Dioxins human exposure

Improper disposal of e-waste has been regarded as the major source of PCDD/ Fs occurring in China s environment [46]. Consequently, e-waste recycling should be somewhat responsible for human exposure to dioxins in China. A comparison of dioxins in human samples from e-waste recycling and reference sites would either confirm or disapprove the notion. The levels of PCDD/Fs (List 4 of Appendix) in human milk samples from a group of pregnant women... 

Ma J, Kannan K, Cheng J, Horii Y, Wu Q, Wang W (2008) Concentrations, profiles, and estimated human exposures for polychlorinated dibenzo-p-dioxins and dibenzofurans from electronic waste recycling facilities and a chemical industrial complex in Eastern China. Environ Sci Technol 42(22) 8252-8259. doi 10.1021/es8017573... 

Young, A.L. and L.G. Cockerham. 1985. Fate of TCDD in field ecosystems assessment and significance for human exposures. Pages 153-171 in M.A. Kamrin and P.W. Rodgers (eds.). Dioxins in the Environment. 

Weisglas-Kuperus, N., Neurodevelopmental, immunological and endocrinological indices of perinatal human exposure to PCBs and dioxins, Chemosphere, 37, 1845, 1998. 

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). 

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. 

However, no studies on fetal exposure are available for setting TEFs. Thus there is a need for dose-response studies of the critical effects, based on synthetic mixtures reflecting the human exposure situation. The WHO TEFs for dioxins, dibenzofurans and PCBs for humans and mammals are given in Table 3. 

Dioxin-contaminated sites, which pose a human health threat, have been the subject of recent analyses by the Centers for Disease Control (CDC) in Atlanta, GA. It has been determined by CDC that 1 ppb of dioxin is detrimental to public health and that people should be dissociated from the hazard. A level of 1 ppb of dioxin (2,3,7,8-TCDD) in soil is recommended as an action level. In cases where soil concentrations exceed 1 ppb, it is recommended by CDC that potential human exposure to the contamination be examined further. If there is human exposure to I ppb or higher on a regular basis, cleanup is indicated. A substance that may be more toxic and hazardous than dioxin is expected to be discovered in the near future. 

Another development is due to the interest in polychlorodibenzofurans, spurred by their occurrence as environmental contaminants. Polychloro-phenols are manufactured in large amounts (150,000 tons per annum) and find a wide range of uses. The usual method of manufacture involves the hydrolysis of chlorobenzenes, and side reactions, favored by high temperature, can lead to the production of polychlorodibenzofurans and poly-chlorodibenzo-p-dioxins. The Seveso incident is well known." Polychloro-biphenyls are also widely used industrial chemicals, particularly in heat exchange systems, and their pyrolysis leads to the formation of polychloro-dibenzofurans. Polychlorodibenzofurans have also been detected in the fly ash and flue gases of incinerators and industrial heating plants. The most toxic of the polychlorodibenzofurans are 2,3,7,8-tetra-, 1,2,3,7,8-penta-, and 2,3,4,7,8-pentachlorodibenzofuran, and an extensive literature exists on the environmental pollution and the results of human exposure to these substances. A particularly tragic example of the latter occurred in 1968 in the Fukuoka prefecture of Japan after consumption of rice oil contaminated with a commercial polychlorobiphenyl. 

Charnley, G., Doull, J., 2005. Human exposure to dioxins from food, 1999-2002. Food Chem. Toxicol. 43, 671-679. 

In spite of their record of producing no detectable harm to humans, the phenoxy herbicides 2,4-dichlorophenoxy acetic acid (2,4-D) and 2,4,5-trichlorophenoxy acetic acid (2,4,5-T) have acquired a less than desirable reputation. This reputation has been the result of their association with low levels of impurities. They have commonly been used as a mixture, which contains trace amounts of highly toxic 2,3,7,8-tetrachlorodibenzo-jj-dioxin, a minor product in the manufacturing of 2,4,5-T. In early production of 2,4,5-T a low level of dioxin was retained. Today s manufacturing process produces 2,4,5-T with no more than 0.1 ppm of the 2,3,7,8 tetrachlorodibenzo-]D-dioxin. This association with toxic dioxin and confusion of the public and the media regarding these issues have led to public distrust in the safety of using phenoxys and to the need to establish clearly the extent of human exposure to these compounds as well as the resulting effects of this exposure. 

Alcock, R.E., PA. Behnisch, K.C. Jones, et al. 1998. Dioxin-like PCBs in the environment—human exposure and the significance of sources. Chemosphere 37 1457-1472. 

The wasting syndrome is a characteristic effect of exposure to 2,3,7,8-TCDD in animals and, in its most severe form, is usually associated with lethality, particularly in rodents. The fact that the wasting syndrome has not been demonstrated in humans does not necessarily indicate that humans are insensitive to this effect of dioxins, but may indicate that human exposure has not approached acutely high enough levels. 

Conso F, Dally S, Cordier S, et al. 1986. Accidental human exposure to polychlorinated dibenzofiirans and polychlorinated dioxins following a transformer fire. Chemosphere 15 1953-1955. 

Ebert E, Price P, Keenan R. 1996. Estimating exposures to dioxin-like compounds for subsistence anglers in North American. In Human exposure, human health risk assessment, and organohalogen compounds, 16th Symposium on Chlorinated Dioxins and Related Compounds, Amsterdam Holland, volume 30, 66-69. 

Gough M. 1991. Human exposure from dioxin in soil-a meeting report. J Toxicol Environ Health 32 205-245. 

Hattemer-Frey HA, Travis CC. 1989. Comparison of human exposure to dioxin from municipal waste incineration and background environmental contamination. Chemosphere 18 643-649. 

Jones KC, Bennett BG. 1989. Human exposure to environmental polychlorinated dibenzo-p-dioxins and dibenzofurans An exposure commitment assessment for 2,3,7,8-TCDD. Sci Total Environ 78 99-116. 

Lundgren K, Andries M, Thompson C, et al. 1986. Dioxin treatment of rats results in increased in vitro induction of sister chromatid exchanges by -naphthoflavone An animal model for human exposure to halogenated aromatics. Toxicol Appl Pharmacol 85 189-195. 

Accidental exposure to dioxins Human health aspects. New York, NY Academic Press, 81-100. 

Rappe C, Nygren M, Marklund S, et al. 1985. Assessment of human exposure to polychlorinated dibenzofurans and dioxins. Environ Health Perspect 60 303-304. 

Travis CC, Hattemer-Frey HA. 1989. Human exposure to dioxin from municipal solid waste incineration. Waste Management 9 151-156. 

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. 

Young AL. 1984b. Determination and measurement of human exposure to the dibenzo-p-dioxins. Bull Environ Contain Toxicol 33 702-709. 

These guidelines and procedures apply to human exposure for direct ingestion of soils contaminated with dioxinand dioxin-like compounds inresidential areas and may not be appropriate for other exposure scenarios. The guidance will be evaluated inview ofnew data that may become available. The scientific basis for the guidelines is outlined in the Background discussion. 

Because the toxicity of dioxin and dioxin-like compounds is assumed to be elaborated through a common receptor-mediated mechanism, levels greater than 50 ppt TEQs are used to determine whether further site-specific evaluation for dioxins is to occur based on the maximum soil concentrations identified at the site. A level of 1 ppb TEQs is used to determine the potential need for public health actions on a site-specific basis andonthe basis of adequate sampling and measured or projected human exposure—past, present, or future—as determined by the health assessor. 

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