| SECONDHAND SMOKE STUDIES: | . |
| . | THE HYPE AND THE DECEIT |
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"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.
DISCUSSIONS:
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Secondhand smoke can triple risk of lung cancer
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by ANDRÉ PICARD / PUBLIC HEALTH REPORTER
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. "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 |
Discussion: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:
Legend
Anti-Smoker 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
cigarettes.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 JunkScience.com
WE CONTINUE WITH...
National Report on Human Exposure to Environmental Chemicals
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March 21, 2001 National Report on Human Exposure to Environmental Chemicals New CDC Chemical Exposure Report Begins to Fill Critical
Data
Show Exposure to Environmental Tobacco Smoke Down
The Centers for Disease Control and Prevention (CDC) today
Advances in a technology known as biomonitoring allow CDC to
"This new resource is a significant development in the field of
This first Report initially measures the exposure of the U.S.
"The Report is a major step toward assessing in the U.S. population
Although the report does not include new information on health
The presence of a chemical in blood or urine does not necessarily
The first Report provides information on the exposure of the U.S.
Metals: lead, mercury, cadmium, cobalt, antimony, barium,
Highlights of the Report
Cotinine
“One significant finding was the more than 75% decrease in serum
Lead
“The good news is that blood lead levels continue to decline among
Next Steps
In addition, CDC will expand the Report to include exposure data
CDC protects people’s health and safety by preventing and
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Discussion on this article: NONE All discussion to follow STUDY ABSTRACT
Major Findings
HighlightsReduced Exposure of the U.S. Population to Environmental
Tobacco SmokeCotinine 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 milliliters4. 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
.05ng/mL)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)
http://www.acsh.org/publications/booklets/traceChem.html"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)
http://www.cdc.gov/nceh/dls/report/Chemicals/cotininegeneral.htm"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."
WE CONTINUE WITH...
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 07/24/2001
Dow Jones Business News
Associated PressCHICAGO -- 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 jama.com)
Discussion:
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."
AND"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.
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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 v
Globe and Mail Article, July
12, 2001 -