1.Arsenic and arsenic intoxication from drinking water
Journal of Medical and Pharmaceutical Information 1999;(6):8-11
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
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Poisoning
3.Arsenic chronically intoxication from tube well water at some areas in Red river and Mekong river delta
Journal of Practical Medicine 2005;519(9):14-17
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
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Poisoning
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Water
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Epidemiology
4.Speckled pigmentation and palmoplantar keratoses leading to the mass detection of chronic arsenic poisoning.
Sheena Maureen T. SY ; Charissa Mia SALUD-GNILO ; Ella Joy NOGAS-PEREZ
Acta Medica Philippina 2017;51(2):146-149
Arsenic is a known human carcinogen and skin manifestations are the earliest and most specific markers of chronic arsenic poisoning. A 43-year-old man from Luzon presented at the Section of Dermatology with a one-year history of hyperkeratotic papules and plaques on the palms and soles. Numerous round hypopigmented macules were scattered on the upper back. Initial 24-hour urine arsenic level was elevated at 288mcg/liter. The patient underwent successful chelation with N-acetylpenicillamine and the palmoplantar keratoses were treated with cryotherapy and topical 20% salicylic acid in white petrolatum. In cooperation with the Department of Health, a comprehensive health and environmental assessment was conducted in the affected communities. This case highlights the role of dermatologists in the diagnosis and management of this public health problem.
Arsenic Poisoning ; Philippines ; Keratoderma, Palmoplantar
5.Relationship between changes of genetic damage and development of disease in patients with arsenism caused by coal-burning.
Xilan WANG ; Aihua ZHANG ; Jingyuan YANG ; Tingting XIE ; Jun LI ; Bixia ZHANG ; Xuexin DONG ; Xiaoxin HUANG
Chinese Journal of Preventive Medicine 2014;48(7):607-611
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.
Arsenic ; Arsenic Poisoning ; Coal ; DNA Damage ; Follow-Up Studies ; Humans
6.Arsenicosis presenting with cutaneous squamous cell carcinoma: A case report.
Marie Len A. CAMACLANG ; Eileen Liesl A. CUBILLAN ; Claudine YAP-SILVA
Acta Medica Philippina 2019;53(2):171-176
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
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Arsenic Poisoning
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Carcinoma, Squamous Cell
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Carcinoma In Situ
8.Study on lead and arsenic poisoning status of workers at Thai Nguyen Color Metal Company.
Journal of Practical Medicine 2004;474(3):32-34
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
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Lead
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Arsenic Poisoning/epidemiology
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Epidemiology
9.Research progress on the regulatory mechanism of non-coding RNA in arsenic toxicity.
Ning BU ; Hai Yan SONG ; Su Hua WANG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2022;40(4):316-320
Arsenic is a non-metallic element, and the International Agency for Research on Cancer has identified arsenic and its compounds as carcinogens. Arsenic and its compounds can be absorbed through the respiratory tract, skin and digestive tract, distributed in the liver, kidney, lung and skin, and cause damage. Non-coding RNAs are closely related to arsenic-induced nervous system disorders, cell necrosis, reproductive toxicity, and carcinogenesis. In recent years, the network regulation of microRNAs (miRNAs) , long non-coding RNAs (lncRNAs) , and circular RNAs (circRNAs) among non-coding RNAs in various diseases induced by arsenic has become a new research field. This paper summarizes the existing scientific research results, and expounds the mechanism of miRNAs, lncRNAs and circRNAs in arsenic toxicity, and provides basic data and theoretical basis for the prevention and treatment of arsenic poisoning.
Arsenic/toxicity*
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Arsenic Poisoning
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Humans
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MicroRNAs/genetics*
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RNA, Circular
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RNA, Long Noncoding/genetics*