458
23 million kg and occupies just under half a million cubic metres. Space is always limited in hospitals. Disposable items require not only shelf upon shelf for storing the necessary variety and volume of instruments and gown and drape packs, but also the local equivalent of rag and bottle banks. Manufacturers can play their part in reducing environmental pollution by use of recyclable plastics with easily separated metal components. If this issue is not addressed we shall have to face something far more serious than the occasional partly incinerated bandage fragment landing on a nearby washing line.
weighs
1. Tieszen
ME, Gruenberg JC. A quantitative, qualitative and critical of surgical waste: surgeons venture through the trash can. JAMA 1992; 267: 2765-68. assessment
Charging for health services
in the
third world Moves towards a greater degree of charging for the use of health services in developing countries are the result of two main factors: (a) the collapse of government funding for health programmes, partly instigated by the fall in commodity prices and the burden of debt repayment; and (b) the general trend towards privatisation. Restraints on government spending, especially on social programmes, have been reinforced by loan conditions imposed by the International Monetary Fund and the World Bank. The issues are complex. Simplistic argument and analogy can be misleading. Reasons why health services are not like other goods have been rehearsed elsewhere,l and problems of inefficient and ineffective services will not be cured by private finance or private provision. Governments, in their commitment to the World Health Organisation’s Health for All, have a responsibility for developing a health policy to maximise access to essential services for effective prevention and treatment of disease, and to promote health. Financing mechanisms should be compatible with achieving such goals. Charges raise revenue but will also affect patient choice. They are sometimes advocated as a means of reducing frivolous use of services by making patients aware of costs. Evidence on the response of patients to charges suggests that demand is generally inelasticie, there is a relatively small response to higher prices. However, it is also clear that the effect of higher charges has a disproportionate effect on the poorest sectors of the population. In Peru and rural Cote d’lvoire, studies have suggested that, for those on very low incomes, a modest rise in charges is likely to reduce use of services substantially, whereas those who are better off remain virtually unaffected.3 Consequently, those whose needs are the least will continue to use services, and those with the greatest needs will be deterred. Some might argue that there is no objection to charges for those who can afford to pay, since their use of services will be largely unchanged. This view ignores the very real difficulties in operating a system that can distinguish those who can and those who
pay.4 The objection is not so much the principle as the feasibility of charges for the relatively affluent. Even though governments should aim to have in place services to meet Health for All goals, there are few fundamental objections to people spending their own money on health services over and above the basic level. Provided they are not removing resources from provision of universal coverage of cannot
basic
there are no losers. However, it is seldom possible to achieve this outcome. Scarce facilities, skilled professionals, and other services provided at public expense are almost always involved in this provision. In particular, it is difficult fully to recover the cost of training for doctors and nurses. Provision of technically advanced services for a minority who can afford to pay is almost always subsidised by governments in some way, and may deprive the rest of the population of key resources.5 Charges affect different types of services to different degrees. Willingness to pay varies and the implications of reduced service use may be more or less important. As Moses and colleagues show in this issue (p 463), the trend to introduce charges for family planning services and services for the treatment and prevention of have communicable disease serious may is Use of services deterred, with consequences. potentially very high costs to the rest of the population. It is hard to justify raising small sums against the increased difficulty in meeting Health for All targets. Economic theory shows the failure of markets when there are "external" costs, and these can be very high in communicable diseases. care
If charges have the effect of moving resources from those with the greatest capacity to benefit to those with lower levels of need, or risk causing outbreaks of communicable diseases, they are hard to justify. However, the effective collapse of government funding for health services in many developing countries leaves a need for alternative sources of funding for basic primary care.2 Some constraints on public expenditure arise from misguided macroeconomic policy and should be resisted. Nevertheless, much of the reduction in health spending has been unavoidable, and tax funding itself has been associated with inefficiency and inappropriate priorities. Clearly new forms of funding are needed. As an interim step, some user charges may help to keep services going, and can have a useful role, especially if revenues generated result in substantial improvements in the quality and availability of services.6 However, in most cases this has not been achieved and user charges have proved inefficient both in terms of incentives and as a mechanism to raise money for health care.7 Models to improve on this performance would rely more on local control and avoid moving resources to the centre and back to the local level. Development of feasible mechanisms for greater risk sharing in the longer term remains a priority if the most regressive effects of charges are to be avoided.
459
1. Normand C. Economics, health and the economics of health. BMJ 1991; 303: 1572-77. 2. Akin J, Birdsall N, De Ferranti D. Financing health services in developing countries: an agenda for reform. Washington, DC: World
Bank, 1987. 3. Gertler P, van der Gaag J. The willingness to pay for medical care: evidence from two developing countries. Washington, DC: World
Bank, 1990. Vogel RJ. Cost recovery in the health care sector: selected country studies in West Africa. Washington, DC: World Bank, 1988. 5. Bennett S. The mystique of markets: public and private health care in developing countries. PHP departmental publication no 4. London: London School of Hygiene and Tropical Medicine, 1991. 6. McPake B, Hanson K, Mills A. Experience to date of implementing the
4.
Barnako initiative: a review and five country case studies. London: London School of Hygiene and Tropical Medicine, 1992. 7. Creese A. User charges for health care: a review of recent experience. Health Policy Plann 1991; 6.
Lymphocyte traffic A reduction in the number of erythrocytes in a blood sample is usually easy to interpret. Red blood cells are produced only in the bone marrow, they remain in the blood for their lifespan, their total number can be calculated, and their main functionoxygen transport-can be deduced. By contrast, it is far more difficult to explain a reduced number of lymphocytes, since these cells are produced in many lymphoid organs and the bloodstream is merely a temporary route on their continuous patrol through the body. Blood contains only about 2% of all lymphocytes.1 Whereas hypoxia results in erythropoietin secretion and increased erythropoiesis, the factors that regulate lymphocyte proliferation are uncertain. Lymphocyte numbers are remarkably constant, especially in view of the need to control proliferation of many clones residing in different compartments of several lymphoid organs. The reason why lymphocyte production returns to normal after immunisation-induced proliferation is unclear. Despite successful characterisation of surface antigens to phenotype lymphocytes and receptors down to the molecular level, very little is understood about lymphocyte kinetics in man. There is no simple measure of the immunological effects of altered numbers of lymphocytes in the blood. Lymphopenia due to reduced numbers of T helper cells and that due to a reduction of all lymphocytes have different effects on immune responses. Is a short increase in natural killer (NK) cells of almost 500%, and in naive CD8 lymphocytes of 200%, after endurance exercise to exhaustion, of any functional importance? It could be a protective mechanism or, conversely, a dangerous imbalance.z2 Age has an important effect on lymphocyte numbers and subset distribution: NK cells comprise 20% of circulating lymphocytes in cord blood but only 11 % in young children.3 Lymphocytes continually leave the blood via different pathways: (a) via specialised endothelium designated high endothelial venules (HEV) in the T-lymphocyte regions of lymph nodes, Peyer’s patches, and tonsils; (b) via sinusoids in lymphoid organs that lack HEV such as the spleen; and (c) via normal vessels in non-lymphoid organs such as lung, liver, and skin. Only the interaction between
and HEV endothelium has been well studied. Numerous adhesion molecules have been characterised, and can broadly be grouped into the immunoglobulin superfamily, the integrin family, and the selectin family.4 The initial hypothesis that there
lymphocytes
homing receptor for peripheral lymph node HEV and another for Peyer’s patch HEV is obviously too simple. There is growing evidence that a cascade of interactions between lymphocytes and endothelial cells and adhesion, regulates triggering, transmigration, and that all these steps can be influenced by cytokines in inflammation.5,6 REV are not static permanent structures: ligation of afferent lymphatics flattens the endothelium and intradermal injection of phytohaemagglutinin or cytokines can induce HEV within hours.’Memory lymphocytes preferentially migrate through peripheral organs such as the skin, and virgin lymphocytes through organised lymphoid organs such as lymph nodes,8 but we do not know what regulates the migration within lymphoid organs to ensure that recirculating lymphocytes come into contact with antigen-presenting cells. This mechanism might also be regulated by adhesion molecules. Similarly, very little is known about the factors responsible for the exit of lymphocytes from lymphoid or other organs. Quantitatively, more lymphocytes leave the blood in organs without HEV, such as the spleen.9 A marginal blood pool of lymphocytes, as described for granulocytes, may be a depot for rapid mobilisation. The lung vascular bed seems to play a central part in this respect. However, no specific adhesion molecules have been identified that regulate homing of lymphocytes to non-HEV organs or to non-lymphoid organs (eg, normal lung or skin).9 When more is known about lymphocyte traffic, one could contemplate the use of migrating lymphocytes as vehicles for toxins in the treatment of cancer, and devise ways of blocking specific homing receptors to stop lymphocytes entering sites of infection and thereby influence the progression to chronic inflammation. was one
1. Westermann
J, Pabst R. Lymphocyte subsets in the blood: a diagnostic window on the lymphoid system? Immunol Today 1990; 11: 406-10. 2. Gabriel H, Urhausen A, Kindermann W. Circulating leucocyte and lymphocyte subpopulations before and after intensive endurance exercise to exhaustion. Eur J Appl Physiol 1991; 63: 449-57. 3. Hannet I, Erkeller-Yuksel F, Lydyard P, Deneys V, DeBruyère M. Developmental and maturational changes in human blood lymphocyte subpopulations. Immunol Today 1992; 13: 215-18. 4. Pardi R, Inverardi L, Bender JR. Regulatory mechanisms in leukocyte adhesion: flexible receptors for sophisticated travellers. Immunol Today 1992; 13: 224-30. JS, Cotran RS. Immunologic interactions of T lymphocytes with vascular endothelium. Adv Immunol 1991; 50: 261-302. 6. Shimizu Y, Newman W, Tanaka Y, Shaw S. Lymphocyte interactions with endothelial cells. Immunol Today 1992; 13: 106-12. 7. Binns RM, Licence ST, Wooding EBP. Phytohemagglutinin induces major short-term protease-sensitive lymphocyte traffic involving high 5. Pober
endothelium venule-like blood vessels in acute-type hypersensitivitylike reactions in skin and other tissues. Eur J Immunol 1990; 20: 1067-71. 8. Mackay CR. T-cell memory: the connection between function, phenotype and memory T cells during activation. Immunol Today
1991; 12: 189-92. 9. Pabst R, Binns RM. Heterogeneity of lymphocyte homing physiology: several mechanisms operate in the control of migration to lymphoid and non-lymphoid organs in vivo. Immunol Rev 1989; 108: 83-109.
23 million kg and occupies just under half a million cubic metres. Space is always limited in hospitals. Disposable items require not only shelf upon shelf for storing the necessary variety and volume of instruments and gown and drape packs, but also the local equivalent of rag and bottle banks. Manufacturers can play their part in reducing environmental pollution by use of recyclable plastics with easily separated metal components. If this issue is not addressed we shall have to face something far more serious than the occasional partly incinerated bandage fragment landing on a nearby washing line.
weighs
1. Tieszen
ME, Gruenberg JC. A quantitative, qualitative and critical of surgical waste: surgeons venture through the trash can. JAMA 1992; 267: 2765-68. assessment
Charging for health services
in the
third world Moves towards a greater degree of charging for the use of health services in developing countries are the result of two main factors: (a) the collapse of government funding for health programmes, partly instigated by the fall in commodity prices and the burden of debt repayment; and (b) the general trend towards privatisation. Restraints on government spending, especially on social programmes, have been reinforced by loan conditions imposed by the International Monetary Fund and the World Bank. The issues are complex. Simplistic argument and analogy can be misleading. Reasons why health services are not like other goods have been rehearsed elsewhere,l and problems of inefficient and ineffective services will not be cured by private finance or private provision. Governments, in their commitment to the World Health Organisation’s Health for All, have a responsibility for developing a health policy to maximise access to essential services for effective prevention and treatment of disease, and to promote health. Financing mechanisms should be compatible with achieving such goals. Charges raise revenue but will also affect patient choice. They are sometimes advocated as a means of reducing frivolous use of services by making patients aware of costs. Evidence on the response of patients to charges suggests that demand is generally inelasticie, there is a relatively small response to higher prices. However, it is also clear that the effect of higher charges has a disproportionate effect on the poorest sectors of the population. In Peru and rural Cote d’lvoire, studies have suggested that, for those on very low incomes, a modest rise in charges is likely to reduce use of services substantially, whereas those who are better off remain virtually unaffected.3 Consequently, those whose needs are the least will continue to use services, and those with the greatest needs will be deterred. Some might argue that there is no objection to charges for those who can afford to pay, since their use of services will be largely unchanged. This view ignores the very real difficulties in operating a system that can distinguish those who can and those who
pay.4 The objection is not so much the principle as the feasibility of charges for the relatively affluent. Even though governments should aim to have in place services to meet Health for All goals, there are few fundamental objections to people spending their own money on health services over and above the basic level. Provided they are not removing resources from provision of universal coverage of cannot
basic
there are no losers. However, it is seldom possible to achieve this outcome. Scarce facilities, skilled professionals, and other services provided at public expense are almost always involved in this provision. In particular, it is difficult fully to recover the cost of training for doctors and nurses. Provision of technically advanced services for a minority who can afford to pay is almost always subsidised by governments in some way, and may deprive the rest of the population of key resources.5 Charges affect different types of services to different degrees. Willingness to pay varies and the implications of reduced service use may be more or less important. As Moses and colleagues show in this issue (p 463), the trend to introduce charges for family planning services and services for the treatment and prevention of have communicable disease serious may is Use of services deterred, with consequences. potentially very high costs to the rest of the population. It is hard to justify raising small sums against the increased difficulty in meeting Health for All targets. Economic theory shows the failure of markets when there are "external" costs, and these can be very high in communicable diseases. care
If charges have the effect of moving resources from those with the greatest capacity to benefit to those with lower levels of need, or risk causing outbreaks of communicable diseases, they are hard to justify. However, the effective collapse of government funding for health services in many developing countries leaves a need for alternative sources of funding for basic primary care.2 Some constraints on public expenditure arise from misguided macroeconomic policy and should be resisted. Nevertheless, much of the reduction in health spending has been unavoidable, and tax funding itself has been associated with inefficiency and inappropriate priorities. Clearly new forms of funding are needed. As an interim step, some user charges may help to keep services going, and can have a useful role, especially if revenues generated result in substantial improvements in the quality and availability of services.6 However, in most cases this has not been achieved and user charges have proved inefficient both in terms of incentives and as a mechanism to raise money for health care.7 Models to improve on this performance would rely more on local control and avoid moving resources to the centre and back to the local level. Development of feasible mechanisms for greater risk sharing in the longer term remains a priority if the most regressive effects of charges are to be avoided.
459
1. Normand C. Economics, health and the economics of health. BMJ 1991; 303: 1572-77. 2. Akin J, Birdsall N, De Ferranti D. Financing health services in developing countries: an agenda for reform. Washington, DC: World
Bank, 1987. 3. Gertler P, van der Gaag J. The willingness to pay for medical care: evidence from two developing countries. Washington, DC: World
Bank, 1990. Vogel RJ. Cost recovery in the health care sector: selected country studies in West Africa. Washington, DC: World Bank, 1988. 5. Bennett S. The mystique of markets: public and private health care in developing countries. PHP departmental publication no 4. London: London School of Hygiene and Tropical Medicine, 1991. 6. McPake B, Hanson K, Mills A. Experience to date of implementing the
4.
Barnako initiative: a review and five country case studies. London: London School of Hygiene and Tropical Medicine, 1992. 7. Creese A. User charges for health care: a review of recent experience. Health Policy Plann 1991; 6.
Lymphocyte traffic A reduction in the number of erythrocytes in a blood sample is usually easy to interpret. Red blood cells are produced only in the bone marrow, they remain in the blood for their lifespan, their total number can be calculated, and their main functionoxygen transport-can be deduced. By contrast, it is far more difficult to explain a reduced number of lymphocytes, since these cells are produced in many lymphoid organs and the bloodstream is merely a temporary route on their continuous patrol through the body. Blood contains only about 2% of all lymphocytes.1 Whereas hypoxia results in erythropoietin secretion and increased erythropoiesis, the factors that regulate lymphocyte proliferation are uncertain. Lymphocyte numbers are remarkably constant, especially in view of the need to control proliferation of many clones residing in different compartments of several lymphoid organs. The reason why lymphocyte production returns to normal after immunisation-induced proliferation is unclear. Despite successful characterisation of surface antigens to phenotype lymphocytes and receptors down to the molecular level, very little is understood about lymphocyte kinetics in man. There is no simple measure of the immunological effects of altered numbers of lymphocytes in the blood. Lymphopenia due to reduced numbers of T helper cells and that due to a reduction of all lymphocytes have different effects on immune responses. Is a short increase in natural killer (NK) cells of almost 500%, and in naive CD8 lymphocytes of 200%, after endurance exercise to exhaustion, of any functional importance? It could be a protective mechanism or, conversely, a dangerous imbalance.z2 Age has an important effect on lymphocyte numbers and subset distribution: NK cells comprise 20% of circulating lymphocytes in cord blood but only 11 % in young children.3 Lymphocytes continually leave the blood via different pathways: (a) via specialised endothelium designated high endothelial venules (HEV) in the T-lymphocyte regions of lymph nodes, Peyer’s patches, and tonsils; (b) via sinusoids in lymphoid organs that lack HEV such as the spleen; and (c) via normal vessels in non-lymphoid organs such as lung, liver, and skin. Only the interaction between
and HEV endothelium has been well studied. Numerous adhesion molecules have been characterised, and can broadly be grouped into the immunoglobulin superfamily, the integrin family, and the selectin family.4 The initial hypothesis that there
lymphocytes
homing receptor for peripheral lymph node HEV and another for Peyer’s patch HEV is obviously too simple. There is growing evidence that a cascade of interactions between lymphocytes and endothelial cells and adhesion, regulates triggering, transmigration, and that all these steps can be influenced by cytokines in inflammation.5,6 REV are not static permanent structures: ligation of afferent lymphatics flattens the endothelium and intradermal injection of phytohaemagglutinin or cytokines can induce HEV within hours.’Memory lymphocytes preferentially migrate through peripheral organs such as the skin, and virgin lymphocytes through organised lymphoid organs such as lymph nodes,8 but we do not know what regulates the migration within lymphoid organs to ensure that recirculating lymphocytes come into contact with antigen-presenting cells. This mechanism might also be regulated by adhesion molecules. Similarly, very little is known about the factors responsible for the exit of lymphocytes from lymphoid or other organs. Quantitatively, more lymphocytes leave the blood in organs without HEV, such as the spleen.9 A marginal blood pool of lymphocytes, as described for granulocytes, may be a depot for rapid mobilisation. The lung vascular bed seems to play a central part in this respect. However, no specific adhesion molecules have been identified that regulate homing of lymphocytes to non-HEV organs or to non-lymphoid organs (eg, normal lung or skin).9 When more is known about lymphocyte traffic, one could contemplate the use of migrating lymphocytes as vehicles for toxins in the treatment of cancer, and devise ways of blocking specific homing receptors to stop lymphocytes entering sites of infection and thereby influence the progression to chronic inflammation. was one
1. Westermann
J, Pabst R. Lymphocyte subsets in the blood: a diagnostic window on the lymphoid system? Immunol Today 1990; 11: 406-10. 2. Gabriel H, Urhausen A, Kindermann W. Circulating leucocyte and lymphocyte subpopulations before and after intensive endurance exercise to exhaustion. Eur J Appl Physiol 1991; 63: 449-57. 3. Hannet I, Erkeller-Yuksel F, Lydyard P, Deneys V, DeBruyère M. Developmental and maturational changes in human blood lymphocyte subpopulations. Immunol Today 1992; 13: 215-18. 4. Pardi R, Inverardi L, Bender JR. Regulatory mechanisms in leukocyte adhesion: flexible receptors for sophisticated travellers. Immunol Today 1992; 13: 224-30. JS, Cotran RS. Immunologic interactions of T lymphocytes with vascular endothelium. Adv Immunol 1991; 50: 261-302. 6. Shimizu Y, Newman W, Tanaka Y, Shaw S. Lymphocyte interactions with endothelial cells. Immunol Today 1992; 13: 106-12. 7. Binns RM, Licence ST, Wooding EBP. Phytohemagglutinin induces major short-term protease-sensitive lymphocyte traffic involving high 5. Pober
endothelium venule-like blood vessels in acute-type hypersensitivitylike reactions in skin and other tissues. Eur J Immunol 1990; 20: 1067-71. 8. Mackay CR. T-cell memory: the connection between function, phenotype and memory T cells during activation. Immunol Today
1991; 12: 189-92. 9. Pabst R, Binns RM. Heterogeneity of lymphocyte homing physiology: several mechanisms operate in the control of migration to lymphoid and non-lymphoid organs in vivo. Immunol Rev 1989; 108: 83-109.
