Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Exhalation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,783 records · Page 99Linked to original sources
PubMed2001

Biological clearance of TEGDMA in guinea pigs.

The excretion of the dental composite component triethylene glycol dimethacrylate (TEGDMA) in feces and urine in vivo and, using the pendular perfusion technique with segments of jejunum and colon, the biliary and enteric excretion in situ were investigated in anesthetized guinea pigs. In the in situ experiments guinea pigs (n = 4) received TEGDMA (0.02 mmol/kg body weight labelled with a tracer dose 14C-TEGDMA 0.7 kBq/g body weight) injected into the jugular vein. In the in vivo experiments guinea pigs (n = 4) received TEGDMA (+14C-TEGDMA; same dose as above) via a gastric tube. Urine and feces were collected for 24 h. In the in situ experiments organs were removed from the guinea pigs 60 min after the beginning of the experiment, and the 14C radioactivity measured. During the 60-min perfusion period the calculated amount of 14C radioactivity excreted into the total jejunum and colon was 0.9 +/- 0.2% and 1.9 +/- 0.1% of the dose administered, respectively (means +/- SEM). Of the 14C-TEGDMA dose, 3.7 +/- 0.2% was found in the bile. A significantly (P < 0.05) higher bile/blood concentration ratio was found 10 min after injection of TEGDMA as compared with the ratios at 20 to 60 min. The following 14C activities (percent of the dose) per total organ were found in guinea pigs (in situ experiment; means +/- SEM): 6.9 +/- 1.7 (muscle), 3.9 +/- 0.5 (kidney), 3.3 +/- 0.1 (skin), 1.4 +/- 0.1 (blood), and 1.2 +/- 0.1 (liver). The 14C activity in all other organs was < 0.4%. The total 14C recovery in all organs tested was 17.5 +/- 1.8%. Over 24 h the amounts of 14C activity excreted in the feces and urine were 0.5 +/- 0.1% and 14.7 +/- 1.8% of the dose administered, respectively (means +/- SEM). The following 14C activities (percent of the dose) per total organ or contents of organs were found (means +/- SEM): 1.4 +/- 0.3 (liver), 0.8 +/- 0.3 (muscle), 0.5 +/- 0.1 (skin), and 0.5 +/- 0.1 (contents of cecum). The 14C activity in all other organs was < 0.2%. The total 14C recovery in all organs tested was 3.9 +/- 0.9%. In a second series of in vivo experiments exhaled air from the animals was captured during the 24-h experimental period. Of the administered dose, 61.9 +/- 4.6% of the 14C (means +/- SEM; n = 4) was exhaled as 14C-carbon dioxide. The results indicate a rapid clearance of 14C-TEGDMA and/or 14C-TEGDMA metabolite(s) from the organism and exhalation is the major route of elimination.

Animals↗
PubMed1998

The disposition and metabolism of 1,3,5-[U-14C]trioxane in male Wistar albino rats.

The present study was designed to investigate 1,3,5-[U-14C]trioxane (TOX) distribution, excretion and metabolism. The experiments were performed on male Wistar albino rats after a single administration of TOX at doses of 40 mg/kg and 400 mg/kg. The exhaled air proved to be the main route of 14C elimination, mainly as 14CO2. During the first 12 h following the administration of 40 mg/kg of TOX the exhalation of 14CO2 was monophasic, with a half-life of 3.5 h. After the administration of 400 mg/kg, TOX was eliminated mainly as 14CO2 with the exhaled air (77%) and unchanged TOX (8%). About 3% of 14C was excreted in the urine as unchanged 1,3,5-trioxane. With regards to TOX elimination from blood plasma for the lower dose, a biphasic process was observed, with half-lives of 4.5 and 72 h. The amount of 14C bound by the erythrocytes was minute compared with the amount in blood plasma. When the higher dose of TOX was administered the efficiency of 14C binding to the erythrocytes was found to be 10 times higher than the respective value for blood plasma. Among the examined tissues the highest concentration of TOX-derived radioactivity was detected in the liver while the lowest was in fat tissue and brain. A subsequent decay of radioactivity occurred in the tissues. The results of the present study indicate that TOX belongs to the group of compounds, which are rapidly eliminated from the organism; hence TOX should not be expected to accumulate within the tissues. The data obtained confirm the assumed pattern of metabolic transformation, according to which 1,3,5-trioxane undergoes enzymatic transformation to formaldehyde, with carbon dioxide and water being the final products.

Animals↗
PubMed2002

Propylene glycol monomethyl ether occupational exposure. 3. Exposure of human volunteers.

OBJECTIVE: Propylene glycol monomethyl ether (PGME) is a widely used additive in industrial and consumer products (paints, inks, diluents, cleaning products, cosmetics.). The aim of the present study was to determine uptake and disposition of PGME alpha-isomer in humans. METHOD: Six healthy male volunteers were exposed to PGME-alpha vapour (15, 50 and 95 ppm) with and without respiratory protection for 6 h including a 30-min break. Free PGME and total PGME (free and conjugated) were analysed in urine. The analytical method involved hydrolysis with HCl (only for the analysis of total PGME in urine), a solid phase extraction on LC-18 columns and a gas chromatograph-flame ionisation detector (GC/FID) analysis after derivatisation with trimethylsilylimidazole. RESULTS: End-exposure levels of free PGME in urine were found to reach 1.3 (+/-0.3), 4.4 (+/-1.6) and 7.9 (+/-2.5) mg/l for 15, 50 and 95-ppm exposure, respectively, without respiratory protection. End-exposure levels of total PGME in urine were found to reach 2.5 (+/-0.8), 6.2 (+/-1.6) and 10.3 (+/-2.3) mg/l for 15, 50 and 95-ppm exposure respectively. Levels of free PGME were also monitored in exhaled air (0.4 (+/-0.1), 1.4 (+/-0.4) and 2.9 (+/-0.9) ppm at the end of 15, 50 and 95-ppm exposure, respectively) and in blood (2.0 (+/-0.9), 4.9 (+/-2.3) and 11.8 (+/-2.4) mg/l at the end of 15, 50 and 95-ppm exposure, respectively). PGME is rapidly excreted in urine and in exhaled air; the half-lives were calculated to be approximately 3.5 h in urine and 10 min in exhaled air. PGME was below detection limits in breath (<0.1 ppm), in blood (<1 mg/l) and in urine (<1 mg/l) after dermal-only exposure to vapour. CONCLUSIONS: This study has demonstrated the relatively high pulmonary uptake compared with the dermal uptake. It has also shown the rapid excretion in urine (3.5 h) and in expired air (10 min). With regard to metabolism, this study has established the presence of conjugated PGME in urine.

Adult↗
PubMed1997

Ethnic differences in biological monitoring of several organic solvents. I. Human exposure experiment.

OBJECTIVES: In order to improve the reliability of biological monitoring and the development of biological limit values, ethnic differences for several organic solvents were studied in Orientals and Caucasians. METHODS: Six Caucasian and six Oriental volunteers were exposed to each organic solvent in an exposure chamber for 6 h. Exposure concentration to each organic solvent studied was 50 ppm for perchloroethylene, 50 ppm for styrene and 100 ppm for m-xylene, respectively. Biological monitoring was carried out for the parent organic solvents in exhaled air and in blood, and for the metabolites in urine during and after exposure. RESULTS: Caucasians showed higher concentrations of perchloroethylene in exhaled air than Orientals after exposure. But Caucasians showed lower concentrations of styrene in the exhaled air than Orientals during the second half of exposure and after it. Orientals showed lower concentrations of urinary metabolites than Caucasians except for mandelic acid. There were no statistically significant differences in the concentrations of solvent in blood for all three solvents. CONCLUSIONS: Implications of these differences in biological levels, under identical exposure conditions, are discussed in the context of biological monitoring.

Adult↗
PubMed1983

In vivo hydroxylation of 3H-acetanilide--evaluation of a new radiospirometric method in the rat.

The proposed in vivo methodology for the investigation of hydroxylation rates consists of of the i.v. administration of tritiated substrates and the collection of tritiated water (HTO) from exhaled air as a measure of HTO accumulation in body water. Specifically, HTO was assessed in exhaled water after i.v. administration of 3H-acetanilide. Over a wide range the half lives of accumulation of HTO in exhaled water (T50) were almost identical with the half lives of elimination of 3H-acetanilide in blood, evaluated by an inverse isotope dilution method (r = 0.96, N = 18). Average T50 amounted to 29 min in controls, was reduced to 20 min after enzyme induction by phenobarbital or 3-methylcholanthrene, and prolonged to 45, 46 and 66 min after bile duct ligation, portacaval shunt and a single dose of ethanol, respectively. It is concluded that the chosen pharmacokinetic approach corrects for the NIH-shift and the results adequately reflect changes in acetanilide hydroxylation related to enzyme induction or inhibition and to liver pathology.

Acetanilides↗
PubMed1985

Excretion pattern and metabolism of hexachlorobutadiene in rats. Evidence for metabolic activation by conjugation reactions.

Excretion, covalent binding and metabolism of hexachloro-1,3-butadiene (HCBD), a nephrotoxic and nephrocarcinogenic compound, have been studied in female rats. Seventy-two hours after administration of a single oral dose of 1 mg/kg [14C]HCBD, 5.3% of the dose were exhaled as unchanged HCBD and 76.3% were metabolized and excreted in urine and feces or exhaled as 14CO2. After a 50 mg/kg dose of [14C]HCBD, the amount of exhaled parent compound was nearly unchanged at 5.4%. At the higher dose the gastro-intestinal absorption of HCBD appeared to be saturated with the result that unchanged HCBD constituted the major portion of the 69% radioactivity eliminated. Covalent binding to proteins in kidney and liver agreed well with the organ-specific toxicity of HCBD: binding was higher in the kidney, independent of the dose. It increased significantly when the rats were pretreated with phenobarbital, an inducer of monooxygenases; it decreased when the inhibitor piperonyl butoxide was given. Urinary radioactivity in 24 hr urine was separated by column chromatography into four fractions. High performance liquid chromatography, radio gas chromatography and gas chromatography/mass spectrometry were used for further separation and identification. Two major metabolites were identified as pentachlorobutadiene methylthio ether and pentachlorobutadiene carboxymethylthio ether. Their formation is plausibly explained via glutathione conjugation, which appears to be the first step in HCBD metabolism. The mechanism of the conjugation at the olefinic double bond of HCBD is explained by an addition-elimination reaction. This pathway, which appears to lead to a destabilization of the HCBD molecule, could explain the distinct nephrotoxic effects of HCBD.

Animals↗
PubMed1988

Volume and pressure during transient added resistance.

Total respiratory resistance (Rrs) can be computed from measurements of flow before and during a brief period of added resistance. This "added resistance' method does not require measurement of total driving pressure (Pt). One of the assumptions of this method is that the change in Pt (delta Pt) is negligible during the time of increased resistance. To evaluate this assumption we measured both the volume exhaled during a brief imposition of an external resistor, and the total respiratory compliance (Crs) of 7 healthy volunteers. The mean volume exhaled was 18.6 ml, and the mean Crs was 88 ml/cm H2O. The volume exhaled divided by Crs gives the change in total static elastic recoil pressure (delta Pel, rs), which is one component of delta Pt. The mean delta Pel, rs was 0.22 cm H2O. Since the pressure exerted by contraction of inspiratory muscles (Pmus,I) opposes Pel, rs, we also estimated delta Pmus,I and subtracted it from delta Pel, rs to obtain delta Pt. The computed mean delta Pt during the time of added resistance was 0.045 cm H2O. This value is quite small in relation to Pt during a spontaneous expiration at rest. We also studied 13 subjects with Chronic Obstructive Pulmonary Disease and found no significant effect of transient added resistance on intraesophageal pressure. We conclude that the assumption of negligible delta Pt should not prevent the added resistance method from being very useful, particularly when simplicity of equipment and testing procedure are important.

Adult↗
PubMed1991

Dynamics of soluble gas exchange in the airways: II. Effects of breathing conditions.

A mathematical model of the airways is developed which focuses on the dynamic exchange characteristics of heat, water and soluble gas. A typical airway segment is divided radially into three regions: the airway lumen, a thin mucous layer of variable thickness coating the airway wall, and an underlying nonperfused tissue layer. A bronchial circulation capillary bed lies beyond the nonperfused tissue layer. The simultaneous exchange of water, heat and soluble gas is dealt with using the model of Tsu et al. (Ann. Biomed. Eng. 16:547-571, 1988). In the case of excretion of ingested ethyl alcohol from the bronchial and pulmonary circulations, the model predicts that during inspiration, because of the alcohol flux from the airway mucosa, a concentration of alcohol in equilibrium with mucus is achieved in the inspired air before the respiratory bronchioles are reached. During exhalation, much of this alcohol redeposits on the airway surface. The net flux of alcohol from the airway surface exceeds the flux of alcohol from the mouth in the exhaled gas indicating that the exhaled alcohol comes from the airways and bronchial circulation rather than from the alveoli and the pulmonary circulation. Alcohol flux moves farther into the airways with oral breathing compared to nasal breathing. Increased ventilation shifts the alcohol flux more alveolarward. Changes in inspired air temperature and humidity have almost no effect on the distribution of alcohol flux in the airways.

Computer Simulation↗
PubMed1995

Determination of DLCO and cardiac output from expired gas slopes with cardiogenic oscillations.

Effects of 'cardiogenic oscillations' on alveolar plateau gas concentration slope measurements, constant expiratory pulmonary capillary blood flow, and DLCO determination have not been previously described. We examined cardiogenic oscillations during constant expiratory maneuvers to assess factors influencing magnitude of oscillations as well as effect of oscillatory phase at the start and end of exhalation measurement period on alveolar gas slope. Five normal volunteers performed repeated single breath constant exhalation vital capacity maneuvers using test gas containing 2 physiologically 'inert' gases: Helium (He Mw 4) and argon (Ar Mw 40). The mixture contained 3 absorbable gases, acetylene (C2H2 Mw 26), carbon monoxide (C18O Mw 30), and oxygen. Alveolar plateau slope, magnitude of cardiogenic oscillations, relative signal to noise ratios, and effect of cardiogenic oscillation phase on measured slope were determined for each gas. Cardiogenic oscillations were present for all inert gases. Oscillations were less evident for CO. However, the effects on calculated Qc and DLCO were negligible. Cardiac oscillations of considerable magnitude are seen during single breath constant exhalation maneuvers and affect constant expiratory gas slope calculations. Cardiogenic oscillation phase does not have a significant effect on measured Qc and DLCO using constant expiratory techniques.

Adult↗
PubMed1983

The uptake and disposition of 1,1-dichloroethylene in rats during inhalation exposure.

The uptake, disposition, and respiratory elimination of 1,1-dichloroethylene (1,1-DCE) during inhalation exposure were evaluated to gain insight into the pharmacodynamics of the halocarbon. Anesthetized male Sprague-Dawley rats inhaled 25, 75, 150, or 300 ppm 1,1-DCE for 3 hr from an aluminized Mylar bag through a miniaturized one-way breathing valve inserted into the trachea. Periodic air samples were taken immediately adjacent to the valve from the separate inhaled air and exhaled breath streams concurrently with blood samples from a cannulated femoral vein and analyzed for 1,1-DCE content by gas chromatography. 1,1-DCE was absorbed very rapidly, in that substantial levels were present in the venous blood at the first sampling time (i.e., 2 min). Percentage systemic uptake decreased over time after initiation of exposure until equilibrium was established. Percentage uptake after reaching equilibrium varied inversely with the exposure concentration. 1,1-DCE venous whole-blood levels in animals exposed to 25, 75, and 150 ppm 1,1-DCE increased rapidly to near steady state within approximately 45 min, as did concentrations of 1,1-DCE in the exhaled breath and alveolar air. Calculation of the amount of 1,1-DCE taken up by the body over the course of the 3-hr exposures revealed that cumulative uptake of the inhaled chemical was statistically linear for the 25-, 75-, and 150-ppm exposures. Accumulation plots for 300-ppm exposed animals, however, were best fitted to a cubic curve form. Although trends toward the establishment of equilibrium were initially seen in the 300-ppm exposed animals, levels of 1,1-DCE in the blood and breath rose progressively during the latter hour of the 3-hr exposure period. Thus, despite increased exhalation of 1,1-DCE, these animals could not prevent systemic accumulation of the chemical.

Animals↗
PubMed1984

Studies on the biochemical effects of nitrogen dioxide. IV. Relation between the change of lipid peroxidation and the antioxidative protective system in rat lungs upon life span exposure to low levels of NO2.

This study examined the relation between lipid peroxidation and the antioxidative protective system in lungs of rats exposed to low levels of nitrogen dioxide (NO2). JCL:male Wistar rats were exposed to 0, 0.04, 0.4, and 4 ppm NO2 for 9, 18, and 27 months. Lipid peroxidation measured by TBA method, increased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. The activity of glutathione peroxidase measured with hydrogen peroxide as substrate decreased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. Furthermore, the activities of two glutathione S-transferases, aryl and aralkyl S-transferase, also decreased in the 0.4 and 4 ppm NO2 groups of the 18-month exposure, but not in any groups of the 9-month exposure. The activity of glutathione peroxidase measured with cumene hydroperoxide as substrate did not show any significant changes in any NO2 group. The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were significantly higher than those in the control group for the 9-month exposure. In the 18-month exposure, however, they showed a tendency to return to control level. The activities of superoxide dismutase and disulfide reductase upon NO2 exposure for 9 and 18 months were not different from control values. To confirm that lipid peroxidation was increased with greater NO2 concentrations and exposure times, ethane and pentane exhalation in breath as an index of lipid peroxidation was examined. Ethane exhalation increased significantly following 0.04, 0.4, and 4 ppm NO2 exposure for 9 and 18 months. Furthermore, ethane formation of rats exposed to 0.04 and 0.4 ppm NO2 for 27 months also increased to twice the control level. On the other hand, after exposure to 4 ppm NO2 for 27 months, ethane levels returned to control level. Pentane formation increased significantly only in the 0.04 and 0.4 ppm groups in the 18-month exposure. Ethane exhalation in rats exposed to 0.04, 0.12, and 0.4 ppm NO2 for 9 and 18 months was similar. These results suggested that the antioxidative protective ability was decreased with prolonged exposure, while formation of cytotoxic lipid peroxides was increased.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Species differences in the disposition of inhaled butadiene.

Recent chronic inhalation carcinogenicity studies of butadiene indicated that B6C3F1 mice are more sensitive to the tumorigenic effects of inhaled butadiene than are Sprague-Dawley rats. Tumors in mice included lymphomas, hemangiosarcomas, alveolar/bronchiolar adenomas and carcinomas, and hepatocellular adenomas and carcinomas whereas in rats tumors included mammary tumors, thyroid follicular cell adenomas, uterine tumors, and exocrine pancreatic adenomas. The purpose of this investigation was to determine if there were differences in the uptake and disposition of inhaled butadiene between rats and mice and if these differences were consistent with the differences in the species susceptibility to inhaled butadiene. Male Sprague-Dawley rats and B6C3F1 mice were exposed nose only to concentrations in the range of 0.14 to 13,000 micrograms [14C]butadiene/liter air (0.08 to 7100 ppm; 25 degrees C, 620 torr) for 6 hr. Blood samples were taken during exposure and urine, feces, and expired air were collected for up to 65 hr after exposure. In both rats and mice there was a significant (p less than 0.001) concentration-related decrease in the percentage of butadiene retained at the cessation of a 6-hr exposure with increasing butadiene exposure concentration, suggesting saturable metabolism of this chemical. At all concentrations of butadiene tested, mice retained about 4 to 7 times the amount (mumol/kg body wt) of butadiene and metabolites than did rats. In both species and at all butadiene concentrations tested, urine and exhaled air were the major routes of excretion of 14C, together accounting for 75 to 85% of the total 14C eliminated. In mice, for all concentrations tested, elimination of 14C in urine, feces, and exhaled air increased with increasing butadiene exposure concentration, although the increase was not proportional to exposure concentration. However, exposure of rats to 13,000 micrograms butadiene/liter air resulted in a leveling off in the amount of 14C that was eliminated in urine and a concomitant increase in exhalation of 14CO2. Analysis of blood samples taken during exposure indicated that the blood of mice contained 2 to 5 times the concentration of 1,2-epoxy-3-butene than did the blood of rats. The data from this study indicate that species differences exist in the amount retained and metabolism of inhaled butadiene.

Absorption↗
PubMed1988

A physiologically based pharmacokinetic model for inhaled carbon tetrachloride.

D.J. Paustenbach et al. (1986, Fundam. Appl. Toxicol. 6, 484-497) have described the pharmacokinetics of inhaled, radiolabeled carbon tetrachloride (14CCl4) in male Sprague-Dawley rats exposed for 8 or 11.5 hr/day for 1- or 2-week periods. These studies provided time-course information for exhaled 14CCl4, the exhaled 14CO2 metabolite, and 14C radioactivity eliminated in the feces and urine. A physiologically based pharmacokinetic (PB-PK) model which incorporated partition characteristics of CCl4 (blood:air and tissue:blood partition coefficients), anatomical and physiological parameters of the test species (body weight, organ weights, ventilation rates, blood flows, etc.), and biochemical constants (Vmax and Km) for CCl4 metabolism was developed to describe these results. The PB-PK model accurately predicted the behavior of CCl4 and its metabolites, both the exhaled CCl4 and 14CO2 and the elimination of radioactivity in urine and feces. The metabolism of CCl4, determined by gas uptake studies, was adequately described by a single saturable pathway. Metabolites were partitioned in the model to three compartments; the amounts to be excreted in the breath (as 14CO2), urine, and feces. Of total CCl4 metabolism, 6.5, 9.5, and 84.0% were formed via the degradative pathways leading to CO2, urinary, and fecal metabolites, respectively. The simplest kinetic explanation of the metabolite time course is that 4% of the initially metabolized CCl4 is directly converted to CO2 (probably via a chloroform intermediate) and the remainder of metabolized CCl4 binds to biological substrates. These adducts appear to be slowly degraded with an average half-life of 24 hr. The breakdown products subsequently appear in the feces and urine (the rate constant for elimination by these two routes is similar) and a small portion is converted all the way to CO2. The PB-PK model successfully described the elimination by all four routes for all four exposure scenarios using a single set of parameters. Vmax and Km were, respectively, 0.65 mg/kg/hr and 0.25 mg/liter. There was no evidence for loss of Vmax with repeated exposure, as would be expected if there was enzyme destruction at these concentrations of CCl4. The model was scaled-up to predict the expected behavior of parent CCl4 in monkeys and humans and the resulting simulations compared very favorably with data collected by McCollister et al. (1951) and Stewart et al. (1961). On the basis of this model and the published data on the rat at 100 ppm about 60% of the inhaled CCl4 is metabolized and the resulting blood levels are already in excess of saturation for the metabolizing enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1991

A model for the uptake of inhaled vapors in the nose of the dog during cyclic breathing.

A model was developed to simulate the uptake of inhaled vapors in the nasal airway of the Beagle dog during cyclic breathing. Input data to the model were morphological and physiological data for the dog, and physiocochemical data for the vapors. The model simulates the nasal airway as a slit-like duct, where air passes between the two airway walls in an ideal plug flow. The thickness of the walls corresponds to the distance between the air interface and the average position where vapor molecules are removed into the capillary blood. All resistance to radial mass transfer is assumed to arise on the liquid side in the diffusion of vapors through the air/blood tissue barrier and in transport by the blood. The model results agreed reasonably well with experimental data. The nasal absorption of vapors on inhalation increased from 1% for a compound with a blood/air partition coefficient of 1 to around 95% uptake for a compound with a partition coefficient of 2000. Desorption from the nasal tissues on exhalation increased from approximately 1% to approximately 30% over the same range of partition coefficients. The nasal uptake over one complete breathing cycle, defined as absorption on inhalation minus desorption on exhalation, was almost zero for low partition coefficient compounds and plateaued at around 65% for high partition coefficient compounds. The model indicates that diffusional resistance and inertia of the nasal tissues result in temporary storage of absorbed vapors upon inhalation, followed by desorption of vapors back into the airstream upon exhalation. An important consequence of this phenomenon is a shift in exposure to inhaled vapors from the lungs to the nasal airway during cyclic flow compared with predictions from experiments and models based on unidirectional flow.

Absorption↗
PubMed1987

Role of lipid peroxidation in the toxicity of T-2 toxin.

Recent reports suggest that lipid peroxidation may be involved in the toxicity of T-2 toxin. In the present study the influence of T-2 toxin on two parameters of lipid peroxidation was examined: the formation of thiobarbituric acid reactive material in isolated hepatocytes and liver homogenates from rats and ethane exhalation in vivo. In isolated hepatocytes there was no significant increase in thiobarbituric acid reactive material, neither after addition of T-2 toxin in vitro nor when the toxin had been applied to the rats 15 hr before preparation of hepatocytes. In liver homogenates the amount of thiobarbituric acid reactive material was increased up to 50% over the controls, depending on the dose of T-2 toxin. The increased values are difficult to interpret, because the extent of the increase depends on the method used for determination of thiobarbituric acid reactive material. Measuring another parameter of lipid peroxidation, i.e. ethane exhalation, there was no difference between the T-2 toxin treated rats and the controls whereas carbon tetrachloride treated rats exhaled high amounts of ethane. These results suggest that lipid peroxidation does not play a major role in T-2 toxin toxicity.

Animals↗
PubMed1985

Radiation exposure in German dwellings, some results and a proposed formula for dose limitation.

The results of our investigations in the Federal Republic of Germany on the indoor and outdoor exposure to natural radiation from gamma rays and radon and thoron daughters are presented. Indoor the median Rn-222 concentration was approximately four times higher than outdoors. A correlation analysis of the data obtained showed that indoors the equilibrium factor F is almost independent of ventilation, Rn-222 concentration and other parameters. The mean equilibrium factor was measured to be F = 0.3 in dwellings and approximately F = 0.4 outdoors. The results of our investigations on diffusion coefficients and exhalation rates showed, that the activity concentration in dwellings and in cellars can generally be explained by the radon exhalation from the building materials. Only in areas of high radon concentrations, the exhalation from the soil was a decisive factor. The mean effective dose equivalent by residence in dwellings amounted to 0.2 - 0.8 mSv/a for Rn-222 daughters and approximately 0.1 mSv/a for Rn-220 daughters. A relationship has been derived which permits the calculation of the expected average radiation exposure in dwellings by gamma radiation and by radon inhalation as function of the radionuclide concentration in building materials.

Construction Materials↗
PubMed1984

Measurement of respiratory tract ammonia in the rabbit and implications to sulfuric acid inhalation studies.

Ammonia (NH3) in the respiratory tract has the potential to neutralize inhaled acid vapors and aerosols. Levels of exhaled (nasal) NH3 were measured in rabbits at different times on the same day, on different days, and in rabbits in a normal fed state, or in a fasted or fed state in which the teeth were brushed and the mouth cleansed. The variability of NH3 levels within any individual rabbit was found to be of the same order as the variability found between different animals. In addition, rabbits which were fasted and had their teeth brushed exhaled significantly less NH3 than did fed animals. Levels in the former group ranged from 4 to 236 micrograms/m3, while those in the latter group ranged from 10 to 758 micrograms/m3. Although brushing the teeth of fed animals compressed the observable range of NH3 levels (22-404 micrograms/m3), this was not a significant reduction compared to fed, unbrushed animals. Thus, fasting likely minimized foodstuff in the mouth; the latter may contribute to NH3 formation through bacterial degradation, which appears to be a significant source of NH3 exhaled through the nose. The NH3 concentrations observed may produce variable degrees of neutralization of inhaled H2SO4 droplets before they deposit in the lungs.

Aerosols↗
PubMed1984

Disposition of [14C]methyl bromide in Fischer-344 rats after oral or intraperitoneal administration.

Methyl bromide is used as a disinfectant to fumigate soil. The intent of our study was to determine the disposition of methyl bromide following a single acute administration. Male Fischer-344 rats were given 250 mumol of [14C] methyl bromide/kg body wt by either oral or i.p. administration. Urine, feces and expired air were collected and at the end of 72 h the rats were sacrificed and tissues analyzed to determine 14C excretion and tissue distribution. After i.p. administration of methyl bromide, the dominant route of excretion was exhalation of 14CO2, with 46% of the dose exhaled as 14CO2. In contrast, urinary excretion of 14C was the major route of elimination (43% of the dose) when methyl bromide was given orally. Very little of the 14C appeared in the feces (less than 3% of the dose) regardless of route of administration. In rats with bile duct cannulations, 46% of an oral dose appeared in the bile over a 24-h period. Collection of bile significantly decreased the exhalation of 14CO2 and 14C excreted in urine compared to controls. At 72 h after oral or i.p. administration, 14-17% of the 14C remained in the rats, with liver and kidney being the major organs of retention. Results indicate that route of administration can affect the pathways for excretion. In addition, excretion of 14C in bile, coupled with the low levels of radioactivity found in the feces, indicates that reabsorption of biliary metabolites from the gut plays a significant role in the disposition of [14C] methyl bromide.

Administration, Oral↗