Search

Objectives. Approximately 13% of all births occur prior to 37 weeks gestation in the U.S. Some established risk factors exist for preterm birth, but the etiology remains largely unknown. Recent studies have suggested an association with environmental exposures. We examined the relationship between preterm birth and exposure to a commonly used herbicide, atrazine, in drinking water.Methods. We reviewed Kentucky birth certificate data for 2004–2006 to collect duration of pregnancy and other individual-level covariates. We assessed existing data sources for atrazine levels in public drinking water for the years 2000–2008, classifying maternal county of residence into three atrazine exposure groups. We used logistic regression to analyze the relationship between atrazine exposure and preterm birth, controlling for maternal age, race/ethnicity, education, smoking, and prenatal care.Results. An increase in the odds of preterm birth was found for women residing in the counties included in the highest atrazine exposure group compared with women residing in counties in the lowest exposure group, while controlling for covariates. Analyses using the three exposure assessment approaches produced odds ratios ranging from 1.20 (95% confidence interval [CI] 1.14, 1.27) to 1.26 (95% CI 1.19, 1.32), for the highest compared with the lowest exposure group.Conclusions. Suboptimal characterization of environmental exposure and variables of interest limited the analytical options of this study. Still, our findings suggest a positive association between atrazine and preterm birth, and illustrate the need for an improved assessment of environmental exposures to accurately address this important public health issue.

Objectives. We examined geographic patterns of lung cancer incidence in Kentucky. Recent research has suggested that the coal-mining industry contributes to lung cancer risk in Appalachia. We focused on the southeastern portion of the state, which has some of the highest lung cancer rates in the nation.Methods. We implemented a spatial scan statistic to identify areas with lung cancer incidence rates that were higher than expected, after adjusting for age, gender, and smoking. The Kentucky Cancer Registry supplied information on cases (1995–2007). The U.S. Census (2000) and several years of Behavioral Risk Factor Surveillance System data (1996–2006) provided county-level population and smoking data. We compared the results with coal-mining data from the Mining Safety and Health Administration and public water utility data from the Kentucky Division of Water.Results. We identified three clusters of counties with higher-than-expected rates. Cluster 1 (relative risk [RR] = 1.21, p<0.01) included 12 counties in southeastern Kentucky. Cluster 2 (RR=1.17, p<0.01) included three nearby counties in the same region. Several of the 15 counties in Cluster 3 (RR=1.04, p=0.01) were part of the Louisville, Kentucky, or Cincinnati, Ohio, metropolitan areas. All of the counties in Clusters 1 and 2 produced significant amounts of coal.Conclusion. Environmental exposures related to the coal-mining industry could contribute to the high incidence of lung cancer in southeastern Kentucky. Lack of evidence for this effect in western Kentucky could be due to regional differences in mining practices and access to public water utilities. Future research should collect biological specimens and environmental samples to test for the presence of trace elements and other lung carcinogens.

Objectives. We identified correlates of exposure to hepatitis B and C viruses among health department clients in Appalachian Kentucky, a rural region noted for high poverty and low education. Additionally, we investigated risk factors for transmission, and the frequency of use of preventive measures.Methods. Patients screened for hepatitis B or C at four county health departments in Appalachian Kentucky were administered a routine prescreening questionnaire and an additional survey designed to obtain detailed personal and behavioral risk factor data. These data were linked to produce a more comprehensive dataset for analysis, including test results, which were attached to the prescreening questionnaire.Results. In total, 92 health department clients participated in the study survey. Of these, test results were available for 80 of the clients. Very few subjects who enrolled in this study tested positive for hepatitis B. Twelve out of 80 participants (15%) tested positive for previous exposure to hepatitis C. No participants reported having human immunodeficiency virus.Conclusions. Transmission of hepatitis C in these rural Appalachian communities is predominantly due to injection drug use. Patients with hepatitis C exposure are similar in their demographic and risk profiles as those seen in urban areas and, despite small numbers, can have a serious impact on small, rural public health systems.

Previous studies demonstrated that tobacco and arsenic exposure are risk factors for bladder cancer. A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure. Information on residential history and lifestyle factors was collected. The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure. Smokers were grouped as ever/never smokers and by pack years of exposure (0, 1-20, >20). Patients were also grouped into four arsenic exposure categories based on the average of the five highest years arsenic concentration in their drinking water: group 1, non-detectable to <10 microg/l (n = 50); group 2, 10-99 microg/l (n = 31); group 3, 100-299 microg/l (n = 35); group 4, >300 microg/l (n = 30). The proportion of tumor samples with p53 mutations and P53 immunopositivity increased strongly with both stage and grade, but not with arsenic exposure or smoking. The prevalence of tumors containing mutational transitions increased markedly with tumor stage (from 14 to 52%, P(trend) = 0.005) and grade (from 11 to 48%, P(trend) = 0.004) and was higher in smokers than in non-smokers (34 versus 18%, respectively, P = 0.10). An increasing trend was observed with pack years of smoking (P = 0.09). The majority of mutations in tumors from both smokers and non-smokers were G-->A transitions, however, in smokers a preference for G-->A transitions at CpG sites was observed (P = 0.07, two-tailed) and a positive trend was observed with pack years of exposure (P = 0.04). A hotspot was found at codon 273 in 12% of the tumors from smokers but was not observed in never smokers (P = 0.05) and a positive trend was observed with pack years of tobacco exposure (P = 0.001). Neither stage nor grade demonstrated a preference for CpG site mutation, suggesting that these changes may be early exposure-related events in carcinogenesis and are not related to tumor progression. Arsenic exposure was not associated with an increased prevalence of p53 mutation or P53 immunopositivity and there was no evidence of interaction between arsenic and smoking with these outcome variables.

This study identified correlates of human papillomavirus (HPV) vaccine acceptance among college-aged women. Data were collected by self-administered questionnaire. In multivariate analyses, women having vaginal sex (past 12 months) were nearly four times more likely to indicate acceptance (P=0.0001). Those reporting ever having a sexually transmissible infection (STI; P=0.03) and those indicating ever having an abnormal Pap test (P=0.03) were more likely to indicate acceptance. Thus, three forms of ?exposure' (having sex, having an STI or abnormal Pap) may be linked to vaccine acceptance among young women attending universities. The findings suggest that opportunities may exist for clinic-based HPV vaccine promotion among this population of women.

Increasing evidence suggests that smoking is associated with cervical cancer mortality. Most previous studies investigating this association have been small. There are no prior reports of population-based survival analyses of smoking and cervical cancer in American women. This population-based survival analysis determined the association between smoking and mortality in 2661 women diagnosed with invasive cervical cancer who were identified in the Kentucky Cancer Registry database between 1995 and 2005. This database was linked to state vital records and the National Death Index. The all cause and cervical cancer specific death rates of known current smokers and nonsmokers were compared using survival analysis with a standard Kaplan–Meier approach and a Cox proportional hazards models to adjust for confounding variables. Adjustments were made for age, ethnicity, rural residence, insurance source, cancer cell type, stage at diagnosis, and treatment received.