Causation in forest decline - ACS Publications - American Chemical

By Richard M. Klein. Statistical and legal proof for the causes ... Woodman and Cowling (/) and others (2-5) have suggested that the causes of forest ...
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Causation in forest decline By Richard M. Klein Statistical and legal proof for the causes of contemporary forest decline and scientific demonstration of its nature, consequences, and sequelae have eluded the scientific community in spite of massive research efforts in Europe and North America. At the same time, the public and legislative bodies are attempting to make decisions of farreaching social and economic importance. Woodman and Cowling ( I ) and others (2-5) have suggested that the causes of forest decline can be demonstrated by application of Koch’s postulates, initially proposed to test the cause-effect relationship of diseases caused by microorganisms. Since the postulates were first formulated by Robert Koch in 1876 (6).fairly precise rules have been developed for the evaluation of diseases caused by biotic agents (7, 8).These require that the presumed causal agent be isolated from affected hosts, that the agent be grown under controlled conditions, that the causal agent induce the same disease when introduced into a new host, and, finally, that the causal agent again be isolated and demonstrated to be identical to the first isolated agent. But even in instances of microbial disease, Koch’s postulates have not always worked. Viruses and obligatory pathogens may not be amenable to cultivation in vitro, and variations in host susceptibility, vigor, age, and other factors profoundly alter clear demonstrations of the postulates. As pointed out by Deumling (9).the postulates require controlled conditions, which are impossible to apply under field conditions, and modifications of the postulates for field studies (IO) cannot provide definitive answers for causation. When there is good reason to suspect that causal factors are not primarily biotic agents, the utility of Koch’s postulates is further diluted. More to the point, the list of potential causal factors in forest decline is large and diverse (11-13). Natural causal factors, which may be acute or chronic, include stresses involving water, temperature, diseases, and insect infestations. Anthropogenic factors include precipitation acidity, the solubilization of indigenous and deposited metals, gaseous components, excess nitrogen, 148 Environ. Sci. Technol., Vol. 22.No. 2. 1988

Richard M. Klein

and other factors. Each of these factors varies in importance in time and space, and each is capable of synergistic interaction with both natural and anthropcgenic factors. Many plant species are declining, and matters of plant age, site factors, and temporal considerations are involved. Hutterman (3) has suggested that a modified Koch’s postuktte formulation could be used to evaluate individual causal factors or stressing

three concentrations with analysis of many structural and functional criteria made over a IO-year period. The medical profession, faced with similar problems and constraints, has developed methods of epidemiology for disease states involving multiple causal factors, the necessity of evaluating natural populations, and the time and space considerations that are analogous to the problems of forest decline. Our current understanding of lung cancer is based on such epidemiological concepts. Incitants include tobacco smoke; asbestos; radiation; viruses; a host of chemical substances in the environment; and matters of life style, age, vigor, sex, genetic factors, and race (14). The time period between initial exposure and disease development is also involved (15). Extrapolations from mice to human populations (as from tree seedlings to forest ecosystems) must be factored into the analysis. The result of such epidemiological evaluations is a probability statement that may be scientifically disappointing and certainly leads to different interpretations.

“Many plant species are declining and matters of plant age, site factors, and temporal considerationsare involved.”

conditions under controlled conditions. Koch’s pOStuhteS, suitably modified, are primarily useful for demonstrating that the factor being tested is unlikely to be involved. Simulation experiments that do not test Koch’s postulates have shown that many of the proposed stressing factors are capable of inducing responses consistent with the hypothesis that the factor is probably involved. It is, however, manifestly impossible to design and conduct a statistically sound multiple-factor test for Koch’s poStulates using mature trees under natural, but controlled, conditions-even with as few as IO presumed causal factors, each presented in only

Given the complexity of the problem, however, probability statements have proved to be adequate guidelines for the formulation of legislation and for the public. As pointed out by Weinberg (16). the questions being asked about cancer research far exceed the capabilities of science; so too for forest decline. The answers go beyond the realm of biological certainty, forcing us into the uncomfortable position of having to operate within a vague framework. Much the same point has been made by Deumling (9). However, epidemiological techniques can, as Koch’s postulates cannot, provide involved people with well-

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documented and adequately supported probability estimates ( I 7, 18). Although subject to modification as additional information becomes available, such probability estimates can be used as a base for critical decisions (19-21). Proposing that decisions be postponed until Koch's postulates are fulfilled is logically doomed to fail.

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Acknowledgments Preparation supported by the Vermont Agricultural Experiment Station, the R. K . Mellon Foundation, and the Robert and Marillyn Wilson Foundation. The advice of Deana Klein, Heiko Liedeker, Helen Myers, Timothy D. Perkins, and Hubert Vogelmann is acknowledged with thanks.

References (1) Woodman, J. N.; Cowling, E.B. Environ. Sci. Technol. 1987.21. 120-26. (2) Adams, D. E J . Air Pollut. Control AsSOC. 1962,13, 360-62. (3) Hutterman, A. Forstarchiv. 1984, 55, 45-48. (4) Last, E T.; Fowlder, D . ; Freer-Smoth, I? H. Forstwiss. Centralbl. 1984, 193, 2048. (5) Cowling, E. B. J . Air Pollut. Control AsSOC. 1985,35, 916-19. (6) Koch, R. Beia Biol. Pflanz. 1876, 2 , 277. (7) Brock, T. D . ; Smith, D. W.; Madigan, M. T. Biology of Microorganisms, 4th ed.; Prentice-Hall: Englewood Cliffs, N . J . , 1984. (8) Davis, B. D. et al. Microbiology, 3rd ed.; Harper & Row: New York, 1980. (9) Deumling, D. Environ. Sci. Technol. 1987,21, 612-13. (10) Woodman, J. N. Tree Physiology, 1987, 3 . 1-5. (1 1) Schutt, €? So Stirbt der Wald; BLV-Verlag: Munich, 1983. (12) World resources: A Report by the Resources Institute for Environment and Development; Mathews, J. T.; Hinricksen, D., Eds.; Basic Books: New York, 1986. (13) Klein, R. M.; Perkins, T. D. Ambio. 1987,16, 89-93. (14) Doll, R.; Peto, R. The Causes of Cancer; Oxford University Press: New York, 1981. (15) Farber, E. Cancer Res. 1984, 44, 546374. (16) Weinberg, A . M. lssues in Science and Technology 1985, I , 59-72. (17) Lilienfeld, A. M.; Lilienfeld, D. E. Foundations of Epidemiology; Oxford University Press: New York, 1980. (18) Miettinne, 0. S. Theoretical Epidemiology: Principles of Occurrence Research in Medicine; Wiley: New York, 1985. (19) Langbeim, L. I.; Lichtman, A . J . Ecological Inference; Sage: Beverly Hills, Calif., 1978. (20) Ruckelshaus, W. D. Science 1983, 221, 1026-28. (21) Ruckelshaus, W. D. Issues in Science and Technology 1985, I , 19-38.

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Richard M.Klein received his Ph.D. in botany and metabolic biochemistry from the University of Chicago. He was A. H. Caspary curator of plant physiology at the New York Botanical Garden before moving to the University of k r mont as a professor of botany. Klein is currently investigating aspects of physiological plant ecology with special reference to contemporary forest decline. Environ. Sci. Technol., Voi. 22, No. 2, 1988 149