title: GSTM1 and GSTP1 and respiratory health in asthmatic children exposed to ozone.
abstract: Acute exposure to ozone has been related to a wide spectrum of health effects in susceptible individuals. Genetic factors may influence interindividual variation in ozone response. The current authors investigated the relationships between common polymorphisms in two genes involved in response to oxidative stress, i.e. glutathione S-transferases M1 (GSTM1) and P1 (GSTP1), and both respiratory symptoms and lung function in response to ozone among childhood asthmatics. A total of 151 asthmatic children, who were participants in a randomised controlled trial of antioxidant vitamin supplementation in Mexico City, were studied. Children were genotyped using PCR methods and followed from October 1998-April 2000. Increases in reported breathing difficulty were associated with ozone exposure in children with GSTM1 null (8%, 95% confidence interval (CI) 1-15%, per 20-ppb increase in 1-h maximum daily average over 7 days) or GSTP1 Valine/Valine (Val/Val) genotypes (14%, 95% CI 5-25%). In children with both GSTM1 null and GSTP1 Val/Val genotypes, the increase in breathing difficulty associated with a 20-ppb increase in ozone exposure was even greater (21%, 95% CI 5-39%). GSTP1 genotypes were not significantly associated with ozone-related lung function changes. In conclusion, asthmatic children with glutathione S-transferase M1 null and glutathione S-transferase P1 Valine/Valine genotypes appear more susceptible to developing respiratory symptoms related to ozone exposure.
authors.affiliation: Instituto Nacional de Salud Publica, 655 Avenida Universidad, Col. Santa Maria Ahuacatitlán, 62508 Cuernavaca, Morelos, México. iromieu@correo.insp.mx
authors.forename: I
authors.initials: I
authors.lastname: Romieu
authors.forename: M
authors.initials: M
authors.lastname: Ramirez-Aguilar
authors.forename: J J
authors.initials: JJ
authors.lastname: Sienra-Monge
authors.forename: H
authors.initials: H
authors.lastname: Moreno-Macías
authors.forename: B E
authors.initials: BE
authors.lastname: del Rio-Navarro
authors.forename: G
authors.initials: G
authors.lastname: David
authors.forename: J
authors.initials: J
authors.lastname: Marzec
authors.forename: M
authors.initials: M
authors.lastname: Hernández-Avila
authors.forename: S
authors.initials: S
authors.lastname: London
mesh_terms: D000397:Air Pollution / Q000009:adverse effects* / Q000032:analysis; D001249:Asthma / Q000235:genetics*; D002648:Child; D004781:Environmental Exposure; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D051549:Glutathione S-Transferase pi / Q000235:genetics* / Q000502:physiology; D005982:Glutathione Transferase / Q000235:genetics / Q000502:physiology; D006801:Humans; D008297:Male; D010126:Ozone / Q000009:adverse effects* / Q000032:analysis; D011110:Polymorphism, Genetic / Q000235:genetics* / Q000502:physiology; D012120:Respiration Disorders / Q000139:chemically induced; D012720:Severity of Illness Index
chemical_list: D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D010126:Ozone; C496556:GSTP1 protein, human