Differential serum inflammatory cytokine elaboration in Nepali brick factory workers

Abstract

Previous studies involving workers at brick kilns in the Kathmandu Valley of Nepal have revealed chronic exposure to hazardous levels of fine particulate matter (PM2.5) common in ambient and occupational environments. Such exposures are known to cause and/or exacerbate chronic respiratory diseases including chronic obstructive pulmonary disease (COPD). However, there is a paucity of data regarding the systemic inflammatory status of exposed workers at brick manufacturing facilities. In the current study, we sought to elucidate systemic inflammatory responses by quantifying the molecular cytokine/chemokine profiles in serum from study participants. A sample of participants (N = 48; 54% female; 31.77±9.76 years-old) were distributed among four different job categories. Blood was procured from participants on-site, allowed to clot at room temperature, and centrifuged to obtain total serum. A human cytokine antibody array was used to screen cytokines/chemokines in serum samples. Comparisons were generated between a control group of administration workers vs. fire master workers, administration vs. green brick hand molders, and administration vs. top loaders. We discovered significantly increased concentrations of eotaxin-1, eotaxin-2, GCSF, GM-CSF, IFN-γ, IL-1γα, IL-1β, IL-6, IL-8, TGF-β1, TNF-α, and TIMP-2 in serum samples from fire master workers vs. administration (p < 0.03). Each of these molecules, with the exception of TIMP-2, were also significantly elevated in the serum from green brick hand molders (p < 0.02). In addition, each molecule was significantly elevated in serum from top loaders compared to administration workers (p < 0.03). With few exceptions, the fire master workers expressed significantly more systemic inflammatory molecular abundance when compared to all other job descriptions. These results reveal an association between pulmonary exposure to PM2.5 and systemic inflammatory responses likely mediated by cytokine/chemokine elaboration. Additional characterization of a broader array of inflammatory molecules may provide valuable insight into susceptibility to lung diseases including COPD. This work was supported in part by funding from Undergraduate Mentoring and a Widtsoe Research Grant from Brigham Young University. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.