Effects of in vitro Exposure of Human Respiratory Epithelial Cells to Formaldehyde

Formaldehyde is the most abundant carbonyl in air. As a by-product of combustion and other natural processes, it is ubiquitous in the environment. Typically, the formaldehyde concentration levels in ambient air are produced by the photochemical oxidation of volatile organic compounds (VOCs), including the major biogenics such as isoprene and methane. Thus, formaldehyde is an important component of atmospheric pollution. Also, it is commonly used in the medical and health fields, in the manufacturing of building materials, and is present in substantial quantities in occupational and home environments. People are likely exposed to low levels of formaldehyde on a daily basis, it has therefore been suggested that formaldehyde exposure may be linked to increased hospital admissions and increased prevalence of inflammatory diseases. Other carbonyl compounds similarly produced and measured in the atmosphere have been shown to produce measurable cytotoxic and inflammatory responses. However, it is largely unknown how exposure to formaldehyde effects specific inflammatory mediator production. To evaluate the potential adverse heath effects elicited by formaldehyde exposure cultured human respiratory epithelial cells (A549) were used as the target of the formaldehyde gas. In cell culture supernatants, cellular distress was measured by the production of pro-inflammatory mediators such as interleukin-8 and Interleukin-6. Cytotoxicity or cellular death was measured by the release of lactate dehydrogenase (LDH). Using permeation tube or large chamber air mixtures, formaldehyde was administered in increasing doses to investigate a dose response of concentrations that have been observed in ambient and occupational environments. Formaldehyde concentrations were measured continuously using a permeable membrane sampler, and detected with fluorometry using an automated Hantzsch derivative reaction (Dasgupta technique). The concentrations in the 3-hr exposures were approximately 55 ppb, 140 ppb, 220 ppb, 390 ppb, and 980 ppb. At the 55 to 220 ppb formaldehyde exposure level, there were virtually no differences between exposed cells and control cells for all endpoints. Cells exposed to 390 and 980 ppb showed no increases in LDH or IL-6, however a concentration dependent decrease was observed in IL-8 expression for both chamber and permeation tube exposures. This data suggests that gaseous formaldehyde does not affect common markers of inflammation or cause cellular death in lung epithelial cells. However the observed decrease in IL-8 expression implies that there may be a mechanism, unknown to us, by which formaldehyde is suppressing the release of IL-8 proteins.Master of Scienc

A Case-Crossover Analysis of Indoor Heat Exposure on Mortality and Hospitalizations among the Elderly in Houston, Texas

Background: Despite the substantial role indoor exposure has played in heat wave&ndash;related mortality, few epidemiological studies have examined the health effects of exposure to indoor heat. As a result, knowledge gaps regarding indoor heat&ndash;health thresholds, vulnerability, and adaptive capacity persist. Objective: We evaluated the role of indoor heat exposure on mortality and morbidity among the elderly (&ge;65&thinsp;years of age) in Houston, Texas. Methods: Mortality and emergency hospital admission data were obtained through the Texas Department of State Health Services. Summer indoor heat exposure was modeled at the U.S. Census block group (CBG) level using building energy models, outdoor weather data, and building characteristic data. Indoor heat&ndash;health associations were examined using time-stratified case-crossover models, controlling for temporal trends and meteorology, and matching on CBG of residence, year, month, and weekday of the adverse health event. Separate models were fitted for three indoor exposure metrics, for individual lag days 0&ndash;6, and for 3-d moving averages (lag 0&ndash;2). Effect measure modification was explored via stratification on individual- and area-level vulnerability factors. Results: We estimated positive associations between short-term changes in indoor heat exposure and cause-specific mortality and morbidity [e.g., circulatory deaths, odds ratio per&thinsp;5&deg;C&thinsp;increase=1.16 (95% CI: 1.03, 1.30)]. Associations were generally positive for earlier lag periods and weaker across later lag periods. Stratified analyses suggest stronger associations between indoor heat and emergency hospital admissions among African Americans compared with Whites. Discussion: Findings suggest excess mortality among certain elderly populations in Houston who are likely exposed to high indoor heat. We developed a novel methodology to estimate indoor heat exposure that can be adapted to other U.S. locations. In locations with high air conditioning prevalence, simplified modeling approaches may adequately account for indoor heat exposure in vulnerable neighborhoods. Accounting for indoor heat exposure may improve the estimation of the total impact of heat on health. https://doi.org/10.1289/EHP6340</p