Original articleAssociations between Multiple Environmental Exposures and Glutathione S-transferase P1 on Persistent Wheezing in a Birth Cohort
Section snippets
Study Participants
The CCAAPS study is a longitudinal birth cohort of high-risk children having at least 1 atopic parent. A complete description of the study's recruitment, methods, and objectives has been published.17 Briefly, infants with at least 1 atopic parent (on the basis of allergy skin prick testing) were enrolled between 2001 and 2003 in a 7-county area of Cincinnati, Ohio. Families were recruited on the basis of the proximity of their home residence to truck and bus traffic by geocoding residential
Subjects, Exposures, and Health Outcomes
Of the 570 study participants, 464 (81.4%) infants were Caucasian, and 106 (18.6%) were non-Caucasian (Table I). Of the non-Caucasian infants, 86.8% were African Americans defined as both parents being African American. Non-Caucasian infants were significantly more likely than Caucasians to have a household income less than $40 000 (69.5% vs 26.7%; P < .001), have higher exposure to DEP ≥0.50 μg/m3 (P < .001), and have visible mold in their homes (P = .01). ETS exposure did not significantly
Discussion
To our knowledge, this study is the first to investigate the impact of complex environmental exposures (DEP, ETS, and mold) along with genetics, specifically GST-P1 on persistent wheezing in children. Our data support that DEP, ETS, or mold exposure are risk factors for wheezing by 24 months of age. Furthermore, the presence of the Val105 allele, which has been shown to significantly lower GST enzyme activity,16 confers susceptibility to these environmental exposures compared with the Ile105
References (32)
- et al.
Biology of diesel exhaust effects on respiratory function
J Allergy Clin Immunol
(2005) - et al.
The development of glutathione S-transferase and glutathione peroxidase activities in human lung
Biochim Biophys Acta
(1986) - et al.
Primary and secondary structural analyses of glutathione S-transferase pi from human placenta
Arch Biochem Biophys
(1990) - et al.
High prevalence of aeroallergen sensitization among infants of atopic parents
J Pediatr
(2006) - et al.
Spatial and temporal variations of PM2.5 concentration and composition throughout an urban area with high freeway density-the Greater Cincinnati study
Atmospheric Environment
(2004) - et al.
Mold damage in homes and wheezing in infants
Ann Allergy Asthma Immunol
(2006) Environmental factors influencing the development and progression of pediatric asthma
J Allergy Clin Immunol
(2002)- et al.
Inflammatory responses in mice after intratracheal instillation of spores of Streptomyces californicus isolated from indoor air of a moldy building
Toxicol Appl Pharmacol
(2001) Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAACThe International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee
Lancet
(1998)- et al.
A comparison of proximity and land use regression traffic exposure models and wheezing in infants
Environ Health Perspect
(2007)
Environmental risk factors of rhinitis in early infancy
Pediatr Allergy Immunol
A study of reactive oxygen species in mainstream of cigarette
Indoor Air
House dust (1-3)-beta-D-glucan and wheezing in infants
Allergy
Effects of glutathione-S-transferase M1, T1, and P1 on childhood lung function growth
Am J Respir Crit Care Med
Polymorphism at the glutathione S-transferase GSTP1 locusA new marker for bronchial hyperresponsiveness and asthma
Am J Respir Crit Care Med
Cited by (58)
Multiple chemical sensitivity: It's time to catch up to the science
2023, Neuroscience and Biobehavioral ReviewsHousehold mold, pesticide use, and childhood asthma: A nationwide study in the U.S.
2021, International Journal of Hygiene and Environmental HealthCitation Excerpt :However, these data were predominantly Caucasian based among restricted age groups (mostly 6–17 years or with no data on specific age groups). On the other hand, longitudinal cohort studies in the U.S. have linked both qualitative and quantitative measures of household mold and its components to asthma or other atopic disease among children mostly in infancy (Behbod et al., 2015; Belanger et al., 2003; Gent et al., 2002; McConnell et al., 2002; Reponen et al., 2011; Rosenbaum et al., 2010; Schroer et al., 2009). These data were also restricted to certain racial/ethnic groups at city or state levels and suffered from varied degrees of residual confounding due to limited data on covariates.
Antioxidant genes and susceptibility to air pollution for respiratory and cardiovascular health
2020, Free Radical Biology and MedicineInteraction of Glutathione S-Transferase M1, T1, and P1 Genes With Early Life Tobacco Smoke Exposure on Lung Function in Adolescents
2019, ChestCitation Excerpt :Studies examining the GSTP1 105 variant reported that associations vary depending on the specific risk alleles of GSTP1.28-30 Similar to our findings, some research exploring second-hand smoke has found no evidence of GSTP1 interaction on asthma outcomes,31-33 but studies investigating lung function were limited. We found no evidence of interaction for GSTP1 genes with early life smoking and lung function impairment or asthma (interaction P > .10) One explanation may be because of the small numbers limiting our power to find associations.
Traffic-related air pollution exposure is associated with allergic sensitization, asthma, and poor lung function in middle age
2017, Journal of Allergy and Clinical ImmunologyCitation Excerpt :GSTT1, GSTM1, and GSTP1 act through a common mechanism involved in managing oxidative stress, where conjugating ROS with glutathione enables detoxification and ultimately protects tissues against oxidative damage.32 Past literature has shown effect modification by GSTs of the effect of TRAP exposure on allergic disease outcomes.33,34 However, very few studies have investigated the effect modification by GSTs on the association between TRAP exposure and allergic sensitization.35,36
Natural History of Allergic Diseases and Asthma
2016, Pediatric Allergy: Principles and Practice: Third Edition
Supported by NIEHS R01 ES11170 and ES10957. The authors declare no conflicts of interest.