Indoor and Personal PM2.5 Samples Differ in Chemical Composition and Alter Zebrafish Behavior Based on Primary Fuel Source.

Fine particulate matter (PM2.5) exposure has been linked to diverse human health impacts. Little is known about the potential heterogeneous impacts of PM2.5 generated from different indoor fuel sources and how exposure differs between personal and indoor environments. Therefore, we used PM2.5 collected by one stationary sampler in a kitchen and personal samplers (female and male participants), in homes (n = 24) in Kheri, India, that used either biomass or liquified petroleum gas (LPG) as primary fuel sources. PM2.5 samples (pooled by fuel type and monitor placement) were analyzed for oxidative potential and chemical composition, including elements and 125 organic compounds. Zebrafish (Danio rerio) embryos were acutely exposed to varying concentrations of PM2.5 and behavioral analyses were conducted. We found relatively high PM2.5 concentrations (5-15 times above World Health Organization daily exposure guidelines) and varied human health-related chemical composition based on fuel type and monitor placement (up to 15% carcinogenic polycyclic aromatic hydrocarbon composition). Altered biological responses, including changes to mortality, morphology, and behavior, were elicited by exposure to all sample types. These findings reveal that although LPG is generally ranked the least harmful compared to biomass fuels, chemical characteristics and biological impacts were still present, highlighting the need for further research in determining the safety of indoor fuel sources.

Potency matters: Impacts of embryonic exposure to nAChR agonists thiamethoxam and nicotine on hatching success, growth, and neurobehavior in larval zebrafish.

Thiamethoxam (TM) is a neonicotinoid insecticide that acts as a nicotinic acetylcholine receptor (nAChR) agonist. While designed to specifically target invertebrate nAChRs, recent studies have reported adverse effects of neonicotinoid exposure in early life-stage fish. This study examined the health and neurobehavioral impacts of chronic exposure to various concentrations of TM or nicotine (NIC) in early life zebrafish (Danio rerio) in conjunction with in-silico molecular docking to compare their ligand-receptor interactions with vertebrate nAChR. Chronic exposure to both reduced survival by approximately 20% (163 µg TM/l) and 25-100% (≥0.49 µg NIC/l). Hatching and growth were impaired following exposure to ≥0.21 µg TM/l or 4.9 µg NIC/l. Both TM and NIC produced morphological and behavioral indicators of neurotoxicity, with more potent effects following NIC exposure. NIC impaired embryonic motor activity by 40% (49 µg NIC/l), while both TM and NIC significantly altered predator escape response in larvae, specifically the latency and the initial burst movement of the response were impacted. Molecular docking predicted variations in the type and strength of interactions that occur between NIC or TM and vertebrate nAChR. These findings demonstrate that chronic exposure to TM might impact general health and neurobehavior of early-stage zebrafish. Our data support hypotheses that TM presents low affinity for vertebrate nAChR but may still pose an adverse risk to larval fish growth and neurobehavior.

Chronic Exposure to Environmentally Relevant Concentrations of Imidacloprid Impact Survival and Ecologically Relevant Behaviors of Fathead Minnow Larvae.

Imidacloprid (IM) has emerged as a contaminant of concern in several areas within the United States due to its frequent detection in aquatic ecosystems and its pseudo-persistence, which pose potential risks to nontarget species. We evaluated the sublethal toxicity of IM to fathead minnow larvae following chronic exposure beginning just after fertilization. Our in silico analysis and in vivo bioassays suggest that IM has a low binding affinity for the vertebrate nicotinate acetylcholine receptor (nAChR), as expected. However, chronic exposure to ≥0.16 µg IM/L reduced survival by 10%, and exposure to ≥18 µg IM/L reduced survival by approximately 20%-40%. Surviving fish exposed to ≥0.16 µg IM/L showed reduced growth, altered embryonic motor activity, and premature hatching. Furthermore, a significant proportion of fish exposed to ≥0.16 µg IM/L were slower to respond to vibrational stimuli and slower to swim away, indicating that chronic exposure to IM has the potential to impair the ability of larvae to escape predation. The adverse health effects we observed indicate that chronic exposure to environmentally relevant concentrations of IM may elicit sublethal responses that culminate in a significant increase in mortality during early life stages, ultimately translating to reduced recruitment in wild fish populations. Environ Toxicol Chem 2023;42:2184-2192. © 2023 SETAC.

Embryonic Exposure to Thiamethoxam Reduces Survival and Alters Neurobehavior of Fathead Minnows.

Thiamethoxam is a commonly used neonicotinoid insecticide that acts as a nicotinic acetylcholine receptor (nAChR) agonist. Although vertebrates are less sensitive to neonicotinoid insecticides than invertebrates, some neonicotinoids have been shown to cause neurobehavioral changes in larval fishes. In the present study, we examine the neurobehavioral toxicity of acute and chronic exposure to environmentally relevant concentrations of thiamethoxam in fathead minnows at two different life stages. Whereas acute exposure of embryos to thiamethoxam does not appear to stimulate spontaneous contractions within 1 min, chronic exposure of embryos to 1.57 µg or more thiamethoxam/L caused increased mortality as well as a subtle increase in spontaneous contraction frequency (SCF), which was negatively correlated with early hatching success. Chronic exposure of embryos to 155 µg thiamethoxam/L impaired predator escape response, and chronic exposure to 0.02-14.61 µg thiamethoxam/L impaired foraging efficiency of some fish. Fathead minnows exposed to thiamethoxam beginning post hatch did not experience changes to measured health or neurobehavioral indicators. Taken together, our findings indicate that embryonic life stages are more sensitive to thiamethoxam exposure than later larval life stages. Because early exposure to thiamethoxam can cause deficits in predatory escape behaviors and may impair foraging success, further study of the potential direct and nondirect impacts of thiamethoxam on wild fish populations is warranted. Environ Toxicol Chem 2022;41:1276-1285. © 2022 SETAC.