1 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
2 Department of Society, Human Development and Health, Harvard School of Public Health, Boston, MA, USA
3 Department of Psychology, Carnegie Mellon University, Pittsburgh, PA, USA
4 Beth Israel Deaconess Medical Center, Boston, MA, USA
Correspondence: Benita Jackson, Channing Laboratory, 181 Longwood Avenue, Boston, MA 02115, USA. E-mail: benita.jackson{at}channing.harvard.edu
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Abstract |
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Methods Participants were from the Coronary Artery (Disease) Risk Development in (Young) Adults (CARDIA) study: 5113 young adults ages 1830 at baseline, approximately balanced within centres across gender, self-identified race/ethnicity (Black, White), and current SES. Childhood SES was ascertained from baseline self-reports of parents' highest completed education. Pulmonary function in young adulthood was measured using FEV1 (forced expiratory volume in one second) and FVC (forced vital capacity), assessed on three occasions over a period of 5 years.
Results Longitudinal analyses suggested that rates of change in both FEV1 and FVC differed in a gradient fashion by childhood SES. As shown by significant childhood SES by time interaction terms, these associations with FEV1 were robust for men (b = 1.59E3, SE = 5.21E4, P < 0.001) and women (b = 1.93E3, SE = 4.80E4, P < 0.001), and adjusted for multiple potential confounders including smoking. Results were similar for FVC. Subsequent examination of the interaction terms suggested that FEV1 and FVC declined for participants in the lowest childhood SES group, showed continued plateau or growth for those in the highest group, and were intermediate for the middle group.
Conclusions Childhood SES may influence men's and women's young adult pulmonary function in two ways. First, individuals with lower childhood SES may not attain as high levels of pulmonary function in early adulthood relative to individuals with higher childhood SES. Second, pulmonary function may decline earlier and faster for individuals with lower childhood SES.
Accepted 16 July 2003
Reduced maximally attained pulmonary function and accelerated rate of pulmonary function decline are risk factors for the development of undesirable health conditions including chronic obstructive pulmonary disease (COPD), cardiovascular disease, and early mortality.1 COPD, for instance, results in poor physical, psychological, and social functioning,2 poses a considerable economic burden,3 and is projected to be the third leading cause of death by 2020.4 Factors contributing to poor pulmonary function have not yet been elucidated fully.
Researchers have conceptualized socioeconomic factors as a fundamental cause of disease.5 However, few studies go beyond considering socioeconomic status (SES) as a confounder when examining pulmonary function.6,7 Those that do suggest low SES is associated with low mean levels of pulmonary function (for a review see ref. 8). Moreover, SES explains pulmonary function differences observed across other social status markers, and beyond effects of smoking.9 Important gaps remain in research linking SES and pulmonary function.
No studies examine how SES influences the trajectory of pulmonary function in young adulthood. Pulmonary capacity is thought to be dynamic, with growth in childhood and adolescence, a plateau during young adulthood, and decline beginning in later adulthood. A recent study examined how early life factors like asthma contribute to level of pulmonary function and change in a sample of young adults, but this study did not consider SES.10 Because childhood SES may be linked with differential exposure to a variety of risk factors (e.g. asthma, allergens, tobacco smoke)11 resulting in childhood respiratory trouble,12 childhood SES may be a critical predictor of adult pulmonary function.13 Young adults are important to study because maximally attained pulmonary function is achieved in young adulthood,14 and higher peak pulmonary capacity serves as a buffer against subsequent decreases in pulmonary function related to ageing and lifetime exposure to environmental toxins. Further, early pulmonary function decline is linked to early mortality. [Wang X et al., Early predictors of chronic obstructive pulmonary disease, submitted manuscript, 2002.]
We examined the association between childhood SES and young adult pulmonary function in the Coronary Artery (Disease) Risk Development in (Young) Adults (CARDIA) study. Based on previous research on SES and health,8,15,16 we hypothesized a gradient relation between childhood SES and young adult pulmonary function at baseline, and also expected to see this gradient persist over time. Finally, we hypothesized that lower childhood SES would be associated with a faster rate of pulmonary function decline.
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Method |
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The study was conducted in four urban centres in the US: Minneapolis, MN; Birmingham, AL; Chicago, IL; and Oakland, CA. The total sample consisted of 5115 participants (2787 women and 2328 men) approximately balanced within each centre across gender, race/ethnicity, and SES. The following participants were included: those who self-identified as Black or as White (US Census Bureau category), with a permanent address in the target area, free of long-term disease or disability, and not pregnant at baseline. Pulmonary function was obtained at baseline (19851986), year 2, and year 5. Data on sociodemographic factors, anthropometry, asthma history, and smoking status were also available. In the public-use data on CARDIA, measurements were deleted when they would have enabled identification of participants (e.g. name, birth date) or were deemed too sensitive to distribute (e.g. illicit drug use). Of eligible participants, 50%, ages 1830 years, participated. Two participants had incomplete data, resulting in 5113 participants for these analyses.
Measures
Childhood SES
Childhood SES was determined by the highest level of education attained between participants' parents. The range available for father's highest education was 11 (11th grade) to 13 (some college or more). More finely grained distinctions for higher levels of father's education were not available. The range for mother's highest education was 11 (11th grade) to 17 (some graduate school or more). A variable was created taking the highest education completed between the participant's father and mother, with values ranging from 11 (11th grade) to 13 (some college or more). Historically, parents' level of one or more markers of SES (income, education, occupation, wealth) has been used as a proxy for childhood SES.18 We used education because it is easily measured, comparable across studies in the US and Western Europe, and a more reliable measure for women than is occupation.19 If the participant had only one parent, that parent's highest education was used to compute childhood SES. Participants missing childhood SES data for both parents (n = 318) were not included.
Pulmonary function
Pulmonary function was assessed with a Collins Survey 8-litre water-sealed spirometer and the Eagle II Microprocessor (Warren E Collins, Inc., Braintree, MA USA) while participants were standing and wearing nose clips. Pulmonary function data were acceptable if at least three reproducible tests of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were taken, with up to five attempts, in accordance with American Thoracic Society standards for pulmonary function. Of the 5113 CARDIA participants, 4861 (95%) yielded acceptable data for FEV1 and FVC.
Other determinants of pulmonary function
Baseline height was measured to the nearest 0.5 cm. Age, gender, current SES, history of asthma (unconfirmed and doctor confirmed), parental (maternal and paternal) smoking status, and participant smoking status were ascertained at baseline by an interviewer-administered questionnaire. Current SES was assessed by number of years of education the participant had completed. Unconfirmed asthma symptoms was ascertained by answering yes to wheezing occasionally apart from colds or most days or nights, and to endorsing breathlessness when hurrying on the level of walking up a slight hill. Doctor-confirmed asthma was defined as answering yes to both have you ever had asthma? and was it confirmed by a doctor?
Analyses
We estimated parameters for the effect of childhood SES on pulmonary function using hierarchical linear modelling (HLM; also known as random effects modelling) using repeated measures analysis in the Statistical Analysis System.20 This allows examination of how people change over time,21 and has been used to examine pulmonary change.22 Multiple observations at different times are viewed as nested within the individual. Each model has two levels: (1) a within subject level that specifies individual time paths, and (2) a between subjects level that considers whether group membership (e.g. low SES versus high SES) accounts for differences in rates of change.21 After examining variance in individual-level intercepts and slopes, a conditional model predicts intercept and slope terms using group as a predictor variable. These models can accommodate missing values of the dependent variable, and allow control for potential confounding variables and baseline pulmonary function when examining rates of decline. Covariates are set as fixed effects in these analyses. The covariance structure was specified using a compound symmetry model which was the best fitting model using Aikaike's Information Criterion and maximum likelihood ratio tests. As we were primarily interested in the between group effects (i.e. childhood SES levels), we present only the data for fixed effects. Values for FEV1 and FVC were divided by height-squared and log-transformed, which has been shown, in this sample, to be the most effective yet parsimonious adjustment for height.23 An age-squared term was added to the models, in addition to linear age, to account for non-linear effects (i.e. growth, plateau, and decline).10 All predictor variables were centred. Thus, the intercept may be interpreted to describe the mean or reference value for each of the other predictor variables. To determine whether childhood SES influenced rate of pulmonary function decline in the mixed regression models, we created an interaction term for childhood SES and time, using linear terms for both.
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Results |
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Using an interaction term of childhood SES and time in Model 1, we examined whether pulmonary function declined faster among participants with low versus higher childhood SES. A significant interaction term for men (b = 1.58E 3, SE = 5.13E 3, P < 0.01) and women (b = 1.89E 3, SE = 4.76E 3, P < 0.001) and subsequent examination of the associations suggested that FEV1 was decreasing most rapidly among those with the lowest childhood SES. For men there was a significant decrease in FEV1 at each level of childhood SES; those with the lowest childhood SES showed the most rapid decrease over the study period. For women there was a significant decrease in FEV1 for the two lower childhood SES levels, but no change over time among those with the highest level. Similarly, a significant interaction term for FVC was seen for men (b = 1.38E 3, SE = 4.22E 4, P < 0.01) and women (b = 1.31E 3, SE = 3.94E 4, P < 0.001). Again, FVC was decreasing most rapidly among those with the lowest childhood SES. For men there was a significant decrease in FVC among those with the lowest childhood SES, whereas there was no change over time for those with higher childhood SES. For women there was no significant change in FVC for those with the lowest childhood SES, but there was significant increased growth among those with higher childhood SES.
Model 2further adjusted for current SES, asthma history, and smoking history (parental and participant's own)suggested that the independent effect of childhood SES remained for both men (b = 0.028, SE = 4.97E 3, P < 0.001) and women (b = 0.020, SE = 4.10E 3, P < 0.001). Similarly, participants with higher levels of childhood SES had higher levels of FVC (Table 3), as evidenced by a significant main effect of childhood SES for both men (b = 0.039, SE = 4.78E 3, P < 0.001) and women (b = 0.028, SE = 4.10E 3, P < 0.001). We again observed an age2 effect for both men (with FVC) and women (with FEV1), such that with a larger age2 there was lower pulmonary function.
The interaction term for childhood SES and time in the fully adjusted Model 2 was consistent with the patterns in Model 1. Again, there was a significant interaction term for men (b = 1.59E 3, SE = 5.21E 4, P < 0.01) and women (b = 1.93E 3, SE = 4.80E 3, P < 0.001) and subsequent examination of the associations suggested that FEV1 was decreasing most rapidly among those with the lowest childhood SES (Figures 1a and 1b). For men there was a significant decrease in FEV1 at each level of childhood SES; those with the lowest childhood SES showed the most rapid decrease over the study period. Similarly, a significant interaction term for men (b = 1.36E 3, SE = 4.29E 4, P < 0.01) and women (b = 1.31E 3, SE = 3.96E 4, P < 0.001) and subsequent examination of the associations suggested that FVC was decreasing most rapidly among those with the lowest childhood SES (Figures 2a and 2b). For men there was a significant decrease in FVC among those with the lowest childhood SES, whereas there was no change over time for those with higher childhood SES. For women there was no significant change in FVC for those with the lowest childhood SES, but there was actually significant increased growth among those with higher childhood SES.
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Some research suggests confounding or interactive effects between race/ethnicity and SES in relation to health outcomes.2426 However, little research to date has looked at these issues in relation to pulmonary function. Ideally to do so one would examine a childhood SES x gender x race interaction over the study period. However, in the current sample, this stratification leads to small cell sizes resulting in unstable estimates due to inadequate statistical power. However, in exploratory analyses we looked within racial groups, controlling for gender, to see if the childhood SES effect was present (data not shown). For all groups, trends suggested that lower SES compared with higher SES was associated with lower pulmonary function.
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Discussion |
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Previous work has suggested that the plateau phase of pulmonary development in young adulthood actually is not a steady-state period.27 Indeed, our FVC findings for women (Figure 2b) suggest that pulmonary function was increasing in the highest while declining in the lowest childhood SES group. Replication of the trajectory we found may suggest underestimation of the length of the growth phase because of failure to consider pulmonary function in the context of SES, and the conditions (e.g. housing, workplace exposures), medical history (e.g. asthma), and behaviours (e.g. smoking) that are shaped by SES.
We included several covariates that may mediate the childhood SESyoung adult pulmonary function relationship. Though we did not conduct formal tests of mediation, our analyses suggest that childhood SES may affect both history of asthma and smoking, which in turn may influence pulmonary function. Indeed, the addition of these terms (along with current SES) substantially reduced the effect on pulmonary function of childhood SES and the interaction of childhood SES with time (Tables 2 and 3), while themselves remaining significant. Notably, those with lower childhood SES were more likely to report undiagnosed asthma symptoms, but less likely to report diagnosed asthma. This may reflect the relationship between SES and both access to healthcare and the management and treatment of asthma.28 In turn, asthma predicted decreases in FEV1 and FVC for both men and women. The relationships among childhood SES, smoking, and pulmonary outcomes were more complicated and warrant further investigation. Of key importance is that while asthma history and smoking may partially mediate the childhood SESyoung adult pulmonary function link, an effect of childhood SES persists beyond the effects of these variables. Even accounting for the effects of asthma history and smoking, projections 15 years from baseline showed the effects of childhood SES on pulmonary function only more pronounced.
It is also noteworthy that after adjusting for all of these covariates, we observed an age2 effect for both men (with FVC) and women (with FEV1), such that with a larger age2 there was lower pulmonary function. Due to different exposures occurring at different times in history, not only that one is 25 years old may influence pulmonary function (age effects), but also when one reaches a given age (cohort effects) is important to consider. Our findings suggest that adjusting for time from baseline (i.e. cohort effects) and other covariates, even across young adulthood in some cases pulmonary function declines more rapidly with age.
Other mechanisms may influence the relationship between childhood SES and young adult pulmonary function.29 For example, children of low SES tend to live in environments exposing them to toxins ranging from air pollution (indoor and outdoor) to interpersonal violence.3032 These toxins may promote respiratory infection; directly, as with air pollution,33 or indirectly through routes like stress, as with interpersonal violence.34 Such exposure may in turn influence later-life pulmonary function.19 Similarly, burgeoning scholarship suggests that psychological factors (e.g. negative emotions, optimism) may be another important route linking social structure and health.35,36 Childhood SES may also shape health behaviours beyond smoking that affect later pulmonary health. For example, nutritional intake of foods high in antioxidants may be protective against pulmonary decline.37
We cannot fully rule out the possibility that there is an unexamined third factor leading to low childhood SES, low pulmonary function, and increased rates of pulmonary function decline. For example, poor health from inherited chronic conditions may influence parents' SES and participants' pulmonary function levels and decline. Though the prospective findings provide important evidence for causation in the direction of childhood SES influencing subsequent pulmonary function and change, we did not test reverse-causal hypotheses in the current study.
Our measure of childhood SES was admittedly limited and subject to recall bias. However, recall of parents' education may be less subject to memory bias than answering more specific questions about living conditions two decades or more earlier. In addition, participants were unaware of our interest in the link between childhood SES and pulmonary function, making a systematic bias in any one direction less likely. Given the restricted range of the childhood SES measure, its significant effect on young adult pulmonary function suggests a robust relationship.
We did not have the power to stratify by race and gender in order to understand childhood SES effects on pulmonary function among black women, white women, black men, and white men, but results were qualitatively similar across these groups. In future work it will be imperative to sample participants in a way to enable the examination of childhood SES x gender x race interactions.
These data add to the growing evidence of SES disparities in physical health. Young adulthood is an under-studied but developmentally critical phase for health because maximum level of pulmonary function is attained during this period, setting the stage for later-life resilience or rapid decline. Our findings suggest that a life-course approach may be usefully applied to pulmonary function in young adulthood. Childhood SES may influence young adulthood pulmonary function in two ways. First, individuals with lower childhood SES may not attain as high levels of pulmonary function in early adulthood relative to individuals with higher childhood SES. Second, pulmonary function may decline earlier and more quickly for individuals with lower childhood SES. Given that pulmonary function decline is progressive, future research is needed to explicate the implications of these findings for later-life health status, as well as the mechanisms linking childhood SES and young adult pulmonary function.
KEY MESSAGES
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Acknowledgments |
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Notes |
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For interpretability of the projections, we adjusted for height2 as a covariate, instead of dividing pulmonary function by height2 and taking the log-transformation. All other parameters used in the models for the projections are as in Model 2 (Tables 2 and 3).
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References |
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2 Engstrom C, Perssson L, Larsson S, Sullivan M. Health-related quality of life in COPD: why both disease specific and generic measures should be used. Eur Respir J 2001;18:6976.
3 Rutten van-Molken M, Feenstra T. The burden of asthma and chronic obstructive pulmonary disease: data from The Netherlands. Pharmacoeconomics 2001;19(Suppl.2):16.
4 Gulsvik A. The global burden and impact of chronic obstructive pulmonary disease worldwide. Monaldi Arch Chest Dis 2001;56:26164.[Medline]
5 Link BG, Phelan J. Social conditions as fundamental causes of disease. J Health Soc Behav 1995;(Extra issue):8094.
6 Blane D, Hart CL, Davey Smith G, Gillis CR, Hole DJ, Hawthorne VM. Association of cardiovascular disease risk factors with socioeconomic position during childhood and during adulthood. BMJ 1996;313:143438.
7 Davey Smith G, Hart C, Blane D, Hole D. Adverse socioeconomic conditions in childhood and cause specific adult mortality: prospective observational study. BMJ 1998;316:163135.
8 Prescott E, Vestbo J. Socioeconomic status and chronic obstructive pulmonary disease. Thorax 1999;54:73741.
9 Abbotts J, Williams R, Ford G. Morbidity and Irish Catholic descent in Britain: relating health disadvantage to socio-economic position. Soc Sci Med 2001;52:9991005.[CrossRef][ISI][Medline]
10 Apostol GG, Jacobs Jr DR, Tsai AW et al. Early life factors contribute to the decrease in lung function between ages 18 and 40: the Coronary Artery Risk Development in Young Adults Study. Am J Respir Crit Care Med 2002;166:16672.
11 Lannerö E, Krull I, Wickman M, Pershagen G, Nordvall S. Environmental risk factors for allergy and socioeconomic status in a birth cohort (BAMSE). Pediatr Allergy Immunol 2002;13:18287.[CrossRef][ISI][Medline]
12 Glezen PW. Antecedents of chronic and recurrent lung disease: childhood respiratory trouble. Am Rev Respir Dis 1989;140:87374.[ISI][Medline]
13 Demissie K, Enrst P, Hanley JA, Locher U, Menzies D, Becklake MR. Socioeconomic status and lung function among primary school children in Canada. Am J Respir Crit Care Med 1996;153:71923.[Abstract]
14 McDonnell WF, Seal E Jr. Relationships between lung function and physical characteristics in young adult black and white males and females. Eur Respir J 1991;4:27989.[Abstract]
15 Anderson NB, Armstead CA. Toward understanding the association of socioeconomic status and health: a new challenge for the biopsychosocial approach. Psychosom Med 1995;57:21325.[Abstract]
16 Hart CL, Hole DJ, Gillis CR, Davey Smith G, Watt GC, Hawthorne VM. Social class differences in lung cancer mortality: risk factor explanations using two Scottish cohort studies. Int J Epidemiol 2001;30:26874.
17 Friedman GD, Cutter GR, Donahue RP et al. CARDIA: study design, recruitment, and some characteristics of the examined subjects. J Clin Epidemiol 1988;41:110516.[ISI][Medline]
18 Berkman LF, Macintyre S. The measurement of social class in health studies: old measures and new formulations. In: Kogevinas M, Pearce N, Susser M, Boffetta P (eds). Social Inequalities in Cancer. Lyon: International Agency for Research on Cancer, 1997, pp. 5164.
19 Prescott E, Lange P, Vestbo J, Group CCHS. Socioeconomic status, lung function and admission to hospital for COPD: results from the Copenhagen City Heart Study. Eur Respir J 1999;13:110914.
20 SAS/STAT Software: Changes and Enhancements Through Release 6.12. Cary, NC: SAS Institute Inc., 1997.
21 Weinfurt KP. Repeated measures analyses: ANOVA, MANOVA, and HLM. In: Grimm LG, Yarnold PR (eds). Reading and Understanding more Multivariate Statistics. Washington DC: American Psychological Association, 2000, pp. 31763.
22 Corey M, Edwards L, Levinson H, Knowles M. Longitudinal analysis of pulmonary function decline in patients with cystic fibrosis. J Pediatr 1997;131:80914.[ISI][Medline]
23 Jacobs DR Jr, Nelson ET, Dontas AS, Keller J, Slattery ML, Higgins M. Are race and sex differences in lung function explained by frame size? Am Rev Respir Dis 1992;146:64449.[ISI][Medline]
24 Kessler R, Neighbors H. A new perspective on the relationships among race, social class, and psychological distress. J Health Soc Behav 1986;27:10715.[ISI][Medline]
25 Williams D. Race/ethnicity and socioeconomic status: measurement and methodological issues. Int J Health Serv 1996;26:483505.[ISI][Medline]
26 Williams D, Lavizzo-Mourey R, Warren R. The concept of race and health status in America. Public Health Rep 1994;109:2641.[ISI][Medline]
27 Robbins D, Enright P, Sherrill D. Lung function development in young adults: is there a plateu phase? Eur Respir J 1995;8:76872.
28 Volmer T. The socio-economics of asthma. Pulm Pharmacol Ther 2001;14:5560.[CrossRef][ISI][Medline]
29 Chen E, Matthews KA, Boyce WT. Socioeconomic differences in children's health: how and why do these relationships change with age? Psychol Bull 2002;128:295329.[CrossRef][ISI][Medline]
30 Faber D, Krieg E. Unequal exposure to ecological hazards: environmental injustices in the Commonwealth of Massachusetts. Environ Health Perspect 2002;110(Suppl.2):27788.
31 Triche E, Belanger K, Beckett W et al. Infant respiratory symptoms associated with indoor heating sources. Am J Respir Crit Care Med 2002;166:110511.
32 Wright RJ, Steinbach SF. Violence: an unrecognized environmental exposure that may contribute to greater asthma morbidity in high risk inner-city populations. Environ Health Perspect 2001;109: 108589.[ISI][Medline]
33 Gauderman WJ, Gilliland GF, Vora H et al. Association between air pollution and lung function growth in Southern California children: results from a second cohort. Am J Respir Crit Care Med 2002;166:7684.
34 Wright RJ, Rodriguez M, Cohen S. Review of psychosocial stress and asthma: an integrated biopsychosocial approach. Thorax 1998;53:106674.
35 Kiecolt-Glaser JK, McGuire L, Robles TF, Glaser R. Emotions, morbidity, and mortality: new perspectives from psychoneuroimmunology. Annu Rev Psychol 2002;53:83107.[CrossRef][ISI][Medline]
36 Kubzansky LD, Wright RJ, Cohen S, Weiss S, Rosner B, Sparrow D. Breathing easy: a prospective study of optimism and pulmonary function in the Normative Aging Study. Ann Behav Med 2002;24:34553.[CrossRef][ISI][Medline]
37 McKeever T, Scrivener S, Broadfield E, Jones Z, Britton J, Lewis S. Prospective study of diet and decline in lung function in a general population. Am J Respir Crit Care Med 2002;165:1299303.