Drs Templeton, Lykissa, and Harbut response on Platinum

[Guest guest]

From a silent sister.

This is very long and techincal. . . but informative -

Something your doctors may be interested in. - Rogene

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Drs Templeton, Lykissa, and Harbut response on

Platinum in Silicone Breast Implants and Implant

Shells.

(Due to the faint copy of this document provided by

the Court, the presentations of Drs. Templeton,

Lykissa, and Harbut have been retyped without

correction of grammar or spelling. Portions that were

unreadable have been noted.)

IV. Responses of Drs. Templeton, Lykissa and Harbut

to Defendant Manufacturer’s Supplemental Submission on

the Chemistry and Toxicology of Platinum.

A. DR. TEMPLETON’S REPLY

Department of Laboratory Medicine and Pathobiology

University of Toronto

100 College St., Toronto, M5G 1LS, Canada

Mr. Doug s

Charfoos and Christensen

5510 Woodward Ave.

Detroit, MI 48202

USA

March 12, 1999

Fax 313-87S.8522

Dear Mr. s:

The following are my comments on the discussion of the

paper by Dr. El Jammal and myself in the Defendants’

Supplemental Submission on the Chemistry and

Toxicology of Platinum, dated March 3, 1999.

The Submission states that “After heating silicone gel

for 18 h ... The recovery experiments show that

recovery of platinum was less reliable at the low end

of the detection limit. 1 ppm (76 + 18%) compared to

the recovery with higher additions of platinum at 10

ppm (96 + 17%). These numbers do not refer to

silicone gel. Rather, under the heading ‘Silicone

oils’ we state that “The recovery of Pt added to the

diluted sample was (76 + 18)% at 1 ug 1-1 and (96 +

17)% at 10 ug1-1 . Addition of 1 mg 1-1 to the

original oil gave a recovery of (l 12 + 9)%.’ This

refers to the oil prior to addition of catalyst and

polymerization, as is clear in our paper.

The recovery from silicone gel under the refined

conditions used for the analyses (remainder of

paragraph is unreadable.)

It is also incorrect to state that a recovery of 76 +

18% (sic) is “less reliable” than a recovery of 96 +

17%. The values are not significantly different

statistically and the variances are comparable

The Submission states “This experiment also clarified

that there are matrix factors, which can artificially

elevate the results or the ICP-MS analysis of

platinum”. I am puzzled why recoveries of less than

100% of an added known amount of Pt would be taken as

demonstrating that the results are artificially

increased. Nevertheless, recovery of Pt from the gel

was (99.2 + 5.2)% indicating the absence of matrix

effects that would increase or decrease the results.

The Submission states that, “The platinum

concentrations given for the blanks in Table 1 of the

article along with the standard deviations in the

actual platinum measurements make it clear that

4 0 to 4. 5 ug of platinum per gram of gel is an upper

limit estimate and may be considered within the range

of 1.0 to 2.0 ppm.” This is mystifying.

The mean + s.d. of the five measurements in aqua regia

given in Table 1 is 4.71 + 0.30. We do not say that

Pt is in the range 4.0 - 4 5 ug/g, but rather that it

is approximately 4.5 ug/g. The average s.d. on the

individua1 measurements is 11% of the individual

value. We state that the value of 4.5 ug/g is “several

orders of magnitude above the method blank for the

procedures”. The calculation is as follows, from line

3 of Table 1: 4.39 mg/kg in 1.2 g of gel is 5.27 ug of

Pt. This was analyzed in 2.00 ml (footnote * to the

Table), so the Pt concentration was 5 2 X (1000/2) =

2635 ug/L. The corresponding method blank was 0.83

ug/L. In summary, our recovery is (99 + 5)%. There is

no e1evating matrix effect, the analytical imprecision

is less than 10% of the measured value, and the blank

contributes less than one part in 3000. The Pt content

of the gel is 4.71 + 0.30 ug/g. or “approximately 4.5

ug/g” and definitely not “within the range or 1.0 to

2.0 ppm”.

Sincerely,

Doug Templeton. PhD. MD

Professor

-------------------------------------------

DR LYKISSA’S REPLY

Baylor

COLLEGE OF

MEDICINE

One Baylor Plaza

Houston, Texas 77030-3498

Department of Pathology

TEL: (713) 798-4661

FAX: (713) 798-5838

Platinum Toxicity Response by Ernest D Lykissa Ph.D.

to Doug s Esq. 3/18/99

Dear Sir,

Complexed Platinum especially in the bound form with

silane moities in the +4 oxidation state do exist as

the evidence of Lipid solubility of these complexes

has shown (Lykissa, 1997). It appears that the

defendants position that the platinum found in the gel

of breast implants is of zero valence is based on the

erroneous assumption that since the platinum is bound

to silane chemical groups, is has no charge available

for further chemical bonding. Once the silane

moities are sheered off the platinum molecule, the +4

charges of the platinum molecule become available. At

this ionic state the platinum molecule may bond with

sulfhydryl groups of the cysteine amino acid residues

of proteins and thus disrupt their structure and

inhibit their functions as enzymes. These may be

vital for maintaining key physiological or biological

functions. This is supported by the data presented by

Agnew et al, in which platinum inhibits the action of

numerous enzymes. Platinum silane complexes are highly

lipophilic due to the absolute absence of any hydroxyl

molecular bonding which would inhibit the catalytic

action that one wants to render so that the

cyclo-polydimethylsiloxane mixture may begin its

crosslinking with neighboring silicon molecule to

neighboring silicon molecule by trapping oxygen from

the water vapor which is fed into the reaction mixture

for this sole purpose. We duplicated this

hydrosilation process at 140 degrees Celcius (sic)

during the production of the distillate and thus we

proved the reversibility of the catalytic action of

the platinum silane catalyst. The platinum-silane

catalyst molecule as it is shown in figure 1

demonstrates the template that the platinum silane

provides, for the seeding of the crossed-linked

cyclosiloxane organic-crystal formation (sic. gel that

breast prosthetic devices were filled with). This

catalytic action during optimum reaction conditions

is absolutely reversible due to the vapor pressure

differential created by aspiration of moist air over

the molten crosslinked gel (Lykissa et al, 1997). The

proof of the valence +4 ionic state of the platinum is

that the platinum silane complex is distillable at 140

degrees Celcius. Noboby (sic) may claim with

scientific merit that platinum metal may be vaporized

at 140 degrees Celcius. We have obtained numerous

distillates of this gel that always contained

platinum-silane as our Inductively Coupled Argon

P1asma-Mass Spectrometric measurements showed in the

same scientific communication by our team.

2me

2me

/

\

Figure 1. 2nIe—Si—Si------O—Si—Si—2me

Pt—Si

Pt

|

/

2me Si—O Si-2me

\ /

2mc S-2me

The publications by Lykissa and his colleagues in 1998

and 1999, attempted to concentrate on the possible

toxic effects of siloxanes. One is the most recent

publication in the DHHS sponsored Environmental Health

Perspectives (Lieberman et al, 1999). In this

communications the data clearly shows that

cyclosiloxane- platinum silane (distilate) is

toxically equivalent to toxins like carbon

tetrachloride (equivalent median lethal dose LD5O).

In addition these cyclosi1oxanes that so easily bleed

through the breast implant envelopes are capable of

resulting into lung congestion among others by

coalescing apparently on the alveolar membranes where

the oxygen-carbon dioxide exchange occurs during

respiration. In the hot breathing living lung the

cyclosiloxanes encounter hot water vapor that makes

them obstruct the membrane surfaces needed for the

vital gas exchange described above. If the dose is

high enough when administered by the intraperitoneal

route, it may result in massive blockage of the

pulmonary alveolar space, and death may ensue. It was

clearly demonstrated that the low molecular silicone

bleed which is complexed with expended platinum silane

catalyst not only accumulate in tissues including

brain, ovaries, kidneys, liver and lungs, but this

silicone-platinum-silane effluent from the breast

implants, is also capable of fatal lung and liver

syndromes in high enough concentrations. (Kala et al

1998. Lieberman et al 1999).

The author(s) of the defendants response assume a

position of authority by labeling Dr. Harbut’s medical

opinion as erroneous though not been medical doctors

or even medical practitioners but rather retired

spectroscopist chemists, (i.e. Dr. Ziegler) or some

other synthetic chemist combination. It is obvious

that even their theoretical assertions have no base

since they do not take in consideration the

reversibility of the process they assumed so stable

and inert till, it was proven by our team otherwise

The evidence presented in the American Journal of

Pathology in March 1998 by Lykissa and his colleagues,

clearly demonstrates the propensity of the

cyclosiloxane-­platinum silane mixture, to accumulate

in the brain tissue of living animals and to persist

there for the duration of one year following a single

administration.

It is highly unlikely, that the rich in lipids

brain tissues, that depend to a great extent on

lipophilicity (lipid solubility) for the transmission

of electric, in nature, nerve impulses are not

affected by high concentrations of very lipid soluble

cyclosiloxane-platinum silane toxins, residing on the

membranes of their constituent cells. The scientific

work of Agnew et al provides a very powerful piece of

evidence that platinum ions in the brain area either

as electrodes carrying an electric charge or platinum

metal in the presence of intense electric discharges

resulted by a living brain.

We have proven that the catalyst is active because the

reaction is reversible when the conditions of

production where emulated with moist air aspirated

(drawn out) instead of pumped into the reaction

mixture.

The defendants figure 1: Hydrosilation Reaction

has one major “overlook”

Pt-silane

SiH + SiCH=CH2 -- --

=SiCH2CH2Si=

The arrows unlike their depiction of a single reaction

arrow, like in every chemical catalytic reaction point

in both directions of synthesis and dissociation

governed by a constant (K equilibrium) of the

reaction. This equilibrium constant is active both

during the formation of the silicone crosslinking for

the creation of the si1icone gel, and the dissociation

of the gel during reversal to its toxic components

cyclosiloxanes and expended platinum-silane catalyst.

Earlier discussed evidence (Lykissa et al 1997, Kala

et al 1998) clearly demonstrate this to be untrue.

Platinum silane does dissolve in fats and is

distributed into the body i.e. brain tissue where it

persists for long periods of time.

The defendants describe a process like I have been

discussing earlier where the hvdrosilation curing of

the gel occurs in the presence of a very active

Platinum +4 molecule which needs to be harnessed in

the presence of excess silane 1:10,000 fold excess.

If the platinum molecule in this reaction is so inert

as they seem to claim, to be in the metal state, then

what was the purpose of such excess silane, if not for

harnessing the high reactivity of platinum.

The various modifications show different methods

of stabilizing and neutralizing various byproducts of

the catalyst manufacture. The clue is in the solvent

solubilizing agent found in Table 1 of the defendants

response.

Butyl Carbitol Acetate produces the evolution of

acetic acid when this catalyst comes in contact with

the other reactive molecules, a very toxic irritant,

similar to very concentrated distilled vinegar. It

also acts as a solvent carrier for a lipophilic

molecular complex. Ethanol was addressing the lipid

solubility of the substance while the neutralization

with sodium-bicarbonate washes was for the purposes of

ridding the mixture of chlorine ions capable of

forming hydrochloric (muriatic) acid in the tissues.

Obviously the manufacturers of MDF-0069 and XY- 173

never addressed the issue of hydrochloric acid or

acetic acid and further additional complex toxic

release issues. Especially when the breast implants

containing this type of gel expended platinum catalyst

were implanted in a human female chest area and begun

to leak their contents in the surrounding tissues.

In the presentation of the data, one finds

reference to the finding, that Platinum silane

catalyzed reactions produce yellow color, and that

yellow hue disappears when large concentrations of

platinum colloidal aggregates are not allowed to form

therefore again we fluid contradictions as to the

presence of colloidal platinum silane. Here the

authors of the defendants offer a hypothetical

assertion at best, that maybe the aggregates are so

fine that no color is seen in the gel.

We stated in our publication that the gel

implants were intact and we ensured ourselves oft-his

fact by washing the outside with water and then

performing a number of wipe test with soft cotton and

never showing any detectable cyclosiloxanes or

platinum by gas chromatography/ mass spectrometry.

This was part of good laboratory practice.

The defendants discuss the failure of Dr. Ash to

find platinum in the urine of women with silicone

breast implants. Based on the evidence we have

presented the lipid solubility of these

platinum-cyclosiloxane complexes are to be excreted in

the sebum (people’s oil) and the feces, and not in the

urine. We have ongoing studies to demonstrate the

validity of this.

The data published by our team in 1998 as we

mentioned earlier clearly shows that these complexes

accumulate in the kidney and brain. These complexes

have been shown by Agnew et al to result in toxic

interactions (inhibitions) of the brain enzymes. But

yet the authors of the defendants choose to ignore the

preponderance of the scientific evidence.

The defendants in their conclusion seem to claim

erroneous facts about the reactivity (valence sate) of

the platinum catalyst and the lack of al1ergic

properties by this substance when very early it was

shown that platinum metal powder in platinum miners is

highly allergenic and results in an asthma-like

syndrome.

In conclusion, I find the defendants supplemental

submission misleading and in significant part, wrong

on the known science.

Very Truly Yours,

Ernest D. Lykissa Ph.D.

(Dr. Harbut’s presentation to the National Science

Panel is faint and was not able to be scanned. It has

been re-typed and no corrections made for spelling or

grammar. The footnotes are unreadable on the copy

provided by the court.)

C. Dr. Harbut’s Reply

CENTER FOR OCCUPATIONAL & ENVIRONMENTAL MEDICINE, P.C.

2225 Greenfield Road, Suite 440

Southfield, Michigan 48075

(248) 559-6663

FAX (248) 559-8234

March 15, 1999

J. s, Esq.

Charfoos & Christenson, P.C.

5510 Woodwaard Avenue

Detroit, Michigan 48202

FAX: 313-875-8522

Dear Mr. s,

Thank you for allowing me to respond to the

“Defendant’s Supplemental Submissions of the Chemistry

and Toxicology of Platinum.”

The available science is in dispute with many of the

defendants’ statements.

I understand that other workers will be contributing

detailed information in regard to the specific

chemical and valence form of the platinum catalyst

involved, but it has been my belief that platinum

catalysts are contained in, and released from both the

silicone shell and gel. This belief is founded in part

in the work of Dr. of the Centers for

Disease Control12, Drs. El_Jammal and Templeton3 of

the University of Toronto, Baylor University’s Dr.

Ernest D. Lykissa4, the work of Dr. Zameroski5,

the expressed beliefs of H. 6, President,

SURGITEK, and the presence of local and systemic

disease consistent with causation by platinum salts in

women with silicone gel breast implants, which will be

discussed later in this letter.

Because of the enormous potency of platinum salts,

NIOSH has set an airborne platinum salt 8 hour

threshold (word unreadable) value at .003mg m3 for

non-sensitized exposed persons. There are no

available data for “safe” levels of platinum

salt-containing devices. Drs. Niezborala and Garner

state, however, in regard to industrial contact. “At

no stage should a worker be able to come into contact

with a solution or a solid containing these particular

complex platinum salts.”7

There is greater than or equal to 2 mg of platinum

catalyst residual in two 250 mg silicone gel breast

implants.

Platinum salts are considered so toxic that the

consensus opinion in Occupational Medicine is that

platinum allergy exists in a worker presenting with

classic allergy symptoms (who is exposed to platinum

salts) until proven otherwise.8

Much of what we know about these classic symptoms have

been as a result of external platinum salt exposure

and have been tabularized to include (1) Rhinorrha (2)

Sneezing (3) Itching of nose, throat, palate (4) nasal

congestion (5) Cough (6) Dyspnes (7) Asthmatic

Wheezing (8) Cyanosis (9) conjunctivitis (10) Edema of

eyes (11) Lacrimation (12) Redness of eyes (13)

Itching of eyes (14) Photophobia (15) Urticaria (16)

Angioedema (17) Contact Dermatitis (18) Pruritia (19)

Lymphocytosis (20) Eosinophilia. 9

“Workers exposed to platinum salts who present with

the signs an symptoms discussed about should be

considered to have platinum allergy until proven

otherwise, and a trial of removal from exposure may be

warranted.” 10

The literature contains other reports of health

effects of platinum salts.

Agnew, et al, injected 10 to 30 micrograms of a 10ppm

solution of 75% PtCl4 and 25% PtCl6 into the brains of

cats. 11 They induced membranous cytoplasmic bodies,

zebra bodies and multiple nucleoli. They noted that

the induction of zebra bodies and MCBs, both of which

are morphologic features of human neurolipidoses

associated with congenital enzyme deficiencies This

pathology suggests an inhibitory effect of platinum on

brain enzymes. In other words, platinum salts cause

brain disease. It is important to not the

concentrations of toxin used here.

Nordlind reported Platinum Chloride (PtCl2) to inhibit

cell DNA synthesis at 10(-4) to 10(-5) Molar

concentration, but to stimulate mainly thymocytes at

10(-5) – 10(-6) Molar concentrations. 12

Dr. Schuppe investigated the requirements for

sensitization to complex salts of platinum in a mouse

model by means of the popliteal lymph node assay. A

single subcutaneous injection of dissolved

hexachloroplatinates without adjuvant induced a

vigorous primary immune reaction in the draining PLN.

Peak reactions were obtained around day 6 post

injection of 90-180 (word unreadable) of Na2(ptCl)6.

Primed mice mounted an enhanced response upon local

re-stimulation with sub-optimal doses of the same, but

not unrelated compounds, indicating a specific

secondary response. For elicitation of a secondary

response to Na2(PTCl)6, one fifth of the primary dose

proved to be sufficient. Compared with most other

drugs and chemicals tested, the amount of halide Pt

salts inducing maximal PLN reactivity was very low.

Compounds eliciting PLN reactions include contact

sensitizers and drugs that can induce various types of

allergy and auto-immunity or both. Schuppe found a

genetic component to the PLN response to

hexachloroplatinate. T cells were required to elicit

PLN reactions to the (Pt Cl6)-2.13

Dr. Bloksma and colleagues reviewed results obtained

with popliteal lymph node assays in rodents and

discussed their ability to detect and analyze

immunotoxic effects of drugs and other low molecular

weight chemicals. They reported on Dr. Schuppe’s work

in support of their thesis, ie: hexachloroplatinate

evokes a primary and secondary immune response, with

T-Cell dependence and B-Cell activation. It is

included as part of an approach to recognize

sensitizing or otherwise immunomodulating chemicals.

14

This work was preceded by Pepys work as far back as

1978 when he confirmed the presence of specific IgE

antibody to platinum salts, but also heat stable,

short term sensitizing antibodies, presumably STS-IgG.

15 By 1988, Seiler had reported that while IgE

antibodies mediate the immediate reaction at

re-exposure, IgG antibodies are responsible for the

delayed effects. 16

As work in the field of platinum salt sensitivity

becomes more sophisticated, the role of IgE levels

have become less predictive of the pathophysiology

induced by platinum salts than previously believed.

Merget and colleagues described the course of

immediate-type occupational asthma after allergen

avoidance. After removal from direct exposure, IgE

dropped but the authors concluded that both

nonspecific and specific bronchial responsiveness do

not decrease after removal from exposure in

immediate-type asthma caused by platinum salts. 17

In fact the variability of RAST testing, skin prick

testing and Serum IgE are so variable and often

insensitive, we are cautioned that negative tests even

in the occupation setting do not exclude platinum

allergy. 18 Merget reported 9 platinum-salt exposed

workers previously without work-related symptoms who

converted from a negative to a positive skin prick

test. Two of the group had a marked increase in total

IgE, but for the whole group, total IgE did not show

an increase at after skin test conversion. 19

There were some specific areas in which the authors of

the defense position on this issue weren’t as clear as

they might have been:

“Platinum metal is non-toxic and non-allergenic.”

Although this is felt to be largely true, there are

reports in the literature of toxicity and

allergenicity of platinum metal. There are reports of

contact stomatitis due to palladium and platinum in

dental alloys, contact dermatitis due to metallic

platinum, and postulate that soluble nonchlorinated

platinum compounds may be allergenic, and that a fine

powdered form of platinum metal may also be

allergenic.20 21 22 23

“Platinum exposure is common in the General

Population”. In this section, the authors state, “Dr.

Ash and his colleagues concluded that ‘urine platinum

is highly unlikely to be increased as a result of

breast implants.”

I have provided the rest of the article with this

letter. The cited paragraph is fundamentally an

explanation of an earlier paragraph which states,

“Indeed, urine would appear to he a poor specimen for

the evaluation of chronic platinum exposure, given

that half of the platinum in blood is eliminated in <3

days and that the affinity of platinum for adipose

tissue is high.’’ 24

Incidentally, it was our facility which first noticed

the incorrect urinary platinum levels being reported

nationally and we sent triple sample to different labs

to attempt to learn the reasons for what we thought

were false elevations. The confirming

correspondence is attached as Appendix A, although

this material was already subpoenaed and provided, as

was our notification of the FDA. Dr. Nuttal later

apologized to me for excluding an acknowledgment.

“Only some platinum salts induce allergic responses”

and ‘Platinum Salt Allergy”. Much of this section has

been rebutted above. Please note the protean

manifestations of ‘platinum salt allergy.” Also please

note the platinum salts which have been associated

with allergic response and are also associated with

silicone breast implants

“There is no evidence of platinum salt allergy in

women with silicone breast implants.” This section

seemed like an excuse to attack my recent work

published in the Israel Journal of Occupational

Health. The authors’ footnote #86 is not very

accurate.

The articles referenced in notes 7, 8, 10, 13, 14, 15,

17 and 22 explain how platinum salts can cause

systemic hypersensitivity as a function of immunologic

initiation rather than irritant epithelial effect.

Furthermore, all of the publication’s cases of asthma

were diagnosed using criteria consistent with both the

ATS and NIH guidelines.

Attached as Appendix B are the results of my Pulmonary

Function Testing of the patient population. Appendix

C is a letter from the National Institute of

Occupational Safety and Health approving the Center

for Occupation and Environmental Medicine to be a

Pulmonary Function Training Facility of the type cited

in the NIH publication. You’ll note that I am the

Course Director.

Additionally, Dr. Froom, the IJOH editor, felt that

Dr. Lykissa’s personal correspondence in regard to the

_expression of the hexachloroplatinate from the

devices was not necessary, that the remainder of the

references provided adequate foundation.

In further support of the presence of

hypersensitizing agent in breast implants, Dr. Tueber

and colleagues published a case report of the

remission of sarcoidosis following the removal of

silicone gel breast implants. An analysis of the

devices and the immunologic activity of platinum salts

demonstrates platinum salts to be the most likely

hypersensitizing agent in those cases. 25

There then is a long discussion of skin patching

using Platinum #2. This testing was conducted in a

non-standardized manner. As described, it is not a

valid approach as described here. Although many

specific details are missing, it is important to note

that the length of time from exposure to sensitization

is longer than that contemplated by the authors of

this study.

Because we already know from previous Dow-Corning

funded, published and commercialized research that

Silicone Gel is biologically active26, it may have

been wiser to apply silicone gel sheeting in a more

standardized fashion to patients who have had silicone

gel implants for a period of time adequate to allow

the initiation of the amnaetic response.

Attached as Appendix D, is an analysis of Silicone Gel

Sheeting, Breast Implant Gel and Breast Implant Shell.

The components are the same. Appendix E is the

pathology report of Joy , MD (along with an

informed consent document) demonstrating mast cells

suggestive of telangiectasia macularis eruptive

perstans at the site of the silicone gel sheeting

patch testing. This positive result, from a properly

performed test, demonstrates what is found when on

properly tests.

The defendant’s platinum report states that there is

no relationship between the devices and neurologic

disease. I included Agnew’s animal work about. If

very tiny amounts of platinum salts reach the

appropriate cerebral tissue, disease will occur.

Platinum has been shown to cross the blood-brain

barrier.

The epidemiological studies cited does not examine

appropriately, if at all, the disease processes

experimentally demonstrated to be associated with

platinum salts.

As a final consideration in this matter, attached as

Appendix E, are the PET scans of two patients, which

were reported as abnormal prior to silicone gel breast

implant explanation (sic). After explanation (sic),

they returned to normal.

In summary, silicone gel and elastomer have (word

unreadable) systemic toxic and allergenic effects.

These effects are likely due to the release of

platonic salts from the devices, or from the release

of colloidal platinum that is reconverted to platinum

salts. Not all implant patients become (word

unreadable) from the devices but some do and some

become very ill.

To help clarify issues of unit conversion and an

attempt to quantify actual amounts of platinum salts,

I have included Appendix F.

In 1995, Dr. J. O’Leary, Vice President of

Epidemiology & Biometrics for the McGhan Medical

Corporation told me that McGhan stopped using platinum

catalyst in their devices in 1987.

Sincerely,

P. Harbut, MD, MPH, FCCP

Diplomate, Occupational Medicine, American Bd. of

Prev. Medicine

Clinical Assistant Professor, Internal Medicine Wayne

State University

V. SUMMARY AND CONCLUSION

The Parties agree that “platinum salts” (aka

chloroplatinic acid) can cause systemic disease in

humans as a result of toxic and/or hypersensitivity

reactions. These toxic and hypersensitivity reactions

can range from asthma, rhinorrhea, tinnitus,

conjunctivitis, urticaria, fatigue syndromes secondary

to impaired oxygen exchange, neurotoxicity, sicca

syndrome, and macular rashes.

The Plaintiffs’ Submission proves that silicone gels

and elastomers do contain unreduced chloroplatinic

acid, i.e.,

“platinum salts.” The Defendants’ internal documents,

the testimony of Defendants’ employees, and the

admissions of the

Defendants in their Supplemental Submission on

Platinum constitute such compelling proofs that a

fairminded scientific review can reach only one

conclusion.

Plaintiffs Submission on Platinum also shows that,

even if one buys the “scientific position” of

Defendants, i.e., that all platinum salts are reduced

to sub micron sized elemental particles in colloidal

suspension) in susceptible individuals, sub-micron

sized elemental platinum, platinum in colloidal

suspension, and platinum metal, can each be a toxin

and/or a hypersensitizer in humans.

Plaintiffs further establish, through the submission

of Dr. Wabeke, that the amount of platinum in silicone

gel

elastomers and implants is not a “small amount” but

rather, a tremendous amount i.e. , as much as “1000 x

the permissible occupational exposure.”

Finally, based on the extensive peer reviewed

research published on elastomer shunts we find a

decades long track record of hypersensitivity disease,

hypersensitivity complications, and elastomer shunt

failures. Because silicone elastomers (e.g., shunts)

have ten times as much platinum catalyst as silicone

gels, the extensive rate of shunt toxicity arid

hypersensitivity complications cannot surprise the

Defendants. Why would we expect a different result

from the gels and elastomers in breast implants?

In conclusion, specifically as to individual patients

with individual signs and symptoms, and generally, as

to the mechanisms of toxicity and hypersensitivity as

outlined in this Submission, a compelling medical and

scientific case is made that platinum salts, as a

residual contaminant in silicone gels and elastomers

are a probable factor, or co-factor, in a variety of

the complaints and diseases presented by women exposed

to silicone gels and elastomers. These facts compel a

conclusion that, silicone gels and elastomers can

cause systemic diseases in humans.