Particulate matter extracted from human anthracotic tissues induces inflammatory markers in co-culture of lung cells and macrophages.

Anthracosis, characterized by black pigmentation in the lungs and tracheobronchial tree due to inhaled carbon particles, has been linked to urban air pollution. This study analyzed the chemical composition of particulate matter extracted from anthracotic tissue (APE) and its effects on human bronchial cells (BEAS-2B) and lung adenocarcinoma cells (A549) in co-culture with M1 or M2 macrophages. Diesel exhaust particles (DEP) served as a positive control. APE was extracted from lung and lymph nodes at Capital Death Verification Service (SVO) and chemically characterized for polycyclic aromatic hydrocarbons (PAHs) and inorganic elements like metals and sulfur. DEP contained more complex PAHs and higher levels of iron, sulfur, and zinc than APE. Pulmonary cell's metabolism decreased after exposure to APE, also co-culture macrophage viability. Macrophage immunophenotyping revealed heterogeneity, with M1 and M2 markers present in mono- and co-cultures, but APE exposure induced a pro-inflammatory M1 profile. Cytokine analysis showed significant increases in IL-1β, TNF-α, IL-6, and IL-8 levels after APE exposure, but not DEP. Gene expression of CYP1A1 and CYP1B1, associated with xenobiotic responses, increased after DEP exposure but remained unaffected by APE. Both APE and DEP caused mild modulation of cell cycle markers p53 and EGFR. These findings suggest APE is a metabolized particle, but not inert, inducing a pro-inflammatory response in pulmonary cells. Differences between APE and DEP effects likely stem from compositional variations: DEP's higher PAHs amount elicited a xenobiotic response, whereas APE's lower-weight PAHs triggered pronounced cytokine release.