TY  - RPRT
AB  - INTRODUCTION: COVID-19 lockdowns led to considerable reductions in air pollutant emissions worldwide, providing a unique opportunity to examine the impacts of reduced air pollution on mortality. This project aimed to quantify changes in nitrogen dioxide (NO2) and fine particulate matter (PM2.5) concentrations due to COVID-19 lockdowns, estimate associations between short-term exposures to these air pollutants and mortality rates, and calculate the attributable changes in mortality in four regions that implemented lockdowns but were mildly affected by the pandemic in early 2020, including Jiangsu Province, China; California, USA; Central and Southern Italy; and Germany. METHODS: To account for meteorological impacts and air pollution time trends, we used a machine learning-based meteorological normalization technique and the difference-in-differences approach to quantify changes in NO2 and PM2.5 concentrations due to lockdowns in early 2020. Using daily air pollution and mortality data from 2015 to 2019, we applied interactive fixed effects models (a causal modeling approach) to estimate associations between day-to-day changes in PM2.5 and NO2 concentrations and all-cause, natural-cause, and cardiovascular mortality rates before the pandemic in each region. Finally, using the quantified air pollution changes and the estimated air pollution-mortality relationships, we calculated the changes in mortality that were attributable to air pollution changes due to the lockdowns. RESULTS: We found that meaningful improvements in air quality occurred during the lockdowns in early 2020 in Jiangsu, China; California, USA; and Central and Southern Italy, with smaller magnitudes of reduction in PM2.5 compared to NO2. We observed no significant reduction in NO2 and a small increase in PM2.5 in Germany. After controlling for unmeasured spatial and temporal confounders, we detected statistically significant associations between short-term increases in PM2.5 and NO2 concentrations and increases in daily all-cause, natural-cause, and cardiovascular mortality rates in all four study regions from 2015 to 2019. Specifically, we determined that lockdown-induced reductions in NO2 resulted in avoiding 1.41 (95% empirical confidence interval [eCI]: 0.94-1.88), 0.44 (95% eCI: 0.17-0.71), and 4.66 (95% eCI: 2.03-7.44) deaths per 100,000 people in Jiangsu, China; California, USA; and Central and Southern Italy, respectively. Mortality benefits attributable to PM2.5 reductions in these regions also were statistically significant, albeit of a smaller magnitude, and resulted in avoiding 0.16 (95% eCI: 0.04-0.29), 0.23 (95% eCI: 0.03-0.43), and 0.91 (95% eCI: 0.09-1.78) deaths per 100,000 people in Jiangsu, China; California, USA; and Central and Southern Italy, respectively. In Germany, the mortality benefits attributable to NO2 changes were not statistically significant (mortality change of -0.11; 95% eCI: -0.25 to 0.03 deaths per 100,000 people), and an observed increase in PM2.5 was associated with an increase in mortality of 0.35 (95% eCI: 0.22-0.48) deaths per 100,000 people during the lockdown. CONCLUSIONS: Using a causal modeling approach, this study contributes to the growing body of evidence that short-term exposures to PM2.5 and NO2 are associated with increased all-cause and cause-specific mortality rates. In areas mildly affected by the COVID-19 pandemic, lockdowns in early 2020 generally improved air quality and led to health benefits, especially in association with NO2 reductions, with notable heterogeneity across regions. This study underscores the importance of accounting for local characteristics when policymakers adapt successful emission control strategies from other regions.
AU  - Chen, K.*
AU  - Ma, Y.*
AU  - Marb, A.
AU  - Nobile, F.*
AU  - Dubrow, R.*
AU  - Stafoggia, M.*
AU  - Breitner-Busch, S.
AU  - Kinney, P.L.*
C1  - 75002
C2  - 57689
SP  - 1-47
TI  - Effect of air pollution reductions on mortality during the COVID-19 lockdowns in early 2020.
JO  - Res. Rep. Health Eff. Inst.
IS  - 224
PY  - 2025
SN  - 1041-5505
ER  - 

TY  - JOUR
AB  - INTRODUCTION: 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. METHODS: 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 diameter < 100 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. RESULTS: 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 with < 3% 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. ONCLUSIONS: 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.
AU  - Rich, D.Q.*
AU  - Peters, A.
AU  - Schneider, A.*
AU  - Zareba, W.*
AU  - Breitner, S.*
AU  - Oakes, D.*
AU  - Wiltshire, J.*
AU  - Kane, C.*
AU  - Frampton, M.W.*
AU  - Hampel, R.*
AU  - Hopke, P.K.*
AU  - Cyrys, J.*
AU  - Utell, M.J.*
C1  - 51533
C2  - 43178
SP  - 5-75
TI  - Ambient and controlled particle exposures as triggers for acute ECG changes.
JO  - Res. Rep. Health Eff. Inst.
VL  - 186
PY  - 2016
SN  - 1041-5505
ER  - 

TY  - RPRT
AB  - Around the world, daily variations in ambient air pollution have been consistently associated with variations in daily mortality. The aim of the study presented here was to assess the effects of ambient air pollution on daily mortality during a period of tremendous changes in air quality in the city of Erfurt, in eastern Germany, from October 1991 to March 2002. Data on particle size distributions were obtained from September 1995 to March 2002 at a research monitoring station. For particles from 0.01 microm to 2.5 microm in diameter, number concentrations (NCs)* and mass concentrations (MCs) were calculated. Particles with diameters less than or equal to 0.10 microm are defined as ultrafine particles (UFP). Data on the gaseous pollutants NO2, CO, SO2, and O3 and on PM10 (particulate matter [PM] with aerodynamic diameter less than or equal to 10 microm) were obtained from a government air-monitoring station. Data on changes in energy consumption, car fleet composition, and population were collected from local authorities. Death certificates of persons living in and dying in Erfurt were abstracted, and daily mortality counts were calculated. Poisson regression models were used to analyze the data, applying penalized splines (also known as P-splines) to model nonlinear relationships in the confounders. Model selection was done without air pollutants in the models, based on a combination of goodness-of-fit criteria and avoidance of autocorrelation in error terms. Final models included P-splines of time trend, meteorologic data, and influenza epidemics as well as day of the week with an indicator variable. Results are presented as change per interquartile range (IQR), i.e., change in the relative risk of mortality associated with a change in the concentration from the 25th to the 75th percentile of a given pollutant. Air pollutants were considered both as linear terms and as P-splines to assess the exposure-response functions. Changes in effect estimates over time were calculated using fully Bayesian time-varying coefficient models. This method was selected over four other approaches tested in simulation studies. Air-pollution concentrations decreased substantially in Erfurt during the decade under observation. The strongest changes were observed for SO2, for which annual concentrations decreased from 64 microg/m3 in 1992 to 4 microg/m3 in 2001. Concentrations of PM10, PM2.5 (particulate matter with aerodynamic diameter less than or equal to 2.5 microm), and CO decreased by more than 50%. NO2, O3, and ultrafine particles also decreased, though to a lesser extent. Based on visual inspection of the data on the changes in ambient air-pollution concentrations during the study period, we defined three study subperiods: A first subperiod from 1991 to 1995; a second, transitional subperiod from 1995 to 1998; and a third subperiod from 1998 to 2002. Generally, air-pollution concentrations decreased substantially from the first subperiod to the second, and some additional decreases occurred from the second subperiod to the third. During the second, transitional subperiod, natural gas replaced coal as the main energy source in Erfurt. In addition, the number of cars with catalytic converters increased over time, as did the number of cars in general. To facilitate the interpretation of the results, we organized the air pollutants into four groups: (1) NO2, CO, and ultrafine particles, (2) PM10 and PM2.5, (3) SO2, and (4) O3. We observed a 1.6% increased risk for daily mortality (CI, -0.4% to 3.5%) for an increase of 19.7 microg/m3 in NO2 (lag day 3), a 1.9% increased risk (CI, 0.2%-3.6%) for an increase of 0.48 mg/m3 in CO (lag day 4), and a 2.9% increased risk (CI, 0.3%-5.5%) for an increase of 9743/cm3 in ultrafine particles (lag day 4). No consistent associations were observed for PM10, PM2.5, or SO2. For O3, a 4.6% increased risk for daily mortality (CI, 1.1%-8.3%) was associated with a 43.8 microg/m3 maximum 8-hr concentration of O3 per day (lag day 2). For all four pollutants, exposure-response functions suggested no deviation from linearity. However, in time-varying models the strongest associations were observed for NO2, CO, and ultrafine particles during the transition subperiod, from 1995 to 1998, when O3 concentrations were lowest. Changes in source characteristics or ambient air-pollution concentrations were not able to explain these observations in a straightforward manner. However, the observations suggested that changes such as the introduction of three-way catalytic converters in cars and the substitution natural gas for coal might have been beneficial. Overall we concluded that: 1. Economic and political changes and the adoption of new technologies in eastern Germany resulted in distinct improvements in ambient air quality; 2. Urban air pollution in Erfurt changed within one decade from the eastern mixture toward that of western Europe ("western mixture"), which is dominated by concentrations of NOx, O3, fine particles, and ultrafine particles with low concentrations of SO2; 3. There was an association between daily mortality and ultrafine particles and combustion-related gases (lag days 3 or 4); 4. Ultrafine particles seemed to be the best pollution indicator and to point to the role of local combustion in the pollution mixture; 5. Regression coefficients showed variation over time for NO2, CO, ultrafine particles, and O3 that could not be explained by nonlinearity in the exposure-response functions; 6. Mortality associated with pollution was lower at the end of the 1990s than during the 1990s, except for mortality associated with O3; and 7. Mortality associated with pollution was strongest in the second, transitional subperiod, from 1995 to 1998, when changes in source characteristics had taken place but the benefits of improved ambient air quality had not yet been completely achieved.
AU  - Peters, A.
AU  - Breitner-Busch, S.
AU  - Cyrys, J.
AU  - Stölzel, M.
AU  - Pitz, M.
AU  - Wölke, G.
AU  - Heinrich, J.
AU  - Kreyling, W.G.
AU  - Küchenhoff, H.
AU  - Wichmann, H.-E.
C1  - 1324
C2  - 26555
CY  - Boston, MA
SP  - 94 S.
TI  - The influence of improved air quality on mortality risks in Erfurt, Germany.
JO  - Res. Rep. Health Eff. Inst.
VL  - 137
PB  - Health Effects Institute
PY  - 2009
SN  - 1041-5505
ER  -