title: Ozone exposure, vitamin C intake, and genetic susceptibility of asthmatic children in Mexico City: a cohort study.
abstract: BACKGROUND
  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 (FEF(25-75)) 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).
  
  
  METHODS
  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.
  
  
  RESULTS
  The change in FEF(25-75) 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 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 FEF25-75 did not differ by vitamin C intake.
  
  
  CONCLUSIONS
  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.
authors: Universidad Autónoma Metropolitana, Unidad Iztapalapa, Avenida San Rafael Atlixco 186, edificio H-001, Col. Vicentina, 09430, D F, México City, Mexico. hmm@xanum.uam.mx
authors: Hortensia
authors: H
authors: Moreno-Macías
authors: Douglas W
authors: DW
authors: Dockery
authors: Joel
authors: J
authors: Schwartz
authors: Diane R
authors: DR
authors: Gold
authors: Nan M
authors: NM
authors: Laird
authors: Juan J
authors: JJ
authors: Sienra-Monge
authors: Blanca E
authors: BE
authors: Del Río-Navarro
authors: Matiana
authors: M
authors: Ramírez-Aguilar
authors: Albino
authors: A
authors: Barraza-Villarreal
authors: Huiling
authors: H
authors: Li
authors: Stephanie J
authors: SJ
authors: London
authors: Isabelle
authors: I
authors: Romieu
mesh_terms: D000367:Age Factors; D000975:Antioxidants / Q000008:administration & dosage*; D001205:Ascorbic Acid / Q000008:administration & dosage*; D001206:Ascorbic Acid Deficiency / Q000188:drug therapy / Q000453:epidemiology; D001249:Asthma / Q000175:diagnosis / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology / Q000517:prevention & control; D002648:Child; D015331:Cohort Studies; D019587:Dietary Supplements; D004311:Double-Blind Method; D004781:Environmental Exposure / Q000009:adverse effects*; D004798:Enzymes / Q000235:genetics*; D005260:Female; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D051549:Glutathione S-Transferase pi / Q000235:genetics; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D016014:Linear Models; D008168:Lung / Q000503:physiopathology; D008297:Male; D008450:Maximal Midexpiratory Flow Rate; D008800:Mexico / Q000453:epidemiology; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000235:genetics; D010126:Ozone / Q000009:adverse effects*; D010641:Phenotype; D011110:Polymorphism, Genetic; D018570:Risk Assessment; D012307:Risk Factors; D014504:Urban Health
chemical_list: D000975:Antioxidants; D001205:Ascorbic Acid; D004798:Enzymes; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D016660:NAD(P)H Dehydrogenase (Quinone); D010126:Ozone; C447479:NQO1 protein, human; C496556:GSTP1 protein, human
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