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Highlights: • An acute exposure to 0.2 ppm ozone impairs odor detection threshold. • The cause is not clear, different modes of action might play at role. • Olfactory threshold seems sensitive to photochemical air pollutants’ effects. Ozone is a ubiquitous and irritant gas. We questioned whether an acute exposure to 0.2 ppm ozone impaired olfactory functioning.
It is suggested that systemic oxidative stress and inflammation play a central role in the onset and progression of cardiovascular diseases associated with the exposure to particulate matter (PM). The aim of this work was to evaluate the time changes of systemic markers of oxidative stress and inflammation, after an acute exposure to Residual Oil Fly Ash (ROFA). Female Swiss mice were intranasally instilled with a ROFA suspension (1.0 mg/kg body weight) or saline solution, and plasma levels of oxidative damage markers [thiobarbituric acid reactive substances (TBARSs) and protein carbonyls], antioxidant status [reduced (GSH) and oxidized (GSSG) glutathione, ascorbic acid levels, and superoxide dismutase (SOD) activity], cytokines levels, and intravascular leukocyte activation were evaluated after 1, 3 or 5 h of exposure. Oxidative damage to lipids and decreased GSH/GSSG ratio were observed in ROFA-exposed mice as early as 1 h. Afterwards, increased protein oxidation, decreased ascorbic acid content and SOD activity were found in this group at 3 h. The onset of an adaptive response was observed at 5 h after the ROFA exposure, as indicated by decreased TBARS plasma content and increased SOD activity. The observed increase in oxidative damage to plasma macromolecules, together with systemic antioxidants depletion, may be a consequence of a systemic inflammatory response triggered by the ROFA exposure, since increased TNF-α and IL-6 plasma levels and polymorphonuclear leukocytes activation was found at every evaluated time point. These findings contribute to the understanding of the increase in cardiovascular morbidity and mortality, in association with environmental PM inhalation. - Highlights: • An acute exposure to ROFA triggers the occurrence of systemic oxidative stress. • Changes in plasmatic oxidative stress markers appear as early as 1 h after exposure. • ROFA induces proinflammatory cytokines release and intravascular leukocyte activation. • PMN activation is a relevant source of reactive oxygen species in this model. • These findings may account for previously described cardiopulmonary alterations.
Acute exposure biological effects on monkeys compared for high energy graphite attenuated protons and Co 60 gamma irradiation
Carfentanil (CRF) is a powerful synthetic opioid that is approximately 100 times more potent than fentanyl and 10,000 times more potent than morphine. CRF originally was intended to be used as a sedative for big game animals in a veterinary setting, but is becoming increasingly common in the illicit drug trade. The increased use of CRF by people has put strain on first responders, who need to administer increased doses of naloxone (Naracan®, Evzio®), an FDA‐approved opioid antagonist, to counteract the effects. First responders may also worry about the potential of self‐exposure through inhalation or dermal contact with CRF. We set out to study the effectiveness of naloxone against a potentially lethal dose of inhaled CRF in male ferrets. Ferrets were implanted with telemetry devices to study cardiac parameters and exposed to aerosolized CRF in a whole‐body plethysmography chamber to record respiratory parameters. We observed profound depression of respiration which resulted in the animals becoming apneic 23% ± 9% of the time during exposure. We also observed cardiac abnormalities, in the form of premature junctional contractions (PJCs), in the ferrets during the apneic periods. At our acute exposure dose, which was lethal in 9% of our animals, ferrets were unresponsive and incapacitated for 105.6 ± 20.0 minutes following the end of exposure. Naloxone, when administered intramuscularly at human equivalent doses ranging from 4 to 40 mg, significantly reduced the time that ferrets were incapacitated following exposure. Although we saw no significant difference in the reduction of time that the animals were incapacitated between the treatment groups (average times between treatment and revival ranged from 6.5 to 9.7 minutes), higher doses of naloxone did revive a portion of the ferrets quicker than the lower doses (some as soon as 1.5–3.5 minutes post‐treatment). We also observed that naloxone was able to significantly reduce the amount of apneic episodes in CRF‐exposed ferrets and resolved the observed cardiac PJCs. Our results suggest that naloxone is a viable treatment against the effects of a potentially lethal dose of inhaled CRF in ferrets. These data have the potential to inform and aid treatment strategies for an acute inhalation exposure to synthetic opioids. Support or Funding Information Opinions, interpretations, conclusions, and recommendations are those of the author and are not necessarily endorsed by the US Army. This research complied with the Animal Welfare Act and implementing Animal Welfare Regulations and adhered to the principles noted in The Guide for the Care and Use of Laboratory Animals. This research was supported by DTRA RD‐CB. M.R. and N.A.A. were supported in part by an appointment to the Postgraduate Research Participation Program at the US Army Medical Research Institute of Chemical Defense administered by the Oak Ridge Institute for Science and Education through an interagency agreement between the US Department of Energy and USAMRMC. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .
Silver nanowires (AgNW) are attractive materials that are anticipated to be incorporated into numerous consumer products such as textiles, touchscreen display, and medical devices that could be in direct contact with skin. There are very few studies on the cellular toxicity of AgNW and no studies that have specifically evaluated the potential toxicity from dermal exposure. To address this question, we investigated the dermal toxicity after acute exposure of polymer-coated AgNW with two sizes using two models, human primary keratinocytes and human reconstructed epidermis. In keratinocytes, AgNW are rapidly and massively internalized inside cells leading to dose-dependent cytotoxicity that was not due to Ag + release. Analysing our data with different dose metrics, we propose that the number of NW is the most appropriate dose-metric for studies of AgNW toxicity. In reconstructed epidermis, the results of a standard in vitro skin irritation assay classified AgNW as non-irritant to skin and we found no evidence of penetration into the deeper layer of the epidermis. The findings show that healthy and intact epidermis provides an effective barrier for AgNW, although the study does not address potential transport through follicles or injured skin. The combined cell and tissue model approach used here is likely to provide an important methodology for assessing the risks for skin exposure to AgNW from consumer products.
The aim of this research was to investigate cardiac autonomic changes associated with acute exposures to airborne particulates. Methods: High fidelity 12-lead ECG (CardioSoft, Houston, TX) was acquired from 19 (10 male / 9 female) non-smoking volunteers (age 33.6 +/- 6.6 yrs) during 10 minutes pre-exposure, exposure and post-exposure to environmental tobacco smoke (ETS), cooking oil fumes, wood smoke and sham (water vapor). To control exposure levels, noise, subject activity, and temperature, all studies were conducted inside an environmental chamber. Results: The short-term fractal scaling exponent (Alpha-1) and the ratio of low frequency to high frequency Heart Rate Variability (HRV) powers (LF/HF, a purported sympathetic index) were both higher in males (p<0.017 and p<0.05, respectively) whereas approximate entropy (ApEn) and HF/(LF+HF) (a purported parasympathetic index) were both lower in males (p<0.036, and p<0.044, respectively). Compared to pre-exposure (p<0.0002) and sham exposure (p<0.047), male heart rates were elevated during early ETS post-exposure. Our data suggest that, in addition to tonic HRV gender differences, cardiac responses to some acute airborne particulates are gender related.
Reactive O{sub 2} species production triggered by particulate matter (PM) exposure is able to initiate oxidative damage mechanisms, which are postulated as responsible for increased morbidity along with the aggravation of respiratory diseases. The aim of this work was to quantitatively analyse the major sources of reactive O{sub 2} species involved in lung O{sub 2} metabolism after an acute exposure to Residual Oil Fly Ashes (ROFAs). Mice were intranasally instilled with a ROFA suspension (1.0 mg/kg body weight), and lung samples were analysed 1 h after instillation. Tissue O{sub 2} consumption and NADPH oxidase (Nox) activity were evaluated in tissue homogenates. Mitochondrial respiration, respiratory chain complexes activity, H{sub 2}O{sub 2} and ATP production rates, mitochondrial membrane potential and oxidative damage markers were assessed in isolated mitochondria. ROFA exposure was found to be associated with 61% increased tissue O{sub 2} consumption, a 30% increase in Nox activity, a 33% increased state 3 mitochondrial O{sub 2} consumption and a mitochondrial complex II activity increased by 25%. During mitochondrial active respiration, mitochondrial depolarization and a 53% decreased ATP production rate were observed. Neither changes in H{sub 2}O{sub 2} production rate, nor oxidative damage in isolated mitochondria were observed after the instillation. After an acute ROFA exposure, increased tissue O{sub 2} consumption may account for an augmented Nox activity, causing an increased O{sub 2}{sup ·−} production. The mitochondrial function modifications found may prevent oxidative damage within the organelle. These findings provide new insights to the understanding of the mechanisms involving reactive O{sub 2} species production in the lung triggered by ROFA exposure. - Highlights: • Exposure to ROFA alters the oxidative metabolism in mice lung. • The augmented Nox activity contributes to the high tissue O{sub 2} consumption. • Exposure to ROFA produces alterations in mitochondrial function. • ΔΨ{sub m} decrease in state 3 may be responsible for the decreased ATP production. • Mild uncoupling prevents mitochondrial oxidative damage.
Hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), a widely used munitions compound, and hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine (MNX), its N-nitroso product of anaerobic microbial nitroreduction, are contaminants of military sites. Previous studies have shown MNX to be the most acutely toxic among the nitroreduced degradation products of RDX and to cause mild anemia at high dose. The present study compares hematotoxicity with acute oral exposure to MNX with parent RDX. Both RDX and MNX caused a modest decrease in blood hemoglobin and ∼ 50% loss of granulocytes (NOAELs = 47 mg/kg) in female Sprague–Dawley rats observed 14 days post-exposure. We explored the possibility that blood cell loss observed after 14 days was delayed in onset because of toxicity to bone marrow (BM) progenitors. RDX and MNX decreased granulocyte/macrophage-colony forming cells (GM-CFCs) at 14, but not 7, days (NOAELs = 24 mg/kg). The earliest observed time at which MNX decreased GM-CFCs was 10 days post-exposure. RDX and MNX likewise decreased BM burst-forming units-erythroid (BFU-Es) at 14, but not 7, days. Granulocyte–erythrocyte–monocyte–megakaryocyte (GEMM)-CFCs were unaffected by RDX and MNX at 7 days suggesting precursor depletion did not account for GM-CFC and BFU-E loss. MNX added to the culture media was without effect on GM-CFC formation indicating no direct inhibition. Flow cytometry showed no differential loss of BM multilineage progenitors (Thy1.1{sup +}) or erythroid (CD71{sup +}) precursors with MNX suggesting myeloid and erythroid lineages were comparably affected. Collectively, these data indicate that acute exposure to both RDX and MNX caused delayed suppression of myelo- and erythropoiesis with subsequent decrease of peripheral granulocytes and erythrocytes. Highlights: ► Acute oral exposure to munitions RDX causes myelosuppression. ► Environmental degradation product MNX is comparable in effect. ► RDX and MNX are cytotoxic to both myeloid and erythroid progenitor cells. ► Myelosuppression is delayed in onset by > 7 days after single exposure.
The circadian timing system (CTS) provides internal and external temporal coordination of an animal's physiology and behavior. In mammals, the generation and coordination of these circadian rhythms is controlled by a neural pacemaker, the suprachiasmatic nucleus (SCN), located within the hypothalamus. The pacemaker is synchronized to the 24 hour day by time cures (zeitgebers) such as the light/dark cycle. When an animal is exposed to an environment without time cues, the circadian rhythms maintain internal temporal coordination, but exhibit a 'free-running' condition in which the period length is determined by the internal pacemaker. Maintenance of internal and external temporal coordination are critical for normal physiological and psychological function in human and non-human primates. Exposure to altered gravitational environments has been shown to affect the amplitude, mean, and timing of circadian rhythms in species ranging from unicellular organisms to man. However, it has not been determined whether altered gravitational fields have a direct effect on the neural pacemaker, or affect peripheral parameters. In previous studies, the ability of a stimulus to phase shift circadian rhythms was used to determine whether a stimulus has a direct effect on the neural pacemaker. The present experiment was performed in order to determine whether acute exposure to a hyperdynamic field could phase shift circadian rhythms.
Carbon dioxide (CO2) originates from human metabolism and typically remains about 10-fold higher in concentration on the International Space Station (ISS) than at the earth's surface. There have been recurring complaints by crew members of episodes of "mental viscosity" adversely affecting their performance, and there is evidence from the ISS that associates CO2 levels with reports of headaches by crewmembers. Consequently, flight rules have been employed to control CO2 below 3 mm Hg, which is well below the existing Spacecraft Maximum Allowable Concentration (SMAC) of 10 mm Hg for 24-hour exposures, and 5.3 mm Hg for exposures of 7 to 180 days. Headaches, while sometime debilitating themselves, are also symptoms that can provide evidence that physiological defense mechanisms have been breached, and there is evidence that CO2 has effects at levels below the threshold for headaches. This concern appears to be substantiated in reports that CO2 at concentrations below 2 mm Hg substantially reduced some cognitive functions that are associated with the ability to make complex decisions in conditions that are characterized by volatility, uncertainty, complexity, ambiguity, and delayed feedback. These are conditions that could be encountered by crews in off-nominal situations or during the first missions beyond low earth orbit. Therefore, we set out to determine if decision-making under volatile, uncertain, confusing and ambiguous circumstances, where feedback is delayed or absent, is correlated with low levels of CO2 during acute exposures (several hours) in crew-like subjects and to determine if additional cognitive domains are sensitive to concentrations of CO2 at, or below, current ISS levels by using a test battery that is currently available onboard ISS. We enrolled 22 volunteers (8 females, 14 males) between the ages of 30-55 (38.8 +/- 7.0) years whose training and professional experience reflect that of the astronaut corps. Subjects were divided among 4 study groups. Exposures occurred in the 20-foot environmental chamber in Bldg 7 at JSC. Each group was exposed to each of four concentrations of CO2 (600, 1200, 2500, and 5000 ppm), and the exposure order was balanced across the groups which were randomly assigned to 4 possible complete exposure orders. Study participants and investigators were blinded to the exposure order. Each exposure lasted 4 hours and occurred on the same day each week for 4 consecutive weeks. Testing included the Strategic Management Simulation (SMS) methodology and the Cognition battery of psychometric measures that are being utilized aboard the ISS. Subjects participated in a familiarization session one week prior to the start of exposure sessions. Each exposure session followed the schedule noted in Figure 1 below. On the morning of each exposure, subjects completed the Cognition battery in a conference room at indoor ambient CO2 levels. Subjects then entered the exposure chamber and were acclimated to the environment for 15 minutes before completing another round of the Cognition battery. After a 20 minute rest, subject completed the approx.80 minute SMS. Subjects were allowed another 20 minute rest period before completing the final Cognition test battery in the exposure chamber. Subjects then returned to the conference room where they completed one final round of Cognition. Data from both testing methodologies are currently being analyzed and will be presented. Study investigators have not yet been unblinded to the coded exposure concentrations, but preliminary results suggest differences.
Micro- and nanoplastics (MPs and NPs) are pervasive environmental pollutants detected in aquatic ecosystems, with emerging evidence suggesting their presence in airborne particles generated by water body motion. Inhalation exposure to airborne MPs and NPs remains understudied despite documented links between occupational exposure to these particles and adverse respiratory outcomes, including airway inflammation, oxidative stress, and chronic respiratory diseases. This study explored the effects of acute NP exposure on a fully differentiated 3D human airway epithelial model derived from 14 healthy donors. Airway epithelium was exposed to aerosolized 50 nm polystyrene NPs at concentrations ranging from 2.5 to 2500 µg/mL for three minutes per day over three days. Functional assays revealed no significant alterations in tissue integrity, cell survival, mucociliary clearance, or cilia beat frequency, suggesting intact epithelial function post-exposure. However, cytokine and chemokine profiling identified a significant five-fold increase in CCL3 (MIP-1α), a neutrophilic chemoattractant, in NP-exposed samples compared to controls. This was corroborated by increased neutrophil chemotaxis in response to conditioned media from NP-exposed tissues, indicating a pro-inflammatory neutrophilic response. Conversely, levels of interleukins (IL-21, IL-2, IL-15), CXCL10, and TGF-β were significantly reduced, suggesting immunomodulatory effects that may impair adaptive immune responses and tissue repair mechanisms. These findings demonstrate that short-term exposure to NP-containing aerosols induces a distinct pro-inflammatory response in airway epithelium, characterized by enhanced neutrophil recruitment and reduced secretion of key immune modulators. These findings underscore the potential for aerosolized NPs to induce oxidative and inflammatory stress, raising concerns about their long-term impact on respiratory health and redox regulation.
The results of recent studies have provided strong evidence for the transgenerational effects of parental exposure to ionising radiation and chemical mutagens. However, the transgenerational effects of parental exposure on survival and fertility remain poorly understood. To establish whether parental irradiation can affect the survival and fertility of directly exposed organisms and their offspring, crustacean Daphnia magna were given 10, 100, 1000 and 10,000 mGy of acute γ-rays. Exposure to 1000 and 10,000 mGy significantly compromised the viability of irradiated Daphnia and their first-generation progeny, but did not affect the second-generation progeny. The fertility of F{sub 0} and F{sub 1}Daphnia gradually declined with the dose of parental exposure and significantly decreased at dose of 100 mGy and at higher doses. The effects of parental irradiation on the number of broods were only observed among the F{sub 0}Daphnia exposed to 1000 and 10,000 mGy, whereas the brood size was equally affected in the two consecutive generations. In contrast, the F{sub 2} total fertility was compromised only among progeny of parents that received the highest dose of 10,000 mGy. We propose that the decreased fertility observed among the F{sub 2} progeny of parents exposed to 10,000 mGy is attributed to transgenerational effects of parental irradiation. Our results also indicate a substantial recovery of the F{sub 2} progeny of irradiated F{sub 0}Daphnia exposed to the lower doses of acute γ-rays. - Highlights: • Viability of irradiated daphnids and their F{sub 1} progeny is compromised. • Viability of the F{sub 2} progeny of irradiated parents is not affected. • Total fertility of irradiated daphnids and their F{sub 1} progeny declines with the dose. • Total fertility of the F{sub 2} progeny of parents exposed to 10,000 mGy is compromised. • The decreased fertility among the F{sub 2} progeny is transgenerational phenomenon.
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