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Review
. 2019 Oct 22;24(1):61.
doi: 10.1186/s12199-019-0816-6.

Chemical intolerance: involvement of brain function and networks after exposure to extrinsic stimuli perceived as hazardous

Kenichi Azuma  1   2 , Iwao Uchiyama  3   4 , Mari Tanigawa  4   5 , Ikuko Bamba  6 , Michiyo Azuma  7 , Hirohisa Takano  8 , Toshikazu Yoshikawa  3 , Kou Sakabe  9
Affiliations
Review

Chemical intolerance: involvement of brain function and networks after exposure to extrinsic stimuli perceived as hazardous

Kenichi Azuma et al. Environ Health Prev Med. .

Abstract

Background: Chemical intolerance (CI) is a chronic condition characterized by recurring and severe symptoms triggered by exposure to low levels of odorous or pungent substances. The etiology of CI has been a controversial subject for a long time. The aim of this review is to summarize findings on the neurological processing of sensory information during and after exposure to low levels of odorous or pungent substances in individuals with CI, focusing on the brain function and networks.

Methods: Scientific studies on CI published between 2000 and 2019 in academic peer-reviewed journals were systematically searched using medical and scientific literature databases. Only peer-reviewed articles reporting original research from experimental human studies directly associated with CI, and involving related neurological responses or brain imaging after exposure to odorous or pungent substances (i.e., in chemical provocation tests), were considered.

Results: Forty-seven studies were found to be eligible for a full-text review. Twenty-three studies met the selection criteria and were included in this review. Evidence indicated that differences between subjects with CI and healthy controls were observed by brain imaging during and after exposure to odorous or pungent substances. Differences in brain imaging were also observed between initial exposure and after exposure to these substances. Neurological processing of sensory information after exposure to extrinsic stimuli in the limbic system and related cortices were altered in subjects with CI. A previous documentable exposure event was likely to be involved in this alteration.

Conclusions: This review documents consistent evidence for the altered neurological processing of sensory information in individuals with CI. Further neurophysiological research exploring the processing of extrinsic stimuli and cognition of sensation through the limbic system and related cortices in CI, and the appearance of symptoms in individuals with CI, are required.

Keywords: Brain imaging; Chemical intolerance; Exposure event; Limbic system; Multiple chemical sensitivity; Odor processing; Prefrontal cortex; Psychosomatic symptoms; Sensory disruption; Susceptibility.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Mechanistic model of the interrelationships among external factors, susceptibility factors, and symptoms (reproduced from Kipen and Fiedler [63] published in Environmental Health Perspectives with permission from the authors)
Fig. 2
Fig. 2
Sensory and cognition model of the interrelationships among stimulus factors, limbic system, cortices, symptoms, and responses. Abbreviations: Amyg, amygdala; EMF, electromagnetic field; Ento, entorhinal cortex; Hipp, hippocampus; PC, piriform cortex; Thal, thalamus
See this image and copyright information in PMC

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MeSH terms

Substances

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