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For the purpose of assessing the human carcinogenic potential of the chlorophenoxy herbicides MCPA, MCPP, and 2,4-DP, the relevant epidemiological and toxicological evidence is reviewed. These compounds have not produced tumours in animal studies conducted under current test guidelines, giving no reason to predict that they would be carcinogenic to humans. Epidemiological studies have been conducted on three continents; greater emphasis is placed on the studies reported from western Europe, however, as this has been the area of more use. Although several of these studies provide suggestive evidence of associations between exposure to chlorophenoxy compounds and increased risks for some uncommon cancers, it is inconsistent and far from conclusive. None of the evidence specifically implicates MCPA, MCPP, or 2,4-DP as human carcinogens.

Available medical and morbidity surveillance findings from 1976 to 1978 for two employee cohorts potentially exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were compared with those of matched unexposed employees. The medical surveillance findings were derived from a screening programme offered to all active employees and included an analysis of various medical history questions and blood chemistry results. Group medical insurance claims served as the source of morbidity surveillance data and the period prevalence of selected diseases was analysed. Few significant differences between the exposed and unexposed were detected. Among the cohort of employees potentially exposed during the manufacture of 2,4,5-trichlorophenoxyacetic acid (2,4,5,-T), a significantly greater frequency of x-ray proved ulcer was reported and significantly more members of this group had diseases of the digestive system diagnosed. Such findings were absent in the more highly TCDD-exposed cohort engaged in 2,4,5-trichlorophenol production, making it unlikely that dioxin was a cause.

The prevalence of selected illnesses and symptoms during 1977-85 was compared between 175 employees potentially exposed to the organophosphate insecticide chlorpyrifos and 335 matched controls with no history of exposure to organophosphates. Subjects were subdivided into three exposure intensity groups on the basis of job title and air monitoring data for dose response testing. This classification scheme was shown roughly to correlate with plasma cholinesterase inhibition in the workers. No statistically significant differences in illness or prevalence of symptoms were observed between the exposed and unexposed groups or among the three exposure subgroups. Potentially exposed employees did report symptoms of dizziness and of malaise and fatigue relatively more often than subjects from the comparison group; however, further analyses by exposure level, process area, or time did not support a relation with exposure. No cases of peripheral neuropathy were seen among the exposed workers. Although the sample size was small and the statistical power limited, the cumulative exposures likely to have been experienced by this workforce exceed those to be expected for individuals using the product as recommended. The absence of exposure related adverse effects, including neurological impairment, is reassuring.

The mortality experience of 371 employees assigned to acrylamide monomer and polymerisation operations was examined with particular emphasis on cancers at sites identified from animal studies such as the central nervous system, thyroid gland, other endocrine glands, and mesotheliomas. A total of 29 deaths was observed up until 1982 (38.0 expected). No statistically significant excesses were noted in the total cohort and no deaths were found for the hypothesised sites of cancer. The observed deaths in the total cohort for the all cancers category were somewhat in excess (11 v 7.9); however, this was due entirely to excess cancers of the digestive tract and respiratory system in the subgroup with previous exposure to organic dyes. Among those employees not exposed to organic dyes, four deaths were due to malignancies versus 6.5 expected. This study does not support a cause effect relation between exposure to acrylamide at this work site and overall mortality, total malignant neoplasms, or any specific cancers.

Mortality is reported to the end of 1982 for 878 chemical workers potentially exposed to 2,4-dichlorophenoxyacetic acid (2,4-D) at any time between 1945 and 1983. Observed mortality was compared with expected levels based on adjusted rates for United States white men and for other male employees from this manufacturing location who were not exposed to 2,4-D. Because of a recently reported increased incidence of astrocytomas in male rats fed the highest dose level of 2,4-D, special attention was given to deaths from brain neoplasms in the cohort. None was observed. The absence of an increased risk of brain cancer in people exposed to 2,4-D is supported by studies of other exposed populations and those studies are briefly reviewed. Moreover, in the present study, analyses by production area, duration of exposure, and cumulative dose showed no patterns suggestive of a causal association between 2,4-D exposure and any other particular cause of death.

Mortality was updated to the end of 1982 for 594 employees exposed to benzene who had been studied previously and for an additional 362 exposed workers not studied previously. Cause specific mortality comparisons were made using United States white male, age, and calendar year adjusted rates. Total mortality was observed to have been significantly below expectation, and this was particularly evident for deaths from accidental causes. Mortality from skin cancer was significantly raised, although there were no unusual or common characteristics among the affected individuals which would suggest a link with exposure to benzene. A non-significant excess of total deaths from leukaemia was noted based on four observed cases; however, all four were myelogenous leukaemias and this represented a significant excess in that subcategory. These and other deaths of possible interest are reviewed in detail. Analyses by work area, duration of exposure, and cumulative dose index did not show patterns suggestive of a causal association between exposure to benzene and any particular cause of death.