Straight Track #94: Asbestos Report

Asbestos: How It's Diagnosed and Why It's Litigated

J. Dillon Hoey
Hoey & Farina Partner

The FELA Reporter and Railroad Liability Monitor, in Vol. 14, No. 12, Dec. 2001, Section 1, wrote an article, "Asbestos: How It�s Diagnosed In Lungs and Why It�s Litigated" (p.3).

We thought it worthwhile to share it with you. The article has been formatted so that you can read it in its entirety, or click to read only those sections that particularly interest you.

What Is Asbestos?

Asbestos is a naturally occurring mineral that was long ago found to have fire retardant properties. Asbestos has been used in production of fire-retardant products such as bricks, pipe coverings, brake linings, ceiling tiles, floor tiles, fire-resistant work clothes, and many others since 1879. From 1890 to 1970, an estimated 25 million tons of asbestos were used in the United States, with two-thirds of this amount in the construction industry (1).

Because in its raw state asbestos is friable, meaning easily broken into microscopically small pieces by ordinary hand action, asbestos can be inhaled into the lungs and can cause damage. Individual asbestos fibers are microscopic in size, with a width much smaller than a human hair. When asbestos is not friable, such as when it is embedded in ceiling tiles or completely encased in pipe coverings, it cannot be inhaled and cannot cause damage. Asbestos-containing materials are known as ACM�s, which can release friable asbestos into the air when broken up by machines, cut, scraped, or sanded.

There are six naturally occurring minerals that are considered asbestos. Three of those minerals � chrysotile, amosite, crosidolite � were commonly used in various products. Three other asbestos minerals � tremolite, actinolite, and anthophyllite � were uncommonly used and are rarely found today.

Today only chrysotile, so-called �white asbestos,� is mined and incorporated into products. However, since asbestos is indestructible, older buildings and products that pre-date the 1970�s may also contain some amosite (brown/off-white) or crocidolite (blue) asbestos.

What Are Ferruginous Bodies?

Individual asbestos fibers cannot be seen under the ordinary (light) microscope. However, once in the lungs, a portion of asbestos fibers usually becomes coated with material that contains iron. The Latin term �ferrous� means of or containing iron. Hence, these coated fibers are called ferruginous bodies.

An individual ferruginous body has a much greater mass than the uncoated fiber and, as a result, can be seen under the light microscope. Ferruginous bodies are often looked for in lung tissue to prove asbestos exposure. When found, they are sometimes referred to as asbestos bodies. However, asbestos is not the only fiber that may be coated with iron in the body; glass and cotton fibers, talc, and graphite also can become coated with iron. When this happens, they are indistinguishable from true asbestos bodies under the light microscope.

Some asbestos claims revolve around the presence or absence of asbestos bodies in lung tissue. Any interpretation of this finding (presence or absence) must be balanced with the claimant�s exposure history and associated lung pathology.

What Is The Harm From Inhaling Asbestos?

Because friable asbestos can be inhaled, the main medical concern is lung or respiratory disease. Disease can come about because of the body�s reaction to the inhaled asbestos, usually the formation of scar tissue. Scar tissue replaces normal lung tissue and, when extensive, can interfere with respiration. In addition, asbestos scar tissue in the lungs can lead to lung cancer.

Generally, asbestos respiratory diseases take two or more decades to develop from the time of first exposure, and then only after extensive or long-term exposure to friable asbestos. The more extensive and longer the exposure, the more risk an individual has for developing asbestos-related disease years later.

Who Is At Risk For Asbestos-Related Disease?

To develop asbestos-related disease, one must have substantial exposure to friable asbestos (2). Usually, such exposure requires working with friable product over a long period of time. Workers at risk for asbestos disease include miners of asbestos, shipyard and power plant workers, brake lining workers, pipe fitters, insulators, boiler makers and repairers, millwrights, and workers in production facilities where asbestos-containing products are manufactured.

It should be noted that while asbestos exposure occurs almost exclusively in the workplace, it might occur else-where in the community, such as in neighborhoods near asbestos mines or even at home. There are several instances of workers� wives developing asbestos disease from cleaning their husbands� asbestos-covered work clothes (3).

What Are The Asbestos-Related Lung and Respiratory Diseases?

Five main respiratory diseases or conditions may occur from asbestos exposure. These include interstitial fibrosis, pleural plaques/fibrosis, benign pleural effusion, lung cancer, and malignant mesothelioma. All of these diseases or conditions also have other causes. The patient�s asbestos exposure history and specific features of the diagnosis often suffice to implicate asbestos as a cause. In many cases, however, the role of asbestos may be in doubt and will be disputed.

Interstitial fibrosis. Lung tissue is very thin, delicate tissue that comprises millions of air sacs surrounded by blood vessels and connective tissue. The portion of the lungs surrounding the air sacs is collectively called the interstitum. If the asbestos fibers get into the interstitium, they can cause scarring, or fibrosis. When this occurs, the disease is called interstitial fibrosis.

Interstitial fibrosis can actually occur from many products and diseases and is by itself a non-specific disorder. Other causes include drug reactions, infections arthritis-related diseases, and chronic heart failure. There is also a specific entity, indiopathic interstitial fibrosis (IPF), that has no known cause.

Asbestosis is interstitial fibrosis specifically due to inhaled asbestos (4). Like any case of interstitial fibrosis, asbestosis can lead to shortness of breath and ultimately can be fatal.

Pleural plaques and pleural fibrosis. Sometimes the scarring is not in the lung tissue itself, but in the outside linings of the lung called the pleura or pleural membranes. These are thin, glistening membranes that completely cover the lungs. When pleural scarring is visible on a chest x-ray, it is termed pleural plaques or pleural fibrosis (5).

Disease confined to the pleural membranes is not asbestosis, which is a diagnosis mistake frequently made by physicians reading chest x-rays. Unlike asbestosis, pleural plaques and fibrosis rarely cause symptoms or any discomfort. Sometimes calcium is deposited into these plaques, and then they are much more easily seen on a chest x-ray because calcium is so dense.

Several other conditions, such as healed tuberculosis and other infections, can cause pleural scarring and calcium deposits. However, a particular distribution of pleural plaques or fibrosis on the chest x-ray (e.g. covering both diaphragm muscles, especially if calcified) can be attributed to asbestos if there is a history of exposure and no other cause is evident.

Asbestos can cause two very different types of pleural effusion � benign and malignant.

Benign pleural effusion. Pleural effusion, a collection of fluid around the lung, is a very common medical problem. Like interstitial fibrosis, there are many potential causes (e.g. pneumonia, congestive heart failure, cancer, kidney disease, rheumatoid arthritis, and tuberculosis).

Malignant pleural effusion is due to either lung cancer or mesothelioma. Benign pleural effusion is not due to cancer but presumably due to the inflammation generated by asbestos (6). When the pleural fluid becomes substantial (usually more than a point or 500 cc), the patient may have symptoms (usually shortness of breath), and the chest x-ray will show the fluid collection.

Asbestos is actually a rare cause of pleural effusion. Pleural scarring and pleural plaques are a much more common result of asbestos inhalation. The only way to reliably diagnosis most causes of pleural effusion is to sample the fluid via a needle in the pleural space and examine it in the lab.

Lung cancer. Lung cancer is the most difficult disease to attribute to asbestos for one principal reason: more than 90 percent of lung cancers are due to cigarette smoking and virtually all lung cancer patients with any asbestos exposure also have a strong smoking history.

Lung cancer is common, with about 180,000 new cases a year in the United States. Since we know asbestos is potentially carcinogenic, every patient with lung cancer and a history of friable asbestos exposure should be evaluated to see what role, if any, asbestos played.

Lung cancer in patients with a history of asbestos exposure frequently leads to litigation. The litigation often ends up pitting expert against expert, all quoting from the abundant literature on the subject (7).

Malignant mesothelioma. This is a cancer of the thin membranes that surround the lungs and abdominal organs (8). Malignant mesothelioma occurs much more commonly in the chest than in the abdomen. Asbestos-caused mesothelioma in the abdomen is thought to arise from fibers entering the lungs and then penetrating through the diaphragm muscles.

Fortunately, mesothelioma is a rare cancer, affecting only about 2,000 people a year in the United States. Unlike lung cancer, it is not due to smoking; in fact, the only known cause of mesothelioma in this country is remote asbestos exposure. (There are other, rare causes of mesothelioma, such as the fibrous material �erionite,� which is mined in Turkey) (9).

The lag time between first exposure to asbestosis and diagnosis of malignant mesothelioma is typically 20 to 50 years. However, in about half the cases there is no history of asbestos exposure, and the cause is unknown. A documented history of asbestos exposure and the diagnosis of malignant mesothelioma will invariably be linked, so in the area of asbestos litigation these cases are straightforward medically, at least.

What Are The Symptoms of Asbestos-Related Lung Disease?

The symptoms are the same as would be seen in any cause of interstitial fibrosis, pleural plaques or fibrosis, benign pleural effusion, lung cancer or mesothelioma. Symptoms generally depend on two factors: extend of the disease (usually determined from the chest x-ray or CT scans) and co-existing conditions, such as smoking-related lung disease.

* In early interstitial fibrosis there are usually no symptoms, but shortness of breath is the principal complaint as the disease advances.

* Benign pleural effusion is asymptomatic when the amount of fluid is small, but in moderate to large effusions shortness of breath is common. Sometimes patients can also complain of chest pain worse with a full breath (so-called pleuritic pain).

* Lung cancer causes no symptom in the early stages, even when it is large enough to be seen on a chest x-ray. In fact, by the time cancer does cause symptoms, it is usually far advanced and incurable. Symptoms from lung cancer can include shortness of breath, coughing up blood, and chest pain. (If lung cancer has spread outside the chest, it can cause other symptoms, depending on location.)

*Mesothelioma generally causes symptoms earlier than lung cancer, because it grows between the lung and the chest wall, an area more sensitive to pain than inside the lung (where lung cancer starts). As a mesothelioma grows, it can cause shortness of breath, chest pain, decreased appetite, and weight loss.

* Pleural plaques/pleural fibrosis cause no symptoms unless the amount of scarring is very extensive, over both lungs; then it can cause shortness of breath. However, extensive scarring of the pleura from asbestos is rare, so the vast majority of workers with pleural plaques or pleural fibrosis have no symptoms.

In summary, the main symptom from asbestos-related lung conditions is either �none� or �shortness of breath.� The medical term for shortness of breath is dyspnea. Dyspnea is such a common symptom, with so many causes, that it has no diagnostic specificity by itself.

Given a randomly chosen, middle-aged man exposed to asbestos in the past, any shortness of breath he has is most likely not from an asbestos-related condition. The most common cause of dyspnea in this population (middle-aged men) are: poor physical fitness with or without obesity; smoking-related lung disease; and heart disease.

Are Asbestos-Related Diseases Treatable?

Asbestosis is not treatable, although symptoms in the worst cases can be ameliorated with oxygen, steroids, and other measures. Pleural plaques and pleural fibrosis are also not treatable, but they cause no symptoms or discomfort except in very rare cases. Pleural effusion is treatable with removal of the fluid; if the fluid comes back, there are procedures that can be taken to keep this from happening.

Lung cancer is curable only by removing the cancer through surgery. However, at the time of diagnosis most lung cancers are not resectable for cure. Instead, treatment will be with radiation or (less commonly) chemotherapy. Radiation and chemotherapy are considered palliative, as they rarely will cure lung cancer, it will only slow its progression.

Malignant mesothelioma is not resectable, since it involves the lining of the lung and the adjacent chest wall. Rarely, in highly selected cases, a surgeon might attempt to remove the entire lung with its lining and parts of the adjacent chest wall. This procedure, called radical pneumonectomy, might prolong survival in a few individuals, but it is not a realistic option for most patients. Radiation and chemotherapy are not effective for mesothelioma, and most patients succumb within 18 months of the diagnosis.

How Does Smoking Affect Asbestos Diseases?

Smoking does not cause asbestosis, pleural scarring, pleural effusion, or mesothelioma. However, there is some evidence that smoking, which since it affects the lungs� natural protective mechanisms, makes people more vulnerable to inhaled asbestos and more likely to develop asbestosis (10). Smoking is the major cause of lung cancer. Since both asbestosis and smoking can independently cause lung cancer, it is important that anyone exposed to asbestos never smoke.

Smoking not only adds to lung cancer risk in some asbestos workers, but it also can heighten the risk, a process known as synergism. This has been demonstrated with certainty only if the worker has lung scarring from the asbestos. Synergism means that if, for example, the risk of developing lung cancer from asbestosis is 1 percent and the risk from smoking is 2 percent, then the risk for a smoking asbestosis patient is significantly higher than 3 percent.

One of the most contentious areas in asbestos claims is whether mere asbestos exposure, without any apparent asbestos scarring in the lungs, also acts synergistically with smoking to increase lung cancer risk. The published evidence suggests that it does not.

Another interesting aspect about smoking is that up to 75 percent of patients with idiopathic interstitial fibrosis are current or former smokers. In large epidemiologic studies, cigarette smoking has been strongly associated with IPF (11). Since asbestosis can appear identical to IPF on a chest x-ray and physical exam, absent a lung biopsy it is possible that some cases of each condition have been misdiagnosed. In one series, IPF was found to be the correct diagnosis in some patients previously diagnosed with asbestosis (12).

What Other Diseases Can Occur From Asbestos?

Other conditions often attributed to asbestos, such as colon cancer and throat cancer, are unproven and are often the subject of litigation when they occur. Common respiratory illnesses, such as asthma, bronchitis, emphysema, and pneumonia, are not due to asbestos.

How Is Asbestos Lung Disease Diagnosed?

There must be a history of substantial exposure to friable asbestos and a lung condition that could be related to asbestos exposure and no evidence for another cause. For example, a positive exposure history and interstitial lung disease on a chest x-ray and the absence of any other cause would be a presumptive diagnosis of asbestosis. However, a long history of asbestos exposure, with a lung condition not associated with asbestos exposure, equals no diagnosis of asbestos-related disease. Likewise, no history of asbestos exposure, with a condition that could otherwise be due to inhaled asbestos, equals no diagnosis of asbestos-related disease.

The vast majority of asbestos lung disease occurs from remote exposure at the workplace. Given a documented history of asbestos exposure, there are three ways to diagnose asbestos lung disease:

1. A chest x-ray or chest CT scan (more detailed than a regular chest x-ray) diagnostic of or consistent with an asbestos-related condition. There are two types of CT scans � the regular resolution scan and the high-resolution scan. The latter is preferable for diagnosing asbestos-related lung disease.

2. A lung biopsy diagnostic of an asbestos-related condition. There are several types of lung biopsies; for asbestos-related disease it must be an open or surgical biopsy, which requires an operation under general anesthesia.

3. An autopsy diagnostic of an asbestos-related condition.

More than 95 percent of asbestos-lung disease cases can be diagnosed with just a history of friable asbestos exposure and an abnormal chest x-ray or chest CT scan. It is rare to make the diagnosis using lung biopsy or autopsy because these exams are rarely obtained.

Obtaining a portion of lung tissue usually requires surgery. While tiny pieces of lung tissue can be obtained without surgery (through an instrument called a bronchoscope), they are usually too small to diagnose asbestos-related diseases. When lung tissue is available, the pathologist will look for ferruginous bodies as well as other signs of asbestos-related pathology.

Surgical biopsy presents some risk to the patient and won�t be attempted unless there is a perceived benefit. For example, since asbestosis is not treatable, physicians won�t recommend a surgical biopsy if only this condition is suspected. On the other hand, a patient may have surgery to remove lung caner, and then there will be sufficient lung tissue to also look for asbestosis.

Autopsy is even more rare than operation for lung tissue, because the vast majority of deaths are no longer autopsied in this country. In fact, most families considering filing suit for an asbestos-related death refuse permission even though an autopsy, because it allows for complete examination of both lungs, is the ultimate way to diagnose asbestos pathology.

Why Is There Controversy Over Diagnosis Of Pleural Plaques?

Pleural plaques from inhaled asbestos are relatively common (compared to other asbestos-related conditions) and are benign. In one study of asbestos-exposed factory workers who had pleural plaques, the size of the plaques averaged 47.9 cm squared, or 2.4 percent of the typical pleural surface area of 2000 cm squared. Interestingly, the size of the plaques was not related to asbestos exposure intensity. Also, the lung function of workers with pleural plaques was the same as a comparable group of workers with no plaques or history of asbestos exposure (13).

Though a marker of remote asbestos exposure, plaques are sometimes difficult to diagnose on a plain chest x-ray because other shadows (particularly overlying body fat) may confuse the picture (14). This is particularly true if the plaques are not calcified. While a chest CT scan can usually separate out pleural plaques from other shadows, CT scans are not routinely done in most asbestos claimants.

Do Pleural Plaques Lead To Cancer?

The only way to answer a question like this is by population studies (i.e., identifying a group with pleural plaques and then following it for a long period of time.) However, since lung cancer is a common condition in smokers and most asbestos-exposed workers have a smoking history, the studies must be carefully controlled for smoking (as well as other variables like the initial chest x-ray interpretation, the subjects� age, and associated lung conditions). Published studies argue both sides of the issue.

In one of several population studies purporting a relationship between pleural plaques and cancer, Hillerdal wrote (1994):

From the general population in the country of Uppsala, Sweden, 1,596 men with pleural plaques fulfilling strict radiologic criteria were identified from 1963 until June 1985. The men have been followed prospectively for 16,369 person-years� The risk for patients with pleural plaques without asbestosis was increased 1.4 times, which was statistically significant (15).

An opposing editorial in the same journal was highly skeptical of Hillerdal�s findings, as well as other studies on the subject (16). Smith pointed out the difficulty of quantifying asbestos exposure and true smoking histories, and of even confirming pleural plaques on the chest x-ray. After providing numerous citations and cogent arguments against Hillerdal�s findings, Smith wrote:

The study of Hillerdal does not demonstrate a significant enough increase in risk to overcome the experimental limitations in his study. This study is just another study that has failed to demonstrate convincing evidence of a significant risk of lung cancer associated with pleural plaques without asbestosis (17).

What Is The Browne Hypothesis?

In 1986, Dr. K. Browne published a paper in the British Journal of Industrial Medicine titled, �Is asbestos or asbestosis the cause of the increased risk of lung cancer in asbestos workers?� (18) Dr. Browne�s basic conclusion was that asbestos per se may not be completely carcinogenic:

"neoplastic change (cancer) may appear only in the wake of inflammation and subsequent fibrosis� it is not asbestos per se but asbestosis which prepares the soil for subsequent malignancy. "

This assessment was based on epidemiologic and biological evidence that lung cancer in asbestos-exposed workers was due to asbestosis and not to asbestos exposure per se. This hypothesis, to put it mildly, is hotly debated (19).

If Browne�s hypothesis is accepted, then simply being exposed to asbestos is not enough to implicate asbestos as a cause of cancer. The history of smoking (almost always the case in lung cancer patients claiming an asbestos cause) should be sufficient to explain the cancer. If Browne�s hypothesis is not accepted, if the worker has no evidence of an asbestos-related disease, but merely the history of exposure, then asbestos could be claimed as a co-contributor of lung cancer, along with cigarettes.

Dozens of articles have appeared since 1986 favoring or disputing the Browne Hypothesis. The issue was put into perspective by a review in the British medical journal Thorax. After surveying the literature the authors wrote:

Asbestos is the most studied of all occupational carcinogens and, apart from tobacco, the most studied cause of lung cancer. It may therefore surprise the general reader that there is an important area of uncertainty about the relationship between inhaled asbestos and the resulting increase in risk of lung cancer. At issue is whether asbestos attributable lung cancers are always associated with asbestos-induced lung fibrosis � that is, asbestosis. This uncertainty has engendered a heated controversy, fueled by important implications for regulation, workers� compensation, and litigation (20).

Jones, et al (21) summarized their assessment of the issues as follows:

* Lung fibrosis of any cause carries increased risk of lung cancer.
* The synergism between asbestos �exposure� and smoking is really a synergism involving asbestosis, and not just asbestos exposure.
* The type of lung cancer does not indicate the cause of the lung cancer.
* Pleural plaques are not proved to definitely indicate increased risk of lung cancer.

In 1999, Dr. William Weiss reviewed 39 English-language reports of cohorts exposed to asbestos in an attempt to address this question of whether lung cancer risk is increased by asbestos exposure alone, or only in the presence of asbestosis. His summary of the data reveals:

The adequately designed studies in the literature support [the Browne] hypothesis. The summary relative risk for lung cancer was 1.00 in seven cohorts with no deaths from asbestosis. In addition, there is a high correlation between asbestosis rates and lung cancer rates in 38 cohorts in contrast to a poor correlation between cumulative exposure data and lung cancer relative risks in eight cohorts with adequate data. The evidence indicates that asbestosis is a much better predictor of excess lung cancer risk than measures of exposure and servers as a marker for attributable cases (22).

Despite these two reviews of the extant literature, there remains heated controversy on the issue. Recognizing the controversy, editors of the journal in which Dr. Weiss� article was published invited an editorial comment by opposing physicians who wrote:

Asbestosis is an indicator of high exposure and contributes additional risk to lung cancer beyond that conferred by sufficient asbestos exposure alone. In our opinion, the hypothesis that the excess lung cancer risk in worker cohorts exposed to asbestos occurs only among those with asbestosis is insufficient to explain this heightened risk of carcinogenicity (23).

Even accepting the Browne Hypothesis, the problem still arises as to how one defines and diagnoses asbestosis.

What Are The Standard Criteria For Diagnosis Asbestosis?

In the mid 1980s, the American Thoracic Society (ATS) helped formulate criteria for diagnosing asbestosis. In the ATS medical journal a group of experts proposed the following criteria for diagnosing asbestosis (24):

* A definite history of exposure to friable asbestos;
* A definite abnormal chest x-ray showing changes typical of asbestosis;
* A definitely abnormal breathing test, showing a certain degree of impairment that could be due to asbestos inhalation; and
* Findings on physical exam of the lungs compatible with the diagnosis and not due to some other condition.

The authors of the ATS article recognized that true asbestosis is a serious disease, for which there is no effective treatment. Patients are short of breath, at on exertion. They have unequivocally abnormal x-rays. They have abnormal breathing tests. The authors specifically chose not to let the diagnosis encompass �healthy� people with equivocal chest x-rays or smokers whose lung impairment was due to smoking.

Not all physicians agreed with these strict criteria, and at the time of publication there was already considerable debate (25). Understandably, some experts do not agree with the ATS criteria. They opine that the disease must be recognized early, before there are symptoms and before the chest x-ray is unequivocally abnormal. However, this position opens up a Pandora�s box of interpretation.

Currently, many physicians will not certify a diagnosis of asbestosis unless the findings meet the strict ATS criteria. However, other physicians will argue just as strong for less restrictive criteria. The result, of course, is not only medical controversy (26), but another reason for litigation.

What Are The Helsinki Criteria?

A group of experts met in Helsinki, Finland in January 1997 to �discuss disorders of the lung and pleura in association with asbestos and to agree upon state-of-the-art-criteria for their diagnosis and attribution with respect to asbestos.� Their report, nicknamed the Helsinki criteria, was published in a Scandinavian medical journal (27).

Prior to the Helsinki criteria, the only published consensus report about clinical diagnosis of asbestos diseases was the ATS article published in 1986. Unfortunately, the Helsinki report does not refer to the ATS article; also, it does not offer any new research or even any references to earlier research or opinion. For these reasons, the Helsinki report does not replace the 1986 ATS report and is at best an editorial comment by a group of international experts.

Principle points raised in the Helinski criteria article include:

* Reliable work histories provide the most practical and useful measures of exposure;
* A high resolution CT scan can facilitate detection of asbestosis and asbestos-related pleural abnormalities but is not recommend as a screening tool;
* New imaging techniques (MRI, gallium scanning, PET scanning) are not recommended for clinical diagnosis; and
* Radiological findings of small opacities, ILO grade 1/0, �are usually regarded as an early stage of asbestosis.� A score of �1/0� means some scarring (1)/ but may be normal (0).

This last point is in contrast to the ATS report, which opined that the threshold of diagnosis should be a radiologic score of 1/1 (i.e. some scarring/definitely not normal). However, the Helsinki report also states, �Smoking effects should be considered in the evaluation of early asbestosis.� This is a very important point often overlooked by people interpreting chest x-rays of known asbestos claimants.

How Are Claims Based Only On The Chest X-Ray?

Asbestosis is defined as lung tissue scarring from inhaled asbestos. Pleural plaques or pleural fibrosis is scarring of the lining of the lungs. These definitions seem straight forward, but how do we actually diagnose this scarring?

As already pointed out, direct examination of lung tissue for evidence of asbestos scarring (lung tissue from surgery or autopsy) is rarely performed. Instead, the vast majority of cases are diagnosed by �shadows� seen on the ordinary chest x-ray or chest CT scan (performed much less commonly than the chest x-ray). In this sense the diagnosis is usually inferential.

Inferential diagnosis is accepted when you have a classic presentation: unequivocal exposure history, unequivocal chest x-ray. Most of these patients were long ago diagnosed and what is left now are tens of thousands of workers and ex-workers whose exposure history and chest x-ray are far from unequivocal.

The majority of the remaining cases are equivocal. When you start with equivocal abnormalities on a chest x-ray, you are entering the realm of subjective interpretation and inherent biases. This is why many cases today often involve significant disagreement over chest x-ray interpretation and, ultimately, diagnosis (28).

Years ago, the US Department of Labor (DOL) set up a special program to train physicians to read chest x-rays of workers (principally coal miners) exposed to coal and silica dust. The goal of the training program was to bring some standards to the reading of the workers� chest x-rays and to identify those with early dust disease. Because these physicians passed Part B of EOL�s training course, they are collectively known as �B-Readers.�

Coal, silica and asbestos dust can all give similar shadows on the chest x-ray. For this reason B-Readers are usually called upon to read the chest x-rays of asbestos workers. There is wide-spread use of B-Readers in litigation involving asbestos claims. Yet studies have shown that B-Readers as a group display enormous variation in chest x-ray interpretation (29).

The problem is manifest most acutely in the thousands of claims that started with screening chest x-rays. This was often done in the 1980s and 1990s under the offer from plaintiff-oriented attorneys to provide free screening chest x-rays to factory workers and ex-workers where asbestos exposure was known. The goal was to look for asbestos-related disease. These chest x-rays were often sent to B-Reader physicians for interpretation. The chest x-ray were read with a mind-set of look for asbestos-related disease.

Whenever a B-Reader�s report indicated the possibility of asbestos disease, the attorney would seek to file suit on behalf of the worker against all the known asbestos suppliers of the worker�s factory. Some analyses of these cases conclude that the chest x-rays were often over-interpreted for asbestos-related disease (30).

What Results From Claims Based Only On The Chest X-Ray?

Much effort and expense is required by both the plaintiff and defendant in cases brought against suppliers for asbestos injury. Plaintiff attorneys claim that workers without symptoms deserve to be compensated if they have significant asbestos in their lungs due to an increased risk of asbestos-related diseases, including cancer. Defendants maintain that many of these cases do not even involve workers with asbestos disease evident on the chest x-ray.

The problem is in the interpretation of the chest x-ray. Smokers can have �shadows� that are often mis-interpreted as asbestos disease (31). Also, many other conditions, such as congestive heart failure, can mimic chest x-ray changes that are mis-interpreted as due to asbestos. This is particularly problematic in situations where the physicians reading the chest x-ray know nothing of the worker�s individual medical history.

Is There A Solution To The Asbestos-Litigation Problem?

Plaintiff attorneys, defense attorneys, medical experts, companies, and individuals exposed to asbestos all have differing opinions on how to resolve the matter. Several organizations have offered possible solutions to the problem.

The National Coalition for Asbestos Resolution presented a solution and a bill was presented to Congress addressing a resolution. The Association of Trial Lawyers of America opposed the Congressional bill. Further discussion will be required to reach a solution.

Notes

1. Levin, S.M., Kann, P.E., Lax, M.D. Medical examination for asbestos-related disease. Amer. J. Indust. Med. 2000; 37:6-22.

2. Mossman, B.T., Churg, A. Mechanisms in the pathogenesis of asbestosis and silicosis. State of the Art. Amer. J. Respir. Crit. Care Med. 1998; 157; 1666-1689.

3. Anderson, H.A., Lilis, R.L., Daum, S.M., et al. Household-contact asbestos neoplastic risk. Ann. NY Acad. Sci. 1976; 272:311-323.

4. Churg, A., Non-neoplastic asbestos-induced disease. Mt. Sinai J. Med. 1986: 53:409-415; Harber, P., Smitherman, J. Asbestosis: diagnostic dilution. J. Occup. Med. 1991; 33:786-93; Becklake, M.R. Asbestos and other fiber-related diseases of the lungs and pleura: distribution and determinants in exposed populations. Chest 1991; 100:248-254; Mossman, B.T., Churg, A. Mechanisms in the pathogenesis of asbestosis and silicosis, supra, note 2.

5. Friedman, A.C., Fiel, S.B., Fisher, M.S., et al. Asbestos-related pleural disease and asbestosis: A comparison of CT and chest radiography. Amer. J. Roentg. 1988; 150:269-275.

6. Gaenler, E.A., Jederlinic, P.J., Churg. A. Idiopathic pulmonary fibrosis in asbestos-exposed workers. Am. Rev. Respir. Dis. 1991; 144:689-696; See also Jones, R.N., Editorial: The diagnosis of asbestosis . Am. Rev. Resp. Dis. 1991; 144:477-478.

7. Selikoff, I.J., Chrug J., Hammond, E.C., Asbestos exposure and neoplasia, JAMA 964; 188:22-26; Selikoff, I.J., Chrug, J., Hammond, E.C. The occurrence of asbestosis among insulation workers in the United States. Ann. NY Acad. Sci. 1965; 132:139-155; Churg, A., Lung cancer cell type and asbestos exposure. JAMA 1985; 253: 2984-85; 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; Edelman, D.A. Does asbestosis increase the risk of lung cancer? Int. Arch. Occup. Environ. Health 1990; 62:345-9; Jones, R.N., Hughes, J.M., Weill, H. Asbestos exposure, asbestosis, and asbestos-attributable lung cancer. Thorax 51, 1996; Weiss, W. Asbestosis: A Marker for the Increased Risk of Lung Cancer Among Workers Exposed to Asbestos. Chest, February 1999; 115(2):536-549.

8. Churg A. Chrysotile, tremoline, and malignant mesothelioma in man. Chest 988: 93:621-628; Hillerdal G. Pleural malignancies including mesothelioma. Curr. Opin. Pulm. Med. 1995; 1:339-43. Metintas M., Hillerdal G., Metintas, S. Malignant mesothelioma due to environmental exposure to erionite: follow-up of a Turkish emigrant cohort. Eur. Respir. J. 1999; 13:523-6.

9. Metinas M., Hillerdal G., Metinas S., supra, note 8.

10. Neuberger, M., Kundi, M. Individual asbestos exposure: smoking and mortality � a cohort study in the asbestos cement industry. Brit. J. Indust. Med. 1990; 47:615-20.

11. Gross, T.J. Hunninghake, G.W. Idiopathic pulmonary fibrorsis. NEJM 2001; 345:517-525.

12. Gaensler, E.A., Jederlinic, P.J., Churg, A., Idiopathic pulmonary fibrosis in asbestos-exposed workers. Am. Rev. Respir. Dis. 1991; 14:689-696; See also Jones, R.N., Editorial: The diagnosis of asbestosis, supra, note 6.

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17. Supra, note 16.

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20. Jones, R.H., Hughes, J.M., Weill, H., supra note 7.

21. Supra, note 20.

22. Weiss, W., supra, note 19.

23. Banks, D.E., et al., supra, note 19.

24. Murphy, R.L.H., Jr., Becklake, M.R., Brooks, S.M., et al. The diagnosis of nonmalignant diseases related to asbestos. Official statement of the American Thoraic Society. Am. Rev. Resp. Dis. 1986, 136:1516-17.

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