Mercury (Hg) has been identified as one of the most toxic nonradioactive materials known to man. Although mercury is a naturally occurring element, anthropogenic mercury is now a major worldwide concern and is an international priority toxic pollutant. It also comprises one of the primary constituents of dental amalgam fillings. Even though dental mercury amalgams have been used for almost two centuries, its safety has never been tested or proven in the United States by any regulatory agency. There has been an ongoing debate regarding the safety of its use since 1845, and many studies conclude that its use exposes patients to troublesome toxicity. In this review, we present in an objective way the danger of dental amalgam to human health based on current knowledge. This dilemma is addressed in terms of an integrated toxicological approach by focusing on four mayor issues to show how these interrelate to create the whole picture: (1) the irrefutable constant release of mercury vapor from dental amalgams which is responsible for individual chronic exposure, (2) the evidence of organic mercury formation from dental amalgam in the oral cavity, (3) the effect of mercury exposure on gene regulation in human cells which supports the intrinsic genetic susceptibility to toxicant and, finally, (4) the availability of recent epidemiological data supporting the link of dental amalgams to diseases such as Alzheimer’s and Parkinson.

African Dust Events (ADE) are a seasonal phenomenon that has been suggested to exacerbate respiratory and proinflammatory diseases in Puerto Rico (PR). Increases in PM₁₀ concentration and the effects of biological endotoxins (ENX) are critical factors to consider during these storms. ENX promote proinflammatory responses in lungs of susceptible individuals through activation of the Toll‐like receptors (TLR2/4) signaling pathways. The objective of the study was to evaluate the toxicological and proinflammatory responses stimulated by ADE PM₁₀ ENX reaching PR using human bronchial epithelial cells. PM₁₀ organic extracts from a rural and urban site in PR (March 2004) were obtained from ADE and non‐ADE and compared. A retrospective data analysis (PM₁₀ concentration, aerosol images, and pediatric asthma claims) was performed from 2000 to 2012 with particular emphasis in 2004 to classify PM samples. Urban extracts were highly toxic, proinflammatory (IL‐6/IL‐8 secretion), and induced higher TLR4 expression and NF‐κB activation compared to rural extracts. ENX were found to contribute to cytotoxicity and inflammatory responses provoked by urban ADE PM₁₀ exposure suggesting a synergistic potency of local and natural ENX incoming from ADE. The contribution of ADE PM₁₀ ENX is valuable in order to understand interactions and action mechanisms of airborne pollutants as asthma triggers in PR.

Fine particles were collected in three indoor environments and an outdoor reference site. Samples were acid and aqueous extracted for metal analyses and cytokine expression study using a BEAS-2B line. Results revealed that the average PM_2.5 concentration indoors was 5.8 μg/m³ while outside, it was 9.4 μg/m³. The airborne metal concentrations in indoor air ranged from 0.01 ng/m³ (Cd) to 620 ng/m³ (Al). All metals analyzed were higher indoors when compared to outdoor (I/O ratio) indicating a contribution from the workplace. Some metals were more efficiently extracted (e.g., Ni, V, As) in the aqueous phase than others (e.g., Fe and Al). Toxicological assays showed that the aqueous extracts at 20% induced IL-6 and subsequently inhibited it at a higher concentration (50%); both IL-8 and MCP-1 were inhibited at 20 and 50%. As, Ni and V concentrations seem to be the most important metals associated with the cytokine induction/inhibition response probably due to the higher bioavailability.