Opposing Effects of Particle Pollution, Ozone, and Ambient Temperature on Arterial Blood Pressure

Hoffmann, Barbara; Luttmann‐Gibson, Heike; Cohen, Allison; Zanobetti, Antonella; Souza, Celine de; Foley, Christopher P.; Suh, Helen; Coull, Brent A.; Schwartz, Joel; Mittleman, Murray A.; Stone, Peter; Horton, Edward S.; Gold, Diane R.

doi:10.1289/ehp.1103647

Cited by 184 publications

(127 citation statements)

References 34 publications

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“…O 3 concentrations are highly correlated with temperature. Hoffmann et al 28 observed that O 3 and higher temperature were associated with decreases in SBP in a study of the short-term effects of ambient air pollution and temperature on arterial BP in 70 people with type 2 diabetes mellitus. Although the combined effects of these 2 factors are not clear, the effect of O 3 exposure on SBP in the study might be masked by an independent temperature effect on SBP.…”

Section: Discussionmentioning

confidence: 99%

Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China

Qian²,

et al. 2013

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http://hyper.ahajournals.org/ Downloaded from Dong et al Effects of Air Pollution on Blood Pressure 579pollution on BP in different parts of the world are unclear but may result from spatial and temporal variability in pollution sources and composition. 17,18 Compared with short-term effects of air pollution, there is little information on the relation between chronic exposure to air pollution and prevalent hypertension. Inconsistent results have also been reported on the association between incident hypertension and air pollution. For instance, Coogan et al 19 showed in a 10-year follow-up for incident hypertension and diabetes mellitus of black women from Los Angeles that NO X (but less PM 2.5 ) borderline increased the risk of becoming hypertensive. However, Sørensen et al 20 reported that longterm exposure (1 and 5 years) to NO X was not associated with incident self-reported hypertension in a Danish cohort. We hypothesized that at the population level, long-term exposure to ambient air pollution is associated with higher BP and higher prevalence of hypertension among humans. In this study, we tested this hypothesis in the 11 Districts Chinese Study, a cross-sectional study of air pollution and adult health in a large, well-characterized population-based sample, residing in northeast China, where there are wide differences in inter-and intracity gradients and ambient pollutant levels, offering a valuable opportunity to assess the associations between exposure and response. Methods Study Cities Selection and Subject RecruitmentMore than 20 million people reside in 14 cities in Liaoning province in northeast China. To maximize the inter-and intracity gradients of the pollutants of interest and minimize the correlation between district-specific ambient pollutants, in April 2009, we selected 3 cities (Shenyang, Anshan, and Jinzhou) based on the results of air pollution measurements between 2006 and 2008. There are 5, well-identified geographic districts in Shenyang, and 3 districts in Anshan and Jinzhou, respectively. Three communities within 1 km of air-monitoring sites were randomly chosen from these districts resulting in 33 locales, and from each of these, 700 to 1000 households were randomly identified. One participant, aged 18 to 74 years, was selected from each household without replacement. Our entry criterion was that the subject should have lived at that place for at least 5 years. The design and conduct of this investigation was reviewed and approved by Human Studies Committee of China Medical University. Before data collection, a written informed consent form was obtained from each participant. Ambient Air PollutionIn each of the selected study districts, there was only 1 municipal air pollution monitoring station, which was located 1 mile from the participants' homes. Measurements of PM 10 , SO 2 , NO 2 , and O 3 concentrations from 2006 to 2008 were obtained at the stations. The measurements were subject to uniform criteria for monitoring, siting, instrumentation, and quality assurance. Thes...

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Section: Discussionmentioning

confidence: 99%

Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China

Qian²,

et al. 2013

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“…28 Short-term exposures to particle pollution (including black carbon and OC) were associated with increases in blood pressure, whereas increases in O 3 were linked to blood pressure decreases in a repeated measures study of patients with type 2 diabetes mellitus. 18 In elderly subjects with coronary artery disease from the Los Angeles, CA, basin, exposure to primary components of fossil fuel combustion (eg, OC) was associated with ST-segment depression 39 and with elevated ambulatory blood pressure. 40 Associations of OC with higher blood pressure were of greatest magnitude among obese participants.…”

Section: Short-term Exposures/acute Effectsmentioning

confidence: 99%

“…102 Many studies have suggested that people with type 2 diabetes mellitus may be more vulnerable to the acute effects of particles on blood pressure and other vascular responses. 18,103 As discussed in our 2008 review, 102 diabetesassociated chronic inflammation and oxidative stress may quench nitric oxide, create imbalances in vasoactive mediators in arterial tissue, change smooth muscle responsiveness as a result of chronic autonomic dysfunction, or impair flowmediated dilation as a result of vascular remodeling. Animal models support obesity and diabetes mellitus as sources of vulnerability to cardiovascular effects of particle mass: Exposure to PM 2.5 increased the risk of insulin resistance in rats fed a high-fat diet but not in those fed a normal-chow diet.…”

Section: Preexisting Chronic Conditions: Diabetes Mellitus and Obesitymentioning

confidence: 99%

“…A repeated measures study of adults with type 2 diabetes mellitus conducted in Boston demonstrated opposing effects of fine particle mass compared with the effects of high temperature or ozone. 18 Whereas increases in PM 2.5 were associated with elevated systolic and diastolic blood pressures, higher temperature and higher ozone levels were linked to a reduction in blood pressure, particularly in those whose mean blood pressure was already within normal limits. Heart rate variability was most reduced when both temperature and ozone were high in the Boston Normative Aging Study.…”

Section: Temperature Pollution and Cardiovascular Riskmentioning

confidence: 99%

“…18 In elderly subjects with coronary artery disease from the Los Angeles, CA, basin, exposure to primary components of fossil fuel combustion (eg, OC) was associated with ST-segment depression 39 and with elevated ambulatory blood pressure.…”

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New Insights Into Pollution and the Cardiovascular System

Gold

Mittleman

2013

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Figure.Odds ratio of ischemic stroke onset for US Environmental Protection Agency categories (good and moderate) of mean ambient fine particulate matter air pollution (PM 2.5 ) levels in the 24 hours preceding stroke onset. Error bars indicate 95% confidence interval. Reproduced from Wellenius et al 5 with permission from the publisher. The increased risk was greatest within 12 to 14 hours of exposure. Update, 2010 to 2012: Cardiac Arrhythmia, Arrhythmia Precursors, and PollutionEvidence continues to be mixed for associations between pollution and documented cardiac arrhythmias or electrophysiological changes such as repolarization abnormalities that may increase the risk of arrhythmias. Even more so than studies of stroke, ascertainment of the timing of the onset of the outcome and the specific electrophysiological nature of the outcome can be challenging to ascertain without personal monitoring, which is absent in studies of administrative data sets, which often report null findings. 6 In their recent review, Link and Dockery 7 concluded that "the incremental risk of air pollution in triggering arrhythmias… is greatest for patients with underlying cardiac disease." A London study examined associations of 11 pollutants with activation of implanted cardioverter-defibrillators, finding mostly weak associations with the elevation of a number of secondary regional pollutants, the strongest of which was the nontraffic particle component sulfate. 8 Increases in premature ventricular counts, atrial fibrillation/flutter, and its precedent, P-wave complexity, were associated with increased PM 2.5 in the previous 1 to 2 hours in a Pennsylvania study of 105 middle-aged healthy nonsmokers with 24-hour ECG and personal particle monitoring.9,10 Ghio et al 11 presented a case report of new-onset atrial fibrillation that occurred 20 minutes into a controlled exposure to concentrated ambient particles and resolved within 2 hours with no sequella. In studies of vulnerable populations who have personal electrophysiological monitoring, ozone has also been considered a risk factor for arrhythmias. An increase in the maximum ozone level predicted increases in bradycardia and apnea in high-risk infants on home monitors. 12Controlled human exposure to 1-hour exposures of diesel exhaust did not influence heart rhythm or variability in a UK study.13 Increased spatial dispersion of myocardial repolarization, but not T-wave alternans, was seen after controlled human exposures to concentrated ambient particles, ozone, or a combination of the 2 exposures.14 Increases in long-term estimated residential PM 2.5 predicted increased odds of QT prolongation without overt ventricular abnormalities in the Multi-Ethnic Study of Atherosclerosis (MESA). 15 Two recent studies (the Table) also suggest acute effects of O 3 on repolarization abnormalities in sensitive subjects. 16,17 Update, 2010 to 2012: Cardiovascular Effects of the Coarse (PM 10-2.5 ) or Ultrafine (<0.1 μm) Fractions of PM 10 Findings on cardiovascular health effects of coarse or ultr...

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Association of Ozone Exposure With Cardiorespiratory Pathophysiologic Mechanisms in Healthy Adults

et al. 2017

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IMPORTANCE Exposure to ozone has been associated with cardiovascular mortality, but the underlying biological mechanisms are not yet understood.OBJECTIVE To examine the association between ozone exposure and cardiopulmonary pathophysiologic mechanisms. DESIGN, SETTING, AND PARTICIPANTSA longitudinal study involving 89 healthy adult participants living on a work campus in Changsha City, China, was conducted from December 1, 2014, to January 31, 2015. This unique quasiexperimental setting allowed for better characterization of air pollutant exposure effects because the participants spent most of their time in controlled indoor environments. Concentrations of indoor and outdoor ozone, along with the copollutants particulate matter, nitrogen dioxide, and sulfur dioxide, were monitored throughout the study period and then combined with time-activity information and filtration conditions of each residence and office to estimate 24-hour and 2-week combined indoor and outdoor mean exposure concentrations. Associations between each exposure measure and outcome measure were analyzed using single-pollutant and 2-pollutant linear mixed models controlling for ambient temperature, secondhand smoke exposure, and personal-level time-varying covariates.MAIN OUTCOMES AND MEASURES Biomarkers indicative of inflammation and oxidative stress, arterial stiffness, blood pressure, thrombotic factors, and spirometry were measured at 4 sessions. RESULTSOf the 89 participants, 25 (28%) were women and the mean (SD) age was 31.5 (7.6) years. The 24-hour ozone exposure concentrations ranged from 1.4 to 19.4 parts per billion (ppb), corresponding to outdoor concentrations ranging from 4.3 to 47.9 ppb. Within this range, in models controlling for a second copollutant and other potential confounders, a 10-ppb increase in 24-hour ozone was associated with mean increases of 36.3% (95% CI, 29.9%-43.0%) in the level of platelet activation marker soluble P-selectin, 2.8% (95% CI, 0.6%-5.1%) in diastolic blood pressure, 18.1% (95% CI, 4.5%-33.5%) in pulmonary inflammation markers fractional exhaled nitric oxide, and 31.0% (95% CI, 0.2%-71.1%) in exhaled breath condensate nitrite and nitrate as well as a −9.5% (95% CI, −17.7% to −1.4%) decrease in arterial stiffness marker augmentation index. A 10-ppb increase in 2-week ozone was associated with increases of 61.1% (95% CI, 37.8%-88.2%) in soluble P-selectin level and 126.2% (95% CI, 12.1%-356.2%) in exhaled breath condensate nitrite and nitrate level. Other measured biomarkers, including spirometry, showed no significant associations with either 24-hour ozone or 2-week ozone exposures.CONCLUSIONS AND RELEVANCE Short-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.

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Opposing Effects of Particle Pollution, Ozone, and Ambient Temperature on Arterial Blood Pressure

Cited by 184 publications

References 34 publications

Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China

Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China

New Insights Into Pollution and the Cardiovascular System

Association of Ozone Exposure With Cardiorespiratory Pathophysiologic Mechanisms in Healthy Adults

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