There is a paucity of studies examining the relationship between diet and asbestos-related diseases. On the other hand, consumers worldwide have become increasingly interested in how diet influences their health and about the nutritional value and safety of the food they eat. Evidence continues to mount that dietary components not only influence the ability to achieve one's genetic potential but also influence physical and cognitive function and the risk of a number of diseases. Unfortunately, there are numerous inconsistencies in the available data, and few, if any, effective strategies to identify those who might benefit from dietary intervention have been identified. Nevertheless, support for the Wynder and Gori (1977)
suggestion more than 30 yr ago that diet was fundamental to determining cancer risk has continued, and recent epidemiological studies clarified the influence of specific food constituents on cancer risk and tumor behavior. The primary health effects of asbestos exposure are related to the lung, ranging from fibrosis to lung cancer and MM. Therefore, the focus of this section is on what is known (or not known) about nutrients and lung disease, and on the little that is known about nutrients and asbestos-related diseases.
In an early case-control study of diet and MM in Louisiana, Schiffman et al. (1988)
reported that consumption of vegetables may have a protective effect on developing this disease, citing an inverse relationship between MM and vegetable intake although a specific food could not be implicated nor could the mechanism be explained. A subsequent report on 94 men and women with MM suggested that tomato or carrot consumption may decrease the risk for MM (Muscat & Huncharek, 1996
). The significant reduction in risk of MM was associated with carrot intake but not other carotene- or vitamin A-containing foods. The decreased risk for MM was associated with consumption of tomatoes or tomato juice but the association did not achieve statistical significance. Nevertheless, Muscat and Huncharek (1996)
indicated that consumption of many vegetables and fruits might have protective effects against MM. No other studies have been identified that further examined the relationship between dietary components and MM. In contrast, interest in the broader relationship between diet and cancer increased over the last two decades, and since lung carcinoma continues to be the most common cancer globally, followed by breast and colorectal cancers, research has focused on the impact of diet and its components on specific types of cancer.
Fortes et al. (2003)
reported on the relationship between components of the Mediterranean diet and lung cancer in a hospital-based, case-control study of patients admitted between 1993 and 1996. Basing nutrient intake on self-administered food frequency questionnaires and controlling for smoking, data demonstrated the protective effects for high consumption of carrots, tomatoes, white meat, exclusive use of olive oil, and regular consumption of sage. Data supported claims that foods rich in antioxidants may reduce the risk for lung cancer. The mechanisms implicated included the protection against oxidative damage to DNA and polyphenolic compounds that prevented interaction of benzo[a]pyrene (BaP) with DNA. Despite this and many other suggestive reports, the effects of diet on cancer development or progression remain contradictory and likely to reflect variation in the ability of food components to reach and/or modify critical cellular targets (Milner, 2006
Cruciferous vegetables (broccoli, cabbage, cauliflower, Brussels sprouts, kale) that are rich in isothiocyanates were postulated to reduce the risk for lung cancer. A recently published systematic review of the epidemiologic literature through December 2007 identified 30 studies on the association between lung cancer and either total cruciferous vegetable consumption or specific cruciferous vegetables and found that the risk for lung cancer among those in the highest category of total cruciferous vegetable intake was 22% lower in case-control studies compared to those in the lowest category of intake (Lam et al., 2009
). Moreover, the strongest inverse relationship was seen among those who were homozygous for GSTM1 and GSTT1 deletions. Of interest is that a review of the relationship between asbestos-related diseases and genetic variability in genes involved in xenobiotic and oxidative metabolism or in DNA repair processes identified increased risk with the GSTM1-null genotype (Neri et al., 2008
). Taken together, these data suggest that components of cruciferous vegetables may modify the risk for asbestos-related disease in individuals with genetic susceptibility, warranting further investigation.
The chemopreventive potential of β-carotene, a provitamin A carotenoid, was supported by a number of observational studies, leading to the initiation of several large-scale randomized chemoprevention trials to determine whether supplementation with β-carotene protected against lung cancer, with disappointing results (Omenn et al., 1996
; Virtamo et al., 2003
). In fact, these trials found that β-carotene supplementation elevated the risk of lung cancer in high-risk populations. Given the importance of clarifying the potential role of carotenoids in the development of lung cancer and the diverse body of evidence, Gallicchio et al. (2008)
conducted a systematic and quantitative review of randomized clinical trials and prospective observational studies and demonstrated that of β-carotene supplementation was not associated with a decrease in the risk of developing lung cancer. The lack of association between lung cancer risk and carotenoid intake was attributed to the likelihood that carotenoid levels were more of a marker of a healthier lifestyle (higher intake of fruits and vegetables) or of residual confounding by smoking. Studies to further examine the effects of carotenoids on lung cancer are not likely to be fruitful.
Another component of food with potential anticancer effects is the phytosterols or plant sterols. Phytoestrols are structurally similar to cholesterol, exist in several forms in plants, and are found in grain legumes (sesame, chickpeas, lentils, and peas), cereal grains (wheat, corn, millet, rye and barley), vegetable oils (e.g., corn), and nuts (pecans, pine, pistachio, peanuts, cashew, and almonds) (Woyengo et al., 2009
). Woyengo et al. (2009)
concluded that phytosterols appear to inhibit the development of various cancers by inhibiting proliferation and promoting apoptosis of cancer cells through the activation of caspase enzymes and may reduce cancer development by lowering blood cholesterol and consequently altering cell membranes. Further study of the potential role of phytosterols in humans is required.
A number of other foods or food components have been studied and not shown to influence cancer risk, including garlic (Kim and Kwon, 2009
) and vitamins A, E, C, and folate (Cho et al., 2006
). Flavonoids, a group of potentially chemoprotective compounds widely distributed in fruit, vegetables, and beverages of plant origin, have also been studied as the potential active ingredient responsible for the reduction of cancer risk. In their analysis of data from the Nurses’ Health Study, Wang et al. (2009)
did not find a significant role for five common flavonols and flavones or selected flavonoid-rich foods in cancer prevention. In a small case-control study, dietary zinc and copper, but not selenium, appeared to be associated with lower risk for lung cancer (Mahabir et al., 2007
Finally, a few words about nutrition in early life: It is well accepted that environmental exposures play a significant role in the etiology of disease. Such exposures usually precede the appearance of clinical disease, often by a prolonged period of time. Besides the role of genetic mutations, epigenetic processes such as DNA methylation and covalent modification of histones are likely to play a role in alterations in gene activity that may contribute to risk for some types of cancer. Burdge et al. (2009)
provided a compelling hypothesis that increased susceptibility to certain disease, including cancer, may have a common origin in developmental changes induced by epigenetic changes induced by environmental exposures, which includes nutrition. The maternal diet, including nutrients known to affect methylation reactions such as folate, vitamin B12, and sulfur amino acids, may impact the developing fetus and contribute to disease susceptibility later in life. This is an important area of future investigation as interest increases with regard to how nutrients influence the development or susceptibility to multiple diseases.
In summary, in the area of the impact of nutrients on asbestos-related diseases, little is known and even less is being investigated. However, because of the increasing awareness that nutrients play an important role in the onset and development of disease and because of the ever-changing food supply as we face a global economy, it seems highly worthwhile to begin to support active research in this area.