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Trachea ulceration

Physiological Effects. The sulfur and nitrogen mustards act first as cell irritants and finally as a cell poison on all tissue surfaces contacted. The first symptoms usually appear in 4—6 h (4). The higher the concentration, the shorter the interval of time between the exposure to the agent and the first symptoms. Local action of the mustards results in conjunctivitis (inflammation of the eyes) erythema (redness of the skin), which may be followed by blistering or ulceration and an inflammatory reaction of the nose, throat, trachea, bronchi, and lung tissue. Injuries produced by mustard heal much more slowly and are much more Fable to infection than bums of similar intensity produced by physical means or by other chemicals. [Pg.398]

Postmortem findings include lymph nodes that are enlarged, fibrotic, and abscessed the nasal cavity, pharynx, larynx, and trachea show nodules, ulcers, and stellate scars the lungs have seed-like (miliary), firm, rounded, encapsulated gray nodules resembling tubercles as well as cutaneous lesions. [Pg.514]

Pathologic exams performed immediately after exposure revealed lesions in the nasal passages, including epithelial degeneration with epithelial cell exfoliation, erosion, ulceration (respiratory epithelium) and epithelial erosion and ulceration of the olfactory epithelium of the dorsal meatus. Less severe changes were observed in the nasopharynx, larynx, trachea, lungs. [Pg.139]

The phyalolt cal action of muKtatd gas may be dasdfied as local and general. The local action results in conjunctivitis or inflammation of the eyes erythema of the skin, which may be followed by blistering or ulceration and inflammatory reaction of the nose, throat, trachea, and bronchi.. . . ... [Pg.226]

Rosenbaum et al. (1998) described two cases of young children (2-3 years old) who bit into ammonia pellets/capsules. Both children drooled and had ulcerative lesions on the tongue and/or on the buccal mucosa. One child had superficial ulcerations on the posterior esophageal wall and the other child had edematous, erythematous upper and lower lips with areas of desquamation, eschar of the hard palate, and edema and erythema of the supraglottic stmctures and upper trachea. Both children recovered without incidence. [Pg.80]

HUMAN HEALTH RISKS EPA group B2 probable human carcinogen Acute Risks inflammation and necrosis of the eyes, mouth and respiratory tract ulceration delirium coma severe blistering conjunctivitis catarrhal inflammation of the mucous membranes, nose, throat, larynx and trachea Chronic Risks damage to the lungs, liver, kidneys, heart and CNS prostration suppression of urine pulmonary edema jaundice hematuria albuminuria. [Pg.89]

HEALTH SYMPTOMS inhalation (irritates skin, eyes, nose, throat, larynx, and trachea) contact (skin ulcerations, necrosis, reddening of the skin). [Pg.89]

Irritates lips, oral mucosa, pharynx produces ulcers and scars, necrosis of trachea, shedding of mucous membrane, edema of glottis Bullae and ulcers of the nasal and buccal mucous membranes and the skin Ulceration and reddish-brown sloughs Irritates the mucous membranes hemorrhages from the nose and mouth... [Pg.254]

His most famous monograph De re metallica (1556) described miners diseases of the lungs as well as of the eyes and the ulcerative effects of ura-ninite down to the bones. Dry pits are more harmful to the miners, since they allow the dust to penetrate much more easily into the trachea and the lungs. Pulmonary ulceration made the affected miners waste away. In some Carpathian mining communities there were women who had married seven times. [Pg.22]

Complications Transverse myelitis, aortic rupture, and ulceration of the trachea and esophagus complicate bronchial artery infusion of chemotherapeutic agents. Fever, malaise, and chemical pneumonitis, in addition to skin necrosis, have also been reported. Hemoptysis has occurred in the absence of residual tumor, presumably related to the infusion itself. These complications have minimized the rewards of infusion. [Pg.219]

However, the trachea is also made of cartilage and can be involved with repetitive cycles of inflammation, ulceration, and scarring that may ultimately present with tracheal stenosis. The two CTDs most often associated with tracheal stenosis include relapsing polychondritis and necrotizing granulomatous vasculitis. Stenosis in both diseases is most common in the subglottic space. [Pg.501]

Obstructive lung disease has been rarely associated with BD as well as trachea-bronchial ulcerations and stenosis. Ulcerative lesions may be found in the trachea and proximal airways. Mucosal edema may result in irregular narrowing of the airway (21-23). [Pg.701]

Rat 6h/day x 3 days 6h/day x 5 days 6h/day x 5 days 9.1 1.02 (TWA) 0.1, 0.5,1.0 2.5 BW 1 marked nasal epithelial degeneration, cell exfoliation, ulceration, and necrosis neutrophil infiltration of epithelium and squamous metaplasia after 5 days milder lesions in pharynx, trachea, and lungs. Nasal inflammation and hyperplasia in squamous and respiratory epithelium (concentration-dependent) but not OE extended to the nasopharyngeal duct at 2.5 ppm. Jiang et al. (1983) George et al. (2010) Jarabek et al. (2010)... [Pg.322]


See other pages where Trachea ulceration is mentioned: [Pg.4]    [Pg.168]    [Pg.549]    [Pg.159]    [Pg.478]    [Pg.71]    [Pg.258]    [Pg.368]    [Pg.284]    [Pg.238]    [Pg.16]    [Pg.379]    [Pg.609]    [Pg.610]    [Pg.322]    [Pg.502]    [Pg.507]   
See also in sourсe #XX -- [ Pg.219 ]




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