Variances were computed with SUDAAN software version 10.0.1 (RTI, Research Triangle Park, North Carolina) using the Taylor series linearization method. To account for the complex NHANES survey design, all analyses used NHANES 2009–2010 MEC sample weights, and thus provided unbiased estimates of behavior and oral HPV prevalence for the civilian, non-institutionalized U.S. Age categories were chosen a-priori to represent generational cohorts who had expected peak sexual exposure around the 1960s, 1970–85, 1986–99 & 2000–10 subjects were divided by age into these corresponding strata of 60–69 yo (called “seniors” hereafter), 45–59 yo (“middle-aged”), 30–44 yo (“adults”), and 20–29 yo (“young adults”). These outcomes were stratified by gender, age-cohort, and race/ethnicity. The primary outcomes of interest were history of ever performing oral sex and number of lifetime oral sex partners. Weighted prevalence estimates were reported. 5,001 individuals of this age completed any part of the 2009–10 ACASI, however, analysis was restricted to the 4,256 (85%) who answered the sexual behavior questions. Subjects <20 years of age were excluded because of more limited sexual data in this group and because their current sexual experience does not reflect their expected cumulative exposure.Īnalysis for this study was restricted to individuals 20–69 yo, as the ACASI was not administered to older individuals. Women ≥60 yo were not asked about number of female (i.e. Participants ≥60 yo were not asked about lifetime number of oral sex partners therefore analysis for this variable was restricted to those between 20–59 yo. Number of lifetime partners reported in this paper is a sum of both male and female partners.
Number of lifetime partners for any kind of sex, vaginal sex, and performing oral sex, were each collected separately. Age at first oral sex was compared to age at first sexual act (referred to as “sexual debut” hereafter) we considered first oral sex to be “at” sexual debut if age at first oral sex was the same as age at first sex. Variables included ever having had any sex, ever performing oral sex (referred to as “oral sex” hereafter), age at first sex, and age first performed oral sex. Sexual behavioral data were collected by audio computer-assisted interview (ACASI). Race and ethnicity were self-identified by participants and reported by NHANES as: Mexican-American, other Hispanic, non-Hispanic white, non-Hispanic black, and other race including multi-racial.
Therefore, we examined differences in sexual behaviors by gender, age-cohort, and race in a nationally representative sample, to explore whether the observed epidemiologic differences in oral HPV infection and OSCC rates reflect differences in sexual behaviors across these groups.ĭemographic data was collected using an interviewer administered survey. Presently, it is unclear whether differences in sexual behavior of men, younger age cohorts, and whites, explain the higher oral HPV infection and HPV-OSCC rates in these groups. Similar to the differences seen in HPV-OSCC rates, oral HPV prevalence in the general population varies by gender, age, and race. – The lower proportion of HPV-OSCC among blacks might be explained by a higher incidence of HPVn-OSCC and/or lower rates of HPV-OSCC among blacks than whites, –. , – Studies consistently report that a significantly higher proportion of white (21–64%) than black (0–35%) OSCC cases are HPV-positive. Indeed, individuals with HPV-OSCC have a distinct demographic profile, tending to be male, younger, and of higher socioeconomic status than those with HPVn-OSCC. is observed among men and whites, but not among women or blacks. , Interestingly, the increase in HPV-OSCC incidence in the U.S. – In addition, ever having performed oral sex varies with age and may differ by race, with oral sex being more prevalent among whites (∼75%) than blacks (∼62%) or Hispanics (∼63%). In recent decades sexual behaviors have changed the age of sexual initiation has decreased, and the lifetime number of sexual partners has increased. By contrast, the recent rise in HPV-OSCC has been speculated to be a result of the sexual revolution coupled with the maturation of the so-called “baby boom” generation. , The decline in HPVn-OSCC has largely been attributed to the success of anti-smoking campaigns.
From 1973 to 2004, the incidence of HPV-positive OSCC (HPV-OSCC) in the United States (U.S.) rose steadily, while the incidence of HPV-negative OSCC (HPVn-OSCC) decreased. Human papillomavirus (HPV), a sexually transmitted infection, causes a subset of oropharyngeal squamous cell cancers (OSCCs).