Document YGr6QZ6KYQ7VdqdmO8MpG8REE

Pitney, Hardin, Kipp & Szuch (MAIL TO) P. O. BOX 1945 MORRISTOWN, NEW JERSEY 07962-1945 ROBERT L. HOLLINGSHEAD ---------OIRECT DIAL NUMBER . (201) 966-8017 (DELIVERY TO) aoo campus drive FLORHAM PARK. NEW JERSEY 07932-0950 ________ FLORHAM PARK (201) 966-6300 NEW YORK (212) 926-0331 October 11, 1993 r o TELEX &420M FACSIMILE (201) 966-1550 Gregory D. Winfree, Esq. Litigation Counsel Union Carbide Corporation Law Department 39 Old Ridgebury Road Danbury, CT 06817-0001 . Re: Colbv v. Union Carbide Corporation Dear Greg: Enclosed please find a copy of Dr. Scoppetuolo's expert report dated September 27, 1993, which has been submitted to plaintiff's counsel on behalf of Union Carbide in this matter. Sincerely, /& RLH:pc Enclosure ROBERT L. HOLLINGSHEAD PRIVILEGED AND "CONFIDENTIAL MATERIAL SUBJECT TO PROTECTIVE ORDER" UCC 075696 a n WINFREE i-t:. ESSEX ONCOLOGY GROUP FAX NO. '-'-ECl _ V < V SSEX ONCOLOGY GROUP, P.A. JAMES M. ORSINlt M.D. MICHAEL SCOPPETUOLO, M.D. 36 NEWARK AVENUE. SUITE 304 BELLEVILLE. NEW JERSEY 07109 TELEPHONE (201) 751-8060 FAX (201) 791-6950 BILLING (2Q1) 751-5757 vi September 27, 1993 Kathryn M. Decker Pitney, Hardin, Kipp & Ssuch P.0. Box 1945 Morrletown, NJ 07962-1945 Dear Ms. Decker: I had the opportunity to review the records you sent In regards to the Lawrence Colby ve. Union Carbide Corporation, Docket Mo. L-1979-91. Specifically, I have reviewed the answers to Interrogatories of Phyllis Colby, certificate of death of Lawrence Colby, post mortem examination of Lawrence Colby, report of Richard Commentuncci, M.D., reports of Roland D. Goodman, M.D., medical records of Mr. Colby's admission to Rlverview Hospital dated April 1981, July 1983, February 1989 and March 1989, office records of Frank Picone, M.D., office records of Brian Boyle, D.O., office records of Dennis Fitzgerald, M.D., office records of A. Pertchlk, M.D., outpatisnt clinic records from Memorial Sloan Kettering Cancer Center, and report of Burton Z. Davidson, Ph.D. I hereby submit this report. Lawrence Colby was a 55-year-old, white male, who presented to Rlverview Hospital in February of 1989 complaining of severe beck end abdominal pain. He also complained of nausea, vomiting, and Increasing abdominal girth. He said this was present for several weeks prior to admission. As noted in the admitting history and physical, the patient carried a history of diabetes mellftus as well as hypertension. Be was known to smoke approximately two packs of cigarettes daily. This has bean well documented back in his medical records. He was also known to be a heavy alcohol abusar. The patient was found to have a tender and enlarged liver that extended approximately five flngerbreadths below the costal margin is the right upper quadrant. He was admitted with the presumptive diagnosis of cirrhosis of the liver. Upon admission to the hospital, the patient was evaluated by a liver/spleen scan which revealed multiple filling defects that were consistent with metastatic disaasa but regenerating hepatic nodules could not be ruled out. A CT scan was suggested. The patient waa evaluated by Dr. Boyle of gastroenterology. A CT scan was recommended aa well as a biopsy for tissue diagnosis. A CT scan of ehs abdomen was performed and this revealed the presence of hepatomegaly with an abnormal appearing liver. There waa evidence UCC 075697 <> CT-3-33FRI 4:35 r'"FX ONCOLOGY GROUP FAX NO. <.ol751895u 2- - of multiple filling defects which were felt to b metastatic deposits but regenerating nodules within the liver could not be ruled out. An ultrasound of the liver was also performed which revealed filling defects In the liver consistent with metastatic diseasa as well as a thickened gallbladder wall. A bone scan was performed which revealed increased radionucleotide uptake in the sixth or seventh rib on the tight side. Whether this represented metastatic dlsaasa remained to be determined. The patient underwent a CT directed needle biopsy and cytology was reported aa positive for malignant calls having a glandular characteristic. It was notad by the pathologist that the cells resembled metastatic adenocarcinoma but a hepatoma could not be ruled out. An alpha feta protein was performed which revealed the level of approximately 20.7, normal being up to 8.5. The hepatitis B profile was performed and this was negative, other tests performed on that admission were a barium enema which was normal and a chest x-ray which revealed no evidence of any primary or metastatic disease. The patient was seen in consultation by Dr. Dennis Fitzgerald of Oncology. It was the feeling of Dr. Fitzgerald that the patient probably had an occult GI cancer with metastatic disease to the liver. He advised adequate analgesia and the beginning of chemotherapy with 5-fluorouracll and leucovorln. Dr. Fitzgerald evaluated the patient with a CA 19-9 antigen which was elevated at 1,940. The patient's CEA was also over 9,000. The patient was then started on chemotherapy with leucovorln, 5-FU by Dr. Fitzgerald. He symptomatically improved on the regimen. During the course of the patient's chemotherapy, he suffered what appeared to ba a cerebral vascular accident in March of 1989. Ha was readmitted to Riverview Medical Center where he underwent an extensive neurological evaluation that included a CT scan of the head, MRI and spinal tap. This entire workup was inconclusive ea to whether neurological event was metastatic or vascular In nature. The patient was treated as if he suffered a cerebral Infarct. During this hospital stay, the patiene was further evaluated and was found to have a normal prostate gland. His chest x-ray was normal and a CT scan of the chest revealed that the lung fields vers clear but there was evidence of metastatic disease within the liver. Vascular studies of the carotid arteries revealed a significant obstruction In the right carotid artery. Because of persistent back pain, ha was evaluated by Dr. Edmond Kwong of radiotherapy for possible radiation to his pancreas. It was the feeling of Dr. Fitzgerald that the patient may have had an occult pancreatic carcinoma. Dr. Kwong evaluated the patient's tests and found that there was no evidence of any pancreatic tumors and felt that radiation was not indicated. The patient was eventually discharged from the hospital to continue on his chemotherapy aa an outpatient. He was then aeeo at Memorial Sloan Kettering Cancer Center by Dr. Ethan Daitrovsky. It was hia conclusion that the patient had an adenocarcinoma of unknown primary with metastatic disease to the liver and concurred in the use of leucovorln, 5-FU. The patient continued under Dr. Fitzgerald's care up until hie death In May of 1989. Causa of death was signed out as metastatic cancer to the liver. The patient eventually underwent a post mortem examination performed at Rlvervlew Medical Center by Vito Gulli, M.D. The findings of the post mortem examination reveal the presence of a primary adenocarcinoma of the lung arising in a scar, with evidence of metastatic disease to the liver, left adrenal gland, bilateral pleural surfaces, small bowel, and perlpaneraatlc and mediastinal lymph nodes. UCC 075698 OCT- 8-93 FRI 4:36 F 'X ONCOLOGY GROUP FAX NO. 2017518950 -3- Therefore, baaed on Chle post mortem examination and my review of the medical records, the cause of death would have been metastatic adenocarcinoma of the lung. Mr. Colby was an employee of OTD from May 1961 to June 1967. It was that this facility that Mr. Colby- worked in the packing and assembly departments for a polyvinyl chloride resin. Ac no time was this facility Involved in the manufacturing of vinyl chloride monomer or polyvinyl chloride itself. It is the contention that this exposure to polyvinyl chloride was directly related to Mr. Colby's eventual development of adenocarcinoma of tha lung. I am specifically asked to comment on the causal relationship of polyvinyl chloride and its monomer In relationship to Mr. Colby's development of adenocarcinoma of the lung. Polyvinyl chloride is considered to be a weak carcinogen. To date, lc has been only associated with the development of a specific liver tumor called angiosarcoma. This appears to be directly related to vinyl chloride monomer and only weakly associated with exposure to polyvinyl chloride. Tha rola of polyvinyl chloride, vinyl chloride monomer and polyvinyl chloride dust has been reviewed in numerous publications. To date, there is no evidence that polyvinyl chloride, its monomer, or polyvinyl chloride dust acts as a carcinogen for the development of any other form of cancer. Smaller studies as well as larger studies have specifically looked at the role of polyvinyl chloride in the development of lung cancer, brain cancer, melanoma and hemopoeclc malignancies. A large study published in 1988 by Doll revealed that polyvinyl chloride and Its monomer are only carcinogenic for angiosarcomas of the liver. They found no evidence to support that polyvinyl chloride or its monomer is carcinogsnic for other forms of cancer. More recent studies published by Wu, et al, In June of 1989, confirmed the face that vinyl chloride was carcinogenic for angiosarcomas of the liver but found no association with polyvinyl chloride, vinyl chloride monomer or polyvinyl chloride dust with the development of lung cancer. A subsequent stupy published in the American Journal of Industrial Medicine in 1993 by Lundberg, confirmed findings of the previous authors in that there was association with Vinyl chloride exposure and development of angiosarcomas, but there was no associated effects with any other forms of cancer except for possibly melanoma. There Was no evidence for an increased risk of lung or brain cancers in this study. It should be noted that in the literature the association with ths development of angiosarcoma appears to be found only in patients that have received high exposure to vinyl chloride monomer and this usually occurs in manufacturing and of polyvinyl chloride. There does not appear to be any association for carcinogenesis of th^se exposed to polyvinyl chloride and its procsssing or packing plants in the abdve studies. This was specifically addressed in the Lundberg publieeelon. Based ijpon the above etudles end the fact that Mr. Colby was not involvsd in tha manufacturing of polyvinyl chloxidt but only in its procsssing and packing, it is my opinion that chare was no causal relationship of his exposure to polyvinyl chloride and his eventual development of adenocarcinoma of the lung. In my opinion, a much more plausible and more Important causal effect) in Mr. Colby's development of lung cancer would have to be hie known smoking history. Mr. Colby was a two pack par day smoker up until the time of his eventual diagnosis of adenocarcinoma in February of 1989. It is well documented that UCC 075699 0CK8-93 FRI 5:04 ET`V ONCOLOGY GROUP FAX NO. (.viToIqOSO F. j! -4- the risk of lung cancer la significantly greater in people who smoke as compared to the general nonsmoking population. It has also been documented! that the amount of cigarettes smoked, as well as the length of time of smoking, significantly increases the risk of development of lung cancer. Baaed on Mr. Colby's age of 55 at the time of diagnosla, and assuming he started smoking at the age of 20, he would have had a 70 pack year history of cigarette smoking. This would significantly Increase his risk for the development of lung cancer, Another factor that would explain the development of lung cancer ip. Mr. Colby, is the relationship between nonsmall cell lung cancers (adenocarcinoma) and scar tissue in the lung. It has been described chat nonsmall cell lung cancers can arrive in an area of lung that had previously been injured and developed scar formation caused by previous infection or trauma. Tha term scar carcinoma describes these nonsmall cell lung cancers chat develop in an area adjacent or directly rslated to a site In tha lung that has been previously injured. This can occur in a smoker as well as in a nonsmoker. It} Mr* Colby's case, the pathologist described bis carcinoma as a rising in the scjar and used the term ''scar" carcinoma. In ? 'mmary, despite Mr. Colby's exposure to polyvinyl chloride, 1 feel that this had no relationship to his eventual development of adenocarcinoma of the lung and his eventual death from this disease. As stated above, studies have shown that there is no relationship with polyvinyl chloride, vinyl chloride monomer, or polyvinyl chloride dust with the eventual development or lung cancer. Vinyl chloride has only been associated with the development of angiosarcomas of the liver and in of itself, is a weak carcinogen. In my opinion, Mr. Colby'a smoking history, and previous lung injury (scar) were responsible fpr his eventual development of adenocarcinoma of the lung. i MSsdf UCC 075700