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The fetus and infant are especially vulnerable to the effects of environmental agents that disrupt developmental processes because their organs are rapidly growing and developing, their metabolism is immature and their intakes can be greater relative to their body weight. In utero and early postnatal stressors, including environmental contaminant exposures, can permanently change the body's structure, physiology and metabolism, predisposing individuals to the development of serious chronic pathologies later in life (eg, cardiovascular, respiratory and neurodegenerative disease), a hypothesis grounded in the Developmental Origins of Health and Disease (DOHaD) paradigm for which there is a growing evidential basis. Up to relatively recently, good epidemiological evidence for early-life developmental effects was available only for a few pollutants, mostly at high-level exposure, such as lead, mercury and polychlorinated biphenyls (PCBs).1 The past decade has seen rapid increase in the study of effects of environmental agents at lower doses on health, growth and development of children. There is now reliable evidence for neurodevelopmental effects of a growing list of industrial agents,2 emerging evidence for the obesogenic effects of endocrine disruptors3 and limited evidence for effects of certain persistent organic pollutants on the developing immune and respiratory systems.4 Most of this new evidence has come from the prospective birth cohort study design: studies starting early in pregnancy, and following child health and development for …
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