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Sökning: WFRF:(Dantoft Thomas Meinertz)

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1.
  • Andersson, Linus, et al. (författare)
  • Chemosensory perception, symptoms and autonomic responses during chemical exposure in multiple chemical sensitivity
  • 2016
  • Ingår i: International Archives of Occupational and Environmental Health. - : Springer. - 0340-0131 .- 1432-1246. ; 89:1, s. 79-88
  • Tidskriftsartikel (refereegranskat)abstract
    • 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 odorantn-butanol using an exposure chamber. The first 10 min constituted blank exposure, after which then-butanol concentration increased and reached a plateau at 11.5 mg/m3.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.
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2.
  • Dantoft, Thomas Meinertz, et al. (författare)
  • Chemical Intolerance
  • 2015
  • Ingår i: Current Rheumatology Reviews. - : Bentham Science. - 1573-3971 .- 1875-6360. ; 11:2, s. 167-184
  • Tidskriftsartikel (refereegranskat)abstract
    • Chemical intolerance (CI) is a term used to describe a condition in which the sufferer experiences a complex array of recurrent unspecific symptoms attributed to low-level chemical exposure that most people regard as unproblematic. Severe CI constitutes the distinguishing feature of multiple chemical sensitivity (MCS). The symptoms reported by CI subjects are manifold, involving symptoms from multiple organs systems. In severe cases of CI, the condition can cause considerable life-style limitations with severe social, occupational and economic consequences. As no diagnostic tools for CI are available, the presence of the condition can only be established in accordance to criteria definitions. Numerous modes of action have been suggested to explain CI, with the most commonly discussed theories involving the immune system, central nervous system, olfactory and respiratory systems as well as altered metabolic capacity, behavioral conditioning and emotional regulation. However, in spite of more than 50 years of research, there is still a great deal of uncertainties regarding the event(s) and underlying mechanism( s) behind symptom elicitation. As a result, patients are often misdiagnosed or offered health care solutions with limited or no effect, and they experience being met with mistrust and doubt by health care professionals, the social care system and by friends and relatives. Evidence-based treatment options are currently unavailable, however, a person-centered care model based on a multidisciplinary treatment approach and individualized care plans have shown promising results. With this in mind, further research studies and health care solutions should be based on a multifactorial and interdisciplinary approach.
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3.
  • Dantoft, Thomas Meinertz, et al. (författare)
  • Multiple chemical sensitivity described in the Danish general population : Cohort characteristics and the importance of screening for functional somatic syndrome comorbidity-The DanFunD study
  • 2021
  • Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 16:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Multiple chemical sensitivity (MCS) is characterized by widespread symptoms attributed to exposure to airborne chemicals. MCS is categorized as a functional somatic syndrome (FSS), and MCS cases often meet the criteria for other types of FSS, e.g. fibromyalgia. The primary aim was to characterize MCS regarding symptom triggers, symptoms, lifestyle and describe demographics, socioeconomics and lifestyle factors associated with MCS. A secondary aim was to examine the implication of FSS comorbidity.Methods: Data were derived from a random sample of the Danish adult population enrolled in the Danish Study of Functional Disorders (DanFunD; n = 9,656). Questionnaire data comprised information used to delimit MCS and four additional types of FSS, as well as data on demographics, socioeconomics and lifestyle. MCS cases (n = 188) was stratified into subgroups; MCS only (n = 109) and MCS with comorbid FSS (n = 73). Information regarding FSS comorbidities were missing for six MCS cases. MCS subgroups and controls without FSS comorbidities (n = 7,791) were compared by means of logistic regression analyses, adjusted for age and sex.Results: MCS was associated with female sex, not being in occupation and low social status, but not with age or education. MCS cases reported normal dietary intake and smoking habits and lower alcohol consumption. Additional associations were found between MCS and low rate of cohabitation, sedentarism, daily physically limitations, and poor quality of sleep. However, subgroup analysis revealed that these findings were primarily associated with MCS with comorbid FSS.Conclusions: MCS was associated with lower socioeconomic status, physically inactivity and poor quality of sleep. Subgroup analysis revealed that several associations was explained by FSS comorbidity, i.e. MCS cases with no comorbid FSS showed normal rate of cohabitation and did not report physical limitations or difficulties sleeping. Overall, our findings emphasise the importance of screening MCS cases for FSS comorbidity both in epidemiological and clinical settings.
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4.
  • Meinertz Dantoft, Thomas, et al. (författare)
  • Inflammatory mediator profiling of n-butanol exposed upper airways in individuals with multiple chemical sensitivity
  • 2015
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10:11
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Multiple Chemical Sensitivity (MCS) is a chronic condition characterized by reports of recurrent symptoms in response to low level exposure to various chemical substances. Recent findings suggests that dysregulation of the immune system may play a role in MCS pathophysiology.OBJECTIVES: The aim of this study was to examine baseline and low dose n-butanol-induced upper airway inflammatory response profiles in MCS subjects versus healthy controls.METHOD: Eighteen participants with MCS and 18 age- and sex-matched healthy controls were enrolled in the study. Epithelial lining fluid was collected from the nasal cavity at three time points: baseline, within 15 minutes after being exposed to 3.7 ppm n-butanol in an exposure chamber and four hours after exposure termination. A total of 19 cytokines and chemokines were quantified. Furthermore, at baseline and during the exposure session, participants rated the perceived intensity, valence and levels of symptoms and autonomic recordings were obtained.RESULTS: The physiological and psychophysical measurements during the n-butanol exposure session verified a specific response in MCS individuals only. However, MCS subjects and healthy controls displayed similar upper airway inflammatory mediator profiles (P>0.05) at baseline. Likewise, direct comparison of mediator levels in the MCS group and controls after n-butanol exposure revealed no significant group differences.CONCLUSION: We demonstrate no abnormal upper airway inflammatory mediator levels in MCS subjects before or after a symptom-eliciting exposure to low dose n-butanol, implying that upper airways of MCS subjects are functionally intact at the level of cytokine and chemokine production and secretory capacity. This suggests that previous findings of increased cytokine plasma levels in MCS are unlikely to be caused by systemic priming via excessive upper airway inflammatory processes.
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