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PubMed2002

Immunohistochemical study on cellular origins of rat lung tumors induced by inhalation exposures to plutonium dioxide aerosols as compared to those by X-ray irradiation.

Immunohistochemical examinations were performed on rat pulmonary tumors induced by inhalation exposures to 239PuO2 aerosols, or by X-ray-irradiation to identify and compare cellular origins or, in turn, target cells at risk for radiation carcinogenesis. Both plutonium-induced and X-ray-induced pulmonary tumors appeared to occur from the lower respiratory tract epithelium through bronchioles into alveoli, and were histopathologically diagnosed as adenoma, adenocarcinoma, adenosquamous carcinoma, and squamous cell carcinoma. Immunohistochemical staining of neoplastic lesions using rabbit polyclonal antibodies to rat surfactant apoprotein A specific for alveolar type II pneumocytes, and Clara cell antigen specific for nonciliated bronchiolar Clara cells, showed that most of the adenomatous and adenocarcinomatous lesions from plutonium-exposed or X-irradiated rats were positive for either or both antigens, while, in contrast, adenosquamous and squamous lesions were mostly negative for both antigens. Even though there were some differences in the proportions and distributions of immunoreactive cells between plutonium- and X-ray-induced tumors and among neoplastic lesions, the results indicate that radiation-induced pulmonary adenomas and adenocarcinomas mostly originate from either alveolar type II pneumocytes or bronchiolar Clara cells, while adenosquamous and squamous carcinomas may be derived from the other epithelial cell components, or might have lost specific antigenicity during their transforming differentiation.

Administration, Inhalation↗
PubMed2006

From dust to dose: Effects of forest disturbance on increased inhalation exposure.

Ecosystem disturbances that remove vegetation and disturb surface soils are major causes of excessive soil erosion and can result in accelerated transport of soils contaminated with hazardous materials. Accelerated wind erosion in disturbed lands that are contaminated is of particular concern because of potential increased inhalation exposure, yet measurements regarding these relationships are lacking. The importance of this was highlighted when, in May of 2000, the Cerro Grande fire burned over roughly 30% of Los Alamos National Laboratory (LANL), mostly in ponderosa pine (Pinus ponderosa) forest, and through areas with soils containing contaminants, particularly excess depleted and natural uranium. Additionally, post-fire thinning was performed in burned and unburned forests on about 25% of LANL land. The first goal of this study was to assess the potential for increased inhalation dose from uranium contaminated soils via wind-driven resuspension of soil following the Cerro Grande Fire and subsequent forest thinning. This was done through analysis of post-disturbance measurements of uranium air concentrations and their relationships with wind velocity and seasonal vegetation cover. We found a 14% average increase in uranium air concentrations at LANL perimeter locations after the fire, and the greatest air concentrations occurred during the months of April-June when wind velocities are highest, no snow cover, and low vegetation cover. The second goal was to develop a methodology to assess the relative contribution of each disturbance type towards increasing public and worker exposure to these resuspended soils. Measurements of wind-driven dust flux in severely burned, moderately burned, thinned, and unburned/unthinned forest areas were used to assess horizontal dust flux (HDF) in these areas. Using empirically derived relationships between measurements of HDF and respirible dust, coupled with onsite uranium soil concentrations, we estimate relative increases in inhalation doses for workers ranging from 15% to 38%. Despite the potential for increased doses resulting from these forest disturbances, the estimated annual dose rate for the public was <1 microSv yr(-1), which is far below the dose limits for public exposures, and the upper-bound dose rate for a LANL worker was estimated to be 140 microSv yr(-1), far below the 5 x 10(4) microSv yr(-1) occupational dose limit. These results show the importance of ecosystem disturbance in increasing mobility of soil-bound contaminants, which can ultimately increase exposure. However, it is important to investigate the magnitude of the increases when deciding appropriate strategies for management and long-term stewardship of contaminated lands.

Air Pollutants, Radioactive↗
PubMed2003

Impact of inhalation exposure modality and particle size on the respiratory deposition of ricin in BALB/c mice.

Ricin is a toxic lectin derived from the seed of Ricinus communis (castor plant). It is lethal in small quantities when disseminated as an aerosol. We determined the impact of using two types of exposure chambers and different particle sizes on the deposition of ricin aerosols in mice. Initially, two types of inhalation exposure chambers (whole-body [WB] or nose-only [NO]) were compared using the same size aerosol (1 micro m) to determine the potential impact upon respiratory deposition and presented dose. We then assessed the role of particle size on deposition by using aerosols with two distinctly sized particle distributions. Selected organs were collected at four time points after exposure and were analyzed by quantitative enyzme-linked immunosorbent assay (ELISA) and epifluorescence microscopy. Results of the exposure chamber comparison, using 1- micro m particles only, indicated approximately 50% of the total ricin in the 4 organs was detected in the lung tissue 1 h after exposure. The trachea and nasopharyngeal region of the animals exposed using the WB chamber contained significantly more ricin than those of animals exposed in the NO chamber. Histopathology indicated an accumulation of ricin in both the tracheobronchial and pulmonary regions with pronounced bronchiolar degradation 48 h postexposure. When particles larger than 3 micro m were used, results indicated a considerable amount of ricin initially detected in the trachea, although this finding was discounted due to the heterodispersity of the particles generated. Interestingly, no animals died as a result of exposure to the equivalent of 4 LD50s (as determined using a 1- micro m particle) when exposed to the larger size distribution of particles. This result indicates a differential lethality that is contingent upon aerosol size.

Administration, Inhalation↗
PubMed2001

Behavioral effects following subacute inhalation exposure to m-xylene or trimethylbenzene in the rat: a comparative study.

Trimethylbenzene (TMB), like xylene (dimethylbenzene), is a significant constituent of some industrial solvent mixtures. In earlier studies, we found that in the rat a subacute low-level inhalation exposure to some of the TMB isomers may result in behavioral alterations detectable weeks after the exposure [Neurotoxicol Teratol 19;1997:327; Int J Occup Med Environ Health 11;1998:319]. The purpose of the present study was to compare m-xylene (XYL) and each of the TMB isomers: 1,2,3-TMB (hemimellitene - HM), 1,2,4-TMB (pseudocumene - PS), and 1,3,5-TMB (mesitylene - MES) with respect to the ability for inducing behavioral effects in the rat. The rats (10-11 animals per group) were exposed repeatedly for 4 weeks (6 h per day, 5 days per week) to XYL (XYL group), HM (HM group), PS (PS group) or MES (MES group) at 100 ppm, or sham exposed (C group) in 1.3 cu/m dynamic inhalation chambers. Starting 2 weeks after exposure the following forms of rat's behavior were assessed: radial maze performance, spontaneous activity in an open field, learning and retention of passive and active (two-way) avoidance response, and heat-induced paw licking before and after a 2 min footshock (a test for assessment of the stress response). None of the solvent-exposed groups differed considerably from the control one with respect to the radial maze performance. Compared to control rats, the rats of the XYL, PS and MES groups, but not those of HM group, showed a significantly higher spontaneous locomotor activity in the open field, an impaired passive avoidance learning and significantly longer paw-lick latencies 24 h after footshock. Acquisition, but not retention, of the two-way active avoidance response was significantly impaired in all solvent-exposed groups. The XYL group did not differ significantly from PS, MES or HM group in any of the behavioral parameters. The above results show that a short-term exposure to any of the TMB isomers or m-xylene at concentration as low as 100 ppm may induce persistent behavioral alterations in the rat.

Administration, Inhalation↗
PubMed1996

Pulmonary fibrogenesis after three consecutive inhalation exposures to chrysotile asbestos.

Previously, this laboratory developed a model of asbestos-induced pulmonary fibrogenesis in rats and mice after a brief (1 to 3-h) inhalation exposure. However, typical human environmental exposures would be repeated, although at lower concentrations than those used in our animal model. Here we have extended this model to encompass repeated exposures and consequent long-term effects. Groups of rats were exposed to chrysotile aerosol (10 mg/m3) for 3- to 5-h periods over 3 consecutive days. Lung fiber burden and pathologic features were studied for as long as 6 mo after exposure. We found that many of the longest (> or = 8 microm) fibers were retained in the lung for at least 6 mo, whereas shorter fibers were cleared more rapidly. The three exposures to chrysotile caused a large increase in DNA synthesis in the epithelium of terminal bronchioles and more proximal airways. When compared with a single exposure, the triple exposure caused an enhanced inflammatory response as well as a prolonged period of increased DNA synthesis in the proximal alveolar region. Hyperplastic, fibrotic lesions subsequently developed in the same region and persisted for at least 6 mo after exposure. These findings will be valuable in directing future studies of the mechanisms of pulmonary fibrosis in this model.

Administration, Inhalation↗
PubMed2003

Relevance of inhalational exposure to food allergens.

PURPOSE OF REVIEW: This review discusses the inhalational route as a clinically important route of exposure to food allergens. RECENT FINDINGS: In childhood, we have recently demonstrated that food allergens can induce both early and late phase bronchial reactions within blinded, placebo-controlled challenges. Additionally, clinically important levels of food allergens have been measured in environmental air samples. SUMMARY: It is well known that the ingestion of food allergens frequently causes respiratory symptoms and that the mechanism of death in fatal anaphylaxis is usually profound bronchospasm. The mechanism by which ingested food allergens induce bronchial reactions is unclear. There are many case reports of bronchial reactions to aerosolized food allergens. Within the food industry the problems have been examined more systematically. From such work it is possible to gain an impression of the potential prevalence of the problem. With 10% of adult asthma being occupational and 10% of occupational asthma being induced by aerosolized food, inhalational exposure to food allergens plays a major role in at least 1% of adult asthma. For a patient with co-existent food allergy and asthma it is important that both dietary and environmental avoidance be practised. The similar pathophysiology of allergic and occupational asthma and the ability of inhaled food allergens to cause the latter raises the question as to whether aerosolized food could play a role in the pathogenesis of childhood asthma.

Allergens↗
PubMed1985

Effects of a two-year inhalation exposure of rats to coal dust and/or diesel exhaust on tension responses of isolated airway smooth muscle.

This study was performed to determine whether chronic inhalation exposure of rats to levels of coal dust (CD) and/or diesel exhaust (DE) similar to those experienced by underground miners affects the pharmacologic characteristics of the animal's airway smooth muscle. Animals were exposed for 2 yr to CD alone (2 mg/m3 of respirable particulates), DE alone (2 mg/m3 of respirable particulates), or CD and DE (CD + DE) in combination (1 mg/m3 CD plus 1 mg/m3 DE). Concentration-response relationships for tension changes induced with acetylcholine, 5-hydroxytryptamine, potassium chloride, and isoproterenol were assessed in vitro on isolated preparations of rat airway smooth muscle (trachealis). Compared with control animals, the maximal contractile responses to acetylcholine of tissues from CD-, DE-, and CD + DE-exposed animals were significantly increased; the effects of CD and DE exposure were additive. The CD + DE exposure, but not the individual treatments, resulted in a significant increase in the maximal relaxation response elicited by isoproterenol; this interaction may have resulted from the addition of, or the synergism between, the nonsignificant effects of CD and DE alone. No treatment altered the sensitivity (EC50 values) of the muscles to the agonists used. The results indicate that chronic exposure to CD, DE, and CD + DE produces differential modifications in the behavior of rat airway smooth muscle. These findings may have some bearing on humans exposed to these substances.

Administration, Intranasal↗
PubMedDate not supplied

Absence of carcinogenic activity in Fischer rats and B6C3F1 mice following 103-week inhalation exposures to toluene.

Toluene, methylbenzene, is used to back-blend gasoline, as a chemical intermediate, and as a solvent; more than 7 million tonnes are produced each year in the United States. Following 14-15-week toxicity studies to estimate appropriate exposure concentrations for the carcinogenesis bioassays, toxicology and carcinogenesis studies of toluene (>99% pure) were conducted by whole-body inhalation exposures of F344/N rats and B6C3F1 mice of each sex for 15 months or two years. Toluene levels were 0 (chamber controls), 600, and 1,200 ppm for rats and 0, 120, 600, and 1200 ppm for mice. Exposures were 6.5 hr/day 5 days/wk. Genetic toxicology studies using Salmonella typhimurium, mouse L5178Y lymphoma cells, and Chinese hamster ovary cells were negative. No chemically related neoplasm was found in male rats, and one nasal, two kidney, and two forestomach neoplasms observed in female rats were considered not to be associated with the toluene exposure. For mice, no biologically important increase was observed for any nonneoplastic or neoplastic lesion. Studies by others had reported carcinogenicity of toluene, especially for total malignant tumors.

Administration, Inhalation↗
PubMed1982

Repeated inhalation exposure of Beagle dogs to 239PuO2: retention and translocation.

Whole-body retention and distribution of 239Pu in selected tissues of Beagle dogs were determined after a series of two or four inhalation exposures to 239PuO2. Exposures were made at half-year intervals with alveolar depositions of about 150 nCi per exposure. Data are reported on dogs followed for one and two years after the first exposure. The plutonium was found to be extremely insoluble; 2-3% of the amount deposited in the alveolar region translocated to tracheobronchial lymph nodes and less than 0.1% translocated to other tissues. The whole-body retention, when compared to retention of 239Pu following a single exposure, supported the hypothesis that each exposure was retained independently with the same retention characteristics. This is in agreement with results reported by other investigators for one human repeatedly exposed by inhalation to low levels of aerosols containing plutonium-uranium fuels.

Aerosols↗
PubMed1988

Comparative toxicity of nickel oxide, nickel sulfate hexahydrate, and nickel subsulfide after 12 days of inhalation exposure to F344/N rats and B6C3F1 mice.

The relative toxicity of nickel oxide (NiO), nickel sulfate hexahydrate. (NiSO4.6H2O), and nickel subsulfide (Ni3S2) was studied in F344/N rats and B6C3F1 mice after inhalation exposure for 6 h/day, 5 days/week for 12 exposure days. Exposure concentrations used (as mg Ni/m3) were 0.9-23.6 for NiO; 0.8-13.3 for NiSO4.6H2O, and 0.4-7.3 for Ni3S2. For each compound there were 5 exposure groups plus a control group. NiSO4.6H2O was the most toxic compound with exposure related mortality seen at exposure concentrations of 13.3 mg/m3 in rats and 1.6 mg/m3 and above in mice. For Ni3S2, mortality was seen in mice (but not in rats) at the highest exposure concentration (7.3 mg/m3). No mortality was seen after NiO exposure. Lesions of the lung and nasal cavity were seen in both rats and mice after exposure to NiSO4.6H2O and Ni3S2 at the 4 highest exposure concentrations. Lesions of the lung were seen primarily at the highest exposure concentrations after NiO exposure. The amount of nickel in the lungs at the end of exposure varied in relation to the water solubility of the compounds. Based on these 2-week studies, the toxicity ranking was NiSO4.6H2O greater than Ni3S2 much greater than NiO. Additional studies are in progress to assess the relative toxicities of these three nickel compounds after 90-day exposures.

Administration, Inhalation↗
PubMed1988

Evaluation of spermatogenesis and sperm quality in the rat following acute inhalation exposure to methyl bromide.

Methyl chloride (MeCl) and methyl bromide (MeBr) have similar target organ specificities in the male F-344 rat, and MeCl is a known reproductive toxicant in that species. Recently, both acute and subchronic inhalation exposures to MeBr were found to produce varying degrees of testicular alteration (S.L. Eustis, S.B. Haber, R.T. Drew, and R.S.H. Yang, 1986, Toxicologist, 6, 54; N. Kato, S. Morinobu, and S. Ishizu, 1986, Ind. Health, 24, 87-103; M.E. Hurtt, K.T. Morgan, and P.K. Working, 1987, Fundam. Appl. Toxicol., 9, 352-365). The present study examined the reproductive effects of MeBr in the male F-344 rat. Adult males (11-13 weeks) were exposed by inhalation to 0 or 200 ppm MeBr 6 hr/day for 5 days (first day of exposure = Day 1). Ten animals from each group were anesthetized with pentobarbital and terminated on Days 1, 3, 5, and 8. Additionally, five males from each group were killed on Days 6, 10, 17, 24, 38, 52, and 73. Plasma testosterone concentration was reduced during and immediately following exposure (Days 1, 3, 5, and 6), but returned to control levels by Day 8. Nonprotein sulfhydryl (NPSH) content of the liver and testis was reduced during exposure but returned to control levels by Day 8 (3 days postexposure). No other reproductive indices, including testis weight, daily sperm production, cauda epididymal sperm count, sperm morphology, percentage motile sperm, linear sperm velocity, and epididymal and testicular histology, were affected by MeBr exposure at any time point examined. Thus, although MeBr causes a transient decrease in plasma testosterone and testicular NPSH concentrations during acute exposure, it has no lasting effect on sperm quality or spermatogenesis in the F-344 rat.

Administration, Inhalation↗
PubMed1995

Gender differences in the metabolism of 1,3-butadiene in Sprague-Dawley rats following a low level inhalation exposure.

1,3-Butadiene (BD), a compound used extensively in the rubber industry, is carcinogenic in the male and female Sprague-Dawley rats after chronic exposures to 1000 and 8000 p.p.m. In terms of incidence of tumors the majority were in mammary tissue, thus the incidence of tumors in female rats exceeded that in males in chronic carcinogenicity studies. In the present study the production and disposition of butadiene monoepoxide (BDO) and butadiene diepoxide (BDO2), mutagenic BD metabolites, were examined in male and female Sprague-Dawley rats following a low level inhalation exposure to BD. The rats were exposed to a target concentration of 62.5 p.p.m. BD by nasal inhalation for 6 h. Immediately after exposure blood, bone marrow, lung and fat samples were removed from all the animals and mammary tissue was removed from females. The samples were prepared by cryogenic-vacuum line distillation and analyzed for the epoxides using multidimensional gas chromatography-mass spectrometry. Levels of BDO in the blood were 25.9 +/- 2.9 and 29.4 +/- 2 pmol/g in male and females respectively. The levels of this metabolite were also similar in males and females in the other tissues examined. The greatest amounts of BDO were in fat (175 +/- 21 and 203 +/- 13 pmol/g in males and females respectively). Levels of BDO2 were approximately 5-fold greater in the blood of female rats compared with male rats. In the other tissues examined BDO2 was also consistently greater in tissues from females. In fat BDO2 was present at a concentration of 7.7 +/- 1.3 and 1.1 +/- 0.1 pmol/g tissue in females and males respectively. Mammary tissue from female rats contained 10.5 +/- 2.4 pmol/g BDO2, a level slightly lower than that observed in blood. The ratios of the two epoxides differed markedly between males and females in all tissues examined. Differences were most pronounced in lung and fat tissues, where BDO/BDO2 ratios were 9 and 0.6 (lung) and 159 and 26 (fat) for males and females respectively. This study is the first to describe a gender difference in the metabolism of BD. The greater production of the highly mutagenic BDO2 in females may play a role in the increased incidence of mammary tumors after chronic exposure to BD.

Administration, Inhalation↗
PubMed1991

Metabolic interaction and disposition of methyl ethyl ketone and m-xylene in rats at single and repeated inhalation exposures.

1. Rats were exposed to m-xylene (300 ppm) and methyl ethyl ketone (MEK, 600 ppm) vapour, separately and in combination. 2. Repeated exposures to m-xylene enhanced liver drug-metabolizing capacity, whereas MEK showed no effects. After mixed exposure the cytochrome P-450-dependent monooxygenase activities were additively or synergistically induced. 3. In the presence of MEK the overall metabolism of xylene was strongly inhibited both after single and repeated exposures, an effect accompanied by elevation of xylene concentration in blood (18-29%) and fat (25-32%). 4. The 24-h excretion of the urine metabolites of m-xylene was decreased by 22-24% in mixed exposures: the excretion of methylhippuric acid was decreased (29%), but that of 2,4-dimethylphenol increased (9-35%). 5. After repeated inhalation exposures the excretion of xylene metabolites in urine was consistently higher, whereas the concentrations of xylene in fat (but not the concentration of MEK) were lower than after a single treatment, conceivably due to accelerated metabolic clearance of xylene. 6. Thioether excretion in urine was enhanced in xylene-treated rats (7-13-fold), but was not influenced by the induced changes in the metabolism of xylene. Xylene inhalation caused liver GSH to decrease slightly (10%), as did inhalation of MEK, but the latter did not enhance the excretion of thioethers. 7. MEK is a potent inhibitor of the side-chain oxidation of m-xylene producing methylhippuric acid, but not of its ring oxidation to 2,4-dimethylphenol, and exhibits a synergistic inducing effect on liver enzymes responsible for the oxidation of m-xylene. The increased ring oxidation of m-xylene was not associated with increased production of reactive metabolites indicated by GSH-depletion or thioether formation.

Administration, Inhalation↗
PubMed1989

Uptake and distribution of 14C during and following inhalation exposure to radioactive toluene diisocyanate.

Inhalation of toluene diisocyanate (TDI) results in toxic responses ranging from pulmonary irritation to immunological sensitization. The use of radioactively labeled isocyanate has made it possible to follow the initial uptake of the compound into the bloodstream independent of the final fate of the isocyanate. This study shows that the rate of uptake into the blood is linear during exposure to concentrations ranging from 0.00005 to 0.146 ppm and that the uptake continues to increase slightly postexposure. It also demonstrates that the radioactivity clears from the bloodstream to a level corresponding to approximately a 100 nM concentration of tolyl group after 72 hr and persists at a nanomolar level even 2 weeks following the exposure. This is similar to the response previously reported by this group for radioactively labeled methyl isocyanate. The initial rate of 14C uptake is also a linear function of the concentration of TDI when expressed either as concentration (ppm) or as concentration multiplied by duration of exposure (ppm.hr). This is discussed in comparison with the toxic responses as a function of both ppm and ppm.hr. Finally, the inclusion of the data on methyl isocyanate indicates that the uptake into arterial blood is a function of exposure concentration, independent of isocyanate structure.

Administration, Inhalation↗
PubMed1995

Effects of inhalative exposure to dioxins in wood preservatives on cell-mediated immunity in day-care center teachers.

The study investigated the effects of chronic inhalative low-level exposure to dioxins in day-care centers containing wood treated with preservatives on (1) the number of peripheral CD4 and CD8 cells and the CD4:CD8 ratio in peripheral blood and (2) the delayed-type hypersensitivity reaction of the skin (Multitest Méreux). The study population consisted of 221 exposed and 189 unexposed employees of day-care centers in or near Hamburg. A status of decreased skin test reagibility was operationalized as hypoergy I (score < 5 mm), hypoergy II (< or = 1 positive reaction), and anergy (no positive reaction). Taking the fading during postexposure time into account, a surrogate for the dioxin burden based on the concentration of dioxins in indoor air (measured using the 2,3,7,8-TCDD TEF followed by the Federal Republic of Germany) was modeled. No effect was found regarding the number of CD4 cells, CD8 cells, and CD4:CD8 ratio. However, some evidence for an increasing dose-response relationship between inhalative exposure to dioxins and the risk of hypoergy and anergy was found, both in the total study population and among subjects with a short postexposure time (< or = 6 months). Subjects with a short postexposure time and a dioxin burden > 0.6 pg/m3 had a significantly higher risk of hypoergy than unexposed subjects (hypoergy I: OR = 9.51, 95% CI = 1.96-42.02; hypoergy II: OR = 2.92, 95% CI = 1.14-7.5). It is concluded that a suppressive effect of inhalative exposure to dioxins in wood preservatives on human cell-mediated immunity cannot be ruled out.

Adolescent↗
PubMed1983

Toxicological effects on mice following inhalation exposures to fluidized-bed coal combustor fly ash.

Toxicological effects of exposure to reaerosolized fly ash from a fluidized-bed coal combustor were evaluated in mice following 500- and 1000-hr inhalation exposures. Alveolar macrophage function, organ histology, and hematopoiesis were assessed following 24-hr/day exposures in two 500-hr experiments. There was little mutagenicity detected by the Ames assay in the samples of the fly ash tested. The chemical characteristics of the fly ash were very similar to those of fly ash produced during conventional coal combustion. However, physical characterization revealed that the fluidized-bed combustion fly ash was not fused as is commonly the case in conventionally combusted fly ash, and as a result had a very large surface area. The function of the alveolar macrophages of exposed mice was impaired, and there were significant changes in the histology of the lung, including cellular infiltration and hyperplasia of bronchiolar and alveolar epithelium. These changes are characteristic of pulmonary responses to chronic irritation of the lung.

Animals↗
PubMed1988

Assessment of inhalation exposure potential from vapors in the workplace.

Quantitative knowledge of human exposure to a chemical represents half of the required input for the health risk assessment process by which occupational health professionals seek to integrate exposure and inherent hazard in clinically meaningful terms. This work reviews and presents explicit methodologies and approaches to the estimation of inhalation exposure to chemicals. Special attention is given to estimating vapor exposures and the critical elements of an indoor air pollution model that assumes conservation of contaminant mass in a specified box of workroom air.

Air Pollutants↗