Debra Dawson v. The Boeing Company, et al.

Case No. 12-10686-GW (JCGX)

Expert Report of Christopher Busby, Ph.D
July 24, 2013

TABLE OF CONTENTS
PAGE(S)
1. Assignment and Professsional Qualifcations ........................................................................ 1
2. Ms. Debra Dawson ............................................................................................................. 6
3. Colorectal Cancer and Radiation ......................................................................................... 9
3.1 Cancer ..........................................................................................................................10
3.2 Colorectal Cancer.........................................................................................................10
3.2.1 Age specific rates and theory of cancer ........................................................10
3.2.2 Ms. Dawsons likelihood of developing the condition. Mark Lindsey ..........12
3.3 Colorectal Cancer: Physiological and Cellular Description ........................................13
3.4 Genomic Instability, Bystander, Field Cancerization ..................................................14
3.5 Ionising Radiation and Colorectal Cancer ...................................................................15
3.5.1 External high dose radiation ........................................................................15
3.5.2 Internal radiation: Uranium and cancer ......................................................18
3.5.3 Summary: does radiation cause cancer of the colon and rectum? ...............20
3.6 Stuart Dyson.................................................................................................................21
4. Radiation and Health: Summary of the Current Situation .................................................... 22
4.1 Evidence of the Failure of the Current (ICRP) Radiation Risk Model; the European
Parliament Petition .................................................................................................25
4.1.1 The Petition basis..........................................................................................25
4.1.2. Childhood cancer near nuclear installations ..............................................26
4.1.3 Infant leukemia after Chernobyl ...................................................................27
4.1.4 Cancer following Chernobyl in Northern Sweden ........................................27
4.1.5 Human sex ratio at birth perturbed by low doses of internal fissionproduct ionising radiation .........................................................................27
4.1.6 Cancer, leukemia/lymphoma and heart disease in Uranium workers ..........28
4.1.7 Secondary Photoelectron Effect ....................................................................28
4.1.8 Cancer and genotoxic effects in Iraq following DU exposure ......................29
4.1.9 Chernobyl effects as reported in the Russian language peer-reviewed
literature ....................................................................................................29
4.2 Uranium .......................................................................................................................29
4.3 Uranium Particle and Uranyl Ion UO2++ Doses to the Crypt Cells of the Colon/
Rectum of Ms. Dawson and Mr. Mark Lindsey ....................................................31
5. Contamination at SSFL and Dispersion Offsite .................................................................. 32
5.1 Contamination ..............................................................................................................32
5.2 The SSFL Environmental Reports ...............................................................................33
5.3 Wind Directions at SSFL and Air Dispersion Modeling .............................................35
5.4 Mechanisms of Exposure .............................................................................................40
6. Uranium Contamination at SSFL....................................................................................... 42
6.1 Environmental Uranium...............................................................................................42
6.2 Uranium Isotope Ratios ...............................................................................................43
6.3 Uranium at SSFL .........................................................................................................46
6.4 Uranium in Water ........................................................................................................47
6.5 Uranium in Soil ............................................................................................................47

6.6 Uranium in the Air .......................................................................................................60

6.7 Boeings Position on Uranium .....................................................................................61
6.8 Uranium in the Los Angeles Water Supply .................................................................62
6.9 Gamma Exposure Rates at SSFL and Historic Contamination ...................................62
6.10 Alpha and Beta Measurements of Contamination. ....................................................67
6.11 Remediation Activity Trends .....................................................................................68
6.12 The Removal of Soil from the SNAP Facility ...........................................................69
6.13 Summary of Section 6 ................................................................................................74
7. Evidence of Offsite Contamination by Uranium ................................................................. 75
7.1 Questionable Procedures ..............................................................................................75
7.2 The Natural Background Gamma Exposure Rates at the SSFL Site and Offsite ........76
7.3 Enriched Uranium at the Background Sites .................................................................80
7.4 Thorium-234 and Thorium-231 ...................................................................................84
7.5 Summary of Section 7 ..................................................................................................84
8. Independent Evidence of Health Effects in Studies of SSFL and Local Populations ............. 85
8.1 Other Examples of Effects ...........................................................................................85
8.2 Morganstern, et al., 2007 .............................................................................................85
8.3 The Childhood Retinoblastoma Cluster .......................................................................88
8.4 Infant Mortality and Cancer in Ventura County ..........................................................88
8.5 Summary of Section 8 ..................................................................................................89
9. The Regulations .........................................................................................................................89
9.1 Offsite Doses ................................................................................................................89
9.2 Summary of Section 9 ..................................................................................................90
10. Overall Summary: Ms. Dawsons Exposure and her Subsequent Cancer ...............................90
11. References ................................................................................................................................92

1. Assignment and Professional Qualifications

1.1 I have been asked by Howarth & Smith and Rose Klein & Marias, LLP to consider
and comment on epidemiological and mechanistic causation in the case of Ms. Debra
Dawson, a hitherto fit and well lady who lived most of her life in the close vicinity of the
Santa Susana Field Laboratory (SSFL) in Ventura County, California and who developed
cancer of the rectum at a relatively early age. This is a classic example of a nuclear site
downwinder cancer risk but there are some unusual aspects in this case relating to
exposure to Uranium.
I have looked at a large number of reports and documents relating to SSFL, which I will
list and refer to, and have concluded that Ms. Dawsons disease was on the basis of
probability more likely than not caused by exposure to radioactive contamination,
including enriched Uranium particulates in contaminated dust released to the air
following remediation work at the SSFL site in the period from 1996 to 2005. All of the
expert opinions I set forth in this report are given to a reasonable degree of scientific
certainty.
1.2. First, I should state my qualifications in this area.1
I have a First Class Honours degree in Physical Chemistry from the University of London
and also hold a Doctorate in Chemical Physics from the University of Kent. I was elected
to the Royal Institute of Chemistry in 1974 and am a member of the International Society
for Environmental Epidemiology. I was until recently Visiting Professor in the
Department of Molecular Biosciences, University of Ulster and am currently Guest
Researcher at the Department of Science and Engineering, Jacobs University in Bremen,
Germany. I am Scientific Director of the environmental consultancy Green Audit and
scientific advisor to the Low Level Radiation Campaign. I was coordinator of the Science
and Policy Group of the EU Policy Information Network for Child Health and
Environment (PINCHE) based in Arnhem, the Netherlands and also the PINCHE
Rapporteur on Radiation and Health in Children and was mainly responsible for the
publication on this issue published in Acta Paediologica [Busby and Fucic, 2006]. I am
Scientific Secretary of the European Committee on Radiation Risk (ECRR) based in
Brussels and senior editor of their reports ECRR2003 Recommendations on the Health
Effects of Ionising Radiation at Low Doses for Radiation Protection Purposes and also
co-editor with Prof Alexey Yablokov of the Russian Academy of Sciences of ECRR2006:
Chernobyl 20-years On report. ECRR2003 has now been published in French, Japanese,
Spanish and Russian and a revised edition was published in 2010 (ECRR2010). This
edition was updated to review and advise on the health effects of Uranium, a matter
which is relevant to the present report on Ms. Dawson. I was a member of the UK
Government Department of Health/ Department of Environment Committee Examining
Radiation Risk from Internal Emitters (CERRIE) and also a member of the UK Ministry
of Defence Depleted Uranium Oversight Board (DUOB) which was set up to examine the
health effects of Depleted Uranium in the Gulf War and Kosovan veterans. I am a
1

I have used English spelling and grammar conventions in this report for the most part, rather than the
American ones.

member of the Ukraine Association Physicians of Chernobyl. My current CV is attached

as Appendix A.
1.3. I have studied the health effects of low dose radiation for more than twenty years. I
have undertaken several research studies, both in the field of radiation epidemiology and
radiation biology and published more than 50 reports and articles on this issue. I have
been invited to give submissions on the health effects of low level internal radiation
exposure to several bodies, including the European Parliament in Strasbourg, and
Brussels, the Royal Society in 2001 and 2002 and also in 2002 the US Congressional
Committee on Veterans Affairs and Security, the Nobel Peace Institute in Oslo,
presentations in the Swedish, Danish and Finnish parliaments, the UK parliament, in
Prague and in Kiev, the New Zealand Royal Society and I was commissioned to advise
the UK Committee on Radioactive Waste Management CoRWM.
1.4. My particular area of expertise is the health effects of internally deposited
radionuclides. I have made fundamental contributions to the science of radiation and
health in this area and have published many articles and reports on this issue. In the last
ten years I have concentrated more on the health effects of Uranium, especially
particulates such as those created artificially following the burning of Uranium in fires or
when deployed as part of a weapon. The current case involves such an exposure.
1.5. It is my expert opinion that Ms. Dawsons cancer was caused by radioactivity in
excess of federal off site limits from the SSFL site. My opinion is based on my academic
background, my professional experience in the field of radiation exposure and cancer
causation, the literature cited herein, the data in this case, the published reports on SSFL
and radiation levels in the area in proximity to SSFL, and my work and analyses of
cancer causation in other matters involving radiation contamination, including, SSFL,
where I have served an as expert consultant, as set forth in this report.
1. Ms. Dawson was an otherwise extremely fit and healthy woman aged 49 when the
cancer developed. Her treating physician, Dr. Bartis, has stated in a declaration
that in his expert opinion, her rectal cancer was caused by radiation exposure from
SSFL. The background colorectal cancer rate in Los Angeles for a woman aged
45-49 is about 25 per 100,000 and the cumulative rate for all ages up to 49 is not
more than 50 per 100,000 individuals, therefore the probability of her developing
the condition without exposure to SSFL radiation is no more than 0.0005. It is
less than this since Ms. Dawson was a fit lady with no family history of the
disease, a person who exercised by running. She did not eat red meat nor was she
a smoker, activities which are known to be linked to the disease.
Ms. Dawsons ex-husband, who lived with her in a residence near SSFL also
developed colorectal cancer. The probability of two individuals living together
both developing the same cancer as a consequence of chance alone is extremely
low; if we take her ex-husbands background rate as 50 per 100,000, the combined
probability of both developing the same condition by chance is less than 1 in 2

million ( 2.5 x 10-7). Therefore, the combined event of two cancers is not a
statistically random one and it is highly probable that they had the same cause.
2. The cause of cancer is almost entirely environmental and is due to exposure to a
mutagen. Cancer is a genetic disease expressed at the cellular level. The
environmental link is particularly clear for colorectal cancer where the association
with diet is strong. Colorectal cancer is known to be the consequence of the
acquisition by a single cell of the basal layer of cells in the colorectal mucosa of
about 6 separate mutations in the cellular DNA. This is the multistage theory of
cancer which for colonic cancer is now generally accepted in the scientific
community. The question is one of probability. It may be simply thought of as a
bingo card with 6 separate numbers necessary to win, or in this case develop
cancer.
3. The incidence of colorectal cancer increases exponentially with age. It is this
knowledge, and quite specifically for colon cancer, which was the platform that
has led to the multistage cancer theories. The time lag or latency period between
exposure to the mutagen and the clinical expression of the disease is between 10
and 20 years but can be less if the dose is high. Thus for Ms. Dawson who was
diagnosed in 2011, a causative exposure to an environmental mutagen in the
period between 1991 and 2001 must be considered.
4. Radiation is a known cause of colorectal cancer. Most of the reported data is from
external irradiation at high doses. However, high cell doses may be delivered
from internal exposures. Radiation causes mutation in the genes of cells which
ultimately acquire the necessary complement to become cancerous. The rate of
acquisition of the necessary mutations is a function of the overall dose and dose
rate at the DNA. Thus the multistage theories predict (and epidemiology shows)
that a higher dose or dose rate results in a more rapid development of the
precursor mutations necessary for the disease and therefore its expression at an
earlier age.
5. For twenty years prior to the diagnosis of her cancer, Ms. Dawson lived within a
few miles of SSFL, and downwind. SSFL is a facility which began releasing
radiation offsite in the 1950s, and has been heavily investigated since the 1980s
for continuing releases of radioactivity and off site migration of radioactivity to
the wider environment.
6. During the period that Ms. Dawson lived downwind, SSFL was involved in a
closure, demolition and remediation operation. This was mainly between 1996
and 2007. In 2007, work was suddenly halted prior to an environmental survey of
the remaining radioactivity on the site. During the remediation period, buildings
and areas in the complex were demolished and topsoil was removed from
radioactive areas and trucked away. This resulted in large amounts of
contaminated dust being generated and blowing downwind and also

contamination along the routes taken by the trucks.

7. Routine measurement of radioactivity in air on the site showed a remarkable and
significant increase in the concentration of Uranium in air which correlated in
time with the remediation works.
8. The Uranium measured in air by filters over this period and reported in the annual
environmental reports was not natural: it was Enriched Uranium and its origin
was therefore the historic activities and contamination of the buildings and ground
at the SSFL.
9. As a result of the releases to air from the remediation work of historic enriched
Uranium contamination annual effective doses to critical members of the public
offsite were in excess of U.S. regulations, namely 10 C.F.R. 20.1301, which
prohibits a total effective dose to individual members of the public in excess of
0.1 rem (1 mSv) per year or 0.002 rem (0.02 millisievert) per hour
10. A significant body of evidence has emerged in the last ten years from research
and from epidemiology that exposure to internal uranium conveys an anomalously
high risk of cancer and genetic damage. This research specifically includes
colorectal cancer.
11. Exposure to Uranium at low dose was found to be the cause of colorectal cancer
by a jury in an official coroners inquest in the UK in 2009 into the death of Stuart
Dyson, a soldier who had been exposed to Depleted Uranium in the first Gulf
War. I was the principal expert witness in this case.
12. Ms. Dawson lived less than three miles from SSFL from approximately 1986 into
1999, within one mile of the SSFL from 2000 into 2001, and within two miles of
the SSFL from 2001 through 2007.
13. Between 1986 and 2000 she lived at 8036 Royer, West Hills, CA (approx 3 miles
from SSFL). Here she maintained a vegetable garden where she grew carrots,
radishes, cucumbers, corn, tomatoes, and lettuce; she consumed these vegetables
as they were in season. Uranium particles from the dust generated by the
remediation work at SSFL were deposited in areas beyond three miles of SSFL
and contaminated gardens, water, houses, animals and people. Ms. Dawson had
exposure paths from all these sources for both external and internal exposure to
Uranium particles from SSFL. The ingested particles passing through Ms.
Dawsons intestinal organs exposed Ms. Dawson to high local doses to cells in the
colorectal tissue.
14. In addition, while living near the site, at the various addresses between 1986 and
2007, Ms. Dawson was exposed to particulate Uranium from dust in the air which
drifted downwind from the SSFL site during the remediation period. These
particulates, after inhalation, most probably were translocated to the lymphatic
4

system or if larger than 1 micron diameter were cleared from the lung and
swallowed. After migration to the intestines, they also more probably than not
caused significant local dose to colorectal epithelia.
15. An epidemiological study of cancer in populations living within 5 miles of SSFL
between 1988-1995 and 1996-2002 showed that there is a significant increased
risk of cancer in these populations in the latter 5-year period when the
remediation was taking place.
16. A study of infant mortality and low birth weight in children born in census tracts
near the SSFL showed significant increases relative to national rates in both
indicators of genetic damage for the period when the remediation was being
carried out.
17. Over the same period of the remediation dust there was a remarkable increase in
the rate of the rare childrens eye cancer retinoblastoma in the area of Los
Angeles downwind of the SSFL. This is a disease associated with exposure to
Uranium in the Navajo nation and also near the Sellafield nuclear reprocessing
site in the United Kingdom where there is significant Uranium contamination.
18. In 2011, results of an extensive EPA commissioned radioactivity survey of areas
near the SSFL were published. The measurements showed that in areas up to 7
miles from the SSFL, external background gamma radiation was significantly
elevated relative both to measurements published by NCRP and the US
Environmental Protection Agency (EPA) for Los Angeles area and also historic
measurements of gamma background reported annually at the perimeter fence and
main gate by SSFL and also the State of California.
19. In the same report, measurements of Uranium in the areas defined as
background areas for the purposes of remediation of the SSFL site showed
clearly that the Uranium in those areas was Enriched, and therefore not from
natural ore deposits. Thus, it is clear from this report that areas as far away from
the SSFL site as 7 miles have been contaminated with enriched Uranium which
resulted partly from the remediation works carried out between 1996 and 2007
and the dispersion of contaminated soil downwind.
20. Thus to summarise, it is my expert opinion that the cause of Ms. Dawsons cancer
was more probably than not exposure of her rectal epithelium to particles of
enriched Uranium which were ingested by her through eating contaminated
vegetables from her garden, and breathing contaminated air from SSFL; in
addition she more probably than not received an excess external radiation dose
from the soil contaminated with material from SSFL. None of the owners of SSFL
monitored the contamination levels off site in local communities. Therefore, it is
not possible to precisely quantify Ms. Dawsons exposure. However, given the
length of time she lived in the area and the multiple exposure pathways from
SSFL radiation, it is my expert opinion that she was exposed at levels in excess of
5

the federal guidelines, specifically 10 C.F.R. 20.1301, which prohibits a total

effective dose to individual members of the public in excess of 0.1 rem (1 mSv)
per year or 0.002 rem (0.02 millisievert) per hour.
2. Ms. Debra Dawson
Ms. Dawson was diagnosed with rectal cancer on or about January 5, 2011, based upon
surgical pathology. Ms. Dawson was living in Castaic, California at the time of her
diagnosis. She is 50 years old and, before contracting rectal cancer, Ms. Dawson was in
exceptional health and worked as a personal physical trainer.
First, it should be appreciated that Ms. Dawson lived for a long time prior to her cancer
very close to the SSFL boundary. Ms. Dawson lived less than three miles from SSFL
from approximately 1986 to 1999, within one mile of the SSFL from 2000 into 2001, and
within two miles of the SSFL from 2001 through 2007. During these periods, Ms.
Dawson ran outside daily, and hiked and biked in and around SSFL several times per
week. She also maintained a vegetable garden where she grew carrots, radishes,
cucumbers, corn, tomatoes, and lettuce; she consumed these vegetables when they were
in season. Often when driving around her residence, she would encounter traffic and find
herself stuck behind large dump trucks from SSFL with Hazardous Materials signs on
them. These were the trucks which were removing radioactively contaminated soil and
other material from the SSFL cleanup. Ms. Dawson resided at the addresses below at the
times indicated in Table 2.1.
It is clear from Table 2.1 and from the map I have created, Fig 2.1, that Ms. Dawson has
lived downwind of the SSFL for most of her life. For 25 years since 1986, she lived
between 1 and 3 miles of the most contaminated area of SSFL, Area IV (see Fig 2.1).
During all of her life the SSFL has been the origin of radioactive releases to the
environment. Between 1996 and 2007 remediation and demolition work at the site caused
a significant increase in the releases from the site. Radioactivity is a known cause of
cancer and indeed of rectal cancer. Ms. Dawson has never used or smoked tobacco
products and has very rarely consumed alcoholic beverages. She has no other known risk
factors for the development of rectal cancer. Ms. Dawson had no history of any kind of
malignancy before her diagnosis. While Ms. Dawsons maternal grandmother had oral
cancer in her jaw, there is no other family history of cancer of any kind.
There is another specific valuable indicator as to the origin of Ms. Dawsons illness.
According to Ms. Dawsons surgeon, Dr. Barstis, her ex-husband also developed rectal
cancer. In a Declaration which I have seen, Dr. Barstis stated:
I have reviewed the pathology report for Ms. Dawsons former husband, Mark Lindsey,
with whom Ms. Dawson lived in proximity to the SSFL between 1986 and 1999, which
report reveals that Mr. Lindsey was also diagnosed with rectal cancer in 2006. This
exposure is also within the latency period for the SSFL exposures. Mr. Lindsey and Ms.
Dawson are not blood relatives and rectal cancer is obviously not a contagious disease.

Table 2.1 Ms. Dawsons addresses between 1986 and 2007 with distances (miles) and
bearings from SSFL Area IV.
Age

Period

(location pin Fig 2.1) Address

44-45

2006-2007

41-44
39-41
38-39

2003-2006
2001-2003
2000-2001

25-39
23-25

1986-2000
1982-1985

23

1984

18-23

1979-1984

(5) 806 Catherine St, Simi

Valley
(4) Birch Street, Simi Valley
(3) Junipero, Simi Valley
(2) 24303 Woolsey Canyon Rd,
West Hills
(1) 8036 Royer, West Hills
8421 Lindley Avenue,
Northridge, CA
16423 Lahey, Granada Hills,
CA
Sepulveda Blvd., West Los
Angeles

12-18
12
10-12

1973-1979
1973
1971-1973

Woodley Ave, Granada Hills

Densmore Ave, Granada Hills
San Juan Capistrano

5-10
2-5
1 -2

1966-1971
1963-66
1963

Densmore Ave, Granada Hills

Colette Ave, Granada Hills
Sepulveda Blvd West LA

0-1

1961-63

Woodgreen Ave, West LA

to
SSFL
2

bearing

2
2
1

NW (046)
NW (046)
ExN (079)

3
10

ESE (103)
087

13

076

More
than 13
miles
13
13
More
than 13
miles
13
13
More
than 13
miles
More
than 13
miles

NW (046)

076
076

076
076

Fig 2.1 Location of the residences of Debra Dawson at different ages near the SSFL, Ventura County, California. Approximate
boundary of SSFL in red. The radioactive area Area IV is indicated. Also shown are bearings of three locations where radioactivity
measurements have been made recently (2011) in order to define background (see text).

3. Colorectal Cancer and Radiation

3.1 Cancer
In order to understand the cause of Ms. Dawsons cancer it is necessary to begin with
some understanding of the cause of cancer.
The body is made up of trillions of living cells. Normal body cells grow, divide into new
cells, and die in an orderly fashion. During the early years of a persons life normal cells
divide faster to allow the person to grow. In adulthood, cells divide only to replace worn
out cells or to repair injuries. Cancer begins when cells in a part of the body start to grow
out of control.
Cancer is overwhelmingly an environmental disease (Doll and Peto 1981). That is to say,
it is a result primarily of exposures to substances which cause mutation in cellular DNA.
This has been shown by comparing cancer rates for different kinds of cancer (organ
cancer sites, breast, colon, stomach etc.) across different populations which emigrate
from one country to another and acquire the rates for that specific cancer of the country
they emigrate to. For a full discussion of cancer and its origins see Busby 1995 and
Busby 2006. This is not to say that there are not genetic pre-dispositions to various kinds
of cancer, but it is clear from twin studies that such genetic pre-dispositions usually
confer only modest excess risks and of course, this begs the question of where the shared
genetic component originated.
Thus, cancer is a genetic disease expressed at the cellular level. The development of a
cancerous tumour is a result of the acquisition by a single cell precursor of a set of
mutations which together are necessary for the cell to ignore territorial constraints and to
replicate itself continuously. The daughter cells then inherit the faulty set of mutations
and also replicate without recognising normal territorial constraints. It is believed from
examination of mosaic characteristics of cells (whether an individual cell is derived at the
embryonic stage from mother or father DNA) that the condition starts with a single cell.
The acquisition of genetic mutations has a highest probability during replication of cells,
and therefore cells which have a high natural replication rate are also those which have
the highest cancer rate. Cells of the surface of tissues, termed epithelial cells, generally
have the highest turnover and cancers are most common in these surface tissues. Of
course, such surface tissue can be inside the body, as is the case of the surface cells of the
large intestine, the colorectal epithelium. It has been known for many years that the
control of development in surface cells is determined by sub-surface tissues
(epidermis/dermis). Very recent work with chimeral transplants (Barcellos Hoff et al
2005) shows that for the tumour to develop there has to be a failure of signalling in the
surrounding sub surface tissue, also shown to be caused by exposure to mutagenic agents
(chemicals or radiation). Exposure of the skin to carcinogenic agents thus causes cancers
of the skin. The famous scrotal cancer excess in chimney sweeps exposed to coal tars
reported by Percival Potts in late Victorian times is a good example, as is the connection
between sunlight and various types of skin cancer. Thus, we would expect that mutagenic
agents which exist in the faeces, in contact with or near to the cells of the colonic/rectal

epithelium, would be the prime environmental cause of colorectal cancer. Evidence from
red meat consumption in different countries bears this idea out and can be seen in Fig 3.1.
From this relationship, it is understood that a carcinogen in the meat in contact with the
colonic/rectal epithelium, where the cells which become cancerous exist, is the primary
cause of the cancer. Furthermore, the majority of colorectal cancers develop in the lower
end of the colon where the solid content of the faecal matter is at its maximum and thus
the concentration of ingested mutagenic agents are also at their maximum (McGee et al
1992, Guyton1988).
Fig 3.1 Age adjusted colon cancer in women and red meat consumption (Armstrong B
and Doll R Int. J.Cancer 15 617-631 1975)

3.2 Colorectal Cancer

3.2.1 Age specific rates and theory of cancer
Much of the work which led to the understanding of the development of cancer as a
multi-stage disease arose from the examination of the enormous increase of cancer rates

10

with age in colorectal cancer. This increases exponentially by more than 1000-fold
between the age of 30 and 80. The death rate from colon cancer in the USA in 1968 is
plotted in Fig 3.2 below.
Fig 3.2 Death rates from colon cancer in the USA in 1968 plotted linearly and
logarithmically (from Cairns 1978).

The various models for cancer development which have been proposed to account for this
exponential increase in cancer with age all have in common the fact that the cancer cell
arises as the end result of a series of steps that have occurred in the life of the patient. The
simplest postulate, and one that is now generally accepted, is that each cell has several
genes which independently restrain it from losing control and that cancer arises when all
of these constraint genes are inactivated by mutation. Because mutation can occur at any
time in the life of a cell or its ancestors (which can, of course, include parental inherited
mutations) the probability of any single cell having a mutation in a particular gene rises
in direct proportion to age. So, the probability that the cell has a mutation in each of N of
its restraining genes will rise as the Nth power of age. Thus, the logarithm of the cancer
incidence should be proportional to the logarithm of the age, and Fig 3.2 shows that this
is indeed the case for colon cancer in women. The number of necessary independent
lesions N in this case is 6.
Certain valuable consequences for the discussion of Ms. Dawsons cancer arise from the
understanding of the mechanism of cancer causation. First, the development of colorectal
11

cancer at the relatively young age of 49 is unusual and more probably than not she had a
significant exposure to a mutagenic substance which she either ingested or inhaled and
was translocated to the gut where it caused mutation in cells of the colorectal epithelium
occurred. Second, (and this also is shown by studies of radiation and cancer reviewed
below) such an exposure more probably than not would have occurred in the period
between 10 and 15 years prior to the diagnosis.
3.2.2 Ms. Dawsons likelihood of developing the condition. Mark Lindsey.
Cancer of the colon and rectum, generally classified as the same disease, is a leading
cause of death in the developed world and is not uncommon. It is the third most common
cancer diagnosed in both men and women in the USA (American Cancer Society) with an
overall risk of developing the disease of 1 in 20. It is, however, largely a disease of the
elderly for reasons which have been discussed. The age specific incidence rates in the
USA for the period 2001-2005 (SEER Incidence rates TableVI-8) are given in Table 3.1
below. From this it can be calculated that the cumulative probability of developing cancer
of the rectum before age 50 for a white US woman is 0.0047, or one in 212. If we make
the same calculation for colon cancer in a man up to age 50 the result is a probability of
0.0084. For comparison, the probability of throwing two sixes on two consecutive dice
throws is obtained by multiplying the individual probabilities, i.e. 1 in 36. Similarly, the
probability of Ms. Dawson and her ex-husband Mr. Mark Lindsey both developing the
same non- communicable disease before age 50 is thus obtained by multiplying these two
probabilities to obtain p = 3.9 x 10-5 or one chance in 25,300 that this combined event
was a random one. It is therefore very likely that these cancers shared a common cause.
If there was a common exposure to a colorectal-cancer-causing mutagen that both these
individuals shared in the period prior to a latency of 10-15 years, then the common cancer
causative agent is highly likely to be the cause of each individual colon cancer. Mr.
Lindsey and Ms. Dawson lived together between 1986 and 1999. This was at 8036
Royer, West Hills, Pin [1] on the map Fig 2.1, some three miles downwind of the SSFL
Area IV during the period that SSFL was engaged in remediation with the generation of
considerable quantities of radioactive dust and where Mr, Lindsey and Ms. Dawson grew
vegetables in their garden for consumption. I will address below the contamination of
these vegetables and of the air they inhaled when living at this address.
Table 3.1 Age specific incidence rates per 100,000 population in USA SEER states
2001-2005.
Age group
25-29
30-34
35-39
40-44
45-49

Colon F
1.1
2.4
4.3
8.3
15.4

Colon M
1.3
2.5
4.6
8.4
16.8

12

Rectum F
0.7
1.4
2.7
5.1
8.9

Rectum M

3.3 Colorectal Cancer: Physiological and Cellular Description

The colon and rectum are parts of the digestive or gastrointestinal system. In the small
intestine food is processed and absorbed; in the large intestine, water is removed and the
waste matter increasingly solidified as it passes though the colon, becoming most solid at
the lowest section, the sigmoid colon which connects with the rectum at the rectosigmoid junction. The waste matter that is left after passing though the colon is called the
faeces. The waste goes finally to the rectum where it is stored until there is sufficiently
enough of it present to initiate a desire to defecate and become excreted though the anus.
The most solid waste exists in the rectum and sigmoid colon where it is in contact with
the epithelial cells lining the organs. The dimensions of the colon and rectum are given in
ICRP 72 Reference Man and are reproduced in Table 3.2. The wall of the colon and
rectum is made up of several layers shown schematically in Fig 3.3. In 95% of cases of
colorectal cancer, the cancer begins in the inner layer, the surface epithelium, shown
convoluted in Fig 3.3. Each convolution consists of an indentation or folded crypt and the
cells comprising the surface mainly produce mucus. If these cells begin to proliferate
abnormally they first produce a non-cancerous polyp on the inside wall of the colon or
rectum. This generally does not develop into a cancer, but nearly all colorectal cancers
originate with such polyps. Almost all colorectal cancers are adenocarcinomas
originating from cells of the epithelium which make mucus, and Ms. Dawsons is no
exception. In the normal intestinal tract epithelial cells are renewed rapidly. Cell turnover
time in the colon is 3 days and mean generation time 16 hours; for the rectum these
values are 13h with a mean transit time of 6-8 days and a cell turnover time of 6-8 days.
Cells are produced by the replication of cells at the basal layer beneath the colonic
epithelium, and it is genetic damage to these cells which eventually results in
uncontrolled proliferation. The evidence that it is the contents of the colon and rectum
that is the origin of the exposure is supported by the observation that 50% of large bowl
cancers arise at the lower end, the sigmoid colon and rectum where the concentration of
solid waste in water is increasing
The purpose of this brief review of colorectal cancer is to identify the position and nature
of the cells which were initially damaged by mutagenic materials in faeces at the lower
end of the colon and rectum so that I can address the exposure associated with radioactive
contaminated food, which more likely than not was the cause of Ms. Dawsons colon
cancer.
Table 3.2 Details of the colon and rectum (ICRP Reference Man 1972, Fisher JK (1982)
Normal colon wall thickness on CT. Radiology 145: 415-418)
Adult
Sigmoid colon
Rectum

Length (cm)
40
15

Diameter of lumen (cm)

4
2.5-5

13

Wall thickness (cm)

0.2
1.8 +-0.4mm

Fig 3.3 Cross section of colon; total wall thickness ca 2mm. Note that cell dimensions are
approximately 0.01mm diameter. Cells at the base of the epithelial crypt are those that
initiate replication and the newly replicated cells then move up the epithelial crypt away
to the surface (from Guyton: Textbook of Medical Physiology and American Cancer
Society information).

3.4 Genomic Instability, Bystander, Field Cancerization

Before turning to radiation and colon cancer I will briefly review the most recent research
evidence on the origin of the cellular mutations that lead to cancer. The evidence
presented in the last section was that the final development of cancer results from a
number of preceding steps and these were, until recently, assumed to be the acquisition of
genetic damage which became incorporated into the cell line or clone of the offspring of
previously damaged cells. In the last ten years evidence has emerged that mutagenic
stress to cells from agents like radiation, besides causing direct genetic damage though
ionisation fragments, also triggers a process termed genomic instability whereby the
cell begins to spontaneously generate random mutations. In addition, damaged cells send
signals to nearby cells which are not exposed to the mutagen causing them to become
unstable and produce random mutations themselves. This is termed the bystander
effect. From these discoveries and by other research it has been found that cells
communicate with one another in local communities, and it seems that a breakdown of
this community signalling is necessary for a single cell to develop out of territorial
controls. These processes are easily accommodated into the mathematics of the original
clonal expansion multistage theories. The conclusions with regard to Ms. Dawson remain
unaltered. An agent localised in her gut which caused a high level of genetic damage to
local cells was the cause of her cancer with a lag period of about 10 to 15 years. The
discovery of field cancerisation, where a number of cancers begin in an area of tissue at
the same time, emphasises the way in which communities of cells control the
development of a cell which has the ability and genetic makeup to develop
uncontrollably. For example, experiments with mouse breast tissue transplanted between
mice and irradiated shows that the prior exposure damage of surrounding cells is critical
to the development of a cancer in transplanted tissue (Barcellos Hoff 2005). Thus, it is

14

high local ionisation density or local dose which is the key precursor condition for cancer
development following initiation.
3.5 Ionising Radiation and Colorectal Cancer
3.5.1 External high dose radiation
Ionising radiation is an accepted cause of cancer of the colon and rectum (BEIRV 1990,
BEIR VII 2005, UNSCEAR 2006). The excess fatal relative risk (ERR) per Sievert,
assuming a linear no threshold dose response and based on the Japanese A-Bomb
external acute dose lifespan studies (LSS), is given by UNSCEAR 2006 as 0.65 per
Sievert. However, this figure relies very heavily on the questionable assumption of
linearity of the dose response. I reproduce in Fig 3.4 Figure IX from UNSCEAR 2006
which gives the data from the LSS for the low dose region. It was reported that 11% of
the cases among exposed cohort members of the Japanese A-Bomb study with colon
doses greater than 5mGy were associated with A-Bomb radiation (Preston et al (2007).
It is clear from Fig 3.4 that the excess colon cancer risk in the LLS begins at the lowest
dose, the data point below 50mSv external dose. These low dose points are treated by the
LSS authors and others as scatter, but the work of Burlakova (Burlakova 2000) has
shown, using objective biomarkers for radiation damage, that the dose response curves
are complex and usually biphasic. Burlakova ascribes these effects to the interplay
between induced DNA repair and an underlying saturatable hogs-back radiation dose
response. Busby (see ECRR 2010, CERRIE 2004b) has a different explanation which is
that cells with different sensitivity are involved due to variation in cell cycle activity in
any population. Thus, cells in the replication phase are hundreds of times more sensitive
to radiation mutagenesis and killing, but these are overwhelmed and killed at some low
dose level resulting in an inverse dose rate effect for a period until, at a higher dose, the
less sensitive non replicating cells become affected and the response increases (for a
discussion see Busby 2012). The initial slope of the graph in Fig 3.4 suggests an Excess
Relative Risk of 1.2/Sv. It is also clear that there is an excess risk from the lowest
external radiation dose.

15

Fig 3.4 Colon dose specific ERR estimates from the Japanese A-Bomb external acute
irradiation studies (LSS) showing the various dose response relationships displayed. Also
drawn in red through the low dose data points is a biphasic relationship of the type
discussed in ECRR 2010 and explained on the basis of the theories of Burlakova and
Busby (see text). (from UNSCEAR 2006 p45).

The Japanese LSS registry incidence analysis for 1958-87 for attained age 50 after
exposure at 30 gave an ERR for colorectal cancer of 1.88 per Sv. Excess colon cancer
risk was also shown from studies of patients irradiated for treatment of benign pelvic
disease including 267 patients followed for average 16 years in which 4 tumours were
observed 1 expected [Brinkley and Haylittle 1969]. A follow up of patients treated for
metropathia haemorrhagica [Smith and Doll 1977] found no excess mortality within 5
years but 21 colon cancer deaths versus 13 expected (RR = 1.6) 5 or more years after
treatment.
UNSCEAR 2006 distinguishes between cancer of the colon and rectum with regard to
radiation stating that the radiation dose response differs. The LSS evidence is clear for
women with an ERR of 0.75 per Gy for exposure at age 30. There was a highly
significant excess (RR = 2.2; p = 0.002) of rectal cancer among cervical cancer patients
treated with radiation (Kleinerman et al 1995). The external doses were high, at 30-60Gy.
Increased incidence of rectal cancer was also found in men irradiated for prostate cancer
(Brenner et al 2000, Baxter et al 2005) RR 2.05 after 10 years of radiotherapy. The
external doses again were high, of the order of 40Gy. In a group of Scottish women
treated with X-rays for uterine bleeding, there was an excess of rectal cancer RR=1.36 at
doses to the rectum assessed at about 5Gy (UNSCEAR 2006). In the UK radiation
workers study (Muirhead et al 1999), there was no excess rectal cancer risk relative to the
national population, but there was significant evidence from relative mortality that this
16

result is a consequence of a healthy worker effect. A dose response relation for the colon
cancer in this study suggested an ERR of 1.7 per Gy. In the Canadian radiation worker
studies, there was no excess rectal cancer risk relative to national populations due to a
healthy worker effect, but in this case there was a strong dose response effect for external
irradiation, suggesting an ERR of 13.8 per Gy (95%CI 3.7, 33.6). The international
Thorotrast study found a Relative Risk of 1.8 between Thorotrast exposed and controls in
Denmark/Sweden, but no dose estimates were made (Travis et al 2003). If we take the
median dose as 100mSv, this gives a risk of about 16 per Sv.
A study published in 2012 of 12,995 women treated for benign gynaecological disorders
in North East USA between 1925 and 1965 attempted to find the median doses associated
with various induced cancers. For colorectal cancer, the median external dose was found
to be 1.7-7.2Gy with evidence for a dose response. Excess relative risks for cancer of the
rectum obtained by Poisson regression were reported to be 0.23/Gy (p= 0.05) external
irradiation (Sakata et al 2012). In a 2012 nested case-control study carried out with
13,048 oncology patients treated by radiotherapy from childhood cancer in Tennessee, 19
cases of colorectal cancer were identified. Poisson regression methods were used to
investigate the magnitude of the radiation related risk, the shape of the dose response,
gender, age at exposure and attained age. The sex averaged ERR per Gy was 0.42. The
estimated lowest external dose range with a significant ERR was 0-200mGy, and there
was no dose threshold. An increased risk of non-cancer illnesses was also observed
(Nottage et al 2012). Increased colorectal cancer risk was found in a study of US
radiotherapy patients published in 2010. Standardised incidence ratio for secondary
colorectal cancer was 10.9 (95%CI 6.6-17.0). The tumour was more likely to be found in
the irradiated section of the colon (SIR 7.7; p = 0.001) and increased by 0.7 per Gy
(Sountoulidesd et al 2010). A study of cancer mortality in French nuclear workers who
were monitored for radiation exposure found a significant positive trend with cumulative
dose for colon cancer (Metz-Flamant et al 2009). In a study of 90,502 endometrial cancer
patients divided into groups, 34,613 individuals who were treated with radiotherapy and
52,182 who were not identified from the US SEER data base, a Poisson regression
approach found that relative risk peaked 10 years after exposure with a 43% excess RR
for colon and rectum cancer combined. (Kuman et al 2008). Research involving a study
of cancer in 200,000 workers using the Canadian National Dose Registry between 19512007 identifies a significant dose response for the incidence of colon cancer with risk per
Gy found to be higher than those shown by the Japanese A-Bomb studies. These were of
relatively low-dose subjects working in the Canadian nuclear industry. (Zeilinski et al
2008). An earlier incidence study of the Canadian National Dose registry subjects found
Excess Relative Risk for cancer of the rectum to be 13.8 per Sv (Sont et al 2001).
Mortality and incidence increases in cancer of the colon and rectum were found in the
Australian participants in the British Nuclear tests in Australia in a study published in
2008. However, the authors decided that the effect was not caused by radiation since
there was no dose trend based on film badges (Gunet et al 2008).

17

3.5.2 Internal radiation: Uranium and cancer

The genotoxic effects of internal radiation exposure cannot be modelled by effects
produced by external irradiation (ECRR2010, ECRR2003, Busby 1995, Busby 2006).
The reason is that cancer and other genotoxic effect of radiation are a function of the
ionisation effects at the target, which is the chromosomal DNA. There are a number of
internal radiation processes, exposures to internal radionuclides that result in a much
higher density of ionisation near the DNA that is predicted by the conventional
assessment of absorbed dose made by the current radiation risk model, which dilutes all
the energy from absorbed radiation into large (generally kilogram) masses of living
tissue. I examine the reasons for this in a separate section below and in Appendix B.
However, the difference between doses from external radiation and internal radiation are
well exemplified by the case of the element Uranium which I l examine and discuss in a
separate section below.
One of the radioactive contaminants released by SSFL which was a substantial
contributing cause to Ms. Dawsons rectal cancer is Uranium. I will review some of the
reports showing that Uranium has anomalously high genetic damage and cancer
producing effects.
I have studied the genotoxic effects of Uranium and was the Chair of the European
Committee on Radiation Risks Uranium effects sub-committee 2003-2010 and edited the
2010 report of Uranium and health which I attach as Appendix C (see
www.euradcom.org/uranium). In this section I briefly review the epidemiological
evidence linking Uranium exposure with cancer. A number of studies of workers at
Uranium processing facilities have indicated that there are significant genotoxic effects
including cancer which occur at low internal doses. Guseva Canu et al have produced
three articles based on studies of French Uranium processing workers, which taken
together indicate anomalous cancer producing effects for Uranium (Guseva Canu et al
2008, 2010, 2012). The authors study lung cancer and lymphoma/leukemia. They found
that very low doses of Uranium exposure by inhalation cause increased hazards out of
proportion to doses. Second, they show that the severity of the risk is a question of the
type of Uranium exposure. By employing the exposure matrix method used by the
authors with their earlier correlation between their exposure matrix and absorbed dose as
calculated by an ICRP based UK Health Protection Agency computer model, it is clear
that the error in the ICRP model shown by the studies is of the order of 2400-fold. That is
to say, there is 2400 times more lymphoma/leukemia than is predicted by the current
radiation risk model.
These results support other findings of the effects of Uranium in workers. A study of a
cohort of uranium workers in the USA exposed to Uranium dust showed highest relative
risks for specific sites for brain tumours (1.57) Oesophagus (1.35) Rectum (1.48) and
colon (1.11) larynx (1.10) and multiple myeloma (1.30) (Dupree Ellis et al 2000). Median
external doses were 15mSv from the sites of the main cancers observed, contact with
Uranium dust seems to be the cause of the excess risks.

18

A study in the UK of workers at the Springfields Uranium fuel production plant showed
(like the Dupree-Ellis study in the USA) that although the workers generally had
comparable or lower level of cancer than the general public (through a healthy worker
effect), for individual sites there was a significant trend with dose. This was true also for
colorectal cancer in the Springfield workers (McGeohegan and Binks 2000). The value of
the AREVA, Springfields and US Mallinkrodt uranium worker studies is that all three
show that Uranium causes cancer at extremely low doses.
These findings support discoveries in Iraq and the Balkans of Uranium effects in those
exposed to weaponised Uranium nanoparticles. These are of particular relevance to the
Dawson case. Three studies were carried out by me and colleagues in Fallujah, Iraq to
investigate the anecdotal evidence of huge increases in cancer rates in Iraq after the 2003
war and its spill-over into a US led attack on the city of Fallujah in 2004. In Busby et al
2010, an epidemiological study identified very high cancer rates in the population of the
city. These were associated with high levels of infant mortality and a sex ratio alteration
at birth which followed one year after the attacks on the city in 2004 in which it was
believed that novel Uranium weapons were employed. There were also high levels of
congenital anomaly rates at birth (Alaani et al 2012). In a follow up where we examined
52 elements in the hair of mothers of children with congenital anomaly, we found
significant excess level of Uranium, which by using long hair samples, we were able to
show increased in the past back to the time of the attacks. There was no other explanation
for the increased indications of genetic damage in the populations. Other studies have
shown high levels of cancer in areas where Uranium weapons were deployed, and I have
presented evidence on this issue to the United Nations Human Rights Council on two
separate occasions and been invited to provide an article on the issue (Busby 2009).
In these and other Uranium weapons and Uranium studies the result is clear: Uranium has
anomalous genotoxic effects and can cause cancer, including colorectal cancer at doses
which are thousands of times lower than those predicted to be necessary to cause cancer
on the basis of acute high dose radiation studies. This fact is also shown by a recent
ecological study of those persons living in census tracts in South Carolina, where
Uranium levels vary (Wagner et al 2011). In this study, groundwater Uranium levels
were mapped and used to define 4 census tract groups with 0.03, 0.08, 0.18 and 0.84ug/l
of Uranium. There was a strong and significant (p=0.01) association between cancer and
Uranium levels. This was true for colorectal cancer. Based on the data in the article, a
ten year exposure is set forth in in Table 3.3. It is clear that Uranium in groundwater
represents a significant hazard for colorectal cancer at very low level of dose, as
conventionally calculated.

19

Table 3.3 10 year cumulative dose (ICRP 72) from drinking water containing Uranium at
level found in groundwater in census tracts in South Carolina (Wagner et al 2011).
Water
Water
concentration activity
ug/l
mBq/l

0.03
0.08
0.19
0.29
trend

2.22
6
13.8
21.6

0.37
1.0
2.3
3.6

10 year
intake Bq*

10y
Cumulative
Colon dose

(cancer incidence
SIR)

ICRP 72
0.15
0.31
0.72
1.12

Referent
0.15
0.22
0.27

ICRP Reference Man, 600l/y; b 5.2 x 10-8 Sv/Bq U-238

3.5.3 Summary: does radiation cause cancer of the colon and rectum?
Cancer of the colon and rectum are shown to be caused by radiation in many studies.
These studies can be divided into external acute high dose studies and internal low dose
studies mostly of groups exposed to the element Uranium. The dose required to cause an
increase in cancer rate is given by the risk factor which is enormously different for
external and internal irradiation. Examples are given in Table 3.4
Table 3.4 Excess Relative Risk factors for colorectal cancer from the literature
(references in text).
Study
Japanese LSS
Cervical
radiotherapy
Prostate
radiotherapy
UK radiation
workers
Canada radiation
workers
USA gynaecological
radiotherapy
Childhood cancer
radiotherapy
Thorotrast
Australian Test

Risk per
Sievert
0.6 to 2
2.2

Exposure

Note

External acute
External acute

Colorectal
Rectum

2.05

External acute

Rectum

1.78

External chronic
monitored
External chronic
monitored

Colorectal

0.23

External acute

Colorectal

0.42

External acute

Colorectal

14(?)
>2000

Internal chronic
Internal chronic

Colorectal; dose not assessed

Rectal

13.8

20

Rectum

veterans
AREVA French
workers
Uranium; USA
Mallinkrodt
Uranium; UK
Springfields
Uranium DU Iraq
Fallujah
S. Carolina ground
water Uranium

2400
>2000
>2000
>5000
>5000

Internal chronic
Enriched Uranium
Internal chronic
Uranium
Internal chronic
Enriched Uranium
Internal chronic
Uranium
Internal chronic
Uranium

Lymphoma/ Leukemia
Colorectal
Various including colorectal
All cancer sites studied
Colorectal

Various conclusions can be drawn from this. First, at high acute doses, either from atom
bombs or from radiotherapy, it is possible to cause cancer of the colon and rectum.
Second, we can see that the dose response for this is not linear. At lower doses, the effect
is proportionately greater. This conclusion is consistent with the mechanism of cancer,
because at higher doses cells are killed and will therefore not mutate. Third, the evidence
is quite clear that for internal irradiation, specifically from exposure to Uranium, the risk
is hundreds of times greater than for external acute exposure. This is confirmed by
several studies. I now turn from reviewing the epidemiology to discussing the causes of
this difference between external and internal; radiation, and particularly the cause of the
health effects of internal Uranium exposure at low doses. In the next section I briefly
consider the mechanism so that I may discuss how it relates to Ms. Dawsons situation.
But, before I do so I will present some details of another case of colon cancer following
exposure to internal Uranium, about which I have personal knowledge and served as an
expert consultant.
3.6 Stuart Dyson
The first Gulf war in Iraq in 1991 saw the introduction to the battlefield of a novel antitank projectile, Depleted Uranium or DU. The US military had begun to employ
penetrators made of solid Uranium which were found to be extremely effective in
penetrating armour, and some 350 tons of this material has been fired on the battlefields
of Iraq causing widespread Uranium contamination of vehicles and the environment,
particularly in the southern part of the country. When a penetrator of DU hits the target
it burns and produces nanoparticle diameter Uranium Oxide which is respirable and
highly mobile. The question of the effects of DU on health forms a complete subject
which is too large to address here. An overview can be found in Busby 2006, 2009 and in
Appendix C. This material contaminated vehicles and also those individuals whose job it
was, after the battles, to clean them. In Iraq, the consequence of the contamination and
the exposures materialized in the form of an increasing cancer rate in those areas which
were contaminated and also increases in congenital malformation and infant mortality
rates in the same areas. One of the British soldiers whose job it was to clean
contaminated vehicles was Stuart Dyson. Shortly after returning to the UK Dyson
became ill, as did many of the veterans of the Gulf war, with a range of symptoms termed
collectively Gulf War syndrome. I have elsewhere opined that this range of illnesses

21

and conditions is a consequence of exposure of the lower brain to Uranium. In 2009, at

the unusually young age of 39, Dyson developed colon cancer and shortly after that he
died. Dyson himself, his wife and many colleagues and veterans believed that the cancer
was caused by the exposure to DU and Her Majestys coroner investigated the issue. The
coroner took evidence from experts appointed by the Ministry of Defence and also from
me; my evidence relating to Mr. Dyson follows closely that presented in this report about
Ms. Dawson. Because of the political implications (thousands of UK servicemen had
been exposed to DU and many were sick) and the many scientific arguments relating to
the effects of DU, the coroner decided to call a jury to deliberate the evidence and
discover the cause of death. The outcome pivoted on the question of whether the
environmental exposure received by Dyson was sufficient to cause his fatal cancer. The
MoD argued, from the position of the radiation risk establishment, that the exposure level
was far too small. This had been the conclusion of a number of official and semi-official
reports into the effects of DU from analyses by the World Health Organisation to the UK
Royal Society. But, all these groups had based their conclusions that the exposure
based on the standard methodology of examining the circumstantial evidence of the
subjects activities likely to have created exposure pathways, was too low on the
conventional risk model, that of the International Commission of Radiological Protection
(ICRP), effectively that of the BEIR committees in the USA and UNSCEAR. These take
their risk factors from the Japanese A-bomb high dose acute exposure studies which, as
we see in Table 3.4, give risk factors for colorectal cancer of between 0.6 and 2 per
Sievert. The Royal Society pointed out in their 2001 report, there is no way that any of
the military personnel could have received a dose greater than about 1 mSv (which
represents an inhalation exposure of several milligrams of DU dust and therefore, even at
a risk of 2 per Sievert (the ICRP give ERR of 0.45), the risk of fatal colon cancer could
not be more than 0.2% (using the ICRP risk factor, 0.05). However, I argued in Court
from the studies of Uranium and also from various theoretical considerations which I will
present, that external and internal radiation is different and that the ICRP model was not
valid for Uranium exposure. The Court accepted my testimony as scientifically sound and
the various experts testified based on the studies, their proper interpretations, the data
found within the studies, the assumptions which could properly be made, the nature of
radiation cancer causing properties, among other things. The jury rejected the evidence of
the MoD and found that Mr. Dysons colon cancer was more probably than not caused by
exposure to Depleted Uranium (REF). The Coroner sent a Rule 43 letter to the Minister
of State and the matter received some media attention. It should be said that even the
MoD did not dispute that there is no level of exposure to radiation, including Uranium,
which cannot cause colon cancer. See, e.g., Committee on the Biological Effects of
Ionizing Radiation, Health Effects of Exposure to Low Levels of Ionizing Radiation, at
398 (Natl Academy Press 1990). There is no threshold limit for radiation exposure and
colon cancer and any exposure can cause an individual cancer. Id.
4. Radiation and Health: Summary of the Current Situation
It is apparent from the discussion of colon cancer and radiation that for internal
radionuclide exposures, particularly Uranium exposure, there are very high risks at very
low doses (Table 3.4). These observations are epidemiological ones. There are many

22

other epidemiological observations of high risks at low doses in the peer review and nonpeer reviewed literature. (Busby 2002). In this section I develop this discussion, since it
is of relevance to the question of the cause of Ms. Dawsons cancer. I present a fuller
account of the history of the science of radiation risk in Appendix B and as it relates to
Uranium in Appendix C.
It must be appreciated that there has been something of a scientific revolution in the
understanding of radiation risk since the radiation risk model of the International
Commission on Radiological Protection was first formulated in 1952 to deal with the
increasing concerns of those being exposed to fallout from nuclear weapons tests. Briefly,
between 1952 and 1990 the dose limits had to be continually reduced following
laboratory research and epidemiology which showed, throughout the period, that low
doses of internal radiation were more hazardous than had been previously thought. By the
late 1960s it had become clear to all who were interested in the subject, that low-level
exposures to radiation carried significant risk of cancer and leukemia. In the 1980s a
series of studies near nuclear sites revealed a risk of child leukemia due to very low doses
below the natural background level. By the 1990s there emerged a number of novel
experimental observations which were able to explain many anomalous epidemiological
observations of significant hazards to health at very low doses. These involve the
discovery of genomic instability and bystander signaling which together are now
referred to as non-targeted effects (Mothershill and Seymour 2012). What they showed is
that (a) organisms and cells are exquisitely sensitive to radiation even at levels below
natural background and (b) the dose response relation is highly complex but mainly
supralinear (hog-backed) at the lowest dose i.e. a greater effect at a lower dose and (c) a
radiation exposure of one cell causes harmful genetic changes in local cells which are not
exposed up to a distance of greater than 500 cells or more. In parallel with these
experimental cell biology discoveries, and from the 1990s onwards there was a further
wealth of epidemiological evidence mainly (but not exclusively) related to Chernobyl
exposures to internal radionuclides. Taken together, these experimental and
epidemiological discoveries made clear that the basis of the current radiation risk model,
that of the ICRP, is fatally flawed for internal radionuclide exposures. The ICRP model
(and others which are based on an averaged absorbed dose like BEIR VII) are the basis
for Health Physics, a discipline that that was developed in the 1950s to calculate the
health outcomes of radiation exposures
The whole assessment of radiation in terms of health has been, and remains, through the
quantity absorbed dose and what can be called the bag-of-water model.
In this bag-of-water model, illustrated in Fig 1, the total energy transferred by the
radiation to living tissue is diluted into a large mass, greater than a kilogram, as if the
effects were uniform throughout the tissue being considered. In Fig 4.1 the tissue mass A
represents an external irradiation by X-rays or gamma rays and here the effects are
uniform across the tissue. But in the case B, for internal irradiation, it is clear that it is
possible, for certain kinds of exposure, for tissue local to the source to receive very large
amounts of radiation energy at the same overall energy transfer to the tissue mass.

23

Fig 4.1 Comparing external and internal irradiation: the ICRP/ ICRU bag of water model.
In case A, external radiation (X-rays or gamma rays) there are 20 events uniformly
spaced throughout the tissue and the absorbed dose (see text) at any microscopic point
is evenly distributed. In case B, for internal irradiation (here from a radioactive particle)
there is a very large transfer of energy to a small tissue volume and the concept of
absorbed dose does not apply (from Busby 2012)

Thus, in the historic (and also the current) system of radiation protection, those experts
who assess radiation risk, Health Physicists, calculate the cumulative absorbed dose in
Grays, i.e. in terms of the total energy in Joules imparted by the beta electron or alpha
particle decays of an internal radionuclide contamination to one kilogram of tissue. The
method derives from its source, the A-Bomb studies and the simplicity of carrying out the
same calculation for external gamma radiation, where the density of energy absorbed
(also delivered as electron tracks) is uniform. For the calculation, the tissue is modeled as
water. For example, those whose body contains 100 Bq of Strontium-90 are assessed, for
the purposes of radiation protection, as having received a cumulative absorbed dose of
100 x w where w is the cumulative (absorbed) dose coefficient, obtained from
measurements of the biological half life of the Strontium in the body and the decay
energy of each decay in Joules. This number w is to be found in a Table published by the
ICRP. In the case of the Strontium-90 contaminated individual, if the person weighed 50
kg, then the mean activity concentration would be 2 Bq/kg. The resulting absorbed dose
would then be 2 x 2.8 x 10-8 (this is the ICRP 72, 1996, dose. In other words, the
committed dose is 5.6 x 108 Sv (0.056
a chest Xdose acute exposure to gamma rays from an atomic bomb linearly scaled to zero dose
(the current way of modeling radiation effects)?
The matter has been discussed in some detail since 1998 by the independent European
Committee on Radiation Risk (ECRR) whose reports (2003, 2010) provide a
methodology for assessing health effects through a system of weighting factors based on
available data. As more and more evidence emerged after 1995 pointing to the face that
something was very wrong with the ICRP absorbed dose approach to internal radiation,
the UK government set up a Committee Examining Radiation Risk from Internal Emitters
(CERRIE). Since there were (and are) political dimensions to the issue, the committee
was composed of scientists and experts from the nuclear industry and the official
radiation protection organizations in the UK. Unfortunately the 4-year process ended in
24

acrimony, legal threats to members of the committee, and failure to agree on a final
report. Two reports were created (CERRIE 2004, 2004b). However, they did agree that
there were reasonable concerns about the safety of employing absorbed dose for certain
internal radionuclide situations, and similar concerns about the safety of the ICRP model
were made in 2005 by the French (2005). The error factor that these discussions led to
was believed by different ends of the CERRIE process to be between 10-fold and 1000fold. More recently, the value put on this error factor by the retired Scientific Secretary
of the ICRP at a meeting in Stockholm in 2009 was two orders of magnitude. What this
means, in our Strontium-90 case above, is that the dose from 100 Bq contamination to the
the risk of fatal cancer is proportionately increased. To put this in perspective, the mean
Sr-90 dose over the period 1959-1963 to individuals in the northern hemisphere was
given as about 1 mSv (UNSCEAR 1977). The ICRP risk model gives a 0.45% per
Sievert excess lifetime cancer risk. Epidemiological studies suggest that the cancer
epidemic which began in the 1980s in areas of high rainfall and fallout is a
consequence of the earlier fallout exposures (Busby 1994). The weighting of dose
necessary to explain this is greater than 300, if calculated from the ICRP Excess Relative
risk factor of 0.45 /Sv (ECRR 2010, Busby 2002). Many other instances of anomalous
health effects from exposure to internal radionuclides require hazard weighting factors of
between 100-fold and more than 2000-fold, and these are consequences of various
mechanisms which depend upon the nuclide being considered and which are discussed
elsewhere (Busby DNA book, ECRR2010).
By 2012, the dissonance between the predictions and explanations of the official
radiation risk models and the perceived reality in terms of human health in populations
exposed to internal radionuclides has become embarrassing to the scientific community .
For the purposes of the current discussion relating to Ms. Dawson I need only to examine
the element Uranium. But before I do this, I will list the main pieces of evidence for the
failure of the current radiation risk model which have been recently presented by
thousands of individuals (including many eminent scientists) as a Human Rights Petition
to the European Parliament and by me in a presentation to the Human Rights Council in
Geneva in October 2012.
4.1 Evidence of the Failure of the Current (ICRP) Radiation Risk Model; the
European Parliament Petition
4.1.1 The Petition basis
1. Radiation exposure is legally controlled in Europe by the Directive EURATOM
96/29 which has been updated in 2012 and either is being or has already been
adopted by Member States.
2. The latest version of this Basic Safety Standards Directive has a clause which
requires a re-justification of all radiation practices if new and important
information which affects the scientific assessment of radiation risk becomes
available.

25

3. The ICRP risk model is formally adopted by this BSS Directive and it depends on
that model for its calculation of the quantity of ill-health (e.g. cancer, leukemia)
caused by any dose.
4. Since 1996, when the BSS was written, there have been many scientific and
epidemiological studies and reports which show the ICRP model to be wrong by a
very large amount. Therefore, the BSS law requires a re-justification of all
radiation practices.
5. The error in ICRP for the kind of internal exposures is between 300 and more
than 1000-fold. This means that between 300 and more than 1000 times more
people develop radiation related cancer than the ICRP model predicts.
The ICRP model is based on the idea of DOSE. This is measured in Milli Gray or Milli
Sievert. It is defined as the absorbed energy per unit mass in Joules per Kilogram. Such a
measure of radiation exposure cannot be used for internal radiation effects from e.g.
plutonium particles since one single particle with a diameter a few micrometers will
impart huge amounts of energy to local cells, but if averaged over large masses of tissue
the DOSE will be almost nothing. This is the origin of the large error factor. A list of
evidence that this is so follows. These are by no means all the instances of the failure of
the current risk model, but science does not require many instances of the failure of a
theory; one instance is enough for the theory to be dismissed as wrong.
4.1.2. Childhood cancer near nuclear installations
There have been reports in peer reviewed journals of increased risk of childhood
leukemia and non-Hodgkin lymphoma near many nuclear sites in Europe. A list and
discussion may be found in ECRR2010. Child leukemia excesses are found near nearly
all the sites that have been examined (ECRR2010) e.g. the reprocessing sites at Sellafield
(Gardner et al 1990), Dounreay UK ( Heasman et al 1986) and La Hague (France) (Viel
and Poubel 1997) near the Atomic Weapons Establishment Aldermaston (UK) ( Busby
and Scott Cato 1997), the Atomic Energy Research Establishment Harwell (UK) ( Busby
and Scot Cato 1997), near Hinkley Point nuclear power station (UK) (Bowie and ewings
1988) and recently, near all the combined nuclear sites in Germany (KiKK study)
(Kaatsch et al 2008, Spix et al 2008) and near all the combined nuclear sites in France
(Sermage-Faure et al 2012), GB (Independent Advisory Group 1984) and Switzerland.
The radiation risk community (COMARE 1996, Independent Advisory Group 1984),
basing calculations on the ICRP risk model, have worked out the dose ranges and say
they cannot be more than a few microSieverts, well below Natural Background. The
ICRP risk model predicts an excess risk of 0.05 cancers per Sievert. 100 microSieverts is
1/10,000 th (10-4 of a Sievert). An Excess Absolute Risk of 0.05/Sv is Excess Relative
Risk (ERR) of 5E-4 for 0-4 y old
children, is 1E-3 per 6 microSv. But, there are twice as many child leukemias as are
expected: a doubling of risk: the ERR observed in the KiKK study was ~ERR=1. So,
ICRP predicts a 1000-fold lower risk than found in the KiKK study. But, we can also
employ the Risk model for child leukemia following obstetric X-rays (Alice Stewarts

26

studies). Stewart found a 40% excess risk after an X-ray dose of 10mSv. That would
suggest a 4% increase after 1mSv, 0.4% after 100uSv. But, we are seeing a 200%
increase at this level. The error is now 200/0.4 = 500-fold. However, the ICRP do not
accept the Stewart findings, or at least they are not incorporated into the model.
4.1.3 Infant leukemia after Chernobyl
Five different groups (Petridou et al 1996, Michaelis et al 1997, Gibson et al 1988,
Ivanov et al 1998, Busby and Scott Cato 2000, Busby 2009) reported a statistically
significant increase in infant leukemia in 5 different countries of Europe in those children
who were in the womb at the time of the Chernobyl Caesium-137 fallout, as measured by
whole body monitoring. The effect was also reported from the USA (Mangano 1997).
Thus, the Chernobyl exposure is the only explanation for the increase. This occurred and
was reported from Greece, Germany, Scotland, Wales, Belarus, USA and the error this
shows in the ICRP model was the subject of two peer reviewed papers in 2000 (Busby
and Scott Cato 2000, and Busby 2009). Using the Alice Stewart relation between dose
and leukemia above, the error is about 400-fold (depending on the country). Using the
ICRP model it is upwards of 1000-fold. This analysis is most relevant since it
unequivocally supports the causal relation revealed by the nuclear site child leukemias,
yet in this case fission product internal radiation can be the only cause.
4.1.4 Cancer following Chernobyl in Northern Sweden
The study by Martin Tondel found an11% increase in cancer for every 100 kBq/sq metre
of Cs-137 from Chernobyl (Tondel et al. 2004). It is possible to calculate that 100
kBq/m2 Cs-137, including a further 100kBq/ m2 of Cs-134 if reduced exponentially due
to rain washout to rivers and lakes with half-life of 6 months, would give a committed
effective dose of about 1 mSv. The ICRP model (ICRP2007) predicts an Excess Relative
Risk of 0.45 per Sv, so the ICRP expected excess relative risk, including a Dose Rate
Reduction Factor of 2 (as used by ICRP) is 0.0225%. The error in ICRP model defined
by Tondels result is thus 490-fold.
4.1.5 Human sex ratio at birth perturbed by low doses of internal fission-product
ionising radiation
Studies by Hagen Scherb and Kristina Voigt (2010) show clear and highly statistically
significant alterations in the human sex ratio at birth (the number of boys born to girls)
after (a) atmospheric bomb testing, (b) Chernobyl and (c) near nuclear facilities. Effects
are shown to be local, European (several countries were studied) and global, supporting
earlier evidence of increases in infant mortality during the period of atmospheric weapons
testing (Sternglass 1971, Whyte 1992). Sex ratio has been accepted as a measure of
genetic damage with the preferential killing of one or other sex depending on the type of
exposure (mothers or fathers). According to Sherb and Voigt, millions of babies were
killed by these effects (Scherb and Voight 2011). Recent re-analysis of the sex ratio
effect in Hiroshima reveals the effect in those populations as well (Padmanabhan 2011),
evidence which was not taken into account by the USA researchers. This evidence

27

objectively confirms the serious genotoxic effect of internal ionising radiation on germ
cells and the exquisite sensitivity of humans and other living creatures to releases from
Uranium fission. Neither the BSS nor the ICRP consider such effects, nor are they
included in any assessment of harm. This is clearly a human rights issue which was not
considered when the BSS was prepared in 1996, and the effects of internal fission nuclide
exposures on the foetus and germ cells have now been confirmed.
4.1.6 Cancer, leukemia/lymphoma and heart disease in Uranium workers
Irina Guseva Canu and co-workers in the French nuclear risk establishment IRSN have
been studying the health effects of Uranium exposure on French nuclear workers who are
exposed only to Uranium. There are three relevant published papers (Guseva Canu et al
2010a, 2010b, 2012). These show a number of things. First, that very low doses of
Uranium exposure by inhalation cause increased hazards of developing lung cancer and
lymphoma/leukemia. Second, they find that the severity of the risk of a question of the
type of Uranium exposure. By employing exposure matrix the method used by the
authors with their earlier correlation between their exposure matrix and absorbed dose, as
calculated by an ICRP based UK Health Protection Agency computer model [29, 30], the
error in the ICRP model shown by the studies is of the order of 2400-fold. That is to say,
there are 2400 times more lymphomas than are predicted by the ICRP risk model. This
finding supports the discoveries in Iraq and the Balkans of Uranium effects in those
exposed to weaponised Uranium nanoparticles.
4.1.7 Secondary Photoelectron Effect
The ability of high atomic number (Z) elements in the body to act as antennas for natural
background gamma radiation was published in 2005 (Busby 2005a, Busby 2005b) and
2008 (Busby and Schnug 2008, Tickell 2008). Briefly, the physical absorption of natural
background gamma radiation by elements is proportional to the fourth power of their
atomic number Z. This means that nano-particles of insoluble high Z elements (Gold,
Platinum, and Uranium) absorb background radiation thousands of times more effectively
than living tissue (mainly water) and then release this energy into tissue as local
photoelectrons. This means that the radiation dose near such particles is extremely high.
Two computer studies by the radiation establishment have conceded that there is an
enhancement of dose near such particles, but both have shown that the enhancement is
finite but modest. The studies are both flawed by the same methodology, which is to
dilute the energy into a large volume of tissue. The experimental measurements with gold
foil (Regulla et al 1998) and gold nanoparticles (Hainfeld et al 2004) and other computer
analyses which examine the dose close to the particles (Howard et al 2009) show quite
clearly that the effects are those of high enhancement of dose largely predicted by theory.
In addition, since Uranium, which has the highest Z of any element, also has a strong
affinity for DNA, the enhancement of hazard from molecular or ionic Depleted Uranium,
shown by a number of studies (Huxley and Zubay 1961, Neilsen et al 1992) is explained.
The SPE has not been incorporated into ICRP risk modeling, and these discoveries (and
others relating to Uranium hazards (Busby 2009, Busby 2010) reported since 1996 falsify
the ICRP risk model which is the basis of the BSS.

28

4.1.8 Cancer and genotoxic effects in Iraq following DU exposure

A series of studies of the population of Fallujah Iraq shown (Alaani et al 2011, Busby et
al 2010, Alaani et al 2012) to have been exposed to Uranium following the 2003-2004
battles have revealed extremely high rates of congenital malformation at birth and cancer
and leukemia/lymphoma in adults. The studies also draw attention to significant sex ratio
effects at birth beginning after 2004. These results, and the increases in genotoxic effects
in the offspring of Gulf veterans support and are supported by the other sets of
observations reviewed above which show that inhaled Uranium nanoparticles represent a
very serious hazard which was not incorporated into the BSS and is entirely overlooked
by ICRP.
4.1.9 Chernobyl effects as reported in the Russian language peer-reviewed literature
The effects of the Chernobyl accident exposures have been reported in the Russian
language peer review literature since 1996. These results have been reviewed by Busby
and Yablokov 2006, Yablokov et al 2010 and Busby et al 2011 (Busby et al 2011), but
have been largely ignored by ICRP. They constitute a very large body of peer reviewed
work which show that the effects of the Chernobyl accident exposures are massive and
extremely serious (Busby et al 2011). They range from cancer and leukemia, to heart
disease, especially in children together with a range of illnesses which can be best
described by the term premature ageing (Malko 1998). They include congenital
transgenerational diseases and are reported in animals and plants which cannot be
affected by the kind of psychological processes (radiophobia) which have been employed
by the radiation risk establishment to account for the early reports coming out of the
affected territories. In addition, there are objective measurements of serious biological
harm to humans and other living creatures affected by the exposures. The germline
mutations found by minisatellite tests (Dubrova et al 1997) in humans were also
associated with real morphological effects and fitness loss in birds (Ellegren et al 1997)
and were shown to have caused significant sex ratio changes in the birds and also
population loss (Moeller et al 2012), which is in agreement with the findings of Scherb
and Voigt (2010) and the infant mortality findings of Sternglass 1971 and Whyte 1992.
The implications for the understanding of the historic effects of the nuclear project on
human health are alarming.
4.2 Uranium
The radiobiological effects of exposure to Uranium have received a great deal of
attention since the mid-1990s following the military use of Uranium weapons (originally
Depleted Uranium DU) in Iraq and the Balkans. Since then, a large number of studies
including animal studies, epidemiology and cell culture studies and also theoretical
studies have shown that Uranium represents a very serious genotoxic hazard, out of all
proportion to its calculated absorbed dose. The matter has been examined by the ECRR
and a report which reviews the area was published in 2010. This is attached as Appendix
C. The committee concluded that for certain kinds of exposure, particularly internal

29

inhalation of particulates, the weighting factor for dose should be 1000. More recent
reports (e.g. the South Carolina study) suggest that this was overcautious and the risk
may be greater than this.
There are a number of genotoxicity enhancement mechanisms that can easily explain the
anomalous hazard from internal Uranium. First, Uranium has a very high affinity for
DNA, binding to the phosphate backbone. This has been known since the 1960s when
Uranyl salts began to be used for staining chromosomal material. . By 1992 the chemical
affinity constant had been measured and was found to be 1010M-1 (Neilsen et al 1992).
Therefore Uranium, an alpha emitter, would preferentially bind to DNA. But, it is now
known that DNA is the main target for radiobiological effects; therefore, we immediately
have a mechanism explaining the enhanced radiotoxicity of Uranium. The concentration
of DNA in a cell is known: it represents a very small fraction of the total material in the
cell. In a 10
2.3 pg deoxyribose, 1.2 pg phosphate. In addition, associated with this macromolecule
are 3.1 pg of bound water and 4.2 pg of inner hydration water (Ward et al 1988). Since
absorbed dose is given as Joules per kilogram, if it were possible to accurately target the
DNA complex alone, a dose to the cell (mass 520 pg) of 1 milliJoule per kilogram (one
milliGray, one milliSievert) would, if absorbed only by the DNA complex (6 pg),
represent a dose of 520/6 = 87 mSv to the DNA. It is possible to imagine the DNA as an
organ of the body, like the thyroid gland or the breast. If this is done, then there should be
a weighting factor for its radiobiological sensitivity of, at minimum, 87 which would be
based on spatial distribution of dose alone. For external photon irradiation, to a first
approximation, tracks are generated at random in tissue. Therefore, only a small
proportion of these tracks will intercept the DNA but the interception will be mainly
uniform, and the health effects from such external exposure may be assumed to be
described by the averaging approach of absorbed dose
The second radiobiological enhancement factor for Uranium arises from a more
interesting source and is unrelated to its intrinsic radioactivity. It is something which I
discovered in 2003 and presented to the CERRIE committee: it is termed the Secondary
Photoelectron Effect (Busby 2005, Busby and Schnug 2009, Howard et al 2009). The
absorption of external gamma radiation by any element is proportional to the fourth
power of its atomic number Z. Uranium (Z=92) has the highest atomic number of any
naturally occurring element. Therefore, its absorption of natural background radiation
will be many thousands of times greater than water or living tissue. The energy absorbed
from the background gamma radiation is converted mainly into photoelectrons and short
range highly ionizing Auger electrons. It follows that a Uranium atom bound to DNA
will not only decay with an alpha particle release, but will continually release
photoelectrons and Auger electrons into the DNA as a result of photoelectron induction
by the external gamma field. This will be particularly harmful for nanometer diameter
particles of Uranium, of the kind released by nuclear sites and following weapons usage.
The effect for particles was modeled by my group at the University of Ulster in 2009 and
the results of a Monte Carlo calculation for a 20nm particle of Uranium (Z=92), Gold
(Z=79) and water (Z=7) are shown in Fig 4.2 below. Enhancement factor in this

30

calculation for 100keV incident photons and the 10nm Uranium particle relative to water
was approximately 8000.
Fig 4.2 Photoelectron tracks emerging from (left to right) 10 nm particles of water
(Z=7.5), Gold (Au; Z =79) and Uranium (U;Z=92) after irradiation with 100keV photons.
Monte Carlo (FLUKA code) analysis. Track numbers are in proportion to the 4th power Z
law (tracks are shown as projections on a flat plane). Note that the model uses 1000
incident photons for Au and U but 10,000 for water [71]

4.3 Uranium Particle and Uranyl Ion UO2++ Doses to the Crypt Cells of the Colon/
Rectum of Ms. Dawson and Mr. Mark Lindsey
From the preceding accounts it has been shown that the ingestion and inhalation of
Uranium particles carry an anomalously high genotoxicity for cells which are local to the
particle. The relevance of this for Ms. Dawsons rectal cancer is that she lived downwind
of a plant which was releasing significant quantities of Uranium contaminated dust. The
period of remediation of the SSFL plant and the period of generation of the Uranium dust
was when Ms. Dawson lived with her husband, Mr. Lindsey, and where they grew
vegetables and ate them in season. One of the exposure pathways more probably than not
was inhalation of the Uranium particle contaminated dust, and for particles larger than
1micron these most probably were removed from the lung by ciliation and swallowed.
Therefore, most probably particles of Uranium have been transported with the food waste
through Ms. Dawsons gut and have ended up in contact with epithelial cells in the
colon/rectal tissue which eventually became damaged and developed into cancer. Slow
dissolving particles most probably resulted in, the local high concentration of Uranyl ion
bound to the DNA in the cells of the colon/rectal epithelium and the local ionisation
density in the DNA of cells will have been very high, as a result of the mechanisms I
have outlined above. Local exposure estimates of this kind have been developed by
ICRP in its ICRP66 lung model. Here, doses from atoms on the surface of lung tissue
have been modeled on the basis of absorption of energy in a layer of surface cells
believed to be the origin of lung cancer. However, the method was not used for any other
exposure to epithelial tissue. The local dose from the alpha decays from the Uranium
particles is modeled, and I show results of such a calculation for some representative
particulates below. It is clear that the alpha dose increases rapidly as the particle size
increases. Environmentally mobile Uranium oxide particles are between 0.05 and 10

31

Uranium from SSFL will impart an average dose of 60mSv a day; a two day
immobilization on the surface of the colonic/rectal epithelium will impart a dose of
120mSv to the cells in the surface tissue.
In addition to this enhancement, there is also the particle secondary photoelectron
enhancement and the Uranium DNA binding effects. These are the cause of the cancer in
the case of Ms. Dawson.
Table 4.1 Alpha doses to local sphere of cells in range of the decay for micron diameter
particles of Uranium Oxide (CERRIE 2004b)
Particle
dia
0.5

Volume
Cm3
6.5 E-14

Mass g
U3O8
5.6E-13

Mass g
U-238
4.8E-13

Activity
Bq
5.9E-9

1.0

5.2E-14

4.3E-12

3.7E-12

8.8E-8

6.5E-11

5.6E-10

4.8E-10

5.9E-6

Hits/day
Dose/day
5.1E-4
0.06mSv
7.6E-3
0.91mSv
0.51
60mSv

Hits/y
Dose/y
0.186
21.9mSv
2.77
332mSv
186
21900mSv

Assumptions: U3O8

5. Contamination at SSFL and Dispersion Offsite

5.1 Contamination
The history of contamination on site at the SSFL was significant. The 2006 report of the
Independent Advisory panel stated (http://www.ssflpanel.org):
Over its lifetime, Area IV of SSFL was home to:
ten reactors
numerous critical facilities (a kind of low-power reactor)
a plutonium fuel fabrication facility
a uranium carbide fuel fabrication facility
a hot lab (purportedly the largest in the country) for remotely cutting up
irradiated nuclear fuel shipped in from around the country from other AEC/DOE
nuclear facilities
a sodium burn pit, in which sodium-coated objects were burned in open-air pits
At least four of the reactors suffered accidents:
the AE6 reactor experienced a release of fission gases in March of 1959
the SRE experienced a power excursion and partial meltdown in July 1959
the SNAP8ER in 1964 experienced damage to 80% of its fuel
the SNAP8DR in 1969 experienced similar damage to a third of its fuel

32

In addition, the Hot Lab suffered a number of fires involving radioactive materials. For
example, in 1957, a fire in the Hot Cell got out of control and not only spread
contamination but damaged some equipment. . . . Because such massive contamination
was not anticipated, the planned logistics of cleanup were not adequate for the
situation. Another radioactive fire occurred in 1971, involving combustible primary
reactor coolant (NaK) contaminated with mixed fission products.
Radioactively and chemically contaminated items were not supposed to be burned in
the Area IV burnpit. Nonetheless, such items were burned there for decades, causing
extensive contamination of soil and groundwater and offsite migration in surface water
runoff.
5.2 The SSFL Environmental Reports
In their environmental reports, Rocketdyne, Boeing and the various operators or agencies
and companies commissioned to record radiation and radioactive substances on the site
and nearby, have a theme which runs through all their literature. It is that the man-made
radiation at the site is below regulatory limits, that radiation exposure doses are below
regulatory limits, and that no water or air leaves the site containing man made radioactive
isotopes at levels that would constitute a hazard to those living nearby. Reports
consistently refer to the presence on the site, in the air or water of natural radioactivity.
When (as often happens) measurements of generic radioactivity, total alpha or total beta
concentrations, appear high, these are ascribed to natural uranium. I make two points in
relation to this. The first is that if the uranium was brought there and contaminated the
SSFL environment, including the soil, the dust, the water, the air, the vegetation, or the
living creatures, it is not natural. That is to say, it was not there before the SSFL
operation, and any health effect produced by it resulted from the persons bringing it
there, releasing it to the environment, and allowing the public to be exposed to it. The
second point is that the uranium measured in the many reports I have examined is not
natural. The operators must have been aware of this but chose to omit any reference to it
from all of the reports I have read. This is a relevant discovery and I will expand upon it.
Natural Uranium has three isotopes U-238, U-235 and U-234. The ratios of these three
isotopes define natural uranium to a very high degree of precision. The uranium routinely
reported as natural at the SSFL, in groundwater, in soil, and in the air by the operators is
not natural. It contains enriched uranium, the material that is made by complex chemical
and physical processing for use in nuclear reactors and bombs. It is uranium that has been
concentrated in the fissionable radioactive isotope U-235 which is normally present at
0.7246%, an atomic ratio of one in 137.88 atoms of U-238 and activity ratio of 21.3. The
standard deviation on the atom ratio due to releases from various nuclear processes,
weapons fallout etc. is less than 1.0. Measurements of uranium isotopes at SSFL show
that the uranium in the area is generally enriched, often significantly enriched. Indeed, the
most recent background radiation studies commissioned by the Environmental
Protection Agency to define the remediation level at SSFL show that the chosen
background sites, up to seven miles from the site are also contaminated with enriched
Uranium and show unusually high gamma radiation levels compared with both historic
background level and measurements made by the State of California near the site itself.
Since this finding helps me to assess the exposure of Ms. Dawson and supports the

33

predictions of the air modeling, which I present below, I will devote a separate section to
the Background Report of November 2011.
The SSFL site itself, and the research and development carried out at the site since the
1950s, employed enriched uranium as a source material for the nuclear fission operations.
In 1970, Rocketdyne had a license from the NRC to hold hundreds of tons of enriched
uranium. The uranium was used in more than ten nuclear reactors. There was a uranium
carbide fuel manufacturing plant. There was a hot lab. There was a sodium reactor
accident in 1959 which produced contaminated material containing uranium, burned in a
pit outside. The operators were consistently criticized by regulators for having a poor
safety record. The material released to the environment over this early period contained
large amounts of enriched uranium. Historically, in the site reports, uranium has been
recorded and tabulated, but SSFL regularly and consistently described this uranium as
natural and marginalized its significance for health. Again, it is scientifically incorrect to
attribute to nature, uranium which was mined elsewhere and physically transported to
another site. Natural background radiation means that which was present before human
activity changed the site by definition. The site appears from maps and aerial photographs
to be built on a plateau, where soil has collected between two rock ridges, one to the
south and one to the north. It is a hollow in the hills: anything produced there and
released builds up in the hollow, in the soil. Therefore, the enriched uranium released has
collected in the ground below the various buildings where these nuclear operations and
accidents occurred or where material was disposed of.
While this uranium-contaminated ground remained undisturbed, only those on the site
would have been exposed, through inhalation of resuspended dust. But, in the 1990s, the
site began to be disturbed for remediation attempts. By 1998, the remediation had
begun in earnest. Huge amounts of SSFL soil began to be dug up. Buildings were
demolished. Contaminated concrete was cut up with high speed tungsten carbide discs.
Photographs show that the area is dry and dusty: dust is generated. The dust contains the
enriched uranium. The dust blows off site. The dust collects in the water and finds its way
into the groundwater. Levels of enriched uranium begin to rise in the groundwater;
uranium concentrations began to rise in the drinking water near the site but also in Los
Angeles (LADWP annual water quality reports, available at www.ladwp.com.) By 2001,
the remediation activity was at its peak. Vast amounts of contaminated soil had been
licensed for removal and trucking to a landfills. The trucks, contaminated with the
uranium dust, drove through the neighbourhoods where Ms. Dawson and her ex-husband
lived and grew their vegetables.
In addition to the uranium problem, the Rocketdyne reports are characterised by scientific
error and perhaps scientific fraud. Their fraudulent methods included reporting
radioactivity after they have subtracted what they term background levels, not given,
and so it is impossible to derive the true levels of contamination from specific isotopes
.The whole of the Rocketdyne site is heavily contaminated: this is shown by gamma
measurements which I use to calculate estimates of the true levels of contamination.

34

5.3 Wind Directions at SSFL and Air Dispersion Modeling

In examining the patterns of contamination offsite from releases and dusts from SSFL it
is necessary to know the distribution of winds at the site. Prior to 2002, the wind from
SSFL was reported to blow mainly from the north-west or the south-east, though the
situation is not entirely clear after 2002. Fig 5.1 gives the wind direction as a percentage
of all wind before 1999 and is reduced from data in the Rocketdyne reports.
There are problems with the Rocketdyne environmental reports where the authors
calculate offsite doses to populations within 16 miles of the site using plume modelling.
The reports list doses to the populations living at various distances and sectors. They
suggest that the highest collective doses are given to those living south of the site.
Collective doses are individual modelled doses multiplied by the population. Therefore,
the numbers can be de-convoluted mathematically based on the populations in each
sector. Based on this data, I have calculated the plume dispersion modes wind rose in a
separate table, in Fig 5.2. It is clear that the Rocketdyne model assumes wind directions
which are not accurate, and which disagree with a wind rose that Rocketdyne itself
published in a separate report. The ATSDR agency report in 1999 states: Finally,
although there are no wind direction data for specific release incidents, the prevailing
wind directions at SSFL blow from the source release areas towards uninhabited areas
around SSFL. (ATSDR 1999). This is simply untrue.
Fig 5.1 Percentage direction of wind blowing from SSFL (reduced from data given in
Boeing reports).

35

Fig 5.2 Assumed direction of wind blowing from SSFL (reduced mathematically from
population and collective dose modelled data given in Boeing reports).

Fig 5.3 Wind rose presented in the MWH Offsite Field Evaluation report 2007 for the
year 2002.

36

The 2002 wind rose is similar to those which are published for years between 1961 and
1999 but show a greater component of winds from the West.
Using accurate computer modelling based upon historical weather data from the USA, I
can examine the wind direction and air mass movements from the SSFL plant on any
period. As an example of this approach, and as an illustration of the point, I use the
NOAA HYSPLIT model averaged over 2 days from 1st November 2002. I first show a
Google Earth satellite photograph of the area with the superimposed air concentration of
unit release of contaminant from SSFL in Fig 5.4
Fig 5.4. Air concentrations up to 50km from release of unit contamination from SSFL
(34.232667N; 118.707167W) on Date: 1st Nov 2002

In addition to this, I can model the destination of air masses leaving the SSFL site on any
day with locations of the air masses at various intervals. I show examples in Fig 5.6, and
Fig 5.7 which employ meteorological data and also relates to time periods when the dust
was generated. It is clear from the model results that at the time, for about half of the 24
hour period following 0800 on 1st December 2003, air masses from the SSFL site mainly
moved from the site to the east. I can also use the system to determine deposition levels

37

and dispersion based on unit release from SSFL. An example is shown in Fig 5.5. Besides
the inhalation route, contaminated dust which is dispersed from the SSFL site will be
deposited on the ground downwind and will find its way into water sources and
vegetation, including the vegetable garden that Ms. Dawson had. The LADWP water
filtration plant lies within the plumes of material generated by SSFL and it is of interest
that levels of uranium began to increase in the water derived from this plant over the
period of the heavy remediation at SSFL 1998-2004.
Fig 5.5. Example of dust deposition plume from unit release over 2 days from SSFL in
November 2002. Blue squares represent the position of maximum deposition in this
simulation and are approximately at the position where Ms. Dawson and her husband
lived and grew vegetables.

As I have noted above, the Boeing environmental reports also employ a plume model to
calculate doses offsite at various radial distances from the SSFL. (Fig 5.2) Their results
for population doses suggest that the main exposures are to the south and north- west.
However, it is clear is from the accurate wind roses, from the HYSPLIT models and from

38

my own modelling, that a significant downwind plume covers the areas where Ms.
Dawson lived some 10-15 years prior to her diagnosis with rectal cancer.
Fig 5.6 Forward tracking air masses generated at the SSFL site between 1st and 2nd
December 2003 beginning at 8am on 1st Dec 2003 for 48 hours: tracks are at 2 hr
intervals. (Draxler, R.R. and Rolph, G.D., 2003. HYSPLIT (HYbrid Single-Particle
Lagrangian Integrated Trajectory: NOAA Air Resources Laboratory, Silver Spring,
MD).

39

Fig 5.7 HYSPLIT model results for 4-hourly releases from SSFL over 24 hours from 8th
Jan 2001 during period that contaminated soil was being loaded and trucked out.
(Draxler, R.R. and Rolph, G.D., 2003. HYSPLIT (HYbrid Single-Particle Lagrangian
Integrated Trajectory: NOAA Air Resources Laboratory, Silver Spring, MD).

5.4 Mechanisms of Exposure

Radioactive material moves offsite in various ways, the most important of which are
listed in Table 5.1 together with the associated human exposure vectors.
Table 5.1 offsite contamination routes for exposures to SSFL releases
Source
Air contamination from
stacks

Contamination
Deposition through plume;
ground/ water/ produce

Air contamination from

remediation generated dust

Deposition through plume;

ground/ water/ produce

40

Exposure
Increased external exposure
Inhalation/ ingestion of
food and drinking water
As above

Air contamination from

natural resuspension
Air contamination by gases
e.g. Tritium, Radon, noble
gases prior to 1988
Highly contaminated dust
from trucking out LL waste

Deposition through plume;

ground/ water/ produce
Inhalation downwind

As above

Local deposition from truck

tyres/ spillage along routes

Increased external exposure

Inhalation/ ingestion of
food and drinking water
All of the above

Resuspension of distant
All of the above
deposited contaminated dust
Ground Water
Drainage of contaminated
contamination from all of
surface
above

Inhalation

Plants/ produce; ingestion/

drinking water

With the development of computers, air source modeling has now become
straightforward, though tedious. It is now possible, with a high degree of certainty, to
show the concentration of any contaminant in any area given metereological data, a
release position, and quantity. The converse can also be done. Given a position, and
historic meteorological data, it can be determined where the air originated over a period
of a few days. We can also examine longer periods on the basis of average metereological
conditions both from the point of view of following an air mass from its source, or the
reverse situation, looking at the sink and predicting the source. The US National Oceanic
and Atmospheric Administration (NOAA) have developed a complex computer model
which employs historic meteorological data to track air masses. Using this system, it is
clear that the places where Ms. Dawson and her husband Mark Lindsey lived were in the
direct plume for releases from the SSFL for a significant proportion of the time that these
releases were high (as I show from analysis of the Environmental Data). This period was
approximately ten years prior to Ms. Dawsons diagnosis, within the accepted latency
period for the colorectal cancer to be initiated and to develop.
The levels of uranium increased in the Los Angeles drinking water over the same period,
according to independent routine measurements made by the LAWPD. Therefore, I
conclude that the water was also a more probable than not exposure pathway as was the
dust contamination from tens of thousands of truck trips carrying contaminated material
away from the site in late 2000, and early 2001.
Ms. Dawson and her ex-husband will not have been alone in suffering the consequences
of these exposures. Other evidence of genetic damage from Uranium exposure should
exist, and indeed it does. I review it in a separate section.

41

6. Uranium Contamination at SSFL

6.1 Environmental Uranium
The element uranium has the highest atomic number of all the naturally occurring
elements on earth. In the last ten years, following its use as a weapon in Iraq and the
Balkans and subsequent closer examination of its biological effects, it has become clear
that it constitutes a serious radiobiological hazard, one not predicted by its intrinsic
radioactivity. I have written at some length about uranium and its anomalous toxicity
(Busy 2005a, 2005b, Busby and Schnug 2009, Howard et al 2009). Uranium has three
main isotopes, listed with some properties in Table 6.1.
Table 6.1 Uranium isotopes of interest
Isotope
U234
U235

U238

Half Life
Years
245
thousand
704
million
4500
million

Atomic
abundance
<0.01%

Mode of decay/

Specific activity

Alpha

230 million Bq/g

Naturally 0.72%
up to 5% if
enriched
99.27%

Alpha

80,000 Bq/g

Alpha (+ short half

life beta- emitter
daughters)

12,400 Bq/g

Uranium is a fairly common element on earth, but in the past, before nuclear activities, it
remained in the ground tied up in uranium ores. Its existence in soils and rocks is one
cause of natural background radiation. Due to its long half life, the main isotope U-238,
which is an alpha emitter, has been conventionally assumed to be a relatively low level
hazard, unless it is ingested or inhaled in some relatively pure or concentrated form. The
gut transfer factor is low, and so even in the few areas where levels in the water or foods
are relatively high, ingestion does not lead to very high body burdens. Levels in different
geological areas are listed in Table 6.2 (from Eisenbud and Gesell, 2000) and levels in
water in Germany (where the element was discovered and occurs at high concentrations)
are shown in Fig 6.1. Some normal levels in groundwater, and air are listed for reference
purposes in Table 6.3 and 6.4 with comparisons with SSFL levels around 2000-2004. It
is the reference levels that define the normal levels of uranium in the normal
environment. I have included the levels of uranium in groundwater at SSFL 2000-2004
which are clearly much higher than any of these reference levels. Both the levels and the
isotopic ratios of uranium at SSFL are not normal.
I must point out that the Rocketdyne reports frequently switch units, making the
estimation of contamination, and trends in contamination difficult to follow even for

42

someone who is familiar with the units employed. Uranium is of interest since it has a
very long half-life, which means that levels which represent radiological hazard have
significant amounts of physical material associated with them. Table 4.2 shows
concentrations in both radiological and mass units. 1 pCi (picoCurie or 10-12 Curie is
0.037Bq (Becquerel or disintegration per second)).
Table 6. 2. Uranium concentrations in rocks and soils in the world. Chatsworth rock
geology is Arkosite sandstone (highlighted bold) according to Rocketdyne reports and
also UCLA reports (from NCRP 1987, also Eisenbud and Gesell 1997)
Material

Uranium-238
Bq/kg (pCi/g)
Igneous Rocks

Basalt (crustal ave.)

Mafic
Salic
Granite

0.5
0.5
3.9
3

7 (0.19)
7 (0.19)
50 (1.35)
40 (1.08)

Shale sandstones
Clean quartz
Dirty quartz
Arkose
Beach sands
Carbonate rocks
a
All rocks (range)
Continental crust ave.
Soil average

Sedimentary rocks
3.7
<1
2-3
1.2
3
2
0.5-4.7
2.8
1.8

40 (1.08)
<10 (<0.3)
40 (1.08)
10-25 (0.3- 0.67)
40 (1.08)
25 (0.67)
7-60 (0.19-1.6)
36 (0.97)
22 (0.6)

6.2 Uranium Isotope Ratios

It is possible to distinguish between natural and anthropogenic uranium on the basis of
isotopic ratios. I have been involved in this area since 1998 in connection with
characterising Depleted Uranium (DU) in the environment. Useful data is given in Table
6.5. Since uranium is enriched in the fissile isotope U235 for nuclear fission in power
reactors, any measurements of isotope ratios that differ from the mean activity ratio of
21.3 (atomic ratio 137.88) define man made uranium. For natural uranium locked up in
rocks or isolated from geochemical and geophysical processes, the U238/U234 ratio
should be exactly 1.00. However, there is a variation around this number even with
natural uranium owing to the fact that the immediate daughter of U238 is the Thorium
isotope Th234, and thorium is far more insoluble than uranium. This results in U234
ratios which are not exactly 1.00 (see NCRP 1987). For this reason, the U234/235 ratio is
what should be used to define the nature of the uranium being measured. If the U238/235 activity ratio is significantly below the reference value of 21.3, the material is
enriched and contains man-made uranium 235. This is the case at SSFL, and as I shall
show, U-235 is both more radioactive than U-238 and is a statutory reportable substance,
unlike natural uranium.
43

Table 6.3 Some comparison levels of Uranium in water (Source: NCRP 1987, Various)
Location

Activity pCi/L

Activity Bq/m3

Concentration

Groundwater All Germany

(mean) N = 400
Groundwater All Germany
(max) N = 400
Atomic Weapons
Establishment AWE
Aldermaston boreholes
AWE surface water
Atomic Energy Research
Establishment Harwell site
UK Groundwater
Rhodia landfill near British
Nuclear Fuels PLC Sellafield,
leachate
Navajo Creek, National
Monument Arizona
Sandia National Laboratory
Arizona, drinking water
(mean)
Drinking water (East USA)
NCRP 87
Abandoned Uranium Mines
project; Four Corners Mine
Area USA
U238
Drinking water (Mid USA)
NCRP 87
Drinking water (West USA)
NCRP 87
Drinking Water Los Angeles
mean 2000
Groundwater in Wagner 2011
S. Carolina study associated
with increased trend risk of
colorectal cancer (Table 3.3)
Groundwater SSFL
Mean 2000-2004
Groundwater SSFL
Max 2000-2004

0.30

11.2

0.9

3.4

125

10

<0.08

<3

<0.25

0.14 0.84
0.135 (.067- 0.8)

5-30
5 (2.5 30)

0.4 2.5

0.06

2.04

0.16

1.0

35

2.8

1.9

40

3.3

0.01

0.4

0.03

2.7

100

0.35

13

8.1 (SD 14.8) on

38 samples; 2
outliers of 201
and 412 omitted
1

3.5

130

10

3.5

130

10

0.1

3.6

0.29

15

570 (520-610)

44

32

1220 (9501500)

94

44

Table 6.4 Some reference levels of uranium in outdoor air compared with SSFL at the
time of the cluster.
Location
Atomic Weapons Establishment, AWE
Berkshire UK, High Volume Air
Samplers (HVAS) 2000-2003
Atomic Energy Research Establishment
AERE Harwell, Oxfordshire, UK HVAS
2000-2003
BNFL Sellafield Nuclear Fuel
Reprocessing Plant, Cumbria, Met. site
and North gate HVAS
2004-2006
SSFL 2000-2002

Activity nBq/m3
155 (SD = 101)
8 samplers, offsite and
onsite; N= 89
250 (SD 405)
4 samplers
N = 22
3,800 (SD 7800)
max 58,000
N = 95
43,000 (SD15,000)

Reference
AWE annual
reports
Harwell Statutory
Monitoring
Reports
Sellafield Statutory
returns to UK
Environment
Agency
Boeing
Annual
Environmental
Reports

Table 6.5 Uranium isotopic ratios in nature and in the environment

Uranium Source

Natural U238/U235

%
Atomic
U235
ratio
enriched
0.3
137.88

Natural U238/U234
0.3
Nuclear reactor U238/U235
3.0
Experimental Reactor
3.0-50
U238/U235
Depleted Uranium U238/U235
a
varies due to solubility of Th234 and recoil

45

Activity
Ratio

Reference

21.3

0.000054 a1.0
32
5
1-32
0.1-5

DUOB 2007
RS2001
DUOB/ RS2001
Eisenbud 1992
Eisenbud 1992

400-500

DUOB/RS2001

Fig 6.1 Uranium in groundwater in the German Federal Republic (courtesy of Prof Ewald
Schnug, Birke et al 2005). The mean level is 0.9

Summary of Part I
The history of radiation risk models shows that the exposure levels permitted by
policymakers have continuously been readjusted throughout the last 80 years as every
new discovery, both in science and in epidemiology, has shown that radiation exposure is
more dangerous than previously thought. This process continues today. Nevertheless, the
current official radiation risk models have not incorporated the most recent discoveries
because to do so would force a complete reappraisal of the current use of nuclear power
and the historic harm done by releases of radioactivity in the past. (Deleted because it
seems misplaced)

6.3 Uranium at SSFL

Uranium levels at the SSFL site have been measured and reported since 1989. The
reports are not continuous: that is to say, the measurements seem rather random and
sporadic from year to year, sometimes giving U235 only, sometimes U234 only and
sometimes U-238. I have not seen any measurements of uranium made at the site before
1989 and have carefully examined all the data publically available. Almost every SSFL
environmental report contains a statement to the effect that only natural background
isotopes exist on the site. Boeing argues in its reports that Chatsworth formation rock is
naturally high in uranium, or that Arkosite sandstone (which is the type of rock)
commonly contains uranium deposits. I have found no mention of this in the relevant
scientific literature; indeed, Arkosite sandstone is listed in the standard work on
environmental radioactivity as having quite modest levels of 10-25Bq/kg (Eisenbud and
Gesell 2000, NCRP 1987). Levels at SSFL are significantly higher than this range.
Levels of uranium in the soil, groundwater and air at the site are very high because of the
work that was conducted there. And isotope ratios show enriched uranium. I have
reduced all the tables in the environmental reports to Tables 6.6 (air), 6.7 (water) and 6.8
(soil) and in these tables I show the U238/U235 ratio which I have calculated from the
data given.
It is not surprising that uranium contamination at SSFL is high. The whole operation is
predicated on experiments with enriched uranium. There were 12 nuclear reactors there,
one of which, a sodium cooled reactor, suffered a serious accident. In 1970 a license was
issued by the US Atomic Energy Commission for Atomics International to hold 5000kg
of U-235 (BNA00439806 License SNM-21). If this was standard 3% enriched uranium,
there was a total of 160 tons of enriched uranium on the site being fed into reactors and

46

generally played with in experiments. The SNAP 10A satellite reactor developed at
building 059 was a U235 powered reactor. The sodium cooled reactor experiments had
sodium flowing around the uranium fuel elements. The sodium was contaminated with
enriched uranium. There were uranium fuel fabrication facilities, and uranium fuel
disassembly facilities. The whole place was awash with uranium, man made, imported,
enriched uranium.
This is clear from examination of the tables 6.6-6.8.
6.4 Uranium in Water
Comparison of the uranium in groundwater at SSFL (Table 6.7) with that in reference
areas show that the levels are both very high and that the isotope ratios define the
material as being slightly enriched. Fig 6.2 shows a histogram and frequency envelope
for the uranium ratio in all the results given from 1989 to 2005. There are clearly some
depleted uranium measurements here, and of course this is what would be expected due
to the burn-up of the U235 in a reactor which leads to the production of depleted
uranium, as is found in material near to Sellafield (Priest et al 2006). Fig 6.2 deconvolutes the frequency distribution into three normal distributions, normal, slightly
enriched and highly enriched. Overall levels (see Table 6.3) show uranium in
groundwater at SSFL to be 200 times higher than the levels at AWE, higher than the
highest level in the whole of Germany (including the area where uranium was discovered
by Klaproth) and 5.6 times higher than the mean level at the abandoned uranium mining
area of Four Corners Mine in USA. This shows that the groundwater is contaminated
with enriched uranium from historic nuclear activities at the site.
6.5 Uranium in Soil
The uranium levels in soil (Table 6.6) can be compared with levels for Arkose sandstone
shown in Table 6.2. They are significantly higher. Also, they are often very high where
we expect them to be, given my conclusions on their origin. For example, in 1992,
2800Bq/kg of highly enriched uranium were reported in soil at the sodium disposal
facility with a highly anomalous U234 ratio. Thus, it is clearly reactor uranium
contaminated sodium that was being disposed of. And because sodium contains lithium,
which is the source of tritium following its reaction with neutrons, we would also expect
tritium to be produced in the reaction with water and sodium. From the early 1990s on,
large amounts of tritium appeared in the groundwater. The most probable explanation is
that this tritium appeared because of the disposal of uranium contaminated with sodium.

47

Fig 6.2 Uranium isotope ratios in groundwater at SSFL 1989-2005; 3 outliers which
occurred in 1991 show highly depleted uranium have been omitted.

Fig 6.3 Uranium ratios in soil at SSFL 1989-2005. Natural Ratio is 21.3 (not 21.7)

48

Uranium Table 6.6 Rocketdyne. Uranium in the air 1989 to 2011, showing values for U-234, 235 and 238 given in annual reports
reduced to fCi/m3 and also total uranium in the air in nBq/m3 calculated from these values. Also given are the U-238/U235 activity
ratios which define whether the material is enriched (E) or highly enriched (EE). The ratio for natural uranium is 21.7.
Year

Location

U234

U235

U238

Enrich Total U*
nBq/M3

Ref

<1989
1989
1989
1989
1990

No uranium measurements in air

//Ambient air sodium burn pit
//RMDF pond
//.T100

NA
NA
NA

0.006
0.012
0.002

0.054
0.085
0.022

9
7.1
11

E
E
E

4200
6734
1700

RI/RD90-132 BC1718
As above
As above
RI/RD91-136 BC 1836

//Ambient air RMDF

//RMDF pond
//RIHL
//T100
//T886
//DS104
//First half 1990 composite
//Ambient average

NA
NA
NA
NA
NA
NA
NA
NA

0.004
.009
.002
.003
.012
.016
0.012
0.004

0.013
.0009
.004
.016
.0007
.03
0.181
0.023

3.25
0.1
2
5.3
.05
1.9
15.1
5.75

EE
EE
EE
EE
EE
EE
E
EE

1110
400
370
1295
495
2800
13800
1850

1991

RI/RD92-138 BC1919 seq

//Ambient air RMDF

0.06

0.027

0.082

3.03

EE

6250

1992

RI/RD93-125 BC2028
None detected (?)

1993

RI/RD94-126 BC2122
Ambient RMDF
RMDF pond
RIHL
T100
886
DS104

.033
.069
.022
ND
.037
.036

ND
ND
ND
ND
ND
ND

.013
.029
.019
.011
.021
.014

49

?
?
?
?
?
?

?
?
?
?
?
?

1702
3600
1500
814
2140
1850

1994
Ambient RMDF pond
DS104

0.022
.022

ND
ND

0.022
.006

?
?

?
?

1600
1040

1995

RI/RD95-153 BC2218 seq

RI/RD96-140 BC2334

Ambient T100

ND

0.001

0.004

EE

330

1996

RD97-134 BC2467
Ambient T100
Ambient average

0.09
0.09

0.065
0.065

0.1
0.1

1.5
1.5

EE
EE

9400
9400

1997

RD98 BC2592
No measurements given

1998

RD99-115
No measurements given

1999

RD00-159
No measurements given

2000
Ambient air RIHL
Ambient average

NA
NA

NA
NA

0.61
0.61

?
?

?
?

45,000
45,000

2001

RD99-152 BC2894
RD02-148 BC3000

Ambient air RMHF

Ambient air T0020
Ambient air average

0.83
0.67
0.75

NA
NA
NA

NA
NA
NA

?
?
?

?
?
?

61,400
50,000
55,500

2002

RD02-148 BC3101
Ambient T020
Ambient average

0.156
0.156

0.286
0.286

NA
NA

0.5
0.5

EE
EE

22,000
22,000

Ambient RMHF
RMHF pond
T020
T100

0.01
0.0266
0.0141
0.0213

NA
0.00761
0.0114
NA

0.003
0.0198
0.0263
0.0167

?
2.6
2.3
?

?
EE
EE
?

480
2000
1900
1400

2003

50

T886
Ambient Average

0.0392
0.0223

NA
0.0095

0.0419 ?
0.0215 2.26

?
EE

3000
1970

2004

RD05-176 BC3301
Ambient RMHF
RMHF pond
T020
T100
T886

0.486
0.350
0.373
0.312
0.278

0.0278
ND
0.0419
ND
ND

0.441
0.247
0.377
0.289
0.263

15.8
?
9.0
?
?

E
EE
?
?

34,300
22,000
29,300
22,200
20,000

2005

RD06 BC3403; ASER

2005 Section 5
Ambient T100
Ambient RMHF

ND
ND

0.243
0.176

ND
ND

?
?

?
?

400,000
140,000

2006

ASER report 2006

Section 5
RMHF
4020
4100

0.27
ND
ND

ND
ND
ND

0.17
0.2
0.09

?
?
?

?
?
?

16,100
14,700
3000

2007

ASER report 2007

Section 5
RMHF
4020
4100

ND
0.051
ND

ND
0.152
ND

ND
0.210
0.21

1.38
?

EE
?

14,000
7080

2008

ASER report 2008

Section 5
RMHF
4020

ND
0.0316

ND
0.0303

ND
ND

51

1.0

EE

3000

2009

ASER report 2009

Section 5
RMHF
4020

0.017
0.0514

ND
0.0126

0.04
?
0.0734 5.8

?
EE

1900
4600

2010

ASER report 2010

Section 5
RMHF
4020

0.034
0.247

ND
ND

0.027
0.027

?
?

2050
9230

2011

ASER report 2011

Section 5
RMHF
4020

ND
ND

0.05
ND

0.14
0.19

2011

2.8
?

EE
?

11,100
12,800
ASER report 2011
Section 5

(* if no U-234 or U238 is given it is assumed present at the same activity as U-238 or U-234 since they are in stochastic equilibrium;
If only U-235 is given it is assumed that the activity ratio 238/235 is natural i.e. 21.7 in order to calculate total Uranium. Note some
readings from these tables // are negative, suggesting background subtraction; note the units change regularly from fCi/m3 to uCi/ml
involving difficulty in determining trends e.g. In 1996 0.09 fCi/m3 became 9 x 10-17 uCi/ml, probably because the levels suddenly rose
by a factor of 10. Note that it seems likely that these ambient measurements are BACKGROUND SUBTRACTED and the real levels
are higher, but there is no way of knowing what has been subtracted.

52

Table 6.7. Groundwater uranium isotopes pCi/L and total uranium mBq/L
Year

Location

U234

U235

U238

1989
1990
1991

SSFL groundwater
SSFL groundwater
SSFL max
SSFL mean
SSFL min

10.4
2.35
ND

0.13
1.4
0.376
.077
-.001

3.43
16.8
194
39
.03

1992

SSFL max
SSFL mean
SSFL min

36.6
10.4
1.22

1.8
.135
nd

1993

SSFL max
SSFL mean
SSFL min

16.3
8.2
0.84

1994

SSFL max
SSFL mean
SSFL min
a
Bldg 059 mean
SSFL max
SSFL mean
SSFL min

1995

Ref

26
12
515
506
?

Enrich Total U*
mBq/L
N
258
E
1295
DD
7580
DD
1533
?
?

41.9
12.2
1.42

23
90
?

N
DD
?

2970
840
?

RD93 BC2026

.78
.39
nd

16.3
9.3
0.88

20.8
23.8
?

N
N
?

1235
662
?

RD94 126 BC 2135

26.4
10.4
ND
3624

2.2
0.8
ND
ND

25.5
9.6
ND
804

11.6
12
?
?

E
E
?
a
EE

2000
770

RD95 153 BC2231

BC2231

15.0
9.8
7.0

0.78
0.57
0.43

15.2
9.1
6.4

19.4
15.9
11.2

N
E
E

1150
720
510

53

160,000

RI RD91 BC1843
RI RD91 BC1843
RD92-138 BC1933

RD96-140 BC2344

1996

SSFLmax
SSFLmean
SSFLmin

11.5
6.9
3.7

.89
.5
.207

10.8
6.4
2.9

12
12.8
14

E
E
E

860
510
250

RD97 134

1997

SSFL max
SSFL mean
SSFL min

16.6
10.8
2.1

0.86
0.51
0.09

15.6
9.9
1.29

18
19
14

E
E
E

1220
780
130

BC2559

1998

SSFL max
SSFL mean
SSFL min

14.2
8.1
0.5

7.9
1.5
0.02

13.3
7.7
-0.01

1.7
5.1
?

EE
EE
?

1310
640
?

RD99 115 BC 2701

1999

SSFL max
SSFL mean
SSFL min

15.7
6.291
0

1.23
0.407
0.011

14
5.678
0.018

11
13.9
1.6

E
E
EE

1140
460
60

RD00-159 BC 2797

2000

SSFL max
SSFL mean
SSFL min

15.1
7.8
1.55

0.8
0.42
0.08

13.2
7.16
1.53

16.5
17.1
19

E
E
N

1075
569
117

RD01-152 BC 2899

2001

SSFL max
SSFL mean
SSFL min

20.59
7.92
2.21

0.72
0.35
0.12

14.8
6.89
1.67

20.5
19.6
13.9

N
N
E

1335
560
150

RD02 148 BC3002

2002

SSFL max
SSFL mean
SSFL min

16.44
8.11
2.87

0.66
0.34
nd

16.38
7.53
1.7

24.8
22.1
?

N
N
?

1240
590
170

RD02 148 BC3103

2003

SSFL max
SSFL mean

20.3
8.42

1.05
0.38

19.3
7.79

18.3
20.5

E
N

1500
610

RD04-170 BC3204

54

SSFL min

1.98

ND

2.02

150

2004

SSFL max
SSFL mean
SSFL min

13.9
7.07
Nd

0.64
0.35
nd

11.2
6.69
nd

17.5
19.1
?

E
N
?

950
520
Nd

RD05-176

2005

SSFL max
SSFL mean
SSFL min

20
7.97
1.39

0.9
0.37
.05

17.9
7.18
1.2

19.9
19.4
24

N
N
N

1440
570
98

BC3405

If the U-224 is much higher than U-238, as it is here, we can assume that it is there as part of enriched Uranium since the U-234 is
removed with the U-235 in the enrichment process owing to its isotopic mass. Higher U-234/238 ratios often signal this but there are
problems in employing this as a test owing to differential solubility of uranium and thorium in water. Th-234 is an intermediate
between U-238 and U234 and can build up relative to the parent U-238 owing to the greater solubility of the uranium. (see e.g.
NCRP94 1987).

55

Rocketdyne Table 6.8 Uranium isotope ratios and total in soil and rock pCi/g and Bq/kg. Natural uranium has activity ratio
U238/U235 = 21.3. (atom ratio is 137.88). This is invariant. Below this is enriched E, above is depleted D. Total levels are deduced
from whatever isotope measurements are available on the basis that the ratio is for natural uranium. Normal levels of total uranium for
Arkosic sandstone which is the geology at SSFL are 10-25Bq/kg (NCRP1987, Eisenbud and Gesell 1997).
Year

Location

U234
pCi/g

U235
pCi/g

U238
pCi/g

Enriched Total
(E, N or U
D)
Bq/kg

Ref

1989

Surface, hot storage room

fission gas tank pit
surface loading dock
runoff channel surface NE liquid waste
facility
runoff channel surface SE liquid waste
facility
runoff channel surface SE RIHL
Surface of site boundary at Bell Creek
Surface at site boundary west of RIHL

NA
NA
NA
NA

0.059
0.054
0.066
0.63

1.03
0.93
1.04
1.01

17.4
17.2
15.7
1.6

E
E
E
EE

78
71
79
98

RD90-132 BC1707

NA

0.049

0.84

17.1

64

NA
NA
NA

0.07
0.063
0.065

1.2
1
1.1

17.1
15.8
16.9

E
E
E

91
76
84

0.11
0.08
0.04

1.4
1.18
1.04

12.7
14.8
26

E
E
D

108
90
78

1990

SSFL max
SSFL mean
SSFL min

1991

Only one measurement made of soil

NA

0.16

NA

270

RD92-138 BC2936

1992

sodium disposal rock/soil max

sodium disposal rock/soil mean
SSFL rocksoil U235 only given max
SSFL rocksoil U235 only given mean

57.9
4.64
NA
NA

13.2
0.62
0.27
0.09

6.16
0.83
NA
NA

0.47
1.34
NA
NA

EEE
EEE
?
?

2860
225
440
146

RD93 BC2028
Note high U234

56

1993

Soil/ rock
SRE soil
Building 023
Building 005
Former Sodium disposal facility max
Former Sodium disposal facility mean

NA
NA
NA
NA
NA
NA

0.07
0.09
0.054
0.103
0.15
0.09

Na
3.74
Na
Na
2.26
0.66

?
42
?
?
15
7.3

?
D
?
?
E
EE

114
146
88
168
173
52

RD94

1994

SSFL soil max

SSFL soil mean

NA
NA

0.11
0.05

1.7
0.83

15.5
16.6

E
E

130
63

RD95

1995

Rock/soil area IV survey max

Rock/soil area IV survey mean
Rock/soil area IV survey min

2.1
0.78
0.36

0.1
0.04
0.02

2
0.79
0.38

20
19.8
19

N
N
N

155
60
28

RD96-140

1996

T064 survey soil data uranium max

T064 survey soil data uranium mean
T064 survey soil data uranium min

9.86
6.7
4.8

0.23
0.05
0.02

2.54
1.82
1.02

11
36
51

E
D
D

470
317
215

RD97
Note high U234

1997

Hot Lab max

Hot Lab mean
Hot Lab min

0.12
0.08
0.04

3.16
2.19
0.5

26
27
12.5

D
D
E

240
165
38

RD98

1998

hot lab soil max

hot lab soil mean
hot lab soil min

1
0.2
0.1

3.2
2.6
1.8

3.2
13
18

EE
E
E

1032
854
730

RD99 BC2706
Note high U234

23.7
20.3
17.8

57

1999

BLDG L85 max

BLDG L85 mean
BLDGL85 min
23rd street max
23rd street mean
23rd street min
T100 trench max
T100 trench mean
T100 trench min

NA
NA
NA
NA
NA
NA
NA
NA
NA

0.143
0.09
0.013
0.532
0.142
0.054
0.164
0.091
0.036

NA
NA
NA
NA
NA
NA
NA
NA
NA

?
?
?
?
?
?
?
?
?

?
?
?
?
?
?
?
?
?

230
150
20
870
230
88
270
150
60

BC2901
U-235 only measured
RD00-159

2000

soil OCY U235 max

soil OCY U235 mean
soil OCY U235 min
soil SRE U235 max
soil SRE U235 mean
soil SRE U235 min
soil 4373 U235 max
soil 4373 U235 mean
soil 4373 U235 min

NA
NA
NA
NA
NA
NA
NA
NA
NA

0.13
0.07
0.04
0.11
0.06
0.03
0.11
0.09
0.07

NA
NA
NA
NA
NA
NA
NA
NA
NA

?
?
?
?
?
?
?
?
?

?
?
?
?
?
?
?
?
?

220
120
70
187
100
50
180
146
114

RD01-152

2001

No soil measured

2002

No soil measured

2003

soil building 4059 max

soil building 4059 mean
Bld 4012 mean
Bld 4012 max

1.04
0.78
0.91
1.1

NA
NA
0.07
0.12

1.04
0.77
0.87
1.08

?
?
12
9

?
?
E
EE

80
60
70
85

RD04-170
BC3209

58

BC3210

2004

soil building 4059 max

soil building 4059 mean

1.07
0.55

0.1
0.04

1
0.52

10
13

E
E

80
40

2005

soil bld 4059 max

soil bld 4059 mean

1.52
1.19

0.34
0.14

1.36
1.09

4
7.8

EE
EE

120
90

59

RD05 176

6.6 Uranium in the Air

Since the contamination present at SSFL is from historic accidents and discharges of man
made enriched uranium from reactors, it would be located in the surface of the soil. It
washed into the groundwater, but would exist in its most definitive isotopic ratio in the
air, since this material is resuspended from the surface. In addition, this is the material
that migrates offsite downwind and is available for exposure though deposition in
downwind communities, or by inhalation in those living downwind like Ms. Dawson.
Table 6.6 shows levels and isotopic ratios of uranium in the air. It also enables me to
present the trend in uranium in air with time. Remediation activities at SSFL in the 1990s
to the present day involved major soil disturbances, such as the cutting up and
compaction of entire buildings, digging, loading and moving of mountains of
contaminated topsoil, spraying of contaminated sodium with water under nitrogen, and a
range of other disturbing activities. These activities moved into a major phase in 19992001. I show the isotope ratio of uranium in air in Fig 6.4 and the trend in uranium in air
in Fig 6.5
Fig 6.4 Uranium isotope ratios in air at SSFL 1989-2004; natural ratio is 21.3 (not 21.7)

60

Fig 6.5 Trend in uranium in air at SSFL 1989-2004 (Source: Rocketdyne Environmental
Reports)

6.7 Boeings Position on Uranium

The Rocketdyne and Boeing reports of uranium and descriptions of uranium, which
language is often quoted by s b DoE and others are that there are high levels on site
naturally, and this has contributed to higher external gamma doses shown on dosimeters
and also the higher than normal levels they present in environmental sampling. This is
misdirection by those concerned. U-235 is regularly reported and is classified as a
special nuclear material. I submit that it is inconceivable that the operators and those
who made measurements at SSFL were unaware of the problem. Indeed, in a slightly late
attempt to cover it up, a survey was commissioned from Cabrera Services and published
in 2007. (Final Status Survey Report, see www.etec.energy.gov/Reading
Room/DDDTable.html)) This study was carried out after all the contaminated soil had
apparently been removed. It majors on uranium isotope ratios. Results from 146 samples
show mean soil levels to be 70Bq/kg with the highest levels about 150Bq/kg. The U-235
distribution is not normal, it is in fact skewed. In what I have come to see as a standard
misdirection on these issues, the authors on p27 state:

61

The U234/U238 ratio was analysed for potential U235 enrichment or depletion different
from natural soil composition, which would be indicative of uranium contamination. The
U234/U238 ratio for naturally occurring uranium is approximately 1.0. Analysis of the
project U234/U238 sample results showed an average ratio of approximately 1.0 which
is indicative of natural uranium.. . . Thus no uranium contamination was identified.
But, besides being quite wrong (see e.g. NCRP 1987) about the U234/U238 ratio in
environmental samples, the results showed a very wide range of U234/U238 ratios,
ranging from 0.7 to 1.3. The U238/U235 ratios should have been used since they
measured U235 in all the samples, but the authors chose not to use them. The remediation
work was stopped in the same year that this report was created.
In 1996, there was an earlier study that also looked at uranium ratios in soil and
multimedia offsite surveys. In this study, results for 161 samples are given in the form
of a cumulative probability plot (RD97-134 BC2500). The mean U238/U235 ratio was
18.6. Authors state (BC2499), The U235 should have activity approximately equal to
4.6% of the U238 activity (i.e. an activity ratio of 21.7, which we know to be slightly
wrong as it happens). They do not, however, comment on the fact that the ratio as given
in their results is 18.6.
6.8 Uranium in the Los Angeles Water Supply
Interestingly, the increases in uranium in the air at SSFL shown in 2000-2002 are
followed by increases in uranium measured in drinking water in Los Angeles, as
measured by the Los Angeles Department of Water and Power and presented as annual
means on their website. Levels in the LA Filtration Plant stream, which was the base
supplier for Ms. Dawson, increased in 2003. Increases were greater for both the northern
wells and the southern wells supplies. I have attempted to obtain the base data from
which these results have been distilled, but despite several phone calls and emails have
had no response to date. The uranium is measured quarterly at various points in the
source line, and analysis of these data might be of interest in connection with the present
study, since the main LADWP filtration plant is downwind from SSFL. Offsite
measurements of uranium in soil at the Chatsworth dry reservoir were made by Essentia
services for LADWP who may have been concerned about the sudden increase of
uranium in drinking water which occurred in 2003. No isotope ratios were made and total
uranium was about 65Bq/kg, three times too high for the type of soil.
6.9 Gamma Exposure Rates at SSFL and Historic Contamination
The levels of contamination at SSFL Area IV, the area where the nuclear activities were
carried out, resulted in increases in the gamma ray background. Radioactive
contamination is measured with a number of instruments designed to respond to the type
of radiation emitted. Traditionally, and certainly in the case of the operators of the SSFL,
focus has been on measuring gamma emitters, gamma rays. This may be partly because
of the penetrating nature of external gamma rays, and partly because they are easy to

62

measure using a variety of devices. Measurements of alpha emitters like uranium are
quite difficult and require special equipment: moreover, because of the short path lengths
in air of alpha particles, surveys will only pick up the few decays which occur on the
extreme surface of any sample. Nevertheless, uranium contamination will give increased
levels of gamma activity to some extent, for U238 through the gamma decay of the
daughters Th234 and Pa 234m, and for U235 through its own decay at photon energy
185keV. The annual environmental reports have recorded overall gamma doses integrated
over long time periods employing thermo-luminescent dosimeters made of various
materials mainly deployed at the perimeters of the site. These have generally shown that
the mean perimeter levels are higher than levels shown in offsite dosimeters. On
occasion, the reports go to some lengths to dispute this obvious fact, but the independent
placement of dosimeters by the State of California showed that this route for disposal of
arguments about risk could not be easily taken. There followed an attempt by Rocketdyne
to show that offsite dosimeter (a new type of aluminium oxide) gave the same annual
doses as the onsite perimeter dosimeters. But the State of California dosimeters did not
agree. Rocketdyne commissioned external dosimetry from the independent McLaren
Hart company. For some time Rocketdyne reports referred to the independent
determination of offsite annual dose (mean 15uR/H) by McLaren Hart (who placed their
dosimeters near approach roads, contaminated with dust from the transport to and from
SSFL). There have been questions about the actual independence of McLaren Hart. The
company was sued for corruption in Louisiana courts and eventually went bankrupt in the
1990s.
Boeings own environmental data show that the mean gamma dose rate over the site is in
excess of historic background. Several Rocketdyne reports concede that the difference
dosimeter measurements to mean values and standard deviations for three periods and
show them in Table 6.9.
I have not been able to find dose rate measurements for the site that I can use to construct
a mean dose rate map for analytical purposes. The closest I have found is the series of
mapped measurements reported for the Radioactive Materials Handling Facility.
I have converted the position of these readings into a coordinate system and plot them as
a dose rate surface in Figs 6.6 and 6.7. However, some interesting data was published in
2011 when a Background Study was created following a project funded by the EPA to
create background levels for the general area that could be employed to define
remediation levels. The statements and text of this document is disturbingly misleading
and it is necessary to look carefully at the data and the implications of the data. In order
to interpret the data correctly from this document, I will devote a separate section to
analyzing it.

63

Table 6.9 Background radiation at SSFL: Rocketdyne SSFL perimeter gamma dosimeters for which continuous periods are available;
reduced to mR/Hr; means and standard deviations; SSL 3 and 4 are combined; SSFL 8 and 9 are combined. 1986-91 omitted due to
Chernobyl fallout. Calculated from data given in each individual annual report. SSFL12 and SSFL 13 are located on the north
perimeter fence near the RMHF.
Year

Offsite
1

All offsite

SSFL 3
/4

SSFL6

SSFL7

SSFL8/9

SSFL11

SSFL12

SSDFL13

1971-85 mean
1971-85 SD
1987
1987 SD
1992-05 mean
1992-05 SD

0.01125
0.0015
0.012
0.008
0.002

0.0113
0.0012
0.016
0.002
0.008
0.002

0.0177
0.004
0.020
0.001
0.0103
0.004

0.0165
0.008
0.017
0.0101
0.002

NA
NA
0.017
0.0103
0.002

0.019
0.0107
0.002

0.0104
0.002

0.0131
0.003

0.0130
0.003

64

Fig 6.6 SSFL: Gamma dose rate surface calculated from measurements made in at
Radioactive Materials Handling Facility RMHF SSFL in 1996

Fig 6.7 SSFL: Gamma dose rate surface truncated at 50uR/H calculated from
measurements made in at Radioactive Materials Handling Facility RMHF SSFL in 1996
Lowest level at perimeter is about 15uR/H.

65

Fig 6.8 Gamma dose rate measurements at RMHF: frequency distribution

Min: 8.00000
1st Qu.: 10.00000
Mean: 17.14286
Median: 13.00000
3rd Qu.: 19.00000
Max: 80.00000
Total N: 288.00000
Std Dev.: 12.23449
It is clear from the figures showing the dose rates in the Radioactive Metals Handling
Facility (RMHF) area, that substantial areas at the perimeter and in the unused corners of
the area have dose rate values consistently as low as 8uR/h. This is in agreement with the
offsite measurements showing a mean background dose rate of 8uR/h and I take 8uR/h as
the mean historic background to be conservative (see later analyses). This defines the
general contamination at SSFL, over the whole site as something capable of delivering an
excess dose rate of 6uR/h. It is possible to make some new calculations of contamination
on this basis.
The general area contamination in Ci/sq metre resulting in a dose rate at 1m of 1R/h for
gamma radiation of various photon energies has been calculated (HRP 1971). For
0.255MeV, which I use as a mean value, the exposure rate above an infinite plane of
gamma source activity of 1Ci/m2 and emitting one gamma photon per disintegration is
7R/h. The linear extrapolation then gives us a mean contamination, assuming 15uR/h, of
2.14 x 106 pCi m-2, or 80000Bq m-2. Of course, the mean excess dose rate on site is
6uR/h, and so the excess contamination from gamma emitting nuclides due to activities at
Rocketdyne, over the whole of Area IV is less than this and equal to 27,000Bq/m2. This
is significant contamination, and of course there are some areas where the contamination

66

is very high, as we see from the dose rate maps of the RMHF. The disturbance of topsoil
contaminated to this degree results in resuspension of some significant radioactivity.
In actuality, it is worse than this because the main isotopes involved here are in fact alpha
emitters, which have very low or absent gamma emissions. I turn to the alpha
measurements in due course.
The photon flat plane approximation I have used can be refined further and I can also
approach this from the point of view of the specific contamination. Rocketdyne tells us
that it is purely natural and mainly natural uranium. NCRP 1987 gives values of
gamma dose rates over land containing natural radionuclides.
Table 6.10 is taken from NCRP 1987.
Table 6.10 Gamma radiation field at 1metre over indicated soil concentrations (pCi/g on
left, Bq/kg on right of column 3) of natural radioisotopes (NCRP1987 Table 5.1)
Radionuclide
K-40
U-238 + daughters
Th-232 + daughters

Soil concentration
1pCi/g
1Bq/kg
1pCi/g
1Bq/kg
1pCi/g
1Bq/kg

Dose rate (uGy/year)

14
0.4
139
4
216
6

Annual reports give us mean levels of all these isotopes in soil. The uranium levels are
between 60 and 150 Bq/kg and this would result in an external dose rate of about
400uGy/year; the K-40 levels are generally constant at about 800 Bq/kg which translates
to 320uGy/y while the Th232 levels are roughly the same as the U-238 levels, giving a
further 600uGy/y. The total theoretical mean gamma dose rate per year over the whole
site is thus 400+320+600 = 1320 uGy/y which is 15uGy/h. Thus, we can be reasonably
secure that the mean levels of contamination over the SSFL site are significant and
involve mean uranium contamination at about 60-150Bq/kg, and that this is between 20
and 110Bq/kg higher than historic background. We can also see that there are places on
the site (e.g. RMHF) that are seriously contaminated. This is the point of this rather
complex gamma analysis of the on-site data.
6.10 Alpha and Beta Measurements of Contamination.
The classical method of measuring contamination by fission products is to measure alpha
and beta emissions from environmental samples. This is more difficult than measuring
gamma emissions and the sensitivity is far lower: nevertheless, for some man made
radioactivity it is the only way. For example, plutonium-239 cannot be measured by
gamma methods, and neither in general can U-238, although it is sometimes possible if
levels are high to use the gamma spectral line from daughter Th-234 as a flag. This
method is, however, rather uncertain for environmental levels owing to differential
solubility of Thorium and Uranium (see e.g. NCRP1987) and I have written elsewhere on
this issue because I was recently involved in making measurements of depleted uranium
in Kosovo and in Lebanon where this problem arose. The only safe way of measuring
uranium isotope ratios is by alpha spectrometry, or more recently by high resolution mass
spectrometry, and I have used both methods.

67

Measurements of gross alpha activity would be valuable to establish a trend, and in

particular to look at the period that is of interest here, 1998-2005, but in the case of
Rocketdyne, these have served no useful purpose because the results given have been
adjusted before reporting. I have carefully examined all the available reported data from
SSFL, from 1959 to the present day, alpha and beta activity in soil, water, air and
vegetation, and conclude that the testing methodology was flawed and unreliable in that it
understates the levels of contamination. Alpha activity in water before 1989 was
unreliable because the method involved filtration, and after that, when levels began to rise
to a level that was actually illegal under statutory guides, the reported levels were backed
off with some unknown quantity of background. This was a common method used at
Rocketdyne and regularly resulted in negative values for contamination, something which
is, of course, impossible.
Table 6.11 shows some of the alpha and beta measurements in groundwater, and I have
also calculated the alpha beta ratio, which is most unusual as there is a very high level of
alpha emitters relative to beta emitters but also that this seems to suddenly change at
times, suggesting that a new input of radioactive material to the groundwater has
occurred. Two things are immediately apparent. First, the overall alpha levels, despite the
back off of background, which began in 1998 are enormously high. Compared with the
alpha activity in groundwater from boreholes at AWE Aldermaston, a facility which
employs uranium and plutonium from assembling bombs, peak levels at SSFL were
routinely thousands of times greater. This is even before the backing off began, and even
higher after the soil disturbances and movements began in 1998 and the groundwater
became further contaminated with radioactive dust containing enriched uranium.
We can see such injections in alterations in the alpha beta ratios in Table 6.11 which
began in 1996 (highlighted in bold) with two further periods after that in 2001-2 and very
recently in 2005. I interpret this as injections of alpha contaminated material from
resuspended dust, but I am cautious as to how far this interpretation can go because the
back off of background will make any ratios after 1998 incorrect. Nevertheless, the
normal alpha beta ratio from natural background materials should be low: at AWE it is
about 0.15. To find alpha levels higher than beta levels, which routinely occurs at SSFL
is most unusual.
The backing off of background alpha has led to some bizarre results. After this behaviour
began, we see total uranium levels in groundwater higher than total alpha levels,
something which is impossible, because uranium isotopes are all alpha emitters. It is not
my aim to attack Rocketdyne and their creative reporting of environmental data: others
have done that. I am merely trying to use their data to approach the truth in this current
matter.
6.11 Remediation Activity Trends
I have attempted to obtain an idea of the activities at the SSFL site from 1989 onwards. I
would like an account of the activities involving digging, cutting, moving of soil and

68

generally disturbing radioactively contaminated buildings, plant, sodium, water and soil
in way that can be quantitatively assessed. I have asked to see details of the
characteristics and quantities of material dug up and trucked out from the site, the route
of the trucks and so forth, but this information has not been available as of yet. In its
absence I have done a preliminary analysis based on the Rocketdyne reports and other
data I have seen. I have made an assessment of the likelihood of generating contaminated
dust on a scale of 1 to 10 by year, based on the activities reported each year in the
Environmental reports. I collect the totals together in Table 6.11 below and present this as
an initial assessment of likely levels of activity likely to generate radioactive (mainly
uranium contaminated) dust. This table and analysis correlates with the measurements of
uranium in air for this period. I also display the trend in Fig 6.10. The remediation index
value I have created from the Environmental Report accurately foretells increases in
alpha beta ratios the following year and fits qualitatively well with the trend in uranium in
air shown in Fig 6.5
The quantities of contaminated material involved are difficult to establish. From the
reports, the main soil removal incident which is quantified is the trucking offsite of the
14,000 tons of soil removed from the Sodium Disposal Facility 2000-2001. Assuming a
density for the soil of 2.1 for sandstone soil (CRC 1989) this represents 7000 cubic
metres which is a pit, 1 metre deep and 26 metres square. This seems rather a small
amount of material given the various maps I have seen of the facilities. Indeed, some light
can be shed on this upon consideration of a map and photograph of the disposal of
contaminated soil from the SNAP facility which occurred in 2003 (although I have not
seen recorded the quantities involved anywhere).
6.12 The Removal of Soil from the SNAP Facility
The Building 4059 Final Status Report (BC27698) provides the results of the Phase A
and Phase B Final Status Survey of the SNAP Ground Prototype Facility, and was
released in 21/4/2006. At this point, the site had been excavated and the soil removed.
The report shows a photograph of the hole where the soil had been removed from, and
also a map showing gamma radiation measurements. There were also some
measurements made of uranium isotope concentrations in the surface soil which was left
behind at the base of the hole. Fig 6.8 shows the photograph of the hole where the soil
was removed and Fig 6.9 the graphic indicating the gamma measurements. The final
demolition of Building 4059 started in 2003. The released portion of the building was
demolished and shipped to a Class 1 hazardous waste disposal site. In 2004 the
remaining test cells and PCR were excavated and disposed of as radioactive waste to the
Nevada Test Site.

69

Fig 6.8 Photograph of SNAP facility area after soil removal (2006 report BC27707). Note
dimension of tracked digger and ladder which give indication of depth of the hole (see
text).

70

Fig 6.9 Gamma exposure rate measured on the surface after removal of contaminated soil
from Building 4059 (T059) SNAP Facility in 2006.

Fig 6.8 enables me to approximate the depth of the excavation. From the ladder rungs and
the size of the tracked digger I am assuming that the excavation is roughly 8 metres deep
in the hole and this hole begins some 8 metres deeper than the perimeter of the area of the
facility. Fig 6.9 gives, besides the gamma dose rates, the latitude and longitude of the site
perimeters, and I can use these to determine the area. The facility is roughly a rectangle
of 6.9m by 11.3 metres with a triangular area of 7.7 metres by 3 metres cut out of it. It is
approximately 5900 square metres overall and I can assume a mean depth of excavation
of approximately 10 metres. This gives a volume of contaminated soil equal to 59,000
cubic metres or 124,000 tons. Using a relatively high natural background gamma level of
10uSv/h, the radiation in the pit and below the SNAP building were still twice
background, an excess gamma exposure rate of about 18uR/h. For background
potassium, uranium and daughters, thorium and daughters , the tables 6.2 and 6.10
permits the construction of the expected exposure rate from the expected natural
background in the Arkose sandstone , which is subtracted to get the excess exposure.
Table 6.11 constructs the background exposure for the type of soil. The result is 85nGy/h
which is approximately what is found (see the section on gamma exposure rates and
mean background). The 7.5 to 10 uR/h (blue) areas on the map in Fig 4.9 represent the
background (in terms of dose this would be about 60 to 80nGy/h because we have to
convert from Roentgens to Grays or Sieverts and I use the factor 0.8 since the photon
71

energy is low). The deep excavation (brown) has material at the bottom of it which is
about 100nGy/h above this. The annual dose from this material would be 87600uSv. For
uranium and daughters this represents activity of 87600/4 = 21,900Bq/kg of Uranium.
For thorium, the amount is slightly less, but still the contamination level is high.
Table 6.11 Constructing the background exposure rate from its soil components. Data
from NRC 1987
Component
K-40
U-238 +
daughters
Th-232 +
Daughters
Cosmic rays at
1000m
All the above
Dose rate

Assumed activity Bq/kg

800
25

Exposure rate uGy/year (NRC 1987)

320
100

24

100 metres

300
744
85nGy/h

Table 6.12 Rocketdyne. Alpha and beta activity in groundwater (Annual Reports). Levels at the
Atomic weapons Establishments Aldermaston are between 10 and 40mBq/m3. Alpha beta ratio
in the water is very unusual (column 6). Ratio of alpha/beta in water at AWE is 0.15 This is in
agreement with the high alpha levels in the groundwater.
Year

1987
1988
1989
1990
1991
1992
1992
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003

Mean alpha
pCi/L
(mBq/L)
1.75 (65)
2.04 (75)
1.23 (45)
5.99 (221)
6.34 (234)
7.97 (294)
5.5
(203)
6.7
(247)
6.6
(244)
7.5
(277)
8.29 (306)
6.8
(251)
7.17 (265)
5.88 (217)
7.97 (294)
8.29 (305)
5.59
(206)

Max alpha
pCi/L(mBq/L)

Mean Beta
pCi/L

Max Beta
pCi/L

Alpha/beta
ratio

3.87 (143)
4.48
(166
3.19
118
28.7
1061
29.1
1076
78
2886
24
888
42.3
1565
25.4
939
53
1961
28
1036
45.8
1694
26.9
995
21
777
59.44
2199
29.36
1086
29.1
1076

4.66
4.18
4.74
5.45
6.38
8.51
9.4
6.8
7.8
6.6
6.3
4.9
9.02
7.22
6.83
4.97
8.23

5.76
5.56
5.83
13.1
43.1
50
38
30.3
34.6
33.7
17.3
18.6
58
28.7
15.9
11.7
17.8

0.38
0.49
0.26
1.09
1.0
0.93
0.58
0.98
0.84
1.13
1.31
1.38
0.79
0.81
1.16
1.66
0.67

72

2004
2005

4.45
6.2

(164)
(229)

21.3
27.9

788
1032

7.72
6.02

16.6
15.9

0.57
1.02

Fig 6.10 Trend in resuspension contamination coefficients associated with remediation 1989
(obtained from Rocketdyne reports).

Table 6.12 Trend in resuspension contamination coefficients associated with remediation 1989
(obtained from Rocketdyne reports) compared with alpha/ beta ratios.
Year

1987
1988
1989
1990
1991
1992
1993
1994

Remediation
work Relative
Index

5
0
2
5
3
2

Alpha/beta ratio in
groundwater
0.38
0.49
0.26
1.09
1.0
0.93
0.58
0.98

73

1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
2005

1
7
9
9
6
20
5
3
8
10
0

0.84
1.13
1.31
1.38
0.78
0.81
1.16
1.66
0.67
0.57
1.02

6.13 Summary of Section 6

Uranium levels and isotope ratios in nature have been well described in the literature. By
comparison with these data, uranium levels at the SSFL site are generally high for the type of
geology (up to eight times greater than the maximum level reported for the type of soil by
standard works) and the material can be shown to be man made from the U238/U235 activity
ratio. When this contaminated soil was disturbed during remediation soil movements from 1997
onwards, resuspension of topsoil resulted in air concentrations of uranium which were
unnaturally high. Groundwater levels of uranium at SSFL were comparable only with levels
found near ex Uranium mines in the USA and the material was enriched and not natural. The
trend in uranium in air is consistent with the disturbance of the contaminated soil during major
remediation from 1999-2004 with a peak at the point at which 4,000 tons of soil were reported
dug up and trucked out between October 2000 to March 2001.
Measurement of gamma exposure doses from Thermoluminescent dosimeters show that the
SSFL site has approximately 6-8uSv/h greater exposure rate than mean offsite background
gamma in the late 1990s and this is supported by analysis of dose rates mapped at the
Radioactive Materials Handling Facility. These excesses reasonably were caused by the
existence of uranium contamination on the site, and calculations using two different methods
support this conclusion. Some unusual measurements of uranium in wells in 2004 require further
examination. Alpha and beta measurements reported by Rocketdyne are criticized for having
been background subtracted without any information on the levels assumed. However, alpha
levels are routinely hundreds of times higher than normal background and alpha beta ratios are
also highly unusual. The alpha beta ratios define injection of new material into groundwater and
the trend correlates with soil removal and remediation activities likely to have caused dust
formation.
Examination of one site which was decontaminated, the SNAP facility, shows that the material
removed from it was over 100,000 tons and was significantly contaminated with radioactivity.
Thus, the site itself is heavily contaminated with enriched Uranium which was resuspended in
the air in the period following 1996.

74

7. Evidence of Offsite Contamination by Uranium

7.1 Questionable Procedures
In Section 6 it was shown that the SSFL site was contaminated with enriched Uranium. The
remediation work which was being carried out from the mid-1990s and which generated very
large amounts of Enriched Uranium measured in the samples on site in the period 1999-2007
was suddenly stopped in 2007. For some reason, it was decided to carry out no further
remediation work but to characterize the contamination at the site so that some limit of
remediation could be agreed upon. After arguments between EPA and DoE the first thing that
happened was that the initial decision to remediate to a level deemed safe by the EPA was
changed to a decision to remediate to a level which would be defined by Natural Background.
This was followed by the EPA commissioning a Background Study of the area surrounding the
SSFL by Hydrogeologic Inc. of New York. The final report was published in Nov 2011. (Final
Radiological Background Study Report Santa Susana Field Laboratory Ventura County,
California. Nov 2011. EPA Contract No.: EP-S3-07-05 Work Assignment Number:
021TATA09QL.; New York: Hydrogeologic Inc.). This is an interesting document which is
misleading as to the true background at SSFL, but gives much useful information to a careful
forensic analysis about the real gamma radiation levels offsite due to offsite contamination. It
also shows that Uranium offsite in the chosen background characterization areas was enriched
and therefore must have originated at SSFL. The company, Hydrogeologic, Inc. chose three
areas near the SSFL site which it stated would be proper areas to characterize backgrounds for:
1. Gamma exposure rates; and
2. Levels (activity concentrations) of 100 radionuclides which might be expected to be
contaminants from SSFL in surface and sub-surface soil.
The three chosen sites are located on the map in Fig 2.1 (which I copy below) were:
1. Lang Ranch
2. Rocky Peak
3. Bridle Path.
The furthest away from SSFL Area IV was the Rocky peak background area which was 7 miles;
the other two were closer, 4 and 5 miles, and community residents apparently expressed concern
that these areas were too close. To address this concern, samples and measurements were taken
from reference sites more than 10 miles away in the four quadrants, NE, NW, SE and SW.
These more distant DTL sites were analysed for Cs-137, Sr-90, Pu-238, Pu-239 and Co-60, but
not for Uranium, a significant omission from a scientific analysis point of view. .
Fig 2.1 (copy) Location and bearing from SSFL Area IV of the three Background Radiation
sites, Lang Ranch, Bridle Path and Rocky Peak chosen by Hydrogeologic Inc. to represent
natural background levels for remediation limits at SSFL (pale blue). Also shown (yellow pins)
locations of Ms. Debra Dawson (see section 2).

75

7.2 The Natural Background Gamma Exposure Rates at the SSFL Site and Offsite
The study was expressly commissioned to analyze the natural background on the SSFL and off
site. Of course, this should have been done before the SSFL was built and before the site had
been contaminated by the transportation to the site of radioactive materials including uranium.
But in any event, the study was supposed to investigate and try to answer what natural
background levels on and off site would have been in the absence of SSFL activities.
Interestingly, the results were tabulated as Counts per Minute and not as exposure rates in
This method of reporting is known to be misleading and to obscure relevant information about
gamma exposure rates. Counts Per Minute (CPM) indicate different exposure rates depending on
the instruments used, are almost useless in scientific analysis, and, particularly in this case,
cannot be compared with previous measurements of gamma exposure rates made onsite and
offsite by Rocketdyne or by the State of California. I have tabulated most of the historic gamma
measurements made by Rocketdyne and (independently) the State of California in this report
(see Section 6 Table 6.9). The mean offsite background and main gate background between
1995 and 2005, measured by Rocketdyne and also on occasion using independent dosimeters by
the State of California, was 0.008mR/h. I will convert the units now to make the discussion

three chosen offsite reference areas and reported in the 2011 Background study were much
per Minute, CPM.
Gamma radiation is measured in a number of ways, with Geiger Counters, Ionisation Chambers
and solid state devices of various types. Often a Thallium doped Sodium Iodide (written-NaI(Tl)) detector is used. This is a scintillation device in which radiation causes light to be
emitted from a crystal and each emission is detected by a photomultiplier tube and amplified to

76

give a click or count. An electronic counter then converts the rate of events to counts per minute
or counts per second. To convert this into gamma exposure Roentgens per hour the system has to
be calibrated against some known radioactive source (usually Cs-137) or against a primary
source such as an ionization chamber. Different sized NaI(Tl) crystals give more or less CPM per
R and so it is necessary to know the size of the crystal and its efficiency. Therefore, for anyone
to understand the meaning of the results (CPM) this calibration has to be provided. In the
Background Report no such calibration was provided. The instrument used was given, however,
as a Ludlum Type 44-20. This is a 3 inch diameter crystal probe which the manufacturer data
accurate within 10% for the specific probe employed) information, I am in a position to convert
the gamma background g
measurements given by Rocketdyne and the State of California, and also historic measurements
made in 1959.
The results for the 3 chosen so called background areas are given in Table 7.1 below. The mean
so called background for the DTL quadrant distant areas are given in Table 7.2. These levels
are much higher than the previously records. The State of California offsite levels and indeed
are higher than the levels reported by Rocketdyne. Obviously, these higher so called background
rates (revisionist history), are not natural background but are higher rates, caused by the
contamination at SSFL.
Table 7.1 Gamma backgrounds at the three chosen comparison sites in the 2011 Background
report converted from Counts per Minute to
and compared with historic background
measurements made at the SSFL gate and offsite by Rocketdyne and by the State of California.
Also shown are results from a 1959 EPA/AEC commissioned aerial survey ARMS I of the Los
Angeles area which included the locations of the Lang Ranch and Bridle Path sites.
Site
BR Lang Ranch CPM
BR Rocky peak CPM
BR Bridle Path CPM
Rocketdyne main gate annual
reports1995-2004
Rocketdyne and State of
California Offsite 1995-2004
Rocketdyne offsite 1975-1988
ARMS I 1959 Lang Ranch

Min
36000
15.6
32000
13.9
38000-40000
16.5-17.4

Max
41000
17.8
36000
15.6
44000-45000
19.1-19.6

Average
39000
17.0
34000
14.8
41000-42000
17.8- 18.3
8
8

7.8

9.1

11
8.5

7.8

9.1

8.5

We see that the newly defined background at Lang Ranch and Bridle Path is about twice what
it was in the SSFL annual reports. If one uses the false higher so called natural background rate
as if it were a true background rate, there is no need to remediate. But this is just wordplay. If

77

you define the background to be artificially high, then you are meeting background by
definition, whatever your contribution to the radiation found at the testing point. But this is not
science. And there is independent data confirming that the older background levels from the
State of California and Rockedyne are closer to the naturaltrue , pre-SSFL levels.
This independent data comes from a histogram of background gamma radiation in the Los
Angeles area published by the NCRP in 1987 (Exposure of population of USA and Canada to
Natural Background Radiation. Washington: NRCP, 1987). I show the histogram in Fig 7.1
Table 7.2 Gamma backgrounds at the four SSFL Background Distant Locations (DTL) sites in
the 2011 converted from Counts per Minute to
Site
Min
Max
Average
11.7
13.3
12.6
9
10
9.3
17.1
15.4
SSFL main gate
8
annual reports
1995-2004
State of California
8
Offsite 1995-2004
Rocketdyne offsite
11
1975-1988

Fig 7.1 Frequency distribution of natural background gamma radiation dose rates in Los Angeles
area (NCRP 1981) bottom right; NCRP refer to Oakley 1972 who in turn uses ARMS 1 and
ARMS 2 data (see text). Note dose (rad/h) rate may be obtained from exposure rate (R/h) by
multiplying by 0.85. A dose rate of 6

78

The histogram in Fig 7.1 is taken by NCRP from a report by T. Oakley written in 1972 for the
US EPA (Natural Radiation Exposure in the United States. Report ORP/SIDS 72-1 Washington
EPA). Oakley employed raw data for an aerial survey carried out in January 1959 for the Los
Angeles area. Kenneth G Books (1959) Aeroradioactivity Survey and related surface geology of
parts of the Los Angeles Region, California (ARMS 1). Civil Effects of Test Operations.
Washington: US Atomic Energy Commission CEX-59.4.16. The report gives details of the aerial
survey in which a DC 3 aircraft equipped with specialised NaI(Tl) scintillation equipment flew
over the 1400 sq miles Los Angeles area at 500ft and mapped the surface radioactivity.
The survey area included two of the three areas chosen in the 2011 Background Survey, Lang
Ranch and Bridle Path, results for which are given in Table 7.1 above. The surveys were carried
out at a time when several nuclear tests had been carried out in the Nevada and Los Alamos sites,
and at a time when the SSFL had been operating for seven years, indeed just around (before) the
time of the sodium reactor meltdown. So any gamma level recorded had some component from
test fallout. The results showed two things. First, that the mean background at the Bridle Part and
area. The second is that a flyover of the SSFL site (the Burro Flats Nuclear Facility) at the time
gave two anomalies: one was twice Natural Background the other four times background.
ly environmental
-2004 as the
fallout components (largely Cs-137) decayed through weathering and physical loss to deeper
ground. The anomalies found in the flyover, at about the time of the sodium reactor meltdown
suggest that by 1959 the site was already extremely contaminated with background gamma
levels up to 48
The importance of these historical data is that as far away as Bridle Path and Lang Ranch (some
5 miles to the West of the site) the gamma background had increased from a mean of about

similar levels at the main gate and in the few offsite locations where they positioned dosimeters
in the period before the remediation, the excess can only be due to radioactivity dispersed from
SSFL during the periods of the remediation 1996-2007, and this radioactivity, as we see from the
other evidence, is mostly from enriched Uranium (and other associated daughter nuclides in the
Uranium-238 and actinide (U-235) series). Since these background sites are to the West, and the
prevailing wind is mainly from the West, more likely than not Ms. Dawson, who lived only 3
miles away to the east suffered more contamination than this and the gamma levels at her
residences were more than this. This exposure alone accounts for more than that allowed by 10
C.F.R. 20.1301, which prohibits a total effective dose to individual members of the public in
excess of 0.1 rem (1 mSv) per year or 0.002 rem (0.02 millisievert) per hour. The data from
Uranium-238 and U-235, and also the Thorium 234 and Thorium 231 measurements at the
background sites show that the Uranium is enriched and not natural.

79

7.3 Enriched Uranium at the Background Sites

Because the contamination causing the excess gamma radiation exposure rate is due to
dispersion of the contaminated dust, and because the contaminated dust, as we have seen from
the on-site air data, is generally highly enriched we can expect that the Uranium isotope ratio
measured in the chosen background areas would also indicate Enriched Uranium. They do.
The frequency distributions of Uranium U238/U235 ratios for the surface material analysed by
Hydrogeologic and reported in the 2011BR are given for Lang Ranch and Bridle Path in Fig 7.2
and 7.3, and for the sub surface samples in Fig 7.4 and 7.5. It is clear that the material is
enriched, though less enriched than the air samples reported from the SSFL site itself.
Fig 7.2 U238/U235 isotope ratio distribution in surface samples (N =27 ) from Lang Ranch
reported in BR 2011. Red line is ratio of Natural Uranium

80

Fig 7.3 U238/U235 isotope ratio distribution in surface samples (N =54 ) from Bridle Path
reported in BR 2011. Red line is ratio of Natural Uranium

Fig 7.4 U238/U235 isotope ratio distribution in sub surface samples (N =10) from Lang Ranch
reported in BR 2011. Red line is ratio of Natural Uranium

81

Fig 7.5 U238/U235 isotope ratio distribution in subsurface samples (N =10) from Bridle Path
reported in BR 2011. Red line is ratio of Natural Uranium

One problem which has emerged in my own work analysing isotopic ratios for Uranium is that
the ratio is highly dependent on the sensitivity of the method for determining U-235. At low
concentrations of U235, the standard error of the ratio becomes large. Therefore, to see if these
indications of enriched Uranium were an artefact of the analytical method, I plot the U238/U235
ratio for the Lang Ranch surface samples against the total U-235 reported in Fig 7.6. It is clear
that the Uranium ratio decreases as the U235 concentration increases, which is evidence that the
enrichment increases as the U-235 concentration increases. Thus, we see that the offsite
contamination is from U-235 and this is to a reasonable degree of scientific certainty the origin
of the high gamma background at these sites.

82

Fig 7.6 Uranium isotope ratio as a function of total U-235 in surface samples at the Lang Ranch
site (BR2011). This shows that the source of the contamination is U-235 from
SSFL.

Total Uranium-238 (median) concentration at both Bridle Path and Lang Ranch sites was about
42Bq/kg which is about 2 to 4 times the expected value for Arkose sandstone geology (see
section 6, Table 6.2). The frequency distribution of U-238 levels at the Lang Ranch site is given
in Fig 7.7. This explains the doubling in background gamma levels seen, especially because the
U-235 is a gamma emitter.

83

Fig 7.7 Frequency distribution of U-238 concentration at the Lang Ranch background site
(surface and subsurface) Bq/kg.

7.4 Thorium-234 and Thorium-231

Further evidence that the Uranium at the Lang Ranch and Bridle Path reference sites is enriched
comes from a similar comparison of the ratio of Thorium-234 and Thorium-231. U-238 decays
to short half life Th-234 which is a weak gamma emitter and can be measured by gamma
spectrometry. U-235 decays to Th-231 which also is a weak gamma emitter and has a very short
half life. Therefore, although U-238 is not a gamma emitter, the two Thorium daughter nuclides
are in secular equilibrium with the parents and can be employed to measure the isotopic ratios.
These Thorium nuclides were in fact reported in the 2011BR and support the conclusions above.
7.5 Summary of Section 7
The 2011 EPA-commissioned so called Natural Background study report shows that the areas
up to 5 miles from the SSFL site are significantly contaminated with Uranium from SSFL which,
from comparison with earlier and historic measurements, indicated that the contamination
occurred after the remediation period 1996-2007. Measurements of gamma radiation exposure
rates and radionuclide contamination at sites chosen to represent Natural Background for the
purposes of remediation were reported. These show that the offsite gamma background of 17the State of California in
the period prior to remediation work in the late 1990s. This is also confirmed by historical data
from the 1959 ARMS1 survey quoted by NCRP 1987. The source of this increased gamma
radiation is shown to be enriched Uranium which has migrated offsite to give a mean value in the
background areas of 42Bq/kg which is twice that expected for the local geology based on
national data. Because the background sites are 4-5 miles mainly upwind of the SSFL site, it is

84

clear that these levels of contamination and gamma dose rates and enriched Uranium
contamination will be higher downwind where Ms. Dawson lived between 1988 and 2001 and
that these exposures more probably than not resulted in exposures in excess of 10 C.F.R.
20.1301, which prohibits a total effective dose to individual members of the public in excess of
0.1 rem (1 mSv) per year or 0.002 rem (0.02 millisievert) per hour.
8. Independent Evidence of Health Effects in Studies of SSFL and Local Populations
8.1 Other Examples of Effects
Ms. Dawsons cancer and that of her ex-husband Mr. Lindsey were caused by exposure to
contamination which occurred in the period of remediation, 1996-2007 more likely than not. Are
there other, examples of effects of such exposure types. There are three examples which I will
now briefly review.
Because solid cancers have a considerable lag period between exposure and diagnosis, usually at
minimum 10 years, what would be required ideally would be a cancer incidence epidemiological
study carried out in the period ten years after the remediation exposures in 1996-2005 i.e. in
2006-2012. But, although the releases were greatest during the remediation, it is clear from
Section 6 (e.g. Fig 6.10 and Table 6.12) that activity from 1989 resulted in the generation of
lesser offsite contamination. Therefore, studies of cancer toward the end of 2000 might be
expected to show some lesser effect, as indeed is the case. As a consequence of anecdotal
concerns about cancer increases in local populations, a study was carried out by Morgenstern et
al and was published in 2007. I will review the findings below.
There are also two other indications that the offsite exposures to Enriched Uranium dust and
other radionuclides carried with it cause health problems. Although the genetic damage caused
by radiation takes about ten to twenty years to cause cancer, this is not true for effects on the
foetus. These would be apparent very soon after birth, or indeed at birth, and show themselves as
infant mortality and childhood cancer. The effects would be contemporaneous with the
exposures, or pretty nearly. The infant mortality rates in census tracts near the SSFL site at the
time of the remediation do in fact show an effect. In addition, there was a cluster of the rare eye
cancer Retinoblastoma in children living downwind of the site in the period of the remediation.
Thus, there are three pieces of evidence which support the conclusion that SSFL emissions
caused Ms. Dawsons cancer:
Morgenstern et al 2007 cancer study
Infant Mortality study
Retinoblastoma cluster in North West Los Angeles
8.2 Morganstern, et al., 2007
Quoting directly from the report:
The investigators of this study explored the rates at which newly diagnosed
cases of cancer occurred in Ventura and Los Angeles Counties between 1988 and 2002 in
relation to distance from SSFL. The two-county region was divided into three exposure areas
(less than 2 miles, 2-5 miles, and greater than 5 miles from SSFL), and the study period was

85

divided into two follow-up periods (1988-1995 and 1996-2002). Data on more than 600,000
cancers and census block-group data for the residential population in the two-county region
were obtained from the California Cancer Registry. Using these data, incidence rates of cancer
were estimated for each exposure area, by category of age, gender, and race/ethnicity (nonHispanic white, Hispanic, and other non-Hispanic).
Because exposure to radiation and chemicals used at SSFL may affect the risk of several
types of cancers, analyses focused on the association between distance from SSFL and 12 adult
cancer outcomesthree general groupings and 9 specific types of cancer. The general
groupings were total cancers (excluding non-melanoma skin cancer), radiosensitive cancers
believed to be affected by ionizing radiation (lung, female breast, thyroid, bone, and leukemias),
and chemosensitive cancers believed to be affected by the types of chemicals used at SSFL
(lung, bladder, liver, kidneys, and bone marrow). The specific cancer outcomes were melanoma,
cancers of the colon and rectum, cancers of blood and lymph tissue (including leukemias,
lymphomas, and multiple myeloma), lung cancer, female breast cancer, bladder cancer, prostate
cancer, thyroid cancer, and cancers of the upper aerodigestive tract (oral and nasal cavities,
pharynx, larynx, and esophagus). Total cancers for children under 15 years were analyzed
separately. For each cancer outcome, the incidence rates for residents living less than 2 miles
and 2-5 miles from SSFL were compared with the incidence rate for residents living more than 5
miles from SSFL. These comparisons were expressed as ratios of incidence rates, i.e., incidence
rate ratios. If environmental hazards originating at SSFL migrated offsite and if community
residents were exposed to those hazards, the expected incidence rate of cancer would likely be
most elevated in the area closest to SSFL, i.e., the expected incidence rate ratio would be greater
than 1 for persons living within 2 miles of SSFL. Estimated incidence rate ratios were corrected
statistically (standardized) for differences between exposure areas in the distribution of age,
gender, and race/ethnicity; i.e., the main results presented in this report, comparing the exposure
areas, were not biased (distorted) by the effects of these three demographic variables on cancer
risk.
The researchers conclusions were that, on the basis of their results there was:
little or no association, for total cancers and radiosensitive cancers among adults; but the
incidence rate of chemosensitive cancers was slightly elevated during both follow-up periods in
the population living within 2 miles of SSFL. Results for the 9 specific cancers revealed some
elevated incidence rates between 1988 and 1995 among persons living within 2 miles of SSFL.
Specifically, the standardized incidence rate ratio was greater than 1.6 for cancers of blood
and lymph tissue, bladder, thyroid, and upper aerodigestive tract. Between 1996 and 2002, the
rate ratio among persons living within 2 miles of SSFL was greater than 1.6 for thyroid
cancer. There were too few childhood cancers to yield informative results.
Conclusion: Despite the methodologic limitations of this study, the findings suggest
there may be elevated incidence rates of certain cancers near SSFL that have been linked in
previous studies with hazardous substances used at Rocketdyne, some of which have been
observed or projected to exist offsite. There is no direct evidence from this investigation,
however, that these observed associations reflect the effects of environmental exposures
originating at SSFL. Given these provocative findings and unanswered questions, it is tempting

86

to recommend further analyses or future studies to address the health concerns of the
community.
Examination of their results tables reveals that these deductions were not really valid. I have
personally carried out several studies of this kind and have written at some length about the
epidemiological methodology which is employed (Busby 1995, 2006). There are a number of
problems. The first is that contamination is not radially distributedit moves with preferred
wind directions and water flows. The second is that the closer you get to the point source,
radially, the smaller the population, and so statistical significance is hard to achieve unless the
effects are large. And this was certainly the case in this study where the inner ring, 0-2miles, was
sparsely populated with the main population not distributed as directly downwind as the larger
populations occupying the areas greater than 5 miles. The population problem is a significant
one. In Morgenstern et als Table 2, which lists cancer rates in the three regions being compared
for 1995-2002, we see that the number of cases in the 0-2 mile radius is only 500 compared with
4623 in the 2-5mile and 278,607 in the > 5 mile ring. What I would do here is to combine the 0-2
and 2-5mile rings and compare these with the >5mile radius population to define two populations
close to and remote from the SSFL. Although it is also clear from the analyses I have carried
out in sections 6 and 7 that contamination carries out further than 5 miles, such an approach
might be expected to show something. Results given in Tables 1 and 2 of Morgenstern et al
2007 give rates/100,000 and numbers of cases, which data enable me to calculate the person year
denominator for the three regions being compared, and these are given for all ages in Table 8.1.
Because these are five year periods, the populations are just 1/5th of these. For the inner ring the
base population in 1996-2002 was a mere 25,195
Table 8.1 Morgenstern et al 2007 total person years for the period 1988-95 and 1996-2002 based
on rates and numbers in their Tables 1 and 2. I combine these to give two regions A and B
Period
1988-95
1996-2002

0-2miles
118,397
125,976

1988-95
1996-2002

2-5miles
1,144,018
1,154,884
0-5 miles Region A
1,262,415
1,280,860

>5miles
74,986,394
80,896,341
>5 miles Region B
74,986,394
80,896,341

I can now compare the two regions, A (0-5 miles) and B (> 5 miles), for all cancers in the two
periods. I do this in Table 8.2.
Table 8.2 Cancer near SSFL 0-5miles (from data in Morgenstern et al 2007).
Period
88-95
96-02

All cancers A
4473
5123

All cancers B
264552
278607

Rate Ratio
1.00
1.16

Statistics
Not Significant
1.12<RR<1.19 ; p<.00000

This shows that there was a highly statistically significant effect of living within 5 miles of the
SSFL in the later of the two periods studied, a period which included the beginning of the
remediation. From the tables various other effects can be found, but most interesting is the

87

apparent increased risk of leukemia/lymphoma and the apparent 25% increased risk of cancer in
children (RR = 1.25) in the period 1996-2002 (19 children in the 0-5 mile group A), an effect
which was not there in the earlier period before the remediation. The childhood cancer excess
shown in the latter period is supported by two other studies which I turn to.
8. 3 The Childhood Retinoblastoma Cluster
Data which is in the public domain show that there was a cluster of 9 or 10 cases of the rare eye
cancer Retinoblastoma in the area of Los Angeles downwind of the SSFL site between 2000 and
2004. The cluster was statistically significant, defined by a 10-fold excess and therefore, not a
chance occurrence. Retinoblastoma, a cancer with a known genetic defect component, is
associated in the literature with exposure to ionising radiation and is notably high in populations
living near Uranium contaminated areas, the Sellafield nuclear reprocessing site in the UK (20fold excess) and the Navajo communities living near Uranium mines (12-fold excess). Thus, the
element Uranium emerges as a likely cause of the cluster. That the remediation contamination
was the cause is also supported by the period of the cluster which coincided with the peak
Enriched Uranium concentrations in the air filters.
8.4 Infant Mortality and Cancer in Ventura County
County data for cancer and infant deaths are available in the USA by county. The genetic and
genomic damage caused by exposure to ionising radiation and Uranium will lead to various
cancers in time, but will also cause effects in the womb which may be looked for in exposurecontemporary infant and perinatal mortality rates and birth weights. Data for infant deaths in
counties in California are obtainable from the Center for Disease Control CDC. I can compare
Ventura County where SSFL is located with other Californian Counties. Table 8.3 gives such a
comparison for periods from 1983 to 2007.
Table 8.3 live births and deaths <1yr in Ventura County compared with other Californian
Counties from 1983 by 5-year periods; Odds Ratio based on 1983-87 = 1.0
Data from US Center for Disease Control and prevention http://wonder.cdc.gov/births
period

Area

Deaths<1y

Live births

1983-7

Ventura
Other Cal
Ventura
Other Cal
Ventura
Other Cal
Ventura
Other Cal
Ventura
Other Cal

380
21428
417
22693
332
17430
288
14132
372
13968

51614
2288859
62588
2865987
59130
2710442
55643
2483982
59882
2653201

1988-92
1993-97
1998-02
2003-07

88

Rate/100,000 OR based
on 1983-87
736
936
1.00
677
791
0.69
561
643
0.59
517
569
0.47
621
527
1.84

From this we can see a trend in falling of infant mortality in line with better healthcare in the
period to 2002 which is suddenly followed by a sharp increase in the period 2002-2007. This
would have been the group most exposed to releases from the peak exposures from the
remediation efforts. I can also look at child cancer using the same system. The latest available
2002-2006 data show that Ventura County has the highest child cancer rate of any of the 18 most
populated counties of California with a rate of 18.8 per 100,000 population (total California
16.6). The same is true for child cancer deaths 0-19 with a rate of 3.643 per 100,000 (total
California 3.063). Finally, from 1988 to 2008 Ventura County had the highest thyroid cancer rate
of all the California Counties with a rate of 18.8 per 100,000 (California 7.08). The thyroid is
known to be the most sensitive organ of the body to ionising radiation. Indeed, Morgenstern et al
found a significant trend of thyroid cancer with distance from SSFL throughout their study
period.
8.5 Summary of Section 8
Three independent examinations of health effects carried out in populations living close to and
downwind of the SSFL all show statistically significant effects which can be ascribed to
exposures to ionising radiation and Uranium. These include the 2007 study of Morgenstern et al,
my own study of a Retinoblastoma cluster and an examination of infant mortality and childhood
cancer in Ventura County employing public data from the Centre for Disease Control. All three
investigations support a peak period of risk around the time that the SSFL was undergoing major
remediation.
9. The Regulations
I was asked to analyse and form an opinion to a reasonable degree of scientific certainty whether
or not Ms. Dawsons exposure, if any, to SSFL contamination was in excess of federal
regulations including 10 C.F.R. 20.1301 and 40 C.F.R. Section 61.92, which governs
Department of Energy facilities. 10 C.F.R. 20.1301 prohibits a total effective dose to individual
members of the public in excess of 0.1 rem (1 mSv) per year or 0.002 rem (0.02 millisievert) per
hour and 40 C.F.R. Section 61.92 prohibits exposure to any member of the public of 10 mrem or
.1mSv per year. It my opinion that Ms. Dawsons exposure to SSFL radioactive contamination
was in excess of federal regulations 10 C.F.R. 20.1301 and 40 C.F.R. Section 61.92. Further, I
was asked to analyse whether or not any such exposure was capable of causing Ms. Dawsons
colorectal cancer and whether it did more likely than not. It is my expert opinion to a reasonable
degree of scientific probability that such exposure is capable of causing and did in fact cause Ms.
Dawsons cancer.
9.1 Offsite Doses
The offsite dose routes include the consequences of releases to air and water. The routes are
listed in Table 5.1. It is not possible, given the lack of data to make hard calculations about the
levels of exposure (a) offsite and (b) to Ms. Dawson. However, it has been shown that
considerable quantities of enriched Uranium dispersed offsite. The simplest calculation is of
annual external dose to populations living and remaining continuously within 5 miles of SSFL.
This is because the data given in the 2011 Background report gives us the difference between the

89

historic gamma background and the mean background at the two closest sites, respectively 4
miles (Lang Ranch) and 5 miles (Bridle Path) from the SSFL Area IV. These two sites were
showing an excess of about 10R/h equal to an excess absorbed dose equivalent of 8.5rem/h
(Section 7.2). This is an annual dose of 75mrem, in excess of the Regulation limit of 10mrem.
That the excess gamma radiation is from SSFL releases is clear from the Uranium isotope ratios.
Lang Ranch and Bridle Path are not downwind, and represent, according to the wind rose in Fig
5.3 about of the frequency of winds that blew towards Ms. Dawsons house at the Royer
address. Thus, conservatively multiplying by a factor of 2 gives an annual external excess dose
to Ms. Dawson of 150mrem (1.5mSv). This alone contravenes the regulations of 10 C.F.R.
20.1301 for exposures from all vectors.
In addition to this, there are inhalation doses from direct air contamination, inhalation doses of
resuspended deposition contamination, inhalation of highly contaminated material from the
30,000 trucks taking the excavated waste to landfills, ingestion of dust from SSFL and from the
trucks, material which had contaminated the produce grown and consumed by locals including
Ms. Dawson, and ingestion of water from sources contaminated by the dust. I have listed these
routes in Table 5.1. The contamination of the ground that led to the increased gamma radiation
in 2011 was due to surface dust, and associated with, initially, a very thin layer. Some of the
material from SSFL (from the Sodium burn pit for example) was extremely contaminated.
Rockedyne contemporaneously did not survey the areas where likely contamination in
surrounding neighbourhoods would be expected to migrate. But the data which is available is
enough to reasonably conclude more probably than not, Ms. Dawsons exposure was from
multiple pathways in excess of the federal guidelines and sufficient to cause her cancer.
To conclude otherwise would require ignoring the data.
9.2 Summary of Section 9
The Regulations for exposures to airborne releases from nuclear licensed sites in the USA give
an annual dose limit of 0.1 rem (1 mSv). See 10 C.F.R. 20.1301. The excess external dose
within 3 miles of the SSFL is shown to be between 75mrem and 150mrem on the basis of 2011
measurements published in the Background report which can be compared with three sets of
independent historical data. SSFL is not allowed to exposure a member of the public, such as
Ms. Dawson to an amount equal to or greater than 0.1 rem (1 mSv) in a year, or 0.002 rem (0.02
millisievert) in any one hour under 10 C.F.R. 20.1301. The SSFL operators have therefore
exceeded the regulation limits.
10. Overall Summary: Ms. Dawsons Exposure and her Subsequent Cancer
My expert opinion is that Ms. Dawson developed cancer of the rectum as a result of her exposure
to radiation and radioactive releases from the SSFL. The arguments have been sequentially
presented in this report and were outlined at the beginning. It is impossible to accurately partition
the contributions of the various exposures suffered by Ms. Dawson, the external, the internal
from food, from water, from inhalation. It is impossible to accurately carry out a numerical dose
reconstruction since there is not enough hard testing information available, and this is always the
case with environmental exposures. However, the data and information does allow

90

reconstruction of a qualitative exposure history with a bottom limit of exposure. Given the
pathways, duration, timing and type of radiation in the environment, an expert opinion can be
reached that Ms. Dawson was exposed at a minimum above federal regulations. Also, the fact
that her cancer diagnosis is unquestionable and that she has colorectal cancer, and metastatic
lung cancer, which is a cancer known to be caused by the type of radiation released by SSFL, it
is scientifically reasonable to form an expert opinion that her exposure to SSFL radiation caused
her cancer. Furthermore, there is a plausible scientific explanation for the mechanism of the
cancer development. The location of the tumor makes it most likely that the main step was the
exposure of the lining of the rectum to waste matter which was contaminated with enriched
Uranium particles which delivered a high dose, in excess of 120mSv (12rem) to the cells of the
colon/rectum adjacent to their location, or even more than this depending on their diameter.
Eating vegetables grown locally was one source. Mr. Mark Lindsey also developed the same
cancer, which cannot be a coincidence. The remediation of the SSFL Area IV in the period 19962005 created huge amounts of enriched Uranium dust and dispersed it downwind, to where Ms.
Dawson lived and grew her vegetables. Tens of thousands of truckloads of very radioactive soil
from the excavations of the buildings and their foundations, from the sodium burn pit and from
other radioactive handling facilities were driven along roads near where she lived, dispersing
dust from the tires and from leaking cargoes. Inhalation of airborne dust by Ms. Dawson will
also have resulted in irradiation of the tissue in the rectum because most particulate matter
entering the respiratory airways is removed by ciliary action and swallowed, unless it has particle
diameter less than 1 micrometer.
I reserve the right to amend or alter this report in the light of new information.

__________________________________
Prof. Dr. Christopher Busby

91

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