Air pollution, genetics increase risks for COPD among patients with asthma
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Key takeaways:
- 8% of patients with asthma developed COPD during follow-up.
- Each 10 µg/m3 increase in particulate matter increased COPD risks by 79%.
- Each 10 µg/m3 increase in nitrogen dioxide increased COPD risks by 13%.
Air pollution and genetic susceptibility increased the risks for progression from asthma to COPD, according to a study presented at the European Respiratory Society International Congress.
Samuel Cai, PhD, lecturer, Centre for Environmental Health and Sustainability at the University of Leicester, and colleagues examined the records of 46,738 patients with asthma who participated in the UK Biobank between 2006 and 2010.
“Globally, around 10% to 60% of asthma patients will develop COPD over time. This patient group, referred as patients with asthma-COPD overlap (ACO), tends to have increased disease severity, incur higher health care cost, and poorer quality of life,” Cai told Healio.
“Apart from the unmodifiable genetic risk, it is really important to identify what risk factors could be prevented to stop this progression,” he continued. “Currently, the role of air pollution is not very well understood, and this study aims to find out to what extent that air pollution poses the risks.”
The researchers estimated individual levels of particulate matter and nitrogen dioxide exposures base on each patient’s home address and calculated genetic risk scores for developing both asthma and COPD for each patient based on eight novel genetic signals indicating ACO in a genome-wide association study.
During the follow-up period, which had a median of 8.1 years, 3,750 (8%) of the patients with asthma at baseline developed COPD.
Hazard ratios for developing COPD among patients with asthma included by 1.56 (95% CI, 1.12-2.17) for each 10 µg/m3 increase in particulate matter at the 2.5 µg scale (PM2.5) and 1.1 (95% CI, 1.04-1.15) for each 10 µg/m3 increase in nitrogen dioxide (NO2).
The researchers noted a dose-response relationship between NO2 and COPD, with adverse effects observed at concentrations as low as 8 µg/m3 for PM2.5 and 12 µg/m3 for NO2.
However, the researchers said, the only significant associations between PM2.5 and COPD were found among those patients with the highest exposures.
“The most significant finding is that the higher level of exposure to PM2.5 or NO2 — both are closely related to traffic in the U.K. — the higher the risk that asthma patients will develop COPD,” Cai said.
“We found that if PM2.5 concentrations increased by 10 µg/m3, such risk will significantly increase by 79%,” he continued.
Similarly, risks for COPD increased by 13% with each 10 µg/m3 increase in NO2 exposure.
“However, these associations were more evident among individuals who carry high genetic risk,” Cai said.
Cai additionally noted how the study’s use of data from the large UK Biobank population database makes it the largest study of its kind to date.
“Also, we have additionally investigated the interplay between air pollution and ACO genetic risk, which had never been done before,” he said.
These findings will provide evidence for physicians to use in informing their patients about the risks that air pollution has for their current condition and help them develop personal prevention strategies as well, Cai continued.
“The use of genetic profiling is particularly useful, as it will enable the doctors to know which patient groups have the highest risk,” Cai said. “Hence, prevention strategies need to be in place.
Reference:
- Cai S, et al. Abstract OA971. Presented at: European Respiratory Society International Congress; Sept. 7-11, 2024; Vienna.
For more information:
Samuel Cai, PhD, can be reached at yc368@leicester.ac.uk.
Perspective
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These findings are not surprising but certainly significant. We know that particulate pollution plays a role in exacerbation of underlying lung disease, cardiovascular disease and other health issues, but this is a unique study that ties the genetic predisposition some have with asthma when exposed to high particulate air pollution to be eventually labeled as ACO.
However, the ongoing debate of what constitutes ACO remains in question. For example, are these asthma patients with long-standing poor control who go on to develop fixed airflow obstruction and who are being labeled as COPD? Alternatively, do these subjects have other findings of COPD on CT scan (such as emphysema changes) or pulmonary function data? Lastly, the burden of cigarette smoking is not accounted for in the data presented.
Still, these findings mainly add to the ongoing literature that COPD and asthma are affected by particulate matter and air pollution. Further research is needed on the development of asthma combined with COPD in relation to environmental exposure.
Certainly, cigarette smoke — including in utero and childhood exposures in particular — would affect lung health and contribute to the development of underlying lung diseases such as asthma and COPD. Along with this, as the authors allude to, genetics play an important role, and there are likely individuals that are prone to development of either of these diseases or both based on their genetic profile.
To improve care for these patients and potentially mitigate or prevent the development of COPD, advocacy would be the first thing that comes to mind, in terms of environmental health. But physicians also can ask patients more about what they are exposed to and educate them about mitigation factors.
Perspective
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The research found that as exposure to either PM2.5 or NO2 increased, there was a corresponding increase in the risk for evolving from asthma to ACO. However, this association was only evident among participants who carried high genetic risk for ACO.
ACO is an important diagnosis for any patient with asthma who is at risk for having their disease evolve to a less reversible condition. For asthma patients who smoke tobacco, or who have exposure to secondhand tobacco smoke, as well as those with long-term poor asthma control, the changes to COPD can signal the need to alter therapy and step up efforts to reduce exacerbations.
While we no longer consider ACO a syndrome (the term ACOS is no longer recommended for use) it is no less important. As described in this work, ACO is used for any patient with diagnosed asthma whose pulmonary function is no longer reversible to the degree it once was. We know that these patients struggle, as typical asthma medications no longer have the same benefit and data have shown that exacerbations are more frequent and often more severe.
As we get a better understanding of the genetic risks and how these risks interact with environmental exposure, we can better help our pulmonary patients discern the optimum course of treatment.
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