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Perennial ryegrass plants (Lolium perenne L.) were exposed in "Closed-Top Chambers" to different ozone concentrations and to charcoal filtered ambient air to study the effect of ozone on the development of pollen. Ozone at ambient (65 nl l(-1), 8h) and elevated (110 nl l(-1), 4h) concentrations affected the maturing of pollen by inhibiting starch accumulation in pollen throughout the anther. Affected pollen persisted in the vacuolated state while normal pollen in the same anther were filled with amyloplasts. The percentage of underdeveloped pollen-determined in transversal sections-was significantly higher in exposed plants than in plants grown in filtered air. Results indicate that ozone stress was responsible for the disrupted development of pollen in L. perenne.

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An experimental procedure is described as a means for assessing the efficiency of skin-protecting measures against the vapors of hazardous substances. Bis(2-chloroethyl)sulfide (S-mustard) is used as the test substance. A continuous flow of S-mustard vapor is conducted through an exposure cell which is attached to the inner side of a rabbit's ear. From the difference in the concentrations measured before and behind the exposure cell, the absorption and the permeation rate of mustard into the skin is calculated. The skin damage, consisting of a reversible erythema, is quantified by measuring the optical transmittance of the exposed skin area during the following days and correlated with the respective absorption (dose) and exposure parameters (ct-product, with c = 3-50 ng/cm3 and t = 60 and 120 min). Reversible, i.e., completely healing, erythema are evoked by ct-products in the range of 250-2000 ng.min/cm3 corresponding to doses from about 0.1 to 1.1 micrograms/cm2. A comparison with older data reveals that human skin, in this respect, is about eight times more sensitive than the inner side of the rabbit's ear.

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The efficacies (ED50) of obidoxime and atropine against paraoxon poisoning in mice were determined by administering the antidotes 5, 20, 40 and 60 min before administration of the organophosphate. With increasing time intervals t between the administration of the antidote and paraoxon, the dose of antidote (ED50), that reduced the lethality of 2 LD50 of paraoxon to 50% increased. The standardized log ED50/t plot was linear and yielded the "efficacy half-life". In addition, the blood concentrations c of the antidotes were measured, resulting in a linear log c/t plot. The "efficacy half-life" was approximately twice the half-life of the antidote in blood. The possible reasons for this phenomenon are discussed.

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The functional set-up of a static inhalation device is described. The closed system consists of a reservoir for the circulating test gas, an inhalator for "nose-only" exposure of 10 rats, and analyzers for the test gas and CO2. It has an overall volume of 200 liters. The following LCt50 values for rats exposed to noxious vapors were determined: DFP 3629, sarin 191, and soman 211 mg X min X m-3. Pretreatment with atropine (10 mg/kg) together with the oximes Toxogonin or HJ6 (each 13 mg/kg) 10 min before the exposure raised the LCt50 of sarin by a factor of 2.5 and 14, respectively. In case of soman poisoning, only HJ6 (50 mg/kg) together with atropine was effective, which increased the LCt50 by a factor of 7.

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From human blood concentrates erythrocyte "ghosts" were prepared. These and an enzyme solution, obtained by Triton X 100 treatment of the ghosts, were reacted with 1.2.2-trimethylpropyl-methyl-phosphonylfluoridate (soman). The rate constants of inhibition of the membrane bound and solubilized acetylcholinesterase (AChE) were determined at 3 degrees C, pH 8 and 9 to be 2 X 10(7) and 1.4 X 10(7) mol-1 min-1, respectively. Ageing of the phosphonylated AChE occurred with rate constants of 3.5 X 10(-2) (ghost bound) and 1.3 X 10(-2) (solubilized) min-1 at 3 degrees C, pH 8. 5 X 10(-4) mol/l atropine decreased the ageing rate by 50%. Reactivation of the non aged phosphonyl-AChE by several pyridinium oximes was enhanced by atropine with the ghost-bound enzyme; the reactivation of the phosphonylated solubilized enzyme, however, was not affected by atropine.

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The rapid development of the natural sciences and the technical progress during the last century have significantly changed our society and environment. During this period the average life expectancy for people in industrialized countries has doubled. A prolongation of life expectancy to this extent, due to for example, understanding of the relationship between various diseases and their corresponding causative agents, had never before occurred in mankind's history. It resulted in specific hygiene precautions. The recognition of such causal relationship was facilitated by the fact that infection diseases generally become apparent after a short incubation time, i.e. that an environmental situation causes health damage. At present, we are searching for origins of diseases of which the causal correlations with environmental influences are far more difficult to recognize than those of infection diseases, since long-term effects have to be observed. Do we have a situation similar to that which we had for infections at the end of the last century ? For diseases such as lung and larynx cancer, there are significant indications of carcinogenic compounds in the environment. Since both types of cancer are about 10 times more common among cigarette smokers who inhale than among non-smokers, a correlation to the risk factor "smoking" is beyond doubt. Living and working in larger cities or highly populated areas are additional factors which many enhance the lung cancer incidence ("urbanisation factor"). The air quality of these areas is supposed to be the reason for this effect. However, the present "bad air quality" at most doubles the disease incidence. A large number of epidemiological studies report on local differences of the incidence rates as well as significant increases or decreases of the mortality rates for some cancer diseases during comparatively short periods. A summary recently has been published by Misfeld (1). As an example, the mortality rate due to lung cancer for males in the F.R.G. has almost doubled during 1955-1975 from 36.5 per 100,000 to 65.9 per 100,000. This holds true for cancer of the rectum which increased from 8.8 per 100,000 to 18.9 per 100,000 during the same period. In contrast, mortality due to stomach cancer decreased from 59.3 to 36.6 per 100,000 and uterine cancer in females decreased from 16.6. to 8.5 per 100,000 (2). The pronounced changes in mortality rates cannot be explained by alterations of the genetic disposition during such a short period. Improved diagnostic and therapeutic techniques might explain decreases but not increases of mortality rates.(ABSTRACT TRUNCATED AT 400 WORDS)

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The influence of pH and temperature upon the dealkylation (aging) of soman-inhibited acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) was investigated. The pH-rate profile, as measured at 5 degrees C, shows a maximum aging rate at pH 5.0 and indicates the involvement of two ionizable groups with pKa values of 6.0 and 4.5. The pH-rate profile was not changed essentially by the two effector compounds, semicarbazide and HH54. the activation energy of aging at pH 7.0 was determined as to 6.12 x 10(4) J/mol; it was lowered by the accelerator of aging semicarbazide to 5.28 x 10(4) J/mol and increased to 9.42 x 10(4) J/mol by the retarding compound HH54.

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By a standard screening in vivo, a series of pyridinium salts were tested for their protective activity against organophosphate poisoning. In order to obtain information about the protective mechanisms, several biochemical properties of these compounds were investigated in vitro, viz., their influence upon the enzymes cholineacetyltransferase and acetylcholinesterase (AChE), reactivation and aging of phosphylated AChE, protection of AChE against phosphylation and their 'direct reaction' with the phosphylating agent. Both in vitro and in vivo several significant structure-activity relationships exist, which in some cases can be correlated, thus allowing an interpretation of the in vivo results on a biochemical basis. Thus the reactivating potency of bispyridinium-4-aldoximes towards diethylphosphoryl-AChE correlates well with the corresponding in vivo results when these compounds are used as antidotes against paraoxon poisoning. In the case of a treatment of soman poisoning the vivo results with a homologous series of oxime-free bispyridinium salts shows a reasonably good correlation with their protective action in vitro. The protective mechanisms of bifunctional bispyridinium monooximes remain uncertain. Several approaches to clarifying this question are discussed in detail.

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The influence of 27 possible effectors, mostly bispyridinium salts, upon the dealkylation (aging) of soman-inhibited acetylcholinesterase (acetylcholine hydrolase, EC 3.1.1.7) was examined at pH 7.6 and 25 degrees C. In the absence of effectors, the rate constant of the aging process was 4.0. 10(-2) min-1. At 2 mM, the strongest inhibitor reduced the rate to 0.8. 10(-2) min-1, whereas it was raised to 8.2. 10(-2) min-1 by the most potent accelerator.

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Mono-quaternary salts Z have been prepared from pyridine-aldoximes and 1,3-dihalogen compounds. These were used to synthesize asymmetrical bis-quaternary pyridine-oximes with three-membered bridge. The effect of reactivation of phosphorylated AChE by these substances is less than that of obidoxim (Toxogonin).

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