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PubMed1986

Effects of inhalation exposure to a high-boiling (288 to 454 degrees C) coal liquid.

Coal liquids have been evaluated in a variety of short-term toxicological assays; however, few studies have been conducted to determine the systemic effects after inhalation exposure to these materials. To extend the data base on potential health effects from coal liquefaction materials, we performed a study with solvent refined coal (SRC)-II heavy distillate (HD). Fischer-344 rats were exposed for 6 hr/day, 5 days/week for 5 or 13 weeks to an aerosol of HD (boiling range, 288 to 454 degrees C) at concentrations of 0.69, 0.14, 0.03, or 0.0 mg/liter of air for the high, middle, low, and control groups, respectively. Survival through 13 weeks of exposure was greater than 90% for all groups; body weights for exposed animals were decreased in a dose-dependent manner. Significant increases in liver weights and decreases in thymus and ovary weights were observed for treated animals compared with controls. There were also significant treatment-related decreases in erythrocytes, hemoglobin, volume of packed red blood cells, lymphocytes, eosinophils, and total white blood cells. After 5 weeks of exposure serum cholesterol concentrations increased in a dose-dependent manner for both sexes and serum triglyceride amounts decreased for males but not for females. After 13 weeks of exposure, high-dose animals had significant increases in cholesterol (males only), triglycerides, blood urea nitrogen, and serum glutamic pyruvic transaminase (SGPT; males) and significant decreases in albumin, SGPT (females), and lactate dehydrogenase (LDH). Examination of bone-marrow preparations from exposed animals demonstrated consistent decreases in the degree of cellularity, suggesting that this organ is a target for HD. Microscopic evaluation of organ sections indicated exposure-related changes for nasal mucosa, pulmonary macrophages, thymus, liver, kidney, bone marrow, ovaries, and cecum. Results from this study indicated dose-dependent increases in the severity of the lesions observed, with few effects in the low-exposure group that were attributable to the exposure.

Animals↗
PubMed1989

Genotoxicity studies on mice after short term inhalation exposure to methyl isocyanate.

Mutagenicity testing is an important aspect of the toxicological evaluation of environmental chemicals for safety. Methyl isocyanate (MIC), a very hazardous chemical used for the manufacture of insecticides, was studied for its genotoxic effects on the somatic cells of mice after inhalation exposure by means of an in vivo micronucleus test and chromosomal analysis of bone marrow cells. Animals were exposed for 10 min to different concentrations (2.40, 4.80 or 7.20 microliters) of MIC in a 22 litre chamber at 0 and 24 h. Bone marrow smears prepared 6 h after the second treatment were examined for the occurrence of micronuclei (MN) in polychromatic (P) and normochromatic (N) erythrocytes. The frequencies of cells with MN and the P/N ratio did not differ significantly from those of the control at all the exposure levels. Chromosomal preparations revealed few structural and numerical abnormalities. Aberrations encountered were of the chromatid type only. Quantitative analyses failed to exhibit any significant increase in aberration rates in the three treated groups. Numerical abnormalities were within the control range.

Administration, Inhalation↗
PubMed1987

Two-hour methyl isocyanate inhalation exposure and 91-day recovery: a preliminary description of pathologic changes in F344 rats.

The accidental release of methyl isocyanate (MIC) in Bhopal, India, was reportedly responsible for the deaths of more than 2,000 people. To study the pathology of acute inhalation exposure to MIC, the tissues of male and female Fischer 344 rats were evaluated immediately after a single 2-hr exposure to 0, 3, 10, or 30 ppm MIC, and through day 91. Early gross pathologic changes in the 30 ppm-exposed rats included a reddish white encrustation around the mouth and nose, a small thymus, and distension of the gastrointestinal tract with gas. Lungs (middle and median lobes) showed consolidation and hemorrhage and failed to deflate when the chest cavity was opened. Microscopic changes in the upper respiratory tract 3 hr after exposure included marked erosion and separation of olfactory and respiratory epithelia from the basement membrane with accumulation of serofibrinous fluid. On day 1, acute inflammation and fibrinopurulent exudate partially blocked the nasal passages. Epithelial cells had sloughed from the nasopharynx, trachea, bronchi, and major bronchioles, leaving the basement membrane covered with fibrin and exudate. Granulomatous inflammation and intraluminal fibrosis of the airways were observed by day 3, with increased intraluminal fibrosis by day 7. Lower airways became blocked by exfoliated cells, mucous plugs, and/or intraluminal fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Retardation of the age-related increase in spontaneous cortical spike-wave discharges (SWD) in rats after a 28-day inhalation (SWD) in rats after a 28-day inhalation exposure to an industrial solvent, pseudocumene (1,2,4-trimethylbenzene).

It has been hypothesized that exposure to neurotoxins may hasten the process of brain ageing. Volatile hydrocarbons are in common use as solvents and their neurotoxic properties are acknowledged. In the rat, the age-related neurodegenerative changes in the brain develop together with an increased occurrence of bursts of spontaneous spike-wave discharges (SWD) in the neocortex. Therefore, the number and/or duration of SWD bursts may serve as an index allowing to distinguish between young and old brains (7). Measuring the SWD activity after exposure may thus reveal the effect of the studied neurotoxicant on brain ageing. Pseudocumene (1,2,4-trimethylbenzene, TMB), is a component of industrial solvent mixtures. The present study investigated the effect of a 4-week (6h/day, 5 days/week) inhalation exposure to TMB at concentrations of 0, 25, 100 or 250 ppm on the occurrence of SWD bursts. EEG recordings were performed before and one day, 30 days and 4 months after exposure. In rats exposed to TMB at 0 and 25 ppm, the level of the SWD activity increased progressively after exposure. In rats exposed to TMB at 100 or 250 ppm, the SWD activity did not increase during the post-exposure period or even dropped below the pre-exposure level. This result indicates that the persistent changes in the rat central nervous system (CNS), following the exposure to TMB, differ in some respects from those which develop in the course of normal ageing.

Administration, Inhalation↗
PubMed1977

Human intoxication following inhalation exposure to synthetic jet lubricating oil.

A previously healthy member of an aircraft flight crew was acutely incapacitated during flight with neurologic impairment and gastrointestinal distress. His clinical status returned to normal within 24 hr. The etiology of his symptoms was related to an inhalation exposure to aerosolized or vaporized synthetic lubricating oil arising from a jet engine of his aircraft.

Adult↗
PubMed2002

Pulmonary granulomas of guinea pigs induced by inhalation exposure of heat-treated BCG Pasteur, purified trehalose dimycolate and methyl ketomycolate.

This study was designed to determine the identity of granulomatogenic substances in Mycobacterium bovis BCG Pasteur. When heat-treated BCG Pasteur bacilli were introduced into the lungs of guinea-pigs by an inhalation exposure apparatus, pulmonary granulomas without necrosis developed. Furthermore, when four kinds of mycolates derived from M. tuberculosis Aoyama B strain were introduced into the lungs by the same method, only trehalose 6,6'-dimycolate (TDM) and methyl ketomycolate induced pulmonary granulomas without central necrosis. The pulmonary granulomas consisted of epithelioid macrophages and lymphocytes. When a mixture of TDM and anti-TDM antibody was introduced into the lungs, development of granulomatous lesions was reduced. These data indicate that TDM and methyl ketomycolate are potent granulomatogenic reagents.

Administration, Inhalation↗
PubMed1992

Delayed effects of acute oral and chronic inhalational exposure to methylparathion on learning and memory in rats.

Impairment of acquisition phase of the learning process was observed in rats even at 3 weeks after single oral exposure to the near-lethal dose of commercial grade methylparathion (MP) followed by atropine resuscitation. Though there was a trend towards memory impairment in this group of animals, memory retention was not significantly affected. Chronic inhalational exposure to MP (one exposure/day for 3 weeks) did not significantly alter learning or memory. No significant alteration in red blood cell or brain acetylcholinesterase levels were observed in either of the two groups. It appears that behavioural effects can persist even 3 weeks after exposure to acute near-lethal doses of the pesticide, as occurs in the clinical situation of suicidal attempts; while repeated exposure to no-observed-effect-level doses as occurs in farm and factory workers, may not be associated with behavioural changes.

Acetylcholinesterase↗
PubMed1996

[A quantitative evaluation of risk associated with occupational inhalation exposure to polycyclic aromatic hydrocarbons in Polish production plants].

In the early eighties, carcinogenic components of polycyclic aromatic hydrocarbons (PAHs) were classified by IARC as potentially carcinogenic to humans, but later epidemiological studies indicate an increased mortality from lung cancer among workers exposed to PAHs. In Poland the highest, although, diversified occupational inhalation exposure to PAHs is observed in the coke production, aluminium metallurgy and steel industries. The cancer risk among workers employed in these industrial plants was assessed in relation to concentrations of benzo(a)pyrene in the air zone of working posts. A wide range of results from 1.11 x 10(-11) to 1.4 x 10(-3), corresponding to the exposure size, was obtained. In order to show the relationship between occupational risk values and environmental exposure risk, both risks were compared using the same multistage model whose coefficients were estimated by employing the maximum likelihood method. It appeared that the occupational risk at working posts with benzo(a)pyrene concentration within allowable values is similar or lower than risk related with cigarette smoking or alimentary exposure (food intake).

Air Pollutants, Occupational↗
PubMed1998

Regional brain dosimetry of trichloroethane in mice and rats following inhalation exposures.

While certain neuroactive volatile organic compounds (VOCs) have been reported to have an uneven distribution in various anatomically distinctive brain regions, this has not yet been reported for the short-chain aliphatic halogenated hydrocarbons. Therefore, the uptake and regional brain distribution of 1, 1, 1-trichloroethane (TRI) in mice and rats following inhalation exposure were examined. Male Sprague-Dawley rats and CD-1 mice were exposed to TRI at either 3500 or 5000 ppm for 10, 30, 60, or 120 min. Seven brain regions from rats and three from mice were sampled, and TRI concentrations in the blood and brain tissues were determined by headspace gas chromatography. In both species, the medulla oblongata was found to have the highest TRI concentrations, while cortex (in both species) and hippocampus (only sampled in rats) contained the lowest TRI concentrations. Substantial differences were also observed between the two species, as the mice exhibited higher capacity to accumulate TRI in the blood as well as in the brain regions. It appears that lipid content is a main factor influencing the differential disposition of TRI among the brains regions. Physiological differences in the respiratory systems of the two species and the physiochemical properties of the chemical favoring diffusion toward lipid-rich compartments could also have been expected to account for the patterns of regional distribution and species differences.

Administration, Inhalation↗
PubMed1992

Application of the EPR spin-trapping technique to the detection of radicals produced in vivo during inhalation exposure of rats to ozone.

Ozone is known to induce lipid peroxidation of lung tissue, although no direct evidence of free radical formation has been reported. We have used the electron paramagnetic resonance (EPR) spin-trapping technique to search for free radicals produced in vivo by ozone exposure. The spin trap alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) was administered ip to male Sprague-Dawley rats. The rats were then exposed for 2 hr to either 0, 0.5, 1.0, 1.5, or 2.0 ppm ozone with 8% CO2 to increase their respiratory rate. A six-line 4-POBN/radical spin adduct signal (aN = 15.02 G and a beta H = 3.27 G) was detected by EPR spectroscopy in lipid extracts from lungs of rats treated with 4-POBN and then exposed to ozone. Only a weak signal was observed in the corresponding solution from rats exposed to 0 ppm ozone (air with CO2 only). The concentration of the radical adduct increased as a function of ozone concentration. After administration of 4-POBN, rats were exposed for either 0.5, 1.0, 2.0, or 4.0 hr to either 0 or 2.0 ppm ozone (with CO2). The radical adduct concentration of the ozone-exposed groups at exposure times of 2.0 and 4.0 hr was significantly different from that of the corresponding air control groups. A correlation was observed between the radical adduct concentration and the lung weight/body weight ratio. These results demonstrate that ozone induces the production of free radicals in rat lungs during inhalation exposure and that radical production may be involved in the induction of pulmonary toxicity by ozone. This is the first direct evidence for ozone-induced free radical production in vivo.

Administration, Inhalation↗
PubMed1982

The biodistribution and metabolic fate of [11C]acrylic acid in the rat after acute inhalation exposure or stomach intubation.

Rats were nose-exposed to an atmosphere containing gaseous [11C]acrylic acid for 1 min and sacrificed 1.5 and 65 min later. At 1.5 min 28% of the administered radiolabel was associated with the snout of the exposed animal. The biodistribution data indicated the gastrointestinal tract as the major site of absorption of acrylic acid after inhalation exposure. Therefore, rats were also stomach intubated with an aqueous solution of [11C]acrylic acid and sacrificed at 1.5, 10, 20, 40, and 65 min after intubation. The absorption of acrylic acid from the stomach was rapid, as was its subsequent metabolism. Carbon-11 was rapidly eliminated from both nose-exposed and stomach-intubated animals as 11CO2, with about 60% of the administered dose eliminated 1 h after administration. A portion of the radiolabel was also eliminated via the renal system.

Acrylates↗
PubMedDate not supplied

Neutral endopeptidase (NEP) and its role in pathological pulmonary change with inhalation exposure to JP-8 jet fuel.

Through a simulated flightline exposure protocol, Fischer 344 rats (F344) were subjected to an aerosol/vapor mix of the military jet fuel, JP-8. Previous studies with this model of lung injury have revealed significant increases in pulmonary resistance, increased alveolar clearance of 99mTcDTPA, and a decrease in bronchoalveolar lavage fluid (BALF) concentration of the neuropeptide substance P (SP). Exposures to JP-8 were nose-only and for one hour daily. Six groups of Fischer 344 rats were exposed for 7, 28, or 56 days at two JP-8 concentrations (low dose = 469-520 mg/m3/hr, high dose = 814-1263 mg/m3/hr). Exposed groups were matched with longitudinal controls. In response to JP-8 inhalation, exposure animals demonstrated a dose-dependent as well as duration-determined reduction in BALF SP concentration. Both JP-8 concentrations caused significant pathological changes in lower pulmonary structures.

Administration, Inhalation↗
PubMed1988

Formaldehyde concentrations in the blood of rhesus monkeys after inhalation exposure.

The effect of subchronic exposure to formaldehyde (HCHO; 6 ppm; 6 hr/day, 5 days/wk for 4 wk) on the HCHO concentration in the blood of three rhesus monkeys was investigated. Immediately after the final exposure, the monkeys were sedated, and blood samples were withdrawn 7 min after the end of exposure. The HCHO concentration in the blood, determined by gas chromatography-mass spectrometry was 1.84 +/- 0.15 micrograms/g blood and did not differ significantly after a further 45 hr without exposure to HCHO (2.04 +/- 0.40 micrograms/g blood). The average concentration of HCHO in the blood of exposed monkeys was also not significantly different from that of three unexposed controls (2.42 +/- 0.09 micrograms/g blood). However, individual monkeys differed significantly from one another with respect to their blood concentrations of HCHO. These results indicate that subchronic inhalation exposure of non-human primates to HCHO has no significant effect on the HCHO concentration in the blood, and that the average concentration of HCHO in the blood of monkeys is similar to that in the blood of humans.

Administration, Inhalation↗
PubMed1994

Development of a cloning assay with high cloning efficiency to detect induction of 6-thioguanine-resistant lymphocytes in spleen of adult mice following in vivo inhalation exposure to 1,3-butadiene.

A cloning assay with high cloning efficiency has been developed to detect spontaneous and induced 6-thioguanine-resistant T-lymphocytes (HPRT mutants) from the spleen of adult mice. The mean cloning efficiency in untreated male mice of 20-22 weeks old was 34.5 +/- 11.2% (SD) and the corresponding mutant frequency 0.7 +/- 0.8 (SD) x 10(-6). The cloning efficiencies obtained in this study are substantially higher than those reported previously by other investigators. Using this assay, it could be demonstrated that inhalation exposure of mice to 200, 500 or 1300 ppm of 1,3-butadiene for 6 h/day on 5 consecutive days caused a statistically significant induction of 6-thioguanine-resistant mutations in T-lymphocytes from spleens of adult mice exposed to 1300 ppm. The exposure to 1300 ppm resulted in a three-fold increase of the spontaneous mutant frequency. The mutant frequency after exposure to 500 ppm was higher than the control but the increase was not significant.

Administration, Inhalation↗
PubMed1994

Nonspecific airway hyperresponsiveness induced by inhalation exposure to sulfuric acid aerosol: an in vitro assessment.

Air pollution may be a factor in the recent increase in severity and prevalence of asthma, but the specific chemical components within the ambient pollutant mix which may be responsible have not been delineated. Acid sulfate aerosols, such as sulfuric acid, have been associated with exacerbation of symptoms in asthmatics and induction of nonspecific airway hyperresponsiveness in normal laboratory animals. This study examined the ability of single (3 hr) inhalation exposures to sulfuric acid to induce nonspecific airway hyperresponsiveness in healthy rabbits. Responsiveness was assessed using an in vitro assay involving administration of increasing doses of acetylcholine or histamine to bronchial and tracheal rings obtained from animals exposed to 50-500 micrograms/m3 sulfuric acid aerosol. Bronchial hyperresponsiveness to both agonists was noted following exposures at > or = 75 micrograms/m3. In addition, sulfuric acid altered the normal response pattern of trachea to histamine. The results provide further support for a role of acid sulfates in the induction of airway hyperresponsiveness, and suggest that effects may be due to modulation of pharmacological receptors involved in maintaining airway tone.

Acetylcholine↗
PubMed1986

The effect of aerosol on estimates of inhalation exposure to airborne styrene.

Exposure to volatile organic contaminants usually is attributed to vapors alone; samples are collected on charcoal tubes or by passive dosimeters. This study demonstrated that aerosols, generated during the spraying of polyester resin solution, can contribute significantly to the exposure to volatile organic contaminants. Four spraying experiments were performed during which 64 samples were collected and analyzed to determine the styrene air concentrations. The results from the four spraying experiments showed that aerosols represented 30% +/- 3% of the total air concentration of styrene. The contribution of aerosols to inhalation exposure needs to be considered in other industrial situations where spray processes are used.

Aerosols↗
PubMed2003

Policy on acute toxic ingestion or dermal or inhalation exposure.

Many nurse practitioners (NPs) practice in emergency and urgent-care settings, and far more practice in remote settings. NPs in each of these settings should be familiar with the assessment, stabilization, and treatment of patients who seek treatment for suspected intentional or accidental poisoning. This month's clinical practice guideline (CPG) column reviews the "Clinical Policy for the Initial Approach to Patients Presenting With Acute Toxic Ingestion or Dermal or Inhalation Exposure."

Acute Disease↗
PubMed1998

Siting criteria based on the prevention of deterministic effects from plutonium inhalation exposures.

Siting criteria are established by regulatory authorities to evaluate potential accident scenarios associated with proposed nuclear facilities. The 0.25 Sv (25 rem) siting criteria adopted in the United States has been historically based on the prevention of deterministic effects from acute, whole-body exposures. The Department of Energy has extended the applicability of this criterion to radionuclides that deliver chronic, organ-specific irradiation through the specification of a 0.25 Sv (25 rem) committed effective dose equivalent siting criterion. A methodology is developed to determine siting criteria based on the prevention of deterministic effects from inhalation intakes of radionuclides which deliver chronic, organ-specific irradiation. Revised siting criteria, expressed in terms of committed effective dose equivalent, are proposed for nuclear facilities that handle primarily plutonium compounds. The analysis determined that a siting criterion of 1.2 Sv (120 rem) committed effective dose equivalent for inhalation exposures to weapons-grade plutonium meets the historical goal of preventing deterministic effects during a facility accident scenario. The criterion also meets the Nuclear Regulatory Commission and Department of Energy Nuclear Safety Goals provided that the frequency of the accident is sufficiently low.

Air Pollution, Radioactive↗