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This article summarises recent discoveries showing how prenatal exposure to alcohol affects the structure and function of the brain and of the individual neurons from which it is built. It explains why this weakens the ability to select activities that are appropriate in the context of current circumstances. It also explains why this reduces the ability to suppress habitual, automatic or impulsive responses when they are inappropriate. These effects of alcohol on the brain lead to enduring impairments in cognition, planning and self-control that become more obvious at later stages of child development. The complexities of these processes and the limitations of current knowledge are acknowledged. The article concludes that many of the enduring cognitive, emotional and social impairments associated with prenatal exposure to alcohol are the expected consequences of the effects that such exposure is known to have on the developing brain.

Introduction: Prenatal exposure to organochlorine compounds (OCs) can increase the risk of reported respiratory symptoms in children. It remains unclear whether these compounds can also impact on lung function. We assessed the association between prenatal exposure to OCs and lung function during childhood. Methods: We included 1308 mother-child pairs enrolled in a prospective cohort study. Prenatal concentrations of p,p′-dichlorodiphenyltrichloroethane [p,p′-DDT], p,p′-dichlorodiphenyldichloroethylene [p,p′-DDE], hexachlorobenzene [HCB], and seven polychlorinated biphenyls [PCBs] were measured in cord blood. Spirometry was performed in the offspring at ages 4 (n = 636) and 7 years (n = 1192). Results: More than 80% of samples presented quantifiable levels of p,p′-DDE, HCB, PCB-138, PCB-153, and PCB-180; p,p′-DDE was the compound with the highest median concentrations. At 4 years, prenatal p,p′-DDE exposure was associated with a decrease in forced expiratory volume in 1 s (FEV1) in all quartiles of exposure (e.g., third quartile [0.23–0.34 ng/mL]: β for FEV1 −53.61 mL, 95% CI −89.87, −17.35, vs. the lowest). Prenatal p,p′-DDE levels also decreased forced vital capacity (FVC) and FEV1/FVC, but associations did not reach statistical significance in most exposure quartiles. At 7 years, p,p′-DDE was associated with a decrease in FVC and FEV1 in only the second quartile of exposure (e.g. β for FEV1 −36.96 mL, 95% CI −66.22, −7.70, vs. the lowest). Prenatal exposure to HCB was associated with decreased FVC and FEV1, but in only the second quartile and at 7 years (e.g. [0.07–0.14 ng/mL]: β for FEV1 −25.79 mL, 95% CI −55.98, 4.39, vs. the lowest). PCBs were not consistently associated with lung function. Conclusion: Prenatal exposure to p,p′-DDE may decrease lung function during childhood, especially FEV1 and at medium levels of exposure. Further and deeper knowledge on the impact of environmental chemicals during pregnancy on lung development is needed. ; Gipuzkoa: This study was funded by grants from Instituto de Salud Carlos III (FIS-PI06/0867 and FIS-PI09/00090), CIBERESP, Department of Health of the Basque Government (2005111093, 2009111069, 2013111089 and 2015111065), and the Provincial Government of Gipuzkoa (DFG06/002, DFG08/001 and DFG15/221) and annual agreements with the municipalities of the study area (Zumarraga, Urretxu, Legazpi, Azkoitia y Azpeitia y Beasain). Sabadell: This study was funded by grants from Instituto de Salud Carlos III (Red INMA G03/176; CB06/02/0041; PI041436; PI081151 incl. FEDER funds; CP16/00128), CIBERESP, Generalitat de Catalunya-CIRIT 1999SGR 00241, Generalitat de Catalunya-AGAUR 2009 SGR 501, Fundació La marató de TV3 (090430), EU Commission (261357). ISGlobal is a member of the CERCA Programme, Generalitat de Catalunya. Valencia: This study was funded by Grants from UE (FP7-ENV-2011 cod 282957 and HEALTH.2010.2.4.5-1), Instituto de Salud Carlos III (G03/176; FIS-FEDER: PI11/01007, PI11/02591, PI11/02038, PI12/00610, PI13/1944, PI13/2032, PI14/00891, PI14/01687, PI16/1288, and PI17/0663; Miguel Servet-FEDER CP11/00178, CP15/00025, and MSII16/00051), Alicia Koplowitz Foundation 2017, and Generalitat Valenciana: FISABIO (UGP 15-230, UGP-15-244, and UGP-15-249).

Objective To examine the effects of prenatal exposure to persistent organic pollutants (POPs) on rapid growth in the first 6 months of life and overweight at 14 months of age. Design and Methods In a Spanish birth cohort study, the POPs dichlorodiphenyldichloroethylene (DDE), hexachlorobenzene (HCB), and polychlorinated biphenyls (PCBs - congeners 153, 138, 180) were measured in maternal serum collected in the first trimester of pregnancy during 2003-2008. Rapid growth was defined as a z-score weight gain >0.67 SD between 6 months of age and birth. Overweight at 14 months was defined as a BMI z-score ≥85th percentile. Generalized linear models examined the association between POPs and rapid growth (N = 1285) and overweight (N = 1198). Results The analysis population included 24% rapid growers and 30% overweight infants. DDE and HCB were positively associated with rapid growth and with overweight. There was some indication that infant sex and exclusive breastfeeding duration may modify the effects of DDE, and that maternal prepregnancy BMI status may influence the effects of HCB. PCBs were not related to postnatal growth. Conclusion Prenatal exposure to DDE and HCB may be associated with early postnatal growth. Further research is needed to evaluate the persistence of these associations at older ages. ; a Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain b Hospital de Mar Medical Research Institute (IMIM), Barcelona, Spain c CIBER Epidemiologia y Salud Pública (CIBERESP), Barcelona, Spain d Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), Barcelona, Spain e Department of Nutrition, Gillings School of Public Health, University of North North Carolina, Carolina, Chapel Hill, United States f Centre for Public Health Research (CSISP-FISABIO), Valencia, Spain g School of Nursing, University of Valencia, Valencia, Spain h Public Health Division of Gipuzkoa, Basque Government, Gipuzkoa, Spain i Donostia Biomedical Research Institute (BIODONOSTIA), Gipuzkoa, Spain j Public Health Laboratory of Gipuzkoa, Gipuzkoa, Spain k Department of Environmental Chemistry, Institute of Environmental Assessment and Water Research (IDÆA-CSIC), Barcelona, Spain l Department of Preventive Medicine and Public Health, University of Oviedo, Asturias, Spain ; Peer reviewed