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Open Access Publications from the University of California

Scholarly Works (13 results)

  • Article
  • Peer Reviewed
UC Irvine Previously Published Works (2013)

Objectives

Geographic Information Systems (GIS) is a powerful tool for assessing exposure in epidemiologic studies. We used GIS to determine the geographic extent of contamination by perfluorooctanoic acid, C8 (PFOA) that was released into the environment from the DuPont Washington Works Facility located in Parkersburg, West Virginia.

Methods

Paper maps of pipe distribution networks were provided by six local public water districts participating in the community cross-sectional survey, the C8 Health Project. Residential histories were also collected in the survey and geocoded. We integrated the pipe networks and geocoded addresses to determine which addresses were serviced by one of the participating water districts. The GIS-based water district assignment was then compared to the participants' self-reported source of public drinking water.

Results

There were a total of 151,871 addresses provided by the 48,800 participants of the C8 Health Project that consented to geocoding. We were able to successfully geocode 139,067 (91.6%) addresses, and of these, 118,209 (85.0%) self-reported water sources were confirmed using the GIS-based method of water district assignment. Furthermore, the GIS-based method corrected 20,858 (15.0%) self-reported public drinking water sources. Over half (54%) the participants in the lowest GIS-based exposure group self-reported being in a higher exposed water district.

Conclusions

Not only were we able to correct erroneous self-reported water sources, we were also able to assign water districts to participants with unknown sources. Without the GIS-based method, the reliance on only self-reported data would have resulted in exposure misclassification.
    Cover page: Assessing the Spatial Distribution of Perfluorooctanoic Acid Exposure via Public Drinking Water Pipes Using Geographic Information SystemsCreative Commons 'BY' version 4.0 license
    • Article
    • Peer Reviewed
    UC Berkeley Previously Published Works (2016)

    Background

    Exposure to some perfluoroalkyl substances (PFAS), such as perfluorohexane sulfonate (PFHxS), perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorononanoic acid (PFNA), may alter levels of sex hormones and insulin-like growth factor-1 (IGF-1) in animals. Human studies on this topic are scarce, and none have been conducted in young children.

    Objectives

    We investigated the relationship between levels of PFAS and estradiol, total testosterone, and IGF-1 in 2,292 children (6-9 years of age) from the C8 Health Project who lived near a chemical plant in the Mid-Ohio Valley (USA) with local contamination from PFOA.

    Methods

    Serum samples were collected in 2005-2006 and analyzed for PFAS, sex hormones, and IGF-1. Results from regression models were expressed as the adjusted percentage difference (95% CI) per sex-specific interquartile range (IQR) increment of each PFAS serum concentration. Analyses by PFAS quartiles were also conducted.

    Results

    Median concentrations of PFHxS, PFOA, PFOS, and PFNA were 8, 35, 22, and 1.7 ng/mL in boys and 7, 30, 21, and 1.7 ng/mL in girls. In boys, PFOA concentrations were significantly associated with testosterone levels (-4.9%; 95% CI: -8.7, -0.8%); PFOS with estradiol (-4.0%; 95% CI: -7.7, -0.1%), testosterone (-5.8%; 95% CI: -9.4, -2.0%), and IGF-1 (-5.9%; 95% CI: -8.3, -3.3%); and PFNA with IGF-1 (-3.5%; 95% CI: -6.0, -1.0%). In girls, significant associations were found between PFOS and testosterone (-6.6%; 95% CI: -10.1, -2.8%) and IGF-1 (-5.6%; -8.2, -2.9%); and PFNA and IGF-1 (-3.8%; 95% CI: -6.4, -1.2%). In both sexes, the magnitudes of the associations decreased monotonically across quartiles for both testosterone and IGF-1 in relation to PFOS, and for IGF-1 and PFNA in girls.

    Conclusions

    To our knowledge, this is the first study suggesting that PFAS are associated with lower levels of IGF-1 and sex hormones in young children.

    Citation

    Lopez-Espinosa MJ, Mondal D, Armstrong BG, Eskenazi B, Fletcher T. 2016. Perfluoroalkyl substances, sex hormones, and insulin-like growth factor-1 at 6-9 years of age: a cross-sectional analysis within the C8 Health Project. Environ Health Perspect 124:1269-1275; http://dx.doi.org/10.1289/ehp.1509869.
      Cover page: Perfluoroalkyl Substances, Sex Hormones, and Insulin-like Growth Factor-1 at 6–9 Years of Age: A Cross-Sectional Analysis within the C8 Health Project
      • Article
      • Peer Reviewed
      UC Irvine Previously Published Works (2014)
      Perfluoroalkyl acids (PFAAs) are persistent, synthetic compounds that are used in a number of consumer products. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) have been associated with cardiovascular risk factors, and changes in gene expression and DNA methylation in animals and cellular systems. However, whether PFAA exposure is associated with LINE-1 DNA methylation, a potential marker of cardiovascular risk, in humans remains unknown. We sought to evaluate the cross-sectional associations between serum PFAAs and LINE-1 DNA methylation in a population highly exposed to PFOA. We measured serum PFAAs twice four to five years apart in 685 adult participants (47% male, mean age±SD=42±11years). We measured percent LINE-1 DNA methylation in peripheral blood leukocytes at the second time point (follow-up), and estimated absolute differences in LINE-1 methylation associated with an interquartile (IQR) shift in mean PFAA serum levels. IQR increases in mean serum PFOA, PFOS, perfluorononanoic acid (PFNA), and perfluorohexane sulfonate (PFHxS) were associated with differences of -0.04 (p=0.16), 0.20 (p=0.001), 0.06 (p=0.19), and 0.02 (p=0.57), respectively, in % LINE-1 methylation at follow-up after adjustment for potential confounders. We observed a monotonic increase in LINE-1 DNA methylation across tertiles of PFOS and PFNA (ptrend=0.02 for both associations), but not across tertiles of PFOA or PFHxS (ptrend=0.71 and 0.44, respectively). In summary, serum PFOS was associated with LINE-1 methylation, while serum PFOA, PFHxS, and PFNA were not. Additional research is needed to more precisely determine whether these compounds are epigenetically active.
        • Article
        • Peer Reviewed
        UC Irvine Previously Published Works (2015)

        Context

        Obesity and diabetes are epidemic in the European Union (EU). Exposure to endocrine-disrupting chemicals (EDCs) is increasingly recognized as a contributor, independent of diet and physical activity.

        Objective

        The objective was to estimate obesity, diabetes, and associated costs that can be reasonably attributed to EDC exposures in the EU.

        Design

        An expert panel evaluated evidence for probability of causation using weight-of-evidence characterization adapted from that applied by the Intergovernmental Panel on Climate Change. Exposure-response relationships and reference levels were evaluated for relevant EDCs, and biomarker data were organized from peer-reviewed studies to represent European exposure and burden of disease. Cost estimation as of 2010 utilized published cost estimates for childhood obesity, adult obesity, and adult diabetes. Setting, Patients and Participants, and Intervention: Cost estimation was performed from the societal perspective.

        Results

        The panel identified a 40% to 69% probability of dichlorodiphenyldichloroethylene causing 1555 cases of overweight at age 10 (sensitivity analysis: 1555-5463) in 2010 with associated costs of €24.6 million (sensitivity analysis: €24.6-86.4 million). A 20% to 39% probability was identified for dichlorodiphenyldichloroethylene causing 28 200 cases of adult diabetes (sensitivity analysis: 28 200-56 400) with associated costs of €835 million (sensitivity analysis: €835 million-16.6 billion). The panel also identified a 40% to 69% probability of phthalate exposure causing 53 900 cases of obesity in older women and €15.6 billion in associated costs. Phthalate exposure was also found to have a 40% to 69% probability of causing 20 500 new-onset cases of diabetes in older women with €607 million in associated costs. Prenatal bisphenol A exposure was identified to have a 20% to 69% probability of causing 42 400 cases of childhood obesity, with associated lifetime costs of €1.54 billion.

        Conclusions

        EDC exposures in the EU contribute substantially to obesity and diabetes, with a moderate probability of >€18 billion costs per year. This is a conservative estimate; the results emphasize the need to control EDC exposures.
          Cover page: Obesity, Diabetes, and Associated Costs of Exposure to Endocrine-Disrupting Chemicals in the European Union
          • Article
          • Peer Reviewed
          UC Irvine Previously Published Works (2010)
          Background: The C8 Health Project was established in 2005 to collect data on perfluorooctanoic acid (PFOA, or C8) and human health in Ohio and West Virginia communities contaminated by a fluoropolymer production facility. Objective: We assessed PFOA exposure via contaminated drinking water in a subset of C8 Health Project participants who drank water from private wells. Methods: Participants provided demographic information and residential, occupational, and medical histories. Laboratory analyses were conducted to determine serum-PFOA concentrations. PFOA data were collected from 2001 through 2005 from 62 private drinking water wells. We examined the relationship between drinking water and PFOA levels in serum using robust regression methods. As a comparison with regression models, we used a first-order, single-compartment pharmacokinetic model to estimate the serum: drinking-water concentration ratio at steady state. Results: The median serum PFOA concentration in 108 study participants who used private wells was 75.7 mu g/L, approximately 20 times greater than the levels in the U. S. general population but similar to those of local residents who drank public water. Each 1 mu g/L increase in PFOA levels in drinking water was associated with an increase in serum concentrations of 141.5 mu g/L (95% confidence interval, 134.9-148.1). The serum: drinking-water concentration ratio for the steady-state pharmacokinetic model was 114. Conclusions: PFOA-contaminated drinking water is a significant contributor to PFOA levels in serum in the study population. Regression methods and pharmacokinetic modeling produced similar estimates of the relationship.
          • 1 supplemental PDF
          Cover page: Private Drinking Water Wells as a Source of Exposure to Perfluorooctanoic Acid (PFOA) in Communities Surrounding a Fluoropolymer Production FacilityCreative Commons 'BY' version 4.0 license
          • Article
          • Peer Reviewed
          UC Irvine Previously Published Works (2011)

          The C8 Health Project was established in 2005 to collect data on perfluorooctanoic acid (PFOA, or C8) and human health in Ohio and West Virginia communities contaminated by a fluoropolymer production facility.

          We assessed PFOA exposure via contaminated drinking water in a subset of C8 Health Project participants who drank water from private wells.

          Participants provided demographic information and residential, occupational, and medical histories. Laboratory analyses were conducted to determine serum-PFOA concentrations. PFOA data were collected from 2001 through 2005 from 62 private drinking water wells. We examined the relationship between drinking water and PFOA levels in serum using robust regression methods. As a comparison with regression models, we used a first-order, single-compartment pharmacokinetic model to estimate the serum:drinking-water concentration ratio at steady state.

          The median serum PFOA concentration in 108 study participants who used private wells was 75.7 μg/L, approximately 20 times greater than the levels in the U.S. general population but similar to those of local residents who drank public water. Each 1 μg/L increase in PFOA levels in drinking water was associated with an increase in serum concentrations of 141.5 μg/L (95% confidence interval, 134.9-148.1). The serum:drinking-water concentration ratio for the steady-state pharmacokinetic model was 114.

          PFOA-contaminated drinking water is a significant contributor to PFOA levels in serum in the study population. Regression methods and pharmacokinetic modeling produced similar estimates of the relationship.

            Cover page: Private drinking water wells as a source of exposure to perfluorooctanoic acid (PFOA) in communities surrounding a fluoropolymer production facility.
            • Article
            • Peer Reviewed
            UC Irvine Previously Published Works (2012)

            Perfluorooctanoic acid (PFOA) is a potential cause of adverse pregnancy outcomes, but previous studies have been limited by low exposures and small study size.

            Using birth certificate information, we examined the relation between estimated PFOA exposure and birth outcomes in an area of West Virginia and Ohio whose drinking water was contaminated by a chemical plant.

            Births in the study area from 1990 through 2004 were examined to generate case groups of stillbirth (n = 106), pregnancy-induced hypertension (n = 224), preterm birth (n = 3,613), term low birth weight (n = 918), term small-for-gestational-age (SGA) (n = 353), and a continuous measure of birth weight among a sample of term births (n = 4,534). A 10% sample of term births ≥ 2,500 g were selected as a source of controls (n = 3,616). Historical estimates of serum PFOA were derived from a previously developed fate and transport model. In a second study, we examined 4,547 area births linked to a survey with residential history data.

            In the analysis based only on birth records, we found no consistent evidence of an association between estimated PFOA exposure and stillbirth, pregnancy-induced hypertension, preterm birth, or indices of fetal growth. In the analysis of birth records linked to the survey, PFOA was unrelated to pregnancy-induced hypertension or preterm birth but showed some suggestion of an association with early preterm birth. Measures of growth restriction showed weak and inconsistent associations with PFOA.

            Based on the analysis using the health survey, these results provide little support for an effect of PFOA exposure on most pregnancy outcomes, except for early preterm birth and possibly fetal growth restriction.

              Cover page: Relationship of perfluorooctanoic acid exposure to pregnancy outcome based on birth records in the mid-Ohio Valley.
              • Article
              • Peer Reviewed
              UC Irvine Previously Published Works (2012)
                Cover page: Relationship of Perfluorooctanoic Acid Exposure to Pregnancy Outcome Based on Birth Records in the Mid-Ohio ValleyCreative Commons 'BY' version 4.0 license
                • Article
                • Peer Reviewed
                UC Irvine Previously Published Works (2013)
                Background: The presence of perfluoroalkyl acids (PFAAs) in breast milk has been documented, but their lactational transfer has been rarely studied. Determination of the elimination rates of, these chemicals during breastfeeding is important and critical for assessing exposure in mothers, and infants., O b jectives: We aimed to investigate the association between breastfeeding and maternal serum, concentrations of perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorononanoic, acid (PFNA), and perfluorohexane sulfonate (PFHxS). For a subset of the population, for, whom we also have their infants' measurements, we investigated associations of breastfeeding with, infant serum PFAA concentrations., Methods: The present analysis included 633 women from the C8 Science Panel Study who had, a child < 3.5 years of age and who provided blood samples and reported detailed information on, breastfeeding at the time of survey. PFAA serum concentrations were available for all mothers and, 8% (n=49) of the infants. Maternal and infant serum concentrations were regressed on duration of, breastfeeding. R esults: Each month of breastfeeding was associated with lower maternal serum concentrations, of PFOA (-3%, 95% CI:-5, -2%), PFOS (-3%, 95% CI:-3, -2%), PFNA (-2%, 95% CI, -2, -1%), and PFHxS (-1%, 95% CI:-2, 0%). The infant PFOA and PFOS serum concentrations, were 6% (95% CI: 1, 10%) and 4% (95% CI: 1, 7%) higher per month of breastfeeding., C onclusions: Breast milk is the optimal food for infants, but is also a PFAA excretion route for, lactating mothers and exposure route for nursing infants.
                  Cover page: Breastfeeding: A Potential Excretion Route for Mothers and Implications for Infant Exposure to Perfluoroalkyl AcidsCreative Commons 'BY' version 4.0 license
                  • Article
                  • Peer Reviewed
                  UC Irvine Previously Published Works (2013)
                    Cover page: Perfluorooctanoic Acid Exposure and Cancer Outcomes in a Contaminated Community: A Geographic AnalysisCreative Commons 'BY' version 4.0 license
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