No description available.

No description available.

No description available.

No description available.

No description available.

No description available.

No description available.

No description available.

No description available.

Fertile White Leghorn (Gallus gallus) and Bobwhite Quail (Colinus virginianus) were subjected to 15 min exposures produced by burning solid rocket motor (SRM) fuel. Comparative mortality data were collected. Chicken eggs were further used to study the effects of exposure on water relations and blood gas parameters. Chicken embryos exposed once on day 19 or incubation demonstrated and LD50 of 204 ppm; the LD50 for quail embryos was 175 ppm. When mortality was regressed on the final exposure concentration, chicken and quail embryos exposed on days 12 and 19 showed LD50's of 127 and 86 ppm respectively, and embryos exposed on days 4, 12, and 19 had LD50's of 75 and 56 ppm. Quail embryos appeared to be more sensitive to SRM exhausts than chicken embryos, probably owing to the larger surface area to volume ration of the egg. Embryos exposed to a small daily concentration had an MLC of 117 ppm and an LD50 of approximately 200 ppm for cumulative exposure concentrations. This suggested that individual exposures were additive in effect. Eggs exposed at temperatures less than 37.5 C showed reduced lethality, while exposures at greater temperatures increased lethality. The rate of water loss from chicken eggs measured over an eight hour period increased 5 times because of a 15 min exposure. Since the increased rate of dehydration occurred during the exposure, the hydroscopic effects of exposure were extreme. When eggs lose the 18% of the initial weight normally lost from evaporation during incubation due to exposure, no more water loss was seen to occur. Blood gas analyses on 12 day embryos showed decreased pH at cumulative exposure concentrations greater than 200 ppm. Carbon monoxide in the exhausts probably increased carboxyhemoglobin, reducing buffering capacity. The acidosis was partially compensated by increased HCO3-, Exogenously derived C1-, plus increased HCO3- may shift intracellular K+, making the serum hyperkatremic. Dehydration effects further increased serum hypertonicity.