Metals in Particulate Pollutants Affect Peak Expiratory Flow of Schoolchildren

Overview

Journal Environ Health Perspect

Date 2007 Apr 14

PMID 17431494

Citations 20

Authors

Yun-Chul Hong

Seung-Sik Hwang

Jin Hee Kim

Kyoung-Ho Lee

Hyun-Jung Lee

Kwan-Hee Lee

Seung-Do Yu

Dae-Seon Kim

Affiliations

Soon will be listed here.

Abstract

Background: The contribution of the metal components of particulate pollutants to acute respiratory effects has not been adequately evaluated. Moreover, little is known about the effects of genetic polymorphisms of xenobiotic metabolism on pulmonary function.

Objectives: This study was conducted to assess lung function decrement associated with metal components in particulate pollutants and genetic polymorphisms of glutathione S-transferase M1 and T1.

Methods: We studied 43 schoolchildren who were in the 3rd to 6th grades. Each student measured peak expiratory flow rate three times a day for 42 days. Particulate air concentrations were monitored every day, and the concentrations of iron, manganese, lead, zinc, and aluminum in the particles were measured. Glutathione S-transferase M1 and T1 genetic polymorphisms were determined using DNA extracted from participant buccal washings. We used a mixed linear regression model to estimate the association between peak expiratory flow rate and particulate air pollutants.

Results: We found significant reduction in the peak expiratory flow rate after the children's exposure to particulate pollutants. The effect was shown most significantly 1 day after exposure to the ambient particles. Manganese and lead in the particles also reduced the peak expiratory flow rate. Genetic polymorphisms of glutathione S-transferase M1 and T1 did not significantly affect peak expiratory flow rate.

Conclusions: This study demonstrated that particulate pollutants and metals such as manganese and lead in the particles are associated with a decrement of peak expiratory flow rate. These effects were robust even with consideration of genetic polymorphisms of glutathione S-transferase.

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