Colleen M Bartman

ResearchCell biologyPulmonologyTherapeutics Open Access | 10.1172/jci.insight.191475 JCI Insight. https://doi.org/10.1172/jci.insight.191475. Copyright © 2026, Bartman et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

1 INTRODUCTION The sensitivity of developing airways to oxygen is well documented both clinically and through numerous laboratory studies. During gestation, the fetus experiences an oxygen tension that creates a relatively hypoxic environment compared to the air we breathe (21% O2 or 160 mmHg): fetal PaO2 (partial pressure of oxygen in the arterial blood) is ~25–50 mmHg and maternal PaO2 is ~80–90 mmHg (Simon & Keith, 2008; Torres-Cuevas et al., 2017).

Although both tobacco and cigarette smoke contain many different components, nicotine is recognized as the addictive substance present in both (1). Since the additional components pose substantial health risks, particularly for cancer, there has been a large gravitation toward the use of nicotine-delivery devices. Therefore, understanding the role of nicotine per se in lung disease is of substantial impact.