No abstract

The lack of a generally accepted case definition for multiple chemical sensitivity (MCS) and the absence of a standardized approach for measuring salient aspects of chemical sensitivity that would permit cross-comparison of findings by different investigators have hindered progress in this area. Based upon findings from an earlier study of 112 persons with self-reported chemical sensitivity who attributed their chemical sensitivity to a well-defined exposure event, we developed an instrument with self-rating scales to assess Symptom Severity, Chemical (Inhalant) Intolerances, Other Intolerances (e.g., foods, medications, alcohol), Life Impact, and Masking (a measure of ongoing chemical exposures). When administered to four patient groups and controls, the scales showed good reliability and validity overall (n = 421) and in each group. Used together, the scales provided sensitivity of 92% and specificity of 95% in differentiating chemically sensitive persons from controls. Our results support use of these scales individually or collectively for a variety of applications including the selection of chemically sensitive subjects and controls for research, assessment of chemical sensitivity in various study populations, cross-comparison of groups studied by different investigators, pre- and post-assessment of therapeutic interventions, clinical evaluation of complex patients who report intolerances, and teaching medical residents and students how to evaluate patients for chemical sensitivity and MCS.

One hundred twelve individuals who reported onset of multiple chemical sensitivity following well-documented exposure to either (1) a cholinesterase-inhibiting organophosphate or carbamate pesticide or (2) remodeling of a building completed mail-out/mail-back questionnaires concerning their exposure, symptoms, sensitivity to ingestants and inhalants, utilization of health-care resources, and impact of their illness on lifestyle. It was hypothesized that if multiple chemical sensitivity resulted from neurotoxic exposure, then organophosphate-exposed respondents should report greater severity of illness resulting from the relatively greater neurotoxicity of this class of chemicals. Pesticide-exposed and remodeling-exposed multiple chemical sensitivity groups reported similar patterns of symptoms and identified similar inhalants and ingestants as triggers for their symptoms; these results suggested a common mechanism (biological and/or psychological) for their conditions. The pesticide-exposed group, however, reported significantly greater symptom severity than did the remodeling-exposed group, especially for neuromuscular, affective, airway, gastrointestinal, and cardiac symptoms. These findings provide evidence for (1) a possible biological basis for multiple chemical sensitivity and (2) a distinct pathophysiology or final common pathway for the condition that, while as yet undefined, appears to be shared by these two groups. Although subjective multisystem health complaints characterize both multiple chemical sensitivity and somatoform disorder, features of this multiple chemical sensitivity sample were inconsistent with somatoform disorder, i.e., onset after 30 y of age in 83%, the predominance of severe cognitive symptoms, and attributions of environmental causation. No group differences were found with respect to lifestyle impact. Eighty-one percent of respondents said they had been working full-time at the time they were exposed, yet at the time of the survey (on average, 7.7 y post exposure) only 12.5% were working full-time. The majority said they had quit their jobs, changed jobs, or changed careers because of their illness. Approximately 40% reported that they had consulted 10 or more medical practitioners. The persistent, disabling neuropsychological symptoms reported by these multiple chemical sensitivity groups are strikingly similar to those reported among individuals exposed occupationally to pesticides and solvents. These parallel findings suggest that the types and levels of exposures associated with extermination and remodeling may not be inconsequential, at least for a subset of the population. Further studies from a variety of perspectives, including human challenge studies and the development of animal models, are needed to define the pathophysiological and psychological mechanisms underlying this costly condition.

No abstract

445-453 (1997)