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PubMed2006

Use of portable microbial samplers for estimating inhalation exposure to viable biological agents.

Portable microbial samplers are being increasingly used to determine the presence of microbial agents in the air; however, their performance characteristics when sampling airborne biological agents are largely unknown. In addition, it is unknown whether these samplers could be used to assess microbial inhalation exposure according to the particle sampling conventions. This research analyzed collection efficiencies of MAS-100, Microflow, SMA MicroPortable, Millipore Air Tester, SAS Super 180, BioCulture, and RCS High Flow portable microbial samplers when sampling six bacterial and fungal species ranging from 0.61 to 3.14 microm in aerodynamic diameter. The efficiencies with which airborne microorganisms were deposited on samplers' collection medium were compared to the particle inhalation and lung deposition convention curves. When sampling fungi, RCS High Flow and SAS Super 180 deposited 80%-90% of airborne spores on agar - highest among investigated samplers. Other samplers showed collection efficiencies of 10%-60%. When collecting bacteria, RCS High Flow and MAS-100 collected 20%-30%, whereas other samplers collected less than 10% of these bioparticles. Comparison of samplers' collection efficiencies with particle inhalation convention curves showed that RCS High Flow and SAS Super 180 could be used to assess inhalation exposure to particles larger than 2.5 microm, such as fungal spores. Performance of RCS High Flow sampler was also reflective of the particle lung deposition pattern when sampling both bacteria and fungi. MAS-100 and SAS Super 180 matched the total deposition curve fairly well when collecting bacterial and fungi species, respectively. For other tested samplers, we observed substantial discrepancies between their performances and particle deposition efficiencies in the lung. The results show that feasibility of applying portable microbial samplers for exposure assessment depends on a particular sampler model and microbial species.

Aerosols↗
PubMed1986

Studies of the temporal and spatial distribution of aerosols in multi-tiered inhalation exposure chambers.

Two multi-tiered whole body inhalation exposure chambers with nominal volumes of 1 m3 (H-1000) and 2 m3 (H-2000) were evaluated for their performance in terms of the temporal and spatial distribution of test aerosols within the chamber. Parameters investigated included chamber type, single-chamber-single-aerosol generator versus two-chamber-single-aerosol generator systems, chamber air supply and exhaust systems, particle size, and aerosol diluter type. Results indicated that: 1) particle size has an effect on chamber aerosol concentration distribution, with the larger particle resulting in a higher variation; 2) the single-chamber-single-generator system is more stable than the two-chamber-single-generator system; 3) the H-2000 chamber has a lower aerosol spatial variability than the H-1000 chamber; and 4) the aerosol distribution within the chamber could be improved with the use of a newly designed diluter.

Aerosols↗
PubMed1980

Ammonia concentrations in an animal inhalation exposure chamber.

Ammonia concentrations in 2.8 m3 chronic inhalation exposure chambers housing either 144 rats or 360 mice were measured by ion chromatography and chemiluminescence to evaluate chamber maintenance procedures. Variables included use of bacteriostatic cageboard, air flow rate, animal species, and age. Ammonia concentrations were lowered by using bacteriostatic cageboard and were inversely proportional to cageboard changing frequency and air flow rate.

Age Factors↗
PubMed2004

Carcinogenicity and chronic toxicity after inhalation exposure of rats and mice to N,N-dimethylformamide.

Carcinogenicity and chronic toxicity of N,N-Dimethylformamide (DMF) were examined by inhalation exposure of groups of 50 rats and 50 mice of both sexes to DMF vapor at a concentration of 0, 200, 400 or 800 ppm (v/v) for 6 h/d, 5 d/wk, for 104 wk. In rats, incidences of hepatocellular adenomas and carcinomas significantly increased in the 400 and 800 ppm-exposed groups and in the 800 ppm-exposed group, respectively. The hepatocellular adenoma did not increase significantly in the 400 ppm-exposed female rats, but its incidence exceeded a range of historical control data in the Japan Bioassay Research Center (JBRC). In mice, incidences of hepatocellular adenomas and carcinomas significantly increased in all the DMF-exposed groups. Incidence of hepatoblastomas significantly increased in the 200 and 400 ppm-exposed male mice, and 4 cases of hepatoblastomas in the 400 ppm-exposed female mice and the 800 ppm-exposed male mice exceeded the range of historical control data of the JBRC. Incidences of altered cell foci increased in the liver of exposed rats and mice in an exposure concentration-related manner, and those foci were causally related to the hepatocellular tumors. Liver weights increased in both rats and mice exposed to DMF at 200 ppm and above. Increased levels of gamma-GTP, ALT, AST and total bilirubin in exposed rats of both sexes and AST and ALT in exposed mice of both sexes were noted. It was concluded that 2-yr inhalation exposure to DMF increased incidences of hepatocellular adenomas and carcinomas in rats and incidences of hepatocellular adenomas, carcinomas and hepatoblastomas in mice, and that hepatocarcinogenicity of DMF was more potent in mice than in rats.

Administration, Inhalation↗
PubMedDate not supplied

Pulmonary responses and recovery following single and repeated inhalation exposure of rats to polymeric methylene diphenyl diisocyanate aerosols.

Acute and repeated inhalation exposures (for 28 days) to polymeric methylene diphenyl diisocyanate (PMDI) were performed in rats. Investigations were made at the end of exposures and after 3, 10 and 30 days of recovery following single acute exposures and after 30 days of recovery following 28 days of exposure. Acute exposures to 10, 30 or 100 mg m(-3) PMDI produced clinical signs in all animals that were consistent with exposure to irritant aerosols. An exposure concentration-related body weight loss and increase in lung weight were seen post-exposure, with complete recovery by day 8. The time course of changes in the lung over the initial days following exposure consisted of a pattern of initial toxicity, rapid and heavy influx of inflammatory cells and soluble markers of inflammation and cell damage, increased lung surfactant, a subsequent recovery and epithelial proliferative phase and, finally, a return to the normal status quo of the lung. During these stages there was evidence for perturbation of lung surfactant homeostasis, demonstrated by increased amounts of crystalline surfactant and increased number and size of lamellar bodies within type II alveolar cells. Repeated exposure over 28 days to the less toxic concentrations of 1, 4 or 10 mg m(-3) PMDI produced no clinical signs or body weight changes, but an increase in lung weight was seen in animals exposed to 10 mg m(-3), which resolved following the 30-day recovery period. Other effects seen were again consistent with exposure to irritant aerosols, but were less severe than those seen in the acute study. Analysis of bronchoalveolar lavage fluid revealed similar changes to those seen in the acute study. At both 10 and 4 mg m(-3) PMDI increased numbers of 'foamy' macrophages in lung lavage cell pellet correlated with the increased phospholipid content of the pellet. Changes in lung lavage parameters and electron microscopic evidence again suggested perturbations in surfactant homeostasis. Histologically, bronchiolitis and thickening of the central acinar regions was seen at 10 and 4 mg m(-3), reflecting changes in cell proliferation in the terminal bronchioles and centro-acinar regions. Almost all effects seen had recovered by day 30 post-exposure. Both acute and subacute studies demonstrate rapid recovery of effects in the lung following exposure to PMDI, with no progression of these effects even at concentrations higher than those shown to produce tumours in a chronic study. These findings add weight to the hypothesis that pulmonary tumours seen following chronic exposure to PMDI are most likely due to a combination of the chronic irritant effects of repeated exposure, coupled with the presence of insoluble polyureas formed by polymerization of PMDI (found in studies reported here and previous chronic studies), and therefore acute or short-term exposures to PMDI are likely to be of little concern for long-term pulmonary health.

Aerosols↗
PubMed1997

32P-postlabelling/HPLC assay reveals an enantioselective adduct formation in N7 guanine residues in vivo after 1,3-butadiene inhalation exposure.

We have established a protocol that allows qualitative and quantitative determination of butadiene monoepoxide-DNA adducts formed as a result of inhalation exposure to 1,3-butadiene. We observed that in this particular case in vivo samples required extensive sample purification to facilitate a low background. Sample preparation included a solid phase extraction carried out with a strong anion exchange column and one-dimensional ion exchange TLC. The ultimate analysis is based on reverse phase HPLC with on-line radioactivity and UV detectors. The qualitative identification and quantitation is based on characterized markers, which are used as external and internal standards. Modified 3'-dGMP markers were used to control labelling efficiency, which varies, and modified 5'-dGMP markers were used as an optical standard to qualitatively assign the products and to determine recovery of the sample preparation. Using this method we were able to demonstrate, for the first time, specific enantio- and regioisomeric adduct formation at the N7 position of guanine residues in liver DNA of rats inhalation-exposed to 1,3-butadiene. The major adduct formed was the C-2 isomer derived from the R enantiomer of butadiene monoepoxide, contributing 47% of all adducts formed at the N7 position of guanine. The relative proportions of the remaining three other adducts detected were 22 (R C-1), 18 (S C-2) and 14% (S C-1) respectively. Inhalation exposure to 200 p.p.m. for 5 days resulted in an alkylation level of 7.2 fmol/10 microg DNA or 2.4 adducts/10(-7) normal nucleotides.

Administration, Inhalation↗
PubMed1990

Species differences in short term toxicity from inhalation exposure to bromobenzene.

Lung, liver and kidney injury were studied in mice, rats and rabbits 48 h after termination of a 4 h inhalation exposure to bromobenzene vapour (250-3400 ppm). Light and electron microscopy of lung tissue revealed injury to Clara cells and adjacent epithelium in mouse bronchioli (bromobenzene concentration 250 ppm and 1000 ppm) and to Clara cells of rat bronchi and bronchioli (1000 ppm bromobenzene) and of rabbit bronchi (2500 ppm and 3400 ppm). Histological and clinicochemical indices of liver damage were found in the same animals, whereas kidney toxicity was observed in mice (two out of ten showed tubular necrosis and elevated concentration of plasma urea) and rats (all had elevated plasma concentrations of creatinine) exposed to 1000 ppm bromobenzene. Inhalation exposure thus produced less kidney injury than expected from previous studies with equimolar doses given intraperitoneally. The mouse was the most severely affected species, followed by the rat, and lastly the rabbit. The animal susceptibility could not be ranked according to the rate of 14C-bromobenzene covalent binding in lung or liver, but it was inversely related to the rate of N-demethylation of benzphetamine (indicative of P450IIB activity) in both lung and liver microsomal preparations. Differences in a P450 mediated detoxification could therefore be of importance in species variability to bromobenzene injury.

Administration, Inhalation↗
PubMed1996

Inhalation exposure to volatilized opioids produces antinociception in mice.

The goal of this study was to determine whether opioids of varying potencies are pharmacologically active via the inhalation route of administration in mice. The opioids evaluated included heroin, morphine, codeine, fentanyl and meperidine; each of these drugs has the potential for abuse in humans. Inhalation exposure to each of these compounds produced antinociception in a dose-dependent manner as assessed in the tall-flick test. No pyrolysis products were detected after heating either morphine or codeine at 250 degrees C for 5 min. Although 6-acetylmorphine was found after heating heroin, it accounted for less than 5% of the recovered sample. Heroin was somewhat less potent by inhalation administration than i.v. injection, with ED50 values of 1.6 and 0.69 mumol/kg, respectively. In contrast, the relative potency of morphine was substantially greater when inhaled than when injected, with respective ED50 values of 0.77 and 3.9 mumol/kg. Whereas the body to brain ratios of [3H]morphine were approximately 8 and 20 for inhalation exposure and i.v. injection, respectively, the ratio for heroin was approximately 5 regardless of administration route. This pattern of results suggests that the increase in morphine potency upon inhalation may have resulted from an increased accessibility to the brain compared with i.v. injection. Finally, naloxone reversed the antinociceptive effects of volatilized heroin, but neither the kappa selective antagonist nor-binaltorphimine nor the delta selective antagonist naltrindole blocked this antinociception, which suggests the involvement of mu opioid receptors. These findings taken together suggest the potential for the abuse of a variety of opioids, in addition to heroin, through the inhalation route of administration by humans.

Administration, Inhalation↗
PubMed1984

The importance of delivered dose in estimating low-dose cancer risk from inhalation exposure to formaldehyde.

Data have recently been obtained on the concentration of formaldehyde covalently bound to the respiratory mucosal DNA of Fischer-344 rats following two 6-hr inhalation exposures to gaseous formaldehyde. These data provide a direct short-term measure of the delivered formaldehyde dose in target tissue as a function of the formaldehyde concentration in ambient air. They also demonstrate that the delivered dose/administered dose relationship is significantly nonlinear. Since chronic inhalation exposure of Fischer-344 rats to high concentrations of gaseous formaldehyde induces squamous cell carcinomas of the nasal cavity, and sine widespread concern exists that formaldehyde exposure may also pose a cancer risk for humans, the implications of this nonlinearity for low-dose risk extrapolation were investigated. The incidence of nasal squamous cell carcinomas in a chronic formaldehyde inhalation bioassay was reanalyzed with several low-dose extrapolation models, using the estimated concentration of formaldehyde covalently bound to respiratory mucosal DNA as the measure of exposure. For this purpose, it was assumed that the short-term observations of covalent binding were representative of steady-state conditions during the course of the chronic study and further, that the covalent binding of formaldehyde to target tissue DNA is an important factor in nasal tumor induction. Resulting maximum likelihood risk estimates and upper 95% confidence bounds were unilaterally lower than the corresponding risk measures based on administered dose, irrespective of the dose-response model employed. Reductions in estimated risk ranged from a factor of 2.5, for the multistage model upper 95% confidence bound, to over 10 orders of magnitude, for the probit model upper 95% confidence bound. These results indicate that the concept of delivered dose can have a significant impact on estimates of low-dose risk and should therefore at least be considered as an alternative dose measure in assessments of human cancer risk from formaldehyde exposure.

Animals↗
PubMed1985

Transmigration of titanium dioxide (TiO2) particles in rats after inhalation exposure.

Titanium dioxide (TiO2) has been used extensively in the manufacturing of white pigment and has generally been regarded as a nuisance dust in animals and man. After inhalation exposure, little is known about transmigration routes and potential toxic effects of translocated particles in other organs. In order to answer these questions, rats were exposed to TiO2 by inhalation exposure at concentrations of 0, 10, 50, and 250 mg/m3 for 2 years. A few free particles were retained in the nasal and tracheobronchial epithelium without any cellular damage, but aggregates of dust-laden macrophages (dust cells) were found in the lymphoid tissue of the submucosa. Inhaled particles were mostly engulfed by alveolar macrophages and confined sharply to the alveolar duct region at 10 and 50 mg/m3, while dust cells were scattered throughout alveoli at 250 mg/m3. A fraction of the inhaled particles was retained in the membranous pneumocytes and interstitial macrophages. A dense accumulation of dust cells was found in the perivascular and peribronchial lymphoid tissue. Some dust cells entered peribronchial lymphatics or pulmonary blood vessels and the general circulation. Dust cells in the hyperplastic peribronchial lymphoid tissue were exposed directly in the luminal surface of the airways and were subsequently eliminated via airways. Massive dust deposition was observed in the tracheobronchial lymph nodes. Dust transmigration was markedly reduced in the cervical lymph nodes, and only a trace amount of dust particles was found in the mesenteric lymph nodes. Some dust cells entered either blood or lymphatic vessels in the lymph nodes and then migrated into the general circulation. The incidence of extrapulmonary dust deposition in the liver or spleen was increased in a dose-related fashion similar to the lung dust burden. Since there was no tissue response to translocated particles in the lymph nodes, spleen, or liver, potential adverse health effects appear to be negligible.

Administration, Intranasal↗
PubMed1994

Extracellular dopamine levels within the striatum increase during inhalation exposure to toluene: a microdialysis study in awake, freely moving rats.

An exposure chamber for microdialysis on awake, freely moving rats during exposure to volatile agents is described. Inhalation exposure to 1000 and 2000 ppm toluene for 2 h was accompanied by an increase in extracellular dopamine levels within the striatum, but did not affect the homovanillic acid level. Neither the dopamine nor the homovanillic acid level was affected by toluene 500 ppm or isoamylacetate. It is suggested that the action of inhaled toluene on the dopamine neuron differs from that of the anaesthetic halothane, possibly by interfering with dopamine reuptake. Microdialysis seems to be a useful tool for studying the effects of volatile agents on brain neurotransmission.

Animals↗
PubMed2005

Bone mass toxicity associated with inhalation exposure to toluene.

The inhalation of a wide range of organic solvents has become popular among young adults. Toluene is one of the most commonly used solvents in industry; it is easily available and convenient to use. Many toxicologic effects on biological systems secondary to deliberate inhalation of toluene have been reported, but investigations on adverse effects associated with bone morbidity is limited. The purpose of this study is to determine bone mineralization and investigate the adverse effects of toluene on bone. The bone mineral density and content of the femoral neck of mice exposed to toluene at 300 ppm for 8 wk were measured by dual X-ray absorptiometry and found significantly reduced compared to the control group. Chronic exposure to toluene was found to affect bone metabolism, and toluene-induced changes could contribute to bone resorption and inhibition of bone formation. Toluene seems to be the responsible component for the demineralizating effects of commonly abused substances, and medical doctors must promote their education about the health hazards in those who abuse solvents especially in areas where inhalant abuse is endemic.

Absorptiometry, Photon↗
PubMed2005

Developmental toxicity of two trimethylbenzene isomers, mesitylene and pseudocumene, in rats following inhalation exposure.

The developmental toxicity of two trimethylbenzene isomers, mesitylene (1,3,5-trimethylbenzene) and pseudocumene (1,2,4-trimethylbenzene) was studied in Sprague-Dawley rats following inhalation exposure. Pregnant rats were exposed whole body to vapours of mesitylene (0, 100, 300, 600, and 1200 ppm) or pseudocumene (0, 100, 300, 600, and 900 ppm), 6h/day, on gestational days (GD) 6 through 20. Significant decrease in maternal body weight gain and food consumption was observed at concentrations of 300 ppm mesitylene, 600 ppm pseudocumene, or greater. Fetal toxicity, expressed as significant reduction in fetal body weight, occurred at 600 and 1200 ppm mesitylene, and at 600 and 900 ppm pseudocumene. There was no evidence of embryolethal or teratogenic effects following inhalation exposure to either of these chemicals. In summary, the no-observed-adverse-effect-level (NOAEL) for maternal toxicity was 100 ppm for mesitylene and 300 ppm for pseudocumene, and the NOAEL for developmental toxicity was 300 ppm for mesitylene and pseudocumene.

Abnormalities, Drug-Induced↗
PubMed2006

Inhalation exposure and risk from mobile source air toxics in future years.

Modeling of inhalation exposure and risks resulting from exposure to mobile source air toxics can be used to evaluate impacts of reductions from control programs on overall risk, as well as changes in relative contributions of different source sectors to risk, changes in contributions of different pollutants to overall risk, and changes in geographic distributions of risk. Such analysis is useful in setting regulatory priorities, and informing the decision-making process. In this paper, we have conducted national-scale air quality, exposure, and risk modeling for the US in the years 2015, 2020, and 2030, using similar tools and methods as the 1999 National-Scale Air Toxics Assessment. Our results suggest that US Environmental Protection Agency emission control programs will substantially reduce average inhalation cancer risks and potential noncancer health risks from exposure to mobile source air toxics. However, cancer risk and noncancer hazard due to inhalation of air toxics will continue to be a public health concern.

Air Pollutants↗
PubMed1990

Epiglottic dysfunction after isocyanate inhalation exposure.

Epiglottic dysfunction due to environmental exposure is a well-known entity. The most common causes of epiglottic dysfunction include trauma (thermal, chemical, and blunt), infection, allergy, neoplasm, and neurologic disorders. We report an unusual case of epiglottic dysfunction due to isocyanate inhalation exposure and review the literature concerning this subject. Following inhalation exposure to diphenylmethane diisocyanate, our patient developed persistent repeated airway obstruction during inspiration. Fiberoptic rhinolaryngoscopy showed that the epiglottis obstructed the glottic airway during each inspiratory cycle. The epiglottic dysfunction was also well demonstrated by barium contrast cineradiography. Total epiglottectomy resulted in resolution of the patient's upper airway obstructive symptoms. Histologically, marked inflammatory changes of the epiglottis were noted, including a focal infiltrative pattern, focal fibrosis, edema, and reactive changes.

Adult↗
PubMed2000

Developmental toxicity of dimethylacetamide in rabbits following inhalation exposure.

(1) Dimethylacetamide was tested for developmental toxicity after inhalation exposure of pregnant Himalayan rabbits. Fifteen female rabbits per main group were exposed to dimethylacetamide vapours at concentrations of 0, 0.2, 0.7 or 2.0 mg/l (equivalent to 0, 57, 199.5 or 570 ppm) and five female rabbits per satellite group to 0 or 2.0 mg/l 6 h/day from day 7 post-insemination (p.i.) to day 19 p.i. All animals were observed until day 29 p.i. (2) No signs of maternal toxicity were seen in the does of the main groups (body weight and gross pathology) or in the does of the satellite groups (body weight, blood chemistry, histopathological findings of the liver). (3) Fetotoxic effects were caused at a concentration of 0.7 mg/l (e.g., increased skeletal variations) and 2.0 mg/l (e.g., significantly decreased fetal and placental weights, increase in soft tissue and skeletal variations). At 2.0 mg/l, there were also signs of a weak teratogenic effect expressed as a marginal, statistically not significant increase in soft tissue malformations (regarding the heart and great vessels). No compound-related effects were observed in the fetuses after exposure to 0.2 mg/l. (4) The highest concentration tested under these conditions (2.0 mg/l) was found to be a no-observable-adverse-effect-level (NOAEL) for the maternal Himalayan rabbit, whereas 0.2 mg/l was defined as the NOAEL for the developing organism.

Abnormalities, Drug-Induced↗
PubMed2001

Long-term effects of low-level sarin inhalation exposure on the spatial memory of rats in a T-maze.

1. To study the influence of low-level sarin exposure on cognitive functions, male albino Wistar rats were exposed to three various low concentrations of sarin (LEVEL 1-3) for 60 minutes in the inhalation chamber. Testing of cognitive functions was carried out using the T-maze evaluating learning and spatial memory. The behavior of sarin-exposed rats in the T-maze was tested several times within five weeks following sarin inhalation exposure to look for any cognitive impairments. The alteration of cognition was evaluated by using a method studying memory elicitation in response to appetitive motivation in a multiple T-maze. 2. Statistically significant, short-term deficiency in the T-maze performance was observed in rats exposed to symptomatic (LEVEL 3) as well as clinically asymptomatic concentration (LEVEL 2) of sarin. The repeated exposure of rats to clinically asymptomatic dose of sarin (LEVEL 2R) did not change the effect of low-level sarin exposure on spatial memory compared to the single exposure to the same dose of sarin. 3. Thus, sarin is able to influence the cognitive functions (e.g. spatial memory) even at low doses that do not cause clinically manifested intoxication following the inhalation exposure. Nevetheless, the alteration of spatial memory lasts for a short time only, in contrast with the severe sarin poisoning.

Administration, Inhalation↗
PubMed2003

Developmental toxicity of N-methyl-2-pyrrolidone in rats following inhalation exposure.

The developmental toxicity of inhaled N-methyl-2-pyrrolidone (NMP) was studied in Sprague-Dawley rats. Pregnant rats were exposed whole body to NMP vapours at concentrations of 0, 30, 60 and 120 ppm, 6 h/day, on gestational days (GD) 6 through 20. Maternal body weight gain was significantly decreased at 60 and 120 ppm on GD 6-13 and maternal food consumption was reduced at 120 ppm on GD 13-21. No significant difference in the gestational weight change corrected for the weight of the gravid uterus was observed, whatever NMP concentration. There were no adverse effects on embryo/fetal viability or evidence of teratogenicity at any concentration tested. Fetal toxicity indicated by reduced fetal weight was observed at 120 ppm. Thus, the no-observed-adverse-effect level (NOAEL) for maternal and developmental toxicity was 30 and 60 ppm, respectively.

Abnormalities, Drug-Induced↗