Dataset Information

Pregnancy exposure to air pollution and early childhood respiratory health in the Norwegian Mother and Child Cohort Study (MoBa).

ABSTRACT: OBJECTIVES:It is unclear whether maternal air pollution exposure during pregnancy induces changes in the developing respiratory system of a child and whether it has consequences for respiratory health in early childhood. We investigated associations between exposure to moderate levels of air pollution during pregnancy and early childhood lower respiratory tract infections (LRTI) and wheezing. METHODS:This study used a subgroup of 17 533 participants in the Norwegian Mother and Child Cohort Study. Air pollution levels at residential addresses were estimated using land use regression models, and back-extrapolated to the period of each pregnancy. Information on LRTI and wheezing and lifestyle factors was collected from questionnaires completed by mothers during pregnancy and when the child was 6 and 18 months of age. RESULTS:Moderate mean levels of NO2 (13.6?µg/m3, range 0.01-60.4) exposure at residential address during pregnancy were not statistically associated with LRTI and wheezing. No association was found per 10?µg/m3 change in NO2 exposure and LRTI before the age of 6 months (adjusted risk ratio (RR) 0.99; 95%?CI 0.84 to 1.17), or between 6 and 18 months of age (adjusted RR 1.05; 95%?CI 0.94 to 1.16). Similarly, we found no association per 10?µg/m3 change in NO2 exposure and wheezing between 6 and 18 months of age (adjusted RR 1.02; 95%?CI 0.97 to 1.07). CONCLUSIONS:There were no statistically significant associations for moderate levels of pregnancy NO2 exposure and respiratory health outcomes during early childhood in overall analyses.

SUBMITTER: Madsen C

PROVIDER: S-EPMC5770814 | biostudies-other | 2017 Dec

REPOSITORIES: biostudies-other

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Pregnancy exposure to air pollution and early childhood respiratory health in the Norwegian Mother and Child Cohort Study (MoBa).

Madsen Christian C Haberg Siri Eldevik SE Magnus Maria C MC Aamodt Geir G Stigum Hein H London Stephanie J SJ Nystad Wenche W Nafstad Per P

BMJ open 20171226 12

<h4>Objectives</h4>It is unclear whether maternal air pollution exposure during pregnancy induces changes in the developing respiratory system of a child and whether it has consequences for respiratory health in early childhood. We investigated associations between exposure to moderate levels of air pollution during pregnancy and early childhood lower respiratory tract infections (LRTI) and wheezing.<h4>Methods</h4>This study used a subgroup of 17 533 participants in the Norwegian Mother and Chi ...[more]

PMID: 29282255

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Project description:Many women drink during pregnancy and lactation despite recommendations to abstain. In animals, alcohol exposure during pregnancy and lactation influences lung and immune development, plausibly increasing risk of asthma and lower respiratory tract infections (LRTIs). Studies in humans are few.In the Norwegian Mother and Child Cohort Study, we examined maternal alcohol intake during pregnancy and lactation in relation to risk of current asthma at 36 months (49,138 children), recurrent LRTIs by 36 months (39,791 children), and current asthma at 7 years (13,253 children). Mothers reported frequency and amount of alcohol intake each trimester and the first 3 months following delivery. We calculated adjusted relative risk (aRR), comparing children of drinkers to nondrinkers, using Generalized Linear Models.A total of 31.8% of mothers consumed alcohol during first trimester, 9.7% during second trimester, and 15.6% during third trimester. Infrequent and low-dose prenatal alcohol exposure showed a modest statistically significant inverse association with current asthma at 36 months (aRRs ~ 0.85). No association was seen with the highest alcohol intakes during the first trimester when alcohol consumption was most common. RRs of maternal alcohol intake during pregnancy with recurrent LRTIs were ~1, with sporadic differences in risk for some metrics of intake, but without any consistent pattern. For current asthma at 7 years, similar inverse associations were seen as with current asthma at 36 months but were not statistically significant. Among children breastfed throughout the first 3 months of life, maternal alcohol intake during this time was not significantly associated with any of the 3 outcomes.The low levels of alcohol exposure during pregnancy or lactation observed in this cohort were not associated with increased risk of asthma or recurrent LRTIs. The slight inverse associations of infrequent or low-dose prenatal alcohol exposure with asthma may not be causal.

Project description:BackgroundOrganophosphate esters (OPEs) are a class of flame retardants in common use. OPEs can easily leach from materials, resulting in human exposure. Increasing concentrations have been reported in human populations over the past decade. Recent studies have linked prenatal OPE exposure to hyperactivity and attention problems in children. Such behaviors are often found among children with attention-deficit hyperactivity disorder (ADHD), however, no study has investigated OPEs in relation to clinically assessed ADHD.ObjectiveTo evaluate prenatal exposure to OPEs as risk factors for clinically assessed ADHD using a case-cohort study nested within the Norwegian Mother, Father, and Child Cohort Study (MoBa).MethodsWe included in the case group 295 ADHD cases obtained via linkage with the Norwegian Patient Registry, and the sub-cohort group 555 children sampled at baseline, irrespective of their ADHD case status. Prenatal concentrations of OPE metabolites were measured in maternal urine collected at 17 weeks of gestation, and included diphenyl phosphate (DPHP), di-n-butyl phosphate (DNBP), bis(2-butoxyethyl) hydrogen phosphate (BBOEP), and bis(1,3-dichloro-2-propyl) phosphate (BDCIPP). We estimated risk ratios and the corresponding 95% confidence intervals [95% CI] using logistic regression, adjusting for season of urine collection, child sex, birth year, and maternal depression, education, and sum of urinary di(2-ethylhexyl) phthalate metabolites (∑DEHP) concentration during pregnancy. To assess the overall impact of simultaneously decreasing exposure to all chemical constituents of an OPE-phthalate mixture, quantile based g-computation was implemented. The mixture constituents included OPE and phthalate metabolites commonly detected in our study. In all models, we considered effect measure modification by child sex and polymorphisms in genes encoding paraoxonase 1 (PON1) and cytochrome P450 (P450) enzymes. Mediation analysis was conducted using thyroid function biomarkers estimated from maternal blood collected at 17 weeks of gestation.ResultsDPHP was detected in nearly all samples (97.2%), with a higher geometric mean among the case group (0.70 µg/L) as compared to the sub-cohort (0.52 µg/L). DNBP was commonly detected as well (93.8%), while BBOEP (52.9%) and BDCIPP (22.9%) were detected less frequently. A higher risk of ADHD was observed in children with greater than median exposure to DPHP during pregnancy (risk ratio: 1.38 [95% CI: 0.96, 1.99]), which was slightly higher among girls (2.04 [1.03, 4.02]) and children of mothers with PON1 Q192R genotype QR (1.69 [0.89, 3.19]) or PON1 Q192R genotype RR (4.59 [1.38, 15.29]). The relationship between DPHP and ADHD (total risk ratio: 1.34 [0.90, 2.02]) was partially mediated through total triiodothyronine to total thyroxine ratio (natural direct effect: 1.29 [0.87, 1.94]; natural indirect effect: 1.04 [1.00, 1.10]; 12.48% mediated). We also observed an elevated risk of ADHD in relation to BDCIPP detection during pregnancy (1.50 [0.98, 2.28]). We did not observe notable differences in ADHD by DNBP (0.88 [0.62, 1.26]) or BBOEP (1.03 [0.73, 1.46]) during pregnancy. Simultaneously decreasing all constituents of common-detect OPE-phthalate mixture, specifically DPHP, DNBP, and 6 phthalate metabolites, by a quartile resulted in an ADHD risk ratio of 0.68 [0.64, 0.72].ConclusionPrenatal exposure to DPHP and BDCIPP may increase the risk of ADHD. For DPHP, we observed potential modification by child sex and maternal PON1 Q192R genotype and partial mediation through maternal thyroid hormone imbalance at 17 weeks gestation.

Project description:BackgroundPrenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of autism spectrum disorder.ObjectivesWe aimed to assess whether prenatal air pollution exposure is associated with childhood autistic traits in the general population.MethodsOurs was a collaborative study of four European population-based birth/child cohorts-CATSS (Sweden), Generation R (the Netherlands), GASPII (Italy), and INMA (Spain). Nitrogen oxides (NO2, NOx) and particulate matter (PM) with diameters of ? 2.5 ?m (PM2.5), ? 10 ?m (PM10), and between 2.5 and 10 ?m (PM(coarse)), and PM2.5 absorbance were estimated for birth addresses by land-use regression models based on monitoring campaigns performed between 2008 and 2011. Levels were extrapolated back in time to exact pregnancy periods. We quantitatively assessed autistic traits when the child was between 4 and 10 years of age. Children were classified with autistic traits within the borderline/clinical range and within the clinical range using validated cut-offs. Adjusted cohort-specific effect estimates were combined using random-effects meta-analysis.ResultsA total of 8,079 children were included. Prenatal air pollution exposure was not associated with autistic traits within the borderline/clinical range (odds ratio = 0.94; 95% CI: 0.81, 1.10 per each 10-?g/m3 increase in NO2 pregnancy levels). Similar results were observed in the different cohorts, for the other pollutants, and in assessments of children with autistic traits within the clinical range or children with autistic traits as a quantitative score.ConclusionsPrenatal exposure to NO2 and PM was not associated with autistic traits in children from 4 to 10 years of age in four European population-based birth/child cohort studies.CitationGuxens M, Ghassabian A, Gong T, Garcia-Esteban R, Porta D, Giorgis-Allemand L, Almqvist C, Aranbarri A, Beelen R, Badaloni C, Cesaroni G, de Nazelle A, Estarlich M, Forastiere F, Forns J, Gehring U, Ibarluzea J, Jaddoe VW, Korek M, Lichtenstein P, Nieuwenhuijsen MJ, Rebagliato M, Slama R, Tiemeier H, Verhulst FC, Volk HE, Pershagen G, Brunekreef B, Sunyer J. 2016. Air pollution exposure during pregnancy and childhood autistic traits in four European population-based cohort studies: the ESCAPE Project. Environ Health Perspect 124:133-140; http://dx.doi.org/10.1289/ehp.1408483.

Project description:BACKGROUND:Air pollution has been related to brain structural alterations, but a relationship with white matter microstructure is unclear. OBJECTIVES:We assessed whether pregnancy and childhood exposures to air pollution are related to white matter microstructure in preadolescents. METHODS:We used data of 2,954 children from the Generation R Study, a population-based birth cohort from Rotterdam, Netherlands (2002-2006). Concentrations of 17 air pollutants including nitrogen oxides (NOX), particulate matter (PM), and components of PM were estimated at participants' homes during pregnancy and childhood using land-use regression models. Diffusion tensor images were obtained at child's 9-12 years of age, and fractional anisotropy (FA) and mean diffusivity (MD) were computed. We performed linear regressions adjusting for socioeconomic and lifestyle characteristics. Single-pollutant analyses were followed by multipollutant analyses using the Deletion/Substitution/Addition (DSA) algorithm. RESULTS:In the single-pollutant analyses, higher concentrations of several air pollutants during pregnancy or childhood were associated with significantly lower FA or higher MD (p<0.05). In multipollutant models of pregnancy exposures selected by DSA, higher concentration of fine particles was associated with significantly lower FA [-0.71 (95% CI: -1.26, -0.16) per 5 μg/m3 fine particles] and higher concentration of elemental silicon with significantly higher MD [0.06 (95% CI: 0.01, 0.11) per 100 ng/m3 silicon]. Multipollutant models of childhood exposures selected by DSA indicated significant associations of NOX with FA [-0.14 (95% CI: -0.23, -0.04) per 20-μg/m3 NOX increase], and of elemental zinc and the oxidative potential of PM with MD [0.03 (95% CI: 0.01, 0.04) per 10-ng/m3 zinc increase and 0.07 (95% CI: 0.00, 0.44) per 1-nmol DTT/min/m3 oxidative potential increase]. Mutually adjusted models of significant exposures during pregnancy and childhood indicated significant associations of silicon during pregnancy, and zinc during childhood, with MD. DISCUSSION:Exposure in pregnancy and childhood to air pollutants from tailpipe and non-tailpipe emissions were associated with lower FA and higher MD in white matter of preadolescents. https://doi.org/10.1289/EHP4709.

Dataset Information

Pregnancy exposure to air pollution and early childhood respiratory health in the Norwegian Mother and Child Cohort Study (MoBa).

Publications

Pregnancy exposure to air pollution and early childhood respiratory health in the Norwegian Mother and Child Cohort Study (MoBa).

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