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Exposure Investigation Report



Biological Samples


Dioxin-like compounds are widespread environmental contaminants and have been detected inhuman blood, adipose tissue, and milk. Using a sensitive analytical methodology, dioxin-likecompounds can be detected in almost all residents of industrialized and non-industrializedcountries. The major source of exposure to dioxin-like compounds in the general population isfrom food (beef, dairy products, and fish), with smaller exposures from air, water, and soil [2]. Based on available data, it has been reported that concentrations of dioxin-like compounds inhumans do not vary significantly by race, gender, or geographic region; however, concentrationsof dioxin-like compounds do increase with age [2].

During the past 20 years, environmental releases of dioxin-like compounds have decreasedbecause of the switch to unleaded automobile fuels, process changes at pulp and paper mills,improved emission controls on incinerators, and reductions in the manufacture and use ofchlorinated phenolic intermediates and products. This has been accompanied by decreases inbody burdens of dioxin-like compounds. In the EPA National Human Adipose Tissue Survey(NHATS), adipose tissue concentrations of CDDs and CDFs decreased by 9 to 96 percent from1982 to 1987 [6]. In Germany, where extensive dioxin biomonitoring has been conducted, blooddioxin levels fell from 45.8 ppt TEQs (lipid-based) in 1988 to 16.1 ppt in 1996 [7]. Also inGermany, breast milk concentrations of dioxins decreased from 32.5 ppt (lipid-based) in 1987 to23.0 ppt in 1991 [8].

To date, no large-scale study of the levels of dioxin-like compounds in a statistically-basedsample of the United States population has been conducted. ATSDR and other researchers haveoften cited reference ranges tabulated from studies conducted in the 1980s [9]. Since dioxinlevels in the environment and in human populations have been decreasing [10], the use of suchstudies to derive comparison ranges for present day populations is not appropriate. Therefore,ATSDR, in collaboration with NCEH, developed comparison levels for blood dioxin levels inthe United States population based on studies conducted in 1995-1998. Some backgroundinformation on these comparison levels is presented in Appendix 1.

As indicated in Table 1, blood dioxin TEQ levels were elevated in the Mossville EI participants. The median (54.8 ppt) and mean (68.3 ppt) concentrations of dioxin TEQs in the EI participantsexceeded the 95th percentile concentration (37.5 ppt) of the comparison population. Furthermore,the concentrations of several individual CDDs and CDFs in the Mossville population wereelevated as compared to the comparison levels. The blood serum levels of 1,2,3,7,8 pentachloro-dibenzo-p-dioxin (PeCDD) in the Mossville residents were particularly elevated. The meanconcentration of PeCDD in the EI participants (28.8 ppt) was more than 3-fold higher than the 95th percentile concentration (9.1 ppt) of the comparison population. The mean concentrations of2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) and the hexachlorodibenzo-p-dioxin congeners inthe EI participants also exceeded the 95th percentile concentrations of the comparison population.

Although the concentrations of many of the dioxin-like compounds were elevated, theconcentrations of some of the congeners were similar to or less than the comparison population. Therefore, the profile of dioxin-like compounds in the EI participants was distinctly differentfrom the comparison population.

One of the EI participants had worked for a chemical company four years prior to the EI. Theblood dioxin TEQ level in this individual was 23 ppt, which is close to the mean of thecomparison population.

The source of dioxin exposures in the Mossville residents is not known. Pentachloro-dibenzodioxins are produced during combustion processes and have been identified in emissionsfrom municipal waste incinerators, cigarette smoke, wood and coal combustion, waste oilfurnaces, and fires of polyvinylchloride (PVC) materials [11, 12]. Hexachlordibenzodioxins(HxCDDs) have been identified in emissions from municipal incinerators and industrial wasteincinerators [12]. Known sources of TCDD include incineration of municipal refuse and certainchemical wastes, chlorine bleaching of wood pulp, and as a byproduct of certain chemicalmanufacturing processes. Laboratory studies have also demonstrated that CDDs and CDFs can be formed from burning PVC-containing materials [13].

In the general population, low level dioxin contamination of foodstuffs is the major contributorto the body burden of dioxins. The State of Louisiana has issued an advisory to limit eating offish from Bayou d'Inde in Calcassieu Parish because of contamination with polychlorinatedbiphenyls, hexachlorobenzene, and hexachlorobutadiene. However, to date, fish from the areahave not been tested for dioxins.

Because dioxins are resistant to metabolism in the body, they bioaccumulate as a person ages. Therefore, blood dioxin levels tend to increase with age. In selecting the EI participants, ATSDRgave preference to older individuals who were long-term residents of the neighborhood, becausethey were at greater risk for cumulative exposures to dioxin. The age of the Mossville residentswho participated in blood testing ranged from 20 to 83, and the average age was 53. Most of theEI participants were long-term residents of Mossville, and the average length of residency in theneighborhood was 32 years.

Regression analyses were conducted to evaluate the relationships between blood dioxin levels,age, and length of residency in Mossville. Age was strongly correlated with blood dioxin level (R2 = 0.657, p < 0.001). Length of residency in Mossville was also correlated with blood dioxinlevel (R2 = 0.252, p < 0.0065), but the correlation was weaker than with age. Using multipleregression analyses, it was determined that if age were controlled for, there was not a significantcorrelation between blood dioxin level and length of residency.

To further assess the relationship between age and blood dioxin level, ATSDR plotted blooddioxin TEQ levels vs. age for the comparison population and the EI participants. Figure 1 showsthat the blood dioxin levels increased in the comparison population as a function of age. Blooddioxin levels in the EI participants also increased with age, but the age-related increase wasgreater in the EI participants than in the comparison population. As shown in Figure 1, theelevations in blood dioxin levels were most pronounced in EI participants who were aged 47 and above.

The reason for the selective elevation in blood dioxin levels in the older EI participants is notknown. One possibility is that older residents have elevated dioxin levels because of exposure todioxins that occurred in the past. Dioxin-like compounds are resistant to metabolic degradation,so after being absorbed into the body, they persist for long periods of time. In occupationally-exposed workers, the biological half-lives of dioxin congeners range from 3.0 to 19.6 years [14]. The half-life of PeCDD, which is a major contributor to the TEQ total in the EI participants, is15.7 years [14]. It has also been reported that the half-lives of dioxin congeners increase as aperson ages and can increase as body fat increases or if a person has liver disease [14]. Therefore, the elevated blood dioxin levels in the EI participants could be the result of exposuresthat occurred many years ago.

Figure 1. Concentration of dioxin TEQs in serum (ppt) vs age

The health significance of the dioxin blood levels measured in this study is unclear. Althoughdioxin is extremely toxic in some animals, humans appear to be more resistant to its toxicologiceffects than most animals in which it has been tested. The primary clinical health effects thathave been observed in humans exposed to high levels of dioxin through occupational oraccidental exposures have been chloracne and transient mild hepatotoxicity (15, 16). Varioustypes of cancer and non-cancer health effects also have been associated with exposure to dioxinin some studies (17). However, study results have been inconsistent in demonstrating theseeffects. In those studies in which a significant association was shown, the increased risk hasbeen relatively small and difficult to interpret due to an inadequate exposure assessment ormultiple chemical exposures.

For example, a recently published study reported a statistically significant association betweenrisk of all cancers combined and occupational exposure to dioxin (18). However, the risk ofcancer was relatively small (i.e., standard mortality ratio generally less than 2.0) and was seen inthe most highly exposed group with estimated exposures 100-1000 times those seen in thegeneral population. The study also notes that some individuals had evidence of significantexposure to other carcinogenic substances, such as asbestos (mesothelioma and lung cancer) or4-amino-biphenyl (bladder cancer), further complicating interpretation. This study and mostpublished dioxin health studies have mainly been limited to an evaluation of exposure to TCDD. It is unclear whether other dioxin congeners are associated with similar types of health effects in humans.

In studies for which exposure data are available, the blood TCDD levels associated withchloracne or increased cancer have been significantly higher than those detected in this EI. Forexample, in humans exposed to dioxin in the workplace, chloracne has been observed at body burdens of 95 to 3,000 ng dioxin/kg body weight [19]; this corresponds to blood dioxin levels of 432 to13,400 ppt (lipid-based). All of the blood dioxin levels in the Mossville test population were below this range.

In occupationally exposed workers, an increased incidence of cancer has been associated withdioxin body burdens of 109 to 7,000 ng dioxin/kg body weight [19]. This dose corresponds to blood dioxin levels of 495 to 31,800 ppt of blood dioxin (lipid-based), which exceed the blooddioxin levels in the Mossville test population.

Although no clinical health effects can be attributed to the levels of dioxin detected in Mossvilleresidents, the levels are elevated as compared to comparison populations. Therefore, it would beprudent public health policy to determine if residents are currently being exposed toenvironmental sources of dioxin and to implement actions to minimize further exposures.

    Breast Milk

Dioxin levels in breast milk tend to decrease with the number of children and the duration offeeding, but increase with the age of the mother [2]. In a study of 42 United States women, theaverage breast milk concentration of dioxin TEQs was 16 ppt (lipid-adjusted) [20]. The dioxinconcentration in the breast milk sample from a Mossville mother was 13.5 ppt (lipid-adjusted),which is less than the cited comparison level. The levels of dioxin detected in breast milk fromthis woman would not pose a health hazard to her infant, and continued breast feeding is encouraged.

Environmental Samples


Surface soil samples were collected from three residential yards located across the street from the chemical plant. The concentrations of dioxin TEQs in the samples ranged from 0.004 to 0.028 ppb. ATSDR set an Action Level of 1 ppb for dioxin contamination in residential soil[21]. The levels of dioxin contamination detected in surface soil from three Mossville yards were 36 to 250 times less than the ATSDR Action Level and do not pose a health hazard.

At one house, surface soil from the front yard contained 0.019 ppb dioxin TEQs, and surface soilfrom the resident's chicken coop contained 0.0006 ppb dioxin TEQs. The owner reported thathe had placed clean sand over the dirt floor of the coop, which may explain the lower dioxinconcentration in surface soil inside the pen.


The concentration of dioxin detected in two chicken eggs from Mossville were about 2 timeshigher than the concentration of dioxin detected in an egg from a Kansas City supermarket. Thesource of the supermarket egg is not known, but it likely came from a commercial farm wherechickens are raised in indoor pens. Such a chicken would have no contact with outdoor, background levels of dioxin contamination, hence the relatively low egg dioxin level.

Low concentrations of dioxin-like compounds are ubiquitous in the environment, so it is notsurprising that low concentrations of dioxin are present in chicken eggs. Other published studies,listed below in Table 3, confirm that low concentrations of dioxin are commonly found in eggs,especially from foraging chickens. Similar concentrations of dioxins have been detected in meatand dairy products from the United States and other industrialized countries [2]. The levels ofdioxin detected in the Mossville egg samples do not pose a health hazard.

Table 3.

Dioxin TEQ concentrations in chicken eggs and soil
  Egg ( pg/g lipid) Soil (pg/g)
Exposure Investigation    
Kansas City supermarket 0.946 --
Mossville # 1 2.09 0.6
Mossville # 2 1.76 0.6
Reference study    
Schuler et al. (Switzerland) [21] 1.3 (caged) -
  3.5 (foraging) 1.4
  6.1 (foraging) 1.3

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