Abstract

Overview

The cellular and molecular mechanisms by which atmospheric pollution from particulate matter and/or electromagnetic fields (EMFs) may prove harmful to human health have not been extensively researched.

Findings

• EMFs and black carbon (BC) particles induced cell damage and a pro-apoptotic response in the HL-60 promyelocytic cell line when exposed to 2.45 GHz radio frequency (RF) radiation in a gigahertz transverse electromagnetic chamber at sub-thermal specific absorption rate levels.
• RF and BC induced moderately significant levels of cell damage in the first 8 or 24 h for all exposure times/doses and much greater damage after 48 h of irradiation and the higher dose of BC.
• Oxidative stress or ROS production increased with time (24 or 48 h of radiation), BC dose, and the combination of both.
• Significant differences between the proportion of damaged and healthy cells were observed in all groups.
• Both radiation and BC participated separately and jointly in triggering necrosis and apoptosis in a programmed way.
• Oxidative-antioxidant action activated mitochondrial anti-apoptotic BCL2a gene expression after 24 h irradiation and exposure to BC.
• Expression of FASR cell death receptors was activated after irradiation for 48 h, leading to pro-apoptotic phenomena and intracellular activity of caspase-3 in the mitochondrial pathways, potentially leading to cell death.

Conclusion

Combined exposure to 2.45 GHz RF and BC over a period of 48 h caused very high levels of toxicity in a HL-60 cell line, triggering an antiproliferative effect dependent on the BC dose and exposure time. Despite the increased expression of antioxidant BCL2a and initial expression of the FAS cell death receptors, cell death occurred predominantly through a caspase-dependent pathway, leading to necrosis and mitochondria-caspase dependent apoptosis. This effect may have implications for antimicrobial, inflammatory, and autoimmune responses in humans. Results underline potential health risks associated with electromagnetic fields and particulate exposure.