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Wenceslaus Murape
Respiratory exposure to hazardous dust can cause pneumoconiosis, a disease that is not curable once it sets in, since the lungs become fibriotic and cannot effectively carry out gas exchange of oxygen into the blood and expelling carbon dioxide from it.
Positive indications on patient assessment are shortness of breath and a chest X-ray may show a characteristic patchy, subpleural, bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing.
In Zimbabwe, workers who work in dusty environments have for long been hoodwinked by employers that taking a pint of milk per day can prevent pneumoconiosis, which is not true.
Once the disease sets in, it will have to be managed for the rest of one’s life. Continual exposure to hazardous dust is associated with certain dusty environments in some industries.
Throughout the world, legislation has been promulgated to assist in the control of human exposure to work-related dust.
In Zimbabwe, the Pneumoconiosis Act Chapter 15:08 seeks to protect those working in dusty occupations from the danger of contracting the disease.
An idea that is still prevalent in Zimbabwe from the early 1970s is that copious consumption of milk removes inhaled dust from the lungs.
The milk became a benefit for workers as it is supplied free at work and sometimes the workers take excessive milk home, which benefits the family.
Industrialists have been happy to bear the cost of providing milk to employees. It is cheaper than having to engineer dust out of the workplace.
Pneumoconiosis cases increased tremendously in the early 1980s to the point that the International Labour Organisation was persuaded to donate a mobile industrial clinic equipped with an X-ray machine to the Ministry of Labour and Social Services and later the National Social Security Authority to monitor pneumoconiosis in Zimbabwe.
The explosive increase in pneumoconiosis cases matched the increase in milk consumption in industry, thereby exposing the fallacy of milk being an antidote for pneumoconiosis.
The fallacy remains so entrenched that many workers, even the enlightened ones, believe that milk has the ability to dislodge inhaled dust.
The basis of this belief is difficult to understand, because physiologically there is nothing to suggest that milk can do this. The route that milk, or any other liquid or food for that matter, takes is through the mouth, down the esophagus (gullet) to the stomach, where the digestion of its protein begins.
The rest of the milk constituents are digested in the small intestines, where protein, fat and sugar are absorbed into the body. Its water content is further absorbed down in the large intestines.
This is not the route taken by a dust particle inhaled in the body. Therefore, the reversal of inhaled dust by swallowing milk is physiologically impossible.
When a person takes a breath, air is drawn in through the nares into the nasopharynx and trachea, then to the conducting system of the lungs. From there it reaches the alveoli (air sacs) by way of various bronchioles and arterial ducts.
Most of the surface of a healthy subject is lined with a film of mucus which is continuously propelled upwards by ciliary action. The velocity of the inhaled air continually slows down so that by the time it reaches the terminal bronchioles, the flow rate is no more than two or three centimeters per second.
The deposition of inhaled particles and the effects of inhaled gases are influenced by the chemical properties of the inhaled agent and by sundry host factors.
The physical properties of importance are size and density, shape and penetrability, surface area, electrostatic charge and hydroscopicity (affinity for water).
Among the more important chemical properties influencing the respiratory tract’s response are acidity and alkalinity of the inhaled agent and its ability to enter into combination with the body constituents.
The respiratory tract is divided into three regions: the nose and extrahopracic airways that extend to the glottis; the conducting airways, that is the dead space or trachea and bronchi to the terminal bronchioles; and the pulmonary parenchyma, where gas exchanges take place.
The nose is an efficient filter and large particles are deposited there. Some small particles reach the dead space, while even smaller particles, called the respirable fraction, of size 0,6 to 6 microns reach the parenchyma, although many of these are deposited in the nose and dead space as well.
Particles sized 0,5 and 2,5 microns are deposited in the alveoli. It is these mi9nute dust particles that cause pneumoconiosis.
It has been shown that an atmospheric concentration of 500 000 particles per millilitre is necessary for every alveoli to receive at least one particle. This is quite heavy and uncommon at work.
The general low level of the dust load in the ambient air of the work environment partly explains the long period of exposure before signs and symptoms of pneumoconiosis manifest themselves.
Host factors in responding to deposited dust particles are divided into genetic, environmental and acquired. The lung defences include ciliary clearance, humoral antibody formation and other factors which may be compromised by the hereditary factors.
The rate of clearance is genetic and immutable for life. Lung defences may be modified by environmental factors, including pollutants, cigarette smoking, drugs, excessive cold and other non-specific factors.
Macrophage (immune system) function, mucociliary clearance and smooth muscle sensitivity may all be affected by extraneous influences. Particles deposited in the dead space are propelled upwards to the nasopharynx, where they are swallowed or spat out.
A normal person produces about 50 to 150ml of mucus daily, which is used to expel particulate matter and other materials. Older people have a slower rate of particulate matter expulsion.
Particles deposited in the alveoli are phagostised (enveloped) by macrophage (large bacteria like cells of the immunity system) and transported to the upper regions (dead space) for expulsion or to the interstitial lung tissue where the macrophage dies, leaving the particles to scar the site of settlement. This is the start of pneumoconiosis.
The practice of giving milk to workers in dusty occupations has no merit in the prevention of pneumoconiosis, since a dust particle inhaled into the body takes a different route from that taken by swallowed milk.
It actually has the opposite effect of promoting pneumoconiosis, as workers remove dust masks because of the false sense of safety from the milk they take.
Online Reporter