The Role of Genetic Polymorphism of IL-4 (C-589T) and TNfa (G-308A) and Regular Passive Smoking in Clinical Manifestations of Pneumonia in Infants

Abstract

Objective: This study set out to investigate the relationship between molecular-genetic mechanisms that modulate cytokine in infants whose parents expose them to cigarette smoke and those that do not expose their infants to cigarette smoke with the possible effects on the severity of pneumonia at presentation to hospital. Exposure to cigarette smoke in infants changed the likelihood of the severity of pneumonia. The results suggest a possible link between the duration of clinical manifestation of pneumonia within infants that are exposed to cigarette smoke. Infants who are exposed to cigarette smoke had higher plasma concentrates in both IgE and CRP. Among infants with the mutant variant of the TNF-α (G-308A) gene, infants from households where both parents smoked or had a father who smoked had longer duration of clinical signs of pneumonia than did infants with no exposure to tobacco smoke. The plasma concentration of IgE in infants in families where one or both parents smoke was significantly higher than in infants with no smoke exposure. The study begins to develop evidence that if the newborn infant is exposed to tobacco smoke either directly from their mother or from others in the household including automobiles, the severity of pneumonia is increased. Both nurses and pediatricians should reinforce the consequences of smoke around the baby to all parents at every opportunity.