April 1, 2024

Lower language - cognition - and motor skills - from marginally higher traffic air pollution


Dept of Integrative Physiology, University of Colorado
Source: Environmental Health, Jan 2023

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Less brain development was seen in children born to mothers living in homes with higher levels of traffic related air pollution. Tests were given to children at age 2 using the Bayley-III Scales of Infant and Toddler Development. The vehicle air pollution particles having the strongest effect for harming brain development were PM10 and PM2.5. For example, pregnant mothers in the highest 25% PM10 group, had children who scored 3 points lower on cognition - compared to children born to mothers in the lowest 25th percentile group. Researchers stated, "If all participants had PM10 levels at the 75th percentile of exposure, the prevalence of cognitive impairment would be predicted to increase to 22%, which highlights the importance of even moderate increases in early-life exposure."

The human brain grows at over 4,000 cells a second begining the 4th week of pregnancy. Cells begin from the center of the brain and move outward and recieve signals not only for growth but for when to stop in their proper location. Proper growth of the human brain requires a crtical balance of communication signals between brain cells through what are called signaling pathways. If signaling pathways are interrupted by external environmental factors (such as from endocrine disrupting chemicals in vehicle exhaust) detrimental changes could be significant. Researchers here also reviewed additional studies with older children but stated a lack of studies in younger children. For example, among school-aged children, exposure in the womb to polycyclic aromatic hydrocarbons (a toxic chemical that forms during engine fuel burning), was found to reduce size of the child's left brain hemisphere white matter surface at age 8. Prenatal PM2.5 exposure was also shown to reduce cortex thickness, altered white matter organization, and reduced blood flow at 6–14 years.[12, 13, 20] Prenatal PM10 exposure was shown to reduce full-scale IQ at ages 4–6 years, and prenatal nitrogen dioxide exposure and traffic density around the home was shown to reduce verbal IQ scores at 7 years of age [10, 11]. Nitrogen dioxide is a primary gas created during fossil-fuel engine combusion. Exposure to this air pollutant resulted in poorer attentional performance in children at 4–5 years of age [14, 15]. Additionally, studies found PM2.5 exposure between weeks 12–40 in pregnancy resulted in lower IQ, slower reaction time, and poorer memory at 6–7 years. [16] In addition, PM10, PM2.5, and NO2 exposure in the late-prenatal and early postnatal periods Late pregnancy and immediately after birth) have been associated with an increased risk of ADHD-like behaviors in children around age 3 [22]. In summary, this research shows a child's developing brain during pregnancy can be damaged from even typical levels of air pollution in society. As this exposure is widespread in society today, the harmful behavioral and economic impacts upon society would be of great concern. The following is the concluding paragraph from the authors of the study, "Prenatal exposure to ambient air pollutants was inversely associated with functional neurodevelopmental outcomes at 2 years, raising concern for child health and future functional impairment. In addition, our findings indicate that exposures during mid to late pregnancy may be especially detrimental to neurodevelopment, which suggests the need for limiting air pollution exposure, especially during the latter half of pregnancy. In summary, this study adds to the growing body of literature cataloging the negative health consequences of both pre- and postnatal ambient air pollution exposure that should be used to inform policy efforts to limit human exposure to air pollutants."

ABSTRACT
Background: Higher prenatal ambient air pollution exposure has been associated with impaired neurodevelopment in preschoolers and school-aged children. The purpose of this study was to explore the relationships between prenatal ambient air pollution exposure and neurodevelopment during infancy.

Methods: This study examined 161 Latino mother-infant pairs from the Southern California Mother's Milk Study. Exposure assessments included prenatal nitrogen dioxide (NO2) and particulate matter smaller than 2.5 and 10 microns in diameter (PM2.5 and PM10, respectively). The pregnancy period was also examined as three windows, early, mid, and late, which describe the first, middle, and last three months of pregnancy. Infant neurodevelopmental outcomes at 2 years of age were measured using the Bayley-III Scales of Infant and Toddler Development. Multivariable linear models and distributed lag linear models (DLM) were used to examine relationships between prenatal exposures and neurodevelopmental scores, adjusting for socioeconomic status, breastfeeding frequency, time of delivery, pre-pregnancy body mass index, and infant birthweight and sex.

Results: Higher prenatal exposure to PM10 and PM2.5 was negatively associated with composite cognitive score (β = -2.01 [-3.89, -0.13] and β = -1.97 [-3.83, -0.10], respectively). In addition, higher average prenatal exposure to PM10 was negatively associated with composite motor (β = -2.35 [-3.95, -0.74]), scaled motor (β = -0.77 [-1.30, -0.24]), gross motor (β = -0.37 [-0.70, -0.04]), fine motor (β = -0.40 [-0.71, -0.09]), composite language (β = -1.87 [-3.52, -0.22]), scaled language (β = -0.61 [-1.18, -0.05]) and expressive communication scaled scores (β = -0.36 [-0.66, -0.05]). DLMs showed that higher prenatal air pollution exposure during mid and late pregnancy was inversely associated with motor, cognitive, and communication language scores.

Conclusions: Higher exposure to air pollutants during pregnancy, particularly in the mid and late prenatal periods, was inversely associated with scaled and composite motor, cognitive, and language scores at 2 years. These results indicate that prenatal ambient air pollution may negatively impact neurodevelopment in early life.

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