Although official efforts to control air pollution have traditionally focused on outdoor air, it is now apparent that elevated contaminant concentrations are common inside some private and public buildings. Concerns about potential public health problems due to indoor air pollution are based on evidence that urban residents typically spend more than 90 percent of their time indoors, concentrations of some contaminants are higher indoors than outdoors, and for some pollutants personal exposures are not characterized adequately by outdoor measurements. Among the more important indoor contaminants associated with health or irritation effects are passive tobacco smoke, radon decay products, carbon monoxide, nitrogen dioxide, formaldehyde, asbestos fibers, microorganisms, and aeroallergens. Efforts to assess health risks associated with indoor air pollution are limited by insufficient information about the number of people exposed, the pattern and severity of exposures, and the health consequences of exposures. An overall strategy should be developed to investigate indoor exposures, health effects, control options, and public policy alternatives.

BACKGROUND.There is anecdotal evidence that the incidence of central nervous system (CNS) metastases in breast cancer patients is increasing. It is unclear whether specific tumor biological properties or the use of systemic therapies influence this risk.METHODS.Using a database of 10,782 patients, 2685 patients were identified who experienced recurrence distantly. Clinical and biological features were analyzed in 2 ways: 1) patients who ever had versus those who never had CNS metastases, and 2) CNS metastases as the first site of recurrence versus those who had other sites. Correlations of survival after CNS metastasis with clinical and biologic features were also analyzed.RESULTS.In the ever versus never analysis, CNS metastases were significantly associated with younger age, premenopausal status, infiltrating ductal carcinoma histology (IDC), estrogen receptor (ER) and progesterone receptor (PR) negativity, low Bcl‐2, high S‐phase, aneuploidy, and altered p53. Tumor size, lymph node status, and use of adjuvant systemic therapy played little role. HER‐2 overexpression was not associated with an increased risk in these patients (none of whom were treated with trastuzumab) (P = .91). However, epidermal growth factor receptor (EGFR) overexpression was associated with increased risk (P = .02). A multivariate analysis revealed ER negativity (odds ratio [OR] 2.8, P<.001), IDC histology (OR 2.5, P = .02), and young age (P<.001) as independent factors for CNS metastases. The clinical and biologic profiles of primary tumors with CNS metastases at first recurrence did not differ from those with CNS metastases after recurrence to other sites, except for HER‐2 status. HER‐2‐positive tumors were not more likely to undergo recurrence initially in the CNS (P = .04). The median survival after CNS metastases was 5.5 months and HER‐2‐positive patients had a shorter survival.CONCLUSIONS.Younger patients with hormone receptor‐negative, highly proliferative, genomically unstable, and p53‐altered tumors were at increased relative risk for CNS metastases. HER‐2 expression and adjuvant systemic therapies did not increase this risk. Cancer 2006. © 2006 American Cancer Society.

We measured volatile organic compound (VOC) exposures in multiple locations for a diverse population of children who attended two inner-city schools in Minneapolis, Minnesota. Fifteen common VOCs were measured at four locations: outdoors (O), indoors at school (S), indoors at home (H), and in personal samples (P). Concentrations of most VOCs followed the general pattern O ≈ S < P ≤ H across the measured microenvironments. The S and O environments had the smallest and H the largest influence on personal exposure to most compounds. A time-weighted model of P exposure using all measured microenvironments and time–activity data provided little additional explanatory power beyond that provided by using the H measurement alone. Although H and P concentrations of most VOCs measured in this study were similar to or lower than levels measured in recent personal monitoring studies of adults and children in the United States, p-dichlorobenzene was the notable exception to this pattern, with upper-bound exposures more than 100 times greater than those found in other studies of children. Median and upper-bound H and P exposures were well above health benchmarks for several compounds, so outdoor measurements likely underestimate long-term health risks from children’s exposure to these compounds.

Two-day average concentrations of 15 individual volatile organic compounds (VOCs) were measured concurrently in (a) ambient air in three urban neighborhoods, (b) air inside residences of participants, and (c) personal air near the breathing zone of 71 healthy, nonsmoking adults. The outdoor (O), indoor (I), and personal (P) samples were collected in the Minneapolis/St. Paul metropolitan area over three seasons (spring, summer, and fall) in 1999 using charcoal-based passive air samplers (3M model 3500 organic vapor monitors). A hierarchical, mixed-effects statistical model was used to estimate the mutually adjusted effects of monitor location, community, and season while accounting for within-subject and within-time-index (monitoring period) correlation. Outdoor VOC concentrations were relatively low compared to many other urban areas, and only minor seasonal differences were observed. A consistent pattern of P > I > O was observed across both communities and seasons for 13 of 15 individual VOCs (exceptions were carbon tetrachloride and chloroform). Results indicate that ambient VOC measurements at central monitoring sites can seriously underestimate actual exposures for urban residents, even when the outdoor measurements are taken in their own neighborhoods.

Air toxics are of particular concern in Greater Houston, home to one of the world’s largest petrochemical complexes and a quarter of the nation’s refining capacity. Much of this complex lies along a navigable ship channel that flows 50 miles from east of the central business district through Galveston Bay and into the Gulf of Mexico. Numerous communities, including both poor and affluent neighborhoods, are located in close proximity to the 200 facilities along this channel. Our aim is to examine the spatial distribution of cumulative, air-pollution-related cancer risks in Houston and Harris County, with particular emphasis on identifying ethnic, economic, and social disparities. We employ exposure estimates from NATA-1999 and census data to assess whether the cumulative cancer risks from air toxics in Houston (and Harris County) fall disproportionately on certain ethnicities and on the socially and economically disadvantaged. The cancer risk burden across Harris County census tracts increases with the proportion of residents who are Hispanic and with key indicators of relative social disadvantage. Aggregate disadvantage grows at each higher level of cancer risk. The highest cancer risk in Harris County is concentrated along a corridor flanking the ship channel. These high-risk neighborhoods, however, vary markedly in relative disadvantage, as well as in emission source mix. Much of the risk they face appears to be driven by only a few hazardous air pollutants. Results provide evidence of risk disparities from hazardous air pollution based on ethnicity and social disadvantage. At the highest levels of risk the pattern is more complex, arguing for a neighborhood level of analysis, especially when proximity to high-emissions industries is a substantial contributor to cumulative cancer risk.

Cumulative risk refers to the combined threats from exposure via all relevant routes to multiple stressors including biological, chemical, physical, and psychosocial entities. Cumulative risk assessment is a tool for organizing and analyzing information to examine, characterize, and possibly quantify the combined adverse effects on human health or ecologic resources from multiple environmental stressors. The U.S. Environmental Protection Agency (EPA) has initiated a long-term effort to develop future guidelines for cumulative risk assessment, including publication in 2003 of a framework that describes important features of the process and discusses theoretical issues, technical matters, and key definitions. The framework divides the process of cumulative risk assessment into three interrelated phases: a) planning, scoping, and problem formulation; b) analysis; and c) interpretation and risk characterization. It also discusses the additional complexities introduced by attempts to analyze cumulative risks from multiple stressors and describes some of the theoretical approaches that can be used. The development of guidelines for cumulative risk assessment is an essential element in the transition of the U.S. EPA risk assessment methodology from a narrow focus on a single stressor, end point, source, pathway, and exposure route to a broader, more holistic approach involving analysis of combined effects of cumulative exposure to multiple stressors via all relevant sources, pathways, and routes.

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