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Human and Ecological Risk Assessment: An
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Is the Ecological Fallacy a Fallacy?
Fritz A. Seiler & Joseph L. Alvarez
Published online: 03 Jun 2010.
To cite this article: Fritz A. Seiler & Joseph L. Alvarez (2000) Is the Ecological Fallacy a Fallacy?, Human and Ecological Risk
Assessment: An International Journal, 6:6, 921-941, DOI: 10.1080/10807030091124365
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Human and Ecological Risk Assessment: Vol. 6, No. 6, pp. 921-941(2000)
1080-7039/00/$.50
2000 by ASP
Is the Ecological Fallacy a Fallacy?
Fritz A. Seiler
1
and Joseph L. Alvarez
2
ABSTRACT
Ecological studies of health effects due to agent exposure are generally consid-
ered to be a blunt instrument of scientific investigation, unfit to determine the
true exposure-effect relationship for an agent. Based on this widely accepted
tenet, ecological studies of the correlation between the local air concentration of
radon and the local lung cancer mortality as measured by Cohen have been criti-
cized as being subject to the Ecological Fallacy and thus producing invalid risk
data. Here we discuss the data that a risk assessment needs as a minimum require-
ment for making a valid risk estimate. The examination of these data and a thought
experiment show that it is Cohens raw ecological data, uncorrected for population
characteristic factors, which are the proper data for a risk assessment. Consequently,
the true exposure-effect relationship is less and less important the more popula-
tion characteristic factors are identified and the larger they are. This reversal of the
usual argument is due to our approach: Here, the prediction of the health effects
in an exposed population is of primary importance, not the shape of the true
exposure-effect relationship. The results derived in this paper hold for ecological
studies of any agent causing any health or other effect.
Key Words: radon, lung cancer, risk assessment, epidemiological studies, ecological fallacy.
INTRODUCTION
In 1995, Cohen published his data on the negative correlation between the
average local air concentrations of radon and the average local lung cancer mortal-
ity rates in U.S. counties (Cohen, 1995; and references therein). Ever since then, his
data have been attacked as being distorted by confounding factors and thus being
subject to the Ecological Fallacy. Following the majority of epidemiologists, many
health physicists and risk assessors seem to agree that ecological studies are not
representative of the true dependence of the lung cancer mortality on the concen-
trations of radon. Consequently, Cohens data have been dismissed from use in risk
1
Sigma Five Consulting, P.O. Box 1709, Los Lunas, NM, 87031-1709, USA. Tel: 505-866-5193;
Fax: 505-866-5197; e-mail: faseiler@nmia.com, to whom all correspondence should be sent
2
Auxier & Associates, 9821 Cogdill Rd., Suite 1, Knoxville, TN, 37932, USA. Tel: 865-675-
3669; Fax: 865-675-3677; e-mail: jalvarez@auxier.com
Submitted Mar. 3, 1999; revised manuscript accepted Sept. 18, 2000
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922 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
assessments; and in countless presentations and papers, these well-measured and
precise data have been ignored.
Recent examples are the report of the BEIR VI committee (NRC, 1999) and two
papers in the journal Health Physics with accompanying discussions (Lubin, 1998 a,b;
Smith et al., 1998; Field et al., 1998; Cohen, 1998 a,b). The reason their authors give
is that an ecological study does not constitute a proper database for the true
exposure-effect function and does not allow the determination of an individual risk.
A matched cohort study is deemed to be the only way to get reliable data for the
determination of the undistorted and thus true exposure-effect function.
It is remarkable that Cohens measurements themselves are not in dispute, only
their use in risk assessment. In fact, these data are the only copious source of
information on the actual incidence of lung cancer fatalities correlated with the air
concentrations of radon. They cover almost the entire population in the contiguous
United States; and in this context we shall call it the test population. These data points
have quite small random errors and show a consistently negative trend with increas-
ing exposure. The important question now is the meaning of these data for risk
assessment.
Another set of available data consists of the same correlation determined for
uranium miners. They were exposed underground to much higher radon levels,
and their exposures were not determined at the time, but much later. These miner
data, with their large errors and doubtful exposures, have been used consistently in
risk evaluations for radon exposures.
It is the purpose of this paper to carefully investigate this situation and to
determine the minimum information needed to make a valid prediction of the risks
for a population exposed to radon and its progeny. In our approach we shall rely
heavily on the Scientific Method, and therefore will give a short discussion of it,
particularly with regard to its application to the problem of the Ecological Fallacy.
It will also be shown that these arguments hold for ecological studies of exposures
to any kind of radioactive or chemical agent, resulting in any kind of a health effect.
THE SCIENTIFIC METHOD AND EXPERIMENTAL RADON DATA
It is not straightforward to summarize our knowledge on the health effects of
inhaling radon and its progeny, because the BEIR IV and BEIR VI Committees have
ignored the Cohen data set. This act is fraught with problems, as we shall discuss in
this section (NRC, 1988, 1999). Also, a strong pro-linear bias is evident in many
publications, represented by the question: Are our data compatible with the linear
model? or by the statement A linear model only was fitted to the data. We will
proceed here by using the Scientific Method (Popper, 1968; Kuhn, 1970; Bunge,
1979; Lett, 1990; Seiler and Alvarez, 1994a). This approach allows us to evaluate the
data without prejudice by asking: What can we learn from the data?
The Scientific Method
The Scientific Method was first formulated by Ren Descartes in 1637 (Descartes,
1968) and lies at the root of the tremendous progress made in science and technol-
ogy since then. It has been adapted to remain current with the development of
mathematics and its application to science, but its essence has remained the same:
200315.pgs 12/12/00, 5:28 PM 922
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 923
Risk Assessment and the Ecological Fallacy
We use experimental observations to formulate a hypothesis, a theory, or a model,
and then subject these ideas to the test with new experimental observations. If the
new data consistently confirm the predictions, we declare a new paradigm and then
look for ways to test it until we discover something new again and have to modify the
model or its theory. If the data consistently contradict the prediction, we have to
drop the paradigm or modify it. This process of changing the paradigm has been
widely discussed in the literature (for instance, Popper, 1968; Kuhn, 1970; Bunge,
1979). The results vary in their approaches, interpretations, and conclusions, but
they all agree on one point: Experimental data are used to either confirm or reject the
predictions of models and theories.
It has been shown that, in order to make this method feasible, the experimental
tests have to be preceded by a modeling effort fulfilling of a number of precondi-
tions (Bunge, 1979; Lett, 1990; Seiler and Alvarez, 1994a). These conditions are
components of what is usually called Doing Good Science. Lett (1990) has put
together a set of five preconditions and one test condition that summarize recent
approaches to this problem. In short, they are:
1. Sufficiency of Observations: Sufficient data have to be available and serve as the
basis to formulate a new hypothesis or model. A lack of sufficient data is often
overcome by making an additional hypothesis but that can lead to wrong
conclusions if the model consists of more assumptions than data. A classical
example of initially insufficient data is the orbit calculation for the Near Earth
Asteroid 1997XF
11
made two years ago, based on a number of data points
closely spaced in time right after the discovery. This led to the prediction of
a close encounter or even a possible collision with earth early in the 21
st
century (Scotti, 1998). The discovery of the same asteroid on some stellar
plates taken eight years before then led to a combined data set which covered
a much larger time interval. It improved the precision of the orbit calculation,
and the probability of a close encounter was found to be smaller but still not
negligible. It finally disappeared for all practical purposes after a more careful
consideration of the uncertainties by three groups of researchers with the
same result.
2. Replicability of Observations: The same and other scientists must be able to
reproduce the original experimental data. Irreproducible results are often the
cause of false models and predictions. As an example, the original Cold
Fusion data could not be reproduced by the authors or any other scientists
(Taubes, 1993), and interest in the effect died away.
3. Comprehensiveness of Data Evaluation: All data in the modeling range must be
compared to the model, not only those which agree with it. Ignoring any set
of experimental data is a highly restrictive act that demands a high level of
justification. We shall see in the following discussions whether dismissing the
Cohen data set from use in radon risk assessment can really be justified.
Another example of ignoring this requirement with severe consequences is
the way Soviet scientist Trofim Lysenko suppressed all data that could and
would have contradicted his Lamarckian theory on the inheritance of ac-
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924 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
quired characteristics by grain. His selectivity led to catastrophic consequences
for Soviet agriculture and its grain harvests for many decades (Friedlander,
1995).
4. Logical Consistency of Model Approach: The set of assumptions and properties of
a theory or model must be free of internal inconsistencies. An example of
failing this requirement are the linear and nonlinear models used in the BEIR
III and BEIR V reports on radiation carcinogenesis in man (NRC, 1980, 1990).
There, the use of event doses instead of total accumulated doses for the
survivors of the nuclear attacks on Japan, leads to logical inconsistencies.
Whereas event doses can be used for the linear model, their use in any
nonlinear model is a mistake. For those models, total accumulated doses must
be used (Seiler and Alvarez, 1994b). This mistake removes the logical founda-
tion for all statements about nonlinear models in both BEIR reports.
5. Scientific Honesty: This is a difficult requirement. We all know that scientists
tend to be faithful to their brainchildren, sometimes beyond all reasonable
doubt (Popper, 1968; Kuhn, 1970). A scientist should admit when his model
has failed and should go on from there. An example is the famous written
wager between Stephen Hawking and Kip Thorne on whether the X-ray source
Cygnus-X1 contains a black hole at its center (Thorne, 1994). When the
experimental evidence became overwhelming, Hawking conceded in good
humor and in writing that Cygnus-X1 does indeed contain a black hole.
Unfortunately, there is another aspect of scientific honesty that has to be
mentioned here. It concerns the integrity of the data presented or evaluated
by a researcher. Recently, we have all become aware of yet another case of
alleged scientific fraud by an investigator (Medical Tribune News Service,
1999). Similar to Lysenko, this investigator is accused of having discarded 93%
of the data in one case because they did not agree with his hypothesis. In this
context, honesty or the lack of it is an integral part of a scientists reputation.
6. Verification of Model: After these five preconditions are met, verification is the
essence of the Scientific Method: Success or failure in predicting the outcome
of an experiment. If the five pre-conditions are not met, however, the outcome
of such an experiment means little, if anything. It must also be noted that all
physical measurements are subject to uncertainties stemming from various
sources. Uncertainties can be classified into two categories: random and sys-
tematic errors.
*
Therefore, success or failure of a model prediction can only
be established statistically within the experimental errors for a given confi-
dence level. Therefore, one experiment alone leads often only to an increase
or decrease of confidence in the model. What is usually required for a com-
*
The term uncertainty is used here as a general expression, covering both random and
systematic errors. This definition runs counter some recent usage in risk assessment, but
it has now been adopted as U.S. National (ANSI) and international (ISO) standard
terminology (Taylor and Kuyatt, 1993, 1994; Seiler and Alvarez, 1998b).
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 925
Risk Assessment and the Ecological Fallacy
plete loss of confidence in the model and an eventual change of paradigm is
a set of results of the same experiment and, even better, failures in one or
more other types of experiment.
This time-proven framework is the basis on which we will judge the data and the
theories for the correlation between the radon concentrations and lung cancer
mortality in U.S. counties.
Information Derived from the Radon Data Available
In the controversy regarding the applicability of Cohens data to risk assessment,
six aspects stand out as important cornerstones for our discussion:
1. Cohens data are derived from a large, statistically robust study. They are so
detailed in radon concentrations that they form a smooth curve of data points,
well within the quite small experimental uncertainties, and without
discontinuities or outliers. All other data (Lubin and Boice, 1997; Lubin,
1998b) are not of comparable quantity and quality, as they are taken at only
a few broadly averaged exposure levels, and have random and systematic
standard errors which are dramatically larger than those of Cohens data
The plot in Figure 1 shows all of the other data together with Cohens
measurements which are given as the diamond symbols with the small errors
between radon concentrations of 20 to 230 Bq m
- 3
. They range from a relative
risk of 1.2 down to about 0.8 near 200 Bq m
- 3
and are clearly nonlinear. It is
also obvious that, within their standard errors, there is no disagreement
between Cohens data and all others, taking into account that standard errors
include a total probability of 68%. The dashed straight line is the linear model
of the BEIR VI Committee, essentially based on an extrapolation of the
uranium miner data at higher exposures. Here, there is a dramatic disagree-
ment of up to twenty standard errors between the BEIR VI Model predictions
and Cohens data (Cohen, 1995, 1998a,b, 1999).
2. Cohen has given a comprehensive evaluation of all potential confounding
factors (Cohen, 1995) to counter various allegations involving confounding
factors. Yet, up to now, his detailed discussions have not been given the
attention they deserve, although the authors of two papers have attempted to
do so (Lubin, 1998a; Smith et al., 1998).
3. In these papers, Lubin and Smith et al. try to show that correlated smoking
corrections of an unspecified magnitude would be needed to make Cohens
data acceptable (Lubin, 1998 a,b; Smith et al., 1998; Field et al., 1998). Cohens
comments on these papers, however, show that these correlations would have
to have implausible magnitudes to bring about differences of twenty standard
errors and more (Cohen, 1998 a,b).
Here we shall approach this problem from a completely different point of
view and make a simple argument in the framework of the Scientific Method.
Non-numerical arguments that show what effects could possibly occur and
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926 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 927
Risk Assessment and the Ecological Fallacy
might somehow lead to a modification of the exposure dependence are not
acceptable as valid evidence (Bunge, 1979; Lett, 1990; Seiler and Alvarez,
1994a). Even worse, this approach is the exact opposite of the basic intent of
the scientific method that is based on the numerical verification of theoretical
or modeling predictions by measurements. The arguments of the proponents
of the linear no-threshold theory criticize Cohens data for not agreeing with
the predictions of their model. They are thus putting the cart before the horse,
and that is scientifically indefensible. It is their job to calculate their predic-
tions in such a manner that they can be compared directly with the experimen-
tal data.
4. Up to the present, nobody has successfully questioned the validity and integ-
rity of Cohens measurements, only their applicability to a risk assessment has
been denied. What is required for a refutation of experimental data is a set of
bona fide contradictory data of roughly equal or better quality. Thus, the only
way to obtain such data is by making new measurements in the same region of
exposures that would contradict Cohens data. No such measurements are
available.
5. Logic dictates that Cohens data set should be used as the null hypothesis when
measurements are made to confirm or contradict it. It is a common but
deplorable practice to exercise all kinds of options when selecting a null
hypothesis. The null hypothesis is at a strong advantage when statistical deci-
sions are made. Instead of even odds of 50:50, the odds are 1:10 and 1:20 in
favor of the null hypothesis for confidence levels of 90% and 95%, respectively.
This is a strong bias in favor of the null hypothesis, and a risk management
decision can be influenced merely by the selection of a favorable null hypoth-
esis.
The Scientific Method offers guidance for such tests in clear and unambigu-
ous terms: We start with our best knowledge and thus with the current para-
digm as the null hypothesis. After all, the model works to a certain extent,
otherwise it would not be the current paradigm. Now we check for deviations
from the paradigm, and it is here that we require rather high standards of the
contradictory data, such as 90% or 95% confidence levels. Only then do we
accept these data as evidence to the contrary and, upon sufficient confirma-
tion, abandon or modify the paradigm.
Thus it becomes clear that the Scientific Method is the only justification for
the use of such highly biased procedures as making decisions based on 90%
or 95% confidence levels. Unfortunately, standard statistics texts do not stress
sufficiently the fact that a cogent reason must be given to justify the selection
of the null hypothesis with its strong biases inherent in high confidence limits.
6. Both Cohens data set and the uranium miner data have serious dosimetry
problems that focus mainly on the time average of the radon concentrations
in air:
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928 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
a. Both sets of data are based on measured exposure concentrations of radon,
which are given in Bq m
-3
or rely on the corresponding total exposures in
Bq s m
-3
, although exposures are often still given in working level months
(WLM). What is actually measured is the concentration of radon in the air.
This concentration is equivalent to an infinite set of different mixtures of
radon and its progeny outside the detector. Also, for the health effects due
to radon and progeny, it is not the radon that matters but its alpha-emitting
progeny, and their concentrations are not measured. The relations be-
tween the measured radon concentrations and the mixture of radon and its
progeny outside the detector are thus multi-valued and undefined. In this
paper, as in most other work, we will discuss the lung cancer mortality in
terms of time-averaged exposures to ambient radon concentrations that are
the only measured quantities. Here, the assumption is made implicitly that
the average isotope mixture is the same everywhere, and that the
time-averaged radon concentrations are a reasonable measure of the
exposures relevant to lung cancer.
b. The miner data involve exposures given in units of WLMs, inferred from
measurements of the exposure concentrations in mines that were made
much later. These data were then used to calculate the concentration
time product of accumulated occupational exposures over years or
decades. Also, for the fit of the linear model to the data, Model I regressions
are used, as if the exposure values had no uncertainties (Sokal and Rohlf,
1981). As we have just shown, they have considerable errors, and it is easy
to demonstrate that, because exposures are difference measurements, their
relative errors are bound to increase as the exposures decrease (Alvarez
and Seiler, 1996; Seiler and Alvarez, 1998a). Clearly, Model II regressions
are required here which treat both mortality rates and exposures as the
stochastic quantities they are (Sokal and Rohlf, 1981; Seiler and
Alvarez, 1994b). When Model I regressions are used despite these facts,
considerable systematic errors may be incurred.
c. For Cohens data, exposures to radon were measured, primarily in the
living areas of residential dwellings. By assuming a more or less constant
average rate of exposure up to the age of the receptors, an average
population exposure could be estimated for every exposure interval. This
argument needs the additional assumption that there is a common set of
factors between the average exposure concentrations in the houses and the
actual time-integrated exposure concentrations of the receptors. These
assumptions could lead to considerable uncertainties

in the values for
effective exposures. However, these conversion factors and their
uncertainties are irrelevant, at least in first order, as long as subsequent
prediction calculations are made using the same experimental method and
the same assumptions to determine the exposure data.
For the case considered in this paper, we will show that the Exposure
Conversion Factors (ECF) involved in the conversion from the radon
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 929
Risk Assessment and the Ecological Fallacy
measurements to exposures or doses and their errors cancel. No such
cancellation of conversion factors and their uncertainties is possible for the
extrapolations of the uranium miner data way down to the low exposures
of the general population. The exposures of miners and of the general
population involve different assumptions and conversion factors that do
not cancel.
This discussion shows that there are significant differences between the informa-
tion derived from the miner data and those from Cohens measurements. It is
important to see that there is no a priori need for a cause-effect model in applying
Cohens data. The data can be used either directly from a data table, or it can be
used indirectly by calculating an interpolating polynomial for convenience. A visual
inspection of Figure 1 shows that a good fit is possible. The miner data, on the other
hand, require the use of a model to extrapolate their information down to much
lower levels of exposure, a much more complex procedure.
As we shall show in the following, only the first, fourth and fifth of these six
arguments are relevant to the problem of predicting health effects. The second,
third and sixth arguments, regardless of their merits, will be shown to have no
bearing on the use of Cohens data for the assessment of risks due to exposures of
humans to radon and its progeny.
MINIMUM REQUIREMENTS FOR A POPULATION RISK ASSESSMENT
Here, we will determine the minimum information required for a prediction of
the number of health effects in an exposed population. To this purpose, we will first
state what a risk assessment does, and what kind of information it needs. Thus, we
seek the most direct connection between exposure and effects data, and will use
time-averaged radon concentrations as measures of exposure. As a next step, we will
then conduct a thought experiment (Gedankenexperiment) in order to clarify
some of the issues mentioned above. Thought experiments are a valuable theoreti-
cal tool, based on a careful step by step evaluation of an experimental procedure
without numbers. Thus it is essentially a dry run of the whole evaluation, carried out
to isolate salient facts.
Minimum Information for a Risk Assessment
The purpose of a risk assessment for the exposure of humans to radon and its
progeny is to estimate the number and type of health effects in a population whose
exposure to radon is known or has been projected. We will call this population the
prediction population. The minimum of information that this risk assessment requires
is thus an effective cause-effect relationship for the prediction population which will
convert the known set of radon exposures of that population directly into a set of
health effects in that population. This is all that is needed, no more.
This minimum requirement has another consequence: The initial goal of the
modeling effort is to predict the number and kinds of health effects in the test
population. The Scientific Method requires a comparison of the experimental data
to the corresponding predictions made by the model. This then leads to a judgment
about the power of the model to predict effects. This is the way that science operates
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930 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
and not the other way around. The ball is thus clearly in the court of the modelers,
and they have to show a successful modeling of the measured risk data for the test
population.
An additional requirement is that both cause-effect relationship and pre-
dicted health effects must be applicable to the prediction population. Note that
all other sets of derived exposure information for the test population, such as
radiation doses to the lung epithelium and so on, may be scientifically interest-
ing and quite useful, but they are not needed to make a valid risk prediction. A
dose-effect relationship for the risk assessment is determined only when it is
convenient and meaningful to do so. Then, the error calculations have to be
done carefully to avoid inserting some errors twice, once when calculating the
cause-effect relationship and again when applying it for a prediction. It is
extremely important to keep these basic facts in mind during the following
discussion.
Preliminary Remarks for the Thought Experiment
From reactions to an earlier version of this paper by some of our friends, and
from the comments of the reviewers of this journal, we have learned that it may be
quite difficult for some readers to let go of some ingrained concepts and well
known facts. In addition, any theoretical thought experiment, such as the one used
here, needs a lot of care in reading and interpretation. However, this is precisely
what we must ask the reader to do.
Also, not being epidemiologists but risk assessors, we will approach these prob-
lems using scientific but not necessarily epidemiological terminology and patterns
of thinking. As an example, ecological studies are not treated as a mere screening
tool, preparatory to a real analysis. These studies furnish data just like any other
data source. We will address the properties of these data, confounding factors and
all, later in this section.
In addition, the idea that the sole purpose of ecological data, and indeed of all
epidemiological data, should be to find the true cause-effect relationship for the
agent, is in our opinion short-sighted and only partly correct. The purpose of any
epidemiological study should be to help make risk predictions for future exposures
of people. A cause-effect relationship is merely a tool often used by risk assessors, but
it is of purely academic interest if it is not needed. We will also show here, that in
this case we do not need this tool at all, not as long as we have good and plentiful
data.
Some readers may have problems with some of the basic and often implicit
assumptions made in risk assessment. Essentially, data from past experience are
used to project risks into the near or far future. Obviously, this cannot be done
without making some assumptions about the transfer of this knowledge from the
past to the future. We will aggregate all needed assumptions into one, an
assumption which is made implicitly or explicitly in every science-based risk
assessment, and that we shall call the Assumption of Equivalent Populations. We will
show that the details of this assumption should not be questioned without really
good numerical evidence, because without this assumption, no risk assessment is
possible.
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 931
Risk Assessment and the Ecological Fallacy
Assumptions for the Thought Experiment
For the thought experiment, we will now make and for the sake of this thought
experiment only four assumptions that cover the situation of health effects due
to radon exposure as it is proposed implicitly by the proponents of the linear theory:
1. The linear model is correct at low exposures and represents the true expo-
sure-effect relationship;
2. The measurements by Cohen accurately report the observable dependence of
the local lung cancer mortality on the local air concentrations of radon in the
populations of U.S. counties;
3. The underlying linear exposure-effect relationship is modified by some factors
characteristic for the test population to such an extent that the result is the
exposure-dependence found in Cohens data; and, finally,
4. The influence of each one of these population characteristic factors is known
exactly.
The implications of the first and the last assumptions for our thought experiment
are obvious, but the second and third need some comment. The second assumption
covers the actually observed health effects in the exposed test population and,
because nobody has been able to invalidate Cohens primary data, these measure-
ments are used here.
The first and second assumptions are of course contradictory, and the third
assumption is needed in order to reconcile them. Actually, the third assumption is
the claim made by the proponents of the linear model in order to save their model.
It states that the total of the confounding factors leads from the true model to the
modified data measured.
To test the logic of this claim, we introduce two factors for every radon
concentration. The first is the Exposure Conversion Factor, ECF, as the usual
straightforward factor converting the radon concentrations C
r
to concentra-
tion time products or some other measures of exposure or dose; and the
second is a new factor which we will call the Factor of Population Characteristics,
FPC (C
r
). It comprises all the population-derived confounding factors, includ-
ing any population influence on the conversion factors such as average resi-
dence time and so on. This FPC (C
r
) leads, as required, from the true cause-
effect relationship to the data found by Cohen. Note that the FPC (C
r
) contains
in particular the entire correlation between smoking and the radon level. Even
more important, it contains the influence of all confounding factors, both
known and unknown, which are introduced by the characteristics of the test
population. In the absence of confounding factors, the FPC (C
r
) is equal to
unity. In the presence of confounding factors, the FPC (C
r
) is representative
of the collective numerical influence of all the confounding factors contribut-
ing to the Ecological Fallacy and more. Therefore, the FPC (C
r
) factor
includes the numerical influence of all the objections to Cohens data voiced
by the proponents of the linear model.
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932 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
It must be stated here that there is, of course, the far more likely explanation that
the discrepancy between the first and second assumptions represents a classical case
of measurements contradicting theoretical or calculated model values. In this case,
the latter are obtained by the questionable extrapolation of a straight line fitted to
uncertain risk values at higher exposures, using a maximum likelihood fitting
procedure that does not take into account the uncertainties of the exposures.
Therefore, Cohens data of the second assumption of our thought experiment
successfully contradict the BEIR VI model values of the first assumption. An excep-
tion would be possible only if the proponents of the linear theory were to show
conclusively that their FPC (C
r
) quantities lead to risks that are numerically compat-
ible with Cohens data (Cohen, 1995). However, it is equally important to realize
that the scientific method puts the responsibility for making a correct prediction of
the data squarely in the lap of the modelers and not in the lap of the experimenters.
However, for the sake of this thought experiment, we will proceed and maintain
that all four assumptions made above are valid.
Results of the Thought Experiment
Now we consider the logical situation created by the four assumptions. The
nationwide measurements of the average local lung cancer mortality and the aver-
age local radon concentrations result in the exposure-mortality correlation m
t e s t
(C
r
) for a radon concentration C
r
in the test population as found by Cohen. In a first
step, we now correct these nonlinear mortality data for the influence of all known
and unknown confounding factors of the test population by multiplying with the
inverse of the population characteristics factor FPC
t e s t
( C
r
) and of the conversion
factor ECF, and, by our assumptions, the result is the underlying true linear
exposure-effect relationship R
t e s t
( C
r
) for the test population,
(1)
It should be noted here that there is really nothing that requires R
t e s t
(C
r
) to be
linear, so that this equation holds for any algebraic form of the true exposure-
effect relationship.
In a second step, we will now assume that it becomes necessary to make a
prediction for the change in lung cancer mortality for an exposed prediction
population, such as the population of an area in and around Denver, CO. The
assumed reason is that this population is suddenly subjected to three times the
normal radon concentration, C
r
= 3 C
r
, a situation which is likely to continue far into
the future. In order to make a prediction for the long-term change in the number
of lung cancer fatalities expected, we now use the true linear model for the
prediction population and apply the population characteristics factor FPC
p r e d
(C
r
)
and the conversion factor ECF, but this time as direct factors. In this manner, we
obtain the appropriately modified expectation values of the lung cancer risk, and
the appropriate cause-effect relationship for the prediction population is,
R C m C
FPC C ECF
test r test r
test r
( ) = ( )
( )

1
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Risk Assessment and the Ecological Fallacy
(2)
It is thus obvious that the two ECFs cancel as previously predicted in item 6.c. of this
paper and that the result therefore is independent of the exposure quantity used
and its uncertainty.
The Assumption of Equivalent Populations
What is usually done implicitly, and what we will here do explicitly, is the transfer
of the information on the test population to the prediction population, a process
sometimes called, a bit imprecisely, the generalization of the data. To this purpose
we make an assumption that is always made, but usually just by implication: the
Assumption of Equivalent Populations. It states that the test population is representative
for the prediction population in all aspects important to the adverse effect. Without
this assumption, no risk predictions can be made for the prediction population.
This assumption is nothing new. In fact, implicitly or explicitly, it has been made
in every science-based numerical risk assessment ever made. The risk of the expo-
sure to any agent that causes an effect is derived from the number of those effects
in an exposed test population and results in an exposure-effect function for that
population. If that function is then to be used to calculate the number of expected
health effects in a prediction population, the assumption is needed that these two
populations react to the agent in exactly the same way. Thus, if we want to use the
data obtained from the test population for a risk projection in the prediction
population the FPCs for the two populations have to be identical,
FPC
pred
(C
r
) = FPC
test
(C
r
) . (3)
This equality, together with Eq. (2), then leads to the final equation,
R
pred
(C
r
) = M
test
(C
r
) . (4)
This means that the risk for the prediction population is given directly by Cohens
risk of lung cancer mortality for the test population. These equations prove the
statement made earlier, and they are also the reason why the Ecological Fallacy
does not matter in going from the test population to the prediction population: the
two identical FPCs cancel, and thus all population characteristic factors, known or
unknown, cancel also.
Actually, we quite often make the assumption of equivalent populations, even
when we know that it is likely to be only partly valid. As an example, we use the
situation of the cancer risk coefficient determined in the BEIR V report (NRC,
1990). The use of this risk coefficient assumes implicitly that the FPC
t e s t
of the
Japanese test population, first at the exposure after 8 years of war deprivations, then
suffering through the post-war chaos, and living only later in times of peace, is
numerically the same as the FPC
p r e d
for the American prediction population 50
R C R C FPC C ECF
m C
FPC C
FPC C
pred r test r pred r
test r
pred r
test r
' '
'
'
( ) = ( ) ( )
= ( )
( )
( )

'
'
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934 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
years later in times of prolonged peace. Then, and only then, can the Japanese
bomb survivor data be used in risk predictions for members of the U.S. population.
In our thought experiment, making the assumption of equivalent populations
means that the predicted values for the Denver population will be numerically equal
to the values of the Cohen data, except for some increase in the systematic un-
certainties due to making this assumption. Thus, as a direct consequence of this
partial equality,
*
the Cohen data can be used directly for the risk assessment. Note
that the assumption of equivalent populations, and thus the equality of the two FPCs,
means that making the smoking correction or any other correction is not necessary,
and that Cohens raw, uncorrected mortality data is the proper data set to be used.
This fact is important with regard to some of the criticisms of the smoking
correction in Cohens evaluation (see, for instance, Field et al., 1998; Archer, 1998;
Cohen, 1998c,d). These criticisms have now become irrelevant for a risk assessment
because these corrections are part of the two identical FPCs, and their influence
cancels.
We are aware that, at first, these conclusions seem counterintuitive. However, it
becomes clear on further consideration that they are a logical consequence of the
minimum data needs for a risk assessment, which is to use the evaluation of actual
effects in the test population to project as directly as possible the actual health
effects in the prediction population. Therefore, the data must include all the
confounding effects, known and unknown, in both populations.
Validity of the Assumption of Equivalent Populations
The radon exposures of the uranium miners and those of the general population
contain a series of substantially different dosimetry factors and lifestyle parameters.
They can give rise to considerable confounding factors, the most important being
the doses derived from measurements made ten years later in a different mining
environment. Here, the validity of the assumption of equivalent populations needs
to be discussed in far more detail than it has been in the past. In the BEIR reports
IV and VI (NCRP, 1988, 1999), the assumption is made a bit more explicitly than
usual but still not in sufficient detail to be convincing.
All the issues raised in discussions about the cause-effect relationships for radon
and other radioisotopes, as well as for whole body irradiation with gamma-radiations
and neutrons, make the conditions for the validity of the assumption of equivalent
populations a bit more complicated. The BEIR and the ICRP reports (ICRP, 1991)
as well as similar reports consider, in varying levels of detail, the different effects of
population characteristics which could affect the assumption of equivalent popula-
tions. Then, however, they do not make the correction, but go on and implicitly
make the assumption of equivalent populations anyway (NCRP, 1980, 1988, 1990,
1999; ICRP, 1991).
When testing for the equality of the factors of population characteristics, we
should remember that the null hypothesis must involve the assumption of equiva-
lent populations because that is the current paradigm in risk assessment. Thus,
according to the Scientific Method, it is the obligation of the proponents of nonzero
*
The term partial equality is used here for two numbers that have
equal values but unequal errors.
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 935
Risk Assessment and the Ecological Fallacy
differences between the two FPCs for the test and prediction population to demon-
strate numerically that a difference between the two FPCs exists and is indeed
significantly different from zero. This would then invalidate Eq. 3 and show that the
calculated corrections to the FPCs need to be made according to Eq. 2, otherwise,
no risk projection is again possible.
Generalization to Other Agents and Health Effects
It is easy to verify, by going again through our thought experiment, that its result
can be generalized, so that it applies regardless of the agent, the health effect, or the
shape of the underlying true exposure-effect relationship. All that matters is the
assumption that the exposure-effect relationship has been modified by the factors
FPCs and ECFs for the test population, resulting in a particular shape. It is this
modified shape that will then predict the actually occurring health effects and which
therefore is relevant for the corresponding risk assessment.
The generalization of the procedure also encompasses its application to inani-
mate objects such as high-pressure steam valves in nuclear or fossil fuel power plants,
for instance. Time to failure data determined for one set of valves can only be
applied to a newer set of the same or similar valves by making the analogue to the
assumption of equivalent populations. Particularly in the case of similar valves, but
also for the same but newer valves, this assumption needs proper justification, or a
prediction of the time-to-failure cannot be made.
This is the main result of our generalized thought experiment: The proper cause-
effect function for predictions is the experimentally found correlation between exposure and
effects (or time and effects), and not the shape of the underlying true exposure-effect function.
It is important to understand here that, for sizeable factors of population char-
acteristics, no underlying true cause-effect function can correctly predict the
actual effects occurring in the prediction population. For correct predictions, the
FPCs specific for the test and prediction populations are needed.
Consequently, the arguments using the concept of Ecological Fallacy may be
relevant to finding the true exposure-effect relationship, but they are completely
irrelevant for a risk assessment. The use of the term Ecological Fallacy therefore
is inappropriate. It is the search for the true exposure-effect relationship which is
problematic and which requires that the confounding factors be quantitatively well
known in order to make valid predictions of the health effects expected in a
prediction population. Unfortunately, and contrary to the fourth assumption in our
thought experiment, most of the confounding factors contributing to the FPCs are
actually not well known numerically, if at all.
POPULATION RISKS AND INDIVIDUAL RISKS
All of Cohens evaluations deal with large numbers of people, not individuals.
That is why the assumption of equivalent populations can be made, and why the
true shape of the cause-effect relationship is of little or no consequence in the
presence of large confounding factors and thus FPCs which are considerably differ-
ent from one. Generally, it is maintained that individual risks cannot be predicted
from epidemiological data unless the study uses matched cohorts, and the true
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936 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
cause-effect relationship can be determined. We will show that this statement is not
correct, and that a statement about the risk for an individual can indeed be made.
Properties of a Fit to the Experimental Data
As we have demonstrated, the risks for a prediction population, given the differ-
ent exposure strata of all subpopulations selected, can be estimated using the
information from the test population. The basis for this estimate is the assumption
of equivalent populations. This means that both the test and the prediction popu-
lation must be large and diverse enough so we are able to rely on the validity of the
assumption. A function of exposure, such as a linear, a linear plus quadratic, or a
U-shaped curve, can then be fitted to the data of the test population by using, for
instance, an inverse-variance-weighted fitting procedure (Brandt, 1976; Lancaster
and Salkauskas, 1986; Bevington and Robinson, 1992). The errors of such a predic-
tion can then be calculated by using the covariance matrix of the fit and either an
analytical approximation of the error propagation equation (Seiler, 1987) or a
corresponding Monte Carlo simulation (Cox and Baybutt, 1981; Kalos and Whitlock,
1986).
A U-shaped curve should be chosen, at least as one option (Luckey, 1991), not
only because Cohens data have that shape but also because a realistic cytodynamic
cancer model of the Moolgavkar type can be fitted to Cohens data (Bogen, 1997).
Also, if Bogens model is fitted to other, independent radon/lung cancer data, it
predicts the U-shaped curve measured by Cohen (Bogen, 1998).
Risk Evaluation for the Prediction Population
For our further discussions, we shall, without loss of generality, limit ourselves to
the properties of linear cause-effect functions. Good examples for linear maximum
likelihood fits are given in standard statistical texts (see, for instance, Walpole and
Myers, 1985). A successful fit to the data results in a set of fitted parameters, and on
that basis two statements can be made. The first is the calculation of the mean
response of the test population for a given exposure (Walpole and Myers, 1985, p.
332). The second is the calculation of the response to the same exposure by any
individual in the test population (Walpole and Myers, 1985, p. 334). For the linear
cause-effect functions assumed here, the correlation matrix is a symmetrical 2

2
matrix. For nonlinear cause-effect functions, such as U-shaped curves, analogous
expressions can be found which involve covariance matrices of the same or higher
dimensions (Brandt, 1976; Lancaster and Salkauskas, 1986; Bevington and Robertson,
1992).
The standard error of the average response in the prediction population is given
by the standard error of the fit value, which decreases roughly as s(1/n) with
increasing sample size n, using the symbol s for the standard deviation of the fit. This
asymptotic behavior is analogous to that of the standard error of a mean as it goes
to very small values for large values of n (Walpole and Myers, 1985, p. 332).
Risk Prediction for an Individual
Using the data of the same fit to the test population, the prediction for the response
of an individual can be made. The procedure yields the same numerical value as the
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Risk Assessment and the Ecological Fallacy
predicted mean response (Walpole and Myers, 1985, p. 334), but it has a much larger
standard error that decreases roughly as s (1+1/n) only. This error decreases asymptoti-
cally with increasing sample size n, not toward very small values, but toward the value of
the standard deviation s of the fit. A similar expression can be obtained for nonlinear
cause-effect functions. Thus, for a member of the test population, the same risk and this
larger error are the correct evaluation of the individual response. If we now apply the
assumption of equivalent populations, we can find in the prediction population a
counterpart for each individual in the test population. For an arbitrary individual in the
prediction population, therefore, the value of the risk and the large standard error
discussed above are the correct estimate of the predicted individual risk.
In other words, the mean risk for the prediction population and the individual
mean risk in that population are partially equal, differing only in the size of their
standard errors. This conclusion can be supported by an inspection of the errors for
each point shown in Figure 1 of Cohens 1995 paper, reproduced also in his recent
papers (Cohen, 1998a, 1999). Note that these are point by point errors and not the
errors of a fit to the data. However, still, the small errors are the standard errors of
the mean and the large ones are the probable errors of the sample (including 50%
probability), given as quartiles.
The large errors of the individual risks can be understood intuitively by analogy:
When we consider a sample of n receptors and ask the question: If we add yet
another receptor and label it n + 1, what will be the mean and the distribution of
our expectation for this measurement? The answer is clearly: It is the sample mean,
and a distribution given, not by the standard error of the mean, but by the standard
deviation of the sample (Seiler and Alvarez, 1995). Therefore, the appropriate error
for an individual risk is much larger than the error of the average risk in the
population, and its variability will include those of all subpopulations and thus from
all members of the prediction population. It is this risk and this error value which
should be used in calculations which involve an individual.
It is important here to be aware that the only condition for the viability of a risk
to an individual is that the individual has to be a bona fide member of the prediction
population. Thus, the individual has all the corresponding probabilities to be a
contributor to the various confounding factors, such as smoking. In other words, the
individual chosen must in all respects be an indistinguishable member of the
prediction population, selected at random.
Risk Prediction for a Particular Individual
A frequently asked question concerns the cancer risk for a particular person X,
taking into account all of the characteristics of the individual, such as age, sex,
smoking status, and other lifestyle parameters. The only way to make such a risk
prediction possible would be to make a successful risk determination for the particu-
lar subgroup of the population that has the same characteristics as individual X. This
subgroup would have to be large enough to produce enough cancer cases so that
a risk determination is possible, and also be large enough to allow making the
assumption of equivalent populations. Thus risks can only be determined for all
members of a meaningful subgroup. For the individual X, however, no personal risk
can be determined.
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938 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
DISCUSSION
In this paper we have demonstrated that, far from being unfit for a risk assess-
ment, Cohens uncorrected measurements of the correlation between the local
exposure concentrations of radon and the local lung cancer mortality are the only
data available which can be used for a risk assessment at low exposures. An explicit
additional condition is that the exposure concentrations of the prediction popula-
tion have to be measured in exactly the same way as the exposure concentrations of
the test population. As we have also shown in our thought experiment, the true
cause-effect function is of use only as long as there are no significant confounding
factors and thus no total FPCs significantly different from one, because these factors
are not known well at all.
The important fact here is that, theoretically, the actual risks can be calculated
without knowing anything about the true cause-effect relationship. Conversely,
the evaluation of the true cause-effect relationship from the data is possible and
useful only if the confounding factors are small and the FPC values lie close to one.
Then, the corrections to be made are small and relatively well known. The evalua-
tions made by Cohen (1995, 1998a,b,d) have shown that for his data, this condition
holds.
It is important to realize at this point that we only use Cohens raw data and not
his corrected data. Clearly, if these corrections were made, the inverse corrections
would have to be made in predicting a risk. As the ECFs and the FPCs, these
corrections also would cancel in a risk assessment.
In their entirety, our statements are a complete reversal of the usual arguments.
This reversal is due to our approach. Our evaluations are based on the minimum
needs of a risk assessment which has one, and one purpose only, and that is to make
a prediction for the actual occurrences of health effects in a prediction population,
based on data for the test population. The true cause-effect function is but a tool
that may or may not be needed. If the FPCs are large, as the proponents of the linear
theory claim, then the true cause-effect function is a practically useless tool.
Considerable progress has been made in the last few years in making plausible
nonlinear models on the basis of the Moolgavkar-Venzon-Knudson two-stage mecha-
nism of carcinogenesis. For the case of radon, and based on new independent radon
exposure data, Bogens CD2-model (Bogen, 1998) was able to predict magnitude
and shape of both Cohens ecological data as well as the lung cancer data for
underground uranium miners. What makes the CD2-model a truly extraordinary
biological model is that, in addition, it independently and correctly predicts an
inverse dose rate effect in non-smoking uranium miners (Bogen, 1998). This is
clearly the way models are tested according to the Scientific Method, particularly
when the predictive power of Bogens CD2-model begins to approach the power of
models used in physics, chemistry, and engineering.
Contrary to the usual statement regarding the impossibility of deriving individual
risks from any kind of ecological studies, it was demonstrated here that such risks
can indeed be estimated from any epidemiological study under properly restrictive
conditions for the individual concerned. The value of the risk is the same as the
average risk for a member of the test population, but the uncertainty is considerably
larger because it must represent the variability of the risk over all members in the
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Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000 939
Risk Assessment and the Ecological Fallacy
prediction population. This means that for a particular individual, the risk can only
be calculated as long as the individual can be regarded as an indistinguishable
member of the test population. For a specific individual X, however, no personal
risk prediction is possible.
What was introduced here as an explicit concept, is the Assumption of Equiva-
lent Populations which holds that the test population is representative for the
prediction population in all aspects which are important for the adverse effect.
In the presence of confounding effects, this means that the FPC for the test
population is identical to the FPC for the prediction population. This property
leads to the prediction of risk values that are equal to the experimental data but
may have slightly larger systematic errors. It also means that the predicted risk
is practically independent of the true cause-effect function. Thus, for a predic-
tion of health effects, the only data needed are a set of carefully made measure-
ments of the effects in the test population, based on a sound experimental
procedure.
For each future application, an explicit set of reasons should be given, stating why
the assumption of equivalent populations should be applicable for this case. If it can
be applied, a valid prediction of health effects is possible; if it cannot be made, no
prediction is possible.
In this paper, we have also shown that the effects of the Ecological Fallacy may
or may not be sizeable, but they are relevant only if the goal is to find the true
cause-effect function. They are, however, irrelevant as long as the goal is the
prediction of health effects in a risk assessment, and the conditions for the assump-
tion of equivalent populations are sufficiently fulfilled. Thus an important result of
this paper is that, when applied to a risk assessment, the Ecological Fallacy is
irrelevant.
What Cohens data did tell us is that the relative risk is at first larger than 1 at
very low concentrations, then it decreases with larger radon exposures until the
relative risk drops significantly below 1. This means that, in that region of air
concentrations, the exposure decreases the risk of lung cancer below the back-
ground level and thus results in a hormetic or beneficial effect. At somewhat
higher exposure concentrations, the risk levels off, begins to rise again, and finally
becomes larger than background above the so-called zero-effects point (Luckey,
1991). Obviously, the structure of all these well-determined nonlinear effects are
nicely hidden in the large uncertainties of the other data, which up to now were
the only ones deemed acceptable by the proponents of the linear model. Note
again that the two data sets are in statistical agreement, but only the Cohen data
with their small errors are able to reveal the finer details of the dependence on
average concentrations. Thus this example is a clear experimental demonstration
of one of the basic tenets of the Scientific Method: If you cannot measure it, you
do not know anything about it!
ACKNOWLEDGMENTS
The authors express their gratitude to Drs. John Auxier, Kenneth Bogen, and
Bernhard Cohen, as well as Mr. James Muckerheide, for a critical reading of the
manuscript and for providing valuable suggestions.
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940 Hum. Ecol. Risk Assess. Vol. 6, No. 6, 2000
Seiler and Alvarez
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