Environmental Asthma: 9 Questions Physicians Often Ask

Environmental Asthma: 9 Questions Physicians Often Ask

The prevalence of asthma in the United States is estimated to be 5% to 8%.1 Asthma is responsible for approximately 5000 deaths annually in this country. It is a leading cause of emergency department (ED) visits, hospitalizations, and school and work absenteeism. The total estimated direct cost of the disease in the United States was $12.7 billion in 1998.2

Asthma is a multifactorial disease with complex genetic and environmental components. It can be exacerbated by exercise, laughter, exposure to allergens and environ- mental tobacco smoke, cold air, viral infections, nitrogen dioxide, sulfur dioxide, ozone, endotoxins, sulfites, and b-blockers.

In this article, we discuss the most important natural and man-made pollutants (other than those associated with occupational asthma) that cause or exacerbate asthma and the most appropriate preventive measures. These contaminants can be classified as either causal pollutants (inhaled allergens) or contributing pollutants (such as tobacco smoke, air pollution, and endotoxins, which irritate the airways). According to the World Health Organization (WHO) estimations, asthma is allergic in more than 50% of adults and in 80% of affected children.3

1. What is responsible for the increase in the prevalence of asthma?

The estimated prevalence of atopic diseases in some developed countries exceeds 30%.1,4 A variety of factors may account for this.5-7

Longer and more concentrated exposure to indoor allergens. Table 1 provides a summary of the most important indoor and outdoor contaminants. Many studies suggest that exposure to indoor allergens is an important factor in the increased incidence and prevalence of allergic diseases. The average person in developed countries spends more than 90% of his or her time indoors; exposure to indoor allergens is therefore more prolonged than it is to outdoor seasonal allergens, and the concentration of most indoor allergens is greater. This exposure of genetically predisposed persons to various allergens, especially indoor allergens during infancy, sensitizes them.8-10

Table 1 -- Pollutants that can cause or exacerbate asthma*

Indoor pollutants+
Allergens: dust mites, cockroaches, animal dander, fungal spores
Tobacco smoke
Endotoxins (potent proinflammatory toxins present in house dust)
Outdoor pollutants
Allergens: pollen, fungal spores
Combustion products: nitrogen dioxide, sulfur dioxide

*The possible role of other pollutants (such as volatile organic compounds) and the existence of
conditions such as "sick building syndrome" and "idiopathic environmental intolerance" ("multiple
chemical sensitivity") remain controversial.
+Outdoor pollutants can also contaminate the indoor environment. Fungi can act as indoor pollutants,
particularly when there is excess moisture, such as from leaking roofs and water pipes and from
malfunctioning air-conditioning systems.

Viral respiratory tract infections, as well as passive exposure to cigarette smoke and other contaminants, can enhance the airway response to inhaled allergens in atopic persons.11,12

More outdoor air pollutants. Epidemiologic studies demonstrate that outdoor levels of air pollutants--including nitrogen dioxide, sulfur dioxide, ozone, and respirable diesel exhaust particles--associated with the use of fossil fuels have progressively increased during the past decade.13,14

In the United States, the National Ambient Air Quality Standards (NAAQs) offer specific standards for air quality, including ozone, particulate matter (both particulate matter 10 [PM10] and particulate matter 2.5 [PM2.5]), sulfur dioxide, nitrogen dioxide, lead, and carbon monoxide. The NAAQs have been recently revised for both ozone and particulate matter based on data that suggested health risks at levels below those established in previous standards.15

Several outcome variables have been used in different studies to investigate a potential association between air pollution and asthma. A comparative study performed in 4 European cities reported an association between levels of nitrogen and sulfur dioxide and ED admissions for asthma in both children and adults.16 An association between nitrogen dioxide and ozone levels and asthma deaths has also been suggested.17 Nitrogen dioxide and PM10 levels have also been associated with lower forced vital capacity and forced expiratory volume in 1 second in children.18

Although an association between air pollution and asthma morbidity seems to be consistent, the possible effects of air pollution on the increased prevalence of asthma in developed countries remain controversial. Studies that compared the former East and West Germany suggested that the prevalence of asthma was greater in West Germany than in East Germany, where air pollution is more severe.19 Another study performed in Australia and New Zealand also indicated that the prevalence of asthma among children in these countries was greater than in countries with much higher levels of air pollution.20

Because traffic exhaust is one of the most important sources of air pollution in developed countries, a number of studies are being conducted to investigate the effects of this type of pollution on asthma. A study of children in the Netherlands reported a significant correlation between physician-diagnosed asthma during the first year of life and several traffic-related pollutants, such as PM2.5, soot, and nitrogen dioxide.21

Altered immune response (the hygiene hypothesis). The hygiene hypothesis suggests that the reduced microbial exposure of children--as a result of westernized lifestyles--is primarily responsible for the increased prevalence of allergic diseases during the past decades in developed countries.

Two main theories have been suggested to explain the hygiene hypothesis. The initial theory suggests that a lack of shifting from helper T cell 2 (TH2) dominance to T-helper T cell 1 (TH1) dominance--which is induced by exposure to immune stimulants, such as viruses, bacteria, and endotoxins, especially during the prenatal period and first years of life--is responsible for the increased prevalence of allergic diseases.22,23 TH1 cells produce interleukin (IL)-2, interferon g (IFN-g), and tumor necrosis factor b (TNF-b); TH2 cells produce IL-4, IL-5, IL-6, IL-10, and IL-13. IL-4, IL-13, and IL-5 promote the production of IgE in response to allergens, and IFN-g suppresses this IgE production. Bacterial and viral infections enhance IL-12 synthesis. IL-12, produced mainly by monocytes and macrophages, induces IFN-g synthesis by TH1 cells, resulting in a suppressed TH2 response.2 A more recent theory emphasizes the role of reduced activity of T regulatory cells (immune suppression) in the increased prevalence of allergic diseases.24

The results of several types of epidemiologic studies support the hygiene hypothesis. The factors that have been studied include parasitic and other infections, exposure to microbial products and cats and dogs, and breast-feeding.

Parasitic infections. The high prevalence of parasitic infections in developing countries protects against allergic diseases.25 Like allergic tissue responses, immune defenses against parasites involve IgE, mast cells, eosinophils, and TH2 lymphocytes. IgE responses are, therefore, immunoprotective against parasites and are not restricted to allergic diseases. This is illustrated by epidemiologic studies in Africa, South America, and Asia that indicate an increased prevalence of asthma associated with population shifts from rural to urban environments. Other studies investigating the effectiveness of anthelmintic treatment on allergic reactivity have demonstrated a decrease of total IgE levels accompanied by an increase in skin reactivity after treatment.

Childhood infections. Infections associated with siblings, day-care attendance, and household crowding protect against allergies and asthma.26-28 The frequency of several allergic diseases has been found to be inversely associated with the number of childhood infections and with the number of siblings and age of day-care attendance, as a measure of exposure to infections. Siblings and day-care attendance promote cross-infections and, thus, the stimulation of TH1 lymphocytes.

Microbial products. Exposure to microbial products associated with farming protects against allergies and asthma.29 It has been suggested that growing up on a farm protects against allergic sensitization in early life. High concentrations of endotoxins (lipopolysaccharide fragments that coat the outer membrane of Gram-negative bacteria) have been reported in farming environments. Endotoxins regulate various processes in the immune system, such as production of IL-12 and IFN-g.

Exposure to cats and dogs. Exposure to these animals in early life may protect against allergies.30 The presence of pets in the home may be associated with increased exposure to endotoxins and other microbial products and, thus, the immune system is indirectly affected.

Breast-feeding. The role of breast-feeding in the development of allergic sensitization is controversial.31 Some epidemiologic studies suggest a protective role of breast-feeding,32,33 and it has been hypothesized that the immunologic components of milk, such as secretory IgA, may account for this protective effect. However, other studies indicate an increased risk of allergy and asthma associated with breast-feeding.34,35

The mechanisms by which breast-feeding may increase allergies and asthma in children have been studied. Exclusively breast-fed infants may have lower levels of Gram-negative enterobacteria in their GI tract than nonbreast-fed infants. In addition, breast-feeding protects against infections.

The majority of studies that support the hygiene hypothesis are cross-sectional and cohort studies, not randomized controlled-intervention studies. Therefore, nonreported confounding factors may partially account for the observation of positive results. Moreover, many observations contradict the hygiene hypothesis and negative findings are less likely to be published than positive findings. The effects of a number of confounding factors on the hygiene hypothesis have been discussed elsewhere.36,37

Dietary influences. Other investigations indicate that dietary changes--such as a decrease in the consumption of fatty fish--may partially account for the increase in asthma.38,39 Epidemiologic studies suggest that omega-3 fatty acids, which are abundant in fish and have anti- inflammatory effects, may decrease symptoms of asthma.40 However, the effectiveness of dietary supplementation with omega-3 fatty acids in the primary prevention of asthma has not been thoroughly investigated.


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