Cadmium-related mortality and long-term secular trends in the cadmium body burden of an environmentally exposed population.
Cadmium-related mortality and long-term secular trends in the cadmium body burden of an environmentally exposed population.
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DOI：
10.1289/ehp.11667
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发表时间：
2008-12
影响因子：
10.4
通讯作者：
Staessen JA
中科院分区：
文献类型：
--
作者：
Nawrot TS;Van Hecke E;Thijs L;Richart T;Kuznetsova T;Jin Y;Vangronsveld J;Roels HA;Staessen JA
很少有人口研究报告体内镉剂量的长期变化和同时发生的死亡率。我们监测了环境暴露人群的血镉（BCd）、24小时尿镉（UCd）和死亡率。从1985年开始，我们从低暴露区（LEA）和高暴露区（HEA）随机招募了476和480名受试者，随访BCd（至2003年）、UCd（至1996年）和死亡率（至2007年）。HEA的最后一家镉生产厂于2002年关闭。从1985-1989年到1991-1996年，LEA和HEA的BCd分别下降了40.3%和18.9%（区间差异p < 0.0001）。从1991-1996年到2001-2003年，HEA的BCd保持不变（+ 1.8%），LEA的BCd增加了19.7% （p < 0.0001）。在整个随访期间，LEA （n = 258）和HEA （n = 203）的BCd年平均下降2.7%和1.8%。从1985-1989年到1991-1996年，高等学校的综合教育费用分别下降了12.9%和16.6% (p = 0.22)，平均每年分别下降2.7% （n = 366）和3.4% （n = 364）。在20.3年（中位数）期间，发生206例死亡（21.5%）。基线时，BCd （14.6 vs. 10.2 nmol/L）和UCd （14.1 vs. 8.6 nmol/24小时）在死亡患者中高于幸存者。基线UCd翻倍的风险（p≤0.04），总死亡率和非心血管死亡率分别为20%和44%，BCd翻倍的风险分别为25%和33%。即使锌镉冶炼厂关闭，历史上的环境污染仍然是一个持续的暴露源。镉环境暴露以无阈值的连续方式增加总死亡率和非心血管死亡率。
Few population studies have reported on the long-term changes in the internal cadmium dose and simultaneously occurring mortality. We monitored blood cadmium (BCd), 24-hr urinary cadmium (UCd), and mortality in an environmentally exposed population. Starting from 1985, we followed BCd (until 2003), UCd (until 1996), and mortality (until 2007) among 476 and 480 subjects, randomly recruited from low- exposure areas (LEA) and high-exposure areas (HEA). The last cadmium-producing plant in the HEA closed in 2002. From 1985–1989 to 1991–1996, BCd decreased by 40.3% and 18.9% in the LEA and HEA, respectively (p < 0.0001 for between-area difference). From 1991–1996 until 2001–2003, BCd remained unchanged in the HEA (+ 1.8%) and increased by 19.7% in the LEA (p < 0.0001). Over the entire follow-up period, the annual decrease in BCd averaged 2.7% in the LEA (n = 258) and 1.8% in the HEA (n = 203). From 1985–1989 to 1991–1996, UCd fell by 12.9% in the LEA and by 16.6% in the HEA (p = 0.22), with mean annual decreases of 2.7% (n = 366) and 3.4% (n = 364). Over 20.3 years (median), 206 deaths (21.5%) occurred. At baseline, BCd (14.6 vs. 10.2 nmol/L) and UCd (14.1 vs. 8.6 nmol/24-hr) were higher in deaths than in survivors. The risks (p ≤ 0.04) associated with a doubling of baseline UCd were 20% and 44% for total and noncardiovascular mortality, and 25% and 33% for a doubling of BCd. Even if zinc–cadmium smelters close, historical environmental contamination remains a persistent source of exposure. Environmental exposure to cadmium increases total and noncardiovascular mortality in a continuous fashion without threshold.
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