Dataset Information

Modeled PFOA exposure and coronary artery disease, hypertension, and high cholesterol in community and worker cohorts.

ABSTRACT:

Background

Several previous studies, mostly cross-sectional, have found associations between perfluorooctanoic acid (PFOA) and high cholesterol levels, but studies of hypertension and heart disease have had inconsistent findings.

Objectives

In this study we examined the association between modeled PFOA exposure and incident hypertension, hypercholesterolemia, and coronary artery disease among workers at a Mid-Ohio Valley chemical plant that used PFOA, and residents of the surrounding community.

Methods

Community- and worker-cohort participants completed surveys during 2008-2011 covering demographics, health-related behaviors, and medical history. Cox proportional hazard models, stratified by birth year, modeled the hazard of each outcome (starting at 20 years of age) as a function of retrospective serum PFOA concentration estimates (generated through fate, transport and exposure modeling), controlling for sex, race, education, smoking, alcohol use, body mass index, and diabetes.

Results

Among 32,254 participants (28,541 community; 3,713 worker), 12,325 reported hypertension with medication, 9,909 reported hypercholesterolemia with medication, and 3,147 reported coronary artery disease (2,550 validated). Hypercholesterolemia incidence increased with increasing cumulative PFOA exposure (sum of yearly serum concentration estimates), most notably among males 40-60 years of age. Compared with the lowest exposure quintile (< 142 ng/mL-years), hazard ratios for subsequent quintiles (ng/mL-years: 142 to < 234; 234 to < 630; 630 to < 3,579; ? 3,579) were 1.24, 1.17, 1.19, and 1.19 overall and 1.38, 1.32, 1.31, and 1.44 among men 40-60 years of age. There was no apparent association between PFOA exposure and hypertension or coronary artery disease incidence.

Conclusions

Higher PFOA exposure was associated with incident hypercholesterolemia with medication, but not with hypertension or coronary artery disease.

SUBMITTER: Winquist A

PROVIDER: S-EPMC4256699 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature

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Publications

Modeled PFOA exposure and coronary artery disease, hypertension, and high cholesterol in community and worker cohorts.

Winquist Andrea A Steenland Kyle K

Environmental health perspectives 20140926 12

<h4>Background</h4>Several previous studies, mostly cross-sectional, have found associations between perfluorooctanoic acid (PFOA) and high cholesterol levels, but studies of hypertension and heart disease have had inconsistent findings.<h4>Objectives</h4>In this study we examined the association between modeled PFOA exposure and incident hypertension, hypercholesterolemia, and coronary artery disease among workers at a Mid-Ohio Valley chemical plant that used PFOA, and residents of the surround ...[more]

PMID: 25260175

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Project description:BackgroundPerfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals. Cross-sectional epidemiologic studies suggest PFOA is associated with liver injury biomarkers.ObjectivesWe estimated associations between modeled historical PFOA exposures and liver injury biomarkers and medically validated liver disease.MethodsParticipants completed surveys during 2008-2011 reporting demographic, medical, and residential history information. Self-reported liver disease, including hepatitis, fatty liver, enlarged liver and cirrhosis, was validated with healthcare providers. Alanine aminotransferase (ALT), ?-glutamyltransferase (GGT) and direct bilirubin, markers of liver toxicity, were obtained from blood samples collected in the C8 Health Project (2005-2006). Historically modeled PFOA exposure, estimated using environmental fate and transport models and participant residential histories, was analyzed in relation to liver biomarkers (n = 30,723, including 1,892 workers) and liver disease (n = 32,254, including 3,713 workers).ResultsModeled cumulative serum PFOA was positively associated with ALT levels (p for trend < 0.0001), indicating possible liver toxicity. An increase from the first to the fifth quintile of cumulative PFOA exposure was associated with a 6% increase in ALT levels (95% CI: 4, 8%) and a 16% increased odds of having above-normal ALT (95% CI: odds ratio: 1.02, 1.33%). There was no indication of association with either elevated direct bilirubin or GGT; however, PFOA was associated with decreased direct bilirubin. We observed no evidence of an effect of cumulative exposure (with or without a 10-year lag) on all liver disease (n = 647 cases), nor on enlarged liver, fatty liver, and cirrhosis only (n = 427 cases).ConclusionResults are consistent with previous cross-sectional studies showing association between PFOA and ALT, a marker of hepatocellular damage. We did not observe evidence that PFOA increases the risk of clinically diagnosed liver disease.CitationDarrow LA, Groth AC, Winquist A, Shin HM, Bartell SM, Steenland K. 2016. Modeled perfluorooctanoic acid (PFOA) exposure and liver function in a Mid-Ohio Valley community. Environ Health Perspect 124:1227-1233;?http://dx.doi.org/10.1289/ehp.1510391.

Project description:Background Although acute coronary syndromes (ACS) are a major cause of morbidity and mortality, relationships with biologically active lipid species potentially associated with plaque disruption/erosion in the context of their lipoprotein carriers are indeterminate. The aim was to characterize lipid species within lipoprotein particles which differentiate ACS from stable coronary artery disease. Methods and Results Venous blood was obtained from 130 individuals with de novo presentation of an ACS (n=47) or stable coronary artery disease (n=83) before coronary catheterization. Lipidomic measurements (533 lipid species; liquid chromatography electrospray ionization/tandem mass spectrometry) were performed on whole plasma as well as 2 lipoprotein subfractions: apolipoprotein A1 (apolipoprotein A, high-density lipoprotein) and apolipoprotein B. Compared with stable coronary artery disease, ACS plasma was lower in phospholipids including lyso species and plasmalogens, with the majority of lipid species differing in abundance located within high-density lipoprotein (high-density lipoprotein, 113 lipids; plasma, 73 lipids). Models including plasma lipid species alone improved discrimination between the stable and ACS groups by 0.16 (C-statistic) compared with conventional risk factors. Models utilizing lipid species either in plasma or within lipoprotein fractions had a similar ability to discriminate groups, though the C-statistic was highest for plasma lipid species (0.80; 95% CI, 0.75-0.86). Conclusions Multiple lysophospholipids, but not cholesterol, featured among the lipids which were present at low concentration within high-density lipoprotein of those presenting with ACS. Lipidomics, when applied to either whole plasma or lipoprotein fractions, was superior to conventional risk factors in discriminating ACS from stable coronary artery disease. These associative mechanistic insights elucidate potential new preventive, prognostic, and therapeutic avenues for ACS which require investigation in prospective analyses.

Project description:ObjectivesTo develop prediction models that better estimate the pretest probability of coronary artery disease in low prevalence populations.DesignRetrospective pooled analysis of individual patient data.Setting18 hospitals in Europe and the United States.ParticipantsPatients with stable chest pain without evidence for previous coronary artery disease, if they were referred for computed tomography (CT) based coronary angiography or catheter based coronary angiography (indicated as low and high prevalence settings, respectively).Main outcome measuresObstructive coronary artery disease (≥ 50% diameter stenosis in at least one vessel found on catheter based coronary angiography). Multiple imputation accounted for missing predictors and outcomes, exploiting strong correlation between the two angiography procedures. Predictive models included a basic model (age, sex, symptoms, and setting), clinical model (basic model factors and diabetes, hypertension, dyslipidaemia, and smoking), and extended model (clinical model factors and use of the CT based coronary calcium score). We assessed discrimination (c statistic), calibration, and continuous net reclassification improvement by cross validation for the four largest low prevalence datasets separately and the smaller remaining low prevalence datasets combined.ResultsWe included 5677 patients (3283 men, 2394 women), of whom 1634 had obstructive coronary artery disease found on catheter based coronary angiography. All potential predictors were significantly associated with the presence of disease in univariable and multivariable analyses. The clinical model improved the prediction, compared with the basic model (cross validated c statistic improvement from 0.77 to 0.79, net reclassification improvement 35%); the coronary calcium score in the extended model was a major predictor (0.79 to 0.88, 102%). Calibration for low prevalence datasets was satisfactory.ConclusionsUpdated prediction models including age, sex, symptoms, and cardiovascular risk factors allow for accurate estimation of the pretest probability of coronary artery disease in low prevalence populations. Addition of coronary calcium scores to the prediction models improves the estimates.

Dataset Information

Modeled PFOA exposure and coronary artery disease, hypertension, and high cholesterol in community and worker cohorts.

Background

Objectives

Methods

Results

Conclusions

Publications

Modeled PFOA exposure and coronary artery disease, hypertension, and high cholesterol in community and worker cohorts.

Similar Datasets

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