808
Oilseed rape not a potent antigen SiR,--0ur experience with oilseed rape (Brassica napus) pollen as an
NUMBERS OF INFANTS GROUPED BY SERUM IgE IN NEONATAL PERIOD AND ATOPIC MANIFESTATION IN FIRSTYEAR
allergen is different from that of Parratt et al,l who found 26 3%
positivity (mild to moderate) to oilseed rape pollen in Dundee and 7-8% positivity (mild to moderate) in Glasgow (p < 0-005) with the ’Phadebas’RAST kits (Pharmacia). Between April, 1989, and July, 1990, we skin-tested 45 male and 36 female atopic children aged 3-14 years for oilseed rape pollen allergy with the ’Solu’ prick solution (ALK, Denmark). Asthma, hay fever, or allergic rhinitis was diagnosed clinically in each child on the basis of history, examination, skin tests, and pulmonary function tests where applicable. Oilseed rape pollen allergy was suspected clinically in all the children investigated. RESULTS OF MOST COMMONLY TESTED AGENTS IN 81 ATOPIC CHILDREN
Oilseed rape has been widely cultivated in the Grampian region of Scotland since 1982 because of European Community subsidies, and contact with the plant cannot be avoided in the countryside. Oilseed rape pollen has been incriminated anecdotally as a cause of asthma, hay fever, and allergic rhinitis, though we can find only one other report of sensitisation.2 The children were tested for 5-15 (mean 8) agents.3 Oilseed rape pollen was weakly positive (flare of up to 5 mm with no wheal) in only 4 of the 81 children, 2 of whom were positive in the pollen season. All 4 children were positive to at least 6 other agents tested. Contrary to Parratt and colleagues’t findings with RAST our skin-tests suggest that oilseed rape pollen causes infrequent and only mild sensitisation, and do not support concern that oilseed rape pollen is - a potent source of sensitisation. The strong perfume emitted or agricultural fungicides and pesticides may well have caused symptoms. TITUS K. NINAN Department of Medical Paediatrics, VALERIE MILNE Aberdeen Children’s Hospital, Royal GEORGE RUSSELL Aberdeen AB9 2ZG, UK
measured by an ultrasensitive ELI SA with a lower limit of detection of 0-02 IU(m1.5 Concentrations of 0-7 IU/ml and over were regarded as raised. 41 of 79 infants (52%) had atopic manifestations in the first year (table). 19 had more than one manifestation. However, only 10% (4/41) had a raised IgE in the neonatal period, and 32% (13/41) had detectable concentrations. Both eczema and a positive skin test were present in 12 infants, none of whom had a raised IgE in the newborn period. Thus application of these strict criteria reduced the prevalence rate to nil (table). In a large Swedish study of 1651 unselected children, 12-6% had raised cord blood IgE (> 0-9 IU/ml), yet the prevalence of "obvious atopic disease" after 7 years’ follow-up was 18-2%. Indeed, only 40% of the atopic children had had raised cord IgE. In another study only 6 % of 5305 newborn babies had a cord blood IgE of over 0-7 IU(rnl,6 whereas atopic disease might be expected in 15%.’ Thus population studies also suggest that many, if not most, children with atopic disease do not have raised IgE in the newborn period. Those who do may represent a special group with especially increased IgE responsiveness. IgE screening may therefore be useful in the selection of such infants for research investigations, but there is certainly no place for generalised screening in clinical practice.2 Furthermore, its use in the identification of candidates for allergy preventive measures when the risk according to family history is intermediate 1-3 (eg, atopy in one parent) cannot be supported because a low IgE in the newborn period can offer no reassurance that the baby will not be affected. Departments of Child Health and Thoracic Medicine, King’s College School of Medicine and Dentistry,
R. G. G. RUIZ
London SE5 9PJ, UK
J. F. PRICE
Department of Allergy and Allied Respiratory Disorders, UMDS, Guy’s Campus, London
D. RICHARDS D. M. KEMENY
Kjellman N-IM, Croner S. Cord blood IgE determination for allergy prediction a follow-up to seven years of age in 1651 children. Ann Allergy 1984; 53: 167-71. 2. Duchateau J, Casimir G. Neonatal serum IgE as predictor of atopy. Lancet 1983; i: 1.
413-14.
Bousquet J, Menardo J-L, Michel F-B. Predictive capacity of cord blood IgE for the development of allergy m infancy and childhood. Ann Allergy 1984; 53: 692-95 4. Matthew DJ, Taylor B, Norman AP, Turner MW, Soothill JF. Prevention of eczema. Lancet 1977; 1: 321-24. 5. Kemeny DM, Richards D, Johannsson A, Durnin S. Ultrasensitive enzyme-linked immunosorbent assays (ELISA) for detection of picogram quantities of IgE and IgE antibodies. J Immunol Meth 1989; 120: 251-58. 6. Kimpen J, Callaert H, Embrechts P, Bosmans E. Influence of sex and gestational age on cord blood IgE. Acta Paediatr Scand 1989; 78: 233-38. 7. Slavin R, Smith LJ. Epidemiologic consideration in atopic disease. In: Bierman CW, Pearlman DS, eds. Allergic disease of infancy, childhood and adolescence. Philadelphia: Saunders, 1980: 165. 3.
G, Saunders C, McSharry C, Cobb S. Oilseed rape as a potent antigen. Lancet 1990; 335: 121-22. 2. Medwinig B. Immediate hypersensitivity to mustard and rape. Contact Dermatitis 1. Parratt D, Thomson
1985; 13: 121-22. 3. Russell G, Jones PS. Selection of skin tests m childhood asthma. Br 70: 104-06.
J Dis Chest 1976;
Lack of relation between IgE in neonatal period and later atopy SIR,-Atopic disease develops in most infants with raised serum IgE in the neonatal period, often in the first year.1-3 However, this does not mean that most atopic infants have high IgE in the neonatal period. We have investigated the relation of IgE in the neonatal period and atopy in infants. Serum was obtained by heel prick at age 7 days during routine screening for phenylketonuria and hypothyroidism in 41 female and 38 male infants. They were selected on the basis of a history of atopy in both parents, with skin-prick test positivity confirmed in at least one. All had full hospital assessments, which included skin-prick testing by the same investigator at 3, 6, and 12 months. They were also seen at home if they had a cough, to check for wheezing. Atopic manifestations were grade 2 or 3 eczema,’ wheezing on at least two occasions, and a positive skin-prick test. Total serum IgE was
Latex
as
aeroallergen
SIR,-Dr Lagier and colleagues’ report (Aug 25, p 517) of a patient in whom asthma developed as a consequence of wearing latex gloves is of considerable interest. They attribute the disease in their patient to exposure to particles of latex in the glove powder. They do not, however, report any investigation of the powder to confirm the presence of such particles. They contrast their patient with one, reported by myself and others,l who also had asthma caused by the use of latex gloves. Our patient, however, reacted only to one make of latex gloves and had no reaction to several others. We measured the vapour given off by the gloves and were able to identify D-carene, which we believed to be a natural contaminant of the latex
Oilseed rape not a potent antigen SiR,--0ur experience with oilseed rape (Brassica napus) pollen as an
NUMBERS OF INFANTS GROUPED BY SERUM IgE IN NEONATAL PERIOD AND ATOPIC MANIFESTATION IN FIRSTYEAR
allergen is different from that of Parratt et al,l who found 26 3%
positivity (mild to moderate) to oilseed rape pollen in Dundee and 7-8% positivity (mild to moderate) in Glasgow (p < 0-005) with the ’Phadebas’RAST kits (Pharmacia). Between April, 1989, and July, 1990, we skin-tested 45 male and 36 female atopic children aged 3-14 years for oilseed rape pollen allergy with the ’Solu’ prick solution (ALK, Denmark). Asthma, hay fever, or allergic rhinitis was diagnosed clinically in each child on the basis of history, examination, skin tests, and pulmonary function tests where applicable. Oilseed rape pollen allergy was suspected clinically in all the children investigated. RESULTS OF MOST COMMONLY TESTED AGENTS IN 81 ATOPIC CHILDREN
Oilseed rape has been widely cultivated in the Grampian region of Scotland since 1982 because of European Community subsidies, and contact with the plant cannot be avoided in the countryside. Oilseed rape pollen has been incriminated anecdotally as a cause of asthma, hay fever, and allergic rhinitis, though we can find only one other report of sensitisation.2 The children were tested for 5-15 (mean 8) agents.3 Oilseed rape pollen was weakly positive (flare of up to 5 mm with no wheal) in only 4 of the 81 children, 2 of whom were positive in the pollen season. All 4 children were positive to at least 6 other agents tested. Contrary to Parratt and colleagues’t findings with RAST our skin-tests suggest that oilseed rape pollen causes infrequent and only mild sensitisation, and do not support concern that oilseed rape pollen is - a potent source of sensitisation. The strong perfume emitted or agricultural fungicides and pesticides may well have caused symptoms. TITUS K. NINAN Department of Medical Paediatrics, VALERIE MILNE Aberdeen Children’s Hospital, Royal GEORGE RUSSELL Aberdeen AB9 2ZG, UK
measured by an ultrasensitive ELI SA with a lower limit of detection of 0-02 IU(m1.5 Concentrations of 0-7 IU/ml and over were regarded as raised. 41 of 79 infants (52%) had atopic manifestations in the first year (table). 19 had more than one manifestation. However, only 10% (4/41) had a raised IgE in the neonatal period, and 32% (13/41) had detectable concentrations. Both eczema and a positive skin test were present in 12 infants, none of whom had a raised IgE in the newborn period. Thus application of these strict criteria reduced the prevalence rate to nil (table). In a large Swedish study of 1651 unselected children, 12-6% had raised cord blood IgE (> 0-9 IU/ml), yet the prevalence of "obvious atopic disease" after 7 years’ follow-up was 18-2%. Indeed, only 40% of the atopic children had had raised cord IgE. In another study only 6 % of 5305 newborn babies had a cord blood IgE of over 0-7 IU(rnl,6 whereas atopic disease might be expected in 15%.’ Thus population studies also suggest that many, if not most, children with atopic disease do not have raised IgE in the newborn period. Those who do may represent a special group with especially increased IgE responsiveness. IgE screening may therefore be useful in the selection of such infants for research investigations, but there is certainly no place for generalised screening in clinical practice.2 Furthermore, its use in the identification of candidates for allergy preventive measures when the risk according to family history is intermediate 1-3 (eg, atopy in one parent) cannot be supported because a low IgE in the newborn period can offer no reassurance that the baby will not be affected. Departments of Child Health and Thoracic Medicine, King’s College School of Medicine and Dentistry,
R. G. G. RUIZ
London SE5 9PJ, UK
J. F. PRICE
Department of Allergy and Allied Respiratory Disorders, UMDS, Guy’s Campus, London
D. RICHARDS D. M. KEMENY
Kjellman N-IM, Croner S. Cord blood IgE determination for allergy prediction a follow-up to seven years of age in 1651 children. Ann Allergy 1984; 53: 167-71. 2. Duchateau J, Casimir G. Neonatal serum IgE as predictor of atopy. Lancet 1983; i: 1.
413-14.
Bousquet J, Menardo J-L, Michel F-B. Predictive capacity of cord blood IgE for the development of allergy m infancy and childhood. Ann Allergy 1984; 53: 692-95 4. Matthew DJ, Taylor B, Norman AP, Turner MW, Soothill JF. Prevention of eczema. Lancet 1977; 1: 321-24. 5. Kemeny DM, Richards D, Johannsson A, Durnin S. Ultrasensitive enzyme-linked immunosorbent assays (ELISA) for detection of picogram quantities of IgE and IgE antibodies. J Immunol Meth 1989; 120: 251-58. 6. Kimpen J, Callaert H, Embrechts P, Bosmans E. Influence of sex and gestational age on cord blood IgE. Acta Paediatr Scand 1989; 78: 233-38. 7. Slavin R, Smith LJ. Epidemiologic consideration in atopic disease. In: Bierman CW, Pearlman DS, eds. Allergic disease of infancy, childhood and adolescence. Philadelphia: Saunders, 1980: 165. 3.
G, Saunders C, McSharry C, Cobb S. Oilseed rape as a potent antigen. Lancet 1990; 335: 121-22. 2. Medwinig B. Immediate hypersensitivity to mustard and rape. Contact Dermatitis 1. Parratt D, Thomson
1985; 13: 121-22. 3. Russell G, Jones PS. Selection of skin tests m childhood asthma. Br 70: 104-06.
J Dis Chest 1976;
Lack of relation between IgE in neonatal period and later atopy SIR,-Atopic disease develops in most infants with raised serum IgE in the neonatal period, often in the first year.1-3 However, this does not mean that most atopic infants have high IgE in the neonatal period. We have investigated the relation of IgE in the neonatal period and atopy in infants. Serum was obtained by heel prick at age 7 days during routine screening for phenylketonuria and hypothyroidism in 41 female and 38 male infants. They were selected on the basis of a history of atopy in both parents, with skin-prick test positivity confirmed in at least one. All had full hospital assessments, which included skin-prick testing by the same investigator at 3, 6, and 12 months. They were also seen at home if they had a cough, to check for wheezing. Atopic manifestations were grade 2 or 3 eczema,’ wheezing on at least two occasions, and a positive skin-prick test. Total serum IgE was
Latex
as
aeroallergen
SIR,-Dr Lagier and colleagues’ report (Aug 25, p 517) of a patient in whom asthma developed as a consequence of wearing latex gloves is of considerable interest. They attribute the disease in their patient to exposure to particles of latex in the glove powder. They do not, however, report any investigation of the powder to confirm the presence of such particles. They contrast their patient with one, reported by myself and others,l who also had asthma caused by the use of latex gloves. Our patient, however, reacted only to one make of latex gloves and had no reaction to several others. We measured the vapour given off by the gloves and were able to identify D-carene, which we believed to be a natural contaminant of the latex
