Diego J Lopez1, Caroline J Lodge1, Dinh S Bui1, Nilakshi T Waidyatillake1, John C Su2,3, Jenny L Perret1, Luke D Knibbs4, Bircan Erbas5, Paul S Thomas6, Garun S Hamilton7,8, Bruce R Thompson9, Michael J Abramson10, E Haydn Walters1,11, Shyamali C Dharmage1, Gayan Bowatte1, Adrian J Lowe1. 1. Allergy and Lung Health Unit, The University of Melbourne, Melbourne, Vic, Australia. 2. Department of Dermatology, Eastern Health and the Population allergy group, Monash University, Clayton, Vic, Australia. 3. Murdoch Children's Research Institute, University of Melbourne, Melbourne, Vic, Australia. 4. Faculty of Medicine, School of Public Health, The University of Queensland, Herston, Qld, Australia. 5. School of Psychology and Public Health, La Trobe University, Melbourne, Vic, Australia. 6. Prince of Wales' Clinical School, and Mechanisms of Disease and Translational Research, Faculty of Medicine, UNSW and Prince of Wales' Hospital, Sydney, NSW, Australia. 7. Department of Lung and Sleep Medicine, Monash Health, Melbourne, Vic, Australia. 8. School of Clinical Sciences, Monash University, Melbourne, Vic, Australia. 9. School of Heath Sciences, Swinburne University of Technology, Melbourne, Vic, Australia. 10. School of Public Health & Preventive Medicine, Monash University, Melbourne, Vic, Australia. 11. Medicine, University of Tasmania, Hobart, TAS, Australia.
Abstract
BACKGROUND: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. METHODS: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2 ], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5 ]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years), and persistence were assessed from surveys, while IgE sensitization was assessed using skin prick tests. The presence or absence of eczema and sensitization was classified into four groups: no atopy or eczema, atopy alone, non-atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. RESULTS: Of 3153 participants in both follow-ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baselineNO2 was associated with increased odds of prevalent eczema (OR = 1.15 [95% CI 0.98-1.36]) and prevalent atopic eczema (OR = 1.26 [1.00-1.59]). These associations were not seen in females (p for interaction = 0.08, <0.01). For both sexes, a 1.6 µg/m3 increase in PM2.5 exposure at follow-up was associated with increased odds of aeroallergen sensitization (OR = 1.15 [1.03-1.30]). CONCLUSION: Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders.
BACKGROUND: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. METHODS: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2 ], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5 ]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years), and persistence were assessed from surveys, while IgE sensitization was assessed using skin prick tests. The presence or absence of eczema and sensitization was classified into four groups: no atopy or eczema, atopy alone, non-atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. RESULTS: Of 3153 participants in both follow-ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baselineNO2 was associated with increased odds of prevalent eczema (OR = 1.15 [95% CI 0.98-1.36]) and prevalent atopic eczema (OR = 1.26 [1.00-1.59]). These associations were not seen in females (p for interaction = 0.08, <0.01). For both sexes, a 1.6 µg/m3 increase in PM2.5 exposure at follow-up was associated with increased odds of aeroallergen sensitization (OR = 1.15 [1.03-1.30]). CONCLUSION: Increased exposure to residential ambient air pollutants was associated with an increased odds of eczema, only in males, and aeroallergen sensitization in both genders.