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Open Access Research article

Non-hispanic whites have higher risk for pulmonary impairment from pulmonary tuberculosis

Jotam G Pasipanodya12, Edgar Vecino1, Thaddeus L Miller1, Guadalupe Munguia1, Gerry Drewyer4, Michel Fernandez14, Philip Slocum3 and Stephen E Weis14*

Author Affiliations

1 Department of Internal Medicine, UNT- Health Science Center at Fort Worth, Fort Worth, TX, USA

2 Department of Internal Medicine, Division of Infectious diseases, UT Southwestern Medical Center at Dallas, Dallas, Texas, USA

3 Department of Internal Medicine, A.T. Still University of Health Sciences, Kirksville, MO, USA

4 Tarrant County Public Health Department, Division of TB Elimination, 1101 S. Main Street, Fort Worth, TX, USA

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BMC Public Health 2012, 12:119  doi:10.1186/1471-2458-12-119

Published: 10 February 2012



Disparities in outcomes associated with race and ethnicity are well documented for many diseases and patient populations. Tuberculosis (TB) disproportionately affects economically disadvantaged, racial and ethnic minority populations. Pulmonary impairment after tuberculosis (PIAT) contributes heavily to the societal burden of TB. Individual impacts associated with PIAT may vary by race/ethnicity or socioeconomic status.


We analyzed the pulmonary function of 320 prospectively identified patients with pulmonary tuberculosis who had completed at least 20 weeks standard anti-TB regimes by directly observed therapy. We compared frequency and severity of spirometry-defined PIAT in groups stratified by demographics, pulmonary risk factors, and race/ethnicity, and examined clinical correlates to pulmonary function deficits.


Pulmonary impairment after tuberculosis was identified in 71% of non-Hispanic Whites, 58% of non-Hispanic Blacks, 49% of Asians and 32% of Hispanics (p < 0.001). Predictors for PIAT varied between race/ethnicity. PIAT was evenly distributed across all levels of socioeconomic status suggesting that PIAT and socioeconomic status are not related. PIAT and its severity were significantly associated with abnormal chest x-ray, p < 0.0001. There was no association between race/ethnicity and time to beginning TB treatment, p = 0.978.


Despite controlling for cigarette smoking, socioeconomic status and time to beginning TB treatment, non-Hispanic White race/ethnicity remained an independent predictor for disproportionately frequent and severe pulmonary impairment after tuberculosis relative to other race/ethnic groups. Since race/ethnicity was self reported and that race is not a biological construct: these findings must be interpreted with caution. However, because race/ethnicity is a proxy for several other unmeasured host, pathogen or environment factors that may contribute to disparate health outcomes, these results are meant to suggest hypotheses for further research.