Aim: Recently, attention has focused on possible early life origins for asthma. We sought to identify whether factors present during pregnancy were associated with development of childhood wheezing phenotypes. Methods: A whole populationbirth cohort (n=1456) on the Isle of Wight, UK, was followed through to age 10 y. Where possible, information regarding environmental exposures and events during pregnancy was obtained from the maternity records (n=1238). Children were seen at ages 1, 2, 4 and 10 y, and wheezing symptoms were used to define wheezing phenotypes in the first decade (n=1034). Results: Risk of early-onset persistent wheeze (onset in the first 4 y, still present at age 10) was increased by environmental tobacco smoke exposure in pregnancy (OR=2.44;95% CI: 1.37-4.34) plus maternal asthma (3.57; 1.84-6.94), but reduced by cat ownership (0.30; 0.13-0.62). Early transient wheeze (onset in the first 4 y, but not present at age 10) was increased by environmental tobacco smoke exposure (1.58; 1.02-2.45),male gender (1.68; 1.09-2.60) and low birthweight (3.65; 1.27-10.52). No environmental factors in pregnancy were associated with lateonset persistent wheeze (onset after age 4 y, still present at 10 y). Conclusion: In addition to genetics, maternal exposures during pregnancy show association with childhood and especially early-life wheezing phenotypes. Aim: Recently, attention has focused on possible early life origins for asthma. We sought to identify whether factors during during pregnancy were associated with development of childhood wheezing phenotypes. Methods: A whole populationirth cohort (n = 1456) on the Isle of Wight, UK, was followed through to age 10 y. Where possible, information regarding environmental exposures and events during pregnancy was obtained from the maternity records (n = 1238). Children were seen at ages 1, 2, 4 and 10 y, and wheezing symptoms were used to define wheezing phenotypes in the first decade (n = 1034). Results: Risk of early-onset persistent wheeze (onset in the first 4 y, still present at age 10) was increased by environmental tobacco smoke exposure in pregnancy = 2.44; 95% CI: 1.37-4.34) plus maternal asthma (3.57; 1.84-6.94) but reduced by cat ownership (0.30; 0.13-0.62). Early transient wheeze (onset in the first 4 y, but not present at age 10) was increased by environmental tobacco smoke expo sure (1.58; 1.02-2.45), male gender (1.68; 1.09-2.60) and low birthweight (3.65; 1.27-10.52). No environmental factors in pregnancy were associated with lateonset persistent wheeze (onset after age 4 y, still present at 10 y). Conclusion: In addition to genetics, maternal exposures during pregnancy show association with childhood and especially early-life wheezing phenotypes.