A Cancer Risk Assessment of Inner-City Teenagers Living in New York City and Los Angeles

BACKGROUND: The Toxics Exposure Assessment Columbia–Harvard (TEACH) project assessed exposures and cancer risks from urban air pollutants in a population of high school teenagers in New York City (NYC) and Los Angeles (LA). Forty-six high school students participated in NYC and 41 in LA, most in two seasons in 1999 and 2000, respectively. METHODS: Personal, indoor home, and outdoor home 48-hr samples of volatile organic compounds (VOCs), aldehydes, particulate matter with aerodynamic diameter ≤ 2.5 μm, and particle-bound elements were collected. Individual cancer risks for 13 VOCs and 6 particle-bound elements were calculated from personal concentrations and published cancer unit risks. RESULTS: The median cumulative risk from personal VOC exposures for this sample of NYC high school students was 666 per million and was greater than the risks from ambient exposures by a factor of about 5. In the LA sample, median cancer risks from VOC personal exposures were 486 per million, about a factor of 4 greater than ambient exposure risks. The VOCs with the highest cancer risk included 1,4-dichlorobenzene, formaldehyde, chloroform, acetaldehyde, and benzene. Of these, benzene had the greatest contributions from outdoor sources. All others had high contributions from indoor sources. The cumulative risks from personal exposures to the elements were an order of magnitude lower than cancer risks from VOC exposures. CONCLUSIONS: Most VOCs had median upper-bound lifetime cancer risks that exceeded the U.S. Environmental Protection Agency (EPA) benchmark of 1 × 10(−6) and were generally greater than U.S. EPA modeled estimates, more so for compounds with predominant indoor sources. Chromium, nickel, and arsenic had median personal cancer risks above the U.S. EPA benchmark with exposures largely from outdoors and other microenvironments. The U.S. EPA–modeled concentrations tended to overestimate personal cancer risks for beryllium and chromium but underestimate risks for nickel and arsenic

Non-Chemical Stressors and Cumulative Risk Assessment: An Overview of Current Initiatives and Potential Air Pollutant Interactions

Regulatory agencies are under increased pressure to consider broader public health concerns that extend to multiple pollutant exposures, multiple exposure pathways, and vulnerable populations. Specifically, cumulative risk assessment initiatives have stressed the importance of considering both chemical and non-chemical stressors, such as socioeconomic status (SES) and related psychosocial stress, in evaluating health risks. The integration of non-chemical stressors into a cumulative risk assessment framework has been largely driven by evidence of health disparities across different segments of society that may also bear a disproportionate risk from chemical exposures. This review will discuss current efforts to advance the field of cumulative risk assessment, highlighting some of the major challenges, discussed within the construct of the traditional risk assessment paradigm. Additionally, we present a summary of studies of potential interactions between social stressors and air pollutants on health as an example of current research that supports the incorporation of non-chemical stressors into risk assessment. The results from these studies, while suggestive of possible interactions, are mixed and hindered by inconsistent application of social stress indicators. Overall, while there have been significant advances, further developments across all of the risk assessment stages (i.e., hazard identification, exposure assessment, dose-response, and risk characterization) are necessary to provide a scientific basis for regulatory actions and effective community interventions, particularly when considering non-chemical stressors. A better understanding of the biological underpinnings of social stress on disease and implications for chemical-based dose-response relationships is needed. Furthermore, when considering non-chemical stressors, an appropriate metric, or series of metrics, for risk characterization is also needed. Cumulative risk assessment research will benefit from coordination of information from several different scientific disciplines, including, for example, toxicology, epidemiology, nutrition, neurotoxicology, and the social sciences

Particle size distributions of lead measured in battery manufacturing and secondary smelter facilities and implications in setting workplace lead exposure limits

<p>Inhalation plays an important role in exposures to lead in airborne particulate matter in occupational settings, and particle size determines where and how much of airborne lead is deposited in the respiratory tract and how much is subsequently absorbed into the body. Although some occupational airborne lead particle size data have been published, limited information is available reflecting current workplace conditions in the U.S. To address this data gap, the Battery Council International (BCI) conducted workplace monitoring studies at nine lead acid battery manufacturing facilities (BMFs) and five secondary smelter facilities (SSFs) across the U.S. This article presents the results of the BCI studies focusing on the particle size distributions calculated from Personal Marple Impactor sampling data and particle deposition estimates in each of the three major respiratory tract regions derived using the Multiple-Path Particle Dosimetry model. The BCI data showed the presence of predominantly larger-sized particles in the work environments evaluated, with average mass median aerodynamic diameters (MMADs) ranging from 21–32 µm for the three BMF job categories and from 15–25 µm for the five SSF job categories tested. The BCI data also indicated that the percentage of lead mass measured at the sampled facilities in the submicron range (i.e., <1 µm, a particle size range associated with enhanced absorption of associated lead) was generally small. The estimated average percentages of lead mass in the submicron range for the tested job categories ranged from 0.8–3.3% at the BMFs and from 0.44–6.1% at the SSFs. Variability was observed in the particle size distributions across job categories and facilities, and sensitivity analyses were conducted to explore this variability. The BCI results were compared with results reported in the scientific literature. Screening-level analyses were also conducted to explore the overall degree of lead absorption potentially associated with the observed particle size distributions and to identify key issues associated with applying such data to set occupational exposure limits for lead.</p

Providing perspective for interpreting cardiovascular mortality risks associated with ozone exposures

AbstractWhen identifying standards for air pollutants based on uncertain evidence, both science and policy judgments play critical roles. Consequently, critical contextual factors are important for understanding the strengths, limitations, and appropriate interpretation of available science, and potential benefits of risk mitigation alternatives. These factors include the relative magnitude and certainty of the risks posed by various factors and the impacts of other risk factors on air pollutant epidemiology study findings. This commentary explores ozone’s status as a risk factor for cardiovascular mortality in contrast with decades of strong and consistent evidence for other established risk factors. By comparison, the ozone evidence is less conclusive, more heterogeneous, and subject to substantial uncertainty; ozone’s potential effects, if any, are small and challenging to discern. Moreover, the absence of a demonstrated causal relationship calls into question efforts to quantify cardiovascular mortality risks attributed to ozone exposures on a population level and highlights the need to explicitly acknowledge this uncertainty if such calculations are performed. These concerns are relevant for other similar policy contexts – where multiple established risk factors contribute to the health impact of interest; exposure-effect associations are relatively small, weak, and uncertain; and a causal relationship has not been clearly established

Ozone exposure and systemic biomarkers: Evaluation of evidence for adverse cardiovascular health impacts

<div><p></p><p>The US Environmental Protection Agency (EPA) recently concluded that there is likely to be a causal relationship between short-term (< 30 days) ozone exposure and cardiovascular (CV) effects; however, biological mechanisms to link transient effects with chronic cardiovascular disease (CVD) have not been established. Some studies assessed changes in circulating levels of biomarkers associated with inflammation, oxidative stress, coagulation, vasoreactivity, lipidology, and glucose metabolism after ozone exposure to elucidate a biological mechanism. We conducted a weight-of-evidence (WoE) analysis to determine if there is evidence supporting an association between changes in these biomarkers and short-term ozone exposure that would indicate a biological mechanism for CVD below the ozone National Ambient Air Quality Standard (NAAQS) of 75 parts per billion (ppb). Epidemiology findings were mixed for all biomarker categories, with only a few studies reporting statistically significant changes and with no consistency in the direction of the reported effects. Controlled human exposure studies of 2 to 5 hours conducted at ozone concentrations above 75 ppb reported small elevations in biomarkers for inflammation and oxidative stress that were of uncertain clinical relevance. Experimental animal studies reported more consistent results among certain biomarkers, although these were also conducted at ozone exposures well above 75 ppb and provided limited information on ozone exposure-response relationships. Overall, the current WoE does not provide a convincing case for a causal relationship between short-term ozone exposure below the NAAQS and adverse changes in levels of biomarkers within and across categories, but, because of study limitations, they cannot not provide definitive evidence of a lack of causation.</p></div