Court Opinion

ID: 9583987
Source: CourtListenerOpinion
Date Created: 2023-08-21 22:43:35.271865+00
Date Added: 2024-06-11T15:06:21.582689
License: Public Domain

Justice EXUM
concurring in result.
I concur in the majority’s decision to remand this case to the Industrial Commission for further proceedings. Since I disagree with much of the majority’s reasoning, I deem it necessary to set out my own views of the case.
First, I disagree with the majority’s apparent notions that Hansel’s occupational disease is simply byssinosis and that she is limited on remand to showing only that her exposure to cotton dust medically aggravated her bronchitis or asthma in order to recover for whatever incapacity for work was caused by the combined effect of all of her pulmonary problems.
As I understand the medical testimony, Hansel actually suffers from chronic obstructive pulmonary, or lung, disease to which several etiological factors could have contributed, ie., cigarette smoking, bronchitis, asthma, and cotton dust exposure. Dr. Harris testified that Mrs. Hansel “has an illness. In general terms, I thought it fitted the pattern of chronic obstructive lung disease .... She has three distinct syndromes that probably contributes [sic] to that impairment. These are asthma, byssinosis, and chronic bronchitis.” Later Dr. Harris also identified cigarette smoking as a possible contributing factor.
*61In addition to this case, we have considered three other so-called “byssinosis” cases. Morrison v. Burlington Industries, 304 N.C. 1, 282 S.E. 2d 458 (1981); Walston v. Burlington Industries, (No. 116, Fall Term 1981); and Wood v. Stevens & Co., 297 N.C. 636, 256 S.E. 2d 692 (1979). The medical etiology of the disease was the primary focus of all the cases except Wood.
Although Morrison claimed benefits for “an occupational disease, to wit: byssinosis . . . caused by exposure to cotton dust,” the medical testimony, the Commission’s findings, and this Court identified her occupational disease as chronic obstructive lung disease. Morrison also suffered from bronchitis, was a cigarette smoker, and could have had emphysema. The Commission found ultimately, however, that her chronic obstructive lung disease was caused at least in part by her cotton dust exposure, a finding which this Court concluded was supported by the evidence.
Walston also claimed benefits for “byssinosis . . . caused by exposure to cotton dust.” The medical testimony again, however, referred to the cause of Walston’s incapacity for work as “pulmonary disease” and “pulmonary problems.” The medical testimony identified the components of his pulmonary disease as “chronic bronchitis, pulmonary emphysema, [and] possible byssinosis.” Dr. Mabe testified, “It is correct as a matter of terminology, to regard the term ‘chronic obstructive lung disease’ as broader in its complications than, say, fibrosis, which can be a localized situation, or emphysema, which can only be general. Chronic obstructive lung disease is the broadest of these terms. It will take them all in. That encompasses all of them in the chronic bronchitis or segmental pulmonary fibrosis.”
It is clear from the medical testimony in Morrison, Walston and this case, and from medical literature on the subject1 that the term “byssinosis” refers simply to the effect, if any, of a worker’s *62exposure to cotton dust on the worker’s overall pulmonary function. The disease, however, which ultimately causes a worker to be incapacitated for work is consistently referred to by the medical witnesses in these cases as chronic obstructive lung disease.2 This disease in its ultimate disabling form may have several components such as bronchitis, asthma, emphysema, and byssinosis. It may, in turn, be caused by one or more environmental factors such as cotton dust exposure or cigarette smoking, or both. The crucial difference between byssinosis, or the effect of cotton dust exposure on the lungs, and other conditions caused by industrial exposures, such as silicosis and asbestosis, is this: The effects of cotton dust exposure (byssinosis) are indistinguishable from the effects of other kinds of lung problems such as bronchitis, or the effects of cigarette smoking; whereas the effects of silicosis and asbestosis are identifiable by biopsy or an autopsy.3
*63Hansel’s claim, therefore, like those of Morrison and Walston, is for the incapacitating effects, if any, of her chronic obstructive lung disease. In this case, therefore, as others in which the worker claims benefits for incapacity to work caused by chronic obstructive pulmonary disease, the central factual inquiry should be first, whether the effects on the pulmonary function caused by cotton dust exposure (byssinosis) significantly contributed to the ultimate medical problem, ie., chronic obstructive lung disease and second, whether and to what extent the chronic obstructive lung disease caused incapacity for work.
I further disagree with the majority’s position that questions three and four can be answered by medical witnesses, for these questions are really conclusions of law to be made by the Commission after it determines certain preliminary factual questions. Whether a particular disease is an occupational disease is ultimately a question of law, for it requires the application of the legal standards set out in G.S. 97-53(13) to the facts. In an occupational disease claim, “[h]aving made appropriate findings of fact, the next question the Commission must answer is whether . . . the illness plaintiff has contracted falls within the definition set out in the statute. This latter judgment requires a conclusion of law.” Wood v. Stevens & Co., supra, 297 N.C. at 640, 256 S.E. 2d at 695-96.
For a disease to be occupational and therefore compensable under G.S. 97-53(13) “two conditions must be met: (1) It must be ‘proven to be due to causes and conditions which are characteristic of and peculiar to a particular trade, occupation or employment’; and (2) It cannot be an ‘ordinary disease of life to which the general public is equally exposed outside of the employment.’ ” Booker v. Medical Center, 297 N.C. 458, 468, 256 S.E. 2d 189, 196 (1979). If there is a greater risk of contracting the disease by workers in a given occupation because of conditions “characteristic of and peculiar” to the occupation, the “nexus between the disease and the employment which” makes the disease occupational and therefore compensable is provided and the sec*64ond condition set out above is satisfied. Id. at 475, 256 S.E. 2d at 200.4 The statute thus insures by its terms that a disease, in order to be compensable, must have the requisite causal connection to the occupation out of which it allegedly arose.
As the majority correctly notes, however, it is not necessary that the occupational “causes and conditions” be the sole cause of the disease. It is enough if these occupational “causes and conditions” are factors which significantly contribute to the development of the disease.5 If occupational “causes and conditions” as defined by G.S. 97-53(13) significantly contribute to a disease’s development, and if the disease itself is not one to which the general public is exposed equally with those engaged in the employment in question, the disease is an occupational disease even though non-occupational causes and conditions also contribute to it. Conversely, a disease is not an occupational disease if the occupational causes and conditions do not contribute to its development in a significant way.
Whether the contribution of occupational “causes and conditions” has been significant or insignificant must largely be determined by evidence relating to the extent and nature of the exposure to the occupational conditions and expert medical opinion relating to the significance of this exposure in light of other factors which may also have contributed to the disease’s development. Significant means, “having or likely to have influence or effect: deserving to be considered: IMPOBTANT, WEIGHTY, NOTABLE.” Webster’s Third New International Dictionary 2116 (Merriam-Webster 1971). “Significant” as we are using it is to be *65contrasted with “negligible,” “unimportant,” “present but not worthy of note,” “miniscule,” “of little moment.” The word has reference not so much to the quantity, in terms of percentage of contribution made by occupational exposure, but more to the quality of its contribution. The factual inquiry, in other words, should be whether the occupational exposure was such a significant factor in the disease’s development that without it the disease would either (1) not have developed or (2) not have developed to such an extent that it results in the incapacity for work for which the worker claims benefits.
To say that occupational causes and conditions must be the sole cause of a disease before it can be considered occupational and therefore compensable is too harsh a principle from the standpoint of the purposes and policies of our Workers’ Compensation Act. This Act “should be liberally construed so that the benefits under the Act will not be denied by narrow, technical or strict interpretation.” Stevenson v. City of Durham, 281 N.C. 300, 303, 188 S.E. 2d 281, 283 (1972).
To say on the other hand that if occupational causes and conditions contribute to the slightest extent, however miniscule or insignificant, to the etiology of a disease, the causation requirement is satisfied places too heavy a burden on industry and tends to compromise the valid principle that our Workers’ Compensation Act should not be transformed into a general accident and health insurance law.
Neither should a disease to which occupational conditions have significantly but not entirely contributed be considered as some kind of pro tanto occupational disease in which an award is made not for the incapacity for work actually caused by the disease but only for so much of such incapacity as corresponds mathematically to the extent of contribution of the occupational conditions. First, the cases in which the point has been considered do not support this view. They either support the significant contribution principle or some less rigorous principle from the worker’s standpoint.6 Second, G.S. 97-52 provides that “[disablement or death . . . resulting from an occupational disease de*66scribed in G.S. 97-53 shall be treated as the happening of an injury by accident within the meaning of the North Carolina Workers’ Compensation Act . . . . ” (Emphasis supplied.) General Statute 97-53(13) provides a generic definition of diseases which may be considered occupational. I believe our legislature intended that a disease either be an occupational disease or that it not be. If it is an occupational disease it is treated like an industrial accident. There is no suggestion in the statutes that a worker could have an occupational disease pro tanto, ie., only to the extent of the contribution of an occupational condition. Third, as I point out below, and as cases from other jurisdictions demonstrate,7 some of these diseases which have dual or multiple causes such as chronic obstructive lung disease, present difficult medical questions regarding the extent to which various causative factors respectively contributed. We ask too much of the medical profession if we require it to assess in terms of mathematical percentages the relative contributions of the various possible causes of such diseases.8 At most the physicians should be asked to determine only whether the occupational conditions, such as cotton *67dust exposure, were or were not in the particular case a significantly contributing factor in the disease’s etiology.
Thus in addressing this industrial disease claim I would require the Commission to consider and resolve several crucial factual issues. The first is whether the employee has a disease and, if so, what is it. “The Commission must determine first the nature of the disease from which the plaintiff is suffering — that is, its characteristics, symptoms and manifestations.” Wood v. Stevens & Co., supra, 297 N.C. at 640, 256 S.E. 2d at 695. Second, the Commission must determine whether any causes and conditions ‘characteristic of and peculiar to’ the occupation in question significantly contributed to, or were significant causative factors in, the disease’s development. Finally, the Commission must determine whether the disease is an ordinary disease of life to which the general public is exposed in the same degree as the worker in question or, in other words, whether the worker is, because of his occupation, exposed to a greater risk of contracting the disease than members of the public generally.
If all of these crucial factual issues are answered favorably to the worker, then the Commission must conclude as a matter of law that the worker has an occupational disease. If any one of them, however, is answered unfavorably to the worker, then the Commission must conclude as a matter of law that there is no occupational disease.
I recognize that we are dealing with a relatively new occupational disease statute which reasonably has been the source of some confusion regarding occupational disease law in this state. This confusion is compounded by the medical complexities involved in chronic lung disease cases. “The causes and development of byssinosis, and the structural and functional changes produced by the disease, are still the subject of scientific debate.” Wood v. Stevens & Co., supra, 297 N.C. at 641, 256 S.E. 2d at 696. A recent carefully controlled study cited in Wood concluded, however, that although the “pathology of the chronic lung disease of textile workers remains unclear,” textile workers, “not only . . . carders and spinners . . . but also . . . yarn preparers and weavers . . .” suffer from “an excess of chronic lung disease” and it “is almost *68certain” that this excess “is caused by dust exposure of the workers in the mills.”9
In view, therefore, of the legal and medical complexities involved, we should remand this matter to the Commission for the taking of further evidence and a new determination of whether Hansel has an occupational disease. I believe there is enough evidence already adduced to indicate that Hansel may be able to prove that her cotton dust exposure significantly contributed to her ultimate chronic obstructive lung disease and that it was this lung disease which ultimately caused her to be incapacitated for work, either partially or totally. I, however, would direct the Commission to proceed in accordance with the principles to which I have referred in this concurring opinion rather than those announced by the majority.
Justice CARLTON joins in this concurring opinion.

. See generally Bouhuys, Schoenberg, Beck and Schilling, Epidemiology of Chronic Lung Disease in a Cotton Mill Community, 5 Traumatic Medicine and Surgery for the Attorney 607, reprinted from Lung — An International Journal on Lungs, Airways, and Breathing, 154(3): 167-186 (1977). The article concludes with the following paragraph:
“There is continuing discussion about the definition of the term ‘byssinosis,’ and confusion about the presumed co-existence of chronic bronchitis and of *62byssinosis among textile workers. To a large extent this debate is one of semantics. Cotton and other textile workers are at risk of acute as well as chronic respiratory symptoms and lung function loss. There can be little doubt that both are caused by exposure to respirable dust in textile mills. The progression from repeated acute insults to the chronic disease has not been traced with certainty, but there is no good evidence against — and much evidence for —such a train of events. It seems most logical to define byssinosis as a dust-induced disease with initial acute responses followed by a stage of chronic lung disease characterized by chronic airway obstruction. This definition is implicit in the description of the clinical stages of byssinosis given by Schilling. For purposes of compensation and prevention, acute responses to textile dust as well as chronic airway obstruction in textile workers should be considered as two stages of one disease syndrome, byssinosis.”

. This is also the term used throughout the Bouhuys article to describe the disabling condition in its ultimate form. Id.

. In Walston, for example, Dr. Williams testified, “There is not specifically any objective finding to say that a man does or doesn’t have byssinosis . . . such as a biopsy or autopsy, such as with silicosis and asbestosis, although in the early stages one can demonstrate a reactivity to the dust by doing pulmonary function studies before and after six hours exposure to the work environment. But in the latter stages, such as one might see with chronic obstructive pulmonary disease, this is no longer valid and these are not specific diagnostic criteria.”
In Morrison, Dr. Sieker testified that there were “two identifiable etiological factors” which contributed to Morrison’s chronic obstructive lung disease. “One is cotton dust exposure, the other is her cigarette consumption.” He said, “[I]n a somewhat arbitrary way but with clinical judgment I assign the etiological factors about 50 percent — 50 to 60 percent for the cotton dust exposure and 40-50 percent for the cigarette smoking and any attendant problems with that. ... At the present time there is no laboratory type of test that would do this. This [assignment of *63etiological factors] had to be based on . . . one’s judgment of the effects of these agents on the respiratory system.”
In the present case Dr. Harris testified that the effects of byssinosis were “indistinguishable from chronic bronchitis.”

. The disease need not be one which originates exclusively from or is unique to the particular occupation in question. Booker v. Medical Center, supra. Nor is the fact that the disease is an ordinary disease of life to which members of the general public also succumb fatal to an occupational disease claim if the "greater risk” nexus is present; for in such cases the public is not exposed to the disease equally with those engaged in the particular employment in question. Id. Thus ordinary diseases of life such as serum hepatitis, tuberculosis and contact dermatitis may be occupational diseases provided that the employee because of his employment has a greater risk of contracting them than does the public generally. Id., and cases cited therein.

. For a full discussion of the significant contribution concept and the authorities upon which it is based see Morrison v. Burlington Industries, 304 N.C. 1, 282 S.E. 2d 458 (1981) (Exum, J., dissenting).

. These cases are collected in my dissent in Morrison v. Burlington Industries, supra.

. These cases are collected in my dissent in Morrison v. Burlington Industries, supra.

. Dr. Harris, for example, testified, “I do not have the ability to separate out any specific symptoms related to byssinosis that this lady has that cannot be explained by the other two conditions that are present.” In his medical report he stated, “It is not possible to quantitate the relative contribution of the various etiological factors in her present respiratory impairment. It is likely that all are involved to some extent.” In Walston v. Burlington Industries, supra, Dr. Williams was unable to testify regarding the relative contributions to Walston’s lung disease made, respectively, by his exposure to cotton dust and his cigarette smoking. He said, “I find it very difficult to answer the question as to . . . what percentage would the cotton dust exposure represent to the pulmonary condition. On the one hand, we have had the opportunity to treat hundreds of patients with this same type of syndrome and findings, in which case it is almost certain the primary etiological agent was cigarette smoking, and this fellow was a smoker. On the other hand, there are figures beginning to emerge to show that it is possible for workers exposed to cotton dust to develop chronic obstructive lung disease even in some instances in non-smokers even though the incident is definitely greater in smokers which accounts for the reason I said it might be a contributory factor, but this is about as close as I can come. I cannot give a percentage. I don’t have an opinion on a specific percentage.”
Although in Morrison, Dr. Sieker did testify to the relative contribution of cigarette smoking and cotton dust exposure in terms of percentages, he conceded that this assessment was made “in a somewhat arbitrary way but with clinical judgment . . . there is no laboratory . . . test that would do this . . . .”

. Bouhuys, Schoenberg, Beck and Schilling, op. cit., supra n. 1. See also IB Larson, supra, § 41.64(b), n. 83.1.