A multidisciplinary research team has identified a faster way to determine which airborne chemicals pose a threat to human lungs. Led by an environmental health researcher with the Texas A&M University School of Public Health , the study shows that lab-grown lung cells that behave like those inside the human body can reliably screen chemicals for respiratory toxicity.
Using this air-liquid interface model , the team examined how two volatile organic compounds — acrolein and formic acid — impact breathing. Acrolein is used in disinfectants, insecticides and pesticides and as a base for animal feed and other items, and formic acid is used for scientific research and in producing leather goods and textiles.
"These common chemicals often spike after disasters like the 2023 East Palestine train derailment , yet there is surprisingly little data on their health risks," said the study's lead author, Olivia Lampe, a doctoral student in the Department of Environmental and Occupational Health and member of Texas A&M's Interdisciplinary Program in Toxicology .
In addition, the study found that inhaling these airborne chemicals can seriously damage the lungs.
The team placed 16HBE bronchial cells in a lifelike model of human lungs to see how they were affected by short-term, high-level exposure to vapors from the two chemicals.
Unlike the standard research process that uses cells submerged in liquid, the air-liquid interface method places cells on a collagen-coated mesh that mimics human lungs when given nutrients. The team developed these cells, then exposed them to different amounts of acrolein or formic acid gas, while a control group was exposed only to clean air.
Statistical analyses found two main results for the cells exposed to acrolein:
- Cell damage. Acrolein only killed cells at very high concentrations. Even at lower doses, however, it penetrated the lung's protective barrier, indicating that acrolein can weaken the lungs without immediately killing the cells.
- Oxidative stress. The cells showed markers of oxidative stress and pro-inflammatory signaling specifically by increasing gene expression of select targets like HMOX-1 and inflammatory markers IL-6 and IL-8.
"These data support that the current government safety guidelines for acrolein are generally effective," Lampe said. "Formic acid, on the other hand, needs more research to determine if current guidelines offer enough protection."
She added that this is because most lab-based health studies focus on formic acid's "parent" chemical, formaldehyde . However, in the real world, formaldehyde stays in the air for only about an hour before turning into formic acid.
The study found two main results for formic acid:
- Loss of barrier integrity. Formic acid saw a dose-dependent increase in barrier permeability independent of cell death. This suggests formic acid is altering the function of tight junction proteins in between cells.
- Cell damage. Like acrolein, formic acid caused significant cell death at high doses.
The study was published in Inhalation Toxicology and was supported by the Texas A&M Superfund Research Center and the T32 Training Program in Toxicology, which are funded by the National Institute of Environmental Health Sciences.
Others involved in the study from the Texas A&M School of Public Health were associate professor Natalie Johnson and postdoctoral research associate Eva Vitucci, along with Carolyn Cannon with the Texas A&M Naresh K. Vashisht College of Medicine and Weihsueh Chiu with the Texas A&M College of Veterinary Medicine and Biomedical Sciences. Johnson, Chiu and Vitucci also are members of the Texas A&M Interdisciplinary Program in Toxicology.
By Ann Kellett, Texas A&M University School of Public Health
