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Assessing the lung cancer risk reduction potential of cMRTPs is hampered by (i) the absence of clinical risk markers that are predictive of future lung cancer development, (ii) the latency of lung cancer manifestation (decades of smoking), and (iii) the slow reduction in excess risk upon cessation and a fortiori upon switching to a cMRTP

Finally, we observed that although early-life CS-induced Cyp1a1 DNAm changes do not persist to 60 wk, acute exposure to CS in adulthood reestablished DNAm patterns observed at 16 wk and was associated with an immune cell infiltration phenotype that was dependent on both early-life and later-life CS exposure

2, 3 Figure 1

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