The effects of obesity on organophosphate pesticide-mediated toxicities, including both cholinergic and non-cholinergic targets, have not been fully elucidated. Therefore, the present study was designed to determine if high fat diet intake alters the effects of repeated exposure to chlorpyrifos (CPS) on the activities of both cholinergic and noncholinergic serine hydrolase targets. Male C57BL/6J mice were placed on either standard rodent chow or high fat diet for four weeks with CPS exposure (2.0 mg/kg) for the last 10 days of diet intake. Exposure to CPS did not alter acetylcholinesterase in the central nervous system, but it did significantly inhibit circulating cholinesterase activities in both diet groups. CPS significantly inhibited hepatic carboxylesterase and fatty acid amide hydrolase and this inhibition was significantly greater in high fat fed animals. Additionally, CPS exposure and high fat diet intake downregulated genes involved in hepatic de novo lipogenesis as well as cytochrome P450 enzymes involved in hepatic xenobiotic metabolism. In summary, the present study demonstrates that high fat diet intake potentiates CPS mediated inhibition of both carboxylesterase and fatty acid amide hydrolase in the liver of obese animals following subacute exposure and suggests obesity may be a risk factor for increased non-cholinergic hepatic CPS toxicity.

Exposure to environmental contaminants and consumption of a high, saturated fatty diet has been demonstrated to promote precursors for metabolic syndrome (hyperglycemia, hyperinsulinemia, and hypertriglyceridemia). The purpose of this study was to determine if exposure to the most prevalent environmental persistent organic pollutants (POPs) would act as causative agents to promote metabolic syndrome independent of dietary intake. We hypothesized that POPs will activate the advanced glycated end‐product (AGE)‐and receptor for AGE (RAGE) signaling cascade to promote downstream signaling modulators of cardiovascular remodeling and oxidative stress in the heart. At 5‐weeks of age nondiabetic (WT) and diabetic (ob/ob) mice were exposed POPs mixtures by oral gavage twice a week for 6‐weeks. At the end of 6‐weeks, animals were sacrificed and the hearts were taken for biochemical analysis. Increased activation of the AGE‐RAGE signaling cascade via POPs exposure resulted in elevated levels of fibroblast differentiation (α‐smooth muscle actin) and RAGE expression indicated maladaptive cardiac remodeling. Conversely, the observed decreased superoxide dismutase‐1 and ‐2 (SOD‐1 and SOD‐2) expression may exacerbate the adverse changes occurring as a result of POPs treatment to reduce innate cardioprotective mechanisms. In comparison, ventricular collagen levels were decreased in mice exposed to POPs. In conclusion, exposure to organic environmental pollutants may intensify oxidative and inflammatory stressors to overwhelm protective mechanisms allowing for adverse cardiac remodeling.

Despite increased awareness and public health initiatives, the incidence of microbial infections related to tattoos has increased since 2000. Building on the first paper in this two-part Series, which detailed the microbiological aspects of tattoo-related infections over the past two centuries from 1820 to 2023, this second paper describes the patterns, causes, and other related epidemiological factors of these infections. Since 2000, bacterial outbreaks, particularly those caused by non-tuberculous mycobacteria, have increased, prompting a re-evaluation of tattoos as a serious public health risk. Insufficient hygiene practices have been the primary cause of microbial infections, with contaminated tattoo inks also contributing substantially, leading to 11 outbreaks and subsequent ink recalls. Although rare, the tattooing process can occasionally lead to life-threatening infections and fatalities. Tattoos by both professional and non-professional artists were associated with infections, suggesting that regulated environments do not necessarily eliminate risk. Additionally, individuals with compromised immune systems, especially those with HIV, were particularly vulnerable to infections such as Leishmania. Although permanent make-up is often perceived as safer than conventional tattoos, infections still occur, with 11 cases reported since 2010. Furthermore, polymicrobial infections involving multiple pathogens have posed challenges for diagnosis and treatment. Overall, these insights highlight the historical and emerging patterns of tattoo-related infections and can inform the development of more effective public health guidelines, enhance preventive measures, and guide future research on reducing the risks associated with tattoos.