clear dose-response relationship was evident. The OR for women with passive 
exposure as a child and as an adult was 1.63 (95% CI 0.8-3.5) and for those only exposed as an adult 1.20 (95%CI 0.5-3.0). Exposure to environmental tobacco smoke only in the workplace was associated with an adjusted OR of 1.27 (95% CI 0.4-4.0). Risks associated with increasing occupational exposure year tertiles were 1.24, 1.71 and 1.71. Total smoker-years of residential and occupational exposure combined resulted in a statistically significant trend (linear test for trend p = 0.05) with ORs for tertiles of exposure of 0.83, 1.54 and 1.82. Our results are consistent with the literature suggesting that long-term, regular exposure to either residential or occupational environmental tobacco smoke is associated with increased lung cancer risk in never-smoking women. © 2001 Wiley-Liss, Inc. 

Received: 27 December 2000; Revised: 2 April 2001; Accepted: 4 April 2001 


Rather than bore you with an essay-like response to this paper, which can lead to a loss of interest, we take you behind the scenes of a real life debate between those who are extremely knowledgeable in the science of epidemiology and those who question their findings and educated opinions.  They proceed to debunk this study posthaste because it is just that bad.  We follow up with another critique by Martha Perske.

Mr. Lauren Colby, an attorney and author of In Defense of Smokers, has studied the tobacco issue, including secondhand smoke studies, intensely for many years.  He is quite qualified to carry on this debate as are some others who have taken the time to become educated in the field of epidemiology and the application of scientific standards.

*This is a colorful insight as to how bias turns so many deaf and blind to the facts:

Smokers' Rights Advocate

 [saying nothing posts Globe And Mail article for review]
 The confidence intervals all straddle 1.0, which means those claims are NOT 
statistically significant. The study proved NOTHING. Any 
claim after this point is a display of incredible chutzpah. 

You don't have to believe me. Go ask a statistician. 

Paul Smith: Sorry, Fork.  Everyone is entitled to an opinion.  Frankly, I'll take the 
IJC's word for it. 

Believe me, I don't believe you.  Do you wonder why?

Jlfork: Because you're a fanatic, I guess. 
I'd think that you'd at least want to find out what a confidence interval is. 
Look it up - it won't take long. When dealing with odds ratios (ORs), the magic 
number is 1.0, the null hypothesis (i.e., no effect). If you can get your CI 
completely above 1.0, you have at least a claim on the effect (although many 
other factors come into that assessment). If the interval is completely below 
1.0, you have an inverse correlation (with the same qualifications). But if the 
interval straddles (or even includes) 1.0, you have squat. That's officially 
called "not significant." This is common for small sample size, which even the 
study authors admitted to. And to claim an upper bound of a CI as the figure of 
merit is either ignorance or deliberate deceit.  (There's another problem with 
retrospective studies and recall bias, particularly when both researchers and 
subjects are eager to cast blame, but we don't have to go that far to dismiss 
these results.) 
Like I said, go ask a statistician. Call an instructor at a local college. Go 
ahead - I dare you.
Larry Colby:  Furthermore, this was a retrospective study. 71 never smoking women with lung 
cancer and 761 healthy, never smoking controls were asked to remember the extent 
of their exposure to second hand smoke. Such studies ALWAYS introduce recall 
bias: the tendency of the lung cancer victims to "remember" (or think that they 
remember) more exposure to smoke than is remembered by the controls. 

At the time of the 1964 Surgeon General's Report, the SG's Committee vowed not 
to use retrospective studies because of the element of recall bias (although, 
perhaps inadvertently, they wound up using quite a bit of retrospective data). 

Given the well known and long recognized problems with these retrospective 
studies, it's surprising that any reputable scientist would take them seriously. 
But this study was funded by the Canadian government, which has an anti-smoking 
bias (see Chapter 6 of my book, on the "LaLonde effect"). They don't care if the 
study is accurate, so long as it scares people into quitting smoking.It isn't necessary that studies prove or disprove anything. 

Paul Smith: Studies support or reject a hypothesis or theory.  This study supports the theory that ETS 
is a causative factor for Lung Cancer and that makes it a worthwhile study.
Larry Colby: The study supports nothing of the kind. At most, it demonstrates that lung 
cancer victims will remember or think that they remember more exposure to second 
hand smoke than people who are not lung cancer victims. That's called "recall 
bias" and is the reason why retrospective studies of this sort are worthless.
Paul Smith: Worthless to who?  Somebody funded the study and found the results useful 
enough to publish.  While it proves nothing, it does support the growing 
body of evidence that ETS is harmful.  Smokers bitch about the uselessness 
or the inaccuracy or the poor design of studies and point out their 
deficiencies but studies continue to be done and they continue to support 
the need for a ban on ETS.
Larry Colby: The only way to remove recall bias is to conduct a prospective study over a 
period of many years, repeatedly interviewing the participants to determine 
their current exposure to primary or secondary smoke, and keeping track of the 
number of lung cancer cases that occur. Doll started out to do something like 
that with his study of British doctors, but his study was thrown off track when, 
in the first few years of the study, practically all of the doctors quit smoking 
Paul Smith:  As I recall, the study indicated that, even taking such confounders into 
consideration, the study still implicated ETS.  Not scientific proof but it 
goes to the preponderance of the evidence overall.
Larry Colby: With all due respect, there is no way in the world to "correct" for recall bias! 
Even if you were studying primary smokers, you'd have to establish a baseline by 
studying the actual smoking habits of the smokers for many, many years, and then 
finding out how much those who fell victim to lung cancer exaggerated, upon 
recollection, the amount that they had actually smoked. The same would be true 
of those exposed to passive smoke, but in that case, the problem is even more 
formidable because you are dealing with somebody's recollection of somebody 
else's smoking habits, over a period of many years. 

It's totally impossible, which is why retrospective studies are worthless.

Paul Smith: I'm so sorry, Larry.  You are obviously correct.  You do, of course, know 
better than the experts, the scientists doing the studies.  I'm sure that 
the readership has noted your expertise and will ignore everything science 
and medicine says from now on.
Larry Colby: Just because somebody has a PH.D. attached to his name doesn't mean that he 
can't make mistakes. Doing a study based upon recall bias is a mistake.
Paul Smith: If so, I cannot fathom that the study would have been frowned upon by 
his/her peers and roundly chastised.  Certainly it wouldn't get published. 
Son of a gun, that doesn't seem to have happened.
Alex: You are singularly naive about the realities of acedemia. 
Any study which appears to confirm current thinking and theories will 
pass peer review.  Nor is the purpose of peer review to determine the 
correctness of the results presented in the stuides, but merely to ensure 
that certain guidelines for scientific procedure have been followed. 
IOW, as long as the formalities have been satisfied, any study could have 
been written by the researcher's dog and it would be passed.
Paul Smith: Oh, you're absolutely correct, Alex.  The studies were a waste of time and 
simply put food on the table and clothes on the back of scientists' 
families.  How silly of me to have missed that.  You are such a smart man, I 
should have known better to take the scientific word over yours.
Larry Colby: These Canadian studies are an example of the LaLonde effect. Marc LaLonde was 
formerly the Canadian Minister of National Health and Welfare. He argued that 
health messages should be vigorously disseminated, and should be "loud, clear 
and unequivocal", even if unsupported by scientific evidence. If a particular 
study showed that smoking might be related to a particular disease, it made no 
difference to him whether the study was seriously flawed, or not. He felt that 
releasing the study was always justified, if it would convince people to stop 
smoking, since everybody knew that smoking was unhealthy.
Paul Smith: There is a HUGE difference between science and politics.  If a politician 
wants to tout bad science, he flirts with the likes of you who just love to 
very publically prove them wrong but they will do it because the ends 
justify the means.  For a scientist to publish tripe to his peers, however, 
is suicide.
Larry Colby: Tripe gets published all the time! Auerbach got his experiment on the beagles 
(in which he "sort of" claimed to have induced lung cancer in the dogs by 
training them to smoke through tracheotomies) published in a scientific journal, 
but, in 40 years, nobody has ever been able to duplicate his results. The cold 
fusion experiments were published in a scientific journal, but nobody has been 
able to duplicate them, either.  The studies that resulted in a ban on DDT were 
published in scientific journals but many scientists now believe that the 
studies were flawed. The journals are full of studies by scientists who believe 
in global warming and others who don't.
*Source of Dialogue:  alt.smokers Newsgroup

Again, to sew things up, we present Martha Perske with a rough draft analysis of the study:

"The results (odds ratios) presented in the Abstract are not statistically significant.

"In every single case, the LOWER number of the confidence interval is below 1.0.

"For example, the odds ratio of 1.21 (a 21% increased risk) from exposure to ETS in the home is followed by a confidence interval of 0.5 to 2.8. Since the lower number (0.5) is below 1.0, this means the finding was not statistically significant.

"Only when BOTH numbers of the confidence interval are above 1.0 is it statistically significant. For example, a confidence interval of 1.5 to 2.8 would be statistically significant.

"Not one of the findings presented in this study reached statistical significance. Including the “dose-response” findings (increased risk with increased exposure). In fact, one of the tables shows that the risk DECREASED with increased exposure.

"Plus, the entire study was based on only 71 cases of nonsmokers with lung cancer. When findings were broken down into subsets the number was even smaller, in some cases only 7.

"Picard [Globe article author] claims “The new research found that when the number of ‘occupational smoker years'...reaches 26, the risk of lung cancer has doubled...When researchers looked at the upper third of workers – those exposed to the most second-hand smoke – they found the lung cancer risk was more than tripled.”

"Okay. So I go to Table III of the study where results are given for 'occupational smoker years' which Picard referred to. Results are given in terms of odds ratios.

"Well, here’s what I find: First off, not one of the increased risks (odds ratios) is statistically significant.

"Second, the odds ratios show a most implausible thing - the reported risk for exposure to 64 or more occupational smoker years was LESS than exposure to 26-64 years.

"Here are the results as reported in the study:

                    Exposure to 1-25 smoker years: Odds ratio 1.16 (based on 10 cases)
                    Exposure to 26-64 smoker years: Odds ratio 1.98 (based on 14 cases)
                    Exposure to 64 or more smoker years: Odds ratio 1.58 (based on 14 cases)

                    (“Occupational smoker years” is defined as the number of employees who smoked
                    regularly in the subject’s immediate work area multiplied by the number of years the
                    subject worked at that job. In other words, if the subject worked with 5 smokers for 10
                    years it would be 50 smoker years.)"

Read more from Martha Perske in her ongoing struggle to obtain a response from the Globe & Mail regarding their unprofessional reporting.  Her subsequent correspondence can be read at

National Report on Human Exposure to Environmental Chemicals


March 21, 2001 
National Report on Human Exposure to Environmental Chemicals

New CDC Chemical Exposure Report Begins to Fill Critical 
Information Gaps in Environmental Health for the U.S. 

            Data Show Exposure to Environmental Tobacco Smoke Down 
                    Dramatically and Levels of Blood Lead Continuing to Decline  

                    The Centers for Disease Control and Prevention (CDC) today 
                    released the first National Report on Human Exposure to 
                    Environmental Chemicals, an important new research tool that will 
                    provide better information on levels of exposure to environmental 
                    chemicals, and, over time, what these levels mean for public health 

                    Advances in a technology known as biomonitoring allow CDC to 
                    measure chemicals directly in blood and urine samples rather than 
                    to estimate population exposures by measuring air, water, or soil 
                    samples. On the basis of this scientific advancement, the new 
                    report provides data on actual levels of chemicals in humans. As 
                    data are collected over the years, researchers will be better able 
                    to determine possible health effects and design appropriate public 
                    health strategies. 

                    "This new resource is a significant development in the field of 
                    environmental health," said Health and Human Services Secretary 
                    Tommy G. Thompson. "It will help us to better track the exposures 
                    of Americans to chemicals in the environment and to measure the 
                    effectiveness of our public health efforts." 

                    This first Report initially measures the exposure of the U.S. 
                    population to 27 environmental chemicals. The Report includes 
                    metals (e.g., lead and mercury), pesticide metabolites, phthalate 
                    metabolites, and cotinine (which tracks exposure to tobacco 
                   smoke). Levels of environmental chemicals were measured in blood 
                    and urine samples collected from participants in CDC's National 
                    Health and Nutrition Examination Survey (NHANES) ---  an ongoing 
                    national health survey of the U.S. population. The Report provides 
                    results from the 1999 survey; data from future years will help 
                    confirm these findings. 

                    "The Report is a major step toward assessing in the U.S. population 
                    which environmental chemicals are present in blood and urine 
                    samples, who is exposed, trends in exposure over time, and 
                    whether interventions to reduce exposure are working," said 
                    Richard J. Jackson, MD, MPH, Director of CDC's National Center for 
                    Environmental Health (NCEH). 

                    Although the report does not include new information on health 
                    risks of exposures or on potential routes of exposures, this is the 
                    first time that national exposure levels of the U.S. population are 
                    known for 24 of these 27 chemicals. CDC previously assessed the 
                    population's exposure to three substances --- lead, cadmium, and 
                    cotinine. The Report provides new data for the 1999 calendar year. 
                    Previously, only limited data were available on which environmental 
                    chemicals were in the U.S. population and at what levels. 

                    The presence of a chemical in blood or urine does not necessarily 
                    indicate that the chemical will cause disease. Additional research is 
                    required to determine whether the levels reported are a cause for 
                    health concern. 

                   The first Report provides information on the exposure of the U.S. 
                    population to these 27 chemicals. The chemicals, grouped into four 
                    categories, are as follows: 

                         Metals: lead, mercury, cadmium, cobalt, antimony, barium, 
                         beryllium, cesium, molybdenum, platinum, thallium, tungsten, 
                         and uranium. 
                         Tobacco smoke: cotinine --- a metabolite of nicotine that 
                         tracks tobacco smoke exposure. 
                         Organophosphate pesticides (Six metabolite 
                         measurements representing exposure to 28 pesticides): 
                         dimethylphosphate, dimethylthiophosphate, 
                         dimethyldithiophosphate, diethylphosphate, 
                         diethylthiophosphate, and diethyldithiophosphate. These 
                         metabolites are generally formed by the breakdown of 28 
                         pesticides, including chlorpyrifos, diazinon, fenthion, 
                         malathion, parathion, disulfoton, phosmet, phorate, 
                         temephos, and methyl parathion. 
                          Phthalate metabolites: mono-ethyl phthalate, mono-butyl 
                         phthalate, mono-2-ethylhexyl phthalate, mono-cyclohexyl 
                         phthalate, mono-n-octyl phthalate, mono-isononyl phthalate, 
                         and mono-benzyl phthalate. 

                    Highlights of the Report 

                    Cotinine is a breakdown product of nicotine after it enters the 
                    body. Levels of cotinine in the body track the amount of exposure 
                    a person has to tobacco smoke. For a nonsmoker, cotinine tracks 
                    exposure to environmental tobacco smoke. CDC measured cotinine 
                    in nonsmokers in the U.S. population as part of a previous survey, 
                    and the Report presents new cotinine data for 1999. 

                    “One significant finding was the more than 75% decrease in serum 
                    cotinine levels for nonsmokers in the United States," said Jim Pirkle 
                    MD, PhD, of CDC’s Environmental Laboratory and coauthor of the 
                    Report. “This decrease documents a dramatic reduction in exposure 
                    of the U.S. population to environmental tobacco smoke since 1991. 
                    However, environmental tobacco smoke remains a major public 
                    health concern since more than half of American youth continue to 
                    be exposed to this known human carcinogen.” 

                    CDC has been measuring the population’s exposure to lead since 
                    1976 through the NHANES surveys. CDC’s Childhood Lead Poisoning 
                    Prevention Program ( works to 
                    reduce exposure of children in the United States to lead. The 
                    Report presents measurements of levels of lead in blood for U.S. 
                    children in 1999. 

                    “The good news is that blood lead levels continue to decline among 
                    children overall,” said Eric Sampson, PhD, of CDC’s Environmental 
                    Laboratory and also a coauthor of the Report.  “However, other 
                    data show that children living in environments placing them at high 
                    risk for lead exposure remain a major public health concern.” 

                    Next Steps 
                    Environmental health is one of the "Leading Health Indicators" in 
                    the U.S. government publication,  Healthy People 2010. Information 
                    on environmental chemical exposures will assist clinicians and public 
                    health officials to better understand the relationship between toxic 
                    exposures and health consequences and will help guide public 
                    health prevention efforts. CDC will add other substances to future 
                    reports on the basis of data obtained from samples collected in 
                    subsequent NHANES surveys. CDC will continue to measure the 27 
                    original substances as well. The goal over the next few years is to 
                    expand the Report to provide information about 100 chemicals. CDC 
                    will monitor trends over time that may help scientists better 
                    understand the impact of environmental chemicals on our health. In 
                    the future, CDC will be able to report exposure levels for more 
                    specific population groups (e.g., children, minority populations, or 
                    women of childbearing age). 

                    In addition, CDC will expand the Report to include exposure data 
                    from studies of people exposed from localized or point-source 
                    exposures (e.g., data on levels of mercury in people who eat 
                    mercury-contaminated fish from a polluted river). For more 
                    information on the Report data, log onto 
           or call 1-866-670-6052. 

                    CDC protects people’s health and safety by preventing and 
                    controlling diseases and injuries; enhances health decisions by 
                    providing credible information on critical health issues; and 
                    promotes healthy living through strong partnerships with local, 
                    national, and international organizations. 

Discussion on this article:  NONE  All discussion to follow STUDY ABSTRACT
CDC ABSTRACT on Findings of Exposure to Cotinine:
Major Findings 

Reduced Exposure of the U.S. Population to Environmental 
Tobacco Smoke 

                    Cotinine is a metabolite of nicotine that tracks exposure to 
                    environmental tobacco smoke (ETS) among nonsmokers; higher 
                    cotinine levels reflect more exposure to ETS. ETS has been 
                    identified as a known human carcinogen. From 1988 through 1991, 
                    as part of the NHANES III survey, CDC determined that the median 
                    level (50th percentile) of cotinine among nonsmokers in the United 
                    States was 0.20 nanograms per milliliter (ng/mL).  Results from the 
                    1999 Report showed that the median cotinine level among people 
                    aged 3 years and older has decreased to less than 0.050 
                    ng/mL-more than a 75% decrease. This reduction in cotinine levels 
                    objectively documents a dramatic reduction in exposure of the 
                    general U.S. population to environmental tobacco smoke since the 
                    period 1988-1991.  However, since more than half of American 
                   youth are still exposed, ETS remains a major public health concern. 

The Report--Major Findings  
           The Report-- Overview 
           The Report-- Results  
           The Report Summary (a PDF file) 
           The Complete Report (a PDF file) 
           The Frequently asked Questions (FAQs) 
           Related Links 

Discussion:  QUESTION - Do the ends justify the effort?

The Centers for Disease Control released the first National Report on Human Exposure to Environmental Chemicals. In a Press Release dated March 21, 2001 they chirped about their new project to measure the amount of 27 chemicals in urine and blood, "a new research tool that will provide better information on levels of exposure to environmental chemicals, and, over time, what these levels mean for public health."

They go on to report a 75% decrease in cotinine levels (a metabolite of nicotine that tracks tobacco smoke exposure).  Judging from the following statement, we can only assume that they are comparing 1999 to 1991, "This decrease documents a dramatic reduction in exposure of the U.S. population to environmental tobacco smoke since 1991."  Well, sure there is a decrease.  In 1991 people were still smoking in their workplace and in most restaurants.  People were still smoking practically everywhere before the health fanatics put an end to that with smoking bans almost everywhere sometime around 1995.  Big surprise!  What on earth are they crowing about?  How to waste our money on silly reports?

One wonders though how they know what the decrease is if they are using random subjects.  Wouldn't it be more substantial if they assessed the same people each time?

Aside from any argument about how much smoking is actually occuring in public areas, the more important questions related to this decrease is how substantial was the exposure prior to reporting a decrease and, once that is understood, what are they actually trying to accomplish by studying this chemical exposure?

Included in their Press Release is the most telling statement of all:

"The presence of a chemical in blood or urine does not necessarily indicate that the chemical will cause disease. Additional research is required to determine whether the levels reported are a cause for health concern."

Now that we finally have it...  that the mere presence of a chemical does not automatically lead to illness, one must also note that not only is that true, but it is a huge understatement in regard to their cotinine measurements:

"From 1988 through 1991, as part of the NHANES III survey, CDC determined that the median level (50th percentile) of cotinine among nonsmokers in the United States was 0.20 nanograms per milliliter (ng/mL).  Results from the 1999 Report showed that the median cotinine level among people aged 3 years and older has decreased to less than 0.050 ng/mL-more than a 75% decrease."

NANOGRAMS!!  Not even a whole nanogram which means they're avoiding using the term PICOGRAM!

Most people are not familiar with these terms in weight and where they fall on the scale.  Here is a weight chart in order to make more sense of just where these weights fall in the grand scheme of things:

          1 gram (g) = 1000 milligrams (mg)
          1 milligram (mg) = 1000 microgram (ug)
          1 microgram (ug) = 1000 nanogram (ng)
          1 nanogram (ng) = 1000 picogram (pg)

To further enhance some visual aid you might require to fathom these measurements, picture a grain of salt.

A grain of salt weighs 100,000 nanograms or 100,000,000 picograms.

We'll proceed to make some conversions in order to bring the full picture into view (keep in mind that we are using their own figures that cotinine levels among nonsmokers in the United States is now 0.05 nanograms per milliliter):

1.  We needed  to convert their decimalized nanograms ( into picograms) (which is really what it is) and did the following:

     One twentieth (.05) of a nanogram (one nanogram being equal to 1000 picograms) is 50 picograms
     [formula: 1000/20=50]

2.  The average weight of a grain of salt is 0.10mg or 0.00010g. (It may vary a little but not enough to make much of a difference when considering such infintismal weights).

Then we had to convert the milligrams into picograms (with the help of the conversion chart):

      One tenth (0.10) of a milligram (one milligram being equal to1000 micrograms) is 100 micrograms.
      [formula: 1000/10=100]

      100 micrograms (a microgram being equal to 1000 nanograms) is100,000 nanograms
      [formula: 100*1000=100,000]

      100,000 nanograms (one nanogram being equal to 1000 picograms) is 100,000,000 picograms
      [formula: 100,000*1000=100,000,000]

Ergo a grain of salt weighs 100,000 nanograms or 100,000,000 picograms.

3.  Next, the study uses milliliters of blood instead of liters ("nanograms per milliliters").  The normal human adult has approximately 5-6 liters of blood in his body.

Since the study is talking more about kids we went with the lower end of 5 and calculated this:

      1 liter = 1000 milliliters
      5 liters x 1000 milliliters = 5000 milliliters

4.  Before reaching the finish line, I wanted to confirm their "75% decrease":

      200 picograms (.20 nanograms) to 50 picograms (.05 nanograms) = difference of 150 which is 75% of 200

5.  We can finally figure out how many nanograms/picograms per entire human blood supply they're really talking about in their given study:

      .05 nanograms x 5000 milliliters = 250 nanograms or 250,000 picograms (End result of their equation of

Our final argument?

That on average, a grain of salt weighs 100,000 nanograms (returning to the larger weight unit).

Their study concludes that the body takes in 250 nanograms of cotinine in comparison.

How ridiculous is that miniscule amount to consider as having a "harmful effect?"

More importantly, before they even saw a reduction of 75%, consider this.  Did .20 nanograms of cotinine in a person's system mean anything of concern to begin with?  That would be 1000 nanograms.
99,000 nanograms less than a grain of salt!

Be especially aware of this trick when you hear a report claiming an increase and the scream, "Something must be done!"  It's just as unmeaningful as it is the other way around.

If only they would adhere to their own scientific standards when it comes to the issue of secondhand smoke, we wouldn't be bombarded with meaningless studies and unnecessary projects that waste the taxpayers' money in order to inflict their version of correct behavior on the unwitting public:

American Council on Science and Health (ACSH)
"The presence in the body of a trace chemical generally signifies occupational or lifestyle-related exposure to that substance. Such a presence alone should not be overinterpreted as necessarily injurious to health, however. For the vast majority of exogenous chemicals (chemicals originating outside the body), there is no evidence to suggest that trace concentrations in the body present a risk to human health."
And for those who scoff at the argument that if ETS is so dangerous then smokers, who are not only exposing themselves to mainstream smoke (directly inhaled) but also to their sidestream smoke should be dropping dead at a greater rate than currently calculated, need to take into account that if the measurement of harm, according to all the health agencies,  is dependant upon the cotinine level in the body of the nonsmoker, which the CDc reports is between <1 ng (typical) - 15 ng (heavy), then it should stand to reason that if smokers always have levels of cotinine higher than 15 ng, up to 500 ng, we should be long dead even before their current estimates for smokers.
The Centers for Disease Control (CDC)
"Cotinine is a major metabolite of nicotine and is currently regarded as the best biomarker for exposure to tobacco; exposure of both active smokers and of nonsmokers to ETS. Cotinine measurement is preferred over measuring nicotine because, although both are specific for exposure to tobacco, cotinine is retained in the body much longer than nicotine. Cotinine can be measured in blood (i.e., in serum), urine, saliva, and hair. Nonsmokers exposed to typical levels of ETS have cotinine levels less than 1 nanogram per milliliter (ng/mL), with heavy exposure to ETS producing levels in the 1 to 15 ng/mL range. Active smokers almost always have levels higher than 15 ng/mL, sometimes over 500 ng/mL."


Study Finds Even Limited Exposure to Secondhand Smoke
Can Harm Arteries

Let's play a game.  Let's see how many times qualifiers (terms such as "may") appear in each article:

Study Finds Even Limited Exposure to Secondhand Smoke Can Harm Arteries 

Dow Jones Business News 
Associated Press 

CHICAGO -- Just half an hour of secondhand smoke can impair normal blood flow to the 
heart, a Japanese study suggests. 

The study examined the effects of spending 30 minutes in a hospital's smoking room on 15 nonsmoking men and 15 smokers. The smokers, whose heart arteries already showed damage, weren't affected. But in nonsmokers, the result was a reduced ability of heart arteries to dilate, which previous research has suggested may be a precursor to hardening of the arteries. 

"This change may be one reason why passive smoking is a risk factor for cardiac disease" and related deaths in nonsmokers, the researchers say in Wednesday's Journal of the American Medical Association. 

The study didn't examine whether the changes from the one-time exposure to smoke were permanent.  

Previous research in smokers has found similar changes that may be reversible if smokers quit, said Dr. David Faxon, president of the American Heart Association. If exposure continues, "gradually, as hardening of the arteries sets in, it's irreversible," he said. 

The study "really sort of confirms prior information that we've had about the adverse effects of secondhand smoke," Dr. Faxon said. 

In the study, Dr. Ryo Otsuka of Osaka City University Medical School and colleagues used blood-pressure tests and an imaging technique called echocardiography to examine the effect on heart arteries' ability to dilate. Measurements were taken before and after exposure to secondhand smoke. 

The smoke appeared to impair the functioning of the endothelium, a lining of cells in the arteries that helps regulate dilation. Scientists believe coronary artery disease may begin when the endothelium becomes damaged, leaving the arteries prone to blockages or narrowing. 

Stanton Glantz, a professor of medicine at the University of California at San Francisco, said the findings add fuel to the debate over secondhand smoke. 

 "People walking into a smoky restaurant, do they want to be clobbering the ability of the 
arteries in the heart to get blood to the heart, even if it's just for a little while?" he said. 

Seth Moskowitz, spokesman for R.J. Reynolds Tobacco Co. (RJR), said the study doesn't 
change the company's belief that there is no scientific evidence establishing that secondhand smoke is a risk factor for lung cancer, heart disease or any other disease in adult nonsmokers. 

Study Finds Evidence of Harmful Effect of Secondhand Smoke on Hearts of Non-Smokers  

CHICAGO, July 22 (AScribe News) -- Just 30 minutes of exposure to secondhand smoke by healthy non-smokers may have a substantial impact on a function in coronary circulation, according to an article in the July 25 issue of The Journal of the American Medical Association (JAMA). 

Ryo Otsuka, M.D., Hiroyuki Watanabe, M.D., and colleagues from Osaka City University 
Medical School, Osaka, Japan, conducted a study from September 2000 to November 
2000 to determine the acute effects of passive smoking on coronary circulation. The study 
included 30 Japanese men who averaged 27 years of age - 15 healthy non-smokers and 15 active smokers without symptoms of disease. None of the men had a history of high blood pressure, diabetes or high cholesterol. 

According to background information cited in the article, passive smoking has been identified as an important risk factor for cardiovascular disease. In 1992, the American Heart Association concluded that the risk of death due to heart disease is increased by about 30 percent among those exposed to environmental tobacco smoke at home, and could be much higher in those exposed at the workplace, where higher levels of environmental tobacco smoke may be present. 

Recent studies have shown that passive smoking may be associated with vascular endothelial dysfunction. However, the acute effects of passive smoking on the coronary circulation in nonsmokers have not been evaluated.  

Normal endothelial cells (cells that line the cavities of the heart and the blood vessels) 
promote vasodilation (an increase in the internal diameter of a blood vessel, causing an increase in blood flow), and inhibit atherosclerosis and thrombosis (formation, development or presence of a blood clot in a blood vessel or the heart). 

Dysfunction of the cells contributes to vasoconstriction (narrowing of blood vessels, 
leading to decreased blood flow), endothelial thrombosis and the process leading to 
development of atherosclerosis. 

The authors used a non-invasive technique called transthoracic Doppler echocardiography to assess coronary flow velocity reserve (CFVR), a measure of endothelial function in the coronary circulation. Echocardiography uses ultrasound waves to make images of the heart chambers, valves and surrounding structures. The authors measured CFVR in each participant before and after a 30-minute exposure to environmental tobacco smoke. 

"Our data revealed that temporary passive smoking abruptly reduced CFVR in 
non-smokers but did not affect CFVR in active smokers. This provides direct evidence of a 
harmful effect of passive smoking on the coronary circulation in non-smokers," the authors write. 

"Mean (average) CFVR in non-smokers was significantly higher than that in active smokers 
before passive smoking exposure (4.4 vs. 3.6, respectively), while CFVR after passive smoking exposure did not differ between groups. Passive smoking exposure significantly reduced mean CFVR in non-smokers (4.4 vs. 3.4, respectively)," they report. 

These substantial changes in endothelial function were not associated with changes in heart rate or blood pressure. 

"The present findings suggest that reduction of CFVR after passive smoking may be caused by endothelial dysfunction of the coronary circulation, an early process of atherosclerosis, and that this change may be one reason why passive smoking is a risk factor for cardiac disease morbidity and mortality in non-smokers," the authors conclude. 

(JAMA. 2001; 286:436-441; available at 


Article on the left has 5 qualifying terms.  Article on the right has 6 qualifying terms.  The article on the left includes a small statement from Mr. Stanton Glantz, the leading lobbyist of anti-smoking regulations in the U.S. In his statement he takes a literal leap in that all these "mays" magically becomes an absolute that not only might acutely affect you but "CLOBBERS" you.  No one could ever accuse Mr. Glantz of not having a vivid imagination.

He goes on to ask if you're willing to be "clobbered" arterially even if for just a short period.  We wonder if that question still applies if we were discussing the effects of smoke from a campfire, barbeque or romantic fireplace, all of which contain the same chemicals as tobacco smoke.  We suggest that this same test, using the same procedures, be conducted on 30 men who are currently out camping in the woods.  That is, if we actually believed this study concludes anything meaningful, which we don't.

Let's not lose sight of what is meaningful about this study, featured in both of these articles:

"The study didn't examine whether the changes from the one-time exposure to smoke were permanent."

"However, the acute effects of passive smoking on the coronary circulation in nonsmokers have not been evaluated. "

One other reference in the article on the right that we cannot let go without question is:

In 1992, the American Heart Association concluded that the risk of death due to heart disease is increased by about 30 percent among those exposed to environmental tobacco smoke at home, and could be much higher in those exposed at the workplace, where higher levels of environmental tobacco smoke may be present

Other than the anti-smoking mouthpiece, Stanton Glantz, no other reputed health agency endorses this claim.  According to the American Council on Science and Health, this claim is "uncertain and controversial."  The Surgeon General, along with the EPA, has never endorsed this claim in any report on smoking and caution everyone to reserve judgement.



  Stanton A. Glantz, PhD; William W. Parmley, MD 

As more and more nonsmokers have come to understand the dangers associated with breathing secondhand smoke,1, 2 the number of 
communities enacting ordinances requiring smoke-free workplaces and public places has increased rapidly. As of May 2001, hundreds of communities had enacted laws requiring smoke-free workplaces, smoke-free restaurants, and smoke-free bars. California requires all workplaces, including restaurants and bars, to be smoke-free.3, 4 The theme for the World Health Organization's World No Tobacco Day in 2001 was "clean indoor air" and communities throughout the world are beginning to clear the air of secondhand smoke. Not only do the laws protect nonsmokers from the toxins in secondhand smoke, but they also create an environment that helps smokers cut down or stop smoking.5 

The tobacco industry's efforts to slow the spread of smoke-free environments has included a systematic effort to attempt to  undermine the scientific evidence that passive smoking causesdisease.6-8 One common theme is that the dose of toxins a nonsmoker inhales is tiny compared with the dose the smoker receives, implying that the risks are trivial or nonexistent. Such statements are based on measuring the delivered dose of 1 or more of the 4000 chemicals in secondhand smoke. The problem with such calculations is they can be manipulated by selecting the particular constituent of smoke to be the one that has low absorption or rapid clearance.1 The real measure of effect should not be the dose of one chemical or another, but rather the biological effect of breathing the 
secondhand smoke. 

The article by Otsuka and colleagues9 in this issue of THE JOURNAL adds substantially to the case that short-term passive smoking adversely affects endothelial function in ways that immediately compromise the cardiovascular system.10 The investigators demonstrated that, in healthy young volunteers, just 30 minutes of exposure to secondhand smoke compromised the endothelial 
function in coronary arteries of nonsmokers in a way that made the endothelial response of nonsmokers indistinguishable from that of habitual smokers. 

The investigators measured blood pressure, heart rate, and coronary flow velocity reserve before and after administering adenosine triphosphate using transthoracic Doppler echocardiography of the left anterior descending coronary artery. This innovative noninvasive approach to measuring coronary endothelial function appears to be ideal in these individuals, who have no evidence of coronary disease. Significantly, these substantial changes in endothelial function were not associated with changes in heart rate or blood pressure. 

Endothelial dysfunction may be at the heart of the development of atherosclerosis. Normal endothelial cells promote vasodilation and inhibit atherosclerosis and thrombosis, in part because of the release of nitric oxide.11 Dysfunctional cells, on the other hand, contribute to vasoconstriction, atherogenesis, and thrombosis. Risk factors contribute individually to endothelial dysfunction and appear to be additive. One possible unifying hypothesis for the effects of risk factors is that they increase oxidative stress that mediates these 
effects.12 Thus, reduction of risk factors improves endothelial function and reduces clinical coronary events. For example, in patients with hyperlipidemia, lipid lowering improves endothelial function both acutely13 and chronically.14 

The findings of Otsuka et al9 are important not only because they illustrate the importance of preventing nonsmokers from any exposure to secondhand smoke, but also because they help to explain the relatively large risk of death and other cardiac events associated with passive smoking compared with active smoking. Passive smoking increases the risk of cardiac death or morbidity about 30%15-21 compared with a doubling to quadrupling of risk associated with active smoking. Thus, the effect of passive smoking is as high as one third the effect of active smoking even though the dose of at least some of the constituents is much less than what the smoker inhales.1 

The first evidence that nonsmokers were sensitive to a component of tobacco smoke came from studies showing that short-term (30-minute) exposure to secondhand smoke activated nonsmokers' platelets to nearly the extent that they were activated in smokers22, 23 and that passive smoking increased the presence of endothelial cell morbidity in the blood.23 These immediate effects on platelets probably act synergistically with the effects on endothelial function. 
The platelet effects convinced epidemiologists that the dose-response curve for cardiovascular effects associated with tobacco smoke exposure was not linear, but exhibited substantial effects at relatively low doses (at least compared with an active smoker; the doses are high when measured against other environmental toxins) that a passive smoker receives.18, 20 In addition, animal studies demonstrated that exposure to the secondhand smoke from a single 
cigarette daily induced atherosclerotic changes.24 The fact that passive smoking does not induce additional effects in smokers9, 22 suggests that the underlying biochemical and cellular processes saturate at the doses involuntary smokers experience. 

While most people think of cancer when they think of active and passive smoking, it is important to emphasize that heart disease is also an important consequence of tobacco smoke exposure. This situation is particularly true for passive smoking; heart disease accounts for about 37 000 of the estimated 53 000 annual deaths attributed to involuntary smoking in the United States.18 Another important difference between the effects of smoking on risk of cancer 
compared with risk of heart disease is that the effects on cancer develop and resolve slowly (over a period of years) whereas the effects of smoking on the cardiovascular system occur rapidly. 

The findings of the study by Otsuka et al9 add to the evidence suggesting that everyone should be protected from even short-term exposure to the toxins in secondhand smoke. Communities should continue to require that workplaces, including restaurants and bars, be smoke-free and mount public education campaigns to encourage smoke-free homes. Not only will everyone breathe better,25 but they will also have healthier hearts. 

Author/Article Information 

Author Affiliation: Division of Cardiology, Department of Medicine, 
University of California, San Francisco. 

Corresponding Author and Reprints: Stanton A. Glantz, PhD, 
Division of Cardiology, University of California School of Medicine, 505 
Parnassus, Room 1317M, Box 0130, San Francisco, CA 94143-0130 

Editorials represent the opinions of the authors and THE JOURNAL 
and not those of the American Medical Association. 


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                                 Surgeon General. 
                                 Washington, DC: US Dept of Health and Human Services, Public 
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                                 National Cancer Institute. 
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                                 report of the California Environmental Protection Agency. 
                                 Smoking and Tobacco Control Monograph No. 10. Bethesda, Md: US 
                                 Dept of Health and Human Services, National Cancer Institute, 
                                 National Institute of Health; 1999. Publication NIH 99-4645. Available 
                                 Accessibility verified June 21, 2001. 

                                 Glantz SA, Balbach E. 
                                 The Tobacco War: Inside the California Battles. 
                                 Berkeley: University of California Press; 2000. 

                                 Magzamen S, Glantz SA. 
                                 The new battleground: California's experience with smoke-free bars. 
                                 Am J Public Health. 

                                 Chapman S, Haddad S, Sindhusake D. 
                                 Do work-place smoking bans cause smokers to smoke "harder"? 
                                 results from a naturalistic observational study. 

                                 Rennie D. 
                                 Smoke and letters. 

                                 Ong E, Glantz S. 
                                 Constructing "sound science" and "good epidemiology:" tobacco, 
                                 lawyers, and public relation firms. 
                                 Am J Public Health. 
                                 In press. 

                                 Bero L, Barnes DE, Hanauer P, et al. 
                                 Lawyer control of the tobacco industry's external research program: 
                                 the Brown and Williamson documents. 

                                 Otsuka R, Watanabe H, Hirata K, et al. 
                                 Acute effects of passive smoking on the coronary circulation in 
                                 healthy young adults. 
                                 ABSTRACT  |  FULL TEXT  |  PDF  |  MEDLINE 

                                 Celermajer D, Adams MR, Clarkson P, et al. 
                                 Passive smoking and impaired endothelium-dependent arterial dilation 
                                 in healthy young adults. 
                                 N Engl J Med. 

                                 Harrison D. 
                                 Cellular and molecular mechanisms of endothelial dysfunction. 
                                 J Clin Invest. 

                                 Oskarsson HJ, Heistad DD. 
                                 Oxidative stress produced by angiotensin too: implications for 
                                 hypertension and vascular injury. 

                                 Tamai O, Matsuoka H, Itabe H, et al. 
                                 Single LDL apheresis improves endothelium-dependent vasodilation in 
                                 hypercholesterolemic humans. 

                                 Treasure CB, Klein JL, Weintraub WS, et al. 
                                 Beneficial effects of cholesterol-lowering therapy on the coronary 
                                 endothelium in patients with coronary artery disease. 
                                 N Engl J Med. 

                                 Wells AJ. 
                                 An estimate of adult mortality from passive smoking. 
                                 Environ Int. 

                                 Wells AJ. 
                                 Passive smoking as a cause of heart disease. 
                                 J Am Coll Cardiol. 

                                 Wells AJ. 
                                 Heart disease from passive smoking in the workplace. 
                                 J Am Coll Cardiol. 

                                 Glantz SA, Parmley WW. 
                                 Passive smoking and heart disease: epidemiology, physiology, and 

                                 Glantz SA, Parmley WW. 
                                 Passive smoking and heart disease: mechanisms and risk. 

                                 Law M, Morris J, Wald N. 
                                 Environmental tobacco smoke exposure and ischaemic heart 
                                 disease: an evaluation of the evidence. 

                                 He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. 
                                 Passive smoking and the risk of coronary heart disease: a 
                                 meta-analysis of epidemiologic studies. 
                                 N Engl J Med. 

                                 Burghuber O, Punzengruber C, Sinzinger H, Haber P, Silberbauer K. 
                                 Platelet sensitivity to prostacyclin in smokers and non-smokers. 

                                 Davis JW, Shelton L, Watanabe IS, Arnold J. 
                                 Passive smoking affects endothelium and platelets. 
                                 Arch Intern Med. 

                                 Penn A, Chen LC, Snyder CA. 
                                 Inhalation of steady-state sidestream smoke from one cigarette 
                                 promotes atherosclerotic plaque development. 

                                 Eisner MD, Smith AK, Blanc PD. 
                                 Bartenders' respiratory health after establishment of smoke-free bars 
                                 and taverns. 

Discussion on this article to be followed by the actual study abstract:

Authors use references to substantiate their claims.  When the references are examined and are shown to be worthless or lacking , that makes the paper worthless or lacking.

Mr. Glantz makes 25 references to support his statements.  Of those 25, six of them (#s 3, 4, 7, 8, 18 & 19) are studies or articles from his own hand.  Hey, who better to call on to support yourself but yourself, right?

Reference #2 is to the CAL-EPA report which relied heavily on the 1992 U.S. EPA report.  The U.S. EPA report has been invalidated and vacated by a federal court judge.  That, in turn, wipes out the CAL-EPA report as a reliable source of information.

Reference #5 has a two-fold problem.  Mr. Glantz has no qualms about asserting the fact that smoking bans are a way for him to control individual behavior.  Never doubt that smoking bans are not about protecting health, they are about forcing you to conform to their smoke-free ideology.  He is also depending upon the laziness of readers not to go and read the abstact he is referring to.  The abstract finds that smokers smoke "harder" when taking a smoking break due to indoor bans than when they do in a social setting where they are free to puff at will.  Their conclusion is frightening:  The individual and public health benefits of reduced smoking frequency engendered by work-place smoking bans may be lessened by policies which allow smokers to take smoking breaks.   Read it again.  What they are saying is that by allowing smoking breaks it is undoing the good of reducing how much we smoke because we can't except for breaks.  In other words, they support not even supplying smoking breaks. This reference has nothing to do with the words which precede it in his editorial, "Not only do the laws protect nonsmokers from the toxins in secondhand smoke, but they also create an environment that helps smokers cut down or stop smoking."  Just an example of how you cannot trust Mr. Glantz's true intentions.

References #6 and #8 to support his wholly unscientific standard he employs to explain why the most basic rule of toxicology, "the dose makes the poison," doesn't apply to cigarette smoke is based on the anti-smoking screeching that the tobacco industry lied and manipulated data.  He wants you to believe that measuring chemicals doesn't matter, that it's simply the effect of cigarette smoke on the body that should be taken into consideration and that the tobacco companies mislead you when they discuss the effect of trace chemicals in the body.  To reiterate his statement, "The real measure of effect should not be the dose of one chemical or another, but rather the biological effect of breathing the secondhand smoke."  The scientific community should drum him out of the field for such a ridiculous statement.  You might as well say it doesn't matter how much heat you're exposed to as long as you sweat.  Babies locked in a car on a very hot day will die.  Babies sitting in a covered stroller in the shade on the same day may break a sweat but they'll be fine.  Mr. Glantz also wants to ignore that the Congressional Research Service, who does not answer to the tobacco industry, has upheld the long held scientific standard that indeed, the dose of the chemical and not what is delivering it, is what matters when discussing any effect on the body.  Oh, and oops, he's failed to list in his reference #8 that he was also one of the researchers... Bero L, Barnes DE, Hanauer P, Slade J, Glantz SA.

Reference #10 is a previous study of the effect of cigarette smoke on the arteries of nonsmokers which Mr. Glantz is using to begin the often heard "mountains of evidence."  He doesn't have just one study but at least two.  Well, he can have 100 studies to point to regarding the effect of smoke on nonsmokers but 100 pieces of junk do not make a case.  This referenced study makes no mention of taking any other lifestyle behavior (ie. diet or occupation) into account before deciding that cigarette smoke impairs endothelium-dependent dilatation.

Reference #15, 16 & 17 are all abstracts attributed to an AJ Wells.  That is one person making claims which Mr. Glantz uses to support information in three instances.  There are hundreds if not thousands of researchers yet it appears that relatively few (you can probably count them on one hand) put forth studies, all if not most based on meta-analysis (cherry picking which studies they want to put together to support their preconceived goal), from which Mr. Glantz can rely on to support his arguments.  #15 is not available for review, #16 uses the now invalidated EPA study's procedures to somehow apply that to heart disease which the EPA study did not address and makes a conclusion.  Hello?  #17 also uses meta-analysis to reach it's conclusion.  The EPA does not endorse any claims made about passive smoking and coronary heart disease.  The largest ever cardiology study, MONICA, funded by the World Health Organization, has failed to find a link between heart attacks and the classic risk factors, such as smoking and high cholesterol levels.

Reference #20 & 21 are more of the same.  They show weak statistical evidence that passive smoking is associated with a small increase in the risk of coronary heart disease and are a product of meta-analysis, no original study.  Association should not be confused with causation.  For every one of Mr. Glantz's references that he says supports the risk of heart disease due to passive smoking, we can produce one that does not.  For the most revealing insight as to how studies that Mr. Glantz relies on to support his claim aren't worth much, one need just read an editorial by Dr. John C. Bailar III where he states that nothing has been proven in the risk assessment of passive smoke on the hearts of nonsmokers.

Reference #22 & 23 make some vague claims about endothelial cell count and platelet aggregate ratio.  There's no mention of confounding factors that were accounted for, nor did either conclusion include studying more than a handful of subjects.  Another violation of scientific standards.  The smaller the group studied (Ref. #23 studied 10 men) the less meaningful the results.  Most importantly, neither of these two reports make any claim that they know what, if any, long term effect there is. For all we know these 10 men were stressed out and that is what caused whatever changes that occured.  This is just more junk for Mr. Glantz to throw out at you and claim there is "mounting evidence" when in fact, each paper reviewed separately does not supply either long term effect information or are statistically weak.

Reference #24 is a study conducted on animals.  Cockerels, to be exact; a young male domestic fowl. We're sorry, but fowl are not people. Saccharin was recently removed from the official carcinogen list after 20 years because it became evident that although studies showed that saccharin caused cancer in animals it never materialized in humans.  And as many stories as you hear about smoking causing cancer, no one has ever been able to induce a tumor in any animal who has been subjected to the amount usually associated with an everyday smoker.  Read up on this little known fact at In Defense of Smokers.

Reference #25 discusses how approximately 53 bartenders felt before and after smoking bans went into effect in their workplace.  You make of it what you will.  They say they took into account personal smoking and recent upper respiratory tract infections but they don't tell you how many of the 53 are smokers themselves and we cannot know what symptoms they say they may have had when smoking was allowed because the study uses a broad term "sensory irritation symptoms."  No one argues that smoke can be an irritant on the eyes for example but that does not mean that you're going to lose an eye because of it.  Also, this report is based on recall bias.  We're sure that if you ask someone how they felt in a smokey environment they're going to give the expected response, even when they didn't experience any symptoms, because it's generally accepted that a lot of smoke is irritating and you assume that you were bothered by it when asked how you felt months ago.  For a real measure of what effect passive smoke has on wait staff, the Oak Ridge National Laboratories conducted a hands-on experiment where they outfitted the subjects with actual air monitors and studied real people, who move from place to place (as opposed to leaving an air monitor in a room which is unrealistic because people do move about) to see exactly how much cotinine (a derivative of nicotine) they inhale.  They concluded that they inhale the equivalent of SIX cigarettes per year.

What was is that Mr. Glantz was trying to prove in his editorial again?

JAMA ABSTRACT on Findings of Acute Effects of Passive Smoking
on the Coronary Circulation:
Acute Effects of Passive Smoking on the Coronary Circulation in Healthy Young Adults  

Ryo Otsuka, MD; Hiroyuki Watanabe, MD; Kumiko Hirata, MD; Kotaro Tokai, 
MD; Takashi Muro, MD; Minoru Yoshiyama, MD; Kazuhide Takeuchi, MD; 
Junichi Yoshikawa, MD 

Context  Recent studies have shown that passive smoking is a risk 
factor for ischemic heart disease and may be associated with vascular 
endothelial dysfunction. The acute effects of passive smoking on 
coronary circulation in nonsmokers are not known. 

Objective  To determine the acute effects of passive smoking on 
coronary circulation using coronary flow velocity reserve (CFVR), 
assessed by noninvasive transthoracic Doppler echocardiography. 

Design, Setting, and Participants 
Cross-sectional study conducted from September 2000 to November 2000 
among 30 Japanese men (mean age, 27 years; 15 healthy nonsmokers and 15 
asymptomatic active smokers) without history of hypertension, diabetes 
mellitus, or hyperlipidemia. 

Main Outcome Measures  Coronary flow velocity reserve, calculated as 
the ratio of hyperemic to basal coronary flow velocity induced by 
intravenous infusion of adenosine triphosphate and measured in each 
participant before and after a 30-minute exposure to environmental 
tobacco smoke. 

Results  Heart rate and blood pressure responses to adenosine 
triphosphate infusion were not affected by passive smoking exposure in 
either group. Passive smoking exposure had no effect on basal coronary 
flow velocity in either group. Mean (SD) CFVR in nonsmokers was 
significantly higher than that in active smokers before passive smoking 
exposure (4.4 [0.91] vs 3.6 [0.88], respectively; P = .02), while CFVR 
after passive smoking exposure did not differ between groups (P = .83). 
Passive smoking exposure significantly reduced mean (SD) CFVR in 
nonsmokers (4.4 [0.91] vs 3.4 [0.73], respectively; P<.001). 

Conclusions  Passive smoking substantially reduced CFVR in healthy 
nonsmokers. This finding provides direct evidence that passive smoking 
may cause endothelial dysfunction of the coronary circulation in 
JAMA. 2001;286:436-441


There is so much information missing from this study that it is hard to know where to begin.  One thing we can say for certain is that as much as we have very little to go on the same can be said for those that claim this is more "proof" of harm from passive smoke.  So little methodology that any conclusion could have been reached, but from the start they knew what they were looking to find, that passive smoke has an effect on non-smokers,  and so they found it.  What most people don't know is that this is not how science is supposed to approach a study.  It is the standard that you begin a study with the hypothesis that you will NOT find an effect.

Since there is little information to base any conclusions on we offer questions, rather than answers, which easily undermine the reliability of this so-called study:

What about the use of the drug adenosine triphosphate (ATP)?

The source of energy for the heart, like all other tissues is ATP or adenosine triphosphate. This high energy molecule is generated by the metabolism of food that you ingest. In the case of the heart, most of the energy at rest is generated by metabolism of fatty acids (approximately 70%) and some carbohydrates. ATP is produced either in the motochondria through a series of enzymatic steps or under certain conditions (when the heart is not getting enough oxygen, a condition called ischemia) by anaerobic glycolysis.

Follow Up Question:  So, ATP occurs naturally depending on what type of food you eat?  Did what the subjects eat that day have anything to do with the results?

The Effects of Electric Currents on ATP Generation, Protein Synthesis, and Membrane Transport ..
Summary: Research shows that ATP (adenosine triphosphate) levels increase with the application of microcurrent and diminish with millicurrent (Cheng 1982). The increase of ATP peaked at 500 microamps and decreased rapidly at higher current levels. Cheng also observed that aminoisobutyric acid uptake increased dramatically beginning at 10 microamps and inhibitory effects began at 750 microamps. The uptake of aminoisobutyric acid which is essential for protein synthesis and membrane transport, showed an increase of 30 - 40%.

Follow Up Question:  Did the use of Doppler echocardiography create a current that affected the effect of the ATP which had been injected into the subjects?

Do we know or did they examine the subjects BEFORE they injected them with adenosine triphosphate?  Our point  being that after ATP was injected, which helps blood flow, it was possible that the nonsmokers where chemically induced to show a greater flow velocity than they naturally have and when or if the ATP wore off (again, no mention of how long the effect lasts) their flow velocity was reduced.

What about Confounding Factors?

Having too much cholesterol isn’t healthy, because when it’s carried by the blood it can build up in arterial walls.
This can narrow the arterial passageways, reduce blood supply to the heart or brain, and set the stage for a heart
attack or stroke.

Follow Up Question:  Did they offer us any indication of weight or diet between the two groups?

Why does this study conflict with others?

Cigarette smoking has been shown to reduce blood flow, especially to the
extremities. Using the ultrasonic Doppler flow meter, Sarin et al[53] concluded that
smoking a single cigarette reduced mean blood flow velocity by 42% in the digital
vessels of male volunteers. Mosely and Finseth[48] showed via angiogram that
smoking a single cigarette produced severe vasoconstriction in a patient.

Follow Up Question:  This one saw a severe vasoconstriction after a smoker smoked one cigarette but the current study in question showed no change for smokers?

Mr. Larry Colby, author of In Defense of Smokers, contributes to the discussion:

The researchers did NOT examine any endothelial cells!!! All they did was to take echocardiograms.  All that they do is to show the degree of dilation or constriction in the arteries. reflected in blood pressure. They measured the blood pressure but the differences in blood pressure before and after "passive smoking" were minuscule, so tiny as to be easily accounted for by the stress induced by the experiment.

I saw another article by Glantz in which he seemed to be saying the exact opposite of what he is saying in the editorial. In that article, he seemed to be saying that the smoke resulted in arterial constriction. For the life of me, I don't understand how you can get arterial constriction without an increase in blood pressure. However, in the editorial, he seems to be arguing that because the smoke reduced endothelial function and "coronary flow velocity reserve" without raising BP or heart rate, it somehow proves that smoking causes heart attacks.

The endothelium is simply the lining of the circulatory system. It is just one cell thick. An echocardiogram is simply an ultrasound view of the heart. It can't possibly resolve structures as small as one cell, so the notion that the researchers were looking at "endothelial cells" is just nonsense.

The term "hyperemic" refers to an excess of blood flow in any part of the body.  Adenosine, according to the Merck Manual, is a powerful (and dangerous) drug used to treat heart arrythmias. In 30 to 60% of patients, it causes dyspnea (difficulty in breathing), chest discomfort and flushing. So, to the extent that they injected adenosine, they were taking chances with the volunteers, but I guess that was an acceptable risk to demonstrate the dangers of smoke (if that's what was demonstrated).

But the key finding here purports to be that the smoke somehow reduced "coronary flow velocity reserve" (CFVR) without impacting blood pressure. I presume that an echocardiagram can measure blood flow in the heart, simply by measuring the volume of blood in the arteries. But I really don't understand how the arteries in the heart can be constricted without constricting other arteries and veins, causing an increase in BP.

The abstract doesn't even tell me in what units CFVR is measured (4.4 WHAT?).  Also, since the study was done in the smoking room of the hospital, we need to know how they controlled for the amount of passive smoke administered to each group. Finally, I note that the passive smoke had no effect on the basal (normal) blood flow in either the smokers or the non-smokers - it only reduced the excess flow induced by the injection of adenosine, So maybe it proves that it's not a good idea for people to go around injecting themselves with adenosine while smoking!

After doing a little more research on the medical terms (which were cleverly used to obfuscate the weaknesses in the experiment), here's how I see it:

They indicate that passive smoking had no effect on normal basal blood flow (as measured by doppler (motion sensing) echocardiography). This means that they tried to find an effect in people exposed to second hand smoke but, without using drugs, they couldn't do so.

Although the abstract doesn't describe the time line, I bet they got the idea of using adenosine to induce hyperemia (excessive blood flow) only after the drug-free experiments failed. Anyway, they measured basal (normal) blood flow before injecting the adenosine. Then they "infused" the adenosine, and measured the excess blood flow, induced by the drug. Then, they exposed the subjects to passive smoke for 30 minutes (meaning, they waited 30 minutes) and measured the blood flow again. In the non-smokers, they reported a drop in the excessive blood flow - they don't say what happened to the excessive blood flow in the smokers.

Now, the Merck manual says that adenosine is a quick acting drug so, the minute that it was injected, the blood flow would almost immediately increase. By the same token, after 30 minutes of waiting, the effects of the drug would wear off, and the blood flow would start returning to normal, whether or not there was any exposure to smoke. Even if they continually "infused" the drug (a dangerous tactic), I'd still expect the blood flow to start dropping off, as the body adjusted to the immediate impact of the drug.

They only tell us that the excessive blood flow tapered off in the non-smokers; they don't tell us what happened in the case of the smokers. Furthermore, they don't seem to have used any controls - people injected with adenosine, not exposed to any smoke at all, and measured again after 30 minutes.  But without controls, they really have no way of saying whether it was the smoke that caused the blood flow to start returning to normal, or
the waiting.

They claim that the excess blood flow, induced by the drug, was greater in non-smokers than in smokers. What this means is uncertain. It could mean simply that the non-smokers were, as a group, younger than the smokers (they don't claim that the two groups were age matched - we're left to make that assumption, but I assume nothing).

So basically, this was an experiment dealing with the effects of a powerful drug, adenosine, on blood flow in the heart, and upon the effects of either passive smoking (or just waiting) on the abnormal blood flow caused by the
drug. Without controls, I don't think it tells us anything at all about anything.

What they did here is to use obscure medical jargon to cover up an experiment that basically failed. Glantz's editorial shows that even he doesn't understand what they did. I didn't understand it either until I looked up such terms as hyperemia, doppler echocardiography, and above all, adenosine.

Actually, this was an invasive experiment. Just to use the doppler, they have to inject a substance into the blood that induces millions of tiny microsopic bubbles, so that the doppler can calculate the velocity of blood flow by looking at the ultra sound reflections from the moving bubbles. Then, they infused the adenosine, which can't be good for you, if it causes chest discomfort, breathing problems, and flushing in up to 60% of the victims.

 The researchers didn't study "normal blood flow" at all, but, instead, used a powerful and dangerous drug (adenosine) to induce an abnormal flow and purported to study the effects of passive smoke in bringing the flow back to normal.

Arguably, if it could be shown that active or passive smoking helps to eradicate the effects of the adenosine, the smoking was good for the participants since it helped to overcome the abnormal effects of the drug and get things back to normal. However, in the absence of any controls, I don't see that they proved anything except that after waiting for 30 minutes, the drug wears off!


In attempting to alarm the public the researchers present a study that fails to take contributing factors into account, does not specify the methods used and cannot determine if there are long lasting effects.  They also disregard medical research that has shown that reduced flow velocity can be controlled, thereby removing any high degree of potential threat of substances that may reduce flow velocity:

Medscape Medline Abstract
N-acetylcysteine improves microcirculatory flow during smoking: new effects of an old drug with
possible benefits for smokers [In Process Citation]

Clin Cardiol 2001 Jul;24(7):511-5    (ISSN: 0160-9289)

Lu Q; Bjorkhem I; Xiu RJ; Henriksson P; Freyschuss A  Department of Medicine, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.

BACKGROUND: Cigarette smoking provokes marked acute changes in the microcirculatory vasculature, including a reduced blood flow velocity. In accordance with the hypothesis that the reduced blood flow is due to an imbalance between pro-oxidants and oxidants, we recently showed that most of the reduction could be reversed by a high dose of vitamin C.
HYPOTHESIS: In the present work we tested the hypothesis that N-acetylcysteine, a mucolyticum and an antioxidant, may have an effect on the smoking-induced changes observed by vital capillary microscopy of the nailfold.
METHODS: In all, 37 healthy volunteers of both genders and with varied smoking habits were treated with N-acetylcysteine 200 mg t.i.d. for 2 weeks. In vivo investigation of the microcirculation by capillaroscopy was performed before and after treatment.
RESULTS: Treatment with N-acetylcysteine significantly reduced the smoking-induced relative decrease in capillary blood flow velocity in a group of volunteers with varied smoking habits (p = 0.0016). The preventive effect was clearly significant in smokers (p= 0.003).
CONCLUSION: Treatment with N-acetylcysteine has a positive impact on microcirculatory flow during smoking, particularly in habitual smokers.

[Not to mention non-smokers too, right?  If smokers can correct for their habit it follows that those exposed to smoke for short periods of time have nothing to worry about, especially if they take a usual dose of Vitamin C per day.  Most people take Vitamin C daily anyway.]

MEDLINE Indexing Date: 200107
Publication Type: Journal Article
PreMedline Identifier: 0011444642
Unique NLM Identifier: 21337544
Journal Code: IM


...research indicates that a large intake of fatty food in one sitting puts enough strain on the cardiovascular system to impair its function. Another study finds that downing a high-fat meal can boost the risk of blood clots.

For 4 hours after a high-fat meal, the body's arteries struggle to let blood flow through them in response to stress, researchers from the University of Maryland School of Medicine in Baltimore report in the Nov. 26 Journal of the American Medical Association.

Impaired vessel function is typically a precursor of atherosclerosis, in which fatty plaques form on the walls of arteries. To test the function of the inner wall of an arm artery in 20 healthy men and women, the scientists strapped a blood pressure cuff around the top of each volunteer's arm, restricted blood flow for 5 minutes, then released the cuff. One minute later, they measured artery size using ultrasound. Normally, the vessel enlarges as the body tries to nourish areas that have been deprived.

In people who hadn't eaten recently, the induced stress enlarged the blood vessel by 20 percent. But in people tested 2 hours after eating a fast-food meal of eggs, sausage, biscuits, and hash brown potatoes, the blood vessel dilated only 12 percent. The dilation response continued to fall for the next 2 hours before improving, says cardiologist and study coauthor Gary D. Plotnick.

Source: "Wretched excess yields double trouble"; Science News Online

Did Glantz and company ask their subjects if they had just eaten?  And if not, should we still alarm everyone for the same effects eating has on cardiovascular circulation as exactly they say to have found with 30 minutes of exposure to cigarette smoke?

In the end what they have "proven" is that they will continue to try to instill fear in an uneducated public with bogus studies and results.

Second-hand smoke linked to crib death, report shows
SIDS victims' lungs found to contain 'much more' nicotine
Second-hand smoke linked to crib death, report shows
            SIDS victims' lungs found to contain 'much more' nicotine 

Helen Branswell 
The Canadian Press 

Babies who are exposed to second-hand smoke are at a higher risk of dying of crib death, 
researchers reported yesterday in the Journal of Pediatrics. 

It had previously been suspected there was a connection, but the researchers, from the 
University of Toronto and University of Maryland, proved the link by comparing the lung tissue of babies who died of sudden infant death syndrome (SIDS) to that of babies who died of other causes. 

"I think maybe it's another small piece in a puzzle why we have to have smoke-free environments around children to start with, and probably around all of us," said principal investigator Dr. Gideon Koren, a senior scientist at the Hospital for Sick Children in Toronto. 

Between three and four babies out of 1,000 succumb to SIDS. 

Medicine has been slow to unravel the mystery behind why some babies never wake up from a nap or a night's sleep. To date, Dr. Koren said, only two factors were shown without doubt to be associated with SIDS. 

The first is the way the child sleeps. It is now known babies who sleep on their stomachs are 
at much greater risk. U.S. public education campaigns instructing parents to put babies down 
on their backs cut the rate of crib deaths by 40%. 

"And the second is really cigarettes," Dr. Koren said. 

But the link, till now, has been based on what are called epidemiological studies, essentially 
oral reports of the environmental factors SIDS babies encountered, as recalled by their 

Such evidence is important in the lack of scientific data, but it is not foolproof. Memories may be faulty. Also, it is well known that people are loath to admit to behaviour they feel embarrassed or guilty about -- a factor that could certainly come into play if a grieving parent felt he or she was being blamed for the death of a child. 

Dr. Koren and his colleagues decided to look for biological markers, solid proof that would 
eliminate the need to rely on reporting from parents. So they looked for nicotine -- a marker of exposure to second-hand smoke -- in the lung tissue of 44 infants who had died of SIDS and 29 babies who had died of other causes. 

"Basically what we found is that SIDS babies had much more nicotine in their lungs," Dr. Koren said. "We did see huge differences." 

Courtesy of FORCES

                         ROOMS - On February 21, Canadian papers printed this "breaking news":
            "Second-hand smoke linked to crib death, report shows - SIDS victims' lungs found
      to contain 'much more' nicotine," announces the National Post. "Secondhand smoke linked to SIDS,"
      echoes the Globe and Mail. In what promises to be yet another junk science machination in the hands of
      the antitobacco mobsters, we can hear the keys to our homes jingling in the hands of the Therapeutic
      State police.

      For a long time Orwellian health nazis have tried to push a "link" between the mysterious SIDS and
      passive smoke, as a way to force themselves into our homes with a sickening lie that makes already
      grieving parents guilty of a trumped-up crime. This newly cooked-up mirage could get the nazis one step
      closer to their goals.

      We have not yet seen the study in question but, judging from what we read on the papers, there is
      nothing to worry about. Science hasn't proven anything here, but there's a lot to worry about how in terms
      of how this will manipulated by he antismoking mob. There are only 44 SIDS cases examined, which make
      this a lightweight report, and having measured nicotine in the lungs does not tell us much. In fact, the
      Globe and Mail itself reports that a 24 nanogram /gram average in the children "exposed" was "nearly
      double" the nicotine concentration in the children "not exposed" – which means that in children "not
      exposed" the concentration was over 12 nanogram/gram. The twisting here is the absurd implication that
      less than a doubling of the concentration of nicotine is "the cause" of SIDS. But there is more nonsense:
      the reports qualify nicotine at an average of 24 nanograms/gram in lung tissue as a "high level" -- a high
      level compared to what, if non-SIDS children had more than half as much already?

      This of course raises fundamental questions that the paper itself is unlikely to answer: namely, how were
      the controls (children "not exposed") selected? Clearly one could pick controls that have no or little
      nicotine in their lungs, and thus produce a study guaranteed to show a difference between cases (children
      "exposed") and controls. There is the question of how the tissue samples were taken: where in the lungs,
      since nicotine concentrates preferentially in fatty tissues; how long after death were the tissues taken; how
      were the samples pickled, in what fluids, in what volumes, for how long time, refrigerated or not; how was
      the analysis done; was it all equally standardized for cases and controls? Other questions abound.

      Indeed, the news reports imply there were differences in nicotine levels among individual samples.
      Nicotine was even absent in the lungs of at least 3 SIDS cases. And surely the study authors could not say
      that nicotine is the cause of SIDS, given that nicotine has been pronounced safe by the US Food and Drug
      Administration, by Health Canada, and countless other regulators around the world that permit the free,
      over-the-counter sales of nicotine patches and gums that any youngster can buy and use. All preparations
      that contain far more nicotine than a pack of cigarettes.

      From a fair scientific point of view, the report is no proof whatsoever that nicotine or other unnamed
      components of passive smoke were or are the cause of SIDS. It is only possible to conclude that the true
      purpose of the "study" is to induce fear and suspicion in unqualified readers, in the time-honored
      deceptive tradition of antitobacco interests.

      If truth be told, the Globe and Mail itself acknowledges that SIDS "… is linked to underdeveloped or
      malformed circuits in the brain that drive respiratory and cardiac function;" which in itself contradicts the
      "cause" proposed by the "study". Could passive smoke be a co-factor in  SIDS? When the causes can be
      many and are unknown, everything is possible or impossible, and we are in the realm of mere
      speculation. The G&M also states that "...having babies sleeping on their backs…reduced cases more than
      30%". Whoa! Have we got a cause and a cure?!

      The literature on SIDS has reported a multitude of associations with SIDS, besides exposure to second
      hand smoke. For the mother it is age, marital status, socioeconomic status, level of education, race,
      urinary tract infections, multiple birth, and prenatal and natal care. For the infant it is age at SIDS, time
      of day at SIDS, season at birth, season at death, sleep position: prone, supine or sideways, birth and
      postnatal pathology, sweating, bed sharing, and breast feeding.For the father it is occupation, education
      level, and smoking habits.For the environment it is housing conditions, density of occupants in
      household, and geographic location.

      As for many other conditions, SIDS is a syndrome associated with many possible risk factors, none of
      which can legitimately be called a "cause", because the possible causal contribution of all or any of these
      factors - if real – is impossible to identify. Prof. Richard Doll, arguably the pope of epidemiology,
      concluded long ago that the epidemiology of multifactorial diseases cannot be a science and can only be
      interpreted... "imaginatively". Prof Kenneth Rothman, another icon of epidemiology, agreed. However he
      went on to say that, although causal inferences are impossible, "…the exigencies of public health demand
      action and despite imperfect knowledge causal inferences must be made." The obvious flaw of this circular
      reasoning is that the "exigencies of public health" would not exist without first having made improper
      causal inferences. What Prof. Rothman should have said is that certain health professionals - and health
      nazis especially - justify their own exigencies to intrude in people’s lives by making up "imaginative"
      causal inferences devoid of defensible justification. Having done so, they hijack government authority and
      demand public compliance simply because they are in power. Some racket indeed.

      So it is that Dr. Aurore Côté cannot be in any rational position to predict that "...parents quitting smoking
      could significantly lower the incidence of SIDS". She must know this or else she should go back to school;
      or perhaps her only intention is to cater to the fraudulent antismoking innuendoes and speculations that
      are served to a naïve public as "conclusive evidence" and "proof positive."

      In fact, the report in question has proven absolutely nothing. Yet, another news item, by Yahoo, reads:
      "Researchers prove second-hand smoke is risk factor for crib death" which must take the prize for
      information twisting. The piece reports that Dr. Koren, head of the "investigation", states that: "To date,
      only two factors were shown without doubt to be associated with SIDS ... the way the child sleeps ... and
      the second is really cigarettes".

      Really? Come-come, some honesty, Dr. Koren! We have come to the conclusion that your piece proves
      absolutely nothing, without even the need to read it. So, either substantiate your statements with some real
      proof, or refrain from misleading people. Why don't you rebut us, Dr. Koren? We are more than willing to
      entertain a public debate on your "proof" on the pages of FORCES, and we will edit not a word of what
      you have to say -- unlike the practice of the antismoking propaganda machine! Dr. Côté, why don't you tell
      the public that yours is also a speculation, as a real scientist should do, or do you prefer to ride the
      professionally safe antismoking horse of junk science?

      Some misguided people forget that we are supposed to live in the 21st century, in an open democracy
      where due process means factual public representations. We believe few would object if after thorough
      observations they said: "It seems that exposure to second hand smoke might be associated with SIDS. We
      do not imply causation here, and likely there is nothing to it, but perhaps you might think it considerate not
      to smoke in the presence of infants." Instead they opt for the strong hand, thinking of themselves as
      possessed by some exclusive knowledge, exempt of explanation because presumably good intentions
      alone justify their arrogance. According to the G&M piece, the antismoker Ms. Vandermeulen advocates
      enforcement to "…monitor what people do in their homes". What a brilliant idea!

      And so it is that the presence of nicotine in the lungs of non-smokers has been played many times in the
      attempt to substantiate antismoking assumptions. The intentional confusion between exposure and
      causality is yet another junk science fraud to mislead the public into thinking that causal proof exists,
      where none can be. It is clear that health nazis look for excuses to get into our homes, perhaps with a
      smoke detector or preferably a camera hooked to a central police station, ready to slam us in the pokey
      should they catch us smoking in the presence of children. George Orwell is here, more than ever and
      totally fulfilled. Today, antitobacco is to science and smokers what yesterday's genetic prejudices were to
      justice and the Jews. Are we ready to be enslaved, or are we prepared to defend ourselves from the
      intrusive lies of the Therapeutic State and its interested acolytes?

Stephen Hartwell of FORCES Toronto adds:

Excuse me ??

3-4 per 1,000 babies succumb to SIDS in All North America ?

400 SIDS babies in Canada out of about 400,000 born every year ?

Isn't that .01 to .04 Per Cent ? How is that any significant Health Risk ?

Milligrams of the same chemicals in babies from the Sydney, Nova Scotia Toxic Pond declared 'safe,' as published in the Globe and Mail the other day, yet nanograms, massively less, in babies is not safe when it comes to SIDS ?

25,000 children die EVERY DAY from poverty globally and this article makes .01% from SIDS in Canada over a whole year sound like it's a pandemic, our entire population is dying shortly after
birth, and it's all the fault of secondhand smoke ?

The generally accepted number of cases for any study is 800 to 1200, yet this study is based on just 44 !?

Cause-and-effect etiology has rarely ever been proven about anything, yet, this study concludes there can be "no doubt" !?

No one knows what causes SIDS, yet a death rate of .01% is a 'significantly higher risk of crib death' from the claimed 2nd ( again - nobody knows what the 1st is ! ) and only other factor - secondhand smoke ?

The only thing Dr. Koren reveals is he does not deserve to be licenced nor called a doctor. Instead, he should be arrested !

Dr. Koren, head of the investigation, is not exactly pure.

How can the general public decide anything when it never gets to read the whole story about anything ?

Include the fact that Koren was suspended for six months in December 2000, for his $ 125,000 part in one of the many Apotex Pharmaceutical scandals:

"Dr. Koren's conduct was very wrong and a serious violation of the university's standards and values," said university president Robert Prichard.

"The severe discipline reflects the university's unequivocal disapproval of his conduct," and forced to resign his head positions at the university.

For $ 125,000 Koren arranged for Apotex to get a Lab at U of T. Dr. Olivieri worked on one of their experimental drugs, and told the test patients and the newsmedia about very potentially dangerous side effects. Koren waged an annomyous letter campaign against her and her supporters to scare them in to silence, and recruited his own supporters in attempts to discredit her and her
supporters the goal being to suppress the data Dr Olivieri was trying to tell people about.

Dr. Nancy Olivieri was vindicated, not just once, but several times over the course of her ordeal.

Koren never was 'vindicated' - he had more charges laid on him, yet he suddenly pops up again,
whitewashed, spiffy clean, and spouting more of his typical junk science, namely this time about SIDS.

Include the fact that the huge majority of family households are now smoke-free, and thereby can not possibly be associated with secondhand cigarette smoke, and that 'No SHS Link to SIDS' was already irrefutably proven numerous times.

Include the fact that the Children's Aid Society has been in a lot of trouble lately for the way it's been handling it's affairs, for removing children without due cause, for violating the Charter of Rights and Freedoms, and Private Property Rights, including possibly causing deaths, such as the young woman who died and may have committed suicide last year, leaving her child without a mother at all.

Ms Vandermeulenof the CAS believes parents have no rights ?

Some CAS chapters ordered the foster parents not to take the kids to visit the grandparents if the grandparents were smokers !

Some CAS chapters ordered the removal of foster children from their long-term foster parents
simply because those parents were tobacco smokers !

The children must have suffered very serious psychological emotional trauma, understandably, when they were told their foster parents were trying to kill them. Potential life-long harmful emotional affects can result, requiring extensive therapy.

Some CAS chapters decided not to disrupt the (family-bond) security of a child already living with smokers, but, not before the devastating emotional damage had already been done, their's and their parents' normal developmental expectations and abilities destroyed.

Is Ms. Vandermeulen claiming only she knows how to raise children ? Has Ms. Vandermeulen even ever had any children ? Or has she just been too busy telling everybody else how to live?

THAT some foster parents who smoke tobacco got their children back, and so far continue to fight off Ms. Vandermeulen's continuing attempts at social engineering, and that the children have suffered psychological emotional trauma as a result proves that Ms. Vandermeulen should be fired, and probably brought up on charges herself.

(Dr.) Koren and Ms. Vandermeullen are the kinds of people we are now supposed to believe about SIDS and secondhand smoke ?

I Don't Think So !

And if the general public were told the whole picture in one single article I believe the vast majority would agree with me.

We all know just how much hospitals, universities and NGO's need every penny they can get. Who doesn't ?

I would like to know how much money those institutions got, and from whom,

Perhaps from
for saying what anti-smokers want said, and scaring the entire public half to death with such blatant indefensible 'horse-hockey' research conclusions.

Stephen Hartwell
Forces Toronto/Forces Canada

IARC Monographs Programme Declares Second-Hand Tobacco Smoke Carcinogenic To Humans
IARC Monographs Programme Declares Second-Hand Tobacco Smoke  
Carcinogenic To Humans 
June 19, 2002

    Additional kinds of cancer linked to smoking 

    World Health Organization 
    International Agency for Research on Cancer 

    WASHINGTON/LONDON/TORONTO, June 19 /PRNewswire/ - A scientific working group of 29 experts from 12 countries convened by the Monographs Programme of the International Agency for Research on Cancer (IARC) of the World Health Organization, Lyon, France, has reviewed all significant published evidence 
related to tobacco smoking and cancer, both active and involuntary. While its 
conclusions unsurprisingly confirmed the cancer-causing effects of active 
smoking, which an earlier working group had considered back in 1986, it now 
concluded its evaluation of the carcinogenic risks associated with involuntary 
smoking, with second-hand smoke also classified as carcinogenic to humans. 

                               ACTIVE SMOKING 

    Disease burden very high 
    In brief, the tobacco epidemic is big - one-half of all persistent 
cigarette smokers are eventually killed by a tobacco-caused disease. Half of 
these deaths occur in middle age (35-69 years), when those killed by tobacco 
lose on average 20-25 years of nonsmoker life expectancy. There is an emerging 
epidemic in females and in developing countries. While annually tobacco 
accounts for millions of cancer deaths worldwide, it causes an even greater 
number of premature deaths from cardiovascular and lung diseases and from 
stroke than from cancer. Nonetheless, tobacco use is the largest cause of 
preventable cancers around the world. 
    Unfortunately, as we continue to examine the cancer risk caused by 
smoking we are learning that it is even greater than previously thought and 
more cancer sites are affected. 

    New cancer sites affected 
    In this monograph, the Working Group added additional cancer sites to the 
already very long list of cancers caused by smoking. Some of these are among 
the most common kinds of cancer around the world, including cancers of the 
stomach, liver, uterine cervix, and kidney (renal cell carcinoma) and myeloid 
leukemia. In addition, the cancer risks of tobacco smoking are greatly 
enhanced for some cancer sites when combined with exposure to other known 

    Not only cigarettes 
    Apart from cigarette smoking, other widely used forms of tobacco smoking, 
such as cigars, pipes and bidis (common in South Asia and growing in 
popularity in the United States), also increase cancer risks for cancer of the 
lung, cancer of the head and neck, and other cancers. 

    The younger one starts, the more significant the risk 
    Risks to smokers are increased greatly the longer they smoke. The 
tendency of youth around the world to start smoking at younger and younger 
ages will predispose them to substantial risks in later life. 

    Don't start smoking, or if you smoke, stop! 
    While it is best never to start smoking, within the next several decades 
the greatest reduction in the number of cancer deaths will be due to the 
reduction in risk for those who stop. Smoking cessation, along with never 
starting to smoke, will remain the best ways to prevent cancer around the 
world in the 21st century. Any possible public health gains from changes in 
cigarette composition would be minimal in comparison. 
    Fortunately, the scientific evidence continues to mount on the benefits 
of cessation at any age. Most of the harmful effect is avoided if smoking is 
stopped in the early 30s, but reduction in risk is obtained even when smoking 
is stopped later in life. Stopping smoking works. 

    Men and women equal 
    The lung cancer risks of smoking are similar in women and men when it has 
been continued equally long and in similar ways. In the United States and the 
United Kingdom (where many women have smoked cigarettes throughout adult 
life), roughly 90% of lung cancers in both men and women are attributable to 
cigarette smoking. 

    Some cancer risks unaffected 
    Tobacco smoking does not cause all cancers. There is now clear evidence 
that smoking causes little or no risk of breast cancer or of endometrial 
cancer. Prostate cancer does not seem to be caused by tobacco smoking either. 


    Second-hand smoke causes lung cancer 
    Nonsmokers are exposed to the same carcinogens as active smokers. Even 
the typical levels of passive exposure have been shown to cause lung cancer 
among never smokers. Second-hand tobacco smoke IS carcinogenic to humans. 
    Concern that breast cancer or any other cancer not caused by active 
smoking might be caused by involuntary smoking is unjustified by the evidence. 

    Uncertainty as to risk to children exposed 
    The evidence for increased cancer risks in later life among children 
exposed to parental and other passive exposures is uncertain at this time.


    The IARC Monographs 
    The IARC Monographs series publishes authoritative independent 
assessments by international experts of the carcinogenic risks posed to humans 
by a variety of agents, mixtures and exposures. Since its inception in 1972, 
the series has reviewed more than 880 agents, and IARC Monographs have become 
well-known for their thoroughness, accuracy and integrity. 

    North American contacts: Marshall Hoffman 703-820-2244 
    Terry Collins 416-538-8712 

     For further details of the Monographs evaluation, please inquire by 
                        e-mail to 

       For more general information, contact Dr Nicolas Gaudin, Chief, 
                      Communications ( 

           World Health Organization       Organisation mondiale de la Sante 
           International Agency for             Centre international de 
             Research on Cancer                 Recherche sur le Cancer 

                150, cours Albert-Thomas, 69008 Lyon, France 

        Telephone: 33 4 72 73 85 67        Facsimile: 33 4 72 73 83 11 

SOURCE World Health Organization - International Agency for 
Research on Cancer 


What counts as "news" in this country has sunk to all time lows.

What they don't tell you here, but has been noted in other reports, is that this study is the result of meta-analysis.  That means no original research was conducted.  It is a pooling of studies already conducted.

News reports such as the one above are conclusion jumped to based on nothing more than the summary of a report that hasn't even been released yet. All they have from which to draw their conclusions are the opinions of the researchers.

If honesty counted for anything in the smoking and secondhand smoke debate you'd be asking yourselves these questions right now:

Are you at all interested in what the report itself says?

Are you at all interested in knowing how they reached their conclusions?

Since this is yet another in a long line of meta-analyses, are you interested to see which studies they disregarded, which numbers they threw away and which data they cherrypicked to fit their conclusions?

Until the actual study is released neither we nor any health organization can ethically say what this report means to any of us.  We'll be awaiting that release and will report in full then.

Researcher hoping for big changes from study tying second-hand smoke to feline lymphoma
Researcher hoping for big changes from study tying
              second-hand smoke to feline lymphoma ^Eds: Antony is CQ  

                  JUSTIN POPE, Associated Press Writer 

 Wednesday, July 31, 2002 
                  (07-31) 03:15 PDT BOSTON (AP) -- 

                  Dr. Antony Moore knows smokers often won't quit to 
                  protect themselves or their children. But he hopes his 
                  new study tying second-hand smoke exposure to the 
                 most common kind of feline cancer will persuade 
                  some people to kick the habit. 

                  "I think there's a lot of people who might not quit 
                  smoking for themselves or their family," said Moore, 
                  a veterinarian at Tufts University. "But they might for 
                  their cats." 

                  In the study, Moore and other researchers at Tufts 
                  and the University of Massachusetts say living in a 
                  household with smokers considerably increases a 
                  cat's risk of acquiring feline lymphoma, which kills 
                  three-quarters of its victims within a year. 

                  The researchers, writing in Thursday's issue of the 
                  American Journal of Epidemiology, studied 180 cats 
                  treated at a Tufts veterinary hospital between 1993 
                  and 2000. They found that, adjusting for age and 
                  other factors, cats exposed to second-hand smoke 
                  had more than double the risk of acquiring the 

                  In households where they were exposed five years or 
                  more, cats had more than triple the risk. In a 
                  two-smoker household, the risk went up by a factor 
                  of four. 

                  It's difficult to say how many cats get feline 
                  lymphoma, believed to be caused by a leukemia 
                  virus, scientists said. Lung cancer rarely strikes 

                  Moore hopes the research will inspire others to take 
                  a closer look at the connection between smoking and 
                  lymphoma in humans. Some studies have suggested 
                  a higher lymphoma risk in children of smokers, but 
                  there has been no definitive work. 

                  Bernadine Cruz, a veterinarian in Laguna Hills, Calif., 
                  isn't surprised by the study's results. She has 
                  warned people for years about respiratory damage 
                  smoke can cause in pets, and has no doubts the 
                  smoke has other effects as well. 

                  "We do know that the environmental stresses put on 
                  our bodies, that often cats and dogs will endure 
                  similar stresses, and they're almost magnified 
                  because their lifespans are so condensed," she said. 

                  The same researchers plan a similar study on dogs. 
                  The source of canine lymphoma is also unclear, 
                  though it's possible cats may be more vulnerable. 

                  "They accumulate a lot on their fur," Moore said. "In 
                  a veterinary clinic if a cat comes in, you can tell if it's 
                  in a smoking household because it smells of 
                  smoke." Dogs, he said, tend to go outside and are 
                  washed more.

Discussion on this article to be followed by the actual study abstract:

The goal is unmasked from the onset of this article.  The researcher hopes that, while smokers don't seem to want to QUIT for other reasons, maybe they'll quit for their pet whose dependence relies solely on its owner and will remain so until its heartbreaking dying day -- unlike children who eventually grow up and become independent.

What we have here is another massaged, manipulated and perverted grasping at straws study (and we use that term loosely) in the continuing saga of the crusade for a smoke-free society.

The entire article is a mass of contradictions and leaps of faith:

"It's difficult to say how many cats get feline lymphoma, believed to be caused by a leukemia virus, scientists said."

They studied 80 cats over 7 years.  No study, human or otherwise, is considered reliable on such a small group of subjects according to epidemiological standards.  There are hundreds of thousands if not millions of cats in the U.S.  Neither has it been peer-reviewed or duplicated -- two other forms of substantiating result reliability.

It's difficult to say how many cats get feline lymphoma?  But magically, when it comes to secondhand smoke, they deduce that the cats they studied can be compared to other cats (lots and lots of them) that they haven't studied and have no idea how many of those not studied have contracted feline lymphoma or from what.

They believe that feline lymphoma is caused by a VIRUS.  Cigarette smoke does NOT cause, or even trigger, viruses. Need we say anything more about that?

Cats ARE NOT people.  To make the leap from feline cancer causers to human cancer is a stretch of enormous magnitude.  There are many who admit that even rats, an animal we've come to accept as evidence for links to human carcinogens, do not replicate the human experience.  Remember saccharin?  That was taken off the human carcinogen list 20 years after they held up a rat and said, "Look. Cancer."  Seems it never materialized in humans. And this study is just too convenient to believe there is definitive evidence that SHS causes cancer in cats anyway.

"They found that, adjusting for age and other factors, cats exposed to second-hand smoke had more than double the risk of acquiring the disease."

What age?  What other factors?  Doubling based on what original number?  If you have 100 cats and 2 normally contract cancer, does 4 now cement the fact that what you hope to have found causes cancer actually does?  Not in any honest science book it doesn't.

"In households where they were exposed five years or more, cats had more than triple the risk. In a  two-smoker household, the risk went up by a factor of four."

As people age, they get sick.  85% of all deaths can be attributed to disease. Cats live approximately one fifth the lifespan of humans.  Can they answer whether disease will strike earlier in a species that lives such a shorter period of time?

And let's not forget that we don't know what original number they are tripling or quadrupling on a disease they say they don't know how many actually get it.

Furthermore, we need to come back to the question: what confounding factors did they consider?  In general, in studies that have actually studied humans who smoke, they find that their diets, economic status and other lifestyle factors leave something to be desired and are contributing factors toward lung cancer. In simple terms -- they generally don't take the best care of themselves and sometimes simply can't take better care due to finances. So how much better care are they taking of their pets?  What kind of food can they afford for them?  How many times are they taken to the vet?  Indeed, what are their vaccination records?  If feline lymphoma is a virus, is it possible that without proper vaccination they are more prone to a viral infection?

And finally:

"Some studies have suggested a higher lymphoma risk in children of smokers, but there has been no definitive work."

But they sure do state with absolute conviction that cats (80 of them out of lots and lots in this country!) in a smoking household are at risk of tripling their chances of acquiring cancer due to secondhand smoke during their "childhood" years. Actually, in 1998 the World Health Organization completed a study that found a 22% decrease in the chances of adults getting cancer who were exposed to smoke as a child.  This was the only statistically significant finding in that study.

AJE ABSTRACT on Environmental Tobacco Smoke and Risk of
Malignant Lymphoma in Pet Cats
Am J Epidemiol 2002; 156:268-273.  
Copyright © 2002 by the Johns Hopkins Bloomberg School of Public Health  
Environmental Tobacco Smoke and Risk of 
Malignant Lymphoma in Pet Cats 

Elizabeth R. Bertone1,2, Laura A. Snyder3 and Antony S. Moore3  

1 Department of Biostatistics and Epidemiology, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA. 
2 Department of Clinical Sciences, Tufts University School of Veterinary Medicine, North Grafton, MA. 
3 Harrington Oncology Program, Tufts University School of Veterinary Medicine, North Grafton, MA.  

Feline malignant lymphoma occurs commonly in domestic cats and may serve as a model for non-Hodgkin’s lymphoma in humans. Several studies have suggested that smoking may increase the risk of non-Hodgkin’s lymphoma. To evaluate whether exposure to household environmental tobacco smoke (ETS) may increase the risk of feline malignant lymphoma, the authors conducted a case-control study of this relation in 80 cats with malignant lymphoma and 114 controls with renal disease diagnosed at a large Massachusetts veterinary teaching hospital between 1993 and 2000. Owners of all subjects were sent a questionnaire inquiring about the level of smoking in the household 2 years prior to diagnosis. After adjustment for age and other factors, the relative risk of malignant lymphoma for cats with any household ETS exposure was 2.4 (95 percent confidence interval: 1.2, 4.5). Risk increased with both duration and quantity of exposure, with evidence of a linear trend. Cats with 5 or more years of ETS exposure had a relative risk of 3.2 (95 percent confidence interval: 1.5, 6.9; p for trend = 0.003) compared with those in nonsmoking households. These findings suggest that passive smoking may increase the risk of malignant lymphoma in cats and that further study of this relation in humans is warranted. Am J Epidemiol 2002;156:268–73.  

Key Words: cat diseases; lymphoma; smoke; smoking; tobacco smoke pollution 

Abbreviations: CI, confidence interval; ETS, environmental tobacco smoke; TUSVM, Tufts University School of Veterinary Medicine.


Questionnaires.  They sent out questionnaires.  In this day and age can you reasonably expect people to answer honestly how much, or whether or not, they smoke?  Smoking has been so demonized that it's entirely more reasonable to expect that any number of smokers will say they do not smoke when they do, skewing the data.

Recall.  Not only do they use questionnaires but they ask about behavior that occurred two years prior. This leads to recall bias.  Memory does NOT serve people well.

Comparitive relevance.  While we're not too sure what the significance is, it does sound like they've compared apples to oranges.  Their case group consisted of  80 cats with malignant lymphoma while their control group consisted of 114 cats with renal disease.

How do you compare subjects with 2 different diseases to reach any reliable result?


While they do not state this in their abstract, this study, according to a helpful gentleman at WABC radio in NYC where this story was aired, was sponsored by (paid for) The Cape Cod Cats Club AND the National Institute of Health.

There is no reason the NIH should study cats.  That is, unless using cats to terrify smokers in order to further their anti-smoking agenda would be useful to them.

Related Material

Flavour of The Times by Number Watch

How does it take two journalists to write guff like this [see AP Article] and then get the numbers wrong? The Trojan Number was actually 194 cats, 80 with lymphoma and 114 controls with renal disease. From this small sample of 80, the “researchers” not only proved that tobacco smoke may cause lymphoma in cats but established a linear trend. Warning: children, do not try this at home; only qualified epidemiologists can perform this feat. It has all the hallmarks of classical epidemiology; anecdotal evidence, wide 95% confidence intervals (1.2 to 4.5) adjustments for age and "other factors", no believable mechanism in terms of concentrations of any possible agents. In a word, Junk. How about an alternative headline: Passive smoking reduces renal disease in cats.


Smoking linked to cavities in kids

UPI Science News
From the Science & Technology Desk
Published 3/11/2003 4:05 PM

ROCHESTER, N.Y., March 11 (UPI) -- Young children exposed to secondhand smoke appear to have a greater risk of developing cavities and tooth decay, a study released Tuesday suggests.

Researchers led by Dr. C. Andrew Aligne, a pediatrician formerly with the University of Rochester and now the founder of Pediathink, a research consulting firm in Rochester, N.Y., examined the connection between secondhand smoke and oral health problems.

The team used data collected from the Centers for Disease Control and Prevention's Third National Health and Nutrition Examination Survey, which was collected from 1988 to 1994. Information on 3,531 children, ages 4 to 11, were analyzed, including blood level measurements of cotinine, a byproduct of nicotine that serves as a marker for environmental tobacco smoke exposure.

As reported in the March 12 issue of Journal of the American Medical Association, study results showed 25 percent of the children had at least one unfilled decayed tooth surface or cavity and 33 percent of the kids had at least one tooth filling, indicating a prior history of cavities.

Researchers also found more than half the study group -- 53 percent -- had cotinine levels indicating secondhand smoke exposure. They reported, however, the association between cotinine levels and cavities was not as statistically significant in children's permanent teeth.

"Passive smoking is known to cause so many health problems in kids, some that are related to cavities," Aligne told United Press International. "It's probably not that cotinine in and of itself in your blood is causing cavities."

Instead, secondhand smoke might cause children to breathe through their mouths more, creating dry mouth. Saliva protects the teeth from decay so dry mouth could increase the risk of cavities, Aligne explained. He added secondhand smoke exposure also might suppress children's immune systems, making them more vulnerable to illness, even oral health illness.

Although the study looked at blood levels of cotinine, the measurements did not indicate how often household members surrounding the child were smoking. "It's difficult to connect that to how many cigarettes Mom is smoking," Aligne said. However, "this is one more piece of evidence that passive smoking harms children."

"Smoking is likely concentrated in people of less education and less affluence," Paul Casamassimo, chairman of pediatric dentistry at Ohio State University College of Dentistry in Columbus and a spokesman for the American Academy of Pediatric Dentistry, told UPI. He said the secondhand smoke link to children's cavities might reflect the association of poverty to children's oral health

If the findings are verified, he said, "this is another nail in the coffin for people not to smoke around children."

Casamassimo noted, however, "you'd think (adult) smokers would have a lot of cavities, but they don't."

Tooth decay is the most common childhood disease in the United States, running up annual treatment costs of about $4.5 billion, according to researchers. Aligne said pediatric tooth decay has declined dramatically over the last 50 years, but it remains a major public health problem for children from low-income families.

Courtesy of FORCES

As the money for loopy "research" becomes scarcer, the grant junkies are scrambling to justify their stipends.  So frenetic have they become that their claims become more bizarre yet more irrelevant simultaneously.  This time secondhand smoke is the culprit for bad oral hygiene in young people.  The usual "risk" is touted, even though it doesn't qualify as risk in its real meaning.  Statistics are shuffled.  Cotinine is again used as a marker for secondhand smoke even though the consumption of potatoes and tomatoes explains why this substance is found in the body.

But the best reason to toss this study down the toilet comes from the researchers themselves.  After many paragraphs devoted to the "link" between secondhand smoke and cavities in the teeth of children "exposed" to secondhand smoke (or tomatoes) the whole theory is quashed:

"Casamassimo noted, however, 'you'd think (adult) smokers would have a lot of cavities, but they don't.'"

Whoops!  No more grants for that researcher!  Never, ever admit that smokers have good teeth and never encourage logic to enter into the equation.  If smokers don't get cavities from running firsthand smoke over their pearly whites hundreds of times per day it is a real far stretch to posit that bystanders, even if children, get cavities from infinitesimally smaller amounts of the stuff.


Smoking Ban Saves Lives in Montana Town

WebMD Medical News
Published 4/1/2003

6 Smoke-Free Months Lead to a 60% Drop in Heart Attacks

April 1, 2003 (Chicago) -- Anti-smoking groups have long contended that smoking bans can have a positive effect on public health, and now they have proof: When Helena, Mont., enacted a smoking ban in public buildings, there was a 60% drop in heart attack admissions at local hospitals.

"What surprised us was how quickly there was an impact from this ordinance," says Richard Sargent, MD, who presented the study at the American College of Cardiology's 52nd Annual Scientific Session. "Also interesting, we found that people from the surrounding area around Helena, where smoking was permitted, still had similar heart attack levels. I liken it to a doughnut. In the hole is smoke-free Helena. In the dough is high-smoke, high-heart-attack surrounding area."

"This striking finding suggests that protecting people from the toxins in secondhand smoke not only makes life more pleasant; it immediately starts saving lives," says co-author Stanton Glantz, PhD, professor of medicine at the University of California, San Francisco, Cardiovascular Research Institute and a statistics authority. "This work substantially raises the stakes in debates over
enacting and protecting smoke-free ordinances."

A similar debate is going on in New York City, where a two-day-old ban forbids smoking in bars, restaurants, and other indoor public places. A more stringent smoking ban will go into effect statewide later this year.

From June 2002 to December 2002, an ordinance in Helena, the capital of Montana, banned smoking in bars, restaurants, casinos, and workplaces in the city. "Helena represents a unique situation," says Glantz. The city of 65,000 people is relatively isolated and is served by one general hospital.

Researchers at St. Peter's Community Hospital reviewed records for the previous four years and determined that about 6.8 admissions for heart attacks occurred each month. During the time of the smoking ban, there were three admissions per month. "That represents a 60% decline in admissions and is highly statistically significant," Glantz tells WebMD.

Though there is a possibility that the findings are due to chance, Glantz says that the odds for this to be a chance occurrence are about 2 in a 1,000.

Sargent says the idea for the study came about when he and a colleague were having a casual conversation about a drop in heart attack admissions. Sargent recalls that his friend said the decline was unbelievable, which led Sargent to search the medical records.

Sargent says the records were meticulously scrutinized to make sure the findings were real. "We believe this is the first time we have been able to show that a smoking ban has resulted in such a reduction in heart attacks."

"This is a small study, so we have to be cautious in how we interpret these results," say Richard Pasternak, MD, associate professor of medicine at Harvard Medical School. "However, the direction of the impact is correct. We know that the smoke from one cigarette can rupture a plaque in blood vessels." That rupture can cause a heart attack or stroke. Pasternak says that secondhand
smoke is also known to have similar impact on people with heart disease.

"So when we have less people exposed to smoke, as was the case in Helena, it makes sense that the hospital admission rate will be decreased," Pasternak says.

Unfortunately, smoke-free Helena is only a memory.

Robert Shepard, MD, of St. Peter's Community Hospital, another co-author, says the smoking ban was overturned by a court ruling. "We are seeing an increase in heart attacks again since December," Shepard says.

In December, there were six heart attacks; eight occurred in January, five in February, and nine in March. He says that in a couple of more months he will be able to confirm that the suspension of the smoking ban can be blamed on causing 14 to 16 heart attacks in the city.

Sargent says the results of the Montana study may be able to help other communities that are attempting to implement smoking bans, such as in the city of Chicago and the states of Delaware and Florida.

SOURCES: American College of Cardiology's 52nd Annual Scientific Session. Richard Sargent, MD, St. Peter's Community Hospital, Helena. Stanton Glantz, PhD, professor of medicine, University of California, San Francisco, Cardiovascular Research Institute. Richard Pasternak, MD, associate professor of medicine, Harvard Medical School. Robert Shepard, MD, St. Peter's
Community Hospital, Helena.


Do smoking bans cut heart attacks in half?
Jacob Sullum, Reason Magazine

April 4, 2003

Cut heart attacks in half! Ban smoking in bars and restaurants!

This is the latest come-on from the busybodies who want to banish smoking from private businesses. The claim, which has been credulously repeated by the news media, is based on a study of heart attacks in Helena, Montana, during the six months after a smoking ban took effect.

The unpublished study is the work of Richard Sargent and Robert Shepard, two local physicians who were leading advocates of Helena's smoking ban, and Stanton Glantz, a well-known anti-smoking activist who directs the University of California at San Francisco's Center for Tobacco Control Research and Education. Sargent says they discovered that the smoking ban "led to an immediate and dramatic decline in the number of heart attacks experienced in Helena."

In truth, the study shows nothing of the kind. The fact that Sargent and his fellow tobaccophobes got away with this kind of prevarication shows how eager journalists are to accept any factoid that helps the anti-smoking cause.

According to data Sargent presented at a recent meeting of the American Academy of Cardiology, St. Peters Community Hospital in Helena saw an average of less than four heart attacks a month from June, when the smoking ban took effect, until December, when the ordinance was suspended because of a legal challenge. From 1998 through 2001, by contrast, the hospital recorded an average of about seven heart attacks a month during the same part of the year.

In a UCSF press release, Glantz declared, "This striking finding suggests that protecting people from the toxins in secondhand smoke not only makes life more pleasant; it immediately starts saving lives."

To a more skeptical eye, this striking finding suggests the perils of drawing conclusions from a single study involving tiny, volatile numbers. As Richard Pasternak, an associate professor of medicine at Harvard, told UPI, "This is a small study, so we have to be cautious in how we interpret these results."

Unless we work for the news service at Glantz's university. The headline on the UCSF press release, which was echoed by news outlets, announced, "Public Smoking Ban Slashes Heart Attack Rate in Community."

A little calculation shows how preposterous this claim is, even if you believe that secondhand smoke causes heart disease. The American Heart Association attributes 35,000 heart disease deaths a year, about 5 percent of the total, to secondhand smoke.

It seems reasonable to assume that the proportion would be similar for heart attacks, fatal or not. So even if a city completely eliminated secondhand smoke (which Helena's ban did not do, since it did not apply to smoking at home), how could that possibly cut heart attacks in half?

Sargent and Glantz note that smoking bans also encourage smokers to cut back or quit. Inconveniently for them, that point suggests that any drop in heart attacks could be due to less smoking rather than less exposure to secondhand smoke.

In any case, the numbers still don't add up. According to the U.S. Centers for Disease Control and Prevention, smoking accounts for about one-fifth of heart disease deaths. So even if every smoker in Helena quit (which no one claims happened), you would not get anything like the drop that Sargent, Shepard and Glantz attribute to the ban.

If smoking bans cut heart attacks in half, it's odd that no one has noticed it before, especially in big cities such as Los Angeles and San Francisco, where an effect of such magnitude should have been obvious. Indeed, why didn't Glantz study hospital data in places within his own state where the samples would have been much bigger and the results more meaningful, instead of focusing on what Sargent calls "a tiny little community in the middle of nowhere"?

California's ban on smoking in workplaces took effect in 1995; it was extended to bars in 1998. Yet according to CDC data, the number of heart disease deaths in California did not drop substantially in either year. If smoking bans cut heart attacks in half, surely the effect would have shown up in these numbers.

Likewise, Delaware should see a sharp drop in heart attacks now that it has banned smoking in all workplaces. So should New York City, where a smoking ban took effect this month, and New York state, which recently passed a ban that takes effect in July. Ditto Boston, Chicago, Dallas and Florida. Or is there something special about hearts in Helena?


Stanton Glantz's Margin of Error
Jacob Sullum, Reason Magazine

Stanton Glantz has written a response to my criticism of his study claiming that Helena, Montana's smoking ban cut heart attacks in half. Among other things, he says the study was not really that small, because "there were over 500 cases included in the analysis." He seems to be referring to the total number of heart attacks in Helena and surrounding areas from 1998 through 2002. But the outcome measure was heart attacks per month in Helena, a very small, highly variable number that ranged from 1 to 13 during the study period.

In response to my suggestion that the effect he attributes to the ban is preposterously large, Glantz says, "The individual risk of heart attack associated with passive smoking is about 30%, which is within the 'margin or error' of the 60% drop we saw in Helena." The 30 percent figure is the increase in risk associated with long-term secondhand smoke exposure in some epidemiological studies. It is itself implausibly high--about one-third the increased risk from smoking, which involves much higher levels of exposure--and it tells us nothing about immediate effects like those Glantz is claiming.

In any case, even completely eliminating secondhand smoke could reduce heart attacks by 60 percent only if exposure to secondhand smoke more than doubled the risk--an increase of 150 percent, compared to the 30 percent figure from the studies to which Glantz alludes. That does seem to be a pretty big difference, no matter what Glantz's margin of error was. And it implies that exposure to secondhand smoke is more dangerous than smoking.

Perhaps realizing how ridiculous and inconsistent this claim is, Glantz hedges by arguing that "when you make workplaces smokefree, many smokers quit or cut down, which reduces their risks of heart attack." But as I pointed out in my column, this effect could not possibly account for a drop of the magnitude Glantz is claiming, even if every smoker in Helena quit.

[NYC C.L.A.S.H. Note:  In its original form, this story contains links to referenced material.  We highly recommend clicking on the link to this piece that we provide in the subject title]


If it Sounds to Good to be True
Angry Bear
Slightly left of center comments on news, politics, and economics from an Economist.

Clearly, cutting heart attacks in half would be a tremendous health benefit, both in terms of quality of life, length of life, and health care expenditures. But of course there's a catch: the authors of the study were also long-time backers of the smoking band in Helena. Kevin points out that the CNN story says that Helena, population 26,000, may be too small a sample from which to draw definitive conclusions. And the CNN story goes on to quote the author of the study as saying "This is a tiny, little community in the middle of nowhere. This study needs to be replicated in New York City."

Kevin points out that we don't need to wait:  But why New York? California has had a statewide indoor smoking ban for years, so there ought to be plenty of data available. And since it's statewide, you don't have to worry about the possibility that smokers all just "went outside city limits" to light up.

As it turns out, California data are readily available on the web. I thought that if the result were true, economists would have already written papers on the subject and if not then I should probably do so. So I took a quick look and found that there was no noticeable change in California's rate of heart attacks after the smoking ban started:
Hospital Discharges for 
"Heart Failure and Shock" 
(DRG 127)
Hospital Discharges for 
"Heart Failure and Shock" 
(DRG 127), 
as a percent of total discharges
The ban in California took effect on January 1, 1998, so if the results from Montana are credible then there should surely be an effect in California in 1998, but there were actually a bit over 5,000 more hospital admissions for heart attacks in 1998 than 1997. Is some of that population growth? Perhaps, but heart attacks as a percentage of hospital admissions also increased in 1998 (note: a death counts as a "discharge", so discharges are essentially equivalent to admissions). California heart attacks fell from 1998 to 1999, but not back to their 1997 (pre-ban) levels--measured either in the number of attacks or attacks as a percentage of discharges.

So what could account for the Helena result? It may simply not be true. Alternatively, the ban lasted from June to December, so it may be that heart attacks are historically lower in that period for some reason. To check this, the doctors should compare the June-December heart attack rate in 2002 to the rate for the same period in 2001. Another story: It might be the result of random statistical variation. Or maybe a new Bally's opened. But, at least in California, there was no pronounced effect on heart attacks following the smoking ban.


Secondhand Smoke Scam
Steven Milloy, Fox News

October 17, 2003

I could only laugh last April when I first heard about a study claiming that a smoking ban in Helena, Mont., cut the city’s heart attack rate by 58 percent in six months.

A prominent op-ed in this week’s Oct. 15 New York Times hailed the Miracle of Helena (search) and urged readers to give it more credit than it deserves.

Citizens of Helena voted in June 2002 to ban smoking in all public buildings, including restaurants, bars and casinos. Doctors at the local hospital soon “noticed,” according to the op-ed, that heart attack admissions had dropped.

Six months later, the ban was rescinded. Heart attack rates allegedly then rebounded to pre-ban levels.

The bottom line is, “Secondhand smoke kills,” according to the op-ed.

That would certainly seem to be a reasonable interpretation -- if all you did was read and believe the op-ed. But, of course, my inquiring mind had a few questions to ask before coming to a “case-closed” conclusion on the Miracle of Helena.

First, the study isn’t easy to evaluate -- but not because it’s rocket science. There simply is no study to evaluate.

The results were issued in typical junk science style via a quick-and-dirty slideshow presentation at the annual meeting of the American College of Cardiology (search). Six months later, the study still is not available to the public.

Slick junk scientists often choose the “science-by-press conference” mode of releasing results because they know their immediate audience likely will not be able to ask probing questions -- a tough thing to do when only sketchy details are hurriedly presented to people with no familiarity of the research conducted.

Even so, anyone paying attention at the presentation should have picked up on the rather obvious problem with the supposed Miracle of Helena.

Assuming the study information presented is accurate, fewer heart attacks seem to have occurred during the six months of the smoking ban.

But a similar short-lived dip in heart attacks rates also occurred in Helena four years earlier in 1998. If whatever caused the 1998 dip happened again in 2002, the Miracle of Helena is really the Mirage of Helena.

I talked to one of researchers about that simple observation. After stumbling and stammering for an explanation, he finally referred me to the “study’s statistician,” Dr. Stan Glantz (search) (more on him later) -- as if some statistical mumbo-jumbo would credibly explain why the 1998 dip in heart attack rates was just an anomaly but the 2002 dip was definitely due to the smoking ban.

Another glaring problem is the researchers’ failure to study any pre- or post-ban patients to medically determine the causes of the reported heart attacks. Given all the genetic, lifestyle and environmental factors that combine to cause heart attacks, it is quite bogus to attribute them to secondhand smoke, especially without examining any patients.

But why let conflicting data and insufficient data get in the way of a politically correct conclusion?

I’m almost surprised that anyone is still trying to link secondhand smoke (search) with heart disease. The University of Chicago’s Dr. John Bailar -- no friend of the tobacco industry-- published in the March 25, 1999, New England Journal of Medicine his quite devastating analysis of the alleged link between secondhand smoke and heart disease.

On the other hand, I’m not surprised to see Stan Glantz’s involvement in the Mirage of Helena.

Glantz’s colleague on the Helena study tried to pass him off to me as “professor of statistics.” But I know better. I’ve observed Glantz for some time. I’ve debated him on the radio. He’s a shameless say-anything, do-anything anti-smoking zealot.

Glantz has a Ph.D. in applied mechanics and engineering economic systems -- whatever that is, it is not statistics. He’s the director of the Center for Tobacco Control Research and Education (search) at the University of California, San Francisco. He’s funded by the federal government to attack the tobacco industry. The National Cancer Institute, for example, gave Glantz $600,000 to “study” tobacco industry lobbying on the state level.

Just what kind of cancer research is that?

It’s been about six months since New York City’s smoking ban went into effect. I asked Dr. Glantz’s colleague if he would be studying whether the NYC smoking ban experience confirmed or contradicted his Helena study claims.

He mumbled something about such a study being too difficult because of all the data involved.

But I can see where anti-tobacco researchers wouldn’t want to have too much data. It just might clear up the smoke they’re blowing in our eyes.


Smoking Out the New York Times Editorial Page
By Dr. Elizabeth M. Whelan, Health Facts and Fears
Elizabeth M. Whelan, Sc.D., M.P.H., is president of the American Council on Science and Health

April 27, 2004

Earlier this week, the New York Times editorial page opined about the effectiveness of banning smoking in public places as a means of cutting down heart disease risk. Citing a very small, six-month study of heart attack admissions to a hospital in Helena, Montana, the Times editors concluded that "a six-month ban on smoking in public places...appears to have sharply reduced the number of heart attacks."

The Times editorial is an example of dozens of news stories and editorials in recent months that uncritically accept the findings that a reduction of heart attack admissions from 40 to 24 in a six-month period was sufficient justification for banning smoking in public places.

The Times should know better.

First, the literature linking secondhand smoke and heart disease reveals that if there is a causal link, environmental tobacco smoke is at best a very weak risk factor. How could the temporary removal of a weak risk factor for heart disease cause a 40% reduction in six months? It defies common sense.

Second, the Times attempts to deflect criticism of its editorial by wrapping around themselves the medical journal that published the Helena, Montana data, noting "the study gains weight from being published in the prestigious British Medical Journal." Not so at all. Prestigious medical journals, unfortunately, do occasionally publish meaningless or misleading data. What makes a study "gain weight" is its being part of a consistent pattern of similar findings. No other study has ever suggested that a short-term reduction in secondhand smoke in public places (which presumably represents exposures of just a few hours a day, maximum) reduces heart disease risk. This study was not "prestigious." It was aberrant.

Third, the Times goes on to acknowledge that "it remains possible that some factor other than the ban was at work in reducing heart attacks." (Like chance, perhaps?) But even while conceding that the smoking ban may not explain the drop in heart attack admissions, the editors still recommend that the "Helena experience should certainly encourage the politicians who have been fighting to keep public places free of cigarette smoke." This is a non sequitur, in essence an argument that the data may be completely flawed but that we should move forward with public policy anyway.

Fourth, if the Times is convinced that smoking bans in public places reduce heart disease risk (convinced enough to dedicate a full editorial to the subject), why did they not wonder in their commentary why similar declines in heart attack admissions did not occur in large cities like New York or Los Angeles following the ban on smoking in bars and restaurants in those places?

The bottom line is that cigarette smoking is annoying and causes a spectrum of deleterious, acute health effects (like upper respiratory distress and earaches). There are lots of good reasons why we should not be subjected to the assault of secondhand smoke in public places. But using the results of dubious scientific studies to justify smoking bans only reinforces the idea that there are "enemies of pleasure" in the public health arena. Policies aimed at protecting our health should be based on sound science, not hype and political correctness.


Smoking, ETS and Heart Disease: Some Stats the Antis Don’t Publicize
Wanda Hamilton, FORCES

May 5, 2004

The death rate from Coronary Heart Disease (CHD) began dropping in the 1950s, before the 1964 Surgeon General’s report on smoking and health, before the smoking rates began dropping, roughly 40 years before there were any smoking bans in “public” places, and 30 to 40 years before the massively-funded “tobacco control” programs.

According to Centers for Disease Control figures (see Table 29 at in 1950 the death rate from heart disease was 586.9.  By 1960 it was 559.0, by 1970 it was 492.7, and by 1980 it was 412.1.  The rate has continued its steady decrease through at least 2001.

This dramatic drop over time is also reflected in the American Cancer Society’s massive CPS I (1959-1965) and CPS II (1962-1968) studies.  Both among smokers and non-smokers the rate of CHD deaths declined by half when the earlier group was compared with the later group.  [Scheidt S, “Changing mortality from coronary heart disease among smokers and nonsmokers over a 20-year interval,” Prev Med 1997 Jul;26(4):441-446].

It is true that the smoking rate for those over 18 dropped from 41.9 in 1965 to 24.6 in 1995, but the drop began when smoking rates (and exposure to ETS) were at an all-time high in the U.S.  Further, the drop in CHD death rates occurred equally for smokers and non-smokers alike.  And certainly it cannot be explained by a drop in exposure to environmental tobacco smoke for non-smokers, since there were virtually no smoking bans until at least the late 1980s and non-smokers encountered ETS almost everywhere.

There have been a number of reasonable explanations for the drop in the CHD death rate, but none of them involve smoking, ETS exposure, smoking bans, smoking cessation drugs, or tobacco control programs.  In an August 12, 1999 letter to the New York Times Dr. Kilmer S. McCully, Chief of Pathology & Lab. Medicine at the Providence V.A. Medical Center, wrote:  “The improvements in smoking cessation, treatment of hypertension and lower blood cholesterol levels cited by the CDC [as the reasons for the drop in the CHD death rate] are more recent than the onset of the decline in heart disease.  A better explanation is the introduction of synthetic folic acid and vitamin B6 into the American food supply beginning in the 1960s.”

An article in 1997 in Hippocrates (Mason M,“Are Heart Attacks Contagious?” 11(12):42-45, 49)  theorized that the drop might be due to the use of broad-spectrum antibiotics:  “The number of deaths from heart attacks, remember, began to fall in the early 1960s.  The American diet hadn’t significantly improved, and exercise had not yet become a priority [not had the elimination of smoking and tobacco smoke].  But something had changed, and chlamydia experts think they know what it was:  Broad-spectrum antibiotics, particularly tetracycline, had come into wide use.”  These antibiotics would kill such microbes as chlamydia pneumoniae which many researchers believe are a substantial cause of heart disease.

Either of these theories seems plausible to explain the drop in CHD death, as does improved diagnostic and therapeutic techniques.  Or it may be the result of increased affluence or any of a host of other variables.

One thing is certain:  No matter how the anti-tobacco establishment tries to spin these statistics with their own tortured data processing  and absurd arguments, the drop in CHD deaths has nothing to do with them, with smoking or with smoking bans.


Where There's Smoke
Sally Satel, Wall Street Journal
Dr. Satel is a resident scholar at the American Enterprise Institute.

May 7, 2004; Page A16

Activists have rushed to embrace a new study that seems to prove, at long last, that secondhand smoke is life-threatening. The British Medical Journal reported that after a smoking ban in Helena, Montana, the heart-attack rate dropped by almost half. In an accompanying editorial, researchers from the Centers for Disease Control heralded the finding. And that prompted the Washington Post to blare, "Second Hand Smoke Poses Heart Attack Risk, Warns the CDC."

In truth, the study is woefully unreliable; but its compatibility with widespread anti-tobacco animus gave it status as "fact." Meanwhile, other solid data that tobacco products can improve the health of smokers go largely ignored.

In June 2002, Helena banned puffing in public places. The prohibition was overturned in December. In the six months it was in effect, there were four heart attacks per month. From June to December of the pre-ban years, the rate was about seven per month. After December 2002, when the ban was lifted, the monthly average jumped back to seven in June-December 2003.

The study has the ring of plausibility. We know that in the laboratory, components of cigarette smoke can cause blood clotting and damage to the lining of blood vessels. But the drop in Helena heart attacks was too dramatic to be explained by reduced exposure to environmental smoke. The reason is that airborne smoke has been shown to have only a weak relationship to heart disease. Moreover, it is difficult to draw meaningful inferences from just a handful of adverse events like heart attacks in a small town over just a half-year.

Still, it would be worth replicating these observations on a much larger scale -- in New York or LA. My guess is that a big-city study would not show such a massive decline in heart attacks. If smoking bans produced such a rapid fall, wouldn't we have noticed by now? With secondhand smoke having declined 75% between the early '90s and 1999, why didn't the national heart-attack rate plummet as it did in Helena?

The stampede to embrace the flimsy Helena study provides an illustration of the double standard surrounding scientific evidence about tobacco. One striking example concerns the virtues of smokeless tobacco. Smokers can dramatically reduce health risks by switching to smokeless products. Consider a Swedish experience: Although 40% of men in Sweden use tobacco products, Swedes have the lowest rate of lung cancer in the EU. Why? Largely because of moist snuff (or snus), which represents half of all the tobacco that Swedish men use. (The other half smoke.) Risks of mouth cancer, depending on the smokeless product used, range from negligible (with snus) to half the risk associated with smoking, for products like chewing-tobacco.

Compare this level of evidence with the study from Helena. Yet anti-smoking advocates embrace that idiosyncratic study while rejecting the growing scientific consensus -- based on replicated, large-scale studies -- that smokeless tobacco can be an effective strategy for harm reduction. A researcher at the National Cancer Institute wrote that "we know little" about "transition to other tobacco products (such as smokeless tobacco) as methods for reducing cancer risk." The surgeon general told Congress that "there is no significant scientific evidence that suggests smokeless tobacco is a safer alternative to cigarettes." Both are patently false.

Assuming that steering people toward better health is the goal here, we need a clear-eyed view of the data -- not a wishful guide to policy that overlooks strong evidence.


Second Hand Joke
Sydney Smith, Tech Central Station
Sydney Smith is a family physician who has been in private practice since 1991. She is board certified by the American Board of Family Practice, and is a Fellow of the American Academy of Family Practice.

May 7, 2004

The rationale for these bans is that smoking in public is not only a nuisance for non-smokers, but a health threat. While it's true that an asthmatic non-smoker may have problems working or relaxing in a smokey bar, anti-smoking advocates have lately drastically stepped up their claims regarding the dangers of second hand smoke. A CDC official, writing in the British Medical Journal warned people with heart disease to avoid all buildings that allowed any smoking, claiming that just thirty minutes of inhaling second hand smoke could cause heart attacks. Apparently, even miniscule amounts of tobacco smoke can turn your coronary arteries from this into this.

The basis of this latest second-hand smoke hysteria is a study in the same issue of the British Medical Journal which purported to find a forty-percent decrease in heart attacks in Helena, Montana, during the six months that the city banned smoking in public places. The data come from St. Peter's Hospital, the one hospital that serves the Helena area, population 68,000. Most of the time, between the months of June and November, St. Peter's gets anywhere from thirty-four to fifty patients with heart attacks. During the six months of the smoking ban, they had only twenty-four. Obviously, the drop in heart attacks must be due to the smoking ban.

Or maybe not. First of all, the number of patients that St. Peter's serves is very small, and the smaller the patient population the more likely disease rates will fluctuate just by chance. Take, for example, my own medical practice. I have around two thousand active patients. Most of the time, I have one or two people in the hospital on any given day. But for the past month, for some reason, I've been averaging four to six patients a day. Is it something about the way I'm practicing medicine? No. I'm practicing the same way I do when I have no patients in the hospital. It's just the nature of illness and populations. Every doctor experiences good months and bad months that are more or less random, (except for bad viral seasons, when patient influx is predictable.) It's not far fetched to think that the same thing is going on at St. Peter's, and if the study had compared heart attacks year to year, rather than six-month period to six-month period, there might not have been such a large difference.

Another problem with the study is that during the six months of the smoking ban, the hospital changed the way it diagnosed heart attacks. Before the smoking ban, heart attacks were diagnosed by testing for an enzyme called creatine phosphokinase. When the heart is damaged, this enzyme leaks into the blood. However, other muscles can leak this enzyme, too, so relying on it exclusively can result in a certain degree of false positives. During the smoking ban, the hospital began testing for another enzyme, called troponin, and enzyme which is specific to heart muscle, and which improves diagnostic accuracy considerably.

It's quite a stretch to look at the data from Helena and conclude that thirty minutes of second hand smoke exposure will kill your heart. It's just too small a sample to make such sweeping conclusions. If banning public smoking really reduced heart attack rates by forty-percent, wouldn't New York city cardiologists have noticed by now? A forty-percent decrease in business is hard to overlook. And wouldn't the city's health department, which believes strongly in the benefits of smoking bans, have noticed, too?

Smoking is bad and smoking around non-smokers without their permission is rude. But exaggerating the dangers that smokers pose to non-smokers is not wise. For one thing, it undermines the credibility of the medical profession. For another, it promotes an attitude of intolerance that should give us pause in a free society. The way things are going, it will be only a matter of time before a smoker is charged with manslaughter for his co-worker's heart attack.


Smoking 'a blight on fertility'

BBC News

Smoking damages almost all aspects of sexual, reproductive and child health, according to a report.
The study, by the British Medical Association, says smoking has caused impotence in 120,000 men aged 30-50.

It is responsible for up to 5,000 miscarriages a year, reduces the chances of successful IVF and is implicated in cases of cervical cancer.

The BMA is calling for tough anti-smoking measures, including help for pregnant women to avoid passive smoke.


The BIG Liars
Numbers Watch

The BMA, long separated from anything approaching real science, has come up with a "report" on, wait for it, smoking and fertility. Not only is it a long winded PC rant, full of the most egregious excesses of the debased statistics that characterise modern epidemiology, but they manage to sully the name of one of the few great names of that branch of science, Sir Austin Bradford Hill. Having taken his name in vain at the very outset, they publish an appendix containing his seven principles by which epidemiology should be conducted, but they add a cavillation to almost every one that completely reverses its intent. Such arrogance! How dare they? One tries to maintain an air of detached amusement at the activities of these politically correct pseudo-scientists, but producing such a travesty of the work of a great man is way beyond the pale. It induces a feeling of impotent anger that they have the ear of the media and the politicians.

It would unbalance a number of the month column to include even a highly abbreviated account of the absurdities in this "report", so it is included in these pages in the form of an FAQ (well, sometimes you have to anticipate the questions before you get overwhelmed).

Related Opinion:  Epidemiology Beyond Its Limits, Tech Central Station, Feb. 23, 2004


Cardiovascular Effects of Secondhand Smoke
Nearly as Large as Smoking

Cardiovascular Effects of Secondhand Smoke  
Nearly as Large as Smoking 

(Circulation. 2005;111:2684-2698.) 
© 2005 American Heart Association, Inc. 

Special Report 

Joaquin Barnoya, MD, MPH; Stanton A. Glantz, PhD 
From the Center for Tobacco Control Research and Education, Cardiovascular Research Institute, and Division of Cardiology, University of California, San Francisco. 

Reprint requests to Stanton A. Glantz, PhD, Professor of Medicine, University of California, San Francisco, 530 Parnassus, Suite 366, San Francisco, CA 94143-1390. E-mail 

Background— Secondhand smoke increases the risk of coronary heart disease by 30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. 

Methods and Results— We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system—platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size—is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. 

Conclusions— The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.


It's too ridiculous to dedicate too much time to.  Here are a few observations -- all that is really needed in response to this junk:

> It's no more than a literature review of old studies and treated it as a new "finding."

> Glantz's cherry-picking is so clever (this full study reads like a 150-count indictment), the sheer number of studies cited is so overwhelming (who cares about the quality, when there's just so MUCH!  And who cares if he mixes in rats and rabbits-- they just add to the "overwhelming evidence" effect-- and his POINT, I believe, is simply to overwhelm-- to flood the synapses of the gullible reader till reader rolls eyes, throws hands up, gives in.)

> Most, if not all, of the cited epidemiology is found in the Cal Epa report and rather easily dismissed.

> One particular logical flaw is in discussing endothelial function.  Glantz first implies it takes 1 to 2 years of non-exposure for a non-smoker's function to return to normal-- and then in the next breath he refers obliquely to Helena (referred to as "epidemiogical studies") as an ostensible example of how helpful creating non-exposure can be.  Except the Helena experiment lasted 6 months. So which is it, Stanton?  ETS is so awful it takes years to recover? Or mere days after a ban all the non-smokers function fine?

This is as much time we wanted to dedicate to this.  But the editor of WebMD subsequently conceded it was questionable as well:

Burning Questions From Our Readers
Our Public Editor Looks at WebMD's Coverage of Secondhand Smoke

By Robert Davis, PhD
WebMD Commentary

July 29, 2005 -- Sometimes the most incisive questions about medical research come not from journalists who cover the beat but from readers who can sense when something doesn't smell quite right.

Take the case of a recent WebMD news article titled "Secondhand Smoke Hurts Heart Like Smoking." It reports on a review of research, published in the journal Circulation, concluding that even brief exposure to secondhand smoke can have physiological effects that are 80% to 90% of those from smoking. The study's authors say that helps explain why secondhand smoke appears to increase the risk of heart disease by about 30% and to account for at least 35,000 deaths annually in the U.S.

A number of WebMD users weren't buying any of it. "I'm sorry," wrote one, "but I just don't accept that report. ... Everyone should quit smoking. Sure. But to use such studies to suggest that smokers are also killing people around them, and in order to pass more laws against smoking, is fraudulent."

What the WebMD article failed to mention -- but what some readers correctly surmised -- is that there's a political agenda behind the research. One of the authors, Stanton Glantz, PhD, of the University of California, San Francisco, is a prominent anti-tobacco activist who for years has been fighting for restrictions on smoking in public places. Glantz and his co-author make it clear that they are not dispassionate scientists but advocates for a cause, when, at the end of their study, they write: "Implementation of smoke-free policies ... would have substantial effects on heart disease morbidity and mortality. ... Physicians, public health advocates, and policymakers can move forward in implementing these policies secure in the knowledge that implementing smoke-free environments to rapidly and substantially improve cardiovascular health rests on a strong scientific foundation."

In fact, the foundation isn't as solid as they would have us believe. The precise effects of secondhand smoke on heart disease are still a matter of some scientific uncertainty and debate, and Glantz's study doesn't add new data. Instead, it selectively reviews human and animal studies that show adverse effects of passive smoke on blood clotting, cholesterol levels, artery narrowing, antioxidant levels, and other indicators of cardiovascular health. Combining the results of these studies, Glantz and his co-author conclude the effects of secondhand smoke are "on average" nearly as large as those of active smoking. But it's not clear exactly how the authors calculated this average, nor do they address possible pitfalls of the research they cite, such as how relevant the animal studies are to humans or how well human experiments in controlled settings replicate real-world conditions.

Controversy Abounds

Even the authors' premise -- that secondhand smoke increases the risk of heart disease by as much as 30% -- is somewhat controversial. John Bailar, MD, PhD, a professor emeritus at the University of Chicago who's a leading expert on research methods, thinks that figure is implausibly high and points to flaws in some of the research on secondhand smoke. Writing in The New England Journal of Medicine about one such study, he concluded that "we still do not know, with accuracy, how much or even whether exposure to environmental tobacco smoke increases the risk of coronary heart disease."

This isn't to say there's no reason to be concerned about secondhand smoke. Common sense dictates -- and research does show -- that breathing it can be harmful. What scientists are still learning is how harmful. [HERE, NYC C.L.A.S.H. DOES NOT SUPPORT THIS STATEMENT.  IT'S A COP OUT STATEMENT IN THE SCIENTIFIC WORLD THAT WANTS TO "BELIEVE."  IT REALLY MEANS "WE CAN'T PROVE IT'S HARMFUL"] That likely varies depending on an array of factors including the level, length, and frequency of exposure; the amount of ventilation; and health status. When someone goes further, though, and makes more sweeping claims that secondhand smoke is almost as dangerous as smoking -- or that it's not dangerous at all -- it should at least give us pause, prompting us to find out who's behind the statements and take a hard look at the supporting evidence. WebMD users instinctively understand this and are right to expect journalists to do likewise. As one put it, "Show the stats ... or shut up."

Given the strong emotions and high stakes involved, simply asking tough questions about secondhand smoke research is enough to thrust you into the fire. Tobacco proponents may cite such scrutiny as evidence that you endorse their views, while anti-tobacco activists may call you an apologist for the tobacco industry. But for journalists, that cannot and should not be a concern. Our job is to tell the truth as best we can discern it and to question what we're told by everyone -- including those promoting a worthy goal like reducing smoking's deadly toll.

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