PT  - JOURNAL ARTICLE
AU  - C Dezateux
AU  - S Lum
AU  - A-F Hoo
AU  - J Hawdon
AU  - K Costeloe
AU  - J Stocks
TI  - Low birth weight for gestation and airway function in infancy: exploring the fetal origins hypothesis
DP  - 2004 Jan 01
TA  - Thorax
PG  - 60--66
VI  - 59
IP  - 1
4099  - http://thorax.bmj.com/content/59/1/60.short
4100  - http://thorax.bmj.com/content/59/1/60.full
SO  - Thorax2004 Jan 01; 59
AB  - Background: Poor fetal growth has been associated with impaired airway function in adult life, but evidence linking birth weight and airway function in early childhood is sparse. We examined the hypothesis that low birth weight for gestation is associated with impaired airway function shortly after birth and that this is independent of impaired postnatal somatic growth. Methods: Airway function was measured using the raised volume technique in healthy white infants of low (⩽10th centile) or appropriate (⩾20th centile) birth weight for gestation and was expressed as forced expiratory volume in 0.4 s (FEV0.4), forced vital capacity (FVC), and the maximal expired flow at 25% of forced vital capacity (MEF25). Infant length and weight, maternal height and weight, maternal report of smoking prenatally and postnatally, and parental occupation were recorded. Results: Mothers of low birth weight for gestation infants (n = 98) were lighter, shorter, and more likely to smoke and have partners in manual occupations. At 6 weeks their infants remained lighter and shorter than those of appropriate birth weight (n = 136). FEV0.4, FVC, and MEF25 were reduced in infants of low birth weight for gestation, in those whose mothers smoked in pregnancy, or who were in manual occupations. After adjusting for relevant maternal and infant characteristics, infants in the low birth weight for gestation group experienced a mean reduction of 11 ml in FEV0.4 (95% CI 4 to 18; p = 0.002), of 12 ml in FVC (95% CI 4 to 19; p = 0.004), and of 28 ml/s in MEF25 (95% CI 7 to 48; p = 0.03). Conclusions: Airway function is diminished in early postnatal life as a consequence of a complex causal pathway which includes social disadvantage as indicated by maternal social class, smoking and height, birth weight as a proximal and related consequence of these factors, and genetic predisposition to asthma. Further work is needed to establish the relevance of these findings to subsequent airway growth and development in later infancy and early childhood.