SYMPOSIUM


Can we be too clean for our own good? The hygiene hypothesis reviewed


BY SHEENAL PATEL, MD, AND REBECCA GRUCHALLA, MD


The hygiene hypothesis began as an attempt to explain the relatively rapid rise in atopic diseases. Strachan’s early hypothesis regarding the role of fam- ily size and exposure to early child- hood infections in the development of atopic diseases has clearly evolved to integrate the possible effects of hy- giene, eradication of parasitic infec- tions, immunizations, improvements in home heating and ventilation, dust mite exposure, breastfeeding duration, diet, parental smoking, pollution, and exposure to pets and farm animals. However, as most of our understand- ing at the current time still comes from observational and epidemiologic stud- ies, further investigations are needed to help uncover which of these genetic and environmental factors are indeed the causes behind the increases in al- lergic rhinitis and asthma.


INTRODUCTION


Since the industrial revolution with the rising prevalence of atopic dis- eases, including allergic rhinitis and asthma, many have sought to explain this trend and the differential in- creases seen in various parts of the world. Although there has been no conclusive evidence identifying any specific causes, numerous epidemio- logic studies have attempted to offer explanations. In 1989, Strachan proposed an ex- planation that has since been famous- ly referred to as the “hygiene hypoth- esis.” He stated, in summary: “These observations ... could be explained if allergic diseases were prevented by infection in early childhood, trans- mitted by unhygienic contact with


54 TEXAS MEDICINE February 2017


older siblings, or acquired prenatally … Over the past century, declining fam- ily size, improved household ameni- ties, and higher standards of personal cleanliness have reduced opportuni- ties for cross-infection in young fami- lies. This may have resulted in more widespread clinical expression of atopic disease.”1


We will review the


evolving body of evidence attempting to explain the rise in allergic diseases and theories behind the hygiene hy- pothesis.


HISTORICAL BACKGROUND


The earliest descriptions of seasonal allergies can be traced back to the 1500s.2


In 1819, John Bostock, MD,


wrote of his own illness and described seasonal symptoms of watery eyes, sneezing, and rhinorrhea. Over the next nine years, he discovered similar symptoms affecting a group of 27 pa- tients.3,4


In 1873, Charles Blackley was


the first to say that pollen grains were the cause of the above symptoms. He also observed agricultural laborers were more likely to be exposed to pol- len but seemed to have fewer cases, and hay fever (allergic rhinitis) also appeared to be more common in the educated compared with the illiter- ate. Interestingly, he predicted that


“as civilization and education advance, the disorder will become more com- mon than it is at the present time.”5 In the 20th century, the prevalence


of allergic rhinitis rose dramatically. In England and Wales, the prevalence of allergic rhinitis was 5 percent in the 1950s but had risen to 20 percent in the 1980s.6


Asthma also became more prevalent, with the earliest re-


ports documenting this increase be- ginning in the 1960s.7,8


However, it


is important to note that this rise in allergic rhinitis appeared to affect certain parts of the world more than others, including rising prevalence in affluent populations, industrialized countries, and in urban areas com- pared with rural areas.9,10 Based on observations of differen-


tial rates in the rise of atopic disease around the world, investigators have sought to seek explanations by exam- ining genetic and environmental fac- tors that have included effects of hy- giene, family size, early life infections, eradication of parasitic infections, im- munizations, improvements in home heating and ventilation, dust mite ex- posure, breastfeeding duration, diet, parental smoking, pollution, and ex- posure to pets and farm animals.11


IMMUNOLOGIC ASPECTS OF THE HYGIENE HYPOTHESIS


One possible theory about the immu- nologic basis of the hygiene hypoth- esis is that both genetic factors and environmental factors may influence immune system development in a way that increases the risk of atopic disease. Different exposures may lead to the production or absence of cyto- kines that may influence the develop- ment of T-helper cells into a pheno- type consistent with tolerance versus a phenotype consistent with atopic disease, including allergic rhinitis and asthma. (See Figure 1.) T-helper lym- phocytes develop from a precursor, Th0 cells, and further differentiate into two subtypes, Th1 and Th2 lym- phocytes. Th1 responses are thought to be protective against a wide variety of microbes. Th2 responses are im- portant in activation, differentiation, and survival of eosinophils. Also, they are important in promoting antibody production by B cells (including IgE) and in growth of mast cells and baso- phils, which are cells involved in the allergic response.12 The hygiene hypothesis suggests that, in the absence of childhood in-


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