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Acknowledgements
I am very much indebted to the work of Dr. J.R. Johnstone on the
previous NHMRC Report (1986). I am also indebted to a variety of writings by Dr. G. Gori,
which have substantially enhanced my understanding of epidemiology. Finally, I am most
appreciative of the suggestions of the reviewers of this paper, several of which have
improved its clarity and the force of its arguments.
- John Luik
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Another kind of credibility is
more worrying. this is rigid, insensitive application of scientific rigour that disregards
the weight of circumstantial evidence, calling into question the validity of
epidemiological findings when it is not in the public interest to do so.
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| John Last
2 |
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For if the trumpet give an
uncertain sound, who shall prepare himself to the battle? (s Corinthians 14.8). The
scientific "yes, but" is essential to research but for modifying the behaviour
of the population it sometimes produces an "uncertain sound" that is all the
excuse needed by many to cultivate and tolerate an environment and lifestyle that is
hazardous to health. |
| The Hon. Marc Lalonde
3 |
The Health Effects of Passive Smoking, the Draft Report of the NHMRC
Working Party represents a careful and sophisticated development of the principles of two
Canadians, Professor John Last, a distinguished epidemiologist, and Marc Lalonde, a
distinguished former minister of National Health and Welfare. Professor Last's principles
are taken from his plenary address to the International Epidemiological Association, while
those of minister Lalonde's are taken from a 1974 document, ' A New Perspective for the
Health of Canadians'. Together, Last and Lalonde provide the unsated but nonetheless
pervasive 'logic' that binds together the Report: namely, the scientific 'yes,but' and the
'insensitive application of scientific rigour' must not be brought to bear in the public
policy process about Environmental Tobacco Smoke (ETS), as it is 'not in the public
interest' to do so. Put most directly, what the Report appears to be is an attempt, no
doubt in the interests of what the authors take to be a good cause, to corrupt the public
policy process with respect to ETS throughout the use of either bad science or corrupt
science.
This response to the Report is divided into two sections. In the
first section, we outline what we mean by the claim that the Report is an instance of
either bad science or corrupt science, and in the second section we examine the
consequences of the use of such instances of bad or corrupt science on the public policy
process.1 - Bad or Corrupt Science
At the outset it is important to define what we mean by bad science
and corrupt science. By bad science we mean incompetent science, science that has
unconsciously failed to do its work properly in some essential sense. Corrupt science, on
the other hand, is bogus science, science that knows that its data misrepresent reality
and its processes are deviant, but nonetheless attempts to pass itself off as genuine
science. It is science that has an institutionalised motivation and justification for
allowing ends to extrinsic to science to determine the findings of science, for allowing
science to be subject to an agenda not its own, for allowing science to tell lies with a
clear conscience. It is essentially science that wishes to claim the public policy
advantages of genuine science without conforming to the scientific process or doing the
work of real science. There are at least four characteristics that mark corrupt science
off from simply incompetent science.
First, corrupt science that moves not from hypothesis
and data to conclusion, but instead from mandated/acceptable conclusion to selected data
back to mandated/acceptable conclusion. That is, to say, it is science that fundamentally
distorts the scientific process through using selected data to reach the 'right'
conclusion, a conclusion that by the very nature of the data necessarily misrepresents
reality.
Second, corrupt science necessarily misrepresents the state of what it
seeks to explain. Rather than acknowledging alternative evidence, or problems with its
evidence that would cast doubt on its conclusiveness, and rather than admitting the
complexity of the issue under review and the limits of its evidence, corrupt science
presents what is at best a carefully chosen partial truth as the whole truth necessary for
public policy. Third, corrupt science not only misrepresents reality but it also
misrepresents its own processes in arriving at its conclusions. Instead of acknowledging
the selectivity of its process and the official compunction of demonstrating the correct
predetermined conclusion, it invests both its process and its conclusions with a mantle of indubitability.
Fourth, and perhaps most importantly,, whereas good science deals with a
dissent an the basis of the quality of it evidence and arguments and considers ad hominem
argument as inappropriate in science, corrupt science seeks to create formidable
institutional barriers to dissent through excluding dissenters from the process of review
and contriving to silence dissent not by challenging its quality, but by questioning its
character and motivation.
These four characteristics manifest themselves in a variety of ways
which include: claiming that a statistical association is a casual relationship; a highly
selective use of data; a highly selective practice of citation and referencing; claiming
that a risk exists regardless of exposure level; assuming that a large number of
statistically non-significant studies constitute a significantly evidentiary trend;
claiming that a series of inconclusive or weak studies justify a strong conclusion;
suggesting that weak evidence warrants decisive regulatory action; being unwilling to
consider seriously non-conforming data; failing to contextualise risk in terms of its
significance; implying that the status of an authority justifies its evidence and policy
recommendations; suggesting that the mean between two Risk Ratios (RRs) is the reasonable
real RR;5 claiming that a finding based on one population is necessarily true of a
different population; confusing the roles of public policy advocate and scientist;
suggesting that certain risks need not conform to the normal public policy process;
advancing public policy measures as 'scientifically justified' without respect to
potential efficacy.
There are at least two major patterns of problems within the Report
that suggest the label incompetent or corrupt science: the Report's understanding of what
counts as evidence and indeed its use of evidence, and the Report's understanding of
logic, particularly coherence and consistency.
Let us begin with the problems of evidence. It is remarkable that a
document published by a body that aims to produce high quality evidence-based information
and advice for use in a range of settings
6 would
proceed without providing its readers with any clear understanding of what its authors
take to be the status of the central scientific discipline, namely epidemiology, upon
which the weight of its evidence is based. It is equally remarkable that the authors would
produce a document that provides no clear position on the assumptions that are employed in
its risk assessments; for example, does it use conservative assumptions and default
options? These two issues, one about the status of epidemiology in general and the other
about risk assessments assumptions in particular are not academic trifles inasmuch as they
go to the heart of two quite central issues- one the issue of whether ETS really does pose
a significant public health problem, and the other the issue of whether the authors are
prepared to be forthright about how certain risk assessment and assumptions can conceal
the uncertainties of the data.
What the authors of the Report appear to believe is that ETS causes
lung cancer based on the weight of epidemiological evidence? For instance the Report
argues that "the evidence that passive smoking causes lung cancer is strong- it
is biologically plausible, reasonably consistent, and demonstrates dose-response
relationships"
8
But apart from the
specific question of whether the evidence adduced in the Report can justify this
conclusion of causality, there is the prior question of whether epidemiology can support
any causal conclusions. As McCormick and Skrabanek have noted in their Follies and
Fallacies in Medicine: It is not uncommon for epidemiological data regarding the
associations to be abused by assuming that an association implies causation. This is
particularly likely in the case of diseases of unknown cause. In modern epidemiology, the
concept of 'cause' has been replaced by statistical associations with so-called risk
factors. As Stehbens point out, risk factors such as high levels of cholesterol in blood
are not causes of coronary heart disease, but associated phenomena such as cough,
shortness of breath, or fever in pneumonia.
9 It is
certainly arguable that the question that the Report seeks to answer is what has been
called a trans-scientific question, a question that goes beyond the powers of science.
10 As Ken Rothman has noted: Despite the philosophic
injunctions concerning inductive interference criteria have commonly been used to make
such inferences, The justification offered has been that the exigencies of public health
problems demand action and that despite imperfect knowledge causal inferences must be
made.
11
Indeed this 'exigencies of public health' approach is precisely the
one taken by the Report,
12 and in doing so it fails
both to warn its readers of the inherent and perhaps insurmountable limitations of
epidemiological evidence and to provide any convincing rationale as to why it should make
a 'judgement about cause and effect'.13 The Report's
reasoning on this point seems utterly specious. For one thing the Hill guidelines14 might provide epidemiological 'causation' but this begs
the question as to whether this is the genuine causation because the reasoning is
transparently circular.: the canons of epidemiology guarantee causation, therefore
causation obtains. Second, the Report's conclusions do not meet even the Hill criteria of
causality, thus there is no justified action that 'must be taken to protect health'.
15 The larger issue, surely, is
whether it is proper to us the word 'cause' in this instance at all,
particularly when the word, at least in the mind of the public, carries a
meaning that appears to confound its epidemiological use?
For instance, when we say that Robert entered the room, pulled out a
gun and shot Sam dead, and conclude that Robert caused Sam's death, we mean 'caused' in
the sense that A caused B to happen. causality in this sense is direct and certain. The
causation of epidemiology is, however, not the causation of 'A caused B' but the
'causation' of statistical association, which can be something quite different. It is
crucially important, therefore for a Report of this sort, one which offers policy advice
to both policy makers and the general public, to be precise about the limitations of its
central evidentiary tool. To this end, the Report should make it clear that its use of the
word 'cause' has two caveats. First, the word is not used in the normal sense of
cause-scientists have not watched ETS enter the lungs of any non-smoker and cause lung
cancer. Second, the epidemiological hypotheses of the possible associations between
multifactorial diseases and low level environmental exposures are extremely difficult to
establish, as opposed to the epidemiological hypotheses about infectious diseases. As the
late Petr Skrabanek has noted:The main preoccupation of
epidemiologists is now the association game. This consists of searching for associations
between 'diseases of civilisation' and 'risk factors'. The 'diseases of civilisation' are
heart disease and cancer. The 'risk factors' studied by epidemiologists are either
personal characteristics (age, sex, race, weight, height, diet, habits, customs, vices) or
situational characteristics (geography, occupation, environment, air, water, sun, gross
domestic product, stress, density of doctors.) Important associations, such as liver
cirrhosis or Korsakoff's psychosis in alcoholism, retinopathy or foot gagarine in
diabetes, aortic lesions or sabre tibias in syphilis, lung cancer in uranium ore miners,
bladder cancer in workers with aniline dyes, are not discovered by epidemiologists but by
clinicians, and they are not called 'associations' but the manifestations, signs, or
complications of diseases which are their causes.
16
This sort of scepticism about the ability to verify the hypotheses of
epidemiology with respect to multifactorial diseases is shared by some of the discipline's
most eminent practitioners. For instance, Sir Richard Doll himself noted that: 'Epidemiological
observations, however, also have serious disadvantages that limit their value. First, they
can seldom be made according to the strict requirements of experimental science, and
consequently the available observations may be open to a variety of interpretations.'
17
The failure of epidemiology to meet the 'strict
requirements of experimental science' lies in the fact that epidemiology does not always
proceed on the basis of randomised trials, which are the unquestioned standard for the
drug studies and other medical research. As Gary Taubes, writing last year in an article
in Science on the limits of epidemiology, observes: 'Assign subjects to random test
and control groups, alter the exposure of the test group to the suspected risk factor, and
follow both groups to learn the outcome. Often, both the experimenters and the subjects
are 'blinded'- unaware who is in the test group and who is a control.'
18
But the 'strict requirements of experimental science'
cannot be used for most risk factors, not simply because of the length of time that would
take and the corresponding expense, but because of the significant ethical objection of
exposing healthy subjects to suspected risks. This means that the epidemiology of
multifactorial diseases must proceed on the basis of observational studies which are
either case-control studies or cohort studies. Case-control studies select a population
that has a particular disease, select a population that does not have the disease and then
systematically compare the two groups for differences. Cohort studies take a large
population, interview them about lifestyle and environment and then follow the population
for a period of time in order to determine who gets which diseases.
But these approaches are themselves open to a series of other
problems- namely, confounders (the unobserved variables in the populations being studied
which are not controlled for) and biases (the problems inherent in the designs of the
studies). For many epidemiologists, these create formidable if not insurmountable
problems. Alvin Feinstein of Yale observes: ' In the laboratory you have all kinds of
procedures for calibrating equipment and standardising measurement procedures. In
epidemiology... its all immensely prey to both the vicissitudes of human memory and the
biases of the interview.'
19 Again as Harvard's
Alex Walker suggests: ' I have trouble imagining a system involving a human habit over
a prolonged period of time that could give reliable estimates if [risk] increases that are
of the order of tens of percent.'
20 These
conclusions are supported by Gio Gori, President of the International Society of
Regulatory Toxicology and Pharmacology, who notes that:
In
studies of local populations, many factors trigger, facilitate, or impede particular
outcomes, and introduce extreme difficulties in reaching specific causal attributions. In
current practice, these difficulties are circumvented by ignoring the multiplicity of
field variables, and by presuming that only the few of contingent interest matter. Adding
uncertainty, most studies of multifactorial conditions are not randomised experiments, but
observational surveys that are virtually impossible to replicate under equal conditions.
Such observational studies are un-testable by the standard rules of the scientific method
and their reports could not be objectively validated... The ethics of science negates the
causal statements of fact if ex perimental predictivity is absent.
21
I am not suggesting that epidemiology is not a science, only that the
epidemiology of multifactorial diseases is plagued with substantial problems which rule
out the use of claims about causation, and about which the readers of the Report deserve
to be informed.
But it is not merely that the Report's authors do not forthrightly
share their epidemiological assumptions, alert the reader to the methodological problems
surrounding the epidemiology of multifactorial diseases, or indicate the special sense in
which 'cause' functions in current epidemiology; it is also that they do not explicitly
expose their risk assessment assumptions, even though such assumptions do function to
determine the Report's directions. For instance, the Report seems to proceed from
conservative assessment assumptions; that is, it is intentionally biased towards finding
more risk. Moreover, it is also driven by a common default option assumption that in the
absence of complete scientific knowledge it will fill the gap between scientific knowledge
and public policy.
22 In this case the Report has
assumed that in the absence of convincing evidence to the contrary, it will proceed as if
there is no threshold of ETS-caused cancer and that the dose response is linear.
23
Only such a default option could explain the Report's
policy recommendations for dealing with ETS. Yet this default is an assumption: it is not
scientific knowledge because it cannot be confirmed or disproved by science. (The default
option does appear to be inconsistent with what the majority of cancer specialists believe
that science knows about carcinogenesis.) The difficulty with such a position is that it
significantly lessens the scientific credibility of the Report inasmuch as it builds into
the Report a non-scientific assumption. Additionally, by avoiding the issue of
conservative assumptions and default options, the Report avoids the most central issue of
risk assessment.
Taken together, the unsatisfactory and misleading discussion of the
limits of epidemiology with respect to the causation and the incorporation of significant
bias throughout the conservative risk assumptions and default options, tend to suggest not
bad science but something closer to corrupt science. It is closer to corrupt science
because it misrepresents the complexity of the issue and the nature of the evidence about
it through failing to acknowledge both its biases and the inherent uncertainties of the
risk assessment exercise itself.
The second evidentiary problem, which again suggests the Report's
proximity to corrupted science, is its uncritical use of the US Environmental Protection
Agency (EPA) 1992 Report. The Report refers to the EPA work as the ' most extensive
recent review of the evidence of passive smoking and lung cancer.'
24 Quite surprisingly, the Report fails to mention the
extensive criticism directed at the EPA's ETS analysis, or the fact that the EPA's
findings are the subject of court action.
25 Given
the uncritical attention devoted to the Epa's work, it is worth noting precisely how
strong the evidence is which suggests that the EPA's science on ETS is corrupt science.
The evidence that the EPA science on ETS is corrupt science falls
into two categories: evidence about the substance of the science, and evidence about the
processes involved in creating and using the science.
A. The
Substantive Issue
The EPA report, Respiratory Health Effects of Passive Smoking: Lung
Cancer and Other Disorders,
26 claims that, 'based on
the weight of the available scientific evidence, the US Environmental Protection Agency
has concluded that the widespread exposure to environmental tobacco smoke in the United
States presents a serious and substantial public health impact.' Is this, in fact, the
case? In order to answer this question one must first know something about the data on
which the Epa decision is based. The EPA report refers to the 30 epidemiological studies
in spousal smoking and lung cancer that have been published from 1982-1990. I t is
important to note that while EPA Administer Reilly in referring to the report spoke about
ETS and cancer in children and in the workplace, and though the report has been used as a
basis for demanding smoking bans both in public places and in workplaces, the EPA did not
examine those studies that look at workplace ETS exposure. The overwhelming majority of
those workplace studies do not find statistically significant exposure to ETS and lung
cancer in non-smokers: a fact that by itself destroys the legitimacy of any harm-based
demand for public or workplace smoking bans.
Thus, to begin with, the EPA's case is based not on workplace or
public ETS exposure, but on the risks of non-smoking spouses contracting lung cancer from
their smoking spouse. But what of the 30 epidemiological studies? Those 30 studies come
from different countries and vary substantially in size. Some have fewer than 20 subjects,
others are based on larger populations, with the largest study involving 189 cancer cases.
Of the 30 studies, 24 reported no statistically significant association, while six
reported a statistically significant association, that is, a positive relative risk for
those non-smoking spouses. Now, relative risks are further classified into strong risks or
weak risks, depending on their magnitude. Within the 30 studies on ETS and lung cancer
none reported a strong relative risk. Moreover, whenever the assessment of relative risk
is weak there is a substantial possibility that the finding, the assessment, is artificial
rather than real. That is to say, there is a strong likelihood that even the weak relative
risk is a reflection not of some real world risk, but of problems with confounding
variables or interpretive bias. There are, for instance, at least 20 confounding factors
ranging from nutrition to socioeconomic status that have been identified as important to
the development of lung cancer. Yet none of the 30 studies attempts to control for these
factors. So, in assessing the global scientific evidence about ETS and lung cancer, the
crucial conclusion is that none of the studies reports a strong relative risk for
non-smokers married to smokers.
Now the EPA report discusses all of these 30 studies, but it limits
its statistical analysis to only 11 U.S. studies of spouses of smokers.What do the 11
studies show? Of the 11, 10 reported no statistically significant association between ETS
exposure and lung cancer while only one reported a statistically significant association.
The EPA analysis of these 11 studies claims that they show a statistically significant
difference in the number of lung cancers occurring in the non-smoking spouses of smokers
such that they suffer 119 such cancers compared with 100 such cancers in non-smoking
spouses of non-smokers. It is this finding of statistical significance, a finding based
only on 11 U.S. studies, 10 of which found no significant association, that is the basis
for the EPA decision to classify ETS as a ' Group A ' carcinogen.
27
In order to arrive at its 'conclusion', the EPA combined the data
from the 11 studies into a more comprehensive data assessment called a 'meta-analysis'.
Meta-analysis is governed by its own rules, as not every included study is a candidate for
such combined analysis. In general, meta-analysis is appropriate only when the studies
being analyzed together have the same structure. The difficulty withe EPA's use of
meta-analysis of the 11 ETS studies is that it has failed to provide the requisite
information about the structure of the 11 studies, information crucial for an independent
assessment of whether the studies are indeed candidates for meta-analysis. Thus, the EPA
conclusion is based on a meta-analysis that is difficult, if not impossible, to verify.
But even more crucial to the question of assessing the quality of the
EPA's ETS science is the issue of confidence intervals, for even by limiting its analysis
ti only 11 studies, and even by lumping these studies together through a meta-analysis,
EPA could not have achieved the 'right' result if it had not engaged in a creative use of
'confidence intervals'. Essentially, confidence intervals express the likelihood that a
reported association could have occurred by chance.
The generally accepted confidence interval is 95%, which means that
there is a 95% confidence that the association did not occur by chance. Inasmuch as most
epidemiologists use the 95% confidence interval, the EPA itself, until the 1992 ETS
report, always used this interval. Indeed every one of the individual ETS studies reviewed
by the EPA used a 95% confidence interval. Curiously, the EPA decided that in this
instance it would use a 90% confidence interval, something that effectively doubles the
chance of being wrong. Without using this 90% standard, the EPA could not have found that
the 11 U.S. studies were 'statistically significant'. Without employing a novel standard,
without, in effect, changing the accepted rules of epidemiological reporting, the EPA
result, already painfully coaxed into existence, would not have existed, and ETS could not
have been labelled a 'Group A' carcinogen.
hus, despite all of its careful selection of the right data, its
meta-analysis and finally its relaxed confidence intervals, the conclusive point remains,
as Huber, Brockie, and Mahajan had already noted in Consumers Research in the United
States, that ' No matter how the data from all of the epidemiological studies are
manipulated, recalculated, 'coked', or 'massaged', the risk from exposure to spousal
smoking and lung cancer remains weak... No matter how these data are analyzed, no-one has
reported a strong risk relationship for exposure to spousal smoking and lung cancer.'
28
B. The Process Issues
While a careful look at the EPA's ETS claims clearly shows why this
science can be called nothing other than corrupt science in that it uses highly selected
data, data that are then further manipulated in breach of accepted scientific norms, all
without cogent explanation, to reach the 'right' conclusion, an examination of the process
underlying this 'science' demonstrates even more clearly its wholly corrupt character.
There are at least nine specific process issues worth noting, each of which highlights a
slightly different dimension of the corrupted character of the EPA's ETS science.
First, EPA science issues from a health promotion perspective that
finds its conceptual home in the Lalonde Doctrine as propounded by Former Canadian
Minister of National Health and Welfare, Marc Lalonde. Lalonde argued that health messages
must be vigorously promoted even if the scientific evidence was incomplete, ambiguous, and
divided. Health messages must be 'loud, clear, and unequivocal' even if the evidence did
not support such clarity and definition. What we have in the EPA is simply the Lalonde
Doctrine as an institutionalised process. Clearly, the substance of the ETS data does not
support its 'Group A' carcinogen status, nor does it support public and workplace smoking
bans on the grounds that ETS threatens the health of non-smokers. But the substance of ETS
data is to be ignored because the Lalonde Doctrine places the process of using such
substance ahead of the substance itself; indeed, it requires that the substance be
portrayed as something that it is not in order to further the health agenda. What this
inevitably does is to build into the heart of the scientific enterprise an
institutionalised motivation and justification for allowing ends extrinsic to science to
determine the findings of science, for allowing science to be subject to an agenda not its
own, for allowing science to tell lies with a clear conscience.Once one has come to see
science as something which of necessity happens within the context of health promotion,
then the process corruptions of the EPA follow quite 'naturally'.
This explains why, at one level, those involved with the EPA decision
on ETS are quite frank about their process. For instance, an EPA official responsible for
the revised ETS risk assessment was quoted as admitting that 'she and her colleagues
engaged in some fancy statistical footwork' to come up with an 'indictment' of ETS.
29 (The footwork to which she referred is the novel 90%
confidence interval.) Or to take another process example, the Science Advisory Board which
reviewed the initial draft risk assessment on ETS, and found the case against ETS based on
its association with lung cancer to be unconvincing, actually urged the EPA staff to
attempt to 'make the case' against ETS on the basis of similarities between ETS and
mainstream smoke.
30 To be fair, the consequences of
the Lalonde Doctrine are not confined to the EPA's anti-smoking agenda. For instance, an
article in the Journal of the American Medical Association in July 1989 reported a study
that claimed to show a link between ETS exposure and increased risk of cervical cancer. In
response to critics who noted that such a link was biologically implausible and that the
study had ignored confounding factors, the authors replied that the study was justified
simply on the grounds that it might reinforce the dangers-of-smoking message: 'While we do
not know of a biologic mechanism for either active...smoking or ETS to be related to
cervical cancer, we do know that cigarette smoking is harmful to health. The message to
the public, as a result of this study, is one that reinforces the message that smoking is
detrimental to health.'
31 It would be difficult to
find a more succinct example of the Lalonde Doctrine at work. There is no compelling
evidence to support their claim, the authors all but admit, but it is important, in the
interests of health promotion, that the public be made to think that there is scientific
evidence of harm.
But second, while those involved in the EPA process are at one level
open about the process, at another level they are profoundly dissembling. For instance,
the EPA fails to mention that the 'Group A' carcinogen status for ETS was arrived at using
a process that violates its own Guidelines for Carcinogenic Risk Assessment. Instead of
accepting that this suggested that the Guidelines for Carcinogenic Risk Assessment be
changed. Given that the 'right' conclusion must be reached and the data do not support
that conclusion, one must manipulate the data and revise the guidelines governing the
process and the conclusion.
Third, the ETS risk-assessment process has been corrupted from the
outset by the fact that it has repeatedly violated the standards of objectivity required
by legitimate science by utilizing individuals with anti-smoking biases. One member of the
group working on the ETS issue at the EPA is an active member of the US anti-smoking
organisations, while the Science Advisory Board that examined the EPA's ETS work included,
not only a leading anti-smoking activist, but several others strongly opposed to tobacco
use. Finally, the EPA contracted some of the work on certain documents related to the ETS
risk assessment to one of the founders of a leading anti-smoking group.
Fourth, the EPA changed the accepted scientific standard with respect
to confidence intervals, without offering any compelling justification, in order to make
it substantive findings statistically significant.
Fifth, the EPA's Workplace Policy Guide which, as a policy document,
would, in the course of normal scientific process, be developed only after the scientific
evidence was in, was actually written before the scientific risk assessment was even
completed, let alone reviewed and finalised.
32 Quite
obviously, science was to be made to fit with policy, rather than policy with science.
Sixth, the EPA fails to note that if the two most recent US ETS
studies were to be included along with its eleven other studies, it would have resulted in
a risk assessment that was not statistically significant, even using the novel 90%
confidence interval. With its entire 'conclusion' at risk, there are exceedingly
compelling process reasons for the EPA to have excluded these two studies from their
analysis.
Seventh, exclusion, however, was apparently insufficient, because the
EPA does simply more than not use studies, it actually refers to them in an appendix
33 and misrepresents one through claiming that it supports
the EPA's ETS conclusions. The study, by Brownson,et all.,
34
which appeared in November, 1992 in the American Journal of Public Health reported no
statistically significant increase in risk between lung cancer and ETS exposure. In order
to get round this politically unacceptable conclusion, the EPA quotes Brownson as
concluding that 'Ours and other recent studies suggest a small but consistent increased
risk of lung cancer from passive smoking.' But this is not the issue, as the EPA well
knows. The question is not whether one observes a small increased risk but whether, in
addition, one can legitimately assert that its magnitude is unlikely to be simply a chance
effect, that is, whether there is a statistically significant risk, which in this case
brownson concluded o could not do. In effect, the EPA misrepresents a scientific finding
through changing the terms of reference from statistical reference to just plain risk.
This penchant for misrepresentation is not, however, just confined to
recent studies. For instance, the EPA analysis consistently makes reference to the
Garfinkel, et all., study. The EPA claims that this study presents at least suggestive
evidence of an association between ETS and lung cancer...
35
But a careful reading of Garfinkel does not confirm this at all. Garfinkel actually says
that 'we found an elevated risk of lung cancer, ranging from 13-31 per cent, in women
exposed to the smoke of others, although the increase was not statistically significant'.
36 The entire question of suggestive evidence is bogus: the
relevant question is whether Garfinkel found a risk that was statistically significant. He
did not, and the EPA misrepresents his finding.
Eighth, the EPA represents its process as a comprehensive and
objective analysis of the ETS data. In the usual course of events, this would imply a
careful examination of the criticisms that have been levelled at the studies used to reach
its conclusions. However, a careful examination of the Bibliography accompanying its
report suggests that this is not the case. Although the note with the Bibliography
indicates that it is not a 'comprehensive list of all references available on the topic'
it is still a list of all the references cited and reviewed for the report. Yet, to take
but one example, one would never know from the report or its Bibliography that the work of
Trichopoulos had been subjected to significant criticism by both Burch and Heller, since
neither is mentioned in the Bibliography. Nor indeed, despite its lengthy examination of
the Hirayama studies, would one learn from either the discussion or the Bibliography that
Hirayama was devastatingly criticised by Rutsch, who noted that one could infer from
Hirayama's data that lung cancer was more common in unmarried non-smoking women than in
the non-smoking wives of smokers-a somewhat curious result.
Now, the possible explanations for such selectivity are that:
- 1) the authors of the study are not familiar with such criticisms,
which would suggest incompetence, or
- 2) they are familiar with the criticisms but have misunderstood them,
ignored them, or discounted them.
But even if one were to discount or ignore them is still odd, if one
is committed to objectivity and openness, not to cite them. Not to cite them suggests that
one wishes to act as if they don't exist and to do this is to give rise to more than the
suspicion that the EPA's ETS work is really an instance of a closed-loop process abuse. In
a closed-loop the circle is never opened up to divergent, dissenting views, views that
challenge the orthodox conclusion. It is not simply that such divergent views are
discounted; it is rather that, as the EPA discussion and their Bibliography indicate, they
simply never are heard-indeed, judging from the Bibliography, they don't exist. What this
demonstrates is a closed-loop process in which voices of dissent are not allowed inside
the decision making circle. The circle is never opened to those who don not share the
agreed perspective.
Ninth, significant difficulties have already been raised about the
quality of EPA science, particularly by the Expert Panel in its report Safeguarding the
Future: Credible Science, Credible Decisions, a report which noted that:
- 1) EPA 'science of uneven quality';
- 2) the 'EPA has not clearly conveyed to those outside or even inside
the Agency its desire and commitment to make high-quality science a priority';
- 3) 'the science advice function-that is the process of ensuring that
policy decisions are informed by clear understanding of relevant science-is not well
defined or coherently organised within the EPA';
- 4) the 'Agency does not have a uniform process to ensure a minimum
level of quality assurance and peer review for all the science developed in support of
Agency decision making';
- 5) the 'Agency lacks the critical mass of externally recognised
scientists needed to make EPA science generally credible to the wider scientific
community.';
- 6) 'science should never be adjusted to fit policy.'
37
Despite this, the EPA process is incapable of correcting itself.
This is perhaps the most significant process corruption of all,
namely a process that is quite conscious of its problems but is unwilling and unable to
address them. Of course, even this characterization is perhaps too kind given that what
the Expert Panel describes as problems are really, for the anti-smoking movement, just the
normal way that science must proceed if it is to make the anti-smoking case. If this is
the case, then there is no conscious sense of process problems. What the Expert Panel's
report actually provides, of course, is another description of corrupted science corrupted
in its substance and its process, science driven by a predetermined policy agenda, science
based on inadequate data,science of uneven quality and inadequately peer reviewed, science
lacking critical validation by outside scientists representative of the 'wider scientific
community', and science, finally,fully aware of its corruption, but unwilling to heal
itself.
This is not to suggest that the NHMRC Report should exclude all
reference to the EPA. It is however, to suggest that it should acknowledge that serious
objections have been raised against the EPA's report, that it should reference those
objections and indicate its own position on such objections. To take but one instance, the
Report could have noted that the EPA's departure from the accepted 95% confidence level is
not accepted epidemiological practice, rather than merely repeating the EPA's self-serving
explanation about a priori hypothesis. The hypothesis is what should have been tested-not
assumed. Are we to assume that the Report's authors countenance as accepted
epidemiological practice the recalculation of the results using a lower significance level
and the declaration that such a new result supports one's case? Not to acknowledge that
objections have been raised and not to give them some attention, with such a fundamental
document in the ETS debate as the EPA analysis is, is to appear to accept the process and
substantive abuses that are the hallmark of corrupted science.
The third evidentiary problem is really a cluster of problems which
relate to the Report's understanding and use of epidemiological evidence. It is also a
series of problems about what the Report chooses not to cite or count as relevant to its
work. These problems have been ably demonstrated by Johnstone,
38
whose account here is fundamental. As he has pointed out, the problem essentially centres
on the fact that the previous NHMRC Report (1986)
39
contained significant errors with respect to the quality of the epidemiological evidence,
errors that go unacknowledged and uncorrected in the 1995 Report. To take one instance,
the 1986 Report considered the work of Trichopoulos
40
but it provided the wrong calculations of risk ratios, even though these had been drawn to
Trichopoulos' attention in 1983 by Heller and accepted by Trichopoulos in 1984.
41 It is astonishing that this error is not mentioned and
that Heller's critique of Trichopoulos is not included in the Report's references. Equally
strange is the fact that Trichopoulos' 1984 paper is not included in the Report's
references. One has the uncomfortable feeling that the Report is not favourably disposed
to acknowledging error in those who argue that the evidence suggests that ETS presents a
health hazard. If this were an isolated instance of incorrectly-cited evidence that failed
to take into account serious questions as to the evidence's validity, it could perhaps be
excused. Instead, one is confronted with what appears to be a pattern of such problems.
Take for instance the work of Hirayama, author of some of the
earliest and most widely quoted studies. Hirayama's 1981 data were analyzed using a test
developed by Mantel. After the publication of Hirayama's paper, Mantel
42 published a criticism of Hirayama's method. In response
to Mantel's criticism, Hirayama produced additional information which Rutsch
43 showed led to the conclusion that lung cancer was more
common for non-smoking unmarried women than for non-smoking wives of smokers. Neither the
NHMRC's 1986 Report nor the present Report mention these significant difficulties with
Hirayama's work. Indeed they do not cite these papers by Mantel or Rutsch. Equally surprising is that the Report's references omit one of
Hirayma's 1981 papers,
44 in which Hirayama
acknowledged, in response to Lee,
45 that his
confidence levels contained errors by factors of over 100%. Of course the Lee paper does
not appear in the references, either. Given that the Report devotes significant attention
to Hirayama's work,, it is nothing less than astonishing that none of these substantial
criticisms of his work is mentioned or referenced. This is precisely what characterises
corrupt science-the unwillingness to acknowledge alternative evidence or problems with
evidence that might undermine its credibility.
A similar reluctance to acknowledge evidentiary mistakes is found in
the fact that the Report fails to acknowledge or correct errors in reporting the results
of Correa, et al.,46 and Garfinkel,et al.,47 that were contained in the 1986 Report. The 1986 Report
claimed that Correa found a positive trend in lung cancer in non-smokers with ETS. Yet
Correa reported no such finding. The 1986 Report also claimed that Garfinkel found a '
positive association in non-smoking females; statistically significant'. But Garfinkel
reports that the elevated risk was not statistically significant and the 1995 Report
nowhere acknowledges its predecessors glaring error.
The fourth evidentiary problem of what, if anything, the 'evidence'
adduced by the Report suggests. The Report's authors believe that the epidemiological
studies 'provide direct empirical evidence of the effect of exposures on the
development of cancer'
48. But this is surely an
impossibility as the language of effect is inextricably linked to the language of cause,
and epidemiological gives us at most statistical associations. But let us leave causal
quibbles aside and focus solely on the question of what the evidence actually shows. Let
us focus on the four largest and most recent case control studies-Kabat
49 , Fontham,
50,
Brownson,
51 and Stockwell,
52 three of which are discussed in the Report. The Report's
discussion of Brownson and Stockwell is curious, if not misleading. The Brownson study
shows no increased average risk. In plain language this means that using only the Brownson
data one should conclude that ETS causes no annual lung cancer deaths. But this crucial
point is not mentioned in the Report. Instead of being provided in the text with this
information we are told that Brownson found 'elevated risks for adult domestic
exposure of greater than 40 pack-years'. But the results of the upward dose response
trend are not definitive and, more crucially, even at the highest exposure levels, risks
are subject to significant uncertainty.
A similarly curious presentation is accorded to Stockwell. The Report
tells us that Stockwell findings are statistically significant.
53
But this is simply untrue as the Stockwell study shows an increased average risk which, at
the 95% level is not statistically significant. What this means is that of the 40 studies
presented in Table 5.2 of the Report only twelve reach statistical significance. Of the
four most recent large studies-Kabat, Fontham, Brownson and Stockwell-two show no
increased average risk (Kabat, Brownson), one shows a barely statistically significant
increased risk (Fontham), and one shows and increased average risk which is nonetheless
not statistically significant at the 95% confidence level (Stockwell).
54 Moreover, if we are to take the Fontham study, which
alone of these four shows a statistically average increased risk, and ask the relevant
question about the degree of risk suggested, then in the words of the Congressional
research Service (CRS), the chance of dying of lung cancer over one's lifetime 'for a
person exposed only to background ETS, the number drops to about 7/100 of one percent'.
55 It is on the strength of this 'evidence' that the Report
concludes that the 'evidence that passive smoking causes cancer is strong'.
56 But this is the conclusion of what can only be described
as corrupted science, science that misrepresents the data, the strength of the data and
what conclusions should be drawn from the data. Indeed, it is difficult not to conclude
that if this 'evidence' were about anything other than tobacco smoke, the suggestion that
it provided the basis for public policy remedies would be immediately dismissed.
This conclusion is strengthened when two additional factors which the
Report mentions are carefully examined: misclassification and the Hill criteria for
causation. there are several sorts of misclassification errors that could occur in the
studies cited in the Report. As the CRS noted: 'It is clear that misclassification and
recall bias plague the ETS epidemiology studies. It is also clear from the simulations
that modest, possible misclassification and recall bias rates can change the measured
relative risk results, possibly in dramatic ways.'
57
This is ignored in the Report's claim that 'Smoker's misclassification is a potential
source of positive....bias which has not been proven to have affected the relevant
epidemiological studies'.
58 But as the CRS notes:
Possible combinations of small rates-below 10 percent-could drive ETS
relative risks in the highest exposure groups to values no longer distinct from 1.0. While
these results are obtained from the Fontham study similar results are likely from the
Brownson study. Even smaller values of these rates- below 3 percent-could be combined to
reduce the lower bounds of the 95% confidence intervals well below 1.0 for these studies.
59
An examination of the Report's use of the Hill criteria reveals a
similarly curious result. Table 5.1 in the Report sets out the Hill criteria for causality
and their application to the studies cited as evidence. What is so surprising about this
table is its consistent misrepresentation of what the data in fact show. For example, with
respect to strength of association, hill argued that a strong association lent greater
credence to a causal claim than a weaker, with a strong association being an RR of at
least three. on this criterion, the Report's RR of 1.3 fails the association test.
Similarly with dose response, the data from Brownson and Stockwell suggest that the
results of the upward dose-response trend are not definitive, and even at the highest
exposure levels, risks are uncertain. As for coherence and consistency, it is difficult to
understand how the evidence presented in the Report if critically examined, as opposed to
the selective discussion of the Report, could lead an independent observer to conclude
that, taken together, the epidemiological evidence consistently and coherently pointed to
ETS as a source of lung cancer. Finally, the claim that the criterion of analogous
reasoning supports causality, inasmuch as exposure to ETS is analogous to active smoking,
is rejected by the EPA.
60
What this means is that there are really two central evidentiary
issues on which the Report clearly founders: the issue of the methodology which supports
the evidence, and the issue of the evidence itself. With respect to the methodology, I
have argued that the epidemiology of multifactorial diseases does not permit the claims
about causation that the Report indulges in and that the Report, far from being forthright
about this limitation, ignores it. With respect to the evidence itself, i have argued
that, leaving aside the question of whether epidemiology can provide us with causal
knowledge about ETS, the evidence provided by the Report itself and taken on its own
terms, does not support its conclusions. Using evidence from the four most recent
case-control studies shows two studies with no increased average risk, one study with a
statistically increased risk and one study with an increased risk that is not
statistically significant at the 95% confidence level. Taken together with the fact that
only twelve of the 40 studies presented in table 5.2 reach statistical significance, it is
readily apparent that the evidence does not support the conclusion that the Hill criteria
of coherence and consistency have been met.
The authors of the Report in part anticipate this line of objection
for they note that the 'RR's which are considered relatively small in epidemiology...can
nevertheless be relatively large in demographic terms. Even a 10% excess in risk may
translate into a considerable number of additional cases if the people carrying that risk
are common in the community'.
61 This reply, however,
misses the point. The question about what the RR shows is really a question about what we
can scientifically know, not a question about the quantity of risk across the population.
Epidemiology is simply too crude a tool to allow us to claim that we know something with
an RR of 1.5 is a risk. In pone sense the discussion about the effect on large populations
is disingenuous, for it begs the question of whether there is any risk. The size of the
population is completely irrelevant to the question of whether we have good evidence that
there is a risk at all.
The second sort of problem which plagues the Report and suggests the
label of corrupted science is its level of logical coherence and consistency. the question
her is, what does the Report's evidence suggest be done as a matter of policy? While we
have argued previously that the Report's evidence will not sustain its findings, at this
point we shall assume that the evidence does not support it. We are concerned now not
about the evidence itself, but whether the Report's policy recommendations cohere with
its findings.
The major problem with the Report's recommendations is that they are
strikingly at odds with its evidence. indeed, it is not wrong to say that the evidence and
the policy recommendations seem completely disconnected. At the very best the
epidemiological evidence suggests and RR which is extremely weak, an RR for never-smoking
women living with smokers of 1.31.
62 the evidence at
best suggests a slight risk in domestic settings, yet the policy recommendations relate to
public settings. This means that if any regulation of ETS is justified it would be
justified on evidentiary grounds solely in homes, not in public places. Indeed, the one
piece of evidence adduced by the Report, the LeVois and Layard meta-analysis, suggests a
workplace ETS exposure and lung cancer RR of only 1.01.
63
Moreover, cotinine levels in non-smokers suggests that residential ETS exposure is
probably more important than workplace exposure.
64
As the CRS concludes: 'If, on average, workplace ETS exposure is lower than residential
exposure, than it is likely that relatively few workers would be exposed to sufficient ETS
to be at increased risk for lung cancer'.
65 All of
this contradicts the Report's claim that 'the nature of the hazard... is likely to be
similar in all enclosed settings, '
66 a claim for
which no scientific evidence is offered.
Here then we come in a different way to see how the Report
demonstrates the qualities of corrupted science. While previously the evidence itself was
misrepresented and misjudged under the guise of objectivity, here the 'evidence' is used
to recommend a course of public policy that is completely incoherent. Not only does the
Report provide no evidence that the alleged hazards of ETS are the same in all enclosed
spaces, but the evidence about the hazards of the workplace that it does present suggests
that the hazard is inconsequential. In the end we are left with a policy that leaves
unregulated the area in which the Report's evidence suggests that there may be a hazard
and regulates the area in which the Report's evidence suggests there is no hazard!
It is, of course, not difficult to understand why such incoherent
policy rationale is advocated. the real justifications for the policy recommendations have
nothing to do with the health threats to non-smokers but instead with two other factors:
the 'loss of amenity' which ETS causes to non-smokers and the 'comprehensive strategy to
control active smoking, both in giving a clear message that non-smoking is normal
behaviour and in protecting young people, in particular, from smoking exemplars'.
67 The Report's authors are to be congratulated for being so
forthright in their reasoning, however repugnant such reasoning might be to both good
sense and democratic values. What emerges from these claims is a clear view of the process
of corrupted science at work: that is, the claim that ETS threatens the health of
non-smokers is only a crude attempt to use a harm-to-others argument to conceal an
offensive and unjustified paternalism. It is not that ETS is harmful, rather it is that
smoking is harmful to smokers and seeing smokers is potentially harmful to young persons.
In reality the science of ETS has nothing to do with the policy
recommendations of the Report since these are not derived from even the inconclusive
evidence that is produced. Controlling ETS is really a policy designed to force smokers to
stop smoking and, further, to stigmatise smokers as morally unacceptable role models. It
is a public policy that is morally reprehensible on at least two grounds: one, that it
attempts to intervene, through manipulation of the facts, in the lives of competent
adults; and two, that it characterises those who engage in a legally permitted behaviour
as inappropriate exemplars for young persons. While it is certainly open to the authors of
the Report to hold these views about the 'exemplar qualities' of smokers, it is not open
to them to attempt to make these subjective moral judgements law in the guise of
legitimate public policy.2 - The Consequences of Corrupted
Science for Society and for Democratic Public Policy
In the first section of this paper I argued that there was
substantial evidence that the Report is an instance of corrupted science. In this second
section, I examine the consequences of using corrupted ETS science in order to frame
public policy.
At the outset it is important to note that, apart from the direct
implications from public policy, there is a wider social issue about the Report and its
claims, namely, the moral questions which it raises.
The first sort of question is obviously the question of the
legitimacy of the misrepresentation, for corrupted science is at bottom science that
misrepresents the state of reality. and what a careful analysis of the scientific claims
of the Report reveals is a profound and systematic disregard for the truth about the
possible dangers from ETS. Not only are data manipulated to produce the desired results
and suppressed or dismissed when they do not fit with the standards of political
correctness, but the fact that accepted standards are changed without justification goes
unnoted. In effect, one has an ethic that legitimises misrepresentation in a good cause-'a
smoke-free society'. But is a smoke-free society a sufficient justification for a public
health movement founded on unreliable science and blatant misrepresentation? The
frightening thing about deceit- whether the allegedly righteous cause of eliminating
smoking, or in the service of any number of worthy ends-is both that it is so easy to
justify and so difficult to restrict its use to the ends that originally justified its
employment.
But there is a second moral question here that goes beyond the
morality of misrepresentation into what might be called the morality of suppressing
dissent. Both the process of producing corrupted science and of utilising it as a basis
for public policy demand a fundamental intolerance of dissent, both scientific and
otherwise. The imperatives of health promotion are such that the ambiguities and
uncertainties that form a legitimate part of science-and, most importantly, the question
about the quality of the evidence, and whether it justifies the proposed public policy
measures-cannot be tolerated. This means that scientific and public policy dissent must be
suppressed through portraying dissenters is either in the pay of the tobacco industry or
at the margins of the scientific establishment, a strategy that raises a host of
subsidiary moral questions. Whatever the cost, 'science' must be seen to provide a
conclusive and united answer to the question of tobacco and harms to the innocent. Thus,
despite the vital role of questions, argument and dissent in science as well as in
democratic life, the process of corrupted science seeks to silence dissent in the interest
of protecting, not the truth, but its misrepresentation of the truth.
By far the most morally objectionable aspect of the Report is its
readiness to use corrupted science to deprive smokers not only of their right to pursue
their pleasure in public, but quite possibly to gain or retain their employment, or
advance their prospects. Put more bluntly, it is the question of whether it is morally
justifiable to use bad science to hurt people. What should never be list sight of in this
debate is that without the alleged scientific justification of harm to innocent parties,
there is no compelling rationale for banning or restricting smoking in public places or
workplaces. Once the corrupted science is stripped away, there simply are no harms, and
without those harms, smoking becomes a self-regarding behaviour, interventions on which
can only be advanced on patiently paternalistic grounds. The Report might still argue that
public and workplace smoking should be banned in order to discourage smokers from smoking,
but this argument loses its compelling harm-to-others character and becomes instead
nothing more than an argument about the State intervening on the private lives of
competent adults.
What is so morally offensive here is that truly morally blameless
people-not the alleged victims of smokers, but smokers themselves-are to be harmed in
significant ways on the basis of bogus science and for no good reason. What makes the
morality of the Report as corrupt as its science is that it is prepared to exploit for its
own ends our readiness to deprive individuals of certain rights, if the exercise of those
rights appears to harm others, by explicitly manufacturing harms to others. In doing so,
the Report simultaneously violates perhaps the two most fundamental moral principles,
first by treating persons, in this case smokers and their alleged harms to others, as
merely means to the end of a smoke-free society and not as ends in their own right, and
second by inflicting substantial pain on an entire class of people without their consent
and for no compelling reason.
But the question of the moral justifiability of using corrupted
science to hurt people goes beyond the question of depriving individuals of their right to
a significant pleasure, or even a job, to something far more crucial, namely, the
justifiability of depriving individuals of their moral standing through stigmatising them
as moral outcasts. In the end, this is, of course, the logical outcome of ETS science, to
make smokers a class of moral miscreants who see themselves, and are seen by others, as so
ruthlessly intent on pursuing their own interests that they are blind to the harm they
inflict on others. it is but a short way from the claim that 'Smoking kills' to the
conclusion that 'Smokers kill'. But then such a conclusion is the public policy
justification for bans on public smoking.
Surely there is nothing more morally loathsome than to attempt to
manipulate public policy to create a class of citizens who, on the basis of bad science,
come to despise themselves for what they mistakenly believe they do to others and who in
turn are despised by their fellow citizens for allegedly threatening their well being. The
ultimate moral corruption of the Report lies in its considered use of corrupted science to
erode the normal standards of respect and tolerance for individual difference. It does
this through attempting to use science to fashion a society which believes that smokers
are thoughtless menaces to the health of their fellow citizens, and that by their
thoughtlessness they place themselves on the periphery of, if not outside, the moral
community.
At the end of the day, the Report's foundation of corrupted science
poses a threat that to that most fragile aspect of social capital-trust. to the extent
that its evidence is shown to be contrived or disconnected from its conclusions, it
lessens every thoughtful citizens trust and respect for both science and government. to
the extent that it misrepresents reality through creating a risk, it makes smokers
distrustful on themselves and their actions while at the same time creating a distrust of
smokers by non-smokers.
For all of the moral problems that the use of corrupted science
raises, the equally, if not far more, disturbing issue that it introduces is the
implications of bad science in the public policy process. What then re the consequences of
introducing corrupted science into the democratic public policy process? In a word,
nothing less than disastrous.
The operative word here is, of course, democratic. We are not
concerned with the uses of bad science in an non-democratic society. In fact, with the
appropriate degree of space we might wish to argue that non-democratic societies, or more
specifically totalitarian societies, might be peculiarly receptive to the use of corrupted
science. Our concern here, however, is with the effects of using corrupted science as a
mechanism for framing and justifying democratic public policy. Our claim is that the
effects of using such science are fundamentally at odds with the character of a democratic
society.
The easiest way to understand the threat that corrupted science poses
to democratic public policy and to democratic life as a whole is to understand what it is
that democratic public policies tries to do. The goal of democratic public policy is to
minimise public harms nsofar as this is possible within the context of such foundational
democratic values as diversity, autonomy, respect, rationality, and fairness.
The Value of Diversity
This is the recognition that the persons who make up democratic
society bring a diversity of beliefs and values to the community, a diversity whose rich
complexity is, more often than not, not captured by the social science theories and data
that are the tools of choice in the public policy process. This diversity, moreover, is
not simply reflected in conflicting notions of what direction society should take, but
more basically in differing pictures of what makes a good personal life. By accepting
diversity as a foundational value, the democratic society and democratic public policy
process accepts it not just as a fact but as something to be encouraged, enhanced and
celebrated as a strength.
The Value of Autonomy
This is the recognition that, subject to the acceptance of certain
minimal core values necessary for any society to exist, the individuals who make up
democratic society are the best judges of the shape that they wish their lives to take and
they should be accorded the maximum liberty, compatible with similar liberty for everyone
else, to think, believe, and live as they choose.
This means that the State will resist the impulse, however
well-intentioned, through the misuse of the public policy process, to undermine and
intrude upon its citizens' capacities and inclinations for self-governance, to engineer
the lives of its citizens through collectivising the conscience into one communal vision
of the good life. The Value of Respect
This is the recognition of the equality of the human and moral
standing with the state that the citizens of a democratic society posses. It is the
recognition that the democratic state sees its citizens as persons of intrinsic worth,
equivalent in dignity and standing with itself, with lives not to be managed or saved, but
to be allowed to develop in ways of their own choosing. It is a recognition that the
State's role should be to encourage its citizens to define themselves and their life
projects in widely varying ways, to foster the development of self-respect through
deferring, to the greatest extent possible, from moral judgments about these
self-definitions and life-projects and to create the conditions which allow its citizens'
lives the greatest possible chance of fulfillment.
The Value of Rationality
This is the recognition that the public policy process must be
grounded on democracy's respect for the rational, that is, adherence to the standards of
rationality with respect to the assumptions that it employs, the evidence that it brigs to
bear on that evidence. None of its elements must be based on irrational considerations:
all must meet the minimal test of reasonableness through being clear, coherent and
compelling. The evidence supporting public policy measures must be substantial. The
measures must be coherent and consistent with what the evidence shows and the measures
proposed must have a significant promise of being effective. At the same time the
recognition of the value of rationality is also the recognition that the truth is
frequently complex, something that places its own limits on the scope of rationality.
Reality will often be richer and denser than evidence and theories, some problems will not
have easily identifiable causes and solutions, but this does not justify public policy
formulated in the absence of reason and on the basis of surmises, hunches or appeals to
emotion or intuition.
The Value of Fairness
This is the recognition that democracy entails a foundational
commitment to elicit, examine and consider, within an objective, open and non-arbitrary
framework, the views of all those whose legitimate interests are likely to be affected by
collective decision making. It is the recognition that a democratic society will not
unfairly discriminate through structuring the power process so as to preclude the
statement and examination of certain perspectives.
* * * * * * * * * * * * *
What this suggests is that both the agenda and the legitimate public
policy in a democracy and the process used to argue about that agenda are constrained by
certain non-negotiable values. What marks certain policy options and certain policy
processes out as illegitimate and non-democratic is their conflict with these core
non-negotiable values. What marks certain policy options and certain policy processes out
as illegitimate and non-democratic is their conflict with these core non-negotiable
values.
To take an example, a public policy that significantly undermined the
autonomy routinely accorded to citizens in a democratic society, or one that tended to
eliminate the diversity and tolerance that are marks of democratic life, or a public
policy process that failed to consider fairly divergent points of view, or used poor
argument or flawed evidence to advance policy options would fail to qualify as legitimate
democratic public policy inasmuch as it conflicted with one or more of the key values on
which not only democratic public policy but democratic society is founded.
Placed within this context it is clear that the Report's use of
corrupted science is a threat, not at some peripheral point, but at the very centre, to
democratic values and to democratic public policy. Corrupted science in the creation of
policy threatens each of the process and substance values-diversity, autonomy, respect,
rationality and fairness- that characterize democratic public policy. And this is
something that should be of concern to everyone, whether non-smoker or smoker.
First, the use of bogus ETS science in attempt to determine the
policy agenda on smoking imperils the distinguishing characteristic of science-its
objectivity-and threatens to render science worthless for public policy purposes. Though
science is never completely objective, if indeed complete objectivity is possible, it at
least, in distinction from much of the political process, professes a fundamental interest
in reason, evidence, and bias-free judgment. In fact, much of science's standing in
contemporary society derives from its objective character, as does much of its usefulness
in the public policy process. In effect, we have a high degree of confidence in the
scientific process as providing a careful, evidenced, and (to some degree) value-free,
assessment of certain questions relating to public policy. And it is precisely this
utility that the use of corrupted science threatens. If science ceases to work outside of
the political and policy process, if it ceases to be a tool available to all sides of an
issue, if it becomes politicised and ideologically sensitive, then it ceases to be
valuable in the policy process because it becomes nothing more than another special
pleading rather than the voice of reason.
In this sense, to use corrupted science, for however allegedly worthy
an end, is inevitably to corrupt science itself. No one who genuinely cares about good
public policy, policy crafted on the basis of careful argument, cogent reasoning, and
compelling data, policy that can stand the test of careful probing and consistent dissent,
will countenance the corruption of science. But the use of bogus science to attempt to
manipulate the public policy debate on smoking threatens not just science, but also the
standards of rationality that distinguish legitimate public policy. Adherence to the norms
of rationality requires that the identification of problems, causes and solutions be based
on empirical evidence of most rigorous sort, evidence that is specific, strong, consistent
and coherent, and on rational arguments that are clear and logically compelling. Problems
and solutions that cannot meet this standard of argument are not allowed a place in the
public policy process. To do so is to abandon commitment to reason as foundational
democratic value. Yet the use of corrupted ETS science as a basis for public policy is
nothing less than an abandonment of rationality as a measure of legitimate public policy.
As we noted above, the Report's ETS 'science' cannot meet any of the tests of rationality
that determine legitimate public policy problems and solutions.
The ETS 'evidence' is not
specific, strong, consistent, or coherent, and if it fails these tests, it cannot provide
compelling rational reasons- as opposed to rhetorical and emotional reasons- for its
public policy recommendations. The use of corrupted ETS science is, however, more than
simply an abandonment of reason in the public policy process, it is also something far
more frightening: the attempt to institutionalize a particular irrational view of the
world as the only legitimate perspective; to replace rationality with dogma as the
legitimate basis of public policy. If the use of corrupted ETS science by the Report
represented simply the abandonment of reason, then their actions would be simply
non-rational. But the Report's efforts go beyond the non-rational to the irrational, to an
assault on reason itself. By refusing to include evidence of scientific dissent from the
officially determined 'truth' about ETS, as evidenced in the omission from key
bibliographies of any references to criticisms of key findings and studies, by
manipulating and misreporting data, the Report's authors tend to appear as enemies of the
open and self-correcting process of reason. In a very real sense, the 'truth' about ETS
ceases to be open to rational assessment and assumes instead the status of revealed dogma.
An d only those who ultimately fear, if not loathe, reason are comfortable with dogma as
the basis of public policy.
There is, however, a third peril that the use of corrupted ETS
science poses to democratic public policy, and that is through its treatment of the
question of risk. The question of risk is central to any modern discussion of harm and
public policy. If everything depends on science, then everything depends on the science of
risk assessment. And this places a special moral burden on those who use the notion of
risk and risk assessment in public policy debates to be certain that the concept isa used
with integrity and not simply as a lever to frighten. In one sense the misuse of the
notion of risk is simply another instance of a fundamental contempt for reason in public
life because it is an attempt to gain, through irrational means, something that careful
argument denies one.
To use the notion of risk with integrity in public policy discussions
would minimally involve:
- 1) stating risk assessment in a way that does not exaggerate harms
and allows for individuals to make their own decisions about balancing the risks and
rewards of various courses of action;
- 2) placing particular risk assessments within a general risk context
in a way that allows one to answer the question of how significant is this risk compared
with other risks associated with everyday living (the question thus becomes not simply 'is
this activity risky', but, 'does it carry a risk level that in other circumstances we
would consider worrisome?'; and
- 3) conveying the full sense of both the inexactness of risk
assessment and the complexity of risk assessment-even in the face of the popular
preference for simplicity.
(As C.P. Snow observed about complexity and ambiguity: 'Even at
the highest level of decision, men do not really relish the complexity of brute reality
and they will hare after a simple concept whenever one shows its head.')
Given the imperatives of the Lalonde Doctrine and the general
aversion of the anti-smoking movement to the individual autonomy, it is obvious that these
standards of responsible risk discussion will be ignored in the ETS debate. Indeed, given
the flimsy nature of the ETS 'science', the last thing that the Report wishes to have is a
careful public policy discussion of the real risks that ETS exposure poses. Everything
hinges on the public thinking that, for example, the non-smoking wives of smoking men have
a 30 per cent increase in their risk of getting lung cancer without stopping to think what
this figure, even if it were true, might mean. As Peter Finch explains, what the figure
means is something quite different, once the risk involved is explained and
contextualized, from what the individuals using the figure want the public to think that
it means:'The annual death rate from lung
cancer among non-smoking wives of non-smoking men is of the order of six per 100,000.
Among non-smoking wives of smoking men the corresponding figure is eight per 100,000. Thus
two in every 99,994 non-smoking wives of smoking husbands die of lung cancer that, it is
claimed, should be attributed to the effects of passive smoking. This is an exposure risk
of almost one in 50,000 about the chance of tossing 16 heads in a row. to put such a small
exposure risk into perspective, note that, in Australia, the death rate from injuries and
poisonings for males aged 15-24 years, at 101 per 100,000 is about 50 times as great...by
emphasising a 30 per cent increase in lung cancer due to passive smoking, health activists
have lead people to think that this is a high risk situation when that is not the case.'
68
Simple statements of risk, even assuming that the risk assessment
itself is reliable, can be significantly misleading. Suppose, for instance, that I wish to
promote the use of a certain heart drug. As a result, I claim that the drug reduces the
death rate among patients from 4 out of every 100 patients, to 3 out of every 100,
something that means the drug has a risk factor of 30 per cent. What I fail to tell you is
that the absolute risk difference is only one percentage point and that I would have to
treat 100 patients to save just one extra life. Although there is some truth to my
original claim of a 25 per cent reduction, my reliance on this figure alone and my failure
to place this reduction in context actually significantly distorts reality.
In effect, the Report's use of corrupted ETS science corrupts the
entire discussion of risk in public policy through failing to not e the inexactness of the
assessment,, through failing to contextualise the risk and compare it with other accepted
forms of risk in everyday life, and through failing to acknowledge the complexity of the
entire issue.
The fourth peril that the use of corrupted ETS science presents for
democratic public policy is that it undermines the value of fairness that is so central to
democratic life. Fairness is undermined in at least two crucial senses. First, the debate
about the nature of the evidence, its complexity and its contentiousness is never fairly
acknowledged. The existence of significant dissent is rarely admitted and truth is made to
appear simple, easy and unambiguously pointing in one policy direction, when in reality,
as we have observed above, none of this is the case. Second, the fundamental requirements
of fairness-the commitment to elicit, examine and consider, within an objective, open and
non arbitrary framework all views, without using the power of authority to suppress and
exclude-these requirements are flouted both in letter and in spirit by the corrupted ETS
science's substance and process. Indeed, perhaps the defining character of corrupted ETS
science is its fundamental non-objectivity, its process unfairness.
The fifth peril that corrupted ETS science presents for democratic
public policy is the existence of an official, State-sanctioned scientific ideology that
is used to morally stigmatise, morally degrade, morally exclude certain citizens from the
civil community. For that is the ultimate public policy purpose of ETS 'science', to
provide a compelling public policy justification for making out certain behaviour as
morally unacceptable. The quite horrible consequences of state sanctioned science that
prescribed certain acceptable ways of living and thinking and which singled out certain
individuals as moral reprobates in our own century should provide warning enough against
the dangers of giving public policy legitimacy to a 'scientific' dogma that morally
degrades and excludes.
Finally, and perhaps most significantly, the use of corrupted ETS
science in the public policy process threatens the central democratic values of autonomy,
respect and diversity. The key to these values is the belief that individuals are equal in
moral standing with the state, that they are the best judges of the shape of their own
lives and should be encouraged to develop genuine diversity, and finally that they are
also capable of understanding and participating in the life of the community, including
choosing those who are to exercise authority. But inasmuch as ETS science is based on a
selective and ultimately untrue reading of reality, and given that it is fundamentally
designed to manipulate both individuals and the policy process into believing and doing
certain things, it is impossible for such science to value autonomy, respect or diversity.
The very nature of corrupted science is such as to deny that individuals can, or at least
can be trusted to, make important and informed decisions about themselves, and most
especially about their health. The agenda of corrupted science is at its core based on the
paternalistic assumption that only a few can think and act correctly, that only a few know
the 'truth', a truth that must be carefully nuanced for the many, that only a few must
ultimately chart one moral or healthy or rational way to live , a way that the State will
in turn enforce. In the end, perhaps paradoxically, corrupted ETS science goes wrong at
the very start, for when it decides that the interests of health promotion and the
interests of a smoke-free society take precedence over the truth, it sets itself on a
course of manipulation, fabrication and misrepresentation that cannot but collide with the
values of autonomy, diversity and respect.
In the final analysis, it is difficult to find anything substantial
in the Report which would tend to mitigate the conclusion that it is an instance of flawed
science and flawed public policy produced by authors who fail to appreciate the difference
between the objectivity of scientific analysis and advice, and the rhetoric and
partisanship of advocacy. Consequently its only usefulness in the public policy process is
as an example of how not to produce legitimate, democratic public policy. |
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