Target and suspect per- and polyfluoroalkyl substances in fish from an AFFF-impacted waterway.

A major source of toxic per- and polyfluoroalkyl substances (PFAS) is aqueous film-forming foams (AFFF) used in firefighting and training at airports and military installations, however, PFAS have many additional sources in consumer products and industrial processes. A field study was conducted on fish tissues from three reaches of the Columbia Slough, located near Portland International Airport, OR, that are affected by AFFF and other PFAS sources. Fishes including largescale sucker (Catostomus macrocheilus), goldfish (Carassius auratus), and largemouth bass (Micropterus salmoides) were collected in 2019 and 2020.

Health-based cyanotoxin guideline values allow for cyanotoxin-based monitoring and efficient public health response to cyanobacterial blooms.

Human health risks from cyanobacterial blooms are primarily related to cyanotoxins that some cyanobacteria produce. Not all species of cyanobacteria can produce toxins. Those that do often do not produce toxins at levels harmful to human health.

Improving the risk assessment of lipophilic persistent environmental chemicals in breast milk.

Lipophilic persistent environmental chemicals (LPECs) have the potential to accumulate within a woman's body lipids over the course of many years prior to pregnancy, to partition into human milk, and to transfer to infants upon breastfeeding. As a result of this accumulation and partitioning, a breastfeeding infant's intake of these LPECs may be much greater than his/her mother's average daily exposure. Because the developmental period sets the stage for lifelong health, it is important to be able to accurately assess chemical exposures in early life.

The anti-inflammatory drug leflunomide is an agonist of the aryl hydrocarbon receptor.

Background: The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates the toxicity and biological activity of dioxins and related chemicals. The AhR influences a variety of processes involved in cellular growth and differentiation, and recent studies have suggested that the AhR is a potential target for immune-mediated diseases.

Methodology/principal Findings: During a screen for molecules that activate the AhR, leflunomide, an immunomodulatory drug presently used in the clinic for the treatment of rheumatoid arthritis, was identified as an AhR agonist.

Activation of aryl hydrocarbon receptor by TCDD prevents diabetes in NOD mice and increases Foxp3+ T cells in pancreatic lymph nodes.

The ligand-activated transcription factor, aryl hydrocarbon receptor (AHR), is a novel inducer of adaptive Tregs. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent AHR ligand, induces adaptive CD4+CD25+ Tregs during an acute graft-versus-host (GvH) response and prevents the generation of allospecific cytotoxic T lymphocytes. TCDD also suppresses the induction of experimental autoimmune encephalitis in association with an expanded population of Foxp3+ Tregs.

Reduction of myeloid suppressor cell derived nitric oxide provides a mechanistic basis of lead enhancement of alloreactive CD4(+) T cell proliferation.

The persistent environmental toxicant and immunomodulator, lead (Pb), has been proposed to directly target CD4(+) T cells. However, our studies suggest that CD4(+) T cells are an important functional, yet indirect target. In order to identify the direct target of Pb in the immune system and the potential mechanism of Pb-induced immunotoxicity, myeloid suppressor cells (MSCs) were evaluated for their ability to modulate CD4(+) T cell proliferation after Pb exposure.

Lead enhances CD4+ T cell proliferation indirectly by targeting antigen presenting cells and modulating antigen-specific interactions.

Although Pb is a well-known immunotoxicant, its mechanism of action is not well understood. Low levels of Pb (approximately 1 microM) markedly enhance the proliferative T cell response in mixed lymphocyte culture (MLC), a process we have termed allo-enhancement. As Pb allo-enhancement occurs whether alloantigen presenting cells (APC) are derived from C57BL/6 or BALB.