Flame retardants are ubiquitous chemicals added to numerous consumer products to prevent the spread of fire. While they are essential in enhancing fire safety, their widespread use has raised concerns about their environmental and health impacts. One such flame retardant, triphenyl phosphate (TPhP), has gained popularity as an alternative to previously restricted compounds. However, recent studies suggest that TPhP may pose risks to both aquatic ecosystems and human health through its potential to disrupt endocrine systems and alter gene expression.
In a study investigating the epigenetic effects of TPhP exposure, researchers examined its impact on embryonic cells derived from steelhead and rainbow trout, known for their relevance in aquatic toxicology and susceptibility to environmental pollutants. The study, published in the Journal of Applied Toxicology, aimed to explore how TPhP exposure influenced epigenetic modifications, particularly DNA methylation and histone modifications, which regulate gene expression.
DNA methylation and histone modifications are epigenetic processes that regulate gene expression without altering DNA sequences. Studying these changes is vital when investigating environmental hazards, as they provide insight into how pollutants affect gene activity, potentially leading to adverse health outcomes in exposed organisms.
In previous blog posts, we’ve explored how contaminants, such as those found in diesel exhaust fumes and formaldehyde, can disrupt DNA methylation and influence post-translational histone modifications, including acetylation and methylation, resulting in cellular changes. Additionally, we’ve highlighted how environmental factors during development, such as maternal diet, stress, and chemical exposure, may induce transgenerational changes in gene expression through epigenetic pathways.
Due to the widespread presence of TPhP in the environment, the researchers of the current study aimed to investigate the potential for epigenetic changes following exposure to TPhP in both trout embryonic and gill epithelial cells. These two cell types were selected to assess the potential for epigenetic changes in both inactive and active developmental cells.
First, the researchers determined sub-lethal concentrations of TPhP that did not cause significant cell death or impair cell proliferation in the trout cells. This was crucial to ensure that observed effects were not simply a result of cellular toxicity. Subsequently, they examined histone modifications, specifically histone H3 acetylation and methylation at lysine 9 (H3K9), as well as global DNA methylation patterns.
The findings revealed that exposure to TPhP led to significant alterations in epigenetic markers in the trout cells. Notably, TPhP exposure was associated with reduced levels of histone H3 acetylation and H3K9 mono-methylation, along with decreased global DNA methylation. These changes suggest potential disruptions in gene expression regulation, which could have implications for the health and development of aquatic organisms.
Interestingly, the study found differential responses between embryonic cells and gill epithelial cells, highlighting the importance of considering cell type-specific susceptibility to environmental toxins. While embryonic cells showed significant alterations in epigenetic markers following TPhP exposure, gill epithelial cells exhibited fewer changes, suggesting varying susceptibilities to TPhP-induced epigenetic modifications.
These findings underscore the need for further research into the broader toxicological consequences of TPhP exposure and its potential impacts on aquatic ecosystems. Understanding the mechanisms by which TPhP disrupts epigenetic regulation can provide valuable insights into its mode of action and aid in developing more targeted risk assessment strategies.
Moreover, given the developmental origins of health and disease hypothesis, which suggests that early-life exposures to environmental factors can predispose individuals to disease later in life, the findings have implications beyond aquatic ecosystems. Epigenetic alterations induced by TPhP exposure during critical developmental windows may have long-term health consequences for both aquatic organisms and humans.
In conclusion, this study sheds light on the epigenetic impacts of TPhP exposure on aquatic organisms and highlights the importance of considering epigenetic mechanisms in assessing the safety of environmental chemicals. Further research is needed to elucidate the specific genes and pathways affected by TPhP-induced epigenetic changes and their potential implications for ecosystem health and human well-being.
Source: Germain L et. al.The flame retardant triphenyl phosphate alters the epigenome of embryonic cells in an aquatic in vitro model.J Appl Toxicol.February 2024.
