Cannon studies

A partial solution to this dilemma could be that a large proportion of the protein-rich foods (meat, eggs) consumed by these people came from animals that were themselves fed a C4 diet. We know that dogs typically share the same diet as humans (Katzenberg 1989 Cannon et al. 1999) and are important components of the diet in some sites (eg., Cuello Hammond 1991 van der Merwe et al, this volume). It is unlikely that all the meat consumed by Maya peoples was derived from pure C4 consumers, however, as we have evidence for at least some C3-based animal bones that are presumed to be waste from food preparation. This should a subject of future study to test for the degree of domestication (and consequent feeding on maize) of meat-supplying animals such as turkeys. 

As Einhellig (48) correctly stated, "Unless cooperative research between chemists and physiologists is conducted, we will continue to be left with the notion that an array of simple phenols cannon to a wide array of soils and situations are the major chemical allelopa-thic agents." As for the importance of the chemical identity, Putnam and Duke (17) expressed it very well "after all chemicals are identified, studies can be made on genetics, specificity, environmental influences and environmental consequences."... 

Mineral Oil and Polyalphaolefin Hydraulic Fluids. No studies were located regarding metabolism in humans or animals after exposure to mineral oil hydraulic fluids or polyalphaolefin hydraulic fluids. It should be noted, however, that hydrocarbons found in mineral oils generally are not expected to undergo extensive metabolism in animals or humans (Cannon 1940 IARC 1984). It may be speculated that polyalphaolefins may undergo limited metabolism of a similar nature. 

Cannon Packing Available in metal only, low pressure drop, low HETP, flooding limit probably higher than Raschig rings. Not much literature data available. Used mostly in small laboratory or semi-plant studies. 

Trulson, M.E., Cannon, M.S., Faegg, T.S., Raese, J.D. Effects of chronic methamphetamine on the nigral-striatal dopamine system in rat brain tyrosine hydroxylase immunochemistry and quantitative light microscopic studies. Brain Res. Bull. 15 569, 1985. 

Cannon, J., Cullinan, P. and Newman-Taylor, A.J., Consequences of a diagnosis of occupational asthma A controlled study. Thorax, 49, 390P, 1994. 

Smith, D.B., Woodruff, L.G., O Leary, R.M., Cannon, W.F., Garrett, R.G., Kilburn, J.E., Goldhaber, M. B. 2009. Pilot studies for the North American Soil Geochemical Landscapes Project - site selection, sampling protocols, analytical methods, and quality control. Applied Geochemistry, in press. 

Lomakin et al., 1996). Surface plasmon resonance studies of the A/ (l—40) /1-amyloid peptide (Cannon et al., 2004) provide even more details of the multiple kinetic steps, and suggest that fibril formation proceeds by reversible addition of a monomer to the tip of the formed fibril, followed by a postbinding, transitional event. 

No studies were located regarding death in humans following inhalation exposure to mirex. No deaths were reported to result from exposure to chlordecone (Cannon et al. 1978 Taylor et al. 

Body Weight Effects. No studies were located regarding body weight effects in humans following inhalation exposure to mirex. Twenty-seven of 133 workers examined as a result of intermediate- or chronic-duration exposures to chlordecone experienced weight loss (Cannon et al. 1978). Weight loss (up to 60 pounds in 4 months) was reported in 10 of 23 workers with blood chlordecone levels in excess of 2 pg/L (Taylor et al. 1978). 

Several studies were presented in Section 2.2.1.2 regarding the systemic effects experienced by workers occupationally exposed to chlordecone (Cannon et al. 1978 Guzelian et al. 1980 Martinez... 

As noted in Section 2.3.1.1, studies have shown that chlordecone is absorbed after occupational exposure (Cannon et al. 1978 Cohn et al. 1978 Taylor 1982, 1985). Although the route of exposure was not specified in the studies, dermal exposures probably constituted a major portion of the exposure in these occupational situations. For a description of the absorption of chlordecone following occupational exposure see Section 2.3.1.1. 

Studies of workers exposed to high levels of chlordecone indicate that pleuritic chest pain was a relatively common complaint (Cannon et al. 1978 Taylor 1982, 1985). Examination of workers with this complaint revealed no cause for the pains. Since oral exposure studies in animals did not identify any respiratory end points that may have been affected following ingestion of chlordecone (Larson et al. 1979b) and no inhalation exposure studies were located, a possible physiological basis for the workers complaints has not been identified. Insufficient information is available to determine whether persons exposed to low levels of chlordecone at hazardous waste sites would experience adverse respiratory effects, but the possibility cannot be discounted. 

The available information indicates that chlordecone is not markedly cardiotoxic in humans (Cannon et al. 1978 Taylor 1982, 1985 Taylor et al. 1978). Rat studies with chlordecone have shown that chronic low-dose ingestion does not cause histologically evident cardiac lesions (Larson et al. 

The only information available for humans exposed to chlordecone pertains to a study of intermediate-to-chronic occupational exposures (exact durations not recorded) of one group of individuals employed at a facility in Hopewell, Virginia. Chlordecone was manufactured in this facility for 21--22 months because of poor hygiene at the facility, exposure by all routes was likely. In addition, concomitant exposure to a precursor was possible. Several studies have been published to describe the toxicity in this human population (Cannon et al. 1978 Taylor 1982, 1985), and results of these studies will be considered here. These results pertain to the chronic-duration exposure also. No deaths were reported (Cannon et al. 1978 Taylor et al. 1978). Skeletal muscle biopsy was conducted on six workers who experienced adverse neurological clinical signs (such as tremors) as well as muscle weakness and incoordination (Martinez et al. 1978). Abnormal histological and biochemical indices were revealed in this tissue. Joint pain was also reported (Taylor 1982, 1985). 

There are no data for intermediate-duration inhalation or dermal exposure of animals to chlordecone, but there are several oral exposure studies (Agarwal and Mehendale 1983a, 1983c Agarwal et al. 1983 Bell and Mehendale 1985 Cannon and Kimbrough 1979 Chu etal. 1980 1981a, 1981b ... 

Further human data should be gathered for intermediate-duration exposure to chlordecone by all routes. Human data were either absent (gastrointestinal, hematological, or renal effects) or limited to a population study with major restrictions (Cannon et al. 1978 Guzelian 1982a Landrigen et al. 

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