Bacteria and material made from corn kernels can clean up PCBs in aquatic environments

Researchers funded by NIEHS demonstrated a new method to clean up aquatic ecosystems using biochar — the carbon-rich byproduct of burning plant matter — and bacteria. Their cost-effective strategy has the potential to destroy polychlorinated biphenyls (PCBs), a group of harmful chemicals that persist in sediments.

Current strategies to remove PCBs from the environment, such as excavating sediments from the bottom of aquatic ecosystems, are costly and can result in water contamination. Remediation strategies that use bacteria to break down pollutants show promise, but bacteria are unable to fully degrade PCBs in the environment. To address this challenge, the team investigated whether adding biochar to solutions with bacteria and PCBs could enhance the performance of a type of PCB-degrading bacteria called Paraburkholderia xenovorans.

The scientists tested different types of biochar, including three natural biochars — made from burning corn kernels, bamboo, and wood — and activated carbon, which is commonly used in water treatment. Next, they measured the effects of each biochar on bacterial growth, bacterial attachment to biochar particles, and expression of bacterial genes that degrade PCBs.

Imaging analysis revealed that bacteria cells attached to the corn kernel biochar in greater numbers compared to the other types of biochar. Bacterial growth was also higher in the solution with the corn kernel material. In addition, there was increased expression of bacterial genes involved in PCB degradation in the corn kernel biochar solution compared with the other materials.

These findings suggest that combining biochar made from corn kernels and PCB-degrading bacteria may provide a cost-effective strategy to clean up contaminated sediments while protecting public and ecosystem health, according to the authors.

Citation: Dong Q, LeFevre GH, Mattes TE. 2024. Black carbon impacts on Paraburkholderia xenovorans strain LB400 cell enrichment and activity: implications toward lower-chlorinated polychlorinated biphenyls biodegradation potential. Environ Sci Technol 58(8):3895-907.

New lab model reveals the underlying mechanisms of PM2.5-induced lung disease

NIEHS-funded researchers developed a new model to study how fine particulate matter (PM2.5) exposure may lead to respiratory disease. The new multicellular model addresses the limitations of current methods, which use only one type of lung cell and are unable to capture the biological complexity of the respiratory system.

Upon breathing in PM2.5 air pollution, tiny particles enter the lung and are deposited in the alveolar capillary region (ACR), where gas exchange occurs. This exposure is linked to respiratory disease; however, the mechanisms are not well understood.

The scientists created a model using three types of lung cells and assembled them to mimic the structure of the ACR. The model included alveolar cells, which cover the surface of the ACR; fibroblasts, which support ACR connective tissue; and endothelial cells, which form the inner lining of blood vessels within the ACR. Then, they exposed the alveolar cells to a type of PM2.5 found in diesel exhaust for 24 hours and analyzed each cell’s response.

PM2.5 altered gene expression in both alveolar cells and endothelial cells. However, endothelial cells had more gene expression changes, despite having indirect contact with the particles. Endothelial cells also developed a type of biological stress, which led them to produce proteins that cause inflammation — an indicator of respiratory disease. Further analysis revealed that a cell signaling pathway in epithelial cells, known as mitogen activated protein kinase, played a key role in the changes observed in the endothelial cells.

The study shows that changes in endothelial cells may play an important role in how PM2.5 exposure leads to lung disease, according to the authors. They also noted that models that include multiple types of lung cells can help expand our understanding of how respiratory disease develops.

Citation: Vitucci ECM, Simmons AE, Martin EM, McCullough SD. 2024. Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure. Part Fibre Toxicol 21(1):15.

New strategy to prioritize PFAS for health risk assessments

An NIEHS-funded team developed a screening method that uses human-derived cells to evaluate how PFAS might affect health. The new approach might help prioritize different PFAS for further testing in efforts to improve health risk assessments.

PFAS are a large group of chemicals widely used in consumer products, but the majority lack toxicity data, making risk evaluation difficult. The most widely accepted approach to assess large numbers of PFAS organizes the chemicals based on structural similarities and then selects a few representative compounds for further testing.

In this study, the team explored a different approach using liver and heart cells grown in a lab and exposing them to 26 different PFAS. They looked at how the chemicals affected cell function and gene expression.

PFAS had minimal effect on liver cell function. In contrast, exposure to eight of the 26 compounds resulted in decreased beating frequency in heart cells. Genetic expression analysis of liver cells showed increased activity in genes that regulate stress and cellular structure, but decreased activity in genes that break down fats. In heart cells, PFAS exposure decreased the expression of genes related to how the heart contracts.

To compare their approach to the traditional structure-based grouping method, the team looked for associations between PFAS molecular weight or chemical structure and the observed biological effects. They found no structural similarities among compounds with similar biological effects.

These results suggest that grouping PFAS by structure alone might not adequately predict individual chemicals’ health effects, according to the authors. Their strategy could guide researchers and policymakers in determining which chemicals to prioritize for future evaluation.

Citation: Tsai HD, Ford LC, Chen Z, Dickey AN, Wright FA, Rusyn I. 2024. Risk-based prioritization of PFAS using phenotypic and transcriptomic data from human induced pluripotent stem cell-derived hepatocytes and cardiomyocytes. ALTEX; [Online 22 Feb 2024].

Inhibiting mitochondria-related protein may protect against neurodegenerative diseases

Partially blocking Drp1, a protein critical for mitochondrial division, may protect against neurodegenerative diseases, according to an NIEHS-funded study. Mitochondria are small cellular structures that produce energy for cells to carry out various functions.

Mitochondrial dysfunction and errors in autophagy, a cellular process that degrades and recycles old cellular components, have been linked to various neurodegenerative disorders, including parkinsonism — an umbrella term for conditions that cause movement symptoms that closely resemble Parkinson's disease. Previous studies have shown that partial reduction of Drp1 may shield against neurodegeneration, but the mechanisms behind this process are not well understood.

First, the scientists used lab-grown cells, derived from human and rat brain cells, to examine the effects of blocking Drp1. Then, they conducted studies in mice with normal Drp1 protein levels and mice that produced approximately one-half the typical amount. They gave the mice either water alone or water containing manganese, a metal implicated in mitochondrial and autophagy impairment, daily for 30 days. Finally, the team analyzed alterations in mouse brain genes and mitochondrial activity.

Results from both cell and animal studies showed that exposure to low nontoxic levels of manganese had no effect on mitochondrial function. However, low-level manganese exposure decreased autophagy rates and increased levels of alpha-synuclein, a protein linked to parkinsonism. In addition, partially blocking Drp1 significantly reduced the damaging effects of manganese on autophagy.

According to the authors, these findings indicate that Drp1 plays an important role in autophagy, independent of mitochondrial activity, and may be a useful target for interventions to treat certain neurodegenerative diseases. Furthermore, the results suggest that exposure to manganese may increase the risk of parkinsonism by increasing the accumulation of alpha-synuclein.

Citation: Fan RZ, Sportelli C, Lai Y, Salehe S, Pinnell JR, Brown HJ, Richardson JR, Luo S, Tieu K. 2024. A partial Drp1 knockout improves autophagy flux independent of mitochondrial function. Mol Neurodegener 19(1):26.