In addition, there are certain categories of joint effects that might more readily provide mechanistic interpretations. The presence of qualitative or pure interaction can highlight components of a complex exposure that might be active in specific conditions. This is illustrated by polymorphisms in genes that metabolize the exposure agent, such as acetylation activity of the NAT2 gene, different kinds of aromatic amines and the etiology of bladder cancer. Studies in the general population consistently show slow acetylation activity increases risk of bladder cancer among smokers, but has no effect among non-smokers [García-Closas, et al. 2005]. In contrast, a study conducted among subjects highly exposed to benzidine, which is rare in the general population, showed slow acetylation activity to be associated with reduced risk of bladder cancer for benzidine-exposed workers [Carreon, et al. 2006]. These studies provided biological insights into mechanisms of actions for different types PAHs on carcinogenesis.
