Clinical and Experimental Allergy, 1995, Volume 25, pages 296-303
REVIEW
Epidemiology of hay fever: towards a community
diagnosis
D. p. STRACHAN
Department of Public Health Sciences, St George's Hospital Medical School, London, UK
Introduction
Symptoms of rhinitis (sneezing, running and blocking of
the nose) occur occasionally in all individuals. However,
the seasonality of allergic rhinitis induced by grass and
tree pollens is characteristic and much of our under-
standing of the epidemiology of allergic rhinitis relies
upon self-reported or doctor-diagnosed 'hay fever'.
Much less is known about the prevalence or distribution
of perennial allergic rhinitis and non-allergic rhinitis [1].
Since exposure to airborne pollen is almost universal in
countries such as Britain, the distribution and determi-
nants of hay fever (other than its seasonal pattern) may
provide an insight into the epidemiology of atopy in
general.
This paper explores the association of geographical,
social and family factors with hay fever as reported by a
national sample of young British adults who had been
followed from birth. The findings are presented in
greater detail than in earlier reports [2-4] and are
discussed in the context of historical and geographical
variations in hay fever prevalence. These epidemiological
observations ('community presentation') will be used to
construct a working hypothesis ('community diagnosis')
to explain why hay fever apparently emerged as a post
industrial revolution epidemic [5] and continues to
increase in prevalence in modern Britain [6,7]. The
implications for future trends in prevalence ('community
prognosis') will be discussed.
Methods
All births in England, Scotland and Wales during 1 week
in March 1958 formed the target sample for a perinatal
morbidity and mortality survey [8]. The National Child
Development Study [9] has attempted to trace and
Correspondence: Dr D. P. Strachan, Department of Public Health
Sciences, St George's Hospital Medical School, Cranmer Terrace,
London SW17 ORE, UK.
Based on an invited contribution to a plenary session at the meeting of
the British Society of Allergy and Clinical Immunology, City
University, London, UK, 7 September 1994.
296
contact all children with the same birth dates who were
resident in Britain during 1965, 1969, 1974, 1981 and
1991 (at ages 7, 11, 16, 23 and 33 years). The following
question was asked in interviews with participants at age
23 years (in 1981): have you suffered from hay fever in
the last 12 months?
A range of potential explanatory variables were col-
lated from the information collected by midwives at birth
and by interviewers at each of the four follow-ups.
Paternal occupation at the birth of the index child was
classified according to the Registrar-General's social
classes used in 1951 [10]. The child's own current or
last occupation at age 23 years was classified by the 1981
social classes [11]. The classes used were I (professional
and managerial), II (intermediate), IIIN (skilled non-
manual), HIM (skilled manual), IV (semi-skilled) and V
(unskilled). The numbers of older and younger children
in the household were determined at the 1969 follow-up,
when most families could be assumed to be complete.
Older children of the family who were currently living
away from home, but aged under 21 years, were included
in the total.
Areas of residence at birth and at age 23 years were
each classified by the region and degree of urbanization.
The local authority areas of birth were classified as
conurbations, county boroughs (outside conurbations)
or administrative counties (predominantly urban or
rural as indicated by their population density at the
1961 census). The counties of residence in 1981 were
classified as conurbations (Greater London and metro-
politan counties) or non-metropolitan counties.
Additional factors which were considered in the
analysis were self-reported cigarette smoking (at age 23
years); parental reports of housing tenure (at age 7
years), shared use of kitchen, bath or toilet with another
household (at age 7 years), housing density (persons per
room at age 11 years), and mode of infant feeding
(reported at the 7-year follow-up); and the following
features of the birth record: sex, birthweight, maternal
age, parity and smoking during pregnancy.
Statistical analysis was performed using SAS [12].
Multiple logistic regression models were fitted by the
method of maximum likelihood using the PLR program
 Epidemiology of hay fever 297

Table 1. Prevalence (%) of hay fever in the past year at 23, by area of residence at 23

Region Conurbations Other areas Whole region

South Eastern 211 (326/1541) 18-6 (309/1671) 19-8(635/3212)

East Anglia 19 0 (214/1129) 19-0 (214/1129)
South Western 17-5 (143/819) 17-5 (143/819)
Wales 14-7 (96/654) 14-7 (96/654)
West Midlands 13-9 (88/632) 17 9 (100/560) 15-8 (188/1192)
East Midlands 15-7 (148/940) 15-7 (148/940)
Yorkshire and Humberside 13 6 (109/801) 13-6 (24/177) 13-6 (133/978)
North Western 14-9 (141/945) 15-9 (73/460) 15-2 (214/1405)
Northern 10 3 (32/311) 12 6 (64/507) 11-7 (96/818)
Scotland 11-5 (63/549) 161 (106/659) 14-0 (169/1208)
All regions 15-9 (759/4779) 16-9 (1277/7576) 16-5 (2036/12355)

in BMDP [13]. These analyses were restricted to 9356
(76%) of the 12 355 respondents at age 23 years, who
had full information on all variables included in the
models.
Results
Geographical variation
Among 12355 cohort members interviewed at age 23,
2036 (16-5%) reported hay fever in the past year. The
prevalence varied substantially across the regions of
Britain, being higher in the south and lower in the north
(Table 1). Comparisons within regions between the major
conurbations and surrounding non-metropolitan counties
did not reveal any consistent urban-rural variation (Table
1). When analysed by area of birth, the prevalence differed
little among those born in rural counties (16-2%, 486/
3009); urban counties (15-6%, 476/3059); county
boroughs (16-1%, 392/2429); and conurbations other
than London (14-7%, 272/1847); but was substantially
higher among those bom in Greater London (22-5%, 358/
1589). The London excess was mainly attributable to the
northwest to south-east gradient regional gradient by area
of birth [3].
Of the responders at age 23 years, 2919 (25%) had
moved from their region of birth. When adjusted by
multiple logistic regression for region of birth and region
of residence at 23, migrants as a group had a high
prevalence of hay fever at 23 (odds ratio 1-22, 95%
confidence interval 1-10-1-35, P < 0-001). After
adjustment for this general migrant effect, and the risk
associated with the region of birth, the risk associated with
the region of residence at 23 had a small independent effect
which was of borderline statistical significance
(0-05 < i ' < 0-10). In contrast, the influence of region of

Table 2. Prevalence (%) of hay fever in the past year at 23, by father's social class and number of children in the household

Number of other children in the household at age 11 '•

Father's social class at birth 0 1 2 3+ Total

I/II 26-1 23-1 18-6 17-4 20-8

(46/176) (175/759) (100/537) (73/419) (394/1891)
III 19-0 19-6 17-3 11-0 16-4
(125/657) (420/2148) (274/1585) (201/1826) (1020/6216)
IV/V 21-0 14-7 15-3 9-7 13-2
(38/181) (83/563) (79/517) (96/998) (296/2249)
Total 20-6 19-5 17-2 11-4 16-5
(209/1014) (678/3470) (453/2639) (370/3233) (1710/10356)

'Includes members of the family under 21 living away from home in 1969.
298 D. P. Strachan

Table 3. Prevalence (%) of hay fever in the past year at 23, by numbers of older and younger children in the household at age 11

Number of younger children in household at 11

Number of older children
in household at 11~ 0 1 2 3-1- Total

0 20-6 21-8 20-4 162 204

(216/1049) (378/1730) (203/993) (113/698) (910/4470)
1 17-3 159 13-7 10-4 15-7
(307/1776) (169/1063) (72/526) (35/338) (583/3703)
2 141 12-8 69 5-5 116
(89/630) (59/462) (14/204) (10/182) (172/1478)
3-1- 107 69 80 81 85
(31/291) (20/289) (14/175) (14/173) (79/928)
Total 17-2 17-7 160 12-4 165
(643/3746) (626/3544) (303/1898) (172/1391) (1744/10579)

'Includes members ofthe family under 21 living away from home in 1969.

birth was strong and independent of both region at 23 and
the general migrant effect (P < 0001).
Family circumstances
Table 2 shows the relationship between hay fever at age
23, household size at age 11 and paternal social class at
birth. The prevalence of hay fever declined with increas-
ing family size and was lower among the offspring of
unskilled and semi-skilled manual workers (IV & V) than
those of skilled workers (III) or professional, managerial
and intermediate groups (I & II). These effects were
independent of each other, with a 25-fold variation in
prevalence across the cells of the Table.
Table 3 shows the joint effects of older and younger
children upon the prevalence of hay fever at age 23
among the index children. Both exerted an independent
effect, but the number of older children appeared to be
the more influential variable.
Independent risk factors
Table 4 shows the variables which made a significant
{P < 0 05) independent contribution to the risk of hay
fever. This 'core' model was based upon 9356 subjects
with complete data, 1548 (16 5%) of whom had hay
fever. Holding other factors constant, hay fever at 23 was
more common among breastfed children of younger,
professional parents, born in the southeast, brought up
in small households living in owner-occupied housing
with sole use of kitchen, bath and toilet. Regular cigar-
ette smokers at 23 reported less hay fever than non-
smokers; subsidiary analyses showed a similar prevalence
in never smokers and ex-smokers at age 23.
Although tests of heterogeneity are presented in Table
4, much of the variation in hay fever by paternal social
class and numbers of older and younger children was
attributable to linear trends in risk, each of which were
highly significant (P < 0 001). The gradients by numbers
of older and younger children in the household were
significantly different from each other (P < 0 001). The
effect of maternal age was of lesser significance
{P < 0 05).
Factors not associated with hay fever at 23 years
Other factors were assessed by adding them individually
to the core model in Table 4. The following variables did
not make a significant independent contribution to the
risk of hay fever at 23: male sex (adjusted odds ratio 1 04,
95% confidence interval (0-93-1-17), birthweight less
than 2500g (1-02, 0-76-1-36), maternal smoking during
pregnancy (0-91, 0-79-1-03), birth in a conurbation or
county borough (1-02, 0-91-1-15), household crowding
(more than one person per room) at age 11 (101, 0-73-
1-38).
Maternal parity and number of older children in the
household at age 11 were highly correlated and their
independent effects could not be estimated with preci-
sion. However, the number of older children in the
household appeared to be the more influential variable.
Discussion
The rising prevalence of hay fever
Anecdotal evidence suggests that hay fever was extremely
rare in Britain before the industrial revolution, and
 Epidemiology of hay fever 299

Table 4. Independent risk factors for hay fever at 23

Number of Adjusted~ 95%

subjects odds ratio C.I. df

Regional SE 3082 100 (Reference)

group at SW 2530 078 067-089 44-3 2
birth # N 3744 0-64 056-073
Father's I 414 100 (Reference)
social II 1288 083 0-63-108
class IIIN 965 080 0-60-106
at HIM 4659 0-72 0-56-0-92 17-5 6
birth of IV 1179 058 0-43-0-78
child V 809 0-74 0-54-1-02
Unclassified 42 041 0-14-1-20
Older 0 3942 1 00 (Reference)
children 1 3323 068 0-60-0-77
(under 21) 2 1301 055 0-46-0-66 83-2 4
in household 3 520 0-45 0-32-0-62
at 11 4+ 270 0-36 0-22-0-58
Younger 0 3354 100 (Reference)
children 1 3151 093 0-82-1-07
in 2 1678 085 0-72-1-01 15-4 4
household 3 714 071 0-55-0-90
at 11 4+ 459 064 0-46-0-88
Age of 30+ 3190 100 (Reference)
mother at 25-29 3168 098 (0-85-1-14) 5-34 3
birth of 20-24 2594 085 (0-72-1-01)
index child <20 404 070 (0-50-0-98)
Breastfed (any duration) 6466 M4 1-01-1-29 4-28 1
Rented housing at 7 5313 086 0-76-0-97 6-25 1
Shared amenities* at 7 1595 079 0-68-0-93 8-13 1
Cigarette smoker at 23 3774 071 0-63-0-80 31-6 1
Total included in model 9356

~ Mutually adjusted by multiple logistic regression.

* Use of kitchen, bath or WC shared with another household. SE. South Eastern, East Anglia, East Midlands. SW. South Western,
Wales, West Midlands. N. Yorkshire & Humberside, North Western, Northern, Scotland.

emerged as a complaint of the urban educated classes in
the 19th century [5]. A large population survey in
Switzerland in 1926 found only 0-28% of 77000 respon-
dents to be suffering from hay fever [14]. At that time, the
prevalence in urban areas was 10 times higher than in
rural areas (1-2% vs 0-13%). A similar survey carried out
in 1985 found a much higher prevalence (10-0%) and
little evidence of urban-rural variation (8-0% vs 10-5%).
The substantial increase in prevalence in Switzerland
parallels that described in serial surveys of American
college students [15], Swedish army recruits [16] and
British teenagers [6,7], which suggest a long-standing
and continuing rise in hay fever prevalence. There is
also evidence of a rise in the prevalence of eczema in
Britain [6,7,17] and Denmark [18]; skin-prick reactions
to common aeroallergens in Britain [19] and USA [20];
and levels of allergen-specific IgE among Japanese
school children [21]. The exception to this general rule
seems to be in Australia, where there was no appreciable
change in the prevalence of self-reported hay fever from
1977-1978 to 1989-1990 [22] nor in the degree of skin-
prick positivity among adults over a similar period [23].
Geographical variations
Estimates of the prevalence of hay fever in different
countries vary widely, from 0-5% to 28% for children
and from 0-5% to 15% for adults [24]. Much of this
variation may be attributable to the methods of sample
selection and case definition, but there is also evidence of
real differences, notably between former east and west
Germany [25]. Regional differences are also apparent
300 D. P. Strachan
within Australia [22], perhaps related to a higher aero-
allergen burden in drier inland districts.
The marked geographical variation in the prevalence
of hay fever in the British 1958 cohort appears to relate
more closely to region of birth than region of residence at
23. This may reflect the distribution of the atopic
genotype, or variations in lifestyle or environmental
exposures (including aeroallergens) in early life. A
study of the birthplace of the parents of children with
and without hay fever would help to distinguish between
these alternative explanations.
Studies of urban-rural variation within countries are
inconsistent. In Tecumseh, USA, probable allergic
rhinitis was found three times more commonly in city
residents than in the surrounding rural areas (75% vs
25%) [26], whereas in Switzerland no urban-rural
variation was evident in recent surveys [14]. The 1958
cohort were born at a time when all cities and most major
towns in Britain experienced winter pollution by coal
smoke and sulphur dioxide at levels comparable to those
in east German cities in the mid-1980s [27]. The absence
of substantial urban-rural variation in hay fever pre-
valence in this large cohort and the low prevalence of hay
fever and allergic sensitization in previously highly
polluted east German cities [25] are evidence against
the hypothesis that irritant air pollution resulting from
industrialization was a major influence in the emergence
of hay fever as a 'post industrial revolution epidemic' in
Britain and elsewhere [28].
There has been concern that the continuing rise in
prevalence of allergic disease in recent decades may have
been due to increased exposure to vehicle-related pollu-
tants such as nitrogen dioxide, ozone and diesel particu-
lates [29]. Two studies have suggested a higher
prevalence of nasal allergy in areas with high traflic
density [30,31]. In modern Britain, ozone levels are
generally higher in urban areas, whereas nitrogen
oxides and diesel particulates are urban pollutants. The
lack of urban-rural variation in the prevalence of hay
fever may thus conceal subtle but counterbalancing
influences of different air pollutants. Nevertheless, it is
clear that exposure to outdoor air pollution cannot
account for the major epidemiological features of hay
fever which emerge from comparisons within popula-
tions, by socioeconomic status and family structure.
Socioeconomic variations
Hay fever has been recognized as a complaint of the
wealthier classes since the 19th century [5], and several
studies suggest that this pattern persists in developed
countries [22,26]. The possibility of differential reporting
and labelling of nasal symptoms in different social
groups was evaluated in a study of adults in south
London [32] which found little difference in the preva-
lence of symptoms or skin-prick reactions by social class,
but a greater use of the hay fever label by doctors among
patients from more privileged social classes.
The socioeconomic gradient in self-reported hay fever
in the British 1958 cohort parallels that seen for eczema
as reported by parents and examined by school medical
officers at ages 7, 11 and 16 [4], and for skin-prick
positivity to common aeroallergens measured at age
34-35 [Strachan DP, unpublished observations]. This
suggests that it is unlikely to be a reporting artifact and
probably reflects an association of aflluence with the
underlying atopic tendency. Socioeconomic variations
in sensitization to common aeroallergens in two large
American surveys [33,34] are consistent with this
interpretation.
Family structure
The strongest association which emerged in this analysis
was between hay fever and the number of older children
in the household. This appeared to be largely independent
of maternal age and parity, suggesting that postnatal
influences were more important than the intrauterine
environment. This would be consistent with the weaker,
but independent, trend by numbers of younger children
in the household.
A similar pattern of decreasing prevalence of hay fever
with increasing numbers of older siblings was found in a
later British birth cohort born in 1970. When studied at
the age of 5 years, 6-0% of the flrstborn children suffered
from hay fever compared with 1-3% of children with
four or more older siblings [35]. In a recent survey of over
18000 teenage school children in SheflSeld, the preva-
lence declined from 18-4% among flrstborns to 11-8%
among children with three or more older siblings
[Strachan DP, unpublished observations]. Total family
size is inversely related to the prevalence of skin-
prick positivity among German children [36], but this
study did not distinguish between older and younger
siblings.
Within the 1958 cohort, the influence of older siblings
is apparent for hay fever or allergic rhinitis ascertained
by parental interview at age 11, and for eczematous
rashes occurring in the first year of life [2]. Skin-prick
tests performed on a sub-sample of the cohort at age
34-35 show a strong, graded and statistically significant
inverse association between number of older siblings and
the prevalence of positive reactions to each of three
common aeroallergens (mixed grass pollen, house
dust mite and cat fur) [37]. These observations
effectively exclude reporting artifacts and suggest

that the relationship between hay fever and house-
hold size reflects the distribution of atopy in general,
rather than organ-specific effects on the nasal
mucosa.
Infant feeding
There has been considerable interest in the possibility
that infant feeding may modulate the development of
allergy, in particular that breastfeeding may have a
protective effect [38]. This debate emerged some years
after the 1958 cohort were born, so it is unlikely that their
mothers had selectively altered their feeding practice
because of a family history of allergy. As in a later
national cohort studied at 5 years of age [35], breastfeed-
ing was actually associated (albeit weakly) with a higher
prevalence of hay fever. However, these findings from
general population samples do not exclude a possible
protective influence of prolonged exclusive breastfeeding
in a small subgroup of infants at particularly high risk of
allergic diseases.
Smoking
Cigarette smoking has been implicated as a cause of
increased serum IgE levels but is associated with a lower
prevalence of cutaneous reactivity to common aeroaller-
gens. This discrepancy has been attributed to a lower
uptake of smoking and a higher rate of smoking cessa-
tion among allergic individuals [39]. In the 1958 cohort,
smoking was less common among respondents with hay
fever at 23 only if hay fever or allergic rhinitis was
reported at age 11 or 16 [Strachan DP, unpublished
analyses]. This suggests that adolescents and young
adults who suffer from hay fever may indeed be less
likely to take up regular cigarette smoking. However, the
similar rates of hay fever among lifelong non-smokers
and former smokers suggest that affected individuals are
not more likely to give up smoking once they have
started.
Higher levels of cord blood IgE in the have been
reported in the offspring of mothers who smoked
during pregnancy [40], but skin-prick positivity was less
common among German children whose mothers
smoked [36]. There is no evidence in the British birth
cohorts that maternal smoking during pregnancy or
childhood is an important determinant of symptomatic
nasal allergy.
Community diagnosis
Hay fever displays a remarkable degree of variation
within and between families in modern Britain. Most
Epidemiology of hay fever 301
of its risk factors are shared by infant eczema and skin-
prick positivity to common aeroallergens, suggesting
that epidemiological variations in each of these three
outcomes reflect the underlying distribution of atopy.
The strongest risk factor to emerge is position in the
household as a child. The apparent protective influence
of older siblings emerges within a few months of birth
(infant eczema) and persists at least to age 35 (skin-prick
responses). This may be seen as an example of biological
'programming' [41].
The precise nature of the programming influence
remains uncertain. A working hypothesis is that allergic
sensitization can be prevented by infections acquired
during early childhood [2]. Evidence is emerging from
in vitro studies that bacterial or viral infections may
stimulate the development of TH-1 lymphocytes and
thus prevent the proliferation of TH-2 cell populations
[42]. Early childhood infections are commonly trans-
mitted by household contact, particularly with older
siblings attending schools and playgroups, but later
infection or reinfection from younger siblings might
have some additional protective effect. The low
prevalence of hay fever among the offspring of poorer
families living in rented housing and sharing household
amenities may reflect unhygienic lifestyles or household
conditions which promote the spread of infection. Wide-
spread use of day nurseries from an early age will
promote cross-infection and may explain the unusually
low prevalence of allergic sensitization in former east
Germany [36]. The slightly increased risk of subsequent
hay fever and eczema [17] among breastfed infants may
reflect a reduced incidence of gastrointestinal infection
during breastfeeding, or more hygienic child rearing
practice in a broader sense.
Community prognosis
The hypothesis that early infection may protect against
atopic disease offers a coherent explanation for both the
past and present epidemiological patterns of hay fever.
Over the past 200 years, reductions in average family
size, improved household amenities and higher standards
of personal cleanliness have reduced the opportunity for
cross-infection within young families. This may have
resulted in more widespread expression of atopy and
the emergence of a 'post industrial revolution epidemic'
of allergic disease, affecting to a greater extent the more
affluent classes and areas of the country.
If the prevalence of hay fever is increasing as a result of
changes in biological programming in early childhood,
then the generations who have been found to be at high
risk of allergic disease while young may carry that
increased susceptibility for much of their lives. Evidence
302 D. P. Strachan
of such a cohort (or generation) effect can be seen in
observations from Tucson, Arizona, where skin-prick
tests to common aeroallergens were performed on the
same population on two occasions, 8 years apart [20]. At
each survey, positive skin tests were most common
among teenagers and young adults, thereafter declining
in prevalence with increasing age. However, the preva-
lence of skin-test positivity was higher on the second
occasion in all age groups, so that in each generation, the
prevalence of this measure of atopy increased with
advancing age. It is therefore likely that the reduced
prevalence of skin-test positivity among the more elderly
subjects reflected a lifelong reduction in allergic respon-
siveness, rather than a biological effect of ageing.
It is likely that over the next few decades hay fever
prevalence in older age groups will continue to rise, as
more susceptible cohorts replace the generations appar-
ently protected by a less affluent upbringing. Future
trends among younger age groups are more difficult to
predict, particularly as living standards and patterns of
child care continue to change. With greater use of pre-
school creche and nursery facilities in developed coun-
tries, it is possible that the risk of allergic sensitization
may decline. As living standards in eastern and western
Europe converge, regional variations in the prevalence
of hay fever may become less marked among future
generations.
Conclusion
Epidemiological variations in reports of hay fever by
young adults appear to be of broader relevance, point-
ing to the underlying distribution of atopy. They sug-
gest that expression of the atopic phenotype may be
programmed by influences operating very early in-
childhood, perhaps before birth. The nature of the
programming influence and the critical period of devel-
opment during which it operates can only be deter-
mined by further clinical and epidemiological studies.
However, if the working hypothesis of a protective
effect of early infection proves to be correct, the remote
possibility of preventing allergic diseases by artificial
inoculation of an infective agent in early infancy
should not be entirely discounted.
Acknowledgements
I wish to thank the Economic and Social Research
Council Data Archive, University of Essex and the
National Child Development Study User Support
Group, City University, London, UK for their assistance
in accessing the National Child Development Study
dataset.
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