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PubMed1988

Natural inhalation exposure to coal smoke and wood smoke induces lung cancer in mice and rats.

In an rural area with a high mortality rate of lung cancer in humans, mice and rats were placed in an environment in which they inhaled coal smoke and wood smoke in indoor air for 15 to 19 months. The incidences of lung cancer in mice in the control group, wood group, and coal group were 17.0% (29/171), 45.8% (81/177), and 89.5% (188/210), respectively: in rats the incidences were 0.9% (1/110), 0 (0/110), and 67.2% (84/125), respectively. In addition, the pollutants in the air were analyzed. The results indicate that coal smoke is a highly significant risk factor for lung cancer in humans in Xuan Wei County of Yun Nan Province in China.

Adenocarcinoma↗
PubMed2004

Systemic immunotoxicity in AJ mice following 6-month whole body inhalation exposure to diesel exhaust.

The purpose of these studies was to determine the effects of subchronic diesel exposure on indicators of systemic immunity in mice. AJ mice were exposed daily for 6 months (6 h/day) to atmospheres containing one of four concentrations (30, 100, 300, and 1000 microg/m(3)) of diluted diesel exhaust (DE) in whole body exposure chambers. The effects of DE were compared to chamber exposure controls receiving fresh air. DE was assessed for effects on systemic immunity by measuring the proliferative response of spleen cells following stimulation with T cell (phytohemagglutinin, or PHA) or B cell (lipopolysaccharide, or LPS) mitogens. The results showed that DE at all exposure levels suppressed the proliferative response of T cells. B cell proliferation was increased at 30 microg/m(3) and was unaffected at the 100, 300, and 1000 microg/m(3) exposures. Polycyclic aromatic hydrocarbons (PAHs) are known to suppress spleen cell mitogenic responses, and it has been hypothesized by several groups that PAHs and perhaps benzo(a)pyrene (BaP)-quinones (BPQs) may be responsible for the effects of DE or diesel exhaust particles (DEP). Therefore, a second purpose of these studies was to determine the effects of in vitro BPQs on AJ mouse spleen cell mitogenic responses and compare to DE in preliminary studies. Unlike DE, BPQs were found to increase T cell proliferation. In addition, analysis of chamber atmospheres showed that there was little if any PAH and BPQs in DE. Therefore, these results demonstrate that because of the absence of BPQs in DE, they are likely not responsible for the immunosuppressive effect of DE on murine spleen cell responses.

Administration, Inhalation↗
PubMed1991

Lung clearance and retention of toner, utilizing a tracer technique, during chronic inhalation exposure in rats.

Male and female F-344 rats were exposed to 6 hr/day, 5 days/week for up to 24 months to a special test toner at 0, 1, 4, and 16 mg/m3, TiO2 at 5 mg/m3, or SiO2 at 1 mg/m3 by the inhalation route. 59Fe-labeled iron oxide and 85Sr-labeled polystyrene particles were periodically inhaled by the nose-only route and used to measure alveolar clearance rates during the course of the study. This method was used to describe a maximum functionally tolerated dose (MFTD). Pulmonary retention of toner and control materials (TiO2 and SiO2) was measured after 3, 9, 15, 21, and 24 months of exposure. The quantity of all three materials retained in the lungs and lung-associated lymph nodes increased with exposure duration and level. The final pulmonary burdens of toner at the three exposure levels were 0.22, 1.73, and 15.6 mg/lung, respectively. Alveolar clearance of both tracers was substantially impaired at the toner high-exposure level, and moderately slowed at the toner middle-exposure level. The excessive quantity of toner retained and the substantially retarded clearance in the toner high-exposure group are indicative of "lung overloading." Alveolar clearance of 85Sr-polystyrene particles was slightly slowed in the TiO2-exposed group and substantially impaired in the SiO2-exposed group. The alveolar clearance of the unexposed rats decreased about 30% during the study, a change ascribed to aging. For a general description of the toxicokinetics of the various dusts, a semiempirical kinetic model was developed, which could generally be useful for the extrapolation of lung retention of insoluble particles from a subchronic to a chronic inhalation study. Both the maximum tolerated dose (MTD) and the MFTD were exceeded at the toner high-exposure level during the study in rats.

Aerosols↗
PubMed1999

Binding of the potent allergen hexahydrophthalic anhydride in the mucosa of the upper respiratory and alimentary tract following single inhalation exposures in guinea pigs and rats.

Hexahydrophthalic anhydride (HHPA; CAS No. 13149-00-3) is a highly allergenic compound commonly used in the chemical industry. Guinea pigs and rats were exposed to [3H2]HHPA by inhalation for 3-8 h and were killed at various intervals during 7 days. The tissue distribution of non-volatile and covalently bound radioactivity was studied by autoradiography. Tissue bound radioactivity was mainly found in the mucosa of the upper respiratory airways, whereas negligible levels were observed in the lungs. In addition, tissue bound radioactivity was present in the gastrointestinal tract and conjunctiva. Moreover, in the cortex of the kidneys in rats, but not in guinea pigs, a low level of tissue bound radioactivity was found. The radioactivity in the tissues persisted for at least 7 days after the end of exposure. Plasma proteins and soluble proteins from trachea, lung, and kidney from [3H2]HHPA-exposed animals were separated by gel filtration. The radioactivity in dialysed plasma was mainly found in the same fractions as albumin. The soluble proteins from trachea, lung, and kidney in both rats and guinea pigs showed a similar pattern as found in blood. The radioactivity in dialysed plasma from both guinea pigs and rats seemed to decay according to a two-compartment model. The non-extractable binding of [3H2]HHPA in the upper respiratory airways and conjunctiva may be of relevance for symptoms in workers with allergy, since they mainly develop symptoms and signs from the nose and eyes.

Administration, Inhalation↗
PubMed1988

[Effects of repeated inhalation-exposure to fenitrothion powder on blood cholinesterase activity in rats].

Effects of repeated exposure to Fenitrothion (Sumithion) powder on erythrocyte membrane acetylcholinesterase (AChE) and plasma cholinesterase (PChE) were studied. Rats (Wistar, male) were exposed to fenitrothion powder for 2 hrs/day, 5 days/week for up to 3 months. The suppression of AChE and PChE increased as the exposure period and exposure concentration increased, although no suppression of AChE was found after a single 4-hr exposure. The persistence of AChE inhibition after the termination of exposure increased with the increase of the exposure period and was longer than that of PChE. Therefore, the AChE activity seems to be useful in examining the response to the repeated exposure to fenitrothion powder.

Administration, Inhalation↗
PubMedDate not supplied

Hepatotoxicity in guinea pigs following acute inhalation exposure to 1,1-dichloro-2,2,2-trifluoroethane.

Groups of 10 male Hartley guinea pigs were exposed to 3.0, 2.0, 1.0, or 0.1% (v/v) 1,1-Dichloro-2,2,2-trifluoroethane (HCFC-123) or 1.0% (v/v) halothane by inhalation for 4 hr. A sixth group of 10 guinea pigs received only air. All animals were sacrificed 48 hr postexposure. Gross and histopathologic examination of the liver, heart, and kidney and routine hematology and clinical chemistry analyses [including isocitrate dehydrogenase (ICDH)] were done on all guinea pigs. Lesions related to HCFC-123 and halothane exposure were limited to the liver and included centrolobular vacuolar (fatty) change, multifocal random degeneration and necrosis, and centrolobular degeneration and necrosis. These lesions were observed in 90-100% of the exposed animals and were absent in the air-only controls. There was significant individual animal variation in susceptibility to both HCFC-123 and halothane, resulting in a spectrum of histologic lesions and clinical chemistry values within each exposure group. Alanine aminotransferase, aspartate aminotransferase, and ICDH were the most significant predictors of hepatocellular damage. Similarities in the response between halothane and HCFC-123 in this guinea pig model suggests that humans susceptible to halothane-induced hepatitis may be susceptible to HCFC-123 by a common mechanism of toxicity.

Administration, Inhalation↗
PubMed1989

Fetal effects of inhalation exposure to cyclohexanone vapor in pregnant rats.

Cyclohexanone (CH), a solvent and thinner that has extensive use in industry, was investigated for developmental effects using pregnant Sprague-Dawley rats exposed to 100, 250 or 500 ppm concentrations in an inhalation chamber for seven hours per day from days 5 through 20 of pregnancy. Controls were exposed to room air. Maternal weight gain at 250 and 500 ppm CH was only slightly lower than in the control dams, and a grey mottling of the lungs was seen in a few of the CH-exposed dams. There were no significant differences between the CH and control groups in fetal weight, resorption sites, fetal death or sex ratio. External and soft tissue examinations revealed no significant incidence of malformations or variations in CH-exposed animals. A slight increase in the mean percent of rudimentary ribs per litter was observed in the 250 and 500 ppm CH-exposed groups. However, no significant numbers of skeletal malformations were noticed in either the CH or room air control groups. It was concluded that respiratory exposure of rats to as much as 500 ppm CH during organogenesis was unlikely to be developmentally toxic.

Administration, Inhalation↗
PubMed1979

Inhalation bioassay chemistry--Walton Horizontal Smoking Machine for inhalation exposure of rodents to cigarette smoke.

Studies of experimental tobacco smoke carcinogenesis have suffered from the lack of a conveniently available and well-characterized device for exposing animals to tobacco smoke for inhalation. The Walton Horizontal Smoking Machine, a commercially available system designed to expose up to 20 mice to the smoke of a single cigarette, may fulfill this need. This system produced a uniform smoke aerosol of predictable concentration and appropriate composition for cigarettes with high delivery of nicotine (40 mg total particulate matter, 2.6 mg nicotine, and 17 cm3 carbon monoxide per cigarette) and with low delivery of nicotine (30 mg total particulate matter, 0.3 mg nicotine, and 17 cm3 carbon monoxide). In this experiment C57BL and DBA/2Bd strains of mice were used. Limitations of the concept of exposing animals to standing smoke were defined.

Animals↗
PubMed1994

Effects of acute combined inhalation exposure to n-butyl alcohol and n-butyl acetate in experimental animals.

The effects of combined exposure to n-butyl alcohol and n-butyl acetate on rotarod performance and hot plate behaviour in rats and respiratory rate in mice were investigated in the condition of an acute inhalation experiment. Rotarod performance and hot-plate behaviour were tested in rats exposed to various concentrations of n-butyl alcohol, n-butyl acetate and their mixture consisting of 50 Vol-% n-butyl alcohol and 50 Vol-% n-butyl acetate immediately after termination of a 4-hour exposure period. The respiratory rate in mice was recorded continuously before the exposure to solvents, during 6 min of exposure and 6 min after termination of exposure using whole body plethysmographic method. Mice were exposed to vapours of single solvents and their 50:50 Vol-% mixture. Both solvents and their mixture caused concentration-dependent disturbances of rotarod performance in rat. The medial effective concentration (EC50) for the effect amounted to 7559 ppm, 8339 ppm and 10672 ppm for n-butyl alcohol, n-butyl acetate and their mixture, respectively. Both solvents and their mixture decreased sensitivity to the pain and changes were concentration-dependent. In condition of combined exposure the results obtained in rotarod and hot-plate behaviour test indicate the summation of individual solvent effects. The tested solvents resulted in concentration-dependent decrease in respiratory rate in mice. n-Butyl alcohol produced maximal decrease in respiratory rate in the first minute of exposure whereas n-butyl acetate in the sixth minute.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Butanol↗
PubMedDate not supplied

Effect of carbon monoxide inhalation exposure in mice on drug metabolism in vivo.

Experiments were undertaken to evaluate the action of carbon monoxide (CO) on the mixed-function oxidase (MFO) system in vivo. Mice were exposed to 500 ppm CO for 8 h per day in an inhalation chamber under dynamic airflow conditions. Hexobarbital (150 mg/kg, i.p.), zoxazolamine (150 mg/kg, i.p.) or ethanol (2 mg/g, i.p.) was given to each group of mice during CO exposure and disappearance of the drug from blood or brain was determined while CO exposure continued. The experiments were repeated with different groups of animals which were exposed to CO for 3 or 5 days. Hexobarbital and ethanol metabolism were not affected by CO following either one day exposure or repeated exposure. There was no statistically significant difference in the brain level of zoxazolamine in animals exposed to CO when compared to control. These studies indicate that in vivo metabolism of hexobarbital, zoxazolamine and ethanol in mice is not affected by exposure to 500 ppm CO under the conditions employed in the present study.

Animals↗
PubMed1991

Hematotoxicity and concentration-dependent conjugation of phenol in mice following inhalation exposure to benzene.

Benzene is metabolized to one or more hematotoxic species. Saturation of benzene metabolism could limit the production of toxic species. Saturation of phase II enzymes involved in the conjugation of the phenolic metabolites of benzene also could affect the hematotoxicity of benzene. To investigate the latter possibility, we exposed male Swiss mice, via the inhalation route, to various concentrations of benzene for 6 h per day for 5 days. Following termination of the final exposure the mice were killed and the levels of phenylsulfate and phenylglucuronide in the blood determined. Spleen weights were recorded and the number of white blood cells counted. At low benzene exposure concentrations phenylsulfate is the major conjugated form of phenol in the blood. At high exposure concentrations, phenylglucuronide is the predominant species. The reductions in spleen weight and white blood cell numbers correlated with the concentration of phenylsulfate in the blood, but are most probably not causally related.

Administration, Inhalation↗
PubMed2004

Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.

While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h. The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 h postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB.

Administration, Inhalation↗
PubMed1992

The contributions to solvent uptake by skin and inhalation exposure.

Solvent exposures were assessed among 97 auto body repair workers in order to determine whether skin contact represented a significant route of exposure. Each subject's cumulative skin exposure was ranked categorically based on simple observation: 49 none, 33 incidental or low, and 15 moderate or high. The median time-weighted average air exposure to solvents was 8.4% of the American Conference of Governmental Industrial Hygienists (ACGIH) combined solvent threshold limit value (TLV) with a range of 0-62% TLV, including toluene (median 4 ppm) and xylenes (median 0.9 ppm). Urine methyl hippuric acids (MHAs, metabolites of xylenes) were low compared to the ACGIH biological exposure index (BEI) with a median of 2% and a range of 0-12% BEI but were strongly correlated with both the level of airborne xylenes and skin exposure when considered simultaneously by using analysis of covariance (R = 0.91, p less than 0.0001). MHA excretion attributable to skin exposure for 15 min or more generally was comparable to or greater than that from associated air exposure over the full work shift. This study had limited ability to assess quantitatively the contributions of toluene exposures, but there was evidence that skin exposures also contributed significantly to toluene absorption. Air sampling will substantially underestimate a worker's total solvent dose in the setting of moderate or high skin exposure. Simple observation was effective in identifying workers in this sample who appeared to have sufficient skin exposure to produce a measurable increase in solvent uptake.

Adult↗
PubMed1992

Developmental toxicity of dimethylformamide in the rat following inhalation exposure.

Dimethylformamide (DMF) is a widely used industrial solvent. DMF has been reported to be a developmental toxin when given to rodents by injection or following dermal administration. In this study, groups of pregnant rats were exposed by inhalation to either 0 (control), 30, or 300 ppm DMF from gestation day 6 through 15. In the 300 ppm rats, both maternal weight gain during gestation and fetal weights were lower than those of the controls. Fetal resorptions were not increased in this group. No significant differences among either maternal or fetal rats were seen in the 30 ppm group compared to controls. Both fetal and maternal toxicity were noted at 300 ppm and the no observed effect level under these experimental conditions was 30 ppm for both the dams and the conceptuses. DMF did not produce malformations in the rat fetus even at a level that was toxic to the dam.

Abnormalities, Drug-Induced↗
PubMed2000

Four weeks' inhalation exposure of Long Evans rats to 4-tert-butyltoluene: effect on evoked potentials, behaviour, and brain neurochemistry.

Long-lasting central nervous system (CNS) neurotoxicity of 4-tert-butyltoluene (TBT) has been investigated using electrophysiology, behaviour, and neurochemistry in Long Evans rats exposed by inhalation to 0, 20, or 40 p.p.m. TBT 6 hr/day, 7 days/week for 4 weeks. Flash evoked potentials and somatosensory evoked potentials were not affected by TBT. In Auditory Brain Stem Response there was no shift in hearing threshold, but the amplitude of the first wave was increased in both exposed groups at high stimulus levels. Three to four months after the end of exposure, behavioural studies in Morris water maze and eight-arm maze failed to demonstrate any TBT induced effects. Exposure was followed by a 5 months exposure-free period prior to gross regional and subcellular (synaptosomal) neurochemical investigations of the brain. TBT reduced the NA concentration in whole brain minus cerebellum. Synaptosomal choline acetyltransferase activity increased and acetylcholinesterase activity was unchanged suggesting increased synaptosomal ability for acetylcholine synthesis. The relative and total yield of synaptosomal protein was reduced suggesting reduced density and total number of synapses in situ, respectively. We hypothesise that a reduced yield of synaptosomal protein reflects a more general effect of organic solvent exposure on the software of the brain. The synaptosomal concentration per mg synaptosomal protein and the total amount of 5-hydroxytryptamine were not affected whereas the total amount of synaptosomal noradrenaline decreased. The concentration and the total amount of synaptosomal dopamine decreased. The noradrenergic and dopaminergic parts of CNS may be more vulnerable to TBT than the serotonergic, and these long-lasting effects may cause or reflect TBT-compromised CNS function.

Acetylcholinesterase↗