Air pollution associated with nonviral asthma attacks among urban youth
Click Here to Manage Email Alerts
Moderate levels of ozone and fine particulate matter were associated with nonviral asthma attacks among children and adolescents living in low-income urban areas, according to a study published in The Lancet Planetary Health.
Exposure to these pollutants also was associated with molecular changes in patients’ airways during nonviral attacks, indicating potential mechanisms behind the attacks, Matthew C. Altman, MD, MPhil, associate professor in the department of medicine, division of allergy and infectious diseases at University of Washington School of Medicine, and colleagues wrote.
“The NIAID Inner City Asthma Consortium has been studying the asthma epidemic in urban children in low-income households for several decades,” Altman told Healio, adding that viral respiratory infections are well known to trigger asthma exacerbations, although other triggers are less understood.
In previous studies, Altman continued, the researchers noted a surprisingly high rate of nonviral asthma exacerbations in urban children, of which they sought to identify the etiology and mechanisms.
“We found the most relevant factor appeared to be local air pollution exposure, especially to fine particulate matter and ozone, even at relatively moderately elevated levels, and found that they caused exacerbations through unique inflammatory pathways,” Altman said.
Study design, results
Altman and colleagues conducted a secondary analysis of 168 children (98 boys) aged 6 to 17 years with exacerbation-prone asthma from Mechanisms Underlying Asthma Exacerbations Prevented and Persistent with Immune-based Therapy Part 1 (MUPPITS1), a prospective and observational cohort study conducted in low-income urban centers of nine U.S. cities. Researchers followed participants between 2015 and 2017 through two respiratory illnesses or for approximately 6 months, whichever came first.
Those who reported a respiratory illness returned to the clinic twice during the 6-day period after their symptoms had begun for nasal sample collection and pulmonary function testing. The researchers categorized each illness as a viral (V+) or nonviral (V–) event and whether it included (Ex+) or did not include (Ex–) an asthma exacerbation.
Also, the researchers downloaded Air Quality Index (AQI) values and individual data for particulate matter at the 2.5 µm (PM2.5) and 10 µm (PM10) scales, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide and lead for each city during the study’s timeframe.
There were 336 respiratory events, including 143 Ex+ and 193 Ex– events.
In the 9 days preceding and following the start of respiratory symptoms, AQI values were significantly higher, indicating poorer air quality, for the Ex+ events than they were for the Ex– events (P < .0001).
Overall, 33.8% events with detailed assessments were V–, including 29.8% of Ex+ events.
Patients who were both V– and Ex+ were exposed to increased AQI values during the 9 days before and after their illness compared with V+/Ex+, V+/Ex–, and V–/Ex–patients (P < .0001), with similar AQI values between the three latter subgroups. Researchers noted these exacerbations occurred after several days of mean sustained increase in AQI.
Also, the V–/Ex+ group experienced higher concentrations of ozone (P < .0001), nitrogen dioxide (P < .0001) and PM2.5 (P = .0006) during this timeframe than the other groups, although the V+/Ex+ group had modestly higher ozone concentrations as well (P = .0014).
There was an association between higher AQI and V–/Ex+ events in the spring and summer (P < .0001) and winter and fall (P = .0003) compared with other events, with the most pronounced differences in spring and summer.
AQI and ozone values also had significant inverse associations with percentage of predicted FEV1 (FEV1%) and FEV1/forced vital capacity ratio during V–/Ex+ events.
Researchers observed a significant association between cumulative AQI values over 3 days and upper airway gene expression modules associated with incipient asthma exacerbations.
Specifically, PM2.5 concentrations were linked to increased epithelial induction of tissue kallikreins, mucus hypersecretion and barrier functions, and ozone concentrations were associated with increased type-2 inflammation.
Comparisons, next steps
The researchers compared these results against data of 419 inner-city youth aged 6 to 20 years with persistent allergic asthma from the randomized, double-blind, placebo-controlled Inner-City Anti-IgE Therapy for Asthma (ICATA) trial. Of 100 asthma exacerbations in this study, 47 were V–.
Like the MUPPITS1 study, patients experiencing V–/Ex+ events also had been exposed to increased AQI, ozone and PM2.5 values compared with the other subgroups (P < .0001), although the effect of nitrogen dioxide was not significant.
Perhaps the most surprising finding, Altman said, was that these pollutants seemed to be associated with asthma exacerbations at only modestly elevated levels by current EPA guidelines.
“This may indicate that measurements underestimate the exposures these children have in their specific urban environments and/or urban children with asthma are more sensitive to these pollutants than has been previously understood/assumed,” he said.
Also, Altman noted that these exacerbations seemed to proceed through distinct inflammatory pathways from viral exacerbations that may not be fully responsive to some current asthma therapies.
Noting that these findings could inform novel asthma management strategies for children in urban areas, the researchers recommended preventive use of personal air quality monitors and air filers around periods of risk.
“Hopefully, this work can help drive the ongoing recognition of need for mitigating air pollution exposure in these urban and other environments,” Altman said, adding that his team is now investigating methods of asthma prevention and treatment in urban children.
“We will incorporate these results into our ongoing and future studies in particular to better understand why some asthma therapies are effective or ineffective in some children and how this may relate to the type of asthma they have and what their environmental exposures are,” he said.
Reference:
- NIH study links specific outdoor air pollutants to asthma attacks in urban children. https://www.nih.gov/news-events/news-releases/nih-study-links-specific-outdoor-air-pollutants-asthma-attacks-urban-children. Published Jan. 4, 2023. Accessed Jan. 5, 2023.
Perspective
Back to Top
These findings are significant, as they demonstrate the substantial effects of various aspects or components of pollution on asthma exacerbations. Importantly, they separate viral infections and, therefore, examine the effects of pollution specifically. Additionally, they look at pulmonary readouts, including biomarkers.
The study strongly implicates air pollution as a substantial contributor to respiratory exacerbations in inner-city children. The identification of inflammatory mechanisms (specific changes including barrier changes, eosinophil responses and lung function) with specific components of pollution (eg, PM2.5 vs. ozone) begins to uncover the pathways or steps triggered by the pollution.
Also, these findings are consistent with clinical experience focused on high rates of asthma and readmission rates among inner-city children. They really solidify the basic principle that pollution has health consequences that already are evident in children.
The vulnerability of inner-city children to this problem calls attention to their need for more careful medical attention, particularly focused on controlling exposure to pollution and managing their lung diseases. This study substantiates and buttresses the need to curtail pollution, which will not only improve lives, but also presumably save money.
Next, I would like to see a comparison of inner city vs. non-inner-city findings. In other words, do these processes and events occur in all children, or do they especially manifest in the inner city? Can we relate these findings to the vulnerability of inner-city children to diseases in general, or is this related to their increased exposure to air pollution? I also would like to see a prospective study to further prove causality.
But overall, these are important results, and the authors and NIH are to be congratulated.
Perspective
Back to Top
There is a wealth of evidence that outdoor air pollution harms children. Indeed, prior studies have documented associations between outdoor air pollution and both increased respiratory infections and asthma exacerbations.
The study by Altman and colleagues contributes further by evaluating the association of the AQI to both viral and nonviral asthma exacerbations among children with persistent asthma receiving asthma controller medications.
Concerningly, the association of the AQI with nonviral-triggered asthma exacerbations occurred in the moderate range (51-100 AQI), for which the EPA advises behavioral changes for persons “unusually sensitive” to air pollution. The moderate range is typically below the National Ambient Air Quality Standard (NAAQS) set by the EPA to provide adequate protection for human health.
It is unknown how many children with asthma are “unusually sensitive” to air pollution, or rather who will experience health harms at pollution levels within moderate AQI ranges. My prior work and results of the current study suggest that many children with asthma are likely to have exacerbations even within the moderate range. Indeed, in the MUPPITS1 cohort, 30% of viral-assessed asthma exacerbation events demonstrated an association in the moderate range, which was validated in a larger cohort of children and young adults with asthma (ICATA, 47%).
An important finding of this study is the association of the AQI and nonviral asthma exacerbations in children with persistent asthma below current NAAQS. Positive associations were found for ozone, PM2.5 and nitrogen dioxide all at levels below current NAAQS (0.07 ppm over 8 hours for ozone, 35 micrograms/m3 over 24 hours for PM2.5, 100 ppb over 1 hour for nitrogen dioxide).
The ozone NAAQS is currently under review by the EPA. Multiple health organizations including the American Thoracic Society support reducing the ozone NAAQS to 0.060 ppm and 24-hour PM2.5 standard to 25 micrograms/m3. Such reductions are supported by the findings of Altman and colleagues.
The association of the AQI with asthma exacerbations supports discussion of the AQI during clinical encounters. Although the AQI was not specifically designed as a tool for persons to learn their own personal susceptibilities to air pollution, the results from Altman and colleagues suggest the AQI might be helpful for children with asthma when used in this way.
Many apps provide an AQI, and the standardized EPA AQI is available hourly on the AirNow.gov website and AirNow smartphone app. For patients using the AQI to learn personal susceptibilities, health care providers should monitor for unintended consequences such as decreased overall physical activity. This may be especially important in regions with a high prevalence of moderate AQI days.
It is important to note that the AQI is an individual behavioral intervention to reduce exposure to air pollution. The best and most equitable way to reduce harm from air pollution is to reduce exposure for everyone. Individual interventions should never be at the expense of sound policy.
The association between the AQI and nonviral asthma exacerbations occurred despite treatment with asthma controller medications. As prior studies have also demonstrated a lack of a protective effective of asthma medications against air pollution exposure, more research is needed to determine optimal asthma management to prevent air pollution harms. Additionally, more research is needed to understand if incorporating the AQI in childhood asthma management improves asthma outcomes.
Reference:
Rosser F, et al. Ann Am Thorac Soc. 2022;doi:10.1513/AnnalsATS.202105-539OC.
Collapse
Read more about
Click Here to Manage Email Alerts