Personal exposure to household air pollution and lung function in rural Bangladesh: A population-based cross-sectional study.

We assessed whether personal exposure to household air pollution [PM2.5 and black carbon (BC)] is associated with lung functions (FEV1, FVC, and their ratio) in non-smoking adults in rural Bangladesh. We measured personal exposure to PM2.5 using gravimetric analysis of PM2.5 mass and BC by reflectance measurement between April 2016 and June 2019. The average 24-hour PM2.5 and BC concentration was 141.0µgm-3 and 13.8µgm-3 for females, and 91.7 µgm-3 and 10.1 µgm-3 for males, respectively. A 1 µgm-3 increase in PM2.5 resulted in a 0.02 ml reduction in FEV1, 0.43 ml reduction in FVC, and 0.004% reduction in FEV1/FVC. We also found a similar inverse relationship between BC and lung functions (9.6 ml decrease in FEV1 and 18.5 ml decrease in FVC per 1µgm-3 increase in BC). A higher proportion of non-smoking biomass fuel users (50.1% of the females and 46.7% of the males) had restrictive patterns of lung function abnormalities, which need further exploration.

Association of household air pollution with cellular and humoral immune responses among women in rural Bangladesh.

Household air pollution (HAP) arising from combustion of biomass fuel (BMF) is a leading cause of morbidity and mortality in low-income countries. Air pollution may stimulate pro-inflammatory responses by activating diverse immune cells and cyto/chemokine expression, thereby contributing to diseases. We aimed to study cellular immune responses among women chronically exposed to HAP through use of BMF for domestic cooking. Among 200 healthy, non-smoking women in rural Bangladesh, we assessed exposure to HAP by measuring particulate matter 2.5 (PM2.5), black carbon (BC) and carbon monoxide (CO), through use of personal monitors RTI MicroPEM™ and Lascar CO logger respectively, for 48 h. Blood samples were collected following HAP exposure assessment and were analyzed for immunoprofiling by flow cytometry, plasma IgE by immunoassay analyzer and cyto/chemokine response from monocyte-derived-macrophages (MDM) and -dendritic cells (MDDC) by multiplex immunoassay. In multivariate linear regression model, a doubling of PM2.5 was associated with small increments in immature/early B cells (CD19+CD38+) and plasmablasts (CD19+CD38+CD27+). In contrast, a doubling of CO was associated with 1.20% reduction in CD19+ B lymphocytes (95% confidence interval (CI) = -2.36, -0.01). A doubling of PM2.5 and BC each was associated with 3.12% (95%CI = -5.85, -0.38) and 4.07% (95%CI = -7.96, -0.17) decrements in memory B cells (CD19+CD27+), respectively. Exposure to CO was associated with increased plasma IgE levels (beta(ß) = 240.4, 95%CI = 3.06, 477.8). PM2.5 and CO exposure was associated with increased MDM production of CXCL10 (ß = 12287, 95%CI = 1038, 23536) and CCL5 (ß = 835.7, 95%CI = 95.5, 1576), respectively. Conversely, BC exposure was associated with reduction in MDDC-produced CCL5 (ß = -3583, 95%CI = -6358, -807.8) and TNF-α (ß = -15521, 95%CI = -28968, -2074). Our findings suggest that chronic HAP exposure through BMF use adversely affects proportions of B lymphocytes, particularly memory B cells, plasma IgE levels and functions of antigen presenting cells in rural women.

Previous tuberculosis disease as a risk factor for chronic obstructive pulmonary disease: a cross-sectional analysis of multicountry, population-based studies.

BACKGROUND: Risk factors for COPD in high-income settings are well understood; however, less attention has been paid to contributors of COPD in low-income and middle-income countries (LMICs) such as pulmonary tuberculosis. We sought to study the association between previous tuberculosis disease and COPD by using pooled population-based cross-sectional data in 13 geographically diverse, low-resource settings. METHODS: We pooled six cohorts in 13 different LMIC settings, 6 countries and 3 continents to study the relationship between self-reported previous tuberculosis disease and lung function outcomes including COPD (defined as a postbronchodilator forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) below the lower limit of normal). Multivariable regressions with random effects were used to examine the association between previous tuberculosis disease and lung function outcomes. RESULTS: We analysed data for 12 396 participants (median age 54.0 years, 51.5% male); 332 (2.7%) of the participants had previous tuberculosis disease. Overall prevalence of COPD was 8.8% (range 1.7%-15.5% across sites). COPD was four times more common among those with previous tuberculosis disease (25.7% vs 8.3% without previous tuberculosis disease, p<0.001). The adjusted odds of having COPD was 3.78 times higher (95% CI 2.87 to 4.98) for participants with previous tuberculosis disease than those without a history of tuberculosis disease. The attributable fraction of COPD due to previous tuberculosis disease in the study sample was 6.9% (95% CI 4.8% to 9.6%). Participants with previous tuberculosis disease also had lower prebronchodilator Z-scores for FEV1 (-0.70, 95% CI -0.84 to -0.55), FVC (-0.44, 95% CI -0.59 to -0.29) and the FEV1:FVC ratio (-0.63, 95% CI -0.76 to -0.51) when compared with those without previous tuberculosis disease. CONCLUSIONS: Previous tuberculosis disease is a significant and under-recognised risk factor for COPD and poor lung function in LMICs. Better tuberculosis control will also likely reduce the global burden of COPD.

Exposure to household air pollutants and endothelial dysfunction in rural Bangladesh: A cross-sectional study.

More than one third of world's population use biomass fuel for cooking that has been linked to an array of adverse health hazards including cardiovascular mortality and morbidity. As part of Bangladesh Global Environmental and Occupational Health (GEO Health) project, we assessed whether household air pollution (HAP) was associated with dysfunction in microvascular circulation (measured by reactive hyperemia index [RHI]). METHODS: We measured exposure to HAP (particulate matter [PM2.5], carbon monoxide [CO], and black carbon [BC]) for 48 hours of 200 healthy nonsmoker adult females who used biomass fuel for cooking. Exposure to PM2.5 and BC were measured using personal monitor, RTI MicroPEM (RTI International, NC) with an internal filter that had been both pre- and post-weighed to capture the deposited pollutants concentration. Lascar CO logger was used to measure CO. Endothelial function was measured by forearm blood flow dilatation response to brachial artery occlusion using RHI based on peripheral artery tonometry. A low RHI score (<1.67) indicates impaired endothelial function. RESULTS: Average 48 hours personal exposure to PM2.5 and BC were 144.15 µg/m3 (SD 61.26) and 6.35 µg/m3 (SD 2.18), respectively. Interquartile range for CO was 0.73 ppm (0.62-1.35 ppm). Mean logarithm of RHI (LnRHI) was 0.57 in current data. No statistically significant association was observed for LnRHI with PM2.5 (odds ratio [OR] = 0.97; 95% confidence interval [CI] = 0.92, 1.01; P = 0.16), BC (OR = 0.85; 95% CI = 0.72, 1.01; P = 0.07), and CO (OR = 0.89; 95% CI = 0.64, 1.25; P = 0.53) after adjusting for potential covariates. CONCLUSIONS: In conclusion, HAP was not associated with endothelial dysfunction among nonsmoking females in rural Bangladesh who used biomass fuel for cooking for years.

Lack of an Association Between Household Air Pollution Exposure and Previous Pulmonary Tuberculosis.

CONTEXT: Observational studies investigating household air pollution (HAP) exposure to biomass fuel smoke as a risk factor for pulmonary tuberculosis have reported inconsistent results. OBJECTIVE: To evaluate the association between HAP exposure and the prevalence of self-reported previous pulmonary tuberculosis. DESIGN: We analyzed pooled data including 12,592 individuals from five population-based studies conducted in Latin America, East Africa, and Southeast Asia from 2010 to 2015. We used multivariable logistic regression to model the association between HAP exposure and self-reported previous pulmonary tuberculosis adjusted for age, sex, tobacco smoking, body mass index, secondary education, site and country of residence. RESULTS: Mean age was 54.6 years (range of mean age across settings 43.8-59.6 years) and 48.6% were women (range of % women 38.3-54.5%). The proportion of participants reporting HAP exposure was 38.8% (range in % HAP exposure 0.48-99.4%). Prevalence of previous pulmonary tuberculosis was 2.7% (range of prevalence 0.6-6.9%). While participants with previous pulmonary tuberculosis had a lower pre-bronchodilator FEV1 (mean - 0.7 SDs, 95% CI - 0.92 to - 0.57), FVC (- 0.52 SDs, 95% CI - 0.69 to - 0.33) and FEV1/FVC (- 0.59 SDs, 95% CI - 0.76 to - 0.43) as compared to those who did not, we did not find an association between HAP exposure and previous pulmonary tuberculosis (adjusted odds ratio = 0.86; 95% CI 0.56-1.32). CONCLUSIONS: There was no association between HAP exposure and self-reported previous pulmonary tuberculosis in five population-based studies conducted worldwide.

Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Low Body Mass Index Is Associated with Higher Odds of COPD and Lower Lung Function in Low- and Middle-Income Countries.

The relationship of body mass index (BMI) with lung function and COPD has been previously described in several high-income settings. However, few studies have examined this relationship in resource-limited settings where being underweight is more common. We evaluated the association between BMI and lung function outcomes across 14 diverse low- and middle-income countries. We included data from 12,396 participants aged 35-95 years and used multivariable regressions to assess the relationship between BMI with either COPD and lung function while adjusting for known risk factors. An inflection point was observed at a BMI of 19.8 kg/m2. Participants with BMI < 19.8 kg/m2 had a 2.28 greater odds (95% CI 1.83-2.86) of having COPD and had a 0.21 (0.13-0.30) lower FEV1 and 0.34 (0.27-0.41) lower FEV1/FVC z-score compared to those with BMI ≥ 19.8 kg/m2. The association with lung function remained even after excluding participants with COPD. Individuals with lower BMI were more likely to have COPD and had lower lung function compared to those in higher BMI. The association with lung function remained positive even after excluding participants with COPD, suggesting that being underweight may also play a role in having worse lung function.

Protein-coding variants implicate novel genes related to lipid homeostasis contributing to body-fat distribution.

Body-fat distribution is a risk factor for adverse cardiovascular health consequences. We analyzed the association of body-fat distribution, assessed by waist-to-hip ratio adjusted for body mass index, with 228,985 predicted coding and splice site variants available on exome arrays in up to 344,369 individuals from five major ancestries (discovery) and 132,177 European-ancestry individuals (validation). We identified 15 common (minor allele frequency, MAF ≥5%) and nine low-frequency or rare (MAF <5%) coding novel variants. Pathway/gene set enrichment analyses identified lipid particle, adiponectin, abnormal white adipose tissue physiology and bone development and morphology as important contributors to fat distribution, while cross-trait associations highlight cardiometabolic traits. In functional follow-up analyses, specifically in Drosophila RNAi-knockdowns, we observed a significant increase in the total body triglyceride levels for two genes (DNAH10 and PLXND1). We implicate novel genes in fat distribution, stressing the importance of interrogating low-frequency and protein-coding variants.

Epidemiology and risk factors of asthma-chronic obstructive pulmonary disease overlap in low- and middle-income countries.

BACKGROUND: Asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) represents the confluence of bronchial airway hyperreactivity and chronic airflow limitation and has been described as leading to worse lung function and quality of life than found with either singular disease process. OBJECTIVE: We aimed to describe the prevalence and risk factors for ACO among adults across 6 low- and middle-income countries (LMICs). METHODS: We compiled cross-sectional data for 11,923 participants aged 35 to 92 years from 4 population-based studies in 12 settings. We defined COPD as postbronchodilator FEV1/forced vital capacity ratio below the lower limit of normal, asthma as wheeze or medication use in 12 months or self-reported physician diagnosis, and ACO as having both. RESULTS: The prevalence of ACO was 3.8% (0% in rural Puno, Peru, to 7.8% in Matlab, Bangladesh). The odds of having ACO were higher with household exposure to biomass fuel smoke (odds ratio [OR], 1.48; 95% CI, 0.98-2.23), smoking tobacco (OR, 1.28 per 10 pack-years; 95% CI, 1.22-1.34), and having primary or less education (OR, 1.35; 95% CI, 1.07-1.70) as compared to nonobstructed nonasthma individuals. ACO was associated with severe obstruction (FEV1 %, <50; 31.6% of ACO vs 10.9% of COPD alone) and severe spirometric deficits compared with participants with asthma (-1.61 z scores FEV1; 95% CI, -1.48 to -1.75) or COPD alone (-0.94 z scores; 95% CI, -0.78 to -1.10). CONCLUSIONS: ACO may be as prevalent and more severe in LMICs than has been reported in high-income settings. Exposure to biomass fuel smoke may be an overlooked risk factor, and we favor diagnostic criteria for ACO that include environmental exposures common to LMICs.

Determinants of Uncontrolled Hypertension in Rural Communities in South Asia-Bangladesh, Pakistan, and Sri Lanka.

BACKGROUND: Uncontrolled blood pressure (BP) is a leading risk factor for death and disability in South Asia. We aimed to determine the cross-country variation, and the factors associated with uncontrolled BP among adults treated for hypertension in rural South Asia. METHODS: We enrolled 1,718 individuals aged ≥40 years treated for hypertension in a cross-sectional study from rural communities in Bangladesh, Pakistan, and Sri Lanka. Multivariable logistic regression model was used to determine the factors associated with uncontrolled BP (systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg). RESULTS: Among hypertensive individuals, 58.0% (95% confidence interval (CI) 55.7, 60.4) had uncontrolled BP: 52.8% (49.0, 56.6) in Bangladesh, 70.6% (65.7, 75.1) in Pakistan, and 56.5% (52.7, 60.1) in Sri Lanka. The odds (odds ratio (95% CI)) of uncontrolled BP were significantly higher in individuals with lower wealth index (1.17 (1.02, 1.35)); single vs. married (1.46 (1.10, 1.93)); higher log urine albumin-to-creatinine ratio (1.41 (1.24, 1.60)); lower estimated glomerular filtration rate (1.23 (1.01, 1.49)); low vs. high adherence to antihypertensive medication (1.50 (1.16, 1.94)); and Pakistan (2.91 (1.60, 5.28)) vs. Sri Lanka. However, the odds were lower in those with vs. without self-reported kidney disease (0.51 (0.28, 0.91)); and receiving vs. not receiving statins (0.62 (0.44, 0.87)). CONCLUSIONS: The majority of individuals with treated hypertension have uncontrolled BP in rural Bangladesh, Pakistan, and Sri Lanka with significant disparities among and within countries. Urgent public health efforts are needed to improve access and adherence to antihypertensive medications in disadvantaged populations in rural South Asia.

Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

In the published version of this paper, the name of author Emanuele Di Angelantonio was misspelled. This error has now been corrected in the HTML and PDF versions of the article.

Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

In the version of this article originally published, one of the two authors with the name Wei Zhao was omitted from the author list and the affiliations for both authors were assigned to the single Wei Zhao in the author list. In addition, the ORCID for Wei Zhao (Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA) was incorrectly assigned to author Wei Zhou. The errors have been corrected in the HTML and PDF versions of the article.

Association between Household Air Pollution Exposure and Chronic Obstructive Pulmonary Disease Outcomes in 13 Low- and Middle-Income Country Settings.

RATIONALE: Forty percent of households worldwide burn biomass fuels for energy, which may be the most important contributor to household air pollution. OBJECTIVES: To examine the association between household air pollution exposure and chronic obstructive pulmonary disease (COPD) outcomes in 13 resource-poor settings. METHODS: We analyzed data from 12,396 adult participants living in 13 resource-poor, population-based settings. Household air pollution exposure was defined as using biomass materials as the primary fuel source in the home. We used multivariable regressions to assess the relationship between household air pollution exposure and COPD outcomes, evaluated for interactions, and conducted sensitivity analyses to test the robustness of our findings. MEASUREMENTS AND MAIN RESULTS: Average age was 54.9 years (44.2-59.6 yr across settings), 48.5% were women (38.3-54.5%), prevalence of household air pollution exposure was 38% (0.5-99.6%), and 8.8% (1.7-15.5%) had COPD. Participants with household air pollution exposure were 41% more likely to have COPD (adjusted odds ratio, 1.41; 95% confidence interval, 1.18-1.68) than those without the exposure, and 13.5% (6.4-20.6%) of COPD prevalence may be caused by household air pollution exposure, compared with 12.4% caused by cigarette smoking. The association between household air pollution exposure and COPD was stronger in women (1.70; 1.24-2.32) than in men (1.21; 0.92-1.58). CONCLUSIONS: Household air pollution exposure was associated with a higher prevalence of COPD, particularly among women, and it is likely a leading population-attributable risk factor for COPD in resource-poor settings.

Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

Genome-wide association studies (GWAS) have identified >250 loci for body mass index (BMI), implicating pathways related to neuronal biology. Most GWAS loci represent clusters of common, noncoding variants from which pinpointing causal genes remains challenging. Here we combined data from 718,734 individuals to discover rare and low-frequency (minor allele frequency (MAF) < 5%) coding variants associated with BMI. We identified 14 coding variants in 13 genes, of which 8 variants were in genes (ZBTB7B, ACHE, RAPGEF3, RAB21, ZFHX3, ENTPD6, ZFR2 and ZNF169) newly implicated in human obesity, 2 variants were in genes (MC4R and KSR2) previously observed to be mutated in extreme obesity and 2 variants were in GIPR. The effect sizes of rare variants are ~10 times larger than those of common variants, with the largest effect observed in carriers of an MC4R mutation introducing a stop codon (p.Tyr35Ter, MAF = 0.01%), who weighed ~7 kg more than non-carriers. Pathway analyses based on the variants associated with BMI confirm enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically supported therapeutic targets in obesity.

Exome-wide association study of plasma lipids in >300,000 individuals.

We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated with total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG). At two loci (JAK2 and A1CF), experimental analysis in mice showed lipid changes consistent with the human data. We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and (iv) TG-lowering alleles involved in hepatic production of TG-rich lipoproteins (TM6SF2 and PNPLA3) tracked with higher liver fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat but decreased risks for both T2D and CAD.

Socioeconomic patterning of chronic conditions and behavioral risk factors in rural South Asia: a multi-site cross-sectional study.

OBJECTIVES: Our aim was to examine relationships between markers of socioeconomic status and chronic disease risks in rural South Asia to understand the etiology of chronic diseases in the region and identify high-risk populations. METHODS: We examined data from 2271 adults in Chennai, Goa and Matlab sites of the Chronic Disease Risk Factor study in South Asia. We report age-sex adjusted odds ratios for risk factors (tobacco, alcohol, fruit-vegetable use and physical activity) and common chronic conditions (hypertension, diabetes, overweight, depression, impaired lung and vision) by education, occupation and wealth. RESULTS: Respondents with greater wealth and in non-manual professions were more likely to be overweight [OR = 2.48 (95% CI 1.8,3.38)] and have diabetes [OR = 1.88 (95% CI 1.02,3.5)]. Wealth and education were associated with higher fruit and vegetable [OR = 1.89 (95% CI 1.48,2.4)] consumption but lower physical activity [OR = 0.52 (95% CI 0.39,0.69)]. Non-manual workers reported lower tobacco and alcohol use, while wealthier respondents reported better vision and lung function. CONCLUSIONS: Ongoing monitoring of inequalities in chronic disease risks is needed for planning and evaluating interventions to address the growing burden of chronic conditions.

Drinking Water Salinity and Raised Blood Pressure: Evidence from a Cohort Study in Coastal Bangladesh.

BACKGROUND: Millions of coastal inhabitants in Southeast Asia have been experiencing increasing sodium concentrations in their drinking-water sources, likely partially due to climate change. High (dietary) sodium intake has convincingly been proven to increase risk of hypertension; it remains unknown, however, whether consumption of sodium in drinking water could have similar effects on health. OBJECTIVES: We present the results of a cohort study in which we assessed the effects of drinking-water sodium (DWS) on blood pressure (BP) in coastal populations in Bangladesh. METHODS: DWS, BP, and information on personal, lifestyle, and environmental factors were collected from 581 participants. We used generalized linear latent and mixed methods to model the effects of DWS on BP and assessed the associations between changes in DWS and BP when participants experienced changing sodium levels in water, switched from "conventional" ponds or tube wells to alternatives [managed aquifer recharge (MAR) and rainwater harvesting] that aimed to reduce sodium levels, or experienced a combination of these changes. RESULTS: DWS concentrations were highly associated with BP after adjustments for confounding factors. Furthermore, for each 100 mg/L reduction in sodium in drinking water, systolic/diastolic BP was lower on average by 0.95/0.57 mmHg, and odds of hypertension were lower by 14%. However, MAR did not consistently lower sodium levels. CONCLUSIONS: DWS is an important source of daily sodium intake in salinity-affected areas and is a risk factor for hypertension. Considering the likely increasing trend in coastal salinity, prompt action is required. Because MAR showed variable effects, alternative technologies for providing reliable, safe, low-sodium fresh water should be developed alongside improvements in MAR and evaluated in "real-life" salinity-affected settings. https://doi.org/10.1289/EHP659.

Rare and low-frequency coding variants alter human adult height.

Height is a highly heritable, classic polygenic trait with approximately 700 common associated variants identified through genome-wide association studies so far. Here, we report 83 height-associated coding variants with lower minor-allele frequencies (in the range of 0.1-4.8%) and effects of up to 2 centimetres per allele (such as those in IHH, STC2, AR and CRISPLD2), greater than ten times the average effect of common variants. In functional follow-up studies, rare height-increasing alleles of STC2 (giving an increase of 1-2 centimetres per allele) compromised proteolytic inhibition of PAPP-A and increased cleavage of IGFBP-4 in vitro, resulting in higher bioavailability of insulin-like growth factors. These 83 height-associated variants overlap genes that are mutated in monogenic growth disorders and highlight new biological candidates (such as ADAMTS3, IL11RA and NOX4) and pathways (such as proteoglycan and glycosaminoglycan synthesis) involved in growth. Our results demonstrate that sufficiently large sample sizes can uncover rare and low-frequency variants of moderate-to-large effect associated with polygenic human phenotypes, and that these variants implicate relevant genes and pathways.

Socioeconomic status and COPD among low- and middle-income countries.

BACKGROUND: Socioeconomic status (SES) is a strong social determinant of health. There remains a limited understanding of the association between SES and COPD prevalence among low- and middle-income countries where the majority of COPD-related morbidity and mortality occurs. We examined the association between SES and COPD prevalence using data collected in Argentina, Bangladesh, Chile, Peru, and Uruguay. METHODS: We compiled lung function, demographic, and SES data from three population-based studies for 11,042 participants aged 35-95 years. We used multivariable alternating logistic regressions to study the association between COPD prevalence and SES indicators adjusted for age, sex, self-reported daily smoking, and biomass fuel smoke exposure. Principal component analysis was performed on monthly household income, household size, and education to create a composite SES index. RESULTS: Overall COPD prevalence was 9.2%, ranging from 1.7% to 15.4% across sites. The adjusted odds ratio of having COPD was lower for people who completed secondary school (odds ratio [OR] =0.73, 95% CI 0.55-0.98) and lower with higher monthly household income (OR =0.96 per category, 95% CI 0.93-0.99). When combining SES factors into a composite index, we found that the odds of having COPD was greater with lower SES (interquartile OR =1.23, 95% CI 1.05-1.43) even after controlling for subject-specific factors and environmental exposures. CONCLUSION: In this analysis of multiple population-based studies, lower education, lower household income, and lower composite SES index were associated with COPD. Since household income may be underestimated in population studies, adding household size and education into a composite index may provide a better surrogate for SES.