Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave., Los Angeles, CA, 90089, USA.
Cousins Center for Psychoneuroimmunology, Department of Psychiatry & Biobehavioral Sciences, Jane & Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA, USA.
Clin Epigenetics. 2022 May 28;14(1):72. doi: 10.1186/s13148-022-01286-8.
Cigarette smoke is a major public health concern. Epigenetic aging may be an important pathway by which exposure to cigarette smoke affects health. However, little is known about how exposure to smoke at different life stages affects epigenetic aging, especially in older adults. This study examines how three epigenetic aging measures (GrimAge, PhenoAge, and DunedinPoAm38) are associated with parental smoking, smoking in youth, and smoking in adulthood, and whether these epigenetic aging measures mediate the link between smoke exposure and morbidity and mortality. This study utilizes data from the Health and Retirement Study (HRS) Venous Blood Study (VBS), a nationally representative sample of US adults over 50 years old collected in 2016. 2978 participants with data on exposure to smoking, morbidity, and mortality were included.
GrimAge is significantly increased by having two smoking parents, smoking in youth, and cigarette pack years in adulthood. PhenoAge and DunedinPoAm38 are associated with pack years. All three mediate some of the effect of pack years on cancer, high blood pressure, heart disease, and mortality and GrimAge and DunedinPoAm38 mediate this association on lung disease.
Results suggest epigenetic aging is one biological mechanism linking lifetime exposure to smoking with development of disease and earlier death in later life. Interventions aimed at reducing smoking in adulthood may be effective at weakening this association.
香烟烟雾是一个主要的公共卫生关注点。表观遗传衰老可能是暴露于香烟烟雾影响健康的一个重要途径。然而，对于暴露于不同生命阶段的烟雾如何影响表观遗传衰老，特别是在老年人中，人们知之甚少。本研究探讨了三种表观遗传衰老指标（GrimAge、PhenoAge 和 DunedinPoAm38）与父母吸烟、青少年时期吸烟和成年时期吸烟之间的关系，以及这些表观遗传衰老指标是否在暴露于烟雾与发病率和死亡率之间的联系中起中介作用。本研究利用了来自健康与退休研究（HRS）静脉血研究（VBS）的数据，这是一项针对美国 50 岁以上成年人的全国代表性样本，于 2016 年收集。共纳入了 2978 名有吸烟暴露、发病率和死亡率数据的参与者。
有两个吸烟的父母、青少年时期吸烟和成年时期的香烟包年数显著增加了 GrimAge。PhenoAge 和 DunedinPoAm38 与包年数有关。这三种指标都在一定程度上中介了包年数与癌症、高血压、心脏病和死亡率之间的关系，GrimAge 和 DunedinPoAm38 也中介了包年数与肺部疾病之间的关系。
研究结果表明，表观遗传衰老可能是将一生中暴露于吸烟与晚年疾病和早逝联系起来的一种生物学机制。旨在减少成年期吸烟的干预措施可能会削弱这种关联。
