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PubMed2003

Toxicity due to 2- and 13-wk inhalation exposures of rats and mice to N, N-dimethylformamide.

In order to better characterize the toxicity of N,N-dimethylformamide (DMF) and to provide its basic toxicity data for risk assessment of workers exposed to DMF, F344 rats and BDF1 mice of both sexes were exposed by inhalation (6 h/d x 5 d/wk) to 100, 200, 400, 800 or 1,600 ppm DMF for 2 wk, and 50, 100, 200, 400 or 800 ppm DMF for 13 wk. Three male and 7 female rats died during the 2-wk exposure to 1,600 ppm DMF, but no death of the exposed rats or mice occurred under any other exposure conditions. Massive, focal and single cell necroses were observed in the liver of DMF-exposed rats and mice. The massive necrosis associated with the centrilobular fibrosis occurred at the highest exposure concentration. The single cell necrosis was associated with fragmentation of the nucleoli as well as an increased mitotic figure. The 13-wk exposures of rats and mice to DMF were characterized by increases in the relative liver weight and the incidence of the centrilobular hepatocellular hypertrophy as well as increased serum levels of AST, ALT, LDH, total cholesterol and phospholipid. Lower confidence limits of the benchmark dose yielding the response with a 10% extra risk (BMDL10) were determined for the relative liver weight and the incidence of hepatocellular hypertrophy of the 13-wk exposed animals. The BMDL10 resulted in 1 ppm for the increased relative liver weight of male rats and mice and 17 ppm for the hepatocellular hypertrophy of male mice.

Amidohydrolases↗
PubMed2005

Effect of water-soluble metal working fluid aerosols on respiratory system after 13 weeks of repeated inhalation exposure in F344 rats.

Three groups of male F344 rats were exposed to a water-soluble metal working fluid (MWF) aerosol at concentrations of 20, 60 or 180 mg/m3 for 6 h/day, five days a week, for 13 weeks in inhalation chambers. The aerosol particles were normally distributed and the mass median aerodynamic diameter was 1.56 microm. Despite the absence of clinical findings or significant changes in body weight during the 13-week exposure period, the numbers of white blood cells and lung weights were significantly higher at the end of the 13-week exposure period. Exposure to 20 mg/m3 of the MWF aerosol was found to have an effect on the respiratory system, including an accumulation of foamy macrophages in the bronchoalveolar lavage (BAL) fluid and thickening of the alveolar walls in the histopathology. The level of histamine and number of polymorphonuclear (PMN) cells were also higher in the BAL fluid from the rats exposed to 60 mg/m3 of the MWF aerosol, while the respiratory inflammation was most pronounced in the rats exposed to 180 mg/m3 of the MWF aerosol, including the accumulation of PMNs and foamy macrophages in the BAL cells, lung weight increase and thickening of the alveolar walls. Immunoglobulin IgG2a level was also lower in the sera from the rats exposed to 180 mg/m3 of the MWF aerosol. Therefore, even though no clinical symptoms were observed in the rats exposed to the high MWF concentration, respiratory inflammation was still induced by a relatively low concentration of the MWF, while the immune system was affected by the high MWF concentration.

Administration, Inhalation↗
PubMed2002

Effects of subchronic inhalation exposure of rats to emissions from a diesel engine burning soybean oil-derived biodiesel fuel.

There is increasing interest in diesel fuels derived from plant oils or animal fats ("biodiesel"), but little information on the toxicity of biodiesel emissions other than bacterial mutagenicity. F344 rats were exposed by inhalation 6 h/day, 5 days/wk for 13 wk to 1 of 3 dilutions of emissions from a diesel engine burning 100% soybean oil-derived fuel, or to clean air as controls. Whole emissions were diluted to nominal NO(x) concentrations of 5, 25, or 50 ppm, corresponding to approximately 0.04, 0.2, and 0.5 mg particles/m(3), respectively. Biologically significant, exposure-related effects were limited to the lung, were greater in females than in males, and were observed primarily at the highest exposure level. There was a dose-related increase in the numbers of alveolar macrophages and the numbers of particles in the macrophages, as expected from repeated exposure, but no neutrophil response even at the highest exposure level. The macrophage response was reduced 28 days after cessation of the exposure. Among the high-level females, the group mean lung weight/body weight ratio was increased, and minimal, multifocal bronchiolar metaplasia of alveolar ducts was observed in 4 of 30 rats. Lung weights were not significantly increased, and metaplasia of the alveolar ducts was not observed in males. An increase in particle-laden macrophages was the only exposure-related finding in lungs at the intermediate and low levels, with fewer macrophages and fewer particles per macrophage at the low level. Alveolar histiocytosis was observed in a few rats in both exposed and control groups. There were statistically significant, but minor and not consistently exposure-related, differences in body weight, nonpulmonary organ weights, serum chemistry, and glial fibrillary acidic protein in the brain. There were no significant exposure-related effects on survival, clinical signs, feed consumption, ocular toxicity, hematology, neurohistology, micronuclei in bone marrow, sister chromatid exchanges in peripheral blood lymphocytes, fertility, reproductive toxicity, or teratology. This study demonstrated modest adverse effects at the highest exposure level, and none other than the expected physiological macrophage response to repeated particle exposure at the intermediate level.

Administration, Inhalation↗
PubMed2000

Inhalation toxicity of 1,6-hexamethylene diisocyanate homopolymer (HDI-IC) aerosol: results of single inhalation exposure studies.

The early acute pulmonary response of female Wistar rats exposed nose-only to a mixture of 1,6-hexamethylene diisocyanate homopolymer (HDI-IC) aerosol was examined. This study was designed to investigate the time course of the relationship between acute pulmonary irritation and ensuing disturbances of the air/blood barrier in rats exposed to concentrations of 3.9, 15.9, 54.3, or 118. 1 mg HDI-IC/m(3). The duration of exposure was 6 h, followed by serial sacrifices 0 h, 3 h, 1 day, 3 days, and 7 days postexposure. Concentrations were selected based on the results of a 4-h acute inhalation study in rats (LC(50) = 462 mg/m(3)). Bronchoalveolar lavage (BAL) fluid was analyzed for markers indicative of injury of the bronchoalveolar region, including phospholipids as proxy of altered surfactant homeostasis. Glutathione (GSH) was determined in BAL fluid and lung tissue. BAL cells with increased intracellular phospholipids were observed on day 1 and especially day 3, with some residual increase on day 7. Increased intracellular phospholipids and activity of acid phosphatases appear to suggest that phagocytized phospholipids may transiently affect lysosomal function. Following exposure to 15.9 mg/m(3), changes returned almost entirely to the level of the air-exposed control on day 7. Especially at higher exposure concentrations, lung weights and total number of cells in BAL were still statistically significantly elevated at this time point. Experimental evidence suggests that markers indicative of a dysfunction of the air/blood barrier, such as angiotensin-converting enzyme, total protein, and phospholipids engulfed by alveolar macrophages, were most sensitive to probe this type of changes. Although GSH in BALF was increased following exposure, there was an apparent depletion of tissue GSH immediately after cessation of exposure. In summary, this study suggests that respirable HDI-IC aerosol appears to cause a transient dysfunction of the air/blood barrier indicated by an increased extravasation of plasma constituents. Despite the remarkable extent of effects observed, most changes were reversible within a postexposure period as short as 7 days. First evidence of increased leakage of pulmonary epithelial barrier was observed at 3.9 mg/m(3). With respect to changes of early markers of pulmonary epithelial barrier dysfunction, approximately 3 mg HDI-IC/m(3) was considered to be the threshold concentration for acute pulmonary irritation.

Acid Phosphatase↗
PubMed2004

Evaluation of bronchoalveolar lavage fluid cytotoxic parameters after inhalation exposure to amosite and wollastonite fibrous dusts combined with cigarette smoke.

The aim of this work was to compare the influence of amosite-asbestos and wollastonite fibrous dusts combined with cigarette smoke on chosen cytotoxic parameters of bronchoalveolar lavage fluid (BALF) in rats. Fisher 344 rats inhaled wollastonite or amosite fibrous dusts (60 or 30 mg x m(-3) air) one hour every two days combined with daily breathing of diluted mainstream tobacco smoke (30 mg of TPM x m(-3) air). The experiment lasted 6 months. After sacrifying the animals bronchoalveolar lavage (BAL) was performed and the viability and phagocytic activity of alveolar macrophages (AM), lactate dehydrogenase (LDH) and alkaline phosphatase activity (in the cell-free BALF), acid phosphatase (ACP) and cathepsin D activity (in cell-free BALF and BAL cell suspension) were examined. Exposure to amosite without tobacco smoke significantly decreased the viability of AM and increased the cathepsin D activity in BAL cells. Exposure to wollastonite significantly increased only the cathepsin D activity in BAL cells. Smoking significantly depressed the phagocytic activity of AM and amplified the amosite-induced increase of lysosomal enzyme activities--especially the activity of cathepsin D in BAL cells.

Animals↗
PubMedDate not supplied

Modeling the effects of water usage and co-behavior on inhalation exposures to contaminants volatilized from household water.

The volatilization of volatile organic chemicals during domestic water usage can result in significant indoor air concentrations, and the subsequent inhalation of these contaminants is an important route of exposure. The magnitude of these exposures is highly dependent on the activities undertaken by the exposed individual, as well as the activities of other occupants of the home. The indoor air quality-exposure Model for the Analysis of Volatiles and Residential Indoor Air Quality (MARVIQ) was used to ascertain the impact of water-use activities on the potential contaminant dose to household members. Human time-activity patterns of various population groups were sampled from the California Air Resources Board database, applying distributions of water-use occurrence and water-use duration to each activity based on survey results. Indoor air concentrations in a sample house and the resulting potential inhalation dose to the occupants were computed for different individuals and pairs of individuals to test for exposure and coexposure effects. The simulated daily exposure is well described by a simplified equation that is a function of the amount of time the individual spends in the shower, the bath, and the bathroom; the total water usage in the home; and the fraction of time the individual is at home. These results can be used to identify high-risk populations, individuals, and households. The study also demonstrates the importance of further research on joint time-activity patterns in multiperson households for assessment of exposure and coexposure effects.

Adult↗
PubMed1997

Twenty-eight-day repeated-dose inhalation exposure of rats to diethylene glycol monoethyl ether.

This study was carried out to provide information on the effects of inhalation of diethylene glycol monoethyl ether, a substance used in industry which may be accidentally inhaled by man. Sprague-Dawley CD rats were exposed by inhalation to a test atmosphere containing diethylene glycol monoethyl ether in a nose-only exposure system for 6 hr a day, 5 days a week for 28 days. Mean exposure levels were 0. 09, 0.27, and 1.1 mg/liter. At the two lowest exposure levels the test substance was present entirely as vapor, but at the highest exposure level the test atmosphere was approximately equally divided by mass into respirable droplets (aerosol) and vapor. A comprehensive battery of toxicological evaluations including food consumption, body weight, clinical signs, hematology, and biochemistry revealed no evidence of a systemic effect of exposure. Histopathological examination showed changes indicative of mild nonspecific irritation in the upper respiratory tract of rats exposed at the two highest exposure levels. These changes consisted of foci of necrosis in the ventral cartilage of the larynx of rats exposed at 0.27 or 1.1 mg/liter and an increase in eosinophilic inclusions in the olfactory epithelium of the nasal mucosa of rats exposed at 1.1 mg/liter. The no observed adverse effect level for systemic effects was 1.1 mg/liter and the no observed adverse effect level for signs indicative of mild nonspecific irritation of the upper respiratory tract was 0.09 mg/liter.

Administration, Inhalation↗
PubMedDate not supplied

[Quantitative assessment of inhalation exposure to various transuranium radionuclide compounds by integral nonstochastic criteria].

The comparison of the danger from inhalation of radionuclide transuranium compounds differently transferred within the body was made by the results of an examination of 169 mongrel dogs and 2000 Wistar rats. Effective and ineffective levels of the radionuclide inhaled were determined by integral nonstochastic criteria, that is, 50 per cent death rate, shortening and increase of the average life and reduction of body mass.

Administration, Inhalation↗
PubMed1998

[Quantification of inhaled exposure to alpha-amylase in 2 bakeries].

BACKGROUND: Baker's asthma and baker's rhinitis are among the most frequent occupational diseases. A major cause is the high exposure to flour dust in the workplace and to allergenic enzymes like alpha-amylase from Aspergillus oryzae (allergen name: Asp o 2). METHODS: To quantify allergen exposure in the workplace, 31 personal dust samples in a conventional small bakery (six workers) and in a biobakery (seven workers) were collected. Using a recently developed two-site enzyme-linked immunosorbent assay based on monoclonal antibodies to alpha-amylase from Aspergillus oryzae, the allergen content of these dust samples was determined. RESULTS: Dust exposure in the biobakery was in the range between 3.5 and 12 mg/m3 (median: 5.2 mg/m3) and in the conventional bakery between 0.9 and 118 mg/m3 (median 8.5 mg/m3). 23 out of 31 exposure measurements showed values higher than 4 mg/m3 (threshold limit value for inhalable dust). In the biobakery, no fungal alpha-amylase could be detected. 15 out of 17 samples taken in the conventional bakery contained fungal alpha-amylase in the range between 0.2 and 88 ng per mg dust. The geometric mean of alpha-amylase exposure in this bakery was 13 ng Asp o 2/m3, and the maximum exposure was 4.8 micrograms/m3. In four cases, fungal alpha-amylase was detected although exposure to dust was below the threshold limit of 4 mg/m3. CONCLUSIONS: This study in two German bakeries shows that preventive measures to reduce contact to allergens have not been sufficiently realised. Relevant alpha-amylase exposure occurred at low dust levels illustrating that dust measurements are not adequate to control alpha-amylase exposure. For fungal alpha-amylase an additional threshold limit should be established.

Aspergillus oryzae↗
PubMed2001

A hybrid computational fluid dynamics and physiologically based pharmacokinetic model for comparison of predicted tissue concentrations of acrylic acid and other vapors in the rat and human nasal cavities following inhalation exposure.

To assist in interspecies dosimetry comparisons for risk assessment of the nasal effects of organic acids, a hybrid computational fluid dynamics (CFD) and physiologically based pharmacokinetic (PBPK) dosimetry model was constructed to estimate the regional tissue dose of inhaled vapors in the rat and human nasal cavity. Application to a specific vapor would involve the incorporation of the chemical-specific reactivity, metabolism, partition coefficients, and diffusivity (in both air and tissue phases) of the vapor. This report describes the structure of the CFD-PBPK model and its application to a representative acidic vapor, acrylic acid, for interspecies tissue concentration comparisons to assist in risk assessment. By using the results from a series of short-term in vivo studies combined with computer modeling, regional nasal tissue dose estimates were developed and comparisons of tissue doses between species were conducted. To make these comparisons, the assumption was made that the susceptibilities of human and rat olfactory epithelium to the cytotoxic effects of organic acids were similar, based on similar histological structure and common mode of action considerations. Interspecies differences in response were therefore assumed to be driven primarily by differences in nasal tissue concentrations that result from regional differences in nasal air flow patterns relative to the species-specific distribution of olfactory epithelium in the nasal cavity. The results of simulations with the seven-compartment CFD-PBPK model suggested that the olfactory epithelium of the human nasal cavity would be exposed to tissue concentrations of acrylic acid similar to that of the rat nasal cavity when the exposure conditions are the same. Similar analysis of CFD data and CFD-PBPK model simulations with a simpler one-compartment model of the whole nasal cavities of rats and humans provides comparable results to averaging over the compartments of the seven-compartment model. These results indicate that the general structure of the hybrid CFD-PBPK model applied in this assessment would be useful for target tissue dosimetry and interspecies dose comparisons for a wide variety of vapors. Because of its flexibility, this CFD-PBPK model is envisioned to be a platform for the construction of case-specific inhalation dosimetry models to simulate in vivo exposures that do not involve significant histopathological damage to the nasal cavity.

Acrylates↗
PubMedDate not supplied

Designs and operational characteristics of inhalation exposure equipment--a review.

The development of equipment for use in the experimental study of the effects of inhalable airborne materials has been reviewed. Reference is made to early descriptions of apparatus employed in the mid-nineteenth century up to the present conventional stainless steel and glass units. Whole body chambers, head only arrangements and face mask devices are described. Factors governing the operational characteristics of chambers when utilized in the static or dynamic mode are discussed. The question of uniformity of distribution of the airborne agent in chamber atmospheres has been examined at some length. It is concluded that unusual arrangements to improve distribution are ineffective or produce only marginal improvements. In addition, brief reference has been made to a number of special areas of investigation and to certain considerations of interest to the operator of inhalation equipment. A list of useful reviews and monographs is provided.

Air Pollutants↗
PubMed2005

Acute inhalational exposure to chlorodifluoromethane (freon-22): a report of 43 cases.

We report 43 cases of chlorodifluoromethane (Freon-22) intoxication that occurred on August 5, 2003 when a freezer in a seafood factory exploded. In this accident, 80 workers were exposed to Freon-22 gas and 43 workers developed symptoms and were transferred to six hospitals. Neurological symptoms including dizziness, headache, and nausea were most frequently observed (40 of 43 patients). One patient was comatose but recovered within 1 h with oxygen inhalation. Airway and respiratory symptoms including dysesthesia of the tongue, pharyngitis, and shortness of breath were also frequently observed (26 of 43 patients). These symptoms disappeared within a few days in all patients. There were no fatalities. Although Freon-22 has been considered to be a chlorofluorocarbon of relatively low toxicity, this incident suggests that potentially significant toxic effects may occur following large exposures.

Accidents, Occupational↗
PubMed1991

Chromosome aberrations in lymphocytes of mice after sub-acute low-level inhalation exposure to benzene.

Male and female CD-1 mice were exposed to near ambient air concentrations of benzene by inhalation for 22 h per day, 7 days per week for 6 weeks. The concentrations were 0, 40, 100 and 1000 ppb. Significant increases in chromosome aberrations in spleen lymphocytes were observed in exposed compared with control mice except in the high-dose group (p less than 0.05 for female mice in 2 experiments and for male mice in 1 experiment; p less than 0.15 for male mice in the second experiment). A lack of increase in aberrations among mice of the high-dose group may be due to an induction of detoxifying enzymes as observed by us in a previous study (Au et al., 1988b). We also found that the female mice were more sensitive to the clastogenic activity of benzene than male mice under our experimental conditions. Our study serves to emphasize the need to conduct subchronic, low-dose in vivo genotoxicity studies using exposure conditions similar to those of humans, for evaluation of potential hazards. Our data suggest that the current occupational exposure concentrations for benzene (less than 1000 ppb) may still be hazardous to humans.

Administration, Inhalation↗
PubMedDate not supplied

Effects of inhalation exposure to hexachlorocyclopentadiene on rats and monkeys.

Hexachlorocyclopentadiene (Hex or C-56) is a highly reactive intermediate used in the production of some insecticides, flame retardants, and resins. The present study was conducted to evaluate the inhalation toxicity of high-purity Hex (97.7%) in rats and monkeys to provide information on the potential hazards of accidental exposure of workers to Hex vapors. Acute, range-finding (14-d), and subchronic (90-d) inhalation studies were conducted with Sprague-Dawley rats and subchronic (90-d) inhalation studies were conducted with cynomolgus monkeys. Both acute and range-finding studies with rats showed a steep dose-response curve, and male rats were more sensitive than females. In the range-finding study with rats the threshold of toxicity for Hex was 0.11-0.5 ppm. Histopathologic examination on rats in the 0.5 ppm group revealed lesions in the olfactory and bronchiolar epithelium and inflammatory exudate in the lumens of the respiratory tract; these changes were consistent with observed impaired respiratory function, confirming the lung as the main target organ. Recovery and regression of lung lesions in rats were noted 2-3 wk after termination of exposure. In the 90-d study, inhalation of Hex vapors at concentrations up to 0.2 ppm for 6 h/d, 5 d/wk, produced no detectable physical or clinical effect and no remarkable gross or histological alterations in rats or monkeys.

Animals↗
PubMed1989

Ethyl chloride: 11-day continuous exposure inhalation toxicity study in B6C3F1 mice.

Groups of seven B6C3F1 mice per sex were exposed for 23 hr/day to 0, 250, 1250, or 5000 ppm ethyl chloride (EtCl) for 11 consecutive days to evaluate the potential toxicity of EtCl under near-continuous exposure conditions. On the day following the last exposure, a neurobehavioral observation battery was performed, samples were obtained for clinical chemistry and hematology, and necropsies were conducted. Histopathologic examination was subsequently performed. The only observed effects were increased relative liver weights and a slight increase in hepatocellular vacuolation (glycogen or fat) in 5000 ppm-exposed mice. Exposures to EtCl were well tolerated despite the unusually long exposure periods.

Administration, Inhalation↗
PubMed1988

Toxicology and pathology of methyl bromide in F344 rats and B6C3F1 mice following repeated inhalation exposure.

The toxicity of methyl bromide was studied in male and female F344 rats and B6C3F1 mice exposed by inhalation to 160 ppm methyl bromide or air 6 hr/day, 5 days/week for up to 6 weeks. The animals were killed after 3, 10, or 30 exposure days, or when 50% mortality was observed in any group. Only female rats survived the entire 30 exposure days at 160 ppm methyl bromide with less than 50% mortality. There were clear species- and sex-related differences in susceptibility of specific organs to methyl bromide. Primary target organs were the brain, kidney, nasal cavity, heart, adrenal gland, liver, and testis. In rats, neuronal necrosis occurred in the cerebral cortex, hippocampus, and thalamus of the brain whereas in mice neuronal necrosis occurred primarily in the internal granular layer of the cerebellum. Nephrosis occurred in all exposed mice, but not rats, and was likely a major cause of moribundity and death. Necrosis of the olfactory epithelium was more severe and extensive in rats than mice. Myocardial degeneration occurred in male and female rats and to a lesser degree in male mice. There was atrophy of the inner zone of the adrenal cortex in female mice and cytoplasmic vacuolation of the adrenal cortex in rats. Testicular degeneration occurred in rats and mice. The target organ specificity of methyl bromide is similar to that of methyl chloride, suggesting that the two monohalomethanes may have a common mechanism of action.

Administration, Inhalation↗
PubMed1998

Measurement and characterization of micronuclei in cultured primary lung cells of mice following inhalation exposure to benzene.

The genotoxic effects of benzene in lung cells of mice exposed to single acute doses by inhalation have been estimated by cytogenetic analysis of micronuclei in primary cultures of lung fibroblasts. Mice were nose-only exposed to 1000 p.p.m. for 30 or 60 min or to 3500 p.p.m. for 30 min and sacrificed 24 h after the end of exposure. Lung fibroblasts were cultured attached to coverslips for 72 h, the last 48 h in the presence of 0.75 microgram/ml cytochalasin B. Micronuclei were scored in binucleate cells. The mechanism(s) of micronucleus induction was characterized by immunofluorescent staining of kinetochore proteins (CREST staining), which allowed micronuclei due to chromosome loss (kinetochore-positive) to be distinguished from those produced by chromosome breakage (kinetochore-negative). Three- and 4-fold statistically significant increases in total micronucleus frequencies were observed in all benzene-exposed mice with respect to unexposed controls. The effect was neither concentration nor time dependent. This is compatible with a plateau dose-effect relationship for the effects on bone marrow, which is explained by saturation of metabolism. Both chromosome loss and chromosome breakage appear to contribute to micronucleus formation, suggesting that in addition to chromosome rearrangements, aneuploidy may be a relevant early genotoxic event associated with benzene carcinogenicity. Under the same treatment conditions no micronucleus induction could be shown in spleen lymphocytes, suggesting that with very short benzene exposures cells at the first contact site with local metabolizing capacity have a higher probability of genetic alterations potentially leading to neoplasia.

Administration, Inhalation↗
PubMed1983

Carcinogenicity of formaldehyde in rats and mice after long-term inhalation exposure.

Groups of approximately 120 male and 120 female Fischer 344 rats and C57BL/6 X C3H F1 mice were exposed by inhalation to 0, 2.0, 5.6, and 14.3 ppm of formaldehyde gas 6 hr/day, 5 days/week, for 24 months. This exposure period was followed by up to 6 months of nonexposure. Interim sacrifices were conducted at 6, 12, 18, 24, 27, and 30 months. Significant formaldehyde-induced lesions were restricted to the nasal cavity and proximal trachea. The distribution and severity of these lesions were concentration dependent. Rhinitis, epithelial dysplasia, and squamous metaplasia occurred in all exposure groups of rats and in the intermediate and high exposure groups of mice. There was regression of rhinitis, dysplasia, and metaplasia at 27 months (3 months postexposure) in the 14.3- and 5.6-ppm groups of mice and in the 2.0- and 5.6-ppm groups of rats. Squamous cell carcinomas were observed in the nasal cavities of 103 rats (52 females and 51 males) and 2 male mice exposed to 14.3 ppm and in 2 rats (one male and one female) exposed to 5.6 ppm of formaldehyde gas. Formaldehyde inhalation was also weakly associated with an increase in the frequency of polypoid adenomas in the nasal cavity of male rats.

Animals↗