Indoor air pollution tied to changes in CF inflammatory markers

Study links elevated fine-particle levels to immune protein shifts

Written by Steve Bryson, PhD |

A boy covers his mouth as clouds of dust rise around him.

Adults with cystic fibrosis (CF) who spent more time in homes with elevated indoor fine-particle levels tended to show changes in circulating inflammatory signaling proteins, a pilot study found.

Researchers measured more than 40 signaling proteins and found that a blood marker linked to tissue repair was significantly associated with greater indoor particulate exposure, which coincided with stove, oven, and fireplace use. However, mean particle exposure levels over time were not tied to these blood protein changes.

“These findings suggest that time spent at elevated indoor [fine particle] concentrations may be relevant to systemic inflammatory signaling in adults with CF and support further investigation into modifiable indoor environmental exposures,” the researchers wrote.

The study, “Associations between household particulate matter and inflammatory cytokines in cystic fibrosis,” was published in Respiratory Medicine.

Outdoor exposure to fine particles has been associated with exacerbations (worsening of lung symptoms), lung function decline, and earlier lung infections in children with CF. But the role of indoor exposures remains poorly understood.

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Because of thick mucus buildup, people with CF are vulnerable to environmental exposures, as impaired lung defenses reduce their ability to clear inhaled particles and mount immune responses.

The researchers investigated a link between household particulate exposure and cytokines, signaling proteins that regulate inflammation and immune activity.

The team enrolled 22 adults with CF, with a mean age of 36.2. Half were women. Participants were non-smokers, not on corticosteroids, and clinically stable, meaning they had gone at least two weeks without an exacerbation and did not have current exacerbation symptoms. All participants were prescribed Trikafta, and none had been exposed to secondhand smoke.

Homes in the study were 11 detached houses (50%), seven townhouses (31.8%), two mobile homes (9.1%), one apartment (4.5%), and one dormitory (4.5%). Seventeen homes (77.3%) had electric cooking stoves, four (18.2%) had gas stoves, and one (4.5%) had no stove.

The researchers monitored each home for four to eleven days, placing a PurpleAir PA-II SD sensor in the main living area to record fine particulate matter (PM2.5, which refers to airborne particles up to 2.5 microns in size, or about 30 times smaller than an average human hair) at two-minute intervals. Participants also kept diaries of particle-generating activities such as heating and cooking. Blood samples were collected at a clinic visit after monitoring.

Exposure was reported as the mean PM2.5 concentration over the monitoring period and the proportion of monitoring time when indoor PM2.5 exceeded 35 micrograms per cubic meter of air (mcg/m3). This threshold was based on the U.S. Environmental Protection Agency 24-hour PM2.5 National Ambient Air Quality Standard.

The mean PM2.5 concentration across homes was 12.4 mcg/m3, while the mean 24-hour average concentration, calculated from complete days alone, was 11.9 mcg/m3. The air in homes spent a mean of 6.4% of the time above the 35 mcg/m3 threshold.

Concentrations showed transient elevations in multiple homes. In four representative homes, peaks coincided with activities such as use of a stove, oven, fireplace, or wood or pellet stove.

The overall mean PM2.5 concentration was not significantly associated with cytokine levels. Still, the proportion of monitoring time above 35 mcg/m3 was associated with variation in four cytokines.

Platelet-derived growth factor AA and BB homodimers (PDGF-AA/BB) showed a moderate, statistically significant positive correlation. These proteins support the growth of connective tissue cells called fibroblasts, the repair of cells that line the airways, and tissue remodeling (reorganizing, degrading, and rebuilding tissue).

These results suggest a “potential relationship between elevated indoor PM2.5 concentrations and systemic repair signaling in [CF patients],” the team wrote.

Blood levels of the pro-inflammatory cytokines interleukin 7, interleukin 8, and TNF-alpha all showed non-significant correlations with exposure time, meaning the differences could have arisen by chance.

The study’s findings “underscore the potential value of high-resolution indoor air monitoring for characterizing patterns of household PM2.5 exposure,” the researchers wrote. “Larger, longitudinal studies incorporating repeated outcome measurements are needed to clarify temporal relationships and to evaluate the clinical implications of indoor particulate exposure in CF.”

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