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 Peters

Charfoos and Christensen

5510 Woodward Ave.

Detroit, MI 48202

USA

March 12, 1999

 

Fax 313-87S.8522

 

 

 

Dear Mr. Peters:

 

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

 

 

 

 

             B            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 Peters 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 Lewis data, one finds reference to the Lewis 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. Douglas Peters, Esq.

Charfoos & Christenson, P.C.

5510 Woodwaard Avenue

Detroit, Michigan 48202

FAX:    313-875-8522

 

Dear Mr. Peters,

 

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. Omar Henderson 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. David Zameroski⁵, the expressed beliefs of David H. Sanders⁶, 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 Taylor, 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. Patrick 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,

 

 

 

Michael 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.