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Costa v. Torrington Company

CASE NO. 4097 CRB-05-99-08

COMPENSATION REVIEW BOARD

WORKERS’ COMPENSATION COMMISSION

JULY 28, 2000

GUIDO COSTA

CLAIMANT-APPELLEE

v.

TORRINGTON COMPANY

EMPLOYER

and

CIGNA

INSURER

RESPONDENTS-APPELLANTS

APPEARANCES:

The claimant was represented by Angelo Paul Sevarino, Esq., 110 Day Hill Road, Windsor, CT 06095-1794.

The respondents were represented by Margaret McGrail, Esq., Pomeranz, Drayton & Stabnick, 95 Glastonbury Boulevard, Glastonbury, CT 06033.

This Petition for Review from the July 26, 1999 Finding and Award of the Commissioner acting for the Fifth District was heard April 14, 2000 before a Compensation Review Board panel consisting of Commissioners Robin L. Wilson, Leonard S. Paoletta and Amado J. Vargas.

OPINION

ROBIN L. WILSON, COMMISSIONER. The respondents1 have petitioned for review from the July 26, 1999 Finding and Award of the Commissioner acting for the Fifth District. They contend on appeal that the medical evidence in this case is insufficient to support the trier’s finding that the claimant’s cirrhotic liver injury was a compensable occupational disease caused by workplace chemical exposure. We disagree with that contention, and affirm the decision of the trial commissioner.

The claimant was employed by the respondent Torrington Company from April 14, 1962 to September 27, 1995. He currently suffers from cirrhosis of the liver, which condition began manifesting itself via esophageal bleeding in 1994. The etiology of that disease was the primary issue facing the trial commissioner. This required two questions to be answered: the level of chemical exposure to which the claimant was subjected, and the probable medical consequences of such exposure.

The claimant attested that, while he was working as a tumbler in the early 1960’s, he was frequently in contact with the chemicals trichloroethylene2 and trichloroethane3, which he would siphon into five-gallon containers from a 55-gallon drum while wearing little or no protective clothing. He also attested that between 1965 and 1980, he worked as a setter in the press room. There, a mixture of chloroethane4 and oil was used as a coolant for the press machines, causing a mist to permeate the air, and continuously exposing the claimant to the machines’ spray, which left a residue on his clothes. He also used the chemicals to wash his hands during work. Joseph Harris, who served as foreman in the press room from 1976 through 1980, agreed that the claimant had been exposed to chloroethane, which he used as a cleanser several times during each work shift.

Once the claimant transferred to the machine shop, he ceased to be directly exposed to chloroethane. The shop foreman, Emilio Zordan, explained that a solvent made from soap and water had replaced chloroethane as the preferred cleanser for both cost and safety reasons. Another longtime employee of the respondent, Angelo Franculli, testified that he had personally used trichloroethane and trichloroethylene degreasers on a regular basis, and that throughout the plant these chemicals had been used extensively and loosely. Eventually, through his union activities and his position on a health and safety committee, Franculli became aware that these substances presented health risks, and his committee began negotiating with the respondent to begin labeling the containers of chemicals that were being used so casually by employees. John Healy, a senior project engineer for the employer, testified that the company switched from trichloroethylene to chloroethane5 in the early 1970’s, and then discontinued the use of chloroethane sometime between 1989 and 1991, when it began using a water soluble product. According to Healy, the change was made for environmental reasons, although the suspected health risks posed by chlorinated solvents were probably an additional factor in the company’s decision to phase out the use of such compounds.

The present claimant had suffered no serious health problems prior to developing cirrhosis of the liver. He had never smoked, had tempered his use of alcohol to an occasional glass of wine, and had no family members with liver-related problems. Dr. Israel, a Hartford gastroenterologist, diagnosed the claimant with cryptogenic cirrhosis. Because the claimant possesses none of the risk factors normally associated with the onset of cirrhosis, Dr. Israel opined that his exposure to chemicals was very likely the cause of his liver disease. The doctor testified that both trichloroethane and trichloroethylene can have a chronic, damaging effect on the liver.

Dr. VanLinda, who is also a gastroenterologist, agreed that the claimant was suffering from cirrhosis of the liver. However, he did not think that his condition could be attributed to any specific cause within a reasonable degree of medical probability. Cirrhosis of the liver develops when a long-term insult to the liver results in necrosis of that organ’s cells. None of the data examined by Dr. VanLinda indicated that exposure to trichloroethylene or trichloroethane caused cirrhosis in male patients. Although acute liver injuries could be caused by exposure to those chemicals, there was no proof that such exposure could lead to cirrhosis. Dr. Israel’s diagnosis differed because he was of the opinion that the claimant had suffered numerous acute liver insults from the chemical exposure, which produced fibrosis each time the liver healed. Over time, the fibrosis accumulated to the point where it resulted in cirrhosis.

The trial commissioner accepted Dr. Israel’s opinion, which he found extremely persuasive. He was less impressed by Dr. VanLinda’s unwillingness to find a causal connection between the claimant’s chemical exposure and his cirrhotic liver condition due to the lack of written literature specifically documenting such a link. In the trier’s view, the doctor seemed to demand a level of almost absolute certainty, which exceeds the evidentiary burden needed to establish compensability. Therefore, he concluded that the claimant’s liver condition was compensable, and ordered the respondents to pay all resulting benefits and medical expenses. The respondents have appealed that decision.

Procedurally, we must first address a motion filed by the claimant that concerns the respondents’ Reasons of Appeal. The respondent-appellants filed their initial Reasons for Appeal on August 13, 1999, listing only one issue: “Whether the Commissioner erred in finding that the claimant sustained a compensable cirrhotic liver injury.” On September 9, 1999, the respondents filed Amended Reasons for Appeal, listing three additional grounds for review, including “Whether the Commissioner erred in denying the Motion to Correct dated August 12, 1999.” The trier had denied that motion on August 16, 1999. In response to the Amended Reasons for Appeal, the claimant moved to dismiss the issue concerning the denial of the Motion to Correct, stating that it was untimely and prejudicial. He contends that the appeal from the denial of the Motion to Correct should have been filed within ten days of the date that motion was denied pursuant to § 31-301(a) C.G.S. and Admin. Reg. § 31-301-1, and that this board now lacks jurisdiction to consider the denial of said motion as part of this appeal.

We do not agree that the respondents’ failure to immediately appeal the denial of the Motion to Correct carries with it the jurisdictional consequences alleged by the claimant, simply because the appellants filed their initial Reasons for Appeal prior to the trial commissioner’s denial of the corrections. Although the language of § 31-301(a) states that an appeal from a decision of the commissioner upon a motion may be made by filing a petition for review within ten days of the date notice of the decision is sent, this board has never required parties to file a separate petition for review from the denial of a Motion to Correct where a timely appeal was filed from the underlying award. Mendoza v. Raposo, 15 Conn. Workers’ Comp. Rev. Op. 155, 157, 2172 CRB-7-94-10 (Jan. 26, 1996). Unlike many other types of motions, under Admin. Reg. § 31-301-4 a Motion to Correct may only be filed in proximity to the entry of an award, and its contents are nothing more than a proposed revision or extension of the original decision. Because of its auxiliary nature, it makes little sense procedurally to require a party to file a separate appeal from this motion, which is usually ruled upon shortly after the original award.

Moreover, Admin. Reg. § 31-301-6 states that the reasons of appeal may assign, in addition to other errors, “that the commissioner erred in refusing to grant a motion to correct the finding or in refusing to find the facts as contained in the motion.” The language of Admin. Reg. § 31-301-7 also contemplates that the denial of a motion to correct may be “made a ground of appeal,” rather than requiring a separate appeal from that ruling. Considering that a party’s initial reasons for appeal are due within ten days of the filing of the petition for review under § 31-301-2, and that a Motion to Correct need not even be filed until two weeks after the filing of the petition for review under § 31-301-4, it would seem that § 31-301-6 and § 31-301-7 contemplate the amendment of the reasons for appeal to incorporate the subsequent denial of a Motion to Correct. Mendoza, supra. In appeals from Superior Court decisions, Practice Book § 63-4(b) allows parties to file amendments to their preliminary statements of issues on appeal, absent undue prejudice to other parties. We perceive no reason to adopt a more restrictive rule in this forum, particularly in light of § 31-301(e), which states that appeals to this board shall be processed in accordance to Supreme Court appellate procedure, where applicable. We also decline to treat the respondents’ filing of a Motion for Extension of Time to file their Reasons for Appeal prior to August 13, 1999 as a waiver of their right to file further amendments to said Reasons. As their conduct here caused no discernible prejudice to the claimant, we deny his Motion to Dismiss.

Turning to the merits, the respondents have raised two related, but nonetheless distinct, points in their appellate brief. First, they contend that ¶ 52 of the Finding and Award misconstrued the testimony of Dr. Israel by glossing over the fact that there is a difference between a chronic exposure that causes an acute injury and a chronic exposure that causes a chronic injury, e.g., cirrhosis of the liver. Paragraph 52 states, “Dr. Israel testified that, after review of two material safety data sheets dated April 10, 1996 involving trichloroethane and trichloroethylene, both documents confirm that these chemicals can have a chronic, damaging effect on the liver.” The respondents contend that, in fact, the safety data sheets confirm only the possibility of acute liver injury, and that Dr. Israel’s opinion on causation was based solely on his own theory of genetic polymorphism (i.e., the capacity of the toxic effects of these chemicals to manifest themselves in different forms) and the potential of repeated acute injuries to cause chronic illness.

After review of the safety data sheets in Claimant’s Exhibits A and C, we do not agree that this information lends itself only to the interpretation urged by the respondents. Among the health risks cited in the toxicity information for trichloroethylene is “damage to liver and other organs from chronic exposure.” Exhibit A, supra. That description does not limit itself to acute liver injuries. Although the health risks listed under 1,1,1-trichloroethane in Exhibit A do not specifically mention liver injuries, they do warn of mutagenic data and gastrointestinal changes, among many possible effects. Exhibit C, meanwhile, does specify that the liver and kidneys are the target organs for irreversible harmful effects, irritation, etc. Dr. Israel specifically stated that in his medical opinion, the cause of the claimant’s cirrhosis was “one or both of the organic solvents that are in those sheets that you showed me and marked an exhibit.” Claimant’s Exhibit B, p. 28. This evidence is substantially consistent with the language of ¶ 52, and we do not believe that the trier erred by refusing to correct this paragraph of his award. Sendra v. Plainville Board of Education, 3961 CRB-6-99-1 (Jan. 20, 2000) (trier evaluates proposed corrections with same discretion that he evaluates credibility of evidence).

The second argument raised in the respondents’ brief is the related, but broader, contention that the medical opinion of Dr. Israel was based upon conjecture, and therefore incapable of providing sufficient proof of a causal connection between the claimant’s chemical exposure and his development of a cirrhotic liver. As the respondents note, the claimant had to introduce competent medical evidence that establishes with a reasonable degree of medical probability a causal tie between his liver condition and his workplace chemical exposure. Struckman v. Burns, 205 Conn. 542, 554-55 (1987); Murchison v. Skinner Precision Industries, Inc., 162 Conn. 142, 151 (1972). As long as the substance of an expert opinion is based upon a reasonable probability rather than mere speculation or conjecture, a trial commissioner may rely upon that diagnosis in his factual findings. Struckman, supra, 555; O’Reilly v. General Dynamics Corp., 52 Conn. App. 813, 817-18 (1999). The respondents contend that Dr. Israel’s diagnosis was in fact cryptogenic cirrhosis (cirrhosis of unknown origin), and that his remarks ascribing the cause of the claimant’s cirrhosis to chemical exposure were unsupported by proper research and were admittedly based on conjecture. See Respondents’ Brief, 10-11. We think that a more favorable interpretation of Dr. Israel’s opinion was readily available as well.

On page 20 of his deposition, Dr. Israel notes that a liver biopsy revealed the presence of macrovesicular fat, which is a symptom consistent with exposure to toxins. The only risk factor for liver disease that he found in the claimant’s history was exposure to trichloroethylene and trichloroethane. Regarding the difficulty of conclusively identifying a cause, he explained, “it’s a process of elimination. Historically there were no alternative candidates, and histopathologically it was most consistent with the toxic exposure.” Id., 23. Though he did not do an “extensive literature search,” Dr. Israel did consult a textbook regarding the pathology of the chemicals in question. Id., 24. He stated that, together with the safety data sheets in Claimant’s Exhibit C, this information confirmed that those chemicals could have a chronic detrimental effect on the liver.

Further, when asked to compare his own opinion with that of Dr. VanLinda, Dr. Israel agreed that one could not demonstrate the cause of the claimant’s cirrhosis with one hundred percent certitude based on the data in the available literature. He thought, however, that “it’s more likely than not a result of exposure to one or both of those organic solvents.” Id., 26-27. When reminded that he could not speculate on this matter, and that he was required to testify within a reasonable degree of medical probability, Dr. Israel reaffirmed his position: “In my medical opinion, the cause of his cirrhosis [is] one or both of those [] organic solvents.” Id., 28. Later, he was challenged by the respondents’ counsel based on the lack of reported cirrhotic liver cases stemming from exposure to the two chemicals identified in the claimant’s workplace. Dr. Israel explained that “this statement ignores the fact that there are reported cases of these chemicals damaging the liver. Cirrhosis is accumulative damage to the liver. So if you have acute damage to the liver, the liver heals, you get fibrosis. . . . You do that enough, and you have got cirrhosis.” Id., 37. In that respect, he compared the claimant’s chemical exposure to the situation of an alcoholic, who continuously subjects his liver to small amounts of acute damage until cirrhosis has set in.

This explanation may have an element of hypothesis in it, but the respondents have hardly demonstrated that the methodology underlying the doctor’s theory was based on an invalid scientific method, or that the opinion was otherwise insufficient to be admitted as competent evidence. See Cabral v. Metropolitan District Employees, 3770 CRB-1-98-2 (May 13, 1999). The doctor’s recitation of the phrase, “my guess is there is some type of genetic polymorphism” does not transform the core of his entire opinion into a primarily speculative notion. Deposition, supra, p. 38. Dr. Israel clearly states his belief that his diagnosis is reasonably medically probable, his thought process is plainly visible from his deposition, and his explanation does not appear to be patently irrational. The trial commissioner unequivocally accepted that explanation over the testimony of Dr. VanLinda. It is well-settled that this board is obligated on review to defer to the trial commissioner’s determinations of evidentiary credibility as long as there is evidence in the record to support his findings. O’Reilly, supra, 818; Fair v. People’s Savings Bank, 207 Conn. 535, 539 (1988). Such evidence exists here. Accordingly, we cannot tamper with the trier’s assessment of the credibility of that evidence on appeal. Funaioli v. New London, 3814 CRB-2-98-5 (June 16, 1999).

The trial commissioner’s decision is hereby affirmed.

Commissioners Leonard S. Paoletta and Amado J. Vargas concur.

1 The trial commissioner noted in his Finding and Award that, during the claimant’s rather lengthy period of employment, there were several different insurers who provided workers’ compensation coverage for the respondent Torrington Company. In response to the claimant’s allegation that he contracted an occupational disease, Forms 43 were filed by the Continental Assurance Company and Kemper Insurance, as well as the respondent Cigna Property and Casualty. Subsequently, the insurers agreed that Cigna and its legal counsel would represent the interests of all of the insurers during these proceedings. BACK TO TEXT

2 Trichloroethylene, or CHClCCl2, is defined by Webster’s Third International Dictionary and the Second College Edition of the American Heritage Dictionary as a heavy, colorless, toxic, nonflammable liquid that is chiefly used to degrease metals, as an extraction solvent for oils and waxes, as an inhalation analgesic or anesthetic, and as a detergent or pesticide. BACK TO TEXT

3 Trichloroethane is defined by Webster’s Third International Dictionary as either of two nonflammable irritating liquid isomeric compounds C2H3Cl3, whose molecular structures vary slightly from each other. One is known as 1,1,1-trichloroethane and is used as the parent compound of DDT and other insecticides, while the other is known as 1,1,2-trichloroethane and is chiefly used as a solvent. BACK TO TEXT

4 Chloroethane, also known as ethyl chloride or C2H5Cl, is defined by Webster’s Third International Dictionary and the Second College Edition of the American Heritage Dictionary as a colorless, pungent compound that is a gas at ordinary temperatures and a flammable, volatile liquid when compressed, used as a solvent, a refrigerant, and a local surface anesthetic. But see note 5, infra. BACK TO TEXT

5 Healy testified that the chemical that the Torrington Company began using in the early 1970’s was called Chlorothene, a trademark for a solvent manufactured by The Dow Chemical Company. See September 3, 1998 Transcript, p. 33. Any references to chloroethane in the record may very well refer to this product rather than the generic substance known as chloroethane, or ethyl chloride, that we defined in note 4, supra. The Material Safety Data Sheets in Claimant’s Exhibit A describe the characteristics of the Dow Chemical solvent in detail; apparently, two versions of the product were used, one of which consisted of 95.1% 1,1,1-trichloroethane, and the other of 96.5% 1,1,1-trichloroethane. BACK TO TEXT

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