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ToxSci Advance Access originally published online on February 27, 2008
Toxicological Sciences 2008 103(2):278-284; doi:10.1093/toxsci/kfn041
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© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Clinical Manifestations and Arsenic Methylation after a Rare Subacute Arsenic Poisoning Accident

Yuanyuan Xu*, Yi Wang*, Quanmei Zheng*, Bing Li*, Xin Li*, Yaping Jin*, Xiuqiang Lv*, Guang Qu{dagger} and Guifan Sun*,1

* Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 {dagger} Department of Gastroenterology, The Central Hospital of Fuxin, Fuxin, Liaoning, PR China 123000

1 To whom correspondence should be addressed at Department of Occupational and Environmental Health, College of Public Health, China Medical University, No. 92 Bei Er Road, Heping District, Shenyang 110001, PR China. Fax: +86-24-2326-1744. E-mail: sungf{at}mail.cmu.edu.cn.

Received December 4, 2007; accepted February 19, 2008


   Abstract

One hundred and four workers ingested excessive levels of arsenic in an accident caused by leakage of pipeline in a copper-smelting factory. Clinical examinations were performed by physicians in a local hospital. Excreted urinary arsenic species were determined by cold trap hydride generation atomic absorption spectrometry. In the initial toxic phase, gastrointestinal symptoms were predominant (83 people, 79.8%). Most patients showed leucopenia (72 people, 69.2%), and increased serum alanine aminotransferase (84 people, 80.8%) and aspartate aminotransferase (58 people, 55.8%). Thirty-five patients (33.6%) had elevated red blood cells in urine. After 17 days of admission, many subjects (45 people, 43.3%) developed peripheral neuropathy and 25 of these 45 patients (24.0%) showed a decrease in motor and sensory nerve conduction velocity. In the comparison of urinary arsenic metabolites among subacute arsenic-poisoned, chronic high arsenic–exposed and control subjects, we found that subacute arsenic-poisoned patients had significantly elevated proportions of urinary inorganic arsenic (iAs) and methylarsonic acid (MMA) but reduced proportion of urinary dimethylarsinic acid (DMA) compared with chronic high arsenic–exposed and control subjects. Chronic exposed subjects excreted higher proportions of iAs and MMA but lower proportions of DMA in urine compared with control subjects. These results suggest that gastrointestinal symptoms, leucopenia, and hepatic and urinary injury are predominant in the initial phase of subacute arsenic poisoning. Peripheral neuropathy is the most frequent manifestation after the initial phase. The biomethylation of arsenic decreases in a dose rate–dependent manner.

Key Words: subacute arsenic poisoning; arsenic methylation; DMPS; urinary arsenic species.


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