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05.09.2014
T? game o i du?ng ph? cho mobile, Hinh ?nh ? game o i du?ng ph? tai game o i du?ng ph? thu? game thi d? o thu? d? khang, game o du?ng ph? a ?. Please use your secure login account to the Patient Portal to send messages or questions to your physician or to request RX refills, appointments, referrals or anything else related to your care. Background: Diabetes is a major threat to public health in the United States and worldwide. Objective: We assessed the epidemiologic literature for evidence of associations between persistent organic pollutants (POPs) and type 2 diabetes.
Methods: Using a PubMed search and reference lists from relevant studies or review articles, we identified 72 epidemiological studies that investigated associations of persistent organic pollutants (POPs) with diabetes.
Conclusions: Heterogeneity of the studies precluded conducting a meta-analysis, but the overall evidence is sufficient for a positive association of some organochlorine POPs with type 2 diabetes.
Key words: chemically induced, diabetes, environment, epidemiology, glucose, hormone, insulin, metabolic syndrome, obesity, persistent organic pollutants, pollution, toxicology.
The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the agencies that sponsored the workshop.
Diabetes is a major threat to public health in the United States and worldwide [Centers for Disease Control and Prevention (CDC) 2011; Danaei et al. Approximately 11% of prediabetic patients who participated in the Diabetes Prevention Program, a large multicenter randomized clinical trial developed by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), developed T2D each year during the average 3 years of follow-up (American Diabetes Association 2011; Knowler et al.
Over the past several years, research addressing the role of environmental chemicals in T2D has rapidly expanded. For the present review we evaluated the literature in terms of consistency, strengths and weaknesses (including power and statistical methods) of the clinical diagnosis, exposure assessment, and study population characteristics in order to identify data gaps and areas for future evaluation and research in the area of POPs exposure and diabetes outcomes.
We identified an additional 17 articles by reviewing the reference lists in the primary literature and review articles, for a total of 43 studies.
Figure 1 – Associations between trans-nonachlor and diabetes in epidemiological studies.
We included a study for consideration if it identified T2D as the outcome and the exposure measure was deemed adequate. Figure 2 – Association between DDE, DDT, or DDD and diabetes in epidemiological studies. Figure 4 – Association between Agent Orange or dioxin and diabetes in studies of Vietnam veterans. Among specific organochlorine chemicals that were evaluated in < 6 studies, including dieldrin, hexachlorobenzene (HCB), ?-hexachlorocyclohexane (?-HCH), lindane (?-HCH), heptachlor epoxide, mirex, and oxychlordane, we found positive patterns of associations (Figure 5). The purpose of this evaluation was not only to assess the epidemiological literature for evidence of associations between POPS and T2D but also to collaboratively identify data gaps and areas for future research in the area of POPs exposure and outcomes related to diabetes.
Figure 5 – Association between miscellaneous organochlorine POPs and diabetes in epidemiological studies. Figure 6 – Association between POPs mixtures and diabetes in epidemiological studies. It is less clear whether studies should use lipid-standardized blood measurement for lipophilic chemicals; several different approaches are currently used in models, including a) wet concentrations without consideration of lipid profiles, b) lipid-standardized concentrations, or c) wet concentrations with lipid adjustment. Adjusting for obesity is controversial in studying the association between POPs and diabetes.
In this sense, the dose–response curves presented in these studies share the low-dose portion of a wide inverted U-shaped association. Figure 7 – Association between brominated compounds and diabetes in epidemiological studies.
Figure 8 – Association between perfluoro­alkyl acids and diabetes in epidemiological studies. Identification of individual chemicals or chemical mixtures that are associated with T2D in epidemiology studies will help direct further toxicity testing. Although our evaluation focused on the epidemiological data, findings from in vitro and animal studies show that TCDD, PCBs, and other chlorinated POPs can cause pancreatic effects (Ebner et al. However, the laboratory animal data on organochlorine-induced changes in glucose and insulin levels are not necessarily consistent with associations between POPs and an increased incidence of T2D reported by epidemiologic studies (Everett et al. Identify biological pathways for diabetes and related disease states, and screen existing POPs for activity in these pathways in high throughput assay systems. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. We evaluated these studies for consistency, strengths and weaknesses of study design (including power and statistical methods), clinical diagnosis, exposure assessment, study population characteristics, and identification of data gaps and areas for future research. The February 2011 Diabetes Strategic Plan (NIDDK 2011) acknowledged the growing science base in this area and cited the need to understand more about the role of environmental exposures as part of future research and prevention strategies. We categorized studies into groups on the basis of study design and nature of the exposure: a) cohort studies with a prospective or nested case–control design, b) cross-sectional studies, c) case–control studies, d) occupational studies, e) ecological studies, f ) studies of maternal exposure, and g) studies of Vietnam veterans.
The POPs literature on diabetes is quite complex, consisting of 72 epidemiological studies that often reported findings for multiple compounds in the same study. We took into account patterns of findings for chemicals or chemical classes if at least three different studies reported diabetes-related outcomes for that chemical or chemical class. However, in many cases the estimates of association reported by individual studies were not statistically significant (Chen et al.
Workshop participants concluded that there was not sufficient evidence for an association between T2D and PBBs or PBDEs (Lee et al.
The resulting list of data gaps includes topics that are related to but not specifically discussed here. The conclusion from our evaluation, that there is an association between POPs and diabetes in Vietnam veterans, differs somewhat from assessments conducted by the Institute of Medicine (IOM) Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (IOM 1994, 2001, 2011). Because POPs circulate with serum lipids, high blood lipids increase measured levels of POPs. There is growing evidence that obesity is on the causal pathway between POPs and diabetes (Lee et al.
Several of the reviewed studies reported evidence of nonmonotonic exposure–response relationships. Varying background exposure distributions may contribute to different forms of the concentration–response curves seen between studies, depending on the relative importance of different POPs in the background mixture.
The workshop participants discussed the possibility of conducting a meta-analysis of existing studies, or a pooled analysis of individual-level data from prospective studies, in particular the five prospective studies of PCB153 and DDE (Lee et al.
Although several organochlorine compounds showed positive associations with T2D, we cannot determine whether these associations are causal in nature based on observational epidemiologic studies alone; additional animal and in vitro mechanistic studies are needed to clarify the role of POPs in metabolic disease development. The combined use of toxicity testing and screening of chemical classes using assays relevant to diabetes will also help epidemiologists determine which chemicals to measure in future studies. On the basis of our review of human epidemiological studies, we conclude that there is support for positive associations between diabetes and certain chlorinated POPs. The economic impact of the disease is enormous, not only in terms of direct medical costs but also on lost productivity.


Initial data mining revealed that the strongest positive correlation of diabetes with POPs occurred with organochlorine compounds, such as trans-nonachlor, dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCBs), and dioxins and dioxin-like chemicals.
Recently, T2D is being diagnosed in individuals earlier in life, including adolescents (NIDDK 2011). To help develop such a research strategy, the National Toxicology Program (NTP) at the National Institute of Environmental Health Sciences (NIEHS) organized a state-of-the-science workshop in January 2011 titled “Role of Environmental Chemicals in the Development of Diabetes and Obesity” (NTP 2011). Aspects of study quality included potential selection bias, possibility of association resulting from reverse causation, or loss to follow-up. To visually assess patterns of primary study findings from this literature, we used a newly developed software program, the Meta Data Viewer (Boyles et al.
We did not consider epidemiological evidence sufficient to determine whether any of the positive associations were causal in nature. For example, we found only one epidemiological study on POPs and T1D, a very important health outcome (Rignell-Hydbom et al. The evidence for an association between exposure to herbicides used during the Vietnam War and long-term health effects in veterans, including diabetes, is assessed every other year by this committee as part of the Agent Orange Act of 1991. Therefore, the failure to account for this relationship may result in the overestimation of relative risks. For example, in the CARDIA (Coronary Artery Risk Development in Young Adults) cohort, estimated associations with diabetes were strongest for the second quartile of exposure to trans-nonachlor, oxychlordane, mirex, highly chlorinated PCBs, and PBB153 (Lee et al.
The inverted U-shaped association has been suspected to be biologically linked to the endocrine-disrupting properties of POPs because an increase from no to low occupancy of hormone receptors has been observed to have linear effects on hormone-mediated phenomena, but that effect sometimes decelerated or even stopped when the dose increased (Vandenberg et al. The structures of chemicals that are associated with diabetes are highly variable, and it is difficult to link them to a common etiologic mechanism.
Therefore, understanding the impact of environmental factors such as chemical exposures is a high-priority research goal (NIDDK 2011). Polychlorinated biphenyl-77 induces adipocyte differentiation and proinflammatory adipokines and promotes obesity and atherosclerosis. Polychlorinated biphenyls affect the activities of gluconeogenic and lipogenic enzymes in rat liver: is there an interference with regulatory hormone actions?
Diabetes in relation to serum levels of polychlorinated biphenyls and chlorinated pesticides in adult Native Americans.
Air pollution and incidence of hypertension and diabetes in black women living in Los Angeles. Plasma organochlorine concentrations and bone ultrasound measurements: a cross-sectional study in peri-and postmenopausal Inuit women from Greenland. Prevalence of self-reported diabetes and exposure to organochlorine pesticides among Mexican Americans: Hispanic Health and Nutrition Examination Survey, 1982–1984.
Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with hyperinsulinemia and insulin resistance. Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on serum insulin and glucose levels in the rabbit.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) alters pancreatic membrane tyrosine phosphorylation following acute treatment.
Biochemical and toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in immature male and female chickens.
2,3,7,8-Tetrachlorodibenzo-p-dioxin causes reduction of glucose transporting activities in the plasma membranes of adipose tissue and pancreas from the guinea pig. TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) causes reduction in glucose uptake through glucose transporters on the plasma membrane of the guinea pig adipocyte. Association of a polychlorinated dibenzo-p-dioxin, a polychlorinated biphenyl, and DDT with diabetes in the 1999–2002 National Health and Nutrition Examination Survey. Biomarkers of pesticide exposure and diabetes in the 1999–2004 National Health and Nutrition Examination Survey. Potential involvement of calcium, CaM kinase II, and MAP kinases in PCB-stimulated insulin release from RINm5F cells. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) reverses hyperglycemia in a type II diabetes mellitus rat model by a mechanism unrelated to PPAR?. Dioxin-like and non-dioxin-like toxic effects of polychlorinated biphenyls (PCBS): implications for risk assessment. Some endocrine and morphological aspects of the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Dose-response and time course of hypothyroxinemia and hypoinsulinemia and characterization of insulin hypersensitivity in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats. Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on adipogenic differentiation and insulin-induced glucose uptake in 3T3-L1 cells.
Chronic consumption of farmed salmon containing persistent organic pollutants causes insulin resistance and obesity in mice. A cross-sectional study of the association between persistent organic pollutants and glucose intolerance among Greenland Inuit.
There is less indication of an association between other nonorganochlorine POPs, such as perfluoroalkyl acids and brominated compounds, and type 2 diabetes. Given the number of people impacted by the disease, an estimated 346 million people worldwide (WHO 2011), and the long-term consequences of diabetes in terms of morbidity, mortality, and economic costs, there is considerable interest in understanding the contribution of “nontraditional” risk factors, such as environmental chemicals, to the diabetes epidemic.
The objective of this workshop was to examine the literature for evidence of associations between certain chemicals and obesity or diabetes.
We conducted an initial search on 24 August 2009 and subsequently updated the search through 15 December 2010. In assessing the PCB studies, we evaluated both total PCBs and PCB153 together because PCB153 is a major contributor to total PCB exposure and is used as an indicator PCB. These aspects were not summarized for each study but were considered during the discussion.
However, the exposure to certain chlorinated POPs can lead to increased levels of serum lipids, and dyslipidemia is involved in the pathogenesis of T2D, suggesting that dyslipidemia may be an intermediate factor in the relationship between POPs and T2D. Combining results from relevant mechanistic and animal studies with findings from epidemiologic studies would enhance our ability to establish a possible causal linkage between POPs and diabetes. Further research to identify all relevant pathways to diabetes will aid in deciphering structure–activity relationships. Exposure to environmental chemicals may be an additional risk factor that, if prevented, could facilitate a reduction in disease incidence and in the overall associated health and economic burden.
Birnbaum,4 Chad Blystone,5 Michael DeVito,5 David Jacobs,6 Josef Kohrle,7 Duk-Hee Lee,8 Lars Rylander,9 Anna Rignell-Hydbom,9 Rogelio Tornero-Velez,10 Mary E. Experimental data are needed to confirm the causality of these POPs, which will shed new light on the pathogenesis of diabetes. Another 35% of people ? 20 years of age are believed to be prediabetic, a condition in which fasting blood glucose, blood glucose following a 2-hr oral glucose tolerance test (OGTT), or plasma HbA1c levels are above normal but not sufficiently elevated to be classified as diabetes (CDC 2011).
Environmental exposures that have been linked to diabetes in at least some study populations include persistent organic pollutants (POPs), arsenic, bisphenol A, phthlatates, organotins, nonpersistent pesticides (Thayer et al.


Epidemiological studies of associations between diabetes and POPs, particularly the halogenated POPs, were considered at the workshop, along with studies of diabetes in association with arsenic, maternal smoking during pregnancy, bisphenol A, phthalates, organotins, and nonpersistent pesticides (Thayer et al. PCB153 is often used as a surrogate measure for total PCBs because it is less expensive to measure (Cote et al. In brief, the Meta Data Viewer is a graphing program that can display up to 15 text columns and graph 1–10 numerical values.
The full list of data gaps and research needs recommended by workshop participants based on the literature review are summarized in Appendix 1.
However, a committee convened by the IOM in 1999 to conduct a specific review of the scientific evidence regarding T2D and Agent Orange in Vietnam veterans concluded that there was limited or suggestive evidence of an association between T2D and exposure to Agent Orange used in Vietnam (IOM 2001). In addition, this relationship is potentially confounded by the consumption of fatty food, which is associated with obesity and with increased POPs levels. Thus, improving understanding of the biological basis for potential nonlinear relationships was considered by the workshop participants to be an important research need (Appendix 1). This new information should be considered by governmental bodies involved in the regulation of environmental contaminants. The prediabetic condition often portends the subsequent development of T2D and is a risk factor for micro- and macrovascular diseases (Tabak et al. We excluded studies from consideration if they were occupational studies, used death certificates to identify T2D, or did not present original data. The input data file is an Excel document, and users can sort, group, and filter data to look at patterns of findings across studies.
This conclusion was maintained in The Veterans and Agent Orange updates in 2001, 2002, 2004, 2006, 2008, and 2010 (IOM 2011). Even though true associations may be somewhere between unadjusted and adjusted results, there is uncertainty about the most appropriate way to deal with lipids. However, adipose tissue serves as a reservoir of POPs, thereby reducing the circulating POPs level (Lim et al. Because of time constraints, we formally assessed only studies with T2D as the outcome, excluding studies with metabolic syndrome as the outcome. Results from studies examining an association between T2D and PBDE153 and PBDE47, which were published after the workshop, are consistent with this initial assessment [Airaksinen et al. In contrast, our conclusion from the present evaluation is that there is evidence for a positive association when the data were considered collectively (Figure 4).
However, the participants concluded that there was too much variation across studies to permit a meta-analysis or pooled analysis. In contrast, in different animal models, TCDD has been shown to cause hypoglycemia (Fried et al. Our search identified 2,752 publications (after removal of duplicates), 72 of which presented original data on diabetes-related studies (see Supplemental Material, Figure S1). Even the categorization of “dioxin-like” or “nondioxin-like” is not sufficient because both categories of PCBs are linked to diabetes (Giesy and Kannan 1998; Lee et al. This effect might have a positive role in limiting the exposure to target tissues for diabetes, such as pancreatic ?-cells. For example, the five studies of PCB153 and DDE mentioned above used different diagnostic strategies and approaches to address confounding, particularly by serum lipid levels (Lee et al. We excluded 28 studies from consideration because the health outcome was not T2D or because the method used to measure exposure or classify T2D was not adequate (see Supplemental Table S1). Meta Data Viewer is a public resource; the program and any associated NTP data files are available for research and publication. Workshop participants also concluded that evidence for an association between T2D and perfluoroalkyl acids, such as PFOS and PFOA, was not sufficient (Costa et al.
1995), or to cause both hyperglycemia and hypoglycemia at different time points during or after dosing (Ebner et al.
Studies on Vietnam veterans were excluded if they were not specific enough to imply exposure to Agent Orange or TCDD; for example, studies comparing veterans who were in Vietnam with those who were not in Vietnam were excluded because they did not specify exposed versus unexposed veterans. We did not consider occupational studies because exposure may be more targeted depending on the occupation, nor did we consider a study by Anderson-Mahoney et al. 2009a) revealed that the risk of diabetes was substantially increased with only small increases within the lower ranges of POPs concentrations, but only slightly increased with higher increases in concentrations of POPs.
Although epidemiology studies tend to show a positive relationship between TCDD body burdens and insulin levels (Cranmer et al. In addition, we chose to limit the introduction of potential biases that are unique to these studies, such as the healthy worker effect.
In a similar manner, an overall pattern of a positive association was apparent in studies of mixtures of organochlorine POPs (Jorgensen et al. We also excluded studies that used death certificates to identify diabetes cases because the prevalence of diabetes is underestimated from mortality data. 1999), TCDD typically causes hypoinsulinemia and increased insulin sensitivity in animals (Ebner et al. For example, in a U.S-based study that characterized the sensitivity and specificity of death certificates for diabetes (Cheng et al. 2008), diabetes was listed as a direct or contributing cause of death on only 6.2% of the death certificates for adults who were known to have diabetes. In addition, temporal and geographic variation among the cohorts resulted in substantial differences in the chemical mixtures to which the populations were exposed as well as the duration and relative concentrations of exposures.
Thus, in animal models, exposure to TCDD mimics the feature of reduced insulin secretion observed in the clinical progression of prediabetes to overt diabetes.
Inhibition of glucose uptake may at least partially explain why hypoinsulinemia is frequently observed in animal studies. In most tissues studied, TCDD inhibits glucose uptake by decreasing the activity or protein level of glucose transporter (GLUT) proteins responsible for transporting blood glucose to adipose, muscular, pancreatic, hepatic, and intestinal epithelial tissue (El-Sabeawy et al. Decreased glucose uptake into the pancreas could mean that pancreatic ?-cells do not sense higher blood glucose levels and therefore do not elicit an insulin response to those levels (Matsumura 1995). The level of glucose-uptake inhibition appears to correlate with the activation of the aryl hydrocarbon receptor, which is required for TCDD-induced toxicological effects (Matsumura 1995; Olsen et al.
However, the dioxin exposures in these in vivo and in vitro studies are approximately 1,000–100,000 times background body burdens observed in the U.S. The in vivo studies are associated with body weight loss, histopathological findings, and significant decreases in thyroid hormones.



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