Is rapeseed really an allergenic plant? popular myths versus scientific realities.
Rapeseed (Brassica napus) is widely blamed for the increased incidence of allergic symptoms since its cultivation has been expanded considerably in recent years. Here, Denis Murphy examines the evidence for the allergenicity of rapeseed, and particularly its pollen, and concludes that it has only a minimal impact on public health.
Published: Immunology Today 20, 511-514, 1999
Author’s declared interests: In 1999, Denis Murphy was Head of the Brassica and Oilseeds Research Department, John lnnes Centre, Norwich Research Park, Norwich. In 2003 Denis Murphy published a booklet (titled GM Free Wales – admirable aspiration or misguided fantasy?) in opposition to the ban on GM crops in Wales advocated by the National Assembly of Wales. Murphy is a scientific researcher, consultant, advisor and educator in plant molecular biology and biotechnology. He advises a number of government agencies on crop biotechnology, both in the UK and overseas. He is currently Head of the Biotechnology Unit at the University of Glamorgan.
Denis Murphy’s current CV
With reference to Murphy’s CV, it is somewhat surprising that Murphy’s article was accepted for publishing in the highly respected scientific journal - Immunology Today. Since the early 1980s Murphy has undertaken extensive biotech research into oilseed rape crops and has published numerous papers. However it would appear that none of Murphy’s research appears to relate to immunology, immunotoxicology or allergy. Murphy has a vested interest in the oilseed and biotech industries and this most certainly would have influenced his decision making and created a biased opinion when reporting on the public health concerns associated with this lucrative dense monoculture. Perhaps if Murphy had at least presented his article in an unbiased way and included specific reference to published literature supporting the view that rapeseed was a public health concern, then this would have went some way to make his article much more palatable and balanced.
Even the article title denigrates the public health complaints by inferring these are popular myths. This is despite the recommendations prioritised in the IEH (Institute of Environment & Health) Assessment A3 published in 1997 in which the scientific committee recommended that much more detailed research should be undertaken to elucidate the public health concerns about oilseed rape.
This article raises serious questions about Murphy’s knowledge of allergy and immunology. If Murphy is fully qualified and experienced in immunology and allergy caused by environmental factors this does not come across in his article.
Murphy states that a popular public perception has been created about rapeseed cultivation being linked to increasing allergic symptoms, particularly among populations in the vicinity of the crop. This is nonsense. Murphy should have instead referred to the existence of published literature that supports the view that rapeseed is linked to increasing allergic type symptoms, particularly among populations in the vicinity of the crop, rather than stating that the public health complaint is merely a public perception (myth). Whilst it is true that agreement has not been reached in the literature regarding the link between rapeseed crops and ill health, one cannot ignore the fact that numerous scientific papers have concluded that oilseed rape is responsible for ill health in both occupationally and non-occupationally exposed individuals.
Murphy goes on to say that the purpose of the article is to examine the results of the latest scientific studies showing that there is no clear evidence that rapeseed has adverse effects on health. It is almost like Murphy has precluded rapeseed from being the cause before examining the literature.
Murphy discusses wind-borne pollen dispersal from rapeseed crops and concluded that the low incidence of out-breeding is evidence of the relative rarity of wind-borne pollen dispersal. This again is nonsense. Whilst it is indeed true that rapeseed is an entomophilous (insect pollinated) crop and as such airborne pollen dispersal is considerably less than wind pollinated plants like grass, a percentage of pollen will indeed become wind-borne and will therefore both contribute to crop pollination and be dispersed down-wind of the rape fields. From the literature, it is clear that wind-borne rapeseed pollen dispersal is not as rare as Murphy would lead us to believe.
On one hand Murphy attempts to dispel concerns that rapeseed pollen may be wind-borne, but yet he goes on to talk about pollen fragment dispersal and its interaction with atmospheric water and makes an analogy to thunderstorm asthma and its causal factors. I believe Murphy is out of his depth speculating about these different theories, particularly since the scientists are still not in agreement about the causal factors in thunderstorm asthma. Furthermore, it has already been established that wind-borne rapeseed pollen generally does not travel more than a few hundred metres from the edge of the field during the flowering phase. It is also generally accepted that rain drops washes out large airborne particles suspended in the airstream. Whilst raindrops can indeed cause dead pollen grains to fragment and become dispersed into the atmospheric aerosol, the biological structure and characteristics of rapeseed pollen released during the flowering phase, so well described by Murphy, does not appear to fit well with Murphy’s hypothesis.
Murphy states that early studies indicating a high incidence of rapeseed allergenicity have been challenged by more recent studies showing that such allergies are uncommon. The wording of this paragraph is misleading and creates the wrong impression. Firstly, all members of the brassica family are highly allergenic, which is well supported in the literature. It is my understanding from reading some of the recent papers that there was little to no standardisation in the plant extracts used for immunological testing for sensitisation in some of the earlier studies. This serious anomaly makes it almost impossible to compare the immunological test results of previous studies. As well as allergenicity, the route of contact, the level of exposure and the distance from source all play an important role in determining whether a person will become sensitised to rapeseed pollen. Primarily, due to physical constraints (i.e. large size of rapeseed pollen grains and its sticky outer-coating) the incidence of respiratory sensitisation is likely to be low in comparison to other smaller and ubiquitous pollen grains. The more recent studies appear to confirm this to be the case.
Murphy states that sensitised individuals tend to be atopic and react to a multiplicity of allergens as well as rapeseed. Whilst this observation is true it is open to misinterpretation and further underlines Murphy’s lack of understanding of IgE antibody-mediated immunological reactions. All IgE reactions by definition, are allergen specific. If an individual is tested and found to have reversible symptoms plus elevated levels of IgE to one type of pollen (e.g. grass pollen) this does not necessarily mean that the individual will also react to other types of pollen (e.g. rapeseed pollen). Murphy’s statement implies that atopic individuals should in some way be discounted from the findings of previous studies on the basis of their reactions to other allergens. This is nonsense. Sensitisation to a specific allergen can occur regardless of whether the individual is atopic. Furthermore, mono-sensitisation to a specific allergen is unusual. Individuals who react to one type of allergen will often react to other allergens. This is due to individual variances in immune system T-cell modulation.
Murphy states that although rapeseed is by no means a potent allergen, rare individuals have been found who exhibit monosensitisation to this pollen. As I said previously this is incorrect, all members of the brassica family are highly allergenic and this is confirmed in the literature.
Murphy discusses the fact that the small proteins from the brassica family are part of the large family of 2S albumins which are among the most abundant proteins found in edible seeds. It would appear that Murphy was trying to build a case that supports the view that rapeseed pollen is no more allergenic than many other types seed and that human cross-reactivity was possible with birch and grass pollen due to similarities in the protein structure and the prevalence of these types of pollen. However, this view is not supported in the literature. From the literature it is clear that IgE cross-reactivity can and does occur relative to foods and chemical derivatives from the brassica family but there is little evidence of IgE cross-reactivity outwith the brassica family. Cross-reactivity has also been reported between exposure to brassicas and the industrial chemical compound isocyanate. This is due to one of the chemicals derived from the brassicas (isothiocyanate) belonging to the isocyanate chemical family. Iothiocyanate is one of the naturally occurring breakdown products of glucosinolate which is released when the plant foliage has been wounded or macerated. Food condiments like mustard contain isothiocyanate, this is what gives mustard its “zing”.
Murphy plays down the allergenicity of rapeseed by stating that it is possible that sensitisation may occur in a small number of those subject to extensive occupational exposure to the plant. This view does not concur with that published in the literature which indicates that occupational exposure to rapeseed is hazardous to health. Fell reported in 1992 that 9 out of 29 (30%) research workers occupationally exposed to rapeseed pollen were skin test positive to the plant. Five of these employees also demonstrated positive nasal challenge and RAST tests to oilseed rape. Rapeseed therefore clearly fits the description of an occupational respiratory sensitiser. Exposure should therefore be controlled as prescribed in the COSHH (control of substances hazardous to health) regulations enforced by HSE (Health & Safety Executive).
Murphy speculates that because patients experiencing allergic symptoms with rapeseed are generally atopic, it is possible that most of the rapeseed allergic pool is a subset of the most extensive pool of patients with grass pollen allergies, who also recognise cross-reacting epitopes in rapeseed pollen. These remarks appear to have been fuelled from similar comments made in the IEH (Institute of Environment & Health) Assessment A3 published in 1997. Such speculation does not appear to have any scientific basis and is not supported in the literature. Brassica, grass and birch pollen may be of similar molecular weight, however, they are derived from different plant families and do not share immunological characteristics.
Murphy plays down the fact that many of the VOCs (volatile organic compounds) and secondary pollutants from rapeseed are classified irritants by the HSE (Health & Safety Executive) and states that these can potentially act as irritants.
Murphy goes on to say that it is unlikely that these compounds ever achieve concentrations high enough to cause physiological effects in humans. Apart from perhaps ozone (secondary pollutant not mentioned by Murphy) Murphy is correct with his observations. However, Murphy fails to take account of other factors like the cumulative effect, synergism and the interaction with other environmental factors. Furthermore many VOCs have the ability to cause haptenic reactions which can cause allergy type symptoms even although no measurable increase in IgE has been recorded.
Murphy is correct that VOCs are emitted from the crop right up until the crop is harvested. However, it is also correct to say that the quantity of VOCs emitted after the flowering phase drops off by a large order of magnitude. This is confirmed in the literature. Technically speaking, it may well be possible to detect the smell of rapeseed after flowering, however, there is no anecdotal evidence of public awareness or reported health concerns regarding this characteristic.
Murphy states that on the basis of the relatively limited clinical studies on the possible effect of VOCs from rapeseed, it can be concluded that there is no direct evidence to suggest that VOCs are responsible for adverse health effects. This is just a matter of semantics. Indeed Murphy is correct, no direct evidence can be found in the literature that suggests that VOCs are responsible for adverse health effects. If there was direct evidence in the literature, there would be no purpose to presenting this critique. My point is; Murphy was unable to locate direct evidence, however, there is strong inference in the literature that the VOCs from rapeseed are responsible. There is considerable direct evidence in the journals of occupational medicine that VOCs are responsible for adverse health effects in both the outdoor and indoor environments. The adverse health effects of VOCs on human health has been the subject of much research and has been found to be the single biggest contributor of symptoms during investigations into tight building syndrome. It would appear that Murphy refuses to look beyond narrow reductionist principles and as a result, this has clouded his judgement when trying to dispel concerns about the effects of rapeseed on human health.
Murphy makes specific reference to some of the conclusions made in the IEH (Institute of Environment & Health) Assessment A3 published in 1997. Murphy is correct to draw attention to the IEH statement that current available data suggests that allergic responses to oilseed rape make very little contribution to the overall burden of allergy in the UK and diagnoses of pollen allergy should be considered in the context of an increased prevalence of allergy in developed and developing countries. Again, this is clear evidence of reductionist principles nailed to the mast. It is disturbing to note such blinkered naivety from a committee of highly respected scientists. Of course the scientists are correct with their conclusions, however, it would appear someone forgot to tell the scientists that the symptoms may be caused by factors other than IgE antibody-mediated allergy and the public health concerns are relative only to areas local to where the crops are grown. It kind of reminds me of being at a children’s pantomime when the kids scream and point at the mad magician “it’s behind you”.
Murphy is correct that despite the IEH conclusions (outlined above) there is strong public perception that rapeseed crops contribute directly to allergic conditions and in particular to respiratory problems. The reasons for this should have been obvious to Murphy. The public see a continuing problem, but the scientists tell them there is no direct evidence of harm. More semantics I fear. “Joe Public” does not know (and quite frankly does not care) about the different types of mechanisms, whether they are immunological or non-immunological. In the eyes of the public, people who live in close proximity to rapeseed crops continue to suffer allergy type symptoms whilst nothing is being done to alleviate public suffering. This is exactly the reason why many allergists advocate that the term ‘allergy’ should be all encompassing as Clemens von Pirquet originally proposed in 1906. If scientists used Pirquet’s original definition of allergy rather than the restricted 1926 definition, the scientists and public would not be in disagreement about the prevalence of allergy in areas where rapeseed is grown in close proximity to dwellings.
Murphy advises that it has been proposed that the public perception of the negative health effects from rapeseed in the UK could be linked to prejudice against Brussels bureaucrats due to subsides from the EU. Apart from Murphy taking Hemmer’s comments out of context, this is a further futile attempt to draw attention away from the real culprit. You don’t have to be a rocket scientist to work out that scientists would not have secured funding to research this subject had there been any doubt about the legitimacy of public health complaints about rapeseed crops. Furthermore, the IEH scientists would not have recommended further detailed research as a priority in IEH Assessment A3 published in 1997.
Murphy suggests that it would be interesting to carry out rigorous epidemiological studies of matched populations in different rape-producing countries in order to assess the role of psychological factors versus clinically provable factors relating to sensitivity to rapeseed. Whilst on face value this appears to be a reasonable suggestion, one has to consider what Murphy is suggesting here. Murphy obviously believes there is a psychological basis and wants an opportunity to test this theory. I don’t believe the psychological aspect needs to be tested, however, should this become a requirement it should not be tested until rapeseed crops have been proven beyond reasonable doubt to be safe and will not present risks to human health. The studying of matched populations in different rape-producing countries will be extremely difficult due to the large number of variable environmental factors and interactions.
Murphy concludes his article with the following statement; “Although it is important to continue to investigate potential health hazards, we should not unnecessarily stigmatise an important and versatile crop that can provide, not only a nutritious edible oil but also a huge spectrum of environmentally friendly, renewable industrial products ranging from lubricants and cosmetics to biodegradable plastics”. This conclusion is not surprising from a person whose career is centred around the development of this lucrative and important oilseed crop. Murphy has obviously failed to consider the duty of care or the legal ramifications of suggesting that research scientists ignore the precautionary principle (EC health and environmental law) that demands that health considerations be put before commercial gain. The stigma that rapeseed is responsible for causing illness in normally healthy rural dwellers should remain until scientists can provide conclusive evidence the rapeseed is not responsible for causing ill health in individuals who live in close proximity to fields of rapeseed.
In a follow-up reply to a letter published in Immunology Today 2000 in which Jones, et al clarify that cross-reactivity between oilseed rape pollen and grass pollen has been ruled out, Murphy reveals his true colours when he attempts to defend his initial comments that rapeseed pollen does cross-react with grass pollen. Murphy promotes GM (genetic modification) technology in a totally in appropriate manner by suggesting that transgenic rapeseed maybe the answer to allergy problems across the world. Murphy even talks of hypoallergenic pollen, which is somewhat astonishing given that this term is solely used to describe ingredients of consumer products like shampoo and other personal hygiene products. Describing pollen of any description (even if it is derived from transgenic crops) as hypoallergenic is simply nonsense and is most certainly not scientific reality.
Copyright - Armitage: 2007