Haemolytic episode in G6 PD deficient workers exposed to TNT.

Abstract

Haemolytic episode in G6 PD deficient workers exposed to TNT. This is a report on three cases of acute haemolytic disease in glucose-6-phosphate dehydrogenase (G6 PD) deficient workers exposed to trinitroluene (TNT). The courses of the haemolytic crises have several features in common, the most striking being the onset of the disease within two to four days after the start of exposure, and the fact that this has been the first and so far the only haemolytic episode in their lives in spite of detailed medical records of past diseases, injuries, and medications during 12 to 16 years preceding the haemolytic crisis and five to nine years following the disease.The lowest haemoglobin levels for the three patients were 4 0, 6-8, and 8-2 g/dl respectively; haematocrit values were 17 and 24 %; reticulocytes rose in case 1 to 26-2 %, in case 2 to 26%, and in case 3 to 10%.Indirect bilirubinaemia was increased in two patients (5-1 and 2-6 mg/100 ml) and stercobilinogen was as high as 2150 mg/24 hr in one patient. The presence of the metabolite monoamino 2-6 dinitrotoluene was proved in the urine of case 3 and reached 21 y %.The possibility of a dose-response relationship is briefly discussed and the risk of exposing G6 PD individuals in chemical processes is mentioned.The exposure of many thousands of workers to TNT, the most commonly used explosive since the first world war, has resulted in the extensive study of its toxicity (von

Sensors—An effective approach for the detection of explosives

“…Deaths from aplastic anemia and toxic hepatitis were reported in TNT workers prior to 1950s [5,6]. Other occasional effects include leukocytosis or leukopenia, peripheral neuritis, muscular pains, cardiac irregularities, renal irritation and bladder tumors [7][8][9]. These compounds are generally recalcitrant to biological treatment and remain in the biosphere, where they constitute a source of pollution due to both toxic and mutagenic effects on humans, fish, algae and microorganisms.…”

Participation of metabolic activation of 2,4,6-trinitrotoluene to 4-hydroxylamino-2,6-dinitrotoluene in hematotoxicity

“…Acute and chronic exposures of workers to TNT have been shown to cause toxicity in the liver, the hematopoietic system and the eye (Härkönen et al, 1983;Hathaway, 1977;Sabbioni et al, 2005). Hematotoxic action of TNT is manifested as hemolysis, destruction of hemoglobin (Hb) in erythrocytes, formation of methemoglobin (metHb), and/or formation of sulfhemoglobin (sulfHb) (Crawford, 1954;Djerassi and Vitany, 1975;Levine et al, 1984). Tenhunen et al (1984) and Savolainen et al (1985) reported that exposure of rats or humans to TNT resulted in the reduction of the enzyme activity responsible for synthesis of delta-aminolevulinic acid which is an intermediate for heme synthesis, but increased the heme oxygenase activity.…”

Health survey of workers in a 2,4,6-trinitrotoluene explosives factory in Fuxin, China

“…Exposure (both acute and chronic) of factory workers to TNT has been shown to lead to toxic effects in the liver, hematopoietic system, and eyes (Harkonen et al, 1983;Hathaway, 1977;Sabbioni et al, 2005). The hematotoxic effects of TNT have been found to be manifested as hemolysis, the destruction of hemoglobin (Hb) in erythrocytes, and the formation of methemoglobin (metHb) (Crawford, 1954;Djerassi and Vitany, 1975;Levine et al, 1984). The authors have previously found that zetacrystallin catalyzes the reductive activation of TNT, which generates reactive oxygen species (Kumagai et al, 2000), and that 4-hydroxylamino-2,6-dinitrotoluene (HADNT), which is an active metabolite of TNT, mediates TNT-induced hematotoxicity through the formation of pro-oxidants such as hydrogen peroxide (Shinkai et al, 2015a).…”