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<?xml version="1.0" ?> <tei> <teiHeader> <fileDesc xml:id="0"/> </teiHeader> <text xml:lang="en"> <p>A NEMIA is a common condition in the elderly<lb/> population and is associated with increased mortality<lb/> <ref type="biblio">(1–3)</ref>. Anemia is more common among non-Hispanic blacks<lb/> <ref type="biblio">(4,5)</ref>, with the National Health and Nutrition Examination<lb/> Survey (NHANES) <ref type="biblio">(4)</ref> showing a threefold greater anemia<lb/> prevalence among blacks as compared to non-Hispanic<lb/> whites. This ethnic/racial difference has also been reported in<lb/> younger adults with lower hemoglobin concentrations (Hb)<lb/> than whites even after considering disease status, behavioral<lb/> risk factors, nutritional intake, and iron status <ref type="biblio" >(6,7)</ref>. These<lb/> results have led to (a) speculation that blacks may have<lb/> a lower set point for Hb than whites <ref type="biblio">(8)</ref> and (b) uncertainty as<lb/> to whether the presence of anemia or lower Hb has adverse<lb/> clinical consequences in blacks similar to those in whites<lb/> <ref type="biblio">(9,10)</ref>. To address this issue, we examined the relationships<lb/> of anemia status and Hb level threshold to all-cause mortality<lb/> in a biracial population of older blacks and whites.<lb/></p> <head>METHODS<lb/></head> <head>Design and Participants<lb/></head> <p>The Chicago Health and Aging Project (CHAP) study<lb/> aims to identify risk factors for Alzheimer's disease. It is<lb/> a prospective, epidemiological study of a geographically<lb/> defined, urban biracial community population in three<lb/> adjacent south side neighborhoods in Chicago: Morgan<lb/> Park, Washington Heights, and Beverly with a reasonable<lb/> distribution of socioeconomic characteristics within each<lb/> ethnic/racial group. More details of the study design have<lb/> been previously published <ref type="biblio">(11,12)</ref>.<lb/></p> <p>Of the 7813 age-eligible residents identified through<lb/> census of the community areas, 6158 (78.9%) were enrolled<lb/> for the baseline population interview. Original data collec-<lb/>tion started in 1993, and data collection occurred in cycles,<lb/> each lasting 3 years, with each cycle ending as the suc-<lb/>ceeding cycle began. As of the third cycle in 2000, CHAP<lb/> began enrolling community residents who had turned 65<lb/> since the inception of the study. CHAP participants were<lb/> randomly selected at each cycle and stratified by age, sex,<lb/> race, and global cognitive function, to undergo a detailed<lb/> clinical evaluation. Details of the stratified randomization<lb/> process have been previously published <ref type="biblio">(11)</ref>. The randomly<lb/> selected participants form the basis of the present study (n ¼<lb/> 1806). Interviews and physical examinations were con-<lb/>ducted with standardized instruments that assess health<lb/> history, physical and cognitive function, and serological<lb/> evaluations of all 1806 participants. Written informed<lb/> consent was obtained, and the study was approved by the<lb/> Institutional Review Board at Rush University Medical<lb/> Center.<lb/></p> <head>Data<lb/></head> <p>Information on vital status was obtained from informants<lb/> at regular follow-up contact and through newspaper obit-<lb/>uaries. All deaths are further verified through matching with<lb/> the National Death Index (NDI). The last date of NDI<lb/> ascertainment was December 2003. Blood samples were<lb/> uniformly collected using sterile technique by phlebotomists<lb/> and nurses. Hb was measured from blood samples using<lb/> a Beckman-Coulter (Wood Dale, IL) LH750 automated<lb/> processor with Coulter reagents. Anemia was defined using<lb/> the World Health Organization (WHO) criteria, as an Hb ,<lb/> 13 g/dL for men or , 12 g/dL for women <ref type="biblio" >(13)</ref>.<lb/></p> <p>Demographic variables used in the analyses included age,<lb/> sex, race, education, and income. Medical conditions,<lb/> including hypertension, diabetes mellitus, stroke, cardiovas-<lb/>cular disease, hip fracture, cancer, Parkinson's disease, and<lb/> thyroid disease, were identified by self-report. Global<lb/> cognitive function was measured by averaging performance<lb/> across the Mini-Mental State Examination <ref type="biblio">(14)</ref>, East Boston<lb/> Memory Test <ref type="biblio" >(15)</ref>, and Symbol Digit Modalities Test <ref type="biblio">(16)</ref>.<lb/> Physical function was assessed using Katz Index of<lb/> Activities of Daily Living <ref type="biblio">(17)</ref>. Cigarette smoking (ever<lb/> smoked in life) and overall health status were assessed based<lb/> on a series of questions derived from the Established<lb/> Population for Epidemiological Studies of the Elderly<lb/> (EPESE) project <ref type="biblio">(18)</ref>. Depressive symptoms were measured<lb/> using a modified version of Center for the Epidemiological<lb/> Study of Depression (CESD; <ref type="biblio">19</ref>). Blood tests included mean<lb/> cell volume (MCV), serum creatinine and cholesterol.<lb/> Glomerular filtration rate (GFR) was calculated using the<lb/> Modification of Diet in Renal Disease (MDRD) equation<lb/> <ref type="biblio">(20)</ref>. Body mass index was calculated by dividing the<lb/> measured weight in kilograms by the square of the measured<lb/> height in meters.<lb/></p> <head>Analytic Approach<lb/></head> <p>Hb level was analyzed in two ways: as a dichotomous<lb/> variable of anemia versus non-anemia using the WHO<lb/> criteria and as a categorical variable of Hb groups above or<lb/> below the anemia cutoff. Cox proportional hazards models<lb/> <ref type="biblio">(21)</ref> were used to test the association between baseline Hb<lb/> and mortality during follow-up, adjusting for other covar-<lb/>iates in blacks and whites separately. All models included<lb/> age, sex, race, and global cognitive function. Hb was added<lb/> to the primary model to test the association to mortality risk.<lb/> Additional models further tested the association of Hb with<lb/> mortality after adding other potential confounders. In the<lb/> first step, income and medical conditions were added to the<lb/> original model. In the second step, physical function and<lb/> depressive symptomatology were added to the model. In our<lb/> final fully adjusted model, we also added smoking status,<lb/> body mass index, GFR, MCV, cholesterol, and self-reported<lb/> health status to our model. Biological measurements were<lb/></p> <figure type="table">Table 1. Selected Characteristics of the Study Population<lb/> Characteristic<lb/> Black N ¼ 897<lb/> White N ¼ 909<lb/> Total (N ¼ 1806)<lb/> Age, mean (SD), y<lb/> 78.9 (6.4)<lb/> 80.9 (6.6)<lb/> 79.9 (6.6)<lb/> Female gender, %<lb/> 533 (59.4)<lb/> 521 (57.3)<lb/> 1054 (58.4)<lb/> Education, mean (SD), y<lb/> 10.9 (3.5)<lb/> 13.8 (3.4)<lb/> 12.4 (3.7)<lb/> Income categories, mean (SD)<lb/> 3.9 (2.0)<lb/> 5.8 (2.6)<lb/> 5.0 (2.5)<lb/> Smoker, %<lb/> 440 (49.1)<lb/> 425 (46.8)<lb/> 865 (47.9)<lb/> Medical conditions<lb/> Coronary artery disease (%)<lb/> 75 (8.4)<lb/> 75 (8.3)<lb/> 150 (8.3)<lb/> Stroke (%)<lb/> 68 (7.6)<lb/> 76 (8.4)<lb/> 144 (7.9)<lb/> Cancer (%)<lb/> 95 (10.6)<lb/> 113 (12.4)<lb/> 208 (11.5)<lb/> Thyroid disease (%)<lb/> 27 (3.0)<lb/> 37 (4.1)<lb/> 64 (3.5)<lb/> Hypertension (%)<lb/> 503 (56.1)<lb/> 330 (36.3)<lb/> 833 (46.1)<lb/> Diabetes mellitus (%)<lb/> 160 (17.8)<lb/> 105 (11.6)<lb/> 265 (14.7)<lb/> Parkinson's disease (%)<lb/> 6 (0.7)<lb/> 9 (0.9)<lb/> 15 (0.8)<lb/> Hip fracture (%)<lb/> 23 (2.6)<lb/> 32 (3.5)<lb/> 55 (3.0)<lb/> Global Cognition, mean (SD)<lb/> À0.238 (0.792)<lb/> 0.184 (0.796)<lb/> À0.025 (0.821)<lb/> MMSE, mean (SD)<lb/> 24.7 (5.3)<lb/> 26.5 (4.7)<lb/> 25.6 (5.1)<lb/> Katz ADL disability . 1 (%)<lb/> 171 (19.1%)<lb/> 144 (15.8%)<lb/> 315 (17.4%)<lb/> CESD, mean (SD)<lb/> 1.9 (2.1)<lb/> 1.3 (1.8)<lb/> 1.6 (2.0)<lb/> Self-Reported Health Status (poor or fair) (%)<lb/> 342 (38.1%)<lb/> 171 (18.8%)<lb/> 513 (28.4%)<lb/> BMI, mean (SD), kg/m 2<lb/> 27.3 (5.7)<lb/> 25.5 (4.9)<lb/> 26.4 (5.4)<lb/> GFR, mean (SD), mL/min per 1.73 m 2<lb/> 65.9 (21.8)<lb/> 61.5 (17.4)<lb/> 63.7 (19.8)<lb/> MCV, mean (SD), fL<lb/> 87.9 (6.4)<lb/> 91.7 (5.0)<lb/> 89.8 (6.3)<lb/> Anemia: WHO criteria (%)<lb/> 350 (39.0%)<lb/> 158 (17.4%)<lb/> 508 (28.1%)<lb/> Hb, mean, g/dL (SD)<lb/> 12.6 (1.5)<lb/> 13.5 (1.5)<lb/> 13.1 (1.6)<lb/> Death, No. all-cause (%)<lb/> 248 (27.6%)<lb/> 282 (31.0%)<lb/> 530 (29%)<lb/> Time to death, mean (SD), y<lb/> 3.7 (2.8)<lb/> 4.0 (2.8)<lb/> 3.9 (2.8)<lb/> Note: SD ¼ standard deviation; ADL ¼ activities of daily living; MMSE ¼ Mini-Mental State Examination; CESD ¼ Center for Epidemiological Study of<lb/> Depression scale; BMI ¼ body mass index; GFR ¼ glomerular filtration rate; MCV ¼ mean cell volume; Hb ¼ hemoglobin concentration; WHO ¼ World Health<lb/> Organization.<lb/></figure> <p>included as continuous variables. We then tested if the<lb/> association between Hb and mortality risk varied between<lb/> blacks and whites for the whole sample by including the<lb/> interaction of race and Hb.<lb/></p> <p>All analyses were done in SAS <ref type="biblio">(22)</ref>, and the figures were<lb/> drawn in S-plus (SAS Institute Inc., Cary, NC). Model<lb/> assumptions were found to be adequately met and assessed<lb/> graphically and analytically.<lb/></p> <head>RESULTS<lb/></head> <head>Baseline Characteristics<lb/></head> <p>The mean age of the 1806 participants was 79.9 years<lb/> (standard deviation [SD] ¼ 6.6 years), with approximately<lb/> 50% blacks and 50% whites (<ref type="table">Table 1</ref>). The proportion of<lb/> participants with anemia according to WHO criteria was<lb/> 28%; 39% among blacks, and 17% among whites. The<lb/> mean (SD) Hb was 13.1 (1.6) g/dL for the entire sample.<lb/> Whites had higher mean Hb values than blacks [13.5 (1.5)<lb/> vs 12.6 (1.5) g/dL].<lb/></p> <head>Hb and Mortality<lb/></head> <p>Participants were followed for a mean of 3.9 years<lb/> (median 3.5 years). A total of 530 deaths (29%) were<lb/> recorded. In our fully adjusted model, anemia was<lb/> associated with a statistically significant 75% increased<lb/> mortality risk for blacks (HR, 1.90; 95% CI, 1.43–2.53)<lb/> (<ref type="table">Table 2</ref>) and for whites (HR, 1.85; 95% CI, 1.32–2.59). In<lb/> analyses stratified by ethnicity/race, among the group with<lb/> GFR , 60 mL/min per 1.73m 2 , increased risk of mortality<lb/> with anemia status was observed both among blacks (HR,<lb/> 1.65; 95% CI, 1.07–2.54) and among whites (HR, 2.23;<lb/> 95% CI, 1.46–3.41). Among the group with GFR ! 60 mL/<lb/> min per 1.73 m 2 , increased risk of mortality with anemia<lb/> was also observed in blacks (HR, 2.14; 95% CI, 1.46–3.13)<lb/> and in whites (HR, 1.87; 95% CI, 1.11–3.16).<lb/></p> <head>Threshold for the Relationship of Hb to Mortality by<lb/> Ethnicity/Race<lb/></head> <p>To examine the Hb threshold that minimized mortality<lb/> risk, we categorized Hb into six groups below and above the<lb/> WHO anemia criteria (Hb . 1 g/dL below, Hb 0–0.9 g/dL<lb/> below, Hb 0.1–1.0 g/dL above, Hb 1–1.9 g/dL above<lb/> [reference group], Hb 2–2.9 g/dL above, and Hb . 3 g/dL<lb/> above). In fully adjusted analyses stratified by ethnicity/<lb/> race, among whites, the point estimates for risk of mortality<lb/> reached statistical significance for all groups having Hb<lb/> below that of the referent group <ref type="table">(Table 2)</ref>. Among blacks,<lb/> Hb . 1 g/dL below the referent group (i.e., Hb , 12.0 g/dL<lb/> for men or , 11.0 g/dL for women) had increased mortality<lb/> risk (HR, 1.95; 95% CI, 1.24–3.06). Similarly, Hb 0–0.9<lb/> g/dL below the reference group showed a statistically<lb/> nonsignificant trend for higher mortality (HR, 1.35; 95% CI,<lb/> 0.88–2.05) compared to the reference group (Hb 1.0–1.9<lb/> g/dL above) <ref type="figure">(Figure 1)</ref>. We then performed further analyses<lb/> to examine the mortality risk for participants having Hb<lb/> 0–0.9 g/dL below the WHO anemia cutoff. When compared<lb/> to participants having a Hb 0.1–0.9 g/dL above the anemia<lb/> threshold, Hb 0–0.9 g/dL below the anemia cutoff was<lb/> associated with an 84% increased risk for mortality among<lb/> blacks (HR, 1.84; 95% CI, 1.21–2.79). Furthermore, Hb<lb/> 0–0.9 g/dL below the anemia cutoff increased the risk for<lb/> mortality among blacks (HR, 2.23; 95% CI, 1.12–4.47)<lb/> compared to an Hb 2.1–3.0 g/dL above the anemia cutoff.<lb/></p> <head>Interaction Between Anemia Status and Hb<lb/> Concentration and Mortality<lb/></head> <p>Although a higher point value for risk of death with<lb/> anemia status was found among blacks compared to whites<lb/> (1.90 vs 1.85 in the fully adjusted models), the statistical<lb/> interaction between race and anemia status was not statis-<lb/>tically significant (p ¼ .88), suggesting that the increased<lb/> mortality of anemia did not differ strongly by race. In<lb/> additional analyses, the interaction term for black ethnicity/<lb/> race with the Hb–mortality relationship was not statistically<lb/> significant except for Hb 0.1–1.0 g/dL above the anemia<lb/> cutoff (<ref type="table" >Table 3</ref>), suggesting that whites had significantly<lb/> higher risk for mortality than blacks within that hemoglo-<lb/>bin group.<lb/></p> <head>DISCUSSION<lb/></head> <p>In this stratified random sample from a population-based<lb/> cohort of older people, we found that anemia is associated<lb/> with an estimated 90% increased mortality in blacks and an<lb/></p> <figure type="table">Table 2. Multivariate-Adjusted Hazard Ratio for Mortality by Race<lb/> Blacks<lb/> Whites<lb/> Hazard Ratio (95% Confidence Interval)<lb/> Anemia Status (World Health Organization [WHO])<lb/> Model A<lb/> 1.96 (1.52–2.53)<lb/> 2.29 (1.74–3.00)<lb/> Model B<lb/> 1.90 (1.43–2.53)<lb/> 1.85 (1.32–2.59)<lb/> Hemoglobin (Hb) concentration (reference group: Hb 1.1–2 g/dL<lb/> above WHO anemia cutoff)<lb/> . 1 g/dL below<lb/> Model A<lb/> 2.15 (1.47–3.16)<lb/> 2.66 (1.74–4.06)<lb/> Model B<lb/> 1.95 (1.24–3.06)<lb/> 2.17 (1.28–3.65)<lb/> 0–0.9 g/dL below<lb/> Model A<lb/> 1.41 (0.96–2.08)<lb/> 2.37 (1.63–3.43)<lb/> Model B<lb/> 1.35 (0.88–2.05)<lb/> 2.14 (1.39–3.30)<lb/> 0.1–1 g/dL above<lb/> Model A<lb/> 0.92 (0.62–1.37)<lb/> 1.37 (0.99–1.88)<lb/> Model B<lb/> 0.86 (0.56–1.32)<lb/> 1.62 (1.13–2.32)<lb/> 2.1–3 g/dL above<lb/> Model A<lb/> 0.76 (0.40–1.45)<lb/> 1.01 (0.69–1.47)<lb/> Model B<lb/> 0.69 (0.36–1.34)<lb/> 1.08 (0.71–1.66)<lb/> . 3 g/dL above<lb/> Model A<lb/> 0.76 (0.18–3.14)<lb/> 1.16 (0.71–1.92)<lb/> Model B<lb/> 0.81 (0.19–3.41)<lb/> 1.41 (0.84–2.39)<lb/> Note: For the models, we adjusted for the following covariates for total<lb/> cohort (for black and white cohorts, race has been removed from the models): A<lb/> (primary model): age, sex, education, race, global cognition; B (fully adjusted<lb/> model): age, sex, education, race, global cognition, income, coronary artery<lb/> disease, diabetes, hypertension, stroke, cancer, hip fracture, Katz Activities of<lb/> Daily Living, Center for Epidemiological Study of Depression scale, smoking<lb/> status, self-reported health status (poor, fair), body mass index, glomerular<lb/> filtration rate, serum cholesterol, mean cell volume.<lb/></figure> <p>85% increased mortality in whites. Racial differences did<lb/> not appear to substantially influence the strong association<lb/> between anemia and increased mortality in this population.<lb/> Among blacks, Hb levels just below the WHO anemia<lb/> threshold of Hb , 13.0 g/dL for men or , 12.0 g/dL for<lb/> women significantly increased mortality compared to Hb<lb/> just above the anemia cutoff.<lb/></p> <p>As with previous studies (4,23), we found a lower average<lb/> Hb among black older adults. Using the WHO criteria,<lb/> Denny and colleagues (9) in the EPESE reported anemia<lb/> prevalence of 34% in blacks and 14% in whites, where as<lb/> Guralnik and colleagues in the NHANES analysis reported<lb/> 28% in blacks and 9% in whites. Racial differences in Hb<lb/> may be in part explained by comorbidity, but Hb has been<lb/> reported to be lower in blacks than in whites even after<lb/> taking into account disease status, behavioral risk factors,<lb/> nutritional intake, and iron status (6,7). One study indicated<lb/> that the trait of a high prevalence of a-thalassemia among<lb/> blacks may account for lower Hb, at least among non-elderly<lb/> individuals (23). These results have led to speculation that<lb/> blacks may have a lower set point for Hb than whites <ref type="biblio">(8)</ref>.<lb/></p> <p>Irrespective of our findings, the clinical significance of the<lb/> lower Hb and anemia status in older blacks remain poorly<lb/> defined. Denny and colleagues <ref type="biblio">(9)</ref> in the Duke EPESE<lb/> reported on mortality and outcomes among 1744 partic-<lb/>ipants, of whom 54% were black. They found an increased<lb/> unadjusted (relative risk [RR] ¼ 1.7; CI, 1.4–2.1) and<lb/> adjusted (RR ¼ 1.4; CI, 1.2–1.8) mortality risk among<lb/> blacks with anemia. The mortality impact of anemia did not<lb/> differ between blacks and whites. In contrast, Patel and<lb/> colleagues <ref type="biblio">(10)</ref> in the Health Aging and Body Composition<lb/> (ABC) Study recently reported that anemia was not<lb/> associated with higher mortality in blacks (HR ¼ 1.15;<lb/> 95% CI, 0.77–1.72)] in contrast to the detrimental impact<lb/> observed in whites. However, the Health ABC Study differs<lb/> from our study in two important ways. First, CHAP is<lb/> a population-based study of persons older than 65 years<lb/> living in the same geographically defined communities<lb/></p> <figure>Figure 1. Hazard ratio (HR) for mortality by hemoglobin (Hb) concentration groups and race.<lb/></figure> <p>regardless of their functional status, whereas the Health<lb/> ABC Study included a healthier cohort who were well<lb/> functioning at baseline. Second, the age range of study<lb/> participants differed: 65 years or older for CHAP and 70–79<lb/> years at baseline for Health ABC. Whether these differences<lb/> account for differences in findings is unclear.<lb/></p> <p>This study builds on prior work by extending the<lb/> population-based finding of the relationship of Hb to<lb/> mortality risk in blacks and whites. Our results showed that<lb/> anemia defined by WHO criteria carries increased mortality<lb/> risk in blacks and whites. Among blacks, even Hb just below<lb/> the WHO anemia threshold (Hb 0–0.9 g/dL below) signifi-<lb/>cantly increased mortality risk when compared to Hb slightly<lb/> above the anemia cutoff (Hb 0.1–1 g/dL above). Among<lb/> whites, Hb below and slightly above (Hb 0.1–1.0 g/dL) the<lb/> WHO anemia threshold carries increased mortality risk.<lb/></p> <p>Whether blacks have significantly different mortality risk<lb/> compared to whites is still unresolved. The point estimate<lb/> for risk of mortality for anemia by WHO was nominally<lb/> higher among blacks (HR ¼ 1.90) than among whites (HR ¼<lb/> 1.85). The statistical interaction term of the Hb–mortality<lb/> relationship with black ethnicity/race was nonsignificant (p<lb/> ¼ .88), suggesting that increased mortality risk of anemia<lb/> did not differ between blacks and whites. Additionally,<lb/> when we categorized Hb above and below the anemia cutoff<lb/> in subgroup analyses, our findings suggested that, for Hb<lb/> 0.1–1 g/dL above the anemia cutoff, but not for any other<lb/> Hb groups, blacks had significantly lower mortality than<lb/> whites (p ¼ .02). Overall, these findings argue against using<lb/> an Hb threshold below the WHO criteria to define anemia in<lb/> blacks when considering anemia as a prognostic marker for<lb/> mortality. However, our findings support considering<lb/> a higher Hb threshold to define the prognostic impact of<lb/> anemia in whites. Further study of the impact of low Hb by<lb/> race on mortality and other health-related measures is<lb/> warranted.<lb/></p> <p>Despite the findings from this and other observational<lb/> studies of older participants showing that lower Hb has<lb/> a strong and independent association with increased<lb/> mortality, the benefits and risks of anemia correction remain<lb/> largely unexplored for older anemic adults. Paradoxically,<lb/> recent data <ref type="biblio">(24)</ref> show that achieving higher Hb (.13 g/dL)<lb/> through pharmacologic treatment with erythropoietin-<lb/>stimulating proteins may increase mortality, at least for<lb/> anemia due to chronic kidney disease. Only clinical trials<lb/> can answer whether anemia treatment affords a benefit.<lb/> This study has several limitations. First, unrecognized<lb/> confounding factors may exist. The comprehensive adjust-<lb/>ment performed and the small changes in multivariate<lb/> analyses in the elevated risk of mortality due to lower Hb<lb/> diminish this possibility. A further limitation is inability to<lb/> differentiate the mortality risks by anemia etiologies. Last,<lb/> our study did not examine repeated measures of Hb over<lb/> time, and cannot address the relationship of change in Hb to<lb/> subsequent mortality.<lb/></p> <p>Our study also has substantial strengths. It is a large,<lb/> population-based study with comprehensive and uniform<lb/> measurement of potentially relevant confounders. Further-<lb/>more, the biracial design permits direct contrasting of two<lb/> racial groups within the study.<lb/></p> <p>Our findings emphasize the importance not only of<lb/> anemia status, but that Hb just below anemia cutoff is<lb/> significantly related to overall mortality in both blacks and<lb/> whites. We believe that our results support the WHO<lb/> threshold of Hb , 13.0 g/dL for men or , 12.0 g/dL as<lb/> reasonable anemia criteria for older blacks, and validate<lb/> other studies showing that a higher Hb threshold may be<lb/> considered for whites. Further research is needed to examine<lb/> the relation of Hb to other important geriatric outcomes in<lb/> racially diverse populations.<lb/></p> <figure type="table">Table 3. Interaction Terms Between Race and<lb/> Hemoglobin (Hb) Concentration<lb/> Coefficient<lb/> Hazard Ratio<lb/> 95% CI<lb/> Anemia Status (World Health Organization)<lb/> Black Participants 3 Anemia Status<lb/> Model A 0.29<lb/> À0.19<lb/> 0.82<lb/> 0.58–1.18<lb/> Model B 0.88<lb/> 0.03<lb/> 1.03<lb/> 0.69–1.55<lb/> Hb Concentration (Categorical Groupings)<lb/> Black Participants 3 Hb Groups<lb/> Hb . 1 g/dL below<lb/> À0.15<lb/> 0.86<lb/> 0.45–1.63<lb/> Hb 0–0.9 g/dL below<lb/> À0.50<lb/> 0.60<lb/> 0.34–1.09<lb/> Hb 0.1–1 g/dL above<lb/> À0.64<lb/> 0.52<lb/> 0.30–0.91*<lb/> Hb 1.1–2 g/dL above<lb/> (Reference)<lb/> 1.0<lb/> Hb 2.1–3 g/dL above<lb/> À0.56<lb/> 0.57<lb/> 0.26–1.24<lb/> Hb . 3 g/dL above<lb/> À0.53<lb/> 0.59<lb/> 0.13–2.69<lb/> Notes: Hazard ratio was adjusted for age, sex, race, education, global<lb/> cognition, income, coronary artery disease, diabetes, hypertension, stroke,<lb/> cancer, hip fracture, Katz Activities of Daily Living, Center for Epidemiological<lb/> Study of Depression scale, smoking, self reported health status (poor, fair), body<lb/> mass index, glomerular filtration rate, serum cholesterol, mean cell volume.<lb/> *p ¼ .023.<lb/> CI ¼ confidence interval.</figure> </text> </tei>