Editorial
Early lung development begins in the fourth week of embryonic gestation and the majority of lung growth is completed in early childhood. As the burden of respiratory disease continues to grow, this window of opportunity is now the focus of increasing interest as researchers explore the factors that affect the future development of lung disease and the possibilities for prevention. In this month’s issue of The Lancet Respiratory Medicine, Janet Stocks and colleagues discuss the substantial effect that fetal and early-life events can have on long-term lung health. Lung function deficits seen in early childhood have been shown to persist into adulthood and predispose those affected to respiratory morbidity and mortality. Research has shown that both maternal and early-life nutrition, as well as exposure to environmental insults such as pollution, smoking, biomass fuels, and allergens, can affect lung function in later life. These external factors do not always cause disease; maternal and childhood susceptibility to a specific insult can greatly affect the size of any effect. Furthermore, such insults act in a multifactorial and interdependent way, making it very difficult to separate and quantify the causal effect of each individual factor. Research into prenatal and postnatal effects on lung development relies heavily on observational epidemiological studies, which assess association but not causation. Multiple confounders, an inability to distinguish between prenatal and postnatal exposures, and fluctuations in the environment over time and by geography all complicate interpretation of the data. Most research into the mechanisms and causes of disease are done in animal models and findings might not translate into studies in human beings. Therefore, prospective, well-designed studies with robust techniques to measure exposures and outcomes are needed, but such studies are huge undertakings that demand collaboration between different centres, have substantial costs attached, and need adequate long-term follow-up data to provide meaningful and clinically useful results. Understanding risk factors and identifying susceptible individuals is only half the battle. The other challenge is applying the knowledge gained to educate the public and the medical profession, as well as finding ways to alter respiratory outcomes in later life. The adverse neonatal outcomes associated with maternal www.thelancet.com/respiratory Vol 1 November 2013
diet, alcohol consumption, and smoking are all potentially avoidable, and public health campaigns to empower mothers to make informed choices that can help to shape their child’s future health are vital. However, other risk factors are not so easy to avoid or modify. In the ESCAPE study, also published in The Lancet Respiratory Medicine this month, data from 74 000 mother-child pairs in 12 European countries were pooled, and exposure to air pollution and traffic during pregnancy was shown to be associated with restricted fetal growth at term, a condition linked to increased risk of respiratory disease later in life. This increased risk of low birthweight at term was recorded at air pollution concentrations lower than the present recommended European Union annual PM2·5 limit of 25 μg/m3. In this context, the 2013 report—Air Quality in Europe—provides worrying data; the European Environment Agency noted that 11 member states had failed to adhere to the recommended limit in 2011, even though it should have been met by 2010. The target for PM2·5 concentrations in 2015 has been set at 20 μg/m3. This goal seems very challenging, especially for eastern Europe, where the pollution levels were highest, and suggests punitive fines will need to be enforced for countries to implement effective pollution control measures. Studies such as ESCAPE, which emphasise the important health benefits to be gained by reducing air pollution, will add weight to the upcoming discussions between policy makers on improving our air quality. Tackling the enormity of some of these environmental and public health issues will demand international cooperation. Encouragingly, on Oct 1, the American Thoracic Society and the European Respiratory Society published a joint statement pledging to reduce disparities in respiratory health and recognising the crucial part that maternal health and early lung development can play. Prenatal and postnatal health are especially vulnerable to social and economic status, and a failure to prioritise research and funding into this area will mean that the health divide continues to expand. As the respiratory community rallies to reduce the burden of lung disease, this crucial time period, during which the fragile new lungs develop, offers an opportunity not to be missed. ■ The Lancet Respiratory Medicine
Bluestone/Science Photo Library
Giving new lungs the best start in life
See Articles page 695 See Review page 728 For the Air Quality in Europe report see http://www.eea. europa.eu/publications/airquality-in-europe-2013 For more on the joint ATS and ERS statement see Am J Respir Crit Care Med 2013; 188: 865–71
663
Early lung development begins in the fourth week of embryonic gestation and the majority of lung growth is completed in early childhood. As the burden of respiratory disease continues to grow, this window of opportunity is now the focus of increasing interest as researchers explore the factors that affect the future development of lung disease and the possibilities for prevention. In this month’s issue of The Lancet Respiratory Medicine, Janet Stocks and colleagues discuss the substantial effect that fetal and early-life events can have on long-term lung health. Lung function deficits seen in early childhood have been shown to persist into adulthood and predispose those affected to respiratory morbidity and mortality. Research has shown that both maternal and early-life nutrition, as well as exposure to environmental insults such as pollution, smoking, biomass fuels, and allergens, can affect lung function in later life. These external factors do not always cause disease; maternal and childhood susceptibility to a specific insult can greatly affect the size of any effect. Furthermore, such insults act in a multifactorial and interdependent way, making it very difficult to separate and quantify the causal effect of each individual factor. Research into prenatal and postnatal effects on lung development relies heavily on observational epidemiological studies, which assess association but not causation. Multiple confounders, an inability to distinguish between prenatal and postnatal exposures, and fluctuations in the environment over time and by geography all complicate interpretation of the data. Most research into the mechanisms and causes of disease are done in animal models and findings might not translate into studies in human beings. Therefore, prospective, well-designed studies with robust techniques to measure exposures and outcomes are needed, but such studies are huge undertakings that demand collaboration between different centres, have substantial costs attached, and need adequate long-term follow-up data to provide meaningful and clinically useful results. Understanding risk factors and identifying susceptible individuals is only half the battle. The other challenge is applying the knowledge gained to educate the public and the medical profession, as well as finding ways to alter respiratory outcomes in later life. The adverse neonatal outcomes associated with maternal www.thelancet.com/respiratory Vol 1 November 2013
diet, alcohol consumption, and smoking are all potentially avoidable, and public health campaigns to empower mothers to make informed choices that can help to shape their child’s future health are vital. However, other risk factors are not so easy to avoid or modify. In the ESCAPE study, also published in The Lancet Respiratory Medicine this month, data from 74 000 mother-child pairs in 12 European countries were pooled, and exposure to air pollution and traffic during pregnancy was shown to be associated with restricted fetal growth at term, a condition linked to increased risk of respiratory disease later in life. This increased risk of low birthweight at term was recorded at air pollution concentrations lower than the present recommended European Union annual PM2·5 limit of 25 μg/m3. In this context, the 2013 report—Air Quality in Europe—provides worrying data; the European Environment Agency noted that 11 member states had failed to adhere to the recommended limit in 2011, even though it should have been met by 2010. The target for PM2·5 concentrations in 2015 has been set at 20 μg/m3. This goal seems very challenging, especially for eastern Europe, where the pollution levels were highest, and suggests punitive fines will need to be enforced for countries to implement effective pollution control measures. Studies such as ESCAPE, which emphasise the important health benefits to be gained by reducing air pollution, will add weight to the upcoming discussions between policy makers on improving our air quality. Tackling the enormity of some of these environmental and public health issues will demand international cooperation. Encouragingly, on Oct 1, the American Thoracic Society and the European Respiratory Society published a joint statement pledging to reduce disparities in respiratory health and recognising the crucial part that maternal health and early lung development can play. Prenatal and postnatal health are especially vulnerable to social and economic status, and a failure to prioritise research and funding into this area will mean that the health divide continues to expand. As the respiratory community rallies to reduce the burden of lung disease, this crucial time period, during which the fragile new lungs develop, offers an opportunity not to be missed. ■ The Lancet Respiratory Medicine
Bluestone/Science Photo Library
Giving new lungs the best start in life
See Articles page 695 See Review page 728 For the Air Quality in Europe report see http://www.eea. europa.eu/publications/airquality-in-europe-2013 For more on the joint ATS and ERS statement see Am J Respir Crit Care Med 2013; 188: 865–71
663
