Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium.
Biometals. 2010 Oct;23(5):769-82. doi: 10.1007/s10534-010-9343-z. Epub 2010 Jun 3.
We focus on the recent evidence that elucidates our understanding about the effects of cadmium (Cd) on human health and their prevention. Recently, there has been substantial progress in the exploration of the shape of the Cd concentration-response function on osteoporosis and mortality. Environmental exposure to Cd increases total mortality in a continuous fashion without evidence of a threshold, independently of kidney function and other classical factors associated with mortality including age, gender, smoking and social economic status. Pooled hazard rates of two recent environmental population based cohort studies revealed that for each doubling of urinary Cd concentration, the relative risk for mortality increases with 17% (95% CI 4.2-33.1%; P < 0.0001). Tubular kidney damage starts at urinary Cd concentrations ranging between 0.5 and 2 μg urinary Cd/g creatinine, and recent studies focusing on bone effects show increased risk of osteoporosis even at urinary Cd below 1 μg Cd/g creatinine. The non-smoking adult population has urinary Cd concentrations close to or higher than 0.5 μg Cd/g creatinine. To diminish the transfer of Cd from soil to plants for human consumption, the bioavailability of soil Cd for the plants should be reduced (external bioavailability) by maintaining agricultural and garden soils pH close to neutral (pH-H(2)O of 7.5; pH-KCL of 6.5). Reducing the systemic bioavailability of intestinal Cd can be best achieved by preserving a balanced iron status. The latter might especially be relevant in groups with a lower intake of iron, such as vegetarians, and women in reproductive phase of life. In exposed populations, house dust loaded with Cd is an additional relevant exposure route. In view of the insidious etiology of health effects associated with low dose exposure to Cd and the current European Cd intake which is close to the tolerable weekly intake, one should not underestimate the importance of the recent epidemiological evidence on Cd toxicity as to its medical and public health implications.
我们关注的是最近的证据，这些证据阐明了我们对镉（Cd）对人类健康的影响及其预防措施的理解。最近，在探索骨质疏松症和死亡率与镉浓度的关系方面取得了实质性进展。环境镉暴露以连续的方式增加总死亡率，而没有证据表明存在阈值，这与肾功能和其他与死亡率相关的经典因素（包括年龄、性别、吸烟和社会经济地位）无关。两项最近的环境人群队列研究的汇总危险率表明，对于每增加一倍的尿镉浓度，死亡率的相对风险增加 17%（95%CI 4.2-33.1%；P<0.0001）。肾小管肾损伤始于尿镉浓度在 0.5 到 2μg 尿镉/g 肌酐之间，最近关注骨效应的研究表明，即使在尿镉低于 1μg Cd/g 肌酐时，骨质疏松症的风险也会增加。不吸烟的成年人群的尿镉浓度接近或高于 0.5μg Cd/g 肌酐。为了减少土壤中镉向植物的转移以供人类食用，应通过将农业和花园土壤的 pH 值保持在接近中性（pH-H 2 O 为 7.5；pH-KCL 为 6.5）来降低植物对土壤镉的生物利用度（外源性生物利用度）。通过保持铁平衡可以最好地降低肠道镉的系统生物利用度。对于铁摄入量较低的人群，如素食者和生育期的女性，这一点可能尤其重要。在暴露人群中，富含镉的房屋灰尘是另一个相关的暴露途径。鉴于与低剂量镉暴露相关的健康影响的隐匿病因以及目前欧洲的镉摄入量接近可耐受每周摄入量，人们不应低估最近关于镉毒性的流行病学证据对其医学和公共卫生意义的重要性。
