Showing posts with label passive smoking. Show all posts
Showing posts with label passive smoking. Show all posts

Sunday, 1 January 2012

Peter Lavac - the whole story

I recently mentioned the bizarre case of Peter Lavac, who blames two people who lived in a flat below him for 18 months for giving him lung cancer and now plans to sue. The whole affair is as fishy as a barrel of haddock, not least because Lavac is a well-known nonsmokers' rights activist and the doctor who claims that his illness was probably caused by secondhand smoke "permeating" his apartment happens to be the chairman of ASH Australia.

My thanks to commenters on the previous post for pointing me to Lavac's testimony to a parliamentary committee on tobacco policy which is dated 1st May 2006. Despite being a member of the Non-Smokers Movement of Australia, Lavac describes himself in this document as a "private citizen". His testimony is filled with anti-smoking clichés and an obvious hatred of smokers.

We have laws to protect us from home invasion by thugs and criminals, yet inadequate laws to protect us from home invasion by toxic carcinogens transmitted by selfish ignorant idiots who do not give a dam [sic] about anyone else ... From the moment these people start sucking on their cancer sticks there is no escape ... Invisible smoking and non-smoking lines make about as much sense as having a non-urinating area in a swimming pool.

His testimony provides some crucial facts that did not appear in the recent news reports, which make a mockery of ASH's claim that his lung cancer (from which he has now recovered) was caused by second, third or fourth-hand smoke. Bear in mind that this testimony was given two years before the cancer was detected, but while he was still living in the apartment.

Not long ago I was diagnosed with a very serious life-threatening illness. One of the first things I did was to purchase a small apartment right on the headland on the edge of a cliff overlooking the ocean to take advantage of the fresh clean air coming off the sea. This, I felt, would be conducive to my recovery and treatment, and give me the best possible chance of beating my illness. The location is idyllic, the view spectacular, the atmosphere tranquil, but, most important of all, the ocean air is pure and pristine.

He does not specify what this life-threatening illness was, but judging by the importance of "fresh clean air", it is reasonable to assume it was some sort of respiratory disorder. Furthermore...

My current health problems are further aggravated and compensated by the fact that I am asthmatic, and have permanent scarring of my lungs from a bout of pneumonia several years ago.

It was at this cliff-side getaway that Lavac encountered two hated smokers who lived in a flat below. According to Lavac, "second-hand smoke constantly permeates my apartment" and according to the Sydney Morning Herald:

Professor Peters told Mr Lavac and his wife to reduce their exposure. After living in their flat for 18 months in 2005-06, they changed address.

And so, within months of giving his testimony to parliament, Lavac had moved house. He had only been there for a year and a half, and it was another 18 months before he fell ill again.

In March 2008, Mr Lavac was in a criminal trial in the Downing Centre, which happened to be filmed for an ABC documentary, On Trial.

"I got pretty sick but at the time I didn't realise just how sick," he said. "I had a bad flu that didn't seem to go away. After the jury verdict I got an X-ray done. I thought I had pneumonia."

A CAT scan detected a small dark shadow at the top of his right lung, and a biopsy confirmed it was cancer.

Here we have a guy with a history of pneumonia, respiratory illness and asthma. A man who had scarred lung tissue long before he moved to his mountain retreat and who had only moved there in the first place because he had a "very serious life-threatening illness".

Both scarred lungs and pneumonia are risk factors for lung cancer:

Tuberculosis and pneumonia can leave scarring on the lungs. The scarring is a risk factor for lung cancer development, specifically adenocarcinoma.

Asthma is also an independent risk factor for lung cancer:

The combined results from five case-control studies--that presented data limited to individuals who had never smoked--showed a 1.8-fold increase in lung cancer risk among asthmatics (95% confidence interval (CI) = 1.3-2.3).

Attributing a case of lung cancer to any single cause is a fool's game—which is why his case will fail if it ever gets to court—but Lavac had at least three identifiable risk factors for the disease which had nothing to do with tobacco. It is plainly nonsense for ASH's chairman to claim that "on the balance of probabilities" Lavac's lung cancer was caused by living for 18 months by the ocean near some people who smoked on the balcony below him. This would be a ludicrous thing to say at any time, but it it is still more absurd when the patient had at least three known risk factors.

You be the judge, because I seriously doubt that a real judge will ever be asked to decide. This is a publicity stunt to launch ASH's campaign against smoking at home. Nothing more, nothing less.

Friday, 30 December 2011

March of the morons

Some pitiful news from Australia:

Cancer sparks legal action over smoking fumes

Peter Lavac, a Sydney lawyer, fitness fanatic and champion surf skier, thought something was wrong when he was not breathing as freely.

Knowing smoke was getting into his air from a flat below where a chain-smoking couple lived, he tried to get them to stop. Unsuccessful, he then approached the body corporate, strata title management and the tenancy tribunal, but to no avail.

He consulted a respiratory specialist, Professor Matthew Peters, who told him to monitor his condition. "From this data and my symptoms, Professor Peters concluded on the balance of probabilities that my symptoms and decrease in lung function were caused by the second-hand cigarette smoke," he said.

No responsible physician would make such a statement. 15% of lung cancers occur in nonsmokers and there are 40 different risk factors for the disease—there is no evidence that being in a flat near another flat where people smoke is one of them. On the contrary, such a hypothesis flies in the face of both science and common sense. What kind of an idiot is this Professor Peters?

Professor Peters, chairman of Action on Smoking and Health, said there was no lower limit for exposure to smoking. "If you can smell smoke, it is hurting you," he said.

Aha! Not just any old doctor, then. This is a guy who has argued for smokers to be denied surgery, who shills for GlaxoSmithKline and who has taken pleasure from hounding smokers out of every conceivable 'public' place in the über-nanny state of Australia. Now, having lied to his patient, he intends to persecute two innocent people who have retreated into their own home—the only place left for them to smoke. Let's not beat around the bush here, friends, this guy is the lowest of the low.

Professor Peters told Mr Lavac, 65, and his wife to reduce their exposure. After living in their flat for 18 months in 2005-06, they moved. In March, 2008, Mr Lavac felt unwell. A CT scan detected a shadow at the top of his right lung, and a biopsy confirmed cancer...

Mr Lavac, who had never smoked, lost a third of his right lung. His surgeon and Professor Peters told him that, on the balance of probabilities, the lesion had been caused by passive smoking.

Yes folks. We live in a world in which professors of medicine tell people that they have developed lung disorders because they lived in a flat for 18 months above people who smoked. This is the state of hypochondria and intellectual retardation we have reached in the last days of 2011.

You can watch this cretin below, if you can stomach it. He mentions that his patient had never smoked and reported no secondhand smoke exposure and so, in his weird little world, it must have been tobacco smoke magically seeping in from a neighbouring building wot done it. At this rate, Australians will be burning wickermen and ducking witches before the end of the decade.




UPDATE:

I didn't want to say too much about Peter Lavac in this post as he has clearly suffered a brush with death. His disbelief at contracting lung cancer is sadly typical of people who think they don't "deserve" to suffer ill health because they have followed all the rules of public health

“How could this possibly happen to me?” asks Peter. “I was at the peak of my physical strength and power. I’d never smoked, I never drank alcohol, I never did drugs, I was an athlete."

However, as Mag points out in the comments, Mr Lavac has a back story himself. He is a member of the Non-Smokers Movement of Australia and lobbied parliament for a draconian smoking ban in 2006.

The coincidences are coming thick and fast, are they not? ASH and the NSMA are both small organisations with limited memberships and yet it just so happens that the "victim" of fourth-hand smoke (or whatever it is) is a prominent lobbyist for NSMA and the doctor who says his story checks out just so happens to be the chairman of ASH.

Gee, what a small world.

Friday, 23 December 2011

The magic 25%

A handful of anti-smoking extremists have long hoped that smoking is linked to breast cancer. The pink ribbon breast cancer campaign is arguably the best-publicised and best-funded initiative in pubic health. Because breast cancer is the most common form of cancer amongst women, even a small association with smoking would allow tobacco control advocates to claim that millions of cases could be prevented by stamping out tobacco.

The problem is that there really isn't any reason to think the two are related. Sixty years of epidemiological research has failed to find a link and, unlike with diseases of the lung and airways, there is no obvious causal mechanism. As recounted in Velvet Glove, Iron Fist (pp. 236-38), neither the International Agency for Research on Cancer (IARC) nor the American Cancer Society believe there is a link and even the otherwise outré Surgeon General's report of 2006 didn't claim smoking to be a cause of breast cancer.

Outside of California, it is generally accepted that breast cancer is not a smoking-related disease. Inside California, things are always a little different. From his pulpit at UCSF, Stanton Glantz has been insisting on a connection for years, and the California Environmental Protection Agency (Cal-EPA) conducted a meta-analysis in 2004 which found an association between breast cancer and passive smoking. When the American Cancer Society expressed reservations about this meta-analysis (amongst other flaws, it excluded a notable cohort study which would have wiped out the association), Glantz went berserk and referred to doubters as "religious fanatics", thus displaying an extraordinary lack of self-awareness.

Glantz has been at it again this month following a review of breast cancer risks conducted by the Institute of Medicine. Getting rather excited at the prospect at linking arms with the pink-ribbon campaign, he overstated the conclusions of the IOM report and announced:

It's time for the large breast cancer advocacy groups to join the tobacco control community.

Glantz seems to think that the IoM report implicated smoking (and passive smoking) as a cause of breast cancer. That is not how I read it, nor is it how the New York Times read it. What the IoM actually found was this:

The evidence also indicates a possible, though currently less clear, link to increased risk for breast cancer from exposure to benzene, 1,3-butadiene, and ethylene oxide, which are chemicals found in some workplace settings and in gasoline fumes, vehicle exhaust, and tobacco smoke.

This was the only reference to tobacco in a 700 word press release. In the report itself, the IoM say that they cannot rule out a link, but that the evidence is equivocal. Tobacco remains a "possible" cause in the same way that mobile phones were found to be a possible cause of brain cancer in a recent IARC report. In other words, the collated evidence does not suggest a causal link, but some studies have found an association.

There are two interesting aspects of the breast cancer/smoking hypothesis. The first is that there was barely a hint of a link for the first 40 years of epidemiological research, as the IoM acknowledge:

Before 1993, more than 50 epidemiologic studies examined the relationship between breast cancer and exposure to tobacco smoke. Although the quality of studies was highly variable, the better conducted studies did not suggest a causal relationship (Palmer and Rosenberg, 1993). An IARC review published in 2004 included studies conducted before 2002, and it relied heavily on a pooled analysis of 53 case–control and cohort studies by the Collaborative Group on Hormonal Factors in Breast Cancer Study (2002) that contended that apparent associations with smoking were confounded by alcohol consumption. The IARC (2004) conclusions were that neither active nor passive smoking was associated with increased risk of breast cancer.

In any other field of research this would be enough to put the matter to bed, but tobacco control was flooded with money in the 1990s and so it continued. This coincided with the rise of ultra-low risk epidemiology and cherry-picked meta-analyses which, in turn, was accompanied by the burden of proof being relaxed in the science to the point where statistically insignificant findings were taken seriously.

Breast cancer is a very common disease and smoking is a very common behaviour. Given these facts, any association between the two should have been evident very early on (by the 1950s, if not even earlier). That no one found an association despite smoking being the most studied risk factor of the twentieth century strongly suggests that none exists. "If smoking was a major cause of breast cancer, we would have found it by now," says Dale Sandler, chief of the NIEHS Epidemiology Branch.

Those who say that smoking (active or passive) causes breast cancer are making an extraordinary claim and, despite efforts being redoubled in the last fifteen years, there is no extraordinary evidence and very little ordinary evidence.

From the IoM report:

Active smoking 

The summary risk ratio was 1.10 (95% CI, 1.07–1.14), indicating a weak association with increased risk for early initiation of smoking. For women who smoked only after a first pregnancy, the summary risk ratio was 1.07, but it was not a statistically significant increase in risk (95% CI, 0.99–1.15). A subsequent report from the NHS found a statistically significant increase in risk associated with greater smoking intensity (i.e., pack-years of smoking) from menarche to a first birth (p for trend <0.001) (Xue et al., 2011). At 1–5 pack-years of smoking before a first birth the hazard ratio (HR) is 1.11 (95% CI, 1.04–1.20); for 16 or more pack-years, the HR is 1.25 (95% CI, 1.11–1.40).

No increase in risk was evident for pack-years smoked from after a first pregnancy to menopause. For 31 or more pack-years, the HR was 1.05 (95% CI, 0.92–1.19). However, pack-years of smoking after menopause may be associated with a slight reduction in risk (p for trend = .02) (Xue et al., 2011). For 16 or more pack-years of postmenopausal smoking, the HR was 0.88 (95% CI, 0.79–0.99).

... For women who started smoking between ages 15 and 19, the HR was 1.21 (95% CI, 1.01–1.44); whereas those who initiated smoking after age 30, the HR was 1.00 (95% CI, 0.76–1.32).

Brown et al. (2010) concluded that their data did not show a consistent association between smoking and significant increases in breast cancer risk among U.S.- or foreign-born Asian women. For example, the results for current smokers showed an OR of 0.9 (95% CI, 0.6–1.3) while ex-smokers had an OR of 1.6 (95% CI, 1.1–2.2).

A study that examined risk for triple-negative breast cancer found no statistically significant increase in risk over nonsmokers based on smoking status, age at initiation, or duration of smoking (Kabat et al., 2011). By comparison, women with estrogen-receptor- positive cancers (ER+) were at significantly increased risk with earlier initiation (< age 20: HR = 1.16, 95% CI, 1.05–1.28) and longer duration of smoking (≥30 years: HR = 1.14, 95% CI, 1.01–1.28).

These relative risks are low or non-existent and even the positive findings are often not statistically significant. The most interesting thing about these associations is that they are actually lower than the associations claimed for passive smoking.

Passive Smoking

A 2005 review by the California Environmental Protection Agency of various health hazards associated with exposure to secondhand smoke included a meta-analysis of 19 epidemiologic studies of breast cancer ... The meta-analysis produced an overall estimate for exposed women of RR = 1.25 (95% CI, 1.08–1.44) (CalEPA, 2005; also reported in Miller et al., 2007). When the analysis was restricted to five studies with more comprehensive exposure assessment, the overall estimate was RR = 1.91 (95% CI, 1.53–2.39).

In 2006, the U.S. Surgeon General’s report The Health Consequences of Involuntary Exposure to Tobacco Smoke, which included consideration of many of the same studies as the California review, concluded, “The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke and breast cancer” (HHS, 2006, p. 13). The conclusion was based on a review of the findings from seven prospective cohort studies, 14 case–control studies, and a meta-analysis of all of these studies. The meta-analysis found that women who had ever been exposed to secondhand smoke (10 studies) were at increased risk of breast cancer (RR = 1.40, 95% CI, 1.12–1.76).

The idea that passive smoking is more dangerous than active smoking is patently absurd, but that didn't stop ASH (USA) hyping Cal-EPA's meta-analysis with this headline in 2005:

Secondhand Tobacco Smoke More Dangerous Than Smoking Itself

It is fitting that an organisation that endorses so much flim-flam should wind up embracing the principles of homeopathy, but any reasonable person understands that the dose makes the poison. In its understated way, the IoM acknowledges that it is a tad unlikely that people who inhale less than 1% of the dose inhaled by smokers would be at greater risk.

For most other smoking-related diseases, the relative risks are much stronger for active smoking than passive smoking. Thus findings of equivalent or stronger relative risks for breast cancer with passive smoking than with active smoking are difficult to explain mechanistically.

And yet these perverse findings exist and they require explanation. At first glance, it seems that the epidemiological research into breast cancer and tobacco don't tell us very much at all. Certainly, they don't tell us very much about the environmental causes of breast cancer, but I think they tell us quite a bit about the state of epidemiology. They show how easy it is to find a relative risk of around 1.25 (ie. a 25% increase) in an observational study. It takes only moderate recall bias or deficiencies in a study's design to come up with such associations. In the case of secondhand smoke and breast cancer we can surmise that the associations are false because there is no link with active smoking, but it is curious that the claimed associations with other diseases also fall in the same ultra-low bracket, regardless of the magnitude of the risk from active smoking.

Smokers are around 1,000 to 2,000% more likely to develop lung cancer. The passive smoker's excess risk is said to be around 25%.

Smokers are around 70% to 100% more likely to develop coronary heart disease. The passive smoker's excess risk is, again, around 25%.

Smokers are not any more likely to develop breast cancer, but the passive smoker's excess risk is said to be—you guessed it—25%.

Despite huge variations in the effects of smoking, the effects of secondhand smoke—if we are to take the epidemiological studies at face value—are remarkably consistent. Consistent with each other, that is. Not consistent with the rest of science.

Monday, 2 May 2011

Passive smoking lowers blood pressure in girls, study reveals

Before retiring to bed last night, I cast a weary, cynical eye on a brief story from The Independent which reported:

Boys who inhale second-hand tobacco smoke at home may experience significant levels of raised blood pressure, a study has found.

But in girls, passive smoking appeared to be associated with a lowering of blood pressure.

These results, if true, suggest that there are dramatic differences between the male and female bodies that make them respond very differently to secondhand smoke. They also imply that there is a new and unlikely form of treatment for girls with high blood pressure: blow smoke at them.

I'm joking, of course, although it is as valid to draw that policy conclusion from the data as it is for the study's author to claim that her work provides "further incentive for governments to support smoking bans". Actually, neither policy would have any effect because the changes in blood pressure were negligible in both cases—a 1% increase/decrease either way, which even the author admits is meaningless for individual health.

An alternative interpretation is that the study found no effect of passive smoking on blood pressure but that by stratifying the results, the researcher was able to find one by chance (in this case, by splitting the group into genders). Or it may be something else; the study only compared cotinine readings with blood pressure readings after all.

The study's author naturally favours the first interpretation:

"These findings support studies suggesting that something about female gender may provide protection from harmful vascular change," said Dr Jill Baumgartner.

Whether there are any biological reasons to explain these contradictory findings, I don't know (... paging #carlvphillips ...). I couldn't possibly comment because—once again—this study has not been published  and it has only been presented at a conference before being press released around the world. It's a PhD dissertation by a student of Population Health and Environment & Resources.

There is an abstract available, however, which shows the increase in boys is not significant while the decrease in girls is significant. Take both genders together and the overall effect of passive smoking on blood pressure is to lower it, although it is unclear whether that association is significant. The abstract also shows a complete lack of a dose-response relationship which is a bit surprising if tobacco smoke was the true cause of the correlation.

What I do know is that it is misleading to report this study under the headline used by both the Daily Mail and The Guardian:

Passive smoking raises blood pressure in boys, study reveals

In fairness to the Mail, they mention the conflicting finding for girls towards the top of the article. The Guardian, to its shame, mentions it towards the bottom. Ben Goldacre recently mentioned an interesting lay experiment which showed how few people bother reading the whole article before making their minds up. Not very many, apparently, which gives The Guardian the horrible distinction of being even worse at reporting science news than the Daily Mail in this instance. (Neither were helped by the study's press release, which only briefly mentions the findings for females.)

We know that the great majority of newspaper readers only ever read the headline, so let's hope the same is not true of blog readers, otherwise the title of this post—which is as technically correct as the Mail and Guardian headlines*—will also give people a mischievously one-sided view of the story.


* Actually, rather more correct since I have at least focused on the statistically significant finding.

(Michael Siegel and Taking Liberties have more on this story.) 




UPDATE:


Carl V. Phillips has a definitive critique on this study over at Ep-ology. Well worth reading.

Wednesday, 2 March 2011

Passive smoking and breast cancer

From the Beeb:

Passive smoking 'raises breast cancer risk'

Er, no. The study does not say that. This is what it says:

Our data suggest that extensive exposure to passive smoking may increase breast cancer risk. However, since risk of breast cancer was restricted to the most extensive passive smoking category with no clear dose response, the association with passive smoking should be considered suggestive only and needs confirmation from other studies.

The statistical association between passive smoking and breast cancer in this study is actually about as suggestive as a burka. The associations are all over the place and none of them achieve statistical significance. The main finding, based on a fairly substantial 1,515 cases, show that nonsmokers exposed to secondhand smoke have a nonsignificant relative risk of 1.08. Has epidemiology really got to the point where anything other than a relative risk of exactly 1.00 is considered "suggestive"? (Chance alone dictates that RRs of 1.00 are rare, but epidemiologists don't believe in chance when they want to make a name for themselves.)

The fact of the matter is that there has never been any good evidence that active smoking causes breast cancer, which makes an association with passive smoking somewhat unlikely, to say the least. Nothing has been more closely studied in the last sixty years than smoking and disease. Since breast cancer is the most prevalent form of cancer in the world, if there was a real association with smoking, it would have been spotted long before now.

It hasn't been for want of trying. Anti-smoking campaigners have always been very keen to find an association because the high incidence of breast cancer would allow them to create even more stratospheric estimates of how many lives are lost to smoking/passive smoking than already exist. But, as I wrote in Velvet Glove, Iron Fist, they have always failed to do so.

A 1994 paper published in the British Journal of Cancer found no link between breast cancer and first or secondhand smoke, nor did a massive assessment of 53 studies that encompassed 55,515 breast cancer patients in the British Journal of Cancer. The Centers for Disease Control, the American Cancer Society, the IARC, the Australian Medical Journal, the British Medical Journal and the US Surgeon General all agreed that there was no link. Geographical and historical spread of cigarette consumption showed no correlation between breast cancer prevalence and smoking, and while lung cancer rates in women began rising in the US from the mid-1960s, breast cancer rates were unaffected by the post-war surge in female smoking.

Velvet Glove, Iron Fist; p. 237

The authors of this new study even acknowledge the lack of evidence for the smoking/breast cancer hypothesis:

...systematic reviews of epidemiological studies published as of 2002 concluded that there was no overall association between active smoking and breast cancer risk, and attributed conflicting results of individual studies in part to the confounding effects of alcohol.

But add that:

However, recent reappraisals of evidence from recent cohort studies have suggested an increased risk of breast cancer that is independent of the effects of alcohol

In other words, decades of research failed to show anything until a few studies were "reappraised" in the era of anything-goes epidemiology in which eager epidemiologists and fevered advocacy groups leap on every finding, no matter how weak. We are now invited to ignore a mountain of evidence built up over decades in favour of single digit relative risks which hover around 1.00, fail to reach significance and fail to display a dose-response relationship. What a state this field of science is in.

If, fifty years ago, you told the scientists who developed the techniques of epidemiology that you thought "passive smoking raises breast cancer risk" because you'd found a statistically insignificant elevated risk of 8% they'd punch you in the face.

That is all.

Friday, 10 December 2010

"It's very scientific"



It was a mark of the crankiness of Victorian-era anti-cigarette campaigners that they claimed cigarettes caused instantaneous death (see Chapter 2, Velvet Glove, Iron Fist). And it was partly because the public became weary of such obvious scare stories that they found it difficult to believe the real truth—several decades later—that chronic smoking could cause fatal diseases in middle- and old-age.

But everything comes full circle and the latest comments from the new Surgeon General, Regina Benjamin, seem designed to take us back at least 100 years. Her predecessor was a tough act to follow. Scientifically illiterate statements like "There is no significant scientific evidence that suggests smokeless tobacco is a safer alternative to cigarettes" and "There is no safe level of secondhand smoke" set new standards of quackery at the Surgeon General's office. But the new incumbent looks up to the job, and when you have an obese Surgeon General serving a president who smokes, all bets are off.

The latest headline claim—breathing a puff of secondhand smoke can kill you instantly—is really just a variation of Carmona's "no safe level" rhetoric. It takes the theoretical possibility that someone at death's door who is critically, terminally ill with heart disease could be finished off by smoking a cigarette, and then extends it to suggest that healthy people are being killed in the street from breathing secondhand smoke.

Benjamin has done nothing to distinguish between these very different situations. Indeed, she has gone out of her way to add to the confusion. This is very clear from her recent interview with Ed Baxter on KGO Radio. Baxter gives her every opportunity to clear up any misunderstanding but Benjamin just keeps piling it up. The transcript is below, and requires little further comment, but I recommend listening to the audio to get a measure of the woman. She doesn't exactly ooze authority. (Listen here - starts at 17.00). My thanks to Becky Johnson for helping with the transcript.

EB: Well, this may be, there have been a lot of warnings about cigarette smoking, but this may be the scariest I've seen. So we really wanted to get it straight from the person who did the study and the survey so we went straight to the top. Surgeon General, Regina Benjamin is on the KGO live line. Thank you for joining us.

RB: Thank you for having me.

EB: If I'm reading this correctly, you're saying your next cigarette could be your last. That's a dramatic way of putting it: "The next cigarette could be your last." This  is a report coming straight out of the Surgeon General's office. Cigarette smoking can cause instantaneous shut down of systems, is that true?

RB: It can certainly cause a heart attack and death, that's true. This report is the 30th Surgeon General's report on tobacco. The previous reports have focused on what diseases are caused by tobacco. But this particular report focuses on how tobacco smoke really damages every organ in your body. One of the things we know is that if you inhale cigarette smoke or inhale passive, second-hand smoke you might have an underlying cardiac disease like heart disease and didn't even know it. When you inhale it, those chemicals, they can irritate the blood vessels, irritate that lining, causing immediate damage. And also cause your blood to be thicker and clot quicker so that can cause an immediate heart attack. So just that one cigarette can cause a heart attack.

JLJ: So even just second hand smoke? Just a whiff of the smoke?

RB: That's correct. We know that cigarettes today have over 7,000 chemicals and chemical compounds. And inhaling those chemicals causes immediate damage to your blood vessels.

EB: And this, of course, would be more severe or traumatic to somebody who has a chronic condition, who has been smoking for a while....

RB: No, it's anyone! Most people who have heart disease, for example, don't even know they have heart disease because they never had any symptoms.

EB: So anyone just walking on a street, a first cigarette or just second hand smoke?
This could be caused by hypertension or any underlining disease, correct?

RB: Any underlying disease or people who may appear to be very healthy and just didn't know it! And also people who are healthy, it affects them as well. It affects your blood vessels and can damage your DNA. We find that people who, particularly women who have reproductive problems, because the DNA is affected by the chemicals in the tobacco. We didn't even know these chemicals existed. We didn't even know that there were 7,000 different chemicals and chemical compounds so these things are new. It's very scientific, but how these chemicals affect your body. Every organ in your body.

EB: We know it causes cancer. It may lead to heart disease. People are talking about chronic diseases. We're talking about instantaneous—and I just want to make sure we're understanding this correctly—instantaneous... your next cigarette or breathing someone's secondhand smoke could cause, basically, an acute episode that could lead to instant death.

RB: That's correct. The other thing is that these cigarettes today are more addicting. The nicotine, the chemical compounds that we now have the science behind—and this report tries to explain how it becomes much more addicting.


Friday, 26 November 2010

Overkill

The big news today is that secondhand smoke causes 600,000 deaths a year worldwide. Anyone tempted to take this figure remotely seriously should bear in mind that the authors of the associated study also believe that "smoke-free laws banning smoking in indoor workplaces rapidly reduce numbers of acute coronary events" and "fully smoke-free policies have a net positive effect on businesses." And, interestingly in the light of the Moral Maze the other night, they consider the main aim of smoking bans to be denormalisation:

Above all, [smoke-free] policies contribute decisively to denormalise smoking, and help with the approval and implementation of other policies that reduce tobacco demand, such as increased tobacco taxes and a comprehensive ban of tobacco advertising, promotion, and sponsorship.

Still, you can't fault their impeccable methodology:

To identify national data for second-hand smoke, the keywords “second hand smoke”, “environmental tobacco smoke”, and “passive smoking” were combined with names of countries or regions, by searching Google and the PubMed database

The spirit of Newton and Darwin lives on, does it not?

What can be said of the 600,000 estimate? Obviously if you extrapolate a relative risk over a larger population, you will get a larger number. That doesn't make the study or studies you are extrapolating from any better, but I won't risk waking this blog's resident troll by going into all that again.

It's interesting that this study appeared in the Lancet because back in the 1990s, Lancet columnist Petr Skrabanek* remarked on the tendency of public health campaigners to use larger and larger populations to get scarier and scarier death counts. He called them "jumbo-jet numbers" because talking about the equivalent number of jumbo-jets that would have to crash for the same death toll sounds more dramatic than explaining that you have to die of something and that most of the people being "killed" were very old. This, from a collection his articles [PDF]:

The intoxication with numbers is another characteristic of the modern crusaders against smoking. They typically use big population blocks as denominators to obtain bigger and bigger numbers. Richard Peto, a leading anti-smoking exponent and a statistician, announced that 'of all children alive today in China under the age of 20 years, 50 million will eventually be killed by tobacco.' This would put the hecatombs of the Second World War in the shade. The British Medical Journal referring to another such statistic, 'typical of the Oxford epidemiologist Richard Peto', quoted that 'about 20 million children now living in Europe will be killed by tobacco in their middle age.' And The Times reported on January 1, 1988, that according to Mrs Risk-factor Epidemiology: Science or Non-science?

Edwina Currie, 'more than a million schoolchildren and 60,000 babies born this year will die of smoking-related diseases such as lung cancer.' Surprisingly, no-one has yet used the population of the whole world as a denominator: this would produce numbers of babies, toddlers, schoolchildren, and other children, killed by tobacco in truly phenomenal ranges. Perhaps the reason for this reticence is the fear of overkill.

Well, now they have. In fact, they've missed a trick by not using the other PR tool of multiplying by years (eg. here). So, to save someone the trouble, here's my study:

'A quantitative, longitudinal assessment of worldwide mortality from environmental tobacco smoke'

Christopher J. Snowdon

Methodology: Google and PubMed of course. I'm a professional.

Results: 600,000 x 10 = 6,000,000

Conclusion: Secondhand smoke will kill 6 million people over the next ten years. Where's my cheque?


[*nb. Petr Skrabanek was a skeptic about—amongst many other things—secondhand smoke. You can probably guess what the anti-smokers' response was. That's right, they accused him of working for the tobacco industry. Which was a lie. He died of a non-smoking related disease in 1994.]

Thursday, 18 November 2010

On a clear day you can still see the evidence

Because of the significance of secondhand smoke (SHS) to the anti-smoking movement in the last thirty years, part of my research when writing Velvet Glove, Iron Fist was to read all the studies relating to SHS and lung cancer. Not just the numerous reports, meta-analyses and summaries which informed the political debate, but the studies themselves which showed the real evidence. Taken together, they provide a far more (for want of a stronger word) equivocal view of the science than is routinely presented by campaigners. In fact, it's difficult to imagine so many conflicting studies showing weak or negative associations being cited as "overwhelming" evidence in a less politicised field of epidemiology.

My annotated list of these studies can be downloaded here and most of the full papers can be read online, so I'll leave the interested reader to make up their own mind, but one question that has been raised is why so many of them are from the '80s and '90s and why are so few of them from the last five years?

The answer, quite simply, is that with SHS popularly recognised as lethal, there is little incentive to carry out further research. Researchers follow research grants and today—with private homes now the focus of anti-smoking campaigns—the big money is to be made in thirdhand smoke, childhood exposure and maternal smoking research.

Studies that produce epidemiological evidence for SHS exposure to adults in normal settings are now few and far between. They tend to include SHS as one possible hazard amongst many and/or receive minimal press attention.

Amongst the first category we might include the very obscure Neuberger study of 2006 ('Risk Factors for Lung Cancer in Iowa Women: Implications for Prevention', Cancer Detection and Prevention) which found that passive smokers were 73% less likely to develop lung cancer than the unexposed group—a finding that the researchers understandably chose not to dwell on.

Amongst the latter category, we could include last year's Tse study ('Environmental Tobacco Smoke and Lung Cancer Among Chinese Nonsmoking Males: Might Adenocarcinoma Be the Culprit?', American Journal of Epidemiology) which found no statistically significant increase in lung cancer risk for passive smokers in either the home or the workplace. As with Neuberger, this 'unhelpful' finding was brushed over in the text of the study by authors, and while they gamely tried to find a stronger (but still nonsignificant) association with adenocarcinoma (which is the type of lung cancer least associated with smoking), this was not a study that received a big press release.

And now—well-spotted by Dick Puddlecote, since it received no press attention—comes another null study. This one (D. Brenner, 'Lung cancer risk in never-smokers: a population-based case-control study of epidemiologic risk factors', BMC Cancer, 2010) found precisely zero increased risk of lung cancer from either childhood or adult exposure to SHS (1.0 95% CI: 0.6-1.8, and 1.0 95% CI: 0.5-2.0 respectively) and no statistically significant increase for workplace exposure (1.2 95% CI: 0.7-2.0). It did, however, find a near-trebling of risk for exposure to paints and solvents (2.8 95% CI: 1.6-5.0) and for exposure to smoke-soot and exhaust (2.8 95% CI: 1.4-5.3). The authors conclude:


Our results support the concept that exposure to exhaust fumes and or soot/smoke (from non-tobacco sources) is a source of carcinogenic exposure.


This study is—or should be—of particular interest since its sample group is unusually large, comprising some 445 lung cancer cases. This puts it high in the rankings of large, well-conducted studies (size being very important when it comes to accurately quantifying risk).

Instead, this study—like most others that fail to support the passive smoking theory—has gone largely unnoticed because, as we all know, 'the debate is over'.

Saturday, 5 June 2010

Free at last


Although completely ignored by the English-speaking media, recent comments by Professor Philippe Even have been widely reported and discussed in his native France. Until recently, Philippe Even was professor emeritus at University of Paris Descartes and the president of the Research Institute Necker. 

As a highly distinguished pulmonologist, he knows a thing or two about respiratory and lung diseases, which is why his comments to Le Parisien have attracted so much attention. This translation comes courtesy of the thoroughly bilingual CAGE Canada:

What do the studies on passive smoking tell us?

PHILIPPE EVEN. There are about a hundred studies on the issue. First surprise: 40% of them claim a total absence of harmful effects of passive smoking on health. The remaining 60% estimate that the cancer risk is multiplied by 0.02 for the most optimistic and by 0.15 for the more pessimistic … compared to a risk multiplied by 10 or 20 for active smoking! It is therefore negligible. Clearly, the harm is either nonexistent, or it is extremely low.

It is an indisputable scientific fact. Anti-tobacco associations report 3,000-6,000 deaths per year in France...

I am curious to know their sources. No study has ever produced such a result.

Many experts argue that passive smoking is also responsible for cardiovascular disease and other asthma attacks. Not you?

They don’t base it on any solid scientific evidence. Take the case of cardiovascular diseases: the four main causes are obesity, high cholesterol, hypertension and diabetes. To determine whether passive smoking is an aggravating factor, there should be a study on people who have none of these four symptoms. But this was never done. Regarding chronic bronchitis, although the role of active smoking is undeniable, that of passive smoking is yet to be proven. For asthma, it is indeed a contributing factor ... but not greater than pollen!

The purpose of the ban on smoking in public places, however, was to protect non-smokers. It was thus based on nothing?

Absolutely nothing! The psychosis began with the publication of a report by the IARC, International Agency for Research on Cancer, which depends on the World Health Organization. The report released in 2002 says it is now proven that passive smoking carries serious health risks, but without showing the evidence. Where are the data? What was the methodology? It's everything but a scientific approach. It was creating fear that is not based on anything.

Why would anti-tobacco organizations wave a threat that does not exist?

The anti-smoking campaigns and higher cigarette prices having failed, they had to find a new way to lower the number of smokers. By waving the threat of passive smoking, they found a tool that really works: social pressure. In good faith, non-smokers felt in danger and started to stand up against smokers. As a result, passive smoking has become a public health problem, paving the way for the Evin Law and the decree banning smoking in public places. The cause may be good, but I do not think it is good to legislate on a lie. And the worst part is that it does not work: since the entry into force of the decree, cigarette sales are rising again.

A maverick? A contrarian? Perhaps, but cui bono? The anti-smoking movement's motive for exaggerating the passive smoking threat is clear enough, but what could a retired pulmonologist have to gain from expressing his scepticism? For me, the most revealing part of the interview was his explanation for why he has waited until retiring before speaking out.

Why not speak up earlier?

As a civil servant, dean of the largest medical faculty in France, I was held to confidentiality. If I had deviated from official positions, I would have had to pay the consequences. Today, I am a free man.



Saturday, 22 May 2010

A tale of two studies


The International Agency for Research on Cancer (IARC) is a well-respected body set up by the World Health Organisation. It has conducted many large epidemiological studies into possible carcinogens. Let's take two of them. We'll call them Product X and Product Y.

There were two major findings for Product X. They were:

Odds ratio: 1.40 (1.03-1.89)

Odds ratio: 1.15 (0.81-1.62)


There were also two major findings for Product Y. They were:

Odds ratio: 0.78 (0.64-0.96)

Odds ratio: 1.16 (0.93-1.44)


You will notice that each study found one small but significant finding and one small but non-significant finding. In the case of Product Y, however, that significant finding suggested a protective effect. 

None of these findings are particularly strong, but—if you had to pick—you would say that Product X was the most likely to be the real carcinogen, right? After all, both findings for Product X show a potential increased risk, and the largest of them is not only statistically significant but is more than twice as large as Product Y's.

But that's not how these findings were reported at all. The WHO issued a press release saying that there was no conclusive evidence that Product X caused cancer and blamed "biases and errors" for the study's findings. The WHO also issued a press release for Product Y, saying that it definitely did cause cancer and blamed weaknesses in the study for its failure to show this more clearly. 

Consequently, the BBC reported that Product X "does not appear to increase the risk" of getting cancer, but reported that Product Y represented "a definite, although small, risk" of getting cancer.

So why would the weakest associations be hyped up while the stronger associations were downplayed?

Product Y is passive smoking. Product X is a mobile phone. 

The World Health Organisation has not decided to wipe mobile phones off the face off the earth.



Wednesday, 7 April 2010

Fruit and veg


The Journal of the National Cancer Institute has just published a very large study which finds that eating fruit and vegetables has, at the most, a very weak effect on cancer risk (see BBC report). This could be seen as yet another example of lifestyle epidemiology contradicting itself—only a few days ago a study reported that eating a fried breakfast was a good way of combatting obesity—but there are good reasons to take this particular paper seriously.

Firstly, it is a very large study, involving over 400,000 subjects. Secondly, it is a cohort (or prospective) study, ie. it follows people over a period of years rather than interviewing people who are already ill. In these two respects, it trumps most of the studies that have found lower cancer risk amongst those who eat their 'five-a-day'.

The JNCI study found a relative risk for those with a high intake of fruit and vegetables to be 0.97 (95% CI = 0.96 to 0.99), ie. a 3% reduction, and there are serious doubts over whether even this extremely modest reduction is genuine or the result of confounding factors. There are few areas of science where a 3% reduction would be taken seriously.

Walter Willett, a prominent figure in the epidemiology of diet, has written a frank editorial to accompany the study, calling the association "very weak" and noting that there is not a single type of cancer that is significantly reduced by eating fruit and veg (full free text). The history of how such a belief came about bears repeating:

During the 1990s, enthusiasm swelled for increasing consumption of fruits and vegetables with the expectation that this would substantially reduce the risk of many cancers. Potential reductions as large as 50% were suggested... 

However, the evidence for a large preventive effect of fruits and vegetables came primarily from case–control studies, which can be readily biased by differences in recall of past diet by patients with cancer and healthy control subjects...

In the late 1990s, the results of large prospective cohort studies of diet and cancer began to accrue, and these did not confirm the strong inverse associations found in most case–control studies. Furthermore, a series of analyses that pooled the data from prospective studies for specific cancer sites confirmed the weak and non-statistically significant associations.

There are clear parallels with the evidence for passive smoking and lung cancer here. In both cases, the largest risks were reported when research was in its infancy (eg. Hirayama, 1981) and most of the evidence came from case-control, rather than cohort, studies. As the years went on, the reported risks diminished, falling from over 2.0 (100% increase) to less than 0.3 (30%). 

Just as the World Cancer Research Fund used a meta-analysis of questionable studies in 2007 to condemn almost everything except fruit and vegetables are carcinogenic, so the EPA and SCOTH conducted meta-analyses based on shaky science to condemn secondhand smoke as carcinogenic.

In both cases, larger and more reliable studies found no risk. In the case of secondhand smoke, one of the most important null studies came from the World Health Organisation's  IARC with Paolo Boffetta as lead author (1998). It found no statistically significant association with lung cancer despite one of the largest sample groups every studied. In the case of fruit and vegetables, the lead author is, again, Paolo Boffetta, and he finds a significant, but very weak, association.

In 1998, the WHO went to the unprecedented lengths of issuing a press release to contradict one of its own studies, so important was passive smoking (and thereby, smoking bans) to the battle against active smoking. It will be interesting to see if there is any backlash against this new study. 

As it is a less heated area, possibly not. Willett concludes his editorial by calling for "heightened efforts to reduce smoking and obesity" which remain the key battlegrounds, but there are many food faddists and vegetarians who will not be happy to hear that their lifestyles are not as healthy as they believed. There will also be many epidemiologists who will (justifiably) feel their work has been discredited.

Ultimately, after a brief period of controversy, the IARC's secondhand smoke report was forgotten about and attention shifted back to the grab-bag of smaller studies which had been favorable to the passive smoking theory. This new study may meet the same fate; already the tiny association it reported is being taken as fact, with all the caveats and doubts ignored:

In any event, a reduced risk of 2.5% should not be dismissed out of hand, the World Cancer Research Fund argues.

"For the UK, this works out as about 7,000 cases a year, which is a significant number," says Dr Rachel Thompson from the charity, which in a major 1997 report said there was "convincing evidence" of the protective effect of fruit and vegetables.

In Velvet Glove, Iron Fist, I described the World Cancer Research Fund's report as "a veritable encyclopedia of weak associations and questionable meta-analyses" (p. 310). Today's JNCI study only reinforces that view. Whatever the truth about this particular issue, basing policy on statistical studies that change like the weather is a fool's errand. 



Sunday, 6 September 2009

Smoking in cars study is misleading


I don't think this will be the last we hear of this...

Secondhand smoke in cars worse than in bars

Jurisdictions around the globe have tried to squash secondhand smoke by banning smoking in public places. But only a few have tried to prevent people from lighting up in their cars -- typically only when children are present.

A new study from Johns Hopkins' school of public health takes on the question car smoking -- just how bad is it?

Pretty bad. The amount of secondhand smoke was significantly higher in cars than in bars and restaurants, the paper found.

This comes from the
Baltimore Sun. The study is unpublished (as is so often the case), but will appear in the October issue of Tobacco Control. That the results are already appearing in the mainstream press is a tribute to the anti-smoking lobby's well-drilled PR machine. Expect to see similar headlines around the world over the next few weeks.

The news angle is evident from the article quoted above - secondhand smoke levels are higher in cars than in bars. The political implications are obvious and the researchers make an open appeal to government in their paper:

These high levels of exposure to SHS [secondhand smoke] support the need for education measures and legislation that regulate smoking in motor vehicles when passengers, especially children, are present.


But the headline is extremely misleading. The study gives an average nicotine level in a car of 9.6µg/m3 (micrograms per cubic metre). There are numerous studies that have measured nicotine levels in bars, so we can see whether the car figure really is 'worse than bars'.

Mulcahy (2005) found a level of 35.5µg/m3 in Irish bars.

Nebot (2005) found levels between 19µg/m3 and 122µg/m3 in bars/discos.

Lopez (2008) measured levels of 32.99µg/m3 in discos/pubs.

All of these readings are far higher than the 9.6µg/m3 reported for cars in this new study. So what's going on? A clue is given in the Mulcahy study which reported a 35.5µg/m3 level before the Irish smoking ban, which fell to 5.95µg/m3 afterwards. 

And then the penny drops. The researchers are comparing the 'smoky' cars with smoke-free bars! It is quite unsurprising, then, that nicotine levels in premises where smoking is completely banned by law are lower than in a car where someone is smoking. Do we really need to pay scientists to tell us such things?

The real finding here is that nicotine levels in 'smoky' cars are much lower than in 'smoky' bars. But that wouldn't make for such a eye-catching headline, would it?



Wednesday, 2 September 2009

1+1=11: James Repace thinks of a number (part 1)

The claim that "tornado-level ventilation" is required to make a building "safe" from secondhand smoke was first made by James Repace, a prominent and fanatical anti-smoking activist since the 1970s. In those days, Repace - who has a degree in physics - was working at the electronics division of Washington's Naval Research Laboratory. By the end of the decade he had written his debut study into secondhand smoke, found a job at the Environmental Protection Agency (1) and soon became a well-known and well-paid anti-smoking spokesman and researcher. In 1998 he set up his own company - Repace Associates, Inc - and became a professional 'secondhand smoke consultant'.

His published papers on the subject of tobacco bear all the hallmarks of the theoretical physicist, with the emphasis heavily on the theoretical. In 2005, he made an effort to convince lawmakers that high tech ventilation systems were not the solution to what he called the "mortal hazard" of secondhand smoke and wrote a paper which concluded that the amount of ventilation required to make a room safe from smokers would be the equivalent of a "veritable indoor tornado." For those of us who have followed the rise of junk science in recent years, this quote has become something of a classic of the oeuvre, but the study from which it came is less well known.

Despite being intuitively ridiculous, the tornado claim has been repeated around the world. In addition to appearing six times on Repace's own website, a quick Google search reveals that it is currently being reported as fact by, amongst many others, ASH, Unison, Cancer Research UK, Americans for Nonsmokers Rights, the Clean Air Coalition, Smokefree Ohio, Stop Smoking Manchester, Smokefree Europe, the World Health Organisation and GASP (although the last three groups have settled for a mere 'hurricane').

The article in question was published in the house journal of the American Society of Heating, Refrigerating and Air-Conditioning Engineers (ASHRAE) in 2005 (2). The publication may be obscure but Repace's decision to submit his paper to it was no accident since ASHRAE issue ventilation guidelines to the building industry. The article is unusually dense with technical jargon which, perhaps deliberately, has the effect of distracting and confusing the casual reader. In its closing paragraph Repace finally gets to the point. He makes two crucial assumptions:

1. The annual US death rate due to secondhand smoke in bars is 15 per 100,000 workers exposed.

2. In a nonsmoking bar, the desirable rate of ventilation is 18 air changes per hour*

Both of these statements are highly contentious but it is not necessary to debunk them individually to show that the tornado claim is nonsense and so, for the purposes of this article, we shall hold our nose and go along with them. Repace - in his roundabout and over-complicated way - multiplies the figure of 18 (the air changes) by 6,750 (which we will come to shortly) to show that a bar that allows smoking requires a whopping 121,500 air changes per hour in order to be as 'safe' as a nonsmoking bar. This equates to 33 air changes per second - a 'veritable tornado' indeed!

The underlying premise for all this is, as Repace wrote, that "since risk is inversely proportional to ventilation rate, the ventilation rate would have to be increased by the ratio of the number of estimated deaths." Doubtless there is some truth in the first part of this sentence. Ventilation surely does reduce risk from air-bound contaminants; this is why it is used in workplaces and scientific laboratories where dangerous chemicals are in the air. This was precisely the message that the hospitality industry, ventilation industry and tobacco industry had been trying to get through to policy makers for years. It was, alas, quite the reverse of the message that Repace and the pro-ban campaigners wanted to send and his tornado calculation hinges on the second part of that sentence ("the ventilation rate would have to be increased by the ratio of the number of estimated deaths.")

But why? What is the correlation? Why on earth should it be assumed that the ventilation rate needs to accelerated by the number of supposed deaths? It is rather like saying that speeding kills 1,000 people a year and therefore the speed limit must be reduced by a thousand to make the roads safe. A speed limit of 0.03mph would certainly make the roads safe but no one would propose such a limit because it is insane to take the correlation between speeding and road accidents quite so literally. In the case of Repace's equation, the very fact that the resulting figure amounts to no fewer than 33 air changes per second would have been enough to make most researchers take a step back and return to the proverbial drawing board. But James Repace is not most researchers and he not only stuck by his conclusion but added, presumably with a straight face, that "even greater airflow rates would apply for air cleaning, which inefficiently removes secondhand smoke gases."

The key number in this calculation is 6,750 (see footnotes for the rest**). Without multiplying 18 by such a high figure, Repace could not have arrived at his terrifying conclusion, so where does it come from? As it turns out, the figure of 6,750 is based on Repace's belief that 15 deaths per 100,000 (per year) are attributable to secondhand smoke amongst exposed workers. He then inflated this number by a factor of ten to arrive at 150 deaths per million and then multiplies that by 45 to represent the 45 years of working life and - voila! - 6,750 deaths. Leaving aside the fact that these estimates are themselves based on highly questionable data, the way in which he arrives at the 6,750 figure reveals that it is completely arbitrary.

It is not even an estimate of the absolute number of US deaths in a year, but an estimate of deaths per million per lifetime. And yet, measuring deaths per million is nothing more than an idiosyncratic statistical device (it is conventional to measure deaths per 100,000). By what twisted logic has it become the gold standard for determining ventilation levels? One might just as easily apply the more common usage of deaths per 100,000 (which would slash the figure to 675) or, since we're picking numbers out of the sky, inflate it further by basing it on deaths per ten million (making it 67,500). Where does it end?

Indeed, considering that he is multiplying it by the number of air changes per hour, it would be more reasonable to also use the estimated number of deaths per hour. This, however, is a figure of just 0.017 and it would have forced him to conclude that 0.3 air changes per hour would render a room safe - the very opposite of a 'veritable tornado'. I am tempted to say that using the hourly rate would make more sense but the whole premise is so absurd that sense does not enter into it. At best it would make it more consistent in its absurdity.

One can argue over whether a room really needs 18 air changes per hour to be 'safe' from environmental contaminants but Repace provides no evidence that this rate of ventilation needs to be increased at all where smoking is permitted, let alone by a factor of nearly seven thousand. What is plainly obvious is that the number Repace multiplies it by is plucked out of thin air. None of the numbers he uses have any relevance to one another except in his own imagination and they are applied to a premise that is, in any case, bereft of rationale. His whole study is based on a series of basic logical errors which, when exposed, bring the rest crashing down.

Postscript

In 1997, the Bellagio hotel and casino opened in Las Vegas with the kind of high-tech ventilation system that Repace claimed was hopelessly ineffective. The Bellagio ventilated its casino several times time every hour with 100% outdoor air. Smoking was permitted throughout, except for the high stakes poker room. In 1999 and again in 2005, air quality assessments found that the air in the casino was as clean or cleaner than that measured outdoors. Respirable suspended particulates (RSP) were found at the barely measurable levels of 12 to 58 micrograms per cubic metre (a microgram is a millionth of a gram) and less than half of the RSP was made up of tobacco smoke. This is far lower than the 400-600 micrograms found in some unventilated bars and is a fraction of OSHA's limit of 5000 micrograms(4)(5). Carbon monoxide levels ranged from 0.8 to 2 parts per million (ppm) - far lower than OSHA's limit of 25ppm. Nitrogen dioxide levels ranged from 0.23ppm to 0.46ppm - well below the permissible 3ppm limit - and nicotine levels were found to be between 3.4 and 9.2 micrograms - a fraction of OSHA's 500 microgram limit (6)(7).

Neither ASHRAE nor OSHA have ever endorsed Repace's study.


* Repace comes up with the figure of 18 air changes an hour by extrapolating from an ASHRAE guideline which stated that this was the amount of ventilation required in a smoky bar. Why Repace then decided he needed to inflate it further is anybody's guess. For the record, the typical ventilation in a bar is between 1 and 2 air changes an hour. In the home, it is even less; ASHRAE recommend private homes receive just 0.35 air changes per hour (3).


**It is worth studying how Repace arrives at the final figure as it provides further evidence of his numerical illiteracy. To do this we must bear two facts in mind:

1. The recommended number of hourly air changes (ACH) is equivalent to 60% of the recommended number of cubic feet per minute per person (cfm/occ) eg. 30 cpm/occ = 18 ACH.

2. There are two ASHRAE guidelines, one for smoky rooms and one for smoke-free rooms. The former requires 30 cfm/occ, the latter 9 cpm/occ.

Repace starts off with the 30 cfm/occ level that applies to smoky rooms and multiplies it by 6,750 = 202,500 cfm/occ. Had he followed this thinking through and worked out the number of air changes, he would have arrived at a figure of 121,500 (which is 60% of 202,500). Instead, he completely changes tack. "However," he writes, "the default ventilation rate for a smoke-free bar under [ASHRAE's] Standard 62.1-2004 is 9 cfm/occ (equivalent to 5.4 ACH)." This is quite true and he proceeds to work out what the 'safe' level would be using the 9 cfm/occ level.

There is a certain logic to using the standard for a smoke-free room since the aim of Repace's study was to find what ventilation is needed to make a room free of smoke. What happens next, however, is very strange.

Instead of multiplying 6,750 by 9 cpm/occ, he takes the figure of 202,500 which he arrived at before and divides it by 9. Why he does this is anybody's guess. This is just plain wrong - he should have divided by 30 and multiplied by 9 - but here, as in much of the rest of the paper, one searches in vain for any semblance of logic. This gives him 22,500, which he then multiplies by the leftover figure of 5.4 for no particular reason and arrives at...121,500 - the exact same number he would have got had he finished off his sums using the 30 cpm/occ figure (above).

A remarkable coincidence? Not a bit of it. Look again at where the crucial figures of 9 and 5.4 came from. 9 ccpm/occ is the ASHRAE indoor air guideline and 5.4 (60% of 9) is the recommended number of air changes pertaining to 9 cfm/occ. Now think of a number, any number. Let's say, for instance, that ASHRAE required a whopping 1,000 cpm/occ indoors and, therefore, 600 air changes per hour. Now do what Repace did. First take the figure of 202,500, divide it by 1,000 ( =202.5) and multiply it by 600. What do you get? That's right: a tornado level of 121,500 air changes per hour. No matter what number you start with, you will always end up with 121,500 because the equation will only ever give you 60% of 202,500. And so, whether ASHRAE requires one cubic foot of fresh air or a million, Repace's equation will always tell you that you need a tornado.

It's like a card trick in which the sleight of hand is executed before you start paying close attention and you end up with the card the magician wants you to have. In this case, the sleight of hand is in the first calculation (6,750 x 30 cfm/occ = 202,500) which looks like a red herring and which Repace appears to disown with a quick "however..." But he has not disowned it and he slips the 202,500 back in as if it were a relevant figure while appearing to be using the more relevant 9 cfm/occ figure. He then employs a final flurry of disorientating calculations, dividing it by 9 and then multiplying by 5.4. The effect is to give us 60% of the first number, which, remember, never belonged in the equation to begin with. It is a very roundabout way of getting there, but this boils down to multiplying 6,750 x 18 = 121,500.

(1) http://www.repace.com/Repace-CV.pdf

(2) http://www.repace.com/pdf/iaqashrae.pdf

(3) http://www.ieqcorp.com/ventilation.htm

(4) http://www.ornl.gov/info/press_releases/get_press_release.cfm?ReleaseNumber=mr20000203-00

(5) http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1637107

(6) www.americangaming.org/assets/files/studies/final_iaq_white_paper_7-7-06.pdf

(7) One nonsmoking visitor to The Bellagio said it has "an air filtration system that makes cigarette smoke almost undetectable, which was a big plus for us and a definate (sic) advantage over other casinos."

1+1=11: Secondhand news (part 2)

[Author's note: When I first wrote this article I had no idea how widespread is the notion than breathing secondhand smoke was more dangerous than smoking. Since putting the article online I have seen the traffic that has come to it by people searching under key words such as 'why is second hand smoke more dangerous than first hand smoke', 'second-hand smoke more dangerous than first-hand smoke', 'the reason second hand smoke is more dangerous than first hand', 'second hand smoking is worse than first because the particles are more concentrated' and 'why second hand smoke causes more harm than first hand'. That is just a very small sample.]

In the second of this series of articles looking at bizarre claims made by the anti-smoking movement, we shall see how the notion came about that secondhand smoke is more 'toxic' than firsthand smoke. As ridiculous as it is, this claim has recently gained considerable currency not only with anti-smoking groups but with the public and even with some politicians. No one individual is directly responsible for this myth arising and no published study has ever explicitly made the claim. Instead, the idea took hold because of a simple misunderstanding and was allowed to flourish because those who should know better had no desire to correct it.

What really started it off was a paper written by Stanton Glantz and Suzaynn Schick in 2005 for the Tobacco Control journal. Stanton Glantz is the high-priest of the anti-smoking movement and this is not the last time we shall encounter him in this series of articles. Having spent ten years studying mechanical engineering, Glantz abandonned the subject in 1973 to embark on a two year course in cardiology. In 1977, he was installed as an assistant professor of medicine at the University of California, San Francisco (1). With his bushy hair, spectacles and array of brightly coloured tee-shirts, Glantz looked every inch the nonconforming West Coast academic. In 1981, he co-founded Californians (later Americans) for Nonsmokers' Rights and set out on his long crusade to portray secondhand smoke as one of most dangerous poisons known to man.

The paper in question - 'Philip Morris toxicological experiments with fresh sidestream smoke: more toxic than mainstream smoke' - is actually perfectly sound for what it is: a straightforward review of a number of obscure experiments conducted by Philip Morris in the 1980s which came to light when the tobacco industry was forced to make its internal documents public in 1998.

The study discusses a series of experiments in which laboratory rats were exposed to very high levels of 'sidestream' and 'mainstream' smoke. Understanding the distinction between the two is crucial in what was to come. Sidestream smoke is, as Glantz correctly described it in the paper, "the smoke that rises from the tip of the burning cigarette between puffs" (2). Mainstream smoke is that which is inhaled and exhaled by the smoker. The definition of mainstream smoke is clumsy and muddled since there is a huge difference between inhaled and exhaled smoke. 1979 Surgeon General's report stated: "When the smoker inhales the mainstream smoke he exhales into the atmosphere less than one-seventh of the amount of volatile and particulate substances that were originally present in the smoke" (3). Exhaled smoke, then, is considerably less 'toxic' than either the smoke that comes from the burning tip or the smoke that is inhaled through the cigarette. That much has always been clear; but the Surgeon General also suggested that inhaled mainstream smoke might be also less toxic than sidestream smoke. It was this hypothesis that inspired the Philip Morris experiments, which began in 1981.

In a secret laboratory in West Germany, rats were placed in tight glass tubes and exposed to extreme concentrations of tobacco smoke on a daily basis. Some of the rats were forced to breathe mainstream smoke, others were given sidestream smoke. The only problem was that inhaled mainstream smoke is very difficult to reproduce and the scientists did so by using a very simple technique: they diluted it with air.



The diagram above was drawn by the scientists who conducted the experiments. The machine on the left is producing sidestream smoke from a smouldering cigarette. The machine on the right is producing mainstream smoke. Notice how the mainstream smoke is coming from the mouth-end of the cigarette and is going down a tube which is open at the top and bottom. This allows the smoke to be diluted by the air. If you look very carefully you can see the words 'dilution air' above it. Contrast that with the sidestream machine which is virtually sealed, thereby forcing concentrated tobacco smoke from the lit end into the tubes.

After three weeks, half the rats given the undiluted sidestream smoke had died; compared to just one from the mainstream smoke group. The hypothesis was proven: sidestream smoke was more toxic than mainstream smoke or, to put it more prosaically, the more smoke is filtered and diluted, the less toxic it becomes.

What could be learnt from this rather mundane and predictable finding? It told us nothing about passive smoking because the doses involved were thousands of times higher than would be inhaled by the heaviest smoker, let alone a passive nonsmoker. The rats that were given the 'sidestream' smoke were being practically asphyxiated with constant, pure tobacco smoke. The difference between the two was underlined by the temperature the rats endured: from a warm 25 degrees celsius in the mainstream smoke tubes to a decidedly toasty 34 degrees in the sidestream smoke tubes.

The scientists who conducted the experiments were well aware that they were not replicating real-life conditions, nor were they trying to. In their report, they stated the obvious: "Under real-life conditions sidestream smoke is diluted in the environment by ambient air and ages through contact and reaction with various surfaces." (4)

It would be several years before Philip Morris scientists began exposing rats to anything approximating real secondhand smoke and when they did so it was with very different equipment. Ageing and diluting the smoke was the key. The apparatus from a typical passive smoking study is shown below.

Note the 'conditioning room' between the cigarettes and the rats and note, too, how much more ventilation has been provided. Even with this dramatically less confined arrangement, those who conducted the experiments estimated that the rats were still being exposed to 10 to 100 times more smoke than any nonsmoker would ever experience, even in the most extreme real life situations. Despite these high doses, which lasted 8 hours a day, every day for up to a year at a time, none of the rats died and there was little evidence of physical harm.

But it was the first set of experiments that were the focus of Glantz and Schick's 2005 paper. The authors used them to show that "whole fresh sidestream smoke is 2-6 times more toxic" than mainstream smoke. The key words in this sentence, however, are "whole" and "fresh"; they were clearly only talking about the smoke that comes off the cigarette at the moment of combustion and not the mixture of sidestream smoke, mainstream smoke and ambient air that makes up secondhand smoke.

Glantz and Schick did not show the diagrams that I have reproduced here, but it should be immediately clear to anyone who views them that the Philip Morris scientists were using a very specific definition of sidestream smoke which had, at best, only a theoretical relevance to real-life human conditions.

It is commonly said that secondhand smoke is 85% sidestream smoke and 15% mainstream smoke. This completely ignores the ambient air which dilutes it. How much it is diluted by depends on the size of the room and the level of ventilation. An article in Regulatory Toxicology & Pharmacology estimated that passive smokers inhale 1/10,000th to 1/100,000th of the respirable tobacco smoke that smokers do. Even if the true figure is as low as 1/1,000th, the real breakdown of what constitutes secondhand smoke would be 0.085% sidestream smoke, 0.015% mainstream smoke and 99.9% ambient air. Once the diluting effect of the air is taken into account, the subtle differences between sidestream and mainstream smoke become largely academic.

The relative toxicity of sidestream and mainstream smoke is, therefore, a red herring. No nonsmoker inhales pure sidestream smoke or anything close to it. They might inhale secondhand smoke but that only contains a tiny amount of sidestream - and exhaled mainstream - smoke which has aged, broken down, clung to surfaces and been greatly diluted before it gets anywhere near them. Many of the constituents of secondhand smoke that people have been taught to fear cannot even be detected in secondhand smoke, even with modern scientific apparatus. Less than 10% of the chemicals that are said to be in mainstream smoke have ever been identified in secondhand smoke (5).

The difference between breathing sidestream smoke and secondhand smoke is rather like the difference between sucking exhaust fumes from a car's tailpipe and standing by a road. You might be being exposed to the same chemicals but the outcome is going to be very different.

For anti-smoking groups, the vast rate of dilution goes unmentioned. Part of the confusion lies in the terminology. Anyone not well-versed in the science could be forgiven for assuming that sidestream smoke is just another word for secondhand smoke. That being the case, it was almost inevitable that anti-smoking activists - whose understanding of science can be shaky at the best of times - would allow their heart to rule their head and assume that passive smoking was more dangerous than smoking.

A look at some typical quotes from anti-smoking websites shows how complex laboratory experiments have been dumbed down for public consumption:

"More than half of the smoke from a burning cigarette is not inhaled by the smoker. Instead this smoke enters into the surrounding environment. This sidestream smoke is inhaled by everyone (including the smoker) in the area. Sidestream smoke has twice as much nicotine and tar as the smoke that smokers inhale. It also has five times the carbon monoxide - a toxic gas that decreases the amount of oxygen in our blood." (6)

"Sidestream smoke is released directly into the air from the burning end of the cigarette. This unfiltered smoke is even more dangerous than mainstream smoke. Some studies have indicated that sidestream smoke contains twice as much tar and nicotine and three times as much carbon monoxide as mainstream. Most of the smoke that a nonsmoker is exposed to is the more dangerous, sidestream smoke." (7)

It would take a lawyer to decide if these statements can be described as technically accurate or not. Generally, anti-smoking groups are smart enough to limit their definition of mainstream smoke to mainstream exhaled smoke. When they do so, they are on safe ground. Smokers absorb most of the toxins in their bodies; consequently, what they breathe out is considerably less toxic than fresh smoke. This distinction, however, will go over the head of many readers, who will likely infer that breathing secondhand smoke is more dangerous than smoking itself.

And these are the more measured statements. There are plenty of other groups who have gone past suggestion and insinuation, and are now openly claiming that smoking is "worse" than smoking:

"Studies have found that secondhand smoke is even more dangerous than inhaled smoke because it burns hotter." (8) [Sidestream smoke actually burns at a lower temperature]

"Second-hand smoke is more dangerous than directly inhaled smoke. It releases the same 4,500 chemicals as smoke that is directly inhaled, but in greater quantity!" (9) [The exclamation mark that concludes this ludicrous sentence is well-deserved]

"Breathing second-hand smoke can be more dangerous than inhaling smoke through a cigarette. It has twice as much nicotine and tar as the smoke that people smoking inhale and five times more carbon monoxide, a deadly gas that starves your body of oxygen." (10)

"It has been scientifically proven that secondhand smokes [sic] are more dangerous to health than firsthand smoke. The smoker, who inhales the (mainstream) smoke "filters" it to some degree before exhaling it, but the non-smoker around him/her inhales the "pure" and more dangerous sidestream smoke. Besides the tar and nicotine in secondhand smoke, there are several cancer-causing substances in secondhand smoke, and in much higher concentration than in mainstream smoke. So, the person who smokes in public, around people, is giving himself/herself a lower dose of poisons, and giving his victims (family members, friends and strangers) around him/her a higher and a more deadly dose of poison." (11)

Once the anti-smoking groups adopted the idea, it was inevitable that the politicians they lobbied would succumb. State Rep. Peter J. Daley of Washington called for legislation to ban smoking in vehicles if one of the passengers was a child, saying: "We know that secondhand smoke is worse than firsthand smoke. The studies are all in, and we really want to protect the health of our children." (12)

And finally the idea took hold amongst the general population. The website Wiki Answers deals with the issue very succinctly: Q: Is second hand smoke worse than first hand?

A: Yes. Second hand smoking is more dangerous than first hand (13)

The myth of nonsmokers being in more danger than smokers is particularly prevalent on internet message boards, blogs and amongst young people in America and Canada who have been fed stories about passive smoking their whole lives. The net result is that secondhand smoke assumes the role of a supernaturally lethal gas and the wheels are greased for the passage of smoking bans. Those who might normally oppose a ban have been persuaded that passive smoking represents a peril too great to ignore.

Take this typical quote from a resident of Scranton, Pennsylvania who, when a smoking ban was brought in, was said to be "thrilled":

"Since they've proved secondhand smoke is worse than firsthand smoke, I'm all for the ban for the health reasons." (14)

In fairness to Glantz and Schick, their 2005 study did not claim that secondhand smoke was more toxic than firsthand smoke, only "fresh sidestream smoke". Nonetheless, Glantz is a shrewd operator who has publicly stated that he only does research if he believes it will help the anti-smoking cause (15). He must have known what he would unleash when he published the sidestream smoke study and, if not, he has certainly fanned the flames since.

What could be more ridiculous than saying that diluted smoke is more dangerous than concentrated smoke? How about saying that diluted smoke gets more dangerous as it gets older?

Step forward Stanton A. Glantz, who, in 2007, returned to the Philip Morris archive with a new article which made that very claim (also published in Tobacco Control). He did so by looking at the five Philip Morris passive smoking experiments mentioned earlier. These provided a wealth of information, even if it wasn't the kind of information anti-smoking groups wanted to hear. One of them, for example, found that "tumors [in the rats exposed to smoke] were similar in number to those seen in the sham-exposed groups." (16) Another reported that: "The test atmosphere had no effect on the general condition and behavior. During the inhalation period one rat died of a technical cause. No test atmosphere related mortality was observed." (17)

Glantz did not comment on the most notable outcome of the experiments - that heavy doses of secondhand smoke did not kill any of the rats - and actually disregarded three of the experiments completely. This left him with two passive smoking experiments, conducted in 1994 and 1997 (the apparatus shown in the second diagram above comes from the report of the 1997 experiment).

He compared these two secondhand smoke studies with the sidestream experiments of the early 1980s, paying particular attention to comments made by those who dissected the rats afterwards. He developed a points system of his own making which purported to measure the physical damage to the rats. These numbers were then entered into a convoluted mathematical equation, along with other data he gleaned or inferred from the written reports. When the calculations emerged from his computer something amazing happened: he was able to show that, pound for pound, the fresh sidestream smoke had caused less damage than the diluted secondhand smoke. Not only that, but the diluted secondhand smoke became more harmful as it got older (18).

This was entering the realms of madness. Half of the rats that had been given fresh sidestream smoke had died for goodness sake! It was hard to see how any more harm could have come to them. By contrast, none of the rats exposed to aged, diluted sidestream smoke had died.

Glantz admitted that he had no idea what "the mechanism for the increased toxicity of aged sidestream smoke" might be, although he seriously suggested that smoke particles absorbed in home furnishings could wait a while before springing back into the air to attack nonsmokers (19).

Glantz also accepted that earlier studies of sidestream smoke had shown "toxicity decreased rapidly in the first 30 seconds of aging." And he noted that, according to his mathematical equation, one experiment had shown that toxicity trebled with ageing and the other showed that it halved. Glantz described this as "remarkable." 'Magical' would have been a better word; the two findings were completely at odds with one another.

If the fact that his hypothesis went against existing toxicological principles was not enough to make Glantz question his own methodology then his own conflicting data should have been. And these were not the only flaws. The experiments Glantz re-examined were conducted years apart, by different scientists, with different apparatus and were designed to study completely different things. The collected reports for these experiments runs to many hundreds of pages, but in none of them is there any suggestion sidestream smoke becomes more toxic with age. In fact, when the results of one of the experiments were published in Toxicological Science in 1998, the authors concluded that the opposite was true: "The results of this study show that room-aging in general reduces the biological activity of FSS [fresh sidestream smoke]." (20)

Not a man crippled by self-doubt, Stanton Glantz ignored all the evidence that he might be wrong and pushed on with his hypothesis:

"If sidestream smoke is approximately three times more toxic than fresh sidestream, and fresh sidestream is approximately four times more toxic than mainstream smoke, then aged sidestream smoke is approximately 12 times more toxic than mainstream smoke."

And there you have it. Sidestream smoke is TWELVE times more deadly than mainstream smoke! So if you're worried about secondhand smoke, make sure you get close to the burning cigarette so it doesn't get too old. If you really want to play it safe, smoke the cigarette yourself.*

* Not really

See http://www.velvetgloveironfist.com/index.php?page_id=38 for references.