Smoking during Pregnancy Affects Speech-Processing Ability in Newborn Infants

BACKGROUND: Tobacco smoking during pregnancy is known to adversely affect development of the central nervous system in babies of smoking mothers by restricting utero–placental blood flow and the amount of oxygen available to the fetus. Behavioral data associate maternal smoking with lower verbal scores and poorer performance on specific language/auditory tests. OBJECTIVES: In the current study we examined the effects of maternal smoking during pregnancy on newborns’ speech processing ability as measured by event-related potentials (ERPs). METHOD: High-density ERPs were recorded within 48 hr of birth in healthy newborn infants of smoking (n = 8) and nonsmoking (n = 8) mothers. Participating infants were matched on sex, gestational age, birth weight, Apgar scores, mother’s education, and family income. Smoking during pregnancy was determined by parental self-report and medical records. ERPs were recorded in response to six consonant–vowel syllables presented in random order with equal probability. RESULTS: Brainwaves of babies of nonsmoking mothers were characterized by typical hemisphere asymmetries, with larger amplitudes over the left hemisphere, especially over temporal regions. Further, infants of nonsmokers discriminated among a greater number of syllables whereas the newborns of smokers began the discrimination process at least 150 msec later and differentiated among fewer stimuli. CONCLUSIONS: Our findings indicate that prenatal exposure to tobacco smoke in otherwise healthy babies is linked with significant changes in brain physiology associated with basic perceptual skills that could place the infant at risk for later developmental problems

Neurodevelopmental Outcomes in the Early CPAP and Pulse Oximetry Trial

BACKGROUND: Previous results from our trial of early treatment with continuous positive airway pressure (CPAP) versus early surfactant treatment in infants showed no significant difference in the outcome of death or bronchopulmonary dysplasia. A lower (vs. higher) target range of oxygen saturation was associated with a lower rate of severe retinopathy but higher mortality. We now report longer-term results from our prespecified hypotheses. METHODS: Using a 2-by-2 factorial design, we randomly assigned infants born between 24 weeks 0 days and 27 weeks 6 days of gestation to early CPAP with a limited ventilation strategy or early surfactant administration and to lower or higher target ranges of oxygen saturation (85 to 89% or 91 to 95%). The primary composite outcome for the longer-term analysis was death before assessment at 18 to 22 months or neurodevelopmental impairment at 18 to 22 months of corrected age. RESULTS: The primary outcome was determined for 1234 of 1316 enrolled infants (93.8%); 990 of the 1058 surviving infants (93.6%) were evaluated at 18 to 22 months of corrected age. Death or neurodevelopmental impairment occurred in 27.9% of the infants in the CPAP group (173 of 621 infants), versus 29.9% of those in the surfactant group (183 of 613) (relative risk, 0.93; 95% confidence interval [CI], 0.78 to 1.10; P = 0.38), and in 30.2% of the infants in the lower-oxygen-saturation group (185 of 612), versus 27.5% of those in the higher-oxygen-saturation group (171 of 622) (relative risk, 1.12; 95% CI, 0.94 to 1.32; P = 0.21). Mortality was increased with the lower-oxygen-saturation target (22.1%, vs. 18.2% with the higher-oxygen-saturation target; relative risk, 1.25; 95% CI, 1.00 to 1.55; P = 0.046). CONCLUSIONS: We found no significant differences in the composite outcome of death or neurodevelopmental impairment among extremely premature infants randomly assigned to early CPAP or early surfactant administration and to a lower or higher target range of oxygen saturation. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Heart, Lung, and Blood Institute; SUPPORT ClinicalTrials.gov number, NCT00233324.

A global perspective on the influence of environmental exposures on the nervous system

Economic and social transitions in the era of globalization warrant a fresh look at the neurological risks associated with environmental change. These are driven by industrial expansion, transfer and mobility of goods, climate change and population growth. In these contexts, risk of both infectious and non-infectious diseases are shared across geographical boundaries. In low- and middle-income countries, the risk of environmentally mediated brain disease is augmented several-fold by lack of infrastructure, poor health and safety regulations, and limited measures for environmental protection. Neurological disorders may occur as a result of direct exposure to chemical and/or non-chemical stressors such as ultrafine particulate matters. Individual susceptibilities to exposure-related diseases are modified by genetic, epigenetic and metagenomic factors. The existence of several uniquely exposed populations, including those in the areas surrounding the Niger Delta or north western Amazon oil operations; those working in poorly regulated environments, such as artisanal mining industries; or those, mostly in sub-Saharan Africa, relying on cassava as a staple food, offers invaluable opportunities to advance the current understanding of brain responses to environmental challenges. Increased awareness of the brain disorders that are prevalent in low- and middle-income countries and investments in capacity for further environmental health-related research are positive steps towards improving human health