Pneumonitis, chemical

Acute exposure to cadmium may lead to chemical pneumonitis and edema, but is rare nowadays (Herber 1994b). Chronic exposure to Cd affects mostly the renal tubules and the lung. Exposure to Cd can take place both in the occupational and environmental area. 

Nitric oxide (NO) is severely irritating to eyes and respiratory system. Effects may be delayed for several hours following exposure. Corrosive. Inhalation may result in chemical pneumonitis and pulmonary edema. Nonflammable. Oxidizer. This product accelerates the combustion of combustible material. 

Inhalation Prompt medical attention is mandatory in all cases of overexposure. Rescue personnel should be equipped with self-contained breathing apparatus. Conscious victims should be carried (not assisted) to an uncontaminated area and inhale fresh air with supplemental oxygen. Quick removal from the contaminated area is most important. Keep the patient warm, quiet, and under competent medical observation until the danger of delayed pulmonary edema has passed (at least for 72 h). Any physical exertion during this period should be discouraged as it may increase the severity of the pulmonary edema or chemical pneumonitis. Bed rest is indicated. Unconscious persons should be moved to an uncontaminated area, and if breathing has stopped, administer artificial resuscitation and supplemental oxygen. Once respiration has been restored they should be treated as above. 

A casualty with known or potential exposure to carbon monoxide blood agents but who shows no signs of neurological or cardiac abnormalities, and does not complain of discomfort (e.g., headache, difficulty breathing, etc.). If available, breath measurement indicates that the blood carbon monoxide level is less than 10%. Anyone with potential exposure to metal carbonyls should be transported to a medical facility for evaluation because of the risk of latent chemical pneumonitis from inhalation of these agents. 

In a gavage study where rats were administered 570, 1,140, or 4,000 mg/kg/day -hexanc for 90-120 days, 3 rats died due to gavage error (chemical pneumonitis immediately following dosing), but no other deaths were reported (Krasavage et al. 1980). 

Respiratory Effects. Pulmonary edema was observed in a patient after an attempted suicide with endrin and was thought to be due to chemical pneumonitis following aspiration of aromatic hydrocarbons contained in the ingested formulation. The authors state that the hydrocarbons may have been the cause of the pulmonary effects (Runhaar et al. 1985), since hydrocarbon-induced chemical pneumonitis is a well established clinical entity. 

Hardy HL, Tabershaw IR Delayed chemical pneumonitis occurring in workers exposed to beryllium compounds. J Ind Hyg Toxicol 28 197-211, 1946... 

Kraut A, Lilis R Chemical pneumonitis due to exposure to bromine compounds. Chest 94 208-210, 1988... 

Nonane could be expected to dry and defat skin, resulting in irritation and dermatitis, by analogy to other liquid paraffin hydrocarbons. Aspiration into the lung could be expected to cause chemical pneumonitis. 

Application of diglycidyl resorcinol ether caused irritation to the eyes and skin of rabbits. Once-monthly intravenous injection of the compound at doses of 100-200 mg/kg bw produced a progressive lowering of the leukocyte count in monkeys. Hyperkeratosis and basal-cell hyperplasia in the forestomach were observed in rats and mice exposed daily to intragastric doses of 12.5 mg/kg bw and higher for 13 weeks. In a two-year study in rats, dose-related bronchopneumonia occurred, which was not consistent with chemical pneumonitis, but was characterized by polymorphonuclear leukocytes in the alveoli. The compound also inhibited the growth of Walker carcinoma in rats (lARC, 1985). The occurrence of forestomach hyperkeratosis and epithelial cell proliferation was confirmed in a two-week study in rats with doses of 25 mg/kg bw, but not with 12 mg/kg bw (Ghanayem et al., 1986). 

Acute effects of exposure to cadmium result primarily from local irritation. After ingestion, the main effects are nausea, vomiting, and abdominal pain. Inhalation exposure may result in pulmonary edema and chemical pneumonitis. 

If the patient has ingested a petroleum distillate (e.g., kerosene, gasoline, or petroleum-based liquid furniture polish), regurgitated hydrocarbons can be aspirated readily and cause chemical pneumonitis. 

Severe skin irritant. Harmful if swallowed, inhaled, or absorbed through skin extremely destructive to the mucous membranes and upper respiratory tract, eyes, and skin. Inhalation may be fatal as a result of spasm, inflammation, and edema of larynx and bronchi, chemical pneumonitis, and pulmonary edema. Skin cancers produced in animals.2 An experimental carcinogen by oral, subcutaneous, intratracheal, and dermal routes.3 Reasonably anticipated to be a human carcinogen.4 Prevent contact with skin, eyes, and clothing. Prevent inhalation of vapor.5 TLV-TWA 0.5 ppm (1.5 mg/m3).6... 

Inhalation of beryllium compounds can cause acute chemical pneumonitis, a very rapidly progressing condition in which the entire respiratory tract, including nasal passages, pharynx, tracheobronchial airways, and alveoli, develops an inflammatory reaction. Beryllium fluoride is particularly effective in causing this condition, which has proven fatal in some cases. 

Occupational exposure to beryllium, a hapten, by inhalation of fumes/dust and/or by skin contact may result in one of two conditions that primarily affect the lungs. In acute berylliosis, which may occur following a high concentration exposure, the metal acts as a direct chemical irritant, causing a nonspecific inflammatory reaction (acute chemical pneumonitis). However, a small percentage of those exposed develop beryllium-specific T-cell-mediated hypersensitivity (Type IV) with proliferation and accu-... 

The most common members of aliphatic hydrocarbons are methane, ethane, n-propane, n-butane, n-pentane, n-hexane, n-heptane, n-octane, n-nonane, and n-decane. In general, after repeated exposure, these compounds cause nausea, vomiting, abdominal discomfort, asphyxia, and chemical pneumonitis. In high concentrations as gas or vapor, these compounds trigger CNS depression and axonopathy. Keeping up the essential requirements of chemical safety to industrial workers, the ACGIH and OSHA have set the threshold limits for many of the aliphatic hydrocarbons. ... 

Asbestosis, alveolar damage, diffuse pleural fibrosis, lung cancer Acute upper airway injury, tracheobronchitis, chemical pneumonitis, beryllosis Upper airway injury, pneumonitis Byssinosis... 

Pulmonary Dyspnea, necrosis of large airway mucosa with sloughing, chemical pneumonitis, pulmonary edema, ARDS, respiratory failure. 

Scarred lung tissue, impaired breathing, chemical pneumonitis Goodpasture s syndrome Hand tremors Weight loss... 

Inhalation. Exposures primarily industrial. Chemical pneumonitis, berylliosis, cancer. 

The major toxicological effects of beryllium are on the lung. Acute exposure to soluble beryllium compounds (e.g., fluoride, an intermediate in the ore extraction process) irritates the entire respiratory tract, may produce acute chemical pneumonitis, and can result in fatal pulmonary edema. Hypersensitivity, which appears to be mediated by the immune system, may also occur following exposure. This means that future exposure to beryllium may produce health effects at concentrations lower than those generally associated with the effect (the individual becomes much more sensitive to beryllium). 

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