Airborne particulate matter and mitochondrial damage: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Oxidative stress generation is a primary mechanism mediating the effects of Particulate Matter (PM) on human health. Although mitochondria are both the major intracellular source and target of oxidative stress, the effect of PM on mitochondria has never been evaluated in exposed individuals.</p> <p>Methods</p> <p>In 63 male healthy steel workers from Brescia, Italy, studied between April and May 2006, we evaluated whether exposure to PM was associated with increased mitochondrial DNA copy number (MtDNAcn), an established marker of mitochondria damage and malfunctioning. Relative MtDNAcn (RMtDNAcn) was determined by real-time PCR in blood DNA obtained on the 1^st(time 1) and 4^thday (time 2) of the same work week. Individual exposures to PM₁₀, PM₁, coarse particles (PM₁₀-PM₁) and airborne metal components of PM₁₀(chromium, lead, arsenic, nickel, manganese) were estimated based on measurements in the 11 work areas and time spent by the study subjects in each area.</p> <p>Results</p> <p>RMtDNAcn was higher on the 4^thday (mean = 1.31; 95%CI = 1.22 to 1.40) than on the 1^stday of the work week (mean = 1.09; 95%CI = 1.00 to 1.17). PM exposure was positively associated with RMtDNAcn on either the 4^th(PM₁₀: β = 0.06, 95%CI = -0.06 to 0.17; PM₁: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the 1^stday (PM₁₀: β = 0.18, 95%CI = 0.09 to 0.26; PM₁: β = 0.23, 95%CI = 0.11 to 0.35; coarse: β = 0.17, 95%CI = 0.09 to 0.26). Metal concentrations were not associated with RMtDNAcn.</p> <p>Conclusions</p> <p>PM exposure is associated with damaged mitochondria, as reflected in increased MtDNAcn. Damaged mitochondria may intensify oxidative-stress production and effects.</p

Is exposure to formaldehyde in air causally associated with leukemia?—A hypothesis-based weight-of-evidence analysis

Recent scientific debate has focused on the potential for inhaled formaldehyde to cause lymphohematopoietic cancers, particularly leukemias, in humans. The concern stems from certain epidemiology studies reporting an association, although particulars of endpoints and dosimetry are inconsistent across studies and several other studies show no such effects. Animal studies generally report neither hematotoxicity nor leukemia associated with formaldehyde inhalation, and hematotoxicity studies in humans are inconsistent. Formaldehyde's reactivity has been thought to preclude systemic exposure following inhalation, and its apparent inability to reach and affect the target tissues attacked by known leukemogens has, heretofore, led to skepticism regarding its potential to cause human lymphohematopoietic cancers. Recently, however, potential modes of action for formaldehyde leukemogenesis have been hypothesized, and it has been suggested that formaldehyde be identified as a known human leukemogen. In this article, we apply our hypothesis-based weight-of-evidence (HBWoE) approach to evaluate the large body of evidence regarding formaldehyde and leukemogenesis, attending to how human, animal, and mode-of-action results inform one another. We trace the logic of inference within and across all studies, and articulate how one could account for the suite of available observations under the various proposed hypotheses. Upon comparison of alternative proposals regarding what causal processes may have led to the array of observations as we see them, we conclude that the case fora causal association is weak and strains biological plausibility. Instead, apparent association between formaldehyde inhalation and leukemia in some human studies is better interpreted as due to chance or confounding

Sinonasal cancer

International audienceSinonasal cancer, the cancer of the nose and paranasal cavities, is rare with an incidence below 2/100,000 person-year; the incidence is lowest among women and with distinct differences between countries. These variations in incidence are mostly explained by differences in occupational exposure, in particular exposure to wood dust, which is by far the major risk factor. This chapter gives an overview of epidemiological studies on sinonasal cancer dealing with epidemiological evidence for various occupational risk factors, exposure characteristics, tumor pathology, findings from experimental and human studies contributing to understanding of cancer mechanisms, and, finally, with molecular alterations observed in sinonasal cancer tissue available as potential molecular markers. The main studies and their findings as well as the principal pathological features of sinonasal tumors are summarized in tables and exemplified in illustrations. © Springer Nature Switzerland AG 2020