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Biomedical subjects

A Muttray

Publications and source records attributed to A Muttray.

At least 19 recordsLinked to original sources
PubMed2006

[Toxic anosmia and rhinitis due to occupational solvent exposure].

A patient's case report documents the development of anosmia and rhinitis caused by occupational exposure to organic solvents, including tetrahydrofuran, cyclohexanone, acetone and other ketones. Physicians should inquire about possible mucosal irritation or prenarcotic symptoms during exposure. If an occupational disease is assumed, notification must be sent to the Institution for Statutory Accident Insurance and Prevention (Berufsgenossenschaft). Some diseases, for example olfactory disorders due to chemical mixtures, are not included in the German list of occupational diseases. In this case, a special law (Sozialgesetzbuch VII) regulates compensation.

Adult↗
PubMed2004

[Olfactory dysfunction. Epidemiology, pathophsiological classification, diagnosis and therapy].

The present manuscript is the result of a collaborative effort within the framework of the Working Group of Olfactology and Gustology of the German Society for ENT, Head and Neck Surgery. It provides a comprehensive overview about the current views on the epidemiology, terminology, diagnostics, and therapy of olfactory dysfunction, and aims to offer a framework for the standardized procedures for the diagnosis and therapy of olfactory disorders.

Algorithms↗
PubMed2002

Effects of an external exposure to 200 ppm methyl ethyl ketone on nasal mucosa in healthy volunteers.

OBJECTIVES: To investigate the effects of an acute exposure to 200 ppm methyl ethyl ketone on the nasal mucosa of healthy volunteers. METHODS: Nineteen healthy non-smoking men were exposed to 200 ppm methyl ethyl ketone and to a sham exposure in an exposure chamber, using a cross-over design. Mucociliary transport time was determined with the saccharine test. Interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor-alpha (TNFalpha) were measured in nasal secretions. Subjective symptoms were assessed by questionnaire. RESULTS: Mucociliary transport time was significantly higher (660 vs. 600 s (medians), P = 0.01) after solvent exposure. Concentrations of IL-1beta and IL-8 were insignificantly elevated after exposure (IL-1beta: 83.8 pg/ml vs. 48.1 pg/ml, medians, P = 0.11; IL-8: 14471 pg/ml vs. 11080 pg/ml, P = 0.12), whereas those of IL-6 and TNFalpha remained unchanged. Subjects did not feel any irritation of nasal mucosa. CONCLUSION: Concentrations of organic solvents not exceeding their MAK values can cause subclinical rhinitis. The secretion of proinflammatory cytokines and impairment of mucociliary transport can explain the development of clinical rhinitis in highly exposed subjects.

Adult↗
PubMed2001

Acute effects on the human EEG after an external exposure to 200 ppm methanol.

OBJECTIVES: Even low concentrations of organic solvents may cause acute effects on the human central nervous system. The German MAK (threshold limit value) of methanol is 200 ppm. The aim of this study was to investigate whether acute exposure to 200 ppm methanol causes adverse effects, measured by EEG, and moreover, whether it is possible to differentiate between sedative and excitatory effects with this method. METHODS: Twelve healthy subjects were exposed for 4 h to 200 ppm and to 20 ppm (control) in an exposure chamber in a cross-over design. The EEG was recorded before (reference) and at the end of each exposure with, the subject's eyes closed and opened and during a choice reaction test (color word stress test). Spectral power was calculated by fast Fourier transformation. Subjective symptoms and effects of blinding with 20 ppm methanol were assessed by questionnaires. RESULTS: The study was a single-blind one. During subjects' exposure to 200 ppm, their scores for prenarcotic and irritating symptoms were not different from controls. In the closed-eye condition of subjects, the spectral power of the theta-band and of some electrodes of the delta-band was significantly less at the end of exposure to 200 ppm, than that of controls. In the open-eye condition and during the color word stress test no significant changes were found. CONCLUSION: The changes in the theta-band suggest a slight excitatory effect of 200 ppm methanol. The effect was weak, as scores of acute symptoms did not change. With respect to our results, it is not necessary for the MAK value to be decreased.

Adult↗
PubMed2000

Acute effects of 200 ppm 1,1,1-trichloroethane on the human EEG.

OBJECTIVES: Even low concentrations of organic solvents used at work may cause acute effects on the human central nervous system. We investigated the acute effects of 200 ppm 1,1,1-trichloroethane on the human EEG. METHODS: 12 healthy subjects were exposed for 4 hours to 200 ppm and to 20 ppm (control) in an exposure chamber in a cross-over design. EEG was recorded before (reference) and at the end of each exposure with eyes closed and open and during the Color Word Stress test. Spectral power was calculated by Fast Fourier transformation and related to reference values (per cent of baseline). Subjective symptoms and effects of blinding with 20 ppm 1, 1,1-trichloroethane were assessed by questionnaire. RESULTS: Blinding was not effective because of the strong smell of 1,1, 1-trichloroethane. The score for tiredness increased slightly during and after exposure to 200 ppm. In the closed eye condition, the median percentage of spectral power increased at all electrodes of the delta -band, significantly at temporo-occipital leads. In the theta-band, the percentage of the median spectral power was elevated at most of the electrodes but the parietal and some temporal ones. As to the alpha subset1-band, the percentage of the median spectral power was lower at the temporo-parieto-occipital electrodes, yielding significance at T subset4. In the alpha subset2-band, the percentage of the median spectral power was lower at all electrodes, significantly at T subset4 and T subset5. The percentage of the median spectral power of the temporo-parieto-occipital electrodes of the beta subset1 -band was lower during exposure to 200 ppm. There were no clear-cut changes in the beta subset2 -band, in the open eye condition and during the Color Word Stress test. CONCLUSION: The changes in EEG and the increased score for tiredness indicate a slight sedative effect of 200 ppm 1,1,1-trichloroethane.

Adult↗
PubMed1999

Saliva as an alternate for blood to measure concentrations of acetone under exposure to isopropanol.

OBJECTIVES: In occupational medicine, blood concentrations are often measured to judge the internal burden of workers at work-place during exposure to a potentially hazardous substance. However, blood-withdrawals are invasive and can often not be taken at work-place due to hygienic reasons. Sampling of saliva is non-invasive and easy to perform even at workplace. In order to substitute blood analysis, analysis of saliva has to be as specific and sensitive as blood investigations. Therefore acetone-concentrations in blood and in saliva during exposure to isopropanol were compared. METHODS: 18 healthy non-smokers were exposed to 360 ppm isopropanol in an exposure chamber over 4 h. Once an hour during exposure and 30 min after, blood and saliva were sampled. Saliva was collected by a cotton plug over 10 minutes and stored in an airtight closed headspace tube. Concentrations of the metabolite acetone were measured by gas chromatography. - RESULTS: The concentrations of acetone in blood and saliva rose continually during exposure and dropped after exposure-cessation. High correlations between concentrations of acetone in blood and saliva were found for each individual and the entire group (entire group: r = 0.8568, p <0.0001, y = 0.8374x - 0.4404). CONCLUSIONS: Acetone-measurement in saliva is a non-invasive, easily conductable and reliable method for estimating the internal burden of isopropanol-exposure. Further studies for the standardization and validation are necessary to impose a threshold limit value on work-place isopropanol-exposure.

2-Propanol↗
PubMed1999

[Obstructive sleep apnea syndrome caused by occupational exposure to solvents].

HISTORY AND ADMISSION FINDINGS: A 52-year-old man working in a chemical laboratory was referred with the possible diagnosis of toxic encephalopathy. For 17 years he had been exposed to high concentrations of perchlorethylene and n-butanol vapours which every day had caused acute symptoms of organic solvent intoxication. Current complaints were autonomic nervous system symptoms, loss of concentration and memory, and fatigue in the second half of the day. The patient was obese but in good general condition. INVESTIGATIONS: Neuropsychiatric examination confirmed the reported loss of concentration and planning ability at work. The polysomnogram indicated an increased number of largely obstructive apnoea attacks. DIAGNOSIS, TREATMENT AND COURSE: As the patients had an obstructive type of sleep apnoea treatment consisted of positive pressure ventilation at night and weight reduction. The occupational exposure to organic solvents was the likely cause. CONCLUSIONS: As the symptoms of encephalopathy and sleep apnoea syndrome overlap, the latter should be considered before an encephalopathy is diagnosed. Because a rare cause of the sleep apnoea syndrome is prolonged and marked occupational exposure to organic solvents this should be asked about in taking the history. If indeed there has been occupational exposure, it should cease at once and be reported.

1-Butanol↗
PubMed1999

The exposure of healthy volunteers to 200 ppm 1,1,1-trichloroethane increases the concentration of proinflammatory cytokines in nasal secretions.

OBJECTIVES: Irritating effects of organic solvents have usually been measured by means of questionnaires. The aim of the present study was to evaluate the sensitivity of different methods of detecting subclinical irritating effects. METHODS: Twelve healthy, non-smoking students were exposed to 200 ppm and to 20 ppm 1,1,1-trichloroethane in an exposure chamber, using a crossover design. The amounts of interleukins (IL)-1beta, IL-6 and IL-8 and prostaglandin E(2) (PGE(2)) in nasal secretions were measured. Mucociliary transport time was determined with the saccharine test. Ciliary beat frequency of nasal epithelial cells was measured with video-interference contrast microscopy. Subjective symptoms were assessed by questionnaire. RESULTS: Concentrations of ILs were significantly elevated after exposure to 200 ppm 1,1,1-trichloroethane (IL-1beta 82.4 vs. 28.8 pg/ml (medians), P=0.003; IL-6 12.2 vs. 7.2 pg/ml, P=0. 01; IL-8 549 vs. 424 pg/ml, P=0.007), whereas the other parameters remained unchanged. CONCLUSION: The interleukins measured proved to be sensitive indicators of irritating effects of 1,1, 1-trichloroethane. The German threshold limit (MAK value) of 200 ppm 1,1,1-trichloroethane does not prevent the subclinical inflammation of nasal mucosa.

Adult↗
PubMed1999

[Anosmia caused by inhaled hazardous substances. Significance for expert assessment general practice].

BACKGROUND: Both environmental and occupational pollutants can affect the functional integrity of the olfactory epithelium or even destroy olfactory tissue. However, occupational hyposmia and anosmia have not been included into the list of occupational diseases. Therefore, compensation of occupationally induced smell disorders is difficult. OBJECTIVE: To evaluate patients with toxic hyposmia for the pollutants involved and to discuss consequences for occupational and environmental medicine. METHODS: A total of 19 patients were evaluated in our departments between 1993 and 1997 for olfactory disorders related to environmental or occupational pollutants. The charts of these patients were retrospectically analyzed and the causative pollutants compared with the literature. RESULTS: A chronical exposure to mixtures of metal dusts and steam, volatile organic substances, and anorganic gases were the most common pollutants involved in occupational dysosmia. Only one case of acute development of an anosmia due to exposure to CO and combustion gases was documented. CONCLUSIONS: Olfactory disorders are underestimated in occupational and environmental medicine. Relevance of olfactotoxic substances for occupational medicine can be postulated in metal and chemical workers, in welding and disinfection. The list of occupational diseases should be completed by olfactory hyposmia and anosmia.

Adult↗
PubMed1998

Immunologic findings in workers formerly exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin and its congeners.

One hundred ninety-two workers in a German pesticide factory who were exposed to polychlorinated dibenzodioxins and -furans (PCDD/PCDF) were investigated for former and present diseases and laboratory changes of the immune system. Moreover, in a subgroup of 29 highly exposed and 28 control persons, proliferation studies were performed. In addition to assays such as blood count, immunoglobulins, serum electrophoresis, monoclonal bands, surface markers, autoantibodies, and lymphocyte proliferation, two new methods, the rise of tetanus antibody concentration after vaccination and the in vitro resistance of lymphocytes to chromate, were used to diagnose the morphologic and functional state of the immune system. There was no stringent correlation of actual PCDD/PCDF concentrations with the occurrence of infections or with one of the immune parameters. In addition, outcomes of the tetanus vaccination and the chromate resistance test were not correlated with PCDD/PCDF. However, the chromate resistance of lymphocytes stimulated by phytohemagglutinin of highly exposed persons was significantly lower than that for the control group. These findings indicate that the function of lymphocytes can be stressed and possibly impaired by high exposure to PCDD/PCDF.

Adult↗
PubMed1997

Blue-yellow deficiency in workers exposed to low concentrations of organic solvents.

OBJECTIVES: To evaluate the effects of low concentrations of organic solvents on color vision. METHODS: Color vision was examined in 24 workers exposed to mixtures of solvents and in 24 control subjects. Exposure to mixtures was below the threshold-limit values. Color vision ability was assessed using the Ishihara plates (to screen for congenital dyschromatopsia), the Farnsworth panel D-15 test, the Lanthony desaturated panel D-15 test, and the Standard Pseudoisochromatic Plates part 2 (SPP2 test). RESULTS: The comparatively less sensitive Farnsworth panel D-15 test failed to show any difference between the groups, but the Lanthony panel D-15 desaturated test as well as the SPP2 test showed a significant impairment in the exposed group. Errors were of the blue-yellow type. CONCLUSION: This study gives further evidence that even mixtures of organic solvents at concentrations below the threshold-limit values may impair color vision.

Adult↗
PubMed1995

Acute changes in the EEG of workers exposed to mixtures of organic solvents.

In a pilot study, 11 workers were exposed to mixtures of organic solvents during the cleaning of printing rolls. The exposure was considered as low to moderate. The "electroencephalogram (EEG)" was recorded before and after the cleaning. The spectral power was calculated by Fast Fourier Transformation in six frequency bands. After exposure the spectral power in particular increased in the alpha-1 band and in the temporooccipital leads of the delta band in the closed-eye condition.

Adult↗
PubMed1995

Effect of subacute occupational exposure to toluene on color vision.

The subacute effect of toluene on color vision was examined in 59 rotogravure workers exposed to toluene. Toluene and ethanol were determined in blood and color vision testing was performed on Monday before shift and on Friday after shift. The battery included the Ishihara plates, the Velhagen plates, the Standard Pseudoisochromatic Plates part 2, the Farnsworth panel D-15 test, and the Lanthony desaturated panel D-15 test. The concentrations of toluene in blood ranged from < 0.22 to 7.37 mg/l. No effect of toluene on color vision could be observed even in a subgroup of highly exposed workers. So their ability to judge colored products was not impaired.

Adolescent↗
PubMed1994

[Encephalopathy following poisoning with an anticholinergic agent].

A 55-year-old chemical laboratory technician developed mydriasis and ocular hypertension, which lasted for 6 weeks, after synthesizing several kilograms of a scopolamine-related test agent with anticholinergic action and then decanting a powdery intermediary substance, the dust of which he may have inhaled. Six weeks later he suddenly had symptoms of an acute intoxication while synthesizing a scopolamine-related substance. The anticholinergic delirium regressed completely within one day requiring no treatment. But subsequently he developed symptoms of a toxic encephalopathy. This only partially regressed over the following 3 years. Its probable cause is thought to have been either the manifestation of an already existing organic cerebral psychiatric syndrome or an as yet unknown effect of the test substance.

Acute Disease↗
PubMed1994

Porphyrin studies in TCDD-exposed workers.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been shown to inhibit uroporphyrinogen decarboxylase activity resulting in chronic hepatic porphyria. From a cross-sectional study of 170 workers in chemical industry 68 showed elevated coproporphyrin levels, interpreted as secondary coproporphyrinuria. Three persons suffered from chronic hepatic porphyria in subclinical stages. None of the workers showed an overt porphyria cutanea tarda. A low-grade zinc protoporphyrinemia was observed in three persons. Forty-three of the 170 workers were evaluable for investigating the effect of TCDD on porphyrin levels. No significant correlation was found between TCDD concentration in adipose tissue and the level of uroporphyrin and coproporphyrin. The influence of a chloracne history is described.

Adipose Tissue↗