Using Sustainable Production Indicators to Measure Progress in ISO 14001, EHS System and EPA Achievement Track

This case study presents results from testing a new tool — indicators of sustainable production (ISPs) — at Acushnet Rubber of New Bedford, Massachusetts. The authors demonstrate how the tool can be used to measure continual improvement and how it fits within the current system for reporting compliance to regulations; and performance under ISO 14001 (environmental management system standard), the environmental, health and safety (EHS) system, and EPA Achievement Track.Developed at the Lowell Center for Sustainable Production (LCSP), this tool includes both core (common for all companies) and supplemental (production-specific) indicators, and aims to raise awareness, support decision-making, and promote continuous improvement toward sustainability. Indicators such as energy use, water use, global warming potential, lost work time case rate, turnover rate, community spending and charitable contributions, among others, were tested at both facility and corporate levels. Results showed the company's progress in EHS as well as the areas that need improvement. The paper concludes with a summary of key lessons learned and recommendations for further use of the tool.     

A Quantitative Estimate of Leukemia Mortality Associated with Occupational Exposure to Benzene3

In 1980, the U.S. Supreme Court vacated a revised occupational standard for benzene, stating that the Occupational Safety and Health Administration (OSHA) had failed to demonstrate that significant health risks existed under the current standard. This decision has been interpreted by OSHA as requiring the consideration of quantitative risk assessments, whenever possible, in the development of regulations for occupational carcinogens. In light of this decision, the available epidemiologic evidence was used to generate a quantitative risk assessment for benzene. Uncertainties regarding the levels and lengths of benzene exposure for the studied cohorts were incorporated into the analysis. Based on the one-hit model, the assessment indicates that a working lifetime exposure to benzene at the current permissible exposure level (10 ppm) poses a substantial excess risk of death from leukemia. This report discusses the calculation of the risk estimates, the basis for relying on certain assumptions, and the inherent limitations of using epidemiologic studies to quantify cancer risks.     

Issues Related to Time Averaging of Exposure in Modeling Risks Associated with Intermittent Exposures to Lead

Typical exposures to lead often involve a mix of long-term exposures to relatively constant exposure levels (e.g., residential yard soil and indoor dust) and highly intermittent exposures at other locations (e.g., seasonal recreational visits to a park). These types of exposures can be expected to result in blood lead concentrations that vary on a temporal scale with the intermittent exposure pattern. Prediction of short-term (or seasonal) blood lead concentrations arising from highly variable intermittent exposures requires a model that can reliably simulate lead exposures and biokinetics on a temporal scale that matches that of the exposure events of interest. If exposure model averaging times (EMATs) of the model exceed the shortest exposure duration that characterizes the intermittent exposure, uncertainties will be introduced into risk estimates because the exposure concentration used as input to the model must be time averaged to account for the intermittent nature of the exposure. We have used simulation as a means of determining the potential magnitude of these uncertainties. Simulations using models having various EMATs have allowed exploration of the strengths and weaknesses of various approaches to time averaging of exposures and impact on risk estimates associated with intermittent exposures to lead in soil. The International Commission of Radiological Protection (ICRP) model of lead pharmacokinetics in humans simulates lead intakes that can vary in intensity over time spans as small as one day, allowing for the simulation of intermittent exposures to lead as a series of discrete daily exposure events. The ICRP model was used to compare the outcomes (blood lead concentration) of various time-averaging adjustments for approximating the time-averaged intake of lead associated with various intermittent exposure patterns. Results of these analyses suggest that standard approaches to time averaging (e.g., U.S. EPA) that estimate the long-term daily exposure concentration can, in some cases, result in substantial underprediction of short-term variations in blood lead concentrations when used in models that operate with EMATs exceeding the shortest exposure duration that characterizes the intermittent exposure. Alternative time-averaging approaches recommended for use in lead risk assessment more reliably predict short-term periodic (e.g., seasonal) elevations in blood lead concentration that might result from intermittent exposures. In general, risk estimates will be improved by simulation on shorter time scales that more closely approximate the actual temporal dynamics of the exposure.     

The Cancer Risk Associated with Residential Exposure to Soil Containing Radioactive Coal Combustion Residuals

Coal combustion residuals (CCRs) are composed of various constituents, including radioactive materials. The objective of this study was to utilize methodology on radionuclide risk assessment from the Environmental Protection Agency (EPA) to estimate the potential cancer risks associated with residential exposure to CCR‐containing soil. We evaluated potential radionuclide exposure via soil ingestion, inhalation of soil particulates, and external exposure to ionizing radiation using published CCR radioactivity values for ²³²Th, ²²⁸Ra, ²³⁸U, and ²²⁶Ra from the Appalachia, Illinois, and Powder River coal basins. Mean and upper‐bound cancer risks were estimated individually for each radionuclide, exposure pathway, and coal basin. For each radionuclide at each coal basin, external exposure to ionizing radiation contributed the greatest to the overall risk estimate, followed by incidental ingestion of soil and inhalation of soil particulates. The mean cancer risks by route of exposure were 2.01 × 10⁻⁶ (ingestion), 6.80 × 10⁻⁹ (inhalation), and 3.66 × 10⁻⁵ (external), while the upper bound cancer risks were 3.70 × 10⁻⁶ (ingestion), 1.18 × 10⁻⁸ (inhalation), and 6.15 × 10⁻⁵ (external), using summed radionuclide‐specific data from all locations. The upper bound cancer risk from all routes of exposure was 6.52 × 10⁻⁵. These estimated cancer risks were within the EPA's acceptable cancer risk range of 1 × 10⁻⁶ to 1 × 10⁻⁴. If the CCR radioactivity values used in this analysis are generally representative of CCR waste streams, then our findings suggest that CCRs would not be expected to pose a significant radiological risk to residents living in areas where contact with CCR‐containing soils might occur.     

Science Policy Choices and the Estimation of Cancer Risk Associated with Exposure to TCDD

United States regulatory agencies use no-threshold models for estimating carcinogenic risks. Other countries use no-threshold models for carcinogens that are genotoxic and threshold models for carcinogens that are not genotoxic, such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD or "dioxin"). The U.S. Environmental Protection Agency has proposed a revision of the carcinogenic potency estimate for TCDD that is based on neither a threshold nor a no-threshold model; instead, it is a compromise between risk numbers generated by the two irreconcilably different models. This paper discusses the revision and its implications.     

Estimating the National Public Health Burden Associated with Exposure to Ambient PM2.5 and Ozone

Ground‐level ozone (O₃) and fine particulate matter (PM_2.5) are associated with increased risk of mortality. We quantify the burden of modeled 2005 concentrations of O₃ and PM_2.5 on health in the United States. We use the photochemical Community Multiscale Air Quality (CMAQ) model in conjunction with ambient monitored data to create fused surfaces of summer season average 8‐hour ozone and annual mean PM_2.5 levels at a 12 km grid resolution across the continental United States. Employing spatially resolved demographic and concentration data, we assess the spatial and age distribution of air‐pollution‐related mortality and morbidity. For both PM_2.5 and O₃ we also estimate: the percentage of total deaths due to each pollutant; the reduction in life years and life expectancy; and the deaths avoided according to hypothetical air quality improvements. Using PM_2.5 and O₃ mortality risk coefficients drawn from the long‐term American Cancer Society (ACS) cohort study and National Mortality and Morbidity Air Pollution Study (NMMAPS), respectively, we estimate 130,000 PM_2.5‐related deaths and 4,700 ozone‐related deaths to result from 2005 air quality levels. Among populations aged 65–99, we estimate nearly 1.1 million life years lost from PM_2.5 exposure and approximately 36,000 life years lost from ozone exposure. Among the 10 most populous counties, the percentage of deaths attributable to PM_2.5 and ozone ranges from 3.5% in San Jose to 10% in Los Angeles. These results show that despite significant improvements in air quality in recent decades, recent levels of PM_2.5 and ozone still pose a nontrivial risk to public health.     

Quantitative Assessment of the Risk of Lung Cancer Associated with Occupational Exposure to Refractory Ceramic Fibers

We present the results of a quantitative assessment of the lung cancer risk associated with occupational exposure to refractory ceramic fibers (RCF). The primary sources of data for our risk assessment were two long-term oncogenicity studies in male Fischer rats conducted to assess the potential pathogenic effects associated with prolonged inhalation of RCF. An interesting feature of the data was the availability of the temporal profile of fiber burden in the lungs of experimental animals. Because of this information, we were able to conduct both exposure–response and dose–response analyses. Our risk assessment was conducted within the framework of a biologically based model for carcinogenesis, the two-stage clonal expansion model, which allows for the explicit incorporation of the concepts of initiation and promotion in the analyses. We found that a model positing that RCF was an initiator had the highest likelihood. We proposed an approach based on biological considerations for the extrapolation of risk to humans. This approach requires estimation of human lung burdens for specific exposure scenarios, which we did by using an extension of a model due to Yu. Our approach acknowledges that the risk associated with exposure to RCF depends on exposure to other lung carcinogens. We present estimates of risk in two populations: (1) a population of nonsmokers and (2) an occupational cohort of steelworkers not exposed to coke oven emissions, a mixed population that includes both smokers and nonsmokers.