Death of humans

No studies were located regarding death of humans after dermal exposure to trichloroethylene. 

Yang LJ, Jeng CJ, Kung HN, et al. Tanshinone IIA isolated from Salvia miltiorrhiza elicits the cell death of human endothelial cells. J Biomed Sci 2005 12 347-361. 

Reactive nitrogen species are another factor of free radical damage in rheumatoid arthritis, although their role is less studied than that of oxygen radicals. Stichtenoth and Frolich [242] pointed out that the inhibition of nitric oxide synthesis had beneficial effects in humans. Mazzetti et al. [243] found that IL-1(3 stimulated NO production in RA chondrocytes. We demonstrated that NO synthase of RA neutrophils generated the enhanced amount of peroxynitrite [234]. Nitric oxide and oxygen radicals are also important inducers of death of human osteoarthritic synoviocytes [244]. 

Cytochrome c oxidase (an enzyme in the mitochondrial respiratory chain) is sensitive to cyanide action (Way 1984). Due to its inhibition, oxygen cannot be utilized, histotoxic hypoxia develops, and this can lead to deaths of humans and animals (see Section 2.3.3). 

Effects reported in humans following dermal exposure to phenol include liver damage, diarrhea, dark urine, and red blood cell destruction. Skin exposure to a relatively small amount of concentrated phenol has resulted in the death of humans. Small amounts of phenol applied to the skin of animals for brief periods can produce blisters and burns on the exposed surface, and spilling dilute phenol solutions on large portions of the body (greater than 25% of the body surface) can result in death. 

In fact, we found that a-tocopherol, an antioxidant hpid-soluble vitamin, prevented geranylgeranoic acid-induced apoptotic cell death of human hepatoma cells. These results are presented in Figure 1 (Shidoji et al, 1997). 

Death can be considered at two different levels death of cells, and death of humans due to old age (which may be described as physiological) or disease. 

Death. There are some data to suggest that lethality may be a public health concern for persons exposed for prolonged periods of time to high levels of 1,4-dichlorobenzene in confined areas (e.g., in homes). The only available information related to the death of humans exposed to 1,4-dichlorobenzene is a case study of a 60-year-old man and his wife who both died of liver ailments after the air in their home had been found to contain increased air concentrations of 1,4-dichlorobenzene (described as saturated ) for 3-4 months (Cotter 1953). However, the exact air concentration of 1,4-dichlorobenzene was not measured or reported, nor was the existence or nature of other possible factors contributing to their deaths (e.g., pattern of alcohol consumption, exposure to other chemicals, or pre-existing medical... 

In the early years there was much interest in the amount of poison necessary to cause sickness and death of humans. From accidental cases of poisoning along the coast of California where catenella commonly blooms, Sommer and colleagues estimated that death of humans resulted from the consumption of about 20,000 HU of poison. However, along the St. Lawrence estuary and Bay of Fundy the Canadians observed death of persons with a consumption as low as 5000 MU. In these areas shellfish become poisonous by feeding on G. tamarensis. 

Also, the reference standard made possible the reporting of the poison content of shellfish as pg per 100 grams of meats and established a basis for an official AOAC mouse assay for the poison (12.13). The Food and Drug Administration set a top limit of 80 micrograms of poison per 100 grams of shellfish meats as marketable for human consumption. This limit is well below the 1 to 4 mg deemed necessary in foods to cause sickness and death of humans. 

Information regarding death of humans after inhalation exposure to DNOC is limited. A case report of a spray operator who inhaled a dense DNOC mist for an unspecified, but apparently acute, duration noted that he died after lapsing into a coma while being treated in a hospital (van Noort et al. 1960). In a survey of 133 spray operators who applied DNOC to cereal crops 5 days per week for 6 weeks, 4 developed signs of acute poisoning (not otherwise specified), one of whom died (Bidstrup et al. 1952). The amount or concentration of inhaled DNOC was not reported in the survey. 

Evdokiou, A., Labrinidis, A., Bouralexis, S., Hay, S., and Findlay, D.M. (2003). Induction of cell death of human osteogenic sarcoma cells by zoledronic acid resembles anoikis. Bone 33 216-228. 

Gordon and Frye (27) collected from the literature reports on 11 deaths of humans considered to be due to atropine. Five of these Involved application of solutions of atropine to the eyes—one person was thought to have received 1.6 mg of atropine and another 18.1 mg. 

Matysiak M, Jurewicz A, Jaskolski D, Sehnaj K (2002) TRAIL induces death of human oligodendrocytes isolated from adult brain. Brain 125 2469-2480. 

The freshwater cyanobacteria Al/f rocvstic aeruginosa produces microcystins. This toxin has been implicated in the death of human dialysis patients (Carmichael 1988). The most common form of microcystins and presumably the biotoxin of choice to be weaponized is microcystin-LR (MCLR). Mice treated with aerosolized MCLR died within hours, and revealed an acute LDjq of 67 /tg/kg (Anon. 1999). Mechanistically, MCLR disturbs cellular function and regulation as a strong inhibitor of protein phosphatases. 

Miller, R. D., and P. Y. Kwok. 2001. The birth and death of human single-nucleotide polymorphisms New experimental evidence and implications for human history and medicine. Hum Mol Genet 10 2195-8. 

Nick Lane breaks out of the mould with a provocative discussion of oxygen s role in evolutionary biology, age-related diseases, and the life and death of human beings... The questions he addresses are of immeasurable practical concern... Lane s exhaustive research is reflected in his tight arguments and crisp prose. ... 

Saleem, M. et al., Lupeol, a fruit and vegetable based triterpene, induces apoptotic death of human pancreatic adenocarcinoma cells via inhibition of Ras signaling pathway. Carcinogenesis, 26 (11), 1956-... 

Xue LY, Chiu SM, Azizuddin K, Joseph S, Olenick NL. The death of human cancer cells following photodynamic therapy apoptosis competence is necessary for Bcl-2 protection but not for induction of autophagy. Photochem Photobiol 2007 83 1016-1023. 

Malik, E, A. Kumar, S. Bhushan, et al. 2007. Reactive oxygen species generation and mitochondrial dysfunction in the apxjp-totic cell death of human myeloid leukemia HL-60 cells by a dietary compxrund withaferin A with concomitant protection by N-acetyl cysteine. Apoptosis 12 (11) 2115-2133. 

Glucose depletion was a principal determinant of hyperoxic (95 % O2) death of human lung-epithelial-like cells (A549), as lactate dehydrogenase activity increased only after glucose was depleted in the medium (Allen and White 1998). 

Chetty, C.S., Vermuri, M.C., Campbell, K., Suresh, C., 2005. Lead-induced cell death of human neuroblastoma cells involves GSH deprivation. Cell Mol. Biol. Lett. 10, 413—423. 

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