Glucose Tolerance and Occupational Exposure to Carbon Disulphide

Franco, Giuliano; Malamani, T; Piazza, Angelo

doi:10.1016/s0140-6736(78)92197-9

Cited by 15 publications

(6 citation statements)

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“…The first environmental contaminant to be associated with an increased diabetes risk was found in the 1970s, when carbon disulfide exposure’s relationship to diabetes was reported (Franco et al , 1978; 2007a). Interest in other environmental contaminants and their potential to increase diabetes risk is relatively recent, and has focused on arsenic, dioxin, and nitrates (Kostraba et al , 1992; Rahman et al , 1996; Rahman et al , 1998; Longnecker and Michalek, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…While the cornerstone of type 2 diabetes prevention programs has focused on weight reduction and increased physical activity, established to reduce the incidence by up to 58% (Knowler et al , 2002), its etiology remains to be elucidated, and the role of environmental pollutants in diabetogenesis has received little attention from the medical and research communities. While it has been known for nearly 30 years that exposure to a variety of environmental toxicants may contribute to diabetes risk (Franco et al , 1978; Longnecker and Daniels, 2001), arsenic has only recently come under scrutiny for its contributing role.…”

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confidence: 99%

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Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

Hill

Wlodarczyk

Mitchell

et al. 2009

Toxicology and Applied Pharmacology

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Background Epidemiological studies have linked environmental arsenic (As) exposure to increased type 2 diabetes risk. Periconceptional hyperglycemia is a significant risk factor for neural tube defects (NTDs), the second most common structural birth defect. A suspected teratogen, arsenic (As) induces NTDs in laboratory animals. Objectives We investigated whether maternal glucose homeostasis disruption was responsible for arsenate-induced NTDs in a well-established dosing regimen used in studies of arsenic’s teratogenicity in early neurodevelopment. Methods We evaluated maternal intraperitoneal (I.P.) exposure to As 9.6 mg/kg (as sodium arsenate) in LM/Bc/Fnn mice for teratogenicity and disruption of maternal plasma glucose and insulin levels. Selected compounds (insulin pellet, sodium selenate (SS), N-acetyl cysteine (NAC), L-methionine (L-Met), N-tert-Butyl-α-phenylnitrone (PBN)) were investigated for their potential to mitigate arsenate’s effects. Results Arsenate caused significant glucose elevation during an I.P. glucose tolerance test (IPGTT). Insulin levels were not different between arsenate and control dams before (arsenate, 0.55 ng/dl; control, 0.48 ng/dl) or after glucose challenge (arsenate, 1.09 ng/dl; control, 0.81 ng/dl). HOMA-IR index was higher for arsenate (3.9) vs control (2.5) dams (p=0.0260). Arsenate caused NTDs (100%, p<0.0001). Insulin pellet and NAC were the most successful rescue agents, reducing NTD rates to 45% and 35%. Conclusions IPGTT, insulin assay, and HOMA-IR results suggest a modest failure of glucose stimulated insulin secretion and insulin resistance characteristic of glucose intolerance. Insulin’s success in preventing arsenate-induced NTDs provides evidence that these arsenate-induced NTDs are secondary to elevated maternal glucose. The NAC rescue, which did not restore maternal glucose or insulin levels, suggests oxidative disruption plays a role.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

Hill

Wlodarczyk

Mitchell

et al. 2009

Toxicology and Applied Pharmacology

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“…That occupational exposure could increase risk, however, has been recognized since the 1970s, when an association with carbon disulfide was reported (6). Here we review the relevant epidemiologic data, which can be categorized as follows: type 1 diabetes in relation to nitrates, nitrites, and nitrosamines, and in relation to polychlorinated biphenyls (PCBs); and type 2 diabetes in relation to arsenic, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and occupational exposures.…”

mentioning

confidence: 99%

“…The concordance rate among monozygous twins is about 30% (9). Whether chemical agents can cause type 2 diabetes in humans is not as clearly established as for type 1 diabetes, though suggestive data exist (6). Many drugs, however, exacerbate type 2 diabetes (20).…”

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confidence: 99%

Environmental contaminants as etiologic factors for diabetes.

Longnecker

Daniels

2001

Environ Health Perspect

170

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For both type 1 and type 2 diabetes mellitus, the rates have been increasing in the United States and elsewhere; rates vary widely by country, and genetic factors account for less than half of new cases. These observations suggest environmental factors cause both type 1 and type 2 diabetes. Occupational exposures have been associated with increased risk of diabetes. In addition, recent data suggest that toxic substances in the environment, other than infectious agents or exposures that stimulate an immune response, are associated with the occurrence of these diseases. We reviewed the epidemiologic data that addressed whether environmental contaminants might cause type 1 or type 2 diabetes. For type 1 diabetes, higher intake of nitrates, nitrites, and N-nitroso compounds, as well as higher serum levels of polychlorinated biphenyls have been associated with increased risk. Overall, however, the data were limited or inconsistent. With respect to type 2 diabetes, data on arsenic and 2,3,7,8-tetrachlorodibenzo-p-dioxin relative to risk were suggestive of a direct association but were inconclusive. The occupational data suggested that more data on exposure to N-nitroso compounds, arsenic, dioxins, talc, and straight oil machining fluids in relation to diabetes would be useful. Although environmental factors other than contaminants may account for the majority of type 1 and type 2 diabetes, the etiologic role of several contaminants and occupational exposures deserves further study.

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“…These discrepancies may be due to differences in various factors such as the degree of exposure, population studied or type of study conducted. Likewise, some authors have suggested that glucose metabolism could be impaired by CS 2 exposure 14,15) , but contradictory null results have also been reported as well 16,17) . In a baseline analysis of this study, glycosylated hemoglobin levels increased in a CS 2 -exposed group compared to a referent group 7) .…”

mentioning

confidence: 99%

Lack of Relationship between Occupational Exposure to Carbon Disulfide and Endocrine Dysfunction: A Six‐year Cohort Study of the Japanese Rayon Workers

Takebayashi

Nishiwaki

Nomiyama

et al. 2003

Journal of Occupational Health

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Lack of Relationship between Occupational Exposure to Carbon Disulfide and Endocrine Dysfunction: A Six-year Cohort Study of the Japanese Rayon Workers: Toru TAKEBAYASHI, et al. Department of Preventive Medicine and PublicHealth, School of Medicine, Keio UniversityObjectives-A six-year prospective cohort study was conducted to clarify whether the current carbon disulfide (CS 2 ) exposure level is low enough to prevent subclinical health impairment and/or to ameliorate health effects due to previous high exposure. This paper describes the follow-up results, exposure assessment, and effects on the endocrine system. Methods-The study subjects were 432 male workers exposed to CS 2 at one of the 11 rayon factories in Japan and 402 referent workers from the same factories, all of whom were examined in 1992-93. 251 CS 2 -exposed, 140 former-exposed and 359 referent workers participated in the follow-up survey (follow-up rate 89.9%) in 1998-99. Urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) at the end of a shift as internal exposure index and the time-weighted average CS 2 concentration as external exposure index were measured twice a year from 1992-1993. By using various blood indices, we evaluated effects on thyroid, hypophysis, and gonad function, as well as effects on glucose metabolism. Information on potential confounding factors, such as age, smoking and alcohol drinking, were collected and adjusted for. ResultsWhen the individual exposure level was represented by arithmetic mean for TTCA and CS 2 concentration, Received July 31, 2002; Accepted Jan 24, 2003 Correspondence to: T. Takebayashi, Department of Preventive Medicine and Public Health, School of Medicine, Keio University, 35 Shinanomachi, Japan geometric means (SD) of CS 2 workers were 1.61 (1.91) mg/g.crea and 5.02 (1.84) ppm, respectively. There were no exposure-related differences in glucose metabolism or any of the endocrinological indices. Conclusions-No biologically significant effects of CS 2 were found on endocrine function in Japanese rayon manufacturing workers when the average internal and external exposure levels were maintained below the current occupational exposure limit. (J Occup Health 2003; 45: 111-118)

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Glucose Tolerance and Occupational Exposure to Carbon Disulphide

Cited by 15 publications

References 1 publication

Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

Environmental contaminants as etiologic factors for diabetes.

Lack of Relationship between Occupational Exposure to Carbon Disulfide and Endocrine Dysfunction: A Six‐year Cohort Study of the Japanese Rayon Workers

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