The purpose of this work was to measure important nutritional status parameters for captive primates, compare those with published data, and look for a link with diet. The nutritional status of nine captive primate species was examined using biochemical analysis. The species were spider monkeys (Ateles geoffroyi), colobus monkeys (Colobus guereza), sooty mangabeys (Cercocebus torquatus), Schmidt's monkeys (Cercopithecus ascanius), mandrills (Papio sphinx), baboons (Papio cynocephalus), chimpanzees (Pan troglodytes), orangutans (Pongo pygmaeus), and gorillas (Gorilla gorilla). Diet information was collected by survey and the estimated nutritional composition of the diet for each species at each institution was compared with non-human primate nutrient requirements. On the average, the captive primates received diets that met or exceeded recommended dietary guidelines for vitamins A, D, and E for non-human primates. Blood samples were collected from 94 primates held at Brookfield Zoo, Fort Worth Zoo, Lincoln Park Zoological Gardens, and North Carolina Zoological Park and analyzed for lipids, vitamins A and E, D metabolites, and carotenoids. Several species showed differences among zoos for some nutrients, but values from any one zoo were not consistently lower. When monkeys were compared with great apes, monkeys had lower serum total cholesterol, triacylglyceride, and measured LDL cholesterol levels, but significantly higher vitamin D metabolite levels. Species differences were found for serum A, E, and carotenoid levels (with the exception of lycopene). Some differences were seen in serum retinol, retinyl *Correspondence to: Susan Crissey, Department of Nutritional Services, Brookfield Zoo, Brookfield, IL 60513. E-mail: znnsouth@ix.netcom.com Received for publication April 29, 1999; Accepted September 20, 1999. 552Crissey et al.palmitate and γ-tocopherol. The relatively large number of animals contributing to this database and the fact that the data were collected from four zoos provide a substantial base for comparing nutritional status. Comparisons of these serum levels with previously published values for selected primates and humans revealed some differences.
Data from population‐based case‐control studies of non‐Hodgkin's lymphoma among white men from Kansas, Nebraska, Iowa, and Minnesota were pooled to evaluate potential risks from environmental exposures in more detail, while controlling for potential confounding factors. These data provided the opportunity to evaluate the risk of non‐Hodgkin's lymphoma from potential exposures to lindane, a pesticide that causes cancer in laboratory animals and has been associated with human cancer in a few epidemiologic investigations. This pooled data set includes 987 individuals with non‐Hodgkin's lymphoma and 2,895 population‐based controls. Information was obtained by telephone or in person interviews, which included detailed questions on farm practices and agricultural use of chemicals. Logistic regression was used to calculate odds ratios (ORs) adjusted for age, state of residence, and subject or proxy interviews. Reported use of lindane significantly increased the risk of non‐Hodgkin's's lymphoma by 50%. Some use characteristics were suggestive of an association. ORs were greater among persons who first used the pesticide 20 years before diagnosis (OR = 1.7) than more recently (OR = 1.3), among those who reported more frequent use (OR = 2.0 for use 5 or more days per year versus 1.6 for fewer than five days per year), and from use on crops (OR = 1.9), rather than from use on animals (OR = 1.3), although these differences were not statistically significant. On the other hand, ORs were lower when based on direct interviews (OR = 1.3) than on data from proxy respondents (OR = 2.1) and adjustment for potential confounding by use of 2,4‐D and diazinon reduced the ORs associated with lindane use from 1.5 to 1.2 and 1.3, respectively. Lindane does not appear to be a major etiologic factor in the development of non‐Hodgkin's's lymphoma, although a small role cannot be ruled out. Am. J. Ind. Med. 33:82–87, 1998. Published 1998 Wiley‐Liss, Inc.
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