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PubMed1980

An apparatus for generation of vapors from liquids of low volatility for use in inhalation toxicity studies.

While it is usually a simple matter to perform inhalation exposures to vapors from low-boiling liquids, inhalation exposures to vapors of high-boiling liquids present problems, especially the risk of decomposing the test substance by use of excessive heat. This work describes a device for the volatilization of high-boiling liquids, in a manner suitable for conducting inhalation exposures, without requiring heat input, which avoids this difficulty. The device is based on counter-current volatilization employing a multi-plate high efficiency distillation column. The column is thermostated below ambient temperature, which increases stability of operation and flexibility of application.

Occupational Exposure↗

PubMed2001

Do EASE scenarios fit workplace reality? A validation study of the EASE model. Estimation and Assessment of Substance Exposure.

Within the framework of European risk assessment of new and existing substances, the EASE model (Estimation and Assessment of Substance Exposure) is often applied to assess inhalative exposure at workplaces. To contribute to the validation of this model, single EASE scenarios were compared with independent measurement data on inhalative exposure to vapors and dusts. For this purpose, workplace measurements obtained in the areas of production, textile printing and coating, screen printing and offset printing, the rubber industry, and the plastics processing industry as well as flame spraying were used. A good correspondence between model estimates and measurement data was found in the case of exposure to vapors for the production of chemical substances in closed systems (EASE scenario: closed system without breaching) and for procedural control works at mainly automated printing workplaces (EASE scenarios: non dispersive use, segregation, low/medium volatility). For the handling of powdery substances measurement results obtained during weighing and filling works, in part semiautomatic, were compared with the EASE estimates for the scenario: dry manipulation, with/without local exhaust ventilation. Good correspondence was estimated if approx. 1 t to 200 t powdery substances were handled per shift. For the EASE scenarios "direct handling with natural ventilation/with local exhaust ventilation," high discrepancies exist between model prediction and measurement results obtained during manual screen printing or the preparation of printing inks.

Air Pollutants, Occupational↗

PubMed1988

Indicators of matrix dependent variation in effective dose for chromium and nickel aerosol exposures.

Inhaled particulates containing Cr and Ni are partially cleared or dissolved thus contributing to short-term internal exposures and partial retention in airways and airspaces. The retained fraction may continuously contribute to internal exposure after external exposure has ceased, through intra- and extracellular chemical processes which continuously liberate various metallic species; i.e. via an active deposit. Recent experiments with Ni and Cr compounds, and freshly produced welding fumes, which contain Ni and Cr, demonstrate a strong dependence of the distribution of these metals on oxidation state, solubility, bioavailability and toxicity as measured by in-vitro bioassay, depending on the collection, storage and analytical technique. It is suggested that exposure limits must consider the wide variation in short- and long-term delivered dose of toxic metals to target tissue with matrix, and that current protocols may be inadequate to protect workers in different industries involving exposures to widely different types of aerosols having only the same chemical element in common.

Aerosols↗

PubMed1994

Evaluation of chemical releases and worker exposures from filter press operations.

The exposures (inhalation and dermal) and releases (air, water, solids, and process streams) associated with the filtration of industrial wastewater sludge from an electronics manufacturing plant were characterized. Chemical releases and worker exposures for a target chemical (total copper) were measured over four operational cycles. Various aspects of the filtration operation believed to influence the measurement values were documented. Worker exposures associated with the discreet stages of the filter operation were measured. Ventilation patterns around the filter press were also monitored. The workers' time-weighted average exposures to total copper during the 113-minute operational cycle ranged from 3.1 to 25 micrograms/m3 (2.2 geometric standard deviation, 6.4 micrograms/m3 geometric mean concentration). The manual removal of filter cake comprised only 15% of the time in an average filtration cycle, but produced 72% of the workers' inhalation exposure. During this cake-removal stage, inhalation exposures ranged from 11 micrograms/m3 to 130 micrograms/m3 (2.5 geometric standard deviation, 30 micrograms/m3 geometric mean concentration). Differences in worker technique may account for the large range of inhalation exposures during the cake-removal stage. Exposures and releases were successfully determined for a single unit operation, as well as for the discreet stages of operation. The data generated will enable EPA to more accurately estimate worker exposures and chemical releases for new chemicals as required by the Toxic Substances Control Act. The approach utilized will benefit industrial hygienists in providing estimates of worker exposures and aid in the targeting of survey sampling.

Air Pollution↗

PubMed1996

Pulmonary effects of machining fluids in guinea pigs and mice.

Acute pulmonary effects of inhalation exposure to (unused) neat and in-use metalworking fluids (MWF) were studied to evaluate the potency of characterized MWF in terms of their effects on breathing and lung inflammation. Inhalation exposure of guinea pigs caused dose-dependent changes in respiratory rate and volume that were used to quantify potency. In-use MWF was consistently more toxic than the corresponding neat MWF. Significant predictors of respiratory responses were whether MWF was neat or in-use (p = 0.0001), exposure concentration (p = 0.022), MWF formulation (p = 0.031), and the particular in-use MWF tested (p = 0.032). Inhalation exposures to MWF biocides resulted in dose-dependent sensory irritation responses. Guinea pig studies revealed significant inflammation resulting from MWF exposure marked by change in bronchoalveolar lavage (BAL) fluid from 3% neutrophils (controls) to 60-79% (MWF-exposed) and 25-fold increase in total BAL cells. The in-use MWF ranged in endotoxin concentration from 280 to 1.7 x 10(5) endotoxin units (EU)/mL. To investigate the role of endotoxin, studies were carried out in mice sensitive (SEN) and resistant (RES) to endotoxin. SEN mice revealed a dose-dependent 10,000-fold increase in BAL neutrophils and a 100-fold increased concentration of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) following inhalation exposure to in-use MWF. This inflammatory response was not observed with exposure to neat MWF or with sham exposure. RES mice demonstrated virtually no response to the inhaled MWF for total cells, neutrophils, IL-6, or TNF-alpha. Removal of microorganisms by filtration of the in-use MWF did not change the responses observed in either strain. These studies demonstrate that lung inflammation may be an important outcome from exposure to in-use MWF and that endotoxin is a toxicant of importance.

Acute Disease↗

PubMed1991

Tumor necrosis factor and interleukin-1 activities in free lung cells after single and repeated inhalation of bacterial endotoxin.

Bacterial endotoxins (lipopolysaccharides), important components of many organic dusts, are known to induce macrophages to produce the inflammatory mediators interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). To investigate the role of these mediators in the early inflammatory responses in the lung, guinea pigs were exposed to an aerosol of bacterial endotoxin. A bronchoalveolar lavage (BAL) was then performed, and TNF-alpha and IL-1 in lysed BAL cells and in the supernatants from BAL cell cultures were studied. The effect of single and repeated LPS inhalation exposures on the activities of TNF and IL-1 was studied, as was the effect of LPS added to the cell culture medium. A single inhalation exposure to LPS caused an increase in the TNF-alpha and IL-1 activities in cell lysate and in the cell culture supernatant. After a second inhalation exposure, cell-associated and extracellular TNF-alpha activity could not be detected, whereas IL-1 activity was markedly enhanced. IL-1 activity was increased when LPS was added to the cell culture medium with or without a prior inhalation exposure. In contrast, TNF-alpha activity was not affected after a second exposure.

Administration, Inhalation↗

PubMed1989

Effect of concentration and cumulative exposure of inhaled sulfuric acid on tracheobronchial particle clearance in healthy humans.

We have previously shown that 1-hr exposures to 0.5 microns sulfuric acid (H2SO4) mist at 100 and 1000 micrograms/m3 produced transient alterations of bronchial mucociliary clearance of monodispersed 7.6 and 4.2 microns mass median aerodynamic diameter gamma-tagged ferric oxide (Fe2O3) in healthy nonsmoking humans in a dose-dependent manner. To determine the role, if any, of the length of exposure, 10 healthy volunteers were exposed to 100 micrograms/m3 H2SO4 for 1 hr and 2 hr on separate occasions, 1 week apart, with measurements of their mucociliary clearance of 5.2 microns Fe2O3 particles inhaled both before and after the inhalation of the H2SO4. Their rate of bronchial mucociliary clearance was markedly reduced for both Fe2O3 aerosols, with slower clearance of the aerosol inhaled after the H2SO4 exposure. For the tagged Fe2O3 aerosol inhaled after exposure for 2 hr at 100 micrograms/m3 H2SO4, the tracheobronchial clearance halftime, (T50), tripled from control, and the reduced rate of clearance was still evident 3 hr after the end of exposure. The 1-hr 100 micrograms/m3 H2SO4 exposure doubled T50 from control, and the reduced rate of clearance lasted for about 2 hr after the end of exposure. These results indicate that the effect of doubling the length of exposure was as great or greater than an order of magnitude increase in the concentration of H2SO4.

Acid Rain↗

PubMed1997

Assessment of health risks due to hazardous air pollutant emissions from electric utilities.

Hazardous air pollutant (HAP) emissions from electric utilities were evaluated. Cancer risks, as well as noncancer effects, due to inhalation exposure were assessed for 67 HAPs. Also, cancer risks due to multipathway exposure to radionuclide emissions were assessed. In addition, an assessment of the fate of mercury (Hg) through various environmental media was included. Results suggest arsenic, chromium, and nickel are the HAPs that present the highest cancer risk due to inhalation exposure. For noncancer effects due to inhalation exposure, hydrogen chloride appears to present the greatest potential concern. The risks due to multipathway exposure to radionuclides are estimated to be of similar magnitude to the risks posed by inhalation of arsenic and nickel. Mercury is of potential concern for multipathway exposures because it persists in the environmental and bioaccumulates in the aquatic food web. The study suggests there is a plausible link between Hg emissions from utilities and the Hg found in soil, water, and freshwater fish.

Air Pollutants↗

PubMed1999

Inflammatory responses of rat alveolar macrophages following exposure to fluoride.

Inhalation exposure to fluoride compounds has been associated with respiratory failure. We have addressed effects of fluoride on alveolar macrophages and lung responses to intratracheally (i.t.) instilled fluoride in rats. I.t. instillation of fluoride at doses of 200 and 400 microg F/rat caused significant polymorphonuclear leukocyte (PMN) infiltration in the rat lung at 20 h post-administration, while 100 microg fluoride did not recruit a significant number of PMNs in the alveolar space. Total RNA was extracted from the lung lavage cells obtained from 5 h post i.t. instillation and mRNA levels of chemokines and proinflammatory cytokines were semi-quantitatively evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). I.t. instillation of fluoride significantly enhanced mRNA expression of cytokines such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory proteins-1alpha and -2. Fluoride-induced augmentation in IL-1beta mRNA expression was also examined by Northern hybridization following in vitro exposure of alveolar macrophages to fluoride. However, the enhancement of IL-1beta mRNA expression following in vitro exposure to fluoride was observed only at 500 microM, a dose higher than the 50% lethal concentration (LC(50)). Non-specific adhesion of alveolar macrophages to the plastic dish was significantly increased following in vitro exposure to fluoride. The fluoride-induced non-specific adhesion was significantly reduced by anti-CD18, suggesting that beta(2) integrin played a role in the increase of adherence. Those results suggest that fluoride activates alveolar macrophages, enhances the production of chemokines and proinflammatory cytokines, and causes PMN infiltration in the lung.

Animals↗

PubMed1999

Upregulation of heme oxygenase gene expression in rat lung epithelial cells following exposure to cadmium.

Inhalation exposure to cadmium (Cd) is associated with inflammatory lesion in the lung. In the present study we have investigated cytotoxic effects of Cd on immortalized rat lung epithelial cells (SV40-T2) and gene expression in those cells following in vitro exposure to sublethal concentrations of cadmium chloride (CdCl(2)). The polymerase chain reaction (PCR)-based subtraction method was used to find differentially expressed genes between control and Cd-exposed SV40-T2 cells. The most prominent cDNA on an agarose gel was identical to a fragment of rat heme oxygenase (HO) gene. Northern blot analysis indicated that the level of HO mRNA expression in SV40-T2 cells was increased to 38-fold of the control value following exposure to 2.5 microM CdCl(2) for 4 h. These results suggest that HO gene expression is one of the most sensitive biomarkers for acute exposure to Cd in the lung.

Animals↗

PubMed2000

Acute inhalation toxicity study of 2-fluoroacetamide in rats.

One of the most potent rodenticides is 2-fluoroacetamide (2-FA). Toxicity of this chemical is well documented. However, its inhalation toxicity data is not available in the literature. Hence, acute inhalation toxicity study was carried out by exposing male and female rats to aerosols of 2-FA at different concentrations for 4 h in a dynamically operated whole body inhalation exposure chamber. During and after the inhalation exposure the rats were less active, and showed mild tremors and convulsions. At higher concentrations the rats died after 2-3 days. The estimated 4-h LC50 for male and female rats was 136.6 and 144.5 mg.m-3 respectively. Exposure to 0.7 LC50 for 4 h duration showed an increase in the liver weight of male and female rats 7 days after exposure. Various haematological and biochemical variables determined were within the normal limits. However, histological findings showed injured lung as indicated by desquamation and necrosis of the epithelium of the respiratory tract. Marked hypertrophy of hepatocytes displaying strong acidophilic granulated cytoplasm was observed. Focal dilatation of renal proximal tubules in kidney with cytoplasmic vacuolation, and irregularly placed pyknotic nuclei were seen. The present study shows that 2-FA is a highly toxic chemical through the inhalation route based on the LC50 value. Consequently necessary precautions should be taken during its handling.

Animals↗

PubMed2004

Thyroid dosimetry in the western trace of the Chernobyl accident plume.

According to World Health Organization guidelines (WHO/SDE/PHE/99.6), the reference level for consideration in stable iodine prophylaxis is based on the inhalation exposure pathway. In the western trace of the Chernobyl accident, the measurement of airborne (131)I fractions (aerosol-associated, gaseous reactive and gaseous organic) indicates that airborne gaseous reactive and, especially, organic (131)I fractions were the major contributors to thyroid exposure due to inhalation. The contribution of inhaled short-lived radioiodines was negligible. To attain more precise thyroid exposure evaluation, (131)I dose factors were determined as a function of age and prevalence of stable iodine deficiency. The results demonstrate that children with a stable iodine deficiency experienced at least two times higher thyroid doses than did children with a dietary iodine sufficiency. The results of these investigations demonstrate that in thyroid dosimetry it is important to know the stable iodine status as well as to have a standardised method for airborne radioiodine measurements, especially for consideration of stable iodine prophylaxis based on the inhalation exposure pathway.

Adolescent↗

PubMed2002

Aniline-induced methemoglobinemia in dogs: pitfalls of route-to-route extrapolations.

Two groups of four beagle dogs each were exposed head-only to aniline vapor in concentrations of 155 or 174 mg/m(3) air for a duration of 4 h in order to attain a targeted total exposure dose of approximately 15 mg aniline/kg body weight. One group of dogs received this calculated dose also by gavage. Dose estimates were made either by the determination of aniline-serum albumin adducts or by repeated measurements of the respiratory minute volume during the inhalation exposure period. The magnitude of methemoglobin (MetHb) produced following each route served as the basis for comparison. MetHb levels were maximal at the end of the inhalation exposure period, attaining approximately 5%, whereas administration by gavage produced a maximum MetHb response of 26%. Measurements of respiratory minute volumes in individual dogs appear to suggest that variability in MetHb formation depends solely on the rate of uptake (ventilation). The concentration of aniline-serum albumin adducts and the extent of MetHb formation showed a nonproportional relationship. In summary, this study demonstrates that for aniline, an agent known to be bioactivated by a hepatic first-pass metabolism, the conversion of findings obtained from oral dosing to inhalation exposure concentrations is subject to overestimating dramatically the magnitude of MetHb formation likely to occur following inhalation exposure. As to whether the fivefold lower potency by inhalation is solely related to the hepatic first-pass bioactivation, to the rate of delivery, or to a less than 100% retention of the inhaled vapor within the respiratory tract remains to be elucidated. This study demonstrates some of the pitfalls that can occur in context with route-to-route extrapolations and reinforces many of the concerns related to such extrapolations.

Administration, Inhalation↗

PubMed2003

Altered surfactant protein A gene expression and protein metabolism associated with repeat exposure to inhaled endotoxin.

Chronically inhaled endotoxin, which is ubiquitous in many occupational and domestic environments, can adversely affect the respiratory system resulting in an inflammatory response and decreased lung function. Surfactant-associated protein A (SP-A) is part of the lung innate immune system and may attenuate the inflammatory response in various types of lung injury. Using a murine model to mimic occupational exposures to endotoxin, we hypothesized that SP-A gene expression and protein would be elevated in response to repeat exposure to inhaled grain dust and to purified lipopolysaccharide (LPS). Our results demonstrate that repeat exposure to inhaled endotoxin, either in the form of grain dust or purified LPS, results in increased whole lung SP-A gene expression and type II alveolar epithelial cell hyperplasia, whereas SP-A protein levels in lung lavage fluid are decreased. Furthermore, these alterations in SP-A gene activity and protein metabolism are dependent on an intact endotoxin signaling system.

Animals↗

PubMed1989

Influence of experimental pulmonary emphysema on the toxicological effects from inhaled nitrogen dioxide and diesel exhaust.

This project examined the influence of preexisting, experimentally induced pulmonary emphysema on the adverse health effects in rats of chronic inhalation exposure to either nitrogen dioxide or automotive diesel-engine exhaust. Previous reports indicated that humans with chronic lung disease were among those most severely affected by episodic exposures to high concentrations of airborne toxicants. There were no previous reports comparing the effects of chronic inhalation exposure to components of automotive emissions in emphysematous and normal animals. The hypothesis tested in this project was that rats with preexisting pulmonary emphysema were more susceptible than rats with normal lungs to the adverse effects of the toxicant exposures. Young adult rats were housed continuously in inhalation exposure chambers and exposed seven hours per day, five days per week, for 24 months to nitrogen dioxide at 9.5 parts per million (ppm)2, or to diesel exhaust at 3.5 mg soot/m3, or to clean air as control animals. These concentrations were selected to produce mild, but distinct, effects in rats with normal lungs. Pulmonary emphysema was induced in one-half of the rats by intratracheal instillation of the proteolytic enzyme elastase six weeks before the toxicant exposures began. Health effects were evaluated after 12, 18, and 24 months of exposure. The measurements included respiratory function, clearance of inhaled radiolabeled particles, pulmonary immune responses to instilled antigen, biochemistry and cytology of airway fluid, total lung collagen, histopathology, lung morphometry, and lung burdens of diesel soot. The significance of influences of emphysema and toxicant exposure, and interactions between influences of the two treatments, were evaluated by analysis of variance. The elastase treatment resulted in pulmonary emphysema that was manifested by enlarged alveoli and alveolar ducts, and by ruptured alveolar septa. There was no accompanying inflammation and no alterations of bronchioles. The emphysema persisted throughout the study period, with little evidence of progression. Lung weight was increased, physiological lung volumes were enlarged, lung compliance was increased, and airflow was obstructed. Nitrogen dioxide exposure of normal rats caused mild epithelial hyperplasia and a thickening of the walls of terminal bronchioles, an extension of bronchiolar epithelium into proximal alveoli, and inflammation in proximal alveoli. Lung volume and weight and the lung collagen content were increased. Airway fluid indicators of cell damage and oxidant protective mechanisms were increased. Similar effects of nitrogen dioxide exposure were superimposed over the effects of emphysema in emphysematous nitrogen dioxide-exposed rats. Several parameters were affected similarly by nitrogen dioxide exposure and emphysema (for example, increased lung volume), and the combined effects tended to be additive.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1984

Follow-up of the antihemolytic effect of toluene inhalation in rats.

The antihemolytic effects of toluene were studied with inhalation exposures in vivo. At a concentration of 2000 ppm the effect seemed to begin 0.5 h after the onset of exposure, and it ended completely 0.5 h after the end of the exposure. There was no significant change in the mean corpuscular volume (MCV), although it increased at first during and also following the exposure. The antihemolytic effect of different toluene concentrations was also tested with inhalation exposures. The inhalation of 300-2000 ppm of toluene caused a significant antihemolytic effect in a 1-h exposure, but it did not change the MCV. The greatest antihemolytic effect was obtained with a concentration of 1500 ppm of toluene. Our results confirm the assumption that the effect of toluene as a membrane-stabilizing agent is a reversible phenomenon that requires the presence of the agent molecules during the hemolytic process. The antihemolytic effect does not seem to be caused by an increase in the MCV.

Animals↗

PubMed1990

Circulating factors that modify lung cell DNA synthesis following exposure to inhaled oxidants. II. Effect of serum and lavage on lung pneumocytes following exposure of adult rats to 1 ppm ozone.

Adult rats were exposed to 1 ppm (1.96 mg/m3) ozone or air for 2 wk. Animals were sacrificed at 3, 5, 7, or 14 d after the onset of exposure, and samples of plasma and lung lavage were obtained. Heat-inactivated plasma and lavage from animals exposed to ozone for 5 or 7 d significantly increased DNA synthesis by lung pneumocytes compared with plasma or lavage from air-exposed animals. Fractionation of plasma and lavage samples indicated that the factor responsible had an isoelectric point of 6.45-6.75, and a molecular weight of 38 +/- 3 kDa. This factor has a dose-dependent effect on lung pneumocyte DNA synthesis in culture. It has no effect on cultured fibroblast DNA synthesis, and is distinct from a previously described factor in the plasma of these ozone-exposed animals that enhances fibroblast DNA synthesis. The factor is detectable within 5 d of exposure, and may hold some promise as a marker of early oxidant lung injury.

Administration, Inhalation↗

PubMed1991

Evidence for the disruption of the bone marrow microenvironment by combined exposures to inhaled benzene and ingested ethanol.

Studies have been performed to investigate the effects of combined in vivo exposures to inhaled benzene and ingested ethanol on the earliest known murine erythropoietic precursor cells, the Burst Forming Unit--Erythroid (BFU-E) and the Colony Forming Unit--Erythroid (CFU-E). Previously we had determined that murine erythropoietic cell populations were particularly susceptible to combined benzene + ethanol treatments. The most striking example of erythropoietic disruption was the transient appearance of large numbers of nucleated red cells (normoblasts) in the circulating blood. In the present studies, male C57Bl/6 mice were exposed to 300 ppm benzene via inhalation for 6 h/d x 5 d/wk x 9 wks. Groups of mice were also exposed to 5% ethanol in the drinking water 4 d/wk x 9 wks. Appropriate controls were also maintained. The hematological assays were performed after 1, 4, and 9 weeks of exposure. After 4 weeks of exposure large numbers of normoblasts appeared in the circulating blood of mice exposed to benzene + ethanol. However, there were no corresponding increases in the numbers of the earliest erythroid progenitor cells in the bone marrow. There were, however, marked increases in the numbers of these cells in the spleen. Previous work in this laboratory had confirmed that the marrow was the source of circulating normoblasts among animals exposed to benzene + ethanol. We conclude, therefore, that circulating normoblasts appear in the peripheral blood because of changes in the bone marrow microenvironment rather than as a consequence of increased erythropoietic proliferation in the marrow.

Administration, Inhalation↗