OR WAIT 15 SECS
What role do environmental exposures play in the rising prevalence and severity of asthma? The authors examine the latest evidence and propose some measures pediatricians can take to protect their patients. Includes a Guide for Parents.
|Jump to:||Choose article section... Causes of asthma The role of infection The indoor environment Outdoor air pollution The Air Quality Index Chemicals in the workplace and home A challenge of infinite variety What can you do for your patients? Web sites for more information|
What role do environmental exposures play in the rising prevalence and severity of asthma? The authors examine the latest evidence and propose some measures pediatricians can take to protect their patients.
Asthma affects between 17 and 26 million people in the United States, nearly a third of whom are children.1,2 Many studies have reported that asthma is increasing in the US and around the world, with a dramatic increase in young children.3 Despite greater awareness of the disease and improvements in treatment, the reported prevalence of asthma among children increased by 58% between 1982 and 1992, and deaths directly attributable to asthma increased by 78% from 1980 to 1993.4 The odds of an adverse outcome (such as intubation, cardiopulmonary arrest, or death) among children hospitalized for asthma in California doubled between 1986 and 1993.5
There is widespread consensus among experts that the increases in asthma are real, and not solely the result of greater awareness of the disease. Possible explanations for the increase in prevalence and severity include environmental exposures.
Asthma is more common in African-Americans and has worse outcomes, with a hospitalization rate about four times higher and a death rate about two times higher than among Caucasians.6,7 The disease is also more common among low-income people living in urban areas. Asthma is the number one chronic health condition and the leading cause of hospitalization among children.8 Pediatricians play a significant role in managing and treating asthma, which should include counseling patients and families about potentially preventable environmental exposures that can cause or exacerbate disease. Moreover, armed with accumulating evidence regarding environmental exposures in children, pediatricians can serve as effective community advocates for a healthy environment.
Asthma has both genetic and environmental components. Atopic people are more likely to develop allergies, eczema, and asthma. In fact, 28% of children whose mothers have asthma have themselves been diagnosed with asthma, compared to only 10% of children of nonasthmatic mothers.3 It is clear, however, that the rapidly increasing rate of asthma in the population cannot be caused by genetic changes because genetic changes occur over many generations. In addition, asthma is increasing among people without atopy or a family history of allergic disease.9
Environmental exposures are known to trigger attacks in people with asthma. Recent research indicates that such exposures may actually cause asthma in some people. Environmental factors associated with asthma include viral infection, contaminants in indoor airsuch as pet dander, dust mites, cockroach feces, fungal contamination, volatile organic compounds (VOCs), and secondhand smokeand pollen and common pollutants (ozone, nitrogen oxides, particulate matter, diesel exhaust) in outdoor air. Some chemicalssuch as isocyanates, methacrylates, epoxy resins, some pesticides, some types of wood dust, and bacterial toxinscan cause or contribute to asthma. Although they are most often associated with occupational asthma, some of them also may be found in the home.
Recent research has begun to uncover important changes in immune function that can set the stage for asthma very early in life.10 Some researchers have discovered that fetuses can become sensitized to environmental contaminants before birth, emerging with a strong predisposition to allergy and asthma. Some, but not all, studies have found that breastfed infants are less likely to develop asthma and allergy than babies who are fed formula.11 Scientists believe that immune modulators in breast milk can help the infant's immune system develop in a way that decreases susceptibility to infectious disease and allergy.
Immunologic research has highlighted the role of T-helper (Th) cells and their subtypes. When the Th1 type of cell is most prevalent, asthma symptoms are not likely to develop. The Th2 type, however, causes secretion of interleukins and other chemical signals that can initiate an allergic or asthmatic reaction.12 A shift in the predominant T-cell population from Th1 to Th2 cells has been associated with asthma. Much current attention focuses on environmental factors that can alter the proportion of Th1 to Th2 cells during infancy and childhood.
Several common diseases of childhood have been associated with airway inflammation, bronchitis, and wheezing.13 Infants infected with respiratory syncytial virus or parainfluenza virus may develop wheezing that can persist as an asthma-like syndrome. In older children, upper respiratory infections often trigger wheezing. These findings have led some scientists to propose that atopic children may develop new-onset asthma following viral infection. Mild, or latent, asthma may be exacerbated by subsequent viral illnesses. Viruses also may produce synergistic effects with environmental allergens, resulting in more severe asthma symptoms.
In contrast, some studies suggest that early childhood infections may reduce the likelihood of asthma. One such study found that children who had had measles were only one-third as likely to develop allergy as children who were vaccinated against measles.14 Similarly, Japanese schoolchildren who had strongly positive tuberculin skin tests, indicating possible direct exposure to tuberculosis, had a lower level of Th2 cytokines and were less likely to have asthma or other allergic illness than children vaccinated against tuberculosis, who demonstrated less of an immune reaction against the disease.15 In possibly related findings, some studies suggest that children exposed to farm animals and endotoxin (a toxin produced by certain kinds of gram-negative bacteria) have a lower risk of asthma, as do children with older siblings and those who attended day care during the first six months of life.16
These findings have been unified in the "hygiene hypothesis," which holds that exposure to childhood diseases, domestic animals, and bacteria protects against asthma and allergies by encouraging the predominance of Th1 cells. In contrast, children living in a modern urban environment, where they have been vaccinated against common diseases, may be at greater risk of developing the Th2-type immune responses associated with asthma.
The hygiene hypothesis, although intriguing, is not consistently supported by the scientific evidence. Recent data from the Children's Health Study indicate that exposure to farm animals and crops or crop dust early in life is, in fact, not protective and is associated with a 60% increase in the risk of asthma. The same study found a higher risk of asthma among children who attend day care.17 The hygiene hypothesis also fails to explain the greater risk faced by African-American children and by lower-income and urban children compared to higher-income and suburban children.
In short, although it is clear that children who already have asthma are likely to suffer exacerbations of the disease when they develop some common childhood infections, the role of childhood infections in causing asthma remains uncertain. Some lines of investigation suggest that infections of the airways in childhood may have a causal role; other studies indicate that some respiratory or nonrespiratory infections may promote a Th1 response that protects against development of asthma. Neither hypothesis adequately describes and explains the geographic and ethnic patterns of asthma seen in the US today.
Children with asthma are more likely than those without asthma to have an allergic response to common household allergens. Asthmatics commonly have a positive skin-prick test to protein extracts from cockroaches, house-dust mites, cat and dog dander, pollen, and common molds. There is no question that exposure to these allergens can trigger an asthma attack in a child who has the disease and is already sensitized to their proteins. Reducing dust mites or other allergens in the home has been shown to decrease the severity of respiratory symptoms in sensitized asthmatics.18
The question of whether indoor allergens actually cause new-onset asthma is more complicated. One large cohort study reported a 70% increase in the risk of developing asthma associated with a humidifier in the home.19 Other studies have reported that children exposed to cockroaches during infancy are twice as likely as their peers to develop asthma by 5 years of age.17 The theory that common household allergens cause new-onset asthma is weakened by three factors:
Data do not suggest any significant increase in indoor allergen concentrations during the last few decades to account for the doubling of the rate of asthma during that time.20
No difference exists between the rate of asthma in geographic areas where house-dust mite and fungal concentrations are low (such as dry, cool regions) and warm, humid areas where concentrations are high.21
Many studies have found that children raised in an environment with low exposure to allergens are less likely to be sensitized to these particular allergens, but most of those studies have not found that these children are less likely to develop asthma.
The data on pets are even more conflicting. In one major southern California study, a pet in the home was associated with a 60% increase in the risk of developing new-onset asthma during adolescence.19 The study concluded that an estimated 32% of new childhood asthma cases might be attributable to household pets. But another recent large study in southern California found no association between pet exposure and childhood asthma by 5 years of age, indicating that more research is needed to better define the relationship.17
Many volatile organic compounds are found in modern buildings, particularly in urban areas. These chemicals include respiratory irritants such as formaldehyde, toluene, and chloroform. VOCs may enter from outside and remain trapped in the indoor environment, or may be released from building materials, carpets, and furniture. They also are found in some household products, including glues, paints, fragrances, and cleaning products. In addition to VOCs, cleaning products contain enzymes and surfactants that can be irritating and cause an immunologic response.22 Homes with an attached garage contain VOCs from evaporated gasoline emitted from parked cars. Some researchers theorize that these chemicals may play a role in asthma.23 Very little evidence exists, however, to help determine whether VOCs or detergents are important variables in causing or exacerbating asthma.
Exposure to secondhand cigarette smoke has been consistently associated with increased frequency and severity of asthma attacks in both children and adults and with the development of asthma in children.24 Infants whose mothers smoke during pregnancy have reduced pulmonary function and are more likely to have persistent wheezing until at least 6 years of age.25 Maternal smoking at least doubles a child's risk of asthma.24 Risk is associated with both prenatal and postnatal exposure to secondhand smoke and is clearly dose relatedincreasing in homes with a greater number of smokers and heavy smokers.
Moreover, smoking and genetics have synergistic effects. Children of nonsmoking parents with asthma and allergies have a 12-fold greater risk of developing early-onset persistent asthma than children of nonsmokers with no family history of asthma or allergies. Maternal smoking in pregnancy interacts with genetic susceptibility to increase the risk an additional threefold.26 Cigarette smoke resembles diesel exhaust and industrial emissions, containing a similar mix of tiny particles, toxic chemicals, and respiratory irritants. Exposure to cigarette smoke and outdoor air pollution may therefore cause a similar asthmatic response.
Asthma is more common in urban areas of industrialized countries, particularly among children living along busy roads and trucking routes.27 A population-based survey of more than 39,000 children in Italy found that those who lived on streets with heavy truck traffic were 60% to 90% more likely to have acute and chronic respiratory symptoms such as wheezing or phlegm and illnesses such as bronchitis and pneumonia.28 A German study of more than 3,700 adolescent students found that those who lived on a street with "constant" truck traffic were 71% more likely to report hay feverlike symptoms and more than twice as likely to report wheezing.29 Studies also have shown that the proximity of a child's school to major roads is linked to asthma and that the severity of asthmatic symptoms increases with proximity to truck traffic.30
Both nitrogen oxides and particulate matter have been linked to a significant decrease in growth of lung function among children living in southern California.31 Although some components of outdoor air pollution have been declining in the US, ozone and fine particle pollution (PM2.5) from diesel engine exhaust are an ongoing and increasing problem.12
Numerous studies have demonstrated an association between specific components in outdoor air and asthma attacks.32 Pollen and mold levels, for example, are associated with asthma exacerbations. Among air pollutants, particulates have been linked to increases in emergency room visits for asthma.33 Nitrogen dioxide (NO2) and sulfur dioxide directly damage the respiratory system. Exposure to sulfur dioxide in laboratory volunteers results in airway constriction, chest tightness, and asthmatic symptoms.34 Elevated levels of NO2 in outdoor air are associated with exacerbations of asthma.35 Because these compounds are potent airway irritants, it is not surprising that they can trigger asthma attacks.
Air pollutants may act in conjunction with common allergens to increase sensitivity to pollen or other common proteins. In laboratory volunteers, combined exposures to levels of ozone, NO2, or diesel exhaust particles found in urban air and low levels of common allergens such as pollen dramatically enhances asthmatic and allergic reactions.36
New data suggest that air pollutants such as diesel exhaust and ozone may actually cause asthma in previously healthy children.37 Diesel exhaust is a major source of ambient PM2.5 and NO2.12 It has been associated with asthma causation by several lines of evidence.12 Several researchers have shown that exposure to diesel exhaust causes direct immunologic changes in the airways that are consistent with the inflammatory changes in asthma and that such exposures shift T-helper cells toward the allergic Th2 cell type.36
One important study has shown that exposure to common urban levels of diesel exhaust can cause people to develop allergic reactions to proteins to which they did not previously react.38 In this study, volunteers were exposed to a concentration of diesel exhaust roughly equivalent to one to three days of breathing Los Angeles air, then exposed to a new allergen. Control subjects exposed to the new allergen alone did not develop antibodies to it, whereas subjects exposed to the allergen and diesel exhaust developed a full-blown allergy. The similarities between the composition of diesel exhaust and secondhand cigarette smoke increases the likelihood that the two pollutants may have similar effects in predisposing exposed children to asthma.
A prospective study of more than 3,500 nonasthmatic school children growing up in southern California found that children who exercised outdoors and lived in an area with a smog problem were at increased risk of developing asthma. In communities with a high ozone concentration, children who played three or more sports faced an asthma risk 3.3 times higher than their peers who played no sports. Sports had no effect in areas of low ozone concentration. In general, time spent outdoors was associated with a 40% higher incidence of asthma in areas of high ozone but not in low-ozone areas.37
The US Environmental Protection Agency (EPA) monitors air pollution in cities throughout the country and reports a daily Air Quality Index (AQI) for five major pollutants: ozone, particulate matter, carbon monoxide, sulfur dioxide, and NO2 . The AQI is reported on a scale of 1 to 500the higher the index value, the greater the level of potential health concern. A value above 100 indicates that pollution levels exceed the national air quality standard and that air quality is considered unhealthy. The AQI divides levels of health concern into the following six categories (Figure 1):
PLEASE NOTE: If you are using Internet Explorer version 6 or higher, after clicking to enlarge the graphic, click the picture icon that appears in the lower right-hand corner of the graphic.
Good (050)air quality poses little or no health risk
Moderate (51100)air quality is "acceptable," although it may be a moderate health concern for a small number of people who are unusually sensitive
Unhealthy for sensitive groups (101-150)sensitive groups such as asthmatics and children may experience health effects
Unhealthy (151-200)everyone may experience health effects, and more sensitive people may experience more serious effects
Very unhealthy (201-300) everyone may experience serious health effects
Hazardous (over 300)everyone is likely to be affected, a public health emergency
The AQI is reported in newspapers (Figure 2) and on television and radio in many cities. Local information is also available on the web at www.epa.gov/airnow. Many cities report a forecast of the next day's AQI to allow residents to plan strenuous activities for times when the air quality is favorable. It is also helpful to know that levels of some pollutants vary in a predictable fashion. The ozone level, for example, tends to rise on summer afternoons because ozone is formed by a chemical reaction of combustion products in sunlight; the carbon monoxide level is higher during cold weather (when car emission controls may be less effective) and morning and evening rush hours.
Chemicals found in the workplace or home can aggravate existing asthma or cause new-onset disease, even in people who are not atopic. Some chemicals cause asthma by means of a powerful irritant effect resulting from a high-level exposure. Corrosive, acid, or alkaline smoke, vapor, or gas, for example, can cause an acute onset of asthma-like disease known as reactive airways dysfunction syndrome (RADS).39 This type of exposure can happen in the home if bleach and ammonia are mixed to create chlorine gas or if drain cleaners or other corrosives are used improperly, or in a house fire.
Chemicals known to cause asthma include the isocyanates, acid anhydrides, methacrylates, complex amines, metalworking fluids, and several metals.39 Isocyanates are found in polyurethane foams, plastics, paints, and varnishes; acid anhydrides are used in epoxy resins and plastics; and complex amines are found in photographic fluids, shellacs, and paints. Methacrylates are used in home hobbies, orthopedic surgery, and dentistry as bonding cement. Metals such as platinum salts, aluminum, cobalt, chromium, and nickel, in dust or aerosol form, are associated with asthma. Some people can become sensitized to a range of organic proteins, including latex, grain dusts, animal proteins, and wood dusts. Although it would be unusual for a young child to be exposed to any of these agents in a sustained manner that would cause an asthmatic response, chemicals used in home hobbies or dusts carried home from work on a parent's clothing could sensitize a child.
Several pesticides are known to cause allergic reactions or airway constriction, raising concerns about children who live near farms or are exposed to the chemicals in household insecticides. Case reports and specific bronchial challenge testing have linked some pesticides with occupational asthma. They include captifol,40 sulfur,41 pyrethrins and pyrethroids,42 tetrachloroisophthalonitrile,43 and several organophosphate and n-methyl carbamate insecticides.44 The organophosphate insecticides, for example, are known to cause increased mucus production and bronchoconstriction.45 The pyrethrin and pyrethroid insecticides are related chemically to chrysanthemum flowers and have been reported to cause allergic sensitization.42 The pyrethroids are increasingly used for household pest control, including control of cockroaches.
A recent large epidemiological study found a statistically significant 2.4-fold increased risk of an asthma diagnosis before 5 years of age among children exposed to pesticides in the first year of life.17 Exposure to pesticides after the first year was not associated with asthma in this group.
There is a potential, though unquantified, risk of environmental exposure related to emissions from a nearby industrial facility or agricultural spraying operation. Although childhood asthma cases have rarely been documented from these types of environmental exposures, the irritant nature of the compounds alone could put an asthmatic child at risk of an attack. It is reasonable, therefore, to ask parents and patients about the proximity of home and school to industrial facilities and farms. It is also important to realize that people may bring agricultural pesticides and industrial chemicals into the home without being aware of the potential hazards to children
Asthma is an illness that has been increasing in frequency and severity among children in most developed countries. It is most common in African-American children who live in an urban area. Although it is clear that some people inherit a genetic predisposition to asthma, the increase in the rate of asthma and its severity almost certainly results from environmental, rather than genetic, factors.
Many common allergens can trigger asthma attacks in people who already have the disease. The most critical question is what environmental factors may cause new-onset asthma. In this area of study, the interactive effects between air pollutants and allergens may be an important clue, raising the possibility that environmental exposures may work together to create asthma. In addition, exposures early in life, including prenatally and during infancy, have been shown to set the stage for later development of asthma. Many chemicals in common use in workplaces and in homes have also been implicated in initiating or exacerbating asthma.
As research elucidates the connection between environmental exposure and health effects, you will continue to play a pivotal role as an educator and an advocate.
1. Rappaport S, Boodram B: Forecasted state-specific estimates of self-reported asthma prevalenceUnited States 1998. Mor Mortal Wkly Rep 1998;47:1022
2. American Lung Association: Asthma in Children Fact Sheet. www.lungusa.org/asthma/ascpedfac99.html Accessed 2/28/02
3. Millar WJ, Hill GB: Childhood asthma. Health Rep 1998;10:9
4. Clark NM, Brown RW, Parker E, et al: Childhood asthma. Environ Health Perspect 1999;107(3):421
5. Calmes D, Leake BD, Carlisle DM: Adverse asthma outcomes among children hospitalized with asthma in California. Pediatrics 1998;101(5):845
6. Eggleston PA, Buckley TJ, Breysse PN, et al: The environment and asthma in U.S. inner cities. Environ Health Perspect 1999;107(Suppl 3):439
7. Von Behren J, Kreutzer R, Smith D: Asthma hospitalization trends in California, 1983-1996. J Asthma 1999;36:575
8. Asthma mortality and hospitalization among children and young adultsUnited States 1980-1993. Mor Mortal Wkly Rep 1996;45(17):350
9. Christie GL, McDougall CM, Helms PJ: Is the increase in asthma prevalence occurring in children without a family history of atopy? Scott Med J 1998;43:180
10. Holt PG, Jones CA: The development of the immune system during pregnancy and early life. Allergy 2000;55:688
11. Chandra RK: Influence of maternal diet during lactation and the use of formula feed and development of atopic eczema in the high risk infants. BMJ 1989;299(6693):228
12. Pandaya RJ, Solomon GM, Kinner A, et al: Diesel exhaust and asthma: Potential hypotheses and molecular mechanisms in action. Environ Health Perspect 2002; 110(Suppl 1):103
13. Gern JE: Viral and bacterial infections in the development and progression of asthma. J Allergy Clin Immunol 2000;105:S497
14. Shaheen SO, Aaby P, Hall AJ, et al: Measles and atopy in Guinea-Bissau. Lancet 1996;347:1792
15. Shirakawa T, Enomoto T, Shimazu S, et al: The inverse association between tuberculin responses and atopic disorder. Science 1997;275:77
16. Ball TM, Castro-Rodriguez JA, Griffith KA, et al: Siblings, day-care attendance, and the risk of asthma and wheezing during childhood. N Engl J Med 2000;343:538
17. Salam MT, Li YF, Langholz B, et al: Early life environmental risk factors for asthma: Findings from the Children's Health Study. Environ Health Perspect online 9 December 2003. Available at http://dx.doi.org/
18. Clark NM, Brown RW, Parker E, et al: Childhood asthma. Environ Health Perspect 1999;107(suppl3):421
19. McConnell R, Berhane K, Gilliland F, et al: Indoor risk factors for asthma in a prospective study of adolescents. Epidemiology 2002;13(3):288
20. Platts-Mills TA, Blumenthal K, Perzanowski M, et al: Determinants of clinical allergic disease. The relevance of indoor allergens to the increase in asthma. Am J Respir Crit Care Med 2000;162:S128
21. Peat JK, Tovey E, Mellis CM, et al: Importance of house dust mite and Alternaria allergens in childhood asthma: An epidemiological study in two climactic regions of Australia. Clin Exp Allergy 1993;23:812
22. Poulson LK, Clausen SK, Glue C, et al: Detergents in the indoor environmentWhat is the evidence for an allergy promoting effect? Known and postulated mechanisms. Toxicology 2000;152:79
23. Larsen GL, Beskid C, Shirnamé-Moré L: Environmental air toxics: Role in asthma occurrence? Environ Health Perspect 2002;110(suppl 4)501
24. Etzel RA: How environmental exposures influence the development and exacerbation of asthma. Pediatrics 2003;112(1 Pt 2):233
25. Martinez FD, Wright AL, Taussig LM, et al: Asthma and wheezing in the first six years of life. N Engl J Med 1995; 332:133
26. London SJ, Gauderman JW, Avol E, et al: Family history and the risk of early-onset persistent, early-onset transient, and late-onset asthma. Epidemiology 2001;12(5):577
27. Brunekreef B, Janssen NA, de Hartog J, et al: Air pollution from truck traffic and lung function in children living near motorways. Epidemiology 1997;8:298
28. Ciccone G, Fostastiere F, Agabati N, et al: Road traffic and adverse respiratory effects in children. SIDRIA Collaborative Group. Occup Environ Med 1998;55:771
29. Duhme H, Weiland SK, Keil U, et al: The association between self-reported symptoms of asthma and allergic rhinitis and self-reported traffic density on street of residence in adolescents. Epidemiology 1996;7:578
30. Pekkanen J, Timonen KL, Ruuskanen J, et al: Effects of ultrafine and fine particles in urban air on peak expiratory flow among children with asthmatic symptoms. Environ Res 1997;74(1):24
31. Gauderman JW, McConnell R, Gilliland F, et al: Association between air pollution and lung function growth in southern California children. Am J Respir Crit Care Med 2000;162:1384
32. Mortimer KM, Neas LM, Dockery DW, et al; The effect of air pollution on inner-city children with asthma. Eur Respir J 2002;19:699
33. 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
34. Balmes JR, Fine JM, Sheppard D: Symptomatic bronchoconstriction after short-term inhalation of sulfur dioxide. Am Rev Respir Dis 1987;136:1117
35. Studnicka M, Hackl E, Pischinger J, et al: Traffic-related NO2 and the prevalence of asthma and respiratory symptoms in seven year olds. Eur Respir J 1997;10:2275
36. Nel AE, Diaz-Sanchez D, Ng D, et al: Enhancement of allergic inflammation by the interaction between diesel exhaust particles and the immune system. J Allergy Clin Immunol 1998;102(4 Pt 1):539
37. McConnell R, Berhane K, Gilliland F, et al: Asthma in exercising children exposed to ozone: A cohort study. Lancet 2002;359:386
38. Diaz-Sanchez D, Garcia MP, Wang M, et al: Nasal challenge with diesel exhaust particles can induce sensitization to a neoallergen in the human mucosa. J Allergy Clin Immunol 1999;104:1183
39. Lombardo LJ, Balmes JR: Occupational asthma: A review. Environ Health Perspect 2000;108(Suppl 4):697
40. Royce S, Wald P, Sheppard D, et al: Occupational asthma in a pesticides manufacturing worker. Chest 1993;103:295
41. Freedman BJ: Sulphur dioxide in foods and beverages: Its use as a preservative and its effect on asthma. Br J Dis Chest 1980;74:128
42. Box SA, Lee MR: A systemic reaction following exposure to a pyrethroid insecticide. Hum Exp Toxicol 1996;15:389
43. Honda I, Kohrogi H, Araki S, et al: Occupational asthma induced by the fungicide tetrachloroisophthalonitrile. Thorax 1992;47:760
44. Underner M, Cazenave F, Patte F: Occupational asthma in the rural environment. Rev Pneumonol Clin 1987;43:26
45. Reigart JR, Roberts JR: Recognition and Management of Pesticide Poisonings, ed 5. US Environmental Protection Agency 735-R-98-003, March 1999
Many questions remain about the exact relationship between environmental pollutants and asthma, but you can undertake some preventive actions to benefit children with asthma, those at risk of asthma, and the health of the community in general:
Evaluate environmental exposures as part of routine asthma management.
Council parents to avoid exposing their children to secondhand smoke; if parents or household members smoke, encourage them to quit and refer them to a cessation program.
Advise limited use of humidifiers when necessary.
Encourage measures to control dust mites, such as pillow and mattress covers, washing bedding in hot water, and using a vacuum cleaner with a high-efficiency particulate air (HEPA) filter.
Teach appropriate control of cockroaches, including sealing of cracks, cleaning up food and water, and using roach baits (such as Roach Motel) instead of pesticide sprays.
Encourage parents to use the Air Quality Index to plan strenuous activities when air quality is best. Physicians and nurses who advise schools and sports teams should be aware of the health implications of an elevated level of air pollution and provide appropriate guidance in conjunction with public health authorities.
Support local and regional measures to improve air quality.
A Guide for Parents will help you educate parents about the relationship between environmental exposures and asthma. A list of "Web sites for more information" is found below.
American Lung Association
Environmental Protection Agency
Contains local outdoor air quality information and ozone maps
Centers for Disease Control and Prevention www.cdc.gov/nceh/airpollution/asthma/default.htm
Information about indoor and outdoor air quality, asthma rates, mold and other possible asthma triggers
The National Asthma Education and Prevention Program (NAEPP) www.nhlbi.nih.gov/about/naepp/index.htm
The NAEPP is administered and coordinated by the National Heart, Lung, and Blood Institute. Fact sheets are available for patients, schools, and health-care providers.
Asthma, your child, and the environmentand how you can make for easier breathing
Asthma is a serious respiratory disease that is more and more common around the world. About 20 million people in the United States have asthmatwice as many as had the disease in 1980. Among children, asthma is the number one chronic health condition and the leading cause of hospitalization. According to a California study, among children who are hospitalized for asthma, the chance of becoming seriously ill or dying has doubled over the past 20 years.
We do not know why more people are getting asthma, nor do we know how to prevent it, but we are learning much more about how exposure to certain things in the environment can cause the disease or make it worse. This guide discusses those exposures and describes what you can do to help reduce your child's risk of asthma or, if you've just found out that your child suffers from asthma, to help prevent attacks.
Many children with asthma also have allergies. Allergies often run in families. Nearly one of every three children whose mother has asthma also has the diseasecompared to one of every 10 children of mothers who do not have asthma. If you know that there is asthma in your family, be sure to tell your pediatrician and other health-care professionals who work with you and your child.
Breastfed infants are less likely to develop asthma and allergies than babies who have been fed infant formula. Scientists believe that substances in breast milk can help the infant's immune system develop in a way that decreases the risk of getting allergies. Breastfeeding is a good way to help prevent asthma.
Viral respiratory (lungs, windpipe, nose) infections, such as the common cold, can be far more severe in children with asthma. Some viruses may even cause asthma in infants who did not have the disease previously. Viral infections can trigger wheezing in children with asthma. To help prevent infections, make sure that everyone in the family washes his or her hands often and gets a flu shot.
Secondhand cigarette smoke may cause asthma or make it worse in children who are exposed to smoke either before or after they are born. Also, a study of California school children found that those who lived in a home with a humidifier had a 70% higher risk of developing asthma.
Children with asthma may wheeze when exposed to cockroaches, animal dander, dust mites, pollen, and common molds. Reducing the level of dust mites or other allergens in the home can decrease the severity of respiratory symptoms in some asthmatics. Here's how you can help prevent attacks:
Asthma is more common in urban areas, particularly among children living along a busy road or a trucking route. Ozone (a major pollutant in smog) and heavy exposure to traffic may cause asthma in previously healthy children and may trigger asthma attacks in children who already have asthma. California school children who play several outdoor sports and live in areas where there is an ozone smog problem, for example, have been found to be three times as likely to develop asthma as children in those communities who don't play sports. Outdoor sports are not associated with asthma in less smoggy areas.
Many substances in outdoor air besides ozone and diesel exhaust can trigger an asthma attack: pollen, mold, smoke, soot, and vehicle exhaust from nondiesel engines, to name a few. Air pollutants such as nitrogen oxides and sulfur dioxide can irritate the respiratory system, causing airway constriction, chest tightness, and asthma symptoms. To help prevent asthma attacks:
Chemicals in the home or the workplace can cause asthma or make it worse. They include chemicals present in:
Although children are not usually exposed to these substances, they may come in contact with the chemicals in home hobby materials or dust that parents bring home from the workplace on their clothing.
Some researchers believe that volatile organic compounds (VOCs) may have a role in asthma. VOCs are irritating chemicals with a strong smell. They may be released from building materials, carpets, furniture, glues, paints, pesticides, cleaning products, and fragrances.
Several pesticides can cause allergic reactions or airway constriction. They include some that are widely used to control cockroaches.
Here's how you can reduce the risk of asthma from chemical exposures:
For additional advice on preventing asthma and asthma attacks, speak with the pediatrician. You'll also find information at the following Web sites:
www.lungusa.org/asthmaThe American Lung Association's asthma home page
www.epa.gov/airnowThe Environmental Protection Agency's AirNow Web site, containing local outdoor air quality information and ozone maps
www.aaaai.org/nab/index.cfm?p=pollenThe American Academy of Allergy, Asthma, and Immunology Web site, containing information about local pollen and mold spore counts
This guide may be photocopied and distributed without permission to give to your patients' parents. Reproduction for any other purpose requires express permission of the publisher, Advanstar Medical Economics Healthcare Communications.
Gina Solomon, Elizabeth Humphreys, Mark Miller. Asthma and the environment: Connecting the dots. Contemporary Pediatrics August 2004;21:73.