Formaldehyde in residences: long-term indoor concentrations and influencing factors.

UNLABELLED: Chronic human exposure to formaldehyde is significantly increased by indoor sources. However, information is lacking on why these exposures appear to persist in older homes with aging sources. We use data from the Relationships of Indoor, Outdoor, and Personal Air study to evaluate 179 residences, most of which were older than 5 years. We assess the dependence of indoor formaldehyde concentrations (C(in)) on building type and age, whole-house air exchange rate, indoor temperature, and seasonal changes. Indoor formaldehyde had mean and median concentrations of 17 ppb, and primarily originated from indoor sources. The factors we analyzed did not explain much of the variance in C(in), probably because of their limited influence on mechanisms that control the long-term release of formaldehyde from aging pressed-wood products bound with urea-formaldehyde (UF) resins. We confirmed that the mitigating effects of ventilation on C(in) decrease with time through the analysis of data for new homes available in the literature, and through models. We also explored source control strategies and conclude that source removal is the most effective way to decrease chronic exposures to formaldehyde in existing homes. For new homes, reducing indoor sources and using pressed-wood with lower UF content are likely the best solutions. PRACTICAL IMPLICATIONS: Formaldehyde concentrations in homes due to indoor sources appear to persist throughout the lifetime of residences. Increases in ventilation rates are most effective in decreasing indoor concentrations in new homes where formaldehyde levels are high or when homes are tight. Consequently, other alternatives need to be promoted such as decreasing the amount of pressed-wood products with urea-formaldehyde (UF) resins in homes or reducing the UF content in these materials.

DNA damage in outdoor workers occupationally exposed to environmental air pollutants.

BACKGROUND: Health concerns about the exposure to genotoxic and carcinogenic agents in the air are particularly significant for outdoor workers in less developed countries. AIMS: To investigate the association between personal exposure to a group of air pollutants and severity of DNA damage in outdoor workers from two Mexican cities. METHODS: DNA damage (Comet assay) and personal exposure to volatile organic compounds, PM(2.5), and ozone were investigated in 55 outdoor and indoor workers from México City and Puebla. RESULTS: In México City, outdoor workers had greater DNA damage, reflected by a longer tail length, than indoor workers (median 46.8 v 30.1 mum), and a greater percentage of highly damaged cells (cells with tail length > or =41 microm); in Puebla, outdoor and indoor workers had similar DNA damage. There were more alkali labile sites in outdoor than indoor workers. The DNA damage magnitude was positively correlated with PM(2.5) and ozone exposure. Outdoor and indoor workers with > or =60% of highly damaged cells (highly damaged workers) had significantly higher exposures to PM(2.5), ozone, and some volatile organic compounds. The main factors associated with the highly damaged workers were ozone, PM(2.5), and 1-ethyl-2-methyl benzene exposure. CONCLUSIONS: With this approach, the effects of some air pollutants could be correlated with biological endpoints from the Comet assay. It is suggested that the use of personal exposure assessment and biological endpoints evaluation could be an important tool to generate a more precise assessment of the associated potential health risks.

The role of information dissemination in sustainability of international partnerships.

The Fogarty-supported International Training Program of the Southwest Center for Occupational and Environmental Health (SWCOEH) at the University of Texas School of Public Health was initiated in 1995, with its activities focused primarily on Latin America. As this program has matured, its participants have been concerned about including elements that increase the likelihood that its trainees and projects will have a sustainable impact on occupational and environmental health in collaborating countries. The Center recently reviewed the experiences of various international organizations and national development agencies with established track records involving donor-supported projects. The authors summarize factors associated with project sustainability and describe how some of them are being incorporated into the SWCOEH program. Particular mention is made of the importance of supporting an infrastructure for broad information dissemination in the language of the intended audience. An example of a project to support a peer-reviewed Spanish-language journal devoted to occupational and environmental health, Salud de los Trabajadores, is presented.

Urban particle-induced apoptosis and phenotype shifts in human alveolar macrophages.

Epidemiological studies report a small but positive association between short-term increases in airborne particulate matter and small increases in morbidity and mortality from respiratory and cardiovascular disease in urban areas. However, the lack of a mechanistic explanation to link particle exposure and human health effects makes it difficult to validate the human health effects. The present study tested the hypothesis that urban particles could cause apoptosis of human alveolar macrophages(AM) and a shift of their phenotypes to a higher immune active state, which would provide a mechanism to explain an inflammatory response. Freshly isolated human AM were incubated for 24 hr with urban particles (#1648 and #1649), Mount Saint Helen's ash (MSH), and residual oil fly ash (ROFA). Cell viability was assessed by trypan blue exclusion and apoptosis was demonstrated by morphology, cell death ELISA, and DNA ladder formation. Additionally, AM were characterized according to RFD1(+) (immune stimulatory macrophages) and RFD1(+)7(+) (suppressor macrophages) phenotypes by flow cytometry. ROFA particles caused AM necrosis at concentrations as low as 10 microg/ml, urban particles had no effect except at 200 microg/ml, and MSH had no effect at 200 microg/ml. ROFA (25 microg/ml) and particles #1648 or #1649 (100 microg/ml) caused apoptosis of AM by all three criteria, but 200 microg/ml MSH had no effect. Finally, 25 microg/ml ROFA and 100 microg/ml particles #1648 or #1649 up regulated the expression of the RFD1(+) AM phenotype, while only ROFA decreased the RFD1(+)7(+) phenotype. Consequently, ROFA and urban particles can induce apoptosis of human AM and increase the ratio of AM phenotypes toward a higher immune active state (i.e., increased RFD1(+):RFD1(+)7(+) ratio). Ifurban particles cause similar changes in vivo, this could result in lung inflammation and possible increased pulmonary and cardiovascular disease.

4-hydroxy-2-nonenal-protein adducts and apoptosis in murine lung cells after acute ozone exposure.

Ozone is a photochemically generated pollutant that can cause acute pulmonary inflammation and induce cellular injury and may contribute to the development or exacerbation of chronic lung diseases. Despite extensive investigation, the mechanisms of ozone and oxidant-induced cellular injury are still uncertain. Ozone has been reported to cause the formation of aldehydes in biological fluids that could explain many of the cellular effects caused by ozone. One of the most toxic aldehydes formed during oxidant-induced lipid peroxidation is 4-hydroxy-2-nonenal (HNE). HNE reacts primarily with Cys and secondarily with Lys and His amino acids, altering protein function and forming protein adducts that can be detected using specific adducts. In this study, we investigated whether ozone could cause the formation of HNE by assaying for HNE-protein adducts in cells isolated by lung lavage from C3H/HeJ mice exposed to 2.0 and 0.25 ppm ozone for 3 hr. Since oxidative stress and HNE have been shown to cause apoptosis we also examined the lung lavage cells for evidence of apoptosis following ozone exposure. Using a specific polyclonal antibody against HNE-amino acid adducts, two principle HNE-protein adducts were detected by Western analysis in cells obtained after ozone exposure at approximately 86-90 and 32 kDa. In addition to cell necrosis, apoptosis of lung cells was significant 3 hr after ozone exposure as detected using a Cell Death ELISA procedure and confirmed with DNA ladder and morphological analysis. The apoptotic cell injury peaked at 6 hr postexposure and decreased by 24 hr. Taken together, these results demonstrate that HNE is formed in vivo following ozone exposure and HNE appears to form specific protein adducts in lung cells. Furthermore, ozone can cause lung cell injury by an apoptotic mechanism in addition to a necrotic mechanism. Since HNE is toxic to cells and is formed as a result of ozone exposure, it may contribute to the lung cell injury following ozone exposure.

Occupational exposure to low frequency magnetic fields in health care facilities.

A characterization of health care workers' exposures to magnetic fields in the 40-1000 Hz range was performed in a multistory research hospital and single-story outpatient surgery unit. Area survey, source, and personal measurements of broadband and frequency-specific magnetic flux densities were performed with frequency analyzer dosimeters; the background static field was measured with a portable magnetometer. Dosimetry measurements were cross-referenced to workers' time/activity patterns. Spot measurements of magnetic flux density in the research hospital varied between 0.8 mG (.08 microT) and 65 mG (6.5 microT). Workers' time-weighted average exposures ranged from 1.2 mG (0.12 microT) to 10.4 mG (1.04 microT), with peak exposures ranging from 8.9 mG (0.89 microT) to 103.7 mG (10.37 microT). Frequency spectra of the exposures were variable and included harmonic bands as well as 60 Hz. The background static magnetic field in the hospital varied between 250 mG (25 microT) and 480 mG (48 microT) suggesting shielding of the geomagnetic field from building materials. These results indicate that health care workers are exposed to 40-1000 Hz magnetic fields during routine patient care. The fields are characterized by a switching (on/off, in/out) pattern of occurrence, variable frequencies that include 60 Hz and harmonic bands, and peak excursions that may occur at regular intervals. These characteristics vary both within and among job categories, suggesting that job title may be a poor surrogate for exposure classification. Although limited in scope, the results indicate that spot measurement of broadband or 60-Hz magnetic fields, or summary indices such as time-weighted average, mean or median, are insufficient to characterize occupational exposures.

A comparative study of respirable particulate microenvironmental concentrations and personal exposures.

Personal monitoring (PM) for respirable suspended particulate matter (RSP) of thirty subjects was performed as part of an air pollution health effects study conducted in Houston, Texas. Parallel RSP measurements were performed in the study subjects' homes and two fixed site monitoring stations. The participants' daytime activities were independently recorded by study techicians. These data were used to characterize RSP concentrations in each microenvironment visited by the participants. Four estimates of daytime exposure to RSP were calculated based on two different microenvironmental models, and home and fixed site mean daytime RSP concentrations. These estimates were compared to mean daytime personal exposure from PM. Hourly estimates of exposure were calculated from a microenvironmental model and mean hourly home RSP concentrations and compared to hourly PM data. The results of the study indicate that, as in the case of NO2, it is important to characterize indoor microenvironmental RSP concentrations according to location, sources, and concurrent activities, both qualitatively and quantitatively. Stratification of concentrations according to sources present and self-reported activity can lead to misclassification of exposures. For RSP and, probably, other pollutants with indoor sources and with short exposure integration times, adequate measures of exposure can only be obtained with very detailed and complex microenvironmental models or comprehensive personal monitoring.