Document zzVmXD9a2VbYG4b7ngjNEEZ23

UNION CARBIDE CORPORATION old rogebury road, danbury, ct dbbi v Corporate Health, Safety end Environmental Affairs Department February 20, 1985 Dr. R.B.K. Tucker 18, Rockridge Road, Parktown, Johannesburg 2193 Republic of S. Africa , Re: Agenda Item 6.1 - 12th Meeting of AIA/MAP: AIA/20/1/2/HAS Asbestos and Simulative Diseases Dear Ron, I have struggled with this item and have produced the attached draft for your consideration. I must confess that I have largely plaguerized the referenced articles (copies of references 1, 2 and 4 are attached hereto) and suppose that, if we decide to publish this, permission would have to be obtained to reproduce the tables and we should indicate our obligation to the referenced authors. I have not sent copies of this draft to anyone else. When you have reviewed the draft, please make any additions, deletions, comments, etc. and forward to AIA for action if you think it would be appropriate. Please let me know what you decide to do. I am not certain about my future as a member of the MAP at the present time and will not know until mid-March whether I will continue to represent the Asbestos Information Association of North America or not. Kind regards to your wife. Sincerely Hilton C. Lewinsohn, MB.BCh., FCCP, MFOM, DIH Assistant Corporate Medical Director HCL:jsh 0111N UCC 010765 THE DIFFERENTIAL DIAGNOSIS OF ASBESTOSIS FROM OTHER FORMS OF INTERSTITIAL LUNG DISEASE DRAFT Introduction The diagnosis of asbestosis can only be made with certainty in the presence of an exposure history. The symptoms of asbestosis are similar to those of other forms of interstitial lung disease and may not be helpful in distinguishing between them. The object of this paper is to focus on the importance of making a distinction between asbestosis in particular and pulmonary fibrosis (interstitial lung disease) in general, since this will affect therapy, medical management, workers compensation and other issues. Definition The term interstitial lung disease is applied to "a heterogeneous group of diseases grouped together because of common clinical, roentgenographic, physiologic and pathologic features. According to Fulmer ^ the most prevalent interstitial diseases are those caused by occupational and environmental inhalants, predominantly due to inorganic dusts. Clinical Features Irrespective of the etiology of the interstitial lung disease, the clinical presentation is virtually the same in all cases. Breathlessness, 0111N UCC 010766 oCj 'i O -2- DRAFT usually first noted on exertion, is the first recognizable symptom in the majority of cases and is invariably present once the disease process has become fairly extensive. The chest x-ray pattern at this stage will be that of a diffuse infiltrative lesion. The pulmonary fibrosis which develops affects the gas exchanging areas of the lung and in some cases a reduction in the carbon monoxide diffusing capacity may be the earliest indication of the disease process. The interstitial lung diseases are characterized by impairment of gas transfer and a restrictive ventilatory defect. The histological appearances in the final stages of the interstitial lung diseases are non-specific and are those of a progressive diffuse chronic pulmonary fibrosis with few, if any, distinguishing diagnostic features. The disease process involves the alveoli and associated connective tissues. VanOrdstrand (2) points out "that there is no occupation in which the worker is immune to nonoccupational diseases". He believes that in some cases the usual routine diagnostic procedures such as work history, chest x-rays and other tests, are not adequate to differentiate occupational from nonoccupational diffuse lung disease. VanOrdstrand feels that there is a place for the use of lung biopsy in such cases. Table I is based on information extracted from Fulmer's^ classification of the Interstitial Lung Diseases combined with information extracted from a similar classification found in Chapter 18 (Interstitial lung disease) in "Color Atlas of Respiratory Diseases" (Edited by D. Geraint James and Peter R. Studdy). (3) The interstitial lung diseases are grouped 0111N UCC 010767 -3- DRAFT according to whether the etiology is known or unknown. According to Fulmer^ one third have a known etiology. Tables 2-6 complement Table I as indicated and are reproduced from James and Studdy's "Color Atlas". VanOrdstrand's approach (2) is to group the radiologic masqueraders of various pneumoconioses in tabular form and Table 7 is in fact his Table 3. Differential Diagnosis Murphy et al. (4) point out that minimal interstitial pulmonary fibrosis caused by the inhalation of asbestos can be difficult to detect. They state that symptomatology is subjective and pulmonary function studies are often nonspecific. X-rays are not able to indicate the etiological factors responsible in the production of diffuse pulmonary fibrotic lesions. Thus, symptoms and signs per se, do not enable asbestosis to be differentiated from other fibrotic lung diseases and it is necessary in each and every case to obtain a detailed medical history and occupational history. There are some features of asbestosis and some details in the medical history which may assist in the differential diagnosis. Fulmer^ discusses the diagnostic approach to patients with interstitial lung disease and emphasizes the need for a systematic approach stating that "A detailed occupational history is mandatory in diagnosing the inorganic dust diseases." Some of the issues which should be covered when taking the medical history include the following few examples: iOr> *;'f L' LJ'. UCC 010768 -4- DRAFT 1. Detailed occupational history - the long latent interval between first exposure to asbestos and development of disease must be recognized and taken into account - contact with household members exposed to asbestos may result in exposure not recognized by the patient - casual workplace exposure may be responsible for the lesions and in some cases living in the neighborhood of a plant may raise suspicions of cause and effect. - farmers' lung and psittacosis may be suggested by a history of exposure to moldy hay or bird droppings respectively - other organic dust exposure possibilities such as use of home humidifiers, vaporizers, saunas - exposure to organic chemicals 2. Detailed drug use history. - Three major groups of drugs are responsible for most drug-induced interstitial diseases. They are listed by Fulmer as the cytotoxic and immunosuppressive agents (bleomycin, nitrosoureas, methotrexate, etc.); the neuroactive and 0111N UCC 010769 vO - 5- DRAFT vasoactive agents (methysergide, Phenytoxin, etc.) and antimicrobial agents (Nitrofurantoin, sulfonamides, etc.). 3. Family history - sarcoidosis - collagen vascular disorders mixed connective tissue disease rheumatoid lung (Skin and eye manifestations of sarcoidosis, collagen-vascular disorders, neurofibromatosis and Wegener's granulomatosis may help in the differential diagnosis). Investigating the patient with an interstitial lung disease may include, in addition to the medical history, interpretation of chest radiographs, and pulmonary function evaluation, special investigations such as serological studies, bronchoalveolar lavage, conjunctival, skin and lymph node biopsy, fiberoptic bronchoscopy and transbronchial biopsy and finally, open lung biopsy may be indicated. In the case of a suspected occupational lung disease, where the diagnosis will determine eligibility for compensation, and where death benefits may be payable to defendants, the opportunity to confirm the clinical diagnosis at autopsy should be vigorously pursued. The chest x-ray is of diagnostic value in only a few types of diffuse interstitial pulmonary fibrosis. Radiographic appearances can be correlated with laboratory data in many instances to yield diagnostic information. According to Fulmer, diffuse interstitial infiltrates with sparing of the 0111N UCC 010770 -6- DRAFT costophrenic angles in a young male is suggestive of histiocytosis-X. In a young black patient in the USA hilar adenopathy with uveitis and skin lesions is thought to be diagnostic of sarcoidosis. Pulmonary function studies are generally not helpful in the differential diagnosis of interstitial disease, including occupational lung diseases. Serological studies are of value in the diagnosis of collagen-vascular disorder and sarcoidosis. Circulating immune complexes or antibasement membrane antibody can also be of use if studied in conjunction with lung tissue or lavage cellular analysis. Interest in the latter procedure has grown recently with regard to the diagnosis of intestitial diseases. Thus far it has proved to be of value only in alveolar proteinosis and the pulmonary hemorrhage syndromes. Hemosiderin-laden macrophages (indicative of pulmonary hemorrhage) and the presence of circulating antibasement membrane antibodies are necessary to diagnose Goodpasture's syndrome. Brocho-alveolar lavage promises to develop into a useful diagnostic procedure. Two distinct cellular patterns have been described. Predominant lymphocytosis is suggestive of sarcoidosis, organic dust disease, acute idiopathic pulmonary fibrosis, certain collagen-vascular disorders, and acute histiocytosis-X. A predominant finding of polymorphonuclear leukocytosis may be seen in inorganic dust diseases, idiopathic pulmonary fibrosis. collagen-vascular disorders and advanced sarcoidosis. Further studies are OlllN UCC 010771 ' - k., * c. }' -7- DRAFT required before this procedure becomes useful in the differential diagnosis of interstitial lung diseases. Transbronchial biopsy may be useful in the diagnosis of interstitial lung disease. Some conditions which may be diagnosed by this procedure are listed in Table 8 (Fulmer's Table 4^). Open lung biopsy is hardly ever justified unless the possibility exists that the outcome will affect treatment of a potentially curable condition. The diagnosis of asbestosis is based upon a history of adequate exposure, radiographic evidence consistent with diffuse interstitial pulmonary fibrosis, a restrictive pulmonary function defect and the presence of bilateral basilar crackles in the lungs. Dyspnoea, cough, sputum production and clubbing of the fingers are usually late, non-specific manifestations. The chest radiograph may provide important clues to the asbestos-related etiology of a case of interstitial lung disease. Pleural plaques are fibrotic areas mainly affecting the parietal pleura. They are usually bilateral, smooth or nodular, and discrete. They are most frequently seen on the posterolateral or anterolateral chest walls, run along the rib margins (most commonly the sixth-tenth ribs) and are also found on the domes of the diaphragm. The apices and costo-phrenic angles are usually clear. Calcification may occur as the years go by. They are considered to be a unique radiographic sign presumptive of asbestos etiology.^ Oil IN UCC 010772 C3S6; -8- DRAFT The small irregular opacities seen on a chest x-ray do not have characteristics which differentiate those seen in cases of asbestosis from those seen in a number of other conditions. Some normal adults will exhibit these radiographic patterns as a part of aging, especially in persons who had repeated pulmonary infections (e.g. bronchitis, pneumonitis). There will be an overlap in the frequency distribution of small opacity profusion in normal and pneumoconiotic individuals at the low levels of profusion.^ Caution must be exercised by the interpreter of radiographs showing such low levels of profusion and unless the exposure history is clear-cut, a positive diagnosis may not be possible without further observation and investigation. Higher levels of profusion of small irregular opacities may also pose problems of interpretation in the absence of an adequate occupational exposure history. Scleroderma, lipoid pneumonia, desquamative interstitial pneumonitis and sarcodosis may produce basal irregular patterns similar to those seen in asbestosis.^ The American College of Radiology's Asbestos Working Group's monograph describes many other diagnosis features of value in making a diagnosis of asbestosis and they point out the differences between early and late findings.^ 0111N UCC 010773 K. Recommendations -9- DRAFT 1. Obtain a detailed medical history, including a meticulous exposure history. 2. In the absence of exposure, a diagnosis of asbestosis can only be made when other etiological agents or conditions have been eliminated to a reasonable degree of certainty. 3. Radiographs must be of good quality, serial films should be available and interpretation should be by a radiologist expert in the diagnosis of pneumoconiosis in particular and chest disorders in general. 4. Pulmonary function tests should only be used to confirm the presence of a restrictive syndrome once there are no specific physiological differences between the many varieties of interstitial lung disorders. 5. Other diagnostic tests should be considered and used in all doubtful cases to rule out conditions which can masquerade as asbestosis. 0111N UCC 010774 G3 x,*} >} r " References: DRAFT 1. Fulmer, Jack D.r The Interstitial Lung Diseases. Chest 1982; 82:172-178. 2. VanOrdstrand, H.S., Pneumoconioses and Their Masqueraders. J. Occup. Med 1977; 19:747-753. 3. Color Atlas of Respiratory Diseases, Chapter 18, pages 161-182 Edited by D. Geraint James and Peter R. Studdy. Published by Year Book Medical Publishers Inc., Chicago. 1982. 4. Murphy, Raymond L.H. et al.. Crackles in the Early Detection of Asbestosis. Am. Rev. Respir Dis. 1984; 129:375-379 5. Asbestos Related Diseases: Clinical, Epidemiologic, Pathologic, and Radiologic Characteristics and Manifestations. Prepared by the Asbestos Working Group (Chairman: Russel H. Morgan). Published by American College of Radiology, 20 North Hacker Drive, Chicago, Illinois 60606 (1982). 6. Morgan, R.H., Donner, M.W., Gayler, B.W., et al.: Decision processes and observer error in the diagnosis of pneumoconiosis by chest roentgenography. Am. J. Roentgenol. 1973; 117:757-764. 0111N UCC 010775 . O'vJ Table 1; Classification of Interstitial Lung Disease* DRAFT Known Etiology Occupational and Environmental Inhalants: Inorganic (see Table 2) Organic (see Table 3) Fumes, gases, vapors, aerosols (see Table 4) Drugs (see Table 5) Poisons Radiation Infectious agents - schistosoma mansoni Pulmonary oedema (cardiac disease) Uremia (metabolic diseases) I | I I I 1 I I 1 I 1 1 I 1 1 I I 1 1 I Unknown Etioloqy Idiopathic pulmonary fibrosis Necrotising angiitis (see Table 6) Collagen disorders - rheumatoid arthritis - progressive systemic sclerosis - Sjogren's syndrome - ankylosing spondylitis Inherited disorders - tuberous sclerosis - neurofibromatosis Miscellaneous - sarcoidosis - pulmonary hemorrhagic syndromes - eosiophilic granuloma - idiopathic hemiosiderosis - amylodosis - veno-occlusive disease - Lymphangioleiomyomatosis *Data compiled from combination of Fulmer's^ Table 1 and James and Studdy's Table on page 161 of "Color Atlas of Respiratory Diseases."^ oiiin UCC 010776 TABLE 2. Causes of occupational Interstitial lung disease. Inorganic dust Industrial hazard Aluminium Asbestos Beryllium 1 Cadmium J Coal Diatomaceous earth Graphite Kaolin Mica Iron oxide (Siderosis) Silica Talc Titanium Grinding Mining Fireproofing Lagging Dock workers Alloys . Electronics Nuclear workers Mining Processing Polishing Welding Mining and manufacturing Drilling, blasting Foundry and glass workers Ceramics and cosmetics Paint UCC 010777 c: 3869 TABLE 3 /Nature and sources of organic dust antigens in extrinsic allergic alveolitis. (Probably IgE mediated obstructive airways disease) Disease Dust exposure Nature of antigen to which precipitin shown Fanners' lung Fog-fever in cattle Bagassosis Mushroom workers' lung Maltworkers' lung Bird fanciers' lung Pituitary snufftakers' lung Wheat weevil disease (Millers' lung) Maple strippers' lung Sequoiosis Suberosis Woodworkers' lung Cheese-washers' lung `New Guinea' lung Smallpox-handlers' lung Paprika splitters' lung Humidifier or forced-air-system lung Coptic lung Poultry handlers' lung Coffee and tea growers' disease Mouldy overheated hay Mouldy hay Mouldy overheated sugar-cane bagasse Mushroom compost dust Mouldy barley or malt Pigeon and budgerigar droppings Wax coating feathers - `pigeon bloom' Powder of porcine and bovine posterior-pituitary extract Infested wheat flour Thermophilic actinomycetes Micropolyspora faeni Thermoactinomyces vulgaris Micropolyspora faeni Mouldy bagasse Thermoactinomyces sacharii Thermophilic actinomycetes (see farmers' lung) Aspergillus fumigatus Aspergillus clavatus Avian serum protein antigens Serum protein and pituitary antigens Sitophilus granarius Maple bark Mouldy redwood sawdust Oak bark, cork dust t Sawdusts of oak, cedar, etc. Moulds on cheese Mouldy thatch dust Smallpox scabs Mouldy paprika pods Fungal spores in air-conditioning ducts and in home humidifiers Cloth wrappings of mummies Poultry feathers and products Green coffee bean Tea fluff Cryptostroma (Coniosporium) corticale Aureobasidium (Putlularia) - pullulans - graphium Mouldy oak bark P. frequentans Sawdust extracts Penicillium casei Extracts of thatch Mucor stolonifer T. candidus T. vulgaris Naegleria gruberi Turkey and chicken proteins UCC 010778 as*5 TABLE 4 Fumes causing interstitial lung disease. Exposure Vapour inhaled Swimming pools Chlorine gas Ore-smelting Sulphur dioxide Nose drops Oil Vineyard spray Bordeaux mixture of copper sulphate and lime Insecticides Pyrethrum UCC 010779 TABLE 5 Causes of drug-induced chronic interstitial lung disease. Busulphan Diphenylhydantoin Bleomycin Gold salts Chlorambucil Nitrofurantoin Cyclophosphamide Paraquat Methotrexate Penicillin Nitrosoureas Procarbazine Vincristine Pentolinium Sulphonamides UCC 010780 1: TABLE 6 Causes of necrotisiiig angiitis. Polyarteritis nodosa - Classical - HBsAg associated in 20 per cent Churg-Strauss eosinophilic granulomatosis Wegener's granulomatosis (see page 155) Systemic lupus erythematosus (see page 145) Behcet's syndrome (see page 146) Henoch-Schonlein purpura Arteritis - Hypersensitivity angiitis - Giant-cell temporal - Takayasu's pulseless aortic - Retinal vasculitis - Rheumatoid arthritis (see page 143) - Rheumatic fever UCC 010781 03893 Table 7: Radiologic Masqueraders of Asbestosis* DRAFT Sarcoidosis Scleroderma Rheumatoid Lung Adult Respiratory distress Syndrome Pse udolymphoma Idiopathic Pulmonary Hemosiderosis Alveolar Proteinosis Thesaurosis Drug Infiltrates Goodpasture's Syndrome Bronchiectasis Universalis Hamman-rich Syndrome Pneumocystis Carinii Chemical Pneumonias Amyloidosis Histiocytosis Parenchymal Hodgkins Disease Pulmonary Edema Inclusion Body Pneumonia Cholesterol Pneumonitis *This is Table 3 in VanOxstrand's publication previously referred to in the text. (reference number 2). 0111N UCC 010782 03SS4 TABLE 8 - INTERSTITIAL LUNG DISEASES THAT CAN BE DIAGNOSED BY TRANSBRONCHIAL BIOPSY.* DRAFT Sarcoidosis Organic dust diseases (hypersensitivity pneumonitides) Histiocytosis-X Pulmonary hemorrhage syndromes Inorganic dust diseases Eosinophilic pneumonias Drug-induced interstitial diseases Lymphangioleiomyomatosis Infectious agents *This list includes diseases in which diagnostic tissue can be obtained, as well as those in which tissue is suggestive put the diagnosis must be made by clinical and laboratory correlation. 0111N UCC 010783 {L' o'*6J*' dr-