Air pollution exposure may impact the composition of human milk oligosaccharides.

Human milk oligosaccharides (HMOs) impact neonate immunity and health outcomes. However, the environmental factors influencing HMO composition remain understudied. This study examined the associations between ambient air pollutant (AAP) exposure and HMOs at 1-month postpartum. Human milk samples were collected at 1-month postpartum (n = 185). AAP (PM2.5, PM10, NO2) exposure included the 9-month pregnancy period through 1-month postpartum. Associations between AAP with (1) HMO diversity, (2) the sum of sialylated and fucosylated HMOs, (3) 6 a priori HMOs linked with infant health, and (4) all HMOs were examined using multivariable linear regression and principal component analysis (PCA). Exposure to AAP was associated with lower HMO diversity. PM2.5 and PM10 exposure was positively associated with the HMO 3-fucosyllactose (3FL); PM2.5 exposure was positively associated with the sum of total HMOs, sum of fucosylated HMOs, and the HMO 2'-fucosyllactose (2'FL). PCA indicated the PM2.5, PM10, and NO2 exposures were associated with HMO profiles. Individual models indicated that AAP exposure was associated with five additional HMOs (LNFP I, LNFP II, DFLNT, LNH). This is the first study to demonstrate associations between AAP and breast milk HMOs. Future longitudinal studies will help determine the long-term impact of AAP on human milk composition.

Developmental Impacts of Epigenetics and Metabolism in COVID-19.

Developmental biology is intricately regulated by epigenetics and metabolism but the mechanisms are not completely understood. The situation becomes even more complicated during diseases where all three phenomena are dysregulated. A salient example is COVID-19, where the death toll exceeded 6.96 million in 4 years, while the virus continues to mutate into different variants and infect people. Early evidence during the pandemic showed that the host's immune and inflammatory responses to COVID-19 (like the cytokine storm) impacted the host's metabolism, causing damage to the host's organs and overall physiology. The involvement of angiotensin-converting enzyme 2 (ACE2), the pivotal host receptor for the SARS-CoV-2 virus, was identified and linked to epigenetic abnormalities along with other contributing factors. Recently, studies have revealed stronger connections between epigenetics and metabolism in COVID-19 that impact development and accelerate aging. Patients manifest systemic toxicity, immune dysfunction and multi-organ failure. Single-cell multiomics and other state-of-the-art high-throughput studies are only just beginning to demonstrate the extent of dysregulation and damage. As epigenetics and metabolism directly impact development, there is a crucial need for research implementing cutting-edge technology, next-generation sequencing, bioinformatics analysis, the identification of biomarkers and clinical trials to help with prevention and therapeutic interventions against similar threats in the future.

Prenatal exposure to ambient air pollution is associated with neurodevelopmental outcomes at 2 years of age.

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 (ß = -2.01 [-3.89, -0.13] and ß = -1.97 [-3.83, -0.10], respectively). In addition, higher average prenatal exposure to PM10 was negatively associated with composite motor (ß = -2.35 [-3.95, -0.74]), scaled motor (ß = -0.77 [-1.30, -0.24]), gross motor (ß = -0.37 [-0.70, -0.04]), fine motor (ß = -0.40 [-0.71, -0.09]), composite language (ß = -1.87 [-3.52, -0.22]), scaled language (ß = -0.61 [-1.18, -0.05]) and expressive communication scaled scores (ß = -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.

Postnatal exposure to ambient air pollutants is associated with the composition of the infant gut microbiota at 6-months of age.

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.

Prenatal exposure to ambient air pollutants and early infant growth and adiposity in the Southern California Mother's Milk Study.

BACKGROUND: Prior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence. However, few studies have assessed changes in infant body composition or multiple pollutant exposures. Therefore, the objective of this study was to examine relationships between prenatal residential AAP exposure with infant growth and adiposity. METHODS: Residential exposure to AAP (particulate matter < 2.5 and 10 microns in aerodynamic diameter [PM2.5, PM10]; nitrogen dioxide [NO2]; ozone [O3]; oxidative capacity [Oxwt: redox-weighted oxidative potential of O3 and NO2]) was modeled by spatial interpolation of monitoring stations via an inverse distance-squared weighting (IDW2) algorithm for 123 participants from the longitudinal Mother's Milk Study, an ongoing cohort of Hispanic mother-infant dyads from Southern California. Outcomes included changes in infant growth (weight, length), total subcutaneous fat (TSF; calculated via infant skinfold thickness measures) and fat distribution (umbilical circumference, central to total subcutaneous fat [CTSF]) and were calculated by subtracting 1-month measures from 6-month measures. Multivariable linear regression was performed to examine relationships between prenatal AAP exposure and infant outcomes. Models adjusted for maternal age, pre-pregnancy body mass index, socioeconomic status, infant age, sex, and breastfeeding frequency. Sex interactions were tested, and effects are reported for each standard deviation increase in exposure. RESULTS: NO2 was associated with greater infant weight gain (ß = 0.14, p = 0.02) and TSF (ß = 1.69, p = 0.02). PM10 and PM2.5 were associated with change in umbilical circumference (ß = 0.73, p = 0.003) and TSF (ß = 1.53, p = 0.04), respectively. Associations of Oxwt (pinteractions < 0.10) with infant length change, umbilical circumference, and CTSF were modified by infant sex. Oxwt was associated with attenuated infant length change among males (ß = -0.60, p = 0.01), but not females (ß = 0.16, p = 0.49); umbilical circumference among females (ß = 0.92, p = 0.009), but not males (ß = -0.00, p = 0.99); and CTSF among males (ß = 0.01, p = 0.03), but not females (ß = 0.00, p = 0.51). CONCLUSION: Prenatal AAP exposure was associated with increased weight gain and anthropometric measures from 1-to-6 months of life among Hispanic infants. Sex-specific associations suggest differential consequences of in utero oxidative stress. These results indicate that prenatal AAP exposure may alter infant growth, which has potential to increase childhood obesity risk.

Specific amino acids but not total protein attenuate postpartum weight gain among Hispanic women from Southern California.

There is a high prevalence of obesity and type 2 diabetes in the United States, particularly among Hispanic women, which may be partly explained by failure to lose gestational weight during the postpartum period. Previous work indicates that protein and amino acids may protect against weight gain; therefore, this study examined the impact of dietary protein and amino acid intake on changes in postpartum weight and the percent of women meeting the Estimated Average Requirement (EAR) for these dietary variables among Hispanic women from the Southern California Mother's Milk Study (n = 99). Multivariable linear regression analysis was used to examine the associations between protein and amino acid intake with change in weight after adjusting for maternal age, height, and energy intake. Women's weight increased from prepregnancy to 1-month and 6-months postpartum (71.1 ± 14.6 vs. 73.1 ± 13.1 vs. 74.5 ± 14.6 kg, p < .0001). Although dietary protein was not associated with weight change (ß = -1.09; p = .13), phenylalanine (ß = -1.46; p = .04), tryptophan (ß = -1.71; p = .009), valine (ß = -1.34; p = .04), isoleucine (ß = -1.26; p = .045), and cysteine (ß = -1.52; p = .02) intake were inversely associated with weight change. Additionally, fewer women met the EAR values for cysteine (11.1%), phenylalanine (60.6%), and methionine (69.7%), whereas most women met the EAR values for tryptophan (92.9%), valine (96.0%), and isoleucine (94.9%). Study results indicate that several essential and conditionally essential amino acids were associated with postpartum weight loss, with a significant portion of women not meeting recommended intake levels for some of these amino acids. These results highlight the importance of postpartum maternal diet as a potential modifiable risk factor.

Exposure to air pollutants and the gut microbiota: a potential link between exposure, obesity, and type 2 diabetes.

Work has shown that increased exposure to air pollutants independently contributes to obesity and type 2 diabetes risk, yet the exact mechanisms underlying these associations have not been fully characterized. The current review summarizes recent findings regarding the impact of inhaled and ingested air pollutants on the gut microbiota. Animal and human studies provide evidence that air pollutants, such as particulate matter, nitrogen oxides, and ozone, have the potential to alter the gut microbiota. Further, studies suggest that such exposure-induced alterations to the gut microbiota may contribute to increased risk for obesity and type 2 diabetes through inflammatory pathways. Future work is needed to fully understand the complex interactions between air pollution, the gut microbiome, and human health. Additionally, advanced sequencing methods for gut microbiome research present unique opportunities to study the underlying pathways that link increased air pollution exposure with obesity and type 2 diabetes risk.