In general, pitfalls in diagnosing OLD arise from one of two basic reasons: physician bias or inadequate evaluation. It would be naive to assume that bias does not play a role in what is inherently an adversarial situation. The "no-fault" nature of workers' compensation does not inhibit litigation, since the employer's Workers' Compensation premiums rise when a claim is sustained. As a result, many, if not most, occupational lung disease claims are contested.
Morgan (1995) has written:
". . . in the U.S. at the present time an attempt is being made to relate virtually all naturally occurring disease to occupational exposure, and suits for all types of so-called occupational injury and illness are extremely common. The present system has done much to undermine the public's faith in the legal and medical professions, but since vast sums of money are involved, it is likely to persist at least for a time."
Thus, in the present litigious climate, one could argue that many of the examples in this paper are not pitfalls at all, that they merely reflect purposeful mis-statements, distortions or omissions to satisfy the hiring attorney's needs: either to turn a non-disease, or a non-occupational chronic disease, into an occupational condition; or to nullify a legitimate occupational condition. Such intentions are probably true some of the time, but more often, I think, the pitfalls discussed in this paper are unintended, and the consequences unwanted.
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There is a lesson here for both physicians and attorneys. Should physicians assume the position of lawyers -- able to take either side of a case and argue it in a way that is provably biased? I don't think so. Physicians should evaluate OLD objectively no matter who is paying for the opinion. Such a position in no way obviates becoming a paid expert. Indeed, "when called upon on behalf of either defendants or plaintiffs, physicians have an obligation and a duty to participate in the justice system as expert witnesses." (ACCP 1990) The author has written reports and testified on behalf of both patients and companies (and, yes, become trapped in a few pitfalls himself!). The point is to evaluate each claim thoroughly and fairly, and not to take a position against one's better medical judgment.
When colleagues in medicine question a diagnosis it is usually in a friendly context. Diagnosis of OLD is different. Inappropriate and unsupported claims can expect to be challenged, and when that happens even the most casual declarative statement will come under intense scrutiny (Richman 1989; Richman 1990). Other physicians will likely be paid to argue against the diagnosis. The physician may be deposed, his or her background explored, credentials examined, integrity called into question. A physician who takes a medically incorrect or obviously biased stand can actually harm the side he is trying to help, especially if his testimony becomes discredited.
The best way for a physician to survive intense scrutiny is to anticipate it. If a physician is asked to review a case of possible OLD, the problem should be approached like a review for a medical journal or a medical grand rounds presentation. What are the facts? Is all the pertinent history included? What is supportable and what is not? Is the assessment consistent with what is currently published about the problem? What conclusion can be comfortably presented to colleagues in an open scientific forum?
Medicine is an art and legitimate controversies exist about many diagnoses, including OLD. The literature is replete with articles about the difficulty in attributing cancer to asbestos exposure (Browne 1986; Cullen 1987; Mossman 1989) or silicosis (Goldsmith 1982; Heppleston 1985); in differentiating occupational from intrinsic asthma (Richman 1990; Chan-Yeung 1988); in deciding if asbestos is the cause of pleural thickening (Rosenstock 1987) or effusion (Epler 1982), etc. Physicians live with uncertainty in both diagnosing and attributing causation in these and many other diseases. It is only in the legal world that physicians are asked to state a diagnosis (or its cause) as "more probable than not" and, if need be, swear to this statement under oath.
The fact that OLD also involves the legal profession should not affect one's objectivity or clinical approach. Physicians have an obligation to themselves and to the larger society to help assure that patients deserving compensation get it, and that claimants without a compensable occupational illness are not unjustly rewarded.
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As for attorneys, they are paid to be advocates. Can they be faulted for relying on a physician's report in favor of the client, no matter how incorrect, sloppy or biased it may be? Yes, in one unarguable aspect: if the report ends up hurting the client, by involving him in a series of futile evaluations, depositions and court dates.
The author has seen, on numerous occasions, claimants put through unnecessary and expensive re-examinations because an attorney sought to justify a diagnosis initially made in a patently shoddy report by an unqualified physician. On many occasions clients have expressed dismay at the multiple series of chest x-rays, blood tests, and doctor visits requested of them, and opined they should never have started the process. I have also been involved in three cases that went to trial lasting, respectively, one day, one week, and two weeks, where there was not a shred of evidence to support any occupational diagnosis. All three cases were predicated on reports full of contradictions and incorrect statements, and the claimant lost in all three instances.
What is the attorney's obligation to his or her client? From a physician perspective, it seems that a smart attorney will know when the expert physician, hired to make a diagnosis, in fact weakens a case. No doubt this realization happens quite often, and many claims are dropped or settled quickly for a small amount. Yet some attorneys seem to drag their hapless claimants through the medical evaluation process, and then through the administrative and civil courts, in a futile attempt to justify a diagnosis without merit. An advocacy position so encumbered can trap not only the physician, but also the attorney and the claimant.
ACCP Guidelines for an expert witness. Chest 1990;98:1006.
Allard C, Cartier A, Ghezzo H, Malo JL. Occupational asthma due to various agents. Chest 1989;96:1046-49.
American Medical Association Guides to the Evaluation of Permanent Impairment, Fourth Edition. American Medical Association, 1993, Chicago.
American Thoracic Society: The diagnosis of nonmalignant diseases related to asbestos. Amer Rev Resp Dis 1986;134:363-68.
American Thoracic Society: Evaluation of impairment/disability secondary to respiratory disorders. Amer Rev Respir Dis 1986;133:1205-9.
Bates DV. Respiratory Function in Disease, 3rd edition. W.B. Saunders Co., Philadelphia, 1989.
Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunction syndrome (RADS); persistent asthma syndrome after high level irritant exposure. Chest 1985;88:376-384.
Browne K. Is asbestos or asbestosis the cause of the increased risk of lung cancer in asbestos workers? Brit J Indust Med 1986;43:145-149.
Brownson RC, Reif JS, Keefe T, et al. Risk factors for adenocarcinoma of the lung. Am J Epidemiol 1987;125:25.
Chan-Yeung M, Lam S, Koerner S. Clinical features and natural history of occupational asthma due to western red cedar (Thuja plicata). Am J Med 1982;72:411-15.
Chan-Yeung M. Evaluation of impairment/disability in patients with occupational asthma. Amer Rev Respir Dis 1987;135:950-51.
Chan-Yeung M. Occupational asthma update. Chest 1988;93:407-411.
Chan-Yeung M. Occupational asthma. Chest 1990;98:148S-161S.
Churg A. Non-neoplastic asbestos-induced disease. The Mt Sinai J Med 1986;53:409-15.
Cockcroft DW, Hargreave FE. Airway hyperresponsiveness. (Editorial). Amer Rev Resp Dis 1990;142:497-500.
Crystal RG, Bitterman PB, Rennard SI, et. al. Interstitial lung diseases of unknown cause. New Engl J Med 1984;310:154-165.
Cullen MR. Controversies in asbestos-related lung cancer. Occupational Medicine: State of the Art Reviews 1987;2:259-272.
Cullen MR, Cherniack MG, Rosenstock L. Occupational Medicine. New Engl J Med 1990;322:594-601.
Davies D, Cotton R. Mica pneumoconiosis. Brit J Indust Med 1983;40:22-27.
Enterline PE. Attributability in the face of uncertainty. Chest 1980;78(suppl):377-379.
Chan-Yeung M, Lam S. State of the Art: Occupational Asthma. Amer Rev Resp Dis 1986;133:686-703.
Epler GR, McLoud TC, Gaensler EA. Prevalence and incidence of benign asbestos pleural effusion in a working population. JAMA 1982;247:617-21.
Fabbri LM, Danieli D, Crescioli S, Bevilacqua P, Meli S, Saetta M, Mapp CE. Fatal asthma is a subject sensitized to toluene diisocyante. Amer Rev Respir Dis 1988;137:1494-98.
Gibbs AR. Pathological Reactions of the Lung to Dust. Chapter 8 in Morgan WKC and Seaton A. Occupational Lung Diseases, Third Edition, W.B. Saunders Co., Philadelphia, 1995; pages 151-152.
Goldsmith DF, Guidotti TL, Johnston DR. Does occupational exposure to silica cause lung cancer? Am J Ind Med 1982;3:423-40.
Hall A, Rumack BH. Clinical toxicology of cyanide. Annals of Emerg Med 1986;15:1067-74.
Hansen JE, Wasserman K. Disability Evaluation. Chapter 33 in: Murray JE, Nadel JA, editors. Textbook of Respiratory Medicine. W.B. Saunders Co., Philadelphia, 1988; pages 699-718.
Heppleston AG. Silica, pneumoconiosis, and carcinoma of the lung. Am J Ind Med 1985;7:285-94.
Hughes JM, Weill H. Asbestosis as a precursor of asbestos related lung cancer: results of a prospective mortality study. Brit J Indust Med 1991;48:229-33.
Kay AB. Eosinophils and Neutrophils in the Pathogenesis of Asthma. Chapter 23, in: Weiss EB, Segal MS, Stein M, eds. Bronchial Asthma, 2nd edition, Little Brown, Boston, 1985.
Kilburn KH, Warshaw RH, Einstein K, et. al. Airway disease in non-smoking asbestos workers. Arch Envir Health 1985;40:293-5.
Lerman Y, Selikoff IJ, Lilis R, Seidman H, Gelb SK. Clinical findings among asbestos workers in U.S.: influence of cigarette smoking. Am J Ind Med 1986;10:449-58.
Malo JL, Cartier A, Ghezzo H, LaFrance M, McCants M, Lehrer SB. Patterns of improvement in spirometry, bronchial hyperresponsiveness, and specific IgE antibody levels after cessation of exposure in occupational asthma caused by snow-crab processing. Amer Rev Respir Dis 1988;138:807-12.
Mapp CE, Corona PC, Marzo ND, Fabbri L. Persistent asthma due to isocyanates: A follow-up study of subjects with occupational asthma due to toluene diisocyante (TDI). Am Rev Respir Dis 1988;137:1326-29.
Martin L. All You Really Need to Know to Interpret Arterial Blood Gases. Williams & Wilkins, Baltimore, 1992.
Merchant JA. Priorities for the management of environmental and occupational asthma. Chest 1990;98(suppl):146S-47S.
Moller DR, Brooks SM, McKay RT, Cassedy K, Kopp S, Bernstein IL. Chronic asthma due to toluene diisocyante. Chest 1986:90494-99.
Morgan WCK, Lapp L, Seaton D. Respiratory disability in coal miners. JAMA 1980;243:2401-04. (See also editorial by Barclay WR, JAMA 1980;243;2427).
Morgan WCK. Legal Aspects of Industrial Disease, in Morgan WCK, Seaton A. Occupational Lung Diseases, 3rd edition; W.B. Saunders Co., Philadelphia, 1995.
Mossman BT, Gee JBL. Asbestos-related diseases. New Engl J Med 1989;320:1721-30.
Oliver LC. Occupational and environmental asthma; legal and ethical aspects of patient management. Chest 1990;98(suppl):220S-224S.
Pattemore PK, Asher MI, Harrison AC, Mitchell EA, et al. The interrelationship among bronchial hyperresponsiveness, the diagnosis of asthma, and asthma symptoms. Amer Rev Resp Dis 1990;142:549-554.
Patterson, et. al. Use of immunologic technology in the diagnosis of environmental and occupational lung disease. Chest 1990;98(suppl):206S-207S.
Pimental JC, Menzes AP. Pulmonary and hepatic granulomatous disorders due to the inhalation of cement and mica dusts. Thorax 1978;33:219-27.
Ramsdale EH, Morris MM, Roberts R, Hargreave FE. Bronchial responsiveness to methacholine in chronic bronchitis: relationship to airflow obstruction and cold air responsiveness. Thorax 1984;39:912-18.
Richman SI. Meanings of impairment and disability. The conflicting social objectives underlying the confusion. Chest 1980;78(suppl):367-71.
Richman SI. Why change? A look at the current system of disability determination and workers' compensation for occupational lung disease. Ann Int Med 1982;97:908-14.
Richman SI. Compensating victims of occupational lung disease: The physician's role in the system. J Occup Med 1989;31:335-38.
Richman SI. Legal treatment of the asthmatic worker. A major problem for the nineties. J Occup Med 1990;32:1-27-31.
Rosenstock L, Hudson LD. The pleural manifestations of asbestos exposure. State of the Art Reviews: Occupational Medicine. Hanley & Belfus, Inc., Philadelphia, 1987; pages 383-407.
Ruppel G. Manual of Pulmonary Function Testing. Mosby Year Book, St. Louis, 1991.
Skulberg DR, Glyseth B, Skaug V, Hanoa R. Mica pneumoconiosis - a literature review. Scand J Work Environ Health 1985;11:65-74.
Smith DD. Medical-legal definition of occupational asthma. Chest 1990;98:1007-11.
Tarlo SM, Broder I. Irritant-induced occupational asthma. Chest 1989;96:297-300.
Yan K, Salome CM, Woolcock AJ. Prevalence and nature of bronchial hyperresponsiveness in subjects with chronic obstructive pulmonary disease. Amer Rev Resp Dis 1985;132:25-29.