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November 11, 2002

 

 

 

Michael J. McFadden

4424 Ludlow St.

Philadelphia, PA 19104

215-386-8430

 

 

A. Gifford Miller
City Hall
New York, NY 10007

 

 

Dear Councilman Miller,

 

I am writing to you about a very serious matter.  There is a powerful and well-funded lobby that has been consistently misleading you with regard to important public policy legislation.

 

The legislation is Mayor Bloomberg’s smoking ban. The lobby is the 880 million dollar a year “tobacco control” industry that has flooded the Council with information carefully designed to mislead and pressure you into voting for an extremist and needless smoking ban.  In this letter I will look at both the needlessness of such a ban and at the sort of deceptions that have been involved in promoting it.

 

First of all, let me point out that despite the amount of rhetoric you have heard to the contrary, the studies examining long term harm to nonsmokers from decades of constant exposure to secondary smoke (ETS) are neither unanimous nor unequivocal.  This letter has three attachments.  Attachment A lists 130 results of studies on ETS and lung cancer.  The studies are listed with their “confidence intervals” in order to show possible statistical significance.  Only a few of these studies confirm the hypothesis that even intense lifelong exposure to ETS has any relation to lung cancer.  You’ll also notice that these numbers stand in stark contrast to the rhetoric you’ve heard from pro-banners.

 

Note that to actually BE statistically significant a confidence interval cannot include the “no-effect” value of 1.0.  Note also that a good number of studies would actually tend to support the OPPOSITE conclusion: namely that ETS might help immunize nonsmokers against lung cancer.  A final important point: even for those studies that meet the test of statistical significance passing that test says nothing about the design validity of the studies themselves, their biases, confounding variables, or causality. Statistical significance is merely a minimum standard to look at before a study should even begin to be considered as possibly indicative of causality.

 

 

 

 

Of particular note is the 1998 World Health Organization study, one of the largest and most prestigious case-control studies ever conducted on this subject.  While the study failed to show any general scientifically significant relationship between ETS and lung cancer it did produce one notable result.  That result, mitigated in the abstract as “no association”, was actually the only significant finding of the study: namely that children of smokers developed cancer later in life at a rate that was 22% less than matched children of nonsmokers!  Take a moment to examine these results and you’ll see that I am not misleading you.

 

Additionally, note that none of these studies was based on the low exposure levels that exist in decent non-smoking dining sections or even in a smoking bar with modern ventilation. The constant repetition of the claim that nonsmokers are inhaling various ridiculous amounts of smoke does not make the claim true.  It is based almost entirely upon a single study using a single approach favored by Antismoking lobbyists because it gives these elevated results.  This approach measures hair nicotine rather than cotinine levels or atmospheric particle exposure.  The results are easily contaminated by such a simple variable as nicotine surface deposition on the hair shafts of both smokers and nonsmokers as opposed to any actual comparison of ingested biological exposure. Thus the inflated results: smokers and nonsmokers would have similar ambient air exposure. 

 

If you consult the actual texts of previous Surgeon General’s Reports (e.g. pp.206-216 of the 1986 Report on ETS) you’ll find that the real levels are a tenth or even a hundredth of what these extremists claim.  Even a simple physical model of lung exchange volume and atmospheric smoke concentrations under varying realistic conditions would often show the expected rate of exposure is only several thousandths of what some ban supporters allege. Indeed, the figures in the new WHO/IARC analysis indicate that it would take about 300 hours for an average worker to ingest the equivalent of a single cigarette at 6 liters/minute of lung exchange, 6 micrograms/m^3, 1 milligram of ingested nicotine.

 

Additional deceptive tactics aimed at you and the Council are illustrated in Attachment B which critically examines NYPIRG testimony given to Councilman Robles’ Subcommittee in early 2000.   My references to that testimony are accurate and can be checked with your files.  Its analysis shows clearly the sorts of rhetorical tricks and factual misrepresentations bombarding you on this issue.  The mountains of information presented by pro-banners may look like solid rock at first glance, but closer examination shows their substance to be closer to that of smelly Swiss Cheese.  Think of how similar criticisms could be leveled at 90% of Tuesday’s testimony. 

 

If you’ve read this far I’m sure you have three questions in mind:  Why would pro-banners lie to you about this matter of public health; How could they have coordinated such a convincingly powerful campaign of deception; and Who the hell am I that I’m taking such effort to communicate with you when I don’t even live in New York?

 

 

 

Why are the ban proponents lying to you?  There are several reasons: idealism, greed, and mistaken beliefs. Some pro-banners simply believe bans are an effective tool to reduce smoking and the number of smokers.  They see this as such a positive goal that they feel fully justified in stretching the truth to make it happen.  Terms such as “massaging the data” and “creative epidemiology” should be anathema to good science.  Attachment C examines a researcher’s fax about the need for such “handling” of the truth.

 

Some are pushing the antismoking agenda out of greed: according to the AMA’s own Tobacco Control Report the tobacco control lobby is receiving over 880 million dollars every year just from state coffers alone… along with untold millions more from other sources.  Many have livelihoods based upon promoting public hysteria about secondary smoke thereby justifying bigger grants from tax increases and increased power and prestige within their organizations after political successes. 

 

And finally, some of those testifying, even some medical personnel relatively untrained in epidemiology, have simply been misled by clever manipulations of truth and statistics.  A high school statistics teacher may actually be more qualified to judge the truth about ETS studies than a brain or even a lung surgeon.

 

How could such a campaign of deception have come about?  Again, money plays an important role.  Antismoking organizations today are well coordinated.   In August of 2000 over 5,000 activists, lobbyists, lawyers, and researchers gathered at a ten million dollar conference in Chicago to plan strategies for the next 20 years to eliminate tobacco use worldwide.  The tactics of focusing on “threats to children”, smoking bans and taxes, smoking in media, “denormalization of smoking”, and depictions of activists like myself as being “shills of the tobacco industry” come directly from such planning sessions.  To avoid attacks upon weak ETS science, lobby organizers urge their membership to simply repeat by rote: “There is no scientific debate. The question has been settled.  Any who question it work for the tobacco industry.”

 

This brings us to the final question above: Who am I and why am I writing to you?  Am I “a shill of the tobacco industry?”  No, I most definitely am not!  I do not now, nor have I ever, had any financial, commercial, or personal relationships with Big Tobacco other than as a customer.  Several years ago I worked with other like-minded citizens to form the Internet Smokers Action Network and have since written extensively on the subject and presented testimony at New York and Philadelphia City Council Hearings. 

 

Two years ago I joined a legal effort to overturn the Master Settlement Agreement between Big Tobacco and the States: no financial expectations were involved.  I have neither tobacco stocks nor any financial interests in the bar/restaurant industry.   My educational background is in statistics, psychology, propaganda analysis, and politics (Manhattan College undergrad, Wharton School of U. of PA. graduate fellow) and I have devoted my life to various forms of citizen activism for peace and social justice.

 

I have been appalled by the misuse of money, the abuse of power, the twisting of statistics, the distortion of language, and the use of manipulative social engineering techniques by Antismokers and I am fighting back in the most effective way I know: with truth and the written word.  This issue is NOT a “public health issue” other than as it relates to a decidedly un-American type of behavior manipulation.  It IS an issue of freedom from the tyranny of a special interest group that has deliberately frightened the public with millions of dollars of scare propaganda. 

 

In the wake of the 70% pro-ban Florida vote, Mayor Bloomberg is now threatening you politically by saying he’ll take the ban to the polls if Council fails to support him.  In Florida the pro-ban lobby spent six million dollars propagandizing the voters while those of us on the other side spent just 1/3000th of that: $2,000.  If both sides had equal voice the vote would have been decidedly different.  If the Mayor tries to coerce NY citizens by using tax money for political lobbying you can be sure the battle will be fought harder and on a more equal footing.

 

One final thought: do not be fooled by pro-ban attempts to cajole you into a “compromise” that exempts private clubs or bars.  This divide and conquer tactic is one they have successfully used elsewhere to whittle down opposition until the remaining minorities, too powerless to stand on their own, finally crumble.  Their goal is a total ban, and anything short of that will simply be used later in an “appeal to level the playing field.”  The fact of the matter is that there simply is NO strong scientific basis for disrupting the lives of millions of New Yorkers and businesses in pandering to these heavily funded extremists.  They do NOT represent most non-smokers who are actually quite happy with the choices offered them already.

 

 

 

 

Sincerely,

 

 

Michael J. McFadden

4424 Ludlow St.

Philadelphia PA 19104

215-386-8430

ISAN: Internet Smokers Action Network: a 100% non-funded all-volunteer citizens group

 

ccs: Councilpeople Quinn, Clarke, Sears, Reed, Gioia, O’Donovan,  and Yassky; Victor Robles, Rudolph Giuliani, selected media and other parties



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ATTACHMENT A

 

ETS Study Results and Commentary

 

 

The details of the codes used in the following table are available in the footnote section at its end.  In general, this is as complete a collection of study results on secondary smoke exposure and lung cancer as you are likely to find anywhere.

 

The studies are divided by type, with workplace and spousal studies generally indicating risk after constant daily exposures lasting for 40 years or even more.  The numbers to pay attention to are the Relative Risk column and the Confidence Interval column.

 

Relative risks below 2.0 or 3.0 are generally viewed with suspicion by epidemiologists because of the risk of contamination of the studies by confounding variables or biases, quite aside from simple statistical error.  An additional point of importance is the notation in the Confidence Interval column indicating whether the CI includes the value of 1.0 between its low and high points.  If it does include 1.0 in that range then the study is said to be NOT statistically significant and should be viewed as affirming the hypothesis that there is no connection between the hypothesized cause and the speculated effect. It should be noted that statistical significance in and of itself is never considered to be sufficient evidence in determining cause and effect: it’s merely a minimum standard used to determine if the results of a study merit further examination and analysis for such things as bias and confounding variables.

 

As you go through these figures, even superficially, you will find two points that stand out strongly as contradictions to Antismokers’ oft-repeated claims that ETS studies are “unanimous and unequivocal” in their condemnation of secondary tobacco smoke.  First of all, the vast majority of the studies are not statistically significant, thus actually supporting the hypothesis that there is NO connection between ETS exposure and lung cancer.  Secondly, and even more amazing given the publicity to the contrary, each of the studies marked by an asterisk in the Relative Risk column actually indicated tendencies of ETS exposure to PROTECT AGAINST lung cancer!   Of course most of those asterisked studies are also non-significant statistically, but as noted in the finishing notes, at least one very important study actually did come up with a scientifically significant finding that early exposure to secondary smoke might protect children from future lung cancers!

 

 


 

 

 

Name

Yr

Local

Type

Sex

Relative Risk

Confidence Interval

 

 

Garfinkel 1 (+)

81

US

Spouse

F

1.18

 .90-1.54

Chan +

82

HK

Spouse

F

0.80 *

 .43-1.30

Correa(+!)

83

US

Spouse

F

2.07

 .81-5.25

Correa(+!)

83

US

Spouse

M

1.97

.38-10.32

Trichopouls(+!)

83

Grk

Spouse

F

2.08

1.20-3.59

Buffler

84

US

Spouse

F

0.80 *

  .34-1.90

Buffler

84

US

Spouse

M

0.51 *

  .14-1.79

Hirayama (+)!

84

Jap

Spouse

F

1.60

1.00-2.40

Hirayama +

84

Jap

Spouse

M

2.24

1.19-4.22

Kabat 1(+)

84

US

Spouse

F

0.79 *

  .25-2.45

Kabat 1(+)

84

US

Spouse

M

 NS  *

0.20-5.07

Garfinkel 2(+)

85

US

Spouse

F

1.23

0.81-1.87

Lam W

85

HK

Spouse

F

2.01

1.09-3.72

Wu(+!)

85

US

Spouse

F

1.40

0.40-4.20

Akiba(+)

86

Jap

Spouse

F

1.50

0.90-2.80

Akiba(+)

86

Jap

Spouse

M

1.80

0.40-7.00

Lee(+)

86

UK

Spouse

F

 NS  *

0.37-2.71

Lee(+)

86

UK

Spouse

M

1.30

0.38-4.39

Bownson 1

87

US

Spouse

F

1.68

0.39-6.90

Gao

87

Chin

Spouse

F

1.19

0.82-1.73

Humble

87

US

Spouse

F

2.20

0.80-6.60

Humble

87

US

Spouse

M

4.82

.63-36.56

Koo

87

HK

Spouse

F

1.64

0.87-3.09

Lam T

87

HK

Spouse

F

1.65

1.16-2.35

Pershagen(+)

87

Swed

Spouse

F

1.20

0.70-2.10

Butler

88

US

Spouse

F

2.20

0.48-8.56

Geng

88

Chin

Spouse

F

2.16

1.08-4.29

Inoue

88

Jap

Spouse

F

2.25

0.80-8.80


 

Shimizu

88

Jap

Spouse

F

1.08

0.64-1.82

Choi

89

Kor

Spouse

F

1.63

0.92-2.87

Choi

89

Kor

Spouse

M

2.73

.49-15.21

Hole

89

Scot

Spouse

F

1.89

.22-16.12

Hole

89

Scot

Spouse

M

3.52

.32-38.65

Svensson

89

Swed

Spouse

F

1.26

0.57-2.81

Janerich

90

US

Spouse

M&F

0.93 *

0.55-1.57

Kalandidi

90

Grk

Spouse

F

2.11

1.09-4.08

Sobue

90

Jap

Spouse

F

1.13

0.78-1.63

Wu-Williams

90

Chin

Spouse

F

0.70 *

0.60-0.90

Liu Z

91

Chin

Spouse

F

0.77 *

0.30-1.96

Brownson 2 ^

92

US

Spouse

F

 NS  *

0.80-1.20

Stockwell ^

92

US

Spouse

F

1.60

0.80-3.00

Liu Q ^

93

Chin

Spouse

F

1.66

0.73-3.78

93

Chin

Spouse

F

1.09

0.64-1.85

Fontham ^

94

US

Spouse

F

1.29

1.04-1.60

Layard

94

US

Spouse

F

0.58 *

0.30-1.13

Layard

94

US

Spouse

M

1.47

0.55-3.94

Zaridze

94

Russ

Spouse

F

1.66

1.12-2.46

Kabat 2 ^

95

US

Spouse

F

1.08

0.60-1.94

Kabat 2 ^

95

US

Spouse

M

1.60

0.67-3.82

Schwartz ^

96

US

Spouse

F

1.10

0.72-1.68

Schwartz ^

96

US

Spouse

M

1.10

0.60-2.03

Sun

96

Chin

Spouse

F

1.16

0.80-1.69

Wang S-Y

96

Chin

Spouse

F

2.53 

1.26-5.10

Wang T-J

96

Chin

Spouse

F

1.11

0.67-1.84

Cardenas ^

97

US

Spouse

F

1.20

0.80-1.60

Cardenas ^

97

US

Spouse

M

1.10

0.60-1.80

Jockel-BIPS

97

Ger

Spouse

F

1.58

0.74-3.38

Jockel-BIPS

97

Ger

Spouse

M

1.58

0.52-4.81

Jockel-GSF

97

Ger

Spouse

F

0.93 *

0.66-1.31

Jockel-GSF

97

Ger

Spouse

M

0.93 *

0.52-1.67

Ko ^

97

Tai

Spouse

F

1.30

0.70-2.50

Nyberg

97

Swed

Spouse

F

1.20

0.74-1.94

Nyberg

97

Swed

Spouse

M

1.20

0.57-2.55

Boffetta(WHO)

98

Eur

Spouse

M&F

1.16

0.93-1.44

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Kabat1 ^

84

US

Work

F

0.70 *

0.30-1.50

Kabat 1 ^

84

US

Work

M

3.30

1.0-10.40

Garfinkel 2 ^

85

US

Work

F

0.93 *

0.70-1.20

Wu ^

85

US

Work

F

1.30

0.50-3.30

Lee ^

86

UK

Work

F

0.63 *

0.17-2.33

Lee ^

86

UK

Work

M

1.61

0.39-6.60

Koo ^

87

HK

Work

F

0.91 *

0.15-5.37

Shimizu ^

88

Jap

Work

F

1.18

0.70-2.01

Janerich ^

90

US

Work

F&M

0.91 *

0.80-1.04

Kalandidi ^!

90

Grk

Work

F

1.39

0.80-2.50

Wu-Williams ^

90

Chin

Work

F

1.20

0.90-1.60

Brownson 2

92

US

Work

F

0.79 *

0.61-1.03

Stockwell ^

92

US

Work

F

 NS  *

NS

Fontham ^

94

US

Work

F

1.39

1.11-1.74

Zaridze

94

Russ

Work

F

1.23

0.74-2.06

Kabat 2 ^

95

US

Work

F

1.15

0.62-2.13

Kabat 2 ^

95

US

Work

M

1.02

0.50-2.09

Schwartz ^

96

US

Work

F&M

1.50

1.00-2.20

Sun

96

Chin

Work

F

1.38

0.94-2.04

Wang T-J

96

Chin

Work

F

0.89 *

0.46-1.73

Jockel-BIPS

97

Ger

Work

F&M

2.37

1.02-5.48

Jockel-GSF

97

Ger

Work

F&M

1.51

0.95-2.40

Ko ^

97

Tai

Work

F

1.10

0.40-3.00

Nyberg

97

Wu

Work

F&M

1.60

0.90-2.90

Boffetta(WHO)

98

Eur

Work

F&M

1.17

0.94-1.45

 

 

 

 

 

 

 


 

 

 

Correa +

83

US

Childhd

F

 NS  *

NS

Kabat &Wyn ^

84

US

Childhd

F

0.92 *

0.40-2.08

Kabat &Wyn ^

84

US

Childhd

M

1.26

0.33-4.83

Garfinkel 2 +

85

US

Childhd

F

0.91 *

0.74-1.12

Wu (+)

85

US

Childhd

F

0.60 *

0.20-1.70

Akiba +

86

Jap

Childhd

F&M

 NS   *

NS

Gao ^

87

Chin

Childhd

F

1.10

0.70-1.70

Koo ^!

87

HK

Childhd

F

1.73

0.60-6.40

Pershagen ^

87

Swed

Childhd

F

 NS  

0.40-2.30

Svensson ^

89

Swed

Childhd

F

3.30

.50-18.80

Janerich ^

90

US

Childhd

F&M

1.09

0.68-1.73

Sobue (^)

90

Jap

Childhd

F

1.28

0.71-2.31

Wu-Will(^)!

90

Chin

Childhd

F

 NS   *

NS

Brownson 2 ^

92

US

Childhd

F

0.80 *

0.60-1.10

Stockwell ^

92

US

Childhd

F

1.10

0.50-2.60

Fontham ^

94

US

Childhd

F

0.89 *

0.72-1.10

Zaridze

94

Russ

Childhd

F

0.98 *

0.66-1.45

Kabat 2 ^

95

US

Childhd

M

0.90 *

0.43-1.89

Kabat 2 ^

95

US

Childhd

F

1.55

0.95-2.79

Sun

96

Chin

Childhd

F

2.29

1.56-3.37

Wang T-J

96

Chin

Childhd

F

0.91 *

0.56-1.48

Jockel-BIPS

97

Ger

Childhd

F&M

1.05

0.50-2.22

Jockel-GSF

97

Ger

Childhd

F&M

0.95 *

0.64-1.40

Ko ^

97

Tai

Childhd

F

0.80 *

0.40-1.60

Boffetta(WHO)

98

Eur

Childhd

F&M

0.78 *

0.64-0.96

 

 

 

 

 

 

 

 

Garfinkel 2

85

US

Social

F

1.42

0.75-2.70

Lee

86

UK

Social

F

0.61 *

0.29-1.28

Lee

86

UK

Social

M

1.55

0.40-6.02

Janerich

90

US

Social

F&M

0.59 *

0.43-0.81

Stockwell

92

US

Social

F

NS *

NS *

Fontham

94

US

Social

F

1.50

1.19-1.89

Kabat 2 (^)

95

US

Social

F

1.22

0.69-2.15

Kabat 2 (^)

95

US

Social

M

1.39

0.67-2.86

Boffetta(WHO)

98

Eur

Social

M&F

1.03

0.82-1.29

 


 

 

Column 1 codes:

^ = Figures from Final Report CA EPA 1997

! = Difference from Forces figures (usually slight, no consistent bias)

+ = 1986 Surgeon General’s Report

( ) = derived/approximate     (WHO) = taken directly from WHO study

 

Unmarked: roughly half the studies noted were not listed in either the California EPA report or the SGR.  Figures for those are from FORCES (a “prosmoking” advocacy group.) For the 66 figures in which cross checking was possible a generally high level of agreement was found with CalEPA and the SGR so there is no reason to believe the FORCES figures are incorrect.  Limiting the chart to only CalEPA and SGR figures would not change the general tendency of the findings.

 

Note: in the case of ranges the chart consistently chooses  from the middle or higher range of exposure for these figures.  For example: in the Janerich ’90 childhood study it uses the figure for up to 25 years of childhood exposure of 1.09 rather than the 2.07 found for more than 25+ years,  while in the Brownson 2 1992 study childhood exposure would have shown a significant negative correlation if exposure was restricted to smoking parents.  Koo 87 “childhood” (actually co-habitant) figures showed a similar effect:  The midrange, which is in the chart, gives 1.73, while the “heavy” exposure of two or more smoking co-habitants gives a lower figure,  1.35.  However in Fontham 94 the lower exposure (1-17 co-habitant exposure) would have yielded a slightly higher (.99) correlation than the higher exposure (18+ years) used (.88).  Many of the studies used differing coding schemes and studied different ranges/sources of exposure.  The chart generally seeks to highlight the middle, or most reasonable ranges rather than highlight the anomalies in either direction.

 

Column 7 codes:

 

* = Studies indicating a NEGATIVE relationship of exposure to secondary smoke and lung cancer.   In these studies, the people that WERE EXPOSED to secondary smoke averaged LOWER rates of lung cancer than those not exposed.

 

NS  *  = Reported by authors only as having no significant relationship or a relationship indicating the SAME rates of lung cancer (i.e. RR = 1.00) among those exposed to secondary smoke and those not exposed.

 

                                       


>>>>>>WHO ABSTRACT<<<<<<<

 

Journal Of The National Cancer Institute, Vol 90, 1440-1450, Multicenter case-control study of exposure to environmental tobacco smoke and lung cancer in Europe.  Authors: P Boffetta et al.

 

BACKGROUND: An association between exposure to environmental tobacco smoke (ETS) and lung cancer risk has been suggested. To evaluate this possible association better, researchers need more precise estimates of risk, the relative contribution of different sources of ETS, and the effect of ETS exposure on different histologic types of lung cancer. To address these issues, we have conducted a case-control study of lung cancer and exposure to ETS in 12 centers from seven Euran countries. METHODS: A total of 650 patients with lung cancer and 1542 control subjects up to 74 years of age were interviewed about exposure to ETS. Neither case subjects nor control subjects had smoked more than 400 cigarettes in their lifetime. RESULTS: ETS exposure during childhood was not associated with an increased risk of lung cancer (odds ratio [OR] for ever exposure = 0.78; 95% confidence interval [CI] = 0.64- 0.96). The OR for ever exposure to Spouse ETS was 1.16 (95% CI = 0.93- 1.44). No clear dose-response relationship could be demonstrated for cumulative Spouse ETS exposure. The OR for ever exposure to workplace ETS was 1.17 (95% CI = 0.94-1.45), with possible evidence of increasing risk for increasing duration of exposure. No increase in risk was detected in subjects whose exposure to Spouse or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to Spouse and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant. CONCLUSIONS: Our results indicate no association between childhood exposure to ETS and lung cancer risk.

We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to Spouse and workplace ETS. There was no detectable risk after cessation of exposure.  Copyright © 1998 Oxford University Press.   Emphasis added

 

(Note that while the author’s interpretation of the childhood figures was simply “no association”, the 22% *reduction* in lung cancer among children of smokers was in fact the only SCIENTIFICALLY SIGNIFICANT result found!  Imagine the publicity this study would have received if the results had been in the opposite direction!  Note also that exposure from “other sources” {e.g. BARS AND RESTAURANTS!} showed NO association to lung cancer!)

 

ATTACHMENT  B

 

 

If I tried to look at every claim that was made by all the antismokers at Wednesday's hearing you'd have a full day of reading ahead of you.  Instead I'm going to look at one particular testimony for the most part and then add a few things beyond that.  I've picked the testimony by the New York Public Interest Research Group for several reasons:

 1)  It holds a special place in my heart (explained below)

2)  It uses many points that were repeated many times in other testimonies.

3)   I know that we both have printed copies so that you can read along with

 me to see that I'm not misrepresenting anything in the material I quote.

 

 

First, as to why NYPIRG is dear to me: For six years I worked with a similar group, going door-to-door raising people's awareness of the dangers of nuclear weapons and collecting contributions.  I know how these groups work and what's important to them.

 

While such groups are sincere in their devotion to the environment, peace or whatever cause, their choice of particular issues is often driven largely by the impact such choices will have on organizational growth and contributions.  When my group was canvassing a conservative neighborhood we would emphasize our concerns about military waste (actually a rather minor point of concern for the group) and de-emphasize our opposition to Star Wars and Reagan's military stance.  In liberal neighborhoods Star Wars spending and Reagan warmongering would be on the top of our clipboards and our tongues.  We weren't lying... just being selective so as to maximize support and contributions (on which our incomes of $5 - $8 an hour or so depended.)

 

NYPIRG works the same way.  The smoking issue is absolutely ideal for canvassing purposes.  If a canvasser smells smoke the issue gets shoved to near invisibility at the bottom of the literature and the fight against chemical spills takes the banner position.  If the canvasser sees American Cancer Society and ASH stickers by the front doorbell the issue of secondhand smoke gets brought to the top and ensures a sizable contribution.

 

Being able to say that "Our lobbyist testified at the NYC Council hearings and convinced hostile Council members to vote for clean air for our children DESPITE the huge monetary and political pressures on Council from Big Tobacco!" ensures a VERY sizable contribution from such a household.


 

I'm telling you the above not to disparage the good work that NYPIRG and other such groups do, but to point out that their purity of motives in pushing this issue is not really all that much different than the purity of motives of the bar owners or even of "Big Tobacco".   As a legislator it's important that you remember that many of the people who come to testify on issues like this have economic interests that are not always readily apparent.  Many billions of dollars from cigarette taxes, lawsuits, and settlements are now being funneled into paying the salaries, expenses and fees of people like the ones who testified on the Anti side at your hearing.  Ten years ago the tobacco companies probably had that advantage.  Today I don't think they're even allowed to spend a cent for that sort of thing under the settlement agreement they signed.

Enough on the background.   Now I'll look at the testimony itself, point by point,  and show you why that mountain of data the antismokers hit you with isn't quite what it appears to be.

 

 

Page One of NYPIRG testimony:

 

After the introduction, NYPIRG says: "Secondhand tobacco smoke is deadly to all who breathe it."   Now, take a moment and think about that. It's actually pure rhetoric, not any sort of scientific statement:  The statement makes it sound as though any human being who has ever breathed a wisp of smoke has died from it while it's obvious that such is not the case.  Still... it sounds good... despite really meaning nothing.

 

They then say: "ETS causes more deaths in the US than all other known environmental toxins combined, and it causes or exacerbates an estimated 300,000 cases of respiratory distress" with the credit for that going to the EPA report and the Surgeon General.  Now it's quite possible that somewhere in the EPA Report such a claim is made about environmental toxins is made, but again, if it is, it is more of a rhetorical claim than any sort of scientific determination of numbers. 

 

As to the second half of their statement, that ETS "causes or exacerbates an estimated 300,000 cases of respiratory distress" note the qualifiers: "causes OR exacerbates"  and "estimated".  Obviously if someone is suffering from severe asthma or acute pneumonia in a smoky environment such will be exacerbated by the smoke (although neither is actually "caused" by the smoke.)  But that 300,000 "estimate" is not from such clearly defined circumstances.  The number is derived from estimates of virtually anyone suffering from bronchitis or pneumonia or asthma who happens to live with a smoker and sees a doctor.  The 300,000 "estimate" also carefully avoids defining what is meant by "respiratory distress"... there's a big difference between someone nearly dying from a severe asthma attack and someone feeling that the smoke in a bar is giving them a runny nose, but both are forms of "respiratory distress".   Without knowing what definitions were used and how the estimates were derived, the claim itself is pretty meaningless DESPITE the fact that it looks so impressive.

 


 

 

 

Similarly with the next claim "up to 11,000 children are sickened and 145 people die each day from ETS."  The words "up to" are a red flag: when you see those words it means that the evidence for whatever claim follows is probably pretty weak and that the person making the statement is leaving a nice legalistic loophole in case the actual number is only 11 (or even zero!) instead of 11,000.  The statement would still technically be "correct". 

 

The wording is also obscure in that we have no idea what sorts of standards are being used to determine what the word "sickened" means in that context.  The claim might be referring to every child who lives with a smoker and catches a cold (caused by a virus!) or simply be a statistical extrapolation from a survey that asked school kids "Are you ever bothered by your parents' smoke?"

 

As to the 145 people dying daily, even the EPA report claimed only a total of 3,000 a year or about 8 people a day; and remember... even THAT claim was thrown out as being fabricated when the report was reviewed by Federal judge William Osteen in 1998 (See Appendix A.) Antismokers like to claim the judge was "pro-tobacco" but that same judge decided AGAINST the tobacco industry in the much more important case putting the industry under FDA regulation.

 

Page Two of NYPIRG testimony:

 

The first sentence claims that the studies on secondhand smoke give evidence that is "unanimous".  This is out and out false.  If you have access to the Surgeon General's Reports take a look at page 71 of the 1986 Report: On that page you'll see the summaries of 13 studies.  Among them you'll find one by Chan and Fung (1982) that found a 20% REDUCTION in lung cancers among spouses of smokers, one by Kabat and Wynder (1984) that found a 10% reduction, several (Koo 1984, Wu 1985, and Garfinkel 1981) that found increased cancer risks but also found that those risks went DOWN with increased exposure, and you'll also find several that show risks so small that the studies were not able to pin them down within acceptable levels of scientific significance (significance usually is taken as meaning that there's less than a five percent chance that the tendency noted was just statistical happenstance).

 

To be fair, the majority of the studies show a tendency, although a very slight one, for an almost immeasurable increase in the absolute rate of lung cancer among people exposed on a heavy daily basis for 30 or 40 or more years.  The percentage increase they sometimes claim (15 - 20%) is only after such decades of exposure. Since lung cancer is rare ( .4% lifetime risk) among nonsmokers to begin with, that translates into about one extra case for every thousand people IF the studies’ findings are not confounded by other factors, and IF all medical science grinds to an immediate halt, and IF no advances are made in cigarette safety or ventilation technology.

 

None of the studies that I know of have addressed the situations of the much smaller exposures of people on a social basis, and quite definitely none have addressed the question of the much lower exposures that would exist in modern environments with higher air quality standards and equipment.   However, the opening statement on Page Two is obviously a complete falsehood: the studies are by NO means "unanimous".  But again... it DID sound impressive, didn't it?

 

 

 

The second sentence contains another outright falsehood: we certainly do NOT "know" that ETS harms children by "causing lung cancer".  The WHO study of 1998 still stands as one of the largest and most authoritative international case control studies of its kind and the ONLY significant finding it made was that children of smokers were 22% *LESS* likely to eventually develop lung cancer than matched children of nonsmokers.  Even the authors had difficulty accepting this finding and interpret it as merely indicating "no association".   Of course if the results had been that strongly in the OTHER direction it would have been trumpeted as absolute proof for the antismoking argument.

 

Page Two, Paragraph Two:  "There is no safe level of exposure to Group A toxins."   I was surprised when I first found out what the scary "Group A" label means: it's NOT something that's "highly" carcinogenic or anything like that: it simply means that a substance has been declared to be carcinogenic in humans as well as in white mice.  OSHA and the EPA do indeed list "safe levels" of exposure to these things: they HAVE to... microscopic quantities of all these things exist all around us!  "Permissible Exposure Limits" specify safe levels for such things.

 

One of the Group A toxins in tobacco smoke is benzene.  According to Lakes Air Toxics Index (http://www.lakes-environmental.com/toxic/ BENZENE.HTML) the OSHA PEL for benzene is 3.26 milligrams per cubic meter of air.  Now in a situation like the Council Hearing Chamber there's roughly ( The chamber being about 30 feet high by 100 wide by 100 long) 9,000 cubic meters of air. According to the 1986 Surgeon General's Report (page 130) a cigarette emits about 330 MICROgrams of benzene ( 330 thousandths of a milligram). To exceed OSHA's Permissible Exposure Limit for this particular Group A carcinogen we'd have to seal the Chamber absolutely airtight and then burn 90,000 cigarettes.   I'm not kidding: do the math yourself.

 

The catch phrase that NYPIRG used was "no safe level of exposure".  What that means is that there's no level of exposure which the EPA will guarantee as *absolutely* safe.  However, as you can see from the above, it would take a hell of a lot of smoking to even APPROACH a level that OSHA still considers acceptable as a daily level of exposure to benzene.

 

Another smoke toxin often held up as "deadly" is arsenic, because we all KNOW arsenic is deadly, right?  The antismokers will point out something like the following: "About five micrograms of arsenic trioxide is inhaled from each cigarette. Three parts of arsenic trioxide per million is the maximum amount permitted in food." (Alton Ochsner, M.D., Smoking and Your Life 1956, p.15)  That sounds pretty bad until you notice that three parts per million means that a single pound of food is thus allowed to contain (454 gms/lb. multiplied by 3 micrograms per gram) 1362 micrograms of arsenic... as much as a smoker inhales from 272 cigarettes!  The trick here was to notice that a "part per million" is the same as a "microgram per gram".

 

So, are nonsmokers forced to inhale deadly arsenic if someone smokes near them?  Yes... but at the rate of 6 cigarettes per year (according to a recent study’s exposure estimate) it would take about 20 years for them to get what they might get in a lunch at McDonald's in a single day!  Similar figuring applied to “safe” urban tap water would equate a 16 ounce tumbler with exposure to the smoke from over 5,000 cigarettes!

 

 

 

 

 

There are lots of other chemicals in smoke.  I could do similar math for most of them.  You've heard about the "4,000 chemicals in smoke".  Well, about 3,900 of those are measurable only in quantities of nanograms and picograms. How big is a picogram?  It's one trillionth of a gram.  There are roughly 10,000 chemicals in the standard American diet if you measure them down to those levels.  Again, it's an impressive sounding but actually meaningless propaganda phrase.

 

Back to the NYPIRG report. The rest of paragraph two continues to say things that sound scary but are not very accurate.  The "3,000" lung cancer deaths a year is from the report that was declared null and void and the NYPIRG people know this full well.  They KNOW  the figure was thrown out, but they repeat it as fact. (as it was repeated in almost every presentation made to you!) The end of the paragraph is totally meaningless: infections are caused by germs, not by smoke, though it's conceivable that heavy exposure to ETS could somehow make one more likely to get infected in some way I guess... but the sentence doesn't even seem to be saying that.

 

Paragraph Three: 90% of nonsmokers encounter smoke at some point.  I can't argue with that... I'd say the figure is probably closer to 100%.  But the second sentence is a CONCLUSION... it starts with the word "Thus" as if something had been proven.  The claim they make in that sentence is that people are at health risk due to the simple fact of being exposed, WITHOUT EVER HAVING SHOWN that such a risk exists!

 

Paragraph Four looks at ETS and children (pretty irrelevant for bars bars).There actually IS some evidence that ETS might cause an increase in SIDS.  I believe the risk is real enough that I'd be concerned about any baby who regularly slept in a smoky bar.  I don't know where the claim in this paragraph about lung cancer and children comes from: as noted earlier, the major study examining that question found REDUCED lung cancer risk… sort of a "vaccination" effect.

 

The final paragraphs cite not scientific findings, but rather declarations by two groups: NIOSH and the AHA.  The declarations sound fairly extreme, and there's a good reason for that: remember... the fear of ETS is seen as VITAL by antismokers  to reduce smoking itself. 

 

Note that the sources cited for the AHA conclusion are papers published in 1991 and 1992. The EPA had these sources if they wanted to use them in their report. The evidence in these papers was so weak though that not even the EPA dared to try to make such a claim in its report after reading them!

 

I won't go into the arguments about the economic effects too deeply.  If the studies were done by activist antismokers like Stanton Glantz (who has devoted his whole life to fighting smoking) they find that bans DON'T hurt business.  If they're commissioned by tobacco companies they find that bans DO hurt.   I'd be inclined to take the word of the restaurant and bar people on this one: they feel it's better for their business if they can make decisions themselves about whether to allow smoking or not.  The only people you see pleading for "a level playing field" (another nice sounding propaganda catch phrase) are the antismokers and those who've been forced by antismokers to ban smoking near a border of a place without such a law.

 

NYPIRG ends by saying  "In sum, the evidence is clear: ETS harms nonsmokers."  If the evidence was actually so clear, why does it appear so cloudy when looked at more closely?


 

ATTACHMENT C

 

 

 

The following two pages are a reproduction of a fax that was sent by an Australian researcher.  It is addressed to the head of the working group that was preparing a meta-analytical report on ETS similar to the one prepared here (and later declared null and void) by the EPA in 1992.

 

Given the poor quality of the fax I will here reproduce several notable sections of that fax.  While this is one of the few documents with this orientation that have reached public eyes, I believe that the tone and concerns are common throughout much of the internal communications that take place within the Antismoking elite when it comes to the “science” of secondary smoke.  While you don’t hear it too often, the recommendation to “massage the data” until it presents the proper conclusions is not unknown to ETS researchers.  Subtler hints of this orientation appear within emails on some of their restricted lists. 

 

 

 

“I am DEEPLY concerned about the implications for the credibility of our whole report arising from the calculations….  If we look at Table 7 in the way any journalist would, in only two age groups (females 60–4 and 65–9 ), do the estimates go over 1 death….  (A) reasonable conclusion will be that the idea that there is ANY lung cancer caused by ETS in Australia will be seen as a huge joke. Journalists… will be hard pressed to write anything other than “Official: passive smoking cleared – no lung cancer” ….  I think we had better get out a thesaurus and find a lot of words to express the words “conservative estimate” in hundreds of different ways….  I think we are looking down the barrell (sic) of a MAJOR public relations problem…. I STRONGLY recommend that we convene another face-to face meeting to discuss what to do about this…. I believe we should alert the NH&MRC to the huge banana skin we are about to put in its path and urge top-level strategic discussion of how to handle this.”  <emphases in original>

 

 

 

 

 

 

 

 

 

 

 

 

Sir George Godber, British Prime Minister of

 

Health, made the following statement while

 

referring to the elimination of smoking in a

 

1975 address to the World Health Organization:

 

 

 

 

“...it would be essential to foster an atmosphere where it was perceived that active smokers would injure those around them, especially their family and any infants or young children who would be exposed involuntarily to ETS.” 

 

 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 



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