Complex Exposures in the Workplace

Complex Exposures and Their Relationship to Work:

Are They Preventable?

By Bill Masters

Wallace, Klor & Mann, P.C.

 

 

  1. “Complex Exposures”

 

“Complex exposures” are exposures to such insidious agents as “immunogens” [molecules that generate an immune response], “antigens” [foreign substances that induce a “specific” immune response], “toxins” [a poisonous substance that directly damages cells and tissues], “teratogens” [substances that result in the development of an abnormal embryo resulting in deformed fetus] or “carcinogens” [substances that increase the risk of development cancer], that is, any substance that can cause humans acute or chronic injury or disease, either directly by incrementally altering or destroying cells or indirectly through the stimulation of a harmful immune response. In the past, complex exposures have involved diseases such as, for example, asbestosis; silicosis; asthma; pulmonary hypersensitivity reactions; skin allergies; radiation; and blood borne diseases, such as hepatitis C.

 

“Complex exposure claims” are those claims in which claimant seeks benefits for health problems owing to purported exposure to “immunogens,” “antigens,” “toxins,” “teratogens,” “carcinogens” or any substance that can cause humans acute or chronic injury or disease, either directly by incrementally and insidiously altering or destroying cells or indirectly through stimulation of a harmful immune response.

 

“Complex exposure claims” typically do not involve what are known as “slam-bang” effects. “Slam-bang” effects are those effects that follow immediately with noticeable magnitude from an exposure. “Slam-bang” effects are usually a tell tale sign of causation. Complex exposure claims are distinguished from simple exposure claims by the difficulty inherent in identifying the cause(s) of claimant’s presenting signs and symptoms.

 

The essence of “complex exposure claims” is that they present a significant prospect for what is called “misclassification bias.” There is a potential for misclassification bias in assessing the exposure and in assessing the effect of exposure.

 

Misclassification Bias As to Exposure

The term ‘exposure” refers to that situation in which people come into contact with something potentially harmful. These potentially harmful things can range from electromagnetic radiation to a variety of biologics, such as viruses and bacteria, and to various harmful man-made agents, such as drugs and devices.

 

At times, an exposure may be described at the level of cells or even molecules. This level of description would provide a degree of precision most helpful in explaining how biologically plausible is a particular theory of causation. But for purposes of litigation that level of precision is not required. What is required is a phenomenological description of the exposure. For instance, did this insomniac ingest L-tryptophan manufactured by this company; or did this shipyard worker inhale asbestos in this ship thirty years ago; or did this pregnant woman ingest Bendectin to palliate symptoms of morning sickness?

 

If what counts as an exposure is not defined carefully and in a way permitting reasonably reliable identification, then what is apt to result is misclassification of what constitutes exposure and non-exposure. That is, a true exposure will be classified as a non-exposure and a true non-exposure will be classified as an exposure.

 

Of these possible kinds of misclassification, the kind most likely to occur, outside litigation, is that in which true exposures will be classified as non-exposures. But in litigation, the reverse is apt to occur because litigants will lie about the nature of their experience in order to become classified as exposed. In either event, the rate of misclassification differs between cases and controls. In the latter example, for instance, controls are more often misclassified as cases than cases are misclassified as controls. For the defense, this is a dangerous phenomenon. It is known as “differential misclassification.”

 

Misclassification Bias As to Effect

Identifying accurately the effect of an exposure is critical. Often the effect will be easily identified. For instance, if the exposure is alleged to cause a form of cancer, that form of cancer can be identified by trained pathologists. Yet, at other times, the effect can be identified only provisionally. This typically occurs when the effect is a syndrome constituted of unspecified subsets of a vast array of non-specific symptoms. Then the defense should be very much concerned with ensuring that the diagnostic criteria for such a syndrome be adequately defined.

 

Timing of Diagnosis

If, after an exposure, the subject in a study group does not manifest symptoms of the disorder for some time, the process of identifying cases may be imprecise and result in misclassifying cases as non-cases. (Generally, this is not a problem for the defense.) In this regard, one should consider the “induction period” and the “latent period” of the disorder. The “induction period” is the period of time from causal action until initiation of disease. The “latency period” is the interval of time between occurrence of the disease and detection of the disease.

 

If what counts as an effect is not defined carefully and in a way permitting reasonably valid and reliable identification, then what is apt to occur is misclassification of what constitutes an effect. That is, a true case will be classified as a non-case and a true non-case will be classified as a case. In the context of litigation, the likelihood is that a true non-case will be classified as a case. This is termed “differential misclassification.”

 

“Complex exposure claims” fall into two basic categories: (1) those in which the harmful agent produces a “signature disease,” such as mesothelioma from asbestos; and (2) those in which a putative harmful agent allegedly produces a constellation of non-specific symptoms not considered to be a signature disease. Often, this second type of “complex exposure claim” arises in advance of proper scientific data either for or against claimant’s claim.

 

Snyder v. Dep’t of Labor & Indus., 40 Wn. App. 566, 699 P.2d 256 (1985).

The worker began employment with the employer in 1979. Before his current employment, he had considerable employment outside the state of Washington, involving welding, grinding, and sandblasting. He had worked with asbestos and was exposed to silicon dust. At his current employment, he was employed as a lead welder in its welding shop. This work exposed him to fumes containing zinc while he was welding seams on large sections of galvanized pipe. The work site did not have an adequate forced-air ventilation system.

 

After working several months in the employer’s welding shop, he began to develop increased and spasmodic coughing, shortness of breath, early fatigue, and sputum. Before he began working for the current employer in 1979, he had not manifested any symptoms of ill health. He was “physically fit, always active and always on the go.”

 

The worker’s expert testified that the worker was suffering from interstitial pulmonary fibrosis (silicosis), welder’s bronchitis, and cigarette bronchitis. The expert testified that the worker had probably contracted the silicosis before his current employment, but was asymptomatic at the time he began working there. He further testified that in his opinion the conditions to which the worker was exposed while working for current employer (i.e., welder’s fumes and dust) aggravated the preexisting silicosis.

 

The court held as follows:

 

In light of the foregoing authority, we hold that aggravation of a preexisting, asymptomatic disease may be compensable as an occupational disease within the meaning of RCW 51.08.140, provided that the employment conditions producing the aggravation are peculiar to, or inherent in, the particular occupation.

 

  1. Complex Exposures in the Workplace

 

A complex exposure in the workplace may cause an “injury” or an “occupational disease.”

 

“Injury”

RCW 51.08.100 defines “injury” as follows:

 

“‘Injury’ means a sudden and tangible happening, of a traumatic nature, producing an immediate or prompt result, and occurring from without, and such physical conditions as result therefrom.”

 

No certain temporal duration is needed to establish “a sudden and tangible happening.” In Garrett Freightlines, Inc. v. Dep’t Labor & Indus., 45 Wn. App. 335, 342-343, 725 P.2d 463, 467 (1986), the court of appeals said that recurrent lifting over the course of a day could have been legally characterized by a jury as an “injury” under the law of industrial insurance.

 

Washington law does not clearly mandate a certain temporal duration to establish “a sudden and tangible happening,” as required by RCW 51.08.100. The statute requires a relation between the injury and “some identifiable happening, event, cause or occurrence capable of being fixed at some point in time and connected with the employment.” Spino v. Department of Labor & Indus., 1 Wn. App. 730, 733, 463 P.2d 256 (1969). The key is not in the establishment of a duration or time frame, as L & I suggests, but in the establishment of causation, the connection between the physical condition, and employment. This causal condition must be established by medical testimony. It is not always necessary, however, to prove every element of such causation by medical testimony. If, from the facts and circumstances and the medical testimony given, a reasonable person can infer that the causal connection exists, the evidence is sufficient.

 

Garrett Freightlines, Inc. v. Dep’t Labor & Indus., 45 Wn. App. 335, 342-343, 725 P.2d 463, 467 (1986); see also, Lehtinen v. Weyerhauser Co., 63 Wn.2d 456, 387 P.2d 760 (1963) (the court said that frequent jolts to claimant while operating equipment over the course of a day could be an injury under the law of industrial insurance); In re: James V. Jacobs, BIIA Dec., 48, 634 (1977) (the BIIA found that activity over the course of a day caused an “injury”); In re: Renford Gallier, BIIA Dec., 89, 3109 (1990) (the BIIA found that a day of lifting boxes resulting in pain and stiffness in the worker’s left shoulder constituted an “injury”).

 

An example of an “injury” in complex exposure claim would be the paper mill worker who is exposed to chlorine gas leak in sufficient dose to burn his lungs.

 

“Occupational Disease”

RCW 51.08.140 defines Aoccupational [email protected] as follows:

A=Occupational disease= means such disease or infection as arises naturally and proximately out of [email protected]

 

The phrase Anaturally arising out of [email protected] is only a requirement in occupational disease (not injury) claims in Washington. RCW 51.08.140. The phrase Anaturally arising out of [email protected] is only a requirement in occupational disease (not injury) claims in Washington. RCW 51.08.140. The phrase has been held to mean the following:

 

  1. AA worker must establish that his or her occupational disease came about as a matter of course as a natural consequence or incident of distinctive conditions of his or her particular employment. The conditions need not be peculiar to, nor [sic] unique to, the worker=s particular [email protected]

 

This requirement–that the worker establish that the occupational disease arose from distinctive conditions of his workplace–would be meaningless if the worker were excused from having to establish what it was particularly in the workplace that caused the occupational disease. If the worker were merely required to prove that he developed certain non-specific symptoms during the time he/she was employed, without establishing what agent was responsible, he/she could not establish and the employer could not disprove that whatever condition the worker developed was distinctive to the workplace—that is, not present also outside the workplace.

 

  1. AThe worker Y must show that his or her particular work conditions more probably than not caused his or her disease or disease-based disability than conditions in everyday life or all employments in general; the disease or disease-based disability must be a natural incident of conditions of that worker=s particular [email protected]

 

  1. AThe condition causing the disease or disease-based disability must be a condition of employment. This is, it is a condition of the workers particular occupation as opposed to conditions coincidentally occurring in his or her [email protected] Dennis v. Dep’t of Labor & Indus., 109 Wn.2d 467, 745 P.2d 1295 (1987).

 

Workers Bringing Their Syndromes/Diseases into the Workplace

A complex exposure in the workplace may cause a new injury or occupational disease or it may light up a latent disease/condition or aggravate a symptomatic disease/condition.

 

Aggravation of Symptomatic Disease/Condition

A complex workplace exposure may cause a symptomatic disease/condition to become temporarily or permanently aggravated. Hurwitz v. Dep’t of Labor & Indus., 38 Wn.2d 332, 229 P.2d 505 (1951). For example, an asthmatic may have symptoms of asthma, such as shortness of breath, that do not cause the worker to miss work but an exposure to workplace fumes may cause the asthma to become debilitating, resulting in a permanent disability.

 

Lighting Up Latent Conditions

If an injury, within the statutory meaning, “lights up” or makes active a “latent” or “quiescent” infirmity or weakened physical condition occasioned by disease, then the resulting disability is to be attributed to the injury, and not to the preexisting physical condition. “If this be true with respect to a weakened physical condition resulting from disease, it must likewise be true with respect to a similar infirmity resulting from some structural weakness of the body.” Miller v. Dep’t of Labor & Indus., 200 Wn. 674, 94 P.2d 764 (1939); Bennett v. Dep’t of Labor & Indus., 95 Wn.2d 531, 627 P.2d 104 (1981). “Quiescent” has been defined as “causing no symptoms.” “Asymptomatic” has been defined as “presenting no subjective evidence of disease.” McDonagh v. Dep’t of Labor & Indus., 68 Wn. App. 749, 845 P.2d 1030, 1034 (1993); Orr v. Dep’t of Labor & Indus., 10 Wn. App. 697, 519 P.2d 1334 (1974).

 

A preexisting condition is not lit up if evidence reveals (1) that the condition was symptomatic before the workplace incident or (2) that the condition was a naturally progressing condition that would have progressed to symptoms without the injury. Austin v Dep’t of Labor & Indus., 6 Wn. App. 394, 492 P.2d 1382, 1384-5 (1971).

 

It is insufficient to show only that a worsening of a pre-existing condition is temporarily lit up by the industrial injury. In re: Arlen Long, BIIA Dec. 94, 2539 (1996).

 

Kallos v. Dep’t of Labor & Indus., 46 Wn.2d 26, 278 P.2d 393 (1955).

The worker contracted silicosis while working outside the state of Washington and before his employment in Washington. The worker’s silicosis was asymptomatic at the time he began working in Washington. In that employment, he was exposed to considerable smoke and dust. Shortly thereafter, the worker began to exhibit the symptoms of silicosis (e.g., shortness of breath, heavy coughing, and early fatigue). The Department contended in Kallos, as it does here, that in order to show entitlement under the occupational disease statute, the claimant “must produce testimony that his disease had its inception in his [current or last] extrahazardous employment, and that a mere showing of aggravation of a preexisting disease due to the conditions of employment is not sufficient.” Kallos, 46 Wn.2d at 29.

 

The court held as follows:

In the instant case, the injury is “such physical condition as results from” a previous nondisabling occupational disease. The proof of the cause of its change from a nondisabling status to a disabling status must satisfy the requirements laid down in Simpson Logging Co. v. Department of Labor & Industries, 32 Wn.2d 472, 202 P.2d 448. The rule of that case may be thus paraphrased to fit the instant case. The condition of the extrahazardous employment must be the proximate cause of the change in the status of the occupational disease for which claim for compensation is made, and the cause must be proximate in the sense that there existed no intervening independent and sufficient cause for the change, so that the change would not have occurred but for the condition existing in the extrahazardous employment.

 

III. Causation

 

Causation is “an event, condition, characteristic, or agent that is a necessary element of a set of other events that produce an outcome, such as disease.” Epidemiology in Reference Manual in Scientific Evidence; K.J. Rothman & S. Greenland. Modern Epidemiology, 7-28 (1998); L. Gordis. Epidemiology, pp. 191-201 (2000); E. Sousa & M. Tooley (eds.) Causation (1998); D. Lewis. Causation as Influence. The Journal of Philosophy, XCVII: 182-197 (2000). As Wittgenstein remarked, “cause isn’t just temporal coincidence but influence.” Wittgenstein, Philosophical Occasions 1912-51, p. 407 (1993).

“Causation” differs from “association.” An “association” is defined as a relation between an exposure and an effect such that the exposure and effect occur together more (or less) frequently than they would strictly by chance. For example, in 1981, in the Women’s Health Study, a relative risk of 1.6 (95% CI 1.4 – 1.9) was reported for users of intrauterine devices (IUD) compared to non-IUD users for pelvic inflammatory disease (PID). This finding is a report of an association, beyond that due to chance, between use of IUDs and PID. That an exposure is statistically associated with an effect is a necessary, but not a sufficient condition for inferring that the exposure causes the effect. For example, in 1994, an epidemiologic study reported a relative risk of 1.38 for breast cancer from exposure to electromagnetic fields. But, today, few would conclude from this association that electromagnetic fields cause breast cancer.

 

In short, an “association” is, at the very least, merely the co-occurrence of two or more events by chance. It is, at the very most, the degree of statistical dependence between two or more events such that they occur together more or less frequently than one would expect by chance.

 

Coincident Association =df as an association between variables owing to chance alone or, less prosaically, “a surprising occurrence of events, perceived as meaningfully related, with no apparent causal connection.”

                       

Statistical Association =df as an association between variables not owing to chance.

 

Correlation =df as a numeric measure of the strength of linear relationship between two random variables or, in general statistical usage, the departure of two variables from independence.

 

That an exposure is statistically associated with an effect is a necessary, but not a sufficient condition for inferring causation. K.E. Stanovich, How to Think Straight About Psychiatry, 75-86 (2001); P. Skrabanek. The Emptiness of the Black Box. Epidemiology, 5: 553-555 (1994). If it cannot be demonstrated that the co-occurrence of an exposure and an effect is a statistical association, it cannot be demonstrated that the exposure causes the effect.

 

The Golden Rule: If it cannot be demonstrated that the co-occurrence of an exposure and an effect is a statistical association, it cannot be demonstrated that the exposure causes the effect.

 

Scientists and epidemiologists are more rigorous in their efforts to establish causation than the judiciary. In this regard, scientists and epidemiologists rely heavily on “inductivism.” “Inductivism” is the epistemological doctrine that science begins with observations and then moves to generalizations about those observations in the form of laws and theories and then to predictions entailed by those theories and then to tests of those predictions with further observations to determine whether the theory is valid. For example, after observing that all ravens they have ever seen are black, ornithologists infer the law that all ravens are black, and predict that all ravens anyone will ever see will be black, and then confirm or disconfirm that prediction through further observations of ravens.

 

To infer causation, scientists and epidemiologists often rely upon inductive criteria. The original inductive criteria fashioned to establish causation from exposure to biological agents are known as the Henle-Koch postulates. Over the years these Henle-Koch postulates were adapted to include a variety of exposures. Currently they have been generalized into widely used set of inductive criteria termed the Bradford-Hill criteria.

 

Here are those nine criteria:

 

  1. Strength of Association: The stronger the association, the more likely the exposure caused the effect. A strong association is unlikely due to one weak unmeasured confounder or other source of modest bias. This criterion is neither necessary nor sufficient for causation.

 

  1. Consistency: Repeated observation of an association in different populations in different circumstances suggests causation. Ideally, many studies with different architecture should produce results that converge. When that occurs, the corpus of epidemiologic evidence can be said to be reliable. Consistency, some say, is not a necessary criterion of causation, but serves only to rule out hypotheses that the association is attributable to some factor that varies across studies.

 

  1. Specificity: Specificity requires that an exposure, if causal, produce a single effect, not multiple effects. This criterion, many epidemiologists recognize, is neither necessary nor sufficient for causation. Simply, single events or conditions may have many effects.

 

  1. Temporality: The cause must precede the effect. This criterion is necessary for causation. But it is not sufficient: As Shakespeare wrote, “I have heard the cock, that is the trumpet to the morn, doth with his lofty and shrill-sounding throat awake the god of day…”.

 

  1. Biologic Gradient: Biologic gradient refers to the presence of a monotonic, that is, unidirectional, dose-response curve. This criterion is neither necessary nor sufficient for causation.

 

  1. Plausibility: Plausibility refers to the biologic likelihood that the exposure caused the effect. This criterion is neither necessary nor sufficient for causation.

 

  1. Coherence: Coherence, like the criterion of bioplausibility, requires that the hypothesis about causation not conflict with what is known about the natural history and biology of the disease. This criterion is neither necessary nor sufficient for causation.

 

  1. Experimental Evidence: Experimental evidence from available sources corroborates the hypothesis of causation. This criterion is neither necessary nor sufficient for causation.

 

  1. Analogy: Analogy refers to the similarity between the association at issue and other associations which are considered more firmly to be cause-and-effect relationships. This criterion is neither necessary nor sufficient for causation.

 

“Despite the apparent simplicity of many of these criteria, many epidemiologists would probably agree that [the Bradford-Hill] criteria are not totally adequate, that they provide few hard and fast rules for making causal inferences.”

 

“Proximate Causation”

In industrial insurance claims, claimant has the burden of proving by a preponderance of the evidence the various elements of his/her claim: (1) he/she has a certain medical condition and (2) this medical condition was proximately caused by an industrial accident event. Spino v. Dep’t of Labor & Indus., 1 Wn App. 730, 463 P.2d 256 (1969).

A cause of a condition is “proximate” if it is related to the condition in two ways: (1) the cause produced the condition in a direct sequence unbroken by any new, independent cause, and (2) the condition would not have happened in the absence of the cause. Sacred Heart Medical Center v. Dep’t of Labor & Indus., 92 Wn.2d 631, 600 P.2d 1015 (1979); Goyne v. Quincy-Columbia Basin Irrigation Dist., 80 Wn. App. 676, 910 P.2d 1321 (1996); Grimes v. Lakeside Industries, 78 Wn. App. 554, 897 P.2d 431 (1995).

 

The cause must be “proximate” in the sense that no intervening independent cause for the disease or disease-based disability existed. That is, but for the workplace conditions to which the employee was exposed, the employee would not have the disease or disease-based disability. Parr v. Dep’t of Labor & Indus., 46 Wn.2d 144, 278 P.2d 666 (1955) (no proximate cause established because employee allergic to all kinds of dust in addition to the wood dust to which he was exposed at work).

 

The claimant must prove that he/she was more probably exposed to that agent in the workplace than in places outside the workplace encountered in everyday life or all employments in general. Parr v. Dep’t of Labor & Indus., 46 Wn.2d 144, 278 P.2d 666 (1955).

           

            Parr v. Dep’t of Labor & Indus., 46 Wn.2d 144, 278 P.2d 666 (1955).

The worker was hypersensitive to dust of various kinds and characters, such as road dust, house dust, and wood dust. That hypersensitivity to dust caused disabling asthma. At work, the employee was required to work in great quantities of wood dust for several hours at a time during certain portions of the year. The worker filed a claim for an occupational disease. Based on a history provided by the worker that related the worker’s exposures at the worksite and nowhere else, the worker’s treating physician testified that the worker’s exposure to these dusts in the workplace caused his asthma. Any dust, whether in the workplace or outside the workplace, would have triggered the worker’s asthma attacks. The worker’s hypersensitivity to dusts did not arise in the first instance from his current employment. The court held that the worker’s asthmatic condition did not arise naturally and proximately from the worker’s employment, and so was not an occupational disease. “We so hold for the reason that the dust allergy could have caused the asthmatic condition regardless of his employment.”

 

General Causation

Proximate causation has two components: “general causation” and “specific causation.” “General causation” concerns the question: As a matter of scientific fact, can a particular agent cause a particular pattern of signs and symptoms in humans? See, e.g., Grant v. Boccia, 135 Wn. App. 176, 137 P.3d 20 (2006); Ruff v. Dep’t of Labor & Indus., 107 Wn. App. 289, 28 P.3d 1, 28-29 (2001); Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1412-13 (D. Or. 1996).

 

General Causation =df as “X is capable of causing Y in the population Z.”

 

A differential diagnosis or a case study should not be acceptable evidence of general causation. An object lesson in the shortcomings of case studies as evidence of causation is the experience of Dr. Benjamin Rush, who lived in the 18th century and was, then, a preeminent physician. Because Dr. Rush was preeminent, people often took his opinions as truth merely because he said it was so [the fallacy of appealing to authority]. In his time, Dr. Rush treated yellow fever by vigorous purging and copious bleeding. “Never before,” he said, “did I experience such sublime joy, as I now felt in contemplating the success of my remedies.” What he was extolling was the evidential force of a case report or case series. By this evidence, he was utterly convinced that he was benefiting his patients [the fallacy “post hoc, ergo propter hoc“]. Moreover, attacks on his methods by some more judicious physicians only made him more assertive that his methods were superior. Today he is known to have been profoundly wrong, and his treatments probably bled many of his patients to death.

 

Specific Causation

Specific causation concerns the question: Given proof of general causation, as a matter of clinical fact, was the claimant exposed to that particular agent in the necessary dose or have the necessary sensitivity and did claimant have the particular pattern of signs and symptoms identified as resulting from exposure to that agent. See Intalco Aluminum Corp. v. Dep’t Labor & Indus., 66 Wn. App. 644, 833 P.2d 390 (1992) rev. denied, 120 Wn.2d 1031, 847 P.2d 481 (1993); cf. Hall, 947 F. Supp. at 1412-13; Ruff v. Dep’t of Labor & Indus., 107 Wn. App. 289, 28 P.3d 1, 28-29 (2001).

 

Specific Causation =df as “X did cause Y in z = Z.”

 

Theoretically, specific causation can be proved two ways: (1) factual proof, either direct or indirect, or (2) statistical proof.

 

            Factual Proof

Factual proof is proof through eyewitness accounts or documents that claimant was exposed to a harmful agent and medical testimony establishes a causative nexus between the exposure and the purported symptoms/disease. For instance, the worker testifies that he was exposed to asbestos at the workplace when working with brake linings and medical testimony establishes through biopsy and histochemcial analysis that he has mesothelioma.

 

            Statistical Proof

Statistical proof amounts to proof that claimant was, epidemiologically, at greater risk for contracting the disease/condition while working in his/her current work environment than while engaged in any of his/her other activities posing a risk for contracting the disease/condition. Sacred Heart Medical Center v. Carrado, 92 Wn.2d 631, 600 P.2d 1015 (1979). Risk is defined, in this context, in relation to the relative [email protected] of the disease/condition in particular activities or categories of activities to the overall prevalence of the disease/condition in the United States. The term [email protected] is a term of medical art. It means the number of affected persons present in the population at a specific time (or during a specific period of time) divided by the number of persons at that time in the total population.

 

            Sacred Heart Medical Center v. Carrado, 92 Wn.2d 631, 600 P.2d 1015 (1979).

Claimant had contracted hepatitis as a result of her employment as a registered nurse in an intensive care unit at a medical center. Expert testimony established that there was a greater probability that a nurse working in a hospital, and particularly in an intensive care unit, will contract the disease than there is that a person employed in some other occupation will do so. Experts agreed that it is virtually impossible to pinpoint the precise source of a given case of hepatitis, since carriers may not display symptoms of the disease. Claimant testified that she had been employed at the medical center for more than the normal period of incubation; that her duties required daily handling of the fluids and excrements of patients; that on one occasion she had been bitten by a patient; and that the handling of needles and other medical equipment resulted in occasional small cuts and punctures on the hands. She also testified that her evenings were usually spent at home, where she lived a quiet life alone, and her attendance at public functions was confined to an occasional movie. She knew of no exposure to the disease which she might have had outside the hospital.

 

The court held as follows:

 

“If, from the medical testimony given and the facts and circumstances proven by other evidence, a reasonable person can infer that the causal connection exists, we know of no principle which would forbid the drawing of that inference. *** Here the medical testimony showed that there is generally a greater probability that a person in the petitioner’s employment will contract hepatitis than there is that someone in another employment will do so. In other words, there is a greater risk of getting the disease when one is employed in a hospital. The Board and the jury were entitled to consider this evidence in conjunction with the petitioner’s uncontradicted and undiscredited testimony that none of her other activities involved such exposure, and to reach the conclusion that, more likely than not, the disease resulted from contact with a carrier in the hospital.”

The test whether an occupational disease has occurred is not whether most workers of reasonable good health would suffer a disabling disease under the same conditions, but rather whether the individual worker with his/her preexisting frailties and bodily infirmities suffered the disease. Simpson Timber Co. v. Wentworth, 96 Wn. App. 731, 981 P.2d 878 (1999).

 

Simpson Timber Co. v. Wentworth, 96 Wn. App. 731, 981 P.2d 878 (1999).

The worker began working for the employer in 1980. All her jobs entailed prolonged standing on cement floors. Over time, the worker developed foot problems. Her doctors concluded that she had plantar fascitis (an inflammation of the underlying connective tissues in the foot). These doctors concluded that her plantar fascitis was aggravated by her work conditions, specifically, standing for long periods of time on cement floors.

 

The court held as follows:

 

While it may be commonplace for workers to stand and move about on hard surfaces, it is certainly less common for workers to do so for prolonged periods of time. While perhaps most workers of reasonably good health may not suffer a disabling disease from prolonged standing, this is not the inquiry or the legal test under the Act. “The worker is to be taken as he or she is, with all his or her preexisting frailties and bodily infirmities.” Dennis, 109 Wn.2d at 471 (citing Wendt v. Department of Labor & Indus., 18 Wn. App. 674, 682-83, 571 P.2d 229 (1977)). Dennis also held that the conditions need not be peculiar to, or unique to, the worker’s employment. 109 Wn.2d at 481.

 

Prolonged standing or movement on cement floors may cause an occupational disease in someone who may be predisposed to foot problems …; we will not hold as a matter of law that it cannot. Whether prolonged standing aggravated [this worker’s] foot condition in this case is a question that was properly left for the trier of fact.

 

  1. Chance Associations Masquerading as an Injury or Occupational Disease

 

When a worker develops symptoms unrelated to a workplace exposure but attributes them to a workplace exposure, from malice or ignorance, the employer has an arduous task in establishing that the workplace exposure did not cause these symptoms. As a practical matter, the employer has the burden of proving the negative–that the workplace exposure did not cause the worker’s symptoms. There are a number of psychological and ideological reasons for this shifting of the burden of proof.

 

Chemical Exposures

The laity is unsophisticated about chemical exposures. Do you agree or disagree with this statement: “For pesticides, it’s not how much of the chemical you are exposed to that should worry you, but whether or not you are exposed at all.” The typical person responds: “It is not how much of the chemical you are exposed to that should worry you, but whether or not you are exposed at all.” The toxicologist (no matter his or her ideological bent) responds: “It’s the dosage that should worry you.” Unlike the lay person, toxicologists endorse the following statements:

 

(1) “Use of chemicals has improved our health more than it has harmed it.”

(2) “Natural chemicals can be just as harmful as man-made chemicals.”

(3) “It is not true that it can never be too expensive to reduce the risks associated with chemicals.”

 

The muddled thinking by lay persons is what the employer needs to combat in chemical exposure cases. The moral: Never under estimate public ignorance! See Kraus, Malmfors, and Slovic. Intuitive Toxicology: Expert and Lay Judgments of Chemical Risks. Risk Analysis, 12(2): 215-32 (1992).

 

Scientific Illiteracy

The fact is, the typical juror is usually incapable of assessing whether or not scientific evidence is valid. Ask any educator; ask any scientist; your typical juror is scientifically illiterate. As a Gallup poll of 1236 adult Americans revealed, those who are apt to decide lawsuits believe in the following absurdities:

 

Astrology 54%
ESP 45%
Aliens Have Landed on Earth 22%
Dinosaurs and Humans Lived Together 41%
Noah’s Flood 65%
Communication With The Dead 42%
Ghosts 35%

 

Polls like this should leave little doubt that a claimant’s attorney, with even modest rhetorical skills, can convince the typical juror that the moon is made of cream cheese or that Elvis can still be seen walking the halls of Graceland.

 

Cognitive Biases

Various cognitive biases may operate in claimant’s favor in claims involving complex exposures. These biases are as follows:

 

Framing Effects—The cognitive bias of drawing different conclusions based on how the data are presented to the decision-maker.

 

Availability Heuristic—Estimating what is more likely to have occurred by what is more available in memory, which is biased toward vivid, unusual, or emotionally charged examples.

 

Availability Cascade—A self-reinforcing process in which a collective belief gains more and more plausibility through its increasing repetition in public discourse (“by repeating something long enough, it will become true”).

 

Confirmation Bias—The tendency to search for or interpret information in a way that confirms one’s preconceptions.

 

Nothing is easier than self-deceit. For what each man wishes, that he also believes to be true.

Demosthenes

 

In defending against a claim for a complex exposure, the employer’s most difficult task is attempting to neutralize the corrosive effects of the various cognitive biases or errors endemic to these kinds of claims. A disturbing cognitive error is found in many administrative rulings (or in the public thinking generally) in favor of claimants on claims involving alleged toxic or allergenic exposures. This cognitive error is known as the “availability heuristic.” E.g., Tversky, A. & Kahneman, D. Availability : A Heuristic for Judging Frequency and Probability. Cognitive Psychology, 5: 207-232 (1973) (a line of cognitive study for which Professor Kahneman won the Nobel Prize in Economics). It is the tendency of a decision-maker to focus on the scenario most easily brought to mind as a basis for inferring that what is true of that easily imagined scenario is true of nearly every similarly situated scenario. Typically, what is most easily brought to mind is the most emotionally charged scenario. This emotionally charged scenario is then considered to be representative or true of the larger group of scenarios being considered.

 

This cognitive error results in a biased assessment of “specific causation” in claims involving alleged toxic or allergic exposures. In those kinds of claims, the claimant asserts that he/she was exposed to any number of fumes, vapors, chemicals, allergens and, therefore, these exposures were responsible for whatever ailment he/she happens to have at the time or at some distant future time. The horror of it! The emotionally charged scenario is that exposures to these strange sounding chemicals causes serious and lasting health problems.

 

“While hard at work, the claimant was [drenched, soaked, covered] in Propiconazole.” [Does it matter that this is a harmless chemical?]

 

“While working in the room where the black liquor was breaking down wood chips into pulp, claimant was gassed with chlorine gas.” [Does it matter that the worker was wearing a gas mask?]

 

The decision-maker, generally being unsophisticated in the action of these chemicals on humans (that is, in the sciences toxicology and immunology), reasons that because these alleged chemicals or allergens might cause problems in some people, they must be causing the problems of which claimant complains. Indeed, anyone exposed to these chemicals cannot help but develop health problems.

 

On two accounts, this emotionally charged possible scenario overrides the evidence—the decision-maker is metaphorically blinded to any other reasonable possibility. On the first account, the decision-maker fails to consider the fact that hundreds of thousands of people (including housewives, house-husbands or house-persons) work at locations where chemicals are present. Only a very small number of those people develop health problems from those exposures. This is due to the fact that (1) many of the chemicals, though strange sounding, are not harmful to humans for a variety of reasons; (2) of the chemicals that might be harmful, the employees do not have exposures to them at doses that are, in fact, harmful (even though they can smell the chemical—skunk scent or sulfur comes immediately to mind, or the smell of chlorine in swimming pools; do all people who swim in, gulp down and breathe in the water in those smelly chlorinated pools die from it?); (3) of the people who do have adverse reactions, very many have a very unusual hypersensitivity to a particular chemical or allergen (such a people with peanut allergies—do all people who eat peanut butter die from it?).

 

On the second account, because of the availability heuristic in this context, the decision-maker gives short shrift to other more likely or statistically prevalent causes of claimant’s symptoms, causes that would be at the forefront of the investigation absent the easily imagined horrors of workplace exposure to some strange sounding chemicals. The entire focus is directed to a cause of injury or disease that can result in compensation for the worker and in happiness for claimant’s counsel and then, in turn, in happiness for claimant’s expert who expects return business for his or her performance.

 

Practice Tip: The employer needs a solid clinical toxicologist and/or industrial hygienists to testify about the realities of chemical exposures.

 

Logical Errors–Affirming the Consequent (Post Hoc; Ergo Propter Hoc)

Arguments in these complex exposure cases typically have the form of the formal fallacy known as “affirming the consequent.” This is the form of that argument:

 

  1. If you are exposed to certain toxins, you can develop certain non-specific symptoms. [That is, the premise is not of the form—”if and only if you are exposed to certain toxins, you can develop certain symptoms.”]
  2. I have developed certain non-specific symptoms.
  3. Therefore, I must have been exposed to certain toxins.

 

In a more abstract form, the argument is as follows:

 

If X is true, then Y is true.

Y is true.

Therefore, X is true.

 

This kind of deductive reasoning is a logical fallacy. The court in Ruff v. Dep’t of Labor & Indus., 107 Wn. App. 289, 28 P.3d 1 (2001) [Division I] disapproved of this kind of argument as a form of proof in toxic exposure cases. The court in Lewis v. Simpson Timber Co., 145 Wn. App. 302, 189 P.3d 178 (2008) [Division II] appears to have endorsed this kind of argument. [More about that case later.]

 

  1. Key Industrial Insurance Cases in Washington—”The Law”

 

Various key points of law need to be asserted in these complex exposures cases.

 

Point of Law: The Worker Must Prove That An Agent Caused The Symptoms/Disease.

 

[1] Identify specific agents in the workplace;

[2] Establish that these agents can cause disease/symptoms;

[3] Establish that claimant was exposed to these agents;

[4] Establish a temporal nexus between exposure to such agents and the onset of the disease/symptoms; and

[5] Rule out other conditions that cause non-specific symptoms alleged to be the disease.

 

Intalco v. Dep’t of Labor & Indus., 66 Wn.App. 644, 833 P.2d 390 (1992). [Division I].

 

[1] Arvin Apol, an industrial hygienist for the National Institute for Occupational Safety and Health (NIOSH). In 1973, NIOSH did an air pollution survey of gasses and particulates at the Intalco plant. At that time, Intalco was in the process of retrofitting the pots with hoods. Apol testified that the air on the unhooded potline was at least twice as dirty as the air on the hooded potline. The survey, which focused primarily on fluoride emissions, found that the threshold limits for that toxin were exceeded on both the hooded and unhooded potlines. However, NIOSH did not measure all of the chemicals present in the Intalco pot room atmosphere, such as aluminum particulates. Apol testified that numerous toxins, including aluminum, benzene solubles, petroleum pitch volatiles, and carbon monoxide would also be present in the pot room atmosphere. He further testified that carbon monoxide and petroleum pitch volatiles had been associated with neurologic disease.

***

[5] The investigation included extensive, systematic medical testing, including nervous system studies, vitamin deficiency tests, and other procedures specifically intended to identify any nonwork-related causes of illness.

 

***

[5] Drs. Longstreth and Rosenstock determined that the patients’ neuropathological process affected their central, rather than peripheral, nervous systems. On the basis of this determination, the physicians eliminated from consideration numerous non-work-related causes. Drs. Longstreth and Rosenstock concluded that the three patients’ illnesses were more probably than not caused by work-related exposures to neurotoxins. They based their conclusion on the similarity of the patients’ symptoms, which were [*653] characteristic of a neurologic disease, and their exposure histories. [3] & [4] Especially in the early years of their employment, all three had intense exposures to a number of toxic substances, including solvents, fluorides, aluminum, and coal tar pitch, and all three were exposed to the same work environment for at least 12 years. [4] & [5] The physicians observed that the patients’ symptoms revealed a neurologic disease that could not be explained as any other known disease or by commonly accepted disease criteria. [2] Finally, they agreed that, as a central nervous system phenomenon, the disease looked like other models of toxin-induced disease known as “central distal axonopathy”.

 

***

[5] Intalco also believes the medical testimony was insufficient because the physicians could not identify the specific toxic agent or agents that proximately caused the claimants’ disease. Intalco’s witness, Mr. Apol of NIOSH, identified several toxins in the pot room, some of which have been associated with neurologic disease. While the physicians could only hypothesize that aluminum could be the specific agent responsible for the claimants’ disease, they firmly concluded that a toxin or a combination of toxins present in the atmosphere of the Intalco pot room more probably than not caused the claimants’ neurologic disease. This conclusion was based on several factors. First, although the clinical findings indicated that the patients suffered from a neurologic disease, their symptoms did not fit the diagnostic criteria of any known disease. [4] Second, the claimants all had similar exposures to known neurotoxins: they had all worked in the pot room for at least 12 years. [5] Third, the physicians’ extensive investigations of the claimants’ medical and work histories revealed no other likely cause of their disease. [2] Finally, while studies of the effects of pot room exposures on the human neurologic system had never been done, animal studies revealed that aluminum exposure could cause symptoms similar to those exhibited by the claimants.

 

Ruff v. Dep’t of Labor & Indus., 107 Wn. App. 289, 305-306, 28 P.3d 1, 9-10 (2001). [Division I]

 

[1] In the workplace, claimant smelled fumes.

[2] Claimant had a relatively immediate physical response to the fumes—cough, watery and burning eyes, dizziness, and a sensation of passing out.

[3] Claimant was diagnosed with an acute allergic reaction.

[4] Before the workplace exposure, claimant had a history of panic attacks producing the symptoms of cough, weakness, dizziness, and nausea.

[5] Claimant’s claim was denied as not due to a workplace exposure because she did not prove required nexus between exposures and symptoms.

 

While in the workplace remodeling a building, the worker smelled fumes and had a relatively immediate physical response of headaches, watery and burning eyes, nausea, cough, weakness, dizziness, and a sensation that she was about to pass out. She went to hospital; the ER doctor diagnosed the worker’s symptoms as an acute allergic reaction. Two days later, the worker returned to work. But after two hours, she felt dizzy and weak. She also experienced numbness in her face and shortness of breath and left work early. Before her workplace exposure to fumes, the worker had a history of head injuries, headaches, depression, and anxiety. She saw a number of doctors for symptoms that included fatigue, sore throat, nausea, nasal congestion, cough, and vomiting. The doctors performed numerous tests. the worker’s test results were all normal. The worker saw her physician about the cough, weakness, dizziness, and nausea she experienced shortly after her workplace exposure. Her physical exam was normal. Her physician opined that the worker had a panic reaction.

 

The court held as follows:

 

The claimants in Intalco worked 12 years at an aluminum pot room. [1] A federal air pollution survey of the pot room established the presence of known neurotoxins such as aluminum particulates and carbon monoxide and petroleum pitch volatiles. The claimants’ doctors diagnosed them with a disorder of the central nervous system and concluded that a toxin or a combination of toxins in the pot room more probably than not caused the disease.

 

The Intalco court rejected the employer’s claim that there was insufficient evidence to support the jury’s finding of proximate cause between the claimants’ disease and their workplace exposure because no physician could identify the specific toxic agent or agents in the pot room that proximately caused the claimants’ disease. [1] The court declined to require proof of the precise chemical that caused the claimants’ disease because several neurotoxins were identified in the pot room, it was undisputed that the neurotoxins cause symptoms similar to that exhibited by the claimants, and [4] & [5] their symptoms did not fit the diagnostic criteria of any known disease. In contrast, no one knows what chemicals Ruff was exposed to during the week-long building remodel.

 

            In re Judy M. Fry, BIIA Dec., 97 3415 (1998).

Claimant was a bookkeeper in an office that was remodeled with new carpeting in July 1993. A few days later, she noticed she had a skin rash. Several months later (September 1993) she saw an osteopath who diagnosed an allergic reaction rather than contact dermatitis. He did no testing for an allergy. The air quality of the workplace was not tested. He had no data concerning what toxins, if any, existed or in what concentrations. He treated claimant with high does of steroids. Claimant’s rash then went into remission. In October 1993, Claimant returned to the workplace for six hours and her rash immediately returned to its original intensity. She returned to work in January 1994 for 15 to 20 minutes and her condition once again flared. Since leaving work for good, her condition improved but had not completely resolved.

 

Claimant’s medical expert opined that claimant’s workplace exposures caused an allergic reaction based on the facts (1) that she had no other exposures or events near the time of the remodel and (2) that on the two occasions that she had returned to the workplace, her condition had flared noticeably. Another medical expert performed patch testing. That testing revealed that claimant was allergic to several formaldehyde resins, bacitracin and nickel. The testing did not reveal she had any allergy to standard glues and resins used in carpets. The expert said claimant had atopic dermatitis and that atopic dermatitis could appear at any time or age with no explanation other than coincidence to so-called exposure in the workplace or elsewhere. The expert said it was improbable that claimant developed the rash from inhaled volatile organic in carpeting and glues. The gassing occurs 24 to 48 hours and then drops off dramatically. The amount of toxins in the ambient atmosphere would be very low.

 

The BIIA noted that “there is no medical or lay testimony concerning what toxins, if any, were present in [claimant’s] workplace during the carpet installation and the painting.” “There is no testimony that rules out any other causation for [claimant’s] skin condition.” “There is no testimony that others in the workplace at that time suffered similar symptoms.” “There is no testimony that toxins that might be found in some carpets and some paint would cause certain conditions or diseases such as [claimant] experienced.” “No one testified about the concentration of toxins in the ambient air.” “No one testified what concentrations might be necessary to give rise to a skin reaction.” “There is also the troubling fact that [claimant’s] condition persisted for years after she was no longer being exposed to the alleged toxins in the workplace.” “Finally, there is no medical testimony that adequately describes how the inspiration of whatever gases may have been given off by the carpet, glues, paint, or cleaners could give rise to a skin condition.”

 

The BIIA remarked, “while the Intalco case removes the necessity for a claimant to show what specific chemical toxin in the workplace gave rise to a condition or disease, it does not do away with the need to show [1] what toxins existed in the workplace, [2] that those toxins are medically known to give rise to the certain conditions or diseases from which the worker actually suffered, and [3] that the toxins existed in a concentration sufficient to cause the deleterious effect.” “The lack of any one of those factors is fatal to a medical opinion on causation.” (Emphasis supplied.)

 

            In re Nancy Lynn Proszek, BIIA Dec., 92 6049 (1995).

Claimant, an airline attendant, while working as a flight attendant on a Boeing 737 suddenly felt hungry and disoriented. Since the flight she has been mentally slow, easily frustrated, and afflicted with memory problems. She contends that she sustained toxic encephalopathy due to carbon monoxide exposure or hypoxic encephalopathy due to deprivation of oxygen during specific flights. She contended that she was deprived of oxygen when the aircraft was flying at 37,000 feet and was pressurized to 8,000 feet. The employer testified that the aircraft was actually flying at 33,000 feet and the cabin had been pressurized to 6000 feet. The aircraft did not use re-circulated air.

 

She had a medical expert testify that to a reasonable degree of medical probability that her mental symptoms indicated a brain injury due to carbon monoxide poisoning or due to a lack of oxygen. He was unaware of any source for the carbon monoxide in the aircraft. He was unaware that the aircraft did not use re-circulated air. He was unaware that the aircraft was pressured to 6000 feet. He was unaware of any literature which associates elevations of 8,000 feet with danger of hypoxia. He offered no opinions on the dangers of hypoxia at 6,000 feet.

 

The BIIA ruled that claimant had presented no objective evidence that she actually was exposed to carbon monoxide or deprived of oxygen while at work. “To exempt her from establishing one [a damaging incident] or the other [an inherently damaging condition in the workplace] would completely relieve her of the burden of establishing a causal relationship between her course of employment and her alleged injury or disease.”

 

Point of Law: Cause-Effect Exposures Must Be Distinct to the Workplace.

 

Dennis v. Dep’t of Labor & Indus., 109 Wn.2d 467, 481, 745 P.2d 1295, 1303 (1987).

 

We hold that a worker must establish that his or her occupational disease came about as a matter of course as a natural consequence or incident of distinctive conditions of his or her particular employment.

 

***

 

The worker, in attempting to satisfy the “naturally” requirement, must show that his or her particular work conditions more probably caused his or her disease or disease-based disability than conditions in everyday life or all employments in general; the disease or disease-based disability must be a natural incident of conditions of that worker’s particular employment.

 

Parr v. Dep’t of Labor & Indust., 46 Wn. 2d 144, 145, 278 P.2d 666, 667 (1955).

When a workman is allergic to dust of various kinds and characters, such as road dust, house dust, wood dust, etc., and that allergy causes asthma, and the asthma becomes permanently disabling (in whole or in part), the fact that his employment required him to work in great quantities of wood dust for several hours at a time during certain seasons of the year, occasioning him great discomfort and causing asthmatic attacks, does not in itself establish that his disabling asthmatic condition arose naturally and proximately out of his employment and hence is an occupational disease within the purview of RCW 51.08.140 [cf. Rem. Supp. 1941, § 7679-1, which was the applicable statute when this claim was filed]. We so hold for the reason that the dust allergy could have caused the asthmatic condition regardless of his employment. St. Paul & Tacoma Lbr. Co. v. Department of Labor & Industries (1943), 19 Wn. (2d) 639, 144 P. (2d) 250.

 

Point of Law: By Objective Means, the Worker Must Establish A Nexus Between the Purported Workplace Exposure and the Symptoms.

 

St. Paul & Tacoma Lumber Company v. Dep’t Labor & Indus., 19 Wn.2d 639, 642-643, 144 P.2d 250, 252-253 (1943).

 

The finding of the joint board that the workman contracted an occupational disease of wood dust asthma from his employment resulting in his death is not sustained by the evidence. There is no evidence of probative value to remove the question of causal relation from the field of speculation and surmise.

 

Appellant widow testified that her husband had been working continuously for respondent employer since March, 1919, and that he had his first attack of serious illness in January, 1940; that for the past five or six years whenever he worked where it was dusty he would have smothering attacks and that whenever he rested from his work and kept away from the dust his condition improved, but that working in the dust at the mill caused him to cough and his breathing became more difficult, whereupon his physicians advised him to go to a drier climate. There was other testimony on the part of workmen, with whom the deceased workman was associated, that in the fuel house where Mr. Higgins was employed it was very dusty and the dust “caused him [Higgins] to do a lot of coughing.” Those workmen, however, did not by reason of their exposure to the dust sustain any disability.

***

The record of the clinic, where the deceased received treatment until he departed for Colorado on his last journey, does not show any complaint of any disability from inhalation of dust. The physician testified further that he did not believe that the physician testified further that he did not believe that the workman had a true “asthma,” and that he did not believe that dust had any bearing on the case.

***

The other physician witness, who is an allergy specialist, examined the deceased first in April, 1941, about two months prior to the death of the workman. He testified that he believed that Mr. Higgins was suffering from an allergy caused by his being “a person peculiarly over-sensitive to a certain substance or substances which may enter his body either in the air that he breathes or in the food that he eats.” He further testified that skin tests (which were never made) and by the reaction of the skin of Mr. Higgins the offending substance, whether it were food, dust from feathers, animals, etc., might be detected. The case history of this workman, the physician testified, indicated the workman suffered less while away from work, but he would not conclude therefrom that the disease was the result of inhalation of dust at respondent’s plant; that the skin tests would have revealed the causative factor of the asthma which may have been dust from wood or other products around him at work or possibly dust around his home or substances in his food in his diet.

“It would only be by the means of such tests that in this case it could be definitely determined as to whether his occupation was the cause of his allergy in spite of the fact that the history seemed to suggest that.”

 

Briefly, the testimony of this physician witness is that the death of Mr. Higgins was attributable to allergic bronchial asthma, but he went no further than to testify that he suspected that deceased was allergic to some substance connected with his employment. He gave a negative answer to the question whether, since the skin tests were not made to determine the cause of the worker’s asthma, he was able to state the cause of the bronchial asthma from which Mr. Higgins suffered. The employees who worked side by side with Mr. Higgins for a number of years experienced no ill effects from their exposure to the wood dust. While the evidence would sustain a finding that the death of Mr. Higgins resulted from bronchial asthma caused by an individual over-sensitiveness to some particular substance, there is no evidence, nothing more than surmise, that that substance was wood dust.

 

McClelland v. ITT Rayonier, Inc., 65 Wn. App. 386, 393-394, 828 P.2d 1138, 1142-1143 (1992). [Division II]

 

Considering the “natural” and “proximate” elements in terms of this case, therefore, we must ask if the evidence shows that McClelland’s major depression and simple phobia were “probably” caused by the distinctive demands of his particular employment, measured objectively, aggravating his preexisting mental problems, or were they caused simply by his own subjective but unrealistic view of the situation at the pulp mill, or by conditions in everyday life.

 

Bearing in mind the holding of Dennis that a compensable occupational disability can result when conditions of employment aggravate a non-work-related disease, and resolving doubts in favor of compensation for the injured worker, we still hold that McClelland failed to create an issue of material fact.

***

McClelland relies primarily on his treating psychiatrist’s testimony that his depression, more probably than not, “mainly related to his work experience and what had happened there.” We are aware that the trier of fact should give “special consideration” to the claimant’s treating physician. Hamilton v. Department of Labor & Indus., 111 Wn.2d 569, 761 P.2d 618 (1988). 1 The doctor’s opinion does not create an issue of fact here, however, because of the longstanding requirement that there must be objective proof of the relationship between the employment and the occupational disease. Favor v. Department of Labor & Indus., 53 Wn.2d at 704-05.

***

Clearly, that is an objective test, not a license for a claimant to rely solely on his subjective impressions of the conditions at his place of employment. Dr. Rice had only his patient’s subjective impressions to go on. We have no doubt that Mr. McClelland suffered depression caused in part by stresses he experienced at work, but those stresses were, unfortunately, self-inflicted and not objectively caused by the work.

 

Point of Law: An expert opinion not based upon full knowledge of all material facts—based that is on only select facts advantageous to the party but omitting proven facts equally material, but not so beneficial to the party–lacks sufficient probative value to support a verdict on the issue of causal relationship.

 

Berndt v. Dep’t of Labor & Indus., 44 Wn.2d 138, 265 P.2d 1037 (1954).

 

“We think that all these circumstances were very material ingredients of a hypothetical question, the purpose of which was to ascertain from a medical expert the causes which had produced plaintiff’s then very serious condition. At the time the question was asked, these facts were all proven, were undisputed, and clearly material. Under such circumstances, a party is not permitted to select facts which may be advantageous to him, and omit proven facts equally material, but not so beneficial to his cause, and upon such partial facts frame a hypothetical question to be submitted to an expert witness. The purpose of all judicial investigation is the ascertainment of truth. Such purpose is wholly frustrated if a party is permitted to exclude from a hypothetical question material undisputed facts.

 

In a civil case all the undisputed facts of the case must be included in a hypothetical question, both as a matter of sound principle and of reason and justice. Neither party has a right to discard an important undisputed fact because the insertion of such fact may alter or vary the answer or opinion of the witness to the prejudice of such party.

 

Parr v. Dep’t of Labor & Indus., 46 Wn.2d 144, 278 P.2d 666 (1955).

 

When a doctor’s examination discloses a disabling disease such as asthma and his knowledge as to the causal relationship between the disease and the conditions of the patient’s employment is entirely dependent upon the history given to him by the patient or others, the value of his opinion as to causal relationship obviously depends upon the extent and accuracy of the information upon which that opinion is based. See discussion in Johnson v. Bangor R. & Electric Co. (1925), 125 Me. 88, 131 Atl. 1.

 

Where the only medical testimony that a workman’s employment was a proximate cause of his disabling disease is the testimony of a doctor, based upon a history given by the workman of recurring attacks of asthma caused by wood dust encountered in the course of his employment, and the doctor has not been advised of a vital element bearing upon causal relationship, i.e., that the workman is allergic to dusts of various kinds, such as road dust, house dust, etc., which also cause him to have asthmatic attacks, such testimony does not have sufficient probative value to support a verdict on the issue of causal relationship. The situation is comparable to that of the expert who answers a hypothetical question from which undisputed material facts have been omitted. See Berndt v. Department of Labor & Industries (1954), 44 Wn. (2d) 138, 265 P. (2d) 1037.

 

Sayler v. Dep’t of Labor & Indus., 69 Wn.2d 893, 421 P.2d 362 (1966).

 

An expert medical opinion concerning causal relationship between an industrial injury and a subsequent disability must be based upon full knowledge of all material facts. An expert opinion given in response to a hypothetical question is without probative value if it is based upon the existence of conditions or facts not included in the question or established by the evidence and not necessarily inferable therefrom. Berndt v. Department of Labor & Indus., 44 Wn.2d 138, 265 P.2d 1037 (1954); Cyr v. Department of Labor & Indus., 47 Wn.2d 92, 286 P.2d 1038 (1955). The same rule applies to medical opinions based upon incomplete or inaccurate medical history. Parr v. Department of Labor & Indus., 46 Wn.2d 144, 278 P.2d 666 (1955). If the doctor has not been advised of a vital element bearing upon causal relationship, his conclusion or opinion does not have sufficient probative value to support an award.

 

Summary of the Case Law

  1. The appellate courts want to reduce the “moral hazard” created when a claim for industrial insurance benefits is founded on claimant’s subjective experience.
  2. The appellate courts do not want claims allowed that are, at their core, merely the claimant’s opportunistic post hoc associations of his/her non-specific symptoms to workplace conditions.
  3. The appellate courts do not want claims allowed where the purported disease is one commonly caused by exposures outside the workplace where the claimant has not clearly eliminated those outside exposures as the cause of his/her disease.

 

Exception To The Summary of Case Law

Division II of the Washington Court of Appeals is not particularly concerned about the moral hazard, as revealed in its recent decision in Lewis v. Simpson Timber Co., 145 Wn. App. 302, 189 P.3d 178 (2008) [Division II].

 

Lewis v. Simpson Timber Co., 145 Wn. App. 302, 189 P.3d 178 (2008) [Division II].

 

The worker was exposed to a chemical in the workplace.

 

“Excess fungicide spray fell down from the main floor into the basement and dripped on [the worker]. At times, her coveralls were soaking wet from the … fungicide… .”

The chemical consisted of propiconazole and unknown solvents.

 

“According to the experts’ testimony, the material safety data sheet (MSDS), showing a product’s potentially hazardous substances, listed only that Mycostat-P and Mycostat-P20 contained propiconazole and other unidentified solvents.”

 

A “solvent” is defined as a liquid that reacts with another substance to bring into solution. So saying that some substance is a “solvent” does not entail that it is harmful. For instance, water is a solvent.

 

“Propiconazole,” a fungicide, was not considered to be harmful. Claimant’s key witness acknowledged that the MSDS for Mycostat did not list any harmful chemical. It merely listed propiconazole and unidentified solvents. Dr. Thomas G. Martin, a well respected occupational medicine specialist at the Occupational Medicine Clinic at University of Washington, opined that the fungicide propiconazole is safe and similar to the fungicide used clinically to treat patients with fungal infections.

 

No one knew what solvents were in Mycostat and, hence, whether they were harmful.

 

Simpson had hired an industrial hygienist to determine the nature of the solvents. He concluded that “one of the challenges [with his investigation] was that [because of] the trade secret solvents that were used [in the Mycostat product, he] never found out exactly what they were.” … [H]e testified:

  1. Now, in assuming what the 80 percent of solvents for the Mycostat[-P]20, were you assuming that xylene was attached to that solvent?
  2. I really have no idea what was in that. As I said earlier, from an agricultural website, they listed solvents that are used and blended with propiconazole. And all of them listed here, including xylene, were listed there. But I don’t know whether xylene is in that product or not.
  3. Have you subsequently reviewed any material that would indicate whether xylene was present in Mycostat-P?
  4. I have–I’ve never received any information from [the manufacturer] or anyone else to tell me that xylene is in it.

 

“Lee also admitted that he did not know whether any of the other compounds that he suggested in his report actually were part of the Mycostat solutions. There was no testimony that xylene or toluene was used at Simpson. Robert Miller, a supervisor, testified that xylene was not used to dilute Mycostat, that he was never told that it was one of the product’s solvents, and that he was not aware of Simpson using it anywhere at its facility.”

 

During the end of the time worker worked for the employer, the worker developed a cluster of non-specific symptoms.

 

[The worker] worked for Simpson for over 30 years. But, in August 2002, she began to experience unexplained symptoms. She had a rash on her arms and chest, bleeding ears, difficulty communicating with others, weight gain, bloody noses, pain when touching others, an asthma-like cough, and difficulty walking. She also experienced digestive problems, ringing in her ears, headaches, tingling under the skin, hallucinations, heart palpitations, and memory loss. In the middle to the end of 2003, she gained about 70 pounds, which she and others described as puffiness and water retention. She also had a marked decrease in energy.

 

When she left the workplace, she said that some of her symptoms abated.

 

[The worker] quit working at Simpson Timber in August 2003. Since that time, her conditions have improved. She has not gained more weight and has no bleeding in the ears, bloody noses, or rashes. Her skin no longer hurts when she is touched and her respiratory symptoms have improved. But she still feels as if she has asthma because, when she becomes ill, her symptoms persist for a much longer duration than they did previously. She still experiences problems with her memory, although she is able to communicate better. She testified that exposure to some smells causes her symptoms to worsen. Those smells are asphalt, gasoline or oil smells, vehicle exhaust fumes, and vehicle air fresheners. When she is exposed to gas fumes, her heart beats very quickly, and she becomes light-headed, dizzy, and tired.

 

Mainstream medical experts found nothing to indicate a harmful chemical exposure. The worker saw her primary care physicians, a family practice physician and an internist. She related to them that she had recently discontinued hormone replacement therapy and had been taking an antidepressant for her menopausal symptoms. These physicians, in an effort to identify what ailed the worker, referred her to a variety of respected specialists. They referred her to a neurologist. He found her to be neurologically normal. They referred her to an eye, ear, nose and throat specialist. He found her to be normal. As of March 2003, the worker had not mentioned to any of these health care providers an exposure to toxins. About this time, in relating to her history to her physicians, the worker began associating her symptoms with her exposure to Mycostat-P. Based on this history, her family physician began exploring the possibility that the worker had an occupational disease from exposure to Mycostat-P.

 

On April 2, 2003, the worker filed an accident report with the employer. On April 28, 2003, her family physician referred the worker to a well respected pulmonologist. He found her to be pulmonologically normal, and opined that she did not have occupationally induced lung disease. On July 11, 2003, her family physician referred her to a well respected occupational medicine specialist at the Occupational Medicine Clinic at University of Washington. He examined her with an associate. Both found her to be physically normal, and opined that she did not have an occupationally induced disorder. This physician noted particularly that, apart from the non-specific symptoms of dizziness, she did not have symptoms consistent with exposure to Mycostat-P, according to data in the National Library of Medical Toxicology. He noted that the fungicide propiconazole is safe and similar to the fungicide used clinically to treat patients with fungal infections. Nor were her symptoms consistent with exposure to xylene. Her family physician then referred her to a neurologist. He found her to be neurologically normal.

 

Brent Burton, M.D., MPH, a board certified specialist in occupational medicine and medical toxicology, after a thorough review of the worker’s medical records, opined, consistently with other examiners that the worker’s constellation of symptoms was inconsistent with a medical condition or with exposure to a toxin or with exposure to Mycostat-P, which is not a neurotoxin, or with the exposure to xylene, which even in significant doses produces only symptoms consistent with short term alcohol intoxication. The worker had an independent medical examination with Dr. Anthony Montanaro, a board certified internist, allergist and immunologist at the Oregon Health Sciences University, where he is a full professor of medicine and Chief of the Division of Allergy and Immunology. Dr. Montanaro opined, consistently with other examiners that the worker did not have symptoms consistent with exposure to a toxic chemical or with exposure to Mycostat-P or Mycostat-P20 or with exposure to xylene.

 

Junk science experts speculated that the worker’s symptoms were caused by exposure to the solvents xylene and toluene. On December 15, 2003, the worker had apparently directed herself to a naturopath, who treated her with various alternative naturopathic therapies. Then, on February 16, 2004, based on a recommendation from her union, the worker had her naturopath refer her to David Buscher, M.D., a self-proclaimed specialist in “environmental medicine,” but without board certification by the American College of Certified Medical Examiners (ACCME). He treated her with an odd assortment of non-medically standard treatments, including supplemental oxygen, ingestion of a powder to “de-toxify her body,” and placement of vials of substances under her tongue to combat potential food allergies. These treatments were described by Brent Burton, M.D., a board certified specialist in occupational medicine and toxicology, as “medical quackery.” Dr. Buscher then referred her to Philip Ranheim, M.D., a family practice physician but not her treating physician, who first saw her April 26, 2005, presumably to lay a foundation for him to testify as a forensic witness.

 

David Buscher, M.D.

Dr. Buscher examined the worker and found her to be normal, except for mild swollen mucus membranes and her subjective complaint of tender muscles. On the issue of specific causation, he opined: “More probably that not, [the worker’s] health problems as described are due to exposures to toxic substances at work … ,” specifically, the solvents of toluene and xylene. Dr. Buscher assumed that the solvents of toluene and xylene were present in an antifungal agent called Mycostat.

 

Asked why an exposure to said solvents would cause the worker’s symptoms, Dr. Buscher testified, “Well, I don’t know. I don’t think we can know for sure. It depends.” Asked why the worker’s symptoms have persisted for years while irritation to her co-workers would last only a few hours, Dr. Buscher replied, “Like I say, I can’t explain it….” Asked whether the worker’s symptoms are necessarily caused by a chemical exposure, Dr. Buscher replied, “No.” He essentially reached his conclusion on specific causation on the basis of the fallacy “post hoc, ergo propter hoc“–that before Mycostat was used, the worker did not complain of her symptoms, after it was introduced into the workplace, she did complain of her symptoms; therefore, something in her workplace caused her symptoms.

 

Dr. Buscher acknowledged that the MSDS for Mycostat did not list any harmful chemical. He further acknowledged that in Washington a MSDS is not required to list non-toxic solvents. The sole reason Dr. Buscher believed that Mycostat contained the solvents of toluene and xylene was that he believed Mr. Lee had identified toluene and xylene as being in Mycostat. In short, Dr. Buscher assumed that Mr. Lee knew what was in Mycostat.

 

  1. “So once the Mycostat was introduced, it is your opinion that that is what caused these symptoms; correct?”
  2. “That’s what I understand, yes.”
  3. “And the reason you say that, that’s based on your understanding that the solvents of toluene and xylene were present in the Mycostat; correct?”
  4. “That’s what I understand; that’s correct.”
  5. And you got that from that report from Mr. Lee, from the industrial hygienist’s report, correct?”
  6. “Yes.”
  7. “And you are assuming that Mr. Lee knew what was in Mycostat in offering the opinions of what was in there; correct?”
  8. “Correct.”

 

Buscher, [the worker’s] treating physician, … reviewed Lee’s report and found it very significant because his “experiences told [him that] this woman was probably exposed to solvents [such as xylene and toluene], but the MSDS said no. So [he] was confused by that. [He] felt there was something missing, and [Lee’s report] confirmed [his] previous suspicion” about his diagnosis of toxic exposure to solvents. He also testified that it was [the worker’s] exposure to solvents that was important, but determining the specific solvent, whether it was xylene, toluene, or another solvent, was not as important to his diagnosis because “if you read a textbook of toxicology, you are going to find a little bit of difference with different solvents and what they do and how they metabolize. But basically they are pretty close [in] how they affect us.” He concluded that “[m]ore probably than not, [the worker’s] health problems as described are due to exposures to toxic substances at work[, which] were most likely the solvents.”

 

Philip Ranheim, M.D.

Dr. Ranheim examined the worker once on April 26, 2003. He never treated her. Her examination was essentially normal, except she had a fungus infection in her toenails; a positive stress Romberg test; and slight asymmetry in her ankle reflexes. On the issue of specific causation, Dr. Ranheim opined that Mycostat caused the worker’s symptoms. He based this opinion on the assumption that constituents of Mycostat included the solvents toluene and xylene. Dr. Ranheim agreed that the Material Safety Data Sheet (MSDS) for Mycostat did not refer to the solvents toluene or xylene. He assumed that Mycostat included the solvents toluene and xylene based on Mr. Lee’s report.

 

“Ranheim also testified that more probably than not [the worker’s] ‘exposure in the workplace caused the symptoms which [she] is experiencing and represents the basis of the injury that she has sustained.’ While Ranheim testified that other factors beside toxic exposure could have explained all of [the worker’s] symptoms and none of his tests showed that she had chemical exposure, his opinion was informed by [the worker’s] self-reported symptoms and chemical exposure, and his review of other physicians’ examinations of her. Ranheim admitted that it is helpful to know what chemical or chemicals to which the patient was exposed, and the patient’s exposure rate to those chemicals, to evaluate a diagnosis, but he testified that physicians must take into account the individual characteristics of the patient, stating, “[i]t’s not the dose [that] makes the poison. It’s the dose plus the host.” But Ranheim testified that Lee’s report, which stated the possible solvents found in the Mycostat solutions, influenced his medical opinion, even though the manufacturer did not supply him with any such information, and he testified that his opinion would have been affected if Mycostat contained only a fungicide and water.”

 

Causation Standard Applied by Division II:

 

“For [the worker] to prove causation, the testimony of medical experts ‘must establish that it is more probable than not that the [exposure to chemicals at the work place] caused the subsequent disability.'” … . And Division One of this court held that, under the IIA, “the claimant [is not required] to identify the precise chemical in the workplace that caused his or her disease” because we liberally construe the IIA and because “the claimant is only required to demonstrate that conditions in the workplace more probably than not caused his or her disease or disability.” Intalco Aluminum, 66 Wn. App. at 658. In addressing the sufficiency of the evidence, it held:

A physician’s opinion as to the cause of the claimant’s disease is sufficient when it is based on reasonable medical certainty even though the doctor cannot rule out all other possible causes without resort to delicate brain surgery. The evidence is sufficient to prove causation if, from the facts and circumstances and the medical testimony given, a reasonable person can infer that a causal connection exists.

 

Intalco Aluminum, 66 Wn. App. at 654-55 (citation omitted).

 

Here, jury instruction 14 stated:

The Worker’s Compensation Act does not require the claimant to identify the precise chemical in the work place that caused his or her disease. However, evidence is not sufficient to prove causation unless, from the facts and circumstances and the medical testimony given, a reasonable person can infer that a causal connection exists.

 

Simpson first argues that instruction 14 misstated Washington law because it did not instruct the jury that [the worker] had to prove that a specific chemical existed in the workplace that she was exposed to and that caused her symptoms. Similar to the employer in Intalco Aluminum, Simpson “cites no authority for the proposition that [the worker] must identify the specific causative agent responsible for [her] occupational disease,” nor could we find any. 66 Wn. App. at 656.

 

Instruction 14 provides that Lewis need not “identify the precise chemical in the work place that caused … her disease.” It instructs the jury that it must find or be able to infer a casual connection. The only reasonable interpretation of the jury instruction is that the cause of [the worker’s] symptoms must have arisen from a chemical or set of chemicals found in her workplace at Simpson. The instruction was not misleading or a misstatement of law.

 

Division II Finds Sufficient Evidence to Persuade a Fair-Minded Rational Person:

 

“In [the worker’s] IIA case, the medical testimony must have established that it was more probable than not that her exposure to chemicals at Simpson caused her occupational disability. *** But although the precise chemical need not be identified, testimony must establish that the presence of a toxin or combination of toxins in [the worker’s] work environment more probably than not caused her medical condition. Intalco Aluminum, 66 Wn. App. at 654-56. “Testimony that goes no further than to indicate that the injury might have caused the condition is insufficient; there must be some evidence of probative value that removes the question of causal relation from the field of speculation and surmise. If there is no evidence of causation beyond a possibility, it is error to submit the case to the jury.”

 

It is undisputed that Mycostat-P and Mycostat-P20 were present at Simpson and that [the worker] was exposed to them. Mycostat-P and Mycostat-P20 contain propiconazole, which is a fungicide used to prevent mold and fungus from growing on the timber. According to the experts’ testimony, the material safety data sheet (MSDS), showing a product’s potentially hazardous substances, listed only that Mycostat-P and Mycostat-P20 contained propiconazole and other unidentified solvents.

 

***

“… Lee’s, Ranheim’s, and Buscher’s testimony provides sufficient evidence to persuade a fair-minded rational person that a combination of toxic chemicals was present in Lewis’s workplace and that those chemicals caused her medical symptoms based on her individual reaction to them.”

 

            Summary of Lewis v. Simpson Timber Company

[1] Worker has contact with a chemical in the workplace.

[2] Expert speculation whether that chemical is harmful.

[3] Reason backward from cluster of non-specific symptoms to a possible harmful chemical exposure.

[4] Have a junk scientist testify that there is a causal nexus between the chemical and the symptoms.

 

            In re James M. Stein, Dckt. No. 99 13234 (September 8, 2000).

Claimant was diagnosed with sarcoidosis, residual erythema nervosa, and arthralgias. He contended that these problems were caused by his workplace exposure to fumes, identified vaguely as organic polymers and acrylic components, including epoxy resin. The BIIA noted that “the evidence in this appeal does not establish the exact chemical agents to which [claimant] was exposed in the workplace.” He was not exposed to beryllium, a substance that had been hypothesized to caused sarcoid like symptoms. He proffered no proof of the extent of his exposure except claimant’s statement that there was a considerable amount of fumes in the air.

 

The BIIA noted that “neither does the evidence establish the quantity or concentration of the chemicals in specific measures, nor the duration of exposure to particular chemicals.” Claimant did proffer evidence that his symptoms worsened while at work and lessened while away from work. The medical experts unable to identify how the workplace played a role with claimant’s sarcoidosis, other than to offer untested hypothesis that “chemical exposure is at least one hypothesis in which medical science is interested.” The experts all agreed that “sarcoidosis is an idiopathic inflammatory disorder caused by an undetermined abnormality of the immune system.”

 

Claimant’s medical experts testified that claimant’s symptoms were a bad cough, burning eyes, pain in his ankles and feet, swelling in his ankles, bumps on his skin, nodules on his arm, and swelling in his joints. The symptoms of a cough and burning eyes began about a month after claimant was hired. The other symptoms developed gradually afterwards. Claimant by history noted that the swelling diminished on weekends and increased while at work. His cough increased while at work. Large doses of steroids (Prednisone) relieved his symptoms dramatically. This was stated to be “the only treatment that will work for allergic toxic exposure responses.” Based essentially on claimant’s history, claimant’s medical experts testified that claimant’s exposures to fumes at work more probably than not aggravated or caused his sarcoidosis.

 

The BIIA remarked that a “claimant is only required to demonstrate that conditions in the workplace more probably than not caused his or her disease or disability.” “The evidence is sufficient to prove causation,” the BIIA further noted, “if, from the facts and circumstances and the medical testimony given, a reasonable person can infer that a causal connection exists.” Because the BIIA was required to construe the IIA liberally in favor of the claimant, it held that “the worker’s compensation statute does not require the claimant to identify the precise chemical in the workplace that caused his or her disease.”

 

Potpourri Theory of Exposures—The Rub

If claimant seeks to argue that by Intalco, he/she does not need to identify the particular agent/irritant out of several possible agents/irritants, then he/she must prove that all of those suspected agents/irritants are not present outside the workplace or that claimant was not exposed to them outside the workplace. In Intalco, none of the suspected toxins were present outside the workplace.

 

The greater the number of members of the class of agents/irritants that the claimant identifies as potentially responsible for his/her symptoms, the greater the burden on claimant to establish that these members of that class are distinct to the workplace.

 

  1. Preventive Measures

 

Before Hiring

As a rule, the employer cannot discriminate against prospective workers based on their preexisting diseases/disorders or propensities to develop various diseases/disorders. But an employer can refuse to hire a worker owing to any sensory, mental or physical handicap if the absence of such a handicap is a “bona fide occupational qualification.” RCW 49.60.180.

RCW 49.60.180(1):

 

“To refuse to hire any person because of the presence of any sensory, mental, or physical disability, unless based upon a bona fide occupational qualification: PROVIDED, That the prohibition against discrimination because of such disability shall not apply if the particular disability prevents the proper performance of the particular worker involved … .”

WAC 162-12-140 (3):

The following examples of fair and unfair preemployment inquiries define what is an unfair practice under RCW 49.60.180(4) and 49.60.200. These examples, however, are not all inclusive. All preemployment inquiries that unnecessarily elicit the protected status of a job applicant are prohibited by these statutes irrespective of whether or not the particular inquiry is covered in this regulation.

 

***

 

  1. Disability

 

Fair Preemployment Inquiries 

[1] Whether applicant is able to perform the essential functions of the job for which the applicant is applying, with or without reasonable accommodation. [2] Inquiries as to how the applicant could demonstrate or describe the performance of these specific job functions with or without reasonable accommodation. Note: Employers are encouraged to include a statement on the application form apprising applicants that if they require accommodation to complete the application, testing or interview process, to please contact the employment office, personnel or human resources department or other office as may be able to assist them.

 

Unfair Preemployment Inquiries 

[1] Inquiries about the nature, severity or extent of a disability or whether the applicant requires reasonable accommodation prior to a conditional job offer. [2] Whether applicant has applied for or received worker’s compensation. [3] Also any inquiry that is not job related or consistent with business necessity.

 

After Hiring

Some prospective workers should not be in some jobs. For example, the asthmatic should not working in the presence or vicinity of irritating gases or dusts.

 

Workers should not be working with substances that can caused adverse physical reactions without proper protective equipment, such as respirators and protective clothing.

 

Identifying Pre-Existing Conditions in Workers

Some prospective workers have preexisting conditions or hypersensitivities that cause them to be susceptible to workplace aggravations or the “lightings up” of latent conditions. In some workplaces, where potential exposures to irritants or environmental triggers exist, these workers are industrial insurance time bombs.

 

Some of the more potentially dangerous potential hires are those with psychological disorders, such as somatoform or anxiety disorders. As Montaigne remarked,

 

“A woman, thinking she had swallowed a pin with her bread, was screaming in agony as though she had an unbearable pain in her throat, where she thought she felt stuck; but because externally there was neither swelling nor alteration, a smart man, judging that it was only a fancy and notion derived from some bit of bread that had scratched her as it went down, made her vomit, and, on the sly, tossed a crooked pin into what she threw up. The woman, thinking she had thrown it up, felt herself suddenly relieved of her pain.”

 

When employers hire workers with preexisting conditions they are often “buying” disabilities associated with that condition. You are also buying the risk of a “false positive” diagnosis incorrectly related to a workplace exposure. Plain and simple, this social cost is being shifted from the public weal to the employer with the help of “progressive” jurists.

 

Washington Law Against Discrimination For Disabilities or Handicaps

In protecting itself from “false positive” complex exposure claims, the employer must tip toe through a minefield of progressive laws designed to protect the worker.

 

RCW 49.60.030(1):

 

“The right to be free from discrimination because of … the presence of any sensory, mental, or physical disability … is … a civil right… .” RCW 49.60.030(1).

 

RCW 49.60.180(1):

 

“It is an unfair practice for any employer: (1) To refuse to hire any person because of … the presence of any sensory, mental, or physical disability… , unless based upon a bona fide occupational qualification: PROVIDED, That the prohibition against discrimination because of such disability shall not apply if the particular disability prevents the proper performance of the particular worker involved: …. (2) To discharge or bar any person from employment because of … the presence of any sensory, mental, or physical disability … .(4) To … use any form of application for employment, or to make any inquiry in connection with prospective employment, which expresses any limitation, specification, or discrimination as to … the presence of any sensory, mental, or physical disability …, or any intent to make any such limitation, specification, or discrimination, unless based upon a bona fide occupational qualification:… .”

 

WAC 162-22-020:

 

“A condition is a ‘sensory, mental, or physical disability’ if it is an abnormality and is a reason why the person having the condition did not get or keep the job in question, or was denied equal pay for equal work, or was discriminated against in other terms and conditions of employment, or was denied equal treatment in other areas covered by the statutes. In other words, for enforcement purposes a person will be considered to be disabled by a sensory, mental, or physical condition if he or she is discriminated against because of the condition and the condition is abnormal.”

 

See also, Phillips v. Seattle, 111 Wn.2d 903, 766 P.2d 1099 (1989).

 

WAC 162-22-025:

 

“It is an unfair practice for any employer, employment agency, labor union, or other person to: (1) Refuse to hire, discharge, bar from employment, or otherwise discriminate against an able worker with a disability or because of the use of a trained dog guide or service animal by an able worker with a disability; or

 

(2) Fail or refuse to make reasonable accommodation for an able worker with a disability… , unless to do so would impose an undue hardship (please see WAC 162-22-065 and 162-22-075); … .”

 

Bona Fide Occupational Qualifications

 

RCW 49.60.180(1):

 

“To refuse to hire any person because of the presence of any sensory, mental, or physical disability, unless based upon a bona fide occupational qualification: PROVIDED, That the prohibition against discrimination because of such disability shall not apply if the particular disability prevents the proper performance of the particular worker involved … .”

 

WAC 162-22-045:

 

“Under the law against discrimination, there is one exception to the rule that an employer, employment agency, labor union, or other person may not discriminate on the basis of protected status; that is if a bona fide occupational qualification (BFOQ) applies. For a complete discussion of BFOQs, please read WAC 162-16-240.”

 

WAC 162-16-240:

 

“Under the law against discrimination, there is an exception to the rule that an employer, … may not discriminate on the basis of protected status; that is if a bona fide occupational qualification (BFOQ) applies. The commission believes that the BFOQ exception should be applied narrowly to jobs for which a particular quality of protected status will be essential to or will contribute to the accomplishment of the purposes of the job. The following examples illustrate how the commission applies BFOQs: (1) Where it is necessary for the purpose of authenticity or genuineness (e.g., model, actor, actress) or maintaining conventional standards of sexual privacy (e.g., locker room attendant, intimate apparel fitter) the commission will consider protected status to be a BFOQ. (2) A 911 emergency response service needs operators who are bilingual in English and Spanish. The job qualification should be spoken language competency, not national origin. (3) An employer refuses to consider a person with a disability for a receptionist position on the basis that the person’s disability “would make customers and other coworkers uncomfortable.” This is not a valid BFOQ… .”

 

“The bona fide occupational qualification applies to all persons with the handicap, even though the particular applicant in fact could perform the job.” Rose v. Hanna Mining Company, 94 Wn.2d 307, 616 P.2d 1229 (1980).

 

“The employer must show that all or substantially all persons who do not possess the qualifications would not be able to perform the work safely and efficiently within the limits of reasonable accommodation.” Fahn v. Cowlitz County, 93 Wn.2d 368, 610 P.2d 857 (1980); Rose v. Hanna Mining Company, 94 Wn.2d 307, 616 P.2d 1229 (1980).

 

“To establish a business necessity defense, an employer must prove by professionally accepted measures that the hiring or promotion test utilized accurately predicts or significantly correlates with the fundamental requirements of job performance. The burden then shifts to the plaintiff to show that other less discriminatory alternatives equally serve the employer’s legitimate business requirements.” Shannon v. Pay ‘N Save Corporation, 104 Wn.2d 722, 709 P.2d 799 (1985).

 

“Application of [RCW 49.60.180] is a two-step process: First, the burden is on the rejected job applicant to establish a prima facie case of handicap discrimination. Second, the burden shifts to the employer to articulate some nondiscriminatory reason for not hiring. It may do so either of two ways. It can show (1) the particular disability prevents the proper performance of the particular worker involved, or (2) a particular worker cannot satisfy a BFOQ.” Blanchette v. Spokane County Fire Protection District No. 1, 67 Wn. App. 499, 836 P.2d 858 (1992).

 

WAC 162-12-140 (3):

The following examples of fair and unfair preemployment inquiries define what is an unfair practice under RCW 49.60.180(4) and 49.60.200. These examples, however, are not all inclusive. All preemployment inquiries that unnecessarily elicit the protected status of a job applicant are prohibited by these statutes irrespective of whether or not the particular inquiry is covered in this regulation.

 

***

 

  1. Disability

 

Fair Preemployment Inquiries 

[1] Whether applicant is able to perform the essential functions of the job for which the applicant is applying, with or without reasonable accommodation. [2] Inquiries as to how the applicant could demonstrate or describe the performance of these specific job functions with or without reasonable accommodation. Note: Employers are encouraged to include a statement on the application form apprising applicants that if they require accommodation to complete the application, testing or interview process, to please contact the employment office, personnel or human resources department or other office as may be able to assist them.

 

Unfair Preemployment Inquiries 

[1] Inquiries about the nature, severity or extent of a disability or whether the applicant requires reasonable accommodation prior to a conditional job offer. [2] Whether applicant has applied for or received worker’s compensation. [3] Also any inquiry that is not job related or consistent with business necessity.

 

Reasonable Accommodations

 

WAC 162-22-065:

 

“(1) Reasonable accommodation means measures that: (a) Enable equal opportunity in the application process; (b) Enable the proper performance of the particular job held or desired; (c) Enable the enjoyment of equal benefits, privileges, or terms and conditions of employment. (2) Possible examples of reasonable accommodation may include, but are not limited to: (a) Adjustments in job duties, work schedules, or scope of work; (b) Changes in the job setting or conditions of work; (c) Informing the employee of vacant positions and considering the employee for those positions for which the employee is qualified.”

 

WAC 162-22-075:

 

“An employer, … must provide reasonable accommodation unless it can prove that the accommodation would impose an undue hardship. An accommodation will be considered an undue hardship if the cost or difficulty is unreasonable in view of: (1) The size of and the resources available to the employer; (2) Whether the cost can be included in planned remodeling or maintenance; and (3) The requirements of other laws and contracts, and other appropriate considerations.”

 

No Retaliation Against Workers

 

RCW 51.48.025:

“(1) No employer may discharge or in any manner discriminate against any employee because such employee has filed or communicated to the employer an intent to file a claim for compensation or exercises any rights provided under this title. However, nothing in this section prevents an employer from taking any action against a worker for other reasons including, but not limited to, the worker’s failure to observe health or safety standards adopted by the employer, or the frequency or nature of the worker’s job-related accidents. … .”

 

Wilmot v. Kaiser Aluminum & Chem. Corp., 118 Wn.2d 46, 821 P.2d 18 (1991).

 

Americans with Disabilities Act

 

42 U.S.C. §12101 et seq.

 

“Title I requires employers with 15 or more employees to provide qualified individuals with disabilities an equal opportunity to benefit from the full range of employment-related opportunities available to others. For example, it prohibits discrimination in recruitment, hiring, … and other privileges of employment. It restricts questions that can be asked about an applicant’s disability before a job offer is made, and it requires that employers make reasonable accommodation to the known physical or mental limitations of otherwise qualified individuals with disabilities, unless it results in undue hardship.”

 

Industrial Hygienists/Toxicologists

Employers can hire experts in industrial toxicology—toxicologists and industrial hygienists–to survey the workplace for potential hazards. This practice has risks. Such surveys can create evidence that the unscrupulous worker can use to build a claim. But given the low threshold of proof necessary these days to prove a claim from complex exposures and the practical reality that employers bear the burden of proving the negative—that claimant was not exposed to a harmful agent—the benefit of such survey outweighs its risks.

 

Cost-Benefit Analyses

Industrial toxicologists seeks to prevent injuries or diseases in workers exposed to potentially harmful industrial agents. They seek to establish what are unacceptable and acceptable health risks in the workplace. They do this by defining what are permissible levels of exposure to industrial agents, such as chemicals. Such levels can be expressed in terms either of allowable atmospheric concentrations or of permissible biologic levels for the chemical. Be aware that these atmospheric or biological allowable concentrations entail some health risk. They are best understood as the level of exposure below which the risk is acceptable.

 

To conclude that a risk is acceptable, the employer must identify and quantify it. That requires knowing the relationship between dose and health effects and the relationship between dose and the prevalence of subjects exhibiting a defined adverse effect. In this regard, the employer must recognize that there is no one single dose-effect relationship but as many as there are exposed workers. Simply, at the acceptable level of risk, some exposed workers will likely develop adverse effects.

 

Simpson Timber Co. v. Wentworth, 96 Wn. App. 731, 981 P.2d 878 (1999).

The test whether an occupational disease has occurred is not whether most workers of reasonable good health would suffer a disabling disease under the same conditions, but rather whether the individual worker with his/her preexisting frailties and bodily infirmities suffered the disease.

 

Periodic Fitness for Duty Examinations

After a worker is hired to work in a workplace with potentially harmful exposures, he/she should have periodic fitness for duty examinations.

 

A monitoring program designed to evaluate the intensity of exposures of workers to industrial chemicals or agents (dust, etc.) must always be complemented by a “health surveillance program.” Such a program is designed to detect as early as possible any adverse biologic and functional effects in exposed workers—effects that are likely to be reversible or that do not progress to significant functional effects when exposure conditions are improved.

 

VII. Defense Strategies in Litigation

 

When preventive measures are insufficient or the worker is unscrupulous or merely confused about cause and effect, the employer will likely find itself in litigation. When that occurs, the employer should roll out its best defense. Following are some important strategies in that effort.

 

Vigorous Discovery of Past Medical History

In litigation, the key weapon in the battle against illegitimate claims is a complete medical history. Hence, the employer’s counsel should vigorously search for all claimant’s medical records. The medical records are the first step. The next step is to be able to see in those records what medical conditions can be responsible for claimant’s symptoms.

 

Practice Tip: A good internist can help in this assessment.

 

General Causation—Exposure and Effect

The employer needs to determine precisely what is the exposure (substance and dose) and what the medical literature identifies as the effect from such an exposure at the estimated doses involved.

 

General Causation–Real Diseases v. Random Symptom Clusters

A Claimant may assert that from the workplace exposure, he/she has developed (1) a signature disease or (2) a clearly identified validated disease or syndrome with established diagnostic criteria or (3) a cluster of non-specific symptoms. Oftentimes, claimant’s symptoms are merely a random assortment of non-specific symptoms from a variety of non-workplace medical conditions. He/she may have shortness of breath and chest tightness from an anxiety disorder; fatigue from depression or the side effects of medication; and an irritated throat from gastroesophageal reflux disorder.

 

A cluster of non-specific symptom should never be accepted as establishing a disease or recognized syndrome. Establishing the existence of a disease or syndrome is never simple—certainly never as simple as a differential diagnosis. Differential diagnosis is merely a process of placing a patient’s clinical profile into an established disease category or syndrome from a set of possibly applicable established disease categories or syndromes. It is a process of instantiation, not of creation. That is, the “hypotheses” (of possibly applicable disease categories) generated in the process of differential diagnosis are not hypotheses about whether a general causative relationship exists between an exposure and an effect. They are rather hypotheses about whether certain generally accepted generally causative relationships (or disease categories or syndromes) apply to a particular individual in the clinic. The process of differential diagnosis simply does not and cannot transmute a novel hypothesis about a general causative relationship into a valid principle of general causation.

 

Symptom Clusters =df as coincident assemblages of symptoms or signs that do not constitute a syndrome or disease.

 

Syndromes =df as disorders without a single identified cause or pathogenesis. E.A Murphy. The Logic of Medicine, p. 132-134 (1997); E.A. Murphy. A Companion to Medical Statistics, pp. 157-161 (1985).

 

Diseases =df as disorders with a single identified cause or pathogenesis. See Taber’s Cyclopedic Medical Dictionary.

 

Typically, at the outset of the process of establishing the existence of a disease or syndrome, scores of symptoms may be implicated, from abasia to zoster. But implicating so many symptoms proves too much. The possible combinations of signs and symptoms, if n represents the total number of signs and symptoms, is 2n-1. (To back out the empty subset, subtract 1 so that the relevant possible combinations of signs and symptoms is 2n-l – 1). Given millions, billions, or even trillions of possible combinations, no expert would have any problem taking any patient–whether or not exposed to the putative toxin or pathogen–and finding some combination of those symptoms which could then be used to diagnose a disease if the patient coincidentally happened to have been exposed to the putative toxin or pathogen. Obviously, if the only thing that distinguishes those with the alleged disorder and those without it is being exposed, no effect has been identified in a cause and effect relationship; all that has been identified is a potential cause, and the issue of causation has been begged.

 

To identify a unique pathology, experts must establish, using multivariate statistical techniques, that this particular cluster of non-specific symptoms is not a random assortment or cluster of signs and symptoms. A group of signs and symptoms is said to be a random cluster or, better, a “random assortment,” when an individual has signs and symptoms from one or more disorders or conditions that have occurred together by virtue of chance or by virtue of what are called processes of “co-morbid disease.” For example, consider a middle aged woman (1) who has depression resulting in symptoms of fatigue, muscle aches, forgetting and difficulty concentrating, and (2) who is taking antidepressants that have the side effect of dry mouth, and (3) who is also perimenopausal, resulting in a variety of well-known symptoms such as joint aches, insomnia, tingling sensations in her extremities, acne rosacea, alopecia (hair loss), dry skin, elevated blood cholesterol, hot flashes, night sweats, headaches, and fatigue. If she reported this constellation of symptoms to her doctor, the doctor, if at all experienced, would not automatically consider them to be manifestations of a “new atypical” disease, but rather to be a random cluster of symptoms from depression, antidepressant medications, and low levels of estrogen.

 

After the purported diagnostic criteria have been developed by multivariate statistical techniques, they are usually refined with data from longitudinal studies and with methods of marshalling expert consensus, such as the “Delphi technique” or the “expert panel.” Kendall, R. E. Clinical Validity. Psychological Medicine, 19: 45-55 (1989); L.C. Morey & J.K. Jones. Empirical Studies of the Construct Validity of Narcissistic Personality Disorders in E.F. Ronningstam (ed.) Disorders of Narcissism (1998); Jones, J. & Hunter, D. Consensus Methods for Medical and Health Services Research. BMJ, 311: 376-380 (1995); Milholland, A.V. et. al. Medical Assessment by A Delphi Group Opinion Technique. NEJM, 288: 1272-1275 (1973); Fink, A. et. al. Consensus Methods: Characteristics and Guidelines for Use. American J. Public Health, 74: 979-983 (1984); Linstone, H.A. & Turoff, M. (eds.) The Delphi Method (1975); Fries, J.F. et al. Criteria for Rheumatic Disease. Arthritis & Rheumatism, 37: 454-462 (1994); Altman, R.D. et al. An Approach to Developing Criteria for the Clinical Diagnosis & Classification of Osteoarthritis. The Journal of Rheumatology, 10(2): 180-183 (1983).

 

Typically, a committee of experts isolates a set of historical, physical and laboratory features of the potential syndrome as potential diagnostic criteria. Next, the “sensitivity” and “specificity” of these features is determined by the Delphi technique of “opinion sampling,” a process designed to use the consensus of experts in situations of uncertainty, by means of anonymity, feedback and iteration. Opinion sampling helps the committee clarify its thinking, usually resulting in a consensus about the potential classification criteria.

 

Then the committee conducts a prospective study, enrolling patients diagnosed with the target disorder and a control group with signs and symptoms that could be confused with those of the proposed disorder. The committee then proposes for further investigation a set of diagnostic variables with more variables than those considered by the experts through the Delphic method. This enlarged set of variables is used by these clinicians (blinded to the status of the case or control group) to diagnose the proposed target disorder. A variable is included in subsequent analyses if it discriminates those with target disorder from those in the comparison group. With this approach, the enlarged set of variables is progressively narrowed to that subset considered most effective in diagnosing the target disorder.

 

Finally, the experts would publish their findings. By publication, other specialists or experts may critique the methods, analyses and conclusions of the study in order for the conclusions, after iterative refinement, to achieve general acceptance in the scientific community.

 

In the world of medicine, these foregoing issues are as basic to the physician as the need to add baking powder to a pie crust to the cook; or the need to ground an electrical wire to the electrician; or the need to keep your eye on the ball to an outfielder; or the need to keep your rifle clean to the soldier; or the need to replace the gas cap to a gas station attendant.

 

Despite these obvious requirements of scientific method, claimants’ experts usually fail to follow them or they fail to reach even consensus about a hypothesis about what is the alleged disease–what are its symptoms and what symptoms occur together. Second, they rarely test clinically an hypothesis to determine whether the yet-to-be-agreed-upon hypothesis is likely to be valid. Even so, some claimants’ experts may concoct and advance an hypothesis about the diagnostic criteria of the alleged disorder. But even then this hypothesis is apt to be ignored by many claimants’ experts; they will continue as though no hypothesis exists. They justify doing so by the accepted clinical practice of diagnosing some patients with a rheumatic disorder who fail to fulfill the formal criteria for that disorder. So when a claimant’s expert testifies that the exposure caused claimant to have a rheumatic disorder, even though claimant does not fulfill the formal criteria, the expert will have solid precedent in clinical practice for that diagnosis.

 

And so, as a practical matter, each expert has concocted his own private set of criteria. (This is reminiscent of Wittgenstein’s remark about a silly method of verification: “Imagine someone saying, ‘But I know how tall I am!’ and laying his hand on top of his head to prove it.”) As a result, this alleged rheumatologic “disorder” will always be an “essentially contested concept,” such as the concepts “social justice”, “the good life,” and “the most beautiful dog.” All are “soft end points”–notions that lack sufficient and necessary criteria and that cannot otherwise be defined by reference to facts about the world.

 

Often, if claimants’ experts fail to reach agreement on an hypothesis about the criteria of this alleged disorder, they either (1) have done the research but kept the results secret because the results are adverse to their position, or (2) have not done the research because they fear the results will likely be adverse to their position, or (3) think, “why do the research when we can buffalo the jurors into thinking that a disorder exists merely because we say it does; let’s not limit the number of possible claimants who can claim to be diseased.” Because claimants’ experts fail to specify the parameters of the alleged disorder, they can and do claim any non-specific symptom or combination of non-specific symptoms can constitute the so-called disorder.

 

Claimants’ experts, of course, do not want to narrow or limit the possibilities; they want to claim that any possible combination of non-specific symptoms is the alleged disease in order to perpetuate their lucrative business of being expert witnesses. In this, claimants’ experts are like fortune tellers or psychics who predict that the weather next week will be either sunny, rainy, snowy, sleeting, clear, or cloudy. Whatever the weather happens to turn out to be, they can take credit for an accurate prediction. As Saint Augustine remarked fifteen hundred years ago,

 

“… [T]here was no art by which the future could be foretold. “They said that guesswork was often borne out by mere chance. If a man made a great many predictions, several of them would later prove to be true…”

 

If the experts do adopt classification criteria, they should explain their rationale for selecting their “cut point,” the dividing line between those criteria that identify the disorder and those that do not. As defense counsel, be particularly attentive to how the cut point establishes the “specificity” of the criteria. “Specificity” is the ability of the criteria to not identify those in a group of people as having the disorder who in fact do not have the disorder. The defense will want the criteria to have a high specificity against other disorders, particularly those based on subjective criteria, such as psychological disorders and “fibromyalgia syndrome.”

 

The defense will also want to know the “positive predictive value” of the classification criteria. Given that the alleged disorder is apt to have a very low prevalence in the general population, even if the criteria have high “sensitivity,” the positive predictive value will be low.

 

Rule 702 & 703 Objections to Medical and Scientific Quackery

Through use of Washington Evidence Rules 702 and 703, the employer needs to exclude from evidence the testimony of medical quacks.

 

Washington Evidence Rule 702:

 

If scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, skill, experience, training, or education, may testify thereto in the form of an opinion or otherwise.

 

Washington Evidence Rule 703:

 

The facts or data in the particular case upon which an expert bases an opinion or inference may be those perceived by or made known to the expert at or before the hearing. If of a type reasonably relied upon by experts in the particular field in forming opinions or inferences upon the subject, the facts or data need not be admissible in evidence.

 

Washington Evidence Rules 702 and 703 are a bulwark against the flow of junk scientists into the courtroom. That rule can be invoked to exclude testimony not based on scientific principles generally accepted in the scientific or medical community. The standard of admissibility of novel evidence in Washington is provided by the “Frye” test. State v. Canaday, 90 Wn.2d 472, 527 P.2d 271 (1974); State v. Copeland, 130 Wn.2d 244, 922 P.2d 1304 (1996); Frye v. United States, 293 F. 1013 (DC Cir 1923). Under the Frye test, scientific evidence will be admitted only if it is “generally accepted in the relevant scientific community.” Id. The core concern of Frye is whether the evidence being offered is based on a scientific methodology generally accepted in the scientific community. The phrase “the scientific community” refers not only to the community of forensic experts but also to the wider scientific community familiar with the theory and its underlying techniques. The court looks for “general” not full acceptance by the community of scientists familiar with the challenged theory. State v. Russell, 125 Wn.2d 24, 40-41, 882 P.2d 747 (1994).

 

Under the Frye test, the court has a two-part inquiry:

 

  1. Is this proffered theory generally accepted in the scientific community? That is, in the abstract, “for all x exposed to z amount of w, it is true that x will develop the property y.” Or, more concretely, “for all people exposed to 5 units of this chemical “gasite” in 4 units of time, then owing to that exposure such people will develop gasitis.”

 

  1. Is this technique or test designed to implement or instantiate the consequences of that theory generally accepted in the scientific community? That is, is the gold standard test or a surrogate test used to determine that plaintiff (as a member of the set of people referred to in the abstract statement of the theory), after he had been exposed to 5 units of gasite in 4 units of time, developed gasitis valid and reliable by the lights of the scientific community? See State v. Cauthron, 120 Wn.2d 879, 888, 846 P.2d 502 (1993). To illustrate, suppose a pathologic examination of a person’s liver for certain organelles “q, r, s” in the cell “z” was the postulated marker or gold standard test for gasitis,” but that inter-observer and intra-observer reliability or concordance for identifying those organelles was less than that of chance, the abstract theory cannot be verified, and perforce cannot be generally accepted in the scientific community given generally accepted scientific methodology. That is to say, the so-called theory is up in the air, and not grounded empirically.

 

An Example of Junk Science: Multiple Chemical Sensitivity Syndrome.

In complex exposure claims,, the likely “junk scientists” will be the advocate of the “chemical sensitivity syndrome.” This junk scientists will parade under the moniker of specialists in so-called “environmental medicine.”

“Multiple chemical sensitivity syndrome” (MCS) has also been called toxic injury, chemical sensitivity, chemical injury, environmental illness, sick building syndrome, and idiopathic environmental intolerance. MCS is not a valid medical diagnosis. It is not found in the International Classification of Diseases (ICD-9-CM). E.g., Bradley v. Brown, 852 F. Supp. 690 (N.D. Ind.), aff’d 42 F.3d 434 (7th Cir. 1994); Cavallo v. Star Enter., 892 F. Supp. 756 (E.D. Va. 1995), aff’d regarding evidentiary holding, 100 F.3d 1150 (4th Cir. 1996); Summers v. Missouri Pac. R.R. Sys., 897 F. Supp. 533 (E.D. Okla. 1995); Valentine v. Pioneer Chlor Alkali Co., 921 F. Supp. 666 (D. Nev. 1996).

 

Both the existence and cause of MCS are hotly disputed. In particular, physicians disagree about whether symptoms are physiologically or psychologically generated or both. MCS has never been clearly defined, no scientifically plausible mechanism has been proposed for it, no diagnostic tests have been substantiated, and not a single case has been scientifically validated. Because of the lack of scientific evidence based on well-controlled clinical trials that supports a cause-and-effect relationship between exposure to very low levels of chemicals and the myriad symptoms reported by clinical ecologists, MCS is not recognized as an established organic disease by the American Academy of Allergy, Asthma, and Immunology, the American Medical Association, the California Medical Association, the American College of Physicians, and the International Society of Regulatory Toxicology and Pharmacology.

 

“Clinical ecologists” who champion MCS describe it as a chronic condition characterized by several adverse and variable affects from exposure to otherwise low levels of substances common in everyday modern human environments. The problem this presents for claimant is that if these chemicals are ubiquitous in his/her everyday environment outside his/her workplace, they cannot be a proximate cause of an occupational disease simply because they are not “distinctive.” AThe worker Y must show that his or her particular work conditions more probably than not caused his or her disease or disease-based disability than conditions in everyday life or all employments in general; the disease or disease-based disability must be a natural incident of conditions of that worker=s particular [email protected] Dennis v. Department of Labor and Industries, 109 Wn.2d 467, 745 P.2d 1295 (1987). AThe condition causing the disease or disease-based disability must be a condition of employment. This is, it is a condition of the workers particular occupation as opposed to conditions coincidentally occurring in his or her [email protected] Dennis, 109 Wn.2d at 467 (1987). MCS, if it is anything, is simply a physical manifestation of a psychosomatic illness.

 

Clinical ecologists are certified by the “American Academy of Environmental Medicine,” founded in 1965 as the Society for Clinical Ecology. It is not a category of medicine certified by the traditional American Board of Medical Specialties. Clinical ecologists are on the very fringe of medicine. They find low-dose effects not generally accepted by mainstream toxicologists. Clinical ecologists have theories and practices severely criticized by courts and by the American Medical Association, the American College of Physicians, the Canadian Psychiatric Association, the International Society of Regulatory Toxicology and Pharmacology, the American Academy of Allergy, Asthma and Immunology, and the American College of Occupational and Environmental Medicine.

 

In short, a clinical ecologist is a purveyor of junk science to the medically unsophisticated. See Sterling v. Velsicol Chemical Corp., 855 F.2d 1188, 1208 (6th Cir. 1988); Bradley v. Brown, 852 F. Supp. 690 (N.D. Ind.), aff’d 42 F.3d 434 (7th Cir. 1994) (Dr. Rea excluded as a junk scientist); Brandon v. First Republicbank Group Medical Plan, [No. CA-7-89-002, Northern District, Texas Nov. 27, 1990] (Dr. Rea excluded as a junk scientist); Hundley v. Norfolk & Western Railway Co., [No. 91C-6127, N.D. Ill., Jan. 31, 1996] (Dr. Rea excluded as a junk scientist); Mullenax v. McRae’s [No. 87-13915-D-3130, Mississippi Worker’s Compensation Commission, March 18, 1993] (Dr. Rea debunked as a junk scientist); Phillips v. Velsicol Chemical Corporation [No. 93-CV-140-J, District of Wyoming, September 19, 1995] (Dr. Rea’s opinions debunked); see also, Cavallo v. Star Enter., 892 F. Supp. 756 (E.D. Va. 1995), aff’d regarding evidentiary holding, 100 F.3d 1150 (4th Cir. 1996); Summers v. Missouri Pac. R.R. Sys., 897 F. Supp. 533 (E.D. Okla. 1995); Valentine v. Pioneer Chlor Alkali Co., 921 F. Supp. 666 (D. Nev. 1996).

 

As the court stated in Bradley:

 

“Even relying wholly upon plaintiffs’ own exhibits, plaintiffs’ fail to establish that the etiology of MCS, accepting arguendo that such a clinical entity exists, is known or tested at this point. Accordingly, Drs. Rea and Johnson’s opinions regarding whether the plaintiffs’ exposure caused their symptoms would be entirely too subjective and speculative. Rea and Johnson are among a group of doctors and scientists known as “clinical ecologists.” *** Rea claims to have seen as many as 20,000 “environmentally sensitive” patients at their Environmental Health Center in Dallas, Texas. See William J. Rea, Chemical Sensitivities Preface (1992). Thirteen percent of those patients “relate the onset of their Sensitivity to a severe acute [chemical] exposure.” This compares, for example, to the nine percent that “identified childbirth as the triggering event.” It is based upon those observations that Rea, and presumably Johnson, base their hypotheses about the etiology of MCS.

 

The problem the court faces here is that Rea and Johnson’s opinions about MCS’s causes are, at best, hypothetical at this point. Rea states frankly in his own recent book that: “We do not know at this time the initial mechanism by which good health gives way to chemical sensitivity.” Accordingly, any opinion that the April 20, 1983 exposure induced MCS in Bradley and Roy would be only slightly diluted speculation. Such a conclusion would necessarily rest on uncontrolled past observations. An example is Rea’s statement that soldiers’ exposure to mustard gas in World War I and Agent Orange in Viet Nam, and citizens’ exposure to cyanate in Bhopal, India after a chemical plant accident there, “all graphically illustrate that chemical sensitivity may be caused by a significant, acute exposure to toxic substances.” There is no indication either in Rea’s book or in other proofs submitted to the court that the victims of these exposures were even diagnosed with MCS. Rea’s contrary conclusion is exempletive of the sort of reasoning that, no doubt, leads many scientists to “dismiss” the work of clinical ecologists as “anecdotal.” See Nicholas Ashford and Claudia Miller, Chemical Exposures: Low Levels and High Stakes 111 (1991). It is a far cry from the tested hypotheses foreseen as the basis of “scientific knowledge” testified to under Rule 702.

 

***
Thus, plaintiffs’ own evidence clearly establishes that the “science” of MCS’s etiology has not progressed from the plausible, that is, the hypothetical, to knowledge capable of assisting a fact-finder, jury or judge. As Daubert recognized, “the scientific project is advanced by broad and wide-ranging consideration of a multitude of hypotheses;” by contract, “in the project of reaching a quick, final, and binding legal judgment . . . about a particular set of events in the past,” the court must weed out the speculative hypothesis from the tested theory. The Court in Daubert recognized and accepted that this gate-keeping function “on occasion will prevent the jury [or the court, in a bench trial] from learning of authentic insights and innovations.” Id. The court recognizes that risk here. Nonetheless, it must answer the question before it based on current knowledge.” Bradley v. Brown, 852 F. Supp. at 699-700.

 

The clinical ecologist has a peculiar clinical approach to diagnosis (for which they have been roundly criticized by the courts in which they have appeared as indicated above). They perform a variety of non-standard tests on blood, tissue and hair. When they identify a chemical in blood or tissue or on hair strand, they proclaim that the patient must have been exposed to this chemical in the workplace; the workplace exposure must have been harmful; that the harm is chronic.

 

This methodology puts the cart before the horse. Usually, in assessing causation, mainstream toxicologists would first identify to what chemical the individual was allegedly exposed and in what dose and then determine whether that chemical was in that person’s system in amounts that satisfied the dose-response threshold and whether the person had objective manifestations of tissue injury from such chemical exposure.

 

The clinical ecologist does not concern himself/herself with the issues such as (1) the fact that what he/she has identified is in trace amounts; (2) that what he/she has found is commonly found in the everyday environment in nearly everyone; (3) whether the patient was actually exposed to that particular chemical in the workplace, (4) the dose of the exposure—that kind of information would put the horse before the cart. It is all irrelevant. To clinical ecologists, dose and toxicity are not related.

 

What the clinical ecologist looks for are present in anyplace, at anytime, in anyone. In fact, that is the keystone to the theories and practice of clinical ecologists—common everyday modern environments are awash in trace amounts of chemicals (pesticides on food; air pollution; water pollution), which in these extremely minuscule amounts can cause a host of symptoms in people. Even though to this special area of practice, all these so-called harmful chemicals are found in everyday life, including, therefore, in any workplace, for clinical ecologists, the preferred focus of exposure is the workplace so that the cost of the clinical ecologists’ treatments will be reliably paid and so that they will continue to be hired as a forensic witnesses to support spurious claims of junk science.

 

The smoking gun to understanding how clinical ecologists approach so-called “chemical sensitivity syndrome” and its causes is what they recommend as treatment. The patient must (1) avoid chemicals in environment (they instruct the claimant to wear cotton gloves extending up the arms and to wear a mask wherever he/she goes); (2) eat organic food to avoid chemicals (pesticides) in and on food; (3) drink filtered (less polluted) water; (4) purify the air in the home; (5) take saunas (“temperature heat therapy”) to rid their bodies of unwanted toxins (never mind that sweat glands are not connected to the liver or any other organ that processes toxins); (6) massage; (7) be injected with “immune boosters;” and (8) be injected with nutrients.

 

Obviously, as this treatment regimen implies, the chemicals with which the claimant is allegedly contaminated are ubiquitous in his/her everyday environment. They are in the air he/she breathes wherever he/she is—in his/her home, in his/her outside environment, everywhere–; they are in the food he/she eats; and they are in the water he/she drinks. This fact presents a problem for claimant. If these chemicals are ubiquitous in his/her everyday environment outside his/her workplace, they cannot be a proximate cause of an occupational disease. This is so simply because they are not thereby “distinctive” to her employment. AThe worker Y must show that his or her particular work conditions more probably than not caused his/her disease or disease-based disability than conditions in everyday life or all employments in general; the disease or disease-based disability must be a natural incident of conditions of that worker=s particular [email protected] Dennis v. Dep’t of Labor & Indus., 109 Wn.2d 467, 745 P.2d 1295 (1987). AThe condition causing the disease or disease-based disability must be a condition of employment. This is, it is a condition of the workers particular occupation as opposed to conditions coincidentally occurring in his or her [email protected] Dennis, 109 Wn.2d at 467 (1987).

 

Warning: Because the test whether an occupational disease has occurred is not whether most workers of reasonable good health would suffer a disabling disease under the same conditions, but rather whether the individual worker with his/her preexisting frailties and bodily infirmities suffered the disease, a claim of MCS may be nothing more than a claim that this particular claimant is hypersensitive to doses of agents to which the vast majority of people would not have an adverse reaction. Simpson Timber Co. v. Wentworth, 96 Wn. App. 731, 981 P.2d 878 (1999).

 

Specific Causation—Consensus Medical Criteria for Disease/Condition

The employer must insist that the worker’s experts identify “consensus medical criteria” for the alleged harmful effect of the alleged complex exposure.

 

Formal medical criteria for diseases and disorders are identified in various authoritative treatises and articles. If left to their own devices, workers’ experts will rarely, if ever, announce or refer to these criteria. They will rather rely on the “ex cathedra” fallacy to establish that the worker has the disease or disorder. The worker has the disorder because I say he/she does—trust me because I have medical expertise or because I am the treating physician.

 

Claimants’ experts should be confronted with these formal criteria. They should be asked to establish the article or treatise from which these criteria were drawn as authoritative.

 

In establishing a defense, the employer’s attorney must refer to authoritative treatises. When presenting claimant’s proof, the claimant’s attorney will not refer to the consensus criteria for a particular disease or disorder. The proof will tend to be vague with what are termed “soft end points.” It will focus more on emotionally laden buzz words. For example,

 

(1) I was “gassed” in 1982–that is, I was exposed to chlorine gas in 1982 [but was wearing a respirator at the time] and was exposed to fumes from 1982 to 1997, [but had no symptoms from these exposures].

(2) Then in 2004 while working in a job that did not expose me to fumes [other than occasional truck diesel fumes] I had a “fit” of chest tightness, coughing and fainting in the morning before going outside to work.

(3) That “fit” must have been caused by some long ago exposure to chlorine gas [rather than my well documented chronic anxiety and panic disorder].

 

Sometimes, the worker’s expert will refer to a specific diagnosis. For example, he/she may testify that the worker has “allergic occupational asthma” without identifying the specific diagnostic criteria for that disorder.

 

The diagnostic criteria for “allergic occupational asthma” are as follows:

 

(1) Claimant did not have asthma before he/she began working;

 

(2) After he/she began working, he had intermittent respiratory symptoms (cough, wheezing, chest tightness, and dyspnea or shortness of breath, and production of sputum);

 

(3) After he/she began working, he/she had physiologic evidence of either reversible/variable airway obstruction [tested by lung volumes] or “hyper-responsiveness,” [increased sensitivity to a variety of non-allergenic stimuli tested by either histamine or methacholine challenge tests]. Balmes, J.R. Occupational Asthma. Chapter 60. In Murray and Nadel’s Textbook of Respiratory Medicine. (4th ed., 2006); Mapp, C.E. et. al. Occupational Asthma. American Journal of Respiratory and Critical Care Medicine, 172: 280-305 (2005); American Thoracic Society. Guidelines for Methacholine and Exercise Challenge Testing. Am. J. Respir. Crit. Care Med., 161: 309-329 (1999).

 

(4) The demonstration of work-relatedness of asthma [causation] by objective means.” Chan-Yeung, M. ACCP Consensus Statement: Assessment of Asthma in the Workplace. Chest, 108: 1084-1117 (1995). [“A history of temporal associations between asthma symptoms and work exposure to a sensitizing agent is not specific for diagnosing occupational asthma.” “Because asthma is a common disease, asthma and exposure to one of the many potential causative agents of occupational asthma can occur together by chance.” Chan-Yeung, M. and Malo, J.L. Occupational Asthma. New England Journal of Medicine, 333: 107-112 (1995).]

 

The employer can anticipate that the worker’s expert will attempt to find various pretexts to disregard one or more of these criteria in reaching a diagnosis. On one pretext or another, the last criteria (the most important criterion) is particularly likely to be excused. For example, I would not subject this worker to testing in the workplace because it would do him/her harm.

 

Specific Causation–Rigorous Differential Diagnosis

The pivotal issue in complex exposures claims is the issue of “alternate causation.” That is, what other exposures or medical conditions can cause the symptoms claimant alleges arose from the workplace exposure? These symptoms are typically “subjective,” meaning that they are mediated through the claimant’s consciousness, and “non-specific,” meaning that they can result from any number of ordinary and extraordinary causes. Here is a partial list of symptoms and signs claimant’s commonly attribute to exposure to a putative toxin: (1) chronic fatigue, (2) cognitive dysfunction, (3) myalgias (muscle aches), (4) arthralgias (joint aches), (5) sicca symptoms (dry eyes and dry mouth), (6) dysphasia (difficulty swallowing), (7) Reynaud’s phenomenon, (8) dyspenia (shortness of breath), (9) night sweats, (10) paresthesias, (11) dysesthesias, (12) sleep disturbance (insomnia), (13) easy bruising, (14) photosensitivity rashes, (15) history of oral ulcers, (16) history of abnormal neurologic testing, such as positive Romberg test, (17) multiple autoantibodies, (18) joint swelling, (19) adenopathy, (20) headaches, and (21) vision problems.

 

Usually, these symptoms are from disorders other than exposure to a chemical in the workplace. In most legal contexts, outside the realm of industrial insurance, the worker would have to establish that the symptoms ABC are from exposure to the chemical, and not from other kinds of more common or prevalent disorders. In the context of industrial insurance, the employer should expect to have to prove that the symptoms ABC are from other kinds of more common or prevalent disorders, not from exposure to the chemical. What is the nature of the employer’s proof that the symptoms ABC are from other kinds of more common or prevalent disorders, not from exposure to the chemical? That proof is typically a thoroughgoing “differential diagnosis.”

 

“Differential diagnosis” is an iterative process (within the hypothetico-deductive model) with four steps designed to establish a particular patient’s clinical diagnosis—(1) listening to the patient describe symptoms and observing signs, (2) generating from those observations hypotheses about a process of disease or symptom formation, (3) gathering additional data to test these hypotheses, and (4) evaluating these hypotheses in light of these data. These four steps are repeated as many times as hypotheses are considered and then rejected, confirmed or set aside for further testing. D. L. Sackett et. al. Clinical Epidemiology, p. 17 (1991); H.C. Sox, et. al. Medical Decision Making, pps. 9-26 (1988); J.P. Kassirer. Diagnostic Reasoning. Annals of Internal Medicine, 110:893 (1989); R.L. Engle, Jr. & B.J. Davis. Medical Diagnosis: Past, Present and Future. Archives of Internal Medicine, 112: 512-543 (1963); F.J. McCartney. Diagnostic Logic. BMJ, 295: 1325-1331 (1987).

 

Differential diagnosis is a form of “proof by exclusion.” In this form of proof, the clinician lists all possible diagnosis given the clinical facts; proves that the list is exhaustive; and then eliminates as unlikely all possible diagnoses but one. That is why if no positive grounds exist for a diagnosis, diagnosis by exclusion is hard to justify logically. E.A Murphy. The Logic of Medicine, p. 201 (1997).

 

Defusing Cognitive Biases/Errors

 

At the end of reason comes persuasion.”

 

  1. Wittgenstein

 

Argument in law is usually not about formal logic–the discovery of clear contradictions, self-refuting statements, fallacies of affirming the consequent or denying the antecedent, the errors so keenly hunted by academic logicians. It is not about linguistic intuitions, those intuitions about which there is the greatest consensus. Rather, arguments in law—to ALJs, judges and juries–appeal to a narrower set of intuitions–to intuitions about cases or experiences about how people live or should live, the kinds of intuitions which often differ from person to person. As Justice Holmes mused in The Common Law, “The life of the law has not been logic: It has been experience.” As Judge Richard Posner recently said, “most judges can handle facts better than they can handle theories.” [R.A. Posner, Legal Reasoning from the Top Down and From the Bottom Up, 59 Univ. Chicago L. Rev. 449 (1992)] That is, the rhetoric of argument concerns how we react emotionally and morally to certain experiences.

 

What influences people of all ages, intellects and personality are stories about people (or animals that seem like people). People cannot help themselves; their social instincts take over. Narratives or stories are intuitively appealing ways of presenting particulars and hence intuitively appealing ways of persuasion. But simply creating a narrative is not enough. The defense also needs a plot, organized usually around the notion of creating sympathy for the employer and antipathy for the worker. The theme, as Professor McElhaney counsels, is not a call to insure justice prevails but a call to right an injustice. “Injustice has the power to stir people’s blood.”

 

Certain plots or narratives have the power to express this theme, to capture the attention and direct the emotions of the audience toward the desired conclusion. Discovering these plots in the facts of each case is the essence of persuasive advocacy, finding, that is, “the same in the different.”

 

For claimant’s counsel the plot of choice is that of claimant as victim, someone against whom the employer has been unjust. In this scenario, claimant is portrayed as the hapless victim of employer’s heartless greed, a state that continues post accident through trial. The jury is implored to effect a reversal of this ill fortune to alleviate an injustice or, more poignantly as claimant’s counsel strives to posture through innuendo, to effect a triumph of good over evil.

 

For the employer’s counsel, a useful plot is that of claimant as clever opportunist exploiting the legal system. In this plotline, the employer is the victim as claimant uses his/her association with the employer as a way to manipulate the biases and indeterminacies of our imperfect legal system to exploit the employer for cash. The jury is implored to set things right.

 

Another plot employer’s counsel may find useful is that of the self-deceived claimant who misattributes the cause of his/her physical complaints. Here the employer portrays claimant as perhaps innocent of mind but nonetheless mistaken, through self-deception, about the employer’s role in denying him/her compensation for his alleged injury. What claimant cannot see is that his/her own emotional forces are responsible for the injury, not the employer’s conduct.

 

Practice Tip: The employer needs to fashion a convincing or plausible theory of alternate causation along with a narrative that stirs some emotional sympathy for the plight of the employer.

 

VIII. Conclusion

 

Complex exposure claims cannot be entirely eliminated but with effort the risk of such claims can be minimized. Given how the current industrial insurance system is administered, that is as much as can be expected.