This study characterizes the personal, indoor, and outdoor PM 2.5 , PM 10 , and PM 2.5 ± 10 exposures of 18 individuals with chronic obstructive pulmonary disease ( COPD ) living in Boston, MA. Monitoring was performed for each participant for six consecutive days in the winters of 1996 or 1997 and for six to twelve days in the summer of 1996. On each day, 12 -h personal, indoor, and outdoor samples of PM 2.5 and PM 10 were collected simultaneously. Home characteristic information and time ± activity patterns were also obtained. Personal exposures were higher than corresponding indoor and outdoor concentrations for all particle measures and for all seasons, except for winter indoor PM 2.5 ± 10 levels, which were higher than personal and outdoor levels. Higher personal exposures may be due to the proximity of the individuals to particle sources, such as cooking and cleaning. Indoor concentrations were associated with both outdoor concentrations and personal exposures ( as determined by individual least square regression analyses ) , with associations strongest for PM 2.5 . Indoor PM 2.5 concentrations were significantly associated with outdoor and personal levels for 12 and 15 of the 17 individuals, respectively. Both the strength and magnitude of the associations varied by individual. Also, personal PM 2.5 , but not PM 2.5 ± 10 , exposures were associated with outdoor levels, with 10 of the 17 subjects having significant associations. The strength of the personal ± outdoor association for PM 2.5 was strongly related to that for indoor and outdoor levels, suggesting that home characteristics and indoor particulate sources were key determinants of the personal ± outdoor association for PM 2.5 . Air exchange rates were found to be important determinants of both indoor and personal levels. Again, substantial interpersonal variability in the personal ± outdoor relationship was found, as personal exposures varied by as much as 200% for a given outdoor level.

Preterm birth is a public health issue of global significance, which may result in mortality during the perinatal period or may lead to major health and financial consequences due to lifelong impacts. Even though several risk factors for preterm birth have been identified, prevention efforts have failed to halt the increasing rates of preterm birth. Epidemiological studies have identified air pollution as an emerging potential risk factor for preterm birth. However, many studies were limited by study design and inadequate exposure assessment. Due to the ubiquitous nature of ambient air pollution and the potential public health significance of any role in causing preterm birth, a novel focus investigating possible causal mechanisms influenced by air pollution is therefore a global health priority. We hypothesize that air pollution may act together with other biological factors to induce systemic inflammation and influence the duration of pregnancy. Evaluation and testing of this hypothesis is currently being conducted in a prospective cohort study in Mexico City and will provide an understanding of the pathways that mediate the effects of air pollution on preterm birth. The important public health implication is that crucial steps in this mechanistic pathway can potentially be acted on early in pregnancy to reduce the risk of preterm birth.

Background: Observed seasonal differences in particulate matter (PM) associations with human health may be due to their composition and to toxicity-related seasonal interactions. oBjectives: We assessed seasonality in PM composition and in vitro PM pro-inflammatory potential using multiple PM samples. Methods: We collected 90 weekly PM 10 and PM 2.5 samples during the rainy-warm and dry-cold seasons in five urban areas with different pollution sources. The elements, polycyclic aromatic hydrocarbons (PAHs), and endotoxins identified in the samples were subjected to principal component analysis (PCA). We tested the potential of the PM to induce tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) secretion in cultured human monocytes (THP-1), and we modeled pro-inflammatory responses using the component scores.

Background: Cooking with biomass fuels on open fires results in exposure to health-damaging pollutants such as carbon monoxide (CO), polycyclic aromatic hydrocarbons (PAHs), and particulate matter.Objective: We compared CO exposures and urinary PAH biomarkers pre- and postintervention with an improved biomass stove, the Patsari stove.Methods: In a subsample of 63 women participating in a randomized controlled trial in central Mexico, we measured personal CO exposure for 8 hr during the day using continuous monitors and passive samplers. In addition, first-morning urine samples obtained the next day were analyzed for monohydroxylated PAH metabolites by gas chromatography/isotope dilution/high-resolution mass spectrometry. Exposure data were collected during the use of an open fire (preintervention) and after installation of the improved stove (postintervention) for 47 women, enabling paired comparisons.Results: Median pre- and postintervention values were 4 and 1 ppm for continuous personal CO and 3 and 1 ppm for passive sampler CO, respectively. Postintervention measurements indicated an average reduction of 42% for hydroxylated metabolites of naphthalene, fluorene, phenanthrene, and pyrene on a whole-weight concentration basis (micrograms per liter of urine), and a 34% reduction on a creatinine-adjusted basis (micrograms per gram of creatinine). Pre- and postintervention geometric mean values for 1-hydroxypyrene were 3.2 and 2.0 μg/g creatinine, respectively.Conclusion: Use of the Patsari stove significantly reduced CO and PAH exposures in women. However, levels of many PAH biomarkers remained higher than those reported among smokers.

Our results suggest that in the Mexico City Metropolitan Area, infants with lower SES (low to medium) are at higher risk of mortality when exposed to ambient PM(10) and O(3).