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Ozone exposure, vitamin C intake, and genetic susceptibility of asthmatic children in Mexico City: a cohort study

Hortensia Moreno-Macías1*, Douglas W Dockery2, Joel Schwartz2, Diane R Gold2, Nan M Laird3, Juan J Sienra-Monge4, Blanca E Del Río-Navarro4, Matiana Ramírez-Aguilar5, Albino Barraza-Villarreal6, Huiling Li7, Stephanie J London7 and Isabelle Romieu8

  • * Corresponding author: Hortensia Moreno-Macías

  • † Equal contributors

Author Affiliations

1 Universidad Autónoma Metropolitana, Unidad Iztapalapa, Avenida San Rafael Atlixco 186, edificio H-001, Col. Vicentina, 09430, D F, México City, Mexico

2 Environmental Health Department, Harvard School of Public Health, Boston, MA, USA

3 Biostatistics Department, Harvard School of Public Health, Boston, MA, USA

4 Hospital Infantil “Federico Gómez”, México City, Mexico

5 Comisión Federal para la Protección contra Riesgos Sanitarios, SSA, México City, Mexico

6 Instituto Nacional de Salud Pública, Cuernavaca, Morelos, Mexico

7 U.S. Department of Health and Human Services, Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, , USA

8 International Agency for Research on Cancer, Lyon, France

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Respiratory Research 2013, 14:14  doi:10.1186/1465-9921-14-14

Published: 4 February 2013



We previously reported that asthmatic children with GSTM1 null genotype may be more susceptible to the acute effect of ozone on the small airways and might benefit from antioxidant supplementation. This study aims to assess the acute effect of ozone on lung function (FEF25-75) in asthmatic children according to dietary intake of vitamin C and the number of putative risk alleles in three antioxidant genes: GSTM1, GSTP1 (rs1695), and NQO1 (rs1800566).


257 asthmatic children from two cohort studies conducted in Mexico City were included. Stratified linear mixed models with random intercepts and random slopes on ozone were used. Potential confounding by ethnicity was assessed. Analyses were conducted under single gene and genotype score approaches.


The change in FEF25-75 per interquartile range (60 ppb) of ozone in persistent asthmatic children with low vitamin C intake and GSTM1 null was −91.2 ml/s (p = 0.06). Persistent asthmatic children with 4 to 6 risk alleles and low vitamin C intake showed an average decrement in FEF25-75 of 97.2 ml/s per 60 ppb of ozone (p = 0.03). In contrast in children with 1 to 3 risk alleles, acute effects of ozone on FEF25-75 did not differ by vitamin C intake.


Our results provide further evidence that asthmatic children predicted to have compromised antioxidant defense by virtue of genetic susceptibility combined with deficient antioxidant intake may be at increased risk of adverse effects of ozone on pulmonary function.

Air pollution; Asthmatic children; Antioxidant genes; Mexico City; Vitamin C