Air Pollution and Postneonatal Infant Mortality in the United States, 1999-2002

Tracey J. Woodruff; Lyndsey A. Darrow; Jennifer D. Parker

Disclosures

Environ Health Perspect. 2008;116(1):110-115. 

In This Article

Abstract and Introduction

Objective: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States.
Methods: We linked county-specific monitoring data for particles with aerodiameter of ≤ 2.5 µm (PM2.5) and ≤ 10 µm (PM10) , ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS) , and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity) , percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths.
Results: After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI) , 1.06-1.27] for a 10-µg/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09-1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category).
Conclusions: This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.

Several studies have found a relationship between particulate matter (PM) air pollution and infant mortality in countries with relatively high levels of PM air pollution as well as in countries with lower pollution levels, such as Canada and the United States (Bobak and Leon 1999; Ha et al. 2003; Lipfert et al. 2000; Loomis et al. 1999; Ritz et al. 2006; Woodruff et al. 1997, 2006) These studies suggest that PM air pollution is more strongly associated with postneonatal mortality (deaths occurring after 28 days of life) than with neonatal mortality (deaths occurring up to 28 days of life) and that the association with postneonatal mortality appears to be specific to respiratory causes (Bobak and Leon 1999; Ha et al. 2003). However, a number of questions remain about the infant mortality and PM air pollution relationship and the role of other air pollutants as either potential confounders of the relationship or as independent predictors of infant mortality.

Until recently, most studies of air pollution and postneonatal infant mortality have focused on larger particles, either measured as total suspended particles or particles with an aerodiameter of ≤ 10 µm (PM10) (Bobak and Leon 1999; Ha et al. 2003; Lipfert et al. 2000; Ritz et al. 2006; Woodruff et al. 1997). Although monitoring of smaller particles measuring ≤ 2.5 µm (PM2.5) has become more widespread, only one study in California has evaluated PM2.5 in relation to respiratory related infant mortality; results support a positive association (Woodruff et al. 2006). Although many studies in adults suggest that PM2.5 is more strongly associated with respiratory and cardiovascular morbidity and mortality than PM10, other studies have found larger particles to be important for certain outcomes (Brunekreef and Forsberg 2005; Pope and Dockery 2006).

In addition, few studies have evaluated the contribution of other pollutants to infant mortality, either on their own or as confounders of the association between particles and infant mortality. A study in the Czech Republic, examining nitrogen dioxide and sulfur dioxide, did not find either pollutant significantly associated with postneonatal respiratory deaths after including the other study pollutants in the model (Bobak and Leon 1999). In a study of U.S. infants born in 1990, controlling for carbon monoxide in the regression models did not affect the observed relationship between PM and infant mortality (Lipfert et al. 2000). Another study in Southern California has found some suggestion of an independent effect of CO on respiratory postneonatal infant mortality and an association between NO2 and sudden infant death syndrome (SIDS) (Ritz et al. 2006).

Finally, although relatively consistent results have been found for PM and respiratory postneonatal infant mortality, varying results have been found for the association between PM and SIDS. PM10 had been found in earlier studies to be associated with SIDS in the United States (Lipfert et al. 2000; Woodruff et al. 1997). However, a study in Canada found that short-term increases in NO2 and SO2, but not PM2.5, were associated with SIDS between 1984 and 1999 (Dales et al. 2004). Similarly, a recent analysis of births in California during 1999-2000 did not find a relationship between PM2.5 and SIDS (Woodruff et al. 2006).

Given the uncertainty in findings for different particle size (coarse vs. fine), the varied findings for studies with multiple pollutants, and the variability in the results for SIDS, further evaluation is warranted. In this study, we addressed these issues and evaluated the role of chronic exposure to gaseous air pollutants (CO, SO2, and ozone) and different particle size (both PM2.5 and PM10) in a more contemporary national data set. We used linked infant birth-death records for infants born in the United States between 1999 and 2002 to examine the relationships between these air pollutants and postneonatal respiratory and SIDS infant mortality.

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