A Geospatial Analysis of CDC-funded HIV Prevention Programs for African Americans in the United States

Given the increase in HIV/AIDS infection rates among racial and ethnic minorities, particularly African Americans, this study was undertaken as part of a larger research effort to examine the distribution of HIV prevention services focusing on African American populations within the United States. Data were gathered via a national survey of community-based organizations (CBOs) funded by the Centers for Disease Control and Prevention (CDC). A geocoded national database was constructed to identify, locate, and map these HIV prevention programs. A total of 1,020 CBOs responded to the survey, yielding a response rate of 70.3%. These CBOs administered a total of 3,028 HIV prevention programs. Data describing intervention types and persons served, combined with the address and service area of responding CBOs, were integrated with census data (2000) and analyzed by using a geographic information system (GIS). The results of our national level analysis show that HIV prevention services for African Americans have fair coverage where African Americans comprise a substantial proportion of the population in urban areas in northeastern states, but that HIV prevention services for African Americans are inadequately distributed in the southeastern states. A local-level analysis was conducted for Alabama, where 68% of HIV/AIDS cases are among African Americans. Specific interventions such as street and community outreach, health communications, and public information are fairly well provided to African Americans in more urban cities in Alabama, however, individual- and group-level interventions have poor coverage in rural areas where a large percentage of African-Americans live. Overall, our study illustrates that the use of GIS adds value when used with other data sources to provide prevention services that are accessible to the populations most in need

A GIS-based method for household recruitment in a prospective pesticide exposure study

<p>Abstract</p> <p>Background</p> <p>Recent advances in GIS technology and remote sensing have provided new opportunities to collect ecologic data on agricultural pesticide exposure. Many pesticide studies have used historical or records-based data on crops and their associated pesticide applications to estimate exposure by measuring residential proximity to agricultural fields. Very few of these studies collected environmental and biological samples from study participants. One of the reasons for this is the cost of identifying participants who reside near study fields and analyzing samples obtained from them. In this paper, we present a cost-effective, GIS-based method for crop field selection and household recruitment in a prospective pesticide exposure study in a remote location. For the most part, our multi-phased approach was carried out in a research facility, but involved two brief episodes of fieldwork for ground truthing purposes. This method was developed for a larger study designed to examine the validity of indirect pesticide exposure estimates by comparing measured exposures in household dust, water and urine with records-based estimates that use crop location, residential proximity and pesticide application data. The study focused on the pesticide atrazine, a broadleaf herbicide used in corn production and one of the most widely-used pesticides in the U.S.</p> <p>Results</p> <p>We successfully used a combination of remotely-sensed data, GIS-based methods and fieldwork to select study fields and recruit participants in Illinois, a state with high corn production and heavy atrazine use. Our several-step process consisted of the identification of potential study fields and residential areas using aerial photography; verification of crop patterns and land use via site visits; development of a GIS-based algorithm to define recruitment areas around crop fields; acquisition of geocoded household-level data within each recruitment area from a commercial vendor; and confirmation of final participant household locations via ground truthing. The use of these procedures resulted in a sufficient sample of participants from 14 recruitment areas in seven Illinois counties.</p> <p>Conclusion</p> <p>One of the challenges in pesticide research is the identification and recruitment of study participants, which is time consuming and costly, especially when the study site is in a remote location. We have demonstrated how GIS-based processes can be used to recruit participants, increase efficiency and enhance accuracy. The method that we used ultimately made it possible to collect biological samples from a specific demographic group within strictly defined exposure areas, with little advance knowledge of the location or population.</p

Effects on the immune system associated with living near a pesticide dump site.

In this paper, we report results of the second phase of a larger study designed to evaluate the effects on the immune system of living near a Superfund site containing organochlorine pesticides, volatile organic compounds, and metals. Phase II was conducted to determine whether living near the site, consisting of six locations in Aberdeen, North Carolina, is associated with higher plasma organochlorine levels, immune suppression, or DNA damage. Each of 302 residents of Aberdeen and neighboring communities provided a blood specimen, underwent a skin test, and answered a questionnaire. Blood specimens were analyzed for organochlorine pesticides, immune markers, and micronuclei. Of 20 organochlorines tested, only DDE was detected in the blood of participants (except for one individual). Age-adjusted mean plasma DDE levels were 4.05 ppb for Aberdeen residents and 2.95 ppb (p = 0.01) for residents of neighboring communities. Residents of 40-59 years of age who lived within a mile of any site, but particularly the Farm Chemicals site, had higher plasma DDE levels than residents who lived farther away. Residents who lived near the Farm Chemicals site before versus after 1985 also had higher plasma DDE levels. Overall, there were few differences in immune markers between residents of Aberdeen and the neighboring communities. However, residents who lived closer to the dump sites had statistically significantly lower mitogen-induced lymphoproliferative activity than residents who lived farther away (p < 0.05). Residential location was not consistently associated with frequency of micronuclei or skin test responses. Although some statistically significant differences in immune markers were noted in association with residential location, the magnitude of effects are of uncertain clinical importance

Acetylation genotype and the genetic susceptibility to postate cancer in a Southern European population

Epidemiologic studies have suggested that environmental factors and diet are important risk factors in the pathogenesis of prostate cancer. The N-acetyltransferases (NAT) are important enzymes in activation and inactivation of various carcinogens, including those found in well-cooked meat and cigarette smoke. METHODS. We analyzed DNA samples from 146 prostate cancer patients and 174 healthy men. We used PCR–RFLP method to analyze NAT1 and NAT2 polymorphisms. RESULTS. We did not find statistically significant differences in NAT1 genotypes frequencies between prostate cancer patients and control group. We observed an association of the slow acetylator genotype, NAT2*6/NAT2*6 with prostate cancer protection (P¼0.017;OR¼0.31, 95% CI 0.11–0.84). Multivariate logistic regression analysis confirmed this association (0.030; OR¼0.32, 95% CI 0.12–0.89). CONCLUSIONS. Our results indicate a role of NAT2 polymorphisms in the carcinogenic pathway of prostate cancer, specifically in a population of Southern Europe

A Prospective Study of Plasma Vitamin D Metabolites, Vitamin D Receptor Polymorphisms, and Prostate Cancer

BACKGROUND: Vitamin D insufficiency is a common public health problem nationwide. Circulating 25-hydroxyvitamin D(3) (25[OH]D), the most commonly used index of vitamin D status, is converted to the active hormone 1,25 dihydroxyvitamin D(3) (1,25[OH](2)D), which, operating through the vitamin D receptor (VDR), inhibits in vitro cell proliferation, induces differentiation and apoptosis, and may protect against prostate cancer. Despite intriguing results from laboratory studies, previous epidemiological studies showed inconsistent associations of circulating levels of 25(OH)D, 1,25(OH)(2)D, and several VDR polymorphisms with prostate cancer risk. Few studies have explored the joint association of circulating vitamin D levels with VDR polymorphisms. METHODS AND FINDINGS: During 18 y of follow-up of 14,916 men initially free of diagnosed cancer, we identified 1,066 men with incident prostate cancer (including 496 with aggressive disease, defined as stage C or D, Gleason 7–10, metastatic, and fatal prostate cancer) and 1,618 cancer-free, age- and smoking-matched control participants in the Physicians' Health Study. We examined the associations of prediagnostic plasma levels of 25(OH)D and 1,25(OH)(2)D, individually and jointly, with total and aggressive disease, and explored whether relations between vitamin D metabolites and prostate cancer were modified by the functional VDR FokI polymorphism, using conditional logistic regression. Among these US physicians, the median plasma 25(OH)D levels were 25 ng/ml in the blood samples collected during the winter or spring and 32 ng/ml in samples collected during the summer or fall. Nearly 13% (summer/fall) to 36% (winter/spring) of the control participants were deficient in 25(OH)D (<20 ng/ml) and 51% (summer/fall) and 77% (winter/spring) had insufficient plasma 25(OH)D levels (<32 ng/ml). Plasma levels of 1,25(OH)(2)D did not vary by season. Men whose levels for both 25(OH)D and 1,25(OH)(2)D were below (versus above) the median had a significantly increased risk of aggressive prostate cancer (odds ratio [OR] = 2.1, 95% confidence interval [CI] 1.2–3.4), although the interaction between the two vitamin D metabolites was not statistically significant (p (interaction) = 0.23). We observed a significant interaction between circulating 25(OH)D levels and the VDR FokI genotype (p (interaction) < 0.05). Compared with those with plasma 25(OH)D levels above the median and with the FokI FF or Ff genotype, men who had low 25(OH)D levels and the less functional FokI ff genotype had increased risks of total (OR = 1.9, 95% CI 1.1–3.3) and aggressive prostate cancer (OR = 2.5, 95% CI 1.1–5.8). Among men with plasma 25(OH)D levels above the median, the ff genotype was no longer associated with risk. Conversely, among men with the ff genotype, high plasma 25(OH)D level (above versus below the median) was related to significant 60%∼70% lower risks of total and aggressive prostate cancer. CONCLUSIONS: Our data suggest that a large proportion of the US men had suboptimal vitamin D status (especially during the winter/spring season), and both 25(OH)D and 1,25(OH)(2)D may play an important role in preventing prostate cancer progression. Moreover, vitamin D status, measured by 25(OH)D in plasma, interacts with the VDR FokI polymorphism and modifies prostate cancer risk. Men with the less functional FokI ff genotype (14% in the European-descent population of this cohort) are more susceptible to this cancer in the presence of low 25(OH)D status

A comparison of sunlight exposure in men with prostate cancer and basal cell carcinoma

Ultraviolet radiation exposure increases basal cell carcinoma (BCC) risk, but may be protective against prostate cancer. We attempted to identify exposure patterns that confer reduced prostate cancer risk without increasing that of BCC. We used a questionnaire to assess exposure in 528 prostate cancer patients and 442 men with basal cell carcinoma, using 365 benign prostatic hypertrophy patients as controls. Skin type 1 (odds ratio (OR)=0.47, 95% CI=0.26–0.86), childhood sunburning (OR=0.38, 95% CI=0.26–0.57), occasional/frequent sunbathing (OR=0.21, 95% CI=0.14–0.31), lifetime weekday (OR=0.85, 95% CI=0.80–0.91) and weekend exposure (OR=0.79, 95% CI=0.73–0.86) were associated with reduced prostate cancer risk. Skin type 1 (OR=4.00, 95% CI=2.16–7.41), childhood sunburning (OR=1.91, 95% CI=1.36–2.68), regular foreign holidays (OR=6.91, 95% CI=5.00-9.55) and weekend (OR=1.17, 95% CI=1.08–1.27) but not weekday exposure were linked with increased BCC risk. Combinations of one or two parameters were associated with a progressive decrease in the ORs for prostate cancer risk (OR=0.54–0.25) with correspondingly increased BCC risk (OR=1.60–2.54). Our data do not define exposure patterns that reduce prostate cancer risk without increasing BCC risk

Inhibitory effects of retinoic acid metabolism blocking agents (RAMBAs) on the growth of human prostate cancer cells and LNCaP prostate tumour xenografts in SCID mice

In recent studies, we have identified several highly potent all-trans-retinoic acid (ATRA) metabolism blocking agents (RAMBAs). On the basis of previous effects of liarozole (a first-generation RAMBA) on the catabolism of ATRA and on growth of rat Dunning R3227G prostate tumours, we assessed the effects of our novel RAMBAs on human prostate tumour (PCA) cell lines. We examined three different PCA cell lines to determine their capacity to induce P450-mediated oxidation of ATRA. Among the three different cell lines, enhanced catabolism was detected in LNCaP, whereas it was not found in PC-3 and DU-145. This catabolism was strongly inhibited by our RAMBAs, the most potent being VN/14-1, VN/50-1, VN/66-1, and VN/69-1 with IC50 values of 6.5, 90.0, 62.5, and 90.0 nM, respectively. The RAMBAs inhibited the growth of LNCaP cells with IC50 values in the μM-range. In LNCaP cell proliferation assays, VN/14-1, VN/50-1, VN/66-1, and VN/69-1 also enhanced by 47-, 60-, 70-, and 65-fold, respectively, the ATRA-mediated antiproliferative activity. We then examined the molecular mechanism underlying the growth inhibitory properties of ATRA alone and in combination with RAMBAs. The mechanism appeared to involve the induction of differentiation, cell-cycle arrest, and induction of apoptosis (TUNEL), involving increase in Bad expression and decrease in Bcl-2 expression. Treatment of LNCaP tumours growing in SCID mice with VN/66-1 and VN/69-1 resulted in modest but statistically significant tumour growth inhibition of 44 and 47%, respectively, while treatment with VN/14-1 was unexpectedly ineffective. These results suggest that some of our novel RAMBAs may be useful agents for the treatment of prostate cancer