Abstract

Background: Secondhand smoke exposes children to numerous toxic chemicals. Passive cigarette smoke causes a number of diseases, such as respiratory disease. Pulmonary arterial hypertension (PAH) is a progressive disease with a dismal prognosis. Some research studies have identified hypoxia and genetic variables as the etiological factors for PAH. As a result, it appears that environmental factors, such as tobacco smoke, disrupt the function of vascular endothelial cells. Objectives: 1) Evaluating the correlation between parental smoking and PAH in infants. 2) Examining the correlation between the number of cigarettes smoked per day by parents and systolic pulmonary arterial pressure (SPAP) during a year. Method: In a cohort study, 140 neonates were classified into smokers and non-smokers. Birth weight and SPAP in neonates were measured in the smoker parental group. Following the measurement of the variables, the second group consisted of neonates with non-smoking parents whose birth weight and SPAP were matched one-to-one with the first group. After one year, we measured SPAP in two groups. Result: At birth, all neonates had normal SPAP. The mean infant SPAP was different between smoker and non-smoker parents; this difference was statistically significant (P-value <0.0001). Over 45 of infants whose parents smoked developed PAH. There was an association between the number of cigarettes that parents smoke daily and infant SPAP levels (P-value <0.0001). There was no association between PAH and the gender of the infants (p-value = 0.497). Conclusion: This research revealed a significant association between parental smoking and PAH in infants. Also, the infant SPAP was significantly linked to the number of cigarettes that the parents smoked per day. © 2024 Elsevier B.V.