Showing papers by "Frederica P. Perera published in 1999"

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

Abstract: 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.

Molecular and genetic damage from environmental tobacco smoke in young children.

Abstract: To assess the risks of early life exposure to environmental tobacco smoke (ETS), we tested whether four biomarkers in peripheral blood were associated with home ETS exposure in Hispanic and African-American children. The biomarkers included cotinine (a metabolite of nicotine) and three indicators of molecular and genetic damage from mutagens/carcinogens, protein adducts formed by the carcinogens 4-aminobiphenyl (4-ABP) and polycyclic aromatic hydrocarbons (PAHs), and sister chromatid exchanges (SCEs). We also explored possible ethnic differences in biomarkers. The study cohort comprised 109 Hispanic and African-American preschool children (1–6 years of age). Plasma cotinine was analyzed by gas chromatography, 4-ABP-hemoglobin adducts by gas chromatography-mass spectroscopy, PAH-albumin adducts by ELISA, and SCEs by cytogenetic techniques. Data on the amount of smoking by mothers (average 10.5 cigarettes per day) and other household members and regular visitors (average 6.5 cigarettes per day) were obtained by interview-administered questionnaires. Cotinine, 4-ABP-hemoglobin adducts, and PAH-albumin were significantly higher ( P < 0.05) in the ETS-exposed children compared with the unexposed. SCEs were marginally higher ( P = 0.076). African–American children had higher levels of cotinine ( P = 0.059) and PAH-albumin ( P = 0.02) than Hispanic children, after controlling for exposure to ETS. These results indicate molecular and genetic damage in minority children with relatively low exposure to ETS. They highlight the need for smoking prevention and cessation programs in women of reproductive age and in families with young children.