Lung function growth in children with long-term exposure to air pollutants in Mexico
Running title: Lung function growth and air pollution
Rosalba Rojas-Martinez1, Rogelio Perez-Padilla2, Gustavo Olaiz-Fernandez1, Laura
Mendoza-Alvarado1, Hortensia Moreno-Macias1,3, Teresa Fortoul4, William McDonnell5,
Dana Loomis6, Isabelle Romieu1
1Instituto Nacional de Salud Publica de México, México, 2 Instituto Nacional de
Enfermedades Respiratorias, México, 3Universidad Autónoma Metropolitana, México,
4Mexico Medical School, UNAM, Mexico, 5Environmental Protection Agency, USA,
6School of Public Health University of North Carolina, USA
Supported by the Mexican Sciences and Technology Council (CONACYT), SALUD-2005-
01-13956, and the National Center for Environmental Health - Centers for Disease Control
and Prevention, Atlanta GA, USA.
Correspondence and requests for reprints should be addressed to Dr. Isabelle Romieu,
Instituto Nacional de Salud Publica, 655 Avenida Universidad, Col. Santa Maria
Ahuacatitlán, Cuernavaca, Morelos 62508, México. Tel: 52-777-101-2935; fax: 52-777-311-
1148; e-mail: email@example.com
Category: 1.18 Air pollution
This article has an online data supplement, which is accessible from this issue’s table of
content online at www.atsjournals.org
Word count: 2,583
AJRCCM Articles in Press. Published on April 19, 2007 as doi:10.1164/rccm.200510-1678OC
Copyright (C) 2007 by the American Thoracic Society.
Rationale: Although short-term exposure to air pollution has been associated with acute,
reversible lung function decrements, the impact of long-term exposure has not been well
established. Objective: To evaluate the association between long-term exposure to ozone
(O3), particulate matter <10 µm in diameter (PM10) and nitrogen dioxide (NO2) and lung
function growth in Mexico City schoolchildren. Methods: A dynamic cohort of 3,170
children aged 8 years at baseline was followed from April 23, 1996 through May 19, 1999.
The children attended 39 randomly selected elementary schools located near 10 air quality
monitoring stations and were visited every 6 months. Statistical analyses were performed
using general linear mixed models. Results: After adjusting for acute exposure and other
potential confounding factors, deficits in FVC and FEV1 growth over the 3-year follow-up
period were significantly associated with exposure to O3, PM10 and NO2. In multi-pollutant
models, an interquartile range (IQR=11.3 ppb) increase in mean O3 concentration was
associated with an annual deficit in FEV1 of 12 ml in girls and 4 ml in boys, an interquartile
range (IQR=36.4 µg/m3) increase in PM10 with an annual deficit in FEV1 of 11 ml in girls
and 15 ml in boys, and an interquartile range (IQR=12.0 ppb) increase in NO2 with an annual
deficit in FEV1 of 30 ml in girls and 25 ml in boys. Conclusion: We conclude that long-term
exposure to O3, PM10 and NO2 is associated with a deficit in FVC and FEV1 growth among
schoolchildren living in Mexico City.
Keywords: lung function growth, air pollution, children
Word count: 247
Epidemiological studies have clearly shown that acute exposure to ambient air pollution is
associated with a range of respiratory events in children1-3. Although there is growing
evidence that air pollution exposure is likely to affect lung growth4-10, there is still
controversy on which pollutant is most harmful to health. Long-term exposure to ozone (O3)
has been associated with significantly decreased lung functions in retrospective and
prospective cohorts of children6,11 and young adults4,5, while the Children’s Health Study
(CHS)7-9 reported that nitrogen dioxide (NO2), acid vapor and elemental carbon had the
The Metropolitan Area of Mexico City experiences significant air pollution problems. O3
levels are high and the average 1-hour daily maximum frequently exceeds 110 ppb (the
Mexican standard)12. Studies conducted among asthmatic children living in Mexico City
have shown a decrement in lung functions and an increase in respiratory symptoms13-16,
suggesting that children with lifelong exposure to a heavily polluted environment, mainly to
ozone pollution, have detectable abnormalities that could be indicative of small airway
disease or decreased total lung capacity.
We therefore conducted a prospective dynamic cohort study to evaluate the long-term effect
of ambient air pollution on the lung function growth of Mexico City schoolchildren. Some of
the results of this study have been previously reported in the form of abstracts17,18.
We selected 10 fixed-site air monitoring stations in Mexico City, then randomly selected 39
elementary schools from among those located within 2 km of the stations. The study cohort
consisted of students of the selected schools who were 8 years of age at the beginning of the
study, had not been diagnosed as asthmatic and whose parents had signed a consent letter. A
substantial number of children entered or left the cohort during the course of the study. At
baseline, a questionnaire was completed by the parents of 1,819 children and a spirometric
test was administered to each child (phase 1). An additional 1,351 participants of the same
age (+/- 1 month) as the previously enrolled children were added to the cohort in subsequent
phases. The cohort was followed every 6 months (spring and fall) for 3 years with
spirometric tests and two questionnaires, one completed by the parents and the other by the
children and their teachers. Lung function testing was conducted by trained technicians
following American Thoracic Society standards19, using computerized dry rolling-seal
spirometers (Model 922, SensorMedics, Yorba Linda, CA, USA). The spirometry quality
control program has been previously reported20.
Air pollution monitoring
We obtained measurements of NO2, SO2, particulate matter with a mass median diameter of
less than 10 µm (PM10), ambient O3 and weather variables (relative humidity and minimum,
maximum and daily average temperature) from 10 government air monitoring stations. We
calculated 8-hour means (between 10 am and 6 pm) for O3 and 24-hour means for PM10 and
NO2 for each day for which hourly data were available for more than 75% of the time. The
selected schools were located within 2 km of 10 fixed-site monitoring stations. Children’s
exposure assessment was based on data from the station closest to their school. Five
monitoring stations (Plateros, Hangares, Taxqueña, Lagunilla and San Agustín) were not
equipped with a TEOM so could not be used to assign PM10 exposure. The PM10 exposure of
children attending the schools concerned was based on data from the nearest station
measuring PM10 (Pedregal, Merced, Cerro de la Estrella, Merced and Tlalnepantla
respectively). The maximum distance between these schools and the PM10 monitoring
stations was 6 km.
Long-term exposure for each day of the study period was estimated as the averages over the
previous 6 months of the daily O3 8-hour mean, PM10 24-hour means and NO2 24-hour
means averaged over the previous 6 months. These averages vary depending on the station
assigned to each school. Only low concentrations of SO2 and CO were registered, so their
effects were not analyzed.
General linear mixed models were used to evaluate the association between air pollutant
concentrations and deficits in lung function growth over time. The outcome variables were
the spirometric parameters FVC, FEV1, FEF25-75%.and FEV1/FVC from a total of 14,545 test
results for 3,170 children. A three-level model was used to distinguish the sources of
variation in the response: a first level to identify the variation between phases within children
nested within monitoring stations, a second level to identify the variation between subjects
within monitoring stations and a third level to identify the variation between monitoring
station variables. We fitted sex-specific models because of the presence of a statistically
significant interaction term between time (study phase) and sex (p<0.001). Annual lung
function growth was defined as the slope obtained from mixed models given by the
coefficient of the interaction term of time with air pollutant concentrations, specifying the
variance-covariance matrix as unstructured with random intercept and slope. Our final model
included the following variables (based on Akaike´s Information Criteria from the model):
time since first test, O3 averaged over 6 months (O3-6), previous-day O3, PM10 averaged over
6 months (PM10-6), previous-day PM10, NO2 averaged over 6 months (NO2-6), previous-day
NO2, interaction terms of study phase with O3-6, PM10-6 and NO2-6, age, body mass index
(BMI), height, height by age, weekday time spent in outdoor activities, and environmental
tobacco smoke (ETS). Longitudinal analysis was performed using the PROC MIXED
procedure of SAS 8.2 (SAS Institute Inc, Cary NC) (for further details of methods used, see
the online data supplement).
Table 1 and E1 present the characteristics of the study population (n = 3,170) by study phase
and sex. Anthropometric measurements and lung function variables increased over time for
both sexes. Figure 1 presents the location of the monitoring stations used in the study. Air
pollutant concentrations over the 3-year study period were higher in spring than fall (Table
E2, online supplement). Over the study period, 8-hour mean O3 concentrations ranged from
60 ppb (SD 25) in the north-east area to 90 ppb (SD 34) in the south-west and 24-hour mean
PM10 concentrations from 53 µg/m3 (SD 32) in the south-west to 97 µg/m3 (SD 49) in the
north-east (Table 2). O3 was negatively associated with PM10 (r = -0.23, p<0.001) and
positively associated with NO2 (r = 0.166, p<0.001).
Table 3 presents O3, PM10 and NO2 means and percentiles of 6-months mean concentrations,
and interquartile range, during the study period. The widest interquartile range was observed
in 6-month mean PM10 concentrations.
Table 4 presents the results by sex of our final mixed models for FVC, FEV1 and FEF25-75%
adjusted for age, BMI, height, height by age, weekday time spent in outdoor activities, ETS
exposure, previous-day mean air pollutant concentration and time since first test. One-
pollutant models showed an association between ambient air pollutants and deficits in lung
growth. In girls, a 11.3 ppb increase (IQR) in O3 was associated with an annual deficit of –35
ml (95% CI –41 to –29) in FVC, -24 ml (95% CI -30 to -19) in FEV1 and -20 ml/s (95% CI -
32 to -8) in FEF25-75%. The annual deficits for boys were -25 ml (95% CI -31 to -19) in FVC,
-16 ml (95% CI -21 to -11) in FEV1 and -8 ml/sec (95% CI -19 to 4) in FEF25-75%. Ambient
PM10 and NO2 concentrations were similarly negatively associated with lung growth. In girls,
a 36.4 µg/m3 increase (IQR) in PM10 was associated with an annual deficit of -39 ml (95% CI
-47 to -31) in FVC and -29 ml (95% CI -36 to -21) in FEV1. The corresponding deficits for
boys were -33 ml (95% CI -41 to -25) in FVC and -27ml (95% CI -34 to -19) in FEV1.
Slightly larger coefficients were observed for the effect of NO2. For a 12.0 ppb increase
(IQR) in NO2, the annual deficits were -48 ml (95% CI -55 to -41) for FVC and -32 ml (95%
CI -39 to -26) for FEV1 in girls and -45ml (95% CI -53 to -37) for FVC and -26 ml (95% CI -
33 to -19) for FEV1 in boys. No significant effect of PM10 and NO2 was observed on FEF25-
75%. Estimates from two-pollutant models were not substantially different. In multi-pollutant
models, the negative association of O3, PM10 and NO2 with lung function growth persisted
but the effect was slightly stronger for O3 in girls than boys. As the observed impact was
greater on FVC than on FEV1, the FEV1/FVC ratio for both sexes tended to increase with
higher pollutant concentrations in all models (see Table 4). When the percentage annual
changes in predicted values were calculated on the basis of the reference equations for
Mexican children21, the results were similar (Table E4, online supplement).
Figures 2a, 2b, and 2c present the estimated growth in FVC (2a), FEV1 (2b) and FEF25-75%
(2c) for the 25, 50 and 75 percentiles of O3, PM10 and NO2 concentrations by sex, obtained
from multi-pollutant models. At the beginning of the study and at each phase of follow-up,
children exposed to lower O3 and PM10 concentrations had better lung function values than
children exposed to higher concentrations.
As FEF25-75%/FVC is a marker of low volume in small airways and this might modify the
effect of O3 on FEF25-75%, we stratified by tertiles of FEF25-75%/FVC. O3 was significantly
related to a deficit in lung growth (-5.1% per 10 ppb; 95% CI -8.7% to -1.5%) among girls
with the lowest FEF25-75%/FVC (lower 2 tertiles). No effect was observed among girls in the
highest tertile or among boys.
Our study revealed significant deficits in lung function growth in children with long-term
exposure to air pollutants. In one-pollutant models, O3, PM10 and NO2 were associated with a
significant deficit in FVC and FEV1 growth in both girls and boys. The FEV1/FVC ratio also
increased, as exposure had a greater impact on FVC than on FEV1. An association between
O3 and a deficit in FEF25-75% growth was observed only among girls with a low FEF25-
75%/FVC ratio. The effect on FEV1 during the 3 years of follow-up was slightly greater than
that reported for exposure to maternal smoking among US children22,23.
A deficit in FVC and FEV1 growth was observed for O3, PM10 and NO2 after adjusting for
the acute effect of these pollutants (previous-day concentrations) and for confounding
factors. In multi-pollutant models O3 and NO2 had the strongest effect among girls. These
results are in part consistent with previous results from the CHS, which observed a deficit in
growth mostly with exposure to PM2.5, NO2 and inorganic acid vapor7,9,15. In the CHS, O3
exposure was associated with a growth deficit in peak expiratory flow rate in fourth graders
followed for only 4 of the 8 years of follow-up8,22. Lower lung functions in children exposed
to higher O3 concentrations have been reported in cross-sectional studies24 including one
based on CHS data which observed lower peak expiratory flow rate (PEFR) and maximal
midexopiratory flow (MMEF) particularly in girls spending more time outdoors25, and in
retrospective 11 and prospective 6 cohort studies. Deficit in lung growth was associated with a
set of pollutants including O3, PM10 and NO2. Their main source, particularly that of NO2 and
O3, is traffic-related: the former is directly emitted from tailpipes while the latter is a
photochemical reaction to exhaust gases26. However, as the pollutants are correlated,
independent effects could not be accurately estimated.
The mechanism of action by which long-term exposure to air pollution produces changes in
lung development has not yet been established. Human and animal studies have
demonstrated several changes in lung morphology related to O3 exposure27-29, particularly
with a predominantly restrictive pattern30. Calderon et al.16 have suggested that chronic and
sustained inhalation of a complex mixture of air pollutants including O3 and PM might be
associated with small airway disease. Recently, oxidative stress resulting from increased
exposure to oxidant compounds (O3, NO2 and particulate components) has been identified as
a major feature underlying the toxic effects of air pollutants31-33. The resulting increased
expression of pro-inflammatory cytokines would lead to an enhanced inflammatory
response32 and potential chronic lung damage. However, it is not clear whether this might
result in permanent loss or whether the pattern of exposure (repeated peak exposure versus
average exposure) is relevant. Because of the shortness of the 3-year follow-up period and
the non-linear pattern of childhood lung function growth34, we were unable to estimate the
impact on lung function attained in early adulthood.
In our study, exposure to pollutants was associated with a higher FEV1/FVC ratio, suggesting
a restrictive pattern similar to that already described in animals30 and humans35. However, the
effect of air pollution on the resulting functional pattern has been inconsistent36,37 and
inflammatory changes in small airways have been observed11.
Several factors need to be considered when interpreting our results. The exposure values used
in studies on the long-term effects of air pollution on lung function growth are usually fixed-
site monitoring station data that has been averaged over communities. To reduce exposure
misclassification, our study was based on schools located within 2 km of the monitoring
stations. In addition, we conducted microenvironmental and personal exposure assessments
in a randomly selected sub-sample of 60 children, using passive O3 samplers and personal
PM10 monitors. PM10 and O3 concentrations from personal, indoor and outdoor monitors
were significantly correlated with the measurements obtained from the fixed-site air
monitoring stations38. Our results were not substantially modified when we adjusted our
models for potential confounding factors. However, we did not have information on variables
such as smoking during pregnancy, birth weight and atopy, which have also been associated
with reduced lung function growth39,40. As socio-economic status might have a differential
distribution across monitoring stations and pollution concentrations and might also be a
determinant of lung function in our population, we tested for interactions between maternal
and paternal education levels and air pollutant effects. None of these interactions were
significant, suggesting that socio-economic status could not explain our results.
Lung function testing was conducted by trained technicians and all spirometry test results
were reviewed by a pulmonologist blinded to the location of the school attended by the child.
The reproducibility of the tests was good and has been previously reported20. In the event of
missing lung function data, if the data was missing in one phase but not in the next the rate of
change could be imputed from the mixed model, as the coefficients obtained from the mixed
model analysis estimated mean effects.
The results of this 3-year study support the hypothesis that long-term exposure to ambient air
pollutants is associated with deficits in lung growth in children. Although we could not
identify specific sources, the effect is likely to be due to vehicular exhaust, as observed in the
CHS9. Although it is still unclear whether the deficits will be permanent, previous studies
have reported long-term deficits in lung function associated with air pollutants9,11. In addition
to the important impact on lung health, early lung function deficits may increase the risk of
developing chronic obstructive lung disease later in life as well as increased cardiovascular
morbidity and general mortality41,42. There is a clear need for stricter air pollution control
measures in Mexico City to protect lung growth in children living there.
Acknowledgments: The authors thank Steve Marshall, Kiros Berhane, James Gauderman,
Nino Kuenzli and Rob McConnell for their important input on this paper; the Mexico City
monitoring network (RAMA) and the field team for providing high quality data, and the
school principals, teachers, students and parents for their participation. They also thank Garth
Evans for reviewing the English manuscript.
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