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

• Main Authors: Moreno-Macías Hortensia, Dockery Douglas W, Schwartz Joel, Gold Diane R, Laird Nan M, Sienra-Monge Juan J, Del Río-Navarro Blanca E, Ramírez-Aguilar Matiana, Barraza-Villarreal Albino, Li Huiling, London Stephanie J, Romieu Isabelle
• Format: Article
• Language: English
• Published: BMC 2013-02-01
• Series: Respiratory Research
• Subjects: Air pollution; Asthmatic children; Antioxidant genes; Mexico City; Vitamin C
• Online Access: http://respiratory-research.com/content/14/1/14

<p>Abstract</p> <p>Background</p> <p>We previously reported that asthmatic children with <it>GSTM1</it> 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 (FEF_25-75) in asthmatic children according to dietary intake of vitamin C and the number of putative risk alleles in three antioxidant genes: <it>GSTM1</it>, <it>GSTP1</it> (rs1695), and <it>NQO1</it> (rs1800566).</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>The change in FEF_25-75 per interquartile range (60 ppb) of ozone in persistent asthmatic children with low vitamin C intake and <it>GSTM1</it> 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 FEF_25-75 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 FEF_25-75 did not differ by vitamin C intake.</p> <p>Conclusions</p> <p>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.</p>