1. How can a person be sure that their asthma symptoms are caused by exposure to something at work? Are there specific tests?

There are three types of work-related asthma. The first type is related to an allergy to something in the workplace. In that case, patients note that the asthma clears up whenever they’re not at work or they’re on vacation. The second type is where there is pre-existing asthma; irritants at the work site will constantly aggravate the existing asthma, so that they always have a lot of minor attacks at work because there may be several things that bother them. The third type is irritant-induced asthma or reactive airways dysfunction syndrome (RADS), reactive airways dysfunction syndrome, which is due to a high level of exposure. In these cases, patients become immediately ill and require medical care, and they would have asthma subsequent to that.

The most common are the first two types. Testing for these would require seeing a specialist, who may do a variety of tests involving specific challenges. For instance, a doctor might do what is called a natural challenge, in which a peak flow meter is used to measure asthma attacks. A peak flow meter is routinely used by family doctors to monitor asthma. By blowing into a cylinder, the meter shows high or low numbers which represent a reliable, objective measurement of the severity of asthma. This device can easily be used at home or in the workplace. Patients can take measurements themselves using a peak flow meter for about two weeks at home, and then go back to work and do the same, to document for the physician if there are differences: this way you can tell if they are really having more asthma at work than at home. By keeping a diary of peak flow measurements, patterns can emerge: asthma may be better or worse at certain times of the day, which may also help in tracking irritants that may be exacerbating the asthma.

2. Are asthma symptoms very different in asthma with latency and asthma without latency?

Basically, asthma is asthma; symptoms are the same whether it is with or without latency. Only the initiation of attacks will be different. Asthma with latency, which is the allergy-related asthma, requires a long exposure of several months or years during which time a person develops an allergy or sensitivity to a chemical in the workplace. This is the type that gets better when the patient is away from work, on the weekends or on vacation. The other type of asthma, without latency, is the high-dose, sudden-onset asthma, which can be put down to a single exposure at one moment in time.

3. Can you explain briefly why you don’t have to be allergic to a substance to have an asthma attack?

Asthma without latency is due to an irritant. The irritant is of such high magnitude that it actually produces injury to the airways of the lung, similar to a respiratory infection or the type of injury induced by an allergic response that causes inflammation of the lungs. This inflammation persists for reasons that aren’t clear, but it is due to this persistent inflammation that they suffer from asthma.

4. Why is taking appropriate asthma medication to keep you on the job site not a good idea?

If you have the type of asthma that is irritant-induced (RADS) or if it is aggravated by some substances at work like cigarette smoke or welding fumes, medication in many cases will allow you to tolerate these exposures and be able to work. In contrast, if you are allergic to something specific, every time you’re exposed to it, your asthma worsens, and continues to increase in severity. There have been a few reports of allergic-type asthma or asthma with latency where the exposure has led to the death of a person. Once you are allergic or sensitized, it is recommended that you have no further exposure to the substance, because it can produce significant worsening and may have serious consequences. In these cases we recommend the person not return to work if the exposure can’t be avoided. This is in contrast to the irritant-type asthma, where the aggravation, even if it is acute and precipitates attacks, doesn’t severely injure the airways. Generally, this type of asthma is not specific to the workplace. In these people, medication seems to improve response to irritants and they can usually stay on the job.

For asthmatics in general, avoiding irritants is probably a good idea, as is getting appropriate medication.

To date, over 200 substances have been linked to occupational asthma with a latency period. Depending on the level of exposure, these triggers lead to asthma by precipitating immune responses characterized by IgE antibodies — the same function that sets off an allergic reaction to ragweed in many people.

Sudden onset of asthma (no latency period) can take place within minutes or hours of exposure, precipitate RADS, and can continue to cause asthma symptoms for years. In most cases, this kind of onset is due to an industrial accident, or ventilation of the workplace being compromised. Documented cases of such asthma attacks were triggered by uranium hexafluoride gas, spray paint with ammonia, fumigants, metal coating remover and smoke inhalation.

By-products of industrial manufacturing are heavily implicated in causing asthma symptoms. Allergic sensitization (associated with a latency period) is commonly caused by such materials as baking products and cotton dust. How much exposure is involved plays a large role in inducing symptoms of asthma, particularly in very dusty types of work. Polyurethane processing and foundry work are notable causes of asthma; millers and bakers exposed to grain dust have an asthma prevalence of up to 40%. If more hazardous activities are added to the list — pouring chemicals, blasting, sawing — the rate goes up even more.

Where the job site is located will affect asthma rates. For instance, western red cedar causes asthma in the western U.S., where it is native, and in Japan, where dock workers are exposed to it while unloading the ships that import the wood. An epidemic of asthma was caused in Barcelona, Spain, when a shipment of soybeans was unloaded in weather conditions that allowed dust from the beans to spread, demonstrating how climate conditions also affect the rate of asthma.

What can be done to reduce the risk factors for asthma in the workplace? Obviously, the ideal solution is to stay away from the kinds of employment that trigger asthma. As this is not always possible, employers should consider adopting strategies such as ensuring proper ventilation, providing personal protective devices (masks), rotating jobs to cut down on the amount of time a worker spends in a particular environment, and enforcing safety measures that eliminate the risk of an accident, such as a chemical spill.

While symptoms may clear up once a worker is no longer exposed to the irritant, many people find that the asthma persists and leads to the chronic airflow problems (hyperresponsiveness) typical of RADS. Further, the longer the exposure, the more chronic the asthma. Once asthma is diagnosed as being occupational in nature, it is not enough to merely open more windows or take a few more puffs on a bronchodilator. A serious discussion regarding options needs to take place between patient and doctor — away from the workplace.

1. What causes a sensitivity to a particular allergen or irritant?

There is a genetic predisposition in some individuals to become immunologically sensitized to different aeroallergens, like cat or house dust mite. The exact mechanism responsible for this genetic predisposition is unknown. It may have to do with the genetic predisposition to have inflammation of the lungs to begin with, which would make it easier for people to become sensitized and induce an immune response against things that they inhale. But this is an active area of research: while we know that the genetic predisposition is there and that it has a strong influence, we don’t know how it is linked to the sensitization process.

2. Briefly, would you explain why asthma and allergies are two distinct disorders, when they are so closely linked?

Asthma is related to inflammation in the airways of the lungs, while allergies result in inflammation of the eyes, skin or nose. Where the inflammation occurs determines whether it’s asthma or something else. Also, many people have both allergies and asthma, and the allergies can enhance the risk of having asthma. On the other hand, you can have allergies and not have a manifestation in the lungs. And you can also have asthma without having allergies. For example, for some kinds of asthma in the workplace, you can become sensitized to a chemical without a history of allergies whatsoever. Yet with repeated exposure to a chemical, you can develop this immunological response or sensitization anyway.

Asthma is such a complex — and confusing — topic because there are many different types of it: with or without allergies, as a result of airway damage from high-level exposure to a chemical, or even as a result of damage done by severe bronchitis.

3. Do pollutants cause allergies? That is, can they be allergens in the same way that house dust mite is an allergen?

This is very unlikely. The gases, the air pollutants like sulphur dioxide and ozone, can in and of themselves cause airway inflammation. But we’re not aware of anyone becoming truly allergic to any of these materials. These material are irritants, and they are much more likely to potentiate asthma in someone who already has a predisposition. For instance, many people think that they’re allergic to cigarette smoke, because every time they get exposed, they get their asthma. But for almost everyone, this is due to the irritant effect of the smoke and not to an allergy. People who have asthma are more sensitive to these irritants — sometimes exquisitely so, but it is not allergy.

4. In your paper you mention that asthma is much more prevalent among blacks than whites. Are your observations on the prevalence of cockroach allergen in the inner city relevant to this statistic?

We don’t really understand all of the epidemiology. Core inner-city people are more likely to have problems with cockroach allergy, and when you go up the social ladder between blacks and whites, the two groups do seem to have different patterns of sensitization. However, accounting for this is also complex and probably depends on factors such as location. Presumably, some years ago here in the northeastern U.S. when heating became much more expensive, people started living in more crowded conditions and had more carpeting and bedding, which increased the population of house dust mites and sensitization to them, which in turn increased the risk of asthma — which came to be seen as an inner city problem.

In a city like Atlanta, Georgia, the environment is very different from the northeast; it’s very wet and humid. The observation made about Atlanta is an interesting one, but as to why sensitization to cockroach is more prevalent there as opposed to house dust mite is still an open question.

Editorial:

This study makes it clear that the environment is a very important factor in asthma, and that different problems occur in different regions and population groups. It’s a very complicated area, in which there are no simple answers. One major aspect that we tried to present in the paper was that while the environment can be a cause of asthma, it can also be a trigger for it, independent of a causative factor. For instance, air pollution doesn’t cause asthma, as best we can tell, but you rarely get exacerbations of asthma outdoors unless you’re exercising — the air pollution worsens the existing asthma. The message here is that the environment is important both in causing and potentiating asthma.

The environment generates countless allergens and irritants, but sorting out which ones have an impact on asthma has important implications for treatment, especially as avoidance is one therapeutic option. The authors of this paper scrutinize environmentally induced asthma from three perspectives: by examining the role of air pollutants such as sulphur dioxide, nitrogen dioxide, and airborne acids; by looking at ways of controlling airborne allergens such as cat dander and dust mite; and by exploring the possibility that interactions between air pollutants and allergens may be responsible for additional detrimental effects on respiratory health.

Air Pollution

Controlled studies show that asthmatics are particularly sensitive to sulphur dioxide. Ordinary people can inhale as much as 5.0 parts per million of sulphur dioxide and experience only slight reductions in airway function. For asthmatics, as little as five minutes of sustained exposure to sulphur dioxide at concentrations of 1.0 parts per million or less produces pronounced bronchoconstriction. Elevated levels of ozone have also been linked to increased visits to the emergency room to treat acute asthma attacks but, interestingly, normal subjects appear to be as susceptible to ozone as asthmatics. However, more studies need to be done, as few to date have compared healthy and asthmatic subjects using the same criteria.

Airborne Allergens

While we know that certain allergens can provoke an acute asthma attack (the average encounter of an asthmatic with a cat will demonstrate this effect), the role of airborne or aeroallergens and chronic asthma can’t be quantified with such assurance. However, there is increasing evidence that chronic asthma and aeroallergens are connected.

Indoor allergens are basic to asthma almost everywhere: house dust mites, mice, cockroaches and pets are common triggers. The usual advice from specialists is to remove — as much as possible — the allergen from the home environment. Studies have demonstrated that this is a very effective method if strictly controlled. For dust mites, all bedding and mattresses should be encased in impermeable covers, bedding should be washed in very hot water (over 130F), and humidity levels kept well in hand. For cat allergen, removing the animal from a household is the best solution. The allergen is produced by the salivary and sweat glands of the cat (which it then carefully washes all over its coat). Cat hairs spreading throughout the household can keep the allergen in the air for months. But as many people are reluctant to give up a cherished pet, weekly washing of the animal and rigourous cleaning and removal of allergen reservoirs such as carpets can be helpful.

Outdoor allergens depend on geography. In Europe, olive trees create seasonal allergies the same way that ragweed does in North America. In Australia, researchers compared samples of dust mite and mould spore aeroallergens in both coastal and inland cities. They found that on the damper coast, house dust mites were much more numerous, and increased the relative risk for asthma by 21 times that for the inland city. Other findings from the U.S. also show that there is a striking relationship between elevated levels of house dust mite aeroallergen and increased prevalence of asthma. This adds further credence to the theory that the level of exposure to an allergen is a determining factor in inducing asthma.

Another factor needs to be added to the mix: socioeconomic class. Researchers are increasingly recognizing that a combination of location and social class has an impact on asthma. For instance, inner city children in Atlanta, Georgia, are generally sensitive to cockroach allergens, and not to cats; however, it was precisely the other way around for their suburban counterparts. Moreover, the major allergen for the inner city poor is not house dust mite, as is common in affluent households, but cockroach. Measures to exterminate cockroaches are available, but for this population, moving to an non-infested building may be difficult.

Sometimes, it is social change that can alter asthma statistics. For instance, asthma is not very common in the Third World, but one population in New Guinea saw their asthma prevalence rise from a scant 0.1% in 1960 to 7% by 1990. In those years, the house dust mite count went up dramatically, probably due to the introduction of cloth bedding.

The Interaction Factor

Do environmental pollutants combine with airborne allergens to exacerbate asthma? While the jury is still out on this question, at least one study has shown a relationship between these two factors. Researchers asked asthmatics who were sensitive to seasonal allergies to breathe in 0.12 parts per million of ozone for one hour; they were then tested for any change in airway function. Although the ozone in itself did not seem to have an effect, the sensitivity of the patients to the inhaled allergen increased significantly, showing that a detrimental interaction was indeed at work.

Such studies highlight new areas to be probed, including analyzing the effect on airways of mixtures of pollutants and allergens in different permutations. As the authors point out, the relationship of asthma to the environment is intricate and will be difficult to clarify. However, the more information about this relationship that becomes available, the better equipped clinicians will be to offer therapeutic solutions.

1. Are oral corticosteroids not effective enough in treating asthma?

The problem is not the effectiveness of corticosteroids. Patients respond to corticosteroids, but because of the toxic effects of the drug, we’re always looking for what we call a corticosteroid-sparing effect. We want to reduce the use of steroids through alternative medication, but it’s not a question of one drug being better than the other.

2. Are you concerned about dependency on corticosteroids, or about other side effects?

Corticosteroids are not like cocaine, which creates a physical dependency. We’re much more concerned about toxicity, particularly in children. Steroids stunt growth, can cause cataracts, high blood pressure, hair all over your body, and can induce a diabetic-like state. But the major concerns are that it stunts growth and weakens bones. Some patients can fracture their ankle just stepping off a curb.

3. What is IgE and why do some people have more of it than others?

Immunoglobulin E or IgE is the allergic antibody, discovered in Denver in the 50s. Clearly, it’s one of the major causes of allergy-induced problems, whether it’s rhinitis (people who have ragweed allergy or hay fever), skin disease such as eczema, or in some cases, asthma. A high percentage of asthmatics manifest this allergic reaction, particularly children. In most cases of asthma it’s the allergy to whatever is in the environment that triggers the allergic response, which in this case targets the airways.

3. Is asthma caused by IgE reactions to allergens harder or easier to treat than non-allergic asthma?

It depends. Some people have what’s called exercise-induced asthma, and they can take a bronchodilator just before they exercise and they’ll be fine. Others have aspirin-sensitive asthma, and as long as they avoid anything containing aspirin, they’ll be fine. It’s not that one is easier or harder to treat. It’s just that one has to identify and then target different mediators and causes with different drugs in the various types of asthma.

4. What is inflammation?

Let’s say that you’re allergic to dogs. Your family has a history of allergy, because there’s a big genetic component to it. You encounter a dog, and inadvertently inhale some of the dog dander. What happens is: the IgE binds to mast cells, which are a type of cell that is present throughout the body’s airways. The allergen also binds to the IgE. The mast cells then degranulate and release a lot of mediators. Other cells, such as lymphocytes (white blood cells), also get activated. This activation process calls in a lot of inflammatory cells. In the case of asthma and other allergic reactions, a major cell that’s called in is the eosinophil. The eosinophils accumulate around the airway, probably releasing their own mediators that break down the epithelium (lining) of the airways. That leads to altered control of some of the nervous functions of the airways. You get smooth muscle hypertrophy (swelling), and contraction and constriction of the airways.

4. Are immune globulin injections as effective in treating asthma as corticosteroids?

One has to think of the therapy of asthma. There are controllers of asthma and there are relievers of asthma. The relievers of asthma are those drugs that go straight to the airway such as beta-agonists — ventolin, for example — where they act to relieve bronchoconstriction. You take the inhaler, and within seconds you get relief. But if you’re looking for a more prolonged effect to keep inflammation down, you need something that’s going to work to keep those inflammatory cells from coming in. The first line therapy is drugs such as cromolyn and nedocromil, which are weak drugs. They may be okay, however, taken as a prophylactic by people with mild asthma. The really effective anti-inflammatory that is available today is corticosteroid; nothing can beat it. But if you take these drugs by mouth, the toxicity is great, particularly if you take it on a continuing basis. Hence the big push to taking steroids by inhalation. The next step after cromolyn or nedocromil is now inhaled corticosteroids. The toxicity is clearly much lower than when taken by mouth, because they act locally with as little systemic absorption as you can get away with. But some patients continue to have inflammatory changes and asthmatic symptoms, so they need oral corticosteroids. And once you’re on oral corticosteroids as a requirement for control, you start to look at experimental therapies for inflammatory control, because you just want to get the patient off the steroids if you can. A lot of what has been tried has followed from the rheumatoid arthritis literature. Arthritis is also an inflammatory disease, and it’s been treated using things like methotrexate, gold and chloroquin. All of these anti-inflammatory drugs have been tried with asthma, without any great success. Also, some of these drugs are themselves quite toxic: methotrexate, for example, is an anti-cancer drug. We were looking for something that had an anti-inflammatory effect without the toxicity, and we were pleasantly surprised to find that gamma globulin (IgG) has that effect. We were able to significantly reduce the need for steroids without losing control of the disease.

Editorial:

This is an experimental therapy. Double-blind, placebo-controlled studies need to be done to determine the efficacy of gamma globulin, and pilot studies have already been done which have supported its efficacy. It’s also a very costly therapy, and that fact is likely to limit its use. But we’re talking about using this therapy in the very small subset of asthmatic patients whose asthma cannot be controlled using conventional methods. Probably no more than one in 100 to one in 500 asthmatics really have severe steroid-dependent asthma. Of course, when you consider that there are 16 million asthmatics in the United States, that’s still a pretty large number of people who stand to benefit.

Immune globulin E (IgE): An antibody that generally makes up only 0.01% or less of the total immune globulin armoury in human blood, but which frequently appears at higher concentrations in allergic people. This antibody is implicated in reactions such as ragweed and hay fever allergies, most food and contact allergies, and allergy-related asthma.

Immune globulin G (IgG): Also known as gamma globulin, this is the most common of the immune globulins, accounting for approximately 80% of all those present in human blood. It is frequently given by injection to boost the immune system prior to possible exposure to infectious diseases (ie. before a visit to the tropics).

Degranulation: The release by cells of lysosomes (small, self-contained bundles of enzymes that normally remove and digest unwanted or deteriorated components of the cell). Once released, the lysosomes turn their attention to foreign material such as bacteria, and stimulate a cascade of immunological reaction.

Eosinophil: A mobile, antiparasitic white blood cell that hunts and kills foreign bacteria. Vital components of the body’s immune system, eosinophils are attracted to the scene of inflammation, where they can aggravate a hypersensitive reaction such as an asthmatic attack caused by allergy.

Immunologists are increasingly coming to view asthma in terms of inflammatory disease. That means that asthma results from a condition known as airway hyperresponsiveness, which involves inflammation prompted partly by the body’s own antibodies, specifically the antibody known as immunoglobulin E (IgE). That inflammation in turn stimulates the production of aggravating substances that cause muscles in the bronchial tract to contract and spasm. “Sensitized” lymphocytes (white blood cells formed in the lymphatic system) are also found in the bronchial fluid of asthmatics, further inflaming the cells of the airway. This is part of an extremely complex inflammatory process involving numerous types of cells and different chains of events, of which the end result is bronchial constriction and reduced air flow.

Corticosteroids are the most effective anti-inflammatory treatment for airway hyperresponsiveness, and are considered safe for use in the inhaled form. But when these fail, it sometimes becomes necessary for physicians to prescribe oral corticosteroids, which have a steroidal effect on the entire system. These drugs can suppress growth in children, cause weight gain, hypertension, cataracts, osteoporosis and even spontaneous bone fractures, and most specialists would use them only in the most extreme and intractable cases of asthma. Naturally, the discovery of a safe and effective anti-inflammatory agent that allowed patients to avoid or limit prolonged use of oral corticosteroids would be a welcome development. Treatments such as methotrexate, dapsone and even gold have shown some benefits, but none has been consistent enough to eliminate the need for systemic corticosteroid use.

As far back as the 1950s, it was noted that monthly injections of immunoglobulin reduced the rate of infections, particularly respiratory infections, in people with gamma globulin deficiency (an immune disease). Intravenous immune globulin (IVIG) has since shown signs of being a potent anti-inflammatory agent in patients with various conditions such as juvenile rheumatoid arthritis. It has the proven capacity to reduce fever and other more sophisticated measurements of inflammation such as levels of C reactive proteins (which are produced in the so-called acute phase response to inflammatory illness or injury). Moreover, IVIG may mimic some of the effects of immunotherapy with known allergens, blocking and neutralizing them before they can get to the IgE bound up in cells and start an allergic reaction. Finally, antibodies found in intravenous immune globulin would seem to limit the production of IgE in the first place. There is known to be a strong link between asthma and allergy, and allergic reactions in the airway are an important factor in many asthmatic attacks. For all of these reasons, IVIG seems a strong possible alternative to systemic corticosteroids.

To test the effectiveness of intravenous immune globulin therapy in asthma, researchers recruited eight steroid-dependent asthmatic children aged from six to 17. Every four weeks, the patients were given 2 g of intravenous immune globulin for each kilogram of body weight. The treatment continued for six months. To assess results, doctors compared symptoms of coughing, wheezing, shortness of breath and chest discomfort before and after IVIG, as well as any changes in medication, and the frequency with which the patients were forced to use beta-agonists to control episodes of exacerbated asthma. Since 40% to 85% of asthmatics tend to test positive for reactions to various common airborne allergens, researchers also carried out some skin-prick tests.

Steroid use among the children declined greatly from an average 154 mg per month before treatment to only 49 mg/month after IVIG. Likewise, use of beta-agonists was halved during IVIG treatment, reflecting the fact that asthmatic symptoms were greatly reduced. Evaluating the severity of six different symptoms such as coughing and nocturnal wheezing on a scale from 0 (no symptoms) to 4 (incapacitating symptoms), average monthly scores decreased from 32 before intravenous immune globulin to 17 after one month of treatment, and remained in the 16 to 18 range as long as therapy was continued.

Confirming the known link between allergy and asthma, seven of eight children had skin reaction to one or more needle-prick tests of common allergens, giving a total of 30 positive reactions before intravenous immune globulin injections began. Following IVIG therapy, only one of those reactions worsened, while two remained unchanged and 27 improved. The average decrease in sensitivity to allergens was a striking hundred-fold. All of these gains were lost when the intravenous immune globulin treatment was suspended for six months, yet when five of the patients restarted intravenous immune globulin therapy six months later their asthma symptoms and steroid requirements once again stabilized and their overall improvement, in fact, surpassed that of the first therapy period.

Perhaps the most notable result was that the average annual cost of hospitalization in the five children who continued with intravenous immune globulin went from over $40,000 to under $3,000. That is a significant change, especially when one bears in mind that asthma is the leading cause of emergency room visits and hospital internment in children. A similar dramatic improvement was seen in three adult patients suffering from a chronic disfiguring skin disease known as atopic dermatitis. Sensitivity to allergens was found to have declined on average thirty-fold, and symptoms of itching, scaling and discolouration retreated rapidly.

More research is needed to learn about the applications of this therapy in a whole range of diseases with both inflammatory and immune components. It remains to be seen what is an optimum dose and what are the limits of intravenous immune globulin. But it is clear that it offers hope to sufferers of many debilitating conditions and may help to free many patients from dangerous steroid dependency.

This new drug is thought to be a safer choice of treatment because it has little effect on other body systems when it is given in doses of up to 16 mg daily. Thus it is seen as having a good safety profile and as being effective in controlling allergy symptoms. The study compared the effectiveness and safety of treating seasonal allergic rhinitis in adolescents using fluticasone propionate (Flovent) versus the use of loratadine tablets, another drug traditionally used in such therapy.

The authors compared the nasal and eye symptoms of 240 adolescents suffering from ragweed-induced allergies, half of whom received fluticasone propionate (Flovent) nasal spray at 200 g daily while the rest were given loratadine tablets, 10 mg daily. Loratadine is an antihistamine which demonstrates little sedative and dehydrating side effects. Patients were asked to record their nasal and eye symptoms on a daily basis.

Overall, fluticasone propionate provided more symptom-free days than did loratadine for nasal problems, but there was no difference between treatments in terms of relieving eye symptoms. Both drugs had the adverse side effects of headache and sore throat. An interesting observation was the diurnal variation in symptom levels, with the morning being the best time of the day for allergy sufferers, regardless of treatment.

Based on these findings, researchers have concluded that fluticasone propionate (Flovent) is an effective means of controlling the symptoms of this specific allergy, without extreme side-effects, and suggest that this treatment be recommended as a first choice for ragweed allergy sufferers.

Questions:

1. Do adolescent allergy sufferers differ from adults? Do allergies intensify with age?

In the case of allergic rhinitis, children and adults are affected in the same way. Allergies do increase with age, due to accumulated exposure to allergens – you can’t be allergic to something you’ve never been exposed to. Very young children tend not to have respiratory allergies (excluding asthma) – these often develop around age six or seven. Both the number of allergies and their intensity generally increase until age 20 or so, then may start to gradually subside. I’m referring to hayfever, not asthma. Of course, people can become allergic to anything at any age.

2. Are there any side effects associated with long-term use of topical intranasal corticosteroids?

Side effects are related to dosage: low doses are well tolerated, but higher doses can cause thinning skin and increased bruising in the elderly, and can interfere with growth in children. They may occasionally lead to yeast infections in the mouth. That’s why we keep patients on the lowest dose possible and follow them carefully. However, 95% of patients have no side effects at all.

3. Do you recommend that people take inhaled corticosteroids only when symptoms arise, or as a preventive measure?

We only prescribe them as needed, never preventively, and at the lowest possible level for effective symptom control.

Comment: I think the most useful development in hayfever treatment in the last 30 years has been the introduction of inhaled corticosteroids. Seasonal use for limited periods (one or two months at a time) is very safe, and the most effective way of keeping symptoms under control. In my practice, every patient who’s troubled by acute ragweed allergy symptoms will get inhaled corticosteroids. However, these must be combined with efforts to minimize exposure to allergens. In the case of ragweed, there’s nothing you can do while outdoors, but at home, keeping windows closed is very important. Air filters are useless if outside air full of pollen is continually coming in. Air conditioning may be needed, with the vents kept closed. This will not only reduce the pollen count, but also the humidity. More people in damp houses are affected by respiratory symptoms, because of increased mould and dust mites. Air conditioning helps both factors.