Cohort study of workers at a New Zealand agrochemical plant to assess the effect of dioxin exposure on mortality.

OBJECTIVES: To describe how the exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) influenced mortality in a cohort of workers who were exposed more recently, and at lower levels, than other cohorts of trichlorophenol process workers. DESIGN: A cohort study. SETTING: An agrochemical plant in New Zealand PARTICIPANTS: 1,599 men and women working between 1 January 1969 and 1 November 1988 at a plant producing the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) with TCDD as a contaminant. Cumulative TCDD exposure was estimated for each individual in the study by a toxicokinetic model. PRIMARY OUTCOME MEASURES: Calculation of cause-specific standardised mortality ratios (SMRs) and 95% confidence intervals (95% CI's) 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 model intercept of 5.1 ppt of TCDD was consistent with background TCDD concentrations in New Zealand among older members of the population. Exposed workers had non-significant increases in all-cancer deaths (SMR=1.08, 95% CI 0.86 to 1.34), non-Hodgkin lymphoma (SMR=1.57, 95% CI: 0.32 to 4.59), soft tissue sarcoma (one death) (SMR=2.38, 95% CI: 0.06 to 13.26), diabetes (SMR=1.27, 95% CI: 0.55 to 2.50) and ischaemic heart disease (SMR=1.21, 95% CI: 0.96 to 1.50). Lung cancer deaths (SMR=0.95, 95% CI: 0.56 to 1.53) were fewer than expected. Neither the stratified SMR nor the proportional hazard analysis showed a dose-response relationship. CONCLUSION: There was no evidence of an increase in risk for 'all cancers', any specific cancer and no systematic trend in cancer risk with TCDD exposure. This argues against the carcinogenicity of TCDD at lower levels of exposure.

Lymphatic and hematopoietic cancers among benzene-exposed workers.

OBJECTIVE: High benzene exposure is related to acute nonlymphocytic leukemia. Recently, myelodysplastic syndrome has been observed at low benzene exposure levels. METHODS: We updated a mortality study of workers with benzene exposure examining acute nonlymphocytic leukemia and myelodysplastic syndrome. We calculated standardized mortality ratios with 95% confidence intervals and examined latency and trends for cumulative exposure levels. RESULTS: All leukemias (standardized mortality ratio = 1.21; 95% confidence interval = 0.74 to 1.97) and acute non-lymphocytic leukemia (standardized mortality ratio = 1.04; 95% confidence interval = 0.34 to 2.44) were at expected levels. We observed one death from myelodysplastic syndrome (standardized mortality ratio = 6.48; 95% confidence interval = 0.17 to 38.15). We observed no trend for cumulative exposure levels. CONCLUSIONS: Our results for all leukemias are consistent with a small increase in risk observed in the lower-exposed subgroups of the Pliofilm study; however, our results are also consistent with no increased risk especially for acute nonlymphocytic leukemia.

Brain Cancer in Workers Employed at a Laboratory Research Facility.

BACKGROUND: An earlier study of research facility workers found more brain cancer deaths than expected, but no workplace exposures were implicated. METHODS: Adding four additional years of vital-status follow-up, we reassessed the risk of death from brain cancer in the same workforce, including 5,284 workers employed between 1963, when the facility opened, and 2007. We compared the work histories of the brain cancer decedents in relationship to when they died and their ages at death. RESULTS: As in most other studies of laboratory and research workers, we found low rates of total mortality, total cancers, accidents, suicides, and chronic conditions such as heart disease and diabetes. We found no new brain cancer deaths in the four years of additional follow-up. Our best estimate of the brain cancer standardized mortality ratio (SMR) was 1.32 (95% confidence interval [95% CI] 0.66-2.37), but the SMR might have been as high as 1.69. Deaths from benign brain tumors and other non-malignant diseases of the nervous system were at or below expected levels. CONCLUSION: With the addition of four more years of follow-up and in the absence of any new brain cancers, the updated estimate of the risk of brain cancer death is smaller than in the original study. There was no consistent pattern among the work histories of decedents that indicated a common causative exposure.

Cancer mortality of workers exposed to styrene in the U.S. Reinforced plastics and composite industry.

BACKGROUND: Epidemiologic studies have reported increased risk of lymphohematopoietic cancers, lung cancer, and pancreatic cancer after exposure to styrene, although findings across studies are not consistent. METHODS: We update a large study of reinforced plastic industry workers with relatively high exposures to styrene, examining cancer risks associated with exposure levels. The study includes 15,826 workers who were exposed between 1948 and 1977 with vital-status follow-up from 1948 to 2008. We examine mortality rates associated with cumulative exposure, duration of exposure, peak exposures, average exposure, and time since first exposure to styrene. Exposure estimates were truncated starting in 1977, the period with the lowest exposures, leaving 27% of the study group with incomplete work histories. RESULTS: The standardized mortality ratios were 0.84 (95% confidence interval = 0.69-1.02) for all lymphatic and hematopoietic cancers combined, 0.72 (0.50-1.00) for non-Hodgkin lymphoma, and 0.84 (0.60-1.14) for leukemia. There was no trend with either cumulative exposure to styrene or number of peaks. Pancreatic cancer deaths were at expected levels (0.96 [0.73-1.22]). There were more lung cancer deaths than expected (1.34 [1.23-1.46]), although with a marked inverse trend with cumulative exposure. CONCLUSION: We found no coherent evidence that styrene exposure increases risk from cancers of the lymphatic and hematopoietic tissue, pancreas, or lung.

Elimination rates of dioxin congeners in former chlorophenol workers from Midland, Michigan.

BACKGROUND: Exposure reconstructions and risk assessments for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins rely on estimates of elimination rates. Limited data are available on elimination rates for congeners other than TCDD. OBJECTIVES: We estimated apparent elimination rates using a simple first-order one-compartment model for selected dioxin congeners based on repeated blood sampling in a previously studied population. METHODS: Blood samples collected from 56 former chlorophenol workers in 2004-2005 and again in 2010 were analyzed for dioxin congeners. We calculated the apparent elimination half-life in each individual for each dioxin congener and examined factors potentially influencing elimination rates and the impact of estimated ongoing background exposures on rate estimates. RESULTS: Mean concentrations of all dioxin congeners in the sampled participants declined between sampling times. Median apparent half-lives of elimination based on changes in estimated mass in the body were generally consistent with previous estimates and ranged from 6.8 years (1,2,3,7,8,9-hexachlorodibenzo-p-dioxin) to 11.6 years (pentachlorodibenzo-p-dioxin), with a composite half-life of 9.3 years for TCDD toxic equivalents. None of the factors examined, including age, smoking status, body mass index or change in body mass index, initial measured concentration, or chloracne diagnosis, was consistently associated with the estimated elimination rates in this population. Inclusion of plausible estimates of ongoing background exposures decreased apparent half-lives by approximately 10%. Available concentration-dependent toxicokinetic models for TCDD underpredicted observed elimination rates for concentrations < 100 ppt. CONCLUSIONS: The estimated elimination rates from this relatively large serial sampling study can inform occupational and environmental exposure and serum evaluations for dioxin compounds.

Cancer incidence of 2,4-D production workers.

Despite showing no evidence of carcinogenicity in laboratory animals, the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) has been associated with non-Hodgkin lymphoma (NHL) in some human epidemiology studies, albeit inconsistently. We matched an existing cohort of 2,4-D manufacturing employees with cancer registries in three US states resulting in 244 cancers compared to 276 expected cases. The Standardized Incidence Ratio (SIR) for the 14 NHL cases was 1.36 (95% Confidence Interval (CI) 0.74-2.29). Risk estimates were higher in the upper cumulative exposure and duration subgroups, yet not statistically significant. There were no clear patterns of NHL risk with period of hire and histology subtypes. Statistically significant results were observed for prostate cancer (SIR = 0.74, 95% CI 0.57-0.94), and "other respiratory" cancers (SIR = 3.79, 95% CI 1.22-8.84; 4 of 5 cases were mesotheliomas). Overall, we observed fewer cancer cases than expected, and a non statistically significant increase in the number of NHL cases.

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.

Mortality rates among workers exposed to dioxins in the manufacture of pentachlorophenol.

OBJECTIVE: We sought to determine if workers exposed to dioxins in pentachlorophenol (PCP) manufacturing were at increased risk of death from specific causes. METHODS: We examined death rates among 773 workers exposed to chlorinated dioxins during PCP manufacturing from 1937 to 1980 using serum dioxin evaluations to estimate exposures to five dioxins. RESULTS: Deaths from all causes combined, all cancers combined, lung cancer, diabetes, and ischemic heart disease were near expected levels. There were eight deaths from non-Hodgkin lymphoma (standardized mortality ratios = 2.4, 95% CI = 1.0 to 4.8). We observed no trend of increasing risk for any cause of death with increasing dioxin exposure. However, the highest rates of non-Hodgkin lymphoma were found in the highest exposure group (standardized mortality ratios = 4.5, 95% CI = 1.2 to 11.5). CONCLUSIONS: Other than possibly an increased risk of non-Hodgkin lymphoma, we find no other cause of death related to the mixture of the dioxin contaminants found in PCP.

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 rates among trichlorophenol workers with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The authors examined 1,615 workers exposed to dioxins in trichlorophenol production in Midland, Michigan, to determine if there were increased mortality rates from exposure. Historical dioxin levels were estimated by a serum survey of workers. Vital status was followed from 1942 to 2003, and cause-specific death rates and trends with exposure were evaluated. All cancers combined (standardized mortality ratio (SMR) = 1.0, 95% confidence interval (CI): 0.8, 1.1), lung cancers (SMR = 0.7, 95% CI: 0.5, 0.9), and nonmalignant respiratory disease (SMR = 0.8, 95% CI: 0.6, 1.0) were at or below expected levels. Observed deaths for leukemia (SMR = 1.9, 95% CI: 1.0, 3.2), non-Hodgkin lymphoma (SMR = 1.3, 95% CI: 0.6, 2.5), diabetes (SMR = 1.1, 95% CI: 0.6, 1.8), and ischemic heart disease (SMR = 1.1, 95% CI: 0.9, 1.2) were slightly greater than expected. No trend was observed with exposure for these causes of death. However, for 4 deaths of soft tissue sarcoma (SMR = 4.1, 95% CI: 1.1, 10.5), the mortality rates increased with exposure. The small number of deaths and the uncertainty in both diagnosis and nosology coding make interpretation of this finding tenuous. With the exception of soft tissue sarcoma, the authors found little evidence of increased disease risk from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Mortality study update of ethylene oxide workers in chemical manufacturing: a 15 year update.

OBJECTIVE: To investigate the long-term mortality patterns of workers with past exposure to ethylene oxide (EO). METHODS: We redefined and updated a cohort of male workers employed in industrial facilities where EO was produced or used. All 2063 men were employed between 1940 and the end of 1988 and were observed for mortality through 2003. Cause specific Standardized Mortality Ratios were calculated. Internal analyses were made by applying Cox proportional hazards models to the data. RESULTS: No indications were found for excess cancer risks from EO exposures, including the lymphohematopoietic malignancies. There were 11 leukemia deaths and 11.8 expected and 12 non-Hodgkin lymphoma deaths and 11.5 expected. Proportional hazards modeling for all cause, leukemia and lymphoid malignancies mortality revealed no trends or associations with cumulative exposure. CONCLUSION: Despite the relatively high EO exposures in the past and extensive mortality follow-up, the cause specific mortality rates are comparable with those of the general US population. The Standardized Mortality Ratio analyses and the proportional hazards modeling for all cause mortality, leukemia and lymphoid malignancies mortality do not indicate exposure related effects in this cohort.

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.

Mortality among chemical workers at Texas City plant: 1940-2001.

OBJECTIVES: To evaluate the mortality experience of workers at a major chemical manufacturing site and to examine brain and liver cancers excesses reported at this site in previous studies. METHODS: This study included 9,730 employees at the Texas City location who worked between 1940 and 2001. Standardized mortality ratios and confidence intervals were calculated. RESULTS: There was less than expected deaths due to all cause mortality and no increase in all cancer mortality. Brain tumor mortality, which did exceed expected rates in past years, was at expected levels in recent years. Liver cancer mortality was greater than expected. CONCLUSION: Brain tumor mortality was either due to chance in the early years or the cause of the brain tumors has been eliminated. Mortality due to liver cancer is higher than expected but only among men hired before 1950.

Chlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyl profiles of workers with trichlorophenol and pentachlorophenol exposures.

We examined the serum lipid adjusted levels of 2,3,7,8-substituted chlorinated dioxins and furans, and four coplanar PCBs for 98 workers. We found workers who worked only in the trichlorophenol units had mean lipid adjusted 2,3,7,8-TCDD levels of 36.8 ppt significantly higher (p<0.05) than 6.0 ppt in the reference group. Workers who worked only in the pentachlorophenol units had mean lipid adjusted levels for 123478-HxCDD of 14.8 ppt, 123678-HxCDD of 156.4 ppt,123789-HxCDD of 23.7 ppt, 1234678-HpCDD of 234.6 ppt, and OCDD of 2,778.2 ppt significantly higher (p<0.05) than the reference group levels for the same congeners of 7.5, 71.8, 8.0, 67.5, and 483.2 ppt, respectively. While we did find 12378-PeCDD levels higher than the reference group in trichlorophenol and pentachlorophenol workers, the differences are small, and could be attributed to normal variation. All furan levels among the trichlorophenol or pentachlorophenol only workers were not significantly different than the reference group. Workers with both trichlorophenol and pentachlorophenol exposures had mean dioxin levels consistent with complex chlorophenol exposures. Tradesmen who worked throughout the plant had congener profiles consistent with both trichlorophenol and pentachlorophenol exposures. PCB 169, 23478-PeCDF, 123478-HxCDF, and 123678-HxCDF levels were also significantly greater (p<0.05) in these tradesmen than in the reference group. We found distinct patterns of dioxin congeners many years after exposure among workers with different chlorophenol exposures. We were effectively able to distinguish past trichlorophenol exposures from pentachlorophenol exposures based on differing serum dioxin profiles among workers.

Factors related to dioxin and furan body levels among Michigan workers.

We evaluated serum concentrations of five selected dioxin, furan, and polychlorinated biphenyls (PCB) congeners among 412 workers at a Midland, Michigan plant that manufactured trichlorophenol and pentachlorophenol (PCP) and formulated chlorophenol-based products. We examined occupational indicators of exposure to these chlorophenols taking into account intrinsic factors such as age and body fat and potential environmental sources of exposure from consumption of local game and fish and other occupations. All five congeners were significantly associated with age and body fat. 2378-TCDD serum concentrations were associated with trichlorophenol operations, total years employed at the plant, as well as working as a hazardous waste worker. 123678-H(6)CDD serum concentrations were related to occupational PCP exposure, chloracne, recent weight loss, eating local game, and working as a hazardous waste worker. Serum concentrations of PCB126 were related to smoking (inversely), and eating local fish or local game. Other factors such as diet and jobs outside of the chlorophenol plant exposures had only a very minor impact on dioxin and furan concentrations in these workers.

Serum concentrations of chlorinated dibenzo-p-dioxins and dibenzofurans among former Michigan trichlorophenol and pentachlorophenol workers.

This study examines serum levels of 2,3,7,8-substituted chlorinated dioxins and furans, and PCBs for 375 Michigan workers with potential chlorophenol exposure, 37 Worker Referents, and 71 Community Referents. The chlorophenol workers were last exposed to trichlorophenol and/or pentachlorophenol 26-62 years ago. Employees working only in the trichlorophenol units had mean lipid-adjusted 2378-tetrachlorodibenzo-p-dioxin (TCDD) levels of 15.9 ppt compared with 6.5 ppt in the Worker Referents. Employees working only in the pentachlorophenol units had mean lipid-adjusted levels for 123478-H6CDD of 16.1 ppt, 123678-H6CDD of 150.6 ppt, 123789-H6CDD of 20.2 ppt, 1234678-H7CDD of 192.6 ppt, and OCDD of 2,594.0 ppt compared with the Worker Referent levels for the same congeners of 7.5, 74.7, 8.6, 68.7, and 509.1 ppt, respectively. All furan and PCB levels among workers in the trichlorophenol and/or pentachlorophenol departments were similar to the Worker Referents. The Tradesmen who worked throughout the plant had dioxin congener profiles consistent with both trichlorophenol and pentachlorophenol exposures. PCB levels and levels of 23478-P5CDF, 123478-H6CDF, and 123678-H6CDF were also greater in these Tradesmen than in the Worker Referents. The Worker Referent group had higher levels of dioxins and furans than the Community Referents indicating the potential for exposure outside the chlorophenol departments at the site. Distinct patterns of dioxin congeners were found many years after exposure among workers with different chlorophenol exposures. Furthermore, past trichlorophenol exposures were readily distinguishable from past pentachlorophenol exposures based on serum dioxin evaluations among workers. These data can be used to better assess dioxin exposures in future health studies.

Mortality study update of acrylamide workers.

OBJECTIVE: The authors examined the long-term health effects of occupational exposure to acrylamide among production and polymerisation workers. METHODS: An earlier study of 371 acrylamide workers was expanded to include employees hired since 1979. In this updated study, 696 acrylamide workers were followed from 1955 through 2001 to ascertain vital status and cause of death. Exposure to acrylamide was retrospectively assessed based on personal samples from the 1970s onwards and area samples over the whole study period. RESULTS: Fewer of the acrylamide workers died (n = 141) compared to an expected number of 172.1 (SMR 81.9, 95% CI 69.0 to 96.6). No cause-specific SMR for any of the investigated types of cancer was exposure related. The authors did, however, find more pancreatic cancer deaths than expected (SMR 222.2, 95% CI 72.1 to 518.5). With respect to non-malignant disease, more diabetes deaths were observed than expected (SMR 288.7, 95% CI 138.4 to 531.0). To assess the influence of regional factors, the analysis was repeated with an internal reference population. The elevated SMR for diabetes persisted. CONCLUSION: This study provides little evidence for a cancer risk from occupational exposure to acrylamide at production facilities. However, the increased rates of pancreatic cancer in this study and another larger study of acrylamide production workers indicate that caution is needed to rule out a cancer risk. The authors believe that the excess of diabetes mortality in this study is most likely not related to acrylamide exposure, because a larger study of acrylamide workers reported a deficit in this cause of death. The authors conclude that the increased SMR for diabetes mortality is probably not related to regional influences.

Body mass index and serum chlorinated dibenzo-p-dioxin and dibenzofuran levels.

Several studies have found that current levels of 2,3,7,8 tetrachlorodibenzo-p-dioxin in serum lipids are related to age with older persons generally having higher levels. To account for this age pattern, reference ranges based on national samples have been established in order to allow determination of background levels for regional studies. In several studies, body mass index (BMI), has also been associated with current 2,3,7,8 tetrachlorodibenzo-p-dioxin levels with increasing body mass index related to increasing levels. We measured lipid-adjusted serum levels for all 2,3,7,8-substituted dioxins and furans in 62 chemical manufacturing workers with chlorophenol exposures and 36 workers without chlorophenol exposures employed at the same location. We then assessed the impact of age and BMI on the serum levels of all these compounds in the presence of other potential confounders. We found that both factors are important independent determinants of serum levels of 2,3,7,8-substituted dioxins and furans. Specifically, age and BMI are both important factors for assessing background levels of 2,3,7,8 tetrachlorodibenzo-p-dioxin, 1,2,3,7,8 pentachlorodibenzo-p-dioxin and the calculated total toxic equivalency. BMI, but not age, is important for assessing background levels of higher chlorinated dioxins and some hexachlorofurans. We conclude that age and BMI are both important considerations when comparing a potentially exposed group to a referent group, or to national norms. Further, age and BMI may also be important in epidemiology studies where back-extrapolation from current dioxin levels is used to assess historical chlorophenol exposure.

Communication of epidemiology study results by industry: the Dow Chemical Company approach.

Communicating epidemiology study results to subjects, affected workers, and community members is an important part of compliance and alignment with our company's policies, industry's Responsible Care Principles, and the doctrines of Good Epidemiology Practices. It is the responsibility of the investigators to interpret their research appropriately for each audience, and to assure that all who have a need or right to know get information in a form meaningful to them. We discuss study communication with examples from a recent evaluation of communication efforts within Dow and our experience with occupational and community studies on dioxin. We also discuss how we currently structure worker and community communication based on this experience. Since each Dow protocol must include a communication plan, when we agree to undertake a study, we are also agreeing to communicate study results. Depending upon the nature and type of the study, there may also be some prestudy communication. We encourage all investigators to share the results of their studies more broadly than just scientific publication and plan for the study communication before the study is initiated.