Prenatal programming of adult disease is well established in animals. In humans the impact of common in utero exposures on long-term offspring health is less clear. We reviewed epidemiology studies of modifiable maternal exposures and offspring blood pressure (BP). Three maternal exposures were identified for review and meta-analyzed where possible: smoking during pregnancy, diet, and age at childbirth. Meta-analysis suggested there was a modest association between higher offspring BP and prenatal exposure to smoke (confounder-adjusted  ϭ 0.62 mm Hg, 95% confidence interval: 0.19 -1.05, I 2 ϭ 16.4%). However, the level of confounder adjustment varied between studies, which in some studies attenuated the association to the null. There was no strong evidence that any component of maternal diet during pregnancy (maternal protein, energy, calcium, and various other nutrients) influences offspring BP. The results of studies of maternal age varied and there was strong evidence of heterogeneity in the pooled analysis. The association with maternal age, if present, was modest (confounderadjusted  ϭ 0.09 mm Hg/y, 95% confidence interval: Ϫ0.03 to 0.21, I 2 ϭ 89.8%). In sum, there is little empirical evidence that the maternal exposures reviewed program offspring BP. Other components of offspring health may be more susceptible to effects of programming in utero. (Pediatr Res 63: 593-598, 2008) P rogramming has been defined as to the process by which a stimulus occurring during a sensitive period of development has lasting effects on development or risk of disease (1,2). Evidence for programming is well established in animals (3) and exposures in humans, such as Rubella infection in utero (4) and inadequate periconceptual folate (5) can also result in structural changes (these might be described as teratogenic effects). However, the relevance of less extreme exposures in humans and their ability to induce adaptive responses is less clear.Interest in the role of early life and later chronic disease developed from early ecological studies by Forsdahl (6) linking infant mortality to subsequent cardiovascular disease mortality. Later studies by Barker and colleagues (1), showing that size at birth was related to adult chronic disease, extended this interest to intrauterine programming. Blood pressure (BP) is strongly and directly associated with mortality from cardiovascular disease (7), and the evidence for associations of low birth weight with adverse outcomes in later life is robust for BP (8) [although this has been disputed (9)]. In addition, there are strong cohort effects for secular changes in BP providing evidence for a role of early exposures (10,11). Thus, we have focused on BP in this review.There are various possible explanations for the association between low birth weight and later disease. These include confounding by socioeconomic position (SEP) (12), shared genes (13) and adjustment for later body size that represents programming in infancy or later in development (14). However, the association be...