A new 18-year nationwide study of US cities found that long term exposure to high levels of ground ozone, a main component of smog, was
linked to significantly higher risk of dying from respiratory diseases.
The study was the work of Dr George Thurston, a professor in the Department of Environmental Medicine at New York University School of Medicine (NYU) School of Medicine, a part of NYU Langone Medical Center, and colleagues, and is published online on 12 March in the New England Journal of Medicine, NEJM.
Many studies have linked atmospheric ozone to poor health, and others have shown that a high-ozone day, for example as a result of city smog, is linked to an increased risk of acute health problems the next day, such as more asthma and heart attacks. However, until this study, the effect of long term exposure to ozone in air pollution (the summertime haze) on health and deaths in particular was somewhat uncertain.
Thurston, who directed the air pollution exposure assessment part of the study, said in a separate press statement that:
"What this study says is that to protect the public's health, we can't just reduce the peaks, we must also reduce long-term, cumulative exposure."
For this study, Thurston and colleagues looked at the potential contribution of exposure to ozone to the risk of death from cardiopulmonary or heart and lung related causes and specifically to death from respiratory causes. It is the first study to separate the effect of ozone from that of fine particulate matter, the tiny particles of pollutant material that cars, factories and power plants release into the atmosphere.
They used data from the American Cancer Society Cancer Prevention Study II and correlated it with air pollution figures for 96 metropolitan areas of the US. They analyzed study records from 448,850 people, including 118,777 deaths over an 18 year period from 1982 to 2000.
The study records included cause of death (where relevant), and things like age, smoking status, body mass index, and diet, plus where the subjects lived, so these potential confounding factors could be taken into account in the statistical analysis.
They were able to find data on daily maximum ozone levels from April 1 to September 30 from 1977 to 2000, and data on fine particles in the air (2.5 microns or smaller in diameter, called PM2.5) for 1999 and 2000.
The researchers found that:
- When they used a single pollutant model, increased levels of either PM2.5 or ozone were significantly linked to increased risk of death from cardiopulmonary causes.
- When they used a two pollutant model, increased PM2.5 was linked to increased risk of death from cardiovascular disease, while ozone was linked to increased risk of death from respiratory causes.
- The risk of dying from respiratory disease was more than 30 per cent higher in metropolitan areas with the highest ozone levels than those with the lowest.
- The estimated risk of dying from respiratory disease went up by 4 per cent for each increase in 10 parts per billion (ppb) of ozone.
- The city with the highest mean daily maximum ozone concentration over the 18 years of the study was Riverside, California (104 ppb).
- This corresponded to about 50 per cent higher risk of dying from lung disease compared to no exposure to ozone.
- Los Angeles came a close second, with an estimated 43 per cent increased risk of dying from lung disease.
- Northeast cities were generally lower in ozone than California.
- For example, Washington DC and New York City, showed a 27 and 25 increased risk of death from respiratory causes linked to ozone exposures.
- The lowest ozone levels were in San Francisco with a 33 ppb long term average daily maximum that was linked to a 14 per cent estimated increase of death from respiratory causes.
- The link between ozone and risk of death from respiratory causes did not change when confounders were taken into account, and neither did it change when they used different statistical models.
"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."
When it is high in the atmosphere, ozone protects us against the harmful UV (ultraviolet) rays of the sun. But at ground level, inhaled ozone causes inflammation of respiratory tissue, according to the Canadian Center for Occupational Health and Safety (CCOHS). Here it is primarily a byproduct of pollution, a secondary pollutant created when nitrogen dioxide from cars, power plants and factories meets with oxygen in the presence of sunshine.
This type of ozone takes time to form and is more likely to be found downwind of cities in suburbs and rural areas, unlike fine particulate matter, a primary pollutant which hangs around where it is produced, in the inner cities, near roads and industrial sites.
Lead author Dr Michael Jerrett, associate professor, Division of Environmental Health Sciences, at the University of California, Berkeley, said that in line with rising death rates from respiratory disease, "background levels of ozone have at least doubled since pre-industrial-revolution times".
Thurston said that even though New Yorkers were breathing air with ozone levels very nearly in compliance with the Environmental Protection Agency short term ozone limit of 75 ppb, their estimates showed they were at a significant 25 per cent higher risk of dying from respiratory causes compared to non exposure.
The researchers said that San Francisco has low levels of ozone pollution because the city is often covered with a blanket of fog that stops the sun coming through to catalyze the photochemical reaction between nitrogen dioxide and oxygen. And Los Angeles, which has high levels, sits in a basin which stops the air pollution from dispersing as rapidly as it does in other cities like San Francisco.
Thurston said the current EPA air quality standards only address the health effects of short-term daily peaks in ozone exposure and do not protect against the long-term cumulative effects. The current EPA level for short term (8-hour) ozone exposure is 75 ppb, which is higher than the 60 ppb recommended by the agency's own scientific advisors, the American Lung Assocation and several other public health bodies. The EPA is going to review the standard in the next 12 months.
Thurston asked, "how do we lower the burden of disease?"
"Do we look only at only those affected by the highest days, or do we look at everyone's exposure over the entire year?"
"Since we all share the same air, paying attention to cumulative exposure shifts the whole exposure distribution for us all, and that's where the health payoff is. A small reduction in everybody's year-round risk benefits us all," he said.
"Long-Term Ozone Exposure and Mortality."
Jerrett, Michael, Burnett, Richard T., Pope, C. Arden, III, Ito, Kazuhiko, Thurston, George, Krewski, Daniel, Shi, Yuanli, Calle, Eugenia, Thun, Michael.
N Engl J Med 2009, 360: 1085-1095.
Published online on March 12, 2009.
Click here for Abstract.
Sources: Journal abstract, NYU Langone Medical Center / New York University School of Medicine, Canadian Center for Occupational Health and Safety.
Written by: Catharine Paddock, PhD