E Flak

Jagiellonian University, Cracovia, Lesser Poland Voivodeship, Poland

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Publications (100)153.96 Total impact

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    ABSTRACT: 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, FEV1, FEV05, and FEF25-75) 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. However, in the group of antihistamine non-users all lung function tests except for FEF25-75 were significantly and inversely associated with prenatal airborne PAH exposure. The results of the study suggest that the intake of antihistamine medications in early childhood may inhibit the negative effect of fetal PAH exposure on lung growth and provides additional indirect evidence for the hypothesis that lung alterations in young children resulting from PAH exposure may be caused by the allergic inflammation within lung. Pediatr Pulmonol. © 2014 Wiley Periodicals, Inc.
    Pediatric Pulmonology 08/2014; · 2.38 Impact Factor
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    ABSTRACT: 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. The relation between cord blood PAH-DNA adducts and airborne prenatal PAH exposure was non-linear. Although cord blood PAH-DNA adducts were significantly associated with the B[a]P exposure categorized by tertiles (non-parametric trend z=3.50, P<0.001), the relationship between B[a]P and maternal blood adducts was insignificant (z=1.63, P=0.103). Based on the multivariable linear regression model, we estimated the effect of the prenatal airborne B[a]P on the level of cord blood adducts. In total, 14.8% of cord blood adducts variance was attributed to the level of maternal adducts and 3% to a higher prenatal B[a] exposure above 5.70 ng/m(3). The calculated fetal/maternal blood adduct ratio (FMR) linearly increased with B[a]P exposure (z=1.99, P=0.047) and was highest at B[a]P concentrations exceeding 5.70 ng/m(3). In conclusion, the results support other findings that transplacental exposure to B[a]P from maternal inhalation produces DNA damage in the developing fetus. It also confirms the heightened fetal susceptibility to prenatal PAH exposure that should be a matter of public health concern, particularly in the highly polluted areas, because DNA adducts represent a pro-carcinogenic alteration in DNA. The continuation of this birth cohort study will assess the possible health effects of fetal DNA damage on the health of children and help in establishing new protective guidelines for newborns.Journal of Exposure Science and Environmental Epidemiology advance online publication, 9 January 2013; doi:10.1038/jes.2012.117.
    Journal of Exposure Science and Environmental Epidemiology 01/2013; · 3.19 Impact Factor
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    ABSTRACT: The goal of the study is to evaluate the importance of maternal atopy as a potential biological source of variability of exhaled FeNO values in healthy children who were non-asthmatic and non-sensitized to common domestic allergens. The study sample consisted of 61 seven-year old children. Fractional exhaled nitric oxide (FeNO) has been measured by NObreath (Bedfont portable device). Children with reported maternal atopy had significantly higher mean FeNO values (geometric mean =10.7 ppb; 95%CI: 6.7-17.1 ppb) than those who denied it (geometric mean =5.2 ppb 95%CI: 3.9-6.9 ppb) (p=0.010). Neither the correlation between FeNO values and gender, respiratory and eczema symptoms, nor ETS exposure in the prenatal and postnatal period or body mass of children were significant. We also found no significant association of FeNO values with the amount of common domestic allergens measured in the households. The results of the ROC analysis suggested 11 ppb as the cut-off point for FeNO to distinguish groups of healthy children with and without maternal atopy. In conclusion, our study provided some evidence suggesting that maternal atopy may affect FeNO level in children independently of asthma and sensitization status to common domestic allergens. The data should be considered in the interpretation of FeNO levels in clinical practice and setting up FeNO screening criteria for identification of eosinophilic airway inflammation.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 06/2012; 63(3):257-62. · 2.48 Impact Factor
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    ABSTRACT: The main goal of the study was to assess possible association between transplacental exposure to genotoxic PAH compounds assessed by the cord blood PAH-DNA adducts and fractional exhaled nitric oxide (FeNO) measured in healthy non-asthmatic children at the age of 7 years. The subjects included the subsample of 89 children who took part in the ongoing population based birth cohort study in Krakow and attended FeNO testing. The effect of transplacental PAH exposure was adjusted for potential confounders, such as maternal allergy and children's specific atopy to common domestic allergens. RESULTS: FeNO values were significantly elevated in children with higher prenatal PAH exposure (gmean = 7.7 ppb; 95% CI: 5.8-10.2 ppb) compared with those at low exposure level (gmean = 3.8 ppb; 95% CI: 2.3-6.3) (P = 0.011). Children with maternal allergy had also significantly higher mean FeNO values (gmean = 13.7 ppb, 95% CI: 8.8-21.4 ppb) compared with the subjects whose mothers denied allergy (gmean = 5.6 ppb, 95% CI: 4.3-7.3 ppb) (P = 0.012). Similarly, FeNO values in atopic children were higher (gmean = 11.2 ppb; 95% CI: 3.8-32.8 ppb) than in non-atopic individuals (gmean = 6.0 ppb; 95% CI: 4.7-7.7 ppb, P = 0.079). The results of the nested multivariable linear regression analysis showed that both maternal allergy and sensitization of children to domestic aeroallergens jointly explained 10.4% of FeNO variance, however, the additional 10.9% was determined by prenatal PAH exposure. CONCLUSION: FeNO is more than a marker useful for screening atopy or symptomatic bronchial inflammation and may also be a proxy for cytokine deregulation and "allergic response" phenotype possibly established in fetal period due to transplacental PAH exposure. Preliminary results of our study should encourage more studies on intrauterine PAH exposure and later respiratory symptoms. Pediatr Pulmonol. 2012. 47:1131-1139. © 2012 Wiley Periodicals, Inc.
    Pediatric Pulmonology 05/2012; 47(11):1131-9. · 2.38 Impact Factor
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    ABSTRACT: 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(2.5)) by personal air monitoring in the second trimester of pregnancy among 431 women, and BP values in the third trimester were obtained from medical records of prenatal care clinics. In the general estimating equation model, the effect of PM(2.5) on BP was adjusted for relevant covariates such as maternal age, education, parity, gestational weight gain (GWG), prepregnancy BMI, environmental tobacco smoke (ETS), and blood lead level. Systolic blood pressure (SBP) increased in a linear fashion across a dosage of PM(2.5) and on average augmented by 6.1 mm Hg (95% CI, 0.6-11.6) with log unit of PM(2.5) concentration. Effects of age, maternal education, prepregnancy BMI, blood lead level, and ETS were insignificant. Women with excessive gestational weight gain (>18 kg) had higher mean SBP parameters by 5.5 mmHg (95% CI, 2.7-8.3). In contrast, multiparous women had significantly lower SBP values (coeff. = -4.2 mm Hg; 95% CI, -6.8 to -1.6). Similar analysis performed for diastolic blood pressure (DBP) has demonstrated that PM(2.5) also affected DBP parameters (coeff. = 4.1; 95% CI, -0.02 to 8.2), but at the border significance level. DBP values were positively associated with the excessive GWG (coeff. = 2.3; 95% CI, 0.3-4.4) but were inversely related to parity (coeff. = -2.7; 95% CI, -4.6 to -0.73). In the observed cohort, the exposure to fine particulate matter during pregnancy was associated with increased maternal blood pressure.
    Cardiovascular toxicology 02/2012; 12(3):216-25. · 2.56 Impact Factor
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    ABSTRACT: We previously reported an association between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and lower birth weight, birth length, and head circumference. The main goal of the present analysis was to assess the possible impact of coexposure to PAH-containing barbecued meat consumed during pregnancy on birth outcomes. The birth cohort consisted of 432 pregnant women who gave birth at term (>36 wk of gestation). Only non-smoking women with singleton pregnancies, 18-35 y of age, and who were free from chronic diseases such as diabetes and hypertension, were included in the study. Detailed information on diet over pregnancy was collected through interviews and the measurement of exposure to airborne PAHs was carried out by personal air monitoring during the second trimester of pregnancy. The effect of barbecued meat consumption on birth outcomes (birth weight, length, and head circumference at birth) was adjusted in multiple linear regression models for potential confounding factors such as prenatal exposure to airborne PAHs, child's sex, gestational age, parity, size of mother (maternal prepregnancy weight, weight gain in pregnancy), and prenatal environmental tobacco smoke. The multivariable regression model showed a significant deficit in birth weight associated with barbecued meat consumption in pregnancy (coeff = -106.0 g; 95%CI: -293.3, -35.8). The effect of exposure to airborne PAHs was about the same magnitude order (coeff. = -164.6 g; 95%CI: -172.3, -34.7). Combined effect of both sources of exposure amounted to birth weight deficit of 214.3 g (95%CI: -419.0, -9.6). Regression models performed for birth length and head circumference showed similar trends but the estimated effects were of borderline significance level. As the intake of barbecued meat did not affect the duration of pregnancy, the reduced birth weight could not have been mediated by a shortened gestation period. In conclusion, the study results provided epidemiologic evidence that prenatal PAH exposure from diet including grilled meat might be hazardous for fetal development.
    Nutrition 11/2011; 28(4):372-7. · 2.86 Impact Factor
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    ABSTRACT: The goal of the study was to test the hypothesis that prenatal Paracetamol exposure increases the risk of developing eczema in early childhood and that this association may be stronger in children who are exposed in fetal period to higher concentrations of fine particulate matter (PM2.5). The study sample consisted of 322 women recruited from January 2001 to February 2004 in the Krakow inner city area who gave birth to term babies and completed 5-year follow-up. Paracetamol use in pregnancy was collected by interviews and prenatal personal exposure to PM2.5 over 48 h was measured in recruited women in the second trimester of pregnancy. After delivery, every three months in the first 24 months of the newborn's life and every 6 months later, a detailed standardized face-to-face interview on the infant's health was administered to each mother by trained interviewers. During the interviews at each of the study periods after birth, a history of eczema was recorded. The incident rate ratio (IRR) for frequency of eczema events over the follow-up was estimated from the Poisson regression model and the overall effect of main exposure variables on eczema was assessed by odds ratios (ORs) by the logistic model. The estimated relative risk of eczema occurring whenever in the follow-up was related significantly neither with prenatal Paracetamol nor higher PM2.5 exposure, however, their joint effect was significant (OR interaction term=6.04; 95%CI: 1.04-35.16). Of potential confounders considered in the analysis only damp/moldy home significantly increased the risk of eczema (OR=1.53; 95%CI: 1.14-2.05). In contrast, there was an inverse significant association between the presence of older siblings and eczema (OR=0.55; 95%CI: 0.35-0.84). The joint effect of the main exposure variables significantly increased frequency of eczema events (IRR=1.78, 95%CI: 1.22-2.61). In conclusion, the findings of the study suggest that Paracetamol use by mothers in pregnancy is not an independent risk factor for eczema in children, however, even very small doses of Paracetamol taken in pregnancy may contribute to the occurrence of allergic symptoms in early childhood if there is prenatal co-exposure to higher airborne fine particulate matter.
    Science of The Total Environment 09/2011; 409(24):5205-9. · 3.26 Impact Factor
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    ABSTRACT: In the last decade, the neurologic effects of various air pollutants have been the focus of increasing attention. The main purpose of this study was to assess the potential impact of early childhood exposure to indoor molds on the subsequent cognitive function of 6-year old children. The results of this study are based on the six-year follow-up of 277 babies born at term to mothers participating in a prospective cohort study in Krakow, Poland. The study participants are all non-smoking pregnant women who were free of chronic diseases such as diabetes and hypertension. The presence of visible mold patches on indoor walls was monitored at regular time intervals over gestation and after birth up to the age of five. The Wechsler Intelligence Scale for Children (WISC-R) was administered to children at age 6. The exposure effect of living in mold-contaminated homes on the IQ scores of children was adjusted for major confounders, known to be important for the cognitive development of children such as maternal education, the child's gender, breastfeeding practices in infancy, the presence of older siblings and the prenatal exposure to lead and environmental tobacco smoke (ETS). The adjusted IQ deficit attributed to longer exposures to indoor molds (>2 years) was significantly lower on the IQ scale (beta coeff.=-9.16, 95%CI: -15.21, -3.10) and tripled the risk of low IQ scoring (OR=3.53; 95%CI: 1.11-11.27) compared with references. While maternal education (beta coeff.=0.61, 95%CI: 0.05, 1.17) and breastfeeding (beta coeff.=4.0; 95%CI: 0.84, 7.17) showed a significant positive impact on cognitive function, prenatal ETS exposure (beta coeff.=-0.41; 95%CI: -0.79, -0.03) and the presence of older siblings (beta coefficient=-3.43; 95%CI: -5.67, -1.20) were associated with poorer cognitive function in children. In conclusion, the results of this study draw attention to the harmful effect of early postnatal exposure to indoor molds on children's cognitive development and provide additional evidence on the role of environmental determinants in human cognitive development.
    Physiology & Behavior 07/2011; 104(5):989-95. · 3.16 Impact Factor
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    ABSTRACT: The main goal of the study was to assess the effect of exclusive breastfeeding on the neurodevelopment of children over a 7-year follow-up period and to test the hypothesis that the observed cognitive gain in breastfed children in the first years of life is a strong predictor of their cognitive development trajectory, which may be continued in later life. The analysis is based on data from the 7-year follow-up of 468 term babies (>36 weeks of gestation) born to non-smoking mothers participating in an ongoing prospective cohort study. The cognitive function of children was assessed by psychometric tests performed five times at regular intervals from infancy through the preschool age. The study included valid neurodevelopmental assessment of the children-443 participants were evaluated least twice; 425, three times; and 307, five times in the follow-up period. The association between the cognitive achievements of preschool age children and exclusive breastfeeding of various durations was performed using the generalized estimating equation longitudinal model, adjusted for major confounders such as maternal education, gender, parity, and weight gain in pregnancy. Children breastfed exclusively for up to 3 months had intelligence quotients (IQs) that were on average 2.1 points higher compared to the others (95% confidence interval (CI), 0.24-3.9); children breastfed for 4-6 months scored higher by 2.6 points (95% CI, 0.87-4.27); and the benefit for children breastfed even longer (>6 months) increased by 3.8 points (95% CI, 2.11-5.45). Other predictors were maternal education, gender of the child, having an older sibling, and weight gain during pregnancy. The results of the study support the WHO expert recommendations on exclusive breastfeeding for 6 months; moreover, they provide evidence that even a shorter duration of exclusive breastfeeding in early infancy produces beneficial effects on the cognitive development of children. The breastfeeding-related IQ gain observed already at the age of 1 was sustained through preschool age, and the difference in terms of IQ score between breastfed children and the reference group (mixed breastfeeding) held constant over the whole preschool period.
    European Journal of Pediatrics 06/2011; 171(1):151-8. · 1.91 Impact Factor
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    ABSTRACT: One of the mechanisms supposed to explain the increasing prevalence of asthma, among children in particular, is the use of antibiotics because they may modify natural microbial exposure and development of the immune system in early childhood. The aim of this study is to investigate the association between the use of various classes of antibiotics (penicillin, cephalosporin and macrolide derivatives) in early childhood and the medical diagnosis of asthma or wheezing reported by mothers over the follow-up after adjustment for potential confounders and respiratory infections. In a population-based sample of 5-year-olds, a part of the ongoing birth cohort study, the standardized interviews on health outcomes, potential confounders (child's gender, maternal atopy, parity, prenatal and postnatal environmental tobacco smoke) and the use of antibiotics were gathered from mothers of 310 children. While the overall use of antibiotics during the early childhood was insignificantly associated with asthma (adjusted OR = 1.65, 95%CI: 0.93 - 2.93), the risk estimates were significant both for macrolide antibiotics (adjusted OR=2.14, 95%CI: 1.16-3.95) and cephalosporins (OR=1.98, 95%CI: 1.14-3.37). The significant excess in IRR (incident risk ratio) of wheezing episodes was related only to the use of macrolide antibiotics (adjusted IRR=1.91, 95%CI: 1.12-3.27). The use of other classes of antibiotics was found not to be associated with the medical diagnosis of asthma or wheezing episodes recorded in the study period. Conclusion: as early childhood use of broad spectrum antibiotics is associated with an increased risk of developing asthma in 5-year-olds, it may be hypothesized that the antibiotic- related suppression of allergic inflammatory responses in the course of treatment may later lead to greater than before atopic immune response in Th2 children or an impairment of Th1 immune responses in early childhood.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 04/2011; 62(2):189-95. · 2.48 Impact Factor
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    ABSTRACT: Gestational weight gain (GWG) is important for health policy as it may be associated with overweight epidemics in childhood and adolescence. The purpose of the study was to perform the risk assessment of joint effects of the excessive GWG and the pregravid maternal BMI on overweight in infancy and childhood. The observations were collected in the ongoing prospective birth cohort study of 482 non-smoking mothers and their newborns in Cracow inner city area. At 5 years of age the subsample of 312 infants were reexamined in order to assess their nutritional status. Body fatness was assessed by means of the weight/length ratio (WLR) in neonates and weight/height ratio (WHR) in 5-year-olds since they showed the strongest correlation with subcutaneous fat mass of young children. In the statistical analysis the binary regression models were applied to identify predictors of overweight. The excessive GWG (>18 kg) increased more than twofold the adjusted relative risk (RR) of neonatal fatness (R=2.7; 95% CI 2.0-3.7) and was also a significant independent risk factor for postnatal body fatness at 5 years of age (RR=2.0; 95% CI: 1.3-3.3). The results confirmed earlier findings that pregravid overweight increased not only the relative risk of neonatal fatness (RR=2.9; 95% CI: 2.2-3.9) but also overweight in early childhood (RR=2.7; 95% CI: 1.7-4.4). The conclusion is that excessive GWG may be a risk factor for overweight in early childhood and should be a focus of public health policy.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 02/2011; 62(1):55-64. · 2.48 Impact Factor
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    ABSTRACT: As there is a scarcity of evidence on potential hazards and preventive factors for infantile eczema operating in the prenatal period, the main goal of this study was to assess the role of prenatal exposure to fine particulate matter and environmental tobacco smoke (ETS) in the occurrence of infant eczema jointly with the possible modulating effect of maternal fish consumption. The study sample consisted of 469 women enrolled during pregnancy, who gave birth to term babies (>36 weeks of gestation). Among all pregnant women recruited, personal measurements of fine particulate matter (PM₂.₅) were performed over 48 h in the second trimester of pregnancy. After delivery, every 3 months in the first year of the newborn's life, a detailed, standardized, face-to-face interview was administered to each mother, in the process of which a trained interviewer recorded any history of infantile eczema and data on potential environmental hazards. The estimated risk of eczema related to higher prenatal exposure to fine particulate matter (PM₂.₅ > 53.0 μg/m³) and postnatal ETS as well as the protective effect of maternal fish intake were adjusted for potential confounders in a multivariable logistic regression model. While the separate effects of higher prenatal PM₂.₅ and postnatal ETS exposure were not statistically significant, their joint effect appeared to have a significant influence on the occurrence of infantile eczema [odds ratio 2.39, 95% confidence interval (CI) 1.10-5.18]. With maternal fish intake of more than 205 g/week, the risk of eczema decreased by 43% (odds ratio 0.57, 95% CI 0.35-0.93). The incidence rate ratio (IRR) for eczema symptoms, estimated from the Poisson regression model, was increased with both higher exposure to prenatal PM₂.₅ and postnatal ETS (IRR 1.55, 95% CI 0.99-2.44) and in children of atopic mothers (IRR 1.35, 95% CI 1.04-1.75) but was lower in girls (IRR 0.78, 95% CI 0.61-1.00). The observed preventive effect of fish consumption on the frequency of eczema symptoms was consistent with the results of the logistic analysis (IRR 0.72, 95% CI 0.52-0.99). The findings indicate that higher prenatal exposure to fine particulate matter combined with postnatal exposure to ETS may increase the risk of infant eczema, while maternal fish intake during pregnancy may reduce the risk of infantile eczema.
    International Archives of Allergy and Immunology 02/2011; 155(3):275-81. · 2.25 Impact Factor
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    ABSTRACT: Several in vivo and in vitro studies have shown that metal-rich particles may enhance allergic responses to house dust mites and induce an increased release of allergy-related cytokines. The main goal of this analysis is to define the possible association of intrauterine exposure to lead and mercury with the occurrence of skin sensitization to common aeroallergens in early childhood. The present study refers to a sample of 224 women in the second trimester of pregnancy recruited from Krakow inner city area who had full term pregnancies and whose children underwent skin prick testing (SPT) at the age of 5. Lead and mercury levels were assessed in cord blood and retested in children at age of 5 years. Aeroallergen concentrations in house dust were measured at the age of 3 years. The main health outcome (atopic status) was defined as the positive SPT to at least one common aeroallergen (Der f1, Der p1, Can f1 and Fel d1) at the age of 5 years. In the statistical analysis of the association between atopic status of children and exposure to metals, the study considered a set of covariates such as maternal characteristics (age, education, atopy), child's gender, number of older siblings, prenatal (measured via cord blood cotinine) and postnatal environmental tobacco smoke together with exposure to polycyclic aromatic hydrocarbons (PAH) as measured by PAH-DNA adducts. In the binary regression analysis, which controlled for the confounders, the risk ratio (RR) estimate for atopic sensitization was significantly associated with the lead exposure (RR=2.25, 95%CI: 1.21-4.19). In conclusion, the data suggest that even very low-level of prenatal lead exposure may be implicated in enhancing sensitization to common aeroallergens in early childhood.
    Environmental Research 01/2011; 111(1):119-24. · 3.24 Impact Factor
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    ABSTRACT: 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. Among pregnant women recruited prenatally to the study, personal measurements of PM(2.5) were performed over 48 h in the second trimester of pregnancy. After delivery, infants were followed for 5 years; the interviewers visited participants in their homes to record children's respiratory symptoms every 3 months in the child's first 2 years of life and every 6 months thereafter. In the fifth year of the follow-up, children were invited for standard lung function testing of levels of forced vital capacity (FVC), forced expiratory volume in 1 s (FEV(1)) and forced expiratory volume in 0.5 s (FEV(0.5)). There were 176 children of non-smoking mothers, who performed at least two acceptable spirometry measurements. Multivariable linear regression showed a significant deficit of FVC at the highest quartile of PM(2.5) exposure (beta coefficient = -91.9, P = 0.008), after adjustment for covariates (age, gender, birthweight, height and wheezing). Also FEV(1) level in children was inversely correlated with prenatal exposure to PM(2.5), and the average FEV(1) deficit amounted to 87.7 mL (P = 0.008) at the higher level of exposure. Although the effect of PM(2.5) exposure on FEV(0.5) was proportionally weaker (-72.7, P = 0.026), it was also statistically significant. The lung function level was inversely and significantly associated with the wheezing recorded over the follow-up. The findings showed that significant lung function deficits in early childhood are associated with prenatal exposure to fine particulate matter, which may affect fetal lung growth.
    Paediatric and Perinatal Epidemiology 09/2010; 24(5):492-501. · 2.16 Impact Factor
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    ABSTRACT: In this prospective cohort study of Caucasian mothers and children in Krakow, Poland, we evaluated the role of prenatal exposure to urban air pollutants in the pathogenesis of neurobehavioral disorders. The objective of this study was to investigate the relationship between prenatal polycyclic aromatic hydrocarbon (PAH) exposure and child intelligence at 5 years of age, controlling for potential confounders suspected to play a role in neurodevelopment. A cohort of pregnant, healthy, nonsmoking women was enrolled in Krakow, Poland, between 2001 and 2006. During pregnancy, participants were invited to complete a questionnaire and undergo 48-hr personal air monitoring to estimate their babies' exposure, and to provide a blood sample and/or a cord blood sample at the time of delivery. Two hundred fourteen children were followed through 5 years of age, when their nonverbal reasoning ability was assessed using the Raven Coloured Progressive Matrices (RCPM). We found that higher (above the median of 17.96 ng/m3) prenatal exposure to airborne PAHs (range, 1.8-272.2 ng/m3) was associated with decreased RCPM scores at 5 years of age, after adjusting for potential confounding variables (n = 214). Further adjusting for maternal intelligence, lead, or dietary PAHs did not alter this association. The reduction in RCPM score associated with high airborne PAH exposure corresponded to an estimated average decrease of 3.8 IQ points. These results suggest that prenatal exposure to airborne PAHs adversely affects children's cognitive development by 5 years of age, with potential implications for school performance. They are consistent with a recent finding in a parallel cohort in New York City.
    Environmental Health Perspectives 09/2010; 118(9):1326-31. · 7.26 Impact Factor
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    ABSTRACT: SUMMARY: The purpose of the study was to check the hypothesis that early wheezing as reported by mothers would be associated with reduced lung function in 4-year olds. Study participants were recruited prenatally, as part of a prospective cohort study on the respiratory health of young children exposed to various ambient air pollutants. After delivery, infants were followed over 4 years and the interviewers visited participants at their home to record respiratory symptoms every 3 months in the child's first 2 years of life and every 6 months in the 3rd and 4th years. In the 4th year of follow-up, children were invited for standard lung function testing by spirometry quantified by forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV(1)), and forced expiratory volume in 0.5 sec (FEV(0.5)) levels. Out of 258 children attending spirometry testing 139 performed at least two acceptable exhalation efforts. Cohort children with acceptable spirometric measurements did not differ with respect to wheezing experience and exposure characteristics from those without. The study shows that episodic wheeze was reported in 28.1% of 4-year olds, 6.5% had transient wheeze, and 4.3% had recurrent wheeze. There was an increased frequency of wheezing symptoms and their duration in transient and recurrent wheezers. Adjusted multivariable regression models for gender and height showed that children who reported more than two episodes of wheezing at any point over the follow-up had FVC values lower by 120.5 ml (P = 0.016) and FEV(1) values lower by 98.3 ml (P = 0.034) compared to those who did not report any wheezing; children experiencing more than 10 wheezing days by age 4 showed FVC deficit of 87.4 ml (P = 0.034) and FEV(1) values of 65.7 ml (P = 0.066). The ratios of FEV(1)/FVC%, and FEV(0.5)/FVC% were neither associated with wheezing episodes nor wheezing days. In recurrent wheezers, lung function decrement amounted to 207 ml of FVC, 175 ml of FEV(1), and 104 ml of FEV(0.5). In conclusion, our findings show that wheezing experience during early postnatal life may be associated with lung function deficit of restrictive character in preschool children and detailed history of wheeze in early postnatal life, even though not physician-confirmed, may help define the high risk group of children for poor lung function testing.
    Pediatric Pulmonology 09/2010; 45(9):919-26. · 2.38 Impact Factor
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    ABSTRACT: 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(2.5)), environmental tobacco smoke (ETS), gender of child, maternal characteristics (age, education and atopy), parity and mould/dampness in the home. The study sample includes 339 newborns of non-smoking mothers 18-35 yr of age and free from chronic diseases, who were recruited from ambulatory prenatal clinics in the first or second trimester of pregnancy. The number of wheezing days during the first 2 yr of life was positively associated with prenatal level of PAH-DNA adducts (IRR = 1.69, 95%CI = 1.52-1.88), prenatal particulate matter (PM(2.5)) level dichotomized by the median (IRR = 1.38; 95%CI: 1.25-1.51), maternal atopy (IRR = 1.43; 95%CI: 1.29-1.58), mouldy/damp house (IRR = 1.43; 95%CI: 1.27-1.61). The level of maternal education and maternal age at delivery was inversely associated with the IRRs for wheeze. The significant association between frequency of wheeze and the level of prenatal environmental hazards (PAHs and PM(2.5)) was not observed at ages 3 or 4 yrs. Although the frequency of wheezing at ages 3 or 4 was no longer associated with prenatal exposure to PAHs and PM(2.5), its occurrence depended on the presence of wheezing in the first 2 yr of life, which nearly tripled the risk of wheezing in later life. In conclusion, the findings may suggest that driving force for early wheezing (<24 months of age) is different to those leading to later onset of wheeze. As we reported no synergistic effects between prenatal PAH (measured by PAH-DNA adducts) and PM(2.5) exposures on early wheeze, this suggests the two exposures may exert independent effects via different biological mechanism on wheeze.
    Pediatric Allergy and Immunology 04/2010; 21(4 Pt 2):e723-32. · 3.38 Impact Factor
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    ABSTRACT: The objective of this study was to assess a hypothesized beneficial effect of fish consumption during the last trimester of pregnancy on adverse birth outcomes resulting from prenatal exposure to fine air particulate matter. The cohort consisted of 481 nonsmoking women with singleton pregnancies, of 18-35 years of age, who gave birth at term. All recruited women were asked about their usual diet over the period of pregnancy. Measurements of particulate matter less than 2.5 mum in size (PM(2.5)) were carried out by personal air monitoring over 48 h during the second trimester of pregnancy. The effect of PM(2.5) and fish intake during gestation on the birth weight of the babies was estimated from multivariable linear regression models, which beside the main independent variables considered a set of potential confounding factors such as the size of the mother (height, prepregnancy weight), maternal education, parity, the gender of the child, gestational age and the season of birth. The study showed that the adjusted birth weight was significantly lower in newborns whose mothers were exposed to particulate matter greater than 46.3 microg/m3 (beta coefficient = -97.02, p = 0.032). Regression analysis stratified by the level of maternal fish consumption (in tertiles) showed that the deficit in birth weight amounted to 133.26 g (p = 0.052) in newborns whose mothers reported low fish intake (<91 g/week). The birth weight deficit in newborns whose mothers reported medium (91-205 g/week) or higher fish intake (>205 g/week) was insignificant. The interaction term between PM(2.5) and fish intake levels was also insignificant (beta = -107,35, p = 0.215). Neither gestational age nor birth weight correlated with maternal fish consumption. The results suggest that a higher consumption of fish by women during pregnancy may reduce the risk of adverse effects of prenatal exposure to toxicants and highlight the fact that a full assessment of adverse birth outcomes resulting from prenatal exposure to ambient hazards should consider maternal nutrition during pregnancy.
    Annals of Nutrition and Metabolism 01/2010; 56(2):119-26. · 1.66 Impact Factor
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    ABSTRACT: The main purpose of the study was to answer the question whether young children without clinical diagnosis of asthma but experiencing early wheezing disorders and therefore being at high risk of developing asthma may have cognitive deficits. In the ongoing birth cohort study wheezing symptoms were recorded postpartum over two first years of age and subsequently cognitive status of children at the age of 3 yr was assessed with the Bayley Mental Development Index (MDI). In the statistical analysis a wide range of modifying and confounding factors (maternal education, gender of children, prenatal exposure to lead and environmental tobacco smoke (ETS) were considered to assess the independent effect of early wheezing phenotypes on cognitive development of children. The MDI score correlated inversely with the number of wheezing days recorded over 24 months (r = -0.13, p = 0.007), lead cord blood concentration (r = -0.12, p = -0.02), number of siblings (r = -0.17, p = 0.0006) and the number of cigarettes smoked daily by other household members at home over the pregnancy period (r = -0.18, p = 0.0002). While the children who experienced wheezing over the first year of age showed deficit of 2 MDI scores (beta coeff. = -2.31, 95%CI: -4.63 to 0.02), those with persistent wheezing had the score deficit of 4 points (beta coeff. = -4.41, 95%CI: -8.27 to -0.55). To our knowledge, it is the first report in the iterature showing that early wheezing is associated the cognitive deficit in a community-recruited very young children. Observed cognitive deficit in early wheezers may be caused by RSV infections or can be related to lower lung function attributed to persistent wheezing, which reducing oxygen supply would affect rapidly developing brain.
    Pediatric Allergy and Immunology 07/2009; 21(3):550-6. · 3.38 Impact Factor
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    ABSTRACT: The primary purpose of this study was to assess the relationship between very low-level of prenatal lead exposure measured in the cord blood (<5 microg/dL) and possible gender-specific cognitive deficits in the course of the first three years of life. The accumulated lead dose in infants over the pregnancy period was measured by the cord blood lead level (BLL) and cognitive deficits were assessed by the Bayley Mental Development Index (MDI). The study sample consisted of 457 children born to non-smoking women living in the inner city and the outlying residential areas of Krakow. The relationship between prenatal lead exposure and MDI scores measured at 12, 24 and 36 months of age and adjusted to a set of important covariates (gender of child, maternal education, parity, breastfeeding, prenatal and postnatal environmental tobacco smoke) was evaluated with linear multivariate regression, and the Generalized Estimating Equations (GEE) longitudinal panel model. The median of lead level in cord blood was 1.21 microg/dL with the range of values from 0.44 to 4.60 microg/dL. Neither prenatal BLL (dichotomized by median) nor other covariates affected MDI score at 12 months of age. Subsequent testing of children at 24 months of age showed a borderline significant inverse association of lead exposure and mental function (beta coefficient=-2.42, 95%CI: -4.90 to 0.03), but the interaction term (BLL x male gender) was not significant. At 36 months, prenatal lead exposure was inversely and significantly associated with cognitive function in boys (Spearman correlation coefficient=-0.239, p=0.0007) but not girls (r=-0.058, p=0.432) and the interaction between BLL and male gender was significant (beta coefficient=-4.46; 95%CI: -8.28 to -0.63). Adjusted estimates of MDI deficit in boys at 36 months confirmed very strong negative impact of prenatal lead exposure (BLL>1.67 microg/dL) compared with the lowest quartile of exposure (beta coefficient=-6.2, p=0.002), but the effect in girls was insignificant (beta coefficient=-0.74, p=0.720). The average deficit of cognitive function in the total sample over the first three years of life (GEE model) associated with higher prenatal lead exposure was also significant (beta coefficient=-3.00; 95%CI: -5.22 to -0.70). Beside prenatal lead exposure, presence of older siblings at home and prenatal environmental tobacco smoke had a negative impact on MDI score. Better maternal education showed a strong beneficial effect on the cognitive development of children. Conclusion: the study suggests that there might be no threshold for lead toxicity in children and provides evidence that 3-year old boys are more susceptible than girls to prenatal very low lead exposure. The results of the study should persuade policy makers to consider gender-related susceptibility to lead and possibly to other toxic hazards in setting environmental protection guidelines. To determine whether the cognitive deficit documented in this study persists to older ages, the follow-up of the children over the next several years is to be carried out.
    Early human development 06/2009; 85(8):503-10. · 2.12 Impact Factor

Publication Stats

777 Citations
153.96 Total Impact Points

Institutions

  • 1996–2014
    • Jagiellonian University
      • • Department of Epidemiology and Preventive Medicine
      • • Medical College
      Cracovia, Lesser Poland Voivodeship, Poland
  • 2005–2013
    • Krakow University Hospital
      Cracovia, Lesser Poland Voivodeship, Poland
  • 2010
    • Columbia University
      • Columbia Center for Children’s Environmental Health
      New York City, NY, United States
  • 1998–2009
    • Akademickie Centrum Komputerowe CYFRONET AGH
      Cracovia, Lesser Poland Voivodeship, Poland
  • 1998–2006
    • Collegium Medicum of the Jagiellonian University
      • Chair of Epidemiology and Preventive Medicine
      Kraków, Lesser Poland Voivodeship, Poland
  • 1987
    • University of Pavia
      • Department of Internal Medicine and Therapeutics
      Pavia, Lombardy, Italy