What Do Patients With Asthma Need to Know About Environmental Control, and What Is the Evidence to Support These Instructions?

Stephen J. McGeady, MD

Environmental control is a vast topic, and an in-depth review is beyond the scope of this chapter. The reader is referred to several excellent reviews if additional information is desired.1-3 The asthmatic patient’s environment includes both the indoors and the outdoors, and potential offending agents may be pollutants that aggravate asthma by their irritant or pro-inflammatory properties or allergens that cause asthma by causing an allergic airway reaction. Some pollutants may also skew immune responses to newly encountered antigens toward allergic responses, thereby expanding the number of potentially offending allergens. The various environmental factors of concern will be considered by primary location and recommended remedies described.

Outdoor pollutants include a large number of compounds, such as sulfur dioxide, nitric oxide, various volatile organic compounds and their metabolites and ozone. There are also particulate materials that may be harmful to asthmatic subjects, and these include diesel exhaust particles from motor vehicles and the particulate effluents of coal and power plants. Although the mechanism is not well-understood, ozone and diesel exhaust particles are able to produce an enhanced allergic response when individuals are exposed to an allergen to which they are sensitive.4 Diesel exhaust particles have also been reported to skew immune responses to newly encountered antigens toward allergy.1 The accumulated evidence that air pollutants encountered outside of the home are harmful to asthmatics is overwhelming, and there is convincing evidence that avoidance of these pollutants can have beneficial effects on asthma.5

Prevention of exposure to these asthma-aggravating pollutants, however, relies almost exclusively on avoidance, and that often includes either remaining indoors while pollutant levels are high or a change of residence out of an area where the pollutant is found. Relocation may not be realistic for some, especially those in lower socioeconomic strata, and this reality may account for part of the poor asthma outcomes seen in impoverished patients. The benefits of avoidance of high levels of air pollution have been documented in several reports. In one such report, the prevalence of respiratory illness in a town in Utah decreased during a strike that closed a steel mill for 1 year. While the mill was inactive, both the level of aerosolized particulates and the prevalence of respiratory disease, including asthma, decreased markedly. When the strike was settled and the mill resumed operation, both particulate levels in the atmosphere and respiratory disease in the community returned to pre-strike levels.5 A similar observation was made when the city of Atlanta decreased motor vehicle traffic during the 1996 Olympics in an attempt to decrease summer ozone. Both the ozone level and asthma morbidity were reduced for the duration of the games.6

Outdoor allergens of concern include all of the aero-allergens that cause increases in asthmatic symptoms by eliciting allergic inflammation. These include primarily pollen and mold allergens, which occur on a seasonal basis. As noted in the earlier discussion of allergic asthma triggers (see Question 5), demonstrating a direct cause-and-effect relationship between these allergens and increased asthma symptoms has been difficult. In some allergic patients, however, there does appear to be a tendency for asthma symptoms to flare up at times when specific aero-allergens are at high levels. It is also a very common complaint that a child’s asthma attacks are precipitated by “weather changes,” and while weather changes involve a series of complicated atmospheric alterations, they may involve increased pollen and mold spore counts as these allergens are pushed ahead of advancing weather fronts. Alternaria mold spores in particular have been reported to be a risk factor for respiratory arrest and for death in children and young adults with asthma in the summer and early fall.7,8

Avoiding outdoor allergens is difficult but can sometimes be achieved by simply remaining indoors. This level of confinement is often impractical, and the negative effect on a child’s psychosocial development and self-esteem should be a consideration before undertaking it. If outdoor exposure is unavoidable or deemed appropriate, it is sometimes possible to control the asthma symptoms with medications. Consideration can also be given to allergen immunotherapy, which may modulate symptoms if an outdoor allergen exposure is the apparent cause of asthma.

Indoor pollutants that may aggravate asthma include environmental tobacco smoke (ETS), which has been associated with several pathologic respiratory conditions and has been clearly connected to asthma exacerbations.9,10 ETS contains a toxic mixture of irritant gases and particulates that are laced with polyaromatic hydrocarbons, which have the potential to generate oxidant species that inflame airway mucosa.1 These compounds also skew immune responses to newly encountered antigens toward allergic responses. The burning of other biomass, such as in fireplaces, may produce a similar array of aerosolized compounds to ETS, although the concentration of these pollutants is almost always lower than that observed in ETS exposure. In addition to the byproducts of biomass incineration, nitrogen dioxide (NO2) is a significant indoor pollutants. The origin of which is usually natural gas-burning appliances, especially when these are poorly maintained or inadequately ventilated. NO2 is a known precursor to ozone in the outdoors, but, indoors, it acts by itself as a promoter of airway inflammation and is well-known to be associated with increased asthma symptoms.11,12 The presence of biologically derived agents, such as endotoxin, has been associated with increased airway inflammation. These compounds are associated with the numbers of animals, including dogs, cats, and humans residing in a given home. The presence of endotoxin from gram-negative bacteria, 1-3 β glucans from molds, and products derived from gram-positive bacteria can cause airway inflammation directly, but may also influence the immune response to potential allergens toward allergic inflammation.13

Intervention to achieve avoidance of indoor pollutants primarily consists of the remediation steps that are obvious. ETS avoidance can best be achieved by discontinuing tobacco smoking altogether or at least confining it to the outdoors. The aerosolized products of wood or other biomass burning can be minimized by ensuring that the fireplace chimney is functioning optimally. NO2 levels can be decreased when natural gas-burning appliances are made to function efficiently and are properly ventilated. Because endotoxin and biologically derived products seem to increase in direct proportion to the number of animals and humans in the home, keeping these inhabitant numbers to a reasonable level that is consistent with the size of the home offers one means of control, while another is maintaining a measure of cleanliness sufficient to prevent accumulation of these potentially harmful compounds.

Indoor allergens that may aggravate asthma include some that are highly airborne, while others are heavier and tend to settle. The best characterized of these heavy allergens are the house dust mites (HDMs). HDMs are found in fabric and bedding in their greatest numbers, and it is the droppings of the HDMs that are the principal source of allergens. The allergenic particles of HDM are heavy, and while they may be briefly aerosolized by dusting or vacuuming, they settle soon after. The greatest exposure to HDM allergen takes place while in bed because HDM are present in largest numbers in bedding, and a considerable fraction of a person’s day is spent sleeping. In contrast to HDM allergen, the allergenic particles from cats and dogs are highly airborne and remain suspended for many hours. The property of remaining airborne together with the inherent allergenicity of dog and cat emanations makes these allergens readily inhaled and a major provoking stimulus in many asthmatic children. The allergens of rodents, which may be present in homes either as vermin or as pets, are not as well studied as are dog and cat, but data from occupational exposures and from the National Cooperative Inner Cities Asthma Study clearly illustrates the potential for rodent allergens to cause or aggravate asthma.14 This same study of asthma in the inner cities has implicated cockroach allergy as being associated with asthma as well.15 Like HDM allergen, cockroach allergen is a weighty particle and is aerosolized primarily during vacuum cleaning of a home infested by these insects. Mold spores are found in all environments both indoor and outdoor, but thrive in the presence of humidity. Thus, homes that have water damage, especially if the water is persistent, will have growing mold colonies and large numbers of airborne mold spores. As noted for outdoor molds, these spores can aggravate asthmatic symptoms.

Intervention to reduce indoor allergen exposure will vary with the specific allergen. As noted, HDM and cockroach allergens are weighty, and, consequently, air filtration with high-efficiency particulate air (HEPA) filters is not effective. Instead, it is recommended that mattresses and pillows be covered with impenetrable covers and bedding be washed at 7- to 14-day intervals in 130°F water. Vacuuming should be done with a double-thickness vacuum collection bag or HEPA filter.15 In attempting to minimize allergen exposure to domestic pets, removal of the animal from the home is best, but seldom acceptable. HEPA air cleaners are helpful in reducing pet allergen exposure due to the aerodynamic properties of these animals’ allergens. More important, however, is the removal, where possible, of reservoirs of allergen such as sofas and carpeting. Last, washing the pet on a frequent basis (eg, weekly) has been shown to diminish the allergen shedding.16 For rodents and cockroaches, the obvious solution is to eliminate the infestation through eradication procedures. Mold remediation can be accomplished with any number of commercially available fungicides, but unless the source of moisture is eliminated, the mold will re-appear.

While published reviews of single interventions in control of indoor allergens have sometimes cast them as ineffective, the more carefully conducted studies have shown efficacy, particularly for HDM control. When a comprehensive approach to improving indoor air quality is carried out, the evidence is that there is a decrease in asthma symptoms and severity.17

References

1.  Peden DB. Air pollution: indoor and outdoor. In: Adkinson NF, Bochner BS, Busse NW, Holgate SF, Laranske JR, Simons FER, eds. Middleton’s Allergy Principles and Practice. 7th ed. St. Louis, MO: Mosby Elsevier. 2009:495-508.

2.  Platts-Mills TAE. Indoor allergens. In: Adkinson NF, Bochner BS, Busse NW, Holgate SF, Laranske JR, Simons FER, eds. Middleton’s Allergy Principles and Practice. 7th ed. St. Louis, MO: Mosby Elsevier. 2009:539-556.

3.  Custovic A. Allergen control in the prevention and management of allergic disease. In: Adkinson NF, Bochner BS, Busse NW, Holgate SF, Laranske JR, Simons FER, eds. Middleton’s Allergy Principles and Practice. 7th ed. St. Louis, MO: Mosby Elsevier. 2009:1447-1458.

4.  Peden DB. The epidemiology and genetics of asthma risk associated with air pollution. J Allergy Clin Immunol. 2005;115:213-219.

5.  Pope CA 3rd. Respiratory disease associated with community air pollution and a steel mill, Utah Valley. Am J Public Health. 1989;79:623-628.

6.  Friedman MS, Powell KE, Hutwagner L, Graham LM, Teague WG. Impact of changes in transportation and commuting behaviors during the 1996 Summer Olympic Games in Atlanta on air quality and childhood asthma. JAMA. 2001;285:897-905.

7.  Denning DW, O’Driscoll BR, Hogaboam CM, Bowyer P, Niven RM. The link between fungi and severe asthma: a summary of the evidence. Eur Respir J. 2006;27:615-626.

8.  O’Hollaren MT, Yunginger JW, Offord KP, et al. Exposure to an aeroallergen as a possible precipitating factor in respiratory arrest in young patients with asthma. N Engl J Med. 1991;324:359-363.

9.  Gergen PJ. Environmental tobacco smoke as a risk factor for respiratory disease in children. Respir Physiol. 2001;28:39-46.

10.  Gold DR. Environmental tobacco smoke, indoor allergens, and childhood asthma. Environ Health Perspect. 2000;(108 Suppl 4):643-651.

11.  Brunekrsef B, Houthuijs D, Dykstra L, et al. Indoor nitrogen dioxide exposure and children’s pulmonary function. J Air Waste Management Assoc. 1990;40:1252-1256.

12.  Neas LM, Dockery DW, Ware JH, Spengler JD, Speizer FE, Ferris BJ Jr. Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary function in children. Am J Epidemiol. 1991;134:204-219.

13.  Virchow JC Jr, Julius P, Matthys H, Kroegel C, Luttmann W. CD14 expression and soluble CD14 after segmental allergen provocation in atopic asthma. Eur Respir J. 1998;11:317-323.

14.  Matsui EC, Simons E, Rand C, et al. Airborne mouse allergen in the homes of inner-city children with asthma. J Allergy Clin Immunol. 2005;115:358-363.

15.  Rosenstreich DL, Eggleston P, Kattan M, et al. The role of cockroach allergy and exposure to cockroach allergen in causing morbidity among inner-city children with asthma. N Engl J Med. 1997;336:1356-1363.

16.  Platts-Mills TA, Vaughan JW, Carter MC, Woodfolk JA. The role of intervention in established allergy: avoidance of indoor allergens in the treatment of chronic allergic disease. J Allergy Clin Immunol. 2000;106:787-904.

17.  Morgan WJ, Crain EF, Gruchalla RS, et al. Inner-city Asthma Study Group. N Engl J Med. 2004;351:1068-1080.

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