Objective. To evaluate whether seasonal early environmental exposures might influence later development of autoimmune disease, by assessing distributions of birth dates in groups of patients with idiopathic inflammatory myopathies (IIMs).Methods. We assessed birth patterns in groups of patients with juvenile-onset IIM (n ‫؍‬ 307) and controls (n ‫؍‬ 3,942) who were born between 1970 and 1999, and in groups of patients with adult-onset IIM (n ‫؍‬ 668) and controls (n ‫؍‬ 6,991) who were born between 1903 and 1982. Birth dates were analyzed as circular data. Seasonal clustering was assessed by the Rayleigh test, and differences between groups by a rank-based uniform scores test.Results. The overall birth distributions among patients with juvenile IIM and among patients with adult IIM did not differ significantly from those among juvenile and adult controls, respectively. Some subgroups of patients with juvenile IIM had seasonal birth distributions. Hispanic patients with juvenile-onset IIM had a seasonal birth pattern (mean birth date October 16) significantly different from that of Hispanic controls (P ‫؍‬ 0.002), who had a uniform birth distribution, and from that of non-Hispanic patients with juvenile-onset IIM (P < 0.001), who had a mean birth date of May 2. Juvenile dermatomyositis patients with p155 autoantibody had a birth distribution that differed significantly from that of p155 antibody-negative juvenile dermatomyositis patients (P ‫؍‬ 0.003). Juvenile IIM patients with the HLA risk factor allele DRB1*0301 had a birth distribution significantly different from those without the allele (P ‫؍‬ 0.021). Similar results were observed for juvenile and adult IIM patients with the linked allele DQA1*0501, versus juvenile and adult IIM patients without DQA1*0501, respectively. No significant patterns in birth season were found in other subgroups.Conclusion. Birth distributions appear to have stronger seasonality in juvenile than in adult IIM subgroups, suggesting greater influence of perinatal exposures on childhood-onset illness. Seasonal early-life exposures may influence the onset of some autoimmune diseases later in life.

ObjectiveIn this review we highlight the need to expand the scope of environmental health research, which now focuses largely on the study of toxicants, to incorporate infectious agents. We provide evidence that environmental health research would be strengthened through finding common ground with the tools and approaches of infectious disease research.Data sources and extractionWe conducted a literature review for examples of interactions between toxic agents and infectious diseases, as well as the role of these interactions as risk factors in classic “environmental” diseases. We investigated existing funding sources and research mandates in the United States from the National Science Foundation and the National Institutes of Health, particularly the National Institute of Environmental Health Sciences.Data synthesisWe adapted the toxicological paradigm to guide reintegration of infectious disease into environmental health research and to identify common ground between these two fields as well as opportunities for improving public health through interdisciplinary research.ConclusionsEnvironmental health encompasses complex disease processes, many of which involve interactions among multiple risk factors, including toxicant exposures, pathogens, and susceptibility. Funding and program mandates for environmental health studies should be expanded to include pathogens in order to capture the true scope of these overlapping risks, thus creating more effective research investments with greater relevance to the complexity of real-world exposures and multifactorial health outcomes. We propose a new model that integrates the toxicology and infectious disease paradigms to facilitate improved collaboration and communication by providing a framework for interdisciplinary research. Pathogens should be part of environmental health research planning and funding allocation, as well as applications such as surveillance and policy development.

The occupations involved in food animal production have long been recognized to carry significant health risks for workers, with special attention to injuries. However, risk of pathogen exposure in these occupations has been less extensively considered. Pathogens are a food safety issue and are known to be present throughout the food animal production chain. Workers employed at farms and slaughterhouses are at risk of pathogen exposure and bacterial infections. The industrialization of animal farming and the use of antimicrobials in animal feed to promote growth have increased the development of antimicrobial resistance. The changed nature of these pathogens exposes workers in this industry to new strains, thus modifying the risks and health consequences for these workers. These risks are not yet recognized by any work-related health and safety agency in the world.

Objective Infection with Campylobacter jejuni, a bacterium carried by poultry and livestock, is the most frequently identified antecedent to the autoimmune neurologic condition Guillain-Barré Syndrome. We used Agricultural Health Study data to assess whether cattle farming was associated with prevalence of neurologic symptoms. Methods Prevalence of self-reported symptoms in cattle farmers (n = 8878) was compared with farmers who did not work with animals (n = 7462), using multivariate regression. Results Prevalence of numbness and weakness were increased for beef and dairy farmers compared with the reference group (P < 0.0001). Of cattle farmers, 48% did not report raising other animal species, and prevalence of numbness and weakness were also increased in this subgroup compared with the reference group (P < 0.02). Conclusions Occupational exposure to cattle was associated with increased prevalence of self-reported symptoms associated with peripheral neuropathy.

IntroductionFoodborne Campylobacter jejuni infection has been associated with an increased risk of autoimmune peripheral neuropathy, but risks of occupational exposure to C. jejuni have received less attention. This study compared anti-C. jejuni IgA, IgG, and IgM antibody levels, as well as the likelihood of testing positive for any of five anti-ganglioside autoantibodies, between animal farmers and non-farmers. Anti-C. jejuni antibody levels were also compared between farmers with different animal herd or flock sizes. The relationship between anti-C. jejuni antibody levels and detection of anti-ganglioside autoantibodies was also assessed.MethodsSerum samples from 129 Agricultural Health Study swine farmers (some of whom also worked with other animals) and 46 non-farmers, all from Iowa, were analyzed for anti-C. jejuni antibodies and anti-ganglioside autoantibodies using ELISA. Information on animal exposures was assessed using questionnaire data. Anti-C. jejuni antibody levels were compared using Mann-Whitney tests and linear regression on log-transformed outcomes. Fisher’s Exact Tests and logistic regression were used to compare likelihood of positivity for anti-ganglioside autoantibodies.ResultsFarmers had significantly higher levels of anti-C. jejuni IgA (p < 0.0001) and IgG (p = 0.02) antibodies compared to non-farmers. There was no consistent pattern of anti-C. jejuni antibody levels based on animal herd or flock size. A higher percentage of farmers (21%) tested positive for anti-ganglioside autoantibodies compared to non-farmers (9%), but this difference was not statistically significant (p = 0.11). There was no significant association between anti-C. jejuni antibody levels and anti-ganglioside autoantibodies.ConclusionsThe findings provide evidence that farmers who work with animals may be at increased risk of exposure to C. jejuni. Future research should include longitudinal studies of exposures and outcomes, as well as studies of interventions to reduce exposure. Policies to reduce occupational exposure to C. jejuni should be considered.