Higher fish consumption in pregnancy may confer protection against the harmful effect of prenatal exposure to fine particulate matter.

BACKGROUND/AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Gender differences in fetal growth of newborns exposed prenatally to airborne fine particulate matter.

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.

Pre-pregnancy dietary vitamin A intake may alleviate the adverse birth outcomes associated with prenatal pollutant exposure: epidemiologic cohort study in Poland.

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.

Fish intake during pregnancy and mercury level in cord and maternal blood at delivery: an environmental study in Poland.

OBJECTIVES: The purpose of this study was to estimate the amount of absorbed mercury (Hg) by mothers and their infants as a result of fish consumption during pregnancy. MATERIALS AND METHODS: The cohort consisted of 313 mother-infant pairs recruited initially from ambulatory prenatal clinics in the first and second trimesters of pregnancy. The customary pattern of fish consumption during pregnancy reported by mothers was correlated with Hg levels in cord and maternal blood at delivery. Blood Hg level was measured using atomic absorption spectrometry. RESULTS: The mean Hg concentration in cord blood was markedly higher than in maternal blood at delivery (1.09 microg/L; 95%CI: 1.00-1.13 microg/L vs. 0.83 microg/L, 95%CI: 0.76-0.91 microg/L). There was significant correlation (r(s)=0.62, 95%CI: 0.55-0.69) between Hg levels in cord and maternal blood. The overall ratio of Hg in cord blood vs. maternal blood was 1.7 (95%C: 1.50-1.89). Fish consumed during the last pregnancy trimester correlated stronger with umbilical cord concentrations (r(s)=0.32; 95%CI: 0.22-0.40) than with Hg in maternal blood (r(s)=0.23; 95%CI: 0.14-0.33). CONCLUSIONS: The study shows that in Poland, babies are exposed to moderate levels of mercury prior to birth and that fish eating in pregnancy significantly contributes to prenatal Hg exposure. The findings also suggest that the level of cord blood Hg should not be used for describing inter-individual differences in maternal exposure to Hg unless a proper correction factor is introduced.

Effects of prenatal exposure to mercury on cognitive and psychomotor function in one-year-old infants: epidemiologic cohort study in Poland.

PURPOSE: The aim of the study is to assess the cognitive and psychomotor status of 1-year-old infants whose mothers were exposed to low, but varying, amounts of mercury during pregnancy. METHODS: Mercury levels in cord and maternal blood at delivery were used to assess prenatal environmental exposure to mercury. Bayley Scales of Infant Development were used to assess neurobehavioral health outcomes. The cohort consisted of 233 infants who were born at 33 to 42 weeks of gestation between January 2001 and March 2003 to mothers attending ambulatory prenatal clinics in the first and second trimesters of pregnancy. Enrollment included only nonsmoking women with singleton pregnancies between the ages of 18 and 35 years who were free from chronic diseases. RESULTS: The geometric mean (GM) for maternal blood mercury level for the group of infants with normal neurocognitive performance was lower (GM = 0.52 mug/L; 95% confidence interval [CI], 0.46-0.58) than that observed in the group with delayed performance (GM = 0.75 mug/L; 95% CI, 0.59-0.94), and this difference was significant (p = 0.010). The GM of cord blood mercury level in the normal group also was lower (GM = 0.85 mug/L; 95% CI, 0.78-0.93) than that observed in the group with delayed performance (GM = 1.05 mug/L; 95% CI, 0.87-1.27), and this difference was of borderline significance (p = 0.070). The relative risk (RR) for delayed performance increased more than threefold (RR = 3.58; 95% CI, 1.40-9.14) if cord blood mercury level was greater than 0.80 mug/L. Risk for delayed performance in the group of infants with greater maternal mercury levels (>0.50 mug/L) also was significantly greater (RR = 2.82; 95% CI, 1.17-6.79) compared with children whose mothers had mercury levels less than 0.50 mug/L. CONCLUSIONS: The results may be of public health importance because delayed psychomotor or mental performance in infants is assumed to be an indicator of later neurocognitive development in children, which may persist into adult life.

Exposure to environmental tobacco smoke in pregnancy and lead level in maternal blood at delivery.

OBJECTIVES: The particular purpose of our study was to assess the impact of environmental tobacco smoke (ETS) on the individual variability of blood lead levels in pregnant women as earlier publications demonstrated the increased blood lead in smokers. MATERIALS AND METHODS: The material consisted of 240 pregnant women who participated in a prospective cohort study on vulnerability of the fetus and infant to environmental hazards. The enrolment included only non-smoking women with singleton pregnancies between the ages of 18-35 years. Whole blood lead concentrations were determined using inductively coupled plasma mass spectrometry. RESULTS: On average, blood-lead measured in pregnant women at delivery was low (GM = 1.7 microg/dL; 95% CI:1.6-1.8 microg/dL) and none of them showed levels above 4.0 microg/dL, but persons reporting exposure to ETS had significantly higher blood lead level (GM = 1.9 microg/dL; 95%CI:1.8-2.1 microg/dL) than those free from this exposure (GM = 1.6 microg/dL; 95%CI:1.5-1.7 microg/dL). In order to single out the effect of the ETS exposure from the confounding variables, we used the stepwise multivariate linear regression for log blood-lead in maternal blood as dependent variable and a set of independent variables, such as age, weight of women before pregnancy and their education level. The results of the analysis showed that all the independent variables included in the model explained 11% of total blood-lead variability among the study women. The strongest component of variance was attributed to ETS exposure (5%), age (3%), education level (2%) and weight (1%). Inclusion into the model of other variables, e.g., residence area and traffic intensity did not improve the proportion of explained variability. CONCLUSIONS: The reason for higher levels of blood-lead in the ETS-exposed women may result from the fact that tobacco smoke contains lead. However, it is possible that inhaled tobacco smoke also increases the absorption of lead from particulate matter deposited in the bronchial tree.