c. Stewart, NYC CLASH, 2003



The War on Smokers
The Anti-Smoking Movement


"Quick and Dirty," 
says Elizabeth Whelan

"Attack the Messenger," 
says Stanton Glantz

Toss the Jargon
(everyone says it)


The EPA Report: 
Lung cancer and Secondhand Smoke

(Understanding the Jargon)

Heart Disease
Secondhand Smoke 
(53,000 "Deaths")



Cigarette constituents 
in the air (OSHA standards)

Table 1: 
constituents, charted

Anti-Smokers sue OSHA...
and say "Never mind."


What else is in 
restaurant air.

"Cooking the Books," a restaurant study

Bartenders' "exposure"

Cotinine as a measure 
(of what?)


For it: The facts

Against it: The Prohibitionists






Categorical statement: There is no such thing as "clean air."

Probably not even on an Alp.  (If the radon doesn't get you, the altitude radiation will.) 

And certainly not in any outdoor environment in any U.S. city. There are,  in city air, according to the New York Times, 320 toxic chemicals spewed out by industry; that, plus emissions being leaked by every car. (It's been said that a non-smoking jogger in Manhattan inhales the equivalent of a pack of cigarettes for every mile she jogs.) And everything out there is coming in here.

Indoor air comes from the same mother as outdoor air, though (and especially in badly-ventilated buildings) indoors can add its own special touches. Aside from whatever's growing in the ventilators (bacteria, fungi, and molds including free-floating penicillin, candida, monilia and 27 others) there's formaldehyde leaking from the foam rubber pillows, volatile compounds leaking from the walls; disinfectants, cleaning solvents, pesticides; wax; ozone from the copying machine, dander from the cat, dust under the scatter rug,  and gas from the stove.

Now add human beings. Not only are they exhaling carbon dioxide -- a pollutant about to be restricted at Kyoto-- but they're shedding all manner of viruses and bacteria.  If they own pets, according to a recent study, they're importing cat and dog dander in on their clothes and sending it into the air. Then too, they're shedding respirable particulates. Yep. That's right. According to OSHA "people contribute millions of particles to the air, primarily through the shedding of skin scales" which OSHA lists among indoor air pollutants. 
- OSHA, Proposed Rule, Federal Register Vol 59, NO. 64, 4/5/94

So-- may we stipulate: "Clean air" does not exist, not even in a smoker-free environment.  And certainly not in a smoker-free restaurant.  Aside from all the above pollutants, possibly the most important source of air pollution and floating carcinogens in restaurants is...


Here's one study among many that nicely makes the point. Conducted by the British government's Health & Safety Executive, in 12 restaurant kitchens, "The Importance of Good Ventilation in Commercial Kitchens and Industrial Cooking Areas" reports restaurant workers are exposed to:

"airborne chemicals including [the carcinogens] heterocyclic amines (HA), nitrosamines, polycyclic aromatic hydrocarbons (PAH), aldehydes, and various volatile organic substances.  Irritants such as acrolein, formaldehyde and acetaldehyde were detected..." as were other respirable particulates.

Nonetheless, all these substances were found to be-- just as are the substances in ETS-- below the airborne OELs (the Brit equivalent of OSHA's PELS, i.e, Permissible Exposure Levels.) 

Home cookers, nonetheless, have been warned by no less than Dr. C. Everett Koop (quoting the American Institute of Cancer Research)  to beware of PAHs emitted into home air from meat fat sputtering and dripping-- as it were-- out of the frying pan and into the fire. 

And the Sacramento Bee warns that  "[cooking] fat, as it decomposes, releases petroleum-based gases into the air that lodge in the lungs." 9/2/94

We wonder seriously if Mssrs. Glantz, Repace, and Cherner would suggest that only the acetaldehydes and acroleins that come from cigarettes, as opposed to those that come from pork chops and burgers, are a threat to human health (even though OSHA says the levels of both are "safe.") 

Applying the same standards to the same carcinogens, one would then have to conclude there's "no safe level of exposure to dinner."

Another danger lurking in restaurant air are those candles, romantically burning on the tables.  Depending, of course, on the size of the candle, as few as 1 to 9 is said to be a risk.   Or to quote the headline from USA Today:

"Candles Might Be Polluting Your Home, EPA Says." 

"Officials say pollutants (particulates) from a burning candle can exceed the standards the Agency sets for outdoor air quality." An EPA spokesman is quoted as saying, "If I  were someone who had a health problem like asthma...candles [are something] I would get rid of."  (June 14, 2001) 


Not that many studies have been done on the health status of restaurant workers. One that's considered the gold standard and often quoted by the health "advocates" is the study conducted by Michael Siegel, who sat at his computer and dredged data from a series of unrelated, unspecific, and often totally irrelevant sets of statistics.

Keeping in mind that this is the same Michael Siegel who was forced to admit to "misrepresenting" facts elsewhere (see Attacking The Messenger), here's an analysis of the Siegel study by independent researcher Martha Perske.

Note: The Siegel study and its methodology are typical of other studies of its ilk.

c. Martha Perske, 2000

In their efforts to ban smoking in restaurants, anti-smokers cite a 1993 study by tobacco-control advocate Michael Siegel, MD, MPH, "Involuntary Smoking in the Restaurant Workplace," published in the Journal of the American Medical Association (JAMA).  Dr. Siegel is with Boston University's School of Public Health.

According to Siegel's study, so say the activists, restaurant and bar workers have a 50% increased risk of lung cancer due to environmental tobacco smoke.

What the public doesn't know is that Siegel's "50% increased risk" was based on six studies that had absolutely nothing to do with environmental tobacco smoke in restaurants or bars or anyplace else for that matter.

Out of the six studies used by Siegel, the only one to even mention environmental tobacco smoke stated that the authors had no information on ETS exposure, and therefore it was "not possible" to do an evaluation (Keller and Howe, 1992.)

Despite the fact that it was "not possible" for the authors of this study to do an evaluation of environmental tobacco smoke, Siegel nevertheless took an increased risk reported in the study for white females currently employed in eating and drinking establishment and-- with no evidence whatsoever-- implied that the increased risk was due to environmental tobacco smoke.

In fact, Siegel extracted data from all six studies that showed small increased risks for lung cancer in food-service workers and implied that the increased risks were due to environmental tobacco smoke, even though there was no evidence in any of the six studies that food-service workers had been exposed to tobacco smoke-- let alone for how long or at what levels.


Siegel concludes, in his study, that the evidence from these six studies "suggested that there may be a 50 percent increase in lung cancer risk among food-service workers that is in part attributable to tobacco smoke exposure in the workplace," and in order "to protect these workers, smoking in bars and restaurants should be prohibited."

"Suggests" that there "may be" an increased risk that is "in part" attributable to tobacco smoke?


In contrast to his cautiously worded conclusion in his study, Siegel told the New York Times that based on his results "it's really a life and death issue" for restaurant workers who breathe smoke for long periods, and that smoking in bars and restaurants should be prohibited. (NY Times, 7/28/93)

Likewise, he told USA Today that secondhand smoke "has a devastating effect" on restaurant workers and smoking in bars and restaurants should be banned. (7/28/93)


Even if Siegel's "50% increased risk" were on solid ground (which it isn't), it only means that the relative risk was 1.50.  According to the National Cancer Institute, relative risks below 2.00 are considered "small" and "may be due to chance, statistical bias, or effects of confounding factors that are sometimes not evident."

Dr. Lynn Rosenberg of the Boston University School of Medicine agrees that "epidemiologists normally take seriously" only relative risks of 3.00 or greater. (Wall Street Journal, 1/3/95)

Indeed, the U.S. Environmental Protection Agency refused to classify electromagnetic fields as a cause of cancer "largely because the relative risks... have seldom exceeded 3.0." (EPA, October 1990, p 6-2, "Evaluation of the Potential Carcinogenicity of Electromagnetic Fields.")

The following, based on material provided by Ms Perske, discusses the 6 studies that Michael Siegel used as the basis for his "50% increased risk." You will now see living examples of How to Bias A Study, and see how ill-founded Mr. Siegel's conclusions are.

KELLER AND HOWE STUDY: Based on 1985-1987 data pertaining to lung cancer and occupation among Illinois non-smokers, this was, in Siegel's words, "unlike the other five studies [in that it] controlled for active smoking by specification, rather than adjustment."  The study authors stated that they had no information on ETS exposure and therefore it was "not possible" to do an evaluation. Nevertheless, Siegel used an increased risk reported on one of the study's tables for white females currently employed in "eating and drinking places" and implied it was due to environmental tobacco smoke.

SCHOENBERG STUDY: Based on 1980-1981 data pertaining to  occupation and lung cancer risk among New Jersey white males.  From this study, Siegel selectively used increased risks reported for bartenders and other food service workers but ignored decreased risks for cooks and food-counter workers. He also ignored the fact that the study classified bartenders, cooks, food-counter workers and other food service workers as "non-high-risk" for lung cancer.  The study did not consider whether these workers were or were not smokers.

ZAHM STUDY: Based on 1980-1986 data pertaining to occupation and type of lung cancer among Missouri white males. The authors of this study said their results may be "statistically unstable" and that the "small numbers, the large proportion of unknown values, and the other limitations suggest that the study's results be interpreted cautiously." Siegel ignored these statements, threw caution to the winds, and used the statistically insignificant relative of risk of 1.8 (based on only 24 cases!) for male "food service workers."

WILLIAMS STUDY: Based on cancer mortality data from the Third National Cancer Survey. This study warned that a "cautious and conservative approach should be followed in interpreting these data...Generally these results should be used only as a research resource for the formulation of hypotheses and planning of studies to follow up leads suggested." (emphasis in original).  Siegel disregarded these warnings and used the lung cancer relative risk of 1.88 (based on only 12 cases) for female "food service workers" (only) as if they were real and attributable to environmental tobacco smoke.

LERCHEN STUDY:  Based on 26 cases of lung cancer among males 
employed in the "eating and drinking establishment industry,' in New Mexico, 1980-1982. From this study, Siegel used the (non-statistically significant) relative risk of 1.6 (based on  26 cases) even though it was noted in this study that it would no doubt take a study of 10,000 lung cancer cases "to evaluate fully occupation and other risk factors for lung cancer."

SINGLETON AND BEAUMONT STUDY: Based on California data from 1979-1981 pertaining to occupation and death due to various causes, including accidents and suicides.  Siegel cherry-picked from this study in that he presented, among other things,  lung cancer results for MALES in the category of "other food service workers" and ignored the significant decreased lung cancer risk for FEMALES in the same category.

It must be underscored that none of these studies had any information        whatsoever on the subjects' exposure to secondhand smoke--how much, how long, of if at all.

Further, despite the claims of the current mayor of New York City that this Siegelian risk was attained after scrupulously adjusting for the subjects' own smoking, this is not the case.

Though Siegel claimed the data from the Zahm study included smoking histories of the subjects, Zahm himself states that the information on smoking represented smoking status at the time of diagnosis only and "may be inaccurate for the time period relevant for carcinogenisis." And considering the circumstances of the interviews, it may be inaccurate, period.

Of the Singleton studies, Siegel admits (within his own paper) that they merely "attempted to control for smoking, alcohol and socioeconomic status indirectly by adjusting for national occupational smoking and alcohol use rates imputed from the National Health Interview Survey data." (emphasis added) Or in other words, he had no real idea whether his subjects smoked, drank, neither or both.

And the Singleton studies account for the largest study population in the whole canon. (260 cases). The number of cases in four other studies are: Lerchen: 20; Schoenberg, 56; Zahm 24; Williams 12, with Keller ringing in with a curt "NA." 


Yet Siegel is treated seriously by legislators everywhere -- mostly because they don't understand what he's about.

In his crusade for Prohibition, the current mayor of New York City has proclaimed--with no citation (he doesn't need one; he's The Mayor!) that bartenders inhale exactly 10 cigarettes per shift.

We can find no source for the claim. 

We can, however, refer once again to the government's figures. According to the NRC, DHHS and EPA, a nonsmoker inhales from 1/10th of 1% to 1% of what's smoked around him. (Op cit)

Therefore: from 1,000 to 10,000 cigarettes would have to be quickly smok-ed in this particular bartender's bar.

Further, if the Mayor can make assertions without citations, we can certainly offer this-- as recently reported by United Press International:

"People who work eight hours a day in heavy-smoking environments had the following CE's (Cigarette Equivalents): Sydney: 0.2; Prague, 1.4; Barcelona, 4.3. That's cigarettes PER YEAR."
-Smokescreens, Bloom, UPI Syndicate 8/22/02

This is actually in line with the findings of other studies (Phillips 1998; Hazelton Labs, 1994). Using personal air monitors on people exposed to smoke in 12 cities in Europe, Phillips reported that non-smokers living with smokers "smoked," on average,  6 cigarettes a year.  The Hazelton study produced 5 cigarettes a year.
-Phillips, To National Toxicology Program, Feb '99; Hazelton: Environment Int'l, Dec 1994

Though all attempts to measure for such "equivalents" pass for iffy (including the ones we like) the iffiest seem to come from the doodlings of Michael Siegel.

To wit, here's Steve Milloy at, discussing Siegel's in-person testimony in 1997 before the Amherst, MA Board of Health, which was considering-- and later voted unanimously for-- a ban. Speaking to the Board:

"Siegel claimed his research shows bartenders who do not smoke themselves inhale the equivalent of one-and-one-half or more packs of cigarettes a day and that '220 bartenders working in the state today, if they continue to work for 40 years, are going to die from their exposure.'

"But Siegel should know better than to make such outlandish statements.

"In 1986, the Surgeon General's report on secondhand smoke devoted a three-page section to the concept of estimating cigarette-equivalents from second hand smoke.  After quantitatively demonstrating how cigarette equivalents can vary as a measure of exposure, the Surgeon General concluded:

...these limitations make extrapolation from atmospheric measures to cigarette equivalents units of disease a complex and potentially meaningless process."

"Why?" Milloy continues. "Secondhand smoke differs greatly from what smokers inhale (i.e., mainstream smoke). Secondhand smoke dilutes rapidly and changes chemically as it ages. Also, smokers inhale mainstream smoke differently (deeper) than nonsmokers inhale secondhand smoke."

Further, Milloy goes on to question exactly which "research" of Siegel's seemed to prove this cigarette-equivalent and death toll for bartenders.  An internet search revealed that no such study authored by Siegel had appeared in print anywhere, or was scheduled for publication. 

But, leave that for a moment; we'll get back to it soon. For now, let's just deal with Siegel's 1997 premise: that  bartenders were inhaling a pack and a half a day. "Or more," to quote him completely.  As revealed by his "study."

For that to be true, using government calculations, we'd then have to postulate exposure to from 3,000 to 30,000 smokes being smoked over 8 hours.

Which, apparently, Siegel did !!

In 1998, Mr. Siegel presented his study. Though it wasn't exactly a study and it wasn't exactly presented.   To this day, it hasn't been published, and it hasn't been peer-reviewed.  Probably on account of it was work as a hired gun for The California Smoke-Free Bar Program (BREATH) and a rehash of old news.
-Siegel, "Smoking and Bars: A Guide for Policy Makers," 1/98, unpublished

In it, Mr. Siegel informs us that a bar is over 4 times as smoky as a house with a single smoker.  He also informs us that "bar workers inhale the equivalent [of] 0.6 cigarettes per day." Or 6/10ths of 1 cigarette.

Far cry from that pack-and-a-half.

So how does he get to a pack-and-a-half a day? By attempting to deduce  a much larger CE for only two of the constituents in secondhand smoke, based on an assumption (revealed through a couple of footnotes) that the bartender in question is exposed to over 3,200 cigarettes per 8-hour shift in a badly-vented environment, where burgers are being fried. (Please refer back to Cooking.) 
-Cudderback Et Al, "Occupational Aspects Of Passive Smoking," Jnl Ind Hyg V 37

Thus, Siegel maintains that for one single constituent (benzo(a)pyrene) which had never been measured in either study he cites, bar workers may inhale the cigarette equivalent of, vaguely, from half a pack to two packs a day. Of this one single element  If they were, in fact, exposed to over 3,000 cigarettes. In bad ventilation, with the hamburger grill on "high." 

This, indeed, is high nonsense.  And no wonder it wasn't published.

Mr. Siegel's calculations also crash against the wall of some recent American studies, conducted by the Oak Ridge National Laboratories (US Dept of Energy) whose findings we report in our section on Ventilation.

The Oak Ridge studies-- in restaurants and taverns in 17 US cities, using 1500 nonsmoking waiters/ waitresses/ bartenders,  showed exposure levels of staff (via personal air monitors and serum cotinine levels) were exceedingly-- in fact, quite surprisingly, low.  And way below statistical estimates by OSHA of what reality is like.

Then, too, there's a  list of studies that attempt to deduce exposure through the levels of serum cotinine, but without checking into the air.

So we need to explain cotinine and how it gets into "serum" (urine, saliva, blood.)


To begin with, by far the most plentiful-- and measurable-- part of a cigarette (either first or secondhand) is simply: the nicotine.  The body then metabolizes nicotine into cotinine.  Smoking, however, isn't the only source of cotinine.  The body also metabolizes foods into cotinine--tomatoes,  potatoes, eggplant, and various teas.

In fact, another study showed that eating a normal (4.9 oz) portion of mashed potatoes produced the same amount of cotinine as 4 hours spent having  drinks in a smoky bar.  And similarly, a rather long lunch with a smoking friend  can be easily equaled by a third of an ounce of eggplant.
-"Relevance Of Nicotine Content Of Common Vegetables To The Identification Of Passive Tobacco Smokers," Domino Et Al, Med. Sci. Res, 1993; 21, 571-2; Similarly, New England Jnl Med, Aug, 1993

Further, too, it's been noted that cotinine is only used as a "marker" (for exposure to  ETS) because it's possible to measure. Even the California EPA has admitted, as most studies do, that the harmless "cotinine does not serve well as a marker for the presence of other tobacco smoke compounds." 

Then too there's this:

"There exists between individuals a genetically determined variation (up to 50 fold) in the level of metabolism to cotinine from a given exposure. " 
-Nyberg Et Al "Misclassification Of Smoking Status,.." Epidemiology, May 1997

And this: 

Men metabolize cotinine faster than women, and whites faster than blacks (by 30%)  This would also apply to the cotinine metabolized out of potatoes.  And would indicate that either-- and/or-- women and blacks would register higher levels than their white / male counterparts to identical exposures.  Further, eating a meal can affect metabolic speed. 
-"Nicotine Metabolism Variables," Ahijevych Et Al/Agency For Health Care Policy & Research (HS07373)

Nonetheless, it's used as a marker.

Okay-- let's get a baseline. Again, according to the government (NIOSH Bulletin 54) a study by Cummings et al in 1990, showed the average concentration of urinary cotinine in a pack a day smoker is approximately 1,200 ng/ml. 

Another study, conducted by the National Research Council in 1986, showed the average amount in a smoker was 1,825 ng/ml.

Another study, also reported by NIOSH,  found that restaurant workers who  themselves didn't smoke, had urine concentrations of 56 ng/ml.  About 1/20th to 1/37th of the cotinine in a smoker.

And please remember that cotinine is a harmless metabolite and a rather poor indicator of anything else in smoke.

Nonetheless, in a recent study (Wortley et al, a study the Mayor likes) the blood levels of cotinine were carefully measured in  50 nonsmoking restaurant  workers,  for a mean serum level of 0.62 (ng/ml.) or 6/10th of a nanogram.  This was higher than the levels recorded in, say, farmers (0.13)

Yes?  And?

People who work in restaurants are exposed to more smoke than, say, a farmer who works in the field.  Um...okay. 

-Wortley Et Al, "Exposure To Secondhand Smoke In The Workplace: Serum Cotinine By Occupation," Jnl OCC & Env Med, 2002; 44 (6) (*) Personal Correspondence w/ Lead Author

Nor is this study a breakthrough in any way.  Remember, the serum measured here is blood, not urine.  According to a study sponsored by ALA, the blood cotinine levels in less than pack-a-day smokers ranged from 182- 249 ng/ml. That's a quantum difference from the 0.62 reported by Wortley among nonsmoking wait staff.
- Ahijevych Et Al,  In "Addiction Behaviors, " Feb, 1999

And yet.

And yet. A study by James Repace measured the urine cotinine in waiters in Hong Kong and projected, solely on the basis of their cotinine, that 150 would die. 
-"Passive Smoking And Risk For Heart Disease And Cancer," Hedley, Repace 

But cotinine (have we mentioned?) is a harmless metabolite that indicates nothing except exposure to nicotine (or nightshade vegetables) But, hey, let's say it again:

"It is not known how levels of cotinine measured relate to the biologically important components of ETS other than nicotine." -Nyberg, Op Cit

Which leaves us with the general workplace studies--all epidemiological-- of which there aren't many.  The largest American study ever done (and sponsored in part by The National Cancer Institute) "Passive Smoking and Lung Cancer in Nonsmoking Women," Brownson et al., 1992, reported:

"... no elevated lung cancer risk associated with passive exposure in the 
-American Jnl Of Public Health, Nov. 1992

Alas, complained EPA, this study (published in November '92) arrived "too late" to be included in their (1993) report.  Had it been so (the largest study ever done!) and been thrown into the hopper, it would have so tilted the weight that ETS could not, not even with lots of fudging, have been classified as a risk or a Class A carcinogen.

As of 1995, there were 8 extant studies that looked into the workplace/ lung cancer data. According to one set of researchers:

"An EPA-style meta-analysis...demonstrates no statistically significant 
association for the data in its entirety--or for any sub-group of American workers. The pooled risk estimate [is] 1.0."
-"ETS Exposure, Lung Cancer And Heart Disease", Sears, Steichen, OSHA 

The studies were pooled into that "EPA-style meta-analysis" because, the authors say, their results were so contradictory and mixed. Two showing a slightly increased risk; two showing a slightly decreased risk, and the rest indeterminate.

The same authors point out that "it is difficult to draw any conclusions concerning heart-disease risk in the US workplace because virtually no such information on the US workplace exists."

None of this, however, prevents the zealots from hollering Wolf or stops them from conjuring baseless death tolls, easily shattered by science and sense.  Take, for example, this crowning lulu from Mayor Bloomberg of NYC.