Chemical Sensitivity Attributed to Pesticide Exposure versus Remodeling

Abstract

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.

Identification of responsible volatile chemicals that induce hypersensitive reactions to multiple chemical sensitivity patients

“…The detailed information is shown in Table 4. These MCS symptoms were similar to those described in previous studies (Miller, 1994;Miller and Mitzel, 1995;Davidoff and Keyl, 1996). For some patients, the symptoms were induced when they stayed in closed rooms (A-1, A-5, C, E-1, E-2, I, J) and/or when they opened doors of closet or hovel (A-3, A-4, C, G, I).…”

“…Once a person acquires MCS, other chemicals as well as some specific chemicals that initiated MCS can trigger the hypersensitive symptoms even at low concentrations (Cullen, 1987). The hypersensitive reactions include memory difficulty, irritation of the respiratory tract, depression, headache, joint pain, muscle pain, fatigue, nausea, dizziness, and so on (Miller, 1994;Miller and Mitzel, 1995;Davidoff and Keyl, 1996).…”

A review of a two-phase population study of multiple chemical sensitivities.

“…This differentiation of symptom severity between subgroups led the authors to conclude that chemical sensitivity has specific physical dynamics inconsistent with somatoform disorders. The results of Mitzel and Miller (1995), therefore, suggest that chemical sensitivity has a physiologic genesis and is not psychogenic.…”

“…Psychogenic theories, however, have been criticized for methodologic weaknesses, such as biased patient selection and the lack of presymptom data (Davidoff and Fogarty 1994). Miller and Mitzel (1995) conducted an experiment that investigated the genesis and other aspects of chemical sensitivity. They divided questionnaires from 112 individuals who had previously reported a chemical sensitivity into two subgroups based on the origin of the condition.…”

The new tapestry of risk assessment

“…In 1995, a paper appeared in Archives of Environmental Health describing 75 people who said they became ill-again, with multi-system symptoms and new-onset intolerances-following remodeling of their home or workplace, and another 37 who said they became ill following an organophosphate or carbamate exposure (Miller and Mitzel 1995). Despite having different initial exposures-pesticides and remodeling volatile organic chemicals-both groups reported similar symptoms and intolerances for structurally unrelated substances.…”