The role of environmental mercury, lead and pesticide exposure in development of amyotrophic lateral sclerosis

被引:124
作者
Johnson, Frank O.
Atchison, William D. [1 ]
机构
[1] Michigan State Univ, Dept Pharmacol & Toxicol, E Lansing, MI 48824 USA
关键词
Methylmercury; Lead; Organophosphates; Paralysis; Amyotrophic lateral sclerosis; Gene-environment; Neurodegenerative disease; GULF-WAR VETERANS; MOTOR-NEURON DISEASE; PARKINSONISM-DEMENTIA COMPLEX; METHYLAMINO-L-ALANINE; PARAOXONASE PON1; SPORADIC ALS; NEURODEGENERATIVE DISEASES; TEMPORAL DETERMINANTS; CLUSTER POLYMORPHISMS; SUPEROXIDE-DISMUTASE;
D O I
10.1016/j.neuro.2009.07.010
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Exposure to an environmental toxicant as a risk factor in the development of amyotrophic lateral sclerosis (ALS) was first hinted at (demonstrated) in the Chamorro indigenous people of Guam. During the 1950s and 1960s these indigenous people presented an extremely high incidence of ALS which was presumed to be associated with the consumption of flying fox and cycad seeds. No other strong association between ALS and environmental toxicants has since been reported, although circumstantial epidemiological evidence has implicated exposure to heavy metals such as lead and mercury, industrial solvents and pesticides especially organophosphates and certain occupations such as playing professional soccer. Given that only similar to 10% of all ALS diagnosis have a genetic basis, a gene-environmental interaction provides a plausible explanation for the other 90% of cases. This mini-review provides an overview of our current knowledge of environmental etiologies of ALS with emphasis on the effects of mercury, lead and pesticides as potential risk factors in developing ALS. Epidemiologic and experimental evidence from animal models investigating the possible association between exposure to environmental toxicant and ALS disease has proven inconclusive. Nonetheless, there are indications that there may be causal links, and a need for more research. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:761 / 765
页数:5
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