Læknablaðið - 01.12.1978, Blaðsíða 69

LÆKNABLAÐIÐ
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was much increased. All histologic sub-
types were seen throughout the whole
period.
Menwhile, Correa and O’Conor,4 utilising
data from Volume I of „Cancer in Five
Continents" had shown that there were at
least three distinct types of epidemiologic
patterns of H.D., the differences lying
principally in the proportion of cases in
childhood. They showed that there was a
reciprocal difference between the child-
hocd peak and the young adult peak. They
showed that socio-economic factors ac-
counted for this and clearly with increasing
affluence, the impact of H.D. shifts from
childhood to young adult life; intermediate
patterns exist as might be expected. This
change with affluence seems very im-
portant because it is shared by no other
childhood cancer. But there are close
parallels in the field of infectious disease
and this made it work considering the
school situations in more detail.
Vianna and Polan had much basic in-
formation to hand from Nassau-Suffolk
where we only had to update and extend
our records of persons under 40 years,
considering only the public but not the
parochial and private schools."’152 Two
methods were used, firstly two sequential
quinquennial periods were compared for
schools with and without H.D. cases. We
found that schools that had cases in the
previous quinquennium almost always had
cases in the second quinquennium, while
only a few cases occurred in school with
no cases in the first quinquennium. In
subsequent criticism of these findings, it
was suggested because we found an annual
incidence rate of only 1.9 per 100.000 per
annum we must have missed cases of H.D.
and that this might explain these find-
ings.:i0 We do not believe cases were missed
to any great extent but that if they were,
that this might negate this finding is ad-
mitted. But it is impossible to believe that
missing cases could affect the other find-
ings using the index-secondary case ap-
proach. Follow up for a decade of all
students in the schools after the index
case had been recognised enabled the
person/years at risk of the school popu-
lation to be calculated and applying the
New York State rates for age we could
obtain rates or alternatively observed to
expected ratios for students; for teachers
an overall rate rather than a specific age
rate had to be applied. The rates and the
ratios both for students and teachers were
remarkably and significantly high and any
missing cases would only raise these rates
far higher. Though indeed we know that
in one school at least there have subse-
quently been cases which would increase
both rates and ratios.54 These findings have
essentially been confirmed in Connecticut
schools.59
Other interesting aspects of this study
were the infrequency of cases in ele-
mentary schools and that the incidence
rates varied significantly with school size.
Thus in schools with less than 1500
students in toto the rates were 5.3/100.000
per annum while with schools of greater
size the rates were 23.8/100.000 per annum.
Moreover, the mean interval in diagnosis
between cases in those school with an
index and at least one secondary case was
3.8 years with a median of 3 years, figures
very close to those found in the Albany
epidemic. This also was very close to thaí
found in our survey of familial cases of
H.D. in New York State.53 These included
family members living in the same house
and those who lived apart. In the latter,
the diagnostic interval was 3.4 years (Mean
4.1, Range 08—8.7 years) whereas for
those living in the same house the interval
was 1 year (Mean 1.2, Range 0.2—2 years),
surely a significant finding. We also found
some other interesting things in this survey
in which familial cases were selected via
the New York State Cancer Bureau to
avoid bias.
We found 23 familial pairs, 46 cases in
all. Following the suggestion of MacMahon
of Harvard30 that if with sib pairs, of
which we had 7, that if the diagnostic
interval was significantly shorter than the
differences between the ages at diagnosis,
this pointed to the likelihood that it was
an environmentally determined disease
rather than a genetic one. Criticism31 was
directed to this suggestion of MacMahons