Peak Expiratory Flow Rate

BackgroundThe 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.ObjectivesThis 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.MethodsWe 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.ResultsWe 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.ConclusionsThis 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.

IntroductionStudies 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.MethodsFifty-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.ResultsAn 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.ConclusionPhthalates, especially DEHP, may worsen pulmonary function and airway inflammation in asthmatic children. To control asthma symptoms, exposure to phthalates needs to be avoided.

The extent to which occupational exposure to ozone in ambient air can affect lung function remains unclear. We conducted a panel study in 43 mail carriers by measuring their peak expiratory flow rates (PEFRs) twice daily for 6 weeks in 2001. The daily exposure of each mail carrier to O3, particulate matter < 10 microm in aerodynamic diameter (PM10), and nitrogen dioxide was estimated by one air monitoring station in the center of the mail carrier's delivery area. Hourly concentrations of air pollutants during their exposure periods were 6-96 ppb for O3, 11-249 microg/m3 for PM10, and 14-92 ppb for NO2. Linear mixed-effects models were used to estimate the association between air pollution exposures and PEFR after adjusting for subject's sex, age, and disease status and for temperature and humidity. We found that night PEFR and the deviation in night PEFR were significantly decreased in association with 8-hr O3 exposures with a lag 0-2 days and by daily maximum O3 exposures with a lag of 0-1 day in our multipollutant models. By contrast, neither PM10 nor NO2 was associated with a PEFR reduction. Daily 8-hr mean concentrations of O3 had greater reduction effects on PEFR than did daily maximum concentrations. For a 10-ppb increase in the 8-hr average O3 concentration, the night PEFR was decreased by 0.54% for a 0-day lag, 0.69% for a 1-day lag, and 0.52% for a 2-day lag. We found that an acute lung function reduction occurs in mail carriers exposed to O3 concentrations below current ambient air quality standards and occupational exposure limits.

BackgroundRespiratory assessments frequently utilize Peak Expiratory Flow Rate (PEFR) as a fundamental measure of lung function. However, standard reference ranges may not accurately represent variations across different demographic groups. This study aims to address this gap by examining the variability of PEFR among healthy Pakistani adults.MethodsThis cross-sectional study was conducted over a six-month period at a tertiary care hospital in Wah Cantt, Pakistan, involving 400 consenting participants. A consecutive sampling technique was employed. Anthropometric measurements, including height and weight, were obtained using a stadiometer and calibrated weighing scale, respectively. Each participant performed three PEFR maneuvers using a peak flow meter, and the highest value was recorded. Additional data, including age and gender, were collected using a structured proforma. Data was analyzed using SPSS.ResultsPEFR showed a strong positive correlation with height (0.616 in males 0.767 in females) and a negative correlation with age (-0.418 in males and -0.115 in females). Male participants exhibited significantly higher PEFR values compared to females.ConclusionThe findings indicate that PEFR is influenced by gender, height, and age. Specifically, males tend to have higher PEFR values; PEFR increases with greater height and decreases with advancing age. These results underscore the importance of considering demographic-specific factors when interpreting PEFR values and support the development of localized reference standards for clinical use.