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1.  Measles, mumps and rubella (MMR) vaccination has no effect on cognitive development in children – the results of the Polish prospective cohort study 
Vaccine  2013;31(22):2551-2557.
The aim of the study was to examine the hypothesis that MMR exposure has a negative influence on cognitive development in children. Furthermore, MMR was compared to single measles vaccine to determine the potential difference of these vaccines safety regarding children’s cognitive development.
The prospective birth cohort study with sample consisted of 369 infants born in Krakow. Vaccination history against measles (date and the type of the vaccine) was extracted from physicians’ records. Child development was assessed using the Bayley Scales of Infant Development (BSID-II) up to 3rd year of life, Raven test in 5th and 8th year and Wechsler (WISC-R) in 6th and 7th year. Data on possible confounders came from mothers’ interview, medical records and analyses of lead and mercury level at birth and at the end of 5th year of life. Linear and logistic regression models adjusted for potential confounders were used to assess the association.
No significant differences in cognitive and intelligence tests results were observed between children vaccinated with MMR and those not vaccinated up to the end of the 2nd year of life. Children vaccinated with MMR had significantly higher Mental BSID-II Index (MDI) in the 36th month than those vaccinated with single measles vaccine (103.8±10.3 vs. 97.2±11.2, p=0.004). Neither results of Raven test nor WISC-R were significantly different between groups of children vaccinated with MMR and with single measles vaccine. After standardization to child’s gender, maternal education, family economical status, maternal IQ, birth order and passive smoking all developmental tests were statistically insignificant.
The results suggest that there is no relationship between MMR exposure and children’s cognitive development. Furthermore, the safety of triple MMR is the same as the single measles vaccine with respect to cognitive development.
PMCID: PMC3684783  PMID: 23588083
children; MMR vaccine; cognitive development
2.  Gender differences in fetal growth of newborns exposed prenatally to airborne fine particulate matter 
Environmental research  2009;109(4):447-456.
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 PM2.5 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 PM2.5 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 PM2.5 exposure. Overall average increase in gestational period of prenatal exposure to fine particles by about 30 μg/m3, i.e., from 25th percentile (23.4 μg/m3) to 75th percentile (53.1 μg/m3) brought about an average birth weight deficit of 97.2 g (95% CI: −201, 6.6) and length at birth of 0.7cm (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 17 g in female newborns; the deficit of length at birth in male infants amounted to 1.1 cm (95% CI: −0.11, −2.04). We found a significant interrelationship between self-reported ETS and PM2.5, however, none of the models showed a significant interaction of both variables. The joint effect of various levels of PM2.5 and ETS on birth outcomes showed the significant deficit only for the categories of exposure with higher component of PM2.5. Concluding, the results of the study suggest that observed deficits in birth outcomes are rather attributable to prenatal PM2.5 exposure and not to environmental tobacco smoke. The study also provided evidence that male fetuses are more sensitive to prenatal PM2.5 exposure and this should persuade policy makers to consider birth outcomes by gender separately while setting air pollution guidelines.
PMCID: PMC3786262  PMID: 19261271
Cohort study; Prenatal exposure; Air pollutants; Fine particles; Gender; Fetal growth deficits
Early human development  2009;85(8):503-510.
The primary purpose of this study was to assess the relationship between very low-level of prenatal lead exposure measured in the cord blood (<5 µg/dL) and possible gender-specific cognitive deficits in the course of the first three years of life. The accumulated lead dose in infants over the pregnancy period was measured by the cord blood lead level (BLL) and cognitive deficits were assessed by the Bayley Mental Development Index (MDI). The study sample consisted of 457 children born to non-smoking women living in the inner city and the outlying residential areas of Krakow. The relationship between prenatal lead exposure and MDI scores measured at 12, 24 and 36 months of age and adjusted to a set of important covariates (gender of child, maternal education, parity, breastfeeding, prenatal and postnatal environmental tobacco smoke) was evaluated with linear multivariate regression, and the Generalized Estimating Equations (GEE) longitudinal panel model. The median of lead level in cord blood was 1.21 µg/dL with the range of values from 0.44 to 4.60 µg/dL. Neither prenatal BLL (dichotomized by median) nor other covariates affected MDI score at 12 months of age. Subsequent testing of children at 24 months of age showed a borderline significant inverse association of lead exposure and mental function (beta coeff. = −2.42, 95%CI: −4.90 to 0.03), but the interaction term (BLL × male gender) was not significant. At 36 months, prenatal lead exposure was inversely and significantly associated with cognitive function in boys (Spearman correlation coefficient = −0.239, p=0.0007) but not girls (r = − 0.058, p = 0.432) and the interaction between BLL and male gender was significant (beta coeff. = − 4.46; 95%CI: −8.28 to −0.63). Adjusted estimates of MDI deficit in boys at 36 months confirmed very strong negative impact of prenatal lead exposure (BLL>1.67µg/dL) compared with the lowest quartile of exposure (beta coeff. = −6.2, p = 0.002), but the effect in girls was insignificant (beta coeff = −0.74, p = 0.720). The average deficit of cognitive function in the total sample over the first three years of life (GEE model) associated with higher prenatal lead exposure was also significant (beta coefficient = − 3.00; 95%CI: −5.22 to −0.70). Beside prenatal lead exposure, presence of older siblings at home and prenatal environmental tobacco smoke had a negative impact on MDI score. Better maternal education showed a strong beneficial effect on the cognitive development of children. Conclusion: The study suggests that there might be no threshold for lead toxicity in children and provides evidence that 3-year old boys are more susceptible than girls to prenatal very low lead exposure. The results of the study should persuade policy makers to consider gender-related susceptibility to lead and possibly to other toxic hazards in setting environmental protection guidelines. To determine whether the cognitive deficit documented in this study persists to older ages, the follow-up of the children over the next several years is to be carried out.
PMCID: PMC3725459  PMID: 19450938
prenatal lead exposure; cognitive function; early childhood; prospective birth cohort study
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 fetus 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 four year follow-up was adjusted for potential confounding factors such as personal prenatal exposure to fine particulate matter (PM2.5), environmental tobacco smoke (ETS), gender of child, maternal characteristics (age, education and atopy), parity, and mold/dampness in the home. The study sample includes 339 newborns of non-smoking mothers 18-35 years 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 two years of life was positively associated with prenatal level of PAH-DNA adducts (IRR = 1.69, 95%CI = 1.52 – 1.88), prenatal particulate matter (PM2.5) 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), moldy/damp house (IRR = 1.43; 95%CI: 1.27 – 1.61). The level of maternal education and maternal age at delivery were inversely associated with the IRRs for wheeze. The significant association between frequency of wheeze and the level of prenatal environmental hazards (PAHs and PM2.5) was not observed at ages 3 or 4 years. Although the frequency of wheezing at ages 3 or 4 years was no longer associated with prenatal exposure to PAHs and PM2.5, its occurrence depended on the presence of wheezing in the first two years 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) are different to those leading to later onset of wheeze. As we reported no synergistic effects between prenatal PAH (measured by PAH-DNA adducts) and PM2.5 exposures on early wheeze, this suggests the two exposures may exert independent effects via different biological mechanism on wheeze.
PMCID: PMC3683604  PMID: 20444151
prenatal exposure to polycyclic aromatic hydrocarbons; biomarkers of exposure; DNA adducts; early wheeze; 4-year olds; birth cohort study
The main purpose of the study was to answer the question whether young children without clinical diagnosis of asthma but experiencing early wheezing disorders and therefore being at high risk of developing asthma may have cognitive deficits. In the ongoing birth cohort study wheezing symptoms were recorded postpartum over two first years of age and subsequently cognitive status of children at the age of 3 years was assessed with the Bayley Mental Development Index (MDI). In the statistical analysis a wide range of modifying and confounding factors (maternal education, gender of children, prenatal exposure to lead and environmental tobacco smoke (ETS) were considered to assess the independent effect of early wheezing phenotypes on cognitive development of children. The MDI score correlated inversely with the number of wheezing days recorded over 24 months (r = −0.13, p=0.007), lead cord blood concentration (r = − 0.12, p = − 0.02), number of siblings (r = − 0.17, p = 0.0006) and the number of cigarettes smoked daily by other household members at home over the pregnancy period (r = − 0.18, p = 0.0002). While the children who experienced wheezing over the first year of age showed deficit of 2 MDI scores (beta coeff. = −2.31, 95%CI: −4.63 to 0.02), those with persistent wheezing had the score deficit of 4 points (beta coeff. = − 4.41, 95%CI: −8.27 to −0.55).
To our knowledge, it is the first report in the literature showing that early wheezing is associated the cognitive deficit in a community-recruited very young children. Observed cognitive deficit in early wheezers may be caused by RSV infections or can be related to lower lung function attributed to persistent wheezing, which reducing oxygen supply would affect rapidly developing brain.
PMCID: PMC3682116  PMID: 19548966
cognitive development; children; wheezing phenotypes; birth cohort study
The Science of the total environment  2011;409(24):5205-5209.
Prenatal Paracetamol (Acetaminophen) has been associated with increased risk of allergic disease in early childhood, an association that could be due to increased altered susceptibility induced by air pollutants. The main 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 is stronger for children who are exposed prenatally 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 over 48 hours was measured in all recruited women in the second trimester of PM2.5 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 a trained interviewer. During the interviews at each of the study periods after birth, a history of eczema was recorded.
By Cox proportional hazard regression, prenatal exposure to Paracetamol increased the risk of eczema by 20% and PM2.5 by 6%, albeit non significantly. However, the the joint exposure to Paracetamol and higher prenatal PM2.5 was significant and doubled the risk of eczema symptoms (HR = 2.07, 95%CI: 1.01 – 4.34). The findings suggest that even very small doses of Paracetamol in pregnancy may affect the occurrence of allergy outcomes such as eczema in early childhood but only at the co-exposure to higher fine particulate matter.
PMCID: PMC3428593  PMID: 21962593
birth cohort study; eczema; children; acetaminophen; pregnancy; prenatal fine particulate matter
7.  Effects of Prenatal and Perinatal Exposure to Fine Air Pollutants and Maternal Fish Consumption on the Occurrence of Infantile Eczema 
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.
PMCID: PMC3047761  PMID: 21293147
Fish consumption; Prenatal exposure to fine particles; Cow's milk allergy; Passive tobacco smoke; Cohort study
8.  Higher Fish Consumption in Pregnancy May Confer Protection against the Harmful Effect of Prenatal Exposure to Fine Particulate Matter 
Annals of Nutrition & Metabolism  2010;56(2):119-126.
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 μm in size (PM2.5) were carried out by personal air monitoring over 48 h during the second trimester of pregnancy. The effect of PM2.5 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 μg/m3 (β 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 PM2.5 and fish intake levels was also insignificant (β = −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.
PMCID: PMC2842166  PMID: 20134157
Air pollutants; Prenatal exposure; Fish consumption; Birth size; Cohort study
Environment international  2009;35(6):877-884.
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 PM2.5 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 two 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 PM2.5 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 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.
PMCID: PMC2709737  PMID: 19394697
wheezing phenotypes; respiratory symptoms; prenatal and postnatal environmental air quality; birth cohort study
10.  Very Low Prenatal Exposure to Lead and Mental Development of Children in Infancy and Early Childhood 
Neuroepidemiology  2009;32(4):270-278.
The primary purpose of the study was to establish a possible association between very low levels of prenatal exposure to lead and mental development of children at 12, 24 and 36 months of age.
The study sample consisted of 444 children born to mothers who attended ambulatory prenatal clinics in Krakow inner city in the first and second trimesters of pregnancy. We assessed exposure to lead by the cord blood lead measurements, and mental development in infancy and early childhood using the Bayley Mental Development Index (MDI). The relationship between prenatal lead exposure and MDI scores at each follow-up period was evaluated with linear multivariate regression. To test the overall effect of maternal exposure to lead during pregnancy on the Bayley test scores at 12, 24 and 36 months of age, we used the generalized estimating equations (GEE) longitudinal panel model as well.
The median lead level in cord blood was 1.23 μg/dl, in the range of 0.44–6.90 μg/dl. An adverse effect of prenatal lead exposure (log-transformed lead concentrations) on MDI scores at 12 months of age was of border significance (β = −5.42, 95% CI: −11.19 to 0.35). Subsequent testing of children at 24 months of age showed a significant inverse association of mental function and lead exposure (β = −7.65, 95% CI: −14.68 to −0.62). A significant deficit in cognitive function due to prenatal lead exposure was also confirmed at 36 months of age (β = −6.72, 95% CI: −12.5 to −0.89). The GEE panel model showed that the average deficit in the cognitive development attributable to lead exposure over 3 years was also significant (β = −6.62, 95% CI: −1.52 to −1.72). Mental function scores of girls were better than boys, and the effect of maternal education remained strongly significant in relation to mental function of 3-year-olds.
The results of the study demonstrate that the neurotoxic impact of very low levels of prenatal lead exposure (below 5 μg/dl) may occur in infants and very young children, and suggest a revision of established health guidelines for prenatal lead exposure criteria.
Copyright © 2009 S. Karger AG, Basel
PMCID: PMC2824585  PMID: 19223686
Prenatal lead exposure; Infant cognitive functioning; Infant psychomotor functioning; Prospective cohort study

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