Publications
124 results found
Nunn AJ, Craigen AA, Darbyshire JH, et al., 1990, Six year follow up of lung function in men occupationally exposed to formaldehyde., Br J Ind Med, Vol: 47, Pages: 747-752, ISSN: 0007-1072
The long term effects of formaldehyde on the respiratory tract have been investigated in a group of 164 workers exposed daily to the chemical during the production of urea formaldehyde resin, together with 129 workers not exposed to free formaldehyde. Exposure was classified as high (corresponding to an eight hour time weighted exposure of more than 2.0 ppm), medium (0.6 to 2.0 ppm), or low (0.1 to 0.5 ppm). Twenty five per cent of workers had had high exposure at some time and 17% moderate exposure. Both the exposed and unexposed groups had an annual assessment that included lung function. The proportion with self reported respiratory symptoms was similar in the two groups, 12% and 16% reporting breathlessness on hurrying and 26% and 20% wheezing. The initial forced expiratory volume in one second (FEV1) was within 0.5 l (approximately one standard deviation (SD)) of the predicted value (by age and height) in 65% of the exposed and 59% of unexposed workers and more than 0.5 l below the predicted value in 9% of exposed and 11% of unexposed workers. The mean decline in FEV1 was 42 ml a year (SD 45) in the exposed group and 41 ml a year in the unexposed group (SD 40 ml a year). The rate of decline showed the expected association with smoking in the unexposed group, but in the exposed group the mean rate of decline in the never smokers was similar to that in current smokers. There were, however, relatively few never smokers and considerable variation in the rates of decline. In the exposed group no association was found between the rate of decline and indices of exposure to formaldehyde. Thus there is no evidence from this study of an excess of respiratory symptoms or decline in lung function in the workers exposed to formaldehyde. The similar rate of decline of FEV1 however in never smokers and smokers of the exposed group is consistent with findings of other studies for workers exposed to formaldehyde and to toluene di-isocyanate.
Venables KM, Newman Taylor AJ, 1990, Exposure-response relationships in asthma caused by tetrachlorophthalic anhydride., J Allergy Clin Immunol, Vol: 85, Pages: 55-58, ISSN: 0091-6749
Four patients with asthma caused by occupational exposure to tetrachlorophthalic anhydride (TCPA) had dust-challenge tests that used eight different levels of TCPA exposure. Measurements of TCPA in the test-cubicle air ranged from 1.3 to 961.1 micrograms/m3. The higher exposures provoked definite late or dual asthmatic responses. Smaller, but statistically significant, responses were observed at low exposures. The late asthmatic-response area had a linear relation to the logarithm of TCPA exposure, but the immediate asthmatic response was less closely related to exposure.
Franklin DM, Guthrie CJ, Chettle DR, et al., 1990, In vivo neutron activation analysis of organ cadmium burdens. Referent levels in liver and kidney and the impact of smoking., Biol Trace Elem Res, Vol: 26-27, Pages: 401-406, ISSN: 0163-4984
In vivo neutron activation measurements of liver and kidney cadmium have been made in 77 exposed workers and 101 referents. Cadmium levels were higher in exposed workers than in referents; both in liver, 25.7 cf. 0.6 micrograms/g, and kidney, 17.9 cf. 2.7 mg. The 19 referents who never smoked had lower mean organ cadmium burdens than the other referents, the difference achieving statistical significance in the kidney, p less than .01. Cigarette smoking was estimated to increase cadmium body burden by 370 +/- 140 micrograms/pack year. These referent cadmium levels are similar to, although slightly below, previous in vivo and autopsy data.
Venables KM, Dally MB, Nunn AJ, et al., 1989, Smoking and occupational allergy in workers in a platinum refinery., BMJ, Vol: 299, Pages: 939-942, ISSN: 0959-8138
OBJECTIVE: To test the hypothesis that smoking increases the risk of sensitisation by occupational allergens. DESIGN: Historical prospective cohort study. SETTING: Platinum refinery. SUBJECTS: 91 Workers (86 men) who started work between 1 January 1973 and 31 December 1974 and whose smoking habit and atopic state (on skin prick testing with common allergens) had been noted at joining. MAIN OUTCOME MEASURES: Results of skin prick tests with platinum salts carried out routinely every three to six months and records of any respiratory symptoms noted by the refinery's occupational health service. Follow up was until 1980 or until leaving refinery work, whichever was earlier. RESULTS: 57 Workers smoked and 29 were atopic; 22 developed a positive result on skin testing with platinum salts and 49 developed symptoms, including all 22 whose skin test result was positive. Smoking was the only significant predictor of a positive result on skin testing with platinum salts and its effect was greater than that of atopy; the estimated relative risks (95% confidence interval) when both were included in the regression model were: smokers versus non-smokers 5.05 (1.68 to 15.2) and atopic versus non-atopic 2.29 (0.88 to 5.99). Number of cigarettes smoked per day was the only significant predictor of respiratory symptoms. CONCLUSION: Smokers are at increased risk of sensitisation by platinum salts.
Venables KM, Davison AG, Newman Taylor AJ, 1989, Consequences of occupational asthma., Respir Med, Vol: 83, Pages: 437-440, ISSN: 0954-6111
Seventy-nine patients attending hospital for follow-up of occupational asthma were interviewed, on average 6 years after asthma developed. Although 90% thought their symptoms had improved, 10% had required a hospital admission (apart from for investigation), 72% still took medication and most reported symptoms in the last 3 months. One-third were currently unemployed and 40-73% reported limitation in everyday activities, such as housework or shopping. Symptoms on waking were used as an index of troublesome asthma. Those 31 in whom this occurred at least once a week reported limitation in everyday activities significantly more commonly than others. This relation was more marked in men than women. Limitation in everyday activities was, however, more frequently reported by women than men, who were also more likely than men to be unemployed, suggesting that factors other than impairment of function also contribute to handicap in occupational asthma.
Venables KM, Davison AG, Browne K, et al., 1989, Pseudo-occupational asthma., Thorax, Vol: 44, Pages: 760-761, ISSN: 0040-6376
A case is reported in which a pattern of work related asthma in a record of peak expiratory flow was artefactual. The patient had pronounced morning dips, which she recorded on working days, when she made the first recording at 0700 h, but not on holiday, when she stayed in bed longer. The case emphasises the need for clear instructions to patients about peak flow records.
Venables KM, Newman Taylor AJ, 1989, Prospective study of asthma in relation to smoking habits., Thorax, Vol: 44, ISSN: 0040-6376
Newman Taylor AJ, Tee RD, 1989, Occupational lung disease., Curr Opin Immunol, Vol: 1, Pages: 684-689, ISSN: 0952-7915
Venables KM, Tee RD, Hawkins ER, et al., 1988, Laboratory animal allergy in a pharmaceutical company., Br J Ind Med, Vol: 45, Pages: 660-666, ISSN: 0007-1072
A cross sectional survey was carried out on 138 workers exposed to laboratory animals. Sixty (44%) had symptoms in a self completed questionnaire that were consistent with laboratory animal allergy (LAA) of whom 15 (11%) had chest symptoms. There was a positive skin prick test to one or more animal urine extracts (rat, mouse, guinea pig, rabbit) in 13% and 38% had a positive radioallergosorbent test to urine extract. LAA chest symptoms were almost five times more common in atopic than non-atopic subjects (who were distinguished by skin test response to common, non-animal aeroallergens). A positive skin test to animal urine was associated with LAA chest symptoms and with atopy. Nose, eye, or skin symptoms without chest symptoms were not associated with atopy. There was an inverse relation between duration of employment at the firm and LAA chest symptoms, suggesting selection of affected people out of employment with animals.
Venables KM, Upton JL, Hawkins ER, et al., 1988, Smoking, atopy, and laboratory animal allergy., Br J Ind Med, Vol: 45, Pages: 667-671, ISSN: 0007-1072
This study examined data from three cross sectional surveys of 296 laboratory workers exposed to small mammals. Four indices of laboratory animal allergy were studied: symptoms suggestive of occupational asthma, symptoms suggestive of any occupational allergy, skin weals to animal urine extracts, and serum binding in radioallergosorbent tests with urine extracts. Pooled data from the three surveys showed an association between smoking and all indices except radioallergosorbent tests; the association was significant for symptoms of occupational asthma. One of the three surveys consistently showed a stronger association of allergy indices with smoking than with atopy (defined on skin tests with non-animal aeroallergens). Associations with smoking persisted after stratifying by atopic status, suggesting that smoking may be a risk factor for laboratory animal allergy.
Newman Taylor AJ, 1988, Occupational asthma., Postgrad Med J, Vol: 64, Pages: 505-510, ISSN: 0032-5473
Occupational asthma is important both as a potentially curable and preventable cause of asthma and as a model of adult onset asthma. It is induced by sensitization to a specific agent inhaled at work; for many of its causes, including inhaled proteins and the low molecular weight chemicals acid anhydrides and reactive dyes, it is probably IgE dependent. The risk of developing specific IgE and associated asthma is markedly increased in cigarette smokers, probably as a consequence of non-specific damage to the respiratory mucosa. Asthma caused by several agents, which include some of its most frequent causes, isocyanates, colophony and plicatic acid (Western Red Cedar) persists in some 50% of cases for years, and possibly indefinitely, after avoidance of exposure. The development of chronic symptomatic asthma seems particularly to occur in those with longer duration of symptomatic exposure.
Tee RD, Gordon DJ, Hawkins ER, et al., 1988, Occupational allergy to locusts: an investigation of the sources of the allergen., J Allergy Clin Immunol, Vol: 81, Pages: 517-525, ISSN: 0091-6749
Allergic symptoms occur commonly in subjects working closely with locusts and are associated with specific IgE antibody. Extracts of intact locusts (Schistocerca gregaria and Locusta migratoria) were used to identify specific IgE antibody, to define the major allergens of the locust and their sources, and to estimate aeroallergen concentration in the working environment. With questionnaire, skin prick tests, and specific IgE measurements, 35 individuals, working in a research center, were surveyed. Of the 15 currently exposed individuals, contact with locusts provoked asthma, rhinitis, and contact urticaria in five, rhinitis and urticaria in three, and rhinitis alone in one individual. Symptoms provoked by locusts and skin test reactions to locust extracts were associated with specific IgE antibody in the serum. The "immunoblot" technique demonstrated the presence of multiple allergens in the locust extracts of approximately 68, 66, 54, 43, 37, 29, and 18 K daltons molecular weight. Locust antigen was identified in the atmosphere by means of an immunochemical method involving elution of high-volume air-sampler filters exposed in the locust breeding room and analysis of eluate allergen content by RAST-inhibition assays. Logit transformation of RAST-inhibition lines demonstrated that the filter extract shared a common slope with the locust extract and with an extract of locust gut. This gut extract also shared a common slope with extracts of locust feces and peritrophic membrane. The major source of allergen appears to be the peritrophic membrane that is present in the gut and is excreted surrounding the feces.
Newman Taylor AJ, 1988, Managing the environment., Br J Clin Pract Suppl, Vol: 59, Pages: 11-16, ISSN: 0262-8767
Newman Taylor AJ, 1987, Respiratory allergy in farmers., Practitioner, Vol: 231, Pages: 1146-1150, ISSN: 0032-6518
Venables KM, Topping MD, Nunn AJ, et al., 1987, Immunologic and functional consequences of chemical (tetrachlorophthalic anhydride)-induced asthma after four years of avoidance of exposure., J Allergy Clin Immunol, Vol: 80, Pages: 212-218, ISSN: 0091-6749
Seven patients with occupational asthma caused by a chemical, tetrachlorophthalic anhydride (TCPA), left their work in 1980. They have subsequently avoided TCPA exposure and have been followed until 1985. One patient died in 1981. The six living patients reported continuing symptoms suggestive of asthma, and five who were studied in 1985 demonstrated mild bronchial hyperresponsiveness (histamine concentration provoking a 20% fall in FEV1 range 2.7 to 12.5 mg/ml). Specific IgE antibody to TCPA conjugated with human serum albumin was measured by a radioallergosorbent test and detected in all patients. After avoidance of exposure, specific IgE fell exponentially with a half-life of 1 year. Specific IgE was still detectable in 1985, and throughout the follow-up period, prick tests with the conjugate elicited immediate skin responses. In 1981 four patients had inhalation tests with TCPA, and specific IgE rose afterward and then fell again.
Docker A, Wattie JM, Topping MD, et al., 1987, Clinical and immunological investigations of respiratory disease in workers using reactive dyes., Br J Ind Med, Vol: 44, Pages: 534-541, ISSN: 0007-1072
A questionnaire survey of over 400 workers handling reactive dyes showed that over 15% had work related respiratory or nasal symptoms. Forty nine employees with symptoms were referred to chest clinics for detailed assessment. It was considered that in 19 the symptoms could be attributed to an irritant response to a variety of chemicals, including hydrochloric acid vapour, sulphur dioxide, and reactive dyes. Symptoms in 24 were attributed to an allergic reaction to a specific agent; in most (21) to one or more reactive dyes. Two patterns of allergic lower respiratory symptoms were identified; an immediate response of short duration and a longer lasting response, usually of several hours, sometimes accompanied by nocturnal asthma. A radioallergosorbent test (RAST) screen containing the most commonly used reactive dyes was used to detect specific IgE. Allergic symptoms to reactive dyes were strongly associated with specific IgE (17/21 employees) and atopy (18/21). Irritant symptoms were also associated with atopy (13/19) but only weakly associated with specific IgE (7/19).
Graneek BJ, Durham SR, Newman Taylor AJ, 1987, Late asthmatic reactions and changes in histamine responsiveness provoked by occupational agents., Bull Eur Physiopathol Respir, Vol: 23, Pages: 577-581, ISSN: 0395-3890
The temporal and quantitative relationship between increases in airway responsiveness and late asthmatic reactions provoked by inhalation challenge with occupational agents was studied in nine individuals who underwent a total of thirteen active inhalation challenge tests with one of the following agents: toluene diisocyanate (TDI), maleic anhydride (MA), trimellitic anhydride (TMA), carmine, or colophony (pine wood resin). Airway responsiveness to inhaled histamine (histamine PC20) was measured before and at approximately 3 and 24 h after control and active challenge exposure, when, on all but four occasions, FEV1 was within 10% of pre-challenge values. Significant increases (p less than 0.02) in histamine responsiveness were present at 3 h following challenge exposures which subsequently provoked a definite late asthmatic reaction (FEV1 decrease greater than 15% 3-11 h post challenge). These increases in histamine responsiveness were significantly greater than those at 3 h following the challenges which provoked an isolated early (FEV1 decrease less than 6% 3-11 h post-challenge) or equivocal late asthmatic reaction (FEV1 decrease 6-15% 3-11 h post-challenge) (p less than 0.03). Although histamine responsiveness remained high at 24 h after challenges provoking late asthmatic reactions (p less than 0.05), this was less than the increase at 3 h and not significantly different from the PC20 at 24 h after challenges provoking either single early or equivocal late asthmatic reactions.(ABSTRACT TRUNCATED AT 250 WORDS)
Johnson NF, Haslam PL, Dewar A, et al., 1986, Identification of inorganic dust particles in bronchoalveolar lavage macrophages by energy dispersive x-ray microanalysis., Arch Environ Health, Vol: 41, Pages: 133-144, ISSN: 0003-9896
This study shows that energy dispersive x-ray microprobe analysis to identify and quantify intracellular particles in macrophages obtained by the minimally invasive method of bronchoalveolar lavage (BAL) can detect inorganic dust exposures of many different kinds. Bronchoalveolar lavage macrophages from 22 patients have been examined. Twelve patients had occupational exposure to asbestos, talc, silica, hard metal or printing ink, while 10 had no known history of dust exposure. X-ray microprobe analysis identified particles which related to the known exposures, superimposed on a background of other particles related to smoking (kaolinite and mica) or to the general environment (silicon, titanium, and iron). The particle identification provided useful objective confirmation of the known exposures, except for silica, which could not be distinguished from the general background levels. X-ray microanalysis using BAL macrophages can be helpful for clarification of mixed dust exposures, to identify particles when light microscopy indicates retained dust in patients with no known history of exposure, and to monitor retained particles after removal from exposure.
Assoufi BK, Dally MB, Newman-Taylor AJ, et al., 1986, Cold air test: a simplified standard method for airway reactivity., Bull Eur Physiopathol Respir, Vol: 22, Pages: 349-357, ISSN: 0395-3890
A simple and standardized test has been developed to measure airway responsiveness to cold dry air. This consists of stepwise increases in ventilation of dry subfreezing air at 10, 20, 40 and 60% of predicted indirect maximum breathing capacity (IMBC). For each step, the inhalation time was 3 min. The optimal time between the steps was 5 min. Exposure ceased when either a fall in forced expiratory volume in one second (FEV1) of more than 20% of baseline occurred or when there was no response after breathing cold air at 60% predicted IMBC. Moderate isocapnic hyperventilation with cold air beyond 3 min induced no further bronchoconstriction. Varying the interval (0, 2 and 5 min) between the steps produced no significant differences in test results. Changing the pattern of breathing had no effect on airway responsiveness, provided that the patient maintained a constant minute-ventilation. This implies that it is not necessary to monitor the rate and depth of respiration continuously in order to achieve a given minute-ventilation, making the technique simpler. In addition, a "CO2 requirement graph" has been constructed at different levels of ventilation. This allows the inspired CO2 concentration to be preset, eliminating the need for elaborate equipment and monitoring of end-tidal CO2 to keep the subject isocapnic during hyperventilation.
Walls AF, Newman Taylor AJ, Longbottom JL, 1985, Allergy to guinea pigs: II Identification of specific allergens in guinea pig dust by crossed radio-immunoelectrophoresis and investigation of the possible origin., Clin Allergy, Vol: 15, Pages: 535-546, ISSN: 0009-9090
An extract of dust from the air-vent filters of a room housing guinea pigs was analysed by quantitative immunoelectrophoretic procedures and compared with extracts of various materials derived from guinea pigs. Crossed radio-immunoelectrophoresis (CRIE) of the dust, performed with sera from twenty asthmatic patients who were positive by skin testing and RAST to guinea pig extracts, identified fourteen IgE-binding constituents. Although responses varied, most sera reacted with four particular allergens, antigens 2, 3, 10 and Sl. The numbers of allergens recognized by individual patients correlated with the RAST score, but not with total serum IgE. All seventeen dust constituents detected by crossed immunoelectrophoresis (and all four major allergens), were also present in extracts of guinea pig dander, fur, saliva and urine; several of these components were absent in an epithelial extract, and there were even less in preparations of shaved pelt, serum or faeces. None of the dust extract antigens were detected in materials used in animal husbandry, dust samples from rooms without guinea pigs, or a D. pteronyssinus extract. These findings suggest that inhalant allergens may be derived predominantly from material shed from the guinea pig coat after contamination with saliva, and possibly to a lesser extent, urine.
Lozewicz S, Davison AG, Hopkirk A, et al., 1985, Occupational asthma due to methyl methacrylate and cyanoacrylates., Thorax, Vol: 40, Pages: 836-839, ISSN: 0040-6376
Five patients had asthma provoked by cyanoacrylates and one by methyl methacrylate, possibly because of the development of a specific hypersensitivity response. Acrylates have wide domestic as well as industrial uses, and inhalation of vapour emitted during their use can cause asthma.
Venables KM, Dally MB, Burge PS, et al., 1985, Occupational asthma in a steel coating plant., Br J Ind Med, Vol: 42, Pages: 517-524, ISSN: 0007-1072
An outbreak of occupational asthma, of unknown cause and extent, was detected in a steel coating plant. In 1979 a cross-sectional study which defined occupational asthma in terms of respiratory symptoms detected 21 people with suggestive symptoms among the 221 studied. They all worked in the coating shop, but the plastic coatings used at the plant contained many potential sensitising agents that might have caused the asthma. All 21 developed their symptoms after 1971, and it was found that in this year a supplier had modified a coating allowing, at the temperatures used in the process, toluene di-isocyanate to be liberated. Two of the symptomatic subjects were tested by inhalation of the isocyanate and showed asthmatic reactions and other subjects were found to have asthma related to periods spent at work by records of peak expiratory flow rate. Over half the 21 had a symptom free latent period after first exposure of three years or less, a pattern not seen in other subjects with respiratory symptoms. After the isocyanate had been removed from the process 17 of these subjects became asymptomatic or improved, a greater proportion than in other subjects with respiratory symptoms.
Walls AF, Newman Taylor AJ, Longbottom JL, 1985, Allergy to guinea pigs: I. Allergenic activities of extracts derived from the pelt, saliva, urine and other sources., Clin Allergy, Vol: 15, Pages: 241-251, ISSN: 0009-9090
Guinea pig-sensitive patients with asthma and rhinitis were skin test positive to extracts of several materials derived from guinea pigs. A radioallergosorbent test (RAST) was developed to measure serum IgE specific for the dander, urine, saliva and also for dust from the air-vent filters of a room housing guinea pigs. A strong correlation was found between positive skin test reactions, and raised serum IgE to these extracts. Furthermore, the relative allergenic potency of extracts was similar when determined by skin-prick testing and by inhibition of the RAST to guinea pig dust. Non-guinea pig-derived extracts such as the hay, sawdust and diet had negligible activity in skin testing and RAST inhibition; and preparations of Dermatophagoides pteronyssinus, house dust and rat dust did not inhibit the RAST for guinea pig room dust. The guinea pig dust, dander, fur, urine and saliva were the more potent extracts; while whole pelt, faeces and serum were considerably less active. Extracts from different sexes were not appreciably different in potency. The results of skin testing, RAST and RAST inhibition suggest cross-allergenicity between the various extracts. Although material shed from the pelt may have been derived from saliva, or even urine, allergenic activities of urinary and salivary preparations were found to be less than those of the dander, fur or dust. This suggests that allergens have become concentrated on the pelt.
Slovak AJ, Newman Taylor AJ, 1985, Allergy to laboratory animals., Br J Ind Med, Vol: 42, Pages: 213-214, ISSN: 0007-1072
Venables KM, Burge PS, Davison AG, et al., 1984, Peak flow rate records in surveys: reproducibility of observers' reports., Thorax, Vol: 39, Pages: 828-832, ISSN: 0040-6376
Records of peak expiratory flow rate (PEFR), commonly used in hospital in the management of asthma, have not been evaluated as a method of identifying cases of asthma in population surveys. Four observers were asked to report on whether asthma was present or absent in 61 graphs of PEFR recorded two hourly for four weeks during surveys of working population. Agreement within individual observers was measured using a subset of 29 graphs which had been copied and distributed at random among the set of 61; agreement was good, from 90% in one observer to 100% in two. Agreement between observers was measured on the basis of all 61 graphs. Agreement occurred between all four observers in 69% of graphs, between at least three out of four in 97%, and, when pairs of observers were examined, between 72% and 93% of graphs. Graphs assessed as showing asthma demonstrated more within day PEFR variability (expressed as the number of days in which the difference between maximum and minimum readings was at least 15%) than graphs assessed as not showing asthma. Some graphs with little within day variability were assessed as showing asthma, apparently because they demonstrated between day PEFR variability.
Coutts IL, Lozewicz S, Dally MB, et al., 1984, Respiratory symptoms related to work in a factory manufacturing cimetidine tablets., Br Med J (Clin Res Ed), Vol: 288, ISSN: 0267-0623
Nagakura T, Lee TH, Assoufi BK, et al., 1983, Neutrophil chemotactic factor in exercise- and hyperventilation-induced asthma., Am Rev Respir Dis, Vol: 128, Pages: 294-296, ISSN: 0003-0805
Elevated levels of the mast-cell-associated serum neutrophil chemotactic factor (NCF) and an increase in blood basophil counts were observed in 6 atopic asthmatics during exercise-induced asthma (EIA). These changes were not found when the same degree of airways obstruction was elicited in the same subjects by isocapnic hyperventilation (ISH) with cold air. The NCF was unlikely to be related to the basophilia alone, because asthmatics without EIA who underwent the same exercise task, produced a similar basophilia but significantly less NCF. These findings suggest that mast-cell-associated (as opposed to basophil-associated) mediators of hypersensitivity are detectable in the bloodstream during the bronchoconstriction induced by exercise, but not by ISH.
Davison AG, Haslam PL, Corrin B, et al., 1983, Interstitial lung disease and asthma in hard-metal workers: bronchoalveolar lavage, ultrastructural, and analytical findings and results of bronchial provocation tests., Thorax, Vol: 38, Pages: 119-128, ISSN: 0040-6376
Five patients with respiratory disorders associated with hard metal exposure are described. In four patients electron microprobe analysis of bronchoalveolar lavage cells or lung tissue was used to show tungsten and other hard-metal components. Three patients had interstitial pneumonia and fibrosis with unusual multinucleate giant cells. Electron microscopy showed that the giant cells comprised both type II alveolar epithelial cells and alveolar macrophages. The multinucleate macrophages formed a distinctive feature of the bronchoalveolar lavage material but the multinucleate alveolar epithelial lining cells were evident only in lung tissue. The other two patients both suffered from work-related asthma, one of whom also had pulmonary opacities. Bronchial provocation tests in these patients supported the diagnosis of hard-metal-induced asthma and implicated cobalt as the agent responsible.
Newman-Taylor AJ, 1982, Laboratory animal allergy., Eur J Respir Dis Suppl, Vol: 123, Pages: 60-64, ISSN: 0106-4347
Newman-Taylor AJ, 1982, Extrinsic allergic alveolitis (hypersensitivity pneumonitis): immunopathology., Eur J Respir Dis Suppl, Vol: 123, Pages: 97-100, ISSN: 0106-4347
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