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Pulmonary toxicity trachea

In vitro exposure of chicken trachea cells to 2,3-benzofuran results in substantial inhibition of ciliary activity (Pettersson et al. 1982), which may indicate that ciliotoxicity is involved in the respiratory effects seen in mice. Certain other furan derivatives exhibit pulmonary toxicity due to metabolic activation by lung P-450 oxygenases (Boyd 1981), but 2,3-benzofuran... [Pg.33]

Acute exposure of rats to high concentrations (up to 40,000 ppm) has resulted in convulsions, pulmonary edema, respiratory arrest, and death. In rats repeatedly exposed at 600 ppm, death was attributed to renal papillary necrosis renal toxicity was not present in rabbits similarly exposed. Exposure of rabbits to 300 or 600 ppm resulted in convulsions and hyperactivity, moderate inflammation of nasal tissues, and some inflammation of the trachea or bronchi. Subchronic studies found that rats exposed at 3 00 ppm had mottled incisor teeth, minimal renal effects, pulmonary histiocytosis, inflammation of nasal tissues, and cerebral vacuolation. [Pg.651]

Respiratory toxicity Upper respiratory system (nose, pharynx, larynx, and trachea) and the lower respiratory system (bronchi, bronchioles, and lung alveoli) Pulmonary irritation Asthma/bronchitis Emphysema Allergic alveolitis Fibrotic lung disease Lung cancer... [Pg.219]

SAFETY PROFILE Moderately toxic to humans by inhalation. Ver irritating by inhalation. Human mutation data reported. Human respirator system effects by inhalation changes in the trachea or bronchi, emphysema, chronic pulmonary edema or congestion. A strong irritant to eyes and mucous membranes. Questionable carcinogen. [Pg.314]

Histopathology did not reveal any abnormalities at exposure dosages of below 500 mg min m. At higher dosages, animals that died or were killed demonstrated hyperemia of the trachea, pulmonary congestion and edema, and pneumonia. These effects were consistent to exposure to pulmonary irritants. DM toxicity values are given in Table 1. [Pg.172]

Aerobiologists at the U.S. Army Medical Research Institute of Infectious Diseases (Fort Detrick, MD) have developed a reproducible, head-only ricin aerosol exposure model for laboratory nonhuman primates (NHP) that yielded acute LCtso values for African green monkeys or rhesus monkeys corresponding to approximately 6-10 or 15 pg/kg, respectively (Wilhelmsen and Pitt, 1996). Exposure of NHP to aerosolized ricin (particle size 1-2 pm) caused a dose-dependent toxicity that is delayed from 8 to 24 h early anorexia and lethargy were frequently observed, followed by gastric distress, hypothermia, hypotension, acute respiratory distress, and death. Rhesus monkeys exposed to the equivalent of approximately 20-40 pg/kg ricin by aerosol died from acute respiratory distress about 36-48 h after exposure necropsy revealed fibrinopurulent pneumonia, acute inflammation of the trachea and airways, and massive pulmonary alveolar flooding (Wilhelmsen and Pitt, 1996). [Pg.437]

Various techniques of particle delivery are used to deduce pulmonary and systemic effects from the wide parameters of potential toxicological influences. The specific techniques that are currently employed in these studies include intratracheal instillation, intratracheal aspiration, and intratracheal inhalation. Of these different delivery techniques, intratracheal installation is a useful technique to assess the potential health effects of different particles efficiently and cost effectively. Intratracheal instillation is characterized by saline suspended particles administered directly into the trachea of the animal being tested. Intratracheal installation provides a relatively easy way to compare the toxicology between different materials. However intratracheal installation is not able to assess particle deposition. Intratracheal aspiration involves droplet administration of suspended particle matter in the form of a puff of air. Intratracheal inhalation is the most relevant for toxicity and risk assessment. Intratracheal inhalation involves nanoparticulate aerosol formation at constant concentrations during the exposure. [Pg.710]

A chemical that causes an aUeigic reaction - that is, can evoke an adverse immune response in a person. See also sensitizer below. Extunple toluene diisocytinate, CAS 584-84-9 Aspiration toxicity includes severe acute effects, such as chemical pneumonia, varying degrees of pulmonary injury or death following aspiration. Aspiration is the entry of a liquid or solid directly through the oral or nasal cavity, or indirectly from vomiting, into the trachea and lower respiratory system. Example turpentine (major component is pinene, C qH, CAS 80-56-8)... [Pg.134]


See other pages where Pulmonary toxicity trachea is mentioned: [Pg.923]    [Pg.391]    [Pg.94]    [Pg.1008]    [Pg.52]    [Pg.187]    [Pg.760]    [Pg.231]    [Pg.106]    [Pg.760]    [Pg.141]    [Pg.43]    [Pg.757]    [Pg.102]    [Pg.701]    [Pg.2305]    [Pg.53]    [Pg.130]    [Pg.478]    [Pg.484]    [Pg.491]    [Pg.368]    [Pg.11]    [Pg.113]    [Pg.486]    [Pg.429]    [Pg.227]    [Pg.820]    [Pg.1712]   
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