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Adverse human health effects caused by fine particulate matter (PM 2.5) were reported; however, source-specific PM 2.5 and its bioreactivity need to be assessed to understand regional human impacts. The objective of this study was to investigate the contributions of PM 2.5 to particle bioreactivity in Taichung City, an urban area of west-central Taiwan. The average mass concentration of PM 2.5 was 44.4 μg m−3 from 21 March to April 22, 2018. PM 2.5 was identified from six distinct sources using a positive matrix factorization (PMF) model. Secondary aerosols were discovered to be the primary contributor to PM 2.5 (25.58%), and were primarily composed of Cl−, NO 3 −, EC, NH 4 +, and SO 4 2−. It was found that approximately 52.20% (23.2 μg m−3) of inhaled PM 2.5 was deposited in the alveolar region after inhalation in the human lungs according to the multiple-path particle dosimetry (MPPD) model. Therefore, human alveolar epithelial A549 cells were exposed to PM 2.5 , which significantly reduced lung cell viability, and increased the cytotoxic lactate dehydrogenase (LDH), reactive oxygen species (ROS), and inflammatory interleukin (IL)-6 (p < 0.05). Next, we discovered positive correlation between secondary aerosols and ROS production, which was further linked to increases in inorganic ions (Mg2+, Cl−, NO 3 −, and SO 4 2−) (p < 0.05). In conclusion, acidic ions from secondary aerosols were positively correlated with ROS production in human alveolar epithelial cells. Our results showed that secondary aerosols could be an important determinant of the deterioration of air quality and human respiratory health in urban areas. [Display omitted] • Secondary aerosol was the primary source of PM 2.5 in Taichung city. • More than half of inhaled PM 2.5 are able to deposit in the alveolar region. • PM 2.5 reduced cell viability and increased cytotoxicity, ROS and IL-6 in vitro. • Acidic ions from secondary aerosol contributed to ROS production. [ABSTRACT FROM AUTHOR]