Incidence, cancer defined

Hazard identification is defined as tlie process of determining whetlier human exposure to an agent could cause an increase in the incidence of a health condition (cancer, birtli defect, etc.) or whetlier exposure to nonliumans, such as fish, birds, and otlier fonns of wildlife, could cause adverse effects. Hazard identification cliaracterizes tlie liazard in terms of tlie agent and dose of the agent. Since tliere are few hazardous chemicals or hazardous agents for wliich definitive exposure data in humans exists, tlie identification of health hazards is often characterized by the effects of health hazards on laboratory test animals or other test systems. ... 

The Chemical Substances Threshold Limit Values Committee classifies certain substances found in the occupational environment as either confirmed or suspected human carcinogens. The present listing of substances that have been identified as carcinogens takes two forms those for which a TLV has b n assigned and those for which environmental and exposure conditions have not been sufficiently defined to assign a TLV. Where a TLV has been assigned, it does not necessarily imply the existence of a biological threshold however, if exposures are controlled to this level, we would not expect to see a measurable increase in cancer incidence or mortality. 

A significant body of data defines the relationship between radiation dose and cancer incidence. This dataset is primarily from a study of the atomic bomb survivors from Nagasaki and Hiroshima, Japan but also includes data from animal studies and other sources of information. While additional data are continuously collected and... 

Kamangar, F., Dores, G. M., and Anderson, W. F. (2006). Patterns of cancer incidence, mortality, and prevalence across five continents Defining priorities to reduce cancer disparities in different geographic regions of the world. /. Clin. Oncol. 24, 2137-2150. 

Although the data are not sufficient to define the shapes of the dose incidence curves in most instances, a markedly increased risk of cancer has been noted in a number of more heavily exposed populations (Ikble 6.5). In 2-naphthylamine distillers, for example, the latency and incidence of bladder cancer have been observed to vary systematically in relation to the duration of exposure (Figure 6.2). In those with exposures lasting more than five years, the cumulative incidence approached 100 percent (Figures 6.2 6.3). 

In contrast to the high degree of specificity of oestrogen receptors, the receptors for androgens are not as well-defined. Nevertheless, a paper published in London more than 200 years ago [492] reported that a high incidence of cancer of the scrotum and testicles was detected among chimney-sweeps. This disease could be associated with the chronic contact with soot. It is well known that the androgen, testosterone, is formed and accumulated mainly in the testes. 

Figure 12.7 Change in incidence of various cancers with migration from Japan to the United States provides evidence that the cancers are caused by components of the environment that differ in the two countries. The incidence of each kind of cancer is expressed as the ratio of the death rate in the populations being considered to that in a hypothetical population of California whites with the same age distribution the death rates for whites are thus defined as 1. (Adapted from J. Cairns, in Readings from Scientific American-Cancer Biology, W. H. Freeman, 1986, p. 13.)...

From studies of human populations exposed to certain chemicals, available data are sufficient to characterize the dose-incidence relationships for some types of cancer at high dose levels. However, as in the case of ionizing radiation, the data are not sufficient to define the dose-incidence relationships precisely for any form of cancer over a wide range of doses and dose rates. Therefore, the probability of cancer induction that may be associated with low doses of chemicals that would be of primary concern in protection of public health can be estimated only by interpolation and extrapolation of data at higher doses and dose rates, based on assumptions about the dose-incidence relationships and mechanisms of toxicity. For the few chemicals for which incidence data are available over a range of doses, the dose-incidence relationship is not inconsistent with linearity, but this result does not constitute proof of linearity. 

Diet and cancer relationships are an area of scientific investigation where the evidence is often vigorously debated, and extrapolation to public policy guidelines elicits much controversy. It is clear that we have not yet obtained incontrovertible evidence to define the benefits and risks which may be derived from specific changes in the fat content of our diet. However many suggest that with respect to cancer prevention, the current state of knowledge, inconclusive as it may be, is sufficient to develop recommendations which may produce significant reductions in the future incidence of certain cancers. 

A critical question concerns the possible value of dietary intervention as a preventive or therapeutic measure. There is little doubt that fat intake influences breast cancer development in rodents at levels which are found in the human diets. However, conclusive evidence is lacking about the quantitative and qualitative aspects of these processes and how fat in diets may be modified to reduce human cancer incidence. It is likely that dietary intervention may prove useful initially as a preventive or therapeutic measure in isolated groups of high risk individuals. As genetic, hormonal, and immunologic risk factors became more clearly defined, individuals at high risk and those with breast cancer may benefit from therapeutic low-fat diets whose efficacy will require assessment in well-designed clinical studies. 

First, the highest appropriate unit cancer risk (UCR) is determined from the tumor data from the most sensitive species, strain, sex, and study (FDA, 2002). Tumor incidences not considered treatment related are omitted from analysis statistical significance is an important tool in evaluating the relationship of treatment to tumor induction. If only one dose was tested and only one type of tumor was induced, then the UCR is defined as the slope of the straight line of tumor incidence versus dose. 

Strength of evidence involves the enumeration of tumours in human and animal studies and determination of their level of statistical significance. Sufficient human evidence demonstrates causality between human exposure and the development of cancer, whereas sufficient evidence in animals shows a causal relationship between the agent and an increased incidence of tumours. Limited evidence in humans is demonstrated by a positive association between exposure and cancer, but a causal relationship cannot be stated. Limited evidence in animals is provided when data suggest a carcinogenic effect, but are less than sufficient. The terms sufficient and limited are used here as they have been defined by the International Agency for Research on Cancer (lARC) and are outlined in 3.6.5.3.I. 

The health effects are further divided and defined on the next level (see Fig. 7). At this level the health effects are described in terms of various diseases and incidence of death. In the case of cancer there are available reliable estimates for the death rates incidence of death is therefore not included explicitly. The description at the lowest level allows quantification of the health effects. 

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