Radiation shielding in dentistry: an update.

The purpose of this article was to review the literature and provide guidelines on the use of radiation protection for patients in the dental setting. There are limited published data on the effects of low radiation doses such as those used in dental radiology. Most of the evidence is subject to bias, with risk models extrapolated from higher dose models such as studies of the Hiroshima bomb survivors. However, the lack of evidence does not denote the absence of risk, as there is no established 'safe' level of radiation exposure. All imaging utilizing ionizing radiation carries a risk for the patient. Hence the patient benefits of imaging must outweigh the potential risk. All diagnostic imaging should adhere to three basic principles, these being justification, optimization and application of dose limits. This article discusses dose reduction techniques and shielding of sensitive organs, particularly the thyroid, during procedures such as intraoral imaging, orthopantomograms and imaging of the pregnant patient.

Thromboxane receptor stimulation associated with loss of SKCa activity and reduced EDHF responses in the rat isolated mesenteric artery.

1. The possibility that thromboxane (TXA(2)) receptor stimulation causes differential block of the SK(Ca) and IK(Ca) channels which underlie EDHF-mediated vascular smooth muscle hyperpolarization and relaxation was investigated in the rat isolated mesenteric artery. 2. Acetylcholine (30 nm-3 microm ACh) or cyclopiazonic acid (10 microm CPA, SERCA inhibitor) were used to stimulate EDHF-evoked smooth muscle hyperpolarization. In each case, this led to maximal hyperpolarization of around 20 mV, which was sensitive to block with 50 nm apamin and abolished by repeated stimulation of mesenteric arteries with the thromboxane mimetic, U46619 (30 nm-0.1 microm), but not the alpha(1)-adrenoceptor agonist phenylephrine (PE). 3. The ability of U46619 to abolish EDHF-evoked smooth muscle hyperpolarization was prevented by prior exposure of mesenteric arteries to the TXA(2) receptor antagonist 1 microm SQ29548. 4. Similar-sized smooth muscle hyperpolarization evoked with the SK(Ca) activator 100 microm riluzole was also abolished by prior stimulation with U46619, while direct muscle hyperpolarization in response to either levcromakalim (1 microm, K(ATP) activator) or NS1619 (40 microm, BK(Ca) activator) was unaffected. 5. During smooth muscle contraction and depolarization to either PE or U46619, ACh evoked concentration-dependent hyperpolarization (to -67 mV) and complete relaxation. These responses were well maintained during repeated stimulation with PE, but with U46619 there was a progressive decline, so that during a third exposure to U46619 maximum hyperpolarization only reached -52 mV and relaxation was reduced by 20%. This relaxation could now be blocked with charybdotoxin alone. The latter responses could be mimicked with 300 microm 1-EBIO (IK(Ca) activator), an action not modified by exposure to U46619. 6. An early consequence of TXA(2) receptor stimulation is a reduction in the arterial hyperpolarization and relaxation attributed to EDHF. This effect appears to reflect a loss of SK(Ca) activity.

Small- and intermediate-conductance calcium-activated K+ channels provide different facets of endothelium-dependent hyperpolarization in rat mesenteric artery.

Activation of both small-conductance (SKCa) and intermediate-conductance (IKCa) Ca2+-activated K+ channels in endothelial cells leads to vascular smooth muscle hyperpolarization and relaxation in rat mesenteric arteries. The contribution that each endothelial K+ channel type makes to the smooth muscle hyperpolarization is unknown. In the presence of a nitric oxide (NO) synthase inhibitor, ACh evoked endothelium and concentration-dependent smooth muscle hyperpolarization, increasing the resting potential (approx. -53 mV) by around 20 mV at 3 microM. Similar hyperpolarization was evoked with cyclopiazonic acid (10 microM, an inhibitor of sarcoplasmic endoplasmic reticulum calcium ATPase (SERCA)) while 1-EBIO (300 microM, an IKCa activator) only increased the potential by a few millivolts. Hyperpolarization in response to either ACh or CPA was abolished with apamin (50 nM, an SKCa blocker) but was unaltered by 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (1 microM TRAM-34, an IKCa blocker). During depolarization and contraction in response to phenylephrine (PE), ACh still increased the membrane potential to around -70 mV, but with apamin present the membrane potential only increased just beyond the original resting potential (circa -58 mV). TRAM-34 alone did not affect hyperpolarization to ACh but, in combination with apamin, ACh-evoked hyperpolarization was completely abolished. These data suggest that true endothelium-dependent hyperpolarization of smooth muscle cells in response to ACh is attributable to SKCa channels, whereas IKCa channels play an important role during the ACh-mediated repolarization phase only observed following depolarization.

Evidence for a differential cellular distribution of inward rectifier K channels in the rat isolated mesenteric artery.

The distribution of functionally active, inwardly rectifying K (K(IR)) channels was investigated in the rat small mesenteric artery using both freshly isolated smooth muscle and endothelial cells and small arterial segments. In Ca(2+)-free solution, endothelial cells displayed a K(IR) current with a maximum amplitude of 190 +/- 16 pA at -150 mV and sensitivity to block with 30 microM Ba(2+) (n = 7). In smooth muscle cells, outward K current was activated at around -47 +/- 3 mV, but there was no evidence of K(IR) current (n = 6). Furthermore, raising extracellular [K(+)] to either 60 or 140 mM, or applying the alpha(1)-adrenoceptor agonist phenylephrine (PE; 30 microM), failed to reveal an inwardly rectifying current in the smooth muscle cells, although PE did stimulate an iberiotoxin-sensitive outward K current (n = 4). Exogenous K(+) (10.8-16.8 mM) both relaxed and repolarized endothelium-denuded segments of the mesenteric artery contracted with PE. These effects were depressed by 100 microM ouabain but unaffected by either 30 microM BaCl(2) or 3 microM glibenclamide. These data suggest that functional, inwardly rectifying Ba(2+)-sensitive channels are restricted to the endothelial cell layer in the rat small mesenteric artery.

Cellular coupling and conducted vasomotor responses.

1. The present brief review examines the concept of spreading vasodilator responses in arteriolar trees, its physiological relevance and possible mechanisms. 2. The most likely mechanisms involve spread of hyperpolarization through tissues in the vessel wall, made possible by electrical coupling between the cells. It is generally agreed that there is coupling between cells within the muscle and endothelial layers, but coupling between the two layers is not always present. 3. The passive electrical properties of arterioles can be modelled, using different techniques depending on the complexity of branching of the arteriolar tree. Comparison of experimental results with the model indicates that hyperpolarization can spread further than expected from passive properties alone, implying that spreading vasodilatation may be an active process.

Activation of endothelial cell IK(Ca) with 1-ethyl-2-benzimidazolinone evokes smooth muscle hyperpolarization in rat isolated mesenteric artery.

1. In rat small mesenteric arteries contracted with phenylephrine, 1-ethyl-2-benzimidazolinone (1-EBIO; 3-300 microM) evoked concentration-dependent relaxation that, above 100 microM, was associated with smooth muscle hyperpolarization. 2. 1-EBIO-evoked hyperpolarization (maximum 22.1+/-3.6 mV with 300 microM, n=4) was endothelium-dependent and inhibited by charybdotoxin (ChTX 100 nM; n=4) but not iberiotoxin (IbTX 100 nM; n=4). 3. In endothelium-intact arteries, smooth muscle relaxation to 1-EBIO was not altered by either of the potassium channel blockers ChTX (100 nM; n=7), or IbTX (100 nM; n=4), or raised extracellular K(+) (25 mM). Removal of the endothelium shifted the relaxation curve to the right but did not reduce the maximum relaxation. 4. In freshly isolated mesenteric endothelial cells, 1-EBIO (600 microM) evoked a ChTX-sensitive outward K-current. In contrast, 1-EBIO had no effect on smooth muscle cell conductance whereas NS 1619 (33 microM) stimulated an outward current while having no effect on the endothelial cells. 5. These data show that with concentrations greater than 100 microM, 1-EBIO selectively activates outward current in endothelial cells, which presumably underlies the smooth muscle hyperpolarization and a component of the relaxation. Sensitivity to block with charybdotoxin but not iberiotoxin indicates this current is due to activation of IK(Ca). However, 1-EBIO can also relax the smooth muscle by an undefined mechanism, independent of any change in membrane potential.

Electrical coupling between smooth muscle and endothelium in arterioles of the guinea-pig small intestine.

Equations describing the steady-state passive electrical properties of arterioles have been derived. The arteriole was modelled as having two thin layers of cells (muscle and endothelium) with strong electrical coupling between cells within a layer and variable coupling between the layers. The model indicated that spread of membrane potential changes was highly dependent on the thickness of cells within the layers. The model was also used to identify the optimal experimental strategy for detecting coupling between the two layers, and experiments were carried out on arterioles from the guinea-pig small intestine. Thickness of the endothelial layer was measured using electron microscopy and was found to be around 0.5 microm. Electrical input resistance was measured in intact arterioles and compared to input resistance of arterioles from which the endothelium had been removed. The experiments confirmed that there was a strong electrical coupling between the muscle and endothelium in these vessels.

Simulating the spread of membrane potential changes in arteriolar networks.

OBJECTIVE: Our aim was to simulate the spread of membrane potential changes in microvascular trees and then make the simulation programs accessible to other researchers. We have applied our simulations to demonstrate the implications of electrical coupling between arteriolar smooth muscle and endothelium. METHODS: A two-layered, cable-like model of an arteriole was used, and the assumptions involved in the approach explicitly stated. Several common experimental situations that involve the passive spread of membrane potential changes in microvascular trees were simulated. The calculations were performed using NEURON, a well-established computer simulation program that we have modified for use with vascular trees. RESULTS: Simulated results show that membrane potential changes would probably not spread as far in the endothelium as they would in the smooth muscle of arterioles. Where feed arteries are connected to larger distributing arteries, passive spread alone may not explain the physiologically observed spread of diameter changes. CONCLUSIONS: Simulated results suggest that the morphology of an arteriole, in which the muscle layer is much thicker than the endothelium, favors electrical conduction along smooth muscle rather than the endothelium. However, it seems that passive electrical spread is insufficient to explain the apparent spread of membrane potential changes in experimental situations. Active responses involving voltage-dependent conductances may be involved, and these can also be included in our simulation.

Electrophysiological basis of arteriolar vasomotion in vivo.

We tested the hypothesis that cyclic changes in membrane potential (E(m)) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (approximately 3 min(-1)) were preceded (approximately 3 s) by oscillations in E(m) of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E(m) were resolved into six phases: (1) a period (6 +/- 2 s) at the most negative E(m) observed during vasomotion (-46 +/- 2 mV) correlating (r = 0.87, p < 0.01) with time (8 +/- 2 s) at the largest diameter observed during vasomotion (41 +/- 2 microm); (2) a slow depolarization (1.8 +/- 0.2 mV s(-1)) with no diameter change; (3) a fast (9.1 +/- 0.8 mV s(-1)) depolarization (to -28 +/- 2 mV) and constriction; (4) a transient partial repolarization (3-4 mV); (5) a sustained (5 +/- 1 s) depolarization (-28 +/- 2 mV) correlating (r = 0.78, p < 0.01) with time (3 +/- 1 s) at the smallest diameter (27 +/- 2 microm) during vasomotion; (6) a slow repolarization (2.5 +/- 0.2 mV s(-1)) and relaxation. The absolute change in E(m) correlated (r = 0.60, p < 0.01) with the most negative E(m). Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO(2) caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E(m) of SMC and EC corresponding with cation fluxes across plasma membranes.

An equation describing spread of membrane potential changes in a short segment of blood vessel.

The spread of membrane potential changes throughout certain cells and tissues plays an important role in their physiology. The attenuation of such changes in any tissue is usually characterized by the cable length constant lambda, which can be determined experimentally if the equations describing membrane potential spread in the tissue are known. Here we derive an equation describing spread of membrane potential changes in a short cable, which is an appropriate model for short segments of blood vessels. This equation is more general than those already published in that the positions of both the current source that gives rise to a potential change, and the point at which the change is measured, can be anywhere along the cable.

Bone mineral density and broadband ultrasound attenuation with estrogen treatment of postmenopausal women.

The purpose of the current study was to determine the changes in lumbar spine, hip, and calcaneus bone mineral density (BMD), and in calcaneus broadband ultrasound attenuation (BUA) in early menopausal women and to assess the effects of estrogen replacement therapy (ERT) on bone mass at these sites over a 2-yr period. Fifty-three Caucasian women who were at least 6 mo postmenopausal were divided into two groups based on estrogen use. Twenty-one women, average age 53.0 +/- 0.6 yr and 2.9 +/- 0.3 yr since menopause, had been receiving estrogen in combination with progesterone for at least 6 mo prior to enrollment in the study. Thirty-two women, average age 52.7 +/- 0.8 yr and 2.8 +/- 0.3 yr since menopause, had never received ERT. During the 2-yr study, women not receiving ERT had significant decreases in BMD of the spine -2.3 +/- 0.6%, femoral neck -2.2 +/- 0.8%, and calcaneus -4.7 +/- 0.9%, and in BUA of the calcaneus -14.3 +/- 1.8%. ERT prevented the decreases in BMD at the spine +0.4 +/- 0.6% and calcaneus -2.3 +/- 1.1%, but did not prevent a significant decrease in bone mass at the femoral neck -1.9 +/- 0.8% and BUA at the calcaneus -17.8 +/- 3.2%. Neither group had significant decreases in total hip BMD. This study demonstrates again that ERT prevents the menopause-associated decreases in spine BMD. However, in this group of women, ERT did not prevent loss in femoral neck BMD or BUA. The results suggest that women being treated with estrogen for maintenance of BMD in early menopause need to be monitored to ensure efficacy of therapy, especially in the maintenance of femoral neck BMD.

Symptoms of hand-arm vibration syndrome in gas distribution operatives.

OBJECTIVES: To survey the prevalence and severity of hand-arm vibration syndrome symptoms (HAVS), and to estimate past and current exposure to hand held vibrating tools in a sample of gas distribution operatives breaking and re-instating road surfaces. METHODS: 153 gas distribution operatives (participation rate 81%) from three company districts were assessed by an administered questionnaire, a clinical examination, and a simple cold challenge test to the hands. Exposure histories were taken aided by a picture album of past and current tools. Information was obtained from several sources on the likely vibratory characteristics of those tools. Estimates were thus obtained of the frequency of blanching and neurological complaints in operatives, and of their lifetime hours of exposure and lifetime dose of vibration. RESULTS: On average, the sample had spent 16 years in employment involving use of vibratory tools. 24% had symptoms or signs of blanching after use of tools in the industry; 46% had troublesome persistent complaints of paraesthesiae or numbness, and these symptoms extended into the hands or arms in 18% of workers. In 5.9% the distribution of symptoms was suggestive of carpal tunnel syndrome; and of ulnar nerve entrapment in a further 3.9%. The risks of blanching and neurological complaints rose significantly with lifetime hours of use of vibrating tools and lifetime dose of vibration. Symptoms were generally mild and apparent only after a prolonged interval, but there were exceptions, and cases had occurred after lower recent exposures. CONCLUSIONS: It has been suggested that aspects of the gas distribution operative's work mitigate against the risk normally anticipated from use of pneumatic road breaking tools. By contrast our data suggest that symptoms of HAVS do occur, given sufficient exposure, a finding relevant not only to gas supply workers, but also to workers from other industries who break and repair road surfaces.

Secular trends in bloodstream infection caused by antimicrobial-resistant bacteria in New Jersey hospitals, 1991 to 1995.

INTRODUCTION: Antimicrobial resistance among bacteria is an increasing public health problem. In 1991, New Jersey was the first state to establish statewide, hospital-based surveillance for antimicrobial-resistant bacteria. METHODS: Each month, all 96 nonfederal New Jersey hospital laboratories complete a form listing the species identity and drug susceptibility results for selected antimicrobial-resistant bacteria isolated from blood cultures from hospital inpatients. Penicillin-resistant Streptococcus pneumoniae and aminoglycoside-resistant gram-negative rods were studied from 1991 to 1995. Vancomycin-resistant enterococci and imipenem-resistant gram-negative rods were studied from 1992 through 1995. RESULTS: From 1992 to 1995, the vancomycin-resistant enterococci bloodstream infection prevalence rate increased from 11 to 29 per 100,000 hospital admissions (p < 0.001); the rate was higher at larger hospitals, urban and inner-city hospitals, and teaching hospitals. From 1991 to 1995, the penicillin-resistant S. pneumoniae bloodstream infection rate increased from 1.1 to 9.9 per 100,000 admissions (p < 0.001). In contrast, bloodstream infection rates did not change significantly for imipenem-resistant (12.5 during 1992 and 14.1 during 1995, p = 0.4) or aminoglycoside-resistant (8.0 during 1991 and 6.8 during 1995, p = 0.4) gram-negative rods. CONCLUSIONS: We found that vancomycin-resistant enterococci and penicillin-resistant S. pneumoniae, but neither of two groups of antimicrobial-resistant gram-negative rods, are increasing rapidly in prevalence in New Jersey. Continued monitoring and interventions to slow these increases are needed.

Ectopic bone formation by marrow stromal osteoblast transplantation using poly(DL-lactic-co-glycolic acid) foams implanted into the rat mesentery.

Porous biodegradable poly(DL-lactic-co-glycolic acid) foams were seeded with rat marrow stromal cells and implanted into the rat mesentery to investigate in vivo bone formation at an ectopic site. Cells were seeded at a density of 6.83 x 10(5) cells/cm2 onto polymer foams having pore sizes ranging from either 150 to 300 to 710 microns and cultured for 7 days in vitro prior to implantation. The polymer/cell constructs were harvested after 1, 7, 28, or 49 days in vivo and processed for histology and gel permeation chromatography. Visual observation of hematoxylin and eosin-stained sections and von Kossa-stained sections revealed the formation of mineralized bonelike tissue in the constructs within 7 days postimplantation. Ingrowth of vascular tissue was also found adjacent to the islands of bone, supplying the necessary metabolic requirements to the newly formed tissue. Mineralization and bone tissue formation were investigated by histomorphometry. The average penetration depth of mineralized tissue in the construct ranged from 190 +/- 50 microns for foams with 500-710-microns pores to 370 +/- 160 microns for foams with 150-300-microns pores after 49 days in vivo. The mineralized bone volume per surface area and total bone volume per surface area had maximal values of 0.28 +/- 0.21 mm (500-710-microns pore size, day 28) and 0.038 +/- 0.024 mm (150-300-microns, day 28), respectively. As much as 11% of the foam volume penetrated by bone tissue was filled with mineralized tissue. No significant trends over time were observed for any of the measured values (penetration depth, bone volume/surface area, or percent mineralized bone volume). These results suggest the feasibility of bone formation by osteoblast transplantation in an orthotopic site where not only bone formation from transplanted cells but also ingrowth from adjacent bone may occur.

Bone formation by three-dimensional stromal osteoblast culture in biodegradable polymer scaffolds.

Bone formation was investigated in vitro by culturing stromal osteoblasts in three-dimensional (3-D), biodegradable poly(DL-lactic-co-glycolic acid) foams. Three polymer foam pore sizes, ranging from 150-300, 300-500, and 500-710 microns, and two different cell seeding densities, 6.83 x 10(5) cells/cm2 and 22.1 x 10(5) cells/cm2, were examined over a 56-day culture period. The polymer foams supported the proliferation of seeded osteoblasts as well as their differentiated function, as demonstrated by high alkaline phosphatase activity and deposition of a mineralized matrix by the cells. Cell number, alkaline phosphatase activity, and mineral deposition increased significantly over time for all the polymer foams. Osteoblast foam constructs created by seeding 6.83 x 10(5) cells/cm2 on foams with 300-500 microns pores resulted in a cell density of 4.63 x 10(5) cells/cm2 after 1 day in culture; they had alkaline phosphatase activities of 4.28 x 10(-7) and 2.91 x 10(-6) mumol/cell/min on Days 7 and 28, respectively; and they had a cell density that increased to 18.7 x 10(5) cells/cm2 by Day 56. For the same constructs, the mineralized matrix reached a maximum penetration depth of 240 microns from the top surface of the foam and a value of 0.083 mm for mineralized tissue volume per unit of cross sectional area. Seeding density was an important parameter for the constructs, but pore size over the range tested did not affect cell proliferation or function. This study suggests the feasibility of using poly(alpha-hydroxy ester) foams as scaffolding materials for the transplantation of autogenous osteoblasts to regenerate bone tissue.

Health and safety behaviour and compliance in electroplating workshops.

Skin problems are reputedly common in electroplaters. To examine the steps taken by employers and employees to prevent or control skin problems, we visited six randomly selected electroplating establishments in Dorset and interviewed the employers and 50 of the employees using structured questionnaires. Several of the companies had not complied with the statutory requirements of the Control of Substances Hazardous to Health (COSHH) Regulations 1988, and deficiencies were evident in assessment, control and health surveillance. A third of the employees had current or recent work-related skin problems, typically dermatitis. Workers were generally ignorant about the hazards of materials handled. They knew about personal protective equipment, but did not always use it, or used gloveware that was deficient or contaminated. Only one in five employees adopted a rudimentary skin care programme; many were unaware of the provision for skin care. There is an urgent need for better training and more attention to skin care in electroplating workshops.

Clinical trials and clinical practice: do doctors use the same criteria to judge outcome?

AIMS: The results of clinical trials often seem to have little influence on the practice of individual doctors. This could be because trial information is presented in the style of a scientific experiment which cannot often be clearly related to the context of everyday patient care. We tested the hypothesis that such framing effects would cause doctors to assess the clinical significance of treatment outcomes differently when presented as clinical trial results rather than as individual patient data. METHODS: Fourteen rheumatologists independently reviewed the same 50 sets of data obtained from patients with rheumatoid arthritis. The data consisted of 10 commonly used clinical and laboratory variables measured before and after a period of treatment. The same data were presented in two formats on two separate occasions. The patient data format was a collection of typed sheets attributing each set of results to an individual patient. The clinical trial format was a professionally printed and bound booklet in which each set of results was laid out as summary results of a small uncontrolled clinical trial. Doctors judged the degree of improvement or deterioration and its clinical importance for each data set for both formats. These changes were converted into units of 'Clinical Importance'. RESULTS: Although some statistically significant differences emerged in the individual doctors' judgements between the formats none of these was of a clinically important size. The median of the mean trial--patient difference between the formats for all 14 doctors was 0.035 units of clinical importance [95% CI -0.244 to 0.074]. CONCLUSIONS: This evidence does not support the hypothesis that framing effects are a major cause of the failure of clinical trials to influence clinical practice.

Respiratory disease in workers exposed to colophony solder flux fumes: continuing health concerns.

The objectives of this study were to establish the prevalence of respiratory, eye, nose and throat symptoms of likely work-relation in workers exposed to colophony solder flux fumes and to assess their lung function. A cross-sectional study was conducted in four medium-sized electronics firms in which control measures to capture solder flux fume were absent or visibly ineffective. All female solders and women working adjacent to soldering stations completed an administered questionnaire concerning symptoms, work history and current soldering frequency. Measurements were made of their forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) during the course of a working shift, using a Vitallograph-Compact portable spirometer. Using weekly hours of soldering as a crude index of current exposure, workers were classified into high (> or = 37 h/wk) and low (< or = 20 h/wk) exposure groups, and their health responses were compared in the analysis. Individuals with symptoms suggestive of work-related asthma were also asked to provide serial peak flow measurements over a further 2-week period, and adequate returns were charted and read by two physicians experienced in the diagnosis of occupational asthma. Data were collected on 152 female workers (overall participation rate = 97%). Symptoms of recurrent, persistent wheeze and/or chest tightness were reported by 75 (49%) of interviewees; 36 (24%) gave a history typical of occupational asthma and six more (4%) a history of pre-existing asthma worsened at work. Twenty-one (14%) of the workforce complained of recurrent breathlessness on moderate exertion; 41 workers (27%) had work-related symptoms of the nose or throat and 25 (16%) had work-related eye symptoms. The odds ratios for 'all wheeze', shortness of breath, and work-related eye, nose and chest symptoms were all significantly greater (raised about 4-5 fold) in women who soldered > or = 37 h/wk when compared with those soldering < or = 20 h/wk. After adjustment by logistic regression for atopy, age and smoking status even higher risk estimates were generally obtained. The odds ratios (OR) and 95% confidence intervals (CI) for high vs. low were: for 'all wheeze', OR = 7.2, CI = 2.5-20.7; for work-related eye symptoms, OR = 5.2, CI = 1.4-19.8; for work-related nasal symptoms, OR = 4.0, CI = 1.4-11.1 and for occupational asthma symptoms, OR = 5.2, CI = 1.4-14.2. Mean FEV1 and FVC percentage difference from expected were slightly lower in full-time solderers than in part-time solderers, but the differences were not significant. Thirty-seven of the 51 workers (73%) who were asked to carry out serial peak flow measurements completed an adequate return: 27 of these records confirmed the presence of asthma, and in all of the cases the history suggested onset post-dating employment in soldering. Eleven peak flow records were indicative of occupational asthma. The health problems associated with colophony solder flux were documented over 18 years ago, but are still clearly apparent in situations where adequate control has not been achieved.