Relationship Between Serum Concentrations of Organochlorine Pesticides and Metabolic Syndrome Among Non-Diabetic Adults

Park, Sun Kyun; Son, Hyo Kyung; Lee, Sung Kook; Kang, Jung Ho; Chang, Yoon Seok; Jacobs, David R.; Lee, Dong Hoon

doi:10.3961/jpmph.2010.43.1.1

Cited by 54 publications

(44 citation statements)

References 18 publications

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“…Significant trends were observed in adjusted log 10 oxychlor, tNONA, HCB and β -HCCH models ( p = 0.056 in the latter) as well. Park et al (2010) found a positive association between β -HCCH and metabolic syndrome in their case-control study; ORs (95% CI) across tertiles 2 and 3 of the compound were 3.2 (1.0–10.3) and 4.4 (1.4–13.5) in a model adjusted for age, sex, alcohol and smoking. The ORs were greatly attenuated when BMI was added to that model and consistent with the effect estimates observed in the Anniston population.…”

Section: Discussionmentioning

confidence: 93%

“…Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzo-furans also were linked to metabolic syndrome in a cross-sectional Taiwanese study (Chang et al, 2010). Associations between organochlorine compounds and metabolic syndrome were observed in a case-control study in Uljin County Korea (Park et al, 2010) and in a second case-control study (nested) from the same community-based cohort (Lee et al, 2014b). Increased organochlorine pesticide levels also have been observed in participants with metabolic syndrome in a small clinical study in India (Tomar et al, 2013).…”

Section: Introductionmentioning

confidence: 97%

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Metabolic syndrome is associated with exposure to organochlorine pesticides in Anniston, AL, United States

Rosenbaum

Weinstock

Silverstone

et al. 2017

Environment International

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The Anniston Community Health Survey, a cross-sectional study, was undertaken in 2005–2007 to study environmental exposure to polychlorinated biphenyl (PCB) and organochlorine (OC) pesticides and health outcomes among residents of Anniston, AL, United States. The examination of potential risks between these pollutants and metabolic syndrome, a cluster of cardiovascular risk factors (i.e., hypertension, central obesity, dyslipidemia and dysglycemia) was the focus of this analysis. Participants were 548 adults who completed the survey and a clinic visit, were free of diabetes, and had a serum sample for clinical laboratory parameters as well as PCB and OC pesticide concentrations. Associations between summed concentrations of 35 PCB congeners and 9 individual pesticides and metabolic syndrome were examined using generalized linear modeling and logistic regression; odds ratios (OR) and 95% confidence intervals (CI) are reported. Pollutants were evaluated as quintiles and as log transformations of continuous serum concentrations. Participants were mostly female (68%) with a mean age (SD) of 53.6 (16.2) years. The racial distribution was 56% white and 44% African American; 49% met the criteria for metabolic syndrome. In unadjusted logistic regression, statistically significant and positive associations across the majority of quintiles were noted for seven individually modeled pesticides (p,p′-DDT, p,p′-DDE, HCB, β-HCCH, oxychlor, tNONA, Mirex). Following adjustment for covariables (i.e., age, sex, race, education, marital status, current smoking, alcohol consumption, positive family history of diabetes or cardiovascular disease, liver disease, BMI), significant elevations in risk were noted for p,p′-DDT across multiple quintiles (range of ORs 1.61 to 2.36), for tNONA (range of ORs 1.62–2.80) and for p,p′-DDE [OR (95% CI)] of 2.73 (1.09–6.88) in the highest quintile relative to the first. Significant trends were observed in adjusted logistic models for log10 HCB [OR = 6.15 (1.66–22.88)], log10 oxychlor [OR = 2.09 (1.07–4.07)] and log10 tNONA [3.19 (1.45–7.00)]. Summed PCB concentrations were significantly and positively associated with metabolic syndrome only in unadjusted models; adjustment resulted in attenuation of the ORs in both the quintile and log-transformed models. In conclusion, several OC pesticides were found to have significant associations with metabolic syndrome in the Anniston study population while no association was observed for PCBs.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 97%

Metabolic syndrome is associated with exposure to organochlorine pesticides in Anniston, AL, United States

Rosenbaum

Weinstock

Silverstone

et al. 2017

Environment International

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“…Previous experiments have demonstrated that exposure to organochlorine pesticides might induce intrauterine growth retardation (IUGR) [38], [39] and obesity in puberty [47], [48], [49], [50]. Prenatal exposure to low doses of MXC reduces the postnatal growth [51].…”

Section: Discussionmentioning

confidence: 99%

Perinatal Exposure to Low-Dose Methoxychlor Impairs Testicular Development in C57BL/6 Mice

Zhang

Liu

et al. 2014

PLoS ONE

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Methoxychlor (MXC), an organochlorine pesticide, has adverse effects on male reproduction at toxicological doses. Humans and wild animals are exposed to MXC mostly through contaminated dietary intake. Higher concentrations of MXC have been found in human milk, raising the demand for the risk assessment of offspring after maternal exposure to low doses of MXC. In this study, pregnant mice (F0) were given intraperitoneal daily evening injections of 1 mg/kg/d MXC during their gestational (embryonic day 0.5, E0.5) and lactational periods (postnatal day 21.5, P21.5), and the F1 males were assessed. F1 testes were collected at P0.5, P21.5 and P45.5. Maternal exposure to MXC disturbed the testicular development. Serum testosterone levels decreased, whereas estradiol levels increased. To understand the molecular mechanisms of exposure to MXC in male reproduction, the F1 testes were examined for changes in the expression of steroidogenesis- and spermatogenesis- related genes. RT-PCR analysis demonstrated that MXC significantly decreased Cyp11a1 and increased Cyp19a1; furthermore, it downregulated certain spermatogenic genes (Dazl, Boll, Rarg, Stra8 and Cyclin-a1). In summary, perinatal exposure to low-dose MXC disturbs the testicular development in mice. This animal study of exposure to low-dose MXC in F1 males suggests similar dysfunctional effects on male reproduction in humans.

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“…It has been reported that exposure to EDCs such as dioxins (39,42), bisphenol A (21), phthalates (37), or p,p=-dichlorodiphenyltrichloroethane (27,40) is highly associated with the increased risk of developing insulin resistance or diabetes, because the subpopulations that have the highest rates of these chronic diseases are also those have greatest exposure to EDCs.…”

mentioning

confidence: 99%

Developmental exposure to di(2-ethylhexyl) phthalate impairs endocrine pancreas and leads to long-term adverse effects on glucose homeostasis in the rat

Lin

Jie

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

152

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-Di(2-ethylhexyl) phthalate (DEHP), a typical endocrine-disrupting chemical (EDC), is widely used as plasticizer. DEHP exposure in humans is virtually ubiquitous, and those undergoing certain medical procedures can be especially high. In this study, we investigated whether developmental DEHP exposure disrupted glucose homeostasis in the rat and whether this was associated with the early impairment in endocrine pancreas. Pregnant Wistar rats were administered DEHP (1.25 and 6.25 mg·kg(-1)·day(-1)) or corn oil throughout gestation and lactation by oral gavage. Body weight, glucose and insulin tolerance, and β-cell morphometry and function were examined in offspring during the growth. In this study, developmental DEHP exposure led to abnormal β-cell ultrastructure, reduced β-cell mass, and pancreatic insulin content as well as alterations in the expression of genes involved in pancreas development and β-cell function in offspring at weaning. At adulthood, female DEHP-exposed offspring exhibited elevated blood glucose, reduced serum insulin, impaired glucose tolerance, and insulin secretion. Male DEHP-exposed offspring had increased serum insulin, although there were no significant differences in blood glucose at fasting and during glucose tolerance test. In addition, both male and female DEHP-exposed offspring had significantly lower birth weight and maintained relatively lower body weight up to 27 wk of age. These results suggest that developmental exposure to DEHP gives rise to β-cell dysfunction and the whole body glucometabolic abnormalities in the rat. DEHP exposure in critical periods of development can be a potential risk factor, at least in part, for developing diabetes.

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Relationship Between Serum Concentrations of Organochlorine Pesticides and Metabolic Syndrome Among Non-Diabetic Adults

Abstract: Despite the small sample size, this study suggests that the background exposure to some OCPs may be associated with metabolic syndrome.

Cited by 54 publications

References 18 publications

Metabolic syndrome is associated with exposure to organochlorine pesticides in Anniston, AL, United States

Metabolic syndrome is associated with exposure to organochlorine pesticides in Anniston, AL, United States

Perinatal Exposure to Low-Dose Methoxychlor Impairs Testicular Development in C57BL/6 Mice

Developmental exposure to di(2-ethylhexyl) phthalate impairs endocrine pancreas and leads to long-term adverse effects on glucose homeostasis in the rat

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