Cigarette Smoke Exposure, Pediatric Lung Disease, and COVID-19

Abstract

The detrimental effects of tobacco exposure on children’s health are well known. Nonetheless, the prevalence of secondhand or direct cigarette smoke exposure (CSE) in the pediatric population has not significantly decreased over time. On the contrary, the rapid incline in use of e-cigarettes among adolescents has evoked public health concerns since increasing cases of vaping-induced acute lung injury have highlighted the potential harm of these new “smoking” devices. Two pediatric populations are especially vulnerable to the detrimental effects of cigarette smoke. The first group is former premature infants whose risk is elevated both due to their prematurity as well as other risk factors such as oxygen and mechanical ventilation to which they are disproportionately exposed. The second group is children and adolescents with chronic respiratory diseases, in particular asthma and other wheezing disorders. Coronavirus disease 2019 (COVID-19) is a spectrum of diseases caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has spread worldwide over the last year. Here, respiratory symptoms ranging from mild to acute respiratory distress syndrome (ARDS) are at the forefront of COVID-19 cases among adults, and cigarette smoking is associated with worse outcomes in this population, and cigarette smoking is associated with worse outcomes in this population. Interestingly, SARS-CoV-2 infection affects children differently in regard to infection susceptibility, disease manifestations, and complications. Although children carry and transmit the virus, the likelihood of symptomatic infection is low, and the rates of hospitalization and death are even lower when compared to the adult population. However, multisystem inflammatory syndrome is recognized as a serious consequence of SARS-CoV-2 infection in the pediatric population. In addition, recent data demonstrate specific clinical patterns in children infected with SARS-CoV-2 who develop multisystem inflammatory syndrome vs. severe COVID-19. In this review, we highlight the pulmonary effects of CSE in vulnerable pediatric populations in the context of the ongoing SARS-CoV-2 pandemic.

Association between prenatal or postpartum exposure to tobacco smoking and allergic rhinitis in the offspring: An updated meta-analysis of nine cohort studies

“…Of course, many smoke compounds cross the placental barrier and can affect the development of the fetus, particularly the immune system 34 - 36 . Exposure to secondhand smoke after birth will have similar impacts on the development of the respiratory and immune systems 37 , 38 . Still, the exact mechanisms are complex and were outside the scope of the present meta-analysis.…”

Environmental inequality: Air pollution and asthma in children

“…73 Moreover, some cigarette smoke derivates may disrupt epithelial cellular junctions, allowing for deeper penetration of toxins and allergens. 73 Oxidate stress related to exposure to tobacco may activate the transcription of factors involved in inflammatory responses, which are responsible for sustained immune cell recruitment and activation. Furthermore, prolonged exposure to tobacco may enhance both Th2-and Th1-mediated inflammatory responses, being associated with a more severe asthma phenotype.…”

“…Exposure to tobacco has been associated with oxidative imbalance and stress, which may change the barrier function of the epithelial layer by reducing ciliary beating and enhancing mucus production, epithelial to mesenchymal transition, and immune dysfunction 73 . Moreover, some cigarette smoke derivates may disrupt epithelial cellular junctions, allowing for deeper penetration of toxins and allergens 73 . Oxidate stress related to exposure to tobacco may activate the transcription of factors involved in inflammatory responses, which are responsible for sustained immune cell recruitment and activation.…”

Environmental inequality: air pollution and asthma in children

“…Exposure to tobacco has been associated with oxidative imbalance and stress, which may change barrier function of the epithelial layer by reducing ciliary beating and enhancing mucus production, epithelial to mesenchymal transition, and immune dysfunction [73]. Moreover, some cigarette smoke derivates may disrupt epithelial cellular junctions, allowing a deeper penetration of toxins and allergens [73].…”

“…Exposure to tobacco has been associated with oxidative imbalance and stress, which may change barrier function of the epithelial layer by reducing ciliary beating and enhancing mucus production, epithelial to mesenchymal transition, and immune dysfunction [73]. Moreover, some cigarette smoke derivates may disrupt epithelial cellular junctions, allowing a deeper penetration of toxins and allergens [73]. Oxidate stress related to exposure to tobacco may activate the transcription of factors involved in inflammatory responses, which are responsible for sustained immune cell recruitment and activation.…”