Long term trends in source apportioned particle number concentrations in Rochester NY.

During the past two decades, efforts have been made to further reduce particulate air pollution across New York State through various Federal and State policy implementations. Air quality has also been affected by economic drivers like the 2007-2009 recession and changing costs for different approaches to electricity generation. Prior work has focused on particulate matter with aerodynamic diameter ≤2.5 µm. However, there is also interest in the effects of ultrafine particles on health and the environment and analyses of changes in particle number concentrations (PNCs) are also of interest to assess the impacts of changing emissions. Particle number size distributions have been measured since 2005. Prior apportionments have been limited to seasonal analyses over a limited number of years because of software limitations. Thus, it has not been possible to perform trend analyses on the source-specific PNCs. Recent development have now permitted the analysis of larger data sets using Positive Matrix Factorization (PMF) including its diagnostics. Thus, this study separated and analyzed the hourly averaged size distributions from 2005 to 2019 into two data sets; October to March and April to September. Six factors were resolved for both data sets with sources identified as nucleation, traffic 1, traffic 2, fresh secondary inorganic aerosol (SIA), aged SIA, and O3-rich aerosol. The resulting source-specific PNCs were combined to provide continuous data sets and analyzed for trends. The trends were then examined with respect to the implementation of regulations and the timing of economic drivers. Nucleation was strongly reduced by the requirement of ultralow (<15 ppm) sulfur on-road diesel fuel in 2006. Secondary inorganic particles and O3-rich PNCs show strong summer peaks. Aged SIA was constant and then declined substantially in 2015 but rose in 2019. Traffic 1 and 2 have steadily declined bur rose in 2019.

The contributions of neonatal inhalation of copper to air pollution-induced neurodevelopmental outcomes in mice.

Exposures to ambient ultrafine particle (UFP) air pollution (AP) during the early postnatal period in mice (equivalent to human third trimester brain development) produce male-biased changes in brain structure, including ventriculomegaly, reduced brain myelination, alterations in neurotransmitters and glial activation, as well as impulsive-like behavioral characteristics, all of which are also features characteristic of male-biased neurodevelopmental disorders (NDDs). The purpose of this study was to ascertain the extent to which inhaled Cu, a common contaminant of AP that is also dysregulated across multiple NDDs, might contribute to these phenotypes. For this purpose, C57BL/6J mice were exposed from postnatal days 4-7 and 10-13 for 4 hr/day to inhaled copper oxide (CuxOy) nanoparticles at an environmentally relevant concentration averaging 171.9 ng/m3. Changes in brain metal homeostasis and neurotransmitter levels were determined following termination of exposure (postnatal day 14), while behavioral changes were assessed in adulthood. CuxOy inhalation modified cortical metal homeostasis and produced male-biased disruption of striatal neurotransmitters, with marked increases in dopaminergic function, as well as excitatory/inhibitory imbalance and reductions in serotonergic function. Impulsive-like behaviors in a fixed ratio (FR) waiting-for-reward schedule and a fixed interval (FI) schedule of food reward occurred in both sexes, but more prominently in males, effects which could not be attributed to altered locomotor activity or short-term memory. Inhaled Cu as from AP exposures, at environmentally relevant levels experienced during development, may contribute to impaired brain function, as shown by its ability to disrupt brain metal homeostasis and striatal neurotransmission. In addition, its ability to evoke impulsive-like behavior, particularly in male offspring, may be related to striatal dopaminergic dysfunction that is known to mediate such behaviors. As such, regulation of air Cu levels may be protective of public health.

IL-17A neutralization fails to attenuate airway remodeling and potentiates a proinflammatory lung microenvironment in diacetyl-exposed rats.

Bronchiolitis obliterans (BO) is a devastating lung disease that can develop following inhalation exposure to certain chemicals. Diacetyl (DA) is one chemical commonly associated with BO development when inhaled at occupational levels. Previous studies in rats have shown that repetitive DA vapor exposures increased lung CD4+CD25+ T cells and bronchoalveolar (BAL) interleukin-17A (IL-17A) concentrations concurrent with the development of airway remodeling. We hypothesized that IL-17A neutralization would attenuate the severity of airway remodeling after repetitive DA vapor exposures. Sprague-Dawley rats were exposed to 200 parts-per-million DA vapor or filtered air (RA) for 6 h/day × 5 days and monitored for 2 wk postexposure. Treatment with IL-17A neutralization (αIL-17A) or IgG (control) began immediately following exposures and continued twice weekly until study's end. Lungs were harvested for histology, flow cytometry, and BAL analyses. Survival, oxygen saturations, and percent weight change decreased significantly in DA-exposed versus RA-exposed rats, but did not differ significantly between DA + αIL-17A versus DA + IgG. Similarly, the number nor severity of airway lesions did not differ significantly between DA + αIL-17A versus DA + IgG rats despite the percentage of lung regulatory T cells increasing with decreased BAL IL-17A concentrations. Ashcroft scoring of the distal lung parenchyma suggested worse parenchymal remodeling in DA + αIL-17A versus DA + IgG rats with increased expression of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß), and nuclear factor-kappa B (NF-κB). Collectively, IL-17A neutralization in DA-exposed rats failed to attenuate airway remodeling with increased expression of pro-inflammatory cytokines TNF-α, IL-1ß, and NF-κB.NEW & NOTEWORTHY Interleukin-17A (IL-17A) neutralization has shown benefit previously in preclinical models of transplant-associated bronchiolitis obliterans (BO), yet it remains unknown whether IL-17A neutralization has similar benefit for other forms of BO. Here, IL-17A neutralization fails to prevent severe airway remodeling in rats exposed repetitively to the flavoring chemical diacetyl, and instead, promotes a proinflammatory microenvironment with increased expression of TNF-α, IL-1ß, and NF-κB within the lung.

Triggering of ST-elevation myocardial infarction by ultrafine particles in New York: Changes following Tier 3 vehicle introduction.

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.

The potential involvement of inhaled iron (Fe) in the neurotoxic effects of ultrafine particulate matter air pollution exposure on brain development in mice.

BACKGROUND: Air pollution has been associated with neurodevelopmental disorders in epidemiological studies. In our studies in mice, developmental exposures to ambient ultrafine particulate (UFP) matter either postnatally or gestationally results in neurotoxic consequences that include brain metal dyshomeostasis, including significant increases in brain Fe. Since Fe is redox active and neurotoxic to brain in excess, this study examined the extent to which postnatal Fe inhalation exposure, might contribute to the observed neurotoxicity of UFPs. Mice were exposed to 1 µg/m3 Fe oxide nanoparticles alone, or in conjunction with sulfur dioxide (Fe (1 µg/m3) + SO2 (SO2 at 1.31 mg/m3, 500 ppb) from postnatal days 4-7 and 10-13 for 4 h/day. RESULTS: Overarching results included the observations that Fe + SO2 produced greater neurotoxicity than did Fe alone, that females appeared to show greater vulnerability to these exposures than did males, and that profiles of effects differed by sex. Consistent with metal dyshomeostasis, both Fe only and Fe + SO2 exposures altered correlations of Fe and of sulfur (S) with other metals in a sex and tissue-specific manner. Specifically, altered metal levels in lung, but particularly in frontal cortex were found, with reductions produced by Fe in females, but increases produced by Fe + SO2 in males. At PND14, marked changes in brain frontal cortex and striatal neurotransmitter systems were observed, particularly in response to combined Fe + SO2 as compared to Fe only, in glutamatergic and dopaminergic functions that were of opposite directions by sex. Changes in markers of trans-sulfuration in frontal cortex likewise differed in females as compared to males. Residual neurotransmitter changes were limited at PND60. Increases in serum glutathione and Il-1a were female-specific effects of combined Fe + SO2. CONCLUSIONS: Collectively, these findings suggest a role for the Fe contamination in air pollution in the observed neurotoxicity of ambient UFPs and that such involvement may be different by chemical mixture. Translation of such results to humans requires verification, and, if found, would suggest a need for regulation of Fe in air for public health protection.

Long-term trends of ultrafine and fine particle number concentrations in New York State: Apportioning between emissions and dispersion.

In the past several decades, a variety of efforts have been made in the United States to improve air quality, and ambient particulate matter (PM) concentrations have been used as a metric to evaluate the efficacy of environmental policies. However, ambient PM concentrations result from a combination of source emission rates and meteorological conditions, which also change over time. Dispersion normalization was recently developed to reduce the influence of atmospheric dispersion and proved an effective approach that enhanced diel/seasonal patterns and thus provides improved source apportionment results for speciated PM mass and particle number concentration (PNC) measurements. In this work, dispersion normalization was incorporated in long-term trend analysis of 11-500 nm PNCs derived from particle number size distributions (PNSDs) measured in Rochester, NY from 2005 to 2019. Before dispersion normalization, a consistent reduction was observed across the measured size range during 2005-2012, while after 2012, the decreasing trends slowed down for accumulation mode PNCs (100-500 nm) and reversed for ultrafine particles (UFPs, 11-100 nm). Through dispersion normalization, we showed that these changes were driven by both emission rates and dispersion. Thus, it is important for future studies to assess the effects of the changing meteorological conditions when evaluating policy effectiveness on controlling PM concentrations. Before and after dispersion normalization, an evident increase in nucleation mode particles was observed during 2015-2019. This increase was possibly enabled by a cleaner atmosphere and will pose new challenges for future source apportionment and accountability studies.

Repetitive diacetyl vapor exposure promotes ubiquitin proteasome stress and precedes bronchiolitis obliterans pathology.

Bronchiolitis obliterans (BO) is a devastating lung disease seen commonly after lung transplant, following severe respiratory tract infection or chemical inhalation exposure. Diacetyl (DA; 2,3-butanedione) is a highly reactive alpha-diketone known to cause BO when inhaled, however, the mechanisms of how inhalation exposure leads to BO development remains poorly understood. In the current work, we combined two clinically relevant models for studying the pathogenesis of DA-induced BO: (1) an in vivo rat model of repetitive DA vapor exposures with recovery and (2) an in vitro model of primary human airway epithelial cells exposed to pure DA vapors. Rats exposed to 5 consecutive days 200 parts-per-million DA 6 h per day had worsening survival, persistent hypoxemia, poor weight gain, and histologic evidence of BO 14 days after DA exposure cessation. At the end of exposure, increased expression of the ubiquitin stress protein ubiquitin-C accumulated within DA-exposed rat lung homogenates and localized primarily to the airway epithelium, the primary site of BO development. Lung proteasome activity increased concurrently with ubiquitin-C expression after DA exposure, supportive of significant proteasome stress. In primary human airway cultures, global proteomics identified 519 significantly modified proteins in DA-exposed samples relative to controls with common pathways of the ubiquitin proteasome system, endosomal reticulum transport, and response to unfolded protein pathways being upregulated and cell-cell adhesion and oxidation-reduction pathways being downregulated. Collectively, these two models suggest that diacetyl inhalation exposure causes abundant protein damage and subsequent ubiquitin proteasome stress prior to the development of chemical-induced BO pathology.

Effects of concentrated ambient ultrafine particulate matter on hallmarks of Alzheimer's disease in the 3xTgAD mouse model.

BACKGROUND: Exposure to air pollution has been identified as a possible environmental contributor to Alzheimer's Disease (AD) risk. As the number of people with AD worldwide continues to rise, it becomes vital to understand the nature of this potential gene-environment interaction. This study assessed the effects of short-term exposures to concentrated ambient ultrafine particulates (UFP, <100 nm) on measurements of amyloid-ß, tau, and microglial morphology. METHODS: Two cohorts of aged (12.5-14 months) 3xTgAD and NTg mice were exposed to concentrated ambient UFP or filtered air for 2 weeks (4-h/day, 4 days/week). Bronchoalveolar lavage fluid and brain tissue were collected twenty-four hours following the last exposure to evaluate lung inflammation, tau pathology, amyloid-ß pathology, and glial cell morphology. RESULTS: No exposure- or genotype-related changes were found with any of the measures of lung inflammation or in the hippocampal staining density of astrocyte marker glial fibrillary acidic protein. The microglia marker, ionized calcium binding adaptor molecule 1, and amyloid-ß marker, 6E10, exhibited significant genotype by exposure interactions such that levels were lower in the UFP-exposed as compared to filtered air-exposed 3xTgAD mice. When microglia morphology was assessed by Sholl analysis, microglia from both NTg mouse groups were ramified. The 3xTgAD air-exposed mice had the most ameboid microglia, while the 3xTgAD UFP-exposed mice had microglia that were comparatively more ramified. The 3xTgAD air-exposed mice had more plaques per region of interest as measured by Congo red staining as well as more plaque-associated microglia than the 3xTgAD UFP-exposed mice. The number of non-plaque-associated microglia was not affected by genotype or exposure. Levels of soluble and insoluble human amyloid-ß42 protein were measured in both 3xTgAD groups and no exposure effect was found. In contrast, UFP-exposure led to significant elevations in phosphorylated tau in 3xTgAD mice as compared to those that were exposed to air, as measured by pT205 staining. CONCLUSIONS: Exposure to environmentally relevant levels of ultrafine particulates led to changes in tau phosphorylation and microglial morphology in the absence of overt lung inflammation. Such changes highlight the need to develop greater mechanistic understanding of the link between air pollution exposure and Alzheimer's disease.

Diesel exhaust particle exposure reduces expression of the epithelial tight junction protein Tricellulin.

BACKGROUND: While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been paid to their effects on the airway epithelial barrier. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems. METHODS: 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 µg/cm2 SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 µg/m3; 2 h per day for 5 days) and changes in the tight junction protein Tricellulin were assessed 2 weeks post exposure. RESULTS: A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran. This reduction in epithelial barrier integrity corresponded to a significant reduction in expression of the tight junction protein Tricellulin. siRNA mediated knockdown of Tricellulin recapitulated changes in barrier function caused by DEP exposure. Neonatal exposure to aerosolized DEP caused a significant reduction in lung Tricellulin 2 weeks post exposure at both the protein and mRNA level. CONCLUSION: Short term exposure to DEP causes a significant reduction in epithelial barrier integrity through a reduction in the tight junction protein Tricellulin. Neonatal exposure to aerosolized DEP caused a significant and sustained reduction in Tricellulin protein and mRNA in the lung, suggesting that early life exposure to inhaled DEP may cause lasting changes in airway epithelial barrier function.

Wavelength-Dependent Photochemistry and Biological Relevance of a Bilirubin Dipyrrinone Subunit.

Phototherapy is a standard treatment for severe neonatal jaundice to remove toxic bilirubin from the blood. Here, the wavelength-dependent photochemistry of vinylneoxanthobilirubic acid methyl ester, a simplified model of a bilirubin dipyrrinone subunit responsible for a lumirubin-like structural rearrangement, was thoroughly investigated by liquid chromatography and mass and absorption spectroscopies, with the application of a multivariate curve resolution analysis method supplemented with quantum chemical calculations. Irradiation of the model chromophore leads to reversible Z → E photoisomerization followed by reversible photocyclization to a seven-membered ring system (formed as a mixture of diastereomers). Both the isomerization processes are efficient (ΦZE ∼ ΦEZ ∼ 0.16) when irradiated in the wavelength range of 360-410 nm, whereas the E-isomer cyclization (Φc = 0.006-0.008) and cycloreversion (Φ-c = 0.002-0.004) reactions are significantly less efficient. The quantum yields of all processes were found to depend strongly on the wavelength of irradiation, especially when lower energy photons were used. Upon irradiation in the tail of the absorption bands (490 nm), both the isomers exhibit more efficient photoisomerization (ΦZE ∼ ΦEZ ∼ 0.30) and cyclization (Φc = ∼0.07). In addition, the isomeric bilirubin dipyrrinone subunits were found to possess important antioxidant activities while being substantially less toxic than bilirubin.

Protein thiol oxidation in the rat lung following e-cigarette exposure.

E-cigarette (e-cig) aerosols are complex mixtures of various chemicals including humectants (propylene glycol (PG) and vegetable glycerin (VG)), nicotine, and various flavoring additives. Emerging research is beginning to challenge the "relatively safe" perception of e-cigarettes. Recent studies suggest e-cig aerosols provoke oxidative stress; however, details of the underlying molecular mechanisms remain unclear. Here we used a redox proteomics assay of thiol total oxidation to identify signatures of site-specific protein thiol modifications in Sprague-Dawley rat lungs following in vivo e-cig aerosol exposures. Histologic evaluation of rat lungs exposed acutely to e-cig aerosols revealed mild perturbations in lung structure. Bronchoalveolar lavage (BAL) fluid analysis demonstrated no significant change in cell count or differential. Conversely, total lung glutathione decreased significantly in rats exposed to e-cig aerosol compared to air controls. Redox proteomics quantified the levels of total oxidation for 6682 cysteine sites representing 2865 proteins. Protein thiol oxidation and alterations by e-cig exposure induced perturbations of protein quality control, inflammatory responses and redox homeostasis. Perturbations of protein quality control were confirmed with semi-quantification of total lung polyubiquitination and 20S proteasome activity. Our study highlights the importance of redox control in the pulmonary response to e-cig exposure and the utility of thiol-based redox proteomics as a tool for elucidating the molecular mechanisms underlying this response.

Natural pseurotins and analogs thereof inhibit activation of B-cells and differentiation into the plasma cells.

BACKGROUND: The frequency of allergic diseases is constantly rising. Dysregulated production of isotype E immunoglobulins is one of the key factors behind allergic reactions and its modulation is therefore an important target for pharmacological intervention. Natural products of the pseurotin family were reported to be inhibitors of IgE production in B-cells. Mechanistic details underlying these effects are however not well understood. PURPOSE: In the present study, we synthesized new analogs of natural pseurotins and extensively investigated their inhibitory effects on activation, proliferation and differentiation of B-cells, as well as on the production of IgE. STUDY DESIGN: Effects of two natural pseurotins (pseurotins A and D) and a collection of fully synthetic pseurotin analogs were studied on mouse B-cells stimulated by the combination of IL-4 and E. coli lipopolysaccharide. The IgE production was determined along with cell viability and cell proliferation. The phosphorylation of selected members of the STAT transcription factor family was subsequently investigated. Finally, the in vivo effect of pseurotin D on the ovalbumin-induced delayed type hypersensitivity response was tested in mice. RESULTS: We discovered that several fully synthetic pseurotin analogs were able to decrease the production of IgE in stimulated B-cells with potency comparable to that of pseurotins A and D. We found that the two natural pseurotins and the active synthetic analogs inhibited the phosphorylation of STAT3, STAT5 and STAT6 proteins in stimulated B-cells, resulting in the inhibition of B-cell proliferation and differentiation into the plasma cells. In vivo, pseurotin D decreased ovalbumin-induced foot pad edema. CONCLUSION: Our results advance the current mechanistic understanding of the pseurotin-induced inhibition of IgE production in B-cells by linking the effect to STAT signaling, and associated modulation of B-cell proliferation and differentiation. Together with our finding that structurally simpler pseurotin analogs were able to reproduce the effects of natural pseurotins, the presented work has implications for the future research on these secondary metabolites in the context of allergic diseases.

Wintertime Wood Smoke, Traffic Particle Pollution, and Preeclampsia.

Previous studies have reported associations between ambient fine particle concentrations and preeclampsia; however, the impact of particulate pollution on early- and late-onset preeclampsia is understudied. Furthermore, few studies have examined the association between source-specific particles such as markers of traffic pollution or wood combustion on adverse pregnancy outcomes. Electronic medical records and birth certificate data were linked with land-use regression models in Monroe County, New York for 2009 to 2013 to predict monthly pollutant concentrations for each pregnancy until the date of clinical diagnosis during winter (November-April) for 16 116 births. Up to 30% of ambient wintertime fine particle concentrations in Monroe County, New York is from wood combustion. Multivariable logistic regression was used to separately estimate the odds of preeclampsia (all, early-, and late-onset) associated with each interquartile range increase in fine particles, traffic pollution, and woodsmoke concentrations during each gestational month, adjusting for maternal characteristics, birth hospital, temperature, and relative humidity. Each 3.64 µg/m3 increase in fine particle concentration was associated with an increased odds of early-onset preeclampsia during the first (odds ratio, 1.35 [95% CI, 1.08-1.68]), second (odds ratio, 1.51 [95% CI, 1.23-1.86]), and third (odds ratio, 1.25 [95% CI, 1.06-1.46]) gestational months. Increases in traffic pollution and woodsmoke during the first gestational month were also associated with increased odds of early-onset preeclampsia. Increased odds of late-onset preeclampsia were not observed. Our findings suggest that exposure to wintertime particulate pollution may have the greatest effect on maternal cardiovascular health during early pregnancy.

Correction to: Term birth weight and ambient air pollutant concentrations during pregnancy, among women living in Monroe County, New York.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Changes in triggering of ST-elevation myocardial infarction by particulate air pollution in Monroe County, New York over time: a case-crossover study.

BACKGROUND: Previous studies have reported that fine particle (PM2.5) concentrations triggered ST elevation myocardial infarctions (STEMI). In Rochester, NY, multiple air quality policies and economic changes/influences from 2008 to 2013 led to decreased concentrations of PM2.5 and its major constituents (SO42-, NO3-, elemental and primary organic carbon). This study examined whether the rate of STEMI associated with increased ambient gaseous and PM component concentrations was different AFTER these air quality policies and economic changes (2014-2016), compared to DURING (2008-2013) and BEFORE these polices and changes (2005-2007). METHODS: Using 921 STEMIs treated at the University of Rochester Medical Center (2005-2016) and a case-crossover design, we examined whether the rate of STEMI associated with increased PM2.5, ultrafine particles (UFP, < 100 nm), accumulation mode particles (AMP, 100-500 nm), black carbon, SO2, CO, and O3 concentrations in the previous 1-72 h was modified by the time period related to these pollutant source changes (BEFORE, DURING, AFTER). RESULTS: Each interquartile range (3702 particles/cm3) increase in UFP concentration in the previous 1 h was associated with a 12% (95% CI = 3%, 22%) increase in the rate of STEMI. The effect size was larger in the AFTER period (26%) than the DURING (5%) or BEFORE periods (9%). There were similar patterns for black carbon and SO2. CONCLUSIONS: An increased rate of STEMI associated with UFP and other pollutant concentrations was higher in the AFTER period compared to the BEFORE and DURING periods. This may be due to changes in PM composition (e.g. higher secondary organic carbon and particle bound reactive oxygen species) following these air quality policies and economic changes.

Term birth weight and ambient air pollutant concentrations during pregnancy, among women living in Monroe County, New York.

Increased ambient air pollutant concentrations during pregnancy have been associated with reduced birth weight, but the etiologically relevant pregnancy time window(s) is/are unclear. In 76,500 singleton births in Monroe County, NY (2005-2016), who were 37-42 gestational weeks at delivery, we used generalized linear models to regress term birth weight against mean gestational month pollutant concentrations, adjusting for mean temperature, and maternal, infant, and medical service use characteristics. Overall, there were no clear patterns of term birth weight change associated with increased concentrations of any pollutant across gestational months. However, among Hispanic women only, increases in all pollutants, except O3, in multiple gestational months, were associated with decreased term birth weight. Each 3.25 µg/m3 increase in PM2.5 concentration in the 6th gestational month was associated with a -20.4 g (95% CI = -34.0, -6.8) reduction in term birth weight among Hispanic women, but a 4.1 g (95% CI = -2.5, 10.8) increase among non-Hispanic mothers (p for interaction < 0.001). Although ambient air pollutant concentrations during pregnancy were not associated with reduced term birth weight among women of all ethnicities living in Monroe County, this observed association in Hispanic mothers may be a result of less exposure misclassification and bias (due to closer residential proximity to the monitoring site).

Spatial-temporal variations of summertime ozone concentrations across a metropolitan area using a network of low-cost monitors to develop 24 hourly land-use regression models.

Ten relatively-low-cost ozone monitors (Aeroqual Series 500 with OZL ozone sensor) were deployed to assess the spatial and temporal variability of ambient ozone concentrations across residential areas in the Monroe County, New York from June to October 2017. The monitors were calibrated in the laboratory and then deployed to a local air quality monitoring site where they were compared to the federal equivalent method values. These correlations were used to correct the measured ozone concentrations. The values were also used to develop hourly land use regression models (LUR) based on the deletion/substitution/addition (D/S/A) algorithm that can be used to predict the spatial and temporal concentrations of ozone at any hour of a summertime day and given location in Monroe County. Adjusted R2 values were high (average 0.83) with the highest adjusted R2 for the model between 8 and 9 AM (i.e. 1-2 h after the peak of primary emissions during the morning rush hours). Spatial predictors with the highest positive effects on ozone estimates were high intensity developed areas, low and medium intensity developed areas, forests + shrubs, average elevation, Interstate + highways, and the annual average vehicular daily traffic counts. These predictors are associated with potential emissions of anthropogenic and biogenic precursors. Maps developed from the models exhibited reasonable spatial and temporal patterns, with low ozone concentrations overnight and the highest concentrations between 11 AM and 5 PM. The adjusted R2 between the model predictions and the measured values varied between 0.79 and 0.87 (mean = 0.83). The combined use of the network of low-cost monitors and LUR modeling provide useful estimates of intraurban ozone variability and exposure estimates that will be used in future epidemiological studies.

Ambient wintertime particulate air pollution and hypertensive disorders of pregnancy in Monroe County, New York.

BACKGROUND: Previous studies have reported associations between ambient fine particle (PM2.5) concentrations and hypertensive disorders of pregnancy (HDP). However, none have examined whether ultrafine particles (UFP; < 100 nm), accumulation mode particles (AMP; 100-500 nm), markers of traffic pollution (black carbon; BC), or wood burning (Delta-C; (30% of ambient wintertime PM2.5 in Monroe County, NY is from wood burning)) are associated with an increased odds of HDP. We estimated the odds of HDP associated with increased concentrations of PM2.5, UFP, AMP, BC, and Delta-C in each gestational month during winter months. METHODS: Electronic medical records and birth certificate data were linked with land-use regression models in Monroe County, New York in 2009-2013 to predict monthly pollutant concentrations during winter (November-April) based on maternal residential address for 16,637 births. Using multivariable logistic regression, we estimated the odds of HDP associated with each interquartile range (IQR) increase in PM2.5, UFP, AMP, BC, and Delta-C concentrations during each gestational month, adjusting for maternal characteristics, birth hospital, temperature, and relative humidity. RESULTS: Each 0.52 µg/m3 increase in Delta-C concentration during the 7th gestational month was associated with an increased odds of HDP (odds ratio (OR) = 1.21; 95% confidence interval (CI) = 1.01, 1.45), with a similar sized estimate in month 8 (OR = 1.18; 95%CI = 0.98, 1.43). Non-statistically significant increased odds of HDP associated with IQR increases in BC concentrations during months 3 (OR = 1.12; 95%CI = 0.98, 1.28) and 7 (OR = 1.12; 95%CI = 0.96, 1.29) were observed. Increased odds of HDP were not observed for PM2.5, UFP, or AMP. CONCLUSIONS: Our findings suggest that maternal exposure to wood smoke in Monroe County during winter is associated with an increased odds of HDP during late gestation. Additional studies are needed to evaluate the effect of wood smoke on HDP and to explore effects on other pregnancy outcomes.

Enantioselective Conjugate Additions of 2-Alkoxycarbonyl-3(2 H)-furanones.

Enantioselective conjugate additions of in situ generated 2-alkoxycarbonyl-3(2 H)-furanones to three distinct types of π-electrophiles (terminal alkynones, α-bromo enones, and α-benzyl nitroalkenes) are reported. Catalysis by a nickel(II)-diamine complex provided alkynone-derived adducts with high enantioselectivity, preferentially as the Z-isomers, and completely suppressed the undesired O-alkylation pathway. A cupreidine-based catalyst enabled extension of the enantioselective conjugate additions to α-bromo enones and α-benzyl nitroalkenes. The densely functionalized adducts that result are useful precursors to synthetic analogs of spirocyclic natural products pseurotins.

Hourly land-use regression models based on low-cost PM monitor data.

Land-use regression (LUR) models provide location and time specific estimates of exposure to air pollution and thereby improve the sensitivity of health effects models. However, they require pollutant concentrations at multiple locations along with land-use variables. Often, monitoring is performed over short durations using mobile monitoring with research-grade instruments. Low-cost PM monitors provide an alternative approach that increases the spatial and temporal resolution of the air quality data. LUR models were developed to predict hourly PM concentrations across a metropolitan area using PM concentrations measured simultaneously at multiple locations with low-cost monitors. Monitors were placed at 23 sites during the 2015/16 heating season. Monitors were externally calibrated using co-located measurements including a reference instrument (GRIMM particle spectrometer). LUR models for each hour of the day and weekdays/weekend days were developed using the deletion/substitution/addition algorithm. Coefficients of determination for hourly PM predictions ranged from 0.66 and 0.76 (average 0.7). The hourly-resolved LUR model results will be used in epidemiological studies to examine if and how quickly, increases in ambient PM concentrations trigger adverse health events by reducing the exposure misclassification that arises from using less time resolved exposure estimates.