Abstract
ObjectivesEarly life environment is essential for lung growth and maximally attained lung function. Whether early life exposures impact on lung function decline in adulthood, an indicator of lung ageing, has scarcely been studied.MethodsSpirometry data from two time points (follow-up time 9–11 years) and information on early life exposures, health and life-style were available from 12862 persons aged 28–73 years participating in the European population-based cohorts SAPALDIA (n = 5705) and ECRHS (n = 7157). The associations of early life exposures with lung function (FEV1) decline were analysed using mixed-effects linear regression.ResultsEarly life exposures were significantly associated with FEV1 decline, with estimates almost as large as personal smoking. FEV1 declined more rapidly among subjects born during the winter season (adjusted difference in FEV1/year of follow-up [95%CI] -2.04ml [-3.29;-0.80]), of older mothers, (-1.82 ml [-3.14;-0.49]) of smoking mothers (-1.82ml [-3.30;-0.34] or with younger siblings (-2.61ml [-3.85;-1.38]). Less rapid FEV1-decline was found in subjects who had attended daycare (3.98ml [2.78;5.18]), and indicated in subjects with pets in childhood (0.97ml [-0.16;2.09]). High maternal age and maternal smoking appeared to potentiate effects of personal smoking. The effects were independent of asthma at any age.ConclusionEarly life factors predicted lung function decline decades later, suggesting that some mechanisms related lung ageing may be established early in life. Early life programming of susceptibility to adult insults could be a possible pathway that should be explored further.
Highlights
Childhood is a critical time window for subsequent lung health
[16] Lung function decline is on one hand a normal ageing process, on the other hand it can be potentiated by risk factors, such as smoking [17, 18] or obesity.[17, 19]
We studied the impact of early life factors on lung function decline in a mixed-effects linear regression model; in a first step, for single early life factors (S1 Table), and secondly, adjusting mutually for all early life exposures
Summary
Adverse childhood environmental exposures can restrain growth[1], modulate lung function [1, 2] and induce changes to gene-expression, modulating airway pathophysiology.[3, 4] The impact of a range of early life factors have been evidenced such as parental life-style [5, 6], nutrition [7] ambient air pollution [8, 9] or viral infections.[10] Epigenetic programming has been suggested as an underlying mechanism leading to less favourable long term respiratory health outcomes. [16] Lung function decline is on one hand a normal ageing process, on the other hand it can be potentiated by risk factors, such as smoking [17, 18] or obesity.[17, 19] Early life impact on adult respiratory health is relatively well documented [20,21,22,23]. For example, shows that a childhood disadvantage score, including childhood asthma, predicted more rapid lung function decline in middle aged adults [21] and Jackson et al evidenced earlier and quicker lung function decline for young adults with lower childhood SES [24] whereas Marossy et al found no significant association between lung function decline in adults age 35–45 and early life respiratory infections.[25]
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