Internal exposure to carcinogenic polycyclic aromatic hydrocarbons and DNA damage

Abstract

In the August issue of the Archives, Kafferlein et al. report no association between occupational exposures to polycyclic aromatic hydrocarbons (PAHs) and deoxyribo nucleic acid (DNA) damage on the individual level (Kafferlein et al. 2012). Internal PAH exposure, assessed in a variety of occupations by means of urinary 3-hydroxy benzo[a]pyrene (3-OH-B[a]P) and 1and 2-naphtol ( P OHNaph), was unrelated with DNA strand break frequencies and the levels of 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodGuo), perhaps with the exception of a small group of converter workers where an uncertain correlation between P OHNaph and 8-oxo-dGuo was observed. Authors discuss reasons for this lack of association suggesting to focus on the individual exposure circumstances. These include possible different routes of exposure and co-exposures and a better understanding and assessment of the kinetics and dynamics of the endpoints. We report here the lack of correlations on the individual level in a group of coke oven non-smoker workers between other endpoints of exposure such as urinary 1-hydroxypyrene (1-OHP) and lymphocyte anti-benzo[a]pyrene diolepoxide DNA adduct (anti-B[a]PDE-DNA) and of genotoxic effect such as lymphocyte micronuclei (MN) frequency. Similar lack of correlations observed when using rather different endpoints call for a discussion on possible common explanations. Whereas co-exposures can be thoroughly investigated, we suspect that the kinetics and dynamics of both exposure and effect endpoints for PAHs are far to be understood. Meanwhile, we propose here that both the results of Kafferlein et al. 2012 and ours could be largely explained by the variable routes of exposure occurring among and within occupational settings.