Oilseed Rape Allergy

THE PRECAUTIONARY APPROACH TO OILSEED RAPE ALLERGY

- NOTE: Refer to Section (E) For Report conclusions -

(A) Is Oilseed Rape’s Reputation for Causing Allergy Justified?

Public concern about allergy symptoms from oilseed rape (OSR) has increased dramatically over the last five years as information filters through to the public via the national newspapers and television [l], suggesting a possible link with the dramatic increase in hay fever and asthma sufferers over the last decade, even horses [2] appear to suffer from OSR allergy (OSRA). However, in March 1993, Professor Seaton of Aberdeen University issued a public statement based on his interim results and advised that OSR's reputation was a media creation with no scientific basis [3].

(B) Are There any Restrictions Controlling The Planting of Oilseed Rape In Close Proximity to Residential Areas and Roadways?

This question was put to the European Commission in 1991 by a Scottish MEP., the Commission's response was as follows [4]: The Commission has not instituted any guidelines, nor does it intend to in the foreseeable future, which would prevent the sowing of OSR crops in close proximity to residential areas and roadways as it is not aware of any conclusive evidence to date indicating that the growing of such seed is harmful to human health. The Commission itself has not carried out any research on potential human health risks associated with exposure to OSR. The only research of which the Commission is aware concerns a three year project on the human health effects of the growing of OSR in progress at Aberdeen University, which was commissioned by the Scottish Office. The Commission awaits the results of this research with interest.

(C) What Aspects Of Oilseed Rape Can Cause Allergy?

The brassica family, which includes oilseed rape, mustard, cabbage and cauliflower, broccoli, brussels sprouts and radish.., is well documented for causing both antibody-mediated allergy and cell-mediated allergy [5].

Brassicas are characterized by a yield of volatile chemicals called isothiocyanates (ITCs) which are derived from biochemicals contained in the plant tissue and released by the plant's natural enzyme myrosinase during degradation of the plant materials [6].

ITCs have been well documented for causing allergic symptoms in patients who have had skin contact with or have ingested brassica derivatives [7]. In France 1987, Dr Gervais reported that patients who had developed occupational asthma due to exposure to isocyanates (organic chemical extensively used by the paint and plastic industries, and it is chemically related to ITC) also developed asthma after eating brassica condiments. This study confirmed that ITCs could also induce asthma [8]. In 1988, Dr Tollsten reported that ITC was one of many volatile substances found in the air space above brassica crops, including OSR [9].

Scientists have reported that OSR pollen (biological allergens) can be transported by wind and may travel in excess of 1km from the source [10]. Furthermore, it is suspected that the airborne pollen may also carry traces of ITCs [11].

Fungal spores thrive on OSR and they also can be transported large distances by the wind. Spores from field fungi are well documented for causing allergy and are particularly hazardous to asthmatics [12].

(D) What Are The Results Of Previous Oilseed Rape Allergy Studies?

The first person to be diagnosed with oilseed rape allergy was a farmer aged 30, from Sweden. The patient was diagnosed by Dr Colldahl in 1954, and was found to be suffering severe rhinitis, conjunctivitis and bronchial asthma when OSR was grown in close proximity to his house. He had no family history of allergy [13].

In Scandinavia 1978, Dr Bucur reported that for several years he had found a large and increasing number of patients who reacted to OSR skin tests. A number of his patients described severe rhinitis, conjunctivitis and asthma when passing by or staying near fields of OSR. Dr Bucur advised that it seemed obvious that sensitisation would occur, and concluded that patients suffering from similar symptoms in OSR regions, should be examined for OSR allergy [4].

In N.America 1979, Dr Lewis reported that 283 atopic patients were skin tested positive when tested with brassica pollen. Though OSR pollen was not specifically mentioned, Dr Lewis qualified this by stating that pollen from the brassica family is all very similar [15].

In Scotland between 1988 and 1993, Dr Parratt led a team of scientists who conducted numerous OSR allergy studies in Tayside region over a period of five years. After a clinical study involving RAST testing (blood testing) of patients in 1989, Dr Parratt reported that his findings supported the general public concern that OSR is a potent source of sensitisation [16].

In Scotland 1990, Prof Ninan reported after skin testing atopic children suspected of having OSR allergy, that his results supported the view that OSR pollen was not a potent allergen. He advised that the chemicals given off from the crops were the likely cause of OSR allergy, and a further study would be required to ascertain their effects on human health [17].

In England 1991, Dr Fell reported that his findings indicated a low prevalence of allergy to OSR pollen unless the subjects were occupationally exposed. Like Prof. Ninan, he too reported that research into the effects of the airborne volatiles was required [18].

In Scotland March 1993, Prof. Seaton reported interim results of his three year study of 2,000 people living in OSR and non-OSR areas. He advised that the results indicated no increase in symptoms in people living in OSR areas in comparison to those living in non-OSR areas. Prof. Seaton concluded that OSRs reputation was a media creation with no scientific basis [3].

It is interesting to note that Prof. Seaton's interim report was based on the results of a questionnaire [19] and had not in fact carried out clinical tests on any of the 2,000 interviewees.

(E) Conclusions and Recommendations

There is no doubt that oilseed rape pollen will cause allergic symptoms in established allergy sufferers who live, travel or work in close proximity to rape fields [20].

Introducing “new” allergens into the environment also creates a window of opportunity in people who have no past history of allergy [21]. The main determining factors in the development of allergy are the concentration of allergen, mode of contact, distance from source, immunocompetence and the total immune stress load [22].

As long as orthodox scientists continue to study and explain oilseed rape allergy using reductionist science, i.e. cause and effect [23], the health of the nation will suffer as scientists fail to identify the causation. Modern science requires modem “lateral thinking” which takes into account all variable interactions (and immune stressors) and their cumulative effects. This is called the precautionary approach [24], which is advocated by the European Commission [25].

The precautionary approach is not new to allergy, clinical ecologists have been studying cell-mediated allergy caused by environmental factors for decades [26] but it is only now that their efforts are coming to fruition, though the “old boy network” of orthodox scientists continue to ignore precautionary science and clinical ecology [27].

It is perhaps noteworthy that the precautionary approach shifts the burden of proof from the clinical ecologist, who previously had to prove that a threat existed, to the accused, who must prove using the same approach that a threat does not exist. When scientists wake up to this “new” way of thinking, the world will become a healthier place for most allergy sufferers [28].

Perhaps a starting point should be government recognition that oilseed rape may indeed be a hazard to human health and it therefore should be taking precautions to protect public health by introducing exclusion zones around residential areas, until at least oilseed rape allergy has been studied using the precautionary philosophy.

Future attempts to exonerate oilseed rape from causing widespread allergy should not be undertaken until both sides of allergy (antibody-mediated and cell-mediated) have been properly addressed by research scientists.

Author: Derek Armitage, February 1994

C.S.A.E.R.

(Community Support Against Exposure to Rapeseed)

Presented and circulated widely to the UK medical, environmental & scientific communities February 1994.

(F) References

1a Hay fever increase., ITN News At Ten broadcast 5/5/93.

1b. Allergy risk from crop., The Times, 15/9/89.

1c. The fields of misery lead to increase in health problems., Christie,B., The Scotsman, 21/5/92.

1d. Pollen count clue as best man dies on eve of wedding., Darlington & Stockton Times, 25/5/93.

2a. Horses may suffer from yellow peril., Young,R., The 25/8/87.

2b. Oilseed rape and equine respiratory disease., Hackett,I.J., The Veterinary Record, 14/7/90, p46.

2c. Pasture-associated seasonal respiratory disease in two horses., Dixon,P.M & McGorum,B .C., The Veterinary Record, 6: 1:90, p9-12.

2d. Headshaking in horses., Mair,T & Lane,G., In Practice, Sept 1990, p183-186.

3a. Scientists say oilseed rape’s yellow peril reputation is unfair., The Scotsman, 4/3/93.

3b. Oilseed rape: experts reject hazard claim., Parry,J., Farming News, 28/5/93.

4. Written Questions Nos 2414191 & 2415/91, Official Journal of The European Communities. No. C159/25,25:6:92., No. C209/14, 15:8:92.

5a. Cutaneous allergy to mustard in a salad maker., Dannaker,C.J & White,I.R., Contact Dermatitis., 1987: 16;212-214.

5b. Anaphylactic shock from mustard after ingestion of pizza., Panconesi,B et al., Contact Dermatitis, 1980:6;294.

5c. Contact Urticaria from cabbage., Calnan,C.D., Contact Dermatitis, 198 1 :7;279. 5d. A cauliflower allergy., Ketel,W.G.van., Contact Dermatitis, 1975:1;324.

5e. Allergic contact & dermatitis from radish., Mitchell,J & Jordan,W.P., British Journal of Dermatology, 197491; 183.

6a. Plants and plant products injurious to the skin., Mitchell,J & Rook,A., Botanical Dermatology .,Vancouver, Greengrass., 1979227.

6b. Item 9a. below, p4014.

7a. Immediate hypersensitivity to mustard and rape., Medwing,B ., Contact Dermatitis, 1985: 13;121-122.

7b. Item 5a. above. c. Item 6. above, p229.

8. The Initiator role of certain respiratory and skin contaminants in food allergies., Gervais,P et al., Allergie et Immunologic, vol19, No 1,1987, p7-11.

9a. Headspace volatiles of whole plants and macerated plant parts of brassica and sinapis., Tollsten,L & Bergstrom,G., Phytochemistry, 1988:27;4013-4018.

9b. Hay fever, the complete guide., Brostoff,J & Gamlin,L., 1993, p120.

10a. Wayward genes play the field., Young,S., New Scientist, 9/9/89, p49-53.

10b. Oilseed rape: “There is no evidence...”, Are we sure?., Cameron,L.A., Angus District Council OSRA Report, 31:8:90., p16-17.

10c. Item 9b. above, p4.

10d. Item 11a. above, p164.

11a. Preliminary observations on inhalation and intradermal challenges of horses with oilseed rape., McGorum,B.C & Dixon,P.M., The Veterinary Record, 1992: 13 1; 166.

11b. Item 10b. above, p17.

11c. Item 18. below, p504.

12a. Micro-organisms & Man., Noble,W.C & Naidoo, J., 1979.

12b. Man meets microbes., Jamison,J.R., 1977.

12c. Item 11a. above, p164.

13. Rape pollen allergy., Colldahl,H., Acta Allergol, 1954:7;367.

14. Rape pollen allergy., Bucur,I & Arner,B., Scandinavian Respiratory Disease, 1978:59;222-227.

15. North American pollinosis due to insect pollinated plants., Lewis,W.H & Vinay,P., Annals of Allergy, 1979:42;309-3 18.

16. Oilseed rape as a potent antigen., Parratt,D et al., The Lancet, 1990:335; 121.

17. Oilseed rape not a potent antigen., Ninan,T.K et al., The Lancet, 1990: 336;808.

18. Oilseed rape; a new allergen?., Fell,P.J et al., Clinical and Experimental Allergy, 1991:22;501-505.

19. Farming Today., Radio 4, broadcasted interview with Seaton, A., (private recording), 8/3/93.

20a Oilseed rape., Seaton,A., Letter published in Scotsman newspaper 13/3/93.

20b. (Private correspondence) Botheroyd, E.M., Health & Safety Executive, 17:9:93. 20c. Item 9b. above, p5.

21a. Allergic to the 20th Century., Taylor,A.N., Horizon transcript, transmitted BBC 1, 10/5/93, p15.

21b. Increase in allergens., Smith,F., Letter published in Scotsman newspaper, 2/6/93. 21c. Item 9b. above, p5.

22a. Overload., Steincamp,J., 1979.

22b. Charles Darwin's health problems: the allergy hypothesis., Smith,F., Journal of The History of Biology, vol 25 No2, Summer 1992, p285-306.

22c. Hypersensitivity, Essential Immunology., Roitt,I.M., 7th edition, 1991, chapter 12.

22d. The big sneeze., Gamlin,L., New Scientist, 2/6/90, p37-41.

22e. Not all in the mind., Mackarness, 1976, p18,77.

22f. Fit to drop., Fitzgerald,A., (BBC fact sheet) 1993.

22g. Item 9b. above, p5.

23a. How science fails the environment., Wynne,B & Mayer,S., New Scientist, 5/6/93, p33-35.

22b. The Rape of Canola, Kneen,B., 1992, p175.

22c. Item 9b. above, p120.

24a. Precautionary principle., Croner’s Environmental Management, April 1992, p1.185.

24b. Item 23a. above, p34.

25. The perils of green pessimism., Milne,A., New Scientist, 12/6/93, p36.

26a. Allergies: Your hidden enemy., Randolph,T & Moss,R., 1981.

26b. Chemical Victims., Mackarness,R., 1980.

26c. Editorial., The Lancet, 3:2:79.

26d. Item 22a.

26e. Item 22b.

27a Allergy and the immune system., Lichtenstein,L.M., Scientific American, Sept 1993; p92.

27b. Dirty air not to blame for asthma., Brown,W., New Scientist, 18:12:93, p5.

27c. Item 3a. above.

27d. Item 22a. above, Guardians for the earth, p206-210.

27e. Item 25. above.

27f. Item 26a above, p217.

28a. Not all in the mind., Mackarness,R., 1976, p38,39,76.

28b. Item 26a. above, 221,222.

28c. Item 26b. above, p25.

4 Replies

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  • Deek,

    I wish I could add some informed comment but my synapses melted after about the 10th para graph!

    -puts dunces cap on and stands in corner!!

    Bluejam.

  • eek I join you ;) in corner

  • Hi Bluejam & April,

    Yeah I do admit the report is a wee bit deep and difficult to read. Unfortunely the paper had to be presented this way to stand up to scientific scrutiny.

    I have added a note at the top of the thread to guide non-wig wearers (LOL) to the conclusions (Section E) where the main thrust of the paper can be found.

    Hope this helps a wee bit.

    Take hair,

    Derek

  • Thanks Deek.

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