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本文引用的文献

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LEAD POISONING IN THE UNITED STATES.
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THE "USPHS" METHOD FOR DETERMINING LEAD IN AIR AND IN BIOLOGICAL MATERIALS.
Am Ind Hyg Assoc J. 1963 Sep-Oct;24:481-91. doi: 10.1080/00028896309343251.
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Blood lead and haemoglobin in lead absorption.铅吸收中的血铅与血红蛋白
Br J Ind Med. 1966 Apr;23(2):105-11. doi: 10.1136/oem.23.2.105.
4
Pathogenesis of hyperuricemia in saturnine gout.铅中毒性痛风中高尿酸血症的发病机制。
N Engl J Med. 1969 May 29;280(22):1199-202. doi: 10.1056/NEJM196905292802203.
5
Nephropathy in chronic lead poisoning.慢性铅中毒中的肾病
Br J Ind Med. 1968 Jul;25(3):196-202. doi: 10.1136/oem.25.3.196.
6
Interlaboratory evaluation of the reliability of blood lead analyses.血铅分析可靠性的实验室间评估。
Am Ind Hyg Assoc J. 1970 Jul-Aug;31(4):412-29. doi: 10.1080/0002889708506268.
7
A micromethod for free erythrocyte porphyrins: the FEP test.游离红细胞卟啉的微量测定方法:FEP试验
J Lab Clin Med. 1973 Jun;81(6):932-40.
8
Mild lead poisoning with an excessively high blood lead.血铅过高导致的轻度铅中毒。
Br J Ind Med. 1972 Oct;29(4):458-60. doi: 10.1136/oem.29.4.458.
9
Pathological effects of lead.铅的病理效应
Int Rev Exp Pathol. 1973;12:1-77.
10
Isolation and properties of a low molecular weight beta-2-globulin occurring in human biological fluids.人生物体液中存在的一种低分子量β-2球蛋白的分离及特性
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美国的职业性铅中毒:与血铅水平相关的临床和生化发现

Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels.

作者信息

Baker E L, Landrigan P J, Barbour A G, Cox D H, Folland D S, Ligo R N, Throckmorton J

出版信息

Br J Ind Med. 1979 Nov;36(4):314-22. doi: 10.1136/oem.36.4.314.

DOI:10.1136/oem.36.4.314
PMID:508643
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1008609/
Abstract

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).

摘要

在两家冶炼厂和一家化工厂的160名铅作业工人中评估了血铅水平与毒性作用之间的剂量反应关系。血铅水平范围为0.77至13.51微摩尔/升(16 - 280微克/分升)。70名工人(44%)有中毒暴露的临床证据,包括33人出现绞痛,12人手腕或脚踝伸肌肌无力,27人贫血(血红蛋白低于8.69微摩尔/升(血红蛋白/4)或14.0克/分升),28人血尿素氮升高(大于或等于7.14毫摩尔/升或20毫克/分升),2人可能患有脑病。血铅水平低于1.93微摩尔/升(40微克/分升)时未检测到毒性。然而,血铅水平为1.93至3.81微摩尔/升(40 - 79微克/分升)的工人中有13%出现伸肌肌无力或胃肠道症状。血铅水平为1.93 - 2.85微摩尔/升(40 - 59微克/分升)的工人中有5%出现贫血,血铅水平为2.90至3.81微摩尔/升(60 - 79微克/分升)的工人中有14%出现贫血,血铅水平大于或等于3.86微摩尔/升(80微克/分升)的工人中有36%出现贫血。长期铅作业工人出现血尿素氮升高。除3名血尿素氮升高的工人外,其余所有工人至少有四年职业性铅暴露史,其中9人接受过口服螯合治疗;该组中有8人肌酐清除率降低,8人肾脏浓缩能力下降。这些数据支持将血铅的允许生物限值设定在1.93至2.90微摩尔/升(40 - 60微克/分升)之间。