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Introduction Bulky DNA adducts are widely accepted as a sensitive biomarker of the biologically effective dose of exposure to genotoxic aromatic compounds, including polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines, from complex environmental exposures, including those in air, tobacco smoke, and diet (de Kok et al. 2002), and may be predictive of cancer risk in adults (Veglia et al. 2008). They provide an overall measure of exposure, absorption, and metabolic activation of a mixture of DNA adduct–forming compounds, integrated with repair of DNA damage of an individual (Farmer 1994; Phillips and Arlt 2007). Bulky adducts have been detected in DNA from pregnant women (Godschalk et al. 2005; Pedersen et al. 2009, 2012a, 2013b; Topinka et al. 2009), placenta (Karttunen et al. 2010; Topinka et al. 2009), and cord blood (Godschalk et al. 2005; Hansen et al. 1993; Kovács et al. 2011; Pedersen et al. 2009, 2013b; Perera et al. 2011; Topinka et al. 2009). However, most of these studies are limited in size, and very little is known so far about modifiable predictors of the in utero formation and repair of these DNA adducts. Maternal smoking (Godschalk and Kleinjans 2008; Hansen et al. 1993; Pedersen et al. 2009), exposure to traffic-related air pollution (Pedersen et al. 2009), and intake of meat with a blackened surface (Pedersen et al. 2012a) have been associated with higher levels of bulky DNA adducts in newborns. Diet is a significant source of exposure to agents that may modulate adduct formation toward either increase or decrease. Possible sources of these adducts are PAHs and other bulky DNA adduct–forming compounds that can be produced during cooking of certain foods such as meats and fish, and they also occur commonly as environmental contaminants especially of leafy plants, cereals, and

Erratum: “Environmental, Dietary, Maternal, and Fetal Predictors of Bulky DNA Adducts in Cord Blood: A European Mother–Child Study (NewGeneris)”