The world of MCS and CIRS research uses specialized terminology that can feel impenetrable. Every term on this page is defined in plain English — no medical background required. Terms are listed alphabetically. Use the letter links to navigate.
A US federal law that prohibits discrimination against people with disabilities in employment, public accommodations, transportation, and government services. The ADA names no conditions. A person whose MCS substantially limits a major life activity is covered, decided case by case, and their employer must then provide reasonable accommodation.
A small, almond-shaped structure in the brain’s limbic system that processes threat signals and regulates fear, anxiety, and emotional memory. Irritation signals from chemicals in the nose travel mainly along the trigeminal nerve, while smell travels through the olfactory bulb; both routes feed the amygdala, and the smell pathway reaches it with fewer relay stations than almost any other sense. In MCS, sensitized amygdala responses contribute to the anxiety, mood changes, and heightened threat detection that accompany chemical exposures.
Any substance — including environmental chemicals, proteins, or microorganisms — that the immune system recognizes and mounts a response to. In MCS, chemical antigens do not trigger the classical IgE-based allergic response; instead, they activate TRPV1/TRPA1 chemosensory pathways. This is why standard allergy tests are negative in MCS patients despite genuine physiological reactivity.
A tick-borne parasite that infects red blood cells, causing a malaria-like illness. Babesia is a common co-infection in patients with Lyme disease and is not detected by standard Lyme testing, which tests only for Borrelia burgdorferi. In MCS patients with multi-susceptible HLA genetics, Babesia biotoxins can drive the same inflammatory cascade as mold biotoxins, stalling CIRS recovery. Diagnosis requires specialty lab testing through facilities such as IGeneX.
A group of intracellular bacteria transmitted primarily by tick bites (and some other vectors) that causes a range of chronic symptoms including neurological effects, fatigue, skin manifestations, and immune dysregulation. Bartonella is the most commonly missed co-infection in Lyme disease patients because standard Lyme panels do not test for it. In patients with MCS and CIRS, Bartonella co-infection can perpetuate inflammatory burden and block recovery. Specialty testing through Galaxy Diagnostics or IGeneX is required for accurate detection.
In the CIRS model, the use of a bile-acid sequestrant (cholestyramine or colesevelam) intended to adsorb biotoxins in the gut and interrupt the proposed enterohepatic recirculation. A prescription treatment whose use, timing and dosing are the prescribing clinician’s; this site states no regimen. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
A measurable biological indicator of a disease state, physiological condition, or response to treatment. In CIRS, specific biomarkers — including TGF-β1, MMP-9, MSH, VIP, C4a, and VEGF — are used to confirm diagnosis, assess severity, and monitor treatment progress. The existence of measurable biomarkers is one of the distinguishing features of CIRS from purely subjective symptom conditions.
A toxin produced by a biological organism. In the context of MCS and CIRS, biotoxins most commonly refers to the mycotoxins produced by water-damaged-building molds (particularly Stachybotrys, Chaetomium, Aspergillus, and others), Lyme disease spirochetes, and other organisms. In genetically susceptible individuals, biotoxins are not cleared normally and recirculate in the body indefinitely, driving chronic inflammation.
A selective membrane that separates circulating blood from the brain and spinal cord, preventing most substances from passing into the central nervous system. The olfactory nerve pathway (nose to brain) bypasses this barrier, which is why inhaled chemicals can have direct neurological effects — particularly relevant to MCS, where VOC exposure produces measurable brain changes visible on imaging.
A validated three-question screener for chemical intolerance. Originally developed from the QEESI, the BREESI can identify patients who warrant full QEESI assessment in under two minutes. It has been validated in primary care settings and is designed to be practical for busy clinical environments. A positive BREESI result indicates that a full chemical intolerance assessment is warranted.
A split product of the complement protein C4. In the CIRS model it is one of the biomarkers the originating group reports as elevated in its patients and uses to track treatment. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
An objective diagnostic test for TRPV1 receptor sensitization. Measured doses of capsaicin — the compound in hot peppers that activates TRPV1 receptors — are inhaled, and the cough response threshold is measured. MCS patients consistently show significantly lower capsaicin thresholds (i.e., they cough at lower doses) than healthy controls. This test has been replicated in independent research groups in Sweden, Denmark, and the United States, and is considered one of the most reliable objective markers for MCS.
The name one research group gives to a multi-system inflammatory illness it attributes to biotoxin exposure — most often water-damaged buildings — in people carrying HLA-DR haplotypes it proposes prevent biotoxin clearance. Defined by that group’s biomarker set and treatment sequence; not validated in mainstream guidelines and not reproduced by independent investigators. This site states no population proportion for it. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page. What is independently established about damp buildings is on Mold, CIRS & chemical sensitivity.
A prescription bile-acid sequestrant, used in the CIRS model as the primary binder intended to interrupt the proposed recirculation of biotoxins through bile and gut. How it is taken relative to food, other medicines and time is the prescriber’s instruction, not this site’s. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
A family of liver enzymes responsible for metabolizing and detoxifying many drugs, chemicals, and environmental toxins. Genetic variants in CYP450 genes affect an individual’s capacity to process specific chemicals. Whether these variants raise the odds of chemical sensitivity is unsettled: the best-known MCS study linked the condition to a faster-acting CYP2D6 variant, not a slower one, and later studies did not consistently confirm it.
A structured neuroplasticity-based recovery program developed by Annie Hopper for conditions including MCS, CIRS, fibromyalgia, and chronic fatigue. DNRS uses structured daily practices to retrain limbic system pathways and reduce the chronic threat response that can amplify chemical sensitivity in some patients. It is not a psychological approach in the dismissive sense — it works with documented neuroplasticity mechanisms. However, DNRS and similar programs help a minority of MCS patients, not the majority. Because MCS has physiological causes, retraining thought and response patterns does not address the root cause for most people. It is most relevant for the subset where conditioned fear responses have become a significant secondary amplifier on top of the biological sensitization. Avoidance of exposures remains the foundation for almost all MCS patients regardless of whether limbic work is also pursued.
The physiological cycle by which substances processed by the liver are secreted into bile, delivered to the intestines, and then reabsorbed back into the bloodstream. Under normal circumstances, biotoxins are tagged by the immune system for clearance and excreted via this pathway. In CIRS patients, whose immune system never signals clearance of biotoxins, enterohepatic recirculation causes indefinite biotoxin recycling — the toxins circulate continuously rather than being eliminated. Binder therapy interrupts this cycle by chemically capturing the biotoxins in the intestine before they can be reabsorbed.
A DNA-based mold testing methodology developed by the US Environmental Protection Agency that measures the relative moldiness of a home or building by analyzing settled dust for the DNA of 36 mold species. ERMI scores provide one measure of relative mold burden, but score thresholds should be interpreted cautiously — no single cutoff reliably distinguishes problem buildings from acceptable ones across all settings, and NIOSH guidance notes that visual inspection and musty odor are often as informative as quantitative testing. ERMI is most useful as one data point in a broader building assessment, not as a standalone verdict. Used in CIRS assessment to evaluate whether the patient’s environment may be a source of ongoing biotoxin exposure.
A brain imaging technique that measures blood oxygen levels as a proxy for neural activity. Used in MCS research to document differences in brain activation patterns during chemical exposures. fMRI studies have identified altered activity in the prefrontal cortex, anterior cingulate cortex, and limbic regions in MCS patients, providing objective neurological evidence of chemical processing differences.
A tripeptide antioxidant produced by the body that plays a central role in Phase II liver detoxification, neutralizing reactive oxygen species and facilitating the excretion of toxins. Glutathione-S-transferase (GST) enzyme variants affect how efficiently glutathione is deployed. Some people with MCS, like many people without it, carry variants that reduce GST activity, and lower glutathione has been measured in some MCS groups. Supplementation strategies aim to support glutathione production through N-acetyl cysteine (NAC), glutathione precursors, and dietary support.
A neuroplasticity-based recovery program developed by Ashok Gupta for conditions including MCS, fibromyalgia, chronic fatigue syndrome, and CIRS. Like DNRS, the Gupta Programme uses structured daily practices to retrain the brain’s amygdala and insula responses, reducing the chronic threat activation that perpetuates chemical sensitivity and related conditions. It operates on documented neuroplasticity principles rather than psychological symptom management alone.
A subset of the ERMI test focusing specifically on the five mold species most associated with CIRS: Stachybotrys chartarum, Aspergillus penicillioides, Aspergillus versicolor, Chaetomium globosum, and Wallemia sebi. The HERTSMI-2 score is used in CIRS management to determine whether a building is safe for a recovering CIRS patient to re-enter. A score of 10 or below is generally considered acceptable; higher scores indicate ongoing biotoxin risk.
A seahorse-shaped brain structure within the limbic system critical for memory formation, spatial navigation, and learning. Chemical exposures in MCS can affect hippocampal function, producing the cognitive symptoms commonly described as “brain fog” — difficulty with word retrieval, short-term memory, concentration, and processing speed. NeuroQuant brain imaging has documented hippocampal volume changes in some CIRS patients.
A protein on the surface of immune cells that presents foreign antigens (including biotoxins) to the immune system for recognition and clearance. Within the CIRS/Shoemaker research literature, certain HLA-DR gene variants are associated with impaired biotoxin clearance; proponents propose that the resulting protein does not effectively recognize and present biotoxin antigens, so carriers do not mount a normal clearance response and biotoxins recirculate rather than being cleared, contributing to CIRS. This specific mechanism and haplotype mapping come from CIRS research and are not independently confirmed in mainstream immunology. HLA-DR genotyping is a one-time blood test that identifies these variants.
The four subtypes of immunoglobulin G, the primary antibody of the adaptive immune system. Standard allergy testing measures IgE (immediate hypersensitivity) and is negative in MCS — which is expected, not diagnostic. The broader immunoglobulin panel including IgA, IgM, and IgG subclasses reveals immune function patterns relevant to MCS and CIRS: IgA deficiency impairs mucosal defense and gut barrier integrity; IgG subclass deficiencies (particularly IgG2 and IgG3) reduce the ability to clear certain pathogens and biotoxins; elevated IgM or IgG patterns can signal chronic infection burden. These tests are standard blood work any physician can order.
A professional medical society for practitioners trained in the diagnosis and treatment of environmentally acquired illnesses, including MCS, CIRS, Lyme disease, and mold-related illness. ISEAI provides practitioner training, conferences, and a practitioner directory. Finding a doctor through ISEAI’s directory is one of the most reliable ways for MCS and CIRS patients to locate a clinician who takes their condition seriously and understands current treatment protocols.
A mast cell stabilizer and antihistamine used in MCAS management to reduce mast cell reactivity and histamine release. Unlike most antihistamines, ketotifen works upstream of histamine release by stabilizing the mast cell membrane itself, preventing degranulation. Often used in combination with H1 and H2 antihistamines as part of a mast cell stabilization protocol. Available by prescription in the US (compounded) and over-the-counter in some countries.
A collection of interconnected brain structures — including the amygdala, hippocampus, hypothalamus, and olfactory bulb — that process emotion, memory, motivation, and sensory input related to survival. The limbic system is sometimes called the “primitive brain” because it handles threat response and emotional regulation rather than higher cognitive functions. In MCS, the direct nasal-to-limbic chemical pathway causes the limbic system to process VOC exposures as threats, triggering fight-or-flight responses at low chemical concentrations.
A general term for structured neuroplasticity-based approaches — including DNRS and the Gupta Programme — that aim to reduce the chronic limbic system threat activation that can amplify chemical sensitivity and related conditions. These programs use daily practices including movement, visualization, and structured cognitive exercises to create new neural pathways and gradually reduce sensitized threat responses. Distinct from standard cognitive behavioral therapy (CBT) in that the target is neurological sensitization rather than belief systems or coping strategies. Limbic retraining is reported (in uncontrolled program surveys) to improve coping, fear and symptom intensity for a minority of MCS patients — those where conditioned fear responses and anticipatory anxiety have become significant secondary amplifiers on top of the underlying physiological condition. For the majority of MCS patients, avoidance of chemical exposures remains the primary and most effective path. Limbic retraining is a secondary tool, not a universal recovery approach, and does not replace avoidance.
A specialty laboratory test that measures specific mycotoxins — including ochratoxin A, aflatoxins, trichothecenes, and gliotoxin — in a urine sample. Unlike CIRS biomarker panels, which measure the downstream inflammatory consequences of biotoxin exposure, mycotoxin urine testing measures the specific toxins themselves, and some practitioners use it to help guide binder selection and track clearance during treatment. Read results with care: mycotoxins are common in food, so many healthy people test positive, and the test cannot tell whether a mycotoxin came from a building or a meal. It has not been validated for diagnosing mold illness. Available through RealTime Labs and Great Plains Laboratory. Interpretation requires a practitioner familiar with mycotoxin testing, as reference ranges are still being standardized across labs.
Antibiotic-resistant coagulase-negative staphylococci that the CIRS model proposes colonize the deep nasal passages when MSH is low and, through biofilm, suppress MSH further. The mechanism has not been studied outside the CIRS practitioner literature. Testing and any eradication treatment are a clinician’s to order; this site describes neither. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
A phenomenon in chemical intolerance where continuous exposure to multiple triggers produces overlapping, chronic symptoms that make it impossible to identify which specific exposures are causing which reactions. The reactions blend together into a persistent background of illness. Unmasking — reducing total chemical exposure load significantly — is necessary before patterns can be identified and specific triggers isolated. Masking is one reason MCS is so difficult to self-diagnose and explain to others.
An immune cell found in connective tissues throughout the body, particularly near nerves, blood vessels, and surfaces that interact with the environment (skin, gut, lungs). Mast cells contain granules packed with histamine, tryptase, heparin, and other inflammatory mediators. When activated, mast cells degranulate — releasing their contents rapidly. Mast cells can be activated by allergens (via IgE), physical stimuli, and chemical exposures including VOCs. In MCS, chronic mast cell activation contributes to the inflammatory environment that lowers the threshold for chemical reactions.
A condition in which mast cells are chronically hyperactivated and degranulate inappropriately, releasing inflammatory mediators across multiple organ systems. Symptoms overlap significantly with MCS and include flushing, hives, GI distress, brain fog, and reactions to foods, chemicals, and environmental stimuli. MCAS and MCS frequently co-occur. Treating MCAS through mast cell stabilization (dietary strategies, antihistamines, mast cell stabilizers like cromolyn and ketotifen) often reduces chemical reactivity. Diagnosis typically requires elevated serum tryptase and/or 24-hour urine histamine/prostaglandin testing.
A chronic condition in which exposure to low-level chemicals — particularly volatile organic compounds (VOCs) such as fragrances, cleaning products, pesticides, and combustion products — triggers symptoms across multiple organ systems. Symptoms may include headache, brain fog, respiratory difficulty, fatigue, nausea, and neurological symptoms. The 1999 Consensus Criteria define MCS as: symptoms reproducible with repeated chemical exposure, a chronic condition, triggered by low exposures, improving when incitants are removed, responding to multiple chemically unrelated substances, and involving multiple organ systems. Biological mechanisms include TRPV1/TRPA1 receptor sensitization and neurological changes documented by brain imaging.
An enzyme that breaks down extracellular-matrix proteins, released as part of inflammatory responses. In the CIRS model it is one of the originating group’s biomarkers, proposed to be elevated in its patients and to affect blood-brain-barrier integrity. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
A pituitary hormone with broad anti-inflammatory effects that also regulates pain sensitivity, sleep quality, immune function, and gut permeability. MSH levels are frequently suppressed in CIRS patients because the biotoxin-driven inflammatory process depletes it. Low MSH creates a cascade of effects: pain sensitivity increases, sleep fragments, and the gut and blood-brain barrier become more permeable. Restoration of MSH is an endpoint of successful CIRS treatment; VIP nasal spray is used in the final protocol step specifically to restore MSH and VIP levels.
A toxin produced by mold (fungi). Not all molds produce mycotoxins, but species common in water-damaged buildings — particularly Stachybotrys chartarum, Aspergillus versicolor, and Chaetomium globosum — produce potent ones including trichothecenes, ochratoxins, and gliotoxins. Mycotoxins can be inhaled, ingested, or absorbed through skin contact. In CIRS-susceptible individuals, they trigger the biotoxin illness cascade. A 2024 report of four cases estimated, from one HLA-DR carrier’s urine samples, clearance half-lives of about 160 days for one mycotoxin and 311 days for ochratoxin A — a single measurement, not a population figure, but consistent with people staying ill for years after leaving a contaminated building.
Software that analyzes standard MRI brain scans to measure the volume of specific brain structures with high precision. In CIRS research, NeuroQuant has documented measurable structural changes including atrophy of the caudate nucleus and swelling of the forebrain parenchyma in biotoxin-affected individuals. NeuroQuant results provide objective structural evidence that cognitive symptoms of biotoxin illness have a measurable neurological basis and can be tracked over time as treatment progresses.
A protein that regulates the growth and maintenance of nerve cells and plays a critical role in maintaining TRPV1 receptor sensitivity. Elevated NGF levels in the nasal secretions of MCS patients have been documented, providing a biochemical explanation for why MCS does not resolve spontaneously without active exposure management. Elevated NGF keeps TRPV1 receptors in a persistently sensitized state; each new chemical exposure stimulates further NGF production, maintaining the cycle.
A non-invasive brain imaging technique that measures blood oxygen levels in the cerebral cortex using near-infrared light. Used in MCS research in Japan to document abnormal prefrontal blood flow patterns during odor stimulation. NIRS studies found that MCS patients show altered prefrontal activation during odor exposure and that brain activation persists 20–30 seconds after the odor stimulus ends — evidence of an abnormally prolonged neural response.
The brain’s capacity to reorganize itself by forming new neural connections throughout life. In the context of MCS recovery, neuroplasticity is the biological basis for limbic retraining programs — the idea that sensitized neural pathways maintaining chronic threat responses can be gradually modified through structured practice. Neuroplasticity is a well-established neuroscience concept, not a metaphor or wishful thinking.
A mycotoxin produced primarily by Aspergillus and Penicillium mold species and found in water-damaged buildings. Ochratoxin A is nephrotoxic (kidney-damaging), immunosuppressive, and potentially carcinogenic. A 2024 report of four cases estimated, from one HLA-DR carrier’s two urine samples taken eighteen months apart, a clearance half-life of about 311 days — roughly ten times slower than expected — with full clearance projected at about 4.3 years without binder therapy. It is a single measurement, not a population figure.
The release of volatile organic compounds (VOCs) from materials into the surrounding air. New materials — carpeting, paint, composite wood furniture, vinyl flooring, mattresses — off-gas at high rates initially and then taper off over weeks to months. For people with MCS, off-gassing from new or recently installed materials is a major exposure risk. Selecting inherently non-emitting materials (solid hardwood, ceramic tile, mineral wool insulation, zero-VOC paint) and allowing adequate ventilation periods (bake-out) before occupancy reduces this risk.
A nuclear medicine imaging technique that measures metabolic activity in tissues by tracking a radioactive glucose tracer. Used in MCS research to document altered brain metabolism during chemical exposures. A Spanish PET study documented frontal deactivation combined with limbic overactivation — consistent with other brain imaging findings across multiple modalities. PET results contribute to the cross-modality convergence of neurological evidence for MCS.
The two-stage liver detoxification system. Phase I (primarily cytochrome P450 enzymes) chemically modifies toxins, usually by oxidation, to make them more water-soluble. Phase II enzymes (including glutathione-S-transferases and sulfotransferases) conjugate the Phase I products to carrier molecules that facilitate excretion. Genetic variants in both Phase I (CYP450) and Phase II (GST, COMT) enzymes affect detoxification efficiency. These variants are common in the general population; whether they are more common in MCS, or help cause it, has not been consistently shown.
The gold-standard validated assessment tool for identifying and quantifying chemical intolerance. Developed from the TILT model by Dr. Claudia Miller and colleagues, the QEESI covers chemical sensitivity, other intolerances (foods, drugs, environmental stimuli), symptom severity, and symptom burden across multiple organ systems. A 2021 validation study found that approximately 1 in 5 primary care patients meets criteria for chemical intolerance on the QEESI. The QEESI is available free at tiltresearch.org and can be self-administered prior to a medical appointment.
An increase in reactivity to a stimulus following repeated exposure. In MCS, chemical exposures sensitize TRPV1/TRPA1 receptors so that they respond at lower and lower concentrations over time. This is the opposite of tolerance (where repeated exposure reduces reactivity). Sensitization is also the basis for the spreading phenomenon — where over time, MCS patients often react to an increasing number of substances — because the sensitized nervous system generates broader threat responses.
The treatment sequence developed by the CIRS model’s originating group: removal from exposure, a bile-acid sequestrant, treatment of nasal colonization where found, stepwise correction of the group’s biomarkers, and in some cases VIP nasal spray, in an order that group sets and a trained clinician interprets from laboratory results. Outcomes are reported by the group in its own treated cohorts; they have not been reproduced independently. This site names the sequence and does not detail it. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
A nuclear medicine imaging technique that measures blood flow in the brain as a proxy for neural activity. SPECT studies of MCS patients have documented measurable differences in brain perfusion patterns during and after chemical exposures, confirming that MCS produces objective, reproducible neurological changes. Results across SPECT studies are consistent with findings from PET, NIRS, and fMRI — contributing to the cross-modality neurological evidence base for MCS.
A cytokine that regulates immune responses, inflammation and tissue repair. In the CIRS model it is one of the biomarkers the originating group reports as elevated in its patients and treats as a target. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
A two-stage disease model developed by Dr. Claudia Miller that describes how MCS develops. Stage 1 (Initiation): a significant chemical exposure — occupational solvent exposure, pesticide application, renovation chemicals, indoor mold — overwhelms the body’s tolerance threshold. Stage 2 (Triggering): after initiation, previously tolerated substances at much lower levels begin triggering symptoms. The TILT model explains why MCS patients often cannot identify a single clear onset event (low-level cumulative exposures can also cross the initiation threshold), and why their symptoms are so diverse (different people lose tolerance to different substances).
Transient receptor potential (TRP) ion channels that detect chemical, thermal, and mechanical stimuli. TRPV1 is activated by capsaicin, heat, and a wide range of VOCs. TRPA1 is activated by irritants including formaldehyde, acrolein, and many fragrances. Both channels are found in sensory nerve endings throughout the body, including the nose, airways, and skin. In MCS, repeated chemical exposures sensitize these channels so that they fire at lower concentrations and generate stronger, more prolonged responses. TRP receptor sensitization is supported by 21+ peer-reviewed studies and is the best-documented biological mechanism for MCS.
The ability to detect differences in contrast — light and dark patterns — at varying spatial frequencies. VCS testing uses standardized printed or computerized patterns to measure this ability. In CIRS, biotoxin-related neurological effects frequently impair visual contrast sensitivity, producing an abnormal VCS test result. Because VCS is objective and measurable, and because CIRS patients consistently show VCS abnormalities that correlate with treatment progress, VCS testing has become a standard component of CIRS assessment and monitoring. The computerized version is available free at survivingmold.com.
A neuropeptide with anti-inflammatory, immune-modulating and neuroregulatory roles. In the CIRS model, the originating group reports low VIP in its patients and uses a compounded VIP nasal spray as the last step of its sequence, reporting improvement in its own cohorts. A prescription treatment; when and whether it is used is the clinician’s. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
Any organic chemical with a high vapor pressure at room temperature, meaning it readily evaporates and enters the air. VOCs are emitted by an enormous range of products — fragrances, cleaning products, paints, adhesives, new furniture, carpeting, vehicle exhaust, and many building materials. Indoor VOC concentrations are typically 4–10 times higher than outdoor levels. For people with sensitized TRPV1/TRPA1 receptors, VOC exposures are the primary triggers of MCS reactions. HEPA filters do not remove VOCs — activated carbon filtration is required.
A prescription bile-acid sequestrant, used in the CIRS model as an alternative binder to cholestyramine; the practitioner literature reports it is often better tolerated. Its use is the prescriber’s to direct. Part of the CIRS model, which comes from one research group and has not been independently confirmed; see the biotoxin science page.
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