Danish Research Centre for Chemical Sensitivities, Copenhagen University Hospital, Gentofte, Denmark.
Department of Biotechnology and Biomedicine, Technical University of Denmark, Lyngby, Denmark.
BMJ Open. 2017 Feb 22;7(2):e013879. doi: 10.1136/bmjopen-2016-013879.
To investigate the pathophysiological pathways leading to symptoms elicitation in multiple chemical sensitivity (MCS) by comparing gene expression in MCS participants and healthy controls before and after a chemical exposure optimised to cause symptoms among MCS participants.The first hypothesis was that unexposed and symptom-free MCS participants have similar gene expression patterns to controls and a second hypothesis that MCS participants can be separated from controls based on differential gene expression upon a controlled n-butanol exposure.
Participants were exposed to 3.7 ppm n-butanol while seated in a windowed exposure chamber for 60 min. A total of 26 genes involved in biochemical pathways found in the literature have been proposed to play a role in the pathogenesis of MCS and other functional somatic syndromes were selected. Expression levels were compared between MCS and controls before, within 15 min after being exposed to and 4 hours after the exposure.
Participants suffering from MCS and healthy controls were recruited through advertisement at public places and in a local newspaper.
36 participants who considered themselves sensitive were prescreened for eligibility. 18 sensitive persons fulfilling the criteria for MCS were enrolled together with 18 healthy controls.
17 genes showed sufficient transcriptional level for analysis. Group comparisons were conducted for each gene at the 3 times points and for the computed area under the curve (AUC) expression levels.
MCS participants and controls displayed similar gene expression levels both at baseline and after the exposure and the computed AUC values were likewise comparable between the 2 groups. The intragroup variation in expression levels among MCS participants was noticeably greater than the controls.
MCS participants and controls have similar gene expression levels at baseline and it was not possible to separate MCS participants from controls based on gene expression measured after the exposure.
通过比较对优化后的化学物质暴露后多发性化学敏感性（MCS）参与者和健康对照者的基因表达，研究导致 MCS 症状发生的病理生理途径。第一个假设是，未暴露且无症状的 MCS 参与者与对照者具有相似的基因表达模式，第二个假设是，基于受控的正丁醇暴露后差异基因表达，MCS 参与者可以与对照者区分开来。
参与者在装有窗户的暴露室内以坐姿暴露于 3.7ppm 的正丁醇中 60 分钟。选择了 26 个涉及文献中发现的生化途径的基因，这些基因被认为在 MCS 和其他功能性躯体综合征的发病机制中发挥作用。在暴露前、暴露后 15 分钟和暴露后 4 小时，将 MCS 和对照者之间的表达水平进行比较。
MCS 和健康对照者是通过在公共场所和当地报纸上发布广告招募的。
36 名被认为自己敏感的参与者接受了资格预审。18 名符合 MCS 标准的敏感者和 18 名健康对照者一起被纳入研究。
有 17 个基因的转录水平足以进行分析。对每个基因在 3 个时间点的组比较和计算的曲线下面积（AUC）表达水平进行了组比较。
MCS 参与者和对照者在基线时的基因表达水平相似，并且无法根据暴露后测量的基因表达将 MCS 参与者与对照者区分开来。
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