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目的通过对循环内皮祖细胞迁移和集落形成单位的测定,探讨细颗粒物PM2.5中镍致心血管疾病的潜在机制。方法选择甘肃某一镍开采和冶炼所致环境空气中镍污染严重地区作为高镍区;位于其上风侧且自然条件与其相近的另一城市作为低镍区;另选择一环境空气中细颗粒物PM2.5浓度较低的自然保护区作为对照区。研究对象为在上述三个地区生活5年以上的60～65岁健康、非吸烟女性居民各10名,采用问卷调查、体格检查和实验室检查(血糖、血脂、肝功及尿蛋白)进行纳入和排除,体格检查和实验室检测指标不合格或已诊断其他疾病包括心血管疾病者均被排除;入选研究对象都按年龄进行配对。分别测定循环内皮祖细胞的迁移情况和集落形成单位数。结果与高镍组比较,低镍组、对照组人群循环内皮祖细胞迁移率和集落形成单位数均较高,差异有统计学意义(P<0.05)。低镍组与对照组人群循环内皮祖细胞集落形成单位数间比较,差异无统计学意义。随着不同地区环境空气中镍浓度的升高,人群循环内皮祖细胞迁移率和集落形成单位数均呈下降趋势。结论细颗粒物PM2.5中的镍可能通过对循环内皮祖细胞功能的抑制而导致心血管疾病的发生。
OBJECTIVE: To investigate the underlying mechanism of nickel-induced cardiovascular disease in PM2.5 PM by measuring the migration and colony forming units of circulating EPCs. Methods Nickel mining and smelting in Gansu were selected as the high-nickel region in the ambient air with high nickel pollution. Another city with its natural conditions on the windward side was selected as the low-nickel region. Another PM2 .5 low concentration nature reserve as control area. Participants were 10 healthy women aged 60-65 years and 10 non-smoking female residents living in these three areas for more than 5 years. Questionnaires, physical exams and laboratory tests (blood glucose, blood lipids, liver function and urine protein) were included And exclusion, physical examination and laboratory test indicators failed or have been diagnosed other diseases, including cardiovascular disease were excluded; selected subjects were paired by age. Circulating endothelial progenitor cells were measured for migration and colony forming units. Results Compared with the high-nickel group, the mobility and the number of colony forming units of circulating EPCs in the low-nickel group and the control group were significantly higher (P <0.05). No significant difference was found in the number of colony forming units of circulating endothelial progenitor cells between low-nickel group and control group. With the increase of nickel concentration in the ambient air in different regions, the migration rate of EPCs and the number of colony forming units in the population all showed a decreasing trend. Conclusion Nickel in fine PM2.5 particles may cause cardiovascular diseases by inhibiting the function of circulating endothelial progenitor cells.