Resources for state health and environment agencies working together to reduce asthma in children. Sponsored by ECOS.

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What are the principal outdoor factors that affect asthma?

Certain outdoor environmental factors are thought to contribute to making asthma worse in people who already have the disease. Sometimes this is called exacerbation of asthma. The term "trigger" refers to something that contributes to an asthma attack in a person who already has asthma. Not all asthmatics respond to all triggers.

In the outdoor environment, both air pollutants (1) and biological allergens (pollens, fungus, molds) can make asthma worse. Pollutants include ozone, particulate matter, sulfur dioxide, carbon monoxide, and nitrogen dioxide. In addition, the World Health Organization identified traffic pollution as a causative influence for asthma (2), and diesel exhaust has also been identified as a possible concern (1, 3).

Biological allergens include pollens, molds, and fungi (4).   Weather conditions including thunderstorms may particularly affect asthmatics (5, 6).

It is less certain what causes the onset of asthma in the first place. There is some evidence that exposure to ozone and biological allergens (particularly certain types of pollens) may contribute to the initial development of asthma, but there is no consensus in the scientific community about this.   Environmental factors may contribute to the onset of asthma, probably in conjunction with other factors including genetic factors.

What Air Pollutants Are Thought to Exacerbate Asthma?

Many studies have reported that higher concentrations of air pollution are associated with higher frequency of asthma reported several ways -- as emergency room visits (7), hospitalizations or hospital discharges, use of medication, increased frequency of symptoms, increased visits to doctors' offices, or increased number of days of school or work missed. Decreased lung function is also reported in some studies.

The results of the studies are not completely consistent, in that not all studies find that the same pollutants are associated with the same effects. Some studies find effects of particulate matter; while other find effects of ozone. Moreover, some studies find no effect. Below, only positive studies are cited.

Particulate Matter

Particles in the air are often referred to as particulate matter or as total suspended particulates. Different studies measure studies of different sizes. "PM 10" refers to particles 10 microns or less in diameter, while "PM 2.5" refers to particles 2.5 microns or less.

Times Series Studies -- Many studies have reported higher frequency of asthma on or shortly after days when particulate matter in the air is high, including increased emergency room visits for adults in Seattle (8, 9) and California (10) and for children (11-13);

Panel Studies -- Studies that follow groups of people over time have reported increased symptoms or severity of asthma to be associated with higher exposures to particulate matter in adults (14), African-American children in Los Angeles (15), children in Southern California (16), fifth and sixth grade students in Utah (17), children in Vancouver (18), children in Seattle (19), and children in Mexico City (20).    Some studies have found reduced lung function in children (20, 21) and in children over 15 (22), and particular susceptibility for asthmatic children (18).

Long-term Studies -- A few studies have reported an association between long-term exposures to PM 2.5 and increased severity or symptoms of asthma in adults (23) and in children (24).

Ozone

Ozone is a gas that is formed from chemical reactions in the lower atmosphere in the presence of light. It is the pollutant most associated with "smog." Ozone at ground level causes adverse health effects, while ozone in the upper atmosphere protects the earth from radiation from the sun.

Times series studies -- Many studies have reported higher frequency of asthma on or shortly after days when ozone concentrations in the air are high, including increased emergency room visits for adults in Seattle (9) and for children (13, 25, 26) ; increased medication use for more severely asthmatic children (15); and increased visits to doctors' offices (27) .

Panel studies -- have reported higher exposures of ozone to be associated with diminished lung function in children over 15 (22) and increased severity of asthma symptoms for children in the US (16, 28), African-American children in Atlanta (29), children in Australia (30), and children in Mexico City (20).    Effects in older children in San Diego were seen particularly when personal exposure to ozone was measured (21, 31). Asthmatics may be considered a susceptible population for effects of ozone (32)

Sulfur Dioxide

Sulfur dioxide is a gaseous pollutant for which the primary sources are related to combustion.

On or shortly after days when particulate matter in the air was high, studies reported increased emergency room visits (11) ; and increased visits to doctors' offices (27) for asthma.

Nitrogen Dioxide

On or shortly after days when nitrogen dioxide in the air is high, studies have reported increased hospitalization or hospital discharges (33) and increased symptoms in African-American children (15).    Some studies have looked at lung function and found that reduced lung function is associated with exposures to higher concentrations of particulate matter. Studies looking at long-term exposures to nitrogen dioxide have reported an association with increased severity or symptoms of asthma in adults (23) and children (24).

Carbon monoxide

On or shortly after days when carbon monoxide in the air is high, studies have reported increased emergency room visits for adults (9) and children (12) and increased asthma symptoms in children (19).    A study of long-term exposures reported an association with increased severity of asthma (23).

What Biological Allergens Exacerbate Asthma?

The outdoor biological allergens that are thought to exacerbate asthma are pollens, molds, and fungus

Pollens

Pollens are released by plants and vary geographically according to the type of vegetation. Pollens are typically monitored by capture in traps placed on roofs, then identification and counting of pollen particles under a microscope (34). Improvements in both collection methods to collect a higher percentage of particles and of identification and counting methods, to better ascertain the amount of allergen contained in the sample, would improve the value of monitoring for prediction of impacts on asthmatics (34). Studies of the relationship between pollen exposures and asthma generally look at either the relationship between sensitization as determined by a skin test and the presence of asthma or exposure to pollen and asthma symptoms (34). The pollens typically identified may not represent those most important to exacerbation of asthma (35)

Molds

Higher exposure to certain molds (Alternaria and Cladosporium) was associated with increased symptoms in a panel of African-American children in Los Angeles (15)

Fungus

A large study of outdoor concentrations of pollens and fungus, as well as air pollutants, found that emergency room visits were associated with higher concentrations of certain kinds of fungus but not pollens (36). A panel study of a few children found that higher concentrations of fungus, but not pollens, were associated with increases severity of symptoms in asthmatic children (4, 31), increased use of medication (4), and reduced lung function (4)

Combined Effects

There is some evidence that the combination of air pollutants and bio allergens may interact to increase the effect on asthmatics. One study reported that exposure to pollens and air pollutants led to heightened response for ozone but not nitrogen dioxide (37).

References Cited

1.             D'Amato G, Liccardi G, D'Amato M. Environmental risk factors (outdoor air pollution and climatic changes) and increased trend of respiratory allergy. Journal of Investigational Allergology and Clinical Immunology 2000; 10:123-8.

2.             WHO. WHO Prevention of Allergy and Asthma Interim Report. Geneva: World Health Organization, Management of Noncommunicable Diseases Department, Chronic Respiratory Diseases and Arthritis, 2000.

3.             Nel AE, Diaz-Sanchez D, Li N. The role of particulate pollutants in pulmonary inflammation and asthma: evidence for the involvement of organic chemicals and oxidative stress. Current Opinion in Pulmonary Medicine 2001; 7:20-6.

4.             Delfino RJ, Zeiger RS, Seltzer JM, Street DH, Matteucci RM, Anderson PR, Koutrakis P. The effect of outdoor fungal spore concentrations on daily asthma severity. Environmental Health Perspectives 1997; 105:622-35.

5.             Girgis ST, Marks GB, Downs SH, Kolbe A, Car GN, Paton R. Thunderstorm-associated asthma in an inland town in southeastern Australia. Who is at risk? European Respiratory Journal 2000; 16:3-8.

6.             Lewis SA, Corden JM, Forster GE, Newlands M. Combined effects of aerobiological pollutants, chemical pollutants and meteorological conditions on asthma admissions and A & E attendances in Derbyshire UK, 1993-96. Clinical and Experimental Allergy 2000; 30:1724-32.

7.             Goldsmith JR, Friger MD, Abramson M. Associations between health and air pollution in time-series analyses. Arch Environ Health 1996; 51:359-67.

8.             Schwartz J, Slater D, Larson TV, Pierson WE, Koenig JQ. Particulate air pollution and hospital emergency room visits for asthma in Seattle. American Review of Respiratory Disease 1993; 147:826-31.

9.             Sheppard L, Levy D, Norris G, Larson TV, Koenig JQ. Effects of ambient air pollution on nonelderly asthma hospital admissions in Seattle, Washington, 1987-1994 [see comments]. Epidemiology 1999; 10:23-30.

10.           Lipsett M, Hurley S, Ostro B. Air pollution and emergency room visits for asthma in Santa Clara County, California. Environmental Health Perspectives 1997; 105:216-22.

11.           Chew FT, Goh DY, Ooi BC, Saharom R, Hui JK, Lee BW. Association of ambient air-pollution levels with acute asthma exacerbation among children in Singapore. Allergy 1999; 54:320-9.

12.           Norris G, YoungPong SN, Koenig JQ, Larson TV, Sheppard L, Stout JW. An association between fine particles and asthma emergency department visits for children in Seattle. Environmental Health Perspectives 1999; 107:489-93.

13.           Tolbert PE, Mulholland JA, MacIntosh DL, Xu F, Daniels D, Devine OJ, Carlin BP, Klein M, Dorley J, Butler AJ, Nordenberg DF, Frumkin H, Ryan PB, White MC. Air quality and pediatric emergency room visits for asthma in Atlanta, Georgia, USA. American Journal of Epidemiology 2000; 151:798-810.

14.           Whittemore AS, Korn EL. Asthma and air pollution in the Los Angeles area. American Journal of Public Health 1980; 70:687-96.

15.           Ostro B, Lipsett M, Mann J, Braxton-Owens H, White M. Air pollution and exacerbation of asthma in African-American children in Los Angeles. Epidemiology 2001; 12:200-8.

16.           Gielen MH, van der Zee SC, van Wijnen JH, van Steen CJ, Brunekreef B. Acute effects of summer air pollution on respiratory health of asthmatic children. American Journal of Respiratory and Critical Care Medicine 1997; 155:2105-8.

17.           Pope 3rd CA, Dockery DW. Acute health effects of PM10 pollution on symptomatic and asymptomatic children. American Review of Respiratory Disease 1992; 145:1123-8.

18.           Vedal S, Petkau J, White R, Blair J. Acute effects of ambient inhalable particles in asthmatic and nonasthmatic children. American Journal of Respiratory and Critical Care Medicine 1998; 157:1034-43.

19.           Yu O, Sheppard L, Lumley T, Koenig JQ, Shapiro GG. Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study. Environmental Health Perspectives 2000; 108:1209-14.

20.           Romieu I, Meneses F, Ruiz S, Sienra JJ, Huerta J, White MC, Etzel RA. Effects of air pollution on the respiratory health of asthmatic children living in Mexico City. American Journal of Respiratory and Critical Care Medicine 1996; 154:300-7.

21.           Delfino RJ. Symptoms in pediatric asthmatics and air pollution: differences in effects by symptom severity, anti-inflammatory medication use and particulate averaging time. Environmental Health Perspectives 1998; 106:751-61.

22.           Rutherford S, Simpson R, Williams G, Mitchell C, McCall B. Relationships between environmental factors and lung function of asthmatic subjects in south east Queensland, Australia. Journal of Occupational and Environmental Medicine 2000; 42:882-91.

23.           Abbey DE, Ostro BE, Petersen F, Burchette RJ. Chronic respiratory symptoms associated with estimated long-term ambient concentrations of fine particulates less than 2.5 microns in aerodynamic diameter (PM2.5) and other air pollutants. Journal of Exposure Analysis and Environmental Epidemiology 1995; 5:137-59.

24.           McConnell R, Berhane K, Gilliland F, London SJ, Vora H, Avol E, Gauderman WJ, Margolis HG, Lurmann F, Thomas DC, Peters JM. Air pollution and bronchitic symptoms in Southern California children with asthma. Environmental Health Perspectives 1999; 107:757-60.

25.           Cody RP, Weisel CP, Birnbaum G, Lioy PJ. The effect of ozone associated with summertime photochemical smog on the frequency of asthma visits to hospital emergency departments. Environmental Research 1992; 58:184-94.

26.           Fauroux B, Sampil M, Quénel P, Lemoullec Y. Ozone: a trigger for hospital pediatric asthma emergency room visits. Pediatric Pulmonology 2000; 30:41-6.

27.           Hajat S, Haines A, Atkinson RW, Bremner SA, Anderson HR, Emberlin J. Association between air pollution and daily consultations with general practitioners for allergic rhinitis in London, United Kingdom. American Journal of Epidemiology 2001; 153:704-14.

28.           Thurston GD, Lippmann M, Scott MB, Fine JM. Summertime haze air pollution and children with asthma. American Journal of Respiratory and Critical Care Medicine 1997; 155:654-60.

29.           White MC, Etzel RA, Wilcox WD, Lloyd C. Exacerbations of childhood asthma and ozone pollution in Atlanta. Environmental Research 1994; 65:56-68.

30.           Jalaludin BB, Chey T, O'Toole BI, Smith WT, Capon AG, Leeder SR. Acute effects of low levels of ambient ozone on peak expiratory flow rate in a cohort of Australian children. International Journal of Epidemiology 2000; 29:549-57.

31.           Delfino RJ, Coate BD, Zeiger RS, Seltzer JM, Street DH, Koutrakis P. Daily asthma severity in relation to personal ozone exposure and outdoor fungal spores. American Journal of Respiratory and Critical Care Medicine 1996; 154:633-41.

32.           Koenig JQ. Effect of ozone on respiratory responses in subjects with asthma. Environmental Health Perspectives 1995; 103 Suppl 2:103-5.

33.           Holmen A, Blomqvist J, Frindberg H, Johnelius Y, Eriksson NE, Henricson KA, Herrstrom P, Hogstedt B. Frequency of patients with acute asthma in relation to ozone, nitrogen dioxide, other pollutants of ambient air and meteorological observations. Int Arch Occup Environ Health 1997; 69:317-22.

34.           Burge HA, Rogers CA. Outdoor allergens. Environmental Health Perspectives 2000; 108 Suppl 4:653-9.

35.           Corsico R, Falagiani P, Ariano R, Berra D, Biale C, Bonifazi F, Campi P, Feliziani V, Frenguelli G, Galimberti M, Gallesio MT, Liccardi G, Loreti A, Marcer G, Marcucci F, Meriggi A, Minelli M, Nardelli R, Nardi G, Negrini CA, Papa G, Piu G, Pozzan M, D'Ambrosio FP, Riva G. An epidemiological survey on the allergological importance of some emerging pollens in Italy. Journal of Investigational Allergology and Clinical Immunology 2000; 10:155-61.

36.           Dales RE, Cakmak S, Burnett RT, Judek S, Coates F, Brook JR. Influence of ambient fungal spores on emergency visits for asthma to a regional children's hospital. American Journal of Respiratory and Critical Care Medicine 2000; 162:2087-90.

37.           Higgins BG, Francis HC, Yates C, Warburton CJ, Fletcher AM, Pickering CA, Woodcock AA. Environmental exposure to air pollution and allergens and peak flow changes. European Respiratory Journal 2000; 16:61-6.