[ RadSafe ] Daniel Fahey Paper on DU testing

[tomhaz at aol.com]

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...........

James,
Of course when you offer your credentials as a critic of scientific 
work, no one will be tempted to laugh.  By the way, uranium won't loose 
its danger in 5 billion years, it will be toxic for ever, as will lead, 
cadmium, mercury,  and a host of other substances that are chemically 
toxic and will remain so.   Where is your anger at being forced to live 
in such an unsafe universe filled with nasty chemicals.  Taking the 
long view, since radioactive materials eventually become non 
radioactive, arn't many of them safer than the chemical poisons?

-----Original Message-----
From: James Salsman <james at bovik.org>
To: radsafe at radlab.nl
Sent: Sat, 18 Mar 2006 19:45:51 -0800
Subject: Re: [ RadSafe ] Daniel Fahey Paper on DU testing

  >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.

 Sincerely,
 James Salsman

  
[1]http://lists.radlab.nl/pipermail/radsafe/attachments/20060317/61dfd541
/2006-Test-Results.pdf

 [2]http://www.bovik.org/du/Wilson61.pdf

 [3]http://www.bovik.org/du/scans/crc.jpg

 [4]http://www.bovik.org/du/aerosol.pdf

  
[5]http://www.annalsofepidemiology.org/article/PIIS1047279701002459/abstr
act

 [6]http://www.bovik.org/du/chromosome-abberations.pdf

 [7]http://www.bovik.org/du/chromosome-abberations.ppt

 --- 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

 Abstract:

 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

 Sincerely,
 James Salsman

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