Bell I R, Baldwin C M, Fernandez M, Schwartz G E
Department of Psychiatry, University of Arizona, Tucson 85723, USA.
Toxicol Ind Health. 1999 Apr-Jun;15(3-4):295-304. doi: 10.1177/074823379901500303.
This paper summarizes theory and evidence for a neural sensitization model of hyperresponsivity to low-level chemical exposures in multiple chemical sensitivity (MCS). MCS is a chronic polysymptomatic condition in which patients report illness from low levels of many different, structurally unrelated environmental chemicals (chemical intolerance, CI). Neural sensitization is the progressive host amplification of a response over time from repeated, intermittent exposures to a stimulus. Drugs, chemicals, endogenous mediators, and exogenous stressors can all initiate sensitization and can exhibit cross-sensitization between different classes of stimuli. The properties of sensitization overlap much of the clinical phenomenology of MCS. Animal studies have demonstrated sensitization to toluene, formaldehyde, and certain pesticides, as well as cross-sensitization, e.g., formaldehyde and cocaine. Controlled human studies in persons with self-reported CI have shown heightened sensitizability in the laboratory to nonspecific experimental factors and to specific chemical exposures. Useful outcome measures include spectral electroencephalography, blood pressure, heart rate, and plasma beta-endorphin. Findings implicate, in part, dopaminergic mesolimbic pathways and limbic structures. A convergence of evidence suggests that persons with MCS or with low-level CI may share some characteristics with individuals genetically vulnerable to substance abuse: (a) elevated family histories of alcohol or drug problems; (b) heightened capacity for sensitization of autonomic variables in the laboratory; (c) increased amounts of electroencephalographic alpha activity at rest and under challenge conditions over time. Sensitization is compatible with other models for MCS as well. The neural sensitization model provides a direction for further systematic human and animal research on the physiological bases of MCS and CI.
本文总结了多重化学物质敏感症（MCS）中对低水平化学暴露反应过度的神经致敏模型的理论和证据。MCS是一种慢性多症状疾病，患者报告在接触许多不同的、结构无关的环境化学物质（化学不耐受，CI）的低水平时会发病。神经致敏是指随着时间的推移，宿主对重复、间歇性刺激的反应逐渐增强。药物、化学物质、内源性介质和外源性应激源都可以引发致敏，并可在不同类型的刺激之间表现出交叉致敏。致敏的特性与MCS的许多临床现象学重叠。动物研究已证明对甲苯、甲醛和某些农药存在致敏现象，以及交叉致敏，例如甲醛和可卡因。对自我报告有CI的人群进行的对照人体研究表明，在实验室中，他们对非特异性实验因素和特定化学暴露的敏感性增强。有用的结果测量指标包括频谱脑电图、血压、心率和血浆β-内啡肽。研究结果部分涉及多巴胺能中脑边缘通路和边缘结构。一系列证据表明，患有MCS或低水平CI的人与在遗传上易患药物滥用的个体可能有一些共同特征：（a）酒精或药物问题的家族史增加；（b）实验室中自主变量致敏能力增强；（c）随着时间的推移，静息和应激条件下脑电图α活动量增加。致敏也与MCS的其他模型相符。神经致敏模型为进一步系统地开展关于MCS和CI生理基础的人体和动物研究提供了方向。
