Editorial Open Access
Copyright ©2010 Baishideng. All rights reserved.
World J Gastroenterol. Jul 28, 2010; 16(28): 3475-3477
Published online Jul 28, 2010. doi: 10.3748/wjg.v16.i28.3475
Colorectal cancer and pollution
AM El-Tawil
AM El-Tawil, Department of Surgery, University Hospital of Birmingham, Birmingham, B15 2TH, United Kingdom
Author contributions: El-Tawil AM is entirely responsible for this article from conception to writing.
Correspondence to: AM El-Tawil, MSc, MRCS, PhD, Department of Surgery, University Hospital of Birmingham, East Corridor, Ground floor, Edgbaston, Birmingham, B15 2TH, United Kingdom. atawil20052003@yahoo.co.uk
Telephone: +44-121-6938231 Fax: +44-121-4466220
Received: March 26, 2010
Revised: April 21, 2010
Accepted: April 28, 2010
Published online: July 28, 2010


The incidence of colorectal carcinoma is increasing in young patients, in contrast to the well established wisdom that it is exclusively diagnosed in patients older than 40 years. In this survey, we examined all possible risk factors, and we recommend a number of measures for early detection in young patients who are at risk of developing this malignant tumor.

Key Words: Colorectal adenocarcinoma, Food contamination, Pesticides, Young patients, Free radicals


Colorectal cancer continues to be one of the most common human malignancies, afflicting nearly one million individuals worldwide every year. The disease can be considered endemic in all western and industrialized countries, but there are indications that, in the near future, colorectal neoplasms will become frequent also in populations that at present show a low incidence of the disease[1]. Reports from Asian and African countries have demonstrated that annual diagnosis of colorectal cancer is increasing[2-5] and cases have been identified in those aged < 40 years old[6]. However, hereditary factors could not be recognized as risk factors in these cases[6] and high dietary intake of meats and fats could not be blamed as risk factors in these developing countries because of a lack of supply of either to the majority of the population[6-8]. Therefore, this phenomenon requires further investigation. It is likely to be due to chemical contamination of food and drink.


It is likely that chlorination of drinking water plays a role in the above phenomenon. During the chlorination process, chlorine reacts with organic materials in the water to produce a complex mixture of halogenated and non-halogenated by-products, the concentration and distribution of which vary with characteristics of the raw water and the treatment process[9]. A large number of halogenated chemical species have been identified, including trihalomethanes, halogenated acetonitriles, halogenated acids, haloketones, and haloaldehydes[10]. Trihalomethanes are the most frequently occurring by-products[11,12] and are routinely measured in public water supplies, thus making them a useful marker for the level of chlorination by-products in treated water. Chronic exposure to disinfected surface waters is considered one of the contributing factors to the development of urinary bladder and colon cancer[13-15]. Mutagenic activity of chlorinated water may be due to the presence of chemicals produced from reactions of chlorine with natural substances released by the breakdown of vegetation in the source water[16]. The chlorinated hydroxyfuranone [e.g. 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone], for example, has been shown to be responsible for a majority of this mutagenic activity[5,12]. 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone has been reported to occur at much lower concentrations in drinking water than other disinfection by-products, yet it might be a significant public health concern because it is the most potent mutagen currently identified in drinking water[17]. Two years of treatment with this compound in drinking water resulted in a multi-organ carcinogenic response in male and female Wistar rats[18]. Moreover, reliable evidence from epidemiological studies has suggested an increase in the risk of urinary bladder, colon, and rectal cancer among people using disinfected drinking water that contains high levels of trihalomethanes[15,19]. King et al[20] have reported that increasing exposure to different drinking water constituents is associated with increasing risk of colon cancer in men. In this population, several halogenated chemical species have shown a tendency for increasing colon cancer risk across different exposure categories due to increasing exposure, which reached at least a 53% elevation in risk for the highest exposure categories. Long-term (approximate 35 years) exposure to trihalomethanes at a level of approximate 75 mg/L was associated with a doubled colon cancer risk among men (OR: 2.10, 95% CI: 1.21-3.66). The highest quartile of cumulative trihalomethanes-years exposure was associated with an OR of 1.74 (95% CI: 1.25-2.43)[20]. The continuous representation of cumulative trihalomethanes exposure was associated with a 17% increase in risk for each 1000 mg/L-years (95% CI: 6-29)[20].


Polychlorinated biphenyls are possible sources of food contamination. They are synthetic organochlorine compounds that are used in industrial and commercial processes[19,21]. However, dioxins, commonly referred to as dibenzodioxins and dibenzofurans, are organochlorine by-products of waste burning, paper lightening, pesticide production, and production of polyvinyl chloride plastics[21,22]. In the United States, major dietary sources of polychlorinated biphenyls and dioxins are beef, chicken, and pork, dairy products, vegetables, fish and shellfish, and eggs[23]. Animal experiments and some evidence in humans have indicated that polychlorinated biphenyls and dioxins are carcinogenic. This is likely to be related to effects on the aryl hydrocarbon receptor, a transcription factor that affects gene expression[24,25].

Food contamination with pesticides is another example. High levels of different types of pesticides in the collected serum samples from patients with colorectal carcinoma and their relatives have been reported[26-29]. However, no significant correlation between these chemicals and development of this neoplasm has been recognized. Also, higher concentrations of these chemicals in the samples from the healthy relatives[29] might have precluded any possibility of any significant link. Nevertheless, there is increasing evidence that systemic oxidative stress plays an important role in the development and progression of cardiovascular disease and cancer[30].

Oxidative stress is defined as a state in which the level of toxic reactive oxygen intermediates (free radicals) overcomes the endogenous antioxidant defenses of the host, such as the lipid-soluble antioxidants. Oxidative stress can result, therefore, from either an excess of free radical production or depletion of antioxidant defenses. For example, in the absence of adequate levels of lipid-soluble antioxidants, increased free radical production may cause functional and structural damage by reacting with lipoproteins, thus resulting in lipid peroxidation with the formation of degradation products, such as malondialdehyde, which are themselves carcinogenic. The mechanism by which overproduction of free radicals can lead to development of a chronic non-infectious disease has been fully described previously[31].

Recent studies have reported that various pesticides can induce oxidative stress in different tissues[32-35]. The significantly reported positive correlation between different tumor stages, concentrations of lipid peroxidation products, and lack of antioxidants in the serum of patients with colorectal cancer[36-38] gives hope for screening those patients who are at risk for development of these tumors, and for detecting these malignancies at an early stage.

The failure to link measurements of pesticides in the serum of patients with diagnosed colorectal adenocarcinoma to other measurements of lipid peroxidation products, (e.g. malondialdehyde) antioxidants, (e.g. vitamin C, zinc) and copper/zinc ratio in the blood likely explains the confusing outcome of the published reports.


Well-structured studies need to be designed to assess a possible link between levels of pesticides in those at risk of developing bowel tumors with the levels of lipid peroxidation products for early tumor detection.


Peer reviewer: Kam-Meng Tchou-Wong, Assistant Professor, Departments of Environmental Medicine and Medicine, NYU School of Medicine, 57 Old Forge Road, Tuxedo, New York, NY 10987, United States

S- Editor Wang YR L- Editor Kerr C E- Editor Lin YP

1.  Ponz de Leon M Colorectal Cancer. New York: Springer-Verlag Berlin Heidelberg 2002; .  [PubMed]  [DOI]  [Cited in This Article: ]
2.  AbdAbdulkareem FB, Abudu EK, Awolola NA, Elesha SO, Rotimi O, Akinde OR, Atoyebi AO, Adesanya AA, Daramola AO, Banjo AA. Colorectal carcinoma in Lagos and Sagamu, Southwest Nigeria: a histopathological review. World J Gastroenterol. 2008;14:6531-6535.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Cancer registration literature update (2006-2008) Asian Pac J Cancer Prev. 2008;9:165-182.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Cronjé L, Paterson AC, Becker PJ. Colorectal cancer in South Africa: a heritable cause suspected in many young black patients. S Afr Med J. 2009;99:103-106.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  Irabor DO, Dongo AE. Anal carcinoma in a tropical low socio-economic population in the new millennium: What has changed? Trop Doct. 2009;39:7-9.  [PubMed]  [DOI]  [Cited in This Article: ]
6.  Abou-Zeid AA, Khafagy W, Marzouk DM, Alaa A, Mostafa I, Ela MA. Colorectal cancer in Egypt. Dis Colon Rectum. 2002;45:1255-1260.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Schmitz PM, Kavallari A. Crop plants versus energy plants--on the international food crisis. Bioorg Med Chem. 2009;17:4020-4021.  [PubMed]  [DOI]  [Cited in This Article: ]
8.  Per Capita Consumption of Meat and Poultry, by Country. Source: U.S. Department of Agriculture, Foreign Agricultural Service, Livestock and Poultry: World Markets and Trade, annual.  Available from: http://www.allcountries.org/uscensus/1370_per_capita_consumption_of_meat_and.html.  [PubMed]  [DOI]  [Cited in This Article: ]
9.  Stevens AA, Moore LA, Slocum CJ, Smith BL, Seeger DR, Ireland JC. By-products of water chlorination at ten operating utilities. Water Chlorination: Chemistry, Environmental Impact and Health Effects. Vol. 6. Chelsea, Michigan: Lewis Publishers, Inc 1990; 579-604.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  Krasner SW, McGuire MJ, Jacangelo JG, Patania NL, Regan KM, Aieta EM. The occurrence of disinfection byproducts in U.S. drinking water. J Am Water Works Assoc. 1989;81:41-53.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Cantor KP. Epidemiologic studies and risk assessment of volatile organic compounds in drinking water. Significance and Treatment of Volatile Organic Compounds in Water Supplies. Chelsea, Michigan: Lewis Publishers, Inc 1990; 465-484.  [PubMed]  [DOI]  [Cited in This Article: ]
12.  International Agency for Research on Cancer IARC Monographs on the Evaluation of Carcinogenic Risk to Humans (52): Chlorinated Drinking-Water; Chlorination By-Products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds. Lyon, France: World Health Organization 1991; .  [PubMed]  [DOI]  [Cited in This Article: ]
13.  Cantor KP, Hoover R, Hartge P, Mason TJ, Silverman DT, Altman R, Austin DF, Child MA, Key CR, Marrett LD. Bladder cancer, drinking water source, and tap water consumption: a case-control study. J Natl Cancer Inst. 1987;79:1269-1279.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Cantor KP, Lynch CF, Hildesheim ME, Dosemeci M, Lubin J, Alavanja M, Craun G. Drinking water source and chlorination byproducts. I. Risk of bladder cancer. Epidemiology. 1998;9:21-28.  [PubMed]  [DOI]  [Cited in This Article: ]
15.  Wigle DT. Safe drinking water: a public health challenge. Chronic Dis Can. 1998;19:103-107.  [PubMed]  [DOI]  [Cited in This Article: ]
16.  Morris RD, Audet AM, Angelillo IF, Chalmers TC, Mosteller F. Chlorination, chlorination by-products, and cancer: a meta-analysis. Am J Public Health. 1992;82:955-963.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Bull RJ, Birnbaum LS, Cantor KP, Rose JB, Butterworth BE, Pegram R, Tuomisto J. Water chlorination: essential process or cancer hazard? Fundam Appl Toxicol. 1995;28:155-166.  [PubMed]  [DOI]  [Cited in This Article: ]
18.  Kronberg L, Vartiainen T. Ames mutagenicity and concentration of the strong mutagen 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone and of its geometric isomer E-2-chloro-3-(dichloromethyl)-4-oxo-butenoic acid in chlorine-treated tap waters. Mutat Res. 1988;206:177-182.  [PubMed]  [DOI]  [Cited in This Article: ]
19.  Komulainen H, Kosma VM, Vaittinen SL, Vartiainen T, Kaliste-Korhonen E, Lötjönen S, Tuominen RK, Tuomisto J. Carcinogenicity of the drinking water mutagen 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone in the rat. J Natl Cancer Inst. 1997;89:848-856.  [PubMed]  [DOI]  [Cited in This Article: ]
20.  King WD, Marrett LD, Woolcott CG. Case-control study of colon and rectal cancers and chlorination by-products in treated water. Cancer Epidemiol Biomarkers Prev. 2000;9:813-818.  [PubMed]  [DOI]  [Cited in This Article: ]
21.  National Center for Environmental Assessment, US Environmental Protection Agency. Dioxin and related compounds.  Available from: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm.  [PubMed]  [DOI]  [Cited in This Article: ]
22.  US Environmental Protection Agency. Polychlorinatedbiphenyls (PCBs).  Available from: http://www.epa.gov/opptintr.  [PubMed]  [DOI]  [Cited in This Article: ]
23.  Schecter A, Cramer P, Boggess K, Stanley J, Päpke O, Olson J, Silver A, Schmitz M. Intake of dioxins and related compounds from food in the U.S. population. J Toxicol Environ Health A. 2001;63:1-18.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  World Health Organization (WHO). Assessment of the health risk of dioxins: re-evaluation of the Tolerable Daily Intake (TDI). WHO Consultation; May 25-29, 1998; Geneva, Switzerland .  [PubMed]  [DOI]  [Cited in This Article: ]
25.  National Center for Environmental Assessment, US Environmental Protection Agency PCBs: cancer dose response assessment and application to environmental mixtures. Washington, DC: US Environmental Protection Agency 1996; .  [PubMed]  [DOI]  [Cited in This Article: ]
26.  Jaga K. Serum organochlorine pesticide levels in patients with colorectal cancer in Egypt. Arch Environ Health. 1999;54:217-218.  [PubMed]  [DOI]  [Cited in This Article: ]
27.  Soliman AS, Smith MA, Cooper SP, Ismail K, Khaled H, Ismail S, McPherson RS, Seifeldin IA, Bondy ML. Serum organochlorine pesticide levels in patients with colorectal cancer in Egypt. Arch Environ Health. 1997;52:409-415.  [PubMed]  [DOI]  [Cited in This Article: ]
28.  Hoar SK, Blair A, Holmes FF, Boysen C, Robel RJ. Herbicides and colon cancer. Lancet. 1985;1:1277-1278.  [PubMed]  [DOI]  [Cited in This Article: ]
29.  Caldwell GG, Cannon SB, Pratt CB, Arthur RD. Serum pesticide levels in patients with childhood colorectal carcinoma. Cancer. 1981;48:774-778.  [PubMed]  [DOI]  [Cited in This Article: ]
30.  Chang D, Wang F, Zhao YS, Pan HZ. Evaluation of oxidative stress in colorectal cancer patients. Biomed Environ Sci. 2008;21:286-289.  [PubMed]  [DOI]  [Cited in This Article: ]
31.  El-Tawil AM. Eastern and Western Nations: Different Prevalence of Chronic-Non-Infectious Diseases, Why? Iranian J Publ Health. 2010;39:96-99.  [PubMed]  [DOI]  [Cited in This Article: ]
32.  Kisby GE, Muniz JF, Scherer J, Lasarev MR, Koshy M, Kow YW, McCauley L. Oxidative stress and DNA damage in agricultural workers. J Agromedicine. 2009;14:206-214.  [PubMed]  [DOI]  [Cited in This Article: ]
33.  Mena S, Ortega A, Estrela JM. Oxidative stress in environmental-induced carcinogenesis. Mutat Res. 2009;674:36-44.  [PubMed]  [DOI]  [Cited in This Article: ]
34.  Muniz JF, McCauley L, Scherer J, Lasarev M, Koshy M, Kow YW, Nazar-Stewart V, Kisby GE. Biomarkers of oxidative stress and DNA damage in agricultural workers: a pilot study. Toxicol Appl Pharmacol. 2008;227:97-107.  [PubMed]  [DOI]  [Cited in This Article: ]
35.  Bartsch H, Nair J. Potential role of lipid peroxidation derived DNA damage in human colon carcinogenesis: studies on exocyclic base adducts as stable oxidative stress markers. Cancer Detect Prev. 2002;26:308-312.  [PubMed]  [DOI]  [Cited in This Article: ]
36.  Biasi F, Tessitore L, Zanetti D, Cutrin JC, Zingaro B, Chiarpotto E, Zarkovic N, Serviddio G, Poli G. Associated changes of lipid peroxidation and transforming growth factor beta1 levels in human colon cancer during tumour progression. Gut. 2002;50:361-367.  [PubMed]  [DOI]  [Cited in This Article: ]
37.  Skrzydlewska E, Stankiewicz A, Sulkowska M, Sulkowski S, Kasacka I. Antioxidant status and lipid peroxidation in colorectal cancer. J Toxicol Environ Health A. 2001;64:213-222.  [PubMed]  [DOI]  [Cited in This Article: ]
38.  Schmid K, Nair J, Winde G, Velic I, Bartsch H. Increased levels of promutagenic etheno-DNA adducts in colonic polyps of FAP patients. Int J Cancer. 2000;87:1-4.  [PubMed]  [DOI]  [Cited in This Article: ]