letters to the editor
Comments on “Isotopic Analysis of Dinosaur Bones” (References for both letters can be found at pubs.acs.org/ac under Supporting Information.)
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econstruction of dinosaur thermophysiology requires the preservation of isotopically unaltered biogenic phosphate. A significant issue affecting the use of stable isotopes from fossil bone and teeth is the possible modification of original in vivo isotope values by mineral and chemical changes in the burial environment (1–4). The preservation of original isotopic composition is required before 18Ophosphate (18Op) qualifies as direct evidence for dinosaur endothermy. In “Isotopic Analysis of Dinosaur Bones” (March 1, 2002, 74, 143 A–150 A), Showers et al. fail to acknowledge a significant body of research that disputes their conclusions. This research suggests that the stable isotopic composition of dinosaur bone may be diagenetically altered during fossilization and therefore does not provide “direct evidence” of dinosaur endothermy in the Tyrannosaurus rex skeleton (Museum of the Rockies specimen #555) analyzed by Barrick and Showers in 1994 (4–6, 9) and that phosphate and carbonate are vulnerable to postmortem chemical and isotopic alteration (5, 9–22). Kolodny et al. argued that pristine micrometer-scale preservation of the internal architecture of dinosaur bones is not a guarantee of pristine geochemistry (5). They demonstrated postmortem diagenesis in the burial environment results in the alteration of original isotope values in fossil bioapatite. They calculated 18O from bioapatite in Cretaceous teleost fish, dinosaurs, and reptiles from the same localities across a latitudinal gradient (Alaska, Wyoming, and Texas). No systematic isotopic offset between these species was preserved, and their data suggested that diagenesis overprinted predicted 18O differences on the basis of contrasting physiology and life history of these animals. The overlapping of 18Op values in modern fish, turtles, and crocodilians in their data set did not support the preservation of original isotopic composition of drinking water or environmental waters inhabited by the species. Kolodny et al.’s findings indicated isotopic equilibration occurred between the fossils and groundwater from the burial environment—“conditions of burial rather than conditions of life.” They concluded that differences in dinosaur 18Op values did not reflect in vivo body temperature variability when the bones were formed, but could more likely be attributed to the chemistry of the burial environment. Chenery et al. showed evidence that early diagenetic recrystallization resulted in the overprinting of the 18O signature of hadrosaurid dinosaur bones buried in Late Cretaceous marine sediments. The strongest argument that Showers, Barrick, and Genna offer in support of unaltered isotope values is the correlation be-
tween 18O of presumed diagenetic calcite cements and structural carbonate. These values are plotted against theoretical 18Op in their Figures 2–4. The rest of the covariance relies on the assumption that the 18O of dinosaur bone phosphate was altered. It would plot in equilibrium with the 18O of the altered calcite, and structural carbonate Giganotosaurus and Camarasaurus 18Op values do not plot in this manner and are considered unaltered by the authors. They acknowledge that Coelophysis isotopic composition is altered. Even if the carbonate and calcite cements are altered, this is not proof that the phosphate oxygen has retained original in vivo 18O values from dinosaur bone more than 100 million years old (14). A linear correlation should exist between cogenetic (same phase) 18Ocarbonate (18Oc) and 18Op values if they are in equilibrium with the same oxygen reservoir (body water) at the same temperature (12). Iacumin et al. demonstrated that isotopic values from T. rex (MOR 555) analyzed by Barrick and Showers (9) failed to meet this minimum criterion for the preservation of original isotopic composition in same-phase carbonate and phosphate (12). If the 18Oc and 18Op values are in equilibrium, the 18Oc and 18Op values reported in their respective temperature equations will yield the same temperature. Unfortunately, this crosscheck cannot be attempted because Showers, Barrick, and Genna provide only “theoretical” phosphate values. As an aside, the y-axis on their Figure 2d appears mislabeled and should be 18Op. [Editor’s note: We apologize for introducing the error during production.] Despite the excellent preservation of micrometer-scale structures in some dinosaur bones and teeth, there is compelling evidence that hydroxylapatite carbonate and phosphate are susceptible to diagenesis and consequent modification of original isotopic composition (4, 6, 7, 14, 23–25). The data presented by Showers, Barrick, and Genna is intriguing and may provide important insights into dinosaur physiology. Stable isotopic geochemistry of fossil bioapatite has great potential as a proxy for interpreting the paleobiology of extinct animals, but not without testable criteria in support of the preservation of original biogenic isotopic values. Until that time, diagenesis is a problem that should not be overlooked. Mark B. Goodwin Universities of California–Berkeley and Davis
[email protected] Graham Bench and Patrick G. Grant Lawrence Livermore National Laboratory J U LY 1 , 2 0 0 2 / A N A LY T I C A L C H E M I S T R Y
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letters to the editor
Reply to Comments on “Isotopic Analysis of Dinosaur Bones”
W
e welcome the comments of Goodwin et al. about the isotopic integrity of fossil bone phosphate (18Op), but it is not true that we have ignored a “significant body of research” concerning bone alteration. We presented data on the coexisting phase relationship between the structural carbonate (18Osc), carbonate cements (18Occ), and 18Op as part of the discussion on bone alteration in T. rex (1). Kolodny points out that all fossil bones are crystalline pseudomorphs (2). It is well known that francolites—apatites that contain CO2 and a small quantity of fluorine—are metastable in the sedimentary environment and exhibit several systematic isomorphous substitutions over time (3). Major and minor ion lattice substitutions, loss of organic and carbonate material, trace element exchange, and precipitation of cements in the fossil bone all result in measurable changes in crystallographic properties and optical indices. However, these changes are not necessarily associated with any isotopic changes (4 –6). Concern has been expressed about the reliability of the 18Op in bone and phosphatic nodules for quite a while (4, 5, 7–10). Even 18Op in bone samples as young as 50,000–650,000 years appear to be altered when partially exposed to groundwater (11). On the other hand, the 18Op of some archaeological samples do not change even after extensive dissolution and diagenesis (12). Metal concentrations, FTIR crystallinity, and carbonate content changes in these samples were not associated with any 18Op changes in bone phosphate. These studies indicate that burial environment and time are important factors for the preservation of bone 18Op. We feel it is well established that changes on the micro- or macroscopic level in bone phosphates are not necessarily associated with isotopic changes at the molecular level. The question is how to reliably determine isotopic alteration at the molecular level. To assess 18Op preservation in fossil bone material at the molecular level, we used the coexisting phase technique introduced by Shemesh (13); however, our approach differed from theirs. Shemesh looked at phosphate nodules and rocks from the early Proterozoic to the Holocene era (2 billion to 10,000 years ago) and found the diagenetic end member (totally altered phosphate) was indicated by a correlation between 18Op and 18Osc. We never found this correlation in vertebrate fossil bone material as old as Jurassic (1, 14–25). Therefore, we assumed that the 18Op was not altered in these specimens. With fossil bone material, we can also examine the cancellous and compact portions to assess partial alteration. The open cancellous portions of the bone are more susceptible to alteration than the compact laminar bone of animals with Haversian bone systems, such as dinosaurs and mammals. If the two types of bones have differences in 18Op, this could indicate the initial stages of alteration or partial alteration. To use this coexisting phase approach, many replicate analyses are required. These replicate analyses also permit intrabone and interbone 18Op variation to be assessed. One of 352 A
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the problems with previous publications that compared fish, dinosaurs, and reptiles from the same formation is that intrabone variation has not been assessed (2). Intrabone variations can be as large as interbone variations depending upon paleophysiology and preservation, or vice versa. There has been some confusion about how to interpret the relationship between 18Osc and 18Op in fossil bones without first finding the diagenetic end member in vertebrate fossil bone. There is a strong correlation between 18Osc and 18Op in bone and tooth samples from modern mammals (10), which suggests that 18Osc and 18Op in bone phosphate start out in equilibrium with body water, meaning that the coexisting phases are originally in equilibrium. Because the coexisting phases (18Osc and 18Op) in fossil bones do not show any correlation, Iacumin and co-workers reason that all fossil 18Osc and 18Op must be altered (2, 10). They suggest that it is quite improbable that a fossil phosphate would ever show a good correlation between the two phases because the carbonate and phosphate phases alter at different rates and will never equilibrate again. They suggest that a lack of correlation between 18Osc and 18Op represents the diagenetic end member of bone phosphate. The comparison of 18Osc and 18Op in a Triassic Coelophysis in the “Isotopic Analysis of Dinosaur Bones” article and in a Permian Dimetrodon (25) demonstrates that the phases are correlated when bone phosphate is totally altered. The intrabone 18Op variation and the 18Op difference between the compact and cancellous bone types increase when the phosphate material is altered (25). Neither is homogenized as suggested by some researchers (2, 10). The Coelophysis and Dimetrodon 18Op data are distinctly different from that of any other dinosaur or articulated vertebrate bone material that has been analyzed using this approach (1, 14–25). Therefore, we argue that diagenetic alteration of biogenic phosphates on a molecular scale over geological time can be detected. Complete alteration not only equilibrates both the carbonate and phosphate phases with the local burial environment but also increases the amount of 18Op variation in the bone phosphate. To detect partial alteration, researchers must compare both the compact and cancellous 18Op. These data demonstrate that altered fossil bone 18Op data cannot be erroneously interpreted as representing homoeothermic metabolism in a fossilized heterothermic animal. We hope that these new techniques will enable a much more extensive examination of diagenetic alteration on a molecular level in fossil bones from several different geological ages by many different groups. Then, paleophysiology studies can continue on well-preserved specimens without the abrogation that the diagenesis controversy has had on this field of study. William J. Showers and Bernard Genna North Carolina State University
[email protected]
