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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.

The authors evaluated the association between ventricular arrhythmias detected by implantable cardioverter defibrillators and ambient air pollution concentrations in the hours immediately before the arrhythmia. Patients given implantable cardioverter defibrillators at the New England Medical Center in Boston, Massachusetts, between mid-1995 and 1999 who lived within 40 km of a central monitoring site (n = 203) were followed until July 2002. The authors used a case-crossover design to study the association between ambient air pollution and up to 798 confirmed ventricular arrhythmias among 84 subjects. The authors found that interquartile range increases in 24-hour moving average particulate matter less than 2.5 mum in aerodynamic diameter and ozone were associated with 19% and 21% increased risks of ventricular arrhythmia, respectively. For each, there was evidence of a linear exposure response, and the associations appeared independent. These associations were stronger than associations with mean concentrations on the same calendar day and previous calendar days. The authors did not find associations with pollutant concentrations less than 24 hours before the arrhythmia. Cases with a prior ventricular arrhythmia within 72 hours had greater risk associated with air pollutants than did cases without a recent arrhythmia. These results confirm previous findings and suggest that matching of pollution periods to arrhythmias is important in detecting such associations.

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 Air pollution exposure has been associated with increased blood pressure in adults. Objective: We examined associations of antenatal exposure to ambient air pollution with newborn systolic blood pressure (SBP). Methods: We studied 1,131 mother–infant pairs in a Boston, Massachusetts, area pre-birth cohort. We calculated average exposures by trimester and during the 2 to 90 days before birth for temporally resolved fine particulate matter (≤ 2.5 μm; PM2.5), black carbon (BC), nitrogen oxides, nitrogen dioxide, ozone (O3), and carbon monoxide measured at stationary monitoring sites, and for spatiotemporally resolved estimates of PM2.5 and BC at the residence level. We measured SBP at a mean age of 30 ± 18 hr with an automated device. We used mixed-effects models to examine associations between air pollutant exposures and SBP, taking into account measurement circumstances; child’s birth weight; mother’s age, race/ethnicity, socioeconomic position, and third-trimester BP; and time trend. Estimates represent differences in SBP associated with an interquartile range (IQR) increase in each pollutant. Results: Higher mean PM2.5 and BC exposures during the third trimester were associated with higher SBP (e.g., 1.0 mmHg; 95% CI: 0.1, 1.8 for a 0.32-μg/m3 increase in mean 90-day residential BC). In contrast, O3 was negatively associated with SBP (e.g., –2.3 mmHg; 95% CI: –4.4, –0.2 for a 13.5-ppb increase during the 90 days before birth). Conclusions: Exposures to PM2.5 and BC in late pregnancy were positively associated with newborn SBP, whereas O3 was negatively associated with SBP. Longitudinal follow-up will enable us to assess the implications of these findings for health during later childhood and adulthood. Citation: van Rossem L, Rifas-Shiman SL, Melly SJ, Kloog I, Luttmann-Gibson H, Zanobetti A, Coull BA, Schwartz JD, Mittleman MA, Oken E, Gillman MW, Koutrakis P, Gold DR. 2015. Prenatal air pollution exposure and newborn blood pressure. Environ Health Perspect 123:353–359; http://dx.doi.org/10.1289/ehp.1307419

Introduction: Atrial fibrillation (AF) is responsible for substantial morbidity and mortality, yet little is known about the environmental factors that may trigger AF episodes. Weather has been proposed as a potential precipitant of paroxysmal AF. Hypothesis: We assessed the hypothesis that changes in outdoor ambient temperature and outdoor absolute humidity may trigger paroxysmal AF in the following 24 hours. Methods: Patients with dual chamber implantable cardioverter defibrillators (ICDs) living in eastern Massachusetts were enrolled between September 2006 and March 2010 from the Tufts Medical Center Cardiac Arrhythmia Clinic (Boston, Massachusetts) and followed prospectively for episodes of paroxysmal AF lasting at least 30 seconds. Arrhythmias documented by the ICD were reviewed and interpreted by an electrophysiologist masked to exposure. The date and time of AF episodes were linked to hourly weather data measured at Boston Logan International Airport. We examined the hypothesis using a time-stratified case-crossover analysis matched on calendar month, day of week and time of day and adjusted for air pollution and barometric pressure. To reduce the possibility of over-representation of clustered events and to reflect the averaging time of the exposure, incident AF episodes were included in the analysis if at least 24 hours had passed since the previous AF episode. Results: Of 200 patients enrolled, 49 experienced at least one AF episode (n = 328 episodes). After excluding events with missing exposure or covariate information, analyses were confined to 230 AF episodes among 47 patients. The 47 patients with paroxysmal AF were followed for an average of 1.9 years, and 32 (68%) were male, 45 (96%) were Caucasian, the mean age was 67 years, 24 (51%) had a history of prior AF episodes, 27 (57%) had a pre-implantation ejection fraction < 35%, and 29 (62%) received the ICD for primary prophylaxis. Outdoor temperature in the previous 24 hours was not associated with AF (odds ratio (OR) = 1.13; 95% confidence interval (CI): 0.89, 1.43, p = 0.32, per interquartile range (IQR) decrease of 6.3°C). Lower absolute humidity in the previous 24 hours was associated with a higher risk of AF onset (OR = 1.33; 95% CI: 1.02, 1.74, p = 0.04, per IQR decrease of 3.5 g/m 3 ); this risk increased slightly for the previous 3 hours (OR = 1.39; 95% CI: 1.06, 1.82, p = 0.02, per IQR decrease of 3.7 g/m 3 ). Conclusions: In conclusion, drier air was associated with a transiently higher risk of paroxysmal AF in the following 24 hours among patients with dual chamber ICDs.

We examine whether ambient air pollution is associated with oxygen saturation in 32 elderly subjects in Steubenville, Ohio.We used linear mixed models to examine the effects of fine particulate matter less than 2.5 μm (PM(2.5)), sulfate (SO(4)(-2)), elemental carbon, and gases on median oxygen saturation.An interquartile range increase of 13.4 μg/m in PM(2.5) on the previous day was associated with a decrease of -0.18% (95% confidence interval: -0.31 to -0.06) and a 5.1 μg/m(3) interquartile range increase in SO(4)(-2) on the previous day was associated with a decrease of -0.16% (95% confidence interval: -0.27 to -0.04) in oxygen saturation during the initial 5-minute rest period of the protocol.Increased exposure to air pollution, including the nontraffic pollutant SO(4)(-2) from industrial sources, led to changes in oxygen saturation that may reflect particle-induced pulmonary inflammatory or vascular responses.

Background Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. The Vitamin D and Omega-3 Trial (VITAL) is randomizing >22,000 U.S. adults >50 years o...

ObjectivesThis study sought to evaluate the association of air pollution with the onset of atrial fibrillation (AF).BackgroundAir pollution in general and more specifically particulate matter has been associated with cardiovascular events. Although ventricular arrhythmias are traditionally thought to convey the increased cardiovascular risk, AF may also contribute.MethodsPatients with dual chamber implantable cardioverter-defibrillators (ICDs) were enrolled and followed prospectively. The association of AF onset with air quality including ambient particulate matter

Background and Aims: Implanted cardioverter defibrillators (ICD) monitor and treat arrhythmias and provide electrocardiographic records of the timing of ventricular and atrial arrhythmias. Diabetes...

Dr. Culic suggests that the associations that we reported [(1)][1] between particulate air pollution (PM2.5) and atrial fibrillation (AF) may be confounded by inadequate control of meteorology. There is a well-developed body of literature suggesting that acute particulate air pollution exposures

Studies of the relationships between low socio-economic status and impaired lung function were conducted mainly in Western European countries and North America. East–West differences remain unexplored. Associations between parental education and lung function were explored using data on 24,010 school-children from eight cross-sectional studies conducted in North America, Western and Eastern Europe. Parental education was defined as low and high using country-specific classifications. Country-specific estimates of effects of low parental education on volume and flow parameters were obtained using linear and logistic regression, controlling for early life and other individual risk factors. Meta-regressions were used for assessment of heterogeneity between country-specific estimates. The association between low parental education and lung function was not consistent across the countries, but showed a more pronounced inverse gradient in the Western countries. The most consistent decrease associated with low parental education was found for peak expiratory flow (PEF), ranging from −2.80 to −1.14%, with statistically significant associations in five out of eight countries. The mean odds ratio for low PEF (

Background: Fine particulate matter (PM2.5) has been associated with physiologic and inflammatory changes related to vascular dysfunction. People with diabetes might be more vulnerable to the cardiovascular effects of air pollution. We examined whether short-term exposure to fine particles is associated[for full text, please go to the a.m. URL], 54. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds)

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.

Inequalities in health between socio-economic groups are a major public health concern. The current authors studied associations between parental socio-economic status (SES) and children's respiratory and allergic symptoms in 13 diverse countries, including the Russian Federation, North America (Canada and the USA), and countries across Eastern and Western Europe. Data of 57,000 children aged 6-12 yrs, originating from eight cross-sectional studies, were analysed. SES was defined by parental education. Respiratory and allergic symptoms were defined by parental questionnaire reports. Multiple logistic regressions showed that low parental education was associated with a decreased risk of inhalant allergy and itchy rash in school children. Furthermore, low parental education was associated with an increased prevalence of wheeze and nocturnal dry cough. No clear association was found between parental education and prevalence of doctor-diagnosed asthma and bronchitis. Part of the difference between socio-economic groups with regard to their children's symptoms was explained by established risk factors, such as parental allergy, smoking during pregnancy, pet ownership, crowding, mould/moisture in the home, use of gas for cooking, and air pollution (particulate matter with a diameter of

Objectives: Adverse effects have been reported of prenatal and/or postnatal passive exposure to smoking on children’s health. Uncertainties remain about the relative importance of smoking at different periods in the child’s life. We investigate this in a pooled analysis, on 53 879 children from 12 cross-sectional studies—components of the PATY study (Pollution And The Young). Methods: Effects were estimated, within each study, of three exposures: mother smoked during pregnancy, parental smoking in the first two years, current parental smoking. Outcomes were: wheeze, asthma, “woken by wheeze”, bronchitis, nocturnal cough, morning cough, “sensitivity to inhaled allergens” and hay fever. Logistic regressions were used, controlling for individual risk factors and study area. Heterogeneity between study-specific results, and mean effects (allowing for heterogeneity) were estimated using meta-analytical tools. Results: There was strong evidence linking parental smoking to wheeze, asthma, bronchitis and nocturnal cough, with mean odds ratios all around 1.15, with independent effects of prenatal and postnatal exposures for most associations. Conclusions: Adverse effects of both pre- and postnatal parental smoking on children’s respiratory health were confirmed. Asthma was most strongly associated with maternal smoking during pregnancy, but postnatal exposure showed independent associations with a range of other respiratory symptoms. All tobacco smoke exposure has serious consequences for children’s respiratory health and needs to be reduced urgently.