Biomarkers of exposure to tobacco smoke and environmental pollutants in mothers and their transplacental transfer to the foetus. Part I: Bulky DNA adducts

Topinka, Jan; Milcová, Alena; Líbalová, Helena; Nováková, Zuzana; Rössner, Pavel; Balaščák, Ivan; Šrám, Radìm J.

doi:10.1016/j.mrfmmm.2009.04.011

Cited by 66 publications

(40 citation statements)

References 31 publications

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“…When toxic organic matter such as polycyclic aromatic hydrocarbons (PAH) is adsorbed onto the surface of PM, associated oxidative stress (Leem et al, 2005) and DNA adducts are formed (Perera et al, 1999). High levels of DNA adducts were associated with reduced gestational length Perera et al, 1998;Perera et al, 1999), and a correlation has been observed between the adduct levels in the mother's and the newborn's blood (Topinka et al, 2009). Newborns with elevated PAH-DNA adducts (which are used as a proxy to measure individual biologically effective dose to PAH) were found to have significantly reduced birth weight and head circumference suggesting that transplacental exposures to PAHs in ambient air may negatively impact on fetal development.…”

Section: Biological Mechanismmentioning

confidence: 99%

Air Pollution and Adverse Pregnancy Outcome

Leem¹,

Ha²

2011

Air Pollution - New Developments

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Section: Biological Mechanismmentioning

confidence: 99%

Air Pollution and Adverse Pregnancy Outcome

Leem¹,

Ha²

2011

Air Pollution - New Developments

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“…PAHs are transported by diffusion across membranes in the respiratory and gastrointestinal tract and are absorbed into the bloodstream. PAHs are capable of crossing the placenta [44, 45]. Umbilical cord blood PAH-DNA adducts have been associated with decreased fetal growth, after adjusting for maternal environmental tobacco smoke exposures in China [46], Krakow, and New York [47, 48].…”

Section: Introductionmentioning

confidence: 99%

Genetic modification of the effect of maternal household air pollution exposure on birth weight in Guatemalan newborns

Thompson¹,

Yousefi²,

Peñaloza³

et al. 2014

Reproductive Toxicology

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Low birth weight is associated with exposure to air pollution during pregnancy. The purpose of this study was to evaluate whether null polymorphisms of Glutathione S-transferases (GSTs), specifically GSTM1 and GSTT1 genes in infants or mothers, modifies the association between high exposures to household air pollution (HAP) from cooking fires and birth weight. Pregnant women in rural Guatemala were randomized to receive a chimney stove or continue to use open fires for cooking. Newborns were measured within 48 hours of birth. 132 mother-infant pairs provided infant genotypes (n=130) and/or maternal genotypes (n=116). Maternal null GSTM1 was associated with a 144 gram (95% CI: -291, 1) and combined maternal/infant null GSTT1 was associated with a 155 gram (95% CI -303, -8) decrease in birth weight. Although there was a trend toward higher birth weights with increasing number of expressed GST genes, the effect modification by chimney stove use was not demonstrated.

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“…The implications are further compounded when the exposed individual is pregnant. Whether the pregnant woman is a smoker or simply exposed to environmental tobacco smoke, the threat of insult to the developing fetus is still cause for concern (1, [17][18][19][20][21][22]. The majority of the compounds found in side stream smoke are the same as those found in mainstream smoke (23)(24)(25)(26)(27)(28)(29).…”

Section: Introduction Tobacco Exposure and Pregnancymentioning

confidence: 99%

“…Polycyclic aromatic hydrocarbons (PAH) are ubiquitous environmental contaminants produced during the combustion of fossil fuels and wood (17). Additionally, PAH such as benzo[a]pyrene, naphthalene, anthracene and pyrene are found in tobacco smoke.…”

Section: Introduction Tobacco Exposure and Pregnancymentioning

confidence: 99%

“…Many PAH are carcinogenic and mutagenic. Benzo[a]pyrene undergoes metabolism by CYP1A1 to epoxides which are further metabolized by epoxide hydrolases to dihydrodiols which can be further activated to the highly carcinogenic benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide ( Figure 1) (17,(53)(54)(55)(56)(57)(58)(59)(60). Of the four possible diol epoxides, (+)-(7R,8S,9S,10S) diol epoxide-2 was found to be the most potent carcinogen.…”

Section: Introduction Tobacco Exposure and Pregnancymentioning

confidence: 99%

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The Relationship between Maternal and Fetal CYP1A1 Genotype in Smokers and Nonsmokers to Benzo(a)pyrene Hemoglobin Adducts

Myers

Barnes

Wright

et al. 2010

Polycyclic Aromatic Compounds

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Numerous methods exist by which we can follow exposure to tobacco smoke in experimental animals as well as in human populations. The simplest method to follow tobacco exposure is by assessing either urinary or serum cotinine levels. Although this provides an accurate assessment of short-term exposure to tobacco, it fails to provide a loan term assessment of exposure over several weeks and/or months. DNA adducts also provide effective means of monitoring exposure to tobacco smoke carcinogens. However, with the use of DNA adducts one deals with repair mechanisms, which may be altered as a result of the initial exposures. The ideal biomarker for use in assessing chemical exposures over a long-term basis is the use of the red cell protein hemoglobin. Formation of electrophilic metabolites of carcinogens has been shown to react with a variety of nucleophilic sites on hemoglobin, therefore forming covalent adducts which persists for the life of the red cell (120 days) and thus can be detected in used as a biomarker of exposure. Tobacco carcinogens must first be activated by a variety of enzymes prior to becoming electrophilic intermediates. Metabolic activation of these compounds proceeds by a number of steps, including the activation via cytochrome enzymes (CYP). Following activation of the carcinogens to a reactive electrophile, the reactive compound can form covalent adducts with DNA and protein. Following activation of the carcinogens, enzymes also are responsible for the detoxification of the reactive electrophilic metabolites. These enzymes help the body handle exposure to these compounds by facilitating detoxification and illumination of those reactive carcinogenic derivatives. The present study examined the relationship between polymorphism of CYP1A1 pharmacogenetics

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Biomarkers of exposure to tobacco smoke and environmental pollutants in mothers and their transplacental transfer to the foetus. Part I: Bulky DNA adducts

Cited by 66 publications

References 31 publications

Air Pollution and Adverse Pregnancy Outcome

Air Pollution and Adverse Pregnancy Outcome

Genetic modification of the effect of maternal household air pollution exposure on birth weight in Guatemalan newborns

The Relationship between Maternal and Fetal CYP1A1 Genotype in Smokers and Nonsmokers to Benzo(a)pyrene Hemoglobin Adducts

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