Towards the development of a systems biology-based risk assessment approach for 
environmental toxicants, including tobacco products in a systems toxicology 
setting such as the "21st Century Toxicology", we are building a series of 
computable biological network models specific to non-diseased pulmonary and 
cardiovascular cells/tissues which capture the molecular events that can be 
activated following exposure to environmental toxicants. Here we extend on 
previous work and report on the construction and evaluation of a mechanistic 
network model focused on DNA damage response and the four main cellular fates 
induced by stress: autophagy, apoptosis, necroptosis, and senescence. In total, 
the network consists of 34 sub-models containing 1052 unique nodes and 1538 
unique edges which are supported by 1231 PubMed-referenced literature citations. 
Causal node-edge relationships are described using the Biological Expression 
Language (BEL), which allows for the semantic representation of life science 
relationships in a computable format. The Network is provided in .XGMML format 
and can be viewed using freely available network visualization software, such as 
Cytoscape.