Heterocyclic amines,meat intake,and association with colon cancer in a population-based study

The authors examined the association between colon cancer and meat intake categorized by level of doneness, cooking method, and estimated levels of heterocyclic amines (HCAs), benzo[a]pyrene, and mutagenicity. Data were collected as part of a population-based, case-control study of colon cancer in North Carolina between 1996 and 2000 that included 701 African-American (274 cases, 427 controls) and 957 White (346 cases, 611 controls) participants. Odds ratios were calculated by using unconditional logistic regression, comparing the fifth to the first quintile levels of intake or exposure. Intake of red meat was positively associated with colon cancer (odds ratio (OR) = 2.0, 95% confidence interval (CI): 1.3, 3.2). Associations with meat intake by cooking method were strongest for pan-fried red meat (OR = 2.0, 95% CI: 1.4, 3.0). Associations with meat intake by doneness were strongest for well-/very well done red meat (OR = 1.7, 95% CI: 1.2, 2.5). The strongest association for individual HCAs was reported for 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) across all levels of exposure, with odds ratios of 1.8-2.0. Overall, sophisticated exposure measures were used to report modest, positive associations between red meat intake and colon cancer consistent with the hypothesis that HCAs may be among the etiologically relevant compounds in red meat.     

Heterocyclic Aromatic Amine [HCA] Intake and Prostate Cancer Risk: Effect Modification by Genetic Variants

The association between heterocyclic aromatic amine (HCA) intake and prostate cancer (PCa) risk may be modified by genetic variation in enzymes involved in HCA metabolism. We examined this question in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition Heidelberg cohort. The study included 204 PCa cases and 360 matched controls. At baseline, participants provided dietary and lifestyle data and blood samples that were used for genotyping. Dietary HCA intake—2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine (PhIP), 2-amino-3,8-dimethylimidazo [4,5-f]quinoxaline (MeIQx), and 2-amino-3,4,8-dimethylimidazo [4,5-f]quinoxaline (DiMeIQx—was estimated using information on meat consumption, cooking methods, and browning degree. Risk estimates for gene × HCA interactions were calculated by unconditional logistic regression. We found inverse associations between PhIP, MeIQx, or DiMeIQx intake and PCa risk when having <2 deletions of the GSTT1 and GSTM1 genes (P _interaction: 0.03, 0.01, and 0.03, respectively), which is supported by analysis of darkly browned meat consumption data. Statistically significant effect modification of both HCA (DiMeIQx) and darkly browned meat intake and PCa risk was observed for allelic variants of MnSOD (rs4880) (P _interaction: 0.02). Despite limitations due to study size, we conclude that the association between HCA intake and PCa risk could be modified by polymorphisms of GSTT1, GSTM1, and MnSOD.     

Polymorphisms in Xenobiotic Metabolizing Genes,Intakes of Heterocyclic Amines and Red Meat,and Postmenopausal Breast Cancer

Heterocyclic amines (HCAs) are mutagenic compounds generated when meats are cooked at high temperature and for long duration. The findings from previous studies on the relation between HCAs and breast cancer are inconsistent, possibly because of genetic variations in the enzymes metabolizing HCAs. To evaluate whether the associations of intakes of estimated HCAs, meat-derived mutagenicity (MDM), and red meat with risk of postmenopausal breast cancer were modified by N-acetyltransferase 2 (NAT2) acetylator genotype or cytochrome P450 1A2-164 A/C (CYP1A2) polymorphism, we conducted a nested case-control study with 579 cases and 981 controls within a prospective cohort, the Nurses’ Health Study. HCAs and MDM intakes were derived using a cooking method questionnaire administered in 1996. NAT2acetylator genotype, the CYP1A2 polymorphism, and intakes of HCAs, MDM, and red meat were not associated with risk of postmenopausal breast cancer. There was also no interaction between NAT2 acetylator genotype or CYP1A2 polymorphism and HCAs and MDM and red meat intake in relation to breast cancer. These results do not support the hypothesis that genetic polymorphisms of xenobiotic enzymes involved in the metabolism of HCAs may modify the associations between intakes of red meat or meat-related mutagens and breast cancer risk.     

Meat intake is not associated with risk of non-Hodgkin lymphoma in a large prospective cohort of U.S. men and women

Meat intake has been inconsistently associated with risk of non-Hodgkin lymphoma (NHL), a heterogeneous group of malignancies of the lymphoid tissue etiologically linked to immunomodulatory factors. In a large U.S. cohort, we prospectively investigated several biologically plausible mechanisms related to meat intake, including meat-cooking and meat-processing compounds, in relation to NHL risk by histologic subtype. At baseline (1995-1996), participants of the NIH-AARP Diet and Health Study completed a diet and lifestyle questionnaire (n = 492,186), and a subcohort (n = 302,162) also completed a questionnaire on meat-cooking methods and doneness levels. Over a mean of 9 y of follow-up, we identified 3611 incident cases of NHL. In multivariable Cox proportional hazards regression models, we found no association between intake of red meat, processed meat, fish, poultry, heme iron, nitrite, nitrate, animal fat, or protein and NHL risk. MeIQx (2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline) and DiMeIQx (2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline), heterocyclic amines formed in meats cooked to well done at high temperatures, were inversely associated with chronic lymphocytic leukemia/small lymphocytic lymphoma [n = 979; HR (95% CI) for the highest vs. lowest quintile of intake: 0.73 (0.55, 0.96) and 0.77 (0.61, 0.98), respectively]. In this large U.S. cohort, meat intake was not associated with NHL or any histologic subtypes of NHL. Contrary to findings in animal models and other cancer sites, meat-cooking and -processing compounds did not increase NHL risk.     

Mutagenicity of food-derived carcinogens and the effect of antioxidant vitamins

The food-derived heterocyclic amines (HCAs) 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) are mutagenic in the Ames test and produce tumors in laboratory animals, including monkeys. These HCAs have also been shown to induce gene mutations in vivo. To assess the antimutagenic effects of dietary antioxidant vitamins, beta-carotene, ascorbic acid (vitamin C), and alpha-tocopherol (vitamin E), on food-borne mutagenes/carcinogens, we evaluated the mutagenic activity of the compounds alone or combined with antioxidant vitamins. We utilized the rat lymphocyte mutation assay at the hypoxanthine guanine phosphoribosyl transferase (Hprt) locus. Female Fischer 344 rats treated with different doses (0, 2.5, 5.0, 25.0, and 50.0 mg/kg) of the carcinogens were sacrificed 5 wk after mutagen treatment. Although IQ and MeIQ slightly increased mutation frequency (MF) at some doses, a significant (P < 0.0009) increase in MF was found in animals exposed to MeIQx at 25 mg/kg. PhIP was the most mutagenic of the HCAs, with increases (P < 0.0001) in MF detected at all dose levels compared with controls. Because PhIP was the most mutagenic, it was selected for studies using the dietary antioxidant vitamins. Addition of antioxidant vitamins, singly or in a mixture, caused a significant (P < 0.0001) decrease in PhIP-induced Hprt MF. Vitamin E was the most effective at decreasing Hprt MF. In addition, we determined whether carcinogen metabolism would be affected by ingestion of vitamins. The activities of endogenous detoxification enzymes, glutathione S-transferase and glutathione peroxidase (GPx), were thus examined. Intake of beta-carotene and vitamin C without the carcinogen resulted in an increase (P < 0.05) in GPx activity. Also a modest increase in GPx activity was seen in animals that received the antioxidant mixture alone. Although the mechanisms of action of the antioxidants remain to be determined, the results indicate that dietary-derived HCA treatment induced MF in rat lymphocytes and suggest that antioxidants in food or taken as supplements could, in part, counteract such mutagenic activities.     

Heterocyclic aromatic amine [HCA] intake and prostate cancer risk: effect modification by genetic variants

The association between heterocyclic aromatic amine (HCA) intake and prostate cancer (PCa) risk may be modified by genetic variation in enzymes involved in HCA metabolism. We examined this question in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition Heidelberg cohort. The study included 204 PCa cases and 360 matched controls. At baseline, participants provided dietary and lifestyle data and blood samples that were used for genotyping. Dietary HCA intake-2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine (PhIP), 2-amino-3,8-dimethylimidazo [4,5-f]quinoxaline (MeIQx), and 2-amino-3,4,8-dimethylimidazo [4,5-f]quinoxaline (DiMeIQx-was estimated using information on meat consumption, cooking methods, and browning degree. Risk estimates for gene × HCA interactions were calculated by unconditional logistic regression. We found inverse associations between PhIP, MeIQx, or DiMeIQx intake and PCa risk when having <2 deletions of the GSTT1 and GSTM1 genes (P(interaction): 0.03, 0.01, and 0.03, respectively), which is supported by analysis of darkly browned meat consumption data. Statistically significant effect modification of both HCA (DiMeIQx) and darkly browned meat intake and PCa risk was observed for allelic variants of MnSOD (rs4880) (P(interaction): 0.02). Despite limitations due to study size, we conclude that the association between HCA intake and PCa risk could be modified by polymorphisms of GSTT1, GSTM1, and MnSOD.     

Effects of marinating with Asian marinades or western barbecue sauce on PhIP and MeIQx formation in barbecued beef

Heterocyclic aromatic amines (HAAs), a group of chemicals formed during high-temperature cooking of meat and fish, are potent mutagens and are suspected to play a role in colorectal cancer. A recent study suggested that marinating meat may offer a way to reduce HAA formation. Hawaii's diverse ethnic populations, which are at various risks of colorectal cancer, often use traditional marinades when cooking meat. We compared the HAA content of beef steaks marinated overnight with teriyaki sauce, turmeric-garlic sauce, or commercial honey barbecue sauce with that of unmarinated steaks. The levels of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) were determined by liquid-liquid extraction and gas chromatography-mass spectrometry. Beef steaks marinated with teriyaki sauce had 45% and 67% lower PhIP level at 10 minutes (p = 0.002) and 15 minutes (p = 0.001) of cooking time as well as 44% and 60% lower MeIQx levels at 10 minutes (p = 0.008) and 15 minutes (p = 0.001), respectively, than unmarinated meat. Lower levels of PhIP and MeIQx were also observed in meat marinated with turmeric-garlic sauce. In contrast, marinating with barbecue sauce caused a 2.9- and 1.9-fold increase in PhIP (p < or = 0.005) and a 4- and 2.9-fold increase in MeIQx (p < or = 0.001) at 10 and 15 minutes, respectively. Differences in the mutagenic activities of marinated and unmarinated steaks, as measured by the Ames assay, paralleled the differences in PhIP and MeIQx levels. Future studies should test the effects of specific ingredients, including the water content of marinades, and the effect of reapplying barbecue sauce during cooking (to reduce charring) on HAA formation.     

Meat consumption, cooking practices, meat mutagens, and risk of prostate cancer

Consumption of red meat, particularly well-done meat, has been associated with increased prostate cancer risk. High-temperature cooking methods such as grilling and barbecuing may produce heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs), which are known carcinogens. We assessed the association with meat consumption and estimated HCA and PAH exposure in a population-based case-control study of prostate cancer. Newly diagnosed cases aged 40-79 years (531 advanced cases, 195 localized cases) and 527 controls were asked about dietary intake, including usual meat cooking methods and doneness levels. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariate logistic regression. For advanced prostate cancer, but not localized disease, increased risks were associated with higher consumption of hamburgers (OR = 1.79, CI = 1.10-2.92), processed meat (OR = 1.57, CI = 1.04-2.36), grilled red meat (OR = 1.63, CI = 0.99-2.68), and well-done red meat (OR = 1.52, CI = 0.93-2.46), and intermediate intake of 2-amino-1-methyl1-6-phenylimidazo[4,5-b]pyridine (PhIP) (Quartile 2 vs. 1: OR = 1.41, CI = 0.98-2.01; Quartile 3 vs. 1: OR = 1.42, CI = 0.98-2.04), but not for higher intake. White meat consumption was not associated with prostate cancer. These findings provide further evidence that consumption of processed meat and red meat cooked at high temperature is associated with increased risk of advanced, but not localized, prostate cancer.     

Plasma Carotenoids and Retinol and Overall and Breast Cancer Risk: A Nested Case-Control Study

Experimental studies suggest that carotenoids and retinol may play a role in carcinogenesis, but epidemiological evidence is lacking. We investigated the prospective associations between plasma concentrations of major carotenoids and retinol, and overall and breast cancer risk. A nested case-control study included all first incident cancer cases diagnosed in the SU.VI.MAX cohort between 1994 and 2002 (n = 159 cases, 1 matched control/case). Baseline plasma concentrations of carotenoids and retinol were measured by high-performance liquid chromatography. Conditional logistic regression was used to assess odds ratios for an increase of 0.1 μmol/L [odds ratio (OR)] and 95% confidence intervals (CI). Plasma β-carotene (OR = 0.95, 95% CI = 0.90–0.99, P_trend = 0.04) and β-cryptoxanthin concentrations (OR = 0.89, 95% CI = 0.81–0.99, P_trend = 0.03) were inversely associated with overall cancer risk. Plasma β-cryptoxanthin concentration was inversely associated with breast cancer risk (OR = 0.83, 95% CI = 0.71–0.96, P_trend = 0.02). The OR between plasma lycopene concentration and overall cancer risk was 1.07 (0.99–1.15), P_trend = 0.06. This association turned significant (P_trend = 0.01) when excluding cancer cases diagnosed during the first year of follow-up. This prospective study suggests an inverse association between plasma concentrations of β-cryptoxanthin and both overall and breast cancer risk, and an inverse association between β-carotene and overall cancer risk. The direct association between lycopene concentration and cancer risk deserves further investigation.     

Feeding of a well‐cooked beef diet containing a high heterocyclic amine content enhances colon and stomach carcinogenesis in 1,2‐dimethylhydrazine‐treated rats

Epidemiologic studies have linked the consumption of red meat and the consumption of highly browned meats containing high levels of heterocyclic aromatic amines (HCAs) to increased risk of colorectal cancer or polyps. The present study determined the effects of long‐term feeding of beef‐containing diets with low and high levels of HCAs (in the context of a low or high beef tallow diet) on a standard 1,2‐dimethylhydrazine (DMH)‐induced colon tumorigenesis protocol. Very lean beef was cooked by a variety of methods at different temperatures, and the levels of the major HCAs (2‐amino‐3,8‐dimethylimidazo[4,5‐f]quinoxaline, 2‐amino‐3,4,8‐trimethylimidazo[4,5‐f]quinoxaline, and 2‐amino‐l‐methyl‐6‐phenylimidazo[4,5‐f]pyridine) were measured by high‐performance liquid chromatogra‐phy. Diets incorporating beef containing low or high levels of HCAs were fed for 12 weeks, during which DMH was administered to induce colon tumors, followed by various dietary regimens as promotional stimuli. Feeding of a beef diet high in HCAs resulted in more DMH‐induced colon adenocarcinomas, but only in the context of a low‐fat diet. The high‐HCA diets increased stomach tumors in all DMH‐treated rats. An apparent interaction of high HCA with a high fat level reduced the colon tumor incidence and tumor numbers in those diets containing both factors. These results support the epidemiologic data linking well‐cooked meat to increased risk for colon and stomach cancer, but the role of dietary fat level remains puzzling.     

The Association between Coffee Consumption and Risk of Colorectal Cancer in a Korean Population

This study was performed to investigate the association between coffee consumption and risk of colorectal cancer in a Korean population and examine whether the association can be altered by adjustment for intake of coffee additives. We conducted a case-control study involving 923 colorectal cancer cases and 1846 controls matched by sex and age (within 5 years). A semi-quantitative food frequency questionnaire was used to assess coffee intakes. High coffee consumption was associated with lower odds of developing colorectal cancer (≥3 cups/day vs. no drinks, OR = 0.68; 95% CI: 0.49–0.96). When we additionally controlled for consumption of coffee additives including sugar and cream, the inverse association became stronger (≥3 cups/day vs. no drinks, OR = 0.22; 95% CI: 0.14–0.33), and a significant inverse linear trend was shown (P_trend < 0.0001). The inverse associations were observed for proximal (P_trend = 0.0001) and distal (P_trend = 0.0003) colon cancer, and rectal cancer (P_trend < 0.0001) in the stratified analysis by anatomical sub-sites. Regarding sex, inverse associations between coffee consumption and colorectal cancer were found for men (P_trend < 0.0001) and women (P_trend = 0.0021). In the stratified analysis by obese status of subjects, inverse linear trends were observed in both non-obese and obese people (P_trend < 0.0001). High coffee consumption may be associated with a lower risk of colorectal cancer in the Korean population and the degree of decrease in the odds of developing colorectal cancer changes by adjustment for intake of coffee additives.     

The effect of rosemary on the mutagenic activity of heterocyclic amines extracted from common food consumed in Saudi Arabia

Meat intake may increase cancer risk as heterocyclic amines (HCAs) are one of the food mutagens produced in meat cooked at high temperature. The consumption of meat in Saudi Arabia is high compared with other developing countries and the incidence of cancer has been increasing during the past 30 years. The present study aimed to quantitatively determine the effect of rosemary on the mutagenic activity and the amount of HCAs formed in beef Shawerma, grilled chicken and fried liver as an attempt to minimize the carcinogenic risk of HCAs formed in these commonly consumed meat dishes. Surprisingly, rosemary extracts (2%, 5%, 10% and 15%) apparently enhanced the total amount of HCAs measured in beef Shawerma, whereas 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) was the only mutagenic amine inhibited by 2% rosemary with a reduction up to 61.6% compared with control. In grilled chicken, the total amount of HCAs measured in 2% rosemary samples was reduced seven-fold lower than the control level, whereas PhIp and 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (TrpP1) were inhibited to non-detectable levels. These data demonstrate that 2% rosemary may play an important role in attenuating the production of PhIP in both Shawerma and fried chicken. In fried liver, HCAs were not detected either in the control or in 2% treated samples whereas augmented levels of TrpP1 were measured in 5%, 10% and 15% rosemary. The mutagenic activity of HCAs extracted from all beef Shawerma and grilled chicken treated samples increased over the control sample using Salmonella typhimurium TA100. In fried liver, the mutagenic activity detected in the control sample was higher than treated samples, which suggests that S. typhimurium TA100 might be less sensitive in detecting the mutagenic response of TrpP1 extracted from the real food system. We believe more research is needed to assess the role of antioxidants in the formation of HCAs in order to optimize both safety and quality of our diets.     

Dietary Iron Intake and Risk of Endometrial Cancer: A Population-Based Case-Control Study in Shanghai,China

Dietary red meat and animal fat have been linked to endometrial cancer (EC) risk, but the impact of bioavailable iron in animal-derived foods has been less well studied. Our objective was to investigate the effects of iron and fats on the risk of EC in a large, population-based, case-control study. The Shanghai Endometrial Cancer Study enrolled 1,204 EC cases and 1,212 controls who completed in-person interviews, including a food frequency questionnaire. Animal-derived iron and fat intakes were calculated from dietary intakes and food composition tables. Logistic regression models were used to evaluate independent and joint effects of iron and fat on EC risk. Animal-derived iron intake was positively associated with EC risk [adjusted OR = 1.9; 95% CI = 1.4–2.7, P _trend < 0.01, highest vs. lowest quartile], predominantly after menopause (OR = 2.2; 95%CI = 1.4–3.4, P _trend < 0.01) and in women with BMI ≥ 25 kg/m ² (OR = 3.2; 95% CI = 1.4–7.5 in postmenopausal obese women, P _trend < 0.01). Animal-derived fat was also associated with postmenopausal EC risk (OR = 1.7; 95% CI = 1.2–2.5, P _trend < 0.01). Multiplicative interactions between animal-derived iron and BMI or animal-derived fat intake were not observed. Animal-derived iron intake is associated with increased risk of EC after menopause and among obese women. Avoidance of animal-derived (heme) iron may reduce the risk of EC in these women.     

Dietary exposure to heterocyclic amines in a Chinese population

Heterocyclic aromatic amines (HAAs) formed in meat during high-temperature cooking have been associated with risk of colorectal and breast cancer. Incidence of these cancers is increasing in Singapore, a country with 77% ethnic Chinese. The purpose of this study was to estimate HAA levels in the Chinese diet and individual levels of exposure to these compounds because little is known. Twenty-five samples (each pooled from three sources) of meat and fish, cooked as commonly consumed, were analyzed by high-performance liquid chromatography for concentrations (ng/g) of 2-amino-3-methylimidazo[4,5-f]quinoline, 2-amino-3, 4-dimethylimidazo[4,5-f]quinoline (MeIQ), 2-amino-3,8- dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-3, 4,8-trimethylimidazo[4,5-f]quinoxaline (4,8-DiMeIQx), 2- amino-3,7,8-trimethylimidazo[4,5-f]quinoxaline, 2-amino -1,6-dimethylfuro[3,2-e]imidazo[4,5-b]pyridine, and 2- amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). Dietary meat consumption data (g/day), including meat type and cooking method, were gathered from food-frequency questionnaires completed by 497 randomly sampled Chinese men and women aged 20-59 yr. PhIP, MeIQx, and 4,8-DiMeIQx were the most abundant HAAs detected. Total HAA concentrations ranged from <0.10 to 6.77 ng/g, of which Chinese-style roasted pork had the highest levels. The estimated mean daily exposure to HAA was 49.95 ng/day (P10 14.0 ng/day, P90 95.8 ng/day); this was 50% higher among younger (20-39 yr) compared with older individuals. Seven specific meat-cooking method combinations contributed 90.1% of this intake, namely, pan-fried fish, pork, and chicken, deep-fried chicken as well as fish, roasted/barbecued pork, and grilled minced beef.     

Cooked meat and risk of breast cancer--lifetime versus recent dietary intake

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs) are carcinogens formed in or on the surface of well-done meat, cooked at high temperature. METHODS: We estimated breast cancer risk in relation to intake of cooked meat in a population-based, case-control study (1508 cases and 1556 controls) conducted in Long Island, NY from 1996 to 1997. Lifetime intakes of grilled or barbecued and smoked meats were derived from the interviewer-administered questionnaire data. Dietary intakes of PAH and HCA were derived from the self-administered modified Block food frequency questionnaire of intake 1 year before reference date. Unconditional logistic regression was used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Modest increased risk was observed among postmenopausal, but not premenopausal, women consuming the most grilled or barbecued and smoked meats over the life course (OR = 1.47; CI = 1.12-1.92 for highest vs. lowest tertile of intake). Postmenopausal women with low fruit and vegetable intake, but high lifetime intake of grilled or barbecued and smoked meats, had a higher OR of 1.74 (CI = 1.20-2.50). No associations were observed with the food frequency questionnaire-derived intake measures of PAHs and HCAs, with the possible exception of benzo(alpha)pyrene from meat among postmenopausal women whose tumors were positive for both estrogen receptors and progesterone receptors (OR = 1.47; CI = 0.99-2.19). CONCLUSIONS: These results support the accumulating evidence that consumption of meats cooked by methods that promote carcinogen formation may increase risk of postmenopausal breast cancer.     

Dietary Fat,Cooking Fat,and Breast Cancer Risk in a Multiethnic Population

Our objective was to examine the association between dietary fat intake, cooking fat usage, and breast cancer risk in a population-based, multiethnic, case-control study conducted in the San Francisco Bay area. Intake of total fat and types of fat were assessed with a food frequency questionnaire among 1,703 breast cancer cases diagnosed between 1995 and 1999 and 2,045 controls. In addition, preferred use of fat for cooking was assessed. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). High fat intake was associated with increased risk of breast cancer (highest vs. lowest quartile, adjusted OR = 1.35, 95% CI = 1.10–1.65, P _trend < 0.01). A positive association was found for oleic acid (OR = 1.55, 95% CI = 1.14–2.10, P _trend < 0.01) but not for linoleic acid or saturated fat. Risk was increased for women cooking with hydrogenated fats (OR = 1.58, 95% CI = 1.20–2.10) or vegetable/corn oil (rich in linoleic acid; OR = 1.30, 95% CI = 1.06–1.58) compared to women using olive/canola oil (rich in oleic acid). Our results suggest that a low-fat diet may play a role in breast cancer prevention. We speculate that monounsaturated trans fats may have driven the discrepant associations between types of fat and breast cancer.     

Red Meat and Processed Meat Consumption and Nasopharyngeal Carcinoma Risk: A Dose-response Meta-analysis of Observational Studies

The purpose of this study is to clarify and quantify the potential dose-response association between the intake of total red and total processed meat and risk of nasopharyngeal carcinoma (NPC). Relevant studies were identified by searching PubMed, EMBASE, and Chinese databases (CNKI and Wanfang). The summary relative risk (RR) with 95% confidence interval (95%CI) was calculated. A total of 15 independent studies with 12,735 subjects were identified. Compared with the low-rank intake, the summary RR of NPC was 1.35 (95%CI, 1.21–1.51) for total red meat and 1.46 (95%CI, 1.34–1.64) for total processed meat. For the moderate-rank intake, the summary RR of NPC was 1.54 (95%CI, 1.36–1.79) for total red meat and 1.59 (95%CI, 1.3–1.90) for total processed meat. The summary RR for high-rank intake was 1.71 (95%CI, 1.14–2.55) for total red meat and 2.11 (95%CI, 1.31–3.42) for total processed meat. The combined estimates showed obvious evidence of statistically significant association between total red and total processed meat consumption dose and risk of NPC (P_trend< 0.01). In conclusion, our data suggest that a high intake of total red or total processed meat is associated with a significantly increased risk of NPC.     

Physical Activity,Diet, and Pancreatic Cancer: A Population-Based,Case-Control Study in Minnesota

Although mounting evidence suggests that insulin resistance is involved in pancreatic carcinogenesis, few epidemiologic studies have comprehensively investigated the role of lifestyle factors influencing this metabolic disorder in the etiology of pancreatic cancer. We sought to examine this problem in a case-control study conducted in 1994–1998 in Minnesota. Cases (n = 186), aged 20 yr or older, were ascertained from all hospitals in the metropolitan area of the Twin Cities and the Mayo Clinic; from the latter, only cases residing in the Upper Midwest of the United States were recruited. Controls (n = 554) were randomly selected from the general population and frequency matched to cases by age (within 5 yr) and sex. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using unconditional logistic regression. After adjustment for confounders, physical activity was associated with a reduced risk, but this protective effect was confined to light activity and moderate activity only (OR = 0.55, 95% CI = 0.30–0.97, P _trend = 0.038 and OR = 0.51, 95% CI = 0.28–0.93, P _trend = 0.07, for highest vs. lowest quartile, respectively). An increased risk was found for dietary intakes of energy and fat but was statistically significant for saturated and polyunsaturated fat only. Of note, no appreciable difference in the magnitude of the associations existed between saturated, monounsaturated, and polyunsaturated fat. Compared with individuals in the lowest quartile of fiber intake, the risk was approximately halved for those in the third (OR = 0.49, 95% CI = 0.26–0.94) and the highest quartile (OR = 0.52, 95% CI = 0.21–1.30). Our study lends support to the hypothesis that dietary and other lifestyle factors influencing insulin resistance modulate pancreatic cancer risk.     

PAHs and PM2.5 emissions and female breast cancer incidence in metro Atlanta and rural Georgia

Environmental chemical exposure could be an important etiologic factor for geographic differences in breast cancer incidence. In this study, we examined emissions of polycyclic aromatic hydrocarbons (PAHs) and PM_2.5 in relation to breast cancer incidence in metro Atlanta and rural Georgia by analyzing data from the Surveillance, Epidemiology, and End Results Program and the Environmental Protection Agency. The results showed that metro Atlanta had a significantly higher age-adjusted annual incidence rate of female breast cancer than rural Georgia (132.6 vs. 113.7 per 100,000) for 1992–2011. Emissions of both PAHs [adjusted β = 0.568 (95 % CI: 0.209, 0.927); p = 0.004] and PM_2.5 [adjusted β = 2.964 (95 % CI: 0.468, 5.459); p = 0.023] were significantly associated with breast cancer incidence in metro Atlanta area. This study suggests that ambient air pollution, especially PAHs and PM_2.5, could have a significant impact on the increased incidence of female breast cancer in urban areas.     

Dairy Products and Cancer Risk in a Northern Sweden Population

Abstract

The role of dairy products in cancer is unclear. We assessed consumption of fermented milk, non-fermented milk, cheese, and butter, estimated from semi-quantitative food frequency questionnaires, in relation to prospective risk of breast, prostate, colorectal, smoking-, and obesity-related cancers in 101,235 subjects, including 12,552 cancer cases, in the population-based Northern Sweden Health and Disease Study. Most analyses (n?=?20) rendered null results. In men, we observed an increased prostate cancer risk among high-consumers of cheese (hazard ratio (HR) for highest vs. lowest quintile (Q5–Q1), 1.11; 95% CI, 0.97–1.27; P^trend?=?0.013). In women, high-consumers of cheese had a decreased risk of overall cancer (HR Q5–Q1, 0.95; 95% CI, 0.88–1.04; P^trend?=?0.039), smoking-related (HR Q5–Q1, 0.84; 95% CI, 0.72–0.97; P^trend ≤ 0.001), and colorectal cancers (HR Q5–Q1, 0.82; 95% CI, 0.63–1.07; P^trend?=?0.048). Butter yielded a weak decreased obesity-related cancer risk in women (HR Q5–Q1, 0.91; 95% CI, 0.81–1.02; P^trend?=?0.049). Fermented milk yielded HRs below zero in women, but with no clear linear associations. In conclusion, this study does not support any major adverse or beneficial effects of fermented milk, non-fermented milk, cheese, and butter in the diet from a cancer risk perspective.