Insulin Resistance and Simultaneous Exposure to Mercury, Dioxins and Furans
At Grassy Narrows and Wabaseemoong First Nations in Ontario, Canada, many people have been diagnosed with Minamata disease (mercury poisoning). Many people in these two communities also have Type II Diabetes.
Both communities were exposed simultaneously to mercury, dioxins and furans from their fish and wild meat. Industrial pollution was the source of the contamination. Although they were tested for mercury, the people were never tested for dioxin or other toxins such as arsenic, cadmium and hexachlorobenzene which have recently been linked to diabetes in a variety of studies. Some of these toxins are still being released by the pulp mill at Dryden, Ontario.
Few studies in the world seem to look at the efects of simultaneous exposures to pollutants. The very recent study below did just that and discovered that simultaneous exposure to mercury. dioxins and furans resulted in increased Insulin resistance. Insulin resistance is a risk factor for Diabetes.
When looking at connections between pollutants and Diabetes, scientists should investigate multiple exposures and the synergistic effect they may have in relation to the onset of Type II Diabetes. All the best to you.
For Land and Life,
John H.W. Hummel
Link to obtain the Full-Text Published Version of this Scientific Paper:
Definition of Insulin Resistance:
Author Jung-Wei Chang
Abstract The neurotoxic effects caused by methylmercury （MeHg） have been well documented in several epidemiologic studies. The most frequent clinical signs and symptoms were color discrimination, incoordination, impaired cognitive performance, cerebellar ataxia and tremor. However, it will also cause adverse health effects, which targets on the liver, kidney function and endocrine system. Besides, several epidemiologic and animal studies have also suggested that polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) would pose the simliar health effects as the methylmercury. Fish consumption was the main and crucial exposure pathway for general population to dioxins and methylmercury. If people consume the polluted fishes and seafood by accident, it might cause higher health risk, which was also the keystone of this study. An-Shun chlor-alkali plant had operated for forty years and manufactured sodium hydroxide, chlorine gas and pentachlophenol (PCP). During the manufactural processes, lots of sludge contained mercury was released into the nearby environment around the factory. The measured data provided evidence that the PCP and untreated wastewater from the factory might had spread via the wastewater and soil into the sea reservoir. Local residents used to catch aquatics such as fish, shrimp and crabs from the reservoir for consumption or vendor. Fish and aquatic organisms consumption from the sea reservoir was the main and crucial pathway for their exposure to dioxins and methylmercury. And the measured data also revealed that the residents had high health effects risk of dioxins and mercury. This study provided a good opportunity to examine the hypothesis that residents co-exposed dioxins and methylmercury might be associated with an increased risk of neurologic and endocrine toxic effects, and even a potential interaction. In Cognitive Abilities Screening Instrument (CASI C-2.0), higher abnormality rates for remote memory (p= 0.036), mental manipulation (p= 0.013), and orientation (p= 0.005) were found in the High-MeHg group than in the Low-MeHg group. The left peroneal motor nerve conduction velocity (NCV) was significantly decreased with serum dioxins (β= -0.86, p= 0.037). We found a slight monotonic increase in the risk for insulin resistance across the serum PCDD/F categories (P for the trend: < 0.001). Groups with serum dioxins higher than 20.5 pg WHO98-TEQDF/g lipid had a higher risk of insulin resistance (adjusted odds ratios of 2.7, 3.5 and 5.0 for 50th to < 75th, 75th to < 90th and 产 90th percentile, respectively) compared with the reference group (< 9.6 pg WHO98-TEQDF/g lipid [< 10th percentile]). Serum dioxins were significantly increased with the number of MetS components (serum PCDD/F levels: 16.9, 20.7, 26.7, 29.5, 28.2, and 24.0 pg WHO98-TEQDF/g lipid, respectively). In factor analysis, four risk factors—lipidemia, blood pressure, body size, and glycemia—accounted for 72.8% of the variance in the 10 core factors in participants and revealed that dioxins were linked to MetS through shared correlations with high blood pressure. After adjusting for confounding factors, participants with higher serum dioxin levels or insulin resistance were at significant risk for having MetS (adjusted odds ratio [AOR] 1.40 [95% CI 1.03-1.90] for dioxins; AOR 6.69 [95% CI 5.03-8.99] for insulin resistance). Participants exposed to higher levels of dioxins and possessed insulin resistance had a much greater risk (AOR 1.80 [95% CI 1.32- 2.48]) of having MetS. High-dose exposure to dioxins is suggested to be a blood pressure-related factor which raised MetS risk by modifying the effect of insulin resistance on metabolic syndrome. After adjusting for confounding factors, residents with higher serum dioxin levels or blood mercury levels (reference: < 25th percentile; higher: > 75th percentile) were at a significant risk for insulin resistance (adjusted odds ratio [AOR] 4.0 [95% CI 2.3-7.3] for dioxins; AOR 2.3 [95% CI 1.5-3.5] for mercury) and HOMA β-cell dysfunction (AOR 2.3 [95% CI 1.3-3.9] only for dioxins). We found a striking multiplicative interaction between dioxins and mercury, even in non-diabetic residents(AOR 2.1 [95% CI 1.1- 4.1]). Accumulated dioxins and mercury may synergistically increase the risk of developing insulin resistance. The Framingham General Cardiovascular Disease score and risk were both significantly increased with serum dioxins (p< 0.001), which shows dioxin might also cause cardiovascular toxic effects.
In our large-scale study with a great deal of variation in PCDD/F and mercury co-exposure, we found that participants—even those without diabetes—co-exposed to higher levels of PCDD/Fs and mercury had a much greater risk of having insulin resistance, which persisted even after we had adjusted for the effect of the other explanatory variables. Our results have important ramifications for public concern, whatever pathophysiologic mechanism underlies the interaction between serum PCDD/Fs and mercury and its association with insulin resistance.
Whether the synergistically increasing risk of insulin resistance leads to a higher prevalence of diabetes deserves more attention and follow-up. In humans, PCDD/Fs and mercury are easily accumulated by eating fish and other seafood. It should concern us that the current Tolerable Daily Intake (TDI) for PCDD/Fs and recommended limits for methylmercury may underestimate the synergistic risk.
In conclusion, we found a significant association between serum PCDD/Fs, blood mercury, and insulin resistance after adjusting for confounding factors: interaction between dioxins, mercury, and insulin resistance exists even in persons without diabetes. Accumulated dioxins and mercury may synergistically increase the risk of developing insulin resistance. Further study is needed to confirm these findings in other persons co-exposed to high levels of PCDD/Fs and mercury. Information about the long-term health implications of insulin resistance should be promptly delivered to those with a history of co-exposure to PCDD/Fs and mercury because of the extra risk of type 2 diabetes, cardiovascular disease, and chronic disease they may incur.
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