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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.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.An increased rate of STEMI was associated with each 3111 particles/cmGreater 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.

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.

Background: Previous work reported increased rates of acute cardiovascular hospitalizations associated with increased PM2.5 concentrations in the previous few days across urban centers in New York State from 2005 to 2016. These relative rates were higher after air quality policies and economic changes resulted in decreased PM2.5 concentrations and changes in PM composition (e.g. increased secondary organic carbon), compared to before and during these changes. Changes in PM composition and sources may explain this difference. Objectives: To estimate the rate of acute cardiovascular hospitalizations associated with increases in source specific PM2.5 concentrations. Methods: Using source apportioned PM2.5 concentrations at the same NYS urban sites, a time-stratified case-crossover design, and conditional logistic regression models adjusting for ambient temperature and relative humidity, we estimated the rate of these acute cardiovascular hospitalizations associated with increases in mean source specific PM2.5 concentrations in the previous 1, 4, and 7 days. Results: Interquartile range (IQR) increases in spark-ignition emissions (GAS) concentrations were associated with increased excess rates of cardiac arrhythmia hospitalizations (2.3%; 95% CI = 0.4%, 4.2%; IQR = 2.56 μg/m3) and ischemic stroke hospitalizations (3.7%; 95% CI = 1.1%, 6.4%; 2. 73 μg/m3) over the next day. IQR increases in diesel (DIE) concentrations were associated with increased rates of congestive heart failure hospitalizations (0.7%; 95% CI = 0.2% 1.3%; 0.51 μg/m3) and ischemic heart disease hospitalizations (0.8%; 95% CI = 0.3%, 1.3%; 0.60 μg/m3) over the next day, as hypothesized. However, secondary sulfate PM2.5 (SS) was not. Increased acute cardiovascular hospitalization rates were also associated with IQR increases in concentrations of road dust (RD), residual oil (RO), and secondary nitrate (SN) over the previous 1, 4, and 7 days, but not other sources. Conclusions: These findings suggest a role of several sources of PM2.5 in New York State (i.e. traffic emissions, non-traffic emissions such as brake and tire wear, residual oil, and nitrate that may also reflect traffic emissions) in the triggering of acute cardiovascular events. Keywords: Cardiovascular hospitalizations, Air pollution, Source apportionment, Traffic emissions

Effect estimates of prenatal exposure to ambient PM

BACKGROUND: Emissions control programs targeting certain air pollution sources may alter PM(2.5) composition, as well as the risk of adverse health outcomes associated with PM(2.5). 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 PM(2.5) 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 PM(2.5) 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 PM(2.5) components and the remaining PM(2.5) mass were also considered to assess the influence of changes in PM(2.5) composition on changes in the risk of CVD and asthma ED visits associated with PM(2.5) over time. RESULTS: The relative risk of CVD ED visits associated with a 10 μg/m(3) increase in 4-day PM(2.5) 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 PM(2.5) 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 PM(2.5) concentrations were observed. These changes could be related to changes in PM(2.5) composition (e.g., an increasing fraction of organic carbon and a decreasing fraction of sulfate in PM(2.5)). Other factors such as improvements in healthcare and differential exposure misclassification might also contribute to the changes.

Rationale: In a previous trial (MOSES [Multicenter Ozone Study of oldEr Subjects]), 3 hours of controlled ozone (O3) exposure caused concentration-related reductions in lung function with evidence ...

Acute respiratory effects of low-level ozone exposure are not well defined in older adults.MOSES (The Multicenter Ozone Study in Older Subjects), although primarily focused on acute cardiovascular effects, provided an opportunity to assess respiratory responses to low concentrations of ozone in older healthy adults.We performed a randomized crossover, controlled exposure study of 87 healthy adults (59.9 ± 4.5 yr old; 60% female) to 0, 70, and 120 ppb ozone for 3 hours with intermittent exercise. Outcome measures included spirometry, sputum markers of airway inflammation, and plasma club cell protein-16 (CC16), a marker of airway epithelial injury. The effects of ozone exposure on these outcomes were evaluated with mixed-effect linear models. A P value less than 0.01 was chosen a priori to define statistical significance.The mean (95% confidence interval) FEVExposure to ozone at near ambient levels induced lung function effects, airway injury, and airway inflammation in older healthy adults. Clinical trial registered with www.clinicaltrials.gov (NCT01487005).

To address limitations of observational epidemiology studies of air pollution and health effects, including residual confounding by temporal and spatial factors, several studies have taken advantage of ‘natural experiments’, where an environmental policy or air quality intervention has resulted in reductions in ambient air pollution concentrations. Researchers have examined whether the population impacted by these air quality improvements, also experienced improvements in various health indices (e.g. reduced morbidity/mortality). In this paper, I review key accountability studies done previously and new studies done over the past several years in Beijing, Atlanta, London, Ireland, and other locations, describing study design and analysis strengths and limitations of each. As new ‘natural experiment’ opportunities arise, several lessons learned from these studies should be applied when planning a new accountability study. Comparison of health outcomes during the intervention to both before and after the intervention in the population of interest, as well as use of a control population to assess whether any temporal changes in the population of interest were also seen in populations not impacted by air quality improvements, should aid in minimizing residual confounding by these long term time trends. Use of either detailed health records for a population, or prospectively collected data on relevant mechanistic biomarkers coupled with such morbidity/mortality data may provide a more thorough assessment of if the intervention beneficially impacted the health of the community, and if so by what mechanism(s). Further, prospective measurement of a large suite of air pollutants may allow a more thorough understanding of what pollutant source(s) is/are responsible for any health benefit observed. The importance of using multiple statistical analysis methods in each paper and the difference in how the timing of the air pollution/outcome association may impact which of these design features is most important is also discussed. Based on these and other lessons learned, researchers may provide a more epidemiologically rigorous evaluation of cause-specific health impacts of an air quality intervention or action. Keywords: Air pollution, Epidemiology, Accountability, Natural experiment, Confounding

The response of respiratory infections to source-specific particulate matter (PM) is an area of active research. Using source-specific PM2.5 concentrations at six urban sites in New York State, a case-crossover design, and conditional logistic regression, we examined the association between source-specific PM and the rate of hospitalizations and emergency department (ED) visits for influenza or culture-negative pneumonia from 2005 to 2016. There were at most N = 14 764 influenza hospitalizations, N = 57 522 influenza ED visits, N = 274 226 culture-negative pneumonia hospitalizations, and N = 113 997 culture-negative pneumonia ED visits included in our analyses. We separately estimated the rate of respiratory infection associated with increased concentrations of source-specific PM2.5, including secondary sulfate (SS), secondary nitrate (SN), biomass burning (BB), pyrolyzed organic carbon (OP), road dust (RD), residual oil (RO), diesel (DIE), and spark ignition vehicle emissions (GAS). Increased rates of ED visits for influenza were associated with interquartile range increases in concentrations of GAS (excess rate [ER] = 9.2%; 95% CI: 4.3%, 14.3%) and DIE (ER = 3.9%; 95% CI: 1.1%, 6.8%) for lag days 0–3. There were similar associations between BB, SS, OP, and RO, and ED visits or hospitalizations for influenza, but not culture-negative pneumonia hospitalizations or ED visits. Short-term increases in PM2.5 from traffic and other combustion sources appear to be a potential risk factor for increased rates of influenza hospitalizations and ED visits.

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 O

Prior work found increased rates for emergency department (ED) visits for asthma and hospitalizations for chronic obstructive pulmonary disease per unit mass of PM(2.5) across New York State (NYS) during 2014 to 2016 after major reductions in ambient PM2.5 concentrations had occurred following implementation of various policy actions and major economic disruptions. The associations of source-specific PM(2.5) concentrations with these respiratory diseases were assessed with a time-stratified case-control design and logistic regression models to identify the changes in the PM(2.5) that have led to the apparently increased toxicity per unit mass. The rates of ED visits and hospitalizations for asthma and COPD associated with increases in source-specific PM2.5 concentrations in the prior 1, 4, and 7 days were estimated for 6 urban sites in New York State. Overall, there were similar numbers of significantly increased (n=9) and decreased rates (n=8) of respiratory events (asthma and COPD hospitalizations and ED visits) associated with increased source-specific PM(2.5) concentrations in the previous 1, 4, and 7 days. Associations of source-specific PM(2.5) concentrations with excess rates of hospitalizations for COPD for spark- and compression ignition vehicles increased in the 2014–2016 period, but the values were not statistically significant. Other source types showed inconsistent patterns of excess rates. For asthma ED visits, only biomass burning and road dust showed consistent positive associations with road dust having significant values for most lag times. Secondary nitrate also showed significant positive associations with asthma ED visits in the AFTER period compared to no associations in the prior periods. These results suggest that the relationships of asthma and COPD exacerbation with source-specific PM(2.5) are not well defined and further work will be needed to determine the causes of the apparent increases in the per unit mass toxicity of PM(2.5) in New York State in the 2014–16 period.

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.

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

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

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

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.

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.

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.

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.

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.

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.

Objectives We explored the association between acute changes in daily mean pulmonary artery (PA) and right ventricular (RV) pressures and concentrations of ambient fine particulate matter [PM with aerodynamic diameter ≤2.5 μm (PM2.5)] as an explanation for previous associations between congestive heart failure (HF) hospital admissions and PM. Materials and methods In the Chronicle Offers Management to Patients with Advanced Signs and Symptoms of Heart Failure (COMPASS-HF) trial, to see whether management of ambulatory HF could be improved by providing continuous right heart pressure monitoring to physicians, the Chronicle Implantable Hemodynamic Monitor (Medtronic, Inc., Minneapolis, MN, USA) continuously measured multiple right heart hemodynamic parameters, heart rate, and activity trends in subjects with moderate/severe HF. Using these trial data, we calculated daily mean pressures, using only those time intervals where the subject was not physically active (n = 5,807 person-days; n = 11 subjects). We then studied the association between mean daily PA/RV pressures and mean ambient PM2.5 concentrations on the same day and previous 6 days. Results Each 11.62-μg/m3 increase in same-day mean PM2.5 concentration was associated with small but significant increases in estimated PA diastolic pressure [0.19 mmHg; 95% confidence interval (CI), 0.05–0.33] and RV diastolic pressure (0.23 mmHg; 95% CI, 0.11–0.34). Although we saw considerable differences in the magnitude of response by COMPASS-HF randomization group (total data access for physicians vs. blocked clinician access), season, left ventricular ejection fraction, and obesity, these effects were not significantly different. Conclusions These pilot study findings provide a potential mechanism for previous findings of increased risk of HF associated with ambient PM. However, because of the small number of subjects, a larger study is needed for confirmation.

Increased particulate matter (PM) air pollutant concentrations have been associated with platelet activation. It was postulated that elevated air pollutant concentrations would be associated with increases in measures of platelet function and that responses would be blunted when taking aspirin and/or fish oil. Data from a sequential therapy trial (30 subjects with type 2 diabetes mellitus), with 4 clinic visits (first: no supplements, second: aspirin, third: omega-3 fatty acid supplements, fourth: aspirin and omega-3 fatty acids) per subject, were utilized. Using linear mixed models, adjusted for relative humidity, temperature, visit number, and season, changes in three platelet function measures including (1) aggregation induced by adenosine diphosphate (ADP), (2) aggregation induced by collagen, and (3) thromboxane B2 production were associated with interquartile range (IQR) increases in mean concentrations of ambient PM2.5, black carbon, ultrafine particles (UFP; 10–100 nm), and accumulation mode particles (AMP; 100–500 nm) in the previous 1–96 h. IQR increases in mean UFP and AMP concentrations were associated with significant decreases in platelet response, with the largest being a –0.43 log(pg/ml) decrease in log(thromboxane B2) (95% CI = –0.8, –0.1) associated with each 582-particles/cm3 increase in AMP, and a –1.7 ohm reduction in collagen-induced aggregation (95% CI = –3.1, –0.3) associated with each 2097-particles/cm3 increase in UFP in the previous 72 h. This UFP effect on thromboxane B2 was significantly muted in diabetic subjects taking aspirin (–0.01 log[pg/ml]; 95% CI = –0.4, 0.3). The reason for this finding remains unknown, and needs to be investigated in future studies.

Background It remains unclear whether fine particulate (PM2.5) exposure affects risk of preterm birth and prelabor rupture of membranes. Unmeasured, poorly measured, and undiscovered individual-level confounders might have introduced bias into past studies that relied on between-women comparisons. Methods This was a longitudinal study of preterm birth and prelabor rupture of membranes in Rochester, NY, 2004-2012 (N = 3,264 women, N = 7,121 singleton births). We used conditional logistic regression to match pregnancies to the same woman and estimate the odds of each outcome associated with average PM2.5 concentrations during each trimester and whole pregnancy. Results For preterm birth, adjusted odds ratios (95% confidence interval) for 1 μg/m increase in PM2.5 in the first trimester, second trimester, third trimester, and whole pregnancy were 1.11 (1.04, 1.18), 1.09 (1.02, 1.16), 1.06 (1.00, 1.13), and 1.17 (1.07, 1.28), respectively. For prelabor rupture of membranes, corresponding odds ratios were 1.00 (0.97, 1.04), 0.99 (0.96, 1.02), 0.99 (0.96, 1.03), and 0.99 (0.94, 1.04), respectively. Conclusion Risk of preterm birth was greater for pregnancies with elevated PM2.5 exposure than other pregnancies to the same women at lower exposure. We did not observe an association between PM2.5 concentrations and prelabor rupture of membranes.

We previously observed increased odds of ST-elevation myocardial infarctions (STEMIs) associated with increased ambient fine particulate matter (PM2.5) in the previous hour. However, data are lacking on the effects of specific PM sources. Using data from 362 patients, a case-crossover design, and conditional logistic regression, we estimated the relative odds of STEMI associated with increased Delta-C (wood smoke), black carbon (BC; traffic), PM2.5, and gaseous pollutants in the previous 1-72 h. We did not observe increased odds of STEMIs associated with increased Delta-C or BC. We did observe increased odds associated with each 7.1 μg/m3 increase in PM2.5 (OR (95% CI): 1.17 (0.99, 1.39)) and each 19.9 p.p.b. increase in ozone (O3; 1.27 (1.00, 1.63)) in the previous hour, and each 0.22 p.p.m. increase in 48-h carbon monoxide (CO) concentrations (1.32 (1.00, 1.73]). Larger relative odds were associated with PM2.5 in May-October, and O3 and CO in November-April. Increased PM2.5, O3, and CO, but not wood smoke or BC, were associated with increased odds of STEMI, and effects may differ by season. Studies using spatially adjusted pollution estimates are needed, as well as studies further examining O3 and CO effects on the risk of STEMI.

1-Nitro-pyrene has been considered a compound specific to diesel combustion emission, while 1- and 2-nitro-napthalene are mainly produced through photochemical conversion of naphthalene released to the atmosphere. Metabolites of these compounds may serve as biomarkers of exposure to traffic related pollutants. We collected urine samples from 111 healthy and non-smoking subjects within (i.e., during the Beijing Olympics) and outside (i.e., before and after the Olympics) a traffic control regime to improve Beijing's air quality. Urines were analyzed for the sum of 1&2-amino-naphthalene (metabolites of 1- and 2-nitro-naphthalene) and 1-amino-pyrene (a metabolite of 1-nitro-pyrene), using an HPLC-fluorescence method. Within the same time periods, PM2.5 mass and constituents were measured, including elemental carbon, sulfate, nitrate, PAHs, carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone, and particle number concentrations. The associations between the urinary metabolites and air pollutants were analyzed using linear mixed-effects models. From the pre- to during-Olympic period, 1&2-amino-naphthalene and 1-hydroxy-pyrene decreased by 23% (p = 0.066) and 16% (p = 0.049), respectively, while there was no change in 1-amino-pyrene (2% increase, p = 0.892). From during- to post-Olympic period, 1&2-amino-naphthalene, 1-amino-pyrene and 1-hydroxy-pyrene concentrations increased by 26% (p = 0.441), 37% (p = 0.355), and 3% (p = 0.868), respectively. Furthermore, 1&2-amino-naphthalene and 1-hydroxy-pyrene were associated with traffic related pollutants in a similar lag pattern. 1-amino-pyrene was associated more strongly with diesel combustion products (e.g. PN and elemental carbon) and not affected by season. Time-lag analyses indicate strongest/largest associations occurred 24–72 h following exposure. 1&2-amino-naphthalene and 1-hydroxy-pyrene can be used as a biomarker of exposure to general vehicle-emitted pollutants. More data are needed to confirm 1-amino-pyrene as a biomarker of exposure to diesel combustion emissions. Controlling creatinine as an independent variable in the models will provide a moderate adjusting effect on the biomarker analysis. Keywords: PAH metabolites, Biomarkers, Diesel exhaust particles, Exposure assessment, Traffic-emitted pollutants

Objectives: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF. Design: We performed a case–crossover study. Participants: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 (n = 203) were followed until July 2002. Evaluations/Measurements: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects. Results: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio = 2.08; 95% confidence interval = 1.22, 3.54; p = 0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon. Conclusions: Increased ambient O3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events.

Epidemiologic studies have demonstrated a consistent link between sudden cardiac deaths and particulate air pollution. We used implanted cardioverter defibrillator (ICD) records of ventricular tachyarrhythmias to assess the role of air pollution as a trigger of these potentially life-threatening events. The study cohort consisted of 203 cardiac patients with ICD devices in the Boston metropolitan area who were followed for an average of 3.1 years between 1995 and 2002. Fine particle mass and gaseous air pollution plus temperature and relative humidity were measured on almost all days, and black carbon, sulfate, and particle number on a subset of days. Date, time, and intracardiac electrograms of ICD-detected arrhythmias were downloaded at the patients' regular follow-up visits (about every 3 months). Ventricular tachyarrhythmias were identified by electrophysiologist review. Risk of ventricular arrhythmias associated with air pollution was estimated with logistic regression, adjusting for season, temperature, relative humidity, day of the week, patient, and a recent prior arrhythmia. We found increased risks of ventricular arrhythmias associated with 2-day mean exposure for all air pollutants considered, although these associations were not statistically significant. We found statistically significant associations between air pollution and ventricular arrhythmias for episodes within 3 days of a previous arrhythmia. The associations of ventricular tachyarrhythmias with fine particle mass, carbon monoxide, nitrogen dioxide, and black carbon suggest a link with motor vehicle pollutants. The associations with sulfate suggest a link with stationary fossil fuel combustion sources.

Background Previously, we reported a 18% increased odds of ST-elevation myocardial infarction (STEMI) associated with each 7.1 µg/m3 increase in PM2.5 concentration in the hour prior to MI onset. We found no association with non-ST elevation myocardial infarction (NSTEMI). We examined if this association was modified by PM2.5 source direction. Methods We used the NOAA HYbrid Single-Particle Lagrangian Trajectory (HYSPLIT) model to calculate each hourly air mass location for the 24 hours before each case or control time period in our previous PM2.5/STEMI case-crossover analysis. Using these data on patients with STEMI (n=338), hourly PM2.5 concentrations, and case-crossover methods, we evaluated whether our PM2.5/STEMI association was modified by whether the air mass passed through each of the 8 cardinal wind direction sectors in the previous 24 h. Results When the air mass passed through the West-Southwest direction (WSW) any time in the past 24 h, the odds of STEMI associated with each 7.1 µg/m3 increase in PM2.5 concentration in the previous hour (OR=1.27; 95% CI=1.08, 1.22) was statistically significantly (p=0.01) greater than the relative odds of STEMI associated with increased PM2.5 concentration when the wind arrived from any other direction (OR=0.99; 95% CI=0.80, 1.22). We found no other effect modification by any other source direction. Further, relative odds estimates were largest when the time spent in the WSW was 8–16 h, compared to ≤7 h or 17–24 h, suggesting that particles arising from sources in this direction were more potent in triggering STEMIs. Conclusions Since relative odds estimates were higher when the air mass passed through the WSW octant in the past 24 h, there may be specific components of the ambient aerosol that are more potent in triggering STEMIs. This direction is associated with substantial emissions from coal-fired power plants and other industrial sources of the Ohio River Valley, many of which are undergoing modifications to reduce their emissions.

Background We and others have shown that increases in particulate air pollutant (PM) concentrations in the previous hours and days have been associated with increased risks of myocardial infarction, but little is known about the relationships between air pollution and specific subsets of myocardial infarction, such as ST-elevation myocardial infarction (STEMI) and non ST-elevation myocardial infarction (NSTEMI). Methods Using data from acute coronary syndrome patients with STEMI (n = 338) and NSTEMI (n = 339) and case-crossover methods, we estimated the risk of STEMI and NSTEMI associated with increased ambient fine particle (

During the 1980s the Republic of Ireland experienced repeated severe pollution episodes. Domestic coal burning was a major source of this pollution. In 1990 the Irish government introduced a ban on the marketing, sale, and distribution of coal in Dublin. The ban was extended to Cork in 1995 and to 10 other communities in 1998 and 2000. We previously reported decreases in particulate black smoke (BS*) and sulfur dioxide (SO2) concentrations, measured as total gaseous acidity, in Dublin after the 1990 coal ban (Clancy et al. 2002). In the current study we explored and compared the effectiveness of the sequential 1990, 1995, and 1998 bans in reducing community air pollution and in improving public health. We compiled records of daily BS, total gaseous acidity (SO2), and counts of cause-specific deaths from 1981 to 2004 for Dublin County Borough (1990 ban), county Cork (1995 ban), and counties Limerick, Louth, Wexford, and Wicklow (1998 ban). We also compiled daily counts of hospital admissions for cardiovascular, respiratory, and digestive diagnoses for Cork County Borough (1991 to 2004) and counties Limerick, Louth, Wexford, and Wicklow (1993 to 2004). We compared pre-ban and post-ban BS and SO2 concentrations for each city. Using interrupted time-series methods, we estimated the change in cause-specific, directly standardized mortality rates in each city or county after the corresponding local coal ban. We regressed weekly age- and sex-standardized mortality rates against an indicator of the post- versus pre-ban period, adjusting for influenza epidemics, weekly mean temperature, and a season smooth of the standardized mortality rates in Coastal counties presumably not affected by the bans. We compared these results with similar analyses in Midlands counties also presumably unaffected by the bans. We also estimated the change in cause-specific, directly standardized, weekly hospital admissions rates normalized for underreporting in each city or county after the 1995 and 1998 bans, adjusting for influenza epidemics, weekly mean temperature, and local admissions for digestive diagnoses. Mean BS concentrations fell in all affected population centers post-ban compared with the pre-ban period, with decreases ranging from 4 to 35 microg/m3 (corresponding to reductions of 45% to 70%, respectively), but we observed no clear pattern in SO2 measured as total gaseous acidity associated with the bans. In comparisons with the pre-ban periods, no significant reduction was found in total death rates associated with the 1990 (1% reduction), 1995 (4% reduction), or 1998 (0% reduction) bans, nor for cardiovascular mortality (0%, 4%, and 1% reductions for the 1990, 1995, and 1998 bans, respectively). Respiratory mortality was reduced in association with the bans (17%, 9%, and 3%, respectively). We found a 4% decrease in hospital admissions for cardiovascular disease associated with the 1995 ban and a 3% decrease with the 1998 ban. Admissions for respiratory disease were not consistently lower after the bans; admissions for pneumonia, chronic obstructive pulmonary disease (COPD), and asthma were reduced. However, underreporting of hospital admissions data and lack of control and comparison series tempered our confidence in these results. The successive coal bans resulted in immediate and sustained decreases in particulate concentrations in each city or town; with the largest decreases in winter and during the heating season. The bans were associated with reductions in respiratory mortality but no detectable improvement in cardiovascular mortality. The changes in hospital admissions for respiratory and cardiovascular disease were supportive of these findings but cannot be considered confirming. Detecting changes in public health indicators associated even with clear improvements in air quality, as in this case, remains difficult when there are simultaneous secular improvements in the same health indicators.

Underlying mechanisms by which air pollutants adversely affect human health remain poorly understood. Oxidative stress has been considered as a potential mechanism that may promote lipid peroxidation by reactive oxygen species, leading to the formation of malondialdehyde (MDA) that is excreted in biofluids (e.g., urine and exhaled breath condensate (EBC)). A panel study was conducted to examine whether concentrations of MDA in EBC and urine were associated, respectively, with changes in air pollution levels brought by the Beijing Olympic air pollution control measures. EBC and urine samples from 125 healthy adults were collected twice in each of the pre-, during-, and post-Olympic periods. Period-specific means of MDA and changes in MDA levels associated with increases in 24-h average pollutant concentrations were estimated using linear mixed-effects models. From the pre- to the during-Olympic period, when concentrations of most pollutants decreased, EBC MDA and urinary MDA significantly decreased by 24% (P < 0.0001) and 28% (P = 0.0002), respectively. From the during-Olympic to the post-Olympic period, when concentrations of most pollutants increased, EBC MDA and urinary MDA increased by 28% (P = 0.094) and 55% (P = 0.046), respectively. Furthermore, the largest increases in EBC MDA associated with one interquartile range (IQR) increases in all pollutants but ozone ranged from 10% (95% CI: 2%, 18%) to 19% (95% CI: 14%, 25%). The largest increases in urinary MDA associated with IQR increases in pollutant concentration ranged from 9% (95%: 0.3%, 19%) to 15% (95% CI: 3%, 28%). These findings support the utility of EBC MDA as a biomarker of oxidative stress in the respiratory tract and urinary MDA as a biomarker of systemic oxidative stress in relation to air pollution exposure in healthy young adults. Both EBC and urine samples can be collected noninvasively in the general population.

Background: A growing body of evidence has associated maternal exposure to air pollution with adverse effects on fetal growth; however, the existing literature is inconsistent. Objectives: We aimed to quantify the association between maternal exposure to particulate air pollution and term birth weight and low birth weight (LBW) across 14 centers from 9 countries, and to explore the influence of site characteristics and exposure assessment methods on between-center heterogeneity in this association. Methods: Using a common analytical protocol, International Collaboration on Air Pollution and Pregnancy Outcomes (ICAPPO) centers generated effect estimates for term LBW and continuous birth weight associated with PM10 and PM2.5 (particulate matter ≤ 10 and 2.5 µm). We used meta-analysis to combine the estimates of effect across centers (~ 3 million births) and used meta-regression to evaluate the influence of center characteristics and exposure assessment methods on between-center heterogeneity in reported effect estimates. Results: In random-effects meta-analyses, term LBW was positively associated with a 10-μg/m3 increase in PM10 [odds ratio (OR) = 1.03; 95% CI: 1.01, 1.05] and PM2.5 (OR = 1.10; 95% CI: 1.03, 1.18) exposure during the entire pregnancy, adjusted for maternal socioeconomic status. A 10-μg/m3 increase in PM10 exposure was also negatively associated with term birth weight as a continuous outcome in the fully adjusted random-effects meta-analyses (–8.9 g; 95% CI: –13.2, –4.6 g). Meta-regressions revealed that centers with higher median PM2.5 levels and PM2.5:PM10 ratios, and centers that used a temporal exposure assessment (compared with spatiotemporal), tended to report stronger associations. Conclusion: Maternal exposure to particulate pollution was associated with LBW at term across study populations. We detected three site characteristics and aspects of exposure assessment methodology that appeared to contribute to the variation in associations reported by centers.

The purpose of the present study was to examine the risk of stillbirth associated with ambient air pollution during pregnancy. Using live birth and fetal death data from New Jersey from 1998 to 2004, the authors assigned daily concentrations of air pollution to each birth or fetal death. Generalized estimating equation models were used to estimate the relative odds of stillbirth associated with interquartile range increases in mean air pollutant concentrations in the first, second, and third trimesters and throughout the entire pregnancy. The relative odds of stillbirth were significantly increased with each 10-ppb increase in mean nitrogen dioxide concentration in the first trimester (odds ratio (OR) = 1.16, 95% confidence interval (CI): 1.03, 1.31), each 3-ppb increase in mean sulfur dioxide concentration in the first (OR = 1.13, 95% CI: 1.01, 1.28) and third (OR = 1.26, 95% CI: 1.03, 1.37) trimesters, and each 0.4-ppm increase in mean carbon monoxide concentration in the second (OR = 1.14, 95% CI: 1.01, 1.28) and third (OR = 1.14, 95% CI: 1.06, 1.24) trimesters. Although ambient air pollution during pregnancy appeared to increase the relative odds of stillbirth, further studies are needed to confirm these findings and examine mechanistic explanations.

Background: Associations between traffic-related air pollutants (TRAPs) and acute cardiopulmonary outcomes may be confounded by psychological stress, noise, and other exposures. Laboratory-based ex...

Previous studies of air pollution and birth outcomes have not evaluated whether complicated pregnancies might be susceptible to the adverse effects of air pollution. It was hypothesised that trimester mean pollutant concentrations could be associated with fetal growth restriction, with larger risks among complicated pregnancies.A multiyear linked birth certificate and maternal/newborn hospital discharge dataset of singleton, term births to mothers residing in New Jersey at the time of birth, who were white (non-Hispanic), African-American (non-Hispanic) or Hispanic was used. Very small for gestational age (VSGA) was defined as a fetal growth ratio0.75, small for gestational age (SGA) asor =0.75 and0.85, and 'reference' births asor =0.85. Using polytomous logistic regression, associations between mean pollutant concentrations during the first, second and third trimesters and the risks of SGA/VSGA were examined, as well as effect modification of these associations by several pregnancy complications.Significantly increased risk of SGA was associated with first and third trimester PM(2.5) (particulate matter2.5 microm in aerodynamic diameter), and increased risk of VSGA associated with first, second and third trimester nitrogen dioxide (NO(2)) concentrations. Pregnancies complicated by placental abruption and premature rupture of the membrane had approximately two- to fivefold greater excess risks of SGA/VSGA than pregnancies not complicated by these conditions, although these estimates were not statistically significant.These findings suggest that ambient air pollution, perhaps specifically traffic emissions during early and late pregnancy and/or factors associated with residence near a roadway during pregnancy, may affect fetal growth. Further, pregnancy complications may increase susceptibility to these effects in late pregnancy.

Implanted cardioverter defibrillators (ICDs) monitor patients for episodes of cardiac arrhythmias and can initiate a therapeutic intervention to restore normal heart rhythm. These devices also record dates, times, and electrograms of these episodes. We examined the effects of air pollution on the incidence of arrhythmias in 195 cardiac patients with ICD devices in the Boston metropolitan area between July 1995 and July 2002. Gaseous air pollutant and meteorologic data were measured on essentially all days, fine particle mass on 80% of the days, and black carbon (BC) on 61% of the days. Date and time of detected arrhythmias, intracardiac electrograms, and therapeutic interventions were downloaded during the patients' regular follow-up visits every 3 months on average. A cardiac electrophysiologist reviewed electrograms recorded before, during, and after the arrhythmias and categorized them into ventricular and supraventricular events. Risk of arrhythmias associated with air pollution was estimated using logistic regression with adjustments for season, temperature, relative humidity, day of the week, and patient. We found increased relative risks of ventricular arrhythmias (VAs) associated with an increase in 2-day mean concentrations for all air pollutants considered, although these associations were not statistically significant. The relative risks of supraventricular arrhythmias (SVAs) increased in association with 2-day mean concentrations for all air pollutants, and this association was significant only for sulfur dioxide (SO2) at 4 ppb (odds ratio [OR] = 1.33; 95% confidence interval [CI] = 1.04, 1.70). The positive associations of VAs and SVAs with particulate matter less than 2.5microm in aerodynamic diameter (PM2.5; also referred to as fine particles), carbon monoxide (CO), nitrogen dioxide (NO2), BC, and SO2 suggest a link with motor vehicle pollutants. We explored patient characteristics that may have identified subjects susceptible to the effects of air pollution. The association of air pollution with SVAs was blunted by regularly prescribed beta-blockers. We found stronger associations of air pollution with VAs for episodes within 3 days of a previous arrhythmia, suggesting that VAs were triggered by air pollution episodes in combination with other factors that raised the patient's underlying risk. Although ICDs are specifically designed to monitor and treat only VAs, these results suggest that air pollution may trigger both VAs and SVAs.

Background: It has previously been reported that the risk of ventricular arrhythmias is positively associated with ambient air pollution among patients with implantable cardioverter defibrillators (ICD) in Boston. Aims: To assess the association of community exposures to air pollution with ventricular arrhythmias in a cohort of ICD patients in metropolitan St Louis, Missouri. Methods: ICD detected episodes reported during clinical follow up were abstracted and reviewed by an electrophysiologist to identify ventricular arrhythmias. A total of 139 ventricular arrhythmias were identified among 56 patients. A case-crossover design was used with control periods matched on weekday and hour of the day within the same calendar month. Conditional logistic regression models were adjusted for temperature, barometric pressure, and relative humidity in the 24 hours preceding the event. Results: There was a significant (24%, 95% CI 7% to 44%) increase in risk of ventricular arrhythmias associated with each 5 ppb increase in mean sulphur dioxide and non-significantly increased risk (22%, 95% CI −6% to 60%; and 18%, 95% CI −7% to 50%) associated with increases in nitrogen dioxide (6 ppb) and elemental carbon (0.5 μg/m3), respectively in the 24 hours before the arrhythmia. Conclusions: These results provide evidence of an association between ventricular arrhythmias and ambient air pollutants in St Louis. This is consistent with previous results from Boston, although the pollutants responsible for the increased risk are different.

Previous studies have investigated the associations between exposure to ambient air pollution and biomarkers of physiological pathways, yet little has been done on the comparison across biomarkers of different pathways to establish the temporal pattern of biological response. In the current study, we aim to compare the relative temporal patterns in responses of candidate pathways to different pollutants. Four biomarkers of pulmonary inflammation and oxidative stress, five biomarkers of systemic inflammation and oxidative stress, ten parameters of autonomic function, and three biomarkers of hemostasis were repeatedly measured in 125 young adults, along with daily concentrations of ambient CO, PM2.5, NO2, SO2, EC, OC, and sulfate, before, during, and after the Beijing Olympics. We used a two-stage modeling approach, including Stage I models to estimate the association between each biomarker and pollutant over each of 7 lags, and Stage II mixed-effect models to describe temporal patterns in the associations when grouping the biomarkers into the four physiological pathways. Our results show that candidate pathway groupings of biomarkers explained a significant amount of variation in the associations for each pollutant, and the temporal patterns of the biomarker-pollutant-lag associations varied across candidate pathways (p