吸煙調查比較容易，不吸煙或吸煙。霧霾調查較難。空中粒子不是均勻分布的。 兩者是蘋果和橘子關係，調查不能比較。
但即便如此，空氣汙染對胎兒影響還是能測的。
http://cebp.aacrjournals.org/content/11/10/1134.full
Cancer Epidemiology, Biomarkers & Prevention
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In Utero DNA Damage from Environmental Pollution Is Associated with Somatic Gene Mutation in Newborns1
Frederica Perera2,
Karl Hemminki,
Wieslaw Jedrychowski,
Robin Whyatt,
Ulka Campbell,
Yanzhi Hsu,
Regina Santella,
Richard Albertini, and
James P. O’Neill
Columbia University School of Public Health, New York, New York 10032 [F. P., R. W., U. C., Y. H., R. S.]; College of Medicine, Jagiellonian University, Krakow 31-034, Poland [K. H., W. J.]; and University of Vermont Genetics Laboratory, Burlington, Vermont 05405 [J. P. O.]
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Abstract
Transplacental exposure to carcinogenic air pollutants from the combustion of fossil fuels is a growing health concern, given evidence of the heightened susceptibility of the fetus. These mutagenic/carcinogenic pollutants include aromatic compounds such as polycyclic aromatic hydrocarbons that bind to DNA, forming chemical-DNA adducts. We have investigated the genotoxic effects of transplacental exposure in humans by analyzing aromatic-DNA adducts and the frequency of gene mutations at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus in umbilical cord and maternal blood samples. Here we show, in a cross-sectional study of 67 mothers and 64 newborns from the Krakow Region of Poland, that aromatic-DNA adducts measured by 32P-postlabeling are positively associated with HPRT mutant frequency in the newborns (β = 0.56, P = 0.03) after controlling for exposure to tobacco smoke, diet, and socioeconomic status. In contrast to the fetus, HPRT mutations and DNA adducts do not reflect similar exposure periods in the mother, and the maternal biomarkers were not correlated. Adducts were higher in the newborn than the mother, indicating differential susceptibility of the fetus to DNA damage; but HPRT mutation frequency was 4-fold lower, consistent with the long lifetime of the biomarker. These results provide the first demonstration of a molecular link between somatic mutation in the newborn and transplacental exposure to common air pollutants, a finding that is relevant to cancer risk assessment.
但即便如此，空氣汙染對胎兒影響還是能測的。
http://cebp.aacrjournals.org/content/11/10/1134.full
Cancer Epidemiology, Biomarkers & Prevention
Skip to main page content
AACR Home
Search CEBP GO
Advanced Search
User Name Password Sign In
Advertisement
In Utero DNA Damage from Environmental Pollution Is Associated with Somatic Gene Mutation in Newborns1
Frederica Perera2,
Karl Hemminki,
Wieslaw Jedrychowski,
Robin Whyatt,
Ulka Campbell,
Yanzhi Hsu,
Regina Santella,
Richard Albertini, and
James P. O’Neill
Columbia University School of Public Health, New York, New York 10032 [F. P., R. W., U. C., Y. H., R. S.]; College of Medicine, Jagiellonian University, Krakow 31-034, Poland [K. H., W. J.]; and University of Vermont Genetics Laboratory, Burlington, Vermont 05405 [J. P. O.]
Next Section
Abstract
Transplacental exposure to carcinogenic air pollutants from the combustion of fossil fuels is a growing health concern, given evidence of the heightened susceptibility of the fetus. These mutagenic/carcinogenic pollutants include aromatic compounds such as polycyclic aromatic hydrocarbons that bind to DNA, forming chemical-DNA adducts. We have investigated the genotoxic effects of transplacental exposure in humans by analyzing aromatic-DNA adducts and the frequency of gene mutations at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus in umbilical cord and maternal blood samples. Here we show, in a cross-sectional study of 67 mothers and 64 newborns from the Krakow Region of Poland, that aromatic-DNA adducts measured by 32P-postlabeling are positively associated with HPRT mutant frequency in the newborns (β = 0.56, P = 0.03) after controlling for exposure to tobacco smoke, diet, and socioeconomic status. In contrast to the fetus, HPRT mutations and DNA adducts do not reflect similar exposure periods in the mother, and the maternal biomarkers were not correlated. Adducts were higher in the newborn than the mother, indicating differential susceptibility of the fetus to DNA damage; but HPRT mutation frequency was 4-fold lower, consistent with the long lifetime of the biomarker. These results provide the first demonstration of a molecular link between somatic mutation in the newborn and transplacental exposure to common air pollutants, a finding that is relevant to cancer risk assessment.
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