2.2　Smoking

Smoking is an independent risk factor for CP.The research has demonstrated acinar cell alterations including cytoplasmic vacuolization and cellular edema could be induced by nicotine.In addition，it also could affect digestive enzymes in the pancreas（Luaces-Regueira et al.2014）.A metaanalysis about smoking and CP reported the pooled risk estimate of CP for smokers vs.never smokers was 2.5（95%CI，1.3-4.6），after adjustment for alcohol consumption（Andriulliet al.2010）.Moreover，it found there was a doseresponse effect on smoking and pancreatic injury.The pooled risk for CP was 3.3（95%CI，1.4-7.9）among those who smoked one or more packs per day and 2.4（95%CI，0.9-6.6）among those who smoked less than one pack per day.The association between smoking and CP was found to be stronger among patients who also consume alcohol（Falk et al.2006；Yadav et al.2010）.A study in experimental animal model provided evidence that smoking and drinking had the synergistic detrimental effects on pancreatitis（Hartwig et al.2000）.(https://www.daowen.com)

Previous studies have shown smoking can accelerate the progression of pancreatic calcification，functional impairment and the progression of acute pancreatitis to CP（Lankisch et al.2009；Imoto and DiMagno 2000；Maisonneuve et al.2005，2006）.Moreover，smoking was correlated with many complications of CP，such as exocrine insufficiency，development of calcifications，and ductal changes（Luaces-Regueira et al.2014）.On the contrary，smoking cessation could slow the development and progression of CP.Result from a meta-analysis showed the risk of CP significantly dropped from 2.8（95%CI，1.8-4.2）in current smokers to 1.4（95%CI，1.1-1.9）in former smokers（Andriulli et al.2010）.The clinical study found smoking cessation in the first years after the clinical onset of CP reduced the risk of developing pancreatic calcifications（Talamini et al.2007）.