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Enclosure and population growth in eighteenth-century England
Explorations in Economic History 12.29-46 (1975)
Enclosure and Population Growth In Eighteenth-Century England GORDON
PHILPOT
Whitman
College
The demographic history of England in the three centuries between 1500 and 1800 may be divided into three phases: (i) From 1500 to about 1650 population grew rapidly; (ii) during the next 100 years it showed no decisive trend; and (iii) about the middle of the eighteenth century there was a sudden fierce acceleration in population growth (Wrigley, 1969a, p. 78). So far no completely satisfactory explanation has been given to account for either the demographic change which occurred at about the midpoint of the seventeenth century, or that which occurred 100 years later. Most research in the area has been concentrated on the second turning point due, no doubt, to its close proximity to the beginnings of the Industrial Revolution. For a while controversy swirled around the question of whether the acceleration in the rate of population growth was a result of a declining death rate or of a rising birth rate and, since the available statistics were not too reliable, both sides could point to some evidence in support of their argument (see, for example, Connell; Deane and Cole, Chap. 3; Habakkuk; McKeown and Brown; and Razzell). Fortunately, not all of the statistics for the period are unreliable. Those of the British peerage, for example, are probably more reliable than any other group’s. Their analysis led T.H. Hollinsworth to the findings that mortality rose in the first half of the seventeenth century while fertility fell. After 1750 there was a sharp drop in both child mortality and adult mortality, and an increase in fertility occurred at about the same time (pp. 70-72).
It might be that the peers were not representative of the population as a whole, but any theory purporting to explain the demographic trends of the period would then have to explain why they were the exception to the general rule. Occam’s razor constrains us, in the absence of evidence to the contrary, to assume that the trends observed in the peerage reflected the underlying demography of the populace as a whole. The high death rates of the late seventeenth and early eighteenth centuries were chiefly attributable to infectious diseases whose incidence was much greater in infancy and childhood than in adult life (Creighton, p. 18). McKeown and Brown investigated three possible causes of the reduction in mortality which occurred in the late eighteenth and early nineteenth 29 Copyright @1975 by Academic Press, Inc. All rights of reproduction in any form reserved.
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centuries: specific medical therapy; changes in the balance between the virulence of the infective organism and its host; and improvements in the environment. They concluded that improvements in the environment were the most acceptable explanation (p. 72). Razzell disagreed with their conclusion and advanced the hypothesis that improvements in medicine, specifically the introduction of inoculation against smallpox, could account for the falling death rate in the eighteenth century (p. 154). Whether the elimination of a single disease would have so great an effect, however, is questionable. Even the extinction of the plague in 1666 caused no immediate fall in the death rate, and Razzell’s hypothesis leaves unanswered the questions of why mortality increased during the seventeenth century and why fertility declined and then rose at the midpoints of the seventeenth and eighteenth centuries. During the 300 years from 1500 to 1800, the great majority of the people of England lived in rural areas.l Any agency which had a major effect on population growth, therefore, must of necessity have worked upon the rural population. If this fact is taken in conjunction with McKeown and Brown’s hypothesis of environmental improvement, the notion is suggested immediately of some kind of change in the rural environment, which leads directly to a consideration of the enclosure movement, the major force for change in eighteenth-century rural England. Certainly there were links between enclosure and population growth. Farey, the agricultural reporter, listed 44 places in Derbyshire in which the total population more than doubled between 1788 and 18 11, a period of widespread enclosure in that county (Chambers, 1957, p. 56). J.D. Chambers writes as follows: The period 178% 1840 saw only a sporadic exodus . . from the rural areas . and side by side with it, an actual filling up of empty spaces and a steady rise in the great majority of established centres of rural population . . This phenomenon of rural fecundity is all the more remarkable since it follows a period marked by enclosure and the consolidation of farms. (1958, p. 82).
It is with the relationship this paper is concerned.
between enclosure and population
growth that
I The Enclosure Hypothesis As a starting point it is necessary to focus attention on one particular area of the medieval English village: the commons or waste, used by the ‘Deane and Cole, p. 7, suggest that between tions of 5,000 or more in 1750.
15 and 16% of the population
lived in concentra-
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villagers as a grazing area for their livestock. As the name suggests, all the animals of the village grazed it in common, the beasts belonging to different owners being mixed together quite indiscriminately. Those villagers who had the privilege of turning out their animals to graze guarded that privilege jealously against the intrusion of strangers. The presence of strange cattle or sheep was strictly prohibited. Villagers who turned out more stock than their proper share were presented at the manorial court and fined, and the limits within which swine could feed were restricted.2 As long as the number of animals permitted to graze on the commons was held within reasonable bounds, they remained relatively healthy. But between 1500 and 1650 the population of England almost doubled (Wrigley, 1969a, p. 78, Fig. 3-3). If the animal population kept pace with the human population the pressures on the limited areas of waste can easily be imagined. Even so, the strict regulation of grazing rights might have continued had it not been for the social upheavals which led to the Civil War (1642-1646). Then the reins of traditional authority were relaxed and the bonds of society weakened. “With many squires taking up arms for Charles I or Parliament, and leaving their locality for years on end, the direct interest of many landlords in farming ceased, and absenteeism became, first a military necessity, then a social habit” (Everitt, pp. 464-465). Along with the breakdown in the social order, the regulation of grazing rights was also a casualty of the Civil War, and the commons in many areas were overstocked. Animal diseases associated with lack of food and overcrowding became prevalent. Because all the animals of the village were turned out on the commons together, it did not take long for one diseased animal to infect all the others. Writing in 1653, Blith complained that “every man laies on at random . . . ” as a result of which “you shall observe such a rot of sheep” that the commoners lose all their flocks.3 In the same year Moore described the commons as “pest-houses of disease for cattle,” and added “Hither come the Poor, the Blinde, Lame, Tired, Scabbed, Mangie, Rotten, Murrainous” (Ernle, p. 128). The situation had not improved in the early eighteenth century when, in many cases, the commons were unstinted. In other cases, while most villagers were restricted as to the number of their stock, one or more of them were restrained by no limit, and not only turned out as many of their own sheep and cattle as they could, but also took in those of strangers (Ernle, p. 158). Even as late as 1794, the cat2Emle, pastures, paper the Vurtler, tion prior
p. 27. Ernie makes a distinction fringed by the untilled wastes.” terms “commons” and “waste” p. 126. Curtler notes that the to 1653, lending support to the
between the two terms, referring to “the common (p. 26) Later the distinction becomes blurred. In this are used interchangeably. problem of overstocking had not received much menhypothesis that it dates from the 1640’s.
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tle and sheep pastured on the Lincolnshire commons were reported to be very unhealthy.4 Disease originating in the fields also affected the cottage and the manor house, either by way of direct contact, or through the agency of milk or meat obtained from infected animals. It goes without saying that in the seventeenth and eighteenth centuries there was no inspection of meat by government officials; no testing of milk for the presence of the tubercle bacillus. The prevailing standards of hygiene are perhaps best illustrated by the example of the master, whose idea of charity was to send to the family of his sick shepherd the carcass of a sheep, which had been found dead in a furrow (Creighton, p. 156n). In 1658, a letter writer refers to disease in the fields together with, not only “a great death of coach horses,” but also much sickness in the human population. In the 1720’s and 1730’s, and again in 1760, cases were reported of disease occurring in horses one or two months before it affected man. During the first half of the eighteenth century, murrain in cattle occurred at the same time as outbreaks of putrid or malignant sore throat and putrid fever in the human population. Indeed, the English throat-distemper of the eighteenth century was identified with the garrotillo of sixteenth- and seventeenth-century Spain, which was linked to preceding murrains of cattle (Creighton, pp. 120, 125, 313, 3455346, 355, 692,735-736 and 736n). Why the breakdown in regulation continued after the turmoil of the seventeenth century was over is not clear. It could have been the result of “social habit” on the part of some absentee squires, but too many eighteenth-century landlords took an intense interest in their land for this to be an acceptable explanation in more than a minority of cases. Perhaps the more progressive squires looked to enclosure as the solution to the problem. At any rate, the enclosure movement did have extremely beneficial Hects on the health of the animal population. After enclosure of the waste, the land was either plowed up or, if still used for grazing, stocked more reasonably. The flocks and herds of different farmers were no longer mixed together indiscriminately, and disease in the animal population was reduced. A correspondent of Arthur Young reported that not one sheep died from the rot on land that had been enclosed whereas, on the same land before enclosure, there were years when not a single sheep escaped the rot. The two enclosed parishes of Childersley and Knapwell both escaped the rot during a period when neighboring parishes were desolated by the disease (Ernle, pp. 236 and 243). As the animal population became healthier, so did the human population, the death rate declined, and the surge in population growth ensued. ‘Ernie, 337-338.
p. 245. For further
evidence
on this point,
see Cutler,
pp. 180 and 230; Gonner,
pp.
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II The Medical Evidence If, prior to enclosure, the pool of infection in an unhealthy animal population occasionally overflowed, to cause epidemics in the human population, then it should be possible to find evidence that diseases which may be transmitted from animals to man were prevalent in the years between the midpoints of the seventeenth and eighteenth centuries. The most common disease of this type, as well as the most common milkborne disease, is brucellosis (Harris, p. 45), which in cattle is known as contagious abortion, and in man as undulant fever, or intermittent fever (Hull, p. 127). There are many references to intermittent fever in the medical writings of the seventeenth and eighteenth centuries, when it was often referred to as the ague, but this cannot be taken as firm proof of the prevalence of brucellosis, since intermittent fever and ague may also be used as synonyms for malaria. Indeed, some modern writers unquestioningly accept the term ague to mean malaria. Razzell, for example, in his paper attributing the growth of population in the eighteenth century to the spread of the practice of inoculation against smallpox, states that no “disease, other than smallpox (due to inoculation), was described as having declined or disappeared, except ague (malaria), which is very frequently mentioned as having disappeared during the latter half of the eighteenth century” (p. 154). J.D. Chambers, while less dogmatic than Razzell, wrote that, “The word malaria is unfamiliar to the student of English epidemiology; but if we call it by the homely name of ague, we shall have no difficulty in recognizing one of the killing diseases of preindustrial England” (1972, p, 98). Creighton, on the other hand, felt that to equate the ague with malaria was an error. Sydenham . . has much to say of agues or intermittents prevalent in town and country for a series of years . . But he does not count these as the agues of the marsh . Sydenham and his learned colleagues were not ignorant of the endemic agues of marshy localities, but they made little account of them in comparison with the aguish or intermittent fevers that came in epidemics all over England (pp. 302-303).
In the last great epidemic period from 1780 to 1786, Jesuit’s bark, the bark of the conchona tree, from which quinine may be derived, was ineffective in the treatment of ague (p. 325), whereas quinine is known to be effective in treating malaria. The inhabitants of high ground fell victim to the ague at a time when those living in nearby valleys escaped. The people of Boston and the neighboring villages in the midst of the fens, for example, were healthy at a time when the ague was epidemic in the more elevated areas of Lincolnshire (p. 367). The reverse would have been true for an outbreak of malaria. Indeed ague was common in districts where anopheline mosquitoes are relatively scarce today. When malaria was introduced into
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England from abroad in the present century by troops returning from the two world wars, no new cases were found after the first winter. Since there is no evidence that the climate in the seventeenth and eighteenth centuries was any more favorable for the overwintering of the malarial plasmodium, it seems unlikely that endemic malaria ever existed in England during that period (McKeown and Brown, p. 47n). If the ague were not malaria, it might well have been the other intermittent fever: brucellosis. Whitmore describes the fatal epidemic ague of 16581659 as so “prodigous in its alterations that it seems to outvie even Proteus himself” (Creighton, p. 367). Compare this with a modern physician’s description of brucellosis: “No disease, not excepting syphilis and tuberculosis, is more protean in its manifestations” (Harris, p. v, Foreword by Simpson). Brucellosis and two other diseases of animal origin, vibriosis and listeriosis, can cause spontaneous abortion and sterility in human females as well as in animals (Harris, p. 198; Hull, pp. 176 and 255). If the ague were brucellosis, therefore, it could account for the decline in fertility which occurred in the seventeenth century when it became prevalent, and for the rise in fertility in the second half of the eighteenth century as it passed from the scene. The ague was also fully capable of explaining the high death rates of the late seventeenth century. The epidemic ague of 1657- 1659, for example, had such an effect on mortality that it was afterwards viewed as a “little plague” comparable to the Great Plague of 1665 (Creighton, p. 314). And a milkborne disease would account for a high rate of child mortality during the period of its prevalency. The second disease of animal origin to merit consideration is tuberculosis. The timing is right. Its incidence increased in the seventeenth century and it reached the peak of its prevalency during the eighteenth (Ackerknecht, p. 104). To be sure, not all tuberculosis is of animal origin. In England in the 1940’s only 23.4% of tuberculosis in man was of the bovine type, but this was a period when the benefits of pasteurization were well known. There is evidence that the proportion of bovine origin is higher in primitive agricultural communities where there is close association between animals and man (Francis, pp. 91 and 95-96), as would be the case in seventeenthand eighteenth-century England. Children are much more commonly infected with the bovine type of the tubercle bacillus than are adults, the incidence being highest among children less than five years of age (Hull, p. 44). Tuberculosis could very well have been, therefore, a source of high child mortality during the late seventeenth and early eighteenth centuries. It continued to be a source of high mortality long after the ague had become extinct, but this may be explained by the relatively long period of residual in-
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fection which is typical of that disease (Hull, p. 37). Finally, in the opinion of at least one medical scholar, the main cause of the fall in mortality due to tuberculosis was environmental improvement (Springett, p. 579), which fits in well with McKeown and Brown’s finding referred to earlier. In considering the third major disease of animal origin, anthrax, we are on less certain ground. It was still prevalent in France, where enclosure came much later than in England, as late as the second half of the nineteenth century (Vallery-Radot, p. 257). Creighton’s “putrid fever” of the middle third of the eighteenth century may well have been anthrax. It occurred at a time of disastrous murrain in cattle, and was reported to be the same disease as one at Rouen, which clearly was anthrax.5 If this assumption is valid, the unenclosed wastes would have been a particular menace to cattle and sheep since, once infected with anthrax, pastures remain contaminated for years. Furthermore, in an era of cottage industry, a large proportion of the rural population would be exposed to the wool and hides of infected animals, and thus to the massive pneumonia of “woolsorters disease” (Hull, pp. 99- 100). It must be emphasized that this is a field in which much research remains to be done, especially by medical historians. For the moment, the part played by anthrax in eighteenth-century medical history must be considered somewhat tentative. III A Question of Timing If the Enclosure Hypothesis is valid, then enclosure, the cause, must have preceded population growth, the effect. In other words, since the acceleration in population growth began about 1750, enclosure should have been getting under way in the first half of the eighteenth century. Yet enclosures were not a purely eighteenth-century phenomenon. Consolidation of the strips in the arable fields, followed by enclosure, was practiced before the fourteenth century, and became prevalent during the period following the Black Death. But the eighteenth century saw a marked increase in the rate of enclosure, of such an order of magnitude, as to make what had gone before seem of only secondary importance. In the 182 years between 1455 and 1637, for example, it is estimated that 744,000 acres were enclosed, or 2.1% of the total area of England (Curtler, p. 148). This represents an average rate of approximately 4,000 acres per annum. Between 1700 and Kreighton, was apparently 1742.”
pp. 120-121. not typhus,
Putrid fever is sometimes used as a synonym for typhus. This fever being described as “interrupted by the typhus epidemic of 1741-
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18 15, on the other hand, about 8125,000 acres, or 22.9% of the total area of England was enclosed, an average rate for the 115-year period of 70,000 acres per annum,6 or 17 times the annual rate of the earlier period. In fact, the difference between the two time periods is even greater. In the sixteenth and seventeenth centuries, both arable and waste had been enclosed, but arable predominated, whereas in the eighteenth century about two-thirds of the land enclosed was waste (Barnes, p. 106), and from the point of view of the Enclosure Hypothesis it is the area of waste enclosed that is the relevant consideration. IV The Statistical Evidence In order to submit the Enclosure Hypothesis to statistical testing, the relevant data for 38 English counties have been assembled in Table 1. The four counties of the London area, Essex, Kent, Middlesex and Surrey, have been omitted on the grounds that over half-a-million people living in a large city have no business in a statistical test of a hypothesis concerning a rural population. Five of the columns in Table 1 have been taken from Deane and Cole’s British Economic Growth, 1688-1959. While the last two columns, which refer to a time period after the first census of 1801, are perhaps fairly reliable, the other three are not, and the techniques by which they have been derived have been criticized by Neal (pp. 643-647) and Flinn (p. 29), among others. Yet data for the eighteenth century is not easy to come by. J. D. Chambers said of Deane and Cole: “They have performed a valuable service and provided economic historians with a number of important tools with which to unlock some of the secrets of the period” (1972, p. 115). It may be that better data will one day be available; until then the economic historian must make do with what he has. The data for the two time periods, 1701-1750 and 1801-1830, have been OThese figures were derived as follows: Curtler (p. 148) estimates that six and a half million acres were enclosed by acts of parliament in the eighteenth and nineteenth centuries. Chambers and Mingay (p. 77) state that nearly three-quarters of the area enclosed by acts was enclosed in the two periods 176@1780 and 1793-1815. Thus three-quarters of six and a half million, or 4,875,OOO acres were enclosed by act of parliament in the period 17W1815. This figure is an over-estimate since they use the phrase “nearly three-quarters,” but it is an underestimate because there was some additional enclosure by acts during the periods 1700-1760 and 178s 1793. If we assume that these two effects cancel each other, the figure of 4,875,OOO is a reasonable one. In addition to enclosure by acts of parliament, there was considerable enclosure by private agreement, especially during the first half of the eighteenth century, when acts of parliament were little used. It is difficult to estimate how much land was enclosed in this way. Chambers and Mingay (p. 78) suggest that it may have amounted to half of the area enclosed by acts. If their estimate is accepted, then one-half of six and a half million, or 3,250,OOO acres were enclosed by agreement, making a total for the period of 8,125,OOO acres.
TABLE y. Area of county enclosed by Act of county Parliament Devonshire 0 Cornwall 0 Lancashire 0 Shropshire 0.3 Monmouthshire 0.4 Cheshire 0.5 Westmorland 0.6 Durham 0.7 Cumberland 1.1 Northumberland 1.7 Sussex 1.9 Staffordshire 2.8 Somerset 3.5 Herefordshire 3.6 Yorks N. Riding 6.3 Hampshire 6.4 Suffolk 7.5 Dorset 8.7 Yorks W. Riding 11.6 Hertfordshire 13.1 Derbyshire 15.9 Worcestershire 16.5 Gloucestershire 22.5 Wiltshire 24.1 Warwickshire 25.0 Berkshire 26.0 Lincolnshire 29.3 Norfolk 32.3 Nottinghamshire 32.5 Buckinghamshire 34.2 Cambridgeshire 36.3 Leichestershire 38.2 Yorks E. Riding 40.1 Oxfordshire 45.6 Bedfordshire 46.0 Rutland 46.5 Huntingdonshire 46.5 Northamptonshire 51.5 ‘Sources: Col. 1, Slater, pp. Deane and Cole, p. 115.
Average death rate 1701-50 (per 1000) 25.7 30.8 26.4 29.2 27.0 33.8 26.3 29.0 21.3 23.0 32.4 30.3 28.4 22.7 25.7 32.7 32.5 29.9 30.2 33.1 25.5 30.3 31.2 26.2 32.0 32.1 38.8 33.2 27.5 35.2 33.4 26.9 39.3 30.0 33.8 28.3 42.5 30.7 14tF7; Cols.
1’
Average birth rate 1701-50 (per 1000) 26.1 34.3 29.1 33.1 32.5 35.8 31.7 33.0 29.1 26.8 39.1 37.2 29.3 28.0 32.3 36.9 34.1 33.0 38.3 34.1 33.4 34.2 34.5 30.1 34.8 36.4 39.0 34.6 31.2 35.8 35.6 32.4 40.8 34.2 32.4 38.1 38.9 33.2 2, 3, 5, and
37
Rate of Average Average migration death rate birth rate 1701-50 1801-30 1801-30 (per 1000) (per 1000) (per 1000) -1.9 21.0 37.5 -1.9 18.2 38.2 24.5 40.6 3.0 -2.5 21.3 36.2 -3.4 18.5 28.4 -0.6 23.1 35.8 -7.6 21.1 38.2 -1.1 22.6 37.1 -10.0 21.8 38.1 -0.6 20.5 33.5 40.5 -7.3 20.0 -4.4 23.2 40.3 -0.2 20.4 34.9 -6.3 19.1 33.1 -8.5 20.0 36.3 0.1 21.7 39.1 -1.8 19.9 37.6 -2.9 19.4 35.4 38.0 -3.4 22.1 21.5 37.0 0.6 -10.4 20.9 37.3 22.7 38.7 -5.3 2.1 19.3 35.3 -3.0 19.6 34.4 2.2 22.9 34.8 -2.0 21.6 37.0 21.8 40.2 -3.3 -3.2 21.1 38.8 22.3 39.2 -4.6 1.0 22.7 37.0 -4.4 24.0 40.5 -2.6 21.5 35.9 -1.0 24.0 40.3 20.9 -3.0 37.0 21.4 2.3 36.6 -15.2 20.6 35.8 2.7 22.7 37.7 -2.5 21.9 35.0 6, Deane and Cole, p. 131; Col. 4,
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pooled, giving 76 observations equations:
PHILPOT
to estimate the parameters of the following
Di = LI + bKi + CEi,
(1)
B, = f - gK, + hDi - jEi,
(2)
where i= i = B, = Bi = Bi = Di = Di = Di = Ei = Ei = Ei = Ki= Ki =
1.. .38 for the period 1701-1750 39.. .76 for the period 1801-1830
County birth rate (per 1,000) Cal. 3 for i = 1 . . . 38 Cal. 6fori = 39 . ..76 County death rate (per 1,000) Cal. 2 for i = 1 . . .38 COI. 5 for i = 39 . . . 76 Percentage area of unenclosed waste in county Col. 1 for i = 1 . . . 38 Ofori = 39...76 lifi= 1...38 Oifi = 39...76
All parameters are positive, a negative effect being shown by a negative sign. Ideally, the dependent variables should be mortality, perhaps expectation of life at birth, and fertility, but the necessary data are simply not available. Death and birth rates must be used in their place. Ki is a dummy variable introduced because the birth and death rates depend not only upon E,, the area of unenclosed waste in the county concerned, but also on the total area unenclosed in the country as a whole. K, thus serves as a proxy for the effect of the nationwide epidemics of ague, which reached far beyond the boundaries of any one country. The use of 1 for the period 1701-1750 and 0 for 1801-1830 may be justified on each of two grounds: (a) The area unenclosed in the whole country was considerably less in 1801-1830 than it was in 1701-1750; and (b) the ague had become extinct in the 1780’s, and so its effects would not be felt in the later time period. 4 is a variable that reflects the percentage area of unenclosed waste in each county. The percentage area of the county enclosed by act of parliament will serve as a proxy variable for this, since almost the entire area enclosed by acts was enclosed after 1750. To be able to be enclosed after 1750, the land must have been given over to the open field system before that date. This measure understates the unenclosed area, since some land was enclosed by nonparliamentary means, even after 1750. On the other hand, the use of zero for the period 1801-1830 is also an understatement, for while the massive burst of enclosure was over by 1815, the process
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continued, though at a much reduced pace, for most of the nineteenth century. To the extent that these understatements balance each other, the effect will be to cause an error in the estimate of the constant term in both equations, but since this term is of no interest to us, no great harm results. Equation (1) shows the death rate depending directly on the two variables K and E, the former reflecting the nationwide epidemics of ague, and the latter the effects of infectious diseases that were. confined within the boundaries of the county: tuberculosis, anthrax, and localized outbreaks of brucellosis. In Eq. (2) the coefficients of K and E have negative signs; the effect of disease originating in the unenclosed waste is to reduce the birth rate through spontaneous abortion and sterility. The variable D appears as an independent variable in this equation because mortality may influence the porportion of women of childbearing age in the population, and thus the birth rate must be a function of mortality as well as of fertility (Flinn, p. 24). Equations (1) and (2) are recursive, and can be estimated independently using ordinary least-squares. The regressions obtained by using this procedure were as follows:
D = 21.36 + (0.49) B = 23.23 (1.82)
6.58K + 0.126E (0.86) (0.029) 8.94K + 0.650 - 0.0018E (0.82) (0.08) (0.0230)
R2 = 0.716,
(1)
R2 = 0.623.
(2)
The statistical evidence is consistent with the Enclosure Hypothesis. In Regression (1) the coefficients of K and E both have the right (positive) sign, and are significant at the 0.01 level. In Regression (2), the coefficients of K and E both have the right (negative) signs, but while the former is significant at the 0.01 level, the latter is not. This might be a result of multicollinearity. The first regression demonstrated a relationship between D and E, and both of these variables appear on the right-hand side of Eq. (2). When E is dropped from the regression, however, the standard deviation of D decreases only from 0.08 to 0.07, and the R* declines hardly at all. The birth rate, therefore, appears not to depend upon the area of unenclosed waste within a county, a result which is in complete harmony with the view that the major cause of low fertility was spontaneous abortion and sterility resulting from the ague, which took the form of nationwide epidemics, and thus would be reflected by the variable K, but not by E. While Regression (1) is consistent with the Enclosure Hypothesis, it is also consistent with an alternative hypothesis: that in the first half of the eighteenth century there was a pattern of migration between the enclosed and the unenclosed counties, which had the effect of reducing death rates in the former, and raising them in the latter, perhaps as farm workers who became unemployed as a result of enclosure moved to unenclosed areas to seek work, and later died there. This alternative hypothesis may be sub-
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jetted to a further test by computing the Spearman coefficient of rank correlation between Column 1 (Percentage area of county enclosed by act of parliament) and Column 4 (Rate of migration, 1701-1750). It turns out to be +0.031, which is statistically insigniticant, and the alternative hypothesis may be rejected. Referring back to Regression (1), the coefficient of determination is 0.7 16, which means that the variables K and E account for 72% of the variation in the death rate, leaving 28% unexplained. This may be due, in part, to the unsatisfactory nature of the proxy variable for E, in representing both some quantitative and some qualitative aspects of what we are trying to measure. As was mentioned earlier, it understates the unenclosed area, but this understatement may be offset to a degree by an equivalent understate ment in the time period 1801-1830. The proxy variable, however, has two additional drawbacks, which are not offset: (a) It is conceptually possible to have two counties with identical percentage areas of unenclosed land, but different percentage areas of waste; and (b) two counties could conceivably have identical percentage areas of waste, but different degrees of strictness in the regulation of pasture rights. An examination of the residuals from Regression (1) may shed more light on this particular problem.’ There are 14 residuals which are greater than +4.00 or less than -4.00. It is reassuring that all of these occur in the range i = 1 . . . 38, since the effects we wish to study should not be operative in the time period 1801-1840. Six counties have residuals which are greater than +4.00, meaning that their death rates are higher in the period 1701-1750 than the regression predicts. These should be areas where stinting was lax or nonexistent, or where the area of waste was high in proportion to the total unenclosed area. The first of these, Cheshire, was dairy country, and thus contact with diseased cattle could be expected to be more frequent than in other, nondairy, areas. A destructive murrain was reported to have caused the death of 30,000 cows in that county in 1751 (Thirsk, p. 83; Creighton, p. 125). In the Weald area of Sussex, manorial control was weak, and the common fields of Hertfordshire were not strictly regulated (Thirsk, pp. 52 and 59). Despite suggestions that the number of animals grazing the pastures of the fen country of Lincolnshire and the East Riding of Yorkshire should be regulated, the commons continued unstinted (Thirsk, pp. 38-39). There remains one county, Huntingdonshire, for which no explanation can be found. Eight counties have residuals which are less than -4.00; their death rates are lower in the period 1701-1750 than the regression predicts. These should be counties in which stinting was successful, or they should have a smaller proportion of waste relative to the total unenclosed area. In two of these counties, Cumberland and Northumberland, the risk of infection was ‘A complete
table of the residuals
may be obtained
upon request
from
the author.
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reduced by the widespread practice of transhumance. “Every summer around Whitsuntide, the herds and flocks from the valleys were led to the higher pastures and fresh grazing, and there the cattle herds, and sometimes the whole community, remained until the hay in the valley was ready to be harvested” (Thirsk, p. 22). Two more, Herefordshire and Derbyshire, had a history of being carefully stinted. Rutland, Nottinghamshire and Leicestershire, were fielden country, the land in whose parishes was highly cultivated. There was no waste left (Thirsk, pp. 92 and 105). In the case of Wiltshire, the discrepancy remains unexplained. V Some Implications of the Enclosure Hypothesis There remains a further method of verifying the validity of a hypothesis: to see if it can explain relevant phenomena in a more satisfactory manner than alternative hypotheses. An interesting case, for example, is Wrigley’s finding that, in the East Devon parish of Colyton, a parish possessing an exceptionally complete parish register, the population history fell into three phases: (i) Before the 1640’s there was usually a substantial surplus of baptisms over burials; (ii) between the 1640’s and the 1780’s burials usually exceeded baptisms; and (iii) After the 1780’s the large surplus of baptisms over burials reappeared. The first and third periods were marked by high fertility levels; the second by low fertility levels. The second period also evidenced a steep rise in child mortality (1969b, pp. 159-160). One cannot help but be struck by the way these dates fit the Enclosure Hypothesis. The 1640’s were the years when the regulation of grazing rights on the waste began to break down; the 1780’s encompassed the last outbreak of ague in England. Add to this the fact that the commons of East Devonshire were stocked without stint (Marshall, p. 135), and one has an explanation which is surely superior to Wrigley’s hypothesis that family limitation was being practiced in the middle period (1969b, p. 174). Hollinsworth also advanced family limitation as a possible explanation for the low fertility level of the British peerage after 1650 (p. 5 1). If the frequency of conception remained the same, but the number of stillbirths increased due to the ague, and the stillbirths were not all recorded, as Hollinsworth suggests was the case (p. 49), then it would appear that births were occurring further apart, giving the impression that family limitation was being practiced. It is significant that the heaviest child mortality and lowest expectation of life at birth for the peerage are found in the cohort born 165&1674, that is after the breakdown in regulation and before the acceleration in the rate of enclosure. Mortality in general was highest about 1660-1672 (p. 53) again in the period that the Enclosure Hypothesis would predict.
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The Enclosure Hypothesis may also account for the growth of the Irish population in the 1780’s. Connell notes that it occurred at a time of extensive reclamation of waste land (p. 38). In an earlier period Ireland was largely a pastoral county and the inhabitants lived on a diet of milk and meat. Some of the reigning diseases were specifically linked to the consumption of meat, and outbreaks of disease in animals preceded their appearance in the human population (Creighton, pp. 345,354355 and 694). The contrast between Germany and France in the first half of the nineteenth century is illuminating. The German population was growing rapidly while common lands were being enclosed; in France population stagnated during a period when progress in enclosure was slow, and anthrax was widespread in the animal population.8 Another finding that has not yet been explained satisfactorily is that the bad harvests in England in 1793-1795 and 1798-1801 did not have as severe effect on death rates as those of earlier periods (Habakkuk, p. 132). If it is accepted that in bad times deaths were caused not by starvation, but because disease was more prevalent in the livestock pastured on the waste, then the enclosure of the preceding 100 years suffices to explain the less severe effects of bad harvests on the death rates. The Enclosure Hypothesis also explains two findings of J. D. Chambers for eighteenth-century Nottinghamshire: (i) The fertility of industrial parishes appears to have been between 20 and 30% higher than that of agricultural parishes (1972, p. 64). The closer contact with the animal population in the latter could well have increased the risk of sterility and spontaneous abortion. (ii) Without family limitation, we should expect seven or eight births per family, but until the last quarter of the eighteenth century the average was no more than four or five (1972, p. 67). Again, epidemics of ague could account for this low fertility, and the extinction of that disease in the 1780’s would account for the increase in fertility thereafter. The relationship between enclosure and industrialization has been a topic of some difficulty for economic historians. Mantoux’s hypothesis that, as a result of enclosure, industry was the “only refuge for thousands of men who found themselves cut off from their traditional occupations,” (p. 182) has been undermined by more recent research which indicates that enclosures actually increased the demand for labor in rural areas (Chambers and Mingay, pp. 98-99). The Enclosure Hypothesis resolves the problem immediately. The increase in population which resulted from the enclosure movement was able to provide for the needs of both the rural areas and the rapidly growing industrial enclaves. Population growth and industrialization have an interesting economic relationship, inasmuch as either could be the cause of the other. Once an 8Bogart, pp. 24, 35, 241 and 250; Vallery-Radot, land was waste as late as 1841.
p. 257. Bogart
notes
that
17% of French
ENCLOSURE
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43
explanation has been found for the increase in population which is independent of industrialization, it becomes possible to postulate that the former was the cause of the latter. Proponents of the view that industrialization was the cause, the population growth the effect, have difficulty in explaining why the balance of baptism and burial altered about 1750 in a rural parish such as Hartland. Hartland was far from the small centres of new industrial growth. Its economic base did not begin to change for many years after the sudden appearance of substantial baptism surpluses. Nor was there any revolutionary change in transport facilities in the area such as might be adduced to explain the action at a distance of the new forces of industrial growth. Yet there were many parishes like Hartland and this fact in turn makes it less easy to accept the view that nascent industrial growth provoked the population changes even in areas close to the new centres of industry (Wrigley, 1969a, p. 156).
The mechanism by which population growth can advance industrialization is a twofold one. First, it leads to an increase in aggregate demand, enabling the benefits of increased specialization and the economies of scale to be realized. Second, through increasing the supply of a scarce factor of production, labor,g it raises the average product of that factor. Both of these mechanisms lead to an increase in income per capita, to more saving, more investment, and finally to a further increase in the demand for labor, so that population grows even more, and the mechanism becomes selfsustaining. Perhaps of equal importance to the growth of population was its increased health. While anthrax might be expected to dispose of its victims relatively quickly, workers suffering from chronic brucellosis or tuberculosis would experience relatively long periods of ill health, which would have adverse effects on their productivity, before they finally became too ill to work at all. Thus the healthier population resulting from the enclosure movement would also be a more productive population. The quality, as well as the quantity, of the labor force speeded along the process of industrialization. This view of population growth as the cause of industrialization meshes neatly with Nef s hypothesis that the Industrial Revolution of the eighteenth century was preceded by one in the period 1540-1640 (p. 8) which was also ODeane and Cole (p. 89) considered that labor scarcity was an outstanding feature of the British economy in the late seventeenth and early eighteenth centuries. Wilson (pp. 371-372) points out that some of the inventions which occurred in the textile industry were specifically directed to the saving of labor, and that as late as 1760 the London Society of Arts offered a prize for a spinning machine, observing that “manufacturers of woolen, linen and cotton find it extremely difficult in the summer season when the spinners are at harvest work to procure a sufficient number of hands.” Chambers (1957, p. 37) states that the labor force was conspicuous by its scarcity in the 1740’s. Scarcity is a relative concept. If labor is scarce, then capital must be abundant, and that abundance tends to be reflected in its price. Wilson (pp. 371-372) suggests that the long term rate of interest bad a general tendency to fall during the hundred years prior to the Seven Years War, while T.S. Ashton (pp. 98-99) emphasizes that, in the early part of the eighteenth century, interest rates were low.
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a century of rapid population growth. The slow down in the hundred years between 1640 and 1740 (p. 15) also matches a period of little or no growth in population. VI The Direction of Future Research Taken by themselves, the individual items of evidence advanced in support of the Enclosure Hypothesis are not completely satisfactory. The strongest piece of statistical evidence was the fact that the coefficient of E was significant at the 0.01 level in the regression with D as the dependent variable but, as was mentioned earlier, the data from which the estimate was derived is suspect. The coefficients of K in both regressions were also significant at the 0.01 level, but K is simply a dummy variable for a time period; the evidence is consistent with other hypotheses than the Enclosure Hypothesis. The fact that the variable E does not affect the birth rate may be consistent with the notion that the ague came in nationwide epidemics, yet as Chambers’ study of eighteenth-century Nottinghamshire shows, differences in fertility did occur between industrial and agricultural parishes. Why not between agricultural parishes? The ague might have been brucellosis, but we cannot be entirely certain that it was not malaria, as other writers have assumed. One is dubious that family limitation was practiced in the seventeenth century; that is not the same thing as saying one is certain that it was not. Yet taken all together, the individual pieces of evidence make for a strong enough case for the advancement of the Enclosure Hypothesis, as at least a tentative explanation for the demographic changes which occured at the midpoints of the seventeenth and eighteenth centuries. Where can we look for more substantial evidence? Medical historians obviously have an important role to play. How important were diseases of animal origin in explaining the high mortality of the late seventeenth and early eighteenth centuries? Were spontaneous abortion and sterility more prevalent during that same time period than before or after? Local historians are the only ones who can make definitive judgments on such matters as how strictly the practice of stinting was enforced in their particular areas, and whether the area of waste was high or low in proportion to the total unenclosed area. Ideally one would like an estimate of the area of unenclosed waste in each county, as distinct from the combined area of waste and arable, say, in 1740, and again in 1840. As was mentioned earlier, the dependent variables in the regressions should be fertility and mortality, rather than birth and death rates. The necessary data on these are presumably to be found in Professor Hollings-
ENCLOSURE
AND POPULATION
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worth’s stack of punch cards, containing data on the fertility and mortality of the British peerage. Once all of these data are available, a definitive statistical test will be possible. If the Enclosure Hypothesis can be validated, then the three major pieces of the puzzle which is the economic history of eighteenth-century England will fit neatly together. And once enclosure, population growth, and industrialization are in place, it becomes a simple matter to fit the minor pieces of the puzzle, a task that remains impossible so long as the major pieces are jumbled. ACKNOWLEDGMENTS The author wishes to thank Professors John D. Bowman, Robert E. Gallman, Donald McCloskey, and James F. Shepherd, as well as Dr. Kenneth Fry, and an anonymous referee, for advice and criticism. The study was financed by a grant from the Aid to Faculty Scholarship Fund of Whitman College. Any errors are attributable solely to the author.
REFERENCES Ackerknecht, E.H. (1965). Hisrory and Geogrophy of the Most Important DLreases. New York. Ashton, T.S. (1955). An Economic Hbtory of England: The 18th Century, London. Barnes, D.G. (1930). A History of the English Corn Lows, New York. Bogart, E.L. (1942). Economic HfitoryofEurope. 1760-1939. New York. Chambers, J.D. (1957). The Vale ofTrent, 1670-1800, London. Chambers, J. D. (1958). “Enclosures and the Rural Population: A Revision,” in Taylor, 74-84. Chambers, J. D. (1972). Population. Economy and Society in Pre-Industrial England, London. Chambers, J. D., and Mingay, G. E. (1966). The Agricultural Revolution, 1750-1880. London. Connell, K.H., “Some Unsettled Problems in English and Irish Population History, l75& 1845,” in Drake, 30-39. Creighton, C. (1965). A History of Epidemics in Britain. Vol. 11, New York. Curtler, W.H.R. (1920). The Enclosure and Redistribution of our Land. Oxford. Deane, P. and Cole, W.A. (1967). British Economic Growth, 1688-1959. Cambridge. Drake, M., Ed., (1969). Populotion in Industrialization. London. Ernie, Lord. (1961). Britlh Forming Past ond Present, Chicago. Everitt, A., “Farm Labourers,” in Thirsk, 396-465. Flinn, M.W. (1970). Britirh Populotion Growth, 170&1850. London. Francis, J. (1958). Tuberculosis in Animals and Mon. London. Gonner, E.C.K. (I9 12). Common Lond and Enclosures, London. Hahakkuk, H.J. (1953). “English Population in the Eighteenth Century,” The Economic HI& tory Review, 117-33. Harris, H.J. (1950). Brucellosis, New York. Hollinsworth, T.H. (1964). “The Demography of the British Peerage,” Populotion Studies. Supplement, 3-108. Hull, T.G. (1963). Diseases Tronsmittedfrom Animals to Mon. Springfield. Mantoux, P. (1961). The Industrial Revolution in the Eighteenth Century, New York. Marshall, W. (1970). Rural Economy of the We+ of England. Vol. II, New York. McKeown, T., and Brown, R.G. “Medical Evidence Related to English Population Changes in the Eighteenth Century,” in Drake, 40-72.
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Neal, L. (197 1). “Deane and Cole on Industrialization and Population Change in the Eighteenth Century,” The Economic History Review, 643-7. Nef, J.U. “Not One, hut Two Industrial Revolutions,” in Taylor, 7-15. Razzell, P.E. “Population Change in Eighteenth-Century England: A Re-Appraisal,” in Drake, 128-56. Slater, G. (1907). The English Peasantry and the Enclosure ofCommon Fields. London. Springett, V.H. (1952). “An Interpretation of Statistical Trends in Tuberculosis,” The Lancer, 521-5and575-80. Taylor, P.A.M., Ed., (1958). The Industrial Revolution in Britain: Triumph or Disaster?, Boston. Thirsk, J., Ed., (1967). Agrarian History of England and Wales. Vol. IV, 15w1640, Cambridge. Vallery-Radot, R. (1923). The Lifeof Pasteur, trans. R.L. Devonshire, New York. Wilson, C. (1965). England’s Apprenticeship, 1603-1763. New York. Wrigley, E.A. (1969a). Population and Hbtory. New York. Wrigley, E. A. (1969b). “Family Limitation in Pre-Industrial England,” in Drake, 157-94.
Enclosure and Population Growth In Eighteenth-Century England GORDON
PHILPOT
Whitman
College
The demographic history of England in the three centuries between 1500 and 1800 may be divided into three phases: (i) From 1500 to about 1650 population grew rapidly; (ii) during the next 100 years it showed no decisive trend; and (iii) about the middle of the eighteenth century there was a sudden fierce acceleration in population growth (Wrigley, 1969a, p. 78). So far no completely satisfactory explanation has been given to account for either the demographic change which occurred at about the midpoint of the seventeenth century, or that which occurred 100 years later. Most research in the area has been concentrated on the second turning point due, no doubt, to its close proximity to the beginnings of the Industrial Revolution. For a while controversy swirled around the question of whether the acceleration in the rate of population growth was a result of a declining death rate or of a rising birth rate and, since the available statistics were not too reliable, both sides could point to some evidence in support of their argument (see, for example, Connell; Deane and Cole, Chap. 3; Habakkuk; McKeown and Brown; and Razzell). Fortunately, not all of the statistics for the period are unreliable. Those of the British peerage, for example, are probably more reliable than any other group’s. Their analysis led T.H. Hollinsworth to the findings that mortality rose in the first half of the seventeenth century while fertility fell. After 1750 there was a sharp drop in both child mortality and adult mortality, and an increase in fertility occurred at about the same time (pp. 70-72).
It might be that the peers were not representative of the population as a whole, but any theory purporting to explain the demographic trends of the period would then have to explain why they were the exception to the general rule. Occam’s razor constrains us, in the absence of evidence to the contrary, to assume that the trends observed in the peerage reflected the underlying demography of the populace as a whole. The high death rates of the late seventeenth and early eighteenth centuries were chiefly attributable to infectious diseases whose incidence was much greater in infancy and childhood than in adult life (Creighton, p. 18). McKeown and Brown investigated three possible causes of the reduction in mortality which occurred in the late eighteenth and early nineteenth 29 Copyright @1975 by Academic Press, Inc. All rights of reproduction in any form reserved.
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centuries: specific medical therapy; changes in the balance between the virulence of the infective organism and its host; and improvements in the environment. They concluded that improvements in the environment were the most acceptable explanation (p. 72). Razzell disagreed with their conclusion and advanced the hypothesis that improvements in medicine, specifically the introduction of inoculation against smallpox, could account for the falling death rate in the eighteenth century (p. 154). Whether the elimination of a single disease would have so great an effect, however, is questionable. Even the extinction of the plague in 1666 caused no immediate fall in the death rate, and Razzell’s hypothesis leaves unanswered the questions of why mortality increased during the seventeenth century and why fertility declined and then rose at the midpoints of the seventeenth and eighteenth centuries. During the 300 years from 1500 to 1800, the great majority of the people of England lived in rural areas.l Any agency which had a major effect on population growth, therefore, must of necessity have worked upon the rural population. If this fact is taken in conjunction with McKeown and Brown’s hypothesis of environmental improvement, the notion is suggested immediately of some kind of change in the rural environment, which leads directly to a consideration of the enclosure movement, the major force for change in eighteenth-century rural England. Certainly there were links between enclosure and population growth. Farey, the agricultural reporter, listed 44 places in Derbyshire in which the total population more than doubled between 1788 and 18 11, a period of widespread enclosure in that county (Chambers, 1957, p. 56). J.D. Chambers writes as follows: The period 178% 1840 saw only a sporadic exodus . . from the rural areas . and side by side with it, an actual filling up of empty spaces and a steady rise in the great majority of established centres of rural population . . This phenomenon of rural fecundity is all the more remarkable since it follows a period marked by enclosure and the consolidation of farms. (1958, p. 82).
It is with the relationship this paper is concerned.
between enclosure and population
growth that
I The Enclosure Hypothesis As a starting point it is necessary to focus attention on one particular area of the medieval English village: the commons or waste, used by the ‘Deane and Cole, p. 7, suggest that between tions of 5,000 or more in 1750.
15 and 16% of the population
lived in concentra-
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villagers as a grazing area for their livestock. As the name suggests, all the animals of the village grazed it in common, the beasts belonging to different owners being mixed together quite indiscriminately. Those villagers who had the privilege of turning out their animals to graze guarded that privilege jealously against the intrusion of strangers. The presence of strange cattle or sheep was strictly prohibited. Villagers who turned out more stock than their proper share were presented at the manorial court and fined, and the limits within which swine could feed were restricted.2 As long as the number of animals permitted to graze on the commons was held within reasonable bounds, they remained relatively healthy. But between 1500 and 1650 the population of England almost doubled (Wrigley, 1969a, p. 78, Fig. 3-3). If the animal population kept pace with the human population the pressures on the limited areas of waste can easily be imagined. Even so, the strict regulation of grazing rights might have continued had it not been for the social upheavals which led to the Civil War (1642-1646). Then the reins of traditional authority were relaxed and the bonds of society weakened. “With many squires taking up arms for Charles I or Parliament, and leaving their locality for years on end, the direct interest of many landlords in farming ceased, and absenteeism became, first a military necessity, then a social habit” (Everitt, pp. 464-465). Along with the breakdown in the social order, the regulation of grazing rights was also a casualty of the Civil War, and the commons in many areas were overstocked. Animal diseases associated with lack of food and overcrowding became prevalent. Because all the animals of the village were turned out on the commons together, it did not take long for one diseased animal to infect all the others. Writing in 1653, Blith complained that “every man laies on at random . . . ” as a result of which “you shall observe such a rot of sheep” that the commoners lose all their flocks.3 In the same year Moore described the commons as “pest-houses of disease for cattle,” and added “Hither come the Poor, the Blinde, Lame, Tired, Scabbed, Mangie, Rotten, Murrainous” (Ernle, p. 128). The situation had not improved in the early eighteenth century when, in many cases, the commons were unstinted. In other cases, while most villagers were restricted as to the number of their stock, one or more of them were restrained by no limit, and not only turned out as many of their own sheep and cattle as they could, but also took in those of strangers (Ernle, p. 158). Even as late as 1794, the cat2Emle, pastures, paper the Vurtler, tion prior
p. 27. Ernie makes a distinction fringed by the untilled wastes.” terms “commons” and “waste” p. 126. Curtler notes that the to 1653, lending support to the
between the two terms, referring to “the common (p. 26) Later the distinction becomes blurred. In this are used interchangeably. problem of overstocking had not received much menhypothesis that it dates from the 1640’s.
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tle and sheep pastured on the Lincolnshire commons were reported to be very unhealthy.4 Disease originating in the fields also affected the cottage and the manor house, either by way of direct contact, or through the agency of milk or meat obtained from infected animals. It goes without saying that in the seventeenth and eighteenth centuries there was no inspection of meat by government officials; no testing of milk for the presence of the tubercle bacillus. The prevailing standards of hygiene are perhaps best illustrated by the example of the master, whose idea of charity was to send to the family of his sick shepherd the carcass of a sheep, which had been found dead in a furrow (Creighton, p. 156n). In 1658, a letter writer refers to disease in the fields together with, not only “a great death of coach horses,” but also much sickness in the human population. In the 1720’s and 1730’s, and again in 1760, cases were reported of disease occurring in horses one or two months before it affected man. During the first half of the eighteenth century, murrain in cattle occurred at the same time as outbreaks of putrid or malignant sore throat and putrid fever in the human population. Indeed, the English throat-distemper of the eighteenth century was identified with the garrotillo of sixteenth- and seventeenth-century Spain, which was linked to preceding murrains of cattle (Creighton, pp. 120, 125, 313, 3455346, 355, 692,735-736 and 736n). Why the breakdown in regulation continued after the turmoil of the seventeenth century was over is not clear. It could have been the result of “social habit” on the part of some absentee squires, but too many eighteenth-century landlords took an intense interest in their land for this to be an acceptable explanation in more than a minority of cases. Perhaps the more progressive squires looked to enclosure as the solution to the problem. At any rate, the enclosure movement did have extremely beneficial Hects on the health of the animal population. After enclosure of the waste, the land was either plowed up or, if still used for grazing, stocked more reasonably. The flocks and herds of different farmers were no longer mixed together indiscriminately, and disease in the animal population was reduced. A correspondent of Arthur Young reported that not one sheep died from the rot on land that had been enclosed whereas, on the same land before enclosure, there were years when not a single sheep escaped the rot. The two enclosed parishes of Childersley and Knapwell both escaped the rot during a period when neighboring parishes were desolated by the disease (Ernle, pp. 236 and 243). As the animal population became healthier, so did the human population, the death rate declined, and the surge in population growth ensued. ‘Ernie, 337-338.
p. 245. For further
evidence
on this point,
see Cutler,
pp. 180 and 230; Gonner,
pp.
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II The Medical Evidence If, prior to enclosure, the pool of infection in an unhealthy animal population occasionally overflowed, to cause epidemics in the human population, then it should be possible to find evidence that diseases which may be transmitted from animals to man were prevalent in the years between the midpoints of the seventeenth and eighteenth centuries. The most common disease of this type, as well as the most common milkborne disease, is brucellosis (Harris, p. 45), which in cattle is known as contagious abortion, and in man as undulant fever, or intermittent fever (Hull, p. 127). There are many references to intermittent fever in the medical writings of the seventeenth and eighteenth centuries, when it was often referred to as the ague, but this cannot be taken as firm proof of the prevalence of brucellosis, since intermittent fever and ague may also be used as synonyms for malaria. Indeed, some modern writers unquestioningly accept the term ague to mean malaria. Razzell, for example, in his paper attributing the growth of population in the eighteenth century to the spread of the practice of inoculation against smallpox, states that no “disease, other than smallpox (due to inoculation), was described as having declined or disappeared, except ague (malaria), which is very frequently mentioned as having disappeared during the latter half of the eighteenth century” (p. 154). J.D. Chambers, while less dogmatic than Razzell, wrote that, “The word malaria is unfamiliar to the student of English epidemiology; but if we call it by the homely name of ague, we shall have no difficulty in recognizing one of the killing diseases of preindustrial England” (1972, p, 98). Creighton, on the other hand, felt that to equate the ague with malaria was an error. Sydenham . . has much to say of agues or intermittents prevalent in town and country for a series of years . . But he does not count these as the agues of the marsh . Sydenham and his learned colleagues were not ignorant of the endemic agues of marshy localities, but they made little account of them in comparison with the aguish or intermittent fevers that came in epidemics all over England (pp. 302-303).
In the last great epidemic period from 1780 to 1786, Jesuit’s bark, the bark of the conchona tree, from which quinine may be derived, was ineffective in the treatment of ague (p. 325), whereas quinine is known to be effective in treating malaria. The inhabitants of high ground fell victim to the ague at a time when those living in nearby valleys escaped. The people of Boston and the neighboring villages in the midst of the fens, for example, were healthy at a time when the ague was epidemic in the more elevated areas of Lincolnshire (p. 367). The reverse would have been true for an outbreak of malaria. Indeed ague was common in districts where anopheline mosquitoes are relatively scarce today. When malaria was introduced into
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England from abroad in the present century by troops returning from the two world wars, no new cases were found after the first winter. Since there is no evidence that the climate in the seventeenth and eighteenth centuries was any more favorable for the overwintering of the malarial plasmodium, it seems unlikely that endemic malaria ever existed in England during that period (McKeown and Brown, p. 47n). If the ague were not malaria, it might well have been the other intermittent fever: brucellosis. Whitmore describes the fatal epidemic ague of 16581659 as so “prodigous in its alterations that it seems to outvie even Proteus himself” (Creighton, p. 367). Compare this with a modern physician’s description of brucellosis: “No disease, not excepting syphilis and tuberculosis, is more protean in its manifestations” (Harris, p. v, Foreword by Simpson). Brucellosis and two other diseases of animal origin, vibriosis and listeriosis, can cause spontaneous abortion and sterility in human females as well as in animals (Harris, p. 198; Hull, pp. 176 and 255). If the ague were brucellosis, therefore, it could account for the decline in fertility which occurred in the seventeenth century when it became prevalent, and for the rise in fertility in the second half of the eighteenth century as it passed from the scene. The ague was also fully capable of explaining the high death rates of the late seventeenth century. The epidemic ague of 1657- 1659, for example, had such an effect on mortality that it was afterwards viewed as a “little plague” comparable to the Great Plague of 1665 (Creighton, p. 314). And a milkborne disease would account for a high rate of child mortality during the period of its prevalency. The second disease of animal origin to merit consideration is tuberculosis. The timing is right. Its incidence increased in the seventeenth century and it reached the peak of its prevalency during the eighteenth (Ackerknecht, p. 104). To be sure, not all tuberculosis is of animal origin. In England in the 1940’s only 23.4% of tuberculosis in man was of the bovine type, but this was a period when the benefits of pasteurization were well known. There is evidence that the proportion of bovine origin is higher in primitive agricultural communities where there is close association between animals and man (Francis, pp. 91 and 95-96), as would be the case in seventeenthand eighteenth-century England. Children are much more commonly infected with the bovine type of the tubercle bacillus than are adults, the incidence being highest among children less than five years of age (Hull, p. 44). Tuberculosis could very well have been, therefore, a source of high child mortality during the late seventeenth and early eighteenth centuries. It continued to be a source of high mortality long after the ague had become extinct, but this may be explained by the relatively long period of residual in-
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fection which is typical of that disease (Hull, p. 37). Finally, in the opinion of at least one medical scholar, the main cause of the fall in mortality due to tuberculosis was environmental improvement (Springett, p. 579), which fits in well with McKeown and Brown’s finding referred to earlier. In considering the third major disease of animal origin, anthrax, we are on less certain ground. It was still prevalent in France, where enclosure came much later than in England, as late as the second half of the nineteenth century (Vallery-Radot, p. 257). Creighton’s “putrid fever” of the middle third of the eighteenth century may well have been anthrax. It occurred at a time of disastrous murrain in cattle, and was reported to be the same disease as one at Rouen, which clearly was anthrax.5 If this assumption is valid, the unenclosed wastes would have been a particular menace to cattle and sheep since, once infected with anthrax, pastures remain contaminated for years. Furthermore, in an era of cottage industry, a large proportion of the rural population would be exposed to the wool and hides of infected animals, and thus to the massive pneumonia of “woolsorters disease” (Hull, pp. 99- 100). It must be emphasized that this is a field in which much research remains to be done, especially by medical historians. For the moment, the part played by anthrax in eighteenth-century medical history must be considered somewhat tentative. III A Question of Timing If the Enclosure Hypothesis is valid, then enclosure, the cause, must have preceded population growth, the effect. In other words, since the acceleration in population growth began about 1750, enclosure should have been getting under way in the first half of the eighteenth century. Yet enclosures were not a purely eighteenth-century phenomenon. Consolidation of the strips in the arable fields, followed by enclosure, was practiced before the fourteenth century, and became prevalent during the period following the Black Death. But the eighteenth century saw a marked increase in the rate of enclosure, of such an order of magnitude, as to make what had gone before seem of only secondary importance. In the 182 years between 1455 and 1637, for example, it is estimated that 744,000 acres were enclosed, or 2.1% of the total area of England (Curtler, p. 148). This represents an average rate of approximately 4,000 acres per annum. Between 1700 and Kreighton, was apparently 1742.”
pp. 120-121. not typhus,
Putrid fever is sometimes used as a synonym for typhus. This fever being described as “interrupted by the typhus epidemic of 1741-
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18 15, on the other hand, about 8125,000 acres, or 22.9% of the total area of England was enclosed, an average rate for the 115-year period of 70,000 acres per annum,6 or 17 times the annual rate of the earlier period. In fact, the difference between the two time periods is even greater. In the sixteenth and seventeenth centuries, both arable and waste had been enclosed, but arable predominated, whereas in the eighteenth century about two-thirds of the land enclosed was waste (Barnes, p. 106), and from the point of view of the Enclosure Hypothesis it is the area of waste enclosed that is the relevant consideration. IV The Statistical Evidence In order to submit the Enclosure Hypothesis to statistical testing, the relevant data for 38 English counties have been assembled in Table 1. The four counties of the London area, Essex, Kent, Middlesex and Surrey, have been omitted on the grounds that over half-a-million people living in a large city have no business in a statistical test of a hypothesis concerning a rural population. Five of the columns in Table 1 have been taken from Deane and Cole’s British Economic Growth, 1688-1959. While the last two columns, which refer to a time period after the first census of 1801, are perhaps fairly reliable, the other three are not, and the techniques by which they have been derived have been criticized by Neal (pp. 643-647) and Flinn (p. 29), among others. Yet data for the eighteenth century is not easy to come by. J. D. Chambers said of Deane and Cole: “They have performed a valuable service and provided economic historians with a number of important tools with which to unlock some of the secrets of the period” (1972, p. 115). It may be that better data will one day be available; until then the economic historian must make do with what he has. The data for the two time periods, 1701-1750 and 1801-1830, have been OThese figures were derived as follows: Curtler (p. 148) estimates that six and a half million acres were enclosed by acts of parliament in the eighteenth and nineteenth centuries. Chambers and Mingay (p. 77) state that nearly three-quarters of the area enclosed by acts was enclosed in the two periods 176@1780 and 1793-1815. Thus three-quarters of six and a half million, or 4,875,OOO acres were enclosed by act of parliament in the period 17W1815. This figure is an over-estimate since they use the phrase “nearly three-quarters,” but it is an underestimate because there was some additional enclosure by acts during the periods 1700-1760 and 178s 1793. If we assume that these two effects cancel each other, the figure of 4,875,OOO is a reasonable one. In addition to enclosure by acts of parliament, there was considerable enclosure by private agreement, especially during the first half of the eighteenth century, when acts of parliament were little used. It is difficult to estimate how much land was enclosed in this way. Chambers and Mingay (p. 78) suggest that it may have amounted to half of the area enclosed by acts. If their estimate is accepted, then one-half of six and a half million, or 3,250,OOO acres were enclosed by agreement, making a total for the period of 8,125,OOO acres.
TABLE y. Area of county enclosed by Act of county Parliament Devonshire 0 Cornwall 0 Lancashire 0 Shropshire 0.3 Monmouthshire 0.4 Cheshire 0.5 Westmorland 0.6 Durham 0.7 Cumberland 1.1 Northumberland 1.7 Sussex 1.9 Staffordshire 2.8 Somerset 3.5 Herefordshire 3.6 Yorks N. Riding 6.3 Hampshire 6.4 Suffolk 7.5 Dorset 8.7 Yorks W. Riding 11.6 Hertfordshire 13.1 Derbyshire 15.9 Worcestershire 16.5 Gloucestershire 22.5 Wiltshire 24.1 Warwickshire 25.0 Berkshire 26.0 Lincolnshire 29.3 Norfolk 32.3 Nottinghamshire 32.5 Buckinghamshire 34.2 Cambridgeshire 36.3 Leichestershire 38.2 Yorks E. Riding 40.1 Oxfordshire 45.6 Bedfordshire 46.0 Rutland 46.5 Huntingdonshire 46.5 Northamptonshire 51.5 ‘Sources: Col. 1, Slater, pp. Deane and Cole, p. 115.
Average death rate 1701-50 (per 1000) 25.7 30.8 26.4 29.2 27.0 33.8 26.3 29.0 21.3 23.0 32.4 30.3 28.4 22.7 25.7 32.7 32.5 29.9 30.2 33.1 25.5 30.3 31.2 26.2 32.0 32.1 38.8 33.2 27.5 35.2 33.4 26.9 39.3 30.0 33.8 28.3 42.5 30.7 14tF7; Cols.
1’
Average birth rate 1701-50 (per 1000) 26.1 34.3 29.1 33.1 32.5 35.8 31.7 33.0 29.1 26.8 39.1 37.2 29.3 28.0 32.3 36.9 34.1 33.0 38.3 34.1 33.4 34.2 34.5 30.1 34.8 36.4 39.0 34.6 31.2 35.8 35.6 32.4 40.8 34.2 32.4 38.1 38.9 33.2 2, 3, 5, and
37
Rate of Average Average migration death rate birth rate 1701-50 1801-30 1801-30 (per 1000) (per 1000) (per 1000) -1.9 21.0 37.5 -1.9 18.2 38.2 24.5 40.6 3.0 -2.5 21.3 36.2 -3.4 18.5 28.4 -0.6 23.1 35.8 -7.6 21.1 38.2 -1.1 22.6 37.1 -10.0 21.8 38.1 -0.6 20.5 33.5 40.5 -7.3 20.0 -4.4 23.2 40.3 -0.2 20.4 34.9 -6.3 19.1 33.1 -8.5 20.0 36.3 0.1 21.7 39.1 -1.8 19.9 37.6 -2.9 19.4 35.4 38.0 -3.4 22.1 21.5 37.0 0.6 -10.4 20.9 37.3 22.7 38.7 -5.3 2.1 19.3 35.3 -3.0 19.6 34.4 2.2 22.9 34.8 -2.0 21.6 37.0 21.8 40.2 -3.3 -3.2 21.1 38.8 22.3 39.2 -4.6 1.0 22.7 37.0 -4.4 24.0 40.5 -2.6 21.5 35.9 -1.0 24.0 40.3 20.9 -3.0 37.0 21.4 2.3 36.6 -15.2 20.6 35.8 2.7 22.7 37.7 -2.5 21.9 35.0 6, Deane and Cole, p. 131; Col. 4,
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pooled, giving 76 observations equations:
PHILPOT
to estimate the parameters of the following
Di = LI + bKi + CEi,
(1)
B, = f - gK, + hDi - jEi,
(2)
where i= i = B, = Bi = Bi = Di = Di = Di = Ei = Ei = Ei = Ki= Ki =
1.. .38 for the period 1701-1750 39.. .76 for the period 1801-1830
County birth rate (per 1,000) Cal. 3 for i = 1 . . . 38 Cal. 6fori = 39 . ..76 County death rate (per 1,000) Cal. 2 for i = 1 . . .38 COI. 5 for i = 39 . . . 76 Percentage area of unenclosed waste in county Col. 1 for i = 1 . . . 38 Ofori = 39...76 lifi= 1...38 Oifi = 39...76
All parameters are positive, a negative effect being shown by a negative sign. Ideally, the dependent variables should be mortality, perhaps expectation of life at birth, and fertility, but the necessary data are simply not available. Death and birth rates must be used in their place. Ki is a dummy variable introduced because the birth and death rates depend not only upon E,, the area of unenclosed waste in the county concerned, but also on the total area unenclosed in the country as a whole. K, thus serves as a proxy for the effect of the nationwide epidemics of ague, which reached far beyond the boundaries of any one country. The use of 1 for the period 1701-1750 and 0 for 1801-1830 may be justified on each of two grounds: (a) The area unenclosed in the whole country was considerably less in 1801-1830 than it was in 1701-1750; and (b) the ague had become extinct in the 1780’s, and so its effects would not be felt in the later time period. 4 is a variable that reflects the percentage area of unenclosed waste in each county. The percentage area of the county enclosed by act of parliament will serve as a proxy variable for this, since almost the entire area enclosed by acts was enclosed after 1750. To be able to be enclosed after 1750, the land must have been given over to the open field system before that date. This measure understates the unenclosed area, since some land was enclosed by nonparliamentary means, even after 1750. On the other hand, the use of zero for the period 1801-1830 is also an understatement, for while the massive burst of enclosure was over by 1815, the process
ENCLOSURE
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GROWTH
39
continued, though at a much reduced pace, for most of the nineteenth century. To the extent that these understatements balance each other, the effect will be to cause an error in the estimate of the constant term in both equations, but since this term is of no interest to us, no great harm results. Equation (1) shows the death rate depending directly on the two variables K and E, the former reflecting the nationwide epidemics of ague, and the latter the effects of infectious diseases that were. confined within the boundaries of the county: tuberculosis, anthrax, and localized outbreaks of brucellosis. In Eq. (2) the coefficients of K and E have negative signs; the effect of disease originating in the unenclosed waste is to reduce the birth rate through spontaneous abortion and sterility. The variable D appears as an independent variable in this equation because mortality may influence the porportion of women of childbearing age in the population, and thus the birth rate must be a function of mortality as well as of fertility (Flinn, p. 24). Equations (1) and (2) are recursive, and can be estimated independently using ordinary least-squares. The regressions obtained by using this procedure were as follows:
D = 21.36 + (0.49) B = 23.23 (1.82)
6.58K + 0.126E (0.86) (0.029) 8.94K + 0.650 - 0.0018E (0.82) (0.08) (0.0230)
R2 = 0.716,
(1)
R2 = 0.623.
(2)
The statistical evidence is consistent with the Enclosure Hypothesis. In Regression (1) the coefficients of K and E both have the right (positive) sign, and are significant at the 0.01 level. In Regression (2), the coefficients of K and E both have the right (negative) signs, but while the former is significant at the 0.01 level, the latter is not. This might be a result of multicollinearity. The first regression demonstrated a relationship between D and E, and both of these variables appear on the right-hand side of Eq. (2). When E is dropped from the regression, however, the standard deviation of D decreases only from 0.08 to 0.07, and the R* declines hardly at all. The birth rate, therefore, appears not to depend upon the area of unenclosed waste within a county, a result which is in complete harmony with the view that the major cause of low fertility was spontaneous abortion and sterility resulting from the ague, which took the form of nationwide epidemics, and thus would be reflected by the variable K, but not by E. While Regression (1) is consistent with the Enclosure Hypothesis, it is also consistent with an alternative hypothesis: that in the first half of the eighteenth century there was a pattern of migration between the enclosed and the unenclosed counties, which had the effect of reducing death rates in the former, and raising them in the latter, perhaps as farm workers who became unemployed as a result of enclosure moved to unenclosed areas to seek work, and later died there. This alternative hypothesis may be sub-
40
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jetted to a further test by computing the Spearman coefficient of rank correlation between Column 1 (Percentage area of county enclosed by act of parliament) and Column 4 (Rate of migration, 1701-1750). It turns out to be +0.031, which is statistically insigniticant, and the alternative hypothesis may be rejected. Referring back to Regression (1), the coefficient of determination is 0.7 16, which means that the variables K and E account for 72% of the variation in the death rate, leaving 28% unexplained. This may be due, in part, to the unsatisfactory nature of the proxy variable for E, in representing both some quantitative and some qualitative aspects of what we are trying to measure. As was mentioned earlier, it understates the unenclosed area, but this understatement may be offset to a degree by an equivalent understate ment in the time period 1801-1830. The proxy variable, however, has two additional drawbacks, which are not offset: (a) It is conceptually possible to have two counties with identical percentage areas of unenclosed land, but different percentage areas of waste; and (b) two counties could conceivably have identical percentage areas of waste, but different degrees of strictness in the regulation of pasture rights. An examination of the residuals from Regression (1) may shed more light on this particular problem.’ There are 14 residuals which are greater than +4.00 or less than -4.00. It is reassuring that all of these occur in the range i = 1 . . . 38, since the effects we wish to study should not be operative in the time period 1801-1840. Six counties have residuals which are greater than +4.00, meaning that their death rates are higher in the period 1701-1750 than the regression predicts. These should be areas where stinting was lax or nonexistent, or where the area of waste was high in proportion to the total unenclosed area. The first of these, Cheshire, was dairy country, and thus contact with diseased cattle could be expected to be more frequent than in other, nondairy, areas. A destructive murrain was reported to have caused the death of 30,000 cows in that county in 1751 (Thirsk, p. 83; Creighton, p. 125). In the Weald area of Sussex, manorial control was weak, and the common fields of Hertfordshire were not strictly regulated (Thirsk, pp. 52 and 59). Despite suggestions that the number of animals grazing the pastures of the fen country of Lincolnshire and the East Riding of Yorkshire should be regulated, the commons continued unstinted (Thirsk, pp. 38-39). There remains one county, Huntingdonshire, for which no explanation can be found. Eight counties have residuals which are less than -4.00; their death rates are lower in the period 1701-1750 than the regression predicts. These should be counties in which stinting was successful, or they should have a smaller proportion of waste relative to the total unenclosed area. In two of these counties, Cumberland and Northumberland, the risk of infection was ‘A complete
table of the residuals
may be obtained
upon request
from
the author.
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reduced by the widespread practice of transhumance. “Every summer around Whitsuntide, the herds and flocks from the valleys were led to the higher pastures and fresh grazing, and there the cattle herds, and sometimes the whole community, remained until the hay in the valley was ready to be harvested” (Thirsk, p. 22). Two more, Herefordshire and Derbyshire, had a history of being carefully stinted. Rutland, Nottinghamshire and Leicestershire, were fielden country, the land in whose parishes was highly cultivated. There was no waste left (Thirsk, pp. 92 and 105). In the case of Wiltshire, the discrepancy remains unexplained. V Some Implications of the Enclosure Hypothesis There remains a further method of verifying the validity of a hypothesis: to see if it can explain relevant phenomena in a more satisfactory manner than alternative hypotheses. An interesting case, for example, is Wrigley’s finding that, in the East Devon parish of Colyton, a parish possessing an exceptionally complete parish register, the population history fell into three phases: (i) Before the 1640’s there was usually a substantial surplus of baptisms over burials; (ii) between the 1640’s and the 1780’s burials usually exceeded baptisms; and (iii) After the 1780’s the large surplus of baptisms over burials reappeared. The first and third periods were marked by high fertility levels; the second by low fertility levels. The second period also evidenced a steep rise in child mortality (1969b, pp. 159-160). One cannot help but be struck by the way these dates fit the Enclosure Hypothesis. The 1640’s were the years when the regulation of grazing rights on the waste began to break down; the 1780’s encompassed the last outbreak of ague in England. Add to this the fact that the commons of East Devonshire were stocked without stint (Marshall, p. 135), and one has an explanation which is surely superior to Wrigley’s hypothesis that family limitation was being practiced in the middle period (1969b, p. 174). Hollinsworth also advanced family limitation as a possible explanation for the low fertility level of the British peerage after 1650 (p. 5 1). If the frequency of conception remained the same, but the number of stillbirths increased due to the ague, and the stillbirths were not all recorded, as Hollinsworth suggests was the case (p. 49), then it would appear that births were occurring further apart, giving the impression that family limitation was being practiced. It is significant that the heaviest child mortality and lowest expectation of life at birth for the peerage are found in the cohort born 165&1674, that is after the breakdown in regulation and before the acceleration in the rate of enclosure. Mortality in general was highest about 1660-1672 (p. 53) again in the period that the Enclosure Hypothesis would predict.
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The Enclosure Hypothesis may also account for the growth of the Irish population in the 1780’s. Connell notes that it occurred at a time of extensive reclamation of waste land (p. 38). In an earlier period Ireland was largely a pastoral county and the inhabitants lived on a diet of milk and meat. Some of the reigning diseases were specifically linked to the consumption of meat, and outbreaks of disease in animals preceded their appearance in the human population (Creighton, pp. 345,354355 and 694). The contrast between Germany and France in the first half of the nineteenth century is illuminating. The German population was growing rapidly while common lands were being enclosed; in France population stagnated during a period when progress in enclosure was slow, and anthrax was widespread in the animal population.8 Another finding that has not yet been explained satisfactorily is that the bad harvests in England in 1793-1795 and 1798-1801 did not have as severe effect on death rates as those of earlier periods (Habakkuk, p. 132). If it is accepted that in bad times deaths were caused not by starvation, but because disease was more prevalent in the livestock pastured on the waste, then the enclosure of the preceding 100 years suffices to explain the less severe effects of bad harvests on the death rates. The Enclosure Hypothesis also explains two findings of J. D. Chambers for eighteenth-century Nottinghamshire: (i) The fertility of industrial parishes appears to have been between 20 and 30% higher than that of agricultural parishes (1972, p. 64). The closer contact with the animal population in the latter could well have increased the risk of sterility and spontaneous abortion. (ii) Without family limitation, we should expect seven or eight births per family, but until the last quarter of the eighteenth century the average was no more than four or five (1972, p. 67). Again, epidemics of ague could account for this low fertility, and the extinction of that disease in the 1780’s would account for the increase in fertility thereafter. The relationship between enclosure and industrialization has been a topic of some difficulty for economic historians. Mantoux’s hypothesis that, as a result of enclosure, industry was the “only refuge for thousands of men who found themselves cut off from their traditional occupations,” (p. 182) has been undermined by more recent research which indicates that enclosures actually increased the demand for labor in rural areas (Chambers and Mingay, pp. 98-99). The Enclosure Hypothesis resolves the problem immediately. The increase in population which resulted from the enclosure movement was able to provide for the needs of both the rural areas and the rapidly growing industrial enclaves. Population growth and industrialization have an interesting economic relationship, inasmuch as either could be the cause of the other. Once an 8Bogart, pp. 24, 35, 241 and 250; Vallery-Radot, land was waste as late as 1841.
p. 257. Bogart
notes
that
17% of French
ENCLOSURE
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POPULATION
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43
explanation has been found for the increase in population which is independent of industrialization, it becomes possible to postulate that the former was the cause of the latter. Proponents of the view that industrialization was the cause, the population growth the effect, have difficulty in explaining why the balance of baptism and burial altered about 1750 in a rural parish such as Hartland. Hartland was far from the small centres of new industrial growth. Its economic base did not begin to change for many years after the sudden appearance of substantial baptism surpluses. Nor was there any revolutionary change in transport facilities in the area such as might be adduced to explain the action at a distance of the new forces of industrial growth. Yet there were many parishes like Hartland and this fact in turn makes it less easy to accept the view that nascent industrial growth provoked the population changes even in areas close to the new centres of industry (Wrigley, 1969a, p. 156).
The mechanism by which population growth can advance industrialization is a twofold one. First, it leads to an increase in aggregate demand, enabling the benefits of increased specialization and the economies of scale to be realized. Second, through increasing the supply of a scarce factor of production, labor,g it raises the average product of that factor. Both of these mechanisms lead to an increase in income per capita, to more saving, more investment, and finally to a further increase in the demand for labor, so that population grows even more, and the mechanism becomes selfsustaining. Perhaps of equal importance to the growth of population was its increased health. While anthrax might be expected to dispose of its victims relatively quickly, workers suffering from chronic brucellosis or tuberculosis would experience relatively long periods of ill health, which would have adverse effects on their productivity, before they finally became too ill to work at all. Thus the healthier population resulting from the enclosure movement would also be a more productive population. The quality, as well as the quantity, of the labor force speeded along the process of industrialization. This view of population growth as the cause of industrialization meshes neatly with Nef s hypothesis that the Industrial Revolution of the eighteenth century was preceded by one in the period 1540-1640 (p. 8) which was also ODeane and Cole (p. 89) considered that labor scarcity was an outstanding feature of the British economy in the late seventeenth and early eighteenth centuries. Wilson (pp. 371-372) points out that some of the inventions which occurred in the textile industry were specifically directed to the saving of labor, and that as late as 1760 the London Society of Arts offered a prize for a spinning machine, observing that “manufacturers of woolen, linen and cotton find it extremely difficult in the summer season when the spinners are at harvest work to procure a sufficient number of hands.” Chambers (1957, p. 37) states that the labor force was conspicuous by its scarcity in the 1740’s. Scarcity is a relative concept. If labor is scarce, then capital must be abundant, and that abundance tends to be reflected in its price. Wilson (pp. 371-372) suggests that the long term rate of interest bad a general tendency to fall during the hundred years prior to the Seven Years War, while T.S. Ashton (pp. 98-99) emphasizes that, in the early part of the eighteenth century, interest rates were low.
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a century of rapid population growth. The slow down in the hundred years between 1640 and 1740 (p. 15) also matches a period of little or no growth in population. VI The Direction of Future Research Taken by themselves, the individual items of evidence advanced in support of the Enclosure Hypothesis are not completely satisfactory. The strongest piece of statistical evidence was the fact that the coefficient of E was significant at the 0.01 level in the regression with D as the dependent variable but, as was mentioned earlier, the data from which the estimate was derived is suspect. The coefficients of K in both regressions were also significant at the 0.01 level, but K is simply a dummy variable for a time period; the evidence is consistent with other hypotheses than the Enclosure Hypothesis. The fact that the variable E does not affect the birth rate may be consistent with the notion that the ague came in nationwide epidemics, yet as Chambers’ study of eighteenth-century Nottinghamshire shows, differences in fertility did occur between industrial and agricultural parishes. Why not between agricultural parishes? The ague might have been brucellosis, but we cannot be entirely certain that it was not malaria, as other writers have assumed. One is dubious that family limitation was practiced in the seventeenth century; that is not the same thing as saying one is certain that it was not. Yet taken all together, the individual pieces of evidence make for a strong enough case for the advancement of the Enclosure Hypothesis, as at least a tentative explanation for the demographic changes which occured at the midpoints of the seventeenth and eighteenth centuries. Where can we look for more substantial evidence? Medical historians obviously have an important role to play. How important were diseases of animal origin in explaining the high mortality of the late seventeenth and early eighteenth centuries? Were spontaneous abortion and sterility more prevalent during that same time period than before or after? Local historians are the only ones who can make definitive judgments on such matters as how strictly the practice of stinting was enforced in their particular areas, and whether the area of waste was high or low in proportion to the total unenclosed area. Ideally one would like an estimate of the area of unenclosed waste in each county, as distinct from the combined area of waste and arable, say, in 1740, and again in 1840. As was mentioned earlier, the dependent variables in the regressions should be fertility and mortality, rather than birth and death rates. The necessary data on these are presumably to be found in Professor Hollings-
ENCLOSURE
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worth’s stack of punch cards, containing data on the fertility and mortality of the British peerage. Once all of these data are available, a definitive statistical test will be possible. If the Enclosure Hypothesis can be validated, then the three major pieces of the puzzle which is the economic history of eighteenth-century England will fit neatly together. And once enclosure, population growth, and industrialization are in place, it becomes a simple matter to fit the minor pieces of the puzzle, a task that remains impossible so long as the major pieces are jumbled. ACKNOWLEDGMENTS The author wishes to thank Professors John D. Bowman, Robert E. Gallman, Donald McCloskey, and James F. Shepherd, as well as Dr. Kenneth Fry, and an anonymous referee, for advice and criticism. The study was financed by a grant from the Aid to Faculty Scholarship Fund of Whitman College. Any errors are attributable solely to the author.
REFERENCES Ackerknecht, E.H. (1965). Hisrory and Geogrophy of the Most Important DLreases. New York. Ashton, T.S. (1955). An Economic Hbtory of England: The 18th Century, London. Barnes, D.G. (1930). A History of the English Corn Lows, New York. Bogart, E.L. (1942). Economic HfitoryofEurope. 1760-1939. New York. Chambers, J.D. (1957). The Vale ofTrent, 1670-1800, London. Chambers, J. D. (1958). “Enclosures and the Rural Population: A Revision,” in Taylor, 74-84. Chambers, J. D. (1972). Population. Economy and Society in Pre-Industrial England, London. Chambers, J. D., and Mingay, G. E. (1966). The Agricultural Revolution, 1750-1880. London. Connell, K.H., “Some Unsettled Problems in English and Irish Population History, l75& 1845,” in Drake, 30-39. Creighton, C. (1965). A History of Epidemics in Britain. Vol. 11, New York. Curtler, W.H.R. (1920). The Enclosure and Redistribution of our Land. Oxford. Deane, P. and Cole, W.A. (1967). British Economic Growth, 1688-1959. Cambridge. Drake, M., Ed., (1969). Populotion in Industrialization. London. Ernie, Lord. (1961). Britlh Forming Past ond Present, Chicago. Everitt, A., “Farm Labourers,” in Thirsk, 396-465. Flinn, M.W. (1970). Britirh Populotion Growth, 170&1850. London. Francis, J. (1958). Tuberculosis in Animals and Mon. London. Gonner, E.C.K. (I9 12). Common Lond and Enclosures, London. Hahakkuk, H.J. (1953). “English Population in the Eighteenth Century,” The Economic HI& tory Review, 117-33. Harris, H.J. (1950). Brucellosis, New York. Hollinsworth, T.H. (1964). “The Demography of the British Peerage,” Populotion Studies. Supplement, 3-108. Hull, T.G. (1963). Diseases Tronsmittedfrom Animals to Mon. Springfield. Mantoux, P. (1961). The Industrial Revolution in the Eighteenth Century, New York. Marshall, W. (1970). Rural Economy of the We+ of England. Vol. II, New York. McKeown, T., and Brown, R.G. “Medical Evidence Related to English Population Changes in the Eighteenth Century,” in Drake, 40-72.
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Neal, L. (197 1). “Deane and Cole on Industrialization and Population Change in the Eighteenth Century,” The Economic History Review, 643-7. Nef, J.U. “Not One, hut Two Industrial Revolutions,” in Taylor, 7-15. Razzell, P.E. “Population Change in Eighteenth-Century England: A Re-Appraisal,” in Drake, 128-56. Slater, G. (1907). The English Peasantry and the Enclosure ofCommon Fields. London. Springett, V.H. (1952). “An Interpretation of Statistical Trends in Tuberculosis,” The Lancer, 521-5and575-80. Taylor, P.A.M., Ed., (1958). The Industrial Revolution in Britain: Triumph or Disaster?, Boston. Thirsk, J., Ed., (1967). Agrarian History of England and Wales. Vol. IV, 15w1640, Cambridge. Vallery-Radot, R. (1923). The Lifeof Pasteur, trans. R.L. Devonshire, New York. Wilson, C. (1965). England’s Apprenticeship, 1603-1763. New York. Wrigley, E.A. (1969a). Population and Hbtory. New York. Wrigley, E. A. (1969b). “Family Limitation in Pre-Industrial England,” in Drake, 157-94.