Abstract Silver, an element of the II(B) Group, is in the second transition series of the periodic table. It is a white, lustrous, relatively soft and very malleable metal. Silver has high thermal and electrical conductivity and resists oxidation in air that is devoid of hydrogen sulfide. Silver is insoluble in water although it can exist in an aqueous environment in three cationic forms, Ag(I), Ag(II), and Ag(III), in addition to its metallic state (AgO). Most silver compounds are made from silver nitrate, which is prepared from silver metal. The toxicological properties of many substances depend on the particular chemical species of that substance, and silver is no exception. Although silver exists in its elemental state and many references within the scientific literature are simply to “silver,” it is important to stress that speciation is critical to understanding the potential for toxicity and subsequent health effects. As with many substances, a discussion of each silver species' toxicological properties would appear rather incomplete due to the lack of information available. Given these factors, it is more logical to discuss silver based on specific target organs or endpoints of concern (i.e., irritation, carcinogenicity) and to provide information on relevant silver species within this context. An explanation for the apparent lack of toxicity information on numerous species of silver is that many of the commonly used forms are insoluble in aqueous media and therefore are not readily tested in laboratory animal species. This property of many silver species may, in part, also explain its apparent lack of acute or chronic toxicity in humans based on years of occupational and workplace experience. Gold is a dense, yet malleable, lustrous, yellow metal widely found in nature as elemental gold or in combination with sulfides in igneous rocks and ores. Gold is very stable and nonreactive and does not burn or oxidize in air. Other than in its atomic state, the metal does not react with oxygen, sulfur, or selenium at any temperature. Gold does react with various oxidizing agents at ambient temperatures provided a good ligand is present to lower the redox potential below that of water. Therefore, gold is not attacked by most acids under ordinary conditions and is stable in basic media. Early uses of gold were in medicinal, antibacterial, and dental applications dating back to the ancient Chinese and Egyptians. Gold salts have been used therapeutically, without notable success in treating several diseases, including asthma, leprosy, syphilis, and tuberculosis. Presently, gold salts have therapeutic usefulness (chrysotherapy) limited to treating rheumatoid arthritis of the peripheral joints and in certain rare skin diseases. Gold salts are most efficacious in the early stages of arthritic disease and reduce the inflammatory process but without inducting any repair process in the joints. Two generally recognized disadvantages to chrysotherapy include relapse following discontinuation of treatment and potential toxicity associated with gold salts. Because of its distribution in the body and short half‐life, colloidal radioactive gold, has been used as a radiation source in treating cancer. As noted for silver, a discussion of the toxicological properties for each gold compound is not practical from the standpoint of available information. Therefore, this discussion on gold and its toxicity potential centers on particular aspects of gold toxicology, and within this framework, where a particular gold compound has been evaluated, it are discussed.

Clustering of health events in or around industrial facilities sometimes leads to worker and community concerns that plant management or local health professionals must address. We provide an eight-step process to deal with these concerns systematically. We emphasize the use of good scientific practices with managerial oversight for effective worker and community communication. This process is directed to plant management and the local health professional and emphasizes the practical aspects of the investigation.

A call for risk assessment approaches that better characterize and quantify uncertainty has been made by the scientific and regulatory community. This paper responds to that call by demonstrating a distributional approach that draws upon human data to derive potency estimates and to identify and quantify important sources of uncertainty. The approach is rooted in the science of decision analysis and employs an influence diagram, a decision tree, probabilistic weights, and a distribution of point estimates of carcinogenic potency. Its results estimate the likelihood of different carcinogenic risks (potencies) for a chemical under a specific scenario. For this exercise, human data on formaldehyde were employed to demonstrate the approach. Sensitivity analyses were performed to determine the relative impact of specific levels and alternatives on the potency distribution. The resulting potency estimates are compared with the results of an exercise using animal data on formaldehyde. The paper demonstrates that distributional risk assessment is readily adapted to situations in which epidemiologic data serve as the basis for potency estimates. Strengths and weaknesses of the distributional approach are discussed. Areas for further application and research are recommended.

The mortality experience of two overlapping cohorts of employees engaged in the manufacture of photographic film support was evaluated to assess the potential chronic health effects of methylene chloride exposure. In the first analysis, we examined causes of death among 1311 men initially employed between 1946 (when the solvent was first used) and 1970; in the second, we updated mortality in a 1964 to 1970 employed cohort of 1013 men. Follow-up was through 1994. The mean exposure among members of the 1946 to 1970 cohort was 39 ppm (8-hour time-weighted average) for 17 years, and the median length of follow-up from first exposure was 34 years. Members of the 1964 to 1970 cohort received an average exposure of 26 ppm for 24 years; median time from first exposure was 35 years. Compared with general population vital statistics, mortality in both cohorts was below expectation for all causes of death, ischemic heart disease, and cancer, including such sites as the lung and liver, which were target organs identified in animal toxicology studies. No statistically significant increases were observed for any cause of death. The combined results of this study and three others in the photographic film and textile fibers industries (approximately 7300 subjects) show that long-term exposure to methylene chloride does not increase the risk of death from any cause including specific diagnoses that have been associated with this widely used solvent.

Mortality in a 1942–1990 cohort of 858 men and 21 women employed in the manufacture and use of hydroquinone was evaluated through 1991. Average exposure concentrations, 1949–1990, ranged from 0.1 to 6.0 mg/m3 for hydroquinone dust and from less than 0.1 to 0.3 for quinone vapor (estimated 8-h time-weighted averages). Compared with general population and occupational referents, there were statistically significant deficits in total mortality and deaths due to cancer. No significant excesses were observed for such hypothesized causes as kidney cancer [2 observed vs 1.3 expected (both control groups), P ∼ 0.39], liver cancer (0 vs 0.8, 1.3), and leukemia (0 vs 2.3, 2.7). Dose-response analyses of selected causes of death, including renal carcinoma, demonstrated no statistically significant heterogeneities or linear trends according to estimated career hydroquinone exposure (mg/m3-years) or time from first exposure.

Risk AnalysisVolume 11, Issue 4 p. 569-571 Response to Tollefson et al.1 F. Terry Hearne, F. Terry Hearne Epidemiology Section, Health and Environment Laboratories, Building 320, Kodak Park, Eastman Kodak Company, Rochester, New York 14652-3615.Search for more papers by this author F. Terry Hearne, F. Terry Hearne Epidemiology Section, Health and Environment Laboratories, Building 320, Kodak Park, Eastman Kodak Company, Rochester, New York 14652-3615.Search for more papers by this author First published: December 1991 https://doi.org/10.1111/j.1539-6924.1991.tb00643.xCitations: 2 1 Manuscript received January 14, 1991. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume11, Issue4December 1991Pages 569-571 RelatedInformation

Mortality findings in a 1964 to 1970 cohort of 1013 hourly-wage men exposed to methylene chloride were substantially unchanged after 4 additional years of observation through 1988. Mean exposure was 26 ppm (8-hour time-weighted average) for 23 years; median follow-up from first exposure was 33 years. A comparison with death rates in both general population and industrial referents showed nonsignificant deficits in observed-expected ratios for such hypothesized causes as lung and liver cancer and ischemic heart disease. Overall mortality from 1964 to 1988 (n = 238) was significantly decreased v both referent groups. The study had 90% power to detect relative risks of 1.7 and 1.3 for lung cancer and ischemic heart disease, respectively; power was inadequate for hepatic cancer. No pancreatic cancer deaths occurred since the 1984 follow-up; eight have been observed v 4.2 expected (P = .13). An analysis of dose response for selected causes of death demonstrated no statistically significant trend according to either career methylene chloride exposure or latency. Similar results were observed when the data were analyzed using Poisson regression modeling.

To assess the potential chronic health effects of methylene chloride, the mortality experience of a maturing 1964 to 1970 cohort of 1,013 hourly men was evaluated through 1984. On average, employees were exposed at a rate of 26 ppm (eight-hour time-weighted average) for 22 years; median latency was 30 years. Compared with the general population, no statistically significant excesses were observed for such hypothesized causes as lung cancer (14 observed v 21.0 expected), liver cancer (0 v 0.8), and ischemic heart disease (69 v 98.1); dose-response relationships based on career methylene chloride exposure and latency were not demonstrated. Among nonhypothesized causes, a significant deficit was reported for total deaths (176 v 253.2). None of the industrial referent comparisons achieved statistical significance. Sufficient power was available to detect relative risks of 1.6 for lung malignancy and 1.3 for ischemic heart disease. In contrast, there was inadequate power to identify meaningful risk levels for hepatic cancer. With 14 combined lung and liver cancer deaths observed v 36.3 predicted (P less than .0001), the mortality estimate projected from a mathematical model derived from an animal bioassay substantially overestimated cancer mortality for these sites. This inconsistency emphasizes the need to incorporate epidemiologic evidence in assessing the human health risks associated with long-term exposure to this widely used solvent.

The mortality experience of a cohort of approximately 9,000 traced men employed at a Tennessee chemical plant was examined between 1972 and 1982. Statistically significant total mortality deficits of 41% to 46% and 14%, respectively, were observed compared with general population and occupational controls. Cancer deaths were 22% (significant) below expectation based on state and national vital statistics, whereas comparison with an employed group showed no difference. Significantly low mortality differentials were also reported for other major causes, including diseases of the circulatory, respiratory, and digestive systems. Analysis of the data by length of employment, payroll status, and chemical production division demonstrated no unusual patterns. The cohort's favorable mortality experience may be attributed to such factors as employee selectivity, health maintenance, accessibility to medical care, and less cigarette smoking.

An epidemiologic investigation of a 1964 cohort of 478 photographic processors in nine Eastman Kodak Color Print and Processing (CP&P) laboratories in the continental United States was undertaken. Analysis of pre-1965 environmental data indicated that chemical exposures were within the standards applicable at the time. The results showed no significant excess mortality, sickness-absence or cancer incidence. The processing cohort's mortality experience after 16 years of follow-up compared favorably with that of two industrial control populations. The present study represents (to our knowledge) the first published occupational epidemiology investigation that specifically examines the health of workers engaged in large-scale commercial photofinishing operations.

Epidemiology Section, Health, Safety and Human Factors, Laboratory, Eastman Kodak Company, Rochester, NY 14650

When determining the generalized T 2 statistics for a sample of n observations using principal components, the occasion may arise where one is interested not in the average of the deviations of a particular component from its aim or standard, but the average of the absolute values of these deviations because it is the magnitude, not the direction. which is of interest. A largesample approximation suitable for quality control applications is proposed to still enable one to include this component in the computation of T M 2. The adequacy of this approximation is examined and a numerical example is included. KEYWORDS: Principal componentsQuality controlAbsolute valuesGeneralized T statistics

This paper discusses, in terms of correlations, the relation between coefficients of the characteristic vectors used in principal component analysis, both within each vector and among vectors. These relationships will be illllstrated with examples (1) where the variates represent a battery of physical tests related to rocket testing and (2) where they represent equally spaced observations on a continuous curve, a case related to film measurements.