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.
An ongoing air quality monitoring program in the Czech Republic has provided nearly continuous data for the concentrations of aerosol and gas-phase pollutants since its inception in February 1992. In addition to PM-2.5 concentrations, the concentrations of sulfate, organic carbon, elemental carbon, trace elements (Al−Pb), and polynuclear aromatic hydrocarbons (PAHs) were also measured. Fine particulate matter (PM-2.5) was composed mainly of organic carbon and sulfate with smaller amounts of trace metals. Coarse particle mass concentrations were typi cally between 10 and 30% of PM-2.5 concentrations. The chemical composition of emissions from power plants, residential space heating, local factories, and motor vehicles was also characterized. The ambient monitoring and source characterization data were then used in receptor modeling calculations, the results of which indicate that residential space heating and power plant emissions ac counted for most of fine particle mass concentrations observed during winter air pollution episodes. Motor vehicles, incinerators, and windblown dust contributed to the balance of the fine particle mass. Peak 24-h average TSP and SO2 concentrations (1100 and 800 μg/m3, respectively) obtained at the main monitoring site at Teplice in northern Bohemia during a severe air pollution episode in 1993 were within a factor of 2 of smoke and SO2 concentrations (1800 and 1600 μg/m3) measured in London during the smog episode of December 5−9, 1952. That pollution episode was thought to have contributed to a substantial increase in mortality.
JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.The relationship between intrauterine growth retardation (IUGR) and exposure to particulate matter < 10 pm (PM10) and particulate matter < 2.5 pm (PM2.5) 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 PM10, PM2.5, 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.
The effect of personal exposure to air pollution on DNA adducts in humans was analyzed in a group (n = 30) of women working outdoors (up to 8 h/day) as postal workers or gardeners in the city of Teplice, Czech Republic (Northern Bohemia), where winter inversions may result in high levels of air pollution from coal combustion. Ten of these women were followed up during the next winter season by repeated personal exposure monitoring and analysis of the DNA adducts in their white blood cells (in four sampling periods). Personal exposure monitoring for respirable particles (< 2.5 microns) was conducted for the 24 h period prior to collection of blood and urine. Particle extracts were analyzed for carcinogenic polycyclic aromatic hydrocarbons (PAH). Urine samples were collected for cotinine analysis to control for exposure to tobacco smoke. DNA isolated from white blood cells was analyzed by 32P-postlabeling with the butanol enrichment procedure. There were 21 non-smokers and nine light smokers in the pilot study (November 1992) and only non-smokers in the follow-up study (winter season 1993/94). In both studies high personal exposure variability between the individuals sampled on the same day was observed. In the pilot study we found a significantly higher (P < 0.05) level of DNA adducts in the 14 non-smoking women sampled on November 24, when their exposure to carcinogenic PAH was also significantly higher (P < 0.05), compared with seven non-smoking women sampled on November 26. We also found a significant correlation (r = 0.541, P < 0.016) between individual exposure to carcinogenic PAH and DNA adducts for the group of non-smokers (n = 21). No significant difference in DNA adduct levels was found between non-smokers and smokers. In the follow-up study, during one sampling period the ambient and personal air monitors exhibited a significantly elevated exposure to respirable particles and carcinogenic PAH. Analyzing data from the follow-up study, a significant effect of personal exposure on DNA adduct levels and their relationship with short-term exposure to carcinogenic PAH was found. The results suggest that DNA adduct levels in white blood cells reflect a short-term environmental exposure.
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