Socioeconomic and racial disparities in cancer risk from air toxics in Maryland

We linked risk estimates from the U.S. Environmental Protection Agency's National Air Toxics Assessment (NATA) to racial and socioeconomic characteristics of census tracts in Maryland (2000 Census) to evaluate disparities in estimated cancer risk from exposure to air toxics by emission source category. In Maryland, the average estimated cancer risk across census tracts was highest from on-road sources (50% of total risk from nonbackground sources), followed by nonroad (25%), area (23%), and major sources (< 1%). Census tracts in the highest quartile defined by the fraction of African-American residents were three times more likely to be high risk (> 90th percentile of risk) than those in the lowest quartile (95% confidence interval, 2.0-5.0). Conversely, risk decreased as the proportion of whites increased (p < 0.001). Census tracts in the lowest quartile of socioeconomic position, as measured by various indicators, were 10-100 times more likely to be high risk than those in the highest quartile. We observed substantial risk disparities for on-road, area, and nonroad sources by socioeconomic measure and on-road and area sources by race. There was considerably less evidence of risk disparities from major source emissions. We found a statistically significant interaction between race and income, suggesting a stronger relationship between race and risk at lower incomes. This research demonstrates the utility of NATA for assessing regional environmental justice, identifies an environmental justice concern in Maryland, and suggests that on-road sources may be appropriate targets for policies intended to reduce the disproportionate environmental health burden among economically disadvantaged and minority populations.     

Assessing exposure to air toxics relative to asthma

Asthma is a respiratory disease whose prevalence has been increasing since the mid 1970s and that affects more than 14.6 million residents of the United States. Environmental triggers of asthma include air pollutants that are respiratory irritants. Air toxics emitted into the ambient air are listed in the 1990 Clean Air Act Amendments as hazardous air pollutants (HAPs) if they can adversely affect human health, including the respiratory tract. HAPs include particulate and gaseous-phase pollutants, individual organic compounds and metals, and mixtures. Associations between asthma exacerbation and both particles and indoor volatile organic compounds (VOCs), often referred to as indoor air quality, have been reported. Studies conducted in the United States, Canada, and Europe over the past two decades have shown that most people living in the developed countries spend the majority of their time indoors and that the air concentrations of many air toxics or HAPs are higher indoors than in the ambient air in urban, suburban, and rural settings. Elevated indoor air concentrations result from emissions of air toxics from consumer products, household furnishings, and personal activities. The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to oversample homes in close proximity to ambient sources, excluding residences where smokers lived, to determine the contribution of ambient emissions to air toxics exposure. The ratios of indoor to outdoor air concentrations of some VOCs in homes measured during RIOPA were much greater than one, and for most other VOCs that had indoor-to-outdoor ratios close to unity in the majority of homes, elevated ratios were found in the paired samples with the highest concentration. Thus, although ambient emissions contribute to exposure of some air toxics indoors as well as outdoors, this was not true for all of the air toxics and especially for the higher end of exposures to most volatile organic air toxics examined. It is therefore critical, when evaluating potential effects of air toxics on asthma or other adverse health end points, to determine where the exposure occurs and the source contributions for each air toxic and target population separately and not to rely solely on ambient air concentration measurements.     

Intersectional inequalities in industrial air toxics exposure in the United States

Environmental justice and health research demonstrate unequal exposure to environmental hazards at the neighborhood-level. We use an innovative method—eco-intersectional multilevel (EIM) modeling—to assess intersectional inequalities in industrial air toxics exposure across US census tracts in 2014. Results reveal stark inequalities in exposure across analytic strata, with a 45-fold difference in average exposure between most and least exposed. Low SES, multiply marginalized (high % Black, high % female-headed households) urban communities experienced highest risk. These inequalities were not described by additive effects alone, necessitating the use of interaction terms. We advance a critical intersectional approach to evaluating environmental injustices.     

Segregation and black/white differences in exposure to air toxics in 1990

I examined non-Hispanic Black and non-Hispanic White differences in exposure to noncriteria air pollutants in 44 U.S. Census Bureau-defined metropolitan areas with populations greater than one million, using data on air toxics concentrations prepared for the U.S. Environmental Protection Agency as part of its Cumulative Exposure Project combined with U.S. census data. I measured differences in exposure to air toxics through the calculation of a net difference score, which is a statistical measure used in income inequality analysis to measure inequality over the whole range of exposures. The scores ranged from 11.52 to 83.60. In every metropolitan area, non-Hispanic Blacks are more likely than non-Hispanic Whites to be living in tracts with higher total modeled air toxics concentrations. To assess potential reasons for such a wide variation in exposure differences, I performed a multiple regression analysis with the net difference score as the dependent variable. Independent variables initially included were as follows: the dissimilarity index (to measure segregation), Black poverty/White poverty (to control for Black/White economic differences), population density and percentage of persons traveling to work who drive to work (alone and in car pools), and percentage of workforce employed in manufacturing (factors affecting air quality). After an initial analysis I eliminated from the model the measures of density and the persons driving to work because they were statistically insignificant, they did not add to the predictive power of the model, and their deletion did not affect the other variables. The final model had an R(2) of 0.56. Increased segregation is associated with increased disparity in potential exposure to air pollution.     

Risk of leukemia in relation to exposure to ambient air toxics in pregnancy and early childhood

There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to toxics in ambient air. In our case–control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children <age 6, and 19,209 controls from California birth records within 2 km (1.3 miles) (ALL) and 6 km (3.8 miles) (AML) of an air toxics monitoring station between 1990 and 2007. Information on air toxics exposures was taken from community air monitors. We used logistic regression to estimate the risk of leukemia associated with one interquartile range increase in air toxic exposure. Risk of ALL was elevated with 3^rd trimester exposure to polycyclic aromatic hydrocarbons (OR = 1.16, 95% CI 1.04, 1.29), arsenic (OR = 1.33, 95% CI 1.02, 1.73), benzene (OR = 1.50, 95% CI 1.08, 2.09), and three other toxics related to fuel combustion. Risk of AML was increased with 3rd trimester exposure to chloroform (OR = 1.30, 95% CI 1.00, 1.69), benzene (1.75, 95% CI 1.04, 2.93), and two other traffic-related toxics. During the child's first year, exposure to butadiene, ortho-xylene, and toluene increased risk for AML and exposure to selenium increased risk for ALL. Benzene is an established cause of leukemia in adults; this study supports that ambient exposures to this and other chemicals in pregnancy and early life may also increase leukemia risk in children.     

An assessment of air toxics in Minnesota

We used monitoring and modeling to assess the concentrations of air toxics in the state of Minnesota. Model-predicted concentrations for 148 hazardous air pollutants were from the U.S. Environmental Protection Agency Cumulative Exposure Project (1990 data). Monitoring data consisted of samples of volatile organic compounds, carbonyls, and particulate matter [Less than and equal to] 10 microm in aerodynamic diameter collected at 25 sites throughout the state for varying periods of time (up to 8 years; 1991-1998). Ten pollutants exceeded health benchmark values at one or more sites by modeling, monitoring, or both (including acrolein, arsenic, benzene, 1,3-butadiene, carbon tetrachloride, chromium, chloroform, ethylene dibromide, formaldehyde, and nickel). Polycyclic organic matter also exceeded the benzo[a]pyrene health benchmark value assumed to represent this class of pollutants. The highest modeled and monitored concentrations of most pollutants were near the center of the Minneapolis-St. Paul metropolitan area; however, many smaller cities throughout the state also had elevated concentrations. Where direct comparisons were possible, monitored values often tended to exceed model estimates. Upper-bound excess lifetime inhalation cancer risks were estimated to range from 2.7 [times] 10(-5) to 140. 9 [times] 10(-5) (modeling) and 4.7 [times] 10(-5) to 11.0 [times] 10(-5) (using a smaller set of monitored carcinogens). Screening noncancer hazard indices summed over all end points ranged from 0.2 to 58.1 (modeling) and 0.6 to 2.0 (with a smaller set of monitored pollutants). For common sets of pollutants, the concentrations, cancer risks, and noncancer hazard indices were comparable between model-based estimates and monitored values. The inhalation cancer risk was apportioned to mobile sources (54%), area sources (22%), point sources (12%), and background (12%). This study provides evidence that air toxics are a public health concern in Minnesota.     

Between-airport heterogeneity in air toxics emissions associated with individual cancer risk thresholds and population risks

Background  

Airports represent a complex source type of increasing importance contributing to air toxics risks. Comprehensive atmospheric dispersion models are beyond the scope of many applications, so it would be valuable to rapidly but accurately characterize the risk-relevant exposure implications of emissions at an airport.     

High-end exposure relationships of volatile air toxics and carbon monoxide to community-scale air monitoring stations in Atlanta,Chicago, and Houston

Evaporative and exhaust mobile source air toxic (MSAT) emissions of total volatile organic compounds, carbon monoxide, BTEX (benzene, toluene, ethylbenzene, and xylenes), formaldehyde, acetaldehyde, butadiene, methyl tertiary butyl ether, and ethanol were measured in vehicle-related high-end microenvironments (ME) under worst-case conditions plausibly simulating the >99th percentile of inhalation exposure concentrations in Atlanta (baseline gasoline), Chicago (ethanol-oxygenated gasoline), and Houston (methyl tertiary butyl either-oxygenated gasoline) during winter and summer seasons. High-end MSAT values as ratios of the corresponding measurements at nearby air monitoring stations exceeded the microenvironmental proximity factors used in regulatory exposure models, especially for refueling operations and MEs under reduced ventilation. MSAT concentrations were apportioned between exhaust and evaporative vehicle emissions in Houston where methyl tertiary butyl ether could be used as a vehicle emission tracer. With the exception of vehicle refueling operations, the results indicate that evaporative emissions are a minor component of high-end MSAT exposure concentrations.     

Inhalation risk upon exposure to emission from industrial enterprises in the town of Magnitogorsk

Based on the risk assessment methodology, the authors gives information on Magnitogorsk priority industrial enterprises; the chemicals contained in their emission from halation risk, which are responsible for moderare and severe risks. Negative health effects due to chronic inhalation exposure and the poorest environmental areas under observation are identified. The directions of application of the findings are specified.     

Addressing community concerns about asthma and air toxics

People with asthma who live near or downwind from a source of toxic emissions commonly express concerns about the possible impact of hazardous air pollution on their health, especially when these emissions are visible or odorous. Citizens frequently turn to their local and state health departments for answers, but health departments face many challenges in addressing these concerns. These challenges include a lack of asthma statistics at the local level, limited exposure information, and a paucity of scientific knowledge about the contributions of hazardous air pollutants to asthma induction or exacerbation. Health agencies are creatively developing methods to address these challenges while working toward improving asthma surveillance data at the state and local levels. Recent community health investigations suggest that hazardous air pollutants that are occupational asthmagens or associated with odors may deserve more attention. In seeking to address community concerns about hazardous air pollution and asthma, community health investigations may also help to fill gaps in our scientific knowledge and identify areas for further research or environmental intervention. The solutions to community problems associated with environmental contamination and asthma, however, require sustained, coordinated efforts by public and private groups and citizens. Public health agencies can make a unique contribution to this effort, but additional resources and support will be required to develop information systems and epidemiologic capacity at the state and local levels.     

Pollutants and asthma: role of air toxics

Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway reactivity to both allergic and nonallergic stimuli. Most asthma exacerbations that result in hospitalization are associated with viral upper respiratory tract infections. Such infections typically induce T-helper type 1 (T(H)1) responses in the airway, involving activation of nuclear factor-kappaB (NF-Kappa B). However, a more recently appreciated cause of asthma exacerbation is exposure to pollutants, including ozone and various components of particulate matter (PM), including transition metals, diesel exhaust, and biologicals such as endotoxin. Although the role of air toxics in asthma pathogenesis remains incompletely examined, many components of PM that are active exacerbants of asthma are also prominent air toxics (metal ions and organic residues). These agents have been observed to activate NF-Kappa B. Reviewed in this article are the actions of specific air pollutants on airway inflammation in humans and potential common response pathways for ozone, PM, and several air toxics.     

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.     

Exposures to multiple air toxics in New York City

Efforts to assess health risks associated with exposures to multiple urban air toxics have been hampered by the lack of exposure data for people living in urban areas. The TEACH (Toxic Exposure Assessment, a Columbia/Harvard) study was designed to characterize levels of and factors influencing personal exposures to urban air toxics among high school students living in inner-city neighborhoods of New York City and Los Angeles, California. This present article reports methods and data for the New York City phase of TEACH, focusing on the relationships between personal, indoor, and outdoor concentrations in winter and summer among a group of 46 high school students from the A. Philip Randolph Academy, a public high school located in the West Central Harlem section of New York City. Air pollutants monitored included a suite of 17 volatile organic compounds (VOCs) and aldehydes, particulate matter with a mass median aerodynamic diameter 相似文献   

Geographic boundaries in breast,lung and colorectal cancers in relation to exposure to air toxics in Long Island,New York

Background  

This two-part study employs several statistical techniques to evaluate the geographic distribution of breast cancer in females and colorectal and lung cancers in males and females in Nassau, Queens, and Suffolk counties, New York, USA. In this second paper, we compare patterns in standardized morbidity ratios (SMR values), calculated from New York State Department of Health (NYSDOH) data, to geographic patterns in overall predicted risk (OPR) from air toxics using exposures estimated in the USEPA National Air Toxics Assessment database.     

GIS modeling of air toxics releases from TRI-reporting and non-TRI-reporting facilities: impacts for environmental justice

The Toxics Release Inventory (TRI) requires facilities with 10 or more full-time employees that process > 25,000 pounds in aggregate or use > 10,000 pounds of any one TRI chemical to report releases annually. However, little is known about releases from non-TRI-reporting facilities, nor has attention been given to the very localized equity impacts associated with air toxics releases. Using geographic information systems and industrial source complex dispersion modeling, we developed methods for characterizing air releases from TRI-reporting as well as non-TRI-reporting facilities at four levels of geographic resolution. We characterized the spatial distribution and concentration of air releases from one representative industry in Durham County, North Carolina (USA). Inclusive modeling of all facilities rather than modeling of TRI sites alone significantly alters the magnitude and spatial distribution of modeled air concentrations. Modeling exposure receptors at more refined levels of geographic resolution reveals localized, neighborhood-level exposure hot spots that are not apparent at coarser geographic scales. Multivariate analysis indicates that inclusive facility modeling at fine levels of geographic resolution reveals exposure disparities by income and race. These new methods significantly enhance the ability to model air toxics, perform equity analysis, and clarify conflicts in the literature regarding environmental justice findings. This work has substantial implications for how to structure TRI reporting requirements, as well as methods and types of analysis that will successfully elucidate the spatial distribution of exposure potentials across geographic, income, and racial lines.     

Ozone and limonene in indoor air: a source of submicron particle exposure

Little information currently exists regarding the occurrence of secondary organic aerosol formation in indoor air. Smog chamber studies have demonstrated that high aerosol yields result from the reaction of ozone with terpenes, both of which commonly occur in indoor air. However, smog chambers are typically static systems, whereas indoor environments are dynamic. We conducted a series of experiments to investigate the potential for secondary aerosol in indoor air as a result of the reaction of ozone with d-limonene, a compound commonly used in air fresheners. A dynamic chamber design was used in which a smaller chamber was nested inside a larger one, with air exchange occurring between the two. The inner chamber was used to represent a model indoor environment and was operated at an air exchange rate below 1 exchange/hr, while the outer chamber was operated at a high air exchange rate of approximately 45 exchanges/hr. Limonene was introduced into the inner chamber either by the evaporation of reagent-grade d-limonene or by inserting a lemon-scented, solid air freshener. A series of ozone injections were made into the inner chamber during the course of each experiment, and an optical particle counter was used to measure the particle concentration. Measurable particle formation and growth occurred almost exclusively in the 0.1-0.2 microm and 0.2-0.3 microm size fractions in all of the experiments. Particle formation in the 0.1-0.2 microm size range occurred as soon as ozone was introduced, but the formation of particles in the 0.2-0.3 microm size range did not occur until at least the second ozone injection occurred. The results of this study show a clear potential for significant particle concentrations to be produced in indoor environments as a result of secondary particle formation via the ozone-limonene reaction. Because people spend the majority of their time indoors, secondary particles formed in indoor environments may make a significant contribution to overall particle exposure. This study provides data for assessing the impact of outdoor ozone on indoor particles. This is important to determine the efficacy of the mass-based particulate matter standards in protecting public health because the indoor secondary particles can vary coincidently with the variations of outdoor fine particles in summer.     

Inhalation exposure in secondary aluminium smelting

Inhalation exposure at seven UK secondary aluminium smelters was investigated to quantify the main exposures and identify their sources. The substances monitored were gases (carbon monoxide, hydrogen sulphide and nitrogen dioxide), total inhalable dust, metals, ammonia, polycyclic aromatic hydrocarbons (PAHs), particulate fluoride salts and acids. The results showed that people were exposed to a range of workplace air pollutants. Personal exposure results for total inhalable dust were between 700 and 5600 microg x m(-3) and the maximum personal exposure result for particulate fluoride salts was 690 microg x m(-3) (as F). The maximum aluminium, total PAH and lead personal exposure results were 900, 19 and 18 microg x m(-3) respectively. The average proportion of aluminium in total inhalable dust samples was 13% and rotary furnace processes generated the most dust. Particulate fluoride salt exposure was more widespread than hydrofluoric acid exposure. The source of the salt exposure was fluoride containing fluxes. The lead exposure source was lead solder contamination in the furnace charge.