Abstract
We aimed to examine the association between parental occupational social contact and hygiene factors on type 1 diabetes (T1D) risk and possible mediation of these effects through child enteroviral infection. We interviewed 333 incident T1D cases and 660 controls from 2008–2011 in Melbourne, Australia. Enteroviral indices (ribonucleic acid by reverse transcription polymerase chain reaction and Coxsackie B virus antibody levels) in peripheral blood were measured in nested case control samples. Parent occupational social contact was assessed by the number of well or sick children, adults or animals contacted daily through work. Higher parental occupational social contact was strongly associated with reduced T1D risk with evidence of dose response (contact with the well or sick score, Adjusted odds ratio (AOR) per category: 0.73 (95% Confidence Interval (CI): 0.66, 0.81); P<0.001 or AOR 0.63 (95% CI: 0.53, 0.75); P<0.001) respectively). Nine of the ten parental social contact indices, were significant mediated through one or more enteroviral indices. The strength of association between enterovirus presence and T1D onset increased with child age (1.2 fold increase per year; P = 0.05). Lower child hand hygiene enhanced the adverse effect of low parental occupational contact with the sick; Synergy Index 5.16 (95% CI: 3.61, 7.36). The interaction between hand washing and parental occupational contact is more consistent with protection against parental enteroviral shedding than the sharing of a protective infectious agent or microbiome.
Highlights
The incidence of paediatric type 1 diabetes mellitus (T1D) has increased over time [1]
Meta-analysis indicates the presence of enterovirus (EV) by polymerase chain reaction (PCR) in peripheral blood is associated with a summary odds ratio of 9.8 (95% Confidence Interval (CI): 5.5, 17.4) for clinical TID onset [3]
EV is markedly more commonly detected among the peripheral blood of family members (63% of parents; 60% of siblings) of incident T1D cases compared to only 3% and 0% of non-family child and adult controls respectively [4]
Summary
The incidence of paediatric type 1 diabetes mellitus (T1D) has increased over time [1]. This autoimmune disease has a first stage of preclinical autoimmunity and a second stage of clinical onset [2]. Meta-analysis indicates the presence of enterovirus (EV) by polymerase chain reaction (PCR) in peripheral blood is associated with a summary odds ratio of 9.8 (95% Confidence Interval (CI): 5.5, 17.4) for clinical TID onset [3]. EV genome can be eliminated relatively quickly from peripheral blood [5]. EV genome may be present in host gut mucosa and pancreatic islets for many years, leading to persistent disease with viral shedding [6] [7]. Prolonged EV elimination in faeces has been postulated to be responsible for T1D clustering among sibsets [4]
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