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Carcinogenic and anticarcinogenic food components / edited by Wanda Baer-Dubowska, Agnieszka Bartoszek, Danuta Malejka-Giganti. p. cm. -- (Chemical and functional properties of food components series) Includes bibliographical references and index. ISBN 0-8493-2096-8 (alk. paper)
1. Carcinogens. 2. Food--Toxicology. 3. Functional foods. 4. Cancer--Diet therapy. I. BaerDubowska, Wanda. II. Bartoszek, Agnieszka. III. Malejka-Giganti, Danuta. IV. Series.
RC268.7.F6C37 2005 616.99'4071--dc2220050500569
Taylor & Francis Group is the Academic Division of T&F Informa plc.
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Preface
Fifty years of research on carcinogenesis have identified multiple cancer risk factors in the human environment, including food. Attempts to counteract carcinogenesis have led to discoveries of many components of plant foods that display biochemical and biological activities capable of preventing cancer. The term “nutraceuticals” has been proposed to describe those food components that exhibit health-promoting properties. Anticarcinogenic food components have become the subject of interest of a relatively new cancer research field called cancer chemoprevention. Although many data on carcinogenic and anticarcinogenic food components have been collected, our understanding of causal mechanisms linking diet and cancer is still evolving. As a result, evaluations of official dietary recommendations are needed on an ongoing basis.
This multidisciplinary book has been designed to provide a broad spectrum of information on both cancer-causing and cancer-preventing food components. Highly qualified and internationally recognized biochemists, toxicologists, epidemiologists, and food scientists have contributed chapters to this book.
Chapter 1 introduces the reader to the basic concepts of food and cancer, and the carcinogenic and anticarcinogenic potentials of food components. The subsequent Chapters 2 and 3 cover the complexities of the molecular and cellular events during the multistage process of chemical carcinogenesis as well as metabolic transformations of mutagens and carcinogens required to convert inert chemical molecules into DNA-reactive agents. In Chapters 4 through 8, a variety of dietary sources of carcinogenic compounds, their abundance in foods, and possible cancer risks are reviewed. Specifically, these chapters cover genotoxic (Chapter 4) and environmental (Chapter 6) contaminants of foods, the impact of food processing on the carcinogen content (Chapter 5), and the presumed roles of anti- and prooxidants (Chapter 7) and polyunsaturated fatty acids (Chapter 8) in carcinogenesis.
The subsequent chapters deal with the cancer-preventive potential of food components. While Chapter 9 familiarizes the reader with basic mechanisms and targets of chemoprevention, the subsequent chapters discuss anticarcinogenic food components of particular current interest. These include phenolic compounds in common spices (Chapter 10), tea and tea constituents (Chapter 11), wine polyphenols and resveratrol (Chapter 12), flavonoids of fruits and vegetables (Chapter 13), carotenoids (Chapter 14), constituents of cruciferous vegetables (Chapter 15), and phytoestrogens (Chapter 16). Chapter 17, the final chapter, provides perspective on the impact of diet on cancer prevention based on human trials and discusses future directions of research in this important field.
This book is designed for professionals employed by the food-processing industry and food scientists involved in research and educational endeavors as well as
students of food science. This book will also be of interest to nutritional and biomedical scientists involved in studies of cancer etiology and prevention. The editors wish to thank all authors for their invaluable contributions.
Wanda Baer-Dubowska Agnieszka Bartoszek
Danuta Malejka-Giganti
The Editors
Wanda Baer-Dubowska, Ph.D., is a professor and head of the Department of Pharmaceutical Biochemistry at the University of Medical Sciences inPozna´n, Poland. She received her M.Sc. and Ph.D. degrees from the same university. As a recipient of French government, Federation of European Biochemical Societies (FEBS), and National Institute of Health Research (INSERM) scholarships, she conducted her postdoctoral studies at the CNRS Institute for Cancer Research in Villejuif, France (1980 to 1982). Later, she was a visiting scientist at the University of Texas M.D. Anderson Cancer Center, Science Park Research Division in Smithville, Texas (1987 to 1989 and 1993 to 1996).
Dr. Baer-Dubowska’s main research interests are chemical carcinogenesis and chemoprevention, particularly by natural products. She is author of numerous peerreviewed and invited publications as well as a reviewer of research articles for several scientific journals.
Dr. Baer-Dubowska is a member of the American Association for Cancer Research, European Association for Cancer Research, International Society for Cancer Prevention, and European Environmental Mutagen Society, for which she is currently serving as the general secretary.
Agnieszka Bartoszek, Ph.D., is an assistant professor in the Department of Pharmaceutical Technology and Biochemistry, Gda´nskUniversity of Technology, Poland. She received her M.Sc. and Ph.D. from the same university. She was a visiting scientist at the Laboratory of Molecular Pharmacology and Drug Metabolism, Imperial Cancer Research Fund in Edinburgh, Scotland (1988 and 1989).
Dr. Bartoszek’s main research interests focus on interactions of antitumor drugs with DNA, chemopreventive properties of selected food components, and dietary intervention during cancer chemotherapy.
Dr. Bartoszek has also been involved with both Polish and American publishers in preparation of several textbooks for students and professionals.
Danuta Malejka-Giganti, Ph.D., is a senior research career scientist at the Veterans Affairs Medical Center, a professor in the Department of Laboratory Medicine and Pathology, and a member of the Cancer Center at the University of Minnesota in Minneapolis. She is a graduate of the School of Pharmacy, Medical Academy, Pozna´n,Poland, where she also received her Ph.D. degree in Pharmaceutical Chemistry. Her postdoctoral studies in cancer research (1960/1961 and 1966/1967) at the University of Florida in Gainesville were sponsored by the fellowships from the National Cancer Institute, National Institutes of Health.
Dr. Malejka-Giganti’s research interests concern mechanisms of liver and mammary gland carcinogenesis by amino and nitro aromatic compounds, including
environmental pollutants, and chemoprevention of mammary gland cancer by modulators of carcinogen and estrogen metabolism. Dr. Malejka-Giganti published numerous research articles in peer-reviewed journals as well as invited research monographs and chapters. She has also served for many years as a member of peerreview committees at the National Cancer Institute and American Cancer Society.
Dr. Malejka-Giganti is a member of the American Association for Cancer Research, American Society for Biochemistry and Molecular Biology, International Society for the Study of Xenobiotics, American Association for the Advancement of Science, and International Society for Preventive Oncology.
Contributors
Seung J. Baek
University of Tennessee Knoxville, Tennessee
Wanda Baer-Dubowska Pozna´nUniversity of Medical Sciences Pozna´n,Poland
Agnieszka Bartoszek Gda´nskUniversity of Technology Gda´nsk,Poland
Marek Biziuk
Gda´nskUniversity of Technology Gda´nsk,Poland
Marcus S. Cooke University of Leicester Leicester, U.K.
Amanda J. Cross
NIH-NCI Rockville, Maryland
Cristina Fortes Institute of Dermatopathology IDI Rome, Italy
Daniel Gackowski
The Rydgier Medical University–Bydgoszcz Bydgoszcz, Poland
Jan Gawecki
Agricultural University of Pozna´n Pozna´n,Poland
Grzegorz Grynkiewicz Pharmaceutical Research Institute Warsaw, Poland
Ewa Ignatowicz Pozna´nUniversity of Medical Sciences Pozna´n,Poland
Elizabeth H. Jeffery University of Illinois at Urbana–Champaign Urbana, Illinois
Tamara P. Kondratyuk
Purdue University West Lafayette, Indiana
Joshua D. Lambert
Rutgers University Piscataway, New Jersey
Janelle M. Landau
Rutgers University Piscataway, New Jersey
Mao-Jung Lee
Rutgers University Piscataway, New Jersey
Joseph Lunec University of Leicester Leicester, United Kingdom
Danuta Malejka-Giganti University of Minnesota Veterans Affairs Medical Center Minneapolis, Minnesota
Zofia Mazerska
Gda´nskUniversity of Technology
Gda´nsk,Poland
Michael F. McEntee
University of Tennessee Knoxville, Tennessee
John A. Milner
NIH-NCI Rockville, Maryland
Nicole Monfilliette-Cotelle
Lille University of Science and Technology Villeneuve d’Asaq, France
Ryszard Oli´nski
The Rydgier Medical University–Bydgoszcz Bydgoszcz, Poland
Adam Opolski
Polish Academy of Sciences
Wrocl/aw,Poland
John M. Pezzuto
Purdue University West Lafayette, Indiana
Elena Shalaev
School of Pharmacy
Purdue University West Lafayette, Indiana
Rashmi Sinha
NIH-NCI Rockville, Maryland
Young-Joon Surh
Seoul National University Seoul, South Korea
K. (Chris) Szyfter
Polish Academy of Sciences Pozna´n,Poland
Natalia Tretyakova
University of Minnesota Cancer Center Minneapolis, Minnesota
Ole Vang
Roskilde University Roskilde, Denmark
Jay Whelan
University of Tennessee Knoxville, Tennessee
Chung S. Yang
Rutgers University Piscataway, New Jersey
Contents
Chapter 1 Food and Cancer: Development of an Association.............................1
K. (Chris) Szyfter and Jan Gawecki
Chapter 2 Molecular Mechanisms of Carcinogenesis........................................13
Danuta Malejka-Giganti and Natalia Tretyakova
Chapter 3 Metabolism of Chemical Carcinogens..............................................37
Chapter 5 Impact of Food Preservation, Processing, and Cooking on Cancer Risk...................................................................................97
Amanda J. Cross and Rashmi Sinha
Chapter 6 Environmental Contamination of Food...........................................113
Marek Biziuk and Agnieszka Bartoszek
Chapter 7 Dietary Anti- and Prooxidants: Their Impact on Oxidative DNA Damage and Cancer Risk.......................................................137
Ryszard Oli´nski,Daniel Gackowski, Marcus S. Cooke, and Joseph Lunec
Chapter 8 Dietary Polyunsaturated Fatty Acids, Eicosanoids, and Intestinal Tumorigenesis..................................................................157
Jay Whelan, Michael F. McEntee, and Seung J. Baek
Chapter 9 Chemoprevention of Cancer: Basic Mechanisms and Molecular Targets.............................................................................177
Wanda Baer-Dubowska and Ewa Ignatowicz
Chapter 10 Chemopreventive Phenolic Compounds in Common Spices..........197
Young-Joon Surh
Chapter 11 Cancer Prevention by Tea and Tea Constituents.............................219
Janelle M. Landau, Joshua D. Lambert, Mao-Jung Lee, and Chung S. Yang
Chapter 12 Cancer Chemoprevention by Wine Polyphenols and Resveratrol........................................................................................239
John M. Pezzuto, Tamara P. Kondratyuk, and Elena Shalaev
Chapter 13 Flavonoids: Common Constituents of Edible Fruits and Vegetables..................................................................................259
Nicole Monfilliette-Cotelle
Chapter 14 Carotenoids in Cancer Prevention...................................................283
Cristina Fortes
Chapter 15 Chemopreventive Potential of Compounds in Cruciferous Vegetables.....................................................................303
Ole Vang
Chapter 16 Phytoestrogens and Their Effects on Cancer..................................329
Grzegorz Grynkiewicz and Adam Opolski
Chapter 17 Diet and Cancer Prevention: Current Knowledge and Future Direction...............................................................................351
1.3Carcinogenic Potential of Food.......................................................................4
1.4Anticarcinogenic Activity of Food..................................................................7
1.5Genetically Determined Variability of Cancer Risk........................................9
1.6Epidemiologic Evidence for an Association between Nutrition and Cancer........................................................................................................9
An association between food intake and life is both evident and banal. Simply, food is essential. Any level of human activity, starting from cellular metabolism (e.g., synthesis of biomolecules) through tissue physiology (e.g., muscle contraction) to organism physiology (e.g., physical labor or sports), requires energy expenditure. The main purpose of nutrition is to provide energy for current and future consumption. Otherwise, food is necessary for body growth, maintenance, and tissue repair. Such an intuitive understanding of nutrition, with no precise knowledge concerning the biology of feeding, was satisfactory for centuries. Acquiring the amount of food sufficient to survive was the main and often the only priority for an individual as well as for a group or population. Regardless of the way the food was gained, be it hunting, agriculture, war, or robbery, a shortage or abundance of food was an indication of poverty or prosperity, of a poor or fortunate life. Populations of early food-gatherers, hunters, farmers, and even well-trained eighteenth-century soldiers (“an army has to feed itself”) repeatedly faced the same problem: a shortage of food during the period preceding the next hunt or harvest. And, given the threat of famine versus that of any negative health effects connected with feeding, the former would always prevail.
A seasonal (in agriculture) or occasional (in hunting, fishery) overproduction of supplies posed the question of food storage. Some of the early techniques of meat or fish storage, such as smoking or salting, as well as those of vegetable and fruit conservation, such as drying, pickling, or souring, have stayed basically the same to the present day. Numerous food additives, mostly herbs, were also known and used in the past. Their assortment and applications varied locally, but the primary purpose was generally the same: to prolong the usability of food products. Spices imported from India, surprisingly popular in Europe during medieval times, were used not only to improve taste but also to cover an unpleasant smell and appearance of food stored for too long a time. Obviously, the present-day understanding of spices as antioxidants and scavengers of free radicals is very far from that of the past, when their use was mostly intuitive.
The above historical remarks concern the early, rather basic and primitive understanding of nutrition. Nutrition as a branch of science, exploiting the achievements of biochemistry, physiology, and recently, genetics, does not go back further than the nineteenth century. The main achievement of that time was establishing a classification of food constituents (proteins, fats, carbohydrates, and minerals), followed by determining how to estimate calorie intake. The role of vitamins as necessary constituents of the human diet was not discovered until the beginning of the twentieth century. The first and primary target of the early period of nutrition science was to propose justifiable recommendations for the required amount of food and its composition. Such recommendations, applicable and needed for group feeding of soldiers and workers, came into practical use in the United States, Canada, Great Britain, and the Soviet Union during the 1930s. However, the optimal dietary recommendations still remain an open question.
1.2NUTRITIONAL NEEDS
To begin a scientific consideration of nutrition, some definitions are needed (Sikorski, 2002; Katan and De Roos, 2003). Nutrients are defined as constituents of food necessary for maintaining normal physiological functions. Essential nutrients are food components required for optimal health. The early dietary recommendations were expected to provide proper and definitely not suboptimal feeding; this can be described by the recently introduced term functional food, understood as a food improving the health or at least the well-being of an individual. This term, to a certain extent, refers to food technology aiming at optimization of food components in a final product without compromising sensory quality (taste, smell, color). Other important questions in nutrition studies besides the design of functional foods for a random population of consumers concern preventive diet and diet as a part of illness treatment.
Work on nutrition optimization involves different aspects and concerns both for the general population and for narrow groups. Construction of the so-called Food Guide Pyramid, performed by the U.S. Department of Agriculture, provides a good example illustrating the need for further work. The pyramid itself is a pictorial model of dietary guidelines calling for a variety of foods and informing the public
about recommended daily proportions (http://schoolmeals.nal.usda.gov/py/ pmap.htm). The general idea underlying the guidelines is to limit the daily intake of fat, replacing it by food rich in polysaccharides, and to enhance the nutritional quality by extensive consumption of fruits and vegetables. One of the recent revisions to these guidelines reflects the recognition of two different types of fats characterized by different levels of aliphatic chain saturation (butter and oil are examples of saturated and unsaturated fats, respectively). The second important revision stems from the appreciation of the function of fiber. It is broadly accepted that bread, oats, and rice can be divided according to their content of dietary fiber into regular, fiber-enhanced (more fiber), and fiber-deficient (e.g., hulled rice) products. On the other hand, results concerning the significance of fiber as an anticarcinogenic agent are still conflicting. It should be admitted that in spite of broad criticism, the Food Guide Pyramid was never officially withdrawn. Finally, there is a tendency to limit meat consumption. Thus, current research efforts aim to provide better guidelines to decision makers, those responsible for collective feeding, and individual consumers.
A relatively new extension of nutrition science reflects the recent expansion of genetics into the biomedical sciences. The genetic information (DNA sequence) specific for the species Homo sapiens is in principle the same for all humans. The full DNA sequence of human genome was published in April 2003. However, a number of subtle sequence variations exist that make each individual unique. Individualization of food requirements and ingestion is one of the manifestations of human population variability. The differences in DNA coding regions and in regulatory sequences are responsible for the occurrence of various forms of proteins and variable patterns of enzymatic activity. Awareness of genetic variability and the unraveling of human DNA inspired researchers to create a new field of science called nutrigenomics (Go et al., 2003; Müller and Kersten, 2003). Nutrigenomics is attempting to investigate a large area including identification of genes involved in the process of nutrition; estimation of interactions between nutrients and genes and their protein products; analysis of metabolic processes associated with nutrition; and recognition of genetically determined individual predispositions to develop nutrition-related diseases. Personalization of diet in relation to an individual’s genetic status seems to be an obvious target for nutrigenomics. Prevention of diet-related diseases could be a specific goal in this regard.
Studies on obesity provide another good example of an impact of gene polymorphism on nutrition. Obesity has been found to be associated with expression of the gene encoding a protein called leptin. The ob (obesity) gene has been identified and localized in the human genome. Ethnic differences in the distribution of ob gene polymorphisms and defects have been determined, and their association with genetically determined obesity confirmed (Gura, 1997). In the course of subsequent studies, it became clear that obesity is not a single-gene condition; many more genes are probably involved (Barsh et al., 2000). DNA polymorphism in another group of genes plays a role in individual differences in the sensitivity to a variety of pathogens, including carcinogens. Thus, genetically determined variability within the human population is recognizable at the nutrition level (Ahima and Osei, 2001).
1.3CARCINOGENIC POTENTIAL OF FOOD
One of the major concerns to be analyzed in a study on carcinogenesis is exposure to exogenous carcinogens, which may be (Ames et al., 1995):
•Present in both natural and polluted human environments
•Associated with working conditions (occupational exposure)
•Attributable to lifestyle (this term primarily covers tobacco smoking or chewing and the consumption of alcoholic beverages)
•Following an intake of cytostatic agents in the course of chemotherapy (paradoxically, drugs designed to eliminate cancer cells can also generate lesions in normal cells)
•Related to diet
According to a rough estimation in a random population of people with cancer, one-third of all cancers are associated with tobacco smoking and one-third with different dietary factors.
The link between diet and cancer is rather complex and definitely not unidirectional. The majority of food products are neutral in relation to carcinogenesis. Only some exhibit pro- or anticarcinogenic properties. Obviously, an abundance of procarcinogenic food constituents is as harmful as a lack of anticarcinogens in the diet. The point, however, is that such a categorization is easily applicable only to a single chemical compound, while dietary products are almost exclusively complex mixtures. Hence, there are numerous situations when a single food product contains, at the same time, some substances that are harmful and some that are beneficial (Willett, 2001; Kritchevsky, 2003).
Let us consider coffee, soy sauce, and red wine as examples:
Caffeine present in coffee beans belongs to a group of so-called oxypurines, capable of intercalating into the DNA helix, which leads to a reversible DNA lesion. Methylglyoxal, another compound found in coffee beans, has been identified as the main mutagen in coffee. On the other hand, it has been shown that an extract from coffee beans exhibits antimutagenic activity against nitrosourea-induced DNA damage.
Soy sauce provides another example of such a bivalent activity. Because it is rich in scavengers of oxygen-derived radicals, soy sauce should be classified as an antimutagenic product. On the other hand, Japanese researchers have shown that soy sauce contains a furanone derivative with DNAbreaking activity; however, this activity is masked by the abundance in soy sauce of antioxidants bearing sulfhydryl groups.
The third example to be mentioned here is red wine. Obviously, it contains up to 18% of ethanol. Ethanol by itself is not mutagenic, but it can act as a cocarcinogen, increasing the genotoxicity of other substances; in addition, acetaldehyde, the first metabolite of ethanol, has the ability to interact with DNA. Furthermore, many brands of wine and beer have been shown to contain traces of one of the heterocyclic amines typically
present in temperature-processed meat and fish and known to be strong mutagens. On the other hand, some of the phenol and alcohol compounds present in red wine have been shown to reduce the DNA damage caused by oxidation and ionizing radiation. These well-documented protective properties along with the acknowledged beneficial influence on digestion are the reason why a moderate consumption of red wine is recommended by nutritionists.
A plethora of carcinogens occurs in food. A categorization of food carcinogens according to their origin has been introduced. The first group includes natural food carcinogens and consists mainly of genotoxins occurring in plants. Their role in nature is to protect plants against fungi, insects, or animals. Examples of such genotoxins are hydrazines (present in mushrooms), safrole (spices in root beer), estragole (dried basil), and psoralens (celery) (Miller and Miller, 1976).
Another group of food carcinogens consists of genotoxic substances that can appear in food because of environmental pollution or in the course of food storage, conservation, and processing.
The term pollution is a very broad one and covers all types of contamination emitted to the ground, surface waters, and atmosphere that could be further acquired by plants, fish, and farm animals. The sources of pollution include industrial waste, diesel exhaust (mostly in the vicinity of roads), and residual amounts of pesticides (Ames et al., 1987; Evangelista de Duffard, 1996).
Dioxins and related compounds (chlorinated hydrocarbons) are of special concern (Kaiser, 2000). Broadly used in the industrial production of chloroorganic chemicals, when emitted to the environment they can easily contaminate food of land animal and fish origin. When dioxins penetrate human bodies, they exert neurotoxic effects and increase cancer risk in many organs. Public attention has been drawn to them as a consequence of several industrial accidents (the best-known example of which was an explosion in Seveso, Italy, in June 1976) that caused serious environmental contamination followed by an increase in morbidity (due to cancer and other diseases) in the population inhabiting the surrounding areas. Dioxins are extremely toxic, and most probably there is no threshold level below which they do not exert carcinogenic potential.
Another example of the effect of environmental pollution on nutrition is contamination of fish by polycyclic aromatic hydrocarbons. Fish living in a polluted aqueous reservoir (e.g., in the vicinity of a petroleum refinery) use the contaminated water to rinse their gills; this ultimately results in the deposition of polycyclic aromatic hydrocarbons in the fish body.
The final example to be mentioned is contamination of foodstuffs by heavy metals. Although some metals are essential for human nutrition, others, including arsenic, cadmium, chromium, nickel, and lead, have been found to pose a potential carcinogenic threat to humans. Arsenic (its main dietary source is fish) and perhaps cadmium appear to be the most harmful.
Food storage/conservation as a source of carcinogens usually reflects improper storage conditions resulting in the occurrence of mycotoxins such as aflatoxins, which are known to be hepatocarcinogens. On the other hand, a number of chemicals
are added to food to extend its storage period. Although many of them are recognized as having carcinogenic properties, they are in common use; the goal is to keep a balance between the increased risk of cancer and extended food usability (Ames et al., 1987; Ferguson, 1999). The preservation of attractive appearance and pleasant aroma of food products is also an important concern for food producers. Examples of additives with potentially carcinogenic properties include ethanol, saccharin, caramel, AF-2 (furylfuramide), nitrate (III), and nitrate (V). The latter two are used as coloring and preservation agents in meat products. Interestingly, some potentially harmful substances, such as derivatives of benzoic acid (used as conservants of processed fruit) or the highly carcinogenic azo dyes, are banned in many countries but still in use in others. This indicates the need for international standardization of food storage and compatibility of the underlying legal regulations.
The last group of food carcinogens to be considered includes those resulting from food processing. Food can be processed in many ways, but perhaps the most frequently used is application of high temperatures (e.g., cooking). The main groups of food carcinogens resulting from high-temperature processing are polycyclic aromatic hydrocarbons (PAH), heterocyclic aromatic amines (HAA), and N-nitrosamines (NOC):
PAH are products of the incomplete combustion of organic matter and therefore occur commonly in temperature-processed foodstuffs (Phillips, 1999). It is not difficult to predict that more PAH would be generated at high temperatures (but not high enough for complete combustion) than at low temperatures. The exact method of heat processing of food is also an important factor. Direct contact with flames (grill, barbecue) drastically increases PAH content, while boiling in water appears to generate the smallest amount of PAH.
HA are products of the pyrolysis of food rich in proteins, especially meat and fish (Robbana-Barnat et al., 1996). HA in animals are carcinogenic primarily for the liver. In humans HA may play a role in several cancers, especially colorectal and breast cancers (Ferguson, 1999).
NOC are generated due to high temperatures in food containing nitrate (III) (cured meat, sausages, ham, smoked and pickled foods); in addition, some nitrous compounds can be converted into NOC under certain processing conditions other than high temperature.
The intake of fat and calories constitutes a separate category that does not fall into the above classification (Ames et al., 1987; Weindruch, 1996; Willett, 2001). Several studies have documented an increased risk of cancers (of the colorectum, breast, and other sites) related to these factors, but some of the results were conflicting. Experiments in laboratory animals exposed to carcinogens have shown a decreased cancer risk in animals kept on a fat- and calorie-restricted diet compared to those fed ad libitum. An extension of life span as a consequence of the restricted diet was also shown in many animal models. The beneficial effect of such dietary restriction on human health and well-being has been considered mostly in the context of coronary disease and arteriosclerosis, but a decrease of cancer risk has also been
noted. Mechanisms of the carcinogenic effect of fat consumed in high amounts are not fully clear. The following processes have been taken into account to explain carcinogenicity of fat:
1.Overproduction of reactive oxygen species paralleling lipid oxidation
2.Deregulation of hormone metabolism
3.Alterations of carcinogen metabolism in the liver, which is the organ primarily responsible for elimination of xenobiotics
4.Changes in molecular and cellular processes involving DNA synthesis, DNA repair, and cell proliferation
Food carcinogens have also been categorized according to their mode of action on the genetic material. The first category includes genotoxic agents causing DNA lesions, as well as clastogenic agents inducing chromosome aberrations. The second category, comprising tumor promoters, mostly includes agents responsible for uncontrolled cell proliferation. Based on the involvement of carcinogens in particular stages of the whole process of carcinogenesis, nutrients with carcinogenic activity can be divided into:
1.Agents initiating the process
2.Agents acting at the stage of cancer progression
1.4ANTICARCINOGENIC ACTIVITY OF FOOD
Having listed the main categories of food-related mutagens/carcinogens, it is also necessary to acknowledge the anticarcinogenic properties of some foodstuffs (Ferguson, 1994). In general, food products rich in antioxidants and free radical scavengers are potential candidates to directly counteract carcinogenesis. Food compounds increasing the processes of detoxification and DNA repair, as well as those decreasing the metabolic activation of procarcinogens, also contribute to anticarcinogenesis, acting indirectly. Anticarcinogenic potential has been documented for fresh fruits and some vegetables such as pepper, which are rich in vitamins; cruciferous vegetables (cabbage, Brussels sprouts, broccoli, etc.), where glucosinolates are responsible for the high detoxifying activity; common spices (especially garlic, also ginger, coumarin, cinnamon, and many others); and coffee (in moderation) as well as black and green tea, with an advantage of the green tea due to a high content of polyphenols, inhibiting activation of many carcinogens.
Categorization of food carcinogens in relation to the progression of carcinogenesis brings about yet another question. Do nutrients with established carcinogenic or anticarcinogenic activity retain the same character throughout the whole process of carcinogenesis? Not many studies have addressed this question, but unexpected results of one of them demonstrated the need for caution in interpreting analogical experiments.
During the mid-1980s, the existing evidence for possible anticancer activity of b-carotene was considered sufficient to justify launching large-scale human intervention trials. These trials were designed to provide final support for the hypothesis that the high consumption of vegetables or fruits containing b-carotene (or of this com-
pound alone) is protective against some types of cancer. Studies were initiated in the United States (4- to 12-year studies completed in 1998 or earlier), China, and Finland.
The Finnish study aimed to determine the influence of dietary intake of bcarotene and vitamin E (separately and together) on the incidence of lung cancer. The study population comprised 29,133 male smokers aged 50 to 69 years. Contrary to what was expected, the group receiving vitamins showed an 18% higher lung cancer incidence and an 8% increase in total mortality. It was consequently assumed that b-carotene, while decreasing the risk of developing tobacco smoke–associated cancer, could increase progression of already-initiated lung cancers. Alternatively, genetic polymorphism was considered as a possible explanation of the Finnish results. The carriers of rare gene variants (presumably more frequent in Finland than in other populations) could have reacted to the anticarcinogenic activity of b-carotene in a different way than the majority of responders do (Charleux, 1996). The experimental attempts to explain a failure of b-carotene preventive activity do not provide a final verdict, but at least two effects have been found (Seifried et al., 2003):
1.A weak prooxidative effect of b-carotene in relation to tobacco smoke
2.An interference of b-carotene with radio- and chemotherapy, affecting treatment efficacy
The findings reported to date leave no doubt that the link between nutrition and cancer initiation should be considered in two opposing contexts: risk increase (consumption of carcinogens present in food) and prevention (intake of food with anticarcinogenic activity).
There is still another point to be raised: can dietary factors influence survival of subjects already treated for cancer? This question is being addressed through chemoprevention studies. Initially, the term “chemoprevention” was used in a narrow sense, concerning a protective activity of some foods towards cancer. Presently, chemoprevention studies and therapeutic attempts focus on three aspects: food intake significance in cancer initiation (already discussed) and cancer progression, and the influence of diet on subjects already treated for cancer, who are at risk for tumor recurrence or development of secondary tumors (De Flora et al., 2001; Sabichi et al., 2003).
Concerning the second and third aspects, there are indications that such factors as fiber, tocopherol, or b-carotene may inhibit cancer growth. At the moment, large clinical trials on the effects of fiber on colon tumor growth inhibition and on the effects of b-carotene, a-tocopherol, and vitamin A on lung cancer are in progress. The uptake of 13-cis-retinoic acid has been shown to decrease the percentage of second primary tumors in head and neck cancer; the occurrence of second primary tumors is among the main failures of treatment in this cancer. Another major focus of chemoprevention diet studies is cancer of the breast (Rock, 2003), the most common tumor site in women. Breast cancer survivors who changed their diet towards fiber-rich and low-fat food, with more fruits and vegetables, were reported to have a lower incidence of secondary cancer events and increased survival. In breast cancer, and to some extent also in head and neck cancer, the risk is also related to hormonal activity. Accordingly, another direction of chemoprevention studies involves investigating the nutritional regulation of hormones.
1.5GENETICALLY DETERMINED VARIABILITY OF CANCER RISK
Another important topic relating to the association between food and cancer is genetic polymorphism. All humans carry the same set of genes. However, some subtle variations exist in their structure, which results in variable enzymatic activity of their protein products. The variability of enzyme activity is usually distributed in a population according to the Gauss (normal) curve. Some genes have more pronounced variants, in which case the distribution of activity is bi- or trimodal (reflecting low/medium/high activity). There are noticeable ethnic differences in the distribution of gene variants. One of the best-known examples is a shift of alcohol dehydrogenase activity to high values in Caucasians compared with low activity in the Japanese population. This results in relatively low tolerance to alcoholic beverages in Japanese people, as compared to Caucasians.
To exert their activity, carcinogens have to penetrate human bodies, cells, and finally cell nuclei to interact with genetic material. Most carcinogens require metabolic activation inside the penetrated cell. The activation of carcinogens helps them become substrates for the process of detoxication; however, at the same time, they acquire DNA-damaging activity. Carcinogen-induced DNA lesions are removed in the course of the DNA repair process. All the mentioned processes (activation, detoxication, DNA repair) are under genetic control executed by enzymes. It has been established that the activity of DNA-metabolizing and DNA-repair enzymes is extremely variable in the human population. Hence, an individual’s susceptibility to carcinogens is determined genetically, and drastic differences are observed among individuals. For some people, even a low exposure to carcinogens could be very harmful, whereas negative health effects are not observed in other people receiving much more extensive exposure (Ames, 1999; Miller et al., 2001).
The consequences of genetic polymorphism have been discussed in relation to exposure to carcinogens. It must be admitted that nutritional needs and food metabolism are also the subject of polymorphic enzymatic activity and therefore are also subject to variation among individuals.
1.6EPIDEMIOLOGIC EVIDENCE FOR AN ASSOCIATION BETWEEN NUTRITION AND CANCER
Finally, we should pose an obvious question concerning a proof for an association between nutrition and cancer at the population level. A partial answer has already been given above; in the following section some more epidemiological evidence will be quoted. When assessing the examples below, one has to bear in mind that humans are not laboratory animals. Looking for the effects that a given diet exerts on health, we have to remember that the subjects are exposed to other carcinogens present in the polluted environment associated with their jobs, medication, and lifestyle. Hence, epidemiological studies must be very carefully designed, and their results must be interpreted with caution. With this in mind, nutrition epidemiologists aim to analyze
precisely defined, preferably large groups, characterized by strict and stable feeding habits, lack of nonnutrient exposures, and uniform ethnicity. Some epidemiological examples of connections between nutrition and carcinogenesis, illustrating the problem’s significance, are presented below.
In Kashmir, an Asian region located along the India/Pakistan border, there is a high incidence of esophageal cancer. At first glance, its association with the high consumption of tea seems rather surprising, given the recognized anticarcinogenic activity of tea. However, the way of preparing tea in Kashmir is quite specific. Instead of being hot water–extracted as in China, Europe, and America, the tea leaves are boiled in salty water for a prolonged time. Under these conditions (high temperature and the presence of salt), alkaloids present in the tea leaves are converted into Nnitrosamines, compounds that are highly carcinogenic toward the esophagus.
Another example comes from Sweden. The traditional diet in Scandinavia included a large amount of well-done red meat; in addition, consumption of fresh vegetables and fruits was rather scanty. As a result, the Swedish people have relatively high incidences of gastric and rectal cancers as compared with those in other parts of Europe. This finding triggered a rational campaign aiming to change the eating habits of the nation.
Interestingly, the highest place in world cancer statistics, both general and concerning some specific types of cancer, such as lung cancer and laryngeal cancer, is held by Hungary. Epidemiologists cannot offer any satisfactory explanation. There have been some hints about socioeconomic reasons. The high level of tobacco smoking has been considered, but given the exceptionally high consumption of pepper, which contains anticarcinogenic vitamins, the cause for the observed incidence of cancer still is not clear.
Migrant people are desirable subjects of investigations for epidemiologists. They provide several variants of dependencies, from traditional eating and food-processing habits (kept or lost in the new location), through environmental and local contamination of food, to ethnic differences in genetic polymorphism. A few examples are presented below.
The incidence of tumors associated with using cycad plants as a source of starch in some of the Japanese islands is rather high, while the cancer risk in migrants from these islands who no longer eat cycad nuts is considerably reduced. The high rate of stomach cancer in Egypt believed to be due to the presence of aflatoxins in inappropriately stored crops is not observed in Egyptian emigrants, who no longer consume contaminated crops. The connection between a high level of fat intake and the risk of developing breast cancer demonstrated for Caucasian women does not apply to Japanese women; this seems to reflect genetically determined differences in these populations.
1.7FINAL REMARKS
Nutritionists recommend the Mediterranean diet because of the associated low risk of cancer development. The reasons for this seem clear: an abundance of fresh fruits and vegetables, preferential usage of plant oil, more fish than meat, lots of spices, and red wine; all of this is within the comprehensive nutrition recommendations.
On the contrary, German, Polish, and Czech diets are rather heavy and rich in fat. Fortunately, these diets include large amounts of cabbage, which seems to be a favorite vegetable in all these nations. Cabbage, together with broccoli, cauliflower, and Brussels sprouts, belongs to the group known as cruciferous vegetables. Their strong anticarcinogenic activity is related to their high content of glucosinolates — compounds that have an ability to stimulate carcinogen-detoxifying enzymes. Fortunately, this anticarcinogenic property of cabbage is not restricted to fresh cabbage but persists in cooked or fermented (e.g., sauerkraut) forms of this vegetable.
Also, some elements of Chinese cuisine could be recommended, e.g., short time of heat processing of meat or fish, abundant usage of spices, a high consumption of green tea.
In general, the amounts of carcinogens taken in with food are rather small. As shown by the epidemiological examples, only a persistently monotonous diet or its elements available as food supplements could be associated with an induction of diet-related cancer. Nevertheless, the question remains: what can be done to reduce the risk of nutrition-associated cancer? Nutritionists offer a very simple recommendation at this point. Its shortest version reads “a varied diet.” In the more extended version, this varied diet is described as rich in fresh vegetables and fruits, with limited usage of meat and fat (preferably vegetable oil), and with the avoidance of alcoholic beverages (except for a moderate amount of red wine).
Bon (but moderate and reasonable) apetit!
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Ames, B.N., Cancer prevention and diet: help from single nucleotide polymorphisms, Proc. Nat. Acad. Sci. USA, 96, 12,216, 1999.
Ames, B.N., Gold, L.S., and Willett, W.C., The causes and prevention of cancer, Proc. Natl. Acad. Sci. USA, 92, 5258, 1995.
Ames, B.N., Magaw, R., and Gold. L.S., Ranking possible carcinogenic hazards, Science, 236, 271, 1987.
Barsh, G.S., Farooqi, I.S., and O’Rahilly, S., Genetics of body-weight regulation, Science, 404, 644, 2000.
Charleux, J.L., Beta-carotene, antioxidant vitamins and their role in preventive nutrition, Nutr. Rev. 54S, 109, 1996.
De Flora, S., Izzotti, A., D’Agostini, F., Balansky, R.M., Noonan, D., and Albini, A., Multiple points of intervention in the prevention of cancer and other mutation-related diseases, Mutat. Res., 480, 9, 2001.
Evangelista de Duffard, A.M. and Duffard, R., Behavioral toxicology, risk assessment, and chlorinated hydrocarbons, Environ. Health Perspect., 104, suppl 2, 353, 1996.
Ferguson, L.R., Antimutagens as cancer chemopreventive agents in the diet, Mutat. Res., 307, 395, 1994.
Ferguson, L.R., Natural and man-made mutagens and carcinogens in the human diet, Mutat. Res., 443, 1, 1999.
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Gura, T., Obesity sheds its secrets, Science, 275, 751, 1997.
Kaiser, J., Just how bad is dioxin? Science, 288, 1941, 2000.
Katan, M.B. and De Roos, N.M., Public health: toward evidence-based health claims for functional foods, Science, 299, 206, 2003.
Kritchevsky, D., Diet and cancer: What’s next? J. Nutrition, 133, 3827S, 2003.
Miller, J.A. and Miller, E.C., Carcinogens occurring naturally in foods, Fed. Proc., 35, 1316, 1976.
Miller, M.C. III, Mohrenweiser, H.W., and Bell D.A., Genetic variability in susceptibility and response to toxicants, Toxicol. Lett., 120, 269, 2001.
Müller, M. and Kersten, S., Nutrigenomics: goals and strategies, Nature Rev./Genetics, 4, 315, 2003.
Phillips, D.H., Polycyclic aromatic hydrocarbons in the diet, Mutat. Res., 443, 139, 1999.
Robbana-Barnat, S., Rabache, M., Rialland, E., and Fradin, J., Heterocyclic amines: occurrence and prevention in cooked food, Environ. Health Perspect., 104, 280, 1996.
Rock, C.L., Diet and breast cancer: can dietary factors influence survival? J. Mammary Gland Biol. Neoplasia, 8, 119, 2003.
Sabichi, A., Demierre, M.F., Hawk, E.T., Lerman, C.E., and Lippman S.M., Frontiers in cancer prevention research, Cancer Res., 63, 5649, 2003.
Seifried, H.E., McDonald, S.S., Anderson, D.E., Greenwald, P., and Milner, J.A., The antioxidant conundrum in cancer, Cancer Res., 63, 4295, 2003.
Sikorski, Z.E., Food components and their role in food quality, in Chemical and Functional Properties of Food Components, Sikorski, Z.E., Ed., CRC Press, Boca Raton, FL, 2002, p. 1.
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2.2Multistage Process of Carcinogenesis...........................................................14
2.2.1Molecular Mechanisms of Mutagenesis and Carcinogenesis...........15
2.2.1.1Role of DNA Damage........................................................15
2.2.1.2Protooncogenes and Tumor Suppressor Genes: Regulators of Cell Growth.................................................18
2.2.2Molecular and Cellular Events during Initiation and Promotion of Carcinogenesis...............................................................................18
2.2.2.1Activation of Oncogenes....................................................18
2.2.2.2Inactivation of Tumor Suppressor Genes...........................20
2.2.2.3Alteration of Genes Regulating Apoptosis.........................21
2.2.3Molecular and Cellular Events during Progression of Carcinogenesis...................................................................................22
2.3Dietary Initiators and Promoters of Carcinogenesis in Humans..................23
2.3.1Examples of Dietary Initiators...........................................................23
2.3.2Examples of Dietary Promoters.........................................................27
2.4Endogenous DNA Damage............................................................................28
In 1775, the London surgeon Sir Percival Pott reported a link between scrotal skin cancer in adult men and their chronic exposure in boyhood, as chimney sweeps, to soot. The significance of this first recognition of the latent nature of cancer was not realized, however, until ~1950, when occupational exposure of workers to aromatic amines in the dyestuff, textile, and rubber industries was shown to be clearly associated with an increased risk of urinary bladder cancer later in life (Gorrod and Manson, 1986). Likewise, positive associations between cigarette smoking and lung cancer (Hoffmann and Hecht, 1990), and exposure to asbestos and lung cancer and mesotheliomas (Mossman and Gee, 1989) were established. Since the latent period
between initial exposure to a carcinogen(s) and clinical manifestation of cancer may take 15 to 25 and in some cases up to 40 years, elucidation of biochemical and molecular changes involved in cancer development has been particularly difficult. Although substantial progress toward understanding the complex process of carcinogenesis has been made during the past 50 years, its intricate mystery is not yet fully unraveled.
Our current knowledge of the process of chemical carcinogenesis has been advanced by the studies in several areas:
1.Testing of hundreds of chemical compounds in laboratory animals, and in bacterial and cell culture systems, led to delineation of the structure–activity relationships within several chemical classes of compounds eliciting carcinogenic and/or mutagenic activities.
2.Studies of the metabolism of chemical carcinogens prompted discoveries of the metabolic pathways yielding electrophilic reactants capable of modifying DNA and inflicting genotoxic damage (Miller and Miller, 1981).
3.Development of two-stage carcinogenesis models in rodents, notably skin carcinogenesis in mice (Slaga, 1984) and liver carcinogenesis in rats (Pitot and Sirica, 1980), demonstrated the irreversible and permanent nature of cancer initiation by a genotoxic carcinogen and the instability or reversibility of promotion by nongenotoxic (epigenetic) compounds.
In classical terms, three stages of the carcinogenesis process are recognized: initiation, promotion, and progression, each involving multiple steps or events. While the development of cancer in animal models can be followed precisely after administration of a single genotoxic carcinogen, human populations are chronically exposed to complex mixtures of carcinogens from environmental, occupational, tobacco smoke, and dietary sources, making it much more difficult to draw a link between carcinogen exposure and carcinogenesis end points.
This review describes the key molecular and cellular mechanisms involved in the multistage process of carcinogenesis and identifies types of DNA damage induced by representative human dietary carcinogens. The complexity and further details of the carcinogenesis process, including the molecular biology of human cancer, are more comprehensively addressed in numerous recent reviews (Cunningham, 1996; Parodi and Mancuso, 1996; Minamoto et al., 1999; Balmain and Harris, 2000; Hanahan and Weinberg, 2000; Loeb and Loeb, 2000; Bertram, 2001; Brennan, 2002; Hahn and Weinberg, 2002a; 2002b; Nebert, 2002; Bignold, 2004).
2.2MULTISTAGE PROCESS OF CARCINOGENESIS
The vast majority of all carcinogens, including those present in diets, require metabolic activation to become reactive toward DNA nucleophiles. It is now generally accepted that an individual’s genotype determines carcinogen-metabolizing enzyme polymorphism, and in turn “low-risk” and “high-risk” individuals with respect to the activation of carcinogens and potentially initiation of carcinogenesis (Graham et al., 1991). Chemical reactions of carcinogen-derived electrophilic species with
nucleophilic sites in DNA produce covalent adducts, thus inflicting DNA damage in normal cells (Miller and Miller, 1981). DNA adducts formed by a genotoxic compound may (Figure 2.1):
1.Undergo complete repair by DNA repair enzymes
2.Block DNA replication and transcription resulting in cell death
3.Remain unrepaired and be bypassed by DNA polymerases, resulting in permanent genetic damage in a new generation of cells
DNA replication in the presence of nonlethal DNA damage is a key requirement for the transformation of a normal cell into a preneoplastic cell and thus, initiation of carcinogenesis. Neoplastic transformation in replicating cells (chiefly the renewing stem cells in tissues) is acquired through mutation(s), which include base substitutions, deletions, translocations, or other modifications that affect the function of proteins involved in control of cell growth and differentiation. These genetic alterations conclude neoplastic transformation, which is sometimes perceived as an intermediate stage preceding promotion (Williams, 2001). Further stages of carcinogenesis, i.e., promotion of a neoplastic cell via clonal expansion to a benign neoplasm, and progression of the latter to a malignant neoplasm (Figure 2.1), involve complex cellular responses. These are prompted by alterations in the expression of cancer-related genes and function of their products.
2.2.1MOLECULAR MECHANISMS OF MUTAGENESIS AND CARCINOGENESIS
2.2.1.1Role
of DNA Damage
Chemical damage to DNA involves the formation of carcinogen–DNA adducts, which itself is not a mutagenic event. Although most DNA damage is repairable, the unrepaired carcinogen–DNA adducts can be misread by DNA polymerases, giving rise to irreversible changes in DNA sequence. The conversion of chemical damage to DNA nucleobases into heritable mutations takes place during cell division. In a normal cell, DNA polymerases generate an accurate and complete copy of the genetic information, using a parent DNA strand as a template. The incoming nucleotides are selected according to their ability to form Watson–Crick base pairs with the bases in the template strand [guanine (G):cytosine (C) and adenine (A):thymine (T)]. Major replicative DNA polymerases have the ability to proofread and remove incorrectly added nucleotides, resulting in a remarkable accuracy (fidelity) of DNA biosynthesis. The typical error rate by DNA polymerases is 1 per 108 to 1010 nucleotides in Escherichia coli and Drosophila, and polymerase fidelity is even greater in mammalian cells (Johnson, 1993).
Covalent binding of carcinogen-derived electrophiles to DNA nucleobases can alter their ability to form correct Watson–Crick base pairs by changing their molecular shape and hydrogen bonding characteristics. For example, O6-alkylated guanine exists as an enol tautomer, leading to a change in H-bonding pattern at N-1 and N-6. As a result, O6-alkylguanine prefers to pair with T rather than with C, guanine’s normal Watson–Crick partner (Figure 2.2). Following the second round of DNA
Detoxification
Excretion
Metabolism
Carcinogen
Growthpromoting protooncogenes
Activation
DNA-reactive electrophile
DNA-adducts
Detoxification
DNA repair
Lethal effect
Replication of chemically modified DNA
Transforming mutation in a critical gene
Tumor suppressor genes
Regulatory genes (apoptosis)
ActivationInactivationAlteration
Expression of altered gene products; loss of regulatory gene products
FIGURE 2.1 Multistage carcinogenesis initiated by a genotoxic carcinogen.
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In rubbing the salt into the pockets be careful to put the salt into every part, otherwise meat will spoil in places missed. Bellies require less salt, the fixed rule being 42%. They are not usually overhauled but are frozen at cure, if shipping is deferred.
Color .
—A great deal depends upon the color of English meats. The trade demands a bright, attractive appearance in same and considerable saltpetre is necessary. Four ounces of saltpetre to the 100 pounds of meat on cuts weighing from three to five pieces per 100 pounds, to as high as six ounces per 100 pounds on smaller cuts, should be used. The salt and saltpetre should be thoroughly mixed before applying.
FIG. 147. SQUARE EXPORT SHORT RIB.
Piling.
—Use extra care to pile meats closely and exclude the air, for they will not develop a desirable color when they are exposed to the air. After the meats are all piled evenly, the edges should be gone over, and any exposed parts covered with a fine sprinkling of salt.
Sides are piled so as to make a cup of the hollow portion with a tendency for the pickle to drain slightly toward the back. Hams are piled shank down on an angle of about 45°.
FIG. 148. WILTSHIRE SIDE.
FIG. 149.—SQUARE SHORT CLEAR.
Overhauling.
—English middles weighing from twenty-three to thirty pounds average, and long cut hams from twelve to fourteen pounds and heavier, should be overhauled at from eight to twelve days old, salting them as before described. Do not overhaul English meats unless necessary in order to hold them after they are cured.
SHIPPING AGE.
Product
Average wt. lbs.
Oct. 15 to March 1 Days March 1 to Oct. 15 Days
Bellies ... 15 to 25 15 to 25
Boneless backs ... 15 to 25 15 to 25
Cumberlands 20-24 20 to 25 20 to 25
Cumberlands 24-30 20 to 25 25 to 30
Cumberlands 30-40 25 to 30 25 to 30
Long clears under 30 20 to 25 20 to 25
Long clears over 30 20 to 25 25 to 30
Dublins and long ribs ... 20 to 25 20 to 25
Long cut hams 10-14 20 to 25 20 to 25
Long cut hams 14-18 25 to 30 25 to 30
ShippingAges.
—The table on the preceding page shows the ages at which English meats can be safely shipped during seasons from October 15 to March 1, and from March 1 to October 15. These ages for shipping should be followed closely, but when necessary the following exception may be made without detriment. From October 15 to March 1, shortest shipping age may be reduced five days.
BoxingMeats.
—Meats to be packed in borax, cured as above, should be put in a plain cold pickle 100-degree strong, then scraped on the skin side and wiped with cloths wrung out of hot water. If the meats are old and have a slippery appearance, they should be scrubbed with a brush in warm pickle and wiped afterwards. They should then be rubbed in borax with the rind placed upon a grating
and the surplus borax brushed off the skin side of the meat, using a fine brush for so doing. It is customary to use from five and one-half to six and one-half pounds of borax per 300 pounds of meat. Meats to be packed in salt should not be washed. The skin and edges of the meat should be thoroughly scraped and then rubbed in fine salt before being put in the boxes. Meats are nailed under heavy pressure so as to exclude all the air possible.
Wiltshires.
—Singed Wiltshires, a cut which was revived during the “Great War,” are made from hogs suitable for Cumberlands. Weights vary by averages. The hogs are singed during slaughter, cured in plain pickle, and shipped on ten days’ pickling, packed in dry salt.
LONG CUT HAMS AND CUMBERLAND TESTS.
Av. wt.
Test. Pig Feet.
—This test may be of service. It shows the percentage of yields of different weight hogs made into long cut hams and Cumberlands, also average weights.
—Usually only the front foot is used as it is a better shaped foot to prepare than the hind foot. The hind feet are more or less disfigured and out of condition by having the gam strings
opened in order to hang the hog on the sticks. The hind foot being used largely for making a low grade of glue. It can, however, be used in boneless pig’s feet.
Preparation.
The feet are scalded, after which the hoofs are removed and the feet are shaved and cleaned, put into a plain salt pickle, 90-degree strong by salometer test, and to this pickle should be added six ounces of saltpetre to each 100 pounds of feet. The feet should be left in this curing pickle for from six to eight days, or until they show a bright red appearance when cooked. If this red appearance does not extend clear through the feet after being cooked, it shows that they are not fully cured. They should not be left in the pickle longer than necessary to fully cure them for if heavily salted it has the effect of making them break in the cooking water.
Cooking.
—After properly cured in the salt pickle the feet should be cooked in a wooden vat (an iron vat discoloring them) provided with a false bottom about six inches above the bottom, so that the direct heat from the steam pipe does not come in contact with the feet. The water should be brought to a temperature of 200° to 206° F. and held at this temperature until the feet are sufficiently cooked. The water should never be brought to the boiling point, as the feet will become badly broken, which greatly injures their appearance.
After the feet are sufficiently cooked and thoroughly chilled in cold water, they should be put into a white wine vinegar pickle 45-degree strong, it being preferable to pack feet which are to be used at once in open vats in a refrigerated room held at a temperature of 38° to 40° F. Where feet are to be held for some months before using it is advisable to put them into barrels or tierces after filling the tierces with vinegar of 45-degree strength. The packages should be stored in a temperature 40° F. When held this way it will be found that the feet have absorbed a great deal of the vinegar and a very marked increase in weight is obtained. There should be a gain of from 10 to 15 per cent in weight at the end of three months.
Tests.
—Prepared pig’s feet at certain seasons of the year are difficult of sale and there are times when it pays better to tank them
or use them for glue purposes. The following tests on rough uncleaned fore and hind feet will show the yield when tanked. Percentages in tests are correct. The prices are those ruling at the time tests were made:
TEST ON TANKED PIGS FEET.
Total weight of front feet tanked 1,070 pounds cooked in tank five hours at forty pounds pressure:
Sixty pounds hock meat, 5.61 per cent, at 3c per pound
Prime steam lard, 138 pounds, 12.90 per cent, at $9.35 per cwt.
(dry basis), 125 pounds, 11.68 per cent, at $17.50 per ton
value, $1.47 per cwt.
Weight hind feet to tank, 996 pounds, cooked in test tank five hours, with forty pounds pressure:
steam lard, 163 pounds, 16.37 per cent, at $9.35 per cwt.
The following tests show costs, in detail, of pig’s feet put up in different sized packages, costs being figured at the regular Chicago market prices at the time these tests were made:
TEST ON 483 PIECES OR 500 POUNDS PIGS FORE FEET.
Debit:
Credit:
Pigs feet oil, 18 pounds at $5.60 per cwt.
$1.00
Pigs feet bones, 58 pounds at ³⁄₄c per pound .43
Pigs feet trimmings, 13 pounds at 1¹⁄₄c per pound .13
Total $1.56
Total net cost of 300 pounds of prepared feet 7.91
Cost per pound, including administrative expense, $0.026. Green weight, 500 pounds; cleaned weight, 450 pounds; split weight, 300 pounds.
Pig Tongues.
—Various uses are made of this piece of meat. They are very extensively used in canning factories where they are put up and known as “lunch tongue”; they are also used in different kinds of sausage, and are put up to quite an extent in vinegar pickle. When handled in the latter manner the following suggestions are of practical value.
The tongues after being trimmed should be cured in a 75-degree plain salt pickle using three ounces of saltpetre to 100 pounds of tongue. After the tongues are fully cured, which will require from eight to twelve days, they are scalded, the outer surface of the tongue being scraped off. In some instances the scalding is done before the tongues are put in the pickle. Either way is proper. After being scraped and cleaned they are cooked as desired and afterward pickled in a white wine vinegar pickle of 45-degree strength. The following tests will show the cost of tongues packed in different sized packages, the cost being determined by the cost of meat and supplies at the time tests were made:
TEST ON 1,000 PIECES, OR 910 POUNDS PIG TONGUES.
Debit:
910 pounds pig tongues, at 6¹⁄₄c per pound $56.88
Scraping at 15c per 100 pieces 1.50
Counting, cooking, etc., three hours at 18c per hour .54
Trimming at 5c per 100 pieces .50 Miscellaneous labor .20
expense, 47c per 100 on 560 pounds produced 2.63
Total $62.25
Credit:
Green weight, 910 pounds; cooked weight, 560 pounds; shrinkage, 38 per cent.
Trimming 112 pounds at 1¹⁄₂c 1.68
Net cost $60.57
Cost per pound, 10⁴⁄₅c; cost handling per cwt., including administrative expense, $0.665 per 100 pounds finished.
COST OF ONE BARREL PIG TONGUES PACKED AT 190 POUNDS NET.
190 pounds pig tongues at 10⁴⁄₅c per pound $20.52
One barrel .78
Packing, one-half hour at 17¹⁄₂c per hour .09
Pickle, ten gallons at 2¹⁄₂c per gallon .25
Coopering, one-sixth hour at 25c per hour .04
Spices, 2c .02
Miscellaneous labor .03
Total cost per barrel $21.73
FormulaforExportHogTonguePickle.
There is at times quite a demand for fresh pig tongues in Liverpool and other foreign points, in which case the trade demands that they arrive there without being salt-cured. The following formula will be found very valuable for this purpose and also point out how to carry tongues without salting them, when it is desired to do so: Use 116 pounds of boracic acid, fifty-eight pounds of borax, twenty-nine pounds of fine salt and seven and one-quarter pounds of saltpetre.
The method of mixing is as follows: The boracic acid and borax are put into a vat containing sixty gallons of water. The vat should be connected with steam supply so that it can be brought to the boiling point, cooking same slowly and stirring it well for half an hour. The salt and saltpetre is then added and should be stirred until thoroughly dissolved. After the solution has been allowed to cool, add sufficient cold water to give it a strength of 21 degrees by salometer test. Chill the solution to a temperature of 38° F. The tongues should be trimmed and thoroughly chilled, it being essential
that they are in perfect condition. They should then be packed in a tierce, after which the tierce is filled with the preservative. Tongue should be shipped in refrigerator cars where the temperature is not allowed to go above 38° F.
Pig Snouts.
—These consist of the snout of the hog together with the upper lips and front part of the nose. During preparation they are handled very much in the same manner as pig’s feet. They are first shaved and cleaned, afterward scalded, removing the outer skin or membrane of the nose. Then they are cured, using a 90-degree plain salt pickle and adding thereto three ounces of saltpetre to 100 pounds of snouts. After they are fully cured, which will require from five to eight days, they should be cooked in a wooden vat to the desired degree of tenderness after which they are chilled in cold water and pickled in white wine vinegar of 45-degree strength. The following tests show the cost of preparing pig snouts in different sized packages:
TEST ON 1,060 PIECES, OR 1,000 POUNDS PIG SNOUTS. Debit:
Cost per pound, 5¹⁄₅c; cost of handling, administrative expense, 85⁶⁄₁₀c per cwt.
