Physical and chemical characterization of airbag effluents.

Objective: This paper describes a study aimed at characterizing the exposure to physical and chemical by-products from the deployment of airbag restraint systems.

Design, Materials And Methods: Specifically, the levels of particulates and the composition of gases and bag fabric speed were measured in the passenger compartment following deployment of either a driver's side or driver's side/passenger's side airbag system.

Measurements: A Fourier transform infrared analyzer (FTIR) and chemiluminescence analyzers were used for gas analysis, a cascade impactor and gravimetric filter measurements for aerosol determination and high-speed films to determine fabric speed.

Role of retinal metabolism in methanol-induced retinal toxicity.

Methanol is a toxicant that causes systemic and ocular toxicity after acute exposure. The folate-reduced (FR) rat is an excellent animal model that mimics characteristic human methanol toxic responses. The present study examines the role of the methanol metabolites formaldehyde and formate in the initiation of methanol-induced retinal toxicity.

A rat model manifesting methanol-induced visual dysfunction suitable for both acute and long-term exposure studies.

A toxic dose of methanol can induce visual dysfunction and metabolic acidosis in humans. However, the methanol dose range capable of inducing such toxicities and the mechanism(s) of visual dysfunction are not clearly understood. Nonprimate laboratory animals do not develop the characteristic human methanol toxicities even after a lethal dose.

Animal model for the study of methanol toxicity: comparison of folate-reduced rat responses with published monkey data.

We attempted to develop a rodent model that exhibits characteristics of human methanol toxicities such as acidosis and visual dysfunction, which are correlated with an accumulation of formate, a toxic metabolite of methanol. Initially three groups of Long-Evans rats with different levels of liver folate were prepared and examined for formate accumulation after methanol administration (3.5 g/kg).

Lack of blood formate accumulation in humans following exposure to methanol vapor at the current permissible exposure limit of 200 ppm.

Accumulation of formate, the putative toxic metabolite of methanol, in the blood and the relationship between pulmonary intake and blood methanol concentration were investigated in six human volunteers following a 6-hr exposure to 200 ppm methanol (the current Occupational Safety and Health Administration 8-hr time-weighted average permissible exposure limit). At the end of a 6-hr exposure to 200 ppm methanol at rest, the blood methanol concentration was increased from a mean of 1.8 micrograms/mL to 7.