Our objective was to characterize the differential relationships between exposure to ambient PM2.5
and its specific components, including metals and EC, and respiratory symptoms in a cohort of very young children living in high-density NYC neighborhoods. We found that Ni and V were associated significantly with wheeze in this cohort during the first 24 months of life after adjusting for sex, ethnicity, ETS, seasonal trends, and copollutants. EC was associated significantly with cough only during the cold/flu season. This study provides new evidence using an individual-level longitudinal study design that specific components of PM2.5
related to residual oil combustion and/or traffic are associated with adverse respiratory health effects in children during the first 2 years of life. PM2.5
, a heterogeneous mix of particles of various chemical constituents from multiple sources, was not associated significantly with wheeze or cough. This latter result suggests that mass-based standards for total PM2.5
may not adequately protect against adverse health effects from exposures to the individual toxic metals and EC components, which are believed to represent approximately only 4 and 3% of the mass, respectively (28
Children participating in this study reside in NYC communities that have very high pediatric asthma prevalence and hospitalization rates (20
) and that contain major trucking thoroughfares, bus depots, and waste transfer stations that emit multiple air pollutants (29
). Traffic emissions, particularly from diesel vehicles, are a dominant source of EC in the atmosphere. Traffic also contributes to ambient metals from direct tailpipe emissions, brake and tire abrasion, and resuspension of roadway dust (9
). Residual oil fuel, which is the major source of ambient Ni and V in NYC, continues to be used for space heating in older residential and commercial buildings that are common in the study area (11
). Concentrations of EC, Ni, V, and Zn are higher at the Bronx monitoring sites in our study area, compared with an average of 87 counties in the United States (7
), and Ni concentrations at the Bronx sites are higher than those at other NYC monitoring sites (11
). These results suggest that metals and EC from heating oil combustion and diesel traffic may be important ambient pollutants that contribute to asthma-related symptoms in these communities.
The largest effect size and most consistent associations were observed between Ni and wheeze. The effects of Ni on wheeze were robust to the inclusion of indicators of traffic emissions such as EC and NO2
. Although NO2
was significantly associated with wheeze in a single-pollutant model, associations became nonsignificant when Ni and EC were included in the model. Therefore, residual oil combustion, an important nontraffic source of ambient Ni in the study area, could be responsible for many asthma-related symptoms among young residents of these communities. Recent studies support a role for Ni in increasing risk of asthma-related outcomes. In a national-scale study, county- and season-specific PM2.5
risk estimates for respiratory and cardiovascular admissions were higher in counties and seasons with a PM2.5
–Ni fraction in the 75th compared with the 25th percentile (5
). Additionally, in reanalyses of the National Mortality and Morbidity Air Pollution Study data, PM10
mortality risk estimates were higher for communities with higher long-term averages of ambient Ni and V (4
), and this effect modification was driven by strong associations observed in NYC (4
). Although these previous studies included adult populations, their findings support the premise that Ni and V may be important airborne pollutants that contribute to adverse respiratory health effects in NYC.
In analyses stratified by the cold/flu season, larger effect estimates for Ni and V on wheeze and significant effects of EC on cough were observed in models containing observations from only the cold/flu season (September 1 to March 31) (). Concentrations of metals and EC are higher in the winter due to emissions from heating sources such as roof-top furnaces and due to lower mixing height in the atmosphere, resulting in diminished dispersion of emitted pollutants (7
). Respiratory symptoms and asthma exacerbations show peaks in the fall and winter and are related to viral infections (30
). In models that excluded the highest 5% of pollutant concentrations, V and EC were no longer associated with wheeze and cough, respectively, suggesting that extreme concentrations occurring primarily during winter may be highly influential in terms of their effects on respiratory symptoms. Nickel remained significantly associated with wheeze after removing the highest 5% measurements. In a study of human airway cells, coexposure to human rhinovirus and nitrogen dioxide (NO2
) or ozone stimulated greater production of the proinflammatory cytokine IL-8 than did exposure to rhinovirus or either pollutant alone (31
). Therefore, significant associations between Ni and V and wheeze and EC and cough during the cold/flu season may occur as a consequence of synergistic effects on airway inflammation induced by exposures to viral infections and airborne Ni. NO2
was significantly associated with wheeze during the noncold/flu season after adjusting for Ni and EC. NO2
concentrations did not display strong seasonal variation (Table E5). Hence, the effects of NO2
on wheeze may have been masked by the larger effects of Ni and/or viral infections exposures during the cold/flu season and became apparent in the absence of exposures to high Ni concentrations and/or viral infections during the noncold/flu season. Unexpected significant negative associations were observed between PM2.5
and wheeze and between Zn and cough that were driven by effects in the cold/flu season. Because these apparent protective effects were observed only in multipollutant models, they are likely explained by the inclusion of copollutants, such as Ni and Fe, that were found to have strong positive effects on symptoms and by higher correlations between pollutants observed in the cold/flu season.
Ambient levels of Ni, V, or EC may serve as surrogates of pollutant mixtures or other individual components from residual oil combustion and/or traffic that are causally associated with respiratory symptoms. Many PM2.5
species evaluated in our models displayed high correlation between sites (Tables E1 and E4) and were highly correlated with other trace elements within sites (Tables E2 and E3), making it difficult to distinguish among the effects of pollutants from common sources. For example, due to the high correlation among Ni and V, we did not include them in the same model to evaluate as potential confounders. Copper (Cu) and iron (Fe) were moderately correlated with Ni, V, and Zn and have been associated with increased mortality (32
) and stimulation of airway inflammation (34
) in the literature. In the current study, however, neither Cu nor Fe was associated with wheeze or cough in single-pollutant models (data not shown), and neither altered the observed associations between Ni or V and wheeze. EC and NO2
, both indicators of traffic tailpipe emissions, were moderately correlated at NYBG but not significantly correlated at IS52. EC was significantly associated with cough during the cold/flu season after adjusting for NO2
and Ni, and NO2
was significantly associated with wheeze during the noncold/flu season after adjusting for Ni and EC. Thus, although traffic emissions appear to contribute to respiratory morbidity, it is difficult to distinguish between the effects of particulate and gaseous pollutants.
We acknowledge several limitations to this study. The study population was comprised of only Dominican and African American children living in Northern Manhattan and the South Bronx, and populations that differ in ethnic composition may differ with respect to the relative strength of association between particular outcomes and exposures. Furthermore, this cohort may differ from the overall population in several other factors, including asthma prevalence, the distribution of traffic- and oil combustion-related pollutants, genetic polymorphisms, and cultural differences that may influence symptom reporting and behaviors relevant to the dose of environmental exposures.
To characterize associations between EC, metals, and PM2.5
and respiratory symptoms, exposures were assigned using data from two monitoring sites located in the study area: IS52 and NYBG. Previously, personal exposures of NYC adolescents to PM2.5
–associated Ni, Zn, and BC were observed to display the greatest spatial variability, whereas exposures to V showed the least spatial variability (35
). In the current study, significant differences were observed in mean concentrations of Ni and EC between sites, and EC was weakly correlated between sites. Small-scale differences in EC, occurring mostly in the winter and spring periods, have been attributed to local stack emissions of EC that cause random spikes in ambient concentrations (Dr. Oliver Rattigan, NYSDEC, personal communication). Using data from existing monitoring stations to represent individual exposures to pollutants with high spatial variability may not represent true exposure as accurately as personal or residential measurements. To incorporate spatial heterogeneity in ambient concentrations of PM2.5
components, exposure estimates were assigned to subjects using inverse-distance weighted pollution measurements from the two stationary monitoring sites. In these longitudinal analyses, relationships between pollutants and symptoms were examined within subjects over time, and previous studies have shown that central site measurements of PM2.5
, EC, and metals are correlated temporally with personal exposures within subjects. Thus, in the current analyses, central site measurements may provide reasonable estimates of exposure (36
). Given the significant spatial differences observed in ambient Ni and EC concentrations, exposure misclassification may be higher for these pollutants. However, such measurement error is likely to be random and would tend to underestimate the effects of Ni and EC on respiratory symptoms.
Symptom data covered a 3-month period and were compared with concurrent 3-month averages of metals, EC, and PM2.5
. Much of the previous evidence regarding the effects of particulate matter or its components pertains to acute (daily) exposures to metals or EC in time-series analyses or to long-term exposures (yearly or multiyear) in cohort studies. For example, deficits in lung function growth have been observed in children in association with community-level pollution exposures between 10 and 18 years of age (16
). In a recent population-level time series study of children 0 to 17 years of age living in Baltimore, Maryland, high ambient Zn levels, measured at a central monitoring site, were associated with increases in asthma emergency department visits and hospitalizations on the following day (17
). From its onset, the Columbia Center for Children's Environmental Health chose the 3-month time interval as the shortest duration in which structured, high-quality questionnaires could be administered to hundreds of women as part of the parent cohort design. The intent was to capture recent chronic (i.e., subacute) exposures and related symptoms. For the purpose of this study, our hypothesis testing was based on determining the effects of subacute environmental exposures on respiratory symptoms, in part to ascertain a signal that goes beyond those related to hourly or daily changes in activities. Given the longitudinal design of our study, collecting data about symptoms on shorter lags (e.g., the previous 7 days) may have improved our characterization of the associations between metals and EC exposures and respiratory symptoms. However, our findings provide evidence that subacute (i.e., 3 months) exposures of very young urban children may be associated with increased probability of respiratory symptoms in addition to acute and long-term exposures to metals and BC or EC that are documented in the literature.
In conclusion, the associations between increases in ambient concentrations of Ni, V, and EC (but not total PM2.5
) and increased probability of respiratory symptoms, after adjusting for copollutants, suggest that specific PM2.5
components related to residual oil combustion and/or traffic may be health-relevant PM2.5
fractions associated with increased respiratory morbidity in children through 24 months of age. Although it has been previously demonstrated that exposures to traffic-related air pollution early in life may be important risk factors for later development of asthma (24
), the current results improve our understanding of the potential deleterious consequences of exposure to specific metals for children in inner cities. Given that metal and EC components of ambient PM2.5
are only indirectly regulated as part of the PM2.5
mass-based standard, improved regulatory action directed at specific sources, such as traffic and residential boilers, or at ambient concentrations of individual components, such as EC and metals, may be needed to help protect young children living in urban areas.