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WORKERS’ COMPENSATION — Expert Testimony — Firefighters — Occupational Disease A-84 September Term 2001; Supreme Court; opinion by Coleman, J.; decided February 11, 2003. On certification to the Appellate Division. [Sat below: Judges Braithwaite and Coburn in the Appellate Division.] DDS No. 39-1-2809 Petitioner Richard Lindquist was employed as a full-time paid fireman with the Jersey City Fire Department from July 1972 until January 1995. He testified that during the first 10 years, he responded to “30 to 60 large fires per year,” “small one-room” fires, car fires, and “dump” fires. When he began his job, each firefighter was given a self-contained breathing apparatus, “but it was just very new and people didn’t seem to use it until 1982.” Although he was exposed to “heavy smoke” for up to 45 minutes to an hour and a half during larger fires, he frequently did not use the apparatus. During smaller outdoor fires, he said he tried to stay upwind but that sometimes he was completely engulfed in smoke. Some of the fires involved burning chemicals, plastics, household cleaners and propane. In 1982, respondent distributed to all firefighters a Scott mask, which provided oxygen to the user. Petitioner testified that the Scott mask “did a pretty good job” of preventing fumes from entering the breathing passages. Nonetheless, he still inhaled smoke that seeped into the mask. He also frequently removed the mask to give orders to other firefighters and to clear moisture that accumulated therein. From 1986 to 1992, petitioner was assigned to supervise the Hazardous Materials Unit of the fire department. During that time, he responded to both residential and industrial fires that included burning plastics and chemicals. Prior to employment with respondent, petitioner had not experienced any problems with breathing or with his eyes, nose or throat. He testified that during his tenure with the fire department, he was taken to the hospital numerous times. On other occasions he was administered oxygen at the scene of a fire. He suffered from shortness of breath, heart palpitations and weakness. Petitioner retired in 1995 at the age of 47, due in part to an early buyout offer and in part to health considerations. At that time, he was less able to perform his responsibilities because his energy and normal breathing capacity gradually had diminished. He testified that he had developed a “post nasal drip which would result in phlegm and coughing” that was “pretty constant” during his employment years. Now, those symptoms occur “[m]aybe two to three times a week.” He also suffers from dry eyes and shortness of breath and is no longer able to play basketball with his son or take long walks with his wife. He is able to walk only one quarter to one half of a mile “before [he begins] breathing heavily.” He cannot perform yard work or house work, such as “building sheds,” without some difficulty. In 1995 or 1996, he began treatment with a bronchodilator one or two times per week, which relieves his symptoms “almost instantly.” Petitioner smoked approximately three-fourths of a pack of cigarettes per day for 22 years, stopping in 1992 or 1994. Dr. Bernard Eisenstein testified on petitioner’s behalf. He specializes in heart and lung medicine and is board-certified in internal medicine. He performed a complete examination of petitioner, a chest X-ray, and pulmonary function studies in January 1995. The physical examination was “essentially negative, except [for] some areas of expiratory wheezing in the thorax.” However, the chest X-ray was “abnormal, [and] revealed increased bronchovascular markings with large lung volume, which . . . is compatible with emphysema.” The results of the pulmonary function studies were “only a little abnormal.” Eisenstein concluded that petitioner suffered from “chronic obstructive pulmonary disease in the form of emphysema.” He attributed the condition primarily to occupational exposure as a firefighter to fire, smoke, hazardous waste, combustion and secondarily to cigarette smoking. However, he was unable to allocate an exact percentage to each cause. He concluded that, “based upon a reasonable degree of medical probability,” petitioner suffered “30 percent of partial total” permanent disability. He admitted that he could not cite any studies in which nonsmoking firefighters developed emphysema. Respondent presented the testimony of Dr. Douglas Hutt, who is board-certified in internal, pulmonary and critical-care medicine. Petitioner told Hutt about his smoking, that his brother and sister suffer from allergies, and that his grandfather had died from emphysema. Hutt performed a complete physical examination of petitioner, including a chest X-ray, which revealed that his lungs were over-inflated and “that the lung fields themselves are very, very big.” Pulmonary function tests showed that petitioner “had some mild airflow obstruction,” that he suffers from “air trapping,” and that his ability to transfer oxygen from the air to the bloodstream was moderately to severely reduced. Hutt concluded that petitioner suffers from emphysema caused by cigarette smoking. He said, “even though only [20%] of people that smoke cigarettes actually get emphysema, that number is [between 70 and 80%] higher if you have relatives that smoke cigarettes and get emphysema which is true in this patient’s family in his grandfather.” He concluded that petitioner suffered “approximately [30%] pulmonary impairment.” Hutt acknowledged that many studies show that firefighters suffer from air flow obstruction and chronic bronchitis; however, he stated that “many of these studies . . . did not account for cigarette smoking” and “[n]one of the studies that [he had] seen . . . demonstrated conclusively or in any way that firefighters are [at] a greater risk for developing emphysema.” In response to questions by the court, Hutt stated that “chemical exposures aren’t generally felt to cause emphysema.” He admitted, however, that he could not say “with 100% certainty . . . that some of the exposure that [petitioner] might have had on his job may [not] have in some small way contributed to the development of the lung disease.” The Judge of Compensation concluded that “petitioner’s occupation[al] disease is due in a material degree to the occupational exposures described” during the trial. The judge also determined that petitioner had suffered an “appreciable impairment of [his] ability to carry on the ordinary pursuits of his retirement lifestyle.” Petitioner was awarded a disability of 30 percent for emphysema. The Appellate Division reversed, concluding that “the evidence of the causal connection between petitioner’s employment and his emphysema is insufficient to sustain the award.” It concluded that Eisenstein’s testimony was “insufficient to show that petitioner’s work exposure exceeded the exposure caused by his smoking cigarettes.” It also observed that he relied “ solely on petitioner’s general characterizations of his work exposures over the years and not on any existing medical, epidemiological or scientific studies establishing causation.” Petitioner argues that the Appellate Division exceeded the scope of its appellate review and ignored testimony that provided an evidentiary basis to support medical causation. He also contends that N.J.S.A. 34:15-43.2 should be interpreted as creating a presumption that his pulmonary disease arose from his employment. By implication, he argues that if the presumption applies, his cigarette smoking and his grandfather’s death from emphysema did not rebut the presumption that his emphysema is causally related to his exposure as a firefighter. Finally, he contends that the higher standard adopted in Fiore v. Consolidated Freightways, 140 N.J. 452 (1995), with respect to dual causation should be limited to cardiovascular injuries and was applied improperly by the Appellate Division. Certain well-established general principles inform the issues here. When the Workers’ Compensation Act, 34:15-1 to 128, was enacted, it provided no coverage for occupational diseases. It was later amended to include nine enumerated occupational diseases. Eventually, it was amended to replace the specific occupational diseases with a definitional phrase, “compensable occupational disease.” The current definition of “compensable occupational diseases” is those diseases established by a preponderance of the credible evidence to have arisen “out of and in the course of employment, which are due in a material degree to causes and conditions which are or were characteristic of or peculiar to a particular trade, occupation, process or place of employment.” 34:15-31a. “Material degree” means “a degree [substantially] greater than de minimis.” Dwyer v. Ford Motor Co., 36 N.J. 487, 493-94 (1962). Another principle of general application is that the act “involved a historic trade-off whereby employees relinquished their rights to pursue common-law remedies in exchange for automatic entitlement to certain, but reduced, benefits whenever they suffered injuries by [compensable] accident.” Millison v. E.I. du Pont de Nemours & Co., 101 N.J. 161, 174 (1985). Consequently, when the Division of Workers’ Compensation and appellate courts are called on to decide whether a particular occupational disease is causally related to a particular employment, they should use the original bargain rationale for workers’ compensation and ergonomics to assist with the determination. Still another well-established principle is “the social policy of liberally construing the Act,” which is social legislation designed “to implement the legislative policy of affording coverage to as many workers as possible.” Brower v. ICT Group, 164 N.J. 367, 373 (2000). The same doctrine is applicable whether the claim involves an accidental injury or an occupational disease, or whether the focus is on a well-established or a modern health condition. But the bargain and the occupational disease statutory history contemplate that what constitutes a compensable occupational disease will be affected by many social and industrial factors that vary across time. Nonetheless, the doctrine of liberal construction does not extend to “the evaluation of credibility, or of weight or sufficiency of evidence.” Oszmanski v. Bergen Point Brass Foundry, Inc., 95 N.J. Super. 92, 95 (App. Div. 1967), certif. denied, 51 N.J. 181 (1968). It is also well-established that a successful petitioner in workers’ compensation generally must prove both legal and medical causation when those issues are contested. Proof of medical causation means proof that the disability was actually caused by the work-related event. Proof of legal causation means proof that the injury is work connected. It is sufficient in New Jersey to prove that the exposure to a risk or danger in the workplace was in fact a contributing cause of the injury. That means proof that the work-related activities probably caused or contributed to the employee’s disabling injury as a matter of medical fact. Direct causation is not required; proof establishing that the exposure caused the activation, acceleration or exacerbation of disabling symptoms is sufficient. Another important principle is that the Rules of Evidence do not apply to workers’ compensation proceedings. N.J.S.A. 34:15-56 provides that when a Judge of Compensation decides a contested case, he “shall not be bound by the rules of evidence.” However, the judge’s determination must be based on competent evidence and there must be substantial credible evidence in the record to support the judgment when the proofs are considered as a whole. In workers’ compensation proceedings, as in toxic-tort litigation involving multiple causations or long-term exposure to toxic substances, it may not be possible scientifically for an injured person to prove decisively the medical cause of the injury. Faced with the need to accommodate the goals of the tort system when the scientific community was in disagreement, Rubanick v. Witco Chemical Corp., 125 N.J. 421 (1991), adopted a less restrictive standard for the admissibility of scientific evidence. That same standard is to be used in weighing the credibility of opinion evidence presented by experts. Given that the only significant distinctions between Rubanick and this case are the forum and the quantum of damages recoverable, the Rubanick standard governing the admissibility and reliability of medical causation evidence should be applied in workers’ compensation cases as well. Rubanick dealt with occupational exposure to PCBs during the course of the plaintiff’s employment with the defendant. Because “scientific knowledge [was] not ‘at a state of the art such that an expert’s testimony could be sufficiently reliable,’” Rubanick “fashion[ed] a broader standard for assessing the reliability of such evidence in [toxic-tort] litigation.” Id. at 432-33. It held, id. at 449, that: “in toxic-tort litigation, a scientific theory of causation that has not yet reached general acceptance may be found to be sufficiently reliable if it is based on a sound, adequately-founded scientific methodology involving data and information of the type reasonably relied on by experts in the scientific field. The evidence of such scientific knowledge must be proffered by an expert who is sufficiently qualified by education, knowledge, training, and experience in the specific field of science. The expert must possess a demonstrated professional capability to assess the scientific significance of underlying data and information, to apply the scientific methodology, and to explain the bases for the opinion reached.” Finally, as to the appropriate standard of appellate review of determinations made in workers’ compensation cases, review is limited to “whether the findings made could reasonably have been reached on sufficient credible evidence present in the record, considering the proofs as a whole, with due regard to the opportunity of the one who heard the witnesses to judge of their credibility.” Close v. Kordulak Bros., 44 N.J. 589, 599 (1965). Deference must be accorded the factual findings and legal determinations made by the Judge of Compensation unless they are “manifestly unsupported by or inconsistent with competent relevant and reasonably credible evidence as to offend the interests of justice.” Perez v. Monmouth Cable Vision, 278 N.J. Super. 275, 282 (App. Div. 1994). The petitioner has the burden to demonstrate by a preponderance of the evidence that his environmental exposure while fighting fires was a substantial contributing cause of his occupational disease. He is not required to “prove that the nexus between the disease and the place of employment is certain.” Magaw v. Middletown Bd. of Educ., 323 N.J. Super. 1, 11 (App. Div.), certif. denied, 162 N.J. 485 (1999). Petitioner was correct that the discussion in Fiore regarding dual causes of cardiovascular injuries requiring a petitioner to prove that his work exposure exceeded the exposure caused by personal factors such as cigarette smoking does not apply to nonheart cases such as this pulmonary case. Fiore acknowledged that it was articulating a “standard to apply in a dual-causation case involving an occupational disease that allegedly has caused coronary-artery disease and an angina attack.” 140 N.J. at 464. A higher standard was adopted for occupational heart cases because 34:15-7.2 was enacted to increase a petitioner’s burden beyond that previously required by Dwyer v. Ford Motor Co., 36 N.J. 487 (1962). Under Dwyer, there was an “assumption that employers take their employees as they find them” and that “ordinary work effort or strain” was sufficient to satisfy the material-degree contribution requirement. Because Fiore does not apply to pulmonary cases, the Appellate Division should not have applied its holding here. The controlling test to be applied here is whether the work exposure substantially contributed to the development or aggravation of emphysema. Petitioner had the burden to demonstrate by a preponderance of the evidence that his environmental exposure while fighting fires was a substantial contributing cause or aggravation of his emphysema. To satisfy that obligation, he was not required to prove that his work exposure exceeded the exposure caused by smoking cigarettes. Nor was he required to “prove that the nexus between the disease and the place of employment is certain” because that would violate the preponderance-of-the-evidence standard. In a case such as this one in which petitioner concedes that his personal risk factor played a significant role in developing emphysema, the Legislature has provided some relief to employers. When there are dual causes of an injury or disease, such as cigarette smoking and employment exposure, 34:15-12(d) requires a credit to “be given [to] the employer or the employer’s insurance carrier for the previous loss of function and the burden of proof in such matter shall rest on the employer.” Ibid. N.J.S.A. 34:15-43.2 creates a presumption that any impairment of the respiratory system of a volunteer firefighter is an occupational disease if the disease first manifests while the firefighter is active and if he had undergone a medical examination on entering the volunteer service that did not disclose the presence of such disease and if the disease first manifests within 90 days of the event medically determined to be the cause thereof. There is no legislative history indicating the Legislature’s intent when enacting the statute. Members of volunteer fire companies were already, at the time, covered by workers’ compensation laws. Paid firefighters as public employees were also covered by the act. Because there is no plausible reason the Legislature would have intended a difference when voluntary and paid firefighters sustained the same pulmonary conditions after fighting the same fire together, it is held that the presumption applies to paid firefighters as well. Further support for this conclusion is the fact that in 1987, the Legislature enacted a rebuttable presumption that cardiovascular and cerebrovascular injury or death to paid and volunteer firefighters sustained while performing fire suppression or medical emergency functions are compensable. 34:15-7.3. The record does not fully disclose whether the statutory preconditions for the presumption have been met here. Assuming, however, that the presumption applies, the existence of such a rebuttable presumption is not dispositive. To rebut the presumption, respondent presented evidence that petitioner smoked and had a family history of emphysema. Because the determination of whether respondent rebutted the presumption is intertwined with whether petitioner sustained his burden of proof on causation, both issues are resolved in petitioner’s favor, infra. Other jurisdictions have addressed the issue of statutory presumptions in favor of the firefighter in one form or another. Thirty states have adopted a presumption that a firefighter’s pulmonary disease or condition is work related, generally following more than five years of such employment. At least one state has been motivated by statistical studies indicating that firefighters are much more likely to suffer from heart and lung diseases due to exposure to smoke and gases under strenuous conditions. Other legislatures have reached the same result without reference to studies, stating that firefighters are “required to work in the midst of and are subject to heavy smoke fumes, and carcinogenic, poisonous, toxic or chemical gases from fires.” 40 Ill. Comp. Stat. Ann. 5/4-110.1. That so many states have created various forms of presumptions of compensability for specified occupational conditions suggests “(1) that a generalized causative link exists between the injury or disease and the workplace and (2) that such a causative link will be difficult to prove.” Solomon, “Fulfilling The Bargain: How the Science of Ergonomics Can Inform the Laws of Workers’ Compensation,” 101 Colum. L. Rev. 1140, at 1174 n.105 (2001). Because so many state legislatures have enacted various presumptions respecting the connection between firefighting and pulmonary and heart conditions, almost “a national consensus emerges regarding” the reliability of that proposition. Hamilton Amusement Ctr. v. Verniero, 156 N.J. 254, 270 (1998). Next considered is whether petitioner’s emphysema is medically related to his work exposure. Emphysema is a “[c]hronic obstructive pulmonary disease (COPD), also called chronic obstructive lung disease[. It] is a term that is used for two closely related diseases of the respiratory system: chronic bronchitis and emphysema.” Div. of Lung Diseases & Office of Prevention, Educ. & Control, Nat’l Insts. of Health, Pub. No. 95-2020, Chronic Obstructive Pulmonary Disease 1 (3d prtg. 1995) (Nat’l Insts. of Health). “In emphysema there is permanent destruction of the alveoli, the tiny elastic air sacs of the lung, because of irreversible destruction of a protein in the lung called elastin that is important for maintaining the strength of the alveolar walls . . . . Emphysema usually develops in older individuals with a long smoking history. However, there is also a form of emphysema that runs in families. People with familial emphysema have a hereditary deficiency of a blood component, alpha-1-protease inhibitor, also called alpha-1-antitrypsin (AAT). If individuals with a severe genetic deficiency of alpha-1-protease inhibitor smoke, they usually have symptoms of COPD by the time they reach early middle age. Some scientists believe that nonfamilial emphysema . . . also results from an imbalance between elastin-degrading enzymes and their inhibitors . . . thought to be a result of the effects of smoking . . . .” Id. at 2-4. Although “[c]igarette smoking is the most important risk factor for COPD . . . [o]ther risk factors include age, heredity, exposure to air pollution at work and in the environment . . . .” Id. at 1. Thus, the National Institutes of Health has recognized that exposure to air pollutants at work can cause both chronic bronchitis and emphysema. Further, “[s]cientists believe that, in addition to smoke-related processes, there must be other factors that cause emphysema in the general population since only 15 to 20 percent of smokers develop emphysema.” Id. at 4. Not only is it well known that industrial pollutants at work can cause or contribute to the development of emphysema, courts in New Jersey have awarded workers’ compensation for emphysema since the current general definition of occupational diseases became effective. Although none of those cases involved firefighters, there are good reasons to infer that many of the workers in those cases were smokers. The point is that some smokers have been awarded workers’ compensation in New Jersey for emphysema based on their occupational exposure. Here, both experts were found to be qualified to render expert opinions under N.J.R.E. 702 by virtue of their knowledge, skill, experience, training or education. Eisenstein’s opinion of causal relationship to employment was based on his many years of experience in examining firefighters, knowledge of pulmonary diseases and special training. He based his opinion of medical causation on the detailed facts concerning the exposure that involved hazardous dump fires, medical history, the X-ray and pulmonary testing, and his own experience in the field and his training. He could point to no study done on firefighters who are nonsmokers and who had emphysema. Hutt testified that although he has read many unspecified studies on lung diseases that included firefighters, none dealt with firefighting and emphysema. He was unaware of any studies linking emphysema to any smoke except cigarette smoke. Hutt admitted that he was aware of “many studies which show that firefighters have worse airflow obstruction and chronic bronchitis . . . [and] may be at somewhat higher risk.” He concluded that, absent any studies that show that firefighters’ “exposure on the job can develop emphysema,” and since petitioner smoked and his grandfather had died of emphysema, petitioner’s emphysema is related to smoking. When, as here, studies of firefighters and other groups have been used to assist experts with the medical causation issue within the Rubanick context, consideration of some or all of those studies would be useful to a reviewing court. Although the studies Hutt said he used were never identified and have not been made part of the record, the Court’s independent research has uncovered many studies. Judicial notice is taken of those studies. They are not nearly as one-sided as was suggested by Hutt. A mortality survey of firefighters in urban Alberta between 1927 and 1987 showed no link between firefighting and chronic pulmonary disease. However, there are other studies to the contrary. The “healthy worker effect,” whereby sick workers leave employment and are not included in studies, complicates most studies of disease in firefighters. To reduce that effect, two studies were performed comparing mortality in firefighters and police officers. Because the socioeconomic background, smoking habits, and health requirements of these groups are similar, any increase in lung disease among firefighters is likely to have been caused by their employment. Both groups of researchers found such an increase. Those studies comparing populations of healthy workers, similar in all relevant respects except fire smoke exposure, present the strongest scientific support for the proposition that firefighting is a significant cause of lung disease. Additional studies support that conclusion. To circumvent some of the limitations surrounding the studies of Alberta firemen, a group of Boston firefighters was studied in 1976 for six weeks as they performed fire suppression functions. The study revealed that although none “of the firefighters [sought] medical attention for smoke inhalation, [there were] acute changes in pulmonary function . . . in more than 30% of fire attendances.” A.W. Musk et al., “Pulmonary Function in Firefighters: Acute Changes in Ventilatory Capacity and Their Correlates,” 36 British J. Indus. Med. 29, 32 (1979). “This study shows that, as a result of his occupation, the respiratory system of the firefighter is subject to frequent episodes of acute irritation . . . [that] may produce cumulative damage manifested by an excessive yearly decline in FEV 1.0 [forced expiratory volume in one second].” Id. at 29, 33. A follow-up study to the Boston study concluded that the previous finding that occupational smoke exposure apparently caused a reduction in ventilatory capacity of firefighters “can no longer be seen.” A.W. Musk et al., “Pulmonary Function in Firefighters: A Six-Year Follow-up in the Boston Fire Department,” 3 Am. J. Indus. Med. 3, 8 (1982). That conclusion, however, was contradicted four years later based on a study of firefighters in the San Francisco Fire Department. That study concluded that routine firefighting is associated with a high incidence of acute decrements in lung function. The most recent study was conducted of New York City firefighters after the collapse of the World Trade Center on September 11, 2001. David J. Prezant, M.D., et al., “Cough and Bronchial Responsiveness In Firefighters at the World Trade Center Site,” 347 New Eng. J. Med. 806 (2002). It “evaluated clinical features . . . of 332 firefighters in whom severe cough developed after exposure [as well as] the prevalence and severity of bronchial hyperreactivity in firefighters without severe cough[, and] classified [them] according to the level of exposure.” Id. at 806. Of the firefighters with severe cough, only three percent were smokers, and 20 percent were ex-smokers. The study revealed that the majority of these firefighters had symptoms of dyspnea (shortness of breath usually associated with serious disease of the heart or lungs), gastroesophageal reflux disease and nasal congestion. Chest X-rays showed no changes in 96 percent of the firefighters studied. However, bronchial hyperactivity was found in a significant number of firefighters without severe cough who had high level to moderate level exposure. The study revealed that airway obstruction in the form of emphysema can occur in firefighters despite normal chest X-rays and virtually normal forced vital capacity and normal forced expiratory volume studies. “Because of the pernicious nature of occupational diseases, the Legislature has been solicitous of workers who suffer from these ailments.” Earl v. Johnson & Johnson, 158 N.J. 155, 166 (1999). Similarly, this Court should be solicitous of firefighters who have demonstrated a substantial likelihood that their fire suppression duties have contributed to the development of emphysema. Courts must not penalize workers suffering from diseases for which science has not yet clearly established causation. “There are areas in which [the] judicial need for certain facts equals or exceeds the scientific community’s ability to establish them. Many cases present issues with respect to which courts have been forced intuitively to make assumptions on the basis of available knowledge . . . .” Rubanick, 125 N.J. at 437. “When the possibility of causal connection is accepted, we cannot deny relief in all cases simply because science is unable decisively to dissipate the blur between possibility and probability.” Dwyer, 36 N.J. at 516. More than a possibility of causal connection exists here. Although the requirement that petitioner must prove his case by a preponderance of the evidence and that his evidence must be scientifically reliable is not relaxed, the evidence must be examined in light of science’s inability to provide conclusive answers to every question of causation. Science has not conclusively proved Eisenstein’s opinion that firefighting can be the primary cause of emphysema in a firefighter who smokes. However, “this [is] not a case where the absence of medical evidence leads to an inference that the proposed medical theory was completely improbable or outlandish.” Magaw v. Middletown Bd. of Educ., 323 N.J. Super. 1, 14 (App. Div.), certif. denied, 162 N.J. 485 (1999). Scientific data has verified what common sense suggests, that acute smoke exposure can damage the lungs. Some articles also have noted a correlation between firefighting and an increased risk of emphysema, but studies simply have not been performed that would conclusively establish causation, perhaps because of the difficulty in designing such a long-term, multivariable study. Additionally, some data indicates that it is unusual for someone of petitioner’s age and smoking history to contract emphysema. More significantly, based on the Judge of Compensation’s finding that petitioner smoked three-fourths of a pack per day for 22 years, his pack-year history was only 16.5 years. That level of past smoking is far below that expected in an emphysema patient. This strongly suggests that some other factors were materially responsible for causing petitioner’s emphysema, although other literature indicates that emphysema can develop more quickly. Hutt suggested that petitioner’s family history could account for his emphysema, and studies do indicate that “familial factors” can increase the risk. However, alpha-1-antitrypsin deficiency causes only about 1 percent of COPD cases. That deficiency is detectible by a blood test that apparently was not performed on petitioner. Therefore the extent to which petitioner’s family history contributed to his emphysema is unknown. Held: Given the current level of scientific knowledge about emphysema, Eisenstein’s testimony was “not a subjective guess or mere possibility.” Sufficient credible evidence exists to support the decision granting petitioner disability benefits. That conclusion is compelled by the principles that the act represents social legislation and is to be interpreted to expand rather than limit coverage, under the social compromise theory it is intended that a petitioner’s burden of proof be lighter than in a common-law tort action, and the studies reveal that although smoking is the most significant risk factor, some other causal factors must exist. Both experts testified that industrial exposure can cause emphysema and that the signs and symptoms have the same manifestation regardless of whether they are caused by cigarette smoking, industrial exposure or a combination of exposures. It is not necessary for petitioner to prove that firefighting was the most significant cause of his disease. He need only show that his employment exposure contributed in a material degree to the development of his emphysema. There is sufficient scientific evidence to support the Judge of Compensation’s conclusion that petitioner sustained his burden of proof. The presumption in favor of compensability has not been rebutted. The judgment of the Appellate Division is reversed. The judgment of the Division of Workers’ Compensation is reinstated. Chief Justice Poritz and Justices Long, Verniero, LaVecchia, Zazzali, and Albin join in Justice Coleman‘s opinion. — Digested by Judith Nallin [The slip opinion is 58 pages long.] For appellant — Thomas W. Polaski (Gary P. Sarlo). For respondent — John H. Geaney (Capehart & Scatchard).

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