Abstract

Arsenic (As) contamination affects hundreds of millions of people globally. Although the number of patients with chronic As exposure is large, the symptoms and long-term clinical courses of the patients remain unclear. In addition to reviewing the literature on As contamination and toxicity, we provide useful clinical information on medical care for As-exposed patients. Further, As metabolite pathways, toxicity, speculated toxicity mechanisms, and clinical neurological symptoms are documented. Several mechanisms that seem to play key roles in As-induced neurotoxicity, including oxidative stress, apoptosis, thiamine deficiency, and decreased acetyl cholinesterase activity, are described. The observed neurotoxicity predominantly affects peripheral nerves in sensory fibers, with a lesser effect on motor fibers. A sural nerve biopsy showed the axonal degeneration of peripheral nerves mainly in small myelinated and unmyelinated fibers. Exposure to high concentrations of As causes severe central nervous system impairment in infants, but no or minimal impairment in adults. The exposure dose–response relationship was observed in various organs including neurological systems. The symptoms caused by heavy metal pollution (including As) are often nonspecific. Therefore, in order to recognize patients experiencing health problems caused by As, a multifaceted approach is needed, including not only clinicians, but also specialists from multiple fields.

Highlights

  • Arsenic (As) has a long history of use as a pigment and as a homicidal agent

  • As the global population increasingly relies on aquifers for drinking water, and because some aquifers are contaminated by heavy metals, the population exposed to As has increased dramatically [2]

  • A small number of acute As exposure patients have been studied in detail, relatively few studies have been performed on a detailed neuropathy of patients chronically exposed to As [4,5,6]

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Summary

Introduction

Arsenic (As) has a long history of use as a pigment and as a homicidal agent. in the past 100 years, As has been used as a pesticide, medicine, and component of a number of products [1]. As the global population increasingly relies on aquifers for drinking water, and because some aquifers are contaminated by heavy metals, the population exposed to As has increased dramatically [2]. A small number of acute As exposure patients have been studied in detail, relatively few studies have been performed on a detailed neuropathy of patients chronically exposed to As [4,5,6]. Patients with chronic As exposure are numerous, their symptoms and clinical courses remain unclear. We describe the research on As toxicity, and clinical aspects and case studies with the goal to make this review useful to physicians who examine patients with arsenicosis as well as to researchers.

Arsenic in the Environment
Metabolic
Toxic LD50 Concentrations
Toxic Mechanisms
Mitochondrial Dysfunction
Lipid Peroxidation
Apoptosis
Increased Calpain
Thiamine Deficiency
Decreased Acetylcholinesterase Activity
Clinical Neurological Symptoms
Acute As Poisoning
Toroku As Pollution
Arsenic Poisoning in Morinaga Dry Milk
Arsenic Contamination in Groundwater
Exposure Dose–Response Relationship in Various Organs
Effect on Children
Factors to Consider
Findings
Conclusions
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