Cancer risk factors, evaluating

Assess the patient for use of HRT by evaluating for the presence of vasomotor symptoms. If the patient is experiencing bothersome vasomotor symptoms, consider the use of HRT only after assessing for risk factors for heart disease and breast cancer. If vasomotor symptoms are tolerable and/or the patient has risk factors for heart disease and/or breast cancer, consider alternative, non-hormonal treatments for vasomotor symptoms. 

Other dietary factors implicated in prostate cancer include retinol, carotenoids, lycopene, and vitamin D consumption.5,6 Retinol, or vitamin A, intake, especially in men older than age 70, is correlated with an increased risk of prostate cancer, whereas intake of its precursor, [3-carotene, has a protective or neutral effect. Lycopene, obtained primarily from tomatoes, decreases the risk of prostate cancer in small cohort studies. The antioxidant vitamin E also may decrease the risk of prostate cancer. Men who developed prostate cancer in one cohort study had lower levels of l,25(OH)2-vitamin D than matched controls, although a prospective study did not support this.2 Clearly, dietary risk factors require further evaluation, but because fat and vitamins are modifiable risk factors, dietary intervention may be promising in prostate cancer prevention. 

Studies in rats reported renal tubular adenomas and adenocarcinomas in male and female animals at doses of 20 mg/kg/day (Kociba et al. 1977a). Metastasis to the lungs was observed. Combined incidences of renal tubular neoplasms in males (9/39, 23%) and in females (6/40, 15%) increased (p <0.05) over controls (males-1/90, females-0/90, 0%). The tumor incidence was not increased in the 0.2 and 2 mg/kg/day dose groups but there were some indications of hyperplasia in animals exposed to 2 m /kg/day. The EPA (1990f) evaluated these data and calculated a human potency factor of 7.8x10 (mg/kg/day) (qi ), representing 95% upper confidence limit of extra lifetime human risk. Based on this value, cancer risk levels of 10, 10, and 10 correspond to exposures of 0.001, 0.0001, 0.00001 mg/kg/day. 

An increased incidence of cancer of the paranasal sinuses was observed in workers at factories where isopropanol was manufactured by the strong-acid process. The risk for laryngeal cancer may also have been elevated in these workers. It is unclear whether the cancer risk was due to the presence of diisopropyl sulfate, which is an intermediate in the process, to isopropyl oils, which are formed as by-products, or to other factors, such as sulfuric acid. Epidemiological data concerning the manufacture of isopropanol by the weak-acid process are insufficient for an evaluation of carcinogenicity (lARC, 1987). 

The AHS, a collaborative research effort between the National Cancer Institute of the National Institutes of Health and EPA, is a prospective occupational study of 89,658 pesticide appliers and their spouses in Iowa and North Carolina assembled between 1993 and 1997 to evaluate risk factors for disease in rural farm populations (Blair et al. 2005). It is being conducted in three phases—phase I (1993-1997), phase II (1999-2003), and phase III (2005)—and includes only limited biomonitoring. Data are gathered with questionnaires to determine pesticide use and exposures, work practices, and other relevant exposures from buccal cell collection with dietary surveys and with interviews to determine updated pesticide exposures (Agricultural Health Study 2005). 

Okrent and Xing (1993) estimated the lifetime cancer risk to a future resident at a hazardous waste disposal site after loss of institutional control. The assumed exposure pathways involve consumption of contaminated fruits and vegetables, ingestion of contaminated soil, and dermal absorption. The slope factors for each chemical that induces stochastic effects were obtained from the IRIS (1988) database and, thus, represent upper bounds (UCLs). The exposure duration was assumed to be 70 y. Based on these assumptions, the estimated lifetime cancer risk was 0.3, due almost entirely to arsenic. If the risk were reduced by a factor of 10, based on the assumption that UCLs of slope factors for chemicals that induce stochastic effects should be reduced by this amount in evaluating waste for classification as low-hazard (see Section 7.1.7.1), the estimated risk would be reduced to 0.03. Either of these results is greater than the assumed limit on acceptable risk of 10 3 (see Table 7.1). Thus, based on this analysis, the waste would be classified as high-hazard in the absence of perpetual institutional control to preclude permanent occupancy of a disposal site. 

Since results from studies with biomedical models indicate potential, there is of obvious interest in the effects of RA consumption in foods on the risk of atherogenesis in humans. The use of surrogate biomarkers for disease risk is more readily achievable for atherosclerosis than for cancer in humans and a number of genetic and environmental risk factors have been identified, with the relative abundance of the different lipoproteins being of primary importance (Lusis, 2000). To date, there have been no epidemiological studies that have examined the intake of CLA derived from foods with the risk of atherosclerosis. However, as discussed in Section 3.6.2.1, the challenge of adequately evaluating the effect of dietary intake of CLA from different food sources presents some special limitations. 

The studies of Nishimoto et al. (1988), Yamada (1974) and Inada et al., (1978) provide strong evidence for a causal link between chemical agent exposure and cancer however, because the workers were exposed to multiple chemicals, it is not possible to state conclusively that the cancers were due solely to sulfur mustard. Furthermore, it should be noted that several possible confounding factors, such as tobacco smoking habits, preexisting health conditions, and post-exposure occupational histories of the workers, were not evaluated. In addition, SMRs themselves may not provide an accurate estimate of relative cancer risk if they do not correlate with tumor incidence rates in exposed and control groups (i.e., if social/economic or other differences between control and exposed groups result in differences in health care which affect survival rates). 

The most conclusive, and most expensive, type of study is a prospective study where the epidemiologist intervenes with the subjects. This type of study is called an intervenKon study. For example, 5(X)0 persons may be given pills containing folic add, while 5000 persons may be given pills containing only filler, where the pills are consumed for 10 years and the subjects are evaluated for cancer. In this manner, the Investigator exerts some control Over the risk factors of interest. 

---