Description

Lead

Lead production. Six lead mines in Missouri, plus five mines in Alaska, Idaho, and Washington, produce lead as a principal product or byproduct, but nearly all lead mine production in the United States has been exported since the last primary lead smelter closed in 2013 (334); 12 secondary refineries in 10 states account for almost all the secondary lead produced.

Lead use. The lead-acid battery industry accounts for the vast majority (about 93%) of U.S. lead consumption (334). Lead-acid batteries are used as starting-lighting-ignition batteries for automobiles, as industrial-type batteries for standby power for computer and telecommunications networks, and for motive power (334).

Lead consumption is declining in the United States for several reasons: (1) a decline in automobile production, (2) increased use of lithium-ion batteries, (3) substitution by plastics for lead in cable covering and cans, (4) use of tin instead of lead in solder for potable water systems, (5) increased use of lead-free solders in the electronics industry, (6) a switch to flat-panel displays that do not require lead shielding, and (7) use of steel and zinc as substitutes for lead in wheel weights (334).

Occupational lead poisoning. Lead exposures historically have been high in mining, ore crushing and sampling, and the smelting and refining of metals where accumulations of ground lead ore cover the floor and machinery surfaces, still finer dust clings to the walls and all projecting surfaces, and lead fumes are dispersed into the ambient air of the workspace (182; 183).

Engineering controls mitigate this somewhat (eg, flared ventilation hoods), but gaps are common where lead ore dust or lead fumes are dispersed in the work areas. Personal protective equipment helps minimize exposure but is often circumvented (eg, removing respirators for convenience because of fogging of the viewing surface or to eat or smoke). Eating and smoking in work areas greatly increases potential lead exposure, in part because of the repetitive hand-to-mouth behavior and the likelihood of contamination of hands or surfaces in the work area.

Other, often unrecognized or underappreciated exposure risks involve professional users (eg, police) and employees of indoor firing ranges (60; 76; 78; 28), foundry workers (183; 284), workers manufacturing batteries (183; 284), workers involved in recycling lead or directly working with lead compounds, and workers manufacturing pottery (183; 150).

Occupational lead poisoning continues to be a significant problem in the United States (04; 05; 28; 59; 60; 61; 63; 64; 65; 66; 67; 68; 69; 70; 71; 72; 73; 74; 75; 77; 79; 80; 81; 82; 83; 84; 85; 86; 87; 181; 201; 349) and other countries (62). Almost two thirds (63%) of adults with very high blood lead levels (BLL 40 µg/dL or higher) have an occupational source of lead, almost one half (32%) have an unknown exposure source, and only 5% have a nonoccupational source (87). Occupational lead poisoning almost always involves inorganic lead.

Although adult blood lead levels have generally declined over the past 30 years, the most recent figures indicate that 20 per 100,000 adults have blood lead levels (BLLs) of at least 10 μg/dL, whereas five per 100,000 adults have BLLs of at least 25 μg/dL (83; 85; 04; 05). Some states have higher rates of adults with elevated blood levels; these include Alabama, Alaska, Iowa, Kansas, Missouri, New Hampshire, New Jersey, New York, North Carolina, Ohio, Pennsylvania, Rhode Island, Wisconsin, and Wyoming, but some others that would likely be among states with higher than average rates did not participate in the Adult Blood Lead Epidemiology and Surveillance (ABLE) program or did not submit data on the number of adults exceeding the stated thresholds. These numbers primarily reflect occupational exposures in the mining and manufacturing sectors.

The Adult Blood Lead Epidemiology and Surveillance (ABLES) Program identified 11,536 adults with at least one very high blood lead level in the United States over the 10-year interval from 2002 to 2011; of these, 2,210 (19%) had persistently high blood lead levels in 2 or more years in that interval (87). Blood lead levels are shown for four of these individuals: three with occupational sources for lead exposure and one with a nonoccupational exposure source (87). Of the three with occupational exposures, one was responsible for recycling grit and steel from bridge painting, one worked in construction and painting, and one worked in battery manufacturing.

Occupations associated with very high blood levels in the United States are shown in Table 1.

Table 1. Occupations Associated with Very High Blood Levels in the United States

Metabolism. Lead in an occupational setting is absorbed primarily via the respiratory route, whereas gastrointestinal absorption is the primary route in nonoccupational settings; transdermal absorption of inorganic lead is negligible. At least 95% of circulating lead is bound to erythrocytes. At a steady state, about 90% of the lead body burden is bound to bone. Although inorganic lead does pass the blood-brain barrier, the concentration of lead in the central nervous system remains comparatively low.

Lead is excreted very slowly from the body (with a half-life of about 10 years), primarily by renal and gastrointestinal routes (both unabsorbed lead and gastrointestinal net excretion). Renal excretion is predominantly (and possibly exclusively) by glomerular filtration. Gastrointestinal excretion includes (1) active secretion or passive loss from salivary glands, the pancreas, and the intestinal wall; (2) shedding of epithelial cells; and (3) biliary excretion.

Lead acts as a cellular toxin, in part by inhibiting mitochondrial respiration.

Occupational exposure limits. The Occupational Safety and Health Administration requires that industries limit airborne lead levels to 50 µg/m3 without reliance or respirator protection through a combination of engineering, work practice, and other administrative controls (Table 2). While these controls are being implemented, respirators must be used to meet the 50 µg/m3 exposure limit (Tables 3 and 4). The action level at which an employer must begin specific compliance activities, including blood lead testing for exposed workers, is 30 µg/m3.

Table 2. Exposure Limits for Inorganic Lead

Table 3. OSHA Respirator Requirements (General Industry Lead Standard)

Table 4. OSHA Respirator Requirements (Construction Lead Standard)

Biologic monitoring. The U.S. OSHA standard for biologic monitoring of workers requires that both blood lead levels and zinc protoporphyrin be monitored on a regular basis (Table 5). The lead level in whole blood provides a direct measure of recent exposure, whereas zinc protoporphyrin and hemoglobin serve as measures of the biochemical effect of exposure. Zinc protoporphyrin is an indicator of average exposure to lead over the last 3 to 4 months but does not reflect recent or acute lead exposure because it does not change quickly when the source of lead exposure is removed. Erythrocyte protoporphyrin accumulates in red blood cells when insufficient iron is present for proper heme synthesis; a small percentage of erythrocyte protoporphyrin is unbound and can be measured as free erythrocyte protoporphyrin, with the remaining erythrocyte protoporphyrin (about 90%) measured as zinc protoporphyrin. Although OSHA does not set limits for zinc protoporphyrin or hemoglobin (which may fluctuate for reasons other than lead exposure), a zinc protoporphyrin of 500 µg/dL can be considered the highest permissible level for a worker with a blood lead level of 50 µg/dL. Confirmed hemoglobin levels less than 11.0 g/dL for men and less than 10.0 g/dL for women warrant investigation.

Table 5. U.S. OSHA Blood Lead Level Compliance Scheme

Organolead (tetraethyl and tetramethyl lead)

Tetraethyllead (tetraethyl lead; TEL; Pb[C2H5]4), and to a lesser extent tetramethyl lead, was used as a fuel additive for much of the 20th century, first being mixed with gasoline beginning in the 1920s as an “antiknock agent” (ie, a gasoline additive that raised the temperature and pressure at which auto-ignition occurs, thus preventing early ignition -- knocking -- before the correctly timed spark). “Leaded gasoline” had an increased octane rating (a measure of a fuel's ability to resist knocking) that allowed engine compression to be raised substantially, improving vehicle performance and fuel economy. Many countries began phasing out the use of tetraethyllead in automotive fuel in the 1970s because of its contribution to environmental lead contamination and its negative impact on brain health, particularly in children, even though this had been opposed and effectively delayed by industry (15; 286; 253; 215; 237; 247; 305; 306; 216; 241), and the risks had been minimalized by government after its use was already established (21; 286). Since 2011, leaded gasoline has been banned in every country as an automobile fuel, although it is still used in certain grades of aviation fuel.

Inorganic mercury

Mercury production. Mercury has not been produced as a principal mineral commodity in the United States since 1992, although mercury is recovered as a byproduct from processing gold-silver ore at several mines in Nevada, and secondary, or recycled, mercury is recovered from batteries, compact and traditional fluorescent lamps, dental amalgam, medical devices, and thermostats, as well as mercury-contaminated soils (334).

Mercury use. Domestic mercury consumption has been declining in the United States for several reasons: (1) reduced use of conventional fluorescent tubes and compact fluorescent bulbs with conversion to LED lighting; (2) substitution of nonmercury-containing products in control, dental, and measuring applications; (3) conversion to nonmercury technology for chloralkali production; and (4) discontinuation of mercury use in most batteries and paints manufactured in the United States (334). Some button-type batteries, cleansers, fireworks, folk medicines, grandfather clocks, pesticides, and skin-lightening creams and soaps may still contain mercury (334).

The leading domestic end users of mercury in the United States are the chlorine-caustic soda (chloralkali), dental, electronics, and fluorescent-lighting manufacturing industries (334). Only two mercury cell chloralkali plants still operate in the United States. Beginning January 1, 2013, the export of elemental mercury from the United States was banned (with some exceptions) under the Mercury Export Ban Act of 2008, and effective January 1, 2020, exports of five additional mercury compounds were banned (334).

Table 6. Work Environments With Risk of Mercury Exposure

Around the world, the most common source of occupational inorganic mercury poisoning is now artisanal and small-scale gold mining (230; 43; 03; 49; 107; 105; 106; 33; 116; 121; 233; 235; 23; 185; 186; 125; 124; 111; 153; 208; 294; 295; 40; 36; 37; 38; 39; 50; 170; 136; 167; 312; 162; 282; 315; 316; 103; 267; 277; 112; 29; 261; 260; 330; 164; 280; 271; 297; 342; 152; 236; 244; 35; 58; 118; 157; 246; 252; 255; 234; 320; 321; 113; 218; 248; 264; 268; 301; 07; 204; 332; 336; 117; 158; 211; 214; 346; 348; 189; 291; 341; 122; 166; 274).

The rapid escalation of gold prices has spurred a new gold rush in developing countries, particularly using artisanal and small-scale gold mining, ie, mining activities that use rudimentary methods to extract and process minerals and metals on a small scale (325). Globally, 14 to 19 million people, typically the poorest and most marginalized, work in artisanal and small-scale gold mining, which produces about 20% of global gold output--the world's largest anthropogenic source of mercury emissions (321). Based on human biomonitoring data, between 25% and 33% of these miners--3.3-6.5 million people globally--suffer from moderate chronic metallic mercury vapor intoxication (321). The resulting global burden of mercury poisoning from artisanal and small-scale gold mining is estimated to range from 1.22 to 2.39 million disability-adjusted life years (321).

Since the 1990s, the most severe problems with mercury poisoning related to artisanal and small-scale gold mining have been in South America's Amazon River Basin (Bolivia, Brazil, Colombia, Ecuador, Guyana, Peru, Suriname, and Venezuela) (Boischio and Cernichiari 1993; 43; 235; 186; 105; 105; 106; 208; 294; 162; 267; 29; 164; 342; 157; 07; 348; 274), Africa (185; 315; 316; 36; 38; 261; 330; 346; 291), Indonesia (36; 37; 246; 264; 204), and the Philippines (23; 125). Most artisanal and small-scale miners in the Amazon work illegally, often in protected areas where mining is prohibited. In Colombia and Venezuela, where organized crime is strongly linked to illegal gold mining, narco-terrorist and guerilla groups have extorted miners to finance their operations (329). Small numbers of cases of inhalational mercury toxicity from artisanal gold extraction continue to occur in the United States (252; 341).

Miners use liquid mercury to separate the gold from either refined ore (concentrate amalgamation) or whole ore without concentration (whole-ore amalgamation, which requires greater quantities of mercury), forming a mercury-gold amalgam. The amalgam is then heated to burn off the mercury, leaving purified gold behind; since at least the 1990s, this is typically done in the open with a blow torch for artisanal and small-scale gold mining (125; 342). Mercury-contaminated slurry is also typically discarded directly into waterways (342). This mercury-dependent gold extraction process exposes miners and their families to harmful mercury vapor and methylmercury (formed from inorganic mercury by the action of microbes that live in aquatic systems and then is bioaccumulated through the food chain) (342; 236; 214; 274).

Release into the environment. Mercury continues to be released to the environment from numerous sources, including (1) mercury-containing car switches (when automobiles produced prior to 2003 are scrapped without recovering them for recycling), (2) coal-fired powerplant emissions, (3) incineration of mercury-containing medical devices, and (4) from naturally occurring sources (334). In many developing countries, mercury used in the recovery of gold in artisanal and small-scale gold mining is burned off with blow torches into the atmosphere or is dumped into waterways.

Occupational mercury poisoning. Occupational mercury poisoning is almost always caused by inhaling mercury vapor and dust of mercury compounds. Skin contact and gastrointestinal absorption are not significant contributors to the absorption of metallic mercury, whereas methyl mercury is almost completely absorbed from the gastrointestinal tract. Some inorganic mercury compounds are nevertheless extremely toxic and corrosive; for example, as little as 1 to 4 gm of mercuric chloride (mercury[II] chloride; mercury bichloride; mercury dichloride; corrosive sublimate; HgCl2) is fatal with corrosive injury of the gastrointestinal tract, acute renal failure, and circulatory collapse (27; 52; 217; 231), whereas mercurous chloride (mercury[I] chloride or calomel, Hg2Cl2) is comparatively harmless and was used as a laxative and as a treatment for syphilis from the 17th to late 19th century.

Occupational exposure limits. Exposure limits for inorganic mercury are provided in Table 7, and NIOSH respirator recommendations based on airborne concentration of mercury vapor or condition of use are provided in Table 8.

Table 7. Exposure Limits for Inorganic Mercury*

Table 8. Respirator Recommendations (CDC/NIOSH)

Biological monitoring. Clinical signs are essential for diagnosis, particularly (1) neurobehavioral changes, (2) intention tremor, and (3) gum changes. A determination of urinary mercury levels, preferably a 24-hour collection, should be made, although the correlation between urinary mercury levels and clinical manifestations is poor. Special mercury-free bottles and stoppers must be used to collect blood and urine specimens.

Interpretation guidelines for urinary mercury levels (μg/L) in workers exposed to inorganic mercury vapor are as follows: normal < 10 μg/L; increased mercury absorption > 50 μg/L; warning level > 100 μg/L; hazardous level (remove from further exposure) > 200 μg/L; symptomatic poisoning likely > 300 μg/L (300).

Organic mercury

Most exposures to organic mercury are environmental rather than directly occupational, but occupational cases do occur.

Dimethyl mercury poisoning. Until 1998, dimethylmercury was the common calibration standard for 199Hg NMR spectroscopy. However, dimethylmercury is extremely toxic, and even an accidental, brief exposure can be fatal. Several deaths were reported among laboratory technicians who synthesized the compound (266; 250).

As a result of a single tragic case in 1998 (140; 250), OSHA issued a Hazard Information Bulletin (256). OSHA guidelines include the following:

Manganese

Manganese ore containing 20% or more manganese has not been produced domestically in the United States since 1970 (334). Manganese ore is consumed mainly by eight firms with plants in the East and Midwest (334). Most ore consumption is related to steel production, either directly in pig iron manufacture or indirectly through upgrading the ore to ferroalloys (334). Additional quantities of ore are used in the production of dry cell batteries, in fertilizers and animal feed, and as a brick colorant (334).

The main source of manganese uptake in occupational manganese poisoning (manganism) is the inhalation of manganese dust or fumes. The primary target organs of toxicity are the lungs and the brain.

Biomarkers. The relationships between manganese biomarkers--including biomarkers in blood, plasma, serum, erythrocytes, urine, bone, toenails, fingernails, hair, and saliva--and both external manganese exposure indices and neurofunctional impairments are limited and inconsistent (313; 283; 207). Laboratory biomarkers of manganese exposure have not been proven to be useful, in part because there is a complex and limited relationship between exposure and blood manganese levels that may depend on exposure attributes and the latency of blood sampling relative to exposure; in particular, plasma and urine manganese levels appear to be of little utility as exposure biomarkers (313). Although one study reported a statistically significant association between a Cumulative Exposure Index for manganese with bone manganese levels, this was not clinically useful as the correlation was only moderate (ρ=0.44) (283).

Occupational exposure limits. Exposure limits for manganese are given in Table 9. What is distinctive about available exposure limits for manganese compared to other neurotoxic metals is the wide disparity from different sources. OSHA does not even provide a permissible exposure level time-weighted average but only a high ceiling level. In 2012, the American Conference of Governmental Industrial Hygienists recommended a 10-fold reduction in the current threshold limit value time-weighted average (TLV-TWA) for inhaled manganese particles measured over an 8-hour shift from 0.2 mg/m3 to 0.02 mg/m3. The National Institute for Occupational Safety and Health recommended exposure limit is now two orders of magnitude higher than the threshold limit value of the American Conference of Governmental Industrial Hygienists (ACGIH). Given the dramatic permanent neurotoxic damage caused by manganese, it would seem prudent to use the most stringent exposure limits, those of the ACGIH.

Table 9. Exposure Limits for Manganese