Particulate air pollution exposure during pregnancy and postpartum depression symptoms in women in Mexico City.
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ABSTRACT:
SUBMITTER: Niedzwiecki MM
PROVIDER: S-EPMC7263529 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:MethodsWe studied associations between prenatal exposure to particulate matter with diameter ≤ 2.5 μm (PM2.5) and postpartum psychological functioning in a lower income, ethnically mixed sample of urban US women enrolled in a pregnancy cohort study. Analyses included 557 mothers who delivered at ≥37 weeks gestation. Daily estimates of residential PM2.5 over gestation were derived using a satellite-based spatio-temporally resolved model. Outcomes included the Edinburgh Postnatal Depression Scale (EPDS) score from 6 or 12 months postpartum and subscale scores for anhedonia, depressive and anxiety symptoms. Associations were also examined within racial/ethnic groups. Distributed lag models (DLMs) were implemented to identify windows of vulnerability during pregnancy.ResultsMost mothers had less than a high school education (64%) and were primarily Hispanic (55%) and Black (29%). In the overall sample, a DLM adjusted for age, race, education, prenatal smoking, and season of delivery, we found significant associations between higher PM2.5 exposure in the second trimester and increased anhedonia subscale scores postpartum. In race stratified analyses, mid-pregnancy PM2.5 exposure was significantly associated with increased total EPDS scores as well as higher anhedonia and depressive symptom subscale scores among Black women.ConclusionsIncreased PM2.5 exposure in mid-pregnancy was associated with increased depressive and anhedonia symptoms, particularly in Black women.
| S-EPMC5905884 | biostudies-literature
Project description:UNLABELLED:Geostatistical interpolation methods to estimate individual exposure to outdoor air pollutants can be used in pregnancy cohorts where personal exposure data are not collected. Our objectives were to a) develop four assessment methods (citywide average (CWA); nearest monitor (NM); inverse distance weighting (IDW); and ordinary Kriging (OK)), and b) compare daily metrics and cross-validations of interpolation models. We obtained 2008 hourly data from Mexico City's outdoor air monitoring network for PM10, PM2.5, O3, CO, NO2, and SO2 and constructed daily exposure metrics for 1,000 simulated individual locations across five populated geographic zones. Descriptive statistics from all methods were calculated for dry and wet seasons, and by zone. We also evaluated IDW and OK methods' ability to predict measured concentrations at monitors using cross validation and a coefficient of variation (COV). All methods were performed using SAS 9.3, except ordinary Kriging which was modeled using R's gstat package. Overall, mean concentrations and standard deviations were similar among the different methods for each pollutant. Correlations between methods were generally high (r=0.77 to 0.99). However, ranges of estimated concentrations determined by NM, IDW, and OK were wider than the ranges for CWA. Root mean square errors for OK were consistently equal to or lower than for the IDW method. OK standard errors varied considerably between pollutants and the computed COVs ranged from 0.46 (least error) for SO2 and PM10 to 3.91 (most error) for PM2.5. OK predicted concentrations measured at the monitors better than IDW and NM. Given the similarity in results for the exposure methods, OK is preferred because this method alone provides predicted standard errors which can be incorporated in statistical models. The daily estimated exposures calculated using these different exposure methods provide flexibility to evaluate multiple windows of exposure during pregnancy, not just trimester or pregnancy-long exposures. IMPLICATIONS:Many studies evaluating associations between outdoor air pollution and adverse pregnancy outcomes rely on outdoor air pollution monitoring data linked to information gathered from large birth registries, and often lack residence location information needed to estimate individual exposure. This study simulated 1,000 residential locations to evaluate four air pollution exposure assessment methods, and describes possible exposure misclassification from using spatial averaging versus geostatistical interpolation models. An implication of this work is that policies to reduce air pollution and exposure among pregnant women based on epidemiologic literature should take into account possible error in estimates of effect when spatial averages alone are evaluated.
| S-EPMC4670782 | biostudies-literature
Project description:BackgroundTo mitigate air pollution-related health risks and target interventions towards the populations bearing the greatest risks, the City Health Outlook (CHO) project aims to establish multi-scale, long-lasting, real-time urban environment and health monitoring networks. A major goal of CHO is to collect data of personal exposure to particulate air pollution through a full profile that consists of a matrix of activities and micro-environments. As the first paper of a series, this paper is targeted at illustrating the characteristics of the participants and examining the effects of different covariates on personal exposure at various air pollution exposure levels.MethodsIn the first campaign, volunteers are recruited to wear portable environmental sensors to record their real-time personal air pollution exposure and routes. After a web-based social media recruitment strategy, 50 eligible subjects joined the first campaign in Beijing from January 8 to January 20, 2018. The mean personal exposures were measured at 19.36, 37.65, and 43.45 μg/m3 for particulate matter (PM) with a diameter less than 1, 2.5, and 10 μm, respectively, albeit with the high spatial-temporal variations.ResultsUnequal distribution of exposures was observed in the subjects with different sociodemographic status, travel behavior, living and health conditions. Quantile regression analysis reveals that subjects who are younger, less educated, exposed to passive smoking, low to middle household income, overweight, without ventilation system at home or office, and do not possess private vehicles, are more susceptible to PM pollution. The differences, however, are generally insignificant at low exposure levels and become evident on bad air quality days.ConclusionsThe heterogeneity in personal exposure found in this the first CHO campaign highlighted the importance of studying the pollution exposure at the individual scale. It is at the critical stage to bridge the knowledge gap of environmental inequality in different populations, which can lead to great health implications.
| S-EPMC6555980 | biostudies-literature
Project description:BackgroundDepression 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.MethodsOne 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.ResultsWe 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).ConclusionsIn 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.
| S-EPMC8626870 | biostudies-literature
Project description:BackgroundParticulate matter ≤10 μm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts.ObjectivesTo evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks.MethodsPM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines.ResultsIn adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 μg/m3) during the second trimester, while negative associations were seen during the second (≥74 μg/m3) and third trimesters (55-65 μg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth.DiscussionAssociations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.
| S-EPMC7525039 | biostudies-literature
Project description:We use individual-level data to estimate the effects of long- and short-term exposure to air pollution (PM2.5) on the probability of dying from COVID-19. To the best of our knowledge, our study is the first to look at this relationship using individual-level data. We find that for Mexico City there is evidence of a positive relationship between pollution and mortality that significantly grows with age and that appears to be mostly driven by long- rather than short-term exposure. By using a rich set of individual- and municipal-level covariates we are able to isolate the effect of exposure to pollution from other crucial factors, thus alleviating endogeneity concerns related to selection. Our results provide yet another reason for the need to implement environmental strategies that will reduce the exposure to air pollution: it is a key element to improve the general population's health. In addition, and considering that at this moment we do not know when the pandemic will stop or if SARS-CoV-2 will become a recurrent threat, the relationship that we uncovered suggests that financial resources should be allocated to improve medical services in those areas where PM2.5 concentrations tend to be high.
| S-EPMC7688431 | biostudies-literature
Project description:Due to their lack of repair capacity mitochondria are critical targets for environmental toxicants. We studied genes and pathways reflecting mitochondrial responses to short- and medium-term PM10 exposure.Whole genome gene expression was measured in peripheral blood of 98 adults (49% women). We performed linear regression analyses stratified by sex and adjusted for individual and temporal characteristics to investigate alterations in gene expression induced by short-term (week before blood sampling) and medium-term (month before blood sampling) PM10 exposure. Overrepresentation analyses (ConsensusPathDB) were performed to identify enriched mitochondrial associated pathways and gene ontology sets. Thirteen Human MitoCarta genes were measured by means of quantitative real-time polymerase chain reaction (qPCR) along with mitochondrial DNA (mtDNA) content in an independent validation cohort (n = 169, 55.6% women).Overrepresentation analyses revealed significant pathways (p-value <0.05) related to mitochondrial genome maintenance and apoptosis for short-term exposure and to the electron transport chain (ETC) for medium-term exposure in women. For men, medium-term PM10 exposure was associated with the Tri Carbonic Acid cycle. In an independent study population, we validated several ETC genes, including UQCRH and COX7C (q-value <0.05), and some genes crucial for the maintenance of the mitochondrial genome, including LONP1 (q-value: 0.07) and POLG (q-value: 0.04) in women.In this exploratory study, we identified mitochondrial genes and pathways associated with particulate air pollution indicating upregulation of energy producing pathways as a potential mechanism to compensate for PM-induced mitochondrial damage.
| S-EPMC5563023 | biostudies-other
Project description:BackgroundStudies have identified associations between air pollution and lipid levels in adults, suggesting a mechanism by which air pollution contributes to cardiovascular disease. However, little is known about the association between early life air pollution exposure and lipid levels in children.MethodsParticipants included 465 mother-child pairs from a prospective birth cohort in Mexico City. Daily particulate matter <2.5 µm in diameter (PM2.5) predictions were estimated using a satellite-based exposure model and averaged over trimesters, the entire pregnancy, and the first year of life. We assessed associations with several lipid measures at 4-6 years of age, including total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non-HDL-C, high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Linear regression models were used to estimate change in lipid levels with each interquartile range increase in PM2.5. We additionally assessed if associations between PM2.5 and lipid levels varied across lipid quantiles using quantile regression. Models were adjusted for maternal education, body mass index, and age, child's age at study visit, prenatal environmental tobacco smoke, and season of conception.ResultsPM2.5 exposure during the third trimester was associated with increases in childhood total cholesterol, LDL-C, and non-HDL-C, and decreases in HDL-C and triglycerides. There was additionally an increasing trend in the effect estimate across higher quantiles of total cholesterol, LDL-C, and non-HDL-C during the third trimester and entire pregnancy period. There were no consistent associations for first year of life exposures.ConclusionIn this longitudinal birth cohort in Mexico City, associations between prenatal PM2.5 and childhood lipid (total cholesterol, LDL-C, non-HDL-C) levels were greater for children at higher lipid quantiles.
| S-EPMC7147392 | biostudies-literature
Project description:BackgroundAlthough the effect of air pollution on various diseases has been extensively investigated, few studies have examined its effect on depression.ObjectivesWe investigated the effect of air pollution on symptoms of depression in an elderly population.MethodsWe enrolled 537 participants in the study who regularly visited a community center for the elderly located in Seoul, Korea. The Korean version of the Geriatric Depression Scale-Short Form (SGDS-K) was used to evaluate depressive symptomatology during a 3-year follow-up study. We associated ambient air pollutants with SGDS-K results using generalized estimating equations (GEE). We also conducted a factor analysis with items on the SGDS-K to determine which symptoms were associated with air pollution.ResultsSGDS-K scores were positively associated with interquartile range (IQR) increases in the 3-day moving average concentration of particulate matter with an aerodynamic diameter ? 10 ?m (PM10) [17.0% increase in SGDS-K score, 95% confidence interval (CI): 4.9%, 30.5%], the 0-7 day moving average of nitrogen dioxide [NO2; 32.8% (95% CI: 12.6%, 56.6%)], and the 3-day moving average of ozone [O3; 43.7% (95% CI: 11.5%, 85.2%)]. For these three pollutants, factor analysis showed that air pollution was more strongly associated with emotional symptoms such as feeling happy and satisfied than with somatic or affective symptoms.ConclusionsOur study suggests that increases in PM10, NO2, and O3 may increase depressive symptoms among the elderly. Of the symptoms evaluated, ambient air pollution was most strongly associated with emotional symptoms.
| S-EPMC3404652 | biostudies-literature
Project description:Particulate matter (PM) exposure has been associated with intestinal disorders. Therefore, there is an urgent need to understand the precise molecular mechanism involved and explore potential prevention strategies. In this study, inhaled PM is shown to activate inflammatory pathways in murine colon. In a panel study, it is found that ambient PM levels are significantly associated with elevated number of fecal white blood cells in healthy subjects. Acting as a promoter, PM exposure accelerates chemical carcinogenesis-induced colonic tumor formation in a murine model. Mechanistically, RNA-seq assays suggest activation of phosphoinositide 3-kinase (PI3K)/AKT cascades in chronically PM-exposed human colon mucosal epithelial cells. Ablation of up-stream driver fibroblast growth factor receptor 4 (FGFR4) effectively inhibits inflammation and neoplasia in PM-exposed murine colons. Notably, dietary curcumin supplement is shown to protect against PM-induced colonic injuries in mice. Collectively, these findings identify that PM exposure accelerates colonic tumorigenesis in a PI3K/AKT-dependent manner and suggests potential nutrient supplement for prevention.
| S-EPMC6548988 | biostudies-literature