Diesel particulate matter (DPM) is a dominant contaminant in fine particulate matters (PM2.5) and has been proved to induce serious harmful effects to human beings, including lung cancer, allergic, and chronic bronchitis. However, little attention has been paid to understand the transgenerational effects of DPM. In the present study, we focused on the transgenerational effects of DPM in the model organism Caenorhabditis elegans (C. elegans) exposed in either maternal generation (F0) or consecutive generations (F0-F5). In maternal exposure manner, 0.1 and 1.0 mu g/mL DPM significantly increased the germ cell apoptosis at F0 generation, while the number of apoptotic germ cells at F1-F5 generation were gradually recovered back to control level. The brood size were significantly reduced by DPM at F2 generation and recovered to control level at F3-F5 generations. In continuous exposure manner, although 0.1 and 1.0 mu g/mL DPM induced significant germ cell apoptosis in F0 generation, there was no difference between F0 and other generations. Continuous exposure to DPM at 0.1 and 1.0 mu g/mL impaired the brood size in F2 to F5 generations. Using a series of loss-of-function mutant strains, we found that cep-1 (w40), hus-1 (op241), and mitogen-activated protein kinase (MAPK) related signaling pathway genes were involved in DPM-induced apoptosis. Our results clearly demonstrated that the adverse effects of DPM could be passed on through long-term multigenerational exposure and DNA damage checkpoint genes and MAPK signal pathway played an essential role in response to DPM induced development and reproduction toxicity