Frequently Asked Questions About Studies on Incinerators
01 - Why does the study on dioxin exposure in the population show that incinerators contribute little to exposure, while the study on cancer incidence near municipal solid waste incineration plants indicates a health impact?
The two studies have different objectives. The study on cancer incidence near municipal waste incineration plants examines the link between the occurrence of cancer and past residence under the plume of an incinerator. The study on dioxin exposure in the population examines the link between dioxin exposure (measured by blood samples) and various contributing factors, including residence within the plume of an incinerator.
The two studies do not cover the same time periods. Pollution from incinerators has decreased over time. In the study on dioxin exposure in the population, the dioxin exposure measurements are recent; they reflect potential cumulative human exposure during the 10 to 15 years preceding the study (the 1990s and 2000s). In fact, the definition of exposed areas through plume modeling is based on cumulative surface deposits from 1994 to 2004. Biological samples were collected from February to June 2005. In the study on cancer incidence near MSW incinerators, a health effect is observed that results from even earlier past exposure, since exposure is defined as extending from the date the incinerator began operation (1972 at the earliest) through 1985, in order to account for the latency period (the time between the start of exposure and the first signs of cancer). This therefore corresponds to the 1970s and 1980s, a period when incinerators were generally more polluting and less regulated than in the 1990s, when regulatory efforts began.Furthermore, in the event that dioxin exposure plays a role in the onset of cancer (as suggested by some studies), the timing of exposure appears to be significant, as shown by animal experiments. Certain periods, particularly developmental periods (including in utero), may be more critical. It cannot be ruled out that even low levels of "excess exposure" occurring during these periods could contribute to an increased risk long afterward.
The two studies do not cover the same geographic areas, incinerators, or populations.Each study had to select its study area and population based on its specific objectives and feasibility. For example, the study on cancer incidence near municipal solid waste incinerators could only be conducted in departments where cancer registries existed. The contamination study had to be conducted in areas where there was a population that consumed locally produced food. In each of the studies, the populations classified as “unexposed” are different, and the “background noise” of their potential environmental contamination is different, which can influence the results. In a mountainous, low-pollution area (e.g., Gilly-sur-Isère), the background level is very low. Therefore, even if there is exposure via the incinerator, the health impact on the population may remain undetectable, which appears to be the case (results of the incidence study conducted in Gilly-sur-Isère).
The health impact measured by the cancer incidence study near MSW incinerators does not determine what, in the incinerator plume, is likely to have caused this impact: it is not just dioxins. The other pollutants emitted by incinerators are numerous: dioxins, furans, PCBs, CO, nitrogen oxides (NOx), sulfates (SOx), hydrochloric acid (HCl), cadmium, lead, chromium, mercury, arsenic, beryllium, aromatic hydrocarbons (PAHs), and particulate matter. Some of these substances are carcinogenic or potentially carcinogenic (PCBs, cadmium, chromium, lead, PAHs), and it is also possible that interactions between these substances play a role.
The health impact measured by the study—cancer incidence near MSW incinerators—does not preclude the route of exposure or the mechanisms that may be involved. Certain contaminants other than dioxins may have an impact via airborne exposure, contact with dust, etc. This therefore represents an overall impact of exposure to the emissions from the older incinerators included in the study, taking into account various potential exposure routes, and does not prejudge the substances or mechanisms involved. Various hypotheses can be proposed. For example, certain cancers such as non-Hodgkin lymphoma (NHL) are partly linked to infectious risk factors (viruses)(1). Exposure from incinerators that contributes to disrupting immune mechanisms could play a role in the increase in the number of NHL cases observed in exposed areas.Another example: a French study (2) showed that women with a specific genetic predisposition (cytochrome P4501B1 polymorphism) who were exposed to emissions from an incinerator for more than 10 years had a 3.26-fold higher, compared to unexposed women who did not have this polymorphism. This illustrates the possibility of gene-environment interactions, a key area of research for understanding the mechanisms of cancer.
The study on dioxin exposure in the population does indeed show a low overall contribution of incinerators to population exposure compared to other factors (age, dietary habits, exposure to other sources, etc.), but it reveals a notable contribution among consumers of local products exposed to incinerators. In the graph on page 12 of the summary, which details different population categories, it is noted that the exposure levels of populations exposed to incinerators are always higher than those of unexposed populations, except in the case of individuals who consume their own produce. Furthermore, the exposure levels of farmers who consume their own local produce in exposed areas are significantly higher than those of other population categories.
In conclusion, there is no contradiction between the two studies, and their results can be interpreted consistently if all the analyzed data are taken into account.
02 - Why is the risk measured in the study on cancer incidence near MSW incineration plants an order of magnitude lower (8.3%) than that measured in 2003 in Jean-François Viel’s study around the Besançon incinerator regarding non-Hodgkin lymphomas (130%)?
We can only speculate on this question, as the studies are different. The exposure-risk relationship observed in the study on cancer incidence near MSW incinerators was determined by taking into account emissions from 16 incinerators, each with different characteristics, whereas Jean-François Viel’s study focused on a specific incinerator—the one in Besançon—which is among the oldest (1971) and known for being particularly polluting. Measurements taken in eggs from hens raised in the vicinity of this incinerator showed very high levels of dioxins, which supports this hypothesis. Furthermore, there are numerous community gardens in the vicinity of this incinerator, and it can be assumed that the consumption of local produce is significant. It would also be necessary to examine dioxin contamination in areas not exposed to this incinerator, which may be particularly low, which would explain, in the event of a causal relationship, a greater contribution from the incinerator in that location. Other hypotheses could also be considered: the existence in this particular area of other unidentified sources of dioxins that may be linked to local practices (e.g., burning, spreading of ashes...), the presence of other risk factors for NHL (infectious factors, other immunotoxic exposures, etc.), or the existence of specific variations not accounted for in the calculation of the reference population between 1980 and 1985, the study period.
03 - The study on dioxin exposure in the population concludes that the route of dioxin exposure via inhalation plays a negligible role compared to the dietary route in the vicinity of incinerators. How, then, can we explain the high levels of dioxins measured in some studies (while others are negative) among workers exposed to dioxins?
Occupationally exposed workers operate in confined spaces and are therefore much more exposed via the respiratory route, but also possibly via the digestive tract (ingestion of dust) or the skin (there is skin absorption because dioxins are lipophilic).
04 - One of the most striking findings of the study on cancer incidence near MSW incinerators is the increased risk of breast cancer in women. Is this the first time this risk has been identified? How can this result be explained, given that this cancer is not typically suspected of being linked to dioxins?
To our knowledge, this is the first time this risk has been identified in connection with exposure to incinerators in the general population. However, this is not the first time a link between dioxin exposure and breast cancer in women has been observed. In a cohort of 981 women exposed to the Seveso accident (1976), a study showed a 2.1-fold increased risk of breast cancer for a 10-fold increase in blood dioxin levels (3). However, the number of cases was low (15 cases). In occupationally exposed cohorts, there are few women, so this cancer has generally not been studied. There is a Russian study showing an excess risk of breast cancer mortality among female employees of a factory that produced herbicides heavily contaminated with dioxins for 30 years (4). In another 1991 study, Manz et al. noted an increased risk of breast cancer in a cohort comprising female workers exposed at a factory in Germany producing herbicides heavily contaminated with dioxins (5). Finally, the previously cited French case-series study on a higher risk of breast cancer (OR=3.26, [1.20–8.884]) among women with a genetic polymorphism who were simultaneously exposed to incinerators, compared to unexposed controls with the complementary polymorphism, illustrates the possibility of a genetic susceptibility linked to environmental exposure to incinerators. In summary: dioxins, by acting on the nuclear AhR receptor, induce the expression of the valCYPP1B1 gene (in individuals with this polymorphism), which leads to an increase in a genotoxic compound resulting from estrogen catabolism, 4-OH catechol-estradiol. Such mechanisms could explain the occurrence of cancers even at low doses in susceptible individuals. The biological plausibility of a role for dioxins in the development of breast cancer is supported by numerous other studies. This plausibility is even suggested in cases of prenatal exposure affecting the next generation. Indeed, animal studies have shown that in utero exposure to dioxins can lead to breast development disorders (6): delayed proliferation and differentiation of the mammary gland, and an increased window of susceptibility to other carcinogens.
A scientific consensus appears to be emerging regarding the classification of dioxins as a multisite carcinogen (a view reaffirmed at the 2006 ISEE/ISEA Congress in Paris), with new studies published since the IARC’s 1997 classification of TCDD as a definite carcinogen seeming to support this conclusion: see a recent review (7). It is therefore not impossible that dioxins are involved in other types of cancer, particularly melanoma, as an increased risk for this tumor has been observed among American soldiers in Vietnam exposed to Agent Orange (8), but this remains to be confirmed.
