In aplastic anemia

The human studies described below show that inhalation exposure to benzene for several months to several years results in pancytopenia or other deficits in the relative numbers of circulating blood cells. Continued exposure to benzene can also result in aplastic anemia or leukemia. 

SAFETY PROFILE Moderately toxic by ingestion. Mutation data reported. An allergen. Implicated in aplastic anemia. A 10 gram dose may be fatal to an adult. Skin contact, inhalation, or ingestion can cause asthma, sneezing, irritation of eyes and nose, hives, and eczema. Combustible when exposed to heat or flame. When heated to decomposition it emits acrid smoke and fumes. 

The dangerous acute dose of the technical mixture has been estimated at about 30 g and the dangerous dose of lindane at about 7 to 15 g. However, as already mentioned, a single dose of 45 mg (or approximately 0.65 mg/kgD of lindane caused convulsions. Lindane shows a marked difference in toxicity to different species. Its toxic effect on laboratory animals compares favorably with that of DDT, but for several domestic animals, notably calves, lindane is more toxic than DDT or dieldrin. On a chronic systemic basis the a, p and y isomers are experimental carcinogens. Has been implicated in aplastic anemia. 

SAFETY PROFILE Moderately toxic by intraperitoneal and intravenous routes. Mildly toxic by ingestion. Experimental reproductive effects. Has been implicated in aplastic anemia. When heated to decomposition it emits very toxic fumes of SOx, NOx, and CT. 

SAFETY PROFILE Human poison by unspecified routes. Moderately toxic to humans and experimentally by ingestion. Experimental poison by intravenous, intraperitoneal, and subcutaneous routes. An experimental teratogen. Human systemic effects by ingestion coma, blood pressure decrease, regional or general arteriolar constriction, dyspnea, cyanosis, respiratory depression, nausea or vomiting, and allergic skin dermatitis. Experimental reproductive effects. Mutation data reported. Implicated in aplastic anemia. Used as a tranquilizer. When heated to decomposition it emits toxic fumes of NOx. See also CARBAMATES. 

DOT CLASSIFICATION 5.1 Label Oxidizer SAFETY PROFILE An experimental teratogen. A powerful oxidizer. Severe irritant to skin, eyes, and mucous membranes. Has been implicated in aplastic anemia. Absorption can cause methemoglobinemia and kidney injury. 

SAFETY PROFILE Poison by intraperitoneal and subcutaneous routes. Moderately toxic by intramuscular route. Human systemic effects sensory change involving peripheral nerves, dermatitis. Experimental reproductive effects. Questionable carcinogen with experimental tumorigenic data. Mutation data reported. Has been implicated in aplastic anemia. 

SAFETY PROFILE Poison by intravenous and subcutaneous routes. Moderately toxic by ingestion and intraperitoneal routes. An experimental teratogen. Human systemic effects by ingestion and intraperitoneal routes change in vestibular functions, blood pressure decrease, eosinophilia, respiratory depression, and pulmonary changes. Human reproductive and teratogenic effects by unspecified routes developmental abnormalities of the eye and ear and effects on newborn including postnatal measures or effects. Toxic to kidneys and central nervous system. Has been implicated in aplastic anemia. Experimental reproductive effects. Human... 

Although bone marrow aplasia has not been related with certainty to either the daily or the total dose of chloramphenicol or to the sex or age of the patients, it has occurred almost exclusively in individuals who were taking prolonged therapy, particularly if they were exposed to the drug on more than one occasion (24). The condition is rare, occurring about once in every 18 000-50 000 subjects in various countries. These variations may in part depend on ethnic factors (25,26). For example, there have been very few cases reported in blacks (27). Bone marrow aplasia due to chloramphenicol has usually resulted in aplastic anemia with pancytopenia other forms, such as red cell hypoplasia, selective leukopenia, or thrombocytopenia, are less common. 

Moore MA, Castro-Malaspina H. Immunosuppression in aplastic anemia—postponing the inevitable N Engl J Med 1991 324(19) 1358-60. 

Slee PH, den Ottolander GJ, de Wolff FA. A case of mer-bromin (Mercurochrome) intoxication possibly resulting in aplastic anemia. Acta Med Scand 1979 205(6) 463-6. 

Guidelines for the appropriate use of hemopoietic growth factors in children have been proposed by a panel of European experts, who carefully summarized the potential indications and recommendations, and concluded that adult guidelines are apphcable to children in most cases (9). The authors considered that growth factors should be used in children for only a hmited number of circumstances prophylaxis or treatment in low-risk patients treated with chemotherapy, routine use in aplastic anemia, and mobilization of peripheral blood progenitor cells in healthy pediatric donors. 

Yunis AA, Miller AM, Salem Z, Arimura GK. Chloramphenicol toxicity pathogenetic mechanisms and the role of the P-NO2 in aplastic anemia. Clin Toxicol 1980 17(3) 359-73. 

S. E. Ball, F. M. Gibson, S. Rizzo, et al. Progressive telomere shortening in aplastic anemia. Blood 91,3582 (1998). 

Vincent PC. In vitro evidence of drug action in aplastic anemia. Blood 1984 49 3-12. 

Antin JH, Smith BR, Holmes W, et al. Phase I/II smdy of recombinant human granulocyte-macrophage colony-stimulating factor in aplastic anemia and myelodysplastic syndrome. Blood 1988 72 705-713. 

Hasegawa M, Matsuki Y, Ozawa S et al. (1968). The role of erythropoietin in aplastic anemia - some aspects of the etiology and treatment of asplastic anemia. Keio J Med, 17, 109-123. 

Lymphocyte immune globulin, an immunoglobulin with inununosuppressive properties (15 mg/kg/day IV for 14 days), is used in the prevention or treatment of acute renal allograft rejection, in aplastic anemia, skin allotransplantation, and in bone marrow allotransplantation (see also Figure 28). 

CHRONIC HEALTH RISKS prolonged contact with skin may cause dermatitis, loss of fingernails, and other abnormalities may cause permanent lung damage implications in aplastic anemia experimental reproductive effects have been reported. 

Table 5. Drugs frequently involved in aplastic anemia. (Adapted from van Arsdel 1978)...

In clinical cases, coproporphyrin I is found to be excreted in increased amounts in conditions of rapid blood regeneration. This fact has been suggested to favor the hypothesis that coproporphyrin I is a by-product of normal protoporphyrin synthesis. Coproporphyrin III is said to predominate over coproporphyrin I in the toxic conditions such as lead poisoning and in aplastic anemias. 

Porphyrinuria may be defined as an increase of ether-soluble porphyrins, such as coproporphyrin, in the urine caused by various disturbances. Coproporphyrin III is said to predominate in lead and chemical poisoning, in aplastic anemia, poliomyelitis, and Hodgkin s disease. Coproporphyrin I is said to predominate in pernicious anemia, leukemia, hemolytic jaundice, nonalcoholic cirrhosis, obstructive jaundice, and infective hepatitis. Some of these effects have been considered in the sections on coproporphyrin and protoporphyrin. 

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