Anthracosis is the term used to describe the black pigmentation of the lungs after long time exposure to biomass smoke and/or air pollution. But it is unknown whether this particulate presence is still capable of causing changes in tissues. Lung and lymph node fragments were collected from autopsies (36) for anthracosis particulate matter (APM) extraction. For detection of polycyclic aromatic hydrocarbons (PAH), gas chromatography coupled with mass spectrometry was performed; Diesel exhaust particles (DEP) was used for comparison. To assess biological effects, BEAS-2B airway cells were cultured with macrophages induced to M1 inflammatory or M2 anti-inflammatory profile and exposed to 50 µg/mL of APM or DEP for 24h. Flow cytometry was performed for macrophages immunophenotyping, culture supernatant was collected for LDH production analysis and RNA for real-time PCR. Studied genes were CYP1A1 and CYP1B1 (P450 family) and AGR2 and TP53 (cell cycle control and repair). Chemical composition showed PAH of low molecular weight (92%), with 2 to 3 rings (91.12%), most naphthalene (3.80±0.02 µg/g) and acenaphthylene (5.26±0.08 µg/g) species. APM or DEP caused no significant change in BEAS-2B LDH production (p=0.101); APM promoted inflammatory profile (M1), both in isolated or co-cultured macrophages; exposure induced the expression of CYP1A1 (DEP) and CYP1B1 (APM and DEP) genes, while a tendency to decrease AGR2 and increase TP53 expression (APM and DEP), both in BEAS-2B and in co-culture. The results suggest that APM has potential to cause immune and inflammatory response.