The environmental predictors of allergic disease,☆☆

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Abstract

The prevalence of allergic diseases has been on the rise for the last 200 years, when hay fever, an easy and obvious-to-recognize illness, was virtually unknown in Europe and North America. Genetic factors are unlikely to explain these rapid increases. Among the potential environmental factors, exposure to ambient air pollution has been intensely debated. Besides passive smoking, which has convincingly been shown to increase the risk for asthma and bronchial hyperresponsiveness among exposed children, the evidence to suggest that outdoor pollution to sulfur dioxide, particulate matter, diesel exhaust, and ozone is causally related with the inception of allergic diseases is poor. Rather, factors associated with the lifestyle of populations or families, such as socioeconomic status, allergen exposure, sibship size, early childhood infections, dietary habits, and growing up in anthroposophic families or a farming environment, may prove to be of greater relevance. The future challenge is to tackle the complex interplay between environmental factors and genetic determinants that will eventually contribute to a better understanding and to better prevention strategies for such multifactorial conditions as asthma and allergies. (J Allergy Clin Immunol 2000;105:9-19.)

Section snippets

AMBIENT AIR POLLUTION

Air pollution is felt by many to be one of the more pressing problems toward the end of this century, posing a potential threat to the health and well-being of entire populations. When an attempt is made to understand the potential adverse effects of air pollution, the distinction between exacerbation of pre-existing disease in already-affected subjects from the potential adverse effects on the inception of newly developing cases of allergic disease seems essential. Although increasing evidence

TRAFFIC EXPOSURE

It has been argued that other types of pollutants that are associated with increasing traffic exposure characteristic of Western cities may be of greater relevance to the inception of allergic diseases than are the traditional type of pollution occurring with burning of coal and other fossil fuels. Diesel exhaust is the single major contributor to particulate matter in most urban areas worldwide, accounting for up to 90% of the total particle mass in some major cities.18 The mass median

OZONE

Single ozone exposure has been shown to evoke cough, breathlessness, and chest pain on inspiration; to result in a restrictive ventilatory defect with decrements in forced vital capacity and FEV1; to induce neutrophilic inflammation of the airway submucosa; and to increase airway reactivity.12 The response to ozone shows large intersubject variability,32, 33 with approximately 10% to 20% of the population sensitive to the development of reductions in lung function after ozone exposure34, 35

ENVIRONMENTAL TOBACCO SMOKE EXPOSURE

There is strong, consistent evidence to suggest that environmental tobacco smoke (ETS) exposure increases the risk of lower respiratory tract illnesses in infancy and childhood.51, 52 A review on adverse health effects of ETS exposure by the US Environmental Protection Agency51 concluded that passive smoke exposure is causally associated with an increased risk of lower respiratory tract infections such as bronchitis and pneumonia, mainly in infants and young children, a small but significant

SOCIOECONOMIC STATUS

High prevalences of childhood asthma and atopic diseases have been found in affluent Western societies. In the developing world a gradient between affluent and poor regions has been seen. In Harare, the capital of Zimbabwe, the prevalence of airway hyperresponsiveness, as assessed by a free-running test, was significantly higher in a wealthier part of the city than in its poorer districts.57 In the United Kingdom high social class was associated with a higher prevalence of atopic eczema.58

NUTRITION

Changes in dietary habits have been implicated as a factor characteristic of societies with increasing affluence, therefore possibly relating to the increase in the prevalence of asthma and atopy seen over the last decades. In some prospective studies breast-feeding has been found to have a transient beneficial effect on the incidence of eczema, food allergy, and early wheezing illnesses in the first 1 to 3 years of life,61, 62 but these findings could not be reproduced by others.63

ALLERGEN EXPOSURE

There is increasing evidence to suggest that the level of allergen exposure is a risk factor for the development of atopic sensitization in children.74, 75, 76 In the German Multicenter Atopy Study76 a large birth cohort following newborn children up to the age of 7 years, house dust mite and cat allergen concentrations in domestic carpet dust were strongly related to the development of atopic sensitization toward that specific allergen in the first 3 years of life. A clear dose-response

FAMILY SIZE

There is increasing consistent evidence that sibship size contributes to the expression of atopy in families. Many authors have shown that the number of siblings is inversely related to the prevalence of self-reported inhalant allergy,82 hay fever,83, 84, 85, 86 atopic eczema,87, 88, 89 skin test reactivity,84, 90, 91, 92, 93 and the presence of specific IgE anitibodies in the serum86, 94, 95 in children, adolescents, and adults. Most reports that were large enough to allow a separate analysis

INFECTIONS

There is still a continuing debate about a potential causal role of virus infections, mainly respiratory syncytial virus (RSV), for the subsequent development of childhood wheezing illness, asthma, and atopy. Two major hypotheses have been proposed to explain the association between respiratory tract infections and subsequent respiratory abnormalities.100 One hypothesis states that viral infections early in life damage the growing lung or alter host immune regulation. The second hypothesis

OUTLOOK

When we speculate about future avenues to reduce our ignorance about the relevant causal factors for the inception of allergic diseases, several issues come to mind. In epidemiology informative study populations must be identified. These may include populations over a broad range of exposure to a suspected risk factor or populations with a significant contrast in the prevalence of allergic diseases. Within the latter group a comparison of environmental influences in ethnically similar groups

CONCLUSIONS

Environmental factors play an important role for the development and manifestation of allergic conditions in genetically predisposed subjects. There is little evidence to suggest that exposure to air pollutants such as sulfur dioxide, particulate matter, traffic exhaust, or ozone is associated with the inception of new cases of atopy or asthma. Rather, lifestyle factors relating to the socioeconomic status of a population or a family, its size, and the number of siblings of a given individual,

References (129)

  • U Wahn et al.

    Indoor allergen exposure is a risk factor for sensitization during the first three years of life

    J Allergy Clin Immunol

    (1997)
  • DP Strachan et al.

    Childhood antecedents of allergic sensitization in young British adults

    J Allergy Clin Immunol

    (1997)
  • PM Matricardi et al.

    Sibship size, birth order, and atopy in 11,371 Italian young men

    J Allergy Clin Immunol

    (1998)
  • RJ Rona et al.

    Family size, atopic disorders in parents, asthma in children, and ethnicity

    J Allergy Clin Immunol

    (1997)
  • D Strachan et al.

    Worldwide variations in prevalence of symptoms of allergic rhinoconjunctivitis in children: the International Study of Asthma and Allergies in Childhood (ISAAC)

    Pediatr Allergy Immunol

    (1997)
  • MB. Emanuel

    Hay fever, a post industrial revolution epidemic: a history of its growth during the 19th century

    Clin Allergy

    (1988)
  • E von Mutius et al.

    Epidemiology of childhood asthma

  • AJ Woolcock et al.

    Evidence for the increase in asthma worldwide

  • International Study of Asthma and Allergies in Childhood Steering Committee

    Worldwide variations in the prevalence of atopic diseases: the International Study of Asthma and Allergies in Childhood (ISAAC)

    Lancet

    (1998)
  • G. Rose

    The strategy of preventive medicine

    (1992)
  • B Burrows et al.

    Association of asthma with serum IgE levels and skin-test reactivity to allergens

    N Engl J Med

    (1989)
  • S. Romagnani

    Human TH1 and TH2 subsets: regulation of differentiation and role in protection and immunopathology

    Int Arch Allergy Immunol

    (1992)
  • E von Mutius et al.

    Familial aggregation of asthma in a South Bavarian population

    Am J Respir Crit Care Med

    (1996)
  • FD Martinez et al.

    Asthma and wheezing in the first six years of life

    N Engl J Med

    (1995)
  • E. von Mutius

    Air pollution and asthma

  • E von Mutius et al.

    Prevalence of asthma and allergic disorders among children in united Germany: a descriptive comparison

    BMJ

    (1992)
  • E von Mutius et al.

    Prevalence of asthma and atopy in two areas of West and East Germany

    Am J Respir Crit Care Med

    (1994)
  • D Nowak et al.

    Prevalence of respiratory symptoms, bronchial hyperresponsiveness and atopy among adults: West and East Germany

    Eur Respir J

    (1996)
  • L Braback et al.

    Atopic sensitization and respiratory symptoms among Polish and swedish school children

    Clin Exp Allergy

    (1994)
  • L Braback et al.

    Risk factors for respiratory symptoms and atopic sensitisation in the Baltic area

    Arch Dis Child

    (1995)
  • S Salvi et al.

    Is diesel a cause for increasing allergies?

    Clin Exp Allergy

    (1999)
  • S Salvi et al.

    Mechanisms of particulate matter toxicity

    Clin Exp Allergy

    (1999)
  • RB Knox et al.

    Major grass pollen allergenn Lol p 1 binds to diesel exhaust particles: implications for asthma and air pollution

    Clin Exp Allergy

    (1997)
  • D Diaz-Sanchez et al.

    Combined diesel exhaust particulate and ragweed allergen challenge markedly enhances human in vivo nasal ragweed-specific IgE and skews cytokine production to a helper cell 2-type pattern

    J Immunol

    (1997)
  • N Terada et al.

    Diesel exhaust particulates enhance eosinophil adhesion to nasal epitheciall cells and cause degranulation

    Int Arch Allergy Immunol

    (1997)
  • D Diaz-Sanchez et al.

    Diesel exhaust particles induce local IgE production in vivo and alter the pattern of IgE messenger RNA isoforms

    J Clin Invest

    (1994)
  • M Wjst et al.

    Road traffic and adverse effects on respiratory health in children

    BMJ

    (1993)
  • H Nitta et al.

    Respiratory health associated with exposure to automobile exhaust, I: results of cross-sectional studies in 1979, 1982, and 1983

    Arch Environ Health

    (1993)
  • A Oosterlee et al.

    Chronic respiratory symptoms in children and adults living along streets with high traffic density

    Occup Environ Med

    (1996)
  • J Edwards et al.

    Hospital admissions for asthma in preschool children: relationship to major roads in Birmingham, United Kingdom

    Arch Environ health

    (1994)
  • G Pershagen et al.

    Air pollution involving nitrogen dioxide exposure and wheezing bronchitis in children

    Int J Epidemiol

    (1995)
  • T Ishizaki et al.

    Studies of prevalence of Japanese cedar pollinosis among the residents in a densely cultivated area

    Ann Allergy

    (1987)
  • TH Hirsch et al.

    Inner city air pollution and respiratory health and atopy in children

    Eur Respir J

    (1999)
  • B Brunekreef et al.

    Air pollution from truck traffic and lung function in children living near motorways

    Epidemiology

    (1997)
  • WS Linn et al.

    A dose-response study of healthy, heavily exercising men exposed to ozone at concentrations near the ambient air quality standard

    Toxicol Ind Health

    (1986)
  • GG Weinmann et al.

    Response to acute ozone exposure in healthy men: results of a screening procedure

    Am J Respir Crit Care Med

    (1995)
  • DH Horstman et al.

    Ozone concentration and pulmonary response relationships for 6.6-hour exposures with five hours of moderate exercise to 0.08, 0.10, and 0.12 ppm

    Am Rev Respir Dis

    (1990)
  • MJ. Hazucha

    Relationship between ozone exposure and pulmonary function changes

    J Appl Physiol

    (1987)
  • WS Linn et al.

    Persistence of adaptation to ozone in volunteers exposed repeatedly for six weeks

    Am Rev Respir Dis

    (1982)
  • BP Farrell et al.

    Adaptation in human subjects to the effects of inhaled ozone after repeated exposure

    Am Rev Respir Dis

    (1979)
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