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Examining the influence of early life socioeconomic position on pulmonary function across the life span: where do we go from here?
  1. B Jackson1,
  2. R J Wright1,2,
  3. L D Kubzansky3,
  4. S T Weiss1
  1. 1Channing Laboratory, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA
  2. 2Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
  3. 3Department of Society, Human Development, and Health, Harvard School of Public Health, Boston, MA, USA
  1. Correspondence to:
    Dr B Jackson
    Channing Laboratory, 181 Longwood Avenue, Boston, MA 02115, USA; benita.jacksonchanning.harvard.edu

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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 age2, asthma, parental smoking, and participant smoking. Although these two studies use quite different samples and different indices for SEP, the findings were consistent with an inverse relationship between childhood SEP and pulmonary function in both young and older adulthood.

FUTURE RESEARCH

To move forward, we need to draw on existing research focused on social disparities and other health outcomes and apply some of the lessons learned from this work to guide future research on SEP and pulmonary function. Building on research on other outcomes, we propose that future research on SEP and pulmonary function should take into consideration the following conceptual and methodological issues:

  • how to measure SEP (in early life as well as adulthood);

  • sample diversity;

  • developmental implications;

  • dose-response effects of SEP;

  • mechanisms linking SEP and pulmonary function; and

  • how best to examine the significance of such research for intervention.

Measuring SEP

There are many ways to measure SEP. Education, income, wealth, and employment type/status have been used individually or in combination. There is no best measure as each has strengths and drawbacks;5,6 rather, different measures are appropriate for different populations. For example, appropriate indicators of SEP depend on the age of the population studied.7,8 Moreover, income would be a poor measure in a population with a high prevalence of unemployment or disability.

A number of factors need to be considered when using SEP of caregivers as a proxy for early life SEP of the study participant. Some argue that the SEP of the father determines family SEP more strongly because men tend to be the primary breadwinner. Others suggest that the SEP of the mother is a better indicator of the child’s early life SEP because mothers tend to be the primary caretakers and thus have more shared environments with children. Using data from both parents may be even more informative but it can be difficult to find a way to combine them appropriately, and assumes that all children live with both their parents and not other caregivers. Others suggest that individual level early life SEP is only one piece of the story and that the larger social context such as the household and neighbourhood in which one lives each also add important insight to understanding the factors that influence health.9,10

Sample diversity

Factors such as race/ethnicity, gender, urban/rural place of residence, and geography may modify the relationship between SEP and life pulmonary function, which underscores the need to examine these questions in diverse populations. For example, educational attainment may not capture the full range of socioeconomic disparities in any given population; there may be differential economic and social returns for women (compared with men) and racial/ethnic minorities (compared with majority whites). Furthermore, the impact of poverty or low SEP may have a greater effect on those with other low social status positions. Even less well understood is whether there is an additive, multiplicative, or other effect of early life SEP in combination with other status indicators.11,12 In future research it will be imperative to sample participants in a way which will make it possible to examine interactions of childhood SEP with gender and race. In secondary analyses of existing large epidemiological studies, measurement of early life SEP is often a function of the availability of measures. However, keeping these general concepts in mind will be helpful in interpreting results.

The even more interesting research question may be whether there is some feature of a particular indicator of SEP that seems to be driving its effects, or whether the general early life milieu matters more for later life health. Lawlor et al used several indicators of SEP: manual childhood social class, no bathroom in the childhood house, no hot water in the childhood house, no access to a car as a child, and having a shared bedroom as a child. Our paper used the highest education completed between the mother and father as a single indicator of SEP. While both papers found generally similar trends, more research focusing on the implications of different definitions of early life SEP on later life pulmonary function is needed.

In the study by Lawlor et al3 childhood SEP was derived from data reported retrospectively. While it is unlikely that pulmonary function influenced the recall of childhood disadvantage, this study design cannot shed light on questions related to the timing of disadvantage. For example, are there critical periods in the life cycle when early life SEP has the greatest effect? Purpose designed studies might track individuals starting at birth, identify childhood SEP using multiple indicators from multiple informants, and then track the development of health and disease over the life cycle.

Developmental implications

Understanding the relationship between SEP and pulmonary function requires a developmental framework.13 SEP—especially those factors related to income—may change over the life span with upward mobility, job loss, or change in marital status.12 Pulmonary function is also dynamic across the life span, with rapid growth in early life, a plateau in young adulthood, and decline in later life. SEP may have stronger effects on pulmonary function during certain periods of childhood than in others.6 To understand whether and how early life SEP influences pulmonary function it is important to examine factors both longitudinally and during different periods in the life cycle (for example, young adulthood versus older adulthood). Prospective longitudinal studies would be particularly valuable in identifying periods of vulnerability related to social status indicators. Low SEP may contribute to accelerated “weathering” of pulmonary function and other health outcomes,14 causing impaired growth and early or rapid decline of pulmonary function.

Dose-response relationship of SEP to pulmonary function and disease outcomes

Is the relationship between childhood SEP and later life pulmonary function better characterised as a threshold or as a continuous graded effect? A threshold effect would mean that, past a certain amount of poverty, the negative effects of deprived early life conditions have no additional effect. Lawlor et al found that, with a greater number of indices of childhood poverty, there was greater lung function compromise. What remains to be studied with their sample is whether at higher levels of childhood SEP there is a gradient effect of childhood SEP on later pulmonary function—that is, is there an incremental improvement in pulmonary function with each step up the SEP hierarchy?15 If so, this would suggest that there is something more than poverty as such that compromises pulmonary function, but also greater harm associated with life experienced at each step down in the social hierarchy.

Mechanisms linking early life SEP and pulmonary function

There may be numerous mechanisms linking early life SEP and later life pulmonary function as reviewed previously.3,4 Although much research has been done on these various factors and how they relate to pulmonary outcomes (pulmonary function and also chronic disease states such as asthma and COPD), less research has examined how they may be shaped by SEP. Here again it is important in future work to take a developmental perspective. That is, the potential impact on a given mediator influenced by early life SEP may change over time as children undergo normal developmental changes. For example, Chen and colleagues6 argue that SEP differences in smoking may increase with age, compatible with the accumulation of negative effects over time.

Examining the significance of the research for intervention

While it is important to understand how these mechanisms operate, it is also important to acknowledge that early life SEP may be a “fundamental cause” of later health and disease.16 Even as interventions are targeted to modify mechanisms piecemeal—for example, reducing parental smoking or air pollution—because of the ubiquitous effects of SEP, new pathways may develop with equally deleterious effects. Thus, in addition to short term health interventions, public health practitioners must also have long term goals for eliminating root causes that contribute to early life deprivation (such as policies to redistribute wealth).17

CONCLUSIONS

Early life factors including social disadvantage are increasingly recognised as important determinants of health across the life cycle, although research focusing on respiratory health related to early life SEP is sparse. The paper by Lawlor et al contributes further to this growing area of scholarship and underscores the need for further studies. We hope that attention to the conceptual and methodological issues noted above will guide research aimed at better understanding these relationships, and inform interventions to ameliorate factors that compromise pulmonary function.

Factors to consider in future research on the relationship between early life socioeconomic position and adult lung function

REFERENCES

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Footnotes

  • 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.

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