Long-Term Ozone Exposure and Mortality

Abstract

BACKGROUND Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution–related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes. METHODS Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are ≤2.5 μm in aerodynamic diameter [PM2.5]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models. RESULTS In single-pollutant models, increased concentrations of either PM2.5 or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM2.5 was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used. CONCLUSIONS In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM2.5 was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

Cardiovascular and Cerebrovascular Emergency Department Visits Associated With Wildfire Smoke Exposure in California in 2015

“…Wildfire smoke contains numerous air pollutants, including particulate matter, ozone, carbon monoxide, polycyclic aromatic compounds, and nitrogen dioxide, all of which have previously been associated with respiratory and cardiovascular outcomes in health studies of air pollution 6, 7, 8, 9, 10. Fine particulate matter (<2.5 μm in diameter [PM 2.5 ]) is a known respiratory irritant and causally related to cardiovascular morbidity 11, 12, 13.…”

“…This has been linked to cardiovascular health impacts such as ischemic heart disease and cerebrovascular events such as ischemic stroke in the ambient air pollutant PM 2.5 literature 11, 15, 16, 17, 18. Other air pollutants in wildfire smoke have also been linked to cardiovascular and respiratory outcomes in urban and ambient air pollution studies, including nitrogen oxides, carbon monoxide, and ozone 7, 8, 9, 10…”

Understanding in situ ozone production in the summertime through radical observations and modelling studies during the Clean air for London project (ClearfLo)

“…The EU air quality guidelines recommend that ozone concentrations do not exceed 60 ppbv for greater than an 8 hour period (http://www.eea.europa.eu/themes/air/ozone), with a 10 ppbv increment in long term exposure to ozone increasing the risk of death from respiratory causes by ~ 3 -4% (Jerrett et al, 2009). Short-term exposure to elevated levels of tropospheric ozone 15 have been associated with several adverse health effects including, for example, exacerbation of asthma in children (Thurston et al, 1997).…”

An integrated assessment of two decades of air pollution policy making in Spain: Impacts, costs and improvements

“…This methodology allows AERIS to provide esti mates on the change in statistical life expectancy per person (Δe c ), the total amount of life years lost (YOLL) and the disability adjusted life years (DALY) for PM 2.5 related cardiopulmonary impacts and the annual cases of premature mortality (Mort) produced by exposure to O 3 . The estimation of health affectations by air pollutants depends on the quan tification of the respective relative risks, whose values in this case stemmed from two epidemiological studies for exposure to PM 2.5 (Pope et al, 2002) and to O 3 (Jerrett et al, 2009;Heal et al, 2013). The estimation of Δe c and YOLL requires the definition of a survival function, which for the case of AERIS was determined from mortality rates which were taken from the World Health Organization (WHO) mortality data and statistics database for cohorts aged between 30 and 60 in Spain, Portugal, Andorra, France, Algeria and Morocco between the years 1990 and 2010 (WHO, 2014 (Mathers et al, 2006).…”