Ryszard Jacek

Krakow University Hospital, Cracovia, Lesser Poland Voivodeship, Poland

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Publications (28)65.83 Total impact

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    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 10/2013; · 2.38 Impact Factor
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    ABSTRACT: 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. Personal samplers of PM2.5 were used to measure fine particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal PM2.5 exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered. RESULTS: The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive significant relationship with the prenatal PM2.5 exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58-2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47-1.73 ppm) and the difference was statistically significant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal PM2.5 and cough severity recorded in the follow-up were related to eCO level. The prenatal PM2.5 exposure represented 5.1%, while children's cough represented only 2.6% of the eCO variability. CONCLUSION: Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fine particulate matter.
    International Journal of Occupational Medicine and Environmental Health 03/2013; · 1.31 Impact Factor
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    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; · 2.64 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: 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: 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 goal of the paper was to assess the pattern of risk factors having an impact on the onset of early wheezing phenotypes in the birth cohort of 468 two-year olds and to investigate the severity of respiratory illness in the two-year olds in relation to both wheezing phenotypes, environmental tobacco smoke (ETS) and personal PM(2.5) exposure over pregnancy period (fine particulate matter). The secondary goal of the paper was to assess possible association of early persistent wheezing with the length of the baby at birth. Pregnant women were recruited from ambulatory prenatal clinics in the first and second trimester of pregnancy. Only women 18-35 years of age, who claimed to be non-smokers, with singleton pregnancies, without illicit drug use and HIV infection, free from chronic diseases were eligible for the study. In the statistical analysis of respiratory health of children multinomial logistic regression and zero-inflated Poisson regression models were used. Approximately one third of the children in the study sample experienced wheezing in the first 2 years of life and in about two third of cases (67%) the symptom developed already in the first year of life. The early wheezing was easily reversible and in about 70% of infants with wheezing the symptom receded in the second year of life. The adjusted relative risk ratio (RRR) of persistent wheezing increased with maternal atopy (RRR=3.05; 95%CI: 1.30-7.15), older siblings (RRR=3.05; 95%CI: 1.67-5.58) and prenatal ETS exposure (RRR=1.13; 95%CI: 1.04-1.23), but was inversely associated with the length of baby at birth (RRR=0.88; 95%CI: 0.76-1.01). The adjusted incidence risk ratios (IRR) of coughing, difficult breathing, runny/stuffy nose and pharyngitis/tonsillitis in wheezers were much higher than that observed among non-wheezers and significantly depended on prenatal PM(2.5) exposure, older siblings and maternal atopy. The study shows a clear inverse association between maternal age or maternal education and respiratory illnesses and calls for more research efforts aiming at the explanation of factors hidden behind proxy measures of quality of maternal care of babies. The data support the hypothesis that burden of respiratory symptoms in early childhood and possibly in later life may be programmed already in prenatal period when the respiratory system is completing its growth and maturation.
    Environment international 05/2009; 35(6):877-84. · 4.79 Impact Factor
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    ABSTRACT: Our primary purpose was to assess sex-specific fetal growth reduction in newborns exposed prenatally to fine particulate matter. Only women 18-35 years of age, who claimed to be non-smokers, with singleton pregnancies, without illicit drug use and HIV infection, free from chronic diseases were eligible for the study. A total of 481 enrolled pregnant women who gave birth between 37 and 43 weeks of gestation were included in the study. Prenatal personal exposure to fine particles over 48 h during the second trimester was measured using personal monitors. To evaluate the relationship between the level of PM(2.5) measured over 48 h in the second trimester of pregnancy with those in the first and the third trimesters, a series of repeated measurements in each trimester was carried out in a random subsample of 85 pregnant women. We assessed the effect of PM(2.5) exposure on the birth outcomes (weight, length and head circumference at birth) by multivariable regression models, controlling for potential confounders (maternal education, gestational age, parity, maternal height and prepregnancy weight, sex of infant, prenatal environmental tobacco smoke, and season of birth). Birth outcomes were associated positively with gestational age, parity, maternal height and prepregnancy weight, but negatively with the level of prenatal PM(2.5) exposure. Overall average increase in gestational period of prenatal exposure to fine particles by about 30 microg/m3, i.e., from 25th percentile (23.4 microg/m3) to 75th percentile (53.1 microg/m3) brought about an average birth weight deficit of 97.2g (95% CI: -201, 6.6) and length at birth of 0.7 cm (95% CI: -1.36, -0.04). The corresponding exposure lead to birth weight deficit in male newborns of 189 g (95% CI: -34.2, -343) in comparison to 17g in female newborns; the deficit of length at birth in male infants amounted to 1.1cm (95% CI: -0.11, -2.04). We found a significant interrelationship between self-reported ETS and PM(2.5), however, none of the models showed a significant interaction of both variables. The joint effect of various levels of PM(2.5) and ETS on birth outcomes showed the significant deficit only for the categories of exposure with higher component of PM(2.5). Concluding, the results of the study suggest that observed deficits in birth outcomes are rather attributable to prenatal PM(2.5) exposure and not to environmental tobacco smoke. The study also provided evidence that male fetuses are more sensitive to prenatal PM(2.5) exposure and this should persuade policy makers to consider birth outcomes by gender separately while setting air pollution guidelines.
    Environmental Research 04/2009; 109(4):447-56. · 3.24 Impact Factor
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    ABSTRACT: The aim of the study was to describe the distribution of house dust mite (HDM) allergens within homes of three‐year‐old children, to identify factors responsible for its variation and to test the hypothesis whether the content of HDM allergens exceeding 2 µg/g dust may be regarded as a risk level of sensitization possibly affecting respiratory health in early childhood. House dust samples were collected in 279 dwellings from the mattresses, children’s bedroom and kitchen floors. In the laboratory, dust samples were analyzed for Der f 1 and Der p 1 using monoclonal antibody enzyme‐linked immunosorbent assays. At the time of the house dust collection, interviews with mothers on the household characteristics and child’s respiratory health were performed. Respiratory outcome variables included running or stuffed nose, cough, barking cough, difficult (puffed) breathing and wheezing or whistling in the chest irrespective of respiratory infection. For each of the symptoms the number of the episodes and duration in days over the past six months were recorded in the questionnaire. In the multivariate Poisson regression analysis, a set of potential confounders has been taken into account such as gender of child, season, maternal education, maternal atopy, older siblings and environmental tobacco smoke. The adjusted rate ratio for episodes of running nose among those exposed to higher HDM exposure was 1.09 (95% confidence interval (CI): 0.98–1.20), for episodes of cough 1.11 (95% CI: 0.99–1.24), barking cough 1.44 (95% CI: 0.99–2.09) difficult breathing 1.31 (95% CI: 0.91–1.92) and for wheezing 1.42 (95% CI: 1.00–2.02). In contrast, rate ratios for the duration of all respiratory symptoms were significantly higher in children exposed to higher HDM level. The corresponding rate ratios for duration of symptoms (in days) were 1.10 (95% CI: 1.06–1.14), 1.06 (95% CI: 1.02–1.11), 1.64 (95% CI; 1.42–1.90), 2.05 (95% CI: 1.79–2.35) and 1.40 (95% CI: 1.21–1.62). The children with positive history of maternal atopy showed a higher risk of wheezing than those without the maternal atopy. The rate ratios for number of wheezing episodes in children of mothers without atopy was insignificant 1.11 (95% CI: 0.94–1.30) while in the group with maternal atopy the risk ratio amounted to 1.47 (95% CI: 1.09–1.96); the corresponding rate ratio estimates for the duration of wheezing were 1.12 (95% CI: 1.04–1.20) and 1.46 (95% CI: 1.29–1.66). The data support the view that exposure to higher level of HDM allergens may affect susceptibility of the bronchi to environmental factors and increase the burden of respiratory diseases in early childhood.
    Early Child Development and Care 01/2009; 179(1):1-16.
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    ABSTRACT: Current understanding on health effects of long-term polycyclic aromatic hydrocarbon (PAH) exposure is limited by lack of data on time-varying nature of the pollutants at an individual level. In a cohort of pregnant women in Krakow, Poland, we examined the contribution of temporal, spatial, and behavioral factors to prenatal exposure to airborne PAHs within each trimester and developed a predictive model of PAH exposure over the entire gestational period. We monitored nonsmoking pregnant women (n = 341) for their personal exposure to pyrene and eight carcinogenic PAHs-benz[a]anthracene, chrysene/isochrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene [B(a)P], indeno[1,2,3-c,d]pyrene, dibenz[a,h]anthracene, and benzo[g,h,i]perylene-during their second trimester for a consecutive 48-hr period. In a subset (n = 78), we monitored indoor and outdoor levels simultaneously with the personal monitoring during the second trimester with an identical monitor. The subset of women was also monitored for personal exposure for a 48-hr period during each trimester. We repeatedly administered a questionnaire on health history, lifestyle, and home environment. The observed personal, indoor, and outdoor B(a)P levels we observed in Krakow far exceed the recommended Swedish guideline value for B(a)P of 0.1 ng/m(3). Based on simultaneously monitored levels, the outdoor PAH level alone accounts for 93% of total variability in personal exposure during the heating season. Living near the Krakow bus depot, a crossroad, and the city center and time spent outdoors or commuting were not associated with higher personal exposure. During the nonheating season only, a 1-hr increase in environmental tobacco smoke (ETS) exposure was associated with a 10-16% increase in personal exposure to the nine measured PAHs. A 1 degrees C decrease in ambient temperature was associated with a 3-5% increase in exposure to benz[a]anthracene, benzo[k]fluoranthene, and dibenz[a,h]anthracene, after accounting for the outdoor concentration. A random effects model demonstrated that mean personal exposure at a given gestational period depends on the season, residence location, and ETS. Considering that most women reported spending < 3 hr/day outdoors, most women in the study were exposed to outdoor-originating PAHs within the indoor setting. Cross-sectional, longitudinal monitoring supplemented with questionnaire data allowed development of a gestation-length model of individual-level exposure with high precision and validity. These results are generalizable to other nonsmoking pregnant women in similar exposure settings and support reduction of exposure to protect the developing fetus.
    Environmental Health Perspectives 12/2008; 116(11):1509-18. · 7.26 Impact Factor
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    ABSTRACT: The purpose of the study was to test the hypothesis whether infants with higher prenatal exposure to fine particles (PM(2.5)) are at greater risk of developing respiratory symptoms and whether fish consumption in pregnancy may modulate the effect. The study was carried out in a cohort of 465 newborns in Krakow (Poland) who have been followed over the first 2 years of life and for whom data on the occurrence of respiratory symptoms and measurements of personal air monitoring in the second trimester of pregnancy were available. The incidence risk ratio (IRR) of respiratory symptoms due to prenatal PM(2.5) exposure were adjusted for potential confounders (gender of child, breastfeeding, parity, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke (ETS), and moulds in households) in the generalized estimating equations (GEE) statistical models. The adjusted risk of coughing was associated significantly with PM(2.5) level (IRR = 2.51; 95% CI: 1.77-3.58), moulds in the household, parity, maternal atopy and postnatal ETS, but was lower in girls, and in infants whose mothers consumed more fish in pregnancy (IRR = 0.85; 95% CI: 0.79-0.91). The risk of wheezing was also correlated significantly with the prenatal exposure to PM(2.5) (IRR = 1.36; 95% CI: 1.29-1.43) but also with the presence of moulds in homes, parity, maternal atopy and postnatal ETS. The occurrence of wheezing was associated inversely with the gender of child, gestational age, and fish consumption in pregnancy (IRR = 0.97; 95% CI: 0.95-0.99). Similarly, the risk of difficult (puffy) breathing increased with prenatal exposure to PM(2.5) (IRR = 1.18; 95% CI: 1.12-1.25) moulds, maternal atopy, and parity. The symptom occurrence was lower in girls and associated inversely with the gestational age, and fish consumption in pregnancy (IRR = 0.94; 95% CI: 0.92-0.97). The results of the study support the hypothesis that fish consumption in pregnancy may mitigate the harmful effect of prenatal or perinatal exposure to components of PM(2.5) resulting in an increased burden of respiratory infections among infants.
    Annals of Nutrition and Metabolism 02/2008; 52(1):8-16. · 1.66 Impact Factor
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    ABSTRACT: The aim of the study was to describe the distribution of house-dust mite (HDM) allergens in homes of three-year-old children and to test the hypothesis whether the content of HDM allergens exceeding 2 microg/g of dust may be regarded as a risk level possibly affecting respiratory health in early childhood. House-dust samples were collected in 275 dwellings from mattresses, children's bedrooms and kitchen floors. In the laboratory, dust samples were analyzed for Der f 1 and Der p 1 using monoclonal antibody enzyme-linked immunosorbent assays (ELISA). At the time of the house-dust collection, mothers were interviewed on the household characteristics and their children's respiratory health. Respiratory outcome variables included wheezing or whistling in the chest irrespective of respiratory infections. The number of the wheezing episodes and their duration in days over the last 6 months were recorded in the questionnaire. In the multivariate Poisson regression analysis on the association between the occurrence of wheezing and exposure, a set of potential confounders, such as child's gender, maternal education, maternal allergy, older siblings, presence of moulds, house dampness, and environmental tobacco smoke (ETS) was taken into account. The adjusted incidence rate ratios (IRR) of wheezing ascribed to a higher HDM level (> 2.0 microg/g dust) were 1.84 (95% CI: 1.45-2.34) for duration of wheezing and 1.56 (95% CI: 0.88-2.75) for episodes. Of the confounders taken into consideration, the presence of moulds had the strongest impact on the risk of wheezing (IRR = 4.24; 95% CI: 3.08-5.84). The data support the view that exposure to a higher level of HDM allergens increases the burden of respiratory diseases in the early childhood and the effect is independent of maternal atopy, ETS, and moulds in homes.
    International Journal of Occupational Medicine and Environmental Health 02/2007; 20(2):117-26. · 1.31 Impact Factor
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    ABSTRACT: This study assessed personal exposure of pregnant women to fine particles (PM(25)) and benzo[a]pyrene (B[a]P) and the relationship between pollutant concentrations in ambient and indoor air. In a group of 78 pregnant women, simultaneous 48 h measurements of personal, indoor, and outdoor exposure to PM(25) and B[a]P were carried out in the second trimester of pregnancy. The results show that participants were exposed to varying concentrations of PM(25) and B[a]P, with higher exposure in the winter season. Overall, the mean personal PM(25) level was 30.4 microg/m(3) and B[a]P 2.1 ng/m(3). The winter/summer ratios for mean personal exposures were 1.4 (35.6 microg/m(3) vs. 25.8 microg/m(3)) and 5.4 (4.9 ng/m(3) vs. 0.9 ng/m(3)), respectively. As for indoor levels, the winter/summer ratios were 1.4 (33.2 microg/m(3) vs. 24.4 microg/m(3)) for PM(25) and 5.4 (4.3 ng/m(3) vs. 0.8 ng/m(3)) for B[a]P, and for outdoor concentrations, the respective values were 1.5 (40.3 microg/m(3) vs. 26.4 microg/m(3), and 6.8 (6.1 ng/m(3) vs 0.9 ng/m(3)). A stronger correlation was found between personal PM(25) exposure and the pollutant concentration indoors (r = 0.89; 95% CI: 0.83-0.93) than outdoors (r = 0.75; 95% CI: 0.64-0.83). The correlations between personal B[a]P exposure and its indoor or outdoor levels were similar (0.95-0.96) and significant. The markedly higher exposure to B[a]P in Kraków in winter than in summer can be explained by the massive use of coal for heating in the cold season. We conclude that although ambient PM(25) measurements provide an adequate indicator of outdoor air quality for use in epidemiologic studies, they may not be adequate for studies on relationship between non-ambient pollution and health effects. Since only about 20% of variability in personal B[a]P exposure could be explained by personal PM(25) level, the extrapolation of personal exposure to B[a]P from personal PM(25) data may be greatly underestimated.
    International Journal of Occupational Medicine and Environmental Health 01/2007; 20(4):339-48. · 1.31 Impact Factor
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    ABSTRACT: The main purpose of the study was to assess the occurrence of wheezing and lung function in non-smoking women exposed to various levels of fine particulate matter(FP) and polycyclic aromatic hydrocarbons (PAH). Out of the total study group, 152 women were included in the lower exposed group (PM2.5 ≤34.3μg/m3 or PAHs ≤ 22.9ng/ m3) and 96 persons in higher concentrations of both air pollutants (PM2.5>34.3μg/m3 and PAHs > 22.9ng/ m3). Except for FVC and FEV1, all lung forced ventilatory flows (PEFR, FEF25% FEF50%, FEF75%, FEF25−75%) were significantly lower in the higher exposed group. The findings suggest bronchoconstriction within the respiratory tract, which may be related to the exposure under study. This was consistent with a higher prevalence of wheezing in more exposed subjects. It was shown that higher levels of both pollutants increased the risk of wheezing by factor 5.6 (95% CI: 1.77–17.8) after accounting for potential confounders such as allergic diseases and exposure to ETS. This study suggests that pollutants in question may have the capacity to promote broncho-constriction and asthmatic symptoms, possibly by bronchial inflammation resulting from the exposure.
    Central European Journal of Medicine 01/2007; 2(1):66-78. · 0.26 Impact Factor
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    ABSTRACT: A cohort study assessed the relationship between dietary intake of vitamin A in 493 healthy mothers before and around conception and adverse birth outcomes associated with environmental toxicant exposures. The cohort, non-smoking women with singleton pregnancies, aged 18-35 years, gave birth at 34-43 weeks of gestation. The women were asked about their diets over one year preceding pregnancy. Measurements of PM2.5 were carried out during the second trimester. Birth outcomes were adjusted for potential confounding factors, including gestational age. Standardized beta regression coefficients confirmed an inverse association between PM2.5 and birth weight (beta = -172.4, p = 0.02), but the effect of vitamin A on birth weight was positive (beta = 176.05, p = 0.05), when the two were adjusted for each other. The negative effect of higher prenatal PM2.5 exposures (above third tertile) on birth weight was significant in women below the third tertile of vitamin A intakes (beta = -185.1, p = 0.00), but not in women with higher intakes (beta = 38.6, p = 0.61). The negative effect of higher PM2.5 exposure on length at birth was significant with lower vitamin A intakes (beta = -1.1, p = 0.00) but not with higher intakes (beta = -0.3, p = 0.56). Prepregnancy nutrition of mothers may modulate the harmful effects of prenatal exposures to pollutants on birth outcomes.
    International journal of occupational and environmental health 01/2007; 13(2):175-80. · 1.18 Impact Factor