w203 Rape

IgE-mediated reactions

Rape seed pollen (and related irritants) can induce asthma, allergic rhinitis and allergic conjunctivitis. (1) 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 (2,3) have been challenged by recent studies showing that such allergies are uncommon, even in areas of intense Rapeseed cultivation. (1,4-8)

Fell et al. reported a low prevalence of allergy to Rape pollen (less than 0.2%), unless subjects were occupationally exposed. (6)

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. (7)

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. (9)

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. (2)

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. (4)

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. (3)

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. (10)

Other reactions

Allergic reactions to Rapeseed and by-products, i.e., Rapeseed flour, have been described.

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. (11,12)

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. (4)

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. (13) These allergens represent cross-reacting homologues of well-known pollen allergens, i.e., calcium-binding proteins, profilin, and high-molecular-weight glycoproteins. (13) 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. (13)

The following allergens have been characterised:

• Bra n 4, a calcium-binding protein, previously known as Bra n 1. (14-19)
• Bra n 7, a calcium-binding protein, previously known as Bra n 2. (4, 18-20)
• Bra n 8, a profilin. (13, 16)
• Bra n Polygalacturonase, a 43 kDa protein. (22)
• Bra n Polygalacturonase was recognised by 5 of 18 Rape seed pollen allergic sera. kDa. (22)

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. (23)

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. (24)

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. (4,5,13,17,25) 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. (26,27)

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. (13, 17, 21)

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). (17) A calcium-binding protein allergen from Olive tree pollen, Ole e 3, exhibits sequence similarity with pollen allergens from Brassica species. (28)

Last reviewed: May 2022