## 4 PAH Occurrence and Formation in Processed Meat, Edible Oils, and Cereal-Derived Products  
Human exposure occurs in an inconsistent manner. Due to their prevalence in the environment, the wide distribution of airborne PAHs renders inhalation one of the major routes of exposure showing increased bioavailability [17]. However, for the non-smoking and non-occupationally exposed population, food consumption accounts for the highest percentage of human exposure to these contaminants [7,84,85]. With respect to the impact of pollution sources on human exposure, food intake of PAHs and derivatives plays an important role in the context of regional/localized contamination through their introduction to the food chain [6,85]. For instance, rural areas exhibit environmental contamination that may result from long-distance atmospheric movement, as evidenced by the corresponding unprocessed food contamination. In addition, the physical and chemical characteristics of PAHs, including solubility, volatility, reactivity, and degradability, highly influence their prevalence in food [2,23]. In this context, the use of contaminated water, crops, and deposition on agricultural food items, among others, contributes greatly to food contamination throughout the processing stages [7,15,84]. In 2002, the Scientific Committee on Food (SCF) established that BaP could be considered a marker for PAH occurrence and carcinogenic effects in food [86]. Harmonized maximum levels (MLs) for BaP were established in 2006 through Commission Regulation (EC) No 1881/2006 [87]. It was later amended by Commission Regulation (EU) No 835/2011 [88] to include Chr, BaA, and Bbf in addition to BaP as a better indicator of total PAHs [89]. In accordance with the EU guidelines [88], the MLs of BaP and PAH4 set for the food categories addressed herein are as follows: 5.0 \(\upmu\)g/kg (BaP) and 30.0 \(\upmu\)g/kg (PAH4) for smoked meat and meat-derived products; 2.0 \(\upmu\)g/kg (BaP) and 10.0 \(\upmu\)g/kg (PAH4) for vegetable oils and fats; and 1.0 \(\upmu\)g/kg (BaP/PAH4) for processed cereal-based foods and baby foods. In spite of the inconsistencies surrounding the maximum levels of PAHs in food, the risk assessment of PAH carcinogenicity has been widely evaluated on the basis of BaP levels. Risk assessment, involving exposure assessment and risk characterization, represents an important aspect in the endeavor to thoroughly monitor PAH concentrations in food. Exposure assessment is generally performed using the toxic equivalency quotient of BaP (TEQBaP) [24]. BaP is used as an indicator to estimate the concentration and toxicity equivalency factor of each congener in the PAH mixture. Subsequently, cancer risk estimates are achieved via the incremental lifetime cancer risk (ILCR) and the margin of exposure (MOE) [24; 90; 91]. The ILCR approach is based on the estimation of the chronic daily intake (CDI) and the cancer risk of BaP. The MOE is estimated based on the benchmark dose lower confidence limit (BMDL) and the CDI [24; 90]. In spite of the modest amounts that they contain, cereals and cereal products were determined to be significant sources of PAH ingestion due to their substantial consumption. Vegetable fats and oils, which have a greater proportion of PAHs than other dietary groups, are another significant factor. Similarly, meat and meat products tend to lead to increased PAH intakes when they make up a significant portion of the diet [2; 89; 23]. Table 1 provides an outline of the representative findings informing on PAH prevalence in meat, vegetable oils, and cereal products.