Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Inhalation Exposure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,711 records · Page 95Linked to original sources

Releases from copper smelters and refineries and zinc plants in Canada: human health exposure and risk characterization.

In these assessments of releases from copper smelters and refineries and from zinc plants as Priority Substances under the Canadian Environmental Protection Act (CEPA), available data were critically evaluated to determine if environmental exposure to selected components of these releases poses a risk to human health. The data on airborne levels of a variety of toxic substances near these facilities in Canada were obtained from the companies or provinces and systematically analyzed. Monitoring of ambient air near the Canadian copper smelters and refineries and zinc plants indicates that releases from these facilities result in increased potential for inhalation exposure of local human populations to several components of releases (As, Cd, Cr, Ni, Pb, SO(2) and PM(10)). Airborne levels in the vicinity of these metal-processing operations overlap those associated with cardiorespiratory effects for PM(10), and exceed health-based guidelines for SO(2) and, near some facilities, Pb. In addition, the margin between levels of As, Cd, Cr and Ni near these facilities in Canada and carcinogenic potency for each of these metals is relatively small near copper smelters, larger near copper refineries, and intermediate near zinc plants. On this basis, the risk to human health from environmental exposure to releases from these facilities is considered to be high compared with other Priority Substances assessed under CEPA, especially for facilities where copper is smelted.

Air Pollutants↗

Radiological health implications of lead-210 and polonium-210 accumulations in LPG refineries.

Radon-222, a naturally occurring radioactive noble gas, is often a contaminant in natural gas. During fractionation at processing plants, Radon tends to be concentrated in the Liquified Petroleum Gas (LPG) product stream. Radon-222 decays into a number of radioactive metallic daughters which can plate out on the interior surfaces of plant machinery. The hazards associated with gamma-emitting short-lived radon daughters have been investigated previously. The present work reports an analysis of the hazards associated with the long-lived daughters; Pb-210, Bi-210, and Po-210. These nuclides do not emit appreciable penetrating radiation, and hence do not represent a hazard as long as they remain on the inside surfaces of equipment. However, when equipment that has had prolonged exposure to an LPG stream is disassembled for repair or routine maintenance, opportunities for exposure to radioactive materials can occur. This paper reports a series of measurements made on an impeller taken from a pump in an LPG facility. Alpha spectroscopy revealed the presence of Po-210, and further measurements showed that the amount on the impeller surface was well above the exempt quantity. Breathing zone measurements made in the course of cleaning the impeller showed that an inhalation exposure equivalent to breathing Po-210 at the Maximum Permissible Concentration (MPC) for 60 hours could be delivered in less than half an hour. It was concluded that maintenance and repair work on LPG and derivitive product stream equipment must be carried out with the realization that a potential radiological health problem exists.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollution, Radioactive↗

Cerebral perfusion impairment in a patient with toluene abuse.

We report the case of a 17-yr-old man diagnosed as a toluene abuser. He had an 8-mo history of toluene inhalation exposure and was admitted to this hospital with symptoms of auditory and visual hallucination. Magnetic resonance imaging (MRI) revealed no structural abnormalities both on T1- and T2-weighted images, whereas SPECT using 99mTc-ethyl cysteinate dimer (ECD) showed multifocally decreased perfusion in the cerebral cortex, basal ganglia and thalami. Our case indicates that SPECT detects early central nervous system injury from toluene inhalation even when neurological examination and neuroanatomic imaging such as MRI are normal.

Adolescent↗

Transgenic mouse mutation assay systems can play an important role in regulatory mutagenicity testing in vivo for the detection of site-of-contact mutagens.

Transgenic mouse mutation assays, such as MutaMouse (lacZ, CD2F1) and Big Blue (lacI, B6C3F1), afford the opportunity to evaluate the mutagenic potential of chemicals in any target organ in vivo. This paper discusses published data collected from the analysis of the skin, stomach and lung DNA after topical, oral and inhalation exposure, respectively. These data indicate that both MutaMouse and Big Blue should play an important part in the evaluation of genotoxicity in vivo, particularly where the endpoint or target tissue available in the more conventional tests is inappropriate. It is concluded that there is a distinct role for this type of assay in genetic toxicology testing. For substances applied to the skin or dosed orally or by inhalation and which are unlikely to reach either the bone marrow or the liver, then data derived from these assays may be more relevant to an assessment of possible risk to man than the currently used unscheduled DNA synthesis in liver and cytogenetics assays in bone marrow or peripheral blood.

Animals↗

Inhalation of resuspended road dust, but not ammonium nitrate, decreases the expression of the pulmonary macrophage Fc receptor.

Pulmonary macrophages (PM) play a key role in the immune defenses of the lung. When stimulated, PM express Fc receptors (FcR) that regulate the immune response. PM were assayed for FcR expression following subchronic inhalation exposure of adult Fischer 344 rats to either 90 micrograms/m3 nitrate (NH4NO3), 300 micrograms/m3 road dust, or clean air, for 4 h/day, 4 days/week, for 8 weeks. PM were lavaged from the lungs and attached to glass coverslips for 18 h. PM FcR were labelled with rat IgG conjugated with cyanine-3. For each exposure, FcR were determined with a Meridian ACAS 570 confocal cytometer by imaging the fluorescence of 50 cells. We found that the IgG binding to FcR (in arbitrary fluorescence units, FU, per cell) for PM from road dust exposed rats was less (835 +/- 39.3 FU/cell) than that for PM from both ammonium nitrate or clean air-exposed rats (1115 +/- 58.0 FU/cell and 1123 +/- 46.6 FU/cell, respectively). While acid incubation conditions in vitro (pH 5.5 for 30 min to simulate the acid environment of ammonium nitrate inhalation) resulted in a 16% decrease in IgG binding (P < 0.05), IgG binding to PM from acid aerosol exposed rats was no different than the IgG bound to PM from clean air-exposed rats. PM exposed to road dust in vivo expressed 25% fewer FcR (P < 0.05). Three-dimensional images of PM failed to show any major alterations in FcR distribution. These preliminary results indicate cellular recognition of antibody-immune complexes may be impaired by subchronic exposure to road dust, which could decrease the immune response of road dust exposed animals.

Animals↗

Intratracheal instillation versus intratracheal-inhalation of tracer particles for measuring lung clearance function.

Effective elimination of particles deposited in the respiratory tract is an important defense function to protect the organism from potentially adverse effects of inhaled particles. Delivery of radioactively labeled tracer particles and subsequent measurement in vivo of their retention in different regions of the respiratory tract provides an adequate method for characterizing this defensive function. However, the delivery of such tracer particles by inhalation may result in some external contamination of the animals and requires specific protective measures while working with radioactive aerosols. In this study, 85Sr-labeled tracer particles (3 microns) were administered to the lower respiratory tract of rats by intratracheal inhalation to avoid external contamination, and also by intratracheal instillation in order to compare the 2 technique with respect to their suitability for measuring normal and impaired particle clearance rates. It was postulated that particle clearance function in the alveolar region can be determined equally well with intratracheally instilled particles despite their uneven distribution in the lung. For both techniques, rats were anesthesized with halothane and the particles were administered via oral intubation. Retention in the lower respiratory tract of about 30 micrograms (inhalation) and 6 micrograms (instillation) of the administered particles was followed over a period of 180 days by external counting of lung 85Sr-activity in a collimated detection system. To impair alveolar particle clearance rates, groups of rats were subjected to 12 weeks of inhalation exposure prior to delivery of the tracer particles as follows: (1) sham-exposed control; (2) pigment-grade TiO2 particles to induce lung overload: (3) ultrafine TiO2 particles: (4) crystalline SiO2 particles (cristobalite). The following results were obtained: The long-term retention half-times (T1/2) of the tracer particles reflecting alveolar clearance consistently showed the same ranking of the treatment groups whether measured after intratracheal inhalation or instillation. Control values were 66 and 72 days, respectively, and significantly prolonged long-term clearance was measured by both methods for pigment-grade TiO2 (117 and 99 days), ultrafine TiO2 (541 and 600 days) and SiO2 (1901 and 1368 days). Comparison of these values between the two modes of administration of tracer particles showed no significant differences. In contrast, the short-term T1/2 (mucociliary clearance) of the intratracheally instilled tracer particles in the different treatment groups were variable and did not accurately reflect particle clearance from the conducting airways. However, short-term T1/2 after intratracheal inhalation of tracer particles were consistent with fast conducting airway clearance, and mucociliary clearance appears to be stimulated when alveolar clearance is significantly impaired due to particle overload or to effects of cytotoxic particles. The results suggest that intratracheal instillation of a low dose (< or = 10 micrograms) of tracer particles in the rat provides an adequate method for reliably determining effects of inhaled toxicants on alveolar particle clearance function. Further, intratracheal inhalation of tracer particles is useful for measuring both short-term (mucociliary) and long-term (alveolar) particle clearance rates in the lower respiratory tract of the rat.

Administration, Inhalation↗

Acute and environmental toxicity studies with hexazinone.

The acute toxicity of hexazinone, a herbicide intended for general noncropland areas and selected crop uses (alfalfa and sugarcane), has been evaluated to establish proper handling guidelines and to measure its potential impact on the environment. The material is slightly to moderately toxic when given as a single oral dose; its LD50 in male rats is 1690 mg/kg, in male guinea pigs 860 mg/kg, and in male dogs greater than 3400 mg/kg although in the dog emesis prevented accurate quantitation. When the material is administered intraperitoneally, the LD50 in rats is 530 mg/kg. Repeated doses (five oral doses per week for 2 weeks) of 300 mg/kg to rats produced slight weight loss in one of two replicate experiments. In both studies, no gross or histologic alterations were apparent. Hexazinone is a moderate to severe eye irritant in the rabbit and produced only mild erythema in rabbit skin at 5278 mg/kg, a dose which did not produce lethality or other clinical signs. Subchronic dermal exposures (10 consecutive doses) to rabbits produced increases in serum alkaline phosphatase and glutamic-pyruvic transaminase at the highest levels tested (680 and 770 mg/kg in two separate experiments) with no effects seen at 150 mg/kg. There were no alterations in livers from treated rabbits examined by light microscopy. No dermal sensitization was produced when concentrations of up to 50% were tested in guinea pigs. One-hour inhalation exposure of up to 7.48 mg/liter did not produce mortality in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗

Vitamin E attenuates acute lung injury in sheep with burn and smoke inhalation injury.

INTRODUCTION: A decrease in alpha-tocopherol (vitamin E) plasma levels in burn patients is typically associated with increased mortality. We hypothesized that vitamin E supplementation (alpha-tocopherol) would attenuate acute lung injury induced by burn and smoke inhalation injury. MATERIALS AND METHODS: Under deep anesthesia, sheep (33 +/- 5 kg) were subjected to a flame burn (40% total body surface area, third degree) and inhalation injury (48 breaths of cotton smoke, < 40 degrees C). Half of the injured group received alpha-tocopherol (1000 IU vitamin E) orally, 24 h prior to injury. The sham group was neither injured nor given vitamin E. All three groups (n = 5 per group) were resuscitated with Ringer's lactate solution (4 ml/kg/%burn/24 h), and placed on a ventilator (PEEP = 5 cmH2O; tidal volume = 15 ml/kg) for 48 h. RESULTS: Plasma alpha-tocopherol per lipids doubled in the vitamin E treated sheep. Vitamin E treatment prior to injury largely prevented the increase in pulmonary permeability index and moderated the increase in lung lymph flow (52.6 +/- 6.2 ml/min, compared with 27.3 +/- 6.0 ml/min, respectively), increased the PaO2/FiO2 ratio, ameliorated both peak and pause airway pressure increases, and decreased plasma conjugated dienes and nitrotyrosine. CONCLUSIONS: Pretreatment with vitamin E ameliorated the acute lung injury caused by burn and smoke inhalation exposure.

Acute Disease↗

Toxicology of coal liquefaction products: an overview.

Repeated exposure to coal liquefaction products produces a broad range of systemic effects. Among these, growth suppression, anaemia, leucocytosis and other haematological disorders are most prominent. Bone marrow, liver and kidney are the target organs affected by treatment. The effects are more severe with heavy distillates and male rats are more sensitive than females. Other changes included increased serum transaminases, alkaline phosphatase and cholesterol. Depending on the route of administration, the skin or lung may also be affected. Inhalation exposure produces the most severe changes, and oral exposure the least. Distillates containing N-PAHs and sulphur-containing PAHs are also more biologically active. Teratological effects were only observed if animals were exposed to the heavy distillate. Similarly, heavy distillates have mutagenic or carcinogenic properties. Teratological effects, as well as mutagenicity and carcinogenicity, of the coal liquefaction distillates seem to be linked to their PAH content, especially the N-PAHs. From the data presented in this review, it should become evident that the potential effects of coal liquefaction products on human health could be severe, especially with long-term exposure. Limited information exists on the occupational effects to coal liquefaction materials because most of the work to date has been with pilot plants. Careful and good judgement is required in order to extrapolate data from pilot plants to commercial-scale production. Experience in health effects of workers in the petroleum industry and coke-oven operations can serve as a guide for the implementation of industrial hygiene programmes for coal liquefaction operations. These programmes include engineering controls, health education, personal monitoring and hygienic practices, medical surveillance and long-term epidemiology studies, and they should be implemented to make coal liquefaction a healthy and environmentally sustainable industry.

Administration, Cutaneous↗

Epidermal growth factor-like activity in bronchoalveolar lavage fluid in experimental silicosis.

We investigated whether development of pulmonary fibrosis following inhalational exposure of mice to silica (quartz) dust was accompanied by enhanced secretion of activity resembling epidermal growth factor (EGF). Mitogenic activity for pulmonary fibroblasts was assessed in bronchoalveolar lavage fluid (BALF) using a serum-free bioassay. Activity in BALF from mice exposed to nonfibrogenic titanium dioxide dust was comparable to that in BALF from normal animals. In contrast, mitogenic activity was significantly increased at 6 and 12 weeks after inhalation of silica particles, coinciding with the appearance of collagenised lesions in the lung. BALF from mice exposed to silica 6 weeks previously had significantly higher concentrations of growth factor(s) able to bind to EGF receptors on pulmonary fibroblasts. In parallel, macrophages within inflammatory lesions in the airspaces acquired immunoreactivity for EGF. The presence of an increased concentration of EGF-like growth factor(s) in BALF might constitute a marker of particle-induced pulmonary fibrosis.

Animals↗

Subchronic inhalation of high concentrations of low toxicity, low solubility particulates produces sustained pulmonary inflammation and cellular proliferation.

Long-term inhalation exposures to high dust burdens can produce tumors or proliferative keratin cysts in the lungs of exposed rats. We hypothesized that dust burdens which overwhelm lung clearance mechanisms are associated with sustained cellular proliferation responses and pulmonary inflammation. Male rats were exposed to titanium dioxide (TiO2) or carbonyl iron (CI) particles for 4 weeks at concentrations of 5, 50 and 250 mg/m3. Following completion of exposure, the lungs of sham and dust-exposed animals were lavaged or assessed for cell proliferation or particle clearance immediately after, as well as 1 week, 1, 3 and 6 months postexposure. Exposures to TiO2 or CI at 250 mg/m3 produced persistent pulmonary inflammatory responses and increased BrdU labeling of terminal airway and pulmonary parenchymal cells. The results of this study clearly demonstrate that exposure to excessive dust concentrations of two low toxicity, low solubility particle-types produced sustained pulmonary inflammation, enhanced pulmonary cell labeling, impairment of particle clearance, and the development of pulmonary lesions.

Administration, Inhalation↗

Toxicokinetics and effects of fibrous and nonfibrous particles.

Chronic inhalation of fibrous and nonfibrous particles by rats at high concentrations results in lung tumor formation if the particles are poorly soluble in the lung. Even rather benign nonfibrous particles such as TiO(2) produce this result. One significant change during a chronic inhalation exposure of poorly soluble particles of low cytotoxicity (PSP) is an impairment of normal clearance mechanisms in the alveolar region of the lung in rats, resulting in a continued buildup to high lung burdens accompanied by chronic alveolar inflammation, fibrosis, and mutational events. Since these are obviously high-dose effects, questions about their extrapolation to humans exposed to much lower concentrations have been raised. Results of key studies reported for chronic inhalation of PSP in rats indicate that mechanisms of PSP-induced lung tumors at high doses do not operate at low dose levels. Furthermore, the existence of two thresholds can be postulated: One is a dosimetric threshold for the endpoint alveolar macrophage-mediated clearance, which is related to lung particle overload. The other is a mechanistic threshold for the endpoint mutation, which is determined by the level of antioxidant defenses to counterbalance reactive oxidant species released by activated inflammatory cells. A no-observed-adverse-effect level (NOAEL) could therefore be based on avoiding alteration of the toxicokinetic of the particles such that the lung burdens stay below the dosimetric threshold. The suggestion that PSP-associated organic compounds (e.g., diesel particulate matter) contribute to the lung tumor responses in rats observed in chronic inhalation studies is not supported by experimental data from in vivo studies. It can be concluded that high-dose rat lung tumors due to PSP should not be used for low-dose extrapolations, and no significant contribution to human lung cancer risk can be predicted from levels of PSP below lung overload. With respect to the pulmonary toxicokinetics of inhaled fibrous particles, the biopersistence of long fibers (>20 microm) which cannot be phagocytized by alveolar macrophages is a key parameter related to long-term carcinogenic effects. Long fibers with a very low biopersistence should not be considered as carcinogenic. Since the clearance kinetics of fibers can generally be described by a biphasic or multiphasic pattern-fast initial and slow final phase-it is essential that the slow phase of the retention kinetics of fibers longer than 20 microm is considered in a biopersistence assay. Based on the results of such assay, fibers can be classified into one of two categories: a biopersistent fiber that cannot be dissolved in the lung within an acceptable time period; or a biosoluble fiber when even long nonphagocytizable fibers will be disappearing rapidly from the lung. However, in addition to biopersistence, it should be mandatory to evaluate fiber toxicity in an appropriate assay relative to a fiber whose long-term effects are well known. Moreover, for organic fibers it is likely that different rules may have to be established for characterization of their toxic and carcinogenic potential.

Administration, Inhalation↗

Pentobarbital-like discriminative stimulus properties of halothane, 1,1,1-trichloroethane, isoamyl nitrite, flurothyl and oxazepam in mice.

Volatile inhalants represent a diverse group of chemicals which pose a public health problem because of their abuse potential and neurobehavioral toxicity. Although relatively little is known about their pharmacology, they share certain pharmacological properties with classic central nervous system depressants. Drug discrimination procedures were used to compare the effects produced by pentobarbital (PB), oxazepam and several inhalants. Mice were trained to discriminate PB from saline injections in a two-lever operant task. Stimulus generalization was examined after 20-min inhalation exposures to halothane (500-8000 ppm), 1,1,1-trichloroethane (500-12000 ppm), isoamyl nitrite (150-1050 ppm), flurothyl (562-1300 ppm) and injections of oxazepam (0.1-20 mg/kg). Halothane, 1,1,1-trichloroethane and oxazepam produced discriminative stimulus effects similar to those produced by PB. Isoamyl nitrite and flurothyl, while decreasing rates of responding, were not consistently generalized from PB. Differences are apparent in the PB-like discriminative effects of inhalants. Toluene, as shown in a previous study, as well as halothane and 1,1,1-trichloroethane have PB-like discriminative effects which are also shared by oxazepam and may be another common effect of central nervous system depressants. Other chemicals, like isoamyl nitrite and flurothyl, are representative of qualitatively different classes of behaviorally active inhalants.

Administration, Inhalation↗

Occupational contact urticaria and late-phase bronchial asthma caused by compositae pollen in a florist.

Insect-pollinated members of the plant family Compositae (Asteraceae) rarely cause immediate-type hypersensitivity disease; however, this may have quite disabling consequences, which is shown by the case of a 42-year-old female florist. She developed contact urticaria later accompanied by rhinoconjunctivitis and bronchial asthma with maximum obstruction occurring some hours after the end of occupational exposure to the causative Compositae pollens of, for example, dandelions, blazing star, golden rod, yarrow, Aster ssp, chrysanthemums, and marguerite. Skin testing revealed immediate-type hypersensitivity to several members of the above-mentioned plant family confirmed by demonstration of specific IgE antibodies. Bronchial provocation testing yielded a positive response with all 4 pollen extracts tested. The patient had to give up work in a flower shop, because sufficient avoidance of airborne inhalant exposure was not considered practical.

Adult↗

Risk factors for adverse health effects following hazardous materials incidents.

To identify risk factors for persistent morbidity, we conducted a prospective study of individuals involved in hazardous materials incidents reported to the Washington Poison Center. Between December 1997 and October 1999, 202 subjects in 87 incidents were surveyed by telephone. Medical symptoms persisting for a minimum of 8 days after the incident were reported in 51 (25%) subjects, and 18 (9%) left work or school for more than 2 days because of the exposure. Medical intervention was reported in 46 (58%) of 79 subjects for whom medical records were available, and objective abnormalities were found in 57 (72%). Multiple logistic regression analysis indicated that subjects with dermal exposures, three or more alcoholic drinks per week, and previous use of psychiatric medications were more likely to report persistent symptoms. Divorced, widowed, or separated subjects, asthmatic subjects, and those having initial dermal symptoms were more likely to miss work or school for more than 2 days. Of patients evaluated at a health care facility, subjects with preexisting hypertension were more likely to receive medical treatment or have objective medical findings, whereas those with inhalation exposures and those decontaminated at the scene were less likely to be treated or have abnormalities. In our study, both incident and individual factors were predictive of adverse health effects, and these findings should be considered in planning the care of patients involved in hazardous materials incidents.

Disasters↗

The acute toxicity of tris(dimethylamino)silane.

The acute handling hazards of tris(dimethylamino)silane [TDMAS] were investigated. The acute male rat peroral LD50 (with 95% confidence limits) was 0.71 (0.51-0.97) ml/kg, and the acute male rabbit percutaneous LD50 was 0.57 (0.35-0.92) ml/kg. The liquid was severely irritating to the rabbit eye and skin, and the vapor severely irritating to the rat eye. The dynamically generated saturated vapor Lt50 in female rats was 12 (9.7-15) min. The effect of varying the atmospheric concentration of vapor from TDMAS on acute inhalation toxicity was investigated by passing ordinary moist air countercurrent to liquid TDMAS metered into a slightly heated glass tube. Based on nominal concentrations, the 4 hr-LC50 for vapor from TDMAS was 734 (603-893) ppm in female rats by this procedure. Stoichiometrically, this accords with toxicity due to liberation of dimethylamine (DMA) from TDMAS. In a subsequent study designed to assess the influence of relative humidity on vapor toxicity, nitrogen was passed over heated liquid TDMAS and the resultant atmosphere was introduced into the air intake duct of the inhalation exposure chamber. Gas chromatographically measured TDMAS concentrations (+/- SD) were 395 +/- 111, 127 +/- 25, 62 +/- 8 and 23 +/- 21 ppm; the corresponding DMA vapor concentrations were 112 +/- 171, 31 +/- 43, 10 +/- 6 and 26 +/- 44 ppm. The 4-hr LC50 (males and females) was 38 (34-43) ppm TDMAS vapor. Thus, TDMAS is of moderate acute peroral and percutaneous toxicity, a severe primary skin and eye irritant, an aspiration hazard, and of high intrinsic acute inhalation toxicity, but in moist air conditions lethal toxicity may be reduced and in such circumstances DMA may be a significant factor in toxicity.

Administration, Inhalation↗

A head-only exposure system for controlled exposures of small rodents.

We have designed a low-cost, compact, head-only exposure system which is easy to use and allows exposure of up to 8 or 16 small rodents depending on the chamber used with the system. Animals are exposed without anesthesia or extreme restraint. Deflection tubes at the chamber inlet and outlet serve to provide turbulent flow within the chamber. Performance of the exposure system was evaluated by analyzing data which was collected during investigations of the kinetics of respirable nickel chloride (NiCl2) and cobalt chloride (CoCl2) aerosols in Sprague-Dawley rats. Acute 2 h exposure to NiCl2 at concentrations ranging from 129 to 1208 micrograms Ni/m3 (MMAD 0.7-0.9 micron, sigma g 1.2-1.5) had a mean run-to-run coefficient of variation (cv) in chamber concentration of 11.6%, and a mean within-run cv of 8.5%. A 26-day repeated exposure of 3 groups of rats to 18.4 micrograms Ni/m3 gave a mean run-to-run cv of 20.9%, mean within-run cv of 10.2%, and within-day cv of 14.5%. Acute exposure studies with CoCl2 at concentrations ranging from 298 to 1371 micrograms Co/m3 (MMAD 0.9, sigma g 1.4) produced a mean run-to-run cv of 8.4% and a mean within-run cv of 7.8%. The repeated exposure of 2 groups of rats for 5 days to CoCl2 at a concentration of 583 micrograms Co/m3 had a mean run-to-run cv of 10.1%, a within-run cv of 7.4% and a within-day cv of 6.8%. The distribution of aerosol within the chamber is shown to have been uniform, and chamber performance was linear over the range tested. This system provides an inexpensive and uniform means of conducting inhalation exposure studies with selected airborne contaminants that might represent a potential health hazard.

Aerosols↗

Protection by extracellular glutathione against sulfur mustard induced toxicity in vitro.

1. The present study characterizes the role of extracellularly added glutathione in protection against sulfur mustard (HD) toxicity in a macrophage monocyte cell line J774. 2. Toxic effects of HD depend on dose and duration of exposure with an ED50 of 50 and 75 microM for dividing and confluent cells respectively. 3. Exposure to HD, 100-200 microM caused approximately 15% decrease in the cellular glutathione (GSH) content 2 h after exposure, pretreatment with GSH, 0.2-10 mM, elevated cellular GSH approximately x 1.5. 4. GSH pretreatment increased cell viability after HD 2-3-fold. Similar protective effects of GSH treatment were found in a human epidermoid carcinoma cell line (KB). 5. Protection by post treatment with GSH was apparent even 60 min post HD exposure. 6. No protection was afforded when the intracellular GSH concentration was elevated prior to exposure and the extracellular GSH had been washed out. However, GSH depleted cells were more sensitive to HD than normal cells, and were also protected by addition of GSH to the growth medium, although the intracellular GSH content remained low. 7. We conclude that it is essential for the GSH to be present extracellularly in order to protect cells from HD toxicity. 8. Our findings have therapeutic implications in particular for the protection of lungs after inhalation exposure to HD vapor.

Cell Line↗