Implicaciones de los hábitos tóxicos en el cáncer

Diego Andrés Chavarro-Carvajal, Elkin García-Cifuentes, Mauricio Acosta

Resumen


Los hábitos nocivos pueden provocar daños a corto o largo plazo. Se clasifican en: hábitos de riesgo y hábitos tóxicos. Esta revisión se enfoca en analizar los hábitos tóxicos y cómo se relacionan con la aparición de procesos neoplásicos. En la literatura, se ha descrito ampliamente la relación que existe entre diferentes agentes químicos o físicos que se asocian con la génesis de neoplasia, enfatizando en el consumo de tabaco, el alcohol (etanol) y el café. El tabaco se produce a partir de las hojas de la Nicotiana tabacum. Su principal forma de consumo es a través de la combustión y aún hoy, 53 años después de que el Comité Asesor del Director General de Sanidad publicara su informe en 1964 advirtiendo de sus efectos nocivos, persiste su aparición como la principal causa de mortalidad prevenible por cáncer. Por otra parte, el alcohol constituye la principal droga consumida en nuestra sociedad. Actualmente, se encuentran todo tipo de bebidas con diferentes concentraciones de alcohol. Se define como consumo moderado la ingesta de una bebida por día para mujeres y dos tragos por día para los hombres; mientras que se concibe como exceso el consumo mayor a tres bebidas cualquier día o siete bebidas por semana en mujeres y más de cuatro bebidas al día o catorce bebidas a la semana en hombres. Adicionalmente, la cafeína se encuentra principalmente en el café, es una sustancia ampliamente consumida y culturalmente aceptada. Los estudios sobre el papel que desempeñan sus componentes han sido controversiales y se plantean diversos retos en su investigación.

 

Cancer toxic habit risks


Abstract

Noxious habits can be harmful in the short and long term. They are classified into risk habits and toxic habits. We focus this review paper on toxic habits and its relation to the onset of neoplastic processes. The relationship between chemical and physical agents and the genesis of neoplasia has been widely described through literature, making emphasis on tobacco, alcohol (ethanol) and coffee. Tobacco is made out of the leaves of the Nicotiana tabacum. It is mainly consumed by the inhalation of its base after combustion, and even now a days 53 years after the Advisory Committee Director General of Health, published its 1964 report, where they warned the community about the tobacco harmful effects, it still remains the main cause of preventable cancer mortality. In addition, alcohol (ethanol) is the most consumed drug in our society; currently all kind of beverages with different concentration of alcohol levels are available. Moderate consumption is defined as no more than one drink per day for females, and two drinks for males, whereas excessive consumption is defined as more than three drinks in one day or more than 7 per week for females, and more than four in one day or more than 14 drinks for males. Furthermore, caffeine is mainly found in coffee, it is a widely consumed and culturally accepted substance. The investigations concerning the role of its components have been controversial, dealing with a variety of challenges during the research.


Palabras clave


hábitos, tabaquismo, alcohol, etanol, cafeína,habits, smoking, alcohol, ethanol, caffeine.

Texto completo:

PDF HTML

Referencias


López AD, Collishaw NE, Piha T. A descriptive model of the cigarette epidemic in developed countries. Tob Control. 1994 Sep; 3 (3): 242- 47. doi:10.1136/ tc.3.3.242

Thun MJ, Carter BD, Feskanich D, Freedman ND, Prentice R, Lopez AD et al. 50-year trends in smoking-related mortality in the United States. N Engl J Med. 2013 Ene; 368 (4): 351- 64. doi: 10.1056/ NEJMsa1211127

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Personal habits and indoor combustions. Volume 100 E A review of human carcinogens. 1a Ed. Lyon: World Health Organization; 2012. 1- 538 pp.

Borgerding M, Klus H. Analysis of complex mixtures- cigarette smoke. Experimental and toxicologic pathology. Exp Toxicol Pathol. 2005 Jul; 57 ( Suppl 1): 43-73.

Rodgman A, Smith CJ, Perfetti TA. The composition of cigarette smoke: a retrospective, with emphasis on polycyclic components. Hum Exp Toxicol 2000 Oct; 19 (10): 573- 95.

Hukkanen J, Jacob P, Benowitz NL. Metabolism and disposition kinetics of nicotine. Pharmacol Rev 2005 Mar; 57 (1): 79 - 115. doi: 10.1124/pr.57.1.3

IARC Working Group on the Evaluation of Carcinoge- nic Risks to Humans. Tobacco smoke and involuntary smoking. IARC Monogr Eval Carcinog Risks Hum. 2004; 83: 1- 1438.

Hecht SS. Progress and challenges in selected areas of tobacco carcinogenesis. Chem Res Toxicol 2008; 21 (1): 160- 71. doi: 10.1021/tx7002068

Ding L, Getz G, Wheeler DA, Mardis ER, McLellan MD, Cibulskis K et al. Somatic mutations affect key pathways in lung adenocarcinoma. Nature 2008 Oct; 455 (7216): 1069-75. doi: 10.1038/nature07423

Schuller HM. Is cancer triggered by altered signalling of nicotinic acetylcholine receptors? Nat Rev Cancer. 2009 Mar; 9 (3): 195-205. doi: 10.1038/nrc2590

Szeliga J, Dipple A. DNA adduct formation by polycyclic aromatic hydrocarbon dihydrodiol epoxides. Chem Res Toxicol 1998 Ene; 11 (1): 1-11. doi: 10.1021/tx970142f

Doll R, Hill AB. Smoking and carcinoma of the lung; preliminary report. Br Med J. 1950 Sep ; 2 (4682): 739-748.

International Agency for Research on Cancer. To- bacco smoking. Monographs on the evaluation of the carcinogenic risk of chemicals to humans. 38. Lyon France: OMS; 1986. 35- 394

Secretan B, Straif K, Baan R, Grosse Y, El Ghissassi F, Bouvard V, et al. A review of human carcinogens- -Part E: tobacco, areca nut, alcohol, coal smoke, and salted fish. The Lancet Oncology. 2009 Nov; 10 (11): 1033- 1034. doi: http://dx.doi.org/10.1016/ S1470-2045(09)70326-2

Öberg M, Woodward A, Jaakkola MS, Peruga A, Prüss-Ustün A. Global estimate of the burden of disease from second-hand smoke. 1. Switzerland: World Health Organization; 2010

Taylor R, Najafi F, Dobson A. Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent. Int J Epidemiol. 2007 Oct; 36 (5): 1048- 59. DOI:10.1093/ije/dym158

Strong KL, Bonita R. Investing in surveillance: a fundamental tool of public health. Soz Praventivmed. 2004; 49 (4): 269- 75. PMID: 15357529

Baan R, Straif K, Grosse Y, Secretan B, El Ghissassi F, Bouvard V, et al. Carcinogenicity of alcoholic beverages. Lancet oncol. 2007 Abr; 8 (4): 292- 3. PMID: 17431955

International Agency for Research on Cancer. Alcohol consumption and ethyl carbamate. Monographs on the evaluation of carcinogenic risks to humans. 96. Lyon France: OMS; 2010. 3- 1383.

Vasiliou V, Pappa A, Estey T. Role of human aldehyde dehydrogenases in endobiotic and xenobiotic metabolism. Drug Metab Rev. 2004 May; 36 (2): 279- 299. doi: 10.1081/dmr-120034001

Jones AW. Urine as a biological specimen for forensic analysis of alcohol and variability in the urine-to- blood relationship. Toxicol Rev. 2006; 25 (1): 15- 35. PMID: 16856767

Chao YC, Wang LS, Hsieh TY, Chu CW, Chang FY, Chu HC. Chinese alcoholic patients with esophageal cancer are genetically different from alcoholics with acute pancreatitis and liver cirrhosis. Am J Gastroenterol. 2000 Oct; 95 (10): 2958- 2964. doi: 10.1111/j.1572-0241.2000.02328.x

Hashibe M, Brennan P, Chuang SC, Boccia S, Castellsague X, Chen C, et al. Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Cancer Epidemiol Biomakers Prev. 2009 Feb; 18 (2): 541- 550. doi: 10.1158/1055-9965.epi-08-0347

Balbo S, Hashibe M, Gundy S, Brennan P, Canova C, Simonato L, et al. N2-ethyldeoxyguanosine as a potential biomarker for assessing effects of alcohol consumption on DNA. Cancer Epidemiol Biomakers Prev. 2008 Nov; 17 (11): 3026- 32. doi: 10.1158/1055- 9965.epi-08-0117

Wang M, McIntee EJ, Cheng G, Shi Y, Villalta PW, Hecht SS. Identification of DNA adducts of ace- taldehyde. Chem Res Toxicol. 2000 Nov; 13 (11): 1149- 57. PMID: 11087437

Maffei F, Forti GC, Castelli E, Stefanini GF, Mattioli S, Hrelia P. Biomarkers to assess the genetic damage induced by alcohol abuse in human lymphocytes. Mutat Res. 2002 Feb; 514 (1- 2): 49- 58. PMID: 11815244

Harkonen K, Viitanen T, Larsen SB, Bonde JP, Lähdetie J. Aneuploidy in sperm and exposure to fungicides and lifestyle factors. ASCLEPIOS. A European Concerted Action on Occupational Hazards to Male Reproductive Capability. Environ Mol Mutagen. 1999; 34 (1): 39- 46. PMID:10462722

Frank A, Seitz HK, Bartsch H, Frank N, Nair J. Immunohistochemical detection of 1,N6-ethenodeoxyadenosine in nuclei of human liver affected by diseases predisposing to hepato-carcinogenesis. Carcinogenesis 2004 Jun; 25 (6): 1027- 31. doi: 10.1093/carcin/bgh089

Druesne-Pecollo N, Tehard B, Mallet Y, Gerber M, Norat T, Hercberg S, et al. Alcohol and genetic polymorphisms: effect on risk of alcohol-related cancer. Lancet Oncol. 2009 Feb; 10 (2): 173- 80. doi: 10.1016/s1470-2045(09)70019-1

Kanda J, Matsuo K, Suzuki T, Kawase T, Hiraki A, Watanabe M, et al. Impact of alcohol consumption with polymorphisms in alcohol-metabolizing enzymes on pancreatic cancer risk in Japanese. Cancer Sci. 2009 Feb; 100 (2): 296- 302. doi: 10.1111/j.1349- 7006.2008.01044.x

Yokoyama A, Omori T. Genetic polymorphisms of alcohol and aldehyde dehydrogenases and risk for esophageal and head and neck cancers. Jpn J Clin Oncol. 2003 Mar; 33 (3): 111- 21. doi: 10.1016/j. alcohol.2005.04.003

Cano-Marquina A, Tarin JJ, Cano A. The impact of coffee on health. Maturitas 2013 May; 75 (1): 7- 21.doi: 10.1016/j.maturitas.2013.02.002




Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.

Academia Nacional de Medicina -  Copyright. Todos los Derechos Reservados

Tel/Fax: (571) - 5550555 Opc. 6  |  Bogotá, Cra. 7ª # 69-11

publicaciones@anmdecolombia.org.co