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Air Pollution Tied to Emphysema, Even in People Who Never Smoked

Allison Inserro
While air pollution has long been associated with cardiovascular and respiratory diseases, this is believed to be the first longitudinal study of air pollution and emphysema progression.
A large-scale study published in JAMA this week showed that air pollution is also linked to the progression of emphysema and may be a factor in rising rates of chronic lung disease in nonsmokers. While air pollution has long been associated with cardiovascular and respiratory diseases, this is believed to be the first longitudinal study of air pollution and emphysema progression.

Emphysema is usually linked with cigarette smoking, and researchers said the study may show why the disease is found in people who never smoked. Without new climate control strategies, this trend is expected to continue, said the researchers, who come from the University of Washington (UW), Columbia University, and the University at Buffalo.

The authors said most of the mortality from chronic lower respiratory disease is due to chronic obstructive pulmonary disease (COPD), which is defined by persistent airflow limitation and emphysema. Emphysema can be seen without spirometric COPD and can be measured on computerized tomography (CT) scans; percent emphysema, or the percentage of emphysema-like lung on CT scans, is linked with increased severity of COPD.

The study was conducted between 2000 and 2018 in 6 urban regions of the United States: New York City, New York; Los Angeles, California; Chicago, Illinois; Baltimore, Maryland; Winston-Salem, North Carolina; and St. Paul, Minnesota. Recruitment for the study began in July 2000 and included 6814 adults aged 45 to 84 years; an additional 257 people were recruited from February 2005 to May 2007 with follow-up through November 2018.

At baseline, the first group of participants were 38% white, 46% were lifelong nonsmokers, and 63% had at least some college education.

Scientists assessed the longitudinal association of outdoor air pollution at the home of each participant—ambient ozone, fine particulate matter (PM2.5), oxides of nitrogen, and black carbon exposure—with change in percent emphysema as determined by CT scans and lung function tests.

Percent emphysema, defined as the percent of lung pixels less than −950 Hounsfield units, was assessed up to 5 times per participant via cardiac CT scan during the first 7 years of the study and in equivalent regions on lung CT scans between 2010 to 2018). Spirometry was performed up to 3 times per participant from 2004 to 2018.

Over a median of 10 years, among the total group of 7071 participants, 5780 were assigned outdoor residential air pollution concentrations in the year of their baseline examination and during the follow-up period and had at least 1 follow-up CT scan; 2772 had at least 1 follow-up spirometric assessment.

“The combined health effect of multiple air pollutants—ozone, fine particles known as PM2.5, nitrogen oxides, and black carbon—was greater than when the pollutants were assessed individually,” explained Bonnie Joubert, PhD, a scientific program director at the National Institute of Environmental Health Sciences, which, along with the National Heart, Lung, and Blood Institute, both part of the National Institutes of Health, funded the study. 

The study—called the Multi-Ethnic Study of the Atherosclerosis (MESA) Air and Lung Studies—also received support from the Environmental Protection Agency, which recently announced plans to reverse the Clean Air Act put into place by former President Barack Obama. This week, attorneys general from 22 states and some of major cities represented by the study (such as New York, California, Maryland, Minnesota, North Carolina) sued the Trump administration over those plans. In July the American Lung Association and the American Public Health Association also said they would sue.

Results showed that median percent emphysema was 3% at baseline and increased a mean of 0.58 percentage points per 10 years.

"We were surprised to see how strong air pollution's impact was on the progression of emphysema on lung scans, in the same league as the effects of cigarette smoking, which is by far the best-known cause of emphysema," the study's senior coauthor, Joel Kaufman, MD, MPH, UW professor of environmental and occupational health sciences and epidemiology in the School of Public Health, said in a statement.

If the ambient ozone level was 3 parts per billion higher where a person lives compared with another location over 10 years, that was linked with an increase in emphysema roughly the equivalent of smoking a pack of cigarettes a day for 29 years. The study determined that ozone levels in some major cities are increasing by that amount, due in part to climate change. The annual averages of ozone levels in study areas were between about 10 and 25 parts per billion (ppb).

"Rates of chronic lung disease in this country are going up and increasingly it is recognized that this disease occurs in nonsmokers," said Kaufman, also a professor of internal medicine and a physician at UW School of Medicine. "We really need to understand what's causing chronic lung disease, and it appears that air pollution exposures that are common and hard to avoid might be a major contributor."

While most of the airborne pollutants are falling due to successful control efforts, ozone is increasing, the study found. Ground-level ozone is mostly produced when ultraviolet light reacts with pollutants from fossil fuels.

"As temperatures rise with climate change ground-level ozone will continue to increase unless steps are taken to reduce this pollutant," said R. Graham Barr, MD, DrPH, MPH, professor of medicine and epidemiology at Columbia University and a senior author of the paper. "But it's not clear what level of the air pollutants, if any, is safe for human health."

Reference

Wang M, Aaron CP, Madrigiano J, et al. Association between long-term exposure to ambient air pollution and change in quantitatively assessed emphysema and lung function. JAMA. 2019;322(6):546-556. doi:10.1001/jama.2019.10255.

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