THOMAS BONCHER (DEC'D), Applicant
BAY ENGINEERED CASTINGS, Employer
UNITED WISCONSIN, Insurer
c/o UNITED HEARTLAND INC
An administrative law judge (ALJ) for the Worker's Compensation Division of the Department of Workforce Development issued a decision in this matter. A timely petition for review was filed.
The commission has considered the petition and the positions of the parties, and it has reviewed the evidence submitted to the ALJ. Based on its review, the commission agrees with the decision of the ALJ, and it adopts the findings and order in that decision as its own.
The findings and order of the administrative law judge are affirmed.
Dated and mailed June 5, 2003
boncher . wsd : 101 : 3 ND § 3.42
/s/ David B. Falstad, Chairman
/s/ James T. Flynn, Commissioner
/s/ Robert Glaser, Commissioner
1. Overview.
The applicant, who is now deceased, claimed permanent and total disability from lung cancer and chronic obstructive pulmonary disease (COPD.) He asserted that these conditions were caused by his employment exposure to airborne silica dust. The defense offered by the employer and its insurer (collectively, the respondent) is that silica exposure, while it causes silicosis, does not cause lung cancer or COPD. The ALJ found for the applicant, and the respondent appeals.
The issue in this case, whether the applicant's employment caused his lung cancer and COPD, has generated substantial expert medical opinion.
2. Expert opinion.
a. The applicant's experts.
The applicant offers the opinion of K.D. Rosenman, M.D. His diagnosis, in July 2002, was severe COPD and a nonresectable lung cancer, which he opined was caused by work directly and by an appreciable period of workplace exposure that was at least a material contributory causative factor in the onset or progression of the conditions. He opined the lung cancer condition was terminal.
Regarding causation, Dr. Rosenman writes:
"...I would conclude within a reasonable degree of medical certainty that [the applicant's] exposure to silica at Bay Engineered Casting was a significant contributor to his development of lung cancer.
"You have asked me to indicate what percentage of lung cancer I attribute to work. Less than 10% of cigarette smokers develop lung cancer. Although there are various hypotheses about how genetics and nutrition might determine why an individual cigarette smoker ends up being one of the 10%, the best data is that certain exposures explain why particular cigarette smokers develop lung cancer. These exposures include arsenic, asbestos, radon gas and silica. A common percentage quoted in the literature is that 80-90% of lung cancer can be attributed to cigarettes. The calculations used to obtain the 80-90% are based on looking at one factor at a time and the total percentages are not intended to add to 100%. For example, in a cigarette smoking asbestos worker who develops lung cancer one can say with equal authority that 80-90% of the individual's lung cancer can be attributed to cigarettes and 80-90 percent attributed to asbestos. One could conclude from these calculations that each contribute 50%. Based on these calculations for asbestos, I would conclude that silica exposure in the foundry was responsible for 50% of Mr. Boncher's lung cancer.
"The literature that silica causes lung cancer is convincing. Authoritative groups such as the International Agency for Research on Cancer (IARC) which receives part of its funding from the U.S. National Cancer Institute and the U.S. National Institute for Occupational Safety and Heath (NIOSH) ha[ve] concluded that silica is a definite human carcinogen. I personally have published a paper based on individuals with silicosis in Michigan and New Jersey who were predominately foundry workers that they had increased risk of lung cancer. [Citation omitted.] The recent NIOSH criteria document just released in 2002 has reviewed the medical literature on silica and cancer and has concluded silica causes lung cancer. [Citation omitted.] The American Thoracic Society concluded that individuals with silicosis are at an increased risk of lung cancer. Work in chipping and grinding is one of the highest risk areas for silica exposure in a foundry. This is the predominate work Mr. Boncher did in the foundries.
"I would also note with a reasonable degree of medical certainty that Mr. Boncher's non-malignant lung disease, silicosis and COPD, were also caused by his exposure to silica in the foundry. Similar to lung cancer, COPD occurs in less than 10% of cigarette smokers. Work exposure, particularly silica, interacts with cigarette smoke and markedly increases the risk of COPD. The fact that Mr. Boncher has advanced silicosis (I interpreted his x-ray as 3/3) and severe COPD complicates his treatment for lung cancer. It reduces the likelihood that surgery could be used to treat him and the reduction in lung reserve from this lung disease worsens the prognosis for his lung cancer.
"Since 1981 I have directed surveillance systems for silicosis. During that time period I have reviewed the medical records and interpreted the radiographs of over 1000 silicotics. I have personally examined hundreds. I have been in 15 or more foundries and reviewed industrial hygiene reports and air samples from at least 50 foundries. I reached my conclusion based on my personal experience, review of the medical literature and review of Mr. Boncher's records. He has three diseases caused by silica (lung cancer, silicosis, COPD). The fact that he smoked cigarettes in no way negates his 34 years of silica exposure. Without the silica exposure it is unlikely he would have developed any of three lung diseases he now has."
Exhibit B, June 17, 2002 report of Rosenman.
The applicant's attorney asked his applicant's oncologist, Anthony Jaslowski,
M.D., to complete a WKC-16-B form, and mark "yes" at box 13 (the causation by
"occupational disease" box) if he agreed with Dr. Rosenman's conclusions.
Dr. Jaslowski instead wrote a letter stating:
"...I have reviewed the information regarding the association with silicosis and lung cancer. I have also reviewed what was supplied by Dr. Kenneth Rosenman. I feel at this juncture that Dr. Rosenman has adequately covered the information and I feel that with my training in medical oncology that my opinion does not add any further information."
Exhibit D, August 7, 2002 letter from Jaslowski.
Dr. Rosenman attaches his article, Rosenman, et al., "Mortality among persons with silicosis reported to disease surveillance systems in Michigan and New Jersey in the United States," Scand J Work Environ Health, 1995; 21(suppl 2):73-76. Exhibit B. This article notes that repeated epidemiologic studies among patients with silicosis have found an increased risk of death from lung cancer. The article states:
"The data do not support the argument that an increased prevalence of smokers among workers with silicosis explains the increased risk of lung cancer.
"The data showed no trend of increasing lung cancer risk among persons with greater silicotic scarring on their x-rays, indicating the increased lung cancer risk did not arise from pulmonary scar tissue.
"The data showed no monotonic trend of increasing risk for lung cancer and all respiratory disease by duration of silica exposure, which was inconsistent with the hypothesis that silica was a direct carcinogen. On the other hand, a statistical increase among men who began work before 1949 suggested that high historical exposures and sufficient latency from the first exposure were associated with lung cancer among silicotics, supporting an effect of silica or some other workplace exposure."
The article's conclusion was that the association between lung cancer and silicosis was supported. The data suggested the association could not be explained by smoking, profusion scores, or a bias from study workers who brought workers compensation claims. The importance of concomitant carcinogens in workplaces using silica could not be ruled out.
The applicant also submits Wagner, "Asbestosis and silicosis," Lancet 1997; 349:1311-1315. Exhibit C. This states flatly:
"Lung-cancer risk is increased in people with silicosis. The International Agency for Research on Cancer has largely determined that respirable crystalline silica found in the workplace is carcinogenic to human beings and categorised it as a group 1 carcinogen."
In addition, Beckett, "Occupational Respiratory Diseases," New England Journal of Medicine, volume 342, number 6 (February 2000) 406, 410 (table 3) lists "crystalline silica (produced by stone cutting, drilling, and tunneling)" as a "selected cause of occupational lung cancer." See exhibit C.
Further, the applicant submitted an article from NIOSH, specifically NIOSH Health Review, "Health Effects of Occupational Exposure to Respirable Crystalline Silica," DHHS (NIOSH) Publication No. 2002-129 April 2002. Exhibit C. The abstract of this article states "occupational exposures to respirable crystalline silica are associated with the development of silicosis, lung cancer, pulmonary tuberculosis, and airways diseases." The article reports that possible carcinogenicity of crystalline silica dust became a subject of intense debate in the scientific community in the 1980s. The article notes that in October 1996, an IARC expert working group "concluded that there `is sufficient evidence in humans for the carcinogenicity of inhaled crystalline silica in the form of quartz or cristobolite from occupational sources.'" Id., at 3.4.1. The article noted, too, that the American
Thoracic Society (ATS) had described the adverse health effects of exposure to crystalline silica, including cancer, finding:
The article went on to state that NIOSH concurs with the conclusions of the IARC working group and the ATS.
The NIOSH article also noted the epidemiologic studies of cancer have mainly investigated workers exposed to respirable crystalline silica in certain industries, including foundries. The article stated, too, that while some of the studies proving the least confounded investigations of an association between occupational exposure to crystalline silica and lung cancer did not find a significant association, most did. Id., at 3.4.2.
Regarding the connection of silica exposure with chronic obstructive pulmonary disease, the applicant submits Hertzberg, Rosenman, et al, "Effect of Occupational Silica Exposure on Pulmonary Function," Chest 2002; 122:721-728, which states:
"The PFT [pulmonary function test] results from our study are consistent with the classical association of silica exposure with restrictive lung disease, as well as the more recent recognition of the occurrence of obstructive changes with silica exposure. However, we only found an association between obstructive changes and cumulative silica exposure in individuals who also smoked cigarettes. The absence of significant obstructive changes in nonsmokers with silica exposure has been reported in some of the studies of South African gold miners, but not others. Some studies have reported obstructive changes among nonsmokers with silica exposure only in the presence of advanced silicosis. We excluded all individuals with radiographic changes of silicosis from this analysis of PFT results. The results of all the studies have concurred that occurrence of obstructive disease is significantly greater among individuals with both silica and tobacco exposure in comparison with either one separately. ...
In addition, Beckett, "Occupational Respiratory Diseases," New England Journal of Medicine, volume 342, number 6 (February 2000) 406, 409 (table 2) lists "crystalline silica" as a "common cause" of chronic airflow limitation.
b. The respondent's experts.
The respondent relies on the report of Stuart Levy, M.D. He notes that since the 1964 Surgeon General's report on smoking was published, "a staggering volume of additional evidence has been accumulated which establishes beyond any doubt that cigarette smoking is causally related to squamous cell carcinoma of the lung, emphysema, and chronic bronchitis." In addition, Dr. Levy characterizes the applicant's condition as "simple silicosis," which is normally asymptomatic, and notes that the applicant's abnormal pulmonary function may thus be attributed to a reasonable degree of medical certainty exclusively to smoking. Regarding the connection between cancer and silica, the doctor writes:
"The issue regarding the association of lung cancer with silica exposure has recently been reviewed at the International Update on Occupational and Environmental Respiratory Disease on March 3, 2002, in Houston, Texas. The representatives from the National Institute of Occupational Safety and Health (NIOSH) who are the strongest proponents for advocating a cause/effect relationship between lung cancer and silica, admitted that the data supporting the association is extremely weak. The studies cited which demonstrated a positive association failed by their own admission to adequately take into account the effect of smoking, bias or other confounding issues, including exposure to other carcinogens including asbestos and radon. A recent superb treatise on the subject (1) ... has convincingly demonstrated that the carcinogenicity of silica in humans has never been demonstrated in any of the quoted studies. The data do not support a causal association between silica exposure, silicosis, and lung cancer. The conclusion that silicosis is associated with a higher than expected increase in lung cancer is not supported by the current literature. [Citation omitted.] Even the often quoted IARC report notes that the carcinogenicity of silica in humans has not been detected in any of the studied industrial circumstances [Citation omitted], but used studies of compensated silicotic patients which is dubious and fraught with selection bias.
In summary, it is my opinion with a reasonable degree of medical probability that had Mr. Boncher not started smoking at age 14 and continued for the next 40 years, he would not have developed lung cancer or chronic obstructive pulmonary disease, regardless of silica exposure. [Footnote added; emphasis in original.]"
Exhibit 3, July 31, 2002 report of Levy.
In a report dated August 21, 2002, the doctor reiterated his opinion that "exposure to silica was not a material contributory causative factor in the causation of lung cancer in Mr. Boncher." Exhibit 17. He also opined that while there was evidence of simple silicosis with slight progression since 1981, that condition did not contribute to the applicant's disability. He also opined that smoking, not silica exposure, was the reason for the applicant's COPD.
The respondent also offers an opinion from Thomas Tolly, M.D., who reviewed the recent x-rays of the applicant's lungs prior to his death. His opinion was that the applicant had simple silicosis. Exhibit 18.
Further, the respondent submits a report from Ross L. Clay, M.D., (exhibit 19) which begins by noting that while the IARC has classified crystalline silica dioxide as a human carcinogen, this is not a well-accepted designation and other reviews of the same data have reached the opposite result. He also indicated that because cancer can be multifactorial, it would be appropriate to look at the question from an "attributable risk" standpoint, that is, assessing the relative contribution of the individual risk factors as "material contributory factors."
Dr. Clay also points out that in assessing the 50/50 smoking-to-silica contribution to lung cancer, Dr. Rosenman is relying on the proven rates for smoking versus asbestos exposure. Dr. Clay states that there is not the same data to back this up with silica exposure, noting that some studies of silica show no association and others a weakly positive association. He states flatly that, unlike the associations showing up for asbestos in a multitude of studies over many years, "no studies show a risk of lung cancer from silica exposure equal to or even anywhere close to the risk of lung cancer due to cigarette smoking." Exhibit 19, November 29, 2001, report of Clay.
Further, Dr. Clay looked at a number of other factors related to cancer in the applicant's case, including a significant history of smoking starting at a young age; a family history of cancer (a brother) and specifically lung cancer (his father); radon exposure (though this is stated in terms of potential exposure if a basement room were regularly used; Dr. Clay noted the applicant's house had been tested and no mitigation done indicating an exposure of below 10pCiL); and secondhand smoke (the applicant's wife smoked). It was Dr. Clay's opinion that the applicant's use of cigarettes, not his silica exposure, caused his condition.
In addition to providing numerous reports indicating that there is a connection for
smoking and radon exposure, the respondent also provides report responding to
the IARC working group's conclusion that crystalline silica is probably
carcinogenic in humans. Exhibit 2, "Silica, silicosis, and lung cancer: a response
to a recent working group report," JOEM, number 42, volume 7, July 2000,
704-720. The thrust of the article is that the data that the IARC relied on does not
sufficiently account for "confounding factors" such as smoking and other potential
industrial carcinogens. While the IARC felt those "confounding factors" were
sufficiently accounted for, the group writing this article did not.
The article concludes by noting that the data demonstrate a lack of association between lung cancer and exposure to crystalline silica in human studies; that silica is not directly genotoxic, and has been shown to be a pulmonary carcinogen only in rats (which is felt not to be a good species for comparison); and "the complex differences between blue collar workers exposed to silica and the general population." The study "was facilitated by a grant ... from the Silica Association."
c. Responses.
Finally, the record includes responses by the medical experts to each other.
Dr. Rosenman begins by noting that three bodies have concluded that silica
causes lung cancer: the IARC, NIOSH, and the American Thoracic Society. He
noted that the JOEM article was written by paid consultants of the industry rather
than a government group; and that the IARC concluded that the vast majority of
studies on registered silicotics reported excess lung cancer risks; and that the
IARC, at least, did not think its studies were confounded. He also described
Dr. Levy's conclusion that silica exposure does not cause COPD as outdated, citing
the Hertzberg, Rosenman article set out above. Exhibit G.
Dr. Levy, for his part, characterizes Dr. Rosenman's characterization of the JOEM article as an "ad hominem" attack. He notes that the consensus at a medical convention audience in Texas was silica has been convincingly demonstrated not to be a carcinogen. Dr. Levy goes on to criticize the Hertzberg, Rosenman article on COPD, as improperly based on company medical screening, noting: "anyone with a modicum of experience in this field knows that company screening testing and pulmonary function data obtained without quality control are notoriously unreliable." Respondent's exhibit 17.
3. Discussion.
The commission must decide whether silica exposure during employment was a material contributory causative factor in the onset or progression of the applicant's disabling COPD and lung cancer. In cases of occupational disease, work exposure does not have to cause the onset of the condition, but only constitute a material contributory factor in its progression. Universal Foundry Co. v. ILHR Department, 82 Wis. 2d 479, 487-88, note 3 (1978).
The commission, like the ALJ, is persuaded that the applicant's work exposure caused his permanent total disability. The commission's review of the medical record establishes that Dr. Rosenman relies on the conclusions of several agencies or organizations (NIOSH, IARC, and the American Thoracic Society) -- as well as articles in Lancet and the New England Journal of Medicine -- that have stated that silica exposure in employment is a carcinogen and causally linked to lung cancer and COPD, at least in workers who, like the applicant here, have silicosis. In rebuttal, Drs. Levy and Clay have established that some experts do not share that view. However, Dr. Levy, at least, largely relies on a report from an industry-sponsored study that indicates the question of whether silica is carcinogen has not been resolved one way or another, and the evidence of audience response at a medical convention in Texas suggesting silica is not a carcinogen. The commission finds the support for Dr. Rosenman's opinion more persuasive.
cc:
Attorney Steven Hitzeman
Attorney Joseph J. Ferris
Appealed to Circuit Court. Affirmed January 13, 2004.
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(1)( Back ) This is the Silica, silicosis, and lung cancer: a response to a recent working group report," JOEM, number 42, volume 7, July 2000, 704-720 article at exhibit 2, discussed below.
uploaded 2003/06/13