Acute Inhalation Toxicity Research Articles

Acute, subacute and 23-day chronic marihuana inhalation toxicities in the rat

The acute, 5-day and 23-day toxicities of Δ 9-THC-impregnated (9% Δ 9-THC) and nonimpregnated marihuana (2.2% Δ 9-THC) cigarettes were determined in Fischer rats. Human smoking conditions were simulated by providing a 50-ml puff of 2-sec duration with a 30-sec exposure interval followed by a 30-sec purge period, each min, through use of an automatic smoking machine. The calculated inhalation doses ranged from 7 to 60 mg/kg acutely from 3.4 to 18.1 mg/kg subacutely, and from 0.7 to 4.2 mg/kg after chronic administration. Acute toxicity was manifested by dose-related hypothermia, hypopnea, loss of coordination, ataxia and prostration. Upon removal from the inhalator, high-dosed animals were depressed and low-dosed animals displayed increased activity rapidly followed by depression. Recovery was nearly complete by 24 hr in the acute trial and by day 6 in the subacute study. Body weights were normal; histopathologic examinations did not reveal any abnormalities. In the 5-day subacute toxicity study rats displayed transitory incoordination, hypothermia, hypopnea and initial increased activity at the lower doses followed by a persistent depression. Rate of body growth was normal, but there was an increase in the weight of reproductive organs. A transient hyperkalemia and hyperproteinemia were seen, but histopathologic examinations gave essentially normal results. Food intake and liver glycogen were increased. When lethality occurred, it was due to respiratory arrest. In the chronic study, there was a dose-related CNS depression and vocalization in the first week of exposure. Low- and middle-dosed animals were hyperactive in the first 10 min post-exposure, but all rats were depressed within 1–2 hr and generally recovered by 6 hr. In the second week of exposure, dose-related ataxia, prostration, “popcorn” response and vocalization were observed; cumulative toxicity occurred in 2 of the high-dosed males. Tolerance to prostration, ataxia, vocalization and exploratory activity developed after 8–12 exposures. After 3 weeks of exposure, hyperactivity and hypersensitivity were seen in low- and middle-dosed groups while high-dosed females exhibited fighting aggression and high-dosed males were depressed or tranquil. During the fourth and last week of exposure, tolerance developed to CNS stimulation in all groups, and animals were either normal or tranquil. Clinical signs were primarily affected in the first week of exposure: a 30–75% dose-related decrease in exploratory activity, hyperthermia at lower doses and hypothermia at the high dose, and a 15–30% decrease in respiration rate at mid and high doses. On day 14, hemochemistry, urinalysis and histopathology were normal but a 10% increase in testes (0.7 mg/kg), and a 15–40% increase in adrenal weights for both sexes was observed, although growth rate was normal. During prolonged exposure, there was a 10% decline in growth rate for males receiving the high dose, but food intake increased 14–29%; in females, body weight was maintained while food consumption fell 5–12%. Generally, continued exposure did not alter rectal temperature, respiration rate, urinalysis or hemochemistry, but a slight decline in hematocrit value was observed at the high-dose level. Histopathologic findings were essentially negative. The inhalation studies reveal that doses of Δ 9-THC, similar to those used by man, rapidly initiate behavioral and physiological changes. Tolerance developed to most of these changes during chronic treatment. Some cumulative toxicity and fighting episodes can occur in the rat after inhalation of marihuana smoke, despite the lack of morphologic changes.

The lack of effects of pretreatment with phenobarbital and chlorpromazine on the acute toxicity of benzene in rats

Female CD rats were injected ip daily for 3 days with either phenobarbital (75 mg/kg) or chlorpromazine (15 mg/kg). On the fourth morning the animals were either subjected to a 4-hr inhalation exposure of benzene or given an ip injection of 50% ( v v ) of benzene and mineral oil. Animals were injected with doses of 1, 2, 3 and 4 g benzene/kg body weight. In the inhalation studies, animals were exposed to 6 levels of benzene ranging from 11,500 to 15,500 ppm. The LD50 for animals injected with benzene and the LC50 for animals inhaling benzene were calculated for control groups and those pretreated with either phenobarbital or chlorpromazine. Neither the LD50 or the LC50 were affected by any of the treatment protocols. In order to determine that the pretreatment was stimulating benzene metabolism, a method for measuring benzene metabolism has been developed using [ 14C]benzene. These studies have shown that phenobarbital and 3-MC do induce benzene metabolism in the liver, that chlorpromazine slightly induces benzene metabolism in the lung, and that pretreatment by these compounds does not affect the acute inhalation toxicity or the ip toxicity of benzene.

Single exposure of rats to the vapors of trace substances in methoxyflurane

The question of the acute inhalation toxicity of real and potential trace substances in methoxyflurane was studied by exposing rats to the vapors of 9 compounds. None of the compounds were of the same order of toxicity as 2,3-dichloro-1,1,1,4,4,4-hexafluoro-2- butene, which was run as a standard. The compounds were found to fall in the following order when ranked from least acutely lethal to most acutely lethal toward rat CClF 2CH 2Cl, CCl 3CClF 2, CF 2CHCl, CH 3OCOOCH 3, CH 3OCF 2CH 2Cl, CClF 2CHCl 2, CHCl 2COOCH 3, CCl 2CF 2, and CH 2ClCOOCH 3.

Toxicology of phosphamidon.

The toxicity of phosphamidon and of its main metabolites, by-products, and formulations has been investigated by means of acute, subacute, and chronic toxicity tests on various vertebrate species in many parts of the world. Particular attention has been paid to acute oral, dermal, and inhalation toxicity testing in mammals, and to the effects of repeated dosing over long periods. Enzymatic and histopathologic investigations were also needed to clarify the mode of action. Special trials covering skin irritation, potentiation, and neurotoxicity provided additional information with regard to public health.

Acute inhalation toxicity of monomethylhydrazine vapor.

Rats, mice, beagle dogs, squirrel monkeys, and rhesus monkeys were exposed to various measured concentrations of monomethylhydrazine (MMH) vapor for specified time periods. Rodents were exposed for 30-, 60-, 120-, and 240-minute periods; dogs and squirrel monkeys, for 15, 30 and 60 minutes; and rhesus monkeys for 60 minutes only. The toxicity of MMH for the five animal species was defined by determinations of LC50 values, pathology, observations of responses, measurements of body weight in rats and mice, and blood chemistry and hematology tests on dogs, and rhesus monkeys. Squirrel monkeys proved to be the most sensitive and rats the least sensitive to the lethal effects of MMH. MMH exposure produced definite but transient, hemolytic changes in dogs and, to a lesser extent, in rhesus monkeys. These experiments show MMH to be a highly toxic compound.

Acute inhalation toxicity of difluoro vapor in mice, rats, dogs, and monkeys

The inhalation toxicity of difluoro (methylphosphonic difluoride) was determined in mice, rats, dogs, and rhesus monkeys exposed for 30 min to various concentrations of the vapor. Most animals showed respiratory distress and were gasping for breath soon after exposure started. Mice and rats usually kept their eyes closed during the exposure; their eyes and noses were irritated. The eyes of dogs were also irritated and showed corneal opacity and miosis. Monkeys were distressed, as they were shaking their heads. They also breathed through their mouths and kept their eyes partially closed. They salivated profusely during the latter part of the exposure. All monkeys lost their appetite after the exposure. A few deaths occurred among all species during the 30-day observation period. Necropsy on dogs revealed the presence of pulmonary congestion and edema. The LCt50 of difluoro vapor for a 30-min total body exposure is 80,000 mg min/m 3 for the mouse, 242,000 mg min/m 3 for the rat, 82,000 mg min/m 3 for the dog, and 91,000 mg min/m 3 for the monkey. The irritating effects of difluoro vapor on the eyes and mucous membranes are sufficiently great that a person will leave a contaminated area, if possible, before a lethal dose in inhaled.

The absorption, distribution, excretion, and toxicity of trifluoroamine oxide

Acute inhalation and intraperitoneal toxicities of trifluoroamine oxide (AMOX) were determined in rats and mice. The LC50's after exposing male rats or mice for 4 hours (deaths within 7 days) were 24.2 ppm and 17.5 ppm, respectively. The LC50's after exposing male rats for 60, 30, or 15 minutes were between 87 and 104 ppm, 119 and 149 ppm, or 202 and 240 ppm, respectively. The intraperitoneal LD50's for male rats or mice (deaths within 7 days) were 51.6 mg/kg and 32.1 mg/kg, respectively. After intraperitoneal injection, females were more susceptible to the lethal effects of AMOX than the males. AMOX produced strong irritations resulting in pulmonary edema and hemorrhage after inhalation, and local denatured changes and accumulation of clear exudate after intraperitoneal injection. AMOX was quickly absorbed after intraperitoneal injection to rats. Fluoride increased quickly in the blood and concentrated in various tissues, especially in the thyroid, bone, and teeth. Most of the fluoride was excreted in the urine, and a considerable amount was recovered also in the feces.

The inhalational toxicity of oxygen difluoride.

Abstract The acute inhalational toxicity of oxygen difluoride in the albino rat has been determined at concentrations of 5 to 40 ppm for 5 to 15 minutes. A CT product (ppm-minutes) of about 100 results in 50% mortality. At the levels studied, gross and microscopic pulmonary damage develop 7 hours after termination of the exposure, and, if death does not intervene, repair begins after the third day. The extreme toxicity of oxygen difluoride and its insidious character make it imperative to exclude its inhalation by personnel.

The acute inhalation toxicity of tetrafluorohydrazine

Summary Rats and dogs were exposed to several concentrations of N2F4 below the previously determined rat 15- and 60-minute LC50's. No histopathologic changes were observed in animals exposed to lethal and sublethal concentrations of N2F4 in the 15- and 60-minute exposures. However, some pathologic changes involving the lungs, spleens, and livers were observed in animals exposed to lethal concentrations in the 4-hour exposures. The toxic signs were cyanosis, hematologic changes, and eye and nasal irritation. Rats showed signs of eye and nasal irritation at concentrations causing no such effects in dogs. However, at these concentrations dogs had a greater increase in methemoglobin than did the rats.

Inhalation toxicity studies with aerosols of sesqui-mustard

Acute inhalation toxicity studies with 1,2-bis(2-chloroethylthio)ethane have been made in mice, rats, guinea pigs, hamsters, pigeons, and dogs. Following exposure, animals show loss of body weight, coughing, dyspnea, ataxia, and diarrhea prior to death. Deaths occurred over a 14-day observation period with a primary peak between the third and sixth day. Pigeons were the least sensitive of the species tested. Tissue damage in most animals was limited to the upper respiratory tract and digestive tract.

The acute inhalation toxicity of heated aerosols of three hydraulic fluids.

Abstract A comparative study was made of the effect of pyrolysis at various temperatures upon the toxicity of aerosols of three aircraft engine hydraulic fluids. Rats and dogs were exposed 4 hours to both unpyrolyzed aerosols and aerosols pyrolyzed at 520°, 1020°, and 1560°F of the following fluids: OS-40, a phosphate ester; XF-408, a mixture of a silicone oil and a fluorohydrocarbon; and MLO-5277, an organosilicate. The toxic signs and pathologic changes produced in exposed animals showed that these compounds and their pyrolytic products were eye and respiratory irritants. OS-40 was the least toxic of the three fluids.

Acute inhalation toxicity of vinyl chloride to laboratory animals.

(1960). Acute Inhalation Toxicity of Vinyl Chloride to Laboratory Animals. American Industrial Hygiene Association Journal: Vol. 21, No. 5, pp. 394-398.

Radiological Appearances of the Chest following Partial Asphyxiation by a Smoke Screen

Radiological Appearances of the Chest following Partial Asphyxiation by a Smoke ScreenP. H. WhitakerP. H. WhitakerSearch for more papers by this authorPublished Online:28 Jan 2014https://doi.org/10.1259/0007-1285-18-216-396SectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail AboutAbstractThe radiological appearances of the chest following asphyxiation by a smoke-screen are recorded, and literature on damage to the lungs by caustic fumes is reviewed. Previous article Next article FiguresReferencesRelatedDetailsCited byThe toxicology of zinc chloride smoke producing bombs and screens11 January 2017 | Clinical Toxicology, Vol. 55, No. 3Zinc Chloride (Smoke Bomb) Inhalation Lung InjuryChest, Vol. 127, No. 6Pulmonary damage after modest exposure to zinc chloride smokeRespiratory Medicine, Vol. 93, No. 12A comparative study of the acute inhalation toxicity of smoke from TiO2-hexachloroethane and Zn-hexachloroethane pyrotechnic mixturesArchives of Toxicology, Vol. 59, No. 3Some Hazards of Accidental Gassing25 June 2016 | Medicine, Science and the Law, Vol. 6, No. 1The Pulmonary Effects of Toxic Gases and Smokes An Experimental Radiographic Investigation*G. M. Ardran28 January 2014 | The British Journal of Radiology, Vol. 23, No. 266The Australian and New Zealand Association of Radiologists28 January 2014 | The British Journal of Radiology, Vol. 23, No. 266 Volume 18, Issue 216December 1945Pages: 369-402 © The British Institute of Radiology History Published onlineJanuary 28,2014 Metrics Download PDF