Impact of Air Pollution to Genome of Newborns

INTRODUCTIONThe effect of in utero environmental exposures on early-life health is growing area of research with major public health implications. Prenatal exposure to certain environmental chemicals, tobacco smoke, and air pollution during critical windows of development can lead to birth defects, low birth weight, impaired growth, immunological disturbances, respiratory symptoms and impaired lung, cognitive and psychomotor development (1, 2). Adverse effects can be significant and lead to lifetime chronic effects (3).Polycyclic aromatic hydrocarbons (PAHs) such as benzo[a] pyrene (B[a]P) are carcinogenic environmental pollutants resulting from incomplete combustion that are commonly found in tobacco smoke, ambient and indoor air, and charbroiled food. PAHs are released to atmosphere from local heating, traffic and various industrial sources. Ambient air exposure to PAHs poses a health risk due to their mutagenic, genotoxic and carcinogenic activity, which was detected only during the last two decades. PAHs are metabolized to form a wide range of products including highly reactive epoxides, which have capacity to bind to DNA, forming PAH-DNA adducts (4, 5) and induce oxidative damage (6). Using acellular system Binkova et al. (7) observed, that the genotoxicity of respirable particulate matter was related to the content of PAHs. Growing body of evidence suggests that ambient air exposure to B[a]P at levels over 1.0 ng/m^sup 3^ induces DNA damage (8). Personal exposure to B[a]P over this value predicts greater genomic frequency of translocations (9), micronuclei (10) and DNA fragmentation in sperm (11).Effect of air pollution seems to be significant to children, who are more sensitive than adults as their organism is in the stage of development. New knowledge about respiratory particles and complex mixtures as represented by PAHs adsorbed on their surface and the use of biomarkers of exposure and effect during the last twenty years were substantial to better understand how air pollution may affect children health already from the beginning of foetal life (12).Prenatal exposure to ambient air polluted by PAHs has been shown to be associated with reduction in birth weight (intrauterine growth restriction-IUGR), an increased likelihood of low birth weight (8, 13-15). B[a]P concentrations in the umbilical cord blood (UCB) correlated with reduced neonatal height and gestational age (16). In addition to inhalation, also dietary exposure is of concern. In the study context, birth weight was assumed to be affected by consuming barbecued meat (17). Also, sufficient evidence exists of a link between the prenatal exposure to mixtures of carcinogenic PAHs and intrauterine growth restriction in humans (10). Study of nonsmoking women from Beijing proved detectable concentrations of PAHs in breast milk, placenta and umbilical cord blood (18).In our recent study (19) we have focused on the effect of exposure to B[a]P to induce changes in DNA adducts, micronuclei and transcriptome in pregnancies from Prague and Ceske Budejovice (CB). Exposure to B[a]P 3 months before delivery was 1.9 ± 0.5 ng/m3 vs. 3.2 ± 0.2 ng/m3 for Prague and CB, respectively (winter 2008/2009). Samples obtained from 35 mothers from Prague and 52 mothers from CB were analyzed, all subjects were nonsmokers. DNA adducts were determined by 32P-postlabeling. Levels of total DNA adducts in cord blood were 0.98 ± 0.89 vs. 1.40 ± 1.31/108 nucleotides (p