Mortality information/rates

Other information on the immunotoxicity of chloroform is limited to one study on effects of chloroform on host resistance in CD-I mice. A single exposure to 10.6 ppm chloroform for 3 hours did not increase the mortality rate after streptococcal challenge and did not alter the ability of alveolar macrophages to destroy bacteria in these mice (Aranyi et al. 1986). After repeated chloroform exposure (3 hours a day for 5 days), the mortality rate significantly increased, but the bactericidal activity of macrophages was not suppressed compared to control animals. 

For keyhole limpet hemocyanine (KLH) both antibody responses and delayed type hypersensitivity (DTH) reactions can be determined [43—45]. In addition several infectious models, including bacterial, viral and parasitic infections may be used to challenge the immune system [18,46]. As survival and eradication of the infections is the primary function of the immune system, these models provide direct information on the functional status of the immune system. Direct immunotoxic compounds will induce immunosuppression and thus an increase in infection rate and/or severity of the infection. The number of infectious agents (bacteria, parasites, or viral colonyforming units), increased morbidity and mortality are indications for an immunotoxic effect. Also a reduction in specific antibody levels in animals treated with the test compound compared to nontreated controls indicates immunosuppression. 

The mortality of 221 workers in a di(2-ethylhexyl) phthalate production plant in Germany was followed between 1940 and 1976. Most subjects (135/221) were hired after 1965 and the process was completely enclosed in 1966. No information on level of exposure was provided. Information on vital status for foreigners [number not stated] was obtained for only 55% of them, but appeared to be complete for the remaining cohort. Reference rates were obtained from local populations (the city of Ludwigshafen, the Rheinhessen-Pfalz land) and national rates. Altogether, eight deaths... 

The U.S. study included mortality records from twelve chemical plants. In only two of those twelve plants was there any information about smoking, and in those two plants the smoking information was collected in the 1980s. To me, it is simply unimaginable that in a study that ended up focused on respiratory cancers so little information was obtained about smoking, which is associated with some 90 percent of respiratory cancer. In particular, there is no information about the smoking rates in men who died before the 1980s, who are, after all, the source of much of the data in a mortality study. 

Mortality associated with acrylonitrile exposure was evaluated as part of a study of 15 643 male workers in a rubber plant in the United States (Akron, Ohio) (Delzell Monson, 1982). Included in the analysis were 327 workers who were employed for at least two years in the plant between 1 January 1940 and 1 July 1971, and who had worked in two departments where acrylonitrile was used, i.e., 81 worked only in the nitrile rubber manufacturing operation where exposures to 1,3-butadiene (see this volume), styrene (lARC, 1994a) and vinylpyridine also occurred and 218 only in the department where the latex was coagulated and dried. [No information on levels of exposure to acrylonitrile was provided ] Mortality among these workers was assessed through 1 July 1978 and compared with age- and calendar-time-specific rates for white men in the United States. SMRs were 0.8 ( = 74 95% CI, 0.7-1.0) for all causes of death, 1.2 ( = 22 95% CI, 0.8-1.9) for all cancers combined, 1.5 ( = 9 95% CI, 0.7-2.9) for lung cancer, 4.0 ( = 2 95% CI, 0.5-14.5) for urinary bladder cancer and 2.3 ( = 4 95% CI, 0.6-5.8) for cancers of the lymphatic and haematopoietic system. SMRs for lung cancer by duration of employment were [1.0] (4 observed, 3.8 expected) [95% CI, 0.3-2.7] for < 5 years, and [3.3] (5 observed, 1.5 expected) [95% CI, 1.1-7.8] for 5-14 years. No case was observed with duration > 15 years. 

Cardiovascular Effects. Information regarding cardiovascular effects in humans after inhalation exposure to chromium and its compounds is limited. In a survey of a facility engaged in chromate production in Italy, where exposure concentrations were 0.01 mg chromium(VI)/m3, electrocardiograms were recorded for 22 of the 65 workers who worked in the production of dichromate and chromium trioxide for at least 1 year. No abnormalities were found (Sassi 1956). An extensive survey to determine the health status of chromate workers in seven U.S. chromate production plants found no association between heart disease or effects on blood pressure and exposure to chromates. Various manufacturing processes in the plants resulted in exposure of workers to chromite ore (mean time-weighted concentration of 0-0.89 mg chromium(ni)/m3) water-soluble chromium(VI) compounds (0.005-0.17 mg chromium(VI)/m3) and acid-soluble/water-insoluble chromium compounds (including basic chromium sulfate), which may or may not entirely represent trivalent chromium (0-0.47 mg chromium/m3) (PHS 1953). No excess deaths were observed from cardiovascular diseases and ischemic heart disease in a cohort of 4,227 stainless steel production workers from 1968 to 1984 when compared to expected deaths based on national rates and matched for age, sex, and calender time (Moulin et al. 1993). No measurements of exposure were provided. In a cohort of 3,408 individuals who had worked in 4 facilities that produced chromium compounds from chromite ore in northern New Jersey sometime between 1937 and 1971, where the exposure durations of workers ranged from <1 to >20 years, and no increases in atherosclerotic heart disease were evident (Rosenman and Stanbury 1996). The proportionate mortality ratios for white and black men were 97 (confidence limits 88-107) and 90 (confidence limits 72-111), respectively. 

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