Association of low income with pulmonary disease progression in smokers with and without chronic obstructive pulmonary disease

Discussion

Individuals with an annual income at or below the US minimum wage level had significantly greater impacts of smoking-related disease. Although the low-income group had less emphysema at baseline, they showed greater disease progression over 5 years in FEV₁ and airway wall thickness. Current smoking was a clear factor predicting disease progression, but the effect of low income on disease progression remained after adjusting for current smoking. The adjusted difference in FEV₁ between the low and higher income groups was 37 mL greater loss in the low-income group. This is a similar magnitude of effect to the adjusted impact of current smoking on FEV₁ at 51 mL loss. These results suggest that low income is important and that factors other than continued smoking are involved in the relationship between low income and disease.

At baseline, low-income subjects had worse quality of life, worse dyspnoea, more chronic bronchitis and a shorter 6MWD, although smoking pack-years were not significantly different. Both current smoking and respiratory exacerbations requiring an emergency room visit or hospitalisation occurred twice as often in the low-income group relative to subjects reporting higher income. Our low-income group was similar in the distribution of disease severity to the higher-income subjects, but had more respiratory symptoms and had greater impairment in 6MWD, despite being significantly younger.

Factors that we considered to explain these results include that our low-income group reported less education, potentially impeding understanding of smoking risks; were less likely to have health insurance; and less likely to get preventative care from a doctor or clinic. In addition, they were more likely to have skipped medical visits or medications due to costs. Although they did report more respiratory exposures, the effect of those exposures on disease progression was not significant after adjusting for other factors. In addition, increased exposure to air pollution may play a role, but we do not have data available to assess that. Higher rates of respiratory medication use in the low-income group may be due to greater symptoms, or it may be the result of inadequate preventive and primary care.

Key social factors associated with low income and SES previously suggested to play a role in worse health include smoking, education, healthcare/insurance and unhealthy living conditions [17]. Smoking is much more prevalent in lower-income individuals [18] and Chetty et al. [1] found local geographic variation in mortality that was associated with smoking behaviour. In the Chetty et al. study, regional increased mortality linked to smoking behaviour was associated with heart disease and cancer, rather than increases in accidents, suicide or homicide. Others have identified associations between low SES and reduced lung function [6], increased hospitalisations [10] and increased mortality from respiratory disease [19]. In a systematic review, Gershon et al. [7] identified consistently negative effects of low SES on COPD symptoms, morbidity and mortality. In that meta-analysis, measures of SES included income, education and occupation. They found that individuals of the lowest SES were twice as likely to have poor outcomes as the higher-income group. Comparing studies across multiple diseases, they found that the negative impact of SES was greatest in COPD relative to diabetes, heart disease, stroke and cancer. Our findings are consistent with these published results and add detail about access to care and impact of low income on decision-making to seek care and comply with treatment.

Our low-income group had a greater proportion of African Americans, but we did not find worse disease at baseline or greater progression in these subjects; in fact, we found less after adjusting for income. The role of race in COPD risk and progression remains unclear, potentially because of the complexities of SES and genetic factors that may influence risk of disease. Eisner et al. [6] in a study of insured health maintenance organisation subjects found that African Americans were not at increased risk of greater COPD severity after adjusting for demographics and physical characteristics. Our population varied in insurance status, but our results suggest that economics rather than race were the major factors predicting progression. African American subjects who experience exacerbations have worse quality of life than non-Hispanic white subjects with exacerbations [20], and they appear to have increased susceptibility to developing disease after smoking exposure [3], yet early work from the COPDGene study showed that African Americans had less emphysema than non-Hispanic white subjects adjusting for smoking pack-years, age and current smoking [4].

Education may influence decisions to continue smoking as well as interactions with the medical profession and compliance with treatment. A Norwegian study showed an association of lower educational level with greater emphysema but not airway wall thickness in COPD patients within a racially homogenous, rural population [21]. A previous COPDGene study relating parental COPD to risk of disease found that race was not significant, but education was an independent predictor of COPD [22]. Persistent smoking is associated with both lower income levels and lower educational attainments [18, 23]. Overall, the complex interplay of income, education, comorbidities and other factors increase the difficulty of defining solutions to continued smoking. The prominent role of continued smoking in low-income individuals suggests that strategies to improve outcomes must be linked to smoking cessation programmes. Smoking cessation programmes should be targeted to the needs and issues of low-income smokers.

Strengths of this study include the large cohort size, geographic diversity of the 21 clinical centres, extensive longitudinal clinical and radiographic data and the enhanced enrolment of African Americans. Limitations to generalisability include a US population that has unique and incomplete insurance coverage. Additionally, income level was documented at the phase 2 visit, not the initial visit when all of the other baseline variables were evaluated. While metrics of SES such as income and education have some stability over time [24], reverse causality cannot be excluded in this analysis. Those with faster disease progression may have been forced to retire, subsequently reducing their income from baseline to the reported level at the phase 2 visit. If they fell into the lowest category, this would bias the estimate of the difference between the low-income and the high-income group away from the null (overestimating the effect). However, the mean social security payment in the US is ∼USD 16 000 per year and retirement will not necessarily result in a drop into the lowest income category.

The information on income, education, comorbid disease, medication use and symptoms are all self-reported. Although verification of income and education would be ideal, it is uncommon to have that type of validation. Since subjects were offered the option to decline to answer these questions, we assume that responses are reflective of their social and economic situation. Although the lower comorbidity score in the low-income group may be accurate (possibly due to the lower average age), there may also be an ascertainment bias in that these subjects have reduced access to primary preventative care and may not have had an opportunity for physician diagnosis of asymptomatic conditions such as hypertension and high cholesterol. Additionally, while we have data on which medications subjects are prescribed, we do not have information on adherence, though our data on accommodations to healthcare costs suggest that low-income subjects may have lower adherence (more likely to not fill prescriptions, more likely to stretch out a prescription). Lower adherence rates may influence exacerbation rates and disease progression.

We chose to study the relationship of low income to a breadth of smokers both with and without spirometric COPD. Smoking impacts on the lung including emphysema, gas trapping and airway wall thickening are identified in smokers without obstruction [25]. We used CT metrics, reported symptoms and spirometry to provide a comprehensive analysis of baseline disease and progression.

The economic burden of smoking-related lung disease and COPD in the United States is sizeable, estimated to be USD 38.8 billion in 2005 [26]. As the third leading cause of death in the United States, there is value in improving outcomes of care for COPD. Worldwide, smoking and other respiratory exposures are common, and COPD is the fourth leading cause of death. Poverty and inadequate education are key issues to consider in order to reduce the burden of respiratory disease. Beyond smoking cessation, we identified a range of factors that could be addressed, including access to primary care and preventive care, access to health insurance and better information about health conditions. Although this study is based on data from the United States, similar associations of low SES to worse COPD have been identified in European cohorts, as well as around the world [7, 10, 21, 27]. Recognising and addressing the role of poverty in increased burden of disease, worse outcomes and more rapid disease progression represents an important strategy for all societies.