Adolescent Tobacco and Cannabis Exposure: Effects on Growth, Bone Health, Endocrine Function, and Reversibility: A Critical Narrative Review

Abstract

Adolescence is a developmentally sensitive interval in which linear growth, pubertal endocrine maturation, body-composition change, and rapid skeletal mineral accrual occur while experimentation with nicotine, tobacco, and cannabis commonly begins. This critical narrative review evaluates whether exposure to combustible tobacco, nicotine-containing electronic products, and cannabis during adolescence alters somatic growth, bone health, endocrine function, and the potential for recovery after cessation. Literature published from 1 January 1980 to 1 July 2026 was identified through multidisciplinary scholarly searching, citation tracing, and verification of bibliographic records and digital object identifiers. Evidence was weighted by developmental directness, design, exposure measurement, control of co-use and lifestyle confounding, and suitability of outcome measures. The most consistent human evidence concerns tobacco and skeletal development: several adolescent and young-adult cohorts associate smoking with lower bone mineral density, reduced cortical dimensions, or slower bone accrual, although newer low-exposure cohorts are less consistent. Associations between adolescent smoking and height or body mass index are heterogeneous and sex-dependent, while post-cessation weight gain is more reproducible than catch-up in stature. Nicotine and cigarette smoke have biologically plausible effects on growth-plate chondrocytes, osteoblasts, osteoclasts, vitamin D status, and endocrine signalling, but evidence from electronic cigarettes remains largely mechanistic rather than clinical. For cannabis, direct adolescent evidence on pubertal timing, final height, endocrine trajectories, and skeletal accrual is strikingly sparse. Adult observational bone studies conflict, and human reproductive-hormone studies do not support a simple model of sustained gonadal suppression. Preclinical studies demonstrate cannabinoid-sensitive endocrine and skeletal pathways but cannot establish adolescent clinical harm. Reversibility is therefore outcome-specific: metabolic changes after tobacco cessation are common, skeletal recovery is plausible but incompletely quantified, and cannabis-related endocrine recovery is supported mainly by animal evidence. Future studies require longitudinal, product-specific exposure measurement, repeated pubertal and endocrine phenotyping, advanced skeletal imaging, and rigorous separation of nicotine–cannabis co-use from causal effects.