Human Exposures to PCDDs and PCDFs

For risk assessment purposes, an important objective in evaluating the environmental fate of PCDD/Fs is predicting the major pathways of human exposure. It is well established that the food chain, especially meat and dairy products, accounts for more than 90% of human exposure to PCDD/Fs and perhaps as much as 99% of human exposure to 2,3,7,8-TCDD.34 In industrialized countries, the average daily intake via food (the major route of exposure to dioxins and furans) ranges from 1.5 to 2.5 pg TEQ kg-1 body weight. 

Other potential pathways of exposure-air inhalation, ingestion of water and soil, and dermal contact with soil-are much less significant to total daily intake of dioxins. PCDD/F intake via air inhalation, water ingestion and soil ingestion is estimated to be 3.2 pg TEQ d 1 (2-3% of total daily intake).38 Dermal contact with soil is negligible, however, constituting an estimated daily intake of 0.15pg TEQ d-1.38 

Ultimate proof of the widespread exposure to TCDD is exemplified by the fact that virtually all human adipose tissue samples contain TCDD at trace levels of 6 ppt.60 Adipose tissue of non-occupationally exposed humans has been found to contain concentrations of 18-122 pg TEQ g 1 fat, with a mean value of 56pg TEQ g 1 fat,43 a value 22 times higher than the concentration in beef fat (2.6 pg TEQ g 1 fat). 

Route/source The Netherlandsa UKb Germanyc USA North Americae 

The EPA has established63 a virtually safe dose of 0.006 pg TEQ kg 1 d1, which represents one excess cancer in a million in exposure population. Many European countries use the World Health Organization value of 10 pg kg 1 d 1 Tolerable Daily Intake (TDI). US daily intake of PCDD/Fs by the general population (1.8 pg TEQ kg 1 d1) greatly exceeds the EPA s virtually safe dose, but falls within the World Health Organization TDI. 

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Human exposure to PCDDs and PCDFs may be due to either specific exposure, mainly of occupational origin, or due to a general exposure of the public. 

The food chain has been shown to be the primary pathway of human exposure to PCDDs and PCDFs (Table 5).34 39 We will examine the accumulation of dioxin in those foods found in the average American diet fruits and vegetables, beef, milk and dairy products, and fish. 

The following example shows how TEQ values are calculated. 2,3,7,8-TCDD has TEE = 1 (asdefined) 2,3,4,7,8-pentachlorodibenzofuran(pentaCDF)has TEF =0.5. Therefore, a mixture of 2 ng TCDD + 6 ng pentaCDF has an assumed toxicity equivalent to 2ng TCDD + (6 x 0.5) ng TCDD, or 5 ng TCDD altogether. Estimates of human exposure to PCDDs and PCDFs in the environments are ca. 0.1 ng TCDD TEQ per person per day, mainly from food. 

Human exposure to PCDD and PCDF occurs mainly via food. As with PCBs, it is expected that dietary intake represents up to 95% of the total amount of PCDD and PCDF. For the purpose of assessing health risks associated with exposure to these POPs, many countries have conducted studies to estimate their daily intake. Examples are given in Table 12.43. Attempts to find a correlation between the amount of PCDD and PCDF in a given area and their contents in human adipose tissue were generally unsuccessful, except in mral areas where a greater proportion of locally produced food is consumed. If an increased contamination is fi om a local source in these areas, higher levels... 

Importantly, past and present human exposure to PCDD/PCDFs and PCBs results primarily from their transfer along the pathway atmospheric emissions air deposition -> terrestrial/aquatic food chains - human diet. Information from food surveys in industrialized countries indicates a daily intake of PCDD/PCDFs on the order of 50-200 pg I-TEQ/person per day for a 60 kg adult, or 1-3 pg I-TEQ/kg bw per day. If dioxin-like PCBs are also included, the daily total TEQ intake can be higher by a factor of 2-3. Recent studies from countries that started to implement measures to reduce dioxin emissions in the late 1980s clearly show decreasing PCDD/PCDF and PCB levels in food and, consequently, a lower dietary intake of these compounds by almost a factor of 2 within the past 7 years. 

Table 1 Carcinogenic and non-carcinogenic effects associated with human exposures to PCDDs/PCDFs...

PCDD/PCDFs are today found in almost all compartments of the global ecosystem in at least trace amounts. They are ubiquitous in soil, sediments and air. Excluding occupational or accidental exposures, most human background exposure to dioxins and PCBs occurs through the diet, with food of animal origin being the major source, as they are persistent in the environment and accumulate in animal fat. 

PCDDs, PCDFs and PCBs are highly fat-soluble and accumulate in adipose tissue. They can also pass through the placenta and are excreted in human breast milk, resulting in exposure of the nursing infant (Table 8.4). The results from UK participants in a WHO inter-laboratory trial showed that the concentrations of PCDDs and PCDFs fell from 29-37 ng I-TEQ/kg milk fat in 1987-1988 to 21-24 ng I-TEQ/kg milk fat in 1993-94.44 Although PCBs were not analysed in 1987-1988, the concentrations in the 1993-94 milk samples were 10-12 ng I-TEQ milk fat. The concentrations were similar to those reported by other European countries and other participants in the WHO trial. 

Wild SR, Harrad SJ, Jones KC. 1993. The influence of sewage sludge applications to agricultural land on human exposure to polychlorinated dibenzo-p-dioxins (PCDDs) and -furans (PCDFs). Environ Pollution 357-369. 

Brouwer A, Ahlbord UG, van Leeuwn FXR, et al. 1998a. Report of the WHO working group on the assessment of health risks for human infants from exposure to PCDDs, PCDFs and PCBs. Chemosphere 37(9-12) 1627-1643. 

PCDD and PCDB are found widespread in the human population in a similar fashion to PCB, DDT and its metabolites, chlorobenzenes, and other common persistent organochlorines. Since food is influenced by environmental residue trends, human residue levels and exposure levels will likely follow environmental trends closely. In the Great Lakes basin area overall trends are not declining for either PCB or PCDD and PCDF except in localized areas. 

Fly ash from municipal waste and industrial waste incinerators contains PCDDs, including TCDD, and PCDFs, which are lipophiles, and heavy metals, including chromium, copper, manganese, vanadium, and lead, which are hydrophiles [29-31]. These chemicals have multiple toxicities, and are known to impact the human liver, immune system, respiratory system, thyroid, male reproductive function, and CNS [32-34]. Several are human carcinogens [32, 35], Enhanced toxic effects are observed for mixtures of some of these [21, 22, 36], The mixtures of toxicants present in fly ash are complex and the mechanisms for their action on the human body are largely unknown. It is known that occupational exposure to fly ash from municipal and industrial waste incinerators increases the blood concentrations of PCDDs and PCDFs [29, 30]. It is also known that heavy metals absorbed from fly ash are translocated from the lungs where they first impact to other body organs where toxic effects are observed [31]. 

Although these reservoirs may be highly contaminated with PCDD/PCDFs, the chemical and physical properties of these compounds imply that dioxins and furans will stay adsorbed to organic carbon in soils or other particles. On the other hand, mobilization can occur in the presence of lipophilic solvents (leaching into deeper layers of soils and/or groundwater) or in cases of erosion or run-off from topsoil (translocation into the neighbourhood). Experience has shown that transport of PCDD/PCDFs due to soil erosion and run-off does not play a major role in environmental contamination and human exposure (Fiedler 1995, 1999). 

Compared to adults, the daily intake of PCDD/PCDFs and PCBs by breastfed babies is 1-2 orders of magnitude higher. A recent field study showed higher mean levels of PCDD/PCDFs and PCBs in human milk in industrialized areas (10-35 pg I-TEQ/g milk fat) and lower levels in developing countries (< 10 pg I-TEQ/g milk fat). Very few studies have been performed on Arctic populations with respect to the exposure of children to these substances. It is likely, however, that the differences in exposure between children and adults demonstrated in many industrialized regions also exist in Arctic regions. 

Polychlorinated dibenzo-y>-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) are chemically classified as halogen-ated (polychlorinated) aromatic hydrocarbons (PHAH). Dioxins are formed as a by-product of chemical processes, whereas PCBs are synthesized by direct chlorination of biphenyls. Due to their lipophilic character, they are concentrated in the food chain and both humans and wildhfe are exposed to them. The major source of human exposure is through the diet, as these substances are concentrated in fatty tissues of beef, poultry, pork and fish, and through cigarette smoking. Moreover, maternal milk contains considerable amounts of PCBs and dioxins. 

Dioxins are a family of the most toxic chlorinated organic compounds known to science, numbering around 75 dioxins and 135 related furans. These can cause cancer and are ECD for humans, even at very low exposure levels, since minute amounts, can bio-accumulate due to their ease of solubility in body fat (dioxins are hydrophobic, water-hating and lipophilic, fat-loving ). Number and position of chlorine atoms in the molecule has a considerable effect on toxicity, and 17 dioxins are classed as highly toxic. These include polychlorinated dioxins (PCDD) and dibenzofurans (PCDF) which are by-products of the chlorine bleaching of paper, the burning of chlorinated hydrocarbons (such as pentachlorophenol, PCB, and PVC) and the incineration of municipal/medical... 

The pressured column chromatographic system is able to process automatically unattended samples in approximately 1 h. It reduces sample manipulation, the risks of human exposure, and the costs of analysis. The whole system is computer controlled and programmed as desired (e.g., volume, flow rates, direction of solvent flow, etc.). The previously filtered n-hexane extracts are loaded and pmnped through individual sets of multilayer silica column and transferred to a basic almnina colmnn. Next, the PCDD/ PCDF is eluted from the alumina column and transferred to the PX-21 carbon column. The interferences are eluted in the forward direction and the PCDD/PCDF is collected in the reverse direction from the carbon columns with toluene. 

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