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Biomedical subjects

J S Puskin

Publications and source records attributed to J S Puskin.

At least 19 recordsLinked to original sources
PubMed2004

The U.S. Environmental Protection Agency's assessment of risks from indoor radon.

The U.S. Environmental Protection Agency has updated its assessment of health risks from indoor radon, which has been determined to be the second leading cause of lung cancer after cigarette smoking. This risk assessment is based primarily on results from a recent study of radon health effects (BEIR VI) by the National Academy of Sciences. In BEIR VI, the National Academy of Sciences fit empirical risk models to data from 11 cohorts of miners, and estimated that each year about 20,000 lung cancer deaths in the U.S. are radon related. A summary, abstracted from the technical report, is given of the EPA's risk assessment results and methods, including some modifications and extensions to the approach used in BEIR VI. Results include numerical estimates of lung cancer deaths per unit exposure, which had not been provided in BEIR VI.

Adolescent↗
PubMed2003

Smoking as a confounder in ecologic correlations of cancer mortality rates with average county radon levels.

Cohen has reported a negative correlation between lung cancer mortality and average radon levels by county. In this paper, the correlation of U.S. county mortality rates for various types of cancers during the period 1970-1994 with Cohen's radon measurements is examined. In general, quantitatively similar, strongly negative correlations are found for cancers strongly linked to cigarette smoking, weaker negative correlations are found for cancers moderately increased by smoking, whereas no such correlation is found for cancers not linked to smoking. The results indicate that the negative trend previously reported for lung cancer can be largely accounted for by a negative correlation between smoking and radon levels across counties. Hence, the observed ecological correlation provides no substantial evidence for a protective effect of low level radon exposure.

Air Pollutants, Radioactive↗
PubMed1995

Estimates of radiogenic cancer risks.

A methodology recently developed by the U.S. EPA for estimating the carcinogenic risks from ionizing radiation is described. For most cancer sites, the risk model is one in which age-specific, relative risk coefficients are obtained by taking a geometric mean of the coefficients derived from the atomic bomb survivor data using two different methods for transporting risks from the Japanese to the U.S. population. The risk models are applied to estimate organ-specific risks per unit dose for a stationary population with mortality rates governed by 1980 U.S. vital statistics. With the exception of breast cancer, low-LET radiogenic cancer risk estimates are reduced by a factor of 2 at low doses and dose rates compared to acute high dose exposure conditions. For low dose (or dose rate) conditions, the risk of inducing a premature cancer death from uniform, whole body, low-LET irradiation is calculated to be 5.1 x 10(-2) Gy-1. Neglecting nonfatal skin cancers, the corresponding incidence risk is 7.6 x 10(-2) Gy-1. High-LET (alpha particle) risks are presumed to increase linearly with dose and to be independent of dose rate. High-LET risks are estimated to be 20 times the low-LET risks estimated under low dose rate conditions, except for leukemia and breast cancer where RBEs of 1 and 10 are adopted, respectively.

Adolescent↗
PubMed1992

Bone cancer risk estimates.

Due to confusion between endosteal (bone surface) dose and average skeletal dose, ICRP 60 has substantially overestimated the risk of radiogenic bone cancer. This confusion apparently stems from an incorrect reading of the BEIR IV report, which does not clearly draw this distinction. It should also be noted that what appear to be summary numerical risk estimates for bone sarcoma induction in BEIR IV and BEIR V refer only to average skeletal dose as calculated for 224Ra.

Bone Neoplasms↗
PubMed1992

An analysis of the uncertainties in estimates of radon-induced lung cancer.

A recent report by the National Academy of Sciences estimates that the radiation dose to the bronchial epithelium, per working level month (WLM) of radon daughter exposure, is about 30% lower for residential exposures than for exposures received in underground mines. Adjusting the previously published BEIR IV radon risk model accordingly, the unit risk for indoor exposures of the general population is about 2.2 x 10(-4) lung cancer deaths (lcd)/WLM. Using results from EPA's National Residential Radon Survey, the average radon level is estimated to be about 1.25 pCi/L, and the annual average exposure about 0.242 WLM. Based on these estimates, 13,600 radon-induced lcd/yr are projected for the United States. A quantitative uncertainty analysis was performed, which considers: statistical uncertainties in the epidemiological studies of radon-exposed miners; the dependence of risk on age at, and time since, exposure; the extrapolation of risk estimates from mines to homes based on comparative dosimetry; and uncertainties in the radon daughter levels in homes and in the average residential occupancy. Based on this assessment of the uncertainties in the unit risk and exposure estimates, an uncertainty range of 7000-30000 lcd/yr is derived.

Adult↗
PubMed1989

EPA's perspective on risks from residential radon exposure.

Indoor radon has been judged to be the most serious environmental carcinogen which the EPA must address for the general public. The optimal strategy for dealing with this problem depends on the magnitude of the risk, how the risk is distributed within the population, as well as the effectiveness and costs of mitigation measures. Based on current exposure and risk estimates, radon exposure in single-family houses may be a causal factor in roughly 20,000 lung cancer fatalities per year. Most of these projected fatalities are attributable to exposures in houses with average or moderately elevated radon levels (below 10 pCi/L). Hence to appreciably reduce radon-induced lung cancers, remediation efforts must include houses not highly elevated in radon. From either an individual risk or a cost-benefit standpoint, reduction of a few pCi/L per home appears to be justified. The optimal strategy for dealing with the indoor radon problem depends on the magnitude of the risk per unit exposure, the distribution of exposures in houses, and the effectiveness and costs of mitigation. EPA's current views with respect to these factors and the associated uncertainties are discussed.

Carcinogens, Environmental↗
PubMed1988

A retrospective look at Rn-induced lung cancer mortality from the viewpoint of a relative risk model.

The potential contribution to U.S. lung cancer deaths from 1930 to 1987 from indoor 222Rn exposures is investigated from the standpoint of a constant relative risk model. Based on this model, which assumes a Rn risk proportional to the baseline lung cancer risk from other causes, the rate of Rn-induced lung cancer mortality has been increasing sharply since 1930. However, the estimated proportion of lung cancer deaths attributable to Rn has remained fairly constant. Applying the range of coefficients the U.S. Environmental Protection Agency employs in assessing the risk from indoor Rn, it is estimated that 8-25% of all current lung cancer deaths are "attributable to" past Rn exposures. The major sources of uncertainty in the estimates are discussed.

Environmental Exposure↗
PubMed1983

Mechanism of sodium independent calcium efflux from rat liver mitochondria.

On the basis of primarily two types of observations, it has been suggested that the Na+-independent Ca2+ efflux mechanism of rat liver mitochondria is a passive Ca2+-2H+ exchanger. First, when a pulse of acid is added to a suspension of mitochondria loaded with Ca2+, a pulse of intramitochondrial Ca2+ is often released, even in the presence of the inhibitor of mitochondrial Ca2+ influx, ruthenium red. Second, at a pH near 7, the stoichiometry of Ca2+ released to H+ taken up by Ca2+-loaded mitochondria, following treatment with ruthenium red, has been observed to be 1:2. This evidence for a Ca2+-2H+ exchanger is reexamined here by studying the release of Ca2+ upon acidification of the medium by addition of buffer, the dependence of liver mitochondrial Ca2+ efflux on external medium pH and intramitochondrial pH, and the Ca2+-Ca2+ exchange properties of the Ca2+ efflux mechanism. These studies show no pulse of mitochondrial Ca2+ efflux when pH is abruptly lowered by addition of buffer. The stoichiometry between Ca2+ and H+ fluxes is found to be highly pH dependent. The reported 1:2 stoichiometry between Ca2+ efflux and H+ influx is only observed at one pH. Furthermore, the rate of Ca2+ efflux from mitochondria is found to increase only very slightly at most as suspension pH is decreased. The rate of Ca2+ efflux is not found to increase with increasing intramitochondrial pH. Finally, no Ca2+-Ca2+ isotope exchange can be demonstrated over the Na+-independent efflux mechanism (i.e., in the presence of ruthenium red). It is concluded that these data do not support the hypothesis that the Na+-independent Ca2+ efflux mechanism is a passive Ca2+-2H+ exchanger.

Animals↗
PubMed1981

A spin label method for measuring internal volumes in liposomes or cells, applied to Ca-dependent fusion of negatively charged vesicles.

A new spin label - broadening agent system for measuring trapped volumes of vesicles or cells is described. The method seems to be more advantageous than existing procedures when volumes of highly negatively charged vesicles are to be determined. The membrane permeable spin label is TEMPONE (2,2,6,6-tetramethyl piperidone-N-oxyl), and the nonpermeable broadening agent is chromium oxalate (K3Cr(C2O4)3). Absolute values for the trapped volumes down to 0.1% in 0.1 ml can be measured with an accuracy of about +/- (1-10%). The method is used to study the final volume of fused phosphatidylserine vesicles as a function of the temperature at which the Ca-induced fusion takes place.

Animals↗