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• W1993118512 abstract "The Naming of Cats is a difficult matter, It isn't just one of your holiday games; You may think at first I'm as mad as a hatter When I tell you, a cat must have three different names [1] The topic of associations between pet exposure and asthma or sensitization is profoundly confusing, and many conflicting and intriguing findings have been published recently. A review of the literature in the late 1990s suggested an increased risk of sensitization in childhood after early pet exposure [2], whereas another found little consistent association between allergen exposure and asthma prevalence [3] and a meta-analysis concluded that pet exposure increased the risk of wheezing in older children [4]. In fact, studies published in the last two years can be used to support just about any viewpoint on the issue: cat exposure increases [5] or decreases [6], and dog exposure decreases [7] or has no effect [8] on the risk of sensitization; asthma is negatively [8] or positively [9] associated with dog exposure, and cat exposure can increase [10] or decrease [6] the risk of asthma, especially in children with allergic heredity. The complexity of the issue of pet exposure may partly be due to different study designs (cohort, case–control, cross-sectional), definitions of exposure (early or current pet ownership or allergen levels), or outcome (sensitization, wheezing, or asthma), as well as selection mechanisms for pet contact. Furthermore, cat and dog allergen is ubiquitous in society and may affect sensitization in predisposed individuals regardless of pet ownership [11, 12]. House dust mite exposure and subsequent sensitization or asthma is slightly less controversial, with a dose–response relation between exposure and sensitization [13] – but even if mite avoidance appears beneficial in already sensitized children, its role in primary causation of asthma is unclear [14, 15]. In an attempt to disentangle the causal relationship between allergen levels, sensitization, and asthma, a longitudinal cohort study where an exposed and an unexposed group are followed prospectively from birth must be considered the best choice of study design. To compare groups with high and low levels of exposure, one must obviously assess allergen exposure accurately. However, this is not an easy task. Equating exposure with ownership of cat or dog may introduce selection bias into a study, as pet ownership may vary with family history of allergic diseases and socio-economy [16, 17]. Determining exposure by measuring allergen levels may be misleading, since cat and dog allergens are largely airborne and the allergen levels in air do not always correlate with those found in dust [18]. Moreover, cat and dog allergens are found in public buildings and accumulation of cat allergen in cat-free environments has been shown to correlate with the number of visitors who have a cat at home or are in regular contact with a cat [5, 19, 20]. All in all, it is virtually impossible to assess personal exposure to cat and dog over time. However, it has been suggested that exposure before birth or in early childhood is crucial in the process of sensitization [21]. Thus, measuring allergen levels longitudinally starting early in life may be the best way to assess personal exposure and its relation to subsequent asthma and allergic disease. This is also a point in time when the risk of information bias and misclassification of exposure and disease is smallest, as the parents have not yet taken any steps to influence exposure subject to their child's disease. Finally, this is also the best time in life to introduce primary prevention strategies aimed at reducing the risk of allergic diseases and asthma. The study by Simpson et al. [22] in this issue of Clinical and Experimental Allergy was designed to investigate how environmental control measures affect levels of mite (Der p 1), cat (Fel d 1) and dog (Can f 1) allergen over a 3.5-year period. It is part of the National Asthma Campaign Manchester Asthma and Allergy Study (NACMAAS), which aims to explore the effect of primary prevention on asthma and allergic diseases early in life. Expectant parents with high risk of allergic diseases (positive skin prick test, no cat or dog at home) were prenatally randomized into a stringent environmental manipulation group (active) and a control group. Prenatal interventions in the active group involved allergen-impermeable bedding in the mother's bed, vinyl floor and no carpets in the baby's room, new cot, allergen-proof mattress and soft toys for the baby, and allergen-impermeable covers when the child later moved into a bed. In addition, the parents were provided with a high-filtration vacuum cleaner, asked to hot wash the bedding, and to damp dust the allergen-impermeable covers once weekly. Considering these strict regimens at a time of life when most families are engaged in a multitude of tasks, it is impressive to note that three years on, more than one-third of the active group were still fully compliant with every aspect of the environmental control measures. Fifty-eight percent of the active families remained in compliance with environmental control in the child's bedroom. Dust samples collected from the child's floor and bed just after birth and when the child was three years old showed that not only were levels of each allergen significantly lower in the active group than in the control group, but the median allergen levels also remained low. This implies that the airborne levels of cat and dog allergen were also low, and that the children in the active group were exposed to fairly low allergen levels during the hours they spent in bed or in their own room. However – and this the authors could not explain – allergen levels on the living room floor did not differ between the two groups at any time point; mite allergens increased over time in both groups, whereas allergens from cat and dog decreased. Since many children spend much of their first years lying, sitting, or crawling on living room floors, this an important exposure site. The similar allergen levels in the active and control group may reflect that many children spend a fair amount of time outside their home, be it in playgroups, in shops, at friends' homes, etc, where they are exposed to allergen levels far above those found in most pet-free homes. These allergens are readily transferred to the homes via clothes, etc [11]. Even if the Simpson study was originally designed to examine the effects of primary prevention on allergic diseases and asthma, it has a suitable design to examine causal relationships between early exposure and later disease. As we cannot possibly randomize children to cat or dog ownership at birth, this is the most feasible alternative. The study has the character of a randomized control trial, the gold standard in epidemiological research. A drawback, however, is that it might be difficult to draw conclusions about what allergen causes what outcome, as all three allergens are lower in the intervention group. The dogma that exposure to pet allergen causes senzitisation, and continued exposure leads to asthma, is being increasingly questioned. Figure 1 attempts to sort out the relations. A close association between sensitization to indoor allergens and asthma (Fig. 1a) has been confirmed in many population-based studies, whereas the causal relationship between early cat or dog allergen exposure and subsequent sensitization (Fig. 1b) or asthma (Fig. 1c) is controversial. Concurrently, from the clinical perspective it is evident that direct or even indirect exposure to cat or dog triggers symptoms in already sensitized individuals with asthma (Fig. 1d) [10, 23, 24]. The strong association between sensitization and asthma in most population-based studies (a) has led to a belief that exposure to pet allergen causes sensitization, and that continued exposure leads to asthma. However, there is no consistent causal relationship between early exposure to pet allergen and sensitization (b) or asthma (c). This apparent lack of a causal relationship might be due to different study designs, definition of exposure and outcome, and confounders – or perhaps there is no causal relationship. What we do know is that pet allergen exposure triggers symptoms in already sensitized children with asthma (d). Reprinted with permission from Elsevier (modified from Grad et al. Lancet 2000; 356:1369–70). The case for a causal relationship between allergen levels, sensitization, and asthma would best be supported by evidence for a dose–response relationship between exposure and symptoms. In the German Multicenter Allergy Study (MAS), a dose–response relationship was reported between levels of both cat and dust mite allergen and subsequent sensitization at three years of age, whereas some years later no relation between early exposure to indoor allergens and wheezing was seen [13, 14]. In contrast, it has been suggested that children who are exposed to high concentrations of cat allergen make a modified Th2 response characterized by the presence of IgG4 antibody to cat proteins without IgE response, whereas moderate exposure should be associated with increased risks of sensitization [25]. This bell-shaped dose–response curve for sensitization could be seen as a form of tolerance. There is also coherent evidence that exposure to a farming environment may protect against atopy and allergic diseases. The protection is not limited to a specific allergen, but rather involves down-regulation of immune responses in individuals exposed to endotoxin [26-28]. A potential causal relationship may easily be distorted, however, since pet allergens are ubiquitous. By identifying non-pet-owning children who report close contacts with cat or dog outside the home, it is possible to distinguish between ‘no’ and ‘any’ exposure, and thus avoid including exposed children in the reference group category and diluting associations between allergen exposure and health effects. This was carried out in the BAMSE birth cohort study including 3596 children of whom 2573 consented to blood samples being drawn at four years of age. Early cat exposure, indirect or direct, turned out to be associated with an increased risk of cat sensitization but not of asthma, whereas there was a decreased risk of asthma and sensitization (to pollen allergens) among the children exposed to dog [5]. Likewise, the Simpson study has good control over its exposure data, and may well provide information on true causal relationships. However, it has been implied that risks of pet ownership can only be studied among individuals without allergic heredity, since those with heredity will develop allergic disease anyway. In the BAMSE cohort study, we found that families with heredity for allergic disease not only kept cats less frequently than others, but also that their indirect cat exposure, indicated by measurable levels of cat allergen in homes without cats, was lower [17]. Those with heredity for allergic disease who avoid pets may nevertheless be indirectly exposed to allergen levels sufficiently high to induce sensitization, with a risk of distorted results even in prospective studies. This may be another reason why dose–response relationships vary in different studies. In causal relationships, temporality is vital: exposure must precede outcome. A prospective study design and adequately posed questions make it possible to assess temporality, whereas a cross-sectional study can only examine the presence or absence of exposure and disease at a certain time point. Moreover, it is important to control for bias (information and selection bias) and confounders (a factor associated with both exposure and outcome, but not directly involved in the causal pathways, e.g. heredity, smoking, breast feeding, socio-economy, etc) [29]. The advantage of a randomized controlled trial is that confounders are equally distributed in the exposed and unexposed groups, reducing the likelihood of bias. There is no gold standard for defining asthma in childhood, which reflects the varying expressions of symptoms, multiple aetiological factors, and heterogeneous response to treatment. In epidemiological studies, wheezing or doctor's diagnosis of asthma are the symptoms most frequently enquired about in questionnaires, although the criteria to define asthma varies between different research groups – in itself a possible reason for differing study results [30]. Sensitization is an easier marker, as it can be measured objectively, but nevertheless, different research groups measure it in different ways: total-IgE, Phadiatop® (Pharmacia CAP SystemTM, Uppsala, Sweden), allergen-specific IgE or skin prick test. The ideal outcome to study a possible causal relationship between allergen exposure and asthma is obviously allergic asthma, where wheezing is combined with sensitization. However, many young children have not yet sero-converted and the samples often turn out to be too small to reach sufficient statistical power. For example, in the BAMSE study only one-third of the 197 children with asthma were sensitized at 4 years. The 1-year follow-up of the NACMAAS group reported that the stringent environmental control measures reduced certain respiratory symptoms among the high-risk infants. In another group of high-risk children with a cat at home, specific cat sensitization appeared slightly more common than in the other groups [31]. Still, the children were very young at the time, and it is with great interest that we now look forward to the report on health effects at three years of age. Ideally, those analyses should report clear and explicable results with well-defined exposures and outcomes, confounding factors, and groups of heredity, with the ultimate aim to suggest primary prevention advice for parents who wish to prevent asthma and allergies in their newborns. So are the causal relationships a thing ‘that no human research can discover’? Maybe there is reason for optimism. Firstly, the NACMAAS study may some day show whether allergen exposure is associated with an increased or decreased risk of sensitization and, more importantly, wheezing and asthma. Secondly, it will provide a possibility to compare health effects in high- and low-risk groups, and also high-risk groups with and without pets. Thirdly, it would be most interesting to see if there is any difference between the health effects on children exposed early in life to cat and to dog allergens. In conclusion, it is apparently possible to decrease levels of allergen in bedrooms by environmental control. It now remains to be seen how this can affect disease in young children. In time, perhaps the role of cat and dog allergens in the development of sensitization and asthma will no longer be as inscrutable as the ‘effanineffable…singular Name’ of T.S. Eliot's cat [1]." @default.
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• W1993118512 title "Cat and dog allergens - can intervention studies solve their inscrutable riddle?" @default.
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