BACKGROUND: Previous interview-based studies have suggested that exposure to neurotoxicants including metals might be related to ALS. METHODS: We evaluated the relation of lead exposure to ALS, using both biological measures and interviews, in a case-control study conducted in New England from 1993 to 1996. Cases (N = 109) were recruited at two hospitals in Boston, MA. Population controls (N = 256) identified by random-digit dialing were frequency-matched to cases by age, sex, and region of residence within New England. RESULTS: Risk of ALS was associated with self-reported occupational exposure to lead (odds ratio [OR] = 1.9; 95% confidence interval [CI] = 1.1-3.3), with a dose response for lifetime days of lead exposure. Blood and bone lead levels were measured in most cases (N = 107) and in a subset of controls (N = 41). Risk of ALS was associated with elevations in both blood and bone lead levels. ORs were 1.9 (95% CI = 1.4-2.6) for each microg/dl increase in blood lead, 3.6 (95% CI = 0.6-20.6) for each unit increase in log-transformed patella lead, and 2.3 (95% CI = 0.4-14.5) for each unit increase in log-transformed tibia lead. CONCLUSIONS: These results are consistent with previous reports and suggest a potential role for lead exposure in the etiology of ALS.
BACKGROUND: Previous interview-based studies have suggested that exposure to neurotoxicants including metals might be related to ALS. METHODS: We evaluated the relation of lead exposure to ALS, using both biological measures and interviews, in a case-control study conducted in New England from 1993 to 1996. Cases (N = 109) were recruited at two hospitals in Boston, MA. Population controls (N = 256) identified by random-digit dialing were frequency-matched to cases by age, sex, and region of residence within New England. RESULTS: Risk of ALS was associated with self-reported occupational exposure to lead (odds ratio [OR] = 1.9; 95% confidence interval [CI] = 1.1-3.3), with a dose response for lifetime days of lead exposure. Blood and bone lead levels were measured in most cases (N = 107) and in a subset of controls (N = 41). Risk of ALS was associated with elevations in both blood and bone lead levels. ORs were 1.9 (95% CI = 1.4-2.6) for each microg/dl increase in blood lead, 3.6 (95% CI = 0.6-20.6) for each unit increase in log-transformed patella lead, and 2.3 (95% CI = 0.4-14.5) for each unit increase in log-transformed tibia lead. CONCLUSIONS: These results are consistent with previous reports and suggest a potential role for lead exposure in the etiology of ALS.
Authors: Ann C McKee; Brandon E Gavett; Robert A Stern; Christopher J Nowinski; Robert C Cantu; Neil W Kowall; Daniel P Perl; E Tessa Hedley-Whyte; Bruce Price; Chris Sullivan; Peter Morin; Hyo-Soon Lee; Caroline A Kubilus; Daniel H Daneshvar; Megan Wulff; Andrew E Budson Journal: J Neuropathol Exp Neurol Date: 2010-09 Impact factor: 3.685
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