BackgroundThe C8 Health Project was created, authorized, and funded as part of the settlement agreement reached in the case of Jack W. Leach, et al. v. E.I. du Pont de Nemours & Company (no. 01-C-608 W.Va., Wood County Circuit Court, filed 10 April 2002). The settlement stemmed from the perfluorooctanoic acid (PFOA, or C8) contamination of drinking water in six water districts in two states near the DuPont Washington Works facility near Parkersburg, West Virginia.ObjectivesThis study reports on the methods and results from the C8 Health Project, a population study created to gather data that would allow class members to know their own PFOA levels and permit subsequent epidemiologic investigations.MethodsFinal study participation was 69,030, enrolled over a 13-month period in 2005–2006. Extensive data were collected, including demographic data, medical diagnoses (both self-report and medical records review), clinical laboratory testing, and determination of serum concentrations of 10 perfluorocarbons (PFCs). Here we describe the processes used to collect, validate, and store these health data. We also describe survey participants and their serum PFC levels.ResultsThe population geometric mean for serum PFOA was 32.91 ng/mL, 500% higher than previously reported for a representative American population. Serum concentrations for perfluorohexane sulfonate and perfluorononanoic acid were elevated 39% and 73% respectively, whereas perfluorooctanesulfonate was present at levels similar to those in the U.S. population.ConclusionsThis largest known population study of community PFC exposure permits new evaluations of associations between PFOA, in particular, and a range of health parameters. These will contribute to understanding of the biology of PFC exposure. The C8 Health Project also represents an unprecedented effort to gather basic data on an exposed population; its achievements and limitations can inform future legal settlements for populations exposed to environmental contaminants.

The life expectancy of persons cycling through the prison system is unknown. The authors sought to determine the 15.5-year survival of 23,510 persons imprisoned in the state of Georgia on June 30, 1991. After linking prison and mortality records, they calculated standardized mortality ratios (SMRs). The cohort experienced 2,650 deaths during follow-up, which were 799 more than expected (SMR = 1.43, 95% confidence interval (CI): 1.38, 1.49). Mortality during incarceration was low (SMR = 0.85, 95% CI: 0.77, 0.94), while postrelease mortality was high (SMR = 1.54, 95% CI: 1.48, 1.61). SMRs varied by race, with black men exhibiting lower relative mortality than white men. Black men were the only demographic subgroup to experience significantly lower mortality while incarcerated (SMR = 0.66, 95% CI: 0.58, 0.76), while white men experienced elevated mortality while incarcerated (SMR = 1.28, 95% CI: 1.10, 1.48). Four causes of death (homicide, transportation, accidental poisoning, and suicide) accounted for 74% of the decreased mortality during incarceration, while 6 causes (human immunodeficiency virus infection, cancer, cirrhosis, homicide, transportation, and accidental poisoning) accounted for 62% of the excess mortality following release. Adjustment for compassionate releases eliminated the protective effect of incarceration on mortality. These results suggest that the low mortality inside prisons can be explained by the rarity of deaths unlikely to occur in the context of incarceration and compassionate releases of moribund patients.

In 1997 the International Agency for Research on Cancer (IARC) classified 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD; the most potent dioxin congener) as a group 1 carcinogen based on limited evidence in humans, sufficient evidence in experimental animals, and extensive mechanistic information indicating that TCDD acts through a mechanism involving the aryl hydrocarbon receptor (AhR), which is present in both humans and animals. The judgment of limited evidence in humans was based primarily on an elevation of all cancers combined in four industrial cohorts. The group 1 classification has been somewhat controversial and has been challenged in the literature in recent years. In this article we review the epidemiologic and mechanistic evidence that has emerged since 1997. New epidemiologic evidence consists primarily of positive exposure–response analyses in several of the industrial cohorts, as well as evidence of excesses of several specific cancers in the Seveso accident cohort. There are also new data regarding how the AhR functions in mediating the carcinogenic response to TCDD. The new evidence generally supports the 1997 IARC classification.

Objectives To determine whether high blood pressure (BP) levels are associated with faster decline in specific cognitive domains. Design Prospective longitudinal cohort. Setting Uniform Data Set of the National Institutes of Health, National Institute on Aging Alzheimer's Disease Centers. Participants One thousand three hundred eighty-five participants with a diagnosis of mild cognitive impairment (MCI) and measured BP values at baseline and two annual follow-up visits. Measurements Neuropsychological test scores and Clinical Dementia Rating Sum of Boxes (CDR Sum) score. Results Participants with MCI with two or three annual occasions of high BP values (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg) had significantly faster decline on neuropsychological measures of visuomotor sequencing, set shifting, and naming than those who were normotensive on all three occasions. High systolic BP values were associated as well with faster decline on the CDR Sum score. Conclusion Hypertension is associated with faster cognitive decline in persons at risk for dementia.

We conducted a case-control study of 325 men ages 30-69 who were diagnosed with end-stage renal disease (ESRD) between 1976 and 1984, and resided in four urban areas of Michigan in 1984. Cases were selected from the Michigan Kidney Registry and excluded men with diabetic, congenital, and obstructive nephropathies. Controls were selected by random-digit dialing and were pair-matched to cases for age, race, and area of residence. Telephone interviews were conducted with 69 percent of eligible cases and 79 percent of eligible controls. Risk of ESRD was significantly related to phenacetin or acetaminophen consumption (odds ratio(OR) = 2.66), moonshine consumption (OR = 2.43), a family history of renal