Teplice program--the impact of air pollution on human health.

275

183

Evidence shows that fetuses and infants are more affected than adults by a variety of environmental toxicants because of differential exposure, physiologic immaturity, and a longer lifetime over which disease initiated in early life can develop. In this article we review data on the effects of in utero exposure to common environmental contaminants, including polycyclic aromatic hydrocarbons (PAH), particulate matter and environmental tobacco smoke (ETS). We then summarize results from our molecular epidemiologic study to assess risks from in utero exposures to ambient air pollution and ETS. This research study, conducted in Poland, used biomarkers to measure the internal and bioeffective dose of toxicants and individual susceptibility factors. The study included 160 mothers and 160 newborns. Ambient air pollution was significantly associated (p < 0.05) with the amount of PAH bound to DNA (PAH-DNA adducts) in both maternal and infant cord white blood cells (WBC). Newborns with elevated PAH-DNA adducts (greater than the median) had significantly decreased birth weight (p = 0.05), birth length (p = 0.02), and head circumference (p = 0.0005) compared to the newborns with lower adducts (n = 135). Maternal and infant cotinine levels were increased by active and passive cigarette smoke exposure of the mother (p < 0.01). An inverse correlation was seen between newborn plasma cotinine (nanograms per milliliter) and birth weight (p = 0.0001) and length (p = 0.003). Adducts were elevated in placental tissue and WBC of newborns who were heterozygous or homozygous for the cytochrome P4501A1 MspI restriction fragment length polymorphism (RFLP) compared to newborns without the RFLP. Levels of PAH-DNA and cotinine were higher in newborns than mothers. These results document that there is significant transplacental transfer of PAH and ETS constituents from mother to fetus; that PAH-DNA adduct levels in maternal and newborn WBC were increased with environmental exposure to PAH from ambient pollution; and that the fetus is more sensitive to genetic damage than the mother. The study also provided the first molecular evidence that transplacental PAH exposure to the fetus is compromising fetal development. If confirmed, these findings could have significant public health implications since a number of studies have found that reduction of head circumference at birth correlates with lower intelligence quotient as well as poorer cognitive functioning and school performance in childhood. Key words: air pollution, cigarette smoking, CYP1A1 MspI RFLP, GSTM1, newborns, PAH-DNA adducts, Poland. -Environ Health Perspect 107(suppl 3): 451-460 (1999). http://ehpnet 1. niehs. nih.gov/docs/1 999/suppl-3/451-460perera/abstract html The context of the work reviewed here is the growing awareness of the vulnerability of the developing fetus and child to certain environmental contaminants, including those commonly found in urban areas around the world. Following a summary of the toxicity and occurrence of polycyclic aromatic hydrocarbons (PAH), partic...

Section: Enhanced Susceptibility Of the Developing Fetus And Infantmentioning

confidence: 99%

Molecular epidemiologic research on the effects of environmental pollutants on the fetus.

Perera

Jedrychowski

Rauh

et al. 1999

275

183

“…Findings from animal studies have provided evidence of an association between air pollution and reproductive and developmental anomalies (Bignzmi et al 1994;Falkner 1986;Kavlock et al 1979Kavlock et al , 1980. Until recently, however, few epidemiologic studies have examined the potential effects of ambient air pollution on birth outcomes (Bobak , 2000Bobak and Leon 1999;Dejmek et al 1999;Dolk et al 2000;Ritz and Yu 1999;Ritz et al 2000;Rogers et al 2000;Sram et al 1996;Wang et al 1997;Woodruff et al 1997;Xu et al 1995).…”

mentioning

confidence: 99%

Association between gaseous ambient air pollutants and adverse pregnancy outcomes in Vancouver, Canada.

Liu

Krewski

Shi

et al. 2003

280

252

The association between ambient air pollution and adverse health effects, such as emergency room visits, hospitalizations, and mortality from respiratory and cardiovascular diseases, has been studied extensively in many countries, including Canada. Recently, studies conducted in China, the Czech Republic, and the United States have related ambient air pollution to adverse pregnancy outcomes. In this study, we examined association between preterm birth, low birth weight, and intrauterine growth retardation (IUGR) among singleton live births and ambient concentrations of sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), carbon monoxide (CO), and ozone in Vancouver, Canada, for 1985-1998. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for such effects. Low birth weight was associated with exposure to SO 2 during the first month of pregnancy (OR = 1.11, 95% CI, 1.01-1.22, for a 5.0 ppb increase). Preterm birth was associated with exposure to SO 2 (OR = 1.09, 95% CI, 1.01-1.19, for a 5.0 ppb increase) and to CO (OR = 1.08, 95% CI, 1.01-1.15, for a 1.0 ppm increase) during the last month of pregnancy. IUGR was associated with exposure to SO 2 (OR = 1.07, 95% CI, 1.01-1.13, for a 5.0 ppb increase), to NO 2 (OR = 1.05, 95% CI, 1.01-1.10, for a 10.0 ppb increase), and to CO (OR = 1.06, 95% CI, 1.01-1.10, for a 1.0 ppm increase) during the first month of pregnancy. In conclusion, relatively low concentrations of gaseous air pollutants are associated with adverse effects on birth outcomes in populations experiencing diverse air pollution profiles. Key words: air pollution, intrauterine growth retardation, low birth weight, preterm birth, risk assessment, sulfur dioxide.

“…We examined the influence of selfreported active and passive smoking on fetal growth in a retrospective epidemiologic study in the frame of a wider project named the Teplice Program (18). The design of the present study enabled us to evaluate the effects of ETS on the fetal growth of infants delivered by nonsmoking mothers as well as by mothers who smoked during the different gestational phases (AS mothers).…”

mentioning

confidence: 99%

The exposure of nonsmoking and smoking mothers to environmental tobacco smoke during different gestational phases and fetal growth.

Dejmek

Podrazilova

et al. 2002

121

We studied the impact of maternal exposure to environmental tobacco smoke (ETS) on birth weight (BW), low birth weight (LBW), and intrauterine growth retardation (IUGR) according to self-reported maternal smoking habits in a sample of 6,866 singleton births. We obtained data about parental characteristics and maternal active smoking (AS) and passive smoking at delivery via maternal questionnaires and medical records. We used three categories of smoking habits (nonsmokers and those who smoked 1-10 or >10 cigarettes per day) and defined ETS exposure as greater than or equal to 5 cigarettes per day smoked by others in the mother's presence. We used multiple regression and logistic regression procedures with adjustment for many associated covariates. We observed a significant reduction of the mean BW in infants of AS mothers. This reduction was only marginal for mothers who stopped smoking after recognizing their pregnancy. ETS exposure in 1,797 of 5,507 nonsmoking mothers reduced the mean BW of their infants by 53 g [95% confidence interval (CI), 24-82 g]. ETS exposure also significantly reduced BW in babies of AS mothers by 92 g (CI, 21-113 g) compared with BW of ETS-nonexposed AS mothers. The adjusted odds ratio (AOR) of LBW for ETS-exposed AS mothers was two times the LBW risk of ETS-nonexposed AS mothers(2.02; CI, 1.11-3.67); the AOR of ETS-exposed nonsmoking mothers was 1.51 (CI, 1.02-2.26). The AOR of IUGR for this group did not differ from unity (1.08; CI, 0.82-1.43). However, ETS exposure increased the AOR of IUGR for AS mothers from 1.64 (CI, 1.06-2.53) to 2.13 (CI, 1.70-2.67). ETS exposure reduced the BW of infants of nonsmoking mothers and contributed to additional BW reduction in infants of AS mothers. ETS exposure increased the risk of LBW but not that of IUGR in babies of nonsmoking mothers.