By Eben van Tonder, 27 April 25

Introduction
Nitrosamines, N-nitroso compounds formed from nitrite and amines, have long been scrutinised due to their carcinogenic potential in animal studies (Lijinsky, 1999). In human diets, cured meats preserved with nitrite have been a major focal point of concern, amid fears that nitrosamines formed during processing, cooking or digestion could elevate cancer risk.
This review critically examines the scientific basis for nitrosamine concerns in cured meats, weighing laboratory findings against human epidemiological data. It highlights evidence that under normal physiological conditions, significant nitrosamine formation in the human stomach is highly unlikely (van Tonder, 2024), especially given the body’s protective mechanisms. It contextualises cured meats as one of many dietary sources of nitrosamines – others include beer and high-heat cooked foods – and questions whether singling out cured meat is warranted.
To provide a balanced perspective, quantitative data on nitrite, nitrate and nitric oxide (NO) in human physiology, particularly during exercise, are reviewed and compared to nitrite doses from typical cured meat consumption. The important biological roles of the nitrate–nitrite–NO pathway in cardiovascular health and exercise performance are also explored. Finally, human and animal evidence on nitrosamine-related cancer risk is evaluated, noting that historical dietary patterns have not produced cancer rates commensurate with the alarm seen in public discourse.
This article prioritises primary literature and official risk assessments, maintaining an objective tone that challenges popular narratives and biases against nitrite in cured meats.
Nitrosamines and Cured Meats: Historical Context and Concerns
Scientific interest in nitrosamines in foods began in the 1960s after nitrosamines were shown to cause cancer in laboratory animals at high doses (Lijinsky, 1999). Investigations detected volatile nitrosamines such as N-nitrosodimethylamine (NDMA) and N-nitrosopyrrolidine (NPYR) in certain cured meats, especially fried bacon, at parts-per-billion levels (Scanlan, 1983).
As a result, regulators implemented strict controls to minimise nitrosamine formation. In the United States, the allowed nitrite dose in bacon was lowered to approximately 120 ppm and it became mandatory to add antioxidants like ascorbate or erythorbate to curing mixtures (Cassens, 1995).
Adding ascorbate has proven highly effective in inhibiting nitrosation reactions (Mirvish, 1995). Likewise, adding tocopherols (vitamin E) to bacon cuts nitrosamine levels several fold (Gray et al., 1991). As a result, modern cured meats, when properly produced, contain only trace, often undetectable, levels of preformed nitrosamines (Sindelar and Milkowski, 2012).
Despite these improvements, concern persists. The International Agency for Research on Cancer (IARC) classified processed meat as a Group 1 carcinogen based on epidemiological correlations with colorectal cancer (IARC, 2015). However, hazard classification does not equate to high risk. The estimated 18% relative increase in colorectal cancer risk per 50g of processed meat consumed daily must be weighed against the low baseline incidence (Bouvard et al., 2015).
Furthermore, nitrite and nitrosamine pathways are only one among several possible causal factors, alongside heme iron and heterocyclic amines formed during cooking (Joosen and Verhagen, 2007).
Formation of Nitrosamines: Chemistry and Physiology
Nitrosation Chemistry in Foods
Nitrosamines form when a nitrosating agent reacts with an amine. Nitrite itself is not directly nitrosating until it forms nitrous acid (HNO₂) or reactive nitrogen oxides under acidic conditions (Lijinsky, 1999). High temperatures, such as those reached during frying, can accelerate nitrosamine formation in the lipid phase of foods like bacon (Scanlan, 1983).
Mitigation strategies using ascorbate and tocopherols target this chemistry effectively (Cassens, 1995; Gray et al., 1991). Regulatory limits on residual nitrite and mandatory inclusion of antioxidants have made modern cured meats safe with respect to nitrosamines.
Endogenous Nitrosation in the Human Stomach
The human stomach is theoretically conducive to nitrosation due to its acidic environment. However, physiological mechanisms strongly inhibit nitrosamine formation. Ascorbate present in foods and gastric secretions reacts with nitrite to prevent nitrosation (Mirvish, 1995).
Experimental studies show that adding ascorbic acid to gastric models reduces NDMA formation fivefold (Vermeer et al., 1979). The presence of lipid in the stomach can influence nitrosation dynamics but, in real-world mixed meals, the overall risk remains low (Vermeer et al., 1979).
Van Tonder (2024) reporting on one study shows that significant nitrosamine formation in the human stomach is unlikely under normal physiological conditions, a view supported by multiple studies.
Dietary Sources of Nitrosamines Beyond Cured Meat
Cured meats are not the sole dietary source of nitrosamines.
Beer and Alcoholic Beverages
Historically, beer was a significant source of NDMA due to malt drying practices. Concentrations reached up to 68 μg/L in the 1970s (Hotchkiss et al., 1981). Modern brewing has greatly reduced this, but beer remains a minor source compared to cured meat today.
High-Temperature Cooking
Grilling, frying and smoking protein-rich foods without added nitrite also produce nitrosamines and related compounds (Joosen and Verhagen, 2007). Smoked fish, in particular, can contain significant nitrosamines, especially if improperly preserved (Scanlan, 1983).
Other Processed Foods
Trace nitrosamines have been detected in cheeses, pickled vegetables and even in natural-cured meats using vegetable nitrates (Honikel, 2008).
Tobacco products remain by far the largest source of human nitrosamine exposure (Hecht, 1999).
Nitrite, Nitrate and NO in Human Physiology: Levels and Beneficial Roles
Baseline Levels and Changes During Exercise
Humans ingest and endogenously produce nitrate and nitrite.
- Plasma nitrate concentration is typically 20–60 µmol/L (Kapil et al., 2014).
- Plasma nitrite is around 0.1–0.5 µmol/L (Lundberg et al., 2008).
- Salivary nitrate can exceed 500 µmol/L and nitrite 200 µmol/L after meals (Govoni et al., 2008).
During exercise, plasma nitrate increases due to NO production, while nitrite serves as a crucial reservoir for NO under hypoxic conditions (Bailey et al., 2010).
Comparison to Cured Meat Intake
A 100g serving of bacon cured with 100 ppm nitrite would contain approximately 10 mg nitrite before cooking, though most degrades during cooking. Ingested nitrite from cured meats is minor compared to daily endogenous nitrate and nitrite turnover (Milkowski et al., 2010).
Role in Exercise and Cardiovascular Health
Dietary nitrate improves blood pressure, endothelial function and exercise performance (Webb et al., 2008; Bailey et al., 2010).
Nitrate supplementation (such as beetroot juice) lowers the oxygen cost of exercise and improves time-to-exhaustion (Bailey et al., 2009). Mouth bacteria are essential for converting nitrate to nitrite, a key step blocked by antiseptic mouthwashes (Govoni et al., 2008).
Thus, nitrate and nitrite are now recognised as important components of cardiovascular health, rather than purely harmful agents.
Health Risk Assessment and Epidemiological Evidence
Animal Studies Versus Human Data
Animal studies consistently show that high doses of nitrosamines cause cancer (Lijinsky, 1999). However, doses used in these studies are many orders of magnitude higher than human dietary exposure (JECFA, 2008).
Endogenous formation of nitrosamines also exceeds dietary intake (SKLM, 2011).
Epidemiology and Population Studies
Countries with high cured meat consumption, such as Austria, do not have elevated colorectal cancer rates compared to the European average (ECIS, 2022).
The relative risk increases seen in cohort studies are small and could be confounded by other lifestyle factors (Bouvard et al., 2015). Screening, healthcare access and other variables have a much greater impact on cancer rates than processed meat intake alone.
Moreover, declining stomach cancer rates globally despite steady nitrite use argue against a major nitrosamine role (Joosen and Verhagen, 2007).
Conclusion
Nitrosamine formation from properly cured meats has been effectively mitigated through regulation and technological interventions. Formation of nitrosamines in the human stomach is unlikely under normal physiological conditions, and humans are adapted to cope with low endogenous nitrosamine formation.
Other dietary sources such as beer, grilled foods and environmental exposures contribute to total nitrosamine intake. Furthermore, nitrate and nitrite are now recognised for their health benefits in cardiovascular and exercise physiology.
The available data do not support the view that occasional consumption of nitrite-cured meats poses a significant cancer risk in the context of a balanced diet and healthy lifestyle.
Caution is warranted, but fear of nitrite-cured meats is not proportionate to the scientific evidence.
References
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