A Perspective on Dioxin Emissions from Municipal Solid Waste Incinerators

This paper discusses the following key issues concerning human exposure to dioxins and furans emitted from typical, modern MSW incinerators: (1) Are MSW incinerators the major source of PCDD/PCDF input into the environment? (2) Are environmental concentrations around MSW incinerators substantially elevated relative to background levels? And (3) are MSW incinerators the major source of human exposure to PCDDs and PCDFs? Current scientific evidence indicates that (1) combustion sources in general (including steel mills, copper smelting plants, motor vehicles, pulp and paper mills, and MSW incinerators) are major sources of PCDD/PCDF input in the environment; (2) environmental concentrations of PCDDs and PCDFs around operating MSW incinerators are not substantially elevated; and (3) 99% of human exposure to PCDDs and PCDFs is from background contamination, even for individuals living near a modern MSW incinerator.     

Consideration of Background Exposures in the Management of Hazardous Waste Sites: A New Approach to Risk Assessment

The current approach to health risk assessment of toxic waste sites in the U.S. may lead to considerable expenditure of resources without any meaningful reduction in population exposure. Risk assessment methods used generally ignore background exposures and consider only incremental risk estimates for maximally exposed individuals. Such risk estimates do not address true public health risks to which background exposures also contribute. The purpose of this paper is to recommend a new approach to risk assessment and risk management concerning toxic waste sites. Under this new approach, which we have called public health risk assessment, chemical substances would be classified into a level of concern based on the potential health risks associated with typical national and regional background exposures. Site assessment would then be based on the level of concern for the particular pollutants involved and the potential contribution of site contaminants to typical background human exposures. While various problems can be foreseen with this approach, the key advantage is that resources would be allocated to reduce the most important sources of human exposure, and site remediation decisions could be simplified by focussing on exposure assessment rather than questionable risk extrapolations.     

Do People Actually Pursue Risk Elimination in Environmental Risk Management?

This study examines whether people pursue the total elimination of environmental risks even if the risk reduction occurs incrementally and requires steadily increasing amounts of money to achieve. Participants' willingness to pay (WTP) was measured for various levels of reduction in the risk of cancer caused by dioxin. Results showed that: (1) people were willing to pay more for an initial reduction in risk than for subsequent reductions, (2) the WTP for the final risk decrement-which achieved total risk elimination-was higher than the WTP for either of the two previous decrements but barely half of that for the first reduction, and (3) the manner in which the questions were framed did not affect participants' responses. These results suggest that the public will not always try to pursue perfect safety at the cost of a large sum of money, but rather may seek a decreasing expenditure as the risk level is reduced.     

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.     

Modeling Receptor-Mediated Processes with Dioxin: Implications for Pharmacokinetics and Risk Assessment

Dioxin (2,3,7,8-tetrachlorodibenzo- p -dioxin; TCDD), a widespread polychlorinated aromatic hydrocarbon, caused tumors in the liver and other sites when administered chronically to rats at doses as low as 0.01 μg/kg/day. It functions in combination with a cellular protein, the Ah receptor, to alter gene regulation, and this resulting modulation of gene expression is believed to be obligatory for both dioxin toxicity and carcinogenicity. The U.S. EPA is reevaluating its dioxin risk assessment and, as part of this process, will be developing risk assessment approaches for chemicals, such as dioxin, whose toxicity is receptor-mediated. This paper describes a receptor-mediated physiologically based pharmacokinetic (PB-PK) model for the tissue distribution and enzyme-inducing properties of dioxin and discusses the potential role of these models in a biologically motivated risk assessment. In this model, ternary interactions among the Ah receptor, dioxin, and DNA binding sites lead to enhanced production of specific hepatic proteins. The model was used to examine the tissue disposition of dioxin and the induction of both a dioxin-binding protein (presumably, cytochrome P4501A2), and cytochrome P4501A1. Tumor promotion correlated more closely with predicted induction of P4501A1 than with induction of hepatic binding proteins. Although increased induction of these proteins is not expected to be causally related to tumor formation, these physiological dosimetry and gene-induction response models will be important for biologically motivated dioxin risk assessments in determining both target tissue dose of dioxin and gene products and in examining the relationship between these gene products and the cellular events more directly involved in tumor promotion.     

Dioxin–An Analysis of the Major Human Studies: Comparison with Animal-Based Cancer Risks

Several major epidemiological studies have reported significant mortality rates (SMRs) for both rare cancers (soft tissue sarcoma, non-Hodgkin's, lymphoma, liver) and the more common cancers (lung, colon, etc), all allegedly caused by TCDD. In this paper, we use the potency of TCDD in animals to establish a plausible worst case cancer risk and ask whether its likely that TCDD is responsible for the epidemiological findings assuming the animal carcinogenic potency is applicable to the conditions of human exposure. Two new features of the technique are the use of measured TCDD blood levels in both animals and humans for dose scale-up and the calculation of an integrated life-time exposure for the exposed workers using measured blood levels. On the basis of the stated assumptions it appears unlikely that any of the major epidemiological studies, with the possible exception of the NIOSH study⁽¹⁾have adequate power to detect the common cancers potentially caused by TCDD.     

TCDD Exposure-Response Analysis and Risk Assessment

We examined the relation between cancer mortality and time-dependent cumulative exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) estimated from a concentration- and age-dependent kinetic model of elimination, and we estimated incremental cancer risks at age 75. Data from the National Institute for Occupational Safety and Health study of 3,538 workers with occupational exposure to TCDD were analyzed using standardized mortality ratios and Cox regression procedures. Analyses adjusted for potential confounding by age, year of birth, and race and considered exposure lag periods of 0, 10, or 15 years. Other potential confounders including smoking and other occupational exposures were evaluated indirectly. To explore the influence of extreme values of cumulative TCDD ppt-years, we restricted the analysis to observations with exposure below the 95th percentile or used logarithmic (ln) transformed exposure values. We applied penalized smoothing splines to examine variation in the exposure-response relation across the exposure range. TCDD was not statistically significantly associated with cancer mortality using the full data set, regardless of the lag period. When we restricted the analysis to observations with exposure below the 95th percentile, TCDD was associated positively with cancer mortality, particularly when a 15-year lag was applied (untransformed exposure data: regression coefficient , standard error (s.e.) = 1.4 x 10(-6), p < 0.05; ln-transformed exposure data: , s.e. = 2.9 x 10(-2), p < 0.05). The estimated incremental lifetime risk of mortality at age 75 from all cancers was about 6 to more than 10 times lower than previous estimates derived from this cohort using exposure models that did not consider the age and concentration dependence of TCDD elimination.     

朱子对"道心"、"人心"的诠释

朱子特别重视伪《古文尚书.大禹谟》中"人心惟危,道心惟微;惟精惟一,允执厥中"之语,视之为"虞廷十六字心传",并且在《中庸章句.序》中对"道心"、"人心"提出完整的诠释,为宋代的道统论奠定了理论基础。他根据自己的义理学系统,对"道心"与"人心"这组概念提出了心性论的诠释,而有别于二程的理气论诠释。其次,他强调"人心"与"人欲"的区别,承认自然欲望之合理性。这说明了朱子的伦理学观点如多数的宋明儒者一样,属于"严格主义",而非"禁欲主义"。