• Wat is MCS ?
    MCS staat voor Multiple Chemical Sensitivity ofwel Meervoudige Chemische Overgevoeligheid.
    Mensen met MCS worden letterlijk ziek van alledaagse chemische stoffen en geuren.

Martin L. Pall

Cases of multiple chemical sensitivity (MCS) are reported to be initiated by seven classes of chemicals. Each of the seven acts along a specific pathway, indirectly producing increases in NMDA activity in the mammalian body. Members of each of these seven classes have their toxicant responses lowered by NMDA antagonists, showing that the NMDA response is important for the toxic actions of these chemicals. The role of these chemicals acting as toxicants, in initiating cases of MCS has been confirmed by genetic evidence showing that six genes that influence the metabolism of these chemicals, all influence susceptibility to MCS. It is likely that chemicals act along these same pathways, leading to increased NMDA activity when they trigger sensitivity responses in MCS patients. The chronic nature of MCS and also related multisystem illnesses is thought to be produced by a biochemical vicious cycle mechanism, the NO/ONOO- cycle, which is initiated by various stressors that increase nitric oxide and peroxynitrite levels (with some but not others acting via NMDA stimulation). The NO/ONOO- cycle is based on well documented individual mechanisms. The interaction of this cycle with
previously documented MCS mechanisms, notably neural sensitization and neurogenic inflammation, explains many of the previously unexplained properties of MCS. This overall mechanism is also supported by physiological correlates found in MCS and related multisystem illnesses, objectively measurable responses to low level chemical exposure in MCS patients, many studies of apparent animal models of MCS and also evidence from therapeutic trials of MCS-related illnesses. Some have argued that MCS is a psychogenic illness, but this view is completely inconsistent with this diverse data on MCS and related illnesses and the literature claiming psychogenesis of MCS is deeply flawed. In addition, two rare predictions that can be used to test psychogenesis both lead to rejection of the psychogenic hypothesis. While the NO/ONOO- cycle mechanism for MCS is supported by many different observations, there are also multiple areas where further study is needed.

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E. Millqvist, U. Bengtsson, O. Löwhagen

Background: In earlier studies, we have shown that patients with a history of sensory hyperreactivity develop asthma-like symptoms when exposed to strong scents, even if they cannot smell any scent.

Methods: For study of possible pathophysiologic mechanisms behind sensory hyperreactivity, the patients' airways and eyes were separately exposed to a common inducing factor, perfume. Eleven patients with a history of hyperreactivity to chemical trigger factors, such as perfume, were provoked single-blindly in a placebo-controlled, randomized study. During airway exposure, the eyes were covered and, during the eye exposure, the patients inhaled fresh air. A special face mask or a nose clip was used to avoid any smell.

Results: During the 30-min exposure to perfume, there was a gradual increase in three main symptoms; i.e., eye irritation, cough, and dyspnea, after both the airway and eye exposures. The increases were significant compared with placebo.

Conclusions: Asthma-like and other symptoms, such as irritation of the eyes, may be induced by exposure of both the airways and the eyes in patients with sensory hyperreactivity. This points to the importance of studying the sensory nervous system, not only in the airways, but also in other organs.

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Hajime Kimata

Plasma levels of substance P, vasoactive intestinal peptide and nerve growth factor, but not histamine, were elevated in patients with self-reported multiple chemical sensitivity (sMCS). Exposure to volatile organic compounds (VOC) increased plasma levels of all parameters in these patients, while it had no effect in normal subjects or patients with atopic eczema/dermatitis syndrome (AEDS). Exposure to VOC also enhanced skin wheal responses induced by histamine in patients with sMCS, while it failed to do so in normal or AEDS subjects. These results indicate that exposure to VOC may enhance neurogenic inflammation with concomitant enhancement of histamine-induced responses.

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William J. Meggs

Department of Emergency Medicine, East Carolina University School of Medicine, Greenville, North Carolina

The reactive airways dysfunction syndrome (RADS), the reactive upper airways dysfunction syndrome (RUDS), the sick building syndrome (SBS), and the multiple chemical sensitivity syndrome (MCS) are overlapping disorders in which there is an intolerance to environmental chemicals. The onset of these illnesses is often associated with an initial acute chemical exposure. To understand the pathophysiology of these conditions, a study of the nasal pathology of individuals experiencing these syndromes was undertaken. Preliminary data indicate that the nasal pathology of these disorders is characterized by defects in tight junctions between cells, desquamation of the respiratory epithelium, glandular hyperplasia, lymphocytic infiltrates, and peripheral nerve fiber proliferation. These findings suggest a model for a relationship between the chronic inflammation seen in these conditions and an individual's sensitivity to chemicals. A positive feedback loop is set up: the inflammatory response to low levels of chemical irritants is enhanced due to the observed changes in the epithelium, and the epithelial changes are propagated by the inflammatory response to the chemicals. This model, combined with the concept of neurogenic switching, has the potential to explain many aspects of RADS, RUDS, SBS, and MCS in a unified way.

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Objective: This study was conducted to confirm the definition of multiple chemical sensitivity (MCS) in actual life: that multiple symptoms are provoked in multiple organs by exposure to, and ameliorated by avoidance of, multiple chemicals at low levels. We used the Ecological Momentary Assessment to monitor everyday symptoms and the active sampling and passive sampling methods to measure environmental chemical exposure.

Methods: Eighteen patients with MCS, diagnosed according to the 1999 consensus criteria, and 12 healthy controls participated in this study. Fourteen patients and 12 controls underwent 1-week measurement of physical and psychologic symptoms and of the levels of exposure to various chemicals. Linear mixed models were used to test the hypotheses regarding the symptom profile of MCS patients.

Results: Some causative chemicals were detected in 11 of 14 MCS patients. Two other patients did not report any hypersensitivity episodes, whereas passive sampling showed far less exposure to chemicals than control subjects. Another subject reported episodic symptoms but was excluded from the following analyses because no possible chemical was detected. Eleven of the 17 physical symptoms and all four mood subscales examined were significantly aggravated in the interview based on “patient-initiated symptom prompts.” On the other hand, there were no differences in physical symptoms or mood subscales between MCS patients and control subjects in the interview based on “random prompts.”

Conclusions: MCS patients do not have either somatic or psychologic symptoms under chemical-free conditions, and symptoms may be provoked only when exposed to chemicals.

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