Mendel strain rats, each consisting of approximate- 
ly 75 adults confined in rooms within which each 
individual had the opportunity of ranging among 
four subareas. Food, water, nesting material, and 
nestboxes were located in each subarea of each 
room. Females born into such already socially 
structured groups frequently exhibited difficulty in 
carrying embryos to term. Following death of 
near term embryos some females died from toxemia 
associated with the large mass of dissolving embry- 
onic tissue. For those females who survived this 
phase, one site of resorbtion of a full-term embryo 
often became the site of an abscess developing 
from the decaying fetus. Death usually ensued by 
the time the abscess reached a diameter of 50mm. 
Several weeks might elapse between death of the 
near-term embryos and the mother’s death. Some 
females were able to resorb near-term fetuses, 
although transient abscesses could be detected by 
palpation. 
Although no such overt symptoms were recog- 
nized among the females of the present study of 
the rats in the Towson enclosure, it nevertheless 
remains a distinct possibility that female physiology 
was impaired as a consequence of resorbing 
embryos. A similar line of reasoning may also 
account for the increased force of mortality charac- 
terizing King’s females. Caged with other adults 
of both sexes they were unable to avoid disturbances 
attendant to this crowded association. Thus from 
the very start of reproductive life they would be 
exposed to alterations of physiology accompanying 
resorbtion of embryos. This leads to a tentative 
hypothesis: Toxic reactions resulting from resorb- 
ing embryos leads to an acceleration of the heredi- 
tary aging process. 
However, most of the mortality curves shown in 
figures 153 and 154 exhibit a force of mortality in 
which the proportion dying doubles each 130-135 
days. When the life table of a species results in 
this form of mortality curve, one must conclude 
that mortality rate is proportional to a physiological 
process of senescence, which begins early in life and 
continues to death. The nature of this process is 
unknown. Physiologically the implication is that 
the older an animal becomes the longer it takes to 
accomplish a unit of function, and furthermore the 
more the function is slowed down by some physio- 
logical antagonism, the greater is the likelihood of 
the antagonizing agent accumulating in the cells. 
Accumulation within the cell of enzyme inhibitors 
(92, 93), whether acquired through foodstuffs or 
280 
resulting from enzymatic activity within the cell 
itself, suggests a mode of origin of such senescence 
[(90), pp. 310-311], 
However, our concern here is not so much with 
the origin of the physiological basis of senescence, 
but rather with the manner in which environmental 
factors interact with the phenomenon of senescence ! 
to produce altered mortality rates. The mortality 
curves for male rats fall into three discrete groups 
Each of the out-of-doors populations (Davis’ and 
Calhoun’s) form a separate group, while the two 
laboratory populations (King’s and Wiesner’s) are 
similar enough to form a single group. 
For a given age the mortality rate of Davis’ rats i 
was approximately seven times that of Calhoun’s, j 
while Calhoun’s was approximately seven times , 
that of King’s or Wiesner’s and Sheard’s. Thus ( 
Davis’ rats exhibited mortality rates about 49 times 
that of King’s and Wiesner’s. When these 
differences are considered along with the similarity [ 
of rate of senescence (i.e. rate of change of mortality ,> 
with age), the following hypothesis is suggested: u 
Mortality rate is proportional to the product of (a) |> 
degree of senescence characteristic of the age in j, 
question and (b) the frequency of intensity of 
deleterious events in the environment. Measure- 
ment of intensity or frequency of all events which j 
favor mortality is difficult. However, provided 
rate of senescence is constant, the ratio of age [ 
specific mortality rates between populations should 
provide an index of the relative severity of the j 
environments. For the comparison Wiesner and 
Sheard:Calhoun:Davis the ratio is 1:7:49. These | 
ratios parallel the observed apparent severity of 1 
environmental conditions contributing to mortal- 
ity. Thus one may conclude that the actual , 
probability of death within a given age span is the 
product of the probability of death from inherent 
aging factors and the probability of encountering 
environmental debilitating factors. It follow 
that even though the force of mortality remains,, 
constant, the greater the severity of the environ 
ment, the shorter will be the life span of any cohort. 
8 . The Significance of Social Class to Sur- 
vival of a Population 
In his review of the relationship between home) 
range and regulation of population density Kalel 
(94) points out that there are three main consequeri-| 
ces of home range development: (1) Emigration 
(2) Death through hypoglycemic shock; (3) Reduc 
