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There has been no clear consensus about whether prenatal exposure to air pollution contributes to the development of wheezing and asthma in children. We conducted a systematic review to analyze the association between exposure to different pollutants during pregnancy and the development of childhood wheezing and asthma.We systematically reviewed epidemiological studies published through June 6, 2017 available in the MEDLINE and Web of Science databases. We included studies that examined the association between prenatal exposure to any air pollutants except tobacco smoke and the incidence or prevalence of “wheezing” or “asthma” from birth to 14 years of age. We extracted key characteristics of each included study using a template of predefined data items. We used the Critical Appraisal Skills Programme checklists to assess the validity of each included study. We conducted overall and subgroup meta-analyses for each summary exposure-outcome association. Pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated by using a random effects model.Eighteen studies met our eligibility criteria. There was notable variability in exposure assessment methods. The overall random effects risk estimates (95% CI) of different pollutants were 1.04 (0.94–1.15) aromatic hydrocarbons (PAH), 1.04 (1.01–1.07) NO2, 1.4 (0.97–2.03) PM2.5 for childhood wheeze and 1.07 (1.01–1.14) NO2, 1 (0.97–1.03) PM2.5, 1.02 (0.98–1.07) SO2, 1.08 (1.05–1.12) PM10 for childhood asthma. Minimal heterogeneity was seen for PAH and SO2, while some heterogeneity was observed for PM10, PM2.5 and NO2.The overall and subgroup risk estimates from the meta-analyses showed statistically significant associations between prenatal exposures to NO2, SO2, and PM10 and the risk of wheezing and asthma development in childhood. There is insufficient evidence to show an effect of prenatal exposure to BC, CO, and O3 on childhood wheezing and asthma. Further studies are needed to examine the individual compounds’ effects.