OBJECTIVE: To quantify the extent to which neighborhood characteristics contribute to racial and ethnic disparities in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) seropositivity in pregnancy.

METHODS: This cohort study included pregnant patients who presented for childbirth at two hospitals in Philadelphia, Pennsylvania from April 13 to December 31, 2020. Seropositivity for SARS-CoV-2 was determined by measuring immunoglobulin G and immunoglobulin M antibodies by enzyme-linked immunosorbent assay in discarded maternal serum samples obtained for clinical purposes. Race and ethnicity were self-reported and abstracted from medical records. Patients' residential addresses were geocoded to obtain three Census tract variables: community deprivation, racial segregation (Index of Concentration at the Extremes), and crowding. Multivariable mixed effects logistic regression models and causal mediation analyses were used to quantify the extent to which neighborhood variables may explain racial and ethnic disparities in seropositivity.

RESULTS: Among 5,991 pregnant patients, 562 (9.4%) were seropositive for SARS-CoV-2. Higher seropositivity rates were observed among Hispanic (19.3%, 104/538) and Black (14.0%, 373/2,658) patients, compared with Asian (3.2%, 13/406) patients, White (2.7%, 57/2,133) patients, and patients of another race or ethnicity (5.9%, 15/256) (P<.001). In adjusted models, per SD increase, deprivation (adjusted odds ratio [aOR] 1.16, 95% CI 1.02-1.32) and crowding (aOR 1.15, 95% CI 1.05-1.26) were associated with seropositivity, but segregation was not (aOR 0.90, 95% CI 0.78-1.04). Mediation analyses revealed that crowded housing may explain 6.7% (95% CI 2.0-14.7%) of the Hispanic-White disparity and that neighborhood deprivation may explain 10.2% (95% CI 0.5-21.1%) of the Black-White disparity.

CONCLUSION: Neighborhood deprivation and crowding were associated with SARS-CoV-2 seropositivity in pregnancy in the prevaccination era and may partially explain high rates of SARS-CoV-2 seropositivity among Black and Hispanic patients. Investing in structural neighborhood improvements may reduce inequities in viral transmission.

OBJECTIVE: We aimed to determine whether coronavirus-disease-2019 (COVID-19) pandemic exposure duration was associated with PTB and if the pandemic modified racial disparities.

STUDY DESIGN: We analyzed Philadelphia births and replicated in New Haven. Compared to matched months in two prior years, we analyzed overall PTB, specific PTB phenotypes, and stillbirth.

RESULTS: Overall, PTB was similar between periods with the following exceptions. Compared to pre-pandemic, early pregnancy (<14 weeks') pandemic exposure was associated with lower risk of PTB < 28 weeks' (aRR 0.60 [0.30-1.10]) and later exposure with higher risk (aRR 1.77 [0.78-3.97]) (interaction p = 0.04). PTB < 32 weeks' among White patients decreased during the pandemic, resulting in non-significant widening of the Black-White disparity from aRR 2.51 (95%CI: 1.53-4.16) to aRR 4.07 (95%CI: 1.56-12.01) (interaction P = 0.41). No findings replicated in New Haven.

CONCLUSION: We detected no overall pandemic effects on PTB, but potential indirect benefits for some patients which could widen disparities remains possible.

Infants born preterm are at risk of neonatal morbidity and mortality. Preterm birth (PTB) can be categorized as either spontaneous (sPTB) or medically indicated (mPTB), resulting from distinct pathophysiologic processes such as preterm labor or preeclampsia, respectively. A growing body of literature has demonstrated the impacts of nitrogen dioxide (NO) and benzene exposure on PTB, though few studies have investigated how these associations may differ by PTB subtype. We investigated the associations of NO and benzene exposure with sPTB and mPTB among 18,616 singleton live births at two Philadelphia hospitals between 2013 and 2017. Residential NO exposure was estimated using a land use regression model and averaged over the patient's full pregnancy. Benzene exposure was estimated at the census tract level using National Air Toxics Assessment (NATA) exposure data from 2014. We used logistic mixed-effects models to calculate odds ratios for overall PTB, sPTB, and mPTB separately, adjusting for patient- and tract-level confounders. Given the known racial segregation and PTB disparities in Philadelphia, we also examined race-stratified models. Counter to the hypothesis, neither NO nor benzene exposure differed by race, and neither were significantly associated with PTB or PTB subtypes. As such, these pollutants do not appear to explain the racial disparities in PTB in this setting.

<p><strong>BACKGROUND: </strong>Among highly exposed populations, arsenic exposure in utero may be associated with decreased birth weight, however less is known about potential effects of arsenic exposure in urban communities without contaminated sources such as drinking water.</p>

<p><strong>OBJECTIVE: </strong>Investigate the association of blood arsenic levels with birth weight-for-gestational age categories within a prospective birth cohort study.</p>

<p><strong>DESIGN/METHODS: </strong>We analyzed 730 mother-infant dyads within the Programming Research in Obesity, GRowth, Environment and Social Stressors (PROGRESS) cohort in Mexico City. Total arsenic was measured in maternal blood samples from the 2nd and 3rd trimesters, at delivery, as well as from infant umbilical cord blood samples. Multivariable, multinomial logistic regression. models adjusting for maternal age at enrollment, pre-pregnancy body mass index, parity, infant sex, socioeconomic position, and prenatal environmental tobacco smoke exposure were used to calculate odds ratios of small-for-gestational age (&lt;10th percentile, SGA) and large-for-gestational age (&gt;90th percentile, LGA) compared to appropriate-for-gestational age (AGA) per unit increase of log-transformed arsenic.</p>

<p><strong>RESULTS: </strong>Median (IQR) blood arsenic levels for maternal second trimester were 0.72 (0.33) μg/L, maternal third trimester 0.75 (0.41) μg/L, maternal at delivery 0.85 (0.70) μg/L, and infant cord 0.78 (0.65) μg/L. Maternal delivery and infant cord blood samples were most strongly correlated (spearman r = 0.65, p &lt; 0.0001). Maternal arsenic levels at delivery were associated with significantly higher odds of both SGA (adj. OR = 1.44, 95% CI: 1.08-1.93) and LGA (adj. OR = 2.03, 95% CI: 1.12-3.67) compared to AGA. Results were similar for cord blood. There were 130 SGA infants and 22 LGA infants. Earlier in pregnancy, there were no significant associations of arsenic and birth weight-for-gestational age. However, we observed non-significantly higher odds of LGA among women with higher arsenic levels in the 3rd trimester (adj. OR = 1.46, 95% CI: 0.67-3.12).</p>

<p><strong>CONCLUSION: </strong>We found that in a Mexico City birth cohort, higher maternal blood arsenic levels at delivery were associated with higher odds of both SGA and LGA. However, sources and species of arsenic were not known and the number of LGA infants was small, limiting the interpretation of this finding and highlighting the importance of future large studies to incorporate arsenic speciation. If our findings were confirmed in studies that addressed these limitations, determining modifiable factors that could be mitigated, such as sources of arsenic exposure, may be important for optimizing fetal growth to improve long-term health of children.</p>