Pneumonitis toxic

Examples Silicosis, asbestosis, pneumonitis, pharyngitis, rhinitis or acute congestion farmer s lung, beryllium disease, tuberculosis, occupational asthma, reactive airways dysfunction S5mdrome (RADS), chronic obstructive pulmonary disease (COPD), hypersensitivity pneumonitis, toxic inhalation injury, such as metal fume fever, chronic obstructive bronchitis, and other pneumoconioses. 

Health and Safety Factors. Boron trifluoride is primarily a pulmonary irritant. The toxicity of the gas to humans has not been reported (58), but laboratory tests on animals gave results ranging from an increased pneumonitis to death. The TLV is 1 ppm (59,60). Inhalation toxicity studies in rats have shown that exposure to BF at 17 mg/m resulted in renal toxicity, whereas exposure at 6 mg/m did not result in a toxic response (61). Prolonged inhalation produced dental fluorosis (62). High concentrations bum the skin similarly to acids such as HBF and, if the skin is subject to prolonged exposure, the treatment should be the same as for fluoride exposure and hypocalcemia. No chronic effects have been observed in workers exposed to small quantities of the gas at frequent intervals over a period of years. 

Pulmonary Oxygen Toxicity Radiation Pneumonitis "Shock Lung"... 

Mineral Oil Hydraulic Fluids. No specific methods were located for interfering with the mechanism of action for toxic effects produced by mineral oil hydraulic fluids. Unstable alveoli and distal airways have been proposed as major factors in the respiratory symptoms that occur after the ingestion of other petroleum-derived materials. Continuous positive airway pressure or continuous negative chest wall pressure, as well as the application of supplemental oxygen, have been recommended to counteract the resultant pneumonitis (Eade et al. 1974 Klein and Simon 1986). 

Mineral Oil Hydraulic Fluids. Aside from the possibility of the development of pneumonitis following the aspiration of ingested mineral oil hydraulic fluid, little is known regarding the toxicity of these materials. Additional animal studies to identify the possible toxic effects of exposure to these materials may provide information relevant to the investigation of methods for reducing the toxic effects. 

Procarbazine -alkylating agent cell cycle independent -bone marrow suppression—prolonged -nausea and vomiting—severe tolerance often develops with repeated dosing -mucocutaneous effects (mucositis, stomatitis, diarrhea) -rash, hives, photosensitivity -interstitial pneumonitis -CNS toxicity—seizures, lethargy, headache, ataxia -flu-like syndrome -azoospermia and amenorrhea almost universal... 

I 12. The answer is b. (Hardman, pp 1264-1265J Dactinomycin s major toxicities include stomatitis, alopecia, and bone marrow depression. Bleomycin s toxicities include edema of the hands, alopecia, and stomatitis. Mitomycin causes marked bone marrow depression, renal toxicity, and interstitial pneumonitis. Plicamycin causes thrombocytopenia, leukopenia, liver toxicity, and hypocalcemia. The latter may be of use in the treatment of hypercalcemia. Doxorubicin causes cardiotoxicity, as well as alopecia and bone marrow depression. The cardiotoxicity has been linked to a lipid peroxidation within cardiac cells. 

Toxicities are GI (stomatitis, diarrhea, nausea, vomiting), hematologic (thrombocytopenia, leukopenia), pulmonary (fibrosis, pneumonitis), and hepatic (elevated enzymes, rare cirrhosis). Concomitant folic acid may reduce some adverse effects without loss of efficacy. Liver injury tests (aspartate aminotransferase or alanine aminotransferase) should be monitored periodically, but a liver biopsy is recommended during therapy only in patients with persistently elevated hepatic enzymes. MTX is teratogenic, and patients should use contraception and discontinue the drug if conception is planned. 

Chemical disasters are not very easy to predict and prevent. Depending on the extent of the accident, they may produce the following health manifestations asphyxiation, central nervous system depression, defeating dermatitis, aspiration pneumonitis, myocardial sensitization and irritability and hepatorenal toxicity. 

Deaths in rats resulting from single-exposure concentration/duration combinations expected to produce 50%-90% mortality usually occurred within 24 hours. These deaths were attributed to cardiac or respiratory failure and were probably a direct effect of 1,2-dibromoethane toxicity. Deaths resulting from exposure concentration/duration combinations expected to produce 0.01%-50% mortality occurred as long as 12 days after exposure and were due to pneumonia. The authors attributed pneumonia to 1,2-dibromoethane-induced lung injury, but this lesion could also have been due to intercurrent bacterial or mycoplasmal pulmonary infection. Rats free of enzootic respiratory infections were not available in 1952. More contemporary inhalation studies of 1,2-dibromoethane using commercially produced rats (Nitschke et al. 1981 NTP 1982) did not report pneumonic lesions or pneumonia-related mortality. 

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