Correlation of ambient pollution levels and heavily-trafficked roadway proximity on the prevalence of smear-positive tuberculosis
ABSTRACT OBJECTIVES: Varying levels of evidence exist for the contribution of indoor air pollution and environmental tobacco smoke as a risk factor for tuberculosis (TB). Despite a similar mechanism of action, the influence of outdoor air pollution exposure as an independent contributor to TB disease has yet to be explored. This area of inquiry is of increasing importance given the level of pollution in the rising economies of many TB-endemic nations. Los Angeles' unique physical environs and traffic patterns mirror other global megacities with a greater burden of TB therefore allowing for preliminary correlative studies. This preliminary study hypothesizes that individuals who reside proximal to elevated pollutant exposures are likely to have a greater burden of disease - as evidenced by sputum smear-positive TB. STUDY DESIGN: Retrospective medical records review. METHODS: Medical records of non-homeless individuals (n = 196) diagnosed with culture positive TB at Los Angeles County and University of Southern California Medical Center Hospital were analyzed from January 2007 to December 2008. The study population was grouped according to acid-fast bacilli (AFB) smear-positive (n = 111) and smear-negative (n = 85) status. Air pollutant exposure was captured using measurements of ozone (O3) and particulate matter with an aerodynamic diameter of less than 2.5 (PM2.5). Individual assignment to O3 and PM2.5 exposures were based on residential proximity to the nearest US Environmental Protection Agency's monitoring station. Proximity of home residences to traffic-related pollutants occurred by measurement of distance to the nearest freeway and major non-freeway road. RESULTS: Single factorial models yielded a significant correlation of smear-positive status and residential exposure to PM2.5. Residential distance to freeways and major arterial roads did not yield an association. CONCLUSIONS: This is the first report linking ambient pollution exposure as a risk factor for TB. PM2.5 may have the potential to impact TB lung pathology as evidenced by the linkage of fine particulate matter levels and smear-positive TB.
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ABSTRACT: Inhalation exposure to indoor air pollutants and cigarette smoke increase the risk of tuberculosis (TB) development. Whether exposure to ambient air pollution particulate matter (PM) alters protective human host immune responses against Mycobacterium tuberculosis (M.tb) has been studied poorly. Here we examined the effect of PM from Iztapalapa, a municipality of Mexico City, with aerodynamic diameters below 2.5μm (PM2.5) and 10μm (PM10) on innate antimycobacterial immune responses in human alveolar type II epithelial cells A549. Exposure to PM2.5 or PM10 deregulated the ability of the A549 cells to express the antimicrobial peptides human β-defensin 2 and 3 (HBD-2 and HBD-3) upon infection with M.tb and increased intracellular M.tb growth (colony-forming units). The observed modulation of antibacterial responsiveness by PM exposure was associated with induction of senescence in PM-exposed A549 cells and unrelated to PM-mediated loss of cell viability. Thus, induction of senescence and downregulation of HBD-2 and HBD-3 expression in respiratory PM-exposed epithelial cells leading to the enhanced M.tb growth represent mechanisms by which exposure to air pollution PM may increase the risk of M.tb infection and TB development. Copyright © 2015, American Society for Microbiology. All Rights Reserved.Infection and immunity 04/2015; 83(6). DOI:10.1128/IAI.03018-14 · 4.16 Impact Factor
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ABSTRACT: High diesel exhaust particle levels are associated with increased health effects; however, knowledge on the impact of its chemical contaminant 1,2-naphthoquinone (1,2-NQ) is limited. We investigated whether postnatal and adult exposures to 1,2-NQ influence allergic reaction and the roles of innate and adaptive immunity. Male neonate (6 days) and adult (56 days) C57Bl/6 mice were exposed to 1,2-NQ (100 nM; 15 min) for 3 days, and on day 59, they were sensitized and later challenged with ovalbumin (OVA). Airway hyper-responsiveness (AHR) and production of cytokines, immunoglobulin E (IgE) and leukotriene B4 (LTB4) were measured in the airways. Postnatal exposure to 1,2-NQ activated dendritic cells in splenocytes by increasing expressing cell surface molecules (e.g., CD11c). Co-exposure to OVA effectively polarized T helper (Th) type 2 (Th2) by secreting Th2-mediated cytokines. Re-stimulation with unspecific stimuli (PMA and ionomycin) generated a mixed Th1 (CD4(+)/IFN-γ(+)) and Th17 (CD4(+)/IL-17(+)) phenotype in comparison with the vehicle-matched group. Postnatal exposure to 1,2-NQ did not induce eosinophilia in the airways at adulthood, although it evoked neutrophilia and exacerbated OVA-induced eosinophilia, Th2 cytokines, IgE and LTB4 production without affecting AHR and mast cell degranulation. At adulthood, 1,2-NQ exposure evoked neutrophilia and increased Th1/Th2 cytokine levels, but failed to affect OVA-induced eosinophilia. In conclusion, postnatal exposure to 1,2-NQ increases the susceptibility to antigen-induced asthma. The mechanism appears to be dependent on increased expression of co-stimulatory molecules, which leads to cell presentation amplification, Th2 polarization and enhanced LTB4, humoral response and Th1/Th2 cytokines. These findings may be useful for future investigations on treatments focused on pulmonary illnesses observed in children living in heavy polluted areas.Archives of Toxicology 02/2014; DOI:10.1007/s00204-014-1212-z · 5.08 Impact Factor
The Korean Journal of Internal Medicine 03/2014; 29(2):170-2. DOI:10.3904/kjim.2014.29.2.170