Two major classes of factors influence the incidence of cancer: hereditary factors and acquired (environmental) factors. Hereditary factors come from our parents and cannot be modified. Environmental factors, which include behavioral choices, are potentially modifiable.

These include tobacco use, poor nutrition, physical inactivity, obesity, certain infectious agents, certain medical treatments, excessive sun exposure, and exposures to carcinogens (cancer-causing agents) that exist as pollutants in our air, food, water, and soil. Some carcinogens occur naturally, and some are created or concentrated by human activity. For example, radon is a naturally occurring carcinogen present in soil and rock; however, occupational radon exposure occurs in underground mines, and substantial exposures also occur in poorly ventilated basements in regions where radon soil emissions are high.

Environmental factors (as opposed to hereditary factors) account for an estimated 75%-80% of cancer cases and deaths in the US. Exposure to carcinogenic agents in occupational, community, and other settings is thought to account for a relatively small percentage of cancer deaths – about 4% from occupational exposures and 2% from environmental pollutants (man-made and naturally occurring). Although the estimated percentage of cancers related to occupational and environmental carcinogens is small compared to the cancer burden from tobacco smoking (30%) and the combination of poor nutrition, physical inactivity, and obesity (35%), the relationship between such agents and cancer is important for several reasons. First, even a small percentage of cancers can represent many deaths: 6% of cancer deaths in the US in 2011 correspond to approximately 34,320 deaths. Second, the burden of exposure to occupational and environmental carcinogens is borne disproportionately by lower-income workers and communities, contributing to disparities in the cancer burden across the US population. Third, although much is known about the relationship between occupational and environmental exposure and cancer, some important research questions remain. These include the role of exposures to certain classes of chemicals (such as hormonally active agents) during critical periods of human development and the potential for pollutants to interact with each other, as well as with genetic and acquired factors.

How Environmental Carcinogens Are Identified

The term carcinogen refers to exposures that can increase the incidence of malignant tumors (cancer). The term can apply to a single chemical such as benzene; fibrous minerals such as asbestos; metals and physical agents such as x-rays or ultraviolet light; or exposures linked to specific occupations or industries (e.g., nickel refining). Carcinogens are usually identified on the basis of epidemiological studies or by testing in animals. Studies of occupational groups (cohorts) have played an important role in understanding many chemical carcinogens – as well as radiation – because exposures are often higher among workers, who can be followed for long periods of time. Some information has also come from studies of persons exposed to carcinogens during medical treatments (such as radiation and estrogen), as well as from studies conducted among individuals who experienced high levels of short-term exposure to a chemical or physical agent due to an accidental or intentional release (such as survivors of the atomic bomb explosions of Hiroshima and Nagasaki). It is more difficult to study the relationship between exposure to potentially carcinogenic substances and cancer risk in the general population because of uncertainties about exposure and the challenge of long-term follow up. Moreover, relying upon epidemiological information to determine cancer risk does not fulfill the public health goal of prevention since by the time the increased risk is detected, a large number of people may have been exposed.

Thus, for the past 40 years, the US and many other countries have developed methods for identifying carcinogens through animal testing using the “gold standard” of a 2-year or lifetime bioassay in rodents. This test is expensive and time-consuming, but it can provide information about potential carcinogens so that human exposure can be reduced or eliminated. Many substances that are carcinogenic in rodent bioassays have not been adequately studied in humans, usually because an acceptable study population has not been identified. Among the substances that have proven carcinogenic in humans, all have shown positive results in animals when tested in well-conducted 2-year bioassays.1 Between 25%-30% of established human carcinogens were first identified through animal bioassays. Since animal tests necessarily use high-dose exposures, human risk assessment usually requires extrapolation of the exposure-response relationship observed in rodent bioassays to predict effects in humans at lower doses. Typically, regulatory agencies in the US and abroad have adopted the default assumption that no threshold level (level below which there is no increase in risk) of exposure exists for carcinogenesis.

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