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Much of the global variation in cancer incidence has been attributed to environmental factors, such as diet. Thus far, one of the constituents of diet that has been most consistently associated with elevated risks of certain cancers is meat, particularly consumption of red and processed meats. Meat intake varies enormously throughout the globe, with some populations consuming relatively little meat, while in some countries, such as Argentina and Australia, meat provides a large percentage of daily caloric intake.
There have been several reviews of the meat and cancer association, including two large consensus reports from the World Cancer Research Fund (1997) and the Committee on Medical Aspects of Food and Nutrition Policy (1998). The recommendation from these reports was to prevent the average level of red meat and processed meat consumption from rising; people consuming high levels (>140 g/day) were advised to reduce their intake. The WCRF report concluded that an association between meat and colorectal cancer was ‘probable.’ In addition, this report concluded that there was a ‘possible’ association between meat and cancers of the pancreas, prostate, breast, and kidney (World Cancer Research Fund, 1997). The WCRF report is being updated; although the publication has not yet been released, it is likely that the recommendation to limit meat consumption will be strengthened.
The amount of epidemiologic evidence on meat intake and cancer risk varies depending on the anatomic site. All of the studies with cancer as an endpoint have been observational cohort and case-control studies rather than clinical trials, although there have been some controlled feeding studies, which is discussed below. This section summarizes the epidemiologic literature for the cancer sites most commonly thought to have risks modifiable by dietary components. The most stable risk estimates are obtained from meta-analyses or pooled analyses, rather than individual studies.
The relationship between meat consumption and cancer of the colorectum has been studied more extensively than that with other cancer sites. In 2001, a meta-analysis pooled results from 13 prospective studies and concluded that an increase of 100 g/day of all meat or red meat was associated with a statistically significant 12–17% increased risk of colorectal cancer, and an increase of 25 g/day of processed meat was associated with a 49% increased risk (Sandhu et al., 2001). The following year, results from 34 case-control studies and 14 cohort studies of meat intake and colorectal cancer were reviewed, of which 15 case-control studies and nine cohort studies examined red meat intake specifically and 22 case-control and seven cohort studies examined processed meat specifically (Norat et al., 2002). This review found a statistically significant increased risk for colorectal cancer for those in the highest quantile of red meat (RR = 1.35; 95% CI = 1.21–1.51) and processed meat (RR = 1.31; 95% CI= 1.13–1.5) (Norat et al., 2002). More recently, a meta-analysis of the prospective studies through March 2006, which included 19 studies, confirmed the positive association in the summary statistics for both red meat (RR = 1.28; 95% CI = 1.15–1.42) and processed meat (RR = 1.20; 95% CI = 1.11–1.31) in the highest versus lowest categories of intake (Larsson and Wolk, 2006).
In contrast, some researchers have questioned the role of meat in colorectal cancer etiology. A pooled analysis of five cohort studies, each with a high proportion of vegetarians, showed no difference in the risk of mortality from colorectal cancer in vegetarians compared with meateaters (Key et al., 1999). However, this study had a high proportion of vegetarians and very few heavy meat-eaters; furthermore, the definition of regular meat-eaters was those who consumed meat just once per week or more.
Esophageal And Gastric Cancer
There is very little known about meat as a risk factor for esophageal cancer. The first cohort study to investigate this association in a Western population was published in 2006 (Gonzalez et al., 2006); this study examined adenocarcinoma of the esophagus and found no association for meat intake overall, but it did report increased risk for those in the highest tertile of processed meat consumption.
With regard to gastric cancer, total meat intake was not associated with risk in three cohorts (Ito et al., 2003; Kneller et al., 1991; Ngoan et al., 2002). Red meat intake was also not associated with gastric cancer risk in two large case-control studies (Boeing et al., 1991; Ji et al., 1998), but was associated with an elevated risk in several other case-control studies (Chen et al., 2002; Correa et al., 1985; Mathew et al., 2000; Ward et al., 1999; Zhang et al., 1997), although only two reached statistical significance (Correa et al., 1985; Ward et al., 1999). Processed meat consumption has also been associated with risk of gastric cancer in several case-control (Boeing et al., 1991; Correa et al., 1985; Ward et al., 1999; Buiatti et al., 1989; Gonzalez et al., 1991; Hoshiyama and Sasaba, 1992; Risch et al., 1985; Ward et al., 1997) and cohort studies (Kneller et al., 1991; Ngoan et al., 2002; Chyou et al., 1990; Nomura et al., 1990; van den Brendt et al., 2003), but not in others (Ito et al., 2003; Galanis et al., 1998; McCullough et al., 2001). None of the studies mentioned above looked separately at cancers of the gastric cardia and non-cardia, the two main subtypes of gastric cancer. Recently, a large, multicentered cohort within Europe published findings for gastric cancer by sub-site; the authors found significantly elevated risks for non-cardia cancer for total meat (3.5-fold risk), red meat (1.7-fold risk), as well as processed meat (2.5-fold risk), but no associations with gastric cardia cancer (Gonzalez et al., 2006).
Meat intake as a risk factor for pancreatic cancer has been investigated in many case-control studies (Bueno de Mesquita et al., 1991; Falk et al., 1988; Farrow and Davis, 1990; Fernandez et al., 1996; La Vecchia et al., 1990; Lyon et al., 1993; Mizuno et al., 1999; Olsen et al., 1989; Raymond et al., 1987; Silverman et al., 1998; Soler et al., 1998; Anderson et al., 2002; Baghurst et al., 1991; Ghadirian et al., 1995; Gold et al., 1985; Ji et al., 1995; Mack et al., 1986; Norell et al., 1986; Tavani et al., 2000), as well as several cohort studies (Coughlin et al., 2000; Hirayama, 1989; Isaksson et al., 2002; Larsson et al., 2000; Mills et al., 1988; Zheng et al., 1993; Michaud et al., 2003; Nothlings et al., 2005; Stolzenberg-Solomon et al., 2002), with mixed results. The majority of studies reported either positive (Falk et al., 1988; Farrow and Davis, 1990; Lyon et al., 1993; Olsen et al., 1989; Soler et al., 1998; Anderson et al., 2002; Ghadirian et al., 1995; Mack et al., 1986; Norell et al., 1986; Tavani et al., 2000; Hirayama, 1989; Larsson et al., 2006; Mills et al., 1988; Zheng et al., 1993; Nothlings et al., 2005) or null results (Bueno de Mesquita et al., 1991; Falk et al., 1988; Fernandez et al., 1996; La Vecchia et al., 1990; Mizuno et al., 1992; Olsen et al., 1989; Raymond et al., 1987; Silverman et al., 1998; Baghurst et al., 1991; Ji et al., 1995; Coughlin et al., 2000; Michaud et al., 2003; Stolzenberg-Solomon, 2002), although few have reported inverse associations (Bueno di Mesquita et al., 1991; Silverman et al., 1998; Gold et al., 1985; Isaksson et al., 2002).
The findings regarding meat intake and prostate cancer are inconsistent, with some studies reporting no relationship (Bosetti et al., 2004; Cross et al., 2005; Gronberg et al., 1996; Hayes et al., 1999; Hirayama, 1979; Hsing et al., 1990; Whittemore et al., 1995) and others reporting positive associations (Deneo-Pellegrini et al., 1999; Gann et al., 1994; Giovannucci et al., 1993; Le Marchand et al., 1994; Michaud et al., 2001; Schuurman et al., 1999; Veierod et al., 1997; Villeneuve, 1999). Most recently, a large U.S. cohort that examined the association between meat and prostate cancer risk separately in whites and African-Americans found no association in white men, but significantly elevated risks in black men. The relative risk estimates comparing the top to the bottom quartile were 2.0 for red meat, 2.4 for processed meat, and 2.7 for cooked processed meat (2.7-fold risk) (Rodriguez et al., 2006). A racial difference in the association between meat and prostate cancer has been observed previously (Hayes et al., 1999).
The evidence for meat intake as a risk factor for breast cancer is also inconsistent. There have been two reviews of the evidence, one meta-analysis of published literature from 22 case-control and nine cohort studies through July, 2003 (Boyd et al., 2003), and one pooled analysis of eight prospective studies (Missmer et al., 2002). The meta-analysis found an overall positive association for meat intake and breast cancer risk (RR = 1.17; 95% CI = 1.06–1.29), with a stronger association for the cohort studies (RR = 1.32; 95% CI = 1.12–1.56) (Boyd et al., 2003). However, the pooled analysis found no association between total meat or red meat intake and breast cancer risk (Missmer et al., 2002). The two most recent prospective studies found elevated risks for breast cancer with high intake of both red and processed meats (Taylor et al., 2007), specifically for estrogen and progesterone-receptorpositive pre-menopausal breast cancer (RR = 1.97; 95% CI = 1.35–2.88) (Cho et al., 2006).
The incidence rates for non-Hodgkin lymphoma (NHL) have increased since the mid-1970s, yet there are few established risk factors. Dietary risk factors have not been extensively investigated, with the majority of studies suggesting a positive association for fat and protein intake, which led to a few studies that examined meat intake. One cohort study (Chiu et al., 1996) and one large case-control study (Purdue et al., 2004) reported elevated risks for total meat intake and NHL risk, although three other casecontrol studies reported null associations (Cross et al., 2006; Tavani et al., 2007; Ward et al., 1994). The results have been inconsistent with respect to red meat; most studies have not found an association for NHL (Tavani et al., 2000; Purdue et al., 2004; Cross et al., 2006; Ward et al., 1994; Chang et al., 2005; Franceschi et al., 1989; Talamani et al., 2006; Zheng et al., 2004), although two female cohorts (Chiu et al., 1996; Zhang et al., 1999) and one case-control study in men (De Stefani et al., 1998) found twoto 2.5-fold elevated risks. Of nine studies (Chiu et al., 1996; Purdue et al., 2004; Cross et al., 2006; Tavani et al., 1997; Ward et al., 1994; Franceschi et al., 1989; Talamani et al., 2006; Zhang et al., 1999; De Stefani et al., 1998) investigating processed meat as a risk factor for NHL, only two found an elevated risk (Purdue et al., 2004; Tavani et al., 1997).
There have been few studies of meat intake in relation to bladder cancer. Two cohort studies have reported elevated, but not statistically significant, risks of bladder cancer for those in the highest category of meat consumption (Chyou et al., 1993; Mills et al., 1991), although other studies have reported null findings (La Vecchia and Negri, 1996; Steinmaus et al., 2000). With regard to red meat specifically, one cohort study found a 2.2-fold increased risk for bladder cancer (Steineck et al., 1988), whereas another found no association (Michaud et al., 2006). Processed meat intake has been associated with bladder cancer risk in one case-control study (Wilkens et al., 1996) and two prospective cohorts combined found a 1.6-fold increased risk for bacon intake (Michaud et al., 2006), whereas another cohort did not (Chyou et al., 1993).
There are several plausible biological mechanisms to explain an association between meat consumption and cancer. Early hypotheses focused on the potential effects of saturated fat or protein in red meat on colon cancer. Subsequent research has implicated other components of meat that could contribute to carcinogenesis such as iron in red meat, mutagens associated with meat preparation, and substances used to preserve meat, as noted below.
Preservation And Processing
Curing meat by adding salt, nitrate, or nitrite or by smoking has been a method of preservation for years. Most of the research regarding meat preservation methods has focused on cancers of the gastrointestinal tract; these studies were summarized by the WCRF report, which concluded that there was ‘possible’ evidence for an association between cured meats and colorectal cancer (World Cancer Research Fund, 1997). Other cancers that have been associated with processed meat consumption include childhood leukemia (Peters et al., 1994) and cancer of the brain (Preston-Martin et al., 1982; Sarasua and Savitz, 1994), oral cavity (Rajkumar et al., 2003), larynx (Levi et al., 2004), prostate (Michaud et al., 2001), and pancreas (Norell et al., 1986; Risch, 2003).
Case-control studies have found a positive association between stomach cancer risk with consumption of salted meat and fish (Boeing et al., 1991; Ward et al., 1999; Buiatti et al., 1989; Haenszel et al., 1972; Kono et al., 1988; Lee et al., 1995; Palli et al., 1992; Ramon et al., 1993); in addition, a cohort study found a two-fold increased risk of stomach cancer with salted fish consumption (Kneller et al., 1991). Salted meat and fish has also been associated with a 2.6-fold increased risk of colorectal cancer (Knekt et al., 1999). Some foods, such as salted fish, are preserved using nitrite salts and are thus a source of both salt and exogenous N-nitroso compounds (NOC) from the reaction between the nitrite and the secondary amines present in the fish. Chinese salted fish, for example, contains high levels of NOCs.
Nitrates/Nitrites And N-Nitroso Compounds (Nocs)
Meat may be associated with cancer risk by contributing to NOC exposure. NOCs are among the most powerful chemical carcinogens; therefore, even small amounts in the human body could be important. The carcinogenicity of NOCs has been tested in 39 different animal species, including six species of primate. Tumors have been induced in all species so far examined at a variety of sites and in a wide range of target cells. Thus, there is no reason to assume that humans are not susceptible to their actions.
There are two major routes of exposure to NOCs, by exogenous routes (from processed meats in particular) and by endogenous formation within the body, which is dose-dependently related to the amount of red meat in the diet. Exogenous exposure to NOCs occurs mainly by the inhalation or consumption of tobacco and preserved or heat-treated foods. Nitrite is added to processed meat as an antibacterial agent against Clostridium botulinum and as a cosmetic agent to react with myoglobin to produce the characteristic red-pink color of cured meats. Nitrate and nitrite are known precursors for NOC formation and, therefore, nitrite added to meat can form NOC in the meat. NOCs have also been detected in foods processed by smoking or direct fire-drying, which uses sufficient heat to oxidize molecular nitrogen to nitrogen oxides, which are able to nitrosate amines present in foods such as meat.
Dietary sources of nitrate and nitrite have not shown consistent associations with cancer risk. Some studies have found a positive association between foods high in nitrite, such as bacon and hot dogs, and esophageal cancer (Rogers et al., 1995), nasopharyngeal cancer (Ward et al., 2000), non-cardia gastric cancer (Mayne et al., 2001), pancreatic cancer (Coss et al., 2004), bladder cancer (Michaud et al., 2006), childhood leukemia, and brain cancer (Peters et al., 1994; Sarasua and Savitz, 1994; Kuijten et al., 1990); however, no association was found for colorectal (Knekt et al., 1999) or gastric cancer risk (Chyou et al., 1990; van Loon et al., 1997). Some studies have estimated overall NOC intake and have found significant positive associations with stomach cancer risk (Correa et al., 1985; Gonzalez et al., 1994; La Vecchia et al., 1995; Pobel et al., 1995), upper aerodigestive tract cancers (Rogers et al., 1995), and brain cancer (PrestonMartin, 1982). Childhood exposure to NOCs has been specifically associated with nasopharyngeal cancer (Ward et al., 2000). A study of esophageal cancer conducted in two different areas of China, a lowand a high-risk area, showed that NOC levels in the diet and daily excretion of NOC were significantly higher in the area at high risk for this cancer (Lin et al., 2002). The association between exogenous NOC exposure and cancer was directly investigated in 73 cases of colorectal cancer in a Finnish cohort of 9985 individuals (Knekt et al., 1999). This study investigated whether N-nitroso-dimethylamine (NDMA) intake or foods rich in N-nitrosamines are predictive for colorectal cancer. NDMA intake came from smoked and salted fish (52%) as well as cured meats and sausages (48%). This study found a significant two-fold increased risk of colorectal cancer in those with a high intake of NDMA (Knekt et al., 1999).
Endogenous NOC formation is thought to occur as a result of nitrosating agents, such as those derived from nitrite, reacting with nitrosatable substrates, the most commonly studied being secondary amines; this reaction can be catalyzed by nitrate reductase, which has an eightfold variation in activity among individuals. A study in rats harboring human fecal flora in their intestine and fed human diets showed a three-fold increase in bacterial nitrate reductase activity with a three-fold increase in meat consumption (Rumney et al., 1993).
Fecal NOC level is measured as apparent total N-nitroso compounds (ATNC), which is a proxy for endogenous N-nitrosation when exogenous NOC exposure is low. When nitrate is given to conventional and germ-free rats, ATNC remains low irrespective of the nitrate dose; however, in conventional rats, the level of nitrate in the water had a marked effect on the fecal ATNC levels (r ¼ 0.95, p < 0.01) (Massey et al., 1988). Furthermore, controlled human feeding studies have demonstrated a clear dose–response effect of red meat on fecal ATNC levels (Hughes et al., 2001). More recently, heme iron was identified as the component responsible for the enhancing effect of red meat on endogenous N-nitrosation (Bingham et al., 2002; Cross et al., 2003). A review of 33 studies considering the effect of iron on colorectal carcinogenesis, which weighted each study according to its design and number of subjects, revealed that the stronger studies did find a positive association between dietary iron or iron stores and colorectal cancer risk (Nelson, 2001). There are no epidemiologic studies assessing the effect of measured heme iron intake from different meats and cancer risk.
Meat Cooking Methods
According to the WCRF report, high-temperature cooking methods, such as pan-frying or grilling/barbecuing, are ‘possibly’ contributing to the risk of both stomach and colorectal cancers (World Cancer Research Fund, 1997). Case-control studies of colorectal adenoma (Gunter, 2005; Probst-Hensch, 1997; Sinha, 1999), colorectal cancer (Butler et al., 2003; Gerhardsson de Verdier et al., 1991; Peters et al., 1989; Wohlleb et al., 1990), and pancreatic cancer (Anderson et al., 2002; Ghadirian et al., 1995; Ji et al., 1995; Norell et al., 1986) have found elevated risks for high-temperature cooking methods. Frying/grilling has also been associated with increased risks of NHL (Chang et al., 2005) as well as pancreatic (Norell et al., 1986), lung (Sinha et al., 1998), and bladder cancer (Steineck et al., 1990). Furthermore, the degree to which the meat is cooked is also thought to affect risk of some cancers. Several case-control studies investigating the role of meat doneness level on the risk of colorectal adenoma (Probst-Hensch, 1997; Sinha et al., 1999) or colorectal cancer (Butler et al., 2003; Gerhardsson de Verdier et al., 1991; Lang et al., 1994; Nowell et al., 2002) have reported elevated risks for wellor very well-done meat consumption. Other studies have found similar associations for well-done meat intake and tumors of the stomach (Ward et al., 1997), prostate (Cross et al., 2005; Norrish et al., 1999), breast (Zheng et al., 1998), and lung (Sinha et al., 1998). However, other studies have not found any associations for high-temperature cooking methods or for well-done meat consumption and colorectal cancer (Augustsson et al., 1999; Kampman et al., 1999; Lyon and Mahoney, 1988; Muscat and Wynder, 1994), pancreatic cancer (Baghurst et al., 1991; Gold et al., 1985; Mack et al., 1986; Stolzenberg-Solomon et al., 2002), or NHL (Chiu et al., 1996; Cross et al., 2006; Chang et al., 2005; Zhang et al., 1999), for example. Relatively large risks are observed when a combination of method and doneness is considered; for example, fried meat with a heavily browned surface increased the risk of colon cancer by 2.8-fold and rectal cancer by six-fold in a Swedish casecontrol study (559 cases and 505 controls) (Gerhardsson de Verdier et al., 1991).
Cooking method and doneness are thought to be surrogates for mutagens formed in meat as a result of the cooking process. Laboratory results have shown that meats cooked at high temperatures contain heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) ( Jagerstad et al., 1991).
Heterocyclic Amines (HCAs)
The most abundant HCAs in cooked meat are PhIP (2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine) and MeIQx (2-amino-3,8-dimethylimidazo(4,5-f )quinoxaline) and, after a cooked meat meal, they are also the two HCAs that are most absorbed (Lynch et al., 1992). In 1993, the International Agency for Research on Cancer found that there was sufficient evidence from experimental animal studies to conclude that the HCAs IQ (2-amino- 3-methylimidazo(4,5-f )quinoline), MeIQ (2-amino-3,4dimethylimidazo(4,5-f )quinoline), MeIQx, DiMeIQx (2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline), and PhIP were carcinogenic (IARC, 1993). Over 20 individual HCAs have been identified, at least ten of which have been found to induce tumors in lab animals at multiple sites. PhIP specifically has been associated with an increased risk of intestinal and mammary adenocarcinomas in rodents, as well as prostate tumors in rats. MeIQx can induce tumors at multiple sites in rodents such as the liver and lung as well as lymphomas and leukemias. In addition, the DNA adducts and mutations from such HCA exposure show similarities between experimental animals and humans; these adducts have been detected in a wide variety of tissues and organs. A small pilot study in humans showed that colonic DNA adducts were formed in a dose-dependent manner after oral administration of a capsule containing MeIQx (Turteltaub et al., 1999). In addition, DNA and protein adducts were formed in the colon and blood, respectively, of humans receiving a dose of PhIP equivalent to the level found in 175 g of very well-done chicken, although the adducts were unstable and declined over 24 h (Dingley et al., 1999).
In more recent studies, questionnaires with detailed cooking and doneness information linked to a HCA database are used to estimate individual HCA intake. The HCA database was created by measuring levels of HCAs in a variety of meats, cooked by different methods to a range of doneness levels (rare, medium, well-done, and very well done) (Knize et al., 1995; Sinha et al., 1995; 1998a,b). Two case-control studies found a significant increased risk associated with HCAs; one found a 1.8-fold increased risk of colon cancer with DiMeIQx intake (Butler et al., 2003), and the other found 2.1to 2.5-fold increased risks for colorectal adenoma with DiMeIQx, MeIQx, and PhIP intake (Sinha et al., 2001). The findings for MeIQx were replicated in a case-control study (157 cases and 380 controls) of colorectal cancer, which showed a significant four-fold increased risk of colorectal cancer in the highest quartile of MeIQx intake (Nowell et al., 2002). One of the most recent studies to publish results on HCA intake and colorectal cancer risk was a population-based study of 620 cases and 1038 controls; this study found that DiMeIQx intake was associated with a 1.8-fold risk, but no associations for MeIQx or PhIP (Butler et al., 2003). Specific HCAs have been investigated in two studies of prostate cancer. The first was a case-control study of 317 cases that found no association (Norrish et al., 1999); the second was a cohort study with 1338 cases, and the authors found PhIP intake to significantly increase the risk for prostate cancer (Cross et al., 2005), which confirms animal findings that suggest PhIP is a prostate-specific carcinogen (Shirai et al., 1999). Furthermore, a case-control study of pancreatic cancer found MeIQx, DiMeIQx, and PhIP were all positively associated with risk (Anderson et al., 2005). However, other studies have shown no association between specific HCA intake and risk of NHL (Cross et al., 2006), colorectal adenoma (Gunter et al., 2005), colorectal cancer, or bladder cancer (Augustsson et al., 1999).
Polycyclic Aromatic Hydrocarbons (PAHs)
PAHs are mutagenic compounds formed in foods processed by smoking, such as meat, as well as in meat cooked by grilling/barbecuing. Meat cooked over a flame results in fat and meat juices dripping onto the hot fire, which yields flames containing a number of PAHs. These PAHs adhere to the surface of the food. Benzo[a]pyrene (B[a]P) is one of the most potent PAH carcinogens in animal studies and can induce leukemia as well as gastric, pulmonary, fore-stomach, esophageal, and tongue tumors in rodents (Culp et al., 1998). Grilled and well-done steak, hamburger, and chicken contain the highest levels of B[a]P, containing up to 4 ng of B[a]P per gram of cooked meat (Kazerouni et al., 2001). Dietary exposure to PAHs is thought to be important, since the intake of well-done meat is more correlated to blood PAH adducts than smoking (Rothman et al., 1990; 1993).
Epidemiologic studies investigating the association between dietary intake of PAHs and cancer have generally proven to be null for colon (Butler et al., 2003) and prostate cancer (Cross et al., 2005). However, case-control studies of colorectal adenoma (Gunter et al., 2005; Sinha et al., 2005) and pancreatic cancer (Anderson et al., 2005) found elevated risks for those in the top, versus bottom, quantile of intake.
Red meat continues to be implicated as a risk factor for carcinogenesis. However, there are limitations to the current literature. Much of the published literature has limited statistical power to examine the relationship of specific types of meat with cancer or within sub-sites. There is a lack of standardization in how meat items are defined, as well as heterogeneity in meat products throughout the globe. Currently, most epidemiologic studies rely on the food frequency questionnaire, which is associated with a degree of measurement error. Furthermore, many of the studies do not include detailed meat-specific components, including information on preparation, cooking methods, and doneness level, in their questionnaires.
Studies have clearly shown that red meat dosedependently increases the endogenous formation of NOCs. However, the carcinogenic potential of such an increase needs to be verified by the characterization of the precise NOC species being formed. Further research is also needed to elucidate the role of iron in cancer risk and to determine whether any such risks associated with iron are the result of a catalytic role in endogenous NOC formation.
It is likely that HCA and PAH intake, determined by meat cooking technique and doneness level, makes a small contribution to cancer risk. However, the normal intake of HCAs is many orders of magnitude below the exposure levels that induce cancer in animal models; the evidence for PAHs also is weaker. Nevertheless, one must consider species differences and the possibility that humans may be more susceptible to the action of these compounds than rodents.
In order to advance the field of meat-related mutagens, the methods of exposure assessment must be further improved. Detailed questionnaires must be used in conjunction with reliable biomarkers in large prospective studies to accurately investigate the associations between meat, meat cooking and preserving methods, and cancer risk.
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