Abstract Current literature states that early-life exposure to smoking produces adverse health outcomes in later life, primarily as a result of subsequent engagements with firsthand smoking. The implications of prior research are that smoking cessation can reduce health risk in later life to levels comparable to the risk of those who have never smoked. However, recent evidence suggests that smoking exposure during childhood can have independent and permanent negative effects on health—in particular, on epigenetic aging. This investigation examines whether the effect of early-life firsthand smoking on epigenetic aging is more consistent with (1) a sensitive periods model, which is characterized by independent effects due to early firsthand exposures; or (2) a cumulative risks model, which is typified by persistent smoking. The findings support both models. Smoking during childhood can have long-lasting effects on epigenetic aging, regardless of subsequent engagements. Our evidence suggests that adult cessation can be effective but that the epigenetic age acceleration in later life is largely due to early firsthand smoking itself.