Long-Term Ozone Exposure Associated with Acceleration of Subclinical Arterial Disease

by | Jan 27, 2020 | 2019, Cardiovascular Health, Environmental Health

Written by Angeline A. De Leon, Staff Writer. Study finds that outdoor O3 concentrations were associated with increased rate of carotid wall thickness progression and risk of new plaque formation.

cardiovascular healthGround-level ozone (O3) is a colorless and highly irritating oxidizing agent formed in the lower atmosphere when primary pollutants (e.g., gasses emitted by power plants, industrial boilers, cars, etc.) react chemically in the presence of sunlight 1. Acute exposure to O3 has been definitively linked to adverse effects in the respiratory system 2, and the effects of long-term O3 exposure have been demonstrated for total mortality 3 and cardiovascular mortality 4. But the specific changes in cardiovascular function caused by long-term O3 exposure are still unclear 5, particularly in relation to subclinical vascular disease 6. The limited amount of research on O3 exposure and vascular disease suggest that prolonged ozone exposure is linked to intima-media thickness of the common carotid artery (IMTCCA), a marker of subclinical arterial disease found to be predictive of heart disease and stroke 5,7,8. To understand the long-term association between O3 exposure and subclinical arterial disease progression, researchers at the University at Buffalo, New York measured IMTCCA, as well as coronary artery calcification (CAC) and carotid plaque (CP) (additional biomarkers of cardiovascular disease, CVD) in a longitudinal cohort 9.

A total of 6,814 healthy subjects (aged 45 to 84 years at baseline) without a history of CVD were followed for approximately 10 years. At baseline and throughout follow-up examinations, data on lifestyle habits, psychosocial factors, and CVD risk factors were collected, and computed tomography (CT) was used to measure IMTCCA, CP, and CAC (for IMTCCA and CP, an average of two measurements were taken over a mean follow-up period of 9 years; for CAC, an average of three measurements were taken over a mean follow-up period of 6.5 years). To estimate long-term outdoor O3 concentration levels, a region-specific saptio-temporal exposure model was developed based on comprehensive monitoring data from the Air Quality System of the U.S. Environmental Protection Agency. Logistic regression models were used to assess longitudinal associations between long-term average O3 exposure and progression of mean IMTCCA, CAC, and CP formation over time. Odds ratios (OR) were also calculated for each parameter.

Mean progression of IMTCCA was 12 +/- 0.5 µm/year and for CAC was 25 +/- 1.4 Agatston units/year. Longitudinal analysis showed that an interquartile range (IQR) increase in long-term average O3 exposure (3 parts per billion, ppb) was associated with a 5.6-µm (95% Confidence Interval: 1.4 to 9.7) faster increase in IMTCCA over a 10-year period. For carotid plaque, a 3-ppb increase in long-term O3 exposure was associated with new CP formation (OR = 1.2, 95% CI: 1.1 to 1.4). No significant association was found between O3 exposure and CAC change.

Study findings elucidate the association between long-term ozone exposure and CVD mortality, suggesting that O3 exposure may contribute to CVD by accelerating the progression of IMTCCA and increasing new plaque formation. The first epidemiological study to examine the longitudinal effects of O3 on IMTCCA, CAC, and CP, the present trial suggests that O3 exposure is linked to arterial injury and progression of atherosclerosis and should be acknowledged as a risk factor for CVD events. Strengths of the study include a relatively large sample size, a relatively long follow-up period, and the use of sensitive measures to estimate residence-specific O3 concentrations. A potential study limitation may be related to the measurement of only outdoor O3 concentrations (instead of both indoor and outdoor levels of O3), which may not be an accurate reflection of individual-level O3 exposure. Cross-sectional studies are warranted to confirm a direct causal tie between O3 exposure and subclinical arterial disease. It would also be valuable to track how subclinical arterial injury relates to clinical outcome and mortality as a function of O3 exposure over time.

Source: Wang M, Sampson PD, Sheppard LE, et al. Long-term exposure to ambient ozone and progression of subclinical arterial disease: the multi-ethnic study of atherosclerosis and air pollution. Environmental Health Perspectives. 2019; 127(5): 57001. DOI: 10.1289/EHP325.

Posted January 27, 2020.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

  1. EPA. Integrated Science Assessment (ISA) of Ozone and Related Photochemical Oxidants 2013 https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=247492. Accessed January 20, 2020.
  2. EEA. Air Quality in Europe 2011. 2011.
  3. Di Q, Wang Y, Zanobetti A, et al. Air pollution and mortality in the Medicare population. New England Journal of Medicine. 2017;376(26):2513-2522.
  4. Turner MC, Jerrett M, Pope III CA, et al. Long-term ozone exposure and mortality in a large prospective study. American journal of respiratory and critical care medicine. 2016;193(10):1134-1142.
  5. Jerrett M, Burnett RT, Pope III CA, et al. Long-term ozone exposure and mortality. New England Journal of Medicine. 2009;360(11):1085-1095.
  6. Breton CV, Wang X, Mack WJ, et al. Childhood air pollutant exposure and carotid artery intima-media thickness in young adults. Circulation. 2012;126(13):1614-1620.
  7. Stein JH, Korcarz CE, Hurst RT, et al. Use of carotid ultrasound to identify subclinical vascular disease and evaluate cardiovascular disease risk: a consensus statement from the American Society of Echocardiography Carotid Intima-Media Thickness Task Force endorsed by the Society for Vascular Medicine. Journal of the American Society of Echocardiography. 2008;21(2):93-111.
  8. Gepner AD, Young R, Delaney JA, et al. Comparison of Coronary Artery Calcium Presence, Carotid Plaque Presence, and Carotid Intima-Media Thickness for Cardiovascular Disease Prediction in the Multi-Ethnic Study of AtherosclerosisCLINICAL PERSPECTIVE. Circulation: Cardiovascular Imaging. 2015;8(1):e002262.
  9. Wang M, Sampson PD, Sheppard LE, Stein JH, Vedal S, Kaufman JD. Long-term exposure to ambient ozone and progression of subclinical arterial disease: the multi-ethnic study of atherosclerosis and air pollution. Environmental health perspectives. 2019;127(5):057001.