Internal exposure of firefighting instructors to polycyclic aromatic hydrocarbons (PAH) during live fire training.

Firefighting instructors in live fire training are inevitably exposed to emissions containing, carcinogenic PAH. The study investigated PAH uptake in a group of firefighting instructors during short-term exposure in live fire training by urinary biomonitoring. Six firefighting instructors (non-smokers) completed five 2 h-training sessions each in a carbonaceous-fired simulation unit using self-containing breathing apparatuses (SCBA). Complying with a minimum time interval of six days between the individual training sessions, the participants provided urine samples before and immediately after, as well as 1, 3, 6, 9, 11, and 18 h after each training session. Samples were analyzed for 10 mono-hydroxylated metabolites of the PAH naphthalene, fluorene, phenanthrene and pyrene using gas chromatography/tandem mass spectrometry. A significant effect of the training sessions on the time course of internal exposure was found (p < 0.0001). The concentration of all parameters clearly increased at the latest 3 h after end of training. After peaking, the concentrations dropped with half-lives between 3.5 and 9.3 h but did not reach the initial levels within 18 h again. Compared to pre-training levels, the increase in metabolite excretion was between 546-933 %. During peak excretion reference values for hydroxynaphthalene (35 µg/L, sum of 1- and 2-isomer) and 1-hydroxypyrene (0.30 µg/L) were exceeded in 64 % (maximum: 381.3 µg/L) and 73 % of the samples (maximum: 1.88 µg/g crea.), respectively. Live fire training is associated with an additional uptake of PAH. Due to the consequent use of SCBA, dermal absorption is assumed as major exposure route. Further measures to reduce PAH exposure should be considered, in particular since higher internal loads caused by accumulation effects are to be expected with daily or more frequent training.

Urine tropenol ester levels in workers handling tiotropium bromide synthesis: implications for exposure prevention and biomonitoring.

Tropenol ester is a highly toxic anticholinergic substance and an intermediate used in industrial production of the bronchodilator tiotropium bromide. The aim of this study was to systematically test workers involved in its production for tropenol ester in urine to identify any exposure pathways and define additional preventive measures. Twelve workers performing tasks involving potential exposure to tropenol ester were repeatedly monitored at the end of each production cycle. Medical exams revealed no symptoms of acute poisoning with tropenol ester, but biological monitoring of urine showed 36 positive findings in 79 samples, with tropenol ester concentrations ranging between the detection limit of 54 pg/mL and 2160 pg/mL. We managed to establish the cause of only one positive finding, which was a hole in a protective glove, whereas the rest most likely occurred due to human error. Because of this, the plant decided to modify the production process by replacing tropenol ester with a safer intermediate. While it is the safest course of action, there where it cannot be taken, biological monitoring can be very helpful in raising awareness about exposure to toxic substances, including the new ones that have not been studied for their adverse potential.

Effects of Visually Induced Motion Sickness on Emergency Braking Reaction Times in a Driving Simulator.

OBJECTIVE: The study explores associations of visually induced motion sickness (VIMS) with emergency braking reaction times (RTs) in driving simulator studies. It examines the effects over the progression of multiple simulated drives. BACKGROUND: Driving simulator usage has many advantages for RT studies; however, if it induces VIMS, the observed driving behavior might deviate from real-world driving, potentially masking or skewing results. Possible effects of VIMS on RT have long been entertained, but the progression of VIMS across simulated drives has so far not been sufficiently considered. METHOD: Twenty-eight adults completed six drives on 2 days in a fixed-base driving simulator. At five points during each drive, pedestrians entered the road, necessitating emergency braking maneuvers. VIMS severity was assessed every minute using the 20-point Fast Motion Sickness Scale. The progression of VIMS was considered in mixed model analyses. RESULTS: RT predictions were improved by considering VIMS development over time. Here, the relationship of VIMS and RT differed across days and drives. Increases in VIMS symptom severity predicted more prolonged RT after repeated drives on a given day and earlier within each drive. CONCLUSION: The assessment of VIMS in RT studies can be beneficial. In this context, VIMS measurements in close temporal proximity to the behaviors under study are promising and offer insights into VIMS and its consequences, which are not readily obtainable through questionnaires. APPLICATION: Driving simulator-based RT studies should consider cumulative effects of VIMS on performance. Measurement and analysis strategies that consider the time-varying nature of VIMS are recommended.

Blue-yellow dyschromatopsia in toluene-exposed workers.

PURPOSE: To evaluate the effects of a chronic occupational exposure to toluene on color vision. METHODS: Color vision was tested in 51 workers exposed to pure toluene and in 51 matched control subjects. Current exposure was determined by biological monitoring. Blood samples were taken at the end of a Friday shift. Color vision ability was assessed using the Ishihara plates (to screen for congenital dyschromatopsia), the Farnsworth panel D-15 test, the Lanthony panel D-15 desaturated test, the Velhagen plates, and the Standard Pseudoisochromatic Plates Part 2. RESULTS: Median toluene concentration was 1.59 mg/l (quartiles 0.78 and 2.65). The whole group of workers did not perform worse than the controls. The same applies to 20 printers, who regularly assessed hues. Assessed with the most sensitive Lanthony panel D-15 desaturated test, color vision of 24 permanently exposed assistants was impaired (median color confusion index of the 1st eyes 1.08 vs. 1.02, p < 0.02; 2nd eyes 1.08 vs. 1.0, p < 0.05; sign test). The assistants made almost exclusively blue-yellow errors. The other color vision tests did not reveal any differences between the groups. CONCLUSION: Changes in the retina are a possible explanation for the observed blue-yellow dyschromatopsia.

Pressure pain thresholds: Subject factors and the meaning of peak pressures.

BACKGROUND: The assessment of pressure pain has become an integral part in pain research. The distribution of pressure under a plunger can be uneven. However, measurements based on conventional devices show the applied force or mean pressure, failing to take local pressure peaks into account. Our main question was whether peak pressures under the probe are responsible for pain onset. METHODS: A force-controlled algometer was fitted with a newly developed pressure-indicating film. Pressure pain thresholds (PPTs) of 100 healthy subjects (57 men, age 18-66 years) were assessed at 29 sites across the body. Each site was measured three times, nonconsecutively and presented in randomized order. Forty subjects were manual labourers. RESULTS: Pressure distributions on hard tissue (bone) were more heterogeneous and showed more prominent peaks beneath the probe when reaching the PPT. Soft tissue (e.g. muscle) created a distinct distribution, with higher pressure especially around the corners of the probe. A high variability of PPTs between subjects and different measurement sites was observed. Men as well as manual labourers had comparatively higher adjusted pressure pain thresholds (force and pressure). CONCLUSIONS: Peak pressures could be relevant for pain onset and should be accounted for in mechanical pain studies. The probe, indentation depth and tissue properties have a major impact on pressure distributions and may therefore affect the perception of pressure pain. Due to higher intra-individual differences regarding peak pressures at the spinous processes, breastbone, forehead and abdomen caution are needed when interpreting those sites. SIGNIFICANCE: This study adds some important considerations for the use of pressure algometers. It was found that during pressure pain thresholds readings distinct peak pressure profiles could arise, which may influence the perception of pain. Peak pressure could be another contributing factor, which may explain some of the high variability in pressure pain readings.

An acute exposure to ozone impairs human olfactory functioning.

INTRODUCTION: Ozone is a ubiquitous and irritant gas. We questioned whether an acute exposure to 0.2 ppm ozone impaired olfactory functioning. METHODS: Healthy, normosmic subjects were exposed according to a parallel group design either to 0.2 ppm ozone (n = 15) or to sham (n = 13) in an exposure chamber for two hours. Possible irritating effects were assessed by questionnaire (range 0-5). The detection threshold of n-butanol was measured with the Sniffin' Sticks test before and after exposure. Olfactory thresholds were logarithmized and a two-way analysis of variance (ANOVA) with repeated measurements was carried out to test the effects of exposure (ozone vs. sham) and time (before vs. after exposure). Additionally, nasal secretions were taken at a preliminary examination and after exposure to determine interleukins 1ß and 8. RESULTS: No irritating effects to the upper airways were observed. In the ozone group, the median score for cough increased from 0 to 2 at the end of exposure (sham group 0 and 0, respectively, p < 0.001). The ANOVA showed a main effect for ozone exposure (F (1, 26) = 27.6, p = 0.0002), indicating higher olfactory thresholds in the ozone group. Concentrations of interleukins in nasal secretions did not increase following ozone exposure. CONCLUSIONS: This study shows a clear impairment of olfactory functioning following an acute exposure to 0.2 ppm ozone.

Measuring mechanical pain: the refinement and standardization of pressure pain threshold measurements.

Pain thresholds are widely used in behavioral research, but unlike other pain modalities, a standardized assessment of pressure pain remains a challenge. In this research, we describe the application of an automatic pressure algometer with a linear increase in force. Ergonomically designed fixation devices were developed to increase the accuracy and to shorten the time of each measurement. Ten healthy volunteers were included in a pilot study to test the algometry method. Pressure pain thresholds (PPTs) were investigated over 2 experimental days in three nonconsecutive runs at 29 measurement sites. During the experiment, subjects reported their subjective sleepiness, level of state-anxiety, psychological status and the perceived pain intensity of each measurement. Pain intensity ratings indicate that instructions were followed. State-anxiety and subjective sleepiness levels were low throughout the experiment. The method has proven to be suitable for standardized PPT measurements across the body in an ergonomic, safe, and user-friendly fashion.

Effect of nighttime aircraft noise exposure on endothelial function and stress hormone release in healthy adults.

AIMS: Aircraft noise disturbs sleep, and long-term exposure has been shown to be associated with increases in the prevalence of hypertension and an overall increased risk for myocardial infarction. The exact mechanisms responsible for these cardiovascular effects remain unclear. METHODS AND RESULTS: We performed a blinded field study in 75 healthy volunteers (mean age 26 years), who were exposed at home, in random order, to one control pattern (no noise) and two different noise scenarios [30 or 60 aircraft noise events per night with an average maximum sound pressure level (SPL) of 60 dB(A)] for one night each. We performed polygraphy during each study night. Noise caused a worsening in sleep quality (P < 0.0001). Noise60, corresponding to equivalent continuous SPLs of 46.3 dB (Leq) and representing environmental noise levels associated with increased cardiovascular events, caused a blunting in FMD (P = 0.016). As well, although a direct comparison among the FMD values in the noise groups (control: 10.4 ± 3.8%; Noise30: 9.7 ± 4.1%; Noise60: 9.5 ± 4.3%, P = 0.052) did not reach significance, a monotone dose-dependent effect of noise level on FMD was shown (P = 0.020). Finally, there was a priming effect of noise, i.e. the blunting in FMD was particularly evident when subjects were exposed first to 30 and then to 60 noise events (P = 0.006). Noise-induced endothelial dysfunction (ED) was reversed by the administration of Vitamin C (P = 0.0171). Morning adrenaline concentration increased from 28.3 ± 10.9 to 33.2 ± 16.6 and 34.1 ± 19.3 ng/L (P = 0.0099). Pulse transit time, reflecting arterial stiffness, was also shorter after exposure to noise (P = 0.003). CONCLUSION: In healthy adults, acute nighttime aircraft noise exposure dose-dependently impairs endothelial function and stimulates adrenaline release. Noise-induced ED may be in part due to increased production in reactive oxygen species and may thus be one mechanism contributing to the observed association of chronic noise exposure with cardiovascular disease.

Further development of a commercial driving simulation for research in occupational medicine.

OBJECTIVES: The purpose of this study was to refine a commercial car driving simulation for occupational research. As the effects of ethanol on driving behavior are well established, we choose alcohol as a test compound to investigate the performance of subjects during simulation. MATERIALS AND METHODS: We programmed a night driving scenario consisting of monotonous highway and a rural road on a Foerst F10-P driving simulator. Twenty healthy men, 19-30 years, participated in a pilot study. Subjects were screened for simulator sickness, followed by training on the simulator one hour in total. Experiments were performed in the morning on a separate day. Participants were randomized into either an alcoholized or a control group. All subjects drove two courses consisting of highway and rural road and were sober for the first course. During a 1 h break the ethanol group drank an alcoholic beverage to yield 0.06% blood alcohol concentration (BAC). Generalized linear mixed models were used to analyze the influence of alcohol on driving performance. Among others, independent variables were Simulator Sickness Questionnaire scores and subjective sleepiness. RESULTS: Subjects did not experience simulator sickness during the experiments. Mean BAC before the second test drive was 0.065% in the mildly intoxicated group. There was no clear-cut difference in the number of crashes between 2 groups. BAC of 0.1% would deteriorate mean braking reaction time by 237 ms (SE = 112, p < 0.05). Ethanol slightly impaired the tracking in the right-hand curves (p = 0.058). Braking reaction time improved by 86 ms (SE = 36, p < 0.05) for the second test drive, indicating a learning effect. CONCLUSIONS: In sum, a clear ethanol effect was observed in the driving simulation. This simulation seems suitable for occupational research and produces little simulator sickness. Controlling for possible learning effects is recommended in driving simulation studies.

The Candy Smell Test in clinical routine.

BACKGROUND: The "Candy Smell Test" (CST) has been introduced as a new testing method for the evaluation of the human sense of smell. In contrast to other established orthonasal smell tests, the CST addresses the retronasal application of odors, typical for food aroma effects during mastication and swallowing. The aim of this study was to evaluate the CST in a clinical setting in patients with olfactory dysfunction and normal controls against the Sniffin' Sticks test. Furthermore, cutoff points for normal and pathological results in the CST should be determined. METHODS: The olfactory performance of 96 patients presenting with olfactory disorders and 71 healthy controls was evaluated with the CST-comprised of 23 different aromatized smell candies and the extended Sniffin' Sticks test (threshold, discrimination, and identification). The control group was gender matched but included also younger persons. RESULTS: The tested subjects could easily understand the procedures and were motivated to participate. The CST correlated well with the Sniffin' Sticks for all tested subjects and for patients (n = 96) and controls (n = 71). The proposed cutoff value to differentiate normosmia from hyposmia in the CST was a score of <16 (i.e., 16 correctly identified odors) of 23. A score below 13 in the CST was the cutoff value for anosmia. CONCLUSION: The CST is an easy-to-handle reliable tool to investigate retronasal olfaction suited for clinical determination of normosmia, hyposmia, and ansomia. In addition, it can be used for investigation where self-application is necessary such as in large survey studies.

The impact of solvent mixtures on neurobehavioral performance: conclusions from epidemiological data.

The review of epidemiological studies investigating the neurobehavioral effects of occupational exposure to solvent mixtures sought to contribute to the following issues: (1) Identification of affected cognitive and motor functions. (2) Identification of sensitive neuropsychological tests. (3) Analysis of exposure-effect relationships. The approach was based on the meta-analytical method of effect size estimates. Fifty-three groups from occupational studies were included in the meta-analysis. Forty-eight neuropsychological performance variables could be analyzed as they were included in at least three studies. Seventeen articles provided detailed information on the constituents of mixtures, thereby enabling the computation of an exposure index that allowed the comparison of different mixtures. Significant negative effect sizes were obtained for 12 test variables measuring attention, memory, motor performance and constructional abilities. The greatest proportion of lower performance scores in the exposed groups was shown by different tests of attention: significant effect sizes between d=-0.16 and -0.46 were calculated. Tests of cognitive processing speed, response alternation and inhibition seemed to be sensitive tools for the detection of poorer performance. Exposure-effect relationships were mainly characterized by inconsistent patterns. Crude and inappropriately calculated exposure measures were blamed for this outcome. A healthy worker effect was suggested more consistently: studies examining groups with longer exposure duration obtained smaller effect sizes. Indications of confounding were observed; however, they did not seem sufficient to question consistent effect size patterns. Paying greater attention to the measurement of exposure and including measures of confounding is advisable for future studies and would enhance the explanatory power of cross-sectional studies and meta-analyses.

Early stress response of human nasal respiratory epithelia after exposure to 1-methoxypropanol-2.

To evaluate the impact of 1-methoxypropanol-2 (MEP) for the stimulation of an inflammatory response in human respiratory mucosa, we exposed 22 primary cell cultures of nasal respiratory epithelia of healthy individuals to MEP concentrations at the level of the German MAK-value (100 ppm) and to the 10-fold concentration (1000 ppm). After 4 and 24h we analyzed the transcription of TNF-alpha, IL-1beta, IL-6, IL-8, MCP-1, GMCSF, Cox-1 and Cox-2 by quantitative PCR as well as the release of the respective cytokines by ELISA. At both MEP concentrations we observed a significant increase of TNF-alpha-, IL-1beta-, IL-6- and Cox-2-transcripts after 4h. After 24h cytokine transcription of TNF-alpha, IL-1beta and IL-6 was normalized, but Cox-2 remained elevated. On the protein level IL-1beta as well as granulocyte macrophages colony stimulating factor (GM-CSF) were decreased after 4h or 24h and uniquely IL-8 levels were increased after 4h. Our data suggest that MEP induces the transcription of genes encoding proinflammatory cytokines and mediators but largely not translation of those. Considering these in vitro data, existing exposure limits seem to be safe with respect to inflammatory responses of the upper respiratory tract. However, the effects of long-term exposures to MEP should be watched closely.

mRNA-induction and cytokine release during in vitro exposure of human nasal respiratory epithelia to methyl methacrylate.

BACKGROUND: Methyl methacrylate (MMA) has been reported to cause histopathological changes in rodent nasal epithelium after inhalation challenges. Data in humans are lacking. METHODS: In this in vitro design 22 primary cell cultures taken from inferior turbinate tissue of healthy individuals were exposed to MMA concentrations of 50 ppm (German MAK-value) and 200 ppm. mRNA expression and cytokine release of inflammatory mediators were quantified after 4h and after 24h. Controls were exposed to synthetic air. Q-PCR analysis was performed for TNF-alpha, IL-1beta, IL-6, IL-8, MCP-1, GMCSF, Cox-1 and Cox-2. ELISA assays were performed from culture supernatants for TNF-alpha, IL-1beta, IL-6, IL-8, MCP-1 and GMCSF. RESULTS: Acute inductions of mRNA after 4h were observed for TNF-alpha, IL-1beta, IL-6, IL-8 and MCP-1 at 50 ppm. ELISA analysis of the described parameters did not reveal any significant upregulations at both concentrations after both 4h and 24h. CONCLUSIONS: The obtained data suggest that exposure of human respiratory epithelia in vitro to 50 ppm and to 200 ppm of MMA does not induce lasting upregulation of the inflammatory mediators measured in this study. The exposure limit of 50 ppm appears safe following these results obtained from human respiratory epithelia.

mRNA induction and cytokine release of inflammatory mediators during in vitro exposure of human nasal respiratory epithelia to acetaldehyde.

Acetaldehyde has been shown to be cytotoxic and carcinogenic to the upper respiratory tract epithelium of rodents following long-term exposure. Most animal studies have concentrated on carcinogenicity and DNA-protein cross-link formation, while less is known about potential dose- and time-dependent induction of aldehyde-induced rhinitis in humans. In this in vitro study, 22 primary cell cultures established from inferior turbinate tissue of healthy individuals were exposed to acetaldehyde concentrations of 50 (German MAK value) or 500 ppm for 4 or 24 h. mRNA expression and protein levels of cytokines and other inflammatory mediators were quantified at the end of the 4- and 24-h exposures. Controls were exposed to synthetic air. Quantitative polymerase chain reaction (Q-PCR) analysis was performed for interleukin (IL)-6, IL-8, IL-1beta, monocyte chemotactic protein (MCP)-1, tumor necrosis factor (TNF)-alpha, GMCSF, Cox-1, and Cox-2. Enzyme-linked immunosorbent assay (ELISA) was performed from culture supernatants for IL-6, IL-8, IL-1beta, MCP-1, TNF-alpha, and GMCSF. Significant inductions of IL-1beta, TNF-alpha, and Cox-1 and Cox-2 mRNA were observed following exposure to > or =50 ppm acetaldehyde for 4 h. IL-6 and MCP-1 were also induced following a 4-h exposure to 500 ppm acetaldehyde. For all these parameters, effects were significantly stronger at the higher concentration. After 24-h of exposure only Cox-2 remained significantly elevated at 500 ppm but not at 50 ppm, while all other mediators had been downregulated. The obtained data suggest that with exposure to 500 ppm and remarkably also at the level of the occupational exposure limit of 50 ppm, an immediate transient upregulation of inflammatory mediator mRNA is induced, possibly leading to subclinical inflammatory effects.

External and internal exposure of wine growers spraying methyl parathion.

Organophosphates, used in agriculture, are readily absorbed through the skin. We investigated the relationship between dermal and inhalative methyl parathion exposure and the plasma levels. Twenty-three healthy wine growers sprayed the insecticide for 50 min. Fluorescent brilliant sulfoflavin was added to the spraying fluids and filter papers were fixed on the subjects. The filter papers were used to evaluate the amount of brilliant sulfoflavine on the unprotected skin fluorometrically. Inhalative exposure was measured with personal air sampler. Plasma concentrations of methyl parathion and its metabolite methyl paraoxon were determined with gas chromatography. Cholinesterase activity in serum and erythrocytes was measured before and after exposure. Some wine growers wore protective clothes, none protective gloves. Dermal exposure ranged up to 12,044 microg, inhalative to 22 microg. Maximum plasma concentration of methyl parathion was 12.1 microg/l. Methyl paraoxon was not detectable. Cholinesterase activity did not decrease. Dermal exposure correlated with the methyl parathion plasma level (Spearman's rho=0.72, p<0.001). In conclusion, dermal exposure exceeded inhalative exposure considerably. Measuring dermal deposition with the brilliant sulfoflavin technique may provide a good estimate of the internal load with methyl parathion. Preventive measures should be improved as toxic effects of repeated exposure to low doses of methyl parathion cannot be excluded.

Acute effects of an organic solvent mixture on the human central nervous system.

OBJECTIVES: At workplaces, organic solvents are often used as mixtures. Nevertheless, there is limited knowledge of their acute effects on human central nervous system. Here we report the effects of a toluene-acetone mixture. METHODS: In a parallel design, subgroups of 12 healthy men each were exposed to a mixture containing 25 ppm acetone and 250 ppm toluene or to air (control) in an exposure chamber for 4.5 hours. Concentrations corresponded to the German TLV (TRGS 403). Concentrations of toluene and acetone in venous blood were measured by headspace gas chromatography. Subjects were sedentary. The following tests were performed before and at the end of exposure: Questionnaires, simple reaction time, vigilance, quantitative analysis of EEG with open and closed eyes and during the Color Word Stress test, and visual evoked potentials (VEP). RESULTS: Blood levels were 0.14 (+/- 0.04 SD) mg toluene/l and 5.43 (+/- 1.37 SD) mg acetone/l at the end of solvent exposure. Scores of neurotoxic and irritating symptoms were not elevated during solvent exposure. Exposed subjects performed as well as control subjects on the simple reaction time test and on the vigilance test, neither reaction time nor number of hits differed significantly. A general linear model on log transformed spectral power values showed insignificant changes in EEG. In the alpha subset2-band an average reduction to 86 % was observed in exposed as compared to non exposed subjects with closed eyes, a reduction to 88 % in the theta-band with open eyes, and a reduction to 92 % in the theta-band during the Color Word Stress test. VEP P 100 latencies and amplitudes did not change. CONCLUSION: The mixture consisting of toluene and acetone did not cause any adverse acute effect. With respect to EEG data, possible subclinical effects on central nervous system cannot be excluded.

Acute effects of low doses of methyl parathion on human EEG.

Biological monitoring of workers exposed to organophosphates consists mainly of measuring serum or erythrocyte cholinesterase activity. However, animal experiments and a field study suggest that quantitative analysis of EEG may be more sensitive. In a parallel group design, 25 farmers were investigated, spraying methyl parathion or water for 50min. EEG was recorded before and after spraying. Serum and erythrocyte cholinesterase activity was compared with intraindividual pre-exposure values. Plasma methyl parathion concentrations ranged up to 12.1µg/l, methyl paraoxon was not detectable. Based on plasma concentrations, two exposed subgroups were defined. In EEG recorded with closed eyes, α(1)-power increased insignificantly (Kruskal-Wallis test) in both subgroups. ß(1)-power was enhanced in both exposed subgroups, reaching significance (p≤0.05) at five of 17 electrodes. Spearman's rank correlation showed a significant association between methyl parathion plasma concentration and the median of ß(1)-band power of the 17 electrodes (rho=0.48, p=0.015). Cholinesterase activity did not decrease. On a group basis, EEG is possibly more sensitive than cholinesterase. EEG changes suggest brain cholinesterase inhibition following low exposure to methyl parathion.

Acute exposure to 50ppm toluene does not increase sleepiness.

The Pupillographic Sleepiness Test (PST) is a new neurophysiological method to assess sleepiness. In an exposure study to a constant exposure level of 50ppm toluene on 20 healthy men, our aim was to find out, if increased sleepiness could be seen with PST. PST was performed before and after 4.5h of exposure. General complaints were assessed with the Swedish Performance Evaluation System (SPES) self-assessment questionnaire, once before and during exposure. Values obtained during exposure were related to pre-exposure values. Parametric cross-over analysis of logarithmic Pupillary Unrest Index (PUI) values did not show an effect of toluene exposure. In a nonparametric cross-over analysis of SPES-scores a significant increase of the scores of unpleasant smell and irritation to the throat, but not of tiredness was found. In conclusion, acute exposure to 50ppm toluene, corresponding to the German threshold limit value, did not increase sleepiness.

Acute effects of 1,1,1-trichloroethane on human olfactory functioning.

BACKGROUND: Animal experiments indicate that 1,1,1-trichloroethane can cause degeneration of the olfactory epithelium. The effects of 1,1,1-trichloroethane on human odor perception still have not been investigated. The goal of this study was to learn more about acute effects of 1,1,1-trichloroethane. METHODS: Twelve healthy, nonsmoking students were exposed to 200 and 20 ppm (control) 1,1,1-trichloroethane in an exposure chamber for 4 hours according to a crossover design. Olfactory functioning was investigated with the Sniffin' Sticks. The test includes the determination of the detection threshold for n-butanol and an odor identification test. RESULTS: After 1 hour of exposure to 200 ppm 1,1,1-trichloroethane, no effects on olfactory functioning were observed. After 4 hours, the olfactory threshold for n-butanol was slightly (p = 0.04) elevated. CONCLUSION: The threshold shift may be caused by different mechanisms, including inflammation of the olfactory mucosa or degeneration of receptor cells.