raveneye

KMA, since you seem to admire the methodology used to conclude that cigarette smoking is harmful, how about showing us an example of a research paper that used good methodology that came to this conclusion.

Then what I will do is show you a research article on SHS that used the same methodology that came to the conclusion that SHS is harmful.

How about it?

KMA-628

You'll have to give me some time on this, but sure. We are talking about research and studies conducted way before the internet (If I remember correctly, the original smoking studies were conducted in the 50's and 60's), so I don't know how much I will find online.

We need to set limits, though....no articles, just studies.

There is one potential fatal flaw here though: I can't concede to a research study that uses the 1992-1993 EPA study as a reference. No matter how hard I would try, I cannot get past the flaws in that study to see anything that uses it as a reference objectively.

It would be the same if I showed you a study that says SHS is safe, and the study happens to be conducted by a scientist employed by RJ Reynolds or Philip Morris--you wouldn't accept that either--the core flaw (in this case, conflict of interest) would prejudice you to any of the results, regardless of whether they are true or not.

Sorry, but I am just being honest about it upfront.

New thread? or in here?

Offline or online?

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

IC3

People blow SHS way out of proportion..Is it unhealthy? Yes, But if all you non-smokers happen to get a whiff walkin down the street..It's not gonna give you cancer. You know how much SHS you would have to take in to even have a fraction of the damage to your body that smokers get from actually smoking? probably more than you guys will ever inhale.

I can't believe that SHS is like some huge plague to you guys, But all the shit factories, Trucks, Cars, Buses spew out into the air every day doesn't seem to be a big deal. If i was a Non Smoker i would preffer to walk down the street and get a whiff of SHS than to have to breathe in that thick black exhaust smoke that comes out of trucks exhausts system and all the other shit that's floating in the air.

Think of those hot summer days when you look over at the downtown skyline, That aint fog..That's smog and isn't exactly healthy to breathe in either..But you can't escape that shit on those summer days. But it's ok right? Cause what generates all the shit that floats around in the air just may be produced by non smokers as well as smokers.

__________________
"To win any battle, you must fight as if you were already dead" -Musashi

KMA-628

raveneye -

In return, I would like something from you.

I don't have the study in front of me, but I will get it when I can--for now, please work on the assumption that I am not making this up.

How is it that a non-smoker who lives with a smoker has a much smaller of getting cancer/heart disease than a person that comes in contact with SHS in public?

The non-smoker, living with the smoker, comes in contact with a whole lot more SHS than the person who is exposed to it in public, yet the person who has the most contact with SHS has less medical problems than the person who has considerably less contact with SHS.

I am stuck on this point--it just doesn't work for me.

My logic goes: If it is as bad as they want us to believe, more exposure should result in more deaths, not less.

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

smooth

You are making a critical assumption about what either of us would accept--an assumption that is simply not true. Neither of us will discredit a study based on its authors, but assess it on its methodology. Find a study by a scientist employed or funded by the tobacco industry and that is fair game to critique, as well.

You never answered me why you think that referencing a study impugns the research of another study. Research does not necessarily (although sometimes it does, but you seem to think that it always does) use the findings of an ealier study and then build on it in the sense you imply. A study might be referenced to say, look this one was faulty, this one was correct, or look we corroberated its findings. Anytime someone or something is mentioned, it has to be referenced. That's all it means--it doesn't mean the later findings are in any way dependent on the earlier research. That's the meaning of independent studies.

Your requirement that no study include the one you find so unpalatable (why? I have to read your whole analysis of it, are you certain that the study was faulty on scientific grounds or legal grounds? -- the courts haven't until recently even given a shit about scientific research, and judges are not trained to make judgements about methodology--just legal judgements. The judge's assessment shouldn't be interpreted to mean the scientific research was faulty, just on what you've posed so far. You could be ripping the quotes you are supplying wildly out of context. For example, if the judge is arguing that the organization made judgements before the research was in, that is a legal concern, but that doesn't impugn the research that was done--and so far, the quotes only discuss the impropriety of making assessments before the research was conducted--not that the research itself was wrong)...but anyway, your requirement is going to be almost, if not absolutely, impossible to meet. All studies are going to reference all the earlier studies because they are required to account for them--even if they find contradictory results. Just because a study lists something in its references doesn't mean it hinges its validity on the ealier study's validity. Even if it is first on the list doesn't mean it is a "primary" reference--it just means it was mentioned first in the paper.

I already explained this to you in an earlier post, but you didn't respond. Perhaps you didn't see that post, because I had some questions in it for you.

__________________
"The theory of a free press is that truth will emerge from free discussion, not that it will be presented perfectly and instantly in any one account." -- Walter Lippmann

"You measure democracy by the freedom it gives its dissidents, not the freedom it gives its assimilated conformists." -- Abbie Hoffman

smooth

KMA, without reading the study, I am going to engage with some of your implicit assumptions.

You are envisioning that SHS inhalers are people who are milling around in bars for a bit of time and go home. Sometimes they are people who go home and their spouse smokes. Sometimes they go to work and are around co-workers who smoke.

Raveneye is less concerned with those people than he is about the worker who inhales SHS all day at the work environment. The reason why you can't wrap your head around that point is because you are comparing someone who has minimal exposure (keep in mind that a lot of people in the home are going to be respectful of their other who doesn't smoke and take measures to minimize exposure--airing the house, going outside, smoking just a few a day, whathaveyou. even though some don't or even if they are chain smokers, it's still just one at a time) to people who are much more likely to experience more dense and prolonged exposure.

Work environmental SHS, however, is denser. A bar waiter(tress), for example, is going to be exposed to hundreds of smokers at once, throughout the workshift. Do you see better why someone who works in a smoky environment would be exposed to more, not less, than a person who lives with a single smoker (even if that person doesn't take measures to limit their spouses exposure)?

__________________
"The theory of a free press is that truth will emerge from free discussion, not that it will be presented perfectly and instantly in any one account." -- Walter Lippmann

"You measure democracy by the freedom it gives its dissidents, not the freedom it gives its assimilated conformists." -- Abbie Hoffman

KMA-628

Yes, in that case I see it.

I haven't seen a study, yet, that breaks down location of exposure as related to illness (except in-home versus public).

With as many bars and restaurants as there are, you would think, if the risk was as "significant" as many claim, there would be a rash of people dying that used to work in a bar and/or restaurant.

We just don't see that, so, I question the correlation.


By the way, here is one of the studies I read last night. It is pre-1993, so I figured I might learn more from a study that didn't rely heavily on the flawed EPA one from 1993.

1986 Surgeon General Report:
The Health Consequences of Involuntary Smoking

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

smooth

KMA, keep in mind that "significant" does not refer to magnitude, just the liklihood of something being due to chance. Your commentary on the amount of bars versus deaths is speculative. Sources already posted indicate that a number of people, ~3,000 by one estimation that you discount, are dying. But we have no idea how that relates to the number of bars and their workers, mainly because to my knowledge neither you nor I have an idea of how many bars and etc are in existence.

Now, I went back and re-read your initial post on the EPA study. It doesn't appear that you read the study itself. The two litigants contest whether the judge's ruling was procedural or scientific. I don't have the briefs, the opinion, or anything in front of me and frankly, I don't want to dig through it. I'm perfectly willing to discard that first study. Their is other independent research that has nothing to do with that study, other than acknowledging its existence.

One of your links didn't even really go into the case at all, but seemed to be some kind of inflammatory political statement comparing Bush to the EPA's misdeeds or something. I don't know, that was the free air canada but maybe I mis-skimmed it.

I did find this valuable however, from the cato insitute:

So they contend that the EPA cherry-picked data and etc. OK, maybe so maybe not. But we need to see these two studies and evaluate them. The article didn't cite them, perhaps an email to the author(s) would net the two they are referring to? Please let me know if you obtain the references and I will pull them from an article database I have access to on campus and we can discuss their methodology and findings. actually, raveneye will do it I hope, finals week is like a few days away and I'm not even supposed to be in politics anymore!!!! my whole plan in exhibition is totally screwed. tecoyah asked that I not permanently take off, just post on occasion so the community didn't lose a valuable member (I'm assuming after a period of inactivity accounts get trimmed) and here I am again posting away every day! LOL.

But I'm totally willing to do what I can and offer some of my, albeit somewhat limited but at least graduate level and not some intro textbook, quantitative methodology training.

__________________
"The theory of a free press is that truth will emerge from free discussion, not that it will be presented perfectly and instantly in any one account." -- Walter Lippmann

"You measure democracy by the freedom it gives its dissidents, not the freedom it gives its assimilated conformists." -- Abbie Hoffman

KMA-628

smooth -

The CDC report I linked above goes into detail more on the "11" studies referenced above from Cato (who, by the way, has a couple more good con SHS articles that I read but won't reference)

There were 13 studies

11 of the 13 found a "positive association with exposure"

6 of the 13 "reached statistical significance" (i.e. greater than 5%).

In other words, of the referenced studies, less than half of them can "prove" SHS is a danger greater than chance.

--Chapter 1, Page 9, Paragraph 2

Anyway, we don't want to see more of you in Exhibition, if you know what I mean. Your avatar alone gets me in trouble with my wife.


BTW - I did read the articles about the EPA study. Rather than just provide one link mentioning the case, I wanted to show that many sources (from the left, middle and right) had mentioned it. After reading the article about the EPA study, I looked up the above study to see what they were referring to.

This is an afternoon discussion for me, not a formal debate (sound familiar???) so I think, given the fact that I am not devoting hours upon hours to this, I have done a healthy amount of research and not just posted soundbites.

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

raveneye

Well if you're excluding all papers that cite studies that are flawed in some way, then I doubt that either one of us will be left with enough studies to count on one hand.

Plus you are using the term "methodology" in a manner that I do not use it and no scientist would use it, since that term by definition does not include any filtering of the identity of references cited, unless the references themselves are a subject of the research.

So let me propose an alternative (since I no longer know what you mean when you use the word "methodology").

Why don't you just specify, in as much detail as you can, exactly what the minimum scientific requirements would be for you to conclude that some risk factor caused harm. For example, we could specify harm as "death" or "contract cancer" or something else.

After you tell us what your minimum requirement is, then I will show you either (1) neither active nor passive smoking studies meet your requirement; or (2) both active and passive smoking studies meet your requirement.

smooth

Don't you mean on one finger?

LOL.
I mean, a basic premise of scientific inquiry is that nothing is ever proven, only disproven; that no one study is conclusive, anyway. They are all flawed in the sense that all can and must be improved upon. That is, I think, the very nature of scienctific exploration and development.


KMA,
I was going to post this to you a bit ago but didn't want it to come across as snarky.
Whenever you write or think "prove" then you need to replace that with "failed to disprove [the null hypothesis]." It may appear symantic, but it's not to statisticians (for some reason, lol, I'm not one).

Has to do with the inability to prove 100% something will occur, so the jargon doesn't even allow that kind of talk, and by extension, thought.

__________________
"The theory of a free press is that truth will emerge from free discussion, not that it will be presented perfectly and instantly in any one account." -- Walter Lippmann

"You measure democracy by the freedom it gives its dissidents, not the freedom it gives its assimilated conformists." -- Abbie Hoffman

Ilow

^^^Furthermore, the fact that the legal and scientific systems run on drastically different criteria may account for the "flawed" EPA study. It frequently occurs that what is statistically significant say at the <.05 level, (meaning that there is less than a 5% chance that the result occured by chance alone) is not the same as PROVING something to a court.

__________________
"Religion is the one area of our discourse in which it is considered noble to pretend to be certain about things no human being could possibly be certain about"
--Sam Harris

KMA-628

You and I could find "flaws" in every study, all day long.

I take exception with this particular study because it has been proven flawed, in a court of law, not because I simply didn't agree with the findings. That is why I stated that I wouldn't be able to accept any study that uses the EPA study as a primary reference.

I'm not following you here.

I see it as this way:

I feel that the studies in the 50's and 60's were done to find out why people were dying of lung cancer, emphysema, etc. They studied it and studied it and found that a connection occurred with smoking. They didn't go into it (at least that's my impression) with the idea of proving smoking was the culprit, rather they went looking for the culprit and found it.

The SHS studies seem to go about it backwards. They were looking to prove that SHS killed a lot of people. And, when evidence didn't agree with them, they excluded the evidence to reach their goal. Then, others hoped on the bandwagon and added on to the already flawed research.

Like I said, I am not disputing that SHS is a dangerous substance. I am disputing the 3,000/45-60,000 deaths each year that they are trying to tie to passive smoke. My feeling is that passive smoke is no more dangerous than the smog most of us breathe on a daily basis, maybe less.

There is no way to quantify exactly what a person breathes in/doesn't breathe in on a daily basis, and the studies admit this....they admit they are guessing.

The #2 cause of lung cancer is Radon exposure, yet I haven't seen anything that takes radon exposure into account for the lung cancer of non-smokers. Since they can't go back in the past and find Radon, there is no way to remove it from the equation--but they do, nonetheless.

I agree that is causes some harm, I haven't argued that at all.

The current claim is that somewhere in the neighborhood of 45-60,000 people die, each year, from heart disease related to exposure to SHS. That seems really, really high to me and difficult to swallow.

I want to know: how is genetics ruled out? How are other environmental/diet/physical aspects ruled out?

How did they come to the conclusion that nothing but SHS caused these hundreds of thousands of people to die?

I want to know why a non-smoker who lives with a smoker dies less than someone who happens to be around SHS? The non-smoker living with a smoker is around SHS every day of the week, every day of the year, yet they are harmed less by it? Saying a few of the smokers are nice and smoke outside doesn't work for me because it is a guess, we don't know, we don't know how much SHS is around this particular non-smoker.

There just seems, to me, to be too many variables to this:

1) When they did their testing they used a machine to simulate smoking - a machine doesn't cover the filter like a human smoker does, thus ETS around a machine (which includes smoke from the "smoker" and smoke directly from the cigarette) will be less toxic than ETS around a human smoker (who has less sidestream smoke than a machine smoker).

2) Each year we discover new things that can kill us. All of these substances, toxins, pollutants, emissions, etc. are around us on a daily basis, how do you remove them as variables in this equation? According to the studies I read, they remove these variables by saying "we know what toxins are in cigarette smoke" and we "know that Person A was around cigarette smoke at some time" so, thus, their disease is related to SHS because they were around it. It almost seems like the study was complete from end to beginning.

3) We are still learning about genetics involving cancer and heart disease (i.e. why does the smoker live to be 90 years old and the health-nut drops dead at age 40 while jogging. I haven't seen anything that takes this into account--I'm not saying it isn't there, I'm saying I haven't seen it. Also, which is more of a contributing factor? If someone has a family history of heart disease and they have a lot of exposure to SHS, which was the contributing factor? How was the other factor removed?

Do you see where I am going with this?

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

KMA-628

That wasn't the issue--it was picking and choosing of information.

In order for the study to have been fair, the EPA should have brought all 13 studies into the mix.

By excluding studies that didn't say what they wanted, they completely tainted their results.

As a result, the EPA then through its entire study into doubt.

Hence my reservation with further studies that use the EPA study as a major reference.

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

Ilow

Not that I am deluded enough to think that any amount of information will convince those who don't wish to be comitted, but here are some interesting things that I found in a quick search: (Mods, please delete if you feel that this is too long for this area, and i can PM it to people individually)

1) Here is an interesting article that among other things documents that the "flawed" EPA study that KMA complains about so vociferously was actually found not to be "flawed" in 2002. It also speaks to the lengths that the tobacco industry will go to in order to protect itself.

Researchers Discover Documents Outlining Tobacco Industry's Political Efforts to Delay Environmental Protection Agency Report on Indoor Second-Hand Smoke

Dateline: ROCHESTER, Minn., April 2 (AScribe Newswire) —
Using previously secret tobacco industry documents, researchers in the current issue of the American Journal of Preventive Medicine, outline the strategies used by the tobacco industry to try to derail the Environmental Protection Agency (EPA) report that led to smoke-free indoor air requirements.
The researchers show for the first time how the tobacco industry attempted to mobilize political pressure on the EPA to delay or stop it from issuing its 1992 risk assessment on environmental tobacco smoke. The assessment concluded that second hand smoke was a Group A human carcinogen and had adverse effects on respiratory health, particularly in children. It also estimated that environmental tobacco smoke causes approximately 3,000 lung cancer deaths annually in nonsmokers.
The documents show the tobacco industry will expend whatever effort is necessary to protect itself from public health policy that would adversely affect cigarette consumption, says Richard Hurt, M.D., director of the Mayo Clinic Nicotine Dependence Center, and an author of the report. In this manuscript, we show that the tobacco industry is constantly trying to stymie public health efforts with regard to second hand smoke and tobacco consumption.
The authors call the environmental tobacco smoke report a seminal event that led to the development of the movement to create smoke-free indoor air.
The researchers obtained the information on the tobacco industry's political strategies based on tobacco company internal documents made public through litigation in the United States. The documents are available at the Minnesota Tobacco Document Depository in Minneapolis and the British American Tobacco (BAT) Document Depository in London. Strategies that are outlined in the journal's report include:
— Lobbying the first Bush Administration to approve an executive order that would impose new risk assessment standards for federal agencies, thus delaying the release of the EPA report.
— Urging the first Bush Administration transfer jurisdiction over environmental tobacco smoke from the EPA to the Occupational Safety and Health Administration, which would have squelched the EPA report.
— Applying enormous political pressure directly by alleging improper procedure and policy at EPA.
Most of the strategies eventually failed, but the authors say the political pressure from U.S. Rep. Thomas Bliley, Jr., R-Va., was a success.
This is the first report showing how a single member of Congress in conjunction with his staff, tobacco industry attorneys and executives worked very aggressively to advance the tobacco industry's interests, Dr. Hurt says.
Bliley, who served 20 years in the U.S. House of Representatives before retiring in 2000, wrote at least 11 letters to EPA Administrator William Reilly touting industry messages of faulty science and flawed procedures, the research says. The letters included attacks on James Repace, one of the journal article's authors, who was then an EPA air policy analyst and staff scientist.
The authors note that the tactics to slow the process were referred to by tobacco industry officials as sand in the gears.
Eventually, the tobacco industry sued the EPA in federal court to nullify the risk assessment as it related to lung cancer. The proceedings took seven years before the suit reached an appeals court hearing. These tactics successfully delayed the EPA risk assessment and placed a cloud over its validity that was not fully vindicated until December 2002 when the U.S. 4th Circuit Court of Appeals overturned the tobacco industry's suit, the authors report.
Ironically, the EPA report and the publicity surrounding its release accelerated the consideration of smoke-free public places and the passage of smoke-free laws in cities, states and even entire countries.
Co-authors of the report are Monique Muggli, an independent tobacco control consultant in St. Paul, Minn., and Repace, visiting clinical professor, Tufts University School of Medicine and Repace Associates, Inc.
American Journal of Preventive Medicine is a journal of the American College of Preventive Medicine and the Association of Teachers of Preventive Medicine. The American Journal of Preventive Medicine publishes articles in the areas of prevention research, teaching, practice and policy.


2)Here are a couple studies that show that you are misinformed in your thinking that second-hand smoke in the home is not harmful. The first relates to children and the second is a detailed study on the effects of briefexposure (I have the references and charts, but cut them out here.)

Title: Kids' Year-Round Asthma Symptoms Triggered by Parent's Second-Hand Smoke; Children's Doctors Should Ask Parents of Asthmatic Children If They Smoke, Counsel Them on Quitting, Researchers Recommend , Ascribe Newswire: Health, 5/5/2004Database: Health Source - Consumer Edition

Kids' Year-Round Asthma Symptoms Triggered by Parent's Second-Hand Smoke; Children's Doctors Should Ask Parents of Asthmatic Children If They Smoke, Counsel Them on Quitting, Researchers Recommend
Dateline: SAN FRANCISCO, May 4 (AScribe Newswire) —Children with asthma whose parents smoke at home are twice as likely to have asthma symptoms all year long than children of non-smokers, a new study shows.Overall, in a nationwide sample of children with asthma, about 13 percent of parents of asthmatic children still smoke - even though second-hand smoke is known to trigger asthma attacks and symptoms in kids.Those findings, made by University of Michigan researchers and scheduled to be presented here on May 4 at the Pediatric Academic Societies Annual Meeting, reinforce the importance of educating parents about how their own smoking can affect their children with asthma. The study is based on data from in-depth phone interviews with 896 parents of asthmatic children ages 2 to 12 years in 10 states.Those interviews were done as part of the Physician Asthma Care Education (PACE) project, which is designed to improve asthma education for physicians, and consequently the health of their young patients who have asthma. The chronic condition affects one in every seven children.The new analysis was conducted by Kathryn Slish, a researcher in the U-M Department of Pediatrics, with assistant professor of pediatrics Michael Cabana, M.D., M.P.H., M.A. The PACE project is led by U-M School of Public Health Dean Noreen Clark, Ph.D., and funded by the Robert Wood Johnson Foundation.We set out to look at children who have seasonal asthma symptoms, but found that a substantial percentage have symptoms year-round, says Slish. We looked more closely and found a strong relationship between parents' smoking status and the likelihood that their child would have problems all year long.It's not rocket science, since it's well known that second-hand smoke can trigger asthma in children, Slish continues. But it's astounding that so many parents smoke around their asthmatic kids, and don't stop even though their children are having trouble breathing all year.The study echoes findings of previous research by the Centers for Disease Control and Prevention, which looked at whether children had had severe asthma symptoms on more or less than 300 days per year, and found a strong correlation to parent smoking among those with more than 300 days.We used a different approach than the CDC, and looked at 90-day blocks of time corresponding to a season, says Cabana. The only other factor that was associated with year-round symptoms was Medicaid insurance coverage.Slish and Cabana note that their findings should provide even more reason for pediatricians, family physicians and nurses to broach the subject of smoking with the parents of any child diagnosed with asthma, and to steer parents who smoke toward resources that can help them quit.By addressing the issue directly, and reminding parents how second-hand smoke can affect their children, perhaps we can cut down on the number of kids having symptoms throughout the year, Cabana says.Even a very brief intervention with physicians encouraging patients to quit smoking has been shown to be successful, adds Clark.Part of the PACE project is teaching physicians how to counsel asthmatic patients and their parents on avoiding asthma triggers - substances in the air that can bring on an asthma attack or lesser symptoms. Triggers include dust, pollen, pet dander, stress, cockroach droppings, mold, air pollution, exercise, cold air - and second-hand smoke. Some triggers, such as pollen, occur only during some times of the year, while others are present year-round and are mainly linked to indoor exposure.The interviews conducted for the current study were part of the baseline data-gathering effort for the PACE project. Parents of young patients of participating doctors were interviewed at length about many factors. They were asked to recall the number of days during each three-month period of the last year that their child experienced daytime asthma symptoms, nighttime asthma symptoms, or limits on their daily activity due to asthma-related precautions or symptoms.If a child had had symptoms on 27 or more days, or seven or more nights, in a 90-day season, he or she was considered to be in peak or persistent asthma symptoms during that time - a definition laid out by the National Heart, Lung, and Blood Institute of the National Institutes of Health.Most of the children - 84 percent - in the study had peaks in none, one, two or three seasons of the past year. But 16 percent of the children had peaks in all four seasons - meaning they were experiencing symptoms nearly one-third of the entire year regardless of what seasonal triggers might be present.Two-thirds of the children in the study were boys, and 12 percent were African-American. The mean age was around 7, and 61 percent used some sort of daily medication to control their asthma. More than 90 percent of the parents interviewed were mothers. Parents were asked directly if they smoked, and 13 percent answered yes.Three-quarters of the households had private insurance, while 14 percent were insured through Medicaid. The remainder had other government insurance or paid for healthcare themselves. Just over 40 percent of the children lived in temperate climates, where differences between seasons were not dramatic.When the researchers performed a statistical analysis to look at which factors were most associated with year-round symptoms, Medicaid status and parental smoking both were linked to a more-than-doubled likelihood.The researchers hope to continue their evaluation of parental smoking behavior as the PACE project continues, and follow-up interviews with parents take place after their children's doctors receive training in evidence-based asthma care and patient communication.For more information, contact Kara Gavin or Krista Hopson, University of Michigan Health System Media Coordinators, at 734-764-2220, or kegavin@umich.edu or khopson@umich.edu.

Transient Decrease of Exhaled Nitric Oxide after Acute Exposure to Passive Smoke in Healthy Subjects



Contents
Materials and Method
Results
Discussion
References
ABSTRACT. Nitric oxide (NO) is produced and detected in the
exhalate from the respiratory tract where it plays important
regulatory functions. Exhaled nitric oxide (eNO) concentrations
are reduced in active cigarette smokers between cigarettes and
in nonsmoking subjects during short-term exposure to
environmental tobacco smoke. In this study, the authors evaluated
eNO before and after an acute exposure to environmental tobacco
smoke in healthy, nonsmoking subjects (n= 12). Baseline eNO
levels were measured by chemiluminescence at baseline (1 hr
before exposure), shortly after the end of exposure, and 10 and
30 min after the end of exposure. Mean room air NO concentration
increased from 3 ppb to 4 ppm (range, 560 ppb-8.5 ppm) during the
exposure period. Carboxyhemoglobin levels were assessed before
and after the exposure with spectrophotometry. All subjects had
decreased eNO with exposure to environmental tobacco smoke (mean
± standard error of the mean: 16.65 ± 1.35 ppb to
13.86 ± 1.33 ppb;p < .001). These concentrations
remained significantly decreased at 10 min and recovered within
30 min. No modifications in airway resistance or increase in
carboxyhemoglobin levels were observed. Exposure to environmental
tobacco smoke transiently—but consistently—decreased
eNO concentration in healthy, nonsmoking subjects, suggesting
that second-hand smoke can directly affect NO in the airway
environment.
<Key words: environmental tobacco smoke, lung, nitric oxide>
CHRONIC EXPOSURE to environmental tobacco smoke (ETS) is a recognized risk factor for respiratory and cardiovascular disease in healthy subjects.[1,2] Second-hand smoke contains several toxic substances that may produce harmful biological effects in exposed subjects—both in airways and in the circulation.[2,3] There is recent evidence linking short-term, acute passive cigarette smoking to endothelial dysfunction in healthy nonsmokers.[4] Nitric oxide (NO), the most important endothelium-derived relaxing factor, is produced and detected in measurable amounts in the respiratory tract, where it plays a part in pulmonary vascular regulation, bronchomotor tone, and host nonspe-cific defense.[5] Exhaled nitric oxide (eNO) is a simple, noninvasive measure of airway NO, which is particularly sensitive to environmental pollution or to pro-inflammatory airway challenges.[6] Decreased eNO has been reported in habitual smokers,[7,8] and reverts after smoking cessation,[9] suggesting an interference of NO-rich cigarette smoke with local antioxidant defenses. The effects of acute, passive smoking on eNO in nonsmokers are not well known; 1 recent study reported decreased eNO levels in nonsmoking subjects during a brief period of smoke exposure.[10] The current study measured eNO in non-smokers after an acute exposure to second-hand cigarette smoke.
Materials and Method
Twelve nonsmoking subjects with no history of disease, asthma, or other chronic airway disorders were recruited from hospital personnel and were enrolled in the study. All subjects lived in smoke-free homes and were advised to avoid environmental smoke exposure during their free time for at least 24 hr before entering the study. The study protocol was approved by the hospital ethics committee, and all subjects gave written informed consent.
NO was detected with a chemiluminescent analyzer (280 NOA Sievers Instruments, Sievers [Boulder, Col-orado]), characterized by a lower limit of detection of 1 ppb and a NO sampling rate of 200 ml/min. Daily 2-point calibration was performed with zero gas (Zero Air Filter, Sievers [Boulder, Colorado]) and a certified NO gas mixture at 1.01 ppm (SIAD [Osio, Italy]). NO was measured from exhaled air with the subjects performing a single, slow, vital capacity maneuver against an expiratory resistance in accordance with the American Thoracic Society guidelines. The breathing circuit comprised a mouthpiece connected to a Hans-Rudolph valve, through which air was inhaled and then exhaled via an expiratory resistance, while targeting a fixed-mouth pressure of 20 mm Hg displayed on a pressure gauge. This technique allows for closure of the velum, thus excluding nasal NO contamination during expiration. All subjects performed a vital capacity maneuver and then a slow (20-sec) exhalation against a 20-cm H[sub2]O mouth resistance, with a resulting expiratory flow rate of 45 ml/sec. The single-breath pattern of eNO showed an initial washout phase followed by a steady plateau.
Airway resistance, expressed as specific airway conductance (SG[subaw]) was determined by a compensated whole-body plethysmograph (6200 Autobox, Sensor Medics [Milan, Italy]). The technique has been described elsewhere.[11] Measurements were made in triplicate, with the subjects panting at 2 Hz.
We assessed baseline eNO concentrations every 20 min for 1 hr to calculate the coefficient of variation for each subject. We also measured SG[subaw] at baseline and again at the end of the exposure period. At the completion of baseline measurements, subjects entered a room with active smokers, where ventilation was 80 m[sup3]. Smokers consumed 22 cigarettes during the 30-min exposure period, during which time we assessed NO levels in the room. At the end of the exposure period, smokers left the room and we assessed eNO concentrations shortly thereafter, and at 10 and 30 min postexpo-sure. Furthermore, we took blood samples at baseline and at the end of the exposure to passive smoke from 5 subjects by venipuncture, using a heparinized syringe for determination of plasma carboxyhemoglobin level (COHb) by spectrophotometry.
Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using analysis of variance (ANOVA) and Student's paired t tests. A value ofp < .05 was considered statistically significant.
Results
NO room levels in the ambient air increased from 3 ppb to 4 ppm (range = 560 ppb-8.5 ppm) during the exposure period. At baseline, the mean eNO concentration was 16.65 ± 1.35; the individual coefficient of variation was < 10% (Table 1). All subjects had a decrease in eNO concentration immediately after the 30-min exposure to passive smoke (13.86 ± 1.33 ppb;p < .001) (Fig. 1); levels remained significantly lower than the baseline value at 10 min (14.93 ± 1.24 ppb;p = .006). Levels of eNO returned to baseline 30 min after the end of the exposure period (16.95 ± 1.47 ppb; p = .452). SG[subaw] did not change significantly between baseline and the end of the passive smoke exposure (0.279 ± 0.009 versus 0.290 ± 0.014 cm H[sub2]O/sec, respectively; p = .174). We observed no significant change in COHb levels following passive smoke exposure.
Discussion
The results of the present study show that passive exposure to cigarette smoke is associated with a reduction in eNO in healthy, nonsmoking subjects. Reductions in eNO occurred after a short (30 min) period of ETS exposure; reductions were completely reversed within 30 min after the exposure was stopped. ETS exposure did not yield significant changes, however, in the COHb blood levels in our subjects. Yates et al.10 recently reported a rapid fall in eNO, both during active smoking and passive cigarette smoke inhalation in normal subjects. The authors noted eNO remained low for 60 min. Our findings generally agree with and further refine those results.
We measured eNO using a single-breath, restricted technique. This method eliminates the contribution of the upper airway, the most important site of NO production in humans,[12] and allows for reproducible NO sampling from the lower airways. Moreover, we calculated eNO values from the plateau curve of the NO concentration, obtained by exhaling against a constant pressure and at a constant expiratory flow rate of 45 ml/sec. This rate is easy to sustain and yields reproducible measurements in the same subject, an important feature as a change in flow rates from 1,000 to 5 ml/sec could cause a 35-fold increase in eNO.[12] During baseline conditions, the technique yielded individual coefficients of variation in eNO in our subjects of < 10%.
It is unlikely that changes in humidity or oxygen ambient tension affected eNO measurement during the smoke exposure period. Nafion drying tubing in the exhalation apparatus minimized an increase in water vapor pressure, which may quench and decrease NO concentration during repeated measurements by chemiluminescence.[13] Inhalation of a hypoxic gas mixture could decrease eNO in humans, but only at very low oxygen concentrations.[14]
The reduction of eNO following smoke exposure could not be related to changes in airway caliber or to the effect of the forced expiratory maneuver.[15] We did not observe a significant change in airway conductance, a sensitive measurement of bronchial tone. The reduction of eNO did not appear to result from carbon monoxide, as the eNO decrease following smoke exposure was not associated with significant changes in COHb absorption. Inhalation of cigarette smoke in concentrations sufficient to raise exhaled carbon monoxide levels to 12 ppm should result in no change in eNO level.[8]
The mechanism for the decrease in eNO with exposure to tobacco smoke remains uncertain. Cigarette smoke contains high concentrations of nitrogen oxides,[16] and the reduction in eNO may result from down-regulation of NO synthase by a negative feedback mechanism.[8] During active smoking in the room, the low baseline ambient NO concentration increased to a median value of 4 ppm. Moreover, in vitro regulation of airway epithelium NO synthesis by smoke extracts takes several hours to change protein expression and is usually irreversible[17]; on the other hand, inhaled heated smoke may lead to a local change in airway osmolarity, which could decrease airway NO concentration.[18]
A recent in vitro study on porcine pulmonary endo-thelial cells suggests that the decreased NO generation seen in response to a solution of cigarette smoke could be related to the NOS gene or to NOS activity.[19] Other possible mechanisms include inactivation of NO by oxidants in cigarette smoke. Perhaps NO reacts rapidly with superoxide, yielding the harmful oxidant peroxyni-trite. Cigarette smoking is associated with lung recruitment and activation of neutrophils[20,21] that produce increased capabilities for the generation of nitrated protein. It is also possible that the decrease in eNO is related to some other substance or combination of substances in cigarette smoke.[4]
Exposure to passive smoke is associated with a number of adverse health effects, and several of these may be explained by reduced NO production. NO production by airway epithelial cells may be important in defending the respiratory tract against infectious agents, because NO has antimicrobial properties.[22] Reduction in the endogenous production of NO by the respiratory tract may increase the risk of infection by several mechanisms; it may contribute to the increased risk of respiratory infection after exposure to passive cigarette smoke.[1]
In conclusion, acute passive smoke exposure causes a transient—but consistent— decrease of lower airway NO in normal subjects, but its clinical significance is unknown. The measurement of eNO after passive smoke exposure may, however, provide a sensitive method for exploring airway response to ETS.


3)And finally for those of you thinking about having kids:

Title: EVEN SECOND-HAND SMOKE IMPAIRS FERTILITY , Better Nutrition, 0405668X, Dec2000, Vol. 62, Issue 12Database: Health Source - Consumer Edition

Section: Health Notes EVEN SECOND-HAND SMOKE IMPAIRS FERTILITY
Studies show that tobacco smoke impairs women's ability to conceive and reduces sperm count in men, and even second-hand smoke can prove damaging to fertility. Dr. Michael Hull and his research team reported in Fertility and Sterility that of the over 14,000 pregnancies looked at in the study, women exposed to smoke were about 15 percent less likely to conceive within the period of a year as those in smoke-free atmospheres. In light of this, Dr. Hull and his colleagues concluded that in couples where the woman is pregnant and in those trying to conceive, smoking by either partner is dangerous.

If anyone is interested in MORE documents on how the tobacco industry is subverting research, let me know.

__________________
"Religion is the one area of our discourse in which it is considered noble to pretend to be certain about things no human being could possibly be certain about"
--Sam Harris

smooth

What are you talking about?

I've pointed out multiple times in this thread that your concept of why something is included as a reference doesn't align with why it is actually ina study.

Yet, you don't answer my question, you just keep repeating yourself.


You want us to show you how researchers go through and determine which factors cause the most damage? (re: radon and people living at home with smokers)
You need to sit in a multiple regression course. We can't adequately explain that for you on an internet board.
If you were willing to concede that we are trained in these types of analyses, and if you had an inkling about them, then we might be able to at least get somewhere in this discussion. But as it is, KMA, you just keep repeating stuff that is simply not true based on a lack of understanding of how scientific experimentation is conducted and the format of resulting research published from such research.

I was trying to be patient and polite, and I hope this doesn't come across as impolite. But you simply don't know what you are talking about on some of your points.


I also don't know how you come to a rapid dismissal of the smokers at home versus public issue. Look, even if you thought that someone's family was sitting inside the home and smoking 24/7, literally, for an entire year, they would not be able to produce the same amount of smoke as an entire (or smoking section) bar or restuarant does in...what? what do you want? a day? a week? a month? surely not a year? apples to apples--year vs. year, who would be exposed to more smoke? this is common sense, but you are demanding some study outlining it. Someone has, it just is increasingly obvious you wouldn't believe it if I dug around and showed it to you.

They might, for all we know, have a wild, preconceived notion that tobacco smoke actually harms people!!! before they conduct the study--which to your mind invalidates the whole thing.

Then you questioned why people weren't dying en masse if SHS was so terrible given the amount of bars in the US. But you question how 3K could die from cancer and 50K could die from heart disease, because, wait, just wait, SHS smoke isn't...X.

This has become a ridiculous conversation that isn't fun, it's not informative, and it's not productive any longer to me. I actually feel baited because you implied you were willing to budge a bit if you were shown the evidence. But you are disqualifying every piece of evidence provided to you on the basis of a very misinformed position. And I'm not talking about your ideological position here--I'm talking about your knowledge of how scientific research is conducted and reported upon. That's the only thing I'm referring to. If you have statistical background, I'm very sorry that I am assuming you don't. But your positions are so far away from anything I've ever heard that I just don't think you have sat in a methods, stats, or regression class.

So don't take any of this personally, please, because it is not about you or your intelligence, or your political viewpoint.

__________________
"The theory of a free press is that truth will emerge from free discussion, not that it will be presented perfectly and instantly in any one account." -- Walter Lippmann

"You measure democracy by the freedom it gives its dissidents, not the freedom it gives its assimilated conformists." -- Abbie Hoffman

KMA-628

llow -

I tried to quote you, but that was way too much of a pain in the ass.

So...

I never said smoking the home wasn't harmful - you need to edit that because it is completely false.

As to the EPA report: EPA was struck down as flawed because they rejected evidence that didn't back up their assertion. I even cited the 13 articles in question. Your article didn't cover that at all. It doesn't matter who challenged them--it only matters that they were challenged. Even the tobacco industry, regardless of what you think of them, has a right to defend themselves.

Does the EPA have a reason for rejecting studies that didn't say what they wanted?

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

KMA-628

I was typing the reply you are referring to while you posted the one about "proof". You gotta at least give me chance to respond before you attack again. Hell, I still haven't read your previous post about "proof".

I am stating my case, in my own way, in a way that makes sense to me. We have discussed that in the past.
If I can't operate up to your standards, then I apologize, but I do what I can and am not really here to please anybody.

And if I contradict myself, just point it out nicely and I will respond--I usually do. I am human, just like all of us and prone to mistakes--at least I admit them when I make them here....my wife can't even get me to do that.

And if "scientific experimentation" means excluding information you don't like, than I want none of it.

Now, I am going to back and read the post you first wrote.....

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

Ilow

Appologies, KMA. To be perfectly clear you insinuated that secondhand smoke in the home was not as harmful as smoke in public places (where you seem to feel that there is little damage occurring) which indicated to me that no harm must be occurring if it is less than a small amount. However, no, you did not specifically state that smoking in the home isn't harmful.
As to the challenges, I think that it matters a great deal who challenges the studies. The EPA study was thoroughly peer reviewed and the "peers" have very little to gain other than the truth, whereas the tobacco companies are protecting their most rudimentary interest, it's quite clear why they would object. Really at this point your holding onto that single study as "evidence" that the detrimental effects of smoking are false is like charging the 82nd armored with a musket. The evidence is overwhelming.

__________________
"Religion is the one area of our discourse in which it is considered noble to pretend to be certain about things no human being could possibly be certain about"
--Sam Harris

KMA-628

No.

I will repeat to clear this up.

In one of the studies I read last night, it said that more people die from SHS outside the home than from SHS inside the home (a lot more).

I still haven't found where I read that, but anyway.....

That didn't make sense to me. I would think it the other way around. Granted I am only guessing here, but it just doesn't make sense.

I have been around second-hand smoke in all types of different locations, and I would say that I found it bothered me inside a house more than anything else (second would be a very smokey bar/restaurant with bad air circulation).

I didn't insinuate anything, rather I said I thought it would be worse inside a house.

__________________
Before you criticize someone, you need to walk a mile in their shoes. That way, if they get angry at you.......you're a mile away.......and they're barefoot.

raveneye

Disputing it on what basis? Your own personal hunches?

And what research paper did you read to come to that conclusion? How can you possibly simply know this? Are you suggesting that we don't need to do any research whatsoever to find out how dangerous SHS is, we can just think about it a little bit and simply know the answer?

Which is the reason that I asked my previous question that you still haven't answered: how many people will you allow it to kill each year before you think it would be justified to ban SHS?

So it sounds like you've already made up your mind, and nothing is going to convince you otherwise. Is that the case?

If it is, say so, and we can call it a day.

smooth

KMA,

None of my last points were even considering my post about "proof." That was simply for your own edification if you ever have the misfortune and displeasure of having to pass a stats class (we all feel that way, as far as a know, "passing" a stats class is not directed at your abilities--it's directed at statistical analyses and the requirement that all grads have to go through it so that, well to be honest, so that we can have these kinds of discussions with each other and critically evaluate one another's work).

My points were really about your repetition of the notion that simply because a study cites an earlier study, flawed or not, that the findings of the latter study are impugned. If the researchers wanted to do a follow-up study, even if they disagreed with the findings, they would have to cite the first study. Even if you found a study straight off the back porch of a tobacco sponsored scientist--as in on the payroll commissioned with the sole purpose of rebutting the 1992 study, guess what? the first thing cited on the references would be the study.

It's called a lit review and you have to consider all the previous studies in it and say what you think is wrong and what you think is right and what you are going to add to the body of scientific knowledge. It doesn't mean you use their data. You still start from your own zero point and find data and analyse it. The difference would be a review or a meta-analysis, which is a broad review of all the studies out in the field, instead of producing their own lab level data.


and then my frustration was exacerbated by you repeating that you can't understand how people sitting at home and exposed to intervals of one or a few smokers per day would be less dangerous than people who are experiencing prolonged exposure in their work environment or, before the bans went into place, lots of smokers in public at one time.

__________________
"The theory of a free press is that truth will emerge from free discussion, not that it will be presented perfectly and instantly in any one account." -- Walter Lippmann

"You measure democracy by the freedom it gives its dissidents, not the freedom it gives its assimilated conformists." -- Abbie Hoffman

raveneye

Let me just clarify what I meant here. I know you believe the study is flawed, but that still doesn't allow you to conclude anything about what the true number of deaths per year is, especially if the range is so large.

Or to put it another way, even if I agree that the interval [3000, 60,000] is an incorrect interval, that knowledge still tells us nothing whatsoever about what the correct interval is.

Any attempt to postulate what the real interval is, independently of controlled scientific studies, is nothing more than a hunch.

tecoyah

I would simply like to point out something......the post you reply to here is the "Feeling" of member, not a stated fact, and it was made clear in his post. The member also stated his "opinion" that SHS is dangerous in several previous posts.

Please let us all read each others statements with an eye towards understanding and respect, rather than pure confrontation.

__________________
Holding onto anger is like grasping a hot coal with the intent of throwing it at someone else; you are the one who gets burned. - Buddha

raveneye

tecoyah, KMA, and others: let me just say that I understand how KMA feels about this (he has let me know in a PM also).

And my post wasn't meant to be pure confrontation, it was seriously meant as a question; i.e. how does one make a decision about what is essentially a purely scientific question, when one has already decided to discard the science as bogus?

But I can see how it could be seen as confrontational, and I apologize to KMA if he was offended (I did try to clarify myself in the post above tecoyah's).

I can get emotional about this, because this is not a theoretical philosophical issue, people are dying from SHS, and there are 10s of thousands of upper respiratory infections every year in children caused by SHS. So for me this really is an important discussion, it's about life and death for many people (including myself who works 10-20 hours per week in bars and clubs).

That's where I'm coming from anyway.

Amnesia620

Let's slap an unaffordable tax upon those that oppose the economy of their own country - technically, it could be viewed as the seeds of terrorism beginning to grow.

In fact, since you made the point, your opinion that you state about "ignorant vehicles and second hand smoke..." causes me undo stress and makes me suffer from undo anxiety - which happens to be dangerous to my health! Negativity is a really disgusting habit. People telling other people how to live, and how to enjoy their own life regardless of how they choose to live it, is a nasty disgusting habit! You do not have the right to make me sick with your filthy nasty disgusting stinking opinions and bossiness...

Gee, that sucks...looks like we all have to learn how to get along, huh? Maybe some should go back to Kindergarten and get a refresher course...

__________________
For example, I find that a lot of college girls are barbie doll carbon copies with few differences...Sadly, they're dumb, ditzy, immature, snotty, fake, or they are the gravitational center to orbiting drama. - Amnesia620