EEG sensitization during chemical exposure in women with and without chemical sensitivity of unknown etiology
- 1 April 1999
- journal article
- Published by SAGE Publications in Toxicology and Industrial Health
- Vol. 15 (3-4), 305-312
- https://doi.org/10.1177/074823379901500304
Abstract
This study tested the sensitization model proposed by Bell et al. [Bell I.R., Miller C.S. and Schwartz G.E. An olfactory-limbic model of multiple chemical sensitivity syndrome: possible relationship to kindling and affective spectrum disorders. Biol. Psychiatry 1992:32:218-242] to study chemical sensitivity. The sensitization model indicates that a pharmacological stimulus or a traumatic event which elicits a strong response can sensitize limbic and/or mesolimbic pathways; and subsequent less intense trauma or stimuli, in the same or different modality, can elicit an amplified response. Three groups of subjects were tested: (1) women who reported chemical sensitivity and no sexual abuse (chemically sensitive, CS); (2) sexually abused (SA) women without chemical sensitivity; and (3) healthy women without chemical sensitivity or sensitivity or sexual abuse history (normal, N). All subjects were exposed to odorant and nonodorous control stimuli once a week for 3 weeks. Electroencephalographic activity was recorded while subjects sniffed the odorant and control stimuli. Results of the study revealed that both the CS and the SA group showed electroencephalogram (EEG) α sensitization across experimental sessions, while the N group showed little change over time. Additionally, EEG findings revealed that the CS group generated significantly greater α activity than the other two groups. Finally, while the groups were different on measures of psychological distress, these differences did not diminish the EEG findings. In summary, these findings suggest that intermittent exposure to chemicals elicits sensitization in CS and SA women without chemical sensitivity, supporting our expectations that chemical sensitivity is, in part, a manifestation of time-dependent sensitization (TDS). Additionally, these EEG findings indicate that CS women are unlike SA and healthy women in the amount of EEG α activity they generate. Finally, these findings indicate that psychological factors as assessed in this study do not explain electrophysiological differences between chemically and non-chemically-sensitive women.Keywords
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