Low frequency noise and stress: bronchitis and cortisol in children exposed chronically to traffic noise and exhaust fumes.

A correlation of respiratory diseases to traffic related air pollution and noise was observed in an interview study. Since in that study the exposure was subjectively assessed, in the present field study nitrogen dioxide as indicator for vehicle exhausts and the mean night-time noise level were measured outside the children's windows in representative locations. Based on these measurements each child was placed in one of the following categories: low, medium or high traffic immission (ambient emissions). The physician contacts due to bronchitis of 68 children were assessed retrospectively from the files of the participating paediatricians. Saliva samples were collected from all children and the cortisol concentration was estimated. Children under high noise exposure (L(night, 8h) = 54-70dB(A)) had in comparison to all other children significantly increased morning saliva cortisol concentrations, indicating an activation of the hypothalamus-pituitary-adrenal (HPA) axis. Analysing a subgroup of children without high noise exposure showed, that children with frequent physician contacts due to bronchitis did not have increased morning saliva cortisol. However, multiple regression analysis with stepwise exclusion of variables showed that bronchitis was correlated more closely to morning salvia cortisol than to traffic immissions. On the other hand, the rate of physician contacts due to bronchitis increased in a dose dependent manner and significantly with increasing traffic immissions. From these results it can be concluded that high exposure to traffic noise, especially at nighttime, activates the HPA axis and this leads in the long term to an aggravation of bronchitis in children. This seems to be more important than the effect of exhaust fumes on bronchitis symptoms. The results of the present study should be subjected to further investigation using specially designed studies.

Respiratory and dermatological diseases in children with long-term exposure to road traffic immissions.

The pathogenesis of allergies can be stimulated by adjuvant effects--i.e. air pollutants such as NO(2) and particles from diesel exhausts as well as noise--the latter especially during night-time. During sleep, noise signals which are associated with danger (i.e. lorry noise) have the potential to trigger stress reactions even if the noise level is low. Increases of cortisol in the first half of the night seem to play an important role. In a blind interview study, the combined effects of chronic exposure to traffic related air pollution and noise, upon the risk of skin and respiratory diseases in children were studied. All children between 5-12 years, who had consulted one of two participating paediatricians were included in the study. The paediatricians diagnoses of 400 children were analysed together with their parents answers regarding the density of road traffic on their street and several confounding factors. Multiple regression analyses resulted in relative risks of asthma, chronic bronchitis and neurodermitis, which increased significantly with increasing traffic load. A comparison with the literature on such effects caused by air pollution alone, showed that traffic noise during the night might have an adjuvant effect on the pathogenesis of the mentioned diseases.

A method for simultaneous evaluation of drug-effects on excitability and inotropy in isolated cardiac preparations.

A method is described which allows determination of the threshold of excitability of electrically stimulated, regularly contracting isolated cardiac preparations. The force of the contraction (CF) is isometrically recorded and serves as feed-back signal indicating effective stimulation. The pulse intensity is decreased monoexponentially as long as contractions are elicited. If the mechanical response does not occur, the pulse intensity is immediately reset to the initial high value and the pulse is delivered with a latency of a few milliseconds. A stimulus intensity just below threshold is recorded as the rectangular pulse threshold (RPT). The method was applied in order to compare the effects of a number of antiarrhythmic drugs including the beta-blocker propranolol on the electrical excitability (1/RPT) and on the contractility of guinea pig left atria stimulated at 3 Hz. In general, the drugs depressed excitability and contractility concomitantly. The rank order of potency with respect to the reduction of excitability was: aprindine greater than propafenone greater than propranolol greater than quinidine greater than mexilitine greater than lidocaine. The Ca-antagonist verapamil reduced contractile force most powerful but had no effect on excitability. Presumably, RPT reflects sodium-channel function. In conclusion, the described method offers an easily operable test of drug effects on the excitability threshold and the contractility of isolated cardiac preparations.

Essential hypertension versus secondary hypertension: discrimination by intracellular electrolytes.

Intracellular activities of sodium and calcium were determined in red blood cells in a group of 106 patients, consisting of essential and renal hypertensives and of normotensives with and without renal insufficiency. Calcium and sodium activities were elevated in essential hypertensives as compared to hypertensives suffering from renal insufficiency. Compared to normotensives without renal insufficiency higher sodium and calcium activities were measured in normotensives without renal impairment. Thus the results suggest that the determination of intracellular electrolytes might be a useful tool for the distinction of secondary hypertension. Furthermore, as yet unidentified humoral factors produced in the kidney might be involved in the regulation of the blood pressure, as a decrease in production of these hypothetic humoral factors (following the destruction of renal tissue) could be the cause for the changes in electrolyte composition.

Intracellular chloride in essential hypertension.

In 25 patients with untreated essential hypertension and 25 healthy controls, erythrocyte intracellular Cl- concentration and activity as well as Na+ activity were measured. Intracellular Cl- concentration in essential hypertensive patients was 70.6 +/- 11.3 as compared with 84.4 +/- 9.5 mmol/l in the controls (P less than 0.001). Intracellular Cl- activity was 77.5 +/- 13.0 mmol/l of cell water in hypertensive patients, the control value being 100.8 +/- 11.0 mmol/l of cell water (P less than 0.001). In the hypertensive group intracellular Na+ activity was 14.3 +/- 4.1 as compared with 7.1 +/- 1.8 mmol/l of cell water in the normotensive group (P less than 0.01). From these results it is suggested that in essential hypertension not only disturbances of cation metabolism, but also of anion metabolism, occur. Possibly the Cl- changes reflect a decreased Cl- inward transport due to an altered Na-K cotransport.

Humoral factors in the pathogenesis of primary hypertension.

In 42 spontaneously hypertensive rats of the Münster strain either parabiosis or cross circulation with normotensive Wistar Kyoto rats was performed. Cross circulation was made through the common carotid arteries and external jugular veins using a peristaltic pump. In parabiosis and in cross circulation experiments hypertension was transmitted from the spontaneously hypertensive rats to normotensive rats. Nephrectomy or adrenalectomy in the spontaneously hypertensive rat before cross circulation abolished this effect. After volume depletion in the hypertensive animals hypertension was not transmitted either. It is concluded that humoral factors causing vasoconstriction play an essential role in the development of hypertension in the spontaneously hypertensive rat.