Autopsy lungs

Stroink, G., Lim, D. and Dunlap, RA. (1987). A Mossbauer-eflect study of autopsied lung tissue of asbestos workers. Phys. Med. Biol. 32, 203-211. 

Kishimoto T, Ono T, Okada K, et al. 1989. Relationship between number of asbestos bodies in autopsy lung and pleural plaques on chest x-ray film. Chest 95 549-552. 

Occurrence in Chiysotile Amphibole asbestos, identified as tremolite asbestos or actinolite asbestos, has been reported to be a minor contaminant in some deposits of chrysotile in Quebec. Part of the evidence that tremolite asbestos exists in certain chrysotile deposits mined in Quebec comes from observations of higher concentrations of tremolite asbestos fibers than chrysotile fibers in autopsied lung tissues of certain miners and millers who were chronically exposed to chrysotile ores (see Case 1994 for review). Inhaled tremolite asbestos fibers are more persistent in lungs than inhaled chrysotile fibers. 

Kunze (50) examined autopsied lung and heart tissue from 340 octogenarians, finding two predominant patterns of amyloid deposits in 49 cases (/) combined vascular and alveolar-septal or (ii) isolated alveolar-septal disease. Typically concurrent heart and lung involvement occurred. The incidence of lung amyloid deposits increased with age, from 2% of cases <80 years old to 10% in cases 80 to 84 years old, and 20% in those older than 85 years. Alveolar-septal deposition always accompanied vascular deposits. Bronchial walls were never involved. 

Fig. 2.1.17. Autopsy lung showing asbestosis (diffuse interstitial fibrosis) in the lower zones, along with a large lung cancer (arrow). The presence of asbestosis allows one to attribute the lung cancer to asbestos exposure. From Churg and Green (1998), used with permission...

Table 2 Types of Mineral Particles in the Airway Walls in Human Autopsy Lungs...

Hydrogen chloride is produced when PVC bums. A series of tests for the Federal Aviation Administration studied this issue. In those studies, test animals were able to survive exposures to hydrogen chloride reaching 10,000 ppm (190). More recent studies indicate less of a potential for delayed effects on lung function than expected (191). In a typical fire, hydrogen chloride levels rarely exceed 300 ppm, a fact confirmed by the Boston Fire Department and Harvard University (192). In hundreds of autopsies conducted on fire victims in the United States, not one death has been linked to the presence of PVC. 

Irregular respiration was observed in both male and female rats after a 4-hour nose-only inhalation exposure to aerosolized endosulfan (Hoechst 1983a). In both male and female rats, dyspnea was observed at the lowest concentrations tested (12.3 and 3.6 mg/m for males and females, respectively). Autopsies of the rats that died revealed dark-red, pinhead-sized foci on the lungs. It is unclear whether these effects represent direct effects of inhaled endosulfan on respiratory tissues or whether they are secondary to central nervous system effects on respiratory function. No treatment-related effects were... 

Boereboom et al. (1998) observed minor lung hemorrhaging and atelectasis at autopsy of a man who ingested approximately 260 mg/kg endosulfan 4 days prior to death. 

Prodromi of anaphylaxis comprise metallic fishy taste, anxiety, sweating, headache, disorientation. Autopsy cases have shown few specific findings sometimes there is inflation of the lung and pulmonary edema with peribronchial eosinophilic... 

Child, 6-year-old, accidently swallowed unknown amount of Gramoxone W (contains paraquat) Residue in urine 6 days after exposure was 3.6 mg paraquat/L death 7 days after onset of symptoms. Autopsy showed ulceration of buccal mucosa, emphysema, severe lung damage, jaundice, and renal failure (Campbell 1968)... 

Weedon et al. (1940) exposed groups of eight rats to a concentration of HCN at 16 ppm for 16 h. No deaths occurred, and rats appeared normal during the exposure. At autopsy of two rats, the lungs of one rat showed pseudotuber-culosis. All other organs in that rat and the other rat were normal. 

Autopsy tissues and other biologic specimens from people fatally poisoned with endrin (by the oral or an unspecified route) were analyzed (Tewari and Sharma 1978). The "fatal period" (presumed to be the time from onset of symptoms until death) for the subjects studied ranged from 1 to 6 hours. As is characteristic of oral administration, highest tissue concentrations were observed in the stomach (1.04-14.5 mg/100 g), intestine (1.31-66 mg/100 g), and liver (0.94-20 mg/100 g), followed by kidney, spleen, heart, and lung. Blood concentrations were low (0.43-0.85 mg/100 g) compared to tissue concentrations. 

Respiratory Effects. Intra-alveolar bleeding, edema of the lungs, and blood in the bronchus were observed at autopsy in a man who had been dead for at least 24 hours after ingesting an unknown quantity of disulfoton (Hattori et al. 1982). This was the only information found regarding respiratory effects in humans after oral exposure to disulfoton. 

Tissue levels of chloroform obtained at autopsy reflected environmental exposure levels in other studies. The levels ranged from 20 to 49 pg/kg of chloroform from adipose tissue extracted into hexane from samples taken from 10 individuals in Florida (Peoples et al. 1979). In 30 autopsy cases in Germany, the adipose tissue contained amean of 23.4 pg/kg wet tissue 24.8 pg/kg perinephric fat 10.8 pg/kg liver tissue 9.9 pg/kg lung tissue and 10 pg/kg muscle tissue (Alles et al. 1988). The maximum chloroform content increased with age and was not dependent on the volume of fat in the tissues. 

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