The Role of Environmental Hazards in Premature Birth Workshop Summary (2003) / Chapter Skim
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4. Preterm Birth - Gene-Environment Interactions
4. Preterm Birth - Gene-Environment Interactions
Pages 46-61
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This chapter summarizes some of the research and research programs that may shed light on environmental causes of preterm birth.
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According to Matthew Longnecker, National Institute of Environmental Health Sciences (NIEHS) , the environmental risk factors for other reproductive outcomes can differ from those for preterm birth.
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It was interesting that the relative risks for environmental tobacco smoke tended to be higher than those for direct smoking. Researchers are beginning to study the relationship between traditional air pollutants and premature birth.
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This suggests that DDE exposure as a risk factor for preterm birth may be more important in those countries where DDT is used for malaria control but not in the United States. Longnecker reviewed a number of other potential risk factors for pre-term birth many of which had few supportive data, conflicting results, or not enough information to make a conclusion.
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Poor maternal health and maternal smoking were important risk factors for poor child health (Chen and Millar, 1999~. Tobacco and Gene-Environment Interactions Wang and colleagues investigated maternal cigarette smoking, metabolic gene polymorphism, and reduced birth weight in a U.S.
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By recording contractions from the myometnum of pregnant rats in a standard organ bath, her laboratory has found that some toxicants, such as PCBs and DDT, can act directly on the myometnum to alter contractions. For example, DDT, which was described above as having a potential role in premature birth, was shown to increase the oscillations (contraction frequency)
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Loch-Caruso concluded that some environmental toxicants can act directly through cellular mechanisms to alter uterine contractions. In vitro approaches using laboratory animal myometrial tissue and cells may prove useful for assessing the potential risks of some environmental chemicals for pregnant women.
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(1995) found that the risk of low birth weight and preterm birth was greatly increased if both the mother and the index child were of low birth weight.
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IMMUNE-DEFICIENT KNOCKOUT MICE AS A MODEL TO ELUCIDATE ENVIRONMENTAL TOXICANTS Participants considered other animal models to begin to understand the effect of environmental toxicants on preterm birth and other reproductive abnor
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During her presentation, Anne Croy of the University of Guelph suggested that if mice lacking lymphocytes are housed under strict microbiological barriers, they are excellent models for reproductive studies because they are immune deficient. The immune system is composed of highly mobile cells that normally circulate in the blood and have the ability to move in and out of tissues.
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From page 56... ...
that focus on uNK cells as indicators of environmental interference in the implantation process and, thus have some effect on the subset of preterm births that may be due to problems of implantation. FEDERAL GOVERNMENT TOXICOLOGY PROGRAMS In addition to the work at academic institutions, the federal government has a number of research and testing programs that are poised to test reproductive and development effects of chemicals.
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The possible types of adverse developmental outcomes include death through early spontaneous abortions, perinatal death, or postnatal deaths; birth defects; altered or reduced growth; and functional deficits, e.g., mental retardation. Related to the work on developmental toxicity is the study of reproductive toxicity that includes adverse effects on the reproductive system, such as changes in gestation, parturition, lactation, onset of puberty, gamete production and transport, and reproductive senescence.
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In concluding, Kimmel noted that the current testing guidelines do include some evaluation of gestation length, but the question remains whether researchers have the appropriate animal models to ask the appropriate questions regarding preterm birth. She suggested that current study designs may be able to be
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The TRCT was originally designed to identify environmental agents that might induce genetic damage in female germ cells or otherwise cause premature cessation of ovulation. The TRCT, as conducted for these purposes, does not capture length of gestation information needed to assess premature birth.
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This assay or study paradigm has many versions that can look at different outcomes (gestational length, average time to litter, cumulative time per litter, numbers of pups per litter, decreased pup weight, altered pup sex ratio, etc.) , and may be applicable for studying preterm birth.
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From page 61... ...
The remaining chemicals listed in this table have been tested but not found to have an effect on either time to litter or gestational length. Ethoxyquin increased the time to litter and sodium selenate increased the gestational length.
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