Nieuwenhuijsen, M. (Mark)
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- Prenatal air pollution exposure and growth and cardio-metabolic risk in preschoolers(Elsevier, 2020) Nieuwenhuijsen, M. (Mark); Irizar, A. (Amaia); Tardón, A. (Adonina); Vioque, J. (Jesús); Fernández-Somoano, A. (Ana); Estarlich, M. (Marisa); Sunyer, J. (Jordi); Fossati, S. (Serena); Martinez, D. (David); Cirach, M. (Marta); Valvi, D. (Damaskini); Guxens, M. (Monica); Vrijheid, M. (Martine); Tamayo, I. (Ibon); Iñiguez, C. (Carmen); Lertxundi, A. (Aitana)Objectives: 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. Methods: 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. Results: 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. Conclusions: 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.
- Prenatal and childhood exposure to air pollution and traffic and the risk of liver injury in European children(2021) Hoek, G. (Gerard); García, E. (Erika); Wright, J. (John); Chatzi, L. (Lida); Vos, M.B. (Miriam B.); Nieuwenhuijsen, M. (Mark); Slama, R. (Rémy); Roumeliotaki, T. (Theano); Aasvang, G.M. (Gunn Marit); Conti, D.V. (David V.); Vafeiadi, M. (Marina); Maitre, L. (Léa); Heude, B. (Barbara); Gómez-Urquiza, J. (José); McEachan, R.R.C. (Rosemary R. C.); McConnell, R. (Rob); Casas, M. (Maribel); Castro, M. (Montserrat) de; Fossati, S. (Serena); Grazuleviciene, R. (Regina); Valvi, D. (Damaskini); Basagana, X. (Xavier); Vrijheid, M. (Martine); Krog, N.H. (Norun Hjertager); Berhane, K.T. (Kiros T.); Stratakis, N. (Nikos); Andrusaityte, S. (Sandra); Varo-Cenarruzabeitia, M.N. (Miren Nerea)Background: Nonalcoholic fatty liver disease is the most prevalent pediatric chronic liver disease. Experimental studies suggest effects of air pollution and traffic exposure on liver injury. We present the first large-scale human study to evaluate associations of prenatal and childhood air pollution and traffic exposure with liver injury. Methods: Study population included 1,102 children from the Human Early Life Exposome project. Established liver injury biomarkers, including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, and cytokeratin-18, were measured in serum between ages 6-10 years. Air pollutant exposures included nitrogen dioxide, particulate matter <10 m (PM10), and <2.5 m. Traffic measures included traffic density on nearest road, traffic load in 100-m buffer, and inverse distance to nearest road. Exposure assignments were made to residential address during pregnancy (prenatal) and residential and school addresses in year preceding follow-up (childhood). Childhood indoor air pollutant exposures were also examined. Generalized additive models were fitted adjusting for confounders. Interactions by sex and overweight/obese status were examined. Results: Prenatal and childhood exposures to air pollution and traffic were not associated with child liver injury biomarkers. There was a significant interaction between prenatal ambient PM10 and overweight/obese status for alanine aminotransferase, with stronger associations among children who were overweight/obese. There was no evidence of interaction with sex. Conclusion: This study found no evidence for associations between prenatal or childhood air pollution or traffic exposure with liver injury biomarkers in children. Findings suggest PM10 associations maybe higher in children who are overweight/obese, consistent with the multiple-hits hypothesis for nonalcoholic fatty liver disease pathogenesis.