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Carbon disulphide exposure affects the response of rat adrenal medulla to hypothermia and hypoglycaemia.

The effects of hypothermia and hypoglycaemia on adrenal catecholamines and dopamine-beta-hydroxylase were compared in control and carbon disulphide (CS2) exposed rats 24 h after the last of ten daily 4 h inhalation exposures to CS2, 2 mg 1(-1) air. Animals were either kept in a cold room (0 degrees C) for 210 min with or without immobilization or were injected with insulin 100 u kg-1. Before these treatments CS2 exposed rats had more dopamine and less adrenaline in their adrenals than controls, and CS2 exposure also elevated the adrenal synthesis of catecholamines. Cold with immobilization or insulin treatment depressed the adrenal adrenaline content and increased the plasma concentrations of noradrenaline and adrenaline. There were no consistent differences between control and CS2 exposed rats. The adrenal dopamine content increased during cold exposure with immobilization or after insulin treatment both in CS2 exposed and control rats. The increase was smaller in CS2 exposed rats but the final dopamine values were nearly identical in the two groups. Exposure to cold (without immobilization) increased the adrenal dopamine content and the rate of catecholamine synthesis in control, but not in CS2 exposed rats. The increase in controls was less than the difference between the pre-cold exposure values of control and CS2 exposed rats. It is concluded that the elevation of adrenal dopamine content and catecholamine synthesis in CS2 exposed rats satisfy part of the demand placed on the adrenal medulla by hypothermia and hypoglycaemia. Consequently the changes induced by the latter treatments were smaller in CS2 exposed than in non-exposed rats. Moreover, when CS2 exposed rats were subjected to cold stress without immobilization their catecholamine synthesis was higher than the level measured in control rats after cold exposure.

3,4-Dihydroxyphenylacetic Acid↗

Acute, 2-week, and 13-week inhalation toxicity studies on dimethylethoxysilane vapor in Fischer 344 rats.

Dimethylethoxysilane (DMES), a volatile liquid, is used by NASA to waterproof the heat-protective silica tiles and blankets on the Space Shuttle. Acute, 2-wk, and 13-wk inhalation exposures to DMES vapor were conducted in male and female Fischer 344 rats. In the acute study, rats were exposed to 4000, 2000, 1000, 500, or 0 (control) ppm DMES for 4 h and observed for 14 days. There were no deaths. Narcosis and ataxia were observed in rats of the two highest concentrations only. These signs disappeared within 1 h following exposure. There were no DMES-related gross or microscopic tissue lesions in rats of all exposure groups. In the 2-wk study, rats were exposed for 6 h/day, 5 days/wk to 3000, 1000, 300, 100, or 0 ppm DMES. During exposure, narcosis was observed in rats of the 3000 and 1000 ppm groups. There was a mild decrease in body weight gain in rats of the 3000 ppm group. A decrease in platelet count, an increase in bile acids, and reduced weights of the thymus, testis, and liver were observed in rats of the 3000 ppm group. Microscopically, hypospermatogenesis and spermatid giant cells were observed in the seminiferous tubules of the testes of rats exposed to 3000 ppm DMES. In the 13-wk study, rats were exposed 6 h/day, 5 days/wk to 2000, 600, 160, 40, or 0 ppm DMES. During exposure, rats of the 2000 ppm group exhibited mild narcosis and loss of startle reflex. Recovery from these central nervous system signs was rapid. Body weights were mildly decreased for rats of the 2000 ppm group. There were no exposure-related effects in hematology, serum chemistry, or urinalysis. Female rats of the 2000 ppm group had delayed estrous cycles (6 days compared to 5 days in control rats). Noteworthy organ weight changes in rats of the 2000 ppm group included decreases in thymus, liver, and testicular weights; however, pathologic lesions were observed in the testes only. Sperm motility, epididymal sperm count, and testicular spermatid count were dramatically reduced. Microscopic lesions included degeneration of the seminiferous tubular cells, pyknosis or absence of germ cells, and hypospermia in the epididymis. Rats of the 600 ppm group had a slight decrease in thymic weight and a transient decrease in body weight. Results of the acute, 2-wk, and 13-wk inhalation studies indicate DMES concentrations of 1000 ppm and higher produce narcosis that rapidly disappears following exposure. Repeated exposure of rats to DMES at either 3000 ppm for 2 wk or 2000 ppm for 13 wk caused testicular atrophy and hypospermia in male rats. Female rats exposed to 2000 ppm for 13 wk had delayed estrous cycles. Toxicological effects in rats of the 600 ppm group were minimal and equivocal. The 160 ppm concentration was a no-observable-effect level (NOEL) for 13 wk of exposure to DMES.

Administration, Inhalation↗

A new dose model for assessment of health risk due to contaminants in air.

The problem of making quantitative assessments of the risks associated with human exposure to toxic contaminants in the environment is a pressing one. This study demonstrates the capability of a new computational technique involving the use of fuzzy logic and neural networks to produce realistic risk assessments. The systematic analysis of human exposure involves the use of measurements and models, the results of which are sometimes used in regulatory decisions or in the drafting of legislation. Because of limited scientific understanding, however, interpretation of models often involves substantial uncertainty. Extensive measurement programs can be very expensive. The high complexity and inherent heterogeneity of exposure analysis is still a major challenge. The approach to this challenge tested here is to use a new model incorporating sophisticated artificial intelligence algorithms. Exposure assessment often requires that a number of factors be evaluated, including exposure concentrations, intake rates, exposure times, and frequencies. These factors are incorporated into a system that can "learn" the relevant relationships based on a known data set. The results can then be applied to new data sets and thus be applied widely without the need for extensive measurements. In this analysis, an example is developed for human health risk through inhalation exposure to benzene from vehicular emissions in the cities of Auckland and Christchurch, New Zealand. Risk factors considered were inhaled contaminant concentration, age, body weight, and activity patterns of humans. Three major variables affecting the inhaled contaminant concentration were emissions (mainly from motor vehicles), meteorology (wind speed, temperature, and atmospheric stability), and site factors (hilly, flat, etc.). The results are preliminary and used principally to demonstrate the technique, but they are very encouraging.

Age Factors↗

Effects of inhalation and cutaneous exposure to styrene on drug metabolizing enzymes in the rat.

The effects of inhalation and cutaneous exposure to styrene on the drug metabolizing enzymes were studied in the rat. Rats were exposed eight hours per day, for seven successive days to 450 ppm concentration of styrene or received one cutaneous dose of styrene daily for seven consecutive days (0.5 and 3.0 g/kg). The animals were killed one day after the last dose. Styrene inhalation increased the activities of epoxide hydrase and UDPglucuronosyltransferase (4-methylumbelliferone as substrate) in liver (1.5- and 1.7-fold, respectively). Ethoxycoumarin deethylation was enhanced 1.7-fold in the kidney. The content of cytochrome P-450 in the liver and the activities of NADPH cytochrome c-reductase, benzpyrene hydroxylase and glutathione S-transferase in the liver and kidney were not altered. No changes in the enzyme activities were detected in the lung. Styrene depressed the epoxide hydrase activity in liver when administered cutaneously. No signs of enzyme induction could be seen after cutaneous administration.

Administration, Topical↗

NTP Toxicology and Carcinogenesis Studies of Dichloromethane (Methylene Chloride) (CAS No. 75-09-2) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

Dichloromethane is widely used in industrial processes, food preparation, and agriculture. In industry, dichloromethane is used as a solvent in paint removers, degreasing agents, aerosol propellants, and triacetate solutions; as a blowing agent in flexible urethane foams; and as a process solvent in the manufacture of steroids, antibiotics, vitamins, and tablet coatings. The use of dichloromethane as an extraction solvent for spice oleoresins, hops, and caffeine from coffee has been approved by the U.S. Food and Drug Administration. Dichloromethane has been used as an inhalation anesthetic and as a fumigant for grain and strawberries. Toxicology and carcinogenesis studies of dichloromethane (99% pure) were conducted by inhalation exposure of groups of 50 male and 50 female F344/N rats and B6C3F1 mice 6 hours per day, 5 days per week, for 102 weeks. The exposure concentrations used (0, 1,000, 2,000, or 4,000 ppm for rats and 0, 2,000, or 4,000 ppm for mice) were selected on the basis of results from 13-week inhalation studies in which groups of 10 rats and 10 mice of each sex were exposed to dichloromethane at concentrations of 525-8,400 ppm 6 hours per day, 5 days per week. During the 2-year studies in rats, body weight gains for exposed males and females were comparable to those of the chamber controls. The survival of exposed male rats was comparable to that of the chamber controls; however, the survival of all groups of males at the termination of the study was low (control, 16/50; low dose, 16/50; mid dose, 17/50; high dose, 9/50). Most of the early deaths among male rats occurred during the final weeks of the study; the survival of male rats through week 86 of the study was 36/50, 39/50, 37/50, and 33/50. This decreased survival is believed to be related to the high incidence of leukemia (34/50; 26/50; 32/50; 35/50). Survival of female rats exposed at 4,000 ppm was reduced relative to that of the chamber controls (30/50; 22/50; 22/50; 15/50); leukemia occurred frequently in all female rat groups. Final mean body weights of high dose male mice and low and high dose female mice were 10%-17% lower than those of the chamber controls; these reductions occurred during the last 16 weeks of the study. The survival of dosed male mice and high dose female mice was reduced relative to that of the chamber controls (male: control, 39/50; low dose, 24/50; high dose, 11/50; female: 25/50; 25/50; 8/50). This reduced survival may have been due to the chemically induced development of liver and lung neoplasia in male and female mice. Increased incidences of benign mammary gland lesions (adenomas and fibroadenomas) occurred in male and female rats exposed to dichloromethane (male: 0/50; 0/50; 2/50; 5/50; female: 5/50; 11/50; 13/50; 23/50). The incidence of malignant mammary gland neoplasms was not increased in female rats (2/50; 2/50; 2/50; 0/50); none was observed in male rats. In addition, integumentary system tumors in the area of the mammary chain occurred with a positive trend in male rats (subcutaneous tissue fibroma or sarcoma: 1/50; 1/50; 2/50; 5/50); the combined incidence of all tumors in the mammary area in male rats was 1/50, 1/50, 4/50, and 9/50. Exposure to dichloromethane was associated with increased incidences of hepatic hemosiderosis, cytomegaly, cytoplasmic vacuolization, necrosis, granulomatous inflammation, and bile duct fibrosis in both male and female rats. There was a positive but marginal trend in the incidence of hepatocellular neoplastic nodules or hepatocellular carcinomas (combined) in female rats (2/50; 1/50; 4/50; 5/50). The incidence of squamous metaplasia of the nasal cavity was increased in female rats exposed at 4,000 ppm (1/50; 2/50; 3/50; 9/50) but not in males (4/50; 5/50; 3/50; 3/50). No nasal cavity tumors were observed in rats. The increased incidences of mononuclear cell leukemia in mid dose and high dose female rats (17/50; 17/50; 23/50; 23/50) were statistically significant by age-adjusted analyses. In male rats, mesotheliomas (arising primarily from the tunica vaginalis) occurred at increas) occurred at increased incidences (0/50; 2/50; 5/50; 4/50). Lung tumors occurred at increased incidences in male and female mice exposed to dichloromethane (alveolar/bronchiolar adenomas: male - 3/50; 19/50; 24/50; female - 2/50; 23/48; 28/48; alveolar/bronchiolar carcinomas: male - 2/50; 10/50; 28/50; female - 1/50; 13/48; 29/48). Cytologic degeneration of the liver was observed at increased incidences in high dose male and dosed female mice (male: 0/50; 0/49; 22/49; female: 0/50; 23/48; 21/48). Incidences of hepatocellular adenomas or hepatocellular carcinomas (combined) were increased in high dose male and dosed female mice (male: 22/50; 24/49; 33/49; female: 3/50; 16/48; 40/48). There were also dose-related increases in the numbers of mice bearing multiple lung or liver neoplasms. Dose-related increases were observed in the incidences of testicular atrophy in male mice and uterine and ovarian atrophy in female mice; these effects are considered to be secondary responses to neoplasia. An audit of the experimental data was conducted for the 2-year studies of dichloromethane. No data discrepancies were found that influenced the final interpretations. Under the conditions of these inhalation studies, there was some evidence of carcinogenicity of dichloromethane for male F344/N rats as shown by an increased incidence of benign neoplasms of the mammary gland. There was clear evidence of carcinogenicity of dichloromethane for female F344/N rats as shown by increased incidences of benign neoplasms of the mammary gland. There was clear evidence of carcinogenicity of dichloromethane for male and female B6C3F1 mice, as shown by increased incidences of alveolar/bronchiolar neoplasms and of hepatocellular neoplasms. Synonyms: DCM; methylene chloride

Journal Article↗

Pulmonary toxicity of inhaled polypropylene fibers in rats.

This study was initiated to assess the pulmonary toxicity of a polyolefin fiber composed of polypropylene in male Fischer 344 rats after 90 days of inhalation exposure. To increase fiber respirability in the rodent, polypropylene fibers were size-selected before aerosolization to have a geometric mean diameter of 1.6 microns (46% < 1 micron) and a geometric mean length of 30.3 microns. Three groups of animals were exposed in nose-only inhalation chambers, 6 hr/day, 5 days/week, for 90 days to 15, 30, or 60 mg/m3 of polypropylene, or filtered air (negative control). Microscopic examination of the polypropylene fiber-exposed lungs revealed that, at all time points examined in the study, there was a dose-dependent increase in pulmonary macrophages. These minimal or mild increases in cellularity appeared to be reversible, especially at the lower doses 30 days post exposure. No fibrosis was observed in any of the groups. A strong correlation was found between the external exposure concentration, the time of exposure, and the lung fiber burden. The number of partially degraded (segmented) fibers within the lung increased with the exposure concentration and period of exposure, as well as with the period of recovery after termination of exposure at 90 days. Fibers were recovered from exposed lungs using a hypochlorite digestion technique.

Administration, Inhalation↗

Biotransformation of perchloroethene: dose-dependent excretion of trichloroacetic acid, dichloroacetic acid, and N-acetyl-S-(trichlorovinyl)-L-cysteine in rats and humans after inhalation.

Chronic exposure of rodents to perchloroethene (PER) increased the incidence of liver tumors in male mice and resulted in a small but significant increase in the incidence of renal tumors in male rats. The tumorigenicity of PER is mediated by metabolic activation reactions. PER is metabolized by cytochrome P450 and by conjugation with glutathione. Cytochrome P450 oxidation of PER results in trichloroacetyl chloride which reacts with water to trichloroacetic acid (TCA) which is excreted. The formation of S-(trichlorovinyl)glutathione (TCVG) from PER results in nephrotoxic metabolites. TCVG is cleaved to S-(trichlorovinyl)-L-cysteine (TCVC) and acetylated to N-acetyl-S-(trichlorovinyl)-L-cysteine (N-ac-TCVC), which is excreted with urine. TCVC is also cleaved in the kidney by cysteine conjugate beta-lyase to dichlorothioketene which may react with water to dichloroacetic acid (DCA) or with cellular macromolecules. The object of this study was to comparatively quantify the dose-dependent excretion of PER metabolites in urine of humans and rats after inhalation exposure. Three female and three male human volunteers and three female and three male rats were exposed to 10, 20, and 40 ppm PER for 6 h, and three female and three male rats to 400 ppm. A dose-dependent increase in the excretion of TCA and N-ac-TCVC after exposure to PER was found both in humans and in rats. A total of 20.4 +/- 7.77 mumol of TCA and 0.21 +/- 0.05 mumol of N-ac-TCVC were excreted in urine of human over 78 h after the start of exposure to 40 ppm PER; only traces of DCA were present. After identical exposure conditions, rats excreted 1.64 +/- 0.42 mumol of TCA, 0.006 +/- 0.002 mumol of N-ac-TCVC and 0.18 +/- 0.04 mumol of DCA. Excretion of N-ac-TCVC in male rats exposed to 400 ppm PER (103.7 nmol) was significantly higher, compared to female rats (31.5 nmol) exposed under identical conditions. N-ac-TCVC was rapidly eliminated with urine both in humans (t1/2 = 14.1 h) and in rats (t1/2 = 7.5 h). When comparing the urinary excretion of N-ac-TCVC, a potential marker for the formation of reactive intermediates in the kidney, humans received a significantly lower dose (3 nmol/kg at 40 ppm) compared to rats (23.0 nmol/kg) after identical exposure conditions. In addition, rats excreted large amounts of DCA which likely is a product of the beta-lyase-dependent metabolism of TCVC in the kidney. The obtained data suggest that glutathione conjugate formation and beta-lyase-dependent bioactivation of TCVC in PER metabolism is significantly higher in rats than in humans. Thus, using rat tumorigenicity data for human risk assessment of PER exposure may overestimate human tumor risks.

Acetylcysteine↗

Metabolism and pharmacokinetics of selected halon replacement candidates.

Metabolism studies were conducted using Fischer 344 and Sprague-Dawley rats following inhalation exposure to 1.0% (v/v) air atmospheres of 1,1-dichloro-2,2,2-trifluoroethane (HCFC-123), 2-chloro-1,1,1,2-tetrafluoroethane (HCFC-124), 1-chloro-1,1-difluoroethane (HCFC-142b), bromochlorodifluoromethane (Halon 1211), and perfluorohexane (PFH) for 2 h. There were no remarkable differences in results between the two strains of rats. Animals exposed to HCFC-123 or HCFC-124 excreted trifluoroacetic acid in their urine. Urinary fluoride concentrations were increased in rats exposed to HCFC-124, and urinary bromide levels were increased in rats exposed to Halon 1211. Small quantities of volatile metabolites 2-chloro-1,1,1-trifluoroethane (HCFC-133a) and 2-chloro-1,1-difluoroethylene were observed in the livers of rats exposed to HCFC-123. Rats exposed to HCFC-142b excreted chlorodifluoroacetic acid in their urine; no volatile metabolites were detected in tissue samples. For PFH studies, no metabolites were detected in the urine or tissues of exposed animals. These results are consistent with proposed oxidative and reductive pathways of metabolism for these chemicals. Pharmacokinetic studies were carried out in rats exposed by inhalation to 1.0%, 0.1%, or 0.01% of HCFC-123. Following exposure, blood concentrations of HCFC-123 fell sharply, whereas trifluoroacetic acid levels rose for approx. 5 h and then declined gradually. Using a physiologically based pharmacokinetic model, saturation of HCFC-123 metabolism was estimated to occur at approx. 0.2% (2000 ppm) HCFC-123.

Animals↗

Effects of acute exposure of toluene and methyl ethyl ketone on psychomotor performance.

Organic solvents are used frequently in industry and workers are often exposed to various combinations of these chemicals. Several are CNS depressants, and the purpose of this experiment was to assess the behavioral effects of 4-hour inhalation exposures to two solvents, toluene and methyl ethyl ketone (MEK) alone and combined. Ethanol at 0.08% blood levels was used as a positive control. A total of 144 paid volunteers were randomly assigned to one of eight treatment combinations in a series of four two-group between subjects studies. Testing was carried out in an exposure chamber, and participants were tested before, during, and after the treatment or control condition on three performance tasks. The tasks measured alertness and psychomotor function and produced a total of 28 measures on each individual over the approximate 8 h of testing. Results indicated that toluene at 100 ppm produced a small but significant impairment on one measure of a visual-vigilance task by lowering the percentage of correct hits. MEK at 200 ppm produced no interpretable significant effects on any of these measures. Additivity was not evident when individuals were exposed to MEK (100 ppm) and toluene (50 ppm) in combination, as no significant performance differences were noted. Ethanol, at 0.08%, affected both the visual-vigilance and a choice-reaction time task at statistically significant levels on two measures, confirming the sensitivity of these two tasks to CNS depressants.

Adolescent↗

A comparative study of biochemical changes induced by inhalation of aerosols of o-Chloroacetophenone & Dibenz (b,f)-1,4-oxazepine in rats.

The biochemical changes in blood samples of rats at different intervals after O-Chloroacetophenone (CN) and Dibenz (b,f)-1,4 oxazepine (CR) were studied. After a single subacute (1/10 LC50) exposure, both the compounds induced hyperglycaemia which was abolished within 24 h. The level of plasma urea was unaltered. CR exposed animals did not show any significant changes in plasma GOT, acid and alkaline phosphatase activities at different intervals. However, in CN exposed animals, a significant elevation of the activities of GOT, GPT, acid and alkaline phosphatase was observed at different intervals. All the parameters became normal within seven days after the exposure. Inhalation of CN aerosols can thus lead to tissue damaging effects in rats.

Aerosols↗

Changes in the rat lung after exposure to radon and its progeny: effects on incorporation of bromodeoxyuridine in epithelial cells and on the incidence of nuclear aberrations in alveolar macrophages.

The aim of this study was to investigate some responses of cells in the rat respiratory tract as a function of time after inhalation exposure to various levels of radon and its progeny. Rats were exposed to a constant concentration of radon and its progeny to give cumulative exposure levels of 120, 225, 440 and 990 working level months (WLM). An additional unexposed group of rats served as controls. The end points selected for investigation were (a) the incorporation of bromodeoxyuridine (BrdU) in epithelial cells of the conducting airways and of the alveolar region of the respiratory tract and (b) the incidence of alveolar macrophages with nuclear aberrations. After exposure, the incidence of epithelial cells incorporating BrdU--the labeling index--increased in all regions of the respiratory tract examined, but the increase occurred later in alveolar than in airway epithelial cells. The highest labeling index was found in bronchial epithelial cells, which probably received the highest radiation dose. After an initial induction period, the incidence of alveolar macrophages with nuclear aberrations also increased. The possibility of using the labeling index of alveolar and airway epithelial cells, and/or the incidence of nuclear aberrations in alveolar macrophages, to estimate the radiation dose to various regions of the respiratory tract after exposure of rats to radon and its progeny is discussed.

Animals↗

Validation of a non-invasive technique to assess immediate or delayed onset of airway hypersensitivity in guinea-pigs.

Conscious Hartley guinea-pigs were sensitized with trimellitic anhydride (TMA) or trimeric hexamethylene diisocyanate biuret (Des-N) by repeated intradermal injections or by inhalation exposure. Immediate- and delayed-onset pulmonary reactions were recorded during/after challenges with the hapten or protein conjugate of the hapten, respectively. The positive control was sensitized and challenged with ovalbumin (OA) by inhalation. Homocytotropic antibodies of the IgG1 type were determined to correlate antibody titres and pulmonary responses. Immediate-onset pulmonary reactions were apparent in guinea-pigs sensitized by inhalation of TMA and OA. Animals sensitized intradermally with TMA demonstrated more vigorous immediate-onset reactions than animals sensitized by inhalation. The measurement of breathing parameters demonstrated that the ability to detect immediate-onset airway hyperreactivity was best when the breathing rate and tidal and minute volumes were measured. None of the measurements for delayed-onset reactions presented conclusive results, since sensitized as well as naive guinea-pigs demonstrated a delayed increase of breathing frequency. Antigen-specific IgG1 antibodies were several orders of magnitude higher in intradermally sensitized animals compared with animals sensitized by inhalation. Although Des-N-sensitized guinea-pigs experienced high IgG1-antibody titres, no response of pulmonary hypersensitivity could be elicited after hapten or conjugate challenge. In summary, it would appear that pulmonary hypersensitivity depends on factors other than IgG1 antibody titres. For the screening of chemicals, the dermal induction and inhalation challenge protocol was revealed to be more sensitive than the inhalation induction and inhalation challenge protocol.

Administration, Inhalation↗

Biological monitoring of controlled toluene exposure.

OBJECTIVES: Widespread exposure to toluene occurs in the printing, painting, automotive, shoemaking, and speaker-manufacturing industries. The relationship between air concentrations and the absorbed dose is confounded by dermal exposure, personal protective devices, movement throughout the workplace, and interindividual differences in toluene uptake and elimination. METHODS: To determine the best biological indicator of exposure we examined the blood and alveolar breath concentrations of toluene as well as the urinary excretion rates of hippuric acid and of o-, m-, and p-cresols from 33 controlled human inhalation exposures to 50 ppm for 2 h. RESULTS: Among the metabolites, o-cresol was least influenced by background contributions, whereas the p-cresol and hippuric acid rates were obscured by endogenous and dietary sources. Toluene levels in alveolar breath proved to be the most accurate and noninvasive indicator of the absorbed dose. A physiologic model described blood and breath data using four measured anthropometric parameters and the fit values of extrahepatic metabolism and adipose-tissue blood flow. CONCLUSIONS: After breathing rate and extrahepatic metabolism had been set to conservative (protective) values (the 97.5th and 2.5th percentiles, respectively) the model predicted that pre-final-shift breath levels of < or =10 micromol/m3 and post-final-shift levels of < or =150 micromol/m3 corresponded to average workplace exposure levels of < or =50 ppm toluene. Alternately, we used the distributions and covariances of the measured and fit model parameters to yield conservative pre-final-shift levels of < or =7.3 micromol/m3 and post-final-shift breath levels of < or =120 micromol/m3 that were reflective of workplace exposure levels of < or =50 ppm toluene.

Adult↗

Inhibition of rat respiratory-tract cytochrome P-450 activity after acute low-level m-xylene inhalation: role in 1-nitronaphthalene toxicity.

The xylenes are commonly used industrial solvents that have been shown to inhibit cytochrome P-450 (CYP450) activities in an organ- and isozyme-specific pattern. This study examined the dose-response and durational effects of m-xylene inhalation on cytochrome P-450 activities in the respiratory tract and liver as well as the effects of these CYP450 alterations on 1-nitronaphthalene (1-NN)-induced respiratory or hepatic toxicity. After m-xylene inhalation exposure there was a dose-related inhibition of all nasal mucosa CYPs examined. At 300 ppm, inhibition was sustained up to 2 days after exposure, but on day 5 all CYP activities were increased. There was also dose-related inhibition of lung CYPs 2B1, 2E1, and 4B1. The activities of these CYPs returned to those of control by day 2 but lung CYP 2B1 was increased 5 days following m-xylene exposure. Hepatic CYP 2E1 activity was increased immediately following m-xylene exposure (300 ppm). CYP 2B1 and CYP 1A2 activities were increased through day 2, all activities returning to control values 5 days postexposure. 1-NN treatment caused severe respiratory toxicity that was prevented by prior m-xylene exposure. Lactate dehydrogenase (LDH) and protein were increased in nasal lavage fluid (NLF) but gamma-glutamyl transferase (GGT) was unchanged. m-Xylene coexposure prevented or ameliorated the increases in LDH and protein but increased GGT. 1-NN-induced increases in bronchoalveolar lavage fluid (BALF) LDH and GGT were attenuated by m-xylene. 1-NN caused pronounced histopathological changes in both respiratory and olfactory regions of the nasal mucosa. Lesions in both regions were characterized by acute epithelial necrosis and exfoliation and suppurative exudate in the airways. These changes were prevented by m-xylene coexposure. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were not changed in animals exposed to 1-NN but were increased by m-xylene coexposure. Low-level m-xylene exposure organ-selectively altered CYP450 isozyme activities and subsequent 1-NN toxicity.

Administration, Inhalation↗

High incidence of malignant lung carcinomas in rats after inhalation of 239PuO2 aerosol.

Female Wistar strain rats were exposed to a single inhalation of a submicron-size aerosol of high-fired 239PuO2 to investigate pulmonary carcinogenesis during lifespan periods. The absorbed lung doses of the exposed animals ranged from 0.6 to 12 Gy and were well correlated with the initial lung deposition (ILD) of 0.1 to 2.3 kBq. Survival and induction of primary lung tumors in 116 exposed rats were compared with those in 56 untreated control rats in respect to lung doses received. Mean survival time was greatly reduced, and the cumulative incidence of total lung tumors was markedly increased to 90-100% in rats that received more than 4 Gy, whereas of the controls only one animal (1.8%) died of primary lung tumors. Primary but benign adenomas were present in exposed animals given 1.0 Gy or less, and the incidence of adenomas was 22-25% at 4-5 Gy, but decreased sharply to 3-5% at 6-8 Gy. In contrast, no malignant carcinomas, including adenocarcinomas, adenosquamous carcinomas and squamous cell carcinomas, developed at a dose of less than 1.0 Gy, whereas they were present in 75% or more of the rats given 4-10 Gy, but only in 55% at 12 Gy. Although there were no clear differences in the dose and time required for induction among the carcinoma types, all tended to develop in earlier periods after inhalation than adenomas. Despite the limited number of exposed animals that received lower doses, results suggest that malignant lung carcinomas are highly and early induced and have a different dose-effect relationship than benign adenomas at doses of more than 1 Gy after inhalation exposure to 239PuO2.

Adenocarcinoma↗

Evaluation of the embryotoxicity of JP-10 in the rat.

The effect of JP-10, the major component of cruise missile fuel, on the development of embryonic rats was evaluated. Pregnant females were exposed via inhalation to 600 ppm or orally dosed with 250, 500 or 1000 mg JP-10/kg on gestation days 6-15. In a separate experiment both fetal and maternal blood levels of JP-10 were monitored during an inhalation exposure. Moderate signs of toxicity including tremors and convulsions were observed in the pregnant females receiving the higher doses. JP-10 was not selectively embryotoxic in the rat when administered by gavage or inhalation. Blood levels of JP-10 in the fetuses were about one half the maternal blood levels at steady state.

Abnormalities, Drug-Induced↗

Distribution, progression, and recovery of acute formaldehyde-induced inhibition of nasal mucociliary function in F-344 rats.

A previous report of inhalation exposure of F-344 rats to formaldehyde gas, using a whole-body exposure system, described the induction of regional inhibition of nasal mucociliary function, with a clear concentration-response relationship. A head-only exposure system was subsequently developed in order to facilitate the present study of reversibility of acute effects of formaldehyde on the nasal mucociliary apparatus. This study also included an examination of more extensive areas of the nose than those reported in the previous work. Male F-344 rats were exposed to 2 or 15 ppm formaldehyde gas for 10, 20, 45, or 90 min or 6 hr with recovery groups examined 1 hr after the end of the 90-min and 6-hr exposures. No effects were observed in rats exposed to 2 ppm formaldehyde. In rats exposed to 15 ppm, the extent of formaldehyde-induced inhibition of mucociliary function detected in specific regions of the nose was time dependent, with increasing areas of mucostasis and ciliastasis being induced during a 6-hr exposure period. A 1-hr room-air exposure, following exposure to 15 ppm formaldehyde, resulted in marked recovery of mucociliary function, indicating the value of a head-only exposure system for rapid examination of mucociliary function following exposure. Recovery of mucociliary function occurred especially in the more posterior areas of affected regions of the nose. However, in areas of recovery mucus flow rate was reduced compared to unexposed control rates, indicating incomplete recovery of function in these areas. Regions of formaldehyde-induced inhibition of mucociliary function correlated well with the previously reported distribution of formaldehyde-induced nasal squamous cell carcinomas, with the exception of effects on the medial aspect of the maxilloturbinate. These findings were considered to provide further support for the proposal that both regional exposure and local tissue susceptibility may be responsible for the distribution of formaldehyde-induced nasal squamous cell carcinomas. It was also postulated, on the basis of mucus flow patterns derived from control animals in this study, that flow relationships between nasal mucus and inspired air form a countercurrent system which may optimize clearance of inhaled air contaminants.

Animals↗

Six-year clinical and immunologic follow-up of workers exposed to trimellitic anhydride.

We report a 6-year study from 1979 through 1985 of workers exposed to trimellitic anhydride (TMA) in three groups of volunteers. Twenty-nine percent of workers (5/17) originally studied had immunologically induced respiratory disease. Subsequent to this evaluation, increased environmental control of TMA exposure was instituted. Since that time, there have been decreasing clinical symptoms and decreasing levels of antibody against TMA conjugated to human serum albumin. These long-term studies originally used radioimmunoassays, but enzyme-linked immunoassays against TMA-conjugated proteins are now demonstrated to be equally appropriate and are more cost-effective. With appropriate clinical and immunologic studies, immunologic airway reactions to TMA may be identified and then prevented by environmental control to decrease inhalation exposure to TMA. This is likely applicable to certain other chemical antigens that immunize by inhalation.

Air Pollutants, Occupational↗