Ozone Exposure in Infants
Ozone Exposure in Infants
Objective: Recent studies indicate that the U.S. Environmental Protection Agency (EPA) ozone standards may not protect sensitive individuals. In this study we examined respiratory effects of ozone in infants who may be vulnerable, particularly if they are children of asthmatic mothers.
Design: Women delivering babies at one of five hospitals in southwestern Virginia between 1994 and 1996 were invited to participate in a cohort study ; 780 women enrolled. Ambient air quality data (ozone and particulate matter) were collected at a central monitoring site.
Participants: This analysis is of 691 infants followed for approximately 83 days between 10 June and 31 August 1995 and/or 1996 ; they contributed a total of 52,421 infant-days of follow-up. Mothers were interviewed at enrollment and approximately biweekly to report infants' daily symptoms. Repeated measures logistic regression models were run separately for wheeze, difficulty breathing, and cough. Ozone metrics included 24-hr average, peak 1-hr, and maximum 8-hr average. Analyses were repeated for the 61 infants whose mothers had asthma.
Results: For every interquartile-range increase in same-day 24-hr average ozone, likelihood of wheeze increased 37% [95% confidence interval (CI) , 284%]. Among infants of asthmatic mothers, same-day 24-hr average ozone increased likelihood of wheeze 59% (95% CI, 1154%) and of difficulty breathing 83% (95% CI, 42136%) . Maximum 8-hr ozone and peak 1-hr ozone were associated with difficulty breathing, but not wheeze, in infants of asthmatic mothers. Ozone was not associated with cough.
Conclusions: At levels of ozone exposure near or below current U.S. EPA standards, infants are at increased risk of respiratory symptoms, particularly infants whose mothers have physician-diagnosed asthma.
Ozone is a common summertime pollutant formed by reactions of ambient nitrogen oxides and volatile organic compounds (VOCs) in the presence of sunlight and heat. Animal and human studies have identified specific effects O3 has on the respiratory system, including alterations in airway epithelium (Bromberg et al. 1991; Devalia et al. 1996; Sandstrom et al. 1991; Wagner et al. 2001), airway hyperresponsiveness (Devalia et al. 1996), airway infiltration by inflammatory cells (Chitano et al. 1995), and enhancement of antigen-associated airway inflammation (Depuydt et al. 2002). Because O3 is a relatively insoluble gas, it tends to pass through the upper respiratory tract and penetrate deep into the lung (Mathieu-Nolf 2002).
O3 has consistently been linked to acute respiratory effects and to hospital admissions in human populations living in highly polluted areas (Ostro et al. 1995, 2001; Romieu et al. 1996, 1997; Thurston et al. 1992). U.S. Environmental Protection Agency (EPA) standards based on peak 1-hr O3 concentrations and maximum 8-hr running averages have been established (U.S. EPA 2006), but recent studies indicate that these standards may not protect sensitive individuals (e.g., children with asthma) from acute respiratory responses (Gent et al. 2003; Mortimer et al. 2000; Thurston et al. 1997).
Young children may be particularly sensitive to O3, because significant lung development continues postnatally (Finkelstein and Johnston 2004). Differences in lung anatomy and physiology, ventilation rates, and organ maturity between children and adults may explain children's greater vulnerability to air pollutants (Mathieu-Nolf 2002). Infants, for whom transient wheeze is common (reported in up to 50% of healthy infants), and infants with a genetic predisposition (e.g., maternal asthma) may be even more sensitive to pollutant effects. There has been a dearth of research examining respiratory health effects of O3 in infants who may be at greatest risk of O3's effects. In this study we examined acute respiratory effects of relatively low O3 levels in infants living in nonsmoking households.
Abstract and Introduction
Abstract
Objective: Recent studies indicate that the U.S. Environmental Protection Agency (EPA) ozone standards may not protect sensitive individuals. In this study we examined respiratory effects of ozone in infants who may be vulnerable, particularly if they are children of asthmatic mothers.
Design: Women delivering babies at one of five hospitals in southwestern Virginia between 1994 and 1996 were invited to participate in a cohort study ; 780 women enrolled. Ambient air quality data (ozone and particulate matter) were collected at a central monitoring site.
Participants: This analysis is of 691 infants followed for approximately 83 days between 10 June and 31 August 1995 and/or 1996 ; they contributed a total of 52,421 infant-days of follow-up. Mothers were interviewed at enrollment and approximately biweekly to report infants' daily symptoms. Repeated measures logistic regression models were run separately for wheeze, difficulty breathing, and cough. Ozone metrics included 24-hr average, peak 1-hr, and maximum 8-hr average. Analyses were repeated for the 61 infants whose mothers had asthma.
Results: For every interquartile-range increase in same-day 24-hr average ozone, likelihood of wheeze increased 37% [95% confidence interval (CI) , 284%]. Among infants of asthmatic mothers, same-day 24-hr average ozone increased likelihood of wheeze 59% (95% CI, 1154%) and of difficulty breathing 83% (95% CI, 42136%) . Maximum 8-hr ozone and peak 1-hr ozone were associated with difficulty breathing, but not wheeze, in infants of asthmatic mothers. Ozone was not associated with cough.
Conclusions: At levels of ozone exposure near or below current U.S. EPA standards, infants are at increased risk of respiratory symptoms, particularly infants whose mothers have physician-diagnosed asthma.
Introduction
Ozone is a common summertime pollutant formed by reactions of ambient nitrogen oxides and volatile organic compounds (VOCs) in the presence of sunlight and heat. Animal and human studies have identified specific effects O3 has on the respiratory system, including alterations in airway epithelium (Bromberg et al. 1991; Devalia et al. 1996; Sandstrom et al. 1991; Wagner et al. 2001), airway hyperresponsiveness (Devalia et al. 1996), airway infiltration by inflammatory cells (Chitano et al. 1995), and enhancement of antigen-associated airway inflammation (Depuydt et al. 2002). Because O3 is a relatively insoluble gas, it tends to pass through the upper respiratory tract and penetrate deep into the lung (Mathieu-Nolf 2002).
O3 has consistently been linked to acute respiratory effects and to hospital admissions in human populations living in highly polluted areas (Ostro et al. 1995, 2001; Romieu et al. 1996, 1997; Thurston et al. 1992). U.S. Environmental Protection Agency (EPA) standards based on peak 1-hr O3 concentrations and maximum 8-hr running averages have been established (U.S. EPA 2006), but recent studies indicate that these standards may not protect sensitive individuals (e.g., children with asthma) from acute respiratory responses (Gent et al. 2003; Mortimer et al. 2000; Thurston et al. 1997).
Young children may be particularly sensitive to O3, because significant lung development continues postnatally (Finkelstein and Johnston 2004). Differences in lung anatomy and physiology, ventilation rates, and organ maturity between children and adults may explain children's greater vulnerability to air pollutants (Mathieu-Nolf 2002). Infants, for whom transient wheeze is common (reported in up to 50% of healthy infants), and infants with a genetic predisposition (e.g., maternal asthma) may be even more sensitive to pollutant effects. There has been a dearth of research examining respiratory health effects of O3 in infants who may be at greatest risk of O3's effects. In this study we examined acute respiratory effects of relatively low O3 levels in infants living in nonsmoking households.
