The mechanisms of action of many environmental agents commonly involve oxidative stress resulting from mitochondrial dysfunction. Zinc is a common environmental contaminant that has been implicated in a variety of oxidant-dependent toxicological responses, although Zn2+ does not directly generate reactive oxygen species. Cheng et al. report on an integrated imaging approach that usd the hydrogen peroxide (H2O2)-specific fluorophore PG1, the mitochondrial membrane potential sensor JC-1, and the mitochondrial redox potential sensor MTroGFP1 in living cells to characterize the role of oxidative stress in zinc-induced toxicity. The authors report that, in A431 skin carcinoma cells, zinc increased H2O2 production, which could be significantly inhibited with the mitochondrial inhibitor carbonyl cyanide 3-chlorophenyl hydrazone. Zinc also caused a loss of mitochondrial membrane potential, which further implicates the mitochondria as the source of the increased H2O2. The authors also reported that zinc induced a rapid loss of reducing redox potential in A431 cell mitochondria and caused rapid swelling of mitochondria isolated from mouse hearts. These findings show a disruption of mitochondrial integrity and H2O2 formation and a shift toward positive redox potential in cells exposed to zinc, and demonstrate the utility of real-time, live-cell imaging to the study of the role of oxidative stress in toxicological responses.
Related News Article: Mitochondrial Mix: Combined Approach to Visualizing Oxidative Stress in Real Time
About half of the world’s population is exposed to smoke from burning biomass fuels at home, and the health burdens of ths exposures have been well described. Burning unprocessed biological material such as wood and dried animal dung may also produce high concentrations of endotoxin, but there is limited information on endotoxin levels in these homes. Semple et al. sampled air in homes burning wood or dried animal dung in 31 homes in Nepal, and wood, charcoal, or crop residues in 38 homes in Malawi. Averaged over 24 hr in Malawian homes, median concentrations of total inhalable endotoxin were 24 endotoxin units (EU)/m3 in charcoal-burning homes and 40 EU/m3 in wood-burning homes. Short-cooking-time samples collected in Nepal produced median values of 43 EU/m3 in wood-burning homes and 365 EU/m3 in dung-burning homes. These results suggest increasing endotoxin levels with decreasing energy levels in unprocessed solid fuels. The authors note that airborne endotoxin concentrations in homes burning biomass fuels are orders of magnitude higher than those found in homes in developed countries where endotoxin exposure has been linked to respiratory illness in children. The authors also note the need for health studies to examine the long-term effects of exposure to endotoxin in children.
Related News Article: Endotoxin from Biomass Burning: An Underestimated Health Hazard?
Recent research indicates that the northward expansion of the tick Ixodes scapularis is associated with the emergence of Lyme disease (caused by Borrelia burgdorferi) in Canada. According to Ogden et al., there is a need to understand the environmental factors that may be associated with increased risk to Lyme disease. Active and passive surveillance for I. scapularis ticks and B. burgdorferi infection indicated that both are increasing in Quebec, possibly facilitated by a warming climate. Multilocus sequence typing of B. burgdorferi in ticks suggested that both the ticks and the bacterium are most likely being introduced from the northeastern United States. Surveillance data indicated that establishment of B. burgdorferi appears to lag a few years behind establishment of the tick population. Increasing numbers of ticks submitted in passive surveillance, as well as clusters of ticks with low infection prevalence, may signal newly established tick populations that have not yet established efficient B. burgdorferi transmission cycles necessary to produce a significant public health risk of Lyme disease. Because both I. scapularis ticks and B. burgdorferi infection may be spreading as a function of changes in the climate, enhanced surveillance may help prevent Lyme disease in humans.
Related News Article: Tracking the Deer Tick: Emerging Lyme Disease Threat in Canada
Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. McConnell et al. evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools. Parent-reported physician diagnosis of new-onset asthma was identified during 3 years of follow-up of a cohort of kindergarten and first-grade children who were asthma- and wheezing-free at study entry into the Southern California Children’s Health Study. Traffic-related pollution exposure was assessed based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO2), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. The authors report an increase in asthma risk with modeled traffic-related pollution exposure from roadways near homes and schools. Ambient NO2 was also associated with increased risk. Models that included both NO2 and modeled traffic exposures suggested independent associations of asthma with traffic-related pollution at school and at home, whereas the estimate for NO2 was attenuated. The authors conclude that traffic-related pollution exposure at school and home may both contribute to the development of asthma.
Related News Article: From Roadways to Wheeze: Child Asthma Associated with Traffic Exposures at Home and at School
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