Serum levels of PCDDs and PCDFs among workers exposed to 2,3,7,8-TCDD contaminated chemicals

Piacitelli, LA; Sweeney, Marie Haring; Fingerhut, M.; Patterson, Donald; Turner, W. E.; Connally, L. Barbara; Wille, Kathleen K.; Tompkins, Brandon T.

doi:10.1016/0045-6535(92)90526-w

Cited by 27 publications

(20 citation statements)

References 10 publications

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“…Concentrations of seven polychlorinated dibenzo-p-dioxin (PCDD) compounds, 10 polychlorinated dibenzofuran (PCDF) and selected polychlorinated biphenyl (PCB) compounds were measured in serum samples donated by 346 individuals (21.6% of the total group) who were employees of the plant for 3 days or more during the time period of trichlorophenol or phenoxyacetic acid manufacture and who resided within 75 km of the plant at the time of the blood draw. TCDD was the only congener that showed elevations above general population background levels, consistent with previous studies of 2,4,5-T manufacturing cohorts and data on product contamination (Nygren et al, 1988;Beck et al, 1989;Papke et al, 1992;Piacitelli et al, 1992;Smith et al, 1992;Ott et al, 1993;Littorin et al, 1994;Flesch-Janys et al, 1996;Heederik et al, 1998;Ryan and Schecter, 2000). The serum study is described in detail in an accompanying publication (Collins et al, 2008).…”

Section: Study Groupsupporting

confidence: 82%

TCDD exposure estimation for workers at a New Zealand 2,4,5-T manufacturing facility based on serum sampling data

Aylward

Bodner

Collins

et al. 2009

J Expo Sci Environ Epidemiol

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Employment in the manufacture of the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) is associated with potential exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and elevated serum lipid TCDD concentrations can be measured in workers for decades after terminated occupational exposure. As part of an epidemiological study of 1599 workers employed at a facility in New Plymouth, New Zealand that manufactured 2,4,5-T, serum TCDD concentrations measured in blood samples from 346 workers were used with work history records and a simple pharmacokinetic model in a linear regression to estimate dose rates associated with specific job exposure groups at the facility. The model was used to estimate serum TCDD concentration profiles over time for each individual in the full study group and accounted for 30% of the observed variance in TCDD concentrations in the serum donor subgroup. The model underestimated measured concentrations substantially for eleven individuals in the study group; examination of questionnaire data revealed a variety of activities apart from routine employment at the facility that may have contributed to the measured serum TCDD concentrations. Estimated serum TCDD concentrations were below 300 p.p.t. for all individuals in the cohort over the entire study time period, lower than estimates for other 2,4,5-T worker populations. This finding is consistent with occupational medicine records, which indicated that no cases of chloracne were ever diagnosed among workers employed on the site. The modeled exposures will be used in an evaluation of mortality patterns of workers at this facility.

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Section: Study Groupsupporting

confidence: 82%

TCDD exposure estimation for workers at a New Zealand 2,4,5-T manufacturing facility based on serum sampling data

Aylward

Bodner

Collins

et al. 2009

J Expo Sci Environ Epidemiol

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“…Dates of employment in TCDD-related processes defined the exposure period (Piacitelli et al 1992). Pregnancies conceived after the father’s first date of exposure were considered exposed, whereas referent pregnancies and pregnancies conceived before the fathers’ exposure at the plants (hereafter referred to as preexposure pregnancies) were considered unexposed.…”

Section: Methodsmentioning

confidence: 99%

Paternal Occupational Exposure to 2,3,7,8-Tetrachlorodibenzo- p -dioxin and Birth Outcomes of Offspring: Birth Weight, Preterm Delivery, and Birth Defects

Lawson

Schnorr

Whelan

et al. 2004

Environ Health Perspect

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Agent Orange is a phenoxy herbicide that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We studied pregnancy outcomes among wives of male chemical workers who were highly exposed to chemicals contaminated with TCDD and among wives of nonexposed neighborhood referents. For exposed pregnancies, we estimated serum TCDD concentration at the time of conception using a pharmacokinetic model. The mean TCDD concentration for workers’ births was 254 pg/g lipid (range, 3–16,340 pg/g). The mean referent concentration of 6 pg/g was assigned to pregnancies fathered by workers before exposure. A total of 1,117 live singleton births of 217 referent wives and 176 worker wives were included. Only full-term births were included in the birth weight analysis (≥37 weeks of gestation). Mean birth weight among full-term babies was similar among referents’ babies (n = 604), preexposure workers’ babies (n = 221), and exposed workers’ babies (n = 292) (3,420, 3,347, and 3,442 g, respectively). Neither continuous nor categorical TCDD concentration had an effect on birth weight for term infants after adjustment for infant sex, mother’s education, parity, prenatal cigarette smoking, and gestation length. An analysis to estimate potential direct exposure of the wives during periods of workers’ exposure yielded a nonstatistically significant increase in infant birth weight of 130 g in the highest exposure group (TCDD concentration > 254 pg/g) compared with referents (p = 0.09). Mothers’ reports of preterm delivery showed a somewhat protective association with paternal TCDD (log) concentration (odds ratio = 0.8; 95% confidence interval, 0.6–1.1). We also include descriptive information on reported birth defects. Because the estimated TCDD concentrations in this population were much higher than in other studies, the results indicate that TCDD is unlikely to increase the risk of low birth weight or preterm delivery through a paternal mechanism.

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“…Total congener concentrations in blood were 35.0 and 42.7 pg TEQ/g fat, respectively. Dioxin concentrations in these cases were largely lower than those observed after accidental releases (15)(16)(17)(18). For example, 2,3,7,8-TCDD concentrations reported by Mocarelli and co-workers (15) ranged from 828 to 56,000 pg TEQ/g of fat in serum of Seveso residents.…”

Section: Resultsmentioning

confidence: 88%

Dioxins and Furans Determination in Postmortem Blood by Gas Chromatography-High-Resolution Mass Spectrometry

Cirimele¹,

Villain²,

Kintz³

2005

Journal of Analytical Toxicology

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]Dioxins and related compounds (furans) are persistent environmental contaminants that cause adverse biological effects. Their influence on humans is still unclear, except for accidental high-dose exposure. However, chronic exposure to these compounds seems to be involved in cancer, endocrine disruption, and neurobehavioral effects. For several years, a large concern about the potential health risks of dioxins is emerging in Europe and United States. Dioxin levels in biological specimens are extremely low and require very sensitive and specific methods of analysis. In this study, gas chromatography coupled to high-resolution mass spectrometry was used to evaluate dioxin body burden of two women deceased from generalized cancer. Fat fraction of blood specimens was obtained after precipitation with ethanol and extraction of both liquid and solid phases spiked with labeled 13C12-dioxin analogues. Organic phases were grouped, washed, and evaporated to weigh the lipid content. Lipids were dissolved in hexane, hydrolyzed with concentrated sulfuric acid, and discarded during water washes. Dioxins purification was achieved using three successive columns: silica, alumina/sodium sulfate, and carbon/Celite. Finally, the toluene eluent was evaporated and the extract injected in the analytical system. After chromatographic separation, detection was achieved in single ion monitoring mode using a high-resolution mass spectrometer operating in electron impact ionization mode (40 eV, minimal resolution of 10,000). Dioxin levels were expressed in pg TEQ/g of fat as defined by the World Health Organization. Quantification limits for each dioxin congener ranged from 2.5 to 12.0 pg/g fat with a relative extraction recovery always higher than 60%. Dioxin concentrations in the blood of the two deceased women were 35.0 and 42.7 pg TEQ/g fat, respectively. These concentrations are largely lower than those observed after accidental releases, but in the range of those observed in the general European population. Therefore, it was not possible to correlate dioxin body burden of the two women as a potential contributor of their cancer pathology. Nevertheless, knowledge of dioxin body burden in the French

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Serum levels of PCDDs and PCDFs among workers exposed to 2,3,7,8-TCDD contaminated chemicals

Cited by 27 publications

References 10 publications

TCDD exposure estimation for workers at a New Zealand 2,4,5-T manufacturing facility based on serum sampling data

TCDD exposure estimation for workers at a New Zealand 2,4,5-T manufacturing facility based on serum sampling data

Paternal Occupational Exposure to 2,3,7,8-Tetrachlorodibenzo- p -dioxin and Birth Outcomes of Offspring: Birth Weight, Preterm Delivery, and Birth Defects

Dioxins and Furans Determination in Postmortem Blood by Gas Chromatography-High-Resolution Mass Spectrometry

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