Mast cell activation may explain many cases of chemical intolerance
Abstract Background This paper explores the relationship between chemical intolerance (CI) and mast cell activation syndrome (MCAS). Worldwide observations provide evidence for a two-stage disease process called toxicant-induced loss of tolerance (TI...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Springer Berlin Heidelberg
2021
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| Online Access: | https://hdl.handle.net/1721.1/138176 |
| _version_ | 1811091877836881920 |
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| author | Miller, Claudia S. Palmer, Raymond F. Dempsey, Tania T. Ashford, Nicholas A. Afrin, Lawrence B. |
| author_facet | Miller, Claudia S. Palmer, Raymond F. Dempsey, Tania T. Ashford, Nicholas A. Afrin, Lawrence B. |
| author_sort | Miller, Claudia S. |
| collection | MIT |
| description | Abstract
Background
This paper explores the relationship between chemical intolerance (CI) and mast cell activation syndrome (MCAS). Worldwide observations provide evidence for a two-stage disease process called toxicant-induced loss of tolerance (TILT) as a mechanism for CI. TILT is initiated by a major exposure event or a series of lower-level exposures. Subsequently, affected individuals report that common chemical inhalants, foods, and drugs (i.e., various xenobiotics) trigger multi-system symptoms.
Purpose
To determine whether MCAS provides a plausible biological mechanism for CI/TILT.
Methods
Using the validated Quick Environmental Exposure and Sensitivity Inventory (QEESI), we compared patients diagnosed with MCAS (n = 147) to individuals who reported chemical intolerances (CI/TILT) following various exposures (n = 345) and to healthy controls (n = 76). Using ANOVA, we compared QEESI scores across groups. Clinical scores for the MCAS patient group were used to predict CI status using logistic regression.
Results
More than half (59%) of the MCAS group met criteria for CI. A logistic regression model illustrates that as the likelihood of patients having MCAS increased, their likelihood of having CI/TILT similarly increased, to a near-perfect correspondence at the high ends of the QEESI and clinical MCAS scores. Symptom and intolerance patterns were nearly identical for the CI and MCAS groups.
Discussion
We present data suggesting that xenobiotic activation of mast cells may underlie CI/TILT. The strikingly similar symptom and intolerance patterns for MCAS and TILT suggest that xenobiotics disrupt mast cells, leading to either or both of these challenging conditions. Faced with patients suffering from complex illness affecting multiple organ systems and fluctuating inflammatory, allergic, and dystrophic symptoms, clinicians can now ask themselves two questions: (1) Could MCAS be at the root of these problems? (2) Could environmental exposures be driving MC activation and mediator release? Increasing our understanding of the connection between TILT and MCs has the potential to expose a new link between environmental exposures and illness, offering new opportunities for improving individual and public health.
Conclusion
The close correspondence between QEESI scores and symptom patterns for MCAS and TILT patients supports xenobiotic-driven mast cell activation and mediator release (i.e., MCAS) as a plausible unifying biological mechanism for CI/TILT, with profound implications for medicine, public health, and regulatory toxicology. |
| first_indexed | 2024-09-23T15:09:27Z |
| format | Article |
| id | mit-1721.1/138176 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T15:09:27Z |
| publishDate | 2021 |
| publisher | Springer Berlin Heidelberg |
| record_format | dspace |
| spelling | mit-1721.1/1381762021-11-23T03:07:05Z Mast cell activation may explain many cases of chemical intolerance Miller, Claudia S. Palmer, Raymond F. Dempsey, Tania T. Ashford, Nicholas A. Afrin, Lawrence B. Abstract Background This paper explores the relationship between chemical intolerance (CI) and mast cell activation syndrome (MCAS). Worldwide observations provide evidence for a two-stage disease process called toxicant-induced loss of tolerance (TILT) as a mechanism for CI. TILT is initiated by a major exposure event or a series of lower-level exposures. Subsequently, affected individuals report that common chemical inhalants, foods, and drugs (i.e., various xenobiotics) trigger multi-system symptoms. Purpose To determine whether MCAS provides a plausible biological mechanism for CI/TILT. Methods Using the validated Quick Environmental Exposure and Sensitivity Inventory (QEESI), we compared patients diagnosed with MCAS (n = 147) to individuals who reported chemical intolerances (CI/TILT) following various exposures (n = 345) and to healthy controls (n = 76). Using ANOVA, we compared QEESI scores across groups. Clinical scores for the MCAS patient group were used to predict CI status using logistic regression. Results More than half (59%) of the MCAS group met criteria for CI. A logistic regression model illustrates that as the likelihood of patients having MCAS increased, their likelihood of having CI/TILT similarly increased, to a near-perfect correspondence at the high ends of the QEESI and clinical MCAS scores. Symptom and intolerance patterns were nearly identical for the CI and MCAS groups. Discussion We present data suggesting that xenobiotic activation of mast cells may underlie CI/TILT. The strikingly similar symptom and intolerance patterns for MCAS and TILT suggest that xenobiotics disrupt mast cells, leading to either or both of these challenging conditions. Faced with patients suffering from complex illness affecting multiple organ systems and fluctuating inflammatory, allergic, and dystrophic symptoms, clinicians can now ask themselves two questions: (1) Could MCAS be at the root of these problems? (2) Could environmental exposures be driving MC activation and mediator release? Increasing our understanding of the connection between TILT and MCs has the potential to expose a new link between environmental exposures and illness, offering new opportunities for improving individual and public health. Conclusion The close correspondence between QEESI scores and symptom patterns for MCAS and TILT patients supports xenobiotic-driven mast cell activation and mediator release (i.e., MCAS) as a plausible unifying biological mechanism for CI/TILT, with profound implications for medicine, public health, and regulatory toxicology. 2021-11-22T13:40:37Z 2021-11-22T13:40:37Z 2021-11-17 2021-11-21T04:22:23Z Article http://purl.org/eprint/type/JournalArticle https://hdl.handle.net/1721.1/138176 Environmental Sciences Europe. 2021 Nov 17;33(1):129 PUBLISHER_CC en https://doi.org/10.1186/s12302-021-00570-3 Creative Commons Attribution https://creativecommons.org/licenses/by/4.0/ The Author(s) application/pdf Springer Berlin Heidelberg Springer Berlin Heidelberg |
| spellingShingle | Miller, Claudia S. Palmer, Raymond F. Dempsey, Tania T. Ashford, Nicholas A. Afrin, Lawrence B. Mast cell activation may explain many cases of chemical intolerance |
| title | Mast cell activation may explain many cases of chemical intolerance |
| title_full | Mast cell activation may explain many cases of chemical intolerance |
| title_fullStr | Mast cell activation may explain many cases of chemical intolerance |
| title_full_unstemmed | Mast cell activation may explain many cases of chemical intolerance |
| title_short | Mast cell activation may explain many cases of chemical intolerance |
| title_sort | mast cell activation may explain many cases of chemical intolerance |
| url | https://hdl.handle.net/1721.1/138176 |
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