BACKGROUND AND OBJECTIVES: It has long been known that airborne polycyclic aromatic hydrocarbons (PAHs) can negatively affect pregnancy and birth outcomes, such as birth weight, fetal development, and placental growth factors. However, similar studies yield divergent results. Our goal was to estimate the amount of monohydroxylated PAH (OH-PAH) metabolites in the urine of pregnant women/mothers and their newborns in relation to birth outcomes, such as placenta weight, Apgar 5', and the growth parameters of children up to the age of two. METHODS: Two cohorts of children born in 2013 and 2014 during the summer and winter seasons in the Czech Republic in the cities Karviná (N = 144) and České Budějovice (N = 198), which differ significantly in the level of air pollution, were studied. PAH exposure was assessed by the concentration of benzo[a]pyrene (B[a]P) in the air and the concentration of 11 OH-PAH metabolites in the urine of newborns and mothers. Growth parameters and birth outcomes were obtained from medical questionnaires after birth and from pediatric questionnaires during the following 24 months of the child's life. RESULTS: Concentrations of B[a]P were significantly higher in Karviná (p < 0.001). OH-PAH metabolites were significantly higher in the mothers' as well as in the newborns' urine in Karviná and during the winter season. Neonatal length was shorter in newborns in Karviná (p < 0.001), but this difference evened out during the next 3 to 24 months. Compared to České Budějovice, newborns in Karviná showed significantly lower weight gain between birth and three months after delivery. The OH-PAH metabolites in mothers' or newborns' urine did not affect birth weight. The presence of seven OH-PAH (top 25% of values of concentrations higher than the median) metabolites in the newborns' urine is associated with decreased length of newborn. Nine OH-PAH metabolites decreased placenta weight, which was the most significant, while seven OH-PAH metabolites decreased Apgar 5'. CONCLUSION: We have shown a possible connection between higher concentration of OH-PAH metabolites in newborns' urine and decreased length, head circumference, placenta weight, and Apgar 5', but not birth weight.

• Keywords
• Birth length, Birth weight, Growth parameters, Head circumference, Monohydroxylated PAH metabolites, Placenta weight, Polycyclic aromatic hydrocarbons,
• MeSH
• Child MeSH
• Humans MeSH
• Mothers MeSH
• Infant, Newborn MeSH
• Placenta MeSH
• Polycyclic Aromatic Hydrocarbons * MeSH
• Birth Weight MeSH
• Pregnancy MeSH
• Prenatal Exposure Delayed Effects * epidemiology   MeSH
• Check Tag
• Child MeSH
• Humans MeSH
• Infant, Newborn MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Polycyclic Aromatic Hydrocarbons * MeSH

Thirty years ago, Northern Bohemia in the Czech Republic was one of the most air polluted areas in Europe. After political changes, the Czech government put forward a research program to determine if air pollution is really affecting human health. This program, later called the "Teplice Program", was initiated in collaboration with scientists from the United States Environmental Protection Agency (US EPA). This cooperation made possible the use of methods on the contemporary level. The very high concentrations of sulphur dioxide (SO2), particulate matter of 10 micrometers or less (PM10), and polycyclic aromatic hydrocarbons (PAHs) present in the air showed, for the first time, the impact of air pollutants on the health of the population in mining districts: adverse pregnancy outcomes, the impact of air pollution on sperm morphology, learning disabilities in children, and respiratory morbidity in preschool children. A surprising result came from the distribution of the sources of pollution: 70% of PM10 pollution came from local heating and not from power plants as expected. Thanks to this result, the Czech government supported changes in local heating from brown coal to natural gas. This change substantially decreased SO2 and PM10 pollution and affected mortality, especially cardiovascular mortality.

• Keywords
• DNA adducts, PAHs, PM2.5, SO2, air pollution, mortality, neurobehavioral changes, pregnancy outcome, sperm abnormalities,
• MeSH
• Air Pollutants * analysis   MeSH
• Humans MeSH
• Particulate Matter analysis   MeSH
• Child, Preschool MeSH
• Pregnancy MeSH
• Health MeSH
• Air Pollution * analysis   MeSH
• Check Tag
• Humans MeSH
• Child, Preschool MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Geographicals
• Czech Republic MeSH
• Europe MeSH
• Names of Substances
• Air Pollutants * MeSH
• Particulate Matter MeSH

Over the last decade or so, a large number of studies have investigated the possible adverse effects of ambient air pollution on birth outcomes. We reviewed these studies, which were identified by a systematic search of the main scientific databases. Virtually all reviewed studies were population based, with information on exposure to air pollution derived from routine monitoring sources. Overall, there is evidence implicating air pollution in adverse effects on different birth outcomes, but the strength of the evidence differs between outcomes. The evidence is sufficient to infer a causal relationship between particulate air pollution and respiratory deaths in the postneonatal period. For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants. For preterm births and intrauterine growth retardation (IUGR) the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies. Molecular epidemiologic studies suggest possible biologic mechanisms for the effect on birth weight, premature birth, and IUGR and support the view that the relation between pollution and these birth outcomes is genuine. For birth defects, the evidence base so far is insufficient to draw conclusions. In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.

• MeSH
• Infant MeSH
• Infant Mortality * MeSH
• Humans MeSH
• Infant, Low Birth Weight * MeSH
• Infant, Newborn MeSH
• Pregnancy MeSH
• Pregnancy Outcome MeSH
• Air Pollution adverse effects   MeSH
• Check Tag
• Infant MeSH
• Humans MeSH
• Infant, Newborn MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

The relationship between intrauterine growth retardation (IUGR) and exposure to particulate matter [less than/equal to] 10 microm (PM(10)) and particulate matter [less than and equal to] 2.5 microm (PM(2.5))( )in early pregnancy was recently studied in the highly polluted district of Teplice (Northern Bohemia). From this observation rose the question about the possible role of the carcinogenic fraction of polycyclic aromatic hydrocarbons (c-PAHs), which are usually bound to fine particles. The impact of c-PAHs and fine particles on IUGR was analyzed in Teplice and in Prachatice, a region with similarly high c-PAH but low particle levels. All European, single live births occurring in a 4-year period in Teplice (n = 3,378) and Prachatice (n = 1,505) were included. Detailed personal data were obtained via questionnaires and medical records. Mean PM(10), PM(2.5,) and c-PAHs levels during the 9 gestational months (GM) were estimated for each mother. Adjusted odds ratios (AORs) of IUGR for three levels of c-PAHs (low, medium, and high) and for continuous data were estimated after adjustment for a range of covariates using logistic regression models. In the present 4-year sample from Teplice, previously published results about increasing IUGR risk after exposure to particles in the first GM were fully confirmed, but no such effects were found in Prachatice. The AOR of IUGR for fetuses from Teplice exposed to medium levels of c-PAHs in the first GM was 1.60 [confidence interval (CI), 1.06-2. 15], and to high levels 2.15 (CI, 27-3.63). An exposure-response relationship was established by analyzing the continuous data. For each 10 ng increase of c-PAHs in the first GM, the AOR was 1.22 (CI, 1.07-1.39). About the same relationship was observed in Prachatice in spite of the low particle levels. The results prove that exposure to c-PAHs in early gestation may influence fetal growth. The particulate matter-IUGR association observed earlier may be at least partly explained by the presence of c-PAHs on particle surfaces.

• MeSH
• Adult MeSH
• Embryonic and Fetal Development MeSH
• Epidemiologic Studies MeSH
• Air Pollutants adverse effects   MeSH
• Humans MeSH
• Polycyclic Aromatic Hydrocarbons adverse effects   MeSH
• Fetal Growth Retardation etiology   MeSH
• Pregnancy MeSH
• Particle Size MeSH
• Pregnancy Outcome MeSH
• Environmental Exposure * MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, U.S. Gov't, Non-P.H.S. MeSH
• Geographicals
• India epidemiology   MeSH
• Names of Substances
• Air Pollutants MeSH
• Polycyclic Aromatic Hydrocarbons MeSH

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.

• MeSH
• Carcinogens analysis   toxicity   MeSH
• Humans MeSH
• Molecular Epidemiology * MeSH
• Mutagens analysis   toxicity   MeSH
• Occupational Exposure statistics & numerical data   MeSH
• Environmental Exposure statistics & numerical data   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Carcinogens MeSH
• Mutagens MeSH