A comparison of the tumors induced by coal tar and benzo[a]pyrene in a 2-year bioassay

Culp, Sandra J.; Gaylor, David W.; Sheldon, Winslow G.; Goldstein, Lawrence S.B.; Beland, Frederick A.

doi:10.1093/carcin/19.1.117

Cited by 251 publications

(256 citation statements)

References 17 publications

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“…40 Epidemiologic studies have directly investigated the association between dietary intake of PAHs and colorectal neoplasms and found a positive association between benzo(a)-pyrene and CRA. 41 The high saturated fat content of red and processed meat is also the proposed culprit for the increased …”

Section: Discussionmentioning

confidence: 99%

Red and processed meat intake and risk of colorectal adenomas: A meta‐analysis of observational studies

Xian

et al. 2012

Intl Journal of Cancer

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Inconsistent results regarding the association between red and processed meat intake and the risk of colorectal adenoma (CRA), the precursor of colorectal cancer (CRC), have been reported. To provide a quantitative assessment of this association, we summarized the evidence from observational studies. Relevant studies were identified in MEDLINE and EMBASE until December 31, 2011. Summary relative risks (SRRs) with 95% confidence intervals (CIs) were pooled with a random-effects model. Between-study heterogeneity was assessed using the Cochran's Q and I 2 statistics. A total of 21 studies (16 casecontrol studies and five cohort/nested case-control studies) were included in this meta-analysis. The SRRs of CRA were 1.36 (95% CI 5 1.17-1.58) for every 100 g/day increase in red meat intake, and 1.24 (95% CI 5 1.12-1.36) for the highest versus the lowest level of red meat intake. Nonlinear dose-response meta-analysis indicated that CRA risk increased approximately linearly with increasing intake of red meat up to~90 g/day, where the curve reached its plateau. Subgrouped analyses revealed that the increased risk of CRA with intake of red meat was independent of geographic locations, design and confounders. The SRRs of CRA was 1.28 (95% CI 5 1.03-1.60) for per 50 g/day increase in processed meat intake, and 1.17 (95% CI 5 1.08-1.26) for the highest versus the lowest level of processed meat intake. Increased intake of red and processed meat is associated with significantly increased risk of CRA.The incidence of and mortality from colorectal cancer (CRC) have been on the rise worldwide. 1 Annually, $1 million new cases of CRC are diagnosed, and nearly 530,000 individuals may die from this disease, equivalent to $8% of all cancer-related deaths worldwide.1 The World Cancer Research Fund (WCRF)/American Institute for Cancer Research (AICR) concluded in a report published in 2007 that high consumption of red and processed meat convincingly increases the risk of CRC.2 In this regard, a more recent meta-analysis of 24 prospective studies of CRC showed an increased risk of 17% (95% confidence interval [CI] ¼ 5-31%) per 100 g/day increased intake of red meat and of 18% (95% CI ¼ 10-28) per 50 g/day increased intake of processed meat.3 One underlying cause might be the formation of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) during cooking or processing of meat, both of which are potent mutagens in rodents and humans. [4][5][6][7] Additionally, heme iron from red meat might be another potential risk factor for CRC development. 8It has been established that most CRCs arise from colorectal adenoma (CRA) by a process referred to as the adenoma-carcinoma sequence.9 On the basis of this theory, we may assume that adenoma and carcinoma share a common etiology and similar epidemiological features. Therefore, better information about risk factors for adenomas might permit more rational development of intervention studies with adenomas as end points.

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Section: Discussionmentioning

confidence: 99%

Red and processed meat intake and risk of colorectal adenomas: A meta‐analysis of observational studies

Xian

et al. 2012

Intl Journal of Cancer

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“…Lung tumors were not observed when BaP was administered in the diet to B6C3F1 mice (Culp et al, 1998). In studies of lung tumor induction by implantation in rats, BaP is more carcinogenic than the benzofluoranthenes or indeno [1,2,3-cd]pyrene (Deutsch-Wenzel et al, 1983).…”

Section: Tobacco Smoke Carcinogens and Cancermentioning

confidence: 99%

“…N-nitrosodiethylamine and N-nitrosopiperidine are two other smoke constituents that could be involved in esophageal tumor induction in smokers. BaP induces some esophageal tumors when administered to mice in the diet (Culp et al, 1998). The risk for esophageal cancer in humans is also enhanced by alcohol consumption (McCoy and Wynder, 1979).…”

Section: Tobacco Smoke Carcinogens and Cancermentioning

confidence: 99%

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

et al. 2002

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It is estimated that cigarette smoking kills over 1 000 000 people each year by causing lung cancer as well as many other neoplasmas. p53 mutations are frequent in tobaccorelated cancers and the mutation load is often higher in cancers from smokers than from nonsmokers. In lung cancers, the p53 mutational patterns are different between smokers and nonsmokers with an excess of G to T transversions in smoking-associated cancers. The prevalence of G to T transversions is 30% in smokers' lung cancer but only 12% in lung cancers of nonsmokers. A similar trend exists, albeit less marked, in laryngeal cancers and in head and neck cancers. This type of mutation is infrequent in most other tumors aside from hepatocellular carcinoma. At several p53 mutational hotspots common to all cancers, such as codons 248 and 273, a large fraction of the mutations are G to T events in lung cancers but are almost exclusively G to A transitions in non-tobacco-related cancers. Two important classes of tobacco smoke carcinogens are the polycyclic aromatic hydrocarbons (PAH) and the nicotine-derived nitrosamines. Recent studies have indicated that there is a strong coincidence of G to T transversion hotspots in lung cancers and sites of preferential formation of PAH adducts along the p53 gene. Endogenously methylated CpG dinucleotides are the preferred sites for G to T transversions, accounting for more than 50% of such mutations in lung tumors. The same dinucleotide, when present within CpGmethylated mutational reporter genes, is the target of G to T transversion hotspots in cells exposed to the model PAH compound benzo[a]pyrene-7,8-diol-9,10-epoxide. As summarized here, a number of other tobacco smoke carcinogens also can cause G to T transversion mutations. The available data suggest that p53 mutations in lung cancers can be attributed to direct DNA damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations.

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“…Parallel treatment with B[a]P induced tumors of the forestomach, esophagus, and tongue. A comparison of the results indicated that the lung and liver tumors appeared to be due to other genotoxic components in coal tar besides B[a]P (Culp et al 1998). Many PAHs have been tested by topical application to the skin of mice or by subcutaneous injection to identify the relationship between structural characteristics of the compounds, their metabolism, and tumorigenic potency.…”

Section: Pahs and Human Carcinogenesismentioning

confidence: 99%

Cancer Risk Assessment, Indicators, and Guidelines for Polycyclic Aromatic Hydrocarbons in the Ambient Air

Boström¹,

Gerde²,

Hanberg³

et al. 2002

Environ Health Perspect

875

459

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A comparison of the tumors induced by coal tar and benzo[a]pyrene in a 2-year bioassay

Cited by 251 publications

References 17 publications

Red and processed meat intake and risk of colorectal adenomas: A meta‐analysis of observational studies

Red and processed meat intake and risk of colorectal adenomas: A meta‐analysis of observational studies

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

Cancer Risk Assessment, Indicators, and Guidelines for Polycyclic Aromatic Hydrocarbons in the Ambient Air

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