Mortality in employees at a New Zealand agrochemical manufacturing site.

BACKGROUND: Previous studies at the Dow AgroSciences (Formerly Ivon Watkins-Dow) plant in New Plymouth, New Zealand, had raised concerns about the cancer risk in a subset of workers at the site with potential exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. As the plant had been involved in the synthesis and formulation of a wide range of agrochemicals and their feedstocks, we examined the mortality risk for all workers at the site. AIMS: To quantify the mortality hazards arising from employment at the Dow AgroSciences agrochemical production site in New Plymouth, New Zealand. METHODS: Workers employed between 1 January 1969 and 1 October 2003 were followed up to the end of 2004. Standardized mortality ratios (SMRs) were calculated using national mortality rates by employment duration, sex, period of hire and latency. RESULTS: A total of 1754 employees were followed during the study period and 247 deaths were observed. The all causes and all cancers SMRs were 0.97 (95% CI 0.85-1.10) and 1.01 (95% CI 0.80-1.27), respectively. Mortality due to all causes was higher for short-term workers (SMR 1.23, 95% CI 0.91-1.62) than long-term workers (SMR 0.92, 95% CI 0.80-1.06) and women had lower death rates than men. Analyses by latency and period of hire did not show any patterns consistent with an adverse impact of occupational exposures. CONCLUSIONS: The mortality experience of workers at the site was similar to the rest of New Zealand.

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

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.

Serum concentrations of chlorinated dibenzo-p-dioxins and dibenzofurans among former New Zealand trichlorophenol workers.

This study examined serum levels of 2,3,7,8-substituted chlorinated dioxins and furans, and 15 PCBs for 346 New Zealand employees who worked at a site that manufactured 2,4,5-trichlorophenol (TCP) and 2,4,5-trichlorophenoxy acetic acid (2,4,5-T). Participants with potential TCP or 2,4,5-T exposures had mean lipid-adjusted 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) levels of 9.9 ng kg(-1) lipid compared to 4.9 ng kg(-1) for workers with no exposure at the site. Among exposed workers, we found evidence of differences in 2,3,7,8-TCDD levels by department and duties. Workers involved in an accidental release had the highest mean 2,3,7,8-TCDD levels, 37.9 ng kg(-1), followed by workers in the trichlorophenol plant, 23.4 ng kg(-1). Workers with potential intermittent exposures to 2,3,7,8-TCDD in construction, maintenance, mechanics, and transport had 2,3,7,8-TCDD levels above New Zealand background levels of 3.9 ng kg(-1), indicating workplace exposures. Among participants with work history indicating no 2,3,7,8-TCDD exposures, we observed some individuals with 2,3,7,8-TCDD levels above background levels. However, in most cases, these workers reported workplace exposures not recorded on their work histories or held other jobs with the potential for 2,3,7,8-TCDD exposures outside the plant. All other dioxin, furan, and PCB levels were similar among the exposed and unexposed workers.

Mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin at a trichlorophenol plant in New Zealand.

OBJECTIVE: We examined the overall mortality rates of 1599 workers employed between 1969 and 1988 at a New Zealand site, which manufactured trichlorophenol. METHODS: We developed exposure estimates for 2,3,7,8-tetrachlorodibenzo-p-dioxin from a serum dioxin evaluation and used standardized mortality ratios (SMR) and proportional hazards models to evaluate risk from exposure. RESULTS: Among exposed workers, deaths from total cancers (SMR = 1.1, 95% confidence intervals [CI]: 0.9-1.4), non-Hodgkin lymphoma (SMR = 1.6, 95% CI: 03-4.7), and ischemic heart disease (SMR = 1.1, 95% CI: 0.9-1.5) were slightly greater than expected, whereas deaths from lung cancer (SMR = 0.8, 95% CI: 0.4-1.5) were less than expected. We observed no significant trends with exposure levels. CONCLUSIONS: Although this study is small, we found no increasing trend of cancer or disease risk with increasing 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure with the possible exception of all cancers combined.