IN THE UNITED STATES DISTRICT
COURT
FOR THE NORTHERN DISTRICT OF
ALABAMA
SOUTHERN DIVISION
IN RE: SILICONE GEL BREAST
IMPLANT PRODUCTS LIABILITY
LITIGATION (MDL-926)
Master File No CV 92-P-10000-S
PLAINTIFFS’ SUPPLEMENTAL
SUBMISSION ON THE CHEMISTRY
AND TOXICOLOGY OF PLATINUM
DATED: March 25, 1999
TABLE OF CONTENTS
Page
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I |
EXECUTIVE SUMMARY |
1 |
|
I |
OVERVIEW OF METAL TOXICITY
AND HYPERSENSITIVITY |
4 |
|
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A: MEDICAL
MECHANISMS OF TOXICITY AND HYPERSENSITIVITY |
4 |
|
I |
B.
THE TOXICOLOGICAL AND HYPERSENSITIVITY RESEARCH ACTIVITIES OF THE DEFENDANTS |
7 |
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THE SCIENTIFIC FACTS OF PLATINUM: METAL, COLLOIDS AND SALTS; IN SILICONE GELS AND ELASTOMERS |
12 |
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A: Unreduced Chloroplatinic Acid (CPA) is in Most
Silicone Gel Implants at the Time
of Implant Insertion in Human Patients |
12 |
|
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B: The Defendants Know that Platinum Leaches Out
of Silicone Elastomers and Gels in Water |
17 |
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C: The Platinum In Silicone Gels and
Elastomers Causes Systemic Allergic Responses in Genetically
Susceptible Humans |
19 |
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1.
There is Good Evidence that Platinum Metal, Especially Sub-Micron Sized Particles
of Elemental Platinum, Including Particles in Colloidal Suspension Convert to
Platinum Salts in Certain Physiologic Conditions |
19 |
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2.
Elemental Platinum Colloid Suspensions, Even Those Not converting to Salts,
Can be Toxic in the Biologic System |
20 |
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3. Genetic Susceptibility |
20 |
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D.
Defendants’ Statement that “Platinum Metal is Non-Toxic And Non-Allergenic” is Probably Not True in
Susceptible Individuals |
21 |
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E.
The Silicone Manufacturers Know that Chloroplatinic Acid (CPA) is
Especially Allergenic in Certain Animal Species and Not in Others |
23 |
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F.
Long-Term Implantation of Silicone Gel or Elastomer Increases Eosinophil Levels in Sensitive Animal
Species And Sensitive Humans |
27 |
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G.
Breast Implant Women Present With Signs and Symptoms Of Platinum and Platinum Salts Toxicity and
Allergy, as reported in the Peer Reviewed Medical Literature |
31 |
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H.
The Pattern of Allergic Responses Seen in Women With Silicone Gel Breast Implants Has Also Been Reported
in Cancer Patients Receiving Platinum Compounds, Contrary to the Assertions
of the Defendants |
34 |
|
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I.
Defendants’ Representation
That Elastomer Shunts and Platinum Electrodes Have Been
Safely Used Without Allergic Complications in Humans is False, and further,
The Peer Reviewed Medical Literature Demonstrates That: --Silicone Elastomer Shunts Provoke Systemic Allergic Responses in
Genetically Susceptible Humans |
|
|
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1. The Problem with Platinum Electrodes |
36 |
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2.
Silicone Elastomer Shunts
Provoke Systemic Allergic Responses in Genetically Susceptible Humans |
38 |
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IV. |
RESPONSES OF DRS. TEMPLETON, LYKISSA AND HARBUT TO DEFENDANT
MANUFACTURER’S SUPPLEMENTAL SUBMISSION ON
THE CHEMISTRY AND TOXICOLOGY OF PLATINUM |
41 |
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A. DR. TEMPLETON’S REPLY |
41 |
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B. DR. LYKISSA’S REPLY |
42 |
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C. DR. HARBUT’S REPLY |
46 |
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V. |
SUMMARY AND CONCLUSIONS |
52 |
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REFERENCES AND APPENDICES TO REPLYS OF DRS. TEMPLETON, LYKISSA AND HARBUT BEGIN AT
EXHIBIT 57, RECORD NO. 7444 (NUMBERED AND LETTERED AS THEY APPEAR IN EACH REPLY) |
55 |
I. EXECUTIVE
SUMMARY
The Parties agree that “platinum
salts” cause both toxicity and systemic hypersensitivity
reactions in humans; but the Defendants contend that there are no
platinum salts” in
silicone gels and elastomers. The
Plaintiffs, in this Submission, prove that platinum salts
are in the completed gels and
elastomers. The Plaintiffs also prove, especially with
genetically susceptible individuals,
that both elemental platinum metal and sub-micron
sized powders of elemental platinum
can also be both toxic and hypersensitizers.
Section II of Plaintiffs’
Supplemental Submission on Platinum identifies the four types of
hypersensitivity responses as well
as the clinical signs and symptoms associated with
each type. This section also reviews
the historical “lack of curiosity” of the Defendants
in pursuing issues of platinum
toxicity and hypersensitivity.
Section Ill, subsection A
establishes that unreduced chloroplatinic acid (platinum salts)
remain in all silicone gels and
elastomers cured with platinum catalyst. Documents and
testimony from the defendants, as
well as a patent held by AT&T, prove Plaintiffs’
assertion that platinum salts remain
in the completed product, and this is confirmatory of
Doctor Lykissa’s positive platinum
salts findings, in vitro.
Subsection B establishes that the
Defendants knew that soluable platinum (i.e., platinum
salts) leaches out of elastomers and
gels in water; and they knew this independent of the
work of Doctor Lykissa.
Subsection C identities the role of
genetic and species variability and susceptibility in the
onset of disease(s) in response to
elemental platinum, sub-micron sized elemental
platinum powders and to platinum
salts.
Subsection D reviews the research in
the area of orthopaedic appliances which
establishes that elemental platinum
metal, as well as other elemental noble metals, can
provoke asthma and other
hypersensitivity responses in genetically susceptible
individuals.
Subsection E demonstrates that the
defendant silicone manufacturers knew that platinum
salts were especially allergenic in
certain animal species and not in others, and this,
explains the “false negative”
results touted by the Defendants in their Supplemental
Submission on Platinum.
Subsection F identifies the
important role played by eosinophils as a marker for certain
allergic diseases as well as reviewing
the Defendants’ historic animal research and the
eosinophil findings in that
research.
Subsection G reviews a comparison of
the signs, symptoms and diseases of women with
breast implants and their
relationship to hypersensitivity and toxic presentations.
Subsection H compares the allergic
responses seen in patients receiving platinum
chemotherapies with the allergic
responses seen in women with silicone gel breast
implants; and,
Subsection I rebuts the assertions
of the Defendants and shows the significant toxic and
hypersensitivity responses to
platinum electrodes and solid elastomer shunts and other
implantable orthopaedic devices.
Section IV contains the responses of
Doctors Templeton, Lykissa and Harbut to the
challenges offered by the Defendants
in their Supplemental Submission on Platinum.
Dr. Templeton’s reply explains his study’s methodology and why the Defendants’
challenge is wrong on the science.
Although his positive platinum findings are adverse to
the Defendants’ position, the legitimacy
of his work stands unchallenged.
Dr. Lykissa’s response details his experimental confirmation (in
vitro) of the presence of
complexed platinum (platinum salts)
in the Defendants’ gel and elastomer products. His
reply also refutes the Defendants’
argument that the platinum catalyst conversion process
is total and irreversible; and he
shows why the resulting platinum residual in Defendants’
gels and elastomers is in an ionic,
not zero valance state.
Dr. Harbut’s reply, and the computation of the amounts of platinum salts
(unreduced
chloroplatinate) present in two 250
cc silicone gel implants (Computed by Roger
Wabeke, MSc, MScChE, CIH, CHMM, PE),
demonstrate an in vivo platinum salts
exposure to platinum in women with
silicone gel implants an amountl000 x greater than
the occupationally allowed limit.
Dr. Harbut’s reply refutes the
Defendants’ challenge to his platinum asthma article
published in the peer reviewed
Israeli Journal of Occupational Health. Dr. Harbut also
identifies the peer reviewed
literature establishing the allergenicity and toxicity of
elemental platinum, and sub-micron
sized elemental platinum powders, as well as
platinum salts. Finally, Dr. Harbut
presents the Pet Scan reports of two patients (with
implants and after explantation).
The abnormal brain findings resolved after explantation.
II. OVERVIEW OF PLATINUM METAL
TOXICITY AND HYPERSENSITIVITY
A. Medical Mechanisms of Toxicity and
Hypersensitivity
Protein-reactive chemicals, metal
salts and drugs, commonly classified as immunological
haptens, are major environmental
noxes targeted at the immune system of mammals.
They may not only interfere with
mammalian defense systems by toxicity, but more
often by evoking hapten-specific
immune responses resulting in allergic and eventually
autoimmune responses.1
The immune status of the individual
exposed, is a variable which must be taken into
account in any consideration of the
factors influencing the metabolism and toxicity of
metals.2 The commonly occurring phenomena
stemming from cellular reactivity to
platinum (and other noble metals)
can be classified into four types of immune response. 3
Type
I: Anaphylactic of Immediate Hypersensitivity
Under this type, an IgE antibody
reacts with the antigen on the surface of mast cells
releasing vasoactive amines.
Clinical reactions, although varied, may consist of
rhinorrhea, conjunctivitis, asthma,
urticaria, or systemic anaphylaxis. The cutaneous,
mucosal, and bronchial reactions to
platinum have been attributed to type I
hypersensitivity, although type III
reactions may also be involved.
Type II: Cytotoxic Hypersensitivity
Type II reactions occur when the
humoral antibody, which is an IgG immunoglobulin,
reacts with an antigen or hapten
bound to the cell surface and fixes complement to
produce cell death. Although these
reactions occur in a variety of
patients, they also can
play a part in multi-system
hypersensitivity diseases, e.g., SLE.
Type
Ill: Immune Complex Hypersensitivity
Type Ill reactions occur when an
antibody combines with soluble antigen and the
complex deposits in tissues,
fixing complement and gives rise to a
polymorphonuclear
inflammatory response. In this type,
the clinical outlook is dependent on the relative
proportions of antigen and antibody,
as well as the genetic sensitivity of the species and
individuals within the species (see
Section 111.0. below). With antibody excess, the
complexes are rapidly precipitated, usually close to the site of
origin of the antigen,
giving rise to an Arthus reaction.
This immune complex reaction is also
responsible for
the systemic reaction known as serum
sickness.
Type
IV: Cell-Mediated Hypersensitivity
Type IV reactions are also known as
delayed-type hypersensitivity. This reaction is
mediated by thymus-dependent
lymphocytes, taking 24-48 hours to develop in sensitized
individuals compared to 1 5-30
minutes for anaphylactic and 4-8 hours for Arthus
reactions. Delayed hypersensitivity
can be transferred by the small number of
specifically sensitized small
lymphocytes present in a lymphocyte suspension.4
The Defendants’ Supplemental
Submission on Platinum fails to recognize that
hypersensitivity is also a toxic
reaction. For patients receiving gold
salt therapy, for
example, skin rash and
hypersensitivity are recognized as the most common drug toxic
manifestations. This reactivity
would be expected for other metal salts, as well.5
Kazantzis’ states that the clinical
effects of metal exposure can be varied, giving rise to
conjunctivitis, rhinitis, asthma,
urticaria, contact dermatitis, proteinuria, nephrotic
syndrome or blood dyscrasia.6 Of these effects, cutaneous hypersensitivity
is the most
common, affecting both industrial
and general population groups. Metal compounds used
in therapeutics and metals used in
orthopeadic prostheses have also been responsible for
hypersensitive reactions. (See
Section III.D. below.)
It should also be recognized that
not all platinum toxic effects are distinct clinical
manifestations,7 but include
tinnitus, nausea, vomiting, leucopoenia, thrombocytapenia,
electrolyte disturbances, seizures
and cardiac abnormalities, in addition to the allergic
type responses.8 Plaintiffs’ previous submissions to
the 706 Science Panel and the Court
identify silica, low molecular
weight cyclics and other co-factors acting alone, or in
synergy, as being capable of
stimulating this type response.
It should be recognized that this
submission on platinum does not claim that platinum, or
platinum salts alone, are
responsible for all clinical manifestations appearing in patients
with silicone gels and elastomers.
However, as presented below, the peer-reviewed
medical and scientific literature
supports Plaintiffs’ claims that platinum metal, sub-
micron elemental platinum particles,
platinum colloides and platinum salts, have proved
their ability to cause systemic
disease in humans (and animals) and are a factor or co-
factor of illness in the Plaintiff
breast implant population.
B. The Toxicological and Hypersensitivity
Research Activities of the Defendants
From the previous submissions of the
defendants, as well as their Supplemental
Submission on Platinum, the
defendants assert that they have done extensive testing on
silicone elastomers and gels,
looking for both toxic and
hypersensitivity responses. The
studies and tests they presented
Science Panel were carefully selected, but incomplete.
Before beginning the substance of
this section, a brief industrial timeline is helpful.
A number of well-respected American
corporations have been involved in the
manufacture of silicone gels and
elastomers for human implantation. During the history
of this industry, the most
scientific, able and sophisticated of
these companies were the
first to drop out of the business of
manufacturing gels and elastomers for
human
implantation. General Electric left
the field in 1976; Minnesota Mining and
Manufacturing (3M) left the field in 1984; years before the
current “breast implant”
litigation. Both of these companies,
as well as Dow Corning, are responsible for some of
the early research on gel and
elastomer toxicity and hypersensitivity.
On June 28, 1 977, 3M employee
Elaine Duncan presented a report to 3M analyzing the
several components of silicone gels and elastomers, including a
spectrographic analysis
of their company’s (McGhan) gels
and elastomers, as well as the gels and
elastomers of
some of their competitors.9 Although
prepared for multiple purposes, this Report found
platinum present at 10 parts per
million in the elastomer, and .8 parts per million in the
gel of Cox-Uphoff. This report also
found 8-10 parts per million of platinum in
McGhan’s elastomer shells.10
On February 17, 1984, Dow Corning’s
William Boley wrote a memo criticizing an
outside researcher’s proposal to
study the “immunogenicity of silicone.”11
In his critique, Boley suggested
that “. . .history has shown that rarely, if ever, does a
patient elicit a ‘hyper-response’ to
silicone. Therefore, it is highly improbable that such a
response will occur for evaluation.”
Of greater interest was Boley’s conclusion that
“...The study...will at best create
the need for a lot more testing. “12
A day earlier, Talmage Holmes, the
Director of Epidemiology at Dow Corning, wrote to
A. H. Rathjen, an executive at Dow Corning, on the subject of the “S.
H. Miller study
protocol.”13 In suggesting that Dow Corning should support
Dr. Miller’s proposed study, Director Holmes expressed concern that “... It seems almost inconceivable that we do not know more
about the human immunologic response to silicone.... 14
Three months later, Dow Corning
employee, Eldon Frisch, in a memo to William Boley,
dated May 9, 1 984, informed Boley
that Dow Corning’s competitor, Baxter, had an
interesting poster exhibit at a
recent biomaterials meeting which demonstrated a cell
culture method developed for the
assessment of immunotoxicity.15 Dow Corning’s Frisch
went on to report that Baxter has
“...tested a number of materials, including silicones,
and have found that many, if not
most, Plastics and elastomers elicit an immunotoxicity
reaction.”16 Dow
Corning’s Frisch went on to suggest that such research might be of
interest to Dow Corning because of
its relationship to “...the alleged case of human
adjuvant disease.”17
The stated objective of the proposed
Miller study which Dow Corning did not fund or
pursue, was to “.. .investigate the possibility of humoral or cellular
immune
hypersensitivity response to one or
more antigenic ligands in the Dow
Corning 360 fluid.”18
As of this time period in 1984, no
one had identified the specific antigenic ligands or
gel/elastomer components that might
be stimulating immune responses in implant
patients. What is clear, however, is
that the industry did not want to look for what it
might find.
On March 12, 1987, Dow Corning’s
Eldon Frisch wrote a memo to Dan Hayes, also of
Dow Corning.19 In his
memo, Frisch reported on his trip to Wayne State University,
School of Medicine, and his meeting
with Professor Heggers. In addition to Heggers,
there were two PhD immunologists and
one PhD clinical chemist present. Dow
Corning’s Frisch reported that, “As
a group, they are firmly convinced that some patients
develop an immune response to
implanted silicone.. .synovitis with bone and joint
implants, infection, ‘rejection
reactions’.... “20
Frisch further reported to his
colleagues at Dow Corning that the people at Wayne State
University “...believed that it
would be possible to develop a testing procedure that could
be conducted rapidly and
inexpensively to pre-test patients to determine which ones had
potential for developing such an
immune response. “21
Dow Corning, for reasons that
one can only speculate, chose not to fund Dr. Heggers’ research (see
Section III.(l)(2)
below).
As of 1987, the hypersensitizing
agent(s) present in gel and elastomer were still not yet
specifically identified.
In the mid 1990’s, after several
years of manufacturer-financed research on a variety of
silicone related subjects, a group
of “industry sensitive” researchers out of the University
of Toronto, Toronto, Canada,
submitted a follow-up grant application to the silicone
manufacturers group they had
previously served. Their multi-faceted proposal was
accepted, solely on the condition,
that they not conduct proposed research on the
hypersensitizing potential of
platinum.22
In his research proposal, Professor
Templeton suggested that platinum.. .commonly used
as catalyst(s) (sic) in the
condensation reactions forming polymeric organosilicones...”
and that “If residual catalyst-
remains… its release as a soluble metal salt would
represent a potential
immunosensitizing stimulus.”23 Dr. Templeton’s published research
in the area of platinum ended with
the publication of his paper “Measurement of
Platinum in Biomedical Silicones by
ICP-MS” in 1995.24
His research on Platinum in
gels and elastomers stopped, and the
silicone industry continued to fund his colleagues’
other directed research.
III. THE SCIENTIFIC FACTS OF PLATINUM: METAL,
COLLOIDS, AND SALTS; SILICONE GELS AND ELASTOMERS.
Unreduced Chloroplatinic Acid (CPA)
is in Most Silicone Gel Implants at the Time of
Implant Insertion in Human Patients.
The scientific/chemical thesis of
Defendants’ Supplemental Submission on the
Chemistry and Toxicology of Platinum
is that the platinum catalyst is 100% unreduced
to a colloidal suspension and that
the process is irreversible. This is a chemically false
premise. In fact, it is axiomatic
that no chemical reaction is 100% complete, and no
reaction is irreversible. Indeed,
even stability, the best that can be hoped for, depends on
the chemical law of equilibrium.
Professor Pauling notes that:
“It must be recognized that
equilibrium is not a situation in which nothing is happening,
but rather a situation in which
opposing reactions are taking place at the same rate, so as
to result in no over-all change.”25
To the extent that variables (e.g.,
electrical charge, heat, friction, macrophage digestion
pressure, etc.) are present, the
equilibrium of the reacted state will be predictably
disrupted. Once the equilibrium has
been disrupted, the reaction may reverse, progress,
or otherwise change. This is
especially true where the initial reaction was not complete
and catalyst (even precursor
catalyst) is present.
Through this submission, the
plaintiffs will prove that unreduced platinum salts (PtCl4,
PtCI6) are in silicone
gel and elastomer implants at the time of human implantation.
The first proof can be found in Defendants’ Supplemental Submission on
Platinum,
pages 38-39, as they try to explain
away the very important Dow Corning 1 996 guinea
pig sensitization study. As the
defendants try to explain away this study, they make a
crucial admission.
On page 39 of Defendants’
Supplemental Submission on Platinum, they state that, “The
1996 guinea pig results are
difficult to reconcile...although Platinum #2 may have
contained a small amount of
unreduced CPA (i.e., chloroplatinic acid).” This significant
admission, which the defendants, in
turn, try to explain away, shows that no chemical
reaction is complete and that
unreduced chloroplatinic acid (CPA) can remain in the
implant. It can further be expected
that this “unreduced CPA” will continue to have a
catalytic, as well as a
hypersensitizing effect, on the breast implant recipient who wears
this dynamic chemical factory for
months, years and even decades.
The second proof that unreduced
chloroplatinic acid remains in “completed” gels and
elastomers can be found in two
articles presented by the Defendants [Record Nos. 8487
and 84911.
The Defendants suggest that the true
catalyst is created after all unreduced chloroplatinic
acid converts to colloidal form; and
this conclusion is based on the research of Lewis and
colleagues [Record Nos. 6241 (1986)
and 2959 (1991)1.
However, when you read the 1997
research of Lewis and colleagues [Record No. 8487]
you find that they recognize a
problem:
“However,
in some cases where silicon-vinyl-containing species were present, the
reaction
product between platinum and a Si-H-containing compound did not give
colloidal
platinum species;...” (at pg. 74).
Accordingly, from the 1997 work of
Lewis and colleagues we see that the presence of
vinyl groups can prevent or block
colloid formation.
From Lewis (above), we look next to
the Dow Corning Corporation Technical Memo
Report presented at Defendants’
Record No. 8491, where we find Dow Corning
explaining that, “The elastomer
formulation used in the envelope manufacture (i.e.,
elastomer) consists of a high
molecular weight PDMS polymer that contains vinyl
functionality. The vinyl groups can
either be in the terminal or pendant positions along
the polymer chain.”
Accordingly, the Defendants’ own
Record references demonstrate a chemical mechanism
which explains the presence of unreduced chloroplatinic acid (CPA) in
completed
elastomers containing vinyl
functionalities.
Plaintiffs’ third proof is found in a letter
dated January 1 4, 1 977, written by David
Sanders, President of Medical Engineering Corporation, a breast implant
manufacturer.26
In President Sanders’ letter to
doctor Sevinor, responding to specific questions from
Sevinor, a Professor from the
University of Florida, President Sanders admits that,
“The only
residual we know of in the mammary prosthesis is the platinum
catalyst...
“27
Plaintiffs’ fourth proof that
active platinum catalyst remains in the completed implant is
found in a December 4, 1 981,
technical report authored by Dow Corning employee
Yolanda Peters.28 in her
report, Yolanda Peters discusses the problem of elastomers
depolymerizing. To explain
this phenomena, she writes:
“J.
Vallender’s report, Dow Corning number 3138, suggested that the reversion is
due to
incomplete neutralization of the basic catalyst used to make the SiOH end
blocked
gums.29
Plaintiffs’ fifth proof is
found in the United States Patent Office. Dr. Wong of AT&T
Technologies. Inc., received a patent on May 1 2, 1 987, for a process that
Stabilized
Silicone Gels.30
In explaining the background of his
invention, Dr. Wong reported that in many cases, the
silicone polymer was formed by
polymarization of a silicone or mixture of silicones in
the presence of a platinum catalyst.
Further, he reported in many cases it is desired to
stop the polymerization process in
order to achieve a silicone polymer with a certain gel
consistency. He explained that this
is true, for example, “...for such things as breast
implants.... “31
Dr. Wong cautions that, “A problem
that has been found to exist with such silicones is
that, with time, the curing process
continues...changing the consistency of the silicone
from the desired consistency to one
that is undesirable.” Of course, Dr. Wong’s invention
was intended to solve the problem of
unreduced chloroplatinic acid and the continuing
catalytic process.
Plaintiffs’ sixth proof is
found in the testimony of a defendant silicone scientist, Wilfred
Lynch. It should be noted here that
Wilfred Lynch is the author of the seminal article
“Polymeric Surgical Implant
Materials,” published in August of 1963.32
Wilfred Lynch
is also a scientist/silicone product
developer with defendant Surgitek Corporation.
At Professor Lynch’s MDL 926
deposition on February 21, 1994, the following
questions and the following answers
were given:
“Q All right. Now would it be fair to say that
this platinum catalyst reaction was used to manufacture all of the gel that was ever used in any MEC breast
implant?
A I would
expect so.
Q . . .the
platinum catalyst was used in all of the shell materials that were used on MEC
gel breast implants, right?
A Yes. Yes.
(Pgs. 114-115)
Q Mr. Lynch,
we were talking before we went off the record a bit about the platinum
catalyst. Do you recall that?
A Yes.
Q I think you
said that it was actually a platinum salt, right?
A Yes.
Q All
right. What, if anything, did Medical Engineering do at the time it began
using that
platinum catalyst to determine if that platinum catalyst had any effect
on the
body?
A We did not do anything about that. (Pgs. 11
6-1 1 7)
***
Q
Okay, I want to ask a couple of questions about the metallic elements in
the gel and the shell material. What,
if any, metallic elements are in the gel material?
A I
don’t know of any, unless you’re referring to the platinum salt catalyst as a
metallic.”33 (Pg. 526)
In conclusion, based on the laws of
general chemistry (i.e., no reaction is “complete” or
“irreversible”), the admission of
the defendants in their “Supplemental Submission,” the
various defendants’ research, Dr.
Wong’s patent, and the testimony of Wilfred Lynch,
only one conclusion can be drawn.
The fair scientific conclusion is that unreduced
platinum salts remain in, and
continue active in, completed implants. This, it
should be noted, is consistent with,
and supplemental to, Lykissa’s finding that platinum
salts leach out of silicone gel
breast implants.
B. The Defendants Know that Platinum
Leaches Out of Silicone Elastomers and Gels in Water.
Aside from the work of Lykissa,34
the defendant implant manufacturers know, or should
know, that soluable platinum leaches
out of silicone elastomers and gel. They also know,
or should know, that this platinum
leaches out in a salt form (i.e., chloroplatinic acid).
The work of Potter and colleagues35
establishes that platinic chloride is a water-soluble
form of the metal that is used
as the preferred catalyst in medical
silicone gels and
elastomers. Their work further
establishes that any soluble platinum
leaching from an
implant would be expected to
distribute in the circulation as a chloroplatinate.
A confirming authority on this
question is Dow Corning researcher Robert Parker.6
What did Robert Parker find?
Dow Corning manufactures silicones
and elastomers for uses other than silicone gel and
elastomer breast implants. They also
make silicone “teets.” “Teets” are also
known as
nipples for babies bottles. To
determine whether platinum leaches out of the elastomers
babies suck on, because The FDA
requires that foods coming in contact with elastomers
not contain certain levels of
contaminants, Dow Corning tested their “teets”. In Parker’s
experiment, tests were run to
determine whether organic bound silicon and platinum
migrated into the food materials and
cow’s milk that might come in contact with these
“teet” materials. The “teet” materials were exposed to water, ethanol in
water, acatic
acid and olive oil. Incredibly,
the platinum leached out of the “teets”
into the water
solution, as well as each of the
other solutions.
As a matter of general chemistry,
one would expect that any soluble platinum leaching
from a “teet” in water would be
leaching out as a water soluble, i.e., as a chloroplatinate,
that is, as a platinum salt. Does
Dow Corning contend that “platinum metal particles”
leach out of its “teets” in water?
C. The Platinum In Silicone Gels and Elastomers Causes Systemic Allergic
Responses In Genetically Susceptible Humans.
Whether platinum is in a metal chunk (See Section M.D. below);
sub-micron sized
particles of elemental platinum, the
latter in an alleged colloidal suspension; or a
platinum salt, egenetic
susceptibility is a prerequisite for systemic allergic response in
humans. Further, each of the proceeding forms of platinum, although to varying degrees,
may cause both toxic and allergic
responses in genetically susceptible humans.
1. There is good evidence that platinum
metal, especially sub-micron sized particles of elemental platinum, including particles in colloidal suspension,
convert to platinum salts in certain physiologic conditions.
The internal environment of the
human body is corrosive and can oxidize stainless steel
orthopedic implants. Voltaric corrosive processes due to ionic exchange in
the body are
well recognized in orthopaedic
surgery. When we consider the
sub-micron size of
alleged colloidal platinum
particles, it is probable they will react within the aggressive
chemical milieu of the macrophage
phagosome, particularly in the presence of an
ongoing tissue response to the biomaterial . 38
It is well known that elemental
platinum is susceptible to reactions with oxidizing agents.
The human body uses agents such as
nitric acid (No) within the macrophage phagosome
during the natural defense
mechanism.39 Accordingly, it would be expected that a certain
percentage of platinum particles
suspended in the alleged colloidal form would react
chemically under such conditions.
For this reason, one can expect, even if one accepts
the Defendants’ argument that
elemental platinum is non-toxic and non-allergenic, that a
certain portion of the elemental
platinum will convert to a salt in the biologic system.
2. Elemental Platinum Colloid
Suspensions, Even Those Not
Converting to Salts, Can Be
Toxic in the Biologic System
The dangers of colloidal toxicity
were established in the groundbreaking research of
Fessenden and Fessenden in 1967.40 In their work, Fessenden and Fessenden focused
on the toxic dangers of crystalline
silica, especially soluble and colloidal
forms of silica.
As these authors reported:
“Colloidal
and soluble silicates…have different biological properties of siliccous dusts.
Especially notable is the greater toxicity of the colloidal and soluble forms.”41
3. Genetic Susceptibility
As more fully discussed below (See
Section lIE. below), there is ample data to
suggest
that certain humans and certain species of animals have a
genetic susceptibility to