期刊论文详细信息
BMC Public Health
Arsenic exposure through drinking water increases the risk of liver and cardiovascular diseases in the population of West Bengal, India
Ashok K Giri7  J Christopher States4  Apurba K Bandyopadhyay7  Papiya Majumder2  Saptarshi Banerjee5  Santanu Basu3  Tanmoy J Sau1  Nilendu Sarma6  Niladri S Majumder7  Nilanjana Banerjee7  Debmita Chatterjee7  Somnath Paul7  Nandana Das7 
[1] Department of Medicine, Calcutta National Medical College, Kolkata, 700 017, West Bengal, India;Tata Main Hospital, Jamshedpur, 831001, Jharkhand, India;Department of General Medicine, Sri Aurobindo Seva Kendra, Kolkata, 700068, West Bengal, India;Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, 40209, USA;Regional Institute of Opthalmology, Calcutta Medical College, Kolkata, 700073, West Bengal, India;Sir Nil Ratan Sircar Medical College and Hospital, Kolkata, 700 014, India;Molecular and Human Genetics Division, CSIR- Indian Institute of Chemical Biology, 4, Raja S. C. Mullick Road, Kolkata, 700 032, India
关键词: Cytokines;    Liver function tests;    Antinuclear antibody;    Arsenic;   
Others  :  1163313
DOI  :  10.1186/1471-2458-12-639
 received in 2012-04-02, accepted in 2012-07-24,  发布年份 2012
PDF
【 摘 要 】

Background

Arsenic is a natural drinking water contaminant affecting 26 million people in West Bengal, India. Chronic arsenic exposure causes cancer, cardiovascular disease, liver disease, neuropathies and ocular diseases. The aims of the present study were to assess bioindicators of hepatocellular injury as indicated by the levels of liver enzymes, to determine the auto immune status, as indicated by the amounts of anti-nuclear antibodies (ANA) and anti-dsDNA antibodies in their serum, and to predict cardiovascular risk in the arsenic exposed population.

Methods

Effect of chronic arsenic exposure on liver was determined by liver function tests. Autoimmune status was measured by measuring ANA and anti-dsDNA in serum. Inflammatory cytokines associated with increased cardiovascular disease risk, IL6, IL8 and MCP-1 were determined.

Results

Our results indicated that serum levels of bilirubin, alanine transaminase, aspartate transaminase, alkaline phosphatase and ANA were increased in the arsenic exposed population. Serum levels of IL6 and IL8 also increased in the arsenic exposed group.

Conclusions

Chronic arsenic exposure causes liver injury, increases the serum levels of autoimmune markers and imparts increased cardiovascular risk.

【 授权许可】

   
2012 Das et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150413094759260.pdf 225KB PDF download
【 参考文献 】
  • [1]Chakraborti D, Das B, Rahman MM, Chowdhury UK, Biswas B, Goswami AB, Nayak B, Pal A, Sengupta MK, Ahamed S, Hossain A, Basu G, Roychowdhury T, Das D: Status of groundwater arsenic contamination in the state of West Bengal, India: A 20-year study report. Mol Nutr Food Res 2009, 53:542-551.
  • [2]World Health Organisation: WHO Guidelines for drinking water quality: Health criteria and other supporting information. Vol. 2. 2nd edition. WHO, Geneva; 1996:940-949.
  • [3]USEPA: EPA Drinking Water News.  ,  ; . http://www.nesc.wvu.edu/ndwc_news_EPA.htm/ webcite (Accessed on May, 2010)
  • [4]Mandal BK, Roy Chowdhury T, Samanta G, Basu GK, Chowdhury PP, Chanda CR, Lodh D, Saha KC, Mukherjee SK, Roy S, Kabir S, Quamruzzaman Q, Chakraborti D: Arsenic in ground water in seven districts of West Bengal, India-the biggest arsenic calamity in the world. Curr Sci 1996, 70:976-986.
  • [5]Banerjee M, Sarkar J, Das JK, Mukherjee A, Sarkar AK, Mondal L, Giri AK: Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosome aberrations. Carcinogenesis 2007, 28(Suppl 3):672-676.
  • [6]States JC, Srivastava S, Chen Y, Barchowsky A: Arsenic and Cardiovascular disease. Toxicol Sci 2009, 107(Suppl 2):312-323.
  • [7]Tseng CH: The potential biological mechanisms of arsenic induced diabetes mellitus. Toxicol Appl Pharmacol 2004, 197:67-83.
  • [8]Ghosh P, Banerjee M, De Chaudhuri S, Chowdhury R, Das JK, Mukherjee A, Sarkar AK, Mondal L, Baidya K, Sau TJ, Banerjee A, Basu A, Chaudhuri K, Ray K, Giri AK: Comparison of health effects between individuals with and without skin lesions in the population exposed to arsenic through drinking water in West Bengal, India. J Expo Sci Environ Epidemiol 2007, 17(Suppl 3):215-223.
  • [9]Guha Mazumder DN: Effect of chronic intake of arsenic-contaminated water on liver. Toxicol Appl Pharmacol 2005, 206:169-175.
  • [10]Banerjee N, Banerjee M, Ganguly S, Bandyopadhyay S, Das JK, Bandyopadhay A, Chatterjee M, Giri AK: Arsenic induced mitochondrial instability leading to programmed cell death in exposed individuals. Toxicology 2008, 246(Suppl 2–3):101-111.
  • [11]Guha Mazumder DN: Chronic arsenic toxicity: clinical features, epidemiology and treatment: experience in West Bengal. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003, 38(Suppl 1):141-163.
  • [12]Basu A, Ghosh P, Das JK, Banerjee A, Ray K, Giri AK: Micronuclei as biomarkers of carcinogen exposure in populations exposed to arsenic through drinking water in West Bengal, India: a comparative study in 3 cell types. Cancer Epidemiol Biomarkers Prev 2004, 13:820-827.
  • [13]Benramdane L, Accominotti M, Fanton L, Malicier D, Vallon JJ: Arsenic speciation in human organs following fatal arsenic trioxide poisoning-a case report. Clin Chem 1999, 45:301-306.
  • [14]Guha Mazumder DN, Haque R, Ghosh N, De BK, Santra A, Chakraborti D, Smith AH: Arsenic in drinking water and the prevalence of respiratory effects in West Bengal, India. Int J Epidemiol 2000, 29:1047-1052.
  • [15]Liu DN, Lu XZ, Li BL, Zhou DX, Li FX, Zheng DH, Wang KH: Clinical analysis of 535 cases of chronic arsenic poisoning from coal burning. Chin J Med 1992, 31:560-562.
  • [16]Zhang AH, Huang XX, Jiang XY, Luo P, Guo YC, Xue SZ: The progress of study on endemic arsenism due to burning arsenic containing coal in Guizhou province. Metal Ions Biol Med 2000, 6:53-55.
  • [17]Lu T, Liu J, LeCluyse EL, Zhou YS, Cheng ML, Waalkes MP: Application of cDNA microarray to the study of arsenic-induced liver diseases in the population of Guizhou, China. Toxicol Sci 2001, 59:185-192.
  • [18]Guha Mazumder DN: Arsenic and Liver diseases. J Indian Med Assoc 2001, 6:311. 314-5, 318-320
  • [19]Arteel GE, Guo L, Schlierf T, Beier JI, Kaiser JP, Chen TS, Liu M, Conklin DP, Miller HL, Montfort C, States JC: Subhepatotoxic exposure to arsenic enhances lipopolysaccharide-induced liver injury in mice. Toxicol Appl Pharmacol 2008, 226:128-139.
  • [20]Straub AC, Stolz DB, Ross MA, Hernandez-Zavala A, Soucy NV, Klei LR, Barchowsky A: Arsenic stimulates sinusoidal endothelial cell capillarization and vessel remodeling in mouse liver. Hepatology 2007, 45:205-212.
  • [21]Styblo M, Hughes MF, Thomas DJ: Liberation and analysis of protein-bound arsenicals. J Chromatogr B Biomed Appl 1996, 677(Suppl 1):161-166.
  • [22]Wanchu AA: Antinuclear antibodies: clinical applications. J Post Grad Med 2000, 46(Suppl 2):144-148.
  • [23]Khuda-Bukhsh AR, Belon P, Biswas SJ, Karmakar SR, Banerjee P, Banerjee A, Guha B, Das JK, Pathak S, Choudhury SC, Bhattacharjee N: Is an elevated antinuclear antibody titer in subjects living in two groundwater arsenic contaminated villages indicative of a time-dependent effect of arsenic exposure. ESAIJ 2007, 2(Suppl 1):10-16.
  • [24]Cooper GS, Miller FW, Germolec DR: Occupational exposures and autoimmune diseases. Int Immunopharmacol 2002, 2:303-313.
  • [25]Baumann H, Gaildie J: The acute phase response. Immunol Today 1994, 15:74-80.
  • [26]Srivastava S, Vladykovskaya EN, Haberzettl P, Sithu SD, D'Souza SE, States JC: Arsenic exacerbates atherosclerotic lesion formation and inflammation in ApoE-/- mice. Toxicol Appl Pharmacol 2009, 241:90-100.
  • [27]Banerjee M, Sarma N, Biswas R, Roy J, Mukherjee A, Giri AK: DNA repair deficiency leads to susceptibility to develop arsenic-induced premalignant skin lesions. Int J Cancer 2008, 123(Suppl 2):283-287.
  • [28]Banerjee N, Banerjee S, Sen R, Bandhyopadhyay A, Sarma N, Majumder P, Das JK, Chatterjee M, Kabir SN, Giri AK: Chronic arsenic exposure impairs macrophage functions in the exposed individuals. J Clin Immunol 2009, 29(Suppl 5):582-594.
  • [29]De Chaudhuri S, Mahata J, Das JK, Mukherjee A, Ghosh P, Sau TJ, Mondal L, Basu S, Giri AK, Roychoudhury S: Association of specific p53 polymorphisms with keratosis in individuals exposed to arsenic through drinking water in West Bengal, India. Mutat Res 2006, 601(Suppl 1–2):102-112.
  • [30]Ghosh P, Basu A, Mahata J, Basu S, Sengupta M, Das JK, Mukherjee A, Sarkar AK, Mondal L, Ray K, Giri AK: Cytogenetic damage and genetic variants in the individuals susceptible to arsenic-induced cancer through drinking water. Int J Cancer 2006, 118(Suppl 10):2470-2478.
  • [31]Mahata J, Basu A, Ghoshal S, Sarkar JN, Roy AK, Poddar G, Nandy AK, Banerjee A, Ray K, Natarajan AT, Nilsson R, Giri AK: Chromosomal aberrations and sister chromatid exchanges in individuals exposed to arsenic through drinking water in West Bengal, India. Mutat Res 2003, 534:133-143.
  • [32]Chatterjee A, Das D, Mandal BK, Roychowdhury T, Samanta G, Chakraborti D: Arsenic in ground water in six districts of West Bengal, India: The biggest arsenic calamity in the world. I. Arsenic species in drining water and urine of the affected people. Analyst 1995, 120:643-650.
  • [33]Buchet JP, Lauwerys R, Roels H: Comparison of the urinary excretion of arsenic metabolites after a single dose of sodium arsenite, monomethylarsonate or dimethylarsinate in man. Int Arch Occup Environ Health 1981, 48(Suppl 1):71-79.
  • [34]States JC, Barchowsky A, Cartwright IL, Reichard JF, Futscher BW, Lantz RC: Arsenic toxicology: translating between experimental models and human pathology. Environ Health Perspect 2011, 119(Suppl 10):1356-1363.
  • [35]Banerjee N, Nandy S, Kearns JK, Bandyopadhyay AK, Das JK, Majumder P, Basu S, Banerjee S, Sau TJ, States JC, Giri AK: Polymorphisms in the TNF-α and IL10 gene promoters and risk of arsenic-induced skin lesions and other nondermatological health effects. Toxicol Sci 2011, 121(Suppl 1):132-139.
  • [36]Kundu M, Ghosh P, Mitra S, Das JK, Sau TJ, Banerjee S, States JC, Giri AK: Precancerous and non-cancer disease endpoints of chronic arsenic exposure: the level of chromosomal damage and XRCC3 T241M polymorphism. Mutat Res 2011, 706(Suppl 1–2):7-12.
  • [37]Thapa BR, Walia A: Liver function tests and their interpretation. Indian J Pediatr 2007, 74:663-671.
  • [38]Friedman SF, Martin P, Munoz JS: Laboratory evaluation of the patient with liver disease. Hepatology, a textbook of liver disease. Saunders publication, Philedelphia; 2003:661-709. 1
  • [39]Kaplan MM: Serum alkaline phosphatase- another piece is added to the puzzle. Hepatology 1986, 6:526-5531.
  • [40]Hagerstrand I: Distribution of alkaline phosphatise activity in healthy and diseased human liver tissue. Acta Pathol Microbiol Scand A 1975, 83(Suppl 5):519-526.
  • [41]Jansen PLM, Muller M: The molecular genetics of familial intrahepatic cholestasis. Gut 2000, 47:1-5.
  • [42]Goswami K, Gachhui R, Bandopadhayay A: Hepatorenal dysfunction in lead pollution. J Environ Sci Eng 2005, 47(Suppl 1):75-80.
  • [43]Halliwell B: Oxidants and human diseases. FASEB J 1987, 1(5):358-364.
  • [44]Ikeda M, Zhang ZW, Shimbo S, Watanabe T, Nakatsuka H, Moon CS, Matsuda-Inoguchi N, Higashikawa K: Urban population exposure to lead and cadmium in east and south-east Asia. Sci Total Environ 2000, 249(Suppl 1–3):373-384.
  • [45]Liu J, Zheng B, Aposhian HV, Zhou Y, Cheng ML, Zhang A, Waalkes MP: Chronic arsenic poisoning from burning high-arsenic containing coal in Guizhou, China. Environ Health Perspect 2002, 110:119-122.
  • [46]Zhou YS, Du H, Cheng ML, Liu J, Zhang XJ, Xu L: The investigation of death from diseases caused by coal-burning type of arsenic poisoning. Chin J Endemiol 2002, 21:484-486.
  • [47]Cooper GS, Gilbert KM, Greidinger EL, James JA, Pfau JC, Reinlib L, Richardson BC, Rose NR: Recent advances and opportunities in research on lupus: environmental influences and mechanisms of disease. Environ Health Perspect 2008, 116(Suppl 6):695-702.
  • [48]Haugbro K, Nossent J, Winkler T, Figenschau Y, Rekvig O: Anti-dsDNA antibodies and disease classification in antinuclear antibody positive patients: the role of analytical diversity. Ann Rheum Dis 2004, 63(Suppl 4):386-394.
  • [49]Olsson AR, Skogh T, Axelson O, Wingren G: Occupations and exposures in the work environment as determinants for rheumatoid arthritis. Occup Environ Med 2004, 61:233-238.
  • [50]Parks CG, Conrad K, Cooper GS: Occupational exposure to crystalline silica and autoimmune disease. Environ Health Perspect 1999, 107(Suppl 5):793-802.
  • [51]Bootsma H, Spronk P, Borg E, Hummel E, de Boer G, Limburg P, Kallenberg C: The predictive value of fluctuations in IgM and IgG class anti-dsDNA antibodies for relapses in systemic lupus erythematosus. A prospective long term observation. Ann Rheum Dis 1997, 56:661-666.
  • [52]Takeuchi K, Turley SJ, Tan EM, Pollard KM: Analysis of the autoantibody response to fibrillarin in human disease and murine models of autoimmunity. J Immunol 1995, 154(Suppl 2):961-971.
  • [53]Mendall MA, Patel P, Asante M, Ballam L, Morris J, Strachan DP, Camm AJ, Northfield TC: Relation of serum cytokine concentrations to cardiovascular risk factors and coronary heart disease. Heart 1997, 78:273-277.
  • [54]Koefler S, Nickel T, Weis M: Role of cytokines in cardiovascular diseases: focus on endothelial responses to inflammation. Clin Sci 2005, 108:205-213.
  • [55]Ridker PM, Rifai N, Pfeffer M, Sacks F, Lepage S, Braunwald E: Elevation of tumor necrosis factor-alpha and increased risk of recurrent coronary events after myocardial infarction. Circulation 2000, 101(18):2149-2153.
  • [56]Asanuma Y, Chung CP, Oeser A, Shiltani A, Stanley E, Raggi P, Stein CM: Increased concentration of pro-artherogenic inflammatory cytokine in systemic lupus erythematos: relationship to cardiovascular risk factor. J Rheumatol 2006, 33(Suppl 3):539-545.
  • [57]Navas-Acien A, Sharrett AR, Silbergeld EK, Schwartz BS, Nachman KE, Burke TA, Guallar E: Arsenic exposure and cardiovascular disease: a systematic review of the epidemiologic evidence. Am J Epidemiol 2005, 162(Suppl11):1037-1049.
  • [58]Wu MM, Chiou HY, Ho IC, Chen CJ, Lee TC: Gene expression of inflammatory molecules in circulating lymphocytes from arsenic-exposed human subjects. Environ Health Perspect 2003, 111(Suppl 11):1429-1438.
  • [59]Morse D, Choi AM: Heme oxygenase-1: the "emerging molecule" has arrived. Am J Respir Cell Mol Biol 2002, 27(Suppl 1):8-16.
  • [60]Fainboim L, Cherñavsky A, Paladino N, Flores AC, Arruvito L: Cytokines and chronic liver disease. Cytokine Growth Factor Rev 2007, 18(Suppl 1–2):143-157.
  文献评价指标  
  下载次数:7次 浏览次数:10次