Air pollution and fuel vapour induced changes in lung functions: are fuel handlers safe?

Automobile exhaust derived air pollutants have become a major health hazard. Coupled with the inhalation of fuel vapour, as occurs in petrol station workers, this may lead to significant impairment of lung function. Spirometric lung functions were studied in 58 petrol station workers to examine this possibility. The forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), forced expiratory flow 25%-75% (FEF25-75) and peak expiratory flow (PEF) were recorded and analysed separately for smokers and non-smokers. The workers were divided into 5 groups for analysis of data based on the number of years of work in the petrol pumps. Outdoor air analysis was also carried out. The FVC, FEV1 and PEF declined significantly with increasing years of work in petrol stations in both smokers and non-smokers. Smoking as an independent variable was found to affect the FEV1 significantly but not FVC or PEF. The FEF25-75 was found to be the most affected spirometric value with a significant reduction with increasing years of work. Smoking as such did not affect it. Oxides of nitrogen (NOx), suspended particulate matter (SPM) and particulate matter less than 10 microns (PM10) in outdoor air were higher than the national ambient air quality standards. Exposure to automobile exhaust and fuel vapour impairs lung function in a time-dependent manner. Cigarette smoking appears to accelerate the decline.

Vasovagal syncope: an enigma.

Syncope is a common clinical problem affecting 3.5% of the general population. About 40% of cases remain undiagnosed and 30% experience recurrent episodes. The article presents an update on the etiopathogenesis and theories of syncope. The pathophysiology of syncope remains elusive. Lewis introduced the term "vasovagal" implying therein that both vasodilatation and bradycardia were involved in the response. Individuals susceptible are unable to maintain adaptive neurocardiovascular responses to upright posture for prolonged periods of time. A complex hemodynamic response develops, with marked hypotension, bradycardia and a loss of consciousness. The "empty ventricle theory", first proposed by Sharpey - Schafer, widely accepted for several years, has been challenged and various other aspects of the vasovagal response have now been studied and implicated in contributing to the episode of unconsciousness. These include baroreflex dysfunction, neuro - endocrine responses, role of respiration and cerebrovascular dysfunction. An episode of syncope represents an episode of unconsciousness. Even a single episode of unconsciousness in the present day lifestyle is a source of distress to a patient, warranting a workup and diagnosis. The etiopathogenesis of the simple faint is complex and we may well be dealing with a constellation of responses and a more detailed classification than hitherto imagined.

OXYGEN TOXICITY.

Oxygen, the gas vital to sustain life, can also destroy it. It may become toxic at an elevated partial pressure, which may be the result of a rise in inspired oxygen concentration, an increase in environmental pressure or a combination of both. The toxicity tends to express itself most recognizably in one of several forms including central nervous system manifestations, pulmonary signs and symptoms and ocular effects, especially in premature infants. Other forms of toxicity should be expected in severe exposure but are difficult to detect and hence are not often considered important limitations for the use of oxygen. The onset and degree of the toxicity vary with the concentration of the gas used and the duration of exposure. Marked variations in individual susceptibility are found. Prevention of its occurrence and early detection of toxicity are called for, the treatment being symptomatic.

Calcium channel blockers and the CVS reflex responses during lower body suction.

Nine normal men (mean age 27.6 yr) were exposed to continuous lower-body suction pressure (LBSP) of -20 to -50 mmHg (for 5 min at each level) on four different occasions after having consumed a single oral therapeutic dose of either diltiazem, nifedipine, verapamil, or a placebo, randomly, in a single blind manner. The suction was applied at 12.30 pm in all experiments, while the medications were administered in such a manner so that their expected peak plasma levels would have been achieved at the time of suction application. The cardiovascular reflex effects commenced at a pressure of -30 mmHg, and peaked at -50 mmHg. The increases in the heart rate for all treatments at -50 mmHg was statistically similar (about 16-20 beats/min). The systolic BP fell by about 9 mmHg for the placebo experiments, and this change was not different from the changes produced by the 3 Calcium channel blocker treatments. The diastolic BP increase was about 3 mmHg. The Cardiac index did not vary significantly. Our results suggest that the commonly used Ca++ channel blockers do not adversely affect orthostatic tolerance.