|Centre||Chulabhorn Research Institute (CRI), Thailand|
|Description of cohort||A follow-up group of 40 male and female children ages 8-10 years from Ron Phibul district of Thailand exposed to arsenic in utero since 2004; and a reference group of 20 children living in the Sao Thong district near Ron Phibul, where arsenic concentration in water has been determined to be very low.|
|Location of cohort||Ron Pibul District of the Nakhon Sri Tammarat Province, located in the southern peninsula of Thailand.|
|Chemicals/Exposures studied||Arsenic in drinking water|
|Health or social effects studied||Cellular and molecular responses to arsenic exposure.|
|Samples collected||Urine, serum, nail and saliva|
|Questionnaires||Yes; Questionnaires were administered
to all participants to obtain personal information regarding residential history, health history and potential confounding factors, birth and pregnancy information (number of births, abortions or complications), use of community drinking water and well water, as well as water and food consumption habits.
|Key Findings||Cohort studies demonstrate the robust impact of a mother’s arsenic consumption on fetal gene expression. Genome-wide expression changes associated with prenatal arsenic exposure showed that the potential biomarker gene set of prenatal arsenic exposure was composed of CXL1, DUSP1, EGR1, IER2, JUNB, MIR21, OSM, PTGS2, RNF149, SFRS5 and SOC3. Biological network analysis showed that the arsenic-associated transcripts could modulate numerous biological pathways, including apoptosis, cell signaling, inflammation and stress response, and ultimately affect health status (Fry et al, 2007).
Hyper-methylation of p53 and a slight decrease in LINE-1 methylation was observed in cord blood of these exposed newborns (Intarasunanont 2012).
Continued exposure to arsenic during early childhood increased level of oxidative DNA damage represented by 8-OHdG, and reduced expression of DNA-repair hOGG1which may lead to initiation of carcinogenesis (Hinhumpatch P, 2013).