Kidney Institute and Division of Nephrology, Department of Internal Medicine, China Medical University Hospital and College of Medicine, China Medical University, Taichung, Taiwan; Big Data Center, China Medical University Hospital, China Medical University, Taichung, Taiwan.
Department of Pediatrics, Chung Shan Medical University, Taichung, Taiwan.
Environ Int. 2018 Sep;118:97-105. doi: 10.1016/j.envint.2018.05.033. Epub 2018 May 31.
Inorganic arsenic (iAs) exposure potentially causes diabetes and cardiovascular diseases in adults. However, its effect on glucose and lipid metabolism in early life remains unknown.
We evaluated the associations between early-life arsenic exposure and profiles of glucose and lipids in a 15-year birth cohort in central Taiwan.
We studied 237 adolescents through 5 waves of follow-up interviews and examinations at ages of approximately 2, 5, 8, 11, and 14 y. We obtained at least one follow-up urine measurement for arsenic species and blood sample collection up to 14 y of age and identified group-based trajectories of serial iAs by semiparametric mixture modeling. Multiple linear and logistic regressions were performed to assess the effect of the arsenic exposure trajectory on serum fasting glucose, total cholesterol (TCHO), triglycerides (TGs), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL).
Three trajectories of postnatal arsenic exposure were identified, namely stable-low (31.4%), stable-high (48.2%), and rising-high (20.4%) groups. Compared with the stable-low trajectory group, the percent changes in TCHO and LDL was 14% (95% confidence interval 4-24%) and 23% (9-38%) for the group with "rising-high" trajectory and was 8% (-1-16%) and 16% (4-29%) for the group with "stable-high" trajectory. The rising-high group was also associated with an increase in the TCHO/HDL ratio by 14% (95% CI 3%-25%). The adjusted odds ratios of high developmental trajectories of TCHO, TG, LDL, and non-HDL levels were 4.0 (95% CI 1.2-13.7), 12.2 (2.2-67), 7.3 (1.8-30), and 3.6 (0.9-14.6), respectively, in the rising-high group (reference: stable-low group).
Our findings suggest that conversion to an atherogenic lipid profile in adolescents may be associated with early-life exposure to environmental arsenic, particularly during the pre-adolescent period. An environmental modification approach for preventing As-related cardiovascular disease is recommended to begin early in life.
无机砷（iAs）暴露可能会导致成年人患糖尿病和心血管疾病。然而，其对生命早期葡萄糖和脂质代谢的影响尚不清楚。
我们评估了台湾中部一个 15 年出生队列中生命早期砷暴露与葡萄糖和脂质特征之间的关系。
我们通过 5 次随访访谈和 2 岁、5 岁、8 岁、11 岁和 14 岁时的检查，对 237 名青少年进行了研究。我们获得了至少一次随访尿液砷物种测量值，并在 14 岁时采集了血液样本，并通过半参数混合模型确定了连续 iAs 的基于群组的轨迹。采用多元线性和逻辑回归来评估砷暴露轨迹对血清空腹血糖、总胆固醇（TCHO）、甘油三酯（TGs）、低密度脂蛋白胆固醇（LDL）和高密度脂蛋白胆固醇（HDL）的影响。
确定了三种产后砷暴露轨迹，即稳定低（31.4%）、稳定高（48.2%）和升高高（20.4%）组。与稳定低轨迹组相比，“升高高”轨迹组的 TCHO 和 LDL 变化百分比分别为 14%（95%置信区间 4-24%）和 23%（9-38%），“稳定高”轨迹组分别为 8%（-1-16%）和 16%（4-29%）。升高高组的 TCHO/HDL 比值也增加了 14%（95%CI 3%-25%）。在升高高组中，TCHO、TG、LDL 和非 HDL 水平高的发育轨迹的调整比值比分别为 4.0（95%CI 1.2-13.7）、12.2（2.2-67）、7.3（1.8-30）和 3.6（0.9-14.6）（参考：稳定低组）。
我们的研究结果表明，青少年中动脉粥样硬化脂质谱的转化可能与生命早期环境砷暴露有关，特别是在青春期前。建议采用环境改善方法，以在生命早期开始预防与砷有关的心血管疾病。
