126
Sick
building syndrome
SIR,-Many people attribute symptoms to the buildings in which they work. Your Dec 14 editorial provides a valuable overview of the many difficulties attributed to so-called sick buildings and the frustrations for those who have to try to resolve them. Employers have the main responsibility for protecting the health of their staff and a strong economic incentive in view of the effects of sick-building problems on morale, performance, and attendance at work. The Health and Safety Executive (HSE) has published advice in its Specialist Inspector Report, number 10. HSE is now aiming to improve knowledge of sick-building syndrome by commissioning a review of the evidence and studies focusing in particular on public-sector buildings. We will also produce simple guidance on prevention aimed at employers and their staff. Unlike more traditional occupational health concerns, inspection and enforcement action are of little use in prevention in sickbuilding syndrome because of the multiple environmental and organisational factors. Both HSE staff and local authority inspectors responsible for enforcing the Health and Safety at Work Act respond to requests for advice. We often find that the difficulty is that management do not listen to the concerns and complaints of staff, or take early action to adjust ventilation, improve housekeeping and cleanliness, or alter the organisation of workrather than a search for the cause. We support your proposition that managers should take heed of staff concerns, make sound judgements on building design, and use occupational health advisers to monitor and propose remedies--or, even better, to prevent their occurrence.
World Health Organisation, Regional Office for Africa, PO Box 6,
Brazzaville, Congo
SANDRO CALVANI
Organization of African Unity. Declaration on African Health Crisis. AHG/DEC L3 (XXVII) Abuja: OAO, 1991. 2. World Health Organisation. Resolutions of the regional committee for Africa. The Bujumbura Appeal: a call for Africa. Bujumbura, WHO: 1991. 3. World Health Organisation—Regional Office for Africa. The creation of a health care financing unit. Brazzaville: WHO, 1991. 4. World Health Organisation Health is not a trade-off against economic development says a new WHO analysis-health dimensions of economic reform. Geneva WHO, 1991. 5. Monekosso GL. Meeting the challenge of Africa’s health in the decade of the nineties 1.
Geneva: WHO, 1991: 57-77. 6. Africa’s unpayable debts. The Economist
1991, Nov 2: 17-18.
N-acetylcysteine and lipoprotein(a)
Health and
Safety Executive, Baynards House,
J.
Westbourne Grove, London W2 4TF,UK
Director, Health Policy Division
T.
CARTER,
Health crisis in African countries SIR,- The tendency to stigmatise the African continent as a never-developing region ("Afropessimism") and the opening up of Eastern Europe are the main factors in the trend to no longer paying attention to important developments in Africa. These factors have also discouraged industrialised countries from reconsidering their lack of response to change in many African countries, even when those changes were demanded as prerequisites to aid by powerful and institutions. Two recent events have emphasised the grave health situation. The Abuja declaration of the summit of the Organization of African Unity on the African health crisis1 stated that "the current economic recession, the debt crisis and the consequent financial constraints have resulted in significant reduction of the health budgets in many countries. Similarly, the ... economic crisis has also aggravated the health crisis". In the same vein, the Bujumbura appeal of the African Ministers of Health of the World Health Organisation (WHO) Africa Region2 has reviewed the efforts by African countries since the 1986 special session of the United Nations General Assembly and noted "the poor quality of health services and the deteriorating health status of the population as a result of the economic crisis". Fortunately, some institutions have not quite abandoned the continent. To complement and support local efforts, a special health fund for Africa has been established by eminent Africans. The WHO Regional Office for Africa has added to this a health-care financing programme.3 WHO has also held an international forum on health’ in Ghana, which was attended by heads of state from all over the world. African leaders have shown the capability to analyse managerial difficulties in health-care delivery and to suggest ways to overcome these and improve services. Monekosso’ has proposed ways to resolve the difficulties; he emphasised enhanced community participation (an exhaustible resource in the continent), grassroots action, and formulation of policy to revive health-care delivery. This would require that funds were directed to the peripheral regions and the districts. states
Most African countries have conformed with the harsh conditions of the Bretton Woods institutions to turn their economy around. These adjustment measures have had negative effects on health, yet the expected promised returns on this tough "investment" have not been forthcoming. According to The Economist, "the case for debt reduction in Africa is watertight... The region is hobbled by debts much heavier, in relation to economic strength, than Latin America’s". Yet the recent Brady plan for debt relief to many third world nations offers no help to African countries.6 I am therefore convinced that it is time that donors, and medical institutions especially, take Africans more seriously. The development partners need to provide and nurture the exceptional cooperation needed to overcome the health crisis facing the continent.
SIR,-Gavish and Bresiow1 reported a 50-70% reduction in plasma lipoprotein(a) (Lp[a]) in two patients taking oral Nacetylcysteine (NAC) at 2 g and then 4 g per day. In contrast, Stalenhoef et aF found that oral NAC at doses of 12-2-4 g daily caused only a very modest reduction in plasma Lp(a). Scanu’s in-vitro datashowing that 2 mmol/1 NAC disrupted antibody recognition of Lp(a), prompted the suggestion that the Lp(a) lowering observed in vivo by Gavish and Breslow might have been an artifact of altered immunoreactivity. In this letter we will attempt to address the issues raised by Stalenhoef et al and Scanu. Upon review of the protocol, we found that the patients studied by Gavish and Breslow in fact received NAC at doses of 2g and 4 g twice daily. Thus the large difference in dose (4-8 g vs 1-2-2-4 g daily) could explain the divergent Lp(a) lowering effects noted by Gavish and Breslow and by Stalenhoef et al, respectively. 9 of the 12 patients studied by Stalenhoef et al were receiving simvastatin, whereas the 2 patients studied by Gavish and Breslow were on no medications other than NAC. In response to drugs such as simvastatin Lp(a) levels increase in some patients,’ and this might offset an Lp(a)-lowering effect of NAC. In Scanu’s study significant alteration of Lp(a) immunoreactivity by NAC was not obtained until the in-vitro concentration was 2 mmol/l. We believe that this has little relevance in vivo. In plasma, NAC occurs in its intact reduced form but also in oxidised forms such as N,N’-diacetylcystine, N-acetylcysteine-cysteine, Nand acetylcysteine-glutathione, N-acetylcysteine-protein complexes. Olsson et als have studied plasma concentrations of intact reduced NAC and total NAC in healthy volunteers after a 400 mg oral dose. This dose led to peak plasma concentrations of intact reduced NAC of 3-5 Nunol/1 and of total NAC of 10 umol/1 30 min after ingestion. The concentration of intact reduced NAC was unmeasurable by 1 -5 h and total NAC was less than 1 umol/1 by 8 h. In another study, Burgunder et al6 fed healthy volunteers 2 g of NAC. They found peak plasma concentration of intact reduced NAC of 9 µmol/1 and total NAC of 67 umol/1 45-60 min after ingestion. Intact reduced NAC levels were unmeasurable and total NAC was 7 pmol/1 at 8 h. In a third study, North et aF fed healthy volunteers 12 g NAC and found peak plasma concentration of intact reduced NAC of 83 umol/1 30 min to 2 h after ingestion. We have done pharmacokinetic modelling of total NAC concentrations, based on the data in Olsson’s paper. This analysis indicated 4 g
Sick
building syndrome
SIR,-Many people attribute symptoms to the buildings in which they work. Your Dec 14 editorial provides a valuable overview of the many difficulties attributed to so-called sick buildings and the frustrations for those who have to try to resolve them. Employers have the main responsibility for protecting the health of their staff and a strong economic incentive in view of the effects of sick-building problems on morale, performance, and attendance at work. The Health and Safety Executive (HSE) has published advice in its Specialist Inspector Report, number 10. HSE is now aiming to improve knowledge of sick-building syndrome by commissioning a review of the evidence and studies focusing in particular on public-sector buildings. We will also produce simple guidance on prevention aimed at employers and their staff. Unlike more traditional occupational health concerns, inspection and enforcement action are of little use in prevention in sickbuilding syndrome because of the multiple environmental and organisational factors. Both HSE staff and local authority inspectors responsible for enforcing the Health and Safety at Work Act respond to requests for advice. We often find that the difficulty is that management do not listen to the concerns and complaints of staff, or take early action to adjust ventilation, improve housekeeping and cleanliness, or alter the organisation of workrather than a search for the cause. We support your proposition that managers should take heed of staff concerns, make sound judgements on building design, and use occupational health advisers to monitor and propose remedies--or, even better, to prevent their occurrence.
World Health Organisation, Regional Office for Africa, PO Box 6,
Brazzaville, Congo
SANDRO CALVANI
Organization of African Unity. Declaration on African Health Crisis. AHG/DEC L3 (XXVII) Abuja: OAO, 1991. 2. World Health Organisation. Resolutions of the regional committee for Africa. The Bujumbura Appeal: a call for Africa. Bujumbura, WHO: 1991. 3. World Health Organisation—Regional Office for Africa. The creation of a health care financing unit. Brazzaville: WHO, 1991. 4. World Health Organisation Health is not a trade-off against economic development says a new WHO analysis-health dimensions of economic reform. Geneva WHO, 1991. 5. Monekosso GL. Meeting the challenge of Africa’s health in the decade of the nineties 1.
Geneva: WHO, 1991: 57-77. 6. Africa’s unpayable debts. The Economist
1991, Nov 2: 17-18.
N-acetylcysteine and lipoprotein(a)
Health and
Safety Executive, Baynards House,
J.
Westbourne Grove, London W2 4TF,UK
Director, Health Policy Division
T.
CARTER,
Health crisis in African countries SIR,- The tendency to stigmatise the African continent as a never-developing region ("Afropessimism") and the opening up of Eastern Europe are the main factors in the trend to no longer paying attention to important developments in Africa. These factors have also discouraged industrialised countries from reconsidering their lack of response to change in many African countries, even when those changes were demanded as prerequisites to aid by powerful and institutions. Two recent events have emphasised the grave health situation. The Abuja declaration of the summit of the Organization of African Unity on the African health crisis1 stated that "the current economic recession, the debt crisis and the consequent financial constraints have resulted in significant reduction of the health budgets in many countries. Similarly, the ... economic crisis has also aggravated the health crisis". In the same vein, the Bujumbura appeal of the African Ministers of Health of the World Health Organisation (WHO) Africa Region2 has reviewed the efforts by African countries since the 1986 special session of the United Nations General Assembly and noted "the poor quality of health services and the deteriorating health status of the population as a result of the economic crisis". Fortunately, some institutions have not quite abandoned the continent. To complement and support local efforts, a special health fund for Africa has been established by eminent Africans. The WHO Regional Office for Africa has added to this a health-care financing programme.3 WHO has also held an international forum on health’ in Ghana, which was attended by heads of state from all over the world. African leaders have shown the capability to analyse managerial difficulties in health-care delivery and to suggest ways to overcome these and improve services. Monekosso’ has proposed ways to resolve the difficulties; he emphasised enhanced community participation (an exhaustible resource in the continent), grassroots action, and formulation of policy to revive health-care delivery. This would require that funds were directed to the peripheral regions and the districts. states
Most African countries have conformed with the harsh conditions of the Bretton Woods institutions to turn their economy around. These adjustment measures have had negative effects on health, yet the expected promised returns on this tough "investment" have not been forthcoming. According to The Economist, "the case for debt reduction in Africa is watertight... The region is hobbled by debts much heavier, in relation to economic strength, than Latin America’s". Yet the recent Brady plan for debt relief to many third world nations offers no help to African countries.6 I am therefore convinced that it is time that donors, and medical institutions especially, take Africans more seriously. The development partners need to provide and nurture the exceptional cooperation needed to overcome the health crisis facing the continent.
SIR,-Gavish and Bresiow1 reported a 50-70% reduction in plasma lipoprotein(a) (Lp[a]) in two patients taking oral Nacetylcysteine (NAC) at 2 g and then 4 g per day. In contrast, Stalenhoef et aF found that oral NAC at doses of 12-2-4 g daily caused only a very modest reduction in plasma Lp(a). Scanu’s in-vitro datashowing that 2 mmol/1 NAC disrupted antibody recognition of Lp(a), prompted the suggestion that the Lp(a) lowering observed in vivo by Gavish and Breslow might have been an artifact of altered immunoreactivity. In this letter we will attempt to address the issues raised by Stalenhoef et al and Scanu. Upon review of the protocol, we found that the patients studied by Gavish and Breslow in fact received NAC at doses of 2g and 4 g twice daily. Thus the large difference in dose (4-8 g vs 1-2-2-4 g daily) could explain the divergent Lp(a) lowering effects noted by Gavish and Breslow and by Stalenhoef et al, respectively. 9 of the 12 patients studied by Stalenhoef et al were receiving simvastatin, whereas the 2 patients studied by Gavish and Breslow were on no medications other than NAC. In response to drugs such as simvastatin Lp(a) levels increase in some patients,’ and this might offset an Lp(a)-lowering effect of NAC. In Scanu’s study significant alteration of Lp(a) immunoreactivity by NAC was not obtained until the in-vitro concentration was 2 mmol/l. We believe that this has little relevance in vivo. In plasma, NAC occurs in its intact reduced form but also in oxidised forms such as N,N’-diacetylcystine, N-acetylcysteine-cysteine, Nand acetylcysteine-glutathione, N-acetylcysteine-protein complexes. Olsson et als have studied plasma concentrations of intact reduced NAC and total NAC in healthy volunteers after a 400 mg oral dose. This dose led to peak plasma concentrations of intact reduced NAC of 3-5 Nunol/1 and of total NAC of 10 umol/1 30 min after ingestion. The concentration of intact reduced NAC was unmeasurable by 1 -5 h and total NAC was less than 1 umol/1 by 8 h. In another study, Burgunder et al6 fed healthy volunteers 2 g of NAC. They found peak plasma concentration of intact reduced NAC of 9 µmol/1 and total NAC of 67 umol/1 45-60 min after ingestion. Intact reduced NAC levels were unmeasurable and total NAC was 7 pmol/1 at 8 h. In a third study, North et aF fed healthy volunteers 12 g NAC and found peak plasma concentration of intact reduced NAC of 83 umol/1 30 min to 2 h after ingestion. We have done pharmacokinetic modelling of total NAC concentrations, based on the data in Olsson’s paper. This analysis indicated 4 g
