Asthma and domestic air quality

PII: S0277-9536(98)00151-8

Soc. Sci. Med. Vol. 47, No. 6, pp. 755±764, 1998 # 1998 Elsevier Science Ltd. All rights reserved Printed in Great Britain 0277-9536/98 $19.00 + 0.00

ASTHMA AND DOMESTIC AIR QUALITY A. P. JONES School of Environmental Sciences, University of East Anglia, Norwich, Norfolk, NR4 7TJ, U.K. AbstractÐIn recent years, there has been a global increase in the prevalence of asthma. This has coincided with many modi®cations to the home environment, resulting in changes to the quality of indoor air. This article considers the links between indoor air pollution and asthma. Exposure to a range of pollutants is examined. Airborne allergens such as those from house dust mites and cockroaches, domestic pets and moulds and fungal spores may be important. Pollution from particulate materials associated with bio-fuel combustion and smoking is discussed, as is the role of chemical vapours and gasses including nitrogen dioxide, formaldehyde and volatile organic compounds. The ecacy of various environmental controls to limit the impact of these pollutants is explored. It is concluded that indoor air pollution may be an important risk for asthma and the health impacts of building design and management require greater recognition and further research. # 1998 Elsevier Science Ltd. All rights reserved Key wordsÐbronchial asthma, indoor environment, housing, pollution, allergens

INTRODUCTION

It is generally agreed that, in recent decades, we have experienced a global increase in asthma prevalence (Burney, 1993; Haahtela et al., 1990). Particularly in more economically developed and rapidly developing countries, rising prevalence has been accompanied by unprecedented changes in both lifestyles and environmental quality. One impact of development has been an upsurge in the proportion of inhabitants living in cities. A repercussion is that an escalating number of the population are exposed to the contaminants of urban air (Lipfert, 1997). Although this has led to concern that outdoor air pollution may be to blame in causing asthma, the ®ndings of many studies are weak or contradictory (for a review, see Brunekreef et al., 1995). Consequently, there has recently been a shift of attention from outdoors to the situation indoors (Hines, 1993). It seems that changes in indoor air quality may be more important in explaining the rise in asthma cases. It is estimated that the average individual born today will spend over 95% of their life inside (Platts-Mills, 1995). In the past, this ®gure was much lower. This trend has coincided with major changes to the home environment, in part driven by alterations to building design which were hastened by high fuel costs during the 1970s energy crisis. Modern homes are much better insulated than was previously the case. Houses with ventilation rates as low as 0.2 to 0.3 air exchanges hÿ1 are now widespread (Platts-Mills et al., 1996). In older properties, particularly those with open ®replaces, ventilation rates above 1 air exchange hÿ1 are more common. Improved insulation has been accompanied by numerous other modi®cations. Many 755

more houses have central heating and sealed-unit double-glazing. For example, although only 29% of British homes were centrally heated in 1970, this ®gure had risen to over 85% by 1995 (ONS, 1996). Fitted carpets have generally replaced loose rugs and advances in construction technology have meant a greater use of synthetic building materials (D'Amato et al., 1994). All these transformations have undoubtedly led to more comfortable living conditions. However, they have also resulted in warmer, more humid houses with a poorer availability of fresh air. These conditions provide an environment in which airborne contaminants are readily produced and may build up to much higher concentrations than typically encountered outside (Hyndman et al., 1994). Of course, many other aspects of the internal and external environment have changed in recent years and it is quite possible that these may partially explain the increasing prevalence of asthma. However, given the amount of time that most individuals spend indoors, it seems that the indoor environment may have an important role to play in allergic disorders. As with all respiratory allergies, asthma is caused by an interaction between genetic and environmental factors (D'Amato et al., 1994). A great number of substances found in the environment can induce allergic respiratory sensitisation and reaction (Lau and Wahn, 1990), while many more precipitate or aggravate respiratory symptoms by non-allergic mechanisms (Salvaggio, 1991; Molina, 1992). Various indoor exposures have been related to asthma, including house dust mites, moulds and fungal spores and nitrogen dioxide (NO2) from gas cooking (Hasselblad et al., 1992). High concentrations of volatile organic compounds and formal-

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A. P. Jones Table 1. Common indoor allergic agents

Source Dust-mite

Cat Dog Rodent Cockroach Fungi

Genus

Species

Allergen

Dermatophagoides Dermatophagoides Euroglyphus Lepidoglyphus Felis Canis Mus Rattus Blattela Periplanetta Alternaria Aspergillus Cladosporium

pteronyssinus farinae maynei destructor domesticus familiaris musculus norvegicus germanica americana alternato fumigatus herbarium

Der p I Der f I Eur m I Lep d I Fel d I Can f I Mus m I Rat n I Bla g I Per a I Alt a I Asp f I Cla h I

dehyde have also been associated with the condition (Wieslander et al., 1997), as has particulate matter from smoking and bio-fuel combustion. Concern over indoor air has now risen to such an extent that the United States Centre for Disease Control has classi®ed indoor pollution as a factor of high environmental risk (CDC, 1994). Domestic air pollution is now seen as a major public health issue and if the asthma problem is to be successfully tackled, it seems that a good understanding of the risks it poses may be vital (Cohen, 1995). This article reviews the current state of knowledge on the relationship between indoor air quality and asthma and outlines some of the interventions that may be required to reduce levels of exposure. INDOOR ALLERGENS

Table 1 summarises the main allergens found in indoor air. House dust mites are present in the dust of all homes built in temperate climates. Droppings from the mite Dermatophagoides pteronyssinus are the principal source of antigens in house dust (Kaliner and White, 1994). Dust mites thrive in soft furnishings, particularly in warm and humid rooms (Table 2). The mites encase their faeces in a coating of intestinal enzymes and it is a protein within these which is the primary allergen (known as Der p I). The estimated number of mite faecal particles in house dust is up to 100 000 per gram. They range from between 10 to 40 mm in diameter (Platts-Mills et al., 1991). Their relatively large size means that they do not remain airborne for long, with an average residence time of less than 30 min (Tovey et al., Table 2. The characteristics of the common house dust mite Size Growth cycle Optimal temperature Minimum temperature Maximum temperature Optimal relative humidity Minimum relative humidity Habitat

250±350 mm1 Egg to adult in 25 d at 258C1 20±308C2 168C3 558C4 70±80%1 50%3 Sofas, fabrics, carpets, sheets, duvets, pillows, mattresses, and other soft furnishings1

Sources: 1D'Amato et al. (1994); (1990); 4Salerno et al. (1992).

2

Jones (1997);

3

Arlain et al.

1981). However, airborne concentrations of mite allergen in disturbed rooms can be more than 1000 times higher than those in undisturbed air (Kalra et al., 1990). A concentration of mite allergen above 2 mg Der p I gÿ1 (equivalent to 100 mites) of dust appears to represent a signi®cant risk factor for mite allergy (WHO, 1995). The ®rst documented observation that mites may be a cause of respiratory symptoms was made over 70 y ago (Ancona, 1923). Today, it is estimated that exposure to mite allergen may trigger attacks in up to 85% of asthmatics (Platts-Mills, 1997). The asthmatic response to exposure is generally in two stages (Cockcroft, 1992). The early or immediate response is an episode of airway obstruction, which peaks between 10±20 min after inhalation and normally resolves with 1±2 h. This response is mostly due to bronchospasm in the lungs. A secondary response may develop some hours after exposure. This is usually associated with airway in¯ammation and may manifest itself as an acute asthma exacerbation, increased airway hyperresponsiveness, or recurrent nocturnal asthma. Studies of the e€ects of dust mite allergen exposure are numerous. Recently, BjoÈrnsson et al. (1995) found that nocturnal breathlessness and other asthma related symptoms were most common in adults inhabiting Swedish homes with large mite populations. In Australian children, Peat et al. (1994) found a positive association between wheezing in the previous year and exposure to dust mite Der p I. As well as being a major trigger of attacks in asthmatics, there is also evidence that exposure to mite allergen, particularly amongst infants, may be an important factor in inducing the onset of asthma itself. In the U.S.A., Call et al. (1992) found that the residents of homes with high concentrations of mites were more likely to be sensitised to mite allergen and this in turn was associated with a higher prevalence of asthma. Sporik et al. (1990) reported that early exposure to mite allergen was an important factor for sensitisation and the early onset of wheezing amongst 68 children living in an area of southern England. In an important study, Arshad et al. (1992) examined the role of early exposure to

Asthma and domestic air quality

dust-mite allergens in the development of allergic disorders amongst infants on the Isle of Wight. 120 infants were randomly allocated to prophylactic and control groups. In the prophylactic group, the infants' bedrooms and living rooms were treated with chemicals to control mites and concentrations of Der p I were monitored. In the control group, no interventions were made. At 12 months the odds ratio for asthma was 4.13 (1.1±15.5) amongst the control group. Like dust mites, cockroaches have been associated with the manifestation of symptoms in individuals with allergic asthma and up to 60% of asthmatics test positive to cockroach allergen (Kuster, 1996). Although cockroaches are generally indigenous to warm tropical climates, some species are able to thrive elsewhere due to the presence of central heating. Sources of cockroach allergens have been found in body parts as well as faecal extracts (Musmand et al., 1995) and the allergen has a di€erent distribution to that from dust mites. In particular it is found in kitchen cabinets, kitchen ¯oor dust, bathrooms and basements (Hannaway, 1993). Rosenstreich et al. (1997) measured concentrations of the allergen in dust taken from 476 homes situated in various inner-city locations in the U.S.A. They discovered that, whilst concentrations of less than 9 units (U) per gram of dust were common, some houses had concentrations of over 1000 U gÿ1. The same authors found that asthmatic children allergic to cockroaches were three times more likely to be hospitalised for their asthma if they lived in a house with a large cockroach population. These children also exhibited signi®cantly more days of wheezing and nights with lost sleep. The authors concluded that the problems of cockroach sensitisation might be particularly severe amongst the residents of poor quality inner city housing, as these homes provide an ideal environment in which cockroaches can thrive. Domestic cats are an important source of allergens in the home, particularly in Northern Europe where the climate is less favourable to dust mites. Cat allergen (Fel d I) is found in saliva and skin. It is generally carried on small particles (<2.5 mm) and hence can be airborne for many hours (Luczynska et al., 1990). Concentrations of cat allergen in domestic dust can be very high, ranging from less than 1 mg gÿ1 to over 10 mg gÿ1 (Luczynska, 1994). Airborne levels of the allergen vary between 2 and 20 ng mÿ3 and Collo€ (1994) found them to be highest in homes with more soft furnishings and ®tted wool carpets. Fel d I can also be detected in homes without a cat (Woodfolk et al., 1992). Recently, it has been proposed that a concentration of Fel d I of over 8 mg gÿ1 in house dust should be considered as a threshold for both atopic (allergic) sensitisation and the development of asthma (D'Amato et al., 1994).

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Because of the small particle size, cat allergen readily enters the lung and can produce a rapid and severe asthmatic response. For example, Pollart et al. (1989) found that 30 out of 188 asthma patients who were admitted to a hospital emergency department with acute attacks were allergic to cats, compared to 1 out of 202 controls. Exposure to other allergens (for example, Can f I from dogs) from animals in the home may be less important for asthma, although can be a signi®cant cause of morbidity in certain asthmatics. Fungus and mould associated respiratory allergies have not been as well studied than those caused by animals (D'Amato et al., 1994). Consequently there is little information available on exact levels of exposure (Burge, 1989), although it is well documented that high levels of humidity favour their growth. The relationship between moulds and house dust-mites means that, as well as being a risk factor for allergic sensitisation, moulds are also thought to be a risk for increased house dust-mite concentrations (Luczynska, 1994). A number of studies have investigated the allergenicity of fungi and moulds. In Sweden, Wickman et al. (1992) found that, compared to non-atopic controls, Penicillium, Alternaria and Cladosporium moulds were more common in the homes of atopic children. Recent work by Neas et al. (1996) examined the association between fungal spore concentrations and lung function amongst a panel of 108 children. They found that morning lung function was inversely associated with Epicoccum and Cladosporium spore concentrations. INDOOR PARTICULATE MATTER

Cigarette smoke is an important source of indoor pollution. The contribution of smoking to indoor air quality has been investigated by studies involving personal monitoring and monitoring of homes for respirable particles. Over several weeks, Spengler et al. (1981) observed respirable particulate concentrations in 80 homes. They found that a smoker of 1 pack a day contributed about 20 mg mÿ3 to 24 h indoor concentrations. Because cigarettes are not smoked uniformly throughout the day, the authors concluded that short-term particulate concentrations of 500 to 1000 mg mÿ3 were likely when cigarettes were actually ignited. Smoking is associated with bronchial hyperresponsiveness. There is little evidence to link smoking in adulthood with the onset of asthma. However, exposure to indoor cigarette smoke has been connected with an increased incidence of atopy and respiratory symptoms in infants. Indeed, amongst very young children, cigarette smoke may be an even more important cause of asthma than house dust mites (Platts-Mills et al., 1996). In Italy, ForastieÂre et al. (1992) examined the self-reported prevalence of asthma in 3239 children

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in the town of Civitavecchia and the city of Rome. They found the prevalence of asthma was elevated in children whose mothers smoked. Similarly, Gortmaker et al. (1982) found the prevalence of parent-reported asthma in children aged 0±17 y increased from 5% to 7.7% for children with a mother or father who smoked and the prevalence of severe asthma increased from 1.1% to 2.2%. Amongst English infants, Arshad et al. (1992) reported an odds ratio for asthma of 3.33 (95% CI 0.8±14.6) if one parent smoked and 11.0 (95% CI 2.5±48.2) if both smoked. Although domestic wood and coal combustion is less common than was once the case, the use of open ®res and woodstoves for cooking and heating can still make a signi®cant contribution to indoor particulate matter concentrations. Traynor et al. (1986) found indoor concentrations of respirable particles were slightly above background (0 to 30 mg mÿ3) during the use of airtight stoves and substantially higher with non-airtight stoves (200 to 1900 mg mÿ3). In general, it appears that homes with airtight woodburning stoves have about 4 mg mÿ3 higher indoor concentrations than homes without stoves. Wood and coal burning in ®replaces also produces particulate pollutants and Moschandreas et al. (1980) found that these concentrations can be much higher than those produced by stoves. Despite the potential for high levels of contamination from domestic bio-fuel combustion, few data are available on smoke and respiratory illness in developed countries. Honicky et al. (1985) conducted a prevalence survey of respiratory symptoms in 62 children in Michigan, U.S.A. They discovered the proportion of children reporting moderate or severe symptoms was much greater for those from homes with woodstoves (84% of children in this group reported at least one severe symptom, compared to 3% of the control group). In their investigation of six US cities, Dockery et al. (1993) found an odds ratio of 1.32 (95% CI 0.99±1.76) for respiratory illness in households with woodburning stoves compared with those using other sources of heating. Likewise, Koenig et al. (1993) reported that infants who were exposed to wood smoke were more likely to exhibit the symptoms of asthma. It is important to note that levels of outdoor air pollution can in¯uence indoor concentrations of particulate pollutants. In homes in Hudders®eld, England, Kingham et al. (1996) examined the relationship between outdoor and indoor levels of particulate pollution from trac. They found a statistically signi®cant association between the two concentrations. However, concentrations were higher outdoors than indoors in all homes studied. This suggests the dispersion of trac related ®ne particles into the home is to some extent limited and particles were not being accumulated indoors.

NITROGEN DIOXIDE FROM GAS APPLIANCES

The use of gas appliances for domestic cooking is common practice in much of Europe and America. In the U.S.A. alone, it is estimated that up to 50% of hot meals are cooked on gas stoves (Gold, 1992). Combustion of gas during cooking and the burning of pilot lights produces NO2. On average, normal use of an unvented gas cooking range adds 25 ppb of NO2 to the background concentration in a home (Samet et al., 1987). During cooking with a gas range, peak levels in the kitchen may reach 200 to 400 ppb (Spengler et al., 1981). In Pisa, Italy, Viegi et al. (1992) examined the e€ects of the home environment on respiratory symptoms of a general population sample. After controlling for potential confounding factors, they found that the use of bottled gas for cooking was associated with increased reporting of cough and phlegm in males. They also discovered that the presence of wheeze and shortness of breath in females was associated with the use of a stove or forced air circulation for heating. Similar results were found in England by Jarvis et al. (1996). They surveyed the association between the use of domestic gas appliances and respiratory symptoms and lung function in adults aged between 20±44 y. Women who reported they mainly used gas for cooking were more likely to mention an attack of asthma or asthma like symptoms in the 12 months prior to the survey. Women who used a gas stove or had an open gas ®re were also found to have reduced lung function and increased airway obstruction. These ®ndings were not made for men. The fact that these studies generally show the greatest e€ect for women might be because women are more susceptible to the products of gas combustion, or they may have greater exposure to high concentrations of these products. Exposure to NO2 may act as a trigger for asthma in one of two ways. One possibility is that the pollutant itself causes a direct e€ect on the lungs by toxic damage. Another is that exposure may sensitise the lungs, making individuals more susceptible to allergic response upon contact with other indoor allergens. The second explanation is particularly pertinent to the home environment, where concentrations of common aeroallergens are high and water produced by gas combustion may favour the growth of mould and dust mite populations. Evidence that the sensitisation mechanism may be important comes from a study by Tunnicli€e et al. (1994). In individuals exposed to 400 ppb of NO2 for 1 h previously, lung function (measured by forced expiratory volume) dropped by 19% within 2 h after the inhalation of house dust-mite Der p I allergen. There was a comparative reduction of just 14% in those exposed only to air.

Asthma and domestic air quality VOLATILE ORGANIC COMPOUNDS (VOCS) AND FORMALDEHYDE

Volatile organic compounds (VOCs) and formaldehyde are irritants produced by many substances in modern homes. Common sources include solvents, ¯oor adhesive, particle board, wood stain, paint, cleaning products, polishes and room fresheners (Xu et al., 1989). Levels of most VOCs can be 5 to 10 times higher indoors than outdoors (Samet, 1990). Both VOCs and formaldehyde are wellknown respiratory irritants. VOC concentrations of 25 mg mÿ3 have been found to induce airway in¯ammation and irritation (Harving et al., 1991; Koren et al., 1992). Typical indoor concentrations of formaldehyde fall in the range of 0.02 to 0.15 ppm (Gold, 1992). Samet (1990) estimates that concentrations in indoor air of over 0.1 ppm can lead to acute upper airway irritation and concentrations above 5 ppm can result in lower airway and pulmonary e€ects. For 88 Swedish subjects aged between 20±45 y, Norback et al. (1995) examined the association between asthmatic symptoms and VOCs and formaldehyde in their dwellings. They found positive associations between the prevalence of reported nocturnal breathlessness and concentrations of both substances. In another Swedish study, Wieslander et al. (1997) examined the association between asthma symptoms and exposure to VOCs and formaldehyde from newly painted indoor surfaces. They found recently painted surfaces were a risk factor for symptoms (Odds ratio 1.5, 95% CI 1.0±2.4). Particularly strong e€ects were associated with newly painted wood details (Odds ratio 2.3, 95% CI 1.2±4.5) and kitchens (Odds ratio 2.2, 95% CI 1.1±4.5). INDOOR ENVIRONMENTAL CONTROLS FOR ASTHMA PREVENTION

The prevention of asthma involves both the prevention of the initial development of the condition (primary prevention) and the prevention of exacerbations in asthmatics (secondary prevention) (WHO, 1995). Although little is currently known

759

about their impact on the prevalence of asthma, primary prevention strategies are obviously attractive. Secondary prevention encompasses interventions designed to avoid and treat the triggers of asthma symptoms. INDOOR ALLERGEN AVOIDANCE

Given the evidence that exposure to allergens in early infancy may precipitate the onset of asthma (Hide et al., 1994), indoor allergen avoidance is probably the most e€ective strategy for the primary prevention of asthma. It also carries obvious bene®ts for secondary prevention. Reducing domestic mite populations is an important, but dicult task. The idea is to remove the habitat of mites and make what remains inhospitable for them. Thus, the main methods are physical measures designed to control the sites that mites grow. A range of short and long term objectives for reducing exposures to house dust mites are outlined in Table 3. Bedding is a prime breeding area for mites. The single most e€ective measure is to cover mattresses and pillows with plastic or vapour permeable fabric covers. This entombs the existing allergen and cuts the mites o€ from their food source (Mudd, 1995). Owen et al. (1990) reported that covering mattresses with vapour-permeable covers reduced the mean concentration of mite allergen on the outside of the mattress from 20.3 to 0.3 mg Der p I gÿ1 of dust. Feather duvets and pillows should be replaced with synthetic ®bre and foam rubber equivalents, as these are less likely to harbour dust-mite populations. Duvets should also be encased with hypoallergenic covers, or regularly washed in hot water (over 558C) to kill mites (Salerno et al., 1992). Cotton and wool blankets should be substituted with synthetic materials, which are less conducive to mite growth. The second priority for mite removal is the ¯ooring and remainder of the bedroom. Whenever possible, the carpet should be replaced by wood or vinyl ¯ooring which can be polished. Cool shampooing carpets has no e€ect on mites and steam cleaning

Table 3. Methods for reducing exposure to house dust-mites Priority objectives * Cover mattresses and pillows. Damp wipe the mattress cover every 2 weeks. * Wash all bedding in hot cycle (0558C) weekly. Replace duvets with dacron or orlon washable material. * Place small objects that accumulate dust in drawers of closed cabinets. Clothing should be stored in closed cupboards or closets. * Vacuum carpets weekly using a vacuum cleaner with an e€ective ®lter. Medium term objectives * If possible, remove carpets from bedrooms. * Replace curtains/drapes with washable cotton curtains or venetian/slat blinds. * Control humidity in the house by increasing ventilation or using central air conditioning. Use dehumidi®ers in basements. * Treat carpets with acaricides or tannic acid. Choice of houses/apartments and ®ttings * Avoid basement ¯ats. Bedrooms should be upstairs. * If possible, avoid houses with carpets ®tted to a concrete slab. All ¯oors should have a primary polished ¯oor (vinyl or wood) and carpets should be movable. * Upholstered sofas and chairs should be avoided. * Ensure air ®lters are kept clean on central heating and air conditioning equipment.

760

A. P. Jones

only reduces the mite allergen for about a month (Mudd, 1995). The carpet is not only a source of airborne allergen, but can also harbour populations of mites which will re-infest bedding. If carpet removal is impractical, a number of di€erent chemical treatments (acaricides and denaturing agents) are available for controlling mite populations. Generally, these are applied as a liquid spray, foam, or powder. However, questions have been raised over the e€ectiveness of these agents, particularly over doses required to have a lasting noticeable e€ect (Platts-Mills et al., 1992). In the rest of the house, high levels of mite allergen can be found in sofas, chairs, carpets, curtains and other materials. Indoor vacuuming is recommended once a week (WHO, 1995). This will help remove dead mite bodies and faecal pellets that are light enough to become airborne when disturbed. However, vacuuming will increase the concentration of airborne allergens in the short term (Platts-Mills, 1997). Consequently, if asthmatics must do the vacuuming, it is preferable to wear a mask and stay out of the room for at least 30 min afterwards. Vacuum cleaners with good suction and extra thick bags may also help, as will the use of units ®tted with high-eciency particulate air (HEPA) ®lters (Reisman et al., 1990). For many areas of the house, the most e€ective treatment for mite populations is a decrease in overall levels of air humidity. Relative humidity indoors should be kept below 50%, but not less than 30% (ACP, 1990). Reductions in humidity can be achieved in several ways. In temperate climates, increasing ventilation (for example from 0.2 air changes per hour to 1 air change per hour) will be e€ective (Platts-Mills et al., 1992). The boiling of kettles and pans should be avoided in poorly ventilated areas and structural faults that allow damp to enter the home should be corrected. The indoor temperature should ideally be maintained at less than 258C, because mites do not reproduce well below this. The eradication of cockroaches from a home can be dicult as they reproduce quickly under ideal conditions. Professional extermination is probably the only method that will control a serious infestation (Kuster, 1996). In an apartment block, even this can be dicult as cockroaches can quickly reinfest from neighbouring apartments. Hence it is important that management practices should aim to keep concentrations of allergen as low as practicable. Kitchen ¯oors and cabinets should be kept clean and free from dust (Pollart et al., 1991). During the night, the maintenance of a kitchen environment that is clear from food and food residues is particularly important, as cockroaches are usually more active during the hours of darkness. Additionally, paper bags and cardboard boxes should not be stored in the home, as cockroaches often live and breed within them (Kuster, 1996).

The elimination of allergens from pets is also important. Obviously, the best avoidance measure is not to keep pets in the home. However, ®nding a new home for a family pet is not always easy. Restricting animals to certain rooms is ine€ective because the allowable rooms act as reservoirs, from which the allergen can be spread throughout the rest of the house (Wood and Egleston, 1992). If the animal cannot be removed, a number of procedures can be adopted for reducing exposure. These include the lifting of carpeted ¯ooring in rooms where dogs and cats will be housed, the adoption of a regime of regular vacuuming, the ®ltration of air and regular washing of the pet (Wood, 1995). Glinert et al. (1990) found that washing cats, combined with the purchase of washable furniture, may reduce levels of cat allergen by around 90%. Despite this, even with regular carpet vacuuming and steam cleaning, it can take many months to achieve a substantial decline in allergen levels. Fungal growth can occur on any surface and is primarily dependent on humidity, plus a source of organic matter. Removing or cleaning mould-laden objects can best reduce the number of fungal spores in indoor air. Surfaces which are especially prone to moulds, particularly in kitchens or bathrooms, should be cleaned with chemicals such as chlorine bleach (Wood, 1995). Moulds grow well in refuse containers and these should be regularly emptied (Mudd, 1995). Maintaining a low relative humidity is also important (Platts-Mills et al., 1996). Bathroom rugs and carpets are also a common source of fungal contamination and should be washed frequently or disposed of as required (Wood, 1995). OTHER MEASURES TO IMPROVE INDOOR AIR QUALITY

It is clear that asthmatics and their families ought to avoid smoking, and try and maintain a smokefree indoor environment as far as possible. Where this cannot be achieved, commercial air puri®cation devices can reduce the particulate load from cigarette smoke. In particular, the use of heating, ventilation, and air conditioning (HVAC) systems ®tted with HEPA ®lters has been shown to lower concentrations of particulate pollutants in indoor air (Antonicelli et al., 1991). However, some concerns have been raised that HVAC systems can become contaminated by fungal growth (Simmons and Crow, 1995). Furthermore, they will not eliminate the constituents of tobacco smoke that are in the gaseous phase, some of which are known respiratory irritants (Samet, 1990). Hence, the avoidance strategy, whilst not always easy, is by far preferable. The management of indoor air quality problems not caused by cigarette smoke is often dicult and, depending on the interventions required, can be costly. Room dehumidi®ers can be useful in helping

Asthma and domestic air quality

prevent mould growth in particularly damp rooms, although there is little research on the ecacy of these devices in reducing asthma symptoms. The principal steps known to reduce exposure to indoor respirable particles from sources other than smoking are venting all furnaces to the outdoors, and maintaining heating systems adequately (WHO, 1995). The use of an airtight wood stove will be preferable to an open stove or an open ®re, and the maintenance of good ventilation is important during operation. The use of ionizers to remove particulate materials from the air is not recommended, because the particles are simply deposited around the ionizer, from where they can easily be re-suspended. Ionizers can also produce ozone, which is a known respiratory irritant. To reduce exposure to NO2, all gas appliances should be regularly serviced, and have sucient ¯ues or ducts. When cooking with gas, it is a good idea to open a window to improve ventilation in the kitchen. Improved ventilation will also help prevent the potential build up of harmful gasses not associated with asthma, such as radon (Radford, 1985). A better indoor environment may be achieved by selecting building construction, building materials, and indoor ®ttings on the principle that the emission of pollutants such as VOCs and formaldehyde should be as low as reasonably achievable. The use of insulation materials that emit formaldehyde should be avoided (Norback et al., 1995). This is often dicult when a new house is being purchased, as few people have any input into the materials used to build their home. The choice of an older property is not necessarily a solution, as it may suffer from structural defects such as rising damp. Despite this, these considerations should be important for asthmatics who are moving home, or planning home alterations. CONCLUSIONS

Over the last century, the design and management of houses has changed considerably. Modern homes are well insulated, warm, and ®lled with soft furnishings and ®tted carpets. These conditions encourage the production and concentration of indoor allergens and air pollutants. These have been associated with asthma, and a range of other allergic diseases. It may be that our immune systems are simply not made for 20th century domestic life. In the past, the conditions prevailing in homes may not have been as comfortable as those we now enjoy, and some characteristics of the indoor environment were less than acceptable. Certainly an increased reliance on wood and coal burning to provide domestic heat meant that particulate pollution from these sources was generally higher than observed today. However, housekeeping practices

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meant that our ancestors were not exposed to the same cocktail of allergens and pollutants that we are. In The House of Mirth, written by Edith Wharton in 1905, it is interesting to note how one of the characters, Mrs Perniston, considers lifting carpets in the summer as one of the cardinal rules of good housekeeping. Nowadays, ®tted carpets mean that such practices are impossible. Complacency over the risks posed by indoor air quality should be avoided; the asthma epidemic is a serious global issue. Yet as Roberts and Dickey (1995) point out, we continue to allow, in many homes, exposures to substances that would not be tolerated on the job or in the outdoor environment. This is simply because most people are not aware of the problem. Allergen avoidance strategies need to be adopted by asthmatics or susceptible individuals. Sensitisation to indoor allergens is strongly associated with the development of asthma. Recent clinical trials have shown that simple avoidance measures are e€ective in reducing asthma morbidity. Such interventions are also ®nancially attractive; in the U.S.A. it has been estimated that an expenditure of just $10 for mite-proof mattress and pillow covers can signi®cantly lower the risk of an asthmatic infant requiring a hospital visit (WSDH, 1994). Patient education is also critical, and the medical practitioner has an important role to play. Good education provides a non-pharmaceutical option to managing asthma, and can be easily taught in the home, or in a primary care, hospital in-patient, or emergency department setting. Avoidance measures provide a simple and e€ective solution to the problems caused by indoor air, and should be the prime focus in any asthma or allergy management programme. In addition, a wider, more long-term, view also needs to be adopted. Managing indoor air is not simply a challenge for the homeowner or the asthma su€erer. Governments need to set and enforce home building standards. Whilst problems with existing homes are dicult to overcome, house designers and builders must be educated so as to create better new structures. However, improved data on the links between house design and health would have to precede the development and enforcement of new standards for building design. At present, we have only limited knowledge in this area. In part, this is due to the lack of gold standards that can be used to assess the quality of indoor air; whilst highly re®ned techniques are available for outdoors, the measurement and reporting of indoor air pollution is less advanced. These technologies must be developed. A change of attitude may also be required with respect to the energy eciency of buildings. Increased fuel costs could be one consequence of improved building design. However, these costs must be o€set against potential reductions in the considerable ®nancial burden from asthma and, for

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asthma prevention programmes to adequately address the problems of indoor air quality, a policy shift from reactive to proactive mode may well be required. AcknowledgementsÐI thank Mr Graham Bentham for his comments on an earlier draft of this manuscript.

REFERENCES

ACP (1990) Mould Spore Allergy. Allergy Control Products Inc., Ridge®eld. Ancona, G. (1923) Asma epidemica da pediculoides ventricosus. Policlinico Sez Med 30, 45±70. Antonicelli, L., Bilo, M. B., Pucci, S., Schou, C. and Bonifazi, F. (1991) Ecacy of an air-cleaning device equipped with a high eciency particulate air ®lter in house dust mite respiratory allergy. Allergy 46, 594±600. Arlain, L. G., Rapp, C. M. and Ahmed, S. G. (1990) Development of Dermatophagoides pteronyssinus. Journal of Medical Entomology 27, 1035±1040. Arshad, S. H., Matthews, S., Gant, C. and Hide, D. W. (1992) E€ect of allergen avoidance on development of allergic disorders in infancy. Lancet 339, 1493±1497. BjoÈrnsson, E., NoÈrback, D. and Janson, C. (1995) Asthmatic symptoms and indoor levels of micro-organisms and house dust-mites. Clinical and Experimental Allergy 25, 423±431. Brunekreef, B., Dockery, D. W. and Krzyzanowski, M. (1995) Epidemiologic studies on short-term e€ects of low levels of major ambient air pollution components. Environmental Health Perspectives 103(Suppl 2), 3±13. Burge, H. A. (1989) Airborne allergenic fungi: classi®cation, nomenclature and distribution. Immunology and Allergy Clinics of America 9, 307. Burney, P. G. J. (1993) Current questions in the epidemiology of asthma. In Asthma, ed. S. T. Holgate, K. F. Austen, L. M. Lichtenstein and A. B. Kay. Academic Press, London. Call, R. S., Smith, T. F., Morris, E., Chapman, M. D. and Platts-Mills, T. A. E. (1992) Risk factors for asthma in inner city children. Journal of Pediatrics 121, 862± 866. CDC (1994) National Health and Nutrition Examination Survey (NHANES III). US Department of Health and Human Services, Atlanta. Cockcroft, D. W. (1992) Allergens. In Asthma: Basic Mechanisms and Clinical Management, 2nd edn., ed. P. J. Barnes, I. W. Rodger and N. C. Thompson, pp. 413± 426. Academic Press, London. Cohen, L. (1995) Indoor air quality a major public health issue, workshop told. Canadian Medical Association Journal 153, 92±93. Collo€, M. J. (1994) Dust-mite control and mechanical ventilation: when the climate is right. Clinical and Experminental Allergy 24, 94±96. D'Amato, G., Liccardi, G. and D'Amato, M. (1994) Environment and development of respiratory allergy. II: indoors. Monaldi Archive of Chest Disorders 49, 412± 420. Dockery, D. W., Pope, C. A., Xu, X., Spengler, J. D., Ware, J. H., Martha, E. F., Ferris, B. G. and Spezier, F. E. (1993) An association between air pollution and mortality in six U.S. cities. The New England Journal of Medicine 329, 1753±1759. ForastieÂre, F., Corbo, G. M., Michelozzi, P., Pistelli, R., Agabiti, N., Brancato, G., Ciappi, G. and Perucci, C. A. (1992) E€ects of environment and passive smoking on the respiratory health of children. International Journal of Epidemiology 21, 66±73.

Glinert, R., Wilson, P. and Wedner, H. J. (1990) Fel d I is markedly reduced following sequential washing of cats. Journal of Allergy and Clinical Immunology 85, 327(Abstract). Gold, D. R. (1992) Indoor air pollution. Clinics in Chest Medicine 13, 215±229. Gortmaker, S. L., Walker, D. K., Jacobs, F. H. and Ruch-Ross, H. (1982) Parental smoking and the risk of childhood asthma. American Journal of Public Health 72, 574±579. Haahtela, T., Lindholm, H., Bjorksten, F., Koskenvuo, K. and Laitinen, L. A. (1990) Prevalence of asthma in Finnish young men. British Medical Journal 301, 266± 268. Hannaway, P. J. (1993) Exposure to high concentration of house dust mites as a possible precipitating factor in near fatal asthma. Journal of Allergy and Clinical Immunology 17, 105±111. Harving, H., Dahl, R. and Mùlhave, L. (1991) Lung function and bronchial reactivity in asthmatics during exposure to volatile organic compounds. American Review of Respiratory Diseases 143, 751±754. Hasselblad, V., Eddy, D. M. and Kotchmar, D. J. (1992) Synthesis of environmental evidence: nitrogen dioxide epidemiology studies. Journal of the Air and Waste Management Association 42, 662±671. Hide, D. W., Matthews, S., Matthews, L., Stevens, M., Ridout, S., Twiselton, R., Gant, C. and Arshad, S. H. (1994) E€ect of allergen avoidance in infancy on allergic manifestations at age two years. Journal of Allergy and Clinical Immunology 93, 842±846. Hines, A. L. (1993) Indoor Air: Quality and Control. Prentice Hall, U.S.A. Honicky, R. E., Osborne, J. S. and Akpom, C. A. (1985) Symptoms of respiratory illness in young children and the use of wood-burning stoves for indoor heating. Pediatrics 75, 587±593. Hyndman, S. J., Brown, D. L., Ewan, P. W., Higenbottam, T. W., Maunder, J. W. and Williams, D. R. R. (1994) Humidity regulation in the management of asthma patients senstized to house dust mites. Quarterly Journal of Medicine 87, 367±372. Jarvis, D., Chinn, S., Luczynska, C. and Burney, P. (1996) Association of respiratory symptoms and lung function in young adults with the used of domestic gas appliances. Lancet 347, 426±431. Jones, A. P. (1997) The main causative factors of asthma, available information on population exposure to those factors, and current measures of control. In Asthma in Europe, pp. 207±301. European Federation of Asthma and Allergy Associations, Holland. Kaliner, M. A. and White, M. V. (1994) Asthma: causes and treatment. Complimentary Therapy 20, 645±650. Kalra, S., Own, S. J., Hepworth, J. and Woodcock, A. (1990) Airborne house dust mite antigen after vacuum cleaning. Lancet 336, 449(letter). Kingham, S., Briggs, D., Elliott, P., Fischer, P., van Reeuwijk, H. and Lebret, E. (1996) Exposure to trac related air pollution: the EC funded Saviah-2 study. In Proceedings of the VIIth International Symposium in Medical Geography, ed. G. Moon, M. Gould and R. Watt. University of Portsmouth, Portsmouth. Koenig, J. Q., Larson, T. V., Hamley, Q. S., Rebolledo, V., Dumler, K., Checkoway, H., Wang, S. Z., Lin, D. and Pierson, W. E. (1993) Pulmonary lung function in children associated with ®ne particulate matter. Environmental Research 63, 26±38. Koren, H. S., Graham, D. E. and Devlin, R. B. (1992) Exposure of humans to volatile organic mixture. III. In¯ammatory response. Archives of Environmental Health 47, 39±44.

Asthma and domestic air quality Kuster, P. A. (1996) Reducing the risk of house dust mite and cockroach allergen exposure in inner-city children with asthma. Pediatric Nursing 22, 297±299. Lau, S. and Wahn, U. (1990) Indoor environments and the development of allergy. ACI News 2, 179±182. Lipfert, F. W. (1997) Air pollution and human health: perspectives for the `90s and beyond. Risk Analysis 17, 137±146. Luczynska, C. M. (1994) Risk factors for indoor allergen exposure. Respiratory Medicine 88, 723±729. Luczynska, C. M., Li, Y., Chapman, M. D. and PlattsMills, T. A. E. (1990) Airborne concentrations and particle size distribution of allergen derived from domestic cats: measurements using a cascade impactor, liquid impinger and two-site monoclonal antibody assay for Fel d I. American Review of Respiratory Disorders 141, 361±367. Molina, C. L. (1992) Respiratory manifestations induced by indoor air. Proceedings of the XVth Congress of EAACI Paris, pp. 377±386. Moschandreas, D. J., Zabransky, J. and Rector, H. E. (1980) The e€ects of woodburning on the indoor residential air quality. Environment International 4, 463± 468. Mudd, K. E. (1995) Indoor environmental allergy: a guide to environmental controls. Pediatric Nursing 21, 534± 536. Musmand, J. J., Horner, W. E., Lopez, M. M. and Lehrer, S. B. (1995) Identi®cation of important allergens in German cockroach extracts by sodium dodecylsulfate-polyacrylamide gel electrophoresis and Western blot analysis. Journal of Allergy and Clinical Immunology 95, 877±885. Neas, L. M., Dockery, D. W., Burge, H., Koutrakis, P. and Speizer, F. E. (1996) Fungus spores, air pollutants, and other determinants of peak expiratory ¯ow rate in children. American Journal of Epidemiology 143, 797± 807. Norback, D., Bjornsson, E., Janson, C., Widstrom, J. and Boman, G. (1995) Asthma. Occupational and Environmental Medicine 52, 388±395. ONS (1996) 1996 Family Spending: A Report on the 1995± 1996 Family Expenditure Survey. Oce for National Statistics, London. Owen, S., Morganstern, M., Hepworth, J. and Woolcock, A. (1990) Control of house dust-mite antigen in bedding. Lancet 335, 396±397. Peat, J. K., Tovey, E., Gray, E. J., Mellis, C. M. and Woolcock, A. J. (1994) Asthma severity and morbidity in a population sample of Sydney schoolchildren. Australian and New Zealand Journal of Medicine 24, 270±276. Platts-Mills, T. A. E. (1995) Is there a dose-response relationship between exposure to indoor allergens and symptoms of asthma? Journal of Allergy and Clinical Immunology 96, 435±440. Platts-Mills, T. A. E. (1997) Asthma and indoor exposure to allergens. The New England Journal of Medicine 336, 1382±1384. Platts-Mills, T. A. E., Ward, G. W., Sporik, R., Gelber, L. E., Chapman, M. D. and Heymann, P. W. (1991) Epidemiology of the relationship between exposure to indoor allergens and asthma. International Archives of Allergy and Applied Immunology 94, 339±345. Platts-Mills, T. A. E., de Blay, F., Ward, G. W. and Hayden, M. L. (1992) Allergen avoidance. In Asthma: Basic Mechanisms and Clinical Management, 2nd edn., ed. P. J. Barnes, I. W. Rodger and N. C. Thompson, pp. 515±526. Academic Press, London. Platts-Mills, T. A. E., Woodfolk, J. A., Chapman, M. D. and Heymann, P. W. (1996) Changing concepts of allergic disease: the attempt to keep up with real changes in

763

lifestyles. Journal of Allergy and Clinical Immunology 98(Suppl), S297±S306. Pollart, S. M., Smith, T. F., Morris, E. C., Gelber, L. E., Platts-Mills, T. A. E. and Chapman, M. D. (1991) Environmental exposure to cockroach allergen: analysis with monoclonal antibody based enzyme immunoassays. Journal of Allergy and Clinical Immunology 87, 505±510. Pollart, S. M., Chapman, M. D., Fiocco, G. P., Rose, G. and Platts-Mills, T. A. E. (1989) Epidemiology of acute asthma: IgE antibodies to common inhalant allergens as a risk factor for emergency room visits. Journal of Allergy and Clinical Immunology 83, 875±882. Radford, E. P. (1985) Potential health e€ects of indoor radon exposure. Environmental Health Perspectives 62, 281±287. Reisman, R. E., Mauriello, P. M., Davis, G. B., Georgitis, J. W. and DeMasi, J. M. (1990) A double-blind study of the e€ectiveness of a high-eciency particulate air (HEPA) ®lter in the treatment of patients with perennial allergic rhinitis and asthma. Journal of Allergy and Clinical Immunology 85, 1050±1057. Roberts, J. W. and Dickey, P. (1995) Exposure of children to pollutants in house dust and indoor air. Reviews of Environmental Contamination and Toxicology 143, 59± 78. Rosenstreich, D. L., Eggleston, P., Kattan, M., Baker, D., Slavin, R. G. and Gergen, P. et al. (1997) The role of cockroach allergy and exposure to cockroach allergen in causing morbidity amongst inner-city children with asthma. New England Journal of Medicine 336, 1356± 1363. Salerno, M. S. R., Huss, K. and Huss, E. W. (1992) Allergen avoidance in the treatment of dust-mite allergy and asthma. Nursing Practitioner 17, 53±65. Salvaggio, J. E. (1991) The impact of allergy and immunology on our expanding industrial environment. Journal of Allergy and Clinical Immunology 85, 689±699. Samet, J. (1990) Environmental controls and lung disease. American Review of Respiratory Diseases 142, 915±939. Samet, J., Marbury, M. C. and Spengler, J. D. (1987) Health e€ects and sources of indoor air pollution. Part 1. American Review of Respiratory Diseases 136, 1486± 1508. Simmons, R. B. and Crow, S. A. (1995) Fungal colonisation of air ®lters for use in heating, ventilating, and air conditioning (HVAC) systems. Journal of Industrial Microbiology 14, 41±45. Spengler, J. D., Dockery, D. W., Turner, W. A., Wolfson, J. M. and Ferris, B. G. (1981) Long-term measurements of respirable particles, sulphates and particulates inside and outside homes. Atmospheric Environment 15, 23±30. Sporik, R., Holgate, T., Platts-Mills, T. A. E. and Cogswell, J. J. (1990) Exposure to house-dust-mite allergen (Der P I) and the development of asthma in childhood. New England Journal of Medicine 323, 502±507. Tovey, E. R., Chapman, M. D., Wells, C. W. and PlatsMills, T. A. E. (1981) The distribution of dust mite allergen in the houses of patients with asthma. American Review of Respiratory Diseases 124, 630±635. Traynor, G. W., Apte, M. G. and Carruthers, A. R. (1986) Indoor Air Pollution Due to Emission from Woodburning Stoves. Lawrence Berkeley Laboratories, Berkeley, CA. Tunnicli€e, W. S., Burge, P. S. and Ayres, J. G. (1994) E€ect of domestic concentrations of nitrogen dioxide on airway responses to inhaled allergen in asthmatic patients. Lancet 344, 1733±1736. Viegi, G., Carrozzi, L., Paoletti, P., Vellutini, M., DiViggiano, E., Baldacci, S., Modena, P., Pedreschi, M., Mammini, U. and di Pede, C. (1992) E€ects of the home environment on respiratory symptoms of a general population sample in middle Italy. Archives of Environmental Health 47, 64±70.

764

A. P. Jones

WHO (1995) Global Strategy for Asthma Management and Prevention. World Health Organisation, Geneva. Wickman, M., Gravesen, S., Nordvall, S. L., Pershagen, G. and Sundell, J. (1992) Indoor viable dust-bound microfungi in relation to residential characteristics, livings habitats, and symptoms in atopic and control children. Journal of Allergy and Clinical Immunology 89, 752±759. Wieslander, G., NorbaÈck, D., BjoÈrnsson, E., Janson, C. and Boman, G. (1997) Asthma and the indoor environment: the signi®cance of emission of formaldehyde and volatile organic compounds from newly painted indoor surfaces. International Archives of Occupational and Environmental Health 69, 115±124.

Wood, R. (1995) Taming Asthma and Allergy by Controlling your Environment. Asthma and Allergy Foundation of America, Baltimore, MD. Wood, R. and Egleston, P. (1992) Management of allergy to animal danders. Immunology and Allergy Clinics of America 12, 69±84. Woodfolk, J. A., Luczynska, C. M., De Blay, F., Chapman, M. D. and Platts-Mills, T. A. E. (1992) Cat allergy. Annals of Allergy 69, 273±275. WSDH (1994) Comprehensive Hospital Abstract Reporting System (CHARS). Washington State Department of Health, Olympia, WA. Xu, Z. Y., Blot, W. J. and Xiao, H. P. (1989) Smoking, air pollution, and the high rates of lung cancer in Shenyang, China. Journal of the National Cancer Institute 81, 1800±1806.