ABSTRACT
BACKGROUND: Studies of prenatal air pollution (AP) exposure on child neurodevelopment have mostly focused on a single pollutant. We leveraged daily exposure data and implemented novel data-driven statistical approaches to assess effects of prenatal exposure to a mixture of seven air pollutants on cognitive functioning in school-age children from an urban pregnancy cohort. METHODS: Analyses included 236 children born at ≥37 weeks gestation. Maternal prenatal daily exposure levels for nitrogen dioxide (NO2), ozone (O3), and constituents of fine particles [elemental carbon (EC), organic carbon (OC), nitrate (NO3-), sulfate (SO42-), ammonium (NH4+)] were estimated based on residential addresses using validated satellite-based hybrid models or global 3-D chemical-transport models. Children completed Wide Range Assessment of Memory and Learning (WRAML-2) and Conners' Continuous Performance Test (CPT-II) at 6.5 ± 0.9 years of age. Time-weighted levels for mixture pollutants were estimated using Bayesian Kernel Machine Regression Distributed Lag Models (BKMR-DLMs), with which we also explored the interactions in the exposure-response functions among pollutants. Resulting time-weighted exposure levels were used in Weighted Quantile Sum (WQS) regressions to examine AP mixture effects on outcomes, adjusted for maternal age, education, child sex, and prenatal temperature. RESULTS: Mothers were primarily ethnic minorities (81% Hispanic and/or black) reporting ≤12 years of education (68%). Prenatal AP mixture (per unit increase in WQS estimated AP index) was associated with decreased WRAML-2 general memory (GM; ß = -0.64, 95%CI = -1.40, 0.00) and memory-related attention/concentration (AC; ß = -1.03, 95%CI = -1.78, -0.27) indices, indicating poorer memory functioning, as well as increased CPT-II omission errors (OE; ß = 1.55, 95%CI = 0.34, 2.77), indicating increased attention problems. When stratified by sex, association with AC index was significant among girls, while association with OE was significant among boys. Traffic-related pollutants (NO2, OC, EC) and SO42- were major contributors to these associations. There was no significant evidence of interactions among mixture components. CONCLUSIONS: Prenatal exposure to an AP mixture was associated with child neurocognitive outcomes in a sex- and domain-specific manner.
Subject(s)
Air Pollutants , Air Pollution , Environmental Pollutants , Prenatal Exposure Delayed Effects , Male , Child , Pregnancy , Female , Humans , Air Pollutants/toxicity , Air Pollutants/analysis , Environmental Pollutants/analysis , Prenatal Exposure Delayed Effects/chemically induced , Prenatal Exposure Delayed Effects/epidemiology , Nitrogen Dioxide/analysis , Urban Population , Bayes Theorem , Air Pollution/adverse effects , Air Pollution/analysis , New England , Particulate Matter/toxicity , Particulate Matter/analysis , Environmental Exposure/analysisABSTRACT
The benefits of nutritional factors on birth outcomes have been recognized, however, limited studies have examined the role of nutritional factors in mitigating the detrimental effects of metals exposure during gestation. We used data collected from 526 mother-infant dyads enrolled in the Programming of Intergenerational Stress Mechanisms longitudinal pregnancy cohort to examine the joint effects of prenatal exposure to metals and maternal nutrition on birth weight for gestational age (BWGA) z-scores. We measured concentrations of twelve metals and trace elements in urine samples collected during pregnancy. Maternal nutritional intake was measured using the Block98 Food Frequency Questionnaire and converted into energy-adjusted consumption of individual nutrients. Using multivariable linear regression and Bayesian Kernel Machine Regression, we found that three metals [cobalt (Co), nickel (Ni), and lead (Pb)] and five metals [barium (Ba), caesium (Cs), copper (Cu), Ni, and zinc (Zn)] were associated with BWGA z-score in male and female infants, respectively. When examining the sex-specific interactions between these metals and nutrient groups [macro nutrients, minerals, A vitamins, B vitamins, anti-oxidant, methyl-donor nutrients, and inflammatory (pro- and anti-)] using a Cross-validated Kernel Ensemble model, we identified significant interactions between the macro nutrients and Co (p = 0.05), minerals and Pb (p = 0.04), and A vitamins and Ni (p = 0.001) in males. No significant interactions were found in females. Furthermore, three minerals (phosphorus, iron, potassium) and vitamin A were found to be more crucial than other nutrients in modifying the association between each respective metal and BWGA z-score in males. A better understanding of the sex-specific interactions between nutrients and metals on birth weight can guide pregnant women to protect their neonates from the adverse health impacts of metal exposures by optimizing nutrient intakes accordingly.
Subject(s)
Metals , Trace Elements , Bayes Theorem , Birth Weight , Female , Humans , Infant , Infant, Newborn , Male , Pregnancy , VitaminsABSTRACT
BACKGROUND: Prenatal exposure to fine particulate matter with a diameter of ≤2.5 µm (PM2.5) has been linked to adverse neurodevelopmental outcomes in later childhood, while research on early infant behavior remains sparse. OBJECTIVES: We examined associations between prenatal PM2.5 exposure and infant negative affectivity, a stable temperamental trait associated with longer-term behavioral and mental health outcomes. We also examined sex-specific effects. METHODS: Analyses included 559 mother-infant pairs enrolled in the PRogramming of Intergenerational Stress Mechanisms (PRISM) cohort. Daily PM2.5 exposure based on geocoded residential address during pregnancy was estimated using a satellite-based spatiotemporal model. Domains of negative affectivity (Sadness, Distress to Limitations, Fear, Falling Reactivity) were assessed using the Infant Behavior Questionnaire-Revised (IBQ-R) when infants were 6 months old. Subscale scores were calculated as the mean of item-specific responses; the global Negative Affectivity (NA) score was derived by averaging the mean of the four subscale scores. Bayesian distributed lag interaction models (BDLIMs) were used to identify sensitive windows for prenatal PM2.5 exposure on global NA and its subscales, and to examine effect modification by sex. RESULTS: Mothers were primarily racial/ethnic minorities (38% Black, 37% Hispanic), 40% had ≤12 years of education; most did not smoke during pregnancy (87%). In the overall sample, BDLIMs revealed that increased PM2.5 at mid-pregnancy was associated with higher global NA, Sadness, and Fear scores, after adjusting for covariates (maternal age, education, race/ethnicity, sex). Among boys, increased PM2.5 at early pregnancy was associated with decreased Fear scores, while exposure during late pregnancy was associated with increased Fear scores (cumulative effect estimate = 0.57, 95% CI: 0.03-1.41). Among girls, increased PM2.5 during mid-pregnancy was associated with higher Fear scores (cumulative effect estimate = 0.82, 95% CI: 0.05-1.91). CONCLUSIONS: Prenatal PM2.5 exposure was associated with negative affectivity at age 6 months, and the sensitive windows may vary by subdomains and infant sex.
Subject(s)
Air Pollutants , Air Pollution , Prenatal Exposure Delayed Effects , Air Pollutants/analysis , Air Pollutants/toxicity , Air Pollution/analysis , Bayes Theorem , Child , Female , Humans , Infant , Male , Maternal Exposure , Particulate Matter/analysis , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Prenatal Exposure Delayed Effects/epidemiology , TemperamentABSTRACT
Rationale: Ambient ultrafine particles (UFPs; with an aerodynamic diameter < 0.1 µm) may exert greater toxicity than other pollution components because of their enhanced oxidative capacity and ability to translocate systemically. Studies examining associations between prenatal UFP exposure and childhood asthma remain sparse. Objectives: We used daily UFP exposure estimates to identify windows of susceptibility of prenatal UFP exposure related to asthma in children, accounting for sex-specific effects. Methods: Analyses included 376 mother-child dyads followed since pregnancy. Daily UFP exposure during pregnancy was estimated by using a spatiotemporally resolved particle number concentration prediction model. Bayesian distributed lag interaction models were used to identify windows of susceptibility for UFP exposure and examine whether effect estimates varied by sex. Incident asthma was determined at the first report of asthma (3.6 ± 3.2 yr). Covariates included maternal age, education, race, and obesity; child sex; nitrogen dioxide (NO2) and temperature averaged over gestation; and postnatal UFP exposure. Measurements and Main Results: Women were 37.8% Black and 43.9% Hispanic, with 52.9% reporting having an education at the high school level or lower; 18.4% of children developed asthma. The cumulative odds ratio (95% confidence interval) for incident asthma per doubling of the UFP exposure concentration across pregnancy was 4.28 (1.41-15.7), impacting males and females similarly. Bayesian distributed lag interaction models indicated sex differences in the windows of susceptibility, with the highest risk of asthma seen in females exposed to higher UFP concentrations during late pregnancy. Conclusions: Prenatal UFP exposure was associated with asthma development in children, independent of correlated ambient NO2 and temperature. Findings will benefit future research and policy-makers who are considering appropriate regulations to reduce the adverse effects of UFPs on child respiratory health.
Subject(s)
Air Pollutants/toxicity , Air Pollution/adverse effects , Asthma/etiology , Maternal Exposure/adverse effects , Particulate Matter/toxicity , Prenatal Exposure Delayed Effects/etiology , Adolescent , Adult , Air Pollutants/analysis , Air Pollution/analysis , Air Pollution/statistics & numerical data , Asthma/epidemiology , Bayes Theorem , Child , Child, Preschool , Female , Humans , Incidence , Infant , Logistic Models , Male , Maternal Exposure/statistics & numerical data , New England/epidemiology , Odds Ratio , Particulate Matter/analysis , Pregnancy , Prenatal Exposure Delayed Effects/epidemiology , Risk Factors , Sex Factors , Young AdultABSTRACT
BACKGROUND: Studies evaluating effects of prenatal polyunsaturated fatty acid (PUFA) intake on childhood asthma reveal mixed results. Inconsistencies may result from not accounting for important modifying factors such as maternal asthma or child sex. OBJECTIVE: To evaluate whether associations between prenatal PUFA intake and childhood asthma are modified by prenatal active maternal asthma or child sex in 412 mother-child dyads. METHODS: Energy-adjusted prenatal dietary and supplement intakes of omega-3 (n-3) and omega-6 (n-6) PUFAs were estimated using the Block98 Food Frequency Questionnaire, administered during pregnancy. Mothers reported asthma in children followed prospectively to 4.0 plus or minus 1.7 years. Generalized additive models with smooth terms for PUFA (n-3, n-6, n-6/n-3 ratio) effects were used to investigate associations between PUFAs and child asthma, without prespecifying the form of these relationships, including effect modification by active maternal asthma or child sex. RESULTS: Among mothers (40% Black, 31% Hispanic), 22% had active asthma in pregnancy; 17.5% of children developed asthma. Lower maternal n-3 PUFA intake was significantly associated with risk of childhood asthma (P = .03), in particular among children of mothers with active asthma and low n-3 PUFA intake (P = .01). This inverse association was more apparent in girls (P = .01) compared with boys (P = .30), regardless of maternal asthma status. For n-6 PUFA and the n-6/n-3 ratio, there was a lower risk of childhood asthma in the midrange of intake and increased risk at higher intake (n-6 PUFA P = .10, n-6/n-3 ratio P = .13). CONCLUSION: Consideration of factors that modify effects of prenatal PUFA intake on childhood asthma has implications for designing intervention strategies tailored to impact those at greatest risk.
Subject(s)
Asthma/pathology , Diet/adverse effects , Fatty Acids, Omega-3/administration & dosage , Fatty Acids, Omega-6/administration & dosage , Adult , Child , Child, Preschool , Fatty Acids, Unsaturated/administration & dosage , Feeding Behavior , Female , Humans , Male , Mothers , Pregnancy , Prenatal Exposure Delayed Effects , Surveys and QuestionnairesABSTRACT
Epidemiological research supports an association between maternal exposure to air pollution during pregnancy and adverse children's health outcomes. Advances in exposure assessment and statistics allow for estimation of both critical windows of vulnerability and exposure effect heterogeneity. Simultaneous estimation of windows of vulnerability and effect heterogeneity can be accomplished by fitting a distributed lag model (DLM) stratified by subgroup. However, this can provide an incomplete picture of how effects vary across subgroups because it does not allow for subgroups to have the same window but different within-window effects or to have different windows but the same within-window effect. Because the timing of some developmental processes are common across subpopulations of infants while for others the timing differs across subgroups, both scenarios are important to consider when evaluating health risks of prenatal exposures. We propose a new approach that partitions the DLM into a constrained functional predictor that estimates windows of vulnerability and a scalar effect representing the within-window effect directly. The proposed method allows for heterogeneity in only the window, only the within-window effect, or both. In a simulation study we show that a model assuming a shared component across groups results in lower bias and mean squared error for the estimated windows and effects when that component is in fact constant across groups. We apply the proposed method to estimate windows of vulnerability in the association between prenatal exposures to fine particulate matter and each of birth weight and asthma incidence, and estimate how these associations vary by sex and maternal obesity status in a Boston-area prospective pre-birth cohort study.
Subject(s)
Bayes Theorem , Child Health , Maternal Exposure , Prenatal Exposure Delayed Effects , Air Pollutants , Air Pollution , Asthma , Bias , Child , Female , Humans , Obesity , Particulate Matter , Pregnancy , Prospective StudiesABSTRACT
OBJECTIVES: To evaluate associations between maternal lifetime traumatic stress and offspring birthweight and examine modifying effects of third trimester cortisol and fetal sex. STUDY DESIGN: Analyses included 314 mother-infant dyads from an ethnically mixed pregnancy cohort. Maternal lifetime trauma was reported via the Life Stressor Checklist-Revised. Fenton birthweight for gestational age z-scores (BWGA-z) were calculated. A 3-cm scalp-nearest maternal hair segment collected at birth was assayed to reflect cumulative third trimester cortisol secretion. Multivariable regression was used to investigate associations between maternal lifetime trauma and BWGA-z and examine 2- and 3-way interactions with cortisol and fetal sex. Because subjects with low or high cortisol levels could represent susceptible populations, varying coefficient models that relax the linearity assumption on cortisol level were used to assess the modification of maternal lifetime trauma associations with BWGA-z as a function of cortisol. RESULTS: Women were primarily minorities (41% Hispanic, 26% black) with ≤12 years education (63%); 63% reported ≥1 traumatic event. Prenatal cortisol modified the association between maternal lifetime trauma and birthweight. Women with higher lifetime trauma and increased cortisol had significantly lower birthweight infants in males; among males exposed to the 90th percentile of cortisol, a 1-unit increase in trauma score was associated with a 0.19-unit decrease in BWGA-z (95% CI, -0.34 to -0.04). Associations among females were nonsignificant, regardless of cortisol level. CONCLUSIONS: These findings underscore the need to consider complex interactions among maternal trauma, disrupted in utero cortisol production, and fetal sex to fully elucidate intergenerational effects of maternal lifetime trauma.
Subject(s)
Hair/chemistry , Hydrocortisone/analysis , Mothers , Stress, Psychological/physiopathology , Adult , Birth Weight , Cohort Studies , Enzyme-Linked Immunosorbent Assay , Female , Gestational Age , Humans , Infant, Low Birth Weight , Infant, Newborn , Male , Multivariate Analysis , Pregnancy , Sex FactorsABSTRACT
BACKGROUND: In utero exposure to particulate matter with an aerodynamic diameter of less than 2.5 µm (PM2.5) has been linked to child lung function. Overlapping evidence suggests that child sex and exposure timing may modify effects and associations may be mediated through glutathione S-transferase P1 (GSTP1) methylation. METHODS: We prospectively examined associations among prenatal PM2.5 exposure and child lung function and GSTP1 methylation in an urban pregnancy cohort study. We employed a validated satellite-based spatiotemporally resolved prediction model to estimate daily prenatal PM2.5 exposure over gestation. We used Baysian distributed lag interaction models (BDLIMs) to identify sensitive windows for prenatal PM2.5 exposure on child lung function and nasal epithelia GSTP1 methylation at age 7 years, and to examine effect modification by child sex. RESULTS: BDLIMs identified a sensitive window for prenatal PM2.5 exposure at 35-40 weeks gestation [cumulative effect estimate (CEE) = - 0.10, 95%CI = - 0.19 to - 0.01, per µg/m3 increase in PM2.5] and at 36-40 weeks (CEE = - 0.12, 95%CI = - 0.20 to - 0.01) on FEV1 and FVC, respectively, in boys. BDLIMs also identified a sensitive window of exposure at 37-40 weeks gestation between higher prenatal PM2.5 exposure and increased GSTP1 percent methylation. The association between higher GSTP1 percent methylation and decreased FEV1 was borderline significant in the sample as a whole (ß = - 0.37, SE = 0.20, p = 0.06) and in boys in stratified analyses (ß = - 0.56, SE = 0.29, p = 0.05). CONCLUSIONS: Prenatal PM2.5 exposure in late pregnancy was associated with impaired early childhood lung function and hypermethylation of GSTPI in DNA isolated from nasal epithelial cells. There was a trend towards higher GSTP1 percent methylation being associated with reduced FEV1. All findings were most evident among boys.
Subject(s)
DNA Methylation/physiology , Glutathione S-Transferase pi/metabolism , Nasal Mucosa/metabolism , Particulate Matter/adverse effects , Prenatal Exposure Delayed Effects/metabolism , Sex Characteristics , Adult , Air Pollutants/adverse effects , Child , Cohort Studies , Female , Humans , Male , Particle Size , Pregnancy , Prenatal Exposure Delayed Effects/diagnosis , Prenatal Exposure Delayed Effects/physiopathology , Prospective StudiesABSTRACT
BACKGROUND: While the distribution of mosquito bed nets is a widely adopted approach for malaria prevention, studies exploring how the usage of a net may be influenced by its source and other factors remain sparse. METHODS: A standardized questionnaire and home-visit observations were used to collect data from 9 villages in Budondo sub-county, Uganda in 2016. Household- and individual-level data were collected, such as bed net ownership (at least one net versus none), acquirement source (free versus purchased), demographics, as well as knowledge of malaria and preventative measures. Net-level data, including alternative uses, and bed net quantity and integrity, were also collected. Mixed effects logistic regression models were performed to identify the key determinants of bed net use. RESULTS: Overall, the proportion of households with at least one bed net was 40%, while bed net availability was only reported among 27% of all household members. Awareness of the benefits of bed net use was statistically significantly associated with ownership of at least one net (OR = 1.72, 95% CI 1.11-2.68, p = 0.02). Among those who own net(s), the odds of a bed net being correctly used (i.e., to sleep under) after adjusting for potential confounders were significantly lower for nets that were obtained free compared to nets that were purchased by the owners themselves (OR = 0.33, 95% CI 0.21-0.51, p < 0.01), resulting in an alternative use of the net. Other factors such as female gender, children ≤ 5 years old, and pregnancy status were also significantly associated with having a net to sleep under (all p < 0.01). CONCLUSION: Understanding inter- and intra-household net-use factors will help malaria control programmes more effectively direct their efforts to increase public health impact. Future studies may additionally consider socioeconomic status and track the lifetime of the net.
Subject(s)
Health Knowledge, Attitudes, Practice , Insecticide-Treated Bednets/statistics & numerical data , Malaria/prevention & control , Mosquito Control/methods , Ownership/statistics & numerical data , Adolescent , Adult , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Insecticide-Treated Bednets/economics , Logistic Models , Male , Mosquito Control/economics , Uganda , Young AdultABSTRACT
RATIONALE: Impact of ambient pollution upon children's asthma may differ by sex, and exposure dose and timing. Psychosocial stress can also modify pollutant effects. These associations have not been examined for in utero ambient nitrate exposure. OBJECTIVES: We implemented Bayesian-distributed lag interaction models to identify sensitive prenatal windows for the influence of nitrate (NO3-) on child asthma, accounting for effect modification by sex and stress. METHODS: Analyses included 752 mother-child dyads. Daily ambient NO3- exposure during pregnancy was derived using a hybrid chemical transport (Geos-Chem)/land-use regression model and natural log transformed. Prenatal maternal stress was indexed by a negative life events score (high [>2] vs. low [≤2]). The outcome was clinician-diagnosed asthma by age 6 years. MEASUREMENTS AND MAIN RESULTS: Most mothers were Hispanic (54%) or black (29%), had a high school education or less (66%), never smoked (80%), and reported low prenatal stress (58%); 15% of children developed asthma. BDILMs adjusted for maternal age, race, education, prepregnancy obesity, atopy, and smoking status identified two sensitive windows (7-19 and 33-40 wk gestation), during which increased NO3- was associated with greater odds of asthma, specifically among boys born to mothers reporting high prenatal stress. Cumulative effects of NO3- across pregnancy were also significant in this subgroup (odds ratio = 2.64, 95% confidence interval = 1.27-5.39; per interquartile range increase in ln NO3-). CONCLUSIONS: Prenatal NO3- exposure during distinct sensitive windows was associated with incident asthma in boys concurrently exposed to high prenatal stress.
Subject(s)
Air Pollution/adverse effects , Asthma/epidemiology , Nitrates/adverse effects , Prenatal Exposure Delayed Effects/epidemiology , Stress, Psychological/epidemiology , Adult , Boston/epidemiology , Causality , Child, Preschool , Comorbidity , Female , Humans , Infant , Male , Pregnancy , Prospective Studies , Sex Factors , Young AdultABSTRACT
Evidence supports an association between maternal exposure to air pollution during pregnancy and children's health outcomes. Recent interest has focused on identifying critical windows of vulnerability. An analysis based on a distributed lag model (DLM) can yield estimates of a critical window that are different from those from an analysis that regresses the outcome on each of the 3 trimester-average exposures (TAEs). Using a simulation study, we assessed bias in estimates of critical windows obtained using 3 regression approaches: 1) 3 separate models to estimate the association with each of the 3 TAEs; 2) a single model to jointly estimate the association between the outcome and all 3 TAEs; and 3) a DLM. We used weekly fine-particulate-matter exposure data for 238 births in a birth cohort in and around Boston, Massachusetts, and a simulated outcome and time-varying exposure effect. Estimates using separate models for each TAE were biased and identified incorrect windows. This bias arose from seasonal trends in particulate matter that induced correlation between TAEs. Including all TAEs in a single model reduced bias. DLM produced unbiased estimates and added flexibility to identify windows. Analysis of body mass index z score and fat mass in the same cohort highlighted inconsistent estimates from the 3 methods.
Subject(s)
Air Pollution/adverse effects , Infant Health , Maternal Exposure/adverse effects , Particulate Matter/adverse effects , Pregnancy Outcome/epidemiology , Bias , Boston/epidemiology , Computer Simulation , Confounding Factors, Epidemiologic , Female , Humans , Infant , Linear Models , Male , Pregnancy , Pregnancy Trimesters , SeasonsABSTRACT
BACKGROUND: Air pollution exposure in childhood is associated with greater incidence and exacerbation of asthma, particularly in children whose parents report high levels of psychological stress. However, this interaction has not been completely elucidated in pregnancy. OBJECTIVE: To examine whether the association between prenatal exposure to particulate matter no larger than 2.5 µm in diameter (PM2.5) and wheeze in children is modified by prenatal stress. METHODS: Mexican women were recruited during pregnancy (N = 552). Residential prenatal daily exposure to PM2.5 was estimated using a satellite-based spatiotemporally resolved prediction model and averaged over trimesters. Maternal stress was indexed by maternal negative life events (NLE) score (range 0-11) ascertained during mid to late pregnancy. NLE scores were dichotomized at the median as low (NLE score ≤ 3) and high (NLE score > 3) stress. Reports of ever wheeze and wheeze in the past 12 months (current wheeze) for children were obtained using the International Study of Asthma and Allergies in Childhood survey at 48 months. The association between prenatal PM2.5 and wheeze was analyzed using a modified Poisson regression and stratified by low vs high stress. RESULTS: Greater PM2.5 exposure during the first trimester was associated with increased risk of current wheeze among children with mothers reporting high prenatal stress (relative risk 1.35, 95% confidence interval 1.00-1.83, per interquartile range increase 3.8 µg/m3) but not among those reporting low stress (relative risk 0.84, 95% confidence interval 0.61-1.16, per interquartile range increase 3.8 µg/m3; P for interaction = .04). CONCLUSION: Increased prenatal stress enhanced the association between PM2.5 exposure in early pregnancy, and child wheeze at 48 months of age. It is important to consider chemical and nonchemical stressors together to more comprehensively characterize children's environmental risk.
Subject(s)
Air Pollutants/analysis , Maternal Exposure , Particulate Matter/analysis , Respiratory Sounds , Stress, Psychological/epidemiology , Adult , Child, Preschool , Environmental Monitoring , Female , Humans , Infant , Infant, Newborn , Male , Mexico/epidemiology , Pregnancy , Prenatal Exposure Delayed Effects , Young AdultABSTRACT
BACKGROUND: Evolving animal studies and limited epidemiological data show that prenatal air pollution exposure is associated with childhood obesity. Timing of exposure and child sex may play an important role in these associations. We applied an innovative method to examine sex-specific sensitive prenatal windows of exposure to PM2.5 on anthropometric measures in preschool-aged children. METHODS: Analyses included 239 children born ≥ 37 weeks gestation in an ethnically-mixed lower-income urban birth cohort. Prenatal daily PM2.5 exposure was estimated using a validated satellite-based spatio-temporal model. Body mass index z-score (BMI-z), fat mass, % body fat, subscapular and triceps skinfold thickness, waist and hip circumferences and waist-to-hip ratio (WHR) were assessed at age 4.0 ± 0.7 years. Using Bayesian distributed lag interaction models (BDLIMs), we examined sex differences in sensitive windows of weekly averaged PM2.5 levels on these measures, adjusting for child age, maternal age, education, race/ethnicity, and pre-pregnancy BMI. RESULTS: Mothers were primarily Hispanic (55%) or Black (26%), had ≤ 12 years of education (66%) and never smoked (80%). Increased PM2.5 exposure 8-17 and 15-22 weeks gestation was significantly associated with increased BMI z-scores and fat mass in boys, but not in girls. Higher PM2.5 exposure 10-29 weeks gestation was significantly associated with increased WHR in girls, but not in boys. Prenatal PM2.5 was not significantly associated with other measures of body composition. Estimated cumulative effects across pregnancy, accounting for sensitive windows and within-window effects, were 0.21 (95%CI = 0.01-0.37) for BMI-z and 0.36 (95%CI = 0.12-0.68) for fat mass (kg) in boys, and 0.02 (95%CI = 0.01-0.03) for WHR in girls, all per µg/m3 increase in PM2.5. CONCLUSIONS: Increased prenatal PM2.5 exposure was more strongly associated with indices of increased whole body size in boys and with an indicator of body shape in girls. Methods to better characterize vulnerable windows may provide insight into underlying mechanisms contributing to sex-specific associations.
Subject(s)
Air Pollutants/analysis , Body Composition , Maternal Exposure , Particulate Matter/analysis , Prenatal Exposure Delayed Effects/epidemiology , Bayes Theorem , Boston/epidemiology , Child, Preschool , Cohort Studies , Female , Humans , Male , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Sex Factors , Urban Population/statistics & numerical dataABSTRACT
INTRODUCTION: While studies have suggested that exposure to manganese (Mn) may be associated with neurodevelopment in school-age children, there is limited information on prenatal and postnatal Mn exposures and tremor or motor function in children. METHODS: We measured Mn levels in dentine of shed teeth, representing prenatal, early postnatal, and cumulative childhood exposure windows, from 195 children (predominantly right-handed, 92%) in Italy. Pursuit Aiming, Luria Nebraska Motor Battery, as well as Tremor and Sway system from Computerized Adaptive Testing System (CATSYS) were administered at 11-14 years old. We examined the relationships of tooth Mn (ln-transformed) with motor function using multivariable linear regressions and generalized additive models, adjusting for age, sex, and socioeconomic status index. Effect modification by sex was also examined. RESULTS: We found that higher prenatal Mn was associated with better body stability in boys in a number of sway tests (including mean sway, transversal sway, sagittal sway, sway area, and sway intensity), while Mn was associated with poorer performance in girls on all of these metrics (all p for Mn × sex interaction < 0.05). Higher prenatal Mn was also modestly associated with better hand/finger and eye-hand coordination in boys compared to girls in sex-stratified analyses, although interaction models did not reach statistical significance. For tremor, on the other hand, higher early postnatal Mn was associated with increased right-hand center frequency in girls (p for interaction < 0.01), but increased Mn level at the later postnatal period was associated with increased center frequency in boys (p for interaction = 0.01). CONCLUSIONS: This study, which used a direct measure of prenatal and childhood Mn exposure, suggested sex-specific critical windows of early life Mn exposure in relation to neuromotor function in adolescents. The sex-specific associations might be strongest with measures of whole body stability, for which the critical exposure window was during the prenatal period.
Subject(s)
Child Development/drug effects , Environmental Exposure , Environmental Pollutants/toxicity , Manganese/toxicity , Nervous System/drug effects , Prenatal Exposure Delayed Effects/epidemiology , Adolescent , Biomarkers/chemistry , Child , Female , Humans , Italy/epidemiology , Male , Nervous System/growth & development , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Sex Factors , Tooth/chemistryABSTRACT
The ten-item Edinburgh Postnatal Depression Scale (EPDS) is one of the most widely used self-report measures of postpartum depression. Although originally described as a one-dimensional measure, the recognition that depressive symptoms may be differentially experienced across cultural and racial/ethnic groups has led to studies examining structural equivalence of the EPDS in different populations. Variation of the factor structure remains understudied across racial/ethnic groups of US women. We examined the factor structure of the EPDS assessed 6 months postpartum in 515 women (29% black, 53% Hispanic, 18% white) enrolled in an urban Boston longitudinal birth cohort. Exploratory factor analysis (EFA) identified that a three-factor model, including depression, anxiety, and anhedonia subscales, was the most optimal fit in our sample as a whole and across race/ethnicity. Confirmatory factor analysis (CFA) was used to examine the fit of both the two- and three-factor models reported in prior research. CFA confirmed the best fit for a three-factor model, with minimal differences across race/ethnicity. "Things get on top of me" loaded on the anxiety factor among Hispanics, but loaded on the depression factor in whites and African Americans. These findings suggest that EPDS factor structure may need to be adjusted for diverse samples and warrants further study.
Subject(s)
Anxiety/diagnosis , Depression, Postpartum/diagnosis , Depression/diagnosis , Ethnicity/psychology , Psychiatric Status Rating Scales , Surveys and Questionnaires , Adult , Anhedonia , Anxiety/psychology , Depression/ethnology , Depression/psychology , Depression, Postpartum/ethnology , Depression, Postpartum/psychology , Ethnicity/statistics & numerical data , Factor Analysis, Statistical , Female , Humans , Postpartum Period/psychology , Poverty , Psychometrics/instrumentation , Psychometrics/statistics & numerical data , Reproducibility of Results , Self Report , Social Class , United StatesABSTRACT
BACKGROUND: Previous studies have suggested an association between particulate air pollution and cardiovascular disease, but the mechanism is still unclear. OBJECTIVE: We examined the association between workplace exposure to vehicle-related particles and cardiovascular disease related systemic inflammatory markers, C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and interleukin-6 (IL-6) in 137 trucking terminal workers (non-drivers) in the U.S. trucking industry. METHODS: We visited two large trucking terminals in 2009 and measured vehicle-related elemental carbon (EC), organic carbon (OC), and particulate matter with aerodynamic diameter ≤2.5µm (PM2.5), for 5 days consecutively at the main work areas. Each participant provided a blood sample and completed a health questionnaire during the sampling period. Individual workplace exposure level was calculated by 12-h time weighted moving averages based on work shift. The association between each blood marker and exposure to each pollutant during 0-12, 12-24, 24-36, and 36-48h before the blood draw was examined by multivariable regression analyses. RESULTS: In general, OC and EC had a positive association with sICAM-1, especially for exposure periods 12-24 (lag12-24) and 24-36 (lag24-36)h prior to blood draw [ß=54.9 (95%CI: 12.3-97.5) for lag12-24 and ß=46.5 (95%CI: 21.2-71.8) for lag12-24; change in sICAM-1 (in ng/mL) corresponding to an IQR increase in OC]. A similar pattern was found for EC and PM2.5. We did not find an association between measured pollutants up to 48h before blood draw and hs-CRP or IL-6. CONCLUSION: In this group of healthy workers, short-term exposure to vehicle-related air pollutants may be associated with sICAM-1. Our findings may be dependent on the exposure period studied.
Subject(s)
Air Pollutants/analysis , Carbon/analysis , Intercellular Adhesion Molecule-1/blood , Motor Vehicles , Occupational Exposure/analysis , Particulate Matter/analysis , Adult , Biomarkers/blood , C-Reactive Protein/analysis , Cardiovascular Diseases/blood , Environmental Monitoring , Female , Gene-Environment Interaction , Glutathione Transferase/genetics , Humans , Interleukin-6/blood , Male , Middle Aged , Vehicle EmissionsABSTRACT
RATIONALE: The influence of particulate air pollution on respiratory health starts in utero. Fetal lung growth and structural development occurs in stages; thus, effects on postnatal respiratory disorders may differ based on timing of exposure. OBJECTIVES: We implemented an innovative method to identify sensitive windows for effects of prenatal exposure to particulate matter with a diameter less than or equal to 2.5 µm (PM2.5) on children's asthma development in an urban pregnancy cohort. METHODS: Analyses included 736 full-term (≥37 wk) children. Each mother's daily PM2.5 exposure was estimated over gestation using a validated satellite-based spatiotemporal resolved model. Using distributed lag models, we examined associations between weekly averaged PM2.5 levels over pregnancy and physician-diagnosed asthma in children by age 6 years. Effect modification by sex was also examined. MEASUREMENTS AND MAIN RESULTS: Most mothers were ethnic minorities (54% Hispanic, 30% black), had 12 or fewer years of education (66%), and did not smoke in pregnancy (80%). In the sample as a whole, distributed lag models adjusting for child age, sex, and maternal factors (education, race and ethnicity, smoking, stress, atopy, prepregnancy obesity) showed that increased PM2.5 exposure levels at 16-25 weeks gestation were significantly associated with early childhood asthma development. An interaction between PM2.5 and sex was significant (P = 0.01) with sex-stratified analyses showing that the association exists only for boys. CONCLUSIONS: Higher prenatal PM2.5 exposure at midgestation was associated with asthma development by age 6 years in boys. Methods to better characterize vulnerable windows may provide insight into underlying mechanisms.
Subject(s)
Air Pollution/statistics & numerical data , Asthma/epidemiology , Maternal Exposure/statistics & numerical data , Particulate Matter/analysis , Prenatal Exposure Delayed Effects/epidemiology , Urban Health/statistics & numerical data , Adult , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Pregnancy , Risk Factors , Sex Factors , United States/epidemiology , Urban Population/statistics & numerical dataABSTRACT
BACKGROUND: Prenatal traffic-related air pollution exposure is linked to adverse birth outcomes. However, modifying effects of maternal body mass index (BMI) and infant sex remain virtually unexplored. OBJECTIVES: We examined whether associations between prenatal air pollution and birth weight differed by sex and maternal BMI in 670 urban ethnically mixed mother-child pairs. METHODS: Black carbon (BC) levels were estimated using a validated spatio-temporal land-use regression (LUR) model; fine particulate matter (PM2.5) was estimated using a hybrid LUR model incorporating satellite-derived Aerosol Optical Depth measures. Using stratified multivariable-adjusted regression analyses, we examined whether associations between prenatal air pollution and calculated birth weight for gestational age (BWGA) z-scores varied by sex and maternal pre-pregnancy BMI. RESULTS: Median birth weight was 3.3±0.6kg; 33% of mothers were obese (BMI ≥30kg/m(3)). In stratified analyses, the association between higher PM2.5 and lower birth weight was significant in males of obese mothers (-0.42 unit of BWGA z-score change per IQR increase in PM2.5, 95%CI: -0.79 to -0.06) ( PM2.5×sex×obesity Pinteraction=0.02). Results were similar for BC models (Pinteraction=0.002). CONCLUSIONS: Associations of prenatal exposure to traffic-related air pollution and reduced birth weight were most evident in males born to obese mothers.
Subject(s)
Air Pollutants/analysis , Birth Weight/drug effects , Maternal Exposure , Pregnancy Outcome/epidemiology , Vehicle Emissions/analysis , Adolescent , Adult , Body Mass Index , Boston/epidemiology , Environmental Monitoring , Female , Humans , Infant, Newborn , Male , Multivariate Analysis , Particulate Matter/analysis , Pregnancy , Sex Characteristics , Soot/analysis , Young AdultABSTRACT
BACKGROUND: Prenatal exposures to stress and physical toxins influence children's respiratory health, although few studies consider these factors together. OBJECTIVES: We sought to concurrently examine the effects of prenatal community-level psychosocial (exposure to community violence [ECV]) and physical (air pollution) stressors on repeated wheeze in 708 urban children followed to age 2 years. METHODS: Multi-item ECV reported by mothers in pregnancy was summarized into a continuous score by using Rasch modeling. Prenatal black carbon exposure was estimated by using land-use regression (LUR) modeling; particulate matter with a diameter of less than 2.5 µm (PM2.5) was estimated by using LUR modeling incorporating satellite data. Mothers reported child's wheeze every 3 months. The effects of ECV and air pollutants on repeated wheeze (≥ 2 episodes) were examined by using logistic regression. Interactions between ECV and pollutants were examined. RESULTS: Mothers were primarily black (29%) and Hispanic (55%), with lower education (62% with ≤ 12 years); 87 (12%) children wheezed repeatedly. In models examining concurrent exposures, ECV (odds ratio [OR], 1.95; 95% CI, 1.13-3.36; highest vs lowest tertile) and black carbon (OR, 1.84; 95% CI, 1.08-3.12; median or greater vs less than median) were independently associated with wheeze adjusting for sex, birth season, maternal atopy, education, race, and cockroach antigen. Associations were similar for PM2.5 (adjusted OR, 2.02; 95% CI, 1.20-3.40). An interaction between ECV with air pollution levels was suggested. CONCLUSIONS: These findings suggest that both prenatal community violence and air pollution can contribute to respiratory health in these urban children. Moreover, place-based psychosocial stressors might affect host resistance such that physical pollutants can have adverse effects, even at relatively lower levels.
Subject(s)
Air Pollution/adverse effects , Maternal Exposure/adverse effects , Respiratory Sounds/etiology , Violence , Child , Female , Humans , Male , Pregnancy , Stress, Psychological/complications , Urban PopulationABSTRACT
RATIONALE: Exploring prenatal factors influencing childhood wheeze may inform programming mechanisms. OBJECTIVES: We examined associations among prenatal maternal cortisol profiles, maternal obesity, and repeated wheeze up to age 2 years (n = 261). METHODS: Salivary cortisol was collected five times per day over 3 days at 29.0 ± 4.9 weeks gestation. Mothers were categorized as obese (body mass index ≥ 30 kg/m(2)) versus nonobese (body mass index < 30 kg/m(2)). Using logistic regression, we examined the influence of log-transformed cortisol metrics (level at each time point, morning rise, diurnal and afternoon slopes) and obesity on wheeze adjusting for covariates. Linear mixed models were implemented to examine associations between cortisol trajectories and wheezing. Interactions between maternal cortisol and obesity were considered. MEASUREMENTS AND MAIN RESULTS: Mothers were primarily minority (56.5% Hispanic, 24.1% African American), 61% had less than or equal to 12 years of education, 34% were obese, and 8.4% of children had repeated wheeze. An interquartile range increase in mean log cortisol at bedtime (odds ratio, 2.2; 95% confidence interval, 1.09-4.09) and maternal obesity (odds ratio, 3.43; 95% confidence interval, 1.26-9.35) were independently associated with wheeze. Linear mixed models revealed an association between a flatter afternoon slope (slower decline in log cortisol per hour) and repeated wheeze in children of obese mothers (children with [-0.017 change] and without [-0.061 change] wheeze [P = 0.009 for time × wheeze interaction]), but not in children of nonobese mothers (with [-0.050 change] and without [-0.061 change] wheeze [P = 0.51]). CONCLUSIONS: Maternal prenatal cortisol disruption and obesity were independently associated with children's wheeze. Obese women with adverse cortisol profiles were most likely to have children with repeated wheeze.