Exposure to phthalates aggravates pulmonary function and airway inflammation in asthmatic children.

Abstract

Studies on the associations between phthalate exposures and respiratory outcomes are limited. We investigated the association of phthalates exposure with pulmonary function and airway inflammation in asthmatic children. Fifty-six children with asthma living in Seoul Metropolitan Area, Korea aged 6-16 years were enrolled. Their pulmonary function including forced expiratory volume in 1 sec (FEV1) and peak expiratory flow rate (PEFR) were measured, and the fractional exhaled nitric oxide (FeNO) as a marker of airway inflammation was examined repeatedly up to four times during the study period. Urinary levels of mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), metabolites for di-(2-ethylhexyl) phthalate (DEHP), and mono-n-butyl phthalate (MnBP), a metabolite of di-n-butyl phthalate (DnBP), were also measured on the same days. The effects of phthalate metabolites on the respiratory symptoms were analyzed using linear mixed effect models with adjustment for potential cofounders. An increase in phthalate metabolites was associated with a decrease in pulmonary function and an increase in FeNO in asthmatic children. As one natural log-unit (ln-unit) levels of urinary MEHHP and MEOHP increased, FeNO levels on the same day increased by 19.47 ppb [95% confidence interval (CI): 9.28, 29.67] and 17.93 ppb (95% CI: 5.86, 30.01), respectively. An increases in the urinary level of MEHHP, MEOHP, and MnBP by one ln-unit was associated with a decrease in PEFR on the next day by 12.17 L/min (95% CI: 2.59, 21.74), 10.80 L/min (95% CI: 0.29, 21.32), and 13.65 L/min (95% CI: 5.07, 22.24), respectively. Phthalates, especially DEHP, may worsen pulmonary function and airway inflammation in asthmatic children. To control asthma symptoms, exposure to phthalates needs to be avoided.