Dose-response relationship between arsenic in drinking water and mortality of urinary cancers in Taiwan.

Ingested arsenic is carcinogenic to the human urinary tract, but uncertainties remain regarding the dose-response relationship. To assess dose-response relationships between arsenic ingestion and urinary cancers, we evaluated the associations between the arsenic level in drinking water and mortality of cancers of the bladder, kidney, and prostate in Taiwan. We utilized the 1971-2000 Taiwan death registry data and calculated the age-standardized mortality rates (ASMRs) using the 1976 world standard population as the reference group. We used the data from a 1974-1976 census survey of wells on the arsenic levels in drinking water conducted by the government to assess exposure levels, which had been divided into three categories: below 0.05 ppm, 0.05-0.35 ppm, and above 0.35 ppm. The data were analyzed using multiple linear regression models and geographical information system. We found no increase in ASMR for all, or any, of the urinary cancers at exposure levels of 0.05-0.35 ppm arsenic, but at exposure levels > 0.35 ppm arsenic was associated with increased ASMR in both males and females for bladder cancer, kidney cancer, and all urinary cancers combined. There was no increased ASMR associated with prostate cancer observed for either exposure category.

Organophosphate pesticides and new-onset diabetes mellitus: From molecular mechanisms to a possible therapeutic perspective.

Organophosphate is a commonly used pesticide in the agricultural sector. The main action of organophosphate focuses on acetylcholinesterase inhibition, and it therefore contributes to acute cholinergic crisis, intermediate syndrome and delayed neurotoxicity. From sporadic case series to epidemiologic studies, organophosphate has been linked to hyperglycemia and the occurrence of new-onset diabetes mellitus. Organophosphate-mediated direct damage to pancreatic beta cells, insulin resistance related to systemic inflammation and excessive hepatic gluconeogenesis and polymorphisms of the enzyme governing organophosphate elimination are all possible contributors to the development of new-onset diabetes mellitus. To date, a preventive strategy for organophosphate-mediated new-onset diabetes mellitus is still lacking. However, lowering reactive oxygen species levels may be a practical method to reduce the risk of developing hyperglycemia.