Prenatal smoke exposure and genomic DNA methylation in a multiethnic birth cohort.

Prenatal smoke exposure and genomic DNA methylation in a multiethnic birth cohort.
复制标题

DOI:
10.1158/1055-9965.epi-11-0553
复制
发表时间:
2011-12
期刊:
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
影响因子:
--
通讯作者:
Terry MB
Terry MB
中科院分区:
其他
文献类型:
--
作者:
Flom JD;Ferris JS;Liao Y;Tehranifar P;Richards CB;Cho YH;Gonzalez K;Santella RM;Terry MB

文献摘要

被引文献

相似文献

暴露于产前烟草烟雾(PTS)与后代的许多健康结果有关,包括一些儿童癌症。较低水平的基因组DNA甲基化也与几种类型的癌症有关。我们研究了PTS是否与后代的整体DNA甲基化水平有关。我们的样本来自纽约市1959年至1963年间出生的女性(n = 90)。我们测量了来自外周血粒细胞的重复元件(Sat2, Alu, LINE-1)的甲基化。我们将前瞻性收集的PTS数据与2001年至2007年(平均年龄43岁)收集的成人流行病学数据和血液样本相结合。我们使用线性回归来评估PTS与重复元件甲基化之间的关系。36%的母亲在怀孕期间吸烟。我们观察到PTS和Sat2甲基化之间呈负相关。即使在调整了包括儿童环境烟草烟雾暴露、出生尺寸、出生后体重和身高变化以及成人吸烟状况和酒精摄入量在内的潜在中介因素后,这种负相关仍然存在(使用对数转化甲基化水平模型,曾经暴露于PTS与从未暴露于PTS的β = - 0.22, 95%置信区间= - 0.40至- 0.03)。PTS暴露与LINE-1或Alu甲基化无统计学意义相关。妊娠期间测量的未回顾性报道的PTS暴露与Sat2甲基化降低有关,但与LINE-1或Alu甲基化无关。如果在更大规模的研究中重复,该研究支持PTS对DNA甲基化水平的持续影响,如Sat2测量,在成年期。
Exposure to prenatal tobacco smoke (PTS) has been associated with a number of health outcomes in the offspring, including some childhood cancers. Lower levels of genomic DNA methylation have also been associated with several types of cancers. We investigated whether PTS was associated with global DNA methylation levels in the offspring. Our sample was drawn from a birth cohort of women born between 1959 and 1963 in New York City (n = 90). We measured methylation of repetitive elements (Sat2, Alu, LINE-1) from peripheral blood granulocytes. We combined prospectively collected data on PTS with adult epidemiologic data and blood samples collected in 2001 to 2007 (mean age, 43 years). We used linear regression to assess the association between PTS and repetitive element methylation. Thirty-six percent of mothers smoked during pregnancy. We observed an inverse association between PTS and Sat2 methylation. This inverse association remained even after adjustment for potential mediators including child environmental tobacco smoke exposure, birth size, postnatal weight and height changes, and adult smoking status and alcohol intake (β = −0.22, 95% confidence interval = −0.40 to −0.03 for ever exposed to PTS vs. never exposed using models of log-transformed methylation levels). PTS exposure was not statistically significantly associated with LINE-1 or Alu methylation. PTS exposure, measured at the time of pregnancy and not retrospectively reported, was associated with a decrease in Sat2 methylation but not LINE-1 or Alu methylation. If replicated in larger studies, this study supports a persistent effect of PTS on DNA methylation levels, as measured by Sat2, in adulthood.