Pulmonary lesion

The filariform larva found in moist soils may be either ingested or penetrate the skin of its host. It is then carried through the circulatory system to the lungs and migrates up the respiratory tree into the digestive tract. The worms feed on intestinal tissue and blood. Some worms may persist in humans as long as nine years. Infestations cause cutaneous reactions, pulmonary lesions, intestinal ulcerations, and anemia. 

Equivalent to 0.11, 0.44, or 1.8 mg Ni m/3 for as long as 13 weeks exposures were 6 h daily and 5 days Dose-dependent increase in pulmonary lesions atrophy of the nasal olfactory epithelium at 0.44 mg/m3 and higher 26... 

No progressive accumulations in tissues. No pulmonary lesions at 50 or 120 mg/kg diet however, 100% of the 250 mg/kg group had pulmonary lesions (Summers 1980)... 

Respiratory Effects. Pulmonary function tests were not affected in workers exposed to hexachloroethane for 5 weeks while wearing protective equipment (Selden et al. 1994). Acute exposure of rats to 5,900 ppm hexachloroethane (a combination of gaseous and microcrystalline material) resulted in interstitial pulmonary pneumonitis (Weeks et al. 1979). These pulmonary lesions were seen after a 14-day recovery period. The entrapment of solid hexachloroethane particles in the lungs could have contributed to the symptoms observed. 

Penha, P. D., and S. Werthamer. Pulmonary lesions induced by long-term exposure to ozone. II. Ultrastructure observations of proliferative and regressive lesimis. Arch. Environ. Health 29 282-189, 1974. 

Plopper, C. G., D. L. Dungworth, and W. S. Tyler. Morphometric evaluation of pulmonary lesions in rats exposed to ozone. Amer. J. Path. 71 395-408, 1973. 

Werthamer, S., L. H. Schwartz, J. J. Carr, and L. Suskind. Ozone-induced pulmonary lesions Severe epithelial changes following sublethal doses. Arch Environ. Health 20 16-21, 1970. 

Examination of 13 individuals 5 years after they were occupationally exposed to a chlorine dioxide leak revealed sensitivity to respiratory irritants and nasal abnormalities. Delayed deaths occurred in animals after exposure to 15 0-2 00 ppm for less than 1 hour. Rats exposed daily to 10 ppm died after 10-13 days of exposure effects were nasal and ocular discharge and dyspnea autopsy revealed purulent bronchitis. Another study reported that two to four 15-minute exposures to 5 ppm for 1 month did not alter the blood composition or lung histology of rats similar exposures to 10-15 ppm caused bronchitis, bronchiolitis, catarrhal alveolar lesions, and peribronchial infiltration. Lesions healed within 15 days after treatment. Rats and rabbits exposed for 30 days to 5 or 10 ppm (2 hours/day) had localized bronchopneumonia with elevated leukocyte counts slight reversible pulmonary lesions were found after exposures of 2.5ppm for 4-7 hours/day. No adverse reactions were... 

Pratt PC, Vollmer RT, Miller JA Epidemiology of pulmonary lesions in nontextile and cotton textile workers—a retrospective autopsy analysis. Arch Environ Health 35 133-138, 1980... 

Chronic exposure (12 months) of rats and mice to 1000 or 5000 mg/m JP-4 did not cause respiratory tract irritation or pulmonary lesions in rats at the end of the exposure or at 12 months after exposure. An increase of interstitial cell tumors was observed in the testis 12 months after exposure. No effect on the incidence of neoplastic tumors was seen in mice in the same study. A 1-year JP-7 exposure study to rats at 750mg/m produced no toxicologi-cally significant treatment-related neoplastic lesions in mice or rats except for a small increase in incidence of C-cell adenomas and kidney adenomas in male rats. However, these tumors are of the type that are considered to be specific to the male rat and not relevant to humans or other animals. The exposure period in these two studies was 1 year, rather than the typical 2-year lifetime period. This time period... 

The progression of symptoms may continue after dust exposure ceases. Although there may be a factor of individual susceptibility to a given exposure to silica dust, the risk of onset and the rate of progression of the pulmonary lesion are clearly related to the character of the exposure (dust concentration and duration). The disease tends to occur after an exposure measured in years rather than in months. It is generally accepted that silicosis predisposes to active tuberculosis and that the combined disease tends to be more rapidly progressive than uncomplicated silicosis. 

Little information is available on the toxicology of pure elemental silicon, which is an inert material that appears to lack the property of causing fibrosis in lung tissue. Silicon dust gave an inert response on intraperitoneal injection into guinea pigs and rats. Another study, however, reported minimal pulmonary lesions in rabbits after the intratracheal injection of silicon dust at a high level of 25 mg. ... 

Paulet and Desbrousses (1970) exposed groups of 10 rats/sex (strain not specified) to chlorine dioxide vapors at a concentrations of 0 or 2.5 ppm (6.9 mg/m ), 7 hours/day for 30 days. The weekly exposure frequency was not reported. Chlorine dioxide-exposed rats exhibited respiratory effects that included lymphocytic infiltration of the alveolar spaces, alveolar vascular congestion, hemorrhagic alveoli, epithelial erosions, and inflammatory infiltrations of the bronchi. The study authors also reported slightly decreased body weight gain and decreased erythrocyte and increased leukocyte levels, relative to controls. Recovery from the pulmonary lesions was apparent in rats examined after a 15-day recovery period. 

Horie A, Tanaka I, Haratake J, et al. 1985. Electron microscopy of pulmonary lesions including carcinoma, induced by inhalation exposure of rats to nickel oxide aerosol. In Brown SS, Sunderman FW Jr, eds. Progress in nickel toxicology. Proceedings of the 3rd International Congress on Nickel Metabolism and Toxicology. Oxford, UK Blackwell, 41-44. 

Hueper WC. 1958. Experimental studies in metal carcinogenesis. IX. Pulmonary lesions in guinea pigs and rats exposed to prolonged inhalation of powdered metallic nickel. Arch Pathol 65 600-607. 

It is called vomiting gas and has been used extensively by the military as a chemical warfare agent. Four ppm is sufficient to render a man unfit for action, and 20 ppm when breathed from 1 to 2 min causes definite bronchial or pulmonary lesions(Ref 5). See also CWA PS under Chemical, Biological and Radiological Agents... 

NO2 is a deep lung irritant capable of producing pulmonary edema. The type I cells of the alveoli appear to be the cells chiefly affected on acute exposure. Exposure to 25 ppm is irritating to some individuals 50 ppm is moderately irritating to the eyes and nose. Exposure for 1 hour to 50 ppm can cause pulmonary edema and perhaps subacute or chronic pulmonary lesions 100 ppm can cause pulmonary edema and death. 

It is known that 02 is potentially toxic as was evident in premature infants where it caused retrolental fibroplasia (2) or in artificial ventilation where it caused pulmonary lesions (3) because of the formation of ROS. 

Nash G, Blennerhasset JB, Pontoppidan H. Pulmonary lesions associated with oxygen therapy and artificial ventilation. N Engl J Med 1967 276 368-374. 

Studies regarding respiratory effects in animals following inhalation exposure to barium are limited to two reports (Hicks et al. 1986 Tarasenko et al. 1977). Pulmonary lesions (perivascular and peribronchial sclerosis and focal thickening of the interalveolar septa) were observed in rats following intermediate inhalation exposure to 3.6 mg barium/m as barium carbonate dust (Tarasenko et al. 1977). Bronchoconstriction was reportedly noted in guinea pigs following inhalation for an unspecified period of time to 0.06 mg barium/m /min as aerosolized barium chloride solution (Hicks et al. 1986). 

Most of the Al absorbed from the respiratory tract accumulates in the lungs. Pulmonary lesions have been described in employees of Al processing or manufacturing industries and encephalopathy after Al inhalation has been reported. Al is widely distributed and has many industrial uses, and toxicity from occupational exposure is assumed to be extremely rare [2, 177]. Nevertheless, a recent study investigating adverse effects on the central nervous system of Al welders found an Al-exposure-related increase in blood and urine Al concentrations, deficits in neuropsychological test performance and mild diffuse EEG abnormalities. Therefore, the potential for Al-induced neurotoxicity in those occupationally exposed to Al fumes may be greater than previously suspected [177]. 

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