Exposure to Ozone Pollution or Wood Smoke Worsens Lung Health of Smokers and Former Smokers


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Over many years, exposure to the levels of ozone and other forms of pollution found in most U.S. cities and some rural communities can take a toll on a person’s health. Two studies led by Johns Hopkins researchers describe the impact of pollution on lung disease, particularly chronic obstructive pulmonary disease (COPD), in the U.S.

In one study, published Dec. 9 in JAMA Internal Medicine, Johns Hopkins researchers found that, among other effects, long-term ozone exposure increases the risk of lung disease — and the severity of that disease — among both former and current smokers. In another study, published Oct. 23 in American Journal of Respiratory and Critical Care Medicine, Johns Hopkins researchers also found that increased neighborhood use of wood as a primary heating source — which releases fine particles into the air — is associated with higher prevalence of lung disease among never-smokers in the community.

“Even if you spend very little time outside, the cumulative effect of pollution over many years seems adequate to have a negative impact on respiratory health,” says Nadia Hansel, M.D., M.P.H., director of the pulmonary and critical care division, professor of medicine and associate dean for research at the Johns Hopkins University School of Medicine and author of both studies.

Ground-level, or tropospheric, ozone is formed when industrial pollutants interact with sunlight, and it is the main ingredient in the smog found around major cities. Ozone is known to irritate the lungs by increasing inflammation, and spikes of very high ozone levels — such as those that occur on hot, sunny days with heavy traffic — can exacerbate lung diseases such as asthma.

Former and current smokers are at high risk of chronic lung diseases and are particularly susceptible to environmental triggers for lung disease flare-ups. Smokers are particularly prone to COPD, a group of diseases including emphysema and chronic bronchitis, characterized by chronic and progressive lung inflammation that leads to shortness of breath and coughing.

In the new JAMA Internal Medicine study, Hansel and her collaborators around the country used data collected from people in several U.S. cities as part of the SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study) air pollution study. Participants in SPIROMICS were former and current smokers ages 40–80. The new analysis included a subset of SPIROMICS participants for whom there was available data on the previous 10 years of ozone exposure — based on where people lived. These 1,874 participants were 54% male, 79% white, 37% current smokers and had smoked an average of 50 pack-years — the equivalent of 25 cigarettes a day for two years, or five cigarettes a day for 10 years.

After adjusting for demographic and socioeconomic factors as well as smoking status and pack-years, the researchers found that people who had been exposed to higher levels of ozone over the previous 10 years were more likely to have COPD. For every 5-parts-per-billion increase in a person’s 10-year ozone exposure, they were 16% more likely to have COPD and 37% more likely to have had a severe exacerbation of the disease in the year prior to study enrollment. The same 5-parts-per-billion increase in ozone exposure was also associated with an increase in the percentage of people with emphysema and a worsening score of the St. George’s Respiratory Questionnaire, which reflects health impairment affecting quality of life.

“What really stood out was that the effect was apparent even among current heavy smokers,” says Hansel. “This means that active smoking doesn’t outweigh this effect of ozone.”

In other words, even people already at the highest risk of COPD had an increased risk with ozone exposure. Moreover, Hansel says, the effect of increasing ozone was apparent even when ozone exposure was at the low end of the spectrum, such as among people living in northeastern cities where dark winters lead to an annual ozone exposure that’s relatively low compared with that of many southwestern locales. 

“I think this adds to increasing evidence that there is probably no healthy level of ozone,” she says. “There are policies that suggest we just need to reach certain targets and everything will be OK, but in my mind that is probably not enough.” Policymakers must develop ways to get ozone as low as possible, she adds, rather than aiming for a particular target number. 

The Centers for Disease Control and Prevention reports that COPD costs the U.S. health care system more than $32 billion, and that there are approximately 7 million COPD-related emergency room visits in the U.S. each year. Hansel and her colleagues calculated that a 5-parts-per-billion decrease in 10-year ozone levels could reduce emergency room visits by 27%, saving a substantial amount of money on COPD care.

While the JAMA Internal Medicine study only measured lung health, previous research has suggested that high levels of ozone can affect cardiovascular health. So Hansel hypothesizes that long-term exposure to ambient levels of ozone may have similar effects on heart disease as it does to lung disease.

“The adverse health effects of ozone likely go beyond what we’ve identified here,” says Hansel. “And we need to keep building evidence of these effects so that it’s not debatable anymore that we need to do more to clean the air.”

In the second paper, researchers including Hansel, associate professor of medicine Meredith McCormack, M.D., M.H.S., and pulmonary and critical care medicine fellow Sarath Raju, M.D., studied data on 8,500 adults enrolled in the National Health and Nutrition Examination Surveys (NHANES), 2007–2012. Of the participants, 19.5% resided in rural areas and 29.6% in urban areas. Rural areas, with a 12.0% prevalence of COPD, had more than double the disease burden seen in urban communities, with a 5.9% prevalence.

By analyzing differences between urban and rural communities that might affect COPD risk, the team discovered that communities with a high rate of solid fuel use — either coal or wood for primary heating — were associated with COPD prevalence. A 1% increase in the number of homes using wood as the primary heating source was linked to 12% higher odds of COPD among people who have never smoked. In rural areas, 4.1% of people used wood as their primary heating source, as opposed to 0.6% in urban areas.

“Wood smoke is a household source of pollution that is associated with high levels of particulate matter and toxic gases,” says Raju, first author of the American Journal of Respiratory and Critical Care Medicine paper. “We hope that this paper raises awareness of the growing epidemic of rural COPD.”

The researchers are now launching further studies that aim to collect individual level — rather than community level — data on environmental exposures that might contribute to COPD. They’re also partnering with other institutions to study COPD rates and risks in rural Appalachia.

Other authors on the JAMA Internal Medicine paper were Han Woo, Roger Peng, Ashraf Fawzy, Nirupama Putcha and Patrick Breysse of Johns Hopkins; Laura Paulin of Dartmouth-Hitchcock Medical Center; Amanda Gassett, Kipruto Kirwa and Joel Kaufman of University of Washington; Neil Alexis of University of North Carolina at Chapel Hill; Richard Kanner, Robert Paine III and Cheryl Pirozzi of University of Utah; Stephen Peters of Wake Forest University; Jerry Krishnan of University of Illinois at Chicago; Mark Dransfield of University of Alabama, Birmingham; Prescott Woodruff of University of California, San Francisco; Christopher Cooper of University of California, Los Angeles; Graham Barr of Columbia University Medical Center; Alejandro Comellas and Eric Hoffman of University of Iowa; MeiLan Han of University of Michigan, Ann Arbor; and Fernando Martinez of Weill Cornell Medicine.

The work described in the JAMA Internal Medicine paper, part of the broader SPIROMICS study, was supported by the National Institutes of Health (HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C, U01 HL137880, R01ES023500, K23ES025781), AstraZeneca/MedImmune, Bayer, Bellerophon Therapeutics, Boehringer Ingelheim Pharmaceuticals Inc., Chiesi Farmaceutici S.P.A., Forest Research Institute Inc., GlaxoSmithKline, Grifols Therapeutics Inc., Inkaria Inc., Novartis Pharmaceuticals Corporation, Nycomed GmbH, ProterixBio, Regeneron Pharmaceuticals Inc., Sanofi, Sunovion, Takeda Pharmaceutical Company, Theravance Biopharma, and Mylan.

Other authors of the American Journal of Respiratory and Critical Care Medicine paper are Emily Brigham, Nirupama Putcha and Aparna Balasubramanian of Johns Hopkins and Laura Paulin of Dartmouth-Hitchcock Medical Center. The AJRCCM paper was supported by the National Institutes of Health (P50MD010431, F32 ES029786-01, R21ES025840, T32 HL007534-36) and the Environmental Protection Agency (R836150).