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Background Multiple chemical sensitivity (MCS) is a chronic condition of unknown etiology. MCS is characterized by recurrent nonspecific symptoms from multiple organ systems in response to chemical exposures in concentrations that are normally tolerated by the majority of the population. The symptoms may have severe impact on patients’ lives, but an evidence-based treatment for the condition is nonexisting. The pathophysiology is unclarified, but several indicators point towards abnormal processing of sensory signals in the central nervous system. Pulsed electromagnetic fields (PEMF) offer a promising new treatment for refractory depression and can be targeted at the brain, thereby activating biochemical cell processes. Methods/Design In a parallel, randomized, double-blind, placebo-controlled trial conducted at the Danish Research Centre for Chemical Sensitivities, the effects of PEMF in MCS patients will be assessed using the Re5 Independent System. Based on sample size estimation, 40 participants will be randomized to either PEMF therapy or placebo. The allocation sequence will be generated by computer. All involved parties (that is, participants, investigators, the research nurse, and the statistician) will be blinded to group allocation. The participants will receive PEMF therapy or placebo applied transcranially 30 minutes twice a day for 7 days a week over 6 consecutive weeks. Outcomes will be measured at baseline, once weekly during treatment, post treatment, and at 2.5-month and 4.5-month follow-up according to a predefined timetable. The primary outcome will be a measurement of the impact of MCS on everyday life. The secondary outcomes will be measurements of MCS symptoms, psychological distress (stress, anxiety or depressive symptoms), capsaicin-induced secondary punctate hyperalgesia, immunological markers in serum, and quality of life. Discussion This trial will assess the effects of PEMF therapy for MCS. Currently, there is no treatment with a documented effect on MCS, and in terms of healthcare there is very little to offer these patients. There is thus a great need for well-conducted randomized trials aimed at assessing possible treatment effects. A positive outcome will pave the way for improved healthcare and understanding of this very disabling and overlooked condition. Trial registration ClinicalTrials.gov, NCT01834781

OBJECTIVES: Multiple chemical sensitivity is a poorly understood syndrome in which various symptoms are triggered by chemically unrelated, but often odorous substances, at doses below those known to be harmful. This study focuses on the process of pavlovian acquisition and extinction of somatic symptoms triggered by odours. METHODS: Diluted ammonia and butyric acid were odorous conditioned stimuli (CS). The unconditioned stimulus (US) was 7.4% CO2 enriched air. One odour (CS+) was presented together with the US for 2 minutes (CS+ trial), and the other odour (CS-) was presented with air (CS-trial). Three CS+ and three CS-exposures were run in a semi-randomised order; this as the acquisition (conditioning) phase. To test the effect of the conditioning, each subject then had one CS+ only--that is, CS+ without CO2--and one CS- test exposure. Next, half the subjects (n = 32) received five additional CS+ only exposures (extinction group), while the other half received five exposures to breathing air (wait group). Finally, all subjects got one CS+ only test exposure to test the effect of the extinction. Ventilatory responses were measured during and somatic symptoms after each exposure. RESULTS: More symptoms were reported upon exposure to CS+ only than to CS-odours, regardless of the odour type. Altered respiratory rate was only found when ammonia was CS+. Five extinction trials were sufficient to reduce the level of acquired symptoms. CONCLUSION: Subjects can acquire somatic symptoms and altered respiratory behaviour in response to harmless, but odorous chemical substances, if these odours have been associated with a physiological challenge that originally had caused these symptoms. The conditioned symptoms can subsequently be reduced in an extinction procedure. The study further supports the plausibility of a pavlovian conditioning hypothesis to explain the pathogenesis of MCS.

We conducted a pilot study using a randomized, single-blind, placebo-controlled exposure among 10 individuals with and 7 without reported chemical sensitivities in a dedicated testing chamber. Objectives of the study were to explore the length of the adaptation period to obtain stable readings, evaluate responses to different substances, and measure the level and type of symptomatic and physiologic reactions to low-level exposures. Reported and observed symptoms, electrodermal response, heart rate, skin temperature, surface electromyogram, respiratory rate, contrast sensitivity, and the Brown-Peterson cognitive test were used and compared between cases and controls and between test substances (glue, body wash solution, dryer sheet) and control substances (unscented shampoo and clean air). Subjects with chemical sensitivities (cases) took longer to adapt to baseline protocols than did controls. After adaptation, despite small study numbers, cases displayed statistically significant responses (all measures, p < 0.02) in tonic electrodermal response to test substances compared with controls and compared with the control substance. Symptoms were also higher in cases than in controls for the body wash solution (p = 0.05) and dryer sheets (p = 0.02). Test-retest showed good agreement for both symptoms and tonic electrodermal responses (McNemar's test, p = 0.32 and p = 0.33, respectively). Outside of skin conductance, other measures had no consistent patterns between test and control substances and between cases and controls. This study shows the importance of using an adaptation period in testing individuals with reported chemical sensitivities and, despite small numbers, raises questions about underlying mechanisms and level of reactivity to low-level chemical exposures in sensitive individuals.

Multiple chemical sensitivity (MCS) is a disorder characterized by nonspecific and recurrent symptoms from various organ systems associated with exposure to low levels of chemicals. Patients with MCS process odors differently than controls do. Previously, we suggested that this odor processing was associated with increased regional cerebral blood flow (rCBF) in the prefrontal area during olfactory stimulation using near-infrared spectroscopic (NIRS) imaging. The aim of this study was to investigate the association of odor thresholds and changes in rCBF during olfactory stimulation at odor threshold levels in patients with MCS. We investigated changes in the prefrontal area using NIRS imaging and a T&T olfactometer during olfactory stimulation with two different odorants (sweet and fecal) at three concentrations (zero, odor recognition threshold, and normal perceived odor level) in 10 patients with MCS and six controls. The T&T olfactometer threshold test and subjective assessment of irritating and hedonic odors were also performed. The results indicated that the scores for both unpleasant and pungent odors were significantly higher for those for sweet odors at the normal perceived level in patients with MCS than in controls. The brain responses at the recognition threshold (fecal odor) and normal perceived levels (sweet and fecal odors) were stronger in patients with MCS than in controls. However, significant differences in the odor detection and recognition thresholds and odor intensity score between the two groups were not observed. These brain responses may involve cognitive and memory processing systems during past exposure to chemicals. Further research regarding the cognitive features of sensory perception and memory due to past exposure to chemicals and their associations with MCS symptoms is needed.

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.

Multiple chemical sensitivity (MCS) patients usually react to odour compounds and the majority of neuroimaging studies assessed, especially at the cortical level, many olfactory-related correlates. The purpose of the present study was to depict sub-cortical metabolic changes during a neutral (NC) and pure (OC) olfactory stimulation by using a recently validated 18 F-2-fluoro-2-deoxy- d -glucose (FDG)-positron emission tomography/computer tomography procedure in 26 MCS and 11 healthy (HC) resting subjects undergoing a battery of clinical tests. Twelve subcortical volumes of interest were identified by the automated anatomical labeling library and normalized to thalamus FDG uptake. In both groups, when comparing OC to NC, the within-subjects ANOVA demonstrated a relative decreased metabolism in bilateral putamen and hippocampus and a relative increased metabolism in bilateral amygdala, olfactory cortex (OLF), caudate and pallidum. The between-groups ANOVA demonstrated in MCS a significant higher metabolism in bilateral OLF during NC. As in HC subjects negative correlations were found in OC between FDG uptake in bilateral amygdala and hippocampus and odor pleasantness scale, the latter positively correlated with MCS subjects’ bilateral putamen FDG uptake in OC. Besides FDG uptake resemblances in both groups were found, for the first time a relative higher metabolism increase in OLF in MCS subjects at rest with respect to HC was found. When merging this aspect to the different subcortical FDG uptake correlations patterns in the two groups, the present study demonstrated to describe a peculiar metabolic index of behavioral and neurological aspects of MCS complaints.

Purpose Multiple chemical sensitivity (MCS) is a prevalent medically unexplained symptom characterized by symptom reactions to everyday chemical exposure below hygienic thresholds. The aim of this study was to investigate the expressions of hyper-reactivity in MCS during whole-body exposure to low concentrations of the odorant n -butanol. Methods We exposed 18 participants with MCS and 18 non-ill controls to a low concentration of the odorant n -butanol using an exposure chamber. The first 10 min constituted blank exposure, after which the n -butanol concentration increased and reached a plateau at 11.5 mg/m 3 . Results MCS participants, compared with controls, reported greater perceived odor intensities, more unpleasantness to the exposure and increasing symptoms over time. MCS participants also expressed higher pulse rate and lower pulse rate variability than controls did. No group differences were found for breathing rate or tonic electrodermal activity responses. Conclusions We conclude that MCS sufferers differ from healthy controls in terms of autonomic responses, symptoms and chemosensory perception during chemical exposure.

Escalating numbers of people throughout the world are presenting to primary care physicians, allergists, and immunologists with myriad clinical symptoms after low-level exposure to assorted everyday chemicals such as smoke, perfumes, air fresheners, paints, glues, and other products. This clinical state is referred to by various diagnostic labels, including multiple chemical sensitivity disorder, environmental intolerance, chemical sensitivity (CS), and sensitivity-related illness, and has been the subject of much controversy within the health care community. The goal of this study was to provide a brief overview of the etiology, pathogenesis, clinical presentation, and management of CS. An evaluation of the medical community's response to this emerging diagnosis was also explored. This review was prepared by assessing available medical and scientific literature from MEDLINE, as well as by reviewing numerous books, toxicology journals, conference proceedings, government publications, and environmental health periodicals. A primary observation, however, is that there is limited scientific literature available on the issue of CS. The format of a traditional integrated review was chosen because such reviews play a pivotal role in scientific research and professional practice in medical issues with limited primary study and uncharted clinical territory. The sensitization state of CS seems to be initiated by a significant toxic exposure, occurring as a 1-time event, or on surpassing a threshold of toxicity after toxicant accrual from repeated lower-level exposures. Once sensitized through a toxicant-induced loss of tolerance, individuals exposed to inciting triggers such as minute amounts of diverse everyday chemicals may experience various clinical and immune sequelae, sometimes involving lymphocyte, antibody, or cytokine responses. Precautionary avoidance of inciting triggers will prevent symptoms, and desensitization immunotherapy or immune suppression may improve symptoms in some cases. Sustained resolution of the CS state occurs after successful elimination of the accrued body burden of toxicants through natural mechanisms of toxicant bioelimination and/or interventions of clinical detoxification. Despite extensive clinical evidence to support the veracity of this clinical state, many members of the medical community are reluctant to accept this condition as a pathophysiologic disorder. The emerging problem of ubiquitous adverse toxicant exposures in modern society has resulted in escalating numbers of individuals developing a CS disorder. As usual in medical history, iconoclastic ideas and emerging evidence regarding novel disease mechanisms, such as the pathogenesis of CS, have been met with controversy, resistance, and sluggish knowledge translation.

Purpose Healthy individuals differ in self-reported chemical intolerance (CI). It is unclear whether this inter-individual variability impacts well-being and performance in environmental and occupational settings with chemical exposures. So far, operational definitions and questionnaires of CI have either emphasized physical symptoms or affective/behavioral disruption. In contrast, this study focused on healthy individuals who reported strong CI which generalized to awareness, physiology, affect, and behavior. We investigated whether generalized self-reported CI is associated with hyper-reactivity and reduced cognitive functioning due to chemosensory-mediated distraction during ammonia exposure. Methods An online sample ( N  = 321) answered established CI questionnaires. Based on the convergent self-reports in these questionnaires, healthy women with generalized CI and healthy female control participants were selected (total N  = 26). Baseline characterization was performed using implicit association, lung and olfactory function tests, health-related self-reports, plasma inflammatory and metabolic markers. Performance in neurobehavioral tasks, perceptual ratings, nasal inflammatory, neuroendocrine, and autonomic nervous system reactivity were examined by means of a 75-min whole-body challenge to ammonia (stepwise increase: 0–10 ppm). Results Correlational analyses confirmed the multidimensionality of CI. Participants with generalized self-reported CI exhibited better olfactory function and reported stronger pungency during the challenge than controls. Cognitive performance and physiological response to the challenge were comparable between the two groups. Conclusions Self-reports of CI are complex and not easily assessed by unidimensional questionnaires. While generalized self-reported CI is associated with altered chemosensory processing, it seems unlikely that it modulates health effects and cognitive functioning during chemical exposure.

Multiple chemical sensitivity (MCS) is characterized by a loss of tolerance to a variety of environmental chemicals. Multiple chemical sensitivity is frequently triggered by exposure to chemical agents, especially insecticides. The aim of the study was to measure the sense of smell and quality of life in patients with MCS compared to the control group. We studied the sense of smell, both sensitive and sensorial characteristics, in female patients with MCS ( n  = 58, mean 50.5 ± 8.5 years) and healthy female volunteers without rhinosinusal pathologies ( n  = 60, mean age 46 ± 10.2 years). Olfactometry (Barcelona Smell Test 24/BAST-24), sinonasal symptoms (visual analogue scale/VAS 0–100 mm), and quality of life (Quick Environmental Exposure and Sensitivity Inventory/QEESI) were assessed. Multiple chemical sensitivity patients showed a significant impairment in smell identification (19 ± 12 %; p  > 0.05) and forced choice (62 ± 18 %; p  > 0.05), but not in smell detection (96 ± 4 %) compared to the control group. Multiple chemical sensitivity patients reported more odours as being intense and irritating and less fresh and pleasant when compared with the control group. Patients scored a high level (40–100) on QEESI questionnaire (symptom severity, chemical intolerances, other intolerances, life impact). In MCS patients, total symptom intensity (VAS/0–700 mm) score was 202 ± 135, while disease severity score was 80 ± 23. The most frequent symptoms were itching and posterior rhinorrhea. Multiple chemical sensitivity patients have an impairment in smell cognitive abilities (odour identification and forced choice, but not for detection) with increased smell hypersensitivity and poor quality of life.