EOHSI

Ironbound Section of Newark, New Jersey

Individuals are exposed to a multitude of environmental factors that, together with genetic inheritance, determine risk of disease. These factors include not only environmental chemical, physical, and biological agents, but also psychosocial stressors that are associated with poverty, race, ethnicity, and other social conditions. Some combination of these factors appears to determine risk for many complex, environment-mediated diseases, such as asthma. Moreover, these risk factors often converge in overly-burdened communities with evident health disparities, including higher rates and severity of asthma. Supported by a new 4-yr, $1.25 million USEPA STAR grant, a team of CEED investigators is working with community members to better understand how chronic psychosocial stress modifies responses to traffic air pollutants among children with asthma in the Ironbound neighborhood of Newark, NJ. CEED investigators Rob Laumbach, Nancy Fiedler, Tina Fan, Howard Kipen, Kathie Kelly-McNeil, and Pam Ohman-Strickland, are working in partnership with members of the Ironbound Community Corporation (ICC), led by Ana Baptista, Co-Investigator.

The project was developed in partnership with the ICC, the largest provider of social services in this diverse, lower-income neighborhood that struggles with a legacy of environmental contamination. Having gotten its name from the railroad tracks that bordered the neighborhood, today the Ironbound neighborhood is bounded by the Port of Newark and Elizabeth, the busiest seaport on the east coast, Liberty Airport, and Routes 1&9, 278, and the NJ Turnpike. Residents are concerned about possible links between the high rates of asthma in the community and the diesel exhaust emitted by trucks servicing the seaport and local industry.

The research project is focused on elucidating the biological modes of action by which chronic stress may interact with traffic pollutants to worsen asthma. Chronic psychosocial stress has detrimental effects on asthma, but the underlying pathophysiology is not clear. On the other hand, acute stressors cause physiologic responses that include dilatation of the airways in preparation for “fight-or-flight.” These responses should help to protect the child during the extreme, acute stress of not being able to breath during an asthma attack. In fact, drugs that mimic the pharmacologic actions of the two main acute stress hormones, norepinephrine and cortisol, are the mainstays of treatment for acute asthma exacerbations. The investigators hypothesize that chronic stress alters the normally protective acute stress response among children with asthma, making them more vulnerable to acute asthma attacks from triggers such as traffic pollutants.

With assistance from the ICC, the investigators will recruit 40 children, aged 9-14, with mild-to-moderate asthma. The team will measure each child’s chronic stress using a validated interview, and acute responses to a laboratory stressor. They will measure personal exposures to black carbon, a marker for diesel exhaust, using small, lightweight monitors that the children will wear for several weeks. These real-time monitors will capture peaks of exposure to diesel exhaust while the children are outdoors. Daily, at-home measurements include symptoms, lung function and levels of nitric oxide in exhaled breath, a marker for airway inflammation. These data will be combined to evaluate how chronic stress modifies associations between worsening asthma and levels of traffic pollutants. The results will inform the assessment of cumulative risk from multiple environmental stressors.

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