Category Archives: Environmental medicine

Sick building syndrome

The World Health Organization has defined the sick building syndrome as an excess of work-related irritation of the skin and mucous membranes (usually eyes, nose and throat) and other symptoms including headache, fatigue and difficulty in concentrating reported by workers in modern office buildings.
In 25% of cases a specific cause has been found, such as contamination of humidification systems, but in the remainder the symptoms have been attributed to reduced rates of ventilation with outdoor air. Increasing the supply of outdoor air does not, however, lower affected workers perception of their environment and some of the symptoms of this syndrome may well be psychological in nature.

Motion sickness

This common problem, particularly in children, is caused by repetitive stimulation of the labyrinth of the ear. It occurs frequently at sea and in cars, but may occur on horseback or on less usual forms of transport such as camels or elephants. Nausea, sweating, dizziness, vertigo and profuse vomiting occur, accompanied by an irresistible desire to stop moving.

Prophylactic antihistamines or vestibular sedatives (hyoscine or cinnarizine) are of some value.

Ultraviolet light

Ultraviolet (UV) light consists of UVB (wavelength 290-320 nm) and UV A (320-400 nm). Wavelengths 100- 290 nm are stopped by the ozone layer.
• UVB causes sunburn.
• UV A and UVB cause skin ageing and skin cancer. Sunscreens absorb UV energy but many preparations only absorb UVB.
The sun protection factor (SPF) is a guide  on the sunscreen performance, but there is no worldwide standard and often the protective effect is only against UVB. With a normal skin, a water-resistant sunscreen of 8-10 containing p-aminobenzoic acid is recommended to avoid sunburn.

Drowning and near drowning

Drowning is a common cause of accidental death, accounting for over 100000 deaths annually worldwide. Approximately 40% of drownings occur in children under 5 years of age. Exhaustion, alcohol, drugs and hypothermia all contribute to the overall problem. In addition, drowning can also occur following an epilepticr attack or after a myocardial infarct whilst in the water.

Dry’ drowning

Between 10 and 15% of drownings occur without aspiration of water into the lungs. Laryngeal spasm is thought to occur with anoxia occurring due to apnoea.

Wet’ drowning

Aspiration of fresh water affects the pulmonary surfactant with alveolar collapse and ventilation-perfusion mismatch leading to hypoxaemia. Aspiration of hypertonic sea water pulls additional fluid into the lungs with further ventilation-perfusion mismatch. In practice, however, there is little difference between salt-water and freshwater drowning as in both groups severe hypoxaemia occurs leading to death in some. Severe metabolic acidosis develops in the majority of survivors. In patients who aspirate more than 22 ml kg-t of water, electrolyte and volume changes do occur, but very few of such patients have survived.

EMERGENCY TREATMENT OF NEAR DROWNING

It must be remembered that patients can survive up to 30 min underwater without suffering brain damage and if the water is near O°C this time can be much longer. The exact reasons for this are not clearly understood, but it is probably related to the protective role of the diving reflex. It has been shown experimentally that submersion
in water causes a reflex slowing of the pulse and vasoconstriction. In addition, hypothermia decreases oxygen consumption of both the heart and brain. Patients should be turned to one side and the mouth cleared of any debris. Mouth-to-mouth respiration should be immediately started together with cardiac resuscitation if this is appropriate. Mouth-to-mouth resuscitation should always be attempted, even in the absence of a pulse and the presence of fixed dilated pupils, as patients can frequently make a dramatic recovery. All patients should be subsequently admitted to hospital for intensive monitoring. Intensive care therapy may be required, and patients are liable to develop the adult respiratory distress syndrome (ARDS).

PROGNOSIS

The prognosis is good if the patient is fully conscious on admission to hospital but poor if the patient is still in a coma.

Noise

The intensity of sound is expressed in terms of the square of the sound pressure. The bel is a ratio and is equivalent to a lO-fold increase in sound intensity; a decibel (dB) is one-tenth of a bel. Sound is made up of a number of frequencies ranging from 30 hertz (Hz) to 20 kHz, with most being between 1 and 4 kHz. When measuring sound, these different frequencies must be taken into account. In practice a scale known as A-weighted sound is used; sound levels are reported as dB(A). A hazardous sound source is defined as one with an overall sound pressure greater than 90 dB(A). Repeated prolonged exposure to loud noise, particularly in the frequency range of 2-6 kHz, causes first temporary and later permanent hearing loss due to damage to the organ of Corti, with destruction of hair cells and, eventually, the auditory neurones. This is a common occupational problem, not only in industry and the armed forces, but also in the home (e.g. from electric drills and sanders), in sport (e.g. motor racing) and in entertainment (pop stars, their audiences and disc jockeys).
Serious noise-induced hearing loss is almost wholly preventable by personal protection (ear muffs, ear plugs); little treatment can be offered once deafness becomes established.

Smoke

Smoke consists of particles of carbon in hot air and gases. These particles are mainly coated with organic acids and aldehydes. Use was widespread of synthetic materials (e.g. polyvinyl chloride) that release other substances, such as carbon monoxide and hydrochloric acid, on combustion. Respiratory symptoms may be immediate or delayed. Patients are dyspnoeic and tachypnoeic. Laryngeal stridor may require intubation. Hypoxia and pulmonary oedema can be fatal. Treatment is to remove the subject from the smoke and give oxygen. Intensive care may be required.

Electric shock

Electric shock may produce clinical effects in three ways:
1 Pain and psychological sequelae. The common ‘electric shock’ is usually a painful, but harmless, stimulus that is an unpleasant and frightening experience. It produces no lasting neurological damage or cutaneous evidence of damage.
2 Disruption of specific biological processes. Ventricular fibrillation, muscular contraction and spinal cord damage follow a major shock. These are seen typically following a lightning strike.
3 Electrical burns. These are either superficial burns (e.g. lightning may cause a fern-shaped burn), or necrosis of subcutaneous tissues due to the heat generated by the electricity.

Ionizing radiation

Ionizing radiation is either penetrating (X-rays, ‘}’-rays or neutrons) or non-penetrating (a or f3 particles). Penetrating radiation affects the whole body, while nonpenetrating radiation only affects the skin. All radiation effects, however, depend on the type of radiation, the distribution of dose and the dose rate.
Absorption of doses greater than 100 rads of y-radiation, e.g. following survival from a nuclear explosion or nuclear power plant accident, causes acute radiation syndromes of varying severity. Long-term effects also occur, sometimes decades after exposure, as radiation increases the rate of mutagenesis.
Radiation dosage is measured in joules per kilogram (J kg-I); 1 J kg” ‘ is also known as 1 gray (1 Gy). This is equivalent to 100 rads. Radioactivity is measured in becquerels (Bq); 1 Bq is equal to the amount of radioactive material in which there is one disintegration per second. 1 curie (Ci) is equal to 3.7 x 1010 Bq. Radiation differs in the density of ionization it causes. Therefore a dose equivalent called a sievert (Sv) is used.
This is the absorbed dose weighted for the damaging effect of the radiation. The annual background radiation is approximately 2.5 mSv.
Excessive exposure to ionizing radiation occurs following accidents in hospitals, industry, nuclear power plants and strategic nuclear explosions.

Mild acute radiation sickness

Nausea, vomiting and malaise follow doses of approximately 1 Gy (75-125 rad). Lymphopenia occurs within several days, followed 2-3 weeks later by a fall in all white cells and platelets. There is a late risk of leukaemia and solid tumours.

Severe acute radiation sickness

Many systems are affected; the extent of the damage depends on the dose of radiation received. The effects of radiation are summarized.

Acute effects

Haemopoietic syndrome

Gastrointestinal syndrome

ENS syndrome
Radiation dermatitis
Delayed effects
Infertility
Teratogenesis
Cataract
Neoplasia
Acute myeloid leukaemia
Thyroid
Salivary glands
Skin
Others

Haemopoietic syndrome

Absorption of doses between 2 and 10 Gy (200-1000 rad) is followed by early and transient vomiting in some individuals, followed by a period of relative well-being. Lymphocytes are particularly sensitive to radiation damage and severe lymphopenia develops over several days. A decrease in granulocytes and platelets occurs 2-3 weeks later as no new cells are being formed by the damaged marrow. Thrombocytopenia with bleeding develops and frequent, overwhelming infections occur, with a very high mortality.

Gastrointestinal syndrome

Absorption of doses greater than 6 Gy (600 rad) causes vomiting several hours after exposure. This then stops, only to recur some 4 days later accompanied by severe diarrhoea. Owing to radiation inhibition of cell division, the villous lining of the intestine becomes denuded. Intractable bloody diarrhoea follows, with dehydration, secondary infection and death.

ENS syndrome

Exposures above 30 Gy (3000 rad) are followed rapidly by nausea, vomiting, disorientation and coma; death due to severe cerebral oedema follows in 36 hours.

Radiation dermatitis

Skin erythema, purpura, blistering and secondary infection occur. Total loss of body hair is a bad prognostic sign and usually follows an exposure of at least 5 Gy (500 rad). Late effects of radiation exposure The survivors of the nuclear bombing of Hiroshima and Nagasaki have provided information on the long-term effects of radiation. The risk of developing acute myeloid leukaemia or cancer, particularly of the skin, thyroid and salivary glands, increases. Infertility, teratogenesis and cataract are also late sequelae of radiation exposure.

TREATMENT

Acute radiation sickness is a medical emergency. Hospitals should be immediately informed of the type and length of exposure so that suitable arrangements can be made to receive the patient. The initial radiation dose absorbed can be reduced by removing clothing contaminated by radioactive materials.
Treatment of radiation sickness is largely supportive and consists of prevention and treatment of infection, haemorrhage and fluid loss. Storage of the patient’s white cells and platelets for future use should be considered, if feasible.
Accidental ingestion or exposure to bone-seeking radioisotopes (e.g. strontium-90 and caesium-137) should be treated with chelating agents (e.g. EDTA) and massive doses of oral calcium. Radioiodine contamination should be treated immediately with potassium iodide 133 mg daily. This will block 90% of radioiodine absorption by the thyroid if given immediately before exposure.

Diving

The increases in ambient pressure to which a diver is exposed at various depths are summarized.
Various methods are used to supply air to the diver. With the simplest, e.g. a snorkel, the limiting factor, which occurs below 0.5 m, is the respiratory effort required to suck air into the lungs. At greater depths this ‘forced negative-pressure ventilation’ ultimately results in pulmonary capillary damage and haemorrhagic pulmonary oedema. Scuba tanks, the method commonly used for sporting diving down to 50 rn, carry compressed air at a pressure balanced with the water pressure.
Divers who work at great depths for commercial purposes or for underwater exploration breathe helium/oxygen or nitrogen/oxygen mixtures delivered by hose from the surface.
A wide variety of complex medical problems may affect divers at all depths. These are summarized below.

PROBLEMS DURING

COMPRESSION (i.e. DESCENT)

Barotrauma

Barotrauma of the middle ear (‘squeeze’) is the commonest disorder in divers. This is caused by an inability to equalize the pressure in the middle ear usually as a result of Eustachian tube blockage. Deafness occurs with eventual rupture of the tympanic membrane followed by acute vertigo.
Paranasal sinus barotrauma (‘squeeze’) is due to dysfunction of the nasal or paranasal sinus with blockage of the sinus ostea. Pain over the frontal sinus occurs. Treatment of both conditions is with decongestants. It can be prevented by avoiding diving when the airways are blocked, e.g. with a respiratory tract infection.

Pressure in relation to sea depth.

Pressure in relation to sea depth.

Nitrogen narcosis

When compressed air is breathed below 30 m the narcotic effects of nitrogen cause impairment of cerebral function with changes of mood and performance that may be lifethreatening. The condition reverses rapidly on ascent. Nitrogen narcosis is avoided by replacing air with helium/oxygen mixtures, which can enable divers to descend to 700 m.
At these great depths neurological disturbances occur that are believed to be the result of the direct effects of pressure on neurones. Tremor, hemiparesis and psychological changes may occur.

Oxygen narcosis

Pure oxygen cannot be used for diving because oxygen becomes toxic to the lungs when the alveolar oxygen pressure exceeds 1.5 atmospheres absolute (5 m of water) and to the nervous system at around 10 m of water. In the lungs, linear atelectasis appears and there is endothelial cell damage with exudation and pulmonary oedema. In the nervous system there is initially a feeling of apprehension, nausea and sweating, followed by muscle twitching and generalized convulsions, which may be fatal underwater.

PROBLEMS DURING

DECOMPRESSION (i.e. ASCENT)

Decompression sickness (‘the bends’) occurs on returning to the surface and is caused by the release of inert gases, usually nitrogen or helium, which form bubbles in the tissues as the ambient pressure falls. It only occurs when the diver ascends too rapidly. Decompression tables are available for calculating the time needed to come to the surface safely from any given depth.

Decompression sickness

This can take a mild form (type 1 ‘non-neurological bends’), with skin irritation, mottling or joint pain only, or be more serious (type 2 ‘bends’), in which a variety of neurological features appear. Patients with type 2 ‘bends’ may develop cortical blindness, hemiparesis, sensory disturbances or cord lesions. If nitrogen bubbles occur in the pulmonary vessels, divers experience retrosternal discomfort, dyspnoea and cough (‘the chokes’). These symptoms develop within minutes or hours of a dive.
Treatment is with oxygen. In addition, all but the mildest forms of decompression sickness (i.e. skin mottling alone) require recompression, usually in a pressure chamber.

A long-term problem is aseptic necrosis caused by infarction due to nitrogen bubbles lodging in nutrient arteries supplying bone. It is seen in 5% of deep-sea divers. Neurological damage may also persist. Lung rupture, pneumothorax and surgical emphysema These emergencies occur principally when divers ‘breathhold’ while making emergency ascents after losing their gas supply. Following lung rupture the patient notes severe dyspnoea, cough and haemoptysis. Pneumothorax and emphysema usually respond to 100% oxygen. Air embolism may occur and should be treated with recompression and hyperbaric oxygen.

High altitudes

The partial pressure of ambient (and hence alveolar and arterial) oxygen falls in a near-linear relationship to altitude.
Below 3000 m there are few important clinical effects. Commercial aircraft are pressurized to 2750 m and the resulting hypoxia causes breathlessness only in those with severe cardiorespiratory disease. The incidence of thromboembolism is, however, slightly greater than at sea level in sedentary travellers on long flights.

Diagram to show the decrease in oxygen and barometric pressure with increasing altitude.

Diagram to show the decrease in oxygen and barometric pressure with increasing altitude.

Above 3000-3500 m, hypoxia causes a spectrum of related clinical syndromes that affect visitors to high altitudes, principally climbers, trekkers, skiers and troops. These conditions, which often coexist, occur largely during the acclimatization process. This may last some weeks, but enables man to live (permanently if necessary) at altitudes up to about 5600 m. At greater heights, although man can survive for days or weeks, deterioration due to chronic hypoxia is inevitable. It has now been demonstrated on several occasions that ascent to the highest of the world’s summits is possible without the use of supplementary oxygen. At the summit of Everest the barometric pressure is 34 kPa (253 mmHg). This enables an acclimatized mountaineer to have an alveolar P02 of 4.0-4.7 kPa (30-35 mmHg)-near the physiological limits of man.

Acute mountain sickness (AMS)

This term is used to describe the malaise, nausea, headache and lassitude that are common above 3500 m. Following arrival at this altitude there is usually a latent interval of 6-36 hours before the onset of symptoms.

Conditions caused by sustained hypoxia.

Conditions caused by sustained hypoxia.

Treatment is rest, with analgesics being given if necessary; recovery is almost invariable.
Prophylactic treatment with the carbonic anhydrase inhibitor acetazolamide is of value in reducing the symptoms of AMS, since these are partly due to the development of alkalosis. Acclimatizing by ascending gradually is the best prophylaxis.
In a minority of cases, the more serious sequelae of high-altitude pulmonary oedema (HAPO) and highaltitude cerebral oedema (HACO) occur. High-altitude pulmonary oedema Predisposing factors include youth, rapidity of ascent, heavy exertion and the presence of mountain sickness. Breathlessness, with frothy blood-stained sputum indicates established HAPO. Unless treated rapidly this leads to cardiorespiratory failure, collapse and death. Milder forms of HAPO are common, presenting with breathlessness that is not severe; it is important to recognize them.

High-altitude cerebral oedema

Cerebral oedema is a poorly understood sequel of hypoxia. It is probably the result of the abrupt increase in cerebral blood flow that occurs even at modest altitudes of 3500-4000 m. Headache is usual, and is accompanied by varying disturbances of cerebral function; drowsiness, ataxia, nystagmus and papilloedema are common. Coma and death follow if the condition progresses.

TREATMENT

Any but the milder forms of AMS require urgent treatment. Oxygen should be given if it is available, and descent to a lower altitude should take place as quickly as possible. Dexamethasone or betamethasone are effective treatments in HAPO or HACO. Diuretics are of little value.

Retinal haemorrhages

Small ‘flame’ haemorrhages in the nerve fibre layer of the retina are common above 5000 m. They are usually symptomless unless they cover the macula, when there is painless loss of central vision. Recovery is usual.

Deterioration

Prolonged residence between 5600 and 7000 m leads to a syndrome of weight loss, anorexia and listlessness after several weeks. Above 7500 m deterioration develops more quickly, although it is possible to survive for a week or more at altitudes over 8000 m.

Chronic mountain sickness

This rare syndrome occurs in long-term residents of high altitudes after several decades. It has been described clearly only in the Andes, but may occur in Tibet and elsewhere in central Asia.

Polycythaemia, drowsiness, cyanosis, finger clubbing, congested cheeks and ear lobes, and right ventricular enlargement occur. The condition is gradually progressive. By way of contrast, coronary artery disease and hypertension are rare in the native populations of high altitudes.