Nonrespiratory mortality and cancer incidence in a cohort of Canadian nickel workers.

Mortality and cancer incidence were examined for an updated cohort of nonsinter nickel workers in Sudbury and Port Colborne, Ontario, Canada. Abstract results are provided for those with ≥ 15 years since first exposure. For circulatory disease mortality, significant elevations were observed overall in many Sudbury work areas and in Port Colborne staff. Underground miners, with first exposure before 1960, displayed significant elevations for pneumoconiosis, as well as silicosis and anthrasilicosis, likely due to crystalline silica. Significant elevations in colorectal cancer incidence were observed in Sudbury underground mining, mining maintenance, and maintenance work areas. Given a case-control study is not practical, the next cohort update should include more detailed occupational exposure assessment, including dust exposure, diesel engine emissions, solvents, various metals, silica, and sulphur dioxide.

Respiratory cancer mortality and incidence in an updated cohort of Canadian nickel production workers.

Respiratory cancer mortality and incidence were examined in an updated cohort of >56,000 Canadian nickel mining and refining workers. There was little evidence to suggest increased lung cancer risk in workers who had no experience in high-risk sintering operations that were closed by 1972, apart from that which would be expected from probable increased smoking prevalence relative to the comparison population. There was no substantive evidence of increased laryngeal cancer risk in the cohort, nor was there evidence of increased pharyngeal cancer risk in nonsinter workers. Nasal cancer incidence was elevated in nonsinter workers, but excess risks appeared to be confined to those hired prior to 1960. These findings lead us to tentatively conclude that occupationally-related respiratory risks in workers hired over the past 45 years are either very low or nonexistent.

Injury mortality in a cohort of mining, smelting, and refining workers in Ontario.

Injury mortality was followed up from 1950 to 2000 in a cohort of 56,576 nickel workers. Injury fatalities were elevated throughout the cohort of never sinter plant workers (SMR = 134, 95% CI [129, 140]). Elevations were also observed in injury mortality subcategories of road, rail, and air (SMR = 137, 95% CI [127, 147]); boating and swimming (SMR = 150, 95% CI [128, 176]); suicide and possible suicide (SMR = 124, 95% CI [114, 135]); and possibly job-related accidents (SMR = 160, 95% CI [145, 175]). The results were largely attributed to underground miners, with 61.4% of all injury mortality (SMR = 162; 95% CI [153, 171]). Occupational etiology could not be ascertained; however, compiled workplace injury fatalities are presented separately. Recommendations include delivery of injury prevention and wellness programs in partnership with the local health unit and other stakeholders.

Reconstruction of historical exposures at a Welsh nickel refinery (1953-2000).

Past epidemiological studies of workers in a nickel refinery in Clydach, Wales, have shown evidence of large excess respiratory cancer mortality risks [lung cancer relative risk (RR) ≈ 3; nasal cancer RR ≈ 140] in those employed prior to 1930, with risks dropping dramatically in workers hired subsequently. The pre-1930 risks have generally been attributed to high exposures to mixtures of nickel compounds. More recent studies of this refinery's workers have focused on those first hired in 1953, when many of the operations that presumably gave rise to the high exposures were no longer in operation. While these studies have shown greatly decreased lung cancer risks overall (RR ≈ 1.4), and no substantive evidence of increased nasal cancer risk, the absence of reliable exposure estimates have made it difficult to ascertain whether the increased lung cancer risks are nickel related or due to other factors. This study uses nickel measurements from the 1970s to the present, documentation of process changes, and dust measurements taken around the 1950s to construct an exposure matrix for the recent cohort. It provides evidence of at least 30-fold decreases in levels of nickel exposure from the 1950s to the present, with estimated inhalable nickel concentrations in the 1950s in excess of 5mg Ni m(-3).

New views on the hypothesis of respiratory cancer risk from soluble nickel exposure; and reconsideration of this risk's historical sources in nickel refineries.

INTRODUCTION: While epidemiological methods have grown in sophistication during the 20th century, their application in historical occupational (and environmental) health research has also led to a corresponding growth in uncertainty in the validity and reliability of the attribution of risk in the resulting studies, particularly where study periods extend back in time to the immediate postwar era (1945-70) when exposure measurements were sporadic, unsystematically collected and primitive in technique; and, more so, to the pre-WWII era (when exposure data were essentially non-existent). These uncertainties propagate with animal studies that are designed to confirm the carcinogenicity by inhalation exposure of a chemical putatively responsible for historical workplace cancers since exact exposure conditions were never well characterized. In this report, we present a weight of scientific evidence examination of the human and toxicological evidence to show that soluble nickel is not carcinogenic; and, furthermore, that the carcinogenic potencies previously assigned by regulators to sulphidic and oxidic nickel compounds for the purposes of developing occupational exposure limits have likely been overestimated. METHODS: Published, file and archival evidence covering the pertinent epidemiology, biostatistics, confounding factors, toxicology, industrial hygiene and exposure factors, and other risky exposures were examined to evaluate the soluble nickel carcinogenicity hypothesis; and the likely contribution of a competing workplace carcinogen (arsenic) on sulphidic and oxidic nickel risk estimates. FINDINGS: Sharp contrasts in available land area and topography, and consequent intensity of production and refinery process layouts, likely account for differences in nickel species exposures in the Kristiansand (KNR) and Port Colborne (PCNR) refineries. These differences indicate mixed sulphidic and oxidic nickel and arsenic exposures in KNR's historical electrolysis department that were previously overlooked in favour of only soluble nickel exposure; and the absence of comparable insoluble nickel exposures in PCNR's tankhouse, a finding that is consistent with the absence of respiratory cancer risk there. The most recent KNR evidence linking soluble nickel with lung cancer risk arose in a reconfiguration of KNR's historical exposures. But the resulting job exposure matrix lacks an objective, protocol-driven rationale that could provide a valid and reliable basis for analyzing the relationship of KNR lung cancer risk with any nickel species. Evidence of significant arsenic exposure during the processing step in the Clydach refinery's hydrometallurgy department in the 1902-1934 time period likely accounts for most of the elevated respiratory cancer risk observed at that time. An understanding of the mechanism for nickel carcinogenicity remains an elusive goal of toxicological research; as does its capacity to confirm the human health evidence on this subject with animal studies. CONCLUDING REMARKS: Epidemiological methods have failed to accurately identify the source(s) of observed lung cancer risk in at least one nickel refinery (KNR). This failure, together with the negative long-term animal inhalation studies on soluble nickel and other toxicological evidence, strongly suggest that the designation of soluble nickel as carcinogenic should be reconsidered, and that the true causes of historical lung cancer risk at certain nickel refineries lie in other exposures, including insoluble nickel compounds, arsenic, sulphuric acid mists and smoking.

Speciation/fractionation of nickel in airborne particulate matter: improvements in the Zatka sequential leaching procedure.

Modifications are reported to the sequential leaching analytical method for nickel speciation/fractionation specified by Zatka so that larger sample masses can be analyzed. Improvements have been made in the completeness of the sulfide/metallic separation during the peroxide-citrate leach step by use of a larger volume of leachant, a longer leach duration and an orbital shaker. Minimal extraction of metallic nickel in this prolonged sulfidic nickel extraction has been confirmed. An increase in the number of samples analyzed simultaneously using these modifications has resulted in substantial productivity improvements and concomitant lower costs. It is critical for practitioners of sequential leaching techniques to recognize potential limitations and to use professional judgment when interpreting results. For example, results obtained may not be biologically relevant in assessing health risks; the acts of sampling and storage may result in changes in fractionation with time; surface coatings/films may alter the ability of a leachant to react with the target compound; and leaching behaviours may be different for samples differing only in particle size distributions.

Species-specific inhalable exposures in the nickel industry: a new approach for deriving inhalation occupational exposure limits.

The American Conference of Governmental Industrial Hygienists (ACGIH) and some regulatory authorities have revised their exposure limits for nickel and nickel compounds in workplaces based upon new sampling standards for inhalable nickel exposures. Others may be in the process of doing so. Safe standards for workplace exposures should utilize the most up-to-date health data on individual nickel species and should incorporate the principles of new sampling conventions that have been developed over the recent decades. The purpose of this paper is to review the basis for setting inhalable occupational exposure standards for the principal inorganic nickel species. It is hoped that this paper will (1) prompt companies in various nickel industry sectors to begin collecting the necessary inhalable aerosol measurements, speciation data, and particle-size information required to implement health-based sampling programs in the future, and (2) encourage regulators to derive species-specific, inhalable-based workplace standards for nickel and its inorganic compounds.