McIntyre Powder and its potential contributions to cardiovascular disease risk: A literature review through the McIntyre Powder historical lens

Abstract

McIntyre Powder (MP) is a fine aluminum powder that was developed to prevent silicosis in gold and uranium mine workers in Ontario, Canada, and was administered to miners there from 1943 to 1979. Mine workers were exposed to high concentrations (35.6 mg/m³ ) of MP for approximately 10 min before every work shift. Contemporary physical and chemical characterizations of this powder have revealed that 12% of the powder is in the ultrafine particle size-range (nanoparticles); and the remaining 88%, in the fine particulate size range (below 2.5 µm in diameter). The confluence of ultrafine particulate (UFP) composition and high airborne concentration of MP would be expected to overwhelm the defense mechanisms of the lung and increase the lung dust burden of the mine worker exposed to respirable dust in the mine. Published studies revealing associations between air pollution particulates and increased risk for cardiovascular disease (CVD) shown a dose-response relationship with ambient PM_2.5 and UFP and suggest that miners exposed to MP may also be at increased risk of CVD. The historical perspective of the use of MP in northern Ontario hard-rock mines and its potential implications for CVD in exposed mine workers are discussed.

Keywords: PM2.5; atherosclerosis; nanoparticles; particle translocation; respiratory inflammation; ultrafine dust exposure.

Figure 1

Microscopy images of fine and ultrafine McIntyre Powder (MP) particles. (A) 1944 electron micrograph of MP particles collected after dispersal in air. Example of particles ~200 nm or below which could not be sufficiently categorized. (B) Transmission electron microscopy image of MP particles in the ultrafine size fraction.

Figure 2

Lung response to inhalation of particulate matter including McIntyre Powder (MP). (A) Particle deposition: Once inhaled, MP makes its way through the respiratory tract to the terminal bronchioles and alveoli, with depth of penetration dependent on particle size. In the process, MP interacts with epithelial cells lining the airways and macrophages in the alveoli (AM), causing activation, and resulting in the release of pro‐inflammatory mediators. (B) Activation of AM by contact with MP: A local inflammatory process is initiated by AM phagocytosis of MP particulates, with release of signaling markers, including chemokines and cytokines. These inflammatory mediators make their way through the alveolar epithelial barrier into the lung interstitium and from there into the circulatory or lymphatic system, resulting in the opportunity for systemic inflammatory effects. (C) Translocation of MP ultrafine particulates (UFPs): UFPs can penetrate the alveolar epithelial barrier directly and travel through the lung interstitium to the capillary where they enter the systemic circulation. Here, acute phase responses include increases in circulating levels of pro‐inflammatory cytokines; increase in thrombogenic activity, with increase in fibrinogen levels and platelet activation and adhesion; and upregulation of endothelin expression. [Color figure can be viewed at wileyonlinelibrary.com]