HAL MORGENSTERN,PHD
Abstract: Despite the widesprcad use of ecologic
analysis in epidemiologic research and health plan-
ning, little attention has been given by health scientists
and practitioners to the methodological aspects of this
approach. This paper reviews the major types of
ecologic study designs, the analytic methods appropri-
ate for each, the limitations of ecologic data for making
causal inferences and what can be done to minimize
these problems, and the relative advantages of ecolog-
ic analysis. Numerous examples are provided to illus-
Ecologic studies are empirical investigation s involving
the group as the unit of analysis. Typically, the group is a
geographically defined arca, such as a state, county, or
census tract. Because they can often be done by combining
existing data files on large populations, ecologic studies are
generally less expensive and take less time than studies
involving the individual as the unit of analysis; ecologic
studiescan also achieve certain objectives generally not met
with nonecologic designs. On the other hand, data on many
variables (e.g.. behaviors. attitudes, and medical histories)
may not be available at the ecologic level, and the results of
ecologic analyses are subject to certain limitations not
applicable to many other study designs.
The purposes of this paper are to show how ecologic
analyses may be used in epidemiologic research and health
planning. and to illustrate some of the advantages and
disadvantagesof this approach. It is important to recognize
that ecologic studies have two major aims: 1) to generate or
test etiologic hypotheses. i.e, to explain disease occurrence;
and 2) to evaluate the effectiveness of population interven-
tions, i.e.. to test the application of our knowledge for
preventing disease and promoting health. In the discussion
that follows. emphasis will be given to the methodological
problems that are especially relevant to the interpretation of
ecologic findings for achieving these two different aims.
The Simple Cohort Study and Ecologic Data
As a basis for comparing and thus interpreting the
results of an ecologic study, we will first review the funda-
---
Address reprint requests to Hal Morgenstern, PhD, Assistant
Professor, Department of Epidemiology and Public Health, Yale
University School of Medicine, 60 College Street, Box 3333, New
Haven, CT 06510. Professor Morgenstern is also affiliated with the
Vale Center for Health Studies, Institution for Social and Policy
Studies. This paper, submitted to the Journal December 21, 1981,
was revised and accepted for publication March 11, 1982.
1) 1982 American.Journal of Public Health
1336
Morgenstern H. Uses of ecologic analysis
1344.
trate the important principIes and methods. A careful
distinction is made between ecologic studies that gen-
erate or test etiologic hypotheses and those that evalu-
ate the impact of intervention prograrns or policies
(given adequate knowledge of disease etiology). Fail-
ure to recognize this difference in the conduct of
ecologic studies can lead to results that are not very
informative or that are misinterpretod by others. (Am J
Public Health 1982; 72: 1336-1344.)
mentals of analyzing a simple cohort study. To simplify the
presentation, we will consider the possible association be-
tween a dichotomous study factor (x = exposed or une x-
posed) a:td a dichotomous disease outcome (y = case or
noncase). On the basis of data obtained from a cohort study
(see Table 1 for notations), epidemiologists usually estimate
at least one of the folIowing parameters:1
1. The risk ratio (or relative risk) is the risk of develop-
ing the disease for exposed persons divided by the corre-
sponding risk for unexposed persons. Using the data nota-
tions in Table 1, we can estimate the risk ratio (RR) as
a/nj
(1)
RR=d;
where aln, is the estimated risk for exposed subjects and c/no
is the estimated risk for unexposed subjects. Under the null
hypothesis (i.e., no association between the study factor and
the disease),the RR is equal to one; a value greater than one
indicates a positive association; and a value less than one
indicates a negative association. Of course, RR can dilfer
from its null value (one), even under the null hypothesis,
becauseof random and nonrandom errors (i.e., chance and
bias, respectively).
2. The Pearson product-moment correlation coefficient
is fue covariance (CXy)of fue study factor (x) and the disease
(y) divided by the square root of the product of the two
variances (V x and V y). The estimated correlation coefficient
(r) from simple cohort data is
r= ~-= ad -bc
= cj>, (2)
vV;-V-; v'mln1oDlnO
For 2 x 2 tables. the correlation coefficient is usually called
the phi «11)coefficient. This measure reflects the extent to
which each variable is able to predict the other. More
specifically. r2 (or <112)
is the proportion of the variance in
..,." each yariable_explained by theother. The vaLue.._ofr can
AJPH December 1982, Vol. 72. No. 12
in epidemiologic r'esearch. Am J Public Health 1982; 72: 1336-

TABLE 1-Data Layout: Cohort Study
Disease Status (y)
-
Study Factor
(x) Case Noncase Total
Exposed a b n,
Unexposed c d no
TOTAL m, mo n
range from negative one (indicating a perfect negative asso-
ciation) to one (indicating a perfect positive association), and
the null value of r is lero.
3. The e/iologic frac/ion (or population attributable risk
per cent) is the proportion of all new cases in the population
due to the exposure. We can estimate the etiologic fraction
(EF) in the source population as
.p (RR -1) (3)
--p EF - (RR -1) + 1 ,
where p is the estimated proportion of exposed persons at
risk in the source population = nI/o, if n is sampled from a
single population. This measure reflects the potential impact
on disease frequency of eliminating the exposure in the
population; thus, it is particularly useful in health planning.
The null value of the EF is zero, and a value of one indicates
that the exposure is a necessary cause of the disease (i.e.,
the RR is infinite).
As shown in Table 2, the key feature of ecologic data,
relative to cohort data, is the lack of information about the
joint distribution of the study factor and the disease within
each group (i.e., unit of analysis). That is, we know the
number of exposed subjects (nlj) and the number of cases
(mlj) within each group, but we do not know the number of
exposed cases (~). In ecologic analysis. the independent
variable (X) is the proportion of exposed subjects within the
group (n¡ynJ, and the dependent variable (Y) is the rate (or
risk) of disease (mlynJ. Notice that both ecologic variables
are continuous, even though the two factors are dichoto-
mous at the individuallevel.
Ecologic Study Designs
The fundamentals of ecologic analysis can best be
presented by dividing ecologic study designs joto tour types.
The simplest of these is the exploratory study in which we
observe geographic ditIerences in the disease rate among
several regions (groups). The objective is tI> search for
spatial patterns that might suggestan environmental etiology
or a special etiologic hypothesis. No exposures are mea-
sured and, generally, no formal data analysis is used. For
example, the National Cancer lnstitute (NCI) mapped the
age-adjustedcancer mortality rates in the US by county for
the period 1950-69.2For oral cancers, they found a striking
ditIerence in geographic patterns by sex: among men. the
AJPH December 1982. Vol. 72. No. 12
USE OF ECOLOGIC ANAL YSIS
mortality rates were greatest in the urban Northeast, which
is consistent with the geographic distributions of known risk
factors (i.e., tobacco smoking and alcohol consumption); bul
among women, the mortality rates were greatest in the
Southeast. These findings led some cancer epidemiologists
at NCI to speculate that snuff dipping, which is common
among rural southern women, mar be a risk factor for oral
cancer.3 In fact, the results of a recent case-control study"
support this hypothesis.
In the multiple-group compari.\"onstudy. we observe the
association between the average exposure level (X) and the
diseaserate (Y) among several groups. We can quantify and
test this ecologic association by regressing y on X, i.e., by
fitting the data to a mathematical model', such as
y = Bo + B.X (4)
where Y is the predicted value of y for any given value of X.
B. is the estimated slope, and Bo is Ihe estimated y.
interceptoTo simpliry the presentation, a simple linear model
will be used throughout this paper; however, the method can
be extended to include several predictors (Xs), polynomial
and interaction terms, and other nonlinear models. What is
most relevant to epidemiologists about this type of analysis
is that the regression coefficients (Bo and B,) mar be used 10
eslimate the same categorical measures normally compuled
from studies conducted at the individuallevel. To eslimale
the RR from ecologic data,6.7we can divide the predicted
rate (Y) where X is set equal to one (all exposed) by Ihe
predicted rate where X is set equal to zero (all unexposed).*
i.e.,
RR = YIX = I
YIX = o =
Bo + B,
= +-B.
Bo
(5)
Bo
The ecologic correlation coefficient (R) is equal to
R = B 1 v-V;¡V-; (6)
where Vx and Vy are the ecologic (between-group) vari-
ances of X and Y. respectively." To estimate the EF. we
simply substitute the above estimate of the RR joto expres-
sion 3. where p is the estimated proportion of exposed
persons in the entire source population. (Note that p may no!
"Notice that. assuming a linear modelo Ihe eslimaled risk
dilJerence (R. -Ro) is equallo the slope (B,).
1337
MORGENSTERN

3
41
...2
~
00
~
>-
~
..
...
:=
...
00
1
00 ...
IX o
~ O
..
"O
u
~
In

Percent Protestant (X)

FIGURE I--.",uicide Rate (per lOSpopulation) by Rellgious Composi-
tion (Per Cent Protestan!) ror Four Groups or Prussian Provlnces,
1883-1890.
*The rour observed poin!s (X, y) on !he graph are: (30, 9.~6),
(4~, 16.36), (78.5, 22.0), and (9~, 26.46). The fitled linc (y) is bascd
on unweigh!ed least squares regression. SOURCE: Durkheim"

be equal to X, the unweighted mean of the proportion

exposed within each group.)
As an illustration of an ecologic comparison study,
consider the work of Emile Durkheim,9 who investigated
suicide in western Europe during the 19thcentury. The data
in Figure 1 represent some of Durheim's findings for four
groups of Prussian provinces between 1883and 1890. The
suicide rate (Y) is regressed on the per cent of each group
that is Protestant (X). Using unweighted** least squares
regression,B, is 24.0 x 10-~and Bo is 36.6 X 10-6, where X
= .62, Vx = .0891,and Vy = 53 X lO-1°. Fromexpression 5,
we calculate RR to be 1 + (24 x 10-5/36.6 x 10-6) = 7.57,
i.e., it appears that Protestants were 71/2times as likely to
commit suicide as were other residents (most of whom were
Catholic). From expression 6, we find R to be 24 x 10-5 x
V.0891/53 X 10-1°= .983. Thus, 97 percent(= .98310fthe
between-group variance in suicide rate is explained by
religious composition of the region. The fact that this value is
so close to one indicates a near perfect lit of the linear
modeloFrom expression 7. assuming that p is equal to X,***
we calculate EF to be .62(7.57 -1)/[.62x (7.57 -1) + IJ =
.803,i.e.. it appears that about 80 per cent of all suicides in
Prussia between 1883and 1890were due to being Protestant
(or to other factors associated with religion).
..Since y is a proportion or rate, the variante of Y may vary
appreciably over values of X. In this situation, it is preferable to use
,,'tighttd least squares regression.
...Since Durkheim did not provide the number of residents in
each group of provinces. we cannot determine p directly from his
data.
1900 1920 1940 1960
FIGURE 2-Time Trends In the Age-Standardlzed Mortallty Rates
(per lo" populatlon) for Two Infectlous Diseasesin Relation to Ihe
Introductlon of a Vacclne: US 1900-1973
Source: McKinlay and McKinlay'O (Reprinted in revised form
by permission of Milbank Memorial Fund Quarterly.)
In the time trend study (or time series study), we
observe the relationship between the change in the average
exposure level (or intervention) and the change in the
diseaserate for a single population. t With time trend studies
involving a sudden change in exposure, such as the start of
an intervention program, we compare the slope in the
diseasetrend before and after the intervention. For example,
in Figure 2, the age-adjusted mortality rates for two infec-
tious diseases are graphed for the period 1900-1973. While
the data suggestthat the introduction of the polio vaccine in
the 1950swas etfective in preventing polio deaths in the USo
it appears that the introduction of the measles vaccine in the
1960shad little or no etfect on measles mortality.loNote that
the measles mortality rate had been declining in this country
since 1910and reached its current low level about 20 yearN
before the vaccine was introduced.
tForrnal statistical analysis oí the relationship between time
trends (Iagged time series regression. cohort analysis. and Fourier
analysis) is beyond the scope of this paper.

AJPH December 1982, Vol. 72, No. 12

1338

c n
o
'"x
~ "t'
5
~
.3
~ that made their water harder than in towns that made their
.:c-
'O
~v ~
~
:c ';;
1940 19~ 1960 1970 1980
FIGURE 3-Tlme Trends In the Age-Standardlzed Coronary Hear!
Dlsease(CHD) Mortallty Rate (per lQ5 populatlon) and Per Capita
Alcohol Consumptlon (gal/yr): US, 1945-1975
Source: Kuller, el a/.'1
With time trend studies involving a gradual change in
average exposure level (observational designs), we must
compare trends in both variables. The objective is to test for
a relationship between trends, taking into account a possible
lag period between a given change in exposure and the
subsequentdisease efIect. For example, Figure 3 shows the
age-adjusted coronary heart disease (CHD) mortality rate
and the per capita alcohol consumption in the US between
1945and 1975.11Since the two trends oppose each other
systematically throughout the periodo we might infer from
these data that alcohol consumption is a protective (nega-
tive) risk factor for CHD. Alternatively. the observed rela-
tionship between the two variables may be due to changes in
diagnostic custom or to trends in other CHD risk factors
associated with changes in alcohol consumption.
A similar analysis of artificial sweeteners and bladder
cancer mortality in the US between 1950and 1967 showed
no relationship between these two trendsl2 for either males
or females. It is possible that the exposure efIect is too weak
to be detected with this type of designo Alternatively.
because of the long latency period of bladder cancer. the
increased use of artificial sweeteners beginning in the early
l%Os
1980sor may not show
1990s. . an efIect on the disease rate until the
In the mixed study, we observe the relationship between
the change in the average exposure level and the change in
the disease rate among several groups. The anaJysis and
interpretation of such data are similar to that of the compari-
son study; the only difIerence is that in the mixed design
both variables are measured as absolute changes between
the same two times (or periods).'Thus, we can estimate the
risk ratio (RR), the correlation coefficient (R), and the
etiologic fraction (EF) from the ecologic regression coeffi-
cients, using expressions 5,6, and 3. Frequently, it is more
convenient or informative to categorize the exposure vari-
able and to compare the changes in disease rate among
groups having difIerent mean exposure levels. For examp)e,
Crawford, et al,!) observed the absolute changes in the
average annual cardiovascular disease (CVD) mortality rate
AJPH December 1982, Vol. 72, No. 12
..-,,=_c --
USE OF ECOLOGIC ANAL YSIS
between 1948 and 1964 for 83 British towns. by sex, age. and
change in water hardness. For al! sex-age groups. espccially
for males. they found an inverse association between trends
in water hardness and CVC mortality. In middle-age men,
for instance, the increase in CVD mortality was less in towns
water softer. Thus. we might infer that water hardnes~
protects one against CVD. In general. the mixed design
provides a better test of an etiologic hypothesis than do the
other ecologic designs. because the results of the mixed
study are less likely to be due to the confounding clfect~ 01"
extraneous risk factors.
The Ecological Fallacy
The major limitation of ecologic analysis for testing
etiologic hypotheses is the potential for substantial bias in
effect estimation. The central problem, known as the "eco-
logical fallacy", 14results from making a causal inference
about individual phenomena on the basis of observations of
groups. In Durkheim's data,9for example, it may have been
Catholics (not Protestants) who were committing suicide in
predominantly Protestant provinces. This alternative expla-
nation is possible, because none of the provinces were
entirely homogeneous with respect to religion. Indeed, it is
quite plausible that members of a certain religious minorilY
might have been more likely to take their own lives than
were members of the majority. tt
The ecological fallacy was first demonslraled mathe-
matically in 1950 by William Robinson," who showed that
the total covariance of two variables can be expressed as the
sum of a within-group component and a between-group
(ecologic) component. Using this form of the "covariance
theorem," Robinson derived the mathematical relation~hip
between the average within-group correlalion coefficient (r)
at thc individual level and the between-group correlation
coefficient (R) at the ecologic level. Several years later.
Duncan, el al,'6extended the covariance theorem to expres~
the relationship between the average within-group and be-
tween-group regression coefficients (bl and B" respective-
Iy).
To understand better the meaning of the ecological
fallacy, we mar partition the bias re~ulting from ecologic
analysis into two components: 1) ag/(reKation hia.\'-due to
the grouping of individuals; and 2) .\'pecificati(Jn hia.\'-due to
the confounding effect of the "group" itself,"" In the (atter
component, either certain extraneou~ risk factors are differ-
entially distributed by group. or some propertY of the group
itself, e.g., social disorganization. affect~ disease occur.
rence" The sum of these components is called cr(I,\",\".le,'('{
ttln CactoDurkheim actually compared suicide rates for Protes-
tants, Catholics, and Jews living in Prussia. From his data. we find
that the rale was about twice as greal among Prolestants as among
other religious groups, suggesting a subslanli.al difference belween
the results obtained at Ihe ecolo~ic level (RR = 7.57) and Ihose
obtained at the individuallevel (RR a 2). Yel Durkheim failed 10
notice Ihis quantitative difference because he did nol actually
eslimale Ihe ma/(nitude of the effect in eilher analysis.
1339
 MORGENSTERN

TABLE 3-Number 01 Subjects, by Exposure Status, Dlsease Status, and Group: Hypothetlcal
Data to Illustrate Cross-Level Bias

Exposed Unexposed
--- ---
Group O) Case Noncase Total Case Noncase Total

1 10 90 100 90 810 900

2 45 255 300 105 595 700
3 100 400 500 100 400 500
4 175 525 700 75 225 300
5 270 630 900 30 70 100
TOTAL 600 1900 2500 400 2100--- 2500

b;a.~, which, in theory, can make the ecologic association
appear stronger or weaker tllan it is at the individual
level.".11 In fact, the two components may cancel each other
out. resulting in no bias in the estimation of effect. However,
in practice. this latter possibility is very infrequent; ordinari-
Iy, cross-level bias exaggerates the magnilude of the true
association.
There will be no cross-level bias when. and only when.
the group mea n of the exposure variable (X) has no etfect on
disease risk (y) at the individual level. controlling for Ihe
individual's exposure value (X).11 Expressed more formally.
there will be no cross-level bias (or ecological fallacy) if the
regression coefficient ~2 (the population parameter) in the
following st~ctural equation is equal t~ zero:
y = ~o + ~IX + ~2X + ~
where the unit of analysis is the individual, X refers to the
average exposure level of the group to which the individual
belongs. and ~ is the error termo Essentially, then, cross-
level bias occurs when an ecologic predictor variable (X)
measuresa ditferent underlying construct(s) than the corre-
sponding variable (x) does at the individ'uallevel, 17'
For a given statistical model at the individual level.
there can be only specification bias. i.e,. confounding; while
for the same model at the ecologic level. there can be both
specification and aggregationbiases. The net effect of group-
ing. therefore. is that a confounding variable at the individual
level may not be confounding at the ecologic level.'" For
example. although the risk of bladder cancer is much greater
for men than for women. sexoas an ecologic variable (per
cent male in each group), will not be very predictive of the
diseaserate (or anything else) acro~~geographically defined
groups. The reason for this difference is that there are
approximately the same proportion of males and females in
all groups. Conversely. a confounding variable at the ecolog-
(7)
ic level may not be confounding at the individual level.'M
This latter discrepancy is greatest for ecologic analyses
involving grouping by the dependent variable. thereby in-
creasing the between-group variance of Y. This type of
grouping will result in confounding due to any correlate of
disease status, even if the corre late is unrelated to the
exposure variable at the individual level (and therefore not
an individual confounder).

¡lllustration 01 Cross-Level Bias

>

The hypothetical data in Table 3 involve 5,000 subjects

..
~
;.. aggregated into five equal-size groups. Using linear regres-
'" sion, as described earlier for multiple-group comparison
c
c studies, we find that B. is .25 and Bo is .075, where X = ..50,
.2
r T .80 + 81 X Vx = .10, and Vy = .00625 (see Figure 4). According to
8-
o /' expression 6, R is equal to .25 V.IO/.00625 = 1.00; thus, the
Lo
Q.
linear model fits the data perfectly, as indicated in Figure 4.
(Note that all observations fall on the fitted line.) From
expression 5, we estimate the RR to be 1 + .251.075= 4.33,
suggestinga fairly strong positive association. The estimated
o .2 .4 .6 .8 I EF. according to expression 3,is .5(4.33 -1)/[.5(4.33 -1) +
1] = .625, where p = .50. That is, of the 1,000 observed
Proportion Exposed (X)
cases,we estimate that 62.5 per cent (625 cases)were due to
FIGURE 4-The Proportion ofDiseased Subjects by the Proportion of the exposure.
Exposed Subjects for Five Groups* (Based on the Hypothetical Data in
Next, we will conduct acrude analysis at the individual
Tahle 3)
level, ignoring group affiliation. According to expression 1,
the estimated crude RR is (600/2500)/(400/2500)= 1.50 (refer
*In this ecologic analysis. the litted line IY) i~ based on least
to the row of "Totals" in Table 3). Thus, the crude associa-
squares regression.

AJPH December 1982. Vol. 72. No. 12

1340

~

tion between the exposure and disease at the individuallevel
is weaker than the ecologic association (1.50 vs 4.33).
Similllrly, thc crudc (zcru-urdcr) currclation cocfficicnt Ir =
<ti)is also smaller than the corresponding ecologic measure
(R). According to expression 2, r is [600(2100) -1900(400)JI
V 1000(4000)(2500)(2500) = .100. Thus, differences in expo-
sure explain only I per cent (=.102) of the variance of
disease status. From expression 3. we estimate the EF to be
.5(1.5 -1)/[.5(1.5 -1) + 1] = .200, which is also less than
the ecologic estimate of .625.
.In the last análysis, we adjust (or standardize) for group
affiliation by controlling for "group" in the individual anal y-
siso The general formula for computing an (internally) stan-
dardized risk ratio' (sRR) is
¿ aj
j
sRR = (8)
¿~
j nOj
where ajand Cjrefer to the number of exposed casesand
unexposed cases, respectively, in the j-th stratum (group)
(refer to Tables \ and 2), sRR is a weigh-ted average of the
RRj, and sRR is also called the standardized morbidity ratio
(SMR). We find that sR'R for the data in Table 3 is 1.00, i.e.,
there is no association between the exposure and the dis-
ease, controlling tor group. In fact, the estimated RRj are
exactly one in every stratum (group). The standardized (or
partial) correlation coefficient is also a weighted average of
the stratum-specific estimates (rj = <l>v,all of which are equal
tu zcru in the example; thus. the partial r is equa\ to zcro.
The standardized EF is estimated from expression 3, substi-
tuting sRR for RR. For the hypothetical data in Table 3,
therefore, thc estimate of the standardized EF is zero.
A summary of results for all threc analyses is given in
Table 4. The dift.erence between estimates for the crude and
standardized analyses is due to the confounding etfect of
extraneous risk factors ditferentially distributed across
groups (specification bias). The ditference between esti-
mates for the ecologic and crude individual analyses is due to
the ditferent units of analysis (aggregation bias). We would
conclude from these data that the exposure is not a risk
factor for the disease. Estimates obtained from the ecologic
analysis are strongly biased as a result of the cumulative
etfects of misspecification and aggregation.
Other Problems with Ecologic Analysis
To compare the results of ecologic studies with the
results of nonecologic studies dealing with the same hypoth-
esized relationship. we must consider the relative accuracy
of our measurementsat each level. since errors in measure-
ment are an important source of bias in the estimation of
etfect.1 In certain situations. aggregate measurements mar
be more accurate than individual measurements. especially
if the phenomenon being measured involves a sensitive
issue. For example. sales or tax record s mar provide a better
estimate of alcohol consumption for an area than asking
AJPH December 1982. Vol. 72. No. 12
USE OF ECOLOGIC ANAL YSIS
TABLE 4-Summary of Results for the Three Analyses, Uslng
the Hypothetical Data in Tabie 3
individuals in that area about their drinking habits. On the
other hand. aggregate measurements mar be less accurate
than individual measurements, especially when the former
are based on small samples within each group. For example.
errors in the measurement of serum cholesterol are likely to
be more extensive at the ecologic level than at the individuitl
level. Thus, we mar conclude that inconsistencies between
the results of ecologic and nonecologic studies mar be due.
at least in part, to differences in the relative accuritcy of
measurements.
Another type of bias that can occur in many types of
observational studies is a reversal of the hypothesized cause
and elfect, i.e., the observed association is due to the direct
or indirect inf1uenceof the disease on exposure status. What
makesecologic studies particularly vulnerable to this error is
that it can occur with prevalence. mortality, or even inci-
dence data. Suppose. for example. we were to observe an
ecologic relationship between the decreasing prevalence of
oral contraceptive (OC) use and the increasing incidence ratt:
of benign breast disease in a population. It is possible that
this inverse association is due to the prescribed termination
of OC use following disease detection. Researchers must use
their knowledge of disease. clinical practice. and human
behavior to rule out this alternative explanation for ecologic
associations involving observational data.
Another problem with ecologic analysis is that certain
predictor variables (especially sociodemographic and envi-
ronmental variables) tend to be more highly correlated with
each other than they are at the individuallevel, 'Ma phenome-
non called multicolinearíty. Consequently, the increased
correlations between these Xs make it particularly difficult
to isolate their etfects on the disease in an ecologic analys;s.
For example. with the water basin area as the unit of
analysis. it is most difficult to separate the etfects of tJilferent
trace elements in water supplies on cancer mortality .I~
Becauseaverage trace element levels are so highly intercor-
related. an estimate of the elfect of one exposure. controlling
for the others, will be very imprecise (or equivalently, the
statistical test of the null hypothesis will be inefficient). In
general. multicolinearity is most problematic for ecologic
studies involving geographically defined units of analysis
that are large and/or few in number .1".2()
1341
MORGENSTERN
Minimizing rhe Problems
Bias and multicolinearity may seriously limit our ability
to test an etiologic hypothesis with ecologic data. Yet there
are a few things that we can do to minimize these problems.
First, as done in the previous illustrations, we should use
ecologic regression-not correlation-to estimate the magni-
tude of the desired association. Although grouping by x does
not result in any aggregation bias of the regression coeffi.
cient (if X is in the model), it does increase the variance of X
relative to the variance of Y. Therefore, the absolute value
of the correlation coefficient will also increase.M,'M,20In other
words, in the situation where groups tend to be homoge-
neous with respect to one of the independent variables,
ecologic regression coefficients, but not ecologic correlation
coefficients, will result in unbiased estimates of their corre-
sponding individual measures. Since grouping by x is very
common in ecologic studies involving geographically defined
groups, the independent variables in an ecologic model mar
easily explain 75 per cent or more of the variance of Y. This
finding does not necessarily indicate that the included varia-
bles are the most important determinants of the disease; it
mar only indicate that, as a result of the grouping process,
we have controlled for the elTects of other important risk
factors.
The second way to minimize inferential problems in
ecologic studies is to make the groups as homogeneous as
possible by using smaller units of analysis, e.g., counties
instead of states, and more groups.'6,21 In theory, this
strategy amounts to grouping by x, thereby ensuring a valid
and more precise estima'te of effect. Unfortunately, this
option is not often feasible because of the limited availability
of data. In addition, grouping on one x included in the model
is likely to create grouping unintentionalIy on another risk
factor not included in the modelo This situation could pro-
duce the opposite effect of what is intended: aggregation bias
might increase.8 By using smalIer groups, the investigator
mar also increase the distorting effects of migration between
regions. This problem is most serious for individual ex po-
sures or diseases that often lead to migration, e.g., asthma-
!ics moving to a drier climate. Furthermore, the use of
smaller units of analysis tends to make the estimates of
disease frequency for groups less stable, which mar become
a serious limitation, since most diseases are "rare" events.
Unstable rate estimates for smalIer groups mar contribute to
less accurate eslimates of effect, if we cannot also increase
the number of groups.
A third way to minimize the problems of ecologic
inference is to assess how our groups were, in fact, formed
and analyze the data accordingly.8 If subjects tend to be
grouped by disease status, ecologic estimates of effect will
be more biased than the corresponding estimates in an
individual analysis. The researcher can, however, eliminate
lhis aggregation bias analyticalIy for ecologic models involv-
ing one or two independent variables. The method, proposed
by Leo Goodman,"is based on a reversal ofindependent and
dependent variables (X is regressed on Y).
Alternatively, we mar believe that subjects are grouped
on a risk factor that is excluded from the ecologic model
1342
(because it has not been measured) or that subjects are
grouped on a correlale of an excluded risk factor. In this
situation. we should include in the model all variables
thought to be related to the grouping process, even if these
variables are not risk factors for the disease.1
The findings of an ecologic analysis can be compared
with the findings of olher observational sludies designed to
test lhe same eliologic hypothesis. If the eslimaled etfect is
consislent across studies involving different designs and
differenl populalions, a causal interprelation is enhanced.
For example. the results of two case-control studies 22.23
linking number of pregnancies to ovarian cancer are consist-
ent with the results of ecologic analyses linking observed
changes in these two vari~bles.2' On the other hand, the
negative ecologic association reported earlier belween water
hardness and CVD mortalityl3 is not consistent with the
results of a case-control study2' and a cohort (mortality)
sludy ,26bOlh of which failed to find a significant association
in lhe hypothesized direclion. Unfortunalely. it is not possi-
ble to determine from lhese results alone lhe extent lo which
lhe ditference in observed effects is due to aggregation bias.
specification bias. other sources of bias. or sampling error.
Therefore. we cannot say which finding is most accurale.
Evaluation o/ lnterventions
In addition to generating and testing etiologic hypothe-
sesoecologic analyses can be used to evaluate the effectiyt'-
ness of population interventions.27Aggregation bias and the
ecological fallacy are moot issues in a population interven-
tion study. if the link between a modifiable risk factor and
the disease has already been established and if modification
of the risk factor can favorably affect disease outcome. i.e..
the treatment is efficacious. In this situation. we do not wish
to make inferences about individuals but about groups-i.e..
we are chiefty concerned with the impact of collective action
on disease rates.U':? An ecologic study in this setting is not
merely an inferior substitute for a nonecologic study; in Cacto
ecologic analysis is preferred for evaluating the effectiveness
of a population intervention. For example. we might assess
the impact of a high blood pressure control program on the
rete of hypertensive-related mortality in a target population.
Many population interventions do not involve direct
manipulation of a risk factor; they involve some collective
action aimed at changing the targeted exp~sure. This feature
applies to all kinds of intervention strategies. including
persuasion or educational approaches. financial incentives
or barriers. and regulatory or legal sanctions. For example.
in the past several years. several states and local jurisdic-
tions have passedlaws requiring smoke detectors in all new.
and sometimes existing. dwelling units.30We might test the
effectiveness of this legislation with a mixed ecologic designo
comparing changes in fire-related death rates during the past
lO years in states or localities with and without such
laws.*** The researchobjective is not to test whether smoke
***This design is based on an unpublished research protocol by
Cyndie B. Gareleck from the Vale Department of Epidemiology and
Public Health.
AJPH Oecember 1982. Vol. 72. No. 12

detectors can indicate the presence of smoke:':-we know
they can. Instead. we want to assess the cumulative impact
of several related factors that determine the success or
failure of the legislation: whether the laws are enforced;
whether the detectors are installed correctly; whether they
are operated and maintained properly by the residents; ando
ultimately. whether they prevent injuries and deaths from
tires. Moreover. the impact of smoke detector laws on tire-
related deaths could not be assessed adequately at the
individual level, because a smoke detector in one unit can
prevent deaths in nearby units or buildings that are them-
selves unprotected.
Another relative advantage of ecologic analysis for
evaluation is that population interventions often have unin-
tended consequences that are not likely to be spotted by
studies conducted at the individuallevel. For example. in an
ecologic comparison study of high school driver education
and motor vehicle fatalities involving teenage drivers. by
state. Robertson and Zador' found no significant associa-
tion between driver education and the cate of fatal crash
involvement among licensed teenagedrivers. However. they
did find that driver education was associated with a substan-
tial increase in the number of licensed teenage drivers. The
net effect was a higher fatal crash involvement cate among all
16-17 year-olds in states with greater proportions of teen-
agers receiving driver education. In other words. given the
current licensure laws for young drivers. the end result uf
publicly funded driver education programs mar be to in-
crease the motor vehicle fatality rate in the population by
increasing the number of licensed teenage drivers.
Summary
This paper has reviewed four types of ecologic study
designs and the analytic methods appropriate for each. In
many ecologic studies. we can estimate the same parameters
that are estimable at the individuallevel for quantifying the
magnitude of the association between the exposure and the
disease. Despite the practical advantagesof ecologic data for
generating and testing etiologic hypotheses. causal inference
about individual events from grouped data is limited by
certain methodological problems. including specification
bias. aggregation Bias, measurement error, ambiguity of
cause and elfect, migration between groups, and multicolin-
earity. To minimize these problems, the researcher can: 1)
use ecologic regression, instead of correlation, including in
the statistical model as many risk factors as possible; 2) use
data that are grouped into the smallest geographic units of
analysis as possible, subject tothe constraints of intergroup
migration and unstable rate estimation; and 3) attempt to
ascertain how the groups were formed and analyze accord-
ingly, which ordinarily means including in the model all
variables thought to be related to the grouping process.
In addition to testing etiologic hypotheses, ecologic
analyses Can also be used to evaluate population interven-
tions. Given adequate knowledge of disease etiology, eco-
logic studies are particularly appropriate for assessing the
impact of collective actions on disease rates and for spotting
AJPH December 1982, Vol. 72, No. 12
USE OFECOLOGIC ANALYSIS
unintended consequences of population intervention~. AI-
though a single ecologic study may be designed to achieve
etiologic and evaluative objectives. the scope of an ecologic
analysis. to be most informative. should be more focused-
either it sheds some new light on our understanding af
disease occurrence. or it test~ the application of our knawl-
edge to controlling the disease in society. Failure to recog-
nize the difference in principIes between etiologic and evalu-
ative research can lead to ecologic results that are not very
informative or that are misunderstood by others.
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MORGENSTERN

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ACKNOWLEDGMENTS
[ would like to thank Dr. Doug Thompson of Ya le University
for his helpful suggestions. An earlier version of this paper wa~
presented at the l09th Annual Meeting of the American Public
Health Association. Los Angeles. CA. November 1-5. 1981. This
work
Grant was
No. supported
5 D04 AH by US Public Health' Service Special Project
0[759-3.

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1344