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PubMed1992

Morphology of nasal lesions induced in Osborne-Mendel rats and B6C3F1 mice by chronic inhalation of allyl glycidyl ether.

Chronic (24-month) inhalation exposure to 5 or 10 ppm allyl glycidyl ether (AGE) induced nasal lesions in Osborne-Mendel rats and B6C3F1 mice. Inflammation, degeneration, regeneration, metaplasia, hyperplasia, and neoplasia were observed in the nasal mucosa. Squamous metaplasia and hyperplasia of the respiratory epithelium and degeneration and regeneration with subsequent squamous and/or respiratory metaplasia of the olfactory epithelium were observed in many AGE-exposed animals. Three primary nasal neoplasms (1 papillary adenoma, 1 squamous cell carcinoma, and 1 olfactory epithelial carcinoma) were observed in rats exposed to 10 ppm AGE, and 1 nasal papillary adenoma was observed in a rat exposed to 5 ppm. Four papillary adenomas and 2 hemangiomas were observed in the noses of mice exposed to 10 ppm AGE. Although the incidence of primary nasal tumors in AGE-exposed rats or mice was not statistically significant compared to the incidence in concurrent controls, the relative rarity of primary nasal tumors in historical controls and the concurrent presence of metaplastic and hyperplastic nasal lesions similar to those reported to be associated with induced tumors of nasal epithelia by other chemicals suggest that the nasal tumors observed may be related to AGE exposure. It was concluded that, in addition to lesions indicating a toxic effect on the nasal mucosa, inhalation exposure to AGE for 24 months resulted in some evidence of carcinogenicity of AGE for male mice, equivocal evidence of carcinogenicity for female mice and male rats, and no evidence of carcinogenicity for female rats.

Administration, Inhalation↗
PubMed2002

Biotransformation of 1,1,1,3,3-Pentafluoropropane (HFC-245fa).

1,1,1,3,3-Pentafluoropropane (HFC-245fa) is being developed as a CFC substitute. 1,1,1,3,3-Pentafluoropropane has a low potential for toxicity: the only remarkable toxic effect seen in rats after inhalation exposure to 1,1,1,3,3-pentafluoropropane in concentrations of up to 50,000 ppm for 90 days was an increased incidence of diffuse myocarditis. To elucidate the possible role of biotransformation in 1,1,1,3,3-pentafluoropropane-induced cardiotoxicity, the biotransformation of 1,1,1,3,3-pentafluoropropane was investigated in rats after inhalation exposure and in rat and human liver microsomes. Male and female rats were exposed by inhalation to 50 000, 10 000, and 2000 ppm 1,1,1,3,3-pentafluoropropane for 6 h, urine was collected for 72 h, and metabolites excreted were identified by 19F NMR spectroscopy and quantified by GC/MS. Trifluoroacetic acid and inorganic fluoride were identified as major urinary metabolites of 1,1,1,3,3-pentafluoropropane; 3,3,3-trifluoropropanoic acid and 1,1,1,3,3-pentafluoropropane-2-ol were minor metabolites. The extent of 1,1,1,3,3-pentafluoropropane biotransformation after inhalation was dependent on exposure concentrations. Neither 3,3,3-trifluoropropanoic acid nor 3,3,3-trifluoropyruvic acid were metabolized to trifluoroacetic acid in vitro or in rats. In rat and human liver microsomes, 1,1,1,3,3-pentafluoropropane was biotransformed by a cytochrome P450-dependent reaction to trifluoroacetic acid and 3,3,3-trifluoropropanoic acid. Rates of trifluoroacetic acid formation were 99.2 +/- 20.5 pmol (mg of protein)(-)(1) min(-)(1) and of 3,3,3-trifluoropropanoic acid formation were 17.5 +/- 4.0 pmol (mg of protein)(-)(1) min(-)(1) in liver microsomes from male rats. In human liver microsomes, rates of trifluoroacetic acid formation ranged from 0 to 11.6 pmol (mg of protein)(-)(1) min(-)(1), and rates of 3,3,3-trifluoropropanoic acid formation ranged from 0.7 to 7.6 pmol (mg of protein)(-)(1) min(-)(1). The results show that 1,1,1,3,3-pentafluoropropane is metabolized at low rates in vivo and in vitro. The toxic effects of 1,1,1,3,3-pentafluoropropane may be associated with the formation of the minor metabolite 3,3,3-trifluoropropanoic acid, which is highly toxic in rats.

Administration, Inhalation↗
PubMed2001

Variations in exposure to inhalable wood dust in the Danish furniture industry. Within- and between-worker and factory components estimated from passive dust sampling.

Variability of exposure to wood dust at large factories in the Danish furniture industry was studied. Three repeated exposure measurements of 292 workers at 38 factories were included in the study. The measurements were carried out by use of personal passive dust monitors. The components of variance were estimated by means of a random effects ANOVA model. The ratio of within- to between-worker variance was 1.07. Based on this result, and three repeated exposure measurements, the observed relation between health outcome and exposure will be attenuated to 74% of the true value. Grouping by factory showed very poor exposure contrast, as the contrast in exposure level among factories was as low as 0.15.

Air Pollutants, Occupational↗
PubMed2001

Health-risk assessment for workers exposed to polycyclic aromatic hydrocarbons (PAHs) in a carbon black manufacturing industry.

This study was established to assess workers' health-risks posed by PAHs exposures via both routes of inhalation and dermal contact. Personal inhalation exposure sampling was conducted on eight wet pelletizing workers and 22 packaging workers, by using a sampling train comprising an IOM personal inhalable aerosol sampler followed by an XAD-2 sorbent tube. Two workers were randomly selected from both exposure groups, and dermal exposures assessed by using soft polypropylene pads attached to the skin for nine different body surface areas for each selected worker. All personal inhalation and dermal samples were analyzed for 21 polycyclic aromatic hydrocarbon (PAH) species, and then converted to benzo[a]pyrene equivalent (BaPeq) concentrations by using the list of toxic equivalent factors (TEFs) suggested by Nisbet and LaGoy [Regul Toxicol Pharmocol 16 (1992) 290]. The resultant inhalation and dermal BaPeq exposure levels were used to estimate lifetime risks for lung cancer and skin cancer by using the BaP unit risks of 7.0 x 10(-2) (microg/m3)(-1) and 37.47(mg/kg bodyweight/day)(-1), respectively. Results show the personal inhalation BaPeq exposure levels for pelletizing and packaging workers were 622 and 774 ng/m3, respectively. The corresponding lifetime lung cancer risks estimated for both exposure groups were 4.35 x 10(-2) and 5.42 x 10(-2) respectively. For dermal exposures, results show personal dermal BaPeq exposure levels for both exposure groups were 0.664 and 0.847 microg/kg per day, respectively. The corresponding estimated lifetime skin cancer risks were 1.13 x 10(-3) and 1.56 x 10(-3), respectively. Although the estimated skin cancer risks were lower than the corresponding lung cancer risks for both exposure groups, however, both were higher than the designated significant risk level (= 10(-3)) which was defined by the US Supreme Court in 1980. Considering the bioavailability of particle-bound PAHs still remains unknown, the health risks obtained from this study could be overestimated and thus require further investigation.

Administration, Cutaneous↗
PubMed1996

Acute exposure to carbon monoxide does not affect plasma lipids, lipoproteins, and apolipoproteins.

STUDY OBJECTIVES: To examine the effects of acute exposure to carbon monoxide and hypoxia on plasma lipids, lipoproteins, and apolipoproteins. DESIGN: Random-order assignment to blinded, inhaled exposures of carbon monoxide and hypoxia. SETTING: Research laboratory of ambulatory subjects. SUBJECTS: 10 elderly, male nonsmokers with chronic stable angina. INTERVENTION: Random-order two-hour inhaled exposure to clean air at sea level, carbon monoxide at sea level, carbon monoxide at high altitude, and clean air at high altitude. MEASUREMENTS: Fasting plasma lipids, lipoproteins, and apolipoproteins before and after exposures. RESULTS: No differences were noted between fasting plasma lipid, lipoprotein, or apolipoprotein levels before and after exposures. CONCLUSION: Acute exposure to carbon monoxide and high altitude does not affect fasting plasma lipid, lipoprotein, or apolipoprotein levels.

Aged↗
PubMed2000

Occupational exposure to inhaled anesthetic. Is it a concern for pregnant women?

QUESTION: Two of my pregnant patients are exposed to inhaled anesthetic on the job. One is an anesthetist, and the other is a veterinarian. They have both expressed concern about this exposure. How should I advise them? ANSWER: Occupational exposure to waste anesthetic gas is not associated with increased risk of major malformations. Risk of spontaneous abortion might be slightly increased, however. This risk can be reduced, if not eliminated, by good gas scavenging systems.

Abortion, Spontaneous↗
PubMed1999

Zinc exposure in Chinese foundry workers.

BACKGROUND: Inhalational exposure to zinc oxide fumes is associated with metal fume fever, a self-limited but very uncomfortable condition closely resembling influenza. Very little is known regarding the toxicokinetics of inhaled zinc, making the interpretation of zinc measurements in serum and urine problematic. METHODS: Twenty workers in a zinc foundry in Baiyin, Peoples' Republic of China, were investigated with serial examinations by a physician, chest radiographs, and spirometry. Exposure assessment consisted of the measurement of zinc in serum, urine, and personal air samples. RESULTS: No cases of metal fume fever were observed during the study period despite exposures to as high as 36.3 mg/m3 over less than 4 hr. In addition, no radiographic or functional changes were noted. Serum zinc levels of all workers were within the reference range and did not correlate with external exposure measurements. However, elevations were noted in urinary zinc levels, which showed a significant association (Spearman's correlation coefficient = 0.47, P = 0.04) between exposure to zinc and urine zinc. CONCLUSIONS: These results provide exposure measurements for zinc at which workers demonstrate tolerance to the development of metal fume fever. Furthermore, they suggest that urine may be the preferred biological medium for the assessment of zinc exposure.

Adult↗
PubMed2004

Assessment of bronchial responsiveness following exposure to inhaled occupational and environmental agents.

Inhalation of a range of agents can result in airway inflammation and/or irritation. This may result in occupational asthma or reactive airways dysfunction syndrome. Reactive airways dysfunction syndrome follows a single large exposure to a chemical agent but is now frequently embraced under the wider term of irritant-induced asthma, a term that also includes asthma due to persistent, lower dose irritant exposures. Bronchial hyperresponsiveness is a hallmark of both occupational asthma and reactive airways dysfunction syndrome, although some patients with occupational asthma may occasionally have typical clinical features without increased bronchial hyperresponsiveness. Following removal of the causal agent in occupational asthma, bronchial hyperresponsiveness generally returns towards normal over a 2-year period, although some individuals demonstrate increased bronchial hyperresponsiveness for longer. Measurement of specific bronchial hyperresponsiveness to the primary causal agent in occupational asthma is used diagnostically but not for assessing prognosis. Bronchial hyperresponsiveness to inhaled methacholine can be measured across individual workshifts to assess work-related change. It may also be measured at the end of a work period when exposure has occurred, and compared with values following a period away from work. There have been no direct, systematic comparisons of changes in methacholine responsiveness in the diagnosis of occupational asthma compared with the more frequently used serial peak flow measurements. Patients with reactive airways dysfunction syndrome classically exhibit non-specific bronchial hyperresponsiveness, which can be readily measured by evaluating responses to inhaled methacholine. Bronchial hyperresponsiveness in reactive airways dysfunction syndrome can persist for many years after initial exposure and serial changes can be used to assess recovery and subsequent disability over time.

Administration, Inhalation↗
PubMed1994

Assessment of respiratory hypersensitivity in guinea-pigs sensitized to diphenylmethane-4,4'-diisocyanate (MDI) and challenged with MDI, acetylcholine or MDI-albumin conjugate.

Guinea-pigs were sensitized to monomeric diphenylmethane-4,4'-diisocyanate (MDI) by two intradermal injections (1-10% MDI, injection volumes of 50-100 microliters/day, on days 0, 2 and 4) or by a single brief high-concentration inhalation exposure (135 or 360 mg/m3, 15 min). Starting with day 21 following sensitization the animals were subjected to inhalation-challenge exposures (30 min) with non-irritating and irritating concentrations of the hapten (MDI). MDI-challenge concentrations ranged from 3.4 +/- 0.9 to 60 +/- 14.3 mg/m3 air. In some groups guinea-pigs were also challenged with acetylcholine (ACh) aerosol or the MDI-guinea pig serum albumin (GPSA) conjugate. Experimental findings indicated that from intradermally sensitized animals an immediate onset respiratory hypersensitivity response could only be elicited with concentrations exceeding the irritant threshold concentration for MDI, i.e. with concentrations greater than approximately 20 mg/m3 air. Guinea-pigs challenged with the MDI-GPSA conjugate (35.3 +/- 2.8 mg/m3 air) also experienced a weak immediate-type respiratory hypersensitivity response. An increased non-specific airway hyper-responsiveness following ACh-challenge was only observed from animals challenged with approximately 60 mg MDI/m3 air. The histopathological evaluation of lungs and lung-associated lymph nodes revealed an association of the increase in eosinophilic granulocytes and concentration of MDI used for challenge exposures. It appeared, in most instances, that this influx was more pronounced in animals sensitized with MDI as compared with concurrent controls challenged with the same MDI concentration. Guinea-pigs sensitized by a single 15-min inhalation exposure to either 135 or 360 mg MDI/m3 air were challenged sequentially with 12 +/- 2.1 mg MDI/m3 air, ACh and MDI-GPSA conjugate. Following the inhalation-induction, an airway hyper-responsiveness was elicited both after challenge with MDI and with the MDI-GPSA conjugate. The influx of eosinophilic granulocytes was more pronounced from animals sensitized by inhalation when compared with guinea-pigs sensitized intradermally and challenged with the same concentration of MDI. Thus, experimental findings suggest that elicitation of respiratory hypersensitivity is concentration-dependent and that challenge concentrations should slightly exceed the threshold concentration for irritation (approximately 20 mg/m3). Sensitization by inhalation increased the susceptibility to irritant stimuli and thus confounds the selection of the most appropriate concentration for challenge. However, the combined assessment of specific pathologic features such as airway eosinophilia and the evaluation of several breathing parameters during hapten- and ACh-challenge make it easier to distinguish effects caused by irritation and respiratory hypersensitivity.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1996

Cardiac sensitization thresholds of halon replacement chemicals predicted in humans by physiologically-based pharmacokinetic modeling.

Human exposure to halons and halon replacement chemicals is often regulated on the basis of cardiac sensitization potential. The dose-response data obtained from animal testing are used to determine the no observable adverse effect level (NOAEL) and lowest observable adverse effect level (LOAEL) values. This approach alone does not provide the information necessary to evaluate the cardiac sensitization potential for the chemical of interest under a variety of exposure concentrations and durations. In order to provide a tool for decision-makers and regulators tasked with setting exposure guidelines for halon replacement chemicals, a quantitative approach was established which allowed exposures to be assessed in terms of the chemical concentrations in blood during the exposure. A physiologically-based pharmacokinetic (PBPK) model was used to simulate blood concentrations of Halon 1301 (bromotrifluoromethane, CF3Br), HFC-125 (pentafluoroethane, CHF2CF3), HFC-227ea (heptafluoropropane, CF4CHFCF3), HCFC-123 (dichlorotrifluoroethane, CHCl2CF3), and CF3I (trifluoroiodomethane) during inhalation exposures. This work demonstrates a quantitative approach for use in linking chemical inhalation exposures to the levels of chemical in blood achieved during the exposure.

Administration, Inhalation↗
PubMed1985

The acute effects of cigarette smoke exposure on experimental skin flaps.

Random vascular patterned caudally based McFarlane-type skin flaps were elevated in groups of Fischer 344 rats. Groups of rats were then acutely exposed on an intermittent basis to smoke generated from well-characterized research filter cigarettes. Previously developed smoke inhalation exposure protocols were employed using a Maddox-ORNL inhalation exposure system. Rats that continued smoke exposure following surgery showed a significantly greater mean percent area of flap necrosis compared with sham-exposed groups or control groups not exposed. The possible pathogenesis of this observation as well as considerations and correlations with chronic human smokers are discussed. Increased risks of flap necrosis by smoking in the perioperative period are suggested by this study.

Animals↗
PubMed1992

Silica-induced pulmonary inflammation and fibrosis in mice is altered by acute exposure to nitrogen dioxide.

The biologic impact of consecutive exposures to two environmental pollutants was examined in mice exposed to silica crystals (SI) by intratracheal (IT) injection followed by an inhalation exposure to nitrogen dioxide (NO2). C57Bl/6 mice received an IT injection of 2 mg SI or sterile saline (SAL) followed by a 2-h inhalation exposure to NO2 at 20 ppm either within 2 h of or 24 h after SI instillation. During acute inflammation (d 3 postsilica), mice exposed to NO2 at either time showed a dramatic and significant reduction in the number of lavaged alveolar neutrophils (PMN) when compared to silica/air-exposed mice. Animals exposed to NO2 24 h after silica also evidenced significant decreases in levels of lavage albumin and lactate dehydrogenase (LDH) 3 d after silica, as well as significant decreases in hydroxyproline content of the lung 30 and 60 d postsilica injection when compared to silica/air-exposed animals. NO2 administration 24 h after silica appeared to shift the appearance of PMN in the lung from d 3 to d 14, but did not otherwise alter chronic cellular inflammation. These data suggest that the marked neutrophil response and collagen deposition induced by SI can be modulated by NO2 exposure and that the time of oxidant gas exposure after silica administration is critical to this modulation.

Acute Disease↗
PubMedDate not supplied

Toxicologic and carcinogenic effects of the type IV phosphodiesterase inhibitor RP 73401 on the nasal olfactory tissue in rats.

RP 73401, a type IV phosphodiesterase inhibitor, caused toxic effects in the nasal olfactory region of Sprague-Dawley rats when administered by either oral or inhalation exposure. A single oral administration of RP 73401 (at a dose of > or = 50 mg/kg) or 5-day inhalation exposure (1 hr/day) at a dose of approximately 1.0 mg/kg per day caused degeneration and sloughing of the olfactory surface epithelium. Degeneration and loss of Bowman's glands were noted in the underlying lamina propria and submucosa. Electron microscopy of these lesions demonstrated that sustentacular cells and the epithelial cells lining Bowman's glands were the primary target cells in the olfactory mucosa. The earliest ultrastructural changes detected in these cells were dilatation and vesiculation of the endoplasmic reticulum, suggesting that metabolic activation is important for the toxic effects. In repeated-dose studies, 13 wk of oral dosing at 2.0 or 6.0 mg/kg per day resulted in subtle disorganization of the olfactory epithelium, whereas basal cell hyperplasia in the olfactory epithelium was identified in a 6-month inhalation study at a dose of 1.0 mg/kg per day. A 2-yr inhalation carcinogenicity study resulted in tumors of the nasal olfactory region in rats treated at 0.5 and 1.0 mg/kg per day. Most tumors were classified as olfactory neuroblastomas, and immunohistochemistry on selected tumors was consistent with their being of neuroectodermal origin. Of the species studied (rat, mouse, and dog), the olfactory toxicity of RP 73401 was confined to the rat, and the toxicity was likely related to metabolic activation by olfactory epithelial cells rather than the phosphodiesterase activity of the compound.

Administration, Inhalation↗
PubMed2003

Scientific principles and pragmatic solutions for the measurement of exposure to inhalable dust.

In order to understand and control the risks presented by inhalation of dust at work, research over many years has been focused on understanding how dust present in the air enters the human nose and mouth during the act of breathing. For health-related dust exposure monitoring, sampling devices are needed that collect the same 'inhalable fraction' of dust as the human head. Mark and Vincent's 1986 paper presented a study that has contributed more than any other to the practical realization of this inhalable dust concept. The authors developed a simple solution--the IOM personal inhalable dust sampler--to what we now know is an extremely complex problem. Although scientific understanding has grown in the years since this paper was published, very few other dust sampling instruments have emerged as being able to meet both the scientific criteria and the practical need for inhalable dust measurement. Both authors have continued to build on this work and have made further contributions to our theoretical and practical understanding in this field.

Air Pollutants, Occupational↗
PubMed1986

A method for direct measurement of systemic uptake and elimination of volatile organics in small animals.

A method was developed which was suitable for toxicokinetic studies requiring direct, repetitive sampling of blood and breath during exposures of small animals to volatile chemicals. Anesthetized male Sprague-Dawley rats were tracheostomized, and a specially fabricated one-way breathing valve was inserted directly into the trachea, in order that the inhaled and exhaled breath streams could be separated and independently sampled. The desired concentration of 1,1,1-trichloroethane was generated in a gas sampling bag, which was connected to the inlet side of the valve for inhalation exposures. Rats dosed with 1,1,1-trichloroethane by gavage inhaled ambient air through the valve. A pneumotachograph was positioned in the influent air stream to measure respiration. Respiratory rate, minute volume, and core temperature were continuously recorded on a physiograph. Samples of inspired and expired air were periodically collected from sampling ports immediately adjacent to the breathing valve and were analyzed for their 1,1,1-trichloroethane content by gas chromatography. Using this system, it was possible to determine percentage systemic uptake at any given time and to monitor cumulative uptake (i.e., total dose received) over the course of inhalation exposures. Alveolar concentrations were calculated by taking into account the respiratory indexes and dead space volume. A femoral vein was cannulated, so that concentrations of the chemical in the blood and breath could be measured concurrently. Data from rats dosed orally and by inhalation with 1,1,1-trichloroethane are presented to illustrate the applicability of the method in kinetics studies of volatile chemicals.

Administration, Inhalation↗
PubMed1985

Air monitoring at the drum bulking process of a hazardous waste remedial action site.

Air monitoring was performed at a hazardous waste remedial action site to measure inhalation exposure at the drum bulking unit processes and ambient emissions downwind from that process. Contaminant concentrations were all well below permissible exposure limits. This study suggests that when workers remain in fixed job locations at hazardous waste sites, occupational inhalation exposure monitoring must consider contaminants generated upwind of the job location as well as contaminants generated at the specific job site. Air sampling must also consider both the particulate and vapor phases of the site contaminants.

Air↗
PubMed2003

Increased susceptibility to RSV infection by exposure to inhaled diesel engine emissions.

Although epidemiologic data strongly suggest a role for inhaled environmental pollutants in modulating the susceptibility to respiratory infection in humans, the underlying cellular and molecular mechanisms have not been well studied in experimental systems. The current study assessed the impact of inhaled diesel engine emissions (DEE) on the host response in vivo to a common pediatric respiratory pathogen, respiratory syncytial virus (RSV). Using a relatively resistant mouse model of RSV infection, prior exposure to either 30 microg/m3 particulate matter (PM) or 1,000 microg/m3 PM of inhaled DEE (6 h/d for seven consecutive days) increased lung inflammation to RSV infection as compared with air-exposed RSV-infected C57Bl/6 mice. Inflammatory cells in bronchoalveolar lavage fluid were increased in a dose-dependent manner with regard to the level of DEE exposure, concomitant with increased levels of inflammatory mediators. Lung histology analysis indicated pronounced peribronchial and peribronchiolar inflammation concordant with the level of DEE exposure during infection. Mucous cell metaplasia was markedly increased in the airway epithelium of DEE-exposed mice following RSV infection. Interestingly, both airway and alveolar host defense and immunomodulatory proteins were attenuated during RSV infection by prior DEE exposure. DEE-induced changes in inflammatory and lung epithelial responses to infection were associated with increased RSV gene expression in the lungs following DEE exposure. These findings are consistent with the concept that DEE exposure modulates the lung host defense to respiratory viral infections and may alter the susceptibility to respiratory infections leading to increased lung disease.

Animals↗