Depressed height gain of children associated with intrauterine exposure to polycyclic aromatic hydrocarbons (PAH) and heavy metals: the cohort prospective study.

Fetal exposure to environmental toxicants may program the development of children and have long-lasting health impacts. The study tested the hypothesis that depressed height gain in childhood is associated with prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and heavy metals (lead and mercury). The study sample comprised 379 children born to non-smoking mothers among whom a total of 2011 height measurements were carried out over the 9-year follow-up period.

Long term effects of prenatal and postnatal airborne PAH exposures on ventilatory lung function of non-asthmatic preadolescent children. Prospective birth cohort study in Krakow.

The main goal of the study was to test the hypothesis that prenatal and postnatal exposures to polycyclic aromatic hydrocarbons (PAH) are associated with depressed lung function in non-asthmatic children. The study sample comprises 195 non-asthmatic children of non-smoking mothers, among whom the prenatal PAH exposure was assessed by personal air monitoring in pregnancy. At the age of 3, residential air monitoring was carried out to evaluate the residential PAH exposure indoors and outdoors.

Prenatal exposure to polycyclic aromatic hydrocarbons and cognitive dysfunction in children.

Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants produced by combustion of fossil fuel and other organic materials. Both experimental animal and human studies have reported the harmful impacts of PAH compounds on fetal growth and neurodevelopment, including verbal IQ of children. Here, we have assessed the association between cognitive function of children and prenatal PAH exposures.

Antihistamine medication may alleviate negative effects of prenatal exposure to polycyclic aromatic hydrocarbons (PAH) on lung function in children. Birth cohort prospective study.

The main purpose of the present study was to test the hypothesis that the depressed lung growth attributable to prenatal exposure to polycyclic aromatic hydrocarbons (PAH) may be modified by the intake of antihistamine medications. Individual prenatal PAH exposure was assessed by personal air monitoring in 176 children who were followed over nine years, in the course of which outdoor residential air monitoring, allergic skin tests for indoor allergens, lung function tests (FVC, FEV(1), FEV(05), and FEF(25-75)) were performed. The analysis with the General Estimated Equation (GEE) showed no association between prenatal PAH exposure and lung function in the group of children who were reported to be antihistamine users.

Separate and joint effects of tranplacental and postnatal inhalatory exposure to polycyclic aromatic hydrocarbons: prospective birth cohort study on wheezing events.

The goal of this epidemiologic investigation was to analyze the associations between prenatal and postnatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and severity of wheeze and recurrent wheeze. The 257 children included in this analysis had a complete set of prenatal and postnatal PAH measurements and attended regular health checkups over a 4-year follow-up period since birth. Transplacental PAH exposure was measured by personal air monitoring of the mothers during the second trimester of pregnancy; postnatal exposure was estimated using the same instruments indoors at the children's residences at age 3.

Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in non-asthmatic children. A population-based birth cohort study.

Objectives: The main goal of the study was to assess possible association between fetal exposure to fine particulate matter (PM2.5) and exhaled carbon monoxide (eCO) measured in non-asthmatic children.

Material And Methods: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków.

Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute broncho-pulmonary infections in early childhood.

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM2.5) on the recurrent broncho-pulmonary infections in early childhood.

The relationship between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) and PAH-DNA adducts in cord blood.

In a birth cohort study, we have assessed the dose-response relationship between individual measurements of prenatal airborne polycyclic aromatic hydrocarbon (PAH) exposure and specific PAH-DNA adducts in cord blood adjusted for maternal blood adducts and season of birth. The study uses data from an earlier established birth cohort of children in Krakow. The final analysis included 362 pregnant women who gave birth to term babies and had complete data on personal exposure in the second trimester of pregnancy to eight airborne PAHs including benzo[a]pyrene (B[a]P), as well as DNA adducts, both in maternal and cord blood.

Prohypertensive effect of gestational personal exposure to fine particulate matter. Prospective cohort study in non-smoking and non-obese pregnant women.

Exposure to fine particulate matter (PM) is a recognized risk factor for elevated blood pressure (BP) and cardiovascular disease in adults, and this prospective cohort study was undertaken to evaluate whether gestational exposure to PM(2.5) has a prohypertensive effect. We measured personal exposure to fine particulate matter (PM(2.

Effect of prenatal exposure to fine particulate matter on ventilatory lung function of preschool children of non-smoking mothers.

Impaired fetal development is associated with a number of adult chronic diseases and it is believed that these associations arise as a result of the phenomenon of prenatal programming, which involves persisting changes in structure and function of various body organs caused by ambient factors during critical and vulnerable periods of early development. The main goal of the study was to assess the association between lung function in early childhood and prenatal exposure to fine particulate matter (PM(2.5)), which represents a wide range of chemical compounds potentially hazardous for fetal development.

Intrauterine exposure to polycyclic aromatic hydrocarbons, fine particulate matter and early wheeze. Prospective birth cohort study in 4-year olds.

The main goal of the study was to determine the relationship between prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) measured by PAH-DNA adducts in umbilical cord blood and early wheeze. The level of PAH-DNA adducts in the cord blood is assumed to reflect the cumulative dose of PAHs absorbed by the foetus over the prenatal period. The effect of prenatal PAH exposure on respiratory health measured by the incidence rate ratio (IRR) for the number of wheezing days in the subsequent 4 yr follow-up was adjusted for potential confounding factors such as personal prenatal exposure to fine particulate matter (PM(2.

Variability of total exposure to PM2.5 related to indoor and outdoor pollution sources Krakow study in pregnant women.

The study is a part of an ongoing prospective cohort study on the relationship between the exposure to environmental factors during pregnancy and birth outcomes and health of newborns. We have measured personal PM(2.5) level in the group of 407 non-smoking pregnant women during the 2nd trimester of pregnancy.