“…While TEQ BaP is directly associated with carcinogenicity, MEQ BaP (mutagenic activity) may not be directly associated with cancer (Zeiger, 1998(Zeiger, , 2001Essumang et al, 2013) and may have implications for other non-cancerous adverse health effects like pulmonary diseases, birth defects, impotency, low intelligent quotient, etc. (DeMarini et al, 2004;Essumang et al, 2013). From the result in Table 6, the TEQ for the seven USEPA priority carcinogens were 0.040 and 0.028 for catfish and solefish smoked traditionally.…”
Section: Cancer and Non-cancer Risk Assessment Of Pahs In Smoked Fishmentioning
confidence: 99%
“…It is known that in mammalian cells, PAHs undergo metabolic activation to diol, and epoxides that bind covalently to cellular macromolecules, including DNA, thereby causing errors in DNA replication and mutations that initiate the carcinogenic process (Rodriguez et al, 1997;Schoket, 1999;Lightfoot et al, 2000;Essumang et al, 2012Essumang et al, , 2013. Polymorphisms causing glutathione transferase deficiencies (GSTM1) may result in elevated breast cancer, lung cancer and other forms of human cancer risk from PAHs (IARC, 1999;Van der Hel et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…PAHs occur as contaminants in different food categories and beverages including water (Belykh et al, 1999), fruit, cereals, oils (Dennis et al, 1983(Dennis et al, , 1991Moret and Conte, 2002), smoked meat (Potthast, 1977;Simko, 2002) and smoked fish (Simko, 1991;Akpan et al, 1994;Lodovici et al, 1995;Moret et al, 1999). Non-processed fish contains low PAHs concentration even when it comes from contaminated water because fishes rapidly metabolize PAHs, resulting in low steady-state level in the tissue (Moret et al, 2000;Chen and Chen, 2005;Wretling et al, 2010;Essumang et al, 2013). The health effects resulting from PAH exposure have recently been discussed extensively in the literature (Shen et al, 2008).…”
) for potential cancer risk. Mean hazard indexes were below 1 (below an acceptable cumulative threshold) ranging from 1.43 x 10 -6 -9.96 x 10 -8 . A significantly high accumulation of PAHs was found in the smoked fish as compared to the non-smoked fish control samples. This study indicates that there is no adverse health effect of PAHs content on consumers of smoked fish species but levels of PAHs present in smoked catfish/solefish prepared using traditional methods may pose elevated cancer risks if consumed at high consumption rates over many years.
“…While TEQ BaP is directly associated with carcinogenicity, MEQ BaP (mutagenic activity) may not be directly associated with cancer (Zeiger, 1998(Zeiger, , 2001Essumang et al, 2013) and may have implications for other non-cancerous adverse health effects like pulmonary diseases, birth defects, impotency, low intelligent quotient, etc. (DeMarini et al, 2004;Essumang et al, 2013). From the result in Table 6, the TEQ for the seven USEPA priority carcinogens were 0.040 and 0.028 for catfish and solefish smoked traditionally.…”
Section: Cancer and Non-cancer Risk Assessment Of Pahs In Smoked Fishmentioning
confidence: 99%
“…It is known that in mammalian cells, PAHs undergo metabolic activation to diol, and epoxides that bind covalently to cellular macromolecules, including DNA, thereby causing errors in DNA replication and mutations that initiate the carcinogenic process (Rodriguez et al, 1997;Schoket, 1999;Lightfoot et al, 2000;Essumang et al, 2012Essumang et al, , 2013. Polymorphisms causing glutathione transferase deficiencies (GSTM1) may result in elevated breast cancer, lung cancer and other forms of human cancer risk from PAHs (IARC, 1999;Van der Hel et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…PAHs occur as contaminants in different food categories and beverages including water (Belykh et al, 1999), fruit, cereals, oils (Dennis et al, 1983(Dennis et al, , 1991Moret and Conte, 2002), smoked meat (Potthast, 1977;Simko, 2002) and smoked fish (Simko, 1991;Akpan et al, 1994;Lodovici et al, 1995;Moret et al, 1999). Non-processed fish contains low PAHs concentration even when it comes from contaminated water because fishes rapidly metabolize PAHs, resulting in low steady-state level in the tissue (Moret et al, 2000;Chen and Chen, 2005;Wretling et al, 2010;Essumang et al, 2013). The health effects resulting from PAH exposure have recently been discussed extensively in the literature (Shen et al, 2008).…”
) for potential cancer risk. Mean hazard indexes were below 1 (below an acceptable cumulative threshold) ranging from 1.43 x 10 -6 -9.96 x 10 -8 . A significantly high accumulation of PAHs was found in the smoked fish as compared to the non-smoked fish control samples. This study indicates that there is no adverse health effect of PAHs content on consumers of smoked fish species but levels of PAHs present in smoked catfish/solefish prepared using traditional methods may pose elevated cancer risks if consumed at high consumption rates over many years.
“…Since individual PAHs have different ability to produce a toxic effect, the toxic equivalency factors (TEFs) (Table 3) are utilized for the estimation of the potential risk of PAH compounds (Essumang et al., 2013; Jiang et al., 2015; Li, Wu et al., 2016). BaP, the most potent carcinogenic and representative PAH, has a reference TEF value of 1.…”
Section: Methodsmentioning
confidence: 99%
“…The sources of PAH in food can come from food processing and preparation, cooking procedures, environmental contamination, and direct contact with nonfood grade mineral oil and contaminated package material (Purcaro et al., 2013). Generally, the amount of PAHs generated during the thermal food processing might cause by many parameters, such as temperature, duration of the treatment, distance from the source of heating, fat content, oxygen accessibility, and the type of combustible used (Akpambang et al., 2009; Essumang, Dodoo, & Adjei, 2013; Lee et al., 2016; Oz & Yuzer, 2016). …”
There is a lack of information regarding the quantitative determination and health risk assessment of polycyclic aromatic hydrocarbons (PAHs) in grilled and fried meat products in Shandong Province of China. The aim of this work was firstly to detect the contamination levels of 15 PAHs in 52 grilled and fried meats consumed by the population of Shandong Province, China. In brief, concentrations of the sum of 15 PAHs in individual samples were ranged from 8.23 to 341 μg/kg with a mean contamination level of 63.3 μg/kg. Moreover, the factors for the formation of PAHs in these samples have been identified and analyzed. One grilled meat sample exceeded the maximum limits of 2 and 12 μg/kg set for BaP and PAH4 by the European Union. For a further step, the mean dietary exposures for total PAHs from grilled and fried meat products were estimated to be 120 and 74.8 ng/kg bw/day, respectively. Finally, the health risk estimation was performed using the incremental lifetime cancer risk (ILCR) approach. The obtained values of four groups were all lower than 10‐4, indicating a slight potential carcinogenic risk of consumer health. This study was the first attempt to provide baseline information of potential health risk of dietary exposure of PAH‐containing grilled and fried meats, which could be useful for health management of the local consumers.
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