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Lindhag v. State10/7/2005
s not asthma, but it may suggest that it's not due to an allergic basis." While Lindhag's eosinophil testing suggested that her symptoms may have lacked an allergic basis, Lindhag's intradermal allergy testing with Dr. Scott revealed an allergic reaction to dust mites. This testing, along with other factors, led Dr. Scott to conclude that Lindhag's sinusitis was likely caused by common household allergens, including dust mites, and that her asthma existed prior to her exposures with DNR. Thus, we cannot conclude that the board erred in favoring Dr. Scott's allergy testing over the inconclusive eosinophil test results.
With respect to antibody testing, Lindhag points to preliminary testing which showed positive IgG antibodies to Trimellitic Anhydride (TMA), an industrial chemical found in items such as carpet adhesive that can possibly cause respiratory disease and asthma. However, Dr. Scott and one of her specialists, Dr. Fireman, opined that the presence of IgG antibodies indicated exposure to TMA, but not necessarily any adverse reaction to it. According to their opinion, the relevant antibody to determine hyper-sensitization, or adverse reaction, is IgE - and the preliminary tests showed that Lindhag's IgE levels were normal. In addition, the testimony suggested that the completed antibody testing was inadequate - Dr. Scott described it as not being clinically interpretable. Dr. Scott went on to testify that more testing along these lines would not have changed her opinion, and that there was no clinical justification to perform more testing. In Dr. Scott's words, "All the IgE antibody testing, if, in fact, it was confirmed, would indicate that at some time she had been exposed to it." In any case, Lindhag's physicians had requested more conclusive testing, but it remained uncompleted because the serum specimen was no longer available. Lindhag bears the burden of proving her claim, and the lack of more conclusive antibody evidence is her own failure of proof. The board did not err in following Dr. Scott's opinions.
Third and finally, Lindhag points to the evidence obtained after the hearing that allegedly disproved the board's finding that a dust mite allergy may have contributed to her symptoms. Whatever the merits of this "newly discovered evidence," it plays no role in the question of whether the board's decision was supported by substantial evidence. The board cannot be expected to deliberate on evidence that was not presented at the hearing. For these reasons, we affirm the board's denial of benefits for nonencephalopathic conditions.
B. The Board Did Not Abuse Its Discretion in Denying Lindhag's Petition for Modification
Lindhag also contends that the board abused its discretion in denying her petition for rehearing and modification. Alaska Statute 23.30.130(a) permits the board to rehear and modify a compensation case " pon its own initiative, or upon the application of any party . . . on the ground of a change in conditions . . . or because of a mistake in its determination of a fact." The board exercises its discretion in deciding whether to grant a rehearing. Lindhag alleges both a mistake in fact and a change in conditions based upon new medical information. We disagree.
The board agreed with Dr. Scott that a dust mite allergy could be a contributing factor for her sinusitis and rhinitis conditions. As mentioned above, Dr. Scott's intradermal allergy testing of Lindhag indicated an allergic reaction to dust mites (D pteronyssinus), which led Dr. Scott to conclude that dust mites were "likely . . . the primary contributing factor to her sinus inflammation and rhinitis." Because Dr. Scott deemed the sinusitis and rhinitis to be chronic and pre
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