Article Text
Abstract
Objectives To describe how 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure influenced mortality in a cohort of workers exposed more recently, and at lower levels, than other cohorts of trichlorophenol process workers.
Methods A cohort study of 1599 men and women working between January 1, 1969 and November 1, 1988 at a plant producing the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5 T) with TCDD as a contaminant.
A toxicokinetic model developed in a previous follow up was updated to estimate cumulative TCDD exposure for each individual in the study. Calculation of cause-specific standardized mortality ratios (SMRs) and 95% confidence intervals (95%CIs) compared those never and ever exposed to TCDD. Dose-response trends were assessed firstly through SMRs stratified in quartiles of cumulative TCCD exposure, and secondly with a proportional hazards model.
Results The toxicokinetic model intercept of 5.1 parts per trillion (ppt) of TCDD was consistent with background New Zealand TCDD concentrations among older members of the population. Exposed workers had non-significant increases in all cancer deaths SMR=1.08, 95% CI 0.86–1.34, deaths from soft tissue sarcoma, SMR=2.38, 95% CI: 0.06–13.26, non-Hodgkin lymphoma, SMR=1.57, 95% CI: 0.32–4.59, diabetes, SMR=1.27, 95% CI: 0.55–2.50 and ischaemic heart disease, SMR=1.21, 95% CI: 0.96–1.50. Lung cancer deaths SMR=0.95, 95% CI: 0.56–1.53, were fewer than expected. Neither the stratified SMR nor proportional hazard analysis showed a dose response relationship.
Conclusion We found neither an excess of all cancers, or any specific cancer, nor a trend with TCDD exposure. This argues against the carcinogenicity of TCDD at lower levels of exposure.