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PubMed1987

Evaluating the toxicity of urban patterns of oxidant gases. I. An automated chronic gaseous animal inhalation exposure facility.

An automated animal inhalation exposure facility was designed to conduct chronic exposures of rodents to gaseous pollutants. The facility consisted of 3 walk-in chambers with modular cages to allow for exposure of up to a maximum of 480 mice or 240 adult rats. Critical parameters of operation, such as relative humidity, pollutant concentration, and temperature, were monitored continuously. Failure of the system to maintain parameters within specified limits activated the alarm system. Distribution of test gases in the chambers was evaluated for homogeneity, and the standard deviation was determined to be within +/- 5% of the target concentrations throughout the chamber. The exposure facility was successfully used to expose 720 rats to diurnal patterns of O3 (baseline of 0.06 ppm for 13 h with an exposure peak to 0.25 ppm over 9 h) and NO2 (baseline of 0.5 ppm for 16 h with an exposure peak to 1.5 ppm over 6 h) for a period of 18 mo.

Administration, Inhalation↗
PubMed2000

[Optimal conditions for establishment of experimental tuberculosis model using an automated inhalation exposure apparatus and its application].

Animal (mouse and guinea pig) pulmonary tuberculosis models were established, using an automated inhalation exposure apparatus (Glas-Col Corp., USA, Model 099CA-4212). This apparatus includes four steps--preheating, nebulization, cloud decay and decontamination. The optimal conditions for M. tuberculosis H37Rv strain infection experiments were as follows: 10(5-6) colony forming unit (cfu) tubercle bacilli; preheating for 15 min.; nebulization for 90 min.; cloud decay for 15 min. and decontamination for 5 min. When 10(4) cfu M. tuberculosis H37Rv strain were introduced into the lungs of interferon (IFN)-gamma knockout mice, using the inhalation exposure apparatus and were followed up for 9 months, the primitive cavitary lesions were observed. This apparatus was also useful for inhalation exposure experiments of guinea pigs. This apparatus can also be utilized for animal inhalation experiments of allergens.

Animals↗
PubMedDate not supplied

Delayed neurotoxic effect of sarin in mice after repeated inhalation exposure.

Delayed neurotoxicity of sarin in mice after repeated inhalation exposure has been studied. Female mice exposed to atmospheric sarin (5 mg m-3 for 20 min) daily for 10 days developed muscular weakness of the limbs and slight ataxia on the 14th day after the start of the exposure. These changes were accompanied by significant inhibition of neurotoxic esterase (NTE) activity in the brain, spinal cord and platelets. Histopathology of the spinal cord of exposed animals showed focal axonal degeneration. These changes were comparatively less than in animals treated with the neurotoxic organophosphate, mipafox. Results from this study indicate that sarin may induce delayed neurotoxic effects in mice following repeated inhalation exposure.

Administration, Inhalation↗
PubMedDate not supplied

Effect of sulphur mustard inhalation exposure on some urinary variables in mice.

The effect of sulphur mustard (2,2'-dichlorodiethyl sulphide) exposure through inhalation at 0.5. 1.0 and 2.0 LC50 (21.2, 42.3 and 84.6 mg m(-3) for 1 h) on some urinary variables was studied in female mice at 6, 24 and 48 h and 7 days post-exposure. The urinary excretion and circulatory blood accumulation of uric acid increased significantly. The level of creatine was also elevated significantly as compared to the control at 2 LC50. It is concluded that sulphur mustard alkylates DNA and triggers catabolism of apurinated purine bases in a very short time. The increase in uric acid excretion in urine can be detected only when the exposure concentration is high.

Administration, Inhalation↗
PubMed1999

Sulphur mustard induced DNA damage in mice after dermal and inhalation exposure.

Sulphur mustard (SM) is a chemical warfare agent of the blistering agent category for which there is still no effective therapy. SM, being a strong electrophile, readily reacts with a wide range of cellular macromolecules including DNA, RNA and protein. Since the main intoxication routes for SM are inhalation and dermal penetration, in the present study we have exposed female mice to different concentrations of SM by dermal and inhalation exposures and estimated the DNA damage in different organs viz., liver, lung, spleen and thymus. SM was applied at 38.7, 77.4, 154.7 mg/kg body weight, on the hair-clipped skin (dermal exposure) equivalent to 0.25, 0.5 and 1.0 of the LD50. Inhalation exposure was carried out at 10.6, 21.2 and 42.3 mg/m3 for 1 h duration equivalent to 0.25, 0.5 and 1.0 LC50. SM induced a dose-dependent DNA damage in all the organs except the lung in dermal exposure. Similarly the inhalation exposure resulted in dose- and time-dependent effect in all the organs including lung. By both routes of exposure liver was the most affected organ followed by spleen, thymus and lung in decreasing order. The quantitative data were corroborated by qualitative analysis of DNA on agarose gel electrophoresis. The genomic DNA analysis of the organs had revealed random nuclear DNA fragmentation resulting in a 'smear' typical of necrotic form of cell death. Since DNA damage is not reversible especially in liver, this can be used as a marker for SM exposure through either the dermal or inhalation route.

Administration, Inhalation↗
PubMed1998

Correlation of lethal doses of industrial chemicals between oral or intraperitoneal administration and inhalation exposure.

Correlations of lethal doses of industrial chemicals between oral or intraperitoneal administration and inhalation exposure in rats and mice were investigated. LC50 values for inhalation exposure and LD50 values for oral and intraperitoneal administration were obtained from the Registry of Toxic Effects of Chemical Substances. LC50 and LD50 values were plotted on ordinate and abscissa, respectively, using logarithmic scales. A correlation coefficient of r = 0.624 (n = 146, p < 0.001) was obtained for LC50 (ppm) and LD50 (mg/kg) values with oral administration (oral LD50) in rats. This correlation was improved by converting the units of LC50 from ppm to ppm h (cumulative dose), and by converting the units of LD50 from mg/kg to mmol/kg. The correlation coefficient was r = 0.742 when ppm*hr and mmol/kg were adopted for LC50 and LD50, respectively. A similar improvement in correlation coefficients by the same unit conversion was also observed between LC50 and LD50 with intraperitoneal (i.p.) administration (i.p. LD50) in rats. Correlations between LC50 and oral LD50 in mice were also improved by the same unit conversion. The correlations between LC50 and i.p. LD50 were higher than those between LC50 and oral LD50 both in rats and mice. In these correlations, coefficients obtained in rats were greater than corresponding coefficients in mice. We calculated equations to estimate LC50 values accompanied by confidence limits from oral or i.p. LD50 values.

Administration, Oral↗
PubMed2006

Acute lung injury following inhalation exposure to nerve agent VX in guinea pigs.

A microinstillation technique of inhalation exposure was utilized to assess lung injury following chemical warfare nerve agent VX [methylphosphonothioic acid S-(2-[bis(1-methylethyl)amino]ethyl) O-ethyl ester] exposure in guinea pigs. Animals were anesthetized using Telazol-meditomidine, gently intubated, and VX was aerosolized using a microcatheter placed 2 cm above the bifurcation of the trachea. Different doses (50.4 microg/m3, 70.4 micro g/m(m3), 90.4 microg/m(m3)) of VX were administered at 40 pulses/min for 5 min. Dosing of VX was calculated by the volume of aerosol produced per 200 pulses and diluting the agent accordingly. Although the survival rate of animals exposed to different doses of VX was similar to the controls, nearly a 20% weight reduction was observed in exposed animals. After 24 h of recovery, the animals were euthanized and bronchoalveolar lavage (BAL) was performed with oxygen free saline. BAL was centrifuged and separated into BAL fluid (BALF) and BAL cells (BALC) and analyzed for indication of lung injury. The edema by dry/wet weight ratio of the accessory lobe increased 11% in VX-treated animals. BAL cell number was increased in VX-treated animals compared to controls, independent of dosage. Trypan blue viability assay indicated an increase in BAL cell death in 70.4 microg/m(m3) and 90.4 microg/m(m3) VX-exposed animals. Differential cell counting of BALC indicated a decrease in macrophage/monocytes in VX-exposed animals. The total amount of BAL protein increased gradually with the exposed dose of VX and was highest in animals exposed to 90.4 microg/m(m3), indicating that this dose of VX caused lung injury that persisted at 24 h. In addition, histopathology results also suggest that inhalation exposure to VX induces acute lung injury.

Acetylcholinesterase↗
PubMed1993

Hepatocyte cell proliferation in mice after inhalation exposure to unleaded gasoline vapor.

Chronic inhalation exposure to unleaded gasoline (UG) induced an increase in liver tumors in female but not male mice. Unleaded gasoline exhibits little, if any, genotoxic activity in vitro or in vivo in the female mouse liver, suggesting that other biological effects such as the induction of cell turnover or altered growth control may play a role in this carcinogenic process. To better understand the role of UG-induced hepatocyte proliferation with respect to the dose- and sex-specific tumor response, male and female B6C3F1 mice were housed in 1-m3 single-pass flow-through inhalation chambers and administered UG under exposure conditions that produced tumors in the chronic studies. Mice were exposed to targeted concentrations of 67, 292, or 2056 ppm PS-6 blend of UG vapor 6 h/d, 5 d/wk, for up to 13 wk. Liver weights were elevated significantly in male and female mice exposed to 2056 ppm UG at wk, 1, 3, 6, and 13. No elevation in liver-specific serum enzymes was noted in treated animals, nor were there any significant histopathological changes in the liver, indicating a lack of overt hepatotoxicity. Hepatocyte proliferation, expressed as nuclear labeling index (Ll), was measured immunohistochemically after 5-bromo-2'-deoxyuridine administration via an osmotic minipump implanted three days before the animals were killed. A 6-to 10-fold increase in Ll compared to controls was observed in male and female mice exposed to 2056 ppm UG at wk 1, with a return to control levels at wk 3, 6, and 13. Mice exposed to 67 or 292 ppm UG did not show any increase in Ll. The mode by which an agent induces cell proliferation is an important consideration in mechanistic studies and the risk assessment process. These data indicate an early transient mitogenic stimulation of cell proliferation, rather than regeneration secondary to cytotoxicity, in the livers of UG-treated mice. The observed proliferative response after UG exposure in the male mouse in the absence of a tumorigenic response suggests that effects in addition to the early transient hepatocyte proliferation response are critical in understanding the sex-specific hepatocarcinogenic response of this complex mixture.

Administration, Inhalation↗
PubMed1992

DNA damage in human white blood cells after inhalative exposure to methylenediphenyl diisocyanate (MDI)--case report.

A workplace-related inhalative exposure test in a challenge chamber was performed on an industrial worker in a methylenediphenyl diisocyanate (MDI) atmosphere from 5 to 20 ppb and the isolated white blood cell DNA was analysed by electrophoresis, anion-exchange chromatography and melting behaviour. The results of electrophoresis indicate that inhaled MDI induces double-strand breaks of DNA. Some of the DNA fragments were estimated to be in the region of 100-500 bp. Anion-exchange chromatography confirmed this finding. Following denaturation and rapid renaturation the results demonstrated that some DNA fragments are cross-linked by MDI. Comparing the melting curves before and after inhalative exposure in the challenge test chamber, genomic DNA revealed differences in the shape of the melting curve (hyperchromic effect). The results suggest that occupational MDI exposure could be associated with white blood cell DNA damage.

Administration, Inhalation↗
PubMed1999

Pharmacological effects of methamphetamine and other stimulants via inhalation exposure.

The effects of methamphetamine-HCl, methcathinone-HCl, cocaine and ephedrine on locomotor stimulation were compared between inhalation exposure and i.v. injection in mice. Methamphetamine-HCl was readily volatilized upon heating at 300 degrees C in a glass pipe with only trace amounts of amphetamine being produced. The ED50 dose (9.4 and 6.5 mumol/kg for inhalation exposure and i.v. injections, respectively) and biodisposition of methamphetamine-HCl were similar for both routes of administration. Methcathinone-HCl and cocaine were readily volatilized. Their dose response profiles also appeared similar for both routes of administration. Ephedrine did not appear to be easily volatilized and was only effective in stimulating locomotor activity after i.v. administration. These findings indicate that inhalation exposure to methamphetamine-HCl, cocaine and methcathinone possess similar pharmacological characteristics as the i.v. route of administration. In particular, this model may have implications in predicting the pharmacological activity of various stimulants via the inhalation route of administration.

Administration, Inhalation↗
PubMed1986

The effect of toluene inhalation exposure on catecholamine contents in rat sympathetic neurons.

Adult male rats were exposed to toluene in short-term exposure by inhalation for 48 h (2000 ppm, continuously), and in long-term inhalation for 3 months (1000 ppm, 8 h daily). The formaldehyde-induced fluorescence (FIF) technique for histochemical demonstration of catecholamines (CA) was used to detect changes in the catecholamine stores. The concentration of CA in the sympathetic neurons of superior cervical ganglia and adrenal medulla was measured by the FIF technique combined with microfluorimetry. The short-term toluene exposure induced a statistically significant reduction of CA contents in sympathetic neurons. After long-term exposure, no change in the CA level could be demonstrated either in sympathetic ganglion or adrenal medulla. In electron microscopic studies no clear pathological changes were detected after toluene exposure.

Adrenal Medulla↗
PubMed1984

Measurement of genotoxic activity in multiple tissues following inhalation exposure to dimethylnitrosamine.

Chemically-induced DNA repair was measured as unscheduled DNA synthesis (UDS) in selected tissues isolated from rats following in vivo exposure to inhaled dimethylnitrosamine (DMN). UDS was evaluated in epithelial cells from rat nasal turbinates and trachea, in hepatocytes and in pachytene spermatocytes from the same treated animal. At nominal concentrations of 500 and 1000 ppm of DMN in air, chemically-induced DNA repair was observed in the epithelial cells of the upper respiratory system. DMN also entered the circulation, as evidenced by a strong DNA-repair response in hepatocytes. No DNA repair was observed in pachytene spermatocytes indicating either that DMN or its active metabolites did not reach the testes in sufficient concentration to induce DNA repair or that the testes lacked the capability to metabolically activate the compound. These results illustrate the potential of this approach to assess the organ-specific genotoxicity of environmental chemicals.

Animals↗
PubMed1984

Effects on the postnatal development of the mouse of preconception, postconception and/or suckling exposure to manganese via maternal inhalation exposure to MnO2 dust.

Female mice were exposed either to MnO2 dust (7 hours/day, 5 days/week) or filtered air (control group) for 16 weeks prior to conception. On day 1 of gestation, half of each of these groups was assigned randomly either to MnO2 dust or filtered air exposure until day 17 of gestation. To separate effects of prenatal maternal exposure to MnO2 from postnatal exposure of offspring to Mn via suckling, a complete fostering/-cross-fostering design was employed. Compared to control mothers, mothers exposed to MnO2 prior to conception produced significantly larger litters. Prenatal exposure resulted in reduced neonatal activity scores and retarded offspring growth that persisted into adulthood. Offspring reared by mothers exposed to MnO2 prior to conception and filtered air postconception had significantly lower day 7 postpartum weights compared to offspring reared by mothers exposed to filtered air both prior to and postconception. Also, offspring reared by mothers exposed to MnO2 prior to conception and filtered air postconception had higher day 12 activity scores compared to offspring reared by mothers exposed to filtered air prior to conception and MnO2 postconception. Prenatal exposure to MnO2 depressed neonate activity and continued exposure, via suckling, intensified this depression. Offspring exposed prenatally to MnO2 were retrieved faster than control offspring. Rearing frequency, exploratory behavior, and scores in tests having an activity component were depressed for sexually mature offspring who had been exposed to MnO2 both in utero and via suckling. Independent of in utero exposure history, sexually mature offspring reared by mothers exposed to Mn had significantly reduced cerebellum + brain stem mitochondrial Mn levels. Also, sexually mature offspring of mothers exposed to filtered air that were reared by MnO2 -exposed mothers had lower cerebral mitochondrial Mn levels than offspring of control mothers reared by control foster mothers.

Animals↗
PubMed2001

A training exercise in subjectively estimating inhalation exposures.

OBJECTIVES: This study examined whether it is possible to train occupational hygienists to estimate inhalation exposures reliably from limited occupational information using a new method and assessed improvements in the quality of the estimate using the aggregate from multiple assessors. METHODS: Five occupational hygienists estimated inhalation exposure for 40 tasks covering a range of chemical hazards using a recently developed subjective modeling technique supplemented by detailed guidance notes. The measured exposure levels were used to determine the validity of the method. The correlation coefficients of the log-transformed data were used to assess the discriminative power of the method, and the ratio of the mean estimate to measured values was used to measure accuracy. RESULTS: There was good-to-excellent agreement between the assessors' estimates and the measured data, the correlation coefficients ranging from 0.73 to 0.85. There was a tendency for assessors to overestimate the exposure levels by, on the average, two- to fourfold. Aggregating the assessors' estimates helped to improve the correlation coefficient to 0.88, the overestimation being 2.6-fold. Using more than three assessors for aggregate estimates did not improve the reliability of the method. CONCLUSIONS: Overall, the assessors found the method to be useful in generating exposure estimates that correlate well with measured levels. The provision of high-quality guidance information is likely to be important in the generation of reliable exposure estimates. The method is likely to be of use in epidemiologic studies in which limited exposure data are available.

Environmental Monitoring↗