RESOLUTION OF A CONTROVERSY DO WASTE TO ENERGY PLANTS CAUSE PUBLIC HEALTH IMPACTS?

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1 RESOLUTION OF A CONTROVERSY DO WASTE TO ENERGY PLANTS CAUSE PUBLIC HEALTH IMPACTS? Paul Chrostowski Sarah Foster CPF Associates, Inc Takoma Avenue Takoma Park MD, 20912, USA pc@cpfassociates.com; sf@cpfassocates.com Abstract: The conversion of municipal solid waste to energy (WTE) has had a significant role in waste management policy for over 30 years. Despite the prevalence and success of this technology, questions continue to be raised regarding the safety of WTE facilities. A recent publication asserts that All incinerators pose considerable risk to the health and environment of neighboring communities as well as that of the general population ; however, there have been hundreds of studies including health risk assessments, epidemiologic studies, and others that should lead to a definitive conclusion regarding the safety of WTE. These studies may be considered to be less than definitive because they are perceived not to address the fundamental question do WTE plants actually cause public health impacts? Rather they are presented as upper bound probabilities or relative risks that many readers feel are difficult to interpret and often equivocal in their outcome. One way to overcome these problems is to organize study results according to formal principles of causation which are widely used in public health practice. This paper presents principles drawn from causation theory and applies them in a case study to analyze claims made by WTE opponents regarding WTE and cancer. The analysis clearly shows that the claims are not substantiated. Keywords: Waste-to-energy, environmental health, epidemiology, causation Introduction Since the inception of the modern age of WTE, questions have been raised about the safety of WTE technologies and facilities. These questions have come from governmental regulatory and public health agencies as well as anti-wte activists and the general public. For example, one organization states without any supporting proof specific to WTE that All incinerators pose considerable risk to the health and environment of neighboring communities as well as that of the general population (Gaia 2012). Another organization asserts living near a waste incinerator increases risks of cancers and other illnesses even from incinerators conforming to the [European] Waste Incineration Directive (CATI 2012). Both CATI (2012) and NTN (2013) have cited epidemiologic studies as evidence that WTE plants cause cancer in proximate populations. On the other hand, industry advocates and many regulatory agencies maintain that WTE is safe and environmentally beneficial (ERC 2013, UKHPA 2010) if constructed and operated in accordance with contemporary laws and regulations. These differences of opinion have spurred the proliferation of scientific studies investigating the hypothetical link between exposure to emissions from these facilities and public health issues. The studies both published

2 and in the gray literature, include epidemiologic studies, risk assessments, environmental monitoring studies, life cycle analyses and others. Most of these studies are valid within the context of their disciplines. For example, a risk assessment will conclude that there is a finite upperbound probability of 7 in one million of contracting cancer under the conditions of exposure (Chrostowski & Foster 2012). An epidemiologic study may conclude that there is a positive but not statistically significant association between MSW incineration and a particular form of cancer. What these studies do not offer is an unequivocal conclusion as to whether the operation of WTE facilities causes a public health impact. One way to overcome these problems is to organize study results according to formal principles of causation which are widely used in public health practice. Environmental Epidemiology and Causation When a general audience thinks of a health study for a proposed or existing waste management technology, they are likely thinking of an environmental epidemiology study. Unlike other environmental health methodologies, epidemiology purports to find relationships ( associations ) between exposures to an etiologic agent and an actual living receptor. Although the term environmental epidemiology has been used since the 1980s, it was given a formal definition by the U.S. National Research Council in 1991 as the study of the effect on humans health of physical, biologic, and chemical factors in the external environment, broadly conceived. By examining specific populations or communities exposed to different ambient environments, it seeks to clarify the relationship between physical, biologic, or chemical factors and human health (NRC 1991). While epidemiologic studies may demonstrate the association between exposure and a health effect, the existence of an association in itself does not necessarily demonstrate that the exposures cause the health effect. This is a critical distinction which forms the basis of this article. The concept of exposure is a necessary component of an environmental epidemiologic investigation. Again to cite the NRC (1991), exposure assessment is a crucial component of environmental epidemiology studies that seek to establish causal relationships between exposure to chemical and physical agents and adverse consequences to human health. As will be seen in the subsequent discussion, exposure is explicit in some criteria for disease causation (temporality, biological gradient), but implicit in many others. We will treat the quality of an exposure assessment within the context of an epidemiologic study as a discrete criterion for causation. Although philosophers had discussed the concept of causation since ancient times, the first exposition of causation using scientific principles was proposed by Robert Koch in Koch developed a series of four postulates to aid microbiologists in determining if exposure to pathogenic bacteria caused a disease. As long as the focus of environmental health was on infectious disease, Koch s postulates were an adequate basis for determinations of disease causation. In the mid-20 th century, however, concerns began to arise regarding potential associations between chemical exposure and disease. Rather than taking a strict experimental approach, environmental health scientists began to rely increasingly on epidemiology to make inferences between chemical exposure and disease. For example, the 1964 report of the US Surgeon General on smoking and health concluded that cigarette smoking caused lung cancer. This conclusion was based on historical associations that met tests of strength, consistency, specificity, temporal relationship and coherence. 2

3 3 British epidemiologist, Sir Austin Bradford Hill (1965) presented a formal system for assisting researchers in determining if an association between chemical exposure and a disease could be considered causal. Hill considered the situation in which observation had revealed an association between two variables perfectly clear-cut and beyond what we would care to attribute to the play of chance and listed nine factors that should be considered: Strength of the association. In epidemiology, the strength of the association is usually measured by the relative risk (or odds ratio). A strong association (high numerical value of a relative risk) supports a hypothesis of causality of the association. A weak relative risk fails to support the hypothesis. Some investigators, and indeed some courts and regulatory bodies, have codified numerical values of relative risk that demark strong or weak in this context, however, none of these limits have been generally accepted. A hypothetical causal relationship is also thought to be more credible if it is precise. Precision in this sense being interpreted as narrow confidence intervals around the relative risk. Consistency. Consistency normally refers to reproducibility of results. In epidemiology, consistency is demonstrated by repeated findings of associations in different population groups or in different settings. Specificity. Specificity often applies to the ability of a particular toxicant to cause a response. In epidemiology, the issue is expressed in the elimination of confounders; in medicine the issue is expressed through the concept of differential diagnosis. Temporality. The exposure must precede the disease. This is a threshold requirement for causation. If a latency period is associated with the development of a particular disease, the duration of the latency should be taken into account. Biological gradient. The biological gradient often is the dose-response relationship in toxicology. An observed dose-response or concentration-response relationship supports a hypothesis of causation. Locational gradients and variable durations of exposure may also be used in causation analysis. Plausibility. The assertion should be biologically plausible. Most investigators use information from field observations, laboratory bioassays, chemical measurements, structure-activity relationships, pharmacokinetics, and in vitro testing to reach as judgment regarding causation. When considered as a whole, these various sources of information should be compatible with each other. Coherence. Hill believed that an interpretation of causality should not conflict with generally known facts of the natural history or biology of the response. Experiment. Experimental evidence results when investigators are able to adequately control the variables in a test. With the exception of a randomized clinical trial, human experimental data are generally not available. With species other than humans, experimental data may be the foundation upon which a determination of causation is made. Analogy. Hill believed that, in some cases, it was possible to draw judgments about causation on the basis of analogy. His examples were birth defects associated with thalidomide and rubella arguing that a similar drug or viral disease could be presumed to have similar effects.

4 4 Susser (1991) critically analyzed scientific thinking concerning causation and developed a refined group of criteria that he felt were most useful and least tautological: Strength is the size of the estimated risk given the constraints of probability levels, confidence intervals, or other measures of likelihood Specificity is the precision with which one variable, to the exclusion of others, will predict the occurrence of another. o Specificity in the cause implies that a given effect has a unique cause o Specificity in the effect implies that a given cause has a unique effect Consistency is the persistence of an association upon repeated testing. o Survivability is the number, rigor, and severity of tests of association o Replicability is the number and diversity of tests of association Predictive performance is the ability of a causal hypothesis drawn from an observed association to predict an unknown fact that is consequent on the initial association. Coherence is the extent to which an hypothesized causal association is compatible with existing knowledge. o Theoretical coherence describes compatibility with existing scientific theory o Factual coherence is compatibility with existing knowledge o Biologic coherence is compatibility with knowledge drawn from a species other than the species from which the causal hypothesis was drawn o Statistical coherence is compatibility with a conceivable model of the distribution of cause and effect. More recently, Shapiro (2008) summarized the state of causation science and enumerated numerous factors that could be used to evaluate epidemiologic causation including: Time order Specification of the study base Specificity (precision) Classification bias Confounding Effect modification Strength of association Statistical stability Dose- and duration-response effects Internal consistency External consistency Analogy Biological plausibility The application of sets of criteria or postulates such as those proposed by Bradford Hill, Susser, or Shapiro has not been without its detractors and is debated frequently in the scientific literature (Kundi 2006, Rothman & Greenland 2005). Regardless of the ultimate outcome of these debates, causation criteria such as those proposed by Bradford Hill, Shapiro, and Susser,

5 especially when used in the context of evidence-based toxicology, are a valuable tool for risk assessors, toxicologists, and epidemiologists to use in evaluating accumulated weight of evidence in complex situations involving multiple and often confounding stimuli and responses, exactly the case with studies of health effects of WTE facilities. Case Study Perhaps the best way to evaluate the application of causation criteria to resolving questions of WTE public health impact is through use of a case study. WTE opponents (NTN 2013) have cited two epidemiologic studies (Garcia-Perez et al and Viel et al. 2000) as evidence that WTE facilities cause cancer. Garcia-Perez et al. (2013) is an ecologic study of cancer mortality in Spanish towns in the vicinity of industrial installations including various types of incinerators. Viel et al. is an ecologic study of the incidence of two types of cancer (non Hodgkin s lymphoma [NHL] and soft-tissue sarcoma [STS]) around a high-emitting incinerator in Besancon, France. In addition to being relied upon by WTE opponents, these studies focus on cancer which is relatively easy to analyze because of a wealth of biological and epidemiological knowledge in addition to being amenable to quantitative risk analysis. Additionally, from a public health epidemiological standpoint, these studies are scientifically sound and published in the peerreviewed scientific literature. Selected causation criteria statistical significance of associations, strength of associations, exposure, and consistency will be applied to the results of the studies to see if they support opponents claims of cancer causation. Before applying various causation criteria, it is necessary to discuss an issue that rarely arises in other aspects of public health epidemiology that of definition of the facilities under study. In many cases, the term incinerator is an umbrella term used in the types of studies we are evaluating here, even though there are substantial differences between different types and ages of waste combustion facilities. This term may apply to a combustor that burns municipal solid waste, non-hazardous industrial waste, hazardous waste, medical waste or other materials with or without energy recovery. In the study of Garcia-Perez et al. (2013), for example, the researchers test hypotheses potentially linking cancer mortality to proximity to an industrial category defined as an incineration. Close inspection of the underlying information base, however, reveals that one of the nine facilities included in this category would be defined as a hazardous waste incinerator in the United States and therefore would not properly fit the category of a WTE plant. Further, many incineration facilities addressed in epidemiological studies were constructed prior to the implementation of U.S. Environmental Protection Agency s (USEPA s) New Source Performance Standards, the European Commission (EC) Waste Incineration Directive (WID), or other equivalent regulatory systems. These older facilities may have operated without significant emission controls and do not reflect facilities operating today or currently proposed for construction. All of the nine incinerators studied by Garcia-Perez et al. were pre-2002 and five were pre The Viel et al. study is even more significant in this respect, because the facility was constructed in 1971 and had measured dioxin itef emissions of 16.3 ng/m 3 which are many orders of magnitude higher than the EC standard of 0.1 ng/m 3. In addition, this facility was not compliant with existing regulations. To insure applicability to actual systems, epidemiologic studies should present a description of the WTE facilities investigated including waste types handled, capacity, combustion temperature, pollution control devices, and stack characteristics. These characteristics are often not reported in the public health literature. Additionally, as a general matter, conclusions from studies of old incinerators cannot be 5

6 6 extrapolated to newer WTE plants that operate under regulatory programs such as the NSPS or WID. Exposure assessment is often the most critical component of an epidemiologic or risk assessment study for health effects potentially associated with waste management alternatives. The topic of exposure assessment is complex. For exposure to occur, a complete exposure pathway linking the source, medium of migration and receptor is necessary (EPA 1989). Exposure assessment involves a quantitative estimate of the amount of a toxic substance that reaches a target tissue. The reliability of the exposure assessment depends to a large extent on the location of the method on a hierarchy (Chrostowski 1994). The top of the hierarchy (most reliable) involves measurements at the target tissue. For example, if one is investigating the topic of the relationship of dioxin to liver cancer, this would involve a measurement of dioxin in a liver biopsy. Other levels in the hierarchy include non-target biological measurements>personal dosimetry>environmental exposure point concentration analysis>refined exposure models>screening exposure models>use of surrogates. In epidemiologic studies, the location on the hierarchy corresponds to the degree of exposure misclassification with the most at the bottom (surrogates) and the least at the top (target organ measurements). Most epidemiologic studies that assess exposure to incinerator emissions rely on surrogates and therefore are of limited reliability. Cordioli et al. (2013) reviewed 41 studies published between 1984 and January 2013 and reported that 30 of the studies relied on surrogates (linear proximity, presence or absence), 11 relied on screening models, and one relied on a refined model. These researchers concluded that there was a notable degree of exposure misclassification caused by the use of distance compared to dispersion modeling. Cordioli et al. recommended that further studies make full use of pollution dispersion models; localize population on a fine-scale; and explicitly account for the presence of potential environmental and socioeconomic confounding.

7 Many epidemiologic studies and most risk assessments of incinerators are concerned with dioxins which particularly complicates the exposure picture. Chlorinated dibenzodioxins and dibenzofurans comprise a family of 210 individual chemical compounds that normally occur together. Each source of dioxins is comprised of a distinct pattern of individual members known as a profile or fingerprint (Cleverly 1997). Because there are many sources of dioxins to the environment, valid exposure measurements should be made on the basis of the profile that is associated with MSW combustion. Dioxin reported as total PCDD/Fs or iteq will normally not reflect exposure to a single source. Additionally, in the case of dioxins and related compounds (e.g. PCBs), it has long been known that exposure through bioaccumulative pathways involving the human food chain is much more significant that airborne exposure (NRC 2000). Therefore, if hypotheses are being addressed that concern exposure to dioxin, modeling should also include atmospheric deposition and food chain biotransfer as well as dispersion. It is instructive to first examine the results of the Garcia-Perez et al. study that are relevant to incineration (eight other categories of industrial facilities were also reported in this study). The authors compared cancer mortality rates for individuals residing 5 km from the facilities compared to those at >5 km distances by calculating relative risk (RR) 1. A relative risk greater than 1 (RR>1) indicates a positive association and a confidence interval (CI) around a RR that includes 1 is conventionally not considered to be statistically significant. Risk ratios may also be negative (RR<1) indicating decreased risk. Bradford Hill considered the strength of an association to be a highly important criterion for causation, and several authors have developed scales for interpreting this risk metric. Shapiro (2008b) notes that RR estimates of 2.0 or less should be considered to be weak or small and any value less than 3.0 should be considered to be tentative. Craun & Calderon (2004) interpret RR of as having no strength, between as weak, and >1.5 as moderate to strong. The danger of a weak RR is that confounding can easily lead to a weak association between exposure and disease that is not related to the exposure under consideration. The data presented by Garcia-Perez et al. show that, out of 44 statistical tests conducted for the incineration category, six had positive associations with weak or no strength; all remaining results were not statistically significant. Garcia-Perez et al. went on to examine potential associations between specific incinerators and cancer mortality. For the category of all cancers, no incinerators had statistically significant associations. This was also true of all other cancer diagnoses evaluated except ovarian cancer for the incinerator designated by PRTR code 2438 (RR 1.95), brain cancer in women only for this same facility (RR 2.05), thyroid cancer in women only for PRTR 467 (RR 2.05), and thyroid cancer for women only for PRTR 4857 (RR 2.04). Two of these incinerators were built in 1975 and the other was built in Using the criteria above, these relative risks would be considered to be weak or tentative (Shapiro) or moderate to strong (Craun & Calderon). In summary, of nine old incinerators, three showed positive associations with various specific cancers in women only. Thyroid cancer was the only cancer with a positive association for more than one facility. Thyroid cancer in women in Spain has a substantially higher background incidence compared to thyroid cancer in men (Ferlay et al. 2013), thus there may be some gender related effects in this cohort. 7 1 Epidemiologists often report study results as rates or ratios of different kinds; relative risk, odds ratio, and standardized incidence ratio are typical of these risk metrics. A good source of information regarding these metrics and other terms used in this article is CDC:

8 Viel et al applied statistical tests for detecting disease clusters around the Besancon incinerator and calculated standardized incidence ratios (SIR) for two cancers (non Hodgkin s lymphoma [NHL] and soft-tissue sarcoma [STS]) rather than relative risks. The basis of calculation of the two metrics is substantially different. A RR compares incidence or mortality in the exposed population to a non-exposed population. A SIR compares incidence in a specific geographical location to that expected based on a larger database. In the case of the Viel study, the expected incidence was calculated based on data from the department of Doubs compared to the area proximate to the Bescancon incinerator. Viel et al. found statistically significant positive but weak SIRs of relationships for NHL and STS, respectively 2. They cautioned that these findings should be confirmed by further investigation. This caveat was not observed when this study was cited by NTN. Garcia-Perez et al. relied on distance (5 km circle) as a surrogate for exposure, a variable corresponding to the highest degree of potential exposure misclassification. Viel et al. also relied on an exposure surrogate (residence in a political jurisdiction), but did recognize the shortcomings of this assumption and proposed future work to refine the exposure assessment. In 2003, this group published results of a follow-up study using screening level air dispersion modeling as a surrogate for exposure, thus moving up a level in the hierarchy (Floret et al. 2003). STS was not reported in this publication and we, therefore, assume that it was not investigated. In the follow-up study, dioxin exposure was arbitrarily assigned to four categories based on the air dispersion modeling very low, low, intermediate, and high. Only the high category showed a statistically significant positive but tentative association (odds ratio (OR) of 2.3) compared to the very low category. Although the dispersion model was the heart of the exposure assessment, details regarding the model were not published. The modeling did not account for non-inhalation exposure and assumed that receptors were stationary. In 2010, this group presented a subsequent analysis based on blood serum measurements of individuals diagnosed with NHL and controls (Viel et al. 2011). In this publication, the authors found statistically significant positive associations between blood levels of the pesticide β-hcch, DDT, PCDD, PCDF, and PCBs. All of the associations were weak; the strongest association was for DDT (OR 1.20). The dioxin measured in the exposed population was not linked to dioxin emitted from the incinerator using environmental forensic techniques. Thus, the sources of exposure are unknown and, as a result, the occurrence of NHL may be a result of exposure from sources other than the incinerator. One of the most significant consequences of weak associations is that they are prone to errors associated with confounding (also see the Bradford Hill criterion of specificity). In the epidemiologic context, confounding exists when a risk factor other than the exposure under study is independently associated with the disease outcome (Shapiro 2008). If an association is strong, these effects are likely to be overcome, however, weak associations may be dominated by confounding. NHL is a case in point since there are many risk factors all associated with relatively weak associations. Bassig et al. (2012) reviewed the state of the evidence for NHL risk factors and uncovered an astounding list of associations that had been reported in the literature. These included smoking, alcohol, radiation, hair dye, diet, occupation, chemicals (solvents, pesticides, PCBs, medications), infectious agents, autoimmune disease, obesity, reproduction and family size, blood transfusion, and genetics. All of these factors would need to 8 2 An apparently anomalous result was a statistically SIR of 3.44 for STS in for the years No interpretation was given by the authors.

9 be controlled for in order to eliminate confounding for a weak association. For example, a recent study by Bulka et al. (2013) shows a statistically significant positive association between NHL and distance from benzene sources. Benzene is a known human carcinogen that is used as a solvent, is a component of gasoline, and is found as a product of combustion of many materials including tobacco. Simon et al. (2004) reported a benzene concentration of 2.2 ug/m 3 in the air of Toulouse for two measurement campaigns. Thus, even though the concentration of benzene in gasoline is limited in France where the Viel studies were performed, it still may be a significant contributor to NHL risk since it is found in the air of at least one French city.. As discussed above, the presence of dioxin as a chemical of potential concern complicates matters substantially. The form of dioxin that is most prevalent in WTE emissions is octachlorodibenzodioxin or OCDD (Cleverly 1997). OCDD exposure does not have a statistically significant positive association with NHL, however (De Roos 2005). This is an important confounding effect for WTE emission exposure that requires elimination for causation to be even considered and is especially relevant to the studies published by Viel and colleagues that attempt to link dioxin exposure to NHL. The final causation criterion to be examined here is that of consistency. Consistency in this context would be demonstrated by associations between exposure to WTE emissions and a health effect that were of similar strength to those in the two studies examined here. Independent studies investigating hypothetical associations between WTE and thyroid, brain, or ovarian cancers (as in the Garcia-Perez study) could not be located, therefore, there is no basis to assess consistency. Ranzi et al. (2011) investigated public health impacts associated with incinerators using air dispersion modeling. The study area contained both an MSW and a medical waste incinerator that were constructed in 1976 and 1991, respectively. Modeled heavy metal concentrations within 3.5 km of the two plants, based on emissions from both facilities combined, were used as a surrogate for exposure. The dispersion model would be characterized as a screening model in the context of the above discussion. These researchers found no statistically significant positive associations between exposure and NHL incidence and mortality among nearby residents compared to the regional population. Some of the associations reported were negative (decreased risk) of a strength characterized as weak to moderate/strong using Craun & Calderon s (2004) descriptors. Pronk et al. (2013) evaluated the risk of NHL at dioxinemitting facilities using a distance surrogate for exposure. MSW incinerators had a moderate to strong negative association (decreased risk) for people residing within either 3 km or 5 km for up to 15 years. As a side note, cement kilns had the strongest positive statistically significant association for NHL (OR 3.8) for people living within 3 km radii of the facilities. Reeve et al. (2013) assessed effects due to potential exposures to five WTE plants in the UK all of which were compliant with the WID. The study compared cancer incidence in 10 km circles around the WTE plants to those in control populations, using a binary exposure surrogate. The statistical modeling of risk was more sophisticated in this effort than normally encountered in epidemiologic studies of waste management options, although the exposure indicator was still based on a proximity-based measure. In comparing potentially exposed circles to control circles, these investigators found a weak and statistically non-significant negative association for NHL. Due to space limitations, not all studies involving NHL are reported here, however, the studies that we examined clearly show a lack of consistency regarding the putative association between WTE and NHL regardless of study type, exposure metric, or methods of data analysis. 9

10 10 Summary and Conclusions Two epidemiologic studies were reviewed using criteria derived from the literature on disease causation. Both studies involved hypotheses regarding exposure to incinerator emissions and human cancer and were scientifically sound from an epidemiologic standpoint. These two studies have been cited by opponents of new WTE facilities as scientific evidence for public health effects of WTE technology. In this article, we focus on three causation criteria strength of association, exposure, and epidemiologic consistency. The associations found in these studies are considered to be weak, the exposure assessment methods are subject to significant uncertainties which can lead to exposure misclassification and the epidemiologic evidence is inconsistent. This exercise reveals that there is no credible scientific evidence from these two studies to support the contentions of the WTE opponents. Thus, although these studies were scientifically sound considering the state-of-the art in environmental epidemiology, they failed to show that public health impacts were caused by WTE plants. Although the case study presented here is limited to a few facilities and cancer endpoints, ultimately these techniques may be used to address the general question of the ability of WTE to cause health effects. Ongoing work in this project includes an expansion to health endpoints other than cancer, application of additional causation criteria, integration of results from epidemiologic and risk assessment studies and expansion to waste management technologies other than WTE. References Bassig, B.A. et al Current understanding of lifestyle and environmental factors and risk of non-hodgkin lymphoma: an epidemiological update. Jour Cancer Epid. doi: /2012/ Bulka, C. et al Residence proximity to benzene release sites is associated with increased incidence of non-hodgkin lymphoma. Cancer, September 15:3309. CATI (Cardiff Against the Incinerator) Peer-reviewed and grey literature on incineration: the current understanding of health impact. January 3, Chrostowski, PC Exposure Assessment Principles. In Patrick, D.R. Toxic Air Pollution Handbook. Van Nostrand Reinhold, NY. Chrostowski, P.C. & Foster, S.A Recent findings from human health and ecological risk assessments of waste-to-energy technologies. SRA Annual Meeting, Baltimore, MD. Cleverly, D. et al The congener profiles of anthropogenic sources of chlorinated dibenzop-dioxins and chlorinated dibenzofurans in the United States. Organohalogen Compounds 32: Cordioli, M. et al A review of exposure assessment methods in epidemiological studies on incinerators. J Environ Public Health. Craun, G.F. & Calderon, R.L How to interpret epidemiological associations. WHO ERC

11 11 Ferlay, J. et al Cancer incidence and mortality patterns in Europe: Estimates for 40 countries in Europ J Cancer 49: Floret, N. et al Dioxin emissions from a solid waste incinerator and risk of non- Hodgkin s lymphoma. Epidemiology 14: GAIA Incinerators: Myths vs. Facts about Waste to Energy. Garcia-Perez, J. et al Cancer mortality in towns in the vicinity of incinerators and installations for the recovery or disposal of hazardous waste. Environ. Inter. 51: Hill, A.B The environment and disease: Association or causation? Proc. Royal Acad Med 58: Kundi, M Causality and the interpretation of epidemiologic evidence. Environ Health Perspect 114: National Research Council Environmental Epidemiology: Public Health and Hazardous Wastes. National Academy Press, Washington, DC. NTN Burning waste for energy: It doesn t stack up. National Toxics Network. NSW, Australia. Pronk, A. et al Residential proximity to industrial combustion facilities and risk of non- Hodgkin lymphoma: a case control study. Environ Health 12:20. Ranzi, A. et al Mortality and morbidity among people living close to incinerators: a cohort study based on dispersion modeling for exposure assessment. Environ Health 10:22. Reeve, NF et al Spatial analysis of health effects of large industrial incinerators in England, : a study using matched case-control areas. Rothman, K.J. & Greenland, S Causation and causal inference in epidemiology. AJPH 95(Suppl 1): S144-S150. De Roos, A.J. et al Persistent organochlorine chemicals in plasma and risk of non- Hodgkin s lymphoma. Cancer Res 2005: Shapiro, S Causation, bias, and confounding: a hitchhiker s guide to the epidemiological galaxy. J Fam Plann Reprod Health Care 34(2) et seq. Simon, V. et al. The impact of reduction in the benzene limit value in gasoline on airborne benzene, toluene, and xylene levels. Sci Total Environ : Susser, M What is a cause and how do we know one? Am J Epidem. 133: UK Health Protection Agency (UKHPA) The Impact on Health of Emissions to Air from Municipal Waste Incinerators: Advice from the Health Protection Agency. February Viel, J-F et al Soft-tissue sarcoma and non-hodgkin s lymphoma clusters around a municipal solid waste incinerator with high dioxin emission levels. Am J. Epid. 152:13-19.

12 12 Viel, J-F., et al Increased risk of non-hodgkin lymphoma and serum organochlorine concentrations among neighbors of a municipal solid waste incinerator. Env. Int.37: