







































Bioarchaeology International


Bioarchaeology International 
Volume 2, Number 1: 44–62 
DOI: 10.5744/bi.2018.1015

Copyright © 2018 University of Florida Press

Broken Childhoods: Rural and Urban  
Non- Adult Health during the Industrial 
Revolution in Northern England  
(Eighteenth– Nineteenth Centuries)
Rebecca L. Gowlanda*, Anwen Caffella,b, Sophie Newmana, 
Alysa Levenec and Malin Holstb,d

aDepartment of Archaeology, Durham University, South Road, Durham DH1 3LE, UK
bYork Osteoarchaeology Ltd, 75 Main St, Bishop Wilton, York YO42 1SR, UK
cOxford Brookes University, School of History, Philosophy and Culture, Faculty of Humanities and 
Social Sciences, Tonge Building, Oxford OX3 0BP, UK

dDepartment of Archaeology, University of York, Kings Manor and Principals House, University of York, 
Exhibition Square, York YO1 7EP

*Correspondence to: Rebecca Gowland, Department of Archaeology, Durham University, South Road,
Durham DH1 3LE, UK

e- mail: Rebecca  .gowland@dur  .ac  .uk

ABSTRACT During the eighteenth and nineteenth centuries, England underwent a period of rapid urbanization and indus-
trialization. The detrimental effects of urban living conditions and child factory labor on the health of children 
during this time has been the subject of considerable debate and investigation by historians. It is generally un-
derstood that growing up in a rural environment was more conducive to healthy growth and development than 
within an industrial town. This study presents the first direct comparison of the bio archae ol o gi cal evidence for 
non- adult health from contemporaneous urban and rural sites from the north of England. Rural skeletal assem-
blages from this period are rare, and most published studies are biased toward urban sites in the south of the 
country. Contrary to expectations, results revealed equal prevalence rates of metabolic and dental disease at both 
sites, but skeletons from the rural site had greater evidence of growth disruption and respiratory disease. Evi-
dence for specific infectious disease and medical care in response to trauma were also identified. Our interpre-
tations of rural/urban health during this period must take into account the dire consequences of social inequalities 
and economic migration. There is a tendency for the latter to be characterized as unidirectional— from country 
to town— without due consideration of rural industry and child migrant workers.

Keywords: child labor; growth; metabolic disease

RESUMEN Durante los siglos XVIII y XIX Inglaterra experimentó un período acelerado de urbanización e industrial-
ización. Los efectos perjudiciales de las condiciones de vida urbana y del trabajo infantil obrero en la salud de 
los niños durante este período han sido objeto de considerables debates e investigación por parte de los histori-
adores. En general, se entiende que el crecer en un ambiente rural era más propicio para un crecimiento y desar-
rollo saludables, en comparación con el ambiente al interior de las ciudades industrializadas. Este estudio presenta 
la primera comparación directa de la evidencia bioarqueológica respecto a la salud de individuos no- adultos pro-
venientes de sitios urbanos y rurales contemporáneos del norte de Inglaterra. Las colecciones de restos óseos 
rurales de este período son escasas, y la mayoría de los estudios publicados están sesgados hacia los sitios ur-
banos del sur del país. Contrario a las expectativas, los resultados revelaron tasas de prevalencia similares en 

Received 10 December 2017
Revised 22 February 2018

Accepted 03 March 2018



Gowland et al. 45

The eighteenth and nineteenth centuries in Britain 
were a period of rapid urbanization and industrializa-
tion; from A.D. 1801 to 1901 the proportion of people 
living in towns increased from one- fifth to four- fifths 
(Wohl 1983). By the mid- nineteenth century almost 
half of the total population of England was under 
20 years of age: “England was awash with children” 
(Humphries 2013:115). Traditionally, children from 
poorer families will always have had to work, either 
within the domestic context or as apprentices and la-
borers. What changed with the Industrial Revolution 
was the nature of that work, with a dramatic increase 
in non- domestic labor by women and children (Goose 
and Honeyman 2013:4). Children of the urban poor in 
the eighteenth and nineteenth centuries have long 
been conceptualized as the passive, exploited victims 
of an insatiable industrial machine, whose wants and 
needs were overlooked by a laissez- faire society fo-
cussed on economy and Empire (Gowland 2015b). In 
a speech to the House of Lords in 1873, Lord Shaftes-
bury famously described children leaving the factory 
gates during the earlier part of the nineteenth century 
as “a set of sad, dejected, cadaverous creatures. . . .  
[T]he sight was most piteous, the deformities incredible. 
They seemed to me, such were their crooked shapes, 
like a mass of crooked alphabets” (Pinchbeck and 
Hewitt 1973:403). This account is borne out by numer-
ous other descriptions of working- class urban chil-
dren at this time (e.g., Engels 1950; Gaskell 1833). By 
contrast, the rural environment during this period 
was conceptualized as much healthier for children, of-
fering fresh, unpolluted air, plenty of sunshine, a 
more varied diet, less overcrowding, and better sani-
tation. As Gaskell (1833:200) observed: “A child from 
an agricultural district, eight or nine years old, bloom-
ing with rosy health, full of vitality, is transported to 
a crowded town . . .  it is exposed to miasmatic evapo-
rations, shut up in a narrow street, its home is damp 
and cold, its food poor and badly cooked: in a few 
months, from the force of these circumstances, the 
Hebe- looking child has become pallid.”

These sentiments were echoed by the nineteenth- 
century physician Francis Sharp (in the Reports from 

the Commissioners on Conditions in Factories, 1833, vol 
XXI, parliamentary papers, pp. 12), who moved from 
a rural practice near Scarborough, North Yorkshire, 
to work in the city of Leeds: “The general appearance 
of the children in Leeds immediately struck me as 
much more pallid, and also the firmness of the fibre as 
much inferior to what I had seen in Scarborough and 
the adjacent country. . . .  If it were not for the individ-
uals who join the mills from the country the factory 
people would soon be deteriorated.”

There was a general anxiety that urban childhoods, 
particularly when spent undertaking factory labor, 
would result in the eventual physiological deterioration 
of the nation. These concerns sparked a number of 
inquiries into the health of urban and factory children, 
and a vast amount of qualitative and anthropom etric 
data was commissioned from across the country. The 
results of these endeavors indicated that rural chil-
dren were, as suspected, on average 3 cm taller than 
their urban counterparts (Kirby 2013). It was con-
cluded, however, that factory labor per se was not re-
sponsible for the “stinted” growth and low life 
expectancy, but rather insalubrious urban conditions 
more generally, combined with the perceived lowly 
habits and morality of the poor (Chadwick 1842). 
There are numerous descriptions of the filthy, over-
crowded, unsanitary, polluted living conditions in 
many of the poorer slum areas. So- called back- to- 
back housing in cities such as Bradford and Leeds also 
allowed very little natural light into the rooms, and 
this combined with severe air pollution meant that 
exposure to sunshine, vital for proper mineralization 
of the bones and immune function in growing chil-
dren, was limited (Brimblecombe 1978; Hudson 1992). 
However, some contemporary accounts of rural life 
also point to inadequate and overcrowded houses, as 
well as polluted water supplies spreading diseases such 
as typhus (Wilkes 2011). The nineteenth- century epi-
demiologist William Farr felt that there was an often 
“fanatical” fixation on the declining conditions of ur-
ban centers, stating that “epidemics desolated the 
country as well as towns, though to less extent” (quoted 
in Young and Handcock 1956:771). Rural populations 

ambos sitios en cuanto a desórdenes metabólicos y enfermedades dentales, pero los esqueletos del sitio rural pre-
sentaron mayor evidencia de alteraciones del crecimiento, y enfermedades respiratorias. También se encontró 
evidencia de enfermedades infecciosas específicas y tratamiento médico como respuesta a traumas. Nuestras 
interpretaciones de la salud rural/urbana durante este período deben tener en cuenta las nefastas consecuencias 
de las desigualdades sociales y la migración económica. Existe una tendencia a caracterizar esta última de manera 
unidireccional— del campo a la ciudad— sin la debida consideración de la industria rural y de los niños traba-
jadores migrantes.



Childhood Health in the Industrial Revolution46

were also highly susceptible to periods of food short-
ages and crop failures, and a series of poor harvests 
could result in poverty and famine (Bogin 1999). Al-
fred Ireson, who was born in 1856, described rural life 
during this period as “a time of trial and difficulty. 
The agricultural workers had long hours, they pay 
barely enough to keep body and soul together. The 
condition of the children in many cases was pitiable. 
Rough food and clothes; everything depended on the 
skill and character of the mother” (quoted in Burnett 
1984:83). While protective measures regarding child 
labor in factories were instigated, those working 
within agriculture and rural cottage industries were 
overlooked until the Education Act of 1876, which de-
creed that children under 10 years of age could no lon-
ger be employed in agricultural work (Burnett 1984; 
Pinchbeck and Hewitt 1973).

The vast majority of research concerning childhood 
health during this period is derived from historical 
data and records (Kirby 2013). While these are ex-
tremely valuable, some of the qualitative reports de-
pict partisan viewpoints and political polemics rather 
than objective observation (e.g., Engels 1950). Recent 
excavations of cemeteries from the eighteenth and 
nineteenth centuries have highlighted the important 
contribution of bio archae ol o gi cal evidence for exam-
ining the direct physiological impact of these environ-
ments on children living at the time (e.g., Brickley 
and Miles 1999; DeWitte et al. 2015; Geber 2016; Lewis 
2002; Mays et al. 2009; Newman and Gowland 2016; 
Pinhasi et al. 2006). Childhood growth and morbid-
ity are multidimensional in etiology but are widely 
documented as being a sensitive indicator of the so-
cioeconomic environment (Lewis 2007). Because so 
few rural sites dating to this period have been exca-
vated, recent bio archae ol o gi cal analyses have been 
strongly biased toward urban population samples. 
Mays et al. (2008) provide a valuable comparison of 
urban Birmingham with rural Wharram Percy, but 
the latter site was in use for a millennium and pre-
dominantly medieval, thus lacking chronological res-
olution. This is important, because rural lifeways were 
not static and unchanging across the last millennium; 
rural industry also developed apace during the late 
eighteenth and early nineteenth centuries.

The aim of this study was to compare and contrast 
rural and urban skeletal evidence for the health and 
mortality of children from two sites in the north of En-
gland in order to assess the historically accepted idea 
that rural environments were more conducive to better 
childhood health. This research provides a rare insight 
into a rural post- medieval assemblage (now reburied) 
and thus also serves to enrich the existing corpus of 
bio archae ol o gi cal knowledge for this period, which has 
so far been largely confined to urban sites. This analysis 

of sites from the north of England also provides an 
important comparative data set given the current bias 
toward sites from the south and midlands. The bio-
archae ol o gi cal data will be integrated with existing 
historical evidence to obtain a richer understanding of 
living and working conditions in both environments.

Materials

Skeletal remains were analyzed from the rural church-
yard of St Michael and St Lawrence, Fewston, North 
Yorkshire, and from the urban site of Coach Lane, 
North Shields, Tyneside (Fig. 1).

Fewston, North Yorkshire

Fewston is a small village located in the Washburn 
Valley, near Harrogate in North Yorkshire. The skele-
tal assemblage was excavated from the parish church-
yard in advance of building work by JB Archaeology 
in 2009 and 2010 (Buglass 2009; Caffell and Holst 2017) 
and was reburied in September 2016. This assemblage 
is exceptional for several reasons:

1. It is one of only a few predominantly post- 
medieval rural skeletal collections.
2. Twenty- one of the excavated individuals were 
confidently identified based on coffin plates and 
grave monuments.
3. The diaries of John Dickinson, a late- nineteenth- 
century resident of the adjacent village of Greater 
Timble, provide important historical insights into 
everyday life in the Washburn Valley. The diaries 
also refer to a number of the identified individu-
als within the skeletal assemblage, thus providing 
unique personal insights.

The Church of St Michael and St Lawrence in Few-
ston was rebuilt in A.D. 1697, most of the medieval 
church having been destroyed in a fire the preceding 
year (Alred 1997:67). The graveyard would have been 
in use from at least the fourteenth century, and some 
of the excavated skeletons could date to the medie-
val period. Only a relatively small area (approximately 
300 m2), however, was subject to excavation, and cof-
fin plates and headstones indicated that the better- 
surviving burials in this location were predominantly 
of nineteenth- century date. The cemetery closed in 
1896, although two individuals who died in the early 
twentieth century did gain permission to be buried 
there. A total of 154 individuals were excavated, in-
cluding 50 non- adults, a category defined here as less 
than 20  years of age. The more usual cutoff age for 
non- adults in bio archae ol o gi cal studies is either 17 or 



Gowland et al. 47

18 years; however, this was extended for the purposes 
of this study in recognition that adversity in early life 
(as evident in many of the skeletons within this sam-
ple) is known to cause delays in the chronological age 
of attainment of skeletal maturation. In the absence of 
a more reliable age from dental development, there-
fore, some of the individuals within the sample may 
have been slightly older than the age that their epiph-
yseal union suggested.

The use of the term non- adult in this context does 
not, of course, reflect nineteenth- century social norms 
regarding the chronological age of attainment of adult 
status, but denotes the skeletal age only. Parish records 
indicate that the social status of those buried within 
the cemetery was mixed, including well- off land-
owners as well as those of lower status, such as labor-
ers. Agriculture was the predominant occupation in 

Fewston during this period, but from the late eigh-
teenth century there was also a textile industry, with 
Westhouse Mill established at nearby Blubberhouses 
in 1791 (Alred 1997:30– 31).

Coach Lane, North Shields

Coach Lane was a former Society of Friends burial 
ground (c. 1711– 1857) located in North Shields, just east 
of Newcastle- upon- Tyne. North Shields in the late 
eighteenth and early nineteenth centuries was a heav-
ily populated shipping, fishing, and coal- mining com-
munity, undergoing rapid development (Proctor et al. 
2016). The town was heavily industrialized, and in a 
government report the environmental conditions were 
considered derisory, with narrow streets described 
as “more justly compared to wells filled with noxious 

Figure 1. The location of the Fewston and Coach Lane, North Shields sites.



Childhood Health in the Industrial Revolution48

emanations” (Second Report of the Commissioners 
1845:19). Numerous epidemics, including cholera, oc-
curred during this period, and air and water pollution 
from the various industries was extensive (Proctor 
et al. 2016). The social status of those buried at the 
Coach Lane cemetery was mixed, with Quakerism 
attracting those from different spheres of life. The 
burial records occasionally document the profession 
of the deceased, and these included “junior painter,” 
“grocer,” “shopkeeper,” “master mariner,” and “linen 
weaver.” There were many prominent, high- status 
Quakers within the northeast during this period, 
some of whom were buried at Coach Lane, along with 
servants (Proctor et al. 2016). The effects of a heavily 
polluted environment, however, would have been det-
rimental to all social classes (Gowland and Newman 
2018). There is direct evidence that at least some of the 
children buried at the site had been engaged in factory 
labor, with the skeleton of one individual (aged 12– 14 
years) possibly exhibiting the notorious occupational 
condition “Phossy Jaw”— osteonecrosis of the mandi-
ble typically caused by exposure to phosphorus during 
match- making (Roberts et  al. 2016). In contrast to 
Fewston, the Coach Lane cemetery was excavated in 
its entirety (Procter et  al. 2016) and consisted of 236 
individuals, 81 of whom were non- adults (under 20 years 
of age).

Methods

Age at death of the non- adults was estimated using 
dental development and eruption, long bone growth, 
and epiphyseal fusion (see Table 1 for details). Follow-
ing convention, dental age was considered more rep-
resentative of the chronological age of the child, as 
tooth development is less affected by environmental 
adversity than skeletal development (Elamin and Liv-
ersidge 2013; Saunders 2008— although see Discussion 
section below). When dental age could not be estab-
lished due to missing teeth, age was instead estimated 
from epiphyseal fusion and metric analysis. Long bone 
diaphyseal lengths were measured and compared to 

age at death estimated from dental age as well as 
Maresh’s (1955) known- age long bone reference data. 
Skeletal growth profiles were constructed from diaphy-
seal lengths of the major long bones using the midpoint 
of the dental age range, whereby an individual with a 
dental age estimate falling between 0.5 to 1.5  years 
would be categorized as 1 year. This follows the practice 
of previous growth studies (see Mays et al. 2008). These 
age categories act as a proxy for known age, and it is 
not intended that the age midpoint should be taken as 
a genuine reflection of the precise chronological age.

Recent methods to detect growth disruption were 
applied, including measurements of vertebral body 
heights (Newman and Gowland 2015), and the left fe-
mur was selected for cortical thickness (CT) measure-
ments (substituted with the right side when necessary) 
(Mays et al. 2009). Radiographs were taken using a 
MPX 10 portable radiography unit set at 70kVp, 
0.500 mAs and with a Carestream Point- of- Care dig-
ital CR reader. Measurements of the total bone width 
(T) and the medullary width (M) were taken from the 
mid- shaft of the femur (Mays et al. 2009). Cortical 
thickness was determined as T –  M, and plotted 
against the dental age (see Newman and Gowland 
2016). Finally, skeletal indicators of puberty were re-
corded following Shapland and Lewis (2013, 2014).

The pathological lesions recorded include rickets 
(vitamin D deficiency), scurvy (vitamin C deficiency), 
cribra orbitalia, dental enamel hypoplasia, dental car-
ies, non- specific periosteal reactions on the major 
long bones, endocranial and ectocranial lesions, max-
illary sinusitis, rib lesions and evidence for tubercu-
losis (Table  1). Rickets was diagnosed through the 
presence of bowed long bones, flared and/or porous 
metaphyses and sternal rib ends, and the presence of 
medial tilting of the distal tibia, while coxa vara and 
flattening deformities in the proximal femur were also 
considered (Brickley and Ives 2008; Mays et al. 2006; 
Ortner and Mays 1998). Scurvy was diagnosed through 
the presence of woven bone in the orbits, porosity 
on the mandible and/or maxilla (especially focused on 
the internal ramus and coronoid process of the man-
dible, and around the infraorbital foramen of the 

Table 1. Methods of analysis used in this study.

Method References

Age at Death dental development Moorrees et al. 1963a, 1963b; Smith 1991
long bone growth Maresh 1955; Scheuer and Black 2000
epiphyseal fusion Scheuer and Black 2000

Growth cortical thickness Mays et al. 2009
vertebral body height Newman and Gowland 2015

Pathologies metabolic disease Brickley and Ives 2006, 2008; Mays et al. 2006; Ortner 2003;  
Ortner and Mays 1998; Stark 2014

cribra orbitalia Stuart- Macadam 1991
dental enamel defects Hillson 1996; Ogden 2008; Ogden et al. 2007
new bone formation Ortner 2003; Roberts and Connell 2004; Lewis 2007



Gowland et al. 49

maxilla), porosity on the greater wing of the sphenoid, 
and porosity in the supraspinous fossa of the scapula 
(Ortner 2003; Stark 2014). The pathological lesions as-
sociated with metabolic disease may be very subtle 
(Brickley and Ives 2008), and this is confounded fur-
ther by the porous appearance of the rapidly growing 
bones of infants and children. All pathologies were 
therefore recorded by two bioarchaeologists working 
side by side (Caffell and Gowland), and the results 
were compared with those of an observer working in-
dependently (Newman). Rickets and scurvy were di-
agnosed as present only when both sets of independent 
observations were positive. If one independent ob-
server identified indicators of rickets or scurvy but 
the other did not, then these skeletons were reexam-
ined and agreement reached. Due to the multiple skel-
etal elements that can display signs of vitamin C or 
vitamin D deficiency, only crude prevalence rates (per 
individual) for these pathologies were calculated; 
however, individuals for whom the diagnostic skeletal 
elements were absent were excluded from the preva-
lence calculations.

All long bones were examined for the presence of 
non- specific periosteal new bone growth in the form 
of woven bone, lamellar bone, and/or abnormal poros-
ity. Likewise, the endocranial and ectocranial sur-
faces and maxillary sinuses were examined for new 
bone formation (woven and/or lamellar) and poros-
ity. All deciduous and permanent teeth (including 
unerupted but observable tooth crowns) were exam-
ined for defects in enamel formation (lines, grooves or 
pits), and the prevalence rates for dental enamel de-
fects were expressed as a percentage of all of the teeth 
present (including observable unerupted teeth). Cribra 
orbitalia was recorded using the Stuart- Macadam 

(1991) system, but only presence or absence is reported 
here, and results are provided as true prevalence rates 
(percentage of preserved orbits affected). The mini-
mum number of ribs present on the left and right side 
for each individual was counted, as was the minimum 
number of ribs showing new bone formation (woven 
or lamellar). The number of un- sided rib fragments 
was counted, along with those exhibiting pathologi-
cal lesions. Crude prevalence rates were calculated for 
the minimum number of ribs affected as a proportion 
of the minimum number of ribs present.

Results

Age at death

The age distribution of the non- adults from Coach 
Lane follows the pattern frequently observed at ar-
chaeological cemetery sites, with a high proportion 
of deaths in those under 6 years of age and relatively 
few deaths during adolescence (Fig. 2). By contrast, 
Fewston presents a more unusual non- adult age dis-
tribution, with higher numbers of adolescent deaths. 
Only two individuals at Fewston were less than 1 year 
of age, one of whom was a named individual. The lack 
of infants is likely to have resulted from the common 
practice of spatial segregation of this age group within 
cemeteries and the fact that only a relatively small area 
was excavated.

The difference in age structure between the two 
sites with respect to the excess of adolescents at Few-
ston is important to consider. Is this unusual age 
profile simply an artifact of the incomplete excava-
tion of Fewston, or could it reflect genuine differences 

Figure 2. The age- at- death distribution of the non- adults from Fewston and Coach Lane.



Childhood Health in the Industrial Revolution50

in age- structure and mortality risks between the 
sites? If the latter, then what was the driving force be-
hind this? We hypothesize that this difference reflects 
genuine mortality risks in this section of the ceme-
tery, which is dominated by nineteenth- century 
burials, and that it is driven by the migration of ado-
lescents from poor urban areas seeking employment 
in rural industry. This will be explored further with 
reference to the results for the pathological lesions 
below. Comparison of the various pathologies be-
tween the two sites will also explicitly consider the 
different age- at- death profiles when inferring aspects 
of the lived experiences of these children.

Growth

Diaphyseal lengths, when plotted against dental age, 
were similar between Fewston and Coach Lane; un-
fortunately, relatively few measurements were possible 
from the former site due to poorer preservation (Fig. 3). 
These values aligned with Maresh’s (1955) data up 

until approximately 10 years of age, after which most 
adolescents drop below the modern values. This 
could relate to the relatively delayed pubertal growth 
spurt in these individuals compared to modern chil-
dren (Fig. 4). In keeping with the findings of Mays 
et al. (2009), cortical thickness appears to be a more 
sensitive indicator of adversity and was compro-
mised in children from both sites. Growth retarda-
tion was observed particularly in children older than 
4 years of age (Fig. 3). While only small numbers of 
femora were available for measurement from Few-
ston, cortical thickness measurements of the humeri 
and tibiae from these sites were similarly reduced when 
compared to modern norms.

Vertebral measurements were taken following the 
protocol outlined by Newman and Gowland (2015), 
which identified measurements from vertebral group-
ings of C5- 6, T6- 8, and L2- 4 as being reliable indica-
tors of potential population differences in growth 
patterns. Due to the C5– C6 group presenting a more 
robust sample within this study for both sites, these 

Figure 3. Femoral diaphyseal lengths and cortical thickness from Fewston and Coach Lane plotted against 
dental age as a proxy for known age and modern comparative data.



Gowland et al. 51

measurements were plotted against dental age (Fig. 5). 
Values for several adolescents from Fewston were 
anomalously low, and an ANCOVA test revealed 
that vertebral body height was statistically different 
(F[1,35] = 13.551, p = 0.001) between the two sites, while 
adjusting for dental age. These adolescents also ex-
hibited a range of skeletal indicators of poor health. 
For example, skeleton 262 had extensive new bone 
formation and severe enamel hypoplasia; skeleton 338 
had severe marrow hyperplasia, woven bone on mul-
tiple skeletal elements, and evidence of scurvy; skele-
ton 208 had sinusitis and cuspal enamel hypoplasia as 
defined by Ogden et al. (2007); and skeleton 331 had 
evidence of scurvy, rickets, enamel hypoplasia, and 
new bone formation on the ribs.

Pathology

A wide range of pathological lesions were observed in 
the non- adult skeletons from both sites. Dental enamel 
defects were common in both the deciduous and per-
manent dentitions. A greater proportion of non- adults 

at Fewston expressed dental defects than at Coach 
Lane (72% compared to 50%), but the true prevalence 
rate for defects was similar at both sites (Table 2), with 
no statistically significant difference between them 
(two sample t- test, p > 0.1).

There were some differences in the type of the den-
tal enamel defects, however, with plane- form and cus-
pal enamel defects more frequent at Fewston (4% of 
all teeth compared to 0.6% at Coach Lane). Deciduous 
as well as permanent teeth were affected by enamel hy-
poplasia at both sites, including pitting defects, but 
cuspal enamel defects in deciduous teeth were not 
common (Supplementary Tables S1– S4). In such in-
stances, the period of stress that produced these le-
sions would have commenced in utero and occurred 
during the formation of both the deciduous and per-
manent dentition.

The crude prevalence of rickets was similar between 
sites and is very high compared to contemporaneous 
sites in London (Lewis 2002). Likewise, the prevalence 
of scurvy was high, and there was no statistically sig-
nificant difference between Coach Lane and Fewston 

Figure 4. Pubertal stages in Coach Lane (n = 11) and Fewston (n = 24) males and females plotted against 
dental age.



Childhood Health in the Industrial Revolution52

(Table 3). Again, this prevalence was higher than at the 
London sites of Chelsea Old Church, St Benet Shere-
hog, and Bow Baptist (ranging from approximately 
4– 10%) but were more comparable with rates seen at 
Cross Bones (37%), a site that was located in a particu-
larly impoverished parish of London during this period 
(Newman and Gowland 2016). Developments in the 
diagnostic criteria for both rickets and scurvy since 
some of these reports were published are partly respon-
sible for the disparity, along with the exclusion of poorly 
preserved skeletons from the prevalence calculations 
in this study. The north of England, however, was a re-
nowned focal point for rickets in the nineteenth cen-
tury (Owen 1889). The prevalence rate of cribra orbitalia 
was, again, high at both sites, but Fewston exhibited 
significantly higher frequencies (Table 3).

Non- adults at both sites showed evidence of maxil-
lary sinusitis and rib lesions, but the prevalence of both 
was significantly higher at Fewston (Table 4, rib lesions 
p < 0.05; sinusitis, p < 0.1) and most particularly in 

children of working age (12– 20  years). By contrast, 
 endocranial and ectocranial new bone was slightly 
higher at Coach Lane, although this was not statisti-
cally significant (Table 4). At Coach Lane, infants from 
1– 12 months were much more likely to exhibit endo-
cranial new bone growth (70%) than other age 
groups, whereas at Fewston higher prevalence rates 
were observed again among the adolescents. Care 
must be taken when interpreting cranial lesions in 
such young infants, because rapid bone growth during 
infancy may be mistaken for pathological lesions 
(Lewis 2007). Periosteal new bone formation was re-
corded for all the major long bones and was much 
more prevalent among the Coach Lane population 
compared to Fewston. Periosteal new bone formation 
at this site was most frequently expressed in the tibiae 
(55%), while at Fewston the femur was more frequently 
affected (22%) (Table 5).

In terms of specific diseases among the non- adults, 
there were three individuals of particular note. The 

Figure 5. Vertebral body height for C5– C6 plotted against dental age.

Table 2. Dental enamel hypoplasia (DEH) at Coach Lane and Fewston.

Age Group

Deciduous Teeth Permanent Teeth

Coach Lane Fewston Coach Lane Fewston

No. teeth  
(no. DEH) % DEH

No. teeth 
(no. DEH) % DEH

No. teeth 
(no. DEH) % DEH

No. teeth 
(no. DEH) % DEH

< 36w 0 0 0 0 0 0 0 0
36w– 1m 34 (0) 0 0 0 0 0 0 0
1– 12m 128 (13) 10 7 (0) 0 3 (1) 33 8 (0) 0
1– 5.9y 382 (66) 17 131 (12) 9 108 (30) 28 202 (28) 14
6– 11.9y 45 (8) 18 67 (7) 10 108 (37) 34 338 (72) 21
12– 19.9y 0 0 3 (0) 0 243 (114) 47 475 (139) 29
Total 589 (87) 14 208 (19) 9 462 (182) 39 1023 (239) 23



Gowland et al. 53

first was skeleton 69 from Coach Lane, who had severe 
osteonecrosis of the mandible accompanied by woven 
bone formation. This has been interpreted as likely due 
to phosphorous poisoning, which was a notorious oc-
cupational condition associated with the match- 
making industry at this time. A detailed description 
of this individual was provided by Roberts et al. (2016).

Skeleton 223 (14– 15- year- old) from Fewston had 
multiple lytic lesions accompanied by new bone for-
mation in the skull. Unfortunately, the skull of this in-
dividual was highly fragmented and only parts of the 
skull, vertebrae, and upper ribs were preserved. Both 
orbital roofs had thick deposits of lamellar bone, with 
woven bone also present in the left orbit. A circular 
lytic lesion approximately 14 mm in diameter, with 
sharp, clear margins, had penetrated the thickness of 
the right orbital roof (Fig. 6). Four further lytic lesions 
were present elsewhere on the cranium. The surround-
ing external surfaces of these generally had scalloped 

roughened areas, with deposits of partially remodeled 
woven bone and lamellar bone (Fig. 7). The body of the 
vomer was enlarged and covered with well- remodeled 
lamellar bone, with a smooth circular depression in 
both lateral walls and the perpendicular plate was 
absent (apparently remodeled). A large, shallow lytic 
lesion was present on the internal surface of the right 
mandibular ramus, and the margins were again 
bounded by thick deposits of partially remodeled wo-
ven bone. Deposits of lamellar bone extended along 
the inferior surface of the right mandibular body, and 
a plaque of lamellar bone was present on the external 
surface of the right ramus. The axis had a lytic lesion 
on the external surface of the left lamina surrounded 
by partially remodeled woven bone. An upper right rib 
had a deposit of porous lamellar bone on the visceral 
surface of the neck. None of the other rib fragments 
had any evidence for lesions, but few of the rib heads 
and necks survived.

Table 3. Crude prevalence rates (CPR) of rickets and scurvy by age group and true prevalence rates (TPR) of cribra orbitalia 
(CO) at Coach Lane and Fewston.

Age Group

Coach Lane Fewston Coach Lane Fewston Coach Lane Fewston

Rickets CPR Rickets CPR Scurvy CPR Scurvy CPR CO TPR CO TPR

36w– 1m 0 (9) 0 0 (0) 0 7 (8) 87.5 1 (1) 100 2 (22) 9 0 (1) 0
1– 12m 7 (12) 58.3 1 (1) 100 10 (12) 83.3 1 (1) 100 2 (20) 10 0 (1) 0
1– 5.9y 11 (25) 44.0 2 (4) 50 7 (27) 25.9 3 (8) 37.5 17 (51) 37 3 (6) 50
6– 11.9y 3 (7) 42.8 6 (9) 66.6 0 (6) 0 4 (13) 30.8 6 (10) 66.6 7 (9) 77.8
12– 19.9y 7 (10) 70 4 (15) 26.6 2 (10) 20 6 (16) 37.5 8 (19) 50 9 (14) 64.3
Total 28 (63) 44.4 13 (29) 44.8 26 (63) 41.2 15 (39) 38.4 35 (122) 32.8 19 (31) 61.3

Table 4. Prevalence rates by age and site for maxillary sinusitis (Sinus), rib lesions (Rib), ectocranial lesions (Ecto) and endocranial lesions (Endo) at 
Coach Lane and Fewston. True prevalence is provided for maxillary sinusitis, while only crude prevalence rates are given for the other pathologies.

Age 
Group

Coach Lane Fewston

Sinus TPR Rib CPR Ecto CPR Endo CPR Sinus TPR Rib CPR Ecto CPR Endo CPR

< 36w 0 (0) 0 0 (1) 0 0 (1) 0 0 (1) 0 0 (0) 0 0 (0) 0 0 (0) 0 0 (0) 0
36w– 1m 2 (2) 100 1 (11) 9.1 3 (13) 23 4 (13) 30.7 0 (0) 0 0 (1) 0 1 (1) 100 1 (1) 100
1– 12m 1 (2) 50 1 (19) 5.3 12 (20) 60 14 (20) 70 0 (2) 0 0 (1) 0 1 (1) 100 1 (1) 100
1– 5.9y 6 (24) 25 1 (25) 4 5 (28) 17.9 12 (28) 42.9 4 (7) 57.1 0 (5) 0 1 (10) 10 4 (10) 40
6– 11.9y 0 (9) 0 0 (4) 0 3 (6) 50 3 (6) 50 4 (12) 33.3 3 (12) 25 0 (13) 0 4 (12) 33.3
12– 19.9y 6 (19) 31.6 4 (9) 44.4 2 (10) 20 2 (10) 20 17 (26) 65.4 5 (12) 41 5 (16) 31.3 5 (14) 35.7
Total 15 (56) 26.8 7 (69) 10.1 25 (78) 32 35 (78) 44.9 25 (47) 53.2 8 (31) 25.8 8 (41) 19.5 15 (38) 39.4

Table 5. True prevalence rates of periosteal new bone formation on the major long bones at Coach Lane and Fewston.

Age Group

Coach Lane Fewston

Hum Rad Ulna Fem Tib Fib Hum Rad Ulna Fem Tib Fib

36w– 1m 10 21 38.9 20 44.4 12.5 0 0 0 0 0 0
1– 12m 32 54.5 50 28 70.8 46.2 20 0 0 0 0 0
1– 5.9y 16 2.4 2.6 38.8 66.7 21 22.2 0 0 20 16.7 33.3
6– 11.9y 11 0 11.1 35.7 8.3 9 6.7 0 0 28.6 25 20
12– 19.9y 27.7 22 27.8 36.8 50 22.2 4 0 16.6 20.8 10.3 15.8
Total 20 15 21 32.8 55 21.9 9.8 0 7.9 22 13.6 18.5



Childhood Health in the Industrial Revolution54

Figure 6. Lytic lesions penetrating the right orbit of skeleton 223.

Figure 7. Lytic lesion and new woven and lamellar bone on the left 
frontal bone of skeleton 223.

Tuberculosis manifested in the skull, while uncom-
mon in adults, can occur more frequently in children 
(Dawson and Robson- Brown 2012; Ortner 2003:247– 
248). Multiple cranial lesions, usually circular, less 
than 20 mm in size, which penetrate the thickness of 
the vault, as observed here, are all features of child-
hood tuberculosis. While bone formation around the 
lesions is not typical, it can occur (Dawson and Robson- 
Brown 2012; Ortner 2003). Chaudhary et al. (2004) and 
Sheikh et al. (2012) state that involvement of the jaw 
is more likely in older individuals (but can occur in 
children) and typically manifests as destructive le-
sions in the mandible, with potential involvement of 
the temporo- mandibular joint. Tuberculosis of the or-
bit is more common in children and is typically uni-
lateral (Dalvin and Smith 2016), as expressed here. 
Blindness is a frequent complication of ocular tuber-
culosis (Dalvin and Smith 2016; Shameem et al. 2009), 

and, given the severity of the lesions, it seems likely 
that skeleton 223 experienced a similar outcome. En-
docranial new bone formation and rib lesions have 
also both been associated with tuberculosis (Lewis 
2004, 2007; Matos and Santos 2006; Roberts and Man-
chester 2005:190; Santos and Roberts 2001, 2006).

Finally, the skeleton of a 12– 14- year- old from Coach 
Lane (skeleton 157) exhibited direct evidence of med-
ical care in the form of cranial surgery in association 
with trauma. The individual had suffered a perimor-
tem blunt- force injury to the left frontal and parietal 
bones along the coronal suture (Fig. 8). Two fracture 
lines radiated anteriorly and posteriorly from the point 
of impact. Two concentric fracture lines extended 
from the anterior fracture from a point located 44 mm 
superior to the left orbit rim and 20 mm anterior to the 
coronal suture. On the ectocranial surface a smoothly 
curved concentric fracture line extended superiorly and 
posteriorly, terminating in the coronal suture 45 mm 
from bregma. The lateral segment was not detached, 
but displaced internally slightly at the inferior/medial 
end. At this inferior part the fracture extends at an 
angle through the bone to the internal surface, where 
a fracture line extends superiorly for 13.6 mm. A neat 
circular perimortem trepanation is located in the left 
frontal squama 11.7 mm medial to the curved fracture 
line, 5.2 mm from the coronal suture, and 12.8 mm from 
the metopic suture. The external diameter (16.7 mm) 
is slightly larger than the internal diameter (14.1 mm) 
(Fig.  8). While the external margins are slightly 
crushed, the internal margins are sharp and the walls 
are smooth. This represents an unsuccessful attempt 
to provide life- saving medical treatment in response 
to the perimortem injury.

Figure 8. Frontal and parietal bone of skeleton 157 with perimortem 
trauma (B), a concentric fracture (A) and evidence for surgical 
intervention (C).



Gowland et al. 55

Discussion

The results initially appeared to contradict the senti-
ments espoused at the time, namely, that urban envi-
ronments were much more damaging to childhood 
health than a rural upbringing. Skeletal remains from 
both places show very high levels of metabolic disease 
and other non- specific indicators of physiological dis-
ruption. The higher prevalence of many of the patho-
logical conditions, together with poorer growth, among 
some of the children from Fewston compared with 
Coach Lane was contrary to expectations and histori-
cal records. Two questions arise from these results: why 
did the children at Fewston suffer so much chronic 
health stress, and why were there so many adolescents 
at this site? Usually, the adolescent age category is one 
of the least well represented within archaeological cem-
etery populations (as observed at Coach Lane), a factor 
lamented in recent studies of puberty in the past (Ar-
thur et al. 2016; Lewis 2016; Shapland and Lewis 2013).

A direct interpretation of this skeletal evidence 
would lead to the conclusion that the rural environ-
ment was at least as deleterious to health as the urban 
environment. Historical evidence for the Washburn 
Valley, in which Fewston is located, does in fact point 
to inadequate, overcrowded, and unsanitary housing 
for some rural dwellers, along with polluted water sup-
plies. For example, local resident John Dickinson 
noted in his diary entry for 13 October 1881: “There is 
part [some] talk about the deficient water supply and 
drainage of the village, and it is thought the sanitary 
authority will take the matter in hand themselves and 
compel the proprietors to alter things. The proprietors 
fear the cost and so it happens that we drink water 
highly polluted with sewage and our sinks [drains] are 
simply beastly” (Caffell 20151). In 1840, Elizabeth and 
William Scaife lost three children (John, aged 2 years, 
Hannah, aged 9  years, and Christiana Eliza, aged 
6 years) within just one week to typhus fever, spread 
via contaminated water during an epidemic that lasted 
from 1838 to 1840.

While such infectious diseases undoubtedly took a 
toll on the morbidity and mortality of the Fewston 
population, they would have proven more fatal to 
younger children, rather than adolescents, as the 
dreadful suffering of the Scaife family attests. These 
diseases are also acute; they will kill quickly and leave 
no visible sign on the skeleton. They are not, therefore, 
responsible for the evidence of chronic disease ob-
served among many of the adolescent skeletons. When 
interpreting the prevalence of pathological lesions, 

1. In addition to the listed reference, an abridged version of this 
diary was published: Harker, R (ed) 1988. Timble Man: Diaries 
of a Dalesman (Nelson, Lancashire).

the younger age- at- death profile of the children at 
Coach Lane should be considered, particularly with 
regard to the osteological paradox (Wood et al. 1992). 
However, given that many of the lesions recorded and 
interpreted at both sites were at least initiated during 
the first few years of life (e.g., enamel hypoplasia, 
rickets, scurvy, and cribra orbitalia), the comparison 
of the two different age- at- death profiles continues to 
have merit.

The presence of documented adults at Fewston has 
made it possible to gather the associated birth and 
death certificates, together with census records. This 
provides a known record of individuals who were 
born, lived, and died in Fewston and its environs— 
that is, the survivors. The skeletons of these adults 
do not show comparable levels of pathological le-
sions (e.g., cuspal enamel hypoplasia), and their stature 
does not appear to have been compromised; indeed, 
for males it was above the average stature for post- 
medieval England (177.3 cm for Fewston males and 
160.4 cm for Fewston females) (Caffell and Holst 2017). 
One could argue that the children in the assemblage 
were non- survivors and that this is why they show a 
higher prevalence of pathology compared to the adults 
(Wood et al. 1992). Another hypothesis (mentioned 
above) is that these adolescents were not local to the 
area and instead represent migrants. This interpreta-
tion will be explored further after a more detailed 
comparison with Coach Lane.

North Shields was widely known to be a heavily in-
dustrialized, polluted, and insalubrious town in the 
nineteenth century (Proctor et al. 2016). The preva-
lence of metabolic, respiratory, and non- specific indi-
cators of health stress at this site was high, as expected. 
In 1889 the British Medical Association estimated that 
vitamin D deficiency in the form of rickets in child-
hood was concentrated in the heavily industrialized 
areas of the northeast, where Coach Lane was located 
(Owen 1889). Vitamin D deficiency at this site is likely 
to have been exacerbated by the more northerly lati-
tude, in conjunction with air pollution from the asso-
ciated industries.

The high levels of vitamin D deficiency observed at 
Fewston, however, were not in keeping with historical 
records. John Snow, the famous nineteenth- century 
spatial epidemiologist, best known for his work on 
cholera, began his medical career as a doctor in a 
North Yorkshire village close to Fewston. Snow (1857) 
observed that rickets was a relatively rare disease in 
Yorkshire when compared to London. He attributed 
this to people from Yorkshire baking their own bread 
due to cheaper fuel sources, in contrast to Londoners 
who almost universally ate shop- bought bread, heav-
ily adulterated with alum. Snow, like his contemporar-
ies, believed that vitamin D deficiency was primarily 



Childhood Health in the Industrial Revolution56

Figure 9. Cuspal enamel hypoplasia on teeth from Fewston.

dietary in origin, rather than due to a lack of sunlight, 
and he thought that alum was responsible for “weak-
ening” the bones. The connection between sunlight 
and vitamin D deficiency was not made until the late 
nineteenth century, and diet was still thought to be 
the predominant cause of the disease even in the 1920s 
(see Findlay and Mellanby 1922). The key point here is 
that the prevalence of rickets at Fewston is contrary 
to Snow’s observations in North Yorkshire.

The prevalence rates of scurvy were also equally 
high in both the rural and urban sites studied here. It 
was expected that scurvy would be less prevalent in 
rural environments due to the increased availability of 
fruit and vegetables. A regional survey of diet and nu-
trition highlights that in rural Yorkshire the working 
classes ate largely bread, oatmeal, some sugar, and 
weak tea, rather than foods rich in vitamin C such as 
potatoes (Horrell and Oxley 2012). Historical records 
have also documented that the diet of women and 
children was more monotonous and less likely to in-
clude meat than the diet of men (Horrell and Oxley 
2012; Humphries 2010).

Dental enamel hypoplasia (DEH) prevalence was 
comparable between the sites. DEH has multiple eti-
ologies (e.g., infectious disease, trauma, malnutrition) 
and is generally regarded as a “non- specific” indicator 
of disease; however, it is worthwhile focusing on the 
type of hypoplastic defects present. While linear 
enamel hypoplasia is by far the most common form 
exhibited in skeletal samples generally, at Fewston 
there are a number of individuals that have “plane- 
form” and “pitted” defects of the type described by 
Ogden et  al. (2007) as “cuspal enamel hypoplasia” 
(Fig. 9). This term describes the combination of pitted 
and plane- form lesions, together with a disruption in 
the pattern of the molar cusps, such that multiple 
small cusps form and develop. Ogden et al. (2007:960) 

noted a relatively high number of individuals with 
such defects (on deciduous and permanent teeth) from 
the post- medieval site of Broadgate in London and ex-
plored a range of reasons for these defects, including 
vitamin D deficiency. Pitting and cuspal enamel hy-
poplasia is also observed on the deciduous teeth at 
Fewston, indicating an in utero insufficiency. Purvis 
et al.’s (1973) clinical study noted an association be-
tween very similar hypoplastic lesions in the decidu-
ous teeth and neonatal tetany, arising from deficiency 
in vitamin D in the mothers during the third trimes-
ter of pregnancy. Their sample was from Scotland, a 
northerly latitude, and they observed an increase in 
frequency during winter and spring when hours of 
sunshine were lowest. They also noted an association 
with increased maternal parity and low social status. 
Similar instances of modern cases of enamel hypopla-
sia associated with nutritional rickets have been re-
ported in the more recent medical literature (e.g., 
Davit- Béal et al. 2014). The presentation of these defects 
is identical to those observed among the Fewston skel-
etons in terms of the teeth affected and location. Vita-
min D deficiency in pregnant women is known to 
result in adverse maternal health and birth outcomes 
affecting the birth weight, bone mass, and immunity of 
the infant (Karras et al. 2016; Paterson and Ayoub 2015).

An early- twentieth- century medical book by Dick 
(1922) focusing on the geographical distribution and 
clinical manifestations of rickets also describes den-
tal lesions, which he argued to be pathognomonic of 
vitamin D deficiency as follows: “There may be only a 
pitting, producing a honeycombed appearance of the 
enamel, or the enamel covering is slight, and the cut-
ting edge of the tooth presents sharp points, giving a 
characteristic appearance to the tooth” (1922:191– 192). 
This description is again consistent with the dental le-
sions observed in some of the Fewston individuals. 
While it is easy to dismiss these early medical texts as 
outdated, particularly when published during a period 
in which the etiology of the condition was only poorly 
understood, it is important to give credit to the fact 
that these observations were made during a time when 
the disease was frequently encountered.

While enamel hypoplasia is generally considered to 
be a non- specific form of stress, in these instances it 
seems likely to have resulted from an insufficiency of 
vitamin D and/or calcium, beginning in utero and ex-
tending until 2  years of age. Vitamin D deficiency 
contributes to hypocalcaemia and hypophosphatemia, 
the latter of which is compounded by hyperparathy-
roidism brought about by hypocalcaemia (Foster et al. 
2014:6– 7). This lack of calcium and phosphorus results 
in developmental and mineralization defects in teeth 
via both direct and indirect mechanisms (Foster 
et al. 2014). It has been observed in clinical studies that 



Gowland et al. 57

vitamin D deficiency can result in inter- globular den-
tine, and this has been identified in archaeological 
teeth of individuals with residual rickets (D’Ortenzio 
et al. 2016). Future analysis of the Coach Lane site may 
benefit from a histological analysis of the teeth, but 
the Fewston skeletons have now been reburied. Of in-
terest is that none of the adults from Coach Lane or 
Fewston exhibited evidence of cuspal enamel hypo-
plasia, indicating a strong association between these 
lesions and the risk of early mortality.

When interpreting the presence of pathological le-
sions and growth disruption early in the life course, it 
is important to consider the significance of maternal 
health for growth and immune status (Gowland 
2015a). Maternal malnutrition, ill health, and exposure 
to toxins within the living or working environment 
during pregnancy will adversely affect the developing 
fetus. Intrauterine growth retardation is strongly as-
sociated with shorter height in childhood and adoles-
cence (Chung and Kuzawa 2014). Furthermore, a 
mother who fails to meet her own genetic potential in 
growth is more likely to have an infant who is small 
for gestational age. Growth deficits early on in life can 
be difficult to recover from, particularly in adverse bi-
olcultural environments (Chung and Kuzawa 2014). 
Indeed, the effects of a poor environment on growth 
could span multiple generations before it is fully re-
versed despite alleviation of environmental stressors 
(Barker 2012).

Finally, when interpreting palaeopathological evi-
dence and delayed growth in terms of the local living 
environments, we must be sure that the pathological 
conditions observed in the skeletons of the children 
from Fewston and Coach Lane do in fact relate to the 
local area. With regard to this period of rapid indus-
trialization and urbanization, migration is often 
conceptualized as unidirectional— from the country-
side to towns. It is important to consider that during 
this period there was a significant amount of rural in-
dustry and that this led in some instances to the ap-
prenticeship of urban children, who were removed to 
the countryside to work as laborers, as domestic ser-
vants, or in textile mills. These individuals were known 
as pauper apprentices: children taken from workhouses 
in cities, usually 10– 12 years of age, and indentured to 
work far from their original home. The children worked 
long hours, 12 to 14 hours per day, and for no pay, but 
were instead “taught a trade” and were housed, fed, 
and given some education (Honeyman 2013; Levene 
2010).

There was a flax mill at Fewston, known as West-
house mill, and historical sources document the em-
ployment of pauper apprentices from the workhouses 
of Lambeth and Shoreditch in London, as well as else-
where in England (Honeyman 2007). It therefore seems 

probable that this excess of adolescents at Fewston, 
with high frequencies of skeletal lesions and stunted 
growth, reflects a poor and destitute childhood in 
London rather than one spent at Fewston. Ives and 
Humphrey’s (2017) study of diaphyseal growth in 
children from the poor London parish of Bethnal 
Green during the nineteenth century also highlights 
severe growth deficits. Social status is one of the stron-
gest determinants of health, and this was particularly 
evident in post- medieval England (Gowland 2018; 
Marmot and Wilkinson 2006). As discussed, the evi-
dence for rickets and enamel hypoplasia at Fewston is 
consistent with the pathological evidence from the 
low- status post- medieval cemetery of Broadgate in 
London (Ogden et al. 2007; Pinhasi et al. 2006). The 
high prevalence of respiratory disease among these 
children at Fewston is also consistent with mill labor, 
in which pulmonary complaints, including byssinosis 
and tuberculosis, were a known occupational hazard 
(Wohl 1983). Further isotopic and archival investiga-
tion is currently being undertaken in order to verify 
the non- local origins of these adolescents (Gowland 
et al. 2017).

Conclusion

While the children at Coach Lane undoubtedly showed 
evidence of adverse living conditions in the form of 
poor skeletal growth and the presence of physiological 
insults to the skeleton, it was surprising and contrary 
to historical evidence that the children from the rural 
site showed comparable health deficits. One explana-
tion is that we need to reevaluate our ideas of rural 
life during this time in terms of it providing a more 
beneficial living environment and diet. Alternatively, 
the health stress observed in some of the Fewston chil-
dren may not relate to the local living environment at 
all but rather to an impoverished urban childhood in 
the workhouses of London and elsewhere. Childhood 
mobility during this period as well as urban- to- rural 
migration should be factored into our interpreta-
tions. Industry was not just an urban phenomenon 
but also a rural endeavor, and we should consider the 
impact of this on the health and population structure 
of Fewston. Finally, poverty has heritable biological 
consequences via poor maternal health status. This 
biological disadvantage then becomes exacerbated by 
poor working and living conditions. The Industrial 
Revolution was a period of relative social mobility, 
with a rise in the middle classes, but for the very poor 
and disenfranchised the inheritance of biological in-
equality in terms of morbidity and mortality risks, in 
addition to social disadvantage, meant that only the 
very tenacious could survive or thrive.



Childhood Health in the Industrial Revolution58

Acknowledgments

The authors would like to acknowledge the British 
Academy (SG132083) for funding this research. We 
would also like to thank Sally and Clive Robinson and 
the volunteers from the Washburn Heritage Centre for 
their contribution and support with the Fewston as-
semblage and Jenny Proctor at Pre- Construct Archae-
ology for access to the Coach Lane collection. I am 
very grateful to Paula Monguí for her translation of 
the abstract.

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Table S1. Coach Lane: dental enamel hypoplasia (DEH; pitting, lines, and grooves).

Age Group

Deciduous Permanent All Teeth

DEH Total % DEH Total % DEH Total %

Foetus < 36w — 0 — — 0 — — 0 — 
Neonate 36w– 1m 0 34 0.00 — 0 — 0 34 0.0
Infant 1– 12m 13 128 10.2 0 3 0.0 13 131 9.9
Young Juvenile 1– 5.9y 61 382 16.0 27 108 25.0 88 490 18.0
Older Juvenile 6– 11.9y 8 45 17.8 37 108 34.3 45 153 29.4
Adolescent 12– 19.9y — 0 — 114 243 46.9 114 243 46.9
Total 82 589 13.9 178 462 38.5 260 1,051 24.7

Supplemental Tables



Gowland et al. 61

Table S2. Coach Lane: cuspal enamel hypoplasia (CEH).

Age Group

Deciduous Permanent All Teeth

CEH Total % CEH Total % CEH Total %

Foetus < 36w — 0 — — 0 — — 0 — 
Neonate 36w– 1m 0 34 0.0 — 0 — 0 34 0.0
Infant 1– 12m 0 128 0.0 1 3 33.3 1 131 0.8
Young Juvenile 1– 5.9y 2 382 0.5 3 108 2.8 5 490 1.0
Older Juvenile 6– 11.9y 0 45 0.0 0 108 0.0 0 153 0.0
Adolescent 12– 19.9y — 0 — 0 243 0.0 0 243 0.0
Total 2 589 0.3 4 462 0.9 6 1,051 0.6

Table S3. Fewston: dental enamel hypoplasia (DEH; pitting, lines, and grooves).

Age Group

Deciduous Permanent All Teeth

DEH Total % DEH Total % DEH Total %

Foetus < 36w — 0 — — — — — 0 — 
Neonate 36w– 1m — 0 — — 0 — — 0 — 
Infant 1– 12m 0 7 0.0 0 1 0.0 0 8 0.0
Young Juvenile 1– 5.9y 12 131 9.2 16 112 14.3 28 243 11.5
Older Juvenile 6– 11.9y 6 67 9.0 53 247 21.5 59 314 18.8
Adolescent 12– 19.9y — 3 — 111 455 24.4 111 458 24.2
Total 18 208 8.7 180 815 22.1 198 1023 19.4

Table S4. Fewston: cuspal enamel hypoplasia (CEH).

Age Group

Deciduous Permanent All Teeth

CEH Total % CEH Total % CEH Total %

Foetus < 36w — — — — — — — 0 — 
Neonate 36w– 1m — 0 — — 0 — — 0 — 
Infant 1– 12m 0 7 0.0 0 1 0.0 0 8 0.0
Young Juvenile 1– 5.9y 0 131 0.0 0 71 0.0 0 202 0.0
Older Juvenile 6– 11.9y 1 67 1.5 12 271 4.4 13 338 3.8
Adolescent 12– 19.9y 0 3 0.0 28 472 5.9 28 475 5.9
Total 1 208 0.5 40 815 4.9 41 1,023 4.0




