Investigating the Effects of Vaping and Nicotine’s Block of Kir2.1 on Humerus and Digital Development in Embryonic Mice

Abstract

Kir2.1 is an ion channel that is important for skeletal development. Nicotine, a common ingredient in electronic cigarettes, blocks Kir2.1. However, little research has been done to investigate how vaping nicotine during pregnancy affects embryonic development. We examined how vaping nicotine during pregnancy would affect embryonic skeletal development in mice. Mice pregnant with embryos of three genotypes—wild‐type, Kir2.1+/KO, or Kir2.1KO/KO—received either no vaping treatment, a 2.4% freebase nicotine vaping treatment, or a 3.6% nicotine salt vaping treatment throughout pregnancy. The embryos were dissected at E18.5, and their skeletons were extracted and stained for imaging. The lengths of the humerus bones and number of digital bones were calculated to quantify differences in bone development between groups. We found significant differences in humerus length between the wild‐type no vape and wild‐type 2.4% freebase nicotine groups, as well as the Kir2.1+/KO no vape and Kir2.1+/KO 2.4% freebase nicotine groups. However, no significant differences were found between wild‐type no vape and wild‐type 3.6% nicotine salt groups, as well as Kir2.1+/KO no vape and Kir2.1+/KO 3.6% nicotine salt groups. We suspect that nicotine salts are metabolized faster than freebase nicotine and thus inhibit Kir2.1’s function for a shorter amount of time, but further research needs to be conducted to test this hypothesis. We conclude that fetal exposure to vaped free base nicotine impacts the development of long bones and reduces long bone length.