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Environmental Health Perspectives Volume 105, Number 6, June 1997

The Relationship between Selected Causes of Postneonatal Infant Mortality and Particulate

Air Pollution in the United States 

Tracey J. Woodruff,1 Jeanne Grillo,2 Kenneth C. Schoendorf2

1U.S. Environmental Protection Agency, Washington, D.C. 20460 USA; 2 National Center

for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, MD 20782 

USA

 Abstract

 Introduction

 Methods

 Results

 Discussion

Abstract

Recent studies have found associations between particulate air pollution and total and adult 

mortality. The relationship between particulate air pollution and mortality among infants has 

not been examined in the United States. This study evaluates the relationship between 

postneonatal infant mortality and particulate matter in the United States. Our study involved 

analysis of cohorts consisting of approximately 4 million infants born between 1989 and 

1991 in states that report relevant covariates; this included 86 metropolitan statistical areas 

(MSAs) in the United States. Data from the National Center for Health Statistics-linked

birth/infant death records were combined at the MSA level with measurements of particulate 

matter 10 m or less (PM10) from the EPA's Aerometric Database. Infants were categorized 

as having high, medium, or low exposures based on tertiles of PM10. Total and causespecific postneonatal mortality rates were examined using logistic regression to control for 

demographic and environmental factors. Overall postneonatal mortality rates were 3.1 

among infants with low PM10 exposures, 3.5 among infants with medium PM10 exposures, 

and 3.7 among highly exposed infants. After adjustment for other covariates, the odds ratio 

(OR) and 95% confidence intervals (CI) for total postneonatal mortality for the high 

exposure versus the low exposure group was 1.10 (1.04, 1.16). In normal birth weight 

infants, high PM10 exposure was associated with respiratory causes [OR = 1.40, (1.05, 

1.85)] and sudden infant death syndrome [OR = 1.26, (1.14, 1.39)]. For low birth weight

babies, high PM10 exposure was associated, but not significantly, with mortality from 

respiratory causes [OR = 1.18, (0.86, 1.61)]. This study suggests that particulate matter is 

associated with risk of postneonatal mortality. Continued attention should be paid to air 

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quality to ensure optimal health of infants in the United States. Key words: air pollution,

infant mortality, particulate air pollution, postneonatal mortality. Environ Health Perspect

105:608-612 (1997)

Address correspondence to T.J. Woodruff, U.S. Environmental Protection 

Agency, 401 M St. SW (2126), Washington, D.C. 20460 USA. 

The authors would like to thank J. Scott Greene and Paul F. Jamason from the 

Center for Climatic Research, University of Delaware, for providing 

temperature data. 

The views expressed in this report are those of the authors, and they do not 

necessarily represent those of the U.S. Environmental Protection Agency. 

Received 8 October 1996; accepted 18 March 1997. 

Introduction

Concerns about the effects of particulate matter air pollution on health date back to the 

historic pollution episodes in London in 1952 when a weather inversion lead to high levels 

of particulate matter air pollution and subsequent increases in mortality and morbidity (1). 

Since then, recent investigations of the relationship between air pollution and mortality in 

the United States have demonstrated an association between particulate air pollution levels 

and mortality at lower air pollution levels. A number of daily time-series studies have 

demonstrated an association between short-term exposure to particulate air pollution and 

mortality (2,3). More recent prospective cohort analyses have also demonstrated an 

association between long-term exposure to particulate air pollution and mortality (4,5). 

However, all the studies conducted in the United States have focused on adults. The original 

investigation in London observed increases in mortality for both adults over 45 years of age 

and children under the age of 1 year (1). Given this result and the number of studies 

showing a positive association between mortality and exposure to particulate air pollution in 

adults in the United States, it is reasonable to hypothesize a similar association might be 

observed in infants in the United States.

This hypothesis is supported by several factors. First, ecological studies in other countries 

have found an association between particulate air pollution and infant mortality (6-8); 

however, it is difficult to apply these results to the United States because particulate matter 

levels in these countries have typically been much higher than in the United States. Second, 

the results of previous studies among adults suggest vulnerable individuals, such as the 

elderly and people with preexisting cardiovascular or respiratory conditions, are more 

susceptible to effects from exposure to particulate air pollution than the rest of the 

population (9). Because of their high mortality rates, infants, particularly those born 

prematurely, may also fall into this group of susceptible individuals. Last, studies have 

found associations between particulate air pollution and respiratory illness in children 

(10,11).

Many studies of adults have examined the association of particulate air pollution with 

overall adult mortality as well as with specific causes of mortality (9,12). However, such an 

inclusive approach may not be appropriate for an analysis of air quality and mortality among 

infants. A majority of infant deaths are unlikely to be influenced by air pollution levels 

because they occur too soon after birth (13) or are due to causes clearly intrinsic to the

infant, such as congenital anomalies (14). To focus only on infant deaths that may plausibly 

be associated with particulate air pollution, we examined the relationship between exposure 

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to particulate air pollution and selected causes of postneonatal mortality in the United States.

Postneonatal death (death of an infant over 27 days of age) is thought to be influenced more 

by the infant's external environment than is mortality earlier in infancy (15). In keeping with 

the previously demonstrated relationship between particulate air pollution and childhood 

respiratory illness (10,11), an association between particulate air pollution and postneonatal 

mortality from respiratory causes can be postulated. Similarly, because several studies have 

suggested that sudden infant death syndrome (SIDS) is associated with exposure to 

environmental tobacco smoke (16,17), a potential association between SIDS and particulate 

air pollution is plausible.

Daily time-series analyses are commonly used to evaluate the relationship between shortterm exposure to particulate air pollution and adult mortality. This method is not appropriate 

for an analysis of postneonatal mortality and pollution because of the small numbers of 

infants who die in a specific location over a short period of time. In adults, cohort analyses 

of specific cities or areas have been used to examine associations between mortality and 

chronic or long-term exposure to particulate matter. While this general approach may be 

feasible for a similar analysis among infants, geographically limited cohort analyses will 

also lack power due to small numbers.

The national-linked birth/infant death records provide a unique database for the examination 

of particulate air pollution and infant mortality. The birth certificate portion of each record 

contains individual level information on parental risk factors for infant mortality, while the 

death certificate portion contains data on the cause and time of death. Thus, potentially 

important confounders can be controlled for in the evaluation of the relationship between

particulate air pollution and infant mortality. The purpose of this study is to examine the 

relationship between chronic exposure to particulate air pollution and postneonatal mortality 

from all causes, from respiratory causes, and from SIDS in the United States.

Methods

In this study, we combined infant mortality data from the National Center for Health 

Statistics (NCHS) with air quality data from the EPA. Information on infant outcome and 

maternal and infant characteristics was obtained from the NCHS-linked birth/infant death 

data files for 1989-1991, the most recent period for which those data were available (18).

Infants born in California, Indiana, Louisiana, Nebraska, New York, Oklahoma, South 

Dakota, and Washington were excluded from the analysis because some of those states did 

not report maternal education and others did not report maternal smoking status on birth 

certificates for the period of interest. Although those states account for 29.5% of births in 

the United States, previous research has demonstrated that infants born in many of those 

states (including California and New York, which contained the majority of excluded births) 

have similar infant mortality characteristics as the nation as a whole (19). Due to federal 

confidentiality constraints, NCHS data files do not contain detailed geographic information

for infants born in counties with populations less than 100,000; therefore, this study was 

limited to infants born in counties with populations of at least 100,000. In addition, only the 

month and year of birth and death are recorded; the exact date of birth or death is not 

available from the NCHS records.

Particulate matter air pollution data were obtained from the EPA's Aerometric Database. 

Monitoring data were obtained for all metropolitan statistical areas (MSAs) that monitored

for particulate matter of 10 m or less (PM10). The infant mortality and PM10 files were 

linked at the MSA level using 1990 Federal Information Processing Standards (FIPS) codes 

common to both files. One hundred and one MSAs from the linked birth/infant death file 

met the geographic and population inclusion criteria previously mentioned, and 86 of those 

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MSAs were included in the EPA database.

PM10 exposure for each infant was based on PM10 levels in the infant's MSA of residence at 

the time of birth. For this study, an infant's exposure was considered to be the mean of the 

PM10 levels for the first 2 months of life. Two months was chosen as the exposure period 

because all infants in the study had PM10 exposure for the month of birth and at least part of 

the next month. The alternative, defining exposure as the average of the PM10 levels over an 

infant's entire lifetime, leads to an overestimate of the influence of PM10 on mortality 

because of declines in PM10 levels in the United States over time. For instance, two infants 

born in the same month in the same MSA will have identical exposures for the first 2 

months of life. If one of the infants should die in his second month and one should survive 

infancy, the survivor will have a lower overall exposure because of the decreasing secular 

trend. Thus, the surviving infant will appear to have a lower exposure, even though the 

infants had identical exposure up to the first infant's death, resulting in an artificially high 

estimate of the association between PM10 and mortality.

For categorical analyses, infants were categorized as having low, medium, or high PM10

exposure depending on whether their 2-month mean exposure was in the bottom one-third, 

middle one-third, or top one-third of the range of exposures. The overall range of infant 

exposures was 11.9-68.8 g/m3. To minimize the influence of outliers, the top and bottom 

1% of exposures were not used in the determination of PM10 exposure category. The

resulting low, medium, and high exposure ranges were <28.0, 28.1-40.0, and >40.1 g/m3.

The outcome of interest in this study, postneonatal mortality, was defined as the death of an 

infant between 1 month and 1 year of age. The postneonatal mortality rate was calculated as 

the number of postneonatal deaths per 1,000 infants who survived the neonatal period (birth 

through 1 month). To focus the analysis on deaths that may plausibly be related to 

particulate matter, our study examined four postneonatal outcomes: 1) all postneonatal 

deaths; 2) normal birth weight (NBW, >=2,500 grams) SIDS deaths; 3) NBW respiratory 

deaths; and 4) low birth weight (LBW, <2,500 grams) respiratory deaths. Respiratory deaths 

are those deaths with a reported underlying cause of death identified by the International 

Classification of Diseases, Revision 9 (ICD-9), codes 460-519. SIDS deaths are those with 

an ICD-9 cause of death of 798.0. Mortality rates by birth weight category were examined 

to test the hypothesis that particulate matter may have a stronger influence among more 

vulnerable populations, specifically among LBW infants. A control disease category of all 

other causes of death was also examined.

Postneonatal mortality rates were calculated within each of the three pollution categories for 

each outcome. Logistic regression was used to adjust for potential confounding variables 

(20,21). These variables were obtained from the birth certificate portion of the NCHS file 

and include maternal education (<12 years, >=12 years), maternal race (black, white, other), 

parental marital status, and maternal smoking during pregnancy (no, yes). Separate models

were run with PM10 levels entered as a categorical variable and as a continuous variable.

Past studies of factors associated with perinatal outcome have shown a differential effect of 

demographic characteristics, such as education, on outcome for black infants and white 

infants (19,22). Accordingly, interaction terms were added to the logistic regression models

to assess potential effect modification. Neither substantial nor significant (all p-values >0.2) 

differential effect by race was observed. Infants with information missing for any of the 

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other variables (e.g., maternal education) were excluded from the analysis. Approximately 

7% of infants were excluded because of missing data.

Climate is also a potential confounder in this analysis because temperature may be related to 

the risk of postneonatal death (SIDS, in particular) and air quality. Monthly temperatures 

throughout the study for each MSA were obtained from the National Center for Climactic 

Research, University of Delaware. For each infant, the average temperature during the first 

2 months of life (analogous to the calculation of PM10 exposure) was entered into the 

logistic models.

The date of birth may also have confounded the relationship between mortality and 

particulate matter in this analysis because both infant mortality and PM10 levels decreased 

during the study period. To control for this possibility, a variable accounting for each 

infant's month and year of birth was entered into the logistic models.

Results

A total of almost 4 million infants residing in 86 MSAs were included in this analysis (Table 

1). Thirty-six percent of all infants were in the low exposure category, 15% had high PM10

exposure, and the remaining 49% of infants were in the middle exposure category. Infants 

with high exposure were the most likely to have low maternal education and unmarried 

parents and to have been exposed to maternal smoking during pregnancy.

Overall postneonatal mortality increased with increasing

PM10 levels, from 3.1 in the low pollution category to 

3.7 in the high category (Table 2). Postneonatal mortality

increased with increasing PM10 exposure for each of the 

birth weight and cause-specific outcomes examined in 

this study. The postneonatal SIDS rate among normal 

birth weight infants with high PM10 exposure was 26% 

higher than among normal birth weight infants with low 

exposure. Normal birth weight infants with high PM10

exposure were 45% more likely to die of respiratory 

causes than normal birth weight infants with low 

exposure. Respiratory mortality among low birth weight 

infants was 35% higher in the high exposure group than 

in the low PM10 exposure group. Conversely, 

postneonatal mortality from all other causes of death did 

not consistently increase with increasing PM10 exposure 

and was only 8% higher among high exposure infants than among low exposure infants. 

Table 1.

Table 2.

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Adjustment for confounding variables weakened the associations between PM10 exposure 

and postneonatal mortality, but substantial differences between the high and low exposure 

groups remained. Table 3 displays the categorical and continuous odds ratios (ORs) for 

mortality by PM10 level after adjustment for maternal education, marital status, maternal 

race, maternal smoking during pregnancy, average temperature exposure, and year and 

month of birth. After adjustment, infants with high levels of PM10 exposure were at 

approximately 10% higher risk of postneonatal death than were infants with low exposure.

Further categorical analysis by cause of death showed a significant relationship between 

PM10 level and SIDS among normal birth weight infants. The adjusted ORs and 95% 

confidence intervals (CI) for infants with medium and high PM10 exposures were 1.09 

(1.01-1.17) and 1.26 (1.14-1.39), respectively. Among normal birth weight infants with high 

PM10 exposure, the adjusted OR for respiratory mortality was 1.40 (1.05-1.85). The 

adjusted ORs for respiratory death among low birth weight infants showed an increased risk 

of approximately 18% for infants with high PM10 exposure compared with infants with low

exposure, although the 95% CI includes 1.0.

The continuous ORs in Table 3 show the relative change in risk of death associated with a 

10 g/m3 increase in PM10 level after adjustment for confounding variables. Overall 

postneonatal mortality increased by 4% for each 10 g/m3 rise in PM10. SIDS among

normal birth weight infants increased by 12% for each 10 g/m3 increase in PM10.

Postneonatal respiratory mortality among normal birth weight infants increased 20% per 

10 g/m3, while postneonatal respiratory mortality among low birth weight infants increased 

by 5%. No association was observed for other causes.

All continuous and categorical models were also run without maternal smoking, 

temperature, and timing of birth. The relationships between PM10 exposure and

postneonatal mortality in those models were virtually identical to the relationships shown in 

Table 3 (data not shown).

Discussion

To our knowledge, this is the first study to concentrate on the relationship between air 

quality and infant mortality in the United States. This analysis demonstrates an association

between PM10 levels and several causes of postneonatal mortality. Specifically, the risk of 

SIDS among normal birth weight infants and respiratory mortality among normal and low 

birth weight infants was higher among infants with high PM10 exposure than among those 

with low exposure, though the adjusted OR for low birth weight respiratory mortality was 

not statistically significant. The risk of postneonatal mortality from any cause was

Table 3.

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approximately 10% higher in infants in the high PM10 category than in those in the low

PM10 category, after adjustment for potential confounders. It appears that the overall 

elevated risk is probably due to the association between PM10 level and SIDS and 

respiratory-related mortality because there was no association with other causes of death.

Previous studies in Taiwan (7) and the Czech Republic (6) have also found an association 

between particulate air pollution and infant mortality. Bobak and Leon (6) used ecological 

analysis to evaluate the relationship between annual infant mortality between 1986 and 1988 

and long-term exposure to several measures of pollution [PM10, SO2, and oxides of nitrogen

(NOx)] in the Czech Republic. They found a consistent positive association between PM10

levels and postneonatal infant mortality, even after adjusting for sociodemographic variables 

and the other pollutants. The associations with the other pollutants were inconsistent.

Knoebel et al. (7) evaluated the relationship between short-term levels of particulate air 

pollution as measured by visibility and SIDS in Taiwan. They found positive significant

associations between SIDS and visibility measured on the day before death and a stronger 

association with 9 days before death after adjusting for a number of covariates. The PM10

levels in the Czech and Taiwan studies (6,7) were much higher than levels in our analysis

[mean of 68.5 in the Czech study (6); values ranged between 36 and 122 g/m3 in the 

Taiwan study (H. Knoebel, personal communication) versus 31 g/m3 in this analysis], yet 

all studies find a consistent, positive association between PM10 levels and postneonatal 

mortality.

While no other study in the United States has examined mortality effects in children, this 

study is consistent with two similarly designed prospective cohort studies of adult mortality 

evaluating the effects of long-term exposure to particulate air pollution: the Harvard Six 

City study (4) and the American Cancer Society study (5). In the Harvard Six City study, 

Dockery et al. (4) analyzed survival of 8,111 adults followed for 14 years in six cities in the 

eastern United States. After adjusting for sociodemographic risk factors, the authors found a 

27% increased risk for mortality between the cities with the highest and lowest levels of 

inhalable particulate matter. Similarly, Pope et al. (5) used 7-year survival data between

1982 and 1988 for over half a million adults in 151 U.S. cities, using the American Cancer 

Society database. After adjusting for sociodemographic risk factors, they found fine particle 

concentrations measured in the beginning of the study, represented by both sulfates and 

particles less than 2.5 m, were associated with a 15% and 17% increase in mortality, 

respectively. Using the results from the logistic model employing a continuous 

representation of PM10, this study estimated a 25% increase in risk of postneonatal death 

between infants exposed to the highest and lowest levels of PM10, after adjustment for

potential confounding factors. This increased risk is similar to the relative risk estimates 

observed in the previous two prospective cohort studies. In addition, the Harvard Six City

study (4) and the American Cancer Society study (5) found higher associations with 

cardiopulmonary related causes, which is similar to this study.

The results of this study are also consistent with the current literature on the mortality and 

morbidity effects associated with particulate matter. In addition to the prospective cohort 

studies, numerous studies have observed associations between mortality and short-term 

exposure to PM10 in adults (2,3,12). Analysis by cause of death finds a stronger relationship 

between PM10 and respiratory-related causes (2,3,12). Also, a number of studies have 

reported positive associations between respiratory-related morbidity and particulate matter

(23-25). In particular, several studies report an association between respiratory effects in 

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children and both short-term and long-term exposure to PM10 (10,11,26).

An intriguing finding of this study is the association between high PM10 levels and SIDS. 

An association between SIDS and environmental tobacco smoke has been demonstrated 

previously, and tobacco smoke contains a substantial proportion of particulate matter (27).

Further exploration is needed to elucidate the observed associations and clarify clues they 

might give as to the etiology and prevention of SIDS.

In this study, the strength of association between PM10 exposure and mortality decreased 

after control for demographic factors and maternal smoking during pregnancy. The logistic 

models used in the analysis were parsimonious, but included the most important variables 

associated with infant mortality that are available from the linked birth/infant death file. 

Similar studies among adults have considered other risk factors such as occupational 

exposures, body mass index, and alcohol consumption. While those specific factors may not 

be relevant to an examination of infant mortality, it is possible that additional characteristics 

of the infant, the parents, or the environment may be confounding the relationships between 

particulate matter and postneonatal mortality observed in this study. It is important to note,

however, that in previous prospective cohort studies, adjustment for additional factors did 

not significantly alter the observed relationships between particulate air pollution and adult 

mortality (4,5).

One difference between particulate matter studies among adults and similar studies among 

children is that the particulate matter levels are more likely to represent a consistent chronic 

exposure among infants than among adults, who are more liable to have moved during their 

lifetime. However, this study has the limitation, as do other epidemiological studies of 

PM10, of only using measured levels to represent ambient concentrations, which do not 

necessarily represent exposure to an individual. A limited number of studies have been 

conducted to assess the relationship between monitored levels of PM10 and personal 

exposures. Studies have found that monitored PM10 levels are highly correlated with levels 

at specific locations (e.g., between a central monitor and one in the backyard of a home) 

within the monitored area (2,28,29). Also, PM10 levels are different, but correlated, between 

indoors and outside (2,28-30). By limiting this study to postneonatal mortality, we hoped to

minimize the influence of mortality among infants who never leave the hospital between 

birth and death and therefore may not have been exposed to the monitored levels of PM10. 

The inclusion of SIDS should further assure a population of infants that is exposed to the 

ambient environment because the diagnosis of SIDS is limited to essentially healthy infants 

who have no medical reason to be confined to the indoors.

There is a high correlation between indoor and outdoor levels of fine particulate matter, 

defined as particles of 2.5 m or less (PM2.5) (28,29). The relationship between PM2.5 and 

adult mortality was examined in both the Harvard Six City study (4) and the American

Cancer Society study (5), both of which found a significant association between mortality 

and chronic exposure to fine particles and sulfates. It is possible that PM10 levels in this 

analysis are a surrogate for fine particles, which includes all particles less than 2.5 m in

size that are components of PM10. There are few PM2.5 and sulfate monitoring data 

available for 1989-1991 so it is not possible to determine if specific components of PM10

account for the associations found in this study.

A number of previous studies have demonstrated a positive association between particulate 

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matter and mortality among adults in the United States. This analysis indicates that

particulate matter may also influence an infant's chance of survival. While further 

examination of this association is needed, the results of this study, combined with results 

from studies examining air pollution and morbidity among children, suggest that continued 

attention must be paid to the nation's air quality to ensure the optimal health of infants and

children in the United States.

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