PRINCIPLES OF TOXICOLOGY

13.9 CANCER AND OUR ENVIRONMENT 315
suggestion, and studies indicate that as the duration of abstinence from smoking increases, a person’s
lung cancer risk actually becomes lower until it eventually approaches the risk faced by a nonsmoker.
For this reason, many have argued that the affect of cigarette smoking is largely one of promotion.
Regardless of whether smoking is largely due to promotion or initiation, it is clearly an avoidable health
hazard and after factoring in the increased risk from cerebrovascular disease due to smoking is arguably
society’s greatest contributor to preventable causes of death.
Alcohol
Alcohol is another clearly avoidable cancer risk. Alcohol consumption is causally related to cancers
of the oral cavity, pharynx, larynx, esophagus, and liver. The combined use of alcohol and tobacco
products also leads to an increased incidence of oral cavity, esophagus, and larynx cancers. Associations
between alcohol and breast cancer have also been proposed. Estimates of the contribution of
alcohol to cancer in the United States range as high as 5 percent; however, it is estimated that there are
some 10 million problem drinkers in the United States, and so, the influence ultimately exerted upon
the national cancer incidence by alcohol might not be fully determined at the present time.
There are several theories regarding the carcinogenic activity of alcohol. Alcohol is known to induce
specific oxidative enzymes and so is suspected of potentially enhancing the initiation activity of certain
carcinogens. It has also been proposed to make tissues more responsive to the action of a carcinogen
by increasing cell permeability or by increasing the effective concentration of a carcinogen intracellularly.
Ethanol is cytotoxic chemical at high doses, and recurrent cellular injury has been suggested
as another possible mechanism for ethanol-induced or enhanced carcinogenesis. The fact that the
development of cirrhosis often precedes and frequently ends in primary liver cancer would tend to
support this hypothesis. Other possible mechanisms include the generation of free radicals (via lipid
peroxidation), and possibly some immunosuppressive effect. Regardless of the mechanism or mechanisms
by which chronic alcohol intake induces cancer or enhances the response of other carcinogens,
it clearly remains as a clearly important, but avoidable, cancer risk factor.
Diet
When Doll and Peto released their statistical analysis of the causes of cancer, many authors noted the
impact that diet had on cancer incidence was as yet unknown, or at best, very much debated. Diet, via
the intake of high quantities of animal fats, can have a decidedly negative impact on a person’s health
and such diets are clearly linked to higher incidences of cancers. However, diet is a double-edged sword
in that it can also be an important moderating influence by providing antioxidants, anticarcinogens,
and other nutritional benefit that helps the body’s detoxification and repair mechanisms to fight off
tumorigenic activity. So, with the possible exception of the cessation of smoking, the improvement of
our diet can have the greatest impact on our own health and the national cancer rate.
It is now well recognized that the plants we consume as part of our diet contain their own natural
pesticides. In fact, certain strains of plants have been cultivated with the purpose of enhancing these
natural defense mechanisms and so require less maintenance and care. However, as was seen with the
increased use of synthetic chemicals, this can enhance the toxicity of the foods we consume. As with
the synthetic chemicals tested in the chronic animal cancer bioassay, the carcinogenic activity of the
“natural” pesticides normally contained in vegetables and fruits is running at roughly 50 percent for
the chemicals tested. Thus, it has been argued that when chemicals are tested in high-dose animal
cancer bioassays one can expect approximately half of the chemicals tested, human-made (synthetic)
or natural, to elicit carcinogenic activity. Based on these projections and on the currently available
data, it has been estimated that 99.9 percent of our total pesticide intake is via the ingestion of natural,
plant-produced pesticides. In fact, it would appear we ingest as much as 1.5 g (1500 mg) of
plant-produced, natural pesticides each day.
Recently, the National Research Council’s (NRC) Board of Environmental Studies and Toxicology
Committee on Comparative Toxicity of Naturally Occurring Carcinogens published a conclusion