Environmental Food Contaminants and Control Recommendations

Environmental contaminants are considered a significant food safety risk. The rising population increased food production and industrialization have accentuated the importance of addressing food contamination. The primary causes of these contaminants in food include agricultural practices, industrial activities, waste management, and air and water pollution. Contamination can occur at various stages of the food chain and can reach consumers.

Various strategies and measures are recommended to prevent and control environmental food contaminants. In this regard, appropriate production systems, the improvement of agricultural practices, and the monitoring of food production systems crucial. Governments and international organizations also play a role in establishing and enforcing food safety standards concerning environmental contaminants.

In conclusion, this brief review addresses significant environmental contaminants such as heavy metals, dioxins, microplastics, nitrite-nitrate, PCBs, and melamine, and highlights potential health issues. Continuous updating of knowledge and strategies in this field through future research and development is essential.

Ensuring food safety is crucial for public health, and consuming safe food is a fundamental human right. The increasing population and the consequent rise in food demand have boosted industrial production. However, foods are at risk of contamination from various environmental sources today. These contaminants can be briefly defined as harmful substances present in the environment that can enter food through various pathways. These contaminants can infiltrate foods through industrial activities, urban development, and agricultural practices, as well as through natural events, posing health risks.

Environmental food contaminants include heavy metals, pesticides, dioxins, Polychlorinated Biphenyls (PCBs), nitrates and nitrites, microplastics, endocrine disruptors, and radioactive substances. These substances can contaminate food at any stage of the food production chain. For instance, agricultural pesticides are directly applied to plants, while plants can absorb heavy metals through water and soil. Similarly, industrial waste and urban pollution can enter water sources, accumulating in seafood. Natural events, such as volcanic eruptions or the erosion of natural mineral deposits, can also release certain contaminants directly into the environment.

The effects of these contaminants on human health are wide-ranging. They can cause serious health issues such as acute poisoning, carcinogenic effects, hormonal imbalances, nervous system damage, and chronic diseases. Vulnerable populations, including children, pregnant women, the elderly, and individuals with weakened immune systems, are particularly sensitive to these contaminants and are therefore, at greater risk. Long-term exposure, even at low doses, can lead to health problems, further increasing the danger posed by these contaminants.

Environmental contaminants can enter food at every stage of the food production chain, from raw material acquisition to the production process and packaging. Pesticides used in agriculture, veterinary drugs in livestock farming, the spread of industrial waste through water and soil, air pollution, and improper food processing methods are major contamination pathways. Additionally, contaminants can migrate from food packaging materials and processing equipment into the food. Therefore, controlling environmental pollution, rigorously monitoring food production processes, and raising consumer awareness are crucial for ensuring food safety.

This review briefly addresses some environmental food contaminants, their routes of contamination, and their effects on health. The aim is to raise awareness on this issue and emphasize the importance of measures related to food safety. Detecting and controlling environmental contaminants is indispensable for public health and food safety.

Dioxins and PCBs (Polychlorinated Biphenyls)

"Dioxins" (Polychlorinated Dibenzo-P-Dioxins [PCDDs] and Polychlorinated Dibenzofurans [PCDFs]) can be unintentionally produced in various chemical processes as well as in nearly all combustion processes [1]. Dioxins are by-products that occur in nearly all combustion processes and many chemical processes, especially during waste incineration, volcanic eruptions, and forest fires [2]. Dioxins refer to a large chemical group containing around 200 different chlorinated compounds [3]. A group with similar physical, chemical, and biological properties to dioxins is the dioxin-like Polychlorinated Biphenyls (PCBs), comprising 12 compounds [4,5].

Dioxins are significant environmental contaminants in food production due to their prevalence in nature and their ability to transfer from air to soil and food, eventually reaching humans through animal-based foods [6]. Their fat-soluble chemical structure allows them to accumulate in the fatty tissues of meat products. The fatty tissues of fish and other animals are particularly important concerning dioxin presence [7]. While the highest dioxin concentrations are detected in fatty fish, animal-derived foods such as meat, eggs, and dairy products are also noteworthy in terms of this contaminant [5]. Additionally, the potential for dioxins to reach the milk of lactating women poses a risk, especially to infants [8,9].

The toxic impact of these compounds accumulating in the human body primarily concerns their effect on health, particularly the disruption of the endocrine system's balance [10]. Acute dioxin exposure primarily causes persistent acne-like skin lesions [7], while chronic exposure can lead to carcinogenic effects [11] and adverse impacts on reproductive and immune systems [7]. Other effects observed in various animal studies include liver enlargement and depression [3]. Dioxin exposure at the same doses results in similar symptoms in both mice and humans [4,9]. The primary method to prevent human exposure to dioxin-like PCBs is to control the release of these chemicals into the environment [12]. Controlling their release into the environment will also minimize food chain contamination [13].

Heavy metals

Heavy metals such as mercury, lead, cadmium, and arsenic are toxic elements that can accumulate in the environment through natural and anthropogenic activities. They can disperse into the environment through natural events, and geological and biological cycles, and accumulate in animal and plant tissues [14]. Human activities such as factory waste, fossil fuel use, mining, and industrialization also contribute to environmental contamination and subsequently affect food [15]. Heavy metals spread into the environment, particularly through soil and water, posing a contamination risk to food.

The most concerning heavy metals as food contaminants are mercury, lead, cadmium, and arsenic. Mercury's primary source for humans is often fish, particularly in contaminated areas, where fish serve as a significant source of methylmercury. In addition to fish, grains also accumulate mercury, which is important for human mercury intake through the food chain.

The release of mercury can also result from activities such as the use of fossil fuels (especially coal), power stations generating electricity, gold and mercury mining, the production of cement, chlorine, caustic soda, mirrors, and medical equipment, industrial spills, dentistry, waste incineration, and the use of pesticides [16] and fungicides [17]. Chronic mercury poisoning can cause neurological and psychological symptoms in humans, affecting the nervous system from all mercury forms [3]. These symptoms disappear once mercury exposure is eliminated [18].

Cadmium's primary source of human exposure is the food chain [19-22]. Due to its extensive industrial use, cadmium can easily contaminate the environment and food [3]. Hence, most foods, even at low concentrations (0.1 mg/kg), contain cadmium, with seafood being a notable source. Fish muscles and livers in cadmium-contaminated areas are reported as significant cadmium sources [23,24]. Other marine organisms such as oysters, scallops, mussels, and shellfish are also important for cadmium contamination [22]. In addition to seafood, animal foods, particularly offal such as kidneys and liver, are significant sources of cadmium [20,25]. Cadmium levels in these tissues can increase with the age of the animals [21]. Studies have shown that leafy vegetables particularly accumulate cadmium [20,26]. Fertilizers used in agriculture, mining activities, cement production, metallurgical processes, fossil fuel usage, and improper management of urban waste are significant sources of cadmium [21].

Cadmium targets the liver and kidneys in the human body [19]. Chronic cadmium exposure in adults (via ingestion or inhalation) can cause damage to the lungs, kidneys, and bones [25]. This toxicity can also lead to cardiovascular issues, emphysema, and kidney disorders [19].

Lead is another significant environmental food contaminant, often found alongside cadmium. The primary source of lead is the lead sulfide ore known as "galena." Smelting and recycling processes also constitute major sources of contamination. Additionally, lead can be found in contaminated drinking water, plant and animal foods, lead-coated containers, water pipes, cosmetics, insecticides, paints, cigarettes, gasoline, leaded toys, lead produced for firearms, and lead acetate in pesticides [27]. Agricultural products are particularly important for environmental lead contamination. In addition to agricultural contamination, food processing and storage containers (especially lead-containing tin cookware, soldered metal cans, glazed bowls, and leaded crystals) can release lead into food [28]. Marine organisms in lead-contaminated waters can also be significant lead sources [29]. In the food cycle, lead can be transported via insects, with poultry tissues becoming contaminated after consuming lead-accumulating insects [30].

Acute lead poisoning symptoms are primarily neurological, including headaches, abdominal pain, irritability, and various nervous system-related conditions [18]. Chronic lead poisoning, however, affects the central and peripheral nervous systems, causing anemia, impaired kidney function, increased amino acid excretion in urine, and weight loss [3,19,31,32].

The use of pesticides in agriculture leads to the formation of arsenic in the soil and the contamination of groundwater [33]. In addition, superphosphate fertilizers contain high levels of arsenic (0.5 mg/100g) [34]. The use of fossil fuels is also considered a major cause of arsenic release [35]. Arsenic, another significant environmental contaminant, generally contaminates soil and water, and through these pathways, it can enter food [18,36]. Arsenic toxicity typically occurs in countries with contaminated groundwater, such as India, Bangladesh, and China [33,37-40].

Chronic arsenic toxicity results from long-term, low-dose exposure and progresses without symptoms [41]. Diseases associated with chronic arsenic toxicity include cancers of the skin, lungs, bladder, kidneys, liver, and uterus [33,42]. The most well-known symptoms of acute arsenic poisoning from high-dose exposure are skin redness, muscle pain, and fatigue [41]. Higher doses can lead to persistent fever, anorexia, melanosis, bloody diarrhea, cardiac arrhythmia, and even death [3,19].

Preventing and controlling the release of heavy metals into the environment is a crucial step in preventing the contamination of food. Monitoring foods according to established heavy metal limits, controlling industrial waste, and regulating every stage of the food chain from raw materials to consumption can be beneficial for improving these processes.

Microplastics

Plastic is frequently used as a packaging material due to its lightweight, flexible, and durable nature. Consequently, microplastics are widespread environmental contaminants across the globe [43]. Microplastics, prevalent in seafood, water, and other food sources, pose significant environmental and health risks due to their pervasive nature and potential for systemic circulation in mammals. These contaminants are widely found in seafood, water, salt, and honey, with particles smaller than 25 µm having the potential to enter the systemic circulation of mammals [44]. Microplastics can cause neurotoxicity, oxidative stress, and inflammation in humans [45]. Additionally, they can have adverse effects on cellular toxicity and the immune system [46].

To prevent microplastics from entering the food chain, proper management of plastic waste and strengthening recycling systems are crucial [47]. Implementing strict controls and regulations to reduce microplastic pollution in the food production chain is also necessary [48]. Raising consumer awareness and paying attention to microplastic content in food packaging can be effective in reducing exposure [49].

Melamine

Melamine, a nitrogen-rich organic compound, is widely used in industries, particularly in fertilizers and plastic production, leading to potential contamination of food during packaging and storage [50]. It becomes a significant contaminant during food packaging and storage processes. Melamine can migrate into food, especially acidic foods, from plastic containers in which it is used. Its use as a fertilizer for crops is also considered an important contamination route [51].

Animal studies have shown that melamine toxicity is related to age, with older animals being less affected due to the completion of organ development [52]. This is similar in humans, where infants are more susceptible to melamine toxicity, which can affect their kidney and urinary systems, sometimes leading to acute kidney failure and death [50,51]

Implementing regulations that limit the use of melamine in fertilizers and food packaging can help reduce contamination. Developing alternative packaging materials and conducting research and development in this area can also help decrease melamine contamination. Prioritizing improvements in products for infants is particularly important.

Nitrate and nitrite

Nitrate and nitrite, commonly found in fertilizers, contaminate food through agricultural practices and water sources [53]. This enriches the soil with these contaminants. Nitrates and nitrites can also be found in water sources, mainly due to human, animal, and industrial waste [54]. Therefore, nitrate and nitrite can naturally occur in many foods. Green leafy vegetables and root crops can absorb nitrate from the soil [55]. Vegetables like beets, celery, lettuce, spinach, and radishes are known to contain over 1000 mg/kg of nitrate. Fruits, however, generally have lower levels of nitrate (10 mg/kg) and nitrite (1 mg/kg) [56]. Studies indicate that a large percentage of the daily intake of nitrate comes from vegetables [57] Processed meat products also expose us to these contaminants due to the use of nitrate and nitrite as additives [58-60]

The acute and chronic health issues caused by nitrate and nitrite are significant. In adults, the consumption of 8-15 g of sodium or potassium nitrate has been linked to severe gastroenteritis, abdominal pain, blood in urine and stool, and general weakness. Nitrite is known to be more toxic than nitrate even at lower levels. The Lethal Dose-50 (LD50) for oral nitrite intake in rats is reported to be 100–200 mg/kg. Acute nitrate toxicity is not a common health issue, but acute nitrite toxicity occurs more frequently and can even result in death. This is because nitrite can rapidly react with hemoglobin in the blood, posing a risk of death [61].

The health risks posed by nitrosamines, formed from the use of nitrate and nitrite [62], are a major concern for public health authorities. The adverse effects of nitrosamines on health were first discovered in the 1950s, when a high incidence of tumors was observed in mink fed with nitrite-containing feed. This led to research showing a link between nitrosamines and cancer [55].

Reducing the presence of these contaminants in food is crucial for public health. Conscious use of fertilizers in agriculture is an essential step. Additionally, proper waste management and preventing human waste from contaminating water sources can reduce the environmental exposure to these contaminants.

Perchlorate

Perchlorate, used extensively in industrial processes [63], can contaminate air [64], soil, and water. Its presence in the air, soil, and water increases the risk of contamination [65]. In areas contaminated with perchlorate, it can transfer from soil and water to plants, especially those with high water content and leafy vegetables, leading to accumulation in these foods [7].

The primary health concern associated with perchlorate intake is its potential to cause thyroid gland issues and indirectly affect the hormone system, body metabolism, and development, especially at high doses [7,66,67]. This is due to the inhibition of iodine uptake by the thyroid glands caused by perchlorate [68].

Reducing perchlorate contamination involves monitoring and managing industrial emissions, improving water treatment processes, and implementing agricultural practices that minimize soil and water contamination. Public health initiatives can also include educating communities about the sources and risks of perchlorate exposure.

To reduce the transfer of environmental pollutants to food, it is crucial to implement controlled agricultural practices, proper industrial waste management, and strict monitoring throughout the food production chain. Foods serve as intermediaries that transfer these contaminants to humans, playing a crucial role in this context. Direct exposure to these toxic elements through food and their absorption during digestion accelerates the toxicity mechanism. As observed in this study, the toxic effects of exposure to environmental contaminants vary widely.

Preventing and controlling environmental food contamination requires a series of strategies and measures. Firstly, careful and controlled use of pesticides and fertilizers in agricultural practices is crucial. Promoting organic farming methods and using biological control agents can help reduce these residues. Additionally, proper management and treatment of industrial waste minimize contaminants that can be transferred through water and soil.

Implementing stringent monitoring and control mechanisms at all stages of the food production chain is essential in reducing contamination risk. Maintaining hygiene standards during food processing and packaging enhances food safety. Furthermore, ensuring that food processing equipment and packaging materials are made from safe and appropriate materials reduces the risk of chemical contamination. Monitoring every stage of the food chain from farm to fork, conducting proper analyses to quickly identify problematic points, and taking corrective measures are critical steps.

Consumer awareness and education are vital for ensuring food safety. By managing their food purchasing and consumption habits consciously, consumers can reduce contamination risks.

Governments and international organizations play a significant role in establishing and enforcing food safety standards. Legal regulations and standards exert pressure on food producers and suppliers, contributing to minimizing environmental contaminants. Furthermore, investing in research and development activities to discover new and effective contamination prevention and control methods should be encouraged.

In conclusion, preventing and controlling environmental food contamination requires a multifaceted and comprehensive approach. Measures taken in agriculture, industry, food processing, and consumption stages will enhance food safety and significantly contribute to public health protection. Continuous review and improvement of the measures and research in this area are crucial for ensuring access to safer foods in the future.

1. Malisch R, Kotz A. Dioxins and PCBs in feed and food--review from European perspective. Sci Total Environ. 2014 Sep 1;491-492:2-10. doi: 10.1016/j.scitotenv.2014.03.022. Epub 2014 May 5. PMID: 24804623.
2. Rivezzi G, Piscitelli P, Scortichini G, Giovannini A, Diletti G, Migliorati G, Ceci R, Rivezzi G, Cirasino L, Carideo P, Black DM, Garzillo C, Giani U. A general model of dioxin contamination in breast milk: results from a study on 94 women from the Caserta and Naples areas in Italy. Int J Environ Res Public Health. 2013 Nov 8;10(11):5953-70. doi: 10.3390/ijerph10115953. PMID: 24217180; PMCID: PMC3863880.
3. Omaye ST. Food and nutritional toxicology. Boca Raton: CRC press; 2004.
4. Assessment of the health risk of dioxins: Re-evaluation of the Tolerable Daily Intake (TDI). Geneva: World Health Organization. 1998.
5. Hoogenboom R, Traag W, Fernandes A, Rose M. European developments following incidents with dioxins and PCBs in the food and feed chain. Food Control. 2015;50:670-683. doi: 10.1016/j.foodcont.2014.10.010.
6. Fiedler H. Dioxins in milk, meat, eggs and fish. D'Mello JP, editor. Food Safety: Contaminants and Toxins. Cambridge: CABI Publishing; 2003.
7. Lawley R, Curtis L, Davis J. The food safety hazard guidebook second edition. Cambridge: Royal Society of Chemistry Publishing; 2012.
8. 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 May 11;63(1):1-18. doi: 10.1080/152873901750128326. PMID: 11346131.
9. Parzefall W. Risk assessment of dioxin contamination in human food. Food Chem Toxicol. 2002 Aug;40(8):1185-9. doi: 10.1016/s0278-6915(02)00059-5. PMID: 12067582.
10. Szajner J, Czarny-Dzialak M, Dziechciaz M, Pawlas N, Walosik A. Dioxin-Like Compounds (DLCs) in the environment and their impact on human health. Journal of Elementology. 2021;26(2). doi: 10.5601/jelem.2021.26.2.2130.
11. Agents classified by the IARC monographs. IARC. 2015
12. Alcock RE, Behnisch PA, Jones KC, Hagenmaier H. Dioxin-like PCBs in the environment-human exposure and the significance of sources. Chemosphere. 1998 Oct;37(8):1457-72. doi: 10.1016/s0045-6535(98)00136-2. PMID: 9753761.
13. On the implementation of the Community Strategy for dioxins, furans, and polychlorinated biphenyls (COM(2001)593)- Third progress report. Brussel. European Commission. 2010.
14. Deshpande S. Handbook of food toxicology. New York: Marcel Dekker Inc; 2002.
15. Özbay S, Dikici E, Soylukan C. Evaluation of biological (feed, water), seasonal, and geological factors affecting the heavy metal content of raw milk. Journal of Food Composition and Analysis. 2023;121:105401. doi: 10.1016/j.jfca.2023.105401.
16. Exposure to mercury: A major public health concern. Geneva: Public Health and Environment / World Health Organization. 2007.
17. Derban LK. Outbreak of food poisoning due to alkyl-mercury fungicide on southern Ghana state farm. Arch Environ Health. 1974 Jan;28(1):49-52. doi: 10.1080/00039896.1974.10666432. PMID: 4586365.
18. Järup L. Hazards of heavy metal contamination. British Medical Bulletin. 2003;68:167-182. doi: 10.1093/bmb/ldg032.
19. Goyer RA, Clarkson TW. Toxic effects of metals. The McGraw-Hill Companies. 2001.
20. Nawrot TS, Staessen JA, Roels HA, Munters E, Cuypers A, Richart T, Ruttens A, Smeets K, Clijsters H, Vangronsveld J. Cadmium exposure in the population: from health risks to strategies of prevention. Biometals. 2010 Oct;23(5):769-82. doi: 10.1007/s10534-010-9343-z. Epub 2010 Jun 3. PMID: 20517707.
21. Pan J, Plant JA, Voulvoulis N, Oates CJ, Ihlenfeld C. Cadmium levels in Europe: implications for human health. Environ Geochem Health. 2010 Feb;32(1):1-12. doi: 10.1007/s10653-009-9273-2. Epub 2009 Aug 18. PMID: 19688602.
22. Exposure of cadmium: A major public health. Geneva: Public Health and Environment World Health Organization. 2010.
23. Amundsen PA, Staldvik FJ, Lukin AA, Kashulin NA, Popova OA, Reshetnikov YS. Heavy metal contamination in freshwater fish from the border region between Norway and Russia. Sci Total Environ. 1997 Aug 18;201(3):211-24. doi: 10.1016/s0048-9697(97)84058-2. PMID: 9241871.
24. Yılmaz F. The comparison of heavy metal concentrations (Cd, Cu, Mn, Pb, and Zn) in tissues of three economically important fish (anguilla anguilla, mugil cephalus and oreochromis niloticus) inhabiting köycegiz lake-mugla (Turkey). Turkish Journal of Science & Technology. 2009;4(1):7-15.
25. Groten JP. Adverse effect of food contaminants. Vries JD. Editor. Food Safety and Toxicity. Boca Raton: CRC Press LLC; 1997.
26. Oymak T, Tokalıoğlu Ş, Yılmaz V, Kartal Ş, Aydın D. Determination of lead and cadmium in food samples by the coprecipitation method. Food Chemistry. 2009;113:1314-1317. doi: 10.1016/j.foodchem.2008.08.064.
27. Thompson LJ, Gupta içinde RC. Veterinary toxicology. 2012:522-526. doi: 10.1016/C2010-0-67763-7.
28. Demirci M, Gıda Kimyası. Tekirdağ: Rebel yayıncılık. 2003.
29. Chi QQ, Zhu GW, Alan L. Bioaccumulation of heavy metals in fishes from Taihu Lake, China. J Environ Sci (China). 2007;19(12):1500-4. doi: 10.1016/s1001-0742(07)60244-7. PMID: 18277656.
30. Zhuang P, Zou H, Shu W. Biotransfer of heavy metals along a soil-plant-insect-chicken food chain: field study. J Environ Sci (China). 2009;21(6):849-53. doi: 10.1016/s1001-0742(08)62351-7. PMID: 19803093.
31. Cramér K, Goyer RA, Jagenburg R, Wilson MH. Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure. Br J Ind Med. 1974 Apr;31(2):113-27. doi: 10.1136/oem.31.2.113. PMID: 4830763; PMCID: PMC1009566.
32. Janssen MM. Contaminantlar. Vries JD, editor. Foof Safety and Toxicity. Boca Raton: CRC Press LLC; 1997.
33. Anawar HM, Akai J, Mostofa KM, Safiullah S, Tareq SM. Arsenic poisoning in groundwater: health risk and geochemical sources in Bangladesh. Environ Int. 2002 Feb;27(7):597-604. doi: 10.1016/s0160-4120(01)00116-7. PMID: 11871394.
34. Erol İ. Gıda hijyeni ve mikrobiyolojisi. Ankara: Pozitif Matbaacılık (In Turkish). 2007.
35. Aposhian HV, Aposhian MM. Newer developments in arsenic toxicity. Journal Of The Amerıcan College Of Toxıcology. 1989;8(7):1297-1305.
36. Goering PL, Aposhian HV, Mass MJ, Cebrián M, Beck BD, Waalkes MP. The enigma of arsenic carcinogenesis: role of metabolism. Toxicol Sci. 1999 May;49(1):5-14. doi: 10.1093/toxsci/49.1.5. PMID: 10367337.
37. Roychowdhury T, Uchino T, Tokunaga H, Ando M. Survey of arsenic in food composites from an arsenic-affected area of West Bengal, India. Food Chem Toxicol. 2002 Nov;40(11):1611-21. doi: 10.1016/s0278-6915(02)00104-7. PMID: 12176088.
38. Duxbury JM, Mayer AB, Lauren JG, Hassan N. Food chain aspects of arsenic contamination in Bangladesh: effects on quality and productivity of rice. J Environ Sci Health A Tox Hazard Subst Environ Eng. 2003 Jan;38(1):61-9. doi: 10.1081/ese-120016881. PMID: 12635819.
39. Ng JC, Wang J, Shraim A. A global health problem caused by arsenic from natural sources. Chemosphere. 2003 Sep;52(9):1353-9. doi: 10.1016/S0045-6535(03)00470-3. PMID: 12867164.
40. Ratnaike RN. Acute and chronic arsenic toxicity. Postgrad Med J. 2003 Jul;79(933):391-6. doi: 10.1136/pmj.79.933.391. PMID: 12897217; PMCID: PMC1742758.
41. Saha JC, Dikshit AK, Bandyopadhyay M, Saha KC. A review of arsenic poisoning and its effects on human healt. 1999;29(3):281-313. doi: 10.1080/10643389991259227.
42. Yoshida T, Yamauchi H, Fan Sun G. Chronic health effects in people exposed to arsenic via the drinking water: dose-response relationships in review. Toxicol Appl Pharmacol. 2004 Aug 1;198(3):243-52. doi: 10.1016/j.taap.2003.10.022. PMID: 15276403.
43. Cverenkárová K, Valachovičová M, Mackuľak T, Žemlička L, Bírošová L. Microplastics in the Food Chain. Life (Basel). 2021 Dec 6;11(12):1349. doi: 10.3390/life11121349. PMID: 34947879; PMCID: PMC8704590.
44. van Raamsdonk LWD, van der Zande M, Koelmans AA, Hoogenboom RLAP, Peters RJB, Groot MJ, Peijnenburg AACM, Weesepoel YJA. Current Insights into Monitoring, Bioaccumulation, and Potential Health Effects of Microplastics Present in the Food Chain. Foods. 2020 Jan 9;9(1):72. doi: 10.3390/foods9010072. PMID: 31936455; PMCID: PMC7022559.
45. Barboza LGA, Vieira LR, Branco V, Figueiredo N, Carvalho F, Carvalho C, Guilhermino L. Microplastics cause neurotoxicity, oxidative damage and energy-related changes and interact with the bioaccumulation of mercury in the European seabass, Dicentrarchus labrax (Linnaeus, 1758). Aquat Toxicol. 2018 Feb;195:49-57. doi: 10.1016/j.aquatox.2017.12.008. Epub 2017 Dec 20. PMID: 29287173.
46. Pironti C, Ricciardi M, Motta O, Miele Y, Proto A, Montano L. Microplastics in the Environment: Intake through the Food Web, Human Exposure and Toxicological Effects. Toxics. 2021 Sep 16;9(9):224. doi: 10.3390/toxics9090224. PMID: 34564375; PMCID: PMC8473407.
47. Prata JC, Reis V, da Costa JP, Mouneyrac C, Duarte AC, Rocha-Santos T. Contamination issues as a challenge in quality control and quality assurance in microplastics analytics. J Hazard Mater. 2021 Feb 5;403:123660. doi: 10.1016/j.jhazmat.2020.123660. Epub 2020 Aug 9. PMID: 33264868.
48. Walkinshaw C, Lindeque P, Thompson R, Tolhurst T, Cole M. Microplastics and seafood: Lower trophic organisms at highest risk of contamination. Ecotoxicology and environmental safety. 2019;190:110066. doi: 10.1016/j.ecoenv.2019.110066.
49. Habib RZ, Kindi RA, Salem FA, Kittaneh WF, Poulose V, Iftikhar SH, Mourad AI, Thiemann T. Microplastic Contamination of Chicken Meat and Fish through Plastic Cutting Boards. Int J Environ Res Public Health. 2022 Oct 18;19(20):13442. doi: 10.3390/ijerph192013442. PMID: 36294029; PMCID: PMC9602623.
50. Pei X, Tandon A, Alldrick A, Giorgi L, Huang W, Yang R. The China melamine milk scandal and its implications for food safety regulation. FoodPolicy. 2011;36(3):412-420. doi: 10.1016/j.foodpol.2011.03.008.
51. Ingelfinger JR. Melamine and the global implications of food contamination. N Engl J Med. 2008 Dec 25;359(26):2745-8. doi: 10.1056/NEJMp0808410. PMID: 19109571.
52. Newton GL, Utley PR. Melamine as a dietary nitrogen source for ruminants. Journal of Animal Science. 1978;47(6):1338-1344. doi: 10.2527/jas1978.4761338x. Pei X, Tandon A, Alldrick A, Giorgi L, Huang W, Yang R. The China melamine milk scandal and its implications for food safety regulation. Food Policy. 2011;36(3):412-420. doi: 10.1016/j.foodpol.2011.03.008.
53. Evans JR, Clarke VC. The nitrogen cost of photosynthesis. J Exp Bot. 2019 Jan 1;70(1):7-15. doi: 10.1093/jxb/ery366. PMID: 30357381.
54. Shukla S, Saxena A. Sources and leaching of nitrate contamination in groundwater. Current Science. 2020;118(6):883-891. doi: 10.18520/cs/v118/i6/883-891.
55. Horsch AM, Sebranek JG, Dickson JS, Niebuhr SE, Larson EM, Lavieri NA, Ruther BL, Wilson LA. The effect of pH and nitrite concentration on the antimicrobial impact of celery juice concentrate compared with conventional sodium nitrite on Listeria monocytogenes. Meat Sci. 2014 Jan;96(1):400-7. doi: 10.1016/j.meatsci.2013.07.036. Epub 2013 Aug 3. PMID: 23973624.
56. Hill MJ. Nitrates and nitrites in food and water (Vol. 7). CRC Press; 1996.
57. Walker R. The metabolism of dietary nitrites and nitrates. Biochem Soc Trans. 1996 Aug;24(3):780-5. doi: 10.1042/bst0240780. PMID: 8878847.
58. Andrade R, Reyes FG, Rath S. A method for the determination of volatile N-nitrosamines in food by HS-SPME-GC-TEA. Food Chemistry. 2005;91(1):173-179. doi: 10.1016/j.foodchem.2004.08.015.
59. Archer DL. Evidence that ingested nitrate and nitrite are beneficial to health. J Food Prot. 2002 May;65(5):872-5. doi: 10.4315/0362-028x-65.5.872. PMID: 12030305.
60. Honikel KO. The use and control of nitrate and nitrite for the processing of meat products. Meat Sci. 2008 Jan;78(1-2):68-76. doi: 10.1016/j.meatsci.2007.05.030. Epub 2007 Jun 27. PMID: 22062097.
61. Lundberg JO, Larsen FJ, Weitzberg E. Supplementation with nitrate and nitrite salts in exercise: a word of caution. J Appl Physiol (1985). 2011 Aug;111(2):616-7. doi: 10.1152/japplphysiol.00521.2011. PMID: 21828255.
62. Özbay S. Investigation of volatile N-nitrosamine contents of hams with different ingredients produced in Turkey. Journal of Food Composition and Analysis. 2024;130:106170. doi: 10.1016/j.jfca.2024.106170
63. Renner R. Perchlorate in food. Environ Sci Technol. 2008 Mar 15;42(6):1817. doi: 10.1021/es0870552. PMID: 18409597.
64. Dasgupta PK, Martinelango PK, Jackson WA, Anderson TA, Tian K, Tock RW, Rajagopalan S. The origin of naturally occurring perchlorate: the role of atmospheric processes. Environ Sci Technol. 2005 Mar 15;39(6):1569-75. doi: 10.1021/es048612x. PMID: 15819211.
65. Blount BC, Valentin-Blasini L, Osterloh JD, Mauldin JP, Pirkle JL. Perchlorate exposure of the US Population, 2001-2002. J Expo Sci Environ Epidemiol. 2007 Jul;17(4):400-7. doi: 10.1038/sj.jes.7500535. Epub 2006 Oct 18. PMID: 17051137.
66. Wolff J. Perchlorate and the thyroid gland. Pharmacol Rev. 1998 Mar;50(1):89-105. PMID: 9549759.
67. Charnley G. Perchlorate: overview of risks and regulation. Food Chem Toxicol. 2008 Jul;46(7):2307-15. doi: 10.1016/j.fct.2008.03.006. Epub 2008 Mar 10. PMID: 18440116.
68. Greer MA, Goodman G, Pleus RC, Greer SE. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Environ Health Perspect. 2002 Sep;110(9):927-37. doi: 10.1289/ehp.02110927. Erratum in: Environ Health Perspect. 2005 Nov;113(11):A732. PMID: 12204829; PMCID: PMC1240994.