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J R Olson

Publications and source records attributed to J R Olson.

67 records · Page 4Linked to original sources
PubMed1969

Congenital mesonephric defects in male infants with mucoviscidosis.

Reports that men with mucoviscidosis were sterile and that portions of their genital tracts were atretic prompted us to investigate the genital tracts of 15 male infants with mucoviscidosis who died within the first year of life and came to necropsy. The genital tracts of all of these infants were abnormal, the abnormalities being confined to mesonephric derivatives. Hypoplastic or absent ducti efferentia, ducti epididymides, or ducti deferentia were found in all 28 specimens of epididymides, and the ducti deferentia were missing from 25 of 27 examples of spermatic cord. The seminal vesicles and the ejaculatory ducts were less frequently hypoplastic or absent. Because these abnormalities of mesonephric derivatives were present so early in life and inflammatory and obstructive changes were absent we believe that they resulted from a failure of development.

Cystic Fibrosis↗
PubMedDate not supplied

Levels of dioxins, dibenzofurans, PCB and DDE congeners in pooled food samples collected in 1995 at supermarkets across the United States.

Food, particularly dairy products, meat, and fish, has been identified as the primary immediate source of intake of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) for the general population. We previously reported PCDD/Fs in individual analyses of food samples from a number of countries, including the U.S., the former Soviet Union, and Vietnam. We also previously estimated daily intake of dioxins and related chemicals in Americans at various ages in these reports. In this paper, the levels of dioxins, dibenzofurans, dioxin toxic equivalents (TEQs), selected dioxin-like PCBs, and DDE (a persistent metabolite of DDT) were measured in 12 pooled food samples from over 90 individual specimens collected from supermarkets throughout the United States during 1995. Samples were pooled by food groups and then analyzed. Food samples were collected in Binghamton, New York; Atlanta, Georgia; Chicago, Illinois; San Diego, California; and Louisville, Kentucky. In addition to the meat, dairy, and fish samples, a vegan (all vegetable, fruit and grain, no animal product) diet, was simulated; this showed the lowest level of dioxins.

Benzofurans↗
PubMedDate not supplied

Cancer risk assessment using blood dioxin levels and daily dietary TEQ intake in general populations of industrial and non-industrial countries.

We previously measured polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in U.S. foods and estimated the daily dioxin toxic equivalent (TEQ) intake to be from 0.3 to 3.0 pg 1-TEQ/kg body weight for adults. These values are similar to values reported in Canada, Germany, England, and the Netherlands. The U.S. Environmental Protection Agency (EPA) Dioxin Reassessment Draft Documents currently propose a cancer risk-specific dose estimate of 0.01 pg TEQ/kg body weight/day (U.S. EPA, 1994). This risk-specific dose estimate represents a lifetime (70 years) dose which results in a plausible upper bound cancer risk of 1 x 10(-6) (the probability of one additional cancer per one million exposed population over a lifetime). The proximate source of almost all dioxin intake in the general population is from food. Using our data for daily dietary dioxin exposure and the EPA's proposed risk specific dose, we estimate that over a lifetime a maximum of 30 to 300 excess cancers per million could result from the ingestion of dioxin containing food products. In the U.S. population of 260 million, a maximum range of 7,800 to 78,000 excess cancers over a lifetime (70 years) or 111 to 1,114 cases/year might be directly linked to dioxin exposure from food. Because these calculations are based on conservative approaches to setting an upper bound, "true" risk is not likely to exceed this value. At present, one-third of all Americans will develop cancer over a lifetime and one in four Americans are likely to die from cancer. For 1995, it was estimated that there would be 1,252,000 new cancer cases in the U.S. From this, we calculate that a maximum between 0.009% and 0.09% (111-1,114 cases/year) of all cancer cases in the U.S. might be directly linked to dioxin intake in food, assuming intakes have remained constant over a lifetime. Previous studies have suggested that as much as 70% of the total cancer risk in humans may be attributable to diet, primarily as a function of caloric and synthetic chemicals in the diet. (NAS, 1996) These figures do not take into account the ingestion of more contaminated food products, other sources of exposure, possible interactions of PCDDs and PCDFs with other chemicals, or increased incidence of cancer from the cancer promoting actions of dioxins. In addition, we reviewed average U.S. general population blood TEQ (ppt, lipid) levels, which reflect body burden, with levels of persons living in less industrialized countries. These data were used to compare the cancer risk of individuals living in the U.S., an industrial country, to those living in selected less industrialized countries. With the assumption that similar populations were being compared, it is estimated that in the non-industrial region of north Vietnam there is one-third the risk of dioxin-related cancer compared with the United States, while Cambodians have a dioxin-related cancer risk that is 14 fold less than the U.S. at this time.

Adult↗
PubMedDate not supplied

Relationship between the murine Ah phenotype and the hepatic uptake and metabolism of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The influence of the Ah locus on the hepatic uptake and metabolism of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied using isolated hepatocytes from Ah responsive C57BL/6J (C57) and nonresponsive DBA/2J (DBA) mice. Hepatocytes from control and TCDD-pretreated C57 and DBA mice were incubated with purified [14C] TCDD (2.2 microM) for 8 hr in the metabolism studies or 2 hr in the uptake studies. Mice were pretreated 7 days prior to hepatocyte isolation with TCDD at doses that maximally induce aryl hydrocarbon hydroxylase activity (C57: 3 micrograms/kg, ip; DBA: 30 micrograms/kg, ip) or at doses approaching the LD50 value (C57: 150 micrograms/kg, ip; DBA: 600 micrograms/kg, ip). Hepatocytes isolated from untreated C57 and DBA mice had similar uptake of [14C]TCDD, and, at all doses, TCDD pretreatment increased [14C]TCDD uptake. The rates of hepatic TCDD metabolism over the first 2 hr of incubation were similar for control C57 and DBA mice, although some qualitative differences in metabolites were detected by HPLC. TCDD pretreatment at doses of 3 and 30 micrograms/kg for C57 and DBA mice, respectively, produced no detectable quantitative or qualitative changes in TCDD metabolism, despite increases in cytochrome P-450 content, 7-ethoxyresorufin O-deethylase (EROD) activity, and benzo[a]pyrene (BaP) metabolism. Pretreatment of C57 and DBA mice with the respective LD50 doses of TCDD decreased the rate of TCDD metabolism by hepatocytes, although cytochrome P-450 content, EROD activity, and BaP metabolism were increased. These results suggest that the uptake and the rate of hepatic metabolism of TCDD do not correlate with genetic differences at the murine Ah locus.

Animals↗
PubMedDate not supplied

Effect of monooxygenase inducers and inhibitors on the hepatic metabolism of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the rat and hamster.

The rat and hamster exhibit about a 100-fold difference in sensitivity to the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), with the hamster representing the most resistant species examined to date. The present study compared the induction and inhibition of hepatic TCDD metabolism in these species using suspensions of isolated hepatocytes. Purified 14C-TCDD or 3H-TCDD (2.2 microM) was incubated for 2-6 hr with hepatocytes isolated from untreated, TCDD-pretreated (5 micrograms/kg, ip), 3-methylcholanthrene-pretreated (3-MC, 50 mg/kg, ip, x 3 days), isosafrole-pretreated (ISO, 150 mg/kg, ip, x 3 days), or phenobarbital-pretreated (PB, 80 mg/kg, ip, x 3 days) rats and hamsters. Untreated rat and hamster hepatocytes metabolized TCDD at a similar rate (0.20 and 0.18 pmol/hr/mg, respectively). In both species, TCDD and 3-MC pretreatments elevated the rate of TCDD metabolism by 5-6-fold, while PB pretreatment had no effect. isosafrole modestly increased (1.8-2.5-fold) TCDD metabolism in each species. Analysis by high performance liquid chromatography indicated similarities in the TCDD-metabolite profiles formed by hepatocytes from both species, with two major metabolite peaks detected following induction by TCDD and 3-MC. The in vitro metabolism of TCDD in hepatocytes from TCDD-pretreated rats and hamsters was inhibited by 7,8-benzoflavone (100 microM), but not by metyrapone (100 microM). The effect of these cytochrome P-450 inducers and inhibitors on the metabolism of 3H-benzo(a)pyrene (BaP) in rat hepatocytes was similar to their effect on TCDD metabolism. However, marked differences were observed in their effects on the metabolism of BaP and TCDD in hamster hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗