Sick leave due to back pain in a cohort of young workers.

PURPOSE: Evidence on risk factors for sick leave from prospective studies in work settings is limited. Furthermore, most available studies focused on workers with substantial low back disorders. These studies consistently report that physical work factors constitute a hindrance to work. However, it remains unclear whether the same risk factors are relevant in workers with less severe conditions or in early phases of the development of back pain. Therefore, this article aims to study risk factors for the occurrence of sick leave due to low back pain (LBP) among young workers with no or a modest history of back pain. METHODS: Participants were 716 young healthcare or distribution workers with no or minimal antecedents of LBP in the year before inclusion. We investigated the role of potential physical, psychosocial and individual risk factors at baseline on the occurrence of sick leave due to LBP 1 year later. To this purpose, we used Cox regression with a constant risk period. RESULTS: Six per cent (95 % CI 4.1-7.6) of the workers reported sick leave 1 year later; they accounted for 12 % of the sick-leave days independent of cause. A non-stimulating psychosocial work environment turned out to be the strongest risk factor for sick leave due to LBP (RR 6.08; 95 % CI 1.42-26.07). Physical factors were not predictive. CONCLUSIONS: In the early phases of back pain and in less severe conditions, the main benefit of interventions lies in targeting the organisation and design of jobs to create a challenging professional environment.

The role of physical workload and pain related fear in the development of low back pain in young workers: evidence from the BelCoBack Study; results after one year of follow up.

AIMS: To study the influence of work related physical and psychosocial factors and individual characteristics on the occurrence of low back pain among young and pain free workers. METHODS: The Belgian Cohort Back Study was designed as a prospective cohort study. The study population of this paper consisted of 716 young healthcare or distribution workers without low back pain lasting seven or more consecutive days during the year before inclusion. The median age was 26 years with an interquartile range between 24 and 29 years. At baseline, these workers filled in a questionnaire with physical exposures, work related psychosocial factors and individual characteristics. One year later, the occurrence of low back pain lasting seven or more consecutive days and some of its characteristics were registered by means of a questionnaire. To assess the respective role of predictors at baseline on the occurrence of low back pain in the following year, Cox regression with a constant risk period for all subjects was applied. RESULTS: After one year of follow up, 12.6% (95% CI 10.1 to 15.0) of the 716 workers had developed low back pain lasting seven or more consecutive days. An increased risk was observed for working with the trunk in a bent and twisted position for more than two hours a day (RR 2.2, 95% CI 1.2 to 4.1), inability to change posture regularly (RR 2.1, 95% CI 1.3 to 3.5), back complaints in the year before inclusion (RR 1.7, 95% CI 1.1 to 2.8), and high scores of pain related fear (RR 1.8, 95% CI 1.0 to 3.1). Work related psychosocial factors and physical factors during leisure time were not predictive. CONCLUSION: This study highlighted the importance of physical work factors and revealed the importance of high scores of pain related fear in the development of low back pain among young workers.

Cadmium: a possible etiological factor in peripheral polyneuropathy.

Uncovering the exact cause of polyneuropathies seems to be impossible in up to 24% of the cases. Experimental studies have shown that cadmium (Cd), which is a well-known occupational and environmental hazard, can be a potent neurotoxicant for the peripheral nervous system. Moreover, Cd has a half-life of more than 15 years in humans. We hypothesize that older workers may be more susceptible to an increased Cd body burden, and may develop a peripheral polyneuropathy (PNP) over time. A blinded epidemiological survey was performed in 13 retired, long-term Cd-exposed workers and 19 age-matched controls. Historical Cd biomonitoring data were available over the last two decades. A neurological clinical examination, nerve conduction studies, and needle EMG were performed, and a standardized questionnaire was given to evaluate polyneuropathy complaints. If two of the following four criteria, i.e. complaints of polyneuropathy, neurophysiological changes compatible with polyneuropathy, distal symmetrical areflexia, or distal symmetrical anesthesia for vibration sense, temperature or blunt-sharp discrimination were present, the diagnosis of PNP was made. Two (11%) of the control and seven (54%) of the retired Cd workers met the PNP criteria OR: 9.92 (95%CI 1.60-61.6), Fisher exact test p=0.015. The existence of a polyneuropathy was related to the level of the Cd body burden as reflected by urinary Cd multiple logistic regression p=0.016, OR=1.26, (95%CI, 1.04-1.51), but not to blood lead (p=0.352). Our findings favour the hypothesis of a promoting role of increased cadmium body burden in the development of PNP at older age.

Comparative urinary excretion of ethoxyacetic acid in man and rat after single low doses of ethylene glycol monoethyl ether.

Male rats were given a single oral dose of ethylene glycol monoethyl ether (EGEE), the dose ranging from plausible human exposures (0.5-1 mg/kg) to doses reported in the literature (100 mg/kg). Urinary excretion of ethoxyacetic acid (EAA) and its glycine conjugate was followed up to 60 h after dosing and compared to data of experimentally exposed human volunteers. In rats, the mean elimination half-life of free as well as conjugated EAA was 7.2 h for all doses. EAA was excreted partly as a glycine conjugate (on average 27%), the extent of conjugation being independent of the dose. The conjugation with glycine showed a clearly diurnal variation, the lowest extent being found during the night. The relative amount of EGEE recovered in urine as EAA was only 13.4% for the lowest dose, but increased as the administered dose of EGEE was higher, indicating that EGEE was metabolised at least in two parallel pathways of which one pathway becomes saturated at relatively low doses. In man, urinary excretion of EAA for equivalent low doses of EGEE differed from that in the rat by a longer elimination half-life (mean 42 h), by the absence of EAA conjugates and by a higher recovery.

Experience with a vocabulary test for workers previously and still exposed to styrene.

OBJECTIVES: This study examined the possible influence of styrene exposure on the results of vocabulary tests because verbal ability is assumed to be relatively resistant to the toxic effects of organic solvents and short vocabulary tests are used as "hold tests" in many neurobehavioral epidemiologic studies, METHODS: To evaluate the chronic neurotoxic effects of styrene, a vocabulary test was administered to a group of still-exposed workers (N=27) and an earlier exposed group of workers (N=90). A self-administered questionnaire was filled out on life events, general health, educational level, and amount of education. The still-exposed group had a mean exposure duration of 4700 hours, and that for the formerly exposed group was 3610 hours. RESULTS: The vocabulary score of the still-exposed group was significantly lower [12.5 (SD 2.9, range 6-18)] than that of their former colleagues [14.3 (SD 3.4, range 8-22)], even though they originally belonged to the same group and had done the same tasks. The exposure duration explained a significant part of the vocabulary results, resulting in decreasing vocabulary scores even when the influence of years of education and age was taken into account. Even after correction for the possible influence of having been laid off or staying at work, there remained a negative influence on the vocabulary score for the duration of styrene exposure. CONCLUSIONS: The use of short vocabulary tests as hold tests in cross-sectional studies of solvent-exposed workers may be limited as they seem to lack the essential toxicity-independent property.

Field study of the urinary excretion of ethoxyacetic acid during repeated daily exposure to the ethyl ether of ethylene glycol and the ethyl ether of ethylene glycol acetate.

The urinary excretion of ethoxyacetic acid (EAA) was studied in a group of five women daily exposed to the ethyl ether of ethylene glycol (EGEE) and the ethyl ether of ethylene glycol acetate (EGEE-Ac) during 5 d of normal production and 7 d after a 12-d production stop. The mean combined exposure concentration of EGEE and EGEE-Ac (expressed in equivalent weight of EGEE) was 14.0 mg/m3 with occasional slight excursions above the current Belgian occupational exposure limit. The daily combined exposure profiles for EGEE and EGEE-Ac were rather constant during the first observation period, but they tended to decrease during the last week. The urinary EAA excretion clearly increased during the work week. Over the weekends the elimination was far from complete, and even after a prolonged nonexposure period of 12 d traces of the metabolite were still detectable. Based on the observations from the first period, a good linear correlation (r = 0.92) was found between the average exposure over 5 d (14.4 mg/m3) and the EAA excretion at the end of the week (105.7 mg/g creatinine). An EAA estimate of 150 +/- 35 mg/g was found to correspond with repeated 5-d full-shift exposures to the respective occupational exposure limit of EGEE (19 mg/m3) or EGEE-Ac (27 mg/m3).

Exposure and inhalation risk assessment in an aluminium cast-house.

To date the exposure, absorption and respiratory health effects of cast-house workers have not been described since most studies performed in the aluminium industry are focused on exposure and health effects of potroom personnel. In the present study, we assessed the external exposure and the absorbed dose of metals in personnel from the aluminium cast house. This was combined with an evaluation of respiratory complaints and the lung function of the personnel. 30 workers from an aluminium casting plant participated and 17 individuals of the packaging and distribution departments were selected as controls. The exposure was assessed by the quantification of total inhalable fume with metal fraction and by the determination of urinary aluminium, chromium, beryllium, manganese and lead concentration. Carbon monoxide (CO), carbon dioxide (CO2), aldehydes and polyaromatic hydrocarbons and man-made mineral fibres concentration were assessed as well. In order to evaluate their respiratory status each participant filled out a questionnaire and their lung function was tested by forced spirometry. Total inhalable fume exposure was maximum 4.37 mg m(-3). Exposure to the combustion gases, man-made mineral fibres and metal fume was well below the exposure limits. Beryllium could not be detected in the urine. The values of aluminium, manganese and lead in the urine were all under the respective reference value. One individual had a urinary chromium excretion above the ACGIH defined biological exposure index (BEI) of 30 microg g(-1) creatinine. There was no significant difference in any of the categories of the respiratory questionnaire and in the results of the spirometry between cast house personnel and referents (Chi-square, all p > 0.05). Exposure in cast houses seem to be acceptable under these conditions. However, peak exposure to fumes cannot be excluded and the potential risk of chromium and beryllium exposure due to the recycling of aluminium requires further attention.

Urinary excretion of ethoxyacetic acid after experimental human exposure to ethylene glycol monoethyl ether.

Ten healthy male subjects were exposed to ethylene glycol monoethyl ether (EGEE) under various conditions of exposure concentration and physical workload and their urinary excretion of ethoxyacetic acid was followed up for 42 hours. Maximal excretion of ethoxyacetic acid was reached three to four hours after the end of the four hour exposure period. Afterwards, ethoxyacetic acid excretion declined slowly with a biological half life of 21-24 hours. Ethoxyacetic acid excretion increased as the uptake of EGEE increased as a consequence of higher exposure concentration or pulmonary ventilation rate during physical exercise. On average, 23.1 +/- 6.3% of EGEE was recovered as ethoxyacetic acid within 42 hours and the recovery did not change as the uptake of EGEE increased. Quantitative relations between ethoxyacetic acid excretion and EGEE uptake were obtained and the relevance of ethoxyacetic acid excretion as a measure for exposure to EGEE is discussed.

Respiratory uptake and elimination of ethylene glycol monoethyl ether after experimental human exposure.

Ten male volunteers were exposed to ethylene glycol monoethyl ether (EGEE) under various conditions of exposure concentration and physical workload. Steady state levels of retention, atmospheric clearance, and rate of uptake were reached immediately after the start of the exposure period for all experimental conditions. Retention was high (64% in resting condition) and increased as physical exercise was performed during exposure. Atmospheric clearance increased as the pulmonary ventilation rate increased. The rate of uptake was higher as exposure concentration or pulmonary ventilation rate, or both, increased. Individual uptake appeared to be governed mainly by transport mechanisms (pulmonary ventilation or cardiac output or both) and not by anthropometric factors. Respiratory elimination of unchanged EGEE accounted for less than or equal to 0.4% of the total body uptake. Postexposure breath concentrations declined rapidly during the first minutes after cessation of exposure, after which a much slower decrease was observed. This slow decrease could be described by a regression equation containing two exponential terms indicating that at least two pharmacological compartments are concerned.

Exposure to ethylene glycol ethers and spermatogenic disorders in man: a case-control study.

A case-control study was conducted among first time patients at a clinic for reproductive disorders. The study group consisted of 1019 cases, defined as patients diagnosed infertile or subfertile on the basis of a spermiogram and 475 controls who were diagnosed as normally fertile by the same procedure. Possible exposure to ethylene glycol ethers was assessed by the presence of the urinary metabolites methoxyacetic acid (MAA) and ethoxyacetic acid (EAA) respectively for 2-methoxyethanol and 2-ethoxyethanol or their acetates. In total, EAA was detected in 39 cases and six controls, with a highly significant odds ratio of 3.11 (p = 0.004). On the other hand, MAA was only found in one case and two controls. The presence of EAA in urine proved to be strongly associated with exposure to preparations containing solvents, especially paint products, and with some groups of occupations, the most important of which were also directly or possibly connected with paint products. The absence of a significant correlation between the concentration of urinary EAA and the various measures of sperm quality could be explained by the expected latent period between exposure and observed effects. Other temporal aspects of the relation between exposure as judged from the presence of urinary EAA and diagnosis are also discussed.

Experimental human exposure to ethylene glycol monomethyl ether.

The uptake of EGME and the urinary excretion of its major metabolite (MAA) was studied in seven male volunteers during experimental exposure to EGME at rest. The exposure concentration was set at 16 mg/m3, the present Threshold Limit Value. A high retention (0.76) remained unchanged during the 4-h exposure period. In combination with a constant pulmonary ventilation and a fixed exposure concentration this resulted in an uptake rate that showed no significant variation in time. The total amount of EGME inhaled corresponded to a dose of only 0.25 mg/kg. During and up to 120 h after the start of the exposure, MAA was detected in the urine. The elimination half-life was on average 77.1 h. The total amount of MAA excreted was calculated by extrapolation and averaged 85.5% of the inhaled EGME. The pharmacokinetic data are compared with those obtained from other human exposure studies to ethylene glycol ethers (EGEE and EGBE).

An improved method for the determination in urine of alkoxyacetic acids.

A sensitive and specific method for the determination in urine of alkoxyacetic acids, the metabolites of ethylene glycol monoalkyl ethers, was developed by combining the advantages of two previously described methods. The acids were determined gas chromatographically as their pentafluorobenzylesters. The alkylation with pentafluorobenzylbromide was performed after dissolving the dry residue of lyophilized urine in methanol. Quantitative derivatization was obtained when the urinary pH was adjusted to pH 7.0, when the reagent concentration was 5% v/v, and when the reaction mixture was heated at 90 degrees C for 3 h. Sample clean-up was performed by adding bidistilled water and the esters were extracted with methylene chloride with high yields (95%). Alkoxyacetic acid concentrations in the range of 0.1 to 200 mg/l could be determined with an average imprecision of +/- 3.5%.

Pulmonary absorption and elimination of ethylene glycol monoethyl ether acetate in man.

Ten male volunteers were exposed to ethylene glycol monoethyl ether acetate (EGEE-Ac) under various conditions of exposure and physical workload. As exposure proceeded, retention, atmospheric clearance, and uptake rate declined slowly to reach steady state levels after three to four hours. Retention increased as a consequence of higher exposure concentrations and of physical workload performed during exposure. Uptake rate was higher as exposure concentration or pulmonary ventilation rate, or both, increased. Subject related factors such as pulmonary ventilation, cardiac output, height, and body fat content also determined individual uptake. During exposure, partial respiratory elimination of EGEE was observed. This finding confirms the hypothesis that EGEE-Ac is first converted to EGEE by (plasma) esterases. The amount of EGEE eliminated at steady state levels correlated more with uptake rate of EGEE-Ac than with exposure concentration. Respiratory elimination of unmetabolised EGEE-Ac accounted for less than or equal to 0.5% of total body uptake. The elimination curves were biexponential indicating that at least two pharmacological compartments are involved. Postexposure breath concentrations were higher as total body uptake increased. Several observations may indicate that the hydrolysis of the ester moiety of EGEE-Ac is hindered by the presence of the natural esterase substrates. With increasing plasma concentrations, however, EGEE-Ac competed more favourably for the available esterase.

Survey of ethylene glycol ether exposures in Belgian industries and workshops.

From 1983 onward, 2654 air samples from 336 different plants from the northern part of Belgium were analyzed for the presence of ethylene glycol ethers. One or more ethylene glycol ethers were detected in 262 air samples (9.9%) covering 78 plants or small establishments (23.2%) from a wide variety of industries. Ethylene glycol ethers were mainly present in establishments or operations where printing pastes, inks, paints and varnishes were used. About one third of the air samples covered various other industries. Car repair shops took a major part of this group. It was not always clear, however, in what precise operation the glycol ethers were involved. The ethylene glycol ethers most frequently identified were ethylene glycol monoethyl ether (EGEE) and its acetate (EGEE-Ac). Furthermore, ethylene glycol monomethyl ether (EGME), its acetate (EGME-Ac), and ethylene glycol monobutyl ether (EGBE) also were present in a large number of air samples. The glycol ethers were not distributed equally among the various groups of operations. Most exposure levels were far below the respective Threshold Limit Value (TLVs) (approximately less than 0.5 x TLV). About 25% of ethylene glycol concentrations, however, were higher than the current TLV. Most of the excursions were slight to moderate, although in selected cases extremely high concentrations were recorded. The majority of air samples revealed complex mixtures of ethylene glycol ethers with other solvents, the glycol ethers often being minor components. The possible implication of these other solvents on glycol ether toxicity and metabolism is discussed.

Ethoxyacetic acid: a metabolite of ethylene glycol monoethyl ether acetate in man.

Urinary excretion of ethoxyacetic acid during and after exposure to ethylene glycol monoethyl ether acetate (EGEE-Ac) was followed up in ten healthy male volunteers. During exposure to EGEE-Ac, ethoxyacetic acid levels appeared with a half life of 2.3 +/- 0.1 h. Ethoxyacetic acid excretion continued to increase after exposure was discontinued reaching maximal levels three to four hours later. The decline afterwards could generally be described assuming a half life of 23.6 +/- 1.8 h. A second maximum excretion of ethoxyacetic acid, however, was noticed about three hours after the first. Redistribution of EGEE-Ac or ethoxyacetic acid, or both, from a peripheral compartment to the central compartment could explain this observation. Ethoxyacetic acid excretion increased with an increase in the uptake of EGEE-Ac due to higher exposure concentrations or pulmonary ventilation rate during physical exercise. On average 22.2 +/- 0.9% of the absorbed EGEE-Ac was recovered within 42 hours. Recovery did not change with a higher intake of EGEE-Ac. At any time after the exposure, quantitative relations between ethoxyacetic acid excretion rate and absorbed dose of EGEE-Ac were found. Monitoring ethoxyacetic acid excretion may therefore be used as a measure of a single exposure to EGEE-Ac.

Gas chromatographic determination of methoxyacetic and ethoxyacetic acid in urine.

Methoxyacetic acid (MAA) and ethoxyacetic acid (EAA), the major metabolites of, respectively, ethylene glycol monomethyl ether and ethylene glycol monoethyl ether and their acetates, are determined by gas chromatography after extraction from urine and methylation using 2-furoic acid (2-FA) as an internal standard. The mean recoveries (n = 30) from urine of MAA, EAA, and 2-FA are 31.4 +/- 7.0%, 62.5 +/- 13.4%, and 58.4 +/- 8.7%, respectively. The recoveries decreased (p less than 0.001), however, as the total amount of acids increased. Standard curves for MAA and EAA in urine are presented. The detection limits of MAA and EAA are 0.15 and 0.07 mg/l. Intra-assay variation for MAA and EAA was 6.0 +/- 2.5% and 6.4 +/- 2.8% and inter-assay variation was 6.2 +/- 2.2% and 8.9 +/- 2.4%. When volunteers were exposed to air containing ethylene glycol monoethyl ether (20 mg/m3), urinary concentration of EAA rose significantly one hour after the exposure period (2.39 +/- 1.03 v less than or equal to 0.07 mg/l, t = 5.2, p less than 0.005).

Experimental human exposure to carbon disulfide. I. Respiratory uptake and elimination of carbon disulfide under rest and physical exercise.

Six human volunteers were exposed to 10 and 20 ppm carbon disulfide at rest and to 3 and 10 ppm carbon disulfide under a 50 W level of physical exercise during four consecutive periods of 50 min. Every 5 min a sample was taken from the mixed exhaled air in which the concentration of carbon disulfide was determined. It was established that only an apparent steady state was reached during this exposure period. The retention values were established as 0.374 (SD = 0.106; n = 239) for exposure to 10 ppm carbon disulfide at rest and as 0.410 (SD = 0.103; n = 239) for exposure to 20 ppm carbon disulfide at rest. During exposure to 10 ppm and 3 ppm carbon disulfide, combined with a 50 W level of physical exercise, the retention values decreased to 0.286 (SD = 0.083; n = 239) and 0.277 (SD = 0.049; n = 239) respectively. Thereby, the measured individual retention values of carbon disulfide show considerable interindividual differences. The respiratory uptake of carbon disulfide (mg CS2) proved significantly influenced by the amount of body fat estimated from skinfold thickness measurements. The respiratory elimination of carbon disulfide in the exhaled air can be described by means of a two-exponential decay.

Experimental human exposure to carbon disulfide. II. Urinary excretion of 2-thiothiazolidine-4-carboxylic acid (TTCA) during and after exposure.

Six human volunteers were exposed to 10 and 20 ppm carbon disulfide at rest and to 3 and 10 ppm carbon disulfide under a 50 W level of physical exercise during four consecutive periods of 50 min. At the start of the experiments, at the end of the exposure periods and during the post-exposure period, urine was sampled and the concentration of 2-thiothiazolidine-4-carboxylic acid (TTCA) was determined. It was established that only a small percentage, ranging from 0.7 to 2.2% of the absorbed carbon sulfide was transformed into TTCA. The excretion rate of TTCA (mumol TTCA h-1) was found to be the best parameter in evaluating the respiratory uptake of carbon disulfide over a range of 37.9 to 163.3 mg CS2 compared to the urinary concentration of TTCA (mole TTCA ml-1) or the creatinine corrected concentration of TTCA (mmol TTCA mol-1 creatinine). The total amount of TTCA (mumol TTCA) excreted proved to be independent of the urinary flow (ml h-1), the estimates of the individual fatty tissue content and the urinary pH. No correlation was found between the respiratory uptake of carbon disulfide (mg CS2) and the excretion rate of TTCA within each exposure condition of 3, 10 or 20 ppm carbon disulfide, respectively.

Neurobehavioural changes and persistence of complaints in workers exposed to styrene in a polyester boat building plant: influence of exposure characteristics and microsomal epoxide hydrolase phenotype.

OBJECTIVES: To investigate neurobehavioural effects and the persistence of complaints in workers exposed to styrene relative to exposure characteristics and the enzyme microsomal epoxide hydrolase (mEH) activity. METHODS: A cross sectional study was performed in a retrospective cohort of workers of a polyester boat building plant 3 years after the main activity shut down in 1989. Workers still currently exposed to a much lower concentration of styrene in air than before (n=27) and formerly exposed workers (n=90) were compared with matched control workers (n=64). Currently and formerly exposed workers laminated 4700 and 3610 hours on average at mean exposure to styrene concentrations of 148 and 157 mg/m(3) respectively. A structured neurological anamnesis into former and present complaints, the NSC-60 questionnaire, and computer assisted neurobehavioural tests (NES) were administered. The mEH phenotype activity was measured in lymphocytes with a novel gas chromatography-mass spectroscopy (GC-MS) method. RESULTS: For the period before 1989, currently and formerly exposed workers reported more complaints than control workers which related well with the mean exposure to airborn styrene concentration (p=0.03). Most complaints disappeared after the end of exposure, although the chest, equilibrium, and somatic category scores of NSC-60 and the number of workers reporting diminished sense of smell remained increased in formerly exposed workers (p

Nocturnal oxygen desaturation, as assessed by home oximetry, in long-term solvent-exposed workers.

Recent studies have suggested that occupational exposure to solvents may be a cause of sleep apnea. Digital oximetry during one night was performed in solvent-exposed offset printers (n = 21) and in a control group (n = 21), using a Palco 400 Pulse Oximeter. The threshold for recording was set at an arterial oxygen saturation (SaO2) of 90%. Furthermore, computerized neurobehavioral tests (NES) and a solvent-related complaints questionnaire (NSC-60) were administered. The mean exposure time was 15 years (SD = 10). Hygiene measurements revealed a large number of different solvents and a cumulative exposure between 15% and 97% of the "cumulative TLV." The exposed workers had more solvent-related complaints, especially regarding mood (analysis of covariance, P = 0.02), than the nonexposed workers. The neurobehavioral tests indicated that hand-eye coordination was significantly worse in the exposed group (analysis of covariance, P = 0.03). The frequency of nocturnal desaturation was significantly higher in the printers (1.7 events/hr +/- SD = 1.5) than in the controls (0.6 events/hr +/- SD = 1.3) (Mann-Whitney test, P < 0.01). Also, the duration of desaturation was longer in the exposed workers: 3.2 min/hr (SD = 3.2) vs 1.2 min/hr (SD = 2.3) (Mann-Whitney test, P < 0.01). In the analysis of covariance, exposure (P = 0.04) and the interaction between smoking and exposure (P = 0.02) were shown to contribute significantly to the excess of nocturnal desaturation in the exposed. The same was true for the mean duration of desaturation (exposure: P = 0.02 and interaction exposure smoking: P = 0.02). The significant interaction was due to a more pronounced effect of solvent exposure among the nonsmoker group. No relation was found between the excess of complaints or the neuroperformance effects and the oximetry data. These data reinforce the presumption that occupational solvent exposure might contribute to sleep-disordered breathing.