Archive for category ‘Clinical Diagnostics‘

Brain dysfunction in MCS – Multiple Chemical Sensitivity

Doctor examining brain Scan

The aim of  the following study was to ascertain whether MCS patients present brain single photon emission computed tomography (SPECT) and psychometric scale changes after a chemical challenge.

This procedure was performed with chemical products at non-toxic concentrations in 8 patients diagnosed with MCS and in their healthy controls. In comparison to controls, cases presented basal brain SPECT hypoperfusion in small cortical areas of the right parietal and both temporal and fronto-orbital lobes.

After chemical challenge, cases showed hypoperfusion in the olfactory, right and left hippocampus, right parahippocampus, right amygdala, right thalamus, right and left Rolandic and right temporal cortex regions(p</=0.01). By contrast, controls showed hyperperfusion in the cingulus, right parahippocampus, left thalamus and some cortex regions (p</=0.01). The clustered deactivation pattern in cases was stronger than in controls (p=0.012) and the clustered activation pattern in controls was higher than in cases (p=0.012).

In comparison to controls, cases presented poorer quality of life and neurocognitive function at baseline, and neurocognitive worsening after chemical exposure. Chemical exposure caused neurocognitive impairment, and SPECT brain dysfunction particularly in odor-processing areas, thereby suggesting a neurogenic origin of MCS.

Reference:  Orriols R, Costa R, Cuberas G, Jacas C, Castell J, Sunyer J., Brain dysfunction in multiple chemical sensitivity, Servei de Pneumologia, Hospital Universitari Vall d’ Hebron, Barcelona, Catalonia, Spain; CIBER Enfermedades Respiratorias (CIBERES), Spain, J Neurol Sci. 2009 Oct 2.

Toxic Sofas, toxic Furniture – An epidemic of furniture-related dermatitis

Toxic-Sofa, toxic Furniture

Toxic Sofas, toxic Furniture – Searching for a cause  

Sitting in new chairs or sofas has elicited dermatitis in numerous patients in Finland and in the U.K. since autumn 2006. The cause of the dermatitis seemed to be an allergen in the furniture materials.

The aim of the following study was to determine the cause of the dermatitis in patients with furniture-related dermatitis. 

Altogether 42 patients with furniture-related dermatitis were studied. First, 14 Finnish patients were patch tested with the standardized series and with the chair textile material. A thin-layer chromatogram (TLC) strip and an extract made from the same textile material were tested in seven Finnish patients. The test positive spot of the TLC and the content of a sachet found inside a sofa in the U.K. were analysed by using gas chromatography-mass spectrometry. All chemicals analysed were patch tested in 37 patients. 

A positive patch test reaction to the chair textile and to its extract was seen in all patients tested, one-third of whom had concurrent reactions to acrylates. Positive reactions to the same spot of the TLC strip were seen in five of seven patients and dimethyl fumarate was analysed from the spot as well as from the sachet contents. Dimethyl fumarate (0.01%) elicited positive reactions in all the patients. The other chemicals analysed did not elicit positive reactions, but one patient in the U.K. had a positive reaction to tributyl phosphate. 

Sensitization to dimethyl fumarate was seen in all the patients with furniture-related dermatitis. Concurrent sensitization or cross-reactions were common among the sensitized patients. 

Reference:   Lammintausta K, Zimerson E, Hasan T, Susitaival P, Winhoven S, Gruvberger B, Beck M, Williams JD, Bruze M.,  An epidemic of furniture-related dermatitis: searching for a cause., Department of Dermatology, Turku University Hospital, PO Box 52, 20521 Turku, Finland, Br J Dermatol. 2009 Jul 20.

Autism – Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?

Autism - Cute little Boy living in his own world

Increased prevalence of the autism spectrum disorders (ASD) and the failure to find genetic explanations has pushed the hunt for environmental causes. These disorders are defined clinically but lack objective characterization.

 To meet this need, we measured neurobehavioral and pulmonary functions in eight ASD boys aged 8 to 19 years diagnosed clinically and compared them to 145 unaffected children from a community with no known chemical exposures. As 6 of 35 consecutive mold/ mycotoxin (mold)-exposed children aged 5 to 13 years had ASD, we compared them to the 29 non-ASD mold-exposed children, and to the eight ASD boys. Comparisons were adjusted for age, height, weight, and grade attained in school. 

The eight ASD boys averaged 6.8 abnormalities compared to 1.0 in community control boys. The six mold-exposed ASD children averaged 12.2 abnormalities. The most frequent abnormality in both groups was balance, followed by visual field quadrants, and then prolonged blink reflex latency. 

Neuropsychological abnormalities were more frequent in mold-exposed than in terbutaline-exposed children and included digit symbol substitution, peg placement, fingertip number writing errors, and picture completion. Profile of mood status scores averaged 26.8 in terbutaline-exposed, 52 in mold exposed, and 26 in unexposed. The mean frequencies of 35 symptoms were 4.7 in terbutaline, 5.4 in mold/ mycotoxins exposed and 1.7 in community controls. 

Reference:   Kilburn KH, Thrasher JD, Immers NB., Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?, Toxicol Ind Health. 2009 Sep 30.

Patients with indoor exposure to molds compared to patients exposed to chemicals

Protection against molds

Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals 

Patients exposed at home to molds and mycotoxins and those exposed to chemicals (CE) have many similar symptoms of eye, nose, and throat irritation and poor memory, concentration, and other neurobehavioral dysfunctions. Aim of a study was to compare the neurobehavioral and pulmonary impairments associated with indoor exposures to mold and to chemicals. 

105 consecutive adults exposed to molds (ME) indoors at home and 100 patients exposed to other chemicals were compared to 202 community referents without mold or chemical exposure. To assess brain functions, the scientists measured 26 neurobehavioral functions. Medical and exposure histories, mood states score, and symptoms frequencies were obtained. Vital capacity and flows were measured by spirometry. Groups were compared by analysis of variance (ANOVA) after adjusting for age, educational attainment, and sex, by calculating predicted values (observed/predicted x 100 = % predicted). And p < .05 indicated statistical significance for total abnormalities, and test scores that were outside the confidence limits of the mean of the percentage predicted. 

People exposed to mold had a total of 6.1 abnormalities and those exposed to chemicals had 7.1 compared to 1.2 abnormalities in referents. Compared to referents, the exposed groups had balance decreased, longer reaction times, and blink reflex latentcies lengthened. Also, colour discrimination errors were increased and visual field performances and grip strengths were reduced. The cognitive and memory performance measures were abnormal in both exposed groups. Culture Fair scores, digit symbol substitution, immediate and delayed verbal recall, picture completion, and information were reduced. Times for peg-placement and trail making A and B were increased. 

One difference was that chemically exposed patients had excess fingertip number writing errors, but the mold-exposed did not. Mood State scores and symptom frequencies were greater in both exposed groups than in referents. Vital capacities were reduced in both groups. Neurobehavioral and pulmonary impairments associated with exposures to indoor molds and mycotoxins were not different from those with various chemical exposures. 

Reference: Kilburn KH, Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals, University of Southern California, Keck School of Medicine (ret.), Pasadena, CA, USA., Toxicol Ind Health. 2009 Sep 30.

A longitudinal study of environmental risk factors for symptoms associated with sick building syndrome

Sick-Building Syndrome realted to toxic materials

Chemicals and Molds often associated with Sick Building Syndrome   

A study was performed to explore possible environmental risk factors, including indoor chemicals, mold, and dust mite allergens, which could cause sick building syndrome (SBS)-type symptoms in new houses. 

The study was conducted in 2004 and 2005 and the final study population consisted of 86 men and 84 women residing in Okayama, Japan. 

The indoor concentrations of indoor aldehydes, volatile organic compounds, airborne fungi, and dust mite allergens in their living rooms were measured and the longitudinal changes in two consecutive years were calculated. 

A standardized questionnaire was used concomitantly to gather information on frequency of SBS-type symptoms and lifestyle habits. About 10% of the subjects suffered from SBS in the both years. 

Crude analyses indicated tendencies for aldehyde levels to increase frequently and markedly in the newly diseased and ongoing SBS groups. Among the chemical factors and molds examined, increases in benzene and in Aspergillus contributed to the occurrence of SBS in the logistic regression model. 

Indoor chemicals were the main contributors to subjective symptoms associated with SBS. A preventive strategy designed to lower exposure to indoor chemicals may be able to counter the occurrence of SBS. 

Reference:  Takigawa T, Wang BL, Sakano N, Wang DH, Ogino K, Kishi R.,    A longitudinal study of environmental risk factors for subjective symptoms associated with sick building syndrome in new dwellings, Sci Total Environ. 2009 Sep 15;407(19):5223-8.