Rape

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Code: w203
Latin name: Brassica napus
Source material: Pollen
Family: Brassicaceae (Cruciferae)
Common names: Rape, Rapeseed, Rape Seed, Oilseed Rape, Rapa

See also: Rape seed f316 (B. napus)

Brassica napus is a variable species, with three subspecies: B. napus oleifera (Rape, Rapeseed etc.) B. napus napobrassica (Rutabagas/Swedes) and B. napus pabularia (Siberian Kale, Hanover Salad, etc.).

Allergen Exposure

Rape is an annual plant similar to Turnip and Rutabaga. It is thought that Brassica napus originated from a hybridisation between the Turnip (B. rapa) and Kale (B. oleracea acephala). Rape originated in northern Europe and was cultivated in the Mediterranean area, but is now grown throughout the world. Canola, a selected genetic variant of Rape, was developed in the late 1970's in Manitoba, Canada, as a more nutritious source of vegetable oil than Rapeseed.

The Rape plant is an annual/biennial growing up to 1.2m, with turnip-like flat leaves 10 to 30cm long, slick, and generally lobed. Unlike Turnips, they have no swollen root, only a thin taproot.

The plant flowers from May to August, producing yellow cross-shaped flowers with four petals. The flowers are hermaphrodite (have both male and female organs) and are primarily insect-pollinated. The plant is also self-fertilising. During the 3- to 4-week flowering period, the crop fields become a conspicuous part of the rural landscape, when bright-yellow flowers are produced and a characteristic odour from the released volatile organic compounds is evident.

The pollen grains are covered with sticky lipoidal substances which result in the grains sticking together. This reduces the ability of the pollen to be airborne for a significant period, and thus this pollen is usually a small fraction of the total atmospheric pollen load. It is possible that dead grains or fragments lacking the sticky coating could become airborne. Sickle-shaped pods containing tiny round seeds are produced.

Rape is cultivated in fields, but the plant may escape and grow on banks of streams, ditches and fields of other crops.

Rape is grown primarily for green livestock fodder, seed oil (called colza oil), and birdseed. The oil contained in the seed of some varieties of this species can be rich in erucic acid, which is toxic. However, modern cultivars have been selected that produce oil almost free of erucic acid, e.g., canola oil.

Allergen Exposure

Characterisation of Rape pollen allergens by immunoblot revealed major allergens of 6/8 kDa and 12/14 kDa, and in the high molecular weight range 33, 42, 51, 58/61 and 70 kDa. These results suggest that Rapeseed pollen is a moderate source of allergy and may sensitise despite low pollen exposure. (1)

A second study identified 2 low-molecular-weight allergens of 6/8 kDa and 14 kD as well as a high molecular-weight cluster (27-69 kDa). The 3 groups of allergens were recognised by 50, 34 and 80% respectively of serum of a group of Rape-allergic patients. (2) These allergens represent cross-reacting homologues of well-known pollen allergens, i.e., calcium-binding proteins, profilin, and high-molecular-weight glycoproteins. (2) The profilin allergens of Rape pollen (6/8 and 14 kDa) could be totally inhibited by Rye pollen and moderately by Birch pollen, while Mugwort had little effect. The 6/8-kDa Rape allergen’s binding could effectively be inhibited by rAln g 2, a calcium-binding protein from Alder. Carbohydrate Determinants appeared to be involved in IgE binding to the 27- to 69-kDa Rape allergens. Furthermore, Timothy Grass pollen proteins appeared to cross-react with the 27- to 69-kDa cluster. The authors suggest that via cross-reactivity, exposure to Rape pollen may be a prolonging and aggravating factor in underlying Birch and Grass pollen allergy. (2)

The following allergens have been characterised:

Bra n 4, a calcium-binding protein, previously known as Bra n 1. (3, 4, 5, 6, 7, 8, 9)

Bra n 7, a calcium-binding protein, previously known as Bra n 2. (2, 7, 8, 9)

Bra n 8, a profilin. (2, 10)

Bra n Polygalacturonase, a 43 kDa protein. (11)

Bra n Polygalacturonase was recognised by 5 of 18 Rape seed pollen allergic sera. kDa. (11)

In a study, a patient sensitive to Brassica pollen reacted to a B. rapa pollen-coat protein of 7.5 kDa, a lipid-binding protein (LTP). This suggests that, due to a taxonomical relationship, the presence of LTP in Rapeseed pollen may be possible. (12)

Potential Cross-Reactivity

An extensive cross-reactivity among the different individual species of the genus could be expected, as well as to a certain degree among members of the family Brassicaceae. (13)

Murphy reports that IgE antibodies, which reacts with most Rapeseed pollen allergens, also cross-reacts with Birch and Grass pollen allergens, which are far more prevalent in the atmosphere than Rapeseed allergens. (1, 2, 6, 14, 15) However, Welch et al. disagree, stating that the allergens of Rape and Grass pollen, although similar in molecular weights, are immunologically distinct and that there is no evidence of cross-reactivity between them, this study was limited to two subjects but indicates that species specific allergens may exist. (16, 17)

Rape pollen contains a profilin and a calcium-binding protein allergen, which may result in cross-reactivity between this plant and other non-Brassicaceae plants containing these panallergens. (2, 6, 10)

A calcium-binding protein allergen from pollen of Bermuda Grass (Cynodon dactylon) also shows significant sequence similarity with the Ca2+ binding pollen allergens from Birch (Bet v 4) and Oilseed Rape (Bra n 1). (6) A calcium-binding protein allergen from Olive tree pollen, Ole e 3, exhibits sequence similarity with pollen allergens from Brassica species. (18)

Clinical Experience

IgE mediated reactions

Rape seed pollen (and related irritants) can induce asthma, allergic rhinitis and allergic conjunctivitis. (19) It is still unclear whether Rape pollen is a common cause of allergic symptoms, or whether volatile organic compounds from Rape are more frequently responsible for these symptoms.

Early studies indicating a high incidence of Rapeseed allergenicity (20, 21) have been challenged by recent studies showing that such allergies are uncommon, even in areas of intense Rapeseed cultivation. (1, 15, 19, 22, 23, 24)

Fell et al. reported a low prevalence of allergy to Rape pollen (less than 0.2%), unless subjects were occupationally exposed. (22)

Soutar et al. took samples from 1000 randomly chosen adults, general practice patients living in two villages surrounded by Rape fields, and from 1000 adults from one village far from such cultivation. On a previously validated questionnaire, there were small but significant excesses of cough, wheeze, and headaches in spring in the Rape area (2.3% v. 1.1%, 6.8% v. 4.6%, and 4.8% v. 2.8%, respectively). Counts of Oilseed Rape pollen were generally low except adjacent to the Rape fields. Oilseed Rape was shown to give off terpenes, and these were detected close to fields. (23)

In a study of patients with a history of reactions to Rape pollen, only 2 of 23 tested showed evidence of allergy to Rape, and only 10 of 23 tested, including these 2, were shown to be atopic. Eye, nasal, and headache symptoms increased in the Rape season in some patients, validating a previous cross-sectional questionnaire. Twelve of 16 cases tested and 7 of 15 controls showed a seasonal fall in PC20; the fall in the cases was significantly greater than in the controls. However, peak flow charts showed no evidence of a fall or of increased variability during the Rape pollen season. The authors conclude that people who complained of symptoms in relation to the flowering of Rape were rarely allergic to the plant and fewer than half were atopic. Nevertheless, they usually showed increased bronchial reactivity during the season, which may have been due in some cases to other allergens but in others to non-specific irritant effects of the air. (25)

These results conflict with those of other studies. In southern and central Sweden, where Rape is cultivated, Rape pollen allergy was reported to occur quite frequently in patients with bronchial asthma and other allergic manifestations. In 366 consecutive patients, IgE antibodies to Rape pollen extracts was found in 23%. Of 54 patients with IgE antibodies to Rape pollen, 81% were positive on Rape pollen provocation tests. (20)

In 4,468 patients with suspected inhalant allergy investigated between June 1994 and May 1995, routine skin-prick testing demonstrated Rape pollen sensitisation in 7.1% of those found to be pollen-allergic. Mono-sensitisation was detected in nine patients. (1)

Twenty-five residents of a small Scottish village reported symptoms when Rape virtually surrounded the village. Symptoms varied during the growing season of the crop and were at their highest coincident with peak flowering. Increased symptoms were reported by 12 of the subjects, though only 7 of these were judged to be atopic. At the same period of the following year when the crop was absent, symptom reporting was significantly lower. The symptoms were sneezing, cough, headache, and eye irritation. The symptoms did not correlate with levels of Oilseed Rape pollen but there was no clear evidence as to which of the other factors associated with the crop might be the cause. (21)

Rape dust, and not pollen, should be considered as an asthma trigger. IgE- mediated occupational asthma was reported in an individual working with Rapeseed in the grain industry. (26)

Other reactions

Allergic reactions to Rapeseed and by-products, i.e., Rapeseed flour, have been described. See Rapeseed f316 for more information.

More than 22 volatile compounds have been identified as being emitted during the flowering period. The main constituents were the monoterpenes limonene, sabinene, beta-myrcene and alpha-farnesene (a sesquiterpene), linalool (a monoterpene alcohol), and the 'green leaf' volatile (E)-3-hexen-1-ol acetate. These compounds constituted between 50 and 87% (mean 68%) of the total volatiles emitted in all of the entrainments carried out with flowering Rape plants. The minor constituents included monoterpenes, sesquiterpenes, short-chain aldehydes and ketones, other 'green leaf' volatiles, and organic sulphides, including the respiratory irritant dimethyl disulphide. (27, 28)

Compiled by Dr Harris Steinman, harris@allergyadvisor.com

References

  1. Hemmer W, Focke M, Wantke F, Jager S, Gotz M, Jarisch R. Oilseed rape pollen is a potentially relevant allergen. Clin Exp Allergy 1997;27(2):156-61.
  2. Focke M, Hemmer W, Hayek B, Gotz M, Jarisch R. Identification of allergens in oilseed rape (Brassica napus) pollen. Int Arch Allergy Immunol 1998;117(2):105-12.
  3. Wopfner N, Dissertori O, Ferreira F, Lackner P. Calcium-binding proteins and their role in allergic diseases. Immunol Allergy Clin North Am 2007;27(1):29-44.
  4. Rozwadowski K, Zhao R, Jackman L, Huebert T, Burkhart WE, Hemmingsen SM, Greenwood J, Rothstein SJ. Characterization and immunolocalization of a cytosolic calcium-binding protein from Brassica napus and Arabidopsis pollen. Plant Physiol 1999;120(3):787-98.
  5. Focke M, Hemmer W, Hayek B, Gotz M, Jarisch R. Identification of allergens in oilseed rape (Brassica napus) pollen. Int Arch Allergy Immunol 1998;117(2):105-12.
  6. Smith PM, Xu H, Swoboda I, Singh MB. Identification of a Ca2+ binding protein as a new Bermuda grass pollen allergen Cyn d 7: IgE cross-reactivity with oilseed rape pollen allergen Bra r 1. Int Arch Allergy Immunol  1997;114(3):265-71.
  7. Toriyama K, Okada T, Watanabe M, Ide T, Ashida T, Xu H, Singh MB. A cDNA clone encoding an IgE-binding protein from Brassica anther has significant sequence similarity to Ca(2+)-binding proteins. Plant Mol Biol 1995;29(6):1157-65.
  8. 24887 Henzl MT, Davis ME, Tan A. Polcalcin divalent ion-binding behavior and thermal stability: comparison of Bet v 4, Bra n 1, and Bra n 2 to Phl p 7. Biochemistry 2010;49(10):2256-68.
  9. 21251 Verdino P, Barderas R, Villalba M, Westritschnig K, Valenta R, Rodriguez R, Keller W. Three-dimensional structure of the cross-reactive pollen allergen che a 3: visualizing cross-reactivity on the molecular surfaces of weed, grass, and tree pollen allergens. J Immunol 2008;180(4):2313-21.
  10. Focke M, Hemmer W, Valenta R, Gotz M, Jarisch R. Identification of oilseed rape (Brassica napus) pollen profilin as a cross-reactive allergen. Int Arch Allergy Immunol 2003;132(2):116-23.
  11. Chardin H, Mayer C, Senechal H, Poncet P, Clement G, Wal JM, Desvaux FX, Peltre G. Polygalacturonase (pectinase), a new oilseed rape allergen. Allergy 2003;58(5):407-11.
  12. Toriyama K, Hanaoka K, Okada T, Watanabe M. Molecular cloning of a cDNA encoding a pollen extracellular protein as a potential source of a pollen allergen in Brassica rapa. FEBS Lett 1998;424(3):234-8.
  13. Yman L. Botanical relations and immunological cross-reactions in pollen allergy. 2nd ed. Pharmacia Diagnostics AB. Uppsala. Sweden. 1982: ISBN 91-970475-09.
  14. Murphy DJ. Is rapeseed really an allergenic plant? Popular myths versus scientific realities. Immunol Today 1999;20(11):511-4.
  15. Hemmer W. The health effects of oilseed rape: myth or reality? No clear evidence that it has adverse effects on health. BMJ 1998;316(7141):1327-8.
  16. Welch J, Jones MG, Cullinan P, Coates OA, Newman Taylor AJ. Sensitization to oilseed rape is not due to cross-reactivity with grass pollen. Clin Exp Allergy 2000;30(3):370-5.
  17. Jones M, Welch J, Cullinan P, et al. Allergenicity of grass and oil rape pollen. Immunology Today 2000;21(3)155.
  18. Batanero E, Villalba M, Ledesma A, Puente XS, Rodriguez R. Ole e 3, an olive-tree allergen, belongs to a widespread family of pollen proteins. Eur J Biochem 1996;241(3):772-8.
  19. Seaton A, Soutar A. Oilseed rape and seasonal symptoms. Clin Exp Allergy 1994;24(12):1089-90.
  20. Bugur I, Arner B. Rape pollen allergy. Scand J Respir Dis 1978;59(4):222-7.
  21. Parratt D, Macfarlane Smith WH, Thomson G, Cameron LA, Butcher RD. Evidence that oilseed rape (Brassica napus ssp. oleifera) causes respiratory illness in rural dwellers. Scott Med J 1995;40(3):74-6.
  22. Fell PJ, Soulsby S, Blight MM, Brostoff J. Oilseed rape--a new allergen? Clin Exp Allergy 1992;22(4):501-5.
  23. Soutar A, Harker C, Seaton A, Brooke M, Marr I. Oilseed rape and seasonal symptoms: epidemiological and environmental studies. Thorax 1994;49(4):352-6.
  24. Ninan TK, Milne V, Russell G. Oilseed rape not a potent antigen. Lancet 1990;336(8718):808.
  25. Soutar A, Harker C, Seaton A, Packe G. Oilseed rape and bronchial reactivity. Occup Environ Med 1995;52(9):575-80.
  26. Suh CH, Park HS, Nahm DH, Kim HY. Oilseed rape allergy presented as occupational asthma in the grain industry. Clin Exp Allergy 1998;28(9):1159-63.
  27. Butcher RD, MacFarlane-Smith W, Robertson GW, Griffiths DW. The identification of potential aeroallergen/irritant(s) from oilseed rape (Brassica napus spp. oleifera): volatile organic compounds emitted during flowering progression. Clin Exp Allergy 1994;24(12):1105-14.
  28. McEwan M, Macfarlane Smith WH. Identification of volatile organic compounds emitted in the field by oilseed rape (Brassica napus ssp. oleifera) over the growing season. Clin Exp Allergy 1998;28(3):332-8.

As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.