The alleged relationship between “lack of circumcision” and genital cancers formerly implicated smegma or smegma-borne pathogens as the causative agent. Only two histologic studies of human smegma ever have been conducted, both of which found it to be perfectly harmless. Smegma is composed of secretions of ectopic sebaceous glands in the prepuce mixed with secretions of the prostate, seminal vesicles, mucin from the urethral glands, and desquamated epithelial cells.10,12
The hypothesis that human male smegma is carcinogenic was first formulated in 1932 by circumcision promoter Abraham L. Wolbarst, M.D.1. Wolbarst also believed that circumcision prevented epilepsy. (In the early part of the 20th Century, the paroxysm of masturbation in children was often misidentified as an epileptic seizure.) Wolbarst wrote: “[Circumcision] diminishes the tendency to masturbation, convulsions and other reflex phenomena of local irritation.” Wolbarst’s beliefs about circumcision were shared by other writers, such as Peter Remondino and Abraham Ravich.
No laboratory or clinical research had been done on the subject at the time. Regardless, Wolbarst’s hypothesis about smegma and cancer found its way into early medical textbooks. In the 1950s a few experiments were done to test the hypothesis by injecting horse smegma into wounds made in the backs of mice. There were clinical studies that attempted to induce cancer by introducing smegma subcutaneously and intravaginally: No carcinomas could be induced.
The smegma hypothesis was finally disproven by an exhaustive study by Reddy2 in 1963. His results were: “The conviction that human smegma is a carcinogen could not be substantiated.”
Preston established quite clearly that there was little evidence to support a relationship between lack of circumcision and penile cancer, cervical cancer, or cancer of the prostate in 1970 but he was unable to identify the causative agent at that time,6 while Leitch7 did the same in Australia.
Gellis (1978) said there are more deaths from circumcision than from cancer of the penis.8
Boczko et al. found numerous reports of penile cancer in circumcised men, thus conclusively disproving Wolbarst’s false claims of protection from penile cancer by circumcision.9
In “Circumcision: An American Health Fallacy,” Edward Wallerstein writes 14: “If infant circumcision reduces penile cancer we could expect to see proportionately less penile cancer in circumcising nations as compared to noncircumcising ones. No such difference is found.” Wallerstein reports that, for various years between 1966 and 1972, the annual rate of new cases of penile cancer was 0.8 for the United States (which circumcises), and 0.5 for Finland, 0.9 for Denmark and 1.1 for both Norway and Sweden (all of which do not). None of these differences is statistically significant. Further, within the same time frame, both France and the United States had the same rate, 0.3, of deaths due to penile cancer.12
The link between the presence of human papillovirus (HPV) and genital cancer was established in the 1980s.15,17,18,19,20 Hellberg et al. (1986) identified tobacco use as another risk factor for cancer of the penis. Poland identified the human papilloma virus (HPV) types 16 and 18 as the cause of penile and cervical cancers in 1990. Cervical cancer has epidemiologic similarities to venereal disease. The human papilloma virus is spread by sexual contact.28 DNA sequences from HPV have been identified in more than 50 percent of cervical cancers tested by 1989.25
In February 1996, representatives of the American Cancer Society stated in a letter to the American Academy of Pediatrics:
The American Cancer Society does not consider routine circumcision to be a valid or effective measure to prevent such [genital] cancers. Research suggesting a pattern in the circumcision status of partners of women with cervical cancer is methodologically flawed, outdated and has not been taken seriously in the medical community for decades.
