TY - JOUR
T1 - Smoking and risk for amyotrophic lateral sclerosis
T2 - Analysis of the EPIC cohort
AU - Gallo, Valentina
AU - Bueno-De-Mesquita, H. Bas
AU - Vermeulen, Roel
AU - Andersen, Peter M.
AU - Kyrozis, Andreas
AU - Linseisen, Jakob
AU - Kaaks, Rudolph
AU - Allen, Naomi E.
AU - Roddam, Andrew W.
AU - Boshuizen, Hendriek C.
AU - Peeters, Petra H.
AU - Palli, Domenico
AU - Mattiello, Amalia
AU - Sieri, Sabina
AU - Tumino, Rosario
AU - Jiménez-Martín, Juan Manuel
AU - Díaz, María José Tormo
AU - Suarez, Laudina Rodriguez
AU - Trichopoulou, Antonia
AU - Agudo, Antonio
AU - Arriola, Larraitz
AU - Barricante-Gurrea, Aurelio
AU - Bingham, Sheila
AU - Khaw, Kay Tee
AU - Manjer, Jonas
AU - Lindkvist, Björn
AU - Overvad, Kim
AU - Bach, Flemming W.
AU - Tjoønneland, Anne
AU - Olsen, Anja
AU - Bergmann, Manuela M.
AU - Boeing, Heiner
AU - Clavel-Chapelon, Francoise
AU - Lund, Eiliv
AU - Hallmans, Goran
AU - Middleton, Lefkos
AU - Vineis, Paolo
AU - Riboli, Elio
PY - 2009/4
Y1 - 2009/4
N2 - Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrolment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2.32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure.
AB - Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrolment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2.32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure.
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U2 - 10.1002/ana.21653
DO - 10.1002/ana.21653
M3 - Article
C2 - 19399866
AN - SCOPUS:65249103010
VL - 65
SP - 378
EP - 385
JO - Annals of Neurology
JF - Annals of Neurology
SN - 0364-5134
IS - 4
ER -