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

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...

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Published inToxicological sciences Vol. 103; no. 2; pp. 278 - 284
Main Authors Xu, Yuanyuan, Wang, Yi, Zheng, Quanmei, Li, Bing, Li, Xin, Jin, Yaping, Lv, Xiuqiang, Qu, Guang, Sun, Guifan
Format Journal Article
LanguageEnglish
Published United States Oxford University Press 01.06.2008
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Online AccessGet full text
ISSN1096-6080
1096-0929
1096-0929
DOI10.1093/toxsci/kfn041

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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.
AbstractList 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.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.
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.
Author Wang, Yi
Xu, Yuanyuan
Zheng, Quanmei
Jin, Yaping
Lv, Xiuqiang
Qu, Guang
Sun, Guifan
Li, Bing
Li, Xin
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  surname: Xu
  fullname: Xu, Yuanyuan
  organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001
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  surname: Wang
  fullname: Wang, Yi
  organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001
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  organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001
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  givenname: Xin
  surname: Li
  fullname: Li, Xin
  organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001
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  organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001
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  givenname: Guang
  surname: Qu
  fullname: Qu, Guang
  organization: Department of Gastroenterology, The Central Hospital of Fuxin, Fuxin, Liaoning, PR China 123000
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  givenname: Guifan
  surname: Sun
  fullname: Sun, Guifan
  email: sungf@mail.cmu.edu.cn, 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. sungf@mail.cmu.edu.cn.
  organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001
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Snippet One hundred and four workers ingested excessive levels of arsenic in an accident caused by leakage of pipeline in a copper-smelting factory. Clinical...
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SubjectTerms Accidents
Adolescent
Adult
Aged
Arsenic - adverse effects
Arsenic - metabolism
arsenic methylation
Arsenic Poisoning - metabolism
Arsenic Poisoning - pathology
Arsenic Poisoning - physiopathology
China
DMPS
Female
Gastrointestinal Diseases - chemically induced
Gastrointestinal Diseases - pathology
Humans
Leukopenia - chemically induced
Leukopenia - pathology
Male
Methylation
Middle Aged
Occupational Exposure
Peripheral Nervous System Diseases - chemically induced
Peripheral Nervous System Diseases - pathology
subacute arsenic poisoning
urinary arsenic species
Water Supply
Title Clinical Manifestations and Arsenic Methylation after a Rare Subacute Arsenic Poisoning Accident
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https://www.ncbi.nlm.nih.gov/pubmed/18308700
https://www.proquest.com/docview/19710020
https://www.proquest.com/docview/69193158
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