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PRINCIPLES OF TOXICOLOGY

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304 CHEMICAL CARCINOGENESIS<br />

TABLE 13.12 Continued<br />

Dimethyl carbamoyl chloride o-Toluidine<br />

1,1-Dimethylhydrazine p-Toluidine<br />

Dimethyl sulfate 1,1,2-Trichloroethane<br />

Dinitrotoluenes Trichloroethylene<br />

Di-sec-octyl phthalate 1,2,3-Trichloropropane<br />

Dioxane Uranium<br />

Environmental tobacco smoke Vinyl bromide<br />

Epichlorohydrin Vinyl chloride<br />

Ethyl acrylate Vinyl cyclohexene dioxide<br />

Ethylene dibromide Vinylidene chloride<br />

Ethylene dichloride Welding fumes<br />

Ethyleneimine Wood dust<br />

Ethylene oxide Zince chromates<br />

Ethylene thiourea<br />

Source: NIOSH Pocket Guide, 1999.<br />

13.9 CANCER AND OUR ENVIRONMENT: FACTORS THAT MODULATE OUR RISKS<br />

TO OCCUPATIONAL HAZARDS<br />

Increased awareness of the ubiquity of synthetic, industrial chemicals in our environment has led a<br />

number of scientists to try to determine what role environmental exposures play in cancer causation.<br />

The USEPA devotes a great deal of its resources to this question as do other federal, international and<br />

private agencies such as the Agency for Toxic Substances and Disease Registry (ATSDR) of the Centers<br />

for Disease Control (CDC), the American Cancer Society (ACS), and the World Health Organization’s<br />

(WHO) International Agency for Research on Cancer (IARC) (see Table 13.14). While each organization<br />

researching the impact of our occupations, lifestyles, diets, and environmental exposures on<br />

cancer have differing agendas and views as to the predicted cancer risks associated with environmental<br />

exposures or our daily routines, there is widespread agreement that the most substantial risks, and the<br />

greatest causes of cancer, are those factors that are controlled by the individual (e.g., diet, smoking,<br />

alcohol intake).<br />

The importance of this fact is twofold: (1) it should be recognized that cancer is a phenomenon<br />

associated with normal biologic processes, and is therefore impacted by those factors that may affect<br />

our normal biologic processes (e.g., diet); and (2) many environmental risk factors exist, and these, in<br />

combination with hereditary risk factors, may frequently provide overwhelming influences in<br />

epidemiological studies of occupational hazards. Thus, the risk factors not being studied (and so<br />

frequently not controlled for) may mask or exacerbate the response being studied and so confound any<br />

study that is not normalized in a manner that removes all potential influences from the association<br />

being studied.<br />

Estimates of the contribution of various factors to the rate of cancer in humans were perhaps first<br />

put forth by Doll and Peto, who produced the results plotted in Figure 13.10. As can easily be seen in<br />

Figure 13.10, the vast majority of the cancers were thought to be related to lifestyle factors; tobacco<br />

and alcohol use, diet, and sexual behavior accounted for 75 percent of all cancers in this initial analysis.<br />

Conversely, industrial products, pollution, and occupation were thought to be related to only 7 percent<br />

of all cancers. Currently, the contributions of diet, disease, and viral agents are still being researched<br />

as perhaps the most common causes of cancer.<br />

In the years following Doll and Peto’s initial assertions, some scientists have questioned whether<br />

such a large proportion of the cancers in humans had such clearly defined causal associations. However,<br />

the most recent evidence accumulated by researchers in this area indicates that less than 1 percent of<br />

today’s cancers result from exposure to environmental pollution, and diet has since been identified as<br />

a key risk factor for cancer in nearly 200 epidemiologic studies. More importantly, the view that there

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