Document MKO3ZJDynvrRm6LNz0aBVDoV

7A i EFFIiCTS-HUMAN HEALTH 42920 lir- ccntiation or dost-, was linear on a logarithmic scale. The 42917 APTIC NO. (.6174 - -ptn JOS r7 O 'n ailal ICS ng as ct, nd at* i7 2 ny equivalent coneentiations and doses of benzene that pioduccd the same inversion of the chronaxia of the antagonistic muscles were found to be 240 mg/cu m and 16,000 mg/I; 120 mg/cu m and KU00 tng/l; 60 mg/cu m and 4000 mg/1; 30 mg/cu m and 2000 mg/1, and 15 mg/cu in and 1000 mg/I. Reduced blood cholinesterase activity, and reduction of the leukocyte, erythrocyte and hemoglobin levels were among the principal symptoms of benzene poisoning. The potentiation of the ef fects of high doses and concentrations of benzene, and the summation effect for lower doses and concentrations were determined, 42915 AFT1C NO. 66240 Chow, C. K., C. J. Dillard, and A, L. Tappel Eddy, T. P. COAL SMOKE AND MORTALITY OF THE ELDERLY. Nature (London), 25l(547l):t36-l38, Scpl. 13. 1974. 13 refs. Mortality from falls in old people is so closely related to mor tality from fractures of long bones, particularly of the prox imal femur, that it seems related to bone fragility. Common contemporary factors may affect mortality and possibly bone fragility for both sexes. Coal smoke may be one such factor. A statistical study was made on British mortality, and death rates from falls were correlated with death rates from bronchitis and domestic smoke pollution. Mortality from falls seemed to be related to domestic smoke pollution independently of the rela tionship to mortality from bronchitis. Since increased smoke he GLUTATHIONE PEROXIDASE SYSTEM AND levels decreased ultraviolet radiation, the effect of smoke on al it- LYSOZYME IN RATS EXPOSED TO OZONE OR NITROGEN DIOXIDE. Environ. Res., 7(3):3U-3I9, June mortality from falls and fractures may have been due to reduced endogenous synthesis by ultraviolet light. 1974. 30 refs. Exposure to rats to low concentrations of ozone (as low as 0.2 42918 APTIC NO. 66386 12 ppm) continuously for 8 days, or intermittently (8 hr/day) for 7 Freeman, Gustave, Laszlo T. Juhos, Nazzareno J. Furiosi, II. r7- days, significantly increased the activities of the glutathione (GSH) peroxidase system in lung tissue. Linear regression analysis showed the increased enzymic activities to be a func Rowena Mussenden, Robert J. Stephens, and Michael J. Evans PATHOLOGY OF PULMONARY DISEASE FROM EXPO tion of ozone concentration. Lysozyme activity was signifi SURE TO INTERDEPENDENT AMBIENT GASES 6. d. cantly increased in lung soluble and plasma, during continu ous, but not intermittent, 03 exposure. The results indicated (NITROGEN DIOXIDE AND OZONE). Arch. Environ. Health, 29(4):203-2l0, Oct. 1974. 27 refs. fs that lipid peroxidation damage occurred in lungs of rats ex Rats in exposure chambers were subjected to mixtures of a posed to relatively high levels of 03. Rats were exposed to nitrogen dioxide and ozone at levels reached in severe smog m relatively higher levels of nitrogen dioxide for 4 days. The ac and were subsequently examined histologically tor injury. The is tivities of GSH reductase and gluco$e-6-phosphatc major site of injury observed was at the level of the junction n dehydrogenase were significantly increased during exposure to of the respiratory bronchiole and the alveolar duct, somewhat .0 a d s 2.3 ppm and 6.2 ppm of N02, respectively. There was no sig nificant increase in the activity of GSH peroxidase in lung soluble, or of lysozyme in the plasma, during exposure to N02. The results suggest that the mechanism of action of N02 is different from that of 03. (Author abstract) more peripheral than the lesion caused by N02 alone. Ozone, the more toxic component, was largely responsible for the in jury at the selected concentrations and for the characteristic fibroblastic activity in that region. The observations suggested that potential injury from ambient smog resulted mainly from 03, whereas injury from tobacco smoke was due largely to its 7 42916 APT1C NO. 66438 relatively high concentration of N02. Smoking and residing in smoggy areas appear to be addilively injurious. (Author ab Dingeon, M. and Collombel stract modified) EVALUATION OF THE NUISANCES CAUSED BY >. ASBESTOS: ASBESTOS USED IN AUTOMOBILES. (Evaluation des nuisances provoquees par I amiante: cas 42919 Fukuie, Noriko APTIC NO. 66247 l de 1 amiante automobile). Text in French. Pollut. Atmos. (Paris), 16(62}:183-190, April-June 1974. 28 refs. BIOLOGICAL EFFECT OF HEAVY METALLIC CATALYST PARTICLES TO BE EXHAUSTED IN THF. i Toxicologic and epidemiologic data on asbestos in occupa AIR. (Jukinzoku shokubai biryushi no seibuisu ni tionally and spontaneously exposed subjects, and the hazards oyobosu eikyo). Text in Japanese. Nippon Jidosha Ken- Ti of asbestos as released by automobile brake linings are kyvjo Kenkyu Sokuho (Res. Lett. Japan Automob. fnst.), discussed. Lung fibrosis, bronchopulmonar cancer, as well as no. 19:63-69, March 1974. i pleural and peritoneal mesothelioma due to inhaled asbestos in Copper, chromium, iron, and aluminum catalysts were ad occupationally' exposed populations were determined. The ministered orally to rats over a 1-month period, followed by latency period of asbestos-induced cancer ranges from 15 to 20 examination of the interna! organs for metal distribution and years. Crocidolile and untophyllite are more powerful car pathological changes in an investigation of the toxicity of the cinogens than chrysolite. The irritation of the respiratory tract heavy metals. No pathological changes were observed, is essential for the formation of lung cancer by asbestos. The carcinogenic effect of different types of asbestos may be due to and be dependent of the presence of impurities, such as chromium.*iron, beryllium, magnesium, nickel, cobalt, and although the point of maximum accumulation rale was dif ferent between Cu and Cr among respective groups of rats. The results indicate that there may be an optimum absorbing concentration for each of the metals. manganese that are carcinogenic, as well as of traces of tar, mineral oil. and benzotalpyrene. The metafile impurities may 42920 APTIC NO. 66379 inhibit the benzotulpyrene hydroxylase activity. The increased Fukuta, Shinji, Toru Yamamoto, Takanari Tokuhisa, Junichi frequency of positive findings of screenings for asbestos m the Mise, and Urizo Fujii lungs p[ city dwellers indicates a minimum, though not nculiui- SERUM IGF LEVEL IN CHRONIC OBSTRUCTIVE hlc hazard, of a\bcsUwis due to asbestos released by brake LUNG DISEASES; WITH SPECIAL REFERENCE TO linings in occupationally" not exposed subjects'.~In~ Hus respect, BRONCHIAL ASTHMA. (Heisokusei bat shikkan ni drum brakes, rct.unlng worn-off asbestos particles practically okeru kcssci IgE chi-kikanshi zensokushorei o chushin to quantitatively inside the brake housing, are less hazardous shite). Text in Japanese. Nihon Kvobu Shikkan Gakkai than disc brakes which release all worn-off asbestos into the Zasshi (Japan. J. Thoracic Dis.), 12\7):386-39l, July 1974. atmosphere in nondenucured form. 24 refs. 93 FMSI-0161