Environmental factors such as air pollution have been linked to the development of cancer, particularly lung cancer. Many outdoor air pollutants—such as arsenic, benzene, hydrocarbons, polyvinyl chlorides, and other industrial emissions as well as motor vehicle exhaust—have been studied for their carcinogenic properties. Indoor air pollution, such as cigarette smoke and radon gas, also poses an increased risk of cancer. In fact, indoor air pollution is considered to be more carcinogenic than outdoor air pollution.

A cigarette smoker’s risk of lung cancer is more than 10 times greater than that of a nonsmoker’s by late middle age. Tobacco smoke contains carcinogens that are known to cause mutations. The risk of lung cancer from cigarette smoking correlates directly with the duration of smoking and the number of cigarettes smoked per day. Research also shows that a person who stops smoking decreases his risk of lung cancer.

Although the risk associated with pipe and cigar smoking is similar to that of cigarette smoking, some evidence suggests that the effects are less severe. Smoke from cigars and pipes is more alkaline. This alkalinity decreases nicotine absorption in the lungs and is also more irritating to the lungs, so that the smoker doesn’t inhale as readily.

Inhalation of secondhand smoke, or passive smoking, by nonsmokers also increases the risk of lung and other cancers. Use of smokeless tobacco, in which the oral tissue directly absorbs nicotine and other carcinogens, is linked to an increase in oral cancers that seldom occur in persons who don’t use the product.

Alcohol consumption is commonly associated with cirrhosis of the liver, a precursor to hepatocellular cancer. The risk of breast and colorectal cancers also increases with alcohol consumption. Heavy use of alcohol and cigarette smoking synergistically increases the incidence of cancers of the mouth, larynx, pharynx, and esophagus. It’s likely that alcohol acts as a solvent for the carcinogenic substances in smoke, thus enhancing their absorption.

Certain occupations that expose workers to specific substances increase the risk of cancer. For example, persons exposed to asbestos are at risk for a specific type of lung cancer, called mesothelioma. Asbestos also may act as a promoter for other carcinogens. Workers involved in the production of dyes, rubber, paint, and beta-naphthylamine are at increased risk for bladder cancer.

Exposure to ultraviolet radiation, including sunlight (UVB) or tanning booths (UVA), causes genetic mutation in the P53 control gene. Sunlight also releases tumor necrosis factor alpha in exposed skin, possibly diminishing the immune response. Ultraviolet sunlight is a direct cause of basal and squamous cell cancers of the skin. The amount of exposure to ultraviolet radiation also correlates with the type of cancer that develops. For example, cumulative exposure to ultraviolet sunlight is associated with basal and squamous cell skin cancer, and severe episodes of burning and blistering at a young age are associated with melanoma.

Ionizing radiation (such as X-rays) is associated with acute leukemia, thyroid, breast, lung, stomach, colon, and urinary tract cancers as well as multiple myeloma. Low doses of radiation can cause DNA mutations and chromosomal abnormalities, and large doses can inhibit cell division. Ionizing radiation can also enhance the effects of genetic abnormalities. Other compounding variables include the part and percentage of the
body exposed, the person’s age, hormonal balance, use of prescription drugs, and preexisting or concurrent conditions.

Sexual practices have been linked to specific types of cancer. The age of first sexual intercourse and the number of sexual partners are positively correlated with a woman’s risk of cervical cancer. Furthermore, a woman who has had only one sexual partner is at higher risk if that partner has had multiple partners. The suspected underlying mechanism here involves virus transmission, most likely human papilloma virus (HPV). Of the approximately 70 types of HPV, types 6 and 11 are associated with genital warts. HPV is the most common cause of abnormal Papanicolaou (Pap) tests, and cervical dysplasia is a direct precursor to squamous cell carcinoma of the cervix, both of which have been linked to HPV (especially types 16 and 31).

Hormones—specifically, the sex steroid hormones estrogen, progesterone, and testosterone—have been implicated as promoters of breast, endometrial, ovarian, or prostate cancer.

Numerous aspects of diet are linked to an increase in cancer, including:

It’s also important to note that childhood obesity may increase the risk of cancer development in later life. Obesity is a prominent risk factor for breast, colon, and prostate cancers. Because cancer is a disease of abnormal cell proliferation, the increased total number of cells in the body associated with obesity undergo a greater number of cell divisions, thereby increasing their susceptibility to abnormal changes and an increased risk of cancer development.

Age is a major determinant in the development of cancer. The longer men and women live, the more likely they are to develop the disease. For example, because of the long natural history of common cancers, prostate cancer may take up to 60 years to become invasive, while colon cancer may take as long as 40 years to develop into an invasive stage. Possible explanations for the increased incidence of cancer with advancing age include:

Genes, through the proteins they encode, are the chemical messages of heredity. Located at specific locations on the 46 chromosomes within the cell’s nucleus, genes transmit specific hereditary traits.

Most cancers develop from a complex interplay among multiple genes and between genes and internal or external environmental factors. Phenomenal progress has been made in the fields of cancer genetics and cytogenetics that has established specific chromosomal changes as diagnostic and prognostic factors in acute and chronic leukemias, as diagnostic factors in various solid tumors, and as indicators for the localization and characterization of genes responsible for tumor development.

Moreover, in the past 25 years, research has identified and characterized many of the genetic alterations that lead to tumor transformation at the chromosomal and molecular cell level. The Human Genome Project, started in 1988 to identify the entire sequence of human DNA, has helped to increase knowledge about genetics and cancer carcinogenesis. The Philadelphia (Ph) chromosome was the first chromosomal anomaly caused by translocation implicated in a human disease (chronic myelocytic leukemia [CML]). However, it’s important to note that not all mutated genes always lead to disease.

As previously discussed, two sets of genes, oncogenes and tumor suppressor genes, participate in the transformation of a normal cell into a malignant cell; however, because multiple, successive changes in distinct cellular genes are required to complete the entire process, the human cell rarely sustains the necessary number of changes needed for tumor transformation. Gene mutations are either inherited from a parent (hereditary or germline mutation) or acquired (somatic mutation). Inheritance accounts for about 10% of all cancers. Acquired mutations are changes in DNA that develop throughout a person’s lifetime. Carcinogenic agents, such as radiation or toxins, commonly are able to damage cellular genes, which are present in the cancer cell genome, thereby triggering cancer development.