Formaldehyde, a chemical widely used in construction, health, and manufacturing industries, was seen to worsen lung inflammation and fibrosis in a mouse model of pulmonary fibrosis (PF), a Brazilian study reports.
In mice lungs, the chemical was found to increase the amount of collagen, a protein responsible for tissue thickening, to lessen the ability of the lungs to expand and contract (called elastance) at rest, and to create a more inflammatory environment.
The research, “Effect of formaldehyde exposure on the development of pulmonary fibrosis induced by bleomycin in mice,” was published in the journal Toxicology Reports.
Formaldehyde — commonly found in products such as glues, press fabrics, and plywood — has been studied as an environmental risk factor in the context of lung diseases like asthma, but not PF.
Other environmental factors, such as cigarette smoke, dust, mold, and gases like ozone and nitrogen dioxide, are linked to a worsening of PF symptoms.
Researchers at the University Nove de Julho and University of São Paulo, both in São Paulo, investigated the effect of formaldehyde exposure in a mouse model of PF and in healthy mice serving as controls.
PF was induced using bleomycin, a compound that causes lung inflammation and impedes the formation of new lung tissue, leading to severe fibrosis.
In each group, some mice inhaled formaldehyde (0.92 milligrams of formaldehyde per 1.000 liters of air) for one hour each day for a total of 10 days (five days a week for two weeks).
Researchers found that formaldehyde exposure in disease mice increased number of granulocytes — a type of immune system white blood cell — in the lungs (23,000 cells) compared to bleomycin-treated mice with no such exposure (15,000 cells). Higher levels of two inflammatory proteins — interleukin 1 beta and interleukin 17 — were also seen in exposed disease mice compared to those who did not inhale formaldehyde.
Other molecules contributing to inflammation were also increased, like C-X-C motif chemokine ligand 1 (CXCL1, a 12-fold increase) and tumor necrosis factor alpha (TNF-alpha, a 3-fold increase), but at the gene level.
Collagen production rose 2.2-fold in the mouse lung, while lung elastance at resting fell by 15 percent.
Researcher found no differences in lung elastance while breathing, or in mucus production, lung thickening and edema (fluid collection in tissues).
“Using an experimental model of PF induced by bleomycin, we showed the effects of formaldehyde exposure in the inflammatory and fibrotic parameters,” the researchers concluded. “This work contributes to understand the effects of pollution in the development of PF.”
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