Dataset Information

Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity.

ABSTRACT: RATIONALE:Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored. OBJECTIVES:To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM2.5 (< 2.5?µm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis. METHODS:Cellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis. MEASUREMENTS AND MAIN RESULTS:In vitro exposure of AM to PM2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1? production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-?) in BAC, and negatively correlated with PPD-induced IFN-? in PBMC. CONCLUSIONS:Inhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis. PM load in AM is correlated with altered M. tuberculosis-induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness.

SUBMITTER: Torres M

PROVIDER: S-EPMC7162557 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Urban airborne particle exposure impairs human lung and blood <i>Mycobacterium tuberculosis</i> immunity.

Torres Martha M Carranza Claudia C Sarkar Srijata S Gonzalez Yolanda Y Osornio Vargas Alvaro A Black Kathleen K Meng Qingyu Q Quintana-Belmares Raul R Hernandez Martha M Angeles Garcia Jose Juan F JJF Páramo-Figueroa Victor Hugo VH Iñiguez-Garcia Marco Antonio MA Flores Jose L JL Zhang Junfeng Jim JJ Gardner Carol R CR Ohman-Strickland Pamela P Schwander Stephan S

Thorax 20190429 7

<h4>Rationale</h4>Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored.<h4>Objectives</h4>To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM<sub>2.5</sub> (< 2.5 µm median aerodynamic diameter) alters human host immune cell responses to <i>Mycobacterium tuberculosis</i>.<h4>Methods</h4>Cellular toxicity (flow cytometry, proliferation assay (MTS as ...[more]

PMID: 31036772

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Project description:Inhalation of halogenated flame-retardants (HFRs) released from consumer products is an important route of exposure. However, not all airborne HFRs are respirable, and thus interact with vascular membranes within the gas exchange (alveolar) region of the lung. HFRs associated with large (>4 µm), inhalable airborne particulates are trapped on the mucosal lining of the respiratory tract and then are expelled or swallowed. The latter may contribute to internal exposure via desorption from particles in the digestive tract. Exposures may also be underestimated if personal activities that re-suspend particles into the breathing zone are not taken into account. Here, samples were collected using personal air samplers, clipped to the participants' shirt collars (n = 18). We observed that the larger, inhalable air particulates carried the bulk (>92%) of HFRs. HFRs detected included those removed from commerce (i.e., polybrominated diphenyl ethers (Penta-BDEs: BDE-47, -85, -100, -99, and -153)), their replacements; e.g., 2-ethylhexyl 2,3,4,5-tetrabromobenzoate (TBB or EH-TBB); bis(2-ethylhexyl) 3,4,5,6-tetrabromophthalate (TBPH or BEH-TEBP) and long-produced chlorinated organophosphate-FRs (ClOPFRs): tris(2-chloroethyl)phosphate (TCEP), tris(1-chloro-2-propyl)phosphate (TCPP or TCIPP), and tris(1,3-dichloro-2-propyl)phosphate (TDCPP or TDCIPP). Our findings suggest estimates relying on a single exposure route, i.e., alveolar gas exchange, may not accurately estimate HFR internal dosage, as they ignore contributions from larger inhalable particulates that enter the digestive tract. Consideration of the fate and bioavailability of these larger particulates resulted in higher dosage estimates for HFRs with log Koa < 12 (i.e., Penta-BDEs and ClOPFRs) and lower estimates for those with log Koa > 12 (i.e., TBB and TBPH) compared to the alveolar route exposure alone. Of those HFRs examined, the most significant effect was the lower estimate by 41% for TBPH. The bulk of TBPH uptake from inhaled particles was estimated to be through the digestive tract, with lower bioavailability. We compared inhalation exposure estimates to chronic oral reference doses (RfDs) established by several regulatory agencies. The U.S. Environmental Protection Agency (EPA) RfD levels for several HFRs are considered outdated; however, BDE-99 levels exceeded those suggested by the Dutch National Institute for Public Health and the Environment (RIVM) by up to 26 times. These findings indicate that contributions and bioavailability of respirable and inhalable airborne particulates should both be considered in future risk assessments.

Dataset Information

Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity.

Publications

Urban airborne particle exposure impairs human lung and blood <i>Mycobacterium tuberculosis</i> immunity.

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