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Factors to consider in future research on the relationship between early life socioeconomic position and adult lung function
Consistent with the Barker hypothesis of the early life origins of adult chronic disease,1 a growing body of research suggests a relationship between social disadvantage in early life and adverse health outcomes.2 In this issue of Thorax a paper by Lawlor et al3 presents evidence for inverse associations between markers of childhood socioeconomic position (SEP) and later life pulmonary function. The authors found that, as the number of indicators of childhood poverty increased, the levels of forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and forced mid expiratory flow rate (FEF25–75) decreased. Limitations of the study included a moderate response rate (60%), possible survivor bias (women from poor backgrounds may be more likely to die prematurely), and recall bias (indicators of childhood SEP were determined retrospectively by self-recall later in life). Yet, because each of these factors would lead to an underestimate of the effect of childhood SEP on pulmonary function in later life, the true effect is probably at least as strong and perhaps even greater than that detected by Lawlor and colleagues.
The analyses presented by Lawlor et al support a cross-sectional relationship between lower SEP in childhood and pulmonary function in adult life. Our group recently completed a longitudinal study of young adult pulmonary function in relation to childhood SEP.4 Using retrospective recall of parental education to examine childhood SEP as a predictor of change in pulmonary function in young adulthood, these longitudinal prospective analyses showed that childhood SEP predicted both baseline and subsequent levels of pulmonary function, as well as rates of decline in young adult women and men, even adjusting for current socioeconomic status, height, age, and age …
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During the preparation of this paper the authors were supported by grants from the National Heart, Lung, and Blood Institute (NHLBI) and Environmental and Health Sciences (ES). B Jackson and S T Weiss were supported by HL07427; R J Wright was supported by K08 HL04187; and L D Kubzansky was supported by ES10932.