EXPOSIÇAO AOS POLUENTES DA QUEIMA DE CANAVIAIS E O RISCO PARA SAUDE

(especial para SIIC © Derechos reservados)
Esta revisão aborda a interação entre o ambiente e a herança genética no aparecimento do câncer, assim como apresenta as ferramentas disponíveis para a detecção do risco de exposição a esses compostos, facilitando a aplicação de estratégias de prevenção da doença.
bosso9.jpg Autor:
Rosa maria Bosso,
Columnista Experto de SIIC

Institución:
Instituto de Biociências, Letras e Ciências Exatas Universidade Estadual Paulista (UNESP)


Artículos publicados por Rosa maria Bosso,
Coautor
Nívea Conforti-Froes.* 
Doutor em Genética, Pós-Doutor em Medicina Preventiva. Universidade Estadual Paulista (UNESP). Instituto de Biociencias, Letras e Ciencias Exatas, campus de Sao José do Rio Preto.*
Recepción del artículo
21 de Abril, 2004
Aprobación
3 de Agosto, 2004
Primera edición
6 de Diciembre, 2004
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
No Brasil, na época da colheita da cana-de-açúcar, costuma-se queimar previamente a plantação para facilitar o corte. No período da safra, os cortadores de cana estão expostos a vários produtos originados da combustão de matéria orgânica, incluindo os hidrocarbonetos aromáticos policíclicos (polycyclic aromatic hydrocarbons [PAHs]), compostos já conhecidos por sua ação mutagênica e/ou carcinogênica. O cortadores de cana também apresentam um aumento de problemas respiratórios, possivelmente resultante da exposição aos poluentes originados da queima de canaviais. Muitas das enzimas envolvidas no processos de ativação e destoxificação dos PAHs são polimórficas. Os polimorfismos genéticos podem desempenhar um papel importante no aumento da suscetibilidade a tumores induzidos por xenobióticos. Esta revisão aborda a interação entre o ambiente e a herança genética no aparecimento do câncer, assim como apresenta as ferramentas disponíveis para a detecção do risco de exposição a esses compostos, facilitando a aplicação de estratégias de prevenção da doença.

Palabras clave
Hidrocarbonetos aromáticos policíclicos, cana-de-açúcar queimada, polimorfismos genéticos, poluentes ambientais, estratégias de prevenção do câncer


Artículo completo

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Abstract
In Brazil, the leaves of the sugar cane are burnt before harvesting in order to make the process of cutting easier. During the harvest time, the sugar cane workers are exposed to various combustion products of organic materials including polycyclic aromatic hydrocarbons (PAHs) which are known to be mutagenic and/or carcinogenic. The workers also have an increased risk of lung respiratory disorders, possibly due to pollutants exposure derived from the practice of burning foliage during the cane-cutting time. Many of the enzymes involved in the activation and detoxification processes of PAHs are genetically polymorphic. Genetic polymorphims can play an important role in increasing susceptibility to xenobiotic-induced tumors. This review approaches the interaction between environmental pollutants and genetic inheritance in the carcinogenic process, as well as the current available tools for risk detection of environmental exposure, thus enabling the application of cancer-prevention public strategies.

Key words
Polycyclic aromatic hydrocarbons (PAHs), sugar cane burnt, genetic polymorphism, environmental pollutants, cancer prevention strategies


Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Medicina del Trabajo, Oncología
Relacionadas: Bioquímica, Epidemiología, Genética Humana, Salud Pública



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Bosso, Rosa Maria
Bibliografía del artículo
  1. UNICA. União da AgroindUstria Canavieira de São Paulo. 2004; http://www.Unica.com.br/pages/sociedade_desenvol1.asp.
  2. UNICA. União da AgroindUstria Canavieira de São Paulo. 2004; http://www.Unica.com.br/files/informacaounica/unica57.pdf.
  3. Schoket B. DNA Damage in humans exposed to environmental and dietary polycyclic aromatic hydrocarbons. Mutat Res 1999; 424(2):143-53.
  4. Van Houdt JJ. Mutagenic activity of airborne particulate matter in indoor and outdoor environments. Atmos Environ 1990;24B:207-20.
  5. Lewtas J, Lewis C, Zweidinger R, et al. Sources of genotoxicity and cancer risk in ambient air. Pharmacogenetics 1992;2(6):288-96.
  6. Hartzell, GE. Overview of combustion toxicology. Toxicology 1996;115:7-23.
  7. Deportes I, Guyod J, Zmirou D. Hazard to man and the environment posed by the use of urban waste compost: a review. The Sci of the Total Environ 1995;172:197-222.
  8. Bartsch H. Studies on biomarkers in cancer etiology and prevention: a summary and challenge of 20 years of interdisciplinary research. Mutat Res 2000;462:255-79.
  9. EPA. Environmental Protection Agency. Method TO-13A determination of polycyclic aromatic hydrocarbons (PAHs) In ambient air using gas chromatography/mass spectrometry (GC/MS). Washington: Environmental Protection Agency: 1999. p.78.
  10. NIOSH. National Institute of Occupational Safe and Health. Polynuclear aromatic hydrocarbons by HPLC: Method 5506. Cicinatti: 1998. p9.
  11. Dipple A, Chaucheng S, Bigger A. Polycycliclic aromatic hydrocarbon carcinogens. Mutag Carcinog Diet 1990:109-27.
  12. Miller E, Miller J. The mutagenicity of chemical carcinogens: correlations, problems and interpretations . In: Hollaender A, editor. Chemical Mutagen. New York:Plenum; 1971.p.83-119.
  13. Vo Dinh T. Chemical analysis of polycyclic aromatic compounds. In: Vicent JH, editor. Aerosol samplim. New York:John Wiley and Sons; 1989. p.17-21.
  14. Kim SJ, Jajoo HK, Kim HY, et al. An efficient route to N6 deoxyadenosine adducts of diol epoxide of csrcinogenic polycyclic aromatic hydrocarbons. Bioorg. Med. Chem 1995;3(6):811-22.
  15. Peltonen K, Dipple A. Polycyclic aromatic hydrocarbons: chemistry of DNA adduct formation. J Occup Environ Med 1995;37(1):52-8.
  16. Dipple A, Moschel R. Chemistry of DNA alkylation and aralkylation. In Mutation and Environmental. Wiley:Liss Inc; 1990. p.71-80.
  17. Doerjer G, Bedell MA, Oesch F. DNA adducts and their biological relevance. In: OBE G, editor. Mutations in Man. Berlin: Springer-Verlag; 1984. p.20-34.
  18. Canella K, Peltonen K, Dipple A. Identification of (+) and (-) anti benzo(a)pyrene dihydrodiol epoxide-nucleic acid adducts by the 32P-postlabeling assay. Carcinogenesis 1991;12:1826-31.
  19. Weston A, Bowman E, Manchester D, Harris C. Fluorescence detection of lesions in DNA. In: Sutherland B, Woodheah A, editores. DNA Damage and Repair in Human Tissues. New York:Plenum; 1990. p.63-81.
  20. IARC. International Agency for Research on Cancer. 2003; http://193.51.164.11/monoeval/crthall.html.
  21. Sakiara KA. Otimização e validação de metodologia para determinação de 1-hidroxipireno em urina [dissertação]. Araraquara (SP): Instituto de Química/UNESP; 2001.
  22. WHO. World Health Organization. Selected non-heterocyclic aromatic hydrocarbons. Genova: 1998. p.883.
  23. Friedberg GC, Walker, GC, Siede, W. DNA repair and mutagenesis. Washington: ASM Press; 1995.
  24. Barret JC. Mechanisms of multistep carcinogenesis and carcinogen risk assessment. Environ Health Perspect 1993;100:9-20.
  25. Lewin, B. Genes VI. Oxford: Oxford University Press; 1997.
  26. Cohen LA. Diet and Cancer. Sci. Am 1987;257:42-8
  27. Yamasaki H, Asby J, Bignami M, et al. Nongenotoxic carcinogens: development of detection methods based on mechanisms: a European project. Mutat Res 1996;353:47-63.
  28. Sikora K. Developing a Global Strategy for Cancer. Eur J Cancer 1999;35:1870-7.
  29. Ramel C. Pollution, carcinogenesis and cancer prevention. Acta Oncol 1991;30:27-33.
  30. Delclos KB, Manjanatha, MG, Li, EE, et al. 32P- postlabelling in studies of arylamine and nitroatomatic hydrocarbon activation and mutagenesis. IARC Sci Publ 1993;124:79-86.
  31. Davidson BJ, Hsu TC, Schantz SP. The genetics of tabacco-induced malignancy. Arch Otolaryngol Head Neck Surg 1993;199:1198-205.
  32. Scully C. Oncogenes, tumor suppressors and viruses in oral squamous carcinoma. J Oral Pathol Med 1993;22:337-47.
  33. Kaderlik KR, Kadlubar FF. Metabolic polymorphism and carcinogen-DNA adduct formation in human populations. Pharmacogenetics 1995;5:108-17.
  34. Ames BN, Gold LS, Willett VC. The causes and prevention of cancer. Proc Natl Acad 1995;92:5258-65.
  35. Motykiewicz G, Michalska J, Pendzich J, et al. A cytogenetic study of men envoronmentally and occupationally exposed to airbone pollutants. Mutat Res 1992;280:253-9.
  36. Hatjian BA, Edwards JW, Harrison J, et al. Ambient, biological and biological effect monitorng of exposure to polycyclic aromatic hydrocarbons (PAHs). Toxicol Lett 1995;77:271-279.
  37. Sato MI, Valent GU, Coimbrão CA, et al. Mutagenicity of airborne particulate organic material from urban and industrial areas of Sao Paulo, Brazil. Mutat Res 1995;335:317-30.
  38. Vargas VMF, Horn, RC, Guidobono RR, et al. Mutagenic activity of. aerborne particulate matter from the urban area of. Porto Alegre, Brazil. Genet Mol Biol 1998;21:247-53.
  39. Zamperlini GCM, Silva MRS, Vilegas W. Identification of polycyclic hidrocarbons in sugar cane soot by gas chromatography-mass spectrometry. Chromatographia 1997;46:655-63.
  40. Bosso RMV. Avaliação da atividade mutagênica da fuligem sedimentável proveniente da queima da cana-de açUcar e da urina dos cortadores de cana através de ensaios com mutação gênica reversa em Salmonella typhimurium [dissertação]. São José do Rio Preto (SP): Instituto de Biociências, Letras e Ciências Exatas/Universidade Estadual Paulista; 2000.
  41. Amre DK, Infante-Rivard C, Dufresne A, et al. Case-Control study of lung cancer among sugar cane farmers in India. Occup Environ Med 1999;56:548-52.
  42. Pavanello S, Clonfero E. Biological indicadors of genotoxic risk and metabolic polymorphisms. Mutat Res 2000;465:285-308.
  43. Jongeneelen F. Methods for routine biological monitoring of carcinogenic PAH- mixtures. Science Total Environ 1987;199:141-9.
  44. Dor F, Dab W, Emperur-Bissonnet P, Zmirou D. Validity of Biomarkers in Environmental Health studies: the case of PAHs and benzene. Crit Rev Toxicol 1999;29(2):129-68.
  45. Singh R, Tucek M, Maxa K, et al. A rapid and simple method for the analysis if 1-hydroxypyrene glucuronide: a potential biomarker for polycyclic aromatic hydrocarbon exposure. Carcinogenesis 1995;16(12):2909-15.
  46. Jongeneelen F. Biological Monitoring of environmental exposure to polycyclic aromatic hydrocarbons: 1-hydroxypyrene in urine of people. Toxicol lett 1994;72:205-11.
  47. Kriek E, Rojas M, Alexandrov K, et al. Polycyclic aromatic hydrocarbon-DNA adducts in humans: relevance as biomarkers for exposure and cancer risk. Mutat Res 1998;400:215-31
  48. Perera FP, Weinstein IB. Molecular epidemiology: recent advances and future directions. Carcinogenesis 2000;21:517-24.
  49. Lang M, Pelkonen O. Metabolism of xenobiotics and chemical carcinogenesis. IARC 1999;148:13-22.
  50. Kawajiri K, Watanabe J, Gotoh O, et al. Structure and drug inducibility of the human cytochrome P-450c gene. Eur J Biochem 1986;159:219-25.
  51. Taningher M, Malacarne D, Izzotti A, et al. Drug metabolism polymorphisms as modulators of cancer susceptibility. Mutat Res 1999;436:227-61.
  52. The human cytochrome P450 (cyp) allele nomenclature committee. 2004; http//www.imm.ki.se/CYPalleles.
  53. Garte S. The role of ethnicity in cancer susceptibility gene polymorphisms: the example of CYP1A1. Carcinogenesis. 1998;19:1329-32.
  54. Kawajiri K, Nakachi K, Imai K, et al. Identification of genetically high risk individuals to lung cancer by DNA polymorphisms of cytochrome P450 1A1 gene. FEBS Let 1990;263(1):131-3.
  55. Hayashi S-I, Watanabe J, Nakachi K, et al. PCR detection of na A/G polymorphismwith exon 7 of the CYP1A1 gene. Nucleic Acid Res 1991;19:47-97.
  56. Hamada GS, Sigimura H, Suzuki I, The heme-binding region polymorphism of cytochrome P4501A1 (CYP1A1), rather than the RstI polymorphism of IIE1 (CYPIIE1), is associated with lung cancer in Rio de Janeiro. Cancer Epidemiol Biomark Prev 1995;4:63-67.
  57. Wormhoudt LW, Commandeur JNM, Vermeulen NPE. Genetic polymorphisms of human N-acetiltransferase, Cytochrome P450, Glutathione-S-Transferase, and Epoxide Hydrolase Enzymes: relevance to xenobiotic metabolism and toxicity. Crit Rev Toxicol 1999;29:59-124.
  58. Abdel-Rahman SZ, El-Zein RA, Anwar, WA, et al. A multiplex PCR procedure for polymorphic analysis of GSTM1 and GSTT1 genes in population studies. Cancer Lett 1996;107:229-33.
  59. Viezzer C, Norppa H, Clonfero E, et al. Influence of GSTM1, GSTT1, GSTP1, and EPHX gene polymorphisms on DNA adduct level and HPRT mutant frequency in coke-oven workers. Mutat Res 1999;431:259-69.
  60. Abdel-Rahman SZ, Anwar WA, Abdel-Aal WE, et al. GSTM1 and GSTT1 genes are potential risk modifiers for bladder cancer. Cancer Detect Prev 1998;22:129-38.
  61. Seidegard J, Pero RW, Markowitz MM, et al. Isoenzyme (s) of glutathione transferase (class Mu) as a marker for the susceptibility to lung cancer: a follow-up study. Carcinogenesis 1990;11:33-6.
  62. Bell DA, Thompson CL, Taylor JA, et al. Genetic monitoring of human polymorphic cancer susceptibility genes by polymerase chain reaction: application to glutathione transferase . Environ Health Perspect 1992;98:113-17.
  63. Rossit AR, Cabral IR, Hackel CB, et al. Polymorphismsin the DNA repair gene XRCC1 and susceptibility to alcoholic liver cirrhosis in older southeastern Brazilians. Cancer Lett 2002;180:173-82.
  64. Hirvonen A, Nylund L, Kociba P, et al. Modulation of mutagenicity by genetically determined carcinogen metabolism in smokers. Carcinogenesis 1994;15:813-15.
  65. Binkovà B, Lewtas J, Mìskova I, et al. Biomarker studies in Northern Bohemia. Environ Health Perspec 1996;104:591-97.
  66. Gabbani G, Hou SM, Nardini B, et al. GSTM1 and NAT2 genotypes and urinary mutagens in coke oven workers. Carcinogenesis 1996;17:1675-81.
  67. Gabbani G, Pavanello S, Nardini B, Influence of metabolic genotype GSTM1 on levels of urinary mutagens in patients treated topically with coal tar. Mutat Res 1999;440:27-33.
  68. Costa DJ, Slott V, Binkova, et al. Influence of GSTM1 and NAT2 genotypes on the relationship between personal exposure to PAHs and biomarkers of internal dose. Biomarkers 1998;3:411-24.
  69. Hemminki K, Dickey C, Karlsson S, et al. Aromatic DNA adducts in foundry workers in relation to exposure, life style and CYP1A1 and glutatione transferase M1 genotype. Carcinogenesis 1997;18:345-50.
  70. Merlo F, Andreassen A, Weston A, et al. Urinary excretion of 1-hydroxypyrene as a marker for exposure to urban air levels of polycyclic aromatic hydrocarbons, Cancer Epidemiol. Biomarkers Prev 1998;7:147-55.
  71. Pavanello S, Gabbani G, Mastrangelo G, et al. Influence of GSTM1 genotypes on anti-BPDE-DNA adduct levels in mononuclear white blood cells of humans exposed to PAHs. Int Arch Occup Environ Health 1999;72:238-46.
  72. Wu MT, Huang SL, Ho CK, et al. Cytochrome P450 1A1 MspI polymorphism and urinary 1-hydroxypyrene concentrations in coke-oven workers, Cancer epidemiol. Biomarkers Prev 1998;7:823-29.
  73. Alexandrie AK, Warholm M, Carstensen U, et al. CYP1A1 and GSTM1 polymorphisms affect urinary 1-hydroxypyrene levels after PAH exposure. Carcinogenesis 2000;21:669-76.

 
 
 
 
 
 
 
 
 
 
 
 
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