St John's Institute of Dermatology, King's College, St Thomas' Hospital, London, SE1 7EH, U.K.
Br J Dermatol. 2014 Jan;170(1):45-51. doi: 10.1111/bjd.12602.
One explanation for the large increase in the prevalence of atopic disease in developed countries during the last 50 years is the 'hygiene hypothesis'. This proposes that a reduced exposure to pathogenic microorganisms at a key period(s) during development results in the maintenance or acquisition of an atopic phenotype. Alternatively, or additionally, we have postulated that increased exposure to chemicals generally, and to irritant/haptenic chemicals in particular, during critical windows of maternal pregnancy/early life have also contributed to changes in the prevalence of atopic disease. Having previously reviewed the potential roles of oral and cutaneous exposure to chemicals on the subsequent diagnosis of atopic disease, we here consider possible evidence of a role for exposure to airborne chemicals as a contributory factor in acquired susceptibility to atopic allergy. After controlling for known confounders, five specific maternal occupations during pregnancy have been implicated as being associated with subsequent atopic disease in the offspring. Each of these occupations is characterized by high and persistent exposure to airborne chemicals. High-level exposure to volatile organic compounds in the domestic environment, either during pregnancy or in early life, is also associated with development of childhood atopic disease. Similarly, sustained exposure to airborne chlorinated chemicals from swimming pools during childhood has been associated with the development of atopic allergy. A possible immunological basis for these associations is that exposure to certain airborne chemicals, even at low levels, can result in the delivery of 'danger' signals that, in turn, bias the immune response towards the selective induction or maintenance of preferential T helper 2-type immune responses consistent with the acquisition of allergic sensitization.
一种解释是，在过去的 50 年里，在发达国家，特应性疾病的流行率大幅上升，这是“卫生假说”。该假说提出，在发育的关键时期（多个时期）减少对致病微生物的接触，会导致特应性表型的维持或获得。或者，或者，我们还假设，在母亲怀孕/生命早期的关键时期，接触一般化学物质，尤其是刺激性/半抗原性化学物质的增加，也导致了特应性疾病流行率的变化。我们之前回顾了口腔和皮肤接触化学物质对随后特应性疾病诊断的潜在作用，在这里我们考虑了暴露于空气中的化学物质可能作为获得特应性过敏易感性的一个因素的可能证据。在控制了已知的混杂因素后，有五项特定的母亲妊娠期间的职业与后代随后的特应性疾病有关。这些职业中的每一种都具有高且持续的空气传播化学物质暴露的特点。怀孕期间或婴儿早期在家庭环境中高水平接触挥发性有机化合物也与儿童特应性疾病的发展有关。同样，儿童时期持续暴露于游泳池中的含氯空气化学物质也与特应性过敏的发展有关。这些关联的可能免疫学基础是，即使接触某些空气传播化学物质（即使水平较低）也可能导致传递“危险”信号，进而使免疫反应偏向于选择性诱导或维持有利于特应性致敏获得的优先辅助性 T 细胞 2 型免疫反应。
