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OCR for page 11
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For biologic markers to be accepted as indicators of the effects of specific air
pollutants, a relationship must be shown to exist between the pollutants (causes) and
the responses (effects) measured by the markers. In approaching its task of evaluating
the potential usefulness of various markers of air-pollution effects, the committee
found it necessary to consider several fundamental criteria for the establishment of
cause and effect in complex environmental relationships. This section reviews those
criteria and suggests guidelines for their application to biologic markers of air-
pollutant stress and damage in forests.
Air pollution affects forests and trees in many ways. Smith ( 1981 ) classified
interactions between air pollutants and forests into three categories. When pollutant
concentrations are low (Class I), forest vegetation and soil serve both as sinks and
sources of pollutants. At intermediate concentrations (Class II), vegetation is subtly
and adversely affected. Acute effects on forests, including morbidity and mortality,
occur at high pollutant concentrations (Class III). Gradations between classes result
in a continuum of effects on forests, occurring from the subcellular to the ecosystem
levels.
Chronic stresses can induce a series of changes (including species impoverish-
ment) that are as systematic as plant succession, although less well recognized. Of the
many examples of the effects of chronic stress, some of the best defined were shown in
experimental studies of the ecologic effects of ionizing radiation (McCormick, 1963;
Woodwell, 1970; Fraley, 1971; Woodwell and Houghton, in press), in which the primary
effect was well defined and measurable, whereas secondary effects, such as insect
damage, were clearly recognized as secondary.
In forest stands affected by regional pollution, where effects of several
stresses might be integrated, cause-and-effect relationships are not as clear as in the
case of ionizing radiation. The challenge of relating specific causes to specific
effects is complicated further by the similarity of patterns of forest changes caused
by a wide variety of toxicants to changes caused by other stresses.
Experimental studies have been designed to investigate the effects of specific
pollutants or combinations of pollutants on forests or trees and to test whether a
particular pollutant might be a factor in damage observed in an existing stand or single
tree. However, in a forested region subjected to a variety of air pollutants and natural
stresses, the effects of each stress are not necessarily unique and identifiable.
Furthermore, simple field studies of affected forest stands cannot yield clear
information about the specific causes of damage--only the general conclusion that the
observed pollutants appear to be associated with the observed damage. The damage might
eventually be noticed as changes in the distribution of species, rather than immediately
as specific physiologic symptoms in individual plants. If an affected species were an
ephemeral or an occasional participant in the community, such changes would be
particularly difficult to recognize and attribute to a cause.
Knowledge of the structure and physiology of forests and trees is now sufficient
to develop a basis for detecting disruption or disturbance from a variety of causes.
Although the task is complicated and efforts are incomplete, the committee's review
suggested some answers to the questions posed during the workshop. The workshop papers
confirmed that many biologic markers of stress are known for trees and forests, but that
few (if any) such markers are unequivocal indicators of single causal agents. Because
many natural and anthropogenic stress factors (summarized in Table 1 ) can combine to
cause changes in the trends of forest metabolism, growth, and mortality (summarized in
Table 2), it is difficult to link causes and effects with certainty. To help to clarify
the links, the committee suggests a set of guidelines for inferring cause-and-effect
relationships in cases of local and regional changes in the health and growth of trees
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and forests. As in much of science, the relationships will be expressed as probabilities
based on current information and experience, not as certainties.
A related problem was addressed by bacteriologist Robert Koch in the nineteenth
century, when the germ theory of disease was gaining wide acceptance (Koch, 1876~. Koch
pointed to the need for systematic and rigorous proof that a disease was caused by a
particular organism.
To establish the cause-and-effect relationship, Koch advanced a set of postulates
that now seem obvious. His postulates, summarized by Yerushalmy and Palmer (1959), were
as follows:
1. The [causative] organism must be found in every case of the disease.
2. [The causative organism] must be isolated from patients and grown in pure
culture.
3. When the pure culture is introduced into a susceptible subject, it must
produce the disease.
These postulates were formulated to deal with bacterial diseases and are widely accepted
in the biomedical sciences. They clearly are inadequate to deal with diseases that have
several etiologic components or to assess cause-and-effect relationships between tree
damage and environmental pollutants. But they can be used to focus thinking about
important questions and can help to rule out particular pathogens as causes.
Hill (1965), Mosteller and Tukey (1977), Cochran (1983), and Holland (1986) have
described various criteria for establishing cause-and-effect relationships. As Holland
pointed out, it is necessary that, "for causal inference, each unit [e.g., each tree,
each stand, etc.] be potentially exposable to any one of the causes.
This committee sought criteria that might help to define the most probable causes
of stress symptoms seen in nature. On the basis of a few common principles, the criteria
for establishing causality that appeared most useful for assessing pollutant effects
on forests are the following:
· Strong correlation. Is there a consistent relationship between the measured
effect and the suspected causers)? This criterion includes the concept of generality
of association or consistency (Koch first postulate) and the concept of strength of
correlation. Mosteller and Tukey (1977) wrote about "a clear and consistent associa-
tion."
· Plausibility or mechanism. Is there a biologic explanation of the mechanism of the
observed association that is reasonable, coherent, or analogous to another case that is
understood? Does it appear to contradict other, known mechanisms? Hill (1965)
cautioned that "what is biologically plausible depends on the biological knowledge of
the day."
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Table 1. Environmental Stress Factors Known to Affect Forests and Trees
Competition for resources:
Growing space
Nutrients
Sunlight
Water
Weather and climate:
Temperature extremes
Drought
High winds
Low humidity
High altitude with high ultraviolet radiation
Heavy loads of ice or snow
Wild fire
Biologic agents:
. -
. rungs
Insects
Nematodes
Bacteria
Viruses and related forms
Parasitic plants
Predators
Lack of essential symbionts
Chemical factors:
Deficiencies or imbalances in essential nutrients
Toxic elements
Allelopathic chemicals
Herbicides
Air pollutants:
Toxic gases
Toxic aerosols
Growth-altering chemicals
Acid deposition leading to direct injury
Atmospheric deposition of toxic particulates
Human disturbances:
Mechanical injury to individual trees
Clearing of forests
Burning of forests
Physical disturbance of soil induced by:
Excessive drainage or flooding
Compaction
Erosion by wind or water
Removal or destruction of organic matter
Mechanical disturbance of soil
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Table 2. Effects or Symptoms of Stress and Damage in Forests and Trees
Effects on Individual Trees
Visible symptoms of injury:
Change in shape, size, color, and number of leaves
Change in normal patterns of growth and development
Change in normal patterns of foliage flushing or senescence
Decreased annual height growth or radial increments
Alteration of physiologic processes:
Photosynthesis
Respiration and metabolism
Transpiration
Mineral nutrition
Transport and allocation of photosynthate
Hormonal control of growth
Symbiotic relationships with other organisms
Changes in susceptibility to other stress factors
Life-history changes:
Decreased longevity; early onset of dieback
Changes in reproductive behavior
Effects on Forests
Decreased productivity of stands
Changes in age-class distribution
Changes in normal patterns of competition and mortality
Changes in normal patterns of community succession
Changes in species composition
Changes in nutrient cycling
Changes in hydrologic behavior, watershed functions, or wildlife habitat
Changes in genetic structure of populations
Responsiveness or experimental replication. Can the effect be duplicated by
Can the effect be stopped or prevented by removing the putative causal
experiment?
agent? Such a result is "strong causal evidence when you can find it" (Holland, 1986~.
This criterion represents Koch's third postulate and includes Hill's (1965) idea of
biologic gradient--i.e., dose-response relationship.
· Temporality. A cause must precede its effect or at least be present at an
appropriate time. Testing this criterion requires adequate histories of exposure and
trends in a forest's growth and composition. It might be difficult to isolate subtle
shifts in the genetic makeup of a tree population that increase the susceptibility of the
population to other stresses.
· Weight of evidence. The individual components of establishing cause-and-effect
relationships--correlation, plausibility, responsiveness, and temporality--do not by
themselves provide sufficient evidence. However, studies that provide information on
Representative terms from entire chapter:
biologic markers
