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PubMed2001

Inhalation toxicity of 4-ethoxyaniline (p-phenetidine): critical analysis of results of subacute inhalation exposure studies in rats.

This article addresses results from a single 4-h and repeated 1- and 4-wk inhalation exposure studies in Wistar rats with vapor and/or aerosol atmospheres of 4-ethoxyaniline (p-phenetidine). Groups of 10 rats/sex were exposed nose-only to mean analytical concentrations of 11.1, 86.2, and 882.6 mg p-phenetidine/m(3) using an exposure regimen of 6 h/day, 5 days/wk for 4 wk. Concentrations were selected based on results from a pilot study in which rats were exposed under identical conditions on 5 consecutive days for 6 h/day to mean analytical concentrations of 38.2, 133.0, and 1247.6 mg/m(3). In repeated exposure studies, the focus of endpoints was on hematotoxicity. The LC50 was not determined, but no rats died following a single 4-h exposure to 5085 mg/m(3) as a mixture of vapor and aerosol. No mortality was observed either in the 1- or 4-wk studies. Rats exposed to 882.6 mg/m(3) and above evoked characteristic signs of toxicity that included cyanosis, with no apparent progression of findings during the exposure period. Animals exposed to 86.2 mg/m(3) and above exhibited a concentration-dependent, significant increase in blood methemoglobin and reticulocyte counts as well as a significant decrease in hemoglobin, hematocrit, and red blood cell counts. Spleen weights were significantly increased in groups exposed to 133.0 mg/m(3) and above. Microscopic changes demonstrated an increased hematopoiesis (bone marrow smears) and splenic hemosiderosis at 86.2 and 882.6 mg/m(3) and a hepatic hemosiderosis only at 882.6 mg/m(3). These data suggest that the toxicity of p-phenetidine is similar to that of its structural analog aniline. Based on the erythrocytotoxicity occurring at 86.2 mg/m(3) and above, including the apparent reactive changes in bone marrow (increased erythropoiesis) and spleen (increased erythroclasia), the no-observed-adverse-effect level (NOAEL) of the 4-wk study was 11.1 mg/m(3) air and that of the 1-wk study was 38.2 mg/m(3) air. This difference in NOAELs is considered to be related to the selection of exposure concentrations rather than cumulative toxicity.

Aerosols↗
PubMed1975

Accumulation and retention of 137Cs-labelled fused aluminosilicate particles by beagle dogs after repeated inhalation exposures.

A group of 12 beagle dogs was given weekly, individual, 10-min inhalation exposures to aerosols of 137Cs-labelled, fused aluminosilicate particles (AMAD approximately equal to 1.8 micron, sigmag approximately equal to 1.6). Whole-body counting was used to assess the pulmonary deposition associated with each exposure and the long-term retention after exposures. Groups of four dogs were removed from further exposures at the end of 10, 20 and 40 exposures, respectively. Two dogs in each group were sacrificed and the other two maintained for long-term retention measurements. The inhaled material was relatively insoluble in body fluids. In each of the sacrificed dogs, approximately equal to 96% of the body burden was in the lung and approximately equal to 1% in the tracheobronchial lymph nodes. The average pulmonary deposition was approximately equal to 20% of the inhaled aerosol for 10, 20 or 30 exposures, a value which was in agreement with previously reported single exposure data. Lower values observed for exposures 31 to 40 were apparently related to differences in respiratory patterns. The long-term, whole-body retentions appear to have effective half-lives ranging from 1200-1800 days in contrast to approximately equal to 400 days seen in singly exposed dogs. Possible reasons are discussed.

Aerosols↗
PubMed1982

Isotoxic oral and inhalation exposure of carbon tetrachloride in Porton-Wistar and Fischer rats.

Male Fischer or Porton-Wistar rats were exposed for 4 h to different atmospheric concentrations of CCl4 or were given increasing oral doses, of CCl4 in order to estimate isotoxic exposures or doses. Animals were killed 20 h after treatment, their serum glutamic-pyruvic transaminase activities were measured and their livers were processed for histological examination. It has been found that the equitoxic oral dose in Wistars is 1.5 times that in Fischer rats and more than 3 times after inhalation. Therefore, the conversion factors from inhalation exposure to oral dose were much higher for Fischer than for Porton-Wistar rats. After oral dosing, the extent of centrilobular damage in Fischer rats was approximately twice that in Porton-Wistar rats. After inhalation exposure, the extent of damage was the same in the two strains, but at least at the two lower exposure levels hydropic degeneration definitely contributed to the size of the damaged areas more in Porton-Wistar than in Fischer rats.

Administration, Oral↗
PubMed2004

The influence of low-level sarin inhalation exposure on the host resistance and immune reaction of inbred BALB/c mice after their infection with Francisella tularensis LVS.

To study the influence of low-level sarin inhalation exposure on immune functions, inbred BALB/c mice were exposed to two low concentrations of sarin for 60 minutes in the inhalation chamber and then infected with Francisella tularensis LVS on the 7th day following the exposure to sarin. 24 hours after infection, the level of some isotypes of antibodies (IgM, IgA) against tularaemia was significantly decreased regardless of the sarin concentration used while the lymphoproliferation was significantly increased regardless of the mitogen and sarin concentration used. Later, the level of some isotypes of antibodies (IgM, IgA) against tularaemia and the vitality of Francisella tularensis LVS was significantly increased in the case of exposure of mice to clinically symptomatic concentration of sarin (7 days after infection) while the lymphoproliferation was significantly decreased regardless of the concentration of sarin when specific tularaemic antigen Ag4 was used as a mitogen (3 weeks after infection). Thus, the results indicate that not only symptomatic but also asymptomatic dose of sarin is able to alter the host resistance and reaction of immune system, especially at 24 hours and 7 days following infection with Francisella tularensis LVS. Nevertheless, the alteration of immune functions following the inhalation exposure to a symptomatic concentration of sarin seems to be more pronounced.

Administration, Inhalation↗
PubMedDate not supplied

Immune activation and autoantibodies in humans with long-term inhalation exposure to formaldehyde.

Four groups of patients with long-term inhalation exposure to formaldehyde (HCHO) were compared with controls who had short-term periodic exposure to HCHO. The following were determined for all groups: total white cell, lymphocyte, and T cell counts; T helper/suppressor ratios; total Ta1+, IL2+, and B cell counts; antibodies to formaldehyde-human serum albumin (HCHO-HSA) conjugate and autoantibodies. When compared with the controls, the patients had significantly higher antibody titers to HCHO-HSA. In addition, significant increases in Ta1+, IL2+, and B cells and autoantibodies were observed. Immune activation, autoantibodies, and anti-HCHO-HSA antibodies are associated with long-term formaldehyde inhalation.

Adolescent↗
PubMed1999

Induction of hepatic xenobiotic metabolizing enzymes in female Fischer-344 rats following repeated inhalation exposure to decamethylcyclopentasiloxane (D5).

Decamethylcyclopentasiloxane (D5) is a cyclic siloxane with a wide range of commercial applications. The present study was designed to investigate the effects of D5 on the expression and activity of selected rat hepatic phase I and phase II metabolizing enzymes. Female Fischer-344 rats were exposed to 160 ppm D5 vapors (6 h/day, 7 days/week, for 28 days) by whole-body inhalation. Changes in the activity and relative abundance of hepatic microsomal cytochromes P450 (CYP1A, CYP2B, CYP3A, and CYP4A), epoxide hydrolase, and UDP-glucuronosyltransferase (UDPGT) were measured. Repeated inhalation exposure of rats to D5 increased liver size by 16% relative to controls by day 28. During a 14-day post-exposure period, liver size in D5-exposed animals showed significant recovery. Exposure to D5 did not change total hepatic P450, but increased the activity of hepatic NADPH-cytochrome c reductase by 1.4-fold. An evaluation of cytochrome P450 (CYP) enzymes in hepatic microsomes prepared from D5-exposed rats revealed a slight (1.8-fold) increase in 7-ethoxyresorufin O-deethylase (EROD) activity, but no change in immunoreactive CYP1A1/2 protein. A moderate increase (4.2-fold) in both 7-pentoxyresorufin O-depentylase (PROD) activity and immunoreactive CYP2B1/2 protein (3.3-fold) was observed. Testosterone 6beta-hydroxylase activity was also increased (2.4-fold) as was CYP3A1/2 immunoreactive protein. Although a small increase in 11- and 12-hydroxylation of lauric acid was detected, no change in immunoreactive CYP4A levels was measured. Liver microsomal epoxide hydrolase activity and immunoreactive protein increased 1.7- and 1.4-fold, respectively, in the D5-exposed group. UDPGT activity toward chloramphenicol was induced 1.8-fold, while no change in UDPGT activity toward 4-nitrophenol was seen. These results suggest that the profile for enzyme induction following inhalation exposure of female Fischer-344 rats to D5 vapors is similar to that reported for phenobarbital, and therefore D5 may be described as a weak "phenobarbital-like" inducer.

Administration, Inhalation↗
PubMed2003

Automated feedback control of an inhalation exposure system with discrete sampling intervals: testing, performance, and modeling.

The application of a proportional-integral-derivative (PID) control algorithm to an inhalation exposure system using a building automation system is described. Previous studies had utilized a control system in which concentration was monitored continuously and adjustments to the generator were made on a continuous basis. In this system, benzene vapor was generated into a chamber, and a gas chromatograph was used to measure the concentration in a chamber at discrete 30-min intervals. Thus only limited opportunities were available to sample and adjust the vapor generator flow rate. A series of tests were conducted in which the generator was operated without control, with control, with an additional load, and with nonoptimal settings. The results showed that the PID control loop could function effectively to restore a system back to the target set point, even with an additional load on the system. With nonoptimal control settings, the system showed oscillatory behavior. A model to simulate operation of the chamber was developed on a spreadsheet program. The model was accurate at simulating the various testing scenarios and useful for selecting the proper control settings. A PID feedback control system operating with a concentration monitoring system that sampled on a 30-min cycle was shown to produce exposures that were accurate in matching the target set point and maintaining a constant concentration.

Algorithms↗
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↗
PubMed2002

Toxicokinetics and metabolism of pseudocumene (1,2,4-trimethylbenzene) after inhalation exposure in rats.

The objective of this study was to evaluate the toxicokinetics and metabolism of pseudocumene after inhalation exposure. Male Wistar rats were exposed to pseudocumene vapors at nominal concentrations of 25,100 or 250 ppm in the dynamic inhalation chambers for 6 h. Blood samples were collected during (between 1st and 6th h) and after exposure (betwen 6th min and 6th h). Blood concentrations of pseudocumene were estimated by gas chromatography using the headspace technique. During a six-hour exposure, the concentration of pseudocumene in blood increased rapidly within the first 2 h reaching then a plateau. The elimination of pseudocumene from blood followed an open two-compartment model. Urine samples were collected from the exposed animals, and metabolites were analyzed by gas chromatography with a flame ionization detector. Three metabolites were measured in the rat urine after hydrolysis: 3,4-dimethylbenzoic acid (3,4-DMBA), 2,4-dimethylbenzoic acid (2,4-DMBA) and 2,5-dimethylbenzoic acid (2,5-DMBA). A significant linear correlation was found between the level of exposure and the concentration of dimethylbenzoic acids. The enzyme kinetics of pseudocumene biotransformation was calculated by Lineweaver-Burk equation. Metabolic constants, Km (mg/l) and Vmax (mg/h/kg), the parameters for pseudocumene biotransformation by rats were estimated (3,4-DMBA - Km = 28, Vmax = 96; 2,4-DMBA - Km = 7, Vmax = 25; 2,5-DMBA - Km = 7, Vmax = 23).

Animals↗
PubMed1989

Effect of repeated benzene inhalation exposures on subsequent metabolism of benzene.

Benzene is a known human leukemogen and animal carcinogen. To better assess the risks associated with benzene exposure, it would be helpful to determine whether repeated inhalation exposures would affect the metabolism of benzene. The purpose of these experiments was to determine if exposure of F344 rats and B6C3F1 mice to 600 ppm benzene, 6 h/day, 5 days/week for 3 weeks, would affect the subsequent in vivo metabolism of inhaled [14C]benzene.

Administration, Inhalation↗
PubMed1986

Lung changes in rats following inhalation exposure to volcanic ash for two years.

Rats were exposed by inhalation to 5 or 50 mg/m3 Mount St. Helens volcanic ash, to 50 mg/m3 quartz (positive controls), or to filtered room air (sham-exposed controls), for 6 hr/day, 5 days/week, for up to 24 months to investigate biological effects of chronic inhalation exposure to volcanic ash under controlled laboratory conditions. Exposure-related lung changes comprised accelerated respiratory frequency; alveolar macrophage accumulation; interstitial reaction; lymphoreticular reaction in peribronchiolar regions and in mediastinal lymph nodes; alveolar proteinosis in the 50- mg/m3 ash- or quartz-exposed groups; increase in fresh lung weights; decreased body weight and increased mortality in the quartz-exposed group; and epidermoid carcinomas especially in the quartz-exposed females and, to a lesser extent, in the 50-mg/m3 ash-exposed females. The observed changes reflect significant dose-response and agent-response relationships.

Aerosols↗
PubMed1987

Inhalation exposure system used for acute and repeated-dose methyl isocyanate exposures of laboratory animals.

Laboratory animals were exposed by inhalation for 2 hr/day (acute) or 6 hr/day (four consecutive days, repeated dose) to methyl isocyanate (MIC). Exposures were conducted in stainless steel and glass inhalation exposure chambers placed in stainless steel, wire mesh cages. MIC was delivered with nitrogen via stainless steel and Teflon supply lines. Chamber concentrations ranged from 0 to 60 ppm and were monitored continuously with infrared spectrophotometers to 1 ppm and at 2-hr intervals to 20 ppb with a high performance liquid chromatograph equipped with a fluorescence detector. Other operational parameters monitored on a continuous basis included chamber temperature (20-27 degrees C), relative humidity (31-64%), static (transmural) pressure (-0.3 in.), and flow (300-500 L/min). The computer-assistance system interfaced with the inhalation exposure laboratory is described in detail, including the analytical instrumentation calibration system used throughout this investigation.

Animals↗
PubMed1985

Acute tubular necrosis after inhalation exposure to methylene chloride. Report of a case.

Nephrotoxic reaction occurred after inhalation exposure to methylene chloride. This exposure is associated with acute renal failure, myoglobinuria, hypocomplementemia, and liver enzyme elevations. Pathologic specimens, both light and electron microscopic, demonstrate renal tubular damage. We conclude that methylene chloride may have potential as both a hepatotoxic and nephrotoxic agent when inhaled at high concentrations over an extended period of time.

Acute Kidney Injury↗
PubMed1987

Experimental T-2 toxicosis in swine following inhalation exposure: effects on pulmonary and systemic immunity, and morphologic changes.

Thirty-four, 9- to 11-week-old, male castrated, crossbred, specific pathogen-free derived pigs were exposed to a T-2 toxin aerosol at a nebulized dose of 0 or 9 mg/kg in pairs, each pair consisting of 1 control and 1 T-2 treated pig which were exposed on the same day. Twenty to 30% of the toxin (1.8 to 2.7 mg/kg) was retained by the pigs. Five pairs were killed on each of 1, 3 and 7 days after dosing. Two pairs of pigs were designated as a 0.33-day group when one T-2 treated pig died and the other was killed in a moribund state at 8 to 10 hours after dosing. The pulmonary and systemic immunity and morphologic changes of the lungs and other organs were examined. Bronchoalveolar lavage was performed to obtain alveolar macrophages (AM) and pulmonary lymphocytes (PL). The phagocytic ability of AM and mitogen-induced blastogenic responses of enriched PL and peripheral blood lymphocytes were evaluated. Clinically, all of the T-2 treated pigs vomited and were cyanotic, anorexic, lethargic and laterally recumbent. In the 0.33-, 1-, and 3-day T-2 treated pigs, there was a marked reduction in AM phagocytosis and mitogen-induced blastogenic responses of PL but not of peripheral blood lymphocytes. Mild to moderate, multifocal interstitial pneumonia was seen in the majority of the T-2 treated pigs. In pigs dying following inhalation of T-2 toxin, there was a more severe pneumonia, as well as marked necrosis of lymphoid tissues, severe necrohemorrhagic gastroenteritis and edema of the gall bladder wall, and multifocal necrosis of the heart and pancreas. Thus, inhalation exposure to T-2 toxin can result in clinical signs and morphologic changes resembling those reported previously in pigs given T-2 toxin intravascularly (iv) at a dose of 1.2 mg/kg (approximate LD50) or greater, as well as death. Mild pulmonary injury as well as transient impairment of pulmonary immunity was present in pigs surviving inhalation exposure.

Administration, Inhalation↗
PubMed2003

Comparisons of pulmonary carcinogenesis in rats following inhalation exposure to plutonium dioxide or X-ray irradiation.

Radiation-induced pulmonary carcinogenesis was compared in female Wistar rats following either inhalation exposure to alpha-emitting (239)PuO(2) aerosols, whole-body or thoracic X-ray irradiation. Dose-dependent survival reduction was correlated with increased malignant lung tumors at doses over 0.45 Gy, reaching the maximum incidence of 90% at 6.6-8.5 Gy in (239)Pu-exposed rats. While the differential dose responses for each histopathological type of tumors were noted, almost 70-80% were carcinomas among all of the primary tumors from (239)Pu-exposed rats. As the dose response curves for lung carcinomas were compared, the slope of the fit linear equation and the calculated relative effectiveness for 50% incidence of lung carcinomas were approximately 11-times as high in (239)Pu-exposure as those of thoracic X-irradiation. The numbers of tumor lesions distributed in the lung per tumor-bearing animal were about 2-fold more in (239)Pu-exposed rats, while the proportions of their histopathological types were similar between (239)Pu-exposure and X-irradiation. These results indicate that the magnitudes of the relative effectiveness or risk for pulmonary carcinogenesis are greater in (239)Pu-exposure than X-irradiation, and that radiation-induced lung tumors appear to originate mostly from the same target epithelial cells.

Adenoma↗
PubMed1996

Quantifying the distribution of inhalation exposure in human populations: distribution of minute volumes in adults and children.

Assessments of inhalation exposure to environmental agents necessitate quantitative estimates of pulmonary ventilation rates. Estimating a range of exposures in a given population requires an understanding of the variability of ventilation rates in the population. Distributions of ventilation rates (Ve) were described based on the results of a large study where Ve were measured while subjects performed a variety of physical tasks. Three distinct ventilation levels were identified using cluster analyses of the mean Ve and then various activities were assigned to the three levels using a k-means procedure. Separate distributions were identified for the three Ve levels for adult males, adult females, and children. The variability of Ve was consistent with a lognormal distribution for all groups. An aggregate daily inhalation rate can be estimated based on the distributions of Ve.

Adolescent↗
PubMed2001

Determination of 2-butoxyethanol emissions from selected consumer products and its application in assessment of inhalation exposure associated with cleaning tasks.

Consumer products are important sources of human exposure to certain chemicals. Recent regulatory requirements for assessing human exposure to three glycol ethers, namely 2-methoxyethanol (ME), 2-ethoxyethanol (EE) and 2-butoxyethanol (BE), have prompted the investigation of these chemicals in consumer products and their emission characteristics. Thirteen products were selected for investigation based on their potential of containing the chemicals. Headspace results indicated that ME and EE were not present in any of the 13 selected products, while BE was detected in the headspace samples of seven products, of which five were household cleaning agents. Other related compounds such as 2-hexyloxyethanol (HE) and 2-(2-butoxyethoxy)ethanol (BEE) were also detected in the headspace samples of some products. BE emissions from five cleaning related products were measured using a field and laboratory emission cell (FLEC) with its subunit to provide emission data for inhalation exposure assessment purposes. These products had initial emission factors ranging from 145 to 938 mg m(-2) h(-1) under the experimental conditions. It was found that the emission factor of BE was inversely proportional to the dilution factor of the products. A good relationship was established between the emission factor of BE and its concentrations in water-based products. Based on product use scenarios developed by US EPA and an assumed "standard room," average daily inhalation exposure levels of a resident as a result of performing cleaning tasks were estimated to be 0.075 and 0.186 mg (kg b.w.)(-1) day(-1) for two all-purpose spray cleaners, and 0.004 and 0.006 mg (kg b.w.)(-1) day(-1) for two-spray glass cleaners, respectively.

Air Pollution, Indoor↗
PubMed2005

Effective dose scaling factors for use with cascade impactor sampling data in tenorm inhalation exposures.

When assessing the effective dose to workers following radio-aerosol inhalation exposures, significant reductions in dose uncertainty can be achieved through direct measurement of the particle-size distribution. The University of Washington Mark III cascade impactor is one such air sampling device that permits the user to determine aerosol mass and radioactivity concentrations as a function of particle size within eight different size intervals (each corresponding to a different impactor stage or end filter). Traditionally, dose assessments made using the LUDEP code or other internal dosimetry software utilize this air sampling information by assigning the radioactivity measured at each stage as concentrated at a single representative size central to the size interval. In this study, we explore more realistic assumptions that the measured radioactivity distributes uniformly, linearly increases, or linearly decreases across the particle size interval for each impactor stage. The concept of an effective dose scaling factor, SF(E), is thus introduced whereby (1) the former approach can be used (which requires less computational effort using the LUDEP code), and (2) the resulting values of effective dose per stage can then be rescaled to values appropriate to a linear radioactivity distribution per stage. For a majority of (238)U-series radionuclides, particle size ranges, and absorption classes, differences in these two approaches are less than 10%, and thus no corrections in effective dose per particle stage are needed. Significant corrections, however, were noted in select cases. For uniform or linearly decreasing radioactivity distributions, end-filter particles (0.03 to 0.35 microm) of type F, M, or S radionuclides were assigned values of SF(E) ranging from 1.15 to 1.44, while 3(rd) stage particles (4.5 to 12 microm) of type M and S radionuclides were assigned values of SF(E) ranging from 1.11 to 1.53. When the cascade impactor measurements indicate a linear increase of activity across a given impactor-stage size range, values of SF(E) range from a high of 1.11 (6(th) stage particles of type F radionuclides) to lows of 0.85 to 0.91 (4(th) stage and end-filter particles of type M and S radionuclides). In these cases, the inhalation dose coefficient varies non-linearly across the particle size range, and the assumption of a mono-size distribution per impactor stage either underestimates (SF(E) > 1) or overestimates (SF(E) < 1) that stage's contribution to the worker effective dose.

Aerosols↗