Elzbieta Mroz

Jagiellonian University, Cracovia, Lesser Poland Voivodeship, Poland

Are you Elzbieta Mroz?

Claim your profile

Publications (70)165.57 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Prenatal polycyclic aromatic hydrocarbon (PAH) exposure has been shown to increase DNA adduct levels and to affect neurodevelopment. Micronutrients may modify the adverse effect of PAH on neurodevelopment. Thus, we examined if micronutrient concentrations modified the association between PAH exposure and neurodevelopmental outcomes. 151 children from a birth cohort who had micronutrient concentrations measured in cord blood and completed the Child Behavioral Checklist (CBCL), between the ages of 6 and 9 years, were evaluated. Prenatal airborne PAH exposure was measured by personal air monitoring. The betas and 95% CI for the associations of antioxidant concentrations and PAH exposure with each of the outcomes of CBCL raw score and dichotomized standardized T-score (based on clinical cutpoints) were estimated, respectively, by multivariable poisson and logistic models. Children below the median for alpha-tocopherol and gamma-tocopherol concentrations, compared to those above, were more likely to have thought problems, aggressive behavior and externalizing problems (p<0.05). Lower carotenoid concentration was associated with more thought problems (MVβ=0.60, p<0.001) and externalizing problems (MVβ=0.13, p<0.05) for the same contrast. No statistically significant associations were observed between retinol concentrations and neurodevelopmental symptoms. Overall, no consistent patterns were observed when we examined the interaction between antioxidants (e.g., alpha-tocopherol) and PAH in relation to CBCL symptoms (e.g., internalizing and externalizing problems, p<0.05). Lower alpha-tocopherol, gamma-tocopherol and carotenoid levels may adversely affect healthy neurodevelopment, even after accounting for PAH exposure. Future research to confirm these findings are warranted given the importance of identifying modifiable factors for reducing harmful PAH effects. Copyright © 2015 Elsevier Inc. All rights reserved.
    Environmental Research 04/2015; 140:136-144. DOI:10.1016/j.envres.2015.03.017 · 3.95 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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. At the age of 5 to 8, children were given allergic skin tests for indoor allergens; and between 5 and 9 years lung function testing (FVC, FEV05, FEV1 and FEF25-75) was performed. The effects of prenatal PAH exposure on lung function tests repeated over the follow-up were adjusted in the General Estimated Equation (GEE) model for the relevant covariates. No association between FVC with prenatal PAH exposure was found; however for the FEV1 deficit associated with higher prenatal PAH exposure (above 37ng/m(3)) amounted to 53mL (p=0.050) and the deficit of FEF25-75 reached 164mL (p=0.013). The corresponding deficits related to postnatal residential indoor PAH level (above 42ng/m(3)) were 59mL of FEV1 (p=0.028) and 140mL of FEF25-75 (p=0.031). At the higher residential outdoor PAH level (above 90ng/m(3)) slightly greater deficit of FEV1 (71mL, p=0.009) was observed. The results of the study suggest that transplacental exposure to PAH compromises the normal developmental process of respiratory airways and that this effect is compounded by postnatal PAH exposure.
    Science of The Total Environment 10/2014; 502C:502-509. DOI:10.1016/j.scitotenv.2014.09.051 · 4.10 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: 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. The study is part of an ongoing, longitudinal investigation of the health effects of prenatal exposure to air pollution on infants and children in Krakow, Poland. The subjects in this report included 170 children whose mothers were enrolled to the study in the first or second trimester of pregnancy whose cord blood were tested for PAH-DNA adducts and who were assessed at age 7 using the Wechsler Intelligence Scale for Children-Revised (WISC-R). The outcome of a priori interest was depressed verbal IQ index (DepVIQ), which is the difference between WISC-R performance and verbal IQ scores. Prenatal PAH exposure was measured by cord blood PAH-DNA adducts, an individual dosimeter, integrating exposure from various sources of exposure over the gestational period. The estimated effect of prenatal PAH exposure on cognitive function was adjusted in multivariable regression for a set of potential confounders (child's gender, parity, maternal education, breastfeeding practice, environmental tobacco smoke (ETS), and postnatal PAH exposure). The prevalence of DepVIQ was significantly higher in children with detectable PAH-DNA adducts compared to those with undetectable adducts (13.7 vs. 4.4 %,). Binary multivariable regression documented that the relative risk of DepVIQ increased threefold with a ln-unit increase in cord blood adducts (relative risk (RR) = 3.0, 95 % confidence interval (CI) 1.3-6.8). Postnatal PAH exposure also increased the risk of DepVIQ (RR = 1.6, 95 % CI 1.1-2.5). Long-term exclusive breastfeeding (at least 6 months) showed a protective effect (RR = 0.3, 95 % CI 0.1-0.9). In conclusion, these results provide further evidence that PAHs are harmful to the developing fetal brain with effects extending through childhood, with implications for the academic success of the children.
    Environmental Science and Pollution Research 09/2014; 22(5). DOI:10.1007/s11356-014-3627-8 · 2.76 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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; 50(5). DOI:10.1002/ppul.23104 · 2.30 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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. Chemical analysis tests were performed to determine airborne concentrations of nine PAH compounds. The results show that both prenatal and postnatal exposure were associated positively with the severity of wheezing days and recurrent wheezing reported in the follow-up. While the incidence rate ratio (IRR) for severity of wheeze and prenatal PAH exposure was 1.53 (95%CI: 1.43-1.64) that for postnatal PAH exposure was 1.13 (95%CI: 1.08-1.19). However, recurrent wheezing was more strongly associated with airborne PAH levels measured at age 3 (OR = 2.31, 95%CI: 1.26-4.22) than transplacental PAH exposure (OR = 1.40, 95% CI: 0.85-2.09), but the difference was statistically insignificant. In conclusion, it appears that prenatal PAH exposure may precipitate and intensify early onset of wheezing symptoms in childhood, resulting from the postnatal exposure and suggest that success in reducing the incidence of respiratory diseases in children would depend on reducing both fetal and childhood exposure to air pollution. Pediatr Pulmonol. © 2013 Wiley Periodicals, Inc.
    Pediatric Pulmonology 02/2014; 49(2). DOI:10.1002/ppul.22923 · 2.30 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND:Airborne polycyclic aromatic hydrocarbons (PAHs) are pollutants generated by combustion of fossil fuel and other organic material. Both prenatal PAH exposure and maternal psychological distress during pregnancy have each been associated with neurodevelopmental problems in children. The goal was to evaluate potential interactions between prenatal exposure to airborne PAHs and maternal psychological distress during pregnancy on subsequent behavioral problems in children.METHODS:In a longitudinal birth cohort study, 248 children of nonsmoking white women in the coal-burning region of Krakow, Poland, were followed from in utero until age 9. Prenatal PAH exposure was measured by personal air monitoring during pregnancy, maternal demoralization during pregnancy by the Psychiatric Epidemiology Research Instrument-Demoralization, and child behavior by the Child Behavior Checklist.RESULTS:Significant interactions between maternal demoralization and PAH exposure (high versus low) were identified for symptoms of anxious/depressed, withdrawn/depressed, social problems, aggressive behavior, internalizing problems, and externalizing problems. The effects of demoralization on syndromes of anxious/depressed, withdrawn/depressed, rule-breaking, aggressive behavior, and the composite internalizing and externalizing scores were seen only in conjunction with high PAH exposure. Fewer significant effects with weaker effect sizes were observed in the low-PAH-exposure group.CONCLUSIONS:Maternal demoralization during pregnancy appears to have a greater effect on child neurobehavioral development among children who experienced high prenatal PAH exposure. The results provide the first evidence of an interaction between prenatal exposure to maternal demoralization and air pollution on child neurobehavioral development, indicating the need for a multifaceted approach to the prevention of developmental problems in children.
    PEDIATRICS 10/2013; 132(5). DOI:10.1542/peds.2012-3844 · 5.30 Impact Factor
  • 03/2013; DOI:10.5645/ghp2013.01.01.04
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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 (PM(2.5)) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM(2.5) exposure and regularly collected data on the occurrence of acute bronchitis and pneumonia diagnosed by a physician from birth over the seven-year follow-up. The effect of prenatal exposure to PM(2.5) was adjusted in the multivariable logistic models for potential confounders, such as prenatal and postnatal ETS (environmental tobacco smoke), city residence area as a proxy of postnatal urban exposure, children's sensitization to domestic aeroallergens, and asthma. In the subgroup of children with available PM(2.5) indoor levels, the effect of prenatal exposure was additionally adjusted for indoor exposure as well. The adjusted odds ratio (OR) for incidence of recurrent broncho-pulmonary infections (five or more spells of bronchitis and/or pneumonia) recorded in the follow-up significantly correlated in a dose-response manner with the prenatal PM(2.5) level (OR=2.44, 95%CI: 1.12-5.36). In conclusion, the study suggests that prenatal exposure to PM(2.5) increases susceptibility to respiratory infections and may program respiratory morbidity in early childhood. The study also provides evidence that the target value of 20μg/m(3) for the 24-h mean level of PM(2.5) protects unborn babies better than earlier established EPA guidelines.
    International journal of hygiene and environmental health 01/2013; DOI:10.1016/j.ijheh.2012.12.014 · 3.28 Impact Factor
  • [Show abstract] [Hide abstract]
    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; DOI:10.1038/jes.2012.117 · 3.05 Impact Factor
  • [Show abstract] [Hide abstract]
    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 11/2012; 47(11):1131-9. DOI:10.1002/ppul.22570 · 2.30 Impact Factor
  • Cancer Research 06/2012; 72(8 Supplement):2643-2643. DOI:10.1158/1538-7445.AM2012-2643 · 9.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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. · 2.72 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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. DOI:10.1007/s12012-012-9157-z · 2.06 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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. DOI:10.1016/j.nut.2011.07.020 · 3.05 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background and Aims: The controversial topic of the early human exposure to mercury is ethylmercury, which is present in the thimerosal-containing vaccines (TCV). The objective of this analysis was to determine the relationship between the neonatal exposure to TCV and cognitive and psychomotor development of children during the first 2 years of life.
    Pediatric Research 11/2011; 70:338-338. DOI:10.1038/pr.2011.563 · 2.84 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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.
    Science of The Total Environment 09/2011; 409(24):5205-9. DOI:10.1016/j.scitotenv.2011.08.068 · 4.10 Impact Factor
  • [Show abstract] [Hide abstract]
    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.
    Physiology & Behavior 07/2011; 104(5):989-95. DOI:10.1016/j.physbeh.2011.06.019 · 3.03 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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. DOI:10.1007/s00431-011-1507-5 · 1.98 Impact Factor
  • [Show abstract] [Hide abstract]
    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. · 2.72 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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. DOI:10.1159/000320376 · 2.43 Impact Factor

Publication Stats

679 Citations
165.57 Total Impact Points

Institutions

  • 1998–2015
    • Jagiellonian University
      • Department of Epidemiology and Preventive Medicine
      Cracovia, Lesser Poland Voivodeship, Poland
    • Akademickie Centrum Komputerowe CYFRONET AGH
      Cracovia, Lesser Poland Voivodeship, Poland
  • 2007–2013
    • Krakow University Hospital
      Cracovia, Lesser Poland Voivodeship, Poland
  • 2008
    • Columbia University
      • Columbia Center for Children’s Environmental Health
      New York, New York, United States
  • 1994–2006
    • Collegium Medicum of the Jagiellonian University
      • Chair of Epidemiology and Preventive Medicine
      Kraków, Lesser Poland Voivodeship, Poland