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Epidemiologic evidence has emerged showing an association between exposure to air pollution and increased risks of gestational diabetes mellitus (GDM). This study examines the effect of low-level air pollution exposure on a subclinical biomarker of hyperglycemia (i.e., HbA1c) in pregnant people without diabetes before conception. We measured HbA1c in 577 samples repeatedly collected from 224 pregnant people in Rochester, NY, and estimated residential concentrations of PM2.5 and NO2 using high-resolution spatiotemporal models. We observed a U-shaped trajectory of HbA1c during pregnancy with average HbA1c levels of 5.13 (±0.52), 4.97 (±0.54), and 5.43 (±0.40)% in early-, mid-, and late pregnancy, respectively. After adjustment for the U-shaped trajectory and classic GDM risk factors, each interquartile range increase in 10 week NO2 concentration (8.0 ppb) was associated with 0.09% (95% CI: 0.02 to 0.16%) and 0.18% (95% CI: 0.08 to 0.28%) increases in HbA1c over the entire pregnancy and in late pregnancy, respectively. These associations remained robust among participants without GDM. Using separate distributed lag models, we identified a period between 8th and 14th gestational weeks as critical windows responsible for increased levels of HbA1c measured at 14th, 22nd, and 30th gestational weeks. Our results suggest that low-level air pollution contributes to hyperglycemia in medically low-risk pregnant people.

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Background: Previous work reported increased rates of cardiovascular hospitalizations associated with increased source-specific PM2.5 concentrations in New York State, despite decreased PM2.5 concentrations. We also found increased rates of ST elevation myocardial infarction (STEMI) associated with short-term increases in concentrations of ultrafine particles and other traffic-related pollutants in the 2014-2016 period, but not during 2017-2019 in Rochester. Changes in PM2.5 composition and sources resulting from air quality policies (e.g., Tier 3 light-duty vehicles) may explain the differences. Thus, this study aimed to estimate whether rates of STEMI were associated with organic carbon and source-specific PM2.5 concentrations. Methods: Using STEMI patients treated at the University of Rochester Medical Center, compositional and source-apportioned PM2.5 concentrations measured in Rochester, a time-stratified case-crossover design, and conditional logistic regression models, we estimated the rate of STEMI associated with increases in mean primary organic carbon (POC), secondary organic carbon (SOC), and source-specific PM2.5 concentrations on lag days 0, 0-3, and 0-6 during 2014-2019. Results: The associations of an increased rate of STEMI with interquartile range (IQR) increases in spark-ignition emissions (GAS) and diesel (DIE) concentrations in the previous few days were not found from 2014 to 2019. However, IQR increases in GAS concentrations were associated with an increased rate of STEMI on the same day in the 2014-2016 period (Rate ratio [RR] = 1.69; 95% CI = 0.98, 2.94; 1.73 µg/m3). In addition, each IQR increase in mean SOC concentration in the previous 6 days was associated with an increased rate of STEMI, despite imprecision (RR = 1.14; 95% CI = 0.89, 1.45; 0.42 µg/m3). Conclusion: Increased SOC concentrations may be associated with increased rates of STEMI, while there seems to be a declining trend in adverse effects of GAS on triggering of STEMI. These changes could be attributed to changes in PM2.5 composition and sources following the Tier 3 vehicle introduction.

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Background. Fish and rice are the main dietary sources of methylmercury (MeHg); however, rice does not contain the same beneficial nutrients as fish, and these differences can impact the observed health effects of MeHg. Hence, it is important to validate a biomarker, which can distinguish among dietary MeHg sources. Methods. Mercury (Hg) stable isotopes were analyzed in hair samples from peripartum mothers in China (n = 265). Associations between mass dependent fractionation (MDF) (δ202Hg) and mass independent fractionation (MIF) (Δ199Hg) (dependent variables) and dietary MeHg intake (independent variable) were investigated using multivariable regression models. Results. In adjusted models, hair Δ199Hg was positively correlated with serum omega-3 fatty acids (a biomarker for fish consumption) and negatively correlated with maternal rice MeHg intake, indicating MIF recorded in hair can be used to distinguish MeHg intake predominantly from fish versus rice. Conversely, in adjusted models, hair δ202Hg was not correlated with measures of dietary measures of MeHg intake. Instead, hair δ202Hg was strongly, negatively correlated with hair Hg, which explained 27-29% of the variability in hair δ202Hg. Conclusions. Our results indicated that hair Δ199Hg can be used to distinguish MeHg intake from fish versus rice. Results also suggested that lighter isotopes were preferentially accumulated in hair, potentially reflecting Hg binding to thiols (i.e., cysteine); however, more research is needed to elucidate this hypothesis. Broader impacts include 1) validation of a non-invasive biomarker to distinguish MeHg intake from rice versus fish, and 2) the potential to use Hg isotopes to investigate Hg binding in tissues.

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BACKGROUND: Influenza healthcare encounters in adults associated with specific sources of PM2.5 is an area of active research. OBJECTIVE: Following 2017 legislation requiring reductions in emissions from light-duty vehicles, we hypothesized a reduced rate of influenza healthcare encounters would be associated with concentrations of PM2.5 from traffic sources in the early implementation period of this regulation (2017-2019). METHODS: We used the Statewide Planning and Research Cooperative System (SPARCS) to study adult patients hospitalized (N = 5328) or treated in the emergency department (N = 18,247) for influenza in New York State. Using a modified case-crossover design, we estimated the excess rate (ER) of influenza hospitalizations and emergency department visits associated with interquartile range increases in source-specific PM2.5 concentrations (e.g., spark-ignition emissions [GAS], biomass burning [BB], diesel [DIE]) in lag day(s) 0, 0-3 and 0-6. We then evaluated whether ERs differed after Tier 3 implementation (2017-2019) compared to the period prior to implementation (2014-2016). RESULTS: Each interquartile range increase in DIE in lag days 0-6 was associated with a 21.3% increased rate of influenza hospitalization (95% CI: 6.9, 37.6) in the 2014-2016 period, and a 6.3% decreased rate (95% CI: -12.7, 0.5) in the 2017-2019 period. The GAS/influenza excess rates were larger in the 2017-2019 period than the 2014-2016 period for emergency department visits. We also observed a larger ER associated with increased BB in the 2017-2019 period compared to the 2014-2016 period. IMPACT STATEMENT: We present an accountability study on the impact of the early implementation period of the Tier 3 vehicle emission standards on the association between specific sources of PM2.5 air pollution on influenza healthcare encounters in New York State. We found that the association between gasoline emissions and influenza healthcare encounters did not lessen in magnitude between periods, possibly because the emissions standards were not yet fully implemented. The reduction in the rates of influenza healthcare encounters associated with diesel emissions may be reflective of past policies to reduce the toxicity of diesel emissions. Accountability studies can help policy makers and environmental scientists better understand the timing of pollution changes and associated health effects.

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Prior studies reported excess rates (ERs) of cardiorespiratory events associated with short-term increases in PM2.5 concentrations, despite implementation of pollution-control policies. In 2017, Federal Tier 3 light-duty vehicle regulations began, and to-date there have been no assessments of population health effects of the policy. Using the NYS Statewide Planning and Research Cooperative System (SPARCS) database, we obtained hospitalizations and ED visits with a principal diagnosis of asthma or chronic obstructive pulmonary disease (COPD) for residents living within 15 miles of six urban PM2.5 monitoring sites in NYS (2014-2019). We used a time-stratified case-crossover design and conditional logistic regression (adjusting for ambient temperature, relative humidity, and weekday) to estimate associations between PM2.5, POC (primary organic carbon), SOC (secondary organic carbon), and rates of respiratory disease hospitalizations and emergency department (ED) visits from 2014 to 2019. We evaluated demographic disparities in these relative rates and compared changes in ERs before (2014-2016) and after Tier 3 implementation (2017-2019). Each interquartile range increase in PM2.5 was associated with increased ERs of asthma or COPD hospitalizations and ED visits in the previous 7 days (ERs ranged from 1.1%-3.1%). Interquartile range increases in POC were associated with increased rates of asthma ED visits (lag days 0-6: ER = 2.1%, 95% CI = 0.7%, 3.6%). Unexpectedly, the ERs of asthma admission and ED visits associated with PM2.5, POC, and SOC were higher during 2017-2019 (after Tier 3) than 2014-2016 (before Tier-3). Chronic obstructive pulmonary disease analyses showed similar patterns. Excess Rates were higher in children (<18 years; asthma) and seniors (≥65 years; COPD), and Black, Hispanic, and NYC residents. In summary, unanticipated increases in asthma and COPD ERs after Tier-3 implementation were observed, and demographic disparities in asthma/COPD and PM2.5, POC, and SOC associations were also observed. Future work should confirm findings and investigate triggering of respiratory events by source-specific PM.

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Increased systemic oxidative stress, implicated in adverse pregnancy outcomes for both mothers and fetuses, has been associated with gestational exposure to air pollutants such as polycyclic aromatic hydrocarbons (PAHs), fine particulate matter (PM2.5), and nitrogen dioxide (NO2). However, it is unclear whether exposure to pollutants at levels below the current air quality standards can increase oxidative stress in pregnant women. In a cohort of 305 pregnant persons residing in western New York, we examined the association between exposure to PM2.5, NO2, and PAHs (measured as urinary 1-hydroxypyrene) and urinary biomarkers of oxidative stress (malondialdehyde [MDA] and 8-hydroxy-2'-deoxyguanosine [8-OHdG]) measured in each trimester. After controlling for gestational stage, maternal age, lifestyles, and socioeconomic factors, each interquartile range (IQR) increase in 1-hydroxypyrene concentration (65.8 pg/ml) was associated with a 7.73% (95%CI: 3.18%,12.3%) higher in MDA levels throughout the pregnancy and in the first and second trimester. An IQR increase in PM2.5 concentration (3.20 µg/m3) was associated with increased MDA levels in the first trimester (8.19%, 95%CI: 0.28%,16.1%), but not the 2nd (-7.99%, 95% CI: 13.8%, -2.23%) or 3rd trimester (-2.81%, 95% CI: 10.0%, 4.38%). The average cumulative PM2.5 exposures in the 3-7 days before urine collection were associated with increased 8-OHdG levels during the second trimester, with the largest difference (22.6%; 95% CI: 3.46%, 41.7%) observed in relation to a one IQR increase in PM2.5 concentration in the previous 7 days. In contrast, neither oxidative stress biomarker was associated with NO2 exposure. Observed in pregnant women exposed to low-level air pollution, these findings expanded previously reported associations between systemic oxidative stress and high-level PM2.5 and PAH concentrations. Further, the first and second trimesters may be a susceptible window during pregnancy for oxidative stress responses to air pollution exposure.

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Understanding health risks from methylmercury (MeHg) exposure is complicated by its link to fish consumption which may confound or modify toxicities. One solution is to include fish intake and a biomarker of MeHg exposure in the same model, but resulting estimates do not reflect the independent impact of accumulated MeHg or fish exposures. In fish-eating populations, this can be addressed by separating MeHg exposure into fish intake and average Hg content of the consumed fish. We assessed the joint association of prenatal MeHg exposure (maternal hair Hg) and fish intake (among fish-eating mothers) with neurodevelopment in 361 eight-year-olds from the New Bedford Cohort (born 1993-1998). Neurodevelopmental assessments used standardized tests of IQ, language, memory, and attention. Covariate-adjusted regression assessed the association of maternal fish consumption, stratified by tertiles of estimated average fish Hg, with neurodevelopment. Associations between maternal fish intake and child outcomes were generally beneficial for those in the lowest average fish Hg tertile, but detrimental in the highest average fish Hg tertile where, for example, each serving of fish was associated with 1.3 fewer correct responses (95% CI: -2.2, -0.4) on the Boston Naming test. Standard analyses showed no outcome associations with hair Hg or fish intake.

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BACKGROUND: Ambient air pollution may be a developmental endocrine disruptor. In animal models, gestational and perinatal exposure to diesel exhaust and concentrated particulate matter alters anogenital distance (AGD), a marker of prenatal androgen activity, in both sexes. Little is known in humans. OBJECTIVES: We examined exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) in relation to human AGD at birth and at 1 year of age, focusing on exposures during critical windows of reproductive development: the male programming window (MPW; gestational weeks 8-14) and mini-puberty (postnatal months 1-3). METHODS: The Infant Development and Environment Study (TIDES) recruited first trimester pregnant women (n=687) at four U.S. sites (Minneapolis, Minnesota; Rochester, New York; San Francisco, California; and Seattle, Washington) from 2010 to 2012. We measured anus to clitoris (AGD-AC) and anus to fourchette (AGD-AF) in female infants at birth; in males, we measured anus to penis (AGD-AP), anus to scrotum (AGD-AS), and penile width at birth and at 1 year of age. Using advanced spatiotemporal models, we estimated maternal exposure to PM2.5 and NO2 in the MPW and mini-puberty. Covariate-adjusted, sex-stratified linear regression models examined associations between PM2.5 and NO2 and AGD. RESULTS: In males, a 1-µg/m3 increase in PM2.5 exposure during the MPW was associated with shorter AGD at birth, but a longer AGD at 1 year of age (e.g., birth AGD-AP: ß=-0.35mm; 95% CI: -0.62, -0.07; AGD-AS: ß=0.37mm; 95% CI: 0.02, 0.73). Mini-pubertal PM2.5 exposure was also associated with shorter male AGD-AP (ß=-0.50mm; 95% CI: -0.89, -0.11) at 1 year of age. Although not associated with male AGD measures, 1-ppb increases in NO2 exposure during the MPW (ß=-0.07mm; 95% CI: -0.02, -0.12) and mini-puberty (ß=-0.04mm; 95% CI: -0.08, 0.01) were both associated with smaller penile width at 1 year of age. Results were similar in multipollutant models, where we also observed that in females AGD-AC was inversely associated with PM2.5 exposure, but positively associated with NO2 exposure. DISCUSSION: PM2.5 and NO2 exposures during critical pre- and postnatal windows may disrupt reproductive development. More work is needed to confirm these novel results and clarify mechanisms. https://doi.org/10.1289/EHP12627.

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BACKGROUND: Consumption of fish yields many nutritional benefits, but also results in exposure to methylmercury (MeHg). The developing brain is known to be particularly susceptible to MeHg toxicity in high doses. However, the potential impact of low-level environmental exposure from fish consumption on children's neurodevelopment remains unclear. METHODS: We investigated postnatal MeHg exposure at 7 years and its association with a battery of 17 neurodevelopmental outcomes in a subset of children (n = 376) from 1535 enrolled mother-child pairs in Nutrition Cohort 2 of the Seychelles Child Development Study (SCDS NC2). Each outcome was modeled in relation to postnatal MeHg exposure using linear regression, adjusting for prenatal MeHg exposure, levels of maternal polyunsaturated fatty acids (PUFA), and several other covariates known to be associated with neurodevelopmental outcomes. RESULTS: Median postnatal MeHg exposure at 7 years was 2.5 ppm, while the median prenatal MeHg exposure was 3.5 ppm. We found no statistically significant associations between postnatal MeHg exposure and any of the 17 neurodevelopmental outcomes after adjusting for prenatal MeHg exposure and other covariates. CONCLUSIONS: These findings are consistent with previous cross-sectional analyses of the SCDS Main Cohort. Continued follow-up of the entire NC2 cohort at later ages with repeated exposure measures is needed to further confirm these findings.

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BACKGROUND: Humans differ in the metabolism of the neurotoxicant methyl mercury (MeHg). This variation may be partially due to variation in genes encoding the transcription factor Nuclear factor E2-related factor 2 (NRF2) and its negative regulator Kelch-like ECH-Associated Protein 1 (KEAP1), which regulate glutathione and related transporter and antioxidant proteins that play a role in the metabolism and neurotoxicity of MeHg. AIM: To elucidate a potential risk from genetic variation in NFE2L2 (encoding NRF2) and KEAP1 toward prenatal mercury exposure and child neurodevelopmental outcomes at 20 months and 7 years of age in a population with variable prenatal exposure to MeHg from maternal fish consumption. MATERIAL AND METHODS: Nutrition Cohort 2 is a mother-child cohort in the Republic of Seychelles. Children were genotyped for NFE2L2 (rs2364723, rs13001694) and KEAP1 (rs8113472, rs9676881) polymorphisms (N = 1285 after removing siblings). Total mercury (Hg) was measured in cord blood as a biomarker for prenatal MeHg exposure. Child neurodevelopmental outcomes included the Bayley Scales of Infant Development II administered at 20 months of age, and outcomes across multiple neurodevelopmental domains from 14 tests administered in children and 3 instruments completed by parents when children were 7 years of age. RESULTS: The mean cord blood MeHg concentration was 34 (95% CI 11, 75) µg/L. None of the four polymorphisms had a significant association (p < 0.05) with either cord MeHg or neurodevelopmental test results at 20 months. There were no significant associations between either NFE2L2 polymorphism and any developmental test scores. At 7 years, children carrying KEAP1 rs8113472 CA showed significantly worse performance on psychomotor function than children with the CC variant (finger tapping, dominant hand: ß - 1.19, SE 0.34; finger tapping, non-dominant hand: ß - 0.92, SE 0.31) and worse social communication (SCQ Total: ß 0.65, SE 0.27). Children carrying rs8113472 AA, versus children with CC, showed significantly better performance on social communication (SRS Total: ß - 8.88, SE 3.60). Children carrying KEAP1 rs9676881 AG, versus children with GG, showed significantly worse performance on psychomotor function (trailmaking A time: ß 8.66, SE 3.37) and cognition (KBIT Matrices: ß - 0.96, SE 0.36). CONCLUSION: No associations between NFE2L2 and KEAP1 polymorphisms and MeHg concentration were identified. However, at 7 years, KEAP1 polymorphisms were associated with differences in neurodevelopmental outcomes in children from a population with high fish intake.

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We characterized mercury and selenium in the fish consumed in the Seychelles Islands to determine if their levels are similar to fish consumed in the US. A secondary aim was to examine whether fish weight and species predict mercury and selenium in fish consumed in the Seychelles. We measured total mercury (THg) and selenium (Se) content of 10 samples from each of the 19 most frequently consumed fish species in Seychelles and for each calculated the Se:Hg molar ratios and the Selenium Health Benefit Value Index (HBV Se). Linear regression models examined associations with weight and species. Average MeHg levels in fish ranged from less than 0.01 ppm (streamlined spinefoot) to 0.7 ppm (bludger trevally) with an overall mean of 0.21 ± 0.23 ppm. Average Se levels ranged from 0.34 ppm (blue-barred parrot fish) to 0.93 ppm (blue-lined large-eye bream) with a mean of 0.54 ± 0.23 ppm. All fish species had a mean Se:Hg molar ratio > 1 and positive mean HBV Se index values. Weight was strongly predictive of MeHg and Se:Hg molar ratio, both across and within most species, but was less predictive of Se and HBV Se. Our study demonstrated that fish consumed in Seychelles have mercury and selenium content similar to that of fish consumed in the US. Fish in both countries have favorable positive values for Se:Hg molar ratios and HBV Se indexes. Because mercury and selenium concentrations in fish are similar to those in the US but fish consumption is substantially higher in Seychelles, the Seychellois make an ideal population in which to determine if there are adverse effects of prenatal, postnatal, and lifetime low dose MeHg exposure from fish consumption.

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BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) are synthetic chemicals found in drinking water and consumer products, resulting in ubiquitous human exposure. PFAS have been linked to endocrine disruption and altered weight gain across the lifespan. A limited and inconsistent body of research suggests PFAS may impact gestational weight gain (GWG) and postpartum body mass index (BMI), which are important predictors of overall infant and maternal health, respectively. METHODS: In the Understanding Pregnancy Signals and Infant Development (UPSIDE/UPSIDE-MOMs) study (n = 243; Rochester, NY), we examined second trimester serum PFAS (PFOS: perfluorooctanesulfonic acid, PFOA: perfluorooctanoic acid, PFNA: perfluorononanoic acid, PFHxS: perfluorohexanesulfonic acid, PFDA: perfluorodecanoic acid) in relation to GWG (kg, and weekly rate of gain) and in the postpartum, weight retention (PPWR (kg) and total body fat percentage (measured by bioelectrical impedance)). We fit multivariable linear regression models examining these outcomes in relation to log-transformed PFAS in the whole cohort as well as stratified by maternal pre-pregnancy BMI (< 25 vs. = > 25 kg/m2), adjusting for demographics and lifestyle factors. We used weighted quantile sum regression to find the combined influence of the 5 PFAS on GWG, PPWR, and body fat percentage. RESULTS: PFOA and PFHxS were inversely associated with total GWG (PFOA: ß = -1.54 kg, 95%CI: -2.79, -0.30; rate ß = -0.05 kg/week, 95%CI: -0.09, -0.01; PFHxS: ß = -1.59 kg, 95%CI: -3.39, 0.21; rate ß = -0.05 kg/week, 95%CI: -0.11, 0.01) and PPWR at 6 and 12 months (PFOA 6 months: ß = -2.39 kg, 95%CI: -4.17, -0.61; 12 months: ß = -4.02 kg, 95%CI: -6.58, -1.46; PFHxS 6 months: ß = -2.94 kg, 95%CI: -5.52, -0.35; 12 months: ß = -5.13 kg, 95%CI: -8.34, -1.93). PFOA was additionally associated with lower body fat percentage at 6 and 12 months (ß = -1.75, 95%CI: -3.17, -0.32; ß = -1.64, 95%CI: -3.43, 0.16, respectively) with stronger associations observed in participants with higher pre-pregnancy BMI. The PFAS mixture was inversely associated with weight retention at 12 months (ß = -2.030, 95%CI: -3.486, -0.573) amongst all participants. CONCLUSION: PFAS, in particular PFOA and PFHxS, in pregnancy are associated with altered patterns of GWG and postpartum adiposity with potential implications for fetal development and long-term maternal cardiometabolic health.

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BACKGROUND: High concentrations of taurine are present in the developing human brain and maternal breast milk. Taurine is thought to influence fetal growth and brain development based on experimental rodent studies. As fish is an important dietary source of taurine, we investigated associations between taurine concentrations and child outcomes in a high fish consuming population. OBJECTIVE: To examine associations between maternal and cord serum taurine concentrations and birth anthropometric measures and cognitive development in children at 20 months of age. METHODS: Pregnant women were recruited between 2008 and 2011 as part of Nutrition Cohort 2 (NC2) of the Seychelles Child Development Study (SCDS). Maternal taurine serum concentrations were measured at 28 week's gestation and in cord serum. Child weight, length and head circumference were measured at birth and neurodevelopment was assessed using Bayley Scales of Infant Development II (BSID-II) at 20 months of age. Associations between taurine status, birth measures and neurodevelopmental outcomes were examined (n = 300) using regression models and adjusted for relevant covariates. RESULTS: Mean (SD) maternal and cord taurine concentrations were 124.9 (39.2) µmol/L (range 28.2-253.9 µmol/L) and 187.6 (60.0) µmol/L (range 55.0-417.4 µmol/L) respectively. We found no associations between maternal taurine concentrations and child anthropometric and neurodevelopmental measures (weight ß = -0.001, SE=0.001; length ß = -0.006, SE=0.006; head circumference ß = -0.002, SE=0.002; MDI ß = -0.005, SE=0.015; PDI ß = -0.004, SE=0.016; all P > 0.05), or between cord taurine concentrations and outcomes (weight ß = -0.001, SE<0.000; length ß = -0.001, SE=0.004; head circumference ß < 0.000, SE=0.002; MDI ß = 0.004, SE=0.010; PDI ß = -0.015, SE=0.012; all P > 0.05). CONCLUSION: The Seychellois population have high maternal and cord taurine concentrations owing to their high fish intake and may be considered taurine replete compared to individuals who consume a Westernised diet. This high taurine status may explain why there were no significant associations between maternal and cord taurine concentrations and outcomes after adjusting for covariates.

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A Bayesian Network (BN) is a probabilistic model that represents a set of variables using a directed acyclic graph (DAG). Current algorithms for learning BN structures from data focus on estimating the edges of a specific DAG, and often lead to many 'likely' network structures. In this paper, we lay the groundwork for an approach that focuses on learning global properties of the DAG rather than exact edges. This is done by defining the structural hypergraph of a BN, which is shown to be related to the inverse-covariance matrix of the network. Spectral bounds are derived for the normalized inverse-covariance matrix, which are shown to be closely related to the maximum indegree of the associated BN.

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Existing statistical methods can estimate a policy, or a mapping from covariates to decisions, which can then instruct decision makers (eg, whether to administer hypotension treatment based on covariates blood pressure and heart rate). There is great interest in using such data-driven policies in healthcare. However, it is often important to explain to the healthcare provider, and to the patient, how a new policy differs from the current standard of care. This end is facilitated if one can pinpoint the aspects of the policy (ie, the parameters for blood pressure and heart rate) that change when moving from the standard of care to the new, suggested policy. To this end, we adapt ideas from Trust Region Policy Optimization (TRPO). In our work, however, unlike in TRPO, the difference between the suggested policy and standard of care is required to be sparse, aiding with interpretability. This yields "relative sparsity," where, as a function of a tuning parameter, λ $$ \lambda $$ , we can approximately control the number of parameters in our suggested policy that differ from their counterparts in the standard of care (eg, heart rate only). We propose a criterion for selecting λ $$ \lambda $$ , perform simulations, and illustrate our method with a real, observational healthcare dataset, deriving a policy that is easy to explain in the context of the current standard of care. Our work promotes the adoption of data-driven decision aids, which have great potential to improve health outcomes.

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Purpose: Suicide risk is higher among violence-involved individuals. Intimate Partner Violence hotline workers are a critical source of support and can potentially be suicide prevention champions. Our primary goal was to examine the effectiveness of disseminating a free, online IPV-Suicide Prevention curriculum, via a randomized control trial, to hotline workers in ten states with the highest suicide and IPV homicide rates. Method: We divided the country into five regions and, based on criterion, chose two states in each region to randomize into the two arms of the study. We examined training participation and engagement between the two approaches: (1) 'dissemination as usual' (control) using a National Domestic Violence Hotline email and a postcard to state/county IPV directors, versus (2) 'enhanced dissemination' (intervention) using a four-point touch method (postcard, phone call, email, and letter) to 'drive' participation. Results: Participation increased in the intervention arm as approaches became more personal (i.e., email and phone calls vs. letters). Results indicate that traditional dissemination strategies such as email announcements and invitations are not as effective as varied and multiple touchpoints for IPV hotline staff. Conclusion: Successful dissemination strategies to promote digital training should consider the value added by personalized connection. Future research is needed to understand how to offer effective and efficient web-based training to those providing IPV and child abuse services.

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BACKGROUND: Maternal exposure to polycyclic aromatic hydrocarbons (PAHs), ubiquitous constituents of air pollution, has been associated with adverse birth outcomes. Yet it remains unclear whether and how socioeconomic status (SES) affects gestational PAH exposure. OBJECTIVE: To examine whether there are socioeconomic disparities in PAHs exposure among pregnant women from Rochester, NY, and if so, to what extent disproportionate proximity to air pollution sources, measured by residential distance to transportation-related sources, contributed to the exposure disparity. METHODS: We measured 1-hydroxypyrene concentrations in 726 urine samples collected from 305 pregnant women up to three samples throughout pregnancy. Residential distances to transportation-related sources were calculated based on participants' home addresses. We used linear mixed-effects models with random intercepts of participants to examine associations between 1-hydroxypyrene, SES indicators, and distance to transportation-related sources. We used structural equation modelling to assess to what extent distance to transportation-related sources contributes to the socioeconomic disparity in 1-hydroxypyrene concentrations. RESULTS: Reduced household income and maternal education level were both significant SES predictors of 1-hydroxypyrene concentrations, after the adjustment for other maternal demographic characteristics. Each interquartile range (IQR) increases in residential proximity to the airport (from 14.3 to 6.0 km), the railroad yard (from 22.3 to 6.0 km), and annual average daily traffic within 300 m (from 3796 to 99,933 vehicles/year) were associated with 15.0% (95%CI: 7.0-22.2%), 15.4% (95%CI: 6.5-23.5%), and 13.6% (95%CI: 4.7-23.3%) increases in 1-hydroxypyrene concentrations, respectively. Proximity to these sources jointly explained 10% (95%CI: 1.6-18.4%) of the 1-hydroxypyrene concentration change associated with decreases in SES as a latent variable defined by both household income and education level. IMPACT STATEMENT: Our findings suggest that efforts to address disproportionate residential proximity to transportation-related sources may reduce the socioeconomic disparity in PAH exposure.

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BACKGROUND: Previously, we found increased rates of ST-elevation myocardial infarction (STEMI) associated with increased ultrafine particle (UFP; <100 nm) concentrations in the previous few hours in Rochester, New York. Relative rates were higher after air quality policies and a recession reduced pollutant concentrations (2014-2016 versus 2005-2013), suggesting PM composition had changed and the same PM mass concentration had become more toxic. Tier 3 light duty vehicles, which should produce less primary organic aerosols and oxidizable gaseous compounds, likely making PM less toxic, were introduced in 2017. Thus, we hypothesized we would observe a lower relative STEMI rate in 2017-2019 than 2014-2016. METHODS: Using STEMI events treated at the University of Rochester Medical Center (2014-2019), UFP and other pollutants measured in Rochester, a case-crossover design, and conditional logistic regression models, we estimated the rate of STEMI associated with increased UFP and other pollutants in the previous hours and days in the 2014-2016 and 2017-2019 periods. RESULTS: An increased rate of STEMI was associated with each 3111 particles/cm3 increase in UFP concentration in the previous hour in 2014-2016 (lag hour 0: OR = 1.22; 95% CI = 1.06, 1.39), but not in 2017-2019 (OR = 0.94; 95% CI = 0.80, 1.10). There were similar patterns for black carbon, UFP11-50nm, and UFP51-100nm. In contrast, increased rates of STEMI were associated with each 0.6 ppb increase in SO2 concentration in the previous 120 h in both periods (2014-2016: OR = 1.26, 95% CI = 1.03, 1.55; 2017-2019: OR = 1.21, 95% CI = 0.87, 1.68). CONCLUSIONS: Greater rates of STEMI were associated with short term increases in concentrations of UFP and other motor vehicle related pollutants before Tier 3 introduction (2014-2016), but not afterwards (2017-2019). This change may be due to changes in PM composition after Tier 3 introduction, as well as to increased exposure misclassification and greater underestimation of effects from 2017 to 2019.

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In many studies of the health effects of toxicants, exposure is measured once even though exposure may be continuous. However, some studies collect repeated measurements on participants over an extended time with the goal of determining a long-term metric that captures the average or cumulative exposure. This can be challenging, especially when exposure is measured at irregular intervals and has some missing values. Here we describe a method for determining a measure of long-term exposure using data on postnatal mercury (Hg) from the Seychelles Child Development Study (SCDS) Main Cohort as a model. In this cohort (n = 779), we incorporate postnatal Hg values that were measured on most study participants at seven ages, three between 6 months and 5.5 years ("childhood"), and an additional four between 17 and 24 years ("early adulthood"). We develop time-weighted measures of average exposure during the childhood and the early adulthood periods and compare the strengths and weaknesses of our metric to two standard measures: overall average and cumulative exposure. We account for missing values through an imputation method that uses information about age- and sex-specific Hg means and the participant's Hg values at similar ages to estimate subject-specific missing Hg values. We compare our method to the implicit imputation assumed by these two standard methods, and to Fully Conditional Specification (FCS), an alternative method of imputing missing data. To determine the accuracy of our imputation method we use data from participants with no missing Hg values in the relevant time window. The imputed values from our proposed method are substantially closer to the observed values on average than the average or cumulative exposure, while also performing slightly better than FCS. In conclusion, time-weighted long-term exposure appears to offer advantages over cumulative exposure in longitudinal studies with repeated measures where the follow-up period for a toxicant is similar for all participants. Additionally, our method to impute missing values maximizes the number of participants for whom the overall exposure metric can be calculated and should provide a more accurate long-term exposure metric than standard methods when exposure has missing values. Our method is applicable to any study of long-term toxicant effects when longitudinal exposure measurements are available but have missing values.

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Bisphenol A (BPA) is a polymer used in the production of polycarbonate plastics and epoxy resins. An estrogen mimic, prenatal BPA exposure has been associated with several behavioral outcomes in children; however, the impact of maternal demographic and economic factors on associations between BPA and child behavioral outcomes have not been examined. The objective of this study was to examine associations between prenatal maternal urinary BPA and behavior in 4-5 year old girls, and to assess whether socio-demographic factors modify this relationship. Mothers enrolled in The Infant Development and Environment Study (TIDES) provided a single spot urine at enrollment (median gestational age 11 weeks) and completed the Behavior Assessment System for Children-2 (BASC-2) and Social Responsiveness Scale-2 (SRS-2) when their daughters were 4-5 years of age. Mother-daughter pairs with complete phthalate, BASC-2, SRS-2, and covariate data were included in this analysis (N = 244). BPA was detectable in 93 % of urine samples. We used multivariable linear regression analyses to estimate associations between maternal urinary log10-transformed BPA concentration and BASC-2 subscale and composite scores and SRS-2 Total Score. To examine the role of socioeconomic and demographic factors associated with study site, we stratified by TIDES center, comparing those enrolled at University of Rochester Medical Center (URMC), a predominately lower socioeconomic population, and those enrolled elsewhere: University of Washington, University of Minnesota, and University of California San Francisco, whose populations share similar higher socioeconomic demographic characteristics. Across all centers, no associations were seen between BPA and BASC-2 or SRS-2 scores. When stratifying by center, BPA was significantly associated with greater social impairment as measured by the SRS-2 Total Score (ß-coefficient [95 % confidence intervals]: 5.1 [1.0, 9.2]) in URMC participants (N = 61). In non-URMC participants (N = 183), BPA was significantly associated with lower BASC-2 Internalizing composite (-3.3 [-6.7, 0.0]) and Depression subscale scores (-3.4 [-6.7, 0.0]) while no associations were seen between BPA and SRS-2 scores. Our findings suggest that sociodemographic factors may modify the impacts of maternal prenatal BPA on developmental endpoints.

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