Beyond the womb: respiratory symptoms in children following acute in utero exposure to fire smoke

Air pollution poses global health, equity, and environmental problems with short and long term consequences

The impact of environmental pollutants from diverse sources on health and well‐being is widely recognised.1 However, much remains unknown, including the relative contributions of specific air pollutants, their size effects, the periods of maximum vulnerability, and the longer term effects of acute and prolonged exposure, particularly in children.2,3 The expected increases in the number and intensity of bushfires, as seen in Australia during the summer of 2019–20, require that the effects of such extreme events on public health be explored.

This issue of the MJA includes the report by Willis and colleagues of a prospective cohort study of infants and young children of mothers living in the Latrobe Valley in Victoria during the 2014 Hazelwood open‐cut coalmine fire (the Latrobe Early Life Follow‐up [ELF] study).4 Two to four years after the fire, parental reports of several indicators were more frequent for the 160 children born to mothers pregnant during the fire (in utero exposure): runny nose or cough (for each 10 μg/m³ increase in mean daily PM_2.5 exposure: relative risk [RR], 1.09; 95% confidence interval [CI], 1.02–1.17), wheeze (RR, 1.56; 95% CI, 1.18–2.07), seeking health professional advice (RR, 1.17; 95% CI, 1.06–1.29), and doctor diagnoses of upper respiratory tract infections, cold or flu (RR, 1.35; 95% CI, 1.14–1.60). These associations were not statistically significant for the 129 children exposed to the fire when 0–2 years old, perhaps because of the small sample size.4 Data on lung function for a subgroup of the ELF cohort (84 children) published elsewhere indicated that increasing mean daily PM_2.5 exposure was modestly associated with reduced respiratory system reactance (per 10 μg/m³ increase: β‐coefficient, 0.26; 95% CI, 0.02–0.50).5

Although the authors took several possible confounders into account (socio‐economic status, background NO₂, tobacco smoke exposure), other possible influences, such as ambient temperature and PM₁₀ and ozone levels, were not examined. The study by Willis and colleagues may also have been limited by the size of the relatively small cohort. In an earlier article,6 the group reported the lack of effect of the fire on fetal growth and maturity outcomes, in contrast to studies of ambient particulate matter exposure in other countries.7,8,9 Further, the cohort in their article4 included only 571 of the 3591 eligible children (16%) in their earlier report,6 and full data were available for only 289 (8%). The mean monthly diary completion rate was possibly suboptimal at 16.2 per participant (62% for the 26‐month study); further, systematic bias was conceivable, as parents with children with symptoms were more likely to complete diaries.

Nevertheless, given the paucity of published data regarding isolated smoke exposure events2,3 and the expected national and global increases in fire events, the findings reported by Willis and her co‐authors are important. The unique nature of the time‐limited exposure of the study cohort produced comparative data for pre‐ and post‐natal exposure to increased PM_2.5 levels. Meta‐analyses have identified an association between ambient air pollution exposure and adverse birth outcomes10,11 — for instance, 15% increase in risk of pre‐term birth per 10 μg/m³ increase in PM_2.511 — but less is known about the long term effects of short term exposure on the future respiratory health of infants and children.2,3 Studies of the effects of Indonesian forest fires on fetal, infant and child mortality found a 20% increase in mortality among children under 3 years of age; at greatest risk were children in poorer areas and infants born to mothers exposed during the third trimester of pregnancy.8

The study by Willis and colleagues4 found that a single large exposure to airborne pollutants not only affects acute health but probably has longer term respiratory consequences, as also reported by others.8,9 This finding is consistent with the reduced lung function and immune dysregulation at adolescence noted in rhesus monkey infants exposed to wildfire smoke.12 Willis and her co‐authors4 did not examine lower respiratory infections, but bronchitis during early childhood (before the age of 2 years) is associated with later deficiencies in lung function.13 This suggests that air pollutant exposure at critical developmental time points (in utero and during early childhood) may have implications for adult respiratory health. While the precise biological mechanisms are largely unknown, the impact of early childhood factors on future adult health (lung function trajectories2) is increasingly recognised. Indeed, it was recently reported that future all‐cause and cardio‐respiratory mortality and morbidity were significantly influenced by lung function impairment (even within the clinically normal range) in a prospective international study of 126 359 adults aged 35–70 years followed for a median 7.8 years.14

Ambient air pollution is different to that caused by wild and coal fires, but the collective impact of acute and chronic air pollutants is now clearer. Air pollutants are not only a health problem, but also problems of global equity8 and environmental sustainability that we all need to address through individual and collective actions.