Robert Goble

The allure of technology: How France and California promoted electric and hybrid vehicles to reduce urban air pollution

All advanced industrialized societies face the problem of air pollution produced by motor vehicles. In spite of striking improvements in internal combustion engine technology, air pollution in most urban areas is still measured at levels determined to be harmful to human health. Throughout the 1990s and beyond, California and France both chose to improve air quality by means of technological innovation, adopting legislation that promoted clean vehicles, prominently among them, electric vehicles (EVs). In California, policymakers chose a technology-forcing approach, setting ambitious goals (e.g., zero emission vehicles), establishing strict deadlines and issuing penalties for non-compliance. The policy process in California called for substantial participation from the public, the media, the academic community and the interest groups affected by the regulation. The automobile and oil industries bitterly contested the regulation, in public and in the courts. In contrast, in France the policy process was non-adversarial, with minimal public participation and negligible debate in academic circles. We argue that Californias stringent regulation spurred the development of innovative hybrid and fuel cell vehicles more effectively than the French approach. However, in spite of the differences, both California and France have been unable to put a substantial number of EVs on the road. Our comparison offers some broad lessons about how policy developments within a culture influence both the development of technology and the impact of humans on the environment.

Distributions of individual susceptibility among humans for toxic effects. How much protection does the traditional tenfold factor provide for what fraction of which kinds of chemicals and effects

Abstract: A significant data base has been assembled on human variability in parameters representing a series of steps in the pathway from external exposure to the production of biological responses: contact rate (e.g., breathing rates/body weight, fish consumption/body weight); uptake or absorption (mg/kg)/intake or contact rate; general systemic availability net of first pass elimination and dilution; systemic elimination or half‐life; active site availability/general systemic availability; physiological parameter change/active site availability; functional reserve capacity‐change in baseline physiological parameter needed to pass a criterion of abnormal function or exhibit a response. This paper discusses the current results of analyzing these data to derive estimates for distributions of human susceptibility to different routes of exposure and types of adverse effects. The degree of protection is tentatively evaluated by projecting the incidences of effects that would be expected for a tenfold lowering of exposure from a 5% incidence level if the population distribution of susceptibility were truly log‐normal out to the extreme tails, and if the populations, chemicals, and responses that gave rise to the underlying data were representative of the cases to which traditional uncertainty factor is applied. The results indicate that, acting by itself, a tenfold reduction in dose from a 5% effect level is associated with effect incidences ranging from slightly less than one in ten thousand, for a median chemical/response, to a few per thousand, for chemicals and responses that have greater human interindividual variability than 19 out of 20 typical chemicals/responses. In practice, for many of the cases where the traditional tenfold factor is applied, additional protection is provided by other uncertainty factors. Nevertheless, the results generate some reason for concern that current application of traditional safety or uncertainty factor approaches may allow appreciable incidences of responses in some cases.

A straw man proposal for a quantitative definition of the RfD.

ABSTRACT This paper discusses the merits and disadvantages of a specific proposal for a numerical calculation of the reference dose (RfD) with explicit recognition of both uncertainty and variability. It is suggested that the RfD be the lower (more restrictive) value of: The daily dose rate that is expected (with 95% confidence) to produce less than 1/100,000 incidence over background of a minimally adverse response in a standard general population of mixed ages and genders, or The daily dose rate that is expected (with 95% confidence) to produce less than a 1/1000 incidence over background of a minimally adverse response in a definable sensitive subpopulation. Developing appropriate procedures to make such estimates poses challenges. To be a viable replacement for current RfDs, a numerical definition needs to be A plausible representation of the risk management values that both lay people and “experts” believe are intended to be achieved by current RfDs, (while better representing the “truth” that current RfDs cannot be expected to achieve zero risk with absolute confidence for a mixed population with widely varying sensitivities), Estimable with no greater amount of chemical specific information than is traditionally collected to estimate current RfD values, Subjected to a series of comparisons with existing RfDs to evaluate overall implications for current regulatory values, A more flexible value in the sense of facilitating the development of procedures to allow the incorporation of more advanced technical information—e.g., defined data on human distributions of sensitivity; information on comparative pharmacokinetic and/or pharmacodynamics in humans vs. test species, etc. The discussion evaluates the straw man proposal in the light of each of these points, and assesses the risks and uncertainties inherent in present RfDs by applying existing distributional information on various uncertainty factors to 18 of 20 randomly-selected entries from IRIS. The analysis here suggests that current RfDs seem to meet the 1/100,000 risk criterion with only somewhat better than 50% confidence. However, the current RfDs appear to generally fall short of the goal of meeting this risk criterion with 95% confidence, typically by an order of magnitude in dose or somewhat more. The single most important uncertainty is the extent of human interindividual variability in the doses of specific chemicals that cause adverse responses. Our major conclusion is that with some important assumptions, it is currently feasible to both specify quantitative probabilistic performance objectives for RfDs and to make tentative assessments about whether specific current RfDs for real chemicals seem to meet those objectives. Similarly it is also possible to make preliminary estimates of how much risk is posed by exposures in the neighborhood of current RfDs, and what the uncertainties are in such estimates. It is therefore possible to harmonize cancer and noncancer risk assessments by making quantitative noncancer risk estimates comparable to those traditionally made for carcinogenic risks. The benefits from this change will be an increase in the candor of public discussion of the possible effects of exposures to chemicals posing non-cancer risks, and encouragement for the collection of better scientific information related to toxic risks in people—particularly the extent and distributional form of interindividual differences among people in susceptibility.

Age-related differences in susceptibility to carcinogenesis: a quantitative analysis of empirical animal bioassay data.

In revising cancer risk assessment guidelines, the U.S. Environmental Protection Agency (EPA) analyzed animal cancer bioassay data over different periods of life. In this article, we report an improved analysis of these data (supplemented with some chemical carcinogenesis observations not included in the U.S. EPA’s original analysis) and animal bioassay studies of ionizing radiation. We use likelihood methods to avoid excluding cases where no tumors were observed in specific groups. We express dosage for animals of different weights on a metabolically consistent basis (concentration in air or food, or per unit body weight to the three-quarters power). Finally, we use a system of dummy variables to represent exposures during fetal, preweaning, and weaning–60-day postnatal periods, yielding separate estimates of relative sensitivity per day of dosing in these intervals. Central estimate results indicate a 5- to 60-fold increased carcinogenic sensitivity in the birth–weaning period per dose ÷ (body weight0.75-day) for mutagenic carcinogens and a somewhat smaller increase—centered about 5-fold—for radiation carcinogenesis per gray. Effects were greater in males than in females. We found a similar increased sensitivity in the fetal period for direct-acting nitrosoureas, but no such increased fetal sensitivity was detected for carcinogens requiring metabolic activation. For the birth–weaning period, we found an increased sensitivity for direct administration to the pups similar to that found for indirect exposure via lactation. Radiation experiments indicated that carcinogenic sensitivity is not constant through the “adult” period, but the dosage delivered in 12- to 21-month-old animals appears a few-fold less effective than the comparable dosage delivered in young adults (90–105 days of age).

Human Interindividual Variability in Susceptibility to Airborne Particles

Part of the explanation for the persistent epidemiological findings of associations between mortality and morbidity with relatively modest ambient exposures to airborne particles may be that some people are much more susceptible to particle-induced responses than others. This study assembled a database of quantitative observations of interindividual variability in pharmacokinetic and pharmacodynamic parameters likely to affect particle response. The pharmacodynamic responses studied included data drawn from epidemiologic studies of doses of methacholine, flour dust, and other agents that induce acute changes in lung function. In general, the amount of interindividual variability in several of these pharmacodynamic response parameters was greater than the variability in pharmacokinetic (breathing rate, deposition, and clearance) parameters. Quantitatively the results indicated that human interindividual variability of breathing rates and major pharmacokinetic parameters-total deposition and tracheobronchial clearance-were in the region of Log(GSD) = 0.1 to 0.2 (corresponding to geometric standard deviations of 10(.1)-10(.2) or 1.26-1.58). Deposition to the deep lung (alveolar region) appeared to be somewhat more variable: Log(GSD) of about 0.3 (GSD of about 2). Among pharmacodynamic parameters, changes in FEV1 in response to ozone and metabisulfite (an agent that is said to act primarily on neural receptors in the lung) were in the region of Log(GSD) of 0.2 to 0.4. However, similar responses to methacholine, an agent that acts on smooth muscle, seemed to have still more variability (0.4 to somewhat over 1.0, depending on the type of population studied). Similarly high values were suggested for particulate allergens. Central estimates of this kind of variability, and the close correspondence of the data to lognormal distributions, indicate that 99.9th percentile individuals are likely to respond at doses that are 150 to 450-fold less than would be needed in median individuals. It seems plausible that acute responses with this amount of variability could form part of the mechanistic basis for epidemiological observations of enhanced mortality in relation to ambient exposures to fine particles.

Roughness effects on urban turbulence parameters

Urban roughness lengths are estimated from measurements of u and u* at one level under neutral conditions, assuming a logarithmic form for the vertical profile of wind velocity. At a given location in the urban area, estimated values show considerable directional variation. The dependence of some turbulence parameters on the urban roughness lengths is experimentally investigated during near-neutral conditions. The ratios Σi/u* decrease with roughness whereas the turbulence intensities Σi/u increase with it. The dependence on roughness is not the same for all components.

Nuclear Waste: Knowledge Waste?

A stalled nuclear waste program, and possible increase in wastes, beg for social science input into acceptable solutions. Nuclear power is re-emerging as a major part of the energy portfolios of a wide variety of nations. With over 50 reactors being built around the world today and over 100 more planned to come online in the next decade, many observers are proclaiming a “nuclear renaissance” (1). The success of a nuclear revival is dependent upon addressing a well-known set of challenges, for example, plant safety (even in the light of improved reactor designs), costs and liabilities, terrorism at plants and in transport, weapons proliferation, and the successful siting of the plants themselves (2, 3).

Age-Related Differences in Susceptibility to Carcinogenesis. II. Approaches for Application and Uncertainty Analyses for Individual Genetically Acting Carcinogens

In an earlier report we developed a quantitative likelihood-based analysis of the differences in sensitivity of rodents to mutagenic carcinogens across three life stages (fetal, birth to weaning, and weaning to 60 days) relative to exposures in adult life. Here we draw implications for assessing human risks for full lifetime exposures, taking into account three types of uncertainties in making projections from the rodent data: uncertainty in the central estimates of the life-stage–specific sensitivity factors estimated earlier, uncertainty from chemical-to-chemical differences in life-stage–specific sensitivities for carcinogenesis, and uncertainty in the mapping of rodent life stages to human ages/exposure periods. Among the uncertainties analyzed, the mapping of rodent life stages to human ages/exposure periods is most important quantitatively (a range of several-fold in estimates of the duration of the human equivalent of the highest sensitivity “birth to weaning” period in rodents). The combined effects of these uncertainties are estimated with Monte Carlo analyses. Overall, the estimated population arithmetic mean risk from lifetime exposures at a constant milligrams per kilogram body weight level to a generic mutagenic carcinogen is about 2.8-fold larger than expected from adult-only exposure with 5–95% confidence limits of 1.5-to 6-fold. The mean estimates for the 0- to 2-year and 2- to 15-year periods are about 35–55% larger than the 10- and 3-fold sensitivity factor adjustments recently proposed by the U.S. Environmental Protection Agency. The present results are based on data for only nine chemicals, including five mutagens. Risk inferences will be altered as data become available for other chemicals.

The Assessment of Radiation Exposures in Native American Communities from Nuclear Weapons Testing in Nevada

Native Americans residing in a broad region downwind from the Nevada Test Site during the 1950s and 1960s received significant radiation exposures from nuclear weapons testing. Because of differences in diet, activities, and housing, their radiation exposures are only very imperfectly represented in the Department of Energy dose reconstructions. There are important missing pathways, including exposures to radioactive iodine from eating small game. The dose reconstruction model assumptions about cattle feeding practices across a year are unlikely to apply to the native communities as are other model assumptions about diet. Thus exposures from drinking milk and eating vegetables have not yet been properly estimated for these communities. Through consultations with members of the affected communities, these deficiencies could be corrected and the dose reconstruction extended to Native Americans. An illustration of the feasibility of extending the dose reconstruction is provided by a sample calculation to estimate radiation exposures to the thyroid from eating radio-iodine-contaminated rabbit thyroids after the Sedan test. The illustration is continued with a discussion of how the calculation results may be used to make estimates for other tests and other locations.

Vulnerability-based spatial sampling stratification for the National Children's Study, Worcester County, Massachusetts: capturing health-relevant environmental and sociodemographic variability

Background The National Children’s Study is the most ambitious study ever attempted in the United States to assess how environmental factors impact child health and development. It aims to follow 100,000 children from gestation until 21 years of age. Success requires breaking new interdisciplinary ground, starting with how to select the sample of > 1,000 children in each of 105 study sites; no standardized protocol exists for stratification of the target population by factoring in the diverse environments it inhabits. Worcester County, Massachusetts, like other sites, stratifies according to local conditions and local knowledge, subject to probability sampling rules. Objectives We answer the following questions: How do we divide Worcester County into viable strata that represent its health-relevant environmental and sociodemographic heterogeneity, subject to sampling rules? What potential does our approach have to inform stratification at other sites? Results We developed a multivariable, vulnerability-based method for spatial sampling consisting of two descriptive indices: a hazards/stressors exposure index (comprising three proxy variables), and an adaptive capacity/sociodemographic character index (five variables). Multivariable, health-relevant stratification at the start of the study may improve detection power for environment–child health associations down the line. Eighteen strata capture countywide heterogeneity in the indices and have optimal relative homogeneity within each. They achieve comparable expected birth counts and conform to local concepts of space. Conclusion The approach offers moderate to high potential to inform other sites, limited by intersite differences in data availability, geodemographics, and technical capacity. Energetic community engagement from the start promotes local stratification coherence, plus vital researcher–community trust and co-ownership for sustainability.