Spring 1972 Conference Issue

For the Homeowner by Alfred W. Boicourt (page 3) Slow-Release Fertilizer for Lawns by Robert W. Schery (4) Sanity in Research and Evaluation of Environmental Health by H.E. Stokinger (7) Turf Conference (10) Recent Developments with Dursban Insecticide for Chinch Bug Control by W.O. Miller (17

Effect of pretreatment of rats with carbon tetrachloride on tolerance development

To evaluate the effect of pretreatment of rats with CCl4 on tolerance development to subsequent exposures, rats were exposed 25-7500 ppm of CCl4 vapor or given CCl4 orally, 3.25 mg/g body weight. Forty-eight hours later these rats were reexposed to a normally lethal 7500 ppm CCl4 concentration. Mortality, blood clotting time, serum bilirubin, serum and liver triglycerides, and CCl4 and CHCl3 concentrations in tissues and in the whole rat were used as a measure of the response to CCl4 exposure. Conversion of CCl4 to CHCl3 in vitro was also determined in normal and pretreated animals. It was found that animals exposed to 4000 ppm for 6 hr or given 3.25 mg/g of CCl4 orally developed tolerance to subsequent normally lethal CCl4 exposures. Serum bilirubin levels in animals protected by CCl4 pretreatment were significantly lower than in those receiving only a single exposure to CCl4. Blood clotting times in protected animals were normal, while in those not protected by pretreatment, they were greatly prolonged. Serum triglyceride levels in protected animals were normal whereas they were considerably depressed in the nonprotected animals. Liver triglycerides were elevated in both protected and nonprotected, but were not as high in the protected animals. Carbon tetrachloride conversion to CHCl3 was slower in protected than in the non-protected animals. Tolerance to CCl4 developed in animals whose ability to metabolize CCl4 had been depressed by pretreatment with the same compound. This suggests that the toxicity of CCl4 is related to its metabolic pathway or to the production of toxic intermediates.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/32734/1/0000103.pd

Inhalation exposure methodology.

Modern man is being confronted with an ever-increasing inventory of potentially toxic airborne substances. Exposures to these atmospheric contaminants occur in residential and commercial settings, as well as in the workplace. In order to study the toxicity of such materials, a special technology relating to inhalation exposure systems has evolved. The purpose of this paper is to provide a description of the techniques which are used in exposing laboratory subjects to airborne particles and gases. The various modes of inhalation exposure (whole body, head only, nose or mouth only, etc.) are described at length, including the advantages and disadvantages inherent to each mode. Numerous literature citations are included for further reading. Among the topics briefly discussed are the selection of appropriate animal species for toxicological testing, and the types of inhalation studies performed (acute, chronic, etc.)

A cellular model for studying accommodation to environmental stressors: A protective response to subtoxic exposure to cadmium

A model is described for testing the effect of exposure to subtoxic challenge upon cellular integrity. The model incorporates Physarum polycephalum as a biological assay system, the ability of the cell to traverse the cell cycle as an indicator of cell integrity, and the use of repeated challenge by cadmium ion as a mechanism for amplifying the response to subthreshold exposure. A sensitivity profile of Physarum, developed by periodic exposure to 5 x 10-4 m Cd2+ for 30 min throughout the cell cycle, contains two peaks of sensitivity resulting in mitotic delay, one in early S and the other in late G2. Physarum accommodates to a subtoxic challenge of Cd2+ by developing a protective response: Exposure to 10-4 m Cd2+ for 30 min in early G2 (0.45 cycle), which does not delay mitosis, protects Physarum against a mitotic delay of 105 min resulting from exposure to 4 x 10-4 m Cd2+ for 30 min in late G2 (0.75 cycle). Protection persists for at least two cell cycles.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/22745/1/0000300.pd

Motion and twisting of magnetic particles ingested by alveolar macrophages in the human lung: effect of smoking and disease

BACKGROUND: Magnetic microparticles being ingested by alveolar macrophages can be used as a monitor for intracellular phagosome motions and cytoskeletal mechanical properties. These studies can be performed in the human lung after voluntary inhalation. The influence of cigarette smoking and lung diseases on cytoskeleton dependent functions was studied. METHODS: Spherical 1.3 μm diameter ferrimagnetic iron oxide particles were inhaled by 17 healthy volunteers (40 – 65 years), 15 patients with sarcoidosis (SAR), 12 patients with idiopathic pulmonary fibrosis (IPF), and 18 patients with chronic obstructive bronchitis (COB). The retained particles were magnetized and aligned in an external 100 mT magnetic field. All magnetized particles induce a weak magnetic field of the lung, which was detected by a sensitive SQUID (superconducting quantum interference device) sensor. Cytoskeletal reorganizations within macrophages and intracellular transport cause stochastic magnetic dipole rotations, which are reflected in a decay of the magnetic lung field, called relaxation. Directed phagosome motion was induced in a weak magnetic twisting field. The resistance of the cytoplasm to particle twisting was characterized by the viscosity and the stiffness (ratio between stress to strain) of the cytoskeleton. RESULTS: One week after particle inhalation and later macrophage motility (relaxation) and cytoskeletal stiffness was not influenced by cigarette smoking, neither in healthy subjects, nor in the patients. Patients with IPF showed in tendency a faster relaxation (p = 0.06). Particle twisting revealed a non-Newtonian viscosity with a pure viscous and a viscoelastic compartment. The viscous shear was dominant, and only 27% of the shear recoiled and reflected viscoelastic properties. In patients with IPF, the stiffness was reduced by 60% (p < 0.02). An analysis of the shear rate and stress dependence of particle twisting allows correlating the rheological compartments to cytoskeletal subunits, in which microtubules mediate the pure viscous (non-recoverable) shear and microfilaments mediate the viscoelastic (recoverable) behavior. The missing correlation between relaxation and particle twisting shows that both stochastic and directed phagosome motion reflect different cytoskeletal mechanisms. CONCLUSION: Faster relaxation and a soft cytoskeleton in patients with IPF indicate alterations in cytoskeleton dependent functions of alveolar macrophages, which may cause dysfunction's in the alveolar defense, like a slower migration, a retarded phagocytosis, a disturbed phagosome lysosome fusion and an impaired clearance