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PubMed1983

Retention of inhaled 238PuO2 in beagles: a mechanistic approach to description.

Groups of Beagle dogs received inhalation exposure to one of three sizes of monodisperse or a polydisperse aerosol of 238PuO2. Periodic sacrifice of pairs of dogs through 4 yr after inhalation exposure provided data on the retention, translocation and mode of excretion of 238Pu. Fragmentation of 238PuO2 particles deposited in lung led to enhanced dissolution, translocation and excretion of 238Pu compared to previous studies using 239PuO2. A mechanistic simulation model was formulated to account for particle dissolution and fragmentation. This model provided adequate prediction of the time course of lung retention, uptake and retention in other organs and excretion. Predictions of the model provided more accurate description of the data than the Task Group on Lung Dynamics model incorporated in the ICRP Publication 30. The mechanistic model provided estimates of cumulative radiation dose to liver and bone that are a factor of five greater and to lung that are a factor of two less than predicted by the Task Group Lung Model.

Aerosols↗
PubMed2001

Risks of fatal cancer from inhalation of 239,240plutonium by humans: a combined four-method approach with uncertainty evaluation.

The risk per unit dose to the four primary cancer sites for plutonium inhalation exposure (lung, liver, bone, bone marrow) is estimated by combining the risk estimates that are derived from four independent approaches. Each approach represents a fundamentally different source of data from which plutonium risk estimates can be derived. These are: (1) epidemiologic studies of workers exposed to plutonium; (2) epidemiologic studies of persons exposed to low-LET radiation combined with a factor for the relative biological effectiveness (RBE) of plutonium alpha particles appropriate for each cancer site of concern; (3) epidemiologic studies of persons exposed to alpha-emitting radionuclides other than plutonium; and (4) controlled studies of animals exposed to plutonium and other alpha-emitting radionuclides extrapolated to humans. This procedure yielded the following organ-specific estimates of the distribution of mortality risk per unit dose from exposure to plutonium expressed as the median estimate with the 5th to 95th percentiles of the distribution in parentheses: lung 0.13 Gy(-1) (0.022-0.53 Gy(-1)); liver 0.057 Gy(-1) (0.011-0.47 Gy(-1)); bone 0.0013 Gy(-1) (0.000060-0.025 Gy(-1)); bone marrow (leukemia), 0.013 Gy(-1) (0.00061-0.05 Gy(-1)). Because the different tissues do not receive the same dose following an inhalation exposure, the mortality risk per unit intake of activity via inhalation of a 1-microm AMAD plutonium aerosol also was determined. To do this, inhalation dose coefficients based on the most recent ICRP models and accounting for input parameter uncertainties were combined with the risk coefficients described above. The following estimates of the distribution of mortality risk per unit intake were determined for a 1-microm AMAD plutonium aerosol with a geometric standard deviation of 2.5: lung 5.3 x 10(-7) Bq(-1) (0.65-35 x 10(-7) Bq(-1)), liver 1.2 x 10(-7) Bq(-1) (0.091-20 x 10(-7) Bq(-1)), bone 0.11 x 10(-7) Bq(-1) (0.0030-4.3 x 10(-7) Bq(-1)), bone marrow (leukemia) 0.049 x 10(-7) Bq(-1) (0.0017-0.59 x 10(-7) Bq(-1)). The cancer mortality risk for all sites was estimated to be 10 x 10(-7) Bq(-1) (2.1-55 x 10(-7) Bq(-1))--a result that agrees very well with other recent estimates. The large uncertainties in the risks per unit intake of activity reflect the combined uncertainty in the dose and risk coefficients.

Administration, Inhalation↗
PubMed1991

[The effect of inhalation of sevoflurane for an hour on the liver of beagles].

The effect of sevoflurane in comparison with that of enflurane and halothane, each at 1.8 MAC, on the liver was examined after inhalation exposure to beagles under controlled respiration for 1 hr. No abnormalities were observed in general conditions in the animals exposed to any of these anesthetics. Recovery time to spontaneous respiration after the end of anesthesia was similar for each group, but the awakening was quickest in sevoflurane exposed group. Blood pressure dropped immediately after the initiation of exposure in each group, but it recovered quickly to preexposure levels after the end of the exposure. Minor and reversible elevations in the values of GOT, GPT, LDH and bilirubin were noted without the organic change of the liver in beagles after the inhalation exposure to 1.8 MAC of each anesthetic. Since similar changes were observed in beagles exposed to enflurane or halothane, we conclude that no change in the liver specifically associated with sevoflurane was found under these experimental conditions.

Anesthesia, Inhalation↗
PubMed1992

Determination of program protection factors for half-mask respirators used at a mineral sands separation plant.

A study was conducted at a mineral sands separation plant to evaluate the workplace performance of half-mask filter cartridge respirators. Inhalation exposure was estimated by measuring the dust and radioactivity concentration inside the respirator while it was worn or hanging around the worker's neck. The program protection factor was determined by simultaneously measuring inside-mask and ambient (outside-mask) concentrations. A total of 27 tests were conducted, covering three brands of half-mask respirators; facial hair on test subjects ranged from clean-shaven to bearded. Program protection factors varied from 1.8 to 13 for dust exposure and 2.5 to 21 for radioactivity exposure. The geometric mean program protection factor over all tests was 5.1 (geometric standard deviation [GSD] = 1.7) for dust exposure and 7.5 (GSD = 1.7) for radioactivity exposure. A minimum program protection factor of 3.5 could be applied to ambient airborne concentration data to obtain a conservative, but more realistic, estimate of inhalation exposure on a worker category basis.

Air Pollutants, Radioactive↗
PubMed1997

CS2-mediated cross-linking of erythrocyte spectrin and neurofilament protein: dose response and temporal relationship to the formation of axonal swellings.

Using model proteins, a mechanism for CS2-mediated covalent cross-linking of proteins has been demonstrated previously. The biologic importance of CS2-promoted protein cross-linking is apparent as a possible dosimeter of CS2 exposure and as a potential mechanism to account for the identical neuropathies produced by 2,5-hexanedione and CS2. The present investigation examines the utility of erythrocyte spectrin cross-linking as a biomarker of effect for inhalation exposure to CS2 and examines the ability of CS2 to cross-link neurofilament proteins, a potential neurotoxic target. Rats were exposed to CS2 via inhalation at control, 50-, 500-, and 800-ppm levels for 2, 4, 8, and 13 weeks and spectrin dimer formation was quantified using denaturing gel electrophoresis and densitometry. Neurofilament preparations were also obtained from spinal cords and examined for cross-linking using Western blotting methods. The results obtained for protein cross-linking were compared to morphologic changes in the cervical and lumbar spinal cord using light and electron microscopy. The spectrin dimer exhibited a cumulative dose response and was detectable at both the 50-ppm level employed that did not produce axonal swellings and prior to the development of axonal swellings for the 500- and 800-ppm levels used. Neurofilament protein cross-linking involved all three subunits and the temporal relationship of cross-linking was consistent with a contributing role in the development of axonal swellings. These results establish the sensitivity of spectrin cross-linking for evaluating inhalation exposures and extend the similarities observed for 2,5-hexanedione and CS2 in both clinical settings and in vitro models to their effects exerted on neurofilaments in the axon.

Administration, Inhalation↗
PubMed1984

Acrylonitrile inhalation in rats: I. Effect on intermediary metabolism.

In male Wistar rats the inhalation exposure to acrylonitrile (AN), 280 mg X m-3, 8 hours a day for five days significantly decreased the serum concentration of cholesterol and triglycerides, but the liver concentrations of phospholipids, and esterified fatty acids were unchanged. The liver microsomal protein and cytochrome P-450 content decreased significantly. On the other hand the levels of glucose, lactate and pyruvate in the blood and brain significantly increased up to 250% of controls. A microscopic examination of the lungs, liver, kidneys and adrenals did not show structural changes and the numbers and enzyme activities of alveolar macrophages were also unaffected. In single 12-hour inhalation exposures the elevation of blood glucose was proportional to the inhaled concentration of AN (average concentrations 57, 125, or 271 mg X m-3); the effect was significant at the lowest AN concentration and was intensified in the glucose tolerance test. The elevation of blood glucose proved to be the most sensitive and dose-related indicator of AN exposure of those observed.

Acrylonitrile↗
PubMedDate not supplied

A physiologically based description of ethylene oxide dosimetry in the rat.

A physiologically based pharmacokinetic (PB-PK) model providing a quantitative description of ethylene oxide (ETO) dosimetry in the rat was developed by integrating information on physiology, tissue solubility of ETO, and rate constants for ETO metabolism and binding. The PB-PK model consisted of nine compartments; liver, lung, testis, brain, fat, venous blood, arterial blood, richly perfused and poorly perfused tissues. The tissue: air partition coefficients of ETO, determined by vial equilibration, were similar among the various tissues (range 44-83). The rate constants for glutathione (GSH) conjugation, hydrolysis, and hemoglobin (Hb)- and DNA-binding were estimated from published data and by conducting in vivo inhalation exposure studies. The model adequately predicted the concentrations of Hb and DNA adducts, hepatic and extrahepatic GSH, and urinary N-acetyl-S-(2-hydroxyethyl)-cysteine following inhalation exposures of 1.2 to 1,200 ppm and intravenous administration of 1 to 100 mg/kg of ETO in male Fischer-344 and Sprague-Dawley rats. There was no evidence of nonlinearity in the overall elimination of ETO in the dose range examined. However, nonlinearities in the components of this first order elimination process (namely GSH conjugation, hydrolysis, exhalation) were found to occur at high exposure concentrations. Characterization of the individual metabolic pathways that affect the tissue dosimetry of ETO is important for interspecies extrapolation and risk assessment for this chemical.

Animals↗
PubMed1993

Molecular epidemiology of lung cancer and the modulation of markers of chronic carcinogen exposure by chemopreventive agents.

Chronic inhalation exposure to environmental carcinogens such as polycyclic aromatic hydrocarbons (PAHs), cigarette smoke, 4-aminobiphenyl (4-ABP), ethylene oxide, and styrene is associated with elevations in biomarkers such as DNA adducts, protein adducts, sister chromatid exchanges (SCEs), chromosomal aberrations, gene mutation, and/or oncogene activation. These biomarkers indicate an increased cancer risk for the exposed population, although quantitative estimates cannot be made with certainty. There is convincing epidemiological evidence that the antioxidant and free radical-scavenging vitamins C and E and beta-carotene (beta-C) protect against cancer of the lung and other epithelial tissues, with somewhat weaker evidence for retinol. Experimental studies demonstrate that these micronutrients are capable of blocking or reducing tumor formation caused by diverse carcinogens. A variety of mechanisms appear to be involved, including suppression of carcinogen activation, enhancement of carcinogen detoxification, induction of cellular differentiation, inhibition of mutagenesis, enhancement of immunologic function, and/or reduction of the formation of carcinogen-DNA adducts, SCEs, micronuclei, and other markers of genotoxic damage. Therefore, we have recently investigated the possible modifying effect of serum vitamins C and E, beta-C, and retinol on a number of such biomarkers in a case-control study of lung cancer, and in a cross-sectional study of heavy smokers. Preliminary results indicate an inhibitory effect of certain vitamins on DNA adduct formation. A significant number of human intervention trials are ongoing involving these vitamins. It appears that biomarkers can provide useful intermediate endpoints for assessment of both the mechanisms and the efficacy of chemopreventive agents.

Animals↗
PubMed1983

The effects of acrolein exposure on pulmonary antibacterial defenses.

Inhalation exposure to acrolein induced a dose-dependent impairment of pulmonary antibacterial defenses in mice. Animals exposed to 3 or 6 ppm of acrolein were increasingly less effective in inactivation of aerogenic challenges of 32P-labeled Staphylococcus aureus. Acrolein concentrations greater than 6 ppm caused increased sensory irritations, but no additional impairment of lung antibacterial resistance. Influenza A viral pneumonia in mice also suppressed pulmonary bacterial activity. Mice convalescing from moderate viral pneumonia became severely deficient in antibacterial defenses when exposed to acrolein. Whether the viral-induced impairment in pulmonary defense delayed the inactivation or allowed the proliferation of bacteria was dependent upon the dose of acrolein. The present study demonstrated that an underlying infectious disease process compounded the pulmonary toxicity of acrolein such that normally moderate toxicity was elevated to a virtual abolition of antibacterial defense mechanisms.

Acrolein↗
PubMed1980

Enhancement of hepatic drug biotransformation by a short-term intermittent turpentine exposure in the rat.

An inhalation exposure of male rats to 300 p.p.m. of a commercial turpentine 6 hrs daily 5 days a week for 8 weeks enhanced the activities of drug biotransformation enzymes of liver microsomes considerably. The activities of NADPH cytochrome c reductase and 7-ethoxycoumarin deethylase, and microsomal content of cytochrome P-450 were increased 35-60% during the first weeks of the experiment, but had a tendency to return towards the control values later on. A similar enhancement of activities was also found in liver microsomal epoxide hydratase and UDP glucuronosyltransferase, but these enzyme activities tended to adapt less during the experiment. The turpentine treatment increased the affinity of liver microsomal cytochrome P-450 to alpha-pinene (the main component of the turpentine). The present data suggests that exposure to turpentine is able to modify considerably the biotransformation of drugs.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1994

A comparison of the acute behavioral effects of alkylbenzenes using a functional observational battery in mice.

The acute neurobehavioral effects of six alkylbenzenes (benzene, toluene, ethylbenzene, propylbenzene, m-xylene, and cumene) were evaluated after 20-min inhalation exposures using a functional observational battery (FOB) in mice. In order to do this, an explicit protocol for the FOB developed for rats by Moser was adapted for use in mice with inhalation exposures. All six alkylbenzenes, in the concentration range of 2000 to 8000 ppm, produced a nearly identical profile of effects, a profile that was also produced by ip administration of the central nervous system depressant drug pentobarbital. These effects included changes in posture, decreased arousal and rearing, increased ease of handling, disturbances of gait, mobility, and righting reflex, decreased forelimb grip strength, increased landing foot splay, and impaired psychomotor coordination. The response to various sensory stimuli was also decreased by the alkylbenzenes and pentobarbital. These acute effects of alkylbenzenes were short-lived, with recovery beginning within minutes of removal from the exposure chamber. The finding that the alkylbenzenes produce a profile of neurobehavioral effects similar to that of pentobarbital is consistent with a growing body of other evidence that many solvents produce a profile of acute effects similar to that of central nervous system depressant drugs and ethanol.

Administration, Inhalation↗
PubMed1983

In vitro and in vivo response after exposure to man-made mineral and asbestos insulation fibers.

The relative in vitro and in vivo toxicity of several types of manufactured fibrous glass insulation and crocidolite asbestos was investigated to aid in selection of a suitable glass fiber for subsequent use in inhalation exposures. The in vitro cytotoxicity to pulmonary alveolar macrophages of small glass fibers from microfiber insulation (count median diameter (CMD) approximately 0.1-0.2 micrometer) was greater than that of the larger fibers from household insulation (CMD approximately 2.4 micrometers). To screen for in vivo pulmonary toxicity, 2-21 mg of glass or asbestos fibers were administered in divided doses to male Syrian hamsters by intratracheal instillation. Animals were sacrificed at 1, 3.5 and 11 months following initial administration of material. One type of glass microfiber [count median diameter (CMD) approximately 0.1 micrometer] caused deaths from pulmonary edema at early times after instillation. High levels of asbestos, a second glass microfiber (CMD approximately 0.2 micrometer) and one type of household insulation fiber (CMD 2.3 micrometers) all resulted in increase in total collagen and mild pulmonary fibrosis at later times after instillation, although microfiber insulation produced a greater response than household insulation. Asbestos insulation produced the greatest response. A five-day inhalation exposure to a high level of glass microfibers deposited in lung less than 10 percent of the lowest instilled amount which elicited indications of lung injury. This amount did not produce significant biological changes at 1 to 12 months after exposure.

Animals↗
PubMed2002

Bronchial challenges with aerosolized food in asthmatic, food-allergic children.

BACKGROUND: Allergic asthma is usually considered to be provoked by aeroallergens. However, we have recently recognized a group of children with food allergies who also develop asthma when exposed to the aerosolized form of the food. METHODS: Between 1997 and 1999 we prospectively identified children with an immunoglobulin (Ig)E-mediated food allergy who develop asthma on inhalational exposure to the relevant food allergen while it is being cooked. Subjects were exposed for 20 min to the aerosolized form of the allergen and the symptoms and the lung function were monitored. Aerosolization was achieved by cooking the food in a small room. Where possible challenges were double-blinded. RESULTS: We identified 12 children with an IgE-mediated food allergy who developed asthma on inhalational exposure to food. The implicated foods were fish, chickpea, milk, egg or buckwheat. Nine out of the 12 children consented to undergo a bronchial food challenge. Five challenges were positive with objective clinical features of asthma. Additionally, two children developed late-phase symptoms with a decrease in lung function. Positive reactions were seen with fish, chickpea and buckwheat. There were no reactions to the seven placebo challenges. CONCLUSIONS: We have presented a prospective series of children with food allergy who developed symptoms of asthma with exposure to aerosolized food allergens. Our data demonstrates that, as in the case of other aeroallergens, inhaled food allergens can produce both early- and late-phase asthmatic responses. This highlights the importance of considering foods as aeroallergens in children with coexistent food allergy and allergic asthma. For these children, dietary avoidance alone may not be sufficient and further environmental measures may be required to limit exposure to aerosolized food.

Aerosols↗
PubMed1992

Pulmonary carcinogenicity of cadmium by inhalation in animals.

Although, the tumorigenic effect of cadmium after subcutaneous and intramuscular injection has been known since 1961, lung tumours after inhalation exposure were reported only more than 20 years later by Takenaka et al. (1983), using cadmium chloride aerosols. Based on these results, aerosols of cadmium sulfate, cadmium oxide and cadmium sulfide pigment were investigated for carcinogenic effects after inhalation exposure in rats, hamsters and mice. All the cadmium compounds tested appeared to have a very similar carcinogenic potency in the rat lung, whereas no exposure-related tumours occurred in hamsters and in mice only cadmium oxide seemed to increase the lung tumour rate. Subsequent analytical investigations of the aqueous suspension of cadmium sulfide used to generate the aerosol showed that it was soluble in water to some extent as a result of photo-oxidation. The exposure atmosphere therefore actually consisted of a mixture of sulfide and sulfate, and the observed lung tumour rate must be attributed to a combined action of the two compounds. For this reason, a clear-cut carcinogenic effect of cadmium sulfide could not be proved by this inhalation study, but because of the high carcinogenic potency of cadmium ions in the rat lung and because cadmium sulfide retained in the lung is bioavailable to a certain extent, aerosols of this compound should be regarded as a probable human carcinogen.

Administration, Inhalation↗
PubMed1977

Toluene concentrations in various tissues of rats after inhalation and oral administration.

The uptake, distribution, and elimination of 3H-toluene in various tissues of rats were studied after inhalation or after gastric intubation. The maximum radioactivity was measured 2--3 h after gastric intubation in tissues, except in white adipose tissue, where the peak radioactivity was reached at 5 h. After inhalation exposure, the uptake to various tissues was very rapid. The maximum radioactivity in most tissues was reached in 15--30 min. The accumulation was slowest in white adipose tissue, where it took 1--2 h. The radioactivity in tissues decreased after inhalation exposure more rapidly than after gastric intubation. Brown adipose tissue and white adipose tissue were different from other tissues in their ability to retain toluene. Twenty-four hours after exposures, only 1% or less of the initial radioactivity was found in tissues other than white adipose tissue, in which the corresponding value was 3.5--5%. The results show a very rapid absorption and distribution of toluene after inhalation and a retention of radioactivity in white adipose tissue. After oral ingestion the distribution showed a similar but much slower pattern.

Adipose Tissue↗
PubMed1996

Diesel exhaust is not a pulmonary carcinogen in CD-1 mice exposed under conditions carcinogenic to F344 rats.

Differences among laboratory animal species in the pulmonary carcinogenicity of chronic inhalation exposure to diesel exhaust have raised several important interpretive issues. Under similar heavy exposure conditions, it is clear that diesel exhaust is a pulmonary carcinogen in rats, but not in Syrian hamsters. Previous reports give conflicting views of the response of mice, which is presently considered equivocal. This report describes carcinogenicity results from a bioassay of CD-1 mice conducted in parallel with a previously reported bioassay of F344 rats (Mauderly et al. (1987) Fundam. Appl. Toxicol. 9, 208-221). Exposure to whole diesel exhaust 7 hr/day, 5 days/week for 24 months at soot concentrations of 0.35, 3.5, or 7.1 mg/m3 caused accumulations of soot in mouse lungs similar to those in lungs of rats and, like the results from rats, did not significantly affect survival or body weight. In contrast to the dose-related neoplastic response of rats, however, the exposures of mice did not increase the incidence of lung neoplasms. This finding is consistent with other data showing that mice, as well as Syrian hamsters, differ from rats in their lung neoplastic and nonneoplastic responses to heavy, chronic inhalation exposure to diesel exhaust soot and several other particles. Although rodents serve as useful indicators of potential human carcinogenic hazards, it is not yet clear which, if any, rodent species have lung neoplastic responses that are useful for quantitative predictions of human lung cancer risk from chronic inhalation of poorly soluble, respirable particles.

Animals↗
PubMed2005

Inhalational and dermal exposures during spray application of biocides.

Data on inhalational and potential dermal exposures during spray application of liquid biocidal products were generated. On the one hand, model experiments with different spraying devices using fluorescent tracers were carried out to investigate the influence of parameters relevant to the exposure (e.g. spraying equipment, nozzle size, direction of application). On the other hand, measurements were performed at selected workplaces (during disinfection operations in food and feed areas; pest control operations for private, public and veterinary hygiene; wood protection and antifouling applications) after application of biocidal products such as Empire 20, Responsar SC, Omexan-forte, Actellic, Perma-forte; Fendona SC, Pyrethrum mist; CBM 8, Aldekol Des 03, TAD CID, Basileum, Basilit. The measurements taken in the model rooms demonstrated dependence of the inhalation exposure on the type of spraying device used, in the following order: "spraying with low pressure" < "airless spraying" < "fogging" indicating that the particle diameter of the released spray droplets is the most important parameter. In addition inhalation exposure was lowest when the spraying direction was downward. Also for the potential dermal exposure, the spraying direction was of particular importance: overhead spraying caused the highest contamination of body surfaces. The data of inhalational and potential dermal exposures gained through workplace measurements showed considerable variation. During spraying procedures with low-pressure equipments, dose rates of active substances inhaled by the operators ranged from 7 to 230 microg active substance (a.s.)/h. An increase in inhaled dose rates (6-33 mg a.s./h) was observed after use of high application volumes/time unit during wood protection applications indoors. Spraying in the veterinary sector using medium-pressure sprayers led to inhaled dose rates between 2 and 24mga.s./h. The highest inhaled dose rates were measured during fogging (114 mg a.s./h) and after-high-pressure applications in the antifouling sector (110-300 mg a.s./h). The potential dermal exposure of spray operators was lowest (dose rates from 0.2 to 7 mg a.s./h) in the areas of food and feed disinfection and private and public hygiene during spraying with low-pressure devices. During fogging, wood protection and antifouling applications, high-potential dermal exposures of the operators were determined. Dermal dose rates varied between 100 and 34,000 mg a.s./h.

Air Pollutants, Occupational↗