Evidence shows a strong association among air pollution, oxidative stress (OS), deoxyribonucleic acid (DNA) damage, and diseases. Recent studies indicated that the ageing, human neurodegenerative diseases and cancers resulted from mitochondrial dysfunction and OS. The purpose of this study is to provide a probabilistic risk assessment model to quantify the atmospheric diesel exhaust particles (DEP)-induced pre-cancer biomarker response and cancer incidence risk for residents in south Taiwan. We conducted entirely monthly particulate matter sampling data at five sites in Kaohsiung of south Taiwan in the period 2002 − 2003. Three findings were found: (i) the DEP dose estimates and cancer risk quantification had heterogeneously spatiotemporal difference in south Taiwan, (ii) the pre-cancer DNA damage biomarker and cancer incidence estimates had a positive yet insignificant association, and (iii) all the estimates of cancer incidence in south Taiwan populations fell within and slight lower than the values from previous cancer epidemiological investigations. In this study, we successfully assessed the tumor incidence for residents posed by DEP exposure in south Taiwan compared with the epidemiological approach. Our approach provides a unique way for assessing human health risk for residences exposed to atmospheric DEP depending on specific combinations of local and regional conditions. Our work implicates the importance of incorporating both environmental and health risk impacts into models of air pollution exposure to guide adaptive mitigation strategies.