Evidence for Errors in Statutory Risk Estimates.
Chris Busby, PhD
Molly Scott Cato, MSc
Aberystwyth, Wales: Green Audit.
Occasional Papers No 98/2; June 1998
Applying ICRP's risk factors to known levels of contamination
Abstract [as published in Energy and Environment]
In an earlier study [1], national statistics were used to show that there had been
increased incidence of leukemia and childhood cancer in the 0-4 age group in both Wales
and Scotland. It was not clear, however that these increases were entirely ascribable to
the effect of Chernobyl, since there was a possible confounding effect in that the birth
cohorts involved were also children of parents who themselves had been exposed at birth
to the weapons testing fallout of the period 1959-65. This above-ground nuclear weapons testing
fallout was associated with increased infant mortality all over the world
[2],[3], including
Wales and Scotland [4]. If this effect was a measure of genetic damage,
then the children
of parents born in this period, would be at higher risk of cancer and leukemia because of
their increased mutation burden.
In order to extend the earlier work, and look more closely at the effect of
Chernobyl this study analyses the trend in incidence of leukemia in the age group 0-1 so
that immediate pre-conception and in utero exposure might be examined.
2. Method
Annual incidence data for all leukemias in the age group 0-1 were obtained from the
Wales Cancer Intelligence Unit or the Information and Statistics Division of the Scottish
Health Services. Population data were obtained from the Welsh Office or Scottish
Office. For comparison purposes the unexposed controls were defined as two groups,
first those aged 0-1 years between 1975 and 1985 and second those aged 0-1 between
1989 and 1991. The exposed birth cohort was taken to be those aged 0-1 in the 18
months between January 1st 1987 and June 30th 1988. Conception in these infants
occurred between April 1st 1985 and September 31st 1987 and most of them will have
been exposed in utero to radioactive isotopes from Chernobyl. We extend the period to
eighteen months because whole body measurements of radioCaesium in humans in the
UK [5] showed that the body content peaked in July 1987 (See Figure 1)
and therefore an
in utero effect from this exposure might be manifest up to April 1988 or later.
The risk
factors used for calculating expected leukemia yields are those adopted by the National
Radiological Protection Board in their various publications, most particularly those used
to assess the risk of childhood leukemia near the Sellafield plant in West Cumbria,
namely, .0065 per Sievert for children age 0-10, 0.0125 for in utero exposure and 0.004
for heritable genetic damage. [6]
These risk factors are broadly similar to those published by the International Commission
on Radiological Protection [7] and the BEIR V committee
[8].
Figure 1
Whole body content of Caesium-137 + Caesium-134 measured in the two
years following Chernobyl. (source: Etherington and Dorrian [5])
3. Exposure Dose Equivalents and Expected Leukemia Increases following
Chernobyl
a = estimate of dose to fathers' testes over pre-conception period
The numbers of recorded cases of infant leukemia in Wales and Scotland over the
period 1975 to 1992 are given in Table 2. In Table 3 we collect together the numbers of
cases, calculated relative risks and Poisson Distribution cumulative probability values
based on the Group 1 1975-85 ten year pre- Chernobyl unexposed populations as
controls. The expected values used in Table 3 were obtained by assuming the average
rate for the control period applied to the exposure period.
Table 2
a = In the period 1st Jan. 1987 to 30th Oct. 1988 there were three cases in Wales and nine
in Scotland.
5. Discussion
Following Chernobyl there have been a number of attempts to examine whether
the incidence of leukemia in children has increased in countries affected by the fallout.
Published studies of trends in leukemia rates in the age group 0-14 in Belarus, Finland
and Sweden, countries badly affected by the pollution reported no significant increases
after April 1986 [11],(12,13). On the other hand, increases in
childhood leukemia have
been reported for parts of Belarus by Savchenko [14]
and others [15]. A
very large study by Parkin et al. [16] on behalf of the World Health Organization examined
the whole of Europe and pooled data from over 20 cancer registries. The latest report of
this group found no significant
step change in childhood leukemia after Chernobyl either in the 0-4 or the 0-14 age
groups. Parkin et al. concluded that the risk factors presently used to predict the effects
of low levels of ionizing
radiation were broadly correct and that the changes in incidence resulting from the
Chernobyl pollution would have been too small to measure, and indeed no increase was
found.
A criticism of the Parkin et al. study is that it involved
a very large number of
different countries each with different populations with different susceptibilities to
leukemia and with a very wide range of exposures to individuals. Since the lag between
exposure and expression is a function of dose (8) it would be predicted
that there might
only be a general average increase throughout the period, an effect which the group
found.
Two earlier studies of Scotland and Wales and Scotland and found modest but
significant increases in leukemia in the 0-4 age group. Gibson et al. 1988
[17]
drew attention to a sharp increase in leukemia in the 0-1 age group in Scotland in 1987 and
Busby, 1996 (18) compared the pre and post Chernobyl cases to show
a significant but
modest increase in Wales in Lymphoid leukemia in the 0-4 age group.
In 1996, Petridou et al. [19] reported a significant ( P = 0.003)
2.6-fold increase in
infant leukemia in Greece, a country where the average Chernobyl exposure dose was
about 2000µSv. Petridou et al.
compared an exposed group born between July 1986 and January 1988 with an
unexposed group born between 1980 and 1986. The total number of infant leukemias in
his exposed group was 12 compared with 22 in their unexposed control. Although they
argued that their results showed an exclusive in utero cause, it is not at all clear how they
came to this conclusion since their exposed period covered eighteen months. Moreover,
almost half of their birth cohort would have received no radiation from Chernobyl in the
first trimester, a period known to be sensitive to radiation damage.
In 1997, Mangano examined the United States for a similar effect
[20] and
demonstrated that even at the low doses involved at this remote distance from Chernobyl,
probably less than 10µSv, there was a
modest increase in infant leukemia of 30% (RR =1.3 P < 0.09). Mangano compared the
birth cohort 1986-87, which he considered exposed to an unexposed cohort which was an
aggregate of 1980-85 and 1988-90.
The results reported here by us show a clear effect with high relative risk values in
the range 3 to 4.4 and a very high degree of statistical significance. This finding supports
the earlier observations of Petridou and Mangano of increases in infant leukemia in two
other countries and show that the effect of the Chernobyl fallout in Wales and Scotland
were significant. The usefulness of the UK data is that good
estimates of the average exposure were available based on many measurements of fallout
isotopes in the air, on the ground, in food, milk and water. It is therefore possible to
examine the accuracy of the presently accepted risk factors for radiogenic leukemia. The
application of these risk factors to the populations of Wales and Scotland predict no
measurable effect.
From Table 1 we see that the fallout exposure to the combined Welsh
and Scottish population of 88 to 110µSv predicts between 0.11 and 0.136 leukemia cases
compared with 12 observed. This shows an error in these risk factors of between 09-fold
and 88-fold respectively. Use of the in utero risk factor of 0.0125 reduces the error to
between 55 and 44-fold but the real number may be much higher since we only have the
0-1 year fraction of the total 70 year prediction. If the cause were pre-conception
exposure to the fathers then the risk-factors for heritable damage of 0.004 may be used
to calculate an error of upwards of 2000-fold.
The NRPB risk factors and those of the other international risk agencies like the
International Commission on Radiation Protection (ICRP), the United Nations Scientific
Committee on the Effects of Atomic Radiation (UNSCEAR) and the Biological Effects
of Ionizing Radiation (BEIR) sub-committee of the US National Academy of Science all
publish broadly similar analyses of leukemia and cancer risk from radiation. These risk
models are almost exclusively based on external acute radiation exposure and have based
their risk factors on the study of the cancer and leukemia yield in the survivors of the
Hiroshima bomb. This model cannot address risk from internal exposure to ingested and
incorporated radionuclides since both the study group and the controls were similarly
contaminated.
Table 3
Relative risk of leukemia in infants born in 1987 and 1988 in Wales and
Scotland and exposed to Chernobyl fallout compared with group born in
the 11 year period 1975-86. Also shown is the risk in the unexposed
group born between 1989 and 1991.
II
Scotland
III Wales and Scotland combined
a Based on the unexposed group (I)
In the last twenty years, and increasingly since the Chernobyl accident, a
significant number of epidemiological and theoretical studies have called into question the accuracy of applying
these external radiation based models to the effects of internal irradiation. Internal irradiation involves
exposure to substances like Plutonium-239 or Strontium-90 which never existed on earth over the period of
evolution and which mimic natural elements. Furthermore the decay scheme of many of these novel
radioisotopes involve sequential disintegrations which have a finite probability of causing sub-lethal cell
damage andsetting up a repair replication cycle. Cells in such a repair replication cycle are hundreds
of times more susceptible to radiation killing and mutagenesis [21], (22)
the basis of cancer radiotherapy where rapidly dividing cells are selectively killed.
Lord et al. [24] have recently reported the induction of leukemia susceptibility in two
different strains of mice following injections of small doses of Plutonium-239 into the fathers fifteen weeks
prior to mating.
In earlier studies in the same series, Lord et al. have calculated effective Relative
Biological Effectiveness factors of several hundred for Plutonium induction of such genetic effects.
This can be seen as a confirmation of suggestions that the phenomenon on genomic instability can assign
'infinite biological effectiveness' to the internal decays from Plutonium-239 suggested in a report
from the Medical Research Council team at Harwell [25].
The main exposures from the Chernobyl pollution in Wales and Scotland were to the
short-lived Iodine-131 and Tellurium-132, and from longer lived Caesium-134 and 137. Tellurium-132 has a
sequentially decaying isotope through its daughter Iodine-132 and is theoretically capable of
inducing Second Event damage [18]. However, most of the Te-132 will have delivered its dose in the
first few weeks and if we approximate a fifteen week period of spermatogenesis in humans then leukemia
in the children would be expected in the birth cohorts from June 1987 to January 1988. This could
conceivably fit the finding of the peak in incidence in Wales occurring in the first half of 1988 since
we are dealing with the whole 0-1 age group at diagnosis. However, the exposure to Caesium-134 and
Caesium-137 would certainly have provided pre-conception irradiation from May 1986 up to mid 1987
(see Fig 1)owing to the use of Caesium contaminated silage cut in the Summer of 1986 as feed for cattle
in the winter of 1987. Without more accurate information on birth dates it is not possible to
distinguish the origin of the leukemia between in utero exposure or pre conception exposure to parents or
a combination.
Since leukemia is a genetic disease, it is of interest that there is some other relevant evidence of general genetic damage to the immediate post Chernobyl in utero irradiated cohort. This comes
from data on very low birth weight babies obtained from the Office of Population Census and Surveys
and reported as a Chernobyl effect in 1995 [21]. There was a significant increase in very low
birth weight babies (<1500g) born in Wales just after Chernobyl, peaking between January 1987 and January
1988.
Fig.2
Increased incidence of childhood leukemia has now been verified near most of the main sources of
radioisotopic pollution in Europe. This includes a ten-fold excess near Sellafield [26],
8-fold near Dounreay [27], fifteen fold near La Hague in France
[28], two fold near Harwell in Oxfordshire and also near the Atomic Weapons Establishment at Aldermaston in Berkshire
[29].
There is further support for the concern that the genetic effects of novel man-made radioisotopes like those in the
Chernobyl fallout and the releases from nuclear sites are much higher than presently modelled. These are the
reports of anomalous increases in human minisatellite mutation rates in children living in territories of
the ex-Soviet Union which were contaminated by the fallout [30].
This present observation of infant leukemia increases associated with a fairly well assessed exposure dose in two countries with good
quality cancer ascertainment and supported by similar observations elsewhere calls into question the risk
models and factors used to assess the cases of the leukemia clusters near sources of radiosiotopic
pollution and places a figure on the error involved in using external Hiroshima based epidemiology to consider
risk from internal exposure from novel radioisotopes. A reassessment of the hazard to health of such
exposure should be the subject of urgent research effort since the problem of risk from such pollution
carries important human health policy decision implications.
(1) C. C. Busby (1996), 'Cancer and leukemia in children born in Wales and Scotland after Chernobyl' ,
Occasional Papers 96/2, Aberystwyth: Green Audit
(2) R.K.Whyte (1992), 'First day neonatal mortality since 1935: a re- examination of the Cross
hypothesis', British Medical Journal, 304: 343-6
(3) E. J. Sternglass (1971), 'Environmental radioactivity and human health', in Proceedings of the Sixth
Berkeley Symposium on Mathematical Statistics and Probability, ed. J.Neyman (Berkeley, Calif.:
University of California Press).
(4) C. C. Busby (1994). Radiation and Cancer in Wales (Aberystwyth:Green Audit).
(5) G. Etherington and M. D. Dorrian (1991), `Radiocaesium levels, intakes, and consequent doses in a
group of adults living in Southern England'. International Atomic Energy Agency Document IAEA-SM-
306/29 (Vienna: IAEA).
(6) J. W. Stather, A. D. Wrixon, J. R. Simmonds (1984, 1986), The Risk of Leukemia and Other Cancers
in Seascale from Radiation Exposure.Document NRPB R-171 and addendum to R-171 (London: HMSO).
(7) International Commission on Radiological Protection (1992), 1990 Recommendations of the
International Commission on Radiological Protection (Oxford: Pergamon Press).
(8) Biological Effects of Ionizing Radiation Committee (BEIR) (1990), Health Effects of Exposure to
Low Levels of Ionizing Radiation, BEIR V (Washington: National Academy Press).
(9) D. M. Smith, G. McAllister, J. Gemill, D. Welham, S. MacLennan (1988), Environmental
Radioactivity Surveillance Programme: Results for the UK for 1985 and 1986. National Radiological
Protection Board (London: HMSO).
(10) D. M. Parkin , E. Cardis, E. Masuyer, et al. (1993), 'Childhood leukemia following the Chernobyl
accident: the European childhood leukemia lymphoma incidence study (ECLIS)', European Journal of
Cancer, 29A(1): 87-95.
(11) E. P. Ivanov, G. Tolochko, V. S. Lazarev, et al. (1993), 'Childhood leukemia after Chernobyl',
Nature, 365-702.
(12) A Auvinen, M. Hakama, H. Arvela, et al. (1994), 'Fallout from Chernobyl and
incidence of Childhood leukemia in Finland 1976-92', British Medical Journal, 309: 151-154.
(13) U. Hjalmars, M. Kulldorf, G. Gustaffson (1994), 'Risk of acute childhood leukemia in Sweden after
the Chernobyl reactor accident', British Medical Journal, 309: 154-157.
(14) V. K. Savchenko (1995), The Ecology of the Chernobyl Catastrophe (Paris: UNESCO).
(15) International Commission on Chernobyl (1996), Chenobyl: Environmental Health and Human
Rights Implications (Geneva: International Peace Bureau).
(16) D. M. Parkin, D. Clayton, R. J. Black et al. (1996), 'Childhood leukemia in Europe after Chernobyl:
5-year follow up', British Journal of Cancer, 73: 1006-1012.
(17) B. E. S. Gibson, O. B. Eden, A. Barrett, et al. (1988), 'Leukemia in young children in Scotland',
Lancet, 1988: 630.
(18) C. C. Busby (1996), contribution to The Health Effects of Low Level Radiation: Proceedings of a
Symposium Held at the House of Commons, Westminster, London, April 24th 1996, ed R.Bramhall
(Aberystwyth: Green Audit).
(19) E. Petridou, D. Trichopoulos, N. Dessypris, et al. (1996), 'Infant leukemia after in utero exposure to
radiation from Chernobyl,' Nature, 382: 352-353.
(20) J. Mangano (1997), 'Childhood leukemia in US may have risen due to fallout from Chernobyl',
British Medical Journal, 314: 1200.
(21) C. Busby (1995), Wings of Death: Nuclear Pollution and Human Health (Aberystwyth: Green
Audit).
(22) W. K. Sinclair and R. A. Morton (1966), 'X-ray sensitivity during the cell generation cycle of
cultured Chinese Hamster Ovary cells', Radiation Research, 29: 450-474.
(23) C. Mothersill and C. B. Seymour (1997), 'Lethal mutations and genomic instability (review)',
International Journal of Radiation Biology, 71: 751-758.
(24) B. I. Lord, L. B. Woolford, L. Wang, et al. (1998), 'Tumour induction by methyl nitroso urea following preconceptional paternal contamination with plutonium-239', British Journal of Cancer, June
issue: in press.
(25) E. G. Wright, S. J. Marsden, S. A. Lorimore, et al. (1994), 'Alpha emitters inducing lesions in stem cells that can result in the transmission of chromosome instability to their progeny', Nature, 335: 6362.
(26) M. J. Gardner, A. J. Hall, M. P. Snee, et al. (1990), 'Methods and basic data of case-control study of leukemia and lymphoma among young people near Sellafield nuclear plant in West Cumbria', British Medical Journal, 300: 29-34.
(27) M. A. Heasman, I. W. Kemp, J. D. Urquhart, and R. Black (1986), `Childhood leukemia in northern Scotland', Lancet, 1986;i: 266.
(28) J.-F. Viel, D. Poubel, and A. Carre (1996), `Incidence of leukemia in young people and the La Hague nuclear waste reprocessing plant: a sensitivity analysis', Statistics in Medicine, 14: 2459-2472.
(29) C. C. Busby and M. Scott Cato (1997) `Death rates from leukemia are higher than expected in areas around nuclear sites in Berkshire and Oxfordshire', British Medical Journal, 315: 309.
(30) A.J.Jeffreys, Y.E.Dubrova, V.N.Nesterov et al (1996) 'Human minisatellite mutation rate after Chernobyl,' Nature 380, 683-6
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and now published in
Energy and Environment Vol. 11 2000, No. 2 127-139
from Chernobyl reveals 100 times less infant leukaemia than actually found.
Sharp increases in infant leukaemia after Chernobyl
have been observed in five countries.
NRPB's head-in-the-sand response (January 2001)
is on this site, with analysis.
After the Chernobyl reactor accident in April 1986, rainfall precipitation caused measurable radioactive contamination of Wales and Scotland. Using risk models developed by themselves and by the International Commission on Radiological Protection, the UK National Radiological Protection Board advised that no measurable increase in leukaemia was predicted at exposures which they estimated from measurements of contamination. However, cancer registry data from both the Wales and Scotland registries show a sharp increase in cases of infant leukaemia age 0-1 in the eighteen month period January 1st 1987 to June 30th 1988. This period is that in which the birth cohort who were in utero in the exposure period following the fallout would be in the age group 0-1. Compared with an "unexposed group" consisting of the period 1975 to 1986 the Wales exposed group had a relative risk (RR) of 4.4 (p=0.004), the Scotland group a RR of 3.7 (p=0.001) and the combined Wales and Scotland group a RR of 3.87 (p=0.0001). A second unexposed group, those aged 0-1 in 1989-91 had no significant increased risk although after 1991 rates increased slightly. This finding supports earlier reports of infant leukaemia effects in Greece, Germany and the U.S. following Chernobyl. The data cannot entirely distinguish between pre-conception or in utero effects but also reported here are increases in very low birthweight births in Wales following Chernobyl, suggesting a genetic component to both effects. The existence of good quality leukaemia and exposure data makes it possible to calculate an error in the presently accepted risk factors for radiation induced leukaemia of about 100-fold or more. The possibility of errors of this magnitude in the contemporary risk estimates of ionising radiation effects suggests that a more cautious approach should be exercised to policy decisions about nuclear power options.
1. Introduction
The explosion at the Chernobyl power station in the Ukraine on 26th April 1986 caused a
release of fission-product radioisotopes to the atmosphere. As a consequence of the
weather prevailing at the time, various quantities of radioactive pollutants from the
release became dispersed as far as the United States. Between 3rd and 5th May, the
radioactive cloud reached the UK and thundery rain caused deposition in parts of Wales,
Scotland, Cumbria and the Yorkshire moors. The National Radiological Protection
Board (NRPB) advised that the levels of exposure were too low to have any measurable
effect on health, and government advice was that food was safe to eat and water and milk
safe to drink. Upland areas of Wales and Cumbria became contaminated and seven
weeks after the event, sheep restrictions were imposed. Many areas of North Wales still
have such restrictions.
The NRPB calculated the 1986 exposure dose equivalent to be
88 µSv [9].
The World Health Organization has given the one-year exposure at 110 µSv.
[10]
The predicted leukaemia yield in the population of infants age 0-1 in Wales is given in Table
1 below.
Risk Factor (/Sv)
1 year exposure (µSv)
Predicted Leukemia yield (cases)b Scotland (pop. 66,100)
Predicted Leukemia yield (cases)b Wales (pop. 38,300)
0.0125 (in utero)
88
1100.07
0.0860.04
0.05
0.0065(age 0 - 10)
88
1100.038
0.0470.022
0.027
0.004 (heritable
damage)
10a
0.0026
0.0015
b = over lifetime of person exposed
4. Observed increases in infant leukemia in Wales and Scotland, 1975-1992
Infant leukaemia (ages 0 - 1) in Scotland and Wales 1975 - 91 (Source Wales Cancer
Intelligence and Surveillance Unit; Scottish Health Services Information and Statistics Office)
Year
Scotland
Wales
1975
1
0
1976
3
0
1977
1
2
1978
2
0
1979
0
0
1980
2
0
1981
4
0
1982
0
1
1983
1
0
1984
3
0
1985
1
1
1986
0
1
a 1987
6
0
a 1988
4
4
1989
2
1
1990
2
1
1991
0
1
I Wales
Group
Observed Cases
Expected Cases
aO/E (Relative Risk: RR)
bCumulative Poisson P
Unexposed (I) 1975 - 86
5
-
1.0
-
Exposed Jan. 1987 to Jun. 1988
3
0.675
4.4**
0.004
1988 alone
4
0.45
8.9**
0.002
1987 and 88
4
0.9
4.5**
0.0135
Unexposed (II)
1989 - 913
1.36
2.2
0.143
Group
Observed Cases
Expected Cases
aO/E (Relative Risk: RR)
bCumulative Poisson P
Unexposed (I) 1975 - 86
18
-
1.0
-
Exposed Jan. 1987 to Jun. 1988
9
2.46
3.7***
0.001
1987 and 88
10
3.28
3.05**
0.002
Unexposed (II)
1989 - 914
4.9
0.8
0.566
Group
Observed Cases
Expected Cases
aO/E (Relative Risk: RR)
bCumulative Poisson P
Unexposed (I) 1975 - 86
23
-
1.0
-
Exposed Jan. 1987 to Jun. 1988
12
3.1
3.87***
0.0001
1987 and 88
14
4.18
3.34***
0.0001
Unexposed (II)
1989 - 917
6.27
1.1
0.47
b Probability assuming a Poisson distribution that the number of observed cases or more than
that number
might occur by chance.
c Significant at the 0.05 level*, the 0.01 level** and the 0.001 level***
Furthermore, the largely physics based radiation exposure models were originally devised
before the
biology of the cell and its complex responses to radiation damage, particularly the repair
and replication
cycle, were discovered. Indeed, many of the linear averaging models still used to predict
radiation action
on cells were devised before the discovery of DNA structure and function.
In the last ten years, interest has focussed on the discovery of radiation induced genomic
instability [23]. It turns out that small doses of ionizing radiation
causes invisible damage to cells which manifests itself in the cell descendants as chromosome instability resulting from a wide range
of different mutations. This work was developed using cell cultures but very recent work has extended it to
animals.
The trend is shown in Figure 2. Monthly data we have obtained from OPCS shows that the peak
months for the birth effect were October November and December 1987 and January 1988. Infant
mortality following radiation exposure from weapons fallout in the period 1959-1963 is well documented
and the effects of internal exposure to radioisotopes on foetal development have been reviewed in
Busby 1995[21].
Trend in very low birth weight babies (<1500g) in Wales over period of
Chernobyl.
Births per 1000 live births (Source: OPCS)
References
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