Pubertal timing refers to the pace at which individuals reach certain stages of puberty relative to their same-age and same-sex peers. The global trend towards earlier pubertal timing is of concern due to its associated adverse health implications including cardiovascular diseases, type Ⅱ diabetes and sex steroid-sensitive cancers(2). In addition, earlier pubertal timing may also lead to increased risky behaviours during adolescence including depression, early sexual activity and substance abuse(2). Therefore, identifying modifiable factors that influence pubertal timing is important to mitigate these adverse outcomes. Studies suggest that passive tobacco smoke exposure is associated with puberty timing, e.g., several birth cohorts have shown that maternal smoking during their third trimester associates with an earlier age of menarche. Life course epidemiology theory may help us understand how passive tobacco smoke exposure relate to pubertal timing. Under this theory, we proposed three life course models to explain the association between passive tobacco smoke exposure and pubertal timing: the critical period model, the risk accumulation model and a compound model of risk accumulation with a sensitive period. The critical period model assumes that exposure during a limited time window has an adverse impact on development, contributing to disease onset in later life, and this impact cannot be modified by subsequent exposures. In contrast, the risk accumulation model posits that as the number and/or duration of exposure increases, there is cumulative damage to biological systems. Additionally, a compound model of risk accumulation with a sensitive period suggests that within the risk accumulation model, there is stronger association between exposure and outcome during a specific developmental period relative to other periods. To our knowledge, no previous study has examined the contribution of passive tobacco smoke exposure during different early life periods (prenatal, infancy and childhood) to pubertal timing.