Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Multiple Chemical Sensitivity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1997

Effects of combined exposure to noise and toxic substances--critical review of the literature.

A number of studies have been conducted in recent years investigating the potential effects on various health endpoints of the combination of noise and a variety of different industrial substances. This review indicates that the information available in both animals and humans on this subject is limited particularly with respect to assessing occupational risk. Most studies have focused on auditory effects in animals, although investigations have been performed for other toxicological endpoints. For some substances, notably toluene, the information from animals studies does suggest an interaction but these were performed only at exposure levels to both noise and chemicals which were each individually ototoxic. Single simultaneous exposure to noise and styrene did not result in any enhancement of auditory impairment above that produced by noise or styrene alone. Single simultaneous exposure to noise and carbon monoxide (CO), however, showed some evidence of enhancement of ototoxicity beyond that produced by noise or carbon monoxide alone, although only at high atmospheric concentrations of CO. When 1,3-dinitrobenzene was administered parentally at neurotoxic dose levels with continuous noise exposure, there was an increased severity of effects in the brain stem. Combined exposure to noise and lead and/or cadmium resulted in histopathological heart lesions of undefined severity, a finding which was not observed for either of those agents in isolation. Dermal exposure to dimethylformamide and noise or inhalation exposure to xylene and noise resulted in some biochemical changes in cardiac muscle which were of doubtful toxicological significance. In developing mice, there was evidence that combined exposure to cadmium sulphate and noise caused an increased incidence of external and skeletal malformations but only at dose levels of cadmium which would have induced developmental effects. Overall, for each of these chemicals and endpoints observed there is a suggestion of some interaction with noise exposure. From the data that are currently available, however, inferences cannot be drawn on whether or not interactions would have occurred at lower, more occupationally relevant, levels of exposure. A number of studies have investigated human populations exposed to both noise and industrial chemicals. Due to confounding factors, however, it was concluded that these data were inadequate for assessing the combined effects of noise and chemical exposure on hearing.

Animals↗
PubMedDate not supplied

The environmental somatization syndrome.

Patients with environmental somatization syndrome (ESS) believe that their symptoms are caused by exposure to tangible components of the external environment or by ergonomic stress at work. ESS is distinguishable by mental contagiousness and by the patients' focus on the external environment as cause of the illness. The presentation is often polysymptomatic, and epidemic outbreaks may appear. The patients usually refuse alternative explanations of their symptoms and discredit and reject any suggestion of a psychogenic etiology. It is important to distinguish between hygienic problems and ESS problems, particularly when poor and inadequate hygienic factors are present simultaneously with an ESS epidemic.

Diagnosis, Differential↗
PubMed1995

Little arrows.

Explore the source record for details and available documents.

Air Pollutants↗
PubMed1996

Little arrows.

Explore the source record for details and available documents.

Air Pollutants↗
PubMed1999

A modeling approach to account for toxicokinetic interactions in the calculation of biological hazard index for chemical mixtures.

Biological hazard index (BHI) is defined as biological level tolerable for exposure to mixture, and is calculated by an equation similar to the conventional hazard index. The BHI calculation, at the present time, is advocated for use in situations where toxicokinetic interactions do not occur among mixture constituents. The objective of this study was to develop an approach for calculating interactions-based BHI for chemical mixtures. The approach consisted of simulating the concentration of exposure indicator in the biological matrix of choice (e.g. venous blood) for each component of the mixture to which workers are exposed and then comparing these to the established BEI values, for calculating the BHI. The simulation of biomarker concentrations was performed using a physiologically-based toxicokinetic (PBTK) model which accounted for the mechanism of interactions among all mixture components (e.g. competitive inhibition). The usefulness of the present approach is illustrated by calculating BHI for varying ambient concentrations of a mixture of three chemicals (toluene (5-40 ppm), m-xylene (10-50 ppm), and ethylbenzene (10-50 ppm)). The results show that the interactions-based BHI can be greater or smaller than that calculated on the basis of additivity principle, particularly at high exposure concentrations. At lower exposure concentrations (e.g. 20 ppm each of toluene, m-xylene and ethylbenzene), the BHI values obtained using the conventional methodology are similar to the interactions-based methodology, confirming that the consequences of competitive inhibition are negligible at lower concentrations. The advantage of the PBTK model-based methodology developed in this study relates to the fact that, the concentrations of individual chemicals in mixtures that will not result in a significant increase in the BHI (i.e. > 1) can be determined by iterative simulation.

Animals↗
PubMed2004

[An auto-iatrogenic disease].

A 55-year-old practitioner from an island in the northern sea felt an increasing hypersensitivity of his entire body to various ambient and nutritional allergens and toxics. He started to treat himself with increasing doses of glucocorticoids and moved to a southern climate in Lanzarote and later on to the Swiss mountains in the grisons. On admission to our hospital in December he was in a disastrous psychotic condition, trying to cool down his body by laying naked on his bed at ambient temperatures around the freezing point. He had consumed on average 250 mg prednisone daily over weeks. As we found out later his personal assistant travelling with him was giving him glucocorticoids through the infusion during his hospital stay. He developed a necrotizing septic phlebitis at the infusion site followed by a Pseudomonas aeruginosa sepsis with fatal multiorgan failure. This case illustrates the dangers of self-treatment by doctors and the difficulties in treating a physician.

Anti-Inflammatory Agents↗
PubMed1999

Provocations with perfume in the eyes induce airway symptoms in patients with sensory hyperreactivity.

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.

Adult↗
PubMed2001

Toxicant-induced loss of tolerance.

Drug addiction and multiple chemical intolerance (abdiction) appear to be polar opposites--the former characterized by craving and dependency, the latter by aversion. However, when the two are viewed in juxtaposition similarities emerge, revealing a common underlying dynamic, one which appears to be a new paradigm of disease. TILT, or toxicant-induced loss of tolerance, bridges the gap between addiction and abduction and has the potential to explain a variety of illnesses, including certain cases of asthma, migraine headaches and depression, as well as chronic fatigue syndrome, fibromyalgia and "Gulf War syndrome". This paper argues that both addiction and chemical intolerance involve a fundamental breakdown in innate tolerance, resulting in an amplification of various biological effects, particularly withdrawal symptoms. While addicts seek further exposures so as to avoid unpleasant withdrawal symptoms, chemically intolerant individuals shun their problem exposures, but for the same reason--to avoid unpleasant withdrawal symptoms. These observations raise critical questions: do addictive drugs and environmental pollutants initiate an identical disease process? Once this process begins, can both addictants and pollutants trigger symptoms and cravings? TILT opens a new window between the fields of addiction and environmental medicine, one that has the potential to transform neighboring realms of medicine, psychology, psychiatry and toxicology.

Avoidance Learning↗
PubMed2001

Idiopathic environmental intolerance: increased prevalence of panic disorder-associated cholecystokinin B receptor allele 7.

BACKGROUND: A growing body of evidence suggests that idiopathic environmental intolerance (IEI) is a psychophysiologic disorder with prominent features of anxiety/panic and somatization, although proponents of a toxicogenic explanation claim, despite a lack of convincing evidence, that symptoms arise from exposure to otherwise nonnoxious environmental agents. Patient behaviour is characterized by strenuous avoidance of perceived triggers to the point of severe impairment of normal social and vocational functioning. IEI proponents claim that previous studies showing a high prevalence of psychopathology in patients with IEI and studies showing panic responses to known panicogenic challenges merely reflect the anxiety-producing result of living with IEI. OBJECTIVE: We explored whether IEI and panic disorder, personality traits, or both shared an underlying neurogenetic basis that would predate the anxiety of IEI symptomatology. The DNA of patients with IEI was examined for the presence of known panic disorder-associated cholecystokinin B (CCK-B) receptor alleles and for personality trait-associated dopamine D4 receptor polymorphisms. METHODS: Eleven patients with typical IEI symptoms were recruited and were individually matched to normal control subjects from an existing bank for age, sex, and ethnic background. Genomic DNA was extracted from peripheral blood samples. CCK-B and dopamine D4 receptor polymorphisms were examined by using standard PCR-based techniques. RESULTS: There was a significantly higher prevalence of the panic disorder-associated CCK-B receptor allele 7 in subjects with IEI (9/22 [40.9%]) compared with control subjects (2/22 [9.1%], P =.037). There was no difference in personality trait-associated polymorphisms of the gene encoding dopamine D4 receptor between patients and control subjects. CONCLUSIONS: These findings provide preliminary evidence that IEI and panic disorder share a common neurogenetic basis, which would predate the anxiety-producing effects of IEI symptoms. Further studies with larger samples are warranted, but these results support previous studies that suggest that panic disorder may account for much of the symptomatology in at least some cases of IEI and provide a basis for rational treatment strategies.

Alleles↗
PubMed2002

MCS: the status of population-based research.

MCS has been studied predominantly in clinical and occupational settings. Since the mid-1990's, a few investigators have examined dimensions of this controversial syndrome in the general population. In this discussion, the role of epidemiology in learning about MCS is presented. Some of the challenges of population-based research on MCS are discussed. Specific studies are presented with regard to study population, case definition, exposure and case classification methods, interpretation, and conclusions.

Epidemiologic Studies↗