Mapping environmental injustices: pitfalls and potential of geographic information systems in assessing environmental health and equity.

Geographic Information Systems (GIS) have been used increasingly to map instances of environmental injustice, the disproportionate exposure of certain populations to environmental hazards. Some of the technical and analytic difficulties of mapping environmental injustice are outlined in this article, along with suggestions for using GIS to better assess and predict environmental health and equity. I examine 13 GIS-based environmental equity studies conducted within the past decade and use a study of noxious land use locations in the Bronx, New York, to illustrate and evaluate the differences in two common methods of determining exposure extent and the characteristics of proximate populations. Unresolved issues in mapping environmental equity and health include lack of comprehensive hazards databases; the inadequacy of current exposure indices; the need to develop realistic methodologies for determining the geographic extent of exposure and the characteristics of the affected populations; and the paucity and insufficiency of health assessment data. GIS have great potential to help us understand the spatial relationship between pollution and health. Refinements in exposure indices; the use of dispersion modeling and advanced proximity analysis; the application of neighborhood-scale analysis; and the consideration of other factors such as zoning and planning policies will enable more conclusive findings. The environmental equity studies reviewed in this article found a disproportionate environmental burden based on race and/or income. It is critical now to demonstrate correspondence between environmental burdens and adverse health impacts--to show the disproportionate effects of pollution rather than just the disproportionate distribution of pollution sources

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation