Litigation Management

DISTINGUISHING BETWEEN ASBESTOSIS AND SILICOSIS:

A Lawyer’s Primer on the Proper Diagnosis of Each Disease

By F. Ford Loker, Esq. and Angela Whittaker-Pion, Esq.
Miles & Stockbridge P.C.

The aim of this paper is to identify a broad range of tests and findings in medical records that defense attorneys will need to masterunderstand in orderand be able to discuss the case inin depth with their chosen expert witnesses, as well as perform effective cross examination of plaintiffs' witnesses. Mentioning any aspect of the diagnosis of asbestos-related or silica-related maladies, particularly the more controversial findings, should not be interpreted as the authors’ endorsement of its relevance or efficacy.

Asbestos-related disease claims have been clogging American courthouses — but not doctors’ offices — since the 1970’s. In the past, progressive judges attempted innumerable “fixes,” none of which succeeded in clearing their dockets permanently. Even the litigants themselves tried to orchestrate a “global” settlement mechanism, but it was rejected by the United States Supreme Court — thus perpetuating the morass.

Now rumors are rife that the United States Congress, at long last, will legislate an end to the litigation crisis before any (or many) more bankruptcies take their toll on the owners, investors, and insurers of some of this country’s largest and most essential businesses. Equally widespread are rumors of the inevitable demise of the “Fairness in Asbestos Injury Resolution Act of 2005” (the “FAIR Act”), because the three chief constituencies affected — former producers of asbestos and asbestos-containing products, their insurers, and organized labor — cannot agree on (1) how many dollars the trust fund will need to compensate potentially hundreds of thousands of claimants; (2) which companies should contribute; (3) what amounts (or tiers) individual payers should contribute; and (4) over what period of time. This may be the classic example of the original proponents regretting what they wished for and launching a circular blame game to explain the impasse.

The Rand Corporation’s Institute for Civil Justice estimated that, through 2002, 730,000 people filed asbestos bodily injury claims, and defendant companies and insurers paid $70 billion in settlements and court judgments — with 59 percent of this amountit going to the attorneys on both sides. One hundred thousand moreAn additional 100,000 asbestos-related lawsuits were filed in 2003, and about 600,000 claims are pending. Actuaries project that, without government intervention, the cost of asbestos injury litigation could reach $265 billion. It is little wonder that certain entrepreneurial lawyers and operators of mobile screening trailers continue to salivate over the potential profits. They are not above testing medical and legal limits to bring more claimants into the system, nor are they above using the same tactics to increase case filings in silica litigation.

Prognosticators at both ends of the trial table suggest that even if “asbestos” goes away tomorrow, “silica” waits in the wings of the mass torts arena. It is precisely this dual disease issue whichissue that has most recently derailed swift passage the FAIR Act.¹

Asbestos and silica have been used since Biblical times in countless industrial, commercial, and residential applications and products. Both are naturally occurring minerals in virtually inexhaustible supply. Both are relatively inexpensive and thus desirable ingredients in many thousands of products. Neither substance, nor the illness claims they spawn, is going to exit the stage of American courtroom drama any time soon. To equip juries with the facts to reach correct verdicts, defense lawyers first must understand which diagnostic tools are employed to differentiate between illnesses caused by asbestos and silica. If the attorneys do not perceive the differences, they cannot educate juries on the subtle differences between asbestosis and silicosis. Uninformed jurors might saddle one industry with paying for the illnesses of the other — or even worse, allow double windfalls for a single, distinct condition.

The relatively recent wave of silica-related lawsuit filings around the country, perhaps not surprisingly, has increased in direct proportion to rumors that the FAIR Act of 2005 would be enacted. So too might the up-tick in silica cases beSimilarly, the up-tick in silica cases might be linked to asbestos-related tort reform legislation in several of the more active and problematic states. For example, in Texas, Mississippi, Georgia, Illinois, Ohio, and Florida, there are ongoing efforts to tighten venue rules, eliminate forum shopping, and require objective indicia signs of impairment before an asbestosis or pleural plaque claim gets receives a trial date. Are the silicosis claims “real,” or are some folks hedging their bets, should an asbestos compensation fund or other tort reforms leave them out in the cold? Paradoxically, silica-related deaths are decreasing,² while silicosis case filings are sky-rocketingskyrocketing. The silica plaintiffs’ bar seems intent on following the path of least resistance by forcing the round peg of silicosis into the square hole of asbestosis. Fitting them both into the same mold will not do justice to either disease and lead to unnecessary frustration and confusion by courts, attorneys, and jurors alike.

Mass screening for asbestos-exposed workers proved so lucrative, that it was little wonder that the same laboratories, the same clinicians, the same x-ray readers, and the same law firms went back to the same well to tap into the same reservoir of alleged dust diseasedust-disease victims. Mobile screening vans, with portable x-ray and spirometry equipment sharing space with the sponsoring lawfirm’s intake desk, were parked at union halls, motels, and shopping centers around the country. Reportedly, the persons screened were not asked to pay for the tests. No one can argue that such a one-stop operation is very “customer-friendly.” Positive test results could turn a patient into plaintiff, before the mobile “lab” drove to its next location.

The screenings focused heavily on chest radiographs that were funneled to a few select “B-readers.” A relatively recent phenomenon has the B-reader who looks for silica exposure also documenting asbestos exposure, and vice versa. If the x-ray is not clear for either mineral, the increasingly popular diagnosis of mixed-dust pneumoconiosis (“MDP”) may be recorded. Re-screening of individuals already diagnosed with a nonmalignant asbestos lung disease (“ALD”) is turning up diagnoses of silicosis or MDP, either in an heretofore missed conjunction of maladies or, even more remarkably, some reports in previously diagnosed cases of ALD find no trace of asbestosis, only evidence of silicosisonly evidence of silicosis and no trace of asbestosis in previously diagnosed cases of ALD. Thise finding has led to a joke making the rounds among counsel handling dust-disease cases: the cure for asbestosis finally has been found, — it’s silicosis!

Although a topic meriting its own article, it bears mentioning here in passing that at least one court is turning an increasingly critical eye upon the legitimacy of mass screenings. Federal District Judge Janis Graham Jack presides over In Re: Silica Products Liability Litigation, MDL No. 1553 (S.D. Texas), encompassing nearly 10,000 silica injury claims. In mid-February Judge Jack conducted three days of well-publicized hearings into the accuracy and propriety of silica screenings.³ She was clearly shocked by the potentially fraudulent practices conducted by several prominent screening outfits and B-readers. Defense lawyers have filed a motion seeking $1.1 million in sanctions from the plaintiffs’ lawyers for “knowingly submitting and advocating bogus diagnoses.” Judge Jack is expected to issue a 100 page100-page opinion on these matters to guide other courts around the country, particularly those courts that may receive the cases on remand. More conscientious jurists like Judge Jack are needed to shut down this mass tort locomotive completely before it leaves the station. Can lessons learned from the wholesale run-up of unimpaired ALD suits be implemented in time to avoid repeating the same mistake for silica exposures?

Despite certain similarities in exposure settings, diagnostic tools, and symptomology, asbestosis and silicosis are quite distinctive forms of pneumoconiosis.⁴ As far as similarities, both asbestos and crystalline silica (quartz) exposure can occur in a wide variety of occupational settings. The development of the respiratory symptoms associated with both of these minerals is dependent upon both the intensity and duration of the exposures (many significantly exposed workers, however, will never develop any occupational lung disease). Thus there are similarities between asbestos and silica, and the nonmalignant diseases associated with them. Yet itIt is the differences between them, however, that isare the focus of the remainder of this article.

Comparison Between Asbestos/Asbestosis and Silica/Silicosis

Significant occupational or environmental exposures to asbestos and silica can cause non-malignantnonmalignant respiratory disease – asbestosis and silicosis, respectively. As mentioned earlier, the size and shape of the dust particle as well as the proximity of the exposed individual to the dust source are key to the development of the illness. Dose is not simply the concentration of asbestos or silica in the atmosphere; rather, it is the number of particles or fibers in the subject’s breathing zone actually inhaled and deposited in the periphery of the bronchial tree. Lungs are not harmed without inhalation of the dust.

Silicosis and asbestosis are both interstitial lung diseases. Interstitial lung disease, or interstitial pulmonary fibrosis, is a generic term that includes a whole hostmultitude of chronic lung disorders, many caused by inhaled particulates, others by genetic abnormalities, and still others of either idiopathic or unknown origin. Virtually all such maladies produce a common patient complaint or symptom — shortness of breath, sometimes reported in medical records as “dyspnea on exertion.” This is simply feeling more breathless than similarly situated persons with healthy lung function, or than the patient experienced prior to the onset of disease. Because these diseases share certain common features, the comparison between these two diseases can generate confusion among lawyers, judges, and juries. Most independent medical experts would agree, however, that, outside of the litigation setting, clinicians are rarely confused in diagnosing silicosis or asbestosis.⁵

Most of the other diseases — particularly the malignancies — associated with either asbestos or silica inhalation lack the common features of the pneumoconioses. Asbestos exposure had been causally associated with diffuse malignant mesothelioma, for example, but silica exposure has not. Silica exposure has been associated with several autoimmune disorders, and even tuberculosis (“TB”). Diseases such as scleroderma, scleraderma systemic lupus erythematosus (SLE), or TB are not caused by asbestos. Lung cancer arguably, especially in the litigation context, may be an area of dual association. Although lawyers may argue that lung cancer can be attributed to either asbestos or silica exposure, unbiased scientists tend to disagree. There is wide agreement among experts in pulmonary diseases that lung cancer in an individual (even a smoker) with full-blown asbestosis can be attributed in part to inhalation of asbestos fibers. However, there is no such consensus over whether exposure to silica has the ability to induce lung cancer.

Silica and Silicosis

Silica — also known as highly purified quartz or silicon dioxide (SiO2) — is the most common and abundant mineral in the earth’s crust. It is common sand. It is, found in abundance in gravel and all types of soils. Our beaches are nothing more than natural silica deposits, and silica is a constituent of the vast majority the earth’s rocks. Silica is also commonly found in mines. Commercial applications of silica are virtually limitless. It has been used as an industrial sand in foundry, sandblasting, and countless other manufacturing operations. If crystals of silica or sand are split into tiny enough particles, they can be inhaled deep into the lungs and later pose health risks.

The most common disease associated with silica exposure is silicosis (nodular pulmonary fibrosis). Silicosis can be asymptomatic and does not inevitably progress in severity. In essence, if an individual breathes in enough microscopic crystals of silica, the natural defense mechanisms of his respiratory system can be overwhelmed.⁶ Silicosis depends upon dose — the intensity and duration of exposure. It is “dose-related,” meaning the higher the amount of inhaled silica, the higher the risk of developing the disease. Confounding the prediction equation, however, is the wild card of individual variation or biosusceptiability among humans. This is seen, for example, in smokers, where the ten yearten-year one-pack-a-day smoker may get develop lung cancer, while the three-pack-a-day smoker shows no signs of illness. Because of differences in dose and variability of hosts, making accurate projections of disease is not possible, from even from known levels of silica exposure. is not possible

Silicosis can occur in three different forms, depending upon the airborne concentration of respirable crystalline silica: chronic silicosis (subdivided into simple or complicated forms), accelerated silicosis, and acute silicosis.

David Weill, M.D., Associate Professor of Medicine in the Pulmonary and Critical Care Division at the University of Colorado Health Sciences Center, in his statement before the Senate Committee on the Judiciary Concerning Asbestos: Mixed Dust and FELA issues, explained:

Chronic simple silicosis is the most common form of the disease in the United States today. Chronic silicosis, in its simple form, typically requires more than twenty years of moderate exposure. It is characterized by rounded nodules, like tiny marbles, principally in the upper lobes of the lungs. In its lower grade forms, simple silicosis does not generally result in respiratory impairment. It may progress, or become more serious over time, especially in workers who continue to be exposed to silica. However, progression tends to be slow and depends on several factors.

In the complicated form of chronic silicosis, the small rounded nodules found in simple silicosis form conglomerate lesions, whose largest diameter exceeds [one] centimeter. Most patients with complicated silicosis have respiratory impairment with abnormal pulmonary function test findings typically indicating lung “restriction” or a reduction in the lungs’ capacity for inhaled air. Accompanying airway obstruction is not uncommon. Rare today, accelerated silicosis results from higher exposure to silica, usually over a period of five to ten years. This form of the disease may progress whether or not continued workplace exposure occurs. Chest x-rays can show either a pattern of small rounded nodules alone or in conjunction with larger conglomerate opacities.

These patterns may be described as small areas of inflammation and / or scarring. “Complicated” silicosis typically occurs in less than five percent of simple silicosis cases. Chronic simple silicosis is the most common diagnosis of those workers bringing claims after a mass screening;, as such, it will be the main focus of the comparison to asbestosis.

“Accelerated” silicosis can develop five to ten years after initial exposure to silica. Individuals with accelerated silicosis can experience breathlessness, weakness, chest pain, cough, and sputum production. The radiographic appearance and symptoms of accelerated silicosis and acute silicosis are similar, but the clinical and radiographic progression of accelerated silicosis is rapid. Unlike chronic silicosis, accelerated silicosis forms an irregular fibrosis appearance. Accelerated silicosis can be serious. When death occurs from accelerated silicosis, it is usually caused by hypoxic respiratory failure.

In his statement before the Senate Committee, Dr. Weill explained acute silicosis (sometimes referred to as “silicoproteinosis”) as:

… [A] rapidly progressive, fatal disease. It occurs after massive exposures, over a relatively short period of time, from several months to a few years. In acute silicosis, the spaces in the lung where oxygen exchange takes place (the “alveoli”) become filled with fluid and cells.

Accelerated and acute silicosis are rarely found in developed countries today, although there have been case reports many years ago of acute silicosis among sandblasters and workers drilling through silica-containing rock.

Some of the typical occupational exposures to silica include: sandblasting, foundry work, refractory work, silica flour work, glass manufacturing, ceramic manufacturing, mining, quarrying or tunneling, stone cutting, abrasive manufacturing, and abrasive blasting.

Asbestos and Asbestosis

“Asbestos” is not a precise scientific term. Rather, it is used to describe certain “families” of fibrous silicates, most with commercial applications. A fiber is characterized as having an aspect ratio where in which the length is three or more times the width. Asbestos-bearing rock requires extensive mining and milling to remove the waste and to separate the fiber bundles into acceptable grades and sizes. It makes an excellent binder or matrix for many products and is an excellent heat insulator. It is flame resistant and impervious to attack by many common acids and corrosives. For years, it was called “The Magic Mineral” and was incorporated into countless products as varied as theatre curtains, oven pads, cigarette filters, and spray-on fireproofing.

There are two main branches in the asbestos family tree: serpentine, where chrysotile (white) is the sole fiber type, and amphibole, consisting of both amosite (brown) and crocidolite (blue) fiber types. These three fiber types have the most commercial uses. The non-commercialnoncommercial amphiboles include anthophyllite, actinolite, and tremolite — the latter being a common contaminant of chrysotile deposits. Serpentine fibers are relatively long and curly. The amphiboles by comparison are shorter and more “spiky.” Size is relative. “Long” might be 25 to 30 microns and short fibers are less than five microns in length. Respirable particles (not fibers) of silica by contrast are generally about ten microns across.⁷ Sophisticated light and electronic microscopy techniques are essential to visualizing individual fibers or particles in either environmental samples or in lung tissue.

Whereas silicosis is characterized by the presence of small nodules of scar tissue, usually in the apex of the lung, asbestosis involves diffuse interstitial fibrosis — typically bilateral at the bases of the lung parenchyma. The lesions form where gas exchange occurs, and the pattern is called intra-alveolar or peribronchiolar scarring. Chest x-rays of lungs of asbestotics show a hazy, ground-glass appearance of irregular, reticular (linear) densities. As its name implies, only “asbestos” causes asbestosis. All forms of asbestos fiber — serpentine and amphibole — are implicated, and all asbestos diseases are dose-related.

Asbestosis most often causes an objectively measurable confirmation of the patient’s complaint of shortness of breath; namely, a “restrictive ventilatory defect” on pulmonary function tests (“PFTs”).⁸ In its recent and somewhat controversial pronouncement, the American Thoracic Society (“ATS”) re-issued diagnostic criteria for nonmalignant asbestos lung disease. This 2004 document indicated that asbestosis also can manifest as an obstructive ventilatory defect — where the rate of air flowairflow, as opposed to the volume of air, is reduced. These new ATS criteriia even permit “mixed restrictive/obstructive” PFT results to support a diagnosis. Only time will tell whether the new ATS criteria will find as wide acceptance as its 1986 version. ⁹ Asbestosis can also lead to a decrease in diffusion capacity (DlCODLCO < 80% of predicted value), although a whole host ofnumerous other pulmonary conditions also impair gas exchange, such as lung damage from cigarette smoking — chronic obstructive pulmonary disease (“COPD”) and emphysema.

Possibility of Having Both Diseases

Dr. Weill’s statement before the Senate Committee echoes the views of Drs. Paul Epstein and Laura Welch at footnote 5 herein:

Although asbestosis and silicosis are different diseases that look different on x-ray films, it is theoretically possible for one person to have both diseases. A person could be exposed to both silica and asbestos in sufficient quantities to cause either disease, but it would be extremely unusual for one person in a working lifetime to have sufficient exposure to both types of dust to cause both diseases.

Elements of the Differential Diagnoses

Overview

In general, because lung tissue often is not available in suspected cases of either silicosis or asbestosis, the diagnosis of either condition is based upon four interrelated clinical criteria: (1) a reliable occupational history, including sufficient latency (the appropriate time interval between exposure and detection of disease) to cause disease; (2) a physical examination; (3) the presence of characteristic chest x-ray evidence, or radiographic abnormalities consistent with the disease; and (4) the exclusion of other pulmonary diseases that can mimic either disease radiographically (e.g., sarcoidosis, fungal disease, berylliosis). Although a physician does not rely solely on a chest film to diagnose either illness, clear distinctions in the appearance and predominance of scarring caused by asbestosis, compared to silicosis, are well known. The chest x-ray alone is the tool whichtool that differentiates the shapes and patterns of opacities. Although several important differences exist that can distinguish radiographically between silicosis and asbestosis, there appears to be a predisposition among certain medical experts to ignore or minimize these differences.

Again, Dr. Weill explained it succinctly:

In evaluating pneumoconioses, chest x-rays are normally interpreted using the International [Labor Office Organization] (“ILO”) radiograph classification system.¹⁰ The purpose of the ILO system was to standardize the interpretation of chest x-rays using descriptions of the size, shape, and degree of involvement (i.e., the profusion) of radiographic abnormalities. The system is used to describe shape (regular or irregular) and size (regular: p, q, r, and irregular: s, t, u) characteristics of radiographic abnormalities. The extent of radiographic abnormalities (profusion) is numbered from normal (or 0) to increasingly abnormal (1, 2, and 3). The ILO classification scheme also addresses which of the six lung zones are involved (upper, middle, and lower in either the right or left lung). Also, particularly important when distinguishing between asbestosis and silicosis, the presence and type of pleural abnormalities are noted.¹¹

As discussed above, chronic (simple) silicosis produces silicotic inflammatory lesions, which appear as tiny round opacities, primarily in the upper zones of both lungs. Dr. Weill explained that:

“[o]n an x-ray, these nodules show up as small, rounded opacities, which would be rated on the ILO form as p, q, or r. In contrast, asbestosis is characterized by linear parenchymal fibrosis, which shows up on an x-ray as small irregular opacities [and rated on the ILO form as] (s, t, or u), primarily in the lower lobes of both lungs.

[c]hronic (complicated) silicosis is even harder to confuse with asbestosis on chest x-rays than is the simple form of the disease. In complicated silicosis, the tiny round nodules found in simple silicosis join together and the opacities that show up on the x-ray film are large…

Asbestosis does not appear on x-ray as similar large opacities or amalgamations of tiny scars that have merged into large ones.

Beyond the x-ray appearance of interstitial changes, asbestos exposure can lead to pleural plaques or pleural thickening. Silica does not lead to these pleural changes. Advanced asbestosis may appear as “honeycombing” of the parenchyma. Silicosis can exhibit a distinctive “eggshell calcification” pattern, and lymph node enlargement is common. Dr. Weill explained:

Not only are these appearances different in individual cases, these two broad radiographic patterns point one toward entirely different diagnostic categories. Diseases other than asbestosis fall into the reticular group. Examples include…idiopathic pulmonary fibrosis, radiation pneumonitis,…chronicpneumonitis…chronic hypersensitivity pneumonitis, chemotherapy-induced lung disease, [and scleroderma]. Diseases other than silicosis fall into the nodular group, including sarcoidosis, berylliosis, coal workers’ pneumoconiosis,…metasticpneumoconiosis…metastatic cancer, [and hystoplasmosishistoplasmosis].

With the right experts, opposing counsel will generate opinions that wrestle inconsistent clinical findings into the diagnosis that fits the lawsuit. There is the safe haven of "inter-reader variability" to explain anomalous findings.¹² The biased expert also can attempt to explain inconsistent findings on the basis of individual susceptibility, much as the ATS now accepts mixed restriction and obstruction on PFTs as evidence of asbestosis. If the courts are effective “gatekeepers,” applying the Daubert test assiduously, such bogus opinions will be stricken. Too often, courts allow such opinions into evidence “for what it is worth” —- small consolation for the defendant in a hostile jurisdiction. In truth, there are clear differences in the manifestation of asbestos- and silica- relatedsilica-related diseases. No honest diagnostician should confuse them. From pathologic, radiographic, and clinical perspectives, asbestosis and silicosis are very distinct diseases.

Differences

ASBESTOS	SICICA
Mesothelioma	No Mesothelioma
No Tuberculosis	Tuberculosis (and other fungal infections; e.g., histoplasmosis, coccidiomycosis)
Laryngeal and certain GI Cancers	Autoimmune Disease (rheumatoid arthritic, lupus, scleroderma, etc.)
Lower lung predominates	Upper and mid lung predominates
Irregular opacities (s, t, u on ILO form)	Rounded opacities (p, q, r on ILO form)
Pleural plaques which may calcify	No calcified plaques
No coalescence of opacities	Coalescence of round opacities
No large opacities	Large opacities
No hilar adenopathy	Hilar adenopathy
No mediastinal adenopathy	Mediastinal adenopathy
No eggshell calcification	Eggshell calcification
Honeycombing	Compensatory emphysema

Finding the Guideposts in Clinical Records

Because (1) silicosis and asbestosis can be found among workers with similar occupational histories, (2) these workers may have been exposed to a multitude of other pneumoconiosis-producing agents on the job, and (3) these workers share other similarities (including widespread tobacco use), it is logical that there be numerous findings for the clinician charged with making the correct diagnosis to tease apartthe clinician charged with making the correct diagnosis would have numerous findings to tease apart. Asbestosis and silicosis are "diagnoses of exclusion," meaning that all other potential causes of the symptoms and clinical findings need to be eliminated. To evaluate the thoroughness of the clinical work-up of either an asbestosis or a silicosis case — regardless of whether it is performed by one of the "entrepreneurial" screening labs, the plaintiff's own family doctor, or the defense IME expert ,— here are the basic elements that should be covered:
1. Chief Complaints
  
  Shortness of Breath
  Dyspnea on Exertion
  Changes in Daily Routines
  Onset of Symptoms, and Associated Activity
  Cough — Dry vs. Productive
  Cough — Chronic (e.g. lasting > 6 weeks) vs. Acute Onset
  Wheezing
  Snoring
2. Past Medical History
  
  Hospitalizations and Surgeries
  Chronic Illnesses
  Cancer
  Allergies
  Accidents (broken ribs)
  Social Habits (alcohol and tobacco)
  Illegal Drug Use
3. Review of Systems
  1. Respiratory
    
    Asthma
    Tuberculosis (positive skin test, exposure to others)
    Pneumonia
    Fungal Infections (raised pigeons or chickens, mold)
    AidsAIDS
    Sleep Apnea
  2. Cardiovascular
    
    Myocardial Infarction (heart attack)
    Bypass Graft / Stent Placement
    Stroke
    Emboli
    Deep Venous Thrombosis
    Angina
    Arrhythmias
    Pace maker / Defibrillator implanted
    Paroxysmal Nocturnal Dyspnea (sensation of waking up, gasping for air, or bolting to sitting position in bed to restore breathing)
    Intermittent Claudication (leg pain/difficulty walking)
    Congestive Heart Failure (ischemic heart disease, pedal edema /(i.e. swollen ankles))
    Orthopnea (sleeping on two or more pillows)
  3. Neurological and Musculoskeletal
    
    Arthritis (Rheumatoid or Degenerative)
    Kyphosis / Scoliosis of the Spine
    Rib Fractures
    Joint Pain or Deformity
    Simple Deconditioning (too painful to walk or regularly exercise, (“out of shape”))
    Obesity
  4. Endocrine
    
    Diabetes Mellitus
    Steroid Therapy
    Hypo- or Hyperthyroidism
4. Family History
  
  Health status of parents/siblings, cause of and age at death
  Cancer clusters among blood relatives
  Residences (from childhood to present, toxins, molds, lead paint, asbestos)
  Secondary or take-home dust exposures
  Exposure to secondhand smoke
  Unusual hobbies, activities (such as model railroads with asbestos “mountains”)
  Dusty hobbies (woodworking)
  Pesticide exposures (agriculture agricultural family)
5. Occupational History ¹³
  
  All jobs
  Direct vs. Indirect Exposures
  Bystander vs. Mechanic
  All harmful agents in work place
  Ventilation
  Regularity, Frequency, Duration, Intensity (of all harmful exposures)
  Periodic or Employment Physicals, X-rays, PFTs
6. Physical Examination
  
  General appearance (in the pink or “sickly”)
  Healthy Complexion and Skin
  Head, Eyes, Ears, Nose
  Mentally Oriented
  Normal Gait and Agility
  Distressed/ /Labored Breathing
  Number and Quality of Respirations
  Vital Signs (pulse, blood pressure, temperature)
  Palpation and Auscultation of the Chest (rales, crackles) Rales or Crackles
  Breath Sounds (wheezes, rasps, distant)
  Heart Sounds (skips, murmurs, gallops, bruits)
  Abdomen (obesity, enlarged liver/, spleen)
  Extremities (clubbing, cyanosis)
  Surgical Scars
  Central nervous system evaluation
7. Laboratory Tests
  1. Chest Radiographs (X-rays, CT Scans, Hi-Resolution CTs)
    
    Current and Historical
    Positioning (AP, PA, Lateral, Supine, Prone)
    Film Quality
    B-reading
    Parenchymal Abnormalities
    Pleural Abnormalities
    Skeletal or Cardiac Abnormalities
    Diaphragmatic Abnormalities
    Bilateral Symmetry or Defect
    Carcinoma/masses
    Accumulation of Fluid
  2. Pulmonary Function Testing¹⁴
    
    Current and Historical
    Historical Consistency or Progression
    Reliable Lad Lab and Equipment
    Experienced Technician
    Raw Data Reproducibility (consistent flow curves from which predicted values selected)
    Accurate Age, Weight, Race and Patient Data Recorded
  3. Spirometry¹⁵
    
    FVC
    FEV1
    FEV1 / FVC
    FEF 25% - 75% — - for small airway function
    FEF 75%
  4. Lung Volumes
    
    Plethysmography (Body Box)
    Helium or Nitrogen Dilution
    TLC
    FRC
    ERV
    RV
    RV/TLC
    AV
  5. Diffusion Capacity
    
    Is volume consistent with other PFTs?
    Is DlCODLCO corrected for alveolar volume (AV)?
8. Invasive Procedures
  
  Bronchoscopy
  Biopsy (needle or open)
  Bronchoalveolar Lavage
  Thoracentesis
  Thoracoscopy
  Closed Pleural Biopsy

Other Pneumoconioses/Mixed Dust Pneumoconioses

The advent of the plaintiffs' bar filing "mixed dust" cases makes discussion of the unusual condition, mixed-dust pneumoconiosis (“MDP”), and other pneumoconioses relevant. Many times, after a screening, a worker will be diagnosed with silicosis, asbestosis, or the common catch all, MDP. Inorganic dusts cause several potentially-relatedpotentially related but different types of lung disease. There are over one hundred causes of diffuse interstitial lung disease. MDPs will occur when lung disease is produced , after inhaling two or more dusts through a number of dust exposures, lung disease is produced. Of course, the first step in determining what, if any, disease may be present requires conducting a differential diagnosis, that is, a determination of which of two or more diseases with similar symptoms is the one from which the person is suffering. A diagnosis of MDP ideally is supported by the identification and quantification of inorganic particulates in lung tissue, and in any event, must include x-rays where mixed dustmixed-dust fibrotic nodules predominate over all other linear and/or rounded opacities.

In December, 2004, researchers of pulmonary diseases produced a consensus paper in the journal, Human Pathology. Authors include numerous internationally prominent experts frequently appearing on both sides of asbestos lawsuits, including Victor L. Roggli, M.D., Jerrold L. Abraham, M.D., and Allen R. Gibbs, M.D. They summarize the main features of MDP in the Abstract:

We defined mixed-dust pneumoconiosis (MDP) pathologically as pneumoconiosis showing dust macules of mixed-dust fibrotic nodules (MDF), with or without silicotic nodules (SN), in an individual with a history of exposure to mixed dust....According to our definition of MDP, therefore MDF should outnumber SN in the lung to make the pathologic diagnosis of MDP....The clinical diagnosis of MDP requires the exclusion of other welldefined pneumoconioses....Irregular opacities are the major radiographic findings in MDP (ILO 1980), in contrast to silicosis, in which small rounded opacities predominate. Clinical symptoms of MDP are nonspecific. MDP must be distinguished from a variety of nonoccupational interstitial pulmonary disorders.

Honma, K. et al., "Proposed Criteria for Mixed-dust Pneumoconiosis: Definition, Descriptions and Guidelines for Pathologic Diagnosis and Clinical Correlation, " HUMAN PATHOLOGY, 35 (2004); 1515-23.

Many of the occupational exposure sites and occupations normally associated with silica and asbestos exposures are also considered potential mixed dustmixed-dust locations, including mines, quarries, steel mills, construction sites, shipyards, gypsum rock mines, zinc mills, foundries, titanium manufacturing facilities, sandblasting operations, and iron working operations. Many timesFrequently, a worker will have mixed exposures, and as a result, it is necessary to be thorough in determining whether (and what) other conditions exist in the worker, and whether injury from silica exposure can be eliminated as a cause.

Numerous substances have been alleged to contribute to mixed- dust pneumoconiosis. In addition to silica and asbestos, some of these substances include: talc (found in certain paints, rubber, ceramics, pharmaceuticals, insecticides, cosmetics, and lubricants), kaolin (China clay, found in certain ceramics, paper, paint, cement, soaps, and sometimes used as a binding agent added to silica sand), fuller's earth (found binder/filler used in refining oils as a binder filler and filler in cosmetics), and mica (aluminum silicates that are sometimes ground up in paper and paint).

Other potential substances include: bentonite (exposures can occur during oil well drilling; and bentonite may also be used as a binding agent added to silica sand), gypsum (plasterboard), vermiculite (insulators), beryllium (metals), cadmium (pigments, paints, ceramics, glass, plastics, and leather), manganese (mining and crushing), and nickel (electroplating, enamels).

Although beyond the scope of this article, when diagnosing lung disease, it is also important to keep in mind that, depending upon the person's exposure history, certain fungal, animal, chemical, bacterial, and unknown causes that are associated with lung injury and mimic those caused by dust also must be ruled out when diagnosing lung disease, in addition to the more traditional diseases associated with exposure to silica, asbestos, and other minerals, elements, or compounds.

CONCLUSION

Of course, engaging the best medical experts in the field of diagnosing pneumoconioses is essential, but legal practitioners will not know whom to call without the basic understanding of the clues buried in a plaintiff’s medical records. Utilization of clinically experienced medical information specialists to uncover, analyze, and summarize these critical pieces of information should be strongly considered. Until defense counsel recognize the key differences between asbestosis and silicosis, and have the underlying factual data to clearly differentiate the two disease processes, they will be significantly limited in their abilitypowerless to cross-examine their adversary's hired gun so as to expose a his bogus diagnosis. Before defendants are subjected to the risk and expense of mass tort litigation over anything as amorphous and commonplace as "dust exposure," appreciating the differences among illness-producing agents is all-important. Was the culprit asbestos, or was it silica? Perhaps the better question would beis: W, was it tobacco, or beryllium, or talc, or kaolin, or mica, or portland cement, or nickel, or rust, or cotton, or coal, or ... any of dozens of other minerals, chemicals and organic compounds commonly found in the American workplace throughout the Twentieth Century?. Applying the appropriate legal analysis to the critical information culled from the underlying medical documentation will ensure the greatest likelihood of success in the defense of these ever expandingproliferating lawsuits.

About the Authors:

F. Ford Loker is a principal in the Baltimore office of Miles & Stockbridge P.C. He maintains a general litigation practice concentrating in mass tort and industry-wide litigation, as well as matters involving class actions, products liability, negligence and insurance. He may be reached at floker@milesstockbridge.com.

Angela Whittaker-Pion is an associate in the Baltimore office of Miles & Stockbridge P.C. Her practice focuses on litigation involving multiple parties, multiple claims, and allocation of liability among related corporate entities. She may be reached at awhittaker@milesstockbridge.com.

The views expressed herein are solely those of the authors and are not made on behalf of any of their clients.

SELECTED REFERENCES

Hearing before the Senate Committee on the Judiciary Condemning Asbestos: Mixed Dust and FELA Issues, 109th Cong. (2005) (Statement of David Weill, M.D., Associate Professor, Division of Pulmonary and Critical Care Medicine, University of Colorado, Health Sciences Center, Denver, Colorado.

Mark Behrens, et al, Silica: An Overview of Exposure and Litigation in the United States (2005).

James P. McFadden, A.B. & Robert Cohen, M.D., The Pathogenesis of Silicosis and Asbestosis:

Similarities and Differences as Shown on Chest X-Ray Films, Harris Martin Columns: Silica (August 2003) at 4.

Thomas J. Tobin, The Closer You Look, the Less You May Know: The Ever-Expanding Universe of Interstitial Lung Disease, Harris Martin Columns: Silica (September 2003) at 2.

Claire Wilkinson & Robert P. Hartwig, Ph.D., An Overview of Silica Liability from the Insurance Information Institute, Harris Martin Columns: Silica (September 2004) at 2.

David Weill, M.D., Silica and Asbestos: Similarities and Differences from a Medical Perspective, Mealey's Litigation Report: Silica Vol. 3, No. 2 (October 2004) at 21.

Fred D. Pooley, "Mineralology of asbestosAsbestos: the Physical and Chemical Properties of the Dusts They Form," Seminars in Oncology, 1981; 8: 243- 49.

American Thoracic Society, "Diagnosis and Initial Management of Nonmalignant Diseases Related to Asbestos," AM. JOUR. of RESPIR. and CRITICAL CARE MED. 2004; 170: 691-715.

American Thoracic Society, "The Diagnosis of Nonmalignant Diseases Related to Asbestos," AM REV RESPIR. DIS. 1986; 134: 363-368.

American Thoracic Society, Committee of the Scientific Assembly on Environmental and Occupational Health, "Adverse Effects of Crystalline Silica Exposure," AM. JOUR. of RESPIR. and CRITICAL CARE MED. 1997; 155: 761 et seq.

American Thoracic Society, Committee of the Scientific Assembly on Environmental and Occupational Health, “Adverse Effects of Crystalline Silica Exposure,” AM. JOUR. of RESPIR. and CRITICAL CARE MED. 1997; 155: 761 et seq.

¹ Greg Gordon, the Star Tribune’s Washington Bureau Correspondent, wrote on February 3, 2005, an article entitled: “Asbestos: Some lawyers accused of double-dipping” in which he stated: “‘It’s no accident that claims over silica dust diseases have soared as Congress has edged toward adopting legislation settling the nation’s asbestos injury suits,’ a legal scholar told Congress on Wednesday. Lester Brickman, a law professor at New York’s Yeshiva University, accused lawyers of engaging in ‘“entrepreneurial, if not fraudulent,’ double-dipping. Appearing before the Senate Judiciary Committee, he cited data showing that 60 percent of 8,629 plaintiffs in a mass silicosis case in Corpus Christi, Texas, had also filed asbestos claims with Johns Manville Corp.’s asbestos bankruptcy trust. Hundreds of companies and their insurers want to permanently cap their mounting asbestos liabilities. But they have voiced concerns that a small number of unscrupulous lawyers could make an end-run around a trust fund by finding doctors willing to label their clients’ illnesses as silicosis or other dust-borne diseases, so they can stay in the court system.”

² Sean F. Mooney included the NIOSH chart attached as Exhibit 1 in Silica: A Litigation Sandstorm, Harris Martin’s Columns: Silica (February, 2005). The chart indicates a dramatic drop in deaths caused (at least in part) by silica between 1968 (1157) and 1996 1999 (187).

³ A blizzard of news reports have has come out of these hearings in Corpus Christi, Texas. Judge Jack is quoted as commenting during the February 17, 2005 examination of Ray Harron, M.D., a B-reader in West Virginia, who had his secretary rubber stamp his signature to over 2500 silicosis diagnoses, that the doctor’s testimony was “raising great red flags of fraud.” See e.g., article by Neal Falgoust in February 18, 2005 edition of Caller-Times, “Case Judge: ‘Red flags of fraud’ are raised.” The hearing was recessed at Dr. Harron’s request to allow him to consult with his personal counsel.

⁴ Pneumoconiosis encompasses any disease causing scarring of the parenchyma of the lung from the inhalation of “dust.” Virtually any dust can cause a pneumoconiosis, if the dust particle is small enough to reach the areas deep within the lung where air exchange occurs and if the dose is sufficient to defeat the body’s several defense mechanisms.

⁵ According to the transcript of the congressional hearing on the FAIR Act of 2005, on February 2, 2005, Paul Epstein, M.D. characterized the “dual occurrences of asbestosis and silicosis are clinical raretyrarity.” Laura Welch, M.D., who frequently is called as a plaintiff’s expert in asbestos trials, testified at the same hearing, “Asbestosis and silicosis really are different diseases, and they’re separable from each other based on the history of exposure, the chest x-ray and pulmonary function test.” Dr. Welch identified herself as the medical director for the Center to Protect Workers’ Rights, an institute affiliated with the building and construction trades of the AFL-CIO.

⁶ All humans have defenses to combat the effects of the ubiquitous “impurities” in the air, such as the mucociliary escalator, the moist linings of the nasal passages and throat, and macrophages — scavenger cells that prowl the alveolar sacs in search of foreign objects like pollen, bacteria, viruses, and dust to engulf and eliminate.

⁷ A micron or micrometer is one millionth of a meter.

⁸ Restriction, as the name implies, is the reduction in the total volume of the lungs of the patient compared to so-called predicted values. The predicted values are based on “normal” populations of persons of similar height, weight, age, gender, and race.

⁹ Based on pProminent pulmonologists publishing letters of criticism or disagreement in the medical literature. See e.g., Martin L., Correspondence, “2004 Asbestos Disease Guidelines Ignore Mass Screening Abuse,” Am. J. Resp. & Critical Care Medicine, 171 (2005); 666-67.

¹⁰ In the United States, the B-reader certification is overseen by the National Institute of Occupational Safety & Health (“NIOSH”), utilizing the standard ILO films.

¹¹ See International LabourLabor Organization, Guidelines for the Use of ILO International Classification of Radiographs of Pneumoconiosis (2000).

¹² "Inter-reader variability" is where two equally credentialed and experienced B-readers arrive at different interpretations of the same films.

¹³ The goal being to determine whether there was or can be an overall exposure assessment calculated in fiber/years or the equivalent.? Was or can there be an assessment of latency?

¹⁴ The goal being to verify consistent measurements of restrictive, obstructive, or mixed ventilatory defects.

¹⁵ Note: It is beyond the space limitations to explain all of the variations on PFTs results to support or refute the written diagnosis in the medical records.

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