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Biomedical subjects

H Mason

Publications and source records attributed to H Mason.

At least 37 records · Page 2Linked to original sources

Occupational hydrocarbon exposure and nephrotoxicity: a cohort study and literature review.

Hydrocarbon exposure has been shown to play an important role in the development of renal dysfunction in several occupational settings. In this study, renal screening was performed in a group of paint sprayers with exposure to hydrocarbon-based paints, recruited from a car manufacturing plant where personal protective equipment was widely used. The hydrocarbon exposure scores and various markers of renal injury were compared between these subjects and a group of paint sprayers from a previous study who did not use personal protective equipment regularly. Cumulative hydrocarbon exposure scores were calculated from a validated questionnaire. Serum creatinine, urinary total protein, albumin, transferrin, retinol-binding protein, and N-acetylglucosaminidase were evaluated, Both groups experienced heavy hydrocarbon exposure but sprayers who regularly used personal protective equipment had significantly reduced exposure scores due to improved skin and respiratory protection. A significant number of sprayers from both groups had elevated levels of serum creatinine. Interestingly, urinary N-acetylglucosaminidase activity, a marker of proximal tubular damage, was abnormal in a significant proportion of sprayers in the unprotected group but normal in those with improved protection. Our results are in keeping with the hypothesis that hydrocarbon exposure through paint spraying may result in active proximal tubular damage which may be reduced by improvement of protection at the worksite. However, renal impairment independent of tubular injury may result from chronic paint exposure, even with improved protection.

Adult↗

Local control of ovarian steroidogenesis.

A number of putative paracrine factors are now thought to interact with FSH in the control of ovarian steroidogenesis. The relative importance of these factors remains to be determined, but the presence of the insulin-like growth factors and their binding proteins and the mechanism of control of the latter through the local production of proteases suggests a role for this system in folliculogenesis. We have demonstrated over-production of steroid hormones in tissue from women with polycystic ovaries. Theca cells in monolayer culture produced excessive amounts of progesterone and androstenedione and granulosa cell oestradiol production was considerably enhanced in response to FSH. Recent evidence points to a genetic defect in the expression or translation of steroidogenic hormones as a cause of excess androgen production, but the gene or genes involved has not been established. Data from our group suggest that granulosa cells from anovulatory polycystic ovaries are prematurely matured and we hypothesize that this is due to the interaction of the raised circulating insulin levels with LH in these follicles, an interaction that results in arrested follicular growth.

Androgens↗

Genetic variants of microsomal metabolism and susceptibility to hydrocarbon-associated glomerulonephritis.

Hydrocarbon (HC) exposure can play a role in the development of chronic glomerulonephritis (GN). Interindividual variations in various metabolizing enzymes may influence HC biotransformation, and hence susceptibility to HC-associated GN. We evaluated the role of human genotypic polymorphism in HC-associated GN, in 41 patients (30 male, 11 female) with primary GN (17 diffuse mesangial proliferative GN, 12 focal segmental GN, 11 membranous GN, one membranoproliferative GN) and 60 (46 male, 14 female) healthy controls. Genotypic polymorphisms of (CYP) P450 2D6 (CYP2D6), glutathione S-transferases mu (GSTM1) and theta (GSTT1) and N-acetyltransferase (NAT-2) were determined using polymerase chain reaction analysis of white-blood-cell DNA. HC exposure scores were determined using a validated questionnaire, and were significantly elevated in GN patients compared to controls. While no significant differences in the various genotypic frequencies were observed in the GN group overall, compared to controls, there was a significant increase in GSTM1 null (n = 10) to GSTM1 wild type (n = 1), and NAT fast (n = 10) to slow (n = 1) acetylators, in the membranous GN group compared to controls (p < 0.05). These results suggest a possible role for GSTM1 null and NAT fast acetylator in the development of HC-associated membranous GN.

Acetyltransferases↗

Granulocyte-macrophage colony-stimulating factor: presence in human follicular fluid, protein secretion and mRNA expression by ovarian cells.

In recent years it has become evident that a leukocyte-cytokine network contributes to the paracrine regulation of ovarian function. The objectives of this study were to examine the presence of a potent lympho-haemopoietic cytokine, granulocyte-macrophage colony-stimulating factor (GM-CSF), in tissues and fluids from human ovaries. In a prospective study, follicular fluid and plasma were collected from naturally cycling women and women undergoing hyperstimulation for in-vitro fertilization (IVF). Granulosa-lutein cells were collected at the time of oocyte recovery for IVF and corpora lutea were collected at the time of hysterectomy for non-ovarian reasons. Culture supernatants from ovarian cell and tissue cultures were harvested on completion of a 48 h incubation. Immunoactive GM-CSF was measured by enzyme-linked immunosorbent assay, and was found to be present at statistically significantly higher levels in follicular fluid (8.9 +/- 0.7 pg/ml) and plasma (11.3 +/- 0.8 pg/ml) of women undergoing hyperstimulation compared to follicular fluid (5.3 +/- 0.3 pg/ml) and plasma (7.1 +/- 0.5 pg/ml) from naturally cycling women. Immunoactive GM-CSF was also detected in culture supernatants of granulosa-lutein cells (47.6 pg/10(5) cells), early luteal phase corpora lutea (0.52 pg/microgram DNA) and mid-luteal phase corpora lutea (0.98 pg/microgram DNA). Furthermore, transcripts for GM-CSF, and both the alpha and beta subunits of the GM-CSF receptor, were detected by reverse transcription polymerase chain reaction (RT-PCR) in granulosa-lutein cell culture preparations and corpora lutea collected during the early, mid- and late luteal phase of the menstrual cycle. These results show that GM-CSF is expressed and secreted by cells within the human ovary, and, together with the finding of expression of mRNA for GM-CSF receptor, suggest a role for GM-CSF in the local regulation of ovarian events.

Adult↗

Serum endothelin concentrations in workers exposed to vibration.

OBJECTIVES: Endothelin 1 (ET1) is one of a newly discovered family of potent naturally occurring vasoconstrictors produced by the endothelium. A few publications indicated that the peptide may have a role in idiopathic Raynaud's phenomenon and Raynaud's phenomenon secondary to connective tissue disease. The aim of this study was to compare serum endothelin concentrations in people with vibration induced white finger (VWF) with those of controls exposed to vibration, and unexposed (pure) controls. SUBJECTS AND METHODS: Male volunteers from a stonemasonry, two quarries, and an insurance company were classified by questionnaire and clinical examination into men with VWF (cases, n = 31), exposed controls (n = 22), or pure controls (n = 36). All subjects were asked to provide two venous blood specimens: a baseline sample after a period of warm equilibration (30 minutes seated in a warm room and 20 minutes with both hands immersed in a water bath at 37 degrees C); and again after cold challenge (both hands immersed in a water bath at 6 degrees C for six minutes). Serum concentrations of the 21 amino acid peptide endothelin ET1-21 were measured by radioimmunoassay. RESULTS: Baseline concentrations of ET1-21 were found to be lower in cases (mean = 12.2 pmol/l) than in the two control groups (mean = 14.7 pmol/l in exposed controls; mean = 14.3 pmol/l in pure controls). Among cases there was a broad inverse relation between severity, as measured by the Griffin blanching score, and baseline ET1-21 (Spearman rank correlation coefficient -0.58, P < 0.001). Cold challenge provoked an overall rise in ET1-21 in all groups, but larger and significant mean absolute and percentage rises were found in cases (4.1 pmol/l and 54%) than in the control groups (2.6 pmol/l and 21% in exposed controls; 1.5 pmol/l and 20% in pure controls). Similar but more obvious differences occurred when controls were compared with those cases who gave a more severe history of disease (Griffin blanching score > or = 24) and those cases found to blanch after cold challenge. In these case subsets baseline ET1-21 was nearly 50% lower than for controls and a four and a half to fivefold greater percentage rise in ET1-21 occurred upon cold challenge. Differences were significant. Close matching for age and smoking did not alter the principal findings. No significant differences, whether in baseline or cold response, were found between unexposed and exposed controls. CONCLUSIONS: Baseline findings seem to contradict various published series and attempts are made to reconcile the differences. It is suggested that a lower baseline ET1-21 in cases may result from a disease compensation mechanism or damage effect. The large relative rise in serum ET1-21 when cases are cold challenged may contribute directly or indirectly to vasospasm, but a simple mechanism is unlikely and interpretation is limited by the absence of measurements of forearm blood flow.

Adolescent↗

Modulation by insulin of follicle-stimulating hormone and luteinizing hormone actions in human granulosa cells of normal and polycystic ovaries.

Anovulation in polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia and insulin resistance, but it has been unclear whether the ovary is insulin resistant in women with PCOS. The aims of this study were, firstly, to determine whether human granulosa cells respond to physiological concentrations of insulin and, secondly, to investigate insulin and gonadotropin interactions in vitro in granulosa cells obtained from normal (N) and polycystic ovaries (PCO). Granulosa cells were incubated with insulin with or without gonadotropins for 48 h. Insulin augmented not only basal production of estradiol and progesterone, but also LH-stimulated steroid accumulation in granulosa cell cultures from N and PCO. Insulin enhanced FSH-stimulated progesterone production by granulosa cells from N and PCO, but the effect on FSH-stimulated estradiol production was variable, ranging from no effect for granulosa cells from N to synergistic for granulosa cells from PCO of anovulatory subjects. Preincubation with insulin for 48 h increased subsequent basal and LH-induced, but not FSH-stimulated, steroid production. These data demonstrate that granulosa cells from PCO respond to insulin despite the association, in vivo, of PCOS with peripheral insulin resistance. Insulin preincubation enhances the subsequent response of human granulosa cells to LH. We propose that in anovulatory women with PCOS, elevated levels of insulin interacting with LH may contribute to the mechanism of anovulation.

Adult↗

Tubular damage in microalbuminuric patients with primary glomerulonephritis and diabetic nephropathy.

Tubular damage as suggested by enzymuria and tubular proteinuria is a recognized feature of glomerulonephritis (GN) with clinical proteinuria and both incipient and overt diabetic nephropathy (DN). However, little is known about the presence of tubulopathy in patients with primary GN, microalbuminuria [albumin excretion (AER) 30-300 mg/d] and microhematuria. Three groups were studied. The GN group comprised 17 (2 F) patients with biopsy-proven GN with microalbuminuria. The DN group comprised 35 (14 F) patients with incipient diabetic nephropathy with AER 30-300 mg/d, and controls comprised 38 (15 F) normal subjects with normal AER < 30 mg/d. Serum creatinine, albuminurinuria, transferrinuria, and markers of tubular damage such as urinary excretion of N-acetyl-glucosaminidase (NAG), leucine aminopeptidase (LAP), gamma-glutamyl transferase (gGT), and retinol binding protein (RBP) were measured. GN and DN had comparable degrees of albuminuria, transferrinuria, and LAP excretion, and these were significantly higher than controls. Serum creatinine was significantly higher in GN than DN and controls. DN had significantly higher NAG and RBP, and lower gGT than GN and controls. In both GN and DN groups, both glomerular proteins correlated with each other and NAG correlated significantly to LAP and gGT. Albuminuria correlated to tubular enzymuria in GN group but not in patients with DN. The results suggest that tubular damage is less marked in microalbuminuric patients with GN than those with DN despite similar degree of glomerular proteinuria. The pattern of tubulopathy is also different in the two groups, indicating differences in the pathogenesis of tubular damage in these two clinical settings.

Acetylglucosaminidase↗

Biochemical markers of basement membrane disturbances and occupational exposure to hydrocarbons and mixed solvents.

To investigate possible mechanisms of hydrocarbon or solvent-induced renal damage, we studied three groups of healthy men employed in a UK manufacturing plant. Group 1 (n = 111) were occupationally exposed to hydrocarbon-based paints, Group 2 (n = 100) were occupationally exposed to petroleum-based mineral oils, and Group 3 (n = 92) had low background occupational exposure to hydrocarbons. Occupational atmospheric exposure levels for toluene, xylene, butanol and oil mist around the time of this study were within UK permissible limits. Group 4 (controls) were males with no known occupational hydrocarbon or solvent exposure (n = 108). Circulating laminin antibodies and the auto-antibody implicated in Goodpasture's syndrome (anti-GBM) were measured, as were serum laminin, a basement membrane turnover marker, and soluble E-selectin, an endothelial activation marker. Group 1 had a significantly greater proportion of subjects with high levels of both anti-laminin antibodies and soluble E-selectin; Group 2 had significantly more subjects with raised anti-GBM antibodies, laminin and soluble E-selectin. Mean levels of soluble E-selectin were increased in Groups 1 and 2. In a small but significant proportion of these workers exposed to hydrocarbons/mixed solvents there are alterations both to basement membranes, resulting in auto-antibody production, and to overlying vascular endothelial cells.

Adult↗

Occupational hydrocarbon exposure and diabetic nephropathy.

Exposure to hydrocarbons has been implicated in the pathogenesis of glomerulonephritis but its role in the development of diabetic nephropathy remains unknown. Three groups of patients with Type 1 diabetes of over 10 years duration were studied. Group 1 comprised 45 patients (23 F) with no diabetic nephropathy (urinary albumin excretion (AER) < 30 mg 24 h-1), group 2 comprised 37 patients (17 F) with incipient diabetic nephropathy (AER between 30-300 mg 24 h-1), and group 3 comprised 31 patients (15 F) with overt diabetic nephropathy (AER > 300 mg 24 h-1). The groups were comparable for age, sex, duration of diabetes, recent glycaemic control, social class, and residential area. Patients were assessed blindly by a validated questionnaire and interview for hydrocarbon exposure, consumption of tobacco, analgesic agents, and alcohol. Exposure scores to hydrocarbons derived from the questionnaire were significantly higher in patients with incipient and overt diabetic nephropathy with smoking adjusted odds ratios of 3.6 and 5.2, respectively. The consumption of alcohol, analgesic agents, tobacco, and smoking habits were similar in the three groups. In conclusion, hydrocarbon exposure may be a key environmental factor in the development of diabetic nephropathy in patients with Type 1 diabetes.

Adult↗

Tubulopathy with macroalbuminuria due to diabetic nephropathy and primary glomerulonephritis.

Tubular damage is a recognized feature of both overt diabetic nephropathy and glomerulonephritis. However, the pattern and mechanism of tubular damage in the two clinical settings remain unclear. Two groups of patients with macroalbuminuria (albuminuria > 300 mg/day) were studied. Group 1 comprised 41 patients with biopsy proven primary glomerulonephritis and group 2 comprised 28 patients with clinical diabetic nephropathy due to insulin dependent diabetes mellitus. Serum creatinine, creatinine clearance, glomerular proteinuria (albuminuria and transferrinuria), markers of tubular damage such as urinary excretion of lysosomal enzyme (N-acetyl glucosaminidase), brush border enzymes (leucine aminopeptidase and gamma-glutamyl transferase) and retinol binding protein (tubular protein) were measured. Both groups were comparable in serum creatinine, creatinine clearance, glomerular proteinuria and excretion of N-acetyl-glucosaminidase. However, a significantly higher degree of tubular brush border enzymuria and a lower level of tubular proteinuria were seen in group 1 than in group 2. In group 1, albuminuria correlated to tubular enzymuria and tubular proteinuria. However, there was no correlation in diabetic patients between parameters of glomerular and tubular damage or dysfunction. The data presented suggested that the pattern of tubulopathy is different in patients with comparable degree of macroalbuminuria due to diabetic nephropathy and glomerulonephritis. Moreover, in diabetic nephropathy contrary to glomerulonephritis, markers of tubular damage are unrelated to glomerular proteinuria. This may suggest different mechanisms of tubular damage in the two clinical settings. We recommended that in all patients with proteinuria, particularly those with diabetic nephropathy, markers of renal tubular damage may be useful in monitoring the course of their disease.

Acetylglucosaminidase↗

Evidence of oxidant injury and tubular damage in early diabetic nephropathy.

Two groups of patients with insulin-dependent diabetes mellitus of > 10 years duration and either persistent normoalbuminuria (group 1, n = 49; albumin excretion < 30 mg/day) or microalbuminuria (group 2, n = 33; albumin excretion 30-300 mg/day) were investigated for evidence of free oxygen radical activity (erythrocytic superoxide dismutase and glutathione peroxidase) and oxidant injury (serum malondialdehyde). Glomerular proteinuria (albuminuria, transferrinuria), tubular proteinuria (retinol-binding protein) and tubular enzymuria (N-acetyl-glucosaminidase and leucine aminopeptidase) were also measured. Healthy controls (n = 38) were matched for age and sex. Groups 1 and 2 were similar in terms of age, sex, duration of diabetes and recent glycaemic control. Serum cholesterol and creatinine were similar in all three groups. Free-radical activity and oxidant injury were significantly higher in groups 1 and 2 than in controls (p < 0.001). Glomerular proteinuria, tubular proteinuria and enzymuria were significantly higher in group 2 than in group 1 and controls (p < 0.01). Group 1 had significantly higher transferrinuria, tubular enzymuria and tubular proteinuria than controls. However, groups 1 and 2 were similar in degree of free oxygen radical generation and oxidant injury. In diabetic nephropathy, oxidant injury and renal tubular damage accompany and may even precede microalbuminuria. The presence of these abnormalities in the absence of glomerular proteinuria favours the hypothesis that alterations first occur in the peritubular microcirculation, which by causing oxidant injury and tubular damage, may initiate diabetic nephropathy.

Adult↗

Relationship between markers of endothelial dysfunction, oxidant injury and tubular damage in patients with insulin-dependent diabetes mellitus.

1. Diabetic nephropathy is a serious microvascular complication in patients with insulin-dependent diabetes mellitus, resulting in end-stage renal disease in 30-45% of such patients. Despite intensive investigation, the pathophysiology of diabetic renal disease has not been fully elucidated. However, several clinical and experimental studies have suggested that endothelial dysfunction and free-radical activity may be important factors. 2. Forty normotensive patients with insulin-dependent diabetes mellitus of between 10 and 20 years duration with persistent normoalbuminuria (albumin excretion < 30 mg/day) and normal renal function were investigated for markers of endothelial dysfunction (plasma von Willebrand factor, soluble thrombomodulin and angiotensin-converting enzyme activity), free oxygen radical generation (erythrocytic superoxide dismutase and glutathione peroxidase) and oxidant injury (serum malondialdehyde). Glomerular proteinuria (albuminuria, transferrinuria), tubular proteinuria (retinol-binding protein) and tubular enzymuria (N-acetyl glucosaminidase and leucine aminopeptidase) were also measured. 3. Patients were divided into two groups. Group 1 comprised 21 patients with elevated markers of endothelial dysfunction, and group 2 comprised 19 patients with normal levels of plasma von Willebrand factor, soluble thrombomodulin and angiotensin-converting enzyme activity. Thirty-eight healthy subjects matched for age and sex acted as controls. 4. Groups 1 and 2 were similar in age, sex, body weight, duration of diabetes mellitus and recent glycaemic control. Serum cholesterol, serum creatinine and glomerular proteinuria were similar in the three groups. Group 1 patients had significantly increased oxidant injury, tubular enzymuria and proteinuria compared with group 2 patients and control subjects (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Hydrocarbon exposure and tubular damage: additional factors in the progression of renal failure in primary glomerulonephritis.

To investigate the role of hydrocarbon exposure in the progression of glomerulonephritis, 68 patients (12 female) with biopsy-proven primary glomerulonephritis (60 proliferative cases, 8 membranous) were blindly assessed for chronic hydrocarbon exposure by a validated questionnaire. Serum creatinine, proteinuria, and urinary excretion of markers of renal tubular damage were measured. Patients were assessed for evidence of progressive renal failure (PRF) (defined as persistent rise of serum creatinine > 50 mumol/l above the baseline) during a mean follow up period of 5 years. Patients were divided according to the presence or absence of PRF, (group 1, n = 29, with PRF) and (group 2, n = 39, without PRF). The two groups were comparable in age, sex, duration of diagnosis (since the time of biopsy) and blood pressure control. The derived chronic hydrocarbon exposure scores were significantly higher in group 1 than 2 (p < 0.001). Moreover, hydrocarbon exposure score since the diagnosis of glomerulonephritis was significantly higher in group 1 than 2 (p < 0.001). In group 1, 73% of patients continued to be exposed to hydrocarbons at their work site after the diagnosis of glomerulonephritis, compared to only 13% in group 2 (p < 0.001). At renal biopsy, group 1 had a significantly higher mean serum creatinine than group 2 but the degree of proteinuria and proportion of patients with hypertension were similar. During follow-up serum creatinine rose significantly in group 1 but not in group 2. In group 2, proteinuria fell significantly during follow-up but remained unchanged in group 1. A higher proportion of patients from group 1 developed hypertension requiring antihypertensive drugs (84% vs. 28%; p < 0.001). Urinary marker secretion data indicated a possible association between tubular damage and renal impairment. These results suggest that chronic hydrocarbon exposure and renal tubular damage are important additional risk factors in the progression of primary glomerulonephritis.

Acetylglucosaminidase↗

Renal impairment with chronic hydrocarbon exposure.

Occupational hydrocarbon exposure is believed by some investigators to play an important role in the development of several non-neoplastic renal diseases. In view of the continuing debate in this area of nephrology we adopted a cross-sectional approach by investigating the prevalence of clinical or sub-clinical renal dysfunction in subjects chronically exposed to hydrocarbons at their work site. Three groups of healthy men working in different and separate areas of a major car manufacturing plant in the North-west of England participated in the study. Group 1 comprised 112 paint sprayers with exposure to paint-based hydrocarbons, group 2 comprised 101 volunteers working in the transmission area of the plant with exposure to petroleum-based mineral oils, and group 3 comprised 92 automated press operators with minimal background exposure to lubricants who acted as internal controls. Early markers of renal dysfunction such as serum creatinine, urinary total protein, albumin, transferrin, retinol binding protein, N-acetyl-glucosaminidase, gamma-glutamyl transferase, and leucine-amino-peptidase excretion were measured. Upper reference values of the parameters measured were derived from 105 comparable laboratory based controls with no occupational exposure to hydrocarbons or heavy metals. Group 1 had a significantly higher prevalence of elevated serum creatinine than the other groups and a higher prevalence of abnormal urinary total protein, N-acetyl-glucosaminidase, gamma-glutamyl transferase, and leucine-amino-peptidase excretion than groups 2 and 3. Group 2 had normal serum creatinine but a significantly higher prevalence of abnormal urinary total protein, transferrin, retinol binding protein, N-acetyl-glucosaminidase, and leucine-amino-peptidase excretion than group 3. Serum albumin was similar in all groups. There was some clustering of abnormal findings but the markers of renal dysfunction used in the study identified 37 individuals in group 1 and 31 subjects in group 2 with at least one abnormal parameter, compared to only five individuals in internal controls. This difference between the two target groups and group 3 was highly significant (p < 0.001). Subjects with chronic paint exposure had renal impairment and tubular dysfunction. Tubular dysfunction was also prominent with petroleum oil exposure. We therefore conclude that chronic hydrocarbon exposure may be associated with clinical and sub-clinical renal dysfunction. We advocate careful monitoring of workers exposure to hydrocarbons and for more effective preventive measures.

Adult↗

A sensitive assay for detection and measurement of neutralising antibody to human immunodeficiency virus.

An assay based on the inhibition of syncytium formation in C8166 cells was developed to measure low levels of neutralising antibody (NT-AB) to human immunodeficiency virus (HIV) and to detect cross-reactivity between virus strains. The relationship between virus challenge and antibody titre was represented by a tripartite curve which was essentially linear over moderate levels of virus input. Based on these findings, antibody titres were standardised against 100 TCID50 of challenge virus. However, lower virus inocula were found to detect minimum levels of antibody. Reproducibility of antibody titres between tests was high, with variation generally lying within one dilution step. The improved sensitivity of the technique allowed detection of NT-ABs in animals immunised with immune-stimulating complexes (ISCOMS) incorporating HIV antigens. Consistent levels of cross-reactivity between HIV strains was demonstrated, indicating the presence of distinct viral groups, from which dominant isolates may be chosen for use in vaccination studies.

Animals↗

The influence of skin structure on permeability: an intersite and interspecies comparison with hydrophilic penetrants.

For reasons that are unclear, skin from various body sites has different permeability properties. We have used hydrophilic penetrants (water, ethanol, mannitol, and paraquat) to study the in vitro permeability of skin from marmoset (eight body sites), man, and rat. Skin structure (stratum corneum thickness and number of cell layers; epidermal and dermal thickness; number and area of hair follicle openings per mm2) was compared with permeability. There was no apparent relationship between skin structure and permeability to the most rapid penetrants, water and ethanol. Follicle area opening was the structural feature that varied most between species and between body sites. Different marmoset body sites showed a threefold range in follicle area but this did not appear to influence the absorption rates of the test penetrants. However, among the species there was an 80-times range in follicle area, which correlated with the observed differences in rate of mannitol and paraquat absorption. Thus, permeability could be related to inter-species differences in skin structure, but only with the relatively slowly absorbed test penetrants, mannitol and paraquat.

Animals↗

Ozone and ultraviolet light act as additive cocarcinogens to induce in vitro neoplastic transformation.

Ozone, a major chemical oxidant in our environment, is an environmental air pollutant with putative carcinogenic action. Using in vitro transformation, we report for the first time that ozone (6 ppm for 10 min) acts in additive fashion with ultraviolet light (4 J/m2) to produce enhanced levels of transformation in hamster embryo cells and mouse C3H/10T-1/2 cells as compared to rats induced by each of the agents alone. The results underscore the hazard of ozone as a toxic pollutant which may have putative carcinogenic effects and interact with other environmental carcinogens.

Air Pollutants↗