Neuromotor Effects of Acute Ethanol Inhalation Exposure in Humans: A Preliminary Study
32
Citation
19
Reference
10
Related Paper
Citation Trend
Abstract:
Neuromotor Effects of Acute Ethanol Inhalation Exposure in Humans: A Preliminary Study: Véronique Nadeau, et al. TOXHUM (Groupe de Recherche en Toxicologie Humaine), Département de Santé Environnementale et Santé au Travail, Université de Montréal, Canada — Ethanol (ETOH) is added to unleaded gasoline to decrease environmental levels of carbon monoxide from automobiles emissions. Therefore, addition of ETOH in reformulated fuel will most likely increase and the involuntarily human exposure to this chemical will also increase. This preliminary study was undertaken to evaluate the possible neuromotor effects resulting from acute ETOH exposure by inhalation in humans. Five healthy non‐smoking adult males, with no history of alcohol abuse, were exposed by inhalation, in a dynamic, controlled‐environment exposure chamber, to various concentrations of ETOH (0, 250, 500 and 1,000 ppm in air) for six hours. Reaction time, body sway, hand tremor and rapid alternating movements were measured before and after each exposure session by using the CATSYS TM 7.0 system and a diadochokinesimeter. The concentrations of ETOH in blood and in alveolar air were also measured. ETOH was not detected in blood nor in alveolar air when volunteers were exposed to 250 and 500 ppm, but at the end of exposure to 1,000 ppm, blood and alveolar air concentrations were 0.443 mg/100ml and 253.1 ppm, respectively. The neuromotor tests did not show conclusively significant differences between the exposed and non‐exposed conditions. In conclusion, this study suggests that acute exposure to ethanol at 1,000 ppm or lower or to concentrations that could be encountered upon refueling is not likely to cause any significant neuromotor alterations in healthy males.Keywords:
Inhalation exposure
Acute exposure
Lung cancer following inhalation in rodents is a major concern regarding exposure to cobalt substances. However, little information is available on adverse effects and toxicity following long-term inhalation exposure to poorly soluble cobalt substances with low bioavailability. Thus, the present study focused on pulmonary effects of the poorly soluble tricobalt tetraoxide (5, 20, 80 mg/m³) in a 28-day inhalation exposure study. Lung weights increased with increasing exposures. Bronchoalveolar lavage fluid analysis and histopathology revealed lung tissue inflammation at the mid-dose with increasing severity in the high-dose group and post-exposure persistency. Markers for cellular damage and cell proliferation were statistically significantly increased. No increase in 8-OH-dG lesions was observed, indicating an absence of oxidative DNA lesions. The primary effect of inhaled Co3O4 particles is inflammation of the respiratory tract strongly resembling responses of inhaled "inert dust" substances, with a NOAEC of 5 mg/m³ under the conditions of this test.
Inhalation exposure
Pulmonary toxicity
Respiratory tract
No-observed-adverse-effect level
Histopathology
Cite
Citations (4)
Vomeronasal organ
Inhalation exposure
Respiratory tract
Cite
Citations (17)
Inhalation exposure
Acute exposure
Cite
Citations (6)
Abstract Inhalation of ZnO particles can cause inflammation of the airways and metal fume fever. It is unclear if different sizes of the particles alter these effects. However, various studies report higher biological activity of other nano-sized particles compared to microparticles. No effects at all were observed after inhalation of micro- and nano-sized zinc oxide (ZnO) particle concentrations of 0.5 mg/m 3 . Studies with different particle sizes of ZnO at higher exposures are not available. Accordingly, we hypothesized that inhalation of nano-sized ZnO particles induces stronger health effects than the inhalation of the same airborne mass concentration of micro-sized ZnO particles. 16 healthy volunteers (eight men, eight women) were exposed to filtered air and ZnO particles (2.0 mg/m 3 ) for 2 h (one session with nano- and one with micro-sized ZnO) including 1 h of cycling at moderate workload. Effect parameters were symptoms, body temperature, inflammatory markers in blood and in induced sputum. Induced sputum was obtained at baseline examination, 22 h after exposure and at the end of the final test. The effects were assessed before, immediately after, about 22 h after, as well as two and three days after each exposure. Neutrophils, monocytes and acute-phase proteins in blood increased 22 h after micro- and nano-sized ZnO exposure. Effects were generally stronger with micro-sized ZnO particles. Parameters in induced sputum showed partial increases on the next day, but the effect strengths were not clearly attributable to particle sizes. The hypothesis that nano-sized ZnO particles induce stronger health effects than micro-sized ZnO particles was not supported by our data. The stronger systemic inflammatory responses after inhalation of micro-sized ZnO particles can be explained by the higher deposition efficiency of micro-sized ZnO particles in the respiratory tract and a substance-specific mode of action, most likely caused by the formation of zinc ions.
Inhalation exposure
Cite
Citations (34)
The objective of this study was to determine the average reduction in inhalation exposures produced by intermittent use of filter cartridge respirators by cadmium workers. Inhalation exposure was estimated by measuring the cadmium concentration inside the respirator while it was worn or hanging around the worker's neck. Air concentrations of cadmium were measured simultaneously inside the respirator and at the worker's lapel with a dual sampling system. Each of nine workers were measured on three consecutive days for a full work shift. The average inhalation exposures ranged from 3 to 67 micrograms/m3 while the TWA lapel concentrations ranged from 19 to 3600 micrograms/m3; respirator use produced a substantial reduction in inhalation exposures when lapel concentrations were above 100 micrograms/m3. On the average, the inhalation exposure was 26% of the lapel concentration, but the effective protection varied widely between individuals and from day to day. If used cautiously, this relationship may be useful for estimating the approximate average inhalation exposure of a group of workers routinely using half mask respirators.
Respirator
Inhalation exposure
Work shift
Cite
Citations (31)
We evaluated the pulmonary pathological features of rats that received a single intratracheal instillation and a 4-week inhalation of a fullerene. We used fullerene C60 (nanom purple; Frontier Carbon Co. Ltd, Japan) in this study. Male Wistar rats received intratracheal dose of 0.1, 0.2, or 1 mg of C60, and were sacrificed at 3 days, 1 week, 1 month, 3 months, 6 months, and 12 months. In the inhalation study, Wistar rats received C60 or nickel oxide by whole-body inhalation for 6 h/day, 5 days/week, 4 weeks, and were sacrificed at 3 days, 1 month, and 3 months after the end of exposure. During the observation period, no tumors or granulomas were observed in either study. Histopathological evaluation by the point counting method (PCM) showed that a high dose of C60 (1 mg) instillation led to a significant increase of areas of inflammation in the early phase (until 1 week). In the inhalation study of the C60-exposed group, PCM evaluation showed significant changes in the C60-exposed group only at 3 days after exposure; after 1 month, no significant changes were observed. The present study demonstrated that the pulmonary inflammation pattern after exposure to well-characterized C60 via both intratracheal and inhalation instillation was slight and transient. These results support our previous studies that showed C60 has no significant adverse effects in intratracheal and inhalation instillation studies.
Inhalation exposure
Intratracheal instillation
Cite
Citations (29)
The inhalation toxicity of carbon nanofibers (CNFs) is not clearly known due to relatively few related studies reported. An acute inhalation study and short-term inhalation study (5 days) were therefore conducted using Sprague-Dawley rats. In the acute inhalation study, the rats were grouped and exposed to a fresh air control or to low (0.238 ± 0.197), moderate (1.935 ± 0.159), or high (24.696 ± 6.336 mg/m3) CNF concentrations for 6 h and thereafter sacrificed at 14 days. For the short-term inhalation study, the rats were grouped and exposed to a fresh air control or low (0.593 ± 0.019), moderate (2.487 ± 0.213), or high (10.345 ± 0.541 mg/m3) CNF concentrations for 6 h/day for 5 days and sacrificed at 1, 3, and 21 days post-exposure. No mortality was observed in the acute inhalation study. Thus, the CNF LC50 was higher than 25 mg/m3. No significant body or organ weight changes were noted during the 5 days short-term inhalation study or during the post-exposure period. No significant effects of toxicological importance were observed in the hematological, blood biochemical, and coagulation tests. In addition, the bronchoalveolar lavage (BAL) fluid cell differential counts and BAL inflammatory markers showed no CNF-exposure-relevant changes. The histopathological examination also found no CNF-exposure-relevant histopathological lesions. Thus, neither acute nor 5 days inhalation exposure to CNFs induced any noticeable toxicological responses.
Inhalation exposure
Acute exposure
Cite
Citations (2)
We performed the two inhalation exposures, whole-body inhalation and nose-only inhalation, to investigate the pulmonary deposition and health effects of the two inhalation methods. In both methods, we exposed rats to the same TiO2 nanoparticles at almost the same exposure concentration for 6 h and compared the deposited amounts of nanoparticles and histopathological changes in the lungs. Rats were exposed to rutile-type TiO2 nanoparticles generated by the spray-dry method for 6 h. The exposure concentration in the whole-body chamber was 4.10 ± 1.07 mg/m3, and that in nose-only chamber was 4.01 ± 1.11 mg/m3. The particle sizes were 230 and 180 nm, respectively. A control group was exposed to fresh air. The amounts of TiO2 deposited in the lungs as measured by ICP-AES after acid digestion just after the exposure were: 42.6 ± 3.5 μg in the whole-body exposure and 46.0 ± 7.7 μg in the nose-only exposure groups. The histopathological evaluation was the same in both exposure groups: no infiltration of inflammatory cells in the alveolar space and interstitium, and no fibrosis. The two inhalation methods using the same material under the same exposure conditions resulted in the same particle deposition and histopathology in the lung.
Inhalation exposure
Intratracheal instillation
Histopathology
Cite
Citations (25)
Polystyrene
Inhalation exposure
Cite
Citations (144)
Rats were exposed for 1 h to increasing concentrations of cadmium (Cd) through inhalation of cadmium chloride aerosol using nose-only inhalation chambers and depositions of Cd in lungs, liver and kidneys were measured. Changes in spontaneous locomotor activities were recorded 2 and 7 d after cessation of exposure. A concentration dependent increase in Cd in lungs, liver and kidneys was accompanied by significant alterations in spontaneous locomotor response that was dependent on the air Cd concentrations and the postexposure duration. The study shows decreased spontaneous locomotor activity due to Cd accumulation in tissues.
Cadmium chloride
Inhalation exposure
Locomotor activity
Acute exposure
Cite
Citations (4)