Select Committee on Science and Technology Sixth Report

CHAPTER 5: Allergy and Our Environment


5.1.As discussed in Chapter 4, allergic disorders in the United Kingdom have now reached epidemic proportions. The environment in which we live, work and learn contributes to both the development (inception) of allergic conditions and the exacerbation of symptoms in those with established allergic disease. This Chapter examines the environmental conditions and everyday situations which may influence allergic disease, the ways in which these factors can be managed, and how the general public is educated about allergy.

The indoor environment


5.2.The extent to which the indoor environment impacts upon allergic diseases is uncertain. Asthma UK reported to us that poor housing could severely exacerbate asthma symptoms and that "damp conditions in particular allow common triggers for allergic asthma such as mould and housedust mites to thrive" (p 290). Professor Burney agreed that "there is quite good evidence that damp housing with mould causes problems, particularly for patients with asthma" (Q 130).

5.3.On the other hand, Professor Warner commented that "everybody lived in damp, cold housing one hundred years ago and there was much less allergy," so poor housing conditions are not necessarily the cause of increasing sensitisation rates (Q 130). Dr Harrison noted, "the fact that somebody is sensitised to housedust mite does not mean, however, that they will show any clinical symptoms" (Q 467). As the development of an allergic condition is not a single, linear process, it is therefore difficult to establish a direct relationship between a particular level of exposure and the development of symptoms.

5.4.In general terms, the points were summed up by Professor Warner, who told us that "once you are allergic and have a problem there is no doubt that living in damp, cold housing makes your problems worse" (Q 130). Although the indoor environment may not itself trigger the development of allergy, some factors may exacerbate symptoms and add to the burden for those already suffering from allergic disorders. It is important to note, as Dr Harrison reminded us, that responses to environmental conditions, for instance the presence of moulds, can also be "sensitivities or intolerances" rather than purely allergic responses" (Q 472).

5.5.In addition to biological triggers, various chemicals within the air can also exacerbate the symptoms of asthma. Professor Burney explained that high levels of nitrogen oxides from gas cooking can have "an adverse effect on patients with asthma" (Q 130) and the Department for Communities and Local Government (DCLG) reported that "as there are probably hundreds (or thousands) of chemical compounds in indoor air, it is not easy to identify the main ones that adversely effect health" (p 14). Professor Warner suggested that "by having energy saving we are creating tight homes which are increasing the levels of nitrogen oxides and volatile organic compounds which might be contributing to enhancing sensitisation in the first place. If we are going to have tighter housing for energy saving then we need proper ventilation systems with heat exchangers in order to achieve benefit for everybody" (Q 130).


5.6.Building Regulations aim to protect the health and safety of people in and around new buildings, but without reference to the occupants. In 2000 the legal requirement of Part F stated that "there shall be adequate means of ventilation provided for people in the building." The accompanying technical guidance (revised in 2006) takes account of energy costs, recommending "between about 0.5 and one air changes per hour," which the DCLG considered sufficient to control the levels of "moisture (to prevent mould growth), nitrogen dioxide, carbon monoxide, total volatile organic compounds and bio-effluents" (p 14).

5.7.The Housing Health and Safety Rating System covers existing housing and allows statutory enforcement of 29 health and safety hazards. Ms Anne Kirkham, from the DCLG, explained that relevant hazards included "damp and mould growth … fuel-combustion products where the impact of nitrogen dioxide and sulphur dioxide is also referenced … volatile organic compounds and the potential allergic responses, and … domestic hygiene, pests and refuse" (Q 83). Thus where an asthmatic person lives in a damp dwelling, "the authority might require a landlord to take more comprehensive or urgent action than it would require in a case involving an able-bodied and less susceptible occupier" (p 15).

5.8.The DCLG contributed to research by Gaia Architects to develop guidance on affordable low-allergy housing and in 2003, 14 affordable low-allergy homes were developed for the Fairfield Housing Cooperative in Perth, Scotland. Fairfield Director, Mr Grant Ager, explained that these homes tested methods to minimise allergy triggers and, by lowering the moisture within the buildings, decreased housedust mite breeding rates. This was done by installing "various ventilation strategies … mechanical heat recovery methods" and "breathing walls" and "breathing ceilings" to control the flow of air and level of water vapour (Q 489). The low allergy houses were also built to what Mr Ager called "non-toxic specifications," with wooden windows instead of Upvc, and which avoided the use of formaldehyde, paints containing volatile organic compounds (VOCs), and gas for cooking or heating (QQ 489, 491).

5.9.Mr Ager commented that residents "with asthma felt better and their reliance on inhalers and other medication decreased," but he also conceded that the sample was not big enough to give a conclusive answer (Q 492). Interestingly, during our visit to Germany, Professor Torsten Zuberbier, Head of the Department of Dermatology and Allergy, Universitätsmedizin Berlin, told us that the European Centre for Allergy Research Foundation granted "quality seals" to hotels with pet-free levels and "allergy-free" rooms, which often had wooden floors, dust mite protective bed covers and other features designed to reduce allergen exposure.[72]

5.10.Professor Warner warned that low allergy housing was very unlikely to "prevent allergy" (Q 132), and Professor Burney commented that "trials of dust mite avoidance in the home have been unsuccessful in reducing asthma symptoms and, paradoxically, may even lead to an increase in allergic sensitisation in children" (p 39). We therefore conclude that there is insufficient evidence to justify the inclusion of low-allergy measures within the Building Regulations at the current time. However, the EAACI noted that interventional studies had often focused on single interventions, "such as provision of mite-proof bedding in adults" and called for "further controlled trials involving multiple interventions … particularly in children" (p 67).

5.11.Chemical pollutants, such as VOCs, have been implicated as possible cofactors in allergy development. Dr Harrison wanted newer "low VOC emitting paints" to be used in the construction industry. He told us that some companies had started to label the emission levels of their products voluntarily and called for "the use of symbols and labels as well as possibly other regulations to encourage the manufacture and use of low emitting products" (Q 488).

5.12.To assess this, the research by Gaia Architects included "a feasibility study of introducing a scheme for labelling construction products according to … VOCs emissions" (p 15). However there also appeared to be a lack of availability of low pollutant-emitting building materials, as Mr Ager reported that it was "hard to source materials in the building centre" for the 14 low-allergy houses, and that the materials used could also be quite expensive (Q 482).

5.13.Asthma UK postulated that "public health policy and housing policy should be well co-ordinated at all levels of Government, and more attention could be paid to the improvement of housing conditions with specific regard to allergy and asthma" (p 290). Mr John Bromley, Head of National Service Reviews at the DH, told us that the Department was involved in "discussions with the trade bodies, the Construction Confederation and the National Federation of Builders" and that it was being proactive in examining how different forms of construction impacted upon inhabitants' health (Q 855). The Department of Trade and Industry was also co-ordinating a strategy for sustainable construction between Government departments and industry, and Mr Lewis suggested that there would be an "opportunity to influence what will come out of that" (Q 854, p 321).

5.14.We recommend that the Department of Health should work with the Department for Communities and Local Government to support and encourage controlled trials involving multiple interventions, to examine the effect of ventilation, humidity and mite-reduction strategies on allergy development and control. As chemicals used in the construction industry may play a role in triggering symptoms in some allergic patients, further evaluation of their role is also required in order to inform procurement policies.

The outdoor environment


5.15.A number of substances are known to exacerbate respiratory allergic diseases—particularly asthma—including ozone, nitrogen dioxide, sulphur dioxide and particulate matter (see Table 4).


Outdoor pollutants and their impact upon allergy
Pollutant SourceKnown health risks
Diesel exhaust particles (DEPs)Diesel engines DEPs can act as non-specific airway irritants and generate oxidants which have a deleterious effect on cells lining the airways. DEPs can also trigger the production of cytokines, chemokines, immunoglobulins and other proteins involved in the allergic response, suggesting that they may also be linked to the inception of allergic disease. People who live in high traffic areas with a high concentration of DEPs have been shown to suffer from enhanced allergic reactions compared to people who live in rural areas, suggesting that there may be an interaction between air pollution and allergens in the air[73]
Particulate matterParticulate matter is a complex mixture of acids, organic chemicals, metals and small particles of dust or soil. It can originate from natural sources such as dust storms and vegetation, or from industry and vehicle emissions of all types Exposure to particulate matter over a long period of time might inhibit lung development.[74] Studies have demonstrated that children living in polluted areas have poorer lung function and are more at risk of developing asthma during adolescence[75]
Ozone (O3)An oxidant pollutant generated at ground level by photochemical reactions involving ultraviolet radiation acting upon atmospheric mixtures of nitrogen dioxide and hydrocarbons from vehicle emissions The inhalation of ozone at high concentrations has been linked to an increased risk of asthma development; ozone can increase airway inflammation and responsiveness and can also potentiate the airway response to inhaled allergens.[76] Children are at greatest risk during the summer, when ozone levels are highest and children spend a greater proportion of time outdoors
Nitrogen dioxide (NO2)An oxidant pollutant, largely produced by vehicle exhaust, although it is also produced by power plants and other sources that burn fossil fuels Not usually associated with notable changes in bronchial function in asthmatic patients, but one study suggested that exposure to nitrogen dioxide increased the prevalence of asthma and rhinitis[77]
Sulphur dioxide (SO2)Largely produced by industry, following the combustion of coal and oil In asthmatic patients sulphur dioxide can induce acute constriction of the bronchi at concentrations much lower than those required to cause constriction in healthy individuals.[78] There is also evidence to suggest that sulphur dioxide can induce the development of asthma[79]

5.16.During the course of our inquiry we did not explore the role of the outdoor environment in great detail; the role it plays in allergy development is still controversial. The DH reported that in 1995 its Committee on the Medical Effects of Air Pollutants (COMEAP) published a report on Asthma and Outdoor Air Pollution, which concluded "with regard to the initiation of asthma … most of the available evidence did not support a causative role for outdoor air pollution. While it was accepted that exposure to air pollutants could produce a worsening of symptoms in those suffering from asthma, factors other than air pollution (diet and the role of infections, for instance) were more likely to have had more of an impact on the number of people suffering from asthma" (p 2).

5.17.However, since this report was produced a growing body of evidence has been published which suggests that urbanization, with its high levels of vehicle emissions, is linked to the rising frequency of respiratory allergic diseases observed in most industrialized countries (see Table 4). Professor Custovic told us that there is "an interesting body of evidence mounting on the potential role of outdoor air pollution … for example the way potentially diesel exhaust particles actually affect pollen grains and pollen allergens making them more allergenic" (Q 478). On our visit to Germany, Professor Heidrun Behrendt, Head, Centre for Allergy and Environment, Technical University Munich, told us that two groups of chemicals, polycyclic aromatic hydrocarbons (PAHs) and VOCs, could act as mediators in the allergic mechanism. Both PAHs and VOCs contain a carbonaceous core to which other compounds, such as diesel exhaust particles, can bind and when this complex in turn interacts with pollen, it acts as a potent sensitiser in allergy development.[80]

5.18.Air pollutants may therefore effect both the development and exacerbation of allergic conditions. COMEAP's report, Does Air Pollution Cause Asthma? is due to be published in 2008 (p 2).


5.19.An important and topical question is whether climate change is increasing the abundance of allergens in the air, such as pollen, which in turn may result in a greater incidence or severity of allergic diseases. There is some evidence that increased atmospheric levels of carbon dioxide fuel the growth of a species of poison ivy, a common cause of contact sensitivity in the United States.[81] In addition, over the last few years global warming has produced milder winters and earlier springs in the United Kingdom, which in turn have caused grass and tree pollen seasons to begin earlier.[82] Looking ahead, research has shown that when ragweed plants are grown under carbon dioxide levels predicted for the future, the plants produce significantly more pollen that when grown under today's conditions.[83]

5.20.Thus if levels of atmospheric carbon dioxide continue to rise, this may have serious consequences for allergy sufferers. With the current international interest in climate change, we therefore felt unable to ignore the consequences that climate change policies may have on allergy. Indeed, the impact of climate change and air pollution on all health is so significant that the Department for Environment, Food and Rural Affairs (Defra) has estimated that the "health effects associated with improved air quality typically account for 80 per cent of the total value of the ancillary effects of greenhouse gas mitigation policies."[84]

5.21.A report produced recently for Defra, Air Quality and Climate Change: A UK perspective, recommended that policies to tackle climate change and air pollution needed to be developed together. It noted that "the Government develops policies to safeguard human health and protect sensitive ecosystems by improving air quality. The Government also develops policies to reduce emissions of pollutants in order to limit climate change. These policies currently operate independently. There are, however, many linkages between the two types of pollution. The pollutants may have common emission sources and some pollutants affect both climate change and human health."[85]

5.22.As climate change and air pollution may significantly impact upon the development of allergic disease, we support the thrust of the recommendations in the report, Air Quality and Climate Change: A UK perspective. We recommend that when developing policies for industry, transport or housing, the Government should take account of the interlinkages between air quality, climate change and human health.

Allergy in the school environment

5.23.In Chapter 4, we outlined the burden that allergic disorders can place upon children at school. The school exam season in the early summer months coincides with the period of high pollen counts, so the examination performance of hayfever sufferers can be severely impaired not only by their symptoms[86] but also, as Professor Custovic noted, by the effects of "sedating antihistamines" which may be taken. He concluded that hayfever could therefore "affect the long term prospects … of quite a substantial proportion of our children" (Q 458), and the Royal College of Paediatrics and Child Health added that this could result in "reduced income" for these individuals (p 117).

5.24.Mr Chris Wells, Deputy Director for Special Educational Needs and Disability, DfES, told us that "the extent to which universities or schools make sure that they use well ventilated rooms, not right by a source of pollen … is a local issue which I cannot regulate for" (Q 82). But other witnesses felt that this issue should be addressed centrally. Ms Joy Winks, Chair of the School Nurses Forum, Royal College of Nursing, argued that "in some areas a child will be allowed to sit an exam at a different time or consideration will be taken of the fact that they have taken medication and in another area that does not happen. There is no consistency and I think that is the major problem" (Q 695). We feel that school nurses should play a role in ensuring that children are not given sedative antihistamines as a first-line therapy for hayfever.

5.25.As Mr Wells noted, the structure of the school year is based upon centuries of history (Q 81). It would not be practical to suggest an alteration of the examination timetable purely to benefit hayfever sufferers, especially as there are also many other non-allergic conditions which can impair children's examination performances. However, we note Mr Wells's comment that "young people do have the right to particular support if they have a condition which is going to seriously affect their likely performance" (Q 82). In light of the large number of children who suffer from hayfever, and the significant impact this can have upon their performance at school, the DfES does not appear to be addressing this issue sufficiently.


5.26.We recommend that the Department for Children, Schools and Families should review the clinical care that hayfever sufferers receive at school, and should reassess the way in which they are supported throughout the examination season. The Department for Children, Schools and Families should also ensure that the provisions made by different schools are fair and consistent.

5.27.In Chapter 4, we also noted that concern has been raised regarding the risks that food allergic children face within the school environment. The Anaphylaxis Campaign has "never been of the opinion that you should ban all nuts and all major [food] allergens in schools," but has expressed particular concern about the Government's recent "Transforming School Food" initiative which recommended that school vending machines should sell nuts and seeds. This contradicts the policy of many schools, especially primary and pre-schools, which "do not have nuts in school deliberately" and ask parents not to send nut, milk or egg products in with packed lunches. Secondary school children are more independent and have control of their own money so "a lot of these snack products will be provided through vending machines" where no advice is provided (Q 446, p 175).

5.28.We accept Mr Wells's general observation that "you cannot ban everything that could give rise to a shock." He commented that parents should "ensure the school understands that the child has … [an] allergy," and felt it was crucial that staff knew how to deal with that allergy appropriately (QQ 75-76). This made it all the more disappointing to receive evidence that allergies were poorly managed within the school environment. Mr Wells commented that "any nurse who administers an immunisation in a school setting will receive anaphylaxis update training on an annual basis" (Q 71). However, a questionnaire study of schools within the Severn area, conducted by the Anaphylaxis Campaign, showed that "44 per cent of the schools with an allergic pupil either did not have staff trained to administer medication or declined to respond to the questionnaire." Another study, conducted in the Nottingham area, identified "gaps in training for both school nurses and school staff … particularly for midday supervisors" (p 174).

5.29.Mr Lewis told us that "most school nurses are employed by Primary Care Trusts … [who] have responsibility for their training," but where a school employs the nurse directly, then the school "has a responsibility to secure adequate training" (Q 872). However, representatives from the School Nurses Forum of the Royal College of Nursing told us of funding problems in both the state and independent sector so "virtually across the nation at the moment school nurses are not being allowed to go on training … places have been cut" (Q 703). In 2006 the Anaphylaxis Campaign piloted a training programme for school nurses and planned to extend this training nationally in 2007-08 subject to "funding becoming available" (p 174). But as Ms Winks noted, it is likely "there will not be a nurse on site in the majority of the mainstream schools" when an anaphylactic emergency occurs (Q 699), so teachers and other staff must also know how to deal with allergic children.

5.30.The Government have made some progress in this area and in 2005 the DH and DfES jointly issued a guidance document named Managing Medicines in Schools and Early Years Settings. This sets out a framework to support children with medical needs and explains the responsibilities at every level from governors and staff to parents and carers. It recommends that an "individual health care plan" should be drawn up in consultation with the parents, child, general practitioner and staff, which details the medication the child should have in school, when it should be administered and by whom. [87]

5.31.The individual care plans assume that teachers and other school staff can deal with children's conditions and administer certain medications, but concern has been raised about the way in which this is assessed. Mr Wells felt it was the responsibility of the head teacher (Q 74) but Ms Winks told us that the head teacher "would not have the knowledge or the skill to be able to say that people are adequately trained." Head teachers therefore had to work "in partnership with somebody from the NHS" (Q 726), which might prove difficult when there is such a limited number of school nurses.

5.32.Finally, part of the problem in managing allergic disorders in schools stems from the fact that children themselves generally have a poor understanding of the conditions. An Australian programme used peer-group educators to teach children about asthma, using games, videos, worksheets or songs, and found it resulted in "an improvement in self reported quality of life in adolescents with asthma" and "a lower number of reported asthma attacks and school absenteeism."[88]

5.33.We support the use of individual care plans for children with medical needs, as described in the Government guidance Managing Medicines in Schools and Early Years Settings. However, we are concerned that many teachers and support staff within schools are not appropriately educated in how to deal with allergic emergencies. We recommend that the Department for Children, Schools and Families should audit the level of allergy training these staff receive, and should take urgent remedial action to improve this training where required.

5.34.An example of where staff education is paramount is the administration of adrenaline autoinjectors (such as Epipens or Anapens). Adrenaline autoinjectors are a prescription-only medicine, specific to each child. Ms Winks was in agreement with the DfES which said that if a child's healthcare plan "identifies that a child carries (or one is held at the school for) an Epipen or adrenaline shot treatment, then there is no reason why the teacher should not deliver it" (QQ 72, 714).

5.35.However, there has been debate regarding the number of autoinjectors prescribed to children. Dr Rosenthal suggested that adrenaline autoinjectors were overprescribed, saying "of countless prescriptions I have written over the last 12 years for such devices only one has ever been used" (p 253). Ms Winks, a school nurse in Sheffield for 15 years, added that although there were 70,000 school children in Sheffield, "I have never known one used" (QQ 702, 716-717). But Professor Hourihane disagreed, stating that all peanut allergic children should carry an autoinjector and that just to provide for peanut allergic children "we would need to increase the number of Epipens by a factor of more than six." He stressed the need for these children to socialise normally "with the extra caution that comes with an appropriate adrenaline kit. We do not want them to ever have to use it but we want them to have it available if they ever have to use it" (Q 674).

5.36.Furthermore, the Anaphylaxis Campaign suggested that it would be useful for schools to keep a stock so that "the generic autoinjector, held by the school, would be available for any child who may need a second dose" (p 179). However, the DfES did not support this idea because teachers "would not have the judgment" to discern whether this treatment was required (Q 72). The Royal College of Nursing agreed that schools should not be given this responsibility (p 271). Nevertheless, Mr Lewis was prepared to review the situation and "make some decisions about what is appropriate" (Q 871).

5.37.We are concerned about the lack of clear guidance regarding the administration of autoinjectors to children with anaphylactic shock in the school environment, and recommend that the Government should review the case for schools holding one or two generic autoinjectors.

Allergy in the workplace


5.38.The HSE reported to us that "chemicals and biological agents used in or arising from work activities can cause the same allergic diseases, and by the same mechanisms, as those in the more general environment" (p 8). The most common agents are shown in Table 3.

5.39.According to the HSE, the most commonly reported respiratory condition is occupational asthma, although "rhinitis and extrinsic allergic alveolitis (EAA) are also important" (p 8). The BOHRF noted that surveillance schemes most commonly received reports of occupational asthma from "paint sprayers, bakers and pastry makers, nurses, chemical workers, animal handlers, welders, food processing workers and timber workers" (p 339). It appears that a significant proportion of occupational asthma cases will have an allergic basis as Professor Newman Taylor told us, "hypersensitivity induced (or allergic) asthma occurs considerably more frequently than irritant induced asthma" (p 92).

5.40.The HSE added that "by far the most common type of work-related skin allergy is allergic contact dermatitis" (p 8). Dr Orton told us that occupational dermatological conditions were most commonly seen in "healthcare workers and hairdressers" as well as workers exposed to "sensitisers in the plastics industry and the construction industry" (Q 264). However, when estimating the incidence of occupational allergic disorders amongst different occupations, it is important to consider the number of workers within each industry. Professor Agius pointed out that although clinicians tended to see many cases of dermatitis reported from healthcare workers, "they constitute a large proportion of the working population and if we took their denominator into account then the risk amongst, say, hairdressers and beauticians is about 10 times higher than the risk amongst healthcare workers" (Q 264).

5.41.The extent to which the occupational agent plays a role in the development of disease, differs for each disorder. Both the BOHRF and HSE made the point that "the risk of sensitisation and occupational asthma is increased by higher exposure" to the occupational agent, although the risk of occupational asthma is increased by the presence of "atopy (in the case of high molecular weight allergens); smoking (low molecular weight allergens); and a particular genotype." In contrast, extrinsic allergic alveolitis is "most often due to a work exposure," is not associated with atopy, is less readily associated with specific genotypes and its risk appears to be reduced with smoking. Less is known about the development of occupational skin disease, but it is thought that "an individual with atopic dermatitis may be more prone to skin allergy and skin irritation in later life" (pp 8-9, 339).


5.42.Although it is difficult to estimate the true number of people who suffer from occupational allergic disorders (see Chapter 3), the prevalence and accompanying burden of occupational allergic conditions has a significant impact upon individual workers and the economy as a whole. The most reliable estimates suggest that the incidence of occupational allergic conditions may be on the decline (para 4.61).

5.43.Unfortunately the general trend of a decline in incidence is not universal across all occupational allergic diseases. Professor Newman Taylor reported that cases of occupational asthma "attributable to isocyanates is now less and the increase in the number of cases caused by latex allergy has decreased since the widespread use of low protein non-powdered rubber gloves. However, a similar decline has not occurred in the number of cases attributed to flour in bakery workers" (p 92).

5.44.The HSE reported that under the Control of Substances Hazardous to Health 2002 (as amended) Regulations (COSHH), employers must prevent or control exposure to harmful substances, and "all employees exposed, or liable to be exposed, to a substance that may cause occupational asthma or severe dermatitis should be under suitable health surveillance" (p 13).

5.45.To enhance the effectiveness of the COSHH regulations, the HSE said it was providing industry with free "task-specific COSHH guidance sheets tailored to a wide range of businesses and employees" (p 13). However, Mr Miguel felt that the COSHH regulations were "procedurally fine" but "identifying the sensitiser" in complex allergy cases could be difficult, and the guidance was too "generic" so did not necessarily help employers (Q 275). New EU regulations—Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH)—require manufacturers and importers of chemicals to provide safety information on substances and to manage their risks safely.[89] Mr Miguel felt that REACH might identify sensitisers in these materials if combined with existing COSHH legislation and "backed up further by UK legislation" (QQ 275, 277).

5.46.Dangerous chemicals are covered by the Chemicals (Hazard Information and Packaging for Supply) Regulations 2002, which require the supplier to "identify the hazards of the chemical, give information about the hazards to their customers and package the chemical safely" but as there was room for improvement, the HSE was "working with suppliers to achieve this." In 2005, specific legislation addressed skin allergens in the workplace, restricting the marketing and use of chromium (VI) in cement which "will have a very significant impact on the incidence of chromium-related skin allergy in workers exposed to cement" (p 13).

5.47.There is a limit to what can be achieved through regulation alone and past experience has shown that simple control measures can make a significant difference to the incidence of disease. For example, Professor Newman Taylor told us that latex allergy problems amongst healthcare workers had been caused by "the powder which the protein from the rubber was absorbing;" the use of gloves with no powder and a low protein content had essentially eliminated the problem. However such a simple solution was not always available for other occupational allergies. For instance, many animal handlers in laboratories develop allergy to proteins in animal urine, but neither these proteins or the animals can be encapsulated to prevent exposure. Instead, it is necessary to find ways to "prevent the urine deposited on the dust in the cage getting into the air and being inhaled" (Q 273).

5.48.In the words of Professor Newman Taylor, the prevention of occupational allergies is made harder by the fact that the structure of industry in the United Kingdom is changing "from manufacturing to service, with smaller workforces, smaller factories and more self-employed people." Whereas big companies might employ "occupational health physicians and safety advisors" to implement safety advice, it is more difficult to ensure safe working practices within businesses such as the "local hairdresser" (Q 273). In fact, the BOHRF noted that "only one in eight of the UK workforce has access to comprehensive occupational health support" (p 341). The key is therefore to raise awareness of occupational allergic conditions and to review the incentives for employers to ensure that "it is in their interests to ensure safe working conditions" (Q 273).

5.49.A number of HSE strategies have been developed to tackle the prevalence of occupational allergies. Occupational asthma and allergic contact dermatitis are priorities within its "Disease Reduction Programme" which aims, from a 2004 baseline, to reduce the incidence of these diseases by 10 per cent by 2008 (p 11). Mr Miguel noted the importance of running campaigns "in combination with the workforce through trade unions and employers" and so commended the Disease Reduction Programme Board which has been established to bring together "trade unions, employers" and "medical people" (Q 273).

5.50.More specifically, Mr Steve Coldrick, Head of the Disease Reduction Programme at the HSE, told us about the first "National Hairdressers' Day" in 2006, which had been organised to decrease dermatitis and change attitudes (Q 63). He told us that as part of the programme, "local authority environmental health officers … [were] visiting about 20,000 hairdressers over the coming year" to demonstrate "the use of gloves and moisturising cream … but later in the programme we will be turning to enforcement" (Q 64). But Professor Agius doubted "the extent to which education alone" would help and felt that efforts should be made to regulate "at the highest level … what manufacturers produce and what employers expect by way of work practices" (Q 275).

5.51.Initiatives to tackle occupational respiratory conditions include the HSE's establishment of an Asthma Project Board with "representatives from unions, industry, an asthma charity and health professionals." This aims to share information and reduce the incidence of occupational asthma by 30 per cent by 2010 compared with the 2000 baseline (p 11). The HSE, in partnership with Asthma UK and others, has produced a 10-step workplace charter to reduce asthma in the workplace,[90] and has also supported BOHRF to produce guidelines on occupational asthma. BOHRF described this work as the "world's first evidence based guidelines for occupational asthma hence the UK is seen as a world leader in this area along with Canada, France and Spain" (p 340).

5.52.The HSE has a planned "programme of evaluation" which will assess how its policies and advice have lowered the prevalence of occupational allergic conditions (p 11); although figures are not yet available, it is probably fair to assume that the work of the Health and Safety Executive has played a significant part.

5.53.We welcome the educational work of the Health and Safety Executive to raise awareness and decrease the risk of occupational allergic disorders amongst employers and staff, and would like to see this work developed. Once allergy centres have been developed (Chapter 9), we recommend that the HSE should liaise with the occupational allergy specialist in each centre to inform its policies and develop strategies to prevent occupational allergic disorders.


5.54.The BOHRF point to strong evidence that "the symptoms and functional impairment of occupational asthma caused by various agents may persist for many years after avoidance of further exposure to the causative agent" (p 339). This was reinforced by the HSE, which noted that those with prolonged exposure and more severe disease before diagnosis were likely to have a "poorer prognosis." In extrinsic allergic alveolitis, "irreversible fibrosis—scarring—of the lung" can develop, so even complete removal of the exposure will not lead to complete remission, although improvement may be seen over a number of years. Workers with skin allergy also need to avoid exposure to "control the progression of the disease and prevent the reoccurrence of symptoms" (p 9). However, Dr Orton added that "persistent post-occupational dermatitis" could sometimes occur where dermatitis persisted even after removal from the exposure (Q 280).

5.55.Diagnosis of occupational allergic conditions is often delayed due to a lack of education amongst general practitioners (Chapter 9), but once an occupational allergic condition is diagnosed, it is often necessary for the worker to give up their current occupation. As explained in paragraph 4.62, Industrial Injuries Disablement Benefit may be paid to workers, whether working or not, whose occupational allergic disorder causes chronic symptoms and a minimum degree of disability for over 90 days. However, this scheme provides benefits for all industrial illnesses in a uniform manner and may not necessarily be the best way to help people suffering from occupational allergic conditions.

5.56.Professor Newman Taylor noted that "if you can identify the disease sufficiently early there is the potential for it to resolve completely" (Q 280). However, it means that the worker will have to find alternative employment which does not involve exposure to that allergen and "there is evidence from a number of studies that those who leave their job because of occupational asthma can remain out of work for several years" (p 93).

5.57.There is therefore a real need to provide the means to support retraining schemes for these workers. In January 2007, the DWP published a consultation document to review the Industrial Injuries Disablement Benefit scheme.[91] The consultation period ended in April 2007, and Ministers have asked for further information on possible options before holding a review seminar, which is planned for October 2007. Professor Newman Taylor felt that "the introduction of a benefit which could support and enable re-training of individuals unable to continue in their current job … to enable them to remain in or return to work should be an important function of a reformed scheme" (p 93). Mr Miguel agreed with this and suggested that a "Government-led training initiative for people with allergies" should be established which involved job centres and employers working together (Q 289).

5.58.We are concerned that employees who are forced to leave work due to an occupational allergic disease can remain unemployed for long periods of time. We recommend that job centres should review the way they work with employers, to improve the way in which they can assist these workers to enter retraining schemes and find alternative employment.

72  Note of the visit to Germany, Appendix 6. Back

73  Riedl and Diaz-Sanchez, Journal of Allergy and Clinical Immunology 115, 2005, "Biology of diesel exhaust effects on respiratory function," pp 221-228. Back

74  Horak et al., European Respiratory Journal 19, 2002, "Particulate matter and lung function growth in children: a 3-yr follow-up study in Austrian schoolchildren," pp 838-845. Back

75  Islam et al., Thorax, 2007, "The Relationship between Air Pollution, Lung Function and Asthma in Adolescents," published online  Back

76  Bernstein et al., Journal of Allergy and Clinical Immunology 114, 2004, "Health effects of air pollution," pp 1116-1123. Back

77  de Marco et al., Clinical Experimental Allergy 32, 2002, "The impact of climate and traffic-related NO2 on the prevalence of asthma and allergic rhinitis in Italy," pp 1405-1412.  Back

78  Sheppard et al., American Review of Respiratory Disease 122, 1980, "Lower threshold and greater bronchomotor responsiveness of asthmatic subjects to sulfur dioxide," pp 873-878. Back

79  Andersson et al., European Respiratory Journal 27, 2006, "Incidence of asthma among workers exposed to sulphur dioxide and other irritant gases," pp 720-725. Back

80  Note of the visit to Germany, Appendix 6. Back

81  Mohan et al., Proceedings of the National Academy of Sciences of the United States of America 103, 2006, "Biomass and toxicity responses of poison ivy (Toxicodendron radicans) to elevated atmospheric CO2," pp 9086-9089. Back

82  Gilmour et al., Environmental Health Perspectives 114, 2006, "How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma,"
pp 627-633. 

83  Rogers et al., Environmental Health Perspectives 114, 2006, "Interaction of the Onset of Spring and Elevated Atmospheric CO2 on Ragweed (Ambrosia artemisiifolia L.) Pollen Production" pp 865-869. Back

84  Department for Environment, Food and Rural Affairs, Ancillary Effects of Green House Gas Mitigation Policies, 2002, p 7. Back

85  Air Quality Expert Group, Air Quality and Climate Change: A UK Perspective, Summary, 2007, Introduction.  Back

86  Walker et al., Clinical and Experimental Allergy 36, 2006, "Hayfever is associated with a significant detrimental impact on exam performance in UK teenagers: case-control study," p 1209. Back

87  DH and DfES, Managing Medicines in Schools and Early Years Settings, 2005.  Back

88  Shah et al., British Medical Journal 322, 2001, "Effect of peer led programme for asthma education in adolescents: cluster randomised controlled trial," (pp 583-587).  Back

89  See Back

90  Asthma UK, Asthma at Work-Your Charter, 2004.  Back

91  See Back

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