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Biomedical subjects

M Lippmann

Publications and source records attributed to M Lippmann.

At least 37 records · Page 2Linked to original sources
PubMed1991

Effects of heavy industrial pollution on respiratory function in the children of Cubatao, Brazil: a preliminary report.

Under a cooperative agreement between New York University and the Environmental Protection Agency, and in collaboration with the University of Sao Paulo (USP), a study is ongoing in Cubatao, Brazil, to try to establish exposure-response relationships on the impact of specific industrial effluents on respiratory function in school-age children. Cubatao, located on the coast about 44 km from the city of Sao Paulo, is surrounded by U-shaped mountains (approximately 800 m) covered with subtropical forests. Its area is approximately 160 km2, and it has a population of approximately 90,000. The geography is such that it causes a consistent diurnal land-sea breeze pattern and the opposite during the night, with low dispersion of the air pollutants. In a small area (approximately 40 km2) against the mountains there is a concentration of over 20 large plants: oil refinery; iron and steel mill; fertilizer, cement, and gypsum production; coke kilns; and chemical, paint, and many other ancillary plants. During the 1988 school year, March through June, August through November, 600 six-year-old children, attending six different kindergarten schools, underwent monthly spirometry tests. Because the children live within a 500 m radius of their school, pollution monitors were located on each of the six schools. Particles were collected using dichotomous stacked filter units placed on 20 m towers to reduce the influence of dust from unpaved roads. The units use different pore size filters for coarse, 2 to 10 microns, and fine particles, (dp) less than 2 microns, and took separate samples for day and nighttime.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗
PubMed1990

1989 Alice Hamilton lecture. Lead and human health: background and recent findings.

This paper, prepared in tribute to Dr. Alice Hamilton on her 120th birthday, reviews her pioneering studies of occupational lead poisoning and its control, her largely unheeded warnings about the possible consequences of widespread lead exposure to the general public through the use of leaded fuel, and the results of recent studies of human exposure to and health effects of lead in the general environment. Evidence is presented for dose-related non-threshold effects for children with blood lead concentrations below 25 micrograms/dl for a variety of effects including verbal IQ; mental development; physical size; and age at physical milestones such as first steps, hearing thresholds, and postural sway. For adults, various studies have produced associations between blood pressure and blood lead concentrations below 35 micrograms/dl, suggesting possible effects on cardiovascular health. While the biological mechanisms responsible for these effects remain poorly understood, recent and current efforts to reduce exposure to lead by the virtual elimination of lead in gasoline and food packaging show that we have learned one of Dr. Hamilton's important lessons, i.e., that the most effective means of reducing excessive exposures are through control of the environmental sources.

Animals↗
PubMed1990

Effects of fiber characteristics on lung deposition, retention, and disease.

There is abundant epidemiologic evidence that asbestos fibers can cause lung fibrosis (asbestosis), bronchial cancer, and mesothelioma in humans, as well as limited evidence for such effects in workers exposed to slag and rockwool fibers. Epidemiological evidence for human disease from inhalation exposures to conventional fibrous glass is negative. While health concerns based on the morphological and toxicological similarities between man-made fibers and asbestos are warranted, it is important to note that most of the toxicological evidence for glass fiber toxicity in laboratory animals is based on nonphysiological exposures such as intratracheal instillation or intraperitoneal injection of fiber suspensions. Man-made fibers have produced lung fibrosis and mesotheliomas in such tests, albeit at much lower yields than asbestos. For all durable mineral fibers, critical length limits must be exceeded to warrant concern about chronic toxicity; i.e., 2 microns for asbestosis, 5 microns for mesothelioma, and 10 microns for lung cancer. Fiber width must be less than 0.1 microns for mesothelioma, and larger than this limit for asbestosis and lung cancer. The human health risks for most fibrous glass products are either low or negligible for a variety of reasons. First, most commercial fibrous glass products have mean fiber diameters of approximately 7.5 microns, which results in mean aero-dynamic diameters approximately 22 microns. Thus, most glass fibers, even if dispersed into the air, do not penetrate into the lung to any great extent. Second, the small fraction of smaller diameter fibers that do penetrate into the lungs are not persistent within the lungs for most fibrous glass products due to mechanical breakage into shorter lengths and overall dissolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Man-made mineral fibers (MMMF): human exposures and health risk assessment.

MMMF are made by spraying or extruding molten glass, furnace slag, or mineral rock. Health concerns are based on the morphological and toxicological similarities between MMMF and asbestos, and the well-documented evidence that asbestos fibers can cause lung fibrosis (asbestosis), bronchial cancer, and mesothelioma in humans. Epidemiological evidence for human disease from inhalation exposures to fibrous glass is largely negative. Some positive associations have been reported for slag and rockwools. Most of the toxicological evidence for MMMF toxicity in laboratory animals is based on non-physiological exposures such as intratracheal instillation or intraperitoneal injection of fiber suspensions. The risks for lung fibrosis, lung cancer, and mesothelioma for industrial exposures to most fibrous glass products are either low or negligible for a variety of reasons. First, most commercial fibrous glass products have mean fiber diameters of approximately 7.5 microns, which results in mean aerodynamic diameters greater than 22 microns. Thus, most glass fibers, even if dispersed into the air, do not penetrate into the lung to any great extent. Second, the small fraction of smaller diameter fibers which do penetrate into the lungs are not persistent within the lungs for most fibrous glass products, due to mechanical breakage into shorter lengths and dissolution. Dissolution is most rapid for the smaller diameters (less than 0.1 micron) capable of producing mesothelioma. The greater hazards for slag and rockwools, in comparison to conventional fibrous glass, appear to be related to their smaller diameters and greater durability within the lungs.

Air Pollutants, Occupational↗
PubMed1989

Tonazocine mesylate in postoperative pain patients: a double-blind placebo controlled analgesic study.

One hundred-fifty post-operative adult patients with moderate to severe pain were enrolled into this analgesic efficacy study comparing single doses of tonazocine mesylate, a new mixed agonist-antagonist opioid analgesic, with morphine. The patients were randomly assigned to five treatment groups: tonazocine mesylate 2, 4, 8 mg; morphine sulfate 10 mg and a placebo group. The results showed mean total pain relief scores for tonazocine 4 mg were nearly identical with that of morphine sulfate 10 mg while 8 mg of tonazocine were superior to 10 mg of morphine. All the active medication groups were superior to the placebo group (P less than 0.02) for both pain intensity and pain relief. Relative potency determined by the dose response indicates that 3.2 mg of tonazocine is equivalent to 10 mg of morphine. Drowsiness was the main adverse reaction seen in all active treatment groups. Tonazocine mesylate appears to be a potent analgesic with promising clinical usefulness and warrants further study.

Adolescent↗
PubMed1989

Health effects of ozone. A critical review.

Health and pollution control professionals and the general public need to develop a more complete understanding of the health effects of ozone (O3) because: 1) we have been unable to significantly reduce ambient O3 levels using current strategies and controls; 2) in areas occupied by more than half of the U.S. population, current peak ambient O3 concentrations are sufficient to elicit measurable transient changes in lung function, respiratory symptoms, and airway inflammation in healthy people engaged in normal outdoor exercise and recreational activities; 3) the effects of O3 on transient functional changes are sometimes greatly potentiated by the presence of other environmental variables; and 4) cumulative structural damage occurs in rats and monkeys exposed repetitively to O3 at levels within currently occurring ambient peaks, and initial evidence from dosimetry models and interspecies comparisons indicate that humans are likely to be more sensitive to O3 than rats. The extent and significance of these effects, and the multibillion dollar costs of ambient O3 controls need to be considered in any future revisions of ambient standards and the Clean Air Act. The transient effects of O3 are more closely related to cumulative daily exposure than to one hour peak concentrations, and future revisions of the ambient standard for O3 should take this into account. The effects of long-term chronic exposure to O3 remain poorly defined, but recent epidemiologic and animal inhalation studies suggest that current ambient levels are sufficient to cause premature aging of the lungs. More research is needed to determine the need for a standard with a seasonal or annual average concentration limit.

Animals↗
PubMed1989

Effect of concentration and cumulative exposure of inhaled sulfuric acid on tracheobronchial particle clearance in healthy humans.

We have previously shown that 1-hr exposures to 0.5 microns sulfuric acid (H2SO4) mist at 100 and 1000 micrograms/m3 produced transient alterations of bronchial mucociliary clearance of monodispersed 7.6 and 4.2 microns mass median aerodynamic diameter gamma-tagged ferric oxide (Fe2O3) in healthy nonsmoking humans in a dose-dependent manner. To determine the role, if any, of the length of exposure, 10 healthy volunteers were exposed to 100 micrograms/m3 H2SO4 for 1 hr and 2 hr on separate occasions, 1 week apart, with measurements of their mucociliary clearance of 5.2 microns Fe2O3 particles inhaled both before and after the inhalation of the H2SO4. Their rate of bronchial mucociliary clearance was markedly reduced for both Fe2O3 aerosols, with slower clearance of the aerosol inhaled after the H2SO4 exposure. For the tagged Fe2O3 aerosol inhaled after exposure for 2 hr at 100 micrograms/m3 H2SO4, the tracheobronchial clearance halftime, (T50), tripled from control, and the reduced rate of clearance was still evident 3 hr after the end of exposure. The 1-hr 100 micrograms/m3 H2SO4 exposure doubled T50 from control, and the reduced rate of clearance lasted for about 2 hr after the end of exposure. These results indicate that the effect of doubling the length of exposure was as great or greater than an order of magnitude increase in the concentration of H2SO4.

Acid Rain↗
PubMed1989

Progress, prospects, and research needs on the health effects of acid aerosols.

Research on human exposure to acidic aerosols and the health effects of such exposures has substantially strengthened the hypothesis that such aerosols are a causal factor for excesses in human mortality and morbidity that have been previously associated with crude exposure indices such as British Smoke, total suspended particulate matter, and sulfur dioxide. Research reported at this symposium also showed that combined exposures to acid aerosols and other ubiquitous air pollutants such as O3, NO2, HNO3, and SO2 produce greater effects in both humans and animals than exposures to each agent separately. The responses reported ranged from physiological functions to lung structure. Furthermore, some of the effects were cumulative with increasing duration of daily exposure and number of repetitive exposures. Critical areas for further research include better definition of the critical temporal parameters affecting exposure and response, effects of mixed pollutant exposures, and pathogenetic mechanisms for acid aerosol-induced chronic lung damage.

Acid Rain↗
PubMed1989

Background on health effects of acid aerosols.

This introduction to the 1987 NIEHS-EPA Symposium on the Health Effects of Acid Aerosols reviews the state of our knowledge on this topic as of the close of the 1984 NIEHS Conference on the Health Effects of Acid Precipitation (Environmental Health Perspectives, Volume 63) and the results of some key studies completed since that time. These studies, together with the results of the studies presented in the papers that follow, provide a substantial increment in our knowledge of the health effects of acid aerosols.

Acid Rain↗
PubMed1989

Reexamination of London, England, mortality in relation to exposure to acidic aerosols during 1963-1972 winters.

Air pollution epidemiology since the 1950s has been able to demonstrate that increases in daily mortality in London, England, were associated with elevated concentrations of index air pollutants, i.e., British Smoke (BS) and sulfur dioxide (SO2). In this work, we reanalyze that portion of the 1958-1972 winter mortality-pollution record for which daily direct acid aerosol measurements were made at a central site in London (St. Bartholomew's Medical College). The purposes of these exploratory analyses are to examine the dataset for indications of a relationship between acid aerosol pollution and human mortality and to compare any noted associations with those for other pollution variables. It is found that the log of acid aerosol concentrations is more strongly associated with raw total mortality in bivariate analyses than is BS or SO2, despite the fact that acid data are available from only one central site (versus seven disperse sites for BS and SO2). The logarithmic nature of the exposure side of the H2SO4-mortality relationship implies a saturation model of pollution effects, possibly due to multiday pollution harvesting influences on a susceptible subpopulation. Moreover, mortality-pollution cross-correlation analyses indicate that mortality effects usually follow pollution in time, supporting a causal relationship between the two. The apparent advantage of H2SO4 over BS in predicting total raw mortality is consistent with the hypothesis that it is the portion of particulate mass of greater health significance and may also allow the development of London mortality results which are more easily transferable to other environments than is the case for existing BS results.

Acid Rain↗