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Is bracken a health hazard?
493
from haemoglobin turnover. Redox reaction iron can initiate many damaging free-radical reactions.1O We contend that exposure of very premature infants to high-intensity light, especially during periods of raised oxygen tension, may initiate ocular damage. Attention should be given to the spectral energy characteristics and the intensity of emission of the ambient illumination in the neonatal environment. University College and Middlesex Hospital School of Medicine,
P. A. RILEY
London W1 Brunel University,
done at 9 weeks’ and DNA was amplified by PCR. (The primer kindly provided by Dr R. Kuijpers, Amsterdam, were slightly modified.) The PCR product was digested with MspI, which yielded three fragments (55, 95, and 150 bp) consistent with the genotype HPA-1(a + b +). In accordance with this finding the father proved to be HPA-1(a + b -) on serological testing. Early typing of the fetus for platelet HPA-1polymorphism can be done by the PCR method. Especially in cases where the father is HPA-1(a + b + ) it is important to establish whether or not the fetus is HPA-1(a + ) because of the possibility of prophylatic treatment or abortion before the 12th week of gestation. was
sequences,
T. F. SLATER
Uxbridge UB8 3PH, UK
1 Riley PA, Slater TF. Pathogenesis of retrolental fibroplasia. Lancet 1969; ii: 265. 2. Slater TF, Riley PA. Free radical damage in retrolental fibroplasia. Lancet 1970; ii: 467. 3. Slater TF. Free radical mechanisms in tissue injury. Biochem J 1984; 222: 1-15. 4 Sies H. Oxidative stress. New York. Academic Press, 1985. 5 Slater TF Free radical mechanisms m tissue injury. London: Pion, 1972. 6 Fliesler SJ, Anderson RE. Chemistry and metabolism of lipids in the vertebrate retina. Progr Lipid Res 1983; 22: 79-131. 7 Burton GW, Joyce A, Ingold KU. Is vitamin E the only lipid-soluble chain-breaking antioxidant m human plasma and erythrocyte membranes? Arch Biochem Biophys
SIR,—The failure of vitamin E to prevent retinopathy of prematurity (ROP) does not exclude free-radical injury as the cause. Too much emphasis on treatment after the damage is done (ie, cryotherapy) distracts from interventions that may eliminate the cause. Many premature infants seem to have essentially no demonstrable plasma antioxidant activity, in part because of a lack of apot-ransferrin.1 If this is of central importance in the aetiology of ROPI,2 it may be possible to prevent this retinopathy in susceptible infants by prophylactic apotransferrin. Susceptibility would be assessed by measuring plasma iron-binding capacity. Alternatively, additional iron-binding capacity might be provided by intravenous administration of polymer-bound forms of desferrioxamine.3 Unmodified desferrioxamine seems to be toxic for premature newborn babiespossibly by causing unacceptable iron losses or by other, unknown mechanisms.4 Laboratory Service, Center,
VA Medical
Charleston, South Carolina 29403, USA
JEROME L. SULLIVAN
1 Sullivan JL. Iron, plasma antioxidants, and the "oxygen radical disease of prematurity". Am J Dis Child 1988; 142: 1341-44. 2 Sullivan JL Retinopathy of prematurity and iron: a modification of the oxygen hypothesis Pediatrics 1986, 78: 1171-72. 3 Hallaway PE, Eaton JW, Panter SS, Hedlund BE. Modulation of deferoxamine toxicity and clearance by covalent attachment to biocompatible polymers. Proc Natl Acad Sci USA 1989; 86: 10108-12. 4 deLemos RA, Roberts RJ, Coalson JJ, deLemos JA, Null DM, Gerstmann DR. Toxic effects associated with the administration of deferoxamine in the premature baboon with hyaline membrane disease Am J Dis Child 1990; 144: 915-19.
PCR for fetal
platelet HPA-1 alloantigen typing
SIR,—Dr Kuijpers and colleagues (Nov 24, p 1319) report typing platelets for HPA-1alloantigens with restriction fragment length polymorphism analysis (RFLP) on DNA prepared from a fetal blood sample taken at 28 weeks. We have used the polymerase chain reaction (PCR) for HPA-1 typing (Zw or PI) on DNA of fetal
prepared from chorionic villus tissue obtained from a 9-week fetus. An alloimmunised HPA-1(a -) woman who had given birth to three thrombocytopenic children (one of whom died in utero after severe haemorrhage) sought advice from the department of obstetrics in the 8th week of pregnancy. A chorionic villus biopsy
ARNE SVEJGAARD
Denmark
Department of Obstetrics and Gynaecology,
JOHANNES BOCK
Rigshospitalet
Is bracken
1983, 221: 381-90 8 Nielsen JC, Naash MI, Anderson RE. The regional distribution of vitamins E and C in mature and premature human retinas. J Invest Ophthalmol Vis Sci 1988, 29: 22-26. 9. Ingold KU, Burton GW, Foster DO, Hughes L, Lindsay DA, Webb A. Biokinetics of, and discrimination between, dietary RRR- and SRR- alpha-tocopherols in the male rat Lipids 1987; 22: 163-72. 10 Halliwell B, Guttendge JMC. Free radicals in biology and medicine, 2nd ed. Oxford: Clarendon Press, 1989
HANS MADSEN ELLEN TAANING JØRGEN GEORGSEN LARS P. RYDER
Department of Clinical Immunology, Tissue Typing Laboratory, Rigshospitalet, DK-2200 Copenhagen N,
a
health hazard?
SIR,—Dr Trotter (Dec 22/29, p 1563) raises several concerns for occupational physicians and rural general practitioners. Large numbers of people work in bracken-infested areas of the UK, many in farming (especially hill sheep farming), national parks, waste disposal, and forestry. Also, teachers may take students on visits to areas of high bracken cover. The evidence that bracken is carcinogenic to man is far from proven, and I am grateful that Trotter acknowledges the lack of evidence. Indeed it would be fair to say that there is no evidence that bracken is a human carcinogen. There are many theoretical carcinogens, for which there is no evidence of a hazard to man.
Lyme disease is another matter. This is present in the UK, and there is evidence of infection amongst countryside workers.1-3 The tick Ixodes ricinus is found inmost bracken-infested areas of the UK, and human tick bites do occur in exposed workers.1 Questioning of park rangers and foresters in Staffordshire has elicited little evidence of tick bites in this admittedly small population who are regularly exposed for 8-12 hours a day for six or seven days a week. Examination of deer carcasses after culling or an accident regularly revealed infestation with ticks. We know of no cases of overt Lyme disease in our working population. Exposed groups have been given information about the condition since late 1989 and protective clothing is supplied. This does not include respiratory protective equipment. Trotter’s claim that bracken "could pose a substantial threat to health in the UK" is unsubstantiated. The ubiquity of bracken in large areas of the UK, and its accelerating spread, because of agricultural changes, would suggest wide exposure of both working, recreational, and remote populations. Bracken is one of the most primitive botanical species known, and has been well established in the UK since prehistoric times; substantial working populations have been exposed with no evidence of a major health hazard. Great care must be taken in the choice of words when advising individuals and populations about the risk. As Trotter says, "to alarm the general public... would be irresponsible". Given the propensity for the media to publish highly selective and often inaccurate reports, rigorous risk assessment must be applied before advice is given. I submit that bracken is unlikely to pose a significant hazard to man.
Staffordshire County Council, Stafford ST16 2LN, UK
1.
E. S. HODGSON
Guy EC, Bateman DE, Martyn CN, et al. Lyme disease: prevalence and clinical importance of Borrelia burgdorferi specific IgG in forestry workers. Lancet 1989; i:
484-86. 2. Nathwani D, Hamlet N, Walker G
72-74. 3. Baird AG, Gillies
Lyme disease: a review. Br J Gen Pract 1990; 40:
JCM, Bone FJ, Dale BAS, Miscampbell NT. Prevalence of antibody indicating Lyme disease in farmers in Wigtownshire. Br Med J 1989; 299: 836-37.
from haemoglobin turnover. Redox reaction iron can initiate many damaging free-radical reactions.1O We contend that exposure of very premature infants to high-intensity light, especially during periods of raised oxygen tension, may initiate ocular damage. Attention should be given to the spectral energy characteristics and the intensity of emission of the ambient illumination in the neonatal environment. University College and Middlesex Hospital School of Medicine,
P. A. RILEY
London W1 Brunel University,
done at 9 weeks’ and DNA was amplified by PCR. (The primer kindly provided by Dr R. Kuijpers, Amsterdam, were slightly modified.) The PCR product was digested with MspI, which yielded three fragments (55, 95, and 150 bp) consistent with the genotype HPA-1(a + b +). In accordance with this finding the father proved to be HPA-1(a + b -) on serological testing. Early typing of the fetus for platelet HPA-1polymorphism can be done by the PCR method. Especially in cases where the father is HPA-1(a + b + ) it is important to establish whether or not the fetus is HPA-1(a + ) because of the possibility of prophylatic treatment or abortion before the 12th week of gestation. was
sequences,
T. F. SLATER
Uxbridge UB8 3PH, UK
1 Riley PA, Slater TF. Pathogenesis of retrolental fibroplasia. Lancet 1969; ii: 265. 2. Slater TF, Riley PA. Free radical damage in retrolental fibroplasia. Lancet 1970; ii: 467. 3. Slater TF. Free radical mechanisms in tissue injury. Biochem J 1984; 222: 1-15. 4 Sies H. Oxidative stress. New York. Academic Press, 1985. 5 Slater TF Free radical mechanisms m tissue injury. London: Pion, 1972. 6 Fliesler SJ, Anderson RE. Chemistry and metabolism of lipids in the vertebrate retina. Progr Lipid Res 1983; 22: 79-131. 7 Burton GW, Joyce A, Ingold KU. Is vitamin E the only lipid-soluble chain-breaking antioxidant m human plasma and erythrocyte membranes? Arch Biochem Biophys
SIR,—The failure of vitamin E to prevent retinopathy of prematurity (ROP) does not exclude free-radical injury as the cause. Too much emphasis on treatment after the damage is done (ie, cryotherapy) distracts from interventions that may eliminate the cause. Many premature infants seem to have essentially no demonstrable plasma antioxidant activity, in part because of a lack of apot-ransferrin.1 If this is of central importance in the aetiology of ROPI,2 it may be possible to prevent this retinopathy in susceptible infants by prophylactic apotransferrin. Susceptibility would be assessed by measuring plasma iron-binding capacity. Alternatively, additional iron-binding capacity might be provided by intravenous administration of polymer-bound forms of desferrioxamine.3 Unmodified desferrioxamine seems to be toxic for premature newborn babiespossibly by causing unacceptable iron losses or by other, unknown mechanisms.4 Laboratory Service, Center,
VA Medical
Charleston, South Carolina 29403, USA
JEROME L. SULLIVAN
1 Sullivan JL. Iron, plasma antioxidants, and the "oxygen radical disease of prematurity". Am J Dis Child 1988; 142: 1341-44. 2 Sullivan JL Retinopathy of prematurity and iron: a modification of the oxygen hypothesis Pediatrics 1986, 78: 1171-72. 3 Hallaway PE, Eaton JW, Panter SS, Hedlund BE. Modulation of deferoxamine toxicity and clearance by covalent attachment to biocompatible polymers. Proc Natl Acad Sci USA 1989; 86: 10108-12. 4 deLemos RA, Roberts RJ, Coalson JJ, deLemos JA, Null DM, Gerstmann DR. Toxic effects associated with the administration of deferoxamine in the premature baboon with hyaline membrane disease Am J Dis Child 1990; 144: 915-19.
PCR for fetal
platelet HPA-1 alloantigen typing
SIR,—Dr Kuijpers and colleagues (Nov 24, p 1319) report typing platelets for HPA-1alloantigens with restriction fragment length polymorphism analysis (RFLP) on DNA prepared from a fetal blood sample taken at 28 weeks. We have used the polymerase chain reaction (PCR) for HPA-1 typing (Zw or PI) on DNA of fetal
prepared from chorionic villus tissue obtained from a 9-week fetus. An alloimmunised HPA-1(a -) woman who had given birth to three thrombocytopenic children (one of whom died in utero after severe haemorrhage) sought advice from the department of obstetrics in the 8th week of pregnancy. A chorionic villus biopsy
ARNE SVEJGAARD
Denmark
Department of Obstetrics and Gynaecology,
JOHANNES BOCK
Rigshospitalet
Is bracken
1983, 221: 381-90 8 Nielsen JC, Naash MI, Anderson RE. The regional distribution of vitamins E and C in mature and premature human retinas. J Invest Ophthalmol Vis Sci 1988, 29: 22-26. 9. Ingold KU, Burton GW, Foster DO, Hughes L, Lindsay DA, Webb A. Biokinetics of, and discrimination between, dietary RRR- and SRR- alpha-tocopherols in the male rat Lipids 1987; 22: 163-72. 10 Halliwell B, Guttendge JMC. Free radicals in biology and medicine, 2nd ed. Oxford: Clarendon Press, 1989
HANS MADSEN ELLEN TAANING JØRGEN GEORGSEN LARS P. RYDER
Department of Clinical Immunology, Tissue Typing Laboratory, Rigshospitalet, DK-2200 Copenhagen N,
a
health hazard?
SIR,—Dr Trotter (Dec 22/29, p 1563) raises several concerns for occupational physicians and rural general practitioners. Large numbers of people work in bracken-infested areas of the UK, many in farming (especially hill sheep farming), national parks, waste disposal, and forestry. Also, teachers may take students on visits to areas of high bracken cover. The evidence that bracken is carcinogenic to man is far from proven, and I am grateful that Trotter acknowledges the lack of evidence. Indeed it would be fair to say that there is no evidence that bracken is a human carcinogen. There are many theoretical carcinogens, for which there is no evidence of a hazard to man.
Lyme disease is another matter. This is present in the UK, and there is evidence of infection amongst countryside workers.1-3 The tick Ixodes ricinus is found inmost bracken-infested areas of the UK, and human tick bites do occur in exposed workers.1 Questioning of park rangers and foresters in Staffordshire has elicited little evidence of tick bites in this admittedly small population who are regularly exposed for 8-12 hours a day for six or seven days a week. Examination of deer carcasses after culling or an accident regularly revealed infestation with ticks. We know of no cases of overt Lyme disease in our working population. Exposed groups have been given information about the condition since late 1989 and protective clothing is supplied. This does not include respiratory protective equipment. Trotter’s claim that bracken "could pose a substantial threat to health in the UK" is unsubstantiated. The ubiquity of bracken in large areas of the UK, and its accelerating spread, because of agricultural changes, would suggest wide exposure of both working, recreational, and remote populations. Bracken is one of the most primitive botanical species known, and has been well established in the UK since prehistoric times; substantial working populations have been exposed with no evidence of a major health hazard. Great care must be taken in the choice of words when advising individuals and populations about the risk. As Trotter says, "to alarm the general public... would be irresponsible". Given the propensity for the media to publish highly selective and often inaccurate reports, rigorous risk assessment must be applied before advice is given. I submit that bracken is unlikely to pose a significant hazard to man.
Staffordshire County Council, Stafford ST16 2LN, UK
1.
E. S. HODGSON
Guy EC, Bateman DE, Martyn CN, et al. Lyme disease: prevalence and clinical importance of Borrelia burgdorferi specific IgG in forestry workers. Lancet 1989; i:
484-86. 2. Nathwani D, Hamlet N, Walker G
72-74. 3. Baird AG, Gillies
Lyme disease: a review. Br J Gen Pract 1990; 40:
JCM, Bone FJ, Dale BAS, Miscampbell NT. Prevalence of antibody indicating Lyme disease in farmers in Wigtownshire. Br Med J 1989; 299: 836-37.