Ecotoxicology and Environmental Safety (Dec 2022)
Association and risk of circulating inflammatory markers with hyperglycemia in coal-burning arsenicosis
Abstract
Background: Several lines of evidence support a significant relationship between exposure to arsenic and diabetes. However, the underlying pathophysiological mechanisms remain incompletely elucidated. Objective: This study examined the association and risk of circulating inflammatory mediators with hyperglycemia in coal-induced arsenicosis. Methods: A cross-sectional study was conducted in the typical coal-burning area in which arsenicosis is endemic in Xingren County, Guizhou, China. A total of 299 arsenicosis subjects and 137 non-arsenic exposed volunteers were recruited for the present study. Participant’s hyperglycemia-related parameters, including fasting blood glucose (FBG), fasting serum insulin (FINS), homeostasis model assessment for both insulin resistance (HOMA-IR) and pancreatic β-cell function (HOMA-β), as well as circulating inflammatory biomarkers i.e., Interleukins-1β (IL-1β), IL- 2, IL − 6, IL-10, IL- 17, IL-18 and TNF-α), were determined and analyzed after completing questionnaire investigation and physical examination. Results: The results clearly showed that coal-burning arsenic exposure was significantly associated with hyperglycemia-related outcomes. Specifically, arsenicosis subjects from the coal-burning endemic area showed a higher level of FBG (median 5.87 mmol/L vs. 4.65 mmol/L) and increased prevalence of hyperglycemia (26.76% vs.16.79%) than reference subjects from the non-arsenic endemic area. Increased HOMA-IR (median 1.93 vs.1.44) and declined HOMA-β (median 96.23 vs. 84.91) were also noted in arsenicosis subjects. Moreover, arsenic exposure was significantly associated with the increased risk of hyperglycemia (adjusted OR = 2.32, 95% CI: 1.37,3.93). In addition, a positive association between arsenic exposure and inflammatory response was observed, and the alteration in circulating inflammatory markers were found to be significantly associated with hyperglycemia-related parameters. Meanwhile, there was a positive relationship between elevated circulating IL-1β, IL-18, IL-6, as well as decreased IL-10 and the increasing risk of arsenic-induced hyperglycemia [adjusted OR = 2.19 (95% CI: 1.26, 3.13);1.13 (95%CI: 1.08, 1.37); 1.19 (95% CI: 1.13, 1.56); 1.15(95% CI: 1.05, 1.36); respectively]. Path analysis further revealed that the mediating effect of IL-1β and IL-18 on the relationship between arsenic exposure and hyperglycemia was closely associated with pancreatic β-cell dysfunction, while those of IL-6 and IL-10 on the association between arsenic exposure and hyperglycemia were partially through insulin resistance. Conclusions: This population-based study indicated that arsenic exposure has a clear disruptive effect on glucose homeostasis, and an elevated inflammatory response was implicated in the risk of arsenic-induced hyperglycemia.
