Radionuclide-induced evolution of DNA and the origin of life.

Artesian groundwaters of high radionuclide concentration are ubiquitous and may have provided the large, sustained energy sources that were required to drive the multistage process of DNA and primordial cell evolution. The rapid, early development of the genetic code as well as its degeneracy can be attributed to exceptionally high radiation-induced mutation rates in this unique environment. The ability of double-strand DNA to direct enzymatic repair of radiation damage to single strands contributed importantly to its selective evolution. It is postulated that the polymerization of nucleotides took place at elevated temperatures within alpha-particle tracks of high ion and free-radical density, followed by rapid quenching to ambient conditions. It also is evident that radiation resistance and ploidy were important selection factors in cellular evolution.

alpha-Radiation dose at bronchial bifurcations of smokers from indoor exposure to radon progeny.

Synergistic interactions of indoor radon progeny with the cigarette smoking process have been evaluated experimentally. Smoking enhances the air concentration of submicron particles and attached radon decay products. Fractionation in burning cigarettes gives rise to the association of radon progeny with large particles in mainstream cigarette smoke, which are selectively deposited in "hot spots" at bronchial bifurcations. Because smoke tars are resistant to dissolution in lung fluid, attached radon progeny undergo substantial radioactive decay at bifurcations before clearance. Radon progeny inhaled during normal breathing between cigarettes make an even larger contribution to the alpha-radiation dose at bifurcations. Progressive chemical and radiation damage to the epithelium at bifurcations gives rise to prolonged retention of insoluble 210Pb-enriched smoke particles produced by tobacco trichome combustion. The high incidence of lung cancer in cigarette smokers is attributed to the cumulative alpha-radiation dose at bifurcations from indoor radon and thoron progeny--218Po, 214Po, 212Po, and 212Bi--plus that from 210Po in 210Pb-enriched smoke particles. It is estimated that a carcinogenic alpha-radiation dose of 80-100 rads (1 rad = 0.01 J/kg = 0.01 Gy) is delivered to approximately equal to 10(7) cells (approximately equal to 10(6) cells at individual bifurcations) of most smokers who die of lung cancer.

Polonium-210: lead-210 ratios as an index of residence times of insoluble particles from cigarette smoke in bronchial epithelium.

Lead-210 and its granddaughter polonium-210 are both natural constituents of cigarette smoke, the 210Pb being enriched in insoluble particles derived from sintered tobacco trichome tips. These particles are stripped of the polonium on combustion, and thus the polonium begins growth at the time of inhalation. Polonium-210 is found in bronchial tissues of smokers, and evidence shows that 210Pb is present at these sites in excess of the polonium. On the assumption that all polonium arises from ingrowth from the insoluble particles, one may calculate from the polonium-lead ratio the mean residence time of these particles. The half-life of polonium (138 days) is almost ideal for this purpose, and its alpha radiation makes measurements of very low concentrations possible. This technique is the first available to assess residence time for inhaled particles in the bronchial epithelium, an important datum because of the vulnerability of bronchial tissues to disease. Measurements from three smokers and two non-smokers show that 210Pb from natural aerosols also is concentrated at bronchial bifurcations, but little 210Pb is associated with this soluble lead. This fact makes estimates of residence time in bronchial epithelium of smokers (3-5 months in these preliminary data) likely to be low.

The sulfur cycle.

Even granting our uncertainties about parts of our model of the sulfur cycle, we can draw some conclusions from it: 1) Man is now contributing about one half as much as nature to the total atmospheric burden of sulfur compounds, but by A.D. 2000 he will be contributing about as much, and in the Northern Hemisphere alone he will be more than matching nature. 2) In industrialized regions he is overwhelming natural processes, and the removal processes are slow enough (several days, at least) so that the increased concentration is marked for hundreds to thousands of kilometers downwind. 3) Our main areas of uncertainty, and ones that demand immediate attention because of their importance to the regional air pollution question, are: (i) the rates of conversion of H(2)S and SO(2) to sulfate particles in polluted as well as unpolluted atmospheres; (ii) the efficiency of removal of sulfur compounds by precipitation in polluted air. And for a better understanding of the global model we need to know: (i) the amount of biogenic H(2)S that enters the atmosphere over the continents and coastal areas; (ii) means of distinguishing man-made and biogenic contributions to excess sulfate in air and precipitation; (iii) the volcanic production of sulfur compounds, and their influence on the particle concentration in the stratosphere; (iv) the large-scale atmospheric circulation patterns that exchange air between stratosphere and troposphere (although absolute amounts of sulfate particles involved are small relative to the lower tropospheric burden); (v) the role of the oceans as sources or sinks for SO(2).