Volume 1 Issue 5
April 1996



The increasing prevalence of and mortality from asthma, especially among minority urban populations, have made it a renewed focus of public health attention. Asthma is considered a chronic condition that is marked by both bronchial hyperresponsiveness and inflammation in the tissues in the airways1.

Asthma hospitalizations among U.S. children increased by 4.5% per year between 1979 and 1987, and the death rate from asthma increased 31% in the same time period2. From 1978 through 1989, asthma mortality in the U.S. increased with a near doubling in the mortality rates in both nonwhites and whites; the mortality rates for nonwhites were 4 times those of whites3.

In contrast, a survey of hospital admissions and death from asthma in Canada found no nationwide increase in death rate from asthma between 1980 and 1989, though the rate of hospitalization for asthma increased greatly in that time period.4 A large cross-sectional study of asthma prevalence in children in Canada indicates that higher asthma rates are found on the east coast. Surveyed parents reported that 4.7% of children overall had physician-diagnosed asthma. Asthma was most common in the two Maritime provinces (7.6%) and least common in British Columbia (3.3%) and Quebec (3.4%)5.

Asthma prevalence has been found to be higher in urban areas. A survey of inner-city children in New York City showed that 14.3% reported ever having asthma, and 8.6% reported current asthma, a rate twice that of the general U.S. population (4.3%)6. A study of asthma mortality in Chicago found an overall asthma mortality rate of 16.42 deaths per million from 1980 to 1988 for persons aged 5 to 34 years; this is approximately three times the rate for the general U.S. population7. Rates were highest among poor black persons. Targonski et al.8 studied asthma mortality among persons aged 5 to 34 years in Chicago from 1968 to 1991, and found a 337% increase in mortality for African Americans, while there was no significant increase among Whites. A study of asthma hospitalization among 5- to 14-year old Medicaid patients in Michigan also found much larger increases among urban black children, from 3.2 per 1000 in 1980 to 7.1 per 1000 in 19849.

The root causes for the continued increases in asthma prevalence and severity are under debate. The environmental factors that have been associated with increased asthma symptoms have generally not increased during recent decades; in the case of outdoor air pollutants, concentrations have decreased in the developed nations. Martinez et al.10 studied a cohort of children from infancy to six years of age, and found that, for most children, wheezing does not increase the risk of asthma later in life. However, for a group of children with elevated immunoglobulin (IgE) levels and a family history of asthma, wheezing appears to be related to a predisposition to asthma. The authors could not determine whether the increased allergic sensitization was due to exposure at an early age or a predisposition to allergic sensitization.



The U.S. Clean Air Act of 1970 established six pollutants as "criteria" pollutants -- sulfur dioxide, nitrogen oxides, carbon monoxide, ozone, particulate matter and lead. The resulting network of monitoring stations has provided a substantial database of pollution levels in many U.S. and Canadian cities which has been used in numerous studies of airborne pollution effects on respiratory function. There is little evidence of associations between asthma and either lead or carbon monoxide; evidence for associations with the remaining four pollutants is summarized below.

Although air pollution levels tend to be higher in urban centers, there is also substantial transboundary movement of pollutants in the Great Lakes region. Researchers in New York and Ontario11 have estimated that regional air pollution transported across the Great Lakes from the U.S. contributed strongly to the high acid aerosol concentrations measured in the city of Toronto.

Particulate Matter. There is considerable evidence that increases in particulate matter are associated with increased respiratory mortality and hospital admissions for asthma. The current U.S. standard for PM10 is 150 ug/m3 (24-hour average); a recent review of epidemiological studies indicates that the lowest observable effect level for asthma is above 50 ug/m3 for PM10 and about 25-75 ug/m3 for PM2.512. A review by researchers at Harvard13 combined results from several studies and concluded that each 10 ug/m3 increase in PM10 was associated with an approximate 3% increase in asthma attacks, bronchodilator use, and lower respiratory symptoms. A recent study at Harvard School of Public Health14 found that both increases in Aparticle-strong acidity@ and a 20 ng/m3 increase in respirable particle (PM2.1) concentration on the previous day were associated with a 0.5 l/min decrease in peak flow rate. However, a study of respiratory effects in 18 U.S. and 6 Canada cities found an increase in bronchitis, but not asthma or wheeze, in cities with higher levels of particle-strong acidity15.

Ozone. As reviewed by Koren16, ozone has been associated with increased hospitalization rates for asthma, but it has been difficult to separate the effects of ozone from those of other pollutants such as acid aerosols. Compared with the current U.S. standard of 0.12 ppm (24-hour average), the recent review by Lebowitz12 indicates that the lowest effect level for asthma occurs at 0.08 ppm. In a recent clinical study,17 asthmatic subjects exposed to 0.16 ppm ozone were signifi-cantly more sensitive to ozone exposure than nonasthmatics.


Sulfur dioxide. Koren16 summarized clinical studies which have indicated that asthmatics may develop significant increases in airway resistance with brief exposures to sulfur dioxide at concentrations as low as 0.25 ppm; the U.S. standard is 0.14 ppm(24-hour). A recent study18 of 14 asthmatics exposed to SO2 while exercizing found increasing symptoms and lung function responses in concentrations above 0.5 ppm. However, Lebowitz12 found that the lowest effect level from two epidemiological studies was 200 ug/m3 (0.08 ppm).


Nitrogen dioxide. Clinical studies , summarized by Koren16, have indicated that some asthmatics are inherently more responsive to NO2 than others. NO2 differs from the other three pollutants in that it may be found in higher concentration indoors, due in part to NO2 production from gas stoves or heaters. A metaanalysis of data from 11 studies showed a significant association between estimated NO2 exposure and illness19. Lebowitz12 reviewed epidemiological studies, and found the results too conflicting to determine a lowest observable effect level.



A number of studies have found that asthma symptoms can be triggered by increases in levels of allergens such as pollens or mold spores.20 In one recent panel study, researchers at Harvard14 collected daily peak flow rates and asthma symptoms from a group of children, along with daily outdoor pollutant and aeroallergen levels. They found, in addition to significant associations between particulate pollution and decreased respiratory function, evidence that mold spore concentration independently reduces lung function. A 10,000 spores/m3 increase in Cladosporium was found to be associated with a 1.0 l/min decrease in morning peak flow rate, while a 60 spores/m3 increase in Epicoccum was associated with a 1.5 l/min decrease in morning peak flow rate.



As described earlier, most research on air pollution and asthma has focused on the criteria pollutants. A team of University of Cincinnati21 researchers reviewed what is known about "air toxics" and asthma, and propose a list of 30 compounds that could have the highest impact on asthma and respiratory health. The list of compounds includes: (1) known occupational asthmagens, such as some isocyanates and aldehydes and several metals; (2) known skin allergens with a potential for inhalation exposure, such as hydrazine or chromium compounds; and (3) respiratory irritants, such as hydrochloric acid and phosphine. The authors report results of a study in which rats were exposed to formaldehyde and acrolein, and found that the effect of an 8-hour exposure was greater that what would be predicted by estimation from effects seen with 2-hour exposures, which emphasizes the need to assess effects from long-term exposures at low pollutant levels.



It has been estimated that people in industrialized nations spend 65% of their time in their homes.22 Some pollutants, including nitrogen dioxide and some organic compounds, can be present in higher concentrations in indoor air than outdoor air. Researchers in Norway23 found that increased bronchial responsiveness was associated with indoor allergens, particularly house dust mites, rather than outdoor allergens. In addition, household characteristics, such as dampness or mold growth, humidifier use, presence of tobacco smoke, presence of wall-to-wall carpet and use of gas or wood stoves, have been found to be significantly associated with asthma and respiratory symptoms in a number of studies.22, 24, 25, 26 Norback et al.22 found asthmatic symptoms to be significantly more common in homes where house dust mites were present (OR=5.3; 95% CI 1.2-22.8).


Although there has been little research on indoor pollutant concentrations and asthma, there is some evidence of an association. Researchers in Sweden22 measured levels of formaldehyde and VOCs, along with other indoor factors, in homes of 47 asthmatics and 41 nonasthmatic subjects. Mean formaldehyde concentrations were 29 and 17 ug/m3 in homes with and without subjects reporting nocturnal breathlessness. The mean levels of total VOCs in the living room were 780 ug/m3 and 300 ug/m3 in homes of subjects with and without reported nocturnal breathlessness. All groups of VOCs (such as terpenes, n-alkanes) were found in significantly higher concentrations in the homes of subjects reporting nocturnal attacks of breathlessness, compared to subjects without nocturnal breathlessness.



Pollutant interactions. The concentrations of criteria pollutants are often correlated, and ambient air nearly always contains a mixture of pollutants. Some recent clinical studies have indicated that pollutants in combination have additive effects. Frampton et al.27 found that asthmatics were significantly (p<0.05) more susceptible to lung function changes when exposed to sulfuric acid aerosol followed by ozone exposure. Liekauf et al.21 suggest that ozone measurements can be used in estimating exposure to toxic air pollutants, especially reactive hydrocarbons.

Pollution/allergens: Gilmour28 reviewed animal and human studies indicating that exposure to pollutants may heighten sensitization to allergens. Increased allergic sensitivity has been found in animal studies with exposure to ozone, nitrogen dioxide or sulfur dioxide; the pollutant exposure levels were higher than those found in ambient conditions. In one clinical study on humans with exposure to 0.12 ppm ozone (the U.S. air quality standard) some subjects showed increased bronchial responsiveness following antigen challenge. However, a second study, using 0.5 ppm ozone, found no significant difference in responsiveness, but it was noted that allergic individuals had much stronger responses than nonallergic individuals. In the author's lab, exposure of rats to 5 ppm nitrogen dioxide (about 100 times the U.S. standard for annual average NO2) resulted in greater immune responsiveness and severity of pulmonary inflammation. The proposed mechanisms for this effect include reduced lung immune response resulting in longer residence time for allergens in the lung, or oxidant-induced release of inflammatory substances in lung tissue resulting in heightened sensitization to allergens.


Rain/Allergens: A recent report from London29 supports previous studies in noting the occurrence of an "epidemic" of emergency room admissions for asthma following a thunderstorm, with a sudden drop in air temperature. Number of lightning strikes, increase in rainfall, fall in temperature, rise in air pressure and relative humidity were associated with increased asthma presentations to the emergency room. A change in pollen concentration (both rise and fall) was also found to be a significant predictor. It has been proposed that rainfall or moisture in the air exacerbates the effects of pollen. As summarized by Knox30, pollen grains rupture by osmotic shock in rainwater, releasing hundreds of starch granules from each grain, and inhalation challenge tests have shown that starch granule suspensions are capable of eliciting immune responses in allergic people.



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3) Arrighi HM. 1995. Ann Allergy Asthma Immunol 74(4):321-326.
4) Wilkins K, Mao Y. 1993. Can Med Assoc J 148(2):185-190.
5) Dales RE, Raizenne M, et al. 1994. Int J Epidemiol 23(4):775-781.
6) Crain EF, Weiss KB, Bijur PE,et al. 1994. Pediatrics 94(3):356-362.
7) Marder, D, Targonski P, Orris P,et al. 1992. Chest 101(6):426S-429S.
8) Targonski PV, Persky VW et al 1994. Am J Public Health 84(11):1830-1833.
9) Gerstman BB, Bosco LA, et al. 1993. J Allergy Clin Immunol 91(4):838-843.
10) Martinez FD, Wright AL, et al. 1995. N Engl J Med 332(3):133-138.
11) Thurston GD, Gorcynski JE,et al. 1994. Environ Res 65:254-270
12) Lebowitz MD. 1996. Eur Respir J 9:1029-1054.
13) Dockery DW, Pope CA III. 1994, Annu Rev Public Health. 15:107-132.
14) Neas LM, Dockery DW, et al. 1996. Am J Epidemiol 143(8):797-807
15) Dockery DW, Cunningham J, et al. 1996 Environ Health Perspect 104(5):500-505.
16) Koren HS. 1995. Environ Health Perspect. 103(Suppl 6):235-242.
17) Horstman DH, Ball BA, et al. 1995. Toxicol Ind Health 11(4):369-385.
18) Gong H, Lachenbruch PA, Harber P, Linn WS. 1995 Toxicol Ind Health 11(5):467-487.
19) Hasselblad V, Eddy DM, Kotchmar DJ. 1992. J Air Waste Manage Assoc. 42:662-671.
20) Lebowitz MD, O
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21) Leikauf GD, Kline S,et al. 1995. Environ Health Perspect 103(Suppl 6):253-271.
22) Norback D, Bjornsson E, et al. 1995. Occup Environ Med 52:388-395.
23) Omenaas E, Bakke P, Eide GE,et al. 1996. Eur Respir J 9:919-925
24) Ostro BD, Lipsett MJ et al. 1995. Am J Respir Crit Care Med 149:1400-6.
25) Peat JK, Tovey E, et al. 1996. Am J Respir Crit Care Med 153:141-6.
26) Infante Rivard C. 1993 Am J Epidemiol 137(8):834-44.
27) Frampton MW, Morrosw PE, Cox C, et al. 1995. Environ Res. 69:1-4.
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29) Celenza A, Fothergill J, Kupek E, Shaw RJ. 1996. BMJ 312:604-7.
30) Knox RB. 1993. Clin Exp Allergy 23:354-9.



A monthly review and summary of the scientific literature on human health effects and environmental pollutants, with an emphasis on pollutants of the Great Lakes ecosystem. Prepared under the direction of the Health Professionals Task Force of the International Joint Commission. This does not represent the official position of the International Joint Commission.

Health Professionals Task Force Secretary: Jim Houston
International Joint Commission
Canada Section
100 Metcalfe Street
Ottawa, Ontario K1P 5M1
phone (613) 995-0230
fax (613) 993-5583
email: houstonj@ijc.achilles.net



Great Lakes Center for Occupational and Environmental Safety and Health
School of Public Health
University of Illinois at Chicago
2121 West Taylor Street
Chicago, Illinois 60612-7260
(312) 996-7887
email: mross1@uic.edu

Project Coordinator:
Mary A. Ross, MA
Senior Science Advisor:
Daniel O. Hryhorczuk, MD, MPH