Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
Department of Medical Research, Ministry of Health and Sports, Yangon, Myanmar.
Environ Health Prev Med. 2019 Apr 23;24(1):23. doi: 10.1186/s12199-019-0781-0.
More than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW).
A cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW.
Residents with ACDW ≥ 10 parts per billion (ppb) had experienced a "feeling of weakness" and "chronic numbness or pain" significantly more often than those with ACDW < 10 ppb. Residents with ACDW ≥ 50 ppb had three types of sensory disturbances significantly more often than those with ACDW < 50 ppb. In children, there was no significant association between symptoms or signs and ACDW.
Subjective symptoms, probably due to peripheral neuropathy, occurred at very low ACDW (around 10 ppb). Objective peripheral nerve disturbances of both small and large fibers occurred at low ACDW (> 50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health.
超过 1.4 亿人饮用含砷地下水。目前尚不清楚导致神经损伤需要多少砷暴露。在这里,我们评估了神经损伤与饮用水砷浓度(ACDW)之间的关系。
采用横断面研究设计。我们对缅甸塔保镇七个村庄的 1867 名居民进行了医学检查。医学检查包括对主观神经症状和客观神经检查(感觉障碍)的访谈。对于主观神经症状,我们确定了嗅觉、视力、味觉和听力缺陷、感觉无力以及慢性麻木或疼痛的存在或不存在。对于客观感觉障碍,我们检查了疼痛感觉、振动感觉和两点辨别力的缺陷。我们分析了主观症状、客观感觉障碍与 ACDW 之间的关系。
饮用水中 ACDW≥10 微克/升(ppb)的居民经历“感觉无力”和“慢性麻木或疼痛”的频率明显高于 ACDW<10 ppb 的居民。饮用水中 ACDW≥50 ppb 的居民出现三种类型的感觉障碍的频率明显高于 ACDW<50 ppb 的居民。在儿童中,症状或体征与 ACDW 之间没有显著关联。
主观症状可能由于周围神经病变而在非常低的 ACDW(约 10 ppb)时发生。小纤维和大纤维的外周神经障碍在低 ACDW(>50 ppb)时发生。这些数据表明砷暴露引起周围神经病的发生存在阈值,并表明饮用水中砷浓度应低于 10 ppb 以确保人类健康。