Cytogenetic studies in lymphocytes of workers exposed to 2,3,7,8-TCDD

Abstract

Chromosome aberrations and sister chromatid exchanges (SCEs) were evaluated in 27 workers with current 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) blood lipid concentrations exceeding 40 parts per trillion (ppt) and in 28 unexposed referents of similar age. No statistical differences were found between the two groups in the percentages of gaps, chromatid or chromosome exchanges, chromatid or chromosome breaks/fragments/deletions, multiple aberrations, or the overall percentage of aberrations including gaps (1.33% in the exposed group vs 1.75% in the referent group) or excluding gaps (0.54% in each group). There was an increased rate of SCEs per cell (P = 0.051) and a higher percentage of cells with more than 10 SCEs (P = 0.064) in the exposed group; however, these associations were no longer significant when smoking status was included as covariate. Additionally, neither current nor back-calculated TCDD concentration was a significant predictor of these parameters based on multiple linear and rank regression analyses.

Cause specific mortality and cancer incidence among employees exposed to 2,3,7,8-TCDD after a 1953 reactor accident.

“…Descriptive accounts of the signs and symptoms experienced after exposure have been reported as well as laboratory studies correlating biomonitoring data with clinical chemistries, immunological variables, and cytogenetic outcomes; mortality follow up studies; and most recently a long term morbidity study based on medical insurance data have been reported.7 [11][12][13][14] These investigations identified 115 cases of chloracne (56 classified as severe) in a cohort of 254 people." Most cases were diagnosed during the early clean up period and no severe cases were found after 1959.…”

Transient increase in micronucleus frequency and DNA effects in the comet assay in two patients after intoxication with 2,3,7,8-tetrachlorodibenzo-p-dioxin

“…In rats, DNA strand breaks were found in vivo in liver and peritoneal lavage cells after TCDD exposure (IARC 1997). In humans, no chromosomal aberrations and SCE were found in 27 workers with TCDD blood lipid concentrations exceeding 40 pg after accidental exposure (Zober et al 1993). Also, no significant difference was observed in the mean SCE rates between ''Yusho'' patients approximately 27 years after the outbreak of the Yusho accident and the general Japanese population (Nagayama et al 2001).…”

Elevated sister chromatid exchange frequencies in New Zealand Vietnam War veterans

“…It is an accepted paradigm that SCEs arise during the period of lymphocyte culture, which would suggest that the veterans have a persistent clastogen still in their bloodstream, or that they possess a common instability. Dioxin, a contaminant of Agent Orange, is known to be an inducer of SCEs (Zober et al, 1993). It is also very persistent and has an average half-life in humans of 7.78 years (Geyer et al, 2002), which suggests that New Zealand Vietnam veterans who were exposed to defoliants more than 30 years ago are still very likely to have elevated dioxin levels when compared to non-veterans.…”

“…The above statement endorses numerous studies where this assay has been used successfully as a bioindicator linking chemical exposure with possible genetic damage (Zober et al, 1993;Garaj-Vrhovac and Zeljezic, 2001;Arias, 2003; Abstract. From July 1965 until November 1971, New Zealand Defence Force Personnel fought in the Vietnam War.…”