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 in | Toxicological sciences Vol. 103; no. 2; pp. 278 - 284 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Oxford University Press
01.06.2008
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Subjects | |
Online Access | Get full text |
ISSN | 1096-6080 1096-0929 1096-0929 |
DOI | 10.1093/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. |
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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 |
Author_xml | – sequence: 1 givenname: Yuanyuan surname: Xu fullname: Xu, Yuanyuan organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 – sequence: 2 givenname: Yi surname: Wang fullname: Wang, Yi organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 – sequence: 3 givenname: Quanmei surname: Zheng fullname: Zheng, Quanmei organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 – sequence: 4 givenname: Bing surname: Li fullname: Li, Bing organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 – sequence: 5 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 – sequence: 6 givenname: Yaping surname: Jin fullname: Jin, Yaping organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 – sequence: 7 givenname: Xiuqiang surname: Lv fullname: Lv, Xiuqiang organization: Department of Occupational and Environmental Health, College of Public Health, China Medical University, Shenyang, Liaoning, PR China 110001 – sequence: 8 givenname: Guang surname: Qu fullname: Qu, Guang organization: Department of Gastroenterology, The Central Hospital of Fuxin, Fuxin, Liaoning, PR China 123000 – sequence: 9 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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Toxicol. doi: 10.1081/CLT-120018263 |
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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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