Zachariah E. M. Morgan’s research while affiliated with University of Colorado Boulder and other places

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 (NO 2 ) and particulate matter smaller than 2.5 and 10 microns in diameter (PM 2.5 and PM 10 , 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 PM 10 and PM 2.5 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 PM 10 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.

Epidemiological studies in adults have shown that exposure to ambient air pollution (AAP) is associated with the composition of the adult gut microbiome, but these relationships have not been examined in infancy. We aimed to determine if 6-month postnatal AAP exposure was associated with the infant gut microbiota at 6 months of age in a cohort of Latino mother-infant dyads from the Southern California Mother’s Milk Study (n = 103). We estimated particulate matter (PM2.5 and PM10) and nitrogen dioxide (NO2) exposure from birth to 6-months based on residential address histories. We characterized the infant gut microbiota using 16S rRNA amplicon sequencing at 6-months of age. At 6-months, the gut microbiota was dominated by the phyla Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria. Our results show that, after adjusting for important confounders, postnatal AAP exposure was associated with the composition of the gut microbiota. As an example, PM10 exposure was positively associated with Dialister, Dorea, Acinetobacter, and Campylobacter while PM2.5 was positively associated with Actinomyces. Further, exposure to PM10 and PM2.5 was inversely associated with Alistipes and NO2 exposure was positively associated with Actinomyces, Enterococcus, Clostridium, and Eubacterium. Several of these taxa have previously been linked with systemic inflammation, including the genera Dialister and Dorea. This study provides the first evidence of significant associations between exposure to AAP and the composition of the infant gut microbiota, which may have important implications for future infant health and development.

BACKGROUND AND AIM: Exposure to ambient air pollutants (AAP) has been linked with the gut microbiome in young adults; however, this relationship has not been studied in infancy. This study aimed to examine the relationships between AAP and the infant gut microbiota. METHODS: This study included 105 infants from the Southern California Mother’s Milk Study. Average exposure to particulate matter (PM2.5, PM10) and nitrogen dioxide (NO2), was examined during the first 6 months of life. The infant gut microbiota was characterized using 16S rRNA sequencing at 6 months. Associations between AAP and the composition of the gut microbiota was examined using a Zero Inflated Poisson Regression (ZIPR), where incidence risk ratios (IRR) and Bonferroni adjusted p-values are reported. Compositionally aware, multinomial models were used to describe associations between AAP and the abundance of each gut microbe, and new methods for visualizing those associations were used to identify an important subset of associated taxa. Based on a directed acyclic graph, models adjusted for sex, breastfeeding frequency, socioeconomic status, birthweight and infant age. RESULTS:Overall, 26, 16 and 22 gut bacterial taxa were associated with exposure to PM10, PM2.5 and NO2, respectively. For example, PM10 and PM2.5 were associated with Enterococcus (IRR=1.08, p0.001) and Actinomyces (IRR=1.46, p0.001) abundances, respectively. Multinomial analysis also revealed that PM10 exposure was associated with the composition of the gut microbiota based on the log-ratio of differentially ranked taxa sub-groups (R2=0.28, p0.001). For example, all microbial genera positively associated with PM10 via ZIPR were also classified as being in the top 35% of differentially ranked taxa positively associated with PM10 exposure. CONCLUSIONS:Early postnatal exposure to AAP was associated with the composition of the infant gut microbiota at 6-months of age. These results suggest that early life exposure to AAP may impact the developing gut microbiome, which may have important implications for infant development.

BACKGROUND AND AIM: Previous research has established an association between postnatal ambient air pollution (AAP) exposure and cognitive development in preschoolers and school-aged children. However, this association has not been examined during infancy, a critical neurodevelopmental window. The purpose of this study was to explore relationships between postnatal AAP exposure and cognitive development in infants. METHODS: This study examined 118 Hispanic mother-infant pairs from the longitudinal Mother’s Milk Study in Southern California. Average individual residential exposure to AAP, including nitrogen dioxide (NO2) and particulate matter smaller than 2.5 and 10 microns in diameter (PM2.5 and PM10 respectively), in the first month of life was estimated from central site monitors. Infant cognitive outcomes at 24-months were measured using the Bailey-III Scales of Infant and Toddler Development. Multivariate linear regression was used to examine relationships between postnatal AAP exposure and age scaled cognitive scores, adjusting for socioeconomic status, breastfeeding frequency, time of delivery (early/late/on-time) as a proxy for gestational age, pre-pregnancy BMI, birthweight, and sex. Effects are reported for each standard deviation increase in exposure. RESULTS:NO2 was negatively associated with fine motor score (β=-0.55, p=0.006), motor score (β=-0.90, p =0.007), and cognitive score (β=-0.55, p=0.01). PM2.5 and PM10 were negatively associated with social emotional scores (β=-0.77, p=0.009 and β=-0.66, p=0.01 respectively). The association between NO2 and cognitive score varied by infant sex (p-interaction = 0.046), where NO2 was negatively associated with cognitive score among females (β=-0.16, p=0.0006) but not males (β=-0.01, p=0.81). CONCLUSIONS:Higher postnatal exposure to AAP in the first month of life was inversely associated with scaled motor, cognitive, and social-emotional scores at 24-months of age. Sex-specific findings for scaled cognitive score may suggest differential impacts of AAP exposure among females. These results indicate that AAP may negatively impact neurodevelopment in early life.