Environmental illness and multiple chemical sensitivity.
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PURPOSE: This study was designed to clarify the definition of sick house syndrome (SHS). METHODS: SHS was defined based on the disease related to habitation as follows. 1. The cause of the onset of a disease relates to house. 2. Symptoms appear within house. 3. Symptoms will be less serious or disappear if patient away from house. 4. If patient goes into house, symptoms will appear repeatedly. When it corresponded to all above, it was defined to SHS, and it classified as MCS (multiple chemical sensitivities) without above conditions. Even if SHS is isolated from similar disease completely, characteristic symptoms of MCS are hard to be detected because MCS are combination of two or more diseases. Based on this working hypothesis, the logistic regression by setting MCS as reference was performed so that characteristic symptoms of SHS show odds ratios with exceeding one. RESULTS: The odds ratios with more than two of characteristic symptoms in SHS were "nausea or vomiting" "Troublesome in everything" and the causative substances to which symptoms get worse was "The smell of a perfume and cosmetics". Characteristic symptoms of an allergy disease were detected by comparison with the allergic conjunctivitis, allergic rhinitis, and bronchial asthma, respectively. CONCLUSION: These results showed that the classification method was appropriate. This definition is not fundamentally differed from the definition of the sick-building syndrome of WHO.
OBJECTIVE: Somatic symptoms that occur in response to odors can be acquired in a pavlovian conditioning paradigm. The present study investigated 1) whether learned symptoms can generalize to new odors, 2) whether the generalization gradient is linked to the affective or irritant quality of the new odors, and 3) whether the delay between acquisition and testing modulates generalization. METHODS: Conditional odor stimuli (CS) were (diluted) ammonia and niaouli. One odor was mixed with 7.4% CO2-enriched air (unconditional stimulus) during 2-minute breathing trials (CS+ trial), and the other odor was presented with air (CS- trial). Three CS+ and three CS- trials were conducted in a semirandomized order (acquisition phase). The test phase involved one CS+-only (CS+ without CO2) and one CS- test trial, followed by three trials using new odors (butyric acid, acetic acid, and citric aroma). Half of the subjects (N = 28) were tested immediately, and the other half were tested after 1 week. Ventilatory responses were measured during and somatic symptoms were measured after each trial. RESULTS: Participants had more symptoms in response to CS+-only exposures, but only when ammonia was used as the CS+. Also, generalization occurred: More symptoms were reported in response to butyric and acetic acid than to citric aroma and only in participants who had been conditioned. Both the selective conditioning and the generalization effect were mediated by negative affectivity of the participants. The delay between the acquisition and test phases had no effect. CONCLUSIONS: Symptoms that occur in response to odorous substances can be learned and generalize to new substances, especially in persons with high negative affectivity. The findings further support the plausibility of a pavlovian perspective of multiple chemical sensitivity.
This article deals with the history of the terminological and nosological development of the concept neurasthenia introduced in 1869 by George Miller Beard and in particular with its reappearance in western medicine in the 1980 s. Beginning with its predecessors in antiquity and continuing with hypochondria, which became a fashionable disease in the 18 th century, the concept neurasthenia reached a high point and world-wide medical acceptance at the end of the 19 th/beginning of the 20 th century. However, between the 1930 s and 1960 s it declined in popularity and gradually disappeared until finally it only had a rudimentary nosological role in the term "pseudoneurasthenia". In the countries of the Far East, on the contrary, the concept of neurasthenia has been in continual use since its importation in the first decades of the last century. In the 1980 s, when an interest in the symptoms of chronic fatigue was reawakened in western medicine, the concept neurasthenia reappeared, this time to define the particular form of a neurotic disorder. Parallel to these developments increasing importance was attached to clinical descriptions of illnesses which on account of their similarity to the symptoms of neurasthenia could be termed modern variants of the concept neurasthenia. These are "Chronic-Fatigue-Syndrome", "Fibromyalgia" and "Multiple Chemical Sensitivities" which have more or less adopted the organic inheritance of Beard's former concept of neurasthenia, despite the fact that so far the question of organicity could not be decisively answered in a single case. In order to clarify possible influences on the development of the concept neurasthenia and its variants, the theories and ideas of E. Shorter, medical historian at the University of Toronto, are discussed in the final part of the article, whereby the particular cultural background in each case has a decisive influence on the manifestation of the psychosomatic symptoms.
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Searching for simple explanations for ill health is as normal as human nature itself. In every era people have suffered varieties of symptoms not readily explained by "known" diseases of the day. To provide explanations and treatment approaches, individuals with symptom complexes were frequently provided a unifying disease label. At the turn of the 20th century, that label was autointoxication. Today, it is multiple chemical sensitivities (MCS). Autointoxication, a popular turn-of-the-century phenomenon illustrates that absent common, reproducible, definable, and measurable findings and consistent, objective endpoints, newly named fad disorders have not survived long term. Autointoxication was a disorder very similar in manifestations to MCS. It was, we now know, a pseudodisease, the treatment of which was based upon an unproven hypothesis. If MCS cannot withstand the probing of scientific investigation, it too will disappear as a diagnosis.
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A clinical algorithm was used to discriminate verifiable chemical sensitivity from psychological disorders in patients referred for evaluation of polysomatic symptoms attributed to hypersensitivity to workplace and domestic chemicals. These patients believed that they were reactive or hypersensitive to low-level exposure to multiple chemicals. Some had previously been evaluated and managed by the tenets of "clinical ecology" and diagnosed as having "multiple chemical sensitivity." Double-blind provocation challenges with an olfactory masker were performed in an environmental chamber on each of 20 patients. A variety of chemicals was employed, one or more per subject, dependent on individual clinical history. Clean air challenges with the olfactory masker were used as placebo or sham controls. As a group, probability analyses of patient symptom reports from 145 chemical and clean air challenges failed to show sensitivity (33.3%), specificity (64.7%), or efficiency (52.4%). Individually, none of these patients demonstrated a reliable response pattern across a series of challenges. Implications for future research in assessment methodology incorporating neurophysiologic and neurobehavioral measures are discussed.