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彭立核, 张学, 何远亮, 李佳昱, 李佳伟, 陈坤, 谢爱萍, 金明娟. 全血铅暴露水平与进展期结直肠肿瘤患病关系病例对照研究[J]. 中国公共卫生, 2023, 39(7): 887-891. DOI: 10.11847/zgggws1139945
引用本文: 彭立核, 张学, 何远亮, 李佳昱, 李佳伟, 陈坤, 谢爱萍, 金明娟. 全血铅暴露水平与进展期结直肠肿瘤患病关系病例对照研究[J]. 中国公共卫生, 2023, 39(7): 887-891. DOI: 10.11847/zgggws1139945
PENG Lihe, ZHANG Xue, HE Yuanliang, LI Jiayu, LI Jiawei, CHEN Kun, XIE Aiping, JIN Mingjuan. Association of whole blood lead level with advanced colorectal neoplasia: a population-based case-control study[J]. Chinese Journal of Public Health, 2023, 39(7): 887-891. DOI: 10.11847/zgggws1139945
Citation: PENG Lihe, ZHANG Xue, HE Yuanliang, LI Jiayu, LI Jiawei, CHEN Kun, XIE Aiping, JIN Mingjuan. Association of whole blood lead level with advanced colorectal neoplasia: a population-based case-control study[J]. Chinese Journal of Public Health, 2023, 39(7): 887-891. DOI: 10.11847/zgggws1139945

全血铅暴露水平与进展期结直肠肿瘤患病关系病例对照研究

Association of whole blood lead level with advanced colorectal neoplasia: a population-based case-control study

  • 摘要:
      目的  了解全血铅暴露水平与进展期结直肠肿瘤患病的关系,为结直肠癌的预防控制提供参考依据。
      方法  采用病例对照研究方法,将2014年4月 — 2016年12月通过浙江省嘉善县结直肠癌早诊早治筛查项目发现的272例进展期结直肠肿瘤患者作为病例组及按病例组同性别、年龄(± 5岁)进行频数匹配的605名同期进行筛查的健康人群作为对照组进行问卷调查、体格检查和实验室检测。
      结果  病例组进展期结直肠肿瘤患者和对照组健康人群全血铅浓度几何均数分别为(28.11 ± 1.64)和(26.87 ± 0.93)μg/L,2组人群全血铅暴露水平差异无统计学意义(P > 0.05)。在调整了性别、年龄、文化程度、吸烟情况、饮酒情况、体育锻炼情况、有无结直肠癌家族史和体质指数(BMI)等潜在混杂因素后,多因素非条件logistic回归分析结果显示,全血铅暴露水平最高五分位组人群进展期结直肠肿瘤的患病风险为最低五分位组人群的1.87倍(OR = 1.87,95%CI = 1.15~3.04);全血铅暴露水平最高五分位组男性人群进展期结直肠肿瘤的患病风险为最低五分位组男性人群的2.12倍(OR = 2.12,95%CI = 1.05~4.30);全血铅暴露水平(经以10为底对数转换后)每增加1个单位,总人群进展期结直肠肿瘤患病风险升高了1.86倍(OR = 2.86,95%CI = 1.28~6.35),男性人群进展期结直肠肿瘤患病风险升高了3.98倍(OR = 4.98,95%CI = 1.62~15.35)。限制性立方样条函数分析结果显示,在调整了性别、年龄、文化程度、吸烟情况、饮酒情况、体育锻炼情况、有无结直肠癌家族史和BMI等潜在混杂因素后,全血铅暴露水平的增加与进展期结直肠肿瘤患病风险的升高呈显著线性关联(χ2整体 = 8.79,P整体 = 0.012;χ2非线性 = 2.17,P非线性 = 0.141)。
      结论  全血铅暴露水平的增加与进展期结直肠肿瘤患病风险的升高有关,铅可能是结直肠癌发生发展的重要环境危险因素。

     

    Abstract:
      Objective   To explore the association between whole blood lead concentration and advanced colorectal neoplasia (CRN) and to provide evidence for colorectal cancer (CRC) prevention and control.
      Methods   The cases of the study were 272 advanced CRN identified from April 2014 to December 2016 in the participants of a CRC early diagnosis and treatment program including face-to-face questionnaire interview, physical examination and laboratory test conducted among the residents of Jiashan county, Zhejiang province; the 605 controls were gender- and age (± 5 years)-frequency matched healthy participants of the program.
      Results   The geometric mean (geometric standard error) of whole blood lead concentration (μg/L) were 28.11(1.64) and 26.87 (0.93) for the cases and controls, without statistically significant difference (P > 0.05). After adjusting for gender, age, education, smoking, alcohol consumption, physical exercise, family history of CRC and body mass index (BMI), unconditional multivariate logistic regression analysis demonstrated that the participants with the highest quintile (Q5) of whole blood lead concentration were at an increased risk of advanced CRN (odds ratio OR = 1.87, 95% confidence interval 95%CI : 1.15 – 3.04) compared to those with the lowest quintile (Q1) and the increased risk was much higher for the male participants (Q5 vs. Q1: OR = 2.12, 95%CI : 1.05 – 4.30). Furthermore after base 10 logarithm conversion, each unit increment in blood lead concentration was associated with a 1.86 (OR = 2.86, 95%CI : 1.28 – 6.35) and 3.98 (OR = 4.98, 95%CI : 1.62 – 15.35) times higher risk of advanced CRN for the all and the male participants, respectively. Restricted cubic spline analysis revealed a significant linear correlation between the increment of whole blood concentration and the increased risk of advanced CRN after adjusting for potential confounders mentioned above (χ2 total = 8.79, Ptotal = 0.012; χ2 non-linearity = 2.17, Pnon-linearity = 0.141).
      Conclusion  Blood lead concentration may be associated with an increased risk of advanced colorectal neoplasia, suggesting a potential role of lead exposure in the etiology of colorectal carcinogenesis.

     

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