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At least 973 records · Page 54Linked to original sources
PubMed1998

Acute effects of 10-minute exposure to hydrogen fluoride in rats and derivation of a short-term exposure limit for humans.

A series of acute inhalation exposures of female rats was conducted with hydrogen fluoride (HF) to establish a concentration-response curve for nonlethal exposures. Durations of 2 and 10 min were used to simulate possible short-term exposures. Concentrations of HF ranged from 593 to 8621 ppm for 2-min exposures and from 135 to 1764 ppm for 10-min exposures. Additional exposures were performed for 60 min at 20 and 48 ppm HF for comparison to existing Emergency Response Planning Guidelines. Animals were evaluated on the day after exposure for changes in parameters of bronchoalveolar lavage, pulmonary function, hematology, serum chemistry, body weight, organ weights, and histopathology. Most exposures were performed with orally cannulated animals to bypass absorption of HF in the nose and achieve maximum delivery of HF to the lower airways. One of the primary uses of the resulting data was to estimate a concentration to which most people could be exposed for 10 min without severe of irreversible health effects. This level was 130 ppm. It was predicted that irritation would occur at this concentration, but the effects on t he respiratory tract would not be "serious" and would be expected to be reversible. The results of this experiment and the subsequent analysis of the data provide an important aid in he planning of responses to an accidental release of HF.

Animals↗
PubMedDate not supplied

Drinking habits and occupational exposure to inhalation anesthetics at low doses.

The aim of this study was to evaluate certain indicators which are an expression of hepatic (serum aminotransferases activities) and hematologic (erythrocyte mean corpuscular volume) changes among health care personnel exposed to inhalation anaesthetics (nitrous oxide and isoflurane). A total of 172 subjects employed in a single hospital were divided into four groups according to exposure and drinking habits: group (i) non drinkers and unexposed subjects, group (ii) drinkers and unexposed subjects, group (iii) non drinkers and exposed subjects, group (iv) drinkers and exposed subjects. No change in aminotransferases activity or in mean erythrocyte size was detected, which could be regarded as the result of anesthetics exposure. Increased aspartate aminotransferase values among unexposed drinkers were related to alcohol intake. This observation was confirmed by the relationship between AST behaviour and quantitative alcohol intake. Hence, when studying any effect involving functions related to the biotransformation of xenobiotics, in which the liver plays a primary role, the importance of establishing the exact daily amount of ethanol intake is stressed.

Adult↗
PubMed1994

Comparisons between operant response and 1,1,1-trichloroethane toxicokinetics in mouse blood and brain.

The effect of 1,1,1-trichloroethane (TRI) inhalation on operant response was evaluated in relation to the concentration of TRI in blood and brain tissue in mice during exposure. Male CD-1 mice were trained to lever-press for an evaporated milk reinforcer on a variable interval (VI 60) schedule for 2 h. Trained mice were then exposed to either 3500 or 5000 ppm TRI for 100 min, and the changes in the schedule-controlled performance were measured. Additional groups of mice were exposed under the same conditions as those used in the behavioral study and sacrificed at various times during exposure, and the blood and brain samples were collected and subsequently analyzed for TRI content by headspace gas chromatography. Uptake of TRI into blood and brain was rapid, with near steady-state levels reached after approximately 40-60 min of exposure. Inhalation of 5000 ppm, but not 3500 ppm TRI was seen to cause inhibition of operant response, starting approximately 30 min following the initiation of inhalation exposure and beginning to recover after 80 min of exposure. The threshold concentrations for the maximal behavioral inhibition were approximately 110 micrograms/g and 130 micrograms/ml in mouse brain and blood, respectively. It appears that in addition to TRI concentrations in blood and brain tissue, the time it takes to reach the apparent threshold TRI concentration was also a determinant for the onset of TRI neurobehavioral depression.

Administration, Inhalation↗
PubMed2001

A dermal model for spray painters. Part II: estimating the deposition and uptake of solvents.

The contribution of dermal exposure to the total body burden of a given chemical is difficult to assess. However, it is possible that as regulatory pressures lead to reductions in inhalation exposure, the proportion of uptake via the dermal route will increase. This study brings together recent work in the field of dermal exposure to provide a model to estimate both exposure and uptake of solvents through the skin. Using spray painters as an example, the process of modelling exposure is described from identifying the determinants of exposure through to calculating the flux of solvent through the stratum corneum and thus the total dermal uptake. Results from a range of exposure scenarios are presented and areas requiring further research and validation are highlighted. The model should allow the estimation of combined dermal and inhalation exposure to solvents in both current work situations and retrospective epidemiological studies. Furthermore, it is envisaged that the model may provide the basis for generic assessment of dermal exposure and uptake.

Air Pollutants, Occupational↗
PubMed1987

Assessment of unscheduled and replicative DNA synthesis in rat kidney cells exposed in vitro or in vivo to unleaded gasoline.

Unleaded gasoline (UG) induces renal toxicity and neoplasia in male but not female rats after chronic inhalation exposure. Before a meaningful determination of the potential human health risk of UG can be made, it is imperative that the mechanism responsible for its carcinogenic action be understood. The purpose of the present investigation was to determine whether the induction of kidney tumors by UG is related to genotoxic or to cell-proliferative effects. Unscheduled DNA synthesis (UDS), as an indicator of genotoxicity, was measured autoradiographically as the incorporation of [3H]thymidine in isolated rat kidney cells following in vivo or in vitro exposure to UG. As an indicator of proliferative activity, cells in S-phase were quantitated in isolated cell preparations obtained from exposed rats. UG was administered to rats by inhalation (2000 ppm) or by gavage (up to 5000 mg/kg). The ability of the in vivo/in vitro kidney cell UDS assay to detect genotoxicants was verified using a variety of compounds. No UDS activity was elicited by UG under any of the conditions employed, including inhalation exposure to a concentration that produced kidney tumors in the 2-year bioassay. A five- to eightfold increase in the percentage of cells in S-phase was observed in male rats exposed to UG for 18 days either by inhalation or by gavage. Cell turnover was not markedly enhanced in identically treated female rats. These data indicate that UG does not evoke UDS in the rat kidney even after exposures that, in all probability, resulted in greater tissue concentrations of UG components than was realized in the long-term inhalation bioassay. The sex-specific induction of replicative DNA synthesis in the kidney paralleled the carcinogenic activity of UG, suggesting that induced cell turnover may be an important factor in the carcinogenic action of this motor fuel.

Alkaline Phosphatase↗
PubMed1983

Bioassay model for estimating body burdens of 241Am from excretion analyses.

A simple bioassay model for predicting the organ burdens of 241Am from excretion rates is presented for inhalation exposures. The model uses three compartments representing lung, liver and skeleton. The model was developed using data from studies in laboratory animals of inhaled or injected 241Am and was validated for people by comparison to cases of accidental inhalation exposures to 241Am. The data for people have a large amount of variability but indicate that the retention half-time of 241Am in liver is approximately 2 yr and in skeleton is approximately 30 yr. These parameters can be used in the model to estimate body and organ burdens from excretion rates after inhalation of 241Am or the model can be fitted to an individual's measured excretion rates.

Americium↗
PubMed2006

Inhalation and dermal exposure to eight antineoplastic drugs in an industrial laundry facility.

OBJECTIVES: The aims of the study were to quantify levels of dermal and inhalation exposure to antineoplastic drugs in an industrial laundry service in the Netherlands and to test the removal efficiency of the washing procedure for removal of antineoplastic drugs. METHODS: During four workdays dermal and inhalation exposure to eight frequently used antineoplastic drugs (cyclophosphamide, ifosfamide, methotrexate, 5-fluorouracil, etoposide, cytarabine, gemcitabine and chlorambucil) were measured for all job titles involved in handling unwashed laundry. To test the removal efficiency of the washing procedure, 10 x 10 cm sections were excised before and after the washing procedure. These sections were taken from 15 bed sheets that were collected in hospitals of patients who were treated with one of the selected antineoplastic drugs. RESULTS: During none of the four measurement days, detectable levels of any of the eight antineoplastic drugs (cyclophosphamide, ifosfamide, methotrexate, 5-fluorouracil, etoposide, cytarabine, gemcitabine, or chlorambucil) were found on workers' skin of hands or in any of the air samples. Only four out of the 15 bed sheets from patients that were treated with antineoplastic drugs appeared to be contaminated with detectable levels of antineoplastic drugs before the washing procedure (range 13.0-3,060 ng/100 cm(2)). After the pre-washing and after the complete washing procedure, no detectable levels of any of the eight antineoplastic drugs were found anymore in the selected bed sheets. CONCLUSIONS: The implementation of guidelines for working with antineoplastic drugs seems to be successful in reducing exposure to antineoplastic drugs of workers in this laundry facility to an acceptable, non-detectable level and to remove antineoplastic drug contamination from bed linen.

Antineoplastic Agents↗
PubMed2000

Appropriate use of animal models in the assessment of risk during prenatal development: an illustration using inorganic arsenic.

BACKGROUND: Assessing risks to human development from chemical exposure typically requires integrating findings from laboratory animal and human studies. METHODS: Using a case study approach, we present a program designed to assess the risk of the occurrence of malformations from inorganic arsenic exposure. We discuss how epidemiological data should be evaluated for quality and criteria for determining whether an association is causal. In this case study, adequate epidemiological data were not available for evaluating the potential effect of arsenic on development. Consequently, results from appropriately designed, conducted, and interpreted developmental toxicity studies, which have been shown to be predictive of human risk under numerous scenarios, were used. In our case study, the existing animal data were not designed appropriately to assess risk from environmental exposures, although such studies may be useful for hazard identification. Because the human and animal databases were deficient, a research program comprising modern guideline toxicological studies was designed and conducted. RESULTS: The results of those studies in rats, mice, and rabbits indicate that oral and inhalational exposures to inorganic arsenic do not cause structural malformations, and inhalational exposures produced no developmental effects at all. The new study results are discussed in conjunction with considerations of metabolism, toxicokinetics, and maternal toxicity. CONCLUSIONS: Based on the available experimental data, and absent contrary findings from adequately conducted epidemiological studies, we conclude that exposure to inorganic arsenic by environmentally relevant routes poses no risk of the occurrence of malformations and little risk of other prenatal developmental toxicity in developing humans without concomitant and near-lethal toxicological effects in mothers.

Abnormalities, Drug-Induced↗
PubMed2003

Low-level sarin-induced alteration of immune system reaction in inbred BALB/c mice.

To study the influence of low-level sarin inhalation exposure on immune functions, inbred BALB/c mice were exposed to low concentrations of sarin for 60 min in the inhalation chamber. Two concentrations of sarin were chosen-asymptomatic concentration (LEVEL 1) and non-convulsive symptomatic concentration (LEVEL 2). The evaluation of immune functions was carried out using phenotyping of CD3 (T-lymphocytes), CD4 (helper T-lymphocytes), CD8 (cytotoxic T-lymphocytes) and CD19 cells (B-lymphocytes) in the lungs, blood and spleen, lymphoproliferation of spleen cells stimulated in vitro by various mitogens (concanavalin A, lipopolysaccharides), phagocyte activity of peritoneal and alveolar macrophages, production of N-oxides by peritoneal macrophages and the measurement of the natural killer cell activity at 1 week following sarin exposure. The results were compared to the values obtained from control mice exposed to pure air instead of sarin. The results indicate that not only symptomatic but also asymptomatic dose of sarin is able to alter the reaction of immune system at 1 week following exposure to sarin. While the number of CD3 cells in the lungs was slightly decreased, an increase in CD19 cells was observed especially in the lungs and blood. The reduced proportion of T-lymphocytes is caused by decay of CD4 positive T-cells. Lymphoproliferation was significantly decreased regardless of the mitogen and sarin concentration used. The production of N-oxides by peritoneal macrophages was stimulated after exposure to LEVEL 2 of sarin whereas their ability to phagocyte the microbes was increased after exposure to LEVEL 1. The natural killer cell activity was significantly higher in the case of inhalation exposure of mice to LEVEL 2 of sarin. Thus, not only organophosphorus insecticides but also nerve agents such as sarin are able to alter immune functions even at a dose that does not cause clinically manifested intoxication following the inhalation exposure. Nevertheless, the alteration of immune functions following the inhalation exposure to a symptomatic concentration of sarin seems to be more pronounced.

Administration, Inhalation↗
PubMed1981

Aryl hydrocarbon hydroxylase activity induced by injected diesel particulate extract vs inhalation of diluted diesel exhaust.

The effects of long-term inhalation of diluted diesel exhaust on aryl hydrocarbon hydroxylase activity (AHH) and cytochrome P-450 content in lung and liver microsomes were investigated in male Fischer-344 rats and compared with repeated parenteral administration of organic solvent extracts of hydrocarbons adsorbed on the diesel particulate surface during the combustion process. The animals were exposed to concentrations of 750 micrograms m-3 or 1500 micrograms m-3 of diesel particulates from a 5.7L GM diesel engine 20 h per day, 5 1/2 days per week for up to 9 months or treated by repeated IP injections of diesel particulate extract (dissolved in corn oil) from the same engine at several dose levels for 4 days. No significant effects of long-term inhalation exposure were observed in liver microsomal AHH activity. A slight decrease in lung microsomal AHH activity was found in rats following 6 months of exposure to diesel exhaust at the particulate concentration of 1500 micrograms m-3. The total mass of particles deposited in the lung during the inhalation exposure was estimated and an equivalent dose of extractable hydrocarbons was administered intraperitoneally; no increase in AHH activity was observed in the lung or liver microsomes. In contrast, 1.4- to 9-fold increases in AHH activity were observed in liver and lung microsomes of rats pretreated by intraperitoneal doses 10-50 times larger than the most conservative estimate of the deposited lung burden. No changes in cytochrome P-450 content were observed in the microsomes of rat liver after inhalation or injection treatment studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1989

Inhalation developmental toxicity study of propylene oxide in Fischer 344 rats.

The developmental toxicity potential of propylene oxide (PO) was evaluated in Fischer 344 rats following inhalation exposure. Four groups of 25 mated female rats were exposed to 0, 100, 300, and 500 ppm of PO for 6 hr per day on Gestation Days 6 through 15, inclusive. Cesarean sections were performed on all females on Gestation Day 20 and the fetuses removed for morphological evaluation. Exposure to propylene oxide did not adversely affect survival, appearance, or behavior at any of the exposure levels tested. Maternal body weight gain and food consumption were reduced significantly among the females at the 500 ppm level during the exposure period. No exposure-related effects were noted with respect to maternal water consumption, organ weights, cesarean section, or fetal morphological observations with the sole exception of increased frequency of seventh cervical ribs in fetuses at the maternally toxic exposure level of 500 ppm. In summation, the no-observable-adverse-effect level (NOAEL) of propylene oxide, when administered to Fischer 344 rats via whole-body inhalation exposure, was considered to be 300 ppm.

Administration, Inhalation↗
PubMed1996

Pulmonary metallothionein expression in rats following single and repeated exposure to cadmium aerosols.

This study examined the expression of metallothionein (MT) isoforms in the lungs of Lewis rats exposed to Cadmium (Cd) aerosols. With the use of isoform-specific oligonucleotide probes and Northern hybridization analysis, we demonstrated that a dramatic, rapid, and coordinate increase occurred in pulmonary MT-1 mRNA and MT-2 mRNA following Cd inhalation exposure. MT mRNAs levels reached a maximum at 2 h post-exposure and remained above control levels at 96 h after exposure. A considerable lag between the time of maximal elevations in MT mRNAs and MT protein accumulation was observed and suggested that regulatory mechanisms in addition to transcriptional control could be involved. MT expression (protein and mRNA) and Cd lung burden were directly related to aerosol Cd concentration. In situ hybridization and immunohistochemistry studies showed good correlation between the localization of MT protein and MT mRNAs. However, staining for MT protein and MT mRNA was not uniformly distributed in the lung. MT was particularly prominent within the alveolar compartment. Even within this area, however, heterogeneity of MT expression was evident. Experiments were subsequently conducted to determine whether prior exposure to Cd modulates the transcriptional activity of MT genes such that there is a greater elevation in gene expression upon reexposure to Cd. Surprisingly, animals pretreated with Cd exhibited a smaller incremental increase in MT mRNA levels in response to subsequent Cd exposure than controls with no prior treatment. Moreover, MT mRNA levels were elevated to a similar extent regardless of whether animals were exposed to Cd aerosols for 1, 2, or 3 weeks (3 h/day; 5 days/week). MT protein and lung Cd burden, on the other hand, exhibited an increasing linear trend as a function of exposure number. In summary, this study has demonstrated that: (1) the lung responds to Cd inhalation exposure by increasing MT mRNA and MT protein levels; (2) MT expression is prominent within alveolar cells but not all cells are MT positive; and (3) Cd-pretreatment does not increase the transcriptional potential of MT genes when the animal is subsequently reexposed to Cd.

Administration, Inhalation↗
PubMed1984

Propylene glycol monomethyl ether acetate (PGMEA) metabolism, disposition, and short-term vapor inhalation toxicity studies.

Male Fischer 344 rats were given a single po dose of approximately 8.7 mmol/kg of [1-14C]propylene glycol monomethyl ether acetate (PGMEA) or exposed to 3000 ppm [1-14C]PGMEA for 6 hr. After dosing, expired air, excreta, and tissues were analyzed for 14C activity, and metabolites in urine were isolated and identified. Approximately 64% of the administered 14C activity was eliminated as 14CO2 and about 24% was excreted in urine within 48 hr after a single po dose of radiolabeled PGMEA. Similarly, 53% was eliminated as 14CO2 and 26% was excreted in urine within 48 hr after the inhalation exposure. Propylene glycol, propylene glycol monomethyl ether (PGME), and the sulfate and glucuronide conjugates of PGME were identified as urinary metabolites after po dosing, as well as after inhalation exposure to PGMEA. The urinary metabolite profile and disposition of [14C]PGMEA were nearly identical to results previously obtained with propylene glycol monomethyl ether (PGME), indicating that PGMEA is rapidly and extensively hydrolyzed to PGME in vivo. A short-term vapor inhalation toxicity study in which male and female Fischer 344 rats and B6C3F1 mice were exposed to 0, 300, 1000, or 3000 ppm PGMEA confirmed that there were no substantial differences in the systemic effects of PGMEA as compared to PGME. However, histopathologic examination did reveal changes in the olfactory portions of the nasal mucosa of rats and mice exposed to PGMEA, which may be related to acetic acid resulting from hydrolysis of PGMEA in the nasal epithelium.

Animals↗