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We examined the effects of three forms of host plant resistance in tomato, Lycopersicon esculentum, on the potato aphid, Macrosiphum euphorbiae. Mi-1.2, a resistance gene (R-gene) in tomato that deters aphid feeding, reduced the population growth of both potato aphid isolates tested, although it appeared to have a greater impact on isolate WU11 than on isolate WU12. The results suggest that there may be quantitative differences in virulence between these two aphid isolates. We also examined two distinct forms of acquired resistance in tomato, jasmonic acid (JA)-dependent and salicylic acid (SA)-dependent induced defenses. Exogenous foliar application of JA triggered expression of a JA-inducible proteinase inhibitor in tomato cultivars with and without Mi-1.2, although the effects of treatment on aphid performance differed between these cultivars. JA-treatment reduced aphid population growth on a susceptible tomato cultivar that lacks Mi-1.2, but did not significantly enhance or inhibit aphid control on a near-isogenic resistant tomato cultivar that carries this gene. Foliar application of an SA analog, benzothiadiazole (BTH), was used to induce SA-dependent defenses. BTH treatment reduced the population growth of both aphid isolates on a susceptible tomato cultivar, and also enhanced aphid control on a resistant cultivar. The results indicate that both SA- and JA-dependent acquired resistance in tomato have a direct negative effect on a phloem-feeding insect. Furthermore, this study demonstrates that acquired resistance and R-gene-mediated resistance can interact for enhanced suppression of insect herbivores.

Methylcyclopentadienyl manganese tricarbonyl (MMT) is effective in raising the octane level of gasoline and is currently used in Canada for that purpose in a maximal concentration of 18 mg Mn/l (slightly less than 0.07 g Mn/U.S. gal). It has been estimated that if MMT were used in all U.S. gasoline in these amounts, the median increase of Mn in ambient air would be not more than 0.05 microgram Mn/m3, with increments generally less than 0.5 microgram Mn/m3 along urban corridors. The scientific literature was reviewed to determine how the increases in environmental manganese predicted from MMT use would relate to the amounts in the natural environment and necessary to life and to the concentrations associated with toxic effects. Even with additional manganese from the use of fuel additives, total Mn intakes would remain within the range of average amounts absorbed from food and water. Respirable manganese in ambient air due to MMT combustion would be many order of magnitude below the concentrations associated with occupational manganism and respiratory problems and also below those reported in isolated episodes of respiratory symptoms in communities near ferromanganese plants. Evidence was reviewed on the possibilities of: (1) increased absorption of inhaled manganese compared with ingested manganese; (2) hypersusceptibility of infants and persons of advanced age; and (3) increased absorption associated with iron deficiency. While relevant to high levels of exposure, these factors would not be expected to lead to toxic effects from the very low concentrations of Mn resulting from MMT use. Experimental animals that inhaled the combustion products of MMT in concentrations of approximately 10, 100, and 1000 micrograms Mn/m3 for 9 mo did not show toxic effects, although there was temporary elevation of tissue levels of Mn. Rhesus monkeys, susceptible to the neurologic effects of Mn, showed no symptoms after inhaling the combustion products of MMT in concentrations of 100 micrograms Mn/m3 for up to 66 wk. Monkeys exposed to 5000 microgram Mn/m3 also showed no symptoms. There is thus a wide margin of safety between the intakes of Mn essential to health and the high concentrations that have been associated with toxic effects. The small amounts of manganese added to the environment by the combustion of MMT used as a fuel additive would be comparable to the normal background and should not create health problems.

The occurrence of several outbreaks of illness among workers handling castor bean pomace at eastern seaports in 1958 and 1959 led to an investigation of the toxicity of a number of commercial preparations. The conventional hemagglutination test and a toxic assay were used to study 14 commercial samples. The agglutination activity may be destroyed by heat without complete destruction of the toxic activity. Four of the samples collected were as toxic as the ricin sample used as the bioassay standard. In view of the potency of the toxin, ricin, and the failure of the agglutinating activity to correlate with the toxic properties of the samples, it is recommended that a toxin assay such as described in this paper be used to evaluate commercial preparations.

The effect of protein insufficiency on immune responsiveness was investigated in inbred mice fed isocaloric diets low and normal in protein. Mice were tested for aberrations of cell-mediated and humoral immunities. Protein insufficiency enhances cell-mediated immunity while depressing or not affecting humoral immunity. Cell-mediated immunity was enhanced in testing: allogeneic skin graft rejection, spleen cell responsiveness to phytohemagglutinin, the graft-vs-host reaction, macrophage function, and resistance to viral and bacterial infections.

A review of chest films from 152 workers who had been employed five or more years in perlite mining or processing showed none with small opacities of profusion 1/0 or higher. There were 14 films with doubtful changes (0/1), but these showed no correlation with type or duration of employment. Pulmonary function was measured in 122 current employees from the same plants. Multiple regression analysis showed no significant association between years of employment in perlite and either forced vital capacity (FVC) or forced expiratory volume (FEV1). There was a significant association between pack-years of cigarettes and both measurements. In 66 workers tested in 1975 and again in 1983, there was an average annual decrease in FVC of 32 mL, with 26 mL predicted by the Knudson formula, which is based on nonsmokers. The average annual decrease in FEV1 was 24 mL with 26 mL predicted. Comparison of groups with differing smoking patterns showed that the decreases in both FVC and FEV1 were associated with smoking. The 28 men who had added four or more pack-years in the interval between tests showed decreases in FVC and FEV1 of 44 mL/year and 31 mL/year, respectively, with 26 mL/year predicted for both groups. Those with less than four added pack-years (which included 26 nonsmokers) had decreases in FVC and FEV1 of 23 mL/year and 19 mL/year with 26 mL/year and 27 mL/year predicted.

Several experiments conducted by our group over a period of 6 years have shown that nutritional stress, especially protein and/or calorie deprivation, leads to many, often dramatic, changes in the immune responses of mice, rats, and guinea pigs. Chronic protein deprivation (CPD) has been shown to create an enhancing effect on the cell-mediated immune responses of these animals. Humoral responses under CPD conditions were most often found to be depressed, but sometimes were unaffected, depending on the nature of the antigen employed. Chronic protein deprivation, consistent with the pattern just mentioned, improved tumor immunity by depressing production of B-cell blocking factors, and, in at least one instance, resistance to development of mammary adenocarcinoma in C3H mice was associated with evidence of increased numbers of T suppressor cells. Profound nutritional deficits (less than 5% protein per total daily food intake) depressed both cellular and humoral immunity. Early, though temporary, protein deprivation caused a long-term depression of both cellular and humoral immunity also, with the humoral component being the first to recover. Manipulation of protein and calories was found to have a profound effect on certain autoimmune conditions. Diets high in fat and low in protein favored reproduction but shortened the life of NZB mice, whereas diets high in protein and low in fat inhibited development of autoimmunity and prolonged life. Chronic moderate protein restriction permitted NZB mice to maintain their normally waning immunologic functions much longer than mice fed a normal protein intake. Further, the low-protein diet was associated with a delay in development of manifestations of autoimmunity. Decreasing dietary calories by a reduction of fats, carbohydrates, and proteins more than doubled the average life span of (NZB X NZW)F1 mice, a strain prone to early death from autoimmune disease. Histopathologic studies using immunofluorescent microscopy revealed that the development of the renal lesions caused by the deposition of antigen-antibody complexes, which is so characteristic of these mice, was markedly delayed.