Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.

Whyatt, Robin M.; Santella, Regina M.; Jędrychowski, Wiesław; Garte, Seymour; Bell, Douglas A.; Ottman, Ruth; Gladek-Yarborough, Alicja; Cosma, Greg; Young, Tie Lan; Cooper, Thomas B.; Randall, Mary C.; Manchester, David K.; Perera, Frederica P.

doi:10.1289/ehp.98106821

Cited by 74 publications

(35 citation statements)

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“…The possible biological mechanisms of air pollution on birth weight might vary according the time of pregnancy, such as the implantation of the fetus and the formation of placenta during the first trimester, as well as important weight gain during the third trimester. Placental abnormalities, DNA damage, disruption of the endocrine system and change of blood coagulability are those potential biological mechanisms, which have been reported (Dejmek et al, 2000;Maisonet et al, 2004;Perera et al, 1999Perera et al, , 2002Whyatt et al, 1998). The finding of a significant effect of PM exposure on LBW during the first trimester is consistent.…”

Section: Window Periodssupporting

confidence: 56%

Air Pollution and Adverse Pregnancy Outcome

Leem¹,

Ha²

2011

Air Pollution - New Developments

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Section: Window Periodssupporting

confidence: 56%

Air Pollution and Adverse Pregnancy Outcome

Leem¹,

Ha²

2011

Air Pollution - New Developments

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“…However, epidemiologic research on this relationship is limited and has been hampered partly because of uncertainties in exposure estimates. Although biologic markers can be useful in understanding the role of environmental contaminants during fetal development (15)(16)(17), research on the effects of prenatal organophosphate exposure has been limited by the lack of biomarkers reflecting cumulative exposures. Available biomarkers, including blood and urine measurements, provide short-term dosimeters only (halflives range from 10 to 30 hr) (18)(19)(20).…”

mentioning

confidence: 99%

Measurement of organophosphate metabolites in postpartum meconium as a potential biomarker of prenatal exposure: a validation study.

Whyatt

Barr

2001

Environ Health Perspect

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144

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Experimental data have linked exposure to prenatal organophosphates to adverse neurocognitive sequalae. However, epidemiologic research has been hampered by lack of reliable dosimeters. Existing biomarkers reflect short-term exposure only. Measurements of pesticides in postpartum meconium may yield a longer-term dosimeter of prenatal exposure. As the initial step in biomarker validation, this research determined background levels, detection limits, and stabilities of six organophosphate metabolites in meconium: diethylphosphate (DEP), diethylthiophosphate (DETP), diethyldithiophosphate (DEDTP), dimethylphosphate (DMP), dimethylthiophosphate (DMTP), and dimethyldithiophosphate (DMDTP). Calibration curves were also constructed. The meconium was collected from 20 newborns at New York Presbyterian Hospital; analyses were undertaken at the Centers for Disease Control and Prevention (CDC). DEP was detected in 19/20 samples (range 0.8-3.2 microg/g) and DETP was detected in 20/20 (range 2.0-5.6 microg/g). DMP and DEDTP were each detected in 1/20 (at 16 and 1.8 microg/g, respectively). DMTP and DMDTP were not detected. Detection limits were comparable to or lower than those in urine; levels were similar to those seen in adult urine in population-based research. Metabolites were stable at room temperature over 12 hr. Calibration curves were linear over the range tested (0.5-400 microg/g); recoveries ranged from 18% to 66%. Using isotope dilution, recoveries of each analyte in individual samples can be corrected automatically based on the recovery of the respective stable isotope-labeled analogue, making this method fully quantitative. Results indicate that measurements of organophosphate metabolites in meconium have promise as biomarkers of prenatal exposure. Further research is needed to determine the time frame of exposure represented by pesticide levels in meconium and to evaluate the dose-response relationship.

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“…CYPlAI affected DNA adducts in newborns (70) and placentas (71) of residents of an air-polluted region; no effect was observed on 1-OH-pyrene in the urine of policemen exposed to air pollution (77) or smokers (92) or on DNA adducts in smokers (92).…”

Section: Discussionmentioning

confidence: 99%

“…These methods were used in 8 studies. DNA adducts were increased in maternal venous and cord blood (70) and in smokers (91)(92)(93)95). No effect was seen for PAH exposure in placenta (71) or for tobacco smoke exposure in placentas (85) and smokers (86).…”

Section: Discussionmentioning

confidence: 99%

“…Surprisingly, of the 12 studies on the effect of tobacco smoke on biomarkers of exposure and effect, only 2 studies evaluated smoking status using cotinine levels in plasma (16,91 There are a limited number of studies on the effect of genotype on biomarkers of exposure and the effect on environmentally exposed groups (Table 2). Knudsen In a cohort of 70 mothers and newborns from Poland, DNA adducts in maternal WBCs were not related to CYPIAJ MspI or GSTM1 polymorphisms, but DNA adducts were significantly higher in newborns who were heterozygous or homozygous for the wild-type genotype of CYPIAJ MspI (70). An investigation of the relationship between PAH-DNA adduct levels and CYPIAI MspI polymorphisms showed that placental PAH-DNA adduct levels were also significantly higher in newborns who were homozygous or heterozygous for the wild-type of CYPIAJ MspI (71,73).…”

Section: Environmental Exposure To Mutagens and Carcinogensmentioning

confidence: 98%

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Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

Srám¹,

Binková²

2000

Environmental Health Perspectives

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Molecular epidemiology is a new and evolving area of research, combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and influence of individual susceptibility with epidemiologic methodologies. Biomarkers evaluated were selected according to basic scheme: biomarkers of exposure-metabolites in urine, DNA adducts, protein adducts, and Comet assay parameters; biomarkers of effect-chromosomal aberrations, sister chromatid exchanges, micronuclei, mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, and the activation of oncogenes coding for p53 or p21 proteins as measured on protein levels; biomarkers of susceptibility-genetic polymorphisms of genes CYP1A1, GSTM1, GSTT1, NAT2. DNA adducts measured by 32P-postlabeling are the biomarker of choice for the evaluation of exposure to polycyclic aromatic hydrocarbons. Protein adducts are useful as a biomarker for exposure to tobacco smoke (4-aminobiphenyl) or to smaller molecules such as acrylonitrile or 1,3-butadiene. Of the biomarkers of effect, the most common are cytogenetic end points. Epidemiologic studies support the use of chromosomal breakage as a relevant biomarker of cancer risk. The use of the Comet assay and methods analyzing oxidative DNA damage needs reliable validation for human biomonitoring. Until now there have not been sufficient data to interpret the relationship between genotypes, biomarkers of exposure, and biomarkers of effect for assessing the risk of human exposure to mutagens and carcinogens. Key words: air pollution, benzene, biomarkers, coke oven, genotypes, occupational exposure, PAHs, pesticides, tobacco smoke. -Envwron Health Perspect 1 08(suppl 1):57-70 (2000). http.//ehpnetl. niehs. nih.gov/docs/2000/suppl-1/57-70sram/abstract. html A new and evolving area of research termed molecular epidemiology attempts to merge sophisticated and highly sensitive laboratory methods (many of them developed during the recent revolution in molecular biology) with analytical epidemiologic methods. Molecular epidemiology bridges basic research in molecular biology and studies of human cancer causation by combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and the influence of individual susceptibility with epidemiologic methodologies (1). The most common view is that the approach represents a natural convergence of molecular biology and epidemiology (2).The number of biomarkers available for evaluating genetic and cancer risk in humans is quite large. Their utility-for human biomonitoring is suggested by the well-known paradigm of environmentally induced cancer, which represents end points for assessing the entire spectrum of human-genotoxicant interactions (3). These biomarkers begin with exposure and include absorption, metabolism, distribution, critical target interaction (i.e., DNA damage and repair), genetic changes, and finally, disease, which is the province of traditional epidemiology. The development of biomarkers has given rise to the field of ...

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Relationship between ambient air pollution and DNA damage in Polish mothers and newborns.

Cited by 74 publications

References 57 publications

Air Pollution and Adverse Pregnancy Outcome

Air Pollution and Adverse Pregnancy Outcome

Measurement of organophosphate metabolites in postpartum meconium as a potential biomarker of prenatal exposure: a validation study.

Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

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