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PubMed1991

Ethanol and food deprivation induced enhancement of hepatotoxicity in rats given carbon tetrachloride at low concentration.

Effects of chronic ethanol consumption and one day food deprivation on the hepatotoxicity of low dose carbon tetrachloride (CCl4; 0 to 100 ppm inhalation for eight hours) in rats were investigated by using biochemical and histopathological methods. Liver malondialdehyde (MDA) contents were significantly increased by exposure to 5 ppm to 50 ppm CCl4 in ethanol treated rats or by exposure to 25 ppm to 50 ppm CCl4 in food deprived rats but not in rats without ethanol or food deprivation. The MDA concentrations reached a maximum at 10 ppm and 50 ppm CCl4 in ethanol treated and food deprived rats, respectively, and decreased to the non-exposed concentration at 100 ppm CCl4. At greater than or equal to 50 ppm CCl4 plasma MDA contents increased significantly only in ethanol treated rats. None of the exposure concentrations influenced plasma glutamic-oxaloacetic transamidase (GOT) and glutamic-pyruvic transaminase (GPT) activities in rats that were only exposed to CCl4 whereas exposure to 10 ppm or higher concentrations combined with ethanol increased both activities. To a lesser extent food deprivation combined with exposure to greater than or equal to 25 ppm CCl4 had the same effect. No histopathological changes were found in the liver of rats exposed to less than or equal to 10 ppm CCl4, and only a few ballooned hepatocytes were seen in centrilobular areas when exposure was 25 ppm or higher. The presence of ballooned and hepatocytes became a regular feature of mid-zonal areas in ethanol treated rats and in the centrilobular areas of food deprived rats after exposure to </= 10 and </=25 ppm CC1(4) respectively. Necrotic hepatocytes were seen in centrilobular areas in liver from ethanol treated and food deprived rats when exposure CC1(4) was >/=25 ppm and >/=50 ppm respectively. These results indicate that consumption of ethanol and food deprivation potentiate CCl(4) induced hepatic damage even at low concentrations of CCl(4) by promoting lipid peroxidation. Thus heavy drinking may be a risk factor for CCl(4) induced hepatic damage even though the CCl(4) concentration is as low as the threshold limit value.

Animals↗
PubMed1992

Chronic neurobehavioural effects of elemental mercury in dentists.

Neurobehavioural tests were performed by 98 dentists (mean age 32, range 24-49) exposed to elemental mercury vapour and 54 controls (mean age 34, range 23-50) with no history of occupational exposure to mercury. The dentists were exposed to an average personal air concentration time weighted average (TWA) of 0.014 (range 0.0007-0.042) mg/m3 for a mean period of 5.5 (range 0.7-24) years and had a mean blood mercury concentration of 9.8 (range 0.6-57) micrograms/l. In neurobehavioural tests measuring motor speed (finger tapping), visual scanning (trail making), visuomotor coordination and concentration (digit symbol), verbal memory (digit span, logical memory delayed recall), visual memory (visual reproduction, immediate and delayed recall), and visuomotor coordination speed (bender-gestalt time), the performance of the dentists was significantly worse than that of the controls. The dentists scored 3.9 to 38.9% (mean 13.9%) worse in these tests. In trail making, digit span, logical memory delayed recall, visual reproduction delayed recall, and bender-gestalt time test scores were more than 10% poorer. In each of the tests in which significant differences were found and in the block design time, the performance decreased as the exposed dose (product of the TWA of air mercury concentrations and the years of exposure) increased. These results raise the question as to whether the current threshold limit value of 0.050 mg/m3 (TWA) provides adequate protection against adverse effects of mercury.

Adult↗
PubMed1992

Dose dependent effects of chronic exposure to toluene on neuronal and glial cell marker proteins in the central nervous system of rats.

The dose dependent effects of chronic exposure to toluene on the neuronal marker proteins (gamma-enolase, calbindin-D28k) and glial cell marker proteins (alpha-enolase, creatine kinase-B, and beta-S100 protein) were investigated in the central nervous system (CNS) of rats. Three groups of animals were exposed to 100 ppm, 300 ppm, or 1000 ppm toluene vapour eight hours a day, six days a week for 16 weeks. The contents of the marker substances were determined with enzyme immunoassays. A significant increase in the three glial cell marker proteins was noted in the cerebellum after exposure to 100 ppm toluene; a more pronounced increase occurred at the higher toluene concentrations. beta-S100 protein also exhibited a dose dependent increase in the brainstem and spinal cord. On the other hand, the two neuronal cell markers did not show a quantitative decrease in the CNS. This means that the development of gliosis, rather than neurone death, is induced by chronic exposure to toluene. The significant biochemical changes induced around the threshold limit value and the concentration dependent alterations suggest that these nerve specific marker proteins may be used to evaluate solvent related damage to the CNS.

Animals↗
PubMed1993

Biological monitoring of occupational exposure to toluene diisocyanate: measurement of toluenediamine in hydrolysed urine and plasma by gas chromatography-mass spectrometry.

Exposure to toluene diisocyanate (TDI) was studied during 48 hours and biological samples from nine subjects were taken in a factory producing flexible polyurethane (PUR) foam. Five PUR workers, two white collar workers, and two volunteers were studied. The concentrations of TDI in air were determined by high performance liquid chromatography with the 9-(N-methylaminomethyl)-anthracene reagent. Urine and plasma samples were collected and the TDI related amines, 2,4-toluenediamine (2,4-TDA) and 2,6-toluenediamine (2,6-TDA), were determined (after hydrolysis) as pentafluoropropionic anhydride (PFPA) derivatives by capillary gas chromatography-mass spectrometry (GC-MS) with selected ion monitoring (SIM) in the negative chemical ionisation mode. The concentration of TDI in air was 1%-10% of the Swedish threshold limit value (TLV) of 40 micrograms/m3. The ratio between 2,4-TDI and 2,6-TDI varied in the air samples in the range of 60%:40%-5%:95%. Calibration plots for human urine spiked with 2,6-TDA and 2,4-TDA in the range of 0.2-12 micrograms/l were produced on eight different occasions during five weeks. The SDS of the calibration plot slopes (n = 8) were less than 4%. Urine and blood samples were taken on six occasions for eight of the studied subjects and on four occasions for one subject during a two day period. The five male PUR workers showed the highest average urinary elimination rate of TDA. Two PUR workers and the two white collar workers had an elimination rate of 20-70 ng on average for the sum of 2,6-TDA and 2,4-TDA per hour and three PUR workers had an average of 100-300 ng TDA per hour. The elimination rate curves for all the studied subjects had a linear relation with exposure to TDI. The concentrations of 2,4-TDA and 2,6-TDA in plasma for the PUR factory employees were virtually stable. No relation between the elimination rates of TDA in urine and plasma concentrations of TDA was found. The five PUR workers showed plasma concentrations of the sum of 2,4-TDA and 2,6-TDA in the range 1-8 ng per ml. The two white collar workers, present only on occasions in the factory, had 0.2- ng TDA per ml plasma. The two volunteers showed an increasing concentration of TDA in plasma with time. At the end of the study their plasma concentrations were 0.6 ng/ml and 0.2 ng/ml plasma. Three subjects had the same concentration of the two TDA isomers in plasma, two subjects had about double, and two subjects had 12 times higher concentrations of 2,6-TDA than 2,4-TDA. The presented study indicates that it is possible to monitor exposure to TDI by monitoring plasma concentrations of TDA.

Adult↗
PubMed1993

Effects of exposure to low concentrations of chlorinated hydrocarbons on the kidney and liver of industrial workers.

An assessment has been made of biochemical alterations in renal and hepatic functions of 73 male operators employed for an average of 8.2 years (range 0.5-23 years) in a chemical plant producing chlorinated hydrocarbons. Exposure to allyl chloride (AC), 1,3-dichloropropene (DCP), epichlorohydrin (ECH), and hexachlorocyclopentadiene (HEX) has regularly been determined by personal air monitoring since 1980. Although exposures to DCP and ECH were well below currently accepted maximum allowable concentrations (MACs), relatively high exposures to AC and HEX, occasionally exceeding the MAC, have been measured. The results of the kidney and liver function tests were compared with those of a control group comprising 35 men employed at the materials division and not occupationally exposed to chemicals. Biochemical alterations of liver function were assessed by determination in serum of alanine and aspartate aminotransferases (ALAT, ASAT), alkaline phosphatase (AP), total bilirubin (BIL), gamma-glutamyltranspeptidase (GGT), lactate dehydrogenase (LDH), and total bile acids (SBA). No differences between the exposed group and the control group were found. Nor were differences found in biochemical tests for renal tubular damage (urinary alanine aminopeptidase (AAP) and N-acetyl-beta-D-glucosaminidase (NAG) and renal tubular function (urinary retinol binding protein (RBP). Total urinary protein and albumin excretion were measured to assess the integrity of the glomerulus. Urinary total protein did not differ between the groups, but urinary albumin, although within normal limits in both groups, was significantly higher (p < 0.02) in the exposed group. This difference in urinary albumin could not simply be explained by exposure to chlorinated hydrocarbons because albumin concentrations did not correlate with the duration of employment. It is concluded that long term exposure to concentrations of AC, DCP, ECH, or HEX below or near the current limit threshold value does not lead to clinically significant effects on kidney and liver.

Adult↗
PubMed1993

Changes in lung function of granite crushers exposed to moderately high silica concentrations: a 12 year follow up.

45 granite crushers and 45 age and smoking matched referents underwent pulmonary function tests in 1976 and 1988. On average, the granite crushers at follow up had worked for 22 years, were 52 (range 36-78) years old, and had inhaled a cumulated amount of 7 mg of silica in the respirable dust fraction. Between 1976 and 1988 the average concentration of respirable quartz in air was 0.16 mg/m3 (threshold limit value (TLV) = 0.10 mg/m3). In 1988 the granite crushers had somewhat lower forced expiratory flows (forced expiratory volume in one second/vital capacity (FEV1/VC) -4.5% and forced midexpiratory flow FEF50 -15%) compared with the referents and a more uneven ventilation distribution (17% higher slope of phase III in the nitrogen single breath curve). Five smoking granite crushers, but none of the referents, had an FEV1 < 80% of the predicted. During the 12 year interval the granite crushers had--compared with the matched referents--a greater decrease in FEV1 (-4.6%), FEV1/VC (-5.4%), maximal expiratory flow, (-8%) and FEF50 (-14%), and a larger increase in phase III and static compliance (p < 0.02 in all variables). The functional changes suggest the presence of airways obstruction and increased compliance of the lungs. Exposure to silica at concentrations of about twice the present TLV was thus associated with airways obstruction and loss of elastic recoil rather than fibrosis and a restrictive function loss as seen in silicosis. The changes were on average small, but in some tobacco smokers more pronounced changes were found.

Adult↗
PubMed1998

Comprehensive evaluation of long-term trends in occupational exposure: Part 2. Predictive models for declining exposures.

OBJECTIVES: To explore the effects of various factors related to the industry, the contaminant, and the period and type of sampling on long term declining trends in occupational exposure. METHODS: Linear regression analyses were used to assess the relation between reductions in exposure and geographical location, industrial sector, type of contaminant, type of monitoring, carcinogenic classification, calendar period, duration of sampling, and number of reductions in the threshold limit value during the sampling period. Both univariable and multivariable models were applied. RESULTS: Based on univariable analyses, the findings suggest that exposures declined more rapidly in manufacturing than in mining, more rapidly for aerosol contaminants than for vapours, and more rapidly when biological, rather than airborne, monitoring was conducted. Exposures collected more recently (first year of sampling in 1972 or later) fell more rapidly than exposures first evaluated during earlier periods. Irrespective of when the data were collected, the results also suggest that the longer the duration of sampling the slower the rate of decline. Taken together, we found that characteristics related to the contaminant, the industry, the sampling period, and the type of sampling explained a substantial proportion of the variability for exposures evaluated before 1972 (R2 = 0.78) and for sites evaluated both before and after 1972 (R2 = 0.91), but explained essentially no variation for data gathered exclusively after 1972 (R2 = 0.04). CONCLUSIONS: By identifying factors that have affected the rates of reduction in a consistent fashion, the results should guide investigators in estimating historical levels when studies assessing exposure-response relations are carried out.

Analysis of Variance↗
PubMed2003

Benzene and naphthalene in air and breath as indicators of exposure to jet fuel.

AIMS: To estimate exposures to benzene and naphthalene among military personnel working with jet fuel (JP-8) and to determine whether naphthalene might serve as a surrogate for JP-8 in studies of health effects. METHODS: Benzene and naphthalene were measured in air and breath of 326 personnel in the US Air Force, who had been assigned a priori into low, moderate, and high exposure categories for JP-8. RESULTS: Median air concentrations for persons in the low, moderate, and high exposure categories were 3.1, 7.4, and 252 microg benzene/m3 air, 4.6, 9.0, and 11.4 microg benzene/m3 breath, 1.9, 10.3, and 485 microg naphthalene/m3 air, and 0.73, 0.93, and 1.83 microg naphthalene/m3 breath, respectively. In the moderate and high exposure categories, 5% and 15% of the benzene air concentrations, respectively, were above the 2002 threshold limit value (TLV) of 1.6 mg/m3. Multiple regression analyses of air and breath levels revealed prominent background sources of benzene exposure, including cigarette smoke. However, naphthalene exposure was not unduly influenced by sources other than JP-8. Among heavily exposed workers, dermal contact with JP-8 contributed to air and breath concentrations along with several physical and environmental factors. CONCLUSIONS: Personnel having regular contact with JP-8 are occasionally exposed to benzene at levels above the current TLV. Among heavily exposed workers, uptake of JP-8 components occurs via both inhalation and dermal contact. Naphthalene in air and breath can serve as useful measures of exposure to JP-8 and uptake of fuel components in the body.

Aerospace Medicine↗
PubMed2003

Municipal waste incinerators: air and biological monitoring of workers for exposure to particles, metals, and organic compounds.

AIMS: To evaluate occupational exposure to toxic pollutants at municipal waste incinerators (MWIs). METHODS: Twenty nine male subjects working near the furnaces in two MWIs, and 17 subjects not occupationally exposed to combustion generated pollutants were studied. Individual air samples were taken throughout the shift; urine samples were collected before and after. Stationary air samples were taken near potential sources of emission. RESULTS: Occupational exposure did not result in the infringement of any occupational threshold limit value. Atmospheric exposure levels to particles and metals were 10-100 times higher in MWIs than at the control site. The main sources were cleaning operations for particles, and residue transfer and disposal operations for metals. MWI workers were not exposed to higher levels of polycyclic aromatic hydrocarbons than workers who are routinely in contact with vehicle exhaust. The air concentrations of volatile organic compounds and aldehydes were low and did not appear to pose any significant threat to human health. Only the measurement of chlorinated hydrocarbon levels would seem to be a reliable marker for the combustion of plastics. Urine metal levels were significantly higher at plant 1 than at plant 2 because of high levels of pollutants emanating from one old furnace. CONCLUSION: While biological monitoring is an easy way of acquiring data on long term personal exposure, air monitoring remains the only method that makes it possible to identify the primary sources of pollutant emission which need to be controlled if occupational exposure and environmental pollution are to be reduced.

Air Pollutants, Occupational↗
PubMed1979

Occupational asthma in an electronics factory.

Workers in a modern electronics factory were surveyed by questionnaire and lung function testing to see if there was evidence of widespread work-related respiratory symptoms. Of the responding workers exposed to solder flux fumes on the shop floor, 22% had work-related breathlessness or wheeze or both. Exposed workers had a lower FEV1 and FVC than unexposed workers. Work-related rhinitis was also present in 22% of exposed workers. The most likely cause for these results is sensitivity to colophony fumes, released from solder flux during soldering. Levels of solder flux fume were below the threshold limit value in this factory during the survey.

Adult↗
PubMed1995

Radio-frequency survey at the bore of a 1.5-T MR imager.

A survey at the bore of a 1.5-T magnetic resonance (MR) imager assessed radio-frequency (RF) exposure. With variable pulse sequences and loading conditions, the RF power density at relevant occupational positions was below measurable limits (less than the threshold limit value for occupational workers of 1 mW/cm2). Exposure to RF fields is below safe limits for personnel who routinely work within an MR imaging suite.

Humans↗
PubMed1976

Occupational type test for the etiological diagnosis of asthma due to toluene di-isocyanate.

An occupational type exposure-test to toluene di-isocyanate (TDI) for the diagnosis of specific respiratory sensitization is proposed. The subjects were tested by exposure to a two-pot polyurethane varnish with and without TDI activator, using a paint-spraying system under standard and controlled conditions, so as not to exceed the threshold limit value of TDI. Forced expiratory volume per second and specific airway resistance (plethysmographic method) were measured before each exposure and during the following 24 h. 47 subjects with clinical symptoms of asthma were examined during their hospital care. For the purpose of this study they were divided into two groups: 42 workers exposed to TDI and 5 not exposed. The preliminary control test, using polyurethane varnish without TDI activator, was always negative and no significant changes in ventilatory parameters were recorded. The spray-painting test, with the same varnish and TDI activator, gave positive responses in 35 out of the 42 exposed workers and negative findings in the group not exposed. This method permits to formulate an accurate diagnosis of TDI respiratory sensitization in the majority of cases (83%). Immediate asthmatic reactions were frequently observed in the exposed subjects with high acetylcholine reactivity. Ten subjects showed a late bronchial reaction (3 h or more after TDI exposure).

Acetylcholine↗
PubMed1997

Hexamethylene diisocyanate induction of transient airway hyperresponsiveness in guinea pigs.

The induction of lung injury and the development of airway hyperresponsiveness (AHR) by exposure to hexamethylene diisocyanate (HDI) were studied in a guinea pig model of occupational lung diseases. In addition to an unexposed control group of 16 guinea pigs (A), two groups (B, C) of 8 animals inhaled HDI atmospheres in the range of the threshold limit value (TLV) of 10 ppb for 6 h/day on 5 days/week over a period of 8 weeks. Airway responses to aerosols of 0.125, 0.25, 0.5, 1.0 and 2.0% acetylcholine (ACH) were measured in exposed as well as in unexposed animals. Basal values of respiratory mechanical and cardiovascular parameters were not significantly altered after 8 weeks of HDI inhalation (group B). Furthermore, additional acute challenge by 10 ppb HDI for a period of 60 min, performed under continuous registration of respiratory and cardiovascular parameters, did not cause any significant changes in functional parameters. After 8 weeks of HDI exposure, the amplitude of airway constriction as a response to 2.0% ACH, indicated by the changes in dynamic elastance (Edyn) rose significantly to almost 5 times the ACH response in group A(p < 0.0005). In group C of 8 guinea pigs, ACH response was evaluated after a latency period of 8 weeks. In this group, changes of airway responsiveness to ACH were significantly smaller than in group B without a latency period. They were comparable to those of group A. In summary, HDI-induced airway hyperresponsiveness to ACH in the guinea pig is reversible within 8 weeks of HDI avoidance. It is assumed that the augmented airway responsiveness indicates an increased risk of developing isocyanate-induced obstructive lung diseases.

Acetylcholine↗
PubMed1983

Impairment of visuo-vestibular interaction in humans exposed to toluene.

15 healthy volunteers were investigated in a vestibulo-oculomotor test battery during toluene exposure. The concentration was comparable to the threshold limit value. The results were compared to an identical air experiment. The intoxication caused an impaired visual suppression during a pseudo-random oscillatory swing test and also an increased saccade speed. Other vestibular-oculomotor parameters were normal. The findings are in accordance with our earlier study on styrene in humans, showing that the visual suppression test and the saccade test are sensitive parameters assessing neurotoxic influences by organic solvents.

Adult↗
PubMed1988

Cobalt exposure and lung disease in tungsten carbide production. A cross-sectional study of current workers.

A cross-sectional study of 1,039 tungsten carbide (TC) production workers was carried out. The purposes were (1) to evaluate the prevalence of interstitial lung disease (ILD) and work-related wheezing, (2) to assess correlations between cobalt exposure and pulmonary disease, (3) to compare lung disease in grinders of hard carbide versus nongrinders, and (4) to evaluate the effects of new and previous threshold limit values for cobalt of 50 and 100 micrograms/m3. We obtained medical and occupational histories, flow-volume loops, single breath carbon monoxide diffusing capacity (DLCO), and chest radiographs. Time-weighted average cobalt levels were determined at every step in the production process. Work-related wheeze occurred in 113 participants (10.9%). Profusion greater than or equal to 1/0 occurred in 26 (2.6%) and interstitial lung disease (defined as profusion greater than or equal to 1M, FVC or DLCO less than or equal to 70%, and FEV1/FVC% greater than or equal to 75) in 7 (0.7%). The relative odds of work-related wheeze was 2.1 times for present cobalt exposures exceeding 50 micrograms/m3 compared with exposures less than or equal to 50 micrograms/m3. The relative odds of profusion greater than or equal to 1/0 was 5.1 times for average lifetime cobalt exposures exceeding 100 micrograms/m3 compared with exposures less than or equal to 100 micrograms/m3 in those with latency exceeding 10 yr. ILD was found in three workers with very low average lifetime exposures (less than 8 micrograms/m3) and shorter latencies. Grinders of hard carbide had lower mean DLCO than nongrinders, even though their cobalt exposures were lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon Monoxide↗
PubMed1992

Delayed effects of NO2 exposure on alveolar permeability and glutathione peroxidase in healthy humans.

Potential toxic effects of prolonged NO2 exposure below the current threshold limit value (TLV) were examined in 14 healthy, nonsmoking adults. The subjects were exposed to 2.3 ppm NO2 and to clean air for 5 h with a 1-wk interval between exposures. Physiologic and biochemical measurements were obtained during the exposures and until 24 h after. A 14% decrease in serum glutathione peroxidase activity (GSH-Px) was observed 24 h after the start of the NO2 exposure, while indications of a 22% decrease in alveolar permeability were found 11 h after the start. There were no indications of mucous membrane irritation or of decreased lung function during or after NO2 exposures. The results support the assumption that a delayed response is a feature of the human reaction to NO2 even below the current TLV of 3 ppm, and they stress the importance of an extended period of observation in future NO2 exposure studies.

Adult↗
PubMed1977

Acute silicosis in tombstone sandblasters.

Four men developed silicosis after sandblasting tombstones for an average of 35 months; 3 of them died an average of 59 months after their first exposure to sandblasting. Lung tissue demonstrated noncaseating granulomas and silicotic nodules involving small arteries and veins in 3 patients and alveolar proteinosis in 2. X-ray energy spectrometry showed primarily elemental silicon in the lung parenchyma. One patient developed lupus erythematosus and another focal glomerulonephritis. Two developed pneumothorax. None had cultural or morphologic evidence of tuberculosis. Pulmonary function studies in all 4 patients revealed a restrictive pattern. Industrial investigations revealed that the patients wore inadequate personal protection equipment and were exposed to 5 times the threshold limit value for respirable silica.

Acute Disease↗
PubMed1977

Longitudinal study of workers employed in the manufacture of toluene-diisocyanate.

Workers at a toluene-diisocyanate manufacturing plant were studied longitudinally to determine the effects of the chemical on their health. Studies included health questionnaire, pulmonary function, environmental monitoring, and immunologic testing. Workers reporting increased lower respiratory symptoms were from the nonsmoker group. Environmental monitoring showed frequent excursions of toluene-diisocyanate concentrations above the threshold limiting value. There was poor correlation between area and personal exposure levels. No exposure-related decline of pulmonary function was demonstrable. Immunologic studies showed development of a positive skin test to a toluene-diisocyanate-human serum albumin conjugate by some persons and an increasing incidence of toluene-diisocyanate-specific IgE antibodies as measured by a radioallergosorbent test. Toluene-diisocyanate did not induce histamine release from leukocytes in vitro but did diminish the in vitro stimulation of cyclic adenosine monophosphate by isoproterenol. Most of the clinically sensitive persons demonstrated adverse bronchial response when challenged by inhalation of toluene-diisocyanate. This response was dose dependent in some persons. When challenged with Mecholyl, clinically sensitive persons showed greater reactivity of airways than nonsensitive persons.

Antibodies↗