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Nitrogen dioxide exposure in school classrooms of inner-city children with asthma - 06/06/18

Doi : 10.1016/j.jaci.2017.08.028 
Jonathan M. Gaffin, MD, MMSc a, b, Marissa Hauptman, MD, MPH b, h, Carter R. Petty, MA c, William J. Sheehan, MD b, d, Peggy S. Lai, MD, MPH b, e, f, Jack M. Wolfson, PhD f, Diane R. Gold, MD, MPH f, g, Brent A. Coull, PhD f, Petros Koutrakis, PhD f, Wanda Phipatanakul, MD, MS b, d,
a Division of Respiratory Diseases, Boston Children's Hospital, Boston, Mass 
c Clinical Research Center, Boston Children's Hospital, Boston, Mass 
d Division of Allergy and Immunology, Boston Children's Hospital, Boston, Mass 
h Division of General Pediatrics, Boston Children's Hospital, Boston, Mass 
b Harvard Medical School, Boston, Mass 
e Massachusetts General Hospital, Boston, Mass 
f Department of Environmental Health, Harvard TH Chan School of Public Health, Boston, Mass 
g Channing Institute of Network Medicine, Brigham and Women's Hospital, Boston, Mass 

Corresponding author: Wanda Phipatanakul, MD, MS, Children's Hospital Boston, Division of Immunology, Fegan 6, 300 Longwood Ave, Boston, MA 02115.Children's Hospital BostonDivision of ImmunologyFegan 6, 300 Longwood AveBostonMA02115

Abstract

Background

Ambient and home exposure to nitrogen dioxide (NO2) causes asthma symptoms and decreased lung function in children with asthma. Little is known about the health effects of school classroom pollution exposure.

Objective

We aimed to determine the effect of indoor classroom NO2 on lung function and symptoms in inner-city school children with asthma.

Methods

Children enrolled in the School Inner-City Asthma Study were followed for 1 academic year. Subjects performed spirometry and had fraction of exhaled nitric oxide values measured twice during the school year at school. Classroom NO2 was collected by means of passive sampling for 1-week periods twice per year, coinciding with lung function testing. Generalized estimating equation models assessed lung function and symptom relationships with the temporally nearest classroom NO2 level.

Results

The mean NO2 value was 11.1 ppb (range, 4.3-29.7 ppb). In total, exposure data were available for 296 subjects, 188 of whom had complete spirometric data. At greater than a threshold of 8 ppb of NO2 and after adjusting for race and season (spirometry standardized by age, height, and sex), NO2 levels were associated highly with airflow obstruction, such that each 10-ppb increase in NO2 level was associated with a 5% decrease in FEV1/forced vital capacity ratio (β = −0.05; 95% CI, −0.08 to −0.02; P = .01). Percent predicted forced expiratory flow between the 25th and 75th percentile of forced vital capacity was also inversely associated with higher NO2 exposure (β = −22.8; 95% CI, −36.0 to −9.7; P = .01). There was no significant association of NO2 levels with percent predicted FEV1, fraction of exhaled nitric oxide, or asthma symptoms. Additionally, there was no effect modification of atopy on lung function or symptom outcomes.

Conclusion

In children with asthma, indoor classroom NO2 levels can be associated with increased airflow obstruction.

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Key words : Asthma, indoor air pollution, obstructive lung disease, nitrogen dioxide, spirometry, exhaled nitric oxide

Abbreviations used : FEF25-75, Feno, FVC, NO2


Plan


 Supported by National Institutes of Health grants K23AI106945 (J.M.G.), R01 AI 073964, R01AI 073964-02S1, K24 AI 106822, U01 AI 110397, U10HL098102 (W.P.), NIH/NIEHS K23ES023700 (P.S.L.), K23AI104780 (W.J.S.), P01 ES009825, and P30ES000002 (D.R.G.). This study was also supported by US Environmental Protection Agency grants RD-834798 and RD-83587201. This work was conducted with support from Harvard Catalyst | Harvard Clinical and Translational Science Center (National Center for Research Resources and the National Center for Advancing Translational Sciences, NIH Award UL1 TR001102) and financial contributions from Harvard University and its affiliated academic healthcare centers. The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard Catalyst, Harvard University and its affiliated academic healthcare centers, or the NIH. This publication was also made possible by EPA grant RD-83479801 and was also funded (in part) by cooperative agreement award no. FAIN: U61TS000237 from the Agency for Toxic Substances and Disease Registry (ATSDR). The EPA supports the Pediatric Environmental Health Specialty Units by providing partial funding to the ATSDR under Inter-Agency Agreement number DW-75-92301301. Its contents are solely the responsibility of the grantee and do not necessarily represent the official views of the ATSDR or EPA. Furthermore, the EPA or ATSDR do not endorse the purchase of any commercial products or services mentioned in the publication. Additional acknowledgment goes to the Allergy and Asthma Awareness Initiative. We thank the following companies for their generous donations: Multi-Test II device, Lincoln Diagnostics, Decatur, Ill; allergenic extracts for skin testing, Greer Laboratories, Lenoir, NC; ImmunoCAP testing, Thermo Fisher, Waltham, Mass; aerochambers, Monaghan Medical, Plattsburgh, NY; and NIOX Machines, Aerocrine, Solna, Sweden.
 Disclosure of potential conflict of interest: J. M. Gaffin and P. S. Lai have received grants from the National Institutes of Health (NIH). M. Hauptman has received grants from the NIH, Environmental Protection Agency (EPA), and Agency for Toxic Substances and Disease Registry. J. M. Wolfson has received a grant and subcontract from the NIH. D. R. Gold has received grants from the NIH and EPA and has received travel support from the NIH. B. A. Coull has received grants from the NIH and EPA. P. Koutrakis has received grants from Boston Children's Hospital/NIH (School Inner-City Asthma Intervention Study). The rest of the authors declare that they have no relevant conflicts of interest.


© 2017  American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
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Vol 141 - N° 6

P. 2249 - juin 2018 Retour au numéro
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