Background noise due to random thermal perturbations of molecules has a disruptive effect on all information handling systems, including cells and organisms. This thermal noise appears to be largely responsible for the spontaneous loss of proliferative cells in cell cultures. The rates at which proliferative cells are lost as a result of heat injury, in cultured hamster cells, have been measured at high temperatures and extrapolated down to 37 C. This gives an expected 0.2% loss per hour due to thermal injury at physiologic temperature. That such a loss does in fact occur can be shown by comparing cell generation time with population doubling time, when these cells are growing at physiologic temperatures. Apparently, internal thermal noise presents a primary hazard to the reliable functioning of the cell quite apart from the insults it receives from its external environment.

Animals↗

PubMed1972

Thermal injury due to normal body temperature.

BY MEASURING THE RATES OF THERMAL INJURY OF HAMSTER CELLS IN CULTURE AT VARIOUS TEMPERATURES WE HAVE FOUND THE FOLLOWING: (1) The number of cells surviving heat injury declines exponentially with time with a characteristic rate constant for each temperature. (2) The temperature dependence of the rate constant follows an Arrhenius law from 46 through 41 C. (3) Extrapolation of the Arrhenius curve to 37 C indicates that over 0.2% of cells are irreversibly lost from the proliferating population each hour as a result of heat injury due to physiologic temperature. (4) The effective activation energy for the thermal destruction of the proliferative capacity of a cell is only 8 eV, which is equivalent to the rupture of less than 50 hydrogen bonds. (5) It is possible to calculate from the Arrhenius law the theoretic upper temperature limit for growth of a cell population. For the cells used in this study, the theoretic limit is 40.6 C.

Animals↗

PubMed1971

DDT in the biosphere: where does it go?

The worldwide pattern of movement of DDT residues appears to be from the land through the atmosphere into the oceans and into the oceanic abyss. Calculations based on the fragmentary data available on. rates of movement and sizes of various pools of DDT residues lead to the conclusion that concentrations in the atmosphere and in the mixed layer of the oceans lag by only a few years behind the amounts of DDT used annually throughout the world. A model suggests that maximum concentrations of DDT residues occurred in air in 1966 and will occur in the mixed layer of the oceans in 1971. The biota probably contains in total less than 1/30 of 1 year's production of DDT during the mid-1960's, a very small amount in proportion to the total potentially available. The reason for the biota's failure to absorb larger quantities and to be affected much more severely is unclear. The analysis suggests that mere good fortune has protected man and the rest of the biota from much higher concentrations, thus emphasizing the need to determine the details of the movement of DDT residues and other toxins through the biosphere and to move swiftly to bring world use of such toxins under rational control based on firm knowledge of local and worldwide cycles and hazards.

Air Pollution↗

PubMed1971