[Aviation fuels and aircraft emissions. A risk characterization for airport neighbors using Hamburg Airport as an example]. / Flugzeugtreibstoffe und Flugzeugemissionen. Eine Risikocharakterisierung für Flughafenanwohner am Beispiel des Hamburger Flughafens.

Aviation fuels are well characterised regarding their physical and chemical properties. Health effects of fuel vapours and of liquid fuel are described after occupational exposure and in animal studies. Exposure of the general population (airport visitors and people living in the vicinity of airports) may occur during fuel supply particularly in warm summers (odour). Aircraft emissions vary with the engine type and the kind of fuel. Combustion of aviation fuel results in CO2, H2O, CO, C, NOx and a great number of organic compounds. Among the emitted polyaromatic hydrocarbons (PAH) no compound characteristic for jet engines (tracer) could be detected so far. Hardly any data exist on the toxicology of jet engine emissions. According to analyses of their chemical composition, however, they contain various toxicologically relevant compounds including carcinogenic substances. Measurements in ambient air around the Hamburg Airport show no elevated pollutant levels. However, no such data exist on aldehydes, black smoke or fine particles. Annoying odours have been stated in some areas around the airport, which were mainly attributed to the aircraft engine emissions rather than to fuel vapours.

Human risk assessment of carcinogens from an administrative perspective.

For evaluation of the carcinogenic potency of an environmental chemical or a mixture of chemicals, epidemiological or workplace studies, animal studies, and in vitro tests are the three major strategies used. Asbestos fibers and 1,2-dichloroethane are chosen as examples. They illustrate that the strategies may enable the implementation of measures by health authorities.

Effects of toxin isolated from the sea anemone Bolocera tuediae on electrical properties of isolated rat skeletal muscle and cultured myotubes.

Electrophysiological effects of a polypeptide toxin isolated from the sea anemone Bolocera tuediae (BTTX II) on isolated fast and slow rat skeletal muscle and on cultured rat myotubes are described in this paper. Nanomolar concentrations of BTTX II cause a concentration-dependent depolarization. This effect is prevented by the presence of tetrodotoxin. Action potential duration is prolonged in all preparations investigated, with the fast muscle being the least sensitive. The positive overshoot and the maximum rate of rise of the action potential is decreased by BTTX II. Cultured myotubes which are less susceptible to the sodium channel blocking activity of tetrodotoxin have the highest sensitivity to all actions of BTTX II. It is further shown that the proportion of spontaneously contracting myotubes is diminished and the frequency of contractions is increased by the toxin. The effects of Bolocera tuediae toxin II resemble those observed with Anemonia sulcata toxin II on mammalian skeletal muscle. From the results it is concluded, that BTTX II may interfere with both the activation and inactivation of sodium channels of the muscle membrane.

Cultured myotubes from skeletal muscle of adult rats. Characterization and action of Anemonia sulcata toxin II.

Mononucleated myogenic cells (satellite cells) were isolated from skeletal muscle of adult rats and grown in culture. These cells replicated and, beginning with the 6th day in culture, they fused and differentiated into multinucleated myotubes, which accumulated creatine kinase and developed cross striation and spontaneous contractions. The differentiation of the excitable membrane and the action of sea anemone toxin ATX II were investigated with microelectrode techniques. Mature myotubes reached a stable membrane potential of -47.3 mV (+/- 6.5 mV) with the 11th day in culture. Action potentials could be generated in all myotubes. During maturation they became faster (increasing rate of rise) and shorter in duration. In spontaneously contracting myotubes spontaneous action potentials were recorded, which were often associated with subthreshold oscillations of membrane potential. ATX II reduced the membrane potential and prolonged the action potential duration with the lowest effective concentrations being 1 nmol/l and 0.5 nmol/l, respectively. Furthermore, ATX II induced electrical activity in quiescent myotubes. After fusion the development of the membrane electrical properties of satellite cell derived muscle cells followed essentially the same pattern as in primary cultures of embryonic myotubes. Electrophysiologically and with respect to their sensitivity to ATX II the mature myotubes resemble denervated muscle fibres.

The effects of Anemonia sulcata toxin II on vertebrate skeletal muscle.

Some effects of the sea anemone toxin, ATX-II, on vertebrate skeletal muscle have been described. At a concentration of 1 X 10(-7)-1 X 10(-6)M, ATX-II caused a sodium-dependent depolarization of the muscle fibres of the rat soleus and extensor digitorum longus, of the mouse soleus and extensor digitorum longus and of the chicken posterior latissimus dorsi. The muscle fibres of the frog sartorius were insensitive to the toxin. Action potentials generated by direct stimulation were prolonged by ATX-II, but the degree of prolongation was variable. Chicken posterior latissimus dorsi muscle fibres were most sensitive in this regard, and mouse extensor digitorum longus were least sensitive. Both denervated and immature muscle fibres were more sensitive to ATX-II than mature innervated muscle fibres. The sensitivity to ATX-II declined rapidly as muscle fibres matured. In some muscles, the prolongation of the action potential was enhanced by repetitive stimulation, but not by the passive depolarization or hyperpolarization of the muscle fibres. The actions of ATX-II could be reversed by washing in all but the innervated soleus of the mature rat.

Effects of sea-anemone toxin (ATX-II) on the frequency of miniature endplate potentials at rat neuromuscular junctions.

Soleus and extensor digitorum longus muscles were isolated from rats. The muscles were exposed to ATX-II, a toxin isolated from extracts of the sea-anemone Anemonia sulcata . The toxin caused a dose-dependent increase in the frequency of miniature endplate potentials in both types of muscle. The increase in frequency could be reversed by the application of tetrodotoxin (TTX), and could be prevented by prior exposure of the muscles to TTX. It is concluded that ATX-II causes a sodium-dependent depolarization of the nerve-terminal membrane.

Venom of the Australian rough-scaled snake, Tropidechis carinatus: lethal potency and electrophysiological actions.

A series of experiments to define the lethal potency (LD50) and electrophysiological properties of the venom of the Australian Rough-scaled Snake (Tropidechis carinatus) are described. Crude pooled venom contains at least five fractions which were separated using liquid chromatography and high pressure liquid chromatography techniques (Fractions I-V). LD50 studies are reported using each of these fractions, with data for both adult and neonatal mice. Fraction I (mol. wt greater than 100,000) was essentially non-toxic. Fraction IV (mol. wt less than or equal to 10,000) and Fraction V (mol. wt less than 1,000) were potent toxic components with LD50'S (s.c. injection; fraction in 0.1% bovine serum albumin and 0.85% saline; neonatal mice) of 0.04 mg/kg and 0.06 mg/kg respectively. LD50'S for the whole crude venom were similar in both adult and neonatal mice. Electrophysiological studies using a Bulbring preparation (rat isolated phrenic nerve-hemidiaphragm) indicated that Fractions I, IIa and IIb were inactive. Fraction IV (mol. wt less than or equal to 10,000) caused rapid neuromuscular blockade which appeared to be irreversible. Neurophysiological experiments with a rat isolated extensor digitorum longus muscle preparation suggested that the major toxic activity of the whole venom resides in Fractions III and IV, and that both of these fractions have presynaptic and postsynaptic action.

Mechanical and electrophysiological effects of sea anemone (Anemonia sulcata) toxins on rat innervated and denervated skeletal muscle.

1 Some effects of the sea-anemone toxin ATX-II on mammalian nerve-muscle preparations have been described. 2 When ATX-II (10(-8)-10(-6) M) was applied to rat hemidiaphragm preparations, both directly and indirectly generated twitch responses were potentiated and prolonged. At the same time the resting tension of the preparations increased. 3 The increase in resting tension caused by ATX-II in innervated muscles was not prevented by curarization, but was reversed by exposure to tetrodotoxin. The increase in denervated muscles was not completely reversed by tetrodotoxin. 4 At concentrations exceeding 1 x 10(-7) M, ATX-II caused a sodium-dependent depolarization of both normal and denervated muscles. The depolarization of the denervated muscles was only partially reversed by tetrodotoxin. 5 In the presence of ATX-II repetitive endplate potentials (e.p.ps) were evoked by single shocks to the motor nerves in many fibres, and in those in which a single e.p.p. was still observed, the quantum content (m) was increased. Miniature e.p.p. frequency was not increased by ATX-II, even when muscle fibres were depolarized by 30 mV. 6 The indirectly and directly elicited action potentials of normal and denervated muscle fibres were much prolonged by ATX-II. The action potentials remained sodium-dependent. The sodium-dependent tetrodotoxin-resistant action potential of the denervated muscle fibre was also prolonged by ATX-II. 7 It is concluded that ATX-II both activates, and delays inactivation of, sodium channels in mammalian skeletal muscle fibres, probably in interacting with the channel "gate'.