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Dioxins
Sources and Health Effects
Terminology. The term "dioxin" or "furan" technically refers to the basic structure of the molecule, which is composed of carbon and oxygen. Through reactions involving halogens, such as chlorine or bromine, dioxins and furans acquire toxic properties. Almost all research on halogenated dioxins and furans has focused on chlorinated species—polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). There are 75 different PCDDs and 135 different PCDFs. Each compound has a distinct number and configuration of chlorine atoms. These differences in chemical structure produce varying levels of toxicity among the PCDD/F family. Although it is technically inaccurate, PCDD/Fs are frequently referred to as dioxins. To minimize confusion, the authors will use the most specific notation available in the literature. The general terms "dioxins" and "dioxin" are assumed to refer collectively to PCDD/Fs.
Sources. PCDD/Fs have no intentional use. They are produced as byproducts of municipal waste combustion, residential coal combustion, secondary aluminum smelting, open barrel burning, and medical waste incineration (1, 2, 3). Recent mass balance analysis suggests that atmospheric formation is also a significant source of PCDD/F deposition (4). However, the researchers note that this mechanism creates congeners with low toxicity, creating little additional risk for people and the environment. The U.S. EPA, in a 1994 draft document, estimated that although only 30 pounds of dioxins are emitted annually, everyone has been exposed to them (5). Other sources suggest that the emission rate is almost 900 pounds per year (6). In 1998, the EPA released its assessment of PCDD/F sources in the United States. According to this report, medical waste incineration is the third largest source of PCDD/Fs (7). Table 1 summarizes the contributions of the top sources.
Table 1: PCDD/F emissions in the United states (I-TEQ/yr).
[Percentages derived from Cleverly et al, 1999.]
Pathways and Exposure. Dioxins degrade very slowly, having an estimated half-life in humans ranging from 7.5 years (1) to 10 years (5). PCDD/Fs are released into the atmosphere, typically attached to particulate matter (2). They redeposit on the land and settle onto plants and soil. When animals ingest plant matter that has dioxin residuals on them, the dioxins bioaccumulate in the animal fat (8). Dioxins are also deposited on bodies of water and then ingested by aquatic organisms, which are in turn eaten by humans. The dioxins are deposited in fatty tissues and bioaccumulate up the food chain. The main route of human exposure is ingestion through fish, meat, and dairy products (1). The most toxic of the PCDD/F group is 2,3,7,8-tetrachlorodibenzo-p-dioxin, or TCDD. The health effects of TCDD have been scrutinized in animal and epidemiological studies since the 1970s.
Animal studies. Earlier animal studies focused on toxicity and carcinogenicity. Toxicological studies in animals have demonstrated carcinogenicity of TCDD in rats, mice, and hamsters. These cancers affected the liver, skin, lung, thyroid, tongue, and hard palate (9).
Recent research has investigated the effects that TCDD may have on the endocrine and immune systems. Studies using significantly lower doses than administered in earlier studies indicate that TCDD has the most profound, long-lasting effect on rats exposed to the substance prenatally. These effects can be seen even at sub-toxic levels. Endocrine system effects include decreased testosterone levels, lowered sperm production, delayed or decreased development of accessory sexual organs, and feminized adult sexual behavior in male offspring exposed prenatally to TCDD (10). Immune system effects include suppression of fetal thymocyte differentiation in mice (11) and inhibition of B cell maturation (12, 13). Some researchers speculate that endometriosis in humans may originate in an altered immune response caused by TCDD (14).
Human studies. Epidemiological studies have focused on the results of occupational and other accidental exposures, mostly focusing on the mortality rate from cancer. Several studies have noted an increased incidence of soft-tissue sarcoma in workers exposed to TCDD through exposure to synthetic chemicals (9, 15, 16). Other studies suggest a potential TCDD link to lymphomas (17) and nasal and nasopharyngeal cancer (18).
To assess the link between TCDD exposure and human cancer risk, the International Agency for Research on Cancer (IARC) undertook a comprehensive analysis of scientific literature on dioxins and furans. Evidence amassed in the IARC study suggests that TCDD acts as a promoter, not as a direct cancer-causing agent. TCDD evidently binds to the Ah receptor in the cell and alters the expression of genes involved in cell growth and differentiation. This mechanism is similar in humans and in experimental animals. Comparable TCDD tissue concentrations were found in the human cohorts who exhibited an increased incidence of cancer and in rats exposed to carcinogenic doses of TCDD. The IARC’s overall evaluation of TCDD was that it is "carcinogenic to humans." The other dioxin compounds were evaluated as "not classifiable as to their carcinogenicity to humans" (1). A subsequent study of the human cohort examined by IARC found statistically significant positive correlations between TCDD exposure and cancer, but only for those workers whose exposure was 100-1000 times greater than that of the general public (19). In June 2000, the U.S. EPA released a draft report reassessing the human health risks posed by dioxin exposure. In response to new evidence, the report included cancer risk estimates that are as much as ten times higher than previous estimates (20).
Consensus in the literature. In contrast to the example of mercury, there is considerable lack of consensus about the severity of health risks associated with dioxin exposure. The first major argument is actual human exposure level. The average TCDD level in human fatty tissue has decreased sharply in the past 20 years (1). Concern over dioxin exposure remains because of more subtle threats to human health than cancer or death. In light of the new evidence that extremely low levels of dioxins can alter the development of fetuses, even this minute concentration may be undesirable.
A second argument revolves around the link between incineration of halogenated plastics and formation of dioxins. The available scientific literature on this topic contains conflicting evidence that a causal relationship exists. Yet it is evident that, since halogens are an essential component of dioxins, some type of halogen (for example, chlorine) must be present in the waste stream to form dioxins.
Healthcare Waste Incineration and Dioxin Production
Use of halogenated plastics in healthcare. Healthcare waste has a distinct material composition that may create significant environmental concerns. Healthcare wastes are known to contain a greater concentration of plastics. Studies that have focused on distinctive departments within healthcare facilities have supported this finding (21, 22). Plastics comprise about 15 percent of healthcare wastes (23). In contrast, the total plastics content of municipal solid waste, before recycling, is only 9 percent (24). This prevalence of plastics in healthcare waste is due to the preference for single-use, disposable products to minimize the possibility of infection.
The most prevalent halogenated plastic in healthcare waste is polyvinyl chloride. Commonly known as PVC or vinyl, this plastic has been in use for over forty years. The versatility of this plastic has led it to be found in as many as 25 percent of all healthcare products (25). Many medical products, including blood and IV bags, dialysis tubing, catheters and inhalation masks, contain PVC (26). Note that PVC is not the dominant plastic used in healthcare facilities. In some cases, the dominant plastic is LDPE, HDPE, PS, or PP. Table 2 lists common applications of various plastics in healthcare. PVC, which is about fifty percent chlorine by weight, is a significant source of chlorine in medical waste streams (6).
Table 2: Types and uses of plastics in healthcare products.
Incineration of PVC and formation of dioxins. The dioxin emissions from medical waste incinerators may be as high as twice the emissions from municipal solid waste incinerators (6). Results of a recent lab-scale reactor study showed that combustion of chlorinated materials produced about ten times more dioxins than combustion of non-chlorinated materials (27). An extensive review of dioxin emission data suggests a causal relationship between the amount of chlorine in an incinerated waste stream and the emissions of dioxins (6).
Most of the relevant experiments have burned municipal solid waste to determine the connection between PVC input and dioxin output; relatively few studies have focused on medical waste incinerators. Some investigators have concluded that the combustion of PVC does not create significant amounts of PCDD/Fs. One well-publicized study found no relationship between chlorine input and dioxin output (28). However, this experiment only measured gas-phase dioxins. Other studies have found that the addition of PVC to municipal waste did not increase PCDD/F emissions upon incineration (29, 30, 31). The combustion formation of halogenated organic compounds like PCDD/Fs is very complex. The following laboratory results, taken together, create a plausible mechanism for PCDD/F formation from PVC combustion.
At temperatures above 300 oC, incineration of PVC leads to production of hydrogen chloride gas (HCl) and chlorobenzene (32). Sufficient evidence exists that chlorinated compounds such as chlorobenzenes and chlorophenols act as precursors, or key intermediates, to PCDD/F formation (33, 34, 35). Combusting PVC with phenol resin at 600 oC in the presence of HCl results in a dramatic increase in PCDD/F production (36). Several studies indicated that there is an exponential relationship between HCl injection and PCDD/F production from hydrocarbon combustion (37, 38).
A wide range of substances can affect the PCDD/F formation reaction. Besides PVC, inorganic chlorine compounds such as HCl, Cl2, KCl, NaCl, CuCl, CuCl2, and FeCl3 can act as source of chlorine (39). Copper compounds are noted as important catalysts for PCDD/F formation (33, 39, 40). The formation of PCDD/F may be inhibited by the absence of oxygen (37, 39). Sulfur has been noted as both an inhibitor (41, 42) and a catalyst (33).
The available literature suggests that the optimal temperature for PCDD/F formation is 250-400 oC (33, 39, 43). While PCDD/F can be destroyed at temperatures above 900 oC, these compounds can also be formed in the postcombustion zone of incinerators, where temperatures are lower. Cooling of the exhaust gases is necessary before entry into pollution control devices, particularly fabric filters. It has been noted that high temperature combustion promotes the formation of PCDD/F precursors such as chlorophenols (33)
Effects of pollution control devices. It is conceivable that when fly ash is captured in devices such as baghouses or electrostatic precipitators (ESPs), conditions favor PCDD/F formation. At low temperatures, carbon structures in fly ash can be broken down, coupled into non-chlorinated dibenzo-p-dioxins and –furans, and chlorinated to form PCDD/Fs (44). This theory is supported by the results of one experiment in which the levels of PCDD/F in fly ash were higher after the baghouse filter than before it. Although overall particle filtration efficiency was greater than 99 percent, PCDD/F particulate removal efficiency was only 50 percent (33). Another study of a full-scale municipal waste combustor exhibited dramatic increases in total PCDD/Fs after the ESPs, supporting the hypothesis of PCDD/F formation in pollution control equipment (45). Recently obtained evidence suggests that substances in the fly ash produced in the incineration process may catalyze dioxin-producing reactions (27).
Some evidence exists that granular activated carbon (GAC) can capture significant amounts of dioxins and furans from the flue gas stream (46). When the GAC supply is exhausted, however, it must be replaced. This creates a solid waste disposal problem that may add to the already high cost of operating a GAC pollution control device. One company has recently developed special catalytic baghouse filters that convert dioxins and furans to water, carbon dioxide, and hydrochloric acid (47). However, hydrochloric acid is a known respiratory and sensory irritant (32).
Healthcare facilities whose medical waste incinerators are equipped with pollution control equipment report significant volumes of ash and lime waste from the equipment that need to be disposed of as solid wastes. At one facility, this waste amounts to more than 400,000 pounds per year. Even though the facility has reduced red bag waste volumes and increased recycling waste volumes, reducing overall actual waste volumes, they have seen a sharp increase in waste going to the landfill. The ash residuals and pollution control device wastes account for that increase (48).
Although as many as 80 percent of on-site medical waste incinerators are predicted to close down due to stricter emissions regulations (49), alternative treatment schemes may be equally problematic. In a situation where medical waste is sterilized and sent to a municipal waste incinerator, problematic materials such as mercury and halogenated plastics remain in the waste. Infectious potential of the waste stream is reduced, but the potential for mercury and dioxin emissions remains.
Even if incinerators are operated at ideal conditions, the potential for dioxin formation may remain, and the amount of pollutants removed must eventually be disposed of. The theory of post combustion PCDD/F formation suggests that the reactions occur on fly ash particles collected in pollution control devices such as fabric filters and ESPs. If this theory holds true, many pollution control devices currently in use are unable to remove significant amounts of PCDD/Fs from the fly ash since the ash collection method encourages PCDD/F formation.
References
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