Association of intrauterine cigarette smoke exposure with indices of fetal lung maturation.

摘要: The timing of fetal lung maturation is regulated, at least in part, by the endocrine milieu, which turn may be influenced environmental factors. Infants smoking mothers are decreased risk neonatal respiratory distress syndrome (RDS), a disease immaturity. Therefore, we measured maturity and cigarette smoke exposure to determine whether lungs smoke-exposed fetuses mature more quickly changes associated with alterations amniotic fluid (AF) cortisol levels. Amniotic lecithin-sphingomyelin ratio (L/S) saturated phosphatidylcholine levels were used as measures maturity, while was assessed measuring AF cotinine, stable nicotine metabolite. Lung advanced (P = .02) L/S .04). Smoke-exposed attained sufficient minimize RDS approximately 1 week earlier than unexposed fetuses. also had higher free, conjugated, total cortisol. Acceleration consistent infants mothers. Maternal could influence directly or indirectly enhancing production and/or secretion Despite RDS, developmental process attain early pulmonary abnormal contribute function increased illness noted