Decision #14/05 - Type: Workers Compensation
Preamble
An Appeal Panel hearing was held on September 3, 2003, at the request of an advocate, acting on behalf of the claimant. The Panel discussed this appeal on several occasions, the last one being December 6, 2004.
Issue
Whether or not the claim is acceptable.
Decision
That the claim is acceptable.
Background
In August 2000, the claimant filed an application for compensation benefits with respect to a condition known as Waldenstroms Macroglobulinemia (WM), a B cell lymphoma confined to bone marrow. The claimant felt that his condition was caused from radiation exposure which took place at work on November 3, 1964 and August 20, 1968.
In order to adjudicate the claim, primary adjudication took into consideration the information that was provided by the employer along with medical information that was received from three of the claimant’s treating physicians. Primary adjudication also consulted with the healthcare branch at the Workers Compensation Board (WCB) to confirm the diagnosis and to determine whether or not it was related to the claimant’s radiation exposure.
In a memo dated November 2, 2000, a WCB internal medicine consultant responded to questions posed by primary adjudication and provided the following information:
- The diagnosis in this case was WM which was established by the claimant’s oncologist after investigating the claimant with bone marrow aspiration, CT of the abdomen and study of the serum electrophoresis.
- WM is one of the malignant lymphoproliferative disorders of small lymphocytes. The disease is more common in men than in women and the incidence increases with age. The median age of diagnosis is around 64 years.
- During research to identify a cause for this rare disorder, he came across no relationship between WM and exposure to isotopes and radiation.
In a letter dated December 22, 2000, primary adjudication informed the worker that his claim had been denied. It was the WCB’s position, based on all the available information that the worker’s condition was not related to his exposure to isotopes and radiation due to the workplace incident of August 20, 1968, on a balance of probabilities. In June 2002, the claimant disagreed with the decision and the case was forwarded to Review Office for consideration.
In a memo to file dated December 10, 2002, a WCB senior medical advisor stated that he had discussed the case with the claimant’s specialist (knowledgeable with occupational radiation injury) who believed that the claimant’s cancer was one type of non-Hodgkin’s lymphoma (NHL) and that in his opinion, this was related to the claimant’s radiation exposure.
On December 16, 2002, the WCB senior medical advisor contacted the treating oncologist. The oncologist stated that WM was one form of NHL which may be related to radiation exposure but she did not know of any study supporting this fact.
On March 20, 2003, the WCB senior medical advisor prepared a memo to file regarding NHL and radiation exposure. He concluded there was nothing to support a link between NHL and radiation exposure.
In a decision dated March 21, 2003, Review Office determined that the claim was not acceptable. Review Office noted that neither of the two WCB physicians were able to reach a conclusion that a cause and effect relationship existed between the claimant’s radiation exposure from the two incidents in the 1960’s and his diagnosis as of April 2000. Review Office noted that the WCB’s healthcare department was unable to conclude that workers in the nuclear industries had been reported to have increased risk of NHL. The published literature did not reveal any conclusive evidence linking NHL to radiation exposure. In June 2003, the claimant appealed Review Office’s decision and an oral hearing was held on September 3, 2003.
At the September 3, 2003 hearing, it was agreed to by all parties that the employer’s representative would respond to the written file presentation and the oral presentation that was made by the claimant’s advocate at the hearing. The Panel asked the employer to provide the Appeal Commission with copies of information discussed at the hearing. The Panel also requested the convening of a Medical Review Panel (MRP) prior to discussing the case further.
As the arrangements to convene a MRP could not be finalized, the Appeal Panel arranged for an independent hematologist to conduct a file review and respond to certain questions posed by the Appeal Panel. A response from the hematologist was later received and his report was forwarded to the interested parties for comment. On December 6, 2004, the Panel met to further discuss the case and considered a submission from the claimant’s advocate dated November 21, 2004 and a submission from the claimant date November 22, 2004.
Legislative Authority:
As an employee of a federal government agency this claimant’s eligibility for compensation benefits is governed by the Government Employees Compensation Act (GECA) which is administered by agreement in Manitoba by the WCB.
Subsection 4(1) of GECA states in part:
Subject to this Act, compensation shall be paid to
- an employee who
- is caused personal injury by an accident arising out of and in the course of his employment, or
Section 2 of GECA states in part:
“accident” includes a wilful and intentional act, not being the act of the employee, and a fortuitous event occasioned by a physical or natural cause;
Reasons
Chairperson Sargeant and Commissioner Day:
In the simplest terms, the issue before the Panel was whether or not there is a cause and effect relationship between the claimant’s exposure to ionizing radiation and the cancer with which he was diagnosed.
For the appeal to be successful, the Panel would have to determine that such a relationship exists. After considerable deliberation, which included further medical review, a majority of the Panel has found in favour of the claimant, concluding that a relationship does exist.
One member of the Panel did not agree with this conclusion. His dissenting opinion is included later in this decision.
We came to our conclusion after conducting a thorough examination of the evidence contained in the claimant’s file, as well as conducting an oral hearing, at which we heard testimony from the claimant, his advocate and representatives of the employer.
We also searched, in other Canadian jurisdictions, for cases where the issue dealt with a possible link between radiation exposure and cancer, specifically NHL. We were successful in finding a case with a very similar fact scenario, a decision of the Ontario Workplace Safety and Insurance Appeal Tribunal (WSIAT).[1]
The majority of the Panel found the reasoning in this decision to be very persuasive and helpful in our deliberations. We have adopted much of that reasoning, applying it to the case before us. This will be set out further in these reasons.
In particular, we rely on that decision’s examination of recent developments in the law of “causation” and how that law applies to compensation cases. This, too, will be described later.
Findings
The following facts are undisputed, in this case:
- In 1964, in the workplace, the claimant was exposed to 19.5 tolerances of radiation. In this incident, the report identifies the material as consisting of fission products.
- In 1968, in the workplace, the claimant was exposed to 17.2 tolerances of radiation. The report, in this incident, lists a number of isotopes with half-lives ranging from 65 days to 27.7 years. The latter refers to Strontium 90, which would require about 280 years until it is no longer radioactive.
- In 2000, it was confirmed that the claimant was suffering from WM, a rare form of NHL.
Both exposures are considered to be very significant. Exposure to 1 tolerance is deemed an “administrative removal level”, by which is meant that the exposed person is removed from that workplace for a period of time.
Medical science has not yet determined that significant exposure to ionizing radiation is a cause of WM or, even, of NHL. Conversely, science has not found that radiation exposure will not cause WM or NHL.
The Evidence
Substantial medical evidence was provided to the panel for its review and consideration.
The Claimant’s Advocate
The claimant’s advocate is a retired industrial physician, who worked for 30 years in the nuclear industry. He presented written and oral testimony to us.
It is his professional opinion that the claimant’s WM was caused by his two exposures to radiation.
In his testimony at the hearing, he stated that, in disease cases, it is necessary “to assemble a series of hard facts in order to produce a credible hypothesis.”
In presenting his case to the Panel, he stated the following:
“The extreme sensitivity of lymphocytes and the lymphocyte precursors, and these are what we are talking about in this kind of lymphoma, the Waldenstrom’s Macroglobulinaemia, the extreme sensitivity of lymphocytes and the lymphocyte precursors in the bone marrow to ionizing radiation is well documented….”
……
“…so after a serious exposure to ionizing radiation, you find a complete collapse of lymphocytes in the blood stream.”
……
“…it is important to understand the second type of contamination, which is the case in [the claimant], that he breathes in very highly radioactive material that is distributed through his body.
“The radiation from the very short range alpha and beta particles may, of course, kill a cell, but the outcome is very different if the irradiated cell, such as a lymphocyte precursor in bone marrow, survives and is modified rather than killed.
“The clone of damaged cells resulting from the reproduction of a modified but damaged cell, but viable cell, may result, after a latent period, in the development of cancer.
“The probability of cancer developing in this way is without a threshold, a low level below which nothing happens …”
……
“Some of these isotopes are going to be excreted in the normal process from the body, but, conservatively, at least 5 percent of them, and this is particularly important in the case of Strontium 90, will be retained.
“The quantities retained in the body may be small, but it must be remembered that one is considering carcinogenic effect without a threshold …”
……
“Waldenstrom’s … arises from changes in the later stages of the lymphocytic precursors, almost before you get to the material lymphocyte. This happens in the bone marrow, an area which, as I have already shown, is uniquely sensitive to ionizing radiation.
“Radiation was cited as a possible cause of non-Hodgkin’s Lymphoma as long ago as 1986 … So what we are suggesting here today is not exactly new.”
……
“We have then fulfilled three of the conditions that I set out. There has been exposure, there has been an appropriate time interval, and there is a disease which is known to be sensitive to ionizing radiation.
“And most importantly … cause/effect relationship is, at the very least, plausible.”
This doctor noted that there is no epidemiological evidence to support his case. But, he further noted that, due to its rarity, there have been no studies relating to WM as a single entity. It has only been included in studies of NHL, which are also few in number.
The WCB Doctors
As noted above in the “Background” section, in November 2000, a WCB internal medicine consultant reported that, after conducting research to identify a cause for this rare disorder, he came across no relationship between WM and exposure to isotopes and radiation. Based on this evidence, the claim was denied.
In March 2003, during a review of the earlier decision, a WCB senior medical advisor wrote a memo, in which he noted the following:
- In December 2002, he contacted the doctor, who later appeared before the Panel in support of the claimant, who informed him that WM was one type of NHL and that, in his opinion, it was related to the claimant’s radiation exposure.
- Later in December 2002, he contacted the claimant’s treating oncologist, who confirmed that WM was one form of NHL which may be related to radiation exposure, but she did not know of any study supporting this fact.
- He had conducted a fairly extensive literature review in respect of any cause/effect relationship between NHL and radiation exposure. He found nothing to support such a link.
- He also reported that he had contacted all the WCBs in Canada and found that there had been no claim accepted for NHL caused by radiation exposure.
[The panel majority notes that this is odd, given the 1995 Ontario decision, already noted and to be discussed further, below.]
Based on these reports of two WCB medical advisors, the claim was again denied.
Other Doctors
As noted above, subsequent to the appeal hearing, the Panel referred the file to an independent medical examiner for a review and response to specific questions.
In brief, he reported the following:
“There is no documented evidence that WM … is related to radiation exposure. … In summary, a causal relationship between ionizing radiation exposure and the development of WM is possible, but not probable.”
……
“… a causal relationship between [the claimant’s] cancer and the accidental exposure to radiation he suffered in 1964 is possible, but not probable.
“… a causal relationship between [the claimant’s] cancer and the accidental exposure to radiation in 1968 is also possible, but not probable.
“According to the papers quoted previously, there is no evidence in the scientific literature available to date that the lifetime occupational exposure to radiation undoubtedly suffered by [the claimant] is causally related to the development of WM.”
Employer
At the appeal hearing, the employer presented little evidence. The panel, however, allowed the employer a period of time, in which to provide a written response to the evidence presented on behalf of the claimant, as well as to provide comments in respect of WSIAT Decision 549/95I2, which was provided to the employer by the panel.
In its response, the employer wrote:
“A principal component of the submission from [the doctor supporting the claimant] is that there is a significant difference between internal and external radiation exposures and that these differences essentially negate the value of epidemiological data in assessing cause and effect between the exposure and the manifestation of the disease. [The doctor] goes on to argue that due to the impossibility of correctly assessing internal radiation exposures (his opinion) one has to rely on biological plausibility in establishing cause and effect.
We argue that, far from being impossible, a good estimate of internal exposure can be made, albeit with uncertainties, which takes into account all of the concerns that [the doctor] expressed. We also argue that the nature of these estimates of internal dose do not render useless the epidemiological data available through international authorities on radiation protection.”
The employer goes on to state that it was able to assess effectively the amount of exposure the claimant incurred, including internally.
In referring to some scientific literature, the employer stated:
“According to the United Nations Scientific Committee on the Effects of Atomic Radiation ‘there is no statistically significant evidence that non-Hodgkin’s Lymphoma is associated with exposure (internal/external) to ionizing radiation’ (UNSCEAR 1994, Annex A, para. 124). The latest report of UNSCEAR (UNSCEAR 2000) again concludes that there are (sic) insufficient data to support any correlation between radiation exposure and NHL incidence.”
We (the panel majority) would note that what is actually written in the UNSCEAR reports is different than as quoted by the employer.
In the 1994 report, it is written: “In general, there is no convincing evidence that non-Hodgkin’s lymphoma is associated with radiation exposure.” There is no reference to statistical significance and none to internal and/or external exposure.
In the 2000 report, UNSCEAR wrote:
“Results from studies of NHL risk groups exposed to external low-LET radiation are mixed. The Japanese atomic bomb survivors as a whole do not show an association, although there is some evidence of an increasing trend in incidence with dose among males (but not females). Findings from other studies are variable, with no clear consistency. Overall, there is little evidence of an association between NHL and external low-LET radiation.” (our emphasis.)
In its response, the employer continued:
“Turning to the issue of biological plausibility, although we can accept the possibility that radiation exposure is the cause of the claimant’s disease cannot be proven to be zero, all available evidence suggests that the probability of this being the case is very low at the committed effective dose levels incurred.”
The Ontario Decision
Facts
In this case, the worker was a chemical engineer employed by a firm which produced uranium and radioisotopes through the processing and refining of uranium ore.
From April 1952 to April 1956, he was exposed to low levels of radioactive materials. In November 1954, he was exposed to dangerous alpha-eminating material, contained in dust which spread throughout the area in which he was working. He had no protection against inhaling or ingesting the dust.
In August 1956, he died from NHL.
The issue before the WSIAT was:
“Does the medical and scientific evidence, when considered in the light of the law respecting the standard of proof, and any presumptions that might apply, establish a connection between the radiation exposure alleged by the appellant and the illness from which the worker died, sufficient to require a finding that the worker's illness and death entitled the worker and his dependants to compensation benefits under the Workers'
Compensation Act?” (WSIAT, para. 50)
This is essentially the same issue as that faced by this panel.
Expert Evidence
Prior to the hearing, the Ontario panel sought input from Dr. Mary K. Gospodarowicz, a leading expert on the carcinogenic effect of radiation exposure. The worker’s advocate sought further comment from Dr. Gordon Atherley, an expert in occupational and environmental health, including, particularly, radiation exposure.
Following are comments from the Ontario panel that are relevant to the case before us:
“As is often the case with epidemiological evidence, the evidence that is available with respect to the relationship, if any, between radiation exposures and NHL is fragmentary and haphazard in its development.” (para. 89)
“The following comment from Dr. Atherley’s report makes the latter point in more technical terms:
‘This [epidemiologic] method works well when substantial numbers of people are exposed and the disease occurs frequently in the exposed group. But when the numbers exposed and the frequency of… disease occurrence may be small, there is a sample size at which even a real difference (in the frequency of disease) between the non-exposed and the exposed group cannot be detected by epidemiology. Thus, epidemiology encounters limits of detection.
Epidemiologists attempt to overcome the limits of detection by combining groups from, say, different locations. But in the process, additional factors enter the picture and act to increase the uncertainty. Thus, in certain circumstances, the method encounters an absolute limit of detection below which no causal effect, however real, can be identified let alone substantiated. This problem of the limit of detection is compounded when multiple factors are involved in the disease causation, as is often the case with carcinogens. This is most certainly the case with NHL.
In practical terms, what this all means is that (a) the absence of statistically significant epidemiological findings is not proof of the absence of cause-effect, and (b) a statistically insignificant finding may even so reflect cause-effect.’” (para. 90)
“In her testimony, Dr. Gospodarowicz indicated that she agreed with the foregoing except that she noted that in the last paragraph there should "also be a (c)" - that is, that statistically insignificant findings may also reflect the absence of a cause and effect relationship.” (para 91)
(emphasis in original)
“From the evidence, it is apparent that a particular problem in assessing the possibility of a causal link between the radiation exposure which this worker is alleged to have encountered and NHL, is that this type of exposure on a scale conducive to such a study is very rare. Accordingly, opportunities for the development of epidemiological evidence on this issue almost never arise.” (para 92)
“Accordingly, since … what actually causes NHL is unknown, when the Hearings Officer concludes, as she did, that the medical literature does not support any relationship between exposure to ionizing radiation and NHL, it is important to remember that she is not saying that the medical evidence proves that NHL is not caused by ionizing radiation. What she is saying is that the little evidence there is does not prove that it can be so caused.” (para 93)
The panel majority note that this is the same scenario as in the case before us, where, both the initial adjudicator and the review officer based their decisions, at least in part, on the advice of medical advisors who could find no support in the medical literature for the premise that NHL may be caused by exposure to ionizing radiation.
“Dr. Atherley's opinion is that ‘the weight of the scientific evidence indicates that the worker's NHL was more likely than not to be due to or to have been exacerbated by his accidental exposure to polonium-210.’ He adds: ‘I do not believe that on the scientific evidence and other information available to me in connection with [the worker's] claim that it is possible to exclude that explanation as the cause of his NHL’. When asked directly to respond to that specific statement, Dr. Gospodarowicz indicated that she did not agree that the weight of the evidence indicates that it is more likely than not that the NHL was caused or exacerbated by the alleged radiation. She does agree, however, that it is not possible to exclude that explanation. She testified that she thinks the likelihood of the radiation exposure contributing to the NHL process to be ‘low’ but that ‘it cannot be excluded’.” (para 148)
“She does, however, agree that the alleged radiation exposure was at least a possible cause.” (para 153)
The panel majority would note that this is not unlike the opinion provided by the independent medical examiner who, in response to Appeal Panel questions, stated that “a causal relationship between ionizing radiation exposure and the development of WM is possible, but not probable.”
Findings
In its “Findings on the Facts”, the Ontario panel noted:
“If the worker's death had been caused by primary lung cancer, or acute leukemia, the experts would have had no difficulty in seeing this exposure as the cause of those diseases. Indeed, we understand Dr. Gospodarowicz's evidence to be that with the inhalation of this level of alpha emitting particles, she would not have been surprised to find lung cancer. (para 177)
“On the basis of Dr. Gospodarowicz's evidence, we also find that a causal relationship between this exposure and the development of the NHL disease is not medically implausible. There is a plausible causal mechanism that could lead from the radiation exposure to the development of NHL through the lowering of the worker's immune system.” (para 178)
Among its findings were:
“It is possible that, if the alleged radiation was not the direct cause of the NHL disease, it could have accelerated the development of a latent NHL through lowering the worker's immune system. While the expert evidence does not go the length of establishing that it is probable that this occurred, this panel finds that that evidence establishes that this is a possibility, and a possibility of some substance - not just mere speculation.
The radiation to which the worker is alleged to have been exposed as a result of the duct accident is a possible, not medically implausible, direct cause of the disease. Here too, while the expert evidence does not establish that the exposure is a probable cause, it does establish a possibility that reflects more than mere speculation. It is a possibility of some substance.” (para 180)
Law of Causation
Following are excerpts from the Ontario panel’s review of the law, which are relevant to our case:
“This case presents the legal system's classic problem of identifying a particular cause of a medical condition when the medical experts can identify a number of things that could have caused the condition but are unable to say which of these in fact caused the condition in the particular case. The presence of multiple, possible causes requires an adjudicator charged with the responsibility of making findings concerning the actual role of a particular potential cause to rely heavily on the law respecting burdens of proof and standards of proof - the law that is sometime referred to as "causation law”. In the past two decades, causation law as it relates to the adjudication of compensation issues in tort cases has been the subject of significant review.” (WSIAT, para 184)
“The leading Canadian decision in the recent review of tort-law causation principles is the decision of the Supreme Court of Canada in Snell v. Farrell (1990), 72 D.L.R. (4th) 291. The Court’s decision in that case was unanimous and it was delivered by the late Mr. Justice, John Sopinka.” (para 189)
“How, then, does the Supreme Court of Canada decision in Snell impact on this Panel's consideration of the cause issue in this case?
We would note, first of all, that the problem of how to ensure fair allocation of the financial burden of an injury in cases involving multiple potential causes is not peculiar to tort cases. It is a problem that is particularly endemic in cases involving the compensation of workers for diseases alleged to have been caused by exposure to hazardous materials in the workplace. In general, therefore, Mr. Justice Sopinka's analysis of the problem in Snell is, implicitly, highly relevant to cases of that kind - of which, of course, this case is one.
The next question is whether the Snell principle that "an inference of negligence may be drawn even though medical or scientific expertise cannot arrive at a definitive conclusion" can or should be applied in workers' compensation cases. Obviously, the equivalent principle in the workers' compensation context would be that an inference of work relatedness may be drawn in a particular case even though medical or scientific expertise cannot arrive at a definite conclusion - i.e. on a balance of probabilities - that work-place exposures in fact caused or contributed to the disease in that case.
In our view, there is nothing unique to the workers' compensation system that would justify our rejecting the Supreme Court of Canada’s direction in respect of that principle.
We hasten to add, however, that, of course, this statement of an adjudicator's authority to draw an inference even though the expert evidence cannot arrive at a definite conclusion does not help in defining the circumstances in which it would be appropriate to do so.
On the latter question, there are other principles that have been clarified in Snell which we believe to be particularly important. The second principle is that the adjudication of the causal issue is not the function of an expert but the function of a lay adjudicator acting as a "jury". Justice Brennan's observations in the Sentilles case, quoted with approval by Sopinka as setting out the appropriate distinction between the "trier of fact" and the expert witnesses, bear repeating.
The jury's power to draw the inference that the aggravation of petitioner's tubercular condition, evident so shortly after the accident, was in fact caused by that accident, was not impaired by the failure of any medical witness to testify that it was in fact the cause. Neither can it be impaired by the lack of medical unanimity as to the respective likelihood of the potential causes of the aggravation, or by the fact that other potential causes of the aggravation existed and were not conclusively negated by the proofs.[2]
It is clear from the context in Snell, that, as far as the adjudication of causal issues is concerned, Sopinka sees no distinction between a trial judge's role in a case where there is no jury (as was the case in Snell) and the role of an actual jury. It may also be noted that this is not a new idea. It has always been considered that the trier-of-fact function may in some cases be assigned to a jury and in some cases to a trial judge sitting without a jury but in either case the function and approach is the same. In administrative justice settings where actual juries are not part of the system, adjudicators may sometimes lose track of this concept. Having the Supreme Court remind us of our role in that respect is, in this Panel's view, helpful.
The third principle to be derived from Snell which, in our opinion, is important and applicable in the workers' compensation system, is that causation is "essentially a practical question of fact which can best be answered by ordinary common sense” and a "robust and pragmatic approach” to the evidence. This is, of course, an articulation of the approach which juries have traditionally been expected to bring to the determination of factual issues.
Finally, Mr. Justice Sopinka's statement that he would be willing to fall back on the Wilberforce principle in the event the practical problems with Lord Bridge's approach … were seen to be resulting in defendants with "substantial connections" to the injury, being relieved of responsibility, must, in our view, be seen as throwing a significant back-light on the nature of the Supreme Court’s approach to causation issues in the circumstances of a case like Snell.” (paras 217 – 225)
Conclusion of the Ontario Panel
“The Panel's question in light of Snell is how would a jury, acting responsibly but with a robust and pragmatic approach to the evidence and exercising its common sense, decide that issue in light of the facts established by the evidence in this case, as set out above.
In our view, on the evidence in this case, such an approach must inevitably lead to the inferring of a causal connection between the radiation exposure and the death of the worker. If the alleged exposures are found to have occurred, the worker would, in our opinion, have to be seen to have suffered a significant workplace accident in which he was exposed to inhaling and ingesting dangerous alpha-emitting particles and thereby incurred a whole-body burden that exceeded twice the permitted burden. The causal connection between such an exposure and the development of NHL is not medically implausible. It is possible. Also, if the worker were suffering incipient NHL when he came to work with the employer in 1952, it is also, on the evidence, possible, in the sense of being medically plausible, that the accidental exposure would have resulted in an acceleration of the pace of the disease development and hastened the worker's death.
Neither of these possibilities are merely speculative. On the evidence they are both substantive.
That these two possibilities are not merely speculative appears from the following. It is true that the medical opinion, which we accept, is that neither of these possible effects was probable or likely. However, Dr. Gospodarowicz agreed that, as compared to individuals who had not been subjected to such exposure, the worker would be seen to have been exposed to an additional risk of contracting NHL. Dr. Gospodarowicz also testified that, in her opinion, the causal connection was not medically implausible. As to the accelerative effect, the evidence establishes that it is not an unknown clinical experience to find the pace of development of a latent cancer condition accelerating as a result of a lowering of the body's immune system caused by a patient's exposure to radiation in the treatment of some other cancer.
Furthermore, the evidence establishes that the type of exposure the worker suffered is very rare. The experts, therefore, had little to work with as far as substantive evidence based on actual clinical experience with equivalent exposures is concerned. Accordingly, the expert opinions either way on this issue of the probable effect of such an exposure on the body's tissues really lie in the area of educated guesses. We do know that this kind of radiation exposure can cause cancer. The medical experts would not have been surprised to find acute leukemia or lung cancer. What appears to stump the experts is how the lungs and blood could have been by-passed and the NHL cancer have been the result. On the other hand, there is little or any clinical experience with this particular type of exposure for them to go on in assessing that mystery.
In evaluating the likelihood of the workplace radiation exposure being implicated in the worker's death, a jury would naturally have to examine any alternative causes. Here, the one other possibility is the worker's exposure as a member of the general population to unknown environmental factors and other unknown causes. As we have seen, however, while that too is not merely a speculative possibility, the odds against any particular member of the general population contracting NHL based on those factors is very high.
When one compares the latter possibility with the other two substantial possibilities, in our view, a robust and pragmatic approach coupled with common sense leads inexorably to the inference – to use the Snell-approved Wilshire language - that the worker's radiation exposure at the time of the duct accident either caused the NHL disease or accelerated the pace of its development. That exposure, if it occurred, must, therefore, be seen to have either caused or hastened the worker's death.” (paras 228 – 234)
Application to this Case
In response to the panel’s request for comments on the Ontario decision, the employer wrote:
“While both cases involve internal exposure to ionizing radiation from the inhalation of radioactive isotopes, purporting to be the cause of a type of cancer grouped under the name of non-Hodgkin’s Lymphoma (NHL) the principal difference is the lack of adequate dosimetry and prompt bioassay follow-up in the WSIAT case no. 549/95, which is in complete contrast to [this claim] where the dose history in general and the dose estimate for the two accidents in particular are well known. In WSIAT 549/95 the board allowed the appeal on the basis of biological plausibility that the exposure either caused the disease or significantly accelerated the development of the cancer. Although the board acknowledged that the probability of cause and effect could not, and probably never would be established with any confidence, they accepted the evidence that the exposure that did take place was very substantial in magnitude and this undoubtedly gave weight to their acceptance of cause and effect. Uncertainties surrounding the timing of the event compared to the first bioassay information obtained and uncertainties in the exact radiological nature of the event itself made it impossible to put a lower limit on the dose received. Even if biological plausibility and cause and effect are accepted in [this case] the estimates of committed effective dose indicate that the probability of the claimant’s disease resulting from his accidental exposure to ionizing radiation is vanishingly small.”
The majority recognizes that we are not bound to follow precedents, especially those from another province. The practice in WCB cases is that each one is decided on its own merits. Nonetheless, the majority has found the reasoning contained in WSIAT 549/95I2 to be both very persuasive and particularly helpful in our deliberation. To that end, we have adopted much of that reasoning into our decision.
Analysis
The employer did not successfully distinguish the case before us from the findings in the Ontario case. They seemed to rest their argument for distinguishing the cases on the fact that the amount of radiation to which the Ontario worker was exposed was unknown, while the dosage experienced in this case was well-recorded.
Our reading of the Ontario case leads us to the view that the only conclusion they made was that “the amount of Polonium 210 absorbed by [the worker] would have been substantial.” (WSIAT 549/95, para 58)
Based on the evidence before us in this case, we (the majority) have concluded that the claimant here was, also, subjected to “substantial” exposures on two occasions.
The employer is not clear in its response to the evidence given by the doctor in support of the claimant. According to the employer, this doctor suggested that, where the exposure was largely internal, this should negate the value of epidemiological data. This seems to suggest that there is a body of epidemiological data which conclusively eliminates radiation exposure as a cause of WM or NHL. This is not so.
If anything is conclusive in this regard, in this case and the Ontario one, it is that there is very little evidence for or against a causal link between radiation exposure and NHL and virtually none in respect of WM.
We find the medical argument presented to the panel by the doctor, who supported the claimant, to be the most persuasive of the various medical opinions presented in this case. Still, it does not definitively establish a causal link between the claimant’s exposures to ionizing radiation and his WM.
To repeat, from the Ontario case, “the type of exposure the worker suffered is very rare. The experts, therefore, had little to work with as far as substantive evidence based on actual clinical experience with equivalent exposures is concerned. Accordingly, the expert opinions either way on this issue of the probable effect of such an exposure on the body's tissues really lie in the area of educated guesses. We do know that this kind of radiation exposure can cause cancer. The medical experts would not have been surprised to find acute leukemia or lung cancer. … On the other hand, there is little or any clinical experience with this particular type of exposure for them to go on in assessing that mystery.”
Conclusion
The majority of the panel concludes that this claimant’s cancer – Waldenstroms Macroglobulinemia (WM – arose out of and in the course of his employment, being a result of his two exposures to ionizing radiation, once in 1964, the other in 1968. We cannot determine the contribution each exposure made to the cancer but are satisfied, on a balance of probabilities, that the exposure in 1968 was a significant contributor.
We have come to this conclusion by following – and adopting some of – the reasoning set out in the Ontario case. The Ontario case – in turn – relied on the law of causation set out in the Snell decision of the Supreme Court of Canada.
The WSIAT panel applied the Snell principle to workers compensation cases, that principle being “that an inference of work relatedness may be drawn in a particular case even though medical or scientific expertise cannot arrive at a definite conclusion - i.e. on a balance of probabilities - that work-place exposures in fact caused or contributed to the disease in that case.”
Applying that Supreme Court-approved principle to the evidence before us leads inexorably to the inference that the claimant’s exposure to ionizing radiation led to the development of WM.
Accordingly, the appeal is allowed.
Footnotes
Panel Members
T. Sargeant, Presiding Officer
A. Finkel, Commissioner
M. Day, Commissioner
Recording Secretary, B. Miller
T. Sargeant - Presiding Officer
(on behalf of the panel)
Signed at Winnipeg this 18th day of January, 2005
Commissioner's Dissent
Commissioner Finkel’s Dissent:
As noted in the background, the claimant has unfortunately been diagnosed with Waldenstroms macroglobulinemia (WM), a rare non-Hodgkins lymphoma-type (NHL) cancer which he feels was caused either by specific major radiation exposure incidents at his workplace in 1964 and/or 1968, or to a more generalized occupational exposure to radiation in his years of work in the nuclear industry. He is appealing the earlier decisions by the WCB that his cancer is not related to his employment in the nuclear industry, and is seeking to have his claim accepted. The claimant was represented at the hearing by an advocate, a doctor with a background in occupational health. The employer also participated at the hearing.
For the claimant to succeed, I would have to find on a balance of probabilities that the claimant’s WM is causally related to his employment. I was unable to reach this conclusion, and my reasons follow.
Legislation:
As indicated by the majority, this claim is adjudicated under the Government Employees Compensation Act (GECA). Certain provisions of the appropriate workers compensation legislation are incorporated into GECA.
In addition to the sections of GECA noted by the majority the following provisions are relevant:
4.(1) Subject to this Act, compensation shall be paid to
a. an employee who
…
ii. is disabled by reason of an industrial disease due to the nature of the employment;
2. In this Act,
“industrial disease” means any disease in respect of which compensation is payable under the law of the province where the employee is usually employed respecting compensation for workmen and the dependants of deceased workmen.
The then-named The Workmen’s Compensation Act defines industrial disease as “any disease that is peculiar to, or characteristic of, an industrial process, trade, or occupation to which Part I applies."
WCB Policy 44.20 provides some assistance in defining the terminology used in the “industrial disease” definition in the old legislation, although this policy refers in general to the current wording of “occupational disease” instead of “industrial disease.” This Policy states, in part:
2. DEFINITIONS RELEVANT TO OCCUPATIONAL DISEASE
A number of terms arise directly from the legislation that require operational definition. For the purpose of this policy the following definitions apply:
a. “peculiar to or characteristic of a particular trade or occupation”
A disease will be described as being peculiar to or characteristic of a particular trade, work process, or occupation if there is a preponderance of scientific evidence to support a conclusion that the nature of the work processes or environment have significantly increased the likelihood of causing a particular disease in the workers who work in that trade or occupation.
b. “peculiar to the particular employment”
A disease will be described as being peculiar to the particular employment if:
1. there are factors identifiable in that workplace that are known to cause the disease, or
2. there is scientific evidence acceptable to the WCB that the particular workplace is the cause of a significantly increased risk of the disease even though the cause has not been identified, or
3. a factor can be identified at the workplace as being the proximate cause of the disease.
Evidence and arguments:
The claimant and his advocate put forward the position that the incidents in 1964 and 1968 led to very heavy and unusual radiation exposures, much of which was inhaled or ingested. They suggest that the measuring tools used were firstly not reliable and secondly were external measuring devices that could not measure internal radiation. They note that while the claimant was required to shower and scrub at length to deal with the external radiation, there was no process available to deal with the substances ingested and that these substances may have remained in his body. They also point out that WM is a rare type of NHL, and that it is not well-understood. They also point to the fact that NHL cancers have been accepted in the United States for workers in the nuclear industry.
The employer’s position focused on an array of scientific studies on radiation exposure dealing with workers in nuclear industries and populations exposed to nuclear explosions or accidents, and argue that these studies do not support that that there is an increased risk for the development of NHL in those populations. The employer notes that WM is a sub-set of the broader category of NHL cancers, and accordingly these studies would also not support that the claimant’s WM arose out of and in the course of the employment.
Regarding the specific exposures in 1964 and 1968, neither party offered direct evidence as to what specific substances were ingested in those incidents, or the quantities or concentrations of those exposures. Both parties acknowledged that the exposures were not planned, were not replicable, and were not directly measurable.
In this case, the panel was not presented with any specific medical evidence connecting the claimant’s cancer to a specific workplace exposure. While there was speculative discussion about the potential impact of ionizing radiation on the lymphatic system, there was acknowledgment that these relationships are hypothesized but not proven. Both parties did, however, present a considerable number of published epidemiological studies dealing with radiation exposures of workers in the nuclear industry, workers using equipment with radiation, as well as people exposed to radiation in the nuclear attacks on Japan in 1945, and Chernobyl.
The panel also had available to it a considerable body of medical reports and opinions, as well as research (and conclusions) undertaken by WCB medical specialists as to relationship of the claimant’s medical condition to his workplace exposures.
Given the complex nature of this claim, the panel chose to send out this matter for the consideration of an independent medical examiner. He was provided with relevant materials from the file, and was asked to undertake such further reviews as necessary, and to provide his opinion regarding the relationship between the claimant’s cancer and the 1960s incidents and/or general workplace exposure.
The tests to be used:
Cases involving industrial or occupational disease rarely have the benefit of clear scientific evidence that can demonstrate a direct biological linkage between the exposure and the disease. In a perfect world, researchers would observe and report that a specific exposure to a chemical or substance for a particular length of time causes a particular change at the cellular level that will in turn lead to a specific disease process. However, as noted by the 1990 Supreme Court of Canada decision in Snell v. Farrell, this type of scientific certainty is not necessary in order to establish a successful claim.
What has evolved to replace this type of scientific certainty in the case of occupational diseases is the use of epidemiological studies – the study of large populations -- to determine if certain diseases are more prevalent for certain types of workers, and thus the basis for the acceptance of the disease as an “accident” under the Act. In this process, large scale studies are done of workers in certain types of industrial or workplace settings to assess whether certain medical conditions are more likely to occur at those workplaces than in the general population.
The idea of a medical condition being “more likely to occur” is a layman’s term for what is really a statistical exercise, in which the study’s authors aggregate their research data, and then use generally accepted statistical tools on their data to determine if the different results between the groups are statistically significant. These cohort studies look for statistically significant increases in the morbidity/mortality of workers in certain workplaces or occupations for certain diseases, in comparison to the control group which is usually a general population.
In cases such as this one, where a particular type of cancer is claimed to be related to an occupational exposure, the WCB and a variety of specialists will scour the scientific literature to determine if the collected studies support a causal relationship between the particular cancer and the workplace.
Where there is a sufficient body of scientific evidence to establish a causal relationship between a particular disease and sufficient exposures in certain occupations, it is open to the WCB or this panel to determine, on a balance of probabilities, that there is a “preponderance of scientific evidence” – in other words, a balance of probabilities -- to establish that the claimant’s cancer was caused by his workplace.
In certain instances, the scientific evidence is so well-established that the WCB has even “codified” certain types of diseases (such as laryngeal cancer and gastro-intestinal cancer) into policies to allow for prompt adjudication of those claims. These policies set out medical diagnoses, the length and types of exposures and the latency periods required, for the link between the disease and the workplace to be established. The presence or absence of a WCB policy dealing with a particular cancer is not relevant to the case at hand, as each case is decided on its merit, and thus it is our responsibility to examine the medical evidence and the scientific research to determine if the causal link can be established.
Of critical importance to the review of the external studies is the idea that there must be a “statistically significant” difference in mortality/morbidity, between the worker’s industry group and the rest of the population.
So what is considered by the medical or scientific community to be a “statistically significant” result, when looking at epidemiological studies? A recent Appeal Commission decision (144/03) dealt with new legislation that codified the entitlement of full time fire fighters to benefits if they were diagnosed with certain types of cancers. The legislation was based on a literature review undertaken by Guidotti and Goldsmith (2002).
In that literature review, the authors provide some interesting insights as to how these large population cohort studies are developed and interpreted. In that case, similar to this one, they were dealing with some cancers that were quite rare. The authors first note that the scientific studies usually group together a number of unique cancers into one category; some of these cancers are very rare and cannot be studied individually (in a statistically meaningful way) in large populations. However, by accumulating these cancers together, there is an accepted recognition that there are likely higher and lower exposure risks for each cancer and that the risk of “brain cancer” represents an averaged risk of this group of cancers. This is the exact situation in the current case, where the claimant’s diagnosed WM cancer is known to be a very rare type of NHL cancer.
Guidotti and Goldsmith then discuss how a scientific presumption (or what the WCB policy describes as a “preponderance of scientific evidence”) is established:
“A presumption assumes that, all other things being equal, most cases of a certain type of cancer will be associated with occupational exposure, even though it is not possible to determine which case is actually caused by the occupation. A presumption is a way of being inclusive in the acceptance of such claims given that it is not possible to distinguish among them. A presumption is usually based on the demonstration that the relative risk exceeds twice that of the general population, because this statistical measure corresponds to even odds, or the notion that the risk arising out of work equals or exceeds that in daily life. In practice, it is impossible to make such a fine distinction. A relative risk of 1.7 or 1.8 (standard mortality ratio, or SMR, of 170 or 180) is usually indistinguishable statistically from one of 2 (a SMR of 200) with any confidence. A presumption is also appropriate when the condition is rare and there is a pattern or strong suggestion of strong association with an occupation that may be concealed by other factors that complicate interpretation of the risk estimate.”
(emphasis added)
By describing the necessary threshold by which workers need to demonstrate a disease compared to the general population, scientists or epidemiologists are effectively drawing a line in the sand, on what constitutes a scientifically meaningful outcome, or a “preponderance of scientific evidence” as required by WCB policy: if the data supports a high relative risk for a particular disease and occupation -- above that line (1.7 or 1.8) – then that qualifies as a “preponderance of scientific evidence” that the workplace exposure is the cause of the worker’s medical condition. At that level of difference between the studied work group and the control group, it becomes reasonable to assume – or presume – that the workplace exposure (as defined in the scientific evidence) led to a particular worker’s disease, and thus an entitlement to benefits.
Analysis:
Although there is an “intuitive” and strongly felt sense expressed by the claimant and his physician that the claimant’s cancer is related to his general or specific workplace exposures, none of the parties have been able to point to any studies demonstrating anywhere near the kinds of morbidity that researchers require, in order to establish a statistically significant link between NHL cancers and the claimant’s workplace.
There have also been many assessments on the file, to determine whether a scientifically accepted causal link can be demonstrated between WM and the claimant’s type of workplace. In particular, I note the following:
- The WCB’s internal medicine consultant prepared a memo on November 2, 2000 in which he cites the extensive file review and literature search that he performed. He then notes:
“Waldenstrom’s macroglobulinemia is one of the malignant lymphoproliferative disorders of small lymphocytes. The disease is more common in men than in women and the incidence increases with age. The median age of diagnosis is around 64 years.
In my search of the literature to identify the cause of this rather rare disorder, I came across no relationship between [WM] and exposure to isotopes and radiation. I am in the process of obtaining an article…”
- A WCB medical advisor prepared a memo on March 20, 2003, in which he noted that the WCB internal medicine consultant had restricted his research to WM. He felt it prudent to review the file again under the broader heading of NHL. He indicates that he contacted all Workers Compensation Boards across Canada and found that no NHL claim related to radiation exposure had been accepted in Canada. He also reviewed a number of major texts regarding cancer epidemiology and the published literature, and found no reports suggesting radiation exposure as a risk factor for the development of NHL.
- The Panel also asked an independent haematologist to consider this matter. The particular physician works in a major cancer facility in Winnipeg, and notes that he has “been responsible for writing and editing five editions of Wintrobe’s Clinical Hematology, the premier textbook in this area. I was assigned special responsibility for the plasma cell dyscrasias which include, among others, the diseases of multiple myeloma and [WM]. My clinical practice at CancerCare Manitoba specializes in these diseases as well.” He was provided with all the job descriptions, scientific, and medical materials on the file, and was encouraged to expand his research. In his report of November 9, 2004, he notes as follows:
“1. There is no documented evidence that [WM] or, indeed, multiple myeloma, a monoclonal gammopathy that is ten times as common as [WM] is related to radiation exposure….As far as [NHL] are concerned, which are similar to [WM] save for the lack of monoclonal gammopathies in most instances, a number of factors have been mentioned as possibly contributing to the current epidemic of [NHL] and these include ionizing radiation, electromagnetic fields, alcohol, tobacco and chronic fatigue syndrome, but the data are very weak and, from a scientific perspective, do not support an association between these factors and an increased risk of [NHL]. In summary, a causal relationship between ionizing radiation exposure and the development of [WM] is possible, but not probable.”
- The haematologist then states that in keeping with his findings, causal relationships between the accidental exposures in 1964 and 1968, are possible but not probable. He finally notes that “according to the papers quoted previously, there is no evidence in the scientific literature available to date that the lifetime occupational exposure to radiation undoubtedly suffered by [the claimant] is causally related to the development of [WM].”
I do wish to comment on an Ontario case (decision 549/95I2) heard by the WSIAT (our counterpart tribunal) in which a claim for NHL for a worker in the uranium processing industry was accepted. This case was cited by the claimant as suggesting that there was indeed an evidentiary precedent for his claim to be accepted. The panel in that case noted that there were two possible causes of the diseases in question (paragraphs 180-181), being a pre-1952 general population exposure, and a post-1952 workplace radiation exposure. In paragraph 182 and 183 they state, “the Panel is satisfied, and so finds that the worker’s NHL was in fact caused by one of the two exposures. The expert evidence does not, in our view, establish either of the causes as the probable cause. Neither does it establish which is the most probable cause. In each case, however, the possibility is a substantive one – not merely speculative. Furthermore, if the general-population exposure were held to be the cause of the worker’s NHL, there is the further possibility that the radiation exposure at the time of the duct accident accelerated the condition and thus advanced the worker’s death.”
There are two matters worth noting regarding the Ontario case. First, there is no “substantive possibility” established by the scientific evidence in the case before us, unlike the WSIAT case. Second, in reading the balance of the WSIAT decision, the Panel seems to suggest that if there are a number of possible causes of a disease, one can add together the series of possibilities and if one of the possibilities involves the workplace, the sum of the possibilities can establish a probability that allows the workplace to be causative of the disease. I find this legal reasoning to be unusual. It is not consistent either with the usual interpretation of the general standard of “balance of probabilities”, nor is it consistent with the WCB policy which requires there to be a “preponderance of scientific evidence to support a conclusion that the nature of the work processes or environment have significantly increased the likelihood of causing a particular disease in the workers who work in that trade or occupation.”
After my full review of this case, I find the compilation of scientific reviews overwhelming in its rejection, at this time, of a causal relationship between the claimant’s specific type of cancer as well as the general class of cancers, and radiation exposure. I accept that the current scientific evidence noted above does not support a linkage, although I am deeply sympathetic to the claimant’s and his physician’s sense that there is indeed a linkage. Accordingly, I find that that the definition of “accident” has not been met, and would deny the claimant’s appeal.
A. Finkel, Commissioner
Signed at Winnipeg, this 18th day of January, 2005.