BackgroundThe United States has the highest incarceration rate in the world which has created a public health crisis. Correctional facilities have become a front line for mental health care. Public health research in this setting could inform criminal justice reform.We determined prevalence rates for mental illnesses and related comorbidities among all inmates in a state prison system.MethodsCross-sectional study using the Iowa Corrections Offender Network which contains health records of all inmates in Iowa. The point prevalence of both ICD-9 and DSM-IV codes for mental illnesses, timing of diagnosis and interval between incarceration and mental illness diagnosis were determined.ResultsThe average inmate (N = 8574) age was 36.7 ± 12.4 years; 17% were ≥50 years. The majority of inmates were men (91%) and white (65%).Obesity was prevalent in 38% of inmates, and 51% had a history of smoking. Almost half of inmates were diagnosed with a mental illness (48%), of whom, 29% had a serious mental illness (41% of all females and 27% of all males), and 26% had a history of a substance use disorder. Females had higher odds of having both a mental illness and substance use disorder. Almost all mental illness diagnoses were first made during incarceration (99%). The mean interval to diagnosis of depression, anxiety, PTSD and personality disorders were 26, 24, 21 and 29 months respectively. Almost 90% of mental illnesses were recognized by the 6th year of incarceration. The mean interval from incarceration to first diagnosis (recognition) of a substance abuse history was 11 months.ConclusionsThere is a substantial burden of mental illness among inmates. Racial, age and gender disparities in mental health care are coupled with a general delay in diagnosis and treatment. A large part of understanding the mental health problem in this country starts at prisons.Electronic supplementary materialThe online version of this article (doi:10.1186/s12889-017-4257-0) contains supplementary material, which is available to authorized users.

Tobacco, alcohol, and human papillomavirus (HPV) are major risk factors for head and neck cancer (HNC), but it is unclear whether there are two distinct HNC risk groups, one associated with HPV and the other with tobacco/alcohol. Because HPV-positive HNC are clinically distinct from HPV-negative cases in treatment response and with more favorable prognoses, determining whether these differences result from infection alone or in association with other HNC risk factors is important for developing future therapeutic strategies. Incident cases of HNC (n = 201) and age-gender frequency-matched controls (n = 324) were recruited to assess anti-HPV VLP (virus like particles) antibodies 16, 18, 31, and 33. Multivariate logistic regression and stratified analyses were used to calculate adjusted odds ratios (OR). HPV-seronegative and seropositive/heavy tobacco users had similar increased adjusted risks of HNC (HPV-seronegative OR = 2.6, 1.4-5.0; HPV-seropositive OR = 2.3, 1.1-4.8), as did HPV-seronegative (OR = 4.3, 2.1-9.1) versus HPV-seropositive/heavy alcohol users (OR = 3.9, 1.6-9.4). Similar HPV/tobacco/alcohol risk profiles also were seen in oropharyngeal and oral cavity tumor sites. Our finding that tobacco/alcohol use increased the risk of HNC in both HPV-seropositive and HPV-seronegative individuals is consistent with the observation that HPV infection is not a sufficient cause of HNC but requires the accumulation of additional cellular changes.

Findings are inconsistent about whether tobacco, alcohol, and human papillomavirus (HPV) are two independent HNC risk factor groups that distinguish an infection-associated cancer from a tobacco/alcohol-associated HNC. We found that cancer in the oral cavity risk was greater in HPV-E6/E7 seropositive/heavy tobacco users (adjusted OR = 3.5) than in HPV-seronegative/heavy tobacco users (adjusted OR = 1.4); and HPV-seropositive/heavy alcohol users (adjusted OR = 9.8) had greater risk than HPV-seronegative/heavy alcohol users (adjusted OR = 3.1). In contrast, the risk of oropharyngeal cancer was greater in the HPV-seronegative/heavy tobacco (adjusted OR = 11.0) than in HPV-seropositive/heavy tobacco (adjusted OR = 4.7) users and greater in HPV-seronegative/heavy alcohol users (adjusted OR = 24.3) compared to HPV-seropositive/heavy alcohol users (adjusted OR = 8.5). Disease-specific and recurrence-free adjusted survival were significantly worse in oropharyngeal HPV-seronegative cases with no survival differences by HPV status seen in oral cavity cases. The association between tobacco/alcohol, HPV, and tumor site is complex. There appear to be distinct tumor site differences in the combined exposure risks, suggesting that different molecular pathways are involved.

We examined antibody response to VLP HPV-16, HPV-16 E6 and E7 antibodies as potential seromarkers of HPV-related head and neck cancer (HNC). The study included 204 HNC cases and 326 controls evaluated for HPV presence in sera using ELISAs for anti-HPV VLP antibodies and HPV-16 E6 and/or E7 antibodies, and in tumor tissue using PCR and DNA sequencing. Anti-HPV-16 VLP was detected in 33.8% of cases and 22.4% of controls, anti-E6 in 20.6% of cases and 0.9% of controls and anti-E7 in 18.6% of cases and 0.6% of controls. HPV-16 DNA was detected in 26.1% of tumors. The adjusted risk of HNC was elevated among those seropositive for HPV-16 VLP (odds ratio (OR) 5 1.7, 1.1-2.5), E6 (OR 5 32.8,. Compared to HPV DNA-negative/seronegative cases, tumor HPV-16 cases had increased risk of detection with anti-VLP antibodies (OR 5 6.8, 3.1-14.9). The odds were more pronounced among cases seropositive for E6 (OR 5 69.0, or E7 (OR 5 50.1, 14.7-171). Antibodies against E6 or E7 were associated with risk of cancer in the oral cavity (OR 5 5.1, 1.2-22.4) and oropharynx (OR 5 72.8,, and with disease characteristics: stage, grade and nodal status. Anti-E6 and/or E7 antibodies were found in 74% of tumor HPV-16 positive cases but in only 5% of tumor HPV-negative cases (K 50.7, 0.6-0.8) suggesting good correlation between the serologic marker and HPV tumor status. Antibodies to HPV-16 E6 and/or E7 represent a more specific biomarker than anti-HPV-16 VLP of an HPV-related HNC. Because of the survival advantage of HPV-related HNC, HPV-16 E6/E7 detection may be useful in therapy targeted for HPV-related tumors. ' 2006 Wiley-Liss, Inc. Key words: head and neck neoplasms; human papillomavirus; HPV E6/E7Virtually all cervical carcinomas and more than 25% of head and neck cancers (HNC) are associated with HPV high-risk (HR) types.1-3 Two serologic markers have been used as surrogates of HPV infection: antibodies to HPV-derived virus-like particles (VLP) and to HPV-16 E6 or E7 oncoproteins. Most investigations have used anti-VLP antibodies which are considered markers of changes that occur early in the development of tumorigenesis and also markers of lifetime exposure to an HPV infection. [4][5][6] Although their presence may not represent a current HPV-related malignancy, the magnitude of risk between the presence of antiVLPs for HPV-16,18 or 33 and cervical cancer is 2-3 fold. 4,5,7 The anti-HPV-16 or 18 E6/E7 antibodies have been evaluated more recently to represent specific markers of a current HPV-associated cancer and they are overexpressed in the tumor. [8][9][10][11] The low prevalence of the anti-E6/E7 antibodies in healthy individuals without an HPV-related tumor has been verified in several large studies of adult populations. 12,13 In these studies only 2-3% of healthy individuals showed serological response to HPV-16 or HPV-18 E6 and/or E7 oncoproteins, whereas these rates increased with severity of cervical dysplasia and have been detected in 25-54% of cases with cervical cancer. 13 However, it remains unclear whether serologic tests...

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