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Prior studies reported that exposure to increased concentrations of fine particulate matter (PM

Background: Previous studies suggest that pathways reducing oxidative stress may have a protective effect against adverse cardiac responses associated with ambient PM. However, few studies have directly assessed total antioxidant capacity (TAC) as a potential effect modifier of cardiac responses to increased ambient PM. Objectives: We examined if TAC modifies the association between ambient PM and markers of heart rate variability (HRV), repolarization, systemic inflammation, and systolic blood pressure (SBP) in post-infarction patients. Methods: We recruited 76 patients with a recent coronary event (myocardial infarction or unstable angina) who participated in a cardiac rehabilitation program from June 2006 to November 2009 in Rochester, New York. Ambient fine particle (PM2.5,≤2.5 μm in aerodynamic diameter), accumulation mode particle (AMP, 100-500 nm) and ultrafine particle (UFP, 10-100 nm) concentrations were measured continuously by fixed-site monitors. Markers of HRV and repolarization were measured by continuous Holter electrocardiogram (ECG) recordings before and during exercise sessions of the rehabilitation program. Blood pressure was measured and venous blood samples were collected before exercise to measure TAC and inflammation markers. We applied linear mixed models to assess changes in markers of HRV, repolarization, systemic inflammation, and SBP associated with increased PM concentrations in the low, medium and high TAC tertile groups, after adjusting for covariates including temperature, calendar time since the beginning of the study, visit number, month of year, and hour of day. Results: Based on subject-visits with available TAC, we observed increases in SBP, C-reactive protein, and fibrinogen, and decreases in rMSSD (square root of the mean of the sum of the squared differences between adjacent normal to normal intervals) and SDNN (standard deviation of normal to normal beat intervals) associated with increased PM2.5, AMP and UFP in the previous 6-120 h (e.g. change in SBP associated with each interquartile range (IQR) increase in PM2.5 lagged 0-5 h was 1.27 mmHg [95%CI: 0.09, 2.46 mmHg]). However, we did not observe a consistent pattern of effect measure modification by TAC for any combination of pollutant and outcome (e.g. changes in SBP associated with each IQR increase in PM2.5 lagged 0-5 h for the low, medium and high TAC tertile groups were 1.93 mmHg [95%CI: 0.23, 3.63 mmHg], -0.31 mmHg [95%CI: -2.62, 2.01 mmHg], and 1.29 mmHg [95%CI: -0.64, 3.21 mmHg], respectively. P for interaction=0.28). Conclusions: In a post-infarction population, total antioxidant capacity does not appear to modify the association between biomarkers of heart rate variability, repolarization, systemic inflammation, and systolic blood pressure and ambient PM concentrations in the previous 6-120 h.

Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, were found to increase central nervous system (CNS) metastasis in mice. Our study investigated in humans whether antidepressants, and specifically SSRIs, increased the relative odds of CNS metastasis. We identified 189 cases of CNS metastasis amongst breast cancer, melanoma, and non-Hodgkin lymphoma subjects who were diagnosed with CNS metastasis or infiltration between January 1, 2005 and September 30, 2013 and 756 controls (patients without CNS metastasis or infiltration). Using logistic regression, we estimated the relative odds of CNS metastasis associated with antidepressant use adjusting for relevant covariates. The prevalence of antidepressants was 28.6 % in cases and 27.5 % in controls, whereas SSRIs were used in 16.9 % of cases and 17.3 % of controls. Among all patients, antidepressants were not associated with CNS metastasis or infiltration. No consistent patterns of association were observed in the analyses of other cancer subsets or exposure measures, with the possible exception of an increased risk of CNS metastasis associated with 'any SSRI use' among breast cancer patients (OR = 1.73, 95 % CI = 0.75, 4.04). We did not observe clear patterns of association, which may be due in part to the small sample size in many of our analyses.

Background Emissions control programs targeting certain air pollution sources may alter PM2.5 composition, as well as the risk of adverse health outcomes associated with PM2.5. Objectives We examined temporal changes in the risk of emergency department (ED) visits for cardiovascular diseases (CVDs) and asthma associated with short-term increases in ambient PM2.5 concentrations in Los Angeles, California. Methods Poisson log-linear models with unconstrained distributed exposure lags were used to estimate the risk of CVD and asthma ED visits associated with short-term increases in daily PM2.5 concentrations, controlling for temporal and meteorological confounders. The models were run separately for three predefined time periods, which were selected based on the implementation of multiple emissions control programs (EARLY: 2005-2008; MIDDLE: 2009-2012; LATE: 2013-2016). Two-pollutant models with individual PM2.5 components and the remaining PM2.5 mass were also considered to assess the influence of changes in PM2.5 composition on changes in the risk of CVD and asthma ED visits associated with PM2.5 over time. Results The relative risk of CVD ED visits associated with a 10 μg/m3 increase in 4-day PM2.5 concentration (lag 0-3) was higher in the LATE period (rate ratio = 1.020, 95% confidence interval = [1.010, 1.030]) compared to the EARLY period (1.003, [0.996, 1.010]). In contrast, for asthma, relative risk estimates were largest in the EARLY period (1.018, [1.006, 1.029]), but smaller in the following periods. Similar temporal differences in relative risk estimates for CVD and asthma were observed among different age and season groups. No single component was identified as an obvious contributor to the changing risk estimates over time, and some components exhibited different temporal patterns in risk estimates from PM2.5 total mass, such as a decreased risk of CVD ED visits associated with sulfate over time. Conclusions Temporal changes in the risk of CVD and asthma ED visits associated with short-term increases in ambient PM2.5 concentrations were observed. These changes could be related to changes in PM2.5 composition (e.g., an increasing fraction of organic carbon and a decreasing fraction of sulfate in PM2.5). Other factors such as improvements in healthcare and differential exposure misclassification might also contribute to the changes.

The northeastern United States has experienced significant emissions reductions in the last two decades leading to a decrease in PM2.5, major gaseous pollutants (SO2, CO, NOx) and ultrafine particles (UFPs) concentrations. Emissions controls were implemented for coal-fired power plants, and new heavy-duty diesel trucks were equipped with particle traps and NOx control systems, and ultralow sulfur content is mandatory for both road and non-road diesel as well as residual oil for space heating. At the same time, economic changes also influenced the trends in air pollutants. Investigating the influence of these changes on ultrafine particle sources is fundamental to determine the success of the mitigation strategies and to plan future actions. Particle size distributions have been measured in Rochester, NY since January 2002. The particle sources were investigated with positive matrix factorization (PMF) of the size distributions (11&ndash, 470 nm) and measured criteria pollutants during five periods (2002&ndash, 2003, 2004&ndash, 2007, 2008&ndash, 2010, 2011&ndash, 2013, and 2014&ndash, 2016) and three seasons (winter, summer, and transition). Monthly, weekly, and hourly source contributions patterns were evaluated.

Rationale: Fine particulate matter air pollution of 2.5 μm or less in diameter (PM2.5) has been associated with an increased risk of respiratory disease, but assessments of specific respiratory infections in adults are lacking. Objectives: To estimate the rate of respiratory infection healthcare encounters in adults associated with acute increases in PM2.5 concentrations. Methods: Using case–crossover methods, we studied 498,118 adult New York State residents with a primary diagnosis of influenza, bacterial pneumonia, or culture-negative pneumonia upon hospitalization or emergency department (ED) visit (2005–2016). We estimated the relative rate of healthcare encounters associated with increases in PM2.5 in the previous 1–7 days and explored differences before (2005–2007), during (2008–2013), and after (2014–2016) implementation of air quality policies and economic changes. Results: Interquartile range increases in PM2.5 over the previous 7 days were associated with increased excess rates (ERs) of culture-negative pneumonia hospitalizations (2.5%; 95% confidence interval [CI], 1.7–3.2%) and ED visits (2.5%; 95% CI, 1.4–3.6%), and increased ERs of influenza ED visits (3.9%; 95% CI, 2.1–5.6%). Bacterial pneumonia hospitalizations, but not ED visits, were associated with increases in PM2.5 and, though imprecise, were of a similar magnitude to culture-negative pneumonia (Lag Day 6 ER, 2.3%; 95% CI, 0.3–4.3). Increased relative rates of influenza ED visits and culture-negative pneumonia hospitalizations were generally larger in the “after” period (P

The United States has experienced substantial air pollutant emissions reductions in the last two decades. Among others, emissions produced by electricity generation plants and industries were significantly lowered. Ultralow (

Prior studies reported that exposure to increased concentrations of fine particulate matter (PM2.5) were associated with increased rates of hospitalization and emergency department (ED) visits for asthma and chronic obstructive pulmonary disease (COPD). In this study, rates were examined from 2005 to 2016 using a case-crossover design to ascertain if there have been changes in the rates per unit mass exposure given substantial reductions in PM2.5 concentration and changes in its composition. PM2.5 concentrations were reduced through a combination of policies designed to improve air quality and economic drivers, including the 2008 economic recession and shifts in the relative costs of coal and natural gas. The study period was split into three periods reflecting that much of the emissions changes occurred between 2008 and 2013. Thus, the three periods were defined as: BEFORE (2005 to 2007), DURING (2008–2013), and AFTER (2014–2016). In general, the number of hospitalizations and ED visits declined with the decreased concentration of PM2.5. However, the rate of COPD hospitalizations and asthma ED visits associated with each interquartile range increase in ambient PM2.5 concentration was larger in the AFTER period than the DURING and BEFORE periods. For example, each 6.8 μg/m3 increase in PM2.5 on the same day was associated with 0.4% (0.0%, 0.8%), 0.3% (−0.2%, 0.7%), and 2.7% (1.9%, 3.5) increases in the rate of asthma emergency department visits in the BEFORE, DURING, and AFTER periods, respectively, suggesting the same mass concentration of PM2.5 was more toxic in the AFTER period.

The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p

Conditional probability functions are commonly used for source identification purposes in air pollution studies. CBPF (conditional bivariate probability function) categorizes the probability of high concentrations being observed at a location by wind direction/speed and investigate the directionality of local sources. PSCF (potential source contribution function), a trajectory-ensemble method, identifies the source regions most likely to be associated with high measured concentrations. However, these techniques do not allow the direct identification of areas where changes in emissions have occurred. This study presents an extension of conditional probability methods in which the differences between conditional probability values for temporally different sets of data can be used to explore changes in emissions from source locations. The differential CBPF and differential PSCF were tested using a long-term series of air quality data (12 years; 2005/2016) collected in Rochester, NY. The probability functions were computed for each of 4 periods that represent known changes in emissions. Correlation analyses were also performed on the results to find pollutants undergoing similar changes in local and regional sources. The differential probability functions permitted the identification of major changes in local and regional emission location. In Rochester, changes in local air pollution were related to the shutdown of a large coal power plant (SO2) and to the abatement measures applied to road and off-road traffic (primary pollutants). The concurrent effects of these changes in local emissions were also linked to reduced concentrations of nucleation mode particles. Changes in regional source areas were related to the decreases in secondary inorganic aerosol and organic carbon. The differential probabilities for sulfate, nitrate, and organic aerosol were consistent with differences in the available National Emission Inventory annual emission values. Changes in the source areas of black carbon and PM2.5 mass concentrations were highly correlated.

Previous studies have reported increased risks of myocardial infarction in association with elevated ambient particulate matter (PM) in the previous hour(s). However, whether PM can trigger mechanisms that act on this time scale is still unclear. We hypothesized that increases in PM are associated with rapid changes in measures of heart rate variability and repolarization. We used data from panel studies in Augsburg, Germany, and Rochester, New York, USA, and two controlled human exposure studies in Rochester. Data included ECG recordings from all four studies, controlled exposures to (concentrated) ultrafine particles (UFP; particles with an aerodynamic diameter 2.5, aerodynamic diameter 2.5 concentrations in the preceding six hours in both panel studies. We did not find consistent associations between particle metrics and T-wave complexity. This study provided consistent evidence that recent exposures to UFP and PM2.5 can induce acute pathophysiological responses.

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

BACKGROUND: Previous studies have reported associations between ambient fine particle (PM(2.5)) concentrations and hypertensive disorders of pregnancy (HDP). However, none have examined whether ultrafine particles (UFP

IntroductionIschemic stroke treatment is time-sensitive, and barriers to providing prehospital care encountered by Emergency Medical Services (EMS) providers have been under-studied.Hypothesis/ProblemThis study described barriers to providing prehospital care, identified predictors of these barriers, and assessed the impact of these barriers on EMS on-scene time and administration of tissue plasminogen activator (tPA) in the emergency department (ED).MethodsA retrospective cohort study was performed using the Get With The Guidelines-Stroke (GWTG-S; American Heart Association [AHA]; Dallas, Texas USA) registry at two hospitals to identify ischemic stroke patients arriving by EMS. Variables were abstracted from prehospital and hospital medical records and merged with registry data. Barriers to care were grouped into themes. Logistic regression was used to identify predictors of barriers to care, and bi-variate tests were used to assess differences in EMS on-scene time and the proportion of patients receiving tPA between patients with and without barriers.ResultsBarriers to providing prehospital care were documented for 15.5% of patients: 29.6% related to access, 26.7% communication, 23.0% extrication and transportation, 20.0% refusal, and 14.1% assessment/management. Non-white and non-black race (OR: 3.69; 95% CI, 1.63-8.36) and living alone (OR: 1.53; 95% CI, 1.05-2.23) were associated with greater odds of barriers to providing care. The EMS on-scene time was ≥15 minutes for 70.4% of patients who had a barrier to care, compared with 49.0% of patients who did not (PConclusionsBarriers to providing prehospital care were documented for a sizable proportion of ischemic stroke patients, with the majority related to patient access and communication, and occurred more frequently among non-white and non-black patients and those living alone. Although EMS on-scene time was longer for patients with barriers to care, the proportion of patients receiving tPA in the ED did not differ.LiT, CushmanJT, ShahMN, KellyAG, RichDQ, JonesCMC. Barriers to providing prehospital care to ischemic stroke patients: predictors and impact on care. Prehosp Disaster Med.2018;33(5):501–507.

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.

Background Previous studies reported triggering of acute cardiovascular events by short-term increasedPM2.5 concentrations. From 2007 to 2013, national and New York state air quality policies and economic influences resulted in reduced concentrations of PM2.5 and other pollutants across the state. We estimated the rate of cardiovascular hospital admissions associated with increased PM2.5 concentrations in the previous 1–7 days, and evaluated whether they differed before (2005–2007), during (2008–2013), and after these concentration changes (2014–2016). Methods Using the Statewide Planning and Research Cooperative System (SPARCS) database, we retained all hospital admissions with a primary diagnosis of nine cardiovascular disease (CVD) subtypes, for residents living within 15 miles of PM2.5 monitoring sites in Buffalo, Rochester, Albany, Queens, Bronx, and Manhattan from 2005 to 2016 (N = 1,922,918). We used a case-crossover design and conditional logistic regression to estimate the admission rate for total CVD, and nine specific subtypes, associated with increased PM2.5 concentrations. Results Interquartile range (IQR) increases in PM2.5 on the same and previous 6 days were associated with 0.6%–1.2% increases in CVD admission rate (2005–2016). There were similar patterns for cardiac arrhythmia, ischemic stroke, congestive heart failure, ischemic heart disease (IHD), and myocardial infarction (MI). Ambient PM2.5 concentrations and annual total CVD admission rates decreased across the period. However, the excess rate of IHD admissions associated with each IQR increase in PM2.5 in previous 2 days was larger in the after period (2.8%; 95%CI = 1.5%–4.0%) than in the during (0.6%; 95%CI = 0.0%–1.2%) or before periods (0.8%; 95%CI = 0.2%–1.3%), with similar patterns for total CVD and MI, but not other subtypes. Conclusions While pollutant concentrations and CVD admission rates decreased after emission changes, the same PM2.5 mass was associated with a higher rate of ischemic heart disease events. Future work should confirm these findings in another population, and investigate whether specific PM components and/or sources trigger IHD events.

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.

Land use regression modeling (LUR) through local scale circular modeling domains has been used to predict traffic-related air pollution such as nitrogen oxides (NOX). LUR modeling for fine particulate matters (PM), which generally have smaller spatial gradients than NOX, has been typically applied for studies involving multiple study regions. To increase the spatial coverage for fine PM and key constituent concentrations, we designed a mobile monitoring network in Monroe County, New York to measure pollutant concentrations of black carbon (BC, wavelength at 880 nm), ultraviolet black carbon (UVBC, wavelength at 3700 nm) and Delta-C (the difference between the UVBC and BC concentrations) using the Clarkson University Mobile Air Pollution Monitoring Laboratory (MAPL). A Deletion/Substitution/Addition (D/S/A) algorithm was conducted, which used circular buffers as a basis for statistics. The algorithm maximizes the prediction accuracy for locations without measurements using the V-fold cross-validation technique, and it reduces overfitting compared to other approaches. We found that the D/S/A LUR modeling approach could achieve good results, with prediction powers of 60%, 63%, and 61%, respectively, for BC, UVBC, and Delta-C. The advantage of mobile monitoring is that it can monitor pollutant concentrations at hundreds of spatial points in a region, rather than the typical less than 100 points from a fixed site saturation monitoring network. This research indicates that a mobile saturation sampling network, when combined with proper modeling techniques, can uncover small area variations (e.g., 10 m) in particulate matter concentrations.

Background Perchlorate and similar anions compete with iodine for uptake into the thyroid by the sodium iodide symporter (NIS). This may restrict fetal growth via impaired thyroid hormone production. Methods We collected urine samples from 107 pregnant women and used linear regression to estimate differences in newborn size and gestational age associated with increases in perchlorate, thiocyanate, nitrate, and perchlorate equivalence concentrations (PEC; measure of total NIS inhibitor exposure). Results NIS inhibitor concentrations were not associated with newborn weight, length, or gestational age. Each 2.62 ng/μg creatinine increase in perchlorate was associated with smaller head circumference (0.32 cm; 95% CI: −0.66, 0.01), but each 3.38 ng/μg increase in PEC was associated with larger head circumference (0.48 cm; −0.01, 0.97). Conclusions These anions may have effects on fetal development (e.g. neurocognitive) that are not reflected in gross measures. Future research should focus on other abnormalities in neonates exposed to NIS inhibitors.

Background To date, there have been relatively few studies of acute cardiovascular responses to controlled ozone inhalation, although a number of observational studies have reported significant positive associations between both ambient ozone levels and acute cardiovascular events and long-term ozone exposure and cardiovascular mortality. Objectives We hypothesized that short-term controlled exposure to low levels of ozone in filtered air would induce autonomic imbalance, repolarization abnormalities, arrhythmia, and vascular dysfunction. Methods This randomized crossover study of 87 healthy volunteers 55–70 years of age was conducted at three sites using a common protocol, from June 2012 to April 2015. Subjects were exposed for 3 h in random order to 0 ppb (filtered air), 70 ppb ozone, and 120 ppb ozone, alternating 15 min of moderate exercise with 15 min of rest. A suite of cardiovascular endpoints was measured the day before, the day of, and up to 22 h after each exposure. Mixed effect linear and logit models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. Site and time were included in the models. Results We found no significant effects of ozone exposure on any of the primary or secondary measures of autonomic function, repolarization, ST segment change, arrhythmia, or vascular function (systolic blood pressure and flow-mediated dilation). Conclusions In this multicenter study of older healthy women and men, there was no convincing evidence for acute effects of 3-h, relatively low-level ozone exposures on cardiovascular function. However, we cannot exclude the possibility of effects with higher ozone concentrations, more prolonged exposure, or in subjects with underlying cardiovascular disease. Further, we cannot exclude the possibility that exposure to ambient ozone and other pollutants in the days before the experimental exposures obscured or blunted cardiovascular biomarker response to the controlled ozone exposures.

Significant changes in emission sources have occurred in the northeastern United States over the past decade, due in part to the implementation of emissions standards, the introduction and addition of abatement technologies for road transport, changes in fuel sulfur content for road and non-road transport, as well as economic impacts of a major recession and differential fuel prices. These changes in emission scenarios likely affected the concentrations of airborne submicron particles. This study investigated the characteristics of 11-500nm particle number concentrations and their size spectra in Rochester, NY during the past 15years (2002 to 2016). The modal structure, diurnal, weekly and monthly patterns of particle number concentrations are analyzed. Long-term trends are quantified using seasonal-trend decomposition procedures based on "Loess", Mann-Kendall regression with Theil-Sen slope and piecewise regression. Particle concentrations underwent significant (p0.05) downward trends. An annual decrease of -323particles/cm

To compare grocery costs between relatively high energy density foods and sugar-sweetened/high-fat beverages and lower energy density foods and more healthful beverages in children's diets.Sixty foods were divided into high and low energy density baskets. Fourteen beverages were designated to either basket based on fat and added-sugar content. Prices were collected at 60 grocery stores and composite costs compared between baskets using Wilcoxon tests.The cost per kilogram of high energy density foods was greater, but the cost per quart of sugar-sweetened/high-fat beverages was lower than more healthful beverages. The cost per 1000 calories and the cost per serving of the high energy density basket were lower.The relative cost of high and low energy density foods in children's diets depends on how cost is quantified. "Pound-for-pound," lower energy density foods and more healthful beverages are generally less expensive, but high energy density foods and less healthful beverages are cheaper per serving. Cost metrics including other factors (e.g. time cost) may further clarify the role of grocery prices in children's diets.

Previously, we reported that increased PM concentrations triggered ST elevation myocardial infarction (STEMI), with the largest rate of MI when pollutant mixtures were high in secondary particles. ...

The development and implementation of effective policies for controlling PM2.5 mass concentrations and protecting human health depend upon the identification and apportionment of its sources. In this study, the PM2.5 sources affecting 6 urban and 2 rural sites across New York State during the period 2005–2016 were determined. The extracted profiles were compared to identify state-wide common profiles. The source contributions provide detailed, long-term quantification of the emission sources across the state during the investigated period (2005–2016). Seven factors were common to all sites: secondary sulfate, secondary nitrate, spark-ignition emissions, diesel emissions, road dust, biomass burning, and pyrolyzed organic (OP) rich. The largest contributors were secondary sulfate, secondary nitrate, spark-ignition (gasoline), diesel, and OP-rich. Secondary sulfate concentrations ranged from 2.3 μg m−3 at Whiteface to 3.2 μg m−3 at Buffalo and the Bronx. The highest secondary sulfate fractional contributions were found at the rural sites (∼46% of PM2.5 mass) also showed the highest OP-rich contributions (∼19%). Secondary nitrate showed the highest concentrations at the urban sites representing ∼17% of PM2.5 mass (1.6 ± 0.3 μg m−3 on average). Urban sites also showed the highest average spark-ignition concentrations (1.7 ± 0.2 μg m−3, ∼18%) and diesel emissions (1.0 ± 0.2 μg m−3, ∼10%). During this period, secondary sulfate concentrations declined likely related to the implementation of mitigation strategies for controlling SO2 emissions and the changing economics of electricity generation. Similarly, diesel and secondary nitrate showed decreases in concentrations likely associated with the introduction of emissions controls and improved quality fuels for heavy-duty diesel on-road trucks and buses. Spark-ignition concentrations showed an increase across the state during 2014–2016 associated with the increase of registered vehicles in New York State.

The performance of a low cost ozone monitor (Aeroqual Series 500 portable gas monitors using a metal oxide sensor for ozone; model OZL) was assessed under field conditions. Ten ozone monitors were calibrated under clean-air laboratory conditions and controlled ozone concentrations of 5 to 100 ppb. Good linearity and response were obtained relative to a research-grade ozone monitor. One monitor was co-located at a regulatory air quality monitoring station that uses a U.S. federal equivalent method (FEM) ozone analyzer. Raw data from the Aeroqual monitor collected over 4 months (June-October) at a 10-minute time-resolution, showed good agreement (r(2)=0.83) with the FEM values but with an overestimation of ~12%. Data were averaged to different time resolutions; 1 h time averaged concentrations showed the best fit with the FEM results (r(2)=0.87). Data analyses suggested the potential of interferences due to temperature, relative humidity, nitrogen oxides, and volatile organic compounds. Correction models using temperature, humidity, and nitrogen dioxide (NO(2)) were tested to relate the monitor concentrations to the FEM values. Temperature and humidity were two readily available variables. The model (#3) that added NO(2) did not provide a substantial improvement in the fit. Thus, the models with only temperature and humidity can be easily developed by any user. The best model explained 91% of the variance and showed statistically significant improvement of the goodness of fits as well as decreased influence of the interfering variables on the diurnal and weekly patterns. The correction models were also able to lower the effect of seasonal temperature changes, allowing the use of the monitors over long-term sampling campaigns. Thus, the Aeroqual ozone monitor can return “FEM-like” concentrations after appropriate corrections. Data provided by a network of monitors could provide intra-urban spatial variations in ozone concentrations and provide more accurate human exposure assessments by reducing exposure misclassification.

Introduction Carboplatin is widely used to treat lung cancer in the United States as an alternative to cisplatin. Several studies have demonstrated that cisplatin-based regimen is associated with a high frequency of thromboembolic complications. However, there has been limited investigation directly comparing the risk of thromboembolic events (TEEs) between cisplatin- and carboplatin-treated patients with lung cancer. Methods All lung cancer patients treated with cisplatin or carboplatin at Wilmot Cancer Center, University of Rochester between 2011 and 2014 were included. Patient characteristics including exposure (cisplatin vs. carboplatin) and outcome (TEEs between the time of the first dose of cisplatin or carboplatin and 4 weeks after the last dose) were collected by reviewing electronic medical records. A Fisher’s exact test was used to compare the proportion of incident TEEs between cisplatin and carboplatin groups. The risk of TEE associated with carboplatin compared to cisplatin was assessed using multiple logistic regression. Results Among 415 subjects, 317 patients (76.4%) received carboplatin and 98 (23.6%) patients received cisplatin. In the carboplatin group, 10.9% (33/302) of evaluable patients developed treatment-related TEEs vs. 14.7% (14/95) in the cisplatin group. There was no significant difference in the risk of developing TEEs between the two groups (P = 0.32). However, 15.2% of carboplatin-related TEEs were arterial thromboses compared to none in the cisplatin group. Conclusions The incidence of carboplatin-related TEEs was high in lung cancer patients without significant difference in the risk of developing TEEs between cisplatin and carboplatin groups. Potential use of prophylactic anticoagulation in all platinum-treated patients should be further investigated.

It is assumed that platelets in diseased conditions share similar properties to platelets in healthy conditions, although this has never been examined in detail for myocardial infarction (MI). We examined platelets from patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) compared with platelets from healthy volunteers to evaluate for differences in platelet phenotype and function. Platelet activation was examined and postreceptor signal transduction pathways were assessed. Platelet-derived plasma biomarkers were evaluated by receiver operator characteristic curve analysis. Maximum platelet activation through the thromboxane receptor was greater in STEMI than in NSTEMI but less through protease-activated receptor 1. Extracellular-signal related-kinase 5 activation, which can activate platelets, was increased in platelets from subjects with STEMI and especially in platelets from patients with NSTEMI. Matrix metalloproteinase 9 (MMP9) protein content and enzymatic activity were several-fold greater in platelets with MI than in control. Mean plasma MMP9 concentration in patients with MI distinguished between STEMI and NSTEMI (area under curve [AUC] 75% [confidence interval (CI) 60-91], P = 0.006) which was superior to troponin T (AUC 66% [CI 48-85, P = 0.08), predicting STEMI with 80% sensitivity (95% CI 56-94), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P 0.0001), and NSTEMI with 50% sensitivity (CI 27-70), 90% specificity (CI 68-99), 70% AUC (CI 54-86, P = 0.03). Platelets from patients with STEMI and NSTEMI show differences in platelet surface receptor activation and postreceptor signal transduction, suggesting the healthy platelet phenotype in which antiplatelet agents are often evaluated in preclinical studies is different from platelets in patients with MI.

Previous studies have examined changes in heart rate variability (HRV*) and repolarization associated with increased particulate matter (PM) concentrations on the same and previous few days. However, few studies have examined whether these health responses to PM occur within a few hours or even less. Moreover, it is not clear whether exposure of subjects to ambient or-controlled PM concentrations both lead to similar health effects or whether any of the subjects' individual characteristics modify any of their responses to PM. The aims of the cur- rent study were to investigate whether exposure to PM was associated with rapid changes (60 minutes or con- current hour up to a delay of 6 hours) in markers of car- diac rhythni or changes in total antioxidant capacity (a marker of protection against oxidative stress) and whether any PM effects on cardiac rhythm markers were modified by total antioxidant capacity, age, obesity, smoking, hypertension, exertion, prior myocardial infarction (MI), or medication.We obtained data from a completed study in Augsburg, Germany (a panel study in N= 109 subjects, including a group with type 2 diabetes or impaired glucose tolerance [IGT; also known as prediabetes]) and a group of other- wise healthy subjects with a potential genetic susceptibil- ity to detoxifying and inflammatory pathways (Hampel et al. 2012b), as well as three completed studies in Rochester, New York (the REHAB panel study of N= 76 postinfarction patients in a cardiac rehabilitation pro- gram [Rich et al. 2012b]; the UPDIABETES study of con- trolled exposure to ultrafine particles [UFPs, particles with an aerodynamic diameter100 nm] of N = 19 patients with type 2 diabetes [Stewart et al. 2010; Vora et al. 2014j; and the UPCON controlled-exposure study of concentrated UFP exposure in N = 20 young, healthy, life- time nonsmokers). Data included 5-minute and 1-hour values for HRV and repolarization parameters from elec- trocardiogram (ECG) recordings and total antioxidant capacity measured in stored blood samples. Ambient con- centrations of UFPs, accumulation-mode particles (AMP, particles with an aerodynamic diameter of 100-500 nm), fine PM (PM2.5, particles with an aerodynamic diameter 2.5 pm), and black carbon (BC) were also available. We first conducted factor analyses in each study to find subgroups of correlated ECG outcomes and to reduce the number of outcomes examined in our statistical models. We then restricted the statistical analyses to the factors and representative.outcomes that were common to all four studies, including total HRV (measured as the standard deviation of normal-to-normal [NN] beat intervals [SDNNj), parasympathetic modulation (measured as the root mean square of the successive differences [RMSSD between adjacent NN beat intervals), and T-wave morphol- ogy (measured as T-wave complexity). Next, we used addi- tive mixed models to estimate the change in each outcome associated with increased pollutant concentrations in the . concurrent and previous 6 hours and with 5-minute inter- vals up to the previous 60 minutes, accounting for the correlation of repeated outcome measures for each subject and adjusting for time trend, hour of the day, temperature, relative humidity, day of the week, month, and visit number. Because multiple comparisons were an issue in our. analyses, we used a discovery-and-replication approach to draw conclusions across studies for each research question.In the Augsburg study, interquartile range (IQR) increases in UFP concentrations lagged 2 to 5 hours were associated with 1%-3% decreases in SDNN (e.g., lagged 3 hours in the group with a genetic susceptibility: -2.26%; 95% confidence interval [CI], -3.98% to -0.53%). In the REHAB study, similarly, IQR increases in UFP concentra- tions in the previous 5 hours were associated with3% decreases in SDNN (e.g., lagged 1 hour: -2.69%; 95% CI, -5.13% to -0.26%). We also found decreases in SDNN associated with IQR increases in total particle count-(a surrogate for UFP) in the UPDIABETES study (lagged 1 hour: -13.22%; 95% CI, -24.11% to -2.33%) but not in the UPCON study. In the Augsburg study, IQR increases in PM2.5 concen- trations in the concurrent hour and lagged 1-5 hours, AMP concentrations lagged 1 and 3 hours, and BC con- centrations lagged 1-5 hours were associated with -1%-5% decreases in SDNN (e.g., PM2.5 lagged 2 hours in the group with diabetes or IGT: -4.59%; 95% CI, -7.44% to -1.75%). In the REHAB study, IQR increases in PM2.5 concentrations lagged 5 and 6 hours and AMP concentra- tions in the concurrent hour and lagged up to 5 hours were associated with 1%-2% decreases in SDNN (e.g., PM2.5 lagged 4 hours: -2.13%; 95% CI, -3.91% to -0.35%). In the Augsburg study, IQR increases in PM2.5 concen- trations in the concurrent hour and BC lagged 1 and 6 hours were associated with 3%-7% decreases in RMSSD (e.g., PM2.5 concurrent hour in the group with diabetes or IGT: -7.20%; 95% CI, -12.11% to -2.02%). In the REHAB study, similarly, increases in PM2.5 concen- trations lagged 4 to 6 hours-though not AMP or BC con- centrations at any lag hour-were associated with -2.5%-3.5% decreases in RMSSD (e.g., PM2.5 lagged 5 hours: -3.49%; 95% CI, -6.13% to -0.84%). We did not find consistent evidence of any pollutant effects on T-wave complexity in 1-hour recordings. For 5-minute record- ings, there was no consistent evidence of UFP effects on SDNN, RMSSD, or T-wave complexity at any 5-minute interval within 60 minutes. We further concluded that these replicated hourly effects of UFP and PM2.5 on short-term measures of SDNN and RMSSD generally did not differ between the groups in the studies (i.e., type 2 diabetes, pre-diabetes/IGT, post- infarction, and healthy subjects). Last, we found no con- sistent evidence of effects of any pollutant on total anti- oxidant capacity and no consistent evidence of modification of our PM2.5-outcome associations by any of the potential effect modifiers.Increased UFP concentrations were associated with decreased SDNN in both of the panel studies and one of the two controlled-exposure studies. We also found that decreased SDNN was associated with both increased PM2.5 and AMP concentrations in the previous 6 hours in the panel studies and that decreased RMSSD was associ- ated with increased PM2.5 concentrations in the previous 6 hours in the panel studies. We therefore concluded that the research questions were replicated. Our findings suggest that both UFPs and PM2.5 are associated with autonomic dysfunction within hours of exposure, which may in part. explain the previously reported risk of acute cardiovascular events associated with increased PM in the previous few hours. Despite the heterogeneity of the study populations,and protocols, our findings provided consistent evidence for the induction of rapid pathophysiological responses by UFPs and PM2.5- The absence of consistent associations between UFPs, PM2.5, and these outcomes when examining shorter time intervals indicates that the 5- to 60-minute responses may be less pronounced than the responses occurring within hours. However, the findings from the 5-minute intervals may have been affected by the variety of proto- cols and conditions from study to study as well as by the potential effects of underlying diseases (e.g., healthy indi- viduals versus individuals with diabetes or a recent cor- onary artery. event), physical activity, circadian rhythms, stress, and/or medications.

Prior work has reported acute associations between ST-elevation myocardial infarction (STEMI) and short-term increases in airborne particulate matter. Subsequently, the association between STEMI and hourly measures of Delta-C (marker of woodsmoke) and black carbon (marker of traffic pollution) measured at a central site in Rochester, NY, were examined, but no association was found. Therefore, land use regression estimates of Delta-C and black carbon concentrations at each patient’s residence were developed for 246 STEMI patients treated at the University of Rochester Medical Center during the winters of 2008–2012. Using case-crossover methods, the rate of STEMI associated with increased Delta-C and BC concentration on the same and previous 3 days was estimated after adjusting for 3-day mean temperature and relative humidity. Non-statistically significant increased rates of STEMI associated with interquartile range increases in concentrations of BC in the previous 2 days (1.10 μg/m3; OR = 1.12; 95% CI 0.93, 1.35) and Delta-C in the previous 3 days (0.43 μg/m3; OR = 1.16; 95% CI 0.96, 1.40) were found. Significantly increased rates of STEMI associated with interquartile range increases in concentrations of BC (1.23 μg/m3; OR = 1.04; 95% CI = 0.87, 1.24) or Delta-C (0.40 μg/m3; OR = 0.94; 95% CI = 0.85, 1.09) on the same day were not observed likely due, in part, to temporal misalignment. Therefore, sophisticated spatial-temporal models will be needed to minimize exposure error and bias by better predicting concentrations at individual locations for individual hours, especially for outcomes with short-term responses to air pollution (

Using a quasi-experimental opportunity offered by greatly restricted air pollution emissions during the Beijing Olympics compared to before and after the Olympics, we conducted the current study to compare ultrafine particles (UFPs) and fine particles (PM2.5) in their associations with biomarkers reflecting multiple pathophysiological pathways linking exposure and cardiorespiratory events. Number concentrations of particles (13.0-764.7 nm) and mass concentrations of PM2.5 were measured at two locations within 9 km from the residence and workplace of 125 participating Beijing residents. Each participant was measured 6 times for biomarkers of autonomic function (heart rate, systolic and diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand, and P-selectin), pulmonary inflammation and oxidative stress (exhaled nitric oxide and exhaled breath condensate pH, malondialdehyde, and nitrite), and systemic inflammation and oxidative stress (urinary malondialdehyde and 8-hydroxy-2'-deoxyguanosine, plasma fibrinogen, and white blood cells). Linear mixed models were used to estimate associations of biomarkers with UFPs and PM2.5 measured 1-7 days prior to biomarker measurements (lags). We found that the correlation coefficient for UFPs at two locations (∼ 9 km apart) was 0.45, and at the same location, the correlation coefficient for PM2.5 vs UFPs was -0.18. Changes in biomarker levels associated with increases in UFPs and PM2.5 were comparable in magnitude. However, associations of certain biomarkers with UFPs had different lag patterns compared to those with PM2.5, suggesting that the ultrafine size fraction (≤ 100 nm) and the fine size fraction (∼ 100 nm to 2.5 μm) of PM2.5 are likely to affect PM-induced pathophysiological pathways independently.

Objectives Increased air pollutant concentrations have been linked to several asthma-related outcomes in children, including respiratory symptoms, medication use, and hospital visits. However, few studies have examined effects of ultrafine particles in a pediatric population. Our primary objective was to examine the effects of ambient concentrations of ultrafine particles on asthma exacerbation among urban children and determine whether consistent treatment with inhaled corticosteroids could attenuate these effects. We also explored the relationship between asthma exacerbation and ambient concentrations of accumulation mode particles, fine particles (≤2.5 micrograms [μm]; PM 2.5 ), carbon monoxide, sulfur dioxide, and ozone. We hypothesized that increased 1–7 day concentrations of ultrafine particles and other pollutants would be associated with increases in the relative odds of an asthma exacerbation, but that this increase in risk would be attenuated among children receiving school-based corticosteroid therapy. Methods We conducted a pilot study using data from 3 to 10 year-old children participating in the School-Based Asthma Therapy trial. Using a time-stratified case-crossover design and conditional logistic regression, we estimated the relative odds of a pediatric asthma visit treated with prednisone ( n =96 visits among 74 children) associated with increased pollutant concentrations in the previous 7 days. We re-ran these analyses separately for children receiving medications through the school-based intervention and children in a usual care control group. Results Interquartile range increases in ultrafine particles and carbon monoxide concentrations in the previous 7 days were associated with increases in the relative odds of a pediatric asthma visit, with the largest increases observed for 4-day mean ultrafine particles (interquartile range=2088 p/cm 3 ; OR=1.27; 95% CI=0.90–1.79) and 7-day mean carbon monoxide (interquartile range=0.17 ppm; OR=1.63; 95% CI=1.03–2.59). Relative odds estimates were larger among children receiving school-based inhaled corticosteroid treatment. We observed no such associations with accumulation mode particles, black carbon, fine particles (≤2.5 μm), or sulfur dioxide. Ozone concentrations were inversely associated with the relative odds of a pediatric asthma visit. Conclusions These findings suggest a response to markers of traffic pollution among urban asthmatic children. Effects were strongest among children receiving preventive medications through school, suggesting that this group of children was particularly sensitive to environmental triggers. Medication adherence alone may be insufficient to protect the most vulnerable from environmental asthma triggers. However, further research is necessary to confirm this finding.

Anti-platelet medications may be less efficacious in certain clinical contexts. Recent studies suggest the need for a gender-specific, personalized approach to anti-platelet therapy. Our goal was to determine whether platelets from women and men activate differently in health and following

We previously reported an increased risk of stillbirth associated with increases in trimester-specific ambient air pollutant concentrations. Here, we consider whether sudden increase in the mean ambient air pollutant concentration immediately before delivery triggers stillbirth.We used New Jersey linked fetal death and hospital discharge data and hourly ambient air pollution measurements from particulate matter ≤ 2.5 mm (PM2.5), carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2) monitors across New Jersey for the years 1998-2004. For each stillbirth, we assigned the concentration of air pollutants from the closest monitoring site within 10 km of the maternal residence. Using a time-stratified case-crossover design and conditional logistic regression, we estimated the relative odds of stillbirth associated with interquartile range (IQR) increases in the mean pollutant concentrations on lag day 2 and lag days 2 through 6 before delivery, and whether these associations were modified by maternal risk factors.The relative odds of stillbirth increased with IQR increases in the mean concentrations of CO (odds ratio [OR] = 1.20, 95% confidence interval [CI] = 1.05-1.37), SO2 (OR = 1.11, 95% CI = 1.02-1.22), NO2 (OR = 1.11, 95% CI = 0.97-1.26), and PM2.5 (OR = 1.07, 95% CI = 0.93-1.22) 2 days before delivery. We found similar associations with increases in pollutants 2 through 6 days before delivery. These associations were not modified by maternal risk factors.Short-term increases in ambient air pollutant concentrations immediately before delivery may trigger stillbirth.

Central-site monitors do not account for factors such as outdoor-to-indoor transport and human activity patterns that influence personal exposures to ambient fine-particulate matter (PM(2.5)). We describe and compare different ambient PM(2.5) exposure estimation approaches that incorporate human activity patterns and time-resolved location-specific particle penetration and persistence indoors. Four approaches were used to estimate exposures to ambient PM(2.5) for application to the New Jersey Triggering of Myocardial Infarction Study. These include: Tier 1, central-site PM(2.5) mass; Tier 2A, the Stochastic Human Exposure and Dose Simulation (SHEDS) model using literature-based air exchange rates (AERs); Tier 2B, the Lawrence Berkeley National Laboratory (LBNL) Aerosol Penetration and Persistence (APP) and Infiltration models; and Tier 3, the SHEDS model where AERs were estimated using the LBNL Infiltration model. Mean exposure estimates from Tier 2A, 2B, and 3 exposure modeling approaches were lower than Tier 1 central-site PM(2.5) mass. Tier 2A estimates differed by season but not across the seven monitoring areas. Tier 2B and 3 geographical patterns appeared to be driven by AERs, while seasonal patterns appeared to be due to variations in PM composition and time activity patterns. These model results demonstrate heterogeneity in exposures that are not captured by the central-site monitor.

Introduction: Increased particulate air pollution (PM) has been associated with increases in fibrinogen while vitamin D and n-3 fatty acids have been studied as modifiable determinants of cardiovas...

Background Laboratory findings have suggested that systemic and vascular inflammation can impair the antiatherogenic function of high-density lipoproteins (HDLs). However, evidence from population studies is sparse. Objective The objective of the study was to assess if blood inflammatory markers modify the risk of recurrent coronary events associated with apolipoprotein A-I (apoA-I) and HDL cholesterol (HDL-C) among postinfarction patients. Methods ApoA-I, HDL-C, and inflammatory markers (C-reactive protein [CRP], serum amyloid A (SAA), fibrinogen, von Willebrand factor [vWF], and D-dimer) were measured from blood samples of 1028 patients drawn 2 months after an index myocardial infarction (MI). Patients were followed up for the composite coronary endpoint (nonfatal MI, coronary death, or unstable angina) for an average of 26 months. Cox proportional hazard models were used to assess effect modifications for the association of apoA-I and HDL-C with coronary risk by each inflammatory marker. Results CRP significantly modified the risk of recurrent coronary events associated with apoA-I. Among the entire population, multivariable-adjusted hazard ratios associated with each standard deviation increase in apoA-I for those with low and high CRP levels were 0.89 and 1.35, respectively ( P value for interaction = .008). vWF was a significant effect modifier of the apoA-I/coronary risk association only among diabetic patients (hazard ratios were 0.56 and 1.43, for diabetic patients with low and high vWF levels, respectively; P value for interaction = .002). No effect modification was observed for the HDL-C/coronary risk association. Conclusion Among stable post-MI patients, CRP modified the risk of recurrent coronary events associated with apoA-I. VWF modified this association only among the diabetic subgroup.

Background Increased particulate air pollution has been associated with both an increased risk of myocardial infarction (MI) and adverse changes in cardiac biomarkers. Up to 30% of ambient wintertime fine particles (PM 2.5 ) in Rochester, NY are from wood burning. Our study examined associations between ambient levels of a marker of wood smoke (Delta-C) and other particulate air pollutants and biomarkers of inflammation, coagulation and thrombosis. Methods We measured blood concentrations of C-reactive protein (CRP), D -dimer, fibrinogen, P-selectin, platelet factor 4 (PF-4), von Willebrand factor (vWF), and myeloperoxidase (MPO) of 135 patients undergoing cardiac catheterization during the winters of 2011–2013. We coupled these data with hourly ambient concentrations of Delta-C, black carbon (BC; marker of traffic pollution), and ultrafine (10–100 nm; UFP), accumulation mode (100–500 nm; AMP), and fine particles ( 2.5 ). Using linear regression models, we estimated the change in each biomarker associated with increased pollutant concentrations at intervals between 1 and 96 h preceding blood collection. Results Each 0.13 µg/m 3 increase in Delta-C concentration in the prior 12 h was associated with a 0.91% increase in fibrinogen levels (95% CI=0.23%, 1.59%), but unexpectedly in the prior 48 h, each 0.17 µg/m 3 increase in Delta-C concentration was associated with a 2.75% decrease in MPO levels (95% CI=−5.13%,−0.37%). We did not see associations between Delta-C concentrations and any other biomarkers. Interquartile range (IQR) increases in PM 2.5, BC, UFP, and AMP concentrations were generally associated with increased CRP and fibrinogen, but not PF4, D -dimer, vWF, or P-selectin. Conclusions In a population of cardiac patients, we noted adverse changes in fibrinogen associated with increased concentrations of a marker of wood smoke. Increases in PM 2.5 , BC, AMP, and UFP concentrations in the previous 96 h were also associated with adverse changes in markers of systemic inflammation and coagulation, but not with markers of endothelial cell dysfunction or platelet activation.

Rationale: Unprecedented pollution control actions during the Beijing Olympics provided a quasi-experimental opportunity to examine biologic responses to drastic changes in air pollution levels.Objectives: To determine whether changes in levels of biomarkers reflecting pulmonary inflammation and pulmonary and systemic oxidative stress were associated with changes in air pollution levels in healthy young adults.Methods: We measured fractional exhaled nitric oxide, a number of exhaled breath condensate markers (H+, nitrite, nitrate, and 8-isoprostane), and urinary 8-hydroxy-2-deoxyguanosine in 125 participants twice in each of the pre- (high pollution), during- (low pollution), and post-Olympic (high pollution) periods. We measured concentrations of air pollutants near where the participants lived and worked. We used mixed-effects models to estimate changes in biomarker levels across the three periods and to examine whether changes in biomarker levels were associated with changes in pollutant concentrations...

Background: Mechanisms underlying previously reported air pollution and cardiovascular (CV) morbidity associations remain poorly understood. Objectives: We examined associations between markers of pathways thought to underlie these air pollution and CV associations and ambient particle concentrations in postinfarction patients. Methods: We studied 76 patients, from June 2006 to November 2009, who participated in a 10-week cardiac rehabilitation program following a recent (within 3 months) myocardial infarction or unstable angina. Ambient ultrafine particle (UFP; 10–100 nm), accumulation mode particle (AMP; 100–500 nm), and fine particle concentrations (PM2.5; ≤ 2.5 μm in aerodynamic diameter) were monitored continuously. Continuous Holter electrocardiogram (ECG) recordings were made before and during supervised, graded, twice weekly, exercise sessions. A venous blood sample was collected and blood pressure was measured before sessions. Results: Using mixed effects models, we observed adverse changes in rMSSD [square root of the mean of the sum of the squared differences between adjacent normal-to-normal (NN) intervals], SDNN (standard deviation of all NN beat intervals), TpTe (time from peak to end of T-wave), heart rate turbulence, systolic and diastolic blood pressures, C-reactive protein, and fibrinogen associated with interquartile range increases in UFP, AMP, and PM2.5 at 1 or more lag times within the previous 5 days. Exposures were not associated with MeanNN, heart-rate–corrected QT interval duration (QTc), deceleration capacity, and white blood cell count was not associated with UFP, AMP, and PM2.5 at any lag time. Conclusions: In cardiac rehabilitation patients, particles were associated with subclinical decreases in parasympathetic modulation, prolongation of late repolarization duration, increased blood pressure, and systemic inflammation. It is possible that such changes could increase the risk of CV events in this susceptible population.

The purpose of this study was to examine the trends in the rates of stillbirth by race and ethnicity and to determine the risk factors of stillbirth.We used New Jersey data (1997-2005) for live births and fetal deaths. Cox proportional hazards model was used to estimate the risk of stillbirth associated with maternal risk factors and pregnancy complications.The rate of stillbirth was 4.4/1000 total births (3.4 for white and 7.9 for black non-Hispanics and 4.4 for Hispanics/1000 total births). The rates of stillbirth decreased from 3.8 in 1997 to 2.7/1000 total births in 2005 for white non-Hispanics but remained unchanged for other race/ethnicity groups. Adjusted relative risks for the risk factors associated with stillbirth were 1.3 (95% CI, 1.2-1.4) for maternal age ≥ 35 years, 1.9 (95% CI, 1.7-2.1) for black non-Hispanics, 2.8 (95% CI, 2.4-3.3) for no prenatal care, 40.2 (95% CI, 36.9-43.9) for placental abruption, 5.3 (95% CI, 3.4-8.2) for eclampsia, 3.5 (95% CI, 2.8-4.3) for diabetes mellitus and 1.7 (95% CI, 1.3-2.2) for preeclampsia.There was a decline in the rate of stillbirth but there were persistent racial disparities with the highest rates of stillbirth for black non-Hispanics.

International audience; BACKGROUND: The findings of prior studies of air pollution effects on adverse birth outcomes are difficult to synthesize because of differences in study design. OBJECTIVES: The International Collaboration on Air Pollution and Pregnancy Outcomes was formed to understand how differences in research methods contribute to variations in findings. We initiated a feasibility study to a) assess the ability of geographically diverse research groups to analyze their data sets using a common protocol and b) perform location-specific analyses of air pollution effects on birth weight using a standardized statistical approach. METHODS: Fourteen research groups from nine countries participated. We developed a protocol to estimate odds ratios (ORs) for the association between particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀) and low birth weight (LBW) among term births, adjusted first for socioeconomic status (SES) and second for additional location-specific variables. RESULTS: Among locations with data for the PM₁₀ analysis, ORs estimating the relative risk of term LBW associated with a 10-μg/m³ increase in average PM₁₀ concentration during pregnancy, adjusted for SES, ranged from 0.63 [95% confidence interval (CI), 0.30-1.35] for the Netherlands to 1.15 (95% CI, 0.61-2.18) for Vancouver, with six research groups reporting statistically significant adverse associations. We found evidence of statistically significant heterogeneity in estimated effects among locations. CONCLUSIONS: Variability in PM₁₀-LBW relationships among study locations remained despite use of a common statistical approach. A more detailed meta-analysis and use of more complex protocols for future analysis may uncover reasons for heterogeneity across locations. However, our findings confirm the potential for a diverse group of researchers to analyze their data in a standardized way to improve understanding of air pollution effects on birth outcomes.

Background Epidemiologic studies consistently demonstrate an association between acute cardiopulmonary events and changes in air pollution; however, the mechanisms that underlie these associations are not completely understood. Oxidative stress and inflammation have been suggested to play a role in human responses to air pollution. The proteasome is an intracellular protein degradation system linked to both of these processes and may help mediate air pollution effects. Objectives In these studies, we determined whether acute experimental exposure to two different aerosols altered white blood cell (WBC) or red blood cell (RBC) proteasome activity in human subjects. One aerosol was fresh diesel exhaust (DE), and the other freshly generated secondary organic aerosol (SOA). Methods Thirty-eight healthy subjects underwent 2-hr resting inhalation exposures to DE and separate exposures to clean air (CA); 26 subjects were exposed to DE, CA, and SOA. CA responses were subtracted from DE or SOA responses, and mixed linear models with F-tests were used to test the effect of exposure to each aerosol on WBC and RBC proteasome activity. Results WBC proteasome activity was reduced 8% (p = 0.04) after exposure to either DE or SOA and decreased by 11.5% (p = 0.03) when SOA was analyzed alone. RBCs showed similar 8–10% declines in proteasome activity (p = 0.05 for DE alone). Conclusions Air pollution produces oxidative stress and inflammation in many experimental models, including humans. Two experimental aerosols caused rapid declines in proteasome activity in peripheral blood cells, supporting a key role for the proteasome in acute human responses to air pollution.

Background Skin cancer is the most common of all cancers and a public health concern of increasing magnitude in the U.S. Purpose A mid-year review of Healthy People 2010 found that the percentage of adults engaging in sun-safe practices increased from 59% in 2000 to 71% in 2005. This paper examines whether this increase in sun-safe practices in adults is an artifact caused by the change from 2000 to 2005 in the operational definition of "sun-safe practices" in the National Health Interview Survey (NHIS). Methods This study analyzed the 2000 and 2005 NHIS data sets in 2009 to examine changes in sun-safe practice prevalence estimates and to estimate the relative odds of practicing sun-safe behaviors associated with gender, age, race/ethnicity, education, and geographic region. Results Contrary to the Healthy People 2010 mid-year review, it was found that engaging in sun-safe practices by adults decreased from 59% (2000) to 55% (2005). A question order effect and use of images for use of sun-safe hats likely caused an artificial change in "cover-up" behavior estimates from 31% (2000) to 18% (2005) and wide-brim hat usage from 27% (2000) to 12% (2005). When eliminating data from these two questions added in 2005, the relative odds of practicing sun-safe behaviors was significantly lower for men in both 2000 and 2005 but were not different for other demographic characteristics. Conclusions The current analyses suggest that the increase in sun-safe behaviors in adults and a notable decrease in "hat use" may be due to methodologic artifacts. When operational definitions change, caution should be used in interpreting estimates over time.

Most previous studies (D’Ippoliti et al. 2003; Peters et al. 2001, 2005; Pope et al. 2006; Zanobetti and Schwartz 2005), but not all (Sullivan et al. 2005), that have investigated the triggering of myocardial infarction (MI) by particulate matter (PM) air pollution concentrations in the hours and days before MI onset have reported an association. Other studies have reported increased mortality due to MI or increased mortality or cardiovascular admissions among MI survivors associated with increases in PM over the previous few days (Braga et al. 2001; von Klot et al. 2005; Zanobetti and Schwartz 2007). Several studies have investigated whether certain subgroups are particularly susceptible and have reported increased cardiovascular effects among those with diabetes (Dubowsky et al. 2006; Goldberg et al. 2001; Liu et al. 2007; O’Neill et al. 2005; Zanobetti and Schwartz 2002) and among patients with chronic obstructive pulmonary disease (COPD) (Naess et al. 2007; Zanobetti and Schwartz 2005; Zanobetti et al. 2000). However, Zanobetti and Schwartz (2005) reported increased susceptibility among patients with COPD but not among persons with diabetes. Numerous researchers have reported that the percentage of infarctions that are nontransmural has been increasing (Goff et al. 2000; Hellermann et al. 2003; Kostis et al. 2007; Myerson et al. 2009; Roger et al. 2006, 2010; Rogers et al. 2008). More recently, Shao (2008) noted a similar secular trend in clinical presentation of MI to emergency departments (EDs) in New Jersey. In short, 72% of persons admitted to hospitals in New Jersey from 1990 through 1992 for MI had had transmural infarctions, and only 28% had had nontransmural infarctions. Since then, however, this pattern has reversed. From 2002 through 2004, most of the admissions for MI were for nontransmural infarctions (63%), with only 37% for transmural infarctions (Shao 2008). These changes may be due in part to improvements in preventive pharmacotherapies (statins, beta blockers, aspirin), interventional procedures [angioplasty, coronary artery bypass graft (CABG)], more sensitive diagnostic tests (troponins), and treatment of the MI upon ED arrival (reperfusion therapy, increased use of antiplatelet agents). It has not been reported whether PM with aerodynamic diameter ≤ 2.5 μm (PM2.5) triggers all infarctions, whether PM–MI associations differ in magnitude, or whether these associations are restricted to PM–transmural or PM–nontransmural infarctions alone. Such investigations may provide insight into the mechanisms by which PM may trigger cardiovascular events. Using the same data as Shao (2008), we attempted to replicate, in New Jersey, previous MI–PM2.5 studies that were conducted in other U.S. and European cities. We hypothesized that increases in mean PM2.5 concentration on the same day and a few days before ED arrival for MI may be associated with increased risk of MI and that these effect estimates would be greater for persons with diabetes and those with COPD than for individuals without these conditions. Further, we explored whether there were differences in risks associated with increases in ambient PM2.5 concentration between transmural and nontransmural infarctions.

Ambient air pollution has been linked to cardiovascular and respiratory morbidity and mortality in epidemiology studies. Frequently, oxidative and nitrosative stress are hypothesized to mediate these pollution effects, however precise mechanisms remain unclear. This paper describes the methodology for a major panel study to examine air pollution effects on these and other mechanistic pathways. The study took place during the drastic air pollution changes accompanying the 2008 Olympics in Beijing, China. After a general description of air pollution health effects, we provide a discussion of panel studies and describe the unique features of this study that make it likely to provide compelling results. This study should lead to a clearer and more precise definition of the role of oxidative and nitrosative stress, as well as other mechanisms, in determining acute morbidity and mortality from air pollution exposure.