Document 3J3mdYrNyNMaNR8nQnebzwXVx

BIPIN H. AVASHIA, M.D. Diplamate American Board of Internal Medicine Diplanate American Board of Preventive Medicine in Occupational Medicine RHONE-POULENC, INC. Institute Plant PO Bax 2831 Charlestonf West Virginia 25330 August 29, 1988 -o 311982 . IfJMWSC ' i H.C. Lewinsohn, M.D. P2590 39 Old Ridgebury Road Danbury, Conn 06817 Dear Hiltons Enclosed is an article on Systemic Sclerosis which pertains to the South Charleston Plant. I am also enclosing very erudite rebuttal which was prepared by a Carbide consultant in rfevmatology. With warm regards. Very truly yours. BHA/kat enclosure B.H. Avashia, M.D. UCC 060778 Systemic Sclerosis Secondary to Occupational Exposure ,Gregory R. Owens, m.d.. Thomas a. meosger, m.d. Pittsburgh &W--t-----c-----p----t----w- -------n--- i "-y 1?- IPflR Systemic sclerosis is a multisystem disease charac autoantibodies were absent (antiterized by widespread fibrotic and degenerative SCl-70, and anti-PM-SCl). The results of other sero changes in the skin, vasculature, and internal organslogic studies, including anti-SM, anti-RNP, and rheu [1], Pulmonary involvement, including either pulmo matoid factor, were negative.* A chest radiograph nary fibrosis [2] or pulmonary arterial hypertension revealed interstitial changes in all lung fields consis due to vascular obliteration [3], is commonly seen in tent with pulmonary fibrosis. Pulmonary function patients with this disorder. The etiology of systemic tests showed a forced vital capacity of 3.09 liters (61 sclerosis is unknown. A number of occupational and percent of predicted), a total lung capacity of 4.36 other exposures have been implicated as potential liters (64 percent of predicted), and a single-breath causes of systemic sclerosis or closely related condi diffusing capacity for carbon monoxide of 4.0 ml/min tions, including silica dust [4], epoxy resins [5], rape- ute/mm Hg (14 percent of predicted). Arterial desatu seed oil [6], carbidopa [7], bleomycin [8], and benzene ration from 92 to 78 percent occurred with minimal (9). We report herein the case histories oftwo chemical exercise. An open lung biopsy procedure revealed pul workers exposed to meta-phenyienediamine in the monary fibrosis with minimal inflammation. No ab same building in whom systemic sclerosis subsequent normality of the pulmonary vasculature was noted. ly developed. Therapy with prednisone 60 mg/day, D-penicilla- CASE REPORTS mine 250 mg/day, and nasal oxygen at 2 litera/minute was started. The patient noted an improvement in Patient 1 respiratory symptoms, but two months later as the This 39-year-old man worked in a restaurant and in corticosteroid dose was decreased to 35 mg/day, short the shipping department of a rayon manufacturing ness of breath worsened and the partial pressure of company. Since 1981, he had been employed as a oxygen at this time was 48 mm Hg. High-dose predni chemical operator in Building 156 in a large chemical sone therapy was re-instituted with symptomatic im company in the Charleston, West Virginia, area where provement. he unloaded and transferred chemicals. During Au gust 1981, he had worked primarily with meta-phenyl- Patient 2 enediamine and had been involved in three accidental This 58-year-old man had worked his entire adult spills with this chemical. In October 1983, Raynaud's life for the same large chemical corporation in the phenomenon, swelling of the hands, and hyperpig Charleston, West Virginia, area as did Patient 1. From mentation of his hands and forearms developed. Fol 1944 to 1948, he worked as a laborer, primarily clean lowing another chemical accident in January 1984, in ing pipes containing vinyl chloride. From 1948 to 1977, which he was exposed to fumes of meta-phenylenedi- he worked as a chemical operator. During this time, he amine, he experienced the sudden onset of a produc was exposed to a variety of chemical compounds, pri tive cough, fatigue, and shortness of breath. He was marily of the amine class, and specifically meta-phe- unsuccessfully treated with bronchodilators and anti nylenediamine. He worked as a supervisor in Building biotics and was referred to our institution. Physical 156 from 1977 to 1981, where he was exposed to the examination revealed normal vital signs, with the ex same amines and, in addition, silicon tetrachloride. He ception of a respiratory rate of 22/minute. Results of retired in 1981 because of health problems. examination of the ears, nose, and throat were normal In January 1980, reflux esophagitis with heartburn Evaluation of the lungs showed a few bibasilar rales. developed, followed one month later by diffuse swell Results of cardiac ana abdominal examinations were ing and redness of both hands. In August 1980, be normal. Periungual erythema and puffy fingers bila noted the onset of Raynaud's phenomenon, shortness terally were present, as were mild skin thickening and of breath, and pedal edema and was treated with furo- hyperpigmentation of the fingers and dorsum of the semide. Bradycardia was detected, and an electrocar forearms. diogram revealed complete heart block. A pacemaker Laboratory evaluation revealed a normal blood ceil was inserted. count, and the erythrocyte sedimentation rate was 7 His condition remained clinically stable until 1983, mm/hour. Levels of electrolytes and creatinine were when shortness of breath worsened such that be could normal, as were the results of liver function tests. An walk only one block without stopping. In addition, be antinuclear antibody was positive at 1:100 with a ho reported the development of a chronic cough produc mogeneous pattern, but all scleroderma-selective tive of scanty amounts of white sputum. He was hospi talized twice in 1983 for pneumonia. In 1984, be was treated with prednisone and a theophylline com From th* Owfeiom o) Pulmonary Median* and RhounutoMey And CMc*l Immunolofy. Department oi Mediant. Unmtnrty a< PtttiburWi. Pittsburgh. Pennjytvenie Requests tor r(jrmts sboUd be addressed to Dr. Gregory R. Owens. University ot Pittsburgh. School ol Miduu. Pension ot Pulmonary pound. He denied chest pain or paroxysmal nocturnal dyspnea. Physical examination in 1984 revealed normal vital Medicine, *40 Scute Hall. 3550 Terrace Street. Pittsburgh. Permsytvinia 15261. Manuscript submitted January 15.1968. and accepted i revised form Apr* 1.I9SS. signs. Examination of the head, eyes, ears, nose, and throat was significant only for telangiectasia of the left cheek and bridge of the nose. The lungs revealed biba- 114 July 1988 The American Journal of Medicine Volume 85 ucc 060779 i t l f II 1 i < < < I i t c I < t c \ r i . C c \ r c f t r ' SYSTEMIC SCLESOSIS/ OWENS AND MEDSGER lilar dry rales. Results of examination of the heart and abdomen were normal. The extremities showed sderodactyly, telangiectasia over the fingers, and diffuse hyperpigmentation. Laboratory evaluation revealed a normal complete blood cell count, and the erythrocyte sedimentation rate was 6 mm/hour. Electrolyte and serum creatinine levels were normal. Serologic studies, including anti nuclear antibody, extractable nuclear antigen, rheu matoid factor, anti-centromere, anti-SCl-70, anti-SM, and anti-RNP, were all negative. The chest radiograph showed bibasilar interstitial markings consistent with pulmonary fibrosis, and an esophagram revealed a mild dilation of the esophagus with gastroesophageal reflux. The electrocardiogram showed complete heart block with a paced rhythm of 70 beats/minute. Pulmo nary function tests revealed a forced vital capacity of 4.37 liters (86 percent of predicted) and a single breath carbon monoxide diffusing capacity of 10.7 ml/ minute/mm Hg (40 percent of predicted). Arterial blood gases showed a pH of 7.46, a partial carbon diox ide pressure of 37 mm Hg, and a partial pressure of oxygen of 76 mm Hg. He was treated with D-penidllamine 500 mg and prednisone 10 mg daily. The patient was seen in follow-up two years later, at which time there was no change in Ids symptoms, pulmonary function, or arterial blood gases. COMMENTS____________ Systemic sclerosis is a disease of multiple organ sys tems that occurs primarily in women and that has an incidence of up to 12 cases per million population per year {10}. Although there is no clear reason for the development of the disease in the majority of patients, exposure to certain chemical agents may be associated with its occurrence. Workers who are exposed to siliceous dusts are pre disposed to the development of systemic sclerosis. A variety of reports have documented an unusually high prevalence of systemic sclerosis in underground gold miners [11], sand blasters [12], and workers in potter ies and foundries [13]. The risk of the development of systemic sclerosis was estimated to be increased 17fold in gold miners from South Africa [11] and in creased 110-fold among German underground coal miners [14]. Systemic sclerosis most commonly devel oped in motormen in the mines who were exposed to the highest concentrations of respirable silica [4], Another circumstance followed by the development of scleroderma after a delay of five to more than 20 years is the injection of foreign substances, usually silicone or paraffin, almost exclusively for breast aug mentation [15], This association has been noted al most exclusively from Japan. Other evidence for an association between chemical agents and scleroderma comes from the epidemic of "toxic oil syndrome" in Spain in 1981 [6]. This epi demic occurred after the ingestion of adulterated cooking oil, rape seed oil. After an acute illness, the victims experienced the development of skin changes reminiscent of scleroderma and sometimes more typi cal ofeosinophilic fasciitis, as well as neuropathies, the sicca syndrome, and pulmonary and esophageal dys function. Exposure to vinyl chloride by inhalation or transcutaneously has also been documented to produce a scle roderma-like disease. In one study, skin changes indis tinguishable from scleroderma developed in 10 of 200 workers who produced vinyl chloride fl6]. However, a number of clinical features suggested that the result ing condition was not typical systemic sclerosis. The skin lesions that were noted tended to be nodular. Clubbing and radiographic evidence of lysis of the dis tal phalanx and erosive sacroiliitis occurred, and he patic fibrosis was evident A genetic susceptibility to this condition has been suspected [18]. Yamakage tt al [5] described a scleroderma-like dis order occurring in men engaged in the polymerization of epoxy resins. This disease occurred after only short term exposure and with a relatively high incidence (six of 233 workers). The authors suggested that a biogenic amine, bis(4 amino-3-methyl-cyclohexyl) methane, was the causative agent Neither of the two workers whose case histories were provided had evidence of pulmonary involvement The same authors also de scribed an association between the development of generalized morphea and exposure to organic solvents [19]. Although these subjects were not studied pro spectively for interna] organ involvement the major ity of the patients had either esophageal dysfunction or pulmonary fibrosis, suggesting a systemic rather than an isolated cutaneous process. The development of other pseudo-sclerodermatous states has been described in persons with elevated lev els of the amine serotonin (L-5-hydroxytryptophan). Both endogenous increases, as seen in the carcinoid syndrome [20], and treatment with exogenous seroto nin for intention myoclonus [7] have been associated with the development ofa scleroderma-like syndrome. The moat pertinent case reports in the literature relate to the development of scleroderma in persons exposed to aliphatic and aromatic hydrocarbon sol vents [19,21-26]. Numerous instances of systemic scle rosis following occupational exposure to trichlorethylene [21-23] or perchlorethylene [24] have been described. Exposure to benzene, an aromatic hydro carbon, may be followed fay disease that tends to be limited to the hands and feet rather than becoming a multisystem disorder [9,25]. Methylene chloride, pre sent in many paint removers, may cause acute pneu monitis [26], a circumstance similar to the disease pre sent in our patients. Thera are several reasons to believe that the devel opment of systemic sclerosis in the two workers re ported in this study is more than coincidental. First, only 20 other men were employed during the time spent in Building 156 by the two workers. Likewise, the onset and explosive progression of disease shortly after several documented chemical accidents in Pa tient 1 reinforces the likelihood of a relationship of disease to the workplace. An epidemiologic survey of the facility would provide a definitive answer to the association of the workplace and the onset of disease. However, it has not been possible to carry out such an evaluation. Elucidating a specific causative exposure in these two patients is more difficult One patient had been exposed to vinyl chloride, a known cause of s sderoderme-like syndrome, in the pest Because of the pro longed delay between the vinyl chloride exposure and the onset of scleroderma, we believe this agent was not a causative one. Likewise, both patients were intermit tently exposed to silicon tetrachloride, which yields hydrochloric add and free silica upon chemical break- Juty 1988 The American Journal erf Medicine Volume 8S 115 ucc i ___ . It it possible that the disease described herein tm precipitated by aa uausual type of exposure to silica, but this seems unlikely. The most attractive potential causative agent is meta-phenylenediamine. In the company facilities, this agent was used most commonly in Building 156. Second, Patient 1 was sub jected to heavy exposure several times shortly before the development of an explosive syndrome, which in cluded lung involvement. Finally, as detailed earlier, other biogenic amines have been implicated in the development of scleroderma-like illnesses. Although chemically induced systemic sclerosis may account for only a small fraction of scleroderma cases, the recognition of specific causative agents may ulti mately lead to an improved understanding of the mechanism of disease induction, including vascular, immunologic, and fibroproliferative events, and possi bly to the development of rational therapy. REFERENCES I. Made* T: Syatemic acJarran (idtrodarma). tcanophlK hoortn and cdckioS. at McC*tyO/>, ad. Artraite anddtedcsndteno, Ml adi Phdartotfcifc tea and Faiattr. 19S* MS-1034. lOagriG, fine G.Martert Catat tetenonaryfcnctennprogateJvaiyMtric arteroait'toiwparteondCHESTtonteteiia tenant with dteaaacterotterma. Chad 1983; S4t 546-550. ]L Shgi A. Swan V, Onam G. Barnes L Rodian G. Madig* T; Pulmonary hypartenson ki tha CHEST wnduna variant d ryJIarmc tdwote. Mhht Iteaum IMS:. 515-524. 4. RodnanG, BanadakT, MadaetrT. Camrraratt It Tha aooaation dpragaaiva aytteric tdveal (sdvudaiiiia) trite coal nnaa' pnaunoconroaa and oMa terra d atom. Ann tetean Mad 1967; 66: 323-334. CYamafcaea A, Shikari H. Sara Y. Hanna! A- Occupation!l idaradaama4ka iSanntarnminfrfinmnarenmriWii|iii!jiTnirTilinrnJTrnnf-rini T*i--iitir tefjea 1980; 161; 33-40. 5.Ataw>46ai A. Zaa MaiaVin A. Salaor-VaSnat J. RocawiotaJ8pal A: Todc at lyndonc a wnduma with teatuaanwteppkgthoaadvanoitt terns dadwy. daatna. Sarin Art*** Rhtum 1986: IS; 200-212. 7. SttnteariE. van WoantM.Youg S. afd'Davatopmant da sdorodarmagia ag dway tharapy ante IShydoaylrypttJphan and caridepa. N Eng J Mad 1980.303:712-787. I FinchW. BorteanG. BuddngwnR. Pnnca R. ririlitaai A: Btecrnycir viducad ad* interna,j Bhaunatd 1980; 7; 661-659. S. Cnnak L Sngri G: Banian* txpmura and tytlaric acterote (latter). Ann Intern Mad 1M7:107; US. 10. Madia* T: Eptdariotegy d pragaiari tyttenac Ktertua. Cln Shaun DS 1979:5:15-25. 13.Era*wa L Sdvudanna in ford nantra in tha tettwataryand with parsed* rateranct te pdmanary mandmattod. 5 Afr J Lab On Mad 1957;3:209-231. 12. Sdand M. teas H, Andaraon A, Santa B, Naibon A. Waipnpadi C; Stem* a ripyard jandbtajtars Environ Raj 1976: t. 237-243. IS. Partea not Otoeatwnai lagdbardn. 2ndad. London; Buttenwriha. 1982: 157. lCMutoki U. Sag* V. Zschunha E. MuntbrS* H. Koppint H: Pragasuva jyjlanic rdaror* nth jtem* >l tha Otrmtn Otinopanc RapctAc. In: Stack C, Myara A, ate. SyWarrvc acteraaia (idaredatma). Now York: Gomr Madicd Pubbhag. 1985; 138-141. 1C KunaMY. Shiofckw Y. Madif*T. Rodtai G: CMcal wadrun d tomtom Sam iteaaH dter cownahe us*y. Otaarvattani on 18 patianti and a rawaw d tea Japanan ttaratua. Arthnta Iteaun 1984; 27:1-12 II IgurItnar-rlw tl "laihim-II ityrifm-iUT "`ratlin1-*T~* *4*~5y1* 7 cNorida dbtaaa: nawdoged ddurtanotk M Ardi Occup Environ Hadte 198C 52 151-157. , 17. VatorwiG. Largo C. Jdg & Stein G. Sadat* V; Cinical maritettatona and esuraa d vinyl (Norite (team. Aral NY Add Sd 1975; 246:6-17. 1C 8hdi C MrW* 1 McMMrter C Matte K. Lauant R; Ganatie ueaplteity te arSrnrtarmt Sw tyndoma in symptomatic and atymptomabc aerharj axpenad vuyi ddohda. j flhaunatd 1986; 111059-1062. lCYkntdi^ A,MteariH:fianaraaadinocphdateaiaafodarmoctirritgin paopla argcaad te orpnic write*. Oarmatoiogca 1962:165; 186-191 MFriat J. Lktdgan J. M t. Sdaradarmatea teaoni and tea carcinoid ayndong. Ante Adam Mad 1971131:550-553 n. Saltan E. Burton J, Ktatan It A now jyndroma dth pignantation. adaredarma. fynaacomntia. Raynaud'* pharamanon. and paripharal nauppatey. Br J Datmatei 197199.437-440. 21 FMMiuan H, bag* H; Sdvodarma aft* occupational atgoiwa to tndvtectStytana andWchtetalhana. Acta Ovtn Vantraol (Stodte) 1987; 67:263-264. 23. Lochty J, Xaty C. Cannon G. Cctey T. Aldridi V. Livagitan G: Pregatwte tyateric tetanwa* anodated vtite ugoJiaa to trichtaraateytena. J Ocog Mad 1987; 29 493-096. M. Sparra* G: A cdnnacliva bswa dbordar tenter to vinyl chiarida dttaaaa ki a patent aapoaad u parchteradiytena. CSn Oarm 1977; 117-21 2C waiter 1 On advant* cauaa Jdarodtnru f kit J Oarmatd 1963:22:157-15C 21. Buia S. Pratt D. May J: OteuM pulmonary vyuy toaowmg pant rynovar axpo- a*. Am J Mad 1986:81:708-704. ---------------- ............^.vriaiuteriteNtetePtetede .^riNikwnga-eatM 8,0Mterite4i4miltete.r4W-rriiii-eMW**>9!ag Ill July 1988 Ths American Journal of Madidne VotemsSS ucc 060781 ariTis case asscca -aCCA 3ovrh 3uffp*r `V* 'JC - ,wC4] v^v'vOOO i I July /, i^rb; ! John L. McClaugherty, Attorney at Law Jackson, Kelly, Holt & O'Farrell 1500 Laidley Fewer ?. 0. 3 ok 553 Charleston, West Virginia 25322 Re: Sherman L. Handley Claim No. 84-49760 rear Mr. McClaugherty: i saw ;his oatlent on 3-5-34 at the racuast t pulmonary disease specialist. Dr. Patel. He java 2 tha t in Octet er of 1933 he had developed s^elli.tt . -- . . --J quite suddenly and he also noticed that his finger purple in the cold. He said ha had been working a temperatures cf minus 5 degrees Farenheit and caug oic and cough. Cn January 23rd he became dyspneic on exarti on and could not climb a flight of stairs. He was seen b y phys ic ia ns and given antibiotics, then he was admitted to the hospi tal and was seen by Dr. Patel who found a pulmonary infiltrate a nd suspected scleroderma with pulmonary involvement. At this time he was very breathless even on walking into the living room; the skin of his hands had become tight; weight had decreased 7 pounds in the hospital; and he had developed indigestion on medications and severe heartburn. While he denied dysphagia, he said he was now unable to drink quickly. He said he was told he had a hiatus hernia. His fingertips were numb. He said he was a chemical operator at Carbide emptying out tanks and that he believed that silicon tetra chloride releasing hydrochloric acid fumes was the cause of all his problems. ucc 060782 1. Me Z liusr.ar' ev a z P'4 When I examined him I found his blood pressure to be 130/90. He "weighed 176 pounds and was 5'10". Thera "were telangiectases ever his chest and he said they had been present 10 years. The lung sounds were normal. The only other finding was of scleroderma of the forearms and hands and left cheek of his face. On 5-3-35 I found harsh breath sounds and fine crackling rales over the right mid zone bilaterally but less on the left. The patient was already taking prednisone, 0 mg daily at breakfast. Other lab tests performed by Dr. Patel had shown a strongly positive antinuclear antibody test at a titer of 1: 611. 1 did net repeat this. A bleed count shrwe ` elevate: white oocnt of 15,300 with / v* /o nt3 'w * * ^, as bedno due : o the high cose prednisone. TMJ-rs sarum cnciest: v-- o -- - izh, again which I interpreted as being caused or azzravat^d bv ednisone. At this point it was clear that patient was s ering frem the disease scleroderma with pu involvement a his pulmonary involvement was his main pro' I told Mr. Handley that there was no treatment known to be safe and effective for this disease but some physicians use a drug called D-penicillamine. I told him that I do not use this drug for that purpose but that the physicians at the University of Pittsburgh see a lot of cases of scleroderma and do use the drug. If he wished I would refer him there. As it turned out, the patient went to Pittsburgh with one disease scleroderma and returned with four diseases, three of them iatrogenic. When he came back he had not only scleroderma but also cushing syndrome secondary to high dose prednisone: recurrent pneumothorax requiring emergency admission to the Charleston Area Medical Center and resulting from open lung biopsy; and the nephrotic syndrome resulting from D-penicillamine medication. I attempted to reduce the prednisone dosage but it was increased again by the Pittsburgh physicians. I also stopped the Penicillamine and the nephrotic syndrome cleared only to return again on restarting a very small dose. (It is also possible that while I was prescribing a very small dose, the patient may have been taking a larger dose since he believed it would save his life). UCC 060783 Beeson end McDermott Textbook of Medicine, :irior., states that there is a 3 to 1 ratio of females to males in this disease. In a 1985 article entitled Pulmonary Involvement in Systemic Sclerosis, Dr. Owens and his colleagues in Pittsburgh fail to mention the percentage of patients who are female. However, in an article entitled Pulmonary Function in Progressive Systemic Sclerosis published in Chest 84-5 1983, they had 33 women and 5 men with CREST syndrome and 67 women and 10 men with diffuse scleroderma. In their article "Interstitial Lung Disease in Scleroderma" Silver and Associates, Arthritis and Rheumatism, - , 254,> 1j- 5- 84 studied 20 oatients with interstitial lung disease its to s tier tearma :n=s e, a were females ar.c II were males, '50% males} . In a: .OU-l taper Cv ittsbureh out. Americ a n ? 77 ic - retorted 69", cf 26 tatier. `ith diffuse sclertderma were f=' . _ ? s >67. of 2^ ja t tents the CREST svndrcrr.e were females, Hew j v r y go on co S3y COc in their `matnocst' that the 22 patients with the CREST syndrome hud been salat tad from 51 tatiants in their research unit over an 13 month interval from June of 1981 through December of 1982. while scleroderma is more often seen in women, it certainly occurs in men too. The true prevalence of any disease in a community is hard to estimate. There have been many attempts to estimate the prevalence of rheumatoid arthritis in various countries and the figures suggest that somewhere between .57. and 27. of the adult population suffers from the common disease rheumatoid arthritis. During the period when I saw 77 patients with scleroderma, I saw 1860 patients with rheumatoid arthritis. Thus, scleroderma is 1/20 as common as the common disease rheumatoid arthritis. It is uncommon but it is not rare. When Dr. Owens learned that Sherman Handley had worked for Carbide, he formed a belief that breathing chemicals must have caused scleroderma in this particular case. When he heard of another patient who had attended the Cleveland Clinic, this solidified his belief. UCC 060784 Jr hr. 1. McC laugher tv, Attorney at lav ~ a ' ?rm= n D . He nd lev I like to distinguish in my own mind between my beliefs and knowledge. Many people used to believe that the world was fiat, today very few believe that. We new have knowledge that it is round. Thus, people's beliefs can sometimes be confirmed as knowledge accumulates but other times beliefs can be demonstrated to be falsa by acquiring new knowledge. Therefore, we have to question Dr. Gwens beliefs and look at his stated reasons for coming to the belief. Dr m one - -- -5 t -O : Cw=ns states that it is unusual for men to get scleroderma rst olacs. He also says that it is very unusual for the o have s very rapid onset of symptoms. So unusual was Ir.arion that Dr. Owens thought that a lung biopsy was The oyuastion then is : How common is scleroderma lung o tan 11 nave a sucuen onset sne crorressrcn? Silver and Associates iris and Rheumatism, 271, 19 Id state that lung disease has a slew gradual deterioration or a rapid downhill course and this is unpredictable by any testing method used at the present time. 3arnett and Coventry, The Medical Journal of Australia, 1040, 1969, report on treatment of 61 personally observed patients with systemic scleroderma seen in Melbourne. They state "these cases presented a very diverse picture, varying from patients with ischemia and sclerotic changes of the fingers only, who lived in good health to old age, to patients rapidly developing skin changes over the whole body who died within a few months or years." Most of us who treat numbers of patients with scleroderma are aware of this peculiar variation in the clinical course of the disease. The first patient I saw in Morgantown in 1974 was an 18 year old girl who died of her disease in less than 12 months. I diagnosed a 75 year old man as suffering from scleroderma of recent onset in November of 1985 and after assuring him that his disease was mild and it was safe for him to take a vacation in Buffalo, New York, I was called by a physician from New York to say that he had been admitted in a crisis and was in pulmonary failure. That patient has returned \JCC 06018s 3\ cd cha Charleston Area Medical Cancer where ha is new on permanent kidney dialysis ana who will clearly dia in Che near future. bast month I saw a middle aged man, a dispatcher working for a iced company, whose onset of disease was explosively sodden in 1933 and in May 1936 he was in the Charleston Area Medical Center having lose 30 pounds weight, unable to swallow feed or to digest ir cr to stand up by himself. These things happen. Scleroderma frequently has an explosive onset in men and in t; rajoricy of patients with scleroderma are housewives. In. . 1 lie: the occupations of men with scleroderma: 100 men eumaccid arteritis; and 3? man with os : soar chr itis '* ^ _ T. ~ ^ 2 "v " "CoTr Carbide, one was Mr. Handley and the otr.er was a mar. sent ever by the Medical Department because of a positive antinuclear antibody test and Raynaud's phenomenon. 'Anile this cces r.ct conform to the ARA criteria for scleroderma, 1 include this as a ccssibla case. Since sc mar.v catients with osteoarthritis have retired, X have examined these employed and expressed in parenthesis the percentage of the total employed under occupation. Thus, we find that of 100 men with rheumatoid arthritis seen in my office between 1984 and 1986 5% worked for Union Carbide. Of 89 men with osteoarthritis seen in the same time period, 49 were still employed and 4% worked for Carbide. The question may now be asked: Is the presence of two Carbide employees among 24 men with scleroderma an unusual event in my practice? _The answer is no. In my practice only the presence of four or more patients with scleroderma who were employed by Union Carbide would have been an unusual or unexpected event. The disease remains a condition seen mostly in housewives and those that occur in males are distributed among the many occupations of the workers of the Kanawha Valley according to the laws of chance. Based upon my examination of Mr. Handley, my review of the literature, and my review of the occupations of men with scleroderma, rheumatoid arthritis or ucc 060786 > John L. McClaugherty, Attorney at La^ ?. e : Sterms r. 1. Harc 1 ey July 7, lr:: Page 6 osteoarthritis seen by me in my office around the time that Mr. Handley 'as seen, I conclude that there is no causal relationship between Mr. Handley's scleroderma and his occupation. Yours sincerely, PLf / l"w' Hnclosure ucc 060787 060788 RHEUMATOID ARTHRITIS OCCUPATION # MALE UHW Office Carpentry Driver Blib, Tnrl'. lujuip. Carbide* DuPont* Allied CliMnicnl* Columbia Our Mechanic Dept. Nat. Rea. A5 25 9 6 5 2 I 1. 3 1 100 Random Male Patients TotaL Rheumatoid Arthritis 1975 - 1986 is 1660 TABLE I PROGRESSIVE SYSTEMIC SCLEROSIS OCCUPATION MALE UMW Office Carbide* Libbey (Kfenr. (Enj' inepr J.ng, Boat) Construei fori Retired Dept. Voo. Rehab. Child 8 5 2 1 A 2 I 1 Total Scleroderma Patients from 1975 - March l, 1986 is 77 - 2A Male 53 Female OSTEOARTHRITIS o o :d OCCUPATION MALE UMW Office Postal Plumbing Carpentry Mechanic Sales Janitor Bus Driver Barber Dentist Unemployed Carbide* Monsanto* Alloy* Elk Metals 13 (27*) 12 (25*) 3 (6*) 3 (6*) 2 (4*) 3 (6*) 2 (A*) 2 (A*) 1 (2*) 1 (2*) 1 (2*) 1 (2*) 2 (A*) 1 (2*) 1 (27.) 1 (2*) Total Male Osteoarthritis in Current Files 1983, 1984, 1985, 1986 - 89 Employed Over 65 49 40 7. Represents Buployed Only * Chemical Tlnnts 6-6-86