ArticlesEffects of maternal smoking during pregnancy and a family history of asthma on respiratory function in newborn infants
Introduction
Important interactions have been demonstrated between early lung function, wheezing illnesses during infancy,1 and symptoms of asthma in later childhood.2 Infants with reduced respiratory function in the first months of life are more likely to develop wheezing lower respiratory illnesses by the age of 1 year and have reduced pulmonary function at age 6 years despite resolution of symptoms.2 These children are more likely to have mothers who smoke. Children with persistent wheezing at age 6 have normal lung function early in infancy but are more likely to have a family history of asthma and high IgE levels as infants.2
Longitudinal studies suggest that early wheezing is a transient phenomenon that resolves in about 60% of children by school-age.2, 3, 4 The findings of Martinez and colleagues2 suggest that this transient condition is associated with reduced airway function soon after birth. The reduced lung function at this age does not seem to predispose to persistent wheezing later in childhood. However, the significance of reduced lung function in early childhood in relation to the development of chronic airflow limitation in adults is unknown. Other observations have suggested that exposure to environmental tobacco smoke predisposes to respiratory illnesses and reduced lung function in infants5, 6, 7 and school-age children.8, 9
One limitation of all these studies is that they could not separate the effects on lung function of direct in-utero exposure and passive postnatal exposure to constituents of cigarette smoke. Even in the studies that included infants,6, 7 measurements of respiratory function were obtained when the babies were a few weeks old, by which time children may have had substantial exposure to environmental tobacco smoke. The patterns of smoking by mothers during and after pregnancy do not facilitate the task of separating in-utero from postnatal effects. Most mothers who smoke during pregnancy continue to smoke postnatally, whereas many who do not smoke during pregnancy start or resume smoking postnatally. Few mothers smoke during pregnancy and then stop afterwards. Despite these difficulties, some investigators have argued that in-utero exposure to the constituents of cigarette smoke results in reduced respiratory function in young infants.6,7 If confirmed, this hypothesis has important implications for lung development, respiratory symptoms during infancy, and the aetiology of various respiratory disorders in later life, including asthma.
Another factor that might significantly affect respiratory function in infancy is genetic predisposition; we found that infants with a family history of asthma have increased bronchial responsiveness.10 The pulmonary function tests available for young babies are complex and time-consuming and most require sedation, so they are unsuitable for use in newborn infants. A simple test of respiratory function that could be applied soon after birth in a large cohort of infants is needed to find out whether there is a significant in-utero effect of maternal smoking, Other potential prenatal effects on early respiratory function, such as a family history of asthma, could be similarly examined.
Martinez and colleagues1 found that an index of tidal expiratory flow was informative about the risk of wheezy lower respiratory illnesses in infants. They found that the time to peak tidal expiratory flow (tPTEF) as a proportion of total expiratory time (tE) was lower in healthy male infants who subsequently developed wheezing than in those who did not. Since tPTEF/tE can be measured simply and without sedation, it is a potentially powerful technique for epidemiological studies. One limitation is the use of a face-mask, which could alter the pattern of breathing. We have described a method for measurement of tPTEF/tE that uses uncalibrated inductance plethysmography and does not require a face-mask.11 This approach reduces the risk that breathing patterns will be altered and is also less alarming for parents of newborn infants. In this study we used this technique to measure tPTEF/tE in a large cohort of newborn infants.
Our hypothesis was that prenatal factors—exposure to cigarette smoke and a family history of asthma—adversely affect respiratory function resulting in low values of tPTEF/tE. We measured tPTEF/tE by respiratory inductance plethysmography in newborn infants of mothers recruited to the Western Australian Pregnancy Cohort Study (WAPCS).
Section snippets
Methods
WAPCS was established to investigate the hypothesis that frequent ultrasound imaging and doppler waveform examinations would reduce neonatal morbidity and rates of preterm birth. 2900 women were enrolled consecutively and randomly assigned imaging at 18, 24, 28, 34, and 38 weeks' gestation (intensive arm) or single imaging at 18 weeks' gestation with additional scans only as indicated clinically (regular arm). Serum cotinine concentrations at 18 weeks' gestation were available for our analysis
Results
500 healthy newborn infants were recruited to the study and had respiratory function measured at a median age of 58 h (range 26-159). All infants were of gestational age greater than 37 weeks at birth. Measurements from 461 (210 male, 251 female) infants were technically adequate for inclusion in the final analysis (table 1). Reasons for exclusion were thoracoabdominal asynchrony and illdefined peak expiratory flow. There were no significant differences in respiratory rate or any of the
Discussion
Previous studies of factors that affect early lung function were unable to examine separate antenatal and postnatal effects. Since we used a technique that allowed us to measure respiratory function in infants soon after birth, we were able to identify antenatal factors that induce changes in respiration in newborn infants independently of any postnatal influences. Although there is controversy about the best method of obtaining and analysing measurements of tPTEF/tE in newborn infants, we have
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