Christensen J M, Poulsen O M
Danish National Institute of Occupational Health, Department of Chemistry and Biochemistry, Copenhagen.
Sci Total Environ. 1994 Jun 30;150(1-3):95-104. doi: 10.1016/0048-9697(94)90134-1.
This paper provides a short overview of cobalt-related diseases with particular reference to the potential carcinogenicity of cobalt compounds, and a review of a 10-year surveillance programme on plate painters exposed to cobalt in two Danish porcelain factories. Clinical experience and epidemiological studies have demonstrated that cobalt exposure may lead to severely impaired lung function, i.e. hard metal lung disease and occupational cobalt-related asthma, contact dermatitis and cardiovascular effects. However, the evidence for the carcinogenicity of cobalt and cobalt compounds is considered inadequate (IARC, 1991). Most frequently, exposure to cobalt occurs simultaneously with exposure to other elements known to pose a health risk, (e.g. nickel, arsenic, chromium, tungsten). The importance of cobalt as sole causal agent in hard metal lung diseases, cardiomyopathy and cancer are still a matter of controversy. In the two Danish porcelain factories, cobalt blue underglaze dyes have been used since 1888. In contrast to the exposure experience of hard metal factories, the exposure of plate painters occurs with only low trace levels of other potentially harmful compounds such as the carcinogenic metals nickel, arsenic and chromium. Consequently, the nearly-pure cobalt exposure makes the plate painters an attractive group for studies on the health effects of cobalt. During the period 1982-1992 the surveillance programme showed a profound reduction in the urine level of cobalt (Co-U) from 100-fold to 10-fold above the median level of the unexposed control subjects. In the same period, the airborne cobalt exposure declined from 1356 nmol/m3 to 454 nmol/m3, the Danish occupational exposure limit being 845 nmol/m3. In 1982, when the cobalt exposure was above the occupational exposure limit, the plate painters showed a chronic impaired lung function. The obstructive effects may be similar to some of the effects observed in hard metal workers. In 1988, a study on the effect of cobalt exposure at low levels revealed no inhibitory effects on thyroid function, but the ratio between T4 and T3 increased, indicating that low cobalt exposure may have an impact on the metabolism of thyroid hormones. Parallel studies were conducted on the metabolism and excretion of cobalt. The gastrointestinal uptake of soluble CoCl was considerably higher than the uptake of insoluble cobalt(II) oxide. In addition, it was demonstrated that ingestion of controlled amounts of the soluble cobalt compound resulted in significantly higher concentrations of cobalt in urine and blood (Co-B) from females compared with males (P < 0.01). Future studies will involve epidemiology and genotoxicity to evaluate the previous and present cancer risk, and detailed process-related exposure assessment studies to select the methods most reliable for surveillance of low-dose cobalt exposure.
本文简要概述了与钴相关的疾病,特别提及钴化合物的潜在致癌性,并回顾了一项针对丹麦两家瓷器厂中接触钴的平板画师的为期10年的监测计划。临床经验和流行病学研究表明,接触钴可能导致严重的肺功能损害,即硬金属肺病和职业性钴相关哮喘、接触性皮炎以及心血管方面的影响。然而,钴及钴化合物致癌性的证据被认为并不充分(国际癌症研究机构,1991年)。最常见的情况是,接触钴的同时也会接触到其他已知对健康有风险的元素(如镍、砷、铬、钨)。钴作为硬金属肺病、心肌病和癌症的唯一致病因素,其重要性仍存在争议。自1888年以来,丹麦的这两家瓷器厂一直使用钴蓝釉下染料。与硬金属工厂的接触情况不同,平板画师接触到的其他潜在有害化合物(如致癌金属镍、砷和铬)的含量仅为痕量水平。因此,近乎纯钴的接触使得平板画师成为研究钴对健康影响的一个有吸引力的群体。在1982年至1992年期间,监测计划显示钴的尿水平(Co-U)大幅下降,从高于未接触对照组中位数水平的100倍降至10倍。在同一时期,空气中钴的接触量从1356 nmol/m³降至454 nmol/m³,丹麦的职业接触限值为845 nmol/m³。1982年,当钴接触量高于职业接触限值时,平板画师表现出慢性肺功能损害。阻塞性影响可能与在硬金属工人中观察到的一些影响相似。1988年,一项关于低水平钴接触影响的研究表明,对甲状腺功能没有抑制作用,但T4与T3的比值增加,表明低水平钴接触可能对甲状腺激素的代谢有影响。同时对钴的代谢和排泄进行了平行研究。可溶性CoCl的胃肠道吸收明显高于不溶性氧化钴(II)的吸收。此外,研究表明,摄入控制量的可溶性钴化合物后,女性尿液和血液(Co-B)中的钴浓度显著高于男性(P < 0.01)。未来的研究将涉及流行病学和遗传毒性,以评估过去和当前的癌症风险,以及详细的与工艺相关的接触评估研究,以选择最可靠的监测低剂量钴接触的方法。