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INTRODUCTION

The seminal observation by Barker that low birth weight was linked to excess risk of cardiovascular disease (CVD) and mortality in adulthood1 led to the concept of “developmental origins of health and disease” (DOHaD). The idea of “programming” during pregnancy development and risk for chronic diseases occurring late in life was first suggested by nutritional experiments inspired by the concept of early “imprinting” of behavior in birds that has been recognized for centuries.2

The programming stimulus exerts long-term effects when applied at a “critical” or “sensitive” period such as the prenatal period, when organs are forming and growing. The fact that in utero exposure to environmental factors may cause permanent injury is of particular interest. There are various examples of how development is very vulnerable in early life to various external stimuli.3 In the late 1950s, the Japanese fishing town of Minamata suffered an epidemic of persistent mental retardation and spastic paresis in children. The children were born from unaffected pregnant mothers who ate seafood contaminated with methylmercury by a factory dumping effluent into Minamata Bay.4 In France in the 1960s, alcohol dependence was found to be very common among the mothers of mentally retarded children at an institution. This finding contributed to identifying the fetal alcohol syndrome, which is characterized by chronic mental health and developmental disorders in the offspring of alcoholic mothers. Other historical examples of the importance of early-life windows of susceptibility include the long-term health effects in the offspring, including several cancers, caused by the widespread use of diethylstilbestrol, a synthetic nonsteroidal estrogen, during pregnancy between the 1940s and 1970s,5 and the Dutch Hunger Winter Families Study (see Box). Studying the long-term structural and functional effects of environmental exposures during fetal and early life (i.e., during the entire childhood, but particularly during the first 2 years of life) is important, given the potential irreversible nature of these health effects and the critical opportunity for prevention during these periods.

In this chapter, we provide a general description of the evidence on early-life exposure to relevant environmental factors that can impact reproductive health, neurodevelopment, respiratory and immune health, growth, obesity, and cardiometabolic health in children (Table 74-1). In this context, “early life” refers to exposure during the prenatal period (fetal life) and postnatal period of childhood. In addition, the chapter covers exposure during adolescence, an important period for development too. This summary of the evidence is not a formal weight-of-evidence analysis. This summary is mainly based on epidemiological literature published between 2008 and 2018, including the review by Vrijheid et al. (2016)6 and other existing reviews and relevant original manuscripts for chemical exposures and air pollution, noise and green spaces (Table 74-2).

TABLE 74-1CHILDREN HEALTH OUTCOMES RELATED TO EARLY-LIFEa EXPOSURES TO CHEMICAL AND PHYSICAL FACTORS

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