Studies exploring the role of diet during pregnancy are still scarce, in part due to the complexity of measuring diet and to the lack of valid instruments. The aim of this study was to examine the ...reproducibility and validity (against biochemical biomarkers) of a semi-quantitative food frequency questionnaire (FFQ) in pregnant women.
Participants were 740 pregnant women from a population-based birth cohort study in Valencia (INMA Study). We compared nutrient and food intakes from FFQs estimated for two periods of pregnancy (reproducibility), and compared energy-adjusted intake of several carotenoids, folate, vitamin B12, vitamin C and α-tocopherol of the FFQ in the first trimester with their concentration in blood specimens (validity).
Significant correlations for reproducibility were found for major food groups and nutrients but not for lycopene (r=0.06); the average correlation coefficients for daily intake were 0.51 for food groups and 0.61 for nutrients. For validity, statistically significant correlations were observed for vitamin C (0.18), α-carotene (0.32), β-carotene (0.22), lutein-zeaxantin (0.29) and β-cryptoxantin(0.26); non-significant correlations were observed for retinol, lycopene, α-tocopherol, vitamin B12 and folate (r≤0.12). When dietary supplement use was considered, correlations were substantially improved for folate (0.53) and to a lesser extent for vitamin B12 (0.12) and vitamin C (0.20).
This study supports that the FFQ has a good reproducibility for nutrient and food intake, and can provide a valid estimate of several important nutrients during pregnancy.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
Background Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results. ...Objectives We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years). Methods First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age <37 weeks) and low birth weight (<2500 g) with childhood asthma outcomes. Results Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma ( P < .05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio OR, 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio pOR, 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27). Conclusion Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPUK
The present study aimed at developing a standardized heat wave definition to estimate and compare the impact on mortality by gender, age and death causes in Europe during summers 1990-2004 and 2003, ...separately, accounting for heat wave duration and intensity.
Heat waves were defined considering both maximum apparent temperature and minimum temperature and classified by intensity, duration and timing during summer. The effect was estimated as percent increase in daily mortality during heat wave days compared to non heat wave days in people over 65 years. City specific and pooled estimates by gender, age and cause of death were calculated.
The effect of heat waves showed great geographical heterogeneity among cities. Considering all years, except 2003, the increase in mortality during heat wave days ranged from + 7.6% in Munich to + 33.6% in Milan. The increase was up to 3-times greater during episodes of long duration and high intensity. Pooled results showed a greater impact in Mediterranean (+ 21.8% for total mortality) than in North Continental (+ 12.4%) cities. The highest effect was observed for respiratory diseases and among women aged 75-84 years. In 2003 the highest impact was observed in cities where heat wave episode was characterized by unusual meteorological conditions.
Climate change scenarios indicate that extreme events are expected to increase in the future even in regions where heat waves are not frequent. Considering our results prevention programs should specifically target the elderly, women and those suffering from chronic respiratory disorders, thus reducing the impact on mortality.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Recent epidemiological research suggests that near road traffic-related pollution may cause chronic disease, as well as exacerbation of related pathologies, implying that the entire "chronic disease ...progression" should be attributed to air pollution, no matter what the proximate cause was. We estimated the burden of childhood asthma attributable to air pollution in 10 European cities by calculating the number of cases of 1) asthma caused by near road traffic-related pollution, and 2) acute asthma events related to urban air pollution levels. We then expanded our approach to include coronary heart diseases in adults. Derivation of attributable cases required combining concentration-response function between exposures and the respective health outcome of interest (obtained from published literature), an estimate of the distribution of selected exposures in the target population, and information about the frequency of the assessed morbidities. Exposure to roads with high vehicle traffic, a proxy for near road traffic-related pollution, accounted for 14% of all asthma cases. When a causal relationship between near road traffic-related pollution and asthma is assumed, 15% of all episodes of asthma symptoms were attributable to air pollution. Without this assumption, only 2% of asthma symptoms were attributable to air pollution. Similar patterns were found for coronary heart diseases in older adults. Pollutants along busy roads are responsible for a large and preventable share of chronic disease and related acute exacerbations in European urban areas.
Perfluoroalkyl substances (PFASs) have been related to neurodevelopmental toxicity in animals. However, human studies are inconclusive.
To evaluate the association between prenatal PFAS exposure and ...neuropsychological development during childhood.
1240 mother–child pairs from the Spanish INMA Project were analyzed. Perfluorohexanesulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), and perfluorononanoic acid (PFNA) were measured in first-trimester maternal plasma. Neuropsychological development was assessed at 14 months, 4–5 and 7 years covering four domains: general cognitive, general motor, attention, and working memory. Associations were studied by means of multivariable regression analyses.
PFHxS, PFOA, PFOS, and PFNA medians were: 0.6, 2.4, 6.1, and 0.7 ng/mL. Higher PFAS prenatal exposure was associated with worse motor development at 14 months, especially in the case of PFHxS (β95%CI: −1.49−2.73, −0.24) and to a lesser extent PFOS (−1.25−2.62, 0.12). There was also a marginal positive association between general cognitive development at 4–5 years and PFOS (1.17−0.10, 2.43) and PFNA (0.99−0.13, 2.12). No clear associations for other neuropsychological outcomes or any sex differences were found.
This study shows no clear-cut evidence of an association between prenatal PFAS exposure and adverse neuropsychological development in children up to the age of 7 years.
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•Study on prenatal PFASs and neurodevelopment up to 7 years (n = 1240, Spain).•Negative pattern between PFASs and 14-month motor development, p < 0.05 for PFHxS.•Some marginal positive associations with 4–5-year-old cognitive development.•No consistent sex modifying effects.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPUK, ZAGLJ, ZRSKP
Results of studies on perfluoroalkyl substances (PFASs) and thyroid hormones (THs) are heterogeneous, and the mechanisms underlying the action of PFASs to target THs have not been fully ...characterized. We examined the relation between first-trimester maternal PFAS and TH levels and the role played by polymorphisms in the iodothyronine deiodinase 1 (DIO1) and 2 (DIO2) genes in this association. Our sample comprised 919 pregnant Spanish women (recruitment = 2003–2008) with measurements of perfluorohexanesulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA), thyroid-stimulating hormone (TSH), total triiodothyronine (TT3), and free thyroxine (FT4), and we genotyped for single-nucleotide polymorphisms in the DIO1 (rs2235544) and DIO2 (rs12885300) genes. We performed multivariate regression analyses between PFASs and THs and included the interaction term PFAS–genotypes in the models. PFHxS was associated with an increase in TSH (% change in outcome 95% CI per 2-fold PFAS increase = 6.09 −0.71, 13.4), and PFOA and PFNA were associated with a decrease in TT3 (−7.17 −13.5, −0.39 and −6.28 −12.3, 0.12, respectively). We found stronger associations between PFOA, PFNA, and TT3 for DIO1–CC and DIO2–CT genotypes, although interaction p-values were not significant. In conclusion, this study found evidence of an inverse association between PFOA and TT3 levels. No clear effect modification by DIO enzyme genes was observed.
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IJS, KILJ, NUK, PNG, UL, UM
The association between air pollution exposure and emotional and behavioural problems in children is unclear. We aimed to assess prenatal and postnatal exposure to several air pollutants and child's ...depressive and anxiety symptoms, and aggressive symptoms in children of 7–11 years.
We analysed data of 13182 children from 8 European population-based birth cohorts. Concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter (PM) with diameters of ≤10 μm (PM10), ≤ 2.5 μm (PM2.5), and between 10 and 2.5 μm (PMcoarse), the absorbance of PM2.5 filters (PM2.5abs), and polycyclic aromatic hydrocarbons (PAHs) were estimated at residential addresses of each participant. Depressive and anxiety symptoms and aggressive symptoms were assessed at 7–11 years of age using parent reported tests. Children were classified in borderline/clinical range or clinical range using validated cut offs. Region specific models were adjusted for various socio-economic and lifestyle characteristics and then combined using random effect meta-analysis. Multiple imputation and inverse probability weighting methods were applied to correct for potential attrition bias.
A total of 1896 (14.4%) children were classified as having depressive and anxiety symptoms in the borderline/clinical range, and 1778 (13.4%) as having aggressive symptoms in the borderline/clinical range. Overall, 1108 (8.4%) and 870 (6.6%) children were classified as having depressive and anxiety symptoms, and aggressive symptoms in the clinical range, respectively. Prenatal exposure to air pollution was not associated with depressive and anxiety symptoms in the borderline/clinical range (e.g. OR 1.02 95%CI 0.95 to 1.10 per 10 μg/m3 higher NO2) nor with aggressive symptoms in the borderline/clinical range (e.g. OR 1.04 95%CI 0.96 to 1.12 per 10 μg/m3 higher NO2). Similar results were observed for the symptoms in the clinical range, and for postnatal exposures to air pollution.
Overall, our results suggest that prenatal and postnatal exposure to air pollution is not associated with depressive and anxiety symptoms or aggressive symptoms in children of 7 to 11 years old.
•We included air pollution data from eight European birth cohorts.•Concentrations of the analysed pollutants varied substantially across Europe.•We assessed emotional and aggressive behaviour symptoms in children of 7–11 years.•Air pollution was not associated with depressive and anxiety symptoms in children.•Air pollution was not associated with aggressive behaviour symptoms in children.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPUK, ZAGLJ, ZRSKP
•Prenatal air pollution exposure was associated with decreased weight and BMI at preschool age.•Prenatal air pollution exposure was associated to a reduced risk of accelerated BMI gain.•Birth weight ...partially mediated the association between PM2.5 and weight and BMI.
We investigated the association between outdoor air pollutants exposure in the first trimester of pregnancy, and growth and cardio-metabolic risk at four years of age, and evaluated the mediating role of birth weight.
We included mother-child pairs (N = 1,724) from the Spanish INMA birth cohort established in 2003–2008. First trimester of pregnancy nitrogen dioxide (NO2) and fine particles (PM2.5) exposure levels were estimated. Height, weight, waist circumference, blood pressure, and lipids were measured at four years of age. Body mass index (BMI) trajectories from birth to four years were identified.
Increased PM2.5 exposure in the first trimester of pregnancy was associated with decreased z-scores of weight (zWeight) and BMI (zBMI) (zWeight change per interquartile range increase in PM2.5 exposure = −0.12; 95% CI: −0.23, −0.01; zBMI change = −0.12; 95% CI: −0.23, −0.01). Higher NO2 and PM2.5 exposure was associated to a reduced risk of being in a trajectory with accelerated BMI gain, compared to children with the average trajectory. Birth weight partially mediated the association between PM2.5 and zWeight and zBMI. PM2.5 and NO2 were not associated with the other cardio-metabolic risk factors.
This comprehensive study of many growth and cardio-metabolic risk related outcomes suggests that air pollution exposure during pregnancy may be associated with delays in physical growth in the early years after birth. These findings imply that pregnancy exposure to air pollutants has a lasting effect on growth after birth and require follow-up at later child ages.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPUK, ZAGLJ, ZRSKP
Fetal smoke exposure is a common and key avoidable risk factor for birth complications and seems to influence later risk of overweight. It is unclear whether this increased risk is also present if ...mothers smoke during the first trimester only or reduce the number of cigarettes during pregnancy, or when only fathers smoke. We aimed to assess the associations of parental smoking during pregnancy, specifically of quitting or reducing smoking and maternal and paternal smoking combined, with preterm birth, small size for gestational age, and childhood overweight.
We performed an individual participant data meta-analysis among 229,158 families from 28 pregnancy/birth cohorts from Europe and North America. All 28 cohorts had information on maternal smoking, and 16 also had information on paternal smoking. In total, 22 cohorts were population-based, with birth years ranging from 1991 to 2015. The mothers' median age was 30.0 years, and most mothers were medium or highly educated. We used multilevel binary logistic regression models adjusted for maternal and paternal sociodemographic and lifestyle-related characteristics. Compared with nonsmoking mothers, maternal first trimester smoking only was not associated with adverse birth outcomes but was associated with a higher risk of childhood overweight (odds ratio OR 1.17 95% CI 1.02-1.35, P value = 0.030). Children from mothers who continued smoking during pregnancy had higher risks of preterm birth (OR 1.08 95% CI 1.02-1.15, P value = 0.012), small size for gestational age (OR 2.15 95% CI 2.07-2.23, P value < 0.001), and childhood overweight (OR 1.42 95% CI 1.35-1.48, P value < 0.001). Mothers who reduced the number of cigarettes between the first and third trimester, without quitting, still had a higher risk of small size for gestational age. However, the corresponding risk estimates were smaller than for women who continued the same amount of cigarettes throughout pregnancy (OR 1.89 95% CI 1.52-2.34 instead of OR 2.20 95% CI 2.02-2.42 when reducing from 5-9 to ≤4 cigarettes/day; OR 2.79 95% CI 2.39-3.25 and OR 1.93 95% CI 1.46-2.57 instead of OR 2.95 95% CI 2.75-3.15 when reducing from ≥10 to 5-9 and ≤4 cigarettes/day, respectively P values < 0.001). Reducing the number of cigarettes during pregnancy did not affect the risks of preterm birth and childhood overweight. Among nonsmoking mothers, paternal smoking was associated with childhood overweight (OR 1.21 95% CI 1.16-1.27, P value < 0.001) but not with adverse birth outcomes. Limitations of this study include the self-report of parental smoking information and the possibility of residual confounding. As this study only included participants from Europe and North America, results need to be carefully interpreted regarding other populations.
We observed that as compared to nonsmoking during pregnancy, quitting smoking in the first trimester is associated with the same risk of preterm birth and small size for gestational age, but with a higher risk of childhood overweight. Reducing the number of cigarettes, without quitting, has limited beneficial effects. Paternal smoking seems to be associated, independently of maternal smoking, with the risk of childhood overweight. Population strategies should focus on parental smoking prevention before or at the start, rather than during, pregnancy.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Our aim was to investigate the relation between PBDEs and fetal growth or newborn anthropometry in a Spanish cohort (2003–2008). PBDE congeners (BDE-47, -99, -153, -154, and -209) were determined in ...serum of 670 mothers at gestational week 12 and in 534 umbilical cord samples. Abdominal circumference (AC), estimated fetal weight (EFW), femur length (FL), and biparietal diameter (BPD) during gestation were measured by ultrasounds. At birth, weight (BW), head circumference (HC), and length (BL) were also measured. We assessed growth in the intervals between 12–20 and 20–34 weeks of gestation and size at birth by standard deviation (SD)-scores adjusted for constitutional characteristics. We conducted multivariate linear regression analyses between PBDE congeners and their sum (ΣPBDEs) and outcomes. We found statistically significant inverse associations between ΣPBDEs and AC, EFW, and BPD at weeks 20–34 and HC at birth. Regarding congeners, the association was clearer with BDE-99, with inverse associations being found with AC, EFW, and BPD at weeks 20–34, and with BW and HC at delivery. These outcomes decreased between 1.3% and 3.5% for each 2-fold PBDE increase. Concerning matrices, we found statistically significant inverse associations with BPD, HC, and BW when using maternal serum, and for AC and EFW with cord serum. In conclusion, PBDEs may impair fetal growth in late pregnancy and reduce birth size.
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IJS, KILJ, NUK, PNG, UL, UM
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