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Objective: The objective of this study was to review 32 studies on firefighters and to quantitatively and qualitatively determine the cancer risk using a meta-analysis., Methods: A comprehensive search of computerized databases and bibliographies from identified articles was performed. Three criteria used to assess the probable, possible, or unlikely risk for 21 cancers included pattern of meta-relative risks, study type, and heterogeneity testing., Results: The findings indicated that firefighters had a probable cancer risk for multiple myeloma with a summary risk estimate (SRE) of 1.53 and 95% confidence interval (CI) of 1.21-1.94, non-Hodgkin lymphoma (SRE = 1.51, 95% CI = 1.31-1.73), and prostate (SRE = 1.28; 95% CI = 1.15-1.43). Testicular cancer was upgraded to probable because it had the highest summary risk estimate (SRE = 2.02; 95% CI = 1.30-3.13). Eight additional cancers were listed as having a "possible" association with firefighting., Conclusions: Our results confirm previous findings of an elevated metarelative risk for multiple myeloma among firefighters. In addition, a probable association with non-Hodgkin lymphoma, prostate, and testicular cancer was demonstrated.

Aims: To extend mortality follow up from 1987 to 1998 for cohort of 18 235 men and women exposed to ethylene oxide., Methods: Standard mortality follow up, life table and Cox regression analysis., Results: There were 2852 deaths, compared with 1177 in the earlier 1987 follow up. There was no overall excess of haematopoietic cancers combined or of non-Hodgkin's lymphoma. However, internal exposure-response analyses found positive trends for haematopoietic cancers which were limited to males (15 year lag). The trend in haematopoietic cancer was driven by lymphoid tumours (non-Hodgkin's lymphoma, myeloma, lymphocytic leukaemia), which also have a positive trend with cumulative exposure for males with a 15 year lag. Haematopoietic cancer trends were somewhat weaker in this analysis than trends in the earlier follow up, and analyses restricted to the post-1987 data did not show any significant positive trends (exposure levels dropped sharply in the early 1980s). Breast cancer did not show any overall excess, although there was an excess in the highest cumulative exposure quartile using a 20 year lag. Internal exposure-response analyses found positive trend for breast cancer using the log of cumulative exposure with a 20 year lag., Conclusions: There was little evidence of any excess cancer mortality for the cohort as a whole, with the exception of bone cancer based on small numbers. Positive exposure-response trends for lymphoid tumours were found for males only. Reasons for the sex specificity of this effect are not known. There was also some evidence of a positive exposure-response for breast cancer mortality.

Low-levels of dioxin cause cancer in animals. In 1997 dioxin was found to be a human carcinogen by the International Agency for Research on Cancer, based largely on four studies of industrial workers exposed to high levels. Recently there has been interest in estimating human cancer risk at low level environmental exposures. Here we review quantitative exposure-response analyses and risk assessment for low environmental levels based on the largest existing cohort of workers exposed to dioxin (the U.S. NIOSH cohort). We estimate that doubling background levels of exposure, which may occur for example by eating a lot of fish which have accumulated dioxin, will increase lifetime risk of cancer death by 0.1 to 1.0%. In the US the background risk of cancer death by age 75 is 12%, so doubling background levels of dioxin exposure would increase this lifetime risk to somewhere between 12.1 and 13.0%. Our results agree broadly with results from a German cohort, which is the only other cohort for which a quantitative risk assessment has been conducted.

Background: In 1997, the International Agency for Research on Cancer classified 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a group 1 human carcinogen, based largely on four highly exposed industrial cohorts that showed an excess of all cancers combined. In this study, we extended the follow-up period for the largest of these cohorts by 6 years and developed a job-exposure matrix., Methods: We did cohort mortality analyses involving 5132 chemical workers at 12 U.S. plants by use of life table techniques (U.S. population referent) and Cox regression (internal referent). We conducted exposure-response analyses for 69% of the cohort with adequate work history data and adequate plant data on TCDD contamination. All P values are two-sided., Results: The standardized mortality ratio (SMR) for all cancers combined was 1.13 (95% confidence interval = 1.02-1.25). We found statistically significant positive linear trends in SMRs with increasing exposure for all cancers combined and for lung cancer. The SMR for all cancers combined for the highest exposure group was 1.60 (95% confidence interval = 1.15-1.82). SMRs for heart disease showed a weak increasing trend with higher exposure (P = .14). Diabetes (any mention on the death certificate) showed a negative exposure-response trend. Internal analyses with Cox regression found statistically significant trends for cancer (15-year lag time) and heart disease (no lag)., Conclusions: Our analyses suggest that high TCDD exposure results in an excess of all cancers combined, without any marked specificity. However, excess cancer was limited to the highest exposed workers, with exposures that were likely to have been 100-1000 times higher than those experienced by the general population and similar to the TCDD levels used in animal studies.