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Exposure to phthalates aggravates pulmonary function and airway inflammation in asthmatic children
Young-Min Kim1,2, Jihyun Kim1,2, Hae-Kwan Cheong3
1Environmental Health Center for Atopic Diseases, Samsung Medical Center, Seoul, Korea.
Insights
Phthalate exposure, particularly di-(2-ethylhexyl) phthalate (DEHP), is linked to reduced lung function and increased airway inflammation in children with asthma. Limiting phthalate exposure may help manage asthma symptoms.
Area of Science:
- Environmental Health
- Pediatric Pulmonology
- Toxicology
Background:
- Limited research exists on the association between phthalate exposure and respiratory health in children.
- Asthma prevalence is increasing globally, necessitating investigation into environmental triggers.
Purpose of the Study:
- To investigate the association between phthalate exposure and pulmonary function in asthmatic children.
- To examine the relationship between phthalate metabolites and airway inflammation markers in pediatric asthma.
Main Methods:
- Fifty-six asthmatic children (aged 6-16) in Seoul, Korea, were enrolled.
- Pulmonary function (FEV1, PEFR) and fractional exhaled nitric oxide (FeNO) were measured.
- Urinary phthalate metabolites (MEHHP, MEOHP, MnBP) were quantified and analyzed using linear mixed-effects models.
Main Results:
- Increased urinary levels of MEHHP and MEOHP correlated with higher FeNO, indicating greater airway inflammation.
- Elevated MEHHP, MEOHP, and MnBP levels were associated with decreased PEFR on the following day.
- Phthalate exposure negatively impacts lung function and airway inflammation in asthmatic children.
Conclusions:
- Di-(2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DnBP) metabolites may exacerbate pulmonary issues in pediatric asthma.
- Reducing exposure to phthalates is recommended for better asthma symptom control in children.
Introduction:
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.
Methods:
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.
Results:
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.
Conclusion:
Phthalates, especially DEHP, may worsen pulmonary function and airway inflammation in asthmatic children. To control asthma symptoms, exposure to phthalates needs to be avoided.
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