Biomarkers of exposure to combustion by-products in a human population in Shanxi, China
Biomarkers of exposure to combustion by-products in a human population in Shanxi, China
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DOI：
10.1038/jes.2009.19
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发表时间：
2010-06-01
影响因子：
4.5
通讯作者：
Donnelly, Kirby C.
中科院分区：
文献类型：
--
作者：
Naufal, Ziad;Li Zhiwen;Donnelly, Kirby C.
多环芳烃（PAH）和其他化合物的复杂混合物排放到环境中对人类健康构成潜在威胁。有关暴露剂量和持续时间的信息对于确定风险程度和识别人群中的敏感受体至关重要。尽管空气中化学物质浓度的测量可用于估计暴露量，但内部生物标记物提供了有关有毒化学物质的暴露剂量和保留量的更准确信息。这项研究是针对接触多种来源的多环芳烃的中国农村人群进行的。研究人群位于已知出生缺陷发生率较高的地区。出生时患有神经管缺陷（NTD）的儿童的父母被招募为病例参与者，出生时没有明显出生缺陷的儿童的父母被招募为对照。该研究旨在检验这样的假设：患有 NTD 的孩子的父母会比没有明显出生缺陷的孩子的父母表现出更高水平的暴露生物标志物。共有 35 名母亲和 32 名父亲被招募为病例参与者，18 名母亲和 19 名父亲被招募为对照参与者。孩子出生后，医院工作人员尽快从研究参与者身上采集静脉血。通过溶剂萃取从全血中分离出 PAH，并从单独的等份血液中分离出 DNA，用于 P-32 后标记以测量大体积加合物。还监测了 II 相酶中的单核苷酸多态性 (SNP)，试图识别敏感受体。病例儿童父母的总 PAH 浓度和致癌 PAH (cPAH) 浓度均升高。母亲中这两个值均显着升高，而父亲中只有 cPAH 浓度显着升高。 DNA 加合物的水平变化很大，并且与血液中的 PAH 水平呈现相反的模式。所评估的多态性均与 PAH 水平或 DNA 加合物无关。对于总 PAH 浓度高于中位浓度的母亲，生出患有 NTD 的孩子的年龄调整优势比 (OR) 为 8.7。尽管这表明 PAH 可能是 NTD 风险的一个影响因素，但与 DNA 加合物缺乏相关性表明可能存在非基因毒性机制。或者，多环芳烃可能是与出生缺陷更直接相关的不同暴露的替代品。结果表明，血液中多环芳烃的水平可用于识别暴露于高浓度燃烧副产品的人群。暴露科学与环境流行病学杂志 (2010) 20, 310-319; doi：10.1038/jes.2009.19； 2009 年 3 月 11 日在线发布
Emissions of complex mixtures of polycyclic aromatic hydrocarbons (PAHs) and other compounds into the environment represent a potential threat to the health of humans. Information regarding the dose and duration of exposure is essential to determine the degree of risk and to identify sensitive receptors within a population. Although measurements of chemical concentrations in air may be used to estimate exposures, internal biomarkers provide more accurate information regarding the dose of exposure and retention of toxic chemicals. This study was conducted in a population in rural China exposed to PAHs from a variety of sources. The study population was located in an area known to have an elevated incidence of birth defects. Parents of children born with a neural tube defect (NTD) were recruited as case participants and parents of children born with no visible birth defect were recruited as controls. The study was designed to test the hypothesis that parents of children born with a NTD would exhibit a biomarker of exposure at higher levels than the parents of a child with no visible birth defect. A total of 35 mothers and 32 fathers were recruited as case participants, and 18 mothers and 19 fathers were recruited as control participants. Venous blood was collected from the study participants by hospital staff as soon as possible following the birth of the child. PAHs were isolated from the whole blood by solvent extraction and DNA was isolated from a separate aliquot of blood for P-32-postlabeling to measure bulky adducts. Single Nucleotide Polymorphisms (SNPs) in phase II enzymes were also monitored in an attempt to identify sensitive receptors. Both total and carcinogenic PAH (cPAH) concentrations were elevated in the parents of case children. Both values were elevated significantly in mothers, whereas only cPAH concentrations were elevated significantly in fathers. Levels of DNA adducts were highly variable and displayed a reverse pattern to that of PAH levels in blood. None of the polymorphisms evaluated were correlated with PAH levels or DNA adducts. For mothers, whose total PAH concentration was above the median concentration, the age-adjusted odds ratio (OR) for having a child with a NTD was 8.7. Although this suggests that PAHs may be a contributing factor to the risk of NTDs, the lack of a correlation with DNA adducts would suggest a possible non-genotoxic mechanism. Alternatively, the PAHs may be a surrogate for a different exposure that is more directly related to the birth defects. The results have shown that blood levels of PAHs may be used to identify populations exposed to elevated concentrations of combustion by-products. Journal of Exposure Science and Environmental Epidemiology (2010) 20, 310-319; doi:10.1038/jes.2009.19; published online 11 March 2009