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These findings, to be presented at AAAAI, may help to expand upon clinicians’ awareness of the mechanics of air pollution’s effect on asthma.
There is a correlation between the expression of specific driver genes connected to T-cell mediated immune processes within the nasal passages and exposure to ozone and fine particulate matter (PM2.5) for asthma patients, new findings suggest.1
These findings are set to be presented at the 2024 American Academy of Allergy, Asthma & Immunology (AAAAI) Annual Meeting held in Washington, DC. The data are the results of a new study involving 167 individuals with different degrees of asthma severity who had been drawn from the New York metropolitan area.
“Poor air quality here in New York and around the world has become increasingly common,” primary author Yoojin Chun, MS, computational biologist at the Icahn School of Medicine at Mount Sinai, said in a statement. “I feel very motivated to study how air pollution drives molecular processes in people with asthma who have an especially hard time breathing when air quality is bad.”
Chun added that the main drivers which the team was able to identify in their research were potentially intervenable targets, and this may end up providing help to patients with asthma.
Chun and colleagues' assessments of levels of air pollutants were gathered from stations located nearest to the home residences of the subjects, and collected by officials with the US Environmental Protection Agency (EPA). After nasal samples were collected from research participants, the team carried out RNA sequencing and then their analyses of differential expression and key driver genes.
The investigators found that, on average, subjects participating in the study received a 16.6 score on the Asthma Control Test. They also noted that 31% exhibited forced expiratory volume (FEV1) percent which had been predicted at under 80%.
The research team were able to point to 6 major driver genes which they linked to ozone exposure, as well as 3 driver genes linked to exposure to PM2.5. The team reported that these genes are likely to impact subsequent reactions among patients.
A notable finding of the team was that FGL2, recognized previously as a major regulator of asthma, was pinpointed as the foremost upstream key driver for PM2.5 as well as ozone. The investigators also reported that TNFRSF10C and CLC were shown to be distinct upstream key drivers for PM2.5 and ozone, respectively.
The investigators also noted that CLC had previously been connected to the co-occurrence of such conditions as dermatitis, asthma, and rhinitis among patients.
The 167 study subjects were noted as being racially and ethnically diverse, with the investigators noting that 18% were Black, 3% were Asian, 38% were White, 34% were Latino, and 8% were labeled as other. Additionally, the team reported that 43% of the subjects were listed as female.
The research team’s results indicated that, overall, exposure to ozone and to PM2.5 among those with asthma had a correlation with the expression of key driver genes in the nasal passages. They added that this was indicative of T-cell mediated immune processes among the patients.
This data also adds to the growing body of research on the topic of pollution and its downstream effects on the body, with research having connected ambient sulfur dioxide (SO2) and particulate matter’s (PM10) link to allergic disease risk and coarse particulate matter pollution to prevalence of asthma in US children.2,3
The current understanding of PM2.5 and ozone as established triggers for asthma exacerbations is enhanced by Chun and colleagues’ findings. By identifying the molecular key drivers behind the effects of ozone and PM2.5 on the airways, this study improves researchers’ mechanistic comprehension of air pollution’s effects on the health of individuals.1
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