Wittman Richard, Hu Howard
Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA.
Environ Health Perspect. 2002 Dec;110(12):1261-6. doi: 10.1289/ehp.021101261.
A 28-year-old female presented for evaluation of left flank pain and polyuria after having been exposed to cadmium in the jewelry manufacturing industry for approximately 3 years. This patient possessed both elevated 24-hr urinary ss2-microglobulin and elevated blood cadmium levels. Approximately 6 months after initial presentation, the patient resigned from her job due to shortness of breath, chest pain, and anxiety. Exposure to cadmium in the jewelry industry is a significant source of occupational cadmium exposure. Other occupational sources include the manufacture of nickel-cadmium batteries, metal plating, zinc and lead refining, smelting of cadmium and lead, and production of plastics. Cadmium is also an environmental pollutant that accumulates in leafy vegetables and plants, including tobacco. Major toxicities anticipated from cadmium exposure involve the renal, pulmonary, and, to a lesser extent, gastrointestinal systems. These include the development of renal proximal tubular dysfunction, glomerular damage with progressive renal disease, and respiratory symptoms including pneumonitis and emphysema. Low-level cadmium exposure has also been associated with increased urinary calcium excretion and direct bone toxicity, effects that recent research suggests may result in the development of osteoporosis. The body burden of cadmium, over half of which may reside in the kidneys, is most often measured through the use of urinary cadmium levels. Blood cadmium measurements generally reflect current or recent exposure and are especially useful in cases with a short exposure period and only minimal accumulation of cadmium in the kidneys. Both ss2-microglobulin and alpha1-microglobulin serve as organ-specific, early-effect biomarkers of tubular proteinuria and thus play a role in identifying early signs of cadmium-induced renal damage in those with potential exposures. In addition to ensuring workplace compliance with Occupational Safety and Health Administration-mandated monitoring and screening measures, it is prudent for those with cadmium exposure to maintain adequate intake of both iron and calcium, appropriate measures even in the absence of exposure.
一名28岁女性因在珠宝制造业接触镉约3年后出现左侧腰痛和多尿前来就诊。该患者24小时尿β2-微球蛋白升高,血镉水平也升高。初次就诊约6个月后,患者因呼吸急促、胸痛和焦虑辞职。珠宝行业接触镉是职业性镉暴露的一个重要来源。其他职业来源包括镍镉电池制造、金属电镀、锌和铅精炼、镉和铅冶炼以及塑料生产。镉也是一种环境污染物,会在包括烟草在内的叶菜类蔬菜和植物中蓄积。镉暴露预期的主要毒性涉及肾脏、肺部,在较小程度上还涉及胃肠道系统。这些毒性包括肾近端小管功能障碍的发展、肾小球损伤伴进行性肾病,以及包括肺炎和肺气肿在内的呼吸道症状。低水平镉暴露还与尿钙排泄增加和直接骨毒性有关,最近的研究表明这些影响可能导致骨质疏松症的发生。镉的身体负荷(其中一半以上可能存在于肾脏中)最常通过测量尿镉水平来衡量。血镉测量通常反映当前或近期的暴露情况,在暴露期短且肾脏中镉蓄积极少的情况下尤其有用。β2-微球蛋白和α1-微球蛋白均作为肾小管蛋白尿的器官特异性早期效应生物标志物,因此在识别有潜在暴露的人群中镉诱导的肾损伤早期迹象方面发挥作用。除了确保工作场所符合职业安全与健康管理局规定的监测和筛查措施外,镉暴露者即使在未暴露的情况下保持充足的铁和钙摄入量也是明智的措施。