Arsenic pollution in tube well water was observed at both Red river and Mekong river deltas with different levels. The average concentrations were determined as 1.3 µg/L; 6.8 µg/L; 72 µg/L; 165 µg/L; 277 µg/L; 421.5 µg/L at Triton (Angiang); Tuliem (Hanoi); Tanhong (Dongthap); Thanhtri (Hanoi); Hoaiduc (Hatay) and Lynhan (Hanam) respectively. Filtration groundwater by sand has removed a major portion of arsenic. The arsenic accumulation in hair sample is useful biomarker for assessment of chronic intoxication of arsenic form drinking and daily use water. It is proved by closely correlation between arsenic contents in hair and consumed water (R2= 0.935). More detail screening of arsenic pollution in tube well water, evaluation of health effect and education for people to use free arsenic water are the most important approaches.
Arsenic ; Poisoning ; Water ; Epidemiology

A description and analysis were realized to determine the intoxication of lead and arsenic in workers who were exposed to various enviromental factors in Thai Nguyen colored metallurgy factories. These workers had > 5 years old professional age in the field of exploiting and processing the metal. Study showed a high level of intoxication. The mean value of urine ALA oscillated in the range from 7.15 – 7.8 mg/l. There were 20-51 cases with pathological manifestation of lead and arsenic intoxication in the years 1998-2000.
Lead Poisoning/epidemiology ; Lead ; Arsenic Poisoning/epidemiology ; Epidemiology

Adult ; Air Pollutants, Occupational ; analysis ; poisoning ; Arsenic Poisoning ; complications ; Causality ; Female ; Humans ; Male ; Maximum Allowable Concentration ; Purpura, Thrombotic Thrombocytopenic ; epidemiology ; Young Adult

OBJECTIVETo explore the level and feature of neonate deformity in water arsenic exposure areas, as to finding out an evidence for the study and prevention of the arsenic exposure.

METHODSThe birth situation of neonate was surveyed from 1998 to 2004 in water arsenic exposure areas according to cross-sectional survey. The results were classified in accordance with ICD-10 and common surveillance of china. The population of Shanyin County served as the common people and the data were analyzed by SPSS 11.5 for windows.

RESULTSThe neonates surveyed were 2467 cases. There were 49 neonates deformity found in this investigation, giving a neonate deformity rate of 198.62 per 10,000 cases, which was shown significantly higher in water arsenic exposure areas than in the normal (U = 3.23, P < 0.01), with types of nervous system deformity, limbs deformity and congenital heart disease as in system classification. There was no significant difference of deformity rate in different sex neonates (chi2 = 0.32, P > 0.05).

CONCLUSIONThe drinking high-arsenic water over a long period of time should be a risk factor of neonate deformity. Prevention and treatment of endemic arsenic exposure should be urgently needed.

Arsenic ; analysis ; Arsenic Poisoning ; complications ; epidemiology ; Congenital Abnormalities ; epidemiology ; etiology ; Cross-Sectional Studies ; Environmental Exposure ; analysis ; Female ; Humans ; Infant, Newborn ; Male ; Water ; analysis ; Water Pollutants, Chemical ; analysis ; Water Supply ; analysis

OBJECTIVETo investigate the effects of mRNA transcriptional and protein expressions of protein kinase Cδ (PKCδ) on the development of arsenic liver injury caused by coal-burning.

METHODSPopulation study:133 arsenic exposures were selected as arsenic exposure groups including the ward non-patient group (25 cases) , no obvious hepatopathy group (38 cases) , mild (43 cases) and moderate to severe hepatopathy group (27 cases) from the area with endemic arsenism in Guizhou province. Another 34 healthy residents were selected as the control group in non-arsenic pollution village. The urine and peripheral blood were collected from the subjects. The arsenic contents in urine and mRNA expressions of PKCδ in peripheral blood were detected. Animal experiment study:thirty wistar rats were randomly by random number table divided into control group, drinking water arsenic poisoning group and coal-burning arsenic poisoning group (i.e., low, medium and high arsenic contaminated grain group) by random number table method, including 6 rats in each group. The control group was fed normally for 3 months, drinking water arsenic poisoning group and coal-burning arsenic poisoning groups were fed respectively with 10 mg/kg As2O3 solution and different concentrations (25, 50 and 100 mg/kg) of arsenic-containing feed which was persisted 3 months. The arsenic contents in urine, mRNA expression levels of PKCδ in peripheral blood and liver tissue and the protein expression levels of phosphorylated protein kinase Cδ(pPKCδ) in liver tissue were detected.

RESULTSThe median(quartile) of arsenic contents in urine were 25.58 (18.62-40.73), 56.66 (38.93-76.77), 64.90 (39.55- 98.37) and 75.47 (41.30-109.70) µg/g Cr respectively for the non-patient group, no obvious hepatopathy group, mild and moderate to severe hepatopathy group. The levels were higher than that in the control group (23.34 (17.84-37.45) µg/g Cr) (P < 0.05), except for the ward non-patient group. The arsenic contents in rat urine were 2223.61 (472.98-3976.73), 701.16 (194.01-1300.27), 1060.94 (246.33-2585.47) and 3101.11 (1919.97-5407.07) µg/g Cr, respectively for the drinking water arsenic poisoning group, the low, medium and high dosage arsenic grain contamination groups, all higher than that in the control group (94.32 (22.65-195.25) µg/g Cr) (P < 0.05) . The protein expressions of pPKCδ in liver tissue were 324.83 ± 25.06, 278.50 ± 30.57, 308.83 ± 34.67 and 326.33 ± 35.09, which were significantly higher than that in the control group (240.17 ± 28.07) (P < 0.05) . The protein expression levels of pPKCδ in liver cell membrane were 0.49 ± 0.06,0.33 ± 0.05,0.37 ± 0.06 and 0.50 ± 0.08, which were significantly higher than that in the control group (0.28 ± 0.04) (P < 0.05) . The protein expression levels of pPKCδ in liver cell cytoplasm were 0.38 ± 0.06,0.31 ± 0.05, 0.35 ± 0.05 and 0.36 ± 0.05, which were significantly higher than that in the control group (0.24 ± 0.05) (P < 0.05).

CONCLUSIONThe arsenic may regulate protein expressions of pPKCδ and induce its membrane translocation, and cause the development of arsenic liver injury caused by coal-burning.

Animals ; Arsenic ; urine ; Arsenic Poisoning ; epidemiology ; metabolism ; Case-Control Studies ; China ; epidemiology ; Coal ; Environmental Exposure ; Female ; Humans ; Liver ; enzymology ; pathology ; Liver Diseases ; enzymology ; etiology ; Male ; Protein Kinase C-delta ; metabolism ; Rats ; Rats, Wistar

OBJECTIVEAnalyses of bladder cancer mortality in the Black Foot Disease (BFD) endemic area of southwest Taiwan conducted by Morales et al. showed a discontinuity in risk at 400 microg/L arsenic in the drinking water in a stratified analysis and no discontinuity in a continuous analysis. As the continuous analysis presentation had been used by both the NRC and the EPA to assess the carcinogenic risk from arsenic ingestion, an explanation of the discontinuity was sought.

METHODSReview of 40 years of published health studies of the BFD-endemic area of SW Taiwan showed that earlier publications had limited their cancer associations with arsenic levels in artesian well waters and that the reports of Morales et al., NRC, and EPA failed to do so. Underlying data for the Morales et al. study were obtained from the appendix to the NRC report. Bladder cancer mortality rates were calculated from case counts and person-years of observation for each study village. Villages were categorized by water source according to the descriptions from the underlying study. Graphic and regression analyses were conducted of the bladder cancer mortality rates using exposure as a continuous variable and simultaneously stratifying by water source.

RESULTSThe median village well arsenic levels ranged from 350 to 934 microg/L for villages solely dependent on artesian well water and from 10 to 717 microg/L for villages not solely dependent on artesian well water. Bladder cancer mortality rates were found to be dependent upon the arsenic level only for those villages that were solely dependent on artesian well water for their water source. Bladder cancer mortality rates were found to be independent of arsenic level for villages with non-artesian well water sources.

CONCLUSIONSThe data indicate that arsenic exposure levels do not explain the bladder cancer mortality risk in SW Taiwan among villages not dependent upon artesian well water. The association for villages dependent upon artesian well water may be explained either by arsenic acting as a high-dose carcinogen or in artesian well water as a co-carcinogen with some other aspect of artesian well water (possibly humic acid). Arsenic exposure level alone appears to be an insufficient exposure measure to describe the risk of bladder cancer mortality in the BFD-endemic area. Risk analyses that fail to take water source into account are likely to misrepresent the risk characterization, particularly at low arsenic levels.

Adolescent ; Adult ; Aged ; Arsenic Poisoning ; complications ; epidemiology ; Child ; Child, Preschool ; Death Certificates ; Environmental Exposure ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Mortality ; trends ; Retrospective Studies ; Risk Assessment ; Taiwan ; epidemiology ; Urinary Bladder Neoplasms ; etiology ; mortality ; Water Supply