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BACKGROUND: Ambient air pollution has been linked to postpartum depression. However, few studies have investigated the effects of traffic-related NOx on postpartum depression and whether any pregnancy-related factors might increase susceptibility. OBJECTIVES: To evaluate the association between traffic-related NOx and postpartum depressive and anxiety symptoms, and effect modification by pregnancy-related hypertension. METHODS: This study included 453 predominantly low-income Hispanic/Latina women in the MADRES cohort. Daily traffic-related NOx concentrations by road class were estimated using the California LINE-source dispersion model (CALINE4) at participants' residential locations and averaged across pregnancy. Postpartum depressive and anxiety symptoms were evaluated by a validated questionnaire (Postpartum Distress Measure, PDM) at 1, 3, 6 and 12 months postpartum. Multivariate linear regressions were performed to estimate the associations at each timepoint. Interaction terms were added to the linear models to assess effect modification by hypertensive disorders of pregnancy (HDPs). Repeated measurement analyses were conducted by using mixed effect models. RESULTS: We found prenatal traffic-related NOx was associated with increased PDM scores. Specifically, mothers exposed to an IQR (0.22 ppb) increase in NOx from major roads had 3.78% (95% CI: 0.53-7.14%) and 5.27% (95% CI: 0.33-10.45%) significantly higher 3-month and 12-month PDM scores, respectively. Similarly, in repeated measurement analyses, higher NOx from major roads was associated with 3.06% (95% CI: 0.43-5.76%) significantly higher PDM scores across the first year postpartum. Effect modification by HDPs was observed: higher freeway/highway and total NOx among mothers with HDPs were associated with significantly higher PDM scores at 12 months postpartum compared to those without HDPs. IMPACT: This study shows that prenatal traffic-related air pollution was associated with postpartum depressive and anxiety symptoms. The study also found novel evidence of greater susceptibility among women with HDPs, which advances the understanding of the relationships between air pollution, maternal cardiometabolic health during pregnancy and postpartum mental health. Our study has potential implications for clinical intervention to mitigate the effects of traffic-related pollution on postpartum mental health disorders. The findings can also offer valuable insights into urban planning strategies concerning the implementation of emission control measures and the creation of green spaces.
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BACKGROUND: Air pollution has been associated with gestational hypertension (GH) and preeclampsia, but susceptible windows of exposure and potential vulnerability by comorbidities, such as prenatal depression, remain unclear. METHODS: We ascertained GH and preeclampsia cases in a prospective pregnancy cohort in Los Angeles, CA. Daily levels of ambient particulate matters (with a diameter of ≤10 µm [PM10] or ≤2.5 µm [PM2.5]), nitrogen dioxide, and ozone were averaged for each week from 12 weeks preconception to 20 gestational weeks. We used distributed lag models to identify susceptible exposure windows, adjusting for potential confounders. Analyses were additionally stratified by probable prenatal depression to explore population vulnerability. RESULTS: Among 619 participants, 60 developed preeclampsia and 42 developed GH. We identified a susceptible window for exposure to PM2.5 from 1 week preconception to 11 weeks postconception: higher exposure (5 µg/m3) within this window was associated with an average of 8% (95% CI, 1%-15%) higher risk of GH. Among participants with probable prenatal depression (n=179; 32%), overlapping sensitive windows were observed for all pollutants from 8 weeks before to 10 weeks postconception with increased risk of GH (PM2.5, 16% [95% CI, 3%-31%]; PM10, 39% [95% CI, 13%-72%]; nitrogen dioxide, 65% [95% CI, 17%-134%]; and ozone, 45% [95% CI, 9%-93%]), while the associations were close to null among those without prenatal depression. Air pollutants were not associated with preeclampsia in any analyses. CONCLUSIONS: We identified periconception through early pregnancy as a susceptible window of air pollution exposure with an increased risk of GH. Prenatal depression increases vulnerability to air pollution exposure and GH.
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Contaminación del Aire , Hipertensión Inducida en el Embarazo , Material Particulado , Humanos , Embarazo , Femenino , Contaminación del Aire/efectos adversos , Adulto , Hipertensión Inducida en el Embarazo/epidemiología , Estudios Prospectivos , Material Particulado/efectos adversos , Los Angeles/epidemiología , Depresión/epidemiología , Preeclampsia/epidemiología , Ozono/efectos adversos , Exposición Materna/efectos adversos , Efectos Tardíos de la Exposición Prenatal/epidemiología , Factores de Riesgo , Dióxido de Nitrógeno/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Adulto JovenRESUMEN
BACKGROUND: Personal exposure to fine particulate matter (PM2.5) is impacted by different sources each with different chemical composition. Determining these sources is important for reducing personal exposure and its health risks especially during pregnancy. OBJECTIVE: Identify main sources and their contributions to the personal PM2.5 exposure in 213 women in the 3rd trimester of pregnancy in Los Angeles, CA. METHODS: We measured 48-hr integrated personal PM2.5 exposure and analyzed filters for PM2.5 mass, elemental composition, and optical carbon fractions. We used the EPA Positive Matrix Factorization (PMF) model to resolve and quantify the major sources of personal PM2.5 exposure. We then investigated bivariate relationships between sources, time-activity patterns, and environmental exposures in activity spaces and residential neighborhoods to further understand sources. RESULTS: Mean personal PM2.5 mass concentration was 22.3 (SD = 16.6) µg/m3. Twenty-five species and PM2.5 mass were used in PMF with a final R2 of 0.48. We identified six sources (with major species in profiles and % contribution to PM2.5 mass) as follows: secondhand smoking (SHS) (brown carbon, environmental tobacco smoke; 65.3%), fuel oil (nickel, vanadium; 11.7%), crustal (aluminum, calcium, silicon; 11.5%), fresh sea salt (sodium, chlorine; 4.7%), aged sea salt (sodium, magnesium, sulfur; 4.3%), and traffic (black carbon, zinc; 2.6%). SHS was significantly greater in apartments compared to houses. Crustal source was correlated with more occupants in the household. Aged sea salt increased with temperature and outdoor ozone, while fresh sea salt was highest on days with westerly winds from the Pacific Ocean. Traffic was positively correlated with ambient NO2 and traffic-related NOx at residence. Overall, 76.8% of personal PM2.5 mass came from indoor or personal compared to outdoor sources. IMPACT: We conducted source apportionment of personal PM2.5 samples in pregnancy in Los Angeles, CA. Among identified sources, secondhand smoking contributed the most to the personal exposure. In addition, traffic, crustal, fuel oil, fresh and aged sea salt sources were also identified as main sources. Traffic sources contained markers of combustion and non-exhaust wear emissions. Crustal source was correlated with more occupants in the household. Aged sea salt source increased with temperature and outdoor ozone and fresh sea salt source was highest on days with westerly winds from the Pacific Ocean.
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We examined the associations between social support and postpartum mental health in 137 U.S. and foreign-born Latinas in the MADRES pregnancy cohort. We also examined whether language, years in the U.S., and country of birth moderates these relationships. Participants were administered PROMIS support measures 1 month postpartum; the Perceived Stress and Postpartum Distress Measure 3, 6, and 12 months postpartum; and the CESD scale 12 months postpartum. Perceived stress was lower at 6 months postpartum for women reporting higher emotional (p = 0.01), informational (p = 0.03), and instrumental support (p < 0.001); and lower at 12 months postpartum for women reporting higher emotional support (p = 0.01). Distress at 6 months was lower in women reporting higher emotional support (p = 0.03). Interactions suggest that associations were stronger for mothers that speak Spanish, spent fewer years in the U.S., and were born in Central America.
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Depresión Posparto , Salud Mental , Embarazo , Femenino , Humanos , Aculturación , Periodo Posparto , Madres/psicología , Hispánicos o Latinos/psicología , Apoyo SocialRESUMEN
Organophosphate esters (OPEs) are increasingly considered neurotoxicants which may impact gross and fine motor development. We evaluated associations between prenatal OPE exposures and infant motor development. Third trimester urinary concentrations of nine OPE metabolites were measured in 329 mother-infant dyads participating in the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) cohort. Child gross and fine motor development at 6, 9, 12, and 18-months were assessed with the Ages and Stages Questionnaire-3 (ASQ-3) and operationalized in models using dichotomous instrument-specific cutoffs for typical motor development. Five OPE metabolites with >60% detection were specific-gravity-adjusted, natural log-transformed, and modeled continuously, while four metabolites with <60% detection were modeled dichotomously (detected/not-detected). We fit mixed effects logistic regression between OPE metabolites and fine/gross motor development and assessed sex-specific effects using a statistical interaction term and sex-stratified models. Among children, 31% and 23% had gross and fine motor scores, respectively, below the ASQ-3 at-risk cutoffs at least once across infancy. A doubling in prenatal diphenyl phosphate (DPHP) exposure was associated with 26% increased odds of potential fine motor delays (ORfine = 1.26, 95% CI: 1.02, 1.57, p = 0.04). We also observed significant interactions by infant sex for associations of detected dipropyl phosphate (DPRP) with gross motor development (pinteraction = 0.048) and detected bis(1-chloro-2-propyl) phosphate (BCIPP) with fine motor development (pinteraction = 0.02). Females had greater odds of potential motor delays for both detected DPRP (females vs males ORgross (95% CI) = 1.48 (0.71, 3.09), p = 0.30 vs 0.27 (0.06, 1.29), p = 0.10) and detected BCIPP (females vs males ORfine (95% CI) = 2.72 (1.27, 5.85), p = 0.01 vs 0.76 (0.31, 1.90), p = 0.56). There were no other significant associations between other metabolites and motor development, despite similar patterns. We found evidence of adverse effects of prenatal OPE exposures on infant motor development with greater adverse effects among female infants with some OPE metabolites.
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Retardadores de Llama , Efectos Tardíos de la Exposición Prenatal , Masculino , Niño , Lactante , Embarazo , Humanos , Femenino , Ésteres/orina , Organofosfatos/metabolismo , Fosfatos , Retardadores de Llama/metabolismoRESUMEN
In-utero exposure to fine particulate matter (PM2.5) and specific sources and components of PM2.5 have been linked with lower birthweight. However, previous results have been mixed, likely due to heterogeneity in sources impacting PM2.5 and due to measurement error from using ambient data. Therefore, we investigated the effect of PM2.5 sources and their high-loading components on birthweight using data from 198 women in the 3rd trimester from the MADRES cohort 48-h personal PM2.5 exposure monitoring sub-study. The mass contributions of six major sources of personal PM2.5 exposure were estimated for 198 pregnant women in the 3rd trimester using the EPA Positive Matrix Factorization v5.0 model, along with their 17 high-loading chemical components using optical carbon and X-ray fluorescence approaches. Single- and multi-pollutant linear regressions evaluated the association between personal PM2.5 sources/components and birthweight, adjusting for gestational age, maternal age, race, infant sex, parity, diabetes status, temperature, maternal education, and smoking history. Participants were predominately Hispanic (81%), with a mean (SD) gestational age of 39.1 (1.5) weeks and age of 28.2 (6.0) years. Mean birthweight was 3295.8 g (484.1) and mean PM2.5 exposure was 21.3 (14.4) µg/m3. A 1 SD increase in the mass contribution of the fresh sea salt source was associated with a 99.2 g decrease in birthweight (95% CI - 197.7, - 0.6), and aged sea salt was associated with a 70.1 g decrease in birthweight (95% CI - 141.7, 1.4). Magnesium, sodium, and chlorine were associated with lower birthweight, which remained after adjusting for PM2.5 mass. This study found evidence that major sources of personal PM2.5 including fresh and aged sea salt were negatively associated with birthweight, with the strongest effect on birthweight from Na and Mg. The effect of crustal and fuel oil sources differed by infant sex with negative associations seen in boys compared to positive associations in girls.
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Contaminantes Atmosféricos , Contaminación del Aire , Masculino , Humanos , Femenino , Embarazo , Anciano , Lactante , Peso al Nacer , Contaminantes Atmosféricos/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Modelos Lineales , Escolaridad , Contaminación del Aire/análisis , Exposición Materna/efectos adversosRESUMEN
Background: Poor sleep quality is associated with weight gain in non-pregnant populations, but evidence in pregnant people is lacking. Our study examined the association between early-to-mid pregnancy sleep quality and weekly gestational weight gain (GWG) rate during mid-to-late pregnancy by pre-pregnancy body mass index (BMI). Method: Participants were 316 pregnant participants from the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) study. During early-to-mid pregnancy, participants reported their sleep quality which was used to construct four categories: very poor, poor, good, and very good. Linear growth curve models examined the association between early-to-mid pregnancy sleep quality and weekly rate of GWG (kg/week) during mid-to-late pregnancy (> 20 weeks gestation), with a three-way cross-level interaction between gestational age, sleep quality, and pre-pregnancy BMI category. Models adjusted for ethnicity by birthplace, hypertensive disorders, perceived stress score, and physical activity level. Results: Overall, poorer early-to-mid pregnancy sleep quality was associated with increased weekly weight gain during mid-to-late pregnancy. For example, amongst normal weight participants, mid-to-late pregnancy weight gain was, on average, 0.39 kg (95% CI: 0.29, 0.48) per week for those with very good sleep quality, 0.53 kg (95% CI: 0.44, 0.61) per week for those with poor sleep quality, and 0.54 kg (95% CI: 0.46, 0.62) per week for those with very poor sleep quality during early-to-mid pregnancy. This difference in GWG rate was statistically significantly comparing very good to poor sleep (0.14 kg/week, 95% CI: 0.01, 0.26) and very good to very poor sleep (0.15kg/week, 85% CI: 0.02, 0.27). This association between sleep quality and GWG rate did not statistically differ by pre-pregnancy BMI. Conclusion: Our study found very poor early-to-mid pregnancy sleep quality was associated with higher mid-to-late pregnancy GWG rate. Incorporating pregnancy-specific sleep recommendations into routine obstetric care may be a critical next step in promoting healthy GWG.
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INTRODUCTION: Secondhand smoke (SHS) exposure during pregnancy is linked to adverse birth outcomes, such as low birth weight and preterm birth. While questionnaires are commonly used to assess SHS exposure, their ability to capture true exposure can vary, making it difficult for researchers to harmonize SHS measures. This study aimed to compare self-reported SHS exposure with measurements of airborne SHS in personal samples of pregnant women. METHODS: SHS was measured on 48-hour integrated personal PM2.5 Teflon filters collected from 204 pregnant women, and self-reported SHS exposure measures were obtained via questionnaires. Descriptive statistics were calculated for airborne SHS measures, and analysis of variance tests assessed group differences in airborne SHS concentrations by self-reported SHS exposure. RESULTS: Participants were 81% Hispanic, with a mean (SD) age of 28.2 (6.0) years. Geometric mean (SD) personal airborne SHS concentrations were 0.14 (9.41) µg/m3. Participants reporting lower education have significantly higher airborne SHS exposure (p=0.015). Mean airborne SHS concentrations were greater in those reporting longer duration with windows open in the home. There was no association between airborne SHS and self-reported SHS exposure; however, asking about the number of smokers nearby in the 48-hour monitoring period was most correlated with measured airborne SHS (Two+ smokers: 0.30µg/m3 vs. One: 0.12µg/m3 and Zero: 0.15µg/m3; p=0.230). CONCLUSIONS: Self-reported SHS exposure was not associated with measured airborne SHS in personal PM2.5 samples. This suggests exposure misclassification using SHS questionnaires and the need for harmonized and validated questions to characterize this exposure in health studies. IMPLICATIONS: This study adds to the growing body of evidence that measurement error is a major concern in pregnancy research, particularly in studies that rely on self-report questionnaires to measure secondhand smoke (SHS) exposure. The study introduces an alternative method of SHS exposure assessment using objective optical measurements, which can help improve the accuracy of exposure assessment. The findings emphasize the importance of using harmonized and validated SHS questionnaires in pregnancy health research to avoid biased effect estimates. This study can inform future research, practice, and policy development to reduce SHS exposure and its adverse health effects.
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BACKGROUND: Evidence suggests organophosphate esters (OPEs) are neurotoxic; however, the epidemiological literature remains scarce. We investigated whether prenatal exposures to OPEs were associated with child neurobehavior in the MADRES cohort. METHODS: We measured nine OPE metabolites in 204 maternal urine samples (gestational age at collection: 31.4 ± 1.8 weeks). Neurobehavior problems were assessed among 36-month-old children using the Child Behavior Checklist's (CBCL) three composite scales [internalizing, externalizing, and total problems]. We examined associations between tertiles of prenatal OPE metabolites (> 50% detection) and detect/non-detect categories (< 50% detection) and CBCL composite scales using linear regression and generalized additive models. We also examined mixtures for widely detected OPEs (n = 5) using Bayesian kernel machine regression. RESULTS: Maternal participants with detectable versus non-detectable levels of bis(2-methylphenyl) phosphate (BMPP) had children with 42% (95% CI: 4%, 96%) higher externalizing, 45% (-2%, 114%) higher internalizing, and 35% (3%, 78%) higher total problems. Participants in the second versus first tertile of bis(butoxethyl) phosphate (BBOEP) had children with 43% (-1%, 109%) higher externalizing scores. Bis(1-chloro-2-propyl) phosphate (BCIPP) and child sex had a statistically significant interaction in internalizing (p = 0.02) and total problems (p = 0.03) models, with 120% (23%, 295%) and 57% (6%, 134%) higher scores in the third versus first BCIPP tertile among males. Among females, detectable vs non-detectable levels of prenatal BMPP were associated with 69% higher externalizing scores (5%, 170%) while the third versus first tertile of prenatal BBOEP was associated with 45% lower total problems (-68%, -6%). Although the metabolite mixture and each CBCL outcome had null associations, we observed marginal associations between di-n-butyl phosphate and di-isobutyl phosphate (DNBP + DIBP) and higher internalizing scores (0.15; 95% CrI: -0.02, 0.32), holding other metabolites at their median. CONCLUSIONS: Our results generally suggest adverse and sex-specific effects of prenatal exposure to previously understudied OPEs on neurobehavioral outcomes in 36-month children, providing evidence of potential OPE neurotoxicity.
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Síndromes de Neurotoxicidad , Efectos Tardíos de la Exposición Prenatal , Femenino , Masculino , Embarazo , Niño , Humanos , Lactante , Preescolar , Teorema de Bayes , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Efectos Tardíos de la Exposición Prenatal/epidemiología , Fosfatos , Organofosfatos , ÉsteresRESUMEN
Background: Air pollution has been associated with gestational diabetes mellitus (GDM). We aim to investigate susceptible windows of air pollution exposure and factors determining population vulnerability. Methods: We ascertained GDM status in the prospective Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) pregnancy cohort from Los Angeles, California, USA. We calculated the relative risk of GDM by exposure to ambient particulate matter (PM10; PM2.5), nitrogen dioxide (NO2), and ozone (O3) in each week from 12 weeks before to 24 weeks after conception, adjusting for potential confounders, with distributed lag models to identify susceptible exposure windows. We examined effect modification by prenatal depression, median-split pre-pregnancy BMI (ppBMI) and age. Findings: Sixty (9.7%) participants were diagnosed with GDM among 617 participants (mean age: 28.2 years, SD: 5.9; 78.6% Hispanic, 11.8% non-Hispanic Black). GDM risk increased with exposure to PM2.5, PM10, and NO2 in a periconceptional window ranging from 5 weeks before to 5 weeks after conception: interquartile-range increases in PM2.5, PM10, and NO2 during this window were associated with increased GDM risk by 5.7% (95% CI: 4.6-6.8), 8.9% (8.1-9.6), and 15.0% (13.9-16.2), respectively. These sensitive windows generally widened, with greater effects, among those with prenatal depression, with age ≥28 years, or with ppBMI ≥27.5 kg/m2, than their counterparts. Interpretation: Preconception and early-pregnancy are susceptible windows of air pollutants exposure that increased GDM risk. Prenatal depression, higher age, or higher ppBMI may increase one's vulnerability to air pollution-associated GDM risk. Funding: National Institutes of Health, Environmental Protection Agency.
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Adverse Childhood Experiences (ACEs) are events that occur before a child turns 18 years old that may cause trauma. In this study, the effect of cumulative ACEs experienced on human maternal DNA methylation (DNAm) was estimated while accounting for interaction with domains of ACEs in prenatal peripheral blood mononuclear cell samples from the Maternal and Developmental Risks from Environmental Stressors (MADRES) pregnancy cohort. The intergenerational transmission of ACE-associated DNAm was also explored used paired maternal and neonatal cord blood samples. Replication in buccal samples was explored in the Children's Health Study (CHS). We used a four-level categorical indicator variable for ACEs exposure: none (0 ACEs), low (1-3 ACEs), moderate (4-6 ACEs), and high (> 6 ACEs). Effects of ACEs on maternal DNAm (N = 240) were estimated using linear models. To evaluate evidence for intergenerational transmission, mediation analysis was used. Analysis of maternal samples displayed some shared but mostly distinct effects of ACEs on DNAm across low, moderate, and high ACEs categories. CLCN7 and PTPRN2 was associated with maternal DNAm in the low ACE group and this association replicated in the CHS. ACE-associated methylation was observed in maternal and neonatal profiles in the COMT promoter region, with some evidence of mediation by maternal COMT methylation. Specific genomic loci exhibited mutually exclusive maternal ACE effects on DNAm in either maternal or neonatal population. There is some evidence for an intergenerational effect of ACEs, supported by shared DNAm signatures in the COMT gene across maternal-neonatal paired samples.
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Background: In-utero exposure to fine particulate matter (PM2.5) and specific sources and components of PM2.5 have been linked with lower birthweight. However, previous results have been mixed, likely due to heterogeneity in sources impacting PM2.5 and due to measurement error from using ambient data. Therefore, we investigated the effect of PM2.5 sources and their high-loading components on birthweight using data from 198 women in the 3rd trimester from the MADRES cohort 48-hour personal PM2.5 exposure monitoring sub-study. Methods: The mass contributions of six major sources of personal PM2.5 exposure were estimated for 198 pregnant women in the 3rd trimester using the EPA Positive Matrix Factorization v5.0 model, along with their 17 high-loading chemical components using optical carbon and X-ray fluorescence approaches. Single- and multi-pollutant linear regressions were used to evaluate the association between personal PM2.5 sources and birthweight. Additionally, high-loading components were evaluated with birthweight individually and in models further adjusted for PM2.5 mass. Results: Participants were predominately Hispanic (81%), with a mean (SD) gestational age of 39.1 (1.5) weeks and age of 28.2 (6.0) years. Mean birthweight was 3,295.8g (484.1) and mean PM2.5 exposure was 21.3 (14.4) µg/m3. A 1 SD increase in the mass contribution of the fresh sea salt source was associated with a 99.2g decrease in birthweight (95% CI: -197.7, -0.6), while aged sea salt was associated with lower birthweight (ß =-70.1; 95% CI: -141.7, 1.4). Magnesium sodium, and chlorine were associated with lower birthweight, which remained after adjusting for PM2.5 mass. Conclusions: This study found evidence that major sources of personal PM2.5 including fresh and aged sea salt were negatively associated with birthweight, with the strongest effect on birthweight from Na and Mg. The effect of crustal and fuel oil sources differed by infant sex with negative associations seen in boys compared to positive associations in girls.
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BACKGROUND: Organophosphate esters (OPEs) are used as flame retardants and plasticizers in various consumer products. Limited prior research suggests sex-specific effects of prenatal OPE exposures on fetal development. We evaluated overall and sex-specific associations between prenatal OPE exposures and gestational age (GA) at birth and birthweight for gestational age (BW for GA) z-scores among the predominately low-income, Hispanic MADRES cohort. METHODS: Nine OPE metabolite concentrations were measured in 421 maternal urine samples collected during a third trimester visit (GA = 31.5 ± 2.0 weeks). We examined associations between single urinary OPE metabolites and GA at birth and BW for GA z-scores using linear regression models and Generalized Additive Models (GAMs) and effects from OPE mixtures using Bayesian Kernel Machine Regression (BKMR). We also assessed sex-specific differences in single metabolite analyses by evaluating statistical interactions and stratifying by sex. RESULTS: We did not find significant associations between individual OPE metabolites and birth outcomes in the full infant sample; however, we found that higher bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) was associated with earlier GA at birth among male infants (p = 0.04), and a nonlinear, inverted U-shape association between the sum of dibutyl phosphate and di-isobutyl phosphate (DNBP + DIBP) and GA at birth among female infants (p = 0.03). In mixtures analysis, higher OPE metabolite mixture exposures was associated with lower GA at birth, which was primarily driven by female infants. No associations were observed between OPE mixtures and BW for GA z-scores. CONCLUSION: Higher BDCIPP and DNBP + DIBP concentrations were associated with earlier GA at birth among male and female infants, respectively. Higher exposure to OPE mixtures was associated with earlier GA at birth, particularly among female infants. However, we saw no associations between prenatal OPEs and BW for GA. Our results suggest sex-specific impacts of prenatal OPE exposures on GA at birth.
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Retardadores de Llama , Organofosfatos , Embarazo , Recién Nacido , Humanos , Masculino , Lactante , Femenino , Teorema de Bayes , Organofosfatos/toxicidad , Organofosfatos/orina , Fosfatos , Retardadores de Llama/toxicidad , ÉsteresRESUMEN
INTRODUCTION AND OBJECTIVES: Research suggests that perceived immigration policy vulnerability has important health implications. Coupled with the mental and physical stressors accompanying the postpartum period and a growing awareness of the discrimination and structural racism experienced by marginalized communities globally, the coronavirus disease 2019 period may have exacerbated stress among vulnerable populations, specifically postpartum Hispanic/Latina women. This study evaluated perceived immigration policy vulnerability (i.e. discrimination, social isolation, and family threats) in early postpartum Hispanic/Latina women in Los Angeles before and during the coronavirus disease 2019 pandemic. METHODS: The Perceived Immigration Policy Effects Scale (PIPES) was administered cross-sectionally at 1 month postpartum to 187 Hispanic/Latina women in the MADRES cohort. Respondents between September 2018 and March 2020 were classified as "pre-pandemic" (N = 128), between March 2020 and July 2020 as "early pandemic" (N = 38), and between August 2020 and November 2021 as "later pandemic" (N = 21). Average PIPES subscale scores were dichotomized into "higher" and "lower" groups (⩽median, >median) and logistic regression models were performed. RESULTS: Approximately half of participants had incomes of <$50,000 (50.3%) and were Latin American born (54.6%). After adjusting for age, nativity, education, income, postpartum distress, and employment status, early pandemic respondents had 5.05 times the odds of a higher score on the perceived discrimination subscale (95% CI: 1.81, 14.11), 6.47 times the odds of a higher score on the social isolation subscale (95% CI: 2.23, 18.74), 2.66 times the odds of a higher score on the family threats subscale (95% CI: 0.97, 7.32), and 3.36 times the odds of a higher total score (95% CI: 1.19, 9.51) when compared to pre-pandemic respondents. There were no significant subscale score differences between later pandemic and pre-pandemic periods. CONCLUSION: Higher perceived immigration policy vulnerability was reported among postpartum women during the early coronavirus disease 2019 pandemic versus pre-pandemic periods. This suggests greater social inequities during the early pandemic period.
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COVID-19 , Emigración e Inmigración , Femenino , Hispánicos o Latinos , Humanos , Pandemias , Políticas , Periodo Posparto , EmbarazoRESUMEN
The aim of this study was to examine the association between adverse childhood experiences (ACEs) and risk for depression among 480 predominantly low-income Hispanic/Latina women in the Maternal and Development Risks from Environmental and Social Stressors pregnancy cohort. Models were fitted to evaluate associations between ACEs and prenatal probable depression measured by the Center for Epidemiologic Studies-Depression Scale adjusting for recruitment site, age, income, race/ethnicity, marital status and parity. The ACEs Questionnaire parameterised experiences as counts (0-10), categories (0, 1-3 and 4+ ACEs) and domains. Participants had a significantly higher likelihood of prenatal probable depression per unit increase in ACEs count or if they reported 4+ ACEs relative to 0 ACEs. Higher likelihood of probable depression was also associated with higher counts of each ACEs domains: abuse, neglect and household dysfunction. Findings suggest systematic screening for depressive symptoms in those with a history of childhood adversities may be important in prenatal care practice.Impact StatementWhat is already known on this subject? Experiencing depression during pregnancy has been associated with later adverse maternal mental and physical health outcomes. Emerging studies indicate that adverse childhood experiences (ACEs) may maintain or increase the predisposition to prenatal depression.What do the results of this study add? Although prenatal depressive symptoms are prevalent among racial/ethnic minority samples including Hispanic/Latinas, research determining whether the association between ACEs and prenatal depression varies by nativity is scarce. Overall, ACEs were common among Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) participants and were associated with a higher likelihood of probable depression during pregnancy. These patterns did not significantly differ among the foreign-born versus U.S.-born Hispanic/Latina women, although the associations were stronger among U.S.-born Hispanic/Latina women.What are the implications of these findings for clinical practice and/or further research? Research should continue to focus on the effects of ACEs in communities that have been historically excluded in perinatal mental health services such as pregnant women from racial and ethnic minority groups. It may be important for clinicians to routinely screen for mental health during pregnancy as an adverse, psychological environment may impact both women and children. These findings suggest a need for improvement in systematic screening for depressive symptoms in those with a history of childhood adversities.
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Experiencias Adversas de la Infancia , Etnicidad , Femenino , Embarazo , Humanos , Niño , Depresión/epidemiología , Depresión/psicología , Grupos Minoritarios , PartoRESUMEN
Breastfeeding may protect women's long-term cardiovascular health; however, breastfeeding-related postpartum lipid changes remain unclear. We aim to examine associations of breastfeeding duration with maternal lipids at 12 months postpartum. In a subsample (n = 79) of the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort, breastfeeding status and duration at 3, 6, and 12 months postpartum were self-reported. Serum levels of lipids, including total cholesterol, triglycerides (TG), high-, low-, and very low-density lipoprotein cholesterol (HDL-C, LDL-C, VLDL-C), were measured from blood samples collected at 12 months postpartum. We used linear regression models to compare lipids by breastfeeding duration, adjusting for potential confounders. Women who were breastfeeding at 12 months had higher HDL-C (mean: 41.74 mg/dL, 95% CI: 37.27−46.74 vs. 35.11 mg/dL, 95% CI: 31.42−39.24), lower TG (80.45 mg/dL, 95% CI: 66.20−97.77 vs. 119.11 mg/dL, 95% CI: 98.36−144.25), and lower VLDL-C (16.31 mg/dL, 95% CI: 13.23, 20.12 vs. 23.09 mg/dL, 95% CI: 18.61−28.65) compared to women who breastfed for <6 months. No lipids were significantly different between women who breastfed for 6−11 months and for <6 months. Each month's increase in breastfeeding duration was significantly, inversely associated with TG and VLDL-C and positively with HDL-C. Adjusting for fasting status, demographics, pre-pregnancy body mass index, breastfeeding frequency, and pregnancy complications did not appreciably change effect estimates. Breastfeeding at 12 months postpartum and a longer duration of breastfeeding in the first year postpartum were both associated with increased HDL-C and decreased TG and VLDL-C at 12 months postpartum.
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Lactancia Materna , Periodo Posparto , Colesterol , Femenino , Hispánicos o Latinos , Humanos , Lípidos , Los Angeles , Embarazo , TriglicéridosRESUMEN
BACKGROUND/OBJECTIVE: Prevalence of pre-pregnancy obesity and excessive gestational weight gain (GWG) are higher among women of color with low SES. Dysregulation of the Hypothalamic-Pituitary-Adrenal (HPA) axis and its end-product, cortisol, during pregnancy is hypothesized to be associated with excessive GWG. However, past studies have produced inconsistent findings and often did not include health disparities populations. This study examined the association between pre-pregnancy body mass index (BMI), third trimester diurnal cortisol, and GWG in low-income, predominantly Hispanic women. SUBJECTS/METHODS: The MADRES study is an ongoing prospective cohort study of primarily Hispanic, low-income pregnant women and their children in Los Angeles, California. Data from 176 participants were included in this study. Total cortisol secretion (area under the curve, AUC) was quantified using four salivary cortisol samples (awakening, 30 min after awakening, afternoon, and bedtime) that were collected at home on one day during the third trimester of pregnancy. Moderation of the association between total cortisol and GWG by pre-pregnancy BMI was tested using multiple linear regression with a multiplicative interaction term. RESULTS: There was no association between total cortisol secretion and GWG overall (p = 0.82), but the association between total cortisol and GWG was stronger for women with class 1 pre-pregnancy obesity compared to women with normal pre-pregnancy BMI (interaction term p = 0.04). CONCLUSIONS: Results suggest that obesity status before pregnancy may be exacerbating the physiological impact of cortisol on GWG.
Asunto(s)
Ganancia de Peso Gestacional/fisiología , Hidrocortisona/análisis , Obesidad/fisiopatología , Tercer Trimestre del Embarazo/sangre , Adulto , Análisis de Varianza , Estudios de Cohortes , Femenino , Edad Gestacional , Humanos , Hidrocortisona/sangre , Los Angeles , Obesidad/sangre , Embarazo , Tercer Trimestre del Embarazo/metabolismo , Tercer Trimestre del Embarazo/fisiología , Mujeres EmbarazadasRESUMEN
BACKGROUND: Depression is the leading cause of mental health-related morbidity and affects twice as many women as men. Hispanic/Latina women in the US have unique risk factors for depression and they have lower utilization of mental health care services. Identifying modifiable risk factors for maternal depression, such as ambient air pollution, is an urgent public health priority. We aimed to determine whether prenatal exposure to ambient air pollutants was associated with maternal depression at 12 months after childbirth. METHODS: One hundred eighty predominantly low-income Hispanic/Latina women participating in the ongoing MADRES cohort study in Los Angeles, CA were followed from early pregnancy through 12 months postpartum through a series of phone questionnaires and in-person study visits. Daily prenatal ambient pollutant estimates of nitrogen dioxide (NO2), ozone (O3), and particulate matter (PM10 and PM2.5) were assigned to participant residences using inverse-distance squared spatial interpolation from ambient monitoring data. Exposures were averaged for each trimester and across pregnancy. The primary outcome measure was maternal depression at 12 months postpartum, as reported on the 20-item Center for Epidemiologic Studies-Depression (CES-D) scale. We classified each participant as depressed (n = 29) or not depressed (n = 151) based on the suggested cutoff of 16 or above (possible scores range from 0 to 60) and fitted logistic regression models, adjusting for potential confounders. RESULTS: We found over a two-fold increased odds of depression at 12 months postpartum associated with second trimester NO2 exposure (OR = 2.63, 95% CI: 1.41-4.89) and pregnancy average NO2 (OR = 2.04, 95% CI: 1.13-3.69). Higher second trimester PM2.5 exposure also was associated with increased depression at 12 months postpartum (OR = 1.56, 95% CI: 1.01-2.42). The effect for second trimester PM10 was similar and was borderline significant (OR = 1.58, 95% CI: 0.97-2.56). CONCLUSIONS: In a low-income cohort consisting of primarily Hispanic/Latina women in urban Los Angeles, we found that prenatal ambient air pollution, especially mid-pregnancy NO2 and PM2.5, increased the risk of depression at 12 months after childbirth. These results underscore the need to better understand the contribution of modifiable environmental risk factors during potentially critical exposure periods.