Chiara Frazzoli and Alberto Mantovani
Attention is considerably rising on direct/indirect interactions between infective and toxicological risk factors in the susceptibility to infectious agents and/or the clinical severity of infectious diseases. In fact, beyond the infectious agent itself, other factors are required to support the onset of an infectious disease, and/or to facilitate its progression or the effectiveness of immune responses. Several endocrine disrupters, mainly dioxin-like compounds, have a recognized ability to alter immune response, e.g. by indirectly altering the response to viral agents, such as influenza viruses (http://www.iss.it/inte/aspe/cont).
Environmentally-relevant exposure levels of widespread contaminants are suspected to jeopardize the effectiveness of antiviral defences. For instance, inorganic arsenic, which is a toxic trace element identified as endocrine disrupter, affects the immune response to infection from the swine flu virus H1N1 in the mouse (http://www.niehs.nih.gov/news/newsletter/2009/june/extramural-papers). Prospective epidemiological studies show a more than multiplicative interaction between infection with hepatitis B virusesand dietary exposure to aflatoxins, e.g. aflatoxin B1, in terms of hepatocellular carcinoma risk (Wild CP, Montesano R, 2009, A model of interaction: Aflatoxins and hepatitis viruses in liver cancer aetiology and prevention. Cancer Lett [Epub ahead of print]). Thus, primary and secondary prevention strategies against food and environmental contaminants are warranted also to support enhanced basal immunity andprevention of infectious diseases.