The act of taking any substance (for example, food, drink, or medications) into the body through the mouth. The term also refers to the process by which certain cells (for example, some white blood cells) surround and then engulf small particles.
The toxin has two components, one having haemagglutinin activity and the other neurotoxic activity which produces most of the symptoms. It has a lethal dose of as little as 1 mg/kg and is highly selective for cholinergic nerves. Thus the symptoms are those of autonomic parasympathetic blockade (dry mouth, constipation, urinary retention, mydriasis, blurred vision) and progress to blockade of somatic cholinergic transmission (muscle weakness). Death results from respiratory muscle paralysis. Treatment consists of supportive measures and 4 aminopyridine and 3, 4 di-aminopyridine, which may antagonise the e?ect of the toxin.... botulism
– although lead-containing paints are no longer used for items that children may be in contact with.
Acute poisonings are rare. Clinical features include metallic taste, abdominal pain, vomiting, diarrhoea, ANOREXIA, fatigue, muscle weakness and SHOCK. Neurological effects may include headache, drowsiness, CONVULSIONS and COMA. Inhalation results in severe respiratory-tract irritation and systemic symptoms as above.
Chronic poisonings cause gastrointestinal disturbances and constipation. Other effects are ANAEMIA, weakness, pallor, anorexia, insomnia, renal HYPERTENSION and mental fatigue. There may be a bluish ‘lead line’ on the gums, although this is rarely seen. Neuromuscular dysfunction may result in motor weakness and paralysis of the extensor muscles of the wrist and ankles. ENCEPHALOPATHY and nephropathy are severe effects. Chronic low-level exposures in children are linked with reduced intelligence and behavioural and learning disorders.
Treatment Management of patients who have been poisoned is supportive, with removal from source, gastric decontamination if required, and X-RAYS to monitor the passage of metallic lead through the gut if ingested. It is essential to ensure adequate hydration and renal function. Concentrations of lead in the blood should be monitored; where these are found to be toxic, chelation therapy should be started. Several CHELATING AGENTS are now available, such as DMSA (Meso-2,3dimercaptosuccinic acid), sodium calcium edetate (see EDTA) and PENICILLAMINE. (See also POISONS.)... lead poisoning
Staphylococcal food poisoning occurs after food such as meat products, cold meats, milk, custard and egg products becomes contaminated before or after cooking, usually through incorrect handling by humans who carry S. aureus. The bacteria produce an ENTEROTOXIN which causes the symptoms of food poisoning 1–8 hours after ingestion. The toxin can withstand heat; thus, subsequent cooking of contaminated food will not prevent illness.
Heat-resistant strains of Cl. perfringens cause food poisoning associated with meat dishes, soups or gravy when dishes cooked in bulk are left unrefrigerated for long periods before consumption. The bacteria are anaerobes (see ANAEROBE) and form spores; the anaerobic conditions in these cooked foods allow the germinated spores to multiply rapidly during cooling, resulting in heavy contamination. Once ingested the bacteria produce enterotoxin in the intestine, causing symptoms within 8–24 hours.
Many di?erent types of Salmonella (about 2,000) cause food poisoning or ENTERITIS, from eight hours to three days after ingestion of food in which they have multiplied. S. brendeny, S. enteritidis, S. heidelberg, S. newport and S. thompson are among those commonly causing enteritis. Salmonella infections are common in domesticated animals such as cows, pigs and poultry whose meat and milk may be infected, although the animals may show no symptoms. Duck eggs may harbour Salmonella (usually S. typhimurium), arising from surface contamination with the bird’s faeces, and foods containing uncooked or lightly cooked hen’s eggs, such as mayonnaise, have been associated with enteritis. The incidence of human S. enteritidis infection has been increasing, by more than 15-fold in England and Wales annually, from around 1,100 a year in the early 1980s to more than 32,000 at the end of the 1990s, but has since fallen to about 10,000. A serious source of infection seems to be poultry meat and hen’s eggs.
Although Salmonella are mostly killed by heating at 60 °C for 15 minutes, contaminated food requires considerably longer cooking and, if frozen, must be completely thawed beforehand, to allow even cooking at a su?cient temperature.
Enteritis caused by Campylobacter jejuni is usually self-limiting, lasting 1–3 days. Since reporting of the disease began in 1977, in England and Wales its incidence has increased from around 1,400 cases initially to nearly 13,000 in 1982 and to over 42,000 in 2004. Outbreaks have been associated with unpasteurised milk: the main source seems to be infected poultry.
ESCHERICHIA COLI O157 was ?rst identi?ed as a cause of food poisoning in the early 1980s, but its incidence has increased sharply since, with more than 1,000 cases annually in the United Kingdom in the late 1990s. The illness can be severe, with bloody diarrhoea and life-threatening renal complications. The reservoir for this pathogen is thought to be cattle, and transmission results from consumption of raw or undercooked meat products and raw dairy products. Cross-infection of cooked meat by raw meat is a common cause of outbreaks of Escherichia coli O157 food poisoning. Water and other foods can be contaminated by manure from cattle, and person-to-person spread can occur, especially in children.
Food poisoning associated with fried or boiled rice is caused by Bacillus cereus, whose heat-resistant spores survive cooking. An enterotoxin is responsible for the symptoms, which occur 2–8 hours after ingestion and resolve after 8–24 hours.
Viruses are emerging as an increasing cause of some outbreaks of food poisoning from shell?sh (cockles, mussels and oysters).
The incidence of food poisoning in the UK rose from under 60,000 cases in 1991 to nearly 79,000 in 2004. Public health measures to control this rise include agricultural aspects of food production, implementing standards of hygiene in abattoirs, and regulating the environment and process of industrial food production, handling, transportation and storage.... food poisoning
Habitat: Native to Mediterranean region; cultivated in North India, Maharashtra and South India.
English: Beet Root, Garden Beet, Chard.Ayurvedic: Palanki.Folk: Chukandar.Action: Leaf—used in burns and bruises, also for diseases of spleen and liver. Tuber and seed— expectorant. Leaf and seed— diuretic. Leaf, tuber and seed— anti-inflammatory. Seed oil— analgesic.
Beet roots are eaten raw as salad or cooked. The leaves are nutritionally superior to roots and are a good source of vitamins and minerals.The plant contains alkaloids ofwhich betaine is a mild diuretic and emme- nagogue.In research, using rats, chard increased regeneration of beta cells in pancreas. Maximum reduction of blood glucose was after 42 days of administration. (J Ethnopharmacol, 2000, 73: 251-259.)Beets are used orally as a supportive therapy in the treatment of liver diseases and fatty liver (possibly due to betaine). Ingestion of large quantities might worsen kidney disease. (Natural Medicines Comprehensive Database, 2007.)... beta vulgarisTreatment Administration of oxygen when available is the most important ?rst-aid management. Rescuers should be trained, must not put themselves at risk, and should use protective clothing and breathing apparatus. In unconscious victims, establish a clear airway and give 100 per cent oxygen. If breathing stops and oxygen is unavailable, initiate expired-air resuscitation. If cyanide salts were ingested, mouth-to-mouth contact must be avoided and a mask with a one-way valve employed instead. Some commercially available ?rst-aid kits contain AMYL NITRATE as an antidote which may be employed if oxygen is unavailable.
Once in hospital, or if a trained physician is on the scene, then antidotes may be administered. There are several di?erent intravenous antidotes that may be used either alone or in combination. In mild to moderate cases, sodium thiosulphate is usually given. In more severe cases either dicobalt edetate or sodium nitrite may be used, followed by sodium thio-sulphate. Some of these (e.g. dicobalt edetate) should be given only where diagnosis is certain, otherwise serious adverse reations or toxicity due to the antidotes may occur.... cyanide poisoning
Severe poisoning from ingestion of fungi is very rare, since relatively few species are highly toxic and most species do not contain toxic compounds. The most toxic species are those containing amatoxins such as death cap (Amanita phalloides); this species alone is responsible for about 90 per cent of all mushroom-related deaths. There is a latent period of six hours or more between ingestion and the onset of clinical effects with these more toxic species. The small intestine, LIVER and KIDNEYS may be damaged – therefore, any patient with gastrointestinal effects thought to be due to ingestion of a mushroom should be referred immediately to hospital where GASTRIC LAVAGE and treatment with activated charcoal can be carried out, along with parenteral ?uids and haemodialysis if the victim is severely ill. In most cases where effects occur, these are early-onset gastrointestinal effects due to ingestion of mushrooms containing gastrointestinal irritants.
Muscarine is the poisonous constituent of some species. Within two hours of ingestion, the victim starts salivating and sweating, has visual disturbances, vomiting, stomach cramps, diarrhoea, vertigo, confusion, hallucinations and coma, the severity of symptoms depending on the amount eaten and type of mushroom. Most people recover in 24 hours, with treatment.
‘Magic’ mushrooms are a variety that contains psilocybin, a hallucinogenic substance. Children who take such mushrooms may develop a high fever and need medical care. In adults the symptoms usually disappear within six hours.
Treatment If possible, early gastric lavage should be carried out in all cases of suspected poisoning. Identi?cation of the mushroom species is a valuable guide to treatment. For muscarine poisoning, ATROPINE is a speci?c antidote. As stated above, hospital referral is advisable for people who have ingested poisonous fungi.... fungus poisoning
Occupational health includes both mental and physical health. It is about compliance with health-and-safety-at-work legislation (and common law duties) and about best practice in providing work environments that reduce risks to health and safety to lowest practicable levels. It includes workers’ ?tness to work, as well as the management of the work environment to accommodate people with disabilities, and procedures to facilitate the return to work of those absent with long-term illness. Occupational health incorporates several professional groups, including occupational physicians, occupational health nurses, occupational hygienists, ergonomists, disability managers, workplace counsellors, health-and-safety practitioners, and workplace physiotherapists.
In the UK, two key statutes provide a framework for occupational health: the Health and Safety at Work, etc. Act 1974 (HSW Act); and the Disability Discrimination Act 1995 (DDA). The HSW Act states that employers have a duty to protect the health, safety and welfare of their employees and to conduct their business in a way that does not expose others to risks to their health and safety. Employees and self-employed people also have duties under the Act. Modern health-and-safety legislation focuses on assessing and controlling risk rather than prescribing speci?c actions in di?erent industrial settings. Various regulations made under the HSW Act, such as the Control of Substances Hazardous to Health Regulations, the Manual Handling Operations Regulations and the Noise at Work Regulations, set out duties with regard to di?erent risks, but apply to all employers and follow the general principles of risk assessment and control. Risks should be controlled principally by removing or reducing the hazard at source (for example, by substituting chemicals with safer alternatives, replacing noisy machinery, or automating tasks to avoid heavy lifting). Personal protective equipment, such as gloves and ear defenders, should be seen as a last line of defence after other control measures have been put in place.
The employment provisions of the DDA require employers to avoid discriminatory practice towards disabled people and to make reasonable adjustments to working arrangements where a disabled person is placed at a substantial disadvantage to a non-disabled person. Although the DDA does not require employers to provide access to rehabilitation services – even for those injured or made ill at work – occupational-health practitioners may become involved in programmes to help people get back to work after injury or long-term illness, and many businesses see the retention of valuable sta? as an attractive alternative to medical retirement or dismissal on health grounds.
Although a major part of occupational-health practice is concerned with statutory compliance, the workplace is also an important venue for health promotion. Many working people rarely see their general practitioner and, even when they do, there is little time to discuss wider health issues. Occupational-health advisers can ?ll in this gap by providing, for example, workplace initiatives on stopping smoking, cardiovascular health, diet and self-examination for breast and testicular cancers. Such initiatives are encouraged because of the perceived bene?ts to sta?, to the employing organisation and to the wider public-health agenda. Occupational psychologists recognise the need for the working population to achieve a ‘work-life balance’ and the promotion of this is an increasing part of occupational health strategies.
The law requires employers to consult with their sta? on health-and-safety matters. However, there is also a growing understanding that successful occupational-health management involves workers directly in the identi?cation of risks and in developing solutions in the workplace. Trade unions play an active role in promoting occupational health through local and national campaigns and by training and advising elected workplace safety representatives.
Occupational medicine The branch of medicine that deals with the control, prevention, diagnosis, treatment and management of ill-health and injuries caused or made worse by work, and with ensuring that workers are ?t for the work they do.
Occupational medicine includes: statutory surveillance of workers’ exposure to hazardous agents; advice to employers and employees on eliminating or reducing risks to health and safety at work; diagnosis and treatment/management of occupational illness; advice on adapting the working environment to suit the worker, particularly those with disabilities or long-term health problems; and advice on the return to work and, if necessary, rehabilitation of workers absent through illness. Occupational physicians may play a wider role in monitoring the health of workplace populations and in advising employers on controlling health hazards where ill-health trends are observed. They may also conduct epidemiological research (see EPIDEMIOLOGY) on workplace diseases.
Because of the occupational physician’s dual role as adviser to both employer and employee, he or she is required to be particularly diligent with regards to the individual worker’s medical CONFIDENTIALITY. Occupational physicians need to recognise in any given situation the context they are working in, and to make sure that all parties are aware of this.
Occupational medicine is a medical discipline and thus is only part of the broader ?eld of occupational health. Although there are some speci?c clinical duties associated with occupational medicine, such as diagnosis of occupational disease and medical screening, occupational physicians are frequently part of a multidisciplinary team that might include, for example, occupational-health nurses, healthand-safety advisers, ergonomists, counsellors and hygienists. Occupational physicians are medical practitioners with a post-registration quali?cation in occupational medicine. They will have completed a period of supervised in-post training. In the UK, the Faculty of Occupational Medicine of the Royal College of Physicians has three categories of membership, depending on quali?cations and experience: associateship (AFOM); membership (MFOM); and fellowship (FFOM).
Occupational diseases Occupational diseases are illnesses that are caused or made worse by work. In their widest sense, they include physical and mental ill-health conditions.
In diagnosing an occupational disease, the clinician will need to examine not just the signs and symptoms of ill-health, but also the occupational history of the patient. This is important not only in discovering the cause, or causes, of the disease (work may be one of a number of factors), but also in making recommendations on how the work should be modi?ed to prevent a recurrence – or, if necessary, in deciding whether or not the worker is able to return to that type of work. The occupational history will help in deciding whether or not other workers are also at risk of developing the condition. It will include information on:
the nature of the work.
how the tasks are performed in practice.
the likelihood of exposure to hazardous agents (physical, chemical, biological and psychosocial).
what control measures are in place and the extent to which these are adhered to.
previous occupational and non-occupational exposures.
whether or not others have reported similar symptoms in relation to the work. Some conditions – certain skin conditions,
for example – may show a close relationship to work, with symptoms appearing directly only after exposure to particular agents or possibly disappearing at weekends or with time away from work. Others, however, may be chronic and can have serious long-term implications for a person’s future health and employment.
Statistical information on the prevalence of occupational disease in the UK comes from a variety of sources, including o?cial ?gures from the Industrial Injuries Scheme (see below) and statutory reporting of occupational disease (also below). Neither of these o?cial schemes provides a representative picture, because the former is restricted to certain prescribed conditions and occupations, and the latter suffers from gross under-reporting. More useful are data from the various schemes that make up the Occupational Diseases Intelligence Network (ODIN) and from the Labour Force Survey (LFS). ODIN data is generated by the systematic reporting of work-related conditions by clinicians and includes several schemes. Under one scheme, more than 80 per cent of all reported diseases by occupational-health physicians fall into just six of the 42 clinical disease categories: upper-limb disorders; anxiety, depression and stress disorders; contact DERMATITIS; lower-back problems; hearing loss (see DEAFNESS); and ASTHMA. Information from the LFS yields a similar pattern in terms of disease frequency. Its most recent survey found that over 2 million people believed that, in the previous 12 months, they had suffered from an illness caused or made worse by work and that
19.5 million working days were lost as a result. The ten most frequently reported disease categories were:
stress and mental ill-health (see MENTAL ILLNESS): 515,000 cases.
back injuries: 508,000.
upper-limb and neck disorders: 375,000.
lower respiratory disease: 202,000.
deafness, TINNITUS or other ear conditions: 170,000.
lower-limb musculoskeletal conditions: 100,000.
skin disease: 66,000.
headache or ‘eyestrain’: 50,000.
traumatic injury (includes wounds and fractures from violent attacks at work): 34,000.
vibration white ?nger (hand-arm vibration syndrome): 36,000. A person who develops a chronic occu
pational disease may be able to sue his or her employer for damages if it can be shown that the employer was negligent in failing to take reasonable care of its employees, or had failed to provide a system of work that would have prevented harmful exposure to a known health hazard. There have been numerous successful claims (either awarded in court, or settled out of court) for damages for back and other musculoskeletal injuries, hand-arm vibration syndrome, noise-induced deafness, asthma, dermatitis, MESOTHELIOMA and ASBESTOSIS. Employers’ liability (workers’ compensation) insurers are predicting that the biggest future rise in damages claims will be for stress-related illness. In a recent study, funded by the Health and Safety Executive, about 20 per cent of all workers – more than 5 million people in the UK – claimed to be ‘very’ or ‘extremely’ stressed at work – a statistic that is likely to have a major impact on the long-term health of the working population.
While victims of occupational disease have the right to sue their employers for damages, many countries also operate a system of no-fault compensation for the victims of prescribed occupational diseases. In the UK, more than 60 diseases are prescribed under the Industrial Injuries Scheme and a person will automatically be entitled to state compensation for disability connected to one of these conditions, provided that he or she works in one of the occupations for which they are prescribed. The following short list gives an indication of the types of diseases and occupations prescribed under the scheme:
CARPAL TUNNEL SYNDROME connected to the use of hand-held vibrating tools.
hearing loss from (amongst others) use of pneumatic percussive tools and chainsaws, working in the vicinity of textile manufacturing or woodworking machines, and work in ships’ engine rooms.
LEPTOSPIROSIS – infection with Leptospira (various listed occupations).
viral HEPATITIS from contact with human blood, blood products or other sources of viral hepatitis.
LEAD POISONING, from any occupation causing exposure to fumes, dust and vapour from lead or lead products.
asthma caused by exposure to, among other listed substances, isocyanates, curing agents, solder ?ux fumes and insects reared for research.
mesothelioma from exposure to asbestos.
In the UK, employers and the self-employed have a duty to report all occupational injuries (if the employee is o? work for three days or more as a result), diseases or dangerous incidents to the relevant enforcing authority (the Health and Safety Executive or local-authority environmental-health department) under the Reporting of Injuries, Diseases and Dangerous Occurrences Regulations 1995 (RIDDOR). Despite this statutory duty, comparatively few diseases are reported so that ?gures generated from RIDDOR reports do not give a useful indication of the scale of occupational diseases in the UK. The statutory reporting of injuries is much better, presumably because of the clear and acute relationship between a workplace accident and the resultant injury. More than 160,000 injuries are reported under RIDDOR every year compared with just 2,500 or so occupational diseases, a gross underestimate of the true ?gure.
There are no precise ?gures for the number of people who die prematurely because of work-related ill-health, and it would be impossible to gauge the exact contribution that work has on, for example, cardiovascular disease and cancers where the causes are multifactorial. The toll would, however, dwarf the number of deaths caused by accidents at work. Around 250 people are killed by accidents at work in the UK each year – mesothelioma, from exposure to asbestos at work, alone kills more than 1,300 people annually.
The following is a sample list of occupational diseases, with brief descriptions of their aetiologies.
Inhaled materials
PNEUMOCONIOSIS covers a group of diseases which cause ?brotic lung disease following the inhalation of dust. Around 250–300 new cases receive bene?t each year – mostly due to coal dust with or without silica contamination. SILICOSIS is the more severe disease. The contraction in the size of the coal-mining industry as well as improved dust suppression in the mines have diminished the importance of this disease, whereas asbestos-related diseases now exceed 1,000 per year. Asbestos ?bres cause a restrictive lung disease but also are responsible for certain malignant conditions such as pleural and peritoneal mesothelioma and lung cancer. The lung-cancer risk is exacerbated by cigarette-smoking.
Even though the use of asbestos is virtually banned in the UK, many workers remain at risk of exposure because of the vast quantities present in buildings (much of which is not listed in building plans). Carpenters, electricians, plumbers, builders and demolition workers are all liable to exposure from work that disturbs existing asbestos. OCCUPATIONAL ASTHMA is of increasing importance – not only because of the recognition of new allergic agents (see ALLERGY), but also in the number of reported cases. The following eight substances are most frequently linked to occupational asthma (key occupations in brackets): isocyanates (spray painters, electrical processors); ?our and grain (bakers and farmers); wood dust (wood workers); glutaraldehyde (nurses, darkroom technicians); solder/colophony (welders, electronic assembly workers); laboratory animals (technicians, scientists); resins and glues (metal and electrical workers, construction, chemical processors); and latex (nurses, auxiliaries, laboratory technicians).
The disease develops after a short, symptomless period of exposure; symptoms are temporally related to work exposures and relieved by absences from work. Removal of the worker from exposure does not necessarily lead to complete cessation of symptoms. For many agents, there is no relationship with a previous history of ATOPY. Occupational asthma accounts for about 10 per cent of all asthma cases. DERMATITIS The risk of dermatitis caused by an allergic or irritant reaction to substances used or handled at work is present in a wide variety of jobs. About three-quarters of cases are irritant contact dermatitis due to such agents as acids, alkalis and solvents. Allergic contact dermatitis is a more speci?c response by susceptible individuals to a range of allergens (see ALLERGEN). The main occupational contact allergens include chromates, nickel, epoxy resins, rubber additives, germicidal agents, dyes, topical anaesthetics and antibiotics as well as certain plants and woods. Latex gloves are a particular cause of occupational dermatitis among health-care and laboratory sta? and have resulted in many workers being forced to leave their profession through ill-health. (See also SKIN, DISEASES OF.)
Musculoskeletal disorders Musculoskeletal injuries are by far the most common conditions related to work (see LFS ?gures, above) and the biggest cause of disability. Although not all work-related, musculoskeletal disorders account for 36.5 per cent of all disabilities among working-age people (compared with less than 4 per cent for sight and hearing impairment). Back pain (all causes – see BACKACHE) has been estimated to cause more than 50 million days lost every year in sickness absence and costs the UK economy up to £5 billion annually as a result of incapacity or disability. Back pain is a particular problem in the health-care sector because of the risk of injury from lifting and moving patients. While the emphasis should be on preventing injuries from occurring, it is now well established that the best way to manage most lower-back injuries is to encourage the patient to continue as normally as possible and to remain at work, or to return as soon as possible even if the patient has some residual back pain. Those who remain o? work on long-term sick leave are far less likely ever to return to work.
Aside from back injuries, there are a whole range of conditions affecting the upper limbs, neck and lower limbs. Some have clear aetiologies and clinical signs, while others are less well de?ned and have multiple causation. Some conditions, such as carpal tunnel syndrome, are prescribed diseases in certain occupations; however, they are not always caused by work (pregnant and older women are more likely to report carpal tunnel syndrome irrespective of work) and clinicians need to be careful when assigning work as the cause without ?rst considering the evidence. Other conditions may be revealed or made worse by work – such as OSTEOARTHRITIS in the hand. Much attention has focused on injuries caused by repeated movement, excessive force, and awkward postures and these include tenosynovitis (in?ammation of a tendon) and epicondylitis. The greatest controversy surrounds upper-limb disorders that do not present obvious tissue or nerve damage but nevertheless give signi?cant pain and discomfort to the individual. These are sometimes referred to as ‘repetitive strain injury’ or ‘di?use RSI’. The diagnosis of such conditions is controversial, making it di?cult for sufferers to pursue claims for compensation through the courts. Psychosocial factors, such as high demands of the job, lack of control and poor social support at work, have been implicated in the development of many upper-limb disorders, and in prevention and management it is important to deal with the psychological as well as the physical risk factors. Occupations known to be at particular risk of work-related upper-limb disorders include poultry processors, packers, electronic assembly workers, data processors, supermarket check-out operators and telephonists. These jobs often contain a number of the relevant exposures of dynamic load, static load, a full or excessive range of movements and awkward postures. (See UPPER LIMB DISORDERS.)
Physical agents A number of physical agents cause occupational ill-health of which the most important is occupational deafness. Workplace noise exposures in excess of 85 decibels for a working day are likely to cause damage to hearing which is initially restricted to the vital frequencies associated with speech – around 3–4 kHz. Protection from such noise is imperative as hearing aids do nothing to ameliorate the neural damage once it has occurred.
Hand-arm vibration syndrome is a disorder of the vascular and/or neural endings in the hands leading to episodic blanching (‘white ?nger’) and numbness which is exacerbated by low temperature. The condition, which is caused by vibrating tools such as chain saws and pneumatic hammers, is akin to RAYNAUD’S DISEASE and can be disabling.
Decompression sickness is caused by a rapid change in ambient pressure and is a disease associated with deep-sea divers, tunnel workers and high-?ying aviators. Apart from the direct effects of pressure change such as ruptured tympanic membrane or sinus pain, the more serious damage is indirectly due to nitrogen bubbles appearing in the blood and blocking small vessels. Central and peripheral nervous-system damage and bone necrosis are the most dangerous sequelae.
Radiation Non-ionising radiation from lasers or microwaves can cause severe localised heating leading to tissue damage of which cataracts (see under EYE, DISORDERS OF) are a particular variety. Ionising radiation from radioactive sources can cause similar acute tissue damage to the eyes as well as cell damage to rapidly dividing cells in the gut and bone marrow. Longer-term effects include genetic damage and various malignant disorders of which LEUKAEMIA and aplastic ANAEMIA are notable. Particular radioactive isotopes may destroy or induce malignant change in target organs, for example, 131I (thyroid), 90Sr (bone). Outdoor workers may also be at risk of sunburn and skin cancers. OTHER OCCUPATIONAL CANCERS Occupation is directly responsible for about 5 per cent of all cancers and contributes to a further 5 per cent. Apart from the cancers caused by asbestos and ionising radiation, a number of other occupational exposures can cause human cancer. The International Agency for Research on Cancer regularly reviews the evidence for carcinogenicity of compounds and industrial processes, and its published list of carcinogens is widely accepted as the current state of knowledge. More than 50 agents and processes are listed as class 1 carcinogens. Important occupational carcinogens include asbestos (mesothelioma, lung cancer); polynuclear aromatic hydrocarbons such as mineral oils, soots, tars (skin and lung cancer); the aromatic amines in dyestu?s (bladder cancer); certain hexavalent chromates, arsenic and nickel re?ning (lung cancer); wood and leather dust (nasal sinus cancer); benzene (leukaemia); and vinyl chloride monomer (angiosarcoma of the liver). It has been estimated that elimination of all known occupational carcinogens, if possible, would lead to an annual saving of 5,000 premature deaths in Britain.
Infections Two broad categories of job carry an occupational risk. These are workers in contact with animals (farmers, veterinary surgeons and slaughtermen) and those in contact with human sources of infection (health-care sta? and sewage workers).
Occupational infections include various zoonoses (pathogens transmissible from animals to humans), such as ANTHRAX, Borrelia burgdorferi (LYME DISEASE), bovine TUBERCULOSIS, BRUCELLOSIS, Chlamydia psittaci, leptospirosis, ORF virus, Q fever, RINGWORM and Streptococcus suis. Human pathogens that may be transmissible at work include tuberculosis, and blood-borne pathogens such as viral hepatitis (B and C) and HIV (see AIDS/HIV). Health-care workers at risk of exposure to infected blood and body ?uids should be immunised against hapatitis B.
Poisoning The incidence of occupational poisonings has diminished with the substitution of noxious chemicals with safer alternatives, and with the advent of improved containment. However, poisonings owing to accidents at work are still reported, sometimes with fatal consequences. Workers involved in the application of pesticides are particularly at risk if safe procedures are not followed or if equipment is faulty. Exposure to organophosphate pesticides, for example, can lead to breathing diffculties, vomiting, diarrhoea and abdominal cramps, and to other neurological effects including confusion and dizziness. Severe poisonings can lead to death. Exposure can be through ingestion, inhalation and dermal (skin) contact.
Stress and mental health Stress is an adverse reaction to excessive pressures or demands and, in occupational-health terms, is di?erent from the motivational impact often associated with challenging work (some refer to this as ‘positive stress’). Stress at work is often linked to increasing demands on workers, although coping can often prevent the development of stress. The causes of occupational stress are multivariate and encompass job characteristics (e.g. long or unsocial working hours, high work demands, imbalance between e?ort and reward, poorly managed organisational change, lack of control over work, poor social support at work, fear of redundancy and bullying), as well as individual factors (such as personality type, personal circumstances, coping strategies, and availability of psychosocial support outside work). Stress may in?uence behaviours such as smoking, alcohol consumption, sleep and diet, which may in turn affect people’s health. Stress may also have direct effects on the immune system (see IMMUNITY) and lead to a decline in health. Stress may also alter the course and response to treatment of conditions such as cardiovascular disease. As well as these general effects of stress, speci?c types of disorder may be observed.
Exposure to extremely traumatic incidents at work – such as dealing with a major accident involving multiple loss of life and serious injury
(e.g. paramedics at the scene of an explosion or rail crash) – may result in a chronic condition known as post-traumatic stress disorder (PTSD). PTSD is an abnormal psychological reaction to a traumatic event and is characterised by extreme psychological discomfort, such as anxiety or panic when reminded of the causative event; sufferers may be plagued with uncontrollable memories and can feel as if they are going through the trauma again. PTSD is a clinically de?ned condition in terms of its symptoms and causes and should not be used to include normal short-term reactions to trauma.... occupational health, medicine and diseases
Shigellosis This form is usually caused by Shigella dysenteriae-1 (Shiga’s bacillus), Shigella ?exneri, Shigella boydii, and Shigella sonnei; the latter is the most benign and occurs in temperate climates also. It is transmitted by food and water contamination, by direct contact, and by ?ies; the organisms thrive in the presence of overcrowding and insanitary conditions. The incubation is between one and seven days, and the severity of the illness depends on the strain responsible. Duration of illness varies from a few days to two weeks and can be particularly severe in young, old, and malnourished individuals. Complications include perforation and haemorrhage from the colo-rectum, the haemolytic uraemic syndrome (which includes renal failure), and REITER’S SYNDROME. Diagnosis is dependent on demonstration of Shigella in (a) faecal sample(s) – before or usually after culture.
If dehydration is present, this should be treated accordingly, usually with an oral rehydration technique. Shigella is eradicated by antibiotics such as trimethoprimsulphamethoxazole, trimethoprim, ampicillin, and amoxycillin. Recently, a widespread resistance to many antibiotics has developed, especially in Asia and southern America, where the agent of choice is now a quinolone compound, for example, cipro?oxacin; nalidixic acid is also e?ective. Prevention depends on improved hygiene and sanitation, careful protection of food from ?ies, ?y destruction, and garbage disposal. A Shigella carrier must not be allowed to handle food.
Entamoeba histolytica infection Most cases occur in the tropics and subtropics. Dysentery may be accompanied by weight loss, anaemia, and occasionally DYSPNOEA. E. histolytica contaminates food (e.g. uncooked vegetables) or drinking water. After ingestion of the cyst-stage, and following the action of digestive enzymes, the motile trophozoite emerges in the colon causing local invasive disease (amoebic colitis). On entering the portal system, these organisms may gain access to the liver, causing invasive hepatic disease (amoebic liver ‘abscess’). Other sites of ‘abscess’ formation include the lungs (usually right) and brain. In the colo-rectum an amoeboma may be di?cult to di?erentiate from a carcinoma. Clinical symptoms usually occur within a week, but can be delayed for months, or even years; onset may be acute – as for Shigella spp. infection. Perforation, colo-rectal haemorrhage, and appendicitis are unusual complications. Diagnosis is by demonstration of E. histolytica trophozoites in a fresh faecal sample; other amoebae affecting humans do not invade tissues. Research techniques can be used to di?erentiate between pathogenic (E. dysenteriae) and non-pathogenic strains (E. dispar). Alternatively, several serological tests are of value in diagnosis, but only in the presence of invasive disease.
Treatment consists of one of the 5nitroimidazole compounds – metronidazole, tinidazole, and ornidazole; alcohol avoidance is important during their administration. A ?ve- to ten-day course should be followed by diloxanide furoate for ten days. Other compounds – emetine, chloroquine, iodoquinol, and paromomycin – are now rarely used. Invasive disease involving the liver or other organ(s) usually responds favourably to a similar regimen; aspiration of a liver ‘abscess’ is now rarely indicated, as controlled trials have indicated a similar resolution rate whether this technique is used or not, provided a 5-nitroimidazole compound is administered.... dysentery
Structure Each tooth is composed of enamel, dentine, cement, pulp and periodontal membrane. ENAMEL is the almost translucent material which covers the crown of a tooth. It is the most highly calci?ed material in the body, 96–97 per cent being composed of calci?ed salts. It is arranged from millions of long, six-sided prisms set on end on the dentine (see below), and is thickest over the biting surface of the tooth. With increasing age or the ingestion of abrasive foods the teeth may be worn away on the surface, so that the dentine becomes visible. The outer sides of some teeth may be worn away by bad tooth-brushing technique. DENTINE is a dense yellowish-white material from which the bulk and the basic shape of a tooth are formed. It is like ivory and is harder than bone but softer than enamel. The crown of the tooth is covered by the hard protective enamel and the root is covered by a bone-like substance called cement. Decay can erode dentine faster than enamel (see TEETH, DISORDERS OF – Caries of the teeth). CEMENT or cementum is a thin bone-like material which covers the roots of teeth and helps hold them in the bone. Fibres of the periodontal membrane (see below) are embedded in the cement and the bone. When the gums recede, part of the cement may be exposed and the cells die. Once this has happened, the periodontal membrane can no longer be attached to the tooth and, if su?cient cement is destroyed, the tooth-support will be so weakened that the tooth will become loose. PULP This is the inner core of the tooth and is
composed of a highly vascular, delicate ?brous tissue with many ?ne nerve-?bres. The pulp is very sensitive to temperature variation and to touch. If the pulp becomes exposed it will become infected and usually cannot overcome this. Root-canal treatment or extraction of the tooth may be necessary. PERIODONTAL MEMBRANE This is a layer of ?brous tissue arranged in groups of ?bres which surround and support the root of a tooth in a bone socket. The ?bres are interspersed with blood vessels and nerves. Loss of the membrane leads to loss of the tooth. The membrane can release and re-attach the ?bres to allow the tooth to move when it erupts, or (to correct dental deformities) is being moved by orthodontic springs.
Arrangement and form Teeth are present in most mammals and nearly all have two sets: a temporary or milk set, followed by a permanent or adult set. In some animals, like the toothed whale, all the teeth are similar; but in humans there are four di?erent shapes: incisors, canines (eye-teeth), premolars (bicuspids), and molars. The incisors are chisel-shaped and the canine is pointed. Premolars have two cusps on the crown (one medial to the other) and molars have at least four cusps. They are arranged together in an arch in each jaw and the
cusps of opposing teeth interdigitate. Some herbivores have no upper anterior teeth but use a pad of gum instead. As each arch is symmetrical, the teeth in an upper and lower quadrant can be used to identify the animal. In humans, the quadrants are the same: in other words, in the child there are two incisors, one canine and two molars (total teeth 20); in the adult there are two incisors, one canine, two premolars and three molars (total 32). This mixture of tooth-form suggests that humans are omnivorous. Anatomically the crown of the tooth has mesial and distal surfaces which touch the tooth next to it. The mesial surface is the one nearer to the centre line and the distal is the further away. The biting surface is called the incisal edge for the anterior teeth and the occlusal surface for the posteriors.
Development The ?rst stage in the formation of the teeth is the appearance of a down-growth of EPITHELIUM into the underlying mesoderm. This is the dental lamina, and from it ten smaller swellings in each jaw appear. These become bell-shaped and enclose a part of the mesoderm, the cells of which become specialised and are called the dental papillae. The epithelial cells produce enamel and the dental papilla forms the dentine, cement and pulp. At a ?xed time the teeth start to erupt and a root is formed. Before the deciduous teeth erupt, the permanent teeth form, medial to them. In due course the deciduous roots resorb and the permanent teeth are then able to push the crowns out and erupt themselves. If this process is disturbed, the permanent teeth may be displaced and appear in an abnormal position or be impacted.
Eruption of teeth is in a de?nite order and at a ?xed time, although there may be a few months’ leeway in either direction which is of no signi?cance. Excessive delay is found in some congenital disorders such as CRETINISM. It may also be associated with local abnormalities of the jaws such as cysts, malformed teeth and supernumerary teeth.
The usual order of eruption of deciduous teeth is:
Middle incisors 6–8 months Lateral incisors 8–10 months First molars 12–16 months Canines (eye-teeth) 16–20 months Second molars 20–30 months
The usual order of eruption of permanent teeth is:
First molars 6–7 years Middle incisors 6–8 years Lateral incisors 7–9 years Canines 9–12 years First and second premolars 10–12 years Second molars 11–13 years Third molars (wisdom teeth) 17–21 years
The permanent teeth of the upper (top) and lower (bottom) jaws.
Teeth, Disorders of
Teething, or the process of eruption of the teeth in infants, may be accompanied by irritability, salivation and loss of sleep. The child will tend to rub or touch the painful area. Relief may be obtained in the child by allowing it to chew on a hard object such as a toy or rusk. Mild ANALGESICS may be given if the child is restless and wakens in the night. A serious pitfall is to assume that an infant’s symptoms of ill-health are due to teething, as the cause may be more serious. Fever and ?ts (see SEIZURE) are not due to teething.
Toothache is the pain felt when there is in?ammation of the pulp or periodontal membrane of a tooth (see TEETH – Structure). It can vary in intensity and may be recurring. The commonest cause is caries (see below) when the cavity is close to the pulp. Once the pulp has become infected, this is likely to spread from the apex of the tooth into the bone to form an abscess (gumboil – see below). A lesser but more long-lasting pain is felt when the dentine is unprotected. This can occur when the enamel is lost due to decay or trauma or because the gums have receded. This pain is often associated with temperature-change or sweet foods. Expert dental advice should be sought early, before the decay is extensive. If a large cavity is accessible, temporary relief may be obtained by inserting a small piece of cotton wool soaked, for example, in oil of cloves.
Alveolar abscess, dental abscess or gumboil This is an ABSCESS caused by an infected tooth. It may be present as a large swelling or cause trismus (inability to open the mouth). Treatment is drainage of the PUS, extraction of the tooth and/or ANTIBIOTICS.
Caries of the teeth or dental decay is very common in the more a?uent countries and is most common in children and young adults. Increasing awareness of the causes has resulted in a considerable improvement in dental health, particularly in recent years; this has coincided with a rise in general health. Now more than half of ?ve-year-old children are caries-free and of the others, 10 per cent have half of the remaining carious cavities. Since the start of the National Health Service, the emphasis has been on preventive dentistry, and now edentulous patients are mainly found among the elderly who had their teeth removed before 1948.
The cause of caries is probably acid produced by oral bacteria from dietary carbohydrates, particularly re?ned sugar, and this dissolves part of the enamel; the dentine is eroded more quickly as it is softer (see TEETH – Structure). The exposed smooth surfaces are usually protected as they are easily cleaned during normal eating and by brushing. Irregular and overcrowded teeth are more at risk from decay as they are di?cult to clean. Primitive people who chew coarse foods rarely get caries. Fluoride in the drinking water at about one part per million is associated with a reduction in the caries rate.
Prolonged severe disease in infancy is associated with poor calci?cation of the teeth, making them more vulnerable to decay. As the teeth are formed and partly calci?ed by the time of birth, the diet and health of the mother are also important to the teeth of the child. Pregnant mothers and children should have a good balanced diet with su?cient calcium and vitamin
D. A ?brous diet will also aid cleansing of the teeth and stimulate the circulation in the teeth and jaws. The caries rate can be reduced by regular brushing with a ?uoride toothpaste two or three times per day and certainly before going to sleep. The provision of sweet or sugary juices in an infant’s bottle should be avoided.
Irregularity of the permanent teeth may be due to an abnormality in the growth of the jaws or to the early or late loss of the deciduous set (see TEETH – Development). Most frequently it is due to an imbalance in the size of the teeth and the length of the jaws. Some improvement may take place with age, but many will require the help of an orthodontist (specialist dentist) who can correct many malocclusions by removing a few teeth to allow the others to be moved into a good position by means of springs and elastics on various appliances which are worn in the mouth.
Loosening of the teeth may be due to an accident or in?ammation of the GUM. Teeth loosened by trauma may be replaced and splinted in the socket, even if knocked right out. If the loosening is due to periodontal disease, the prognosis is less favourable.
Discoloration of the teeth may be intrinsic or extrinsic: in other words, the stain may be in the calci?ed structure or stuck on to it. Intrinsic staining may be due to JAUNDICE or the antibiotic tetracycline. Extrinsic stain may be due to tea, co?ee, tobacco, pan (a mixture of chuna and betel nuts wrapped in a leaf), iron-containing medicines or excess ?uoride.
Gingivitis or in?ammation of the gum may occur as an acute or chronic condition. In the acute form it is often part of a general infection of the mouth, and principally occurs in children or young adults – resolving after 10–14 days. The chronic form occurs later in life and tends to be progressive. Various microorganisms may be found on the lesions, including anaerobes. Antiseptic mouthwashes may help, and once the painful stage is past, the gums should be thoroughly cleaned and any calculus removed. In severe conditions an antibiotic may be required.
Periodontal disease is the spread of gingivitis (see above) to involve the periodontal membrane of the tooth; in its ?orid form it used to be called pyorrhoea. In this, the membrane becomes damaged by the in?ammatory process and a space or pocket is formed into which a probe can be easily passed. As the pocket becomes more extensive, the tooth loosens. The loss of the periodontal membrane also leads to the loss of supporting bone. Chronic in?ammation soon occurs and is di?cult to eradicate. Pain is not a feature of the disease but there is often an unpleasant odour (halitosis). The gums bleed easily and there may be DYSPEPSIA. Treatment is largely aimed at stabilising the condition rather than curing it.
Dental abscess is an infection that arises in or around a tooth and spreads to involve the bone. It may occur many years after a blow has killed the pulp of the tooth, or more quickly after caries has reached the pulp. At ?rst the pain may be mild and intermittent but eventually it will become severe and a swelling will develop in the gum over the apex of the tooth. A radiograph of the tooth will show a round clear area at the apex of the tooth. Treatment may be by painting the gum with a mild counter-irritant such as a tincture of aconite and iodine in the early stages, but later root-canal therapy or apicectomy may be required. If a swelling is present, it may need to be drained or the o?ending teeth extracted and antibiotics given.
Injuries to teeth are common. The more minor injuries include crazing and the loss of small chips of enamel, and the major ones include a broken root and avulsion of the entire tooth. A specialist dental opinion should be sought as soon as possible. A tooth that has been knocked out can be re-implanted if it is clean and replaced within a few hours. It will then require splinting in place for 4–6 weeks.
Prevention of dental disease As with other disorders, prevention is better than cure. Children should be taught at an early age to keep their teeth and gums clean and to avoid re?ned sugars between meals. It is better to ?nish a meal with a drink of water rather than a sweetened drink. Fluoride in some of its forms is useful in the reduction of dental caries; in some parts of the UK natural water contains ?uoride, and in some areas where ?uoride content is low, arti?cial ?uoridation of the water supply is carried out. Overcrowding of the teeth, obvious maldevelopment of the jaw and persistent thumbsucking into the teens are all indications for seeking the advice of an orthodontist. Generally, adults have less trouble with decay but more with periodontal disease and, as its onset is insidious, regular dental inspections are desirable.... teeth
It stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas, thus facilitating the digestive process.... cholecystokinin
In severe cases, the enamel develops brown stains.
Such cases occur mostly where the fluoride level in water is far greater than the recommended level or when additional fluoride supplements are taken.... fluorosis
Clinical course The incubation period of enteric fever is 7–21 days. Early symptoms include headache, malaise, dry cough, constipation and a slowly rising fever. Despite the fever, the patient’s pulse rate is often slow and he or she may have an enlarged SPLEEN. In the second week of illness, organisms invade the bloodstream again and symptoms progress. In general, symptoms of typhoid fever are more severe than those of paratyphoid fever: increasing mental slowness and confusion are common, and a more sustained high fever is present. In some individuals, discrete red spots appear on the upper trunk (rose spots). By the third week of illness the patient may become severely toxic, with marked confusion and delirium, abdominal distension, MYOCARDITIS, and occasionally intestinal haemorrage and/or perforation. Such complications may be fatal, although they are unusual if prompt treatment is given. Symptoms improve slowly into the fourth and ?fth weeks, although relapse may occur.
Diagnosis Enteric fever should be considered in any traveller or resident in an ENDEMIC area presenting with a febrile illness. The most common di?erential diagnosis is MALARIA. Diagnosis is usually made by isolation of the organism from cultures of blood in the ?rst two weeks of illness. Later the organisms are found in the stools and urine. Serological tests for ANTIBODIES against Salmonella typhi antigens (see ANTIGEN) (the Widal test) are less useful due to cross-reactions with antigens on other bacteria, and diffculties with interpretation in individuals immunised with typhoid vaccines.
Treatment Where facilities are available, hospital admission is required. Antibiotic therapy with chloramphenicol or amoxyacillin is e?ective. However, the potential toxicity of the former and the widespread resistance that has developed to both these antibiotics has led to the use of QUINOLONES such as CIPROFLOXACIN as the initial therapy for enteric fever in the UK and in areas where resistant organisms are common. A few individuals become chronic carriers of the organisms after they have recovered from the symptoms. These people are a potential source of spread to others and should be excluded from occupations that involve handling food or drinking-water.
Prolonged courses of antibiotic therapy may be required to eradicate carriage.
Prevention Worldwide, the most important preventive measure is improvement of sanitation and maintenance of clean water supplies. Vaccination is available for travellers to endemic areas.... enteric fever
METABOLIC DISORDERS such as URAEMIA and pancreatitis (see PANCREAS, DISORDERS OF)
Bowel infarction
Drug ingestion
Massive blood transfusion, transfusion reaction (see TRANSFUSION OF BLOOD), CARDIOPULMONARY BYPASS, disseminated intravascular coagulation
Treatment The principles of management are supportive, with treatment of the underlying condition if that is possible. Oxygenation is improved by increasing the concentration of oxygen breathed in by the patient, usually with mechanical ventilation of the lungs, often using continuous positive airways pressure (CPAP). Attempts are made to reduce the formation of pulmonary oedema by careful management of how much ?uid is given to the patient (?uid balance). Infection is treated if it arises, as are the possible complications of prolonged ventilation with low lung compliance (e.g. PNEUMOTHORAX). There is some evidence that giving surfactant through a nebuliser or aerosol may help to improve lung e?ectiveness and reduce oedema. Some experimental evidence supports the use of free-radical scavengers and ANTIOXIDANTS, but these are not commonly used. Other techniques include the inhalation of NITRIC OXIDE (NO) to moderate vascular tone, and prone positioning to improve breathing. In severe cases, extracorporeal gas exchange has been advocated as a supportive measure until the lungs have healed enough for adequate gas exchange. (See also RESPIRATORY DISTRESS SYNDROME; HYALINE MEMBRANE DISEASE; SARS.)... indirect insult
Causes The cause of fever is the release of fever-producing proteins (pyrogens) by phagocytic cells called monocytes and macrophages, in response to a variety of infectious, immunological and neoplastic stimuli. The lymphocytes (see LYMPHOCYTE) play a part in fever production because they recognise the antigen and release substances called lymphokines which promote the production of endogenous pyrogen. The pyrogen then acts on the thermoregulatory centre in the HYPOTHALAMUS and this results in an increase in heat generation and a reduction in heat loss, resulting in a rise in body temperature.
The average temperature of the body in health ranges from 36·9 to 37·5 °C (98·4 to 99·5 °F). It is liable to slight variations from such causes as the ingestion of food, the amount of exercise, the menstrual cycle, and the temperature of the surrounding atmosphere. There are, moreover, certain appreciable daily variations, the lowest temperature being between the hours of 01.00 and 07.00 hours, and the highest between 16.00 and 21.00 hours, with tri?ing ?uctuations during these periods.
The development and maintenance of heat within the body depends upon the metabolic oxidation consequent on the changes continually taking place in the processes of nutrition. In health, this constant tissue disintegration is exactly counterbalanced by the consumption of food, whilst the uniform normal temperature is maintained by the adjustment of the heat developed, and of the processes of exhalation and cooling which take place, especially from the lungs and skin. During a fever this balance breaks down, the tissue waste being greatly in excess of the food supply. The body wastes rapidly, the loss to the system being chie?y in the form of nitrogen compounds (e.g. urea). In the early stage of fever a patient excretes about three times the amount of urea that he or she would excrete on the same diet when in health.
Fever is measured by how high the temperature rises above normal. At 41.1 °C (106 °F) the patient is in a dangerous state of hyperpyrexia (abnormally high temperature). If this persists for very long, the patient usually dies.
The body’s temperature will also rise if exposed for too long to a high ambient temperature. (See HEAT STROKE.)
Symptoms The onset of a fever is usually marked by a RIGOR, or shivering. The skin feels hot and dry, and the raised temperature will often be found to show daily variations – namely, an evening rise and a morning fall.
There is a relative increase in the pulse and breathing rates. The tongue is dry and furred; the thirst is intense, while the appetite is gone; the urine is scanty, of high speci?c gravity and containing a large quantity of solid matter, particularly urea. The patient will have a headache and sometimes nausea, and children may develop convulsions (see FEBRILE CONVULSION).
The fever falls by the occurrence of a CRISIS – that is, a sudden termination of the symptoms – or by a more gradual subsidence of the temperature, technically termed a lysis. If death ensues, this is due to failure of the vital centres in the brain or of the heart, as a result of either the infection or hyperpyrexia.
Treatment Fever is a symptom, and the correct treatment is therefore that of the underlying condition. Occasionally, however, it is also necessary to reduce the temperature by more direct methods: physical cooling by, for example, tepid sponging, and the use of antipyretic drugs such as aspirin or paracetamol.... fever
An overdose of paracetamol is a common choice of those attempting to commit suicide. Since the government restricted the number of paracetamol tablets an individual may purchase over the counter, the incidence of people taking the drug in overdose with the intention of taking their lives has fallen sharply.... paracetamol poisoning
A localised (focal) form of liver disease in all tropical/subtropical countries results from invasive Entamoeba histolytica infection (amoebic liver ‘abscess’); serology and imaging techniques assist in diagnosis. Hydatidosis also causes localised liver disease; one or more cysts usually involve the right lobe of the liver. Serological tests and imaging techniques are of value in diagnosis. Whilst surgery formerly constituted the sole method of management, prolonged courses of albendazole and/or praziquantel have now been shown to be e?ective; however, surgical intervention is still required in some cases.
Hepato-biliary disease is also a problem in many tropical/subtropical countries. In southeast Asia, Clonorchis sinensis and Opisthorchis viverini infections cause chronic biliary-tract infection, complicated by adenocarcinoma of the biliary system. Praziquantel is e?ective chemotherapy before advanced disease ensues. Fasciola hepatica (the liver ?uke) is a further hepato-biliary helminthic infection; treatment is with bithionol or triclabendazole, praziquantel being relatively ine?ective.... liver disease in the tropics
The principal function of saliva is to aid in the initial processes of digestion, and it is essential for the process of mastication (chewing), whereby food is reduced to an homogeneous mass before being swallowed. In addition, the ptyalin in the saliva initiates the digestion of starch in the food.
An excessive ?ow of saliva known as salivation occurs as the result of taking certain drugs. Salivation also occurs as the result of irritation in the mouth – as for instance, in the teething child – and from DYSPEPSIA. De?ciency of saliva is known as XEROSTOMIA.... saliva
Habitat: Western Himalayas at 1,800 and Kashmir at 2,400 m, also grown in gardens.
English: Holy Thistle, Milk Thistle.Action: Seeds—liver protective, gallbladder protective, antioxidant. Used in jaundice and other biliary affections, intermittent fevers, uterine trouble, also as a galactagogue. Alcoholic extract used for haemorrhoids and as a general substitute for adrenaline. Seeds are used for controlling haemorrhages. Leaves—sudorific and aperient. Young leaves and flowering heads are consumed by diabetics.
Key application: In dyspeptic complaints. As an ingredient of formulations for toxic liver damage; chronic inflammatory liver disease and hepatic cirrhosis induced by alcohol, drugs or toxins. (Expanded Commission E Monographs, WHO.)The seeds gave silymarin (flavanol lignin mixture), composed mainly of silybin A, silybin B (mixture known as silibinin), with isosilybin A, isosilybin B, silychristin, silydianin. In Germany, Milk Thistle has been used extensively for liver diseases and jaundice. Sily- marin has been shown conclusively to exert an antihepatotoxic effect in animals against a variety of toxins, particularly those of death cap mushroom, Amanita phalloides. Silybin, when given by intravenous injection to human patients up to 48 hours after ingestion of the death cap, was found to be highly effective in preventing fatalities.Silymarin has been used successfully to treat patients with chronic hepatitis and cirrhosis; it is active against hepatitis B virus, and lowers fat deposits in the liver in animals.(For hepatic cirrhosis: 420 mg per day; for chronic active hepatitis 240 mg twice daily—extract containing 7080% silimarin.)... silybum marianumThe symptoms depend upon the site of the infection. General symptoms such as fever, weight loss and night sweats are common. In the most common form of pulmonary tuberculosis, cough and blood-stained sputum (haemoptysis) are common symptoms.
The route of infection is most often by inhalation, although it can be by ingestion of products such as infected milk. The results of contact depend upon the extent of the exposure and the susceptibility of the individual. Around 30 per cent of those closely exposed to the organism will be infected, but most will contain the infection with no signi?cant clinical illness and only a minority will go on to develop clinical disease. Around 5 per cent of those infected will develop post-primary disease over the next two or three years. The rest are at risk of reactivation of the disease later, particularly if their resistance is reduced by associated disease, poor nutrition or immunosuppression. In developed countries around 5 per cent of those infected will reactivate their healed tuberculosis into a clinical problem.
Immunosuppressed patients such as those infected with HIV are at much greater risk of developing clinical tuberculosis on primary contact or from reactivation. This is a particular problem in many developing countries, where there is a high incidence of both HIV and tuberculosis.
Diagnosis This depends upon identi?cation of mycobacteria on direct staining of sputum or other secretions or tissue, and upon culture of the organism. Culture takes 4–6 weeks but is necessary for di?erentiation from other non-tuberculous mycobacteria and for drug-sensitivity testing. Newer techniques involving DNA ampli?cation by polymerase chain reaction (PCR) can detect small numbers of organisms and help with earlier diagnosis.
Treatment This can be preventative or curative. Important elements of prevention are adequate nutrition and social conditions, BCG vaccination (see IMMUNISATION), an adequate public-health programme for contact tracing, and chemoprophylaxis. Radiological screening with mass miniature radiography is no longer used.
Vaccination with an attenuated organism (BCG – Bacillus Calmette Guerin) is used in the United Kingdom and some other countries at 12–13 years, or earlier in high-risk groups. Some studies show 80 per cent protection against tuberculosis for ten years after vaccination.
Cases of open tuberculosis need to be identi?ed; their close contacts should be reviewed for evidence of disease. Adequate antibiotic chemotherapy removes the infective risk after around two weeks of treatment. Chemoprophylaxis – the use of antituberculous therapy in those without clinical disease – may be used in contacts who develop a strong reaction on tuberculin skin testing or those at high risk because of associated disease.
The major principles of antibiotic chemotherapy for tuberculosis are that a combination of drugs needs to be used, and that treatment needs to be continued for a prolonged period – usually six months. Use of single agents or interrupted courses leads to the development of drug resistance. Serious outbreaks of multiply resistant Mycobacterium tuberculosis have been seen mainly in AIDS units, where patients have greater susceptibility to the disease, but also in developing countries where maintenance of appropriate antibacterial therapy for six months or more can be di?cult.
Streptomycin was the ?rst useful agent identi?ed in 1944. The four drugs used most often now are RIFAMPICIN, ISONIAZID, PYRAZINAMIDE and ETHAMBUTOL. Three to four agents are used for the ?rst two months; then, when sensitivities are known and clinical response observed, two drugs, most often rifampicin and isoniazid, are continued for the rest of the course. Treatment is taken daily, although thrice-weekly, directly observed therapy is used when there is doubt about the patient’s compliance. All the antituberculous agents have a range of adverse effects that need to be monitored during treatment. Provided that the treatment is prescribed and taken appropriately, response to treatment is very good with cure of disease and very low relapse rates.... nature of the disease tuberculosis has
Habitat: Native to North Africa; commonly grown in North Western India.
English: Broad bean, Windsor bean.Unani: Baaqlaa.Action: Fresh beans—cooked alone or with meat, are prescribed in Unani medicine for cough, also for resolving inflammations. Externally, the bean and flowers are used as a poultice for inflammations, warts and burns.
A number of harmful principles are reported in the broad beans. A large amount of Dopa, mainly in free state and partly in the form of its beta- glucoside; and gluco alkaloids, vicine and convicine, have been isolated.Ingestion of fresh, uncooked or partially cooked beans is not recommended.The seeds gave positive test for hydrocyanic acid and also contain arsenic.The fresh beans exhibit an oestro- genic activity. Phytoalexins of the immature seeds exhibit antifungal activity.Malic, citric and glyceric acids are the principal organic acids present in the pods (also present in the hulls). The glyceric acid on subcutaneous injection produced a marked diuresis in rabbit. (A decoction of the leaves and stems of the field bean, Faba vulgaris Moench, is used as a diuretic.)An aqueous extract of the root nodules exhibited vasoconstricting activity on rabbits.... vicia fabaThe concept of the dose-response is important for understanding the risk of exposure to a particular substance. This is embodied in a statement by Paracelsus (c.1493–1541): ‘All substances are poisons; there is none which is not a poison. The right dose di?erentiates a poison and a remedy.’
Poisoning may occur in a variety of ways: deliberate – SUICIDE, substance abuse or murder; accidental – including accidental overdose of medicines; occupational; and environmental
– including exposure during ?re.
Ingestion is the most common route of exposure, but poisoning may also occur through inhalation, absorption through the skin, by injection and through bites and stings of venomous animals. Poisoning may be described as acute, where a single exposure produces clinical effects with a relatively rapid onset; or chronic, where prolonged or repeated exposures may produce clinical effects which may be insidious in onset, cumulative and in some cases permanent.
Diagnosis of poisoning is usually by circumstantial evidence or elimination of other causes of the clinical condition of the patient. Some substances (e.g. opioids) produce a characteristic clinical picture in overdose that can help with diagnosis. In some patients laboratory analysis of body ?uids or the substance taken may be useful to determine or con?rm the o?ending agent. Routine assays are not necessary. For a very small number of poisons, such as paracetamol, aspirin, iron and lead, the management of the patient may depend on measuring the amount of poison in the bloodstream.
Accurate statistics on the incidence of poisoning in the UK are lacking. Mortality ?gures are more reliable than morbidity statistics; annually, well over 100,000 cases of poisoning are admitted to hospital. The annual number of deaths from poisoning is relatively small – about 300 – and in most cases patients die before reaching hospital. Currently, CARBON MONOXIDE (CO) is by far the most common cause of death due to poisoning. The most common agents involved in intentional or accidental poisoning are drugs, particularly ANALGESICS, ANTIDEPRESSANT DRUGS and SEDATIVES. Alcohol is also commonly taken by adults, usually in combination with drugs. Children frequently swallow household cleaners, white spirit, plant material – such as belladonna (deadly nightshade) and certain mushrooms; for example, death cap and ?y agaric – aftershave and perfume as well as drugs. If possible, the suspect container, drug or plant should be taken with the victim to the hospital or doctor. The use of child-resistant containers has reduced the number of admissions of children to hospital for treatment. Bixtrex® is an intensely bitter-tasting agent which is often added to products to discourage ingestion; however, not everybody is able to taste it, nor has any bene?cial e?ect been proven.
Treatment of poisoning usually begins with decontamination procedures. For ingested substances this may involve making the patient sick or washing the stomach out (GASTRIC LAVAGE): this is usually only worthwhile if performed soon after ingestion. It should be emphasised that salt (sodium chloride) water must never be given to induce vomiting, since this procedure is dangerous and has caused death. For substances spilt on the skin, the affected area should immediately be thoroughly washed and all contaminated clothing removed. Following eye exposure, the affected eye/s should be thoroughly irrigated with saline or water.
Treatment thereafter is generally symptomatic and supportive, with maintenance of the victim’s respiratory, neurological and cardiovascular systems and, where appropriate, monitoring of their ?uid and electrolyte balance and hepatic and renal function. There are speci?c antidotes for a few substances: the most important of these are PARACETAMOL, iron, cyanide (see CYANIDE POISONING), opioids (see OPIOID), DIGOXIN, insecticides and some heavy metals. Heavy-metal poisoning is treated with CHELATING AGENTS – chemical compounds that form complexes by binding metal ions: desferrioxamine and pencillinamine are two such agents. The number of people presenting with paracetamol overdose – a common drug used for attempted suicide – has fallen sharply since restrictions were placed on its over-thecounter sales.
When a patient presents with an illness thought to be caused by exposure to substances at work, further exposure should be limited or prevented and investigations undertaken to determine the source and extent of the problem. Acutely poisoned workers will usually go to hospital, but those suffering from chronic exposure may attend their GP with non-speci?c symptoms (see OCCUPATIONAL HEALTH, MEDICINE AND DISEASES).
In recent years, legislation has been enacted in the UK to improve safety in the workplace and to ensure that data on the hazardous constituents and effects of chemicals are more readily available. These o?cial controls include the Control of Substances Hazardous to Health (COSHH) and the Chemicals (Hazard Information and Packaging) Regulations (CHIP) and are UK legislation in response to European Union directives.
The National Poisons Information Service is a 24-hour emergency telephone service available to the medical profession and provides information on the likely effects of numerous agents and advice on the management of the poisoned patient. The telephone numbers are available in the medical literature. In the UK this is not a public-access service. People who believe they, or their relatives, have been poisoned should seek medical advice from their GPs or attend their local hospital.
Toxbase The National Poisons Information Service provides a primary clinical toxicology database on the Internet: www.spib.axl.co.uk. This website provides information about routine diagnosis, treatment and management of people exposed to drugs, household products and industrial and agricultural products.
(See also APPENDIX 1: BASIC FIRST AID.)... poisons
Other deficiencies. Muscle cramps, spasms, tremors, nervousness, insomnia, joint pains.
Body effects. Healthy teeth and bones, blood clotting, nerve and muscle resilience.
Calcium helps reduce risk of fracture particularly in menopausal women who may increase intake to 1500mg daily. Calcium citrate malate is regarded as more effective than calcium carbonate. Calcium and Magnesium are essentials.
Sources. Dairy products, fish, sardines, salmon, watercress, hard drinking water, spinach. Dried skimmed milk may supply up to 60 per cent of the recommended daily amount.
Herbs. Chamomile, Clivers, Dandelion, Horsetail, Coltsfoot, Meadowsweet, Mistletoe, Plantain, Scarlet Pimpernel, Silverweed, Shepherd’s Purse, Toadflax. Taken as teas, powders, tablets or capsules.
Herbal combination to increase intake. Comfrey 3, Horsetail 6, Kelp 1, Lobelia 1, Marshmallow root 2, Oats 4, Parsley root 1. Tea: 1 heaped teaspoon to each cup boiling water; infuse 15 minutes; 1 cup morning and evening.
Calcium tablet supplements should first be pulverised before ingestion and taken in honey, bread bolus, or other suitable vehicle. Vitamin D assists absorption – 400-800 international units daily. ... calcium
Typical combination. Magnesium carbonate 200mg; Calcium carbonate 240mg. Uses. Mineral deficiencies, osteoporosis, to maintain healthy teeth.
Note: Not used by the elderly or those with digestive weakness.
Dolomite supplements should first be pulverised before ingestion, taken in honey, a bread bolus or other suitable vehicle. ... dolomite
Multiple causes: diseases of the gut; strictures, fistulas, Crohn’s disease, obstructions, parasites, infections, drugs, X-rays, endocrine disease, gastric surgery. A common cause is gluten sensitivity due to ingestion of gluten foods (wheat, oats, rye, barley).
Symptoms: Wasting of muscles, weight loss, flatulence, loss of appetite, distension, fat in the faeces, large pale frothy stools, vitamin and mineral deficiencies.
Alternatives. Teas: Alfalfa, Agrimony, Gotu Kola, Meadowsweet, Red Clover, Oats.
Decoctions: Irish Moss, Dandelion root, Fenugreek seeds, Bayberry bark. Calamus or Gentian, in cold infusion.
Formula. Dandelion 1; Echinacea 2; Saw Palmetto 1; few grains Cayenne or drops Tincture Capsicum. Dose: Liquid Extracts: 1 teaspoon. Tinctures: 1-2 teaspoons. Powders: 500mg (two 00 capsules or one- third teaspoon). Thrice daily.
Irish Moss, strengthening. Echinacea to sustain natural powers of resistance. Diet. Gluten-free. Soya products. Avoid dairy products. Slippery Elm gruel. Vitamins: B-complex, B1, B6, B12, Folic acid, PABA, C, E.
Minerals: Calcium, Iron, Copper, Zinc. ... malabsorption syndrome
Bites from dog fleas are an occasional nuisance. Ticks and mites from dogs, including a canine version of the scabies mite, are other common problems. The fungi that cause tinea infections in dogs can be caught by humans.
Some people become allergic to animal dander (tiny scales from fur or skin). They may, for example, have asthma or urticaria when a dog is in the house. (See also zoonoses.)... dogs, diseases from
Many erosions result from ingestion of alcohol, iron tablets, or aspirin.
The physical stress of serious illness, such as kidney failure, or of burns may bring on an erosion.
Often there are no symptoms, but erosions may bleed, causing vomiting of blood or blood in the faeces.
Persistent loss of blood may lead to anaemia.
Gastric erosions are diagnosed by gastroscopy.
They usually heal in a few days when they are treated with antacid drugs and ulcer-healing drugs.... gastric erosion
The infestation is generally confined to dogs and sheep, but may be passed on to humans through accidental ingestion of worm eggs from materials contaminated with dog faeces.
The cysts grow slowly, and symptoms may not appear for some years. In many cases, there are no symptoms. Cysts in the liver may cause a tender lump or lead to bile duct obstruction and jaundice. Cysts in the lungs may press on an airway and cause inflammation; rupture of a lung cyst may cause chest pain, the coughing up of blood, and wheezing. Cysts in the brain may cause seizures. Ruptured cysts may rarely cause anaphylactic shock, which can be fatal.
Diagnosis of hydatid disease is by CT scanning or MRI. The cysts are usually drained or removed surgically.... hydatid disease
Symptoms begin soon after ingestion and include restlessness, stiffness of the face and neck, increased sensitivity of hearing, taste, and smell, and photosensitivity, followed by alternating episodes of seizures and floppiness. Death may occur from respiratory arrest.
The victim is given intravenous injections of a tranquillizer or a barbiturate, with a muscle-relaxant drug if needed.
Breathing may be maintained by a ventilator.
With prompt treatment, recovery usually occurs in about 24 hours.... strychnine poisoning
Worm diseases found in developed countries include threadworm infestation, ascariasis, whipworm infestation, toxocariasis, liver-fluke infestation, and various tapeworm infestations. Those occurring in tropical regions include hookworm infestation, filariasis, guinea worm disease, and schistosomiasis.
Worms may be acquired by eating undercooked, infected meat, by contact with soil or water containing worm larvae, or by accidental ingestion of worm eggs from soil contaminated by infected faeces.
Most infestations can be easily eradicated with anthelmintic drugs.... worm infestation
FAMILY: Rutaceae
SYNONYMS: C. vulgaris, C. bigaradia, Seville orange, sour orange bigarade (oil).
GENERAL DESCRIPTION: An evergreen tree up to 10 metres high with dark green, glossy, oval leaves, paler beneath, with long but not very sharp spines. It has a smooth greyish trunk and branches, and very fragrant white flowers. The fruits are smaller and darker than the sweet orange. It is well known for its resistance to disease and is often used as root stock for other citrus trees, including the sweet orange.
DISTRIBUTION: Native to the Far East, especially India and China, but has become well adapted to the Mediterranean climate. It also grows abundantly in the USA (California), Israel and South America. Main producers of the oil include Spain, Guinea, the West Indies, Italy, Brazil and the USA.
OTHER SPECIES: There are numerous different species according to location – oils from Spain and Guinea are said to be of superior quality.
HERBAL/FOLK TRADITION: ‘Oranges and lemons strengthen the heart, are good for diminishing the coagubility of the blood, and are beneficial for palpitation, scurvy, jaundice, bleedings, heartburn, relaxed throat, etc. They are powerfully anti-scorbutic, either internally or externally applied.’. The dried bitter orange peel is used as a tonic and carminative in treating dyspepsia.
In Chinese medicine the dried bitter orange and occasionally its peel are used in treating prolapse of the uterus and of the anus, diarrhoea, and blood in the faeces. Ingestion of large amounts of orange peel in children, however, has been reported to cause toxic effects.
ACTIONS: Anti-inflammatory, antiseptic, astringent, bactericidal, carminative, choleretic, fungicidal, sedative (mild), stomachic, tonic.
EXTRACTION: An essential oil by cold expression (hand or machine pressing) from the outer peel of the almost ripe fruit. (A terpeneless oil is also produced.) The leaves are used for the production of petitgrain oil; the blossom for neroli oil.
CHARACTERISTICS: A dark yellow or brownish-yellow mobile liquid with a fresh, dry, almost floral odour with a rich, sweet undertone.
PRINCIPAL CONSTITUENTS: Over 90 per cent monoterpenes: mainly limonene, myrcene, camphene, pinene, ocimene, cymene, and small amounts of alcohols, aldehydes and ketones.
SAFETY DATA: Phototoxic; otherwise generally non-toxic, non-irritant and non sensitizing. Limonene has been reported to cause contact dermatitis in some individuals.
AROMATHERAPY/HOME: USE See sweet orange.
OTHER USES: Used in certain stomachic, laxative and carminative preparations. Employed as a fragrance component in soaps, detergents, cosmetics, colognes and perfumes. Extensively used as a flavouring material, especially in liqueurs and soft drinks. Also utilized as a starting material for the isolation of naturallimonene.... orange, bitter
FAMILY: Rutaceae
SYNONYMS: C. aurantium var. dulcis, C. aurantium var. sinensis, China orange, Portugal orange.
GENERAL DESCRIPTION: An evergreen tree, smaller than the bitter variety, less hardy with fewer or no spines. The fruit has a sweet pulp and non-bitter membranes. Another distinguishing feature is the shape of the leaf stalk: the bitter orange is broader and in the shape of a heart.
DISTRIBUTION: Native to China; extensively cultivated especially in America (California and Florida) and round the Mediterranean (France, Spain, Italy). The expressed oil is mainly produced in Israel, Cyprus, Brazil and North America; the distilled oil mainly comes from the Mediterranean and North America.
OTHER SPECIES: There are numerous cultivated varieties of sweet orange, for example Jaffa, Navel and Valencia. There are also many other subspecies such as the Japanese orange (C. aurantium var. natsudaidai). See also bitter orange.
HERBAL/FOLK TRADITION: A very nutritious fruit, containing vitamins A, B and C. In Chinese medicine the dried sweet orange peel is used to treat coughs, colds, anorexia and malignant breast sores. Li Shih-chen says: ‘The fruits of all the different species and varieties of citrus are considered by the Chinese to be cooling. If eaten in excess they are thought to increase the “phlegm”, and this is probably not advantageous to the health. The sweet varieties increase bronchial secretion, and the sour promote expectoration. They all quench thirst, and are stomachic and carminative.’.
ACTIONS: Antidepressant, anti-inflammatory, antiseptic, bactericidal, carminative, choleretic, digestive, fungicidal, hypotensive, sedative (nervous), stimulant (digestive and lymphatic), stomachic, tonic.
EXTRACTION: 1. Essential oil by cold expression (hand or machine) of the fresh ripe or almost ripe outer peel. 2. Essential oil by steam distillation of the fresh ripe or almost ripe outer peel. An oil of inferior quality is also produced by distillation from the essences recovered as a byproduct of orange juice manufacture. Distilled sweet orange oil oxidizes very quickly, and anti-oxidant agents are often added at the place of production. (An oil from the flowers is also produced occasionally called neroli Portugal or neroli petalae; an oil from the leaves is also produced in small quantities.)
SYNONYM: 1. A yellowy-orange or dark orange mobile liquid with a sweet, fresh fruity scent, richer than the distilled oil. It blends well with lavender, neroli, lemon, clary sage, myrrh and spice oils such as nutmeg, cinnamon and clove.
2. A pale yellow or colourless mobile liquid with a sweet, light-fruity scent, but little tenacity.
PRINCIPAL CONSTITUENTS: Over 90 per cent monoterpenes, mainly limonene. The cold expressed oil also contains bergapten, auraptenol and acids.
SAFETY DATA: Generally non-toxic (although ingestion of large amounts of orange peel has been known to be fatal to children); non-irritant and non-sensitizing (although limonene has been found to cause dermatitis in a few individuals). Distilled orange oil is phototoxic: its use on the skin should be avoided if there is danger of exposure to direct sunlight. However, there is no evidence to show that expressed sweet orange oil is phototoxic although it too contains coumarins.
AROMATHERAPY/HOME: USE
Skin care: Dull and oily complexions, mouth ulcers.
Circulation muscles and joints: Obesity, palpitations, water retention.
Respiratory system: Bronchitis, chills.
Digestive system: Constipation, dyspepsia, spasm.
Immune system: Colds, ’flu.
Nervous system: Nervous tension and stressrelated conditions.
OTHER USES: Sweet orange peel tincture is used to flavour pharmaceuticals. Extensively used as a fragrance component in soaps, detergents, cosmetics and perfumes, especially eau-de-colognes. Extensively used in all areas of the food and drinks industry (more so than the bitter orange oil). Used as the starting material for the isolation of naturallimonene.... orange, sweet
FAMILY: Lamiaceae (Labiatae)
SYNONYMS: Pulegium, European pennyroyal, pudding grass.
GENERAL DESCRIPTION: A perennial herb up to 50 cms tall with smooth roundish stalks, small, pale purple flowers and very aromatic, grey-green, oval leaves. Like other members of the mint family, it has a fibrous creeping root.
DISTRIBUTION: Native to Europe and parts of Asia; it is cultivated mainly in southern Spain, Morocco, Tunisia, Portugal, Italy, Yugoslavia and Turkey.
OTHER SPECIES: There are several different varieties of pennyroyal according to location: in Britain the ‘erecta’ and ‘decumbens’ types are most common. The North American pennyroyal (Hedeoma pulegoides), which is also used to produce an essential oil, belongs to a slightly different species, though it shares similar properties with the European variety.
HERBAL/FOLK TRADITION: A herbal remedy of ancient repute, used for a wide variety of ailments. It was believed to purify the blood and also be able to communicate its purifying qualities to water. ‘Pennyroyal water was distilled from the leaves and given as an antidote to spasmodic, nervous and hysterical affections. It was also used against cold and “affections of the joints”.’.
It is still current in the British Herbal Pharmacopoeia, indicated for flatulent dyspepsia, intestinal colic, the common cold, delayed menstruation, cutaneous eruptions and gout.
ACTIONS: Antiseptic, antispasmodic, diaphoretic, carminative, digestive, emmenagogue, insect repellent, refrigerant, stimulant.
EXTRACTION: Essential oil by steam distillation from the fresh or slightly dried herb.
CHARACTERISTICS: A colourless or pale yellow liquid with a very fresh, minty herbaceous odour. It blends well with geranium, rosemary, lavandin, sage and citronella.
PRINCIPAL CONSTITUENTS: Mainly pulegone, with menthone, iso-menthone, octanol, piperitenone and trans-iso-pulegone. Constituents vary according to source – the Moroccan oil contains up to 96 per cent pulegone.
SAFETY DATA: Oral toxin. Abortifacient (due to pulegone content). Ingestion of large doses has resulted in death.
AROMATHERAPY/HOME: USE None. ‘Should not be used in aromatherapy whether internally or externally.’.
OTHER USES: Used as a fragrance material mainly in detergents or low-cost industrial perfumes. Mainly employed as a source of natural pulegone.... pennyroyal
FAMILY: Lauraceae
SYNONYMS: S. officinale, Laurus sassafras, S. variifolium, common sassafras, North American sassafras, sassafrax.
GENERAL DESCRIPTION: A deciduous tree up to 40 metres high with many slender branches, a soft and spongy orange-brown bark and small yellowy-green flowers. The bark and wood are aromatic.
DISTRIBUTION: Native to eastern parts of the USA; the oil is mainly produced from Florida to Canada and in Mexico.
OTHER SPECIES: There are several other species, notably the Brazilian sassafras (Ocotea pretiosa) which is also used to produce an essential oil (also highly toxic). See also Botanical Classification section.
HERBAL/FOLK TRADITION: It has been used for treating high blood pressure, rheumatism, arthritis, gout, menstrual and kidney problems, and for skin complaints. ‘Sassafras pith – used as a demulcent, especially for inflammation of the eyes, and as a soothing drink in catarrhal affection.’. The wood and bark yield a bright yellow dye.
ACTIONS: Antiviral, diaphoretic, diuretic, carminative, pediculicide (destroys lice), stimulant.
EXTRACTION: Essential oil by steam distillation from the dried root bark chips.
CHARACTERISTICS: A yellowy-brown, oily liquid with a fresh, sweet-spicy, woody camphoraceous odour. (A safrol-free sassafras oil is produced by alcohol extraction.)
PRINCIPAL CONSTITUENTS: Safrole (80–90 per cent), pinenes, phellandrenes, asarone, camphor, thujone, myristicin and menthane, among others.
SAFETY DATA: Highly toxic – ingestion of even small amounts has been known to cause death. Carcinogen. Irritant. Abortifacient.
AROMATHERAPY/HOME: USE None. ‘Should not be used in therapy, whether internally or externally.’.
OTHER USES: Sassafras oil and crude are banned from food use; safrol-free extract is used to a limited extent in flavouring work. Safrol is used as a starting material for the fragrance item ‘heliotropin’.... sassafras
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