N° 14 | July 2007

Preserved and non-preserved vegetables: Differing associations with nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is a rare form of cancer in most regions of the world. The incidence of NPC is dramatically higher in selected regions, however, such as in Southern China and in Hong Kong1. Elevated rates of occurrence are also seen in other parts of Southeast Asia1.

One risk factor for NPC is being infected with the Epstein-Barr Virus (EBV)2. However, this is such a common infection among most human populations that there are likely to be “triggers” that contribute to the cancer-causing effects of EBV infection. This has led to hypotheses that dietary factors could potentially play a role in this regard. For example, intake of Cantonese-style salted fish has consistently been found to be associated with an increased risk of NPC3. Cantonese-style salted fish contains high levels of volatile nitrosamines produced during the preservation process that have been shown in animal and laboratory studies to be both mutagenic and carcinogenic.

Preserved vegetables: a risk factor?

Although protective associations between fresh fruit and vegetable intake and many malignancies have been observed, the consumption of preserved fruits and vegetables have aroused suspicion as another dietary factor that may contribute to the risk of NPC. By preserved vegetables, we refer to produce that has been salted, dried, canned, fermented, or pickled. It is conceivable that the process of preservation could result in the production of cancer-causing agents. The preservation processes used to prepare these types of vegetables are also thought to increase the levels of carcinogenic nitrosamines4.

A review of the epidemiologic evidence showed that when compared to individuals who consumed the least amount of preserved vegetables, those who ate the most had double the risk of NPC5. When looking at types of vegetables, a similar magnitude of association was seen for green leafy vegetables, all non-starchy vegetables, and cruciferous vegetables. Furthermore, there was a dose-response trend, with a higher risk of NPC for greater amounts of preserved vegetables consumed5.

The increase in NPC risk with the intake of preserved vegetables is biologically plausible based on the higher concentrations of nitrates and nitrosamines associated with the preservation processes. Nitrosamines are known mutagens and animal carcinogens that induce the formation of DNA adducts which, if not repaired, may lead to point mutations and a greater likelihood of cancer.

Fresh vegetables: protective factor?

For non-preserved vegetables, highest-versus-lowest categories of consumption in adulthood were associated with an approximate 40% decrease in the risk of NPC5. Dose-response trends were not consistently observed, but were present in the majority of studies that reported these findings. A protective association of similar magnitude was also seen in groups of types of vegetables (green leafy, non-starchy roots and tubers, all non-starchy vegetables)5.
The inverse association between non-preserved vegetable intake and NPC risk is consistent with what is known about the protective effect of vegetable intake on the development of cancer of other types. The protective effects of vegetables are thought to be mediated by multiple components, including beta-carotene, alphatocopherol, retinoids, phytoestrogens, and folate. These components are involved in numerous biological processes that may alter cancer risk, including the inhibition of cell growth, the normal synthesis and methylation of DNA, and protection against oxidative stress and DNA damage.


Currently, the evidence indicates that preserved vegetable intake increases NPC risk whereas eating fresh vegetables reduces NPC risk. Both of these associations are strong, appear not to be specific to any type of vegetable, and the observations across studies have been consistent. However, because studies have not accounted for consumption of both types of vegetables in the same analyses, it is difficult to draw definitive links. This is because we do not know if eating fresh vegetables actually protects against NPC, or it merely acts as a marker of eating less preserved vegetables. Similarly, we do not know if eating preserved vegetables increase NPC risk, or distinguishes those who eat less fresh vegetables. While it will be important to clarify these issues, the present evidence suggests a complex role between vegetable consumption and NPC: fresh vegetables are associated with substantially reduced risk of disease, whereas vegetables that have been preserved in specific ways may actually increase NPC risk. These findings are most relevant to countries in Asia where preserved vegetables comprise a substantial portion of the diet. This differing pattern of associations based on preservation raises the broader issue that certain preservation techniques may be so potent that they are capable of transforming vegetables from healthenhancing factors to factors that actually contribute to the pathogenesis of disease.

  1. GLOBOCAN 2000: Cancer Incidence, Mortality and Prevalence Worldwide. Version 1.0. Version 1. Lyon, France: IARCPress, 2001.
  2. Yu MC, Henderson BE. Nasopharyngeal cancer. In: Schottenfeld D, Fraumeni JF. Cancer epidemiology and prevention, 2nd ed. New York: Oxford University Press, 1996:603-18
  3. Yu MC, Ho JH, Lai SH, Henderson BE. Cantonese-style salted fish as a cause of nasopharyngeal carcinoma: report of a case-control study in Hong Kong. Cancer Res. 1986;46:956-61
  4. Yu MC, Yuan JM. Epidemiology of nasopharyngeal carcinoma. Semin Cancer Biol. 2002;12:421-9
  5. Gallicchio L, Matanoski G, Tao X, Chen L, Lam TK, Boyd K, Robinson KA, Balick L, Mickelson S, Caulfield LE, Herman JG, Guallar E, Alberg AJ. Adulthood consumption of preserved and non-preserved vegetables and the risk of nasopharyngeal carcinoma: a systematic review. International Journal of Cancer. 2006; 119: 1125-1135.