tained from 37 incinerator workers in four facilities and from 35 water-treatment plant workers in eight facilities. When the first urine samples were compared, incinerator workers had positive mutagen assays four times more often than water-treatment workers; the difference was statistically significant. Although the frequency of mutagens was higher among incinerator workers for the second and third urine samples, the differences from frequencies in the water-treatment workers were no longer statistically significant. With microsomal activation, the proportions of incinerator workers who had positive mutagen assays declined in the three urine samples—from 21.6% to 15.2% and then 8.3%. The authors speculated that the trend might be explained in two ways. One is that incinerator workers began to take measures to reduce their exposures. The other is that exposures to mutagenic substances in incinerator plants was highly variable. The authors pointed out that the presence of mutagens in the urine does not establish that mutations are taking place in the cells of these workers, but they did recommend that measures be taken to reduce occupational exposures of incinerator workers to potential mutagens in their work environments.

Angerer et al. (1992) measured concentrations of various organic substances in the blood and urine of 53 workers at a municipal-waste incinerator in Germany and 431 men and women “who belong to different subgroups,” also in Germany. No information is provided in the report on the extent of industrial-hygiene controls in the incinerator facility. Statistically significantly higher concentrations of urinary hydroxypyrene, 2,4- and 2-5-dichlorophenol, and 2,4,5-trichlorophenol, and of plasma hexachlorobenzene (HCB) were found among incinerator workers, whereas the controls had higher concentrations of urinary 4-monochlorophenol and tetrachlorophenol. No statistically significant differences between the two groups were found for blood benzene (after stratification on cigarette-smoking), plasma polychlorinated biphenyls, or urinary 2,4,6-trichlorophenol or pentachlorophenol. Urinary hydroxypyrene was measured because it is a metabolite of pyrene and has been shown to be a good indicator of internal dose of PAHs. Plasma PCBs and HCB and urinary chlorophenols were measured because these chemicals, when combusted, are precursors of dioxins and furans, and because they are easier to measure in biological material than the dioxins and furans. The lack of consistent findings between the incinerator and comparison groups for PCBs, HCB, and chlorophenols means this study provides no conclusive evidence on the exposure, absorption, or metabolism of combustion precursors of the PCDDs and PCDFs, and so allows no inference about exposures to PCDDs and PCDFs. However, the higher concentrations of hydroxypyrene might indicate that incinerator workers had higher exposures to PAHs.

Schecter et al. (1994) measured polychlorinated dioxins and dibenzofurans in pooled samples of blood from 85 workers at a relatively old incinerator in New York City and pooled blood from 14 matched controls in the same city. Higher concentrations of several of the dioxin and furan congeners, except TCDD, were found in the blood of incinerator workers. The authors comment that the

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