Association of low-level environmental exposure to cadmium and lead with gout flare using a cohort study design
Association of low-level environmental exposure to cadmium and lead with gout flare using a cohort study design
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使用队列研究设计研究低水平镉和铅环境暴露与痛风发作之间的关联。
DOI：
10.1016/j.chemosphere.2021.130648
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发表时间：
2021
期刊：
影响因子：
8.8
通讯作者：
Changgui Li
中科院分区：
文献类型：
--
作者：
Hui Zhang;Hailong Li;Am;a Phipps Green;Ming Wang;Fei Yan;Maichao Li;Yuwei He;Wenyan Sun;Xuan Yuan;Jie Lu;Mingshu Sun;Tony R. Merriman;Changgui Li
镉（Cd）和铅（Pb）是具有内分泌干扰特性的有毒重金属。我们在一项队列研究中调查了低水平镉/铅环境暴露与痛风状态（临界期痛风、痛风发作和合并痛风）的关系。采用电感耦合等离子体质谱法（ICP-MS）测定了408例痛风患者血液和346例痛风患者尿液中Cd和Pb的含量（Cd-B和Pb-B）和尿中Cd和Pb的含量（Cd-U和Pb-U）。痛风发作组中Cd-B和Pb-B的中位数水平（μg/L）分别为0.87（范围0.41-2.49）和31.54（25.38-41.46），痛风发作组中Cd-U和Pb-U的中位数水平分别为1.05（0.69-1.91）和3.86（3.49-4.44）。这些中位数均显著高于对照组和临界组（P< 0.05）。在模型3下调整后，与参考三分位1相比，三分位2（T2）的Cd-B和三分位3的Cd-U水平与痛风发作状态显著相关（OR分别为4.3，P = 0.041和OR = 25.1，P = 0.002）。对于Pb-U，在模型3下，与T1相比，T2中痛风发作状态的风险显著更高（OR = 51.0，P = 0.002）。我们的研究结果表明，在痛风发作组中，Cd-B、Pb-B、Cd-U和Pb-U的中位数水平显著高于无痛风或痛风但处于临界期的参与者。我们提供的证据表明，痛风发作状态的风险与镉水平增加有关，血液和尿液中的镉水平是痛风发作状态的危险因素。
Cadmium (Cd) and lead (Pb) are toxic heavy metals with endocrine-disrupting properties. We investigated the associations of low-level environmental exposure to Cd/Pb and gout status (intercritical gout, gout flare and combined gout) in a cohort study. We measured by ICP-MS the levels of Cd and Pb in blood (Cd–B and Pb–B) and urine (Cd–U and Pb–U) from 408 participants with blood and 346 participants with urine samples recruited from a hospital gout clinic. The median levels of Cd–B and Pb–B (in μg/L) in the gout flare group were 0.87 (range 0.41–2.49) and 31.54 (25.38–41.46), respectively, and the median levels of Cd–U and Pb–U in the gout flare group were 1.05 (0.69–1.91) and 3.86 (3.49–4.44), respectively. These medians were significantly higher than those in the control or intercritical groups (P< 0.05). For Cd–B in tertile 2 (T2) and Cd–U in tertile 3, Cd levels were significantly associated with gout flare status compared to the reference tertile 1 (OR = 4.3,P= 0.041 and OR = 25.1,P= 0.002, respectively) after adjustment under Model 3. For Pb–U, the risk of gout flare status was significantly higher in T2 (OR = 51.0,P= 0.002) compared to the T1 under Model 3. Our results show that median levels of Cd–B, Pb–B, Cd–U and Pb–U in the gout flare group were significantly higher than participants without gout or with gout but in the intercritical period. We provide evidence that the risk of gout flare status is associated with increased Cd levels, and that blood and urine levels of Cd are a risk factor for gout flare status.