{"id":{"repo_id":"arizona-thes","oai_identifier":"oai:repository.arizona.edu:10150/282608"},"canonical_url":"https://search.dev.ndltd.org/etd/arizona-thes/oai:repository.arizona.edu:10150/282608","repository":{"repo_id":"arizona-thes","name":"University of Arizona","base_url":"https://repository.arizona.edu/oai/request"},"display":{"title":"EEG measures of subjects with idiopathic chemical sensitivity: A test of the sensitization model","abstract":"This study tested the sensitization model proposed by Bell, Miller & Schwartz (1992) to study multiple chemical sensitivity (MCS). The sensitization models indicates that a traumatic event which elicits a strong response can sensitize limbic and/or mesolimbic pathways and future 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; (2) sexually abused women without chemical sensitivity; and (3) healthy woman without chemical sensitivity nor sexual abuse history. All subjects were exposed to odorant and nonodorant control stimuli once a week for three weeks. Electroencephalographic (EEG) activity was recorded while subjects sniffed the odorant and control stimuli. Based on the sensitization model, it was hypothesized that subjects who reported chemical sensitivity as well as subjects who reported a history of sexual abuse would show increases in the amplitude spectrum in the alpha frequency band across experimental sessions during exposure to odorant stimuli. Additionally, it was hypothesized that the healthy control subjects would show little or no changes over time. As predicted, the chemically sensitive and the sexually abused groups showed sensitization across experimental sessions. Additionally, the healthy control subjects showed habituation across experimental sessions. These findings indicate that individuals with chemical sensitivity show evidence of sensitization and that sensitization is not specific to MCS.","abstract_html":"This study tested the sensitization model proposed by Bell, Miller &amp; Schwartz (1992) to study multiple chemical sensitivity (MCS). The sensitization models indicates that a traumatic event which elicits a strong response can sensitize limbic and/or mesolimbic pathways and future 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; (2) sexually abused women without chemical sensitivity; and (3) healthy woman without chemical sensitivity nor sexual abuse history. All subjects were exposed to odorant and nonodorant control stimuli once a week for three weeks. Electroencephalographic (EEG) activity was recorded while subjects sniffed the odorant and control stimuli. Based on the sensitization model, it was hypothesized that subjects who reported chemical sensitivity as well as subjects who reported a history of sexual abuse would show increases in the amplitude spectrum in the alpha frequency band across experimental sessions during exposure to odorant stimuli. Additionally, it was hypothesized that the healthy control subjects would show little or no changes over time. As predicted, the chemically sensitive and the sexually abused groups showed sensitization across experimental sessions. Additionally, the healthy control subjects showed habituation across experimental sessions. These findings indicate that individuals with chemical sensitivity show evidence of sensitization and that sensitization is not specific to MCS.","abstract_has_math":false,"creators":["Fernandez, Mercedes, 1963-"],"institution":"The University of Arizona.","degree_name":"Ph.D.","degree_level":"doctoral","degree_discipline":"Graduate College","degree_department":null,"school":null,"contributors":[],"advisors":["Schwartz, Gary E."],"committee_chairs":[],"committee_members":[],"year":1998,"date_issued":"1998","date_published":"1998","updated_at":"2026-07-24T00:56:34Z","subjects":["Health Sciences, Pathology.","Psychology, Physiological."],"languages":["en_US"],"rights":["Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10150/282608","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Schwartz, Gary E."]},{"key":"dc:creator","label":"Author","values":["Fernandez, Mercedes, 1963-"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2013-04-18T09:54:30Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2013-04-18T09:54:30Z"]},{"key":"dc:date.issued","label":"Date","values":["1998"]},{"key":"dc:publisher","label":"Institution","values":["The University of Arizona."]},{"key":"dc:type","label":"Dc Type","values":["text","Dissertation-Reproduction (electronic)"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Graduate College","Psychology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Arizona"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Health Sciences, Pathology.","Psychology, Physiological."]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_US"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10150/282608"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["This study tested the sensitization model proposed by Bell, Miller & Schwartz (1992) to study multiple chemical sensitivity (MCS). The sensitization models indicates that a traumatic event which elicits a strong response can sensitize limbic and/or mesolimbic pathways and future 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; (2) sexually abused women without chemical sensitivity; and (3) healthy woman without chemical sensitivity nor sexual abuse history. All subjects were exposed to odorant and nonodorant control stimuli once a week for three weeks. Electroencephalographic (EEG) activity was recorded while subjects sniffed the odorant and control stimuli. Based on the sensitization model, it was hypothesized that subjects who reported chemical sensitivity as well as subjects who reported a history of sexual abuse would show increases in the amplitude spectrum in the alpha frequency band across experimental sessions during exposure to odorant stimuli. Additionally, it was hypothesized that the healthy control subjects would show little or no changes over time. As predicted, the chemically sensitive and the sexually abused groups showed sensitization across experimental sessions. Additionally, the healthy control subjects showed habituation across experimental sessions. These findings indicate that individuals with chemical sensitivity show evidence of sensitization and that sensitization is not specific to MCS."]},{"key":"dc:title","label":"Title","values":["EEG measures of subjects with idiopathic chemical sensitivity: A test of the sensitization model"]}]}],"canonical_facts":{"dc:contributor.advisor":["Schwartz, Gary E."],"dc:creator":["Fernandez, Mercedes, 1963-"],"dc:date.accessioned":["2013-04-18T09:54:30Z"],"dc:date.available":["2013-04-18T09:54:30Z"],"dc:date.issued":["1998"],"dc:description.abstract":["This study tested the sensitization model proposed by Bell, Miller & Schwartz (1992) to study multiple chemical sensitivity (MCS). The sensitization models indicates that a traumatic event which elicits a strong response can sensitize limbic and/or mesolimbic pathways and future 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; (2) sexually abused women without chemical sensitivity; and (3) healthy woman without chemical sensitivity nor sexual abuse history. All subjects were exposed to odorant and nonodorant control stimuli once a week for three weeks. Electroencephalographic (EEG) activity was recorded while subjects sniffed the odorant and control stimuli. Based on the sensitization model, it was hypothesized that subjects who reported chemical sensitivity as well as subjects who reported a history of sexual abuse would show increases in the amplitude spectrum in the alpha frequency band across experimental sessions during exposure to odorant stimuli. Additionally, it was hypothesized that the healthy control subjects would show little or no changes over time. As predicted, the chemically sensitive and the sexually abused groups showed sensitization across experimental sessions. Additionally, the healthy control subjects showed habituation across experimental sessions. These findings indicate that individuals with chemical sensitivity show evidence of sensitization and that sensitization is not specific to MCS."],"dc:identifier.uri":["http://hdl.handle.net/10150/282608"],"dc:language.iso":["en_US"],"dc:publisher":["The University of Arizona."],"dc:rights":["Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. 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