5

Environmental medicine
Michael L Clark

Disease and the environment 51

Environmental temperature 51
Heat injury 51
Cold injury 52
Hypothermia 52
Peripheral cold injury 53
High altitude 54
Diving 55
Problems during descent 55
Problems during and following ascent 55
Drowning 56
Air pollution 56
Ionizing radiation 57
Electric shock 59
Lightning strike 59
Smoke 59
Noise 59
Bioterrorism/biowarfare 60
Potential pathogens 60
Emergency planning 60
 Travel 60
Building-related illnesses 61
Non-specific building-related illness 61
Specific building-related illness 61

Disease and the Environment

The incidence and prevalence of disease and causes of death within a community
are a reflection of interrelated factors:
• Genetic predisposition.
• Nutrition, poverty and affluence (see p. 183), some countries having a grossly
uneven distribution between rich and poor. This leads to chronic disease such
as diabetes and obesity mainly in the cities, with malnutrition and infectious
disease in the rural areas.
• Purity of water sources and sanitation facilities (see p. 47).
• Atmospheric pollution.
• Environmental disasters and accidents.
• Background ionizing radiation and man-made radiation exposure, deliberate
or accidental.
• Environmental temperature.
• Patterns of infective disease (see p. 222).
• Political forces determining levels of healthcare, preventative strategies and
effects of war on civilian populations (see p. 49).
Some of these environmental effects have been clearly documented within the
last decade: for example, the massive civilian mortality and morbidity during the
Afghan war, previous Iraq wars and current military action in the Middle East.
Loss of life and disease prevalence following the 2006 tsunami, the earthquakes
in Szechuan (2008) and Haiti (2010), and cyclone Nargis in the Irawaddy delta
have been huge. Aspects related to global health are discussed in more detail in
Chapter 4.
Flooding caused by El Niño in East Africa resulted not only in an increase in
breeding sites for mosquito vectors but also in a major outbreak of Rift Valley
fever due to the enforced close proximity of cattle and humans.
Tobacco use (active and passive), obesity (see pp. 206–212) and excess
alcohol consumption also play a significant role in disease. Physical inactivity
has an effect on mortality that is equivalent to tobacco use or obesity. Worldwide
health programmes have been established in most countries to reduce these
effects.

Further reading
Van Rooyen MS. Medical complications associated with earthquakes. Lancet
2012; 379:748–757.

Environmental Temperature
Climate change is an unquestionable phenomenon due mainly to increased
carbon dioxide production and changes in our habitat.
The effect of environmental temperature (TEnv) is paramount in infective
diseases; increases as small as 1°C cause major changes in disease vectors.
Patterns of infective disease are likely to change radically within the next
20 years. Climate effects are already becoming apparent, such as:
• changes in the patterns of malaria in South-east Asia
• the occurrence of dengue fever in southern Italy
• outbreaks of cholera, and seasonal variation in diarrhoea and vomiting.
Research into the effect of climate change on the changing patterns of
infective diseases will point to potential ways in which national and international
efforts can be targeted.

Heat Injury
Body core temperature (TCore) is maintained at 37°C by the thermoregulator
centre in the hypothalamus, which integrates information from skin temperature
sensors with core temperatures from receptors in the brain and in the walls of
large blood vessels.
Heat is produced by cellular metabolism and is dissipated through the skin by
both vasodilatation and sweating, and in expired air via the alveoli. When the
environmental temperature (TEnv) is >32.5°C, profuse sweating occurs.
Sweat evaporation is the principal mechanism for controlling TCore following
exercise or in response to an increase in TEnv.
 Heat acclimatization takes place over several weeks. The sweat volume
increases and the sweat salt content falls. Increased evaporation of sweat reduces
TCore.

Heat cramps
Painful muscle cramps, usually in the legs, often occur in fit people when they
exercise excessively, especially in hot weather. Cramps are probably due to low
extracellular sodium caused by excess intake of water over salt. They can be
prevented by increasing dietary salt. They respond to combined salt and water
replacement, and in the acute stage to stretching and muscle massage. TCore
remains normal.

Heat exhaustion
At any environmental temperature (especially with TEnv of >25°C), and with a
high humidity, strenuous exercise in clothing that inhibits sweating, such as a
wetsuit or military uniform, can cause an elevation in TCore in less than
15 minutes. Weakness/exhaustion, cramps, dizziness and syncope, with TCore
>37°C, define heat exhaustion. Elevation of TCore is more critical than water and
sodium loss. Heat exhaustion may progress to heat stroke, a serious emergency
(see below).

Management
Reduce (TEnv) if possible and cool the patient with sponging and fans. Give O2 by
mask. Other causes of high TCore, such as malaria, should be ruled out if
appropriate.
Oral rehydration with both salt and water (25 g of salt per 5 L of water/day) is
given in the first instance, with adequate replacement thereafter. In severe heat
exhaustion, intravenous fluids are needed; 0.9% saline is given. Monitor serum
sodium and correct secondary potassium loss.

Heat stroke
Heat stroke is an acute life-threatening situation in which TCore rises >41°C.
There is headache, nausea, vomiting and weakness, progressing to confusion,
coma and death. The skin feels intensely hot to the touch. Sweating is often
absent but not invariably so.
Heat stroke can develop in unacclimatized people in hot, humid, windless
conditions, even without exercise. Sweating may be limited by prickly heat
(plugging or rupture of the sweat ducts, leading to a pruritic, papular,
erythematous rash).
Excessive exercise in inappropriate clothing, such as exercising on land in a
wetsuit, can lead to heat injury in temperate climates. Diabetes, alcohol and
drugs, such as antimuscarinics, diuretics and phenothiazines, can contribute.
Heat stroke can lead to a fall in cardiac output, lactic acidosis and intravascular
coagulation.

Prevention
Acclimatization, fluids, avoidance of inappropriate clothing and common sense
are required.

Management
• Apply standard life support measures (ABCDE).
• Reduce TEnv if possible.
• Arrange cold water immersion if facilities are available. Otherwise, cool the
patient with sponging, icepacks or fanning.
• Give O2 by mask.
• Move the patient to a medical facility. Manage in intensive care: monitor
cardiac output and respiration; measure biochemistry, clotting and muscle
enzymes.
• Give fluids intravenously so the intravascular volume remains normal.
Prompt treatment is essential and can be curative, even with a TCore of >41°C.
Morbidity and mortality are directly related to the duration of the high TCore.
Complications are hypovolaemia, intravascular coagulation, cerebral oedema,
rhabdomyolysis, and renal and hepatic failure.

Malignant hyperpyrexia
See page 889.

Further reading
Hajat S, O'Connor M, Kosatsky T. Health effects of hot weather: from
awareness of risk factors to effective health protection. Lancet 2010; 375:856–
863.

Cold Injury
Cold injury may be divided into hypothermia, which is whole-body cooling, and
peripheral cold injury (Box 5.1).

 Box 5.1
Cold injury
• Hypothermia is defined as a core temperature of <32°C
• Peripheral cold injury includes:
– Frostbite: the local cold injury that follows freezing of tissue
– Non-freezing cold injury: the damage – usually to feet – following
prolonged exposure to a TEnv between 0° and 5°C, usually in damp
conditions

Hypothermia
Hypothermia occurs in many settings.
At home. Hypothermia can occur when TEnv is <8°C, if there is poor heating,
inadequate clothing and poor nutrition. Depressant drugs, such as hypnotics, as
well as alcohol, hypothyroidism or intercurrent illness also contribute.
Hypothermia is commonly seen in the poor, frail and elderly. The elderly have a
diminished ability to sense cold and also have little insulating fat.
Neonates and infants become hypothermic rapidly because of a relatively
large surface area in proportion to subcutaneous fat.
Outdoors on land. Hypothermia is a prominent cause of death in climbers,
skiers and polar travellers, and in wartime. Wet, cold conditions with wind chill,
physical exhaustion, injuries and inad​equate clothing are contributory. Babies
and children are at risk because they cannot take action to warm themselves.
Cold water immersion. Dangerous hypothermia can develop following
immersion for more than 30 min to 1 hour in water temperatures of 15–20°C. In
TWater <12°C, limbs rapidly become numb and weak. Recovery takes place
gradually, over several hours following rescue.

Clinical features
Mild hypothermia (TCore <32°C) causes shivering and initially intense
discomfort. However, the hypothermic subject, though alert, may not act
appropriately to rewarming: for example, by huddling, wearing extra clothing or
exercising. As the TCore falls below 32°C, severe hypothermia causes impaired
judgement – including lack of awareness of cold – and drowsiness and coma.
Death follows, usually from ventricular fibrillation.

Diagnosis
Diagnosis is straightforward, if a low-reading thermometer is available. If not,
rapid clinical assessment is reliable. Someone who feels icy to the touch –
abdomen, groin, axillae – is probably substantially hypothermic. If the person is
clammy, uncooperative or sleepy, TCore is almost certainly <32°C.

Sequelae
Pulse rate and systemic blood pressure fall. Cardiac output and cerebral blood
flow are low in hypothermia and can fall further if the upright position is
maintained or the thorax restrained by a harness, or by hauling during
evacuation. This is why helicopter and lifeboat winch rescues are often carried
out with a stretcher rather than a chest harness.
Respiration becomes shallow and slow. Muscle stiffness develops; tendon
reflexes become sluggish, then absent. As coma ensues, pupillary and other
brainstem reflexes are lost; pupils are fixed and may be dilated in severe
hypothermia. Metabolic changes are variable, with either metabolic acidosis or
alkalosis. Arterial PO2 may appear normal: that is, falsely high.
There is shift of the oxygen dissociation curve (see p. 90) to the left because
of the reduction in temperature of haemoglobin. Thus, if an arterial blood sample
from a hypothermic patient is analysed at 37°C, the PO2 will be falsely high.
Within the range 37–33°C, this factor is around 7% per degree centigrade. Many
blood gas machines also calculate the arterial saturation; this too will be falsely
high. When a patient is monitored using a pulse oximeter, the level of arterial
oxygen saturation (SaO2) will, however, be correct, but if SaO2 is then converted
by calculation to PaO2, a downward correction must be applied – simply due to
hypothermia.
Bradycardia with ‘J’ waves (above the isoelectric line at the junction of the
QRS complex and ST segment; Fig. 5.1 ) are pathognomonic of hypothermia.
Prolongation of PR and QT intervals and the QRS complex also occurs.
Ventricular dysrhythmia (tachycardia/fibrillation) or asystole is the usual cause
of death.

FIGURE 5.1 Electrocardiogram showing J waves in hypothermia.

Management
• Maintain the patient horizontal or slightly head-down.
• Rewarm gradually.
• Correct metabolic abnormalities.
• Anticipate and treat dysrhythmias.
• Check for hypothyroidism (see pp. 1202–1204).
If the patient is awake, with a core temperature of >32°C, place in a warm
room, use a foil wrap and give warm fluids orally. Outdoors, add extra dry
clothing, huddle together and use a warmed sleeping bag. Rewarming may take
several hours. Avoid alcohol: this adds to confusion, boosts confidence
factitiously, causes peripheral vasodilatation and further heat loss, and can
precipitate hypoglycaemia.

Severe hypothermia
In severe hypothermia, people look dead. Always exclude hypothermia before
diagnosing brainstem death (see p. 1172). Warm gradually, aiming at a 1°C/hour
increase in TCore. Direct mild surface heat from an electric blanket can be helpful.
Treat any underlying condition promptly, such as sepsis. Monitor all vital
functions. Correct dysrhythmias. Check for sedative drugs.
Give warm intravenous fluids slowly. Correct metabolic abnormalities.
Hypothyroidism, if present, should be treated with liothyronine. Various methods
of artificial rewarming exist: inhaled warm humidified air, gastric or peritoneal
lavage, and haemodialysis. These are rarely used. Hypothermia is frequently
lethal when TCore falls below 30°C. Survival with full recovery has, however,
been recorded with a TCore of <16°C.

Prevention
Hypothermia in the field can often be prevented by forethought and action. For
the elderly, improved home heating and insulation, central heating in bedrooms
and electric blankets are helpful in cold spells. This can be expensive and
unaffordable for some people, so supplemental finance is required.

Peripheral cold injury

Frostbite
Ice crystals form within skin and superficial tissues when the temperature of the
tissue (TTissue) falls to −3°C: TEnv generally must be below −6°C. Wind chill is
frequently a factor. Typically, fingers, toes, nose and ears become frostbitten.
Frostbitten tissue is pale, greyish and initially doughy to the touch. Later,
tissue freezes hard, looking like meat from a freezer. Frostbite can easily occur
when working or exercising in low temperatures and typically develops without
the patient's knowledge. Below a TEnv of 5°C, hands or feet that have lost their
feeling are at risk of cold injury.
 Management
Transport the patient – or if this is impossible, make them walk, even on
frostbitten feet – to a place of safety before commencing warming. Warm the
frozen part by immersion in hand-hot water at 39–42°C, if feasible. Assess
hypothermia. Continue warming until obvious thawing occurs; this can be
painful. Vasodilator drugs have no part in management. Blisters form in a few
days and, depending on the depth of frostbite, a blackened shell – the carapace –
develops as blisters regress or burst. Dry, non-adherent dressings and aseptic
precautions are essential, though hard to achieve. Frostbitten tissues are
anaesthetic and at risk from further trauma and infection. Recovery takes place
over many weeks and may be incomplete. Surgery may be needed, but should be
avoided in the early stages.

Chilblains
These are small, purplish itchy inflammatory lesions, occurring on toes and
fingers. They occur in cold, wet conditions. They are more common in women
and heal in 7–14 days. Prevention is by keeping warm and wearing gloves and
warm footwear.

Non-freezing cold injury

Non-freezing cold injury (NFCI, trench foot) describes tissue damage following
prolonged exposure, usually for several hours or more, at TEnv around or slightly
above freezing, but without frostbite. Wet socks and boots are the usual cause.
There is severe vasoconstriction, and blotchiness of the lower limbs, with pain
and oedema on rewarming. Recovery usually follows over several weeks. There
may be a prolonged late susceptibility to cold. NFCI is a prominent cause of
morbidity in troops operating in low temperatures and is a subsequent cause of
litigation.
Prevention of frostbite and NFCI is largely by education and common sense:
avoid damp feet and wet boots. Always carry spare dry socks, gloves and
headgear.

Further reading
Sheridan RL, Goldstein MA, Stoddard FJ Jr et al. Case records of the
 Massachusetts General Hospital. Case 41-2009. A 16-year-old boy with
hypothermia and frostbite. N Engl J Med 2009; 361:2654–2662.
Wira CR, Becker JU, Martin G et al. Anti-arrhythmic and vasopressor
medications for the treatment of ventricular fibrillation in severe hypothermia.
Resuscitation 2008; 78:21–29.
http://www.hypothermia.org Hypothermia prevention, recognition and
treatment.

High Altitude
The partial pressure of atmospheric oxygen – and hence alveolar and arterial
oxygen – falls in a near-linear relationship as barometric pressure drops with
increasing altitude (Fig. 5.2).

FIGURE 5.2 The decrease in oxygen and barometric pressure with increasing altitude.

Commercial aircraft are pressurized to around 24 000 m (lowering the oxygen

saturation by 3–4%). This trivial reduction is not noticed by healthy individuals.
Air travel is discussed on page 61.
On land, below 3000 m there are few clinical effects. The resulting
hypoxaemia causes breathlessness only in those with severe cardiorespiratory
disease. Above 3000–3500 m, hypoxia causes a spectrum of related syndromes
that affect high-altitude visitors, principally climbers, trekkers, skiers and troops
(Box 5.2), especially when they exercise. These conditions occur largely during
acclimatization, a process that takes several weeks; once completed, this can
enable humans to live – permanently, if necessary – up to about 5600 m. At
greater heights, although people can survive for days or weeks, deterioration due
to chronic hypoxia is inevitable.

 Box 5.2
Conditions caused by sustained hypoxia

Condition Incidence (%) Usual altitude (m)

Acute mountain sickness 70 3500–4000

Acute pulmonary oedema 2 4000
Acute cerebral oedema 1 4500
Retinal haemorrhage 50 5000
Deterioration 100 ≥6000
Chronic mountain sickness Rare 3500–4000

The world's highest railway runs to Lhasa in Tibet, reaching altitudes of over
5000 m. Emergency oxygen is provided in the carriages. Roads at similar
altitudes in Central Asia are used extensively but since road passengers do not
exercise, serious altitude-related illnesses are unusual. Climbing the world's
highest summits is just possible without supplementary oxygen, though it is
often used on peaks above 7500 m. At the summit of Mount Everest (8848 m),
the barometric pressure is 34 kPa (253 mmHg). An acclimatized mountaineer has
an alveolar PO2 of 4.0–4.7 kPa (30–35 mmHg) – near humans' absolute
physiological limit. In 2007, arterial blood samples from acclimatized doctors on
Everest at altitude 8400 m, breathing air, showed an average PO2 of 24.6 mmHg
(3.3 kPa).

Acute mountain sickness

Acute mountain sickness (AMS) describes malaise, nausea, headache and
lassitude that affect the majority of people for a few days, above 3500 m.
Following arrival at this altitude, there is usually a latent interval of 6–36 hours
before symptoms begin. Treatment is rest, with analgesics if necessary. Recovery
is usually spontaneous over several days.
Prophylactic treatment with acetazolamide, a carbonic anhydrase inhibitor and
respiratory stimulant, is of some value in preventing AMS. Acclimatizing – that
is, ascending gradually – provides better and more natural prophylaxis.
In the minority, more serious sequelae – high-altitude pulmonary oedema and
high-altitude cerebral oedema – develop.

High-altitude pulmonary oedema

Predisposing factors include youth, rapidity of ascent, heavy exertion and severe
AMS. Breathlessness, occasionally with frothy blood-stained sputum, indicates
established oedema. Unless treated rapidly, this leads to cardiorespiratory failure
and death. Milder forms are common. Breathlessness at rest should raise the
suspicion of pulmonary oedema.

High-altitude cerebral oedema

Cerebral oedema is the result of an abrupt increase in cerebral blood flow that
occurs even at modest altitudes of 3500–4000 m. It is unusual below 4500 m,
and occurs typically in the first 2 weeks, during acclimatization. Cerebral
oedema can also develop suddenly in well-acclimatized climbers above 7000 m.
Headache is followed by drowsiness, ataxia and papilloedema, with coma and
death if brain oedema progresses.

Management
Any but the milder forms of AMS require urgent treatment. Oxygen should be
given by mask if available, and descent should take place as quickly as possible.
Nifedipine reduces pulmonary hypertension and is used in pulmonary oedema.
Dexamethasone is effective in reducing brain oedema. Portable pressure bags
inflated by a foot pump are widely used; the patient is enclosed in the bag.

Retinal haemorrhage
Small flame haemorrhages within the retinal nerve fibre layer are common
above 5000 m and usually symptomless. Rarely, a haemorrhage will cover the
macula, causing painless loss of central vision. Recovery is usual.

Deterioration
Prolonged residence between 6000 and 7000 m leads to weight loss, anorexia
and listlessness after several weeks. Above 7500 m, the effects of deterioration
become apparent over several days, although it is possible to survive for a week
or more at altitudes near 8000 m without supplementary oxygen.

Chronic mountain sickness

Chronic mountain sickness occurs in long-term residents at high altitudes,
usually after several decades, and is seen in the Andes and in Central Asia.
Headache, polycythaemia, lassitude, cyanosis, finger clubbing, congested
cheeks and ear lobes, and right ventricular enlargement develop. Chronic
mountain sickness is gradually progressive.
Coronary artery disease and hypertension are rare in high-altitude native
populations.

Further reading
Grocott MP, Martin DS, Levett DZ et al. Arterial blood gases and oxygen
content in climbers on Mount Everest. N Engl J Med 2009; 360:140–149.
Imray CH, Grocott MP, Wilson MH et al. Extreme, expedition and
wilderness medicine. Lancet 2015; 386:2520–2525.
Wilson MH, Habig K, Wright C et al. Pre-hospital emergency medicine.
Lancet 2015; 386:2526–2534.
http://www.thebmc.co.uk Union Internationale des Associations
d'Alpinisme (UIAA) Mountain Medicine Data Centre leaflets, available from
British Mountaineering Council, 177–179 Burton Road, Manchester M20
2BB, UK.
http://www.wms.org Wilderness Medical Society Information, PO Box
2463, Indianapolis, Indiana 462206, USA.

Diving
Free diving by breath-holding is possible to around 5 m, or with practice to
greater depths. Air can be supplied to divers by various methods.
A snorkel provides air to a depth of about 0.5 m; inspiratory effort is the
limiting factor. At depths >0.5 m – that is, with a longer snorkel tube, forced
negative-pressure ventilation can cause pulmonary capillary damage with
haemorrhagic alveolar oedema.
 Scuba divers – recreational sports divers descending to 30 m – carry bottled
compressed air or a nitrogen–oxygen mixture.
Commercial divers who work at great depths breathe helium–oxygen or
nitrogen–oxygen mixtures, delivered by hose from the surface.
Ambient pressures at various depths are shown in Box 5.3.

 Box 5.3
Depth and pressure

Pressure
Water depth (m)
Atmospheres mmHg

0 1 760
10 2 1520
50 6 4560
90 10 7600

Problems during descent

Middle ear barotrauma (squeeze) is common and is due to an inability to
equalize pressure in the middle ear; Eustachian tube blockage is the usual cause.
Pain and hearing loss occur, sometimes with tympanic membrane rupture and
acute vertigo.
Sinus squeeze is intense local pain due to blockage of the nasal and paranasal
sinus ostia.
Management is by holding the nostrils closed and swallowing, or similar
manœuvres, as well as use of decongestants. Diving with a respiratory or sinus
infection should be avoided.

Oxygen narcosis
Pure oxygen is not used for diving because of oxygen toxicity. Lung atelectasis,
endothelial cell damage and pulmonary oedema occur when alveolar oxygen
pressure exceeds 1.5 atmospheres, at depths of around 5 m. At around 10 m, the
central nervous system (CNS) becomes affected: apprehension, nausea and
sweating are followed by muscle twitching and generalized convulsions.
 Nitrogen narcosis
When compressed air is breathed below 30 m, the narcotic effects of nitrogen
begin to impair brain function. Poor judgement is hazardous; this also occurs
with nitrogen–oxygen mixtures in recreational diving. Nitrogen narcosis is
avoided by replacing air with helium–oxygen mixtures, enabling descent to
700 m. At these extreme depths, the direct effect of pressure on neurones can
cause tremor, hemiparesis and cognitive impairment.

Problems during and following ascent

Free divers who breath-hold often hyperventilate deliberately prior to plunging
in. This drives off CO2, reducing the stimulus to inspire. During the subsequent
breath-hold, PaCO2 rises and PaO2 falls. On surfacing, decompression lowers
PaO2 further. This can lead to syncope, known as a shallow water blackout.
Since loss of consciousness can take place in the water, this can lead to fatalities.

Decompression sickness
Decompression sickness (the bends) is caused by the release of bubbles of
nitrogen or helium and follows too rapid a return to the surface. Decompression
tables indicate the duration for safe return from a given depth to the surface. In
general, no decompression is necessary for diving above 30 m; at 30–60 m,
decompression is necessary.
Bends can be mild (type 1, non-neurological bends), with skin irritation and
mottling and/or joint pain. Type 2, neurological bends, are more serious and
involve the development of cortical blindness, hemiparesis, sensory disturbances
or cord lesions.
If bubbles form in pulmonary vessels, divers experience retro​sternal
discomfort, breathlessness and cough, known as the chokes. These develop
within minutes or hours of a dive. Decompression problems do not only occur
immediately on reaching the surface; they may take some hours to become
apparent. Over the subsequent 24 hours, further ascent, such as air travel, can
occasionally provoke the bends.
Other problems during ascent include paranasal sinus pain and nosebleeds –
medically minor but dramatic, with excruciating pain and a mask full of bloody
fluid. Toothache can be caused by gas bubbles within rotten fillings.
 Management
All but the mildest forms of decompression sickness, such as skin mottling
alone, require recompression in a pressure chamber, following strict guidelines.
Recovery is usual. A long-term problem is aseptic necrosis of the hip due to
nitrogen bubbles causing infarction. Focal neurological damage may persist, but
complaints of fatigue and poor concentration are issues compounded by
litigation that commonly follows diving accidents. Objective, evidence-based
assessments are essential.

Lung rupture, pneumothorax and surgical emphysema

These emergencies occur when divers breath-hold during emergency ascents
after gas supplies become exhausted. There is dyspnoea, cough and haemoptysis.
Pneumothorax and surgical emphysema resolve with 100% oxygen. Air
embolism can also occur and is treated with recompression.

Further reading
Brubakk A, Neuman TS. Bennett and Elliott’s Physiology and Medicine of
Diving, 5th edn. London: WB Saunders; 2002.
Edmonds C, Thomas B, McKewzie B et al. Diving Medicine for Scuba
Divers; 2012; available at http://www.divingmedicine.info.
Lynch JH, Bove AA. Diving medicine: a review of current evidence. J Am
Board Fam Med 2009; 22:399–407.
http://www.diversalertnetwork.org/ Divers Alert Network (DAN).
http://www.divingmedicine.info/ Diving Medicine for Scuba Divers.

Drowning
Drowning is defined as a process resulting in primary respiratory impairment
from submersion or immersion in a liquid medium. Terms such as ‘near-
drowning and ‘wet drowning’ should not be used.
Drowning is a common cause of accidental death worldwide. In the UK, some
40% of drownings occur in children under 5 years of age. Drowning can also
follow a seizure or a myocardial infarct. Exhaustion, alcohol, drugs and
hypothermia all contribute to deaths following submersion.
Fresh or seawater aspiration destroys pulmonary surfactant, leading to
alveolar collapse, ventilation/perfusion mismatch and hypoxaemia. Aspiration of
hypertonic seawater (5% NaCl) pulls additional fluid into the alveoli with further
ventilation/perfusion mismatch. In practice, there is little difference between
saltwater and freshwater aspiration. In both, severe hypoxaemia develops
rapidly. Severe metabolic acidosis develops in the majority of survivors.

Management and prognosis

Clearance of the airway and ventilation are the major requirements for
submerged people, and bystanders should start resuscitation immediately once
the person is stable on land. Rescue breaths and chest compression come before
the initiation of standard cardiopulmonary resuscitation as used in cardiac arrest
(see pp. 956–959). Patients have survived for up to 30 minutes under water
without suffering brain damage – and sometimes for longer periods if TWater is
near 10°C. Survival is probably related to the protective role of the diving reflex;
submersion causes bradycardia and vasoconstriction. Oxygen consumption is
also decreased by hypothermia.
Resuscitation should always be attempted, even with absent pulse and fixed
dilated pupils. Patients frequently make a dramatic recovery. All survivors
should be admitted to hospital for intensive monitoring, as acute respiratory
distress syndrome (ARDS) can develop during the subsequent 48 hours.
Recovery is frequently complete if consciousness is regained within several
minutes of commencing resuscitation but poor if a patient remains stuporose or
in coma at 30 minutes.

Prevention
This includes making sure that all people can swim, particularly young children.
Any water can be dangerous, and swimming should only be undertaken in
supervised areas.

Further reading
Szpilman D, Bierens JJ, Handley AJ et al. Drowning. N Engl J Med 2012;
366:2102–2110.
Vanden Hoek TL, Morrison LJ, Shuster M et al. Part 12: Cardiac arrest in
special situations: 2010 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
 Circulation 2010; 122:S829.

Air Pollution

Epidemiology
Air pollution is one of the biggest problems facing the world currently. It has
become a public health emergency as it leads to chronic diseases and exacerbates
respiratory, cardiac and other medical problems. According to the United
Nations, air pollution is the cause of 3.7 million premature deaths per year, most
of which are from heart attacks and strokes. Annually, pollution is the cause of
1.4 million deaths in China, 645 000 in India and 110 000 in Pakistan, and
figures are rising. It is also the single largest environmental risk in Europe,
causing 430 000 premature deaths. It has been estimated that air pollution kills
more people in a year than malaria and HIV combined and about ten times more
deaths than road accidents in some countries. Atmospheric air pollution, due to
the burning of coal for energy and heat, has been a feature of urban living in
developed countries for at least two centuries. It consists of black smoke and
sulphur dioxide (SO2) and, from combustion of hydrocarbon fuels in motor
vehicles, nitrogen oxides (NO and NO2), diesel particulates, polyaromatic
hydrocarbons and ozone, a secondary pollutant generated by photochemical
reactions in the atmosphere. Levels of NO2 can be high in poorly ventilated
kitchens and living rooms where gas is used for cooking and in fires.
Particulate matter consists of coarse particles (10–2.5 µm in aerodynamic
diameter), produced by construction work and farming, and fine particles
(<2.5 µm) generated from burning fossil fuels. Fine particulates (PM2.5) remain
airborne for long periods and are carried into rural areas. Several respiratory and
cardiac problems are exacerbated by these very small particles.
The World Health Organization (WHO) global air-quality guidelines suggest
24-hour values of <25 µg/m3 for PM2.5 for the short term and 10 µg/m3 in the
long term. In Europe, 70% of the particulates present in urban air result from the
combustion of diesel fuel, providing a background concentration of 3–5 µg/m3.
The WHO estimates that air pollution causes 800 000 premature deaths
worldwide every year.
Deaths from respiratory and cardiovascular disease occur mainly in older
populations; air pollution mainly causes bronchitis in children. Pollution from
motor vehicles has been linked to increased hospital admissions, reduced lung
function in children and younger adults, and an increase in lung cancer
(polyaromatic hydrocarbons). Although it has been proposed that air pollution
may cause asthma and other allergic diseases, there is no current evidence for
this (Box 5.4). However, air pollution does adversely affect lung development in
teenage children, while both NO2 and ozone enhance the nasal and lung airway
responses to inhaled allergen in people with established allergic disease.

 Box 5.4
Air pollutants and their health effects

Average
Poor air
Pollutant concentrati Susceptible individuals Mechanisms of health effects
quality
on
Sulphur 5–15 ppb >125 ppb Asthmatics Bronchoconstriction through neurogenic
dioxide mechanism
(SO2)
Ozone (O3) 10–30 ppb >90 ppb All affected, particularly Restrictive lung defect
during exercise Airway inflammation
Enhanced response to allergen
Nitrogen 25–40 ppb >100 ppb Allergic individuals Airway inflammation
dioxide Enhanced response to allergen
(NO2)

Particulate
matter
 PM10 25–30 µg/m3 >65 µg/m3 Elderly Airway and alveolar inflammation
Allergic individuals Enhanced selective production of the
allergy antibody (IgE)
 PM2.5 3–5 µg/m3 >10 µg/m3 Those with cardiac and Airway inflammation
respiratory disease

ppb, parts per billion.

Management
When air quality is poor, asthmatics are advised to avoid exercising outdoors and
to increase their anti-inflammatory medication (i.e. inhaled corticosteroids).
Short- and long-term measures are required to reduce air pollution, particularly
diesel particulates (which are predicted to increase as more diesel engines are
used). Such measures include increased motor engine efficiency, catalytic
converters, diesel particulate traps and decreased reliance on cars and trucks.

Further reading
Editorial. Short-lived climate pollutants: a focus for hot air. Lancet 2015;
386:1707.
Beelen R, Raaschou-Nielsen O, Stafoggia M et al. Effects of long-term
exposure to air pollution on natural-cause mortality: an analysis of 22
European cohorts within the multicentre ESCAPE project. Lancet 2014;
383:785–795.

Ionizing Radiation
Ionizing radiation is either penetrating (X-rays, γ-rays or neutrons) or non-
penetrating (α- or β-particles). Penetrating radiation affects the skin and deeper
tissues, while non-penetrating radiation affects the skin alone. All radiation
effects depend on the type of radiation, the distribution of dose and the dose rate.
Dosage is measured in joules per kilogram (J/kg): 1 J/kg = 1 gray (1 Gy) = 
100 rads.
Radioactivity is measured in becquerels (Bq); 1 Bq is defined as the activity
of a quantity of radioactive material in which one nucleus decays per second;
3.7  ×  1010 Bq = 1 curie (Ci), the older, non-SI unit.
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. A chest X-ray delivers 0.02 mSv, and CT of the
abdomen/pelvis about 10 mSv (see Box 17.5). A cumulative risk of cancer
following repeated imaging procedures has been established and X-ray
exposures should be reduced if possible.
Excessive exposure to ionizing radiation follows accidents in industry, nuclear
power plants and hospitals, and deliberate nuclear explosions designed to
eliminate populations – and exceptionally, by poisoning, with polonium, for
example.

Mild acute radiation sickness

Nausea, vomiting and malaise follow doses of approximately 1 Gy.
Lymphopenia occurs within several days, followed 2–3 weeks later by a fall in
all white cells and platelets.

Acute radiation sickness

Many systems are affected; the extent depends on the dose of radiation (Box
5.5).

 Box 5.5
Systemic radiation effects
Acute effects
• Haemopoietic syndrome
• Gastrointestinal syndrome
• CNS syndrome
• Radiation dermatitis
Delayed effects
• Infertility
• Teratogenesis
• Cataract
• Neoplasia:
– Acute myeloid leukaemia
– Thyroid
– Salivary glands
– Skin
– Others

Haemopoietic syndrome
Absorption of 2–10 Gy is followed by transient vomiting in some individuals,
followed by a period of improvement. Lymphocytes are particularly sensitive to
radiation damage; severe lymphopenia develops over several days. A decrease in
granulocytes and platelets follows 2–3 weeks later, since no new cells are formed
in the marrow. Thrombocytopenia develops with bleeding and frequent
overwhelming infections; there is a high mortality.
Gastrointestinal syndrome
Doses >6 Gy cause vomiting several hours after exposure. This then stops, only
to recur some 4 days later, accompanied by diarrhoea. The villous lining of the
intestine becomes denuded. Intractable bloody diarrhoea follows, with
dehydration, secondary infection and sometimes death.

CNS syndrome
Exposures of >30 Gy are followed rapidly by nausea, vomiting, disorientation
and coma. Death due to cerebral oedema can follow, usually within 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 >5 Gy.

Late effects of radiation exposure

Survivors of the nuclear bombing of Hiroshima and Nagasaki in 1945 provided
data on long-term radiation effects. Risks of acute myeloid leukaemia and
cancer, particularly of skin, thyroid and salivary glands, increase. Infertility,
teratogenesis and cataract are also late sequelae, developing years after exposure.

Major nuclear power plant accidents

Two high-level nuclear accidents have occurred: the first in 1986 in Chernobyl
in the Ukraine (part of the Soviet Union at the time), and the second in 2011 in
Fukushima in Japan.
In Chernobyl, 30 people died in the first 3 months due to radiation and other
factors. The majority of the people in the area received only a very low dose of
radiation and only cancer of the thyroid has been found as a long-term
consequence.
In the Fukushima disaster, which occurred following an earthquake that
generated tsunamis along the east coast of Japan, radiation release was 10–30%
of that released in Chernobyl. There were no immediate deaths due to radiation
and the long-term effect of radiation is thought likely to be small.
The major problems caused by both disasters relate to psychological and
social effects, as a result of the populations' evacuation and removal from their
homes for years following the accidents, as well as a general concern about the
effects of radiation on themselves and their children.
 Figure 5.3 shows the measures needed in a nuclear disaster.

FIGURE 5.3 General disaster and nuclear disaster cycle. The measures shown in
boxes refer to a programme specifically for a nuclear disaster. Those not in boxes are
measures required for any large-scale disaster. (From Ohtsuru A, Tanigawa K, Kumagai A et al. Nuclear
disasters and health: lessons learned, challenges, and proposals. Lancet 2015; 386:489–499, with permission.)

Therapeutic radiation
The sequelae of therapeutic radiation – early, early-delayed and late-delayed
radiation effects – are discussed on page 604. Focusing techniques are used to
target radiation towards the field being treated, so that radiosensitive structures,
such as the ovaries, are protected by shielding.

Management
Acute radiation sickness is an emergency. Absorption of the initial radiation dose
can be reduced by removing contaminated clothing.
Management is largely supportive: prevention and treatment of infection,
haemorrhage and fluid loss. Harvesting of blood products is sometimes carried
out.
Accidental ingestion of, or exposure to, bone-seeking radio-isotopes (e.g.
90
strontium and 137caesium) is treated with chelating agents, such as EDTA and
massive doses of oral calcium. Radio-iodine contamination should be treated
immediately with potassium iodide to block radio-iodine absorption by the
thyroid.

Further reading
Christodouleas JP, Forrest RD, Ainsley CG et al. Short-term and long-term
health risks of nuclear-power-plant accidents. N Engl J Med 2011; 364:2334–
2341.
Clancey G, Chhem R. Hiroshima, Nagasaki and Fukushima. Lancet 2015;
386:405–406.
Ohtsuru A, Tanigawa K et al. A nuclear shadow from Hiroshima and
Nagasaki to Fukushima. Lancet 2015; 386:403.

Electric Shock
Electric shock can produce:
• Pain and psychological sequelae. The common domestic electric shock is
typically painful, but rarely fatal or followed by serious sequelae. Nevertheless,
it is an unpleasant and intensely frightening experience. A brief, immediate
jerking episode can occur, which is not an epileptic seizure. There is usually no
lasting neurological, cardiac or skin damage.
• More serious effects. These are distinctly rare following accidents in the home
or in industry, but claims by survivors following industrial accidents are
frequently made.
• Cardiac, neurological and muscle damage. Ventricular fibrillation, muscular
contraction and spinal cord damage can follow a major shock.
• Electrical burns. These are commonly restricted to the skin. Muscle necrosis
and spinal cord damage can also occur.
• Electrocution. This means death following ventricular fibrillation, either
accidentally, or deliberately as a method of execution. In the USA, at
executions, an initial voltage of >2000 volts was applied for some 15 s in the
electric chair, causing loss of consciousness and ventricular fibrillation, before
 the voltage was lowered. The TCore during the execution process would
sometimes reach >50°C, leading to severe damage to internal organs.

Lightning Strike
Cloud-to-ground lightning originating in thunderstorms. Human tissues are
directly damaged by the high-voltage DC current of >10 million volts that lasts
only for a few milliseconds. The result is cardiac arrest due to asystole.
Fern-shaped burns are seen on the skin. The victim's clothes explode off the
body and the person is pulseless, not breathing and in coma. The only chance of
survival at this stage is bystander cardiopulmonary resuscitation. The mortality
is high and those who survive are left with variable CNS damage.

Further reading
Davis C, Engeln A, Johnson E et al. Wilderness Medical Society practice
guidelines for the prevention and treatment of lightning injuries. Wilderness
Environ Med 2012; 23:260.

Smoke
Smoke is air containing toxic and/or irritant gases and carbon particles, coated
with organic acids, aldehydes and synthetic materials. Carbon monoxide, sulphur
dioxide, sulphuric and hydrochloric acids, and other toxins may also be present.
The highly toxic polyvinyl chloride is no longer used in household goods. Air
pollution is discussed on page 56.
On smoke inhalation, patients become breathless and tachypnoeic
immediately. Choking and stridor may require intubation. Pulmonary oedema
and hypoxia can be fatal.
Breathing through a wet towel or clothing is the best emergency treatment.
Remove the victim from the scene as rapidly as possible. Give oxygen and
arrange ITU support.
Prevention. Smoke alarms, regularly checked, should be installed in every
household.

Noise
Sound intensity is expressed as the square of sound pressure. The bel is the ratio
equivalent to a 10-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 Hz to
20 kHz, most being between 1 and 4 kHz. 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 of >90 dB(A).
Repeated, prolonged exposure to loud noise, particularly between 2 and
6 kHz, causes first temporary and later permanent hearing loss, by physically
destroying hair cells in the organ of Corti and, eventually, auditory neurones.
Noise-induced hearing loss is a common occupational problem, not only in
industry and the armed forces, but also in the home (drills and sanders), in sport
(motor racing) and in entertainment (musicians, DJs and their audiences).
Serious noise-induced hearing loss is almost wholly preventable by personal
protection (ear muffs, ear plugs). Little can be offered once hearing loss has
become established.

Other effects of noise

Noise is intensely irritative, increasing or producing anxiety and anger.
Excessive, repetitive noise is used in torture. Excess noise possibly affects child
development and reading skills.

Further reading
Basner M, Babisch W, Davis A et al. Auditory and non-auditory effects of
noise on health. Lancet 2014; 383:1325–1322.

Bioterrorism/Biowarfare
Interest in biological warfare and bioterrorism intensified during the 1991 Iraq
war and later, following the destruction of the Twin Towers in New York in
2001. The potential of bacteria as weapons is illustrated by a suggestion that
several kilograms of anthrax spores might kill as many people as a Hiroshima-
sized nuclear weapon.

Potential pathogens
The US Centers for Disease Control and Prevention in Atlanta, Georgia, have
developed a classification of potential biological agents (Box 5.6).
  Box 5.6
Critical biological agents

Category
A. Very infectious and/or readily disseminated organisms: high
mortality with a major impact on public health
B. Moderately easy to disseminate organisms: moderate morbidity
and mortality
C. Emerging and possible genetically engineered pathogens
Pathogens
Smallpox, anthrax, botulism, plague,
tularaemia, viruses
Q fever, brucellosis, glanders, food-/water-
borne pathogens, influenza
Viral haemorrhagic fevers, encephalitis
viruses, drug-resistant tuberculosis

(Adapted from Khan AS, Morse S, Lillibridge S. Public health preparedness for biological
terrorism in the USA. Lancet 2000; 356:1179–1182, with permission.)

Smallpox
Smallpox is a highly infectious disease with a mortality of >30%. There is no
proven therapy but there is an effective vaccine. Universal vaccination was
stopped in the early 1970s; the vast majority of the world's population is now
unprotected against the variola virus (see p. 251). The potential exists for a
worldwide epidemic of smallpox, possibly initiated by a bioterrorist act.
Smallpox has an incubation period of around 12 days, allowing any initial
source of infection to go undetected until the rash (Fig. 5.4), similar to that of
chickenpox, develops on the second or third day of the illness. Infection is
transmitted by the airborne route; the patient becomes infectious to others 12–
24 hours before the rash appears, thus allowing a potential infected volunteer to
pass infection to others before being recognized as suffering from smallpox. If
vaccines were to be administered widely to those potentially infected within
3 days of contact, an epidemic might well be prevented. Smallpox virus is stored
in two secure laboratories: in Russia and in the USA. Supplies of vaccine are
potentially available worldwide.
 FIGURE 5.4 Smallpox rash.

Anthrax
In late 2001, anthrax organisms (see p. 287) were sent through the US mail and
infected 22 individuals. Of these, 11 developed pulmonary anthrax, 5 of whom
died; 11 suffered from cutaneous anthrax.
A simulated anthrax attack postulated release of anthrax powder from a truck
passing a sports stadium with 74 000 spectators; 16 000 were estimated to have
become infected, with a death rate of 25%. In Russia, following accidental
release of anthrax from a bioweapons factory, the death rate was substantial in
those nearby, especially downwind.

Botulism
The toxin produced by Clostridium botulinum is one of the most potent poisons
known (see p. 280).
As a bioweapon, botulinum toxin could be transmitted in food or by air: for
example, from a crop-spraying light aircraft. The toxin is inactivated by chlorine
in domestic water supplies. There is no vaccine available.

Plague
Plague (see p. 291) could potentially be used as a bioweapon either by airborne
dissemination or by transmission by infected rats. Immunization is of limited
value.
 Other potential infective agents are listed in Box 5.6.

Emergency planning
Many countries have plans to deal with bioterrorist attacks. These include
training of healthcare staff and police. Such plans indicate the governments'
awareness of the possibility of these threats. Stockpiling of vaccines, antibiotics
and protective clothing is essential.

Further reading
Adaja AA, Toner A, Inglesby TV. Clinical management of potential
bioterrorism-related conditions. New Engl J Med 2015; 372:954–962.
Berkelman RL, Hartley DM. Syndromic surveillance and bioterrorism-
related epidemics. Emerg Infect Dis 2003; 10:1197–1204.

Travel

Motion sickness
This common problem is caused by repetitive stimulation of the labyrinth.
Motion sickness occurs frequently at sea and in cars (especially in children), but
also with less usual forms of transport such as camels or elephants. Nowadays,
motion sickness is rare during commercial flights, but it is a problem during
space travel and on airships – one reason why the airship industry has not
flourished.
Nausea, sweating, dizziness, vertigo and profuse vomiting occur, accompanied
by an irresistible desire to stop moving. Prostration and intense incapacitating
malaise can develop: for example, in seasickness.
Prophylactic antihistamines, vestibular sedatives (hyoscine or cinnarizine) and
stem ginger are of some value.

Air travel
The incidence of deep venous thrombosis and pulmonary embolism is slightly
greater in sedentary passengers on long-haul flights than in a similar population
at sea level. Dehydration and alcohol probably contribute. Prophylactic aspirin is
not recommended but moving the legs regularly and walking around the cabin
every hour may be beneficial.
Commercial aircraft cabins are pressurized (see p. 54). Patients with
respiratory disease, particularly chronic obstructive pulmonary disease, may well
require oxygen therapy. They should seek advice from their airline.
All patients must be sure to take tablets and other therapy with them in the
cabin in case they are required during the flight. Always consult the airline if
there is any concern regarding health issues.

Inflight medical emergencies

Half of inflight emergencies are attended by doctors. The main problems are
syncope, chest symptoms (cough and pain) and gastrointestinal symptoms. Most
patients are managed successfully but approximately 25% require hospitalization
on arrival at their destination.

Jet-lag
Jet-lag (circadian dyschronism) is the well-known phenomenon that follows
travelling through time-zones, particularly from west to east. Intense insomnia,
fatigue, poor concentration, irritability and loss of appetite are common.
Headaches may occur. Symptoms last several days.
Mechanisms relate to the hypothalamic body clock within the suprachiasmatic
nuclei. The clock is regulated by various Zeit​gebers (time-givers), such as light
and melatonin.
Management of jet-lag includes its acceptance as a phenom​enon causing poor
performance – and thus waiting for 3–5 days to recover, drinking plenty of fluid
and avoiding alcohol. Various hypnotics can help insomnia but their value is
disputed. Oral melatonin is widely used to reduce jet-lag but is not available on
prescription in the UK. Melatonin probably hastens resetting of the body clock.

Further reading
Peterson DC, Mortongill C, Guyetta FX et al. Outcomes of medical
emergencies on commercial aircraft flights. New Engl J Med 2013; 368:2075–
2083.
Sack R. Jet lag. N Engl J Med 2010; 362:440–447.
Silverman D, Gendeau M. Medical issues associated with commercial
flights. Lancet 2009; 373:2067–2077.
 Waterhouse J, Reilly T, Atkinson G. Jetlag: trends and coping strategies.
Lancet 2007; 369:1117–1129.

Building-Related Illnesses
Non-specific building-related illness
Multi-storey buildings typically have a controlled environment, often with
automated heating and air-conditioning, and no ready access to external
ventilation. More than half the adult workforce in developed countries works in
such buildings.
Headache, fatigue and difficulty concentrating, sometimes in epidemics, are
the main complaints but these have become less frequent. Psychological factors
are thought to play a substantial role. Temperature, humidity, dust, volatile
organic compounds, such as paints and solvents, and even low-level carbon
monoxide toxicity have all been blamed, none with any scientific foundation.

Specific building-related illness

Legionnaires' disease (see p. 1105) can follow contamination of air-
conditioning systems.
Humidifier fever (see p. 1117) is also due to contaminated systems, probably
by fungi, bacteria and protozoa. Many common viruses are potentially
transmissible in an enclosed environment, such as the common cold, influenza
and, rarely, pulmonary tuberculosis. Allergic disorders, like rhinitis, asthma and
dermatitis, also occur following exposure to indoor allergens such as dust mites
and plants. Office equipment – for example, fumes from photocopiers – has also
been implicated. Passive smoking (see p. 1075) is no longer an issue in Europe
and North America, following legislation against smoking.