SUMMARY
Nickel is a naturally occurring element that exists in nature mainly in the form of sulfide, oxide, and silicate minerals. Because it is ubiquitous, humans are constantly exposed to nickel in various amounts. "Zero exposure" to nickel is neither possible, nor desirable. Nickel has been shown to be an essential element in certain microorganisms, animals, and plants. The generally held view is that nickel is probably an essential element for humans as well.
Nickel is an extremely important commercial element. Factors which make nickel and its alloys valuable commodities include strength, corrosion resistance, high ductility, good thermal and electric conductivity, magnetic characteristics, and catalytic properties. Stainless steels are particularly valued for their hygienic properties. In some applications, nickel alloys are essential and cannot be substituted with other materials. Given these many beneficial properties, nickel is used in a wide variety of products discussed below.
1.2 PRODUCTION AND USE
Nickel in one form or another has literally hundreds of thousands of individual applications. Annual world production of nickel products in recent years has averaged in excess of 900 kilotonnes. Primary nickel products are classified by the amount of nickel they contain. Class I products contain almost 100 percent nickel, whereas Class II products vary widely in their nickel content.
Most primary nickel is used in alloys, the most important of which is stainless steel. Other uses include electroplating, foundries, catalysts, batteries, welding rods, coinage, and other miscellaneous applications. The list of end-use applications for nickel is, for all practical purposes, limitless. Nickel is found in transportation products, electronic equipment, chemicals, construction materials, petroleum products, aerospace equipment, durable consumer goods, paints, and ceramics. From this list, it is evident that nickel is a critical metal to industrialized societies.
1.3 SOURCES OF EXPOSURE
Given its many uses and applications, the potential for exposure to nickel, its compounds, and alloys is varied and wide ranging. With respect to occupational exposures, the main routes of toxicological relevance are inhalation and, to a lesser extent, skin contact.
Workers engaged in nickel production - which may include mining, milling, concentrating, smelting, converting, hydrometallurgical processes, refining, and other operations - are exposed to a variety of nickel minerals and compounds depending upon the type of ore mined and the processes used to produce intermediate and primary nickel products. Generally, exposures in the producing industry are to moderately soluble and insoluble forms of nickel. In the producing industry, soluble nickel compounds are more likely to be found in hydrometallurgical operations. Exposures in nickel-using industry sectors vary according to the products produced and include both soluble and relatively insoluble forms of nickel.
In the past, airborne nickel concentrations were believed to have been quite high (> 10 mg Ni/m3) in certain producing operations, with some estimates of exposures as high as 100 mg Ni/m3 or more for Ni3S2 sintering (sometimes referred to as "matte" sintering). More recent estimates of exposure (post-1960) are much lower, with current measurements generally averaging > 1 mg Ni/m3. Exposures to nickel species in user industries have historically been much lower than in producing industries, with estimates generally averaging well below 1 mg Ni/m3.
1.4 PHARMACOKINETICS OF NICKEL
The major routes of nickel intake are dietary ingestion and inhalation. In most individuals, diet constitutes the main source of nickel intake. Recent studies indicate that average dietary intake is approximately 0.15 mg Ni/day. Nickel in drinking water (averages ranging from < 0.001 to 0.01 mg Ni/L) and ambient air (averages ranging from 1 to 60 ng Ni/m3) is generally quite low. Other sources of nickel exposure include contact with nickel-containing articles such as jewelry, medical applications, and tobacco smoke.
For individuals occupationally exposed, total nickel intake is likely to be higher than that of the general populace. Whether diet or workplace exposures constitute the main source of nickel in workers depends upon a number of factors. These factors include the aerodynamic size of the particles and whether the particles are inhalable, the concentration of the nickel that is inhaled, the minute ventilation rate of a worker, whether breathing is nasal or oronasal, the use of respiratory protection equipment, personal hygiene practices, and general work patterns.
Toxicologically speaking, inhalation is the most important route of nickel exposure in the workplace, followed by dermal exposure. Deposition, absorption, and retention of nickel particles in the respiratory tract will depend on many of the factors noted above for intake. Not all particles are inhalable. Humans inhale only about half of the particles with aerodynamic diameters > 30 µm, and it is believed that this efficiency may decline rapidly for particles with aerodynamic diameters between 100 and 200 µm. Of the particles inhaled, only a small portion with aerodynamic diameters larger than 10 µm are deposited in the lower regions of the lung, with deposition in this region predominantly limited to particles £ 4 µm.
Factors such as the amount deposited, solubility, and surface area of the particle will influence the behavior of particles once they are deposited in the lung. The smaller and more soluble the particle, the more rapidly it will be absorbed into the bloodstream and excreted. The residence time of nickel-containing particles in the lung is believed to be an important component of toxicity.
With respect to skin absorption, divalent nickel has been shown to penetrate the skin fastest at sweat ducts and hair follicles; however, the surface area of these ducts and follicles is small. Hence, penetration through the skin is primarily determined by the rate at which nickel is able to diffuse through the horny layer of the epidermis. Although the actual amount of nickel permeating the skin from nickel-containing materials is unknown, in studies using excised human skin, the percent permeation was small, ranging from 0.23 (non-occluded skin) to 3.5 percent (occluded skin) of an administered dose of nickel chloride. Marked differences in the rate of nickel permeation have been reported for nickel solutions, with nickel sulfate solutions permeating the skin at a rate 50 times slower than nickel chloride solutions.
Analyses of human tissues from autopsy studies have shown highest concentrations of nickel in the lungs, thyroid gland, and adrenal gland, followed by lesser concentrations in kidney, liver, heart, spleen, and other tissues. Excretion of absorbed nickel is mainly through urine, whereas unabsorbed nickel is excreted mainly in feces. Nickel also may be excreted in sweat, hair, and human breast milk.
1.5 SUMMARY OF THE TOXICITY OF NICKEL COMPOUNDS
Just as the pharmacokinetics of chemical nickel species are influenced by their physical and chemical properties, concentration, and route of exposure, so, too, are the toxic effects of nickel. Although a number of nickel-related effects, including renal and reproductive effects, have occasionally been reported, the main effects noted in humans are respiratory and dermal. Consequently, the major routes of toxicological relevance in the workplace are inhalation and skin contact.
In most work environments, the potential chronic toxicity of various nickel species is likely to be of more concern than acute effects, with the exception of nickel carbonyl. Long-term exposures to some nickel compounds have been associated with excess lung and nasal sinus cancers. The major source of evidence for this association comes from studies of workers who were employed in certain nickel-refining operations. On the whole, these workers were generally exposed to higher concentrations of nickel than those that prevail in many workplaces today. These workers were also exposed to a variety of other potentially carcinogenic substances, including arsenic compounds, polyaromatic hydrocarbons (PAHs), and sulfuric acid mists. These concurrent exposures make a direct cause and effect interpretation of the data difficult, although in some instances, the animal data help to shed light on the potential carcinogenic role, if any, played by different nickel species. Summarized below are the respiratory and dermal effects associated with exposure to individual nickel species.
1.5.1 Summary of the Toxicity of Metallic Nickel
A determination of the health effects of metallic nickel is based mainly upon epidemiological studies of over 40,000 workers from various nickel-using industry sectors (nickel alloy manufacturing, stainless steel manufacturing, and the manufacturing of barrier material for use in uranium enrichment). These workers were examined for evidence of carcinogenic risk due to exposure to metallic nickel and, in some instances, accompanying oxidic nickel compounds and nickel alloys. No nickel-related excess respiratory cancer risks have been found in any of these workers. Animal data on carcinogenicity are largely in agreement with the human data. Early studies on the inhalation of metallic nickel powder, although somewhat limited with respect to experimental design, are essentially negative for carcinogenicity.
Data relating to respiratory effects associated with short-term exposure to metallic nickel are very limited. One case report of a fatality has been recorded in a man spraying nickel using a thermal arc process. However, the relevance of the case is questionable since the reported exposure to total nickel was extremely high (382 mg Ni/m3). Nevertheless, special precautions to reduce inhalation exposure to fine and ultrafine powders should be taken.
Collectively, animal and human data present a mixed picture with respect to the potential role that metallic nickel may play in non-malignant respiratory disease. A few cases of asthma or fibrosis have been reported in humans and certain inflammatory effects have been noted in animals. However, the overall literature shows that past exposures to metallic nickel have not resulted in excess mortality from such diseases. Additional studies on such effects would be useful.
Skin sensitization to nickel metal can occur wherever there is leaching of nickel ions from articles containing nickel onto exposed skin. Occupational exposures involving direct and prolonged skin contact with metallic nickel may elicit cutaneous allergy (allergic contact dermatitis) in nickel-sensitized workers. However, nickel dermatitis occurs mainly as the result of non-occupational exposures.
1.5.2 Summary of Nickel Metal Alloys
Each type of nickel-containing alloy is a unique substance with its own special physico-chemical and biological properties that differ from those of its individual metal constituents. The potential toxicity of a nickel alloy (including carcinogenic effects) must, therefore, be evaluated separately from the potential toxicity of nickel metal itself and other nickel-containing alloys.
While there are no studies of nickel workers exposed solely to nickel alloys in the absence of metallic or oxidic nickel, studies on stainless steel and nickel alloy workers (who would likely have low level nickel alloy exposures) suggest an absence of nickel-related excess cancer risk. In the main, intratracheal studies on animals have also shown an absence of cancer risk in animals exposed to nickel alloys. Collectively, these studies suggest that nickel alloys do not act as respiratory carcinogens. For many alloys, this may be due to their corrosion resistance that results in reduced release of the metal ions to target tissues.
With respect to non-carcinogenic respiratory effects, no animal data are available for determining such effects, and the human studies that have looked at such endpoints have generally shown no increased mortality due to non-malignant respiratory disease.
Because alloys are specifically formulated to meet the need for manufactured products that are durable and corrosion resistant, an important property of all alloys and metals is that they are insoluble in aqueous solutions. They can, however, react (corrode) in the presence of other media. Of particular importance to dermal exposures are the potential of individual alloys to corrode in sweat. The potential for nickel alloys to elicit an allergic reaction in occupational settings will depend on both the sweat resistant properties of the alloy and the amount of time that a worker is in direct and prolonged skin contact with an alloy. Alloys that release less than 0.5 µg /cm2/week are generally believed to be protective of the majority of nickel-sensitized individuals, when in direct and prolonged skin contact. Alloys that release greater than 0.5 µg /cm2/week of nickel may not, in and of themselves, be harmful. They may be used safely when not in direct and prolonged contact with the skin or where ample protective clothing is provided.
1.5.3 Summary of the Toxicity of Soluble Nickel
The precise role of soluble nickel in human carcinogenicity is uncertain. Although there is some association of soluble nickel with respiratory cancer, this association may reflect the ability of soluble nickel to enhance the carcinogenicity of other agents rather than a direct carcinogenic effect. Epidemiologic information suggests that an increased risk of respiratory cancer associated with refinery process exposure to soluble nickel compounds primarily occurs at levels in excess of 1 mg Ni/m3. However, a few recent studies have noted that exposures slightly lower than this (around 0.5 mg Ni/m3) may have been associated with the excess respiratory cancers observed in workers exposed to soluble nickel.
Well-conducted inhalation animal studies where rats and mice were exposed to soluble nickel at workplace equivalent concentrations up to 2-6 mg Ni/m3 did not show any evidence of carcinogenicity. However, at workplace equivalent levels above 0.1 mg Ni/m3, chronic respiratory toxicity was observed in animal studies. Respiratory toxicity due to soluble nickel exposures may have enhanced the induction of tumors by less soluble nickel compounds or other inhalation carcinogens seen in refinery workers. This mode of action is in agreement with mechanistic information indicating that nickel ions from soluble nickel compounds will not be bioavailable at target respiratory nuclear sites because they have inefficient cellular uptake and are rapidly cleared from the lungs.
With respect to non-malignant respiratory effects in humans, the evidence for soluble nickel salts being a causative factor for occupational asthma, while not overwhelming, is more suggestive than it is for other nickel species. Such evidence arises mainly from a small number of case reports in the electroplating industry and nickel catalyst manufacturing. It should be noted, however, that exposure to soluble nickel can only be inferred in some of the cases and confounding factors (exposure to chromium, cobalt, and plating solutions of low pH) often have not been taken into account.
Aside from asthma, the only other non-carcinogenic respiratory effect reported in nickel workers exposed to soluble nickel is that of fibrosis. Evidence that soluble nickel may act to induce pulmonary fibrosis comes from a recent study of nickel refinery workers that showed modest abnormalities in the chest x-rays of workers. An association between the presence of irregular opacities (ILO >1/0) in chest x-rays and cumulative exposures to soluble nickel, sulfidic nickel, and possibly metallic nickel, was reported. The significance of these results for the clinical diagnosis of fibrosis remains to be determined.
Historically, workplaces where prolonged contact with soluble nickel has been high, have shown high risks for allergic contact nickel dermatitis. For example, nickel dermatitis was common in the past among nickel platers. Due to improved industrial and personal hygiene practices, however, over the past several decades, reports of nickel sensitivity in workplaces, such as the electroplating industry, have been sparse.
1.5.4 Summary of the Toxicity of Oxidic Nickel
Like the above-mentioned species of nickel, the critical health effect of interest in relation to occupational exposure to oxidic nickel is respiratory cancer. Unlike metallic nickel, which does not appear to be carcinogenic, and soluble nickel, whose carcinogenic potential is likely to be promotional in nature, the evidence for the carcinogenicity of certain oxidic nickel compounds is more compelling. That said, there is still some uncertainty regarding the forms of oxidic nickel that induce tumorigenic effects. Although oxidic nickel is present in most major industry sectors, it is of interest to note that epidemiological studies have not consistently implicated all sectors as being associated with respiratory cancer. Indeed, excess respiratory cancers have been observed only in refining operations in which nickel oxides were produced during the refining of sulfidic ores and where exposures were relatively high (> 5 mg Ni/m3). At various stages in this process, nickel-copper oxides may have been formed. In contrast, no excess respiratory cancer risks have been observed in workers exposed to lower levels (< 2 Ni/m3) of oxidic nickel free of copper during the refining of lateritic ores or in the nickel-using industry.
A high calcining temperature nickel oxide administered to rats and mice in a two-year inhalation study did show some evidence of carcinogenicity in rats. In intraperitoneal studies, nickel-copper oxides have appeared to be as potent as nickel subsulfide in inducing tumors at injection sites. There is, however, no strong evidence to indicate that black (low temperature) and green (high temperature) nickel oxides differ substantially with regard to tumor-producing potency.
There is no single unifying physical characteristic that differentiates oxidic nickel compounds with respect to their in vitro genotoxicity or carcinogenic potential. Some general physical characteristics which may be related to carcinogenicity include: particle size £ 5 µm, large particle surface area, presence of metallic or other impurities and/or amount of Ni (III), and the ability to induce reactive oxygen radicals. Phagocytosis appears to be a necessary, but not sufficient condition for carcinogenesis. Solubility in biological fluids will also affect how much nickel ion is delivered to target sites (i.e., cell nucleus).
With respect to non-malignant respiratory effects, oxidic nickel compounds do not appear to be respiratory sensitizers. Based upon numerous epidemiological studies of nickel-producing workers, nickel alloy workers, and stainless steel workers, there is little indication that exposure to oxidic nickel results in excess mortality from chronic respiratory disease. In the few instances where excess risks of non-malignant respiratory disease did appear-for example, in refining workers in Wales-the excesses were seen only in workers with high nickel exposures (> 10 mg Ni/m3), in areas that were reported to be very dusty. With the elimination of these dusty conditions, the risk that existed in these areas seems largely to have disappeared by the 1930s. In two studies of nickel workers using lung radiographs, there was no evidence that oxidic nickel dusts caused a significant fibrotic response.
Dermal exposures to oxidic nickel are believed to be of little consequence to nickel workers. While no data are directly available on the effects of oxidic nickel compounds on skin, due to their low water solubility, little skin absorption of nickel ions is expected.
1.5.5 Summary of the Toxicity of Sulfidic Nickel
Of all the nickel species examined in this document, a causal relationship for respiratory cancer can best be established for nickel subsulfide. The human data suggest that respiratory cancers have been primarily associated with exposures to less soluble forms of nickel (including sulfidic nickel) at concentrations in excess of 10 mg Ni/m3. Animal data unequivocally point to nickel subsulfide as being carcinogenic.
Relative to other nickel compounds, nickel subsulfide may be the most efficient at inducing the heritable changes needed for the cancer process. In vivo, nickel subsulfide is likely to be readily phagocytized and dissolved by respiratory epithelial cells resulting in efficient delivery of nickel (II) to the target site within the cell nucleus. In addition, nickel subsulfide has relatively high solubility in biological fluids which results in the release of nickel (II) ions, with subsequent induction of cell toxicity and inflammation. Chronic cell toxicity and inflammation may enhance tumor formation by nickel subsulfide or other carcinogens (as discussed for soluble nickel compounds).
The evidence for non-malignant respiratory effects in workers exposed to sulfidic nickel has been mixed. Mortality due to non-malignant respiratory disease has not been observed in Canadian sinter workers, but has in refining workers in Wales. With the elimination of the very dusty conditions that likely brought about such effects, the risk of respiratory disease disappeared in the Welsh workers by the 1930s. In a recent study of Norwegian nickel refinery workers, an increased risk of pulmonary fibrosis was found in workers with cumulative exposure to sulfidic and soluble nickel. The significance of these results for the clinical diagnosis of fibrosis remains to be determined.
No relevant studies of dermal exposure have been conducted on workers exposed to sulfidic nickel. Likewise, no animal studies have been undertaken.
1.5.6 Summary of the Toxicity of Nickel Carbonyl
The human data unequivocally show that nickel carbonyl is an agent which is extremely toxic to man; the animal data are in agreement with respect to this acute toxicity.
It is not possible to assess the potential carcinogenicity of nickel carbonyl from either human or animal data. Unless additional, long-term carcinogenicity studies in animals can be conducted at doses that do not exceed the Maximum Tolerated Dose (MTD) for toxicity, the database for the carcinogenicity of nickel carbonyl will remain unfilled. This issue may only be of academic interest since engineering controls and close monitoring of nickel carbonyl exposure to prevent acute toxicity greatly limit possible exposures to this compound.
Exposures to nickel carbonyl are usually confounded with exposures to other nickel compounds. However, for acute nickel carbonyl exposures urinary nickel can be used as a health guidance value to predict health effects and the need for treatment. Reasonably close correlations between the clinical severity of acute poisoning and urinary concentrations of nickel during the initial three days after exposure have been established as follows:
| Symptoms |
18-hr urine specimen(µg Ni/l) |
| Mild |
60-100 |
| Moderate |
100-500 |
| Severe |
>500 |
These values, however, are only relevant when urinary nickel is not elevated due to other nickel compound exposures.
Recent experience at a nickel carbonyl refinery has shown that the clinical severity of the acute nickel carbonyl exposure can also be correlated to nickel levels in early urinary samples (within the first 12 hours of exposure). The use of an 8-hour post exposure urinary nickel specimen may also be helpful in categorizing cases and determining the need for chelation therapy.
1.6 ASSESSING THE RISKS OF WORKERS EXPOSED TO NICKEL
Any efforts to evaluate occupational health risks such as those identified above must start with good data collection. This includes not only monitoring workplace exposures (discussed in greater detail in the next section), but assessing the health of individual workers with the ultimate goal of keeping the worker healthy and reducing the overall risks in the work environment. It is not enough to periodically monitor workers, but programs must be implemented in ways that allow for the systematic collection of data that can be used in epidemiological studies and, subsequently, risk assessment. In some countries, implementation of a health surveillance program is obligatory. In such instances, any company-based surveillance program should be in compliance with the relevant local/national guidelines. Developing infrastructure and systems that support consistent data collection and storage requires effort, careful planning, and an adequate allocation of resources.
The general steps involved in the assessment of risks include:
- Determining the population at risk.
- Identifying the hazards.
- Assessing exposures and health outcomes.
- Developing data collection and management systems.
- Training and benchmarking.
For purposes of risk assessment, records should be kept on most, if not all, workers employed in the nickel industry. This includes not only production workers, but office workers and support staff as well. Consideration should also be given to contractors, such as temporary workers or long-term maintenance crews employed at factories, as some of these workers may be employed in potentially high exposure jobs. Companies should assign a unique identifier to each individual.
It is also important to identify all potentially harmful substances in a workplace and to monitor and control exposures in order to manage the risk. All the nickel species present in an industrial setting should be identified, and a complete inventory of raw materials used, materials produced, by-products, and contaminants should be taken. Consideration should be given to monitoring these materials not only under normal operations, but also when short-term peak exposures occur (e.g., during maintenance). In addition, a record should be made of all procedures and equipment used (including control equipment such as local exhaust ventilation and respirators), changes in processes, and changes in feed materials. Complementing this description of the worksite should be a description of each worker's employment history, both past and present.
With respect to exposures, two types of exposure data are required: those that pertain to the ambient environment (e.g. workplace air) and those that pertain to the internal environment of the worker (e.g. health surveillance). To be of use in risk assessment, each must be linked to the other. Health surveillance may be used to evaluate an individual's health prior to, during, and at termination of employment. Occasionally, it also may be used during retirement. Considerable clinical skill and judgment are required to assess work-related health effects. Consultation with properly trained personnel is critical. Issues such as the invasiveness, sensitivity, and accuracy of testing procedures must be considered carefully, as should the rights of the workers. Laws regarding discriminatory practices in hiring and job placement should be strictly followed, as should laws regarding recordkeeping. Any health data gathered and recorded should be subject to rigorous quality control.
In structuring a health surveillance program, consideration ideally should be given to the following components:
Pre-placement assessment. Of particular importance is the identification of pre-existing medical conditions in target organs (notably the respiratory system and skin, but also reproductive and renal systems) that potentially might be affected by nickel and its compounds. A pre-placement assessment should typically include, but not necessarily be limited to: baseline health data, a detailed history of previous disease and occupational exposures, present or past history of allergies (particularly nickel-related) including asthma, identification of personal habits (most notably, smoking) and hobbies, a physical examination (which may include chest X-rays and other pulmonary tests), and evaluation of the suitability of a worker to wear respiratory protection equipment.
Periodic assessment. Such an assessment generally consists of an update of the above, but may also include more extensive testing. Unless mandated more frequently by law, measurements of respiratory function and chest x-rays should be considered around every 5 years. Depending on the age, the smoking status, and the job task (nature and level of exposure), more frequent chest X-rays may be appropriate.
Skin patch testing is not recommended as a routine pre-employment procedure because there is a possibility that such test may sensitize the applicant. However, in special circumstances, such testing may be warranted for purposes of clinical diagnosis. Patch testing should only be undertaken by persons experienced in the use of the technique.
In many industrial health surveillance programs, workers may be monitored for markers of exposure in body fluids, with the intent of establishing a correlation between external exposure, internal exposure (as measured by the marker), and effect. However, in the case of nickel, a biological monitoring program should be implemented only after careful consideration of the facts and limitations of such a program. While of some value as a marker of exposure, nickel in urine, blood, and other tissues or fluids (with the exception of nickel carbonyl) has not been shown to be predictive of health risks. Given that biological monitoring reflects only the amount of solubilized nickel present in biological materials and not true body burden, its utility is questionable as an early warning device of potential health effects that are generally organ-specific, long-term, and accumulative in nature.
If implemented, a biological monitoring program should augment both environmental monitoring and industrial hygiene programs. It should never be implemented as a "stand alone" program. Given the above limitations, biological monitoring may have a place, but mainly in specific situations, e.g. where exposures are to soluble nickel compounds, fine nickel metal powders, or nickel carbonyl. It is less useful in situations where exposures are predominantly to insoluble compounds of larger particle size or where exposures are mixed. If biological monitoring is undertaken, urinary sampling is generally preferred over serum sampling because it is less invasive and easier to conduct.
It is preferable that any health surveillance program implemented be administered by qualified occupational health specialists. However, once a proper data collection system is in place, non-expert staff, with appropriate training, can help to collect some of the data on a day-to-day basis.
Lastly, any surveillance program that is implemented should be evaluated to know how well it is working. This entails establishing sound database management systems, filling recognized data gaps, and setting goals against which future evaluations can be made.
1.7 WORKPLACE SURVEILLANCE
Knowledge of general exposure conditions within the workplace is another element of a good worker protection program. Workplace surveillance entails understanding applicable legislative/regulatory occupational exposure limits and implementing an air monitoring program that allows for the comparison of worker exposures to these limits. It is necessary for the employer to keep abreast of current recommended and mandated exposure limits regarding nickel and its compounds and to assure that workplace exposures comply with these limits.
Components of an air monitoring program are:
- development of a sampling strategy,
- purchase or rental of sampling equipment and supplies,
- calibration of equipment,
- sample collection,
- sample analysis,
- calculation of exposure concentrations,
- determination of compliance status,
- notification of employees of the results, and
- documentation and recordkeeping.
Specific requirements for each of these components may differ from country to country therefore, employers should consult the appropriate government agency and/or code for detailed procedures on establishing an air monitoring program. Air monitoring is not an end in itself but should be considered part of an overall program of risk assessment and management. It is necessary to evaluate monitoring results and decide whether any action is required to modify the sampling procedures or working environment.
When monitoring, it is important that the sampling strategy be flexibly designed to account for differences in worker and job variability. This means that different sampling strategies may need to be employed in different areas of a plant. It is also important to note that while either personal or static sampling devices may be used (provided that regional regulations do not stipulate a particular method), personal sampling is best suited to evaluating worker exposure while static sampling is a preferred tool for data collection for engineering controls. In all cases, the employees' support should be sought by explaining the reason for sampling and asking for their participation.
Recently, the search for a more rational, health-related aerosol sampling has resulted in the development of an inhalable sampler at the Institute of Occupational Medicine. This sampler takes into consideration the efficiency of inhalation of the human head and the deposition of particles in the nasopharyngeal, thoracic and alveolar regions of the respiratory tract.
Side-by-side comparisons of the inhalable sampler to "total" aerosol samplers (such as the 37 mm sampler) have shown the inhalable sampler to consistently measure 2-3 more aerosol than the "total" sampler. The observed biases tended to be greater for workplaces where aerosols are coarser.
As noted above, health effects associated with nickel exposures may be dependent upon a number of factors including chemical form (speciation), particle size, and solubility within biological fluids. Research projects currently underway are designed to provide new methods and means for collecting biologically-meaningful aerosol fractions. In fact, the American Conference of Governmental Industrial Hygienists (ACGIH) have proposed setting their Threshold Limit Value (TLV) recommendations for nickel compounds based upon the "inhalable" particulate fraction. Once these recommendations become final, countries that use the ACGIH TLVs to set their own Occupational Exposure Limits will be likely to make the appropriate changes. In the interim, it may be prudent to begin a program of evaluating the use of an inhalable dust fraction sampler, obtain measurements of particle size distribution, and to determine nickel species in samples when reasonably practicable.
Good industrial hygiene practice requires that an employer provide the sampled employees (and those unsampled employees whose exposures they are deemed to represent) with their personal sampling results and an explanation of their meaning. Group results should also be shared with the workforce. Where the results of sampling a "representative" individual(s) are made available to other workers, consideration should be given to withholding personal identifiers. Exposure recordkeeping requirements may vary from country to country; hence, it is advisable to consult with the appropriate authority for details on possible mandatory requirements. Like health data, exposure monitoring data should be subject to rigorous quality control.
1.8 CONTROL MEASURES
Whenever conditions suggest high exposures or monitoring indicates a potential for overexposure, measures to control exposures should be taken. Control options fall into four categories:
- engineering controls,
- administrative controls,
- control through work practices, and
- personal protective equipment (PPE).
Typically, engineering, administrative, and work practice controls are preferred over PPE when feasible. Since regulatory authorities may differ in their definition of "feasible" controls, employers should contact their respective authority for specific guidelines.
Three categories of engineering controls generally are considered - substitution, enclosure, and ventilation. Of these three options, ventilation is probably the most widely employed as a means of controlling exposures, although it is not necessarily the most effective in all situations. In choosing among options, consideration should be given to the nature of the operation (e.g. is the operation likely to be continuously dusty), the materials handled, feasibility, and regulatory requirements.
When employed, exhaust fans and exhaust ventilation (i.e., exhaust hoods at the source of exposure) are preferred over intake fans for work area ventilation. Ventilation design is complex and should be undertaken only by suitably trained engineers. The designer should consider both the regulations that govern exposure to workplace contaminants and the process operation itself, including the materials being used and the frequency with which they are handled.
Administrative controls, such as employee rotations and workshift modification, can also be used to reduce individual exposures, but such practices should be secondary to engineering controls.
In any industrial setting, it is important to engage in good housekeeping and personal hygiene practices. In the nickel industry, special care should also be taken to reduce the risk of contact dermatitis (e.g. by wearing protective clothing and gloves) and the risk of inhaling nickel in excess of permissible limits. Because smoking is the most common cause of respiratory cancer, it should be discouraged, if not banned.
Personal protective equipment (PPE) ordinarily is the last control option considered. Use of PPE should occur under a properly administered program. When the use of respirators is involved, a written program should be established which describes management and employee responsibilities, respirator selection, fitting, and fit-testing, employee instruction and training, medical screening, and program evaluation. Because recommendations on the use of respirators and other protective equipment may vary from country to country, employers should contact their appropriate authority for guidance.
1.9 LIMIT VALUES AND HAZARD COMMUNICATION
A number of countries and jurisdictions have established specific regulatory requirements for hazard communication relating to the use, handling, and presence of chemicals in the workplace. Such information must be relayed to workers and sometimes to a variety of "end-users" of the chemical, as well as any other parties that may be affected by exposure to the chemical.
Generally speaking, three components comprise a hazard communication program: labeling, Material Safety Data Sheets (MSDS), and worker training. The producer/supplier is responsible for preparing labels and MSDSs and seeing that these are delivered to its customer. Worker training is the responsibility of all employers, regardless of industry sector. As important differences may exist between jurisdictions, employers should contact their relevant authorities for further detailed information on such programs and any specific requirements pertaining to nickel.
