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Do Ambient Ozone or Other Pollutants Modify Effects of Controlled Ozone Exposure on Pulmonary Function?
Rich, DQ, Thurston, SW, Balmes, JR, Bromberg, PA, Arjomandi, M, Hazucha, MJ, Alexis, NE, Ganz, P, Zareba, W, Thevenet-Morrison, K, et al
Annals of the American Thoracic Society. 2020;(5):563-572
Abstract
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 of airway inflammation and injury, but without convincing evidence of effects on cardiovascular function. However, the subjects' exposures to indoor and outdoor air pollution in the hours and days before each controlled O3 exposure may have modified biomarker responses to the controlled O3 exposures.Objectives: We sought to determine whether personal measures of nitrogen dioxide (NO2) and O3, or ambient concentrations of O3, particulate matter ≤2.5 μm in aerodynamic diameter, NO2, carbon monoxide (CO), and sulfur dioxide (SO2) in the 72 and 96 hours before the exposure visit modified biomarker responses to controlled O3 exposure.Methods: MOSES subjects were exposed for 3 hours in random order to clean air containing 0 ppb O3, 70 ppb O3, or 120 ppm O3, alternating 15 minutes of moderate exercise with 15 minutes of rest. Cardiovascular and pulmonary endpoints (biomarkers of autonomic function, repolarization, ST segment change, arrhythmia, prothrombotic vascular status, systemic inflammation, vascular function, pulmonary function, oxidative stress, and lung injury) were measured on the day before, the day of, and up to 22 hours after each exposure. We evaluated whether ambient pollutant concentrations in the 96 hours before the pre-exposure visit modified pre- to post-exposure lung function biomarker responses to the controlled O3 exposures, using tertiles of passive personal exposure samplers (PES) of O3 and NO2, ambient air pollutant concentrations, and mixed effects linear regression. We also similarly explored the effect modification of controlled O3 effects on biomarkers of other MOSES outcome groups in the same way. Although we used P < 0.01 to define statistical significance, we did not formally correct for multiple comparisons.Results: The effects of MOSES controlled O3 exposures on forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) were modified by ambient NO2 and CO, and PES NO2. Reductions in FEV1 and FVC were observed only when these concentrations were in the "medium" or "high" tertile in the 72 hours before the pre-exposure visit. There was no such modification of the effect of controlled O3 exposure on any other cardiopulmonary outcome group.Conclusions: Reductions in markers of lung function, but not other pathways, by the MOSES controlled O3 exposure were modified by ambient NO2 and CO, and PES NO2, and these reductions were observed only when these pollutant concentrations were elevated in the hours and days before the pre-exposure visit.Clinical trial registered with ClinicalTrials.gov (NCT01487005).
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Association Between Exposure to Ambient Air Pollution and Thyroid Function in Korean Adults.
Kim, HJ, Kwon, H, Yun, JM, Cho, B, Park, JH
The Journal of clinical endocrinology and metabolism. 2020;(8)
Abstract
CONTEXT Although a significant relationship has been reported between air pollution and thyroid function in limited samples or regions, few studies have addressed this association in the general population. OBJECTIVE Using a nationwide sample of Korean adults, we investigated the association between exposure to air pollution and thyroid function, and whether this association differed between subgroups stratified according to age or body mass index (BMI). METHODS We included 4704 adults in the final analysis and used each person's annual average exposure to 4 air pollutants, namely, particulate matter with an aerodynamic diameter less than or equal to 10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide, and carbon monoxide (CO). We measured serum thyrotropin (TSH) and free thyroxine (FT4) concentrations as indicators of thyroid function according to age and BMI. RESULTS The annual average exposure to NO2 and CO was significantly associated with an elevated TSH and reduced FT4 concentration after adjusting for possible confounding factors (all P < .05). In men, in addition to these 2 pollutants, PM10 exposure was positively associated with TSH level (P = .03). Age-stratified analysis showed stronger effects of NO2 and CO exposure in older than in younger adults. Exposure to these air pollutants was related to serum TSH and FT4 concentrations in people with overweight or obesity but not in those of normal weight. CONCLUSIONS This study provides the first evidence that air pollution exposure is linked to thyroid function in the general population and that this association may be stronger in older or overweight or obese adults.
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Air pollution in relation to very short-term risk of ST-segment elevation myocardial infarction: Case-crossover analysis of SWEDEHEART.
Sahlén, A, Ljungman, P, Erlinge, D, Chan, MY, Yap, J, Hausenloy, DJ, Yeo, KK, Jernberg, T
International journal of cardiology. 2019;:26-30
Abstract
OBJECTIVE Studies have related air pollution to myocardial infarction (MI) events over days or weeks, with few data on very short-term risks. We studied risk of ST-segment elevation MI (STEMI) within hours of exposure to air pollution while adjusting for weather. METHODS We performed a case-crossover study of STEMI cases in Stockholm, Sweden (Jan 2000-June 2014) based on SWEDEHEART. Exposures during hazard periods up to 24 h prior to admission were compared to bidirectionally sampled control periods. Risks attributable to sulphur dioxide (SO2), nitrogen dioxide (NO2), ozone and particulate pollutants (PM2.5, PM10) were studied in conditional logistic regression models for interquartile range increments. RESULTS Risk of STEMI (n = 14,601) was associated with NO2 (strongest at 15-h lag) and with PM2.5 (strongest at 20-h lag), in single-pollutant models adjusting for air temperature and humidity (NO2: odds ratio (OR; 95% confidence interval) 1.065 (1.031-1.101); PM2.5: 1.026 (1.001-1.054)). After adjusting models for atmospheric pressure (significantly associated with STEMI risk at 14-24-h lags), NO2 remained highly statistically significant (1.057 (1.022-1.094)) but not PM2.5 (1.024 (0.997-1.052)). No associations were seen for SO2, ozone or PM10. CONCLUSION Risk of STEMI rises within hours of exposure to air pollutants, with strongest impact of NO2. These findings are complementary to earlier reports which have not acknowledged widely the importance of very short-term fluctuations in air pollution.
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Mediterranean Diet and the Association Between Air Pollution and Cardiovascular Disease Mortality Risk.
Lim, CC, Hayes, RB, Ahn, J, Shao, Y, Silverman, DT, Jones, RR, Thurston, GD
Circulation. 2019;(15):1766-1775
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Abstract
BACKGROUND Recent experimental evidence suggests that nutritional supplementation can blunt adverse cardiopulmonary effects induced by acute air pollution exposure. However, whether usual individual dietary patterns can modify the association between long-term air pollution exposure and health outcomes has not been previously investigated. We assessed, in a large cohort with detailed diet information at the individual level, whether a Mediterranean diet modifies the association between long-term exposure to ambient air pollution and cardiovascular disease mortality risk. METHODS The National Institutes of Health-American Association for Retired Persons Diet and Health Study, a prospective cohort (N=548 845) across 6 states and 2 cities in the United States and with a follow-up period of 17 years (1995-2011), was linked to estimates of annual average exposures to fine particulate matter and nitrogen dioxide at the residential census-tract level. The alternative Mediterranean Diet Index, which uses a 9-point scale to assess conformity with a Mediterranean-style diet, was constructed for each participant from information in cohort baseline dietary questionnaires. We evaluated mortality risks for cardiovascular disease, ischemic heart disease, cerebrovascular disease, or cardiac arrest associated with long-term air pollution exposure. Effect modification of the associations between exposure and the mortality outcomes by alternative Mediterranean Diet Index was examined via interaction terms. RESULTS For fine particulate matter, we observed elevated and significant associations with cardiovascular disease (hazard ratio [HR] per 10 μg/m3, 1.13; 95% CI, 1.08-1.18), ischemic heart disease (HR, 1.16; 95% CI, 1.10-1.23), and cerebrovascular disease (HR, 1.15; 95% CI, 1.03-1.28). For nitrogen dioxide, we found significant associations with cardiovascular disease (HR per 10 ppb, 1.06; 95% CI, 1.04-1.08) and ischemic heart disease (HR, 1.08; 95% CI, 1.05-1.11). Analyses indicated that Mediterranean diet modified these relationships, as those with a higher alternative Mediterranean Diet Index score had significantly lower rates of cardiovascular disease mortality associated with long-term air pollution exposure ( P-interaction<0.05). CONCLUSIONS A Mediterranean diet reduced cardiovascular disease mortality risk related to long-term exposure to air pollutants in a large prospective US cohort. Increased consumption of foods rich in antioxidant compounds may aid in reducing the considerable disease burden associated with ambient air pollution.
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Association of Air Pollution Exposures With High-Density Lipoprotein Cholesterol and Particle Number: The Multi-Ethnic Study of Atherosclerosis.
Bell, G, Mora, S, Greenland, P, Tsai, M, Gill, E, Kaufman, JD
Arteriosclerosis, thrombosis, and vascular biology. 2017;(5):976-982
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OBJECTIVE The relationship between air pollution and cardiovascular disease may be explained by changes in high-density lipoprotein (HDL). APPROACH AND RESULTS We examined the cross-sectional relationship between air pollution and both HDL cholesterol and HDL particle number in the MESA Air study (Multi-Ethnic Study of Atherosclerosis Air Pollution). Study participants were 6654 white, black, Hispanic, and Chinese men and women aged 45 to 84 years. We estimated individual residential ambient fine particulate pollution exposure (PM2.5) and black carbon concentrations using a fine-scale likelihood-based spatiotemporal model and cohort-specific monitoring. Exposure periods were averaged to 12 months, 3 months, and 2 weeks prior to examination. HDL cholesterol and HDL particle number were measured in the year 2000 using the cholesterol oxidase method and nuclear magnetic resonance spectroscopy, respectively. We used multivariable linear regression to examine the relationship between air pollution exposure and HDL measures. A 0.7×10-6 m-1 higher exposure to black carbon (a marker of traffic-related pollution) averaged over a 1-year period was significantly associated with a lower HDL cholesterol (-1.68 mg/dL; 95% confidence interval, -2.86 to -0.50) and approached significance with HDL particle number (-0.55 mg/dL; 95% confidence interval, -1.13 to 0.03). In the 3-month averaging time period, a 5 μg/m3 higher PM2.5 was associated with lower HDL particle number (-0.64 μmol/L; 95% confidence interval, -1.01 to -0.26), but not HDL cholesterol (-0.05 mg/dL; 95% confidence interval, -0.82 to 0.71). CONCLUSIONS These data are consistent with the hypothesis that exposure to air pollution is adversely associated with measures of HDL.
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Lack of association between air pollutant exposure and short-term risk of ischaemic stroke in Lyon, France.
Mechtouff, L, Canoui-Poitrine, F, Schott, AM, Nighoghossian, N, Trouillas, P, Termoz, A, Porthault-Chatard, S, David, JS, Chasles, V, Derex, L
International journal of stroke : official journal of the International Stroke Society. 2012;(8):669-74
Abstract
BACKGROUND Some observational and experimental studies have suggested a short-term relationship between air pollutants and ischaemic stroke; however, the results conflict. AIMS The objective of this study was to investigate the association between particulate matter less than 2·5 and 10 microns in aerodynamic diameter, nitrogen dioxide, sulphur dioxide and ozone, and short-term risk of ischaemic stroke in Lyon, France. METHODS The AVC69 study was a multicenter cohort study in which all consecutive adult patients admitted to one of the emergency or neurological departments of the Rhône area for suspicion of stroke were included during a seven-month period. Only patients with ischaemic stroke living within the study area, composed of Lyon and 18 neighbouring communities with homogenous air pollutants exposure, formed the basis of our study. We adopted a time-stratified case-crossover design to analyse the short-term effect (up to two-days) of air pollutants on ischaemic stroke incidence. Models were adjusted for temperature, variation of atmospheric pressure, minimal relative humidity, influenza epidemics, pollen count, and holidays. Stratified analyses by gender and class age were performed. Different lag times were analysed. RESULTS 376 patients were included. Mean age was 76·6 years (± 13·7). 53·7% were women. No association was observed between air pollutants and short-term risk of ischaemic stroke after adjustment for main confounding factors. Results remained unchanged whatever the gender or age. CONCLUSIONS These results suggest a lack of association between air pollutant exposure and short-term risk of ischaemic stroke in a French urban area.