Lung function growth trajectories in non-asthmatic children aged 4-9 in relation to prenatal exposure to airborne particulate matter and polycyclic aromatic hydrocarbons - Krakow birth cohort study.

BACKGROUND: Patterns of lung function development during childhood can be helpful in understanding the pathogenesis of respiratory diseases. A variety of environmental and lifestyle factors, present from the prenatal period to adulthood, may affect or modulate lung function growth. The aim of this study was to investigate, the associations between individual growth trajectories of children's lung function during childhood and prenatal exposure to airborne fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAH), which were hypothesized to adversely affect spirometry parameters. MATERIAL AND METHODS: The study group comprised 294 non-asthmatic, full term children from the Krakow birth cohort, who underwent annual spirometry testing at the ages of 4-9 years. Individual personal air monitoring of PM2.5 and PAH were performed over 48 h in the second trimester of pregnancy. Possible confounders or modifiers such as child's gender, height, atopic status and exposure to environmental tobacco smoke (ETS) were considered. Polynomial multilevel mixed models were used to assess the growth rates of children's lung functions. RESULTS: Lung function trajectories differed significantly for boys and girls for FVC, FEV1 and FEF25-75. Girls had lower rates of increase than boys: - 20.5 (95%CI: - 32.4; - 8.6) ml/year (FVC); - 19.9 (95%CI: -30.7;-9.0) ml/year (FEV1); and - 32.5 (95%CI: - 56.9; - 8.2) ml/year (FEF25-75). Spirometry functions increased with age; however the growth rate decelerated over time. Significant lung function impairment (lower FVC and FEV1 levels) was observed from 4 to 9 years among subjects prenatally exposed to higher levels of PM2.5 as well as PAH, but not in the case of FEF25-75. No significant differences were observed in the rates of increase over time in relation to prenatal PM2.5 and PAH exposure. CONCLUSION: Our results indicate that in non-asthmatic children high prenatal exposure to airborne PM2.5 and PAH is associated with lower trajectories of FVC and FEV1, but not the rate of increase over time, suggesting that the initial effect is not diminishing in time.

Urinary polycyclic aromatic hydrocarbon metabolites among 3-year-old children from Krakow, Poland.

Polycyclic aromatic hydrocarbons (PAHs) are widespread in the environment and can adversely affect human health. The aim of the present study is to describe the level of PAHs exposure in children living in Kraków, one of the most polluted cities in Poland, and to determine the relationship of urinary biomarkers with environmental PAHsexposure. Urinary monohydroxy metabolites (OH-PAHs) of 20 PAHs were assessed in 218 three-year old children, of which only 10 were present in nearly all the samples: monohydroxy metabolites of naphthalene, fluorene, phenantrene and pyrene. Of the metabolites analyzed, hydroxynaphthalenes were predominant and constituted almost 73% of total excreted OH-PAHs, while 1-OH-PYRene was the least abundant (2.3% of total OH-PAHs). All measured urinary OH-PAHs were statistically significantly correlated with each other (R = 0.165-0.880) but the highest correlation coefficients with other individual OH-PAHs and with total OH-PAHs were observed for 2-OH-FLUOR. Children exposed at home to environmental tobacco smoke (ETS) had higher concentrations of fluorene and pyrene urinary metabolites compared to those without ETS exposure; and those exposed to gas-based appliances used for cooking or heating water had higher levels of fluorene and phenanthrene metabolites than children not exposed. The use of coal, wood or oil for heating was associated with elevated levels of 1-OH-PYRene. Urinary PAHs metabolites only modestly reflect high molecular weight carcinogenic PAHs exposures such as those monitored in air in the present study. None of the measured PAHs metabolites was correlated with airborne PM2.5 and only two were slightly correlated with measured higher molecular mass airborne PAHs. The average concentrations of these specific metabolites in Polish children were much higher than observed in other pediatric populations living in developed countries. Our findings suggest that to capture various sources of PAHs, in addition to 1-OH-PYRene, biomonitoring of PAHs exposure should include 2-OH-NAP and 2-OH-FLUOR.

What mother know about vaccine preventable diseases?

INTRODUCTION AND OBJECTIVE: The improving epidemiological situation of the most of communicable diseases causes, that the real and potential risks attributable to them have been forgotten. The aim of study was to determine the mothers knowledge about vaccine preventable diseases MATERIALS AND METHODS: A survey was conducted among 177 randomly selected mothers. The interviews with mothers hospitalized after childbearing in two hospitals in Krakow and Myslenice were conducted at the end of 2014 and in 2015 RESULTS: The assessment of risk to develop an infectious diseases in unvaccinated children significantly varied among mothers. Individual respondents claimed that the risk does not exist regarding each of considered disease. The highest percentage of that kind of answers was related to poliomyelitis ­ 3.9% of mothers assessed that unvaccinated children have no risk to become ill. The similar percentage of respondents assessed a risk as remote probable regarding poliomyelitis, pertussis and hepatitis A - 16.8%, 15.2% and 16.3%, respectively. The highest risk was attributed to varicella ­ 50.6% mothers gave that answers. Mothers could not state a risk of disease developing mostly with regard to poliomyelitis, diphtheria, hepatitis A and pertussis ­ 42.7%, 38.2%, 33.7% and 33.2%, respectively. Relatively high percentage of respondents stated a mild course of that kind of diseases like varicella, mumps, rubella, infectious diarrhea and measles - from 17.4% with respect to measles to 34.3% regarding varicella. To life-threating category mothers primarily included sepsis (74.2%), meningitis and tick-borne encephalitis (each obtained 68.5% answers) CONCLUSIONS: Mothers knowledge about vaccine preventable diseases varied depending on the type of disease. The lack of awareness of the risk related to communicable diseases regarded not only those diseases which have not been occurred in Poland for many years but also those ones that still represent significant epidemiological problem. The society too often has an opinion that some diseases like varicella, mumps or rubella are the mild diseases what can conduce to easy withdrawal from those vaccinations

Opinions about vaccination among mothers who delivered newborns in two hospitals in Krakow and Myslenice

INTRODUCTION AND OBJECTIVE: Campaigns against vaccinations in Poland have been increasingly more frequently observed in recent years, that was the reason of bigger number of parents refusing a consent for their children immunization. The aim of study was to determine the sources of information which significantly influence mothers' opinions about vaccinations. MATERIALS AND METHODS: A survey was conducted among 154 randomly selected mothers hospitalized after childbearing in two hospitals in Krakow and Myslenice at the end of 2014 and in 2015. The research tool was the author's structured questionnaire interview. RESULTS: The majority of mothers regarded vaccinations as an efficient method of children protection against infectious diseases. Nevertheless, a few percent of women admitted that it is not efficient method or had no opinion about it. The mothers' confidence was higher for vaccines known for many years compared to new formulations ­ 23.7% did not trust them and 22.4% had no statement on it. The most of respondents claimed that the safety of polyvalent vaccines is lower than single formulas, and were convinced that children receive too many vaccines. About 54.6% of mothers had no opinion and 13.6% admitted that children with chronic diseases should not be vaccinated. Depending on the question content from 3.2% to 54.6% respondents had no opinion about included vaccination issues. The pediatricians and family doctors were the main and the most reliable source of information about vaccinations. The reliability of doctors was assessed higher by citizens of big city compared to women living in rural area (statistically significant). Above 50% of mothers used mass media as a source of information about vaccination but less than 8% regarded them as reliable. CONCLUSIONS: Despite the wide access to different source of information, the newborns' mothers too often had the knowledge and opinions about vaccination inconsistent with data derived from medical facts. Furthermore, significant group of mothers had no opinions about important issues with respect to vaccinations. At the beginning of infants life when parents decide of their child immunization, the reliable knowledge about that issue should be delivered by GPs because the other sources of information are assessed as much less reliable.

Significant interactions between maternal PAH exposure and single nucleotide polymorphisms in candidate genes on B[ a ]P-DNA adducts in a cohort of non-smoking Polish mothers and newborns.

Polycyclic aromatic hydrocarbons (PAH) are a class of chemicals common in the environment. Certain PAH are carcinogenic, although the degree to which genetic variation influences susceptibility to carcinogenic PAH remains unclear. Also unknown is the influence of genetic variation on the procarcinogenic effect of in utero exposures to PAH. Benzo[ a ]pyrene (B[ a ]P) is a well-studied PAH that is classified as a known human carcinogen. Within our Polish cohort, we explored interactions between maternal exposure to airborne PAH during pregnancy and maternal and newborn single nucleotide polymorphisms (SNPs) in plausible B[ a ]P metabolism genes on B[ a ]P-DNA adducts in paired cord blood samples. The study subjects included non-smoking women ( n = 368) with available data on maternal PAH exposure, paired cord adducts, and genetic data who resided in Krakow, Poland. We selected eight common variants in maternal and newborn candidate genes related to B[ a ]P metabolism, detoxification, and repair for our analyses: CYP1A1 , CYP1A2 , CYP1B1 , GSTM1 , GSTT2 , NQO1 , and XRCC1 . We observed significant interactions between maternal PAH exposure and SNPs on cord B[ a ]P-DNA adducts in the following genes: maternal CYP1A1 and GSTT2 , and newborn CYP1A1 and CYP1B1 . These novel findings highlight differences in maternal and newborn genetic contributions to B[ a ]P-DNA adduct formation and have the potential to identify at-risk subpopulations who are susceptible to the carcinogenic potential of B[ a ]P.

Prenatal polycyclic aromatic hydrocarbon (PAH) exposure, antioxidant levels and behavioral development of children ages 6-9.

PURPOSE: 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. METHODS: 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. RESULTS: 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 (MVß=0.60, p<0.001) and externalizing problems (MVß=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). CONCLUSIONS: 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.

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

Fetal exposure to environmental toxicants may program the development of children and have long-lasting health impacts. The study tested the hypothesis that depressed height gain in childhood is associated with prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and heavy metals (lead and mercury). The study sample comprised 379 children born to non-smoking mothers among whom a total of 2011 height measurements were carried out over the 9-year follow-up period. Prenatal airborne PAH exposure was assessed by personal air monitoring of the mother in the second trimester of pregnancy and heavy metals were measured in cord blood. At the age of 3 residential air monitoring was done to evaluate the level of airborne PAH, and at the age 5 the levels of heavy metals were measured in capillary blood. The effect estimates of prenatal PAH exposure on height growth over the follow-up were adjusted in the General Estimated Equation (GEE) models for a wide set of relevant covariates. Prenatal exposure to airborne PAH showed a significant negative association with height growth, which was significantly decreased by 1.1cm at PAH level above 34.7 ng/m(3) (coeff.=-1.07, p=0.040). While prenatal lead exposure was not significantly associated with height restriction, the effect of mercury was inversely related to cord blood mercury concentration above 1.2 µg/L (coeff.=-1.21, p=0.020), The observed negative impact of prenatal PAH exposure on height gain in childhood was mainly mediated by shorter birth length related to maternal PAH exposure during pregnancy. The height gain deficit associated with prenatal mercury exposure was not seen at birth, but the height growth was significantly slower at later age.

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

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

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

The main goal of the study was to test the hypothesis that prenatal and postnatal exposures to polycyclic aromatic hydrocarbons (PAH) are associated with depressed lung function in non-asthmatic children. The study sample comprises 195 non-asthmatic children of non-smoking mothers, among whom the prenatal PAH exposure was assessed by personal air monitoring in pregnancy. At the age of 3, residential air monitoring was carried out to evaluate the residential PAH exposure indoors and outdoors. 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 37 ng/m(3)) amounted to 53 mL (p=0.050) and the deficit of FEF25-75 reached 164 mL (p=0.013). The corresponding deficits related to postnatal residential indoor PAH level (above 42 ng/m(3)) were 59 mL of FEV1 (p=0.028) and 140 mL of FEF25-75 (p=0.031). At the higher residential outdoor PAH level (above 90 ng/m(3)) slightly greater deficit of FEV1 (71 mL, 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.

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

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

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

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

Prenatal exposure to air pollution, maternal psychological distress, and child behavior.

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.

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

OBJECTIVES: The main goal of the study was to assess possible association between fetal exposure to fine particulate matter (PM2.5) and exhaled carbon monoxide (eCO) measured in non-asthmatic children. MATERIAL AND METHODS: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. 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.

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

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM2.5) on the recurrent broncho-pulmonary infections in early childhood. The study included 214 children who had measurements of personal prenatal PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 level (OR=2.44, 95%CI: 1.12-5.36). In conclusion, the study suggests that prenatal exposure to PM2.5 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 PM2.5 protects unborn babies better than earlier established EPA guidelines.

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

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

Fractional exhaled nitric oxide in healthy non-asthmatic 7-year olds and prenatal exposure to polycyclic aromatic hydrocarbons: nested regression analysis.

UNLABELLED: 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.

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

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

Effect of exclusive breastfeeding on the development of children's cognitive function in the Krakow prospective birth cohort study.

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.

Impact of barbecued meat consumed in pregnancy on birth outcomes accounting for personal prenatal exposure to airborne polycyclic aromatic hydrocarbons: Birth cohort study in Poland.

OBJECTIVE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: In conclusion, the study results provided epidemiologic evidence that prenatal PAH exposure from diet including grilled meat might be hazardous for fetal development.

Effect of prenatal exposure to fine particulate matter and intake of Paracetamol (Acetaminophen) in pregnancy on eczema occurrence in early childhood.

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.