Connective tissue cells responding to wounding of the periodontal ligament of the lower first molar in mice were studied using the techniques of radioautography and grain counting. Animals were given an intraperitoneal injection of 2 uCi 1g 3H‐Tdr 1 hr before being killed at either 30, 72 or 120 hr after wounding. The ligament in 1 um plastic sections was divided into compartments on the basis of distance from the wound, and the relative number of labelled cells in each compartment was assessed at 30, 72 and 120 hours after wounding. The distance of each labelled cell from the closest blood vessel was also measured at each time to detect relative movement of labelled cells away from blood vessels. In a Parallel experiment, haematogenous progenitors of macrophages were depleted by irradiating the animals with 800rads prior to woundilng to determine if mistakes in identification between fibroblasts and marophages could significantly affect the results. The ultrastructural characteristics of 150 of the 3H‐Tdr labelled cells was examined in thin sections of wounded periodontal ligament prepared for elctron microcope radioautography, The majority of cells lebelled 30 hours after wounding were confirmed to be paravascular, and most of them were found to be located within 200 μ of the wound margin. Some of these cells appreared to have divided a number of times between 30 and 72 hours after wounding, and to have migrated into the wound between 70 and 120 hours after wounding. Examination of the irradiated material and the electron microscope radio‐autographs suggested that significant numbers of macrophages had not been included in the counts of labelled cells. The elctron microscope radioautographs also suggested that cells which exhibited different degrees of cytodifferentiation had incorporated 3H‐Tdr.

We measured the spatial pattern of particle number (PN) concentrations downwind from the Los Angeles International Airport (LAX) with an instrumented vehicle that enabled us to cover larger areas than allowed by traditional stationary measurements. LAX emissions adversely impacted air quality much farther than reported in previous airport studies. We measured at least a 2-fold increase in PN concentrations over unimpacted baseline PN concentrations during most hours of the day in an area of about 60 km2 that extended to 16 km (10 miles) downwind and a 4- to 5-fold increase to 8–10 km (5–6 miles) downwind. Locations of maximum PN concentrations were aligned to eastern, downwind jet trajectories during prevailing westerly winds and to 8 km downwind concentrations exceeded 75 000 particles/cm3, more than the average freeway PN concentration in Los Angeles. During infrequent northerly winds, the impact area remained large but shifted to south of the airport. The freeway length that would cause an impact equivalent to that measured in this study (i.e., PN concentration increases weighted by the area impacted) was estimated to be 280–790 km. The total freeway length in Los Angeles is 1500 km. These results suggest that airport emissions are a major source of PN in Los Angeles that are of the same general magnitude as the entire urban freeway network. They also indicate that the air quality impact areas of major airports may have been seriously underestimated.

Most published epidemiology studies of long-term air pollution health effects have relied on central site monitoring to investigate regional-scale differences in exposure. Few cohort studies have had sufficient data to characterize localized variations in pollution, despite the fact that large gradients can exist over small spatial scales. Similarly, previous data have generally been limited to measurements of particle mass or several of the criteria gases. The Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) is an innovative investigation undertaken to link subclinical and clinical cardiovascular health effects with individual-level estimates of personal exposure to ambient-origin pollution. This project improves on prior work by implementing an extensive exposure assessment program to characterize long-term average concentrations of ambientgenerated PM 2.5 , specific PM 2.5 chemical components, and co-pollutants, with particular emphasis on capturing concentration gradients within cities. This paper describes exposure assessment in MESA Air, including questionnaires, community sampling, home monitoring, and personal sampling. Summary statistics describing the performance of the sampling methods are presented along with descriptive statistics of the air pollution concentrations by city. Supporting Information is available on-line that presents more details of the measurement methods and quality control/quality assurance procedures and outcomes. This information is available free of charge via the internet at

A desirable feature of an implant surface which penetrates epithelium would be that the surface impedes epithelial downgrowth. Previous experiments have shown that the micromachined, horizontally oriented grooves on the percutaneous implant surface can impede epithelial downgrowth (Chehroudi et al., J. Biomed. Mater. Res., 22, 459 (1988) and 23, 1067 (1989)). However, little is known of the effect of varying groove parameters such as depth, spacing, and orientation on epithelial downgrowth and attachment of epithelial (E)-cells and fibroblasts (F) to percutaneous implants in vivo. Grooves were produced with a 30-micron pitch and depths of 22 microns, 10 microns, or 3 microns. In addition, 10-microns- and 3-microns-deep grooves were made with pitches of 39 microns and 7 microns, respectively. Implants with grooves oriented either horizontally or vertically to the long axis of the implant as well as smooth control surfaces were coated with 50 nm of titanium and placed in the parietal area of rats for a period of 7 days. Close attachment of E-cells was found on the smooth, 10-microns- and 3-microns-deep, horizontally or vertically aligned grooved surfaces; in contrast, E-cells bridged over the 22-microns-deep, horizontally oriented grooves. F formed a capsule on the smooth surface as well as the 10-microns- and 3-microns-deep horizontally oriented grooves, but F inserted obliquely into the 22-microns-deep, horizontally aligned grooved surface. Histomorphometric measurements indicated that the epithelial downgrowth was greatest on the vertically oriented grooved and smooth surfaces and was shortest on the 22-microns-deep and 10-microns-deep horizontally aligned grooved surfaces. These differences indicate that epithelial downgrowth was accelerated on the vertically oriented grooved surfaces and inhibited on the horizontally oriented grooved surfaces. Moreover, the mechanism of inhibition of the epithelial downgrowth may differ among these surfaces. E-cells bridged over the 22-microns-deep grooves and their migration appeared to be inhibited by the F that inserted into the implant surface. In the shallower horizontal grooves, however, epithelial downgrowth was probably inhibited by contact guidance because there was no evidence of F inserting obliquely into the implant surface.