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Perinatal environmental exposures affect mammary development, function, and cancer risk in adulthood.

Annual review of pharmacology and toxicology

United States, Animals, Body Weight, Breast, drug effects, pathology, Breast Neoplasms, chemically induced, Diet, Endocrine Disruptors, toxicity, Environmental Exposure, analysis, Environmental Pollutants, Female, Humans, Perinatal Care, Puberty, physiology, Puberty, Precocious, Reproduction, Risk Factors, Rodentia, growth & development

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      Abstract

      Puberty is an important transition that enables reproduction of mammalian species. Precocious puberty, specifically early thelarche (the appearance of breast "buds"), in girls of multiple ethnic backgrounds is a major health problem in the United States and other countries. The cause for a continued decrease in the age of breast development in girls is unknown, but environmental factors likely play a major role. Laboratory and epidemiological studies have identified several individual environmental factors that affect breast development, but further progress is needed. Current research needs include increased attention to and recording of prenatal and neonatal environmental exposures, testing of marketed chemicals for effects on the mammary gland, and understanding of the mammary gland-specific mechanisms that are altered by chemicals. Such research is required to halt the increasing trend toward puberty at earlier ages.

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      Most cited references 122

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      Fetal origins of adult disease: strength of effects and biological basis.

      Low birthweight has been consistently shown to be associated with coronary heart disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life-death, hospital treatment and the need for medication. Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924-1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic disease are documented. The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension. Coronary heart disease and type 2 diabetes may originate through two widespread biological phenomena-developmental plasticity and compensatory growth.
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        Variations in the Pattern of Pubertal Changes in Boys

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          The timing of normal puberty and the age limits of sexual precocity: variations around the world, secular trends, and changes after migration.

          During the past decade, possible advancement in timing of puberty has been reported in the United States. In addition, early pubertal development and an increased incidence of sexual precocity have been noticed in children, primarily girls, migrating for foreign adoption in several Western European countries. These observations are raising the issues of current differences and secular trends in timing of puberty in relation to ethnic, geographical, and socioeconomic background. None of these factors provide an unequivocal explanation for the earlier onset of puberty seen in the United States. In the formerly deprived migrating children, refeeding and catch-up growth may prime maturation. However, precocious puberty is seen also in some nondeprived migrating children. Attention has been paid to the changing milieu after migration, and recently, the possible role of endocrine- disrupting chemicals from the environment has been considered. These observations urge further study of the onset of puberty as a possible sensitive and early marker of the interactions between environmental conditions and genetic susceptibility that can influence physiological and pathological processes.
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            Author and article information

            Journal
            22017681
            3477544
            10.1146/annurev-pharmtox-010611-134659

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