The Johns Hopkins School of Medicine, Division of Pediatric Pulmonology, Department of Pediatrics, Children's Hospital Los Angeles, Rubenstein Child Health Building, 200 N. Wolfe Street, 3rd Floor, Baltimore, MD 21287, USA. Electronic address: .
Public health (Impact Factor: 1.43). 02/2013; 127(3). DOI: 10.1016/j.puhe.2012.12.030
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.
[Show abstract][Hide abstract] 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; 88(8). DOI:10.1007/s00204-014-1212-z · 5.98 Impact Factor
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