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2,3,7,8-Tetrachlorodibenzo-p-dioxin alters lipid metabolism in animals; however, evidence for such an effect in humans is conflicting. This conflict was addressed using data from a cross-sectional medical study conducted between 1987 and 1988. The exposed participants had been employed at least 15 y earlier in the manufacture of 2,4, 5-trichlorophenol or one of its derivatives at two chemical plants in the United States. A total of 281 workers and 260 unexposed referents participated. Workers had substantial exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin, evidenced by a median serum 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration of 406.6 femtograms/gram of serum (fg/g serum), compared with 36.9 fg/g serum among the referents. A slight association between triglyceride concentration and serum 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration was found (p = .05). Over the range of observed 2,3,7,8-tetrachlorodibenzo-p-dioxin values (i.e., 37-19 000 fg/g serum), triglyceride concentration increased only about 0.4 mmol/l. No association was found between an abnormally elevated triglyceride (i.e., > 2.82 mmol/l) concentration and serum 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration. An association was also found between serum 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration and an abnormal high-density lipoprotein concentration (p = .09). In summary, there was evidence of an effect on lipid metabolism in a group of workers with high serum 2,3,7,8-tetrachlorodibenzo-p-dioxin concentrations. The influence of serum 2,3,7,8-tetrachlorodibenzo-p-dioxin on lipid concentrations, however, was small, compared with the influence of other factors., DISORDERS of lipid metabolism, characterized by the presence of hyperlipidemia (i.e., hypercholesterolemia and hypertriglyceridemia), are major risk factors for the development of coronary heart disease.[1,2] rom primary inborn errors of [...]

The toxic chemical 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is produced during the manufacture of fungicides and herbicides such as 2,4,5-trichlorophenol (TCP) and agent orange, respectively. TCDD is extremely potent and is toxic to the liver. Studies performed in laboratory animals have shown that TCDD can damage the lungs, causing physiological changes that are similar to those seen in humans with chronic bronchitis. These findings prompted an investigation to determine if workers exposed to TCDD have an increased risk of developing chronic bronchitis or other forms of chronic obstructive pulmonary disease (COPD). The study included 281 workers who were exposed to substantial levels of TCDD 15 years ago during the manufacture of sodium TCP and 260 workers who were not exposed to TCDD. Complete medical histories, medical examinations and pulmonary (lung) function tests were performed on each subject. Chronic bronchitis was diagnosed in 11 of 271 (4.1 percent) exposed workers and 13 of 253 (5.1 percent) of those who were not exposed to TCDD. Similarly, COPD was diagnosed in 11 of 233 (4.7 percent) workers who were exposed to substances contaminated with TCDD and 7 of 226 (3.1 percent) unexposed workers. Lung function was similar in both groups of workers and there was no difference in the incidence of chest or lung abnormalities between the two groups. In this population of workers exposure to substances contaminated with TCDD was not associated with impaired lung function or an increased risk of developing chronic bronchitis or COPD. (Consumer Summary produced by Reliance Medical Information, Inc.)

Background: In 1997, the International Agency for Research on Cancer classified 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD) as a group 1 human carcinogen, based largely on four highly exposed industrial cohorts that showed an excess of all cancers combined. In this study, we extended the follow-up period for the largest of these cohorts by 6 years and developed a job-exposure matrix. Methods: We did cohort mortality analyses involving 5132 chemical workers at 12 U.S. plants by use of life table techniques (U.S. population referent) and Cox regression (internal referent). We conducted exposure-response analyses for 69% of the cohort with adequate work history data and adequate plant data on TCDD contamination. All P values are two-sided. Results: The standardized mortality ratio (SMR) for all cancers combined was 1.13 (95% confidence interval = 1.02-1.25). We found statistically significant positive linear trends in SMRs with increasing exposure for all cancers combined and for lung cancer. The SMR for all cancers combined for the highest exposure group was 1.60 (95% confidence interval = 1.15-1.82). SMRs for heart disease showed a weak increasing trend with higher exposure (P = .14). Diabetes (any mention on the death certificate) showed a negative exposure-response trend. Internal analyses with Cox regression found statistically significant trends for cancer (15-year lag time) and heart disease (no lag). Conclusions: Our analyses suggest that high TCDD exposure results in an excess of all cancers combined, without any marked specificity. However, excess cancer was limited to the highest exposed workers, with exposures that were likely to have been 100-1000 times higher than those experienced by the general population and similar to the TCDD levels used in animal studies. [J Natl Cancer Inst 1999;91:779-86]

Examines if exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin may be associated with adverse effects on the cardiovascular system.