The essential mission of occupational health and safety is to protect and enhance the health, well-being and productivity of workers, individually and collectively. That mission cannot be accomplished without an understanding of stress and the mechanisms through which it affects individuals and organizations, and without a well-planned programme that will both alleviate its deleterious effects and, more important, prevent them.
Stress is an inescapable ingredient of the lives of all people everywhere. It stems from—and simultaneously affects—individuals’ inner sense of well-being; their relationships with family, friends, co-workers and strangers; and their capacity to function in the home, the workplace and the community. When excessive, it leads to physical or psychological symptoms and, when prolonged, it may lead to disability and disease. It modifies individuals’ perceptions, feelings, attitudes and behaviour and affects the organizations whose activities they direct or carry out. The subject of stress is covered extensively elsewhere in this Encyclopaedia.
Designing a Stress Management Programme
The effective workplace stress management programme will contain a number of overlapping elements operating concurrently. Some are formalized under the designation of a stress management programme while others are simply part of general organizational management even when they are explicitly aimed at controlling stress. Some of these are aimed at employees individually and in groups; others are aimed at stressors arising in the workplace; and still others address the stressors impinging on the organization as an entity in itself which inevitably filter down to affect some or all of the employees. The elements of a workplace stress management programme will be examined under the following headings.
1. Managing stress-related symptoms. This element deals with individuals already suffering from the effects of stress. Labelled the “medical model,” it attempts to identify individuals with signs and symptoms and to persuade them to come forward voluntarily or accept referral to professionals able to evaluate their problems, diagnose the causes and offer appropriate treatment. It may be based in the employee health service or in the employee assistance programme, or it may be associated with any other counselling services provided by the organization. The services may cover a broad range extending from one-on-one interviews and examinations to telephone “hot-lines” for emergency situations to comprehensive centres with multidisciplinary staffs of qualified professionals. It may be served by full- or part-time professionals or by contractual or casual referral arrangements with professionals who come to the worksite or are based in nearby facilities in the community. Some units deal with any and all problems, while others may more or less focus on such specific stress-related syndromes as hypertension, backache, alcoholism, drug abuse or family problems. The contributions of these service elements to the stress management programme are based on the following capabilities:
2. Reducing individual vulnerability. The most common elements in stress management programmes are those that help individuals to cope with stress by reducing their vulnerability. These include series of seminars and workshops, supplemented by audiotapes or videotapes and pamphlets or other publications that educate employees to cope with stress more effectively. Their common denominators are these:
Some of the tools they employ are listed in figure 1. For those not familiar with the term, “rap sessions” are meetings of groups of employees, with or without supervisors being present, in which experiences and problems are discussed and complaints freely ventilated. They are analogous to the shop meetings held under union auspices.
Figure 1. Some approaches to reducing vulnerability.
3. Interpersonal relations in the workplace. Organizations are being increasingly made aware of stressors emanating from the diversity of the workforce and the interpersonal problems they often present. Prejudice and bigotry do not stop at the gates of the worksite and are often compounded by insensitive or discriminatory behaviour on the part of managers and supervisors. Sexual and racial bias may take the form of harassment and may even be expressed in or evoke acts of violence. When rampant, such attitudes demand prompt correction through enunciation of an explicit policy that includes disciplinary actions against those who are guilty, coupled with protecting victims emboldened to complain against reprisals.
4. Managing job-related stressors. It is the organization’s responsibility to minimize job-related stressors that may have an adverse effect on employees’ capacity to function effectively. It is most important to ensure that supervisors and managers on all levels receive appropriate training to recognize and to deal promptly and effectively with the “people problems” that will inevitably arise in the workplace.
5. Managing the organization’s stress. The organization as an entity is exposed to stressors which, if not properly managed, filter down through the workforce, inevitably impinging on employees on all levels. This state of affairs requires the establishment of challenging but attainable goals and objectives, early identification and assessment of potential stressors that may thwart those plans, coordination of the organization’s capacities to deal with them and the communication of the results of those efforts to the workforce. The last-mentioned need is particularly critical at times of economic stringency, when employee collaboration and optimal productivity are especially important in dealing with such crises as changes in top management, threatened mergers and takeovers, plant closings or relocations. and downsizing.
6. Helping to manage personal stressors. While the management of stressors arising in the home and in the community is fundamentally a problem for the individual, employers are discovering that the stress they generate is inevitably brought into the workplace where, either on their own or in conjunction with job-related stressors, they often affect employees’ well-being and compromise their work performance. Accordingly, employers are finding it expedient (and in some instances, necessary) to establish programmes designed to assist employees to cope with stressors of this sort. A list of the most common personal stressors and workplace programmes aimed at them is presented in figure 2.
Figure 2. Stressors in the workplace and workplace programmes to help with them.
Basic Principles of the Programme
In establishing a worksite stress management programme, some basis principles must be emphasized.
First, it must be remembered that there are no boundaries between stress arising in the workplace, in the home and in the community. Each individual presents a unique composite of all of the factors which are carried wherever he or she may go. This means that while the programme must focus on those problems arising in the workplace, it must recognize that these continue to affect the worker’s outside life, nor can it ignore those originating off the job. Indeed, it has been shown that work itself and the support derived from co-workers and the organization may have a therapeutic value in dealing with personal and family problems. In fact, the loss of this support probably accounts for much of the disability associated with retirement, even when it is voluntary.
Second, stress is highly “contagious”. It not only affects particular individuals but also those about them with whom they must relate and collaborate. Thus, dealing with stress is simultaneously therapeutic and preventive.
Third, coping with stress is inherently an individual responsibility. Troubled employees can be identified and offered counselling and guidance. They can be given support and encouragement and taught to improve their coping skills. When necessary, they can be referred to qualified health professionals in the community for more intensive or prolonged therapy. But, in the last analysis, all this requires the consent and participation of the individual which, in turn, depends on the structure of the programme, its status in the organization, the competence of its staff and the reputations they earn, and its accessibility. Perhaps the most important determinant of programme success is the establishment of and strict adherence to a policy of observing the confidentiality of personal information.
Fourth, control of workplace stress is fundamentally a managerial responsibility. The programme must be based on an explicit organizational policy that places high value on employee’s health and well-being. And that policy must be reflected in the day-to-day operations by the attitudes and behaviour of managers on all levels,
Fifth, employee involvement in the programme’s design and operation and, particularly, in identifying stressors and devising ways to control them is an important ingredient of programme success. This is facilitated in many workplaces where safety and health joint labour-management committees function or where worker participation in managerial decision-making is encouraged.
Finally, a successful stress management programme requires an intimate understanding of the employees and the environment in which they work. It is most successful when stress-related problems are identified and resolved before any damage is done.
The essential mission of occupational health and safety is to protect and enhance the health, well-being and productivity of workers, individually and collectively. That mission cannot be accomplished without an understanding of stress and the mechanisms through which it affects individuals and organizations, and a well-planned programme that will both alleviate its deleterious effects and, more important, prevent them.
In this era of multinational organizations and ever-expanding international trade, employees are being increasingly called upon to undertake travel for business reasons. At the same time, more employees and their families are spending their holidays in travel to distant places around the world. While for most people such travel is usually exciting and enjoyable, it is often burdensome and debilitating and, especially for those who are not properly prepared, it can be hazardous. Although life-threatening situations may conceivably be encountered, most of the problems associated with travel are not serious. For the holiday traveller, they bring anxiety, discomfort and inconvenience along with the disappointment and added expense involved in shortening a trip and making new travel arrangements. For the business person, travel difficulties may ultimately affect the organization adversely on account of the impairment of his or her work performance in negotiations and other dealings, to say nothing of the cost of having to abort the mission and sending someone else to complete it.
This article will outline a comprehensive travel protection programme for individuals making short-term business trips and it will briefly describe steps that may be taken to circumvent the more frequently encountered travel hazards. (The reader may consult other sources—e.g., Karpilow 1991—for information on programmes for individuals on long-term expatriate assignments and on programmes for whole units or groups of employees dispatched to workstations in distant locales).
A Comprehensive Travel Protection Programme
Occasional seminars on managing the hazards of travel are a feature of many worksite health promotion programmes, especially in organizations where a sizeable proportion of employees travels extensively. In such organizations, there often is an in-house travel department which may be given the responsibility of arranging the sessions and procuring the pamphlets and other literature that may be distributed. For the most part, however, educating the prospective traveller and providing any services that may be needed are conducted on an individual rather than a group basis
Ideally, this task is assigned to the medical department or employees’ health unit, where, it is to be hoped, a knowledgeable medical director or other health professional will be available. The advantages of maintaining in-house medical unit staff, apart from convenience, is their knowledge of the organization, its policies and its people; the opportunity for close collaboration with other departments that may be involved (personnel and travel, for example); access to medical records containing health histories of those assigned to travel assignments, including details of any prior travel misadventures; and, at least, a general knowledge of the kind and intensity of work to be accomplished during the trip.
Where such an in-house unit is lacking, the travelling individual may be referred to one of the “travel clinics” that are maintained by many hospitals and private medical groups in the community. The advantages of such clinics include medical staff specializing in the prevention and treatment of the diseases of travellers, current information about conditions in the areas to be visited and fresh supplies of any vaccines that may be indicated.
A number of elements should be included if the travel protection programme is to be truly comprehensive. These are considered under the following heads.
An established policy
Too often, even when a trip has been scheduled for some time, the desired steps to protect the traveller are taken on an ad hoc, last-minute basis or, sometimes, neglected entirely. Accordingly, an established written policy is a key element in any travel protection programme. Since many business travellers are high-level executives, this policy should be promulgated and supported by the chief executive of the organization so that its provisions can be enforced by all of the departments involved in travel assignments and arrangements, which may be headed by managers of lower rank. In some organizations, the policy expressly prohibits any business trip if the traveler has not received a medical “clearance”. Some policies are so detailed that they designate minimal height and weight criteria for authorizing the booking of more expensive business-class seating instead of the much more crowded seats in the economy or tourist sections of commercial aircraft, and specify the circumstances under which a spouse or family members may accompany the traveller.
Planning the trip
The medical director or responsible health professional should be involved in planning the itinerary in conjunction with the travel agent and the individual to whom the traveller reports. The considerations to be addressed include (1) the importance of the mission and its ramifications (including obligatory social activities), (2) the exigencies of travel and conditions in the parts of the world to be visited, and (3) the physical and mental condition of the traveller along with his or her capacity to withstand the rigours of the experience and continue to perform adequately. Ideally, the traveller will also be involved in such decisions as to whether the trip should be postponed or cancelled, whether the itinerary should be shortened or otherwise modified, whether the mission (i.e., with respect to number of people visited or number or duration of meetings, etc.) should be modified, whether the traveller should be accompanied by an aide or assistant, and whether periods of rest and relaxation should be built into the itinerary.
Pre-travel medical consultation
If a routine periodic medical examination has not been performed recently, a general physical examination and routine laboratory tests, including an electrocardiogram, should be performed. The purpose is to ensure that the employee’s health will not be adversely affected either by the rigours of transit per se or by other circumstances encountered during the trip. The status of any chronic diseases needs to be determined and modifications advised for those with such conditions as diabetes, autoimmune diseases or pregnancy. A written report of the findings and recommendations should be prepared to be made available to any physicians consulted for problems arising en route. This examination also provides a baseline for evaluating potential illness when the traveller returns.
The consultation should include a discussion of the desirability of immunizations, including a review of their potential side-effects and the differences between those that are required and those that are only recommended. An inoculation schedule individualized for the traveler’s needs and departure date should be developed and the necessary vaccines administered.
Any medications being taken by the traveller should be reviewed and prescriptions provided for adequate supplies, including allowances for spoilage or loss. Modifications of timing and dosage must be prepared for travellers crossing several time zones (e.g., for those with insulin-dependent diabetes). Based on the work assignment and mode of transport, medications should be prescribed for the prevention of certain specific diseases, including (but not limited to) malaria, traveller’s diarrhoea, jet lag and high altitude sickness. In addition, medications should be prescribed or supplied for on-the-trip treatment of minor illnesses such as upper respiratory infections (particularly nasal congestion and sinusitis), bronchitis, motion sickness, dermatitis and other conditions that may be reasonably anticipated.
For the traveller who does not wish to spend valuable time searching for a pharmacy in case of need, a kit of medications and supplies may be invaluable. Even if the traveller may be able to find a pharmacy, the pharmacist’s knowledge of the traveller’s special condition may be limited, and any language barrier may result in serious lapses in communication. Further, the medication offerred may not be safe and effective. Many countries do not have strict drug labelling laws and quality assurance regulations are sometimes non-existent. The expiration dates of medications are often ignored by small pharmacies and the high temperatures in tropical climates may inactivate certain medications that are stored on shelves in hot shops.
While commercial kits stocked with routine medications are available, the contents of any such kit should be customized to meet the traveller’s specific needs. Among those most likely to be needed, in addition to medications prescribed for specific health problems, are drugs for motion sickness, nasal congestion, allergies, insomnia and anxiety; analgesics, antacids and laxatives, as well as medication for haemorrhoids, menstrual discomfort and nocturnal muscle cramps. The kit may furthermore contain antiseptics, bandages and other surgical supplies.
Travellers should carry either letters signed by a physician on letterhead stationery or else prescription blanks listing the medications being carried and indicating the conditions for which they have been prescribed. This may save the traveller from embarrassing and potentially long delays at international ports of entry where customs agents are especially diligent in looking for illicit drugs.
The traveller should also carry either an extra pair of eyeglasses or contact lenses with adequate supplies of cleansing solutions and other necessary appurtenances. (Those going to excessively dirty or dusty areas should be encouraged to wear eyeglasses rather than contact lenses). A copy of the user’s lens prescription will facilitate the procurement of replacement glasses should the traveller’s pair be lost or damaged.
Those who travel frequently should have their kits checked before each trip to make sure that the contents have been adjusted to the particular itinerary and are not outdated.
In addition to notes confirming the appropriateness of the medications being carried, the traveller should carry a card or letter summarizing any significant medical history, findings on his or her pre-travel health assessment and copies of a recent electrocardiogram and any relevant laboratory data. A record of the traveller’s most recent immunizations may obviate the necessity of submitting to mandatory inoculation at the port of entry. The record should also contain the name, address, telephone and fax numbers of a physician who can supply additional information about the traveller should it be required (a Medic-Alert type of badge or bracelet can be useful in this regard).
A number of vendors can supply medical record cards with microfilm chips containing travellers’ complete medical files. While often convenient, the foreign physician may lack access to the microfilm viewer or a hand lens powerful enough to read them. There is also the problem of making sure that the information is up-to-date.
Some countries require all arriving travellers to be vaccinated for certain diseases, such as cholera, yellow fever or plague. While the World Health Organization has recommended that only vaccination for yellow fever be required, a number of countries still require cholera immunization. In addition to protecting travellers, the required immunizations are also intended to protect their citizens from diseases that may be carried by travellers.
Recommended immunizations are intended to prevent travellers from contracting endemic diseases. This list is much longer than the “required” list and is enlarging annually as new vaccines are developed to combat new and rapidly advancing diseases. The desirability of a specific vaccine also changes frequently in accord with the amount and virulence of the disease in the particular area. For this reason, current information is essential. This may be obtained from the World Health Organization; from government agencies such as the US Centers for Disease Control and Prevention; the Canada Health and Welfare Department; or from the Commonwealth Department of Health in Sydney, Australia. Similar information, usually derived from such sources, may be obtained from local voluntary and commercial organizations; it is also available in periodically updated computer software.
Immunizations recommended for all travellers include diphtheria-tetanus, polio, measles (for those born after 1956 and without a physician-documented episode of measles), influenza and hepatitis B (particularly if the work assignment may involve exposure to this hazard).
The amount of time available for departure may influence the immunization schedule and dosage. For example, for the individual who has never been immunized against typhoid, two injections, four weeks apart, should produce the highest antibody titre. If there is not enough time, those who have not been previously inoculated may be given four pills of the newly developed oral vaccine on alternate days; this will be considerably more effective than a single dose of the injected vaccine. The oral vaccine regimen may also be used as a booster for individuals who have previously received the injections.
Health Insurance and Repatriation Coverage
Many national and private health insurance programmes do not cover individuals who receive health services while outside of the specified area. This can cause embarrassment, delays in receiving needed care and high out-of-pocket expenses for individuals who incur injuries or acute illnesses while on a trip. It is prudent, therefore, to verify that the traveller’s current health insurance will cover him or her throughout the trip. If not, procurement of temporary health insurance covering the entire period of the trip should be advised.
Under certain circumstances, particularly in undeveloped areas, lack of adequate modern facilities and concern over the quality of the available care may dictate medical evacuation. The traveller may be returned to his or her home city or, when the distance is too great, to an acceptable urban medical centre en route. A number of companies provide emergency evacuation services around the world; some, however, are available only in more limited areas. Since such situations are usually quite urgent and stressful for all those involved, it is wise to make preliminary stand-by arrangements with a company that serves the areas to be visited and, since such services may be quite expensive, to confirm that they are covered by the traveller’s health insurance programme.
A medical consultation soon after return is a desirable follow-up to the trip. It provides for a review of any health problems that may have arisen and the proper treatment of any that may not have entirely cleared up. It also provides for a debriefing on the circumstances encountered en route that can lead to more appropriate recommendations and arrangements if the trip is to be repeated or undertaken by others.
Coping with the Hazards of Travel
Travel almost always entails exposure to health hazards that, at the least, present inconvenience and annoyance and can lead to serious and disabling illnesses or worse. For the most part, they can be circumvented or controlled, but this usually requires a special effort on the part of the traveller. Sensitizing the traveller to recognize them and providing the information and training required to cope with them is the major thrust of the travel protection programme. The following represent some of the hazards most commonly encountered during travel.
Rapid passage across time zones can disrupt the physiological and psychological rhythms—the circadian rhythms—that regulate the organism’s functions. Known as “jet lag” because it occurs almost exclusively during air travel, it can cause sleep disturbances, malaise, irritability, reduced mental and physical performance, apathy, depression, fatigue, loss of appetite, gastric distress and altered bowel habits. As a rule, it takes several days before a traveller’s rhythms adapt to the new location. Consequently, it is prudent for travellers to book long-distance flights several days prior to the start of important business or social engagements so as to allow themselves a period during which they can recover their energy, alertness and work capacities (this also applies to the return flight). This is particularly important for older travellers, since the effects of jet lag seem to increase with age.
A number of approaches to minimizing jet lag have been employed. Some advocate the “jet lag diet,” alternating feasting and fasting of carbohydrates or high protein foods for three days prior to departure. Others suggest eating a high carbohydrate dinner prior to departure, limiting food intake during the flight to salads, fruit plates and other light dishes, drinking a good deal of fluids before and during the trip (enough on the plane to require the hourly use of the rest room) and avoidance of all alcoholic beverages. Others recommend the use of a head-mounted light that suppresses the secretion of melatonin by the pineal gland, the excess of which has been linked to some of the symptoms of jet lag. More recently, small doses of melatonin in tablet form (1 mg or less—larger doses, popular for other purposes, produce drowsiness) taken on a prescibed schedule several days before and after the trip, have been found useful in minimizing jet lag. While these may be helpful, adequate rest and a relaxed schedule until the readjustment has been completed are most reliable.
In addition to jet lag, travel by air can be difficult for other reasons. Getting to and through the airport can be a source of anxiety and irritation, especially when one has to cope with traffic congestion, heavy or bulky luggage, delayed or cancelled flights and dashing through terminals to make connecting flights. Long periods of confinement in narrow seats with insufficient leg room are not only uncomfortable but may precipitate attacks of phlebitis in the legs. Most passengers in well-maintained modern aircraft will have no difficulty breathing since cabins are pressurized to maintain a simulated altitude below that of 8,000 feet above sea level. Cigarette smoke may be annoying for those seated in or near the smoking sections of planes that have not been designated as smoke-free.
These problems can be minimized by such steps as prearranging transfers to and from the airports and assistance with baggage, providing electric carts or wheel chairs for those for whom the long walk between the terminal entrance and the gate may be troublesome, eating lightly and avoiding alcoholic beverages during the flight, drinking plenty of fluids to combat the tendency toward dehydration and getting out of one’s seat and walking about the cabin frequently. When the lattermost alternative is not feasible, performing stretching and relaxing exercises like those demonstrated in figure 1 is essential. Eye shades may be helpful in trying to sleep during the flight, while wearing ear plugs throughout the flight has been shown to decrease stress and fatigue.
Figure 1. Exercises to be performed during long airplane trips.
In some 25 countries, including Argentina, Australia, India, Kenya, Mexico, Mozambique and New Zealand, arriving aircraft cabins are required to be sprayed with insecticides before passengers are allowed to leave the plane The purpose is to prevent disease-bearing insects from being brought into the country. Sometimes, the spraying is cursory but often it is quite thorough, taking in the entire cabin, including the seated passengers and crew. Travellers who find the hydrocarbons in the spray annoying or irritating should cover their faces with a damp cloth and practice relaxation breathing exercises.
The United States objects to this practice. Transportation Secretary Federico F. Peña has proposed that all airlines and travel agencies be required to notify passengers when they will be sprayed, and the Transportation Department plans to bring this controversial issue before the International Civil Aviation Association and to cosponsor a World Health Organization symposium on this question (Fiorino 1994).
Mosquitoes and other biting pests.
Malaria and other arthropod-borne diseases (e.g., yellow fever, viral encephalitis, dengue fever, filariasis, leishmaniasis, onchocercosis, trypanosomiasis and Lyme disease) are endemic in many parts of the world. Keeping from getting bitten is the first line of defence against these diseases.
Insect repellents containing “DEET” (N,N-diethyl-meta-toluamide) may be used on the skin and/or clothing. Because DEET can be absorbed through the skin and may cause neurological symptoms, preparations with a DEET concentration over 35% are not recommended, especially for infants. Hexanediol is a useful alternative for those who may be sensitive to DEET. Skin-So-Soft®, the commercially available moisturizer, needs to be reapplied every twenty minutes or so to be an effective repellent.
All persons travelling in areas where insect-borne diseases are endemic should wear long-sleeve shirts and long trousers, especially after dusk. In hot climates, wearing loose-fitting thin cotton or linen garments is actually cooler than leaving the skin exposed. Perfumes and scented cosmetics, soaps and lotions that may attract insects should be avoided. Lightweight mesh jackets, hoods and face guards are particularly helpful in highly infested areas. Mosquito bed netting and window screens are important adjuncts. (Before retiring, it is important to spray the inside of the bednetting in case undesirable insects have become trapped in it.)
Protective clothing and nets may be treated with a DEET-containing repellent or with permethrin, an insecticide available in both spray and liquid formulations.
Despite decades of mosquito eradication efforts, malaria remains endemic in most tropical and subtropical regions of the world. Because it is so dangerous and debilitating, the mosquito control efforts described above should be supplemented by prophylactic use of one or more antimalarial drugs. While a number of fairly effective antimalarials have been developed, some strains of the malaria parasite have become highly resistant to some if not all of the currently used drugs. For example, chloroquine, traditionally the most popular, is still effective against strains of malaria in certain parts of the world but is useless in many other areas. Proguanil, mefloquine and doxycycline are currently most commonly used for chloroquine-resistant strains of malaria. Maloprim, fansidar and sulfisoxazole are also used in certain areas. A prophylactic regimen is started prior to entering the malarious area and continued for some time after leaving it.
The choice of the drug is based on “up to the minute” recommendations for the particular areas to be visited by the traveller. The potential side-effects should also be considered: for example, fansidar is contraindicated during pregnancy and lactation, while mefloquine should not be used by airline pilots or others in whom central nervous system side-effects could impair performance and affect the safety of others, nor by those taking beta-blockers or calcium-channel blockers or other drugs that alter cardiac conduction.
Contaminated tap water may be a problem all over the world. Even in modern urban centers, defective pipes and faulty connections in older or poorly maintained buildings may allow the spread of infection. Even bottled water may not be safe, particularly if the plastic seal on the cap is not intact. Carbonated beverages are generally safe to drink provided they have not been allowed to go flat.
Water can be disinfected by heating it to 62ºC for 10 minutes or by adding iodine or chlorine after filtering to remove parasites and worm larvae and then allowing it to stand for 30 minutes.
Water filtration units sold for camping trips are usually not appropriate for areas where the water is suspect since they do not inactivate bacteria and viruses. So-called “Katadyn” filters are available in individual units and filter out organisms larger than 0.2 microns but must be followed by iodine or chlorine treatment to remove viruses. The more recently developed “PUR” filters combine 1.0 micron filters with exposure to a tri-iodine resin matrix that eliminates bacteria, parasites and viruses in a single process.
In areas where the water may be suspect, the traveller should be advised not to use ice or iced drinks and to avoid brushing the teeth with water that has not been purified.
Another important precaution is to avoid swimming or dangling limbs in fresh-water lakes or streams harboring the snails carrying the parasites that cause schistosomiasis (bilharzia).
Food may be contaminated at the source by the use of “night soil” (human body wastes) as a fertilizer, in passage by a lack of refrigeration and exposure to flies and other insects, and in preparation by poor hygiene on the part of cooks and food handlers. In this respect, the food prepared by a street vendor where one can see what is being cooked and how it is being prepared may be safer than the “four star” restaurant where the posh ambience and clean uniforms worn by the staff may hide lapses in the storage, preparation and serving of the food. The old adage, “If you can’t boil it or peel it yourself, don’t eat it” is probably the best advice one can give the traveller.
Travellers’ diarrhoea is encountered worldwide in modern urban centres as well as in undeveloped areas. While most cases are attributed to organisms in food and drink, many are simply the result of strange foods and food preparation, dietary indiscretions and fatigue. Some cases may also follow bathing or showering in unsafe water or swimming in contaminated lakes, streams and pools.
Most cases are self-limited and respond promptly to such simple measures as maintaining an adequate fluid intake, a light bland diet and rest. Simple medications such as attapulgite (a clay product that acts as an absorbent), bismuth subsalicylate and anti-motility agents such as loperamide or reglan may help to control the diarrhoea. However, when the diarrhoea is unusually severe, lasts more than three days, or is accompanied by repeated vomiting or fever, medical attention and the use of appropriate antibiotics are advisable. Selection of the antibiotic of choice is guided by laboratory identification of the offending organism or, if that is not feasible, by an analysis of the symptoms and epidemiological information about the prevalence of particular infections in the areas visited. The traveller should be provided with a pamphlet such as the one developed by the World Health Organization (figure 2) that explains what to do in simple, non-alarming language.
Prophylactic use of antibiotics has been suggested before one enters an area where water and food are suspect, but this is generally frowned upon since the antibiotics themselves may cause symptoms and taking them in advance may lead the traveller to ignore or become lax towards the precautions that have been advised.
Figure 2. A sample of a World Health Organization educational pamphlet on traveller’s diarrhoea.
In some cases, the onset of the diarrhoea may not occur until after the return home. This is particularly suggestive of parasitic disease and is an indication that the appropriate laboratory tests be made to determine whether such an infection exists.
Travellers to mountainous regions such as Aspen, Colorado, Mexico City or La Paz, Bolivia, may have difficulty with the altitude, particularly those with coronary artery disease, congestive heart failure or lung diseases such as emphysema, chronic bronchitis or asthma. When mild, altitude sickness may cause fatigue, headache, exertional dyspnoea, insomnia or nausea. These symptoms generally subside after a few days of diminished physical activity and rest.
When more severe, these symptoms may progress to respiratory distress, vomiting and blurred vision. When this occurs, the traveller should seek medical attention and get to a lower altitude as quickly as possible, perhaps meanwhile even inhaling supplementary oxygen.
Crime and civil unrest.
Most travellers will have the sense to avoid war zones and areas of civil unrest. However, while in strange cities, they may unwittingly stray into neighbourhoods where violent crime is prevalent and where tourists are popular targets. Instructions on safeguarding jewelry and other valuables, and maps showing safe routes from the airport to the centre of the city and which areas to shun, may be helpful in avoiding being victimized.
Simple fatigue is a frequent cause of discomfort and impaired performance. A good deal of the difficulty attributed to jet lag is often the result of the rigours of travel in planes, buses and automobiles, poor sleep in strange beds and strange surroundings, overeating and alcohol consumption, and schedules of business and social engagements that are too full and demanding.
The business traveller is often bedevilled by the volume of work to clear up prior to departure as well as in preparing for the trip, to say nothing of catching up after the return home. Teaching the traveller to prevent the accumulation of undue fatigue while educating the executive to whom he or she reports to consider this ubiquitous hazard in laying out the assignment is often a key element in the travel protection programme.
With the increase in travel to strange and distant places for business and for pleasure, protecting the health of the traveller has become an important element in the worksite health promotion programme. It involves sensitizing the traveller to the hazards that will be encountered and providing the information and the tools needed to circumvent them. It includes medical services such as the pre-travel consultations, immunizations and provisions of medications that are likely to be needed en route. Participation by the organization’s management is also important in developing reasonable expectations for the mission, and making suitable travel and living arrangements for the trip. The goal is successful completion of the mission and the safe return of a healthy, travelling employee.
Prevention and control of infectious diseases is a central responsibility of the employee health service in areas where they are endemic, where work entails exposure to particular infectious agents to which the population may be singularly susceptible, and where community health services are deficient. In such circumstances, the medical director must act as the public health officer for the workforce, a duty that requires attention to sanitation, potable food and water, potential vectors of infection, appropriate immunization when available, as well as early detection and prompt treatment of infections when they occur.
In well-developed urban areas where employees are relatively healthy, concern over infectious diseases is usually eclipsed by other problems, but prevention and control of infectious diseases remain, nonetheless, important responsibilities of the employee health service. By virtue of their prevalence among all age groups (obviously including those most likely to be employed) and because of their fundamental capacity to be spread through the close contacts characteristic of the typical work environment, infectious diseases are an appropriate target for any employee health promotion programme. However, the efforts of employee health units to respond to the problem they pose are not often discussed. In part, this lack of attention may be attributed to the view that such efforts are a matter of routine, taking the form, say, of seasonal influenza immunization programmes. Additionally, they may be overlooked because they are activities not necessarily associated with broad health promotion initiatives but, instead, are woven into the fabric of the comprehensive employee health programme. For example, the individual counselling and treatment of employees undergoing periodic health evaluation often includes ad hoc health promotion interventions directed at infectious illnesses. Nonetheless, all these represent meaningful activities which, with or without formal designation as a “programme”, may be combined into a cohesive strategy for the prevention and control of infectious diseases.
These activities may be divided among a number of components: dissemination of information and employee education; immunizations; response to outbreaks of infection; protecting the health of travellers; reaching family members; and keeping up-to-date. To illustrate how these may be integrated into a comprehensive employee health programme serving a large urban, largely white-collar workforce, this article will describe the programme at J.P. Morgan and Company, Inc., based in New York City. While it has unique features, it is not dissimilar from those maintained by many large organizations.
J.P. Morgan & Company, Inc.
J.P. Morgan & Company, Inc., is a corporation providing diverse financial services throughout the world. Headquartered in New York City, where approximately 7,500 of its 16,500 employees are based, it maintains offices of various sizes elsewhere in the United States and Canada and in major cities of Europe, Asia, Latin America and Australia.
In-house medical departments were present in each of its immediate parent organizations from the early part of this century and, following the amalgamation of J.P. Morgan with Guaranty Trust Company, the employee health unit has evolved to provide not only standard occupational medical activities but a broad range of free services to employees, including periodic health evaluations, immunizations, outpatient primary care, health education and promotion and an employee assistance programme. The effectiveness of the medical department, which is based in New York City, is enhanced by the concentration of the bulk of Morgan’s workforce in a limited number of centrally located facilities.
Dissemination of Information
Dissemination of relevant information is usually the cornerstone of a health promotion programme and it is arguably the simplest approach whether resources are limited or abundant. Providing accurate, meaningful, and understandable information—modified as needed according to employees’ age, language, ethnicity and educational level—serves not only to educate but also to correct misconceptions, inculcate effective prevention strategies and direct employees to appropriate resources within or outside the worksite.
This information can take many forms. Written communications can be directed to employees at their workstations or to their homes, or can be distributed at central worksite locations. These may consist of bulletins or publications obtained from government or voluntary health agencies, pharmaceutical companies or commercial sources, among others or, if resources permit, they can be developed in-house.
Lectures and seminars can be even more effective particularly when they allow employees to pose questions about their individual concerns. On the other hand, they present the drawback of requiring accessibility and a greater time commitment on the part of both employer and staff; they also breach anonymity, which sometimes may be an issue.
Our own experience with the dissemination of health information on HIV infection can be viewed as an example of this activity. The first cases of the illness were reported in 1981 and we first became aware of cases among our employees in 1985. In 1986, in large measure because of local media attention to the problem, the employees in one of our European offices (where no cases of the illness had yet surfaced) requested a programme on AIDS. The speakers included the corporate medical director and an expert on infectious diseases from a local university hospital. The audience consisted of almost 10% of that unit’s entire workforce of whom 80% were women. The emphasis of these and subsequent presentations was on transmission of the virus and on strategies for prevention. As one might assume from the composition of the audience, there was considerable concern about heterosexual spread.
The success of that presentation facilitated the development of a far more ambitious programme at the New York headquarters the following year. A newsletter and brochure anticipated the events with a brief discussion of the illness, posters and other advertisements were utilized to remind employees of the times and places of presentations, and managers strongly encouraged attendance. Because of the commitment of management and general concerns about the illness in the community, we were able to reach between 25 and 30% of the local workforce in the multiple presentations.
These sessions included a discussion by the corporate medical director, who acknowledged the presence of the illness among employees and noted that the corporation was committed to their continuing employment as long as they remained well enough to work effectively. He reviewed the corporation’s policy on life-threatening illnesses and noted the availability of confidential HIV testing through the medical department. An educational videotape on the illness was shown, followed by an expert speaker from the local municipal health department. A period of questions and answers followed and, at the close of the session, everyone was given a packet of information materials on HIV infection and prevention strategies.
The response to these sessions was very positive. At a time when other corporations were experiencing workplace disruptions over employees with HIV infections, Morgan had none. An independent survey of employees (and those of several other corporations with similar programmes) found that programme participants thoroughly appreciated the opportunity to attend such sessions and found the information provided was more helpful than that available to them from other sources (Barr, Waring and Warshaw 1991).
We held similar sessions on HIV infection in 1989 and 1991, but found that attendance diminished with time. We attributed this, in part, to perceived saturation with the subject and, in part, to the illness shifting its impact to the chronically unemployed (in our area); indeed, the number of employees newly infected with HIV who came to our attention dramatically declined after 1991.
Meanwhile, Lyme disease, a bacterial illness transmitted by the bite of the deer tick in suburban and local vacation environments has become increasingly prevalent among our employees. A lecture on this subject supplemented by printed information attracted considerable attention when it was given in 1993. Points emphasized in this presentation included recognition of the illness, testing, treatment and, most important, prevention.
In general, programmes designed to disseminate information whether written or in lecture form, should be credible, easily understandable, practical and relevant. They should serve to elevate awareness, especially with regard to personal prevention and when and how to obtain professional attention. At the same time, they should serve to dissipate any inappropriate anxieties.
Immunizations at the worksite address an important public health need and are likely to provide tangible benefits, not only to the individual recipients but to the organization as well. Many employers in the developed world who do not have an employee health service arrange for outside contractors to come to the worksite to provide a mass immunization programme.
While most immunizations provide protection for many years, influenza vaccine must be administered annually because of continuing changes in the virus and, to a lesser extent, waning patient immunity. Since influenza is a seasonal illness whose infectiousness is typically widespread in the winter months, the vaccine should be administered in the autumn. Those most in need of immunization are older employees and those with underlying illnesses or immune deficiencies, including diabetes and chronic lung, heart and kidney problems. Employees in health care institutions should be encouraged to be immunized not only because they are more likely to be exposed to persons with the infection, but also because their continuing ability to work is critical in the event of a serious outbreak of the illness. A recent study has shown that vaccination against influenza offers substantial health-related and economic benefits for healthy, working adults also. Since the morbidity associated with the illness can typically result in a week or more of disability, often involving multiple employees in the same unit at the same time, there is sufficient incentive for employers to prevent the resultant impact on productivity by offering this relatively innocuous and inexpensive form of immunization. This becomes especially important when public health authorities anticipate major changes in the virus and predict a major epidemic for a given season.
Probably, the main barrier to the success of influenza (or any other) immunization programmes is the reluctance of individuals to participate. To minimize their hesitation, it is important to educate employees on the need for and availability of the vaccine and to make the immunization readily accessible. Notices should go out through all available means, generically identifying all those in special need of immunization emphasizing the relative safety of the vaccine, and explaining the procedure through which it can be obtained.
Time and the inconvenience of travel to visit a personal physician are potent disincentives for many individuals; the most effective programmes will be those that provide immunizations at the worksite during working hours with minimum delays. Finally, cost, a major barrier, should either be held to a minimum or absorbed entirely by the employer or the group health insurance programme.
Contributing to employee acceptance of immunizations are such additional factors as community publicity and incentive programmes. We have found that media reports of a threatening influenza epidemic will regularly increase employee acceptance of the vaccine. In 1993, to encourage all employees to have their vaccination status evaluated and to receive needed immunizations, the medical department at Morgan offered those who accepted these services participation in a lottery in which company stock was the prize. The number of employees seeking immunization in this year was half again as great as the number seen during the same period in the prior year.
Other immunizations advised for healthy adults of typical employment age are diphtheria-tetanus and, possibly measles, mumps, and rubella. Diphtheria-tetanus immunization is recommended every ten years throughout life, assuming that one has had a primary series of immunizations. With this interval, we find immune status most easily confirmed and the vaccine most easily administered during our employees’ periodic health evaluations (see below), although this can also be accomplished in a company-wide immunization campaign such as the one used in the incentive programme mentioned above.
Public health authorities recommend measles vaccine for everyone born after 1956 who does not have documentation of two doses of measles vaccine on or after the first birthday, a history of measles confirmed by a physician, or laboratory evidence of measles immunity. This immunization can readily be administered during a pre-employment or pre-placement health evaluation or in a company-wide immunization campaign.
Public health authorities recommend that everyone have medical documentation of having received rubella vaccine or laboratory evidence of immunity to this illness. Adequate rubella immunization is especially important for health care workers, for whom it is likely to be mandated.
Again, adequate rubella immunity should be ascertained at the time of employment or, absent this possibility, through periodic immunization campaigns or during periodic health evaluations. Effective immunity can be conferred on persons in need of rubella or rubeola vaccine by administration of MMR (measles-mumps-rubella) vaccine. Serologic testing for immunity can be undertaken to identify the immune status of an individual prior to immunization, but this is not likely to be cost-effective.
In so far as hepatitis B is transmitted through sexual intimacy and by direct contact with blood and other body fluids, initial immunization efforts were directed at populations with elevated risks, such as health professionals and those with multiple sexual partners. Additionally, the increased prevalence of the illness and carrier state in certain geographic areas such as the Far East and sub-Saharan Africa has given priority to immunization of all newborns there and of those who frequently travel to, or remain for extended periods in, those regions. More recently, universal immunization of all newborns in the United States and elsewhere has been proposed as a more effective strategy for reaching vulnerable individuals.
In the work environment, the focus of hepatitis B immunization has been on health care workers because of the risk of their exposure to blood. Indeed, in the United States, government regulation requires informing such personnel and other likely responders to health care emergencies of the advisability of being immunized against hepatitis B, in the context of a general discussion of universal precautions; immunization must then be provided.
Thus, in our setting at Morgan, information about hepatitis B immunization is conveyed in three contexts: in discussions on sexually transmitted diseases such as AIDS, in presentations to health care and emergency service personnel on the risks and precautions relevant to their health care work, and in interventions with individual employees and their families anticipating assignments in areas of the world where hepatitis B is most prevalent. The immunization is provided in conjunction with these programmes.
This illness, typically transmitted by contaminated food or water, is much more prevalent in developing nations than in industrialized countries. Thus, protection efforts have been directed at travellers to areas of risk or those who have household contact or other very close contact with those newly diagnosed with the illness.
Now that a vaccine to protect against hepatitis A has become available, it is administered to travellers to developing countries and to close contacts of newly diagnosed, documented cases of hepatitis A. If there is insufficient time for antibody levels to develop prior to the departure of travellers, serum immune globulin may be administered simultaneously.
As an effective, safe hepatitis A vaccine is available, immunization efforts can be directed to a significantly larger target group. At a minimum, frequent travellers to and residents in endemic areas should receive this immunization, and food handlers should also be considered for immunization because of the risk of their transmitting the illness to large numbers of people.
Prior to any immunization, careful attention should be paid to possible contraindications, such as hypersensitivity to any vaccine component or, in the case of live vaccines such as measles, mumps, and rubella, immune deficiency or pregnancy, whether present or soon anticipated. Appropriate information on possible vaccine risks should be conveyed to the employee and signed consent forms obtained. The limited possibility of immunization-related reactions should be anticipated in any programme.
Those organizations with existing medical staffs can obviously utilize their own personnel to implement an immunization programme. Those without such personnel may arrange for immunizations to be provided by community physicians or nurses, hospitals or health agencies or by government health agencies.
Response to Outbreaks
Few events arouse as much interest and concern among employees in a particular work unit or an entire organization as awareness that a co-worker has a contagious illness. The essential response of the employee health service to such news is to identify and appropriately isolate those who are ill, both the source case and any secondary cases, while disseminating information about the illness that will allay the anxiety of those who believe that they may have been exposed. Some organizations, hoping to minimize potential anxiety, may limit this dissemination to possible contacts. Others, recognizing that the “grapevine” (informal communication among employees) will not only spread the news but will probably also convey misinformation that could unleash latent anxiety, will seize the event as a unique opportunity to educate the entire workforce about the potential for spread of the disease and how to prevent it. At Morgan, there have been several episodes of this type involving three different diseases: tuberculosis, rubella, and food-borne gastroenteritis.
Tuberculosis is justifiably feared because of the potentially significant morbidity of the illness, especially with the increasing prevalence of multiple drug resistant bacteria. In our experience, the illness has been brought to our attention by news of the hospitalization and definitive diagnosis of the index cases; fortunately at Morgan, secondary cases have been rare and have been limited to skin test conversions only.
Typically with such cases, public health authorities are notified, following which contacts are encouraged to undergo baseline tuberculin skin testing or chest x-rays; the skin tests are repeated ten to twelve weeks later. For those whose skin tests convert from negative to positive in the follow-up testing, chest x-rays are obtained. If the x-ray is positive, employees are referred for definitive treatment; if negative, isoniazid prophylaxis is prescribed.
During each stage of the process, informational sessions are held on both a group and individual basis. Anxiety is typically disproportionate to risk, and reassurance, as well as the need for prudent follow-up, are the primary targets of the counselling.
Morgan’s cases of rubella have been identified on visits to the employee health unit. To avoid further contact, the employees are sent home even if there is only a clinical suspicion of the illness. Following serologic confirmation, usually within 48 hours, epidemiological surveys are conducted to identify other cases while information about the occurrence is disseminated. Although the major targets of these programmes are female employees who may be pregnant and who might have been exposed, the outbreaks have served as an opportunity to verify the immune status of all employees and to offer vaccine to all those who might need it. Again, local public health authorities are advised of these occurrences and their expertise and assistance are utilized in addressing organizational needs.
A single experience with a food-related illness outbreak occurred at Morgan several years ago. It was due to staphylococcal food poisoning which was traced to a food handler with a skin lesion on one of his hands. Over fifty employees who utilized the in-house dining facilities developed a self-limited illness which was characterized by nausea, vomiting and diarrhoea, appearing approximately six hours after ingesting the offending cold duck salad, and resolving within 24 hours.
In this instance, the thrust of our health education efforts was to sensitize the food handlers themselves to the signs and symptoms of illness that should influence them to leave their work and seek medical attention. Certain managerial and procedural changes were also implemented:
Recently, two neighbouring organizations also experienced food-related illness outbreaks. In one, hepatitis A was transmitted to a number of employees by a food handler in the company dining room; in the other, a number of employees developed salmonella food poisoning after consuming a dessert prepared with raw eggs in a restaurant off the premises. In the first instance, the organization’s educational efforts were directed at the food handlers themselves; in the second, information on various foods prepared from raw eggs—and the potential hazard that this entailed—was shared with the entire workforce.
While the three experiences described above follow the typical health promotion format of reaching out to the entire employee population or, at least, to a substantial subset, much of the health promotion activities of organizations like Morgan with respect to infectious diseases takes place on a one-on-one basis. These include interventions that are made possible by pre-placement, periodic, or retirement health evaluations, inquiries about international travel, and incidental visits to the employee health service.
Individuals examined at the time of employment are typically young and healthy and are unlikely to have had recent medical attention. They are often in need of such immunizations as measles, rubella, or diphtheria-tetanus. Additionally, those scheduled to be placed in areas of potential disease transmission such as in health or food services receive appropriate counselling about the precautions that they should observe.
Periodic medical examinations.
Similarly, the periodic health evaluation provides the opportunity to review immunization status and to discuss the risks that may be associated with specific chronic illnesses and the precautions that should be undertaken. Examples of the latter include the need for annual influenza immunization for individuals with diabetes or asthma and instruction for diabetics on the appropriate care of the feet to avoid local infection.
Recently reported news about infectious diseases should be discussed, particularly with those with known health problems. For example, news of outbreaks of an E. coli infection attributed to eating inadequately cooked ground meat would be of importance to all, while the danger of contracting cryptosporidiosis from swimming in public pools would be especially relevant to those with HIV disease or other immune deficiencies.
Employees who are examined in relation to retirement should be urged to obtain pneumococcal immunization and advised about annual influenza immunization.
The increasing globalization of work assignments coupled with the heightened interest in international travel for pleasure have contributed to a continuing expansion of the population needing protection against infectious diseases not likely to be encountered at home. A pre-travel encounter should include a medical history to reveal any individual health vulnerabilities that may increase the risks associated with the anticipated travel or assignment. A good—and not uncommon—example of this is the pregnant woman considering travel to an environment with chloroquine-resistant malaria, since the alternative forms of malaria prophylaxis may be contraindicated during pregnancy.
Comprehensive information on the infectious illnesses prevalent in the areas to be visited should be provided. This should include methods of transmission of the relevant illnesses, avoidance and prophylactic techniques, and typical symptoms and strategies for obtaining medical attention if they develop. And, of course, indicated immunizations should be provided.
Visits to the employee health service.
In most occupational health settings, employees may receive first aid and treatment for symptoms of illness; in some, as at Morgan, a broad range of primary care services is available. Each encounter offers an opportunity for preventive health interventions and counselling. This includes providing immunizations at appropriate intervals and alerting employee-patients about health precautions relative to any underlying illness or potential exposure. A particular advantage of this situation is that the very fact that the employee has sought this attention suggests that he or she may be more receptive to the advice given than may be the case when the same information is received in a broad educational campaign. The health professional should capitalize on this opportunity by ensuring that appropriate information and necessary immunizations or prophylactic medications are provided.
Reaching family members.
Although the main thrust of occupational health is to assure the health and well-being of the employee, there are many reasons to see that effective health promotion efforts are conveyed to the employee’s family as well. Obviously, most of the objectives noted earlier are equally applicable to other adult members of the household and, while the direct services of the occupational health unit are generally not available to family members, the information can be conveyed home through newsletters and brochures and by word of mouth.
An additional consideration is the health of children, especially in view of the importance of early childhood immunizations. It has been recognized that these immunizations are often overlooked, at least in part, not only by the economically disadvantaged, but even by the children of more affluent US corporate employees. Seminars on well-baby care and printed information on this subject, provided either by the employer or by the employer’s health insurance carrier may serve to minimize this deficiency. Additionally, modifying health insurance coverage to include such “preventive” measures as immunizations should also serve to encourage appropriate attention to this matter.
Although the introduction of antibiotics in the middle of the twentieth century led some to believe that infectious diseases would soon be eliminated, actual experience has been very different. Not only have new infectious diseases appeared (e.g., HIV and Lyme disease), but more infectious agents are developing resistance to formerly effective medications (e.g., malaria and tuberculosis). It is imperative, therefore, that occupational health professionals keep their knowledge of developments in the field of infectious diseases and their prevention current. Although there are many ways of doing this, periodic reports and bulletins emanating from the World Health Organization and national health agencies such as the US Centers for Disease Control and Prevention are particularly useful.
High among employers’ responsibilities for the health of the workforce is the prevention and control of infectious diseases among employees. This includes identification, isolation and appropriate treatment of individuals with infections together with prevention of their spread to co-workers and dependants and allaying the anxieties of those concerned about potential contact. It also involves education and appropriate protection of employees who may encounter infectious diseases while at work or in the community. The employee health service, as illustrated by the above description of activities of the medical department at J.P. Morgan and Company, Inc., in New York City, may play a central role in meeting this responsibility, resulting in benefit to individual employees, the organization as a whole and the community.
As the epidemic of HIV infection worsens and spreads, increasing numbers of workplaces, labour unions, employers and employees are being affected by the threat of HIV infection and AIDS (collectively to be termed HIV/AIDS). The effects are often particular and highly visible; they can also be insidious and somewhat hidden. Over the relatively brief lifetime of the HIV epidemic, the direct and indirect consequences of AIDS for the business sector and for the workplace in general (as distinguished from its health care aspect), remain for the most part a peripherally acknowledged component of the severity and magnitude of AIDS.
The attitudes and opinions of employees about AIDS are of pivotal importance, and must be assessed if a workplace programme is to be planned and managed effectively. Employee ignorance and misinformation can represent major obstacles to an educational programme, and if misjudged or handled poorly, can lead to distrust and disruption, and can aggravate already-prevalent biases and fears about AIDS.
In the United States, “AIDS has generated more individual lawsuits across a broad range of health issues than any other disease in history”, notes Lawrence Gostin of the HIV Litigation Project. A 1993 national survey of employee attitudes about AIDS by the National Leadership Coalition on AIDS reports that many working Americans continue to hold negative and potentially discriminatory attitudes toward HIV-infected co-workers, and the survey finds that most employees either don’t know how their employers would react to HIV- or AIDS-related situations in their workplaces, or they think that their employer would dismiss an employee with HIV infection at the first sign of illness. Discriminating against employees based solely on disability is expressly forbidden in the United States by the Americans with Disabilities Act (ADA), which includes under its protection people with HIV infection and AIDS. The Americans with Disabilities Act requires employers of more than 15 people to make “reasonable accommodations”, or adjustments in the job for their employees with disabilities, including HIV infection and AIDS.
For example, 32% of working Americans in the survey thought an employee with HIV infection would be fired or placed on disability leave at the first sign of illness. Clearly, if an employer moved to dismiss an employee with HIV infection solely on the basis of the diagnosis alone, that employer would be breaking the law. Such widespread employee ignorance of an employer’s legal responsibilities clearly makes employers—and by extension, their managers and employees—vulnerable to potentially costly discrimination lawsuits, work disruptions and employee morale and productivity problems.
Misperceptions about the epidemic can also fuel discriminatory attitudes and behaviour among managers and employees and can place an employer at risk. For example, 67% of workers surveyed thought that their colleagues would be uncomfortable working with someone with HIV infection. Left unchecked, such attitudes and the sorts of behaviour consistent with them can place an employer at considerable risk. Managers may erroneously assume that discriminatory treatment against those with HIV infection or AIDS, or those perceived as being infected, is acceptable.
HIV/AIDS Management Challenges
The medical, legal, financial, and workplace developments arising from the epidemic pose a host of challenges for people with HIV infection and AIDS, their families, their unions and their employers. Labour leaders, business executives, human resource professionals and front-line managers face increasingly complicated duties, including controlling costs, protecting the confidentiality of employees’ medical information and providing “reasonable accommodations” to their employees with HIV infection and AIDS, in addition to protecting people with HIV infection and AIDS and those perceived as having the illness from discrimination in hiring and promotion. People infected with HIV are remaining at work longer, so that employers need to plan how best to manage HIV-infected employees fairly and effectively over a longer period of time, and often with little or no training or guidance. Effectively managing employees with AIDS requires keeping abreast of emerging health care options, health insurance and health care costs, and legal and regulatory requirements, shaping effective “reasonable accommodations”, and managing concerns about confidentiality and privacy, discrimination issues, employee fears, harassment of infected workers, customer concerns, work disruptions, lawsuits, declines in worker productivity and morale—all the while maintaining a productive and profitable workplace and meeting business goals.
That is a large and somewhat complex set of expectations, a fact that underscores one of the essential needs in setting about to provide workplace education, namely, to start with managers and to train and motivate them to view AIDS in the workplace as part of long-term strategies and goals.
Amid the barrage of questions and concerns about the epidemic and how to manage its impact on the workplace, employers can take cost-effective steps to minimize risk, cut health care costs, protect their company’s future and, most important, save lives.
Step one: Establish a workplace HIV/AIDS policy
The first step toward effectively managing the workplace issues arising from the HIV epidemic is to put in place a sound workplace policy. Such a policy must set forth clearly the ways a business will deal with the host of complex but manageable challenges generated by HIV/AIDS. (“A sound workplace policy that accounts for an employer’s responsibilities to infected and affected workers will help keep a business from becoming a test case,” says Peter Petesch, a Washington, DC–based labour lawyer interested in the issue of AIDS and its workplace ramifications.)
Of course, a workplace policy itself will not remove the difficulties inherent in managing an employee with a fatal and often stigmatized illness. Nonetheless, a written workplace policy goes a long way towards preparing a company for its efforts to manage AIDS by minimizing risks and protecting its workforce. An effective written policy will include among its aims the need to
Effective HIV/AIDS policies should cover and provide guidance on compliance with the law, nondiscrimination, confidentiality and privacy, safety, performance standards, reasonable accommodation, co-worker concerns and employee education. In order to be effective, a policy must be communicated to employees at every level of the company. Moreover, it is crucial to have the outspoken, highly visible support of upper-level management and executives, including the chief executive, in reinforcing the urgency and importance of the messages outlined above. Without this level of commitment, a policy that exists just “on paper” runs the risk of being simply a lion with no teeth.
There are two general approaches to developing HIV/AIDS policies:
Step two: Train managers and supervisors
Managers and supervisors should be thoroughly familiarized with the employer’s workplace HIV/AIDS policy guidelines. One should ensure that every level of management is supplied with clear and consistent guidance on the medical facts and the minimal risk of transmission in the general workplace. In countries with anti-discrimination laws, managers must also be thoroughly familiar with their requirements (e.g., the Americans with Disabilities Act and its reasonable accommodation requirements, nondiscrimination, confidentiality and privacy, workplace safety and employee performance standards in the United States).
Also, all managers must be prepared to field questions and concerns from employees about HIV/AIDS and the workplace. Often the front-line managers are the first ones called on to provide information and referrals to other sources of information and to provide in-depth answers to employee questions about why they should be concerned about HIV infection and AIDS and about how they are expected to behave. Managers should be educated and prepared before employee education programmes are instituted.
Step three: Educate employees
Workplace-based education programmes are inexpensive and cost-effective ways to minimize risk, protect workers’ lives, save money on health care costs and save lives. MacAllister Booth, CEO of the Polaroid Corporation, recently said that the AIDS education and training for all Polaroid employees cost less than the treatment costs of one case of AIDS.
Workplace wellness programmes and health promotion are already an established part of the world of work for more and more workers, particularly among labour organizations and larger businesses. Campaigns to reduce medical costs and days missed due to preventable illnesses have focussed on the importance of stopping smoking and of exercising and following a healthier diet. Building on efforts to increase the safety of workplaces and the health of the workforce, workplace wellness programmes are already established as cost-effective and appropriate venues for health information for employees. HIV/AIDS education programmes can be integrated into these ongoing health promotion efforts.
Further, studies have shown that many employees trust their employers to provide accurate information about a broad range of topics, including health education. Working people are concerned about AIDS, many lack understanding of the medical and legal facts about the epidemic, and they want to learn more about it.
According to a study by the New York Business Group on Health (Barr, Waring and Warshaw 1991), employees generally have a positive opinion of employers who provide information about AIDS and—depending on the type of programme offered—found the employer to be a more credible source of information than either the media or the government. Further, according to the National Leadership Coalition on AIDS’ survey of working American’s attitudes about AIDS, 96% of employees who received AIDS education at work supported workplace-based HIV/AIDS education.
Ideally, attendance at employee education sessions should be mandatory, and the programme should last at least one and a half hours. The session should be conducted by a trained educator, and should present materials in an objective and nonjudgemental way. The programme should also allow for a question-and-answer period and provide referrals for confidential assistance. Initiatives taken with regard to AIDS in the workplace should be ongoing, not one-shot events, and are more effective when linked with such public acknowledgements of the importance of the problem as World AIDS Day observances. Finally, one of the most effective methods for discussing AIDS with employees is to invite a person living with HIV infection or AIDS to address the session. Hearing first-hand how someone lives and works with HIV infection or AIDS has been shown to have a positive impact on the effectiveness of the session.
A thorough workplace AIDS education programme should include a presentation of these matters:
Studies caution that attitudes about AIDS can be negatively reinforced if an education or training session is too brief and not sufficiently thorough and interactive. Similarly, simply handing out a brochure has been shown to increase anxiety about AIDS. In a brief, cursory session, attendees have been found to absorb some of the facts, but to leave with unresolved anxieties about the transmission of HIV, anxieties which have, in fact, been aroused by the introduction of the subject. Thus it is important to allow sufficient time in a training session for in-depth discussion, questions and answers, and referrals to other sources of confidential information. Optimally, a training session should be compulsory because the stigma still associated with HIV infection and AIDS will prevent many from attending a voluntary session.
Some Union Responses to HIV/AIDS
Some leading examples of union HIV/AIDS education and policy initiatives include the following:
Although the unions and companies responding constructively to the day-to-day workplace challenges of HIV/AIDS are in the minority, many have provided the models and a growing body of knowledge that is readily available to help others effectively address HIV as a workplace concern. The insight and experience gained over the past ten years demonstrate that well-planned AIDS policies, workplace standards and practices, leadership and ongoing labour, management and employee education are effective methods for addressing these challenges.
As trade unionists, industry groups and business associations recognize the growing consequences of AIDS for their sectors, new groups are forming to address the particular relevance of AIDS to their interests. The Thai Business Coalition on AIDS was launched in 1993, and appears likely to stimulate similar developments in other Pacific Rim countries. Several business and trade groups in Central and Southern Africa are taking the initiative in providing workplace education, and similar undertakings have become visible in Brazil and in the Caribbean.
The World Development Report (1993) was devoted to “Investing in Health” and examined the interplay between human health, health policy and economic development. The report provided a number of examples of the threat which AIDS poses to development strategies and accomplishments. This report indicates that there is a growing opportunity to utilize the skills and resources of global finance and development, working in closer harmony with public health leaders around the world, to form more effective action plans for confronting the economic and business challenges stemming from AIDS (Hammer 1994).
Unions and employers find that implementing AIDS policies and employee education programmes before confronting a case of HIV helps reduce workplace disruptions, saves money by protecting the health of the workforce, averts costly legal battles, and prepares managers and employees to respond constructively to the challenges of AIDS in the workplace. The tools needed to manage the multiple and complex day-to-day issues associated with the disease are readily accessible and inexpensive. Finally, they can save lives and money.
F. William Sunderman, Jr.
Occurrence and Uses
Metal carbonyls have the general formula Mex(CO)y, and are formed by combination of the metal (Me) with carbon monoxide (CO). Physical properties of some metal carbonyls are listed in table 1. Most are solids at ordinary temperatures, but nickel carbonyl, iron pentacarbonyl and ruthenium pentacarbonyl are liquids, and cobalt hydrocarbonyl is a gas. This article focuses on nickel carbonyl, which, because of its volatility, exceptional toxicity and industrial importance merits special attention in regard to occupational toxicology. Since iron pentacarbonyl and cobalt hydrocarbonyl also have high vapour pressures and potential for inadvertant formation, they warrant serious consideration as possible occupational toxicants. Most metal carbonyls react vigorously with oxygen and oxidizing substances, and some ignite spontaneously. Upon exposure to air and light, nickel carbonyl decomposes to carbon monoxide and particulate nickel metal, cobalt hydrocarbonyl decomposes to cobalt octacarbonyl and hydrogen, and iron pentacarbonyl decomposes to iron nonacarbonyl and carbon monoxide.
Table 1. Physical properties of some metal carbonyls
*Decomposition starts at temperature shown.
Source: Adapted from Brief et al. 1971.
Metal carbonyls are used in isolating certain metals (e.g., nickel) from complex ores, for producing carbon steel, and for metallizing by vapour deposition. They are also used as catalysts in organic reactions (e.g., cobalt hydrocarbonyl or nickel carbonyl in olefin oxidation; cobalt octacarbonyl for the synthesis of aldehydes; nickel carbonyl for the synthesis of acrylic esters). Iron pentacarbonyl is used as a catalyst for various organic reactions, and is decomposed to make finely powdered, ultra pure iron (so-called carbonyl iron), which is used in the computer and electronics industries. Methycyclopentadienyl manganese tricarbonyl (MMT) (CH3C5H4Mn(CO)3) is an antiknock additive to gasoline and is discussed in the article “Manganese”.
The toxicity of a given metal carbonyl depends on the toxicity of carbon monoxide and of the metal from which it is derived, as well as the volatility and instability of the carbonyl itself. The principal route of exposure is inhalation, but skin absorption can occur with the liquid carbonyls. The relative acute toxicity (LD50 for the rat) of nickel carbonyl, cobalt hydrocarbonyl and iron pentacarbonyl may be expressed by the ratio 1:0.52:0.33. Inhalation exposures of experimental animals to these substances induce acute interstitial pneumonitis, with pulmonary oedema and capillary damage, as well as injury to the brain, liver and kidneys.
Judging from the sparse literature on their toxicity, cobalt hydrocarbonyl and iron pentacarbonyl rarely pose health hazards in industry. None the less, iron pentacarbonyl can be formed inadvertently when carbon monoxide, or a gas mixture containing carbon monoxide, is stored under pressure in steel cylinders or fed through steel pipes, when illuminating gas is produced by petroleum reforming, or when gas welding is carried out. Presence of carbon monoxide in emission discharges from blast furnaces, electric arc furnaces and cupola furnaces during steel-making can also lead to the formation of iron pentacarbonyl.
Safety and Health Measures
Special precautions are mandatory in the storage of metal carbonyls; their handling must be mechanized to the maximum degree, and decanting should be avoided wherever possible. Vessels and piping should be purged with an inert gas (e.g., nitrogen, carbon dioxide) before being opened, and carbonyl residues should be burnt or neutralized with bromine water. Where there is an inhalation hazard, workers should be provided with airline respirators or self-contained breathing apparatus. Workshops should be fitted with down-draught ventilation.
Nickel carbonyl (Ni(CO)4) is mainly used as an intermediate in the Mond process for nickel refining, but it is also used for vapour-plating in the metallurgical and electronics industries and as a catalyst for synthesis of acrylic monomers in the plastics industry. Inadvertent formation of nickel carbonyl can occur in industrial processes that use nickel catalysts, such as coal gasification, petroleum refining and hydrogenation reactions, or during incineration of nickel-coated papers that are used for pressure-sensitive business forms.
Acute, accidental exposure of workers to inhalation of nickel carbonyl usually produces mild, non-specific, immediate symptoms, including nausea, vertigo, headache, dyspnoea and chest pain. These initial symptoms usually disappear within a few hours. After 12 to 36 hours, and occasionally as long as 5 days after exposure, severe pulmonary symptoms develop, with cough, dyspnoea, tachycardia, cyanosis, profound weakness and often gastrointestinal symptoms. Human fatalities have occurred 4 to 13 days after exposure to nickel carbonyl; deaths have resulted from diffuse interstitial pneumonitis, cerebral hemorrhage or cerebral oedema. In addition to pathologic lesions in the lungs and brain, lesions have been found in liver, kidneys, adrenals and spleen. In patients who survive acute nickel carbonyl poisoning, pulmonary insufficiency often causes protracted convalescence. Nickel carbonyl is carcinogenic and teratogenic in rats; the European Union has classified nickel carbonyl as an animal teratogen. Processes that use nickel carbonyl constitute disaster hazards, since fire and explosion can occur when nickel carbonyl is exposed to air, heat, flames or oxidizers. Decomposition of nickel carbonyl is attended by additional toxic hazards from inhalation of its decomposition products, carbon monoxide and finely particulate nickel metal.
Chronic exposure of workers to inhalation of low atmospheric concentrations of nickel carbonyl (0.007 to 0.52 mg/m3) can cause neurological symptoms (e.g., insomnia, headache, dizziness, memory loss) and other manifestations (e.g., chest tightness, excessive sweating, alopecia). Electroencephalographic abnormalities and elevated serum monoamine oxidase activity have been observed in workers with chronic exposures to nickel carbonyl. A synergistic effect of cigarette smoking and nickel carbonyl exposure on the frequency of sister-chromatid exchanges was noted in a cytogenetic evaluation of workers with chronic exposure to nickel carbonyl.
Safety and Health Measures
Fire and explosion prevention. Because of its flammability and tendency to explode, nickel carbonyl should be stored in tightly closed containers in a cool, well-ventilated area, away from heat and oxidizers such as nitric acid and chlorine. Flames and sources of ignition should be prohibited wherever nickel carbonyl is handled, used or stored. Nickel carbonyl should be transported in steel cylinders. Foam, dry chemical, or CO2 fire extinguishers should be used to extinguish burning nickel carbonyl, rather than a stream of water, which might scatter and spread the fire.
Health protection. In addition to the medical surveillance measures recommended for all nickel-exposed workers, persons with occupational exposures to nickel carbonyl should have biological monitoring of nickel concentration in urine specimens on a regular basis, typically monthly. Persons who enter confined spaces where they might possibly be exposed to nickel carbonyl should have self-contained breathing apparatus and a suitable harness with lifeline tended by another employee outside the space. Analytical instruments for continuous atmospheric monitoring of nickel carbonyl include (a) Fourier-transform infrared absorption spectroscopes, (b) plasma chromatographs and (c) chemiluminescent detectors. Atmospheric samples can also be analysed for nickel carbonyl by (d) gas chromatography, (e) atomic absorption spectrophotometry and (f) colourimetric procedures.
Treatment. Workers suspected to have been acutely exposed to nickel carbonyl should be immediately removed from the exposure site. Contaminated clothing should be removed. Oxygen should be administered and the patient kept at rest until seen by a physician. Each voiding of urine is saved for nickel analysis. The severity of acute nickel carbonyl poisoning correlates with the urine nickel concentrations during the first 3 days after exposure. Exposures are classified as “mild” if the initial 8-h specimen of urine has a nickel concentration less than 100 µg/l, “moderate” if the nickel concentration is 100 to 500 µg/l, and “severe” if the nickel concentration exceeds 500 µg/l. Sodium diethyldithiocarbamate is the drug of choice for chelation therapy of acute nickel carbonyl poisoning. Ancillary therapeutic measures include bed rest, oxygen therapy, corticosteroids and prophylactic antibiotics. Carbon monoxide poisoning may occur simultaneously and requires treatment.
Mercury combines readily with sulphur and halogens at ordinary temperatures and forms amalgams with all metals except iron, nickel, cadmium, aluminium, cobalt and platinum. It reacts exothermically (generates heat) with alkaline metals, is attacked by nitric acid but not by hydrochloric acid and, when hot, will combine with sulphuric acid.
Inorganic mercury is found in nature in the form of the sulphide (HgS) as cinnabar ore, which has an average mercury content of 0.1 to 4%. It is also encountered in the earth’s crust in the form of geodes of liquid mercury (in Almadén) and as impregnated schist or slate (e.g., in India and Yugoslavia).
Extraction. Mercury ore is extracted by underground mining, and mercury metal is separated from the ore by roasting in a rotary kiln or shaft furnace, or by reduction with iron or calcium oxide. The vapour is carried off in the combustion gases and is condensed in vertical tubes.
The most important uses of metallic mercury and its inorganic compounds have included the treatment of gold and silver ores; the manufacture of amalgams; the manufacture and repair of measurement or laboratory apparatus; the manufacture of incandescent electric bulbs, mercury vapour tubes, radio valves, x-ray tubes, switches, batteries, rectifiers, etc.; as a catalyst for the production of chlorine and alkali and the production of acetic acid and acetaldehyde from acetylene; chemical, physical and biological laboratory research; gold, silver, bronze and tin plating; tanning and currying; feltmaking; taxidermy; textile manufacture; photography and photogravure; mercury-based paints and pigments; and the manufacture of artificial silk. Some of these uses have been discontinued because of the toxic effects that the mercury exposure exerted upon workers.
Organic Mercury Compounds
Organic compounds of mercury may be considered as the organic compounds in which the mercury is chemically linked directly to a carbon atom. Carbon-mercury bonds have a wide range of stability; in general, the carbon-to-mercury bond in aliphatic compounds is more stable than that in aromatic compounds. According to one reliable estimate, more than 400 phenyl mercurials and at least that number of alkyl mercury compounds have been synthesized. The three most important groups in common usage are the alkyls, the aromatic hydrocarbons or aryls and the alkoxyalkyls. Examples of aryl mercury compounds are phenylmercuric acetate (PMA), nitrate, oleate, propionate and benzoate. Most available information is about PMA.
Uses. All the important uses of the organic mercury compounds depend on the biological activity of these substances. In medical practice organic mercury compounds are used as antiseptics, germicides, diuretics and contraceptives. In the field of pesticides they serve as algicides, fungicides, herbicides, slimacides and as preservatives in paints, waxes and pastes; they are used for mildew suppression, in antifouling paints, in latex paints and in the fungus-proofing of fabrics, paper, cork, rubber and wood for use in humid climates. In the chemical industry they act as catalysts in a number of reactions and the mercury alkyls are used as alkylating agents in organic syntheses.
Absorption and effects: Inorganic and metallic mercury
Vapour inhalation is the main route for the entry of metallic mercury into the body. Around 80% of inhaled mercury vapour is absorbed in the lung (alveoli). Digestive absorption of metallic mercury is negligible (lower than 0.01% of the administered dose). Subcutaneous penetration of metallic mercury as the result of an accident (e.g. the breakage of a thermometer) is also possible.
The main routes of entry of inorganic mercury compounds (mercury salts) are the lungs (atomization of mercury salts) and the gastrointestinal tract. In the latter case, absorption is often the result of accidental or voluntary ingestion. It is estimated that 2 to 10% of ingested mercury salts are absorbed through the intestinal tract.
Skin absorption of metallic mercury and certain of its compounds is possible, although the rate of absorption is low. After entry into the body, metallic mercury continues to exist for a short time in metallic form, which explains its penetration of the blood-brain barrier. In blood and tissues metallic mercury is rapidly oxidized to Hg2+ mercury ion, which fixes to proteins. In the blood, inorganic mercury is also distributed between plasma and red blood cells.
The kidney and brain are the sites of deposition following exposure to metallic mercury vapours, and the kidney following exposure to inorganic mercury salts.
The symptoms of acute poisoning include pulmonary irritation (chemical pneumonia), perhaps leading to acute pulmonary oedema. Renal involvement is also possible. Acute poisoning is more often the result of accidental or voluntary ingestion of a mercury salt. This leads to severe inflammation of the gastrointestinal tract followed rapidly by renal insufficiency due to necrosis of the proximal convoluted tubules.
The severe chronic form of mercury poisoning encountered in places like Almadén up until the early 20th century, and which presented spectacular renal, digestive, mental and nervous disorders and terminated in cachexia, was eliminated by means of preventive measures. However, a chronic, “intermittent” poisoning in which periods of active intoxication are interspersed between periods of latent intoxication can still be detected among mercury miners. In the latent periods, symptoms remit to such a degree that they are visible only on close search; only the neurological manifestations persist in the form of profuse sweating, dermographia and, to some extent, emotional instability.
A condition of “micromercurialism” characterized by functional neurosis (frequent hysteria, neurasthenia, and mixed forms), cardiovascular lability and secretory neurosis of the stomach has also been described.
Digestive system. Gingivitis is the most common gastrointestinal disorder encountered in mercury poisoning. It is favoured by poor oral hygiene and is accompanied by an unpleasant, metallic or bitter taste in the mouth. Ulceromembranous stomatitis is much less common and is normally found in persons already suffering from gingivitis who have accidentally inhaled mercury vapours. This stomatitis commences with the subjective symptoms of gingivitis with increased salivation (mercurial ptyalism) and coating of the tongue. Eating and drinking produce a burning sensation and discomfort in the mouth, the gums become increasingly inflamed and swollen, ulcers appear and there is spontaneous bleeding. In acute cases, there is high fever, inflammation of the submaxillary ganglions and extremely fetid breath. Alveolodental periostitis has also been observed.
There may be a bluish line on the tooth edge of the gums, in particular in the vicinity of infected areas; this line is, however, never encountered in persons without teeth. Slate-grey punctiform pigmentation of the oral mucosae—the vestibular side of the gums (usually those of the lower jaw), the palate, and even the inside of the cheeks—has also been observed.
Recurrent gingivitis affects the supporting tissues of the teeth, and in many cases the teeth have to be extracted or merely fall out. Other gastrointestinal disorders encountered in mercury poisoning include gastritis and gastroduodenitis.
Non-specific pharyngitis is relatively common. A rarer manifestation is that of Kussmaul’s pharyngitis which presents as a bright-red coloration of the pharynx, tonsils and soft palate with fine arborisation.
Nervous system involvement may occur with or without gastrointestinal symptoms and may evolve in line with two main clinical pictures: (a) fine-intention tremor reminiscent of that encountered in persons suffering from multiple sclerosis; and (b) Parkinsonism with tremor at rest and reduced motor function. Usually one of these two conditions is dominant in the over-all clinical picture which may be further complicated by morbid irritability and pronounced mental hyperactivity (mercurial erethism).
Mercurial Parkinsonism presents a picture of unsteady and staggering gait, absence of balance-recovery reflexes and hypotonia; vegetative symptoms are slight with mask-like facies, sialorrhea, etc. However, Parkinsonism is usually encountered in milder forms, in particular as micro-Parkinsonism.
The most frequently encountered symptoms resemble those presented by persons with multiple sclerosis, except that there is no nystagmus and the two conditions have a different serology and different clinical courses. The most striking feature is tremor which is usually a late symptom but may develop prior to stomatitis.
Tremor usually disappears during sleep, although sudden generalized cramps or contractions may occur; however, it always increases under emotional stress and this is such a characteristic feature that it provides firm grounds for a diagnosis of mercury poisoning. Tremor is particularly pronounced in situations where the patient feels embarrassed or ashamed; often he or she will have to eat in solitude since otherwise he would be incapable of raising food to his lips. In its most acute form, the tremor may invade all the voluntary muscles and be continuous. Cases still occur in which the patient has to be strapped down to prevent him falling out of bed; such cases also present massive, choreiform movements sufficient to wake the patient from his sleep.
The patient tends to utter his words in staccato fashion, so that his sentences are difficult to follow (psellismus mercurialis); when a spasm ceases, the words come out too fast. In cases more reminiscent of parkinsonism, speech is slow and monotonous and the voice may be low or completely absent; spasmodic utterence is, however, more common.
A highly characteristic symptom is a desire for sleep, and the patient often sleeps for long periods although lightly and is frequently disturbed by cramps and spasms. However, insomnia may occur in some cases.
Loss of memory is an early and dementia a terminal symptom. Dermographia and profuse sweating (for no obvious reason) are frequently encountered. In chronic mercury poisoning, the eyes may show the picture of “mercurialentis” characterized by a light-grey to dark, reddish-grey discoloration of the anterior capsule of the crystalline lens due to the deposition of finely divided particles of mercury. Mercurialentis can be detected by examination with a slit-lamp microscope and is bilateral and symmetrical; it usually appears some considerable time before the onset of general signs of mercury poisoning.
Chronic mercury poisoning usually starts insidiously, which makes the early detection of incipient poisoning difficult. The main target organ is the nervous system. Initially, suitable tests can be used to detect psychomotor and neuro-muscular changes and slight tremor. Slight renal involvement (proteinuria, albuminuria, enzymuria) may be detectable earlier than neurological involvement.
If excessive exposure is not corrected, neurological and other manifestations (e.g., tremor, sweating, dermatography) become more pronounced, associated with changes in behaviour and personality disorders and, perhaps, digestive disorders (stomatitis, diarrhoea) and a deterioration in general status (anorexia, weight loss). Once this stage has been reached, termination of exposure may not lead to total recovery.
In chronic mercury poisoning, digestive and nervous symptoms predominate and, although the former are of earlier onset, the latter are more obvious; other significant but less intense symptoms may be present. The duration of the period of mercury absorption preceding the appearance of clinical symptoms depends on the level of absorption and individual factors. The main early signs include slight digestive disorders, in particular, loss of appetite; intermittent tremor, sometimes in specific muscle groups; and neurotic disorders varying in intensity. The course of intoxication may vary considerably from case to case. If exposure is terminated immediately upon the appearance of the first symptoms, full recovery usually occurs; however, if exposure is not terminated and the intoxication becomes firmly established, no more than an alleviation of symptoms can be expected in the majority of cases.
Kidney. There have been studies over the years on the relationships between renal function and urinary mercury levels. The effects of low-level exposures are still not well documented or understood. At higher levels (above 50 μg/g (micrograms per gram) abnormal renal function (as evidenced by N-acetyl-B-D-glucosaminidase (NAG), which is a sensitive indicator of damage to the kidneys) have been observed. The NAG levels were correlated with both the urinary mercury levels and the results of neurological and behavioural testing.
Nervous system. Recent years have seen the development of more data on low levels of mercury, which are discussed in more detail in the chapter Nervous system in this Encyclopaedia.
Blood. Chronic poisoning is accompanied by mild anaemia sometimes preceded by polycythaemia resulting from bone marrow irritation. Lymphocytosis and eosinophilia have also been observed.
Organic Mercury Compounds
Phenylmercuric acetate (PMA). Absorption may occur through inhalation of aerosols containing PMA, through skin absorption or by ingestion. The solubility of the mercurial and the particle size of the aerosols are determining factors for the extent of absorption. PMA is more efficiently absorbed by ingestion than are inorganic mercuric salts. Phenylmercury is transported mainly in blood and distributed in the blood cells (90%), accumulates in the liver and is there decomposed into inorganic mercury. Some phenylmercury is excreted in the bile. The main portion absorbed in the body is distributed in the tissues as inorganic mercury and accumulated in the kidney. On chronic exposure, mercury distribution and excretion follow the pattern seen on exposure to inorganic mercury.
Occupational exposure to phenylmercury compounds occurs in the manufacture and handling of products treated with fungicides containing phenylmercury compounds. Acute inhalation of large amounts may cause lung damage. Exposure of the skin to a concentrated solution of phenylmercury compounds may cause chemical burns with blistering. Sensitization to phenylmercury compounds may occur. Ingestion of large amounts of phenylmercury may cause renal and liver damage. Chronic poisoning gives rise to renal damage due to accumulation of inorganic mercury in the renal tubules.
Available clinical data do not permit extensive conclusions about dose-response relationships. They suggest, however, that phenylmercury compounds are less toxic than inorganic mercury compounds or long-term exposure. There is some evidence of mild adverse effects on the blood.
Alkyl mercury compounds. From a practical point of view, the short-chained alkyl mercury compounds, like methylmercury and ethylmercury, are the most important, although some exotic mercury compounds, generally used in laboratory research, have led to spectacular rapid deaths from acute poisoning. These compounds have been extensively used in seed treatment where they have been responsible for a number of fatalities. Methylmercuric chloride forms white crystals with a characteristic odour, while ethylmercury chloride; (chloroethylmercury) forms white flakes. Volatile methylmercury compounds, like methylmercury chloride, are absorbed to about 80% upon inhalation of vapour. More than 95% of short-chained alkyl mercury compounds is absorbed by ingestion, although the absorption of methylmercury compounds by the skin can be efficient, depending on their solubility and concentration and the condition of the skin.
Transport, distribution and excretion. Methylmercury is transported in the red blood cells ( 95%), and a small fraction is bound to plasma proteins. The distribution to the different tissues of the body is rather slow and it takes about four days before equilibrium is obtained. Methylmercury is concentrated in the central nervous system and especially in grey matter. About 10% of the body burden of mercury is found in the brain. The highest concentration is found in the occipital cortex and the cerebellum. In pregnant women methylmercury is transferred in the placenta to the foetus and especially accumulated in the foetal brain.
Hazards of organic mercury
Poisoning by alkyl mercury may occur on inhalation of vapour and dust containing alkyl mercury and in the manufacture of the mercurial or in handling the final material. Skin contact with concentrated solutions results in chemical burns and blistering. In small agricultural operations there is a risk of exchange between treated seed and products intended for food, followed by involuntary intake of large amounts of alkyl mercury. On acute exposure the signs and symptoms of poisoning have an insidious onset and appear with a latency period which may vary from one to several weeks. The latency period is dependent on the size of the dose—the larger the dose, the shorter the period.
On chronic exposure the onset is more insidious, but the symptoms and signs are essentially the same, due to the accumulation of mercury in the central nervous system, causing neuron damage in the sensory cortex, such as visual cortex, auditory cortex and the pre- and post-central areas. The signs are characterized by sensory disturbances with paresthaesia in the distal extremities, in the tongue and around the lips. With more severe intoxications ataxia, concentric constrictions of the visual fields, impairment of hearing and extrapyramidal symptoms may appear. In severe cases chronic seizures occur.
The period in life most sensitive to methylmercury poisoning is the time in utero; the foetus seems to be between 2 and 5 times more sensitive than the adult. Exposure in utero results in cerebral palsy, partly due to inhibition of the migration of neurons from central parts to the peripheral cortical areas. In less severe cases retardation in the psychomotor development has been observed.
Alkoxyalkyl mercury compounds. The most common alkoxyalkyl compounds used are methoxyethyl mercury salts (e.g., methoxyethylmercury acetate), which have replaced the short-chain alkyl compounds in seed treatment in many industrial countries, in which the alkyl compounds have been banned due to their hazardousness.
The available information is very limited. Alkoxyalkyl compounds are absorbed by inhalation and by ingestion more efficiently than inorganic mercury salts. The distribution and excretion patterns of absorbed mercury follow those of inorganic mercury salts. Excretion occurs through the intestinal tract and the kidney. To what extent unchanged alkoxyalkyl mercury is excreted in humans is unknown. Exposure to alkoxyalkyl mercury compounds can occur in the manufacture of the compound and in handling the final product(s) treated with the mercurial. Methoxyethyl mercury acetate is a vesicant when applied in concentrated solutions to the skin. Inhalation of methoxyethyl mercury salt dust may cause lung damage, and chronic poisoning due to long-term exposure may give rise to renal damage.
Safety and Health Measures
Efforts should be made to replace mercury with less hazardous substances. For example, the felt industry may employ non-mercurial compounds. In mining, wet drilling techniques should be used. Ventilation is the main safety measure and if it is inadequate, the workers should be provided with respiratory protective equipment.
In industry, wherever possible, mercury should be handled in hermetically sealed systems and extremely strict hygiene rules should be applied at the workplace. When mercury is spilt, it very easily infiltrates into crevices, gaps in the floor and workbenches. Due to its vapour pressure, a high atmospheric concentration may occur even following seemingly negligible contamination. It is therefore important to avoid the slightest soiling of work surfaces; these should be smooth, non-absorbent and slightly tilted towards a collector or, failing this, have a metal grill over a gutter filled with water to collect any drops of spilt mercury which fall through the grill. Working surfaces should be cleaned regularly and, in the event of accidental contamination, any drops of mercury collected in a water trap should be drawn off as rapidly as possible.
Where there is a danger of mercury volatilizing, local exhaust ventilation (LEV) systems should be installed. Admittedly, this is a solution which is not always applicable, as is the case in premises producing chlorine by the mercury cell process, in view of the enormous vaporization surface.
Work posts should be planned in such a way as to minimize the number of persons exposed to mercury.
Most exposure to organic mercury compounds involves mixed exposure to mercury vapour and the organic compound, as the organic mercury compounds decompose and release mercury vapour. All technical measures pertaining to exposure to mercury vapour should be applied for exposure to organic mercury compounds. Thus, contamination of clothes and/or parts of the body should be avoided, as it may be a dangerous source of mercury vapour close to the breathing zone. Special protective work clothes should be used and changed after the workshift. Spray painting with paint containing mercurials requires respiratory protective equipment and adequate ventilation. The short-chained alkyl mercury compounds should be eliminated and replaced whenever possible. If handling cannot be avoided, an enclosed system should be used, combined with adequate ventilation, to limit exposure to a minimum.
Great care must be exercised in preventing the contamination of water sources with mercury effluent since the mercury can be incorporated into the food chain, leading to disasters such as that which occurred in Minamata, Japan.
Occurrence and Uses
Manganese (Mn) is one of the most abundant elements in the earth’s crust. It is found in soils, sediments, rocks, water and biological materials. At least a hundred minerals contain manganese. Oxides, carbonates and silicates are the most important among manganese-containing minerals. Manganese can exist in eight oxidation states, the most important being +2, +3, and +7. Manganese dioxide (MnO2) is the most stable oxide. Manganese forms various organometallic compounds. Of major practical interest is methylcyclopentadienyl manganese tricarbonyl CH3C5H4Mn(CO)3, often referred to as MMT.
The most important commercial source of manganese is manganese dioxide (MnO2), which is found naturally in sedimentary deposits as pyrolusite. Two other types of deposit can be distinguished: carbonate accumulations, which are usually composed mainly of rhodocrosite (MnCO3), and stratiform deposits. However, only the sedimentary deposits are significant, and those are usually worked by opencast techniques. Sometimes underground mining is necessary, and room and pillar extraction is carried out; seldom is there any call for the techniques used in deep metal mining.
Manganese is used in the production of steel as a reagent to reduce oxygen and sulphur and as an alloying agent for special steels, aluminium and copper. It is used in the chemical industry as an oxidizing agent and for the production of potassium permanganate and other manganese chemicals. Manganese is used for electrode coating in welding rods and for rock crushers, railway points and crossings. It also finds use in the ceramics, match, glass and dyestuff industries.
Several manganese salts are used in fertilizers and as driers for linseed oil. They are also utilized for glass and textile bleaching and for leather tanning. MMT has been used as a fuel-oil additive, a smoke inhibitor, and as an antiknock gasoline additive.
Absorption, distribution and excretion
In occupational situations manganese is primarily absorbed by inhalation. Manganese dioxide and other manganese compounds which occur as volatile by-products of metal refining are practically insoluble in water. Thus, only particles small enough to reach the alveoli are eventually absorbed into the blood. Large inhaled particles may be cleared from the respiratory tract and swallowed. Manganese may also enter the gastrointestinal tract with contaminated food and water. The rate of absorption can be influenced by a dietary level of manganese and iron, the type of manganese compound, iron deficiency and age. However, the risk of intoxication by this route is not great. Absorption of manganese through the skin is negligible.
After inhalation, or after parenteral and oral exposure, the absorbed manganese is rapidly eliminated from the blood and distributed mainly to the liver. The kinetic patterns for blood clearance and liver uptake of manganese are similar, indicating that these two manganese pools rapidly enter equilibrium. Excess metal may be distributed to other tissues such as kidneys, small intestine, endocrine glands and bones. Manganese preferentially accumulates in tissues rich in mitochondria. It also penetrates the blood-brain barrier and the placenta. Higher concentrations of manganese are also associated with pigmented portions of the body, including the retina, pigmented conjunctiva and dark skin. Dark hair also accumulates manganese. It is estimated that the total body burden for manganese is between 10 and 20 mg for a 70 kg male. The biological half-life for manganese is between 36 and 41 days, but for manganese sequestered in the brain, the half-life is considerably longer. In the blood, manganese is bound to proteins.
The organic compound MMT is rapidly metabolized in the body. The distribution seems to be similar to that seen after exposure to inorganic manganese.
Bile flow is the main route of excretion of manganese. Consequently, it is eliminated almost entirely with faeces, and only 0.1 to 1.3% of daily intake with urine. It seems that biliary excretion is the main regulatory mechanism in the homeostatic control of manganese in the body, accounting for a relative stability of manganese content in tissues. After exposure to the organic compound MMT, excretion of manganese goes to a large extent with urine. This has been explained as a result of biotransformation of the organic compound in the kidney. As a metalloprotein compound of some enzymes, manganese is an essential element for humans.
Intoxication by manganese is reported in mining and processing of manganese ores, in the production of manganese alloys, dry-cell batteries, welding electrodes, varnishes and ceramic tiles. Mining of ore can still present important occupational hazards, and the ferromanganese industry is the next most important source of risk. The operations that produce the highest concentrations of manganese dioxide dust are those of drilling and shotfiring. Consequently, the most dangerous job is high-speed drilling.
Considering the dependence of deposition sites and solubility rate of particle size, the dangerous effect of exposure is closely related to the particle size composition of manganese aerosol. There is also evidence that aerosols formed by condensation may be more harmful than those formed by disintegration, which can be connected again with the difference in particle size distribution. The toxicity of different manganese compounds appears to depend on the type of manganese ion present and on the oxidation state of manganese. The less oxidized the compound, the higher the toxicity.
Chronic manganese poisoning (manganism)
Chronic manganese poisoning can take either a nervous or pulmonary form. If the nervous system is attacked, three phases can be distinguished. During the initial period, diagnosis may be difficult. Early diagnosis, however, is critical because cessation of exposure appears to be effective in arresting the course of the disease. Symptoms include indifference and apathy, sleepiness, loss of appetite, headache, dizziness and asthenia. There may be bouts of excitablity, difficulty in walking and coordination, and cramps and pains in the back. These symptoms can be present in varying degrees and appear either together or in isolation. They mark the onset of the disease.
The intermediate stage is marked by the appearance of objective symptoms. First the voice become monotonous and sinks to a whisper, and speech is slow and irregular, perhaps with a stammer. There is fixed and hilarious or dazed and vacant facies, which may be attributable to an increase in the tonus of the facial muscles. The patient may abruptly burst into laughter or (more rarely) into tears. Although the faculties are much decayed, the victim appears to be in a perpetual state of euphoria. Gestures are slow and awkward, gait is normal but there may be a waving movement of the arms. The patient is unable to run and can walk backwards only with difficulty, sometimes with retropulsion. Inability to perform rapid alternating movements (adiadochokinesia) may develop, but neurological examination displays no changes except, in certain cases, exaggeration of the patellar reflexes.
Within a few months, the patient’s condition deteriorates noticeably and the various disorders, especially those affecting the gait, grow steadily more pronounced. The earliest and most obvious symptom during this phase is muscular rigidity, constant but varying in degree, which results in a very characteristic gait (slow, spasmodic and unsteady), the patient putting his or her weight on the metatarsus and producing a movement variously described as “cock-walk” or “hen’s gait”. The victim is totally incapable of walking backwards and, should he or she try to do so, falls; balance can hardly be preserved, even when trying to stand with both feet together. A sufferer can turn round only slowly. There may be tremor, frequently in the lower limbs, even generalized.
The tendinous reflexes, rarely normal, become exaggerated. Sometimes there are vasomotor disorders with sudden sweating, pallor or blushing; on occasion there is cyanosis of the extremities. The sensory functions remain intact. The patient’s mind may work only slowly; writing becomes irregular, some words being illegible. There may be changes in the pulse rate. This is the stage at which the disease becomes progressive and irreversible.
Pulmonary form. Reports of “manganese pneumoconiosis” have been contested in view of the high silica content of the rock at the site of exposure; manganese pneumonia has also been described. There is also controversy over the correlation between pneumonia and manganese exposure unless manganese acts as an aggravating factor. In view of its epidemic character and severity, the disease may be a non-typical viral pneumopathy. These manganic pneumonias respond well to antibiotics.
Pathology. Some authors maintain that there are widespread lesions to the corpus striatum, then to the cerebral cortex, the hippocampus and corpora quadrigemina (in the posterior corpora). However, others are of the opinion that the lesions to the frontal lobes provide a better explanation for all the symptoms observed than do those observed in the basal ganglia; this would be confirmed by electroencephalography. The lesions are always bilateral and more or less symmetrical.
Course. Manganese poisoning ultimately becomes chronic. However, if the disease is diagnosed while still at the early stages and the patient is removed from exposure, the course may be reversed. Once well established, it becomes progressive and irreversible, even when exposure is terminated. The nervous disorders show no tendency to regress and may be followed by deformation of the joints. Although the severity of certain symptoms may be reduced, gait remains permanently affected. The patient’s general condition remains good, and he or she may live a long time, eventually dying from an intercurrent ailment.
Diagnosis. This is based primarily on the patient’s personal and occupational history (job, length of exposure and so on). However, the subjective nature of the initial symptoms makes early diagnosis difficult; consequently, at this stage, questioning must be supplemented by information supplied by friends, colleagues and relatives. During the intermediate and full-blown stages of the intoxication, occupational history and objective symptoms facilitate diagnosis; laboratory examinations can provide information for supplementing the diagnosis.
Haematological changes are variable; on the one hand, there may be no changes at all, whereas, on the other, there may be leucopenia, lymphocytosis and inversion of leucocyte formula in 50% of cases, or increase in haemoglobin count (considered as the first sign of poisoning) and slight polycythaemia.
There is diminished urinary excretion of 17-ketosteroids, and it may be assumed that the adrenal function is affected. Albumin level in the cerebrospinal fluid is increased, often to a marked degree (40 to 55 and even 75 mg per cent). Digestive and hepatic symptoms are non-indicative; there is no sign of hepatomegalia or splenomegalia; however, accumulation of manganese in the liver may result in metabolic lesions which seem to be related to the patient’s endocrinological condition and may be influenced by the existence of neurological lesions.
Differential diagnosis. There may be difficulty in distinguishing between manganese poisoning and the following diseases: nerve syphilis, Parkinson’s disease, disseminated sclerosis, Wilson’s disease, hepatic cirrhosis and Westphal-Strümpell’s disease (pseudo-sclerosis).
Safety and Health Measures
The prevention of manganese poisoning is primarily a question of suppression of manganese dusts and fumes. In mines, dry drilling should always be replaced by wet drilling. Shotfiring should be carried out after the shift so that the heading can be well ventilated before the next shift starts up. Good general ventilation at source is also essential. Airline respiratory protection equipment as well as independent respirators have to be used in specific situations to avoid excessive short-term exposures.
A high standard of personal hygiene is essential, and personal cleanliness and adequate sanitary facilities, clothing and time must be provided so that compulsory showering after work, a change of clothes and a ban on eating at the workplace can be effected. Smoking at work should be prohibited as well.
Periodic measurements of exposure levels should be performed, and attention should be given to the size distribution of airborne manganese. Contamination of drinking water and food as well as workers’ dietary habits ought to be considered as a potential additional source of exposure.
It is inadvisable for workers with psychological or neurological disorders to be employed in work associated with exposure to manganese. Nutritional deficiency states may predispose to anaemia and thus increase susceptibility to manganese. Therefore workers suffering from such deficiencies have to be kept under strict surveillance. During the anaemic state, subjects should avoid exposure to manganese. The same relates to those suffering from lesions of the excretory organs, or from chronic obstructive lung disease. A study has suggested that long-term manganese exposure may contribute to the development of chronic obstructive lung disease, particularly if the exposure is combined with smoking. On the other hand impaired lungs may be more susceptible to the potential acute effect of manganese aerosols.
During the periodic medical examinations the worker should be screened for symptoms which might be connected with the subclinical stage of manganese poisoning. In addition, the worker should be examined clinically, particularly with a view to detecting early psychomotor changes and neurological signs. Subjective symptoms and abnormal behaviour may often constitute the only early indications of health impairment. Manganese can be measured in blood, urine, stools and hair. Estimation of the extent of manganese exposure by means of manganese concentration in urine and blood did not prove to be of great value.
The average manganese blood level in exposed workers seems to be of the same order as that in non-exposed persons. Contamination during sampling and analytical procedures may at least partly explain a rather wide range found in literature particularly for blood. The use of heparin as an anticoagulant is still quite common although the manganese content in heparin may exceed that in blood. The mean concentration of manganese in urine of non-exposed people is usually estimated to be between 1 and 8 mg/l, but values up to 21 mg/l have been reported. Daily manganese intake from human diets varies greatly with the amount of unrefined cereals, nuts, leafy vegetables and tea consumed, owing to their relatively high content of manganese, and thus affects the results of normal manganese content in biological media.
A manganese concentration of 60 mg/kg of faeces and higher has been suggested as indicative of occupational exposure to manganese. Manganese content in hair is normally below 4 mg/kg. As the determination of manganese in urine, which is often used in practice, has not yet been validated enough for assessment of individual exposure, it can be used only as a group indicator of the mean level of exposure. Collection of the stool and the analysis of manganese content is not easy to perform. Our present knowledge does not include any other reliable biological parameter which might be used as an indicator of individual exposure to manganese. Thus the assessment of workers’ exposure to manganese still has to rely on manganese air levels. There is also very little reliable information about the correlation between the manganese content in the blood and urine and the findings of neurological symptoms and signs.
Persons with the signs of manganese intoxication should be removed from exposure. If the worker is removed from exposure shortly after the onset of symptoms and signs (before the fully developed stage of manganism) many of the symptoms and signs will disappear. There may be some residual disturbances, however, particularly in speech and gait.
Magnesium (Mg) is the lightest structural metal known. It is 40% lighter than aluminium. Metallic magnesium can be rolled and drawn when heated between 300 and 475 ºC, but is brittle below this temperature and is apt to burn if heated much above it. It is soluble in, and forms compounds with, a number of acids, but is not affected by hydrofluoric or chromic acids. Unlike aluminium, it is resistant to alkali corrosion.
Occurrence and Uses
Magnesium does not exist in a pure state in nature, but is generally found in one of the following forms: dolomite (CaCO3·MgCO3), magnesite (MgCO3), brucite (Mg(OH)2), periclase (MgO), carnallite (KClMgCl2·6H2O) or kieserite (MgSO4·H2O). In addition, it is found as a silicate in asbestos and talc. Magnesium is so widely distributed over the earth that facilities for processing and transporting the ore are often the determining factors in selecting a site for mining.
Magnesium is used, mainly in alloy form, for components of aircraft, ships, automobiles, machinery and hand tools for which both lightness and strength are required. It is used in the manufacture of precision instruments and optical mirrors, and in the recovery of titanium. Magnesium is also extensively used in military equipment. Because it burns with such intense light, magnesium is widely used in pyrotechnics, signal flares, incendiary and tracer bullets, and in flash bulbs.
Magnesium oxide has a high melting point (2,500 ºC) and is often incorporated into the linings of refractories. It is also a component of animal feeds, fertilizers, insulation, wallboard, petroleum additives and electrical heating rods. Magnesium oxide is useful in the pulp and paper industry. In addition, it serves as an accelerator in the rubber industry and as a reflector in optical instruments.
Other important compounds include magnesium chloride, magnesium hydroxide, magnesium nitrate and magnesium sulphate. Magnesium chloride is a component of fire extinguishers and ceramics. It is also an agent in fireproofing wood and textile and paper manufacture. Magnesium chloride is a chemical intermediate for magnesium oxychloride, which is used for cement. A mixture of magnesium oxide and magnesium chloride forms a paste which is useful for floors. Magnesium hydroxide is useful for the neutralization of acids in the chemical industry. It is also used in uranium processing and in sugar refining. Magnesium hydroxide serves as a residual fuel-oil additive and an ingredient in toothpaste and antacid stomach powder. Magnesium nitrate is used in pyrotechnics and as a catalyst in the manufacture of petrochemicals. Magnesium sulphate has numerous functions in the textile industry, including weighting cotton and silk, fireproofing fabrics, and dyeing and printing calicos. It also finds use in fertilizers, explosives, matches, mineral water, ceramics and cosmetic lotions, and in the manufacture of mother-of-pearl and frosted papers. Magnesium sulphate increases the bleaching action of chlorinated lime and acts as a water-correcting agent in the brewing industry and a cathartic and analgesic in medicine.
Alloys. When magnesium is alloyed with other metals, such as manganese, aluminium and zinc, it improves their toughness and resistance to strain. In combination with lithium, cerium, thorium and zirconium, alloys are produced which have an enhanced strength-to-weight ratio, along with considerable heat-resisting properties. This renders them invaluable in the aircraft and aerospace industries for the construction of jet engines, rocket launchers and space vehicles. A large number of alloys, all containing over 85% magnesium, are known under the general name of Dow metal.
Biological roles. As an essential ingredient of chlorophyll, the magnesium requirements of the human body are largely supplied by the consumption of green vegetables. The average human body contains about 25 g of magnesium. It is the fourth most abundant cation in the body, after calcium, sodium and potassium. The oxidation of foods releases energy, which is stored in the high-energy phosphate bonds. It is believed that this process of oxidative phosphorylation is carried out in the mitochondria of the cells and that magnesium is necessary for this reaction.
Experimentally produced magnesium deficiency in rats leads to a dilation of the peripheral blood vessels and later to hyperexcitability and convulsions. Tetany similar to that associated with hypocalcaemia occurred in calves fed only milk. Older animals with magnesium deficiency developed “grass staggers”, a condition which appears to be associated with malabsorption rather than with a lack of magnesium in the fodder.
Cases of magnesium tetany resembling those caused by calcium deficiency have been described in humans. In the reported cases, however, a “conditioning factor”, such as an excessive vomiting or fluid loss, has been present, in addition to inadequate dietary intake. Since this tetany clinically resembles that caused by calcium deficiency, a diagnosis can be made only by determining the blood levels of calcium and magnesium. Normal blood levels range from 1.8 to 3 mg per 100 cm3, and it has been found that persons tend to become comatose when the blood concentration approaches 17 mg per cent. “Aeroform tumours” due to the evolution of hydrogen have been produced in animals by introducing finely divided magnesium into the tissues.
Toxicity. Magnesium and alloys containing 85% of the metal may be considered together in their toxicological properties. In industry, their toxicity is regarded as low. The most frequently used compounds, magnesite and dolomite, may irritate the respiratory tract. However, the fumes of magnesium oxide, as those of certain other metals, can cause metal fume fever. Some investigators have reported a higher incidence of digestive disorders in magnesium plant workers and suggest that a relationship may exist between magnesium absorption and gastroduodenal ulcers. In foundry-casting magnesium or high-magnesium alloys, fluoride fluxes and sulphur-containing inhibitors are used in order to separate the molten metal from the air with a layer of sulphur dioxide. This prevents burning during the casting operations, but the fumes of fluorides or of sulphur dioxide could present a greater hazard.
The greatest danger in handling magnesium is that of fire. Small fragments of the metal, such as would result from grinding, polishing or machining, can readily be ignited by a chance spark or flame, and as they burn at a temperature of 1,250ºC, these fragments can cause deep destructive lesions of the skin. Accidents of this type have occurred when a tool was sharpened on a wheel which was previously used to grind magnesium alloy castings. In addition, magnesium reacts with water and acids, forming combustible hydrogen gas.
Slivers of magnesium penetrating the skin or entering deep wounds could cause “aeroform tumours” of the type already mentioned. This would be rather exceptional; however, wounds contaminated with magnesium are very slow to heal. Fine dust from the buffing of magnesium could be irritating to the eyes and respiratory passages, but it is not specifically toxic.
Safety and Health Measures
As with any potentially hazardous industrial process, constant care is needed in handling and working magnesium. Those engaged in casting the metal should wear aprons and hand protection made of leather or some other suitable material to protect them against the “spatter” of small particles. Transparent face shields should also be worn as face protection, especially for the eyes. Where workers are exposed to magnesium dust, contact lenses should not be worn and eyewash facilities should be immediately available. Workers machining or buffing the metal should wear overalls to which small fragments of the metal will not adhere. Sufficient local exhaust ventilation is also essential in areas where magnesium oxide fumes may develop, in addition to good general ventilation. Cutting tools should be sharp, as blunt ones may heat the metal to the point of ignition.
Buildings in which magnesium is cast or machined should be constructed, if possible, of non-flammable materials and without ledges or protuberances on which magnesium dust might accumulate. The accumulation of shavings and “swarf” should be prevented, preferably by wet sweeping. Until final disposal, the scrapings should be collected in small containers and placed apart at safe intervals. The safest method for disposal of magnesium waste is probably wetting and burying.
Since the accidental ignition of magnesium presents a serious fire hazard, fire training and adequate firefighting facilities are essential. Workers should be trained never to use water in fighting such a blaze, because this merely scatters the burning fragments, and may spread the fire. Among the materials which have been suggested for the control of such fires are carbon and sand. Commercially prepared firefighting dusts are also available, one of which consists of powdered polyethylene and sodium borate.
Adapted from ATSDR 1995.
Occurrence and Uses
Lead ores are found in many parts of the world. The richest ore is galena (lead sulphide) and this is the main commercial source of lead. Other lead ores include cerussite (carbonate), anglesite (sulphate), corcoite (chromate), wulfenite (molybdate), pyromorphite (phosphate), mutlockite (chloride) and vanadinite (vanadate). In many cases the lead ores may also contain other toxic metals.
Lead minerals are separated from gangue and other materials in the ore by dry crushing, wet grinding (to produce a slurry), gravity classification and flotation. The liberated lead minerals are smelted by a three-stage process of charge preparation (blending, conditioning, etc.), blast sintering and blast furnace reduction. The blast-furnace bullion is then refined by the removal of copper, tin, arsenic, antimony, zinc, silver and bismuth.
Metallic lead is used in the form of sheeting or pipes where pliability and resistance to corrosion are required, such as in chemical plants and the building industry; it is used also for cable sheathing, as an ingredient in solder and as a filler in the automobile industry. It is a valuable shielding material for ionizing radiations. It is used for metallizing to provide protective coatings, in the manufacture of storage batteries and as a heat treatment bath in wire drawing. Lead is present in a variety of alloys and its compounds are prepared and used in large quantities in many industries.
About 40% of lead is used as a metal, 25% in alloys and 35% in chemical compounds. Lead oxides are used in the plates of electric batteries and accumulators (PbO and Pb3O4), as compounding agents in rubber manufacture (PbO), as paint ingredients (Pb3O4) and as constituents of glazes, enamels and glass.
Lead salts form the basis of many paints and pigments; lead carbonate and lead sulphate are used as white pigments and the lead chromates provide chrome yellow, chrome orange, chrome red and chrome green. Lead arsenate is an insecticide, lead sulphate is used in rubber compounding, lead acetate has important uses in the chemical industry, lead naphthenate is an extensively used dryer and tetraethyllead is an antiknock additive for gasoline, where still permitted by law.
Lead alloys. Other metals such as antimony, arsenic, tin and bismuth may be added to lead to improve its mechanical or chemical properties, and lead itself may be added to alloys such as brass, bronze and steel to obtain certain desirable characteristics.
Inorganic lead compounds. Space is not available to describe the very large number of organic and inorganic lead compounds encountered in industry. However, the common inorganic compounds include lead monoxide (PbO), lead dioxide (PbO2), lead tetroxide (Pb3O4), lead sesquioxide (Pb2O3), lead carbonate, lead sulphate, lead chromates, lead arsenate, lead chloride, lead silicate and lead azide.
The maximum concentration of the organic (alkyl) lead compounds in gasolines is subject to legal prescriptions in many countries, and to limitation by the manufacturers with governmental concurrence in others. Many jurisdictions have simply banned its use.
The prime hazard of lead is its toxicity. Clinical lead poisoning has always been one of the most important occupational diseases. Medico-technical prevention has resulted in a considerable decrease in reported cases and also in less serious clinical manifestations. However, it is now evident that adverse effects occur at exposure levels hitherto regarded as acceptable.
Industrial consumption of lead is increasing and traditional consumers are being supplemented by new users such as the plastics industry. Hazardous exposure to lead, therefore, occurs in many occupations.
In lead mining, a considerable proportion of lead absorption occurs through the alimentary tract and consequently the extent of the hazard in this industry depends, to some extent, on the solubility of ores being worked. The lead sulphide (PbS) in galena is insoluble and absorption from the lung is limited; however, in the stomach, some lead sulphide may be converted to slightly soluble lead chloride which may then be absorbed in moderate quantities.
In lead smelting, the main hazards are the lead dust produced during crushing and dry grinding operations, and lead fumes and lead oxide encountered in sintering, blast-furnace reduction and refining.
Lead sheet and pipe are used principally for the constructon of equipment for storing and handling sulphuric acid. The use of lead for water and town gas pipes is limited nowadays. The hazards of working with lead increase with temperature. If lead is worked at temperatures below 500 °C, as in soldering, the risk of fume exposure is far less than in lead welding, where higher flame temperatures are used and the danger is higher. The spray coating of metals with molten lead is dangerous since it gives rise to dust and fumes at high temperatures.
The demolition of steel structures such as bridges and ships that have been painted with lead-based paints frequently gives rise to cases of lead poisoning. When metallic lead is heated to 550 °C, lead vapour will be evolved and will become oxidized. This is a condition that is liable to be present in metal refining, the melting of bronze and brass, the spraying of metallic lead, lead burning, chemical plant plumbing, ship breaking and the burning, cutting and welding of steel structures coated with paints containing lead tetroxide.
Routes of entry
The main route of entry in industry is the respiratory tract. A certain amount may be absorbed in the air passages, but the main portion is taken up by the pulmonary bloodstream. The degree of absorption depends on the proportion of the dust accounted for by particles less than 5 microns in size and the exposed worker’s respiratory minute volume. Increased workload therefore results in higher lead absorption. Although the respiratory tract is the main route of entry, poor work hygiene, smoking during work (pollution of tobacco, polluted fingers while smoking) and poor personal hygiene may considerably increase total exposure mainly by the oral route. This is one of the reasons why the correlation between the concentration of lead in workroom air and lead in blood levels often is very poor, certainly on an individual basis.
Another important factor is the level of energy expenditure: the product of concentration in air and of respiratory minute volume determines lead uptake. The effect of working overtime is to increase exposure time and reduce recovery time. Total exposure time is also much more complicated than official personnel records indicate. Only time analysis in the workplace can yield relevant data. The worker may move around the department or the factory; a job with frequent changes in posture (e.g., turning and bending) results in exposure to a great range of concentrations. A representative measure of lead intake is almost impossible to obtain without the use of a personal sampler applied for many hours and for many days.
Particle size. Since the most important route of lead absorption is by the lungs, the particle size of industrial lead dust is of considerable significance and this depends on the nature of the operation giving rise to the dust. Fine dust of respirable particle size is produced by processes such as the pulverizing and blending of lead colours, the abrasive working of lead-based fillers in automobile bodies and the dry rubbing-down of lead paint. The exhaust gases of gasoline engines yield lead chloride and lead bromide particles of 1 micron diameter. The larger particles, however, may be ingested and be absorbed via the stomach. A more informative picture of the hazard associated with a sample of lead dust might be given by including a size distribution as well as a total lead determination. But this information is probably more important for the research investigator than for the field hygienist.
In the human body, inorganic lead is not metabolized but is directly absorbed, distributed and excreted. The rate at which lead is absorbed depends on its chemical and physical form and on the physiological characteristics of the exposed person (e.g., nutritional status and age). Inhaled lead deposited in the lower respiratory tract is completely absorbed. The amount of lead absorbed from the gastrointestinal tract of adults is typically 10 to 15% of the ingested quantity; for pregnant women and children, the amount absorbed can increase to as much as 50%. The quantity absorbed increases significantly under fasting conditions and with iron or calcium deficiency.
Once in the blood, lead is distributed primarily among three compartments—blood, soft tissue (kidney, bone marrow, liver, and brain), and mineralizing tissue (bones and teeth). Mineralizing tissue contains about 95% of the total body burden of lead in adults.
The lead in mineralizing tissues accumulates in subcompartments that differ in the rate at which lead is resorbed. In bone, there is both a labile component, which readily exchanges lead with the blood, and an inert pool. The lead in the inert pool poses a special risk because it is a potential endogenous source of lead. When the body is under physiological stress such as pregnancy, lactation or chronic disease, this normally inert lead can be mobilized, increasing the lead level in blood. Because of these mobile lead stores, significant drops in a person’s blood lead level can take several months or sometimes years, even after complete removal from the source of lead exposure.
Of the lead in the blood, 99% is associated with erythrocytes; the remaining 1% is in the plasma, where it is available for transport to the tissues. The blood lead not retained is either excreted by the kidneys or through biliary clearance into the gastrointestinal tract. In single-exposure studies with adults, lead has a half-life, in blood, of approximately 25 days; in soft tissue, about 40 days; and in the non-labile portion of bone, more than 25 years. Consequently, after a single exposure a person’s blood lead level may begin to return to normal; the total body burden, however, may still be elevated.
For lead poisoning to develop, major acute exposures to lead need not occur. The body accumulates this metal over a lifetime and releases it slowly, so even small doses, over time, can cause lead poisoning. It is the total body burden of lead that is related to the risk of adverse effects.
Whether lead enters the body through inhalation or ingestion, the biologic effects are the same; there is interference with normal cell function and with a number of physiological processes.
Neurological effects. The most sensitive target of lead poisoning is the nervous system. In children, neurological deficits have been documented at exposure levels once thought to cause no harmful effects. In addition to the lack of a precise threshold, childhood lead toxicity may have permanent effects. One study showed that damage to the central nervous system (CNS) that occurred as a result of lead exposure at age 2 resulted in continued deficits in neurological development, such as lower IQ scores and cognitive deficits, at age 5. In another study that measured total body burden, primary school children with high tooth lead levels but with no known history of lead poisoning had larger deficits in psychometric intelligence scores, speech and language processing, attention and classroom performance than children with lower levels of lead. A 1990 follow-up report of children with elevated lead levels in their teeth noted a sevenfold increase in the odds of failure to graduate from high school, lower class standing, greater absenteeism, more reading disabilities and deficits in vocabulary, fine motor skills, reaction time and hand-eye coordination 11 years later. The reported effects are more likely caused by the enduring toxicity of lead than by recent excessive exposures because the blood lead levels found in the young adults were low (less than 10 micrograms per deciliter (μg/dL)).
Hearing acuity, particularly at higher frequencies, has been found to decrease with increasing blood lead levels. Hearing loss may contribute to the apparent learning disabilities or poor classroom behavior exhibited by children with lead intoxication.
Adults also experience CNS effects at relatively low blood lead levels, manifested by subtle behavioural changes, fatigue and impaired concentration. Peripheral nervous system damage, primarily motor, is seen mainly in adults. Peripheral neuropathy with mild slowing of nerve conduction velocity has been reported in asymptomatic lead workers. Lead neuropathy is believed to be a motor neuron, anterior horn cell disease with peripheral dying-back of the axons. Frank wrist drop occurs only as a late sign of lead intoxication.
Haematological effects. Lead inhibits the body’s ability to make hemoglobin by interfering with several enzymatic steps in the heme pathway. Ferrochelatase, which catalyzes the insertion of iron into protoporphyrin IX, is quite sensitive to lead. A decrease in the activity of this enzyme results in an increase of the substrate, erythrocyte protoporphyrin (EP), in the red blood cells. Recent data indicate that the EP level, which has been used to screen for lead toxicity in the past, is not sufficiently sensitive at lower levels of blood lead and is therefore not as useful a screening test for lead poisoning as previously thought.
Lead can induce two types of anaemia. Acute high-level lead poisoning has been associated with hemolytic anaemia. In chronic lead poisoning, lead induces anemia by both interfering with erythropoiesis and by diminishing red blood cell survival. It should be emphasized, however, that anemia is not an early manifestation of lead poisoning and is evident only when the blood lead level is significantly elevated for prolonged periods.
Endocrine effects. A strong inverse correlation exists between blood lead levels and levels of vitamin D. Because the vitamin D-endocrine system is responsible in large part for the maintenance of extra- and intra-cellular calcium homeostasis, it is likely that lead impairs cell growth and maturation and tooth and bone development.
Renal effects. A direct effect on the kidney of long-term lead exposure is nephropathy. Impairment of proximal tubular function manifests in aminoaciduria, glycosuria and hyperphosphaturia (a Fanconi-like syndrome). There is also evidence of an association between lead exposure and hypertension, an effect that may be mediated through renal mechanisms. Gout may develop as a result of lead-induced hyperuricemia, with selective decreases in the fractional excretion of uric acid before a decline in creatinine clearance. Renal failure accounts for 10% of deaths in patients with gout.
Reproductive and developmental effects. Maternal lead stores readily cross the placenta, placing the foetus at risk. An increased frequency of miscarriages and stillbirths among women working in the lead trades was reported as early as the end of the 19th century. Although the data concerning exposure levels are incomplete, these effects were probably a result of far greater exposures than are currently found in lead industries. Reliable dose-effect data for reproductive effects in women are still lacking today.
Increasing evidence indicates that lead not only affects the viability of the foetus, but development as well. Developmental consequences of prenatal exposure to low levels of lead include reduced birth weight and premature birth. Lead is an animal teratogen; however, most studies in humans have failed to show a relationship between lead levels and congenital malformations.
The effects of lead on the male reproductive system in humans have not been well characterized. The available data support a tentative conclusion that testicular effects, including reduced sperm counts and motility, may result from chronic exposure to lead.
Carcinogenic effects. Inorganic lead and inorganic lead compounds have been classified as Group 2B, possible human carcinogens, by the International Agency for Research on Cancer (IARC). Case reports have implicated lead as a potential renal carcinogen in humans, but the association remains uncertain. Soluble salts, such as lead acetate and lead phosphate, have been reported to cause kidney tumors in rats.
Continuum of signs and symptoms associated with lead toxicity
Mild toxicity associated with lead exposure includes the following:
The signs and symptoms associated with moderate toxicity include:
The signs and symptoms of severe toxicity include:
Some of the haematological signs of lead poisoning mimic other diseases or conditions. In the differential diagnosis of microcytic anaemia, lead poisoning can usually be ruled out by obtaining a venous blood lead concentration; if the blood lead level is less than 25 μg/dL, the anaemia usually reflects iron deficiency or haemoglobinopathy. Two rare diseases, acute intermittent porphyria and coproporphyria, also result in haeme abnormalities similar to those of lead poisoning.
Other effects of lead poisoning can be misleading. Patients exhibiting neurological signs due to lead poisoning have been treated only for peripheral neuropathy or carpal tunnel syndrome, delaying treatment for lead intoxication. Failure to correctly diagnose lead induced gastrointestinal distress has led to inappropriate abdominal surgery.
If pica or accidental ingestion of lead-containing objects (such as curtain weights or fishing sinkers) is suspected, an abdominal radiograph should be taken. Hair analysis is not usually an appropriate assay for lead toxicity because no correlation has been found between the amount of lead in the hair and the exposure level.
The probability of environmental lead contamination of a laboratory specimen and inconsistent sample preparation make the results of hair analysis difficult to interpret. Suggested laboratory tests to evaluate lead intoxication include the following:
CBC with peripheral smear. In a lead-poisoned patient, the haematocrit and haemoglobin values may be slightly to moderately low. The differential and total white count may appear normal. The peripheral smear may be either normochromic and normocytic or hypochromic and microcytic. Basophilic stippling is usually seen only in patients who have been significantly poisoned for a prolonged period. Eosinophilia may appear in patients with lead toxicity but does not show a clear dose-response effect.
It is important to note that basophilic stippling is not always seen in lead poisoned patients.
Blood lead level. A blood lead level is the most useful screening and diagnostic test for lead exposure. A blood lead level reflects lead’s dynamic equilibrium between absorption, excretion and deposition in soft- and hard-tissue compartments. For chronic exposures, blood lead levels often underrepresent the total body burden; nevertheless, it is the most widely accepted and commonly used measure of lead exposure. Blood lead levels srespond relatively rapidly to abrupt or intermittent changes in lead intake (e.g., ingestion of lead paint chips by children) and, within a limited range, bear a linear relationship to those intake levels.
Today, the average blood lead level in the US population, for example, is below 10 μg/dL, down from an average of 16 μg/dL (in the 1970s), the level before the legislated removal of lead from gasoline. A blood lead level of 10 μg/dL is about three times higher than the average level found in some remote populations.
The levels defining lead poisoning have been progressively declining. Taken together, effects occur over a wide range of blood lead concentrations, with no indication of a threshold. No safe level has yet been found for children. Even in adults, effects are being discovered at lower and lower levels as more sensitive analyses and measures are developed.
Erythrocyte protoporhyrin level. Until recently, the test of choice for screening asymptomatic populations at risk was erythrocyte protoporphyrin (EP), commonly assayed as zinc protoporphyrin (ZPP). An elevated level of protoporphyrin in the blood is a result of accumulation secondary to enzyme dysfunction in the erythrocytes. It reaches a steady state in the blood only after the entire population of circulating erythrocyles has turned over, about 120 days. Consequently, it lags behind blood lead levels and is an indirect measure of long-term lead exposure.
The major disadvantage of using EP (ZPP) testing as a method for lead screening is that it is not sensitive at the lower levels of lead poisoning. Data from the second US National Health and Nutrition Examination Survey (NHANES II) indicate that 58% of 118 children with blood lead levels above 30 μg/dL had EP levels within normal limits. This finding shows that a significant number of children with lead toxicity would be missed by reliance on EP (ZPP) testing alone as the screening tool. An EP (ZPP) level is still useful in screening patients for iron deficiency anaemia.
Normal values of ZPP are usually below 35 μg/dL. Hyperbilirubinaemia (jaundice) will cause falsely elevated readings when the haematofluorometer is used. EP is elevated in iron deficiency anaemia and in sickle cell and other haemolytic anaemias. In erythropoietic protoporphyria, an extremely rare disease, EP is markedly elevated (usually above 300 μg/dL).
BUN, creatinine and urinalysis. These parameters may reveal only late, significant effects of lead on renal function. Renal function in adults can also be assessed by measuring the fractional excretion of uric acid (normal range 5 to 10%; less than 5% in saturnine gout; greater than 10% in Fanconi syndrome).
Organic lead intoxication
The absorption of a sufficient quantity of tetraethyllead, whether briefly at a high rate or for prolonged periods at a lower rate, induces acute intoxication of the CNS. The milder manifestations are those of insomnia, lassitude and nervous excitation which reveals itself in lurid dreams and dream-like waking states of anxiety, in association with tremor, hyper-reflexia, spasmodic muscular contractions, bradycardia, vascular hypotension and hypothermia. The more severe responses include recurrent (sometimes nearly continuous) episodes of complete disorientation with hallucinations, facial contortions and intense general somatic muscular activity with resistance to physical restraint. Such episodes may be converted abruptly into maniacal or violent convulsive seizures which may terminate in coma and death.
Illness may persist for days or weeks, with intervals of quietude readily triggered into over-activity by any type of disturbance. In these less acute cases, fall in blood pressure and loss of body weight are common. When the onset of such symptomatology follows promptly (within a few hours) after brief, severe exposure to tetraethyllead, and when the symptomatology develops rapidly, an early fatal outcome is to be feared. When, however, the interval between the termination of brief or prolonged exposure and the onset of symptoms is delayed (by up to 8 days), the prognosis is guardedly hopeful, although partial or recurrent disorientation and depressed circulatory function may persist for weeks.
The initial diagnosis is suggested by a valid history of significant exposure to tetraethyllead, or by the clinical pattern of the presenting illness. It may be supported by the further development of the illness, and confirmed by evidence of a significant degree of absorption of tetraethyllead, provided by analyses of urine and blood which reveal typical findings (i.e., a striking elevation of the rate of excretion of lead in the urine) and a concurrently negligible or slight elevation of the concentration of lead in the blood.
Lead Control in the Working Environment
Clinical lead poisoning has historically been one of the most important occupational diseases, and it remains a major risk today. The considerable body of scientific knowledge concerning the toxic effects of lead has been enriched since the 1980s by significant new knowledge regarding the more subtle subclinical effects. Similarly, in a number of countries it was felt necessary to redraft or modernize work protective measures enacted over the last half-century and more.
Thus, in November 1979, in the US, the Final Standard on Occupational Exposure to Lead was issued by the Occupational Safety and Health Administration (OSHA) and in November 1980 a comprehensive Approved Code of Practice was issued in the United Kingdom regarding the control of lead at work.
The main features of the legislation, regulations and codes of practice emerging in the 1970s concerning the protection of the health of workers at work involved establishing comprehensive systems covering all work circumstances where lead is present and giving equal importance to hygiene measures, ambient monitoring and health surveillance (including biological monitoring).
Most codes of practice include the following aspects:
Some regulation, such as the OSHA lead standard, specifies the permissible exposure limit (PEL) of lead in the workplace, the frequency and extent of medical monitoring, and other responsibilities of the employer. As of this writing, if blood monitoring reveals a blood lead level greater than 40 μg/dL, the worker must be notified in writing and provided with medical examination. If a worker’s blood lead level reaches 60 μg/dL (or averages 50 μg/dL or more), the employer is obligated to remove the employee from excessive exposure, with maintenance of seniority and pay, until the employee’s blood lead level falls below 40 μg/dL (29 CFR 91 O.1025) (medical removal protection benefits).
Safety and Health Measures
The object of precautions is first to prevent the inhalation of lead and secondly to prevent its ingestion. These objects are most effectively achieved by the substitution of a less toxic substance for the lead compound. The use of lead polysilicates in the potteries is one example. The avoidance of lead carbonate paints for the painting of the interiors of buildings has proved very effective in reducing painters’ colic; effective substitutes for lead for this purpose have become so readily available that it has been considered reasonable in some countries to prohibit the use of lead paint for the interiors of buildings.
Even if it is not possible to avoid the use of lead itself, it is still possible to avoid dust. Water sprays may be used in large quantities to prevent the formation of dust and to prevent it from becoming airborne. In lead smelting, the ore and the scrap may be treated in this way and the floors on which it has been lying may be kept wet. Unfortunately, there is always a potential source of dust in these circumstances if the treated material or floors are ever allowed to become dry. In some instances, arrangements are made to ensure that the dust will be coarse rather than fine. Other specific engineering precautions are discussed elsewhere in this Encyclopaedia.
Workers who are exposed to lead in any of its forms should be provided with personal protective equipment (PPE), which should be washed or renewed regularly. Protective clothing made of certain man-made fibres retains much less dust than cotton overalls and should be used where the conditions of work render it possible; turn-ups, pleats and pockets in which lead dust may collect should be avoided.
Cloakroom accommodation should be provided for this PPE, with separate accommodation for clothing taken off during working hours. Washing accommodation, including bathing accommodation with warm water, should be provided and used. Time should be allowed for washing before eating. Arrangements should be made to prohibit eating and smoking in the vicinity of lead processes and suitable eating facilities should be provided.
It is essential that the rooms and the plant associated with lead processes should be kept clean by continuous cleaning either by a wet process or by vacuum cleaners. Where, in spite of these precautions, workers may still be exposed to lead, respiratory protective equipment should be provided and properly maintained. Supervision should ensure that this equipment is maintained in a clean and efficient condition and that it is used when necessary.
Both the toxic properties of organic lead compounds, and their ease of absorption, require that contact of the skin of workers with these compounds, alone or in concentrated mixtures in commercial formulations or in gasoline or other organic solvents, must be scrupulously avoided. Both technological and management control are essential, and appropriate training of workers in safe work practices and the use of PPE is required. It is essential that atmospheric concentrations of alkyl lead compounds in the workplace air should be maintained at extremely low levels. Personnel should not be allowed to eat, smoke or keep unsealed food or beverages at the workplace. Good sanitary facilities, including showers, should be provided and workers should be encouraged to practise good personal hygiene, especially by showering or washing after the work shift. Separate lockers should be supplied for working and private clothes.
Iridium (Ir) belongs to the platinum family. Its name derives from the colours of its salt, which are reminiscent of a rainbow (iris). Although it is very hard and the most corrosion-resistant metal known, it is attacked by some salts.
Occurrence and Uses
Iridium occurs in nature in the metallic state, usually alloyed with osmium (osmiridium), platinum or gold, and it is produced from these minerals. The metal is used to manufacture crucibles for chemical laboratories and to harden platinum. Recent in vitro studies indicate the possible effects of iridium on Leishmania donovani and the trypanocidal activity of iridium against Trypanosoma brucei. Ir is used in industrial radiology and is a gamma emitter (0.31 MeV at 82.7%) and beta emitter (0.67 MeV at 47.2%). 192Ir is a radioisotope which has also been used for clinical treatment, particularly cancer therapy. It is one of the most frequently used isotopes in interstitial brain irradiation.
Very little is known about the toxicity of iridium and its compounds. There has been little opportunity to note any adverse human effects since it is used only in small amounts. All radioisotopes are potentially harmful and must be treated with appropriate safeguards required for handling radioactive sources. Soluble iridium compounds such as iridium tribromide and tetrabromide and iridium trichloride could present both toxic effects of the iridium or the halogen, but data as to its chronic toxicity are unavailable. Iridium trichloride has been reported to be a mild irritant to the skin and is positive in eye irritation test. Inhaled aerosol of metallic iridium is deposited in the upper respiratory ways of rats; the metal is then quickly removed via the gastrointestinal tract, and approximately 95% can be found in the faeces. In humans the only reports are those concerning radiation injuries due to accidental exposure to 192Ir.
Safety and Health Measures
A radiation safety and medical surveillance programme should be in place for persons responsible for nursing care during interstitial brachytherapy. Radiation safety principles include exposure reduction by time, distance and shielding. Nurses who care for brachytherapy patients must wear radiation monitoring devices to record the amount of exposure. To avoid industrial radiography accidents, only trained industrial radiographers should be allowed to handle radionuclides.