Atmospheric fine particulate matter (PM 2.5 ) was collected to investigate its dispersion in simulated lung fluid (SLF) and its interaction with model cell membranes. Organic acids, NH 4 + , SO 4 2 − and NO 3 − were detected in PM 2.5 soluble fraction, and heavy metals were detected from the total mass. The insoluble fraction contained kaolinite, CaCO 3 , aliphatic carbons, aromatic rings, carboxyl and hydroxyl groups reflected by the infrared spectra. Proteins dispersed PM 2.5 in SLF, resulted in smaller hydrodynamic diameter ( d H ) and slower sedimentation rate. Conversely, phospholipids increased d H value and accelerated sedimentation rate. Giant unilamellar vesicles (GUVs) and supported lipid bilayers (SLBs) were used as model cell membranes. PM 2.5 adhered on and disrupted the membrane containing positively-charged lipids but not the membrane containing neutrally- and negatively-charged lipids, which was monitored by microscopy and a quartz crystal microbalance with dissipation (QCM-D). The cationic sites on membrane were necessary for PM 2.5 adhesion, but membrane should be disrupted by the combined action of electrostatic forces and hydrogen bonds between PM 2.5 oxygen containing groups and the lipid phosphate groups. Our results specified the roles of proteins and phospholipids in PM 2.5 dispersion and transport, highly suggested that the health hazard of PM 2.5 was related to the biomolecules in the lung fluid and the particle surface groups. [ABSTRACT FROM AUTHOR]