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- Guxens, Monica, et al.
(författare)
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Air pollution exposure during pregnancy and childhood autistic traits in four European population-based cohort studies : the ESCAPE project
- 2016
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Ingår i: Environmental Health Perspectives. - Stockholm : Karolinska Institutet, Dept of Medical Epidemiology and Biostatistics. - 0091-6765 .- 1552-9924.
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Tidskriftsartikel (refereegranskat)abstract
- Background: Prenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of autism spectrum disorder. Objectives: We aimed to assess whether prenatal air pollution exposure is associated with childhood autistic traits in the general population. Methods: Ours 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 μm (PM2.5), ≤ 10 μm (PM10), and between 2.5 and 10 μm (PMcoarse), 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. Results: A 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‑μg/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. Conclusions: Prenatal 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.
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| 2. |
- Khashan, Ali S, et al.
(författare)
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Gestational age and birth weight and the risk of childhood type 1 diabetes : a population-based cohort and sibling design study
- 2015
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Ingår i: Diabetes Care. - Stockholm : Karolinska Institutet, Dept of Medical Epidemiology and Biostatistics. - 0149-5992 .- 1935-5548.
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: We investigated the effects of gestational age, birthweight, small for gestational age (SGA) and large for gestational age (LGA) on childhood type 1 diabetes. Methods: We conducted a population-based cohort study of all singleton live births in Sweden between 1973-2009 and a sibling-control study. Perinatal data were extracted from the Swedish Medical Birth Register. Children with type 1 diabetes diagnosis were identified from the Swedish National Patient Register. Log-linear Poisson regression and conditional logistic regression were used for data analysis. Results: The study cohort consisted of 3,624,675 singleton live births (42,411,054 person-years). There were 13,944 type 1 diabetes cases during the study period. The sibling-control study consisted of 11,403 children with type 1 diabetes and 17,920 siblings. Gestational age between 33-36 weeks (RR=1.18; [95%CIs: 1.09, 1.28) and 37-38 weeks (RR=1.12; [95%CIs: 1.07, 1.17]) was associated with type 1 diabetes in the cohort study and remained significant in the sibling-control study. SGA (RR=0.83; [95%CIs: 0.75, 0.93]) and LGA (RR=1.14; [95%CIs: 1.04, 1.24]) were associated with type 1 diabetes in the cohort study. The SGA association remained unchanged in the sibling study while the LGA association disappeared. Very low birthweight was associated with a reduced risk of type 1 diabetes. Conclusions: The findings suggest a small association between gestational age and type 1 diabetes that is not likely due to familial confounding factors. Gestational age and type 1 diabetes may be related to insulin resistance due to early life growth restriction or altered gut microbiota in preterm babies.
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| 3. |
- Khashan, Ali S, et al.
(författare)
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Mode of obstetrical delivery and type 1 diabetes : a sibling design study
- 2014
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Ingår i: Pediatrics. - Stockholm : Karolinska Institutet, Dept of Medical Epidemiology and Biostatistics. - 0031-4005 .- 1098-4275.
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: We investigated the association between cesarean section (CS) and type 1 diabetes (T1D), and if the association remains after accounting for familial confounding by using a sibling-control design. METHODS: We conducted a population-based cohort study of all singleton live births in Sweden between 1982 and 2009, followed by sibling-control analyses. T1D diagnoses were identified from the Swedish National Patient Register. Mode of delivery was categorized into unassisted vaginal delivery (reference group), instrumental vaginal delivery (IVD), emergency CS, and elective CS. The statistical analysis was conducted in 2 steps: firstly log-linear Poisson regression with aggregated person-years by using the full cohort; secondly, conditional logistic regression for sibling-control analyses. The sibling analysis included siblings who were discordant for both mode of delivery and T1D. RESULTS: In the cohort analyses (N = 2 638 083), there was an increased risk of childhood T1D among children born by elective CS (adjusted relative risk [RR] = 1.15 [95% confidence interval: 1.06-1.25]) and IVD (RR=1.14 [1.06-1.23]) but not emergency CS (RR = 1.02 [0.95-1.11]) when compared with children born by unassisted vaginal birth. However, the effect of elective CS and IVD on childhood T1D almost disappeared and became nonsignificant in the sibling-control analyses. CONCLUSIONS: The present findings suggest a small association between elective CS and IVD and T1D. The sibling-control results, however, suggest that these findings are not consistent with causal effects of mode of delivery on T1D and may be due to familial confounders such as genetic susceptibility and environmental factors.
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