"Asleep at the Wheel": The Special Menace of
Inherited Afflictions from Ionizing Radiation. Fall 1998.
John W. Gofman, M.D., Ph.D., Professor Emeritus of
Molecular & Cell Biology, University of California at Berkeley, and
Egan O'Connor, Executive Director, CNR.
- Part 1 — "Asleep at the Wheel" due to a "Famous Failure"
- Part 2 — Dramatic Difference between Two Concepts
- Part 3 — Which Afflictions Are Irregularly Inherited?
- Part 4 — The Build-Up of Mutations during 1,000+ Years
- Part 5 — Inherent Limits of the A-Bomb Genetics Program
- Part 6 — Only 8 Inherited Effects Covered by Bomb Study
- Part 7 — "Fragile" Foundation Acknowledged by Neel and Colleagues
- Part 8 — The Health-Menace of a False Perception
- Part 9 — Why "The Radiation Concept" Is So Credible
- Part 10 — Can Natural Radiation Explain the Mutation Rate?
- Part 11 — The Specific Evidence from Low-Dose Radiation
- Part 12 — Is the Evidence "Screaming" at Humanity?
Part 1 "Asleep at the Wheel" due to a "Famous Failure"
topic which consumes Parts 5,
6, 7 of this
article is the famous failure to detect (at a statistically
significant level) any extra frequency of inherited
afflictions, in the Japanese children of the Atomic Bomb
main importance of the "famous failure" has
been its power to render much of the environmental and medical
communities "asleep at the wheel," with respect to the menace
of inherited afflictions caused by ionizing radiation. Some
environmentalists even talk about "giving nuclear power a
second chance." And some people in medicine are so relaxed,
about low-dose radiation, that their customers have to fight
in order to obtain shielding of their ovaries and testes from
suspect that hardly one-percent of
environmentalists and medical professionals know (a) that
when the A-Bomb Genetics Program was initiated, it was already
acknowledged that, in all probability, it would be inherently
incapable of producing statistically significant results (see
Para.5b), and (b) that very few
inherited effects were even explored in that Program (see
Part 6). One purpose of this
article is to document statements (a) and (b).
other purpose of this article is to set forth
a scientifically credible warning that ionizing radiation is
probably the single most menacing mutagen to which people
everywhere are exposed --- and by itself is probably the
mutagen which accounts for one-quarter or more of humanity's
inherited afflictions (Para.2b). This
warning is tied to three types of relevant human evidence (Parts
Part 2 Dramatic Difference between Two Concepts
renowned British biologist, J.B.S. Haldane, suggested in
1948 that perpetual exposure to natural background radiation
might account for most of humanity's accumulated burden of
inherited afflictions (Haldane 1955,
p.115). The great bulk of such afflictions are in the
class called "Irregularly Inherited Disorders"
reality-check, on evidence accumulated since
1955, suggests that the share due to natural background
radiation is very probably 25% or more --- maybe as high as
50%. So, it is time to consider the following scientifically
credible proposition: Natural background radiation is the
mutagen which accounts for 25% or more of those cases of
Irregularly Inherited Afflictions which occur because of
inherited predisposition. For brevity in this article, we
can refer to the proposition as "The Radiation Concept" (The
Radiation Concept of Irregularly Inherited Afflictions).
Radiation Concept" differs dramatically from
a notion which became the operative concept during the "Atoms
for Peace" program --- namely, that it would be
inconsequential if nuclear pollution were to double the dose
from natural background radiation. This operative notion is
embedded in such numbers as a "permissible annual radiation
dose" of 0.1 rad (100 milli-rads), and it is the premise of
current discussions which refer to 0.1 rad per year as a dose
too small to bother about at all (for instance, see
Billen 1990 and Health
Physics 1996). We and others call this "The
De Minimis Concept.
Radiation Concept" can neither be validated
nor invalidated by the A-Bomb Genetics Program --- as we will
explain --- but three other types of evidence make it a very
credible warning, scientifically (Part 9).
Part 3 Which Afflictions Are Irregularly Inherited?
afflictions and inherited mutations are
not the same thing, of course. Mutations are a cause,
afflictions are a result. Many different kinds of mutations
may result in the same affliction.
mutations can be loosely divided by
their consequences: (1) Those which confer a certainty of
some affliction (for instance, a malformed heart, a mental
handicap, or a disease like hemophilia), (2) those which
confer an elevated chance of negative consequences --- a
predisposition, vulnerability, susceptibility, (3) those which
are biologically inconsequential, and (4) those which are
beneficial. With respect to group (4), the BEIR Committee of
the National Research Council has stated the "general wisdom"
in this field: "It must be emphasized again that virtually
all mutations have harmful effects" (BEIR
(2), above, is the key to a vast group of
afflictions --- from mild to devastating --- called
"Irregularly Inherited Disorders" (also called, "Disorders of
are some of the Irregularly Inherited
Afflictions? They range from dyslexia to Alzheimer's Disease.
By 1990, the BEIR Committee included the following afflictions
as an illustrative selection of Irregularly Inherited
Disorders (BEIR 1990, p.70, p.89):
disease, cancer, diabetes mellitus,
schizophrenic psychoses, affective psychoses (uni-polar and
bi-polar), multiple sclerosis, epilepsy, glaucoma, asthma,
psoriasis, rheumatoid arthritis, Grave's disease, gout,
allergic rhinitis, idiopathic procto-colitis, gallstones, and
mineral deposits in the kidneys. There are many, many more.
The Irregularly Inherited Disorders are so common that every
person is thought to have at least one (BEIR
1990, p.70). Logic insists that inherited predisposing
mutations create problems in every major system: immune, endocrine,
reproductive, nervous, respiratory, digestive, urinary ...
one yet knows (a) what share of cases of the
Irregularly Inherited Afflictions occurs because of
predisposing inherited mutations and (b) what share of cases
of the same afflictions would happen "anyway." Estimates of
(a) have been 50% or lower, in reports sponsored by the
government (history in BEIR 1990 +
NRC 1991). We predict that
nearly all cases require some predisposing mutations (Gofman
1994, Chapter 7, Part 2). However, "The Radiation Concept" is
independent of that prediction. Whatever the share turns out
to be, "The Radiation Concept" (Para.2b)
says that 25% or more of such cases are the result of humanity's
perpetual exposure to natural background radiation.
when we speak of Irregularly Inherited
Afflictions, we mean all the cases which occur because of an
inherited predisposition and not cases which would have
occurred "anyway" under the same circumstances.
Part 4 The Build-Up of Mutations during 1,000+ Years
definition, an inherited mutation is present in
every cell of an offspring's body --- including the
lymphocytes circulating in the blood. Some inherited
mutations are so harmful that the recipient always dies before
ever having any children. Because such mutations can not be
passed along to the next generation, they never accumulate in
the population. By contrast, most inherited mutations never
cause early death, and so they can be passed along to the next
generation. These are the mutations which accumulate in a
population. People inherit so many mutations that it is an
enormous task (now in its early stages) to figure out which
inherited mutations produce harmful consequences and which
ones are biologically inconsequential (Para.3b).
an offspring inherits a particular mutation,
and the same mutation is not found in the lymphocytes of one
of the parents, it means that the mutation occurred newly in a
germ cell of a parent who did not inherit it from his or her
ancestors. (Germ cells are the precursors of "eggs" and
sperm.) Such a mutation in the offspring is called a "de
novo" mutation. By contrast, if the same mutation is found in
the lymphocytes of one of the parents, the offspring's
mutation is called a "parental mutation" --- meaning that one
parent has it in every cell. Many, many earlier generations
may have had it in every cell, too.
that Paul has inherited three parental
plus one de novo mutation called D.
Suppose that his wife Mary has inherited three parental mutations
plus one de novo mutation called
H. Their daughter Alice may inherit
as parental mutations plus J as a
de novo mutation, while her brother Edward may inherit
as parental mutations plus K as a
de novo mutation. In this "scenario," de novo mutations keep adding to the
inventory. And indeed, de novo mutations are the only possible
source of humanity's accumulated inventory of inherited
"mutation rate" in a population refers to the
rate of de novo mutations per generation, and not to the
population's very much higher incidence rate of parental
mutations, already accumulated during 50 or 100 previous
generations. The ratio of "de novo to parental" mutations is
low, and this unfavorable "signal to noise ratio" has been an
obstacle to conclusive epidemiologic research in this field.
Part 5 Inherent Limits of the A-Bomb Genetics Program
of the most important statements, in the
world's professional literature on inherited afflictions, was
published by the National Academy Press in 1991 (Neel
1991). The statement occurs in the "Orientation" section (at p.2) of
the 518-page book entitled The Children of Atomic Bomb
Survivors: A Genetic Study, edited by James V. Neel and
William J. Schull --- two of the principal investigators in
1946, knowledge both of the doses of radiation
sustained by survivors [of the atomic bombings] and the
sensitivity of the mammalian genome to radiation was far
inferior to the present situation. Nevertheless, as the
preliminary data on post-atomic bomb Hiroshima and Nagasaki
emerged, it became very likely, given the number of survivors
in the two cities and their probable gonadal doses, as well as
the indicators one would be forced to pursue in any study,
that even a very major effort would not yield a statistically
significant difference between the children of survivors
receiving increased radiation at the time of the bombings
(ATB) and the children of suitable controls.
other words, when the study was initiated, it
was expected in advance that such a study would be inherently
incapable of detecting the radiation-induction of inherited
afflictions at any statistically significant level. The
famous negative "findings" were built-in before the study
began. And yet the negative findings were described in 1990
as follows --- in the highly influential journal Science:
[A-Bomb Study] researchers have found no
evidence of any genetic effects at all in the children who
were conceived after the blast --- no genetic diseases,
cancer, or congenital abnormalities. And they have scoured
the data with a fine-toothed comb, even scanning protein
sequences for any telltale variation that would indicate a
genetic mutation" (Roberts 1990).
of the Roberts description could easily
say "Case closed." But the researchers who did the work have
quite a different view. Seven leading analysts in the A-Bomb
Genetics Program wrote in 1990 (Neel 1990, p.1061):
take it as a given that the exposure [to the
atomic bombs] resulted in mutations in some survivors of the
atomic bombings, inasmuch as, without exception, under
controlled laboratory conditions, ionizing radiation has
produced mutations in every properly studied plant and animal
species." And (Neel 1990,
p.1063): "Again we reiterate the
point that, unless humans differ from every other properly
studied animal, as well as from plants, mutations must have
been produced by this exposure." See also Para.7a.
statements are emphatic warnings --- widely
unknown or ignored --- that of course ionizing radiation
(regardless of its source) contributes to inherited human
Part 6 Only 8 Inherited Effects Covered by Bomb Study
one appreciates the vast range of afflictions,
to which inherited mutations contribute, then one can better
appreciate the limitations of the A-Bomb Genetics Program with
respect to radiation-induced inherited afflictions in
offspring of A-Bomb Survivors. Only the following eight
"indicators" were studied, in an effort to detect a
statistically higher rate of de novo mutation in offspring
having at least one parent exposed to bomb radiation, compared
with offspring having neither parent exposed to bomb radiation
(details in Neel 1990). As predicted
(Para.5b), for none of
the eight indicators was a statistically significant
difference found (Neel 1990, p.1053).
1 - Untoward pregnancy outcome (an infant stillborn
and/or exhibiting major congenital malformation and/or dying
within the first 2 weeks of life expectancy).
2 - Death (except from cancer) before an average age of
28.8 Years (age in Neel 1991,
p.403); age 39 was the oldest.
3 - Occurrence of malignancy before age 20 (age at
p.1057, Neel 1990).
4 - Frequency of de novo chromosomal translocations and
inversions: Blood samples were taken from offspring at an average
age of 23-24 years (Awa 1987, p.346). Searches for
balanced translocations (reciprocal and Robertsonian) and
pericentric inversions were done without any molecular
techniques, such as "FISH."
5 - Frequency of sex-chromosome aneuploidy (wrong number
of sex chromosomes).
6 - Frequency of de novo mutation in 30 selected
protein-coding genes (Neel 1988 + Neel 1990, p.1059-1060):
Out of an estimated 50,000 to 100,000 genes in the genome, 30
were selected for study, indirectly. The protein products of
30 genes were studied electrophoretically, for alteration of
electric charge, and a subset of nine enzymes was examined for
a partial loss of activity (Neel 1988, pp.664-66).
7 - Sex-ratio among children of exposed mothers.
8 - Height, weight, circumference of head, chest.
Part 7 "Fragile" Foundation Acknowledged by Neel and Colleagues
do Neel and co-workers conclude from their eight specific
indicators? They acknowledge (Neel 1990,
p.1063) that "Each of the eight estimators of a genetic effect
of the bombs which we have been able to generate is associated
with a relatively large error term, and individually these
estimators are fragile reeds on which to lean in building a
Neel and co-workers combine five of
their eight indicators (#1, 2, 3, 5, 6, from above), and
calculate an estimate of the dose of bomb-radiation which
would double the mutation rate for these five indicators.
Their estimate (Neel 1990, p.1064
text): About 200 rems (approx. 200 rads). Since the
error-term on each of the five indicators is larger than
its slope (Neel 1990, Table 5), their estimate of 200 rems
is consistent with very different values. Neel and
co-workers decline, appropriately, to suggest any specific
confidence limits (Neel 1990, p.1064).
Part 8 The Health-Menace of a False Perception
responsible people become familiar with the
basis of the estimated 200-rem doubling dose, they will
recognize how unreliable and virtually irrelevant it is. This
is not the fault of Neel and colleagues. From the outset,
their study was expected to be inherently unable to produce
any meaningful evaluation of the impact of ionizing radiation
on inherited afflictions (Para.5b). What
is such a menace to human health is the perception that
the results are meaningful when they are not.
and co-workers partly acknowledge the
irrelevancy of their 5-indicator estimate, when they state
(Neel 1990, p.1063; emphasis is in the
original): "Ideally, the genetic doubling dose is calculated
as that amount of radiation which increases the total
impact of spontaneous [de novo] mutation by 100%.
statement is correct. And we add that the
Irregularly Inherited Disorders represent the overwhelming
share of the potential impact. When the A-Bomb Study
addressed cancer before age 20 (very rare), it essentially
addressed the issue of inherited predisposition to cancer not
at all. As for the multitude of other Irregularly Inherited
Afflictions (Para.3e), the A-Bomb Genetics Program has
addressed only the very rare disorders which were fatal before
an average age of 28.8 years of age. The overwhelming share,
of the potential impact from exposure to ionizing radiation,
is simply not addressed by that Program.
Part 9 Why "The Radiation Concept" Is So Credible
Radiation Concept" was defined in Paragraph
2b. It assigns a very large role to natural background
radiation --- an assignment based on three types of human
is the fact that today's incidence rate of Irregularly
Inherited Afflictions (Para.3g) is the result of
many centuries of build-up, because the responsible mutations
rarely kill their carriers before child-bearing age
(Para.4a). Therefore, the
chemical "revolution" after World
War Two can not explain very much of humanity's current
incidence of such inherited afflictions. A very large share
of the current incidence has to be explained by mutagens which
have "always been with us." Natural background radiation
certainly qualifies on that requirement.
is the emerging evidence --- thanks to recently developed
laboratory techniques in "molecular" cytogenetics --- that
structural chromosomal mutations are extremely important causes
of inherited diseases and "birth defects" (as we predicted in
Gofman 1970 and
1981). We have described some of the
evidence and references elsewhere (Gofman 1992,
1994). Such chromosomal mutations are often
called "I/D/R events" in the biomedical literature.
important are they? In 1989, Mohrenweiser and 2 co-workers
stated (Mohrenweiser 1989, p.242): "[Recent]
molecular studies of human genetic diseases indicate that
insertion/deletion/re-arrangement [I/D/R] events are the
molecular basis for many genetic alterations ... The latter
group of variants may be of greater health significance than
base substitutions as most of the mutations in the I/D/R
class, if they involve functional loci, should result in the
loss of a functional gene product" --- the same point made in
Gofman 1981 (p.787). Elsewhere, Neel
and 7 co-workers acknowledge:
"... a surprising frequency of spontaneous mutations are being
found to be deletions" (Neel 1988,
p.666). Hemophilia-A is an example. Youssoufian reported in
1987 that more deletions than point mutations have been
identified as causing hemophilia-A
(Youssoufian 1987, p.3772).
is the evidence --- some of it available for decades (e.g.,
Kucerova 1972, Evans
1978) --- that ionizing radiation is a "champion
clastogen." Clastogen means "chromosome breaker." Breakage of
both opposing strands of
DNA, in the double helix, is the key requirement for
production of all varieties of structural chromosomal
mutations --- including dicentric translocations, insertions,
and deletions. There are many mutagens beside ionizing
radiation which can cause single strand breaks, but ionizing
radiation can also deliver the biologically unnatural amounts
of energy which readily break both strands (discussion of the
uniquely violent properties of ionizing radiation, in
Part 4). The
double-strand breaks are far more difficult for a cell to repair
correctly than single-strand breaks.
only is ionizing radiation a particularly
potent chromosome breaker, but also chromosomal mutations are
more likely --- per mutation --- to have biological
consequences than non-chromosomal mutations. For instance,
one of the most common chromosomal mutations (the deletion)
actually removes segments of the genetic code, whereas a
single base-change does not. Even the smallest deletion can
scramble the genetic code along major segments of DNA.
is scientifically very credible to predict that
chromosomal mutations cause at least half of humanity's
current incidence of Irregularly Inherited Afflictions (with
the other half caused by non-chromosomal mutations such as
base-changes, etc.) and that ionizing radiation causes at
least half of the de novo chromosomal mutations
Part 10 Can Natural Radiation Explain the Mutation Rate?
have proposed "The Radiation Concept
(Para.2b) because there is enough
dose from natural background radiation to cause 25% or more of
the Irregularly Inherited Afflictions
(details in Part 11).
sea-level, natural background radiation
exposes everyone to about 0.1 rad per year of absorbed
radiation dose (the dose is is slightly higher at higher
altitudes). This means that, ever since the beginning of
humanity, the germ cells in our ancestors have accumulated a
radiation dose of about 0.1 rad per year. At what age did
people have children in the past? We can not ignore past
practices (Para.9b). If
we say that ages 15-20 (or 17.5 years
on the average) have been common, then the average accumulated
gonadal dose would be about 1.75 rads for each parent.
the question becomes: Could an average
gonadal dose of only 1.75 rads suffice to account for half of
the de novo mutation rate for chromosomal mutations? By
accounting for half of all chromosomal mutations, natural
background radiation would account for one-fourth of all the
afflictions --- if half of the afflictions are due to
non-chromsosomal mutations (Para.9g).
question can be explored by study of
chromosomal mutations in human blood. Such studies are highly
relevant, because every chromosomal mutation inflicted by
ionizing radiation on lymphocytes can also be inflicted by
radiation on the chromosomes of human germ cells.
Blood-studies have been done for decades. Although the
methods reveal only the easily visible mutations, the
non-detected chromosomal mutations occur in proportion to the
detected ones, since all types begin with chromosome breakage.
dicentric translocation is the chromosomal
mutation on which blood-studies generally rely most heavily.
With the use of common methods, about 1 dicentric is detected
in 1,000 cells from an adult blood-donor. This frequency
reflects the fact that the dicentric mutation occurred after
conception --- because the same dicentric would have to appear
in every cell if it were inherited. There is no question that
blood-studies are counting de novo dicentrics.
we really would like to count, with respect
to "The Radiation Concept," is the frequency of de novo
dicentrics typically found in the blood of people at age 17.5
years, when their accumulated gonadal dose from natural
background radiation is about 1.75 rads. Then, we would
irradiate samples of their blood with an extra 1.75 rads. If
we found that the experimental dose of 1.75 extra rads doubled
the pre-experimental count of de novo dicentrics, we would
have to conclude that natural background radiation caused all
of the pre-experimental dicentrics in the blood.
If 1.75 extra rads can add as many de novo
dicentrics as were already present before the extra 1.75 rads
--- in other words, if 1.75 rads can double the frequency of
dicentrics --- this would be evidence that 1.75 rads from
natural background radiation are sufficient to cause all of
the pre-experimental de novo dicentrics. There would be no
"room" for a contribution, to the pre-experimental count of
dicentrics, by any other clastogen except the inescapable
natural background radiation.
because natural background radiation
has access to the gonads, we could reasonably infer that
natural background caused all of the de novo chromosomal
mutations in the germ cells, too.
such studies establish that an extra
dose of 3.5 rads is required in order to double the
pre-experimental number of de novo dicentrics at age 17.5
years? Then we would conclude that natural radiation
causes about half of the de novo chromosomal mutations
which accumulate during the child-bearing years
Part 11 The Specific Evidence from Low-Dose Radiation
quote from the BEIR-5 Report (BEIR 1990,
p.385): "In areas of high natural background radiation, an
increased frequency of chromosome aberrations has been noted
1983, Tonomura and 2 co-workers at the Tokyo
Medical and Dental University reported their blood-study of 96
adults (49 females; 47 males) who had neither previously
received any exposure to ionizing radiation from their jobs
nor any significant exposure from medical procedures, as well
as of 23 newborn infants whose mothers had not received
medical radiation during pregnancy. The age-distribution of
the blood-donors and the number of cells examined were
(Tonomura 1983, Tables 28-1 and 28-2):
Age 20: 12,495 cells from 13 donors.
Age 30: 20,322 cells from 20 donors.
Age 40: 21,560 cells from 22 donors.
Age 50: 18,546 cells from 21 donors.
Age 60: 19,544 cells from 20 donors.
Newborn: 15,325 cells from 23 donors.
et al report (p.605) that "the incidence
of dicentrics showed a linear increase with age." The
frequency detected in newborns was zero. The frequency at age
20 --- when about 2.0 rads of gonadal dose have accumulated
from natural background radiation --- was 0.0007 (9 de novo
dicentrics in 12,495 cells). The frequency at age 40 (when an
additional 2.0 rads of gonadal dose from natural background
radiation have accumulated) was 0.0012 (25 dicentrics in
21,560 cells). Because the additional 2 rads added 70% to the
rate of 0.0007 already present at age 20, it is credible that
less than 2 rads could account for 50% or more of the
dicentrics observed at age 17.5.
Radiation Concept" and the Tonomura data are therefore in
harmony (see Para.10i). It would be very
enlightening to have some larger studies of the Tonomura type,
but we are unaware of any. We note that in 1979, Evans also
reported that de novo chromosomal mutations increase with age.
Citing "unpublished evidence" and one 1968 Russian study, Evans
writes (1979, p.532): "We have evidence
from studies on a variety of populations for an increase in the
spontaneous frequency of [chromosomal] aberrations --- in the
absence of known radiation exposure [other than natural
background] --- with increasing age.
1992, results were published from one of the
largest and most reliable blood-studies
(Lloyd 1992). Blood
samples were drawn from 20 donors of various ages, with an
average age of 30.1 years (Lloyd 1992, Table 8). Two of the
20 donors were smokers. Each blood sample was divided into
four portions: One portion (the control) received no extra
radiation. The second portion received an extra radiation
dose of 0.482 rad (4.82 mGy). The third portion received an
extra dose of 2.85 rads (28.5 mGy). The fourth received an
extra dose of 28 rads (280 mGy). The blood was irradiated
with xrays of defined quality (169 keV ISO wide series)
produced by an xray machine operated at 250 kVp with a
half-value layer of 4.3 mm Cu (Lloyd 1992, p.336).
for blood samples receiving 28 rads, 3,000
cells were "scored" at each dose-level from each of the 20
donors (for example, 60,000 cells were scored for the control
group). Even though this was a much bigger study than
Tonomura's, counts varied considerably from one donor to
another, both before and after the extra irradiation
(Lloyd Table 8) --- which illustrates
the reason not to rely heavily on small studies.
of "The Radiation Concept," our interest
is in comparing the counts of de novo chromosomal mutations in
the Control Group (which must have accumulated a dose from
natural background radiation of about 3.0 rads by age 30) with
the counts from the blood which received an extra 3.0 rads
(actually, 2.85 rads). The counts below, from the 20 donors
combined, come from Lloyd 1992, Table
8. Dic=dicentrics. CR=centric rings. AF=acentric fragments.
Control: 49 Dic. 1 CR 134 AF
Extra 2.85 rad: 88 Dic. 12 CR 211 AF
extra 2.85 rads added 80% to the control's
frequency of de novo dicentrics and added about 60% to the
fragments. (We can ignore the centric rings, because a
measurement of 1 is very unstable.) If we assume, reasonably,
that the counts of dicentrics and fragments in the control
samples would have been lower, if the average age had been
17.5 years instead of 30.1 years, then it would be very
reasonable indeed to believe that (a) 2.85 rads is enough
approximately to double such control values, and (b) that 1.75
rads of gonadal dose, received by age 17.5 years from natural
background radiation, is enough to cause half of all the de
novo chromosomal mutations.
Part 12 Is the Evidence "Screaming" at Humanity?
Radiation Concept" is in harmony with the
Tonomura data and the Lloyd data on low-dose radiation. And
that is because "The Radiation Concept" is not a mere
speculation drawn from thin air. It is a scientifically
credible concept based on relevant real-world evidence of the
types described in Part 9.
radiation from any source (natural or
man-made) is well-established as a particularly potent cause
of chromosomal mutations and other complex genetic mutations.
This is just not in dispute. And there are solid biological
reasons for the unique mutagenic potency of ionizing radiation
(discussion and references in Gofman 1997).
population dose of 0.1 extra rad per year, due
to human activities, would be the equivalent of doubling the
annual gonadal dose from natural background radiation. We
have shown above that such an annual increment, if received
generation after generation, could ultimately add 25% to the
incidence of the Irregularly Inherited Afflictions --- a
consequence of breath-taking size. Indeed, adding that extra
dose for just one generation would have a very large aggregate
impact on future generations, because no one can issue "a
recall" on the mutations, which are transmitted from that one
generation to future generations (quantitative analysis in
Gofman 1994, Chapter 7.)
if the extra dose comes from nuclear
pollution, it is impossible to limit such dose to a single
generation, because many of the radioactive species persist in
the biosphere for centuries and millennia. For example, half
of the carbon-14 created in nuclear power plants today will
still be around 5,700 years from now. And half of the radium,
already "liberated" by mining nuclear fuel, will still be
around 1,600 years from now.
very low doubling-dose for radiation-induced
chromosomal mutations, and confirmation of the importance of
such mutations in inherited disorders, combine almost to
scream at humanity: "Do not permit increases in nuclear
pollution. At enormous expense, you can recapture only a
small part of what you let loose. Irrevocable nuclear
pollution inevitably increases humanity's rate of inherited
people will also consider the possibility that
chromosomal mutations are the cause of more than half
of humanity's inherited afflictions (Para.9g). Such
a prospect is not rendered "improbable" by current knowledge.
Moreover, the measurements discussed in Part 11 have
error-bands, which means that natural background radiation
could turn out to explain almost all the mutation rate for
chromosomal mutations. In other words, today's evidence does
not rule out the possibility that very low-dose ionizing
radiation, from natural background, explains 50% or more of
the inherited afflictions.
bottom line is: Even "The Radiation Concept"
presented in this article (Para.2b) may rather severely
underestimate the impact of low-dose ionizing radiation on
inherited afflictions. It is far from prudent, for anyone in
environmental or medical circles to be "asleep at the wheel."
# # # # #
>>>>> Reference List <<<<<
- Awa 1987 (Akio A.) + 9 colleagues: "Cytogenetic Study
of the Offspring of Atomic Bomb Survivors," pp.344-361 in
- BEIR 1990: Committee on the Biological Effects of
Ionizing Radiation, Health Effects of Exposure to Low Levels
of Ionizing Radiation. National Academy Press. ISBN 0-309-03995-9.
- Billen 1990 (Daniel): "Spontaneous DNA Damage and Its
Significance for the `Negligible Dose' Controversy in
Radiation Protection," Radiation Research 124: 242-245.
Responses by Keith F. Baverstock and John F. Ward in 1991,
Radiation Research 126: 383-387.
- Evans 1978 (H.J.) + David C. Lloyd (editors),
Mutagen-Induced Chromosome Damage in Man. University Press,
- Evans 1979 (H.J.) + 3 co-workers: "Radiation-Induced
Chromosome Aberrations in Nuclear Dockyard Workers," Nature
277: 531-534. Feb. 15.
- Gofman 1970 (John W.) + Arthur R. Tamplin: "Questions
for Dr. Paul Tompkins, Director of the Federal Radiation
Council," pp.1538-1559 in Underground Uses of Nuclear Energy,
Hearings on S.3042 before Senate Committee on Public Works, Air
& Water, August 5, 1970. See also
Chapter 3 in
1971 by Gofman + Tamplin. ISBN 0-87857-004-7.
- Gofman 1981 (John W.): Radiation and Human Health.
ISBN 0-87156-275-8. Sierra Club Books. Still in print.
- Gofman 1992 (John W.): Radiation-Inducible
Chromosome Injuries: Some Recent Evidence on Health
Consequences --- Major Consequences. On Internet at:
- Gofman 1994 (John W.): Chernobyl Accident: Radiation
Consequences for This and Future Generations. Russian
language. Vysheishaya Shkola Publishing House, Minsk. ISBN
- Gofman 1997 (John W.): "The
Free-Radical Fallacy about Ionizing Radiation: Demonstration That
a Popular Claim Is Senseless." On Internet at:
- Haldane 1955 (John Burdon Sanderson): "Genetical
Effects of Radiation from Products of Nuclear Explosions,
Nature 176: 115.
- Health Physics 1996: Position Statement of the Health
Physics Society, "Radiation Risk in Perspective," by Kenneth
F. Mossman + 5 colleagues, in Health Physics Newsletter, March
- Kucerova 1972 (M.) + A.J.B. Anderson + K.E. Buckton +
H.J. Evans, "Xray Induced Chromosome Aberrations in Human
Peripheral Blood Lymphocytes," International Journal of Radiation
Biology 21: 389-396.
- Lloyd 1992 (David C.) + 10 co-workers: "Chromosomal
Aberrations in Human Lymphocytes Induced in Vitro by Very Low
Doses of Xrays," International Journal of Radiation Biology 61:
- Mohrenweiser 1989 (Harvey W.) + Robert D. Larsen +
James V. Neel: "Development of Molecular Approaches to
Estimating Germinal Mutation Rate," Mutation Research 212:
- Neel 1988 (James V.) + 7 co-workers: "Search for
Mutations Altering Protein Charge and/or Function in Children
of Atomic Bomb Survivors: Final Report," American Journal of
Human Genetics 42: 663-676. Also in Neel 1991,
- Neel 1990 (James V.) + 6 co-workers: "The Children of
Parents Exposed to Atomic Bombs: Estimates of the Genetic
Doubling Dose of Radiation for Humans," American Journal of
Human Genetics 46: 1053-1072. Also in Neel
- Neel 1991 (James V.) + William J. Schull, editors:
The Children of Atomic Bomb Survivors: A Genetic Study.
ISBN 0-309-04488-X. National Academy Press.
- NRC 1991 (Nuclear Regulatory Commission): "Health
Effects Models for Nuclear Power Plant Accident Consequence
Analysis, Addendum One to Nureg/CR-4214.
- Roberts 1990 (Leslie): "British Radiation Study
Throws Experts into a Tizzy," Science 248: 24-25. April 6.
- Tonomura 1983 (Akira) + Kunikazu Kishi + Fumiko
Saito: "Types and Frequencies of Chromosome Aberrations in
Peripheral Lymphocytes of General Populations," Chapter 28
(pp.605-616) in Radiation-Induced Chromosome Damage in Man,
edited by Takaaki Ishihara + Masao S. Sasaki. ISBN
0-8451-2404-8. Pub: Alan R. Liss Inc, New York City.
- Youssoufian 1987 (Hagop) + 5 co-workers:
"Characterization of Five Partial Deletions of the Factor VIII
Gene," Proceedings of the National Academy of Sciences (USA) 84:
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