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Neurodevelopmental regression (NDR) is an enigmatic event associated with autism spectrum disorder (ASD) during which a child loses previously acquired skills and develops ASD symptoms. In some, a trigger which precedes the NDR event, such as a fever, can be identified, but in many cases no trigger is obvious. We hypothesize that air pollution (PM2.5) may trigger NDR, especially in those children without an identified trigger. Average daily PM2.5, ozone, precipitation and maximum temperature (Tmax) were derived from Environmental Protection Agency models and National Oceanic and Atmospheric Administration monitors based on zip-code information from 83 ASD participants during the six-weeks following the onset month of an NDR event and a reference period defined as one year before and one year after the event. Seasonally adjusted logistic regression (LR) and linear mixed models (LMM) compared cases (with a history of NDR) and matched controls (without a history of NDR). LR models found that the risk of NDR was related to higher PM2.5 during 3 to 6 weeks of the NDR event period, particularly in those without a trigger. Overall, both models converged on NDR being related to a higher PM2.5 and lower Tmax both during the NDR event period as well as the reference period, particularly in those without a known trigger. This temporal pattern suggests that environmental triggers, particularly PM2.5, could be related to NDR, especially in those without an identifiable trigger. Further studies to determine the underlying biological mechanism of this observation could help better understand NDR and provide opportunities to prevent NDR.

In recent years, there has been growing interest in developing air pollution prediction models to reduce exposure measurement error in epidemiologic studies. However, efforts for localized, fine-scale prediction models have been predominantly focused in the United States and Europe. Furthermore, the availability of new satellite instruments such as the TROPOsopheric Monitoring Instrument (TROPOMI) provides novel opportunities for modeling efforts. We estimated daily ground-level nitrogen dioxide (NO2) concentrations in the Mexico City Metropolitan Area at 1-km2 grids from 2005 to 2019 using a four-stage approach. In stage 1 (imputation stage), we imputed missing satellite NO2 column measurements from the Ozone Monitoring Instrument (OMI) and TROPOMI using the random forest (RF) approach. In stage 2 (calibration stage), we calibrated the association of column NO2 to ground-level NO2 using ground monitors and meteorological features using RF and extreme gradient boosting (XGBoost) models. In stage 3 (prediction stage), we predicted the stage 2 model over each 1-km2 grid in our study area, then ensembled the results using a generalized additive model (GAM). In stage 4 (residual stage), we used XGBoost to model the local component at the 200-m2 scale. The cross-validated R2 of the RF and XGBoost models in stage 2 were 0.75 and 0.86 respectively, and 0.87 for the ensembled GAM. Cross-validated root-mean-squared error (RMSE) of the GAM was 3.95 μg/m3. Using novel approaches and newly available remote sensing data, our multi-stage model presented high cross-validated fits and reconstructs fine-scale NO2 estimates for further epidemiologic studies in Mexico City.

To examine the association between exposure to radiation from computed tomography (CT) studies and the incidence of cataract. In a nested case–control study, all cataract cases and their matched controls were sampled from a retrospective cohort of Israeli residents who underwent CT scans or ultrasonic tests in Soroka Medical Center, Beer-Sheva, Israel, between the years 1996 and 2014. The risk of cataract associated with head, neck or the rest of the body CT was assessed using Poisson survival analysis. The nested matched sample included 3841 cataract cases and their age- and sex-matched controls (n = 228,743). CT radiation exposure was more frequent in the cataract group, with 9.7% head CT, 1.2% neck CT and 6.6% other CT, compared to 5%, 0.7% and 3.7% among person-years without cataract (p

Type 2 diabetes is a major public health concern. Several studies have found an increased diabetes risk associated with long-term air pollution exposure. However, most current studies are limited in their generalizability, exposure assessment, or the ability to differentiate incidence and prevalence cases. We assessed the association between air pollution and first documented diabetes occurrence in a national U.S. cohort of older adults to estimate diabetes risk. We included all Medicare enrollees 65 years and older in the fee-for-service program, part A and part B, in the contiguous United States (2000–2016). Participants were followed annually until the first recorded diabetes diagnosis, end of enrollment, or death (264, 869, 458 person-years). We obtained annual estimates of fine particulate matter (PM2.5), nitrogen dioxide (NO2), and warm-months ozone (O3) exposures from highly spatiotemporally resolved prediction models. We assessed the simultaneous effects of the pollutants on diabetes risk using survival analyses. We repeated the models in cohorts restricted to ZIP codes with air pollution levels not exceeding the national ambient air quality standards (NAAQS) during the study period. We identified 10, 024, 879 diabetes cases of 41, 780, 637 people (3.8% of person-years). The hazard ratio (HR) for first diabetes occurrence was 1.074 (95% CI 1.058; 1.089) for 5 μg/m3 increase in PM2.5, 1.055 (95% CI 1.050; 1.060) for 5 ppb increase in NO2, and 0.999 (95% CI 0.993; 1.004) for 5 ppb increase in O3. Both for NO2 and PM2.5 there was evidence of non-linear exposure-response curves with stronger associations at lower levels (NO2 ≤ 36 ppb, PM2.5 ≤ 8.2 μg/m3). Furthermore, associations remained in the restricted low-level cohorts. The O3-diabetes exposure-response relationship differed greatly between models and require further investigation. In conclusion, exposures to PM2.5 and NO2 are associated with increased diabetes risk, even when restricting the exposure to levels below the NAAQS set by the U.S. EPA. Type 2 diabetes is a major public health concern. Several studies have found an increased diabetes risk associated with long-term air pollution exposure. However, most current studies are limited in their generalizability, exposure assessment, or the ability to differentiate incidence and prevalence cases. We assessed the association between air pollution and first documented diabetes occurrence in a national U.S. cohort of older adults to estimate diabetes risk. We included all Medicare enrollees 65 years and older in the fee-for-service program, part A and part B, in the contiguous United States (2000–2016). Participants were followed annually until the first recorded diabetes diagnosis, end of enrollment, or death (264, 869, 458 person-years). We obtained annual estimates of fine particulate matter (PM2.5), nitrogen dioxide (NO2), and warm-months ozone (O3) exposures from highly spatiotemporally resolved prediction models. We assessed the simultaneous effects of the pollutants on diabetes risk using survival analyses. We repeated the models in cohorts restricted to ZIP codes with air pollution levels not exceeding the national ambient air quality standards (NAAQS) during the study period. We identified 10, 024, 879 diabetes cases of 41, 780, 637 people (3.8% of person-years). The hazard ratio (HR) for first diabetes occurrence was 1.074 (95% CI 1.058; 1.089) for 5 μg/m3 increase in PM2.5, 1.055 (95% CI 1.050; 1.060) for 5 ppb increase in NO2, and 0.999 (95% CI 0.993; 1.004) for 5 ppb increase in O3. Both for NO2 and PM2.5 there was evidence of non-linear exposure-response curves with stronger associations at lower levels (NO2 ≤ 36 ppb, PM2.5 ≤ 8.2 μg/m3). Furthermore, associations remained in the restricted low-level cohorts. The O3-diabetes exposure-response relationship differed greatly between models and require further investigation. In conclusion, exposures to PM2.5 and NO2 are associated with increased diabetes risk, even when restricting the exposure to levels below the NAAQS set by the U.S. EPA.

BACKGROUND: Many studies have reported that long-term air pollution exposure is associated with increased mortality rates. These investigations have been criticized for failure to control for omitted, generally personal, confounders. Study designs that are robust to such confounders can address this issue. METHODS: We used a self-controlled design for survival analysis. We stratified on each person in the Medicare cohort between 2000 and 2015 who died, and examined whether PM(2.5), O(3) and NO(2) exposures predicted in which follow-up period the death occurred. We used conditional logistic regression stratified on person and controlled for nonlinear terms in calendar year and age. By design slowly varying covariates such as smoking history, BMI, diabetes and other pre-existing conditions, usual alcohol consumption, sex, race, socioeconomic status, and green space were controlled by matching each person to themselves. RESULTS: There were 6,452,618 deaths in the study population in the study period. We observed a 5.37% increase in the mortality rate (95% CI 4.67%, 6.08%) for every 5 μg/m(3) increase in PM(2.5), a 1.98% (95% CI 1.61%, 2.36%) increase for 5 ppb increment in O(3), and a 2.10% decrease (95% CI 1.88%, 2.33%) for a 5ppb increase in NO(2). When restricted to persons whose PM(2.5) exposure never exceeded 12 μg/m(3) in any year between 2000 and 2015, the effect size increased for PM(2.5) (12.71% (11.30, 14.15)), and the signs of O(3) and NO(2) reversed (−0.26% (−0.88, 0.35) for O(3) and 1.77% increase (1.40, 2.13) for NO(2)). Effect sizes were larger for Blacks (e.g. 7.71% (5.46, 10.02) for PM(2.5)). CONCLUSION: There is strong evidence that the association between annual exposure to PM(2.5) and mortality is not confounded by individual or neighborhood covariates, and continues below the standard. The effects of O(3) and NO(2) are difficult to disentangle.

Stroke is the second most common cause of death and disability in the world. Many studies have found fine particulate matter (PM2.5) exposure to be associated with an increased risk of atherosclerotic cardiovascular disease, mostly focusing on ischemic heart disease and acute myocardial infarction. In a national analysis conducted in Israel—an area with unique climate conditions and high air pollution levels, we estimated the association between short-term PM2.5 exposure and ischemic stroke, intracerebral hemorrhage (ICH), or transient ischemic attacks (TIA). Using the Israeli National Stroke Registry, we obtained information on all stroke cases across Israel in 2014–2018. We obtained daily PM2.5 exposures from spatiotemporally resolved exposure models. We restricted the analytical data to days in which PM2.5 levels did not exceed the Israeli 24 h standard (37.5 µg/m3). We repeated the analysis with a stratification by sociodemographic characteristics and comorbidities. For all outcomes, the exposure–response curves were nonlinear. PM2.5 exposure was associated with a higher ischemic stroke risk, with larger effect estimates at higher exposure levels. Although nonsignificant, the exposure–response curve for TIA was similar. The associations with ICH were nonsignificant throughout the PM2.5 exposure distribution. The associations with ischemic stroke/TIA were larger among women, non-Jewish individuals, older adults, and individuals with diabetes, hypertension, and ischemic heart disease. In conclusion, short-term PM2.5 exposure is associated with a higher risk for ischemic stroke and possibly TIA, even when PM2.5 concentrations do not exceed the Israeli air quality guideline threshold. Vulnerability to the air pollution effects differed by age, sex, ethnicity, and comorbidities.

BackgroundType 2 diabetes is a major public health concern. Studies show that both genetics and environmental exposures play a significant role in developing the disease. We assessed the association between air pollution and first documented diabetes occurrence in a national U.S. cohort of older adults to estimate diabetes risk.MethodsWe included all Medicare enrollees 65 years and older in the fee-for-service program, part A and part B, in the contiguous United States (2000-2016). Participants were followed annually until the first recorded diabetes diagnosis, end of enrollment, or death (264,869,458 person-years). We obtained annual estimates of fine particulate matter (PM2.5), nitrogen dioxide (NO2), and warm-months ozone (O3) exposures from highly spatiotemporally resolved prediction models. We assessed the simultaneous effects of the pollutants on diabetes risk using survival analyses. We repeated the models in cohorts restricted to ZIP codes with air pollution levels not exceeding the national ambient air quality standards (NAAQS) during the study period.ResultsWe identified 10,024,879 diabetes cases of 41,780,637 people (3.8% of person-years). The hazard ratio (HR) for first diabetes occurrence was 1.074 (95% CI 1.058; 1.089) for 5 µg/m3 increase in PM2.5, 1.055 (95% CI 1.050; 1.060) for 5 ppb increase in NO2, and 0.999 (95% CI 0.993; 1.004) for 5 ppb increase in O3. Both for NO2 and PM2.5 there was evidence of non-linear exposure-response curves with stronger associations at lower levels (NO2 ≤ 40 ppb, PM2.5 ≤ 9 µg/m3). Furthermore, associations remained in the restricted low-level cohorts. The O3-diabetes exposure-response relationship differed greatly between models and require further investigation.ConclusionExposures to PM2.5 and NO2 are associated with increased diabetes risk, even when restricting the exposure to levels below the NAAQS set by the U.S. EPA.

Background:Congenital Heart Defects (CHD) are the most common structural defects of newborns. Southern Israel’s population is comprised of Jews (75%) and Arab-Bedouins (25%). The latter has a high rate of consanguinity and low abortion rate compared with the Jewish population, which led us to suspect a higher CHD prevalence in this population. Our aim was to compare maternal risk factors that are associated with CHD in these populations.Methods:All births during 1991–2011 in Soroka University Medical Center (n = 247, 289) with 6078 newborns having CHD were included. To account for same-woman deliveries, general estimating equation models adjusted for ethnicity, gender and birth number were used.Results:The total prevalence of CHD was 24.6/1000 live births, with 21.4 and 30 among Jewish and Bedouin populations, respectively, (p = 0.001). Multi-variant analysis of risk factors for CHD revealed that risk factors common to both populations included conception with fertility medications, sibling CHD, maternal CHD, diabetes mellitus, hypertension and anaemia. Risk factors that were specific for the Bedouin population were – maternal age over 35 years, recurrent pregnancy loss and in vitro fertilisation. However, sibling CHD was more common as a CHD risk factor in the Jewish compared with the Bedouin population (Adjusted OR 10.23 versus 3.19, respectively).Conclusions:The prevalence of CHD is higher in both the Bedouin and Jewish populations than previously reported. Several maternal factors were associated with CHD specifically for a certain population. Risk factors for CHD vary in populations residing in the same geographic area.

Background Birthweight is a strong predictor of normal growth, healthy development, and survival. Several studies have found associations between temperature, fine particulate matter (PM2.5), and birth weight. However, the relevant timing of exposures varies between studies and is yet unclear. Therefore, we assessed the difference in term birthweight (TBW) associated with weekly exposure to temperature and PM2.5 throughout 37 weeks of gestation. Methods We included all singleton live term births in Massachusetts, U.S between 2004 and 2015 (n = 712,438). Weekly PM2.5 and temperature predictions were estimated on a 1 km grid from satellite-based models. We utilized a distributed lag nonlinear model (DLNM) to estimate the difference in TBW associated with weekly exposures from the last menstrual period to 37 weeks of gestation. Results We found a nonlinear association with prenatal temperature exposure. Larger effects were observed in warmer temperatures, where higher temperatures were negatively associated with TBW. Temperature effects were larger in the first and final weeks of gestation. We observed a negative difference in TBW associated with PM2.5 exposure. Overall, a 1 µg/m3 increase in prenatal exposure was associated with 3.9 g lower TBW (95% CI −5.0 g; −2.9 g). PM2.5 effects were larger in the final weeks of gestation. Conclusion We found heat and PM2.5 exposure to be related to lower TBW. Our findings suggest that women are more susceptible to both exposures towards the end of pregnancy. Susceptibility to heat was higher in the initial weeks of pregnancy as well. These critical windows of susceptibility can be communicated to pregnant women during routine prenatal visits to increase awareness and target interventions to reduce exposures.

This exploratory study was aimed to investigate the link between toxic metal content in women’s urine and their morbidity 2 years before and 6 years after the test. Concentrations of 25 metals in urine were analyzed for 111 pregnant women collected prior to delivery. All women were of Arab-Bedouin origin. Information on primary care and hospital visits during the study period was obtained. In a Poisson regression model, a health outcome was regressed over metal exposure and other factors. A Weighted Quantile Sum Regression (WQS) approach was used to indicate metals dominating in their possible impact on women's morbidity. Obesity was the most frequently diagnosed condition in this population (27.9%). Diagnoses in a neurological category accounted for 36.0%, asthma or respiratory—25.2%, psychiatric—12.6%, cardiovascular—14.4% and cancer or benign growth—for 13.5%. Based on WQS analysis, cancer and benign growth were mostly attributed to the increased levels of cadmium, cardiovascular outcomes were linked with lead, and obesity was found associated with elevated levels of nickel. Hematological, neurological and respiratory outcomes were attributed to multiple non-essential metals. The health and exposure profile of women in the study warrants a periodic biomonitoring in attempt to identify and reduce exposure to potentially dangerous elements.

Background The majority of studies linking exposure to metals with certain health outcomes focus on known toxic metals. Alternatively, this study assesses the extent to which exposure to a wider range of metals during gestation is associated with childhood morbidity. Methods We analyzed the concentrations of 25 metals found in urine samples of 111 pregnant women of Arab-Bedouin origin collected prior to birth. In addition, we collected medical records on their offspring for six years following birth, including every interaction with HMOs, local hospitals, and pharmacies. Results The main types of morbidities diagnosed and treated during this period were preterm births, malformations, asthma-like morbidity, cardiovascular and behavioral problems, and obesity. Multivariable analysis showed that offspring born before term were more likely to have been exposed to elevated maternal concentrations of zinc, thallium, aluminum, manganese, and uranium, all with adjusted relative risk above 1.40 for an increase by each quintile. Likewise, children with asthma had been exposed to higher levels of magnesium, strontium, and barium at gestation, while behavioral outcomes were associated with elevated biometals, i.e., sodium, magnesium, calcium, selenium, and zinc, as well as higher levels of lithium, cobalt, nickel, strontium, cadmium, vanadium, arsenic, and molybdenum. A heatmap of adjusted relative risk estimates indicates the considerable implications that exposure to metals may have for preterm birth and developmental outcomes. Conclusions The current study shows that perinatal exposure to metals is adversely associated with pediatric morbidity. Further such analyses on additional samples are warranted.

Background Many vulnerable populations experience elevated exposures to environmental and social stressors, with deleterious effects on health. Multi-stressor epidemiological models can be used to assess benefits of exposure reductions. However, requisite individual-level risk factor data are often unavailable at adequate spatial resolution. Objective To leverage public data and novel simulation methods to estimate birthweight changes following simulated environmental interventions in two environmental justice communities in Massachusetts, US. Methods We gathered risk factor data from public sources (US Census, Behavioral Risk Factor Surveillance System, and Massachusetts Department of Health). We then created synthetic individual-level datasets using combinatorial optimization, and probabilistic and logistic modeling. Finally, we used coefficients from a multi-stressor epidemiological model to estimate birthweight and birthweight improvement associated with simulated environmental interventions. Results We created geographically-resolved synthetic microdata. Mothers with the lowest predicted birthweight were those identifying as Black or Hispanic, with parity > 1, utilization of government prenatal support, and lower educational attainment. Birthweight improvements following greenness and temperature improvements were similar for all high-risk groups and were larger than benefits from smoking cessation. Significance Absent private health data, this methodology allows for assessment of cumulative risk and health inequities, and comparison of individual-level impacts of localized health interventions.

BACKGROUND: Although long-term exposure to particulate matter17.4 μg/m(3)) to low-pollution zip code-days with similar background characteristics. Then, we estimated the percent change in admissions attributable to high pollution. We repeated the models restricting the analysis to zipcode-days with PM(2.5) below of 35 μg/m(3). RESULTS: We observed significant increases in all-cause hospital admissions (2.53% in PD and 2.49% in AD/dementia) attributable to high PM(2.5) exposure. The largest observed effect for common causes was for pneumonia and urinary tract infection. All the effects were larger in CDBD compared to the general Medicare population, and similarly strong at levels of exposure considered safe by the EPA. CONCLUSION: We found Medicare beneficiaries with CDBD to be at higher risk of being admitted to the hospital following acute exposure to PM(2.5) levels well below the National Ambient Air Quality Standard defined as safe by the EPA.

Numerous studies have found higher cardiovascular (CVD) risk associated with particulate matter smaller than 2.5 μm in diameter (PM2.5) ([1][1]). Most studies have used classical regression methods, which are limited in their ability to establish causality. Alternatively, causal inference analyses

Neighborhood demographic polarization, or the extent to which a privileged population group outnumbers a deprived group, can affect health by influencing social dynamics. While using birth records from 2001 to 2013 in Massachusetts (n = 629,675), we estimated the effect of two demographic indices, racial residential polarization (RRP) and economic residential polarization (ERP), on birth weight outcomes, which are established predictors of the newborn&rsquo, s future morbidity and mortality risk. Higher RRP and ERP was each associated with higher continuous birth weight and lower odds for low birth weight and small for gestational age, with evidence for effect modification by maternal race. On average, per interquartile range increase in RRP, the birth weight was 10.0 g (95% confidence interval: 8.0, 12.0) higher among babies born to white mothers versus 6.9 g (95% CI: 4.8, 9.0) higher among those born to black mothers. For ERP, it was 18.6 g (95% CI: 15.7, 21.5) higher among those that were born to white mothers versus 1.8 g (95% CI: &minus, 4.2, 7.8) higher among those born to black mothers. Racial and economic polarization towards more privileged groups was associated with healthier birth weight outcomes, with greater estimated effects in babies that were born to white mothers than those born to black mothers.

To examine the association between exposure to radiation from computed tomography (CT) studies and the incidence of cataract.In a nested case-control study, all cataract cases and their matched controls were sampled from a retrospective cohort of Israeli residents who underwent CT scans or ultrasonic tests in Soroka Medical Center, Beer-Sheva, Israel, between the years 1996 and 2014. The risk of cataract associated with head, neck or the rest of the body CT was assessed using Poisson survival analysis.The nested matched sample included 3841 cataract cases and their age- and sex-matched controls (n = 228,743). CT radiation exposure was more frequent in the cataract group, with 9.7% head CT, 1.2% neck CT and 6.6% other CT, compared to 5%, 0.7% and 3.7% among person-years without cataract (p 0.001). In a multivariate analysis, a similar increased risk of cataract associated with head (hazard ratio (HR): 1.24, 95% confidence interval (CI): 1.11; 1.38) and other CT (HR: 1.25, 95% CI: 1.10; 1.43) was found. No association with neck CT (HR: 1.07, 95% CI: 0.80; 1.43) was observed.In our study population, a similar risk of cataract with head, neck or the rest of the body CT was detected.

Background Particulate matter Objective We jointly investigated the association of short and long-term exposures to PM2.5 and temperature with hospital admissions, and explored the modification of the associations with the short-term exposures by one another and by temperature variability. Methods Daily ZIP code counts of respiratory, cardiac and stroke admissions of adults ≥65 (N = 2,015,660) were constructed across New-England (2001−2011). Daily PM2.5 and temperature exposure estimates were obtained from satellite-based spatio-temporally resolved models. For each admission cause, a Poisson regression was fit on short and long-term exposures, with a random intercept for ZIP code. Modifications of the short-term effects were tested by adding interaction terms with temperature, PM2.5 and temperature variability. Results Associations between short and long-term exposures were observed for all of the outcomes, with stronger effects of long-term exposures to PM2.5. For respiratory admissions, the short-term PM2.5 effect (percent increase per IQR) was larger on warmer days (1.12% versus −0.53%) and in months of higher temperature variability (1.63% versus −0.45%). The short-term temperature effect was higher in months of higher temperature variability as well. For cardiac admissions, the PM2.5 effect was larger on colder days (0.56% versus −0.30%) and in months of higher temperature variability (0.99% versus −0.56%). Conclusions We observed synergistic effects of short-term exposures to PM2.5, temperature and temperature variability. Long-term exposures to PM2.5 were associated with larger effects compared to short-term exposures.

To (a) evaluate the risk for placenta accreta following primary cesarean section (CS), in regard to the stage of labor, the cesarean section was taken (elective prelabor vs. unplanned during labor); and (b) investigate whether the association between placenta accreta and maternal and neonatal complications is modified by the type of the primary CS. In a population-based retrospective cohort study, we included all singleton deliveries occurred in Soroka University Medical Center between 1991 and 2015, of women who had a history of a single CS. The deliveries were divided into three groups according to the delivery stage the primary CS was carried out: ‘Unplanned 1’ (first stage—up to 10 cm), ‘Unplanned 2’ (second stage—10 cm) and ‘Elective’ prelabor CS. We assessed the association between the study group and placenta accreta using logistic generalized estimation equation (GEE) models. We additionally assessed maternal and neonatal complications associated with placenta accreta among women who had elective and unplanned CS separately. We included 22,036 deliveries to 13,727 women with a history of one CS, of which 0.9% (n = 207) had placenta accreta in the following pregnancies: 12% (n = 25) in the ‘Unplanned 1’ group, 7.2% (n = 15) in the ‘ Unplanned 2’ group and 80.8% (n = 167) in the ‘elective’ group. We found no difference in the risk for subsequent placenta accreta between the groups. In a stratified analysis by the timing of the primary cesarean delivery, the risk for maternal complications, associated with placenta accreta, was more pronounced among women who had an unplanned CS (OR 27.96, P

To analyze in a retrospective cohort study the outcomes of pregnancies with isolated oligohydramnios at the late preterm period (34-36.6 weeks of gestation).This retrospective cohort study included three groups of women: (1) Women with isolated oligohydramnios whose pregnancy was managed conservatively (n = 33 births); (2) women with isolated oligohydramnios who were managed actively (i.e. induction of labor) (n = 111 births); and (3) a control group including women with normal amount of amniotic fluid who had a spontaneous late preterm delivery (n = 10,445 births). Maternal and fetal characteristics and obstetrics outcomes were collected from a computerized database of all deliveries at Soroka University Medical Center during the study period.Our cohort included 10,589 births. The rate of inducing labor was higher in the oligohydramnios groups compared to the controls (p .001). There was an increase in the rate of cesarean section (CS) in the conservative treatment group (p .001), compared with the other groups. Conservative management was associated with higher rates of maternal infection (p = .026), chorioamnionitis (p = .01), and transitory tachypnea of the newborn (p = .02). After controlling for confounding factors, mal presentation (OR = 19.9), and a prior CS (OR = 2.4) were independently associated with an increased risk for CS, while induction of labor was associated with a reduced risk for CS (OR = 0.28).Women with late preterm isolated oligohydramnios had a higher rate of induction of labor than women with a normal amount of amniotic fluid. Induction of labor seems to be beneficial to both the neonate and the mother as seen by a lower rate of CS conducted in this group, as well as lower maternal and neonatal morbidity in comparison to the conservative group. Therefore, women with oligohydramnios at late preterm may benefit from induction of labor.

Rational: Several studies have found higher risks for childhood respiratory illness, associated with exposure to particulate matter (PM) less than 10 μm in diameter (PM10) and PM2.5 and gaseous pollution.Objectives: We analyzed the association between air pollution and hospitalizations due to bronchiolitis, an obstructive pulmonary disorder, commonly caused by respiratory syncytial virus infant infection.Methods: Data were obtained from a local tertiary medical center providing services for a population of 700,000 comprising two ethnic groups: predominantly urban Jews and rural Bedouin Arabs. The latter group includes 30% residing in unrecognized villages in a temporary dwelling. We included all infants (0–2 yr) hospitalized with bronchiolitis between 2003 and 2013. Daily PM estimates were obtained from a satellite-based model incorporating daily remote sensing data and assigned to the family residence locality. Other air pollutants and meteorological parameters were obtained from a local monitoring site....

Background: Numerous studies show associations between exposure to Particulate Matter and Cardiovascular disease (CVD). Current cardiovascular equations incorporate the major risk factors for CVD. The patients' environment, however, is not incorporated in these equations. Methods: In a retrospective analysis, we assessed the contribution of neighborhood greenness and particulate matter (coarse-PM and PM0.2. The c-statistics slightly improved from 77.30%–77.40% for the prediction of MI (p=0.004) and from 75.60%–75.76% for the prediction of stroke (p=0.027). Calibration was fair in all models. The associations were partially mediated through the patients' comorbidities. Conclusion: The negligible improvement in the prediction performance, despite significant associations with PM and NDVI, may be due to partial mediation of these associations through the conventional cardiovascular risk factors, suggesting the importance in assessing the environmental effects on more basic physiological pathways when addressing the contribution to the cardiovascular risk. Keywords: Air pollution, Neighborhood greenness, Cardiovascular risk, Stroke, Myocardial infarction

Few studies examined the impact of maternal socioeconomic status and of its combined effects with environmental exposures on birthweight. Our goal was to examine the impact of maternal homelessness (mothers ever homeless or who lived in shelters during pregnancy) and participation in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) during pregnancy in conjunction with air pollution exposure on birthweight in the Boston-based Children’s HealthWatch cohort from 2007 through 2015 (n = 3366). Birthweight was obtained from electronic health records. Information on maternal homelessness and WIC participation during pregnancy were provided via a questionnaire. Prenatal fine particulate matter (PM2.5) exposures, estimated at the subject’s residential address, were calculated for each trimester. We fit linear regression models adjusting for maternal and child characteristics, seasonality, and block-group-level median household income and examined the interactions between PM2.5 and each covariate. Prenatal maternal homelessness was associated with reduced birthweight (−55.7 g, 95% CI: −97.8 g, −13.7 g), while participating in WIC was marginally associated with increased birthweight (36.1 g, 95% CI: −7.3 g, 79.4 g). Only average PM2.5 during the second trimester was marginally associated with reduced birthweight (−8.5 g, 95% CI: −19.3, 2.3) for a 1 µg/m3 increase in PM2.5. The association of PM2.5 during the second trimester with reduced birthweight was stronger among non-Hispanic Black mothers and trended toward significance among immigrants and single mothers. Our study emphasizes the independent and synergistic effects of social and environmental stressors on birthweight, particularly the potentially protective effect of participating in WIC for vulnerable populations.

Background: Radon is an inert gas formed from the decay of naturally-occurring materials in the earth's crust. It infiltrates into homes from soil, water, and construction materials. Its decay products are radionuclides, which attach to ambient particles. Residential radon is one of the leading risk factors for lung cancer. The scarce evidence for associations with other mortality causes originates mostly from occupational studies. Methods: In a cohort study with 14 years of follow-up (2000−2013), we evaluated the association between chronic radon exposure and all-cause mortality, and explored whether there are subpopulations who are more vulnerable to radon effects. We included 87,296,195 person-years of follow-up from all Medicare beneficiaries in the Mid-Atlantic and Northeastern U.S. states. We examined the association between the logarithm of county-averaged radon (ln(Rn)) and mortality and assessed effect modification by chronic conditions. Results: An interquartile range increase in the ln(Rn) was associated with a 2·62% increase (95% CI 2·52%; 2·73%) in mortality, independent of PM2.5 exposure. Larger mortality risks were observed among individuals with respiratory, cardiovascular and metabolic diseases, with the highest associations observed among those with diabetes (4·98% increase), heart failure (4·58% increase), and chronic obstructive pulmonary disease (4·49% increase). Conclusion: We found an increased risk for all-cause mortality associated with increased radon exposure. The risk was enhanced among susceptible individuals with chronic conditions. We believe this is the first cohort study to identify populations at higher risk for non-malignant health consequences of radon exposure. Due to the limitations in exposure assessment and availability of individual confounders, these findings should be interpreted with caution. Keywords: Radon, Radiation, Mortality, PM2.5

Background: Dozens of cohort studies have associated particulate matter smaller than 2.5 µm in diameter (PM2.5) exposure with early deaths, and the Global Burden of Disease identified PM2.5 as the fifth-ranking mortality risk factor in 2015. However, few studies have used causal modeling techniques. We assessed the effect of annual PM2.5 exposure on all-cause mortality rates among the Medicare population in the Northeastern and mid-Atlantic states, using the difference-in-differences approach for causal modeling. Methods: We obtained records of Medicare beneficiaries 65 years of age or more who reside in the Northeastern or mid-Atlantic states from 2000 to 2013 and followed each participant from the year of enrollment to the last year of follow-up. We estimated the causal effect of annual PM2.5 exposure on mortality rates using the difference-in-differences approach in the Poisson survival analysis. We controlled for individual confounders, for spatial differences using dummy variables for each ZIP code and for time trends using a penalized spline of year. Results: We included 112,376,805 person-years from 15,401,064 people, of whom 37.4% died during the study period. The interquartile range (IQR) of the annual PM2.5 concentration was 3 µg/m3, and the mean annual PM2.5 concentration ranged between 6.5 and 14.5 µg/m3 during the study period. An IQR incremental increase in PM2.5 was associated with a 4.04% increase (95% CI = 3.49%, 4.59%) in mortality rates. Conclusions: Assuming no omitted predictors changing differently across ZIP codes over time in correlation with PM2.5, we found a causal effect of PM2.5 on mortality incidence rate.

Features of the environment may modify the effect of particulate matter &le, 2.5 &micro, m in aerodynamic diameter (PM2.5) on health. Therefore, we investigated how neighborhood sociodemographic and land-use characteristics may modify the association between PM2.5 and cardiovascular mortality. We obtained residence-level geocoded cardiovascular mortality cases from the Massachusetts Department of Public Health (n = 179,986), and PM2.5 predictions from a satellite-based model (2001&ndash, 2011). We appended census block group-level information on sociodemographic factors and walkability, and calculated neighborhood greenness within a 250 m buffer surrounding each residence. We found a 2.54% (1.34%, 3.74%) increase in cardiovascular mortality associated with a 10 &micro, g/m3 increase in two-day average PM2.5. Walkability or greenness did not modify the association. However, when stratifying by neighborhood sociodemographic characteristics, smaller PM2.5 effects were observed in greener areas only among cases who resided in neighborhoods with a higher population density and lower percentages of white residents or residents with a high school diploma. In conclusion, the PM2.5 effects on cardiovascular mortality were attenuated by higher greenness only in areas with sociodemographic features that are highly correlated with lower socioeconomic status. Previous evidence suggests health benefits linked to neighborhood greenness may be stronger among lower socioeconomic groups. Attenuation of the PM2.5&ndash, mortality relationship due to greenness may explain some of this evidence.

Background Previous reports indicate an association between ambient temperature (Ta) and air pollution exposure during pregnancy and preterm birth (PTB). Nevertheless, information regarding the association between environmental factors and specific precursors of spontaneous preterm birth is lacking. We aimed to determine the association between Ta and air pollution during gestation and the precursors of spontaneous preterm parturition, i.e. preterm labor (PTL) and preterm prelabor rupture of membranes (PPROM). Methods From 2003 to 2013 there were 84,476 deliveries of singleton gestation that comprised the study cohort. Exposure data during pregnancy included daily measurements of temperature and particulate matter Results There is an association of environmental exposure with the precursors of spontaneous preterm parturition; PPROM was more sensitive to Ta fluctuations than PTL. This effect was modified by the ethnicity, Bedouin-Arabs were susceptible to elevated Ta, especially within the last day prior to admission with PPROM (Relative Risk (RR) =1.19 [95% CI, 1.03; 1.37]). Jews, on the other hand, were susceptible to ambient pollutants, two (RR=1.025 [1.010; 1.040]) and one (RR= 1.017 [1.002; 1.033]) days prior to spontaneous PTL with intact membranes resulting in preterm birth. Conclusion High temperature is an independent risk factor for PPROM among Bedouin-Arabs; ambient pollution is an independent risk factor for spontaneous PTL resulting in preterm birth. Thus, the precursors of spontaneous preterm parturition differ in their association with environmental factors.

Many studies have reported that PM2.5 was associated with mortality, but these were criticized for unmeasured confounding, not using causal modeling, and not focusing on changes in exposure and mortality rates. Recent studies have used propensity scores, a causal modeling approach that requires the assumption of no unmeasured confounders. We used differences in differences, a causal modeling approach that focuses on exposure changes, and controls for unmeasured confounders by design to analyze PM2.5 and mortality in the U.S. Medicare population, with 623, 036, 820 person-years of follow-up, and 29, 481, 444 deaths. We expanded the approach by clustering ZIP codes into 32 groups based on racial, behavioral and socioeconomic characteristics, and analyzing each cluster separately. We controlled for multiple time varying confounders within each cluster. A separate analysis examined participants whose exposure was always below 12 μg/m3. We found an increase of 1 μg/m3 in PM2.5 produced an increased risk of dying in that year of 3.85 × 10−4 (95% CI 1.95 × 10−4, 5.76 × 10−4). This corresponds to 14,000 early deaths per year per 1 μg/m3. When restricted to exposures below 12 μg/m3, the increased mortality risk was 4.26 × 10−4 (95% CI 1.43 × 10−4, 7.09 × 10−4). Using a causal modeling approach robust to omitted confounders, we found associations of PM2.5 with increased death rates, including below U.S. and E.U. standards.

Evidence from recent decades supports a causal association between air pollution (particulate matter10 μm in diameter [PM10] and PM2.5 μm in diameter [PM2.5]) and oxidative stress, possibly involving impaired metabolism of glucose and lipids.Using a satellite based model to assess PM exposure at 1-km spatial resolution, we examined the associations between PM and glucose, hemoglobin A1c (HbA1c), and lipids.Population-based retrospective cohort study of a 10-year period.Members of the largest health care provider in Southern Israel.We included all serum glucose, HbA1c, and lipids tests of subjects with known cardiovascular diseases and risk factors. Subjects' glycemic status was defined as normal or diabetes.Log-transformed glucose, HbA1c, and lipid values were explored by mixed models, with adjustment for personal and seasonal confounders.We assessed 73 117 subjects with over 600 000 samples. Three-month average concentration of PM10, but not 1- to 7-d exposure, was associated with increases of serum glucose, HbA1c, low-density lipoprotein and triglycerides, and decrease of high-density lipoprotein. The strongest associations were observed among subjects with diabetes (percent increase [95% confidence interval], for interquartile range increase of PM10 and PM2.5): 3.58% (1.03%; 6.20%) and 2.93% (0.35%; 5.59%) increase in HbA1c and 2.37% (2.11%; 2.63%) and 1.54% (1.26%; 1.83%) increase in low-density lipoprotein. Antidiabetic medications (other than insulin) attenuated the air pollution effect on serum glucose.Intermediate-term, but not short term, exposure to PM is associated with alterations in glucose, HbA1c, and lipids, especially among people with diabetes.

BackgroundThe aetiology of conotruncal heart defects is poorly understood and the birth prevalence varies geographically. The known risk factors for developing conotruncal heart defects are as follows: CHD in siblings, genetic chromosomal abnormalities, paternal age >30 years, high parity, low birth weight, prematurity, and maternal diabetes.ObjectiveThe aim of this study was to characterise conotruncal heart defects, birth prevalence, mortality, and morbidity in the population of southern Israel, of whom 75% are Jewish and the rest are mostly Bedouin Arabs.MethodsThe data were obtained from Soroka University Medical Center database of births and newborns. Conotruncal heart defects cases were identified by ICD9 codes.ResultsDuring 1991–2011, there were 247,290 singleton live births and 393 conotruncal heart defects in Soroka University Medical Center. The birth prevalence per 10,000 live births of tetralogy of Fallot, transposition of the great arteries, and truncus arteriosus was 9.5, 5, and 1.8, respectively. In the multivariate analysis, Bedouin descent (adjusted odds ratio 2.40, p35 years (1.66, p=0.004), and siblings with congenital heart defects (1.98, p=0.005) were associated with tetralogy of Fallot, and Bedouin descent (1.61, p=0.05), siblings with congenital heart defects (2.19, p=0.004), and diabetes mellitus (7.15, pConclusionWe observed higher birth prevalence of conotruncal heart defects compared with the birth prevalence reported worldwide, specifically among the Bedouins, a population characterised with high consanguinity rate. Therefore, genetic counselling and early fetal echocardiograms should be encouraged, especially in high consanguinity rate populations. Naturally, further educational efforts are needed in order to decrease consanguinity and its related consequences.