Modification of the association between lead exposure and amyotrophic lateral sclerosis by iron and oxidative stress related gene polymorphisms

Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration

Volumn 16, Issue 1-2, 2015, Pages 72-79

  Eum, Ki Do ^a   Seals, Ryan M ^a   Taylor, Kathryn M ^a   Grespin, Matthew ^a   Umbach, David M ^b   Hu, Howard ^c   Sandler, Dale P ^b   Kamel, Freya ^b   Weisskopf, Marc G ^a  

^a HARVARD SCHOOL OF PUBLIC HEALTH   (United States)

^b NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES   (United States)

^c UNIVERSITY OF TORONTO   (Canada)

Author keywords

Amyotrophic lateral sclerosis; Epidemiology; Hemochromatosis; Iron metabolism; Oxidative stress

Indexed keywords

GENOMIC DNA; GLUTATHIONE TRANSFERASE P1; IRON; LEAD; TRANSFERRIN; GSTP1 PROTEIN, HUMAN;

ADULT; AGED; AMYOTROPHIC LATERAL SCLEROSIS; ARTICLE; ATOMIC ABSORPTION SPECTROMETRY; CASE CONTROL STUDY; COMPARATIVE STUDY; CONTROLLED STUDY; ENVIRONMENTAL EXPOSURE; FEMALE; GENOTYPE; HEMOCHROMATOSIS; HUMAN; LEAD BLOOD LEVEL; MAJOR CLINICAL STUDY; MALE; MULTIPLEX POLYMERASE CHAIN REACTION; OXIDATIVE STRESS; PATELLA; PRIORITY JOURNAL; SINGLE NUCLEOTIDE POLYMORPHISM; TIBIA; UNITED STATES; WILD TYPE; X RAY FLUORESCENCE; BONE; GENETIC ASSOCIATION; GENETIC POLYMORPHISM; GENETICS; LEAD POISONING, NERVOUS SYSTEM; METABOLISM; MIDDLE AGED;

ADULT; AGED; AMYOTROPHIC LATERAL SCLEROSIS; BONE AND BONES; FEMALE; GENETIC ASSOCIATION STUDIES; GENOTYPE; GLUTATHIONE S-TRANSFERASE PI; HEMOCHROMATOSIS; HUMANS; IRON; LEAD; LEAD POISONING, NERVOUS SYSTEM; MALE; MIDDLE AGED; OXIDATIVE STRESS; POLYMORPHISM, GENETIC; SPECTROPHOTOMETRY, ATOMIC; TRANSFERRIN;

EID: 84925667751     PISSN: 21678421     EISSN: 21679223     Source Type: Journal    
DOI: 10.3109/21678421.2014.964259     Document Type: Article

References (36)

1. Barber SC, Shaw PJ. Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. Free Radic Biol Med. 2010; 48: 629-41.
2. Johnson FO, Atchison WD. The role of environmental mercury, lead and pesticide exposure in development of amyotrophic lateral sclerosis. Neurotoxicology. 2009; 30: 761-5.
3. Sutedja NA, Veldink JH, Fischer K, Kromhout H, Heederik D, Huisman MH, et al. Exposure to chemicals and metals and risk of amyotrophic lateral sclerosis: a systematic review. Amyotroph Lateral Scler. 2009; 10: 302-9.
4. Factor-Litvak P, Al-Chalabi A, Ascherio A, Bradley W, Chio A, Garruto R, et al. Current pathways for epidemio-logical research in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Frontotemporal Degener. 2013; 14 (Suppl 1): 33-43.
5. Kamel F, Umbach DM, Munsat TL, Shefner JM, Hu H, Sandler DP. Lead exposure and amyotrophic lateral sclerosis. Epidemiology. 2002; 13: 311-9.
6. Fang F, Kwee LC, Allen KD, Umbach DM, Y e W, Watson M, et al. Association between blood lead and the risk of amyotrophic lateral sclerosis. Am J Epidemiol. 2010; 171: 1126-33.
7. Vonk WI, Klomp L W. Role of transition metals in the patho-genesis of amyotrophic lateral sclerosis. Biochem Soc Trans. 2008; 36: 1322-8.
8. Feder JN. The hereditary hemochromatosis gene (HFE): a MHC class I-like gene that functions in the regulation of iron homeostasis. Immunol Res. 1999; 20: 175-85.
9. Hall EC, Lee SY, Mairuae N, Simmons Z, Connor JR. Expression of the HFE allelic variant H63D in SH-SY5Y cells affects tau phosphorylation at serine residues. Neuro-biol Aging. 2011; 32: 1409-19.
10. Lee SY, Patton SM, Henderson RJ, Connor JR. Consequences of expressing mutants of the hemochromatosis gene (HFE) into a human neuronal cell line lacking endogenous HFE. FASEB J. 2007; 21: 564-76.
11. Namekata K, Oyama F, Imagawa M, Ihara Y. Human trans-ferrin (Tf): a single mutation at codon 570 determines Tf C1 or Tf C2 variant. Hum Genet. 1997; 100: 457-8.
12. Hayes JD, Strange RC. Glutathione S-transferase polymorphisms and their biological consequences. Pharmacology. 2000; 61: 154-66.
13. Brooks BR. El Escorial World Federation of Neurology criteria for the diagnosis of amyotrophic lateral sclerosis. Subcommittee on Motor Neuron Diseases/Amyotrophic Lateral Sclerosis of the World Federation of Neurology Research Group on Neuromuscular Diseases and the El Escorial 'Clinical limits of amyotrophic lateral sclerosis'workshop contributors. J Neurol Sci. 1994; 124 (Suppl): 96-107.
14. Weisskopf MG, Weuve J, Nie H, Saint-Hilaire MH, Sudarsky L, Simon DK, et al. Association of cumulative lead exposure with Parkinson's disease. Environ Health Perspect. 2010; 118: 1609-13.
15. Aro A, Amarasiriwardena C, Lee ML, Kim R, Hu H. Validation of K-X-ray fluorescence bone lead measurements by inductively coupled plasma mass spectrometry in cadaver legs. Med Phys. 2000; 27: 119-23.
16. Aro AC, Todd AC, Amarasiriwardena C, Hu H. Improvements in the calibration of 109Cd K-X-ray fluorescence systems for measuring bone lead in vivo. Phys Med Biol. 1994; 39: 2263-71.
17. Nie H, Hu H, Chettle DR. Application and methodology of in vivo K-X-ray fluorescence of Pb in bone (impact of KXRF data in the epidemiology of lead toxicity, and consistency of the data generated by updated systems) X-Ray Spectrometry Volume 37, Issue 1. X-Ray Spectrometry. 2008; 37: 69-75.
18. Wilker E, Korrick S, Nie LH, Sparrow D, Vokonas P, Coull B, et al. Longitudinal changes in bone lead levels: the VA Normative Aging Study. J Occup Environ Med. 2011; 53: 850-5.
19. Kim R, Landrigan C, Mossmann P, Sparrow D, Hu H. Age and secular trends in bone lead levels in middle-aged and elderly males: three-year longitudinal follow-up in the Normative Aging Study. Am J Epidemiol. 1997; 146: 586-91.
20. Kleinbaum DG, Klein M. Logistic regression: a self-learning text: Springer; 2010.
21. Morimoto LM, White E, Newcomb PA. Selection bias in the assessment of gene-environment interaction in case-control studies. Am J Epidemiol. 2003; 158: 259-63.
22. Wacholder S, Chatterjee N, Hartge P. Joint effect of genes and environment distorted by selection biases: implications for hospital based case-control studies. Cancer Epidemiol Biomarkers Prev. 2002; 11: 885-9.
23. Vanderweele TJ, Mukherjee B, Chen J. Sensitivity analysis for interactions under unmeasured confounding. Stat Med. 2012; 31: 2552-64.
24. Rothman KJ. No adjustments are needed for multiple comparisons. Epidemiology. 1990; 1: 43-6.
25. Goldberg M, Silbergeld E. On multiple comparisons and on the design and interpretation of epidemiological studies of many associations. Environ Res. 2011; 111: 1007-9.
26. Yen AA, Simpson EP, Henkel JS, Beers DR, Appel SH. HFE mutations are not strongly associated with sporadic ALS. Neurology. 2004; 62: 1611-2.
27. Sutedja NA, Sinke RJ, van Vught PW, van der Linden MW, Wokke JH, van Duijn CM, et al. The association between H63D mutations in HFE and amyotrophic lateral sclerosis in a Dutch population. Archives of Neurology. 2007; 64: 63-7.
28. Goodall EF, Greenway MJ, van Marion I, Carroll CB, Hardiman O, Morrison KE. Association of the H63D polymorphism in the hemochromatosis gene with sporadic ALS. Neurology. 2005; 65: 934-7.
29. Restagno G, Lombardo F, Ghiglione P, Calvo A, Cocco E, Sbaiz L, et al. HFE H63D polymorphism is increased in patients with amyotrophic lateral sclerosis of Italian origin. J Neurol Neurosurg Psychiatry. 2007; 78: 327.
30. He X, Lu X, Hu J, Xi J, Zhou D, Shang H, et al. H63D polymorphism in the hemochromatosis gene is associated with sporadic amyotrophic lateral sclerosis in China. European Journal of Neurology: the official journal of the European Federation of Neurological Societies. 2011; 18: 359-61.
31. Praline J, Blasco H, Vourc'h P, Rat V, Gendrot C, Camu W, et al. Study of the HFE gene common polymorphisms in French patients with sporadic amyotrophic lateral sclerosis. J Neurol Sci. 2012; 317: 58-61.
32. van Rheenen W, Diekstra FP, van Doormaal PT, Seelen M, Kenna K, McLaughlin R, et al. H63D polymorphism in HFE is not associated with amyotrophic lateral sclerosis. Neurobiol Aging. 2013; 34: 1517.
33. Mitchell RM, Lee SY, Simmons Z, Connor JR. HFE polymorphisms affect cellular glutamate regulation. Neurobiol Aging. 2011; 32: 1114-23.
34. Mitchell RM, Lee SY, Randazzo WT, Simmons Z, Connor JR. Influence of HFE variants and cellular iron on monocyte chemoattractant protein-1. J Neuroinflammation. 2009; 6: 6.
35. Nandar W, Connor JR. HFE gene variants affect iron in the brain. The Journal of Nutrition. 2011; 141: S729-39.
36. Onalaja AO, Claudio L. Genetic susceptibility to lead poisoning. Environ Health Perspect. 2000; 108 (Suppl 1): 23-8.