Reassessment of the Long-term Mortality Risks
of Active and Passive Smoking
1) “The Long-term Mortality Risks of Active Smoking
and the Need for a Reassessment”
James E. Enstrom, Ph.D., UCLA
2) “Reassessment of the Mortality Risks of Passive
Smoking in the United States”
Geoffrey C. Kabat, Ph.D., Einstein College of Medicine, New York
3) “Silencing of Science: The Phenomenon and Its
Impact on Passive Smoking Epidemiology”
Sheldon B. Ungar, Ph.D., University of Toronto
4) Additional Discussion: “Trofim Denisovich Lysenko
and Pseudoscience in the Soviet Union (1927-1962)”
1
Rationale for Symposium
1) Important epidemiologic findings regarding
active and passive smoking have been ignored or
mischaracterized in prior assessments
2) Rigorous scientific principles require that all
epidemiologic findings must be fairly and
consistently assessed
3) “Silencing” of politically incorrect epidemiologic
findings is ethically and scientifically wrong
4) The credibility of epidemiology is seriously
damaged when ideology and politics replace
rigorous scientific principles
2
Goals for Symposium
1) To present evidence that the long-term mortality
risks of active smoking are greater than generally
believed and the long-term mortality risks of
passive smoking are less than generally believed
2) To establish the credibility of this largely ignored
or mischaracterized epidemiologic evidence
3) To make the case that future research and future
assessments need to be conducted objectively
and transparently, free of ideology and politics
3
17 May 2003 British Medical Journal
4
Background on Enstrom
33 years of epidemiologic research at UCLA
28 years of conducting and/or analyzing prospective
epidemiologic cohorts:
California Mormons
California Physicians
Prevention Magazine Subscribers
Alameda County Study Cohort
United States Veterans Cohort
NHANES Epidemiologic Followup Study Cohort
California Cancer Prevention Study Cohort
Themes: low-risk subgroups and different perspectives
5
California Cancer Prevention Study
1) 1,078,000 total subjects in 25 states enrolled by
American Cancer Society with late 1959 questionnaire
and followed for mortality during 1960-1972 (CPS I)
2) 118,000 California subjects followed for mortality
during 1960-1998 and a 1999 questionnaire survey--at
UCLA with special permission from ACS (CA CPS I)
3) This is the largest epidemiologic cohort followed for at
least 39 years
6
Need for Reassessment
Regarding Active Smoking
1) BMJ Table 10 shows strong 39-year relationship
between active smoking and lung cancer
2) 90% reduction in US tar-adjusted per capita
cigarette consumption
3) Continuing high US lung cancer death rate with
160,000 deaths per year
4) Population impact of smoking cessation not fully
understood or evaluated
7
BMJ Table 10
1960-1998 Active Smoking and Lung Cancer Deaths
Late 1959
smoking status
Males
RR (95% CI)
Females
RR (95% CI)
Never
Former
Current
1-9 cpd
10-19
20
21-39
40-80
1.0
3.5
1.0
1.5
4.1
7.9
12.5
16.4
18.7
(2.9-5.8)
(6.1-10.1)
(10.0-15.6)
(13.0-20.8)
(14.5-24.0)
All current
11.9
(9.6-14.7)
(2.8-4.4)
2.0
5.1
9.1
15.1
15.8
6.2
(1.1-2.0)
(1.5-2.6)
(4.2-6.1)
(7.7-10.8)
(12.3-18.7)
(11.8-21.1)
(5.4-7.2)
8
1900-2005 U.S. Per Capita Cigarette Consumption
and Tar-Adjusted Consumption
Number of cigarettes
5000
4500
4000
3500
Per capita
3000
2500
2000
Tar adjusted
1500
1000
500
0
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000
Year
Data source: Tobacco Outlook Report, Economic Research Service, U.S. Dept. of Agriculture.
9
1930-2005 U.S. Age-adjusted Lung Cancer Death Rates
Deaths per 100,000
70
60
Total population
50
40
30
20
10
Never smokers
0
1930
1940
1950
1960
1970
1980
1990
2000
Year
Data Source: NCHS Vital Statistics; Death rates are age-adjusted to 2000 US standard population.
10
Conventional Benefits of Smoking Cessation
(Enstrom & Heath EPIDEMIOLOGY 1999)
CA CPS I Males
Lung cancer death rate ratios by smoking status at entry
Late 1959 smoking status
Current
Former
Quit < 1 year (1959)
Quit 1-4 years (1955-58)
Quit 5-9 years (1950-54)
Quit 10-19 years (1940-49)
Quit 20+ years (<1939)
Never
1960-1969
Death Rate Ratio
12.3
13.0
8.9
4.7
2.7
1.8
1.0
11
Natural Experiment of Smoking Cessation
(Enstrom & Heath EPIDEMIOLOGY 1999)
Cigarette smoking prevalence among CA CPS I subjects who
smoked in late 1959, based on follow-up surveys of survivors.
Sex
1959
1965
1972
1999
Males
100%
74%
51%
7%
Females
100%
86%
66%
7%
12
Natural Experiment of Smoking Cessation
(Enstrom & Heath EPIDEMIOLOGY 1999)
Relative risk of lung cancer death in CA CPS I cohort:
41,000 current cigarette smokers as of late 1959 compared with
50,000 never smokers
Follow-up period (by decade)
Sex
1960-1969
1970-1979
1980-1989
1990-1997
Males
12.6
(7.9-20.2)
12.1
(8.1-18.0)
12.5
(8.5-18.4)
10.2
(6.1-17.0)
2.5
(1.7-3.8)
6.3
(4.7-8.3)
7.0
(5.4-9.0)
7.8
(5.8-10.4)
Females
13
Additional
Natural Experiments of Smoking Cessation
1) US Veterans Study: 106,000 males followed 1954-1979
(Enstrom J Clin Epi 1999)
2) NHEFS: 700 males & 1100 females followed 1971-1992
(Enstrom J Clin Epi 1999)
3) Iowa Women’s Health Study: 37,000 women 1986-1999
“decline in excess lung cancer risk among former smokers is
prolonged compared with other studies . . . excess lung cancer risk
persisted up to 30 years”
(Ebbert, et al. J Clin Oncol 2003)
14
Randomized Controlled Trials With
A Smoking Cessation Intervention
1) Whitehall Civil Servants Study
1,445 high risk male smokers from London advised in 1970
(JECH 1978, JECH 1982, JECH 1992)
2) Multiple Risk Factor Intervention Trial (MRFIT)
12,866 high risk US males enrolled in 1972
(JAMA 1982, Circulation 1996, Ann Epi 1997)
3) Lung Health Study (LHS)
5,887 US/CN male and female smokers enrolled in 1986
(JAMA 1994, AJRCCM 2002, AIM 2005)
15
Smoking cessation in three RCTs:
intervention group (I) versus control group (C)
Study
Intervention
period (years)
Average Cessation
during intervention period
Intervention
Control
Whitehall
1
~60%
~25%
MRFIT
6
~45%
~20%
LHS
5
~35%
~15%
16
Initial RCT lung cancer deaths and
relative differences, (I-C)/C, and 95% CI (%)
Study Follow-up years
Whitehall*
Lung cancer deaths (I-C)/C & 95% CI
I
C
(%)
10.5
22
~24*
MRFIT
7
34
28
+21.4
LHS
5
20**
19
+ 5.3
76
71
+ 7.0 (-15.5 to +33.7)
TOTAL
- 8.3
*deaths & incident cases, which are scaled (714/731)
**only “special intervention—placebo” group included
17
Full RCT lung cancer deaths and
relative differences, (I-C)/C, and 95% CI (%)
Study Follow-up years
Lung cancer deaths (I-C)/C & 95% CI
I
C
(%)
Whitehall*
20
45
~50*
- 10.0
MRFIT
16
135
117
+15.0
89
- 13.5
256
+ 0.4 (-11.5 to +13.5)
LHS
TOTAL
14.5
77**
257
*deaths & incident cases, which are scaled (714/731)
**only “special intervention—placebo” group included
18
Tobacco Smoke and Involuntary Smoking
IARC Monographs on the Evaluation of
Carcinogenic Risks to Humans, Volume 83
May 2004
1452 pages
Coverage of Smoking Cessation
1) Standard comparison of lung cancer rates among
former smokers, current smokers, and never smokers
2) Nothing on population impact versus successful quitters
3) Nothing on “natural experiments”
4) Nothing on randomized controlled trials
19
THE HEALTH BENEFITS OF
SMOKING CESSATION
A Report of the Surgeon General 1990
(628 pages)
PREFACE BY THE SURGEON GENERAL
“Taken together, the evidence clearly indicates that smoking
cessation has major and immediate health benefits for men and
women of all ages.”
MAJOR CONCLUSIONS
“ the health consequences of smoking cessation for those who
quit smoking in comparison with those who continue to smoke:
1.
Smoking cessation has major and immediate health
benefits for men and women of all ages.”
20
SUMMARY: Active Smoking & Cessation
Long-term mortality risk of lung cancer due to active smoking is
greater than generally believed because it less reversible by
cessation than generally believed based on evidence presented
1) The lung cancer mortality risk ratios for self-selected former
smokers compared with never smokers do not accurately
reflect the population impact of smoking cessation
2) Long-term “natural experiments” in cohorts within the United
States do not show convergence of smoker and never smoker
death rates in spite of substantial smoking cessation
3) Randomized controlled trials involving smoking cessation do
not show a significant reduction in lung cancer deaths in the
intervention groups relative to the control groups
21
Factors Impeding Reassessment
1) Complex Issue: population impact of cessation
versus focus on successful quitters
2) “Wrong Message”: negative findings supposedly
discourage smokers from quitting
3) Uncertainty: implies lung cancer etiology and
benefits of cessation are not completely understood
4) “Silencing”: ignored in major consensus reports
and general information to the public
5) “Conflict of Interest”: some of the above research
has been funded by the tobacco industry
22
May 2006 EPIDEMIOLOGY
Lead Editorial:
“On Conflicts of Interest”
Five Commentaries:
“Kafka's Truth-seeking Dogs”
“What to Declare and Why?”
“He Who Pays the Piper, Calls the Tune…”
“Why Focus Only on Financial Interests?”
“A Conflict-of-Interest Policy for Epidemiology”
23
Conflict of Interest & BMJ Paper
1) Because the final portion of the funding for the CA CPS I study came
from the tobacco industry, attention was diverted from the substance of
the BMJ paper to allegations of tobacco industry influence
2) Because the BMJ findings do not fit the anti-smoking advocacy
agenda, the ACS and key anti-smoking activists have conducted an
ongoing campaign of ad hominem attack, character assassination,
and “silencing” with regard to Enstrom & Kabat
3) Most troubling are the false and misleading statements made about
the BMJ paper by certain powerful US epidemiologists, which will be
presented following the discussion of Lysenko & Soviet pseudoscience
4) The Enstrom & Kabat experience illustrates the difficulty of
conducting “politically incorrect” tobacco epidemiology
24
Reassessment of the Mortality
Risks of
Passive Smoking in the United
States
Geoffrey C. Kabat, Ph.D.
25
26
Background

ETS contains many carcinogens and toxins

exposure is widespread and involuntary

active smoking is a major cause of
avoidable morbidity and mortality
27
Environmental tobacco smoke



ETS is a mixture of sidestream smoke from the
burning tip of the cigarette (70-90%) and
exhaled mainstream smoke (10-30%). Over
time the mixture ages and is deposited on
surfaces.
ETS is both different qualitatively and much more
dilute than the smoke the active smoker inhales
-- how much more dilute? 1/10th? 1/100th?
1/1,000th?
the effects of ETS can only be studied in never
smokers
28
Need for reassessment of passive
smoking



implausible that ETS could cause a 30% increase
in CHD risk given that ETS is much more dilute
than actively inhaled smoke and RR for active
smoking is ~1.8-2.0
strength of association depends on which studies
are included in meta-analysis
issue is difficult to assess objectively because of
enormous political stakes
29
Meta-analyses of ETS and LC
RR
95% CI
US EPA (1992) – US studies
1.19
(1.04-1.35)*
Hackshaw et al. BMJ (1997)
1.23
(1.13-1.34)
IARC (2004) -- females
1.24
(1.14-1.34)
IARC (2004) – males
1.37
(1.02-1.83)
*90% CI
30
Meta-analyses of ETS and CHD
RR
95% CI
Law et al. BMJ (1997)
1.30
(1.22-1.38)
He et al. NEJM (1999)
1.25
(1.17-1.32)
Thun et al. EHS (1999)
1.25
(1.17-1.33)
31
Estimates of US deaths due to ETS
Lung cancer
3,000 -- 5,000
CHD
35,000 – 60,000
32
Follow-up of California CPS I cohort




followed for mortality from 1960 through 1998
118,094 adults, of whom 35,561 were neversmokers with a spouse
ETS exposure based on smoking status of the
spouse in 1959, 1965, & 1972
7,159 respondents to 1999 questionnaire
provided assessment of their self-reported total
ETS exposure
33
34
Deaths for analysis of active and passive
smoking – 1960-1998
Total cohort
Never smokers
CHD
19,485
5,932
Lung Cancer
2,970
156
COPD
2,243
264
35
Active smoking and CHD death, 1960-1998
Males
Active smoking status




RR
95% CI
Females
RR
95% CI
Never smoked
Former smoker
Current smoker
• 1-9 cpd
• 10-19
• 20
• 21-39
• 40-80
1.0
1.2
--(1.1-1.3)
1.0
1.0
1.2
1.4
1.6
1.8
1.9
(1.1-1.3)
(1.3-1.5)
(1.5-1.7)
(1.6-1.9)
(1.7-2.1)
1.1
1.4
1.8
2.0
2.4
(1.0-1.2)
(1.3-1.5)
(1.7-1.9)
(1.8-2.3)
(2.0-2.9)
All current smokers
1.5
1.5
(1.4-1.6)
(1.5-1.6)
--(0.9-1.1)
36
ETS and CHD death, 1960-1998
All 1959 participants
followed 1960-98
Never
Former
Current
1-9 cpd
10-19
20
21-39
40+
RR
Males
95% CI
1.00
--0.94 (0.78-1.12)
0.94 (0.75-2.22)
0.97
0.86
0.92
1.16
1.29
(0.78-1.21)
(0.70-1.05)
(0.74-1.15)
(0.79-1.69)
(0.75-2.22)
Females
RR
95% CI
1.00
1.02
1.01
--(0.93-1.11)
(0.93-1.09)
1.13
1.03
1.04
0.95
0.83
(0.97-1.33)
(0.91-1.17)
(0.92-1.16)
(0.80-1.12)
(0.65-1.06)
37
Active smoking and lung cancer death, 1960-1998
Active smoking status




RR
1.0
3.5
Males
95% CI
Never smoked
Former smoker
Current smoker
• 1-9 cpd
• 10-19
• 20
• 21-39
• 40-80
--(2.8-4.4)
4.1
7.9
12.5
16.4
18.7
(2.9-5.8)
(6.1-10.1)
(10.0-15.6)
(13.0-20.8)
(14.5-24.0)
All current smokers
11.9
(9.6-14.7)
RR
Females
95% CI
1.0
1.5
--(1.1-2.0)
2.0
5.1
9.1
15.1
15.8
(1.5-2.6)
(4.2-6.1)
( 7.7-10.8)
(12.3-18.7)
(11.8-21.1)
6.2
(5.4-7.2)
38
ETS and lung cancer death, 1960-1998
Males
RR
95% CI
Females
RR
95% CI
All 1959 participants
followed 1960-98
Never
Former
Current
1.00
--0.92 (0.37-2.30)
0.69 (0.34-1.39)
1.00
1.08
0.93
--(0.73-1.60)
(0.65-1.33)
39
Summary of BMJ results



exposure to spousal smoking was not associated with
increased mortality from lung cancer or CHD (3 follow-up
intervals)
exposure was weakly associated with increased mortality
from COPD
active smoking showed strong dose-response relationships
with lung cancer, CHD, and COPD (BMJ table 10)
40
Conclusion of BMJ paper
“The results do not support a causal relationship
between ETS and mortality, although they do not
rule out a small effect. The association between
ETS and CHD and lung cancer may be
considerably weaker than generally believed.”
41
American Cancer Society


ACS cohort studies CPS I and CPS II account for
the vast majority of data on ETS and CHD
ACS contends that CPS I cannot be used to
address passive smoking because in 1960s
everyone was exposed
42
Response to ACS criticisms

not true that everyone was exposed to
ETS

majority of women in CA CPS I cohort
were “homemakers”


in their 1999 meta-analysis, Thun et al.
saw fit to include 2 cohort studies initiated
in the 1960’s
ACS has the ability to check our analysis
for 1960-1972
43
Misclassification of ETS exposure
spousal exposure may not reflect total ETS
exposure since there are other sources of
exposure
misclassification was lower in certain sub-groups
1999 questionnaire showed that smoking status
of spouses was directly related to a history of
total exposure to ETS
misclassification was not sufficient to obscure a
true association between ETS & CHD, particularly
in women
44
Spousal smoking vs. self-reported ETS exposure
among CA CPS I never smokers -- females
1959 spousal smoking
Never
Current 1-19 cigs/day
Current 20-39 cigs/day
Current 40+ cigs/day
History of regular ETS exposure
as of 1999 (%)
None
Light Moderate Heavy
62
26
20
16
24
29
21
13
11
39
41
48
3
6
18
24
Enstrom & Kabat, BMJ 2003
45
ETS and CHD: comparison of CA CPS I and CPS II
Females
Spousal smoking
Never
Former
Current
1-19 cpd
20 cpd
21-39 cpd
40+
Current – total
Ever
Enstrom (CA CPS I)
Steenland (CPS II)
1.00
--1.02 (0.93-1.11)
1.00
--1.00 (0.90-1.48)
1.07
1.04
0.95
0.83
1.01
1.01
1.15
1.07
0.99
1.04
1.10
1.04
(0.96-1.19)
(0.92-1.16)
(0.80-1.12)
(0.65-1.06)
(0.93-1.09)
(0.94-1.08)
(0.90-1.48)
(0.83-1.40)
(0.67-1.47)
(0.67-1.61)
(0.96-1.27)
(0.95-1.15)
46
New meta-analysis US CHD studies
Enstrom & Kabat, Inhalation Toxicology
(2006).

includes published studies of CPS I and CA CPS I

applies consistent criteria for inclusion of results
RRcurrent/never = 1.04 (0.99-1.10)
RR ever/never
=
1.04 (0.99-1.10)
Thun et al., Environ Health Perspect (1999)
RRexposed/not exposed = 1.22 (1.13-1.30)
47
Meta-analysis of US lung cancer studies


case-control & cohort studies
includes Enstrom & Kabat, 2003
RRever/never = 1.10 (1.00-1.21)
48
Jenkins, “16 Cities Study”
(1993-94)



100 nonsmokers in each of 16 metro areas
collected 24-hr air samples both at work and
away from work using personal monitoring
participants filled out questionnaires about their
exposures and gave a pre- and post- saliva
sample
samples were analyzed for 10 markers of ETS,
including RSP and nicotine
49
50
Estimates of ETS exposure


Jenkins (1996): mean ETS exposure ~ 8
cigarette equivalents/year
Phillips (1998): housewives with heaviest
exposure could inhale up to 11 cigarette
equivalents/year
51
Richard Peto testimony before House of Lords
Feb. 14, 2006
Question:
“Sir Richard, I wanted to start by asking if you could give us
your assessment of the health risks associated with passive
smoking in the home or at work and in other public places.
It would be helpful if you could give us an indication of both
absolute and relative magnitudes of the health risks and
also the degree of uncertainty attached to the available
statistical evidence.”
Peto’s response:
“I am sorry, I know that is what you would like to be given,
but the point is that these risks are small and difficult to
measure directly. What is clear is that cigarette smoke itself
is far and away the most important cause of human cancer
in the world – that is, cigarette smoke taken in by the
smoker – and passive smoking, exposure to other people’s 52
smoke, must cause some risk of death from the same
diseases. Measuring that risk reliably and directly is
Factors impeding reassessment of
effects of ETS on mortality

incomplete analysis of largest available
data sets (CPS I and CPS II)

minimal research funding

publication bias against null findings

ideological and political agendas
53
Conclusions


Estimates of the association of ETS with CHD
and lung cancer appear to have been overstated.
From the scientific and public health viewpoints,
the focus should be on the very large and certain
effects of active smoking rather than on the very
small and highly uncertain effects of passive
smoking.
54
View of Major ETS Reports
NAS 1986
 Surgeon General 1986
 US EPA 1992
 California EPA 1986
 IARC 2004
 California ARB 2005

55
56
Additional slides—to be
used during Lysenko
session
57
Silencing of Science:
The Phenomenon and Its
Impact on Passive Smoking
Epidemiology
Shelly Ungar
University of Toronto
58
Consider this…


1 in 3 Americans is convinced
Darwinian evolution is “definitely
false”
1 in 7 is convinced it’s true
59
George Bush on Intelligent Design

“Teach the debate”

Bumper sticker:
• “God Said It, I Believe It, and That
Settles It.”
60
Scientists as Secular Shamans

Deliver the goods
• Invested with authority

But scientific authority is precarious
• No infallible source

Ideally open to debate and revision
• Internal disinterested debate

BUT…
61
Vulnerable to “agenda science”

Partisans
• Not disinterested, or truth-seeking

unreasoned allegiance to belief or cause or
$
• aim to conscript science to own ends

use of a wide range of tactics
• Publication bias

Selective disclosure
• silencing
62
Silencing


efforts to prevent the making of
specific scientific claims in arenas in
which these claims are typically
reported.
Range from gagging to publication
bias
• Can morph into fraud

(Note too: not all claims of silencing are
valid)
63
State Silencing

USSR


Denmark


Lomborg, The Skeptical Environmentalist
US



Lysenkoism
Climate Scientists
Reproductive issues
Canada

Climate Scientists
64
Corporate Silencing

Pharmaceutical industry



Vioxx
Paxil
Food corporations

aspartame
65
Silencing by scientists

Lomborg,


The Skeptical Environmentalist
Climate Scientists

skeptics

AIDS research (?)

Tobacco research
66
Silencing by advocates

Environmentalists



Climate change
Lomborg
Health authorities (& laypersons)

Second-hand smoke
67
Enstrom, J., & Kabat, G.
Environmental tobacco smoke
and tobacco related
mortality in a prospective study of
Californians, 1960-98.
British Medical Journal, 2003:
326, 1057-1100.
68
Silencing skirmishes start
BMJ turns tabloid:
Thanks for turning back the clock on public
health decades or more. We don’t need
this kind of negligence from what used to
be a professional medical publication. I
seriously wonder who got paid off at BMJ
to publish this utter garbage.
Dale Jackman
Seriously Annoyed
I won’t dignify this rag with my
credentials
69
Number of Rapid Responses on BMJ Web Site
18
16
14
12
# Rapid
Responses
/Day
10
8
6
4
2
0
15
17
19
21
23
25
27
29
31
2
4
6
8
10
12
14
16
18
20
22
24
Dates (May 15-June 24)
70
Level of Expertise
Evaluation of
Publication
Decision
Expert
Knowledgeable
Layperson
*
Total
Positive
5
12
11
28
Negative
20
44
19
83
Neutral
6
12
5
23
Total
31
68
35
134
* Includes those who
provide no credentials
71
“Irresponsible Journalism”
I was genuinely shocked to see this splashed across the
front page of this week’s BMJ, tabloid-style. An industrysponsored, methodologically flawed study with inconclusive
results but with major potential public health implications
especially once the press get hold of it.
“Passive smoking may not kill.” How much would the
tobacco industry pay for such a soundbite in a major peerreviewed journal? Since when did I pay my subscription
so that you could do their dirty work for them?
72
Level of Expertise
Target of
Negative
Evaluations
Expert (N=20)
"Knowledgeable"
(n=44)
Layperson (n=19)
Article per se
4
10
5
Flaw in the article
15
13
5
Tobacco/Authors
10
22
13
Journal/Editor
1
24
11
Media/Public
3
21
8
Total
33
90
42
73
“From hero to pariah in one easy jump”
Richard Smith BMJ Editor May 18, 2003
“We long ago decided that we would not have a blanket policy of refusing
to publish research funded by the tobacco industry, as some journals
have done. Our argument was that a ban would be antiscience,
systematically distorting the scientific record. . . . Once the research has
been done it should be published, and if it passes our peer review process
it can be published in the BMJ. . . .
I find it distrubing that so many people and organisatons -including the BMA, our owners-- refer to the flaws in the study
without specifying what they are. . . .
We judged this paper to be a useful contribution to an important debate.
We may be wrong as we are with many papers. That’s science. But I
remain convinced that it would have been wrong to reject the paper simply
because it was funded by the tobacco industry.”
74
Fear of Media Coverage
“The study has already been widely
cited by the lay press and is being
used by the tobacco industry to block
public health efforts to enact smokefree policies.”
75
& Use by Tobacco Industry
“As the industry is already
demonstrating, this ‘result’ will be
pumped throughout the globe in
industry PR, in the mouths of its
front organizations, as ‘controversy’
over passive smoking.”
76
Multi-pronged search of
international newspaper coverage

Not even a “blip” of coverage
• Silencing by media


About 60 articles worldwide
Minor papers
• Gwinnett Daily Post, Georgia.
77
Interactive research
Email:
“I can tell you that I have closely
followed the effects of this article in
the Dutch press. It's incredible how
little newspapers have reported on
this study. Only two Dutch
newspapers have published it… this
E&K study looks to be self-censored
by the public Dutch media”
(Maessen, Forces).
78
Not “balanced” coverage
“A new study downplaying the effects
of secondhand smoke on the health
of smokers’ spouses is being
condemned even before it has
appeared in print…”
[It’s a] “pretty crappy piece of
science”
(California)
Sacramento Bee
79
4 articles defend publication
“To believe that second-hand smoke
may not be very harmful has become
a thought-crime almost akin to
Holocaust denial. Those who dare
express doubts must expect
hysterical abuse from every point of
the PC compass.”
(Toronto)
National Post
80
Misuse of the Study?

Tobacco companies


Not trumpet it heavily
Smoker’s rights groups

Enshrine as proof that threat is exaggerated
81
The Washington
Times
Ban the bans
By Jay Ambrose
Published March 26, 2006
…nonsmokers with easily offended nostrils and who are probably
mostly ignorant of the most exhaustive research project ever
completed on secondhand smoke.
The study involved 118,000 Californians. It followed their health
history for four decades, and was conducted by highly respected
scientists and published in the highly respected British Medical
Journal. Here is what it said: There is no evidence of a "causal
relationship" between "exposure" to tobacco smoke in the air around
you and death. A "small effect" cannot be ruled out, the scientists
reported, but that's it. Period.
82
Misunderstand science

No single study definitive
• Especially when dealing with “small risks”
research
• Same overestimation of ‘outlier’ climate studies
83
Mismeasure of science

Not covered by media because…
• Changes nothing

“regime of truth” surrounding smoking
• Cannot be intelligibly questioned
• Not about dueling scientists
84
Smokers are deviants of choice

Secondhand smoke
created a moral
panic
• Smokers as folk
devils
85
Google Alert Secondhand…

Study Finds DNA Risk From Secondhand Casino Smoke

Secondhand smoke can affect pets' health

Exposing infants to secondhand smoke could contribute to cancer risks
later in life

STAT Medical News: Secondhand Smoke Detectable in Babies

Cigarette smoke, even secondhand smoke, can weaken bones

Stroke Prevention…avoid exposure to secondhand smoke

Secondhand smoke linked to acting out [by children]

Small children exposed to secondhand smoke are more likely to develop
ear infections, upper respiratory infections and asthma.

A link exists between secondhand smoke and type 2 diabetes.
86
Eurobarometer poll, 2005




95% said smoking in the presence of a
pregnant woman could harm the baby
75% said they would not smoke in the
presence of a child
75% said they were aware smoke could
be dangerous for non-smokers
53% of people aged 15 to 24 were worried
about second-hand smoking
87
Eurobarometer poll, 2005

SUPPORT FOR BANS
• Office/indoor workplace: 86%
• Any indoor public space: 84%
• Restaurants: 77%
• Bars or pubs: 61%
88
89
Ministers accused of exaggerating risks of
passive smoking
By JANE MERRICK, Daily Mail 08:50am 7th
June 2006
Peers said the ban was not justified by the
relatively low risks of passive smoking
Ministers exaggerated the risk of passive
smoking to force through a blanket ban on
lighting up in public, a report has claimed.
The Government ignored scientific research
on the effects of secondhand smoke in
enclosed public places, according to the
report from the Lords economic affairs
committee.
It says that the smoking ban, which comes
into effect in all pubs, clubs and
workplaces next summer, was a political
decision by Labour's nanny state tendency
- and not justified by the relatively low risk
of passive smoking.
90
pariah.
We long ago decided that we would not have a blanket policy of refusing to publish
research funded by the tobacco industry, as some journals have done. (1) Our argument
was that a ban would be antiscience, systematically distorting the scientific record.
I would try to dissuade anybody from accepting tobacco company money, and I
resigned from Nottingham because it did so. Isn't it thus hypocritical to publish research
funded by the industry? To my mind it isn't. With some difficulty, I'm setting the ethic
that all science should be published above the ethic that you shouldn't take money from
the tobacco industry. Once the research has been done it should be published, and if it
passes our peer review process it can be published in the BMJ.
Our way of making decision on research papers is first to ask if we are interested in the
question. We are certainly interested in the question of whether passive soming kills,
and it's clear to us that the question has not been definitively answered. Indeed, it may
well never be answered definitively. It's a hard question,and our methods are
inadequate. We then peer review the study. Two top epidemiologists-- including George
Davey-Smith--reviewed the paper. Then the paper went to our hanging committee,
which always includes a statistician as well as practising doctors and some of us.
Everybody reads every word of every paper. We asked for extensive changes to the
paper, and the paper we published was different from the paper submitted--which is
usually the case.
We are planning to post on our website all the comments of the reviewers, our
statistician, and the hanging committee. I hope that they will be up soon after the
weekend.
Of course the paper has flaws --all papers do-- but it also has considerable strengths-91
long follow up, large sample size, and more complete follow up than many such studies.
Trofim Denisovich Lysenko &
Pseudoscience in the Soviet Union
(1927-1962)
92
Trofim Denisovich Lysenko was a self-promoting Soviet agronomist
who invented a procedure called vernalization, which he claimed
would lead to dramatically increased crop yields.
Lysenko's claims violated Mendelian genetics and never faced a
rigorous test. However, Joseph Stalin was impressed because
Lysenko promised improved agricultural output unbounded by
hereditary constraints.
Lysenko was portrayed as a genius and rose rapidly in power and
prestige with the backing of Stalin and the media. He was especially
skillful at denouncing geneticists who disagreed with him as enemies
of the state. The result was purges that sent hundreds of dissenting
Soviet scientists to the gulags or killed.
93
Lysenko and his theories dominated Soviet biology for over thirty years.
However, vernalization never increased crop yields and there were two major
famines that killed millions. Current Russian biology still has not entirely
recovered from the Lysenko era.
This episode dramatizes the dangers of political ideology influencing
science and of uncritical media promoting false concepts. A crude
analogy can be made with certain aspects of tobacco epidemiology.
With the goal of reducing smoking, activists exaggerate the dangers
of passive smoking and attack scientists want to do objective work in
this area. In this climate attention is diverted from the real dangers of
active smoking and from a complete understanding of lung cancer
etiology. And the lung cancer epidemic continues.
94
Statement of Major Points of Symposium
1) all epidemiologic findings must be evaluated in a
fair and consistent manner in order to obtain an
accurate assessment of the mortality risks of active
and passive smoking
2) epidemiologic findings must be judged on their
merits and not on extraneous factors
3) additional epidemiologic research in this area
needs to be conducted free of partisanship.
95