Exposure, dioxin

There have been suggestions of alterations in sex ratios following accidental environmental exposure to dioxin in Seveso, Italy, in 1976. Between 1977 and 1984, 74 births occurred in the most heavily contaminated zone which showed an excess of females (26 males and 48 females born). Preliminary evidence suggests that the excess was associated with high dioxin exposure in both parents. Over a later period, between 1985 and 1994, the ratio declined (60 males and 64 females) and was no longer statistically significant. 

Although the effects of chronic exposure of humans to low levels of POPs are difficult to predict, some biological effects have been described. For example, exposure of children to PCBs and PCDD/Fs may be linked to an elevated risk for infectious diseases. Exposure of pregnant women to PCDD/Fs may cause lower fertility in their male offspring. The adverse effects to human health of acute and chronic exposure of high concentrations of POPs, especially among industrial workers exposed to daily intakes of chemicals, are more evident. Elevated concentrations of DDE and TCDD have been associated with the development of cancers such as breast cancer, leukaemia and thyroid cancer. Dioxin exposure may also be associated with immunotoxicity, reproductive diseases and neurotoxicity. Extreme exposure to chlorinated compounds has resulted in death [101]. 

Barber, T.R., D.J. Chappie, D.J. Duda, P.C. Fuchsman, and B.L. Finley. 1998. Using a spiked sediment bioassay to establish a no-effect concentration for dioxin exposure to the amphipod Ampelisca abdita. Environ. Toxicol. Chem. 17 420-424. 

Funatake, C.J. et al., 2004. Early consequences of 2,3,7,8-trtrachlorodibenzo-p-dioxin exposure on the activation and survival of antigen-specific T cells. 

The Air Force scientists who direct the Ranch Hand study concluded, in 1997, that dioxin exposure is associated with increased risk of adult-onset diabetes,12 which is the only disease that they link to dioxin. In their most recent comment on the possible dioxin-diabetes link, the Air Force scientists state that the evidence for a connection is weaker in the data collected in the 1997 exams than in the data from the 1992 exams.131 doubt that... 

Institute of Medicine, Veterans and Agent Orange Herbicide/Dioxin Exposure and Type 2 Diabetes (Washington, D.C. National Academy Press,... 

IOM s conclusion about a link between herbicides and respiratory cancer depends on studies of highly exposed workers in which exposures have been verified by body burden measurements. Thomas Starr analyzed the relationships between dioxin exposures and cancer rates in those workers.56 Although exposures varied over a 1,500-fold range, cancer rates did not increase at higher dioxin exposures, providing no support for an association. 

One of the most sensitive mammals to dioxin-like PCB and dioxin exposure is the mink. Effects have been documented in both farmed mink [65,66] and wild mink [67-72], Extensive work was done in the 1970s and 1980s by Auerlich, Ringer, and colleagues [65,66,73-76] that documented the impact of feeding Great Lakes fish to mink. These impacts included reproductive... 

S100A9 Knock-out No functional abnormalities. Absence of S100A8 protein. Myeloid cells with reduced density. No functional abnormalities in vivo. Absence of S100A8 protein. Reduced response to chemoattractant stimuli in vitro. Stimulation of myeloid cells with ATP results in a stronger increase of intracellular free Ca2+. No emigration of CD4-CD8 double-negative thymocytes upon tetrachlorodibenzo-p-dioxin exposure. 

Emond, C, J.E. Michalek, L.S. Birnbaum, and M.J. DeVito. 2005b. Comparison of the use of a physiologically based pharmacokinetic model and a classical pharmacokinetic model for dioxin exposure assessment. Environ. Health Perspect. 113(12) 1666-1668. 

Fiedler, H., Buckley-Golder, D., Coleman, P., King, K., Peterson, A., 1999. Compilation of EU dioxin exposure and health data Environmental levels. Organohalo. Compd. 43, 151-154. 

Some possible toxicological effects such as endocrine disruption continue to be uncertain, particularly for DDT, DDE, dieldrin and dioxin exposures. The history of environmental health shows that safe levels are uncertain and vary as knowledge improves. The long-term trend is often towards lower levels as uncertainties decrease. This should be considered when accounting for the public benefits of further reducing POPs residues and wastes in the Australian environment. 

Eskenazi B University of California, Berkeley CA Endometriosis and Dioxin Exposure in Females of Seveso National Institute of Environmental Health Sciences... 

Bertazzi PA, Zocchetti C, Guercilena S, et al. 1997. Dioxin exposure and cancer risk A 15-year mortality study after the "Seveso Accident". Epidemiology 8 646-652. 

Fingerhut MA, Halperin WE, Honchar PA, et al. 1984. An evaluation of reports of dioxin exposure and soft tissue sarcoma pathology among chemical workers in the United States. Scand J Work Environ Health 10 299-303. 

Jones K. 1995. Diesel engine emissions and the link to human dioxin exposure. Dioxin 95 Secretariat, Edmonton AB Canada Organohalogen Compounds 24 69-74. 

MMWR. 1988. Preliminary report 2,3,7,8-tetrachlorodibenzo -p-dioxin exposure to humans - Seveso, Italy. Morbidity and Mortality Weekly Report 37(48) 733-736. 

Pluim HJ, van der Goot M, Olie K, et al. 1996. Missing effects of background dioxin exposure on development of breast-fed infants during the first half year of life. Chemosphere 33 1307-1315. 

Pohl H, DeRosa C, Holler J. 1995. Public health assessment for dioxins exposure from soil. Chemosphere 1995 31(l) (2437-2454). 

Zober A, Papke 0. 1993. Concentrations of PCDDs and PCDFs in human tissue 36 years after accidental dioxin exposure. Chemosphere 27 413-418. 

Franc MA, Pohjanvirta R, Tuomisto J, Okey AB. Persistent, low-dose 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure effect on aryl hydrocarbon receptor expression in a dioxin-resistance model. Toxicol Appl Pharmacol 2001 175 43-53. 

Embryonic age Neural tube defects from retinoic acid, arsenic, and valproic acid (Adams, 1993 Bennett Finnell, 1998) Decreased fertility in female rats exposed to dioxin (TCDD) (Gray Ostby, 1995) Hydronephrosis with dioxin exposure during embryonic or fetal periods in rats (Couture-Haws et al., 1991 Bimbaum, 1995) ... 

Neonate Infant Exposure of juvenile mice to pesticides caused Parkinson-like declines in dopaminergic neurons in adulthood (Cory-Slechta et al., 2005) Hydronephrosis with dioxin exposure during neonatal and infantile periods in rats (Bimbaum, 1995) Maternal grooming affects ability to respond to stress in adulthood in rats (Gilbert, 2005)... 

American Hospital Association, Comments from the American Hospital Association on the United States Environmental Protection Agency Dioxin Exposure and Health Effects Documents, AHA, Chicago, IL, January 13, 1995. 

The food chain is the primary pathway of human exposure to dioxin, with meat (38%) and dairy products (28%) dominating. Fish ingestion can be a significant contributor in countries with high fish consumption (26% of total intake in the Netherlands), but is not an important factor in the US. The exact contribution of fruits and vegetables is unclear, but vegetable oil does appear to play a role in human dioxin exposure. Inhalation and consumption of contaminated water and soil are not major sources of human exposure to TCDD. 

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