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      Impact of Environmental Chemicals on Lung Development

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          Disruption of fundamental biologic processes and associated signaling events may result in clinically significant alterations in lung development.


          We reviewed evidence on the impact of environmental chemicals on lung development and key signaling events in lung morphogenesis, and the relevance of potential outcomes to public health and regulatory science.

          Data sources

          We evaluated the peer-reviewed literature on developmental lung biology and toxicology, mechanistic studies, and supporting epidemiology.

          Data synthesis

          Lung function in infancy predicts pulmonary function throughout life. In utero and early postnatal exposures influence both childhood and adult lung structure and function and may predispose individuals to chronic obstructive lung disease and other disorders. The nutritional and endogenous chemical environment affects development of the lung and can result in altered function in the adult. Studies now suggest that similar adverse impacts may occur in animals and humans after exposure to environmentally relevant doses of certain xenobiotics during critical windows in early life. Potential mechanisms include interference with highly conserved factors in developmental processes such as gene regulation, molecular signaling, and growth factors involved in branching morphogenesis and alveolarization.


          Assessment of environmental chemical impacts on the lung requires studies that evaluate specific alterations in structure or function—end points not regularly assessed in standard toxicity tests. Identifying effects on important signaling events may inform protocols of developmental toxicology studies. Such knowledge may enable policies promoting true primary prevention of lung diseases. Evidence of relevant signaling disruption in the absence of adequate developmental toxicology data should influence the size of the uncertainty factors used in risk assessments.

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          Most cited references 123

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          Effect of in utero and early-life conditions on adult health and disease.

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            The origins of the developmental origins theory.

             Fred G Barker (2007)
            Current orthodoxy states that coronary heart disease results from the unhealthy lifestyles of westernized adults together with a contribution from genetic inheritance. This does not provide a secure basis for prevention of the disease. Geographical studies gave the first clue that the disease originates during intra-uterine development. Variations in mortality from the disease across England and Wales were shown to correlate closely with past differences in death rates among newborn babies. In the past most deaths among newborns were attributed to low birthweight. This led to the hypothesis that undernutrition in utero permanently changes the body's structure, function and metabolism in ways that lead to coronary heart disease in later life. The association between low birthweight and coronary heart disease has been confirmed in longitudinal studies of men and women around the world. The developmental model of the origins of the disease offers a new way forward.
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              Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales.

              Although the rise in ischaemic heart disease in England and Wales has been associated with increasing prosperity, mortality rates are highest in the least affluent areas. On division of the country into two hundred and twelve local authority areas a strong geographical relation was found between ischaemic heart disease mortality rates in 1968-78 and infant mortality in 1921-25. Of the twenty-four other common causes of death only bronchitis, stomach cancer, and rheumatic heart disease were similarly related to infant mortality. These diseases are associated with poor living conditions and mortality from them is declining. Ischaemic heart disease is strongly correlated with both neonatal and postneonatal mortality. It is suggested that poor nutrition in early life increases susceptibility to the effects of an affluent diet.

                Author and article information

                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                August 2010
                5 May 2010
                : 118
                : 8
                : 1155-1164
                [1 ] Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, Oakland, California, USA
                [2 ] Pediatric Environmental Health Specialty Unit, University of California–San Francisco, San Francisco, California, USA
                Author notes
                Address correspondence to M. Miller, Office of Environmental Health Hazard Assessment, 1515 Clay St. 16th Floor, Oakland, CA 94612 USA. Telephone: (510) 622-3159. Fax: (510) 622-3210. E-mail: mmiller@

                The authors declare they have no actual or potential competing financial interests.

                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.


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