AUTOPSY

Acute toxicoses, as well as potential long-term effects of aflatoxki ingestion, have been extensively reported (93). Autopsy reports have noted a positive correlation between aflatoxki B and victims of Reye s Syndrome ki Thailand (94), but this evidence should only be considered as suggestive and preliminary (95). 

The inorganic tin compound that has received the most study from a toxicological viewpoint is stannic oxide. Autopsies performed on workers in the tin mining and refining industry, who inhaled tin oxide dust for as long as 20 yr, disclosed no pulmonary fibrosis (57). Inhalation for long periods produces a benign, symptomless pneumoconiosis with no toxic systemic effects (58). 

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. 

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

Toxicity of 2-Ghloroethanol. Ethylene chlorohydrin is an irritant and is toxic to the Hver, kidneys, and central nervous system. In addition, it is rapidly absorbed through the skin (73). The vapor is not sufficiently irritating to the eyes and respiratory mucous membranes to prevent serious systemic poisoning. Contact of the Hquid in the eyes of rabbits causes moderately severe injury, but in humans corneal bums have been known to heal within 48 hours. Several human fataUties have resulted from inhalation, dermal contact, or ingestion. One fatahty was caused by exposure to an estimated 300 ppm in air for 2.25 hours. In another fatal case, autopsy revealed pulmonary edema and damage to the Hver, kidneys, and brain (73). 

The specimens analyzed are the punctures of human liver. This provides the life-time investigation of elemental metabolism in liver of patient. This is very important aspect, because the information obtained from autopsy is distorted because of fast processes in the liver post mortem. 

Let s begin the analysis, or autopsy with the physical evidence on the component. seal parts. 

Autopsies of animals in the Meuse Valley, Donora, and London episodes described in Chapter 16, Section III, revealed evidence of pulmonary edema. Breathing toxic pollutants is not, however, the major form of pollutant intake for cattle ingestion of pollution-contaminated feeds is the primary mode. 

Jacques, J. (1987) Bertlielot Autopsie d un Mythe (Belin, Paris). 

Tewari SN, Harplani SP. 1972. Detection of organo-phosphorus pesticide residues in autopsy tissues by thin layer chromatography. Proc Nat Acad Sci India 42(A) 287-292. 

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... 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

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. 

No lesions of the spleen were evident on autopsy of a man who ingested a dose of approximately 260 mg endosulfan/kg (Boereboom et al. 1998). 

Similarly, convulsive seizures and a sustained epileptic state persisted after stomach contents were pumped and activated charcoal and anticonvulsive medication were administered in a 43-year-old man who ingested approximately 260 mg/kg endosulfan (Boereboom et al. 1998). At 4 days after exposure, the man was pronounced brain dead, and autopsy revealed cerebral hernia from massive cerebral edema. Eight additional accidental and/or intentional cases of acute poisoning with endosulfan resulting in adverse neurological effects have been reported in more recent studies, six by Blanco-Coronado et al. (1992), one by Lo et al. (1995), and one by Pradhan et al. (1997) two out of the eight resulted in death. Tonic-clonic convulsions were seen in the Blanco-Coronado et al. (1992) cases, whereas Lo et al. (1995) reported the development of muscle fasciculations and episodes of convulsions in their case. In the case reported by Pradhan et al. (1997), the patient had consumed about 75 mL of hquid endosulfan (35% w/v). In this case, in addition to tonic-clonic seizures and myoclonic jerks, the patient developed... 

Diarrhea was observed in rats exposed for 5 days, 6 hours/day to both lethal and sublethal doses of P-endosulfan ( 250 mg/kg/day for males and i6 mg/kg/day for females) (Hoechst 1989b). Autopsy of animals from this study revealed that the mesenteric blood vessels of one of the surviving females exposed to 16 mg/kg/day were distended with blood, and that the small intestines of animals dying as a result of exposure were filled with a reddish fluid (500 mg/kg/day for males and 31.25 for mg/kg/day females). In contrast, no treatment-related effects were revealed by routine gross and histopathological examination of gastrointestinal tissues (stomach, small and large intestines, and pancreas) from rats exposed to doses of 27 mg/kg/day (females) and 81 mg/kg/day (males) for 30 days, 6 hours/day,... 

Studies in animals and autopsy findings of endosulfan and metabolites in various tissues in humans suggest that absorbed endosulfan is most readily distributed to adipose and brain tissue, but that the liver and kidney may be longer-term repositories of endosulfan and its metabolites. Endosulfan residues were found in fat of hospitalized Spanish children (Olea et al. 1999), but no studies were located regarding known or suspected differences between children and adults with respect to endosulfan distribution. 

Renal Effects. Hemorrhage of the medullary layer of the kidneys was observed in an early report of three fatal cases of acute oral poisoning with endosulfan (Terziev et al. 1974). More recent studies have reported acute renal failure after ingestion of endosulfan as a major contributing cause of death in two individuals in both cases, postmortem examination showed extensive tubular necrosis (Blanco-Coronado et al. 1992 Lo et al. 1995). Neither case discussed the possible mechanism of endosulfan-induced acute renal failure, but in one case, the authors of the report indicate that the renal lesions may relate to sepsis and shock (Blanco-Coronado et al. 1992). Ingested doses were not determined in any of these cases, and it is not totally clear that the effects observed at autopsy were a direct result of endosulfan exposure, although based on results from acute animal studies, it seems likely. 

Williams DT, Le Bel GL, Junkins E. 1988. Organohalogen residues in human adipose autopsy samples from six Ontario municipalities. J Assoc Off Anal Chem 71 410-414. 

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... 

Settipane GA, Newstead GJ, Boyd GK Frequency of Hymenoptera venom allergy in an atopic and normal population. J Allergy Clin Immunol 1972 50 146-150. Nall TM Analysis of 677 death certificates and 168 autopsies of stinging insects deaths. J Allergy Clin Immunol 1985 75 207. 

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