HANOVER, New Hampshire – Adults with cystic fibrosis (CF) who spent more time exposed to elevated levels of indoor fine particulate matter showed changes in certain blood proteins involved in inflammation and tissue repair, according to a pilot study. The findings suggest that short-term exposure to indoor air pollution may influence inflammatory signaling in people with CF, although average particulate levels were not significantly associated with changes in these proteins.
The study, titled “Associations between household particulate matter and inflammatory cytokines in cystic fibrosis,” was published in Respiratory Medicine.
Indoor air pollution and cystic fibrosis
People with CF are particularly vulnerable to environmental pollutants because thick mucus buildup impairs the lungs’ natural defenses, making it harder to clear inhaled particles and respond effectively to potential threats.
Previous research has linked outdoor exposure to fine particulate matter with worsening lung symptoms, declining lung function, and earlier lung infections in children with CF. However, the effects of indoor particulate exposure remain poorly understood.
To investigate this relationship, researchers examined whether household exposure to fine particulate matter was associated with changes in cytokines, signaling proteins that regulate inflammation and immune activity.
How the study was conducted
The study included 22 clinically stable adults with CF, with an average age of 36.2 years. Half of the participants were women. All were prescribed Trikafta, did not smoke, had no exposure to secondhand smoke, and were not taking corticosteroids. Participants had also gone at least two weeks without a pulmonary exacerbation, or worsening of respiratory symptoms.
The researchers monitored indoor air quality in participants’ homes for four to 11 days. A PurpleAir PA-II SD sensor was placed in the main living area of each home to measure fine particulate matter, known as PM2.5, every two minutes.
PM2.5 consists of airborne particles measuring 2.5 microns or less in diameter, approximately 30 times smaller than an average human hair. These particles can originate from activities such as cooking, heating, and burning wood.
Participants recorded activities that could generate particles, including cooking and heating. Following the monitoring period, blood samples were collected during a clinic visit to measure more than 40 inflammatory signaling proteins.
Researchers assessed exposure in two ways: the average indoor PM2.5 concentration throughout the monitoring period and the proportion of time concentrations exceeded 35 micrograms per cubic meter of air (µg/m³). The threshold was based on the U.S. Environmental Protection Agency’s 24-hour PM2.5 air quality standard.
Cooking and heating contributed to particle spikes
Across the monitored homes, the average PM2.5 concentration was 12.4 µg/m³. The average 24-hour concentration, calculated using complete monitoring days, was 11.9 µg/m³.
Indoor PM2.5 levels exceeded 35 µg/m³ for an average of 6.4% of the monitoring period. Although overall concentrations were generally below this threshold, several homes experienced temporary spikes in particulate levels.
In four representative homes, these peaks coincided with activities such as using a stove, oven, fireplace, or wood- or pellet-burning stove. The findings highlight how everyday household activities can cause short-term increases in indoor particle exposure.
Elevated exposure time linked to a tissue-repair marker
The researchers found no statistically significant association between average PM2.5 concentrations and cytokine levels. However, the amount of time participants spent in homes with PM2.5 concentrations above 35 µg/m³ was associated with changes in four cytokines.
The strongest finding involved platelet-derived growth factor AA and BB homodimers (PDGF-AA/BB), proteins involved in the growth of fibroblasts, repair of airway-lining cells, and tissue remodeling. Higher exposure time was moderately and significantly correlated with changes in these tissue-repair signaling markers.
According to the researchers, this finding suggests a potential relationship between elevated indoor PM2.5 levels and systemic tissue-repair signaling in people with CF.
The study also examined three pro-inflammatory cytokines: interleukin-7 (IL-7), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α). Although their blood levels showed correlations with exposure time, none of these associations reached statistical significance. The observed differences could therefore have occurred by chance.
Further research needed
The researchers emphasized that the findings are preliminary and do not establish that indoor particulate exposure causes inflammatory changes or worsens CF symptoms.
They noted that high-resolution indoor air monitoring could help researchers better understand how household activities contribute to patterns of PM2.5 exposure.
“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,” the researchers wrote.
Further research involving larger groups of participants and repeated measurements over time will be needed to determine whether short-term indoor pollution exposure has meaningful effects on inflammation, tissue repair, and respiratory health in adults with CF.
Contact
Laura M. Paulin
Dartmouth Hitchcock Medical Center