Acute lung injury, acute respiratory distress syndrome and inhalation injury: an overview.

Acute Lung Injury (ALI) and the Acute Respiratory Distress Syndrome (ARDS) are severe respiratory diseases that have a very poor prognosis and have numerous causes. Despite a great deal of research and investigation since the initial description of ARDS 30 years ago many questions about the pathogenesis, treatment and outcome of the disease remain unanswered. Although there is evidence to suggest that outcome of ALI and ARDS is improving, the reasons why are unknown and there is not yet a well developed treatment for these diseases.

Aerosol deposition modeling using ACSL.

An aerosol deposition model has been written for inclusion into physiologically based pharmacokinetic (PBPK) models, allowing PBPK model based risk assessments to be performed for aerosolized materials. Previously, PBPK models could only treat inhaled gases and vapors. The deposition model employs a semi-empirical equation to describe extrathoracic deposition and employs data concerning the geometry of the thoracic conducting airways as well as that of the gas exchange regions of the lung to compute the deposited aerosol mass based on aerosol diffusion, sedimentation, and impaction.

Breathing zone particle size and lead concentration from sanding operations to remove lead based paints.

The relationship between lead concentration in the dry film of lead based paints applied to steel bulkheads aboard ship, the lead concentration found in the air when the paint is removed by mechanical means, and blood lead concentrations of workers involved in lead based paint removal has not been well characterized. Intuitively a direct relationship must exist but confounding factors confuse the issue. Simultaneous sampling procedures from the same paint removal operation may differ by several orders of magnitude.

Tissue distribution, metabolism, and clearance of the convulsant trimethylolpropane phosphate in rats.

The distribution, metabolism, and clearance of trimethylolpropane phosphate (TMPP), a potent, bicyclophosphate, gamma-aminobutyric acid-ergic convulsant, were studied in male Fischer-344 rats. Intraperitoneal administration of TMPP was compared with oral gavage with respect to rates of absorption, distribution, and clearance. Distribution of TMPP to major body tissues was evaluated for the first 24 hr after administration or, in the case of regional brain distribution, immediately after the first TMPP-induced clinical seizure.

Acute effects of a bicyclophosphate neuroconvulsant on monoamine neurotransmitter and metabolite levels in the rat brain.

Naive male Sprague-Dawley rats were injected intraperitoneally (i.p.) with the bicyclophosphate convulsant trimethylolpropane phosphate (TMPP) at dose levels from 0.

Trimethylolpropane phosphate (TMPP) perfusion into the nucleus accumbens of the rat: electroencephalographic, behavioral and neurochemical correlates.

The infusion (0.13 mumol/infusion) of the convulsant trimethylolpropane phosphate (TMPP) into the nucleus accumbens (NA) of adults Sprague-Dawley rats reliably induced subclinical seizures, hyperlocomotor activity, and integrated stereotypies. Observation of these behaviors was temporally correlated with the appearance of EEG paroxysms, as well as with significant decreases in extracellular concentrations of both dopamine (DA) and norepinephrine (NE) in the NA.

Environmental degradation of polyacrylamides. II. Effects of environmental (outdoor) exposure.

The environmental fate of a polyacrylamide thickening agent (PATA), formulated without and with a glyphosate-surfactant herbicide (GH), was examined under various environmental situations: formulation in surface water and ground water, volatility, and soil mobility. Environmental Fate of PATA in Surface Water and Ground Water: PATA was formulated at four concentrations in distilled-deionized water, three surface water samples, and two ground water samples, without and with a GH. Solutions were placed in glass bottles, covered with plastic wrap, and exposed to environmental (outdoor) conditions for 6 weeks.

Evaluation of the respiratory tract after acute exposure to a pyrotechnically generated aerosol fire suppressant.

Fischer 344 rats (250-300 g) were exposed to the resulting aerosols from the pyrolysis of Spectrex Fire Extinguishant (SFE) Formulation A, a pyrotechnically generated aerosol fire suppressant, at a loading equivalent of 50 or 80 g m(-3) air for 15 or 60 min. Exposures were conducted in a 700-1 whole-body inhalation chamber under static conditions. The chamber atmosphere was analyzed for mass aerosol concentration and size distribution.

An overview of the development, validation, and application of neurobehavioral and neuromolecular toxicity assessment batteries: potential applications to combustion toxicology.

Currently, there are few alternatives to the use of animals in toxicology for human risk assessment. Neurobehavioral toxicology is an emerging area in which complex performance capacity is evaluated during or following toxicological exposure. While a number of single tests and a few more complex neurobehavioral batteries exist, no fully validated and comprehensive neurobehavioral toxicity assessment battery has yet been developed.

Environmental degradation of polyacrylamides. 1. Effects of artificial environmental conditions: temperature, light, and pH.

A polyacrylamide thickening agent (PATA) was formulated at four concentrations in distilled-deionized water, without and with a glyphosate-surfactant herbicide (GH). Over a 6-week period, these mixtures were exposed to various controlled temperature and light conditions. Acrylamide concentration, ammonium concentration, and pH were measured at weekly intervals to assess the degradation of polyacrylamide and acrylamide.

Risk assessment policy for evaluating reproductive system toxicants and the impact of responses on sensitive populations.

Risk assessment policy for evaluating environmental chemicals for their potential to produce reproductive system failures is similar to policy for evaluating cancer-causing effects. The objective of reproductive system risk assessment is to expand on the test standards that primarily focus on fertility endpoints and birth defects by using mechanism-of-action studies and quantitative risk assessment methods. An understanding of the sensitivity of reproductive system insult between animal species and from animal models to man is critical to developing risk assessment policy and test standards.

Evaluation of shipboard formation of a neurotoxicant (trimethylolpropane phosphate) from thermal decomposition of synthetic aircraft engine lubricant.

MIL-L-23699 lubricants that are composed principally of trimethylolpropane triheptanoate (TMP) and tricresyl phosphate (TCP) have been shown to form a neurotoxicant, trimethylolpropane phosphate (TMPP), during pyrolysis and/or combustion. Mechanistically, TMPP is thought to irreversibly inhibit the GABA-mediated inhibitory response and thereby produce epileptiform clonic/tonic seizures with convulsions followed by death. Thermal decomposition of MIL-L-23699 lubricant produces TMPP under laboratory conditions, but this product has not been detected in the workplace following actual fires.

Acute toxicity, distribution, and metabolism of 2,4,6-trinitrophenol (picric acid) in Fischer 344 rats.

Picric acid (2,4,6-trinitrophenol) is widely used in industry, by the military, and as a research/clinical chemistry reagent. Characterization of the toxicity of this chemical has been limited. Thus the acute toxicity, distribution, and metabolism of picric acid were investigated using Fischer 344 rats.

In vitro activation of lipophilic tributyltins by superoxide produces tributylstannyl superoxo radicals, proposed initiators of lipid peroxidation: an EPR model study.

Tri-n-butyltin(TBT) compounds having the chemical formula (C4H9)3SnX are broad-spectrum biocidal agents whose toxic effect is primarily at the membrane level. Red blood cells (RBC) exposed to micromolar concentrations of tributyltin compounds (TBTX) undergo morphological changes and hemolysis. Determination of the mechanism of action whereby TBT elicits membrane damage continues to be a challenging endeavor.