Early life influences on the development of chronic obstructive pulmonary disease

Abstract

There is increasing evidence that chronic obstructive pulmonary disease (COPD) is not simply a disease of old age that is largely restricted to heavy smokers, but may be associated with insults to the developing lung during foetal life and the first few years of postnatal life, when lung growth and development are rapid. A better understanding of the long-term effects of early life factors, such as intrauterine growth restriction, prenatal and postnatal exposure to tobacco smoke and other pollutants, preterm delivery and childhood respiratory illnesses, on the subsequent development of chronic respiratory disease is imperative if appropriate preventive and management strategies to reduce the burden of COPD are to be developed. The extent to which insults to the developing lung are associated with increased risk of COPD in later life depends on the underlying cause, timing and severity of such derangements. Suboptimal conditions in utero result in aberrations of lung development such that affected individuals are born with reduced lung function, which tends to remain diminished throughout life, thereby increasing the risk both of wheezing disorders during childhood and subsequent COPD in genetically susceptible individuals. If the current trend towards the ever-increasing incidence of COPD is to be reversed, it is essential to minimize risks to the developing lung by improvements in antenatal and neonatal care, and to reduce prenatal and postnatal exposures to environmental pollutants, including passive tobacco smoke. Furthermore, adult physicians need to recognize that lung disease is potentially associated with early life insults and provide better education regarding diet, exercise and avoidance of smoking to preserve precious reserves of lung function in susceptible adults. This review focuses on factors that adversely influence lung development in utero and during the first 5 years of life, thereby predisposing to subsequent COPD.

Secreted Phosphoprotein 1 Is a Determinant of Lung Function Development in Mice

“…Severe impairments during any (82). However, mild structural or functional defects due to aberrant lung development (83) may increase susceptibility to respiratory diseases (COPD, cystic fibrosis, or asthma) that may be clinically detectable only during childhood or later in life through pulmonary function testing (84)(85)(86)(87). Therefore, it is important to detect genetic abnormalities that can affect early fetal and postnatal lung development; postnatal lung growth and maturation; and lung injury, repair, and remodeling processes (84)(85)(86)(87)(88)(89)(90).…”

“…However, mild structural or functional defects due to aberrant lung development (83) may increase susceptibility to respiratory diseases (COPD, cystic fibrosis, or asthma) that may be clinically detectable only during childhood or later in life through pulmonary function testing (84)(85)(86)(87). Therefore, it is important to detect genetic abnormalities that can affect early fetal and postnatal lung development; postnatal lung growth and maturation; and lung injury, repair, and remodeling processes (84)(85)(86)(87)(88)(89)(90). In mice, alveolarization takes place between P5 and P30 and is controlled by finely integrated and mutually regulated networks of transcriptional factors, growth factors, matrix components, and physical forces (9,(89)(90)(91)(92).…”

Early growth characteristics and the risk of reduced lung function and asthma: A meta-analysis of 25,000 children

“…Airway caliber is a key 243 determinant of total airway resistance and reduced caliber is a prominent feature of asthma 244 and chronic obstructive pulmonary diseases (5-7). Lower lung function in early life is likely to 245 lead to lower peak lung function in early adulthood, and the natural decline in FEV1 from that 246 point onwards will be accelerated by any additional adverse exposures (41). Thus, lung 247 function during the lifecourse seems to be programmed at least partly in early life.…”

Early-life origins of chronic respiratory diseases: understanding and promoting healthy ageing

“…A growing number of studies suggest that not only cigarette smoke but also several other factors are involved in the pathogenesis of COPD. Alongside those taking effect in adulthood, the role of perinatal and early-infancy factors, including prematurity and BPD, has recently been stressed [161,162], and an association has been suggested between low birth weight and both airflow limitation in adulthood [163,164] and death due to COPD [165]. Likewise, it has been demonstrated that some childhood disadvantages (parental asthma, childhood asthma, childhood respiratory infections and maternal smoking) have much the same impact on adult lung function and the risk of COPD as heavy smoking [50], suggesting that COPD can be seen as a disease of childhood that becomes manifest in adults [124,166].…”