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Chromosomal aberrations induced by e...

Bocskay, Kirsti A.

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Chromosomal aberrations induced by environmental pollutants.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Chromosomal aberrations induced by environmental pollutants./
作者:	Bocskay, Kirsti A.
面頁冊數:	172 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2369.
Contained By:	Dissertation Abstracts International65-05B.
標題:	Health Sciences, Public Health. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3133533
ISBN:	0496807722

Chromosomal aberrations induced by environmental pollutants.
Bocskay, Kirsti A.

Chromosomal aberrations induced by environmental pollutants. - 172 p.

Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2369.

Thesis (Ph.D.)--Columbia University, 2004.

Molecular and traditional epidemiology studies have indicated a possible relationship between in utero environmental exposures and increased risk for childhood cancers, especially acute leukemias. Chromosomal aberrations have been associated with environmental exposures and cancer risk in adults. Moreover, these exposures may be targeting specific chromosomes for damage. In order to more clearly define the association between prenatal exposures and chromosomal aberrations as a marker of potential cancer risk, whole chromosome probe FISH (fluorescence in situ hybridization) for chromosomes 1--6 and Giemsa-staining were used to measure aberration frequencies in 60 newborns from the Columbia Center for Children's Environmental Health (CCCEH) Prospective Cohort Study. The study population comprises African-American or Dominican, non-smoking mother-newborn pairs exposed to varying levels of polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and the residential pesticides, chlorpyrifos and propoxur. Prenatal exposures were assessed by questionnaire, prenatal air monitoring, and biomarkers in cord blood. African-American newborns had a significantly higher level of stable chromosomal aberration frequencies in cord blood than did Dominicans. Multivariate regression demonstrated a significant positive association of PAHs, as measured by personal air monitoring during the third trimester, with stable aberration frequencies (p = 0.0066). No significant increases in aberration frequencies were seen for ETS, propoxur, or chlorpyrifos exposures. FISH for stable aberrations was found to be a more sensitive measure for detecting changes in aberrations, compared to FISH for unstable aberrations or Giemsa-staining for aberrations. Breaks in chromosomes 1--6 were not randomly distributed by chromosome size or DNA content, which has never been documented in a population with exposures only to environmental pollutants such as the CCCEH cohort.

ISBN: 0496807722Subjects--Topical Terms:

1017659
Health Sciences, Public Health.

Chromosomal aberrations induced by environmental pollutants.
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500 $a Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2369.
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502 $a Thesis (Ph.D.)--Columbia University, 2004.
520 $a Molecular and traditional epidemiology studies have indicated a possible relationship between in utero environmental exposures and increased risk for childhood cancers, especially acute leukemias. Chromosomal aberrations have been associated with environmental exposures and cancer risk in adults. Moreover, these exposures may be targeting specific chromosomes for damage. In order to more clearly define the association between prenatal exposures and chromosomal aberrations as a marker of potential cancer risk, whole chromosome probe FISH (fluorescence in situ hybridization) for chromosomes 1--6 and Giemsa-staining were used to measure aberration frequencies in 60 newborns from the Columbia Center for Children's Environmental Health (CCCEH) Prospective Cohort Study. The study population comprises African-American or Dominican, non-smoking mother-newborn pairs exposed to varying levels of polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and the residential pesticides, chlorpyrifos and propoxur. Prenatal exposures were assessed by questionnaire, prenatal air monitoring, and biomarkers in cord blood. African-American newborns had a significantly higher level of stable chromosomal aberration frequencies in cord blood than did Dominicans. Multivariate regression demonstrated a significant positive association of PAHs, as measured by personal air monitoring during the third trimester, with stable aberration frequencies (p = 0.0066). No significant increases in aberration frequencies were seen for ETS, propoxur, or chlorpyrifos exposures. FISH for stable aberrations was found to be a more sensitive measure for detecting changes in aberrations, compared to FISH for unstable aberrations or Giemsa-staining for aberrations. Breaks in chromosomes 1--6 were not randomly distributed by chromosome size or DNA content, which has never been documented in a population with exposures only to environmental pollutants such as the CCCEH cohort.
520 $a A complementary in vitro study was performed to further assess the correlation between chromosomal aberrations and environmental pollutants, or their metabolites. Lymphocyte cultures from 10 volunteers were challenged with benzo[a]pyrene diol epoxide (BPDE), 1,2,4-benzenetriol, and propoxur. There was significant inter-individual variability in response to each treatment. Only BPDE demonstrated a modest increase in the mean and median levels of stable and total aberration frequencies. The data suggested that the distribution of breaks within chromosomes 1--6 was not random. Moreover, each treatment generated a different pattern of cytogenetic damage.
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