Impact of bushfire smoke on infant lungs

THIS summer’s catastrophic bushfires saw much of eastern Australia blanketed in smoke and ash, including our major cities. The associated poor air quality and high levels of air pollution were unfamiliar and concerning to many Australians.

Bushfires create smoke that suspends particulate matter usually smaller than 2.5 micrometres (PM_2.5) in the air. These particles are small enough to be inhaled deep into the lungs. Governments and public health authorities in both New South Wales and Victoria have been quick to highlight health warnings for the most vulnerable in our community, including infants and pregnant mothers.

For the developing lung, there is no safe level of air pollution, but fortunately, the risks from exposure to bushfire smoke are most likely mild and short term for most infants. In the recent fire season, bushfire haze lasted from days (Melbourne) to weeks (Sydney and northern NSW), rather than the year-round, multiyear exposure to air pollution in some cities.

Globally, environmental air pollution is not new. The direct and indirect impacts of air pollution exposure on the fetus and infant have been previously described. In utero pollutant exposure can cause systemic inflammation in the mother and placental insufficiency. The fetus can be exposed to increased oxidative stress from maternal effects and/or direct particle effects. This may exert an epigenetic change and postnatally influence lung function, birth weight, and cognitive and immune development. Similar effects can occur from direct postnatal exposure.

Why are infants at greater risk?

The infant lung is small and infants breathe at a faster rate than adults. More importantly, early life is a critical period for lung development. Lung growth commences in the womb, well before it is responsible for gas exchange. Fetal lung growth branches from the trachea into smaller and more complex parts. It is not until 34 weeks of pregnancy that the fetal lung has developed enough alveoli to safely support independent breathing. The growth of new alveoli does not stop at birth, with alveolarisation continuing well into later childhood and even early adult life. Alveolarisation occurs in tandem with the immune development of the respiratory system. Together they provide the infant lung with remarkable abilities to adapt to challenges. Unfortunately, it also means the infant and fetal lung is susceptible to inflammation and injury at a time of ongoing change.

Work from the Murdoch Children’s Research Institute on the long term respiratory outcomes of infants born preterm and of those with chronic illnesses such as asthma and cystic fibrosis has shown that disrupting the normal process of lung growth and differentiation impacts lung function into later life. More worrying is that lung injury in early life may also slow the trajectory of lung growth in later childhood.

What are the short term risks?

Due to the small size, faster respiratory rate and growing lungs, infants cannot manage the same exposure load to airborne particulate matter. Infants’ airways are also more reactive to new insults and challenges. For most infants, the bushfire smoke will likely have minimal impact; irritating the airways and increasing the risk of coughing and respiratory infections, and thus potentially increasing health care visits. Infants with pre-existing illness, especially those born preterm or with congenital heart defects, are at greater risk of respiratory complications or exacerbation of existing chronic lung problems.

While not dismissing the short term impact of smoke exposure, the potential long term impact on later lung function is of greater significance.

Is the bushfire smoke likely to impact on infant lung growth long term?

Unfortunately, many children worldwide are raised in environments of increasingly high pollution. Caution should be applied to extrapolating the known effects of chronic exposure to air pollution on uterine growth, infant mortality, cognitive development and childhood lung function to the shorter term situation resulting from bushfires in Australia. Air pollution is not simple. Pollutant materials differ in composition and size and, thus, in airway delivery or distribution. Much of our knowledge has arisen from large studies of chronic exposure in urban environments. These studies have been further limited by non-standardised air pollution models and poor differentiation of indoor from outdoor exposure.

Much less is known about exposure to bushfire smoke. Bushfire smoke is a fine particulate matter compared with other air pollutants. This means it is more likely to be inhaled deep into the alveoli. Bushfire smoke may also contain other pollutants depending on the location of the fire and agents used to fight it. Historically, smoke exposure has been short. The Centre for Air Pollution, Energy and Health Research has been following the respiratory outcomes from previous large bushfires in Australia. They identified a potential link between prolonged exposure to bushfire smoke from the 2014 Hazelwood fire in infancy (less than 2 years old) with greater respiratory tract infections and altered lung mechanics in children (increased resistance and reactance measured using forced-oscillation technique) 3 years after exposure, even after accounting for maternal smoking. The increase in lung resistance was relatively minor, and less than the effect of antenatal tobacco smoke exposure. This study was limited in size (84 of 203 originally recruited infants) and the Hazelwood fire was unique being a coal mine fire. There was also no assessment of the effect of smoke exposure on the developing immune system, which is an important contributor to long term respiratory health.

Compared with other respiratory risks (such as smoking) or chronic air pollution in other parts of the world, it is unlikely that the current bushfire smoke will cause serious adverse health outcomes for infants.

There is still much we do not know. The recent call for projects from the Medical Research Futures Fund to better understand the impact of bushfires on our health is welcome. Well designed large cohort studies are needed to determine the effect of bushfire smoke exposure to the healthy and already diseased infant lung. The outcome measures need to be long term, meaning that the impact will not be known for many years.

Generation Victoria (GenV), a new Victoria-wide longitudinal cohort study due to commence in 2020, capturing pregnancy and postnatal clinical, demographic and biological data from all infants born in the state, is ideally suited to address this and other child health questions that may result from impact of climate change events in early life. This research platform will, for example, enable researchers to compare the long term respiratory health of any infants exposed to bushfire smoke compared with those less exposed.

Such studies are essential before we can determine the longer term impact of bushfire smoke on the lung health of vulnerable infants.

Associate Professor David Tingay is a neonatologist in the Department of Neonatology at The Royal Children’s Hospital Melbourne; NHMRC CDF Research Fellow and Co-Leader, Neonatal Research at Murdoch Children’s Research Institute; Principal Fellow, Department of Pediatrics, The University of Melbourne.

 Professor Sarath Ranganathan is Group Leader of the Respiratory Research Group at the Murdoch Children’s Research Institute. He is a full-time specialist in paediatric respiratory medicine at the Royal Children’s Hospital Melbourne.

Dr Shivanthan Shanthikumar is a consultant paediatric respiratory specialist who works at the Royal Children’s Hospital in Melbourne. He is completing his PhD at the Murdoch Children’s Research Institute which aims to identify epigenetic biomarkers of cystic fibrosis lung disease severity. He is also interested in a wide range of childhood respiratory disorders including asthma, lung infections and respiratory complications of childhood cancer.

The statements or opinions expressed in this article reflect the views of the authors and do not represent the official policy of the AMA, the MJA or InSight+ unless so stated.