Health Effects of Acid Aerosols on North American Children: Respiratory

Symptoms

Douglas W Dockery,12 Joan Cunningham,1 Andrew L. Damokosh,1 Lucas M. Neas,12'3 John D. Spengler,1 Petros

Koutrakis,1 James H. Ware,4 Mark Raizenne,15 and Frank E. Speizer 1,2

'Department of Environmental Health, Harvard School of Public Health, 2Channing Laboratory, Brigham and Women's Hospital,

Harvard Medical School, 3Department of Epidemiology, Harvard School of Public Health, and 4Department of Biostatistics, Harvard

School of Public Health, Boston, MA 02115 USA; 5Environmental Health Directorate, Health Canada, Ottawa, K1AOL2 Canada

We min e respiratoryea effe of esur to aidic air pi among 1369

white childee St12 ye Iarsldfmm"C 24cmmn tie n h United.State.: ndCnada'L between,

1988 and 1991. Each child's parent or udi completed a questnnie. Air qual and

meteorologywere measd in-each community for a 1-year period. We usd a two-stage logistic

regression model to analyze the dat, adjusting for e ef of history of aergies parental ama, panta eduction, nd current snomking in the home.

Chil4renIiX,in in the commnt withth highes Is of patcetog acdt wee snft one-isdI of bnhit pea tyear oaedtwo children lI i l l

co ny Fine aice te was aso a ia wth h er repor of bron ti (OR

- 1.65;95% CI 1.12-2.42). No other respiratorly symptoms were Sinfatl higher in asoi

-on wih any of the Iirpoluret No eni bgruIps were id ified Rpotedl

brnhts bulnithe asthma i;hes cuh norjbem were asoitd with levl of prt}!

cle atrnizj8a;xdsty.for these child... living Sina nostuif. envsronniestt*R.. u.rm.i. ac.d aerosols,

air polla.tSio bronchitis, children respiao^ symptom. 'srnsem

iO4:550050l9X6)

Although there has been much public and

scientific debate about acid rain and its precursors, the focus in the past was largely on

ecological effects and secondary health effects

related to mobilization of toxic metals.

Concern about the possible adverse human

health effects resulting from exposure to acid

aerosols has been more recent (1,2).

Experimental studies of sulfur dioxide

and total suspended particulates have shown

adverse health effects in both animals (3) and

human subjects (4). In epidemiologic studies, particulate pollution has been associated

with decrements in lung function (5), higher

prevalence of respiratory symptoms and illness (6-8), and higher rates of hospitalizations (9,10) and mortality (11), even at the

levels currently found in many urban areas.

Fine particles, which penetrate deeply

into the lungs, are produced by direct emissions from combustion sources or atmospheric reactions of gaseous pollutants.

These fine particles are often very acidic.

The observed health effects associated with

particulate pollution may be attributable at

least in part to the acidity of the fine particles (12,13). Previous population-based

studies lacked direct measures of ambient

aerosol acidity, but recent improvements in

atmospheric monitoring techniques have

made it possible to directly measure particle

strong acidity (14).

In children from the Six Cities Study,

reported bronchitis and chronic cough were

associated with total suspended particles (7)

and with particulate matter less than 15

pm in aerodynamic diameter (8). In a later

analysis of children from the same six communities plus Kanawha County, West

Virginia (15), the city-specific summertime mean of particle strong acidity was

associated with significantly higher risk of

bronchitis and chronic cough.

This study was specifically designed to

examine the relationship between longterm, intermittent exposure to particle

strong acidity and the respiratory health of

children (16). In this article, we describe

the associations between particle strong

acidity and respiratory symptoms.

Methods

Air monitoring. We selected 24 communities on the basis of previously measured

sulfate and ozone concentrations and

demographic characteristics (17). The

study included 18 sites in the United

States and 6 sites in Canada to provide a

wide range of expected particle strong acidity and ozone levels. Communities were

predominantly suburban or rural with

homogeneous, relatively stable populations

and no major local sources of air pollution.

Air pollution measurement methods

and calibration procedures are described

in an accompanying paper (17). Air pollution monitoring began at each site before

the summer high acid-ozone exposure

period and continued for at least 11

months. Particulate pollutants were sampled for 24 hr every other day. Inhalable

particulate matter with an aerodynamic

diameter >10 pm (PM1O) was sampled

using a Harvard Impactor (18). Fine particulate matter with an aerodynamic diameter >2.1 pm (PM2.1) was sampled using a

glass impactor/filter pack system. Fine particle strong acidity, fine particle sulfate,

and gaseous acids (nitrous and nitric acids)

were sampled using the Harvard EPA

Annular Denuder System (HEADS) in 21

communities (19-21). In three communities with expected low levels of gas-phase

acidity, the Harvard Impactors with

ammonia denuders were used. Strong acidity was measured by pH analysis (20) and

sulfate was measured by ion chromatography of the extracted particles. Ozone was

monitored continuously.

We grouped the 24 communities by the

sources of particulate mass and acidity (17).

The Sulfate Belt was defined as the 11 sites

with high sulfate and acidity concentrations

lying generally along the Appalachian Plateau

and the Allegheny Mountains. The Transport Region induded communities north and

east of the Sulfate Belt, which are generally

downwind of the principal sulfur emissions

in the United States. The remaining commuAddress correspondence to D.W. Dockery,

Environmental Epidemiology Program, Department of Environmental Health, Harvard School of

Public Health, 665 Huntington Avenue, Boston,

MA 02115 USA.

We thank C. Franklin, D. Villeneuve, and R.

Burnett for their advice and support. This study was

possible because of the hard work of M. Fay, A.

Jemas, E. Donahue, C. Fischer, S. Hanig, L. Kern,

J. L. McClelland, C. Panek, B. Phelps, E. Solomon,

J. Mortimer, K. Wilby, and J. Moore, E. Graham,

E. Haynes, M. Ramsey, the air monitoring staff at

the Harvard School of Public Health, and the field

staff at the various locations. We thank the school

administrators, teachers, and especially the parents

and children in the participating communities. This

paper was presented in part at an international conference sponsored by the American Thoracic Society

in San Francisco, California, 18 May 1993. This

study was supported in part by National Institute of

Environmental Health Science grants ES-04595

and ES-0002, U.S. Environmental Protection

Agency cooperative agreement CR 816071, and

Health Canada. L. M. N. and J. C. were supported

in part by a National Institute of Health National

Research Service Award (HL-07427).

Received 21 August 1995; accepted 22 January

1996.

500 Volume 104, Number 5, May 1996 - Environmental Health Perspectives
Articles * Acid aerosols and respiratory symptoms in children

nities were grouped as West Coast (three

sites) and Background (four sites).

Respiratory health questionnaire. The

study protocol and methods were approved

by the Institutional Review Board at the

Harvard School of Public Health and also

by the local health department and school

board(s) in each community. We contacted

principals of selected schools directly and

invited them to participate. In communities with fewer than 750 children in the

fourth and fifth grades, all schools with at

least 10 students in each grade were

approached. In larger communities, selection of schools was based either on proximity to the air monitoring station or on random selection, depending on the geography of the school district(s). We distributed standard respiratory health questionnaires to the children at participating

schools in September and October of 1988

(eight communities), 1989 (nine communities), and 1990 (seven communities).

Children were instructed to have the questionnaire completed by a parent or

guardian and to return it to school the following day. Classroom (but not individual)

incentives were used to encourage participation, and questionnaires were distributed

multiple times over several weeks. The

overall response rate (returned questionnaires plus written refusals) was 91%, with

a range of 85-99% for the individual communities (Table 1).

Later in the school year, each school was

visited again and the pulmonary function of

children who had their parents' permission

to participate was measured. The results of

the analysis of pulmonary function are

reported in an accompanying article (23).

Definition of respiratory symptoms.

Children's respiratory symptoms in the previous year were determined from questionnaire responses defined as follows: 1) asthma: ever diagnosed with asthma by a physician plus asthmatic symptoms present in the

past year; 2) attacks of wheezing: episodes of

shortness of breath with wheezing and/or

episodes of wheezing after playing hard or

exercising; 3) persistent wheeze: wheeze

apart from colds and/or wheeze for 3 or

more days out of the week for a month or

longer; 4) chronic cough: cough first thing

in the morning for as long as 3 months in a

row and/or cough at other times during the

day or night for as long as 3 months in a

row; 5) chronic phlegm: congestion in the

chest or bringing up phlegm other than with

colds for as long as 3 months in a row; 6)

bronchitis: a chest illness diagnosed as bronchitis; 7) asthmatic symptoms: asthma,

attacks of wheezing, and/or persistent

wheeze; and 8) bronchitic symptoms:

chronic cough, chronic phlegm, and/or

bronchitis. Only reports of symptoms in the

past 12 months were considered.

Statistical methods. Previously reported

analyses of city-specific health outcomes

have demonstrated a larger between-city

variation than would be predicted by

interindividual variation (7,8). In the present study, we used a two-step analysis to

correct for any excess between-city variability. In the first step, city-specific-adjusted

logits of symptom prevalence were calculated from a logistic regression model for the

respiratory symptom of interest controlling

for sex, child's history of diagnosed allergies, parental history of diagnosed asthma

(for either biological parent), parental posthigh school education (for either parent),

and current smoking in the home. In the

second step, these city-specific-adjusted

logits were regressed against the city-specific annual mean air pollution concentrations using weights inversely proportional

to the sum of the between-city and withincity variances of the adjusted logits.

Analyses were done using the SAS software

(SAS Institute, Inc., Cary, North

Carolina). We scaled the regression coefficients from the second step to the range of

the city-specific means for the air pollutant

of interest (highest to lowest; Table 1) and

expressed them as odds ratios (OR) and

95% confidence intervals (95% CI).

To assess the consistency of the evidence and to search for sensitive subgroups,

the analyses were repeated stratifying for

sex; history of a severe chest illness before

the age of 2; use of a humidifier in the

home; lung function in the lowest quartile

of forced vital capacity (FVC); current

exposure to environmental tobacco smoke

at home; exposure to maternal smoking

during pregnancy; year of study; country;

and eastern versus western cities.

Results

The city-specific ranges in the annual pollutant means (Table 1) were 51.9 nmol/m3

for particle strong acidity, 6.8 pg/m3 for

sulfate particles, 14.9 pg/m3 for respirable

particulate matter (PM21), and 17.3 pg/m3

for inhalable particulate matter (PM1O).

The gaseous acids (HNO2 and HNO3)

were measured in all but three communities and together had a range of 111

nmol/m3. City-specific mean particle

strong acidity was moderately correlated

with PM1O [Pearson's correlation coefficient (r) = 0.47], strongly correlated with

sulfate (r= 0.90) and PM2.1 (r= 0.82), and

essentially uncorrelated with gaseous acids

(r = 0.07). Three exposure parameters were

considered for the annual mean ozone concentration: the average maximum 1-hr

mean (range 46 ppb), the average daytime

8-hr (1000-1800 hr local time) mean

(range 39 ppb), and the average daily 24-hr

mean (range 19 ppb). All three ozone parameters were highly correlated across the 24

communities with Pearson correlation

coefficients ranging from 0.74 to 0.98. By

design, city-specific mean particle strong

acidity was only weakly correlated with the

three ozone parameters; the strongest correlation was with the average 1-hr maximum

ozone concentration (r = 0.37).

A total of 17,008 children were eligible

to participate in the study, of whom

15,523 children (91%) returned a questionnaire. Children who were reported to

have cystic fibrosis, a history of a chest

Table 1. Summary of city-specific annual mean air pollution concentrations: 24 communities, United

States and Canada, 1988-1991

Pollutant Grand mean SD Minimum Maximum Range

Particulate matter

Inhalable (pg/m3) 23.8 5.0 15.4 32.7 17.3

Respirable (pg/m3) 14.5 4.2 5.8 20.7 14.9

Sulfate particles (pg/m3)a 4.7 2.2 0.7 7.4 6.8

Particle strong acidity (nmol/m3) 27.5 16.2 0.0 51.9 51.9

Gaseous pollutants

Ozone, 1-hr max. (ppb) 46.5 8.5 26.9 72.5 45.6

Ozone, 8-hr daytime avg. (ppb) 38.4 7.5 21.0 60.4 39.4

Ozone, 24-hr avg. (ppb) 27.8 5.1 16.3 34.8 18.5

Sulfur dioxide (ppb)b 4.8 3.5 0.2 12.9 12.7

Ammonia (ppb)b 1.3 1.4 0.1 5.8 5.7

Nitrous acid (ppb)b c 0.6 0.4 0.1 1.4 1.3

Nitric acid (ppb)bc 0.9 0.4 0.3 2.1 2.7

Acidityb

Particle strong acidity (nmol/m3) 31.1 14.0 8.5 51.9 43.4

Gaseous acids (nmol/m3)d 59.4 28.4 22.7 134.0 111.3

Total (nmol/m3) 90.6 33.9 38.0 150.5 112.5

al pg/m3 = 10.4 nmol/m3.

bExcluding Egbert, Ontario; Yorkton, Saskatchewan; and Aberdeen, South Dakota.

Cl ppb = 40.9 nmol/m3.

dGaseous acids = nitrous + nitric acid.

Environmental Health Perspectives . Volume 104, Number 5, May 1996 501
Articles * Dockery et al.

Table 2. Distribution of covariates used in the respiratory symptoms model by community: 13,369 children, 24 comunities, United States and Canada, 1988-1991

Parental Current

Site Participation No. of children Females Allergy Parental post-high school smoking in

code (%) Excluded Included (%) history (%) asthma (%) education (%) the home (%)

Sulfate Belt

Hendersonville, TN HEN 85 59 504 56 40 13 68 55

Oak Ridge,TN OAK 96 119 540 46 41 15 83 42

Morehead, KY MOR 93 48 393 50 30 14 52 61

Blacksburg, VA BLB 94 124 666 48 37 16 74 37

Charlottesville, VA CHV 91 171 522 46 24 12 45 53

Zanesville, OH ZAN 90 122 647 51 26 16 50 61

Athens, OH ATH 88 82 609 53 29 13 69 52

Parsons, WV PAR 91 50 580 51 28 13 43 56

Uniontown, PA UNT 94 63 584 48 24 10 46 62

Penn Hill, PA PEN 90 119 566 49 32 11 80 44

State College, PA STC 91 97 601 51 31 16 89 30

Transport Region

Leamington, ON LEM 93 111 586 51 30 10 54 55

Newtown, CT NEW 92 50 458 52 37 16 89 38

Egbert, ON EGB 90 76 618 49 37 13 63 62

Pembroke, ON PMB 96 55 530 49 33 9 53 64

Dunnville, ON DUN 89 37 442 50 29 15 51 58

South Brunswick, NJ SBK 88 131 329 48 42 11 79 46

West Coast

Simi Valley, CA SIM 88 129 539 49 31 17 78 40

Livermore, CA LIV 84 102 582 52 46 18 87 36

Monterey, CA MTY 90 92 642 52 32 17 91 29

Background

Springdale, AK SPG 91 58 506 53 38 13 50 61

Aberdeen, SD ABD 96 71 676 51 26 11 77 49

Yorkton, SK YOR 95 82 628 47 39 10 58 58

Penticton, BC PCT 95 106 621 47 33 13 65 52

All 24 communities 91 2154 13369 50 33 13 67 50

Table 3. Adjusted prevalence of respiratory symptoms by community and symptom: 13,369 children, 24 communities, United States and Canada, 1988-1991a

Asthmatic symptoms (%) Bronchitic symptoms (%)

Attacks of Persistent Any asthmatic Chronic Chronic Any bronchitic

Asthma wheeze wheeze symptoms Bronchitis cough phlegm symptoms

Sulfate Belt

Hendersonville, TN 3 5 4 7 6 5 2 10

Oak Ridge, TN 5 7 7 10 10 3 2 13

Morehead, KY 5 7 7 9 5 4 3 9

Blacksburg, VA 5 9 9 12 10 5 3 13

Charlottesville, VA 5 8 6 9 9 5 3 12

Zanesville, OH 6 9 7 12 7 6 5 13

Athens, OH 6 8 8 11 7 5 4 12

Parsons, WV 7 7 7 11 7 5 1 11

Uniontown, PA 5 6 7 10 7 5 2 12

Penn Hill, PA 8 10 10 12 9 5 4 14

State College, PA 11 11 12 16 7 9 4 15

Transport Belt

Leamington, ON 5 7 6 10 4 7 3 12

Newton, CT 6 8 8 11 5 6 3 10

Egbert, ON 9 11 10 14 4 8 5 12

Pembroke, ON 5 8 8 11 4 7 3 11

Dunnville, ON 9 10 10 14 5 8 3 10

South Brunswick, NJ 7 7 7 10 7 7 4 13

West Coast

Simi Valley, CA 10 10 9 14 7 6 3 12

Livermore, CA 7 8 8 11 3 5 3 9

Monterey, CA 7 8 9 11 8 5 3 14

Background

Springdale, AR 4 6 6 8 5 5 2 9

Aberdeen, SD 7 9 10 12 8 5 3 14

Yorkton, SK 10 9 9 15 4 4 2 8

Penticton,BC 5 7 6 9 5 4 1 9

aAdjusted for sex, history of allergies, parental asthma, parental education, and current smoking in the home. See text for definition of symptoms.

502 Volume 104, Number 5, May 1996 * Environmental Health Perspectives
Articles - Acid aerosols and respiratory symptoms in children

operation, serious chest injury, or heart disease, or who were reported to have received

oxygen for more than 2 weeks as newborns

were excluded (n = 790). Other exclusions

were based on age (not 8-12 years; n = 14),

race (not white; n = 1013), and missing

information on covariates of interest (n =

337). A total of 13,369 children in 24

communities were included in this analysis.

Overall, half (50%) of the subjects were

girls, 33% had a history of diagnosed allergies, 13% had at least one parent with a

history of asthma, 67% had at least one

parent with some post-high school education, and 50% were currently exposed to

environmental tobacco smoke at home.

The prevalence of these factors varied by

community (Table 2). After adjusting for

these factors, the community-specific

prevalence of asthma was 3-11%; attacks

of wheeze, 5-1 1 %; persistent wheeze,

4-12%; any asthmatic symptoms, 7-16%;

bronchitis, 3-10%; chronic cough, 3-9%;

chronic phlegm, 1-5%; and any bronchitic

symptoms, 8-15% (Table 3).

Particle strong acidity was associated

with significantly higher reporting of bronchitis in the past year (Fig. 1 and Table 4;

OR = 1.66, 95% CI, 1.11-2.48 for the

range of 52 nmol/m3), as was annual mean

sulfate (OR = 1.65, 95% CI, 1.12-2.42 for

the range of 7 pg/m3).

None of the particulate pollutants was

associated with significantly higher reporting of asthma, attacks of wheeze, persistent

wheeze, chronic cough, or chronic phlegm

(Table 4). There was a significant inverse

association between chronic cough and

PM O. Gaseous acids were associated with a

significantly higher risk of asthma (OR =

2.00; 95% CI, 1.14-3.53) and showed a

positive association with higher reporting of

attacks of wheezing, persistent wheeze, and

any asthmatic symptoms (Table 4). Ozone

was not associated with a significantly higher risk of any of the respiratory symptoms

of interest, regardless of the averaging time

used (Table 4). There was a suggestion of a

higher risk of chronic cough associated with

24-hr average ozone (OR = 1.29; 95% CI,

0.87-1.91). Ozone for all three averaging

times showed some association with higher

reporting of bronchitis.

The association between particle strong

acidity and bronchitis was similar when the

sample was stratified by sex (Fig. 2). The

association was sensitive to the inclusion of

the Canadian sites, which tended to have

low bronchitis prevalence and low to moderate particle strong acidity. Thus, much

weaker associations were found when the

sample was restricted to U.S. cities or cities

studied in the second year, which were predominantly U.S. cities (Fig. 2). No sub12

10

WI1

C3

.0

0

C)

160

100.

10

St

=-

8

6

4

0

0 10 20 30 40 50 60

Particle strong acidity (annual mean in nmol/m3)

Figure 1. Association of bronchitis with particle strong acidity adjusted for sex, child's history of atopy,

parental education, parental asthma, and current smoking in the home: 24 cities, United States and

Canada, 1988-1991. One-half 95% Cls for each city-specific bronchitis prevalence are shown. Site codes

are provided in Table 2.

These results are consistent with earlier

reports from the Six Cities Study (7,8,15),

which noted higher rates of reported bronchitis, but not asthma or wheeze, in association with total suspended particles (7),

with particulate matter < 15 pm in aerodynamic diameter (8), or with levels of particle strong acidity (15). In these earlier studies, reporting of chronic cough was higher,

but not significantly so, in association with

these pollutants.

Prior controlled exposure studies of

animals and humans provide support for a

relationship between acid aerosols and

bronchitis. Short-term exposures to acid

aerosols have been shown to result in alterations of mucociliary clearance in rabbits,

mice, donkeys, and humans (24). Thus it

is reasonable to suspect that chronic exposure to moderate levels of acidic air pollution may affect children's nonspecific

defense mechanisms adversely, increasing

their risk of respiratory illness.

groups appeared to be markedly more sensitive to particle strong acidity than the

overall sample of children with respect to

their risk of bronchitis (Fig. 3). The risk of

bronchitis among children who were in the

lowest quartile of FVC was not associated

with level of particle strong acidity.

Discussion

This study was designed to determine

whether long-term exposure to acidic

aerosols, estimated by annual mean concentrations, was associated with differences

in reported respiratory symptoms in children. The data from this study indicate

that adjusted prevalence of bronchitis in

children aged 8-12 years was significantly

associated with particle strong acidity concentrations. Asthma, persistent wheeze,

chronic cough, and chronic phlegm were

not significantly associated with higher levels of acid aerosols. No sensitive subgroups

were identified.

Environmental Health Perspectives * Volume 104, Number 5, May 1996 503
Articles * Dockery et al.

Table 4. Association of air pollutants with respiratory symptoms by symptom and pollutant: 13,369 children, 24 communities, United States and Canada, 1988-1991 a

Particle strong acidity

(52 nmoVm3)

Sulfate particles

(6.8 pg/iM3)

Respirable particulate matter

(14.9 pg/m3)

Inhalable particulate matter

(17.3 pg/M3)

Gaseous acids

(2.7 ppb)

Total acid

(1 14 nmol/m3)

Max. ozone,

1-hr avg. (45.6 ppb)

Sulfur dioxide

(12.7 ppb)

OR

95% Cl

OR

95% Cl

OR

95% Cl

OR

95% Cl

OR

95% Cl

OR

95% Cl

OR

95% Cl

OR

95% Cl

Asthma

0.71

0.43-1.16

0.80

0.50-1.29

0.72

0.40-1.28

0.77

0.44-1.35

2.00

1.14-3.53

1.64

0.98-2.73

1.02

0.44-2.33

1.05

0.57-1.93

Attacks of

wheeze

0.79

0.59-1.06

0.93

0.70-1.24

0.82

0.58-1.15

0.79

0.57-1.08

1.40

0.99-1.99

1.26

0.92-1.73

0.99

0.61-1.60

1.07

0.75-1.55

Persistent

wheeze

0.83

0.60-1.15

0.96

0.70-1.31

0.80

0.55-1.16

0.75

0.53-1.07

1.34

0.87-2.05

1.24

0.86-1.79

0.90

0.52-1.54

1.19

0.80-1.79

Any asthmatic

symptoms

0.81

0.60-1.10

0.91

0.67-1.24

0.79

0.55-1.12

0.75

0.54-1.05

1.34

0.91-1.96

1.24

0.89-1.72

0.89

0.53-1.50

1.16

0.80-1.68

Bronchitis

1.66

1.1 1-2.48

1.65

1.12-2.42

1.50

0.91-2.47

1.50

0.93-2.43

1.18

0.67-2.08

1.43

0.89-2.28

1.49

0.72-3.12

1.56

0.95-2.56

Chronic

cough

0.92

0.64-1.31

1.04

0.74-1.47

0.82

0.54-1.23

0.69

0.48-0.99

1.02

0.64-1.61

0.98

0.66-1.45

1.13

0.62-2.04

1.02

0.66-1.58

Chronic

phlegm

0.95

0.60-1.49

1.29

0.84-1.96

1.02

0.61-1.73

1.05

0.64-1.72

1.48

0.90-2.43

1.40

0.91-2.15

1.12

0.53-2.39

1.55

1.01-2.37

Any bronchitic

symptoms

1.19

0.92-1.53

1.27

1.01-1.61

1.08

0.80-1.46

1.07

0.80-1.43

1.11

0.80-1.53

1.18

0.90-1.55

1.17

0.76-1.81

1.29

0.98-1.71

aSymptoms adjusted for sex, history of allergies, parental asthma, parental education, and current smoking in home. Odds ratio (OR) represents relative risk over

the range of city-specific air pollution; Cl, confidence interval.

The higher reporting of bronchitis, in

contrast to asthma, persistent wheeze, or

chronic cough, is consistent with an

increased susceptibility to illness in association with particle strong acidity.

Alternatively, there may be more misclassification of relatively subjective symptoms

like cough and wheeze in contrast to diagnosed bronchitis. Such misclassification

may have limited our ability to observe

associations of symptoms with air pollution.

Although these data indicate an association between particulate air pollution,

specifically particle strong acidity, and

bronchitic symptoms, there is no evidence

for higher reporting of asthmatic symptoms

associated with these pollutants. Similar

results in which particulate air pollution

was associated with bronchitic symptoms

but not with any indicator of asthma have

been reported in the Six Cities Study (7, 8)

for the United States and in German studies (25). Children in Leipzig with high sulfur dioxide and particle exposures were

compared to children in Munich with

much lower exposures to these pollutants.

Bronchitic symptoms were elevated in the

high sulfur dioxide/particle exposures, but

asthmatic symptoms were decreased in

Leipzig, the community with higher particle and sulfur dioxide pollution. The

authors suggested that asthmatic symptoms

were associated with higher ozone concentrations in Munich. However, in the current data the association between asthmatic

symptoms and measures of chronic ozone

exposure were very slight. No association

was found between ozone and respiratory

symptoms in the Six Cities Study (7,8).

The observed association of asthma and

Geography l

All cities

U.S. cities

Eastern cities

Year of study

Year

Year 2

Year 3

Gender

Males

Females

1 2 3

Adjusted odds ratios

Figure 2. Odds of bronchitis and 95%confidence

intervals for a 52 nmol/m3 increment in particle

strong acidity for stratified samples of children or

cities adjusted for sex, child's history of atopy,

parental education, parental asthma, and current

smoking in the home: 24 cities, United States and

Canada, 1988-1991. Dashed line indicates overall

estimated effect.

asthmatic symptoms with gaseous acids

must be interpreted with caution because

this association appears to be driven by

only one community. The annual mean for

gaseous acid in Simi Valley was one-third

higher than the mean for the next highest

community (17), and Simi Valley also had

the second highest rate of reported asthma.

If Simi Valley is excluded from consideration, the association between gaseous acid

levels and asthma is no longer significant.

All children r

Any chest illness 1_.

before age 2

Persistent wheeze, attacks

of shortness of breath

with wheeze, or asthma

Lowest quartile of forced

vital capacity (RVC) (n = 22)

Parental asthma

Maternal smoking

during pregnancy

ETS in the home

Any use of humidifiers

1 2 3

Adjusted odds ratios

Figure 3. Odds of bronchitis and 95% confidence

intervals for a 52 nmol/m3 increment in particle

strong acidity for potentially sensitive subgoups

of children or cities adjusted for sex, child's history of atopy, parental education, parental asthma,

and current smoking in the home: 24 cities, United

States and Canada, 1988-1991. Dashed line indicates overall estimated effect.

There appears to be no evidence that the

prevalence of asthma or asthmatic symptoms

in children is associated with chronic exposure to particulate, sulfur oxide, or ozone air

pollution. This does not imply that acute air

pollution episodes do not trigger or exacerbate asthmatic attacks, as has been shown in

multiple studies. However, air pollution does

not appear to contribute to the increased

prevalence of new cases of asthma, as is often

claimed in the popular press.

504 Volume 104, Number 5, May 1996 * Environmental Health Perspectives
Articles * Acid aerosols and respiratory symptoms in children

In this study, at least 11 months of air

monitoring data were used to calculate

annual means of pollutants as a surrogate

for lifetime exposure. The validity of such a

monitoring scheme depends on the representativeness of the selected year's aerometrics. Brook and Spengler (26) have examined historical aerometric data and concluded that community air pollution levels

have been relatively stable over these children's lifetimes and that the relative rankings of the communities with respect to

particle strong acidity, ozone, and PM1O

were not likely to have changed. Although

it is possible that the children differed in

their personal activity and exposure patterns between communities, these differences were not likely to be related to annual means of acid air pollution.

Particle strong acidity, sulfate, and fine

particulate matter are all formed in secondary reactions of the emissions from fossil fuel combustion. They have similar

regional and temporal distributions. The

strong correlations of several pollutants in

this study, especially particle strong acidity

with sulfate (r = 0.90) and PM2.1 (r =

0.82), make it difficult to distinguish the

agent of interest. This study was designed

to have a low correlation of particle strong

acidity with ozone, and although high

ozone was positively associated with reporting of bronchitis, the association was not

statistically significant.

The sampled children in each community were selected to have a narrow range of

age and race. Communities also were selected to have similar demographic characteristics. We adjusted for differences among communities in the distributions of sex, child's

allergy history, parental education, parental

asthma, and current smoking in the home in

the first stage of the two-stage model. No

evidence of effect modification was observed

among these children. The association of

bronchitis with particle strong acidity was

similar regardless of sex, year of study, country, home characteristics, or child's health

history. The only exception was for children

in the lowest quartile of FVC, who had no

association between a higher risk of bronchitis and particle strong acidity.

These data indicate that chronic exposure to acid aerosol pollution may have

observable negative consequences for the

health of children. Although the long-term

consequences of bronchitis in these children

remain unclear, respiratory illnesses in

childhood may be a risk factor for chronic

obstructive disease. These children also may

be at a higher risk from other environmental and occupational exposures later in life.

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Environmental Health Perspectives * Volume 104, Number 5, May 1996 505