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The effects of 6 weeks of thrice weekly training on glycaemic control were assessed in 20 sedentary Type 2 (non-insulin-dependent) diabetic patients and 11 control subjects matched for previous physical activity. References1.Jarrett RJ, Keen H, Chakrabarti R (1982) Diabetes, hyperglycaemia and arterial disease. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser.
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Objectives: We studied autoimmune diseases in relation to level of exposure to perfluorooctanoic acid (PFOA), which was introduced in the late 1940s and is now ubiquitous in the serum of residents of industrialized countries. Discussion: To our knowledge, this is the first study of associations between this common environmental exposure and autoimmune diseases in humans. This research was funded by the C8 Class Action Settlement Agreement (Circuit Court of Wood County, West Virginia) between DuPont and Plaintiffs, which resulted from releases into drinking water of the chemical perfluorooctanoic acid (PFOA, or C8). In the present study, we focused on a large cohort (n = 32,254) that had been exposed to high levels of PFOA, a perfluorinated compound introduced into the environment in the 1950s. The autoimmune diseases considered here are ulcerative colitis, Crohn’s disease, rheumatoid arthritis, multiple sclerosis, lupus, and type 1 diabetes.
Although it is likely that different autoimmune diseases have separate etiologies, the fact that several genes have been linked to more than one autoimmune disease also suggests that they may have some aspects in common (Delgado-Vega et al. This study is one of a series of studies conducted by the C8 Science Panel, a three-person panel of epidemiologists set up pursuant to a 2004 legal settlement between plaintiffs and DuPont (C8 Science Panel 2013; Frisbee et al.
Most adult C8HP participants (74% of participants ? 20 years of age) consented to participate in a follow-up study. Two rounds of surveys were conducted, the first from August 2008 to April 2010 and the second from May 2010 to May 2011.
To estimate past exposures, we developed historical yearly serum PFOA estimates for community residents based on the estimated intake of PFOA-contaminated drinking water, assuming low background exposure. Estimates of annual serum PFOA levels for workers in different jobs were developed by the C8 Science Panel (Woskie et al.
We estimated associations with cumulative exposure to PFOA, which was calculated by summing estimated yearly serum concentrations during follow-up and modeled as a time-dependent variable in Cox regression. Other analyses were restricted to person-time after the C8HP was established in 2005–2006 (prospective analysis), with participants reporting a history of any of the autoimmune diseases before participation in the C8HP (prevalent cases) being excluded to restrict the analysis to incident cases diagnosed after 2005–2006.
Table 1 – Cohort characteristics based on the most recent survey and measured serum PFOA levels in 2005–2006 [n (%)]. Numbers of validated cases of each autoimmune disease are shown along with mean at diagnosis and sex in Table 2. Of the 342 self-reported cases of type 1 diabetes, 69 were validated as either type 1 diabetes or insulin-dependent diabetes (type 1 diabetes is also known as insulin-dependent diabetes), and we found another 91 validated cases (as either insulin-dependent or type 1) among subjects who reported that they had diabetes but did not know what kind. The known higher incidence of rheumatoid arthritis, lupus, and multiple sclerosis among women compared with men is reflected in our data (Table 2). Sensitivity analyses using either exposures beginning in the “qualifying year” or without background added in, were similar to those shown in Table 3 (data not shown). Only ulcerative colitis (n = 30) and rheumatoid arthritis (n = 56) had ? 25 cases diagnosed after participation in the original C8HP (2005–2006) or 1 July 2006 (for those enrolled in the worker cohort who did not participate in the C8HP). Table 4 – Prospective survival analysis results, follow-up 2005–2006 through 2008–2011, for selected outcomes (? 30 cases) [RR (95%)]. For all six autoimmune diseases considered here, the prevalence in the Mid-Ohio Valley conformed broadly with that expected from the U.S. Cumulative PFOA exposures were associated with ulcerative colitis, but not Crohn’s disease, in our study population. Both ulcerative colitis and Crohn’s disease have a genetic component, but twin studies suggest this component is relatively modest for ulcerative colitis. A growing body of evidence suggests inflammatory bowel disease may be due, in part, to deficiencies in innate immunity and an impaired intestinal epithelial barrier, resulting in damaging inflammatory responses to the microbial environment of the gastrointestinal tract (Baumgart and Carding 2007; Gersemann et al. It is possible that increased gut absorption of PFOA in subjects with ulcerative colitis (including possibly early still undiagnosed ulcerative colitis) could lead to higher measured serum PFOA levels, which could create a false appearance of a causal association, if measured levels were used to predict current (or even subsequent) ulcerative colitis. Other limitations include possible inaccuracies in disease validation and ascertainment, including under-ascertainment of cases that were not self-reported by participants, lack of validation of the absence of disease among those who did not report autoimmune disease outcomes, and the possible exclusion of cases that could not be verified because of a lack of consent or inability to obtain appropriate medical records. Another limitation is that exposures were classified according to estimated historical serum levels based on predicted water concentrations and predicted air concentrations using an environmental fate and transport model, individual residential histories, and maps of public water supply networks, coupled with a one-compartment absorption and excretion model (Shin et al.
DisclaimerPublication of articles in EHP does not mean that the National Institute of Environmental Health Sciences (NIEHS) condones, endorses, approves, or recommends the use of any products, services, materials, methodology, or policies stated therein. A prospective analysis of ulcerative colitis diagnosed after the baseline 2005–2006 survey (n = 29 cases) suggested a positive but non-monotonic trend (ptrend = 0.21).
Steenland, Rollins School of Public Health, Emory University, 1518 Clifton Rd., Atlanta, GA 30322 USA. PFOA (also known as C8) is ubiquitous at low levels (nanograms per milliliter) in the serum of virtually all residents of industrialized countries (Lindstrom et al. In humans it is thought to be stored in the liver, kidney, and serum, and has an elimination half-life of approximately 3.5 years (Olsen et al. For these six diseases we had data on self-reported occurrence, for which we then sought validation through medical records review. Surveys were completed over the phone (63%) or online (37%), and most participants completed both rounds of surveys. The estimates of drinking-water PFOA concentrations were based on the amount of PFOA released from the DuPont plant, wind patterns, river flow, groundwater flow, and the residential address history provided by each participant (Shin et al.
In addition to the community cohort, we studied a cohort of 4,391 past and current workers at the DuPont plant using the same survey completed by the community cohort participants, including a residential history.
2012) and combined with estimated annual serum levels from residential exposure to contaminated drinking water that were derived as described above for the community cohort. Community residents and workers were combined to form a final population of 32,254 persons for whom we could study the relationship between past PFOA serum levels and subsequent disease.
Participants were asked whether a doctor or other health professional had ever told them they had an autoimmune disease, with specific categories listed for lupus, multiple sclerosis, myasthenia gravis, Sjogren’s syndrome, vasculitis, Addison’s disease, or other. Associations between PFOA exposure and each outcome were conducted using separate survival analyses (Cox regression) with age as the time variable. Person-time for participants in the C8HP started on the date of their C8HP blood draw and interview, which varied from July 2005 to July 2006. The median year of birth of the cohort was 1957, 54% were female, 20% were current smokers, 27% were current drinkers, 18% had a college education or more, and 36% were obese (BMI > 30) (BMI, smoking, and drinking assessed at time of last interview).
Validated cases (based on medical record review) included 346 participants who reported rheumatoid arthritis for which they were taking medication (25% of the 1,292 who reported taking medication), 72 participants with lupus (39% of 187 self-reported cases), and 98 with multiple sclerosis (65% of 150 self-reported cases).
Of the 160 validated cases, 85 were validated specifically for type 1 diabetes, while the remaining cases were validated as “insulin-dependent.” We conducted analyses for both the group of 160 validated cases and also for the subgroup of 85 cases specifically validated as type 1 diabetes. Ulcerative colitis showed a significant positive association with cumulative PFOA exposure, with monotonically increasing rate ratios for both the unlagged and lagged exposures and significant trends based on models of log-transformed cumulative exposure. All RRs for ulcerative colitis were elevated after the first quartile, but without a monotonic trend, based on this prospective analysis (ptrend = 0.21, unlagged analysis) (Table 4). Ulcerative colitis and Crohn’s disease are clinically distinct conditions, with distinguishing clinical, anatomical, and histological findings. The concordance of ulcerative colitis in monozygotic twins is 10%, and 3% in dizygotic twins, compared with 37% and 7%, respectively, for Crohn’s disease (Baumgart and Carding 2007).
However, in our data we estimated associations with cumulative PFOA exposure predicted by a model that did not incorporate measured PFOA concentrations, hence “reverse causality” (by which disease might increase measured serum levels rather than serum levels preceding disease) is not relevant here. Our cohort was largely a survivor cohort, with community members having to have been alive in 2005–2006 at the time of a baseline survey. We also lacked data on other potential environmental toxicants in the serum of Mid-Ohio Valley residents that could have confounded associations with PFOA, and given the limited information on the causes of autoimmune diseases, we cannot rule out possible confounding by other unmeasured exposures or characteristics. We studied a well-defined cohort with documented high exposure to a chemical that has been reported to suppress the immune system in animals.


The ideal candidate will have a scientific background in a field relevant to EHP’s scope of coverage and experience in translating highly complex scientific information for a general audience, social media, and art direction or graphic design. Conclusions and opinions are those of the individual authors and advertisers only and do not reflect the policies or views of the NIEHS. Edward Arnold, London, pp 179–2032.Kannel WB, McGee DL (1979) Diabetes and cardiovascular disease — the Framingham Study.
Disease history was assessed retrospectively from 1952 or birth (if later than 1952) until interview. The settlement mandated a baseline survey of 69,000 persons who lived or who had lived in six water districts where water had been contaminated with PFOA (called the C8 Health Project, or C8HP). We studied a Mid-Ohio Valley community-based population that comprised persons who lived or worked in any of six PFOA-contaminated water districts and participated in the C8HP baseline survey in 2005–2006 (Frisbee et al. Both surveys included the same questions regarding demographic information and medical history, including questions about whether the participants had ever been told by a doctor that they had specific chronic diseases. This group was a subset of a cohort of 6,027 workers employed at the DuPont chemical plant between 1948 and 2002 who were previously studied for mortality (Leonard et al. We estimated combined residential and occupational exposure for 3,713 workers who completed a follow-up survey (84%), including 1,890 (51%) who also had participated in the 2005–2006 C8HP. Our model-based exposure predictions were well correlated with serum PFOA measurements obtained in 2005–2006 for community cohort members (r = 0.67) (Shin et al.
Participants who reported that they had been told they had one of the specific chronic diseases of interest were then asked the age at first diagnosis and for consent to review medical records as well as for consent to contact the relevant health care provider. Follow-up began in 1952 (the approximate date of first emissions of PFOA from the DuPont plant), or date of birth, whichever came later. We conducted analyses by quartile of cumulative exposure, with cut points for each outcome determined from the cumulative exposure of the cases of that outcome at time of diagnosis, and separate cut points derived for lagged and unlagged exposures. This eliminated prior nonexposed person-time before cohort eligibility, and resulted in a loss of about 10–15% of cases, depending on the outcome being evaluated. For members of the worker cohort who did not participate in the C8HP (n = 1,823), person-time at risk began on 1 July 2006. There were 151 validated cases of ulcerative colitis (25% of self-reported cases), and 96 validated cases of Crohn’s disease (53% of self-reported cases) (10 cases were validated for both ulcerative colitis and Crohn’s disease). The mean age for type 1 diabetes (combining insulin-dependent and specifically type 1) is younger than the mean age at onset for the other diseases, reflecting the fact that some of these cases occur among juveniles, although in recent years the majority of type 1 diabetes now occurs among adults. No such trend was evident for Crohn’s disease or for any of the other autoimmune diseases examined.
Crohn’s disease can occur in any part of the gastrointestinal tract, although most cases start in the end of the small bowel. In contrast, current smoking is negatively associated with ulcerative colitis, though former smoking is a risk factor. Experimental findings also suggest PPAR-? activation may lead to reprogramming of tissue macrophages towards an M2 antiinflammatory phenotype, which may contribute to decreased vaccine efficacy or immunosuppression in diseases dependent on cytotoxic T-cell responses (DeWitt et al. If community residents with autoimmune disease were less likely to have survived until 2005–2006, they would have been less likely than other residents to have enrolled in the study, possibly biasing our results.
Model-estimated levels were correlated with measured levels in 2005–2006 (rS = 0.67), based on 45,000 participants.
Disease outcomes were confirmed through medical records review, with relatively large numbers for many autoimmune diseases.
Recent insights in the epidemiology of autoimmune diseases: improved prevalence estimates and understanding of clustering of diseases. Immunotoxicity of perfluorooctanoic acid and perfluorooctane sulfonate and the role of peroxisome proliferator-activated receptor alpha. Perfluorinated compounds—exposure assessment for the general population in Western countries. Recent trends in the prevalence of Crohn’s Disease and ulcerative colitis in a commercially insured US population. Retrospective cohort mortality study of workers in a polymer production plant including a reference population of regional workers.
Epidemiology of environmental exposures and human autoimmune diseases: findings from a National Institute of Environmental Health Sciences Expert Panel Workshop.
Half-life of serum elimination of perfluorooctanesulfonate, perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. High-dose, short-term exposure of mice to perfluorooctanesulfonate (PFOS) or perfluorooctanoate (PFOA) affects the number of circulating neutrophils differently, but enhances the inflammatory responses of macrophages to lipopolysaccharide (LPS) in a similar fashion.
From symptom to diagnosis: clinical distinctions among various forms of intestinal inflammation.
Environmental fate and transport modeling for perfluorooctanoic acid emitted from the Washington Works Facility in West Virginia. Retrospective exposure estimation and predicted versus observed serum perfluorooctanoic acid concentrations for participants in the C8 Health Project. Differential activation of nuclear receptors by perfluorinated fatty acid analogs and natural fatty acids: a comparison of human, mouse, and rat peroxisome proliferator-activated receptor-?, -?, and -?, liver X receptor-?, and retinoid X receptor-?. Design, methods and population for a study of PFOA health effects among highly exposed Mid-Ohio Valley community residents and workers. Survival and cause-specific mortality in ulcerative colitis: follow-up of a population-based cohort in Copenhagen County. Retrospective exposure assessment of perfluorooctanoic acid serum concentrations at a fluoropolymer manufacturing plant. Oral and intravenous glucose tolerance determined 72 h after the last exercise period showed only minimal improvement. Although information on population trends in autoimmune disease rates is limited, concerns have been raised that autoimmune disease incidence rates may be increasing as a result of increasing exposures to xenobiotics (Miller et al. Human exposure to PFOA occurs via many sources, including food, drinking water (Shin et al. PFOA is a rodent carcinogen and causes fetal loss in mice at dietary levels of approximately 20 ppm (Lau et al. For most other autoimmune diseases we did not have self-reported data, or the numbers of cases were too small to analyze. The settlement also created the C8 Science Panel, which was charged with determining whether it is more probable than not that PFOA is linked to (associated with) any human disease. For participants who died after the completion of the C8HP survey in 2005–2006 or who were not capable of completing a follow-up survey, we surveyed their next-of-kin (4% of the cohort had next-of-kin interview).
Each estimated yearly serum concentration took into account new exposure during the year and the estimated amount of PFOA remaining in the body after partial excretion during the prior year. Approximately 60% of the cohort reported having had a disease of interest; 79% percent of these consented for us to review their medical history.
In a separate question, participants were asked whether a doctor or health professional had ever told them they had had inflammatory bowel disease, excluding irritable bowel syndrome.
Rate ratios (RR; the ratio of disease rates) were estimated for the second, third, and fourth quartiles relative to the first quartile, which was the referent group. The proportional hazard assumption of a constant hazard ratio for cumulative exposure over time was verified based on the nonsignificance of an interaction term between time (age) and cumulative exposure.
Second, we estimated associations with cumulative exposures above background levels only, so that exposure began at year of first exposure to contaminated water or work in the DuPont plant (above background analysis). For all but two of the autoimmune diseases—rheumatoid arthritis and ulcerative colitis—there were insufficient cases to conduct a prospective analysis.
The median length of follow up was 53 years (birth to end of follow-up); the median length of follow-up after the earliest year living or working in a contaminated water district was 29 years. Crude prevalences for validated cases per 100,000 adults (? 20 years of age) in our cohort in 2008–2001 were 410, 300, 1,080, 500, 230, and 310 for ulcerative colitis, Crohn’s disease, rheumatoid arthritis, type 1 diabetes (including insulin-dependent), lupus, and multiple sclerosis, respectively.
Animal models and human studies suggest that PFOA toxicity includes systemic suppression of adaptive immunity and antibody production (DeWitt et al.


However, two factors argue against this as an explanation for our positive findings for ulcerative colitis. Nonetheless, our finding of a positive association between cumulative serum PFOA concentration and incident ulcerative colitis, and a lack of associations with other autoimmune diseases, are based only on one study and need replication.
Plasma glucose levels were, however, significantly lower at 12 h than 72 h after exercise in eight subjects tested at both time points. Cumulative exposure to PFOA was derived from estimates of annual mean serum PFOA levels during follow-up, which were based on plant emissions, residential and work history, and a fate-transport model. The most common autoimmune diseases include inflammatory bowel disease (consisting of ulcerative colitis and Crohn’s disease), rheumatoid arthritis, celiac disease, multiple sclerosis, systemic sclerosis, systemic lupus, type 1 diabetes, and two types of thyroid disease (Grave’s disease and Hashimoto’s thyroiditis) (Cooper et al. Self-reported cases of Graves’ disease and Hashimoto’s thyroiditis are not included in this analysis because they were difficult to distinguish from other (non-autoimmune) forms of hyperthyroidism and hypothyroidism. The C8 Science Panel conducted 11 studies over the course of 5 years to make this determination. The principal route of exposure for this population was via PFOA-contaminated drinking water. The Emory University Institutional Review Board reviewed and approved all aspects of this study, including consent forms and surveys. The final community cohort comprised 28,541 community residents who had estimated historical PFOA serum concentrations and had never worked at the DuPont plant.
Professional medical abstractors obtained records documenting the disease in question from medical providers by mail or by in-person office visit. They were then asked to specify whether the inflammatory bowel disease was ulcerative colitis or Crohn’s disease.
Tests for trend were based on the p-value of the coefficient of the natural log of cumulative exposure modeled as a continuous time-dependent variable in a Cox regression model that included the same covariates as the corresponding model of cumulative PFOA exposure as a categorical variable.
Data from the United States and Western Europe based on both hospital and non-hospital data suggest comparable patterns but lower prevalences for adults and children combined, with ranges of 140–300, 100–200, 310–830, 340–570, 30–150, and 50–360, respectively, for these same diseases (Cooper et al. Ulcerative colitis affects the mucosa (epithelial lining of the gut), whereas Crohn’s disease affects the whole bowel wall.
Positive risk factors include prior gastrointestinal infections and oral contraceptive use, while protective factors include appendectomy and breastfeeding. First, life expectancy for those with ulcerative colitis is about the same as the general population (Davoli et al.
These data suggest that an exercise programme can produce a significant decrease in glycosylated haemoglobin levels in Type 2 diabetic males probably due, in great measure, to the cumulative effect of transient improvements in glucose tolerance which follow each individual period of exercise.
Cox regression models were used to estimate associations between quartiles of cumulative PFOA serum levels and the incidence of autoimmune diseases with ? 50 validated cases, including ulcerative colitis (n = 151), Crohn’s disease (n = 96), rheumatoid arthritis (n = 346), insulin-dependent diabetes (presumed to be type 1) (n = 160), lupus (n = 75), and multiple sclerosis (n = 98). Rodent studies have reported evidence of immunosuppressant effects including lymphoid organ atrophy and decreased de novo antibody production in certain strains of mice (DeWitt et al. C8HP participants (n = 69,030) had their PFOA serum levels measured and provided a medical history.
Overall, we were able to find a medical record relevant to the reported disease for 92% of those consenting to medical record review (Winquist et al. In another question, participants were asked whether a doctor had ever told them they had arthritis, and if yes, whether it was rheumatoid or osteoarthritis.
For each outcome, follow-up ended at time of last interview, at time of disease occurrence, or at time of death, whichever occurred earliest. However, there is no definitive diagnostic method to distinguish between them in about 10% of cases (Hanauer 2006; Sands 2004).
Until recently, PFOA has been used in manufacturing a wide variety of consumer products, such as Gore-tex™, Teflon®, and Scotchgard™ (Shin et al. Approximately 80% of the current residents who had participated in the 2005–2006 survey in the six districts participated in the C8HP (Frisbee et al. Finally, participants were asked if they had ever had diabetes, with specific categories of type 1 or type 2 (excluding pregnancy-induced diabetes). On the other hand, a recent study based on medical claims data (n = 12 million) reported prevalences of 263 and 241 per 100,000 U.S. However, with regard to oral contraceptives and breastfeeding, we analyzed our data separately for men and women, and found little difference between these analyses (data not shown). One TH2-type cytokine [interleukin (IL)-13] is thought to play a unique and critical role in ulcerative colitis in gut mucosal inflammatory response (Mannon and Reinisch 2012); however, PFOA-related effects on IL-13 expression have not been described. For three diseases—multiple sclerosis, rheumatoid arthritis, and lupus—we were also able to use supplemental data from the C8HP (2005–2006), which conducted its own medical record validation, to confirm some cases that had been self-reported to us but for whom were unable to obtain a medical record.
Participants who self-reported an outcome that was not validated were excluded from the analysis for that outcome.
Many PFOA-related immune effects may be mediated through activation of peroxisome proliferator–activated receptors (PPAR)-?, PPAR-?, or other receptors expressed in the colon, but non–receptor-mediated changes may also occur (DeWitt et al. Ultimately, the context of the microbial environment may be especially relevant in explaining PFOA-related effects on ulcerative colitis.
To our knowledge, there are no prior studies of associations between PFOA and autoimmune disease in humans.
The cohort studied here was exposed primarily via drinking water contaminated with PFOA that originated from emissions from a nearby chemical plant that used PFOA in the manufacture of Teflon®. To date, information about PFOA in relation to immune function in humans is limited to a few cross-sectional studies of relatively insensitive immune markers (reviewed by Steenland et al. Data are largely lacking for other autoimmune diseases (Baumgart and Carding 2007; Bogdanos et al. These data also indicate that the prevalences of both types of adult inflammatory bowel disease have been slightly increasing over the 6-year period studied (2004–2009).
Although PFOA-related activation of human PPAR-? has not been established (Takacs and Abbott 2007; Vanden Heuvel et al.
2006), activation of PPAR-? through endogenous and exogenous ligands appears to have antiinflammatory effects in colitis models and is being explored for therapeutic potential (Dubuquoy et al.
2012) Together, these findings suggest that the association between PFOA and ulcerative colitis in the present study (in contrast with a lack of clear associations with Crohn’s or any of the other autoimmune diseases examined), might be explained by effects of PFOA on responses to bacterial exposures and other unique aspects of lower gastrointestinal toxicity that may not be reflected by systemic or other organ-specific immune effects. Genetic studies, including recent genomewide association studies (GWAS), have identified a number of genes that may contribute to autoimmune diseases, particularly genes of the major histocompatibility complex (MHC) that have associated with rheumatoid arthritis, systemic sclerosis, and lupus (Delgado-Vega et al. However, a recent study of children in the Faroe Islands reported a significant decrease in childhood antibody levels to diphtheria and tetanus at 7 years of age in association with elevated serum levels of PFOA and another fluorocarbon, perfluoroctane sulfonic acid (PFOS) (Grandjean et al. These findings seem to contradict our finding of a positive association between PFOA and ulcerative colitis.
To our knowledge, there are no published data on autoimmune disease in relation to PFOA in animals or humans. However, specific gastrointestinal and local immune effects of PFOA are not described in the literature. McGraw-Hill, New York p 84413.National Diabetes Data Group (1979) Classification and dignosis of diabetes mellitis and other categories of glucose tolerance. Academic Press, New York, pp 1205–121417.Wide L (1969) Radioimmunoassays employing immunosorbents.
In: Waldhausl WK (ed) Proceedings of the 10th Congress of International Diabetes Federation Vienna, Austria. Acta Med Scand 205–227–23026.Hilsted J, Galbo H, Christensen NJ (1979) Impaired cardiovascular responses to graded exercise in diabetic autonomic neuropahy.



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