Airway Alveolar Attachment Points and Exposure to Cigarette Smoke In Utero

Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Perth, Western Australia; and Department of Respiratory Medicine, Royal Children's Hospital, Melbourne, Victoria, Australia

	ABSTRACT

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

 
The harmful effects of in utero cigarette smoke exposure include increased asthma symptoms and reduced lung function during the neonatal period, increased airway responsiveness to inhaled stimuli, and an increased risk of sudden infant death syndrome. Altered lung function may result from altered airway/lung structure. Airway dimensions, alveolar attachment points, and parenchymal elastin content were measured in 32 infants who died from sudden infant death syndrome and were grouped according to their perinatal cigarette smoke exposure. Compared with those without any exposure to cigarette smoke, the distance between alveolar attachments on airways was greater (p < 0.001) in infants exposed to cigarette smoke only in utero or both in utero and during the postnatal period but not different in those with only postnatal exposure. The percentage of elastin within the alveolar walls was similar in all the exposure groups. These findings suggest that in utero cigarette smoke exposure may result in abnormal airway function due to a reduction of the forces opposing airway narrowing.

　

Key Words: alveolar attachments • in utero cigarette smoke exposure • sudden infant death syndrome

	INTRODUCTION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

 
Maternal cigarette smoking during pregnancy is known to be a significant health risk to infants (1, 2). It is associated with restricted growth (3), reduced respiratory function at birth (4, 5) that persists into childhood (6), increased airway responsiveness (7), an increased likelihood of developing wheeze and asthma (8, 9), and an increased risk of sudden infant death syndrome (SIDS) (10–14). Epidemiologic studies that have adjusted for the effects of postnatal smoke exposure suggest that increased responsiveness in these infants is primarily associated with cigarette smoke exposure in utero (6, 15, 16). Gilliland and coworkers (8) have shown that although cigarette smoke exposure in utero increases the occurrence of doctor-diagnosed asthma and wheeze in school children, postnatal exposure operates as a cofactor that triggers wheezing attacks.

The mechanisms that result in abnormal postnatal lung function due to exposure to cigarette smoke in utero are unknown. The exposure is a unique form of passive smoke exposure in that there is no direct exposure to the fetal lung. However, components of cigarette smoke such as cotinine can cross the placental barrier (17). Prenatal subcutaneous administration of nicotine to pregnant monkeys results in decreased expression, but increased function, of