ETHYLENE-OXIDE - AN ASSESSMENT OF THE EPIDEMIOLOGIC EVIDENCE ON CARCINOGENICITY

Citation
Re. Shore et al., ETHYLENE-OXIDE - AN ASSESSMENT OF THE EPIDEMIOLOGIC EVIDENCE ON CARCINOGENICITY, British Journal of Industrial Medicine, 50(11), 1993, pp. 971-997
Citations number
46
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
00071072
Volume
50
Issue
11
Year of publication
1993
Pages
971 - 997
Database
ISI
SICI code
0007-1072(1993)50:11<971:E-AAOT>2.0.ZU;2-M
Abstract
Mortality from cancer among workers exposed to ethylene oxide (EtO) ha s been studied in 10 distinct cohorts that include about 29800 workers and 2540 deaths. This paper presents a review and meta-analysis of th ese studies, primarily for leukaemia, non-Hodgkin's lymphoma, stomach cancer, pancreatic cancer, and cancer of the brain and nervous system. The magnitude and consistency of the standardised mortality ratios (S MRs) were evaluated for the individual and combined studies, as well a s trends by intensity or frequency of exposure, by duration of exposur e, and by latency (time since first exposure). Exposures to other work place chemicals were examined as possible confounder variables. Three small studies by Hogstedt initially suggested an association between E tO and leukaemia, but in seven subsequent studies the SMRs for leukaem ia have been much lower. For the combined studies the SMR = 1.06 (95% confidence interval (95% CI) 0.73-1.48). There was a slight suggestion of a trend by duration of exposure (p = 0.19) and a suggested increas e with longer latency (p = 0.07), but there was no overall trend in ri sk of leukaemia by intensity or frequency of exposure; nor did a cumul ative exposure analysis in the largest study indicate a quantitative a ssociation. There was also an indication that in two studies with incr eased risks the workers had been exposed to other potential carcinogen s. For non-Hodgkin's lymphoma there was a suggestive risk overall (SMR = 1.35, 95% CI 0.93-1.90). Breakdowns by exposure intensity or freque ncy, exposure duration, or latency did not indicate an association, bu t a positive trend by cumulative exposure (p = 0.05) was seen in the l argest study. There was a suggested increase in the overall SMR for st omach cancer (SMR = 1.28, 95% CI 0.98-1.65 (CI 0.73-2.26 when heteroge neity among the risk estimates was taken into account)), but analyses by intensity or duration of exposure or cumulative exposure did not su pport a causal association for stomach cancer. The overall SMRs and ex posure-response analyses did not indicate a risk from EtO for pancreat ic cancer (SMR = 0.98), brain and nervous system cancer (SMR = 0.89), or total cancer (SMR = 0.94). Although the current data do not provide consistent and convincing evidence that EtO causes leukaemia or non-H odgkin's lymphoma, the issues are not resolved and await further studi es of exposed populations.