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PubMed1989

Effects of inhaled municipal refuse incinerator fly ash in the guinea pig.

Fly ash was collected from two municipal refuse incinerators. It was analyzed for heavy metals, elements, and a wide range of toxic organics. It was resuspended in air for inhalation exposure of guinea pigs. These animals were exposed at high concentrations of each ash 6 h/d for 5 d, and tissues were taken 45 d after the exposure. Following the first exposure and after each daily exposure the ventilatory response of these animals upon challenge with CO2 was found to be depressed. Recovery occurred following exposure. Heavy metals, cadmium, lead, zinc, and mercury were elevated in the lungs of these animals. Histologic evaluation of pulmonary tissue revealed multifocal pneumoconiosis. Interstitial infiltration by macrophages and smooth muscle hypertrophy of blood vessels and bronchioles were also observed. There was no evidence of a dioxinlike toxic effect following inhalation of these ashes.

Air Pollutants↗
PubMed2002

On the risk of mortality to primates exposed to anthrax spores.

Current events have heightened the importance of understanding the risks from inhalation exposure to small numbers of spores of Bacillus anthracis. Previously reported data sets have not been fully assessed using current understanding of microbial dose response. This article presents an assessment of the reported primate dose-response data. At low doses, the risk to large populations of low doses of inhaled spores (e.g., < 100) is not insignificant.

Administration, Inhalation↗
PubMed1987

Discriminative stimulus properties of toluene in the mouse.

Little is known about the nature of the acute intoxication produced by exposure to high concentrations of toluene such as that which occurs with spills and in solvent abusers. The intoxication may be similar to that produced by classic central nervous system depressants such as the barbiturates. To investigate this hypothesis, drug discrimination procedures were used to compare the acute effects produced by toluene and pentobarbital (PB). Mice were trained to discriminate toluene (100 mg/kg, ip) from vehicle in a two-lever task in which responding was under the control of a fixed-ratio 20 (FR20) schedule of food presentation. Generalization tests were conducted after 20-min inhalation exposures to toluene (150-3600 ppm) and 20 min after injections with either PB (5-30 mg/kg) or morphine (3-20 mg/kg). Most mice generalized to inhaled toluene and to PB in a concentration- or dose-related fashion, but not to morphine. These results show that the effects of injected toluene can be established as a discriminative stimulus in mice, and that these stimulus effects are independent of route of administration. Shared discriminative stimulus properties with PB suggest that toluene produces an acute intoxication like that of other classic CNS depressants.

Administration, Inhalation↗
PubMedDate not supplied

Occupational exposure to elemental constituents in fingerprint powders.

Fingerprint detection is an essential component of any crime detection agency. Little information is available regarding the elemental constituents of powders that are available currently. One recent case of lead poisoning coupled with many complaints from the Vancouver identification Squad members initiated a study regarding the elemental composition of, and the occupational exposure to, these powders. Multi-elemental analysis of the powders investigated showed that all contained varying amounts of aluminum, calcium, zinc, iron, magnesium, manganese, and nickel. One powder, however, contained 41% lead. The time spent at the scene of crime during a normal working shift averaged 95.5 min. Assessment of inhalation exposure during this period by personal air sampling pumps never exceeded the occupational exposure standards for these elements. Secondary exposure from dust-contaminated police vehicles and clothing can be an important contributor to overall exposure.

Air Pollutants↗
PubMed1994

Oxygen metabolites from lavage and interstitial lung cells after inhalation of endotoxin in guinea pigs.

Airborne endotoxins play a role in a variety of occupational diseases such as byssinosis and humidifier's disease and are associated with pulmonary and systemic symptoms. An excess generation of oxygen free radicals (including superoxide anion, O2-) by inflammatory cells has been suggested in endotoxemia. We have studied the release of superoxide from guinea-pig lung lavage and interstitial cells and blood monocytes (BMs) at different times after an acute inhalation exposure to bacterial endotoxin. O2- generation was measured by the O2- dismutase-inhibitable reduction of ferricytochrome c, after stimulation with phorbol-myristate-acetate (PMA) or opsonized zymosan (OZ). After endotoxin exposure, the spontaneous release of O2- remained unchanged for the three cell types. From 4 h after exposure until 48 h afterwards, lung lavage cells produced more O2- after PMA or OZ stimulation than did cells from unexposed guinea pigs. The pattern of O2- generation by interstitial cells followed that of lung lavage macrophages. O2- production remained unchanged in BMs at all times. These results suggest that endotoxin inhalation induced a priming of lavage and interstitial cells, mainly macrophages, associated with an increase in O2- production. As O2- production by BMs remained unchanged, this cell is unlikely to be responsible for the systemic symptoms seen after endotoxin inhalation.

Administration, Inhalation↗
PubMed1985

Teratogenic potential of inhaled dichlorobenzenes in rats and rabbits.

Orthodichlorobenzene (ODCB) and paradichlorobenzene (PDCB) were evaluated for teratogenic potential in rats (ODCB only) and rabbits. Groups of bred rats and inseminated rabbits were exposed to 0, 100, 200, or 400 ppm of ODCB; groups of inseminated rabbits were exposed to 0, 100, 300, or 800 ppm of PDCB. Animals were exposed for 6 hr/day on Days 6 through 15 (rats) or 6 through 18 (rabbits) of gestation. Maternal toxicity, as evidenced by a significant decrease in body weight gain, was observed in all groups of ODCB-exposed rats and liver weight was significantly increased in the 400-ppm ODCB-exposed group. Slight maternal toxicity was observed in groups of rabbits exposed to 400 ppm ODCB or 800 ppm PDCB as indicated by significantly decreased body weight gain during the first 3 days of exposure. Inhalation of up to 400 ppm of ODCB was not teratogenic or fetotoxic in rats, and neither ODCB nor PDCB was teratogenic or fetotoxic in rabbits at exposure levels up to 400 or 800 ppm, respectively.

Abnormalities, Drug-Induced↗
PubMed1995

Clastogenic effects of 1,3-butadiene and its metabolites 1,2-epoxybutene and 1,2,3,4-diepoxybutane in splenocytes and germ cells of rats and mice in vivo.

Clastogenicity of 1,3-butadiene (BD), 1,2-epoxybutene (EB), and 1,2,3,4-diepoxybutane (DEB) was studied in splenocytes and germ cells of rats and mice by means of micronucleus assays (cytokinesis-block method for splenocytes, suspension method for germ cells). Inhalation exposure of mice to 200, 500, or 1,300 ppm BD (6 h/d; 5 days) induced significant chromosome damage in spermatocytes at the preleptotene stage. EB and DEB induced significant amounts of clastogenic damage in splenocytes and spermatocytes of rats and mice. The lowest tested effective doses for mice and rats were, respectively, 40 and 80 mg/kg for EB, and 15 and 30 mg/kg for DEB. In splenocytes, 80 mg EB/kg induced 3.6 times more MN in mice than in rats, whereas 30 mg DEB/kg induced the same amount of damage in both species. Damage in germ cells of mice was induced in early spermatocytes treated with 40 and 80 mg EB/kg, and in late spermatocytes exposed to 30 mg DEB/kg. In rats, 40 mg EB/kg induced damage in early spermatocytes, whereas 80 mg EB/kg induced chromosomal damage in early and late spermatocytes. In rats treated with DEB, clastogenic damage was induced in spermatocytes at preleptotene, zygotene, diplotene, and diakinesis stages. When the clastogenic potential of EB and DEB in splenocytes and germ cells of mice and rats was compared, DEB always showed a stronger effect than EB. Body weight, testis weight, ratio of testis weight to body weight, and ratio of Golgi to Golgi + cap phase spermatids were used as parameters for toxicity. Exposures to 500 and 1,300 ppm BD were somewhat toxic to mice. Doses of 80 mg EB/kg and 30 mg DEB/kg exhibited toxic effects in mice and rats.

Administration, Inhalation↗
PubMed1983

Absorption, distribution, and retention of inhaled selenious acid and selenium metal aerosols in beagle dogs.

We studied the distribution and retention of inhaled selenious acid and selenium metal aerosols which were similar in size and chemical form to selenium aerosols that may be produced during fossil fuel combustion. Beagle dogs were given 10 to 61 micrograms Se/kg of body weight by inhalation. Aerosols generated for the inhalation exposures were also collected and instilled into the upper respiratory tracts or stomachs of additional dogs to measure systemic absorption at these sites. Selenium-75, incorporated into the aerosols, was used to determine the Se content in the whole animal, excreta, and individual tissues as a function of time. Virtually all of the inhaled selenious acid aerosol was rapidly absorbed into the blood from the lungs, gastrointestinal tract, and the nasal membranes. Selenium metal aerosols were less rapidly absorbed. Selenium that was absorbed into the blood was translocated to the liver, kidney, spleen, and heart. Selenium-75 in these organs had a biological half-life of 30 to 40 days. Approximately 50% of the deposited Se was eliminated with a biological T1/2 of 1.2 days. Urine was the major route of excretion, accounting for 70 to 80% of the excreted Se. The long-term component of the whole-body retention function for both inhaled aerosols had a half-life of about 34 days and accounted for about 20% of the initial Se dose. The data suggested that although absorption of selenious acid into blood following inhalation was more rapid than absorption of selenium metal, once absorbed the disposition of both compounds was similar.

Aerosols↗
PubMed1979

Effects of intermittent styrene inhalation, ethanol intake and their combination on drug biotransformation in rat liver and kidneys.

The modifying effects of daily ethanol ingestion in the drinking water as a 15 % solution (v/v) on drug biotransformational changes induced by inhalation exposure to styrene (300 ppm or 1260 mg/m3, 6 h daily, 5 d/week, up to 17 weeks) were studied in rat liver and kidney. The drug hydroxylation activities (7-ethoxycoumarin O-deethylase and 2,5-diphenyloxazole hydroxylase) both in liver and in kidneys were increased more by ethanol ingestion than by styrene inhalation. When administered in combination, styrene and ethanol exerted mostly an additive enhancing effect. However, hepatic NADPH-cytochrome c reductase activity was reduced both in styrene and in ethanol-treated rats. Hepatic styrene oxide hydratase activity was virtually unaffected by styrene treatments. The depression of glutathione concentration in liver was greater after styrene-ethanol than after styrene treatment alone. The hepatic UDPglucuronosyltransferase activity was enhanced slightly both in styrene and in styrene-ethanol rats. The binding affinity of styrene towards cytochrome P-450 was increased after styrene inhalation as shown by lowered K8 values. The perirenal fat concentration of styrene showed a rough inverse relationship to the overall monooxygenation activities in liver and kidney. Despite the additively induced enzyme activities in styrene-ethanol-treated rats the accumulation of styrene in fat of these animals was on the whole somewhat greater, suggesting that these two solvents in vivo also have mutual inhibitory effects on biotransformation.

Animals↗
PubMed1992

[The acute toxicity of the microbial preparation bulmoscide].

The acute toxicity of a new Bulgarian microbial preparation bulmoscid on the basis of Bacillus thuringiensis H-14 in the conditions of oral, dermal, inhalation and intraperitoneal introduction in experimental animals is determined. The assessment of toxicity is made by using toxicometric, integral, hematologic, histologic and microbiologic methods in accordance with Bulgarian and international criteria and standards. It is established, that the preparation bulmoscid introduced orally in dose 5500 mg.kg-1 (6.6.10(10) cell kg-1), applied dermally in dose 6000 mg/kg-1 (7.2.10(10) cells kg-1) and in concentrations 18 mg.m-3 (2.2.10(8) cells m-3) for 14 day inhalation exposure, provokes no lethal exit and symptoms of intoxication and leads to no changes in the integral, hematologic and histologic investigations on experimental animals. The preparation belongs to the practically nontoxic substances. The studies of the acute toxicity show, that the microbial preparation bulmoscid offers no danger for appearing of oral, dermal and inhalation poisonings when observing the regulations for its production and use.

Acute Disease↗
PubMed1997

Serum liver function profiles in coking workers.

Coking workers are regularly exposed to coke oven emissions (COE), which consist mainly of polycyclic aromatic hydrocarbons and volatile organic compounds. In a previous cross-sectional study, we found that coking and by-product workers with heavy exposure to COE in the older of two coke operation areas in Taiwan had higher serum activities of hepatic aminotransferase than the controls. In this study, we further examine the relationship of exposure to COE with liver function profiles in coking workers. Liver function profiles included serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), alkaline phosphatase (ALP), and total bilirubin (BIL). The exposed group included 88 workers working 3 months or more in the older coke oven plant. Fifty-nine referents, not visiting the coke operation areas in the last 3 months, came from the administrative area in the same company. Each participant wore a personal monitor that was used to measure benzene soluble fraction (BSF) of total particulates, as a surrogate of COE, for 3 consecutive days between August 1995 and February 1996. Serum liver function profiles, hepatitis B surface antigens, and anti-hepatitis C antibodies were examined in the morning following the exposure measurements. Exposure levels were categorized by exposure situations (high, medium, low) among coking workers. The high exposure group (n = 23) worked topside of the oven. The medium exposure group (n = 44) worked at the sideoven for more than 4 hr/day, whereas the low exposure group (n = 21) worked at the sideoven for less than 4 hr/day and mostly remained in the control rooms. The low exposure group was used as an internal comparison group. The median BSF concentrations for various exposure situations were as follows, high exposure group: 372 micrograms/m3, medium exposure group: 61 micrograms/m3, low exposure group: 49 micrograms/m3, and referents: 10 micrograms/m3. The coking workers (n = 88) did not significantly differ from the referents (n = 59) in any of the liver function profiles. Excluding the referents, workers in the high exposure group had a mean AST level that was 31% higher (95% confidence interval (CI) = 9-57%) and a mean ALT level that was 46% higher (95% CI = 7-98%) than those in the low exposure group after adjusting for appropriate confounders in multivariate models. The prevalence of an abnormal hepatocellular pattern (AST > 37 IU/L or ALT > 39 IU/L) was more common in the high exposure group than in the low exposure group (adjusted odds ratio = 4.4; 95% CI = 0.9-22.6). However, these associations were not found in GGT, ALP, or BIL. After controlling for the possible effects of nonoccupational factors on serum activity of AST and ALT, we conclude that increased AST and ALT levels among topside coking workers may be caused by heavy inhalation exposure to COE. Additionally, the adverse hepatic effect seems to be caused by a mixture of hazards, rather than a unique identifiable chemical.

Adult↗
PubMed1990

Decrease in the rat bronchial acetylcholinesterase activity after toluene diisocyanate inhalation.

Acetylcholinesterase (AChE) activity was measured in bronchial tissue homogenate and blood from rats subjected to single and repeated 4-h daily inhalation exposure to toluene diisocyanate (TDI) or control atmospheres. A single 4-h exposure to TDI in the concentration range of 0.7-4.3 ppm did not decrease AChE activity in bronchial tissue but a 4-h exposure to 0.6 ppm TDI, or greater, for two consecutive days did reduce this activity (19% to 33% of the controls). Increasing the level of exposure to TDI for two consecutive days from 0.6 to 4.0 ppm and extending the length of exposure to 1.2 ppm TDI from 2 to 4, 9 or 14 days produced no further decrease in bronchial ACHE activity. Throughout these experiments, blood AChE activity remained unchanged. In rats exposed to 0.3 or 1 ppm TDI for 3 weeks, staining of the bronchial smooth muscle for AChE was reduced (36% of the controls) after exposure to 1 ppm TDI. These results support, for the first time, in vivo and localized anti-AChE activity by TDI.

Acetylcholinesterase↗
PubMed1997

Short-term inhalation and in vitro tests as predictors of fiber pathogenicity.

A wide range of fiber types was tested in two in vitro assays: toxicity to A549 epithelial cells, as detachment from substrate, and the production of the proinflammatory cytokine tumor necrosis factor (TNF) by rat alveolar macrophages. Three of the fibers were also studied in vivo, using short-term inhalation followed by a) bronchoalveolar lavage to assess the inflammatory response and b) measurement of cell proliferation in terminal bronchioles and alveolar ducts, using incorporation of bromodeoxyuridine (BrdU). The amount of TNF produced by macrophages in vitro depended on the fiber type, with the man-made vitreous fibers, and refractory ceramic fibers being least stimulatory and silicon carbide (SiC) whiskers providing the greatest stimulation. In the epithelial detachment assay there were dose-dependent differences in the toxicity of the various fibers, with long amosite being the most toxic. However, there was no clear relationship to known chronic pathogenicity. Fibers studied by short-term inhalation produced some inflammation, but there was no clear discrimination between the responses to code 100/475 glass fibers and the more pathogenic amosite and SiC. However, measurements of BrdU uptake into lung cells showed that amosite and SiC produced a greater reaction than code 100/475, which itself caused no more proliferation than that seen in untreated lungs. These results mirror the pathogenicity ranking of the fibers in long-term experiments. In conclusion, the only test to show potential as a predictive measure of pathogenicity was that of cell proliferation in lungs after brief inhalation exposure (BrdU assay). We believe that this assay should be validated with a wider range of fibers, doses, and time points.

Administration, Inhalation↗
PubMed2005

Epidemiology of hydrogen phosphide exposures in humans reported to the poison center in Mainz, Germany, 1983-2003.

BACKGROUND: Poisonings with rodenticides containing hydrogen phosphide-releasing compounds may lead to deleterious organ dysfunction and death. Since data of hydrogen phosphide poisonings is limited to case reports/series, this study was intended to elucidate hydrogen phosphide poisonings based on a 20-year data collection. METHODS: Explorative data analysis of the Poison Center Mainz database looking for route of exposure, symptoms, and severity using the Poisoning Severity Score. RESULTS: From 1983-2003, 188 hydrogen phosphide poisonings were reported. Sixty-five percent of these were unintentional residential, 28% attempts to commit suicide (intentional), 5% occupational, and 2% undetermined. In the majority of intentional poisonings the poison was ingested, whereas in unintentional poisoning of adults inhalation exposure dominated, caused by inappropriate self-protection from the released hydrogen phosphide gas during usage. Frequently observed symptoms in unintentional poisonings were nausea, vomiting, pain, coughing, and dizziness with no further worsening of symptoms. In intentional poisonings frequent symptoms were vomiting, somnolence, seizures, coma, and shock with two initially fatal poisonings. Follow-up on these cases showed a significant worsening of symptoms and a two-fold increase in fatal poisonings. CONCLUSION: Route of exposure, severity of symptoms, and the necessary treatment differs substantially between unintentional and intentional poisonings. In this study, two initially symptomatic intentional poisonings were later reported fatal. Careful monitoring is recommended in symptomatic intentional poisonings.

Adolescent↗
PubMed2006

Increases in amphetamine-like discriminative stimulus effects of the abused inhalant toluene in mice.

RATIONALE: Toluene, an abused solvent, shares behavioral and pharmacological effects with abused depressant drugs. These effects include ethanol- and pentobarbital-like discriminative stimulus effects. There is also emerging evidence that this abused inhalant may share stimulus effects with abused central nervous system (CNS) stimulants. OBJECTIVE: To further explore the discriminative stimulus effects of one abused inhalant, this experiment evaluated the amphetamine-like discriminative stimulus effects of toluene. MATERIALS AND METHODS: Mice were trained to discriminate between d-amphetamine (1.0 mg/kg) and saline in a two-lever drug discrimination procedure in which responding was under the control of a fixed-ratio 15 schedule. Mice were tested after 10-min inhalation exposures to air or toluene (500-6,000 ppm) and stimulus generalization was examined at 0, 15, 30, 45, 60, and 75 min post-exposure. RESULTS: Concentration-related increases in amphetamine-lever responding were observed for amphetamine doses >0.56 mg/kg with full substitution occurring immediately after testing for 1.0 and 1.78 mg/kg. Partial amphetamine-lever responding was observed for all concentrations of toluene across the 75-min post-exposure test trials. Response rates that had decreased immediately after all toluene exposures recovered within 15-min post exposure. CONCLUSION: This partial substitution of toluene for amphetamine suggests that studies of the effects of abused solvents on brain dopaminergic systems need to be included in the study of possible CNS mechanisms.

Administration, Inhalation↗
PubMed1994

Mutagenicity of 1,3-butadiene inhalation in somatic and germinal cells of mice.

Inhalation exposure of mice to 50, 200, 500 or 1300 ppm of 1,3-butadiene for 6 h per day for 5 consecutive days caused micronuclei in mouse bone marrow and peripheral blood erythrocytes. The dose response was non-linear. The slope of the curve flattened with increasing exposure concentration. Coat color spots were found in the mouse spot test after exposure of pregnant females on pregnancy days 8-12 to 500 ppm of 1,3-butadiene. Dominant lethal mutations were induced in spermatozoa and late spermatids after exposure of male mice to 1300 ppm with the 5-day exposure regimen. Thus, in the mouse 1,3-butadiene is a somatic and germ cell mutagen.

Administration, Inhalation↗
PubMed2000

[Relationship between lung cancer and aflatoxin B1].

The relationship between aflatoxins and liver cancer is well established. In addition the inhalation exposure to carcinogen aflatoxin B1 (AFB 1) is considerable. Genotoxic chemical is known to react with DNA either directly or after metabolic activation to form adducts, a step thought to be relevant with respect to chemical carcinogenesis. The presence and the amount of specific DNA adducts provide a good indication of chemical exposure and genetic damage resulting the exposure to carcinogens and account for same of factors affecting individual susceptibility to cancer. Analysis of DNA adducts requires that the sensitivity of the methods to be sufficient high to allow detection of about 1 adduct/109 normal nucleotides. Most suitable method is based in physiochemical technique such as HPLC. Because circumstantial epidemiological evidence suggests that AFB1 inhalation may cause primary lung cancer. We investigate AFB1 by HPLC in three different tobacco sources, and in 39 patients with compatible lung cancer or chronic bronchitis. The patients were divided by clinical manifestations in lung cancer (n: 25) and chronic bronchitis (n: 14). Twenty-three of 25 patients presented epidermoid lung cancer within smoking habit, and 2 of 25 presented adenocarcinoma without smoking habit. In chronic bronchitis group 12 of 14 cases presented smoking habit. The control PBS liquid was negative to AFB1; the different tobacco sources, a) Virginia of Jujuy, b) Brasilero and c) black of Salta presented AFB1 positive determinations respectively. The bronchial tissues obtained by lung biopsies presented positive AFB1 in lung epidermoid cancer at 0.68 +/- 0.82 mg/L. The adenocarcinoma presented AFB1 negative determinations. In chronic bronchitis patients with smoking habit (n: 12) presented AFB1 positive with a level less than the epidermoid lung cancer group, 0.21 +/- 0.109 mg/L, p < .025.

Adenocarcinoma↗