Critical windows of exposure for children's health: cancer in human epidemiological studies and neoplasms in experimental animal models.

Critical windows of exposure for children's health: cancer in human epidemiological studies and neoplasms in experimental animal models.
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DOI:
10.1289/ehp.00108s3573
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发表时间:
2000-06
影响因子:
10.4
通讯作者:
Roman E
Roman E
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Anderson LM;Diwan BA;Fear NT;Roman E

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在人类中,癌症可能是由遗传和环境暴露引起的;然而,在大多数情况下,暴露的关键时间窗口的识别是有问题的。在孕前时期暴露与儿童或成年期癌症有关的证据是模棱两可的。与儿童癌症以及在子宫内受到辐射的成人癌症肯定有关的物质包括:母亲在怀孕期间受到电离辐射以及儿童白血病和某些其他癌症,母亲在怀孕期间使用己烯雌酚以及其女儿的阴道透明细胞腺癌。在围产期/产后期间发生的可能增加癌症风险的环境暴露清单正在增加,但迄今为止的证据不一致,也不确定。在动物模型中,各种类型的辐射和化学物质都证明了孕前致癌作用,从胎儿生殖细胞到减数分裂后生殖细胞的所有阶段都表现出敏感性。经胎盘和新生儿癌变在某些情况下表现出明显的个体发育阶段特异性。机制性因素包括处于危险中的细胞的数量、细胞分裂的速率、分化特征的发展,包括激活和解毒致癌物的能力、干细胞的存在以及可能的其他因素。通过对不止一个物种的这些因素进行研究,并侧重于具体的人类风险问题,将加强人类风险估计的准确性。
In humans, cancer may be caused by genetics and environmental exposures; however, in the majority of instances the identification of the critical time window of exposure is problematic. The evidence for exposures occurring during the preconceptional period that have an association with childhood or adulthood cancers is equivocal. Agents definitely related to cancer in children, and adulthood if exposure occurs in utero, include: maternal exposure to ionizing radiation during pregnancy and childhood leukemia and certain other cancers, and maternal use of diethylstilbestrol during pregnancy and clear-cell adenocarcinoma of the vagina of their daughters. The list of environmental exposures that occur during the perinatal/postnatal period with potential to increase the risk of cancer is lengthening, but evidence available to date is inconsistent and inconclusive. In animal models, preconceptional carcinogenesis has been demonstrated for a variety of types of radiation and chemicals, with demonstrated sensitivity for all stages from fetal gonocytes to postmeiotic germ cells. Transplacental and neonatal carcinogenesis show marked ontogenetic stage specificity in some cases. Mechanistic factors include the number of cells at risk, the rate of cell division, the development of differentiated characteristics including the ability to activate and detoxify carcinogens, the presence of stem cells, and possibly others. Usefulness for human risk estimation would be strengthened by the study of these factors in more than one species, and by a focus on specific human risk issues.