Outbreak of Fatal Arsenic Poisoning Caused by Contaminated Drinking Water

Abstract

An outbreak of subacute poisoning occurred among nine members of a family; eight were ill with gastrointestinal symptoms, four developed encephalopathy, and two died. Abnormal liver function tests and leukopenia were common laboratory findings. Epidemiologic and environmental investigations traced the source of arsenic exposure to a farm well with water containing 108 ppm arsenic. The soil adjacent to the well was also contaminated with arsenic, possibly from waste pesticide. Presumably, arsenic gained access to the well through obvious leaks in the well's casing. To our knowledge, this is only the second reported outbreak of fatal arsenic poisoning from contaminated drinking water and one of few instances where illness followed exposure to a toxic substance which was disposed of, or possibly disposed of, in an indiscriminate manner.

Association of Clinical Complications with Nutritional Status and the Prevalence of Leukopenia among Arsenic Patients in Bangladesh

“…Rodent models of arsenic exposure have also demonstrated disturbances in heme biosynthesis, characterized particularly by an increased urinary uroporphyrin excretion [26,27]. These observations explain the possible reason for 26% of our patients suffering from anaemia, also reported by previous workers [8,9]. However, we have seen a far higher prevalence of anaemia in the female patients than males, 26 out of 30; 14 of these female patients represented the underweight nutritional group.…”

“…These effects may be due to both a direct, cytotoxic or hemolytic effect on the blood cells [8,10] and a suppression of erythropoiesis [10]. The magnitude of exposure to patients examined by these researchers is not specified, although arsenic concentration in some of the wells in the area exceeded 1000 µg/L.…”

“…Several studies have found that anaemia, leukopenia and thrombocytopenia are common effects of arsenic poisoning in humans following acute [8] and chronic oral exposures [9] at doses of 50 µg/Kg/day or more. These effects may be due to both a direct, cytotoxic or hemolytic effect on the blood cells [8,10] and a suppression of erythropoiesis [10].…”

Molecular and ionic mimicry and the transport of toxic metals

“…Numerous studies have shown that this metal has deleterious effects on the respiratory (Civantos et al, 1995;Dunlap, 1921;Lundgren, 1954;Morton and Caron, 1989;Pinto and McGill, 1953;Sandstrom et al, 1989), neurological (Armstrong et al, 1984;Blom et al, 1985;Civantos et al, 1995;Feldman et al, 1979;Lagerkvist and Zetterlund, 1994), and cardiovascular (Cullen et al, 1995;Jensen and Hansen, 1998;Lagerkvist et al, 1986Lagerkvist et al, , 1988 systems. The most common and well-characterized sign of As poisoning is the development of skin lesions and warts (Bickley and Papa, 1989;Dunlap, 1921;Holmqvist, 1951;Lagerkvist et al, 1986;Mohamed, 1998;Perry et al, 1948;Pinto and McGill, 1953).…”

Effect of arsenic trioxide along with tannic acid, di-sodium hydrogen phosphate, alum and effects of sand-charcoal-iron-filter bed filtrated water along with alum on body weight and some hematological parameters in rabbit

“…The haematopoietic system was also affected by both short-and long-term arsenic exposures. Anemia and leukopenia were common effects of poisoning and have been reported as resulting from acute, intermediate and chronic oral exposures (Armstrong et al, 1984). These effects might be due to a direct haemolytic or cytotoxic effect on the blood cells (Lerman et al, 1980).…”