Acute pain pathways: protocol for a prospective cohort study.

INTRODUCTION: Opioid analgesics are often used to treat moderate-to-severe acute non-cancer pain; however, there is little high-quality evidence to guide clinician prescribing. An essential element to developing evidence-based guidelines is a better understanding of pain management and pain control among individuals experiencing acute pain for various common diagnoses. METHODS AND ANALYSIS: This multicentre prospective observational study will recruit 1550 opioid-naïve participants with acute pain seen in diverse clinical settings including primary/urgent care, emergency departments and dental clinics. Participants will be followed for 6 months with the aid of a patient-centred health data aggregating platform that consolidates data from study questionnaires, electronic health record data on healthcare services received, prescription fill data from pharmacies, and activity and sleep data from a Fitbit activity tracker. Participants will be enrolled to represent diverse races and ethnicities and pain conditions, as well as geographical diversity. Data analysis will focus on assessing patients' patterns of pain and opioid analgesic use, along with other pain treatments; associations between patient and condition characteristics and patient-centred outcomes including resolution of pain, satisfaction with care and long-term use of opioid analgesics; and descriptive analyses of patient management of leftover opioids. ETHICS AND DISSEMINATION: This study has received approval from IRBs at each site. Results will be made available to participants, funders, the research community and the public. TRIAL REGISTRATION NUMBER: NCT04509115.

Patient-Reported Opioid Analgesic Use After Discharge from Surgical Procedures: A Systematic Review.

OBJECTIVE: This systematic review synthesizes evidence on patient-reported outpatient opioid analgesic use after surgery. METHODS: We searched PubMed (February 2019) and Web of Science and Embase (June 2019) for U.S. studies describing patient-reported outpatient opioid analgesic use. Two reviewers extracted data on opioid analgesic use, standardized the data on use , and performed independent quality appraisals based on the Cochrane Risk of Bias Tool and an adapted Newcastle-Ottawa scale. RESULTS: Ninety-six studies met the eligibility criteria; 56 had sufficient information to standardize use in oxycodone 5-mg tablets. Patient-reported opioid analgesic use varied widely by procedure type; knee and hip arthroplasty had the highest postoperative opioid use, and use after many procedures was reported as <5 tablets. In studies that examined excess tablets, 25-98% of the total tablets prescribed were reported to be excess, with most studies reporting that 50-70% of tablets went unused. Factors commonly associated with higher opioid analgesic use included preoperative opioid analgesic use, higher inpatient opioid analgesic use, higher postoperative pain scores, and chronic medical conditions, among others. Estimates also varied across studies because of heterogeneity in study design, including length of follow-up and inclusion/exclusion criteria. CONCLUSION: Self-reported postsurgery outpatient opioid analgesic use varies widely both across procedures and within a given procedure type. Contributors to within-procedure variation included patient characteristics, prior opioid use, intraoperative and perioperative factors, and differences in the timing of opioid use data collection. We provide recommendations to help minimize variation caused by study design factors and maximize interpretability of forthcoming studies for use in clinical guidelines and decision-making.

Sex steroid hormone metabolism in relation to risk of aggressive prostate cancer.

BACKGROUND: The combined action of androgens and estrogens-specifically their balance-may play a role in prostate carcinogenesis, but existing evidence is sparse and inconsistent. We investigated associations between serum sex steroid hormones, including estrogen metabolites, and risk of aggressive prostate cancer. METHODS: In a case-control study nested within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort, we measured serum estrone, estradiol, and 13 estrogen metabolites, in the 2-, 4-, or 16-hydroxylation pathways, using an LC/MS-MS assay. Cases (n = 195) were non-Hispanic white men ages 55 to 70 years when diagnosed with aggressive prostate cancer (stage III or IV and/or Gleason ≥7). Controls (n = 195) were non-Hispanic white men without prostate cancer who were frequency matched to cases by age and year at blood draw, and time since baseline screen. Only men with serum testosterone and sex hormone-binding globulin measured previously were eligible. Logistic regression models were used to estimate ORs and 95% confidence intervals (95% CI). RESULTS: Risk of aggressive prostate cancer was strongly inversely associated with estradiol:testosterone ratio (OR4th quartile vs. 1st = 0.27; 95% CI, 0.12-0.59, Ptrend = 0.003) and positively associated with 2:16α-hydroxyestrone ratio (OR4th quartile vs. 1st = 2.44; 95% CI, 1.34-4.45, Ptrend = 0.001). Individual estrogen metabolites were unrelated to risk. CONCLUSIONS: Our findings suggest that sex steroid hormones, specifically the estrogen-androgen balance, may be important in the development of aggressive prostate cancer. IMPACT: Improved understanding of the hormonal etiology of prostate cancer is critical for prevention and therapeutic interventions.

Non-steroidal anti-inflammatory drugs use is associated with reduced risk of inflammation-associated cancers: NIH-AARP study.

BACKGROUND: Chronic inflammation has been linked to cancers, and use of non-steroidal anti-inflammatory drugs (NSAIDs) has been associated with reduced risk of several cancers. To further refine the magnitude of NSAID-related associations, in particular for cancers related to inflammation, such as alcohol-, infection-, obesity-, and smoking-related cancers, as well as for less common cancers, we evaluated the use of NSAIDs and cancer risk in a very large cohort. We used propensity scores to account for potential selection bias and hypothesized that NSAID use is associated with decreased cancer incidence. METHODS: We conducted a prospective study among 314,522 participants in the NIH-AARP Diet and Health Study. Individuals who completed the lifestyle questionnaire, which included NSAID use, in 1996-1997 were followed through 2006. Information on cancer incidence was ascertained by linking to cancer registries and vital status databases. FINDINGS: During 2,715,994 person-years of follow-up (median 10.1 person-years), there were 51,894 incident cancers. Compared with non-users of NSAIDs, individuals who reported use in the 12 months prior to interview had a significantly lower risk of all inflammation-related cancer, alcohol-related, infection-related, obesity-related, and smoking-related cancers [hazard ratio (HR) (95% CI)) 0.90 (0.87-0.93), 0.80 (0.74-0.85), 0.82 (0.78-0.87), 0.88 (0.84-0.92), and 0.88 (0.85-0.92) respectively)]. CONCLUSIONS: After accounting for potential selection bias, our data showed an inverse association between NSAID use and alcohol-related, infection-related, obesity-related, and smoking-related cancers and support the hypothesis that inflammation is related to an increased risk of certain cancers.

Prospective evaluation of serum sarcosine and risk of prostate cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.

Metabolomic profiling has identified, sarcosine, a derivative of the amino acid glycine, as an important metabolite involved in the etiology or natural history of prostate cancer. We examined the association between serum sarcosine levels and risk of prostate cancer in 1122 cases (813 non-aggressive and 309 aggressive) and 1112 controls in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Sarcosine was quantified using high-throughput liquid chromatography-mass spectrometry. A significantly increased risk of prostate cancer was observed with increasing levels of sarcosine (odds ratio [OR] for the highest quartile of exposure [Q4] versus the lowest quartile [Q1] = 1.30, 95% confidence interval [CI]: 1.02, 1.65; P-trend 0.03). When stratified by disease aggressiveness, we observed a stronger association for non-aggressive cases (OR for Q4 versus Q1 = 1.44, 95% CI: 1.11, 1.88; P-trend 0.006) but no association for aggressive prostate cancer (OR for Q4 versus Q1 = 1.03, 95% CI: 0.73, 1.47; P-trend 0.89). Although not statistically significant, temporal analyses showed a stronger association between sarcosine and prostate cancer for serum collected closer to diagnosis, suggesting that sarcosine may be an early biomarker of disease. Interestingly, the association between sarcosine and prostate cancer risk was stronger among men with diabetes (OR = 2.66, 95% CI: 1.04, 6.84) compared with those without reported diabetes (OR = 1.23, 95% CI: 0.95-1.59, P-interaction = 0.01). This study found that elevated levels of serum sarcosine are associated with an increased prostate cancer risk and evidence to suggest that sarcosine may be an early biomarker for this disease.

Neuropsychiatric events in varenicline and nicotine replacement patch users in the Military Health System.

AIM: To determine the rate ratio of neuropsychiatric hospitalizations in new users of varenicline compared to new users of nicotine replacement therapy (NRT) patch in the Military Health System (MHS). DESIGN, SETTING AND PARTICIPANTS: Varenicline (n = 19,933) and NRT patch (n = 15,867) users who initiated therapy from 1 August 2006 to 31 August 2007 within the MHS were included in this retrospective cohort study. After matching according to propensity scores, 10,814 users remained in each cohort. The study population included those with and without a history of neuropsychiatric disease. MEASUREMENTS: Patients were followed for neuropsychiatric hospitalizations defined by primary neuropsychiatric discharge diagnosis using ICD-9 codes from in-patient administrative claims. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated after propensity score matching on exposure for socio-demographic factors, health-care utilization, comorbidities, medication history and neuropsychiatric history. FINDINGS: There was no increase in the rate of neuropsychiatric hospitalizations in patients treated with varenicline compared to NRT patch when followed for 30 days (propensity-score matched HR = 1.14, 95% CI: 0.56-2.34). Results were similar after 60 days of follow-up. CONCLUSIONS: There does not appear to be an increase in neuropsychiatric hospitalizations with varenicline compared with nicotine replacement therapy patch over 30 or 60 days after drug initiation.

The association between inflammation-related genes and serum androgen levels in men: the prostate, lung, colorectal, and ovarian study.

BACKGROUND: Androgens and inflammation have been implicated in the etiology of several cancers, including prostate cancer. Serum androgens have been shown to correlate with markers of inflammation and expression of inflammation-related genes. METHODS: In this report, we evaluated associations between 9,932 single nucleotide polymorphisms (SNPs) marking common genetic variants in 774 inflammation-related genes and four serum androgen levels (total testosterone [T], bioavailable T [BioT]; 5α-androstane-3α, 17ß-diol glucuronide [3αdiol G], and 4-androstene-3,17-dione [androstenedione]), in 560 healthy men (median age 64 years) drawn from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Baseline serum androgens were measured by radioimmunoassay. Genotypes were determined as part of the Cancer Genetic Markers of Susceptibility Study genome-wide scan. SNP-hormone associations were evaluated using linear regression of hormones adjusted for age. Gene-based P values were generated using an adaptive rank truncated product (ARTP) method. RESULTS: Suggestive associations were observed for two inflammation-related genes and circulating androgen levels (false discovery rate [FDR] q-value <0.1) in both SNP and gene-based tests. Specifically, T was associated with common variants in MMP2 and CD14, with the most significant SNPs being rs893226G > T in MMP2 and rs3822356T > C in CD14 (FDR q-value = 0.09 for both SNPs). Other genes implicated in either SNP or gene-based tests were IK with T and BioT, PRG2 with T, and TNFSF9 with androstenedione. CONCLUSION: These results suggest possible cross-talk between androgen levels and inflammation pathways, but larger studies are needed to confirm these findings and to further clarify the interrelationship between inflammation and androgens and their effects on cancer risk.

A reproducible and high-throughput HPLC/MS method to separate sarcosine from α- and ß-alanine and to quantify sarcosine in human serum and urine.

While sarcosine was recently identified as a potential urine biomarker for prostate cancer, further studies have cast doubt on its utility to diagnose this condition. The inconsistent results may be due to the fact that alanine and sarcosine coelute on an HPLC reversed-phase column and the mass spectrometer cannot differentiate between the two isomers, since the same parent/product ions are generally used to measure them. In this study, we developed a high-throughput liquid chromatography-mass spectrometry (LC-MS) method that resolves sarcosine from alanine isomers, allowing its accurate quantification in human serum and urine. Assay reproducibility was determined using the coefficient of variation (CV) and intraclass correlation coefficient (ICC) in serum aliquots from 10 subjects and urine aliquots from 20 subjects across multiple analytic runs. Paired serum/urine samples from 42 subjects were used to evaluate sarcosine serum/urine correlation. Both urine and serum assays gave high sensitivity (limit of quantitation of 5 ng/mL) and reproducibility (serum assay, intra- and interassay CVs < 3% and ICCs > 99%; urine assay, intra-assay CV = 7.7% and ICC = 98.2% and interassay CV = 12.3% and ICC = 94.2%). In conclusion, this high-throughput LC-MS method is able to resolve sarcosine from α- and ß-alanine and is useful for quantifying sarcosine in serum and urine samples.

Dietary carbohydrate, glycemic index, glycemic load, and risk of prostate cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort.

OBJECTIVE: To evaluate the associations between dietary carbohydrate, glycemic index (GI), glycemic load (GL), and incident prostate cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort. METHODS: Between September 1993 and September 2000, 38,343 men were randomized to the screening arm of the trial at one of 10 PLCO centers. A food frequency questionnaire administered at baseline assessed usual dietary intake over the preceding 12 months. Prostate cancer was ascertained by medical follow-up of suspicious screening results and annual mailed questionnaires and confirmed with medical records. Cox proportional hazards regression was used to model the associations of carbohydrate, GI, and GL with prostate cancer risk. RESULTS: During follow-up (median = 9.2 years), 2,436 incident prostate cancers were identified among 30,482 eligible participants. Overall, there were no associations of baseline carbohydrate, GI, or GL with incident prostate cancer in minimally or fully adjusted models. There were no associations when the 228 advanced and 2,208 non-advanced cancers were analyzed separately. CONCLUSIONS: Dietary carbohydrate, GI, and GL were not associated with incident prostate cancer in PLCO. The narrow range of GI in this cohort may have limited our ability to detect associations, an issue that future studies should address.

Association between genetic variants in the 8q24 cancer risk regions and circulating levels of androgens and sex hormone-binding globulin.

BACKGROUND: Genome-wide association studies have identified multiple independent regions on chromosome 8q24 that are associated with cancers of the prostate, breast, colon, and bladder. METHODS: To investigate their biological basis, we examined the possible association between 164 single nucleotide polymorphisms (SNPs) in the 8q24 risk regions spanning 128,101,433-128,828,043 bp, and serum androgen (testosterone, androstenedione, 3alphadiol G, and bioavailable testosterone), and sex hormone-binding globulin levels in 563 healthy, non-Hispanic, Caucasian men (55-74 years old) from a prospective cohort study (the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial). Age-adjusted linear regression models were used to determine the association between the SNPs in an additive genetic model and log-transformed biomarker levels. RESULTS: Three adjacent SNPs centromeric to prostate cancer risk-region 2 (rs12334903, rs1456310, and rs980171) were associated with testosterone (P < 1.1 x 10(-3)) and bioavailable testosterone (P < 6.3 x 10(-4)). Suggestive associations were seen for a cluster of nine SNPs in prostate cancer risk region 1 and androstenedione (P < 0.05). CONCLUSIONS: These preliminary findings require confirmation in larger studies but raise the intriguing hypothesis that genetic variations in the 8q24 cancer risk regions might correlate with androgen levels. IMPACT: These results might provide some clues for the strong link between 8q24 and prostate cancer risk.

Androgen receptor CAG repeat length and risk of biliary tract cancer and stones.

Biliary tract cancers, encompassing cancers of the gallbladder, extrahepatic bile ducts, and ampulla of Vater, are rare but highly fatal. Gallstones represent the major risk factor for biliary tract cancer, and share with gallbladder cancer a female predominance and an association with reproductive factors and obesity. Although estrogens have been implicated in earlier studies of gallbladder cancer, there are no data on the role of androgens. Because intracellular androgen activity is mediated through the androgen receptor (AR), we examined associations between AR CAG repeat length [(CAG)(n)] and the risk of biliary tract cancers and stones in a population-based study of 331 incident cancer cases, 837 gallstone cases, and 750 controls from Shanghai, China, where the incidence rates for biliary tract cancer are rising sharply. Men with (CAG)(n) >24 had a significant 2-fold risk of gallbladder cancer [odds ratio (OR), 2.00; 95% confidence interval (CI), 1.07-3.73], relative to those with (CAG)(n) < or = 22. In contrast, women with (CAG)(n) >24 had reduced gallbladder cancer risk (OR, 0.69; 95% CI, 0.43-1.09) relative to those with (CAG)(n) < or = 22; P interaction sex = 0.01, which was most pronounced for women ages 68 to 74 (OR, 0.48; 95% CI, 0.25-0.93; P interaction age = 0.02). No associations were found for bile duct cancer or gallstones. Reasons for the heterogeneity of genetic effects by gender and age are unclear but may reflect an interplay between AR and the levels of androgen as well as estrogen in men and older women. Further studies are needed to confirm these findings and clarify the mechanisms involved.

Measuring serum melatonin in epidemiologic studies.

BACKGROUND: Epidemiologic data on serum melatonin, a marker of circadian rhythms, and cancer are sparse due largely to the lack of reliable assays with high sensitivity to detect relatively low melatonin levels in serum collected during daylight, as commonly available in most epidemiologic studies. METHODS: To help expand epidemiologic research on melatonin, we assessed the reproducibility and refined a currently available melatonin RIA, and evaluated its application to epidemiologic investigations by characterizing melatonin levels in serum, urine, and/or plasma in 135 men from several ethnic groups. RESULTS: Reproducibility was high for the standard 1.0-mL serum [mean coefficient of variation (CV), 6.9%; intraclass correlation coefficient (ICC), 97.4%; n = 2 serum pools in triplicate] and urine-based (mean CV, 3.5%; ICC, 99.9%) assays. Reproducibility for the 0.5-mL refined-serum assay was equally good (mean CV, 6.6%; ICC, 99.0%). There was a positive correlation between morning serum melatonin and 6-sulfatoxymelatonin in 24-hour urine (r = 0.46; P = 0.008; n = 49 subjects). Melatonin levels in serum-plasma pairs had a high correlation (r = 0.97; P < 1x10(-4); n = 20 pairs). Morning serum melatonin levels were five times higher than those from the afternoon (before 9 a.m. mean, 11.0 pg/mL, versus after 11 a.m. mean, 2.0 pg/mL). Chinese men had lower melatonin levels (mean, 3.4 pg/mL), whereas Caucasian, African-American, and Ghanaian men had similar levels (mean, 6.7-8.6 pg/mL). CONCLUSIONS: These results suggest that melatonin can be detected reliably in serum samples collected in epidemiologic studies in various racial groups. IMPACT: With improved assays, it may be possible to investigate the role of melatonin and the emerging circadian rhythm hypothesis in cancer etiology in epidemiologic studies.

Diabetes genes and prostate cancer in the Atherosclerosis Risk in Communities study.

There is a known inverse association between type 2 diabetes (T2D) and prostate cancer (PrCa) that is poorly understood. Genetic studies of the T2D-PrCa association may provide insight into the underlying mechanisms of this association. We evaluated associations in the Atherosclerosis Risk in Communities study between PrCa and nine T2D single nucleotide polymorphisms from genome-wide association studies of T2D (in CDKAL1, CDKN2A/B, FTO, HHEX, IGF2BP2, KCNJ11, PPARG, SLC30A8, and TCF7L2) and four T2D single nucleotide polymorphisms from pre-genome-wide association studies (in ADRB2, CAPN10, SLC2A2, and UCP2). From 1987 to 2000, there were 397 incident PrCa cases among 6,642 men ages 45 to 64 years at baseline. We used race-adjusted Cox proportional hazards models to estimate associations between PrCa and increasing number of T2D risk-raising alleles. PrCa was positively associated with the CAPN10 rs3792267 G allele [hazard ratio (HR) 1.20; 95% confidence interval (CI), 1.00-1.44] and inversely associated with the SLC2A2 rs5400 Thr110 allele (HR, 0.85; 95% CI, 0.72, 1.00), the UCP2 rs660339 Val55 allele (HR, 0.84; 95% CI, 0.73, 0.97) and the IGF2BP2 rs4402960 T allele (HR, 0.79; 95% CI, 0.61-1.02; blacks only). The TCF7L2 rs7903146 T allele was inversely associated with PrCa using a dominant genetic model (HR, 0.79; 95% CI, 0.65-0.97). Further knowledge of T2D gene-PrCa mechanisms may improve understanding of PrCa etiology.

Impact of treatment and socioeconomic status on racial disparities in survival among older women with breast cancer.

OBJECTIVE: To examine racial/ethnic disparities in mortality and survival in a large nationwide and population-based cohort of women with breast cancer after simultaneously controlling for differences in comorbidity, treatment, and socioeconomic status. METHODS: A cohort of 35,029 women with stage I-IIIA breast cancer at age > or = 65 from 1992 to 1999 was identified from the surveillance, epidemiology, and end results-medicare linked databases with up to 11 years of follow-up. Cox proportional hazard regression analysis was performed to determine the risk of all-cause and breast cancer-specific mortality. RESULTS: African-American women with breast cancer were more likely to live in the poorest quartiles of socioeconomic status at the census tract level than whites (73.7% versus 20.7%, P < 0.001). Those living in communities with the lowest socioeconomic status were 11% more likely to die than those in the highest (hazard ratio, 1.10; 95% confidence interval, 1.04-1.16). The risk of dying changed slightly after controlling for race/ethnicity (1.11; 1.05-1.18). Compared with white women with breast cancer, crude hazard ratios of all-cause and breast cancer-specific mortality were 1.35 (1.27-1.45) and 1.83 (1.56-2.16) for African-Americans. After adjusting for treatment and socioeconomic status, hazard ratio of all-cause mortality was no longer significant in African-Americans (1.02; 0.84-1.10), whereas the risk of breast cancer-specific mortality was marginally higher in African-Americans (1.21; 1.01-1.46). CONCLUSIONS: Racial disparities in overall survival between African-American and white women with breast cancer were not present after controlling for treatment and socioeconomic status. Efforts to eliminate these barriers have important public health implications for reducing disparities in health outcomes.

Adherence to recommendations for follow-up to abnormal Pap tests.

OBJECTIVE: To evaluate whether timely adherence rates differ by race among women with abnormal Pap tests participating in a cost-free or reduced-cost program. METHODS: Eligible subjects included women aged 47-64 years who received a referral for follow-up care after an abnormal Pap test from 1999 to 2002 in South Carolina (n=330). Adherence was measured as days to receipt of follow-up care after an abnormal Pap test. Cox proportional hazards modeling was used to estimate risk factors associated with time to adherence within 60 and 365 days by race. RESULTS: African-American and non-Hispanic white women had similar adherence to follow-up. Among white women, those with high-grade lesions were less likely to adhere in a timely manner relative to those with low-grade lesions (hazard ratio 0.6, 95% confidence interval [CI] 0.4-1.0). For African-American women, rural residence (hazard ratio: 0.5, 95% CI 0.2-0.9) and history of abnormal Pap tests (hazard ratio 0.6, 95% CI 0.3-1.0) were associated with decreased adherence, whereas less education (hazard ratio 2.3, 95% CI 1.3-3.9) was associated with increased adherence. CONCLUSION: Adherence rates do not differ by race. However, risk factors for adherence within race are variable. Interventions tailored to the differential needs of racial and ethnic groups may prove effective toward increasing timely adherence rates. LEVEL OF EVIDENCE: II.

Meta-analysis of racial disparities in survival in association with socioeconomic status among men and women with colon cancer.

BACKGROUND: Few studies have addressed racial disparities in survival for colon cancer by adequately incorporating both treatment and socioeconomic factors, and the findings from those studies have been inconsistent. The objectives of the current study were to systematically review the existing literature and provide a more stable estimate of the measures of association between socioeconomic status and racial disparities in survival for colon cancer by undertaking a meta-analysis. METHODS: For this meta-analysis, the authors searched the MEDLINE database to identify articles published in English from 1966 to August 2006 that met the following inclusion criteria: original research articles that addressed the association between race/ethnicity and survival in patients with colon or colorectal cancer after adjusting for socioeconomic status. In total, 66 full articles were reviewed, and 56 of those articles were excluded, which left 10 studies for the final analysis. RESULTS: The pooled hazard ratio (HR) for African Americans compared with Caucasians was 1.14 (95% confidence interval [95% CI], 1.00-1.29) for all-cause mortality and 1.13 (95% CI, 1.01-1.28) for colon cancer-specific mortality. The test for homogeneity of the HR was statistically significant across the studies for all-cause mortality (Q=31.69; P<.001) but was not significant across the studies for colon cancer-specific mortality (Q=7.45; P=.114). CONCLUSIONS: Racial disparities in survival for colon cancer between African Americans and Caucasians were only marginally significant after adjusting for socioeconomic factors and treatment. Attempts to modify treatment and socioeconomic factors with the objective of reducing racial disparities in health outcomes may have important clinical and public health implications.

West Nile virus infection among the homeless, Houston, Texas.

Among 397 homeless participants studied, the overall West Nile virus (WNV) seroprevalence was 6.8%. Risk factors for WNV infection included being homeless >1 year, spending >6 hours outside daily, regularly taking mosquito precautions, and current marijuana use. Public health interventions need to be directed toward this high-risk population.

A case-control study of farming and prostate cancer in African-American and Caucasian men.

OBJECTIVE: To determine the risk of prostate cancer associated with farming by duration, recency and specific activities among African-Americans and Caucasians. METHODS: This population-based case-control study had information on farming-related activities for 405 incident prostate cancer cases and 392 controls matched for age, race and region in South Carolina, USA, from 1999 to 2001. Cases with histologically confirmed, primary invasive prostate cancer who were aged between 65 and 79 years were ascertained through the South Carolina Central Cancer Registry. Appropriately matched controls were identified from the Health Care Financing Administration Medicare Beneficiary File. Data were collected using computer-assisted telephone interviewing, and adjusted odds ratios (aOR) were estimated using unconditional logistic regression. RESULTS: Farming was associated with increased risk of prostate cancer in Caucasians (aOR 1.8; 95% confidence interval (CI) 1.3 to 2.7) but not in African-Americans (aOR 1.0; 95% CI 0.6 to 1.6). Regarding specific farming activities, farmers who mixed or applied pesticides had a higher risk of prostate cancer (aOR 1.6; 95% CI 1.2 to 2.2). Increased risk of prostate cancer was observed only for those farming <5 years. CONCLUSIONS: Increased risk of prostate cancer for farmers in this study may be attributable to pesticide exposure. Racial differences in the association between farming and prostate cancer may be explained by different farming activities or different gene-environment interactions by race.

What predicts adherence to follow-up recommendations for abnormal Pap tests among older women?

OBJECTIVE: To address socio-demographic factors associated with adherence to follow-up recommendations in a high-risk population of women referred for follow-up care after an abnormal Pap test. METHODS: 486 women aged 46-64 served by BCCEDP in two southeastern states between 1999-2002 and referred for follow-up care after an abnormal Pap test were the sampling frame for this cross-sectional study; 204 women completed a phone-based interview in 2004. Cox proportional hazards modeling was used to determine the association of various risk factors with time to adherence. RESULTS: Among those completing the phone interview (interview rate=61.4%) the mean age was 53.3 years, 64.7% were African-American women, 81.9% had low-grade cervical lesions, and all were either uninsured or under insured. Over 95% received follow-up care for an abnormal Pap test within 365 days of referral. When the BCCEDP criteria of follow-up within 60 days were applied, 52.9% were adherent. Rates of self-reported and program documented adherence differed significantly by state. After adjusting for state of residence, women who reported having symptoms of a chronic disease were more likely to be adherent within 365 days (aHR=1.42; 95% CI=1.00, 2.04). Neither age, race, lesion severity, education, number of dependent adults or children, self-perceived physical health, nor smoking status was associated with time to adherence. CONCLUSIONS: Findings suggest that institutional factors may be more important than individual factors in predicting time to adherence for an abnormal Pap test.