Environmental factors play an important role in the pathophysiology of infl
ammatory bowel disease. There is a strong and consistent association betwee
n smoking and Crohn's disease, and between nonsmoking and ulcerative coliti
s. Despite extensive research, the exact pathophysiological mechanisms for
these associations remain unclear. In spite of this, some clinical trials w
ith nicotine-patches showed beneficial effects for the treatment of ulcerat
ive colitis. Associations of Crohn's disease and ulcerative colitis with ot
her environmental factors are weaker like the association with use of oral
contraceptives ol those less well investigated such as the association with
childhood hygiene. Most studies suggesting a potential pathogenetic role o
f Mycobacterium paratuberculosis or an effect of tuberculostatic therapy in
Crohn's disease could not be reproduced by others. Perinatal or childhood
infections by viruses like measles are heavily debated, but not proven to b
e causal for inflammatory bowel disease. Coagulation disorders have been de
scribed as protecting from inflammatory bowel disease, suggesting hypercoag
ulability to be a pathogenetic factor. Some studies described that appendec
tomy may prevent the onset of ulcerative colitis in man and mice. Other env
ironmental factors such as hydrogen sulfide, tonsillectomy, diet, blood tra
nsfusions, and Listeria also require confirmation. There are, however, conv
incing data from genetic animal models and twin studies that environmental
factors as the intestinal bacterial flora interact with susceptible hosts t
o cause inflammatory bowel disease. Inflammatory bowel diseases have multif
actorial etiologies, which require a differentiated approach for treatment
and prevention.