Article about occupational asthma
Doctors first linked certain occupations with respiratory problems during the eighteenth century. Today, we know that at least 350 agents used in the workplace may trigger occupational asthma. For example, Henneberger and colleagues remark that high levels of biological dust increase the likelihood of an asthma exacerbation almost four-fold. Low levels of biological dust and high levels of mineral dust almost double the risk.
As occupational asthma often shows a clear pattern of onset and the symptoms frequently improve when exposure to the trigger ceases (such as during holidays), many cases are potentially preventable. Certain countries – including the UK and some parts of the USA – monitor occupational lung diseases, including asthma. Nevertheless, estimates of the number of people affected by work-related asthma vary widely. Scientists who study patterns of diseases (epidemiologists) suggest that work-related factors probably cause between a tenth and a quarter of asthma cases among adults. However, Henneberger and colleagues point out that doctors may have diagnosed only a third of occupational asthma cases. And people who suffer respiratory symptoms may voluntarily change job, leading epidemiologists to further underestimate the true risk.
Occupational asthma - technical article
Parental occupation and childhood asthma
Certain parental occupations seem to increase the likelihood that their children will wheeze or suffer asthma. Parents can transport potential hazards – including pesticides, organic solvents and allergens (such as wheat, latex and dander from laboratory animals) from work to home. This potentially exposes children and other household members to the trigger.
The three routes to occupational asthma
Broadly, occupational factors can trigger asthma in three ways. First, certain allergens sensitize the immune system and prompt production of large amounts of specific IgE. This takes time. So asthma symptoms arising from sensitization to occupational allergens tend to emerge several months or even years after exposure starts.
Once the worker’s immune system generates specific IgE, exposure to very low levels of the occupational trigger can provoke symptoms.
Second, chemicals that irritate the lining of the lung, damage the bronchial wall or increase the number of inflammatory cells can trigger asthma. Indeed, a single exposure to high levels of some airway irritants can cause this ‘non-allergic’ occupational asthma. In one case, Kern reports, 21 per cent of hospital workers exposed to high levels of acetic acid following a spill developed irritant-induced asthma. This compared with 3 per cent of those with medium levels of exposure to acetic acid and none of those exposed to low levels. Similarly, exposure to high levels of gas and fumes increases the risk of suffering asthma two and a half times. One study found that a fire, mixing cleaning agents and a chemical spill each trebled asthma risk.
In contrast to the allergic form, this form of asthma develops minutes or hours after a usually recognizable incident (such as a fire or chemical spill) during which the worker was exposed to high levels of a respiratory irritant. In many cases, the person had not previously suffered respiratory disease. Indeed, workers often report many years of exposure to low levels of the agent without suffering symptoms. In other cases, frequent lower-intensity exposures to certain chemicals may induce asthma, although further studies need to determine how many cases arise from this mechanism.
Finally, various non-specific factors – such as dust, cold air and physical exercise – at work can provoke pre-existing asthma or undermine lung function. Images of a cloud of dust sweeping through Manhattan’s streets following the terrorist attacks on the World Trade Center on September 11, 2001, remain unforgettable. Not surprisingly, lung function declined markedly in rescue workers exposed to the dust. Aldrich and colleagues found that in the year after the attack, mean FEV1 fell by 439 ml and 267 ml in fire fighters and emergency medical service workers respectively who had never smoked. Lung function improved little during the next six years. After six years, 13 per cent of fire fighters and 22 per cent of emergency medical service workers showed FEV1 below the lower limit of the normal range. This extreme example illustrates that chemically and biologically ‘inert’ dust can still cause considerable lung damage.
Cigarette smoking further increases the risk of sensitization or asthma symptoms in several workforces, while some chemicals may directly contract bronchial smooth muscle. Finally, people with manual jobs may find that exercise triggers symptoms. In these cases, the treatments for exercise-induced asthma may help.
Common causes of occupational asthma
Almost every occupation is at risk of exposure to factors that trigger or exacerbate asthma, even that of office worker – some printers produce ozone, for example. Nevertheless, people working in certain occupations are at especially high risk of developing work-related asthma, as the following examples illustrate.
Bakers and flourmill workers
The Italian physician Bernardino Ramazzini first linked asthma with working in a bakery in his book De Morbis Artificum Diatriba [Diseases of Workers] published in 1713. Doctors now know that numerous factors in a bakery can cause sensitization and, in some cases, asthma; these include: wheat, rye, barley, oat and other flours; α-amylase (an enzyme that helps yeast work); and contaminants such as mites and fungi. Indeed, in dusty areas of bakeries and flourmills, up to 20 per cent of airborne allergen particles are small enough to deposit in bronchioles and alveoli.
The variety of allergens responsible for occupational asthma among bakers continues to expand. Most people think of lupins as ornamental flowers. But lupins belong to the legume family of plants, alongside peanuts, peas, chicked in the Roman Empire. Today, lupin products – such as flour – are increasingly used to manufacture bread, pasta and pastries and to thicken soup.
Campbell and Yates point out that, despite centuries of its use, the first reports of occupational sensitization to lupin emerged only in 2001. Since then, studies have suggested that between 21 and 29 per cent of people who inhale lupin at work become sensitized. Lupin allergies can cause asthma, conjunctivitis (an inflammatory reaction on the outermost surface of the eye and the inside of the eyelid) and rhinitis. As this example illustrates, it’s important to remain vigilant for changes in asthma patterns when your company introduces new processes.
Detergent manufacturers, food processors (including bakers), research staff and healthcare professionals use enzymes, which, as they’re proteins, can evoke allergic reactions. Workers manufacturing enzymes and detergent products seem to be at the highest risk. But even lower levels can cause respiratory symptoms. Kitchen staff using papain to tenderize meat can become sensitized and develop respiratory disease, for example. Indeed, any protein that can become airborne and is of a size that can deposit in the lower airways could probably induce occupational asthma in some people.
Numerous chemicals can cause or trigger asthma, including complex platinum salts (used in the refining of precious metals, the chemical and pharmaceutical industries) and a group of compounds called diisocyanates. Many of these chemicals are much smaller than protein allergens. However, platinum salts, diisocyanates and some other chemicals seem to bind to, and change the shape of, proteins produced naturally by the body. The immune system produces antibodies against these altered proteins. And some chemicals – such as certain diisocyanates – may contract the muscles around the airways.
Diisocyanates are used to manufacture polyurethane. As polyurethanes are widely used, workers can be exposed to diisocyanates when applying certain paints (such as aircraft and car spray paints) and from some inks and adhesives, for example. There are several diisocyanates, each of which can cause occupational asthma. In Europe, hexamethylene diisocyanate used in spray paints probably accounts for most cases of occupational asthma caused by this group of chemicals. Sensitive workers can react to minute amounts of diisocyanates. For example, workers sensitized to toluene diisocyanate may develop asthma after exposure to concentrations as low as one part in a billion.
Wood dust is another potential cause of occupational asthma. For example, Schlünssen and colleagues found that 1.7 and 3.1 per cent of woodworkers in furniture factories showed IgE to pine and beech respectively. Although the risk was relatively low, the likelihood of being sensitized rose as exposure to wood dust increased.
Similarly, Campo and colleagues found that 54 per cent of carpentry apprentices had work-related respiratory symptoms caused by wood dust, 15 per cent due to diisocyanate and 9 per cent to both. Those who suffered from rhinitis were roughly twice as likely to develop respiratory symptoms due to wood dust exposure compared to those without rhinitis. In asthmatic apprentices, the risk of respiratory symptoms due to wood dust was almost three times higher. In this study, 9 per cent of participants showed specific IgE to wood.
Workers handling animals
Dander and other allergens from domestic pets are common causes of allergic asthma. Allergens in urine, pelt, hair and blood also contribute to occupational asthma among people working with animals. Indeed, 28 per cent of airborne allergens liberated from rat urine in animal laboratories are tiny enough to deposit in the small airways. Larger particles may deposit in the nose, which can provoke occupational rhinitis.
Overall, around 15 per cent of workers become sensitized and about 2 per cent develop asthma during their first year of working with animals. Another way to look at the risk calculates the number of cases per person-month: so, 12 people working for one month and one person working for 12 months both represent 12 person-months. Positive skin tests to rat urine develop at a rate of approximately 2.5 new cases per 1,000 person-months.
Latex is the milky sap from the rubber tree. Manufacturers process latex to create, among many other products, adhesives, foam, carpet backings, medical gloves, catheters, condoms and balloons. Unfortunately, natural latex contains numerous allergens that sensitive people may inhale or absorb through their mucosa – such as people who need indwelling urinary catheters – and possibly skin. People who need to change latex gloves regularly (such as healthcare workers) seem to be at higher risk of developing sensitivity to latex. Furthermore, people sensitive to natural rubber latex may cross-react to several foods and plants, including avocados, bananas and the weeping fig (Ficus benjamina).
Colophony, a resin produced by pine trees, is used as a solder flux and, less commonly, as a coolant, in bitumen and in poultry processing. Soldering releases a fume of acids and other chemicals that can, when inhaled, trigger asthma in some patients. In one study, around a fifth of patients working in areas of a factory with high levels of colophony fumes developed work-related respiratory symptoms. This compared to between 4 and 16 per cent in other parts of the factory. However, exactly how colophony triggers asthma isn’t clear.
Not surprisingly, given its importance as an allergen in the general population, pollen can trigger asthma among people working in horticulture. Patiwael and colleagues, for example, found that, over eight years, 9 per cent of people working growing bell (sweet) peppers in greenhouses produced IgE to the pollen. Furthermore, 19 per cent showed work-related rhinitis. In this study, atopy (a genetic tendency to develop allergies) and smoking increased the risk of developing occupational rhinitis by approximately six and four times respectively. Moreover, 8 per cent of workers in horticulture showed work-related asthma symptoms, with atopy and smoking increasing the risk by five and almost twelve times respectively.
Pollen isn’t the only potential occupational trigger in horticulture. For example, spider mites – a pest affecting various crops grown in greenhouses and fruit orchards – can trigger allergy and asthma in greenhouse workers, farmers and children living in rural areas. Because of concerns about the safety of pesticides among consumers, some growers have started using predatory mites to hunt down the pests. However, anti-pest mites can prove allergenic. Kronqvist and colleagues found that 36 per cent of people working in greenhouses growing cucumbers and tomatoes were sensitized to at least one predatory or pest mite species. Of these, 35 per cent had asthma and 47 per cent suffered from rhinitis and conjunctivitis.
Diagnosing occupational asthma
It’s vital to get the diagnosis right: people suffering from occupational asthma usually need to change their job or may even face unemployment. On average, according to Ayres and co-authors, changing jobs because of occupational asthma typically reduces income by between 22 and 50 per cent. Indeed, between 20 and 80 per cent of those who change job suffer some loss of income.
Unfortunately, you can’t rely on your inhalers to continue working properly at work. Standard asthma treatments may not work optimally if the allergen exposure continues. Protective equipment – such as air-fed helmet respirators – may improve or abolish symptoms in some employees. However, these can be uncomfortable and cumbersome.
So how can you tell whether you encounter the trigger for your asthma at home, at work or at play? If you suffer asthma symptoms (e.g. cough and chest tightness) at work but these are absent or less severe after work, at weekends or while on holiday, you may suffer from occupational or work-exacerbated asthma.
However, this pattern isn’t infallible. The late-phase reaction means that asthmatic symptoms can occur during the evening or night following exposure. Furthermore, on repeated exposure, people with oc-cupational asthma take longer to recover. So symptoms may not improve over the weekend, but abate only after you’ve been on holiday for several days. To complicate matters further, non-specific triggers – including cold air, tobacco smoke, exhaust fumes and the vapours of paint or perfumes – can cause symptoms at home, even if the cause is work-based.
If the doctor suspects that you suffer from work-related asthma, you’ll probably be asked to measure your lung function at home and at work. And it’s a good idea to keep a diary of your known exposures at work. You may also undergo a challenge test or other investigations (such as a skin prick test) to see if you have become sensitized.
Tests to detect specific IgE antibodies can support the diagnosis. But used alone the tests are rarely sufficient to diagnose asthma. Antibodies indicate only that the person is ‘sensitized’ and not that the particular trigger causes your symptoms. Many more people are sensitized than develop asthma or other allergic symptoms. Nevertheless, doctors may suggest a diagnosis of occupational asthma based on very high antibody levels (called titres) in people with a characteristic pattern of symptoms. The next article considers these tests.
Most occupational asthma improves once exposure to the allergen ends. But while many recover completely, some find that their asthmatic symptoms and airway hyper-reactivity do not resolve. And some people who develop work-related asthma endure persistent symptoms despite avoiding the occupational allergen.
One group of researchers, led by Rachiotis, examined 39 studies investigating outcomes in occupational asthma. A third of people recovered completely from their asthma over an average of 31 months. However, in individual studies recovery rates varied from zero to 100 per cent. Furthermore, 73 per cent of patients showed non-specific bronchial hyper-responsiveness. Workers with the longest durations of employment or symptomatic exposure were the least likely to recover, possibly reflecting the impact of airway remodelling.
Not surprisingly, doctors and employers have looked for ways to reduce the risk of occupational asthma. The 30 to 40 per cent of the population who are atopic are especially likely to develop occupational asthma from, among others triggers, allergens in a bakery, animals, detergent enzymes, certain dyes and some seafoods. However, most atopic subjects will develop neither sensitization nor asthma symptoms. So, for example, in order to prevent one asthma case a laboratory would need to exclude seven atopic employees who could handle the animals. The difficulty predicting who is at risk means asthma remains an occupational hazard for millions of workers.