<< Back to Silica, Crystalline

Disclaimer: This is not DOL or OSHA controlled material and is provided here for reference only. We take no responsibility for the views, content, or accuracy of this information.

Lawrence Martin, M.D.

1. Making an unsupported medical diagnosis (looking for a "quick fix")

Settlement of an occupational lung disease claim takes time. The treating physician may want to oblige his or her patient by making a quick (unsupported) diagnosis in the chart or in a letter to plaintiff's attorney. Although an unsupported diagnosis may help initiate a claim it will only get in the way if the claim is contested.

A 56 year-old man with a long smoking history was being treated for exacerbation for chronic obstructive pulmonary disease (COPD). Noting that the patient "works in a foundry," his family physician wrote in the chart: "Dx. COPD - occupational asthma." A worker's compensation claim was filed, supported solely by the physician's statement (reiterated on the claim form without any supporting information). Ultimately the claim was disallowed, but only after two year's of legal wrangling and several experts had independently evaluated the patient.

If the treating physician cannot be the patient's advocate all the way through a claim, the patient should be referred to someone who can. The above claim might not have been filed had the treating physician referred the patient to a specialist from the beginning.

The "quick fix" pitfall sometimes occurs when the claimant's physician is asked by an attorney to certify OLD "so Mr. C. can pursue his claim." Even though the physician never considered OLD in Mr. C., he feels an obligation to help and, with some prompting by the attorney, writes: "It is more probable than not that my patient, Mr. C, has occupational asthma." If uncontested, such a statement may be all that is needed to pursue a scheduled award. If contested, however, the following facts will emerge: the doctor is not an expert in the field; he has treated the patient on numerous occasions but never made any connection between asthma symptoms and OLD before the claim; his first mention of OLD appears in his letter to the claimant's attorney. The result in such a situation is usually nullification of the treating doctor's testimony and delay in resolving the patient's claim.

This type of pitfall also occurs when a physician is hired specifically to certify a diagnosis in multiple claimants with similar exposure history. To save time the physician may adopt a "uniform" approach, in which every letter reads the same, irrespective of the facts of the case.

A large number of ex-foundry workers were sent to one physician to certify that they had OLD from their remote foundry work. Since most of the workers had no lung disease of any type, certification required coming up with a quick-fix diagnosis. Thus every letter from the physician included the following boilerplate statement, irrespective of the evidence: "His symptoms, clinical examination, employment history, and chest x-rays are consistent with the diagnosis of Asbestosis and or Asbestos exposure related disease." In fact, in almost every case nothing about the patients' exams, test results or chest x-rays were consistent with the stated diagnoses. Lacking evidence to support these conditions, no claim was allowed at the administrative level. When a few of these cases were adjudicated in the courts, the identical nature of the letters harmed the physician's credibility.

2. Echoing an unsupported diagnosis made by someone else

Many diagnoses appear on the chart without adequate documentation, only to have the never-substantiated diagnosis repeated over and over throughout the patient's clinical record.

A patient with COPD had a brief history of foundry work. His physician wrote "R/O asbestosis" on a chest x-ray request form. A radiologist read the film as: ". . .Severe COPD...some fibrotic streaks not typical of asbestosis but cannot rule out that diagnosis." The patient was later hospitalized and at some point "R/O asbestosis" simply became "asbestosis" in the hospital chart. This unsubstantiated diagnosis was echoed by numerous other physicians and listed along with "COPD," "Cor Pulmonale" and, ultimately, "Respiratory Failure." The patient died of COPD-related respiratory failure. No autopsy was done. A claim was made for asbestosis as the cause of death. Repetition of the incorrect diagnosis in the hospital chart gave the impression that asbestosis had been established. Review of the records showed the diagnosis traceable to the single radiology report. There was never any radiologic evidence for asbestosis.

A form of ECHO diagnosis also occurs when a patient receives compensation for a disease not present by the usual medical criteria. For example, the medical and legal criteria for coal worker's pneumoconiosis are different (Richman 1989; Richman 1982; Hansen 1988). Under the 1969 Federal Coal Mine Health and Safety Act, many coal workers met criteria for compensation only because they smoked cigarettes or had non-respiratory disability such as heart disease, hypertension or obesity (Morgan 1980). The result is that many ex-miners hospitalized for exacerbation of COPD with clear lung fields on chest x-ray are erroneously noted throughout the chart as having "coal worker's pneumoconiosis." This type of ECHO diagnosis fosters confusion about terminology and clinical causation.

3. Inadequate clarification of 'impairment' and 'disability'

Impairment is purely a medical condition, such as loss of physiologic function or anatomic loss, e.g. percent decrease in FEV-1 or loss of a limb. Disability is a broader term, meaning overall effect of impairment on the individual and his or her ability to work and function in society (ATS 1986). A worker with respiratory impairment may or may not be disabled for a particular job. Two workers with identical impairment may have varying degrees of disability, by virtue of factors such as age, sex, education and socioeconomic status (ATS 1986).

Notwithstanding the accepted definitions, the two terms are often used inter-changeably and have at times generated much confusion (Richman 1980). The physician should not be faulted for using one term when he or she means the other. Rather, the pitfall comes from using either term as a substitute for clearly stating the worker's limitation or characterizing the patient's impairment/disability in some useful fashion.

A physician evaluating a patient for "percentage of disability" found the FEV-1 approximately 15% below predicted. He wrote that the patient had "15% impairment of the body as a whole," implying a modest degree of fixed impairment and therefore disability. However, he did not address the fact that the patient: a) was taking daily bronchodilator medication, without which the FEV-1 would likely have been much lower; b) had much worse lung function during exacerbations, as documented in emergency department records; and c) was completely disabled for gainful employment because of airway hyper-responsiveness and lack of any skill outside the dusty trades. The physician substituted a precise but limited statement on impairment for a fuller characterization of the patient's true disability.

A related pitfall is stating a percentage of impairment (or disability) on an arbitrary basis. Workers' compensation agencies frequently ask for "the amount of disability stated in a definite percentage." Physicians evaluating pulmonary disorders can use lung function tests (FEV-1, FVC, diffusing capacity), resting arterial blood gases and/or exercise test results as a guide (ATS 1986; AMA Guides). Alternatively, the degree of bronchial hyper-responsiveness and/or the documented minimal amount of medications necessary to control asthma symptoms can be used (Chan-Yeung 1987). Some physicians, unfortunately, seem to just pull a percentage out of 'thin air.'

A patient was evaluated by two different physicians a month apart; each had access to the same data, and the patient's clinical status was unchanged in the interval. One physician found the claimant to have "20% permanent partial disability;" the other found "80% permanent partial disability." Neither physician explained the stated percentage.

After evaluating a patient with chronic rhinitis who also had some history of occupational dust exposure, an otolaryngologist wrote: ". . .it is reasonable to assume that a component of her nasal problems is due to her occupational exposure . . . it is, in reality, a multifactorial problem . . . I feel the chronic irritative environmental exposure would account for 60-70% of her nasal symptoms." The physician provided no explanation as to how he arrived at "60-70%."

4. Ignoring or minimizing relevant medical history

This is perhaps the most common pitfall. Medical history that would be prominent in a routine clinical presentation is often ignored in an occupational claim.

A patient alleging silicosis had a documented history of congestive heart failure (CHF), with CHF-related pleural effusions; she used three different cardiac medications. Her chest x-ray showed cardiomegaly with some vascular redistribution of blood flow and nothing to suggest pneumoconiosis. The physician evaluating her as an outpatient, on the question of OLD, read her chest x-ray as showing "interstitial disease" and concluded she had "silicosis." In an otherwise detailed report the physician made no mention of her cardiac history.

Medical history that appears in a physician's treatment records often disappears when that same physician is asked to certify an occupational illness.

A physician at a tertiary referral center saw a 38-year-old female patient in 1983 for what he noted in the chart to be "shortness of breath and chronic nonproductive cough x 2 yrs. . ." Similar complaints had been recorded by other physicians. No specific diagnosis was made and the patient was lost to followup. Between April 1984 and February 1987 the patient worked for Company X soldering computer boards. During this period her cough continued, on occasion exacerbated by exposure to epoxy fumes. Two methacholine challenge tests were normal and at no time did she manifest airway obstruction or wheezing. Her complaints continued after leaving the company, without any objective evidence for asthma. After re-evaluating the patient in 1989 this same physician wrote her attorney that the diagnosis was "asthmatic bronchitis...of occupational origin" from work at Company X. He made no mention of having evaluated her for identical symptoms in 1983, before she ever started working for the company.

Selective reporting is particularly common as regards smoking history. I have encountered several situations where patients were diagnosed as having occupationally-induced chronic obstructive lung disease with no mention made of an extensive smoking history.

In September 1987 a 55-year-old man was hospitalized for what his physician noted in the chart as: "Exacerbation of chronic obstructive pulmonary disease. . . He has a 30 pack year history of smoking and quit two or so years prior to this admission." The patient had worked in a paper mill for several years and lately had become bothered by fumes at work. After discharge from the hospital an occupational claim was made. In October 1987 the same physician completed a Workers' Compensation 'Statement of Occupational Disease' form for his patient. Under "What is the Diagnosis?" the physician wrote: "Occupational asthma; chronic bronchitis, COPD." Under "What in your opinion is the cause of the disease?" the physician wrote "Allergen at work." No mention was made of the smoking history, or of how an "allergen" might have caused the COPD.

5. Arguing against yourself

This is a rare pitfall, but one that can trap the unwary expert.

A 59-year-old man died in 1985 of pulmonary fibrosis. He had a documented history of extensive work exposure to asbestos during the 1960s and 1970s. Pulmonary fibrosis first became manifest in 1975, in a pattern typical of asbestosis. The autopsy revealed extensive pulmonary fibrosis and at least one asbestos body per high power field. The patient's employer, who was sued on the claim of asbestosis, stated through experts that the claimant died of "idiopathic pulmonary fibrosis." In 1988 the company's pathology expert wrote that he found "A single ferruginous body, possibly an asbestos body was demonstrated [but] the overall [histologic] pattern is that of an end stage lung with fibrosis of a nonspecific nature...on the basis of the evidence I do not consider this disease process to be asbestosis...the pulmonary disease should be placed in the category of idiopathic pulmonary fibrosis...[the diagnosis] is...clearly...not...asbestosis."

This same expert had previously published, in a specialty medical journal (statement paraphrased):

asbestos bodies are not always observable because they are cleared from the lung and undergo dissolution with time, and therefore particle counts do not correlate directly with the severity of pulmonary parenchymal disease.

The pitfall in this case was the expert's conclusion, directly contrary to his own published work (as well as others; see Churg 1986), that the available data indicated a diagnosis 'clearly not asbestosis.' Unchallenged, such a statement would seem to be conclusive. Critically challenged (principally by citing his own published work), defendant's expert appears highly biased. One wonders what this expert would have written had he been retained by the plaintiff's attorney.

6. Ignoring the possibility of a rare or unusual diagnosis

A 59-year old man developed pneumoconiosis from close exposure to mica while working for a gun shell manufacturer between 1975 and 1982. Prior to this job he had no respiratory history and was a non-smoker. Chest x-ray showed bilateral interstitial nodular infiltrates consistent with pneumoconiosis (lung scarring from inhaled dusts, such as asbestos and silica). Pulmonary function studies showed moderate to severe restrictive impairment; after three minutes of treadmill exercise his oxygen saturation fell from 98% to 87%. An open lung biopsy in 1983 showed "severe interstitial fibrosis [with] honeycomb lung...no asbestos body is identified." Electron microscopic analysis of the lung tissue revealed "elemental composition of aluminum, potassium, and silicon [as] found in mineral silicates, commonly referred to as mica." Thus the diagnosis was unequivocal mica pneumoconiosis, of which a few cases had been reported up to that time (Pinmental 1978; Davies 1983). Despite this evidence, a prominent expert hired by the company wrote in October 1984: "Although [the patient's] history would appear to clearly indicate a significant degree of mica dust work exposure, I must say that from my own years of experience as a lung specialist, his physical and x-ray findings are to me classically those of a non-occupational work problem which is defined by some as idiopathic pulmonary fibrosis...This non-occupational condition has caused a marked degree of impairment of [his] lung function and does limit his present work ability . . ."=

Taking advantage of the relative rarity of pure mica pneumoconiosis, this expert attempted to use his own prominence to refute an obvious case of occupationally-related interstitial fibrosis. (An article appeared the following year reporting 66 cases of apparent mica pneumoconiosis; the authors found causation by mica exposure alone reasonably convincing in 26 of the cases [Skulberg 1985].) The expert compounded his mistake by claiming that the alternative diagnosis, idiopathic pulmonary fibrosis (IPF), is "classically" characterized by certain "physical and x-ray findings," yet the literature available at the time strongly emphasized the non-specificity of these findings (Crystal 1984).

Along the same line, some experts erroneously rule out the possibility of occupational asthma (OA) because no familiar causative compound is identified. About one patient with classic symptoms of OA who worked around several identified chemicals, an expert wrote: "I know of nothing this patient was exposed to that can cause asthma." Over 200 chemicals and compounds have been implicated in occupational asthma (Chan-Yeung 1986; Chan-Yeung 1990; Smith 1990) and the list grows yearly (Cullen 1990). In many cases a specific sensitizing agent cannot be identified (Smith 1990). For the individual patient, finding a specific agent is less important than documenting temporal changes in lung function that implicate some causalfactor from which the patient can be removed (Cullen 1990).

7. Not obtaining or reviewing independent chest x-rays and reports

The vast majority of physicians today rely on independent radiologists to both take and interpret chest x-rays on their patients. However, some non-radiology trained physicians operate x-ray machines in their office and then formally interpret the claimant's chest x-ray. This practice can lead to over-interpretation.

In a letter to an attorney a pulmonologist formally interpreted his patient's outpatient chest x-ray as showing interstitial lung disease from pneumoconiosis; there was no interpretation by a radiologist. During the same year the claimant had other chest x-rays during a hospitalization; all were read as normal by independent radiologists ignorant of the occupational claim.

Sometimes a chest x-ray already interpreted by a hospital-based radiologist will be reinterpreted without reference to the radiologist's report. Certainly there can be honest differences of opinion. More often, however, the 're-interpreter' has simply ignored the radiology report rather than disagreed with it.

A 70 year old man with severe COPD had a series of chest x-rays over five years. All films were read, by various radiologists, as consistent with bullous emphysema; a few "fibrotic streaks" were noted and commented on as consistent with bullous emphysema. No mention was made in the radiology reports of interstitial lung disease (ILD), OLD, or pneumoconiosis. (Also, no mention was made in the clinician's brief history, provided on the x-ray request forms, of any ILD or occupational lung concern.) A pulmonary expert was asked by the claimant's attorney to evaluate the patient and all his chest x-rays. The physician wrote the attorney that the "chest x-rays are indicative of interstitial fibrosis and [occupationally-related] pneumoconiosis." The physician made no mention of the formal radiology reports or of any difference of opinion he had with the radiologists' interpretations.

Often a "B-reader" will be hired by plaintiff's attorney to "prove" a patient has pneumoconiosis. A B-reader is a physician (not necessarily a radiologist) who has taken a course on reading pneumoconiosis x-rays according to the standards of the International Labor Organization (ILO), and passed a timed x-ray interpretation test. Since interpretation of all x-ray films is partly subjective, it may be difficult to argue with a reading of "minimal" pneumoconiosis (1/1 or 1/0 on the ILO scale). However, if a B-reader ignores extant x-rays reports he might enter a pitfall as did the radiologist and pulmonologist in the next case.

On March 4 Dr. W., a certified B-reader, interpreted a PA and lateral chest x-ray as showing interstitial lung disease of profusion 1/1, consistent with occupational pneumoconiosis. Based on this interpretation, a pulmonologist wrote plaintiff's attorney a letter stating the patient had asbestosis. However, both the radiologist and the pulmonologist ignored records readily available (in their own hospital), which included 15 prior chest x-rays and 3 chest CT scans. None of the prior x-rays or CT scans were interpreted as showing any interstitial lung disease, which meant that the condition was unequivocally non-existent. More damaging to the plaintiff's case, however, was the fact that one of the earlier chest x-rays and one of the chest CT scans had actually been interpreted as negative by the same B-reader expert - Dr. W.

8. Attributing causation with certainty when it is unwarranted by the facts

A physician stated that his patient's severe emphysema was caused by work as a garage mechanic. The patient was a heavy smoker and had no history of specific occupational illness (i.e., no history of occupational asthma, no pneumoconiosis.) A review of the medial literature found no evidence whatsoever for association of emphysema with low level exposure to garage fumes.

This example is easier to analyze than situations where there is more than one known cause for a disease. A good case in point is the causation of lung cancer when a patient was both a heavy cigarette smoker and also exposed to asbestos. Enterline has written that no opinion about the tumor's etiology can be certain, and that to attribute the lung cancer to asbestos with certainty would mean that asbestos exposure blocked the possible effects of all other cancer-causing agents, a scientifically untenable position (Enterline 1980). Rather than reach an unwarranted conclusion 'with certainty,' the physician could point out the multi-factorial causation and venture a probability for each factor (based on smoking history, asbestos exposure history, etc.; Enterline 1980). The pitfall is in trying to mold an uncertain situation into a statement that, in order to become legally acceptable, becomes medically invalid.

An example of a medically invalid statement was prepared by an oncologist who had treated lung cancer in a 69-year-old man with a history of heavy smoking.

Over several months of chemotherapy, the oncologist made no mention in numerous letters and chart notes regarding asbestos as a cause of his patient's lung cancer, instead attributing the cancer solely to cigarette smoking. Two years after the patient died, the plaintiff's attorney asked the oncologist to write a letter about causation of the cancer in light of "new" information - supplied by the attorney - that the patient had been continuously exposed to asbestos in his job as an automobile service manager. Without any corroborating evidence of actual asbestos exposure, and despite the fact that the patient never had any asbestos-related disease, the physician obliged, writing the attorney: "There is a large body of knowledge relating to the health risks of both asbestos and cigarette smoking because of the economic implications of these carcinogens. It is certainly within reasonable medical probability that both of these carcinogens [cigarettes and lung cancer] played a part in Mr. X's disease."

This "quick fix" attempt by the oncologist (Pitfall 1) failed because it was based on undocumented asbestos exposure information, and also because the conclusion was medically incorrect. There must be confirmation of some asbestos-related pathology to implicate the mineral as a cause of lung cancer (Browne 1986; Gibbs 1995; Hughes and Weill 1991).

Another variation of the 'certainty' pitfall occurs when physicians state that an occupational illness "substantially accelerated a patient's death" when there were many causes, including natural aging. It is not uncommon to see "substantial acceleration" of death claimed for patients who died after age 75, and of medical problems unrelated to their occupation. Notwithstanding the medical facts in such a case, can physicians credibly claim "substantial acceleration of death" when a patient lives well beyond his life-expectancy?

9. Relying on a claimant's own smoking history

Many OLD claimants say they don't smoke. In our lab we routinely do co-oximetry all arterial blood gases, and this test includes measurement of blood carbon monoxide (Martin 1992). Carbon monoxide (CO) is elevated in the blood of all current cigarette and cigar smokers, usually to a level between 5% and 10% (in non-smokers it is less 2.5%). On many occasions CO is elevated in professed "non-smokers," indicating current smoking (the half-life of CO in the blood is about six hours). When the claimant is confronted with this laboratory information he or she will often revise the history and admit to "smoking some but not as much as before." If blood gas measurements are not done (the test requires a sample of arterial blood), a CO level can be checked in a venous blood sample, or even in a sample of air exhaled by the claimant.

A variation of this pitfall is relying on a standard questionnaire instead of interviewing the claimant or reviewing available medical records. One physician wrote in his report that the claimant was a "life-long non-smoker," and based this statement on negative answers to simple "yes" or "no" questions the claimant made on an occupational history questionnaire. Yet this claimant, who had been previously examined numerous times by other physicians for a chronic heart condition, had a clear history of smoking heavily in the past, and would probably have admitted this history had he been asked directly. The expert's erroneous assertion about the smoking history undermined his testimony when the claim came to trial.

The importance of an accurate smoking history is obvious. Many conditions claimed to be occupational in origin are instead more likely to occur, or be aggravated from, smoking.

10. Mis-interpreting pulmonary function and arterial blood gas tests

Pulmonary function tests are standard tests of lung function performed in most hospitals and in many physicians offices. They require the subject to blow forcefully through a tube, plus perform other maneuvers that can give valuable information about lung function. Arterial blood gas test is done on a sample of arterial blood, and checks for (among other parameters) the patients level of oxygenation. The results of these tests are interpreted as to both the existence and type of abnormality by a physician with specialized training (usually a pulmonologist). Frequently, however, in cases reviewed for compensation the test results are mis-interpreted. Four common errors include:

a) interpreting a low diffusing capacity (DLCO) as indicative of diffusion impairment without accounting for the patient's hematocrit or carbon monoxide level (both can affect the DLCO (Ruppel 1991).

b) interpreting improvement in either FEF25-75% or maximal voluntary ventilation (MVV), after inhaled bronchodilator, as indicative of hyper-reactive airways disease or asthma (FEF25-75% is too sensitive a measurement to gauge bronchial hyperresponsiveness; also, sequential FEF25-75% measurements must be made at the same lung volume for valid comparison (Ruppel 1991). MVV is effort-dependent and bears a fixed relationship to FEV-1 (Ruppel 1991); if MVV improves without concomitant change in FEV-1 the patient's initial test likely reflected suboptimal effort).

c) equating an abnormal methacholine challenge response with a diagnosis of asthma. A drop in FEV-1 of 20% after inhaling methacholine indicates only airway hyperresponsiveness, which can be found in many other conditions (Ramsdale 1984; Yan 1985; Pattemore 1990).

d) interpreting a low resting PaO2 as indicative of "diffusion block" and therefore interstitial lung disease; pure diffusion impairment is rare and does not cause significant reduction of resting PaO2 (Bates 1989).

11. Missing the real cause of a patient's complaint

Physicians who evaluate patients for a third party (lawyer or government agency) do not have a true doctor-patient relationship. For example, there is no obligation to treat and/or followup on the patient's problem. However, physicians do have an obligation call it ethical or moral to help the patient medically if that is possible at the time of evaluation.

A 46-year-old woman filed a Workers' Compensation claim for "industrial bronchitis." Her main symptom was chronic cough for a year. She had worked as an assembler of motors and claimed that dust and fumes in the factory caused her problem. She was using oral theophylline plus both a beta-adrenergic and a steroid inhaler, all without apparent benefit. A physician was asked to evaluate her "on the claim of industrial bronchitis." Based on her symptoms (chronic cough, post nasal drip) the physician suspected chronic sinusitis; sinus x-rays confirmed bilateral maxillary sinusitis with air fluid levels. She was referred to an otolaryngologist.

Although the physician was only asked to evaluate the claim of industrial bronchitis, that clearly was not the cause of her cough. One does not have to become a treating physician to make the correct diagnosis or steer the claimant in the direction of proper therapy.

Along the same line, physicians should encourage any patient they see, no matter what the referral source, to quit smoking. I have seen numerous OLD claimants who still smoke. Without a trace of irony, many of them opined that their cough or shortness of breath was solely related to prior occupational exposure. Physicians should use the opportunity to remind claimants that, irrespective of the merits of their claim, cigarettes are harming their health and may be causing their symptoms.

12. Diagnosing occupational lung disease without attempting to remove the patient from the cause

Physicians also have an obligation to help remove workers from harmful environments. It may not be feasible (for economic and other reasons) to relocate the patient, but every attempt should be made to remove him or her from the offending agent(s) (Chan-Yeung 1990; Merchant 1990). Workers cannot rely on respirators and face masks to prevent further inhalation damage. One death has been reported in a patient with documented toluene diisocyante asthma who continued to work with the compound (Fabbri 1988). Studies of patients with occupational asthma who remain in the same industry show that they either do not recover or continue to deteriorate (Chan-Yeung 1990). If a physician suspects OLD, steps should be taken to remove the patient from the cause.

13. Confusion over basic terminology and pathophysiology in OLD

There are many controversies in the field of OLD. This pitfall refers to statements which are factually incorrect, i.e., not considered a matter of opinion. Among the more common mis-statements made by physicians:

a) 'continued asthma symptoms after a patient has left the workplace rules out occupationally-caused asthma' [not true; see Chan-Yeung 1990; Chan-Yeung 1982; Moller 1986; Cockcroft 1990; Mapp 1988; Malo 1988; Allard 1989].

b) 'absence of prior sensitization rules out occupational asthma' (i.e., reversible airways obstruction with bronchial hyperresponsiveness) [not true; see Brooks 1985; Tarlo 1989].

c) 'blood eosinophilia in asthma is specific for allergy' [not true; see Kay 1985].

d) 'antibody to an inhaled compound (e.g., trimellitic acid) is diagnostic of occupational asthma from that compound' [not true; see Patterson 1990].

e) 'the presence of pleural thickening/pleural plaques on the chest x-ray indicates asbestosis' [not true; see ATS 1986; pages 363-68].

f) 'adenocarcinoma of the lung is not smoking-related' [not true; see Brownson 1987].

g) 'large-airway obstruction with emphysema is explained by asbestos inhalation' [no evidence for; see Churg 1986; Kilburn 1985; Lerman 1986].

Regarding this pitfall, one attorney experienced in OLD litigation has written: "I have frequently witnessed occasions in which medical experts ignore or reject the published diagnostic standards and instead employ peculiar nomenclatures and diagnostic criteria in a regrettable litigation tactic calculated to confuse" (Richman 1989). A good medical expert does not want to confuse anyone, least of all a jury hearing the case.

A smoker with COPD worked as a paint sprayer. He was treated in an emergency department April 3 for COPD exacerbation, and released; he returned to work the next day. A month later he learned that the paint he used in early April contains some cyanide compound. An attorney referred him to a physician, who ordered a cyanide blood level; it was 25 ng/ml, a value in the expected range for cigarette smokers. (Cyanide causes mild symptoms when the level is above 50 ng/ml; depressed level of consciousness begins at 100 ng/ml and death occurs above 300 ng/ml [Hall 1986]. At no time was there any documentation of shock, acidosis or cerebral hypoxia. All of the patient's symptoms were consistent with previously-documented COPD. Nonetheless, the physician wrote to the attorney that the patient "suffered an episode of acute cyanide toxicity on April 3, and now suffers from chronic low-level cyanide toxicity." Subsequently a claim was made in civil court for "acute and chronic cyanide toxicity." The case was ultimately dismissed.

14. Using sloppy or incorrect language, including misspelling

It is amazing how often physicians send out reports with obviously incorrect spelling, syntax, terminology and even the claimant's name. This type of mistake can weaken the physician's credibility and harm the side he or she is trying to help. The usual reason, I suspect, is that many physicians do not read over what they dictate or make no attempt to edit their report. A few examples I have encountered (the intended word is in brackets):

"The patient has a long-standing history of tobaggism [tobaccoism]."

"I believe it entirely impossible [possible] that it caused also an irreversible airway obstructive syndrome leading to the state now where she is a total pulmonary cripple."

"After careful review of his records and noting the progressive nature of his/her [his] subjective symptoms..."

"I evaluated Mr. Brown on October 14, 19--. . . Past medical history indicates that Mr. Jones [Mr. Brown]..."

15. Not saying "I don't know," when you don't

It is entirely proper to say there is not enough information, that the diagnosis is inconclusive, and let the chips fall where they may. If you find you need more information to reach a valid conclusion hospital records, additional tests, whatever that should be stated in your report. It is better to be forthright and uncertain than certain and wrong.