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SKELETAL EVIDENCE OF STRESS IN SUBADULTS: TRYING TO COME OF AGE AT GRASSHOPPER PUEBLO (ARIZONA).

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Authors HINKES, MADELEINE JOYCE.

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Hinkes, Madeleine Joyce

SKELETAL EVIDENCE OF STRESS IN SUBADULTS: TRYING TO COME OF AGE AT GRASSHOPPER PUEBLO

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University Microfilms International

SKELETAL EVIDENCE OF STRESS IN SUBADULTS: TRYING TO

COIlE OF AGE AT GRASSHOPPER PUEBLO

Madeleine Joyce Hinkes

A Dissertation Submitted to the Faculty of the

DEPAR'rnENT OF ANTHROPOi.(.

In Partial Fulfillment of the Requirements For tbe Degree of

DOCTOR OF PHILOSOPHY

In the Graduate College

THE UNIVERSITY OF ARIZONA

1 983

As members of the Final Examination Committee, we certify that we have read the dissertation prepared by Madeleine Joyce Hinkes enti tled SKELETAL EVIDENCE OF STRESS IN SUBADULTS: TRYING TO COME OF

AGE AT GRASSHOPPER PUEBLO

and recommend that it be accepted as fulfilling the dissertation requirement

·"J--Q-1r3 Date 12.12.83 Date ~q, 1C,1:3 Date /O::;z;;r n Date

Date

Final approval and acceptance of this dissertation is contingent upon the candidate's suJ::mission of the final copy of the dissertation to the Graduate College.

I hereby certify that I have read this dissertation prepared under my direction and recommend that it be accepted as fulfilling the dissertation requiremeryt. /./ (

Date STATDlENT BY AllTIIOR

This dissertation has been submitted. in partial fulfillment of requirements for an advanced degree at The University of ArizoDa and is depoei ted in the UniverBi ty Library to be made available to bor rowers un~ar rules of the Library.

Brief quotations from this dissertation are allowable without special permission. provided that accurate acknowledgment of source is made. Requests for permission for extended quotation from or reproduction of this manuscript in whole or in part may be granted by the copyright holder. ACKJIOWLEIJG!IENS

Many individual.s have been involved. in the successful compl.e tioD. of this dissertation. I would especially like to thank the four mellbera of my cOIIIIIlittee, who interrupted their busy schedules 80 that

I could meet mine. My chairman, Dr. "'alter Birkby, provided unl.imited access to his personal. library. Dr. M. E. Horbeck guided me through the long and sometimes painful process of revising and editing the written produot. Dr. Jeff Reid shared with me his theoretical ouUook on Grasshopper Ruin, and continually offered h~8 encouragement and positive reinforcement. Dr. William Stini, whose duties 88 department chairman prevented major participation on his part, nevertheless was always available to ciiscuea my dissertation research and professional p].tuIS.

Other persons are deserving of acknowledgment. Notable among these is Dr. Jane Bulkstra, my undergraduate advisor at Northwestern

University, whose innuence in my formative years as a physical anthro pologist has stayed with me and was instrumental in formulating this research design. Drs. Michael Pitt, M.D., Diagnostic Radiology,

Arizona Health Sciences Center, and Steve Wagner, D.D.S., Dental

Oncology, Universit,. of New Mexico Hospital, have been extremely help

ful in the diagnosis and interpretation of skeletal. and dental con ditions.

iii iv

For their friendship and faith in me, I warmly thank Drs. Stan

Rhine, Claire Gordon, Doug Hanson, and Laura Kosakowsky.

A number of other individuals have contributed in meaningful ways, for which I am grateful. Hazel Gillie typed the final manuscript,

Craig Montgomery and Kathi Froede drew the figures, Alison Galloway taught me the ways of the word processor.

All research at Grasshopper is made possible under an agreement with the White Mountain Apache Tribal Council, whose interest and hos pitality is greatly appreciated. Financial support for the field school has been obtained from The National Science Foundation (GE-46Ol, GE-?781,

GZ-22, GZ-397, GZ-745, GZ-1113, GZ-1493, GZ-1924, GS-2566~ G8-33436,

SOC-72-05334, SOC-74-23724), The Wenner-Gren Foundation, The National

Geographic Society, and The State Historic Preservation Officer.

This research in particular has been funded by The UniverSity of Arizona Graduate Student Development Fund, Sigma Xi, and the Depart ment of Anthropology, University of Arizona.

In closing, I dedicate this dissertation to my loving and patient family. TABLE OF CONTENTS

Page

LIST OF TABLES ...... vii

LIST OF ILLUSTRATIONS

ABSTRACT ...... xii

1. INTRODUCTION.

Anthropological Value of Subadult Remains Goals of This Research .. Description Analysis .... Explana tiOD

2. GRASSHoPPER PUEBLO .. 10

The Skeletal Remains .. 14 Sample Validity 15

3. METHODOLOGY ••••••• 23

Building the Biological Profile 27 Age Estimates ...... 27 Sex Assignments ...... 32 Demographic Profile ...... 36 Long Bone Gro .... th ...... '" ...... 38 Evaluation of Skeletal and Dental Variants .. 41 Assessing Skeletal Stress ...... 42 Specific Pathologies ...... 43 General Responses to Stre&s ...... 45 Statistical Evaluation ...... 71

4. COMPARATIVE DATA FROM RECENT AMERICAN INDIAN GROUPS 73

Weaning stress ...... 73 Disease stress ...... 77 Ecological Stress .. 79

5. RESULTS.AND DISCUSSION .. 84

Mortality .. .. 84 Fetation ...... 86 vi

TABLE OF CONTENTS ... ~

Page

Infancy. • • 86 Childhood • • 87 Adolescence • 88 Sex Ratio • • 88 Adulthood • • 91 Growth VariabUity • 91 Skelet&l and Dental Variants 100 Postcranial Skeleton 100 Cranial. Skeleton 102 Dental Variants. • • • • 1fYl S~...... 116 Skeletal Pathologies •••• 117 Postcranial. Pathologies • 117 Cranial Pathol.ogies • 120 Skeletal Stress Markers • 124 Cortical Bone Loss • 124 Porotic Hyperostosis 127 Cribra Orbi ta11a •• l.2B Growth Retardation • 131 Harris Lines ••••• 133 Linear Enamel Hypoplasia • 135 Co-occurrence of Stress Markers • • • 138 SU111111817 • • • • • • • • • • • • • • • • • 143

6. IN'l'RA-8I'l'E ANALYSIS OF CHANGE IN STRESS LEVElS 150

Derin! tiOD of Groupings • 152 The Hypotheses • • • • • 157 The Test of Time •••• 159 Demographic Factors • 159 Stress Markers ••• 162 Summary. • • • • • • 166 The Test of Space • • • • 169 Demographic Features 169 Stt"ess Markers 173 Summary • • • • 177 Evaluation •••• 179

7. CONCLUDING STATEMENTS • 183

APPENDIX A. TDIPORAL AND CULTURAL AFFILIATION OF SITES MENTIONED IN TEXT • 187

APPENDIX B. SKELETAL INVENTORY • 189

LIST OF REFERENCES ••••••• 198 LIST OF TABLES

Table Page

1. Age and sex distribution of Grasshopper skeletal remains. 16

2. Percentage of subadults in large archaeological populations • ...... 17

3. Methods of age and sex estimation used in this research .. 24

4. Underlying causes of death in children under 5 years, in Monterrey, Mexico, 1968-1970 ...... 80

5. Chi-square tests of observed versus expected sex distributions of adults and subadul ts ...... " ...... 90

6. Correlations between dental age estimates and the maximum diaphyseal length of long bones ...... 92

? Individuals with femoral diaphyseal lengths one standard deviation above or below the mean for their age groups 96

8. Femoral diaphyseal. length by sex ...... 98

9. Long bone diaphyseal lengths: dental age as computed by Weaver (1977) • • • • • • • • • • • • • • • • • • • • • 99

10. Location and frequency of fused teeth for fifteen eub- adults ...... 111

li. Location and frequency of paramo1ar tubercles for seven subadul.ts ...... 114

12. Frequency of pegged teeth for Grasshopper Ruin Bubadul ts. 114

13. Frequency of dental caries for Grasshopper Ruin Bubadults 123

14.. Frequency of subadults by age falling below the average cortical index for the femur and/or humerus .. 126

15. Frequency and distribution of Harris lines ...... 134

16.. The association of tibial transverse line frequency and age of line formation ...... • ...... • ...... 134

vii viti

LIST OF TABLES-~

Table Page

17. Frequency and distribution of hypoplastic teeth 136

18. Total occurrenoe of each stress marker for each age group. 139

19. Co-occurrence of stress markers ...... 141.

20. Chi-square tests of associations between stress markers • 142

2l. Chi... square test of dental pathologies and skeletal stress markers ...... 145

22. Presence/absence of stress markers by age and sex 147

23. Chi-square test of sex and stress markers ...... 149

24. Temporal classification of rooms and subadult burials 154

25. Spatial classifioation of rooms and sub.:t.dul t burials .. 156

26. Temporal-spatial matrix of subadul t burials ...... 158

27. Age distribution of subaduHs from temporal groups.. 160

28. Frequency of stress markers for individuals in temporal groups. • ...... • .. • .. • • .. • • .. • .. ... 163

29. The association of tibial transverse line frequency and age of 1ine formation for temporal. groups ...... 165

30. Number of individual.s with stress markers in temporal groups...... • ...... • • ...... 167

31. Age distribution of subadults from spatial groups ... 170

32. Kolmogorov-Smirnov tests of mortality age distributions 172

33. FrcG.uency of stress markers for individuals in spatial groups.. • • • ...... • ...... • ...... 174 34. The association of tibial transverse line frequency and age of line formation for spatial groups. .. • ...... 176

35. Number of individuals with stress markers in spatial. group;; 178

36. Probability of stress marker incidence among outlier subadul ts ...... • ...... • ...... • .. • .. • .. .. • .... 178 ix

LIST OF TABLES~

Table Page

37. Frequency of stress markers for components of late group. • • • • • • • • • • • • • • • • • • • • • • • 180 LIST OF ILLUSTRATIONS

Figure Page

1. Areal location of Grasshopper Ruin.. 11

2. Map of Grasshopper Pueblo ...... 12

3. Sample dental chart, from 5-6 year.. old girl from Burial. 130 ••••••••••••••••••••••••••• 26

4. Sequence of formation and eruption of teeth among American Indians (from Ubelaker 1978:47) ...... 30

5. Comparison of porotie hyperostosis (right) and non- pathological sutural hyperostosis (left) 51

6. Measurement of bone cortical thickness ...... fJ7

7. Scale model of template used to calculate the age of occurrence of Harris lines in the tibia ...... 64

8. Tooth development chronology for assessment of formative times of linear enamel hypoplasia (from MassIer et ale 1941: 40) • • • • • • • • • • • • • • • • 68

9. Mortality curve for Grasshopper Pueblo.. 85

10. Mortality curves separated by sex ...... 89

11. Comparison of femoral diaphyseal lengths for seven age groups from Grasshopper, Indian Knoll., and Arikara sites r 101

12. Kerckring's ossicle from chi1.d in Burial 220 • • • • • •• 104

1.3. Unusual bregmatic configuration from child in Burial 628. 105

14. Cranium of adolescent female from Burial 611 'With evidence of possible scalping • • • • • • • • • • • • • • • • 108

15. Dental frequencies in subadu1ts; totals include all erupting and erupted teeth from 248 children • • 109

16. Perthes' Disease affecting left femur and ilium 118 xi

LIST OF ILLUSTRATIONS-~

Figure Page

17. Frontal 1esioD from child in Burial 172 • 121

18. Index of cortical thickness for femur BDd humerus at ..idshaft •••••••••••••• 125

19. Incidence of porotic hyperostosis. 129

20. Incidence of su.tural hyperostosis. 130

21.. Incidence of cribra orb! tal.ia • • • 132

22. Prevalence of stress markers by age • 1"

2,. Mortality curves for temporal groups 161 24. Mortality curves for spatial groups • 1'71 ABSTRACT

The human skeletal remains from Grasshopper RuiD, Arizona, constitute an excellent series for the stud,. of gE"OWth and development.

A total of 390 aubadults, fetal through 18 years of age, have been recovered, in a mortality distribution comparable to that observed in most anthropologioal populations.

Children are extremel.,. sensitive to metabolic upsets during the growth process, and an individual's history of illness 1s often recorded in his bones and teeth. This research is concerned with read ing this record and deftloping a picture of the biological quality of life during pueblo occupation.

On the whole, incidence of skeletal stres/; markers is low.

Just 145 children have one or more markers, indicating a low disease load for the Bubadul t community. Based on ethnographic and clinical records of disease among Southwestern Indians, it is believed that most children without visible stress markers were victims of common and virulent gastrointestinal and upper respiratory infections. Those children with stress markers appear to have been subject to underlying morbid conditioDS (par&.sitism, dietary deficiencies) which would have intensified the effects of infectious diseases.

In order to determine whether a particular sector of the com munity was at greater risk, the skeletal sample is partitioned into temporal and spatial groups. The impetus for this analysis derives xii xiii from a long-standing archaeological research focus: the factors pre cipitating abandonment. MOst eYidence points to an environmenta1 change and subsequent shortfall in the noral. food supply. Behavioral responses to this stress have been documented, but until this research, no direct measure of the effect on puebl.o inhabitants had been devised.

Differences in stress marker frequency among temporal groups reveal no clear pattern. When spatial groups are aDalyzed, chUdren from outliers are found to have significantly greater prevalence of

Harris lines, implying a pervasive, recurring stress. These findings are interpreted in l.ight of the unique temporal. and. spatial placement of outliers, and are believed to be due to a combination of factors inclUding depletion of resOIU'ces, differential access to resources, and increasing contamination of site environs. CIIAP'l'ER 1

IN'1'RODUCTION

Skeletal maturation, boDY' responses to acute and chronic develop mental upsets, and the form aDd distribution of pathologies renect the abUity of a human group to resolve the universal problems of nutrition and disease (Buikstra 1981). The age pattern of mortality also has important implications for an understanding of the past population which produced the skeletal. series (Cook 1981; Howell 1982). The mortality' of children can be viewed as a sensitive marker of a popu1ation's success in coping with stress (Mul.inski 1976). Death is, after all, the ul.ti mate example of maladaptation (Huss-Ashmore t Goodman and Armelagos

1982).

Children, due to insufficient nutrient stores in the face of extreme physiol.ogical demands of growth, are the first to register metabol.ic disturbances. The developing skeleton provides an excellent record of adverse genetic, nutritional, epidemiological, and environ mental factors affecting growth and development. This skeletal record of stress is easily retrievable and can be interpreted in light of what is known of the population's cul. tural ecological setting.

An abundance of biologicall,.-meaningful. information can be derived from an analysis of the skeletal remains of chil.dren. This information complements that which can be dari ved from adult skeletal remains. Analyses of both types of remains are equally significant and relevant to an understanding 0 f the human biology of a prehistoric

population. In the study undertaken here, a large collection of 1ittle_

studied subadu1 t skeletal remains from Grasshopper Ruin is used to

devel.op a picture Qf the biol.ogical quality of life at both an individual. and a community l.eve1 within this 14th century Arizona pueblo.

Anthropo10sical Value of Subadult Remains

As the method and theory of physical anthropology have changed.

immature skel.etal material. has gradually come to be recognized as an-

thropol.ogically useful. For the first half of this century, the orien-

tation of i?hysical anthropology was towards description, classification, measurement, and speculation (Washburn 1951). The conventional. inves-

tigations of comparative craniometry and racial divergence required complet09 adult crania (for example , Hrdli~ke. 1940; Hooton 1930; Snow

1948; Neumann 1952). This preoccupation with typological studies re-

tarded the development of analyses for investigations, microevo1utioD, behavioral patterns, and the biol.ogical effect of extrabiological. variables (Robbins 1977). Booton (1930: 15) succinctly stated the prevailing sentiment of his time:

In the case of infants and immature individuals, the cartila ganous state of epiphyses and the incomplete ossification of sutures, as well as the fragility of the bones themselves usually results in crushing and disarticulation. In any event, the skeletons of oun sub ects are of co arativel little anthropological value emphasis adde •

While the remains of infants may have been recovered, once they were counted they were ignored (Johnston 1968). In some Cases, the remains of infants were not recognized as such. Robbins (1977) has found human fetal bones in bags of animal bones at one major site, and

personal experience tells me that this is not an isolated case.

Washburn's (1951) delineation of the "new" physical anthropology

served to stimul.ate a new phase of research, characterized by attempting

to understand process, divising and testing hypotheses, rep1acing specu

lation with theory, and suggesting that anthropometry be viewed as only

one of many possible anaJ.ytical teChniques and not an end in itself

(Blakely 1977). The advent of multidisciplinary studies and the wide

spread availabil.ity of X-ray units and other more sophisticated analy

tical devices have greatly advanced the frontiers of physical anthro

pology.

The first major application to subadults of the theory of the

new physical anthropology came two decades ago, with Johnston's analyses

(1961, 1962, 1968, 1969) of the juvenile skeletal remains from Indian

Knoll, an Archaic she1l Dlidden in south-central Kentucky. His pioneering

work is notable for both its rationale and its methods. Adult skeletal

series from various sites Were routinely compared for stature differ

ences, but consistently overlooked were the effects of diet and disease

on statural attainment. Johnston felt that the growth process should

be studied first in children before making these comparisons since "the

major component of variation among adults is due to variation in the

growth process" (Johnston 1969: 335).

Johnston (1968) found an almost complete absence of knowledge

concerning features of growth of any pre-19th century gl'OUp. The Indian

Knoll skeletal collection provided 420 subadul t remains for his analysis.

His methods included devising an age estimate for each child, measuring the long bone lengths of all. those under six years of age, and esti mating growth velooity, the rate of bone length maturation. He found that, when compared to American White children, Indian Knoll children shoved a similar direction but a lower rate of growth. He attributed this to genetic and environmental factors. He suggested (Johnston

1962) that the values he obtained might prove useful as a means to age other American Indian skeletal material.. Examination of long bone growth rates has now become nearly standard procedure in many skeletaJ. anaJ.yses (Y'Edynak 1976; Merchant and Ubelaker 1977; Weaver 1977; Ube1aker 1978).

A second analytic focus for Johnston was the sequence of epiphy seal union in older juveniles in this same population, since all previous studies of this topic had been performed on modern White popu lations. Johnston found that, as seen in many other populations, females matured skeletally two years earlier than males. and that the ages of epiphyseal union at Indian Knoll fell wi thin the White range

(Johnston 1961). The skeletal material from Indian Knoll has since been used in other biological. research (Cassidy 1972; Sundick 1972. 1977. 1978).

The research potential of subadul t skeletons need not be limited to bone growth studies, as recent pUblications demonstrate. A small but prolific group of researchers are examining the sensitivity of the young skeleton to the effects of subsistence changes (Rose 1977, Rose,

Armelagos and Lalla 1978; Lalla and Rose 1979; Cook 1979, 1981, in press;

Cook and Buikstra 1979; Clarke 1980; HUBs-Ashmore et al. 1982 j Milner

1982). Since we can learn a great deal about how or how well a 5 population lived by the ways in which its mellbers died, it is vital to study those who died at a )"CUDg age. "The fact that a person died young presupposes illness. injury, or other deficiency which prevented his reaching adulthood" (Johnston 1962:249). If a child had been stressed by disease, nutritional deprivations, or an unfavorable social. or natural environment, there should be documentation of these insults in the bones and teeth, in the form of growth disruption markers, herein after referred to as "stress markers."

This type of stud,. is new to the Southwest (Palkovich 1980).

Eastern Woodlands subadul t remains have been well-surveyed (Johnston

1962, 1968, 1969; Cassidy 1972; Sundick. 1972i Ortner and. Corruccini

1976; Rose at al. 1978; Cook 1979. 1981, in preSB; Cook. and Buikstra

1979; Lalla and Rose 1979; Clarke 1980; Milner 1982). In the Southwest, by contrast, physical. anthropologists have instead concentrated on bio logical distance (Spuhl.er 1954; Hanna. 1962; Corruccini 1972; Birkby 1m. 1982; E1-Najjar 1974; McWilli..... 1974; Miller 1981; Shiplll8l1 1982) and paleopatho1081 studies (Osborne and MUes 1965; Kunitz 1970; Kunitz and Euler 19'72; J. H. Miles 1975), both of which ignore children.

The Grasshopper series has been used in this and other osteo logical research. B:irkby, Miller and Shipman all examined biolOgical relationships as perceived frOID frequencies of certain nonmetric trai ta, but each author had a slightly different orientation. Birkby (1973,

1982) used cranial nonmetric traits to measure biological. relationships among the adults of Grasshopper, Point of Pines, Turkey Creek, and

Kinishba, and also defined two different social units at Grasshopper, suggesting a male exogamous mating pattern with an uxorilocal residence rule. Shipman (1982) studied these same four sites, using poatcrBDial nOJll!l8trics and cranial and postcranial metrics. Miller (1981) analyzed the biological re1atioDShips of seven central Arizona sites, i!lC1udiDg

GrasshOpper, but emphasizing Chavez Pasa. Cassella (1972) looked at artificia1 cranial defoi'matiOD among Grasshopper adul ta in aD attempt to correlate types of deformation with social status. Blaok (19'781,) and

Weaver (19'77) used juvenile ske1etal remains from Grasshopper to deviae or teat methods of sexing and aging children; their methods and resul.ts will. be discussed in a 1ater chapter. Mul.inski (19'76) analyzed fetal remains to see if he cou1d document changes oyer tillle in the number of fetal deaths. Sumner (n.d.) is currently investigating the relatioDBhip between bone growth and biomechanics of the femur using the Grasshopper ske1etBl series. Final.ly, several researchers have examined Grass- hopper (predominantl.y adult) skeletal remains in as yet unpublished surveys of various pathologies.

Goals of This Research

Rather than focusing on the sociological illplications of m0r tuary data (Clark 1969; Griffin 1967; and Wh1 ttlesey 1978), this research concentrates on the biological individual as represented in the skeletal remains. The basic research question is the impact of stress on growth. disease, and death patterns. The concern is with demonstrating that tM analysis of immature ske1etu remains contributes to the understanding of a particular prehistoric comwni ty and of biocultural adaptations general1.7 among prehistoric inhabitants of the Southwest.

This research differs from other biological analyses using

Grasshopper skeletal material. in that it examines only the subadult portion of the local population, although it has regional. implications.

This research differs from other growth and deyelopment analyses of pre historie material in that it encompasses a narrow time span with rela tively fine-scale temporal control, and it is limited to a single

Southwestern site with a large subadul t component.

The three goals of this research are descriptive, analytical, and explanatary.

Description

The immature skeletal remains from Grasshopper have never been subjected to intensive study, although the collection has been accumu lating for nearly 20 years and now includes 456 juveniles. Phe descrip tive aspect of this study will focus on physical development as evaluated by means of osteological and odontological analyses. It is emphasized that every human skeleton, no matter how young, is importantj

8S an individual and as a representative of society, each child has something to tell us by his or her presence in the mortuary record.

Specific questions to be addressed include:

1. What are the demographic characteristics of the skeletal sample?

2. What evidence of disease or other stress has been recorded in the skeletal remains?

3. What is the impact of disease on subadult mortality?

4. Are the various stress markers which have been analyzed in other skeletal series of value in this series?

5. Hew does the health status of children at Grasshopper compare wi th that of other prehistoric groups? 6. How can ethnographic and modern evidence of disease among South western Indian groups contribute to an appreciation of the health ambiance at Grasshopper?

Analysis

Some archaeologists working at Grasshopper have identified what they believe to be behavioral responses to environmenteJ. stress occur:... ring late in the occupation span (Reid 19?3. 1978; Ciolek-Torrello and

Reid 19?4; Ciolek-Torrello 19?8; Whittlesey 1978; Reid and Whittlesey

1982). Others reject this view (Graves. Longacre and Holbrook 1982).

As of yet, there is no archaeological proof of stress or changing stress levels over time. The analytic skills of physical anthropology may be able to provide that proof, if differences can be observed in the types and frequency of various skeletal and dental. stress markers, parti tioning the skeletal sample into temporal and spatial groups. and determinin~; significant patterns. A more complete discussion of the rationale behind this analysis is presented in Chapter 6.

Explana tiOD

Evaluation of the analysis endeavors to answer the following questions: Which stress marker is the most sensitive within this skeletal series? Do differences in the type and severity of :physio.., logical stress exist across s:PBce and time at this "itc? What do these differences mean? What im:plications does a physical. anthropological interpretation of these results have for an understanding of human be havior? Can the success of adaptations at Grasshopper be judged by their effect on health, nutritional status, and mortality of the popu lation in question?

The human skeletal remains are used as an independent data source to test hypotheses previously developed and tested by archaeo logical methods. As a contribution to ongoing research at Grasshopper, this analysis Dlay provide a new way of looking at old problems. If there is evidence of physiological stress imprinted on growing bone, it \ may be related to the environmental stress which is believed to have precipitated abandonment. CHAP_ 2

GRASSHOPPER PUEBLO

Grasshopper Ruin is a large Mogollon pueblo located ten miles west of Cibecue, Arizona, on the Fort Apache Indian Reservation (Fig. 1).

The sandstone masonry pueblo contains more than 500 one-and-two story rooms, arranged in three major room blocks and several outliers to the weat, east, and north of the _in ruin (Fig. 2). There are three plazas, one of which was roof~d to form the Great Kiva. Tree-ring analysis indicates occupation of the locality beginning around A.D. l275 and ending at about A.D. 1400. Maximum habitation of Grasshopper Pueblo was from A.D. 1300 to circa A.D. 1350.

Pueblo const.ruction history has been studied in detail

(Scarborough and Shimada 1974; Reid 1973; Longacre 1916; Graves at ale

1982; Reid and Sh1!11ada 1982; Wilcox 1982). Starting from two small and one larger cl.uster of core rooms, the pueblo grew rapidly until A.D.

1330. with sporadic building episodes thereafter. These original clus ters may represent three founding groups (Graves et ale 1982). Subse quent population growth was rapid, due both to biological expansion of the 10c81 population and to immigration from other small dispersed settlements. Longacre (19'76) has estimated a peak population size of just over 1000 persons; Graves and others (1982) have revised that estimate downwards to approximately 600 persons.

10 11

Figure 1. Areal loeation of Grasshopper Ruin. -- Map, eourtesy Longaere, Holbrook and Graves 1982, Multidisciplinary Research at Grasshopper Pueblo. 12

(y<:¢ :z ", il ,,'", , ~, .,

..j

J:!l] .0 [tJ

c:J '.'' ~. ,":. 13 The past and present environmental setting of Grasshopper ie

well described (Holbrook 1982; Holbrook and Graves 1982; Kelso 1982).

Briefly, the ruin is lC1cated in a meadow astride the old channel of Salt

River Draw, surrounded by Ponderosa pine forest with oak. and juniper, lit

an elevation of 1800 meters.

Since 1963 The University of Arizona Field School. has excavated

96 rooms, the Great Kiva, and several test trenches and pits in the

plazas and extramural areas. Extramural testing 'Was carried out to

define the stratigraphy of the site and to uncover buried human remains.

For the most part, these extramural areas contained the skeletal. remains

of adults, while the remains of children were more often found beneath

room noors. This is a buria1 treatment often reported for children in

historic and prehistoric Southwest pueblos (Parsons 1939; Vhite 1942,

1962; Lange 1959; Robinson and Sprague 1965; Ellis 1968, Griffin 1969).

Grasshopper is an ideal laboratory for the study of prehistoric

pueblo organization because of its relatively short occupation, the

fine-scale temporal control of major construction events, ita large mor

tuary collection, and the large number of domestic artifacts abandoned on occupation surfaces (Longacre and Reid 1974; Ciolek-Torrello 1978;

Reid and Whittlesey 1982). The occupation of Grasshopper coincides with

the greatest population in the region; within aradius orl2 miles of this

pueblo were at least nine contemporaneous pueblos with 35 or more rooms

(Graves et al. 1982; Tuggle, Reid and Cole 1983).

Residents of the pueblo followed a mixed subsistence strategy

composed of agriculture, h·.mting, and collecting. Domesticated plants

include corn, beans, squash, and cotton. Agricultural fields were 14

small t and a rainfall-dependent technol.ogy was practiced, with no evi

dence of water diversion or major land modification (Tuggle et al.

1983). Avian and especially mammalian remains comprise 99.75% of sJ.1.

recovered nonhuman bone. Deer were hunted extensively (Olsen 1980).

Wild plant remains include manzanita, sunflower, squawbush, walnut,

juniper, prickly pear, grape, and various members of the chenopod group

(Bohrer 1982). No major changes in subsistence practice over the course

of occupation bave been observed (Reid 1978).

Much of the recent research at Grasshopper has focused on

dimensions of social structure and organization: household identifi

cation (Ciolek-Torrello and Reid 1974; Reid and Whittlesey 1982), com

munity growth and organization (Tuggle 1970; Reid 1973, 19?8; Longacre

1976), the mortuary program (Clark 1969; Griffin 1967; 'Whittlesey 1978),

and room function (Sullivan 1974.; Ciolek-Torrell~ 1978). Perhaps the

most startling aspect of Grasshopper Pueblo is its complete and perma nent abandonment circa A.D. 1400. There is no evidence for rl;lids or warfare, sweeping epidemics, or environmental violence. A mild cli

matic alteration -- below-average precipitation for a number of years -

is suspected (Tugglp. et ale 1983).

The Skeletal Remains

Grasshopper provides an ideal archaeo1.ogical si tuation for the

physical anthropologist. Six hunch-ed sixty-tour burial numbers have

been assigned and a total of 674 individuals have been counted, making

this one of the largest single-site series ever unearthed in North

America. The alkaline soil at the site preserved even the smallest and moat fragile bones; the archaeologists did not selectively recover 15 remains; and once the skeletal remains arrived at the laboratory, they were treated carefully to prevent "post-exhumation sttrition!! (Birkby

1973). Consequently, the Grasshopper skeletal. collection is among the finest in the Southwest.

After each fiel.d season, the skeletal remaiDS were broupt to the Human Identification Laborato17 of the Arizona State Museum, Tucson, to be treated and stored under the supervision of Dr. Walter Birk'b7.

In the lab, the bones were washed in water, air dried, and preserved with 2!!!!. a pol.yvin71 acetate resin, to prevent deterioration. Ribs were not treated in ~t but were bagged separately for possible future serological anal.ysis. BODe fragments were reconstructed where possible with ~ cement. Each skeleton was then label.ed, boxed, and stored in the l.aboratory.

The age distribution of the Grasshopper series is presented in

Table 1. Two-thirds of the series are subadults: fetuses, children, adolescents. This research focuses on this component of the mortuary population and includes all individuals younger than 18 years of age, a total of 456 Bubadults. Sixty-six. of these remains were so fragmen tary and incomplete as to be analytically useless, learing aD effective sampJ.e size of '90.

Sample Validity

Because demographic studies are only as good as the data upon which they are based (Milner 1982), it is crucial for any human osteol ogist to estimate the representativeness of the skeletal sample under study. The Grasshopper series is unusual among prehistoric sitea in the high percentage of subadults (Table 2). This table presents 16

Table 1. Age and sex distribution of Grasshopper skeletal remains.

Sample Percent Females Undeterm.

Fetal 40 6.6 40 Neonatal. 60 9.9 60 0-6 m 26 4.3 26 6-12 m 30 4.9 3 26 12-1B m 43 7.1 10 26 lB-24 m 33 5.4 B lB 2-3 y 30 4.9 10 11 3-4 'I 29 4.B 4 19 6 4-5 'I 15 2.5 3 7 5 5-6'1 25 4.1 9 6-B y 26 4.3 13 4 B-l0y 10 1.6 5 0 10-12 Y 4 0.6 3 0 12-14 'I 1.0 o 14-16 'I 1.5 3 0 16-18 '1.'" 0.6 2 0 lB-2O 'I 17 2.B 12 0 20-25 " 30 4.9 22 0 25-30 Y 27 4.4 12 15 0 30-35 'I 33 5.4 13 20 0 35-40 'I 25 4.1 11 14 40-45 y 26 4.3 14 12 0 45 + 'I 60 9.9 20 40 TOTALS 60B3 99.9 148 229 231 1. Methods for aging subadults are listed in Table 3. Ages for adults on file in Human Identification Lab, Arizona State Museum. 2. Methods for sexing subadul ts are listed in Table 3. Sexes for adul.ts on file in Human Identification Lab, Arizona State HuseWD. 3. Number of individuals recovered = 674. Number of unusable aub adults (see text) = 66. Effective sample size for total site = 608. "Limits of this study. Effective sample size for subadults = 390. 17

Table 2. Percentage of subadults in large archaeological populations.

Size of Skeletal. ~~ sitel Samp~e Total N <2l yr. Reference

Indian Knoll, KY B73 48% 29;li Johnston and Snow 1961

Point of Pines, AZ 42B 41 31 Bennett 197'a

Pecos Pueblo, NM 5B7 }O 16 Goldstein 1963

Mesa Verde, CO 202 40 12 Bennett 1975

Ledders, IL 1BB 61 61 Droessler 1981

Schild, IL 346 58 66 Droessler 1981

Koster Mounds, IL 229 4~ 61 Droessler 1981

Libben, 08 12B9 59 40 Lovejoy et &1.. 1977

Grasshopper t AZ GoB 67 75 Hinkest this paper 1. Cultural information on these and other sites referred to :in text can be found in Appendix A. 18

demographic information for nine sites, widely plaoed. in space and time,

chosen for their large skeletal eeries. The Grasshopper seriee does

indeed stand out for its subadult component. For purposes of this

table, age 21 was used as the point separating adulthood and subadult- hood, because this is how many of the researchers oi ted therein have arranged their data. Cultural information for these sites and others mentioned in the text can be found in Appendix A.

Confidence in the 'Ya1idity of the large subadult sample at

Grasshopper is based in part on demographic data of developing coun

tries. Studies designed to investigate child mortality in Latin America have documented a fetal death rate of 1.8.~ and a 26-28% mortality in

children under five years (Burke, York and Sande 1979). Death rates as

such cannot be computed for prehistoric series since the number of live births is never known. but demographic surveys document a tremendous loss of the youngest children. Puffer and Serrano (1973) found that of children dying before age five, 78.6% of these died during their first year and 12.4% during their second year of life. In an earlier census of two New Mexican pueblos I Aberle (1932) found that by the end of their second year. one-third of the children in these pueblos .... ere dead.

In a 1949-53 Gambian study. 187 live births were recorded. The mor

tality rate of children under age seven reached 43%, with a peak at 9 to 14 months. There 'Were 54 neonatal deaths. This "prodigious wastage of life" in young children occurred despite the availability of medical intervention (McGregor. Bi11ewicz and Thomson 1961:1664).

Death rates for modern U.S. White children are not comparable.

Pratt and associates (1978) recorded a mortality rate in the first five 19 years of only l.06/loo~ooo in a 1960 ce218US.. It should be kept in mind that the dramatic ful in childhood death rates in Western countries is largely due to the availability of effective preventative and. thera peutic medicines, which are less accessible in Third World countries and nonexistent in prehistoric pueblos.

Further support for confidence in sample validity is drawn from an examination of the excavation methodology. Nearly ~ of all juvenile skeletal remains came from rooms t vi th the remainder recovered from test pits in plazas and trash areas. Had Bubnoor pits not been defined and excavated, the number of subadult burials recovered would have been much lower. Ninety-six rooms (2~ of the pueblo total) have been exca vated, and 65 of these rooms contained the burials of children, ..... ith an average of six children per room. All factors being equal, we can hypothesize that if the total pueblo ..... ere to be excavated, 350 of the

500 .:."'ooms should contain child burials, yielding a potential skeletal sample of over 2000 subadults ..

Because all. roem blocks as '.Jell as extramural areas have been sampled, it seems reasonable to assume, unless the residents of Grass- hopper subscribed to a mortuary prCigl"am substantially different from that kno..... n elsewhere, that the skeletal collection is a reasonably representative proportion of the total mortuary population interred at the pueblo. This is not to say, however, that the pueblo has been ran dolllly sampled or that the burials are evenly distributed. On the contrary, much archaeological work has focused on the Great Kiva and surrounding rooms in Room Block 2. These rooms contained an average of 20

6.56 child skeletons each, while the average for Room Block 1 is 4 .. 48 and for Room Block 3, 6.13.

It is an undeniable fact that we will never know how representa ti ve the excavated skeletal sample is of the total mortuary population or, more importantly, of the total. population once living at this or any ai te. Even total excavation would not guarantee complete confidence in the representa.ti veness of the skeletal remains recovered (Howell

1982). At Grasshopper, the infant and chil.d mortality appears greater than that recorded for other prehistoric populations since archaeologi cal recovery is good, and this theoretically-high infant mortality is a more accurate representation of demographic reality.

A number of other dilemmas face any researcher involved in a study of prehistoric skeletal remains. The first of these is that in most excavations, the physical anthropologist has no input into the sampling strategy, which is often done for purposes unrelated to the recovery of skeletal remains. The remains are usually removed by personnel untrained in osteology. Consequently, the skel.etal sample may be small, fragmentary, and incompl.ete.

A second problem is that because the remains are a mortuary sample, any analysis is based on pathological specimens, not on a

'normal,' healthy group. A similar situation would arise were a re searcher to use hospital patients to represent the average inhabitants of a city. It is overl.y-simplistic to assume that the frequency of stress indicators and developmental. disturbances in a mortuary sample directly reflects the experience of the living popul.ation which buried these individual.s (Cook and Buikstra 1979). Stress indicators tend to 21 be more frequent in living individuals with a history of malnutrition or disease; higher frequencies of these indicators would then be expected in individuals dying at younger ages. Consequently, comparisons of frequencies of stress indicators should be age-structured. Care must be taken to investigate thoroughly all the complex interactions of disease and development within a specific cultural milieu (see Cook

1981 for a particularly insightful discussion of this problem).

The fact that the remains are skeletal is the third problem

(Johnston 1962). The anthropologist has only bones and teeth with which to work and therefore has no record of the many pathologic processes which may have affected only the soft tissues. Of the diseases which can elicit skeletal responses, many are indistinguishable from one another as to the nature of the response. Lacking supplementary clinical information, it is rare that a bony condition can be said to be pathognomonic of a particular disease. Disease frequencies can be compared only with modern groups or with other prehistoric samples, of which were exposed to exactly the same stresses (Cook 1981). It is often difficult to ascertain age and sex of skeletal remains. Precision is not possible in the face of unknown variability. Modern comparative growth and maturation standards may be inapplicable due to racial dif ferences or secular trends in recent generations (Garn 1965; Sundick 1977).

A final problem is that the sample, as with all archaeological samples, is cross-sectional j each individual can be viewed only once.

Disease progressions and developmental rates cannot be followed •

• • • we can see an early individual at only one moment of his existence--the moment of death. It is a snap-shot, not a moving picture. It is true that from the structure and 22 pathology -present in the skeleton at that moment much can be inferred about what led up to the final appearanee, but that is quite different from being granted a diachronic or per specti ve view of a person at seYeral stages of his life histo:ry (1Ie1161967:39O).

These limi ting factors will always exist in an anal.ysis of prehistoric skeletal remains, but they should not deter study of these remains. "If such material. is to be of use at all," stated Johnston

(1962: 249), z.these lilllitatio~ must be borne graciously and realized analytically.II CHAPTER 3

METHODOLOGY

The initial step in the analysis of subadul ts from Grasshopper

was to eXaMine the skeletal remains of each individual. Index cards were used to record burial number, provenience, age and sex assignments

(see Table 3), lengths of complete long bones, any observed dental and

s..l{eletal pathologies and anomalies, whether a dental chart had been made, and whether radiographs had been taken of long bones. Appendix B

summarizes these data for each individual. Measurements and observa

tions were verified at random during analysis.

If increased magnification were needed to scan dental or bony

features, a Bauach and Lomb dissecting microscope was used. Length measurements of all complete long bones were taken to the nearest milli meter with an osteometric board or sliding calipers, depending on the

size of the bone.

Radiographs were taken of all complete long bones for evalua

tion of Harris lines and cortical bone loss. The long bones of 21

subadults had previously been radiographed by W. H. Birkby, and these

films were incorporated into this study. Teeth or other bones which

required diagnosis of pathological or anomalous condi tiona were also radiographed. Radiography of long bones was done on 14 x 17 inch

Cronex-4 film in cardboard cassettes, with an exposure setting of 78

KV, 60 MAS, and a tube-film distance of 40 inches. The long bones of

23 24

Table}. Methods of age and sex estimation used in this resear~h.

~ Fetal, Neonatal. Cranial maturity Hesdorf!er and Scammon Secondary ossifieation 1928 eenters Pierce t Mainen and Dental. ealeification Bosman 1977 Fazekas and Koaa 1978 Tanner 1978 Scheuer 1 Musgrave and Evans 1980

6mto12,. Dental eruption Ube1aker 1978

12 to 18 ,. Epiphyseal fusion GOBS 1973 Mackay chart n.d.

6mto18,. Metrics of dentition Black 1978&, 1978b

12 to 18 ,. Pelvic conformation Krogman 1962 Phenice 1969 25 several uall children fit on each sbeet of film. To prevent distortion of the X-ray image caused by femoral curvature and torsion in an anterio-posterior Yiev. the anterior surface of the bone was laid aD the film holder for a poaterio-anterior view, as recommended by Trotter and

Peterson (1967). Lateral radiographs were taken on a ~ .eample of long bones to Yerii'y observatiOllS in the p-a view. Dental radiographe were

DIIlde on Kodak. type DF-58 dental fil., 1.25 x 1.62; inches, at a setting of 56 ltV, 10 MAS, and a tube-film distance of 15 inches. FUm was de

,"loped by hand, using Kodak X-ray developer and fixer, and then air dried. All radiosr:aphic equipment is located in the Human Identifica tion Lab of the Arizona State Museum.

Dental. charts were compiled for each individual. over six months of age who had at least five erupted teeth among the remains, resulting in 212 charts. Dental observations could be made on an additional }If children for whom dental charts vere not constructed. Features noted for each dentition include: which deciduous or permanent teeth were present (fully calcified or not, in bone or isolated), antemortem or postmortem loss ot teeth, stage ot eruption (unerupted but visible, not fully' erupted, completely erupted), dental variants (see below tor description), attrition, caries, and any other pathological conditions

(fractures, abscesses). Figure' presents a sample chart. Dental. maturation sequences were used to estimate an age for each child in the sample (see Age Estimates, below).

For purposes of the presea.t research, ODly nondestructive tech niques were used. Other researchers have used sections of bones or teeth to evaluate bone mineral content (Lambert, Szpunar and Buikstra 1~ _I: l:I:I:I"lp!'lUYJ

I; 1~ ItOO;I;I¥I; 1;1

Figure 3. Sample dental chart, from 5-6 yeat'-old girl from Burial 130. __ " = tooth present; c = tooth calcifying; P :;;:: pegged tooth; FI' = fused teeth; MP = tooth missing postmortem.

~ 27

1979; Lambert et ale 1982) t bone microstructure (Armelagos et al. 1972;

Richman, Ortner and Schulter-Ellis 1979; Huss-Ashmore et ale 1982). and

dental microdefects (Rose 1977; Rose et ale 1978; Lalla and Rose 1979;

Cook 1981). Since there has been no previous analysis of Grasshopper

subadul.te, no sectioning or destruetion of hard tissue was undertaken

at this time. These microscopic and spectroscopic techniques are,

however, quite promising for future work at Grasshopper.

Building the Biological Profile

Age Estimates

Techniques for aging juveniles rely on dental development (cal

cificatioD, root completion, eruption) t epiphyseal closure t and long

bone lengths. It is generally held (Hoarreeat Fanning and Hunt 1963;

Garn, Lewis and Kerewaky 1965; Johnsto!:' 1968; Sundick 1972; Anderson,

Thompson and Popovich 1976; Ube1aker 1978; Hoffman 1979) that of thesee

dental development is the closest approximator of chronological reality.

This topic has received much study (Massler, Schour and Foncher

1941; Brauer and Bahador 1942; Robinow, Richards and Anderson 1942;

Meredith 1946; Hurme 1948; Hunt and Gleiser 1955; Falkner 195?i A. E. W.

Miles 1963; Kraus and Jordan 1965; Noble 1976). Sundick (1972) gives

an excellent S\lJIII!Iary of the strong and weak points of many of these

studies. Unfortunately, there have been only three suoh analyses on

American Indian material (Hrdlif:ka 1908; Steggerda and Hill 1942;

Dahlberg and Menegaz-Bock 1958). There is some evidence for differing

tooth formation and eruption sequences between Whi tee and Indians. In

Whites, the permanent upper and lower central incisors erupt before 28 laterals. In Indians, eruption of all lower permanent incisors precedes that of uppers (Sundick 1977). Among Pima Indians, the anterior per manent teeth erupt later and the posterior teeth earlier than do those of \lhites, possibly due to heavy wear on the deciduous molars (Dahlberg and Menegaz-Bock 1958:1136).

Part of the problem encountered when trying to evaluate archae ol.ogical remains by the pUblished standards is dealing with missing teeth. Standards using a tooth-by-tooth assessment will be more useful. than those which require a summation of whole-mouth data. Calcification progressions are difficult to evaluate, because the tiny tooth ·pre.. forms' Dlay be overlooked in the field or rinsed down the drain by an energetic bone-washer. Developing teeth that do remain embedded in the

jaws may be accessible only radiographically (Demirjian, Goldstein and

Tanner 1973).

The aging task is simplified if tooth eruption sequences are used, and this is the aging method employed in this research. The most frequently used standards are those of Schour and Massler (1941, 1944).

Other standards are avails.ble (for axample, Moorrees et ale 1963; D.

Marshall 1976) and may actually be more realistic in terms of showing

Yariability, but the Schour and Massler chart is by far the simplest to employ. An independent verificatiOn of this chart was performed by

Brauer and Bahador (1942) on 415 young patients in dental clinics at

Iov.5l State University Hospital.. In nearly 50% of the individuals they examined, chronological, calcification, and eruption ages corresponded exactly to the Schour and Hassler chart. 29

Ubelaker (1978) has devised a similar chart, based on 18 pub lie:hed sources, of the sequence of formation and eruption of teeth among

American Indians. His chart, reproduced in Figure 4, is used in the present study to age children. The method of use involves making a visual comparison between an individual's jaws and teeth and the chart, which lists an age range for each stage of tooth development. The actual result of aging unknowns by dental eruption intervals is to sequence individuals relative to each other, since it is developmental age, not chronological age, which is being evaluated. The numerical

'age' is more or les6 a convenient label.

In this research, the primary goal in assigning ages is to arrive at a workable age distribution and not to try for false pre cision by using every possible means of age estimation. Therefore, I found it sufficient to rely on gross evaluation of dental eruption.

Some researchers who have attempted more complex forms of dental aging

(for example, Sundick 1972) have later decided it yielded no additional information (R. Sundick, personal communication 1981). unless one is specifically interested in dental development as an end in itself.

Ages for fetuses and neonates were estimated in a somewhat more subjective manner. Age assessments were based on bone maturity. Cri teria included: texture of the bone tissue. ossification patterns of temporal and occipital bones, configuration of borders of cranial vault bones. presence of secondary ossification centers of long bonest and degree of dental calcification (Hesdorffer and Scammon 1928; MassIer and others 1941; Pierce et al. 1977; Fazekas and Kosa 1978; Tanner

1978j Scheuer et a1.. 1980) .. ~5MONTKS ..~ ;NtU;~gS) ~''''''~(!8MOS) f) 0 7Y[ARS ~(J 't. _!1MONTliS _g (_30,",051 ~INUTERO C) " ...,,' (:0.: 12 MOS) '~e:lOOJI81I1T" ~ G 12 YEARS ", t;;;:;;"0d:9I I!: :I MDS) CJ • '" 5 ',"'" '"'"''' t:::::I 1_2""'05) :;So;,0;rg,."", ~ "'DO,O 1!.3MOSI A <9 0 ~""'" ~~~ao , "'OHTIIS _'(3 &: ~"""''' ~DO~ (~3MOS) _

~atlO'E'l <0 ~ YEAJtS r;;; ~;;:':"'. "'S "'" '''' .,,' "'"'' ~""'''' 0 C3 ~01 8 ISMOlnllS 35 YEARS !!61,10S)G.Q£ 'YEARS (t 30101051 ~~ 0<9 ,n •• ,,' • Q " Figure 4. Sequence of formation and eruption of teeth among American Indians (from Ubelaker 1978:47). """'. \'J 31 For individuals appearing older than 12 years, a combination of dental eruption and long bone epiphyseal union was used to arrive at an age estimate. Two standards of' epiphyseal union sequence have been derived specifically from prehistoric American Indians CT. D~ Stewart

1934; Johnston 1961). These figures indicate no statistical evidenoe of racial differences. In this instance. the error that may be in.. valved in using dental age instead of known ohronologioal age does not seem to be significant. In any case, chronological age is notoriously unreliable as an indicator of deyelopmental maturity (Marshall 1976) ..

The actual. times of appearance and union of epiphyses can be found in an anatomy book or atlas (Pyle and Hoerr 1969; GOBS 1973; Platzer 1978) and are neatly tabulated in Todd (1930), Flecker (1942), Krogman (1962), and Mackay (n.d.). I found the Mackay pictorial chart particularly helpful.

The age intervals presented in Table 1 are uneven. Infants can be gl"ouped in six-month intervals because their developmental. rates are much more distinctive, as evidenced by the small error factors listed by Ubelaker (1978) in his dental chart, rsp::"oduced in Figure 4. As variability increases, so does the size of the designated age interval.

Children older than six years are assigned to two-year intervals, partly to compensate for smaller 68ltlple sizes.

Long bone diaphyseal lengths are not used as an age indicator in this research, although it is frequently done (Maresh 1955; Johnston

1962; Sundick 1972; Y'Edynak 1976; Merchant and Ube1aker 1977; Weaver

1977; Hoffman 1979). One reason this method was not used here is that gl"owth rates vary widely within and among popUlations (Ubelaker 1978). 32

All but two of the studies listed above examined long bone growth based on prehistoric skeletal remains, for which age was inferred from dental

features, thus compounding error factors. The two studies of living children (Maresh 1955; Hoffman 1979) are based on serial radiographs, which may not be perfect records of actual bone dimensions. A second reason this method was not used here is that since part of this research involves developing a measure of long bone growth in t?e Grasshopper series, it would be misleading to age this sample by means of long bone lengths developed from other skeletal samples.

Sex Assignments

There are few reliable means of distinguishing between the sexes in the skeletal. remains of young individuals. since skeletal sexual dimorphism is not pronounced until after puberty. Many physical anthro pologists simply do not attempt this task. Bennett (1973a) assumes a

50:50 ratio in individuals l.ess than 16 years of age. Studies on aborted fetuses indicate a slight predominance of males (McMillen 1979), al.though these results have been qUestioned (Lowry, Lindl.ey and Migeon

1979). The usual ratio at birth seems to be 105 males to 100 females

(Howell 1982).

Other anthropologists have devised their own methods for sex determination, with varying degrees of success. Seven of these methods are discussed here, along with potential drawbacks for use on the Grass hopper series.

The earliest studies are those of Reynolds (1945, 1947) and

Boucher (1957). Both u.sed pel'i'i;:: iiiea;;u.~iii6nt5 taken from radiographs 33

of live children (Reynolds 19lf.5. 1947) and fetuses (Boucher 1957). The

probl.em here is that while these infants have articulated pelves with

cartil.age, it is quite another matter to derive comparable measurements

from dry t disarticulated bones.

JobDston and SUOV' (1961) attempted to deterlline the sex of 361

Indian Knoll children (0 to 14 :rears of age). Al though the,. are not specific as to the method they used, it was based on obseM'ations of pelvic conformation and general. size of the teeth (Snow 1948). Their resu1.ts were 174 males. 150 females, and Yl indetermiaate.

Chai and Trotter (1970) used tetal material (16-44 fetal weeks) in :tactor and diseriminant analyses to look at sex and race (Whi teo-Negro) differences. '!'heir 21 variables illYolved ratios of the lover limb lengtba to upper limb lengths. Significant sex differences were dis covered, with two factors describing 8", of the variance. '!heir stan dards are not applicable to older indiViduals, though, and a comparable reference collection of children's skeletons of known sex is not available ('l'. D. Stewart 1962).

Y'Edynak: (1976) and Weaver (1977) have devised standards from prehistoric populations. Y'Edynak used a sample of 109 pre.. 19th century

Aleu:ts and EakilllOB ranging in age trOll 0 to 19.9 years. Using sciatic notch "idth, pubo.. ischial index, fa~eJ. neck lensth, and presence or absence of a pre.. auricular sulcus, she isolated '+7 lIl8les and 47 females, with 15 indeterminate.

Weaver (1977) used 105 children, fetal to six years of age,

frOll! Grasshopper. Be applied a principal. components analysis to six metric and one nonmetric character of the pelvis. '1'hree components were derived with binomial distribution. By observing which vaxiable(s) was most heavily loaded for each eigenvector, he interpreted that one

component corresponded to size, while the other tvo vere associated with

sex differences. His results indicated 41 males, 45 females, and 13

indeterminate. The present research did not attempt to verify W~ave!"'s

assignments; that task has previously been accomplished by Black

(1978b) t as discussed below.

The problem with the studies of Weaver and Y'EdYDak is that

they deal with prehistoric, and hence unknown, material; there is no

way to check on what percentage of the sample was correctly sexed be ..

cause true sex is not known. The fact that these two researchers were

able to distinguish two sub... groups within their respective samples in..

dicates that some factor(s) is operating to produce a dichotomy, and in

all probability that factor is sexual dimorphism. The similarity of

their resul.ts is interesting in that their ratios are 60 close to

Bennett's assumed 50:50 distribution.

A seventh method, and the one used in this research, is based

on live chil.dren of known sex (n = l},). It uses measurements of decid..

uous teeth, it is applicable to young children, and it promises up to

7% accuracy, a definite advantage over an earlier method devised on

permanent teeth by Bailit and Hunt (1964). The method is a discriminant

analysis of mesiodistal and buccolingua1 tooth crown dimensions (Black

19788" 1978b) t developed on a sample of White children from the Univer

sity of Michigan University School Growth Study. In 15 out of 20

measurements, the male mean exceeds the female mean. This fact is due 35 to an absolutely longer period of amelogenesis in males (Pindborg 1970;

Moss and Moss-Sa1entijn 1977).

Black applied his derived standards to Grasshopper subadults and was able to assign a sex to 142 children, 58 males and 84 females (Black

1978:Table 75). He notes that, in his modern sample, females were more often misclassified than males, although misclassification on the whole was not frequent. I have made use of Black's results and, after testing the consistency of my measurements with his, applied his method to the six juvenile skeletons excavated since his study was completed. Sex assignments of an additional 11 adolescents were based on features of pelvic conformation (Krogman 1962; Phenice 1969). Combining Black's and my results yields a sex ratio of 65 males, 94 females, and 231 in determinate. Over half of the individuals in the indeterminate group are fetuses, neonates, and perinatal infants.

Black's (1978b) and Weaver's (1977) studies overlap only slightly t since few children in the Grasshopper series had both the dentition required by Black and the pelvic bones required by Weaver.

Thirty children from Weaver's sample are duplicated in Black's, and of these 30, the assigrunents of sex agreed in 20 cases. In the ten con flicting cases, I preferred to use Black's assignments. Since his technique was derived from a known semple, I felt it 'Wou1.d be more re liable when applied to unknowns.

Studies on living children have shown that the sexes can mani fest differential response to stress, a fact which may prove significant at Grasshopper. It could be predicted either that males would have more growth disruptions, since the growing male is more sensitive to stress, or that females would have more growth disruptions, since females are often less cul turally buffered from stress (Goodman, Armelagos and Rose

1980). In a study of a rural village in Colombia, Stini (1969) showed that the long-term effects of a protein deficiency were more pronounced in males, who were unable to generate catch-up growth in early ado lescence. Cook and Hanslip (1964) demonstrated the unusually unfavor able mortality and poorer nutrition of girls under five years of age as compared with boys in Greater Syria. Preferential infanticide and neglect are not likely explanations, as thf' deaths are reported. Rather, it appears that there may be an unwitting but significant resource dis tribution favoring maJ.es.

Demographic Profile

Opinions differ as to whether a skeletal sample approxi.mates a living population, amenable to the construction of life tables and survivorship curves. On one hand, it is believed that there is a regular pattern to vital events, such as birth and death rates (Weiss 1973,

1975, 1976; Howell 1976), so that what is observed in modern populations is applicable to prehistoric ones as Yell. The larger the cemetery population, the less 'noise' there will be in the pattern (Lovejoy et al.

1977). Various statistical smoothing teChniques can be applied to eliminate the 'noise.' At best though, skeletal demography is but a general estimate of conditions, and results should not be taken abso lutely (Weiss 1975; Moore, Swedlund and Armelagos 1975).

On the other hand, a prehistoric skeletal series does not meet the assumptions necessary to generate a life table. These include: 37 that it be a biologically stable population, that it represent a single generation cohort, that death rates be even at all ages after infancy

(Angel 1968). Since cemeteries include individuals who were never simultaneously alive and thus had a zero probabi1ity of mating, the cemetery 'population' is not a population (deme) in the true biological sense (eadien et al.. 1974). Burials can at times be sequenced relative to one another, but there is no possible way to draw a line between generationst especially if the cemetery were used over a long period of time. Stabil.ity of an extinct population cannot be guaranteed. If, as in the case of Grasshopper, we are looking for evidence of a people under stress, population instability may be that very evidence.

A life table measures 6urvh'orship, relative to the number of people living at each age. This assumes that the number of people living at each age is known. In an archaeological sample, what is known is the number of people dying at each (estimated) age who 'Were buried at the site and whose remains were recoyered. With such a large potential for error, it is risky to assume that a skeletal sample will approximate the average lineage of its source population. Archaeologi cal skeletal data yield too few facts to have much theoretical import.

Therefore, a life table should be viewed as a means of generating, not testing, hypotheses (Petersen 1975; Mobley 1980).

A stellar example of misinterpretation can be Been in a recent re-evaluation by Howell (1982) of the Libben Site life table constructed by Lovejoy and associates (1977). According to the life table, 83% of the population of Libben died before age 30 and 98% died before the age of 45. The infant mortality (20% died before the age of five) is lower 38

and the adult mortality higher than expected from living populations,

although this is a pattern often reported for prehistoric series.

Lovejoy and associates emphasize that all skeletal material vas re

covered in the near-total excavation of the site I 80 this distribution

is not an artifact. Vltat they do not contemp1ate is that infants may

have received a mortuary treatment which ~ould preclude their recovery

at the site. If this life table is accurate, Howell (1982) points out,

Libben had many orphans, few grandparents, and an over-worked young

sdul t sector -- small wonder they died early. Either their lifestyle

was extremely difficult, or the life table is based on doubtful age

techniques or basic principles (Bocquet-Appel and Masset 1982).

Because of the many problems inherent in the construction and

use of life tables and because this research is particularly concerned with nonadult remains, demographic data are presented in the form of a

mortality curve. Mortality experience. rather than survivorship. is

the demographic data Bet most readily obtainable from an analysis of

the human skeletal remains from a prehistoric site. The distribution

of age at death displayed in a mortality curve "serves to identify the

age when individuals experience the greatest risk of succumbing to

potentially fatal, and often interrelated. external and internal stimulill

(Milner 1982:19). The Grasshopper mortality curve will be presented

and discussed in Chapter 5.

Long Bone Growth

The Grasshopper 6ubadul t skeletal sample contained 1478 intact

long bones without fusing epiphyses and 109 intact long bones with

fusing epiphyses. These figures represent one-third of the total number 39

of long bones to be expected if all 390 Bubadul ts had a complete set of 1.2 long bones (n = 4680). Some of' the missing long bones were not re

cover2d ~hen the skeletal. remains ....ere excavated, and many of' those long

bones which were recovered were incomplete or too fragmentary to recon

struct.

The maxilllUlil diaphyseal lengths of the 1478 bones are used to

study linear growth in the Grasshopper sample. These measurements are

presented in Tabl.e 6 t p. 92, which lists for each of the six l.ong bones

the estimated (dental, epiphyseal) age, ~ample size. mean length in mID,

standard deviation, and range. Should additional. subadult skeletal

remains be recovered from Grasshopper, a child could be aged by measur

ing a selected long bone, turning to the appropriate line of the table,

and reading the corresponding age.

Since females are more mature skeletally than males at a given

a~, their bone development outpaces dental development while the two are concordant in males (Hunt and Gleiser 1955i D. Marshall 1976; W. A.

Marshall 1977). This statement was tested on a sample of 80 subadults

from Grasshopper, those individuals having intact femora and for whom

a sex assignment could be made. Results are preB~nted in Table 8,

p. 98.

Weaver (1977) analyzed growth in 688 long bones from Grasshopper

children fetal to six years of age. His sample is contained wi thin the

current one. The tables generated in the present reaearch will be com

par,;ld with his results and will expand them in terms of sample size and

age range. An attempt is made to isolate growth spurts and the age

range of greatest growth variability. A cross-sectional study, as is 40

this one, is more effective than a longitudinal study in estimating

population values, since all members of the population are independent

of each other (Marshall 1977). Since each child can be measured only

once, though, this research CBr.not elicit data as to variations in

growth ra tea.

A second comparison will be made I between the Grasshopper table

developed here and similar tables developed for Indian Knoll (Johnston

1962) and Arikara (Ubelaker 1978) subadults. The galls of this com

parison are to evaluate inter-site differences, and secondarily to

illustrate why such tables are not the best means of estimating age.

Indian Knoll and Grasshopper are separated by 1500 miles and 4500 years,

while Grasshopper and the Arikara sitea are separated by 1000 miles and

just 350 years.

A growth curve as such will not be constructed for the Grass hopper sample, for the philosophical reason mentioned above. Previously,

Weaver (1977) constructed a growth curve based on his measurements of

long bones in the Grasshopper sample. He compared the Grasshopper curve

to those derived by others from akeletal samples of Arikara, Indian

Knoll, Dickson Mounds, tvo New Mexican prehistoric pueblos, and to one

derived from Denver Whites (Maresh 1955) and found no significant dif-

ferences.

Ubelaker notes that derived growth curves !lshow little vari

ability in rates of growth among Indian populations, when allowance is

made for variation attributable to the use of different methods of

aging\! (Ubelaker 1978:48). Both Ube1aker and Johnston (1%2) have

found growth rates of American Indians to be somewhat slower than those 41

of Whites, which is to be expected when adult statures are compared.

Estimated stature for prehistoric Indian groups compared in this text

ranges from 163.6 em for Grasshopper males tc 165.99 em for Arikara

males (Bass, Evans a...~d Jantz 1971); the average American male of today

measures circa 175.0 em in stature.

Evaluation of Skeletal and Dental Variants

A number of skeletal and dental anoma1ies were observed in the

course of analysis. While these are not indicative of physiOlogical

stress, they do serve to characterize this population and so are dis-

cussed from a descriptive standpoint. The etiology, heritability,

and distribution of these anomalies were researched, 60 that hypotheses

of familial relationships at Grasshopper might be offered. Burial in

the same or a connecting room of the pueblo is used here to suggest

relatedness.

Skeletal variants noted include Kerckringts ossicle, bregmatic

configuration, early closure of cranial sutures, extra vertebrae, fused

ribs, and the discrete traits of Inca bones end atlanta-occipital

fusion. These variants were evaluated primarily by means of anatomy

books (Schaeffer 1953; Goss 1973i Platzer 1978) and articles on spe-

cific topics, to be cited in the discussion.

Dental variants observed include: fused teeth, retained decid-

uous teeth, supernumerary teeth, pegged teeth, lingual and paramolar

tubercles, and Carabelli' s cusps. Their frequencies among the Grass-

hopper sample are compared with other prehistoric and modern population 42 frequencies. It should be noted that morphological. characteristics of the deciduous dent! tioD are not often studied in prehistoric skeletal series. A number of dental anatomy references proved to be quite help ful in eValuation and interpretation of tbese features, notably Diamond

(1952) t Wheeler (1962), Kraus, Jordan and Abrams (1969) I Garlin and

Goldman (19'70) t Pindborg (1.970) t stewart and Prescott (1976) I and

Bhaskar (1980).

Attrition rates of the deciduous dentition were also noted.

Dental attrition is the gradual and regular loss of tooth substance as a result of natural mastication (Pindborg 1970). If the normal rate is increased, the attrition is termed "intensified.. " Moderate attrition may be protectivej it reduces and removes the occlusal stagnation areas that generally predispose to caries (Van Reenen 1966).

Attri tion is a mechanical process, reflecting daily and intimate contact of prehistoric peoples with their environment (Perzigian 1977).

The teeth of Mesa Verde inhabitants, for example, ahow spectacular wear due to grinding of corn on sandstone rocks (Wells 1975). Excessive wear is characteristically seen in older adults, but the deciduous molars may show intensified attrition. The enamel of deciduous teeth is thinner than that of permanent teeth (Kraus et &1. 1969; Bhaskar 1980), and due to the smaller size of the primary molars, there is a greater ratio of chewing per surface area.

Assessing Skeletal stress

Evaluation of disease in a prehistoric population is best under_ taken wi thin an anthropological rather than a medical perspective, since all the I patients' are deceased, and most of the literature on disease and malnutrition focuses on the survivors. The physical anthropologist is more accustomed to looking at bare bones without supplementary clinical information and accepts the fact that only in rare instances can a specific disease name be applied to a skeletal pathology.

Analysis of morbidity among the sKeletal remains of Grasshopper subadults is based on the directive that the reconstruction of disease states from skeletal evidence requires careful consideration of the nature of observable pathologies and the range of disease processes which induce these skeletal responses (Palkovich 1980). There are two levels of observable pathologies to be discussed here, specific and general.

Specific Pathologies

This first level is concerned with specific pathologies, those derived from trauma or a circumscribed disease episode, even though the disease or source of the trauma might not be identifiable. Included are fractures, congenital malformations, bony reactions in a very limited area of the skeleton, such as a scalp wound or a single bone infection

(osteitis) t and dental caries. In the Grasshopper sample, evidence for this type of pathology is drawn from gross macroscopic examination of all skeletal remains. with radiographic 'Yerification when necessary. A number of published descriptions are used as aids in identification, in cluding Ortner and Putschar (198l) and Steinbock (1976). Both of these books present prehistoric as well RS historic evidence of pathologies, accompanied by medical descriptions and references to facilitate inter pretation of the diseases and injuries obserTed in the skeleton. Infectious diseases (for exampl.e, influenza and other upper respiratory infections and gastrointestinal. disorders) by their very nature are sel.dom identifiable in skeletal remains, but are in fact the major killers of young children (see discussion in Chapter It.). Occur rence of such disease episodes in a child's life can precipitate the formation of stress markers which may be identif'iabl.e in skeletal remains, as discussed below.

Oral. Pathol.ories. If the skeletal SJStem indicates a poor state of health, the teeth may al.ao renect poor health. Eyidence for oral pathology, such as caries and abscesses, is noted macroscopically during the compilation of dental charts.

Caries has been described as an "infectious and tranamissabl.e disease in which progressive destruction of tpoth structures is ini tiated by microbial activity on the tooth Urface" (Pindborg 1970:256).

This occurs as a direct result of lytic activity by bacteria, the lIacidogenicti theory (Mandel 1979). Factors which affect caries fre quency include: the chemical composition and physical. consistency of the diet. the genetics of dental microstructure and salift, and oral hygiene. Caries rates rise nearly in proportion to the increase of cereal carbohydrates in the diet (Wells 197.5).

Untreated caries result in ultimate destruction of the entire crown and significant portions of the root. Exposure of the pulp cham ber leads to a high risk of infection with the almost inevi table sequelae of abscess and destruction of supporting tissues (Ortner and

Putschar 1981). This infection may be carried to other parts of the 45 body via hematogenous dissemination. Ortner and Putscbar illustrate a

possible correlation between a large deciduous abscess and osteomyelitis

of the long bonee in a six year old child from 16th century Virginia

(Ortner and Putschar 1981: 122-123).

Caries generally affect the permanent dentition, although the

deciduous dentition is by no means immune. Twelve percent of the

children at Pecos Pueblo had deciduous caries (Hooton 1930). In a study

of 528 Guatemalan chil.dren, aged six months to se~en years, the fre

quency of deciduous caries was twice that of United States Whites, with

boys more commonly afflicted. Linear enamel. hypoplasia (LEH) was a pre

disposing factor (Infante and Gillespie 1976, 1977). Circular caries

also appear to be related to LEH; severe hypoplastic lesions often be

come carious, leaving transverse bands of decay on labial and buccal

surfaces of the tooth (Cook 1979; Cook and Buikstra 1979). It should

be noted that "circular caries" is an anthropological, not an odonto

logical, term.

The teething process produces an acute inflammatory response in

the adjacent connective tissue, characterized by pain. a slight fever,

and a general malaise in the affected child (Bhaskar 1980). Undoubtedly,

infants at Grasshopper suffered from teething pain, though there is no

record of the extent of their ordeal.

General Responses to Stress

The second level of pathologies includes generalized bony and

dental responses to a metabolic or systemic stress. "Stress" as used

bere is "the extent to ",bich an individual experiences deprivation or 46 injury because, by his own biological and cultural criteria, his: access to important resources is too limited or too unreliable" (Cowgill 1975:

127). stress is a physiologic response, involving activation of the pituitary-adrenal cortical axis and the sympathetic-adrenal medul.lary axis with increased release of adrenal cortical and medullary hormones.

In simpler terms, a stress is a mental or physical pressure which strains an individual' B biological resources, leading to weakness or injury. Individual physiological changes resulting from stress maY' cause populational inereases in morbidity and mortality, coupled with decreases in productive and reproductive capacities (Goodman et 81.

1980).

Bony response to stress is less dramatic than the responses elicited from other organ systems (Huss-Ashmore et ale 1982), since the skeleton is frequently the last system to register an insult. The conservative nature of the skeletal system reinforces its role as a storehouse of minerals, to be tapped only as a last resort.

The source of the stress may be chronic (such as nutritional deficiency) or acute (a single disease episode). Each type of stress may leave a representative trademark or 'stress marker.' Chronic poor health may be characterized skeletally by gradual proliferation or dis integration of bone mass, resulting in porotic hyperostosis, cribra orbitalia, cortical bone loss, and growth retardation (Palkovich 1980).

Acute attacks may leave stop-and-start growth lines on bones and teeth ..

These are known as Harris lines in bones and linear enamel hypoplasia in teeth. Not all stress markers have equal utility for assessing morbidity. Fo!" example, the markers most often associated with malnutrition are linear enamel hypoplasia, porotic hyperostosis, and cortical bone loss (Huss-Ashmore et 81. 1982). The six stress markers discussed here were selected for use in this research because they have proven useful to other anthropologists attempting to evaluate skeletal respoDSe to stress at other ai tes.

Porotic HYperostosis. As seen on the akull t porotic hyperos tosis pr.esents as bony changes resulting from increased proliferation of hematopoietic tissue in the bone marrow', characterized radiographi cally by widening of the diploic spaces and displacement externally of the outer table, which may be thinned or completely atrophied (Moseley

1965a, 1965b). The diploic trabeculae may assume a position perpen dicular to the inner table in a radial configuration which, when advanced, has a hair-on-end appearance (Cockburn 1977). Externally, a sieve-like porosity is seen on the fiat bones of the calvarium, usually in a bilaterally symmetric distribution.

Various conditions have been blamed for porotic hyperostosis; there does not appear to be a single etiology. but all of those proposed affect blood and associated tissues. The hereditary hemolytic anemias, especially thal.assemia. have most often been implicated (Moseley 1965b;

Angel 1967; Steinbock 1976). In the New \lorld. however, these abnormal hemoglobin variants do not occur natively. Instead, it is iron deficiency anemia which appears responsible for porotic hyperostosis among American Indians, iron 'being the core of the hemoglobin molecule. steinbock (1976) lists iroD-deficiency as the most common cause of anemia worldwide at presentj others rank iron-deficiency anemia as a 48 maj:lr United States health problem (Heddy et al.. 1974; OVen and Lippman

1977). Despite the high incidence of thid particular anemia, accompany_ ing bony changes are less frequently seen in modern populations and do not reflect the severity of the anemia (Lanzkoweky 1968; Watson,

Grossman and Meyers 1973).. However, if an iron-deficiency anemia is accompanied by a protein deficiency, the resulting oateomal.acia predis poses to further osseous changes (Shahidi and Diamond 1960; Cockburn

1977; Mensforth et al. 1978).

Infants and very young children (7-18 months) are at highest risk for iron deficiency because of their rapid growth rate (Haddy et ala 1974). Neonatal. iron stores are depleted by six months of age, and even earlier in premature infants and twins. Milk is a poor dietary source of iron, and many Indian groups prolong breastfeeding or supple ment it with only a non-nutritious starchy gruel (Corbett 1968). In fants are prone to gastrointestinal disorders which severely decrease absorption of iron, as well as other nutrients. A sick child is more likely to eat poorly. Intestinal parasites, which induce internal bleeding, severely deplete iron stores and may be a significant causal factor in anemia (Darby et al. 1956; Faust and Russell 1957; McGregor et al. 1961; Carlson, Armelagos and Van Gerven 1974; Mensforth et al. 1978).

It is a simple matter to measure hemoglobin concentration and hematocrit in living children, but bone is the only residuum of the iron-storing system that is archaeologically retrievable. While there have been few studies of the actual iron content of the bone itself

(Zaino 1968), there has been much notice taken of the bony changes of 49

porotic hyperostosis within skeletal. populations fl-om Indian Xnoll,

Kentucky (Snow 1948). Libban, Ohio (Mensforth'"et ale 1978). Dickson

Mounds, Illinois (Lallo, Armelagos and Mensforth 1977), Pecos Pueblo,

New Mexico (Hooton 1930), Chichen Itza (Hooton 1962) and Altar de

Sacrifioios, Mexico (Saul 1973). Canyon de Chelly, Arizona, and the

Chaco area of New Mexico eEl-Najjar et al. 1976). among other New World

sites.

Von Endt and Ortner (1982) have performed an amino acid analysis

gn affected bone from a Pueblo Bonito child, comparing it with unaffected

bone from the same site and with modern unaffected bone. They found

the porotic bone to have 25' les8 of certain amino acids necessary for

bone protein synthesis. SUch altared protein bioS)'llthesis could be due

to insufficient protein intake or to lack of an enzyme cofactor, a vitamin or lIIineraJ.. These findings are not incODsistent with the hy

pothesis of iron-deficiency.

The cause of iron deficiency is thought to be a result of maize

agriculture; pre-agricul tural groups or those supplementing agricultura!

products with a variety of resources eas at Grasshopper) shOW' a much lower incidence of porotic hyperostosie eEl-Najjar et al.. 1976; Lall0

et ale 1977). Maize contains only a moderate amount of iron. Two

thouBElD:d grams of cornmeal contain 4,. of the USDA recommendation of

15 mg of iron, but its absorption is inhibited by the high phJtic acid

content. The ratio of phytate to iron i8 on the order of 32 mg per kg

(Kuhnlein 1981), but the exact cbelating capacity of' phy'tate is not known. Corn i8 low in other nutrients, al.tbough its value of niacin

and amino acids is greatly enhanced by alkali processing techniques (Katz, Hediger and Vallero,. 1974). The biological value of corn protein

is only ~; a growing child would have to ingest 450 g of corn or 800 g (nearly two pounds) of tortillas per day, were this his only source

of protein (Be'har 1968).

In the Southwest in general and at Grasshopper in particular,

the natural clays and rocks are themselves rich sources of iron, since

there is no acid leaching of soil nutrients. How mueh of this might be

incorporated into the corn plant is not known. Clay is sometimes eaten

by young children, and groundstone IIaIlOS and metates release more iron

into the corn meal than would cooking in an iron kettle (Kuhnlein and

Calloway 1979; Kuhnlein 1981). It is said (Wells 1975) that one Ameri-

can Indian consumes -three manoa and tva metates in his lifetime. Un

fortunately, the clay and groundstone themselves contain che1ators, so

there is probably little net gain in dietary iron, but a 1arge gain in

dental attrition.

Prevalence of porotic hyperostosis among the young inhabitants of Grasshopper is noted by means of visual. observation and radiography where warranted. The working definition of porotic hyperostosis for

this research inc1udes its appearance only on Squamosal portions of cranial bones. Intense hyperostosis along ectocranial. and endocranial.

surfaces of the metopic, sagittal, and lambdoidal. ~ -is also ob

served in this sample (see Fig. 5). This porosity in areas when and where rapid growth takes place may vell be an inseparable and non

pathological, though little noted, feature of the cranial Tault growth

process. Hrdli~ka stated that porotic hyperostosis as such specifically avoids the sutures (cited in Moseley 1965&, 1965b). Radiographic Figure 5. Comparison of porotic hypp.Tostosia (right) and non pathological sutural hyperostosis (left).

~ 52 studies of porotic hyperostosis in the living (Lanzkowsky 1968; WatsoD,

Grossman and Meyers 1973) make DO mention of sutural. hyperostosis. It has been rrry experience that areas of active bone grovth. such as alveolar and long bone metaphyseal regions, usually exhibit porosity.

For these reasons, sutural. hyperostosis, in this research, will. ~ be counted as porotic hyperostosis. In the absence of expl.ici t defini tiona of porotic hyperostosis in other skeletal analyses, it is not possible to determine which recorded high frequencies of porotic hyperostosis are high because they include sutural as well as squamosal hyperostosis.

Thus, comparabil.ity among skeletal aeries may not be a realistic under taking.

Lalla and associates (1977) were abl.e to correlate incidence of porotic hyperostosiS with that of infectious disease, as manifested by periosteal reaction in l.ong bones, among skeletal remains from three occupation phases at Dickson Mounds and one occupation at Eiden, Ohio.

In most cases, the infection appears to have preceded the hyperostosis.

Both cranial. hyperostosis and periosti tis were more common in Eiden and

Dickson agricultural. populations than in Dickson hunter-gatherers.

Among children younger than 15 years of age, 36.6% had porotic hyperos tosis, but since the authors make no age subdivisions in this group, it is not possible to analyze age-related changes in finer detail..

Mensforth and associates (1978) found a similar correlation of porotic hyperostosis and periostitis at the Libben Site. One-half of infants under 12 months of age (n = 90) shO'tl'ed periosteal innammation, while the peak occurrence of hyperostosis was at about three years.

This suggests that infectious disease may precipitate nutritional 53 deficienciea. Porotic hyperostosis vas seen in 44.~ of chUdren under ten years of age (n = 97) at that sit••

At Arr010 Hondo. New Mexico, Palkovich (1980) found an incidence of porotic hnMtrostoais of 2~ among infants under one ,.ear of age and of 1" among one to five-year olds. Among these children, hyperostosis W&8 associated with endocranial lesioDS, cribra orbital!.a, and general ized skeletal porosity, all of which have elsewhere been related to iron-deficiency anemia.

Crib!"a Orbita11a. Cribra orbitalia is a bilateral condition of sieve-like perforations of the bOJl1 orbit, caused by h)tpertrophy' and hyperplasia of the diploe in the orbital roof (Hengen 1m). Some investigators feel that cribra IIlaY' be the initial. manii"estatiOD of porotic hyperostosis; the orbital roof degenerates earlier than the cranium because its thin external table is more easily eroded by inten sified activity in the diploic zone (Steinbock 1976; Lallo et al. 1977).

Cribra is poorly-documented in l.iving populations, and may not be visible radiographically on a ful.ly-neshed skull.

Cribra is clearl.y visible in the orbits of some members of the

Grasshopper aample. Its prevalence and severity will be visually appraised, and distinguished from post-mortem damage due to soil ero sion or weathering.

Parasitic anemias appear to be the most pervasive cause of cribra, and young chUdren are most susceptible to worm infestations.

Parasitic diseases are more serious and preyal.ent cl.oser to the equator. so it is no surprise that Hengen (1971:66) found the incidence of cribra to increase with decreasing geographic latitude. Lacrlmal gland irri

tation, scalp infestation, xerophthalmia, and trachoma have also been

offered as possible etiologies (Frost 1965; steinbock 1976; Cook and

Buikstra 1.979), and al.l affect young chi1.dren.

Nathan and Haas (1966) have documented mild cribra in the crania

of young apes and monkeys from museum collections. Six of 16 apes

(gorillas, orangs, and chimps) were affected, as was one out of 18 mon keys (baboons, macaques), with females more so than males. No data were available on the lives of these primates, so no etiological ~.lg

gestiona are offered. Their observations do open up an interesting

avenue of experimentation.

Carlson, Armelagos and Van Gerven (1974) found a strong associ ation between deficient iron intake, parasitism, and cribra in their

Nubian series. Thirty-two percent of children under age ten had cribra; no postcranial (periosteal) involvement was observed.

Ctoulski (1977) examined 454 crania from four tribes of post contact Indians of the British Columbian coast. There was a high fre quency of cribra in children six to 18 years, with females affected three times more frequently than males. Dietary iron was high, with a diet of fish, marine and land mammals, but females may have had less

Recess to these resources. Cybulski feels that the incidence of cribra might be due to postcontact disruption and disease epidemics.

Growth Retardation. Shortened stature due to a slowed rate of growth is the body's way of adapting to decreased amounts of building materials. The effects of protein deprivation on the hormones which 55 control growth are not yet fully understood (Dreizen at al. 1958; Newman

1960; B~har 1968; Stini 1974; Owen and Lippman 1977). In dealing 'With prehistoric skeletal remains, however, there is no good way of deter mining how tall people would have been barring any interference, except by comparisons with growth standards from extant populations. Even then, secular trends may akew the results. Since the skeletal sample is cross.. sectiona1., it is impossible to differentiate between ehildren short from birth and those who experience growth retardation later on.

It is known that the primary effect of undernutri tiOD in late fetation is growth retardation (HUBs-Ashmore and others 1982).

Intra-group comparisons may be more profitable for prehistoric samples, and such a comparison is formulated for the Grasshopper analysis. This research examines individuals within each age group, to Bee if those children showing a greater number or severity of growth dis ruptions may have shorter long bones than the seemingly healthier children.

Cook (1979) analyzed gro';1th in Illinois Woodland juvenile skeletal. remains. When femur length versus dental age was plotted for juvenile skeletal remains from Middle and Late Woodland sites, it was observed that for the pre-agricu1tural Middle Woodland group, femora are longer at a given dental age; that is, growth was more rapid for the theoretical.1y better-nourished Middle Woodland children (Cook 1979).

Cortical Bone Loss_ Besides measuring linear growth, bone breadth can also be measured. and may be more revealing as to health status (Johnston 1968; Huss-Ashmore and others 1982). Bone is a dynamic system, constantly forming and remodeling in response to hor

monal, mechanical, and other factors (Frost 1972a, 1972b; Ruff and Hayes

1983). The osteob1asts of the periosteum on the surface of a long bone lay down new bone in the form of subperiosteal circumferential layers

parallel to the bone surface. To prevent an overly-thick mass of com

pact bone from forming as the bone grows in width, bone is resorbed at

the endosteal surface bordering the marrow cavity (Weinmann and Sicher

1947; Arnold and others 1966; Garn, Guzman and Wagner 1969; Crelin

1981). The balance between rates of deposition and resorption regulates an increase or decrease in skeletal mass.

One way to quantify this skeletal density is to measure the width of the bone cortex, the dense bone fabric which surrounds and protects the marrow cavity, from radiographs of the bones. Other methods include densitometry or microradiography using the bone itself.

The value of such studies to an analysis of prehistoric skeletal remains

is that bone density is intimately innuenced by diet and nutritional status, as well as by other metabolic -processes (Smithgall and others

1966; Martin and Armelagos 1979; Richman et 81. 1979; Huss-Ashmore and others 1982). Under conditions of poor nutrition, minimal new bone is

formed, but older bone is more rapidly removed, resulting in cortical

bone losa. This demineralization occurs as certain amino acids and

other nutrients stored in bone are mobilized and redirected to rescue more important organ systems (Huss-Ashmore et al.. 1982).

On radiographs (see Fig. 6), bone cortical thickness (C) is

quantified by Bubtracting the diameter of the medullar:,· cavity (M) from

the total subperiosteal diameter (T), as measured in a frontal plane 57

E-M -! -T-

Figure 6. Measurement of bone cortical thickness. -- As determined from radiographs, C = bone cortical thickness, Ii = diameter of medullary cavity, T = total subperiosteal diam~ter. 58

(Garn 1970). The equation reads! C = T-M. The percent cortical I area'

(elr x 100) is a measure of relative bone density. The ontogenetic pattern is of an initial neonatal gain, then a loss, a juvenile gain including an adolescent spurt, and then a slight gain until age 50 or

50, when C decreases, leading to osteoporosis Or bone demineralization

(Gar. 1970).

For the Grasshopper aeries, cortical thickness is measured from radiographs of all complete femora and humeri at midshaft, using a

Wolfe micrometer eyepiece calibrated in 0.1 mm. These bones were se lected because they ar~ nearly circular at midshaft and are relatively large in infant skeletons. The right femur and humerus were measured for each child; lacking them, the bone(s) from the left side were used, giving a sample size of 189 femora and 178 humeri, representing 228 children. Results are expressed as cortical diameter over total diameter (cIT), Nordin' s Index~.

Garn prefers to measure cortical thickness on the second meta carpal because, of the tubular bones, it is the most regular in cross section and the least subject to morphological variation. Measurement of the metacarpal cortical thickness of 91 Guatemalan boys with protein calorie malnutri tiOD revealed a slight but significant increase in total width of subperiosteal and medullary cavity diameters (T and M), but a marked reduction at the endosteal surface, in cortical area, and in percent cortical. area (Garn et ale 1969). This situation indicates continuing subperiosteal apposition with a dramatic excess of endosteal resorption (Garn 1970), resulting in a thinned cortex. 59 Only a few studies have examined cortical bone dynamics in archaeological samples, rut it has been found to be a useful measure of chronic stress. Cook (1979) used this technique as one means of quanti fying subsistence changes between Middle and Late Woodland groups living in the lower Illinois River valley in the first millenium A..D. Because immature metacarpals are small and can be easily overlooked during excavation, Cook Measured the cortical thickness on radiographs of immature femora. She found a significant difference in cortical thick ness at midshaft in children of weaning age between, the two samples, with the earlier hunter-gatherer group showing greater thickness than the later agricultural group. She interpreted these reaul ts to mean that weaning age nutri tiOD was poorer in the Late Woodland agricu1- turalists, thus contributing to increased mortality at that age.

Huss-Ashmore and associates (1982), in an analysis of 75 pre historic Nubian juveniles, age newborn to 14 years, found a striking decrease in femoral cortical thickness after age ten. The percent cortical area was maintained at a low level throughout chil.dhood, in contrast to Garn's (1970) observed pattern. Apparently, lung bone growth in these Nubians was supported at the expense of cortical thick ness. These conclusions were verified microscopically by Huss-Ashmore.

Active resorption spaces 'Were observed, 'With resorption greatly exceed ing formation. This suggested to the researchers that increased bone turnoyer may accompany the shift to maize horticulture, due to secondary hyperparathyroidism induced by a calcium-deficient maize diet.

Harris Lines. Radiopaque transverse lines of long bones may reaul t from any severe metabolic insul t during the time of bone growth 60

(Harris 1933). Long bone, growth in chil.dren is characterized by a lengthening of the diaphysis and an enlargement of the epiphyses. The site of most activity is the growth plate, that cartilagenou8 area be

tween the metaphysis and the epiphysis. Cartilage grows continually on the side of the growth plate facing the epiphysis, while on the side

facing the metaphysis, cartilage breaks down and is replaced by bone.

The growth plate persists during the entire postnatal growth period, after which time the epiphyses are fused to the diaphysis and linear

growth is complete (Weinmann and Sieher 1947; Crelin 1981).

A metabolic or traumatic insult during the growth period could cause a temporary slowing or cessation of the rate of invasion by the osteoblastic cells into the cartilage. This process is accompanied by a thickening of the temporary zone of calcification in the adjacent cartilage. When invasion of this zone by the osteoblasts is resumed or accelerated, a narrow, heavily mineralized area is left in the shaft of

the bone as new bone is formed beyond it (Sontag 1938; Park 1954, 1964).

This area appears on the reontgenogram as a white line, a1 though the

"line" is actually a three-dimensional phenomenon. The lines form especially at fast-growing ends of the femur, tibia. and radius, and may be incomplete, unilateral, or bilateral (Park 1954, 1964; Dreizen et al. 1.956, 1958; Dreizen. Spirakis and Stone 1964; Huss-Ashmore et a1..

1982). Lines may differ in thickness and density. Remodeling and dif

ferential line erasure can and does occur during the individual's

lifetime, as part of the normal sequence of bone cell turnover.

Harris lines are of great value to the paleopathologist, because

they can serve as age-specific markers of metabo1.ic insu1 ts in an 61

indiTidual' s health histOl7 and perhaps that of a population. The

average number of lines per boDe yields an index of morbid! t,.. useful

for comparative purposes (Vel.ls 1967i Clarke 1980). The timing of the

1.1nes can be satiated by measuring the distance from the line to the

ends of the bone aDd relating these distances to the average birth length of the bone (WeUs 1967; Allison, Mendoza and Pessia 1974).

Most lines are visible about one year after the precipitating event

(Marshall 1968).

Potential obstacles to the use of Harris lines as chronologie

stress markers include the foll.owing: the lines themselves give no

clue as to the nature of the stress encountered. Since lines form and disappear, the number of lines does not equal. the amount of illness

6uffered (Dreizen at ale 1956). Because lines do not form until growth has resumed, a chronic stress wil.l produce fewer (or no) l.ines than a repetitive, acute stress. Finally, no ODe has ever deve10ped a measure of how much stress is required to cause lVowth cessation and subsequent line formation. The association between disease and 1ine formation is high, but predictability is low (Gindhart 1969). Individual responses vary widely. As indicators of nutritional stress, the aignificance of

Harris 1inea is debatab1e, and requires other supporting evidence (Huss

Ashmore at sl. 1982).

On a more positive note, anal.ysia of Harris lines in living chi1dren lends credence to their use in paleopathological studies.

Lines are seen fetal.J.y and neonatally (Harris 1933), although V.Us

(1967) questions whether these are true Harria lines. Sontag (19,8) documented lines in the tarsal bones of one month old infants; theae 62 particular lines echoed the outline of the bones at birth. Sontag attributed this reaction to the shock of labor and birth itself: pres sure on the cranium, fluid loss, sudden respiratory and gastrointestinal functioning. massive endocrine readjustment.

Lines are common in well- and poorly-nourished children, with a peak value in preschoolers, according to Dreizen and associates (1964), who radiographically followed 679 children from birth to skeletal ma. turi ty. In another study (Gindhart 1969), 201 subjects from the Fels longi tudinal series were documented from one month of age to young adulthood. Of these, 199 developed transverse lines at the distal tibia. One child had a total of 19 such lines. The greatest frequency was in the 2 to 2.5 year age group, which coincides with a peak in occurrence of the common childhood diseases. Males appeared more sus ceptible to line formation, due to their longer period of growth, but the lines persisted longer in females.

In the Grasshopper analysis, the frequency of Harris lines is derived from radiographs of all complete femora, tibiae, and radii, from a total of 267 ehildren. Lines are counted for the right distal femur, distal and proximal tibia, and distal radius. If the bones frOID the right side 'Were not present, the left bone(s) was used. The standard used to identify a Harris line is that the line must extend at least one-third of the diameter of the bone (Gindhart 1969; Buikstra 1976).

A liberal standard such as this will take into account the effects of bone and line remodeling over time. To ensure that the lines observed are three-dimensional Harris 'lines' and not spicules or trabecular irregularities, lateral radiographs were taken of those long bones showing transverse lines in posterio-anterior view. In all cases, lines visible in the posterio-anterior view are also visible in the lateral view. The position and periodicity of the lines is noted, in order to

estimate whether the precipitating stress might have been cyclical or

intermi ttant. Bilaterality of the lines is examined in all cases where

both the right and left bones aI'e pi'esent.

Estimations of the ages of line occurrence for each individual

are made using the technique of Allison and associates (1974). The

bone of choice is the tibia; due to its more symmetric shape its growth

pattern is more regular than that of the femur. A template was devised

to illustrate annual growth increments (Fig. 7). The longest tibia with

fused epiphyses was measured in DUD and the presumed birth length was

subtracted. For this series, 64 ram was selected as the average birth

length, based on information in Table 6, p. 92. The remainder of the

bone length was divided into three-fifths for growth at the proximal

end and two-fifths for growth at the distal end. Each of these dis

tances was subdivided into 16 equal parts, representing the 16 years of

gt"owth from birth to epiphyseal fusion. Individual bone growth does,

of course, vary from this template, but the error factor should be con

stant for this series. Exact chronological ages are not assigned, but

it is possible to derive an estimate within an age group (NB-2 y, 2-'+ y,

4-8 y, 8-12 y, 12-18 y). The template is placed over a radiograph on a

viewing box and centered so that the bone to be appraised is located

between the corresponding proximal and distal growth increments. A

general age of occurrence can then be assigned to each transverse line

or portion thereof. 64

® 8-12y

Proximal 3/5 @ 4-8y

Average Birth Length

Distal 2/5

Figure 7. Model of template used to calculate the age of occurrence of Harris lines in the tibia. 65 McHenry (1968) counted the transverse lines in the distal. femora of prehistoric adult Indians from three temporal groups in the San

Joaquin valley of California. The average number of lines per bone was

8.01. Those individuals dyiDg at younger ages had more lines. The earlier group of Indians, subsisting by hunting. had more lines than the later group, who hunted, fished, e..'!d collected acorns.. Because these people stored acorns, it is suggested that there was leas of a seasonal fluctuation in food supply_

Two studies comparing hunter-gatherers and agriculturalists have produced results similar to each other. Cassidy (1972) compared

Indian Knoll to Hardin Village, a protohistoric Kentucky settlement, and found the latter agrionl tural group to show nearly three times as many lines of stress. Cook (1979) demonstrated more Harris lines in the same agricultural Late Woodland group which showed decreased cortical thick ness, as discussed earlier.

Allison and associates (1974) compared prehidoric Peruvian coastal inhabitants to those living in the mountains. Coastal residents had more lines, perhaps due to the stress of malaria. A modern coastal group showed the same relative frequency of lines, but that sample con sisted of 19 hospital patients.

Linear Enamel Hypoplasia. The developing tooth is nearly as plastic a structure as bone, and, consequently, also responds to en vironmental stresses encountered during growth (Perzigian 1977). As with Harris lines, hypoplastic lines on teeth provide a 'memory' of systemic growth disruption and stress in young children (Goodman et ale

1980). LEH provides a better record, because the dental lines are 66

neither remodeled nor resorbed, as are Harrie lines. It is not clear

which tooth is the most sensitive indicator of stress (Huss... Ashm.ore

et aJ.. 1982). This will depend on the timing of the stress and which

tooth is forming when the insult occurs.

Enamel is laid down in a regular pattern of incremental bands

beginning at the cusp tip and moving outwards to the cementa-enamel

junction in a two-part process (Cook 1981). The first stage is for

mation of the matrix, followed by minera1.ization and maturation of hard

tisaue. The layers of enamel and dentin in a developing tooth are ex

tremely sensitive to variations in metabolic processes during formation

and calcification. If the maturation phase is disrupted, areas of

chalky bypocalcification develop, but enamel contours are normal. If

the formative phase is disrupted, a hypoplastic enamel defect occurs

(Bhaskar 1980). There is a lack of enamel production at those incre

mental intervaJ.s of the teeth that were forming during the time of a

systemic disturbance, resulting in pits, lines. or bands of hypomineral

ization (Sarnat and Schour 1942).

There are also a variety of heredity enamel defects (Winter and

Brook 1975), but chronologie enamel aplasia appears to be environmen

tally induced. Hypoplastic enamel on a single tooth may be due to

localized trauma. or in the case of a permanent tooth, to local. sepsis

of an abscessed deciduous root (Diamond 1952).

The distance of a line from the cementa-enamel. junction of a

tooth can indicate the age at which the stress is likely to have

occurred (Goodman and others 1980). In their study of Guatemalan chil

dren. two to three years of age, Sweeney and his associates found that 67 31 of 73 children had LEH on one or more deciduous maxillary incisors.

The presence of a line seemed to correlate with reported infections during the first month of life -- diarrhea, thrush, conjunctivitis

(Sweeney et 81. 1969). Nearly one-fourth of the children with LEH in this sample had reen premature. In a second Guatemalan study of chil dren visiting health care facilities, it was found that children with advanced malnutrition had a 73.1% frequency of LES, and children with milder malnutrition had a 42.% frequency (Sweeney, Saffir and de Leon

1971).

Sar::mt and Schour (1942), examining a group of 1000 Chicago schoolchil.dren, related the origin of two-thirds of LEH incidence to a period spanning three weeks to 12 months, with the other one-third from

13-34 months. Permanent lateral incisors and premolars were most fre quently affected. Just six percent of their sample had LEH, and in over half of these cases, medical records provided no clue as to etio logic factors.

LEH is evaluated in the Grasshopper series by means of visual inspection of all teeth. The prevalence of stains, pits, and lines is noted, as are the number of affected teeth per individual. A' dento chronology' chart of the times of dental calcification (Mass1er et al.

1941:40), as reproduced in Figure 8, is used to estimate the age of the individual at the time of the presumed precipitating stress.

LEH has been observed in other prehistoric groups. A sample of 111 adults from three occupation phases at Dickson Mounds (A.D. 950-

1300) revealed an increasing frequency of LEX as reliance on maize agriculture increased: 4,5% LEH frequency in Late Woodland, 6D.' in 68

Figure 8. Tooth development chronology for assessment of formative times of linear enamel hypoplasia (from Hassler et al.. 1941: 40). 69

W'oodland-Miseissippian (Goodman et al. 1980). The pattern of linee on teeth in this series seems to indicate a repetitive annual stress cycle.

Teeth most commonly affected were lower caniDes and upper central incisors.

A metric and morphologic analysis of 58 deciduous dentitiona from several Ohio Valley sites (2000 B.C. to A.D. 1000) indicated that many individuals were stressed prenatally (Sciulli 1977). Linear enamel hypoplasia was observed on portions of teeth which calcify in utero.

Perhaps this is a renectioD of an upset in maternal mataboliem, but the upset was not severe enough to induce abortion (Shaw 1970).

After extensive examination of prehistoric juvenile skeletal remains from the l.ower Illinois valley, Cook and Buikstrf'l (1979) have noted a significant association between prenatal dental defects and bol'Q' evidence for anemia and infectious disease. Children with enamel defects appear to have had a relatiftly greater weaning-age mortality than unaffected children, as the former are more freq,uentl,. represented in the sample.

McHenry and Schulz (19'76) examined the association between LEI! and Harris lines. Since their mechaDisms of development partiall,. over lap, is there a regular co-occurrence? It would be of interest to know, as these are two independent body tissues, vi th distinct formation chronol.ogies and differential preservation. The authors examined the perlll8!lent canines and femora of 147 hunter-gatherer sub- and young adults. Co-ocourrence (the presence of both traits at the same age in the same individual) was seen, but to no significant extent. The pres ence of LEH without Harris lines could be expl.Bined by' remodeling of the lines (Park 1964; Gindhart 1969). lneidence of Harris lines 70 without LEI! can be explained 'b7 the importance of the recovery factor in Harris line formation. According to Park (1964), radiopaque transverse lines do not form until bone lP"owth resumes after the metabolic insult has ended. No such recovery factor has been found to exist for LEH formation.

Clarke (1980) conducted a similar study on skeletal remains from Mesa Verde and DicksoD Mounds. He found the age of incidence of trannerae lines to peak about one year earlier than .enamel ~asia. and related both to weaning stress. He suggests that the linea in bone may derive from an initial infection, while the enamel l.eaioDS derive from subsequent malnutrition and diarrhea. Another explanation might be that amelogenesis i8 a Blower process than osteogenesis (Bhaskar

1980), but no exact comparison rates were found in the literature.

Co-occurrence of Stress Markers: Most researchers studying stress markers in prehistoric skeletal series have observed that the presence of one stress marker is usuall,. correlated with the presence of one or more of the others. Harris lines have been BSsocia ted with cortical bone 10s8 (Cassidy 19'72; Cook 1979), with linear enamel hno pluia (Wells 1967; Cassidy 1972; McHenry and Schul.tz 1976; Clarke

1980). with retarded growth (Cook 1979). Retarded growth has simi1ar1y been associated with cortical bone loss (Cook 1979; Huss-Ashmore and others 1982) and LEH (Cook 1981). Linear enamel hypoplasia is alao seen in conjuDction with cribra orbital.ia (Cook and Buikstra 1979). Both cribra orbi talia and porotic hyperostosis have been associated with postcranial periostitis (Carlson and others 1974; Lallo and others 1977;

Mensforth and others 1978; Palkovich 1980). 71

Prenatal stress, as documented by LEH on deciduous teeth

(Sciulli 1977; Cook and Buikstra 1979), may reduce an individual's

ability to cope with subsequent nutritional and disease stress encoun

tered in infancy and early childhood, lea.ding to a diminished life

expect.wey (Wells 1967; Sweeney and others 1971). Repeated systemiC

stress at a young age has been shown to have a detrimental effect on

survival (Cook and Buikstra 1979; Cook 1981).

Implications of these findings for Grasshopper Bubadults are

investigated. The number, type, periodicity, and severity of growth

disruptions, as measured by the six stress markers, are appraised for

each child. Comparisons are then made wi thin and across age groups and

by sex, to see which stress markers are most frequently correlated with

which others, whether the presence of one predisposes to others, whether

a child can recover from the effects of prenatal stress or if his con

stitution appears to be permanently impaired. If possible, this a.nS.ly

sis will isolate the particular group of children appearing to be at highest risk; according to most studies cited herein, this high-risk

group should center on weanlings.

Statistical Evaluation

This research examines .the effect of nutritional status and

disease on the growth and development of subadul ts from Grasshopper

Pueblo. Comparisons are made within and among groups divided along the

lines of age, sex, temporal and spatial. provenience. Descriptive sta

tistics are used to present results (mean, standard deviation, range of

variation) • 72 Certainly this is a multivariate problem, but the design of this

study permits it to be treated as a series of bivariate problems. Ini

tially, prevalence of stress markers is considered along dimensions of

age and sex. Later, prevalence of stress markers is considered in

dimensions of time and space. Segmenting the analysis in this manner

will retain an adequate sample size for each group. Scoring stress

markers as present or absent facilitates the use of the Chi-square

statistic (Mather 1966; ROBcoe 1975) to test for the degree of rela

tionship betveen variables in a 2 x 2 contingency table.

When the data are continuous, as in an age distribution, the

Kolmogorov-Smirnov test of goodness of fit can be used instead of Chi

square. K-S is actually the more powerful nonparametric test and is

more reliable with smaller sample sizes (Siegel 1956).

Considering the nature of the skeletal sample, meaningful

differences are more likely to occur in patterns, rather than in fre

quencies, of stress markers (Cook and Buikstra 1979). CHAPTER 4

COMPARATIVE DATA. FROM RECENT AMERICAN INDIAN GROUPS

One specific question to be answered through this research is:

What factor(s) might have been responsible for the infant and child mortality at Grasshopper? Apparently fatal trauma, congenital malformations, and bone infections have been documented in other prehistoric populations 'Whitney 1886; Osborne and Miles 1965; Roney 1965; Kunitz and Euler 1972; Miles 1975). A pair of child's crutches was recovered from Mesa Verde (Osborne and Miles 1965). These artifacts aside, we are usually left with skeletons showing no bony reactions or on1y very general. ones open to many interpretations. Fortunately, physical anthropologists in the Southwest have access to an abundance of ethnographic and modern evidence of specific diseases affecting the native population, diseases which due to their etiology or viruJ.ence would not affect calcified tissues. Ma~ of these diseases were not precipitated by European contact and may have been significant in the lives of young children at Grasshopper Pueblo. Interpretation of morbidity and mortality among subadults in this series will draw on the data presented here.

Weaning stresS

Moriquand, a modern French pediatrician, has designated three factors \.hich operate with variable intensity in a child's life: "le 74 danger alimentaire, 1e danger infectieux, 1e danger congenital" (cited in Behar 1964). In developed countries, perinatal death is due mainly to congenital malformations and genetic disorders, since prompt medical. attention can often alleviate the other "dangerstl (Scrimshaw 1968;

Morison 1970; Milunsky 1982). In contrast, preindustrial. countries have a high death rate in children under five years of age and especially in children of weaning age due to nutritional and infectim16 diseases

(Moore, Silverberg and Read 1972; Puffer and Serrano 1973; Burke and others 1979). Since weaning is such a critical period in a child's life, it will be examined in greater detail. Major points to be covered include nutritional adequacy, exposure to pathogens, and the synergistic interaction between malnutrition and infection.

In underdeveloped countries, weaning usually occurs in the second year of life, 12-24 months. One-third to one-ha1f of the total infant mortality of a group may occur during this period (Welbourn 1955;

Wolstenholme and O'Connor 1964), as environmental and host factors are at their high and low points, respectively (Scrimshaw 1964; Gordon,

Wyon and Ascoli 1967). An infant less than 12 months of age is pro tected by adequate breast feeding and passively-acquired immunities

(Scrimshaw 1964; Gordon and others 1967). After the first year, there is often inadequate dietary suppl.ementation and increased exposure to new pathogens as, rel.eased from the confines of the cradleboard, the toddl.er begins to expl.ore his environment. In most vill.ages, sanitation and personal. hygiene are questionable; food and water may be contami nated (Scrimshaw 1964, 1968).. Nutritional adequacy is further threat ened by a scarcity of protein-rich foods of high biological value, 75 maternal ignorance of nutritional needs, and food prejudices or other faulty dietary habits (Aberle 1932; Galdston 1960; Stini 1971).

The archaeological record at Grasshopper and elsewhere reveals nothing about the diets of babies and SJDall. chUdren, but recent

Indians show a diversity of weanling diets, as seen in the following examples. According to Hrdli~ka (1908), the basic weanling diet in the

Southwest consisted of coffee, soup, tortillas, and fruit. These foods are deficient in protein just when a growing child needs it most. In

Zia Pueblo, for example, children are weaned at two years of age on black coffee and cereal gruel. Papago add broth and plant juices to the diet at six months, followed by coffee, mashed beans or potatoes, pieces of tortilla or orange sections. When a Yuman child begins to walk, his diet is supplemented by pre-chewed corn, mashed peaches, and juniper berries (Moore et 81. 1972). The Otomi of Mexico give babies pulque (Anderson et 81. 1946), not especia11y nutritious but high in vi tamin C -- and likely to reduce teething pain.

Protein-calorie malnutrition and kwashiorkor are serious prob lema in weaning-age children in many areas of the world (Aberle 1932;

McGregor and others 1961; Scrimsbaw, Taylor and Gordon 1968; Stini

1%9, 1974; Scrimshaw and Tejada 1970; Jelliffe 1975; Van Duzen et al.

1976; Jelliffe and Jelliffe 19'78). A deficient nutritional state is the most important cause of excessive mortality in developing areas

(Burnet and White 1972; Puffer and Serrano 1973). But, since nutri tional status of a group is best evaluated by correlating tbe results of dietary, clinical, and biochemical studies with anthropometrics 76

(Owen and Lippman 1977) t we are handicapped in studying prehistoric populations ..

Malnutri tiOD lowers resistance of the host to infection, just as infectious disease exacerbates existing malnutrition. Infectious stress lowers the ability to eat and absorb nutrients and hastens ni tro gen excretion. Nutritionally-induced determinants of this synergism include; reduced capacity of host to form specific antibodies; de creased phagocytic activity of micro- and macrophages; interference with production of nonspecific protective substances; reduced nonspecific resistance to bacterial toxins; al teratioDs in tissue integrity; de creased inflammatory response and alterations in wound healing and collagen formation; effects originating in alterations of intestinal flora; variations in endocrine activity (Scrimshaw et al. 1968; Stini

1971). A malnourished child does. not even have an intact skin as a defense mechanism (Keusch 1975).

By thus weakening resistance, malnutrition appears to broaden the spectrum of microorganisms which can cause disease at a time when the child is encountering large numbers and varieties of microorganisms to which he has no acquired immunity. In rural Guatemala, for example, a child must develop in the first five years of life a resistance to several strains of ~ • .2.2!i,more than 20 Shigella, several~, measles, chickenpox, Whooping cough, and dozens of other respiratory infections. Lack of success is apparent in a death rate in children under five of 46.6 per 1000, as compared with 19.3 per 1000 in Mexico and 1.1 per 1000 in the United states (Wolstenholme and O'Connor 1964). 77 There also seems to be a psychological stress associated with weaning (Lallo and ROBe 1979). As the mother's constant presence is no longer required for breaetfeeding, the young chil.d must deal with what

he considers to be maternal neglect (Aberle 1932) II A new sibling may now be the center of attention.. Physiological effects of such separa tion anxiety are extremely dif:ficul t to evaJ.uate, especially in skeletal. remains, but it is known that emotional stress does increase suscepti bility to disease (Goodman and others 1980; Wood 1983).

Disease Stress

The most common communicable diseases, respiratory infections and Bcute diarrheal diseases, are the least understood. In many areas, respiratory diseases are the chief cause of illness, especially in the youngest infants (Clements 1931~ Kraus 1954). There are over 100 dif ferent serotypes of rhinoviruses capable of infecting man (Burnet and

White 1972j Beeson and McDermott 1975). The situation is not helped by the fact that parents are often unaware their child is ill, or else they accept illness as a natural phase of development (McGregor and others

1961). In many Indian groups, children are seldom bathed, and minimal attention is paid to cleanliness of the mouth, ears, and nose (Aberle

1932).

The World Health Organization ranks acute diarrheal diseases among the top five killers, as a regular and prominent feature of infant and child deaths, due to their high virulence and communicability

(Abramaon 1950j Goodwin et alo 1960; B~har 1964; Scrimshaw et 81. 1968;

Puffer and Serrano 1973; Woodward et al. 1971.;). Scrimshaw and associates 78 (1962) cite a village epidemic in which no child between the ages of 6 and 18 months escaped sickness.

Some researchers feel that gastroenteritis of infancy may be but a temporary clinical upset which accompanies the acquisi tiOD of new strains of coliform organisms in the we8D1ing gut (Gordon et ale 1967;

Otten 1%7; Ironside 1973). In any case, the ultimate cause of death is likely to be electrolyte imbe:.l.ance stemming from severe dehydration and substantial protein loss (Stini 1971).

Along with the various enteric and respiratory diseases that are so abundant among Indian groups today, there is an impressive list of other diseases contributing to the morbidity profile. One of the diseases most frequently recorded among Southwestern Indians is trachoma

(Hrdli~ka 1908; Kraus 1954; Hadley;' 1955; Darby et al. 1956; Sievers

1966; Chase et 81. 1971; Rabin, Anthony and Harrison 1972; Lee et al.

1974). Trachoma is a chronic infectious disease of the eye; it thrives in hot dry areas with a shortage of available water and poor hygiene

(Beeson and McDermott 1975). Although common on Southwest reservations~ it is not severe. Trachoma has, however, been cited as a potential cause of cribra orbitalia (Frost 1965; Cook and Buikstra 1979; steinbock

1976) • It would seem that whenever toddlers are not putting foreign objects in their mouths, they are rubbing their eyes with soiled hands.

otitis media (middle ear infection) is a frequent bacterial com plication of upper respiratory infections (W. M. Moore et Bl. 1972; Lee et al. 1.974; u.s. Government Printing Office 1976). It is characterized by swelling of mucous membranes in the naso-pharynx which obstructs 79 drainage of the eustacbiaD tubes. Bony evidence for otitis media is DOt definitive (Titche et ill. 1981).

Other diseasea often reported at Southwestern Indian haspitala include: coccidioidomycosis (Sievers 1964; Woodbury 1965). dental in

-fections (Kraus 1954; Darby et al. 1956; Moore at ale 1972; Wells 1975;

Chase at al. 1971), clinical protein-calorie malnutrition and vitamin deficiencies (French 1967; Van Duzan at al. 1969; Wetls 1975), skin infections (Kraus 1954; Darby at al. 19'76; Chase at al. 1971). smallpox, measles, chickenpox, whooping cough (Hrdli~ka 1908; Salomon, Mata and

Gordon 1968), and millaria (Hrd1il!ka 1908. Giglic1i 1968). Tab1e 4, adapted from Puffer and Serrano (197': 422), presents a recent BIlrvey of causes of death for young children from Monterrey, Mexico.

Ecological stress

Clinical disease depends on the interaction of an agent, a host, and an environment. Public health officials are concerned with agents; skel.etal biologists consider the compromised host. Attention must alBO be given to the environment and ecol.ogical factors. Mortality during infancy i8 notoriously susceptible to these environmental influences

(Burnet and White 1972).

Evaluation of the environment includes Beveral variables: loca tion and type of Wtltel' source, excreta disposal, fly densities, esthetics of house and surroundings, structural quality of house, availability and purity' of water for wasbing and cooking, and personal. hygiene (stewsrt et al. 1955; Arme1agos and Dewey 1970; Puffer and

Serrano 1973). Where some or all. of these variables are unfavorable, 80

Table 4. Underlying causes of death in children under 5 years, in Monterrey, Mexieo, 1968-1970. -- Adapted from Puffer and Serrano (1973: 422) •

Total Infants Children Under Under 28 d.- --r---T-li Cause 5 yr. Total. 28 d. 11 mo. Yr. Yr.

All causes 3953 3220 1377 1842 421 312 Infective and Parasitic Disease 1790 1364 226 1138 253 173 Amebiasis 156 110 8 102 22 24 Diarrheal disease 1063 950 130 820 75 38 Other ihtestinal disease 56 50 14 36 3 3 Tuberculosis 62 17 0 17 21 24 Diphtheria 3 a a 0 a 3 Whooping cough 26 14 0 14 8 4 Tetanus 14 14 14 a a a Septicemia 68 65 55 10 2 1 Measles 297 120 0 120 113 64 Congeni tal syphilis 2 2 1 1 a a Moniliasis 4 4 4 0 a a Helminthiases 8 a 0 a 4 4 Other 31 18 0 18 5 8 Neoplasms 17 1 0 1 5 11 Nutri tional Deficiency 91 44 1 43 28 19 Protein malnutrition 49 10 a 10 25 14 Nutri tional marasmus 23 18 a 18 2 3 Other 19 16 1 15 1 2 Endocrine &: Metabolic Disease 3 2 a 2 a 1 Deficiency anemias a a a a a a Other blood diseases 2 a 0 a 1 1 eNS inflammation 59 48 5 43 8 3 Other eNS and sensory disease 3B 26 2 24 5 7 Disease of Circulatory system 4 3 a 3 a 1 Pneumonia, Influenza 481 415 133 282 46 20 Other respiratory disease 161 loB 6 102 34 19 Disease of digestive system 14 12 3 9 a 2 Diseas~ of g-u system 19 11 a 11 1 7 Disease of akin 19 15 7 8 4 a Disease of musculoskeletal. system a a 0 0 0 0 Congeni tal. anomalies 253 227 121 106 13 13 Nervous System 91 80 53 27 5 6 Circulatory system 82 74 25 49 5 3 Digestive system 47 42 27 15 3 2 Other 33 31 16 15 a 2 Certain perinatal. causes B12 812 804 8 a a Sudden death 26 25 2 23 1 Other 95 83 61 22 5 External causes 69 24 6 18 17 28 81 disease vectors thrive. A case in point is the area around the Little

Gila River, Arizona, whose vater is ueed for irrigation, SWimming, house hold needs, and drinking; " ••• home privy ••• serves only to con centrate the putrid contents of thi~ pit in a convenient breeding spot for fiies and maggots which, during adulthood, contributed mightily to the extremely high infant mortality rate and the 'warm weather diarrheas'" (Git1.itz 1950:44). After indoor plumbing was installed in the Hopi village of Moenkopi, the number of hospital visits for diarrhea was cut in half (Rubenstein et ale 1969).

The rise of agriCUlture has been blamed for deterioration of the environment on a small scale (Braidwood and Reed 1957; Polunin

1967; Alland 196B; Brothwell 1969; Yudkin 1969; Armelagos and Dewey

1970; Cockburn 1971). A hunting-gathering way of life is characterized by smal.l group size, little intergroup contact, minimal permanent en vironmental disturbance, mobility, and a diverse diet (Dunn 1968).

Agriculture has led to increased population, frequent contact, and aggregation. For example, incidence of acute diarrheas among the Zuni are highest in August which coincides with the Gallup Indian Ceremonial, when large numbers of people come together (Lasersohn 1965). Pueblo

Indian families living as they do in one or two rooms in a small, con gested community, resemble in some respects both urban and rural popu lations. During the night they are as crowded as are people in the tenements, but during the day most of their time is spent outdoors

(Aberle 1932).

Decreased mobility of the groups as a whole, brought about by the need to tend crops, and basic agricultural practices are the factors 82 contributing most to disease frequencies. Density-dependent bacilli, streptococci, and parasites are able to establish themselves. Endo parasites include tapeworms and nematodes; ectoparasites include ticks, mites, fleas, and lice; free-living p3.t'asites include fiies, mosquitos, and gnats (Faust and RUBsell 1957; 'tIoodbury 1965). Parasi tea tend to accommodate to populations in which they have existed for a long time.

Increased human resistance implies decreased parasite noxiousness

(Alland 1968), although sub-clinical infestation may still be influen tial in the overall disease picture. Hookworm ini'est&tion has been

01 ted 8S a significar..t causal factor in many anemias (Faust and Russell

1957; McGregor et al. 1961; Ho!ngen 1971; Wood 1983).

Animals, both wanted and unwanted, are added to the ecological picture, contributing their diseases, parasites, and waste products

(U.S. Department of Health, Education and Welfare 1<)68; Kunitz 1970;

Kunitz and Euler 1972). At Grasshopper Pueblo, there is osteological evidence of domesticated dogs and turkeys in the pueblo (Olsen 1980).

Stored grain is subject to infestation and contamination by rodents and microorganisms. In some cases, however t the microorganisms may prove to be helpful, as with the tetracycline-producing Strepto mycetes in Neolithic Nubia (Bassett et ale 1980). The practice of draining swamps, use of feces fertilizer, and irrigation provide new breeding areas for disease agents. The choice of crops is also a sig nificant factor, in terms of protein versus carbohydrate content, pres ence and availability of other nutrients, and perhaps even pollen levels. The high frequency of allergies to wheat and milk is often 8} cited as evidence that humankind is not even yet fully adapted to an agricultural. lifestyl.e (Yudkin 1969).

The length of time settlements are occupied can influence health by providing an environment conducive to the transmission of infectious diseases through a fecal-oral route (Cockburn 1971). A pueblo can be victimized by its own IIsanitary indiscretions" (Kunitz and Euler 1972:

20) t as occupation span lengthens.

Climatic factors may be important; hot summers and cold winters in a pueblo at high a1 titude do not make pleasant living condi tiona.

When the ground is frozen, waste material and dead bodies are not easily disposed of. Increased use of fires for warmth yields smoke and par ticulate matter which may contribute to increased upper respiratory infections at this time. Finally, "not a few children die each winter from the results of exposure and other privations, and in summer from the eating of unripe fruit or other injurious food" (Hrdli'6ka 1908:180). CHAPTER 5

RESULTS AND DISCUSSION

Resul ts of the biological. analysis of 390 subadul ts from Grass hopper ar~ presented here. After construction of the biological profile, the prevalence of stress markers is discussed along with their signifi cance within this skeletal series. Age and sex differences are evaluated. Provenience information is given in instances where Buch information may suggest familial relationships. Unless otherwise indi c<.::.ted, the sample size is 390.

Mortality

The mortality curve for the Grasshopper skeletal series is shown in Figure 9. The general shape of this curve corresponds to those seen for many undeveloped countries (Weiss 1973). This pattern is ODe of very high infant mortality, high but declining mortal.ity from ages one to five, and a steadily decreasing rate until the ages of 10 to 15, the time of lowest mortality. Trying to come of age at this pueblo appar ently was not easy, and the rigors took their toll among young children.

The mortality sample of 390 subadults includes 100 fetuses and neonates

(25.6% of the sample), 162 infants, postnatal to three years (41.%) I

105 children, three to ten years (26.cm). and 23 adolescents, ten to

18 years (5.9%). Clearly, infants are at highest risk.

84 85

\ \ \ \

'" 45

40 :;~ is ~ 35

F N I 2 3 4 5 6 8 10 12 14 16 IS 20 25 30 35 40 45 50-1- '-FtT.L 1I·1+f~.I.T"L AGE AT DEATH IN YEARS

Figure 9. Mortality curve for Grasshopper Pueblo .. 86

Fetation

The inferred high fetal and neonatal death rate is not surpris ing given the primitive, unsanitary living conditions (and, presumably, birthing conditions) and the lack of maternal pre- and perinatal medical care. Premature and other low birth weight infants, if not stillborn, rarely survive their first hazardous day under such conditions (Puffer and Serrano 1973). Fetal immaturity is apparent at Grasshopper; six of

40 fetuses appear to be less than five fetal months of age, in terms of my assessment of bone development. Premature births, spontaneous abor tions, and neonatal deaths have elsewhere been attributed to nutrition al stress in the mother (Ebbs and associates 1942j Herrenkohl 1979).

One possible set of twins has been identifieil, in Burial 385A and 385B. Both individuals are neonates, found in the same pit, and the lengths of their long bones are nearly identical. Another possible set of twins may be in Burial l.21A and l2lB t the remains of two young fetuses. Two complete sets of long bones were recovered, with frag ments of two sets of cranial bones. Two fetuses (Burials 9313 and 377B) had each been buried with a woman of reproductive age, but it was not possible to tell from field notes exactly how the skeletal remains were associated (for example, whether the women might have died in childbirth) •

Infancy Surviving birth, the first serious disease threat comes to

Grasshopper infants in their first two years, the time of weaning. The second yeaJ' of life can be the most hazardous, especially if the nutri tional state is suboptimal, as it is in most weanling diets (Puffer and 87

Serrano 1973). A high proportion of Grasshopper weanlings succumbed, 8S documented by the peak mortality experience during this period.

It has been suggested that those children ~ho survive this ordeal are somehow toughened to enable them to fight disease better throughout their lives. Based on an 18th century Connecticut mortality sample, Meindl (1982) and Meindl and Swedlund (1977) propose that wide_ spread childhood infectiouB disease does strengthen survivors in a developmental manner, and perhaps also eliminates les6 fit individuals.

The process is one of weeding out genetically inadequate infants by otherwise trivial infections (Burnet and White 1972). The hypothesis certainly applies at Grasshopper; once the critical threshcld of wean ing was successfully crossed, a long life vas possible. A similar situation is seen at Arroyo Hondo, New Mexico (Palkovich 1980).

Childhood

Toddlers are confined to the limited area of site periphery and cannot escape the contamination of occupational refuse; thus the poten tial for disease contraction may be high. Older children are more mobile and can venture beyond pueblo boundaries. Their infectious disease load correspondingly lessens, as does their death rate (Puffer and Serrano 1973; Pratt et al. 1978; Burke et 81. 1979). For modern middle class children, on the other hand, the first serious disease threat may come at this time, when they begin school and are exposed to other children and their germs (Burnet and White 1972).

Accidental deaths might play an increasingly important part in childhood mortality, because the child is exploring the natural environ ment outside pueblo walls. Drowning, exposure t and the 88

like would not leave marks on the skeleton although animal attacks

might.

Adolescence It has been suggested that the 10-12 year age group really is

the prime of life (Buxnet and White 1972). This is the low point on the

Grasshopper mortality curve. The fact that a high number of these

children show healing of the osseous lesions which plagued their younger

relations demonstrates the potential survivability of the precipitating

infectious attacks.

Sex Ratio

Figure 10 presents the mortality curve separated, after eight

years of age, into males and females. Eight years was selected because

only after this age could all individuals be sexed. Sex assignments

could be made on less than ~ of the 6ubadults below eight years, and

of these, females outnumber males nearly 1.5 to 1. After age eight (8

to 18 years) there are 17 males and 16 females. The total subadult sex ratio stands at 65 males to 94 females (.69), which is not significant at the .01 level (see Table 5). If the 231 indeterminates are parti

tioned in a similar proportion, the sex ratio is 159:231, which is aig nifican-t at the .01 level (Table 5). The degree of misclassification

is, of course, unknown.

Although it might be tempting to suggest female infanticide to

account for this hypothesized subadul t sex ratio (Robbins 1977), there

is no supporting evidence. The sex of the youngest infants could not be determined. No traumatic injuries were observed in the youngest in..

fants, nor do the field notes indicate irregularities in burial 89

"- o " ~ !!z .."

,--F • I I'_TAL AGE AT DEATH IN YEARS

Figure 10. Mortality curve separated by sex. 90

Table 5. Chi-square tests of observed versus expected sex distributions of adults and subadul ts.

Males Females Total

~ Observed 65 94 159 Expected 79.5 79.5 159 Difference -14.5 14.5 X2 = 5.28, approximate level of significance = 0.05. df = 1

Subadults. including partitioned indeterminates Observed 159 2,1 390 Expected 195 195 390 Difference - 36 36 X2 = 13.29, approximate level of significance = 0.01.

~ Observed 135 218 Expected 109 109 218 Difference - 26 26 X2 = 12.40, approximate level of significance = 0.01. 91 treatment. If more females of all ages are dead and buried at the

pueblo, it can be assumed that more females also lived at the pueblo.

This assumption is logical. in light of the theorized social structure of

the pueblo: male exogamy with uxorilocal residence (Birkby 1973. 1982) t

the Bocial pattern often seen at Southwestern pueblos (Dozier 1965;

Longacre 1976). At Grasshopper; the age at which a boy is Bent to his

future wife's place of residence is not known.

Adulthood The apparent overabundance of females in bur:i.als continues into

adulthood, at a similar ratio of 83: 135 (.61) t significant at the .01

level (Table 5). In most archaeological series, it is males who are

overenumerated due to biases in methods of sexing (Weiss 1973). At

Grasshopper, residence patterns may be an important factor. There is no

evidence at this site that the cemeteries sampled thus far are sex

specific. The predominance of females remains a problem.

A high adult female mortality is usually attributed to compli

cations of pregnancy and stresses of childbearing, and the shape of

the mortality curve attests to this. With nearly 18,l: of the skeletal

sample being fetal or neonatal, this stressful. situation is highlighted

for both mother and baby. A fuller discussion of adult mortality

patterns must await a more comprehensive analysis of the adult skeletal remains.

Growth Variabili ty

Data on long bone diaphyseal lengths are presented in Table 6.

Since sample sizes are greatest for the femur (299) and humerus (329) t 92

Table 6. Correlations between dental age estimates and the maximum diaphyseal l.ength of long bones.

Estimated Size of Mean Standard Range of Age (yrs) Sample Length (rom) Deviation Variation (mm)

Femur -,.eta! 56 57.43 10.48 26-69 Neonatal 69 73.14 1.74 70-76 PN-0.5 27 84.00 7.48 73-99 0.5-1.0 19 107.26 9.13 96-125 1.0-1.5 23 118.96 10.68 91-137 1.5-2.0. 13 131.85 9.94 120-150 2-3 14 146.43 11.86 125-160 3-4 18 169.78 21.0 130-201 4-5 8 190.50 21.77 170-225 5-6 14 211.64 15.86 184-240 6-7 20 221.75 19.01 184_248 7-8 9 243.67 30.75 205-285 8-10 9 273.33 4.44 266-277 10-12 0 Tibia ----retal 51 50.57 10.02 25-62 Neonatal 59 64.00 2.03 59-69 PN-0.5 25 73.72 5.60 65-83 0.5-1.0 24 88.96 7.08 81-108 1.0-1.5 23 118.96 10.68 92-120 1.5-2.0 9 109.22 5.61 103-112 2-3 8 126.22 6.43 120-138 3-4 18 169.78 21.0 108-163 4-5 8 190.5 21.77 152-189 5-6 14 211.64 15.86 152-185 6-7 14 182.43 16.02 153-208 7-8 7 204.86 25.75 1'/6-233 8-10 9 225.33 10.49 203-236 10-12 2 270.00 25.45 252-288 Fibula FeW. 31 48.84 27-58 Neonatal 29 61.62 ~:~ 57-67 PN-O.5 19 64.53 21.03 6"-80 0.5-1.0 14 87.71 8.10 76-102 1.0-1.5 12 100.00 8.29 90-116 1.5-2.0 5 102.8 8.47 95-112 2-3 6 125.00 9.51 112-136 3-4 9 140.67 19.08 106-162 4-5 3 162.66 13.43 153-178 5-6 4 164.75 2.99 161-168 6-7 6 169.00 33.61 106-205 7-8 3 220.33 21.94 195-233 8-10 4 225.25 4.11 220-230 10-12 93 Table 6--continued

Estimated Size of Mean Standard Range of Age (yr.) 'Sample Length (mm) Deviation Variation (mm)

Humerus ---retaI 55 49.91 8.54 28-63 Neonatal 87 62.32 6.53 59-65 PN-0.5 26 72.58 5.06 66-80 0.5-1.0 2; 83.44 16.84 93-101 1.0-1.5 22 94.18 8.57 87-109 1.5-2.0 17 106.88 6.19 101-121 2-3 17 108.12 24.91 103-127 3-4 20 132.15 9.10 122-150 4-5 13 142.00 10.72 133-165 5-6 13 153-54 8.53 135-171 6-7 14 161.5 14.70 138-181 7-8 9 186.11 13.29 170-203 8-10 9 196.44 6.54 183-206 10-12 2 237.00 1.41 2)6-238 Ulna --""Fetal 42 47.95 9.29 26-61 Neonatal 56 59.89 1.77 57-66 PN-0.5 20 66.75 5.22 54-74 0.5-1.0 17 76.82 6.38 69-91 1.0-1.5 21 85.14 5.37 78-99 1.5-2.0 10 89.8 5.35 83-96 2-3 8 102.87 5.25 96-113 3-4 13 10B.00 5.86 97-116 4-5 7 124.28 11.66 111-142 5-6 7 129.00 9.36 114-145 6-7 6 144.00 9.27 132-154 7-8 6 153.00 13.59 143-171 8-10 3 179.67 5.77 163-173 10-12 2 183.00 183 Radius --rew 47 42.68 7.56 24-51 Neonatal 61 52.31 2.08 49-58 PN-0.5 14 59.28 5.28 49-67 0.5-1.0 15 6B.73 4.61 64-78 1.0-1.5 21 76.57 5.11 70-91 1.5-2.0 10 81.9 4.56 76-86 2-3 8 85.87 10.72 69-97 3-4 10 100.9 5.82 94-109 4-5 4 119.5 13.40 106-132 5-6 6 118.83 3.87 113-122 6-7 9 129.11 11.06 110-11.0 7-8 6 143.5 11.52 133-155 8-10 4 146.25 7.09 140-155 10-12 167.00 167 94 this discussion will concentrate on these two bonea. Little bilateral aSy1!llIIetry is observed until after six months of age t when infants would begin to express increased mechanical function. For most children past

this age, the bones of tha right side are 1-3 rom longer than the bones of the left side.

The greatest mean increase in growth per year is observed during the first year. The femur grows from a neonatal. 73.14 mm to

107.26 mm, and has nearly doubled its birth length by the end of the second year. An increase of this magnitude is not seen again until 8 to 10 years, the beginning of an adolescent growth spurt (Marshall

1977).. Growth of the humerus is slower. Birth size is not doubled until the fourth year, but the humerus does not attain the ultimate length of a femur. The adolescent spurt is clearly visible in the 10-12 year group.

Of the long bones available for measurement, two sets were re markable. The humeri from Burial 23 (0 to 6 months) show extremely well-developed muscle markings. The 18 to 24 month old child from

Burial 570 is generally robust. His femur, when compared to that of the 'average' child from his age group, is nearly four mm wider in mid shaft cross-section. There appears to be no obvious familiar relation.. ship, since one child is from Room Block 1 and the other is from an

Outlier.

Variability in the growth process is evident from an examination of standard deviations and ranges. For femoral growth, the most dis persed measures are those of 7-8 year olds. For the humerus, the greatest variance is in the 2-3 year age group. There is a considerable 95 overlap of ranges throughout the table, which highlights the dit:ic"'epancy

between dental development and bone growth. In two instances, mean bone length decreases with increasing age. The mean tibial length of chil

dren 5 to 6 years of age is longer than the tibia of children 6 to 7 years of age. The radius of 4-5 year old children is longer than that of 5-6 year aIds. The pooling of the sexes in this table may account

for much of the variation.

'Taller than average' and 'shorter than average' children are

identified as those children with long bone diaphyseal. lengths greater

than one standard deviation above the mean and less than one standard

deviation below the mean, respectively, for their age group. Using

femoral standards, a total of 16 children, postnatal to ten years of age, demonstrate accelerated growth, while 17 children within the Game age range demonstrate retarded growth (see Table 7). Just 12% of these

subadults are beyond one Gtandard deviation of the mean femoral length;

the skeletal sample is remarkably homogeneous in this respect.

Of the 16 children taller than average, 11 show stress markers

or some other pathology. Apparently, an excellent state of health is not the contributing factor to accelerated growth. The most economical

explanation would be that what these 16 children have in common is re

tarded dentition.. One of these children is the infant from Burial 23,

descr:i.bed above as being particularly muscular.. Sex could be determined

for 10 out of the 16. There are seven females and three males. Since

female bone age tends to exceed dental age, girls should be taller (that

is, have greater long bone diaphyseal lengths) for their dental ages.

The neatness of this supposition is sullied by the observation that of 96

Table 7. Individuals with femoral diaphyseal lengths one standard deviation above or below the mean for their age groups.

No. of No. of Individuals Individuals Sample Size Age Group with Longer with Shorter for Eaeh (yr.) Bones (sex) Bones (sex) Age Group

PN-l.O 5" 2F,OM,31 6" IF,CM,51 56 1.0-2.0 4" OF,lM,31 4" 2F,OM,21 76 2.0-3.0 2" 2F,OM,OI 2' OF,OM,21 30 3.0-4.0 I' IF,OM,OI 2' IF ,OM ,1I 29 4.0-5.0 IF,CM,OI 0 15 5.0-6.0 2' IF,lM,OI I' IF,OM,OI 25 6.0-7.0 I' OF,lM,OI I' IF,OM,OI 15 7.0-8.0 0 0 11 8.0-10.0 0 IF,OM,OI 10 16 17 267

Each * indicates an individual with other stress markers. Sex: F = female, M = male, I = indeterminate. 97 those children showing retarded growth, seven are female and ten are of indeterminate sex.

When femoral diaphyseal. length is compared between the sexes, as in Table 8, a number of observations can be made. Boys have l.onger femora in 7 out of 15 age groups, girls have l.onger femora in 5 groups, and no comparison can be made in 3 groups. Girls start out smaller, then catch up with and temporarily overtake boys. Boys are ultimately taller. There are not enough subjects to evaluate adolescent growth spurts.

A useful. project for future research might be to re-examine

Table 6 in an inter- and intra-limb proportional study, as illustrated by BU8chang (1982). He examined qualitative shape changes in a sample of 85 upper middle cl.ass children, two months to 11 years of age. Such a detail.ed analysis of growth is beyond the scope of this research, but is currently underway by Sumner (n.d.).

In a comparison of long bone diaphyseal lengths fioom Tabl.e 6 with Weaver's (1977) resul.ts, dispJ.ayed in Table 9. it is seen that for ten sets of measurements (fetal. to six years) for the femur and for the humerus, Weaver's lengths are consistently greater in all but two cases.

The difference ranged from 0.16 to 13.6 mm. The lower end of the scale may be attributabl.e to interobserver error.. For both bones, JIt9 sample size is more than twice his, which undoubtedly has introduced added variance. But OD the whole, the two sets of tables do not diverge in a major way.

The femur is used in Figure 11 to illustrate some interrelated aspects of the data presented in three tabl.es of dental age and 98

Table 8. Femoral diaphyseal length by sex.

Female MaJ.e Age Group Sample Mean Range Sample Mean Range

6-12 m 110.5 96-125 102.0 12-18 m 5 114.4 108-121 117.0 110-130 18-24 m 120.0 139.5 2-3 Y 150.0 136-165 0 3-4 y 8 161.0 130-201 3 181.5 171-194 4-5y 3 201.25 176-225 1 188.0 5-6y 216.4 184-240 4 210.5 200-234 6-7 y 219.9 184-241 3 228.7 205-248 7-8 y 221.8 205-251 266.0 249-285 8-10 y 274.0 266-279 272.0 267-277 10-12 y 293.0 292-294 12-14 y 348.0 329,0 325-333 14-16 y 376.5 0 14-16 y. 385.0 406.7 380-470 16-18 y. 426.3 416-432 442.7 440-445

-epiphyses fused 99 Table 9. Long bone diaphyseal lengths: dental age as computed by Weaver (1977).

Estimated Age in Femur Rumerus Years n Mean n Mean Fetal 17 60.6 6.98 21 54.1 6.67 Newborn 40 73.3 4.4 51 65.6 3.4 .5 92.33 7.97 76.25 6.5 1.0 14 ll1.14 8.31 20 90.4 7.04 1.5 7 125.29 8.38 9 103.56 5.79 2.0 134.67 17.7 5 114.2 11.48 2.5 7 148.57 12.21 8 114.13 7.86 3.0 165.8 21.79 4 129.25 11.59 3.5 2 166 24.04 2 129 14.14 4.0 4 178.5 8.1 3 133.3 5.39 4.5 185.5 5.48 4 139.75 3.61 5.0 207 2 148.5 1.5 5.5 1 140 6.0 212.33 18.38 7 154.29 5.9 Taken from Weaver 19??:Table ll. 100 diaphyseal length relationships (Johnston 1963:251; Ubelaker 1978: 48-49; this research, Table 6). In the first six years of life, the Arikara mean femoral length exceeds those of either Grasshopper or Indian Knoll, which are actually quite similar to each other. A child from Grass hopper aged by Arikara long bone standards would appear younger than if aged dentally. This pattern is consistent with what is known of adult stature in the three skeletal series: Arikara adults are tallest (Bass and others 1971).

Figure 11 demonstrates why these tables should not be randomly used to determine the age of unknown skeletal material. Disparate results are obtained with each table, as seen by the spread of means and ranges. These discrepancies are due in part to different methods of the researchers, and in part to variability across time and space.

Inter-site variability is not unexpected, given the range of intra-site variability. Long bone growth rates are simply more inconsistent and population-specific than dental development rates (MassIer et al. 19'+1) and more subject to environmental forces. The deciduous dentition

"appears nonchalan'i::!y independent of most usually correlated develop mental processes" (Falkner 1957: 390).

Skeletal and Dental Variants

Postcranial Skeleton

Two postcranial anomalies were observed. The adolescent female from Burial ,56'+ has 25 presacral vertebrae along with fused first and second right ribs. The 6 to 7 year old boy from Burial 27 shows the nonmetric trait of atlanto-occipital fusion, the bilateral joining of 101

:~ ...... ,

IDO ·. 'j . ... j I :··,1.1 lUTAl SAMPLE SIZES . j 8RASSHOPPER ,'5 WIMAN ICIO...L. .. -145 .. 1·.--..... ;...... ,. MIURA .-116 t· "'_"...... ""-.

0.0.5 o.s-1.5 L5-2.5 2,.5-3.5 5.5-4.5 4.S·5J11h AGE GROUPS

Figure 11. Comparison of femoral diaphyseal lengths for seven age groupe from Grasshopper, Indian Knoll, and Arikara sites. 102

the first cervical vertebra to the occipital. condyles. This fusion

occurs only rarely, and is al.so seen in two adults in this series.

Cranial Skeleton

~. Three examples (3/390) of true Inca bones are seen,

from Burials 446. 542, and 652. These bones received their name frOID

their assumed high frequency among ancient Peruvians. A true Inca bone extends from asterion to asterion, in contrast to lambdoidal cesicles, which may also be quite large (as observed in crania from Burials 31,

117. 256B). The Inca bone of Burial 446 is bipartite. Among adul.ts at

Grasshopper. Birkby (1973' found Inca bones in the frequency of 2/57 males and 0/104 females. Since there is an established genetic basis

to Inca bone prevalence (Hepburn 1908) t a spatial. relationship W88 sought among the individuals showing this trait. Two children are from

Outliers and one is from Room Block 1.

At Pecos Pueblo, this trait was observed in 2/:IXJ adult crania; at Point ot" Pines, 11/13'; at Mesa Verde, 11/58 (Bennett and Hulse

1966; Bennett 1973b). These frequencies may be misl.eading because

Bennett does not distinguish between true Inca bones and 1arge lamb doidal ossie1es (Bennett 1mb: 20-21).

Kerckringl s Ossicle. These 08sie1es are formed in the process

of occipital ossification. "For many weeks two deep lateral. fissures

separate the interparietal and. supra-occipital portions, and a mem branous space extending from the center of the squamous portion to the

foramen magnum partially separates the lateral portions of the 103

supra-occipital. This space is partly occupied later by a spicule of

bone (ossicle of Kerckring)1I (Morris 1953:144). This is illustrated in

Figure 12e

Seven children at Grasshopper have this 08sicle (Burials 220,

234, 240, 343B, 396, 484, 562); they range in age from neonatal to four

years old. Two children are from the same room and a third is from a

nearby room in RB 2; three children are from neighboring rooms in RB 1

and the seventh child is from RB ·3.

Since this trait has not been reported at other sites, no com

parisons can be made.

Bregma Configurations. Bregma is the site of the junction of coronal, sagittal, and metopic sutures, and also the location of the anterior fontanelle. This fontanelle is usually trapezoidal in shape with the long axis running anterio-posterior. The fontanelle oloses during the seoond year, by which time the metopic suture also has fused.

Four young ohildren (Burials 234, 613, 628, 648) show an open bregma, indioating presenoe of the fontanelle in life. The metopic suture is. patent in Burial 234 (12 to 18 months). The shape of the area in the six to 12 month infant from Burial 628 is unusual. -- squared rather than trapezoidal. (see Fig. 13). The other two children are both

18 to 24 months of age. Three ohildren are from RB 3 and the fourth is from BB 1.

Early Suture Closure. The purpose of the cranial sutures is to aJ.low bone movement and growth and expansion of the brain. These sutures close over time at documented rates, beginning at about age 20 (stewart 104

Figure 12. Kerckringl B ossicle from child in Burial 220. 105

Figure 13. Unusual bregmatic configuration from child in Burial 628. 106

1979). Premature suture closure is treated as a cranial anomaly in this study, although the underlying cause may be pathological (Bennett 1967).

The skull grows secondarily to the brain (Weinmann and Sieher

194-7). When cranial growth is limited in one area, there is compensa tory growth at open sutures, leading to disfigurement, termed cranio stenosis (Knudson and Flaherty 1960; Gordon 1959). Increased intracranial pressure can cause exophthalmos or blindness. The most serious effect may be mental retardation, if the sutures close before brain growth is complete. Over ~ of the ultimate brain volume is attained by age ten, and actually there is little gr"owth after age three (Weinmann and Sieher 1947).

Studies among extant populations, as cited by Gordon (1959) and

Knudson and Flaherty (1960) I suggest that closure of sutures between four and six years of age is a variant of normal and not uncommon. It is rare, in these studies, for an individual to seek medical care because of a complaint related to early suture closure. Gordon (1959) indicates a strong hereditary tendency, favoring males.

Fifteen subadults in the Grasshopper series showed complete closure and obliteration of the sagittal suture. Nine are over age ten

(four males, five females), and there does not appear to be any notice able disfigurement. Six other affected individuals range in age from two to eight years (two males, two females, two indeterminate) and do ahow the characteristic craniostenosis. Two children are from adjacent rooms in Room Block 2, three are from neighboring roams in Room Block

1, one child is from the Great Kivaj the remainder are from plazas and test trenches. 107

Bennett (1967) documents cases of craniostenosis at Navajo

Mountain, Vandal Cave, Tuzigoot, Point of Pines, Turkey Creek, and other

Southwestern 6i tea. Rohenthal and Brooks (1960) describe a case from

California.

Possible Scalping. The adolescent female from Buria1 611 ex hibits what may be marks of sCalping. Faint cut marks, resembling de fleshing or butchering marks, can be seen along the zygomatic process of the frontal, the temporal-parietal border, and just above the mastoid process (see Fig. 14).. Similar marks are observed on the crania of two adul t skeletons from Burials 10 and 543. These markings might imply that cuttings were made across the forehead, above the ears, and across the base of the skull. The marks on the cranium of Burial 611 are not immediately obvious, unlike the massive trauma illustrated in Ortner and Putschar (1981:92-93).

Early explorers to the pueblos of Arizona and New Mexico make no mention of scalping. Later reports imply that scalping 'Was a custom of long-standing, "though practiced in a primitive and less striking form" (Friederici 1906:129).

Dental Variants

Of the 248 children for whom dental counts could be taken, 18 had only permanent teeth and 139 had only deciduous teeth. The re mainder had mixed denti tiona. Figure 15 presents the frequency of each tooth in the Grasshopper sample. A variety of uncommon dental features have been observed in the dental ma terial ~ and most of these in the 108 1'5S 1'!9I"'I"'I'lll13++.llT61·15s1 ~~~MMg~~ @~8t1t1 t1f1lif!1~ R L @~bBB B8b8l® HM~~~ ~~~MM

Figure 15. Dental frequencies in subadul ts; totals include all erupting and erupted teeth from 248 children. -_ Deciduous teeth are counted in 226 children and permanent teeth are counted in 84 children.

g 110

deciduous dentition. Seven of these variants are discussed, along with

what is known of their prevalence in other populations.

Fused Teeth. Gemination and fusion are two developmental pro

cesses aff~ctiDg primarily the milk teeth. Gemination results from a

single tooth bud that splits incompl.etely, while fusion is the end

product of two tooth buds which join. A related pi'ocess is twinning,

the complete splitting of a tooth bud into mirror-image teeth (Pindborg

1970). Fusion occurs most frequently in the anterior mandibular teeth

and results in a reduced number of teeth in the dental arch. It may be

followed by a similar reduction in tooth number (hypodontia) in the

succeeding permanent dent! tien.

There is a hereditary nature to fused teeth, according to

stewart and Prescott (1976). Siblings have a 2% greater incidence than

the general population. A Japanese study showed a ~ incidence, which

was ten times greater than that found in a Swedish study. In general.,

the incidence in Caucasian populations has been found to be less than

0.%. A three-family study, carried through four generations, showed

that 12 of the 17 affected individuals were femal.e (Moody and Montgomery 1934). Out of the 226 individuals having deciduous teeth in the

Grasshopper sample, 14 (6.2';\n had fused teeth. The distribution is shown in Table 10. This table also includes a neonate from Burial 156, whose fused incisors are still unerupted. Dental radiographs of the other 13 ehildren reveal complete fusion of roots as well as teeth, and also show that the proper number of permanent teeth are present in in all cases. Seven of tl,e 15 ehildren 111

Table 10. Location and frequency of fused teeth for fifteen sUbadults.

Teeth Right Left Bilateral

Deciduous mandibular i1 and i2

Deciduous mandibular i2 and c Q 112 coul.d be sexed; all are female. As for spatial. rela.tionships, six chil dren are from Room Block 2, three are from Room Block 3. and three are from Room. Block 1.

One instance of true gemination was seeD, in Burial 658. The permanent right l.ower lateral incisor has attempted to divide, causing formation of a supernumerary tooth. This individual is also a female, from Room Block l.

In a study of deciduous dentitions from the Ohio valley. Sciul.li

(1.977) found 2/58 cases of fusion, both of the lower lateral incisor and canine. Sundick (personal cormaunication 1981) noticed fusion only of mandibular incisors at Indian Knoll. One case, seen at Pecos

Pueblo, was of a fused right central. and lateral mandibular incisor

(Hooton 1930). None were observed at Point of Pines (Snyder 1959).

Paramolar Tubercles. The paramolar tubercle of Bolk (Balk's cusp) is a buccal elaboration of the parastyl.e and protostylid (Krogman

1960). occurring on both deciduous and permanent molars. It is fel t by some that these extra cusps are remnants of the cingulum found in primitive primates and mammals (Kustaloglu 1962; Pindborg 1970). Balk

(cited by Dahlberg 1945) believed that the deciduous dentition once had more teeth in each quadrant, teeth which have 'treen lost through evolu tion. These lost teeth are represented in modern populations by the occasional. appearance of a supernumerary tooth; these supernumerary teeth are sometimes fused to the molar, with only an extra cusp as evidence of former presence.

This feature is rare in Caucasians and Negros, and shows a genetic basis within Mongol.oids. A 1976 study by Stewart and Prescott 113 has shown a 2-3% incidence among Malaysians and American Indians in general, but a 31% incidence among Pima Indians. This high frequency in Southwestern Indians was earlier demonstrated by Kustaloglu (1962), who examined 345 deciduous upper molars and found ?/l~ (4.~) to have a paramolar tubercle Oil dm1 and 7/195 (3.6%) on dm2.

Seven Grasshopper chil.dren have paramolar tubercles, as seen on upper right drol, lower right dml, upper 1eft dml, and lower right dm2

(see Table 11 for frequencies). In one case, tubercles were seen bi laterally in right and left upper dml. In another child, tubercles were seen in corresponding teeth in upper and lower arches: right upper and lower dml. Three of the seven children are from neighboring rooms in Room Block 2, two other children are from Room Block 3.

Lingual Tubercles. Elaboration of the lingual tubercle is most often seen on permanent upper lateral incisors, and again is attributed to the Cingulum (Pindborg 1970). This particular tooth is the most variable in the anterior complement and the most studied tooth in the human dentition (Klatsky 1956; Stewart and Prescott 1.976).

In the Grasshopper sample, three individuals, all from Room

Block 3, had this variant, as follows: Burial 611, right upper 12;

Burial 407, left upper I2; Burial 441, bil.ateral upper 12. Two out of

200 individuals at Point of Pines had this variant. Among modern Pima, incidence of these ~ ~ runs as high as 86% (Snyder 1959).

Pegged Teeth. Twenty-one out of the 248 individuals wi th observable dentition have one to four pegged teeth, including permanent incisors, and deciduous incisors and canines (see Table 12). Pegged 114

Table 11. Location and frequency of paramolar tubercles for seven Bub adults.

Teeth Right Left Bilateral.

Deciduous maxillary ml Deciduous mandibular ml o o Deciduous mandibular M2 o

·One child shows trait in upper and lower arches on right side.

Table 12. Frequency of pegged teeth for Grasshopper Ruin subadults.

Tooth Right Left

Deciduous maxillary i2 1/22 2/132 Deciduous mandibular i2 1/134 0/142 Deciduous maxillary c 6/151 9/146 Deciduous mandibular c 6/153 5/146 Permanent maxillary 12 2/37 5/32

Total number affected subadul ts = 21 Total number affected teeth = 37 115 deciduous canines are extremely rare (Gorlin and Goldman 1970). but the

Grasshopper sampl.e contains four chileJren having pegging of all four primary canines. No spatial relationship could b~ established for these four.

Seven individual.s had just ODe pegged tooth, nine had two to four pegs, and five had at least one; due to missing teeth, bilaterality coul.d not be observed in these individuals. Seven are males, four are females, and ten are of indeterminate sex. Room Blocks 1. and 2 each contain eight affected children.

At Point of Pines, five individuals had a total of eight pegged teeth (Snyder 1959).

Supernumerary Teeth. Hyperodontia, an increased number of teeth, is manifested by supernumerary teeth. The young boy from Burial.

413 at Grasshopper has an extra tooth between the upper left di2 and dc.

In the general population, prevalence of supernumerary teeth runs about

"', with males affected twice as often as females (Gorlin and Goldman

1970; Pindborg 1970).

Retained Teeth. Two children, both seven to nine years of age, have retained their right upper dil after full eruption of the permanent incisors. Both children are from Room Block 1 i one is male and one i9 female. As a matter of course, retention of dil is rare (Gorlin and

Goldman 1970). A Finnish sampl.e showed a ~ frequency of persistent teeth, with de and upper dm2 most commonly retained (Pindborg 1970).

Carabelli's CuSP. First defined in 1842, the Carabelli's cusp is an accessory cusp which generally occurs bilaterally on the anterior 116 medial aspect of the lingual surfaces of the maxillary pe:rmanent and deciduous molars. This trait has long been considered a Caucasian race marker, yet it occurs with appreciable frequency among Mongoloids. In these instances, presence of the trait is usually correlated with genetic admixture (Kraus 1951, 1959; Snyder and others 1969), a highly unlikely prospect at Grasshopper.

At Grasshopper, Carabelli I s cusps were seer~ bilaterally on the permanent Ml and deciduous m2 of two individuals, 0.5% of the subadults.

These two individuals are a female from an Outlier and a male from Room

Block 2. In terms of tooth frequency, the cusp was seen on 1.1% of all dm2 and 0.% of all Ml in the sample. Hanihara (1967) found a trait frequency of 11.9}6 in a Japanese popUlation. Snyder and associates

(1969) found the trait in nearly their entire Tarahumara and Mestizo sample. Carabelli's cusps were seen in almost 9% of Pecos Pueblo in.. habitants (Krogman 1960).

Dental Attrition. Intense dental attrition is noted on the deciduous molars of all children six years or older, but no attempt was made to classify the wear by degrees.

Summary

Nine of the thirteen traits described above are believed to have a genetic basis (Inca bones" early suture closure, fused teeth, para molar tubercles, lingual tubercles, pegged teeth, supernumerary teeth, retained deciduous teeth, and Carabelli's cusp). These traits occur with greatest frequency in subadults from Room Block 2, which has 21 occurrences in the 89 subadults recovered from that area. This 117 incidence of 0.24 is compared with an incidence of 0.17 in Room Block 1.

(19 occurrences out of 112 subadults), 0.1.3 in Room Block :5 (10/78), and

0.13 in the Outliers (4/30). This finding may indicate a closer degree

of genetic relatedness among residents of Room Block 2.

Skeletal Pathologies

None of the pathologies to be discussed below is indicative of

the actual cause of death. 'Cause of death' refers to whatever disease,

syndrome, morbid state, or pathological condition may' have been directly

or indirectly involved in the process of death (Puffer and Serrano

1973). Instead, these pathologies reflect underlying disease processes which may have left their mark on the developing skeleton and which may

have contributed to an overall debilitated state of health.

Postcranial Pathologies

Parthest Disease. The left femur of the adolescent male from.

Burial 191 shows evidence of an aseptic ischemic necrosis of the femoral

epiphyseal. head, or Perthes' Disease (see Fig. 16). This is an uncommon'

disease of childhood and adolescence, with an incidence in boys four

times that in girls.

According to Weinmann and Sicher (1947) and Ortner and Putschar

(1981) t the degenerative process begins when the blood supply to the

epiphysis is disturbed. This can occur in several ways: from an. ex

ternal force, from trauma or repetitive trauma, or from an internal.

abnormal tension of vessels and connective tissue wi thin the articular

capsule. The epiphysis becomes flattened and irregular in outline and 118

Figure 16. Perthes' Disease affecting left femur and ilium. -_ A = affected bones; B = unaffected right femur and ilium. All bones shown in posterior view. 119 fuses to the femoral neck. Necrotic bone is replaced by a course, fibrillar-type bone, which has little resistence to mechanical stress.

Regeneration is not likely to take place if the mechanical forces which originally disrupted normal vascularity remain. This condi tien is not itself fatal, but is conducive to secondary infections.

The individual from Burial 191 shows evidence of mild infection.

There does appear to have been some physical handicap. This boy prob ably walked with an abnormal abducted gait, as suggested by the over development of ~ intermedius attachments.

other Postcranial Pathologies. The neonate from Burial 118 presents a diagnostic problem. The sternal ends of ribs one through eight are bilaterally expanded and irregular. The changes are not de generative, nor do the:v resemble the ribs of rickets or scurvy. There is new bone formation due perhaps to periosteal stimulation. Radio graphically, the cortex is intact; this new bone is external to it.

There are ten small separate segments of this same type of bone, re sembling the ossified costal cartilage of mature adults. It is possible that whatever caused the rib problems may have also caused respiratory problems.

Among the rest of the skeletal sample t no evidence was seen of healed fractures or bone infections. Perimortem fractures could not be distinguished from those occurring immediately postmortem, but breakage cccurring in the course of excavation was identifiable by the clean appearance of the broken edges and the absence of soil in the break lines. 120

Cranial Pathologies

The three to four year old girl from Burial 172 exhibits a cir cular, raised lesion on the left rear of the frontal bone. This lesion measures 2 by 2 em and is located 1. em left of the midline and 2 em anterior to the coronal. suture (Fig. 17). The inner table is not in volved, nor is the lesion apparent radiographioally. The vascularity of the lesion supports two possible diagnoses: a sequitur of a scalp lesion, or a hemangioma, a benign tumor characterized by the prolifera tion of newly-formed blood vessels. It may have been asymptomatic.

The three to four year old female from Burial 320 shows what may be an old depressed fracture on the right side of the frontal bone.

There is increased vascularity in this area and also in the right parietal bone.

The two to three year old girl from Burial 368 shows a 4 by 2 em depression in the right parietal, which bulges into the inner table.

Although no fracture is visible radiographically I the likeliest inter pretation is an old healing trauma to the head which, due to youthful elasticity of the bone, did not result in breakage.

The six to seven year old boy in Burial 432 presents a lesion to the left frontal bone, 8 em above the zygomatic arch. The lesion is

5 cm long, 2 em across, and barely crosses the coronal border to the left parietal. Both tables are intact, and the bone in this area is darkened on the outer table. Radiogra:;;hy !'~'!e~l!; n!:' ,e.!;!~~:r.eb:·y !:'f yascu- larity between left and right sides. The lesion appears -Co be like that of Burial 368, an old healing trauma to the head. 121

Figure 17.. Frontal lesion from child in Burial 172. 122

Milnar (1982) found similar cranial injuries in his Illinois skeletal sample. These are small diameter, healed depressions in the outer table. He attributes them to crushing blows, with localized 60ft tissue infection.

Dental Caries. Caries are observed in 72 teeth, 66 deciduous and 6 permanent, distributed among 39 individuals. No child had caries in both deciduous and permanent teeth. Table 13 presents the frequency of carious teeth in this sample. Twenty-two children each had one carious tooth, 10 children each had two carious teeth, and eight chil dren each had three or more carious teeth.

All caries are occlusal and occur, with few exceptions, in molars. The tooth most often showing caries is maxillary dml. The youngest child with deciduous caries is in the 18 to 24 month age group.

Peak occurrence is in the five to six year age group. The permanent first molars are not affected to any great degree. This is the tooth wi th the longest potential life in the mouth; it is encouraging that at

Grasshopper they did not decay early on.. The four children who do have carious Ml are over 12 years of age.. Since the diet at Grasshopper was not solely agricultural tit was perhaps not particularly cariogenic

(Wells 1975; Mandel 1979) ..

Abscesses resulting from severe caries are noted in six decid uous and one permanent molar, including the molar of a two-three year old child. It is possible that such an infection may have been a con tributory cause of death for these seven children.

At Point of Pines, 56/350 persons and 166/3677 teeth were cari ous, including 12 deciduous incisors and first molars (Snyder 1959). 123

Table 13. Frequency of dental caries for Grasshopper Ruin subadults.

Tooth Right/upper Left/upper Righ t/lower Left/lower

Frequency = ~~~~r o~!e~~:~~~:!i~:=Sible

Deciduous il 0/143 0/133 0/114 0/134 Deciduous i2 1/122 0/132 0/134 0/142 Deciduous c 0/151 1/146 0/146 0/153 Deciduous ml 15/179 11/176 9/188 6/149 Deciduous m2 4/158 6/155 8/165 5/133 Permanent Ml 4/63 1/71 0/68 1/65

Total. number affected subadulte = 39 Total number affected teeth = 72 124

Skeletal Stress Markers

Cortical Bone Loss

Figure 18 presents the index of cortical thickness at midahaft

for 189 femora and 178 humeri from 228 children. Range, mean, and one

standard deviation are indicated for each age interval. The pattern

evident here is similar to that discussed earlier by Garn and 8660ci-

ates (1969)and Carlson, Armelagos and Van Gerven (1976). An initial

neonatal gain is seen followed by a weanling 106s, and a juvenile gain

wi th an adolescent spurt. The largest observable range is in the

youngest group, which includes fetuses, neonates, and infants under 12

months of age. Since the skeleton grows vigorously in utero and during

the first postnatal year t this spread is not unexpected (Marshall 1977).

One observation should be clarified. It would appear that in

the humeri of three to six year olds, there are children with tremen

dously thick cortices. In fact, two children register cortical indices

of 0.51 and one child registers 0.80. This dimension is due to a rela

tive excess of periosteal bone accumulation (Frost 1972b), though

nei ther the cause nor the significance of this bone modeling error is

known. One of these children is included among the group having longer

than average femora. None of the three is free from other stress mar kers. Two have Harris lines, one has cribra orbitalia. All are female.

The numbers of individuals in each age group falling below the

limit of 'normal' bone thickness are presented in Table 14. The two

age groups with the greatest percentage of affected members are 9-12

year alds and 12-15 year olds. These are children in their growth spurt 125

F F F

F H ...K CO F ~ IfttH

.25 tt t::;~ .z

.15

o 0-1 1-2 2-3 3-6 6-9 9-12 12-15 -I AGE!,..,,) 14/1'2 25/25 DIG I!Iia3 "13 5/8 fI8 7/& SAMPLE SIZE (Flft'lur/Humlruc)

Figure 18. Index of cortica1 thickness for femur and humerus at midshaft. 126

Table 14. Frequency of subadul ta by age falling below the average cortical index for the femur and/or humerus.

No. of Affected Both Bones Femur Humerus Age Individuals· Affected Only Only

F-12 m. 20/92 1-2 yr. 6/30 3 2-3 yr. 4/20 3-6 yr. 3/41 1 6-9 yr. 5/22 9-12 yr. 3/8 12-15 yr. 2/6 0 15-18 yr. 0/9 0 0 Total number of affected indi vidual.s = 43.

Total number of individuals upon whom observations could be made is 228: 52 have femur only, 40 have humerus only, 136 have both. "'Number of affected individuals/number in age group for whom observatior.s could be made. 127

(Krogman 1972; Marshall 1977; Tanner 1978). for whom iDcreases in bone

breadth may not have kept pace with increases in bone length. The

least affected age groups are 3-6 year alds and 15-18 year ol.ds.

In ten instances, thinned cortex is associated with the presence

of cribra orbi talia. The two children mentioned previously as having

particularly robust skeletons fall in the low range for both humerus

and femur. Their muscular frames are not augmented by thickened cor

tices.

Cook (1919) found a mean femoral index of approximately 0.65-0.68

for her newborn to three month age group. Her one to two and two to

three year group averages are slightly greater than those of the com

parable Grasshopper groups (12-21f m. = index of 3.5; 24-36 m. = index

of 3.5-4). It is difficult to determine the degree of pathology represented

by cortical bone loss, since its prevalence in this skeletal. sample is

low. It may be more meaningful to note that 26 of the 43 children with

cortical bone loss show other stress markars, and that of the ten chil

dren having three or four stress markers, seven show cortical. bone loss.

Porotic Hyperostosis

Fifteen cases of classic porotic hyperostosis were seen among

the 390 subadults, less than t.,,; of the sample. Bones involved included

the parietals and, in four instances, the temporal squama. No child

older than four years had this condition, implying either that this con

dition is associated with early death or that healing and remodeling can occur. Both implications seem warranted, as older children do in

fact show healing or healed hyperostosis. 128

The peak age of occurrence is birth to six months (see Fig. 19), with four affected infants out of the 30 in that age group. But the most severe case is seen in the three to four year old girl from Burial. 320 t the only such afflicted child in that age group. Radiographs of this girl t s parietal and frontal. bones show extreme hyperostosis and an ex panded diploic space.

The fact that very few and very young children 'Were affected suggests this is not a .... idespread dietary problam, but r:".ther that the porotic hyperostosis may be a complication of infectious disease or parasitism, although the cause-effect mechanism is not known.

No association was noted between porotic hyperostosis and post cranial infection, as Lallo and associates (1977) had observed in their

Mississippian sample. In the Grasshopper sample, in 8 out of 15 cases, there was no association with any other cranial, dental, or postcranial disease or stress marker. Of the seven cases in which associations were seen, the most common associations are with cortical bone lOBS and cribra orbitalia. Porotic hyperostosis does not appear to be a signifi cant pathological condition at Grasshopper t and the 3.8% incidence is perhaps the lowest documented frequency in a prehistoric skeletal col lection of this size. Eighty-four individuals (21.5%) showed Butural hyperostosis which, in this research, is not considered pathological.

The age distribution of these children is shown in Figure 20. Incidence is closely linked to times of cranial growth.

Cribra Orbitalia

Cribra is the most common stress marker in the Grasshopper sample, yet affects only 54 (14%) subadults, in the age distribution 129

AGE ~le:LE 5 4

Figure 19. Incidence of porotic hyperostosis. --

% incidence = ~:~:~ ~~ ~:~:r~:r i:~:~gup 130

AGE ~,t~ 1-1.5 1.5·2 2~3 3-4 4-{) 5-6 6-8 8-10 kHZ 12-14

~~lELE 2 16 16 16 :84

Figure 20. Incidence of sutural hyperostosis. -- % incidence = ::::~ ~~ ~~~:r:rp::e a:O:oup 131 shown in Figure 2l. The greatest incidence is from 12 to 18 months, and may thus be attributable to nutritional compromises during weaning.

An al. ternate or supplementary explanation is to attribute cribra to conjunctivitis or trachoma, infectious diseases of the eye which spread rapidly and which have been linked both to cribra and to children of this age group (Frost 1965; steinbock 1976).

Co-occurrence of cribra and porotic hyperostosis is observed in four individuals, three females and one of indeterminate sex, all be tween six e-nd 18 months of age. It does not appear that at Grasshopper cribra is a precursor of porotic hyperostosis (Lalla and associates

1977). Exactly one-half of cribra cases are unassociated wi th other stress markers.

Growth Retardation

Growth retardation is discussed in terms of the femur. The number of children with at least one femur totals 199. Seventeen of these children, seven females and ten of indeterminate sex, aged post natal to ten years, fall below one standard deviation of the mean femoral diaphyseal lengths for their respective at!:e groups, as was shown in Table 7. Eleven of these children (65%) show other stress markers as well, including porotic hyperostosis, cribra, cortical bone loss, Harris lines, and linear enamel hypoplasia. Gindhart (1969) found that Harris lines did not significantly decrease diaphyseal length.

A similar percentage of tall children (69)6) show other stress markers. Of the ten children with three or four stress markers, six are short for their dental ages. But since fewer than l~ of postnatal 132

Figure 2l. Incidence of cribra orbitalia. --

% incidence = ::~:~ ~~ ~:~~~;:r;r a:t;oup 133 children have short femora for their age, this does not appear to be a

significant stress marker in the Grasshopper skel.etal series.

Harris Lines

Among the 267 subadults for whom radiographs could be examined,

transverse lines are observed in the long bODes of 53, at the sites of

distal. femur, proximal and distal. tibia, and distal radius, in the d18-

tribution shown in Table 15. Although observations were made on the

bones of the right side where possible, two-thirds of these individua1s had bones of both sides present. In those cases in which bilaterality . could be observed, the transverse l.ines are seen in corresponding posi- tiona in left and right bones.

Al. though Harris lines are the second most common stress marker in this skeletal series, lines in general are not frequent nor are they patterned. The average number of l.ines per individual in all bones is

7.4, with a high of 27 lines (Burial 191) and a low of one l.ine (Burial

442). The high incidence of lines in the boy from Burial 191 is believed to be related to the Perthes' Disease from which he suffered.

Nineteen children in the 5-7 year age group account for 41% of all lines.

Using the tibial template illustrated in Figure 7. the approxi mate age of line occurrence was ca1culated for 43 subadults with trans verse 1.ines in the tibia. '!ab1.e 16 shows the number of lines forming

in particul.ar periods. Lines which may have been quickl.y remodeled,

of course, were not present to be counted. Nearly three-quarters of tibial lines appeared during early and especially middl.e chUdhoCld, comparabl.e t? We1.1s' (1967) findings on Saxon skeletons. The youngest chil.d with l.ines is in the 6-1.2 month age group, the oldest is 1.6-1.8 134

Table 15. Frequency and distribution of Harris lines.

Number of 8i te of Lines Affected Distal Proximal Distal Distal Individuals Femur Tibia Tibia Radius

0 25 3

Tot. 53 Total number lines per site 121 116 131 22 Mean number lines per site 3.10 2.70 2.44

Observat ions based on sample size of 267.

Table 16. The association of tibial transverse line frequency and age of line formation.

Age at Ase of Line Formation Death 0 .. 2 y 24 Y 4-8 y 8-12 y 12-18 Y Total

0-2 y ( 5) 20 lines 20 (.08) 2-4 Y ( 9) 15 39 54 (.22) 4-8 y (20) 7 32 88 127 (.51) 8-12 Y ( 4) 10 21 (.08) 12-18 Y ( 5) 1 4 17 25 (.10) Total (43) 44 72 101 27 247 lines (.18) (.29) (.41) (.11) (.01) (100)

Interpretation: For example t the five children in the 0-2 year age group have 8.% of all Harris lines, but 18% of all lines have their origin in this infancy period. 135 years of age. The 4-8 year old children experience both the peak number

of lines and the peak time of line formation. The 20 children in this

group have a total of 127 lines, 88 of 'Whieh are of recent origin.

Forty-one percent of tibial. lines formed during this age period.

Acquisi tiOD of lines appears to be closely associated with age

at death. Most lines are counted in the same age period as that in which

the child died. One conclusion to be drawn is that the stress(es) pre_

cipitating line formation contributed to an-overal.l debilitation of the

child. Wells (1967) attributed line formation to winter bronchitis,

summer dysenteries, and periodic famines, all of which could apply to

Grasshopper subadults as well.

Twenty-eight of the 53 subadul ts with Harris lines show only

this particular stress marker. The remaining 25 children show one or

more other stress markers, most commonly cortical bone loss. One-half

(26) of the subadults with transverse lines are female; 17 are male, and

nine are of indeterminate sex.

Linear Enamel Hypoplasia

Dental hypoplasia is observed in one or more teeth of 28 of the

248 children whose dentition could be examined. Eighteen cases involved

deciduous teeth and ten cases involved permanent teeth. No child had

hypoplastic lesions on both the deciduous and permanent dentition, be

caUse with one exception, all children with deciduous lesions died

prior to eruption of the permanent teeth. Table 17 displays the dis

tribution of affected teeth.

Determining the age at which hypoplasia Was induced may be

instrumental in suggesting an etiology for the stress. In order for 136 Table 17. Frequency and distribution of hypoplastic teeth.

Right Left Right Left Upper Upper Lower Lower

~ central incisor 12/14} n/1}} 5/114 4/1}9 lateral incisor 10/122 1}/1}2 }/134 }/142 canine 5/151 6/146 0/153 0/146 first molar 7/179 7/176 5/188 5/149 second molar 2/158 }/155 1/165 1/1}} (18 affected chil.dren, 10} affected teeth, 5.72 affected teeth/chUd)

Permanent central incisor }j40 4/3} 0/50 0/47 lateral incisor 1/37 1/32 0/40 0/35 canine 1/21 2/22 4/27 2/2} first premolar 2/21 2/22 0/22 0/21 second premolar 1/21 0/16 0/18 0/17 first molar l/63 1/71 0/68 0/65 (25 affected teeth, 10 affected children, 2.5 affected teeth/child)

Frequencies expressed as :~~!i ~~~::~:~~~n6 possible 137 the deciduous denti tieD to be so affected while leaving the permanent

denti tiOD untouched, the stress must have been prenatal (MassIer et al.

194-1; chart reproduced in Figure 8). Placement of lesions for :.:he child

from Burial 502, for example, suggests an early fetal. stress, since lesions are seen only at the transverse midline of the upper central incisors and the tips of the upper lateral incisors. Other children suggest a late fetal stress, as lesions are observed on upper incisors and dml, but not the canines or dm2. A systemic etiology is suspected

because seven of these children have at least seven, with a high of 14, affected teeth.

Among the 103 affected deciduous teeth in the Grasshopper sample,

24 are stained, 28 show hypoplastic lines, and 51 show loss of enamel due to caries, the "circular caries" described by Cook and Buikstra

(1979) .. Upper deciduous incisors, which calcify first, appear to be the most sensitive. Of the 11 children having the most severe carious lesions, eight died before they reached the age of two years. As in the Illinois Woodland samples, these children do appear to have been selected against (Cook and Buikstra 1979j Cook 1981) .. As stated earlier, premature birth has been linked to a predisposition towards linear enamel hypoplasia (Sweeney and others 1969) ..

Future research on LEH at Grasshopper should include a micro

structural analysis of sectioned dental 'pre-forms' recovered with fetal

skeletal material, to investigate whether dental lesions can be observed at this early stage of development.

Six of the individuals with the most severe deciduous lesions are evenly distributed in three rooms of the pueblo, two in RB 1. and one in RB 2, a teasing suggestion towards a genetic predisposition to

poor enamel formation.

Of the 25 affected permanent teeth, 16 "'how faint lines and nine

are stained. The affected teeth, incisors and canines primarily, are

those which would be forming during the weaning period.

One individual is remarkable, the adolescent female from Burial

108. Teeth affected are the upper right premolars. PMl has a hypo

plastic line (and an occlusal caries). PM2 is somewhat smaller than

its counterpart on the left side and is denected slightly towards MI.

Since the defect is so isolated, it may be due to some mechanical

trauma, perhaps a blow to the cheek, while the teeth were forming.

This girl shows no other stress markers.

LEH is associated with other stress markers in 20 individuals,

and unassociated in eight. It appears to be primarily a stress of

young children.

Co-occurrence of Stress Markers

Most prevalent of the stress markers are cribra orbi talia and

Harris lines, affecting 54 and 53 individuals, followed by cortical.

bone loss in 43 and linear enamel hypoplasia in 28. Growth retardation

(17) and porotic hyperostosis (15) are not common in this group of

children.

Each stress marker favors certain age groups (Table 18). Cribra

affects predominantly those in the 12-18 month range, while Harris lines

are found especially in 6-8 year aIds. This group also registers the

most enamel hypoplasia, but of the younger children (18-24 m.) having Table 18. Total occurrence of each stress marker for each age group.

Age Group Number of Individuals with Each stress Marker and Purotic Cribra Cortical Enamel Harris Growth Total Number Sample Size Hyperostosis Orbi taIia Bone Loss Hypoplasia Lines Retardation Stress Markers· Fetal (60) Neonatal (40) 0-6 m. (26) 11 6-12 m. (0) 15 2 30 12-18 m. (43) 15 4 30 18-24 m. (3) 8 3 6 23 2-3 y. (0) 4 23 3-4 y. (29) 18 4-5 y. (15) 5-6 y. (25) 1 17 6-8 y. (26) 4 14 31 8-10 y. (10) 4 7 10-12 y. ( 4) 3 12-14 y. ( 6) 14-16 y. ( 9) 7 16-18 y. ( 4) 1 1 Totals (390) 15 54 43 28 53 17 210 ·The total number of affected individuals is 145; the total number of stress markers is greater than that because 50 individuals have more than one stress marker. f-' '" 140 enamel. hypoplasia, each is more severely affected. Decreased cortical thickness, porotic hyperostosis, and growth retardation affect primarily the very young. None of these distributions is surprising if normal growth and development patterns (Krogman 1972; MaJ.iua 1975) and basic mechanics of these stress ril8rkers are understood.

Analysis of the association of stress markers wi thin an indi vidual may yield information as to the cumulative effects of repeated insults to the growing child as renected in the skeleton. Stress

IIIElrkers are observed in 145 out of the 390 subadults in the Grasshopper sample. Ninety-five children have just one stress marker. Of the re maining 50 children, 40 have two stress iD8I'kers, seven have three stress markers, and three children have four stress markers. These associations are shown in Table 19 and calculation of their significance is shown in Table 20.

All three children having four associated stress markers are under three years of age. Four of the seven children with three associ ated stress markers are also less than three years of age; the remaining three children are between six and eight years of age.

Porotic hyperostosis is the stress marker most frequently observed alone, followed by Harris lines and cribra orbital.is. Linear enamel. hypoplasia is the stress marker most often associated with other stress markers, and the most common association is between IEH and cribra orbi ta1ia. The most common associations overall are those of cortical. bone loss with cribra orbi taUa and Harris lines.

Five of the 14 associations are significa.,t. Significant co occurrences are seen between cortical. bone loss and growth retardation, Table 19. Co-occurrence of stress markers.

Cortical. t-inear Stress Growth Porotic Cribra Harris Bone Enamel Markers Retardation Hyperostosis Orbitalia Lines Loss H:lEoElasia

Cortical. (17) bone loss

Growth (6) retardation 7"

Porotic (8) hyperostosis 5"

Cribra 10 (28) orbi talia 6"

Harris (28) lines 10"

Linear enamel 0 9" (8) hypoplasia

Total occurrences 43 17 15 54 53 28

·Significant associations at < .05 (unassociated occurrences)

...... Table 20. Chi-square tests of associations between stress markers.

Linear Enamel Porotic Growth Cortical Harris Lines Hypoplasia Hyperostosis Retardation Bone Loss

P T P A T P T P A T P A T ·.:I p7 4653 P 9 45 54 P 4 50 54 P 6 48 54 P 10 44 54 ~ ~ A 47 284 331 A 19 308 327 A 11 321 332 A 11 319 330 33 293 326 "~T 54 330 384 T 28 353 381 T 15 371 386 T 17 367 384 T 43 337 380 )(2 = 0.04 <.90 )(2 = 8.02 <.01 )(2 = 2.08 < .20 )(2 = 6.63 < .01 )(2 = 3.25 <.10 Linear Enamel. Porotic Growth Harris Lines Hypoplasia Hyperostosis Retardation PAT P A T P A T P A T ..,~p 1033 43 P 4 39 43 P 5 38 43 p 7 36 43 ,~.., A 43 315 358 A 24 319 343 A 10 332 342 A 10 330 340 tgT 53348 ltol. T 28 358 386 T 15 370 385 T 17 366 383 "'" )(2 = 4.23 <.05 )(2 = 0.30 <.70 )(2 = 7.73 <.01 )(2 = 16.01 <.001 Linear Enamel Porotic Linear Enamel Porotic Harris Lines Hypoplasia Hyperostosis Hypopl.asia Hyperostosis § P T P A T P T • P A T P T :5 ~ P 4 13 17 P 1 16 17 P 2 15 17 ,~ P 7 46 53 p 2 51 53 e~ A 49 321 370 A 27 345 372 A 13 358 371 ~ A 22 310 332 14 323 337 "~T53334387 T 28 361 389 T 15 373 388 ~ T 29 356 385 T 16 374 390 0: 2 )( = 1.45 <.30 )(2 = 0.05 <.90 )(2 = 2.98 <.10 ",)(2 =,2.84 < .10 X2 :=I 0.02 <.90

Key: P = trait present; A = trait absent; T = total.; df = 1; X2 = chi-square value; <.10 = significance level. ~ 143 porotic hyperostosis, and Harris lines, and between cribra orbita1ia and growth retardation, and cribra and LEH. These associations may be better understood if looked at in age-specific terms (see Fig. 22).

With the exception of Harris lines, all are stress markers of the first two years of 1ife, the time period with the greatest mortality at Grass hopper. It should be kept in mind that these stl'aes markers do not appear overnight. Rather, they may take up to a year to develop. It has been shown that some of the precipitating stresses, such as LEH, have a prenatal origin.

An attempt was made to cOITelate dental disease, as reflected in caries and LEH, with cranial. and postcranial stress markers, to see if poor skeletal health was associated with poor dental health. A sig nificant association is seen (Table 21), reinforcing the idea that the precipitating stresses are systemic.

Six children have skeletal pathologies other than stress markers.

Two of these children (Burials 118 and 368) had no strees markers. The boy from Burial 191, along with Perthee' Disease, had Harris lines and dental caries. Three other chUdren with cranial lesions also had severe porotic hyperostosis (Burial 320), caries and cribra (Burial

172). and Harris lines (Burial 432).

Summary

Subadults from Grasshopper Pueblo seem to have had a low disease load. and few children evidence histories of acute attacks or chronic deprivations. The diet at Grasshopper was potentially excellent, but there may have been differential access to food. Nearly two-thirds ,.....-----...PlEVALI!tICE ~ MOST INTENSE I'ClROTIC HYP£ROSTOSISI

CRIBRA OIIIITALIA - COIITICAL lONE LOSS

~TION

HARRIS LINES

ENAMEL HYI'OPLASIA

F N ...... 0-6 6-12 12-18 18-24 ,. 2-3 3-4 4-5 5-6 6-8 8-10 KH2 12-14 14·16 1&.-18 ~a....

Figure 22. Prevalence of stress markers by age. _ Among Grasshopper subadultB, the age group most affected by each etress i marker is labeled Umoat intense." Table 2l. Chi-square test of dental pathologies and skeletal stress markers.

Dental Skeletal Stress Markers Pathologies Present Absent Total

Present 30 33 63 Absent 107 240 347

Total 137 273 320 )(2 = 16.47, approximate level of significance = 0.001, df = 1. 146

(245 or 63%) of the 390 subadults show no stress markers whatsoever.

Of the 37% with stress markers (145), an average of 1.45 stress markers

per person are recorded.

Absence of stress markers is especially common in the youngest

members, as seen in Table 22. One fetus, two neonates, and seven peri

natal infants show pathological conditions of the hard tissues. Since

it has been shown that prenatal dental defects are frequent in this

sample, it stands to reason that for many individuals the uterine en

vironment was not a pleasant place. Sickly or very young mothers pro

duce babies les6 likely to survive and thrive. Those term infants

surviving the birth trauma may have succumbed to hypoxic or other stress

due to immature organ systems and lack of medical intervention to meet

"Ie danger congenital." Infants who might have survived for a few months simply did not have enough time to register any stress on the

skeleton and may have died from a single severe attack of diarrhea or

upper respiratory infection. Thus, an early weeding out period may be postulated for infants of hypothesized poor constitution.

Older infants begin to show signs of chronic stress, most likely as the result of repeated attacks of these same infections, and perhaps

underlain by marginal nutrition as weaning is begun. The physiological

stressfulness of this period has been well-documented previously. Over

the next two years, more and more children begin to show stress markers

although they remain temporarily successful in fighting off pathogens.

Children both with and without signs of cumulative stresses died in

childhood. For those children unscarred by previous metabolic insults, 147

Table 22. Presence/absence of stress markers by age and sex.

Age Group Unaffected Affected Totals Group Size M F I M F I Unaff. (%5 Aff. (%5 Fetal 40 39 39 98 Neonatal. 60 58 58 97 3 0-6 m. 26 19 19 73 27 6-12 m. 30 9 17 9 30 21 70 12-18 m. 43 13 13 21 49 22 51 18-24 m. 33 10 3 8 20 61 13 39 2-3 y. 30 15 50 15 50 3-4 y. 29 10 15 52 14 48 4-5 y. 15 4 12 80 20 5-6 y. 25 12 48 13 52 6- y. 26 12 0 35 17 65 8-10 y. 10 0 4 0 40 6 60 10-12 y. 4 0 50 50 12-14 y. 6 0 67 33 14-16 y. 1 0 0 56 44 16-18 y. 1 0 0 50 50 Totals 390 32 43 170 33 51 61 245 63 145 37 148 a single acute disease episode may have overpowe?'ed their defenses.

But a gTeater proportion of children in their second and third years show no stress markers.

Most children surviving their first three years presumably went on to adulthood, as older age groups are not well represented in the subadult mortality sample. Older children do show lesion remodeling and healing, supporting the hypothesis that those of stronger constitutions survive.

In the absence of bony evidence to the contrary, common infec tious diseases of the respiratory and gastrointestinal systems are assumed to have been the primary killers of Bubadults at Grasshopper, a situation not at all unexpected considering the ecological picture of the pueblo and what has been demonstrated of disease stress among modern

American Indians.

Of the 13 individuals recovered who died between ages 14 and

18, more females than males lack stress markers. Like many women of their mothers' generation, these young women may have lost their lives due to complications of pregnancy and thus contributed to the fetal mortality complement as well.

No significant relationship was found between sex and the presence/absence of stress markers (see Table 23). However, it must be borne in mind that sex assignments could be made on just 159 out of

390 subadults, and females predominate. No statement can be made as to whether males or females are more prone to certain stress markers. Table 23. Chi-square test of sex and stress markers.

Sex Present Absent Total

Male 33 32 65 Femal.e 51 43 94

Total. 84 75 159

X2 = .187, approximate level of significance = 0.70, df = 1. CHAPTER 6

INTRA ..SITE ANALYSIS OF CHANGE IN STRESS LEVELS

Search for the circumstances surrounding the abandonment of

Grasshopper Pueblo has underlain archaeological research at the ruin.

A number of changes in behavioral patterns towards the end of the aeou- pation period have been defined and are believed to be adaptive responses to a period of decreased rainfall, which certainly would have affected the subsistence base (Reid 1973, 1978; Longacre 1976; Tuggle and others 1983). Ciolek-Tarrelia and Reid (1974) have observed that over time household si:!.e, as approximated from hearth size, decreased at the pueblo. Similarly, the number of imported goods decreased. Reid

(1973, 1978) believes that added diversity in resources exploited by the pueblo inhabitants may be another response to a strain on the habitual subsistence base. He suggests an increased emphasis on hunting and collecting over time, but the sample of plant and animal data is such that no quantitative statements can yet be made (Olsen 1980).

Ciolek-Torrello (1978) and Reid (1973) have documented a simpli- fication of community organization units over time, from large, well- planned early construction units to the small dispersed outliers of the late period. In a like manner, Whittlesey sees a decline tbrough time in the elaborateness of burial treatment: HHigh energy grave treatment declines in burials associated" with later-constructed portions of the

150 151 pueblo. The absolute quantity of burial. goods and the ratio of arti facts per burial also decline through time" (Whittlesey 1978:226).

A second view, held by Grave.::, Longacre and Holbrook (1982:201), suggests that abandonment was preeipi tated largely by the failure of the community to adapt its socio-cultural organization as population size and density increased. They believe that abandonment of Grasshopper and contemporary pueblos "reflects the collapse of an entire system of in terdependent communities," and that collapse is not directly attributable to climatic fluctuations.

Thus far, no direct measure of environmental stress or its effect on Grasshopper residents has been devised. The behavioral re sponses defined in the archaeological record are several steps removed from the stress itself. Environmental fluctuations directly affect the food supply, which directly affects the health of the people, which may result in behavioral adaptations. When early attempts (Reid 1973, 1978) to test human responses over time to conditions of stress produced in conclusive results, this problem was temporarily set aside pending better environmental and skeletal data. Analysis of the hUl71an skeletal remains from Grasshopper brings the research one significant step closer to an answer.

The preceding chapter discussed the profile of morbidity and mortality for the subadults at Grasshopper. Skeletal evidence for physiological stress has been documented in just over one-third of these individuals. This analysis now partitions the skeletal sample into temporal and spatial groups to look for inter-group differences in 152 the type and severity of stress markerst from which much can be inferred about the nature of the precipitating stress.

Defini tieD of Groupings

Burials and the human skeletal remains contained wi thin are sequenced relative to one another by the construction history of the room in which the interment is provenienced. Tree-ring dates have fixed in time some of this history. Fourteen room construction phases have been delineated, based in large part on wall types (Reid, personal. com_ munication 1982; Reid and Shimada 1982). Most building was accomplished from A.D. 1300 to 1330, which includes construction phases (CP) 1. through 6 and ends with the conversion of Plaza 3 into the Great Kiva.

Construction phases 5 and 6 are over-represented in the archaeological record~ because the Great Kiva and surrounding rooms have been com pletely excavated. Room abandonment sequences have been determined based on the number of whole pots on the last utilized floor and the number of sherds per square meter of fill (Reid 1973j Ciolek-Torrello

1978). Early-abandoned rooms have little refuse on the last noor, but a high density of secondary refuse in the room fill. The situation is reversed in late-abandoned rooms. Two-thirds of the rooms excavated thus far have been designated as late-abandoned (Reid 1973, 1978j

Ciolek-Torrello 1978). stratigraphy of burial pits suggests that most room interments took place during occupation or shortly before abandon ment of the room.

The Great Kiva and rooms of early construction (cP 1 through 6) and early abandonment are, in this test, early rooms and the burials 153

contained within are early burial.s. Late-constructed (CP 7 through 14),

late-abandoned rooms yield late burials. Early-constructed, late

abandoned rooms are here labeled long term rooms. The j!lstification for

making a separate long term grouping 0 f rooms and burials, aside from

the temporal factor, is two-fold. It is suggested, since these rooms

were constructed early and maintained or reorganized through time appar

ently by the same household (Ciolek... Torrello and Reid 1974; Ciolek

Torrello 1978), that the inhabitants might somehow be privileged with

respect to resources. Other long term rooms seem to have retained a

single utilitarian function, such as Room 280, identified as a turkey

farm by the presence of eggshell fragments and the high frequency of

the bones of immature birds (Olsen 1980).

Plazas 1 and 2, test trenches, and outlying room blocks are

more difficult to sequence, though the outliers are generally considered

to have been constructed later than the main p'leblo (Reid 1973; Ciolek

Terrello 1978; Reid and Whittlesey 1982). There is no good architec

tural evidence by which to order Plazas 1 and 2, neither of which has

been more than half excavated, although it has been suggested that the

origins of Plaza 2 lie below the building surface assigned to CP 8 and

9 (Whittlesey 1978). A similar problem arises in reference to the

various extramural test trenches. To circumvent this difficulty,

skeletal material from plazas and test trenches is not included in this

phase of the intra-site analysis, and the 44 subadult burials within

are designated 'unclassified.' Table 24 lists the frequency of rooms

for each time period and the total number of subadul t interments which

are assigned to each period. 154

Table 24. Temporal classification of rooms and aubadul t burials.

No. of Excavated P.OO!!!5 wi th Subadul t Size of Subadult Time Period Burials Skeletal Sample

Early 13 108

Late 26 100

Long Term 26 138

Unclassified 44

Totals 65 390 155 Spatial groupings are less complex to delineate. There are

three main room blocks, ten small outliers, three plazas, one of which

is the Great Kiva, and several test trenches. Table 25 lists the fre

quency of rooms and burials for each spatial group_ Each of the three

main room blocks appears to have been established. hJ a distinct social

group, differing from each other with respect to architecture styles,

patterns of cranial deformation, mortuary :;ustoms, and distribution of

ceramic and artifact types (Graves and others 1982; Reid and \,lhittlesey

1982), as well as biological heritage (Birkby 1973, 1982). Room Block

2 is believed to be the residence of the pivotal 60cial group, as the

Great Kiva and the most sumptuous burials are located there (Reid and vlhittlesey 1982). Its large core construction unit (21 rooms) may

represent the movement of an entire village to what would become Grass hopper Pueblo (Graves and others 1982). It stands to reason, then,

that children in each social (that is, spatial) group may have been

exposed to different diets, diseases, and physical microenvironments.

Members of a kin group may share a susceptibility to certain conditions.

Differences across space may be as significant as differences through

time.

Two comparisons of spatial groupings are undertaken. The first

compares the subadults of Room Blocks 1, 2, and 3 to each other. The

second comparison pools these three groups under the guise of main

pueblo and contrasts this large group with the outliers.

Temporal and spatial groupings of rooms and skeletal remains

cannot be entirely separated from each other, since space (location of a room) is very much a function of time. All rooms in Room Block 2, 156

Table 25. Spatial classification of rooms and 6ubadult burials.

No. of Excavated Rooms with Subadul t Size of Subadul t Spatial Group Burials Skeletal Sample

Room Block 1 26 112

Room Block 2 15 89

Room Block 3 14 78

Outliers 10 30 Plazas. Great Kiva 0 58

Test Trenches 0 23

Totals 65 390 157 for example, are early-constructed and most are long term (Table 26), suggesting that this choice location was settled early on and remained under the control. of the founders and their descendants. All. outliers are l.ate-constructed and may have been built by young families budding off from the main pueblo. What is being measured then is a combination of factors, but this shoul.d not greatly affect the validity of the analysis. Rarely is just one factor responsible for change. Even if less food or less quality food were available as time went by. there would always be some social sector which had greater access to it. It is impossible to isolate the individual. effects of temporal and social or spatial factors. But it is these compl.ex interrelationships that make the study of the adaptability of a prehistoric community so inter esting.

The HYpotheses

The working hypothesis for this test is that skeletal. and dental stress markers will be more frequent or renect more severe metabolic upsets in subadults derived from the late period of occupation. Alter nate hypotheses recognize greater stress in the early period, or no differences between temporal. periods. If the working hypothesis is proven, a powerful measure of support is given to the archaeological suppod tion of increased stress. If the working hypothesis cannot be accepted on the basis of skel.etal biol.ogy. biocul tural exp1anations will be sought.

The second phase of the test involves an examination of spatial groups to see whether differences exist in response to stress among 158

Table 26. Temporal-spatial matrix of 6ubadul t burials.

Main Ruin Test BEl RB2 RB3 Plazas Out1.iers Trenches Total

Early 39 25 7 (GK)37 0 108

Late 39 0 31 30 0 100

Long Term 34 64 40 0 138

Unclassified 0 21 23 44

Total 112 89 78 58 30 23 390 159 room blocks or between the main pueblo and the outliers. Based on what is known archaeologically of these groups, it is expected that Room

Block 2 and the outliers should be most different from each other. Evi dence is gathered from data on demography and pathology. Again it is emphasized that correlations and differences which are not statistically significant may still be valuable if they highlight particular patterns within -the data.

The Test of Time

Demographic Factors

The age distribution for three temporal groups is presented in

Table 27 and illustrated by a mortality curve in Figure 23. To make the curve mot'e meaningful with small sample sizes, frequencies are expressed as percentages of each sample. The late curve is the most divergent, with a significantly lower percentage of infants and greater percentage of young children than expected. In the total subadult series of 390 individuals, 60% died in their first two years of life. Similar results are seen in the early sample (64%) and the long term sample (6%).

Infant mortality is markedly lower in the late group (49%). The decrease in infant deaths in this group is compensated for by an increase from ages three to six, so that by age six, mortality rates are more even.

The frequency of children under six years of age is 8% in the total sample, 80)6. in the early sample, 88% in the late sample, and 90% in the long term sample.

Mortality age distributions for early versus late are tested by the Kolrnogorov-Smirnov statistic. When children postnatal to 18 years 160

Table 27. Age distribution of subadults from temporal groups.

Early Late Long Term Age Group Period Period % Period %

Fetal 8.3 7.0 17 12.3 Neonatal 20 18.5 16 16.0 22 16.0 PN-l y. 18 16.7 13 13.0 24 17.4 1-2 y. 22 20.3 13 13.0 32 23.2 2-3 y. 4.6 8 8.0 11 8.0 3-4 y. 7 6.5 14 14.0 8 5.8 4-5 y. 2.8 7 7.0 2.9 5-6 y. 2.8 10 10.0 5.1 6-8 y. 10 9.3 7.0 4.3 8-10 y. 2.8 1.0 1.4 10-12 y. 0.9 1.0 o 12-14 y. 3 2.8 2.0 14-16 y. 3 2.8 1.0 3 2.2 16-18 y. 0.9 2 1.4 Totals 108 100 138

Kolmogorov-Smirnov Two-Sample Test Early v. Late n = 79 n = 77 D = 0.168 D.05 = 0.151 reject Ho of PN-18 yr.. (1-2 yr.) similar dis tribution

Early v. Late n = 39 n = 51 D = 0.304 D.05 = 0.213 reject Ho of 2-18 yrs. (5-6 yr.) similar dis tribution

D =Largest difference in relative cumulative frequencies. D.05 = Tabled value significant at .05 level. 161

••••••• EARl.Y ---- LATE 0-0 LONG TERM 20

F N 456 8 10 ~ K ~ ~ F-FETAL N-NEONATAL AGE IN YEARS

Figure 23. Mortality curves for temporal groups. 162 of age are compared, the maximum cumulative difference is seen at 1-2 years and is significant at p = .05. When the "noise" of infants is removed and children 2-18 years are compared, the maximum cumulative difference is seen at 5-6 years and is aga~n significant at p = .05. There is a statistically significant difference between mo!"tality age distributions of early and late groups. The implications of these dis tri butions become more clear as prevalence of the stress markers is examined.

The average number of subadul ts interred in a room decreased over time. Early rooms contain 5.46 children, long term rooms contain

5.31 children, and late rooms contain an average of 3.85 children. If indeed household size shrank over time (Reid 1973; Ciolek-Terrello and

Reid 1974j Ciolek-Torrello 1978; Reid and Whittlesey 1982), then these figures are not surprising.

Stress Markers

The prevalence of porotic hyperostosis, cribra orbi talia, tical bone loss, growth retardation, Harris lines, and linear enamel hypoplasia is noted for each temporal group, as summarized in Table 28 and briefly discussed below.

Poro'i:ic HYperostosis. Of the 15 children with porotic hyper ostosis, four are early, three are late, and eight are long term. Since less than 4% of the entire Grasshopper sample showed evidence of hyper ostosis, these figures, not surprisingly, are not significant.

Cribra Orbitalia. Fifty-four children had bony indications of cribra. Thirteen of these children are from early rooms, 13 are late, Table 28. Frequency of stress markers for individuals in temporal groups.

S tress Markers Total # Temporal Group Porotic Cribra Cortical Growth Harris Enamel Stress and Sample Size Hyperostosis Orbi talia Bone L088 Retardation Lines Hypoplasia Markers

Early (108) 4 (4/108,4%) 13 (12%) 13 (12%) 5 (%) 18 (17%) 7 (6%) 60

Late (100) 3 <:3%) 13 (1%) 10 (1(1%) 2 (2%) 17 (17%) 7 (7%) 52

Long Term (138) 8 (6%) 19 (14%) 16 (12%) 8 (6%) 12 ( 9%) 10 (7%) 73

.... !:.' 164

and 19 are long term. It is of interest to note that all four children

with co... occurrence of porotic hyperostosis and cribra orbitalia are from

l.ong term rooms, but this may be a function of larger sampl.e size and a

higher proportion of infants, the age group most affected by porotic

hyperostosis and cribra.

Cortical. Bone Loss. Of the 43 children identified as having

thinned femoral or humeral. bone cortex, 13 are early, 10 are late, and

16 are long term, proportionately lO.. l~ of the chi1dren in each group.

Wi thin each temporal. group t as in the subadul. t sample as a whole, the greatest proportion of children with cortical bone loss are

less than 12 months of age t and the long term group shows the greatest

percentage (10/1.6) of affected individuals in that young group.

Growth Retardation. Seventeen children are identified as having

femora significantly shorter than average. Included in this group are

five early children, two late children, and eight long term children.

Harris Lines. Transverse lines are observed in 17% of early and late children and ~ of long term children. Early and late groups can be distinguished by the index of morbidity, as calculated from the

tibia. The number of lines per bone is highest for late children (6.07)

and lowest for early children (4.64). Long term children fall in be

tween, at 5.6 lines per bone.

Table 29 displays the age of formation of Harris lines in the

three temporal samples. The maximum number of lines is observed among late children, and especially among 4-8 year aIds. Though this period 165

Table 29. The association of tibial transverse line frequency and age of 1ine formation for temporal groups.

Temporal AD of "Line Formation Total. -# Group 0-21 2-4Y' 4-8 y 8-12 y 12-18 Y Lines

Early (",,18) 13 (.20) 7 (.11) 23 (.35) 19 (.29) 3 (.05) 65

Lat. (",,17) 5 (.06) 26 (.31) 45 (.53) 9 (.11) 0 85

Long Term 12 (.21) 18 (.32) 26 (.46) 0 0 56 (",,12)

Number of l.ines formed in each period is given along with.percentage of total lines counted for each teniporal group_ 166 is alao the peak time of line formation in early and long term children, a smaller percentage of total lines are formed then.. Early and long term are distinguished from late by having nearly one-quarter of lines forming in the first two years, but this can be explained by the fact that these two skeletal samples contain more infants (Table 27). A sizeable proportion of lines form in late childhood in the early sample, but 10/19 of these lines belong to one child, the boy with Perthes'

Disease from Burial 191. The early group is the only one showing line formation in adolescence, but of the three groups, the early sample c::rhtains the greatest proportion of subadul ts in that age group.

Linear Enamel HyPoplasia. Among early children, four are affected with LEH in the decidu,DllS and three in the permanent dentition.

Late children show five affected deciduous dentitions and two permanent.

Long term children are affected in eight sets of deciduous teeth and two sets of permanent. Of the six most severe cases of deciduous LEH, two children are from each temporal group.

Summary

Table 30 displays the number and proportion of subadults in each temporal group with 0, 1-2, or 3-4 stress-induced pathologies. The long term group is most different, having the greatest proportion of members with no stress markers. On the whole, children in the long term sample are younger than those in either the early or late samples, and may not have had enough time to develop stress markers. But four children in the long term group have 14 stress markers among them. The ratio of stress markers per person is consequently greatest for long term 167 Table 30. Number of individuals with stress markers in temporal groups.

o stress 1-2 Stress 3.... Stre.. Temporal Group Markers % Markers % Markers % Total

Early 63 58 43 40 loB Late 58 58 41 41 1 100 Long Term 88 64 46 33 4 3 138 168 children, 1.46, followed by 1.33 for early children, and 1.24 for late children.

If the stress markers are considered in age-specific terms as was illustrated by Figure 22, then it can be said that long term chil dren have the highest frequency of stress markers of infancy, and late children have the highest frequency of stress markers of young child hood. Children from the early group are more varied.

The main thrust of this comparison is between children dying early in pueblo history and children dying late in the occupation. Dif ferences exist, but they are Bubtl.e and not one-sided. In demographic terms, the sample sizes are nearly equal, but the early group has sig nificantly more 1-2 year aIds, while 5-6 year aIds are more common in the late group_ The relative abundance of young children in the late group may account for the frequency of stress markers of childhood documented for this group. Late children are more severely affected by

Harris lines; fewer children have lines but there are more lines per affected child. Although it has not been demonstrated that the level of stress was higher in later times, it may be that there was a quali tative rather than a quantitative change in stress, a difference in type rather than in level of stress. Since the late group contains children who lived at a pueblo which had been intensively occupied for at least 50 years, we may be seeing the effects of resource depletion, short-term food shortages, or an ell-time low in sanitation, any of which could lead to increased disease frequency. 169

To better understand the nature of stress and physiological response in Grasshopper Pueblo subadults, it is necessary to look at spatial groups which, in most cases, crosscut temporal gt'Oups.

The Test of Space

Demographic Features

Table 31 and Figure 24 present the age distribution of five spatial groups, Room Blocks 1, 2, and 3, the plazas including the Great

Kiva, and the outliers. The percentage of subadults below the age of two years in each group is ~ for HE 1, 71% for RB 2, 6% for RB 3,

5:% for plazas, and 47% for outliers. The percentage of subadults below the age of six years is 84% for RB 1, 91% for RB 2, 91% for RB 3, 71% for plazas, and 90% for outliers. The plazas contain a slightly older group of children, a1 though all the young ages are represented in the sample. It can be seen that the peak at three to four years in the late mortality curve (Fig. 23) is due in large part to the children from out liers; 20'% of the children recovered from outliers are between three and four years of age. To test the likelihood of chance distribution, the Kolrnogorov-Srnirnov statistic was used to compare mortality profiles of room blocks and outliers to each other. Results are presented in

Table 32, tests 1-6. Test 1 is significant, tests 3 and 5 nearly so at p = .05. The similarity of RB 2 and 3 (test 2) may be attributed to the fact that both are in the large West Room Block, Which could also explain the difference between these room blocks and RB 1 (tests 1 and

3). Test 5 proved equivocal. These two proveniences (RB 2 and outliers) should be most different, based on archaeological and biological 170

Table 31. Af!.e distribution of 6ubadults from spatial groups.

Room Room Room Age Block 1 % Block 2 % Block 3 % Plazas % Outliers % Fetal 12 10.7 9.0 10 12.8 3.4 6.7 Neonatal 16 14.3 17 19.0 16 20.5 13.8 13.3 PN-l y. 15 13.4 18 20.2 9 11.5 15.5 20.0 1-2 y. 18 16.1 20 22.5 19 24.3 12 20.7 6.7 2-3 y. 10 8.9 6 6.7 3 3.8 3.4 13.3 3-4 y. 8.0 6 6.7 5 6.4 6.9 20.0 4-5 y. 7.1 2.2 3.8 1.7 0 5-6 y. 5.4 4.5 7.7 5.2 10.0 6-8 y. 10 8.9 1.1 3.8 12.1 10.0 8-10 y. 6 5.4 2.2 3 5.2 0 10-12 y. 0.9 1.3 0 0 12-14 y. 0 1.3 3.4 14-16 y. 0 3.4 2.6 6.9 16-18 y. 0.9 2.2 1.7 0

Totals 112 89 78 58 30

Does not include 23 individuals from test trenches. 1'/1

25 0

ROOMBLOCK I ROOMBLOCK 2 0--0 IOOOM9lOCK 3 20 '" PLAZAS '" OUTLIERS ..... Z '"~ 15 '"Cl. '"

F N 4 5 I. f-FETAl It_NEONATAL AGE IN

Figure 24. Mortality curves for spatial groups. 172

Table 32. Kolmogorov-Smirnov tests of mortaJ.i ty age distributions.

Test No. Comparison D.05 Ho

BE l:RB 2 .164 .142 reject n = 112, 89 Fetal-1S yr.

R'fI 2:RB 3 .052 .151 retain n = 89, 78 Fetal-18 yr.

3. HE l:RB 3 .148 .151 equivocal n = 112, 78 Fetal-18 yr.

4. HE 1:0utliers .077 .242 retain n = 112, 30 Fetal-18 yr.

5. RB2:0utliers .241 .242 equivocal n = 89, 30 Fetal-18 yr.

6. RE 3:0utliers .225 .242 retain n = 78, 30 Fetal-IS yr.

7. HE 2:0utliers .283 .242 reject n = 84, 30 Fetal-IO yr.

8. RB l:Outliers .15 .242 retain n = 110, 30 Fetal-IO yr.

9. RB 3:0utliers .263 .242 reject n "" 74, 30 Fetal-IO yr.

D = Largest difference in relative cumulative frequencies. D.05 = Tabled value significant at .05 level. Ho = No significant differences in sample distributions. 173 evidence. The test was recomputed counting only children less than 10

years of age, since no child older than that was recovered from out

liers. This time. a significant result was obtained (test 7). The test

was similarly recomputed for BE 1 and 3 (tests 8 and 9), yielding one

significant reaul t. In sum, Room Blocks 2 and 3 are most similar to

each other, both are different from RB 1. Room Block 2 and outliers are

most dissimilar.

Besides having the smallest sample size (30) and the least

number of rooms excavated (10), the outlier group also has the lowest

ratio of Buhadult interments per room (3). The highest figure is from

Room Block 2, with an average of 5.93 children per room. Room Block 1

averages 4.31 and Room Block 3 averages 5.57 children per room. Room

Block 1 has the most excavated rooms (26). Outlying rooms are notice

ably smaller (Reid and Whittlesey 1982). Again, it is evident that the

outliers contribute most to the configuration of the late group. stress Markers

Table 33 displays the prevalence of each stress marker for the

spatial groups, the results of which are discussed below.

Porotic Hyperostosis. Ten children from Room Block 1, four

from Room Block 2 and one from Room Block 3 have this condition. Porotic hyperostosis is not seen in children from outliers or plazas.

Cribra Orbi talia. Cribra is seen in 18 children from RB 1 t 12

children from RB 2, and 10 children from RB 3. Two children from out

liers and seven from plazas also have cribra. Of the four children Table 33. Frequency of stress markers for individuals in spatial groups.

stress Markers Total # Spatial Group Porotic CrUra Cortical Growth Harris Enamel Stress and Sample Size Hyperostosis Orbitalia Bone Loss Retardation Lines Hypoplasia Markers

RB1 (112) 10 (10/112=9%) 18 (1$%) 13 (12%) 4 (4\1» 15 (1:%) 8 ( '/%) 68

BB 2 ( 89) 4 (4\1» 12 (1:%) 7 ( &>\) 7 (&>\) 9 (1OJi) 2 ( 2%) 41

RB3 ( 78) 1 (1%) 10 (1:%) 9 (12%) 2 (:%) 5 ( $%) 8 (10%) 35

Plazas (;8) 0 7 (12%) 9 (1$%) 2 (:%) 9 (19)1) 5 ( 9%) 32

Outliers (30) 0 2 ( '/%) 4 (1:%) 0 10 0:%) 5 (10%) 19

~ 175 with co-occurrence of cribra and porotic hyperostosis, two each are from Room Blocks 1 and 2.

Cortical Bone Loss. Thinned cortex was earlier defined as being one standard deviation below the mean cortex width for the humerus and femur. Included in this category are 13 children from HB 1, seven from

RB 2, nine from RB 3, four from outliers, and nine from plazas.

Growth Retardation. The greatest proportion of children with short femora derive from HB 2, with seven affected children. Room Block

1 has four short-boned children, RB 3 has two, and the plazas have two.

No child from outliers had short femora for his dental age. This could imply that children from outliers have retarded dental development, but in all likelihood, the lack of children with this stress marker is due to a small sample size. Just 17/390 subadults are classified as growth retarded, so the probability of an outlier child showing this stress marker is minute.

Harris Lines. Transverse lines are especially common in out liers, affecting one-third of children in that sample. This is the greatest incidence of a stress marker for any temporal or spatial group.

Nineteen percent of total Harris line incidence is found in children from outliers, who constitute less than 8% of the total skeletal sample.

Nevertheless, outlier children do not show the greatest index of mor bidity. The maximum number of lines per tibia is seen in RB 1 (5.85), followed by outliers (4.8), RB 2 (4 .. 22), and RB 3 (2.6).

Lines appear to form later and stop earlier in outlier children

(Table 34), but no child older than eight years of age has been 176

Table 34. The association of tibial transverse l.ine frequency and age of line formation for spatial groups.

Spatial A~ of Line Formation Total # Group 0-2 y 2-4 Y 1;:8 y 8-12 y 12-18 Y Lines

Room Block 1. 4 (.05) 27 (.35) 32 (.42) 13 (.17) 76 (n = 13) Room Block 2 11 (.29) 12 (.32) 14 (.37) 0 0 37 (n = 9)

Room Block 3 7 (.54) 3 (.23) 2 (.15) 1 (.08) 0 13 (n = 5)

Outliers 4 (.08) 30 (.42) 24 (.50) 1 (.02) 0 59 (n = 10)

Number of lines formed in each period is given aJ.ong with percentage of total lines counted for each spatial group. 177 recovered from outliers. The skeletal sample from HE 3 contains more lines formed in infancy, RB 1 shows more lines formed in late childhood.

Linear Enamel HyPoplasia. LEI{ was observed in eight children from RB 1, two children from RB 2, eight children from RB 3. three children from outliers, and five children from plazas. Of the six most severely affected deciduous denti tiona, two are from each room block.

Summary·

The greater percentage of the skeletal sample from RB 2, HB 3. and the plazas have no stress markers (Table 35), and no child from

HE 3 had more than two stress markers. The average number of stress markers per person is greatest for the plazas (1.60) and lowest for

Room Block 3 (1.3). The other groups fall in between: RB 2 = 1.58,

RB 1 = 1.45, outliers = 1.36. The outlier group, with one-half the popUlation of the plazas, one-third the popUlation of RB 2, and one fourth the population of RB 1, actually has proportionately more stress markers. Table 36 presents the probabilities of outlier children having any of the stress markers, based on their frequency in the total sub .. adult popUlation. With only a 0.011 chance of having even the most com mon stress marker, the morbidity picture of outlier children becomes even more impressive.

It is apparent that the configuration of stress markers in the late group is greatly influenced by the outliers. To test this more directly, it may be useful to subdivide the late group of 100 subadults into two components, main pueblo (n = 70) and outliers (n = 30). 178

Table 35. Number of individuals with stress markers in spatial gt"oups.

o Stress 1-2 Stress 3 .. 4 Stress Spatial Group Markers % Markers % fJfarkers % Total

RBl 6~ 57 ~5 40 3 112 RB 2 63 71 22 25 89 RB3 51 65 27 35 0 78 Plazas 38 65 19 33 58

Outliers 16 53 13 ~, 3 }O

Table 36. Probability of stress marker incidence among outlier sub adul.ts.

Occurrence in Actual stress Grasshopper Theorized Occurrence Occurrence in Marker Sample in Outlier Sample Outlier Sample

Porotic Hyperostosis 15/390 = .038 (15/390)(}o/390) = .003

Cribra Orbitalia ~/390 = .138 (~/390)(30/390) = .on .067·

Cortical Bone Loss ~3/390 = .no (~3/390)(}o/390) = .008 .133'

Linear Enamel Hypoplasia 28/390 = .072 (28/390)(}o/390) = .005 .100·

Growth Retardation 17/390 = .0~3 (17/390)(}o/390) = .003

Harris Lines 53/390 = .136 (53/390)(}o/390) = .010 .333'

·Used in computation of chi-square comparison of observed versus expected occurrence. )(2 = 1~.~8 )(2.05 at df = 3 = 7.815 Ho = reject 179 Table 37 displays the now familiar matrix of provenience and stress markers, tallying the occurrences of each stress marker for in dividuals in each spatial group. Fourteen children from outliers are affected as compared to 26 affected children from the main pueblo, which yields a stress marker to person ratio of 1.36 for outliers and

1.27 for the main pueblo. One child from the outliers is the only late child with 3-4 stress markers (the child from Burial 503 has three markers). Were late main p'jeblo children affected in the same propor tion as outlier children, 33 main pueblo children should have stress markers, seven more than observed.

~ The goal of this analysis has been to elucidate differences in stress marker occurrence and severity among temporal and spatial group ings of subadul t skeletal material from Grasshopper Ruin. The analysis was formulated to test hypotheses developed by archaeologists which suggest that life at the pueblo became increasingly stressful as occu pation span lengthened. In all likelihood, a major component of this stress was an environmental change. No attempt has been made here to define the nature of the environmental stress. The focus has instead been on physiological, rather than behavioral, responses to that stress, as recorded in the bones and teeth of growing children.

No clear pattern emerged among temporal groups, although acute stress markers, especially Harris lines, are more severe in late chil dren. Striking differences between early and late should not be expected, however, because the early settlers of Grasshopper were the Table 37. Frequency of stress markers for components of late group.

stress Markers Total # Spatial. Group Porotic Cribra Cortical Growth Harris Enamel Stress and Sample Size Hyperostosis Orbitalia Bone Loss Retardation Lines Hypoplasia Markers

Outliers (30) 0 2 ( 7Ji) 4 (13%) 10 (33%) 3 (10;11) 19

Main Pueblo RB 1 and 3 (70) 3 ("%) 11 (16%) 6 ( 9%) 2 (3%) 8 (10;11) 4 ( 6%) 38

~ 181 late residents of their former pueblo(s). The events l.eading to abandon_ ment of their prior home may have been similar to those which eventually led to the abandonment of Grasshopper, and there may have been similar physiological stresses.

More information is gained if spatial groups are analyzed, especially spatial components of the late group. Children from out liers show a disproportionate amount of stress. Again, Harris lines are the most striking, reflecting a qualitative rather than quantitative change in stress patterns and affecting especially children 4 .. 8 years of age. All temporal and spatial groups are more or less equally affected by chronic stresses, especially those of infancy. Outlier children show more acute stress, in a repetitive but not ,cyclical pat tern. The physiological stress may be traceable to increased contami nation of site environs, increased susceptibility of nutri tionally compromised children, or a combination of these and other factors.

The biological data suggest that the spatial provenience of the outliers is a more influential factor than is the temporal provenience t since children from late rooms of the main pueblo do not suffer a com parable morbidity. The lateness of the outliers implies that important resources may have been depleted or unavailable due to environmental changes. The segregated spatial placement of the outliers suggests that their inhabitants were somehow different and perhaps low on the social register. Architectural evidence from outliers indicates that jacal walls were built upon low masonry foundations (Reid 1973; Ciolek

Torrello 1974). At that elevation, occupation of outliers would cer tainly have been confined to the warmer seasons. Perhaps an important 182

aspect of the stress inflicted on children buried in outliers has to do

with yearly migrations between Grasshopper Pueblo and their winter habitation site (Reid 1973; Graves and others 1982).

This physical anthropological analysis has augmented what is

currently known about life at Grasshopper Pueblo and how it changed over

time. The aforementioned behavioral responses are better understood

when seen in conjunction with increased severity of childhood illness

over time and especiallY in the outliers. Additional skeletal and

cultural evidence from the Dutliers is necessary to formulate stronger

statements of stress and response.

The situation at Grasshopper is not unique, but what distin

guishes this 6i te is the multidisciplinary investigation. This analysis has been the first to test physiological responses to stress as a part

of this ongoing research program. Having demonstrated the validity of

such an approach, it is anticipated that human skeletal remains will

increasingly be used as an independent data source to test other archaeological hypotheses. CllAPTER ?

CONCLUDING STATEMENTS

The purpose of this dissertation research has been to evaluate the measurable skeletal indicators of physiological stress in growing children from. Grasshopper Pueblo and to use this information to develop a broader picture of community health. In particular, this research has tested an archaeologically-deri'T,'ed hypothesis which suggests that increased enviromnental stress towards the end of the occupation span led to eventual. abandonment of the pueblo.

The test was initiated by dividing the Bubadu1t sample into temporal and spatial groups, based on cultural evidence, and observing patterns of disease stress. Once the kinds of disease stress had been identified, their l.ikel.y causes could be inferred, with the help of ethnographic and clinical reports of health and sickness. It was an tiCipated that, if the archaeological hypotheSis is accurate, increased evidence of malnutri tiOD or disease would be imprinted on growing bone of later inhabitants.

Infant mortality in all groups was high, a not unexpected find ing, given that high death rates in the first two years of life are reported in most undeveloped areas today. Weaning on inappropriate foods t corresponding gastrointestinal upsets, and upper respiratory infections are most often cited as causes of death, and there is no 184 reason not to believe that these factors were as common or more so in a

14th century pueblo. Otherwise, the disease l.oad appears to have been light. Just 37% of Bubadul ts had one or more of the six stress markers evaluated here, suggesting that chronic or acute poor health was not pervasive.

Among the temporal and spatial groups, skeletal indicators of chronic physiological stress due to malnutrition or parasitism, remain fairly constant. But in children from the late period, and especially those recovered from outliers, the frequency of Harris lines, markers of recurrent acute stress, is unexpectedly high. Both the temporal and the social setting of the outliers aid in interpretation of this find ing. Influential factors include an increased population density at the main pueblo, environmental fluctuations which would affect the type and availability of food, probable seasonal occupation of outliers, and localized contamination of site environs. Disease incidence must have risen, as physiological resistance weakened.. These conclusions are subtle and suggestive, whether considered on their own merits or added to cultural changes previously documented by archaeologists, but the small sample size of human skeletal remains from outliers impedes a stronger statement ..

The significance of this research obtains at Grasshopper and in the Southwest as a culture area, since local prehistory is filled with episodes of pueblo establishment and abandonment. This dissertation represents a major effort to· integrate biological and archae ological data, synthesizing the results of skeletal analysis with what is known of settlement patterns, social organization, subsistence 185 strategy, and environmental conditions at this site. Such an analysis has been possible with the Grasshopper skeletal material becauee of the rnul tidiscipli:il8.Ty nature of ongoing research and because archaeologists at Grasshopper have followed an enlightened program of burial recovery t making this series one of the finest and certainly the best cared for prehistoric collection west of the Mississippi. Southwestern archae ology suffers from a definite I ceramicocentrism .. I Such an attitude is not surprising, as ceramics are plentiful and beautiful, but it can prove detrimental to the recovery of htllilan skeletal remaina. Oftentimes, reaching the room noor terminates excavation, and little attempt is made to identify eubfloor burial pits. Other times, when burials are recovered, they are thought of more as recepticles for grave goods than for human remains. It is hoped that this dissertation will alert other archaeologists and physical anthropologists to the mutual research benefit of joining forces.

Since it appears unlikely that this skeletal collection will be increased, even though excavation continues, and since the future of many such collections is threatened by uninformed excavation or reburial policies, it is imperative to make full use of this and other skeletal series for the .... eal th of scientific kno .... ledge they hold about past popu lations. The research potential of this series has barely been tapped.

Some suggestions for future work follow.

1. An intensive biological analysis is needed of adults in these same temporal and spatial groups, to observe the effects of childhood disease on adult health and longevity. 186 2. A D':ultivariate analysis of the many intercorrelatioDS of age,

sex, provenience, and stress markers could be undertaken, in order to make stronger statements of distribution and possible predisposition to

physiological effects of external stress.

3. A continuation of the demographic simul.ation studies begun by

Longacre (1976) might allow an estimation of actual mortality rates and measurement of the effects of immigration.

4. When sectioning of bone and teeth is undertaken, studies can be made of bone densitometry and trace mineral content. Microscopic analysis may reveal patterns of lesion development and severity.

This dissertation could well serve as a model for work at other sites and with other skeletal series. APPENDIX A

TEMPORAL AND CULTURAL AFFILIATION OF SITES MENTIONED IN TEXT

187 Grasshopper Pueblo, AZ A.D. 1275-1400 Mogollon agriculture, hunt, collect Indian Knoll, KY 8000-2000 B.P. Archaic shell midden hunt, collect Libben, OB A.D. 800-1100 Late Woodland hunt, marginal agriculture Eiden, OB A.D. 1~90 t 55 agriculture Dickson Mounds, IL Woodland component A.D .. 900-1050 hunt, collect Transi tional 1050-1150 Mississippian 1150-1,50 agriculture Arroyo Hondo Pueblo, NM A.D. 1,00-1~20 agriculture Hardin Village, KY A.D. 1500-1675 Fort Ancient Tradition agriculture Pecos Pueblo, NM several components A.D. 1100-1838 agriculture Mesa Verde, CO A.D. 1100-1450 Anas8zi agrioul ture Point of Pines, AZ A.D. 1250-1450 Mogollon agriculture Turkey Creek pueblo, AZ A.D. 1000-1250 Mogollon agriculture Kinishba Pueblo, AZ A.D. 1250-1325 Mogollon agricu1 ture Chavez Pass, AZ A.D. 1200-14-50 (Pueblo) agriculture Arikara Sites, SD A.D. 1700-1750 agriculture Nubian Cemeteries, Sudan Meroi tic component 350 B.C.-A.D. 350 agr:f.cul ture X-Group A.D. 350-550 agricu1 ture Christian A.D. 550-1400 agriculture Lower Illinois Valley Sites Middle Woodland component 100 B.C.-A.D. 500 incl. Klunk, Gibson, Gay hunt, collect Late Woodland component A.D. 500-1000 incl. Ledders, Schild, Klunk, Gibson, Gay, Koster, Yokem transition to agrioul ture Mississippian component A.D. 1000-1650 inola Schild, Yokem agrioul ture 8i APPENDIX B

SKELETAL INVEN'l'ORY

!!l' N = neonate, M = Male, F = Female, LT = Long term, GK = Great Kiva, HI. = Rarris Lines, CO = cribra orbitalia, PH = porotic hyperostosis, LEH = linear enamel hypoplasia, OBI. = cortical bone loss, GR = growth retardation, P = other pathology, A = other anomal.y, RIYr = retained deciduous teeth, FT = fused teeth, PI' = pegged teeth, ESC = early suture closure, C = dental caries, PMT = paramolar tubercles, LT = l.iDgual tubercles, SST = supernumerary tooth, CC = Carabelli's cusp, I = Inca bone, KO = Kerckringl 8 ossicle.

Burial Dental Number Age &- Sex Chart X-ray Anomalies PatholOgies Provenience

4 3-4y F IlL Test pit 11 12-1& M Broadside 12 18-24m F CO Broadside 13 5-6y x CO, HL Broadside 18 3-4y F x RB 1, Late 21 8-9y M x x RIl'l' IlL RB 1, Late 22 3-4y F x x OUt, Late 23 o-6m x CBL Out, Late 24 3-4y F x IlL Out, Late 27 6-7Y M x LEII Test pit 28 6-12m x CBL RB 1, LT 29 0-600 x RB 1, Late 31 12-1Bm x x For cm. Out, tate 32 6-7y F x x LEII, IlL Out, Late 33 12-1Bm M x CO RB 1, LT 34 18-24m x Broadside 368 5-6y F x Ct CO Broadside 37 18-24m M x IlL Broadside 44 N x Broadside 45 4-5Y F x RB 2, LT 46 N x RB 2, LT 47 0-6m x 1m 2, LT 48 12-1Bm F x RB 2, LT 49 12-1Bm F RB 2, LT 54 6-7Y F x x IlL RB 1, Early 55 N x RB 2, LT 58 7-8y x PT CO,IIL RB 1, tate

189 190

Buria1 Danta1 Rumbe!" Age & Sex Chart X-ray Anomalies Pathologies Provenience

59 12-1Bm F x RB 1, Late 60 5-6y M x HL RB 1, Late 61 6-12m " liB 1, Late 62A Fetal x RB 1, Late 66 o-6m F PH,CO,CBL 1m 1, LT 67 6-7y F x "x HL,CBL,GR RB 1, LT 69 l?-lBm x CO GK, Earl.y 7C 12-1Bm x GK, Early 71 12-1Bm F x CO GK, Early 72 6-7y F x x ESC CBL GK, Early 73 12-147 H x x Pr GK, Early 75 Fetal OK, Early 78 9-107 F x x C GK, Early 85 0-6.. Plaza 1 86 N RB 2, Early 87 5-6y x Plaza 1 90 3-4y F x FT GR Test Pit 92 8-9y M x Plaza l. 9311 Fetal x Plaza l. 94 6-7y F x x C, CO, HI. Pl.aza 1 95 N x Git, Early 96 0-6m x PH 1m 2, Early 97 12-24m F x x CO, CBL GK, Early 99 N x Plaza 1 lOCA N x OK, Early 100B 12-18m x GK, Early 102 6-12m GK, Early 106 18-24m x GK, Early 107 18-24m x x me, EarJ.,. 109 7-87 M x x C, HL Plaza l. no 6-12m x FT RB 2, Early nl 3-4y F x x FT GK, Early 117 7-Sy M x x RB 2. Early u8 N x x P RB 2; L-T 119 N x GK, Early l2lA Fetal 1m 2, L-T 122 6-12m x CBL GK, Early 123 18-24m F x x GR,HI. GK. Earl.y 124 3-57 x PMT C RB 2, L-T 125 18-24m F x PMT 1m 2, L-'r l28A 15-167 F x GK, Early 130 5-67 F x x FT,Pr HL. eBI. RB 2, L-T 131 6-12m x RB 2, L-T 132 5-6y M x x PT GR, Early 134 12-1Bm x x RB 2, L-T 136 12-1Bm x GK, Early 137 12-1Bm PT RB 2, L-T 191-

Burial. Dental Number Age &: Sex Chart X-r~ Anomalies Patho1ogies Provenience

138 II :rm 2, L-T 139 Fetal. " RB 2, 1.-'1' 146 o-6m " GK, Early 147 5-6m F x " x BL lIB 2, L-T 148 II x CBL, GR RB 2, L-T 149 12-1Bm F RB 2, L-T 151A o-6m " x" RB 2, L-T 15lB 0-6. GR RB 2, L-T 152 15-17)' M x " LEB,C,BL GK, Early 153 6-7)' F x " LEB,CO,HL GK, Early 154 6-1211 " GR RB 2, L-T 156 II " FT RB 2, L-T 157 6-1211 " CBL RB 2, L-T 159 o-6m "x FT RB 2, L-T 160 0-611 GK, Early 161 6-12. " RB 2, L-T 167 6-1211 PH,CO,CBL,GR RB 2, 1.-'1' 170 18-2411 M x " RB 2, 1.-'1' 172 3-4y F "x C, CO, P RB 2, L-T 173 o-6m " x CBL, GR GK, Earl.y 176 II OK, Early 179 2-37 F "x C, LEH, CBL OK, Early 181 12-18m x GK, Early 182 6-7y M x C, HL, CBL GK, Earl,. 183 6-120 " GK, Early 186 5-6y GK, Early 189 12-1Bm M " x GK, Early 191 12-14y M x x C, HL, P GK. Early 192 II x GK, Early 193 6-7y x C t m. GK. Early 197 16-17y F x x" HI. GK, Early 202 5-6y Test Pit 204 2-37 x CO,m.,CBL,GR Test Pit 207 II RB 2, Earl,. 213 6-12m CBL RB 2, Early 214 5-6y M C, HI. RB 2, L-T 215 II x RB 2, Earl.y' 218 II x RB 2, Early 219 II RB 2, Early 220 12-1Bm x" KO RB 2, L-T 221 18-2411 co RB 2, L-T 223 Fetal RB 2, Early 224 4-51 x CO RB 2, Early 229 6-1211 "x CO RB 2, Early 234 12-18m M KO CO 1m 2, L-T 235 0-6m M x" RB 2, L-T 192

Burial Dental Number Age & Sex Chart X-ray Anomalies Pathologies Provenience

237 6-7y M x HI. RB 2, L-T 238 N RB 2, L-T 239 6-12m RB 1. Late 240 3-4y F x KO RB I, Late 241 18-24m x PMT PH,HI. RB 2, Early 242 5-6y F x C RB 2, L ..T 243 24-3Om F x Fl' RB 1, Late 244 Fetal RB 1, Late 247 18-24m F RB 2, L-T 248 14-17y M c RB 2, L-T 249 3-3.5y C RB 1, Late 250 9-1Oy F RB 1, Late 251 Fetal RB I, L-T 256A N RB 1, Early 25GB 2.5-3y CO, GEL RB 1, Early 259 8.9y M co RB I, Late 261 2-3y M HB 2, L-T 265 11-12y F co Test Pit 266 6-12m Test Pit 268 Fetal Test Pit 273 12-14y F Test Pit 277 Fetal Test Pit 281 18-24m F Test Pit 282A 18-24m Test Pit 282B 2-2.5y M Test Pit 284 9-1Oy F HI. HB 1, Late 285 7-8y F C RB 1, Late 289 18-24m M x PT LEH, CO RB 1, Early 290 9-10y F x C, GR RB 1, Early 292 N x RB 1, Late 293 0-6m x RB I, Early 294 Fetal RB I, Early 297 3-4y F RB 1, Late 300 6-12m RB I, Late 301 4-5y F Fl' HB 1, Late 303A 4-5y RB I, Late 304 6-12m CO RB I, Late 305 7-8y F ESC C RB I, Early 3Q6 5-6y x c RB I, Late 308 N x RB I, L-T 309 6-7y F C, CBL HB I, Late 310 Fetal RB 1, L-T 313 6-12m PH, eBL RB I, Early 315 4-5y Pr RB I, Late 316 12-18m CO RB I, Late 320 3-4y F x PH, P RB I, L-T 321 3-4y F x HI. RB 1, L-T 193

Burial Dental Number Age &: Sex Chart X-ray Anomalies Pathologies Provenience

322 9-1Oy F x HL, eBL RB 1, Earl.y 332 1O-11y M x Test Pit 334 3-4y F Plaza 2 337 5-6y F BE 1, Late 338 16-18y F x RB 1, L-T 339 4-5y c BB 1, L-T 34C 6-12m PK RB 1, L-T 342 2.5-3y RB 1, L-T 343A N x BE 1, Late 343B 0-6m x KO PM RB 1, Late 347 Fetal x HE 1, LooT 348 6-12m HE 2, L-T 349 N BB 1, Early 350 12-18m M x PMT RB 1, Early 351 Fetal RB 1, Early 360 Fetal RB 1, Early 361 9-1Oy F x ESC, PT C, HI.. Test Pit 362 12-18m x RB 2, L-T 363 17-19y M LEI! Teet Pit 365 N RB 1, Early 366 2-3y M CO BB 1, Late 368 2-3y F P RB 1, Late 369 2-3y M ESC HL RB 1, Early 370 5-6y F CO, GR RB 1, Late 371C 5-6y RB 1, Early 376 2-3y FT co HE 1, Late 37% Fetal BE 1, Early 378 N RB 2, L-T 379 4-5y x HE 1, Late 384 3-4y M x PT e, HL RB 1, Late 385A N RB 1, Late 385B N RB 1, Late 387 Fetal RB 2, L-T 389 2-3:\' PH RB 1, Late 390 N RB 1, Late 394 N RB 2, L-T 395 12-18m M co, eBL RB 1, L-T 396 N KO RB 1, L-T 397 12-18m x PT RB 1, L-T 398 6-12m M eEL RB 1, L-T 401 18-24m LEH, co RB 1, L-T 402 N HE 1, LooT 403 N RB 1, L-T 404 Fetal RB 1, L-T 407 11-12y F LT RB 3. Late 408B 6-7Y RB 1, L-T 194

Burial Dental Number Age & Sex Chart X-r~ Anomalies Pathologies Provenience

lfo9 12-1Bm PH RB 1, L-T 411 2.5-31 x x" C 1m 1, L-T 41} 4-57 M x x ESC ,SST CO RB 1, L-or 414 5-4,- M x pr RB 1, L...Jr 418 5-6y x C, LEU 1m 3. Late 419 2-31 M x LESt CO 1m 1, L-T 420 5-47 x " pr at co RB 3. Late 421 Fetal. x 1m 2, Early' 422 12-1Bm F x x IlL 1m 1, Early 42} 10-117 F x x CBL, BL RB 1, Early 424 5-67 x CO RB 3. Late 425 5-47 F x x CO RB 2, Early 427 1m 1, Early 428 II "x PH lIB 1, Early 429 "Fetal RB 1, Early 4}O 4-57 F x "x pr RB 1, Earl,. 4}1 O.. 6m x CBL 1m 1, Early 4}2 6-7'1 M x x P, IlL RB 1, Ear17 4}} RB 1, Early 4}4 "12-18m x x CBL 1m 1, Early 4}6 II x RB 3. Late 4}8 II x RB 1, Early 439 5-67 x x ESC,PT CO RB 3. Late 440 12-1Bm x LEU 1m 3. Late 441 14-157 M x " x Lor HL, CBL 1m 3. Late 442 12-1Bm H x pr PH,IIL 1m 3, Late 443 5-47 M x "x IlL RB 3. Late 444 Fetal RB 3, Late 445 0.6m " RB 1, Earl.,. 446 5-67 F x " x CO, HI. RB 1, Early 449 6-7'1 M RB 3. Late 451 o-6m RB 3. Late 452 18-24m x RB 1, Early 454 5-4,- F x x RB 1, Early 455 4-57 H x C RB 3. Late 456 II x RB 3. Late 461 II x RB 3, Ear17 462 II x RB 2, Early 463 18-24,. x F'r,P'r RB 2, Early 464 }-'ty F x x RB 3. Late 465 2-31 x x P'r GR,CO,HI. RB 2, Early 466 14-167 M x C, IlL RB 2, Earl:,. 467 12-1Bm F "x RB 2, Early 469 Fetal RB 3. Late 470 12-18,. x LEE, CO RB 3. Late 472 H x RB 2, Early 474A 12-1Bm x x CBL, GR RB 3, Late 195

Burial Dental Number Age & Sex Chart X-ray Anomalies Pathologies Provenience

474B 6-12m x RB 3, Late 475A N x RB :S, Late 476 Fetal CBL RB 3. Late 478 2-3y RB 2, Early 479 Fetal RB 3. L-T 480 5-6y M C RB 3. L-T 481 12-181:11 CO HB 3. L-T 482 0-6m BB 2, Early 483 N RB ,. Late 484 12-18m FT,KO BE 3. Late 485 2-3y M RB 2, Early 486 18-24m 1m 3, Early 487 2-3y M Out, Late 488 2-3y C out, Late 489 2-3y F x ESC HI. RB 3. L-T 490 12-18m x RB 3. Late 493 18-24m RB 3, L-T 494 N BE 3. Late 495 N HE 3. Late 496 5-6y M RB 3, L-T 497 7-8y M c HB 3. L-T 498 12-18m co RB 3, L-T 500A 3-4y Out, Late 502 6-12m LEH,CBL BE 3, L-T 503 7-8y F CC LEH,CBL,HL out, Lat'9 504 6-12m Out, Late 510 N Out, Late 511 3-4y F x CO Out, Late 512 12-18m F x CO RB ,. L-T 513 3-4y F x RB 3. L-T 514 18-24m LEH RB 3. L-T 515 N x RB 3. L-T 517A 0-6m x Out, Late 517B 5-6y F x x HI. Out, Late 518 2-3y F Out, Late 519 Fetal RB 2, L-T 520 6-12m F CBL, HL RB 3, L-T 521 Fetal RB 3. L-T 523 9-1Oy M RB 2, L-T 524 16-18y M RB 2, L-T 529 N RB 3, L-T 530 2-3y M x PMT CO RB 3, L-T 531 14-16y M x Pr RB 2, L-T 532 N RB 3, L-T 533 12-18m x Pr LEH,CO,GR RB 2, L-T 535 Fetal. x RB 2, L-T 537 18-24m M RB 2, L-T 196

Burial Dental Number Age & Sex Chart X-ray Anomalies Pathologies Provenience

538 2-3y F x x HL RB 2, L-T 539 2-3y M x x c t LEH, IlL RB 2, L-T 541A lB-24m F CO RB 2, L-T 541B N x RB 2~ L-T 542 3-4y x HL, eBL Out, Late 544 2-3y M "x x CBL RB 2, L-T 546 lB-24m x x PMT HL Out, Late 54B Fetal Out, Late 549 6-12m F PH,CO,CBL,GR RB 2, L-T 550 IB-24m M Out, Late 552 N Out, Late 553 3-4y F CO Out. Late 554 0-6m Out, Late 555 5-6y M IlL Out, Late 556A O-Gm Out, Late 556B 2-3Y F IlL Out, Late 557 5-6y F FT C, IlL Out, Late 558 IB-24m F HE 2, L-T 562 o-6m KO RB 2, L-T 563 Fetal RB 2, L-T 564 l5-l7y F RB 2, L ...T 565 3-4y M RB 2, L-T 566 5-6y M RB 2, L-T 567 6-l2m x GR RB 1, Early 570 lB-24m x LEH, CO RB 1, Early 571 lB-24m LEH, co RB I, Early 574 4-5Y F C Plaza 2 577 9-l0y M C Plaza 2 57B 6-l2m CBL Plaza 2 5B5 7-By M x Plaza. 1 586 6-12m CO. CBL Plaza 2 5B7 N Plaza 2 58B l4-l6y M PT CBL Plaza 1 594 3-4y F Plaza 2 596 0-6m RB 3. Early 599 Fetal. RB 3, L-T 600 Fetal RB 3. L-T 602 N Plaza 2 603 l2-1Bm LEH, CO Plaza 2 604 12-18m RB 3. Early 606 2-3y GR HB ;S, L-T 607 3-4y F CO RB 3, Early 609 N x RB 3. L-T 611 11-13y F x LT RB 3, Early 613 lB-24m CO, eBL RB 3, L-T 615 N Plaza 1 616 3-4y F RB 3, L-T 197

Burial Dental Number Age & Sex Chart X-ray Anomalies Pathologies Provenience

618 18-24m F FT RB 3, L-T 619 Fetal HE 3. LooT 62l 3-4y RB 3. L-T 623 3-4y x Plaza 1 625 11-13y M x CBL RB 3. Late 626 0-6m RB 3. LooT 627 N RB 3. L=T 628 6-12m RB :;, LooT 630 4-5y F x LEH t eBL RB 3. Late 632 18-24m M x HE 3. LooT 633 4-5y F x RB 3. Early 634A N x RB :;. Late 636 Fetal RB 3. LooT 638 12-18m RB 3, Late 640 Fetal R5 3, LooT 642 N RB 3, LooT 643 N HB 3. LooT 644 N RB 3, LooT 645 0-6m RB 3. Early 646 18-24m M x HB 3. LooT 648 l8-24m x PMT LEH RB 3, LooT 649 7-8y F LEH, HL RB 3. L-T 651 6-12m CBL RB 3. L-T 652 7-8y Out, Late 653 N Out, Late 654A N x Out, Late 654B Fetal x Out, Late 656 6-12m F LEH RB 1, L.. T 657 7-8y F HIlT LEH t HL RB 1, LooT 658 6-7Y F FT,SST LEH HE 1, Early 659 2-3y F RB 1, LooT 660 0-6m x PH RB 1, L-T 661 12-1Bm F x PH ,CO ,CBL RB 1, LooT 662 Fetal RB 1, Early 663 3-4y HE 1, Early LIST OF REFERENCES

ABERLE, S. D. 1932 Child Mortality Among Fueblo Indians. American Journal. of Physical Anthropoloe;y. Vol. 16, pp. 339-349.

ABRAMSON, H. 1950 Acute Diarrheal Disorders of Newborn Infants. American Journal of Diseases of Children, Vol. 79. pp. ~

ALLAND, A. A. 1968 Popul.ation Control. Factors: Infanticide, Disease, Nutrition, and Food Supply. (Discussion) in Man the Hunter, edited by R. B. Lee and I. DeVore, pp. 243-245. Aldine Publishing Co., Chicago.

ALLISON, M. J. t D. MENDOZA and A. PEZZIA 1974 A Radiographic Approach to Childhood lllness in Pre-Columbian Inhabitants of Southern Peru. American Journal of Physical Anthropology, Vol. 40, pp. 409-416.

ANDERSON, D. L., G. W. THOMPSON and F. POPOVICH 1976 Age of Attainment of Mineralization stages of the Permanent Dentition. Journal of Forensic Science, Vol. 21, pp. 191- 200.

ANDERSON, R. K., J. CALVO, G. SERRANO and G. C. PAYNE 1946 A Study of the Nutritional Status and Food Habits of Otomi Indians in the Mezquital Valley of Mexico. American Journal of Public Health, Vol. 36, pp. 883-903.

ANGEL, J. L. 1967 Porotic Hyperostosis or Osteoporosis Symmetriea. In Diseases in Antiguity, edited by D. Brothwell and A. T. Sandis~ Charles C. Thomas, Springfield.

1.968 The Bases of Paleodemography. American Journal. of Physical Anthropology, Vol. 30. pp. 427-438.

ARMELAGOS, G. J. and J. R. DEWEY 1.970 Evo1utionary Responses to Human Infectious Diseases. ~, Vol. 20, pp. 271-275.

198 199

ARMELAGOS, G. J. t J. H.. MIELKE, K. H. OWEN, D. P. VAN GERVEN, J. R. DEWEY and P.. E. MAHLER 1972 Bone Growth and Develop!!,ent in Prehistoric Populations from Sudanese Nubia. Journal of Human Evolution, Vol. 1, pp. 89- 119.

ARNOLD, J. Soo, M. H. BARTLEY, S. A. TON'!' and D. P. JENKINS 1966 Skeletal Changes in Aging and Disease. Clinical Orthopedics, Vol. 49, pp. 17-38.

BAILIT, H. L. and E. E. HUNT, JRs 1964 The Sexing of Children's Skeletons from Teeth Alone and Its Genetic Implications. American Journal of PhYsical Anthro ~. Vol. 22, pp. 171-174.

BASS, 'tI. M., D. R. EVANS and R. L. JANTZ 1971 The Leavenworth Site Cemetery: Archaeology and Physical Anthropology. University of Kansas Publications in Anthro ~,2. Lawrence, Kansas.

BASSETT, E. J. t M. S. KEITH, G. J. ARMELAGOS. D. L. MARrIN and A. R. VILLANUEVA 1980 Tetracycline-Labeled Human Bone from Ancient Sudanese Nubia (A.D. 350). ~,Vol. 209, pp. 1532-1534.

BEESON, P. B. and W. HcDERMOl'T 1975 Textbook of MediCine, 2 Vols. W. B. Saunders Co., Philadel phia. , BEHAR, M. 1964 Death and Disease in Infants and Toddlers of Preindustrial. Countries. American Journal of Public Hea1.th, Vol. 54, pp. 1100-1105.

1968 Food and Nutrition of the Maya Before the Conquest and At the Present Time. In Biomedical Challenges Presented by the American Indian, edited by Pan American Heuth Organization. WHO Scientific Publication No. 165, Washington, D.C.

BENNETT, K. A. 1967 Craniostenosis: A Review of the Etiology and a Report of New Cases. Allerican Journal of Physical Anthropology, Vol. 27. pp. 1-10.

1973a On the Estimation of Some Demographic Characteristics of a Prehistoric Population from the American Southwest. American Journal of Physieal Anthropo1og, Vol. 39. pp. 223-23-2.---

1973b The Indians of Point of Pines, Arizona. Anthropological Papers of the University of Arizona, 23. Tucson. 200

BENNETT9 K. A. 1975 Skeletal Remains from Mesa Verde National Park, Colorado. USDI. NPA Publications in Archaeology 7F. Wetherill Mesa ~. BENNETT, K. A. and F. S. HULSE 1966 Microevolution at Mesa Verde. XXXVI CODla"eSS Internacional de Americanistas, Vol. 2, pp. 369-376. Sevilla.

BHASKAR, S. N. (Ed.) 1980 Orban's Oral HistologY and Embryologr. C. V. Mosby Co., St. Louis.

BIRKBY, W. H. 1973 Discontinuous Morphologica1 Traits of the Skull as Population Merkers in the Prehistoric Southwest. Doctoral Dissertation, University of Arizona, 'l'ueson.

1982 Bio6ocial Interpretations from Cranial Nonmetric Trai te of Grasshopper Pueblo Skel.etal Remains. In Multidisciplinary Research at Grasshopper Pueblo, Arizona, edited by W. A Longacre, S. J. Holbrook and M. W. Graves. Anthropological Papers of the University of Arizona, 40. Tucson.

BLACK, T. K., III 1.978a Sexual Dimorphism in the Tooth-Crown D:;'ameters of the Decid uous Teeth. American Journal of Physical Anthropology, Vol. 48, pp. 77-82.

1978b A Method for Determining the Sex of Immature Human Skeletal Remains from Odontometric Dimensions. Doctoral dissertation, Universi ty of Michigan, Ann Arbor.

BLAKELY, R. L. 1977 Introduction: Changing Strategies for the Biological Anthro pologist. In Biocultural Adaptations in Prehistoric America, edited by R. L. Blakely, pp. 1-9. Southern AnthropolOgical Society Proceedings, 11. Athens, Georgia.

BOCQnEl'-APPEL, J. P. and C. MASSET 1982 Farewell to Paleodemography. Journal of Human Evolution, Vo1. n, pp. 321-333.

BOHRER, V. L. 1.982 Plant Remains from Rooms at Grasshopper Pueb1.o. In Multi disciplinary Research at Grasshopper Pueblo. Arizona, edited by W. A. Longacre, S. J. Holbrook and M. W. Graves, pp. 97- 106. Anthropological papers of the University of Arizona, 40, Tucson. 201

BOUCHER, B. J. 1955 Sex Differences in the Foetal. Sciatic Notch. ~ Forensic Medicine, Vol. 2, pp. 51-54.

BRAIDWOOD, R. J. and C. A. REED 1957 The Achievement and Early Consequences of Food-Production: A Consideration of the Archaeological and Natural-Historical Evidence. Cold Spring Harbor Symposia on Quantitative Biology. Vol. xxii.

BRAUER, J. C. and M. A. BAHADOR 1942 Variations in Calcification and Eruption of the Deciduous and Permanent Teeth. Journal of American Dental Association, Vol. 42, pp. 1373-13B7.

BROTRWELL, D. R. 1969 Dietary Variation and the Biology of Earlier Ruman Popula tions. In The Domestication and Exploitation of Plants and Animals, edited by P. J. Ucko and G. W. Dimbleby. Aldine, C'iii'CiiO ..

BUIKSTRA. J. E. 1976 The Caribou Eskimo: General and Specific Diseases. American Journal of Physical Anthropology, Vol. 45, pp. 351-3~

1981 Mortuary Practices, Palaeodemography and Palaeopatho1ogy: A Case Study from the Koster Site (Illinois). In The Archaeology of Death, edited by R. Chapman, I. Kinile'8, and K. Randsborg, pp. 123-132. Cambridge University Press.

BURKE, M., M. YORK and I. SANDE 1979 Mortality in Childhood. Pan American Health Organization Scientific Publications 386. Washington, D.C.

BURNET, M. and D. C. WHITE 1972 Natural History of Infectious Disease. Cambridge University Press.

BUSCHANG, P. H. 1982 Differential Long Bone Growth of' Children between Two Months and Eleven Years of Age. American Journal of Physical Anthropology, Vol. 58, pp. 291-295.

CADIEN, J. D., E. F. HARRIS, W. P. JONES and L. J. MANDARINO 1974 Biological Lineages, Skeletal Populations, and Microevolution. Yearbook of Physical AnthropoloS! 18.

CARLSON, D. S.t D. J. ARMELAGOS and D. P. VAN GERVEN 1974 Factors Innuencing the Etiology of Cribra Orbi talia in Prehistoric Nubia. Journal of' Human Evolution, Vol. 3. pp. 405-410. 202

CARLSON, D. S., G. J. ARMELAGOS and D. P. VAN GERVEN 1976 Patterns of Age-Related Cortical Bone toss (Osteoporosis) Within the Femoral Diaphysis. Human Biology, Vol. 48, pp. 295-31".

CASSELLS, E .. s. 1972 A Test Concerning Artificial Cranial Deformation and statue from the Grasshopper .site. East-Central Arizona. Kiva, Vol. 37. pp. 8.... 93. --

CASSIDY I C. M. 1972 A Comparison of Nutrition and Health in Pre-Agricultural and Agricultural Amerindian Skeletal Popul.ations. Doctoral dissertation, University of 'Wisconsin, Madison ..

CHASE, H. P., V. KOMER, J. M. DODDS, M. E. SAWBARLICH, R. M. HUNTER, R. S. BURTON and V .. SPALDING 1971 Nutritional Status of Preschool Mexican-American Migrant Farm Children. American Journal of Diseases of Childhood, Vol. 122, pp. 316-324.

CHOI, S. C. and M. TROTTER 1970 A Statistical Study of the Multivariate structure and Race Sex Differences of American White and Negro Fetal Skeletons. American Journal of PhYsical Anthropolog, Vol. 33, pp. 307- 312.

CIOLEK_TORRELLO, R. S. 1978 A Statistical Analysis of Activity Organization, Grasshopper pueb10, Arizona. Doctoral dissertation, University of Arizona, Tucson.

CIOLEK-TORRELLO, R. S. and J. J. REID 1974 ~~r. in Household Size at Grasshopper. .!S.!!!. Vol. 40, pp.

CLARK, G. A. 1969 A Preliminary Analysis of Burial Clusters at the Grasshopper Site, East-Central Arizona. ~t Vol. 35, pp. 57-86.

CLARKE, S. K. 1980 Early Childhood Morbidity Trends in Prehistoric Populations. Human Biology, Vol. 52, pp. 79-85.

CL»!ENTS, F. 1931 Racial Differences in Mortality and Morbidity. Human Biology, Vol. 3. pp. 397-419.

COCKBURN, T. A. 1971 Infectious Diseases in Ancient Populations. Current Anthro ~, Vol. 12, pp. 45-62. 203

COCKBURN. E.. (Ed.) 1977 Porotic Hyperostosis: An Enquiry. Paleopathology Associ ation Monograph 2, Detroit.

COOK, D. C. 1979 Subsistence Base and Health in Prehistoric Illinois Valley: Evidence from the Human Skeleton. Medical Anthropoloe;:y. Vol. 3. pp. 109-124.

1981 Mortality, Age structure and Status in the Interpretation of stress Indicators in Prehistoric Skeletons: A Dental Example from the Lower Illinois Valley. In The Archaeolog:y of Death, edited by R. Chapman. I. Kinnes and K. Randsborg, pp. 1:;:3- 145. Cambridge University Press.

In Human Growth: A Perspective on Subsistence Base Change. Press Northwestern University Archaeological Program Scientific Papers. Evanston.

COOK, D. C. and J. E. BUIKSTRA 1.979 Health and Differential Survival. in Prehistoric Populations! Prenatal. Dental Defects. American Journal of Physical Anthropology. Vol. 51, pp. 64g...664.

COOK, R. and A. HANSLIP 1964 Nutrition and Mortality or Females under 5 Years of Age Com pared with Males in the "Greater Syria" Region. Journal of Tropical Pediatrics, Vol. lO~ pp. 76-81. ----

CORBETT, T. H. 1968 Iron Deficiency Anemia in a Pueblo Indian Village. ~ of American Medical Association, Vol. 205, p. 186.

CORRUCCINI, R. S. 1972 The Biological Rel.atioDships of Some Prehistoric and Historic Pueblo Popul.ations. American Journal of Ph:raical. Anthro ~, Vol. 57, pp. 373-388.

COWGILL, G. L. 1975 Popul.ation Pressure as a Non-Explanation. American Antiquity ~ 30, pp. 12?-13l.

CRELIN, E. S. 1981 Development of the Musculoskeletal System. CIBA Clinical Symposia, Vol. 33, No. l~

CYBULSKI, J. S. 1977 Cribra Orbi taJ..ia, A Possible Sign of Anemia in Ear1y Historic Native Populations of the Bl'itish Columbia Coast.. American Journal of Physical. Anthropolosy, Vo1. 47, pp. 31-4-0-.-- 204

DAHLBERG, A. A. 1945 The Paramolar Tubercl.e (Balk). AmericaD Journal. of PltTsical Anthropolo&y. Vol. 3, pp. 97-103.

DAHLBERG, A. A. and R. M. MENEGAZ-BOCK 1958 Emergence of the Permanent Teeth in Pima Indian Children. Journal of Dental. Research, Vol. 37, pp. 1123-1140.

DARBY, W. J. t C. G. SALISBURY, W. J. McGONITY, H. F. JOHNSON. E. B. BRIllGFORTI! and H. R. SANDS'l'EAD 1956 A study' of the Dietary Background and Nutriture of the Navajo IndiBD. Journal of Nutrition, Vol. 60, Supplement 2. m:HIRIJIAN, A. , H. GOLDSTEIN and J. M. TANNER 1973 A New System of Dental Age Assessment. Human Biologr. Vol. 45, pp. 211-227.

DIAMOND, M. 1952 Dental Anatom;r. MacMillan and Co., New York.

DOZIER, E. P. 1965 Southwestern Social Units and ArchaeoloSY'_ ~ Antiquity, Vol. 31, pp. 38-47.

DRElZEN, S., C. CURRIE, E. J. GILLEY and T. D. SPIES 1956 Observations on the Association between Nutritive Failure, Skeletal Maturation Rate. and Radiopaque Transverse Lines in the Distal End of the Radius in Children. American Journal of Roeot.nol0gY, Vol. 76, pp. 482-487.

DREIZEN, S., R. M. SNODGRASSE, H. WEBB-PEPLOE and T. D. SPIES 1958 The Retarding Effect of' Protracted Undernutrition on the Appearance of the Postnatal Ossification Centers in the Hand and Wrist. Human Biology, Vol. 30. pp. 253-263.

DRElZEN. S., C. N. SPIRAKIS and R. E. STONE 1964 The Influence of Age and Nutri tiona! Status aD "Bone Scar" Formation in the Distal. End of the Growing Radius. American Journal of PhYsical Anthropolog, Vol. 22, pp. 295-~

DROESSLER, J. 1981 Craniometry and Biological Distance: Biocultural Continuity and Change at Late WooiUand-Mlssl.ss1pplan Interrace. CGn+'e'P for American Archaeolog, Evanston, Illinois.

DUNN, F. L. 1968 Epidemiological Factors: Health and Disease in Hunter Gatherers. In Man the Hunter, edited by R. B. Lee and I. DeVore, pp. 221-228. Aldine, Chicago. 205

EBBS, J. H., W. A. seoTI', F. F. TISDALL, W. J. HOYLE and M. BELL 1942 Nutrition in Pregnaney. Canadian Medical Association Journal, Vol. 1!6, pp. 1-6.

ELLIS, F. H. 1968 An Interpretation of Prehistoric Death Customs in Terms of Modern Southwestern Parallels. In Collected Papers in Honor of L:rndon Lane Hargrave! Papers of Arachaeologica1 Society of New Mexico 1. University of New Mexico Press, Santa Fe.

EL... NAJJAR, M. Y. 19'74 People of Canyon de Chelly: A Study in their Biology and and Culture. Doctoral Dissertation, Arizona state University, Tempe.

EL-NAJJAR, M. Y., O. J. RYAN, C. G. TURNER, II and B. LOZOFF 1976 The Etiology of Porotic Hyperostosis Among the Prehistoric and Historic Anasazi Indians of Southwestern United States. American Journal of PhYsical Anthropology. Vol. 44, pp. 477-488.

FALKNER, F. 1957 Deciduous Tooth Eruption. Archives of Diseases of Childhood, Vol. 32, pp. 386-391.

FAUST .. E~ C., 9!ld P .. F~ RUSSELL 1957 Craig and Faust's Clinical Parasitology. Lea and Febiger, Philadelphia.

FAZEKAS, I. GY. and F. KOSA 1978 Forensic Fetal Osteology. p..kademiai Kiado, Budapest.

FLECKER, H. 1942 Time of Appearance and Fusion of Ossification Centers as Observed by Roentgenographic Methods. American Journal of Roentgenology, Vol. 47, pp. 97-159.

FRENCH, J. G. 1967 Relationship oi Morbidity l;O the FeeCiing P8.ttei'ij,5 of Navajo Children from Birth through Twenty-Four Months. American Journal of Clinical. Nutrition, Vol. 20, pp. 375"~

FRIEDERICI, G. 1906 Scalping in America. Smithsonian Institute Annual Report, pp. 423-438.

FROST, H. M. 1965 Morphometry of Bone in Paleopathology. In HUman Paleopath ~, edited by S. Jarcho, pp. 1}1-174. Proceedings of a Symposium on Human Paleopathology, Washington, D.C. 206

FROST, H. M. 1972a Bone Remodeling and Its Relationship to Metabolie Bone ~. Charles C. Thomas, Springfield.

19?2b Bone Modeling and Skeletal Modeling Errors. Charles c. Thomas t Springfield.

GALDSTON, I. (Ed.) 1960 Human Nutrition, Historic and Scientific. International Universities Press, Inc., New York.

GARN, S. M. 1965 The Applicabili.ty of North American Growth Standards in Developing Countries.. Canadian Medical Association Journal, Vol. 93. pp. 914-919.

1970 The Earlier Gain and the Later Loes of Cortical Bone in Nutritional Perspective. Charles C. Thomas, Springfield.

GARN, S. M., M. A. GUZMAN and B. WAGNER 1969 Subperiosteal Gain and Endosteal LOSB in Protein-Calorie Malnutrition. American Journal of PhYsical AnthropologY', Vol. 30, pp. 153-156.

GARN, S. M., A. B. LEWIS and R. S. KEREWSKY 1965 Genetic, Nutritional, and Maturational Correlates of Dental Development. Journal of Dental Research, Vol.. 44, pp. 228- 243.

GIGLIOLI, G. G. 1968 Malaria in the American Indian. In Biomedical Challenges Presented by the American Indian, edited by Pan American Health Organization, pp. 104-113. WHO Scientific Publication, Vol. 165. Washington, D.C.

GINDHART, P. S. 1969 The Frequency of Appearance of Transverse Lines in the Tibia in Relation to Chil.dhood Illness. American Journal of Physical Anthropologv, Vol. 31, pp. 17-23.

GITLITZ, I. 1.950 Diarrheal Disease on an Indian Reservation. Arizona Medicine t Vol. 7. pp. 42-44.

GOLDSTEIN, M. S. 1963 Some Vital Statistics Based on Skeletal Material. ~ Biology, Vol. 35, pp. 3-12. GOODMAN, A. H., G. J. ARMELAGOS and J. C. ROSE 1980 Enamel Hypop1asias as Indicators of Stress in Three Prehis toric Populations from Illinois. Human BiologY, Vol. 52, pp. 515-528. 2W

GOOI1WIN t M. R., JR., D. C. MUCKEL, R. S. GANELIN, R. E. WEAVER and F. J. PAYNE 1960 Observations on Etiology of Diarrheal Diseases in Arizona. American Journal of Tropical Medicine and Hygiene, Vol. 9, pp. 336-342.

GORDON, H. 1959 Craniostenosis. British Medical Journal, Vol. 5155, w. 792-795.

GORDON, J. E. , J. B. wrON and W. ASCOLI 1967 The Second Year Death Rate in Less Developed Countries. American Journal of Medical Science, Vol. 254. pp. 357-380.

GORLlN, R. J. and H. M. G()LDJIAN 1970 Thoma's Oral Pathology (2 vols.), C. V. Mosby, St. Louis.

GOSS, C. M. (Ed.) 1973 Gray's Anatomy of the Human Body. Lea and Febiger, Phila delphia.

GRAVES, M. W., W. A. LONGACRE and S. J .. HOLBROOK 1982 Aggregation and Abandonment at Grasshopper Pueblo, Arizona. Journal of Field Archaeology. Vol. 9. pp. 193-206.

GRIFFIN, P. B. 1967 A High Status Burial from Grasshopper Ruin, Arizona.. ~, Vol. 33, pp. 37-53.

1969 Late Mogollon Readaptation in East-Central Arizona.. Doctoral dissertation, University of Arizona, Tucson.

HADDY, T. B., C. JURKOWSKI, M. BRODY, D. J. KALLEN and D. M. CZAJKA NARINS 1974 Iron Deficiency With and Without Anemia in Infants and Chil dren. American Journal of Diseases of Children, Vol. 28, pp. 787-792.

HADLEY, J. N. 1955 Health Conditions Among Navajo Indians. Public Health Reports, Vol. 70, pp. 831-836.

RANIHARA, K. 1967 Racial Characteristics in the Dentition. Journal of Dental ~, Vol. 46 (supplement to 5), pp. 923-925.

HANNA, B. L. 1962 The Biological Relationships Among Indian Groups of the Southwest; Analysis of Morphological Traits. American Journal of Physical Anthropology, Vol. 20, PP.~. 208

HARRIS, H. A. 1933 Bone Growth in Health and Disease. Oxford University Preas, London.

HENGEN, o. P. 1.971 Cribra Orbitalia: Pathogenesis and Probable Etiology. ~. Vol. 22, pp. 57-75.

HEPBURN, D. 1908 Anomal.ies in the Supra-Inial PortioD of the Occipital Bone, Resulting from Irregularities of the Ossification, with Con sequent Variations of the Interparietal Bone. Journal of Anatomy, Vol. 42, pp. 88-92. ----

HERRENKOHL. L. R. 1979 Prenatal stress Reduces Fertility and Fecundity in Femal.e Offspring. ~,Vol. 106, pp. 1097-1099.

HESDORFFER, M. B. and R. E. SCAMMON 1928 Growth of Long-bones of Human Fetus as Illustrated by the Tibia. Society of Experimental Biology and Medicine Pro ceedings, Vol" 25. pp. 638-641.

HOFFMAN, J. M. 1979 Age Estimations from Diaphyseal Lengths: Two Months to Twelve Yp.ars. Journal of Forensic Science, Vol. 24, pp. 461-469.

HOHENTHAL~ w. D. and S. T. BROOKS 1960 An Archaeological Scaphocephal from California. American Journal of PhYsical AnthropologY, Vol. 18, pp. 59~

HOLBROOK, Se J. 1982 Prehistoric Environmental Reconetruction by Mammalian Micro fauna1 Analysie, Grasshopper Pueblo. In Multidisciplinary Research at Grasshopper Pueblo. Arizona, edited by \rI. A. Longacre, S. J. Holbrook and M. W. Graves, pp. 73-87. Anthropological Papers of the Uni versi ty of Arizona 40, Tuceon.

HOLBROOK, S. J. and M. 'fl. GRAVES 1982 Modern Environment of the Grasshopper Region. In Multidisci plinary Research at Grasshopper Pueblo. Arizona, edited by W. A. Longacre, S. J. Holbrook and M. W. Graves, pp. 5-12. AnthropolOgical Papers of the University of Arizona 40, Tucson.

HOOTON, E. A. 1.930 The Indians of Pecos Pueblo. Yale University Press, New Haven. ---~~-..

1.962 Skeletons fr.)m the Cenote of Sacrifice at Chichen Itza. In The Maya and Their Neighbors, elii ted by C. L. Hays and others, pp. 272-280. University of utah Press, Salt Lake City. 2())

HOWELL, N. 1976 Toward a Uniformitarian Theory of Human Paleodemography. Journal of Human Evolution, Vol. 5. pp. 25-40.

1982 Village Composi tiOD Implied by a Paleodemographic Life Table: The Libben Site. American Journal of PhYsical Anthropologl. Vol. 59. pp. 263--0269.

HRDLICKA, A. 1908 Physiological and Medical Observations ;'mong the Indians of Southwestern United states and Northern Mexieo. BAE Bulletin 34, "ashington, D.C.

1940 Catalogue of Human Crania in the United States National Museum Collections: Indians of the Gulf States. Proceedings of National Museum, S.l •• Vol. 87, pp. 315-464.

HUGHES, D. R. 1968 Skeletal Plasticity and Its Relevance in the Study of Earlier Populations. In The Skeletal Biology of Earlier Human Populations, edited by D. R. Erothwell, pp. 31-55. Symposia of the Society for the Study of Human Biology viii. Pergamon Press, London.

HUNT, E. E. t JR. and I. GLEISER 1955 The Estimation of Age and Sex of Preadolescent Children from Bones and Teeth. American Journal of Physical Anthropology, Vol. 13, pp. 479-11·~7_

HURKE, V. C. 1948 Standards of Variation in the E::.-uption of the First Six: Permanent Teeth. Child Development, Vol. 19, "pp. 213-231.

HUSS-ASHMORE, R., A. H. GOODMAN and G. J. ARMELAGOS 1982 Nutritional Inference from Paleopathology. In Advances in Archaeological Method and Theory, edited by M. B. Schiffer, Vol. 5, pp. 395-474. Academic Press.

INFANTE, P. F. and G. M. GILLESPIE 1976 Dental Caries Experience in the Deciduous Dentition of Rural Guatemalan Children Ages 6 Months to 7 Years. Journal of Dental. Research, Vol. 55, pp. 951-957. ----

1977 Enamel Hypoplasia in Relation to Caries in Guatemalan Children. Journal of Dental Research, Vol. 56, pp. 493-498.

IRONSIDE, A. G. 1973 Gastroenteritis of Infancy. British Medical Journal, Vol. 1, pp. 284-286. 210

JELLIFFE, D. B. and E. F. P. JELLlTFE 1978 Human Milk in the Modern World. Oxford University Press, Fairlawn, New Jersey.

JELLIFFE, E. F. P. 1975 Protein-Galorie Malnutrition of EarlY Childhood: Two Decades of Malnutri tieD (A Bibliography). Commonwealth Bureau of Nutri tieD, Aberdeen.

JOHNSTON, F. E. 1961 Sequence of Epiphyseal Union in a Prehistoric Kentucky Popu lation from Indian Knoll. Human Biology, Vol. 33, pp. 66-81.

1962 Growth of the Long Bones of Infants and Young Chi1dren at Indian Knoll. American Journal of Physical AnthropologY, Vol. 20, pp. 249-254.

1968 Growth of the Skeleton in Earlier Populations. In The Skeletal Biology of Earlier Human Populations, editedby D. R. Brothwell, pp. 57-66. Symposia of the Society for the Study of Human Biology viii. Pergamon Press, London.

1969 Approaches to the Study of Developmental Variability in Human Skeletal Populations. American Journal of Physical Anthro ~, Vol. 3J., pp. 335-342.

JOHNSTON, F. E. and C. E. SNOW 1961 The Reassessment of the Age and Sex of the Indian Knoll Popu lation: Demographic and Methodological Aspects. American Journal of Physical Anthropology, Vol. 19, pp. 237~

KATZ, S. H. f M. L. HEDIGER and L. A. VALLEROY 1974 Traditional Maize Processing Techniques in the New World. ~t Vol. 184, pp. 765-773.

KATZ, S. H. and A. F. C. WALLACE 1974 An Anthropological Perspective on Behavior and Disease. American Journal of Public Health, Vol. 64, pp. 1050-1052.

KELSO, G. K. 1982 Two Pollen Profiles from Grasshopper Pueblo. In Multidisci plinary Research at Grasshopper Pueblo, Arizona, edited by - W. A. Longacre, S. J .. Holbrook and M.. W. Graves, pp. 106-110. Anthropological Papers of the University of Arizona 40, Tucson.

KEUSCH, G. T. 1975 Malnutrition and Infection: Deadly Allies. Natural History Vol. 84, pp. 27-34.

KLATSKY t M. 1956 The Incidence of Six Anomalies of the Teeth and Jaws. ~ Biology, Vol. 28, pp. 420-428. 211

KNUDSON, H. W.. and R. A. FLAHERTY 1960 Craniosynostosis. American Journal of Roentgeno1.ogy, Vol. 84, pp. 454-460.

KRAUS, B. S. 1951 Carabelli's Anomaly of the Maxillary Molar Teeth~ ~ Journal of Human Genetics, Vol. 3, pp. 3'+8-355.

1954 Indian Health in Arizona. Tucson: Bureau of Ethnic Research Second Annual Report. University of Arizona.

1959 Occurrence of the Carabelli Trait in Southwest Ethnic Groups. American Journal of Physical Anthropol.ogy, Vol.. 17, pp. 117- 123.

KRAUS, B. S. and R. E. JORDAN 1965 The Human Dentition Before Birth. Lea and Febiger, Phila delphia.

KRAUS, B. SiI, R. E. JORDAN and L. ABRAMS 1969 Dental Anatomy and Occlusion. Williams and Wilkins Co., Baltimore.

KROGMAN, \II. M. 1960 Oral Structures Genetically and Anthropologically Considered. Annals of New York Academy of Science, Vol. 85, pp. 17-41.

1962 The Human Skeleton in Forensic Medicine. Charles C. Thomas, Springfield.

1972 Child Growth. University of Michigan, Ann Arbor.

KUHNLEIN, H. V. 1981 Dietary Mineral Ecology of the Hopi. Journal of Ethnobiology, Vol. 1, pp. 84-94.

KUHNLEIN, H. V. and D. H. CALLOWAY 1979 Adventitious Mineral Elements in Hopi Indian Diets. ~ of Food Science, Vol. 44, pp. 282-285.

KUNITZ, S. J. 1970 Disease and Death Among the Anasazi. ~,Vo1. 76, pp. 17-22.

KUNITZ, S. J. and R. C. EULER 1972 Aspects of Southwestern Paleoepidemiology. Prescott College Anthropological Reports 2, Prescott.

KUSTALOOLU, O. A. 1962 Paramolar Structures of the Upper Denti tion. ~ Dental Research, Vol. 41, pp. 75-83_ 212

LALLa, J. Woo, G.. J. AHMELAGOS and R. P. MENSFORTH 1977 The Role of Diet, Disease, and Physiology in the Origin of Porotic Hyperostosis. Human Biology, Vol. 49, pp. 471-483.

LALLO, J. \I. and J. C. ROSE 1979 Patterns of Stress, Disease and Mortality in Two Prehistoric Populations from North America. Journal. of Human Evolution, Vol. 8, pp. 323-335.

LAMBERT, J. B., C. B. SZPUNAR and J. E. BUIKSTRA 1979 Chemical Analysis of Excavated Bone from Middle and Late Woodland Sites. Archaeometry. Vol. 21, pp. 115-129.

LAMBERT, J. B., S. M. VLASAK, A. C. THOMETZ and J. E. BUIKSTRA 1982 A Comparative Study of the Chemical Analysis of Ribs and Femurs in Woodland Populations. American Journal of Physical AnthropologY, Vol. 59, pp. 289-294.

LANGE, C. H. 1959 Cochiti: A New Mexican Pueblo. University of Texas Press, Austin.

LANZKOWSKY t P .. 1968 Radiological Features of Iron-Deficiency Anemia. American Journal of Diseases of Children, Vol. 116, pp. l6-~

LASERSOHN, W. 1965 Acute Diarrheal Diseases in a Zuni Community. Public Health Reports, Vol. 80, pp .. 457-461.

LEE, M., J. A. BIRKBECK, I. D. DESAI, M. J. MILLER, G. R. MEALY and W. P. REED 1974 Dia osis and Treatment of Prevalent Diseases of North American Indian Populations 2 vols. • MSS Information Corp, New York.

LONGACRE, W. A. 1976 Population Dynamics at the Grasshopper Pueblo, Arizona. In ~:m~~::h~~b~~!~;:~l~~:l§tnt~!~;!;:i :~p~~a~::6 Me:~~!e:r:!s, Albuquerque.

LONGACRE, W. A. and J. J. REID 1974 The University of Arizona Archaeological Field School at Grasshopper: Eleven Years of Multidisciplinary Research and Teaching. Kiva, Vol. 40, pp. 3-38.

LOVEJOY t C. 0., R. S. MEINDL, R. R. PRYZBECK, T. S. BARTON, K. G. HEIPLE and D. KO'!'TING 1977 Paleodemography of the Libben Site, Ottawa County, Ohio. ~, Vol. 198, pp. 291-293. 213

LOWRY, J .. Too, M. LINDLEY and B. R. MIGEON 1979 Fetal Mortality and Sex Ratio. ~t Vol. 206, p. 1428.

MACKAY t R. H. n.d. Chart--Skeletal. Maturation. Eastman Kodak, New York.

MALINA, R. M. 1975 Growth and Devel.opment, The First Twenty Years in Man. Burgess Publishing Co., Minneapolis.

MA.NDEL, I. D. 1979 Dental Caries. American Scientist, Vol. 67. pp. 680-688.

MARESH, M. M. 1955 Linear Growth of Long Bones of Extremities from Infancy through Adolescence. American Journal of Diseases of Children, Vol. 89. pp. 725-742.

MARSHALL t D. 1976 Radiographic Correlation of Hand, Wrist and Tooth Development. Dental RadiographY and PhotographY, Vol. 49. pp. 51-72.

MARSHALL, W. A. 1968 Problems in Relating the Presence of Transverse Lines in the Radius to the Occurrence of Disease. In The Skeletal Biology of Earlier Human PopulatioDsy edited by D. R. Brothwell, pp. 245-261. London: Symposia of the Society for the Study of Human Biology viii. Pergamon Press.

1977 Human Growth and Its Disorders. Academic Press, New York.

MARTIN, D. L. and G. J. ARMELAGOS 1979 Morphometrics of Compact Bone: An Example from Sudanese Nubia. American Journal of Physical Anthropology. Vol. 51, pp. 571-578.

MASSLER, M., I. SCROUR and H. PONCHER 1941 Developmental Pattern of the Child as Reflected in the Ca1ci fication Pattern of the Teeth. American Journal of Diseases of Children, Vol. 62, pp. 33-67.

MATHERy K. 1966 statistical Analysis in Biology. Methuen & Co., London

McGREGOR, I. A., W. Z. BILLEWICZ and A. M. THCMSON 1.961. Gro.... th and Mortality in Children in an African Village. Bri tish Medical Journal, Vol. 2, No. 5268, pp. 1661-1666.

McHENRY, H. 1968 Transverse Linea in Long Bones of Prehistoric California Indians.. American Journal of Physical Anthropology, Vol. 29, pp. 1-18. 214

McHEJ:fRY t H. M. and P. D. SCHULZ 1976 The Association Between Harris Lines and Enamel Hypoplasia in Prehistoric California Indians. American Journal of Ph:ysical Anthropology, Vol. 44, pp. 507-512.

McMILLEN, M. M. 1979 Differential Mortality by Sex in Fetal and Neonatal Deaths. Science, Vol. 204, pp. 89-91.

McWILLIAMS, K. R. 1974 Gran Quivira and Biological Distance in the United States Southwest. Doctoral dissertation, Arizona State University, Tempe.

MEINDL, R. S. 1982 Components of Longevity: Developmental and Genetic Responses to Differential Childhood Mortality. Social Science and Medicine, Val.. 16, pp. 165-174.

MEINDL, R. S. and A. C. SWEDLUND 1977 Secular Trends in Mortality in the Connecticut Valley, 1700- 1850. Human Biolo51, V01. 49, pp. 389-414.

MENSFORTH, R. P., C. o. LOVEJOY, J. W. LALLO and G. J. ARMELAGOS 1978 The Role of Constitutional Factors, Diet, and Infectious Disease in the Etiology of Porotic Hyperostosis and Periosteal Reactions in Prehistoric Infants and Children. Medical Anthropology, Vol. 2, pp. 1-59. ---

MERCHANT, V. L. and D. H. UBELAKER 1977 Skeletal Growth of the Protohistoric Arikara. American Journal of Ph.vsical. Anthropology, Vol. 46, pp. 61-72. MEREDITH, R. V. 1946 Order and Age of Eruption for the Deciduous Dentition. Journal of Dental. Research, Vol. 25, pp. 43-66.

MILES. A. E. W. 1963 Dentition in the Estimation of Age. Journal of Dental ~, Vol. 42, pp. 255-263.

MILES, J. M. 1975 Orthopedic Problems of the Wetherill Mesa Populations. USDI, NPS, publications in Archaeolog;y ?a. Wetherill Mesa ~. Washington, D.C.

MILLER, R. J. 1981 Chavez Pass alLd Biological. Relationships in Prehistoric Central. Arizona, Doctoral dissertation, Arizona State University, Tempe. MILNER, G. R •. 1982 Measuring Prehistoric Levels of Health: A Study of Mississippian Period Skeletal Remains from the American Bottom, Illinois. Doctoral dissertation, Northwestern University, Evanston.

MILUNSKY t A. 1982 Fetal Malformations and Environmental Influence. American Journal of Forensic Medicine and Pathology, Vol. 3, pp. 329- 334.

MOBLEY, C. M. 1980 Demographic Structure of Pecos Indians: A Model Based on Life Tables. American Antiquity, Volo 45. pp. 518-530.

MOODY, E. and L. B. MONTGOMERY 1934 Hereditary Tendencies in Tooth Formation. Journal of American Dental Association, Vol. 21, pp. 1774-1776.

MOORE, J. A., A. C. SWEDLUND and G. J. ARMELAGOS 1975 The Use of Life Tables in Pa1eodemography. American Antiquity, Vol. 40, No.2, Part 2, pp. 57-70-.---

MOORE, \II. M., M. M. SILVERBERG and M. S. READ 1972 Nutrition, Growth and Development of North American Indian Children. DREW Publication (NIH) 72-66. Washington, D.C.

MOORREES, C. F. A., E. A. FANNING and E. E. HUNT, JR. 1963 Formation and Resorption of Three Deciduous Teeth in Children. American Journal of Physical AnthropologY, Vol. 21, pp. 205- 2l3.

MORISON, J. E. 1970 Foetal and Neonatal PathologY. Appleton-Century-Crofts, New York.

MOSELEY, J. E. 1965a Radiographic Studies in Hematologic Bone Disease: Implica tions for Paleopathology. In Human Paleopatho1ogY t edited by S. Jarcho, pp. 121-130. Proceedings of a Symposium on Human PaJ.eopathology. W1ashington, D.C.

1965b The Paleopathologic Riddle of "Symmetrical Osteoporosis." American Journal of Roentgenology, Vol. 95, pp. 135--142.

MOSS, M. L. and L. MOSS-SALENTIJN 1977 Analysis of Developmental Processes Possibly Related to Human Sexual Dimorphism in Permanent and Deciduous Canines. American Journal of PhYSical AnthropologY, Vol. 46, pp. 407- 414. MULINSKI, T. M. J. 1976 The Use of Fetal Matel":i.a1 as a Measure of Stress at Grass hopper Pueblo. Unpublished paper presented to Society for American Archaeology meeting, St. Louis.

NATHAN, H. and N. HAAS 1966 On the Presence of Cr1bra Orbitalia in Apes and Monkeys. American Journal of Physical AnthropologY, Vol. 24, pp. 351- 360.

NEUMANN, G. K. 1952 Archeology and Race in the American Indian. In Archeology of the Eastern United States, edited by J. B. Griffin, pp. 13- 34. University of Chicago Press, Chicago.

NEWMAN, M. T. 1960 Adaptations in the Physique of American Aborigines to Nutritional Factors. HUman Biology, Vol. 32, pp. 288-313.

NOBLE, H. W. 1976 The Estimation of Age from the Dentition. In Dental Identi fication and Forensic Odontology, edited by W. Harvey. Henry Kimpton Publishers, Longon.

O~, J. w. 1980 A Zooarchaeological Analysis of Vertebrate Faunal Remains from the Grasshopper Pueblo, Arizona. Doctoral dissertation, University of California, Berkeley.

ORTNER, D. J. and R. S. CORRUCCINI 1976 The Skeletal Biology of the Virginia Indians. American Journal of PhYsical Anthropology, Vol. 45, pp. 717-722.

ORTNER, D. J. and W. G. J. PUTSCHAR 1981 Identification of Pathological Conditions in Human Skeletal Remains. Smithsonian Contributions to AnthropologY 28. Washington, D.C.

OSBORNE, D. and J. S. MILES 1965 Diseases Encountered at Mesa Verde, Colorado. In Human Paleopatholosy, edited by S. Jarcho, pp. 85-97. Proceedings of a Symposium on Human Paleopathology, Washington, D.C.

OTTEN, C.. M. 1967 On Pestilence, Diet, Natural Selection, and the Distribution of Microbial and Human Blood Group Antigens and Antibodies. Current Anthropology, Vol. 8, pp. 209-226.

OWEN, G. and G. LIPPMAN 1977 Nutritional Status of Infants and Young ChUdren: USA. Pediatric Clinics of North America, Vol. 24, pp. 211-217. 217

PALKOVICH I A. M. 1980 The Arroyo Hondo Skeletal and Mortuary Remains. School. of American Research Press, Santa Fe.

PARK, E. A. 1954 Bone Growth in Health and Disease. Archives of Diseases of ~, Vol. 29, pp. 269-281 ..

1964 The Imprinting of Nutritional Disturbances on the Growing Bone. ~t Vol. 33 (suppl.ement), pp. 815-862.

PARSONS, E. C. 1939 Pueblo Indian Religion. University of Chicago Press, Chicago.

PERZIGIAN, A. J. 1977 Teeth as Tools for Prehistoric Studies. In Biocultural Adaptations in Prehistoric America, edited by R. L. Blakely, pp. 101-114. Southern Anthropological Society Proceedings 11, Athens.

PETERSON t w.. 1975 A Demographer's View of Prehistoric Demography. ~ Anthropology. Vol. 16, p1'. 227-245.

PHENlCE, T. W. 1969 A Newly Developed Visual Method of Sexing the Os Pubis. American Journal of Physieal Anthropolosy. Vol. 30, pp. 297- 301.

PIERCE, R. H., M. W. MAINEN and J. F .. BOSMAN 1977 The Cranium of the Newborn Infant. Department of Health, Edueation, and Welfare, Bethesda.

PINDBORG, J. J. 1970 PathologY of the Dentlu. Hard Tissues. W. B. Saunders Co •• Philadelphia ..

PLATZER, w. 1978 Loeomotor System. (Vol. 1 of Color Allas and Textbook of Human AnatoMY). Yearbook Medical Publishers, Chicago.

POLUNIN t I. V. 1967 Health and Disease in Contemporary Primitive Societies. In Diseases in Antiquity, edited by D. Brothwell and A. T. Sandison, pp. 69-97. Charles C. Thomas, Springfield.

PRA'l"I', M. W., V. L. HUTCHINS, Z. L. JANUS and D. P. BODYCOMBE 1978 Infant and Perinatal Mortality Rates by Age and Race. Maternal and Child Health Studies Project, Information Science Research Institute, Washington, D.C. PUFFER, R. R. and C. V. SERRANO 1973 PatterDS of Mortality in Childhood. Pan American Health Organization Sdenee Publication 262.

PYLE, S. I. and N. L. HOERR 1969 A Radiovaphic Standard of Reference for the GrowiD! Knee. CharJ.es C. Thomas, Springfield.

RABIN, D., B. ANTHONY and S. HARRISON 1972 Health Problems of U.S. and North American Indian populations. MSS Informatie Corp., New York.

REID, J. J. 1973 Growth and Response to stress at Grasshopper Pueblo, Arizona. Doctoral dissertation, University of Arizona, Tucson.

1978 Resp~e to stress at Grasshopper Pueblo, Arizcma. In Discovering Past BehaTior, edited by P. Grebinger, pp. 195- 213. Gordon and Breach Science Publishers, Inc., New York.

19B2 Personal communication. Assistant Professor of Anthropology, University of Arizona, Tucson.

REID, J. J. and I. SHIMADA 1982 Pueblo Growth at Grasshopper: Metbods and Models. In MultidisciplinarY' Research at Grasshopper Pueblo, Arizona, edited by W. A. Longacre, S. J. Holbrook. and M. W. Graves, pp. 12-19. Anthropological Papers of the Universi tv of ~ 40, Tucson.

REID, J. J. and S. M. WHITTLESEY 1982 Households at Grasahopper Pueblo. American Behavioral ~. Vol. 25. pp. 687-'703.

REYNOLDS, E. L. 1945 The Bony Pelvic Girdle in Earl,. Infancy. American Journal of Phlsical Anthropolofg', Vol. 3, pp. 32l-354.

1947 The Bony Pelvis in Prepuberal Childhood. American Journal of Physical AnthropoloQ', Vol. 5, pp. 165-200.

RICHMAN, E. A., D. J. ORTNER and F. P. SCHULTER-ELLIS 1979 Differences in Intra-Cortical Bone Remodel.ing in Three Aboriginal. American. Populations: Possible Dietary Factors. Calcified Tissue International, Vol. 28, pp. 209-214.

ROBBINS, L. M. 19?7 The Stor,. of Life Revealed b,. the Dead. In Biocul.tural Adaptations in Prehistoric America, edited by R. L. Blakely, pp. 10-26. Southern Anthropological. Society Proceedings U, Athens. 219 ROBINOW, M., T. W. RICHARDS and M. ANDERSON 1942 'rhe EruptioD. of DeciduouB Teeth. ~. Vol. 6, pp. 127-133.

ROBINSON. W. J. ODd R. SPRAGUE 1965 Disposal of the Dead at Point of PiDes, Arizona. ~ Antiquity. Vol. 30. pp. 442-453.

RONEY, J. G. , JR. 1965 Palaeoepidemiology: An Example from California. In Humau Paleopathology • edited by S. Jarcho, pp. 99-120. ProCeed ings of a Symposium on Human Pa1.eopathology, Washington, D.C.

ROSCOE, J. T. 1975 Fundamental Research Statistics for the Behavioral Sciences. Holt, Rinehart and Wiaston, Inc., New York.

ROSE, J. C. 1977 Defective Enamel Histology of Prehistoric Teeth from nlinois. American Journal. of Physical Antbropol.O&. Vol. 46. pp. 439- 446.

ROSE, J. C. t G. J. ARMELAGOS end J o We LALLO 1978 Histological Enamel Indicator of ChUdhood Stress in Pre historic Skeletal Samples. American Journal of PhYsical Anthropol~~, Vol. 49, pp. 511-516.

RUBENSTEIN, A., J. BOYLE. C. L. ODOROFF and S. J. KUNITZ 1969 Effect of Improved Sanitary Facilities on Infant Diarrhea in a Hopi Village. Public Health Reports, Vol. 84, pp. 1093-1097.

RUFF. C. B. and W. C. HAYES 1983 Cross-sectional Geometry of Pecos Pueblo Femora and Tibiae - A BioDlechanical. Investigation. American Journal of Physical Anthropologr. Vol. 60, No.3, pp. 359-400.

SALOMON, J. B., L. J. MATA and J. E. GOROON 1968 Malnutrition and the CODIIIIon Communicable Diaeases of Child hood in Rural Guatemala. American Journal of Public Health, Vol. 58. pp. 505-515.

SARNAT, B. G. and I. SCHOUR 1942 Enamel Hypoplasia (Chronologie Enamel Hypoplasia) in Relation to Systemic Disease: A Chronologic, Morphologic and Etiologic Classification. Journal of American Denta1 ASBOci ~. Vol. 29. pp. 67-75.

SAUL. F. P. 1973 Disease in the Maya Area: The Pre-Columbian Evidence. In The Classic Maya Collapse, edited by T. P. Culbert, pp. 301-324. University of New Mexico Press. Albuquerque. SCARBOROUGH, R. and I. SRnlADA 1974 Geologic Analysis of Wall Composition at Grasshopper with Behavioral Implications. !!!!, Vol. 40. pp. 49-67.

SCHAEFFER, J. P. (Ed.) 1953 Morris' Ruman Anatomy. Blakiston Co., New York. SCHEUER, J. L., J. H. MUSGRAVE and S. P. EVANS 1980 The Estimation of La.te Fetal and Perinatal Age from Limb Bone Length by Linear and Logari trunic Regression. Annals of Human Biology, Vol. 7, pp. 257-265. ---

SeROUR, L. and M. HASSLER 1941 The Development of the Ruman Dentition. Journal of American Dental Association, Vol. 28, pp. 1153-1160.

1944 Chart - The Development of the Human Dentition. American Dental Association.

SCIULLI, P. W. 1977 A Descriptive and Comparative Study of the Deciduous Dentition of Prehistoric Ohio Val.ley Amerindians. American Journal of Physical AnthropologY, Vol. 47, pp. 71-86.

SCRIMSHAW IN. S. 1964 Ecological Factors in Nutritional Disease. American Journal of Clinical Nutrition, Vol. 14, pp. 112-121.

1968 The Death Rate of l-Year Old Children in Underdeveloped Countries. Archives of Environmental Health, Vol. 17. pp. 691-692.

SCRnlSHAw, N. S., H. A. BRUCH. W. ASCOLI and J. E. GORDON 1962 Studies of Diarrheal Disease in Central America. American Journal of Tropical Medicine and Rygiene, Vol. ll,~- 409.

SCRIMSHAW, N. S., C. E. TAYLOR and J. E. GORDON 1968 Interactions of Nutrition and Infection. WHO Monograph ~ 57. Geneva.

SCRIMSHAW, N. S. and C. TEJADA 1970 Pathology of Living Indians as Seen in Guatemala. In Handbook of Middle American Indians, edited by T. D. Steward, V~ University of Texas Press, Austin.

SHAHIDI, N. T. and L. K. DIAMOND 1960 Skull Changes in Infants vith Chronic Iron-Deficiency Amemia. New England Journal of Medicine, Vol. 262, pp. 137-139. 221

SHAW, J. B .. 1970 Preeruptive Effects of Nutrition on Teeth. Journal. of Dental. ~, Vol. 49, pp. 1238-1250.

SHIPMAN, J. H. 1982 Biological Relationships among Prehistoric Western Pueblo Groups Based on Metric and Discrete Traits of the Skeleton. Doctoral dissertation, University of Arizona, Tucson.

SIEGEL, S. 1956 Nonpararnetric Statistics for the Behavioral Sciences. McGraw Hill Book Co., New York.

SIEVERS, M. L. 1964 Coceidioidomycosis Among Southwestern American Indians. Annual Review of Respiratory Diseases, Vol. 90, pp. 920-926.

1966 Disease Patterns Among Southwestern Indians. Public Health Reports, Vol. 81, pp. 1075--1083.

SMITHGALL, E. B., F. E. JOHNSTON, R. M. MALINA and M. A. GALBRAITH 1966 Developmental Changes in Compact Bone Relationships in the Second Metacarpal. Human Biolog. Vo1.. 38, pp. 141.-151. SNOW, C. E. 1.948 Indian Knoll Skeletons. University of Kentucky Reports in Anthropology, Vol. 4, No.3, Part 2. Lexington. SNYDER, R. G. 1.959 The Dental Morphology of the Point of Pines Indians., Doctoral dissertation, University of Arizona, Tucson.

SNYDER, R. G. t A. A. DAHLBERG, C. C. SNOW and T. DAHLBERG 1969 Trait Analysis of the Dentition of th.e Tal"'ahumara Indians and Mestizos of the Sierra Madre Occidental, Mexico. American Journal of Physical AnthropologY, Vol. 31, pp. 65-76. ---

SONTAG, L. W. 1.938 Evidence of Disturbed Prenatal and Neonatal Growth in Bones of Infants Aged One Month. American Journal of Diseases of ~. Vol. 55, pp. 1248-1256.

SPUHLER: t J. N. 1.954 Some Problems in the Physical Anthropology of the American Southwest. American Anthropologist, Vol. 56, pp. 604-625.

STEGGERDA, M. and T. HILL 1942 Eruption Time of Teeth Among Whites, Negroes, and Indians. American Journal of Orthodontic and Oral Surgery, Vo1.. 28, pp. 361-370. 222

STEINBOCK, R. T. 1976 Paleopatholorical Diagnosis and Interpretation. Charles C. Thomas, Springfield.

STEWART, B. E. and G. R. PRESCOTT 19'76 Oral Facial Genetics. C. V. Mosby, St. Louis.

STEWART, T. D. 1934 Sequence of Epiphyseal Union, Third Molar Eruption and Suture Closure in Eskimos and American Indians. American Journal of Phtsical Anthropolop;!". Vol. 19. pp. 43~

1962 Comments on the Reassessment of the Indian Knoll Skeletons. American Journal of Physical Anthropology, Vol. 20, pp. 143- 147.

1979 Essentials of Forensic Anthropolop_ Charles C. Thomas, Springfield.

STEWART, W. H. t L. J. McCABE, E. C. HEMPHILL and T. DeCAPI'l'O 1955 The Relationship of' Certain Environmental Factors to the ~r;;~~c:e:ic~H!:i:::!o;~. 'r,r!;:n ~8:;~ of STINI. W. A. 1969 Nutri tiona! Stress and Growth: Sex Differences in Adaptive Response. American Journal of PhySical Anthropologl. Vol. 31. pp. 417-426.

1971 Evolutionary Implications of Changing Nutritional Patterns in Human Populations. American Anthropologist, Vol. 7:5, pp. 1019-1030.

1974 Adaptive Stroategies of Human Populations Under Nutritional. Stress. In Biosocial Interrelations in Population Adaptation, ed! ted by F. E. Johnston and E. S. Watts, pp. 19-41. World Anthropology Series, Mouton, The Hague.

SULLIVAN, A. P., III 1974 Problems in the Estimation of Original Room Function: A Tentative Solution from the Grasshopper Ruin. Kiva, Vol. 40, pp. 9,-101. --

SUMNER, D. R. n.d. Size t Shape and Bone Mineral Content of the Human Femur in Growth and Aging. Doctoral dissertation, University of Arizona, Tucson.

BUNDICK, R. I,. 1972 Human Skeletal Growth and Dental Development as Observed in the India11 Knoll Population. Doctoral dissertation, Univer sity of Toronto, Toronto. SUNDICK, R. I. 19?? Age and Sex Determination of Subadul t Skeletons. ~ Forensic Science, Vol. 22, pp. 141-144.

1978 Human Ske1etal Growth and Age Determination. HCMO, Vol. 29, pp. 228-249. --

1981 Personal. communication. Profel!lsor of Anthropology, Western Michigan Univerait1.

SWEENEY, E. A., J. CABRERA, J. URRUTIA and L NATA 1969 Factors Associated with Linear Hypoplasia of HumlUl Deciduous Incisors. Journal. of Dental Research, Vol. 48, pp. 1275-1279.

SWEENEY, E. A., A. J. SAFFIR and M. de I:£ON 1971 Linear Hypoplasia of Deciduous Incisor Teeth in Malnourished Children. American Journal of Clinical Nutrition, Vol. 24, pp. 29-31.

TANNER, J. H. 1978 Foe-tus Into Man: Physical Growth from Conception to Maturity. Open Books Publishing, Ltd., London.

TITCHE, L. L., R. D. WACHTER, W. W. COULTHARD and L. L. HARRIES 1981 Mastoiditis in Prehistoric Arizona Indians. Arizona Medicine, Vol. 38. pp. 712-714. TODD, T. W. 1930 The Anatomical Features of Epiphyseal Union. Child Develop ment, Vol. 1, pp. 186-194.

TROTl'ER, M. and R. R. PETERSON 1967 Transverse Diameter of the Femur: On Roentgenograms and on Bones. Clinical OrthopediCS, Vol. 52, pp. 2'3-.239.

TUGGLE, H. D. 1970 Prehistoric Community Relationsbips in East-Central Arizona. Doctoral dissertation, University of Arizona, Tucson.

TU~83H·F~t;;n~; :!~;;dM:~iio;~~i?uiture in the Grasshopper Region of Arizona. Ms, Department of Anthropology, University of Arizona, Tucson.

UBELAKER, D. H. 1978 Human Skeletal Remains: Excavation, Analysis, Interpretation Aldine Publishing Co., Chicago. 224 u.s. DEPAR'lMENT OF HEALTH, EDUCATION AND WELFARE 1968 Tracking Diseases from Nature to Man. National Communicabl.e Disease Center, PHS, Atlanta. u.s. GOVEBNMENT PBINTING OFFICE 1976 Report on Indian Health

VAN DUZEN, J., J. P. CARTER, J. SECONDI and C. FEDERSPIEL 1969 Protein and Calorie Mal.nutri tiCD Among Preschool Navajo Indian Children. American Journal of Clinical Nutri tieD, Vol. 22, pp. 1362-1370.

1976 Protein-and Calorie Malnutri tiCD Among Preschool. Navajo Indian Children: A Follow-up. American Journal. of Clinical ~, Vol. 29, pp. 657-662.

VAN REENEN, J. F. 1966 Dental Features of a Low-Caries Primitive Population. Journal of Dental Research, Vol. 45, pp. 703-713.

VON ENDT, D. W. and D. J. ORTNER 1982 Amino Acid Analysis of Bone from a Poasible Case of Pre historic Iron Deficiency Anemia from the American Southwest. American Journal of PhYsical AnthropologY, Vol. 59. pp. 377-385.

WASHBURN, S. L. 1951 The New Physical Anthropolog'fo, Transactions of New York Academy of Sciences, Series II, Vol. 13. pp. 298-304.

WATSON, R. C., H. GROSSMAN and M. A. MEYERS 1973 Radiologic Findings in Nutritional Disturbances. In Modern Nutrition in Health and Disease, edited by Goodhart a~ Shils, pp. 547-571.

WEAVER, D. S. 1977 New Methods for the Determination of Sex, Age, and Rates of Growth of Infant and Child Skeletal Remains in Prehistoric American Indian Populations. Doctoral dissertation, University of New Mexico, Albuquerque.

YlEINMANN, J. P. and H. SICRER 1947 Bone and Bones. C. V. Mosby Co., St. Louis.

WEISS, K. M. 1973 Demographic Models for Anthropology. American Antiquity, Vol. 38, No.2, Part 2.

1975 Demographic Disturbances and the Use of Life Tables in Anthropology. American AntiQuity, Vol. 40, No.2, Part 2, pp. 46-56. 225

WEISS, K. M. 1976 Demographic Theory and Anthropological Inference. ~ Review of AnthropologY, Vol. 5, pp. 351-375.

WELBOURN, H. F. 1955 The Danger Period During Weaning, Part iii. ~ Tropical Pediatrics, Vol. I, pp. 161-173.

WELLS, c. 1967 A New Approach to Palaeopathology: Harris Lines. In ~;:~~:~:t i;p~;~{e~: eg~!;~e:Yc~· ~~:::e~~r~:f~;l~:

1975 Prehistoric and Historical Changes in Nutritional. Diseases and Associated Conditions. Progress in Food and Nutrition Science, Vol. 1, pp. 729-779.

WHEELER, R. C. 1962 An Atlas of Tooth Form. W. B. Saunders Co •• Philadelphia.

WHITE, L. 1942 The Pueblo of Santa Ana, New Mexico. American Anthropological Association Memoir 60.

1963 The Pueblo of Sia, New Mexico. Bureau of American Ethnology ~184.

WHITNEY, W. F. 1886 Notes on the Anomalies, Injuries and Diseases of the Bones of the Native Races of North America. Reports of the Peabody ~ III, No.5, pp. 433-448. Cambridge.

WHITTLESEY, S. M. 1978 status and Death at Grasshopper Pueblo: Experiments toward an Archaeological Theory of Correlates. Doctoral disserta tion, University of Arizona, Tucson.

Wn.COX, D. R. 1982 A Set-Theory Approach to Sampling Pueblos: The Implicationi::'i of Room-Set Additions at Grasshopper Pueblo. In Multi disciplinary Research at Grasshopper Pueblo, Ariz'Oiia":pp. 19-28. AnthropolOgical Papers of the University of Arizona 40, Tucson.

WINTER, G. B. and A. H. BROOK 1975 Enamel Hypoplasia and Anomalies of the Enamel. ~ Clinics of North America, Vol. 19, pp. 3-24.

WOLSTENHOIME, G. E. W. and M. O'CONNOR (Eds.) 1964 Diet and Bodily Constitution. Little Brown & Co., Boston. 226

WOOD, C. s. 1983 Early Childhood, The Critical stage in Human Interactions with Disease and Culture. Social Science and Medicine, Vol. 17, No.2, pp. 79-85.

WOODBURY, A. M. 1965 Notes on the Human Ecology of Glen Canyon. University of Utah Anthropological Papers 74. Salt Lake City.

WOODWARD, W. E. , N. HIRSCHHORN, R. B. SACK, R. A. CASH, I. BROWNLEE, G. H. CHICKADONZ, L. K. EVANS, R. H. SHEPARD and R. C. WOODWARD 1974 Acute Diarrhea on an Apache Indian Reservation. American Journal. of Epidemiolog;y, Vol. 99, pp. 281-290. ---

Y'EDYNAK, G. 1976 Lon'g Bone Growth in Western Eskimo and Aleut Skeletons. American Journal. of Physical Anthropol.oftV, Vol. 45, pp. 569- 574.

YUDKrn, J .. 1969 Archaeology and the Nutritionist. In The Domestication and Exploitation of Plants and Animals, edited by P. J. Ucko and G. W. Dimbleby. Aldine, Chicago.

ZA'INO, E. C. 1968 Elemental Bone Iron in the Anasazi Indians. American Journal of PhYsical Anthropo1o&, Vol. 29, pp. 433-436.