Severe maternal morbidity associated with endometriosis: a population-based, retrospective cohort study.

OBJECTIVE: To evaluate the association between endometriosis and the risk of severe maternal morbidity (SMM) as defined by the Centers for Disease Control and Prevention. DESIGN: This was a population-based, retrospective cohort study using the California Office of Statewide Health Planning and Development Linked Birth File with hospital discharge International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) diagnoses between 2007 and 2012. SETTING: Population-based. PATIENT(S): A total of 3,098,578 pregnancies from 2007 to 2012. INTERVENTION(S): Prior diagnosis of endometriosis identified using the ICD-9-CM codes 617.0-617.9. MAIN OUTCOME MEASURE(S): The primary outcome of interest was SMM, which was defined as having been diagnosed with any of the ICD-9-CM codes corresponding to 25 peripartum conditions listed by the Centers for Disease Control and Prevention. The secondary outcomes of interest were each individual condition. RESULT(S): Of the 3,098,578 pregnancies analyzed, 2,910 pregnancies were among women with a prior diagnosis of endometriosis. There were 45,655 pregnancies complicated by at least 1 SMM; 158 pregnancies (54.3 per 1,000 pregnancies) were in women with endometriosis and 45,497 (14.7 per 1,000 pregnancies) were in women without endometriosis. Women with pregnancies complicated by endometriosis were 2.41 times more likely to develop SMM than women who did not have endometriosis (adjusted odds ratio [aOR], 2.41; 95% confidence interval [CI], 2.03-2.87). There was an increased risk of disseminated intravascular coagulation (aOR, 2.46; 95% CI, 1.65-3.66), heart failure during a procedure or surgery (aOR, 2.58; 95% CI, 1.69-3.94), pulmonary edema (aOR, 3.02; 95% CI, 1.11-8.17), blood transfusion (aOR, 2.17; 95% CI, 1.75-2.68), and hysterectomy (aOR, 2.46; 95% CI, 1.58-3.85). When the association was stratified by delivery mode, the risk of SMM was higher for vaginal delivery (aOR, 4.59; 95% CI, 2.73-7.71) than for cesarean delivery (aOR, 1.64; 95% CI, 1.37-1.97) (P-interaction<.0001). CONCLUSION(S): This study demonstrated that endometriosis is a major risk factor for SMM, especially among those who deliver vaginally. Furthermore, precautions should be taken before delivery in anticipation of potential complications.

Outcomes of labor induction at 39 weeks in pregnancies with a prior cesarean delivery.

BACKGROUND: The optimal timing of induction for those undergoing a trial of labor after cesarean section has not been established. The little data which supports the consideration of induction at 39 weeks gestation excludes those with a history of prior cesarean section. OBJECTIVE: To determine the risks and benefits of elective induction of labor (IOL) at 39 weeks compared with expectant management (EM) until 42 weeks in pregnancies complicated by one previous cesarean delivery. STUDY DESIGN: This is a retrospective cohort analysis of singleton non-anomalous pregnancies in the United States between January 2015 and December 2017. Data was provided by the CDC National Center for Health Statistics, Division of Vital Statistics. Analyses included only pregnancies with a history of one previous cesarean delivery (CD). Perinatal outcomes of pregnancies electively induced at 39 weeks (IOL) were compared to pregnancies that were induced, augmented or underwent spontaneous labor between 40 and 42 weeks (EM). Unlabored cesarean deliveries were excluded. Outcomes of interest included: cesarean delivery, intra-amniotic infection, blood transfusion, adult intensive care unit (ICU) admission, uterine rupture, hysterectomy, 5-minute Apgar score ≤3, prolonged neonatal ventilation, neonatal ICU (NICU) admission, neonatal seizure, perinatal/neonatal death. Log-binomial regression analysis was performed to calculate the relative risk (RR) for each outcome of interest, adjusting for confounding variables. RESULTS: There were 50,136 pregnancies included for analysis with 9,381 women in the IOL group. Compared with EM, IOL at 39 weeks decreased the risk of intra-amniotic infection (1.7% vs 3.0%, p < .001; aRR: 0.58, 95% CI: [0.49-0.68]), blood transfusion (0.3% vs. 0.5%, p = .03; aRR: 0.66, 95% CI: [0.45-0.98]), and low 5-minute Apgar score (0.31% vs 0.47%, p = .031; aRR: 0.66, 95% CI: [0.44-0.97]). Conversely, IOL increased the risk of cesarean delivery (49.0% vs 27.6%, p < .001; aRR: 1.72, 95% CI: [1.68-1.77]). Furthermore, in the EM group, 919 pregnancies developed preeclampsia and 42 progressed to eclampsia. There were no differences in other perinatal outcomes. CONCLUSION: In pregnancies complicated by one previous cesarean delivery, elective induction of labor at 39 weeks reduced the risk of intra-amniotic infection, blood transfusion, and low 5-minute Apgar score while increased the risk of repeat cesarean delivery.

The joint effects of obesity and pregestational diabetes on the risk of stillbirth.

Objective: Obesity and pregestational diabetes (PGDM) may interact to further increase the risk of stillbirth than either risk factors independently. The objective of this study was to determine the risk of stillbirth in pregnancies complicated by both conditions.Method: This was a retrospective cohort analysis of singleton nonanomalous births using the updated Texas vital records database between 2006 and 2014. Gestational diabetes and hypertensive diseases were additionally excluded from analysis. Analysis was stratified into 10 strata based on BMI class: underweight, normal weight, overweight, obese and morbidly obese, and PGDM. Furthermore, gestational age was stratified into the four periods for analysis: 24-33, 34-36, 37-39, and 40-42 weeks. The rate of stillbirth per 10,000 pregnancies were calculated for each stratum. The risks of stillbirth associated with each BMI class and PGDM were compared to normal weight nondiabetic pregnancies for each gestational period using proportional hazard regression models.Result: After all exclusions, 3,097,123 births remained for analysis, including 5997 stillbirths. The overall rate of stillbirth increased from 15.0 per 10,000 pregnancies in normal weight pregnancies to 26.7 per 10,000 pregnancies in the morbidly obese group. The rate of stillbirth further increased with coexistence of PGDM to 119.9 per 10,000 pregnancies in the normal weight group and 209.8 per 10,000 pregnancies in the morbidly obese group. Compared to normal weight nondiabetic pregnancies the overall adjusted hazard ratio (aHR) of stillbirth associated with morbid obesity without PGDM was 1.57 [1.38, 1.79]. However, when further complicated by PGDM, the aHR was 6.67 [5.05, 8.81] in normal weight pregnancies and 12.86 [9.36, 17.67] in morbidly obese pregnancies. The highest risk of stillbirth was seen between 37 and 39 weeks, when the aHR in the diabetic normal weight group was 9.63 [5.65, 16.40] and the aHR in the diabetic morbidly obese group was 25.34 [15.58, 41.22].Conclusion: PGDM and obesity both independently increased the risk of stillbirth. The joint effect of obesity and PGDM is stronger than the summation or multiplication of the individual effects of each risk factor.

The association between maternal lipid profile after birth and offspring risk of autism spectrum disorder.

PURPOSE: Maternal obesity has been consistently associated with offspring risk for ASD, as well as lipid metabolism derangements. However, few ASD studies have examined maternal lipids in conjunction with maternal prepregnancy body mass index (BMI). METHODS: This nested case-control study was based on the Boston Birth Cohort, a prospective cohort study of mother-child dyads recruited at the Boston Medical Center. Maternal blood samples were collected shortly after delivery and analyzed for total plasma cholesterol, HDL, and triglyceride (TG) concentrations. Low-density lipoprotein (LDL) was subsequently calculated by the Friedewald equation. Cases were identified using ASD diagnoses in children's medical records. The odds of ASD were estimated with continuous lipid levels for a linear relationship, and we further explored the nonlinear relationship using the tertile of each lipid analyte with the highest tertile as the reference group. Logistic regression was used to estimate the risk of ASD adjusting for potential confounders. The analyses were performed separately for mothers with normal weight and overweight/obese based on maternal prepregnancy BMI. RESULTS: One standard deviation decrease in postpartum maternal LDL was associated with increased odds of ASD aOR 1.35 [1.04-1.75]. There was no association between postpartum maternal HDL and TG levels and ASD risk. Decreasing levels of LDL were not associated with ASD risk in normal-weight mothers (aOR 1.2 [0.83-1.75]), but the ASD risk was more pronounced in overweight and obese mothers (aOR 1.54 [1.03-2.27]). Follow-up analysis of nonlinear association models showed that, when compared to the highest tertile, lower maternal LDL concentrations were associated with approximately two times increased risk of ASD (first tertile: aOR 2.49 [1.27-4.87] and second tertile: aOR 2.79 [1.42-5.48]). A similar pattern was observed with overweight/obese mothers but not in normal-weight mothers. CONCLUSIONS: Lower maternal postpartum plasma LDL concentration was associated with increased odds of ASD in offspring among children born to overweight and obese mothers. Our findings suggest that both maternal BMI and lipids should be considered in assessing their role in offspring ASD risk, and additional longitudinal studies are needed to better understand maternal lipid dynamics during pregnancy among normal-weight and overweight/obese mothers.

Meconium androgens are correlated with ASD-related phenotypic traits in early childhood in a familial enriched risk cohort.

BACKGROUND: Prenatal exposure to increased androgens has been suggested as a risk factor for autism spectrum disorder (ASD). This hypothesis has been examined by measurement of steroids in amniotic fluid, cord blood, saliva, and blood with mixed results. METHODS: To provide an orthogonal measure of fetal exposure, this study used meconium, the first stool of a newborn, to measure prenatal androgen exposure from infants in the Early Autism Risk Longitudinal Investigation (EARLI). EARLI is a familial-enriched risk cohort that enrolled pregnant mothers who already had a child with an ASD diagnosis. In the younger child, we investigated the association between meconium unconjugated (u) and total (t) concentrations of major androgens testosterone (T), dehydroepiandrosterone (DHEA), and androstenedione (A4), and ASD-related traits at 12 and 36 months of age. Traits were measured at 12 months with Autism Observation Scale for Infants (AOSI) and at 36 months with total score on the Social Responsiveness Scale (SRS). One hundred and seventy children had meconium and AOSI, 140 had meconium and SRS, and 137 had meconium and both AOSI and SRS. RESULTS: Separate robust linear regressions between each of the log-transformed androgens and log-transformed SRS scores revealed three-way interaction between sex of the child, sex of the proband, and testosterone concentration. In the adjusted analyses, t-T, u-A4, and u-DHEA (P ≤ 0.01) were positively associated with AOSI scores, while u-T (P = 0.004) and u-DHEA (P = 0.007) were positively associated with SRS total score among females with female probands (n = 10). Additionally, higher concentrations of u-T (P = 0.01) and t-T (P = 0.01) predicted higher SRS total score in males with male probands (n = 63). Limitations Since we explored three-way interactions, this resulted in a limited sample size for some analyses. This study was from an enriched-risk cohort which may limit generalizability, and this study used ASD-assessment scales as outcomes instead of diagnostic categories. Additionally, the novel use of meconium in this study limits the ability to compare the results in this cohort to others due to the paucity of research on meconium. CONCLUSIONS: This study supports the utility of meconium for studies of endogenous fetal metabolism and suggests the sex of older siblings with autism should be considered as a biological variable in relevant studies.

A meta-analysis of two high-risk prospective cohort studies reveals autism-specific transcriptional changes to chromatin, autoimmune, and environmental response genes in umbilical cord blood.

Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder that affects more than 1% of children in the USA. ASD risk is thought to arise from both genetic and environmental factors, with the perinatal period as a critical window. Understanding early transcriptional changes in ASD would assist in clarifying disease pathogenesis and identifying biomarkers. However, little is known about umbilical cord blood gene expression profiles in babies later diagnosed with ASD compared to non-typically developing and non-ASD (Non-TD) or typically developing (TD) children. Methods: Genome-wide transcript levels were measured by Affymetrix Human Gene 2.0 array in RNA from cord blood samples from both the Markers of Autism Risk in Babies-Learning Early Signs (MARBLES) and the Early Autism Risk Longitudinal Investigation (EARLI) high-risk pregnancy cohorts that enroll younger siblings of a child previously diagnosed with ASD. Younger siblings were diagnosed based on assessments at 36 months, and 59 ASD, 92 Non-TD, and 120 TD subjects were included. Using both differential expression analysis and weighted gene correlation network analysis, gene expression between ASD and TD, and between Non-TD and TD, was compared within each study and via meta-analysis. Results: While cord blood gene expression differences comparing either ASD or Non-TD to TD did not reach genome-wide significance, 172 genes were nominally differentially expressed between ASD and TD cord blood (log2(fold change) > 0.1, p < 0.01). These genes were significantly enriched for functions in xenobiotic metabolism, chromatin regulation, and systemic lupus erythematosus (FDR q < 0.05). In contrast, 66 genes were nominally differentially expressed between Non-TD and TD, including 8 genes that were also differentially expressed in ASD. Gene coexpression modules were significantly correlated with demographic factors and cell type proportions. Limitations: ASD-associated gene expression differences identified in this study are subtle, as cord blood is not the main affected tissue, it is composed of many cell types, and ASD is a heterogeneous disorder. Conclusions: This is the first study to identify gene expression differences in cord blood specific to ASD through a meta-analysis across two prospective pregnancy cohorts. The enriched gene pathways support involvement of environmental, immune, and epigenetic mechanisms in ASD etiology.

Placental gross shape differences in a high autism risk cohort and the general population.

A growing body of evidence suggests that prenatal environment is important in Autism Spectrum Disorder (ASD) etiology. In this study, we compare placental shape features in younger siblings of children with ASD, who themselves are at high ASD risk, to a sample of low risk peers. Digital photographs of the fetal placenta surface and of the sliced placental disk from 129 high ASD risk newborns and from 267 newborns in the National Children's Study Vanguard pilot were analysed to extract comparable measures of placental chorionic surface shape, umbilical cord displacement and disk thickness. Placental thickness measures were moderately higher in siblings of ASD cases. The placentas of ASD-case siblings were also rounder and more regular in perimeter than general population placentas. After stratification by sex, these across-group differences persisted for both sexes but were more pronounced in females. No significant differences were observed in cord insertion measures. Variations in placental shape features are generally considered to reflect flexibility in placental growth in response to changes in intrauterine environment as the placenta establishes and matures. Reduced placental shape variability observed in high ASD risk siblings compared to low-risk controls may indicate restricted ability to compensate for intrauterine changes.

The association between gestational weight gain and risk of stillbirth: a population-based cohort study.

PURPOSE: To estimate the risk of stillbirth associated with excessive and inadequate weight gain during pregnancy. METHODS: Retrospective cohort study using the Texas vital records database between 2006 and 2011, with 2,230,310 births (5502 stillbirths) was included for analysis. Pregnancies were categorized as adequate weight gain, excessive weight gain, inadequate weight gain, or weight loss based on the Institute of Medicine 2009 recommendations. Hazard ratios (HRs) for stillbirth were estimated for each gestational weight-gain stratum using adequate weight gain as the comparison group. The analysis was performed separately for each body mass index (BMI) class. RESULTS: Both inadequate weight gain and weight loss were associated with an increased risk of stillbirth for all BMI classes except the morbidly obese group. Highest risk was seen in weight-loss groups after 36 completed weeks (normal weight: HR = 18.85 [8.25-43.09]; overweight: HR = 5.87 [2.99-11.55]; obese: HR = 3.44 [2.34-5.05]). Weight loss was associated with reduced stillbirth risk in morbidly obese women between 24 and 28 weeks (HR = 0.56 [0.34-0.95]). Excess weight gain was associated with an increased risk of stillbirth among obese and morbidly obese women, with highest risk after 36 completed weeks (obese: HR = 2.00 [1.55-2.58]; morbidly obese: HR = 3.16 [2.17-4.62]). In contrast, excess weight gain was associated with reduced risk of stillbirth in normal-weight women between 24 and 28 weeks (HR = 0.57 [0.44-0.70]) and in overweight women between 29 and 33 weeks (HR = 0.62 [0.45-0.85]). Analysis for the underweight group was limited by sample size. Both excessive weight gain and inadequate weight gain were not associated with stillbirth in this group. CONCLUSIONS: Stillbirth risk increased with inadequate weight gain and weight loss in all BMI classes except the morbidly obese group, where weight demonstrated a protective effect. Conversely, excessive weight gain was associated with higher risk of stillbirth among obese and morbidly obese women but was protective against stillbirth in lower weight women.

Umbilical cord blood androgen levels and ASD-related phenotypes at 12 and 36 months in an enriched risk cohort study.

BACKGROUND: Autism spectrum disorder (ASD) affects more than 1% of children in the USA. The male-to-female prevalence ratio of roughly 4:1 in ASD is a well-recognized but poorly understood phenomenon. An explicit focus on potential etiologic pathways consistent with this sex difference, such as those involving prenatal androgen exposure, may help elucidate causes of ASD. Furthermore, the multi-threshold liability model suggests that the genetic mechanisms in females with ASD may be distinct and may modulate ASD risk in families with female ASD in the pedigree. METHODS: We examined umbilical cord blood from 137 children in the Early Autism Risk Longitudinal Investigation (EARLI) cohort. EARLI is an ASD-enriched risk cohort with all children having an older sibling already diagnosed with ASD. Fetal testosterone (T), androstenedione (A4), and dehyroepiandrosterone (DHEA) levels were measured in cord blood using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Robust linear regression models were used to determine associations between cord blood androgen levels and 12-month Autism Observation Scales for Infants (AOSI) scores and 36-month Social Responsiveness Scale (SRS) scores adjusting for potential confounders. RESULTS: Increasing androgens were not associated with increasing 12-month AOSI score or 36-month total SRS score in either boys or girls. However, the association between T and autistic traits among subjects with a female older affected sibling was greater at 12 months (test of interaction, P = 0.008) and deficits in reciprocal social behavior at 36 months were also greater (test of interaction, P = 0.006) than in subjects whose older affected sibling was male. CONCLUSIONS: While increased prenatal testosterone levels were not associated with autistic traits at 12 or 36 months, our findings of a positive association in infants whose older ASD-affected siblings were female suggests an androgen-related mechanism that may be dependent on, or related to, genetic liability factors present more often in families containing female ASD cases. However, this initial finding, based on a small subgroup of our sample, should be interpreted with considerable caution.

The Changing Epidemiology of Autism Spectrum Disorders.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with lifelong impacts. Genetic and environmental factors contribute to ASD etiology, which remains incompletely understood. Research on ASD epidemiology has made significant advances in the past decade. Current prevalence is estimated to be at least 1.5% in developed countries, with recent increases primarily among those without comorbid intellectual disability. Genetic studies have identified a number of rare de novo mutations and gained footing in the areas of polygenic risk, epigenetics, and gene-by-environment interaction. Epidemiologic investigations focused on nongenetic factors have established advanced parental age and preterm birth as ASD risk factors, indicated that prenatal exposure to air pollution and short interpregnancy interval are potential risk factors, and suggested the need for further exploration of certain prenatal nutrients, metabolic conditions, and exposure to endocrine-disrupting chemicals. We discuss future challenges and goals for ASD epidemiology as well as public health implications.

Differences in testosterone and its precursors by sex of the offspring in meconium.

Prenatal metabolism exerts profound effects on development. The first stool of the newborn, meconium, provides a window into the prenatal metabolic environment. The objective of this study was to examine the feasibility of meconium as a novel matrix to quantify prenatal steroid levels. We quantified parameters of analytical interest regarding the use of meconium, including sample stability. We hypothesized that meconium steroid content would differ by sex, prompting analysis of meconium to test effects of prenatal steroid metabolism. Meconium from 193 newborns enrolled in the Early Autism Risk Longitudinal Investigation (EARLI) study, including 107 males, and 86 females, were analyzed by isotope dilution-liquid chromatography-high resolution mass spectrometry (ID-LC-HRMS) while blinded to identity for testosterone (T), androstenedione (AD), and dehydroepiandrosterone (DHEA). Steroid levels were compared by sex, and investigations of potential trends resulting from sample storage or processing was conducted. The unconjugated steroid content of meconium in ng/g (mean, standard deviation) was for males: T (2.67, 8.99), AD (20.01, 28.12), DHEA (13.96, 23.57) and for females: T (0.82, 1.63), AD (22.32, 24.38), DHEA (21.06, 43.49). T was higher in meconium from males (p=0.0333), and DHEA was higher in meconium from females (p=0.0202). 6 female and 3 male T values were below the limit of detection. No extreme variability in hydration or trend in steroid levels by storage time was detected. Sexually dimorphic levels of hormones may reflect gestational differentiation, and future studies should consider meconium analysis.

The effects of maternal obesity on perinatal outcomes among those born small for gestational age.

BACKGROUND: Maternal obesity has been associated with higher birth weight. Small for gestational age (SGA) neonates born to obese women may be associated with pathological growth with increased neonatal complications. METHODS: This was a retrospective cohort study of all non-anomalous singleton neonates born in Texas from 2006-2011. Analyses were limited to births between 34 and 42 weeks gestation with birth weight ≤10th percentile. Results were stratified by maternal pre-pregnancy BMI class. The risk for stillbirth, neonatal death, neonatal intensive care unit (NICU) admission and five minute Apgar scores <7 were estimated for each obesity class and compared to the normal weight group. Multivariable logistic regression analyses were performed to control for potential confounding variables. RESULTS: The rate of stillbirth was 1.4/1000 births for normal weight women, and 2.9/1000 among obese women (p < 0.001, aOR: 1.83 [1.43, 2.34]). The rate of neonatal deaths among normal weight women was 4.3/1000 births, whereas among obese women it was 4.7/1000 (p = 0.94, aOR: 1.10 [0.92, 1.30]). A dose-dependent relationship between maternal obesity and stillbirths was seen, but not for other neonatal outcomes. CONCLUSION: Among SGA neonates, maternal pre-pregnancy obesity was associated with increased risks for stillbirth, NICU admission and low Apgar scores but not neonatal death.

Use of meconium in perinatal epidemiology: potential benefits and pitfalls.

PURPOSE: Meconium is a biomarker matrix that can be used to assess cumulative exposures in epidemiologic studies of prenatal risk factors. Depending on when meconium is collected, different exposure windows during pregnancy can be measured. However, little guidance exists regarding the extent to which timing of meconium collection will influence resulting effect estimates. METHODS: We performed a simulation study of prenatal tobacco smoke exposure (assessed from meconium nicotine) and birth weight. We discuss four typical meconium collection methods capturing different exposure windows and assess the biases induced by these methods. RESULTS: In simulations assuming that exposure to tobacco smoke only during late gestation was of etiologic relevance to birth weight, use of a meconium collection method that captured exposure windows other than late gestation resulted in biased estimates of the true nicotine-birth weight association. CONCLUSIONS: Using meconium collection methods that do not reflect an exposure window of etiologic relevance can lead to biased results and erroneous conclusions regarding the nature of prenatal exposure-outcome associations. Understanding how prenatal exposure patterns vary across the pregnancy and exposure windows of etiologic relevance is essential in determining when and how to collect meconium for use in biomarker studies of prenatal exposure.

Obesity and the risk of stillbirth: a population-based cohort study.

OBJECTIVE: Obesity is a known risk factor for stillbirth. However, this relationship has not been characterized fully. We attempted to further examine this relationship with a focus on delivery near and at term. STUDY DESIGN: We designed a retrospective cohort study of singleton nonanomalous live births and stillbirths in the states of Washington and Texas to examine the associations of maternal prepregnancy body mass index (BMI) and risk of stillbirth. Confounder-adjusted hazard ratio of stillbirth in relation to BMI was estimated through Cox proportional hazards regression model. The hazard ratio was used to estimate the population-attributable risk. We also estimated the fetuses who were at risk for stillbirth based on gestational age. RESULTS: Among 2,868,482 singleton births, the overall stillbirth risk was 3.1 per 1000 births (n = 9030). Compared with normal-weight women, the hazard ratio for stillbirth was 1.36 for overweight women, 1.71 for class I obese women, 2.00 for class II obese women, 2.48 for class III obese women, and 3.16 for women with a BMI of ≥50 kg/m(2). The fetuses who are at risk for stillbirth increased after 39 weeks' gestation for each obesity class; however, the risk increased more rapidly with increasing BMI. Women with a BMI of ≥50 kg/m(2) were at 5.7 times greater risk than normal weight women at 39 weeks' gestation and 13.6 times greater at 41 weeks' gestation. Obesity was associated with nearly 25% of stillbirth that occurred between 37 and 42 weeks' gestation. CONCLUSION: There is a pronounced increase in the risk of stillbirth with increasing BMI; the association is strongest at early- and late-term gestation periods. Extreme maternal obesity is a significant risk factor for stillbirth.

World Trade Center disaster: assessment of responder occupations, work locations, and job tasks.

BACKGROUND: To date there have been no comprehensive reports of the work performedby 9/11 World Trade Center responders. METHODS: 18,969 responders enrolled in the WTC Medical Monitoring and Treatment Program were used to describe workers' pre-9/11 occupations, WTC work activities and locations from September 11, 2001 to June 2002. RESULTS: The most common pre-9/11 occupation was protective services (47%); other common occupations included construction, telecommunications, transportation, and support services workers. 14% served as volunteers. Almost one-half began work on 9/11 and >80% reported working on or adjacent to the ''pile'' at Ground Zero. Initially,the most common activity was search and rescue but subsequently, the activities of most responders related to their pre-9/11 occupations. Other major activities included security; personnel support; buildings and grounds cleaning; and telecommunications repair. CONCLUSIONS: The spatial, temporal, occupational, and task-related taxonomy reported here will aid the development of a job-exposure matrix, assist in assessment of disease risk, and improve planning and training for responders in future urban disasters.