No abstract available.
Arsenic*

This study introduced the arsenic and arsenic intoxication in the world, especially in arsenic contaminated drinking water in Bangladesh. The study on the 1,200 samples of drinking water from drilling well in Hanoi and surround areas of river delta by the Center for Fresh Water and Environmental Hygiene of the Ministry of Agriculture and Rural Development found that there was a high contaminated level for the geological layer Holocene in the river delta.
Arsenic ; Poisoning

No abstract available.
Arsenic* ; Keratosis*

Arsenic ; toxicity ; Arsenic Poisoning ; Ecotoxicology

No abstract available.
Arsenic ; Parkinsonian Disorders

Study on vegetables, fruits and tubers surround Thai Nguyen Colour Metal Refinery Factory showed that: levels of lead and arsenic in the vegetable, fruits and tubers were higher than allowed standards. These levels were higher 2-5 times than these in the control were
Lead ; Arsenic ; Food Contamination

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

To elucidate arsenic-induced oxidative DNA damage, the genotoxicity of arsenic in human cells was comparatively studied with single cell gel electrophoresis (SCGE) assay in combination with the observation of the protective effects of dimethyl sulfoxide (DMSO) and catalase. Arsenic, at the concentration of 2.4 μM by coincubation for 24 hours, significantly induced DNA damage in HL60, a human promyelocytic leukemia cell line. In contrast, significant DNA damage was found in human mononucleocytes at the concentration of 4.8 μM or above. The cells were incubated separately with DMSO (12 mM/l), a well-known hydroxyl radical (OH-) scavenger, and catalase (1,300 U/ml), a hydrogen peroxide (H2O2) scavenger, for 6 hours and then further coincubated with various concentrations of arsenic for 24 hours at 37°C and 5% CO2. The findings showed that both DMSO and catalase significantly reduced the arsenic-induced tail moment, a parameter of total damaged DNA, in HL60 and mononucleocytes. Hence our findings indicate that arsenic, with micromolar concentrations, induces typical and various extents of DNA damage in human cells via reactive oxygen species in a dose-dependent manner.
Human ; DNA Damage ; Arsenic ; Dimethyl Sulfoxide ; Arsenic measurement

OBJECTIVETo investigate the changes of genetic damage in patients with arsenism caused by coal-burning in 9 years. To analyze the relationship between the changes of genetic damage and disease progression and provide a basis for condition monitoring.

METHODSOf 206 arsenism patients from the area with endemic arsenism in Guizhou province were tracking surveyed in February 1998 and divided into 4 groups, including suspicious, mild, moderate and severe poisoning group. Another 67 healthy residents from a neighbour township 12 km away where arsenic was not prevalent were surveyed. Over a 9-year follow-up, 131 arsenism patients and 45 controls with the complete biochemical indexes among them were selected as subjects in December 2006. Arsenic (As) concentration of urine and hair were detected by silver diethyldithiocarbamate spectrophotometry (Ag-DDC). Micronucleis (MN) and chromosome aberrations (CA) were analyzed by conventional methods. DNA single-strand breaks of peripheral blood were measured by single cell gel electrophoresis (SCGE), and the tail lengths of comet were used to measure DNA damage.

RESULTSAmong the control, suspicious, mild, moderate and severe arsenic poisoning group, the As contents of urine and hair were respectively (34.16 ± 10.25), (52.35 ± 22.41), (62.26 ± 31.13), (71.43 ± 49.92), (78.45 ± 50.64) µg/L and (1.37 ± 0.56), (3.69 ± 1.78), (4.88 ± 3.49), (5.21 ± 3.10), (6.25 ± 4.04) µg/g in 2006, which were lower than that 9 years before (urine as contents were (36.07 ± 20.70), (73.65 ± 41.33) , (90.92 ± 82.14) , (126.55 ± 107.31) and (139.44 ± 90.90) µg/L, and hair As contents were (1.41 ± 1.18), (4.85 ± 4.20), (5.72 ± 4.07) , (6.43 ± 4.32) and (7.19 ± 4.68) µg/g, respectively, F value was 10.63, 7.72, 14.66, 11.00 respectively, all P values were < 0.05). Except for suspicious poisoning group, the differences of urine As contents in the other groups all showed significance (P < 0.05). The incidences of MN were (0.238 ± 0.130) %, (0.268 ± 0.192) %, (0.283 ± 0.157) % and (0.391 ± 0.233)%; the incidences of CA were (14.36 ± 5.44) %, (18.09 ± 6.49) %, (19.38 ± 5.63)% and (19.83 ± 5.84) %; the tail lengths of comet were (29.88 ± 13.81) , (29.84 ± 12.80) , (34.50 ± 9.88) and (41.58 ± 12.98) µm respectively in 2006 for all poisoning groups; which were higher than that 9 years before(the incidences of MN were (0.163 ± 0.051) %, (0.186 ± 0.117) %, (0.196 ± 0.104) % and (0.273 ± 0.142) %; the incidences of CA were (13.18 ± 5.17)%, (14.48 ± 6.61)%, (15.67 ± 8.49) % and (16.90 ± 8.38) %; the tail lengths of comet were (15.07 ± 12.93) , (19.57 ± 8.80) , (27.03 ± 10.77) and (34.71 ± 14.95) µm) , except for the incidences of MN and CA in suspicious poisoning group and of MN in mild poisoning group , the differences of the three indexes in the other groups were significant (P < 0.05) . The state of illness of arsenic poisoning patients aggravated 9 years later. With the increase of urine and hair As contents and the development of arsenism, the incidences of MN, CA and the tail lengths of comet of all poisoning groups increased. There were positive correlations among them (r values were respectively 0.212, 0.316, 0.232, 0.263, 0.321, 0.654 and 0.760) (P < 0.05).

CONCLUSIONThe exacerbation of genetic damage was related to constantly high arsenic loads. The accumulation of genetic damage and its irreversibility might be one of the important reasons of the development of arsenism and cancer.

A 29-year-old male with eleven-year history of hyperkeratotic papules and speckled pigmentation developed cutaneous squamous cell carcinoma. Arsenicosis was confirmed by elevated hair arsenic level, and histopathologic findings of arsenical keratosis and one lesion showing carcinoma-in-situ. Chronic arsenic exposure has been found to activate inflammatory and carcinogenic pathways leading to development of pre-malignant and malignant lesions. A multi-disciplinary approach involving healthcare specialists and environmentalists is crucial in source control and management of long-term complications.
Arsenic ; Arsenic Poisoning ; Carcinoma, Squamous Cell ; Carcinoma In Situ