|
|
The correlation between blood chloroform and diabetes and related glycemic and lipid metabolic parameters based on NHANES database#br# |
LI Jiayi1, LIU Xuekui2, GENG Houfa1,2, LIANG Jun1,2 |
(1. Graduate School of Bengbu Medical College, Bengbu Anhui 233000; 2. Department of Endocrinology, Xuzhou Central Hospital, Xuzhou Jiangsu 221000, China)
|
|
|
Abstract Objective: To explore the correlation between blood chloroform concentration in the human body and the risk of diabetes, and provide a basis for the prevention and control of diabetes. Methods: The data, extracted from 2017—2018 year of the United States National Health and Nutrition Examination Survey database, was used for the study. After excluding pregnant women, teenagers under 18 years old, participants with missing chloroform concentrations, and incomplete diabetes survey, a total of 622 participants were included for further analysis. The participants were divided into T1 (<0.011 μg/L), T2 (≥0.011, and <0.017 μg/L), and T3 (≥0.017 μg/L) groups based on their blood chloroform concentrations using the quartile method. The logistic regression was used to analyze the incidence rate of diabetes among the three groups, and a cubic spline graph was utilized to demonstrate the correlation between chloroform and the risk of diabetes. Results: The risk of developing diabetes increases with the increasing of chloroform concentration (the T3 group was 1.23 times higher than the T1 group). The results of restricted cubic spline analysis showed that chloroform exposure was positive correlation with fasting blood glucose, homeostatic model assessment of insulin resistance (HOMAIR), which was an index for insulin resistance. Furthermore, partial correlation analysis also indicated that there was a positive correlation between chloroform concentration and both fasting blood glucose levels and HOMAIR. Additionally, the risk of developing diabetes was found to be positively associated with chloroform concentration. In addition, subgroup analysis results also showed that blood chloroform was a risk factor for diabetes. Conclusion: Chloroform exposure is an independent risk factor for diabetes, which can increase insulin resistance and thereby increase the risk of developing diabetes.
|
Received: 19 April 2023
|
|
|
|
[1]Bommer C, Heesemann E, Sagalova V, et al. The global economic burden of diabetes in adults aged 20-79 years: a costofillness study[J]. Lancet Diabetes Endocrinol, 2017, 5(6): 423-430.
[2]Sun H, Saeedi P, Karuranga S, et al. IDF Diabetes Atlas: Global, regional and countrylevel diabetes prevalence estimates for 2021 and projections for 2045[J]. Diabetes Res Clin Pract, 2022, 183: 109119.
[3]European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO). EASLEASDEASO Clinical Practice Guidelines for the management of nonalcoholic fatty liver disease[J]. J Hepatol, 2016, 64(6): 1388-1402.
[4]Tancredi M, Rosengren A, Svensson AM, et al. Excess mortality among persons with type 2 diabetes[J]. N Engl J Med, 2015, 373(18): 1720-1732.
[5]Chatterjee S, Khunti K, Davies MJ. Type 2 diabetes[J]. Lancet, 2017, 389(10085): 2239-2251.
[6]Kahn SE, Cooper ME, Del Prato S. Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future[J]. Lancet, 2014, 383(9922): 1068-1083.
[7]Richardson SD, Plewa MJ, Wagner ED, et al. Occurrence, genotoxicity, and carcinogenicity of regulated and emerging disinfection byproducts in drinking water: a review and roadmap for research[J]. Mutat Res, 2007, 636(1/3): 178-242.
[8]Ritter L, Solomon K, Sibley P, et al. Sources, pathways, and relative risks of contaminants in surface water and groundwater: a perspective prepared for the Walkerton inquiry[J]. J Toxicol Environ Health A, 2002, 65(1): 1-142.
[9]Bove F, Shim Y, Zeitz P. Drinking water contaminants and adverse pregnancy outcomes: a review[J]. Environ Health Perspect, 2002, 110(Suppl 1): 61-74.
[10]Tardiff RG, Carson ML, Ginevan ME. Updated weight of evidence for an association between adverse reproductive and developmental effects and exposure to disinfection byproducts[J]. Regul Toxicol Pharmacol, 2006, 45(2): 185-205.
[11]Windham GC, Waller K, Anderson M, et al. Chlorination byproducts in drinking water and menstrual cycle function[J]. Environ Health Perspect, 2003, 111(7): 935-941; discussion A409.
[12]Constan AA, Sprankle CS, Peters JM, et al. Metabolism of chloroform by cytochrome P450 2E1 is required for induction of toxicity in the liver, kidney, and nose of male mice[J]. Toxicol Appl Pharmacol, 1999, 160(2): 120-126.
[13]Gemma S, Vittozzi L, Testai E. Metabolism of chloroform in the human liver and identification of the competent P450s[J]. Drug Metab Dispos, 2003, 31(3): 266-274.
[14]Testai E, De Curtis V, Gemma S, et al. The role of different cytochrome P450 isoforms in in vitro chloroform metabolism[J]. J Biochem Toxicol, 1996, 11(6): 305-312.
[15]Mansuy D, Beaune P, Cresteil T, et al. Evidence for phosgene formation during liver microsomal oxidation of chloroform[J]. Biochem Biophys Res Commun, 1977, 79(2): 513-517.
[16]Smith JH, Maita K, Sleight SD, et al. Mechanism of chloroform nephrotoxicity. Ⅰ. Time course of chloroform toxicity in male and female mice[J]. Toxicol Appl Pharmacol, 1983, 70(3): 467-479.
[17]Blount BC, Aylward LL, Lakind JS, et al. Human exposure assessment for DBPs: factors influencing blood trihalomethane levels[M]// Nriagu JO. Encyclopedia of Environmental Health: Vol 3. Amsterdam: Elsevier, 2011: 100-107.
[18]Demarini DM. A review on the 40th anniversary of the first regulation of drinking water disinfection byproducts[J]. Environ Mol Mutagen, 2020, 61(6): 588-601.
[19]Ashley DL, Blount BC, Singer PC, et al. Changes in blood trihalomethane concentrations resulting from differences in water quality and water use activities[J]. Arch Environ Occup Health, 2005, 60(1): 7-15.
[20]Caro J, Gallego M. Assessment of exposure of workers and swimmers to trihalomethanes in an indoor swimming pool[J]. Environ Sci Technol, 2007, 41(13): 4793-4798.
[21]Gngler S, Waldenberger M, Artati A, et al. Exposure to disinfection byproducts and risk of type 2 diabetes: a nested casecontrol study in the HUNT and Lifelines cohorts[J]. Metabolomics, 2019, 15(4): 60.
[22]Andra SS, Charisiadis P, Makris KC. Obesitymediated association between exposure to brominated trihalomethanes and type Ⅱ diabetes mellitus: an exploratory analysis[J]. Sci Total Environ, 2014, 485-486: 340-347.
[23]Lim GE, Stals SI, Petrik JJ, et al. The effects of in utero and lactational exposure to chloroform on postnatal growth and glucose tolerance in male Wistar rats[J]. Endocrine, 2004, 25(3): 223-228.
[24]Kaiser JP, Lipscomb JC, Wesselkamper SC. Putative mechanisms of environmental chemicalinduced steatosis[J]. Int J Toxicol, 2012, 31(6): 551-563.
[25]Fruci B, Giuliano S, Mazza A, et al. Nonalcoholic fatty liver: a possible new target for type 2 diabetes prevention and treatment[J]. Int J Mol Sci, 2013, 14(11): 22933-22966.
[26]Anstee QM, Targher G, Day CP. Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis[J]. Nat Rev Gastroenterol Hepatol, 2013, 10(6): 330-344.
|
[1] |
. [J]. Journal of Jiangsu University(Medicine Edition), 2023, 33(04): 359-363,368. |
|
|
|
|