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Spatial variation in particulate matter–related health and toxicological outcomes is partly due to its composition. We studied spatial variability in particle composition and induced cellular responses in Mexico City to complement an ongoing epidemiologic study. We measured elements, endotoxins, and polycyclic aromatic hydrocarbons in two particle size fractions collected in five sites. We compared the in vitro proinflammatory response of J774A.1 and THP-1 cells after exposure to particles, measuring subsequent TNFα and IL-6 secretion. Particle composition varied by site and size. Particle constituents were subjected to principal component analysis, identifying three components: C1 (Si, Sr, Mg, Ca, Al, Fe, Mn, endotoxin), C2 (polycyclic aromatic hydrocarbons), and C3 (Zn, S, Sb, Ni, Cu, Pb). Induced TNFα levels were higher and more heterogeneous than IL-6 levels. Cytokines produced by both cell lines only correlated with C1, suggesting that constituents associated with soil induced the inflammatory response and explain observed spatial differences.

Background Human alveolar macrophages are first-line cellular responders to inhaled particulate matter (PM) and microbial pathogens in the lungs. We examined whether PM exposure affects human bronchoalveolar and peripheral blood mononuclear cell responses to Mycobacterium tuberculosis. Methods Bronchoalveolar and peripheral blood mononuclear cells were obtained from 30 healthy adult volunteers living in Mexico City, Mexico. Proportions of alveolar macrophages with PM and areas of cytoplasm occupied by inhaled PM within alveolar macrophages were evaluated in 50 bronchoalveolar cells from each donor by ImageJ (version 1.49) on 1000× digital bright field microscopy cytospin images. Ambient PM 2.5 (aerodynamic diameters <2•5 µm) was collected with high-volume samplers at the Instituto Nacional de Ecología y Cambio Climático, Mexico City. Frequencies of interleukin 1β, tumour necrosis factor (TNF) α, interleukin 6, and interferon-γ-producing bronchoalveolar and peripheral blood mononuclear cells stimulated with M tuberculosis (strain H37Ra at multiplicities of infection [MOI] of 1 and 10), lipopolysaccharide, 6 kDa early secretory antigenic target (ESAT-6), purified protein derivative, and PM 2.5 were enumerated by ELISPOT assays.

Particulate matter may promote cardiovascular disease, possibly as a consequence of its oxidative potential. Studies using susceptible animals indicate that particulate matter aggravates atherosclerosis by increasing lipid/macrophage content in plaques. Macrophage lipid uptake requires oxidized low-density lipoprotein and scavenger receptors; same receptors are involved in particulate matter uptake. We studied in vitro particulate matter potential to oxidize low-density lipoproteins and subsequent cell uptake through scavenger receptors. Particulate matter-induced low-density lipoproteins oxidation was evaluated by the thiobarbituric acid assay. Binding/internalization was tested in wild type and scavenger receptor–transfected Chinese hamster ovary cells, and in RAW264.7 cells using fluorescently labeled low-density lipoproteins. Dose-dependent binding/internalization only occurred in scavenger receptor–transfected Chinese hamster ovary cells and RAW264.7 cells. Competition binding/internalization using particles showed that particulate matter induced decreased binding (~50%) and internalization (~70%) of particle-oxidized low-density lipoproteins and native low-density lipoproteins. Results indicate that particulate matter was capable of oxidizing low-density lipoproteins, favoring macrophage internalization, and also altered scavenger and low-density lipoproteins receptor function.