Identifying indoor and outdoor pollutants can help control the severity of asthma exacerbations.
By Jennifer Vavra
The exact origins of asthma remain unclear; however, it is thought that asthma is caused by an interaction between environmental and genetic factors.1 On the basis of this suggested causation standard, investigations of environmental factors have been launched. Environmental tobacco smoke is the only air pollutant that has been identified as a causative agent in the development of asthma.2 While there is no clear evidence correlating the development of asthma with other environmental pollutants, research results1-12 do suggest that environmental pollutants and allergens seem to exacerbate asthma attacks or symptoms by acting as triggers, aggravators, and/or irritants.
Environmental pollutants vary in source and location. There are two major categories: outdoor and indoor. While these distinctions represent the major locations of pollutants, some outdoor pollutants can be found indoors, and vice versa. Aggravating allergens exist both outdoors and indoors and are often considered pollutants, but should be thought of as allergens.
When air pollution is mentioned, a few outdoor suspects usually come to mind. Nitrogen dioxide, sulfur dioxide, chlorofluorocarbons, triatomic oxygen (lower-atmosphere ozone),5 and particulate matter are usually thought of immediately; the results of automobile exhaust, construction, and industry, these outdoor pollutants can be powerful asthma irritants and aggravators. Harold Nelson, MD, of the National Jewish Medical and Research Center, Denver, says, “There is no question that outdoor air pollution increases the symptoms of asthma, visits to the emergency department, and hospitalizations. Oxides of nitrogen, sulfur dioxides, and ozone all have adverse effects. Possibly the most harmful outdoor pollutant to asthma patients is fine particulate matter of less than 10 µm. While outdoor pollution is capable of aggravating asthma, it is hard to connect outdoor pollutants with the cause of asthma or to blame the increase of reported asthma on outdoor pollutants.”
Nitrogen dioxide is a by-product of smoking, volcanic activity, lightning, bacteria, power generation, fossil-fuel–burning industries, and automobile exhaust. Of these sources, the most insidious are power generation (with 35% of nitrogen dioxide production) and automobiles (with 45%). Unfortunately, environmental levels of nitrogen dioxide are rising.3 In addition, nitrogen dioxide converts to ozone during the summer months when strong sunlight, low winds, and high temperatures are present. In the absence of strong sunlight, nitrogen dioxide is not converted to ozone and remains in the atmosphere.3
In addition to being an outdoor pollutant, nitrogen dioxide is also categorized as an indoor pollutant, resulting from improperly ventilated gas stoves and kerosene lamps. In fact, nitrogen dioxide is found at higher levels indoors. Regardless of the location, nitrogen dioxide is less reactive than ozone. Due to the low solubility of nitrogen dioxide, it penetrates to the periphery of the lung. More than 60% of nitrogen dioxide may be deposited in the lung periphery.12 Exposure to nitrogen dioxide can increase the accumulation of protein in the alveoli and pulmonary cells, which could, in turn, lead to decreased elasticity and poor gas exchange.3 It has been reported that high levels of nitrogen dioxide, sulfur dioxide, and ozone result in elevated antigen perfusion from the lungs to the blood, which could result in systemic reactions to allergens.3 It has also been hypothesized that the oxidizing nature of nitrogen dioxide causes reduced alveolar macrophage phagocytosis, which could permit the antigen to remain in the lungs longer.3 Koenig2 reported on a meta-analysis of 20 studies that were designed to address the effects of nitrogen dioxide on bronchial hyperresponsiveness and found that it increased an average of 60% in asthma patients after controlled exposure to nitrogen dioxide.
Sulfur dioxide originates from volcanoes, industrial sources, domestic heating, and vehicles.3 In a controlled exposure study reported by Koenig,2 it was found that a 2.5-minute exposure to sulfur dioxide was enough to cause bronchoconstriction in subjects with asthma. Sulfur dioxide causes a decrease in forced expiratory volume in 1 second (FEV1) and an increase in total lung resistance. Sulfur dioxide does not produce a direct antigenic response, and asthma patients are sensitive to lower concentration of sulfur dioxide than are people without asthma. Findings suggest that sulfur dioxide acts as a direct irritant.
It is possible that sulfur dioxide may decrease lung function by causing epithelial cell damage and an irritation response in the airways. It has also been suggested that sulfur dioxide may activate sensory nerves in the airways, resulting in wheeze and cough; these, in turn, would result in bronchial irritation. Sulfur dioxide is mostly absorbed in the upper airways when the body is at rest, due to deep ventilation. Exercise also seems to create the risk of lower-airway damage due to deep ventilation. In general, sulfur dioxide provokes bronchoconstriction accompanied by wheezing and shortness of breath in asthma patients. Of the common pharmaceutical agents used to treat asthma, albuterol was shown to be the most effective in blocking or mitigating the effects of sulfur dioxide.2 Like nitrogen dioxide, sulfur dioxide requires strong sunlight, low winds, and high temperatures for its conversion to ozone to take place. If not converted to ozone, sulfur dioxide remains in the atmosphere.3
Chlorofluorocarbons destroy upper-atmosphere (good) ozone, allowing exposure to harmful ultraviolet radiation and causing global warming. This is detrimental for two reasons. First, a decrease in good atmospheric ozone has been correlated with an increase in reported skin cancers. Second, Zoidis12 suggests that increased ultraviolet radiation and global warming can lead to an increased production of triatomic oxygen. Other means of production of ozone involve the conversion of nitrogen dioxide and sulfur dioxide from automobile exhaust and combustion sources.3
Inhaled ozone is associated with damage to the mucosa of airways caused by the activation of inflammatory cells through a cytokine-mediated mechanism.12 Exposure to ozone is a major health concern for asthma patients due to bronchial response, as measured by decreasing pulmonary-function levels.12 It has been reported3 that a strong three-way interaction of ozone, particulate matter, and temperature results in lowered peak expiratory flow rate readings. Ozone, by increasing polymorphonuclear (PMN) cell counts, has also been associated with decreases in the amount of allergen needed to cause a reaction.3 It appears that ozone is capable of stimulating eosinophils and attracting PMNs to the airways.3 There is also a possibility that mast-cell-driven mediators like leukotrienes, histamine, or prostaglandin D are released, which could lead to heightened inflammation of the airways. In the late-phase reaction this could result in hyperactivity, which can be very risky for asthma patients.3 On the basis of these findings, Bielory and Deener3 reported an in vitro study that found that ozone is capable of inducing release of an immune regulatory cytokine and capable of deploying fibroblasts to the lungs (and arousing their twofold to threefold devision). It was also found that ozone has cytotoxic effects on epithelial cells. In general, ozone exposure is associated with airway inflammation, decreased lung function, and enhanced response to aeroallergens; these effects result in more emergency department visits and hospitalizations.2
Particulate matter is an extremely diverse mixture of smoke, soil particles, tire particles, engine oil, sulfate, construction dust, and nitrates.3 Gravel pits and the salt used on roads in winter are also sources.13 Therefore, it is very difficult to reproduce particulate matter in a controlled laboratory setting in order to get reliable results. Although there is strong evidence linking particulate matter and adverse effects on the respiratory system, the exact agents causing the negative effects and their mechanisms of action have yet to be explained.13 One form of particulate matter, however, is common in Canada and the United States and is easily reproduced: sulfuric acid.2
Due to the ease of reproducing sulfuric acid, many studies of particulate matter have been based on inhaled concentrations of this type. The results of these studies suggest that asthma patients are more sensitive to all concentrations of sulfuric acid and that they display decreased FEV1 and forced vital capacity.2 Particulate matter is generally associated with increased symptoms of respiratory distress, lowered lung function, increased use of asthma medications, and increased visits to the emergency department and hospitalizations, especially in children.2,8
The negative health effects of particulate matter become more severe when the particulates themselves become smaller. Particulate matter that is less than or equal to 10 µm in diameter is especially dangerous. Because the particles are so small, they are not filtered out by the respiratory tract’s defenses. These particles are small enough to be inhaled into the lower airways, where they can plug the gas-exchange system. While no complete reports have been conducted on fatalities and daily air pollution, evidence does exist that links particulate matter with increased mortality of individuals more than 65 years old who had preexisting cardiac or respiratory disease.2
There are numerous studies reviewing the significance of outdoor allergens in asthma development and aggravation. Many epidemiological studies agree that pollen sensitivity poses only a minimal risk for the development of asthma in the general population.7 Other research focuses on allergens as aggravators, not sources, of asthma development. Pollen seems to trigger an inflammatory response in the airways, causing bronchoconstriction. In order for pollen to act as a trigger, however, the subject needs to be exposed to a high concentration of the allergen, as the pollen itself is large enough to prevent it from penetrating to the level of the lower airways readily.7 Studies7,10 link large amounts of allergens, namely grass and birch, with increased lower-respiratory inflammation, allergic rhinitis, and asthma exacerbation.
Alternaria spp are common outdoor molds that can cause respiratory irritation. Alternaria and other outdoor molds cause degranulation of mast-cell inflammatory mediators through the cross-linking of mold surface antigens with immunoglobulin E (IgE) antibodies on the mast cell.3 If this happens in the bronchioles, the airways swell, greatly impeding the passage of air. If the reaction occurs in the gas-exchange area of the lung, pulmonary function can cease, with fatal results. Immunotherapy can have some very beneficial effects on those who have outdoor mold allergies. Sensitivity to Alternaria has been correlated with increased bronchial responsiveness and risk for asthma.7 The effects of outdoor allergens can be exacerbated when combined with outdoor pollutants.
With the exception of nitrogen dioxide, most outdoor pollutants have been decreasing. The decrease of outdoor pollutants in the United States can be attributed to the Clean Air Act of 1970 and the formation of the National Ambient Air Quality Standards Board. These entities have helped regulate industry practices and have contributed to the development of automobiles that burn fuel more cleanly. Despite the drop in outdoor pollutants, the cases of diagnosed and reported asthma are on the rise. This has provoked the study of indoor pollutants and allergens.
It has been reported3 that the average US resident spends 22 hour a day indoors. Indoor pollutant concentrations are very high due to tightly sealed housing, which is characterized by insulation, decreased ventilation, wall-to-wall carpeting, and high indoor temperatures.3 This indoor environment provides a kind of vacuum seal for airborne pollutants and allergens.
Environmental Tobacco Smoke
Possibly the most visible indoor pollutant is environmental tobacco smoke. While people may encounter environmental tobacco smoke in an outdoor setting and experience it as an asthma irritant or aggravator, the majority of the research on environmental tobacco smoke concerns indoor exposure. The mechanism of action of environmental tobacco smoke is not entirely known, yet its health effects are undeniable. The US Environmental Protection Agency estimates that environmental tobacco smoke increases asthma symptoms in 200,000 to 1 million children each year. Evidence3 suggests that environmental tobacco smoke may exert its effects by altering the permeability of epithelial cells. Direct inflammatory effects involving lymphocyte function, cytokine induction, increases in total serum IgE levels, and increases in airway responsiveness have been noted.
Most of the research on environmental tobacco smoke has focused on maternal smoking in utero and during early childhood. It has been suggested3 that mothers who smoke while their children are in utero create a twofold to threefold increase in the risk that their children will develop asthma. Maternal smoking has a significant influence on asthma development in children up to 2 years old, but the risk decreases as the child gets older. Researchers estimate that maternal environmental tobacco smoke is responsible for exacerbating 7.5% of the total annual cases of symptomatic asthma in children.3
Volatile Organic Compounds
Volatile organic compounds are another type of indoor pollutant. These come from a variety of sources, including particleboard, solvents, cleaning products, floor adhesive, wood stain, paint, polishes, room fresheners,1 furniture, water supplies, fuel combustion, and building materials.4 Volatile organic compounds exist at concentrations that are five to 10 times greater indoors than outdoors and act as respiratory irritants.1
Formaldehyde is another indoor pollutant that can result from environmental tobacco smoke, chipboard, construction materials, insulating materials, water-based paints, fabrics, plywood, disinfectants, cleaning agents, and cooking and heating practices.4 Burr reports that peak expiratory flow rates and formaldehyde concentrations are inversely related in children, with the most noted effects found in children with asthma. Formaldehyde is a respiratory irritant that can contribute to upper-respiratory irritation in small concentrations and to lower-airway and pulmonary effects in larger concentrations.1 Nocturnal breathlessness has been reported when concentrations of volatile organic compounds and/or formaldehyde are present in an environment.1
Ventilation of housing can greatly reduce volatile organic compounds and other indoor pollutants. Ron Burke, deputy director of the American Lung Association (ALA) of Metropolitan Chicago, comments, “Indoor air-quality testing rarely happens on a regular basis outside industrial settings where standards need to be met. The key to maintaining good indoor air quality is source reduction. By including proper ventilation and reducing pollution sources (such as by not allowing smoking, limiting harsh cleaning supplies, and finding alternate pest-control methods), indoor air quality can be achieved and maintained.”
Add allergens to an already somewhat hostile breathing environment and major respiratory health problems can develop. Increased indoor temperatures provide a healthy environment for the growth of mold. Indoor mold can flourish in bathroom areas, as well as due to humidifiers, leaky roofs, and potted plants. It has been noted that some people can have severe reactions to mold, including allergic bronchopulmonary aspergillosis, which requires steroid treatment.10
A frequent indoor allergen is the fecal material of the house dust mite. Dust mites feed primarily on human dander and skin. Therefore, they are most commonly found in bedding, pillows, and mattresses.10 Dust mites flourish in warm temperatures with high humidity and have a low native population in areas of high altitude, although they can be introduced into such environments by furniture imported from lower altitudes. Dust mites can also live in arid climates if the household environment is unusually humid.14 Older homes that absorb moisture have the highest concentration of dust mites. High levels are also found in newer homes with low ventilation and wall-to-wall carpeting. Dust mite droppings act as allergens, causing asthma symptoms evidenced by wheezing.3 Dust mites can be controlled using a few simple measures such as providing the mattresses and pillows with covers that are impermeable to dust mites and having bedding materials laundered regularly.1
Approximately 60% of US residents own pets.6 Unfortunately, pet dander is another source of inhaled indoor allergens. These allergens can act as potent asthma triggers.6Both cat and dog dander are common allergens. They can be controlled by removing the pet from the home environment or by keeping the pet out of the bedroom to avoid nighttime breathing distress due to the deep inhalation that accompanies sleep. Weekly bathing of the animal can also reduce the dander allergen.6
Cockroach fecal matter and saliva6 are allergens that can be found throughout the house, but are seen in the highest concentrations in the kitchen (or where food is stored). Emergency department visits and hospitalizations have been correlated with cockroach allergies.10 A few steps are recommended for controlling this allergen. Pesticides will add to the level of indoor pollution and should be avoided. Bait traps are a healthy alternative that can be used to rid the area of cockroaches. Remove all cockroach bodies and residues from the environment. Repair or plug any openings leading outdoors or into wall interiors. Store food in sealed containers and keep surface areas clean.6 If they are followed with persistence and consistency, these steps should rid the environment of cockroaches.
Controlling allergy symptoms can drastically reduce poor health. “There is no question that if someone has an allergy that aggravates asthma, prevention of exposure can drastically reduce the symptoms,” Nelson comments. As with outdoor and indoor pollutants, the key to preventing exposure comes through identifying the aggravator, educating the person about the asthma aggravator or irritant, and avoiding the identified aggravator or irritant. As asthma and allergies are usually diagnosed in childhood, early identification of allergens is vital.
It is difficult to control indoor and outdoor pollutants and allergens. Ideally, it should not be so difficult to control asthma effectively. Burke says, “If the nation applies the same energy to controlling and preventing asthma as it did to tuberculosis, I believe we can vastly reduce asthma morbidity and mortality rates. The ALA is committed to this effort and greatly encourages broad participation.”
Jennifer Vavra is a contributing writer for RT Magazine. For further information contact [email protected]
- Jones AP. Asthma and domestic air quality. Soc Sci Med. 1998;47:755-764.
- Koenig JQ. Air pollution and asthma. J Allergy Clin Immunol. 1999;104:717-722.
- Bielory L, Deener A. Seasonal variation in the effects of major indoor and outdoor environmental variables on asthma. J Asthma. 1998;35:7-48.
- Burr ML. Indoor air pollution and the respiratory health of children. Pediatr Pulmonol. 1999;18:S3-S5.
- Gong H Jr. Ozone’s ill effects. RT. 1996;9(5):23-28,102.
- Mitchell T. The great indoors. RT. 1998;11(4):39-43.
- Nelson HS, Szefler SJ, Jacobs J, et al. The relationship among environmental allergen sensitization, allergen exposure, pulmonary function, and bronchial hyperresponsiveness in the childhood asthma management program. J Allergy Clin Immunol. 1999;104:775-785.
- Norris G, Young-Pong SN, Koenig JQ, et al. An association between fine particles and asthma emergency department visits for children in Seattle. Environ Health Perspect. 1999;107:489-493.
- O’Neill MS. Helping schoolchildren with asthma breathe easier: partnership in community-based environmental health education. Environ Health Perspect. 1996;104:464-466.
- Roberts RL. Seasonal effects on asthma. RT. 1999;12(4):45-48,85.
- Thompson G. Asthma and ozone. RT. 1999;12(5):42.
- Zoidis JD. The impact of air pollution on COPD. RT. 1999;12(6):43-45,63.
- Kanner RE. Fine particulate air pollution: what are the effects on human health? RT. 1996;9(6):37-38,166.
- Nelson HS, Fernandez-Caldas E. Prevalence of house dust mites in the Rocky Mountain states. Ann Allergy Asthma Immunol. 1995;75:337-339.