Hyunok Choi1, Miroslav Dostal2, Anna Pastorkova2, Pavel Rossner3, Radim J Sram4, Shuk-Mei Ho5. 1. Departments of Environmental Health Sciences, Epidemiology, and Biostatistics, University at Albany School of Public Health One University Place, Rm 153, Rensselaer, NY 12144-3456, USA. Electronic address: hchoi@albany.edu. 2. Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine, Czech Academy of Sciences, Vídeňská 1083, 142 20 Prague 4, Czech Republic. 3. Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine, Czech Academy of Sciences, Vídeňská 1083, 142 20 Prague 4, Czech Republic. Electronic address: prossner@biomed.cas.cz. 4. Department of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine, Czech Academy of Sciences, Vídeňská 1083, 142 20 Prague 4, Czech Republic. Electronic address: sram@biomed.cas.cz. 5. Department of Environmental Health, University of Cincinnati, Cincinnati, OH, USA. Electronic address: hosm@ucmail.uc.edu.
Abstract
BACKGROUND: Sexually dimorphic risk of obesity-associated asthma is posited to accelerate around puberty. Yet, the role of air pollution on the lean and obese asthmatic children has never been examined. OBJECTIVE: To compare whether a unit exposure to airborne benzo[a]pyrene (B[a]P) is associated with altered risks of asthma across the overweight/obese (OV/OB) control, lean asthmatic, and OV/OB asthmatic children, respectively, compared to the lean controls, before and after adjusting for oxidant stress markers (i.e. 15‑F2t‑IsoP, 8‑oxo‑dG, and Carbonyl). METHODS: Asthmatic and healthy control children, recruited from polluted urban and rural areas, were matched to ambient concentration of B[a]P. A unit increase in B[a]P and multinomial logistic regression on OV/OB control, lean asthmatic, and OV/OB asthma were compared across the sex- and age-groups. RESULTS: The median B[a]P was associated with a linear increase among the female children, according to OV/OB and asthma, respectively, and together, compared to the lean control girls (p = 0.001). While B[a]P was associated with positive relationship with 15‑F2t‑IsoP level among the OV/OB boys, the same exposure-outcome association was inverse among the OV/OB girls. One natural log-unit increase in ambient B[a]P was associated with 10.5-times greater odds (95% CI, 2.6-39.6; p = 0.001) the adolescent OV/OB boys, compared to the unit odds among the lean controls. In contrast, the adolescent OV/OB girls were associated with highest adjusted odds of the asthma (aOR = 15.4; 95% CI, 2.9-29.1; p < 0.001) compared to the lean control girls. An adjustment for 15‑F2t‑IsoP, and Carbonyls was associated with greater odds of asthma per unit exposure for the adolescent OV/OB girls (aOR = 16.2; 95% CI, 1.4-181.8; p = 0.024). CONCLUSIONS: B[a]P exposure was associated with a leap in the odds of asthma among the OV/OB adolescents, particularly the girls, after adjusting for 15‑F2t‑IsoP and Carbonyls.
BACKGROUND: Sexually dimorphic risk of obesity-associated asthma is posited to accelerate around puberty. Yet, the role of air pollution on the lean and obese asthmatic children has never been examined. OBJECTIVE: To compare whether a unit exposure to airborne benzo[a]pyrene (B[a]P) is associated with altered risks of asthma across the overweight/obese (OV/OB) control, lean asthmatic, and OV/OB asthmatic children, respectively, compared to the lean controls, before and after adjusting for oxidant stress markers (i.e. 15‑F2t‑IsoP, 8‑oxo‑dG, and Carbonyl). METHODS: Asthmatic and healthy control children, recruited from polluted urban and rural areas, were matched to ambient concentration of B[a]P. A unit increase in B[a]P and multinomial logistic regression on OV/OB control, lean asthmatic, and OV/OB asthma were compared across the sex- and age-groups. RESULTS: The median B[a]P was associated with a linear increase among the female children, according to OV/OB and asthma, respectively, and together, compared to the lean control girls (p = 0.001). While B[a]P was associated with positive relationship with 15‑F2t‑IsoP level among the OV/OBboys, the same exposure-outcome association was inverse among the OV/OBgirls. One natural log-unit increase in ambient B[a]P was associated with 10.5-times greater odds (95% CI, 2.6-39.6; p = 0.001) the adolescent OV/OBboys, compared to the unit odds among the lean controls. In contrast, the adolescent OV/OBgirls were associated with highest adjusted odds of the asthma (aOR = 15.4; 95% CI, 2.9-29.1; p < 0.001) compared to the lean control girls. An adjustment for 15‑F2t‑IsoP, and Carbonyls was associated with greater odds of asthma per unit exposure for the adolescent OV/OBgirls (aOR = 16.2; 95% CI, 1.4-181.8; p = 0.024). CONCLUSIONS: B[a]P exposure was associated with a leap in the odds of asthma among the OV/OB adolescents, particularly the girls, after adjusting for 15‑F2t‑IsoP and Carbonyls.