Distribution of nickel in lungs from former nickel workers

Objective: The purpose of this work was to study the distribution of nickel within lung tissue obtained from nickel-exposed people and to evaluate the␣use of only one single sample for determination of the nickel burden of the lung. Methods and materials: The material used was lung tissue obtained from 15 former nickel refinery workers who had been exposed to a variety of nickel compounds such as Ni₃S₂, NiO, Ni⁰, NiSO₄, and NiCl₂. Ten samples taken from different locations of the lung as well as from the right and left bronchus and from the right lower lobe (total 13 samples per individual) were analyzed for nickel by electrothermal atomic absorption spectrometry. Samples obtained from ten people not connected to the refinery served as a reference group. Results: The arithmetic mean value ± SD for nickel concentration was 50 ± 150 μg g⁻¹ dry wt. Biopsies collected on the center of the lower right lobe had an average nickel concentration of 82 ± 252 μg g⁻¹. The average nickel concentration detected in the right and left bronchus was 5.9 ± 11.6 and 3.8 ± 6.0 μg g⁻¹, respectively. Lung tissue obtained from ten people not connected to the refinery had an average nickel concentration of 0.74 ± 0.44 μg g⁻¹. Conclusions: The significant findings based on log-normal distribution of the nickel concentration were as follows: (1) samples obtained from the right lung showed no significant difference from samples taken from the left lung–a comparison of the nickel concentration detected in all the lung lobes showed that no single lobe differed from another; (2) the concentration of nickel found in the main bronchus of the refinery workers, although elevated, was significantly lower than the concentration detected in the remaining tissue; and (3) one single biopsy did not reflect the nickel burden of the lung. Received: 20 November 1997 / Accepted: 21 April 1998     

Update of cancer incidence among workers at a copper/nickel smelter and nickel refinery

Objectives: To assess cancer risk among nickel-exposed workers. Methods: We updated cancer incidence among 1388 workers employed for at least 3 months at a copper/nickel smelter and nickel refinery in Harjavalta, Finland. There were 1155 workers exposed to nickel during the period 1960–1985 in the smelter (566 workers), repair shop (239 workers), or refinery (418 workers). Cancer incidence was followed through the files of the Finnish Cancer Registry up to 31 December 1995. For overall cancer and for a priori selected specific cancer types the ratio of observed to expected numbers of cases was computed as a standardized incidence ratio (SIR), controlled for age, gender, and calendar period and using the region-specific rates as a reference. Results: The overall cancer incidence among both nickel-exposed and unexposed subcohorts was at the expected level. A small increase in lung cancer incidence, which reached statistical significance among workers with a latency exceeding 20 years, was observed among the smelter workers exposed to insoluble nickel compounds. Among workers in the refinery, who were exposed primarily to nickel sulfate at levels below 0.5 mg/m³ as well as to low concentrations of other nickel compounds, there was an increased risk for nasal cancer (SIR 41.1, 95% CI 4.97–148), positively associated with latency and duration of employment, and an excess risk for stomach (SIR 4.98, 95% CI 1.62–11.6) and lung (SIR 2.61, 95% CI 0.96–5.67) cancers. Conclusions: Since elevated nasal and lung cancer risks were confined to the refinery, where the primary exposure was to nickel sulfate, it is likely that nickel sulfate is mainly responsible for the elevated respiratory cancer risk. We cannot rule out whether the excess stomach cancer risk is a chance finding, or related to the working environment. Received: 11 September 1997 / Accepted: 17 October 1997     

Cancer risk among workers at a copper/nickel smelter and nickel refinery in Finland

Summary A total of 1388 workers employed for at least 3 months at a copper/nickel smelter and nickel refinery were followed up for cancer from 1953 to 1987 through the Finnish Cancer Registry. There were 1339 male and 49 female workers, making a total of 27130 and 706 person-years, respectively. All of the women worked in the refinery, which opened in 1960, the same year the smelting of nickel began. A total of 67 cancers were diagnosed among the men, the standardized incidence ratio for all cancers being 1.0. No cancer was found among the women (1.8 expected). The risk of cancer among men was analysed according to primary site, exposure to nickel, type of work, years since first exposure and age at diagnosis. In the subcohort of nickel refinery workers, one case of sinonasal cancer was observed, against 0.02 expected, but otherwise no significantly increased risks of cancer were found. In addition to the small size of the cohort, the non-positive finding concerning lung cancer might be related to the relatively low arsenic exposure and, perhaps, to the late commencement of nickel production.     

Mortality experience among employees at a hydrometallurgical nickel refinery and fertiliser complex in Fort Saskatchewan, Alberta (1954-95)

OBJECTIVE—To study the mortality experience of workers at a hydrometallurgical nickel refinery and fertiliser complex in Fort Saskatchewan, Alberta, Canada.
METHODS—A total of 1649 male employees of Sherritt International who worked for at least 12 continuous months during the years 1954 to 1978 at the Fort Saskatchewan, Alberta hydrometallurgical nickel refinery and fertiliser complex were followed up for an additional 17 years. Mortality was ascertained from the Canadian mortality data base maintained by Statistics Canada and covered the years 1954-95. Statistics were analysed with Monson's computer program.
RESULTS—Total mortality, when compared with the Canadian population, was significantly below expectation. Fewer deaths were found for circulatory disease, ischaemic heart disease, respiratory disease, neoplasms, digestive cancer, and accidents, poisonings, and violence. Among the 718 men in the group exposed to nickel, there were no deaths due to nasal cavity or paranasal sinus cancer. Fewer deaths were found for all causes, circulatory disease, ischaemic heart disease, neoplasms and digestive cancer. Lower death rates were observed than expected for respiratory malignancies and cancer of the bronchus and lung.
CONCLUSION—No association was found in this study between exposure to nickel concentrate or metallic nickel in the hydrometallurgical refining process and the subsequent development of respiratory cancer.


Keywords: epidemiology; nickel workers; mortality     

Persisting risk of nickel related lung cancer and nasal cancer among Clydach refiners

Objective

To evaluate the risk of lung cancer and nasal cancer among workers employed at the Clydach nickel refinery, South Wales since 1930 by combining data from the two most recently published papers on this cohort.

Methods

Observed and expected numbers of cancer deaths were extracted for workers who had a minimum of five years service and were employed for the first time between 1902 and 1992. Standardised mortality ratios (SMR) were calculated for subgroups according to year of employment, time since first employment, and process work.

Results

A persisting excess of respiratory cancer was found for workers employed in the period 1930–92, with a lung cancer SMR of 133 (95% CI 103 to 172) and a SMR for nasal cancer of 870 (95% CI 105 to 3141). The lung cancer excess was most clearly seen 20 years or more after first employment and seemed to be confined to process workers. There was no indication of a further reduction in risk since 1930.

Conclusion

The extreme nickel related cancer hazard at the refinery before 1920 was greatly reduced during subsequent years. Some of the carcinogenic exposures seem to have remained after 1930, producing an elevated risk of nasal cancer and a 30% excess of lung cancer in the workforce. There was evidence of a persisting risk among process workers first employed since 1953.     

Mortality of workers at a nickel carbonyl refinery, 1958-2000

Background: Excess risks of respiratory cancer have been shown in some groups of nickel exposed workers. It is clear, however, that not all forms of nickel exposure are implicated in these excess risks.

Aim: To determine whether occupational exposures received in a modern nickel carbonyl refinery lead to increased risks of cancer, in particular nasal cancer and lung cancer.

Methods: The mortality experienced by a cohort of 812 workers employed at a nickel refinery was investigated. Study subjects were all male workforce employees first employed in the period 1953–92 who had at least five years' employment with the company. Observed numbers of cause specific deaths were compared with expectations based on national mortality rates; SMRs were also calculated by period from commencing employment, year of commencing employment, and type of work.

Results: Overall, standardised mortality ratios (SMRs) were close to 100 for all causes (Obs 191, SMR 96, 95% CI 83 to 111), all neoplasms (Obs 63, SMR 104, 95% CI 80 to 133), non-malignant diseases of the respiratory system (Obs 18, SMR 97, 95% CI 57 to 153), and diseases of the circulatory system (Obs 85, SMR 94, 95% CI 75 to 116). There were no significantly increased SMRs for any site of cancer. There was a non-significant excess for lung cancer (Obs 28, Exp 20.17, SMR 139, 95% CI 92 to 201), and in subgroup analyses a significantly increased SMR of 231 (Obs 9) was found for those 142 workers with at least five years' employment in the feed handling and nickel extraction departments. In the total cohort there was a single death from nasal cancer (Exp 0.10).

Conclusions: The non-significant excess of lung cancer deaths may well be a chance finding, but in light of previous studies some role for nickel exposures cannot be excluded.

     

Exposure to soluble nickel in electrolytic nickel refining

Past and present exposure to nickel was studied in an electrolytic nickel refinery, where an increased incidence of nasal cancer had been reported, using nickel analyses in air, blood and urine. Genotoxic effects were studied using analysis of micronuclei from acridine orange-stained smears from the buccal mucosa of the workers. Workers used respirators or masks in tasks where the exposure was expected to be high. Inside the mask, nickel concentrations were 0.9–2.4 μg m⁻³ in such tasks. In those tasks where masks were not used, nickel concentrations in the breathing zone were 1.3–21μgm⁻³. Air-borne nickel concentrations (stationary sampling) varied between 230 and 800μg m⁻³ in 1966–1988 with no systematic change; thereafter lower concentrations (170–460μg m⁻³) have been observed. After-shift urinary concentrations of nickel were 0.1–2 μmoll⁻¹ they showed no correlation with nickel concentrations in the air. Concentrations of nickel in the urine were still elevated after a 2–4 week vacation. The frequency of micronucleated epithelial cells in the buccal mucosa of nickel refinery workers was not significantly elevated by comparison with referents. No relationship was observed between micronucleus frequencies and levels of nickel in air, urine or blood.     

Lung cancer in workers in a nickel refinery

ABSTRACT This study is an analysis of the occurrence of lung cancer in nickel workers, particularly with regard to development time, histological types and tobacco smoking, in addition to specific exposure to nickel dust and fumes. It is a continuation of previous work in this field (Kreyberg, 1954a, b; 1962, 1969). The series consists of 44 cases of lung cancer occurring during the years 1948-74 in people currently or previously employed at Falconbridge nickel refinery. A seven-year period of reduced activity during the war enables lung cancer in workers who took up employment in 1927-39 to be compared with that in workers who started in or after 1946. It is confirmed that exposure to nickel dust and fumes increases the risk of developing lung cancer. However, all subjects with small cell anaplastic carcinoma and at least 25 out of 28 subjects with epidermoid carcinoma had been tobacco smokers. Four smokers and four non-smokers had Group II tumours. The mean age at diagnosis of lung cancer in the nickel workers corresponds closely with that of male subjects with lung cancer in general, in spite of the very wide differences in the development time, if this is related to the employment time in the refinery alone. The mean age at diagnosis is, however, consistent if the development time is related to the length of tobacco smoking. Tobacco smoking is an important factor in the development of lung cancer in nickel workers, and under the conditions described in this study the reduced carcinogenic influence may be attributable to reduced exposure to nickel and possibly also to tobacco.     

Investigations on the quantitative determination of nickel and chromium in human lung tissue

Summary Nickel (Ni) and some of its relatively insoluble compounds as well as chromates may be able to induce cancer in the region of the lungs, as well as in the nose and paranasal sinuses after occupational exposure. Latency periods may amount to 20 years and more. The results of recent investigations have shown that these metals cumulate in the lung tissue after inhalation of relatively insoluble chromium and nickel compounds. The quantitative detection of these heavy metals in samples of pulmonary tissue hence permits the amount of past exposure to be estimated. To establish the normal values, samples of pulmonary tissue from 30 normal subjects were investigated for chromium and nickel content. The samples were taken from different segments and lobes of the lungs, taking topographical anatomical criteria into consideration. In addition, 15 persons who had formerly been exposed to nickel and/or chromium (11 nickel refinery workers, of whom 10 had died of lung cancer, 2 stainless steel welders, 1 foundry worker, 1 electrical technician) were also investigated. From the results of 495 tissue samples from the normal group, median chromium concentrations between 130 and 280 ng/g were calculated, with median nickel concentrations of 20–40 ng/g (wet weight). If these values are related to the nickel concentrations measured in refinery workers, values 112-5,860 times higher were found. The concentrations were about 500 times higher than normal for nickel, and about 60 times higher than normal for chromium in the stainless steel welders. For the foundry workers who died of lung cancer, chromium and nickel concentrations in the normal range were calculated, with the exception of the nickel concentrations in the upper and lower lobes of the right lung. The very high nickel concentrations found in the samples of lung tissue from former nickel refinery workers should be regarded as a guideline with regard to the appraisal of the causal relationship between lung cancer and occupational exposure to relatively insoluble nickel compounds. This result is also supported by epidemiological investigations on this subgroup and must thus be considered etiologically conclusive. For the welders, chromium and nickel concentrations were found that were markedly above normal, but as yet there is no epidemiologically reliable verification for the increased occurrence of malignancies in this occupational group. On the basis of present scientific knowledge, no indications were found of relevant chromium and/or nickel exposure of the lung tissue that might be able to induce lung cancer in either foundry workers or for electric technicians.Dedicated to Professor V. Becker on his 65th birthday     

Exposure to nickel compounds and smoking in relation to incidence of lung and nasal cancer among nickel refinery workers.

OBJECTIVES: To investigate the relation between occupational hazards among nickel refinery workers and their exposure to different forms of nickel over time and the interaction between smoking and total exposure to nickel. METHODS: The cohort consisted of 379 workers with first employment 1916-40 and at least three years of employment and 4385 workers with at least one year of employment 1946-83. Data on smoking (ever or never) were available for almost 95% of the cohort. Two analyses were used, indirect standardisation from observed and expected numbers and Poisson regression. RESULTS: During the follow up 1953-93, 203 new cases of lung cancer were observed v 68 expected (standardised incidence ratio (SIR) 3.0, 95% confidence interval (95% CI) 2.6-3.4) and 32 cases of nasal cancer were observed v 1.8 expected (SIR 18.0, 95% CI 12-25). The Poisson regression analysis showed an excess risk of lung cancer in association with exposure to soluble forms of nickel, with a threefold increase in relative risk (RR) (P < 0.001) and a multiplicative effect of smoking and exposure to nickel. The RRs were 1.1 (95% CI 0.2-5.1) for exposed workers who had never smoked and 5.1 (95% CI 1.3-20.5) for exposed workers who smoked. CONCLUSION: It is not possible to state with certainty which specific nickel compounds are carcinogenic, but a significant excess risk was found for workers exposed to soluble nickel alone or in combination with other forms of nickel. The present study suggests a multiplicative effect of smoking and nickel exposure.     

Biomonitoring of nickel and chromium in human pulmonary tissue

Nickel (Ni) and chromium (Cr) and some of its compounds may be able to induce cancer in the lungs as well as in the nose and paranasal sinuses after occupational exposure. Latency periods amount to 20 years and more. Therefore objective exposure data are not available in the most cases and expert evaluation of the causal connection is often difficult. Recent investigations have shown, that Ni and Cr can cumulate in human lung tissue after occupational exposure. For the evaluation of normal Ni- and Cr-values a total of 495 human lung tissue samples of 30 occupationally non-exposed persons were analysed by AAS including ZEEMAN-compensation after wet oxidative digestion. Additional samples of 10 deceased persons who have been occupationally exposed to nickel in previous times by nickel-refining and welding, especially flame spraying have been investigated. The median Ni- and Cr- concentrations in the lungs of the non-exposed persons ranged between 20–40 resp. 133–277 ng/g (wet weight). In nickel refinery workers Ni- concentrations were found which exceeded the normal range about 1,000. In welders, especially flame sprayers, also values more than 100 times higher could be analysed for Ni and Cr. Partially these concentrations were found years after the end of the inhalative exposure.     

Evidence of carcinogenicity in humans of water-soluble nickel salts

Background  

Increased risks of nasal cancer and lung cancer in nickel refiners have been investigated scientifically and discussed since they were detected in the 1930s. Nickel compounds are considered to be the main cause of the cancer excess. Parts of the nickel producing industry and their consultants oppose the classification of water-soluble nickel salts as human carcinogens, and argue that the risk in exposed workers should be ascribed to other occupational exposures and smoking.     

Asbestos-related cancers in refinery workers in the Australian petroleum industry

In this study of the incidence of asbestos-related cancer in the Australian petroleum industry, the authors traced a cohort of 16,543 petroleum industry workers for a total of 226,989 person-years. There were 18 cases of pleural mesothelioma; 12 occurred in refinery nonoffice workers, for whom the Standardized Incidence Ratio was 3.77 (95% confidence interval = 1.95-6.59). The incidence of lung cancer was significantly lower than that in the general male population. Lung cancer incidence was higher in maintenance workers than in nonmaintenance workers, but the excess was not statistically significant, as it was based on small numbers with wide confidence intervals. Lung cancer rates in refinery workers did not increase with duration of employment; however, they did tend to be higher in workers hired in earlier decades. Excess mesothelioma incidence in refinery workers is confirmed, but it is likely that there are few if any asbestos-related lung cancers.     

Cardio-respiratory studies on glass bangle workers

Summary Cardio-respiratory functions were recorded in 18 glass bangle workers (Belanias) who worked near the belan furnace continuously for 2 h. The workers were exposed to high ambient temperature (tDB 38.2°C ± 3.4°C) and thermal radiation (tG 46.2°C ±5.1°C) during their work. The physiological responses recorded after the work spell at 1(R₁) 3 (R₃) and 5 (R₅) minute intervals exhibited incomplete recovery. The oral temperature remained significantly high (0.74°F ±0.27°F) even at RS and never reached pre-work value. Similarly the heart rate values remained very high (26.4 ± 5.4 beats/min) at R₁, (10.7 ± 3.9 beats/min) at R₃ and (4.01 ± 2.4 beats/min) at R₅ periods during recovery, thereby showing that heart rate did not regain the pre-work status. The incomplete recovery in heart rate revealed cardiac stress in the exposed workers. Besides the cardiac stress, the cardiac cost of the work under the prevailing hot conditions in the glass bangle industry was very high, adding further to circulatory strain in these workers. Almost all the exposed workers were found to have hyperventilation syndrome characterized by increased respiratory frequency and tidal volume resulting in ventilatory stress induced by physical and physiological heat.     

Polycyclic aromatic hydrocarbons (PAHs): a possible cause of lung cancer mortality among nickel/copper smelter and refinery workers.

A retrospective industrial hygiene investigation was undertaken to explain the cause of a statistically significant excess lung cancer mortality observed in a subset of a large cohort of nickel workers involved in mining, smelting, and refining of nickel and copper in Ontario. The focus of this paper is to demonstrate how an industrial hygiene follow-up assessment of an epidemiologic finding can help to identify a likely cause. Polycyclic aromatic hydrocarbons (PAHs) alone or in association with particulate and gaseous contaminants (e.g., SO2) were likely the causative agents of the excess lung cancer observed among the lead welders, cranemen, and arc furnace workers of the copper refinery.     

Can lung cancer risk among nickel refinery workers be explained by occupational exposures other than nickel?

BACKGROUND: Exposures in nickel refineries represent complex chemical mixtures, but only the effect of nickel has been evaluated quantitatively in epidemiologic studies of nickel workers. METHODS: For a Norwegian refinery, time- and department-specific exposure estimates were developed for arsenic, sulfuric acid mists, and cobalt in air on the basis of personal measurements and chemical data on raw materials and process intermediates. Exposure to asbestos, as well as employment in high-risk occupations outside the refinery, were assessed. We conducted a case-control study nested in a cohort of refinery workers, with 213 cases (diagnosed 1952-1995) and 525 age-matched controls. We analyzed lung cancer risk, adjusted for smoking, by cumulative exposure and duration of work. RESULTS: There was a substantial association between cumulative exposure to water-soluble nickel and lung cancer risk. Weaker effects were suggested for exposure to arsenic at the refinery and for occupational exposures outside the refinery for 15 years or more. No detectable excess risk was found for refinery exposure to asbestos or sulfuric acid mists, and no dose-related increase in risk was seen from cobalt. CONCLUSIONS: Exposure to water-soluble nickel remained the most likely explanation for the excess lung cancer risk in the cohort. Other occupational exposures did not confound the strong dose-related effect of nickel to any appreciable degree.     

Relationship between atmospheric and urinary nickel in workers manufacturing electrical resistances using nickel oxide: role of the bioavailability of nickel

The daily concentrations of nickel in total (ie inhalable) andrespirable airborne dust (personal sampling) and in post-shiftand pre-shift urine samples were monitored during five consecutivework days in 20 workers exposed to NiO in a workshop manufacturingelectrical resistances. The individual daily atmospheric nickelconcentrations ranged from 0.5 to 9586 µg Ni/m³ (geometricmean 22.9) for total dust and from 0.2 to 332 µg Ni/m³(geometric mean 3.5) for respirable dust. The results of theurinary excretion of nickel suggested that the occupationally-relatedsystemic absorption of nickel strongly differed in one subject(worker E) compared to the other 19 workers. In the latter groupthe nickel concentration in urine never exceeded 5 µgNi/g creatinine, it did not differ between post-shift and pre-shiftsamples (geometric means: 1.1 versus 1.2 µg Ni/g creatinine),and it was only slightly higher than that measured in a groupof 17 non-exposed subjects (mean 0.5 µg Ni/g creatinine;range 0.1–1.7); furthermore their nickel elimination inurine did not change during the days off or after two weeksof holiday. In worker E, the nickel concentration ranged from21 to 101 µg Ni/g creatinine in post-shift urine, thenext morning (after 16 h) it had dropped on average by 50 percent, it decreased further during the days off, and amountedstill to 4.4 µg Ni/g creatinine after two weeks of holiday.These divergent patterns of elimination of nickel in urine aremost likely related to differences in the nature of exposureto airborne nickel involving both particle size and bioavailabilityof nickel. Worker E was exposed to NiO powder of 1–8 µmparticle size resulting in nickel levels of the respirable fractionon average about 50 times that measured for the 19 other workers(3 µg Ni/m³). Transformation of the initial NiO powderinto particles of 150 to 600 µm size and associated changesin physicochemical properties of NiO in the particles of therespirable fraction may explain why the urinary excretion ofnickel in the 19 workers is hardly influenced by their occupationalexposure to this metal. The pattern of urinary nickel eliminationin worker E, however, most likely reflects very recent exposureto NiO, suggesting that the degree of bioavailability of nickelfrom this particular physicochemical form of NiO powder is muchhigher than that usually accepted for poorly soluble nickelcompounds.     

Respiratory cancer in a cohort of nickel sinter plant workers.

A study was undertaken of a cohort of nickel refinery workers from a sinter plant that operated from 1948 to 1962. A complete follow-up of the 495 workers has been carried out by searching death records and other measures. Incidence cases known to the Workmen's Compensation Board of Ontario have been included. Fifty-four cases of lung cancer and eight of sinus cancer (including two in men who subsequently developed primary lung cancer) were located. The risk of lung and sinus cancer was much higher in the earlier days of operation of the plant, with an increase rate of over 40% for those employed in the first year of operation. The dose-response relationship has been examined by regressions of standardised morality ratios (SMR) and standardised incidence ratios (SIR). The SIR suggests that the risk doubled at levels of exposure of 12 months (six months in the earlier years).     

More evidence of unpublished industry studies of lead smelter/refinery workers

Background

Lead smelter/refinery workers in the US have had significant exposure to lead and are an important occupational group to study to understand the health effects of chronic lead exposure in adults. Recent research found evidence that studies of lead smelter/refinery workers have been conducted but not published. This paper presents further evidence for this contention.

Objectives

To present further evidence of industry conducted, unpublished epidemiologic studies of lead smelter/refinery workers and health outcomes.

Methods

Historical research relying on primary sources such as internal industry documents and published studies.

Results

ASARCO smelter/refinery workers were studied in the early 1980s and found to have increased risk of lung cancer and stroke in one study, but not in another.

Conclusions

Because occupational lead exposure is an on-going concern for US and overseas workers, all epidemiologic studies should be made available to evaluate and update occupational health and safety standards.     

Dust exposure and impairment of lung function at a small iron foundry in a rapidly developing country

OBJECTIVES—A cross sectional prospective study was carried out among iron foundry workers (exposed) and soft drink bottling and supply company workers (unexposed) to assess their occupational exposure to ambient respiratory dust in their work environment and its effect on their lung function profile.
PARTICIPANTS—Lung function was measured in 81 exposed and 113 unexposed workers. Personal respirable dust concentrations were measured for all the exposed and the unexposed workers. Information on respiratory signs and symptoms was also collected from the participants.
RESULTS—Among the exposed workers, midexpiratory flow (FEF_25-75), forced expiratory volume in 1 second (FEV₁), peak expiratory flow (PEF), FEV₁/FVC, and FEV₁/VC ratios were significantly lower whereas the vital capacity (VC) and forced vital capacity (FVC) were non-significantly higher. Job at the iron foundry was a significant predictor of lung function. Exposure to high concentration of respirable dust at the iron foundry was also a significant predictor. Workers working in high exposure areas (general works, furnace, continuous casting areas, and fabrication workshop) had lower lung function values than workers in medium and low exposure areas. Smoking did not enhance the effects of exposure to dust on lung function.
CONCLUSIONS—Exposure to respirable dust was higher among the iron foundry workers; and among these, general, furnace, rolling mill, and fabrication workers had higher exposures to dust than did workers in continuous casting, the mechanical workshop, and the bottling plant. Job type and exposure to dust were significant predictors of lung function. Implementation of industrial hygiene and proper and efficient use of personal protection equipment while at work could help to protect the respiratory health of industrial workers.


Keywords: lung function; dust exposure; foundry; smoking; personal protection