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Published in Jamie Bartram, Rachel Baum, Peter A. Coclanis, David M. Gute, David Kay, Stéphanie McFadyen, Katherine Pond, William Robertson, Michael J. Rouse, Routledge Handbook of Water and Health, 2015
Lisa Smeester, Andrew E. Yosim, Rebecca C. Fry
Mechanistically, there is a concern that the formation of N-nitroso compounds through endogenous nitrosation of nitrates and nitrites may contribute to carcinogenesis. Epidemiological studies have not demonstrated an association between nitrate/nitrite contaminated drinking water and cancers of the gastrointestinal system (esophagus, stomach, bladder and colon), nevertheless nitrate and nitrite are classified as group 2A probable carcinogens based on animal studies (IARC, 2010). It should also be noted that while epidemiological studies have shown a positive correlation between levels of nitrate and hypertrophy of the thyroid gland (van Maanen et al., 1994), effects on thyroid hormone dysregulation have been inconclusive as nitrate was associated with lowered thyroid stimulating hormone (TSH) among women (van Maanen et al., 1994), while increased levels of TSH was reported in a children’s cohort (Tajtakova et al., 2006).
Endogenous Formation of Nitrosamines and Oxidative DNA-Damaging Agents in Tobacco Users
Published in Roger O. McClellan, Critical Reviews in Toxicology, 2017
J. Nair, H. Ohshima, U. J. Nair, H. Bartsch
Tobacco habits such as smoking, snuff dipping, and chewing of tobacco alone or with betel quid (BQ) ingredients have been causally associated in man with malignancies of the upper aerodigestive tract, pancreas, and renal pelvis.1,2 About one-third of all cancers worldwide can be attributed to various tobacco habits,3,4 and hence could be preventable by the cessation of the habits. Tobacco smoke contains several known classes of carcinogens such as polycyclic aromatic hydrocarbons, volatile and tobacco-specific nitrosamines (TSNA), and aromatic amines,5 whereas in unburnt tobacco, very high concentrations (up to milligrams per gram of product) of TSNA have been reported.6–8 Based on rodent bioassays that demonstrated the carcinogenicity of TSNA9,10 and epidemiological studies that have causally associated tobacco habits to human cancer,1,2 it is strongly suggested that TSNA contribute to the causation of human neoplasms.11 In addition to the preformed nitroso compounds present in tobacco and tobacco smoke, nitrosamines could also be formed endogenously from nitrosatable alkaloids such as nornicotine, anatabine, and anabasine (present in hundreds of milligrams per gram of tobacco), and from nitrosatable amines such as pyrrolidine. Evidence is also accumulating for the endogenous synthesis of nitrosamines from nitric oxide (NO)-mediated reactions that are generated during inflammatory processes via nitric oxide synthase.12 In addition, nitrosation modifiers such as thiocyanate (in saliva) and aldehydes (in smoke) may catalyze the nitrosation process in the body. The formation of reactive oxygen species (ROS) has been demonstrated from BQ ingredients such as areca nut and catechu, which are used frequently in India and other countries from Micronesia.13 Several experimental studies have demonstrated that ROS can lead to DNA-base damage such as 8-hydroxydeoxyguanosine (80H-dG) and thymine glycol, which are implicated in mutagenesis and carcinogenesis.14 The following article reviews the current evidence for the formation of nitroso compounds in the human body, following the use of tobacco by various habits and by nitrosation processes that may also be enhanced during chronic cellular inflammatory conditions via the formation of NO. The role of endogenous formation of ROS and derived DNA damage, possibly acting synergistically with TSNA in the etiology of oral cancer, is also discussed.
Ground/drinking water contaminants and cancer incidence: A case study of rural areas of South West Punjab, India
Published in Human and Ecological Risk Assessment: An International Journal, 2021
Gursharan Kaur, Ravishankar Kumar, Sunil Mittal, Prafulla Kumar Sahoo, Upma Vaid
Like the U and As, drinking high levels of anions NO3– also cause cancers of various types such as bladder and digestive system. The ADI value of NO3– was higher among all parameters in the current study. Schullehner et al. (2018) carried out an extensive epidemiological study of NO3– exposure through drinking water in 2.7 million adults during the year 1978 to 2011 and reported 5,944 number of colorectal cancer cases suggesting a strong relationship between the two. The mechanism involved is endogenous reduction of NO3– into nitrite by nitrosation reactions and formation of highly carcinogenic N-nitroso compounds in the stomach, large intestine, colon, and bladder (Weyer et al. 2001; De Roos et al. 2003; Bryan et al. 2012). N-nitroso compounds are the most potent known carcinogens which act systemically and cause cancer in these organs.
Nitrates in industrial and traditional tomato paste from Arsenjan City, Iran: a health risk assessment study
Published in International Journal of Environmental Health Research, 2023
Amin Mohammadpour, Ehsan Gharehchahi, Mohammad Reza Narooie, Zahra Derakhshan, Aynura Aliyeva, Amin Mousavi Khaneghah
Ingestion exposure to NO3– and nitrites (NO2–) primarily occurs through food and drinking water, with 80% of NO3– coming from vegetables (Karwowska and Kononiuk 2020). Ingestion exposure to NO3– and NO2– can harm human health. Infants under three months can acquire methemoglobinemia (Blue Baby Syndrome). NO3− toxicity arises from its conversion into NO2– and nitric oxide (NO) by reductase enzymes. Some oral bacteria, such as facultative anaerobes, could convert NO3– and NO2– into NO and other nitrogen-containing compounds, which can then participate in various physiological and pathological processes. Additionally, bacteria within the intestinal tract can convert NO3– to NO2– and finally to NO, potentially playing a role in forming cancer-causing N-nitroso compounds (Hezel and Weitzberg 2015). The WHO has established an acceptable daily intake (ADI) of NO3– and NO2– of 3.7 and 0.07 mg per kg of BW per day, respectively (Keller et al. 2020). Based on the IARC, ingested NO3– or NO2– under circumstances that lead to endogenous nitrosation is classified as probably carcinogenic to humans (Group 2A) (Loprieno 1975). Substantial evidence links NO3– ingestion and thyroid disease and neural tube abnormalities. Recent studies have shown that short-term exposure to high levels of NO3– may decrease the risk of hypertension and heart disease in people over 60. The human body absorbs NO3– rapidly, but more than 90% of excretion occurs by urine. Antioxidant compounds in certain foods, such as vitamin C and green tea, can lower the body’s formation of N-nitroso compounds (NOCs) (Organization and U 2004). Therefore, health risk assessment of exposure to NO3– in the diet is challenging.