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No fire without smoke: Are the children really out of the woods?
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- 자료유형학술지논문
- 저자명Bush, Andrew,Sonnappa, Samatha
- 학회/출판사/기관명John Wiley & Sons Ltd
- 출판년도2020
- 언어영어
- 학술지명/학위논문주기RESPIROLOGY
- 발행사항Vol.25No.2[2020]_x000D_
- ISBN/ISSN
- 소개/요약There is increasing recognition that the time between conception and the first day at school represents a period of vulnerability for the developing respiratory tract. Antenatal and early life exposure to pollutants, including nicotine and air pollution, leads to impaired lung function, which largely tracks into the sixth decade.1 It is increasingly realized that chronic obstructive pulmonary disease (COPD) will not be prevented by adult life interventions; the action occurs very early on. In a recent publication in Respirology, Shao et al. followed up a cohort of children who were transiently exposed to high levels of atmospheric pollution as a result of serious fires.2 At 3‐year follow‐up, they demonstrated impairment of peripheral lung mechanics as measured by the forced oscillation technique (FOT). As a positive control, the authors were also able to detect the effects on FOT indices of maternal smoking during pregnancy. As in many real‐world studies, there are data issues that mandate caution in drawing strong conclusions. Follow‐up was incomplete (84/203, 41%), which could have led to an inadvertent selection bias, as discussed by the authors.2 A comparison of FOT results in infants exposed to the fire with unexposed controls or with those older than 2 years of age during the fire would have added value to the study. Furthermore, the area of reactance (Ax) is regarded as a small airway index that is sensitive to changes in the bronchomotor tone.3, 4 The results would have been more informative had there been additional measurements of bronchodilator response compared to normal controls. On univariable analysis, the authors report the average PM2.5 (10 μg/m3 increase) for the β‐coefficient of Z (AX) to be 0.241 (0.035, 0.447) and maternal smoking during pregnancy to be 0.613 (0.112, 1.115). It is intriguing that, instead of this association becoming diluted in a multivariable analysis where maternal smoking during pregnancy (a significant confounder) was adjusted for in the model, the β‐coefficient for Z (AX) is higher at 0.260, while there were no significant associations seen with either respiratory system resistance or reactance. In addition, the lung function changes reported by Shao et al. are relatively minor and close to the noise of the measurement; a more sophisticated evaluation, perhaps when the children are older, would help capture the full extent of the impact of this transient heavy smoke exposure. However, there may be more to heavy smoke exposure during critical time windows than just impaired lung function. First, in another such natural experiment, an outdoor‐housed colony of rhesus macaque monkeys that were exposed to ambient pollution from a series of Californian wildfires in the first 3 months of life were studied in adolescence.5 There were two bursts of exposure lasting 4–6 days, and PM2.5 peaked at 78 μg/m3. This was lower than in the present study (median and interquartile range (IQR) peak: 103.4 (60.6, 150.7), with a staggering top value of 731, nearly 30 times higher than the national average). In adolescence, when compared with controls born a year later, infant monkeys that were exposed to the fires had impaired lung function which were dissimilar to the results reported here. However, there were more than just physiological changes; the monkeys also exhibited gender‐specific immunological changes. Both genders exhibited changes in toll‐like receptor (TLR) pathways. Female monkeys had reduced peripheral blood mononuclear cell synthesis interleukin (IL)‐8 in response to flagellin or lipopolysaccharide, with male monkeys demonstrating additional decrements in TLR pathways and reduced transcription factor expression. In humans, antenatal exposure to tobacco is also associated with immunological changes in cord blood mononuclear cells.6, 7 The smoke‐exposed children may therefore also have been set up for subsequent increased vulnerability to infection, and this might be the subject of a future study. Second and very importantly, it is becoming increasingly clear that a reduced forced expiratory volume in the first second (FEV1) has long‐term implications beyond the respiratory tract. The association of low initial FEV1 with COPD is well known,8 but what is becoming appreciated is that a low FEV1 is associated with increased all‐cause mortality as early as the third decade of life.9, 10 It is speculative, but could this early smoke exposure lead, in the future, to an increased risk of cardiometabolic co‐morbidities in particular? Again, ongoing follow‐up of these children would be informative. So, what is the overall message of Shao et al.'s study2? Clearly, we know that big fires are not good for anybody, but what the manuscript does stress yet again is the vulnerability of preschool children to environmental insults. Importantly, they could not demonstrate a safe threshold for exposure. Paediatricians need to continue to press home this point to politicians and urge strong action; Shao et al.'s study2 adds to the evidence that we are literally playing with fire if we do not do our utmost to protect little lungs from all outdoor (and indoor) pollutants.
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