Arsine Poisoning

Fowler, Bruce A.; Weissberg, Joseph B.

doi:10.1056/nejm197411282912207

Cited by 105 publications

(43 citation statements)

References 26 publications

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“…5,6 According to Fowler et al, in renal tubular damage by arsenic, lysosomes were suggested to be the place in which arsenic-hemoglobin complexes were sequestered for long periods. 9 Therefore, we also considered that dense granules in the vacuolar structures might be the arsenic-hemoglobin complexes.…”

Section: Discussionmentioning

confidence: 99%

Acute Kidney Injury by Arsine Poisoning: The Ultrastructural Pathology of the Kidney

et al. 2012

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Arsenic is a terribly poisonous material. There have been many reports of arsine poisoning in workers, and a few have discussed acute kidney injury by arsine. But literatures which investigated the pathologic findings are uncommon, and especially, the ones describing ultrastructural findings are rare. Here, we report an incident of acute arsine poisoning complicated by acute kidney injury and suggest the characteristics of the renal pathology in arsine-induced renal injury, especially the ultrastructural findings.

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Section: Discussionmentioning

confidence: 99%

Acute Kidney Injury by Arsine Poisoning: The Ultrastructural Pathology of the Kidney

et al. 2012

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“…Arsine exposure by humans was found fatal without proper therapy. Arsine breaks down in the body to inorganic arsenic and methylated derivatives which was less toxic than arsine (Fowler and Weissburg, 1974). The mechanism of hemolysis involved depletion of intracellular GSH, resulting in oxidation of sulfhydryl groups in the hemoglobin from ferrous to ferric in mice and rats.…”

Section: Effect On Hematological Parameters 321 Total Erythrocyte mentioning

confidence: 99%

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

Ahmed¹,

Siddiqui

Islam³

et al. 2016

Asian J. Med. Biol. Res

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Abstract:The effect of arsenic trioxide along with tannic acid, di-sodium hydrogen phosphate (DSHP), alum and effects of sand-charcoal-iron-filter (SCIF)-bed filtrated water along with alum on body weight and some hematological parameters were carried out on a total of 30 (01 month old) adult Newzealand white rabbits. The Rabbits were randomly divided in to 6 equal groups (A,B,C,D,E & F) at the ratio of three males and two females in each group, rats of group A was kept as control without giving any treatment, rabbits of group B received arsenic trioxide@100 ppm, group C received arsenic trioxide @ 100 ppm plus tannic acid @100 ppm, group D received arsenic trioxide @ 100 ppm plus di-sodium hydrogen phosphate @100 ppm, group E received arsenic trioxide @100 ppm plus alum @100 ppm orally daily for 60 days in all cases and group F received alum @100 ppm in SCIF-bed filtrated water orally daily for 60 days. The result showed that body weight gain of control group (A) per week per rabbit was found to increase but in treated group B (arsenic trioxide@100ppm orally daily) the mean body weight of group B were decreased gradually and significant (P<0.05) decrease in body weight was observed at 40 days of feeding and at day 60 it was highly significant (P<0.01). Rabbits of group C, D and E were apparently normal and mild body weight reductions were observed which was statistically insignificant. No body weight loss was observed in rabbit of group F. TEC, Hb and PCV were slightly reduced in group C, D, E and F but highly significant (P< 0.01) reduction of TEC, Hb and PCV were observed in group B. ESR values were slightly increased in group C, D, E and F but highly significant (P< 0.01) increased of ESR value was observed in group B. Leukocytosis was observed in rabbits of group B. In this study, it was concluded that treatment with arsenic oxide at low doses has harmful effects on experimental animals including hematological alterations.

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“…Death is caused by acute renal failure, apparently the result of massive tubular damage induced principally by the intratubular precipitation of hemoglobin (10). Standards limiting occupational exposure to arsine have, for the most part, been intended to prevent acute toxicity (1).…”

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confidence: 99%

“…Chronic inhalation of arsine in concentrations below those required to produce acute toxicity would appear however to be widespread in modern industry. Potentially exposed workers include metal smelters and refiners, metallurgists, solderers, lead platers, battery makers, and manufacturers of semiconductors (10,45). In such workers, inhaled arsine is rapidly removed from lung tissue (35) and is oxidized to form elemental trivalent arsenic (As+3) and arsenous oxide (arsenic trioxide, AS 2 0;l) (10,27).…”

mentioning

confidence: 99%

“…Potentially exposed workers include metal smelters and refiners, metallurgists, solderers, lead platers, battery makers, and manufacturers of semiconductors (10,45). In such workers, inhaled arsine is rapidly removed from lung tissue (35) and is oxidized to form elemental trivalent arsenic (As+3) and arsenous oxide (arsenic trioxide, AS 2 0;l) (10,27). Both of these species of arsenic have been shown to be human carcinogens (26).…”

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confidence: 99%

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Occupational exposure to arsine. An epidemiologic reappraisal of current standards.

Landrigan¹,

Costello²,

Stringer³

1982

Scand J Work Environ Health

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LANDRIGAN PJ, COSTELLO RJ, STRINGER WT. Occupational exposure to arsine: An epidemiologic reappraisal of current standards. Scand j work environ heaLth 8 (1982) 169-177. In an evaluation of chronic occupational exposure to arsine (AsHg), an epidemiologic survey was conducted at a lead-acid battery manufacturing plant. Personal (breathing zone) air samples were obtained for the measurement of exposure to arsine and particulate arsenic (As), and area air samples were also collected for the determination of arsenic trioxide (AS20g) vapor concentrations. For the quantification of arsenic absorption, total arsenic content was determined in duplicate 24-h urine samples. Arsine in 177 breathing-zone air samples ranged from nondetectable to 49 ,ug/m 3 . The highest levels were found in the battery formation area, where arsine is generated by the reaction of battery acid with lead-arsenic alloy. 'Exposures to particulate arsenic (maximum 5.1 ,ug/m 3 ) and to AS20g (maximum 0.44 ,ug/m 3 , expressed as As) were generally lower. Urine analysis showed that eight (20.5 0/0) of 39 production workers had urinary arsenic concentrations (corrected to a specific gravity of 1.024) of 50 ,ug/l (0.67 ,umol/l) or above, indicating increased arsenic absorption. None of eight office staff had elevated urinary arsenic levels. A close correlation was found between urinary arsenic concentration and arsine exposure (N = 47; r = 0.84; P = 0.0001). Arsine levels above 15.6 flg/m 3 were associated with urinary arsenic concentrations in excess of 50 ,ug/l (0.67 flmol/l). No correlation was found between urinary arsenic content and exposures to particulate arsenic or to AS20g. Consumption of neither seafood, red wine, tobacco, nor contaminated drinking Water accounted for urinary arsenic excretion. It was concluded that the current arsine exposure standard, 200 flg/m 3 , fails to prevent chronic increased absorption of trivalent arsenic from the inhalation of arsine.

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Arsine Poisoning

Cited by 105 publications

References 26 publications

Acute Kidney Injury by Arsine Poisoning: The Ultrastructural Pathology of the Kidney

Acute Kidney Injury by Arsine Poisoning: The Ultrastructural Pathology of the Kidney

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

Occupational exposure to arsine. An epidemiologic reappraisal of current standards.

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