[ RadSafe ] Daniel Fahey Paper on DU testing

James Salsman james at bovik.org
Sat Mar 18 21:45:51 CST 2006

 >Date: Sat, 18 Mar 2006 15:17:30 -0800
 >From: James Salsman <james at bovik.org>
 >To: Spratt, Brian G <b.spratt at imperial.ac.uk>
 >CC: ... duweapons at hotmail.com....

Dear Dr. Spratt:

I have learned from Dan Fahey [1] that you have submitted a
paper to Critical Reviews in Chemistry claiming that the
Depleted Uranium Oversight Board's measurements of uranium
exposure from urine isotope ratio studies, which assume that
substantial exposure must be from insoluble uranium oxides,
are accurate.  Sadly, they are not accurate because of the
assumption, that uranium combustion product exposure will
result in residual amounts of insoluble oxides remaining in
the lungs, is not correct.  (I note also that Fahey's paper
inexplicably ignores the use of 30 mm incendiary DU ammunition
fired from Apache helicopters.)

I will be urging the editors of Critical Reviews in Chemistry
to reject your manuscript, and to admonish you for your
negligence in the field of epidemiology.  I have repeatedly
informed you that uranyl oxide, including as a gas vapor, is
produced by uranium burning in air.  You, in turn, dismissed
my concerns in a most unscientific manner.

Please see Wilson, W.B. (1961) "High-Pressure High-Temperature
Investigation of the Uranium-Oxygen System," in the Journal Of
Inorganic and Nuclear Chemistry, 19, 212-222 [2], on page 213:

         1/3 U3O8(s) + 1/6 O2(g) --> UO3(g)

Again, absorption of UO3(g) is immediate and small U3O8 particles
(which comprise 75% of the particulate combustion products,
according to Gilchrist, Glissmyer, and Mishima, 1979) dissolve
readily to uranyl ions, so uranium contamination from pyrophoric
uranium munitions by way of their UO3(g) would not necessarily
be detected urine studies which reflect only lung contamination
with the dioxide dust particles which settle more quickly and
travel less distance. [3, 4]  There is no hypothesis which explains
the observed increased incidence of birth defects in the military
[5] and civilian populations of which I am aware, other than uranyl
compound inhalation.  Mustard gases would be accompanied by the
increased cancer rates seen in those near sites of known nerve
gas exposure, but not most U.S. and U.K. troops.  Uranium
combustion products are the only viable explanation.

And let us not forget the words of your colleague, Simon Cotton,
who has stated in that the aerial oxidation of uranium results,
eventually, in the formation of a uranyl compound. ("Lanthanides
and Actinides," New York: Oxford University Press, 1991, page 127.)
Therefore, the urine isotope ratio studies are only vaguely
correlated with soluble uranyl exposure, and you know it.  Your
assertions to the contrary are most unprofessional.

Again, I hope you will please join me in advocating that uranium
contamination be measured by chromosome abberation analysis
instead of urine isotope analysis.  White blood cell karyotyping
is essentially the same test as are used for amniocentesis and
biopsies in most hospitals regularly. [6, 7]

And I hope that you will also please join me in asking that the
DoD Birth and Infant Health Registry include epidemiological
statistics particular to the exposed 1991 population in their
annual reports currently in preparation instead of omitting
any mention of the exposed subset as they do in their current
draft annual reports.

James Salsman








--- from previous message ---
I thought you would be interested in this new peer-reviewed article:

Rita Hindin, Doug Brugge and Bindu Panikkar, "Teratogenicity
of depleted uranium aerosols:  A review from an epidemiological
perspective," Environmental Health, vol. 4 (26 August 2005),
pp. 17:  http://www.ehjournal.net/content/4/1/17


BACKGROUND: Depleted uranium is being used increasingly often as a
component of munitions in military conflicts. Military personnel,
civilians and the DU munitions producers are being exposed to the DU
aerosols that are generated. METHODS: We reviewed toxicological data on
both natural and depleted uranium. We included peer reviewed studies and
gray literature on birth malformations due to natural and depleted
uranium. Our approach was to assess the "weight of evidence" with
respect to teratogenicity of depleted uranium. RESULTS: Animal studies
firmly support the possibility that DU is a teratogen. While the
detailed pathways by which environmental DU can be internalized and
reach reproductive cells are not yet fully elucidated, again, the
evidence supports plausibility. To date, human epidemiological data
include case examples, disease registry records, a case-control study
and prospective longitudinal studies. In aggregate the human
epidemiological evidence is consistent with increased risk of birth
defects in offspring of persons exposed to DU. DISCUSSION: The two most
significant challenges to establishing a causal pathway between (human)
parental DU exposure and the birth of offspring with defects are: i)
distinguishing the role of DU from that of exposure to other potential
teratogens; ii) documentation on the individual level of extent of
parental DU exposure. Studies that use biomarkers, none yet reported,
can help address the latter challenge. Thoughtful triangulation of the
results of multiple studies (epidemiological and other) of DU
teratogenicity contributes to disentangling the roles of various
potentially teratogenic parental exposures. This paper is just such an
endeavor. CONCLUSIONS: In aggregate the human epidemiological evidence
is consistent with increased risk of birth defects in offspring of
persons exposed to DU.

Full text:  http://www.bovik.org/du/du-teratogenicity.pdf

James Salsman

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