Occupational exposure to inhalational anaesthetics.
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Air Pollutants, Occupational↗
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Estimation of absorption of trihalomethanes and carbon tetrachloride in low-level exposure by inhalation pharmacokinetic analysis in rats.
Inhalation pharmacokinetics of the environmental contaminants chloroform, bromodichloromethane, chlorodibromomethane, and carbon tetrachloride were evaluated, and their absorption amounts were estimated in rats to obtain fundamental data for risk assessment of chronic low-level exposures. Measured amounts of the substances were injected into a closed chamber system in which a rat had been placed, and the concentration changes in the chamber were examined. The pharmacokinetics of the substances were evaluated on the basis of the concentration-time courses using linear or nonlinear compartment models. The metabolic elimination amounts at various exposure concentrations were extrapolated using the estimated pharmacokinetic parameters. With exposure to chloroform, the fraction of the elimination amount at 1 ppb exposure (low concentration) against the exposure concentration was estimated to be 1.1 times higher than the fraction at 10 ppm exposure (high concentration). With exposure to low concentrations (1 ppb), extrapolation showed that more chloroform (0.33 nmol/h/kg) was absorbed by the rats than chlorodibromomethane (0.11 nmol/h/kg), bromodichloromethane (0.072 nmol/h/kg), and carbon tetrachloride (0.053 nmol/h/kg). Our findings revealed differences in the absorption amounts among the substances for the same exposure concentrations.
Absorption↗
Clinical approach to chronic beryllium disease and other nonpneumoconiotic interstitial lung diseases.
Exposures in the workplace result in a diverse set of diseases ranging from the pneumoconiosis to other interstitial lung diseases to acute lung injury. Physician awareness of the potential disease manifestations associated with specific exposures is important in defining these diseases and in preventing additional disease. Most occupational diseases mimic other forms of lung disease, including pulmonary fibrosis, sarcoidosis, adult respiratory distress syndrome (ARDS), and bronchiolitis. A "sarcoidosis"-like syndrome, usually limited to the lungs, may result from exposure to bioaerosols and a number of metals. Exposure to beryllium in the workplace produces a granulomatous lung disease clinically indistinguishable from sarcoidosis, chronic beryllium disease (CBD). Beryllium's ability to produce a beryllium-specific immune response is used in the beryllium lymphocyte proliferation tests to confirm a diagnosis of CBD and exclude sarcoidosis. Exposure to other metals must also be considered in the differential diagnosis of sarcoidosis. When an individual presents acutely with ARDS or acute lung injury, an acute inhalational exposure must be considered. Exposure to a number of irritant substances at high levels may cause a "chemical pneumonitis" or acute lung injury, depending on the solubility and physicochemical properties of the substance. Some of the most notable agents include nitrogen and sulfur oxides, phosgene, and smoke breakdown products. Ingestion of paraquat may also result in an ARDS syndrome, with pulmonary fibrosis eventually resulting. Bronchiolitis is a rare manifestation of inhalational exposures but must also be considered in the clinical evaluation of inhalational exposure.
Adult↗
Lung exposure from inhalation of radon progeny: calculated from in vivo measurements of 210Pb in the skull.
To calculate the radiation dose to the lungs from the inhalation of radon and its short-lived progeny, an accurate estimate of cumulative exposure is necessary. In this preliminary study, the content of 210Pb in the skeleton is used to obtain a measure of integrated exposure to the lungs of people living in homes with above average concentrations of radon. Measurements of skeletal 210Pb made in vivo allow the exposed individuals to become, in effect, their own "samplers" and "dosimeters" through the normal physical and physiological processes of inhalation, deposition, and retention. 210Pb measurements have been made on 40 subjects whose homes have above average levels of radon. These data are used to obtain their cumulative lung exposures, defined as RLM (Respiratory Level Months). RLM is calculated from the numbers of atoms of RaA, RaB, and RaC,C' deposited in their respiratory systems over the time periods lived in the surveyed homes. The RLM values obtained are not significantly different than conventional WLM exposures calculated for the same time periods.
Adult↗
Two-week (ten-day) inhalation toxicity and two-week recovery study of phenol vapor in the rat.
The toxicity of phenol vapor was evaluated in male and female Fischer 344 rats (20/sex/group) via flow-past nose-only inhalation exposure. The test animals were exposed to target concentrations of 0 (air control), 0.5, 5.0, or 25 parts per million (ppm) of phenol in air for 6 hours/day, 5 days/week, for 2 weeks. High pressure liquid chromatography (HPLC) measurement of phenol test atmospheres determined mean (+/- standard deviation) analytical concentrations of 0.0 +/- 0.0, 0.52 +/- 0.078, 4.9 +/- 0.57, and 25 +/- 2.2 ppm, respectively. After 2 weeks of exposure, 10 test animals/sex/group were sampled for clinical chemistry and hematology parameters, and then sacrificed. Histopathological examination included the nasopharyngeal tissues, larynx, trachea, lungs with mainstem bronchi, kidney, liver, and spleen. The remaining 10 animals/sex/group were retained for a 2-week recovery period. Recovery groups of animals were evaluated as described previously and then sacrificed. No signs of toxicity in clinical observations (including overt neurological signs), body weights, food consumption, clinical pathology, organ weights, macroscopic pathology or microscopic pathology were seen during the exposures or at either sacrifice interval. In conclusion, 2-week inhalation exposures to phenol vapor at concentrations up to and including 25 ppm did not produce any adverse effects.
Administration, Inhalation↗
A comparison of worker exposure to inhalable and total dust, inorganic arsenic, and borates using two types of particulate sampling assemblies in a borate mining and processing facility.
This study describes a comparison of worker exposure to total and inhalable dust, inorganic As, and borates using two types of particulate sampling assemblies as part of a comprehensive industrial hygiene evaluation in a borate mining and processing facility. Employees were segmented into similar exposure groups (SEG) based on work location within the facility, job classification, and type of chemical agent. Approximately 10% of the employees from each SEG wore two personal sampling devices simultaneously for the purpose of collecting total and inhalable particulate fractions using a closed face, 37-mm mixed cellulose ester matched-weight filters (MMW), and Institute of Occupational Medicine (IOM) sampling assembly. Sample results indicated that the IOM concentrations were consistently higher than the corresponding MMW concentrations for all three agents. An analysis was performed to investigate a relationship between MMW and IOM. The data revealed correlation coefficient values of 0.72, 0.82, and 0.84 for total dust (n = 197), inorganic As (n = 137), and borates (n = 194), respectively. These positive correlation coefficients indicate that the IOM and MMW measurements are consistent with each other, and can be used for predicting exposure levels. The total dust and borate large mean ratios should be considered in developing inhalable fraction-based regulatory standards.
Air Pollutants, Occupational↗
The automated bioaerosol exposure system: preclinical platform development and a respiratory dosimetry application with nonhuman primates.
INTRODUCTION: Well-characterized inhalation exposure systems are critical for preclinical testing and pathogenesis studies. The automated bioaerosol exposure system (ABES) provides a microprocessor-driven inhalation platform that provides exquisite data acquisition and control over all aspects of inhalation exposures. Because this represents a new technology, the development and characteristics of the ABES are thoroughly discussed. In addition to control over homeostatic and aerosol conditions, the ABES incorporates a dosimetry function based on respiratory performance of the test animal during inhalation. METHODS: To test the system, rhesus macaques were initially sham-exposed using the ABES in a head-only inhalation configuration. The ABES was subsequently used under biosafety level (BSL)-III conditions in a vaccine efficacy challenge using aerosolized staphylococcal enterotoxin B (SEB) toxin, again using the real-time dosimetry function of the system. RESULTS: Sham exposure results indicated significant departures from corresponding whole-body plethysmography (WBP) respiratory function estimates taken before the inhalation procedure. The results of the SEB exposure demonstrated the utility of using the ABES to generate consistently accurate and precise inhalation dose. DISCUSSION: Taken together, the results of the sham and toxin challenge experiments demonstrate that the dosimetry function of the ABES improves the precision and accuracy of inhaled dose delivery and calculation as compared to predictive WBP conducted before the exposure. The ABES represents a highly adaptable platform for the design of inhalation systems to suit the requirements of a variety of animal models.
Administration, Inhalation↗
Two generation reproduction study of ethylbenzene by inhalation in Crl-CD rats.
BACKGROUND: This study was conducted to evaluate the potential adverse effects of ethylbenzene (EB) on reproductive capability from whole-body inhalation exposure of F0 and F1 parental animals. METHODS: Four groups of Crl:CD(SD)IGS BR rats (30/sex/group for F0 and 25/sex/group for F1) were exposed to 0, 25, 100, and 500 ppm EB for 6 hr/day for at least 70 consecutive days before mating. Inhalation exposure for the F0 and F1 females continued throughout mating, gestation through gestation day (GD) 20, and lactation days (LD) 5-21. On LD 1-4, females received EB in corn oil via oral gavage at dose levels of 26, 90, and 342 mg/kg/day (divided into three equal doses, approximately 2 hr apart), as calculated from a physiologically-based pharmacokinetic (PBPK) model to provide similar maternal blood area-under-concentration (AUC) as provided by inhalation. Pups were weaned on postnatal day (PND) 21 and exposure of the F1 generation started on PND 22. Estimates of internal exposure were determined by measuring EB concentrations in blood collected from F1 dams (4/group) and their culled pups 1 hr after the last gavage dose on PND 4. On PND 22, blood was collected from these same F1 dams and their weanlings for EB analysis 1 hr after a 6-hr inhalation exposure. The remainder of the F2 generation was not directly exposed. RESULTS: EB exposure did not affect survival or clinical observations. Male rats in the 500 ppm group in both generations gained weight more slowly than the controls. There were no indications of adverse effects on reproductive performance in either generation. Male and female mating and fertility indices, pre-coital intervals, spermatogenic endpoints, ovarian follicle counts, reproductive organ weights, lengths of estrous cycle and gestation, live litter size, pup weights, developmental landmarks, and postnatal survival were unaffected. No adverse exposure-related macroscopic pathology was noted at any level. CONCLUSIONS: Increased liver weights were found in the animals exposed to 500 ppm. F1 maternal whole blood EB concentrations of 0.49, 3.51, or 18.28 mg/L were found 1 hr after administration of a composite oral dose of 26, 90, or 342 mg/kg/day, respectively, but no detectable EB was found in blood samples of their F2 PND 4 culled pups. F1 maternal mean whole blood EB levels 1 hr after a 6-hr inhalation exposure on postpartum day (PPD) 22 was 0.11 mg/L (25 ppm), 0.56 mg/L (100 ppm), and 11 mg/L (500 ppm). For the offspring exposed with their dams on PND 22, F2 pup blood EB concentrations ranged from 0.017-0.039 mg/L (25 ppm), 0.165-0.465 mg/L (100 ppm), and 8.82-15.74 mg/L (500 ppm). Because decreased weight gain in the 500 ppm males was transient and no histopathological changes were associated with the increased liver weights in the 500 ppm male and female groups, these changes were not considered adverse. Therefore, for parental systemic toxicity, 100 ppm was considered a NOEL and 500 ppm a NOAEL in this study. The 500 ppm exposure concentration was considered a NOAEL for F0 and F1 reproductive toxicity and offspring developmental endpoints.
Administration, Oral↗
Prolonged exposure to inhalational anesthetic nitrous oxide kills neurons in adult rat brain.
Short-term exposure of adult rats to nitrous oxide (N2O), an inhalational anesthetic and NMDA (N-methyl-D-aspartate) antagonist, causes a reversible neurotoxic vacuole reaction in neurons of the posterior cingulate/retrosplenial cortex (PC/RSC) which resembles that caused by low doses of other NMDA antagonists. Since high doses or prolonged exposure to other NMDA antagonists can cause neurons to die, we assessed whether prolonged N2O exposure might also cause neuronal cell death. Adult female Sprague-Dawley rats were exposed to 150-vol% N2O (approximately EC50 for N2O anesthesia in rats) for various durations from 1 to 16 h. The time course for onset and disappearance of the reversible vacuole reaction was studied, as was the time course and dose requirement for triggering cell death. A maximum vacuole reaction was observed in PC/RSC neurons in brains examined immediately after 3 h of 150-vol% N2O exposure and the same magnitude of vacuole reaction was observed when brains were examined immediately after a longer period of N2O exposure. When N2O was terminated at 3 h and the rats were killed 1 h later, the vacuole reaction was markedly diminished and if the rats were killed 3 h later the vacuole reaction had completely disappeared. Prolonged exposure to 150-vol% N2O (for 8 h or more) caused neuronal cell death which was detectable by silver staining 32 h later. Concurrently administered GABAergic agents, diazepam (an i.v. anesthetic), or isoflurane (an inhalational anesthetic), prevented this cell death reaction. Our findings demonstrate that short-term exposure of adult rats to N2O causes injury to PC/RSC neurons that is rapidly reversible, and prolonged N2O exposure causes neuronal cell death. These neurotoxic effects, including the cell death reaction, can be prevented by coadministration of GABAmimetic anesthetic agents. Duration of NMDA receptor blockade appears to be an important determinant of whether neurons are reversibly injured or are driven to cell death by an NMDA antagonist drug.
Analysis of Variance↗
Chronic cadmium exposures associated with kidney function effects.
A follow-up study was conducted on 27 workers with a median of 25 years exposure to airborne cadmium. Two exposure groups had been selected a low exposure group of office, laboratory and supervisory personnel (n = 11, average urinary cadmium 13.1 micrograms/l); and a high exposure group of production workers with long histories of work in areas with substantial airborne cadmium (n = 16, average urinary cadmium 45.7 micrograms/l). An estimate of each subject's time-weighted-average inhalation exposure to cadmium was calculated from personal sampling data (1973-1976) and area sampling data (1943-1976). Based on the findings of another study, the average inhalation exposures in each of the work areas were adjusted for use of personal protective masks (respirators). Comparison of kidney function status between the high and low exposure groups showed a significant reduction in creatinine clearance, and increased uric acid and beta microglobulin excretion by the high group. Significant renal effects were associated with estimated average inhalation exposures of 63 micrograms/m3 over a 25 year period. The relationship between urinary cadmium excretion and cumulative exposure changed for higher exposures; this was consistent with the "critical concentration" model of cadmium's effects on the kidney.
Air Pollutants, Occupational↗
Evaluation of the teratogenic potential and reproductive toxicity of coal-derived naphtha.
Liquids which are derived from coal liquefaction processes and boil above approximately 250 degrees C have induced terata in rats. However, few studies have addressed the teratogenic potential of coal liquids which boil below 250 degrees C. The present studies evaluated the reproductive and teratogenic potential of EDS hydrotreated naphtha, a refined coal liquid boiling below 177 degrees C. These studies were conducted by inhalation exposures with Sprague-Dawley rats at target vapor concentrations of 0.2, 1.0, and 5.0 g/m3. The first study assessed teratogenesis. There was no evidence that inhalation exposures for 6 hr per day between Days 6 and 19 of gestation induced maternal toxicity, fetal toxicity, or malformation. In a second study, rats were exposed for 6 hr per day, 5 days per week for 13 weeks, and then mated to assess reproductive toxicity. There was little evidence that inhalation exposure to EDS hydrotreated naphtha adversely affected reproductive performance or fetal development in Sprague-Dawley rats. A low incidence of malformations was observed in treated groups, but these malformations were probably not treatment related.
Abnormalities, Drug-Induced↗
Resuspension studies in the Marshall Islands.
The contribution of inhalation exposure to the total dose for residents of the Marshall Islands was monitored at occasions of opportunity on several islands in the Bikini and Enewetak Atolls. To determine the long-term potential for inhalation exposure, and to understand the mechanisms of redistribution and personal exposure, additional investigations were undertaken on Bikini Island under modified and controlled conditions. Experiments were conducted to provide key parameters for the assessment of inhalation exposure from plutonium-contaminated dust aerosols: characterization of the contribution of plutonium in soil-borne aerosols as compared to sea spray and organic aerosols, determination of plutonium resuspension rates as measured by the meteorological flux-gradient method during extreme conditions of a bare-soil vs. a stabilized surface, determination of the approximate individual exposures to resuspended plutonium by traffic, and studies of exposures to individuals in different occupational environments simulated by personal air sampling of workers assigned to a variety of tasks. Enhancement factors (defined as ratios of the plutonium-activity of suspended aerosols relative to the plutonium-activity of the soil) were determined to be less than 1 (typically 0.4 to 0.7) in the undisturbed, vegetated areas, but greater than 1 (as high as 3) for the case studies of disturbed bare soil, roadside travel, and for occupational duties in fields and in and around houses.
Administration, Inhalation↗
Occupational exposure through spraying remedial pesticides.
A total of 20 surveys at 15 sites of remedial in-situ timber and masonry treatment took place in the latter half of 1996. Two of these surveys concerned wall washes (biocides), the remainder were non-agricultural pesticides. The purpose was to measure the surface deposition and inhalation exposure of the operatives to the pesticide spray fluids used. The diluted spray fluids were found to have significantly different concentrations from those intended by the sprayer. The pesticides were applied at pressures between 320 and 1050 kPa. Deposition rates for spray fluid on coveralls covered a wide range, with more than 30 fold difference between the median and the highest results (median 209 mg/minute; range 27.4 to 6550 mg/min). Contamination of coveralls occurred in all surveys, with the pesticide getting beneath the coveralls in 95% of surveys, with a median 5% contamination beneath the overall. The averaged and normalised deposition pattern was 75% legs, 11% arms, 12% torso and 2% head. Exposure of hands to pesticide (expressed as spray fluid) beneath protective gloves occurred in 89% of surveys (median 5.78 mg/minute; range 0.23 to 358 mg/min) and contamination of socks by spray fluid in 78% of surveys (median 2.08 mg/minute; range 0.12 to 260 mg/min). Exposure by inhalation to spray fluid was measurable in 72% of surveys (median 53.5 mg/m3 TWA; range 4.33 to 1320 mg/m3; 2 data excluded). Inhalation exposure and deposition on coveralls rose markedly at spray pressures above 700 kPa (100 psi).
Agricultural Workers' Diseases↗
Exposure of farmers to phosmet, a swine insecticide.
OBJECTIVES: The goal of this study was to measure dermal and inhalation exposures to phosmet during application to animals and to identify what determinants of exposure influence the exposure levels. METHODS: Ten farmers were monitored using dermal patches, gloves, and air sampling media during normal activities of applying phosmet to pigs for insect control. Exposures were measured on the clothing (outer), under the clothing (inner), on the hands, and in the air. Possible exposure determinants were identified, and a questionnaire on work practices was administered. RESULTS: The geometric mean of the outer exposure measurements was 79 microg/h, whereas the geometric mean of the inner exposure measurements was 6 microg/h. The geometric mean for hand exposure was 534 microg/h, and the mean air concentration was 0.2 microg/m3. Glove use was associated with the hand and total dermal exposure levels, but no other determinant was associated with any of the exposure measures. The average penetration through the clothing was 54%, which dropped to 8% when the farmers wearing short sleeves were excluded. The farmers reported an average of 40 hours a year performing insecticide-related tasks. CONCLUSIONS: Farmers who applied phosmet to animals had measurable exposures, but the levels were lower than what has been seen in other pesticide applications. Inhalation exposures were insignificant when compared with dermal exposures, which came primarily from the hands. Clothing, particularly gloves, provided substantial protection from exposures. No other exposure determinant was identified.
Animal Husbandry↗
Measurements of carbonyls in a 13-story building.
BACKGROUND, AIM AND SCOPE: Formaldehyde and acetaldehyde are emitted by many mobile and stationary sources and secondary aldehydes are intermediates in the photo-oxidation of organic compounds in the atmosphere. These aldehydes are emitted indoors by many materials such as furniture, carpets, heating and cooling systems, an by smoking. Carbonyls, mainly formaldehyde and acetaldehyde, have been studied because of their adverse health effects. In addition, formaldehyde is a suspected carcinogen. Therefore, the concentrations of formaldehyde and acetaldehyde were determined to assess the inhalation exposure doses to carbonyls for people who work in a 13-story building and in order to evaluate the cancer hazard. METHODS: Carbonyl compounds in indoor and outdoor air were measured at a 13-story building located in Mexico City. The mezzanine, fifth and tenth floors, and the third level-parking garage were selected for sampling. Samples were collected in two sampling periods, the first from April 20 to 29, 1998 and the second from December 1 to 20, 1998. Carbonyls were sampled by means of DNHP-coated cartridges at a flow rate of 1 l min(-1) from 9:00 to 19:00 hours, during 2-hour time intervals and analyzed by HPLC with hours, during 2-hour time intervals and analyzed by HPLC with UV/VIS detection. RESULTS: Mean carbonyl concentrations were highest in the 3rd level-parking garage, with the formaldehyde concentration being the highest ranging from 108 to 418 microg m(-3). In working areas, the highest carbonyl arithmetic mean concentrations (AM) were observed on the 5th floor. Acetone and formaldehyde concentrations were highest in April ranging from 161 to 348 microg m(-3) (AM = 226) and from 157 to 270 microg m(-3) (AM = 221), respectively. Propionaldehyde and butyraldehyde were present in smaller concentrations ranging from 2 to 25 and 1 to 28 microg m(-3), respectively, considering all the samples. Mean indoor/outdoor ratios of carbonyls ranged from 1.8 to 9.6. A reduction of inhalation exposure doses of 41% and 45% was observed in the fifth floor air after the air conditioning systems had been repaired. Formaldehyde and acetaldehyde concentrations were higher in smoking environments. CONCLUSION: Indoor carbonyl concentrations were significantly greater than outdoor concentrations. Tobacco smoke seems to be the main indoor source of formaldehyde. After the air conditioning system was maintained and repaired (as was recommended), an important reduction in the emission of formaldehyde and acetaldehyde was achieved on all floors, except for the 3rd level parking garage, thereby reducing the inhalation exposure doses. RECOMMENDATION: The results obtained in this research demonstrated that maintenance of air conditioning systems must be carried out regularly in order to avoid possible adverse effects on health. Additionally, it is mandatory that isolated smoking areas, with air extraction systems, be installed in every public building.
Acetaldehyde↗
Exposure to inhalable flour dust in Canadian flour mills.
In 1999, the American Conference of Governmental Industrial Hygienists (ACGIH(R)) proposed a Threshold Limit Value (TLV(R)) of 0.5 mg/m(3) for flour dust with a sensitization notation. The Labour Program of the Department of Human Resources Development Canada (HRDC), following notice of the intention to set a TLV, conducted a study of the levels of exposure to flour dust in flour mills across Canada to verify existing conditions, as well as to decide whether to adopt the proposed TLV or reference some other value. As part of the study, a relationship between flour dust concentrations obtained by using Institute of Occupational Medicine (IOM) samplers and closed-face 37-mm cassettes was examined and the literature on the health effects of exposure to flour dust was reviewed. A total of 104 millers, packers, sweepers, bakery mix operators, and others (mixed tasks) from 14 flour mills were sampled over an 8-hour work shift using IOM samplers. The results indicate that 101 employees (97.1%) were exposed to levels exceeding 0.5 mg/m(3), 66 employees (67.3%) to levels exceeding 5 mg/m(3), and 44 employees (42.3%) to levels exceeding 10 mg/m(3). For comparison purposes, flour dust measurements were also taken in a highly automated flour mill using state-of-the-art technology. The results suggest that even with the most up-to-date technology and proper cleaning operations in place, the flour milling industry may not be able to reduce the flour dust levels to below the TLV of 0.5 mg/m(3). According to the measurements of inhalable and total dust concentrations, the IOM sampler appears to be a more efficient collector of inhalable airborne particles up to 100 microm than the closed-face 37-mm cassette.
Air Pollutants, Occupational↗
Exposure to inhalable dust and endotoxins in agricultural industries.
Endotoxin is a well-known bacterial toxin that causes several health effects. Animal faeces and plant materials contaminated with bacteria have been identified as important determinants of organic dust related endotoxin exposure. Although high exposure to organic dust and endotoxins has been described regularly in agricultural industries, a detailed overview of levels of airborne exposure to endotoxins in the agricultural industry, as well as a systematic comparison between several specific branches using the same exposure assessment protocols are lacking. In this study, personal endotoxin exposure in a broad spectrum of agricultural industries was investigated and possible determinants of exposure were explored. 601 personal inhalable dust samples were taken in 46 companies of three agricultural industrial sectors: grains, seeds and legumes sector (GSL), horticulture sector (HC) and animal production sector (AP), with 350 participating employees. Dust and endotoxin levels were determined gravimetrically and by using the Limulus Amoebocyte Lysate (LAL) assay, respectively. Basic descriptive analysis and elaborate analysis of variance were performed. Mean exposure levels were high, with large differences between sectors and between companies within the sectors. Highest dust and endotoxin exposures were found in companies of the GSL sector. In all three sectors exposure was higher in the primary production part compared to the (industrial) products processing part of the sector. The Dutch proposed health based occupational exposure limit (50 EU m(-3)) and temporary legal limit (200 EU m(-3)) for endotoxin were often exceeded. Differences in exposure between workers were larger than the day-to-day variability. Identified determinants increasing exposure levels were company, dustiness of the product and contact with animals/faeces. 'Wet' processes resulted in less dusty working environments and thus lowered endotoxin exposure. Overall, exposure to endotoxins over the whole range of agricultural industries is high. A 10-1,000 fold reduction in exposure is needed to reduce endotoxin related health risks.
Agriculture↗
Inhalation toxicity of propineb. Part II: Results of mechanistic studies in rats.
Previous repeated inhalation exposure studies revealed two independent organotropic effects of inhaled propineb dust: One was restricted to the lung, the other to muscle weakness of hindlimbs. These effects were believed to be causally related to the principle decomposition products of this type of dithiocarbamate in the biological milieu and related to zinc and carbon disulfide. Two mechanistic 1-wk inhalation studies were performed, each focusing on one of these findings. The 7 x 6-h/day repeated-exposure inhalation study analyzed whether the nature of the response occurring at the alveolar level is "adaptive" or "early adverse" and whether soluble zinc is the causative agent. Groups of 18 female rats were exposed nose-only to mean concentrations of 0, 1.1, 5.5, and 25.8 mg propineb/m(3) and 6.9 mg ZnO/m(3). On postexposure days 1, 3, and 15 the time course of responses was analyzed by bronchoalveolar lavage (BAL), including quantification of Zn and metallothionein (MT) in BAL cells. Clinical evidence of muscular weakness was investigated separately in 20 female Wistar rats exposed to 70 mg propineb/m(3) on 5 consecutive days (6 h/day), followed by a 2-wk postexposure period. Clinical signs, body weights, and feed and water consumption were recorded as frequently as technically feasible. Fifty percent of rats received an oral cysteine supplementation to verify/refute the hypothesis that the incapacitation observed in previous studies is the cause of emaciation and associated impairment of CS(2) detoxification. The findings of the first study are consistent with this hypothesis, namely, that soluble Zn triggers a series of pulmonary events that is consistent with the homeostasis of this essential metal. It is concluded, accordingly, that the adjusted maximal workplace level for ZnO is also valid for propineb to preclude Zn-mediated responses to occur in the lung. With respect to muscular effects, this mechanistic study demonstrates further that the increased detoxification capacity afforded by oral supplementation of cysteine mitigates markedly the toxic potency of propineb. Procedural variables specific to the inhalation bioassay appear to be decisive for the elicitation of muscular effects. The major variable is considered to be the large drop in body weights associated with each exposure session and the concomitantly decreased uptake of essential nutritional factors (e.g., cysteine) involved in the detoxification of this compound. Accordingly, the muscular deficits elicited by high concentrations of propineb are viewed to be secondary effects in an animal species likely to be more susceptible to this type of change than humans (Pauluhn & Rosenbruch, 2003).
Administration, Inhalation↗