Para-occupational poisoning …

Douglas J Lanska MD MS MSPH

Neurotoxicology

Updated 06.16.2024
Expires For CME 06.16.2027

Para-occupational poisoning

Author: Douglas J Lanska MD MS MSPH

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Para-occupational poisoning

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Introduction

Overview

Para-occupational ("take-home") poisonings derive from occupations and industries but affect individuals who are not themselves workers in the occupation or industry. Routes of para-occupational poisoning include transmission of toxic substances to bystanders without a human vector (ie, humans do not transmit the pathogen), transmission of toxic substances from workers to nonworkers, and germline mutations in workers affecting offspring. Transmission without a human vector may be by environmental contamination, particularly near the responsible industry or toxic dumpsite, or by transmission to bystanders at work, especially with cottage industries.

Transmission of toxic substances from workers to nonworkers may be via breast milk or other bodily fluids, transplacental transmission, or via fomites (ie, a substance, such as clothing, capable of adsorbing and transmitting an agent of disease). Para-occupational poisonings with major neurologic effects include lead, mercury, and organophosphorus pesticide poisonings.

Key points

	• Para-occupational ("take-home") poisonings derive from occupations and industries but affect individuals who are not themselves workers in the occupation or industry.
	• Routes of para-occupational poisoning include transmission of toxic substances to bystanders without a human vector (ie, humans do not transmit the pathogen), transmission of toxic substances from workers to nonworkers, and germline mutations in workers affecting offspring.
	• Transmission of para-occupational poisoning without a human vector may be by environmental contamination, particularly near the responsible industry or toxic dumpsite, or by transmission to bystanders at work, especially with cottage industries.
	• Transmission of toxic substances from workers to nonworkers may be via breast milk or other bodily fluids, transplacental transmission, or via fomites (ie, a substance, such as clothing, capable of adsorbing and transmitting an agent of disease).
	• Para-occupational poisonings with major neurologic effects include lead, mercury, and organophosphorus pesticide poisonings.

Historical note and terminology

Para-occupational poisoning has likely existed since antiquity, particularly as miners and smelters brought lead dust home on their clothing and bodies, and lead white was the most widely produced and used white pigment until the late 19th century. Later, lead was employed in other artisanal activities (eg, ceramic glazes in pottery from the 16th century).

French Huguenot potter, hydraulics engineer, and craftsman Bernard Palissy (c 1510–1589) was famous for having struggled (unsuccessfully) for 16 years to imitate Chinese porcelain.

Bernard Palissy inspecting the lead glaze on an example of his pottery

(Source:"Travailleurs et hommes utiles," avec préface de Léon Chauvin: Librairie nationale d'Education et de Récréation. Limoges: Eugène Ardant et Cie, 1899. Public domain. Edited by Dr. Douglas J Lanska.)
"Bernard de Palissy in his workshop" (1843)

By French painter Joseph-Nicolas Robert-Fleury (1797-1890). (Courtesy of the Amsterdam Museum, Amsterdam, The Netherlands. Public domain. Edited by Dr. Douglas J Lanska.)

Around 1539, Palissy was shown a white enameled cup that astonished him, and he began concerted experimental efforts to determine how it was produced. At that time, pottery covered with a white tin glaze and painted with various enamels was manufactured in Italy, Spain, Germany, and southern France. His family was reduced to poverty as he burned his furniture and the floorboards of his house to feed the fires of his kiln.

"Bernard Palissy, inventor of enamelled pottery"

Japanese print shows Palissy, apparently in a frenzy, burning chairs to keep the furnace going as his wife, who is breastfeeding a baby, and a boy run in fear. (Source: Japanese Department of Education [between 1850 and 1900]. ...

Although Palissy failed to discover the secrets of Chinese porcelain or maiolica (ie, tin-glazed pottery), he nevertheless created a style of rustic lead-glazed pottery called "Palissy ware" for which he is now famous.

Bernard Palissy self-portrait in lead-glazed earthenware

(Source: From the collection of Baron Anthony de Rothschild in London. Hand-colored lithograph from Sauzay A, Delange H. Monographie de l'œuvre de Bernard Palissy, suivie d'un choix de ses continuateurs ou imitateurs. Paris: E ...
Lead-glazed earthenware dish by Bernard Palissy (1550)

(Source: Museum für Angewandte Kunst à Cologne. Public domain.)

Analyses of extant examples of his pottery demonstrate that Palissy used colored lead glazes derived from lead silicates using as colorants various oxides of transition metals (copper, cobalt, manganese, and iron) plus a small addition of the oxide of the post-transition metal tin (25). Whether Palissy's use of lead glazes contributed to the maniacal pursuit that thrust his family into poverty is unclear, but it is at least plausible.

Description

Routes of para-occupational poisoning. Para-occupational exposures may occur by various routes (Table 1). For example, para-occupational exposures may occur by transmission of toxic substances to bystanders without a human vector (ie, humans do not transmit the pathogen). This occurs with either environmental contamination, particularly near an industry or toxic dumpsite, or by direct contamination of bystanders at the worksite, especially with cottage industries. Para-occupational exposures may also occur by transmission of toxic substances from workers to nonworkers either via breast milk, across the placenta (in maternal-fetal transmission), or via fomites (ie, a substance, such as clothing, capable of adsorbing and transmitting an agent of disease). Finally, para-occupational exposures may occur through germ-line mutations in workers affecting offspring. Examples of all these modes of transmission have been documented for various substances (39; 61; 145; 70; 87; 104).

Table 1. Routes of Para-Occupational Poisoning

	1. Transmission of toxic substances to bystanders without a human vector (ie, humans do not transmit the pathogen)
		a. Environmental contamination, particularly near the responsible industry or toxic dumpsite
		b. Bystanders at work, especially with cottage industries
	2. Transmission of toxic substances from workers to nonworkers
		a. Via breast milk or other body fluids
		b. Transplacental
		c. Via fomites (ie, a substance, such as clothing, capable of adsorbing and transmitting an agent of disease)
	3. Germline mutations in workers affecting offspring

Routes of environmental contamination may not always be obvious. For example, exposure to solvent vapors resulted in a sensory neuropathy and mild encephalopathy in a 44-year-old female cook through a ventilation system cross-connection between her restaurant and an adjacent upholstery shop (13).

Numerous studies have evaluated the placental transfer of neurotoxins that can be para-occupational or environmental poisons, including lead, mercury, and manganese (40; 27; 97; 169; 147; 92; 119; 137; 73; 152; 82; 91; 99; 68). An infant's blood lead at birth closely follows that of its mother, even at high values (40; 91), whereas mercury and manganese accumulate in the fetus, resulting in a 1.5- to 2-fold increase in fetal manganese levels compared to maternal blood manganese levels (92; 99) and a more than 3-fold increase in fetal compared to maternal blood mercury levels (91). Prenatal exposure to mercury and lead poses a health threat, particularly to the developing brain (73). Polymorphisms in iron metabolism genes might modify maternal-fetal lead transfer via the placenta (82). In particular, the maternal hemochromatosis HFE C282Y gene variant is associated with greater reductions in placental transfer of lead as the maternal blood lead level increases (82).

A fomite refers to inanimate objects that can carry and spread disease and infectious agents. Para-occupational disease transmission by fomites can include toxic substances and various infections (94; 113).

Para-occupational poisonings with major neurologic effects include lead, mercury, and organophosphorus pesticide poisonings.

Clinical applications

	• For para-occupational lead poisoning, the proven routes of exposure are limited to environmental contamination, direct exposure of nonworking bystanders (particularly in cottage industries), transplacental transmission, and exposure to fomites carried home by workers.
	• Lead poisoning has been documented in persons living in environmentally contaminated areas near industries involved in primary and secondary lead smelting, battery manufacturing, mining, pottery, electric cable splicing, and various cottage industries.
	• Numerous cases of lead poisoning in nonworking family members have been reported in which exposures occurred from occupational processes performed in the home, including recycling exhausted automobile batteries, pottery production, operating a target range, cutlery production where the cutlery is quenched in a bath of molten lead, printing operations, recovery of gold and silver from jeweler's waste, battery repair, and processing gold ore rich in lead (breaking, grinding, and drying ore) inside family compounds.
	• The rate of spontaneous abortions is increased in women lead workers compared with the rates in those women before beginning lead work and compared with the rates for comparable employees not exposed to lead. In addition, fetal exposure can cause adverse neurologic effects in utero or during postnatal development.
	• To minimize fomite-related para-occupational lead exposures, multiple steps are necessary: (1) protective work clothing should be provided by the company; (2) work clothing should not be transported home; (3) work clothing should be cleaned by an industrial laundry; (4) street clothes should not be worn under work clothes; (5) street clothes should be stored in clean lockers separate from the lockers used to store work clothes; (6) workers should always shower and shampoo their hair before going home; and (7) vehicles driven to work should be regularly washed and vacuumed.
	• Minamata disease (methylmercury poisoning) occurred in two separate epidemics in Japan: the first was noted in 1953 in Minamata and the second in 1965 in Niigata Prefecture. Both spread much more widely as the toxin was bioaccumulated and dispersed from the original sites of toxic wastewater dumping that caused the original epidemics.
	• The rapid escalation of gold prices has spurred a new gold rush in developing countries, particularly using artisanal and small-scale gold mining (ASGM), ie, mining activities that use rudimentary methods to extract and process minerals and metals on a small scale.
	• The 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 bioaccumulated through the food chain).

Para-occupational lead poisoning. Para-occupational lead poisoning is the best studied form of para-occupational poisoning.

For para-occupational lead poisoning, the proven routes of exposure are limited to environmental contamination, direct exposure of nonworking bystanders (particularly in cottage industries), transplacental transmission, and exposure to fomites carried home by workers (Table 2).

Table 2. Occupations and Exposure Routes in Para-occupational Lead Poisoning

	Para-occupational exposure
Occupation	Environmental contamination	Bystander exposure	Transplacental	Fomites
Primary lead smelting (from ore)	+	+		+
Secondary lead smelting (eg, old batteries, lead scrap)	+	+	+	+
Storage battery manufacture and repair	+			+
Metal founding				+
Automobile radiator and body repair				+
Firearms instructors and target range attendants				+
Pottery production		+	+
Cutlery manufacture		+	+
Jewelry manufacture		+	+
Electrical parts manufacture				+
Printing		+

Occupations associated with para-occupational lead poisoning. Lead poisoning has been documented in persons living in environmentally contaminated areas near industries involved in primary and secondary lead smelting (130; 144; 96; 95; 98; 15; 54; 173; 107; 110; 109; 108; 170; 09; 08; 10; 07; 11; 38; 37; 176; 154; 165; 166; 167; 55; 181; 164; 29; 78; 105; 65; 155; 184), battery manufacturing (106; 178; 115), mining (130; 116), pottery (56), electric cable splicing (142), and various cottage industries (125).

Hughlett's Smelting Furnace, Galena, Illinois, 1866

after A R Waud?) Note that Galena, Illinois, is named for the mineral galena, the natural mineral form of lead(II) sulfide. (Source: “Harper's New Monthly Magazine” 1866;32:687. Courtesy of the U.S. Library of Congress, Prints ...
Bunker Hill Lead Smelter, Bradley Rail Siding, Kellogg, Shoshone County, Idaho

In foreground, from left to right, plant dry, slag fuming plant, blast furnace, smelter office, lead and silver refineries are visible. High-velocity flue leads from the lower plant to the bag house and stacks at the top of the...
Lead Smelter, Flat River, St. Francois County, Missouri

(Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Stereograph of a lead-smelting plant, Leadville, Colorado

(Source: Keystone View Company,1928. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Jumbo blocks of lead weighing 2500 pounds each at a large smelting operation at the Eagle-Picher plant near Cardin, Oklahoma

(Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
View of the Homestake Mines and the big mining town, Lead City, South Dakota, c 1891

(Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Old lead mine, reopened to aid the war effort during World War II, to supply needed lead and zinc

(Source: Photographer Andreas Feininger [1906-1999] for the U.S. Office of War Information. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Chance Mine, c 1909

Five miners in a lead mine, possibly in the Coeur d'Alene region of Idaho. (Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Crushing lead ore, Creedo, Colorado, 1942

(Source: Photographer Andreas Feininger [1906-1999] for the U.S. Office of War Information. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Lead and silver mining, Creedo, Colorado, 1942

Using a pick axe and shovel to extract lead ore, which is transported out of the mine in metal ore cars. (Source: Photographer Andreas Feininger [1906-1999] for the U.S. Office of War Information. Courtesy of the U.S. Library o...
Lead and silver mining, Creedo, Colorado, 1942 (1)

The man is facilitating the flow of lead ore. (Source: Photographer Andreas Feininger [1906-1999] for the U.S. Office of War Information. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D....
Lead and silver mining, Creedo, Colorado, 1942 (2)

The man is facilitating the flow of lead ore. Note that he is smoking; this repetitive hand-to-mouth behavior increases the ingestion and inhalation of lead dust. (Source: Photographer Andreas Feininger [1906-1999] for the U.S....
Hoisting ore and lowering miners, Lead Homestake Mine

(Source: Detroit Publishing Co between 1900 and 1910. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Rookwood Pottery, Cincinnati, Ohio

Source: Detroit Publishing Co. between 1900 and 1906. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Moravian Pottery and Tile Works, Doylestown, Bucks County, Pennsylvania (1)

(Source: Jet Lowe, 1987. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Kiln at First Moravian Pottery and Tile Works, Doylestown, Bucks County, Pennsylvania, 1901

(Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Moravian Pottery and Tile Works, Doylestown, Bucks County, Pennsylvania (2)

(Source: Photographer Carol M Highsmith between 1980 and 2006. Carol M. Highsmith Archive, U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)

Lead levels in air, surface soil, dust, and vegetation are frequently dangerously elevated near smelting operations, battery manufacturing facilities, and other industries and then decrease with distance from them (144; 96; 95; 98; 54; 60).

The Port Pirie Cohort Study. A longstanding cohort study of the effects of lead exposure on pregnancy outcome and early childhood development in the lead smelting city of Port Pirie and surrounding areas of South Australia has been ongoing since the 1980s (107; 110; 109; 108; 170; 09; 08; 10; 07; 11; 181; 176; 154; 165; 166; 167; 55; 181; 164; 93; 105; 155).

Over 600 children, originally recruited during antenatal life, underwent serial blood lead estimations up to 2 years of age (181). A formal developmental assessment (Bayley Scales of Infant Development) was carried out at the age of 24 months. Blood lead concentrations measured antenatally (maternal), at delivery (maternal and umbilical cord), and postnatally at 6, 15, and 24 months were negatively correlated with mental development at the age of 24 months. When multiple covariates, including maternal IQ, were controlled for in multiple regression analysis, a statistically significant inverse association was observed between blood lead concentration measured at 6 months of age and mental development at 2 years of age. From this analysis, a child with a blood lead concentration of 30 micrograms/dl at the age of 6 months will have an estimated deficit of 3.3 points (approximately 3%) on the Bayley Mental Development Scale relative to a child with a blood lead concentration of 10 micrograms/dl.

Low-level exposure to lead during early childhood was inversely associated with neuropsychological development through the first 7 years of life (08). IQ scores were measured in 494 7-year-old children who had developmental deficits associated with elevated blood lead concentrations at the ages of 2 and 4 years. Exposure to lead was estimated from the lead concentrations in maternal blood samples drawn antenatally and at delivery as well as from blood samples drawn from the children at birth (umbilical cord blood), at the ages of 6 and 15 months and 2 years, and annually thereafter. IQ at the age of 7 years was inversely associated with both antenatal and postnatal blood lead concentrations. After adjustment for maternal IQ, parental education level, socioeconomic status, quality of the home environment, and other factors, the inverse relationship between IQ and lead exposure was still evident for postnatal blood samples, particularly within the age range of 15 months to 4 years. An increase in blood lead concentration from 10 micrograms per deciliter (0.48 μmol per liter) to 30 micrograms per deciliter (1.45 μmol per liter), expressed as the average of the concentrations at 15 months and 2, 3, and 4 years, produced an estimated reduction in IQ of 4.4 to 5.3 points, an approximate deficit in IQ of 4% to 5%.

Exposure to environmental lead during the first 7 years of life was associated with cognitive deficits that persist into later childhood (165), but these deficits appear to be only partially reversed by a subsequent decline in blood lead level (166).

Most of the average blood lead level of 6-month-old infants can be accounted for by normal infant and family behaviors (93). A 4-month-old infant can absorb up to 4 microg of lead a day (equivalent to a blood lead level of up to about 2.4 microg/dl) by mouthing their fingers, about two-thirds of all exposure routes identified. Lead uptake via inhalation accounts for about 0.5% to 3% of an infant's blood lead level at 5 microg/dl.

The total cohort involved 723 infants born in or around Port Pirie (155). At all childhood assessments, postnatal lead levels (particularly those reflecting cumulative exposure) showed significant small associations with outcomes, including cognitive development, IQ, and mental health problems. Furthermore, average childhood blood lead levels showed significant small associations with some adult mental health problems, including anxiety problems and phobia for females. There did not appear to be any age of greatest vulnerability or threshold of effect. Because the magnitude of these effects was generally small in this cohort, they were not discernible at an individual level but instead represent a population health concern.

Environmental contamination. Although overt lead toxicity is uncommon, blood lead levels are commonly elevated in exposed individuals living (130; 144; 96; 95; 98; 54; 173; 38) or working near (37) lead-based industries, and one study documented a significant negative correlation between levels and motor nerve conduction velocities in children living near a lead smelter (95). The highest blood lead levels are typically found in children aged 1 to 6 years (130; 96; 38). The elevated blood lead levels are not explained by differences in ingestion of either lead-based paint or lead-contaminated food or water (144; 96; 54; 38). Chronic oral ingestion and gastrointestinal absorption of particulate lead from dust, and inhalation and pulmonary absorption of airborne particulate lead are the major sources of lead uptake in exposed individuals (96; 159). Soil lead is relatively immobile and less accessible for absorption (96) but may be an important source of ingested lead for children between the ages of 2 and 7 (173).

Bystander exposure. Direct lead exposure to nonworking industrial bystanders at industrial sites occurs, particularly in cottage industries (130; 90; 112; 47; 136; 83; 84; 111; 102; 103; 62; 01; 139; 114; 18; 71; 12). Numerous cases of lead poisoning in nonworking family members have been reported where exposures occurred from occupational processes performed in the home. The occupations involved have included the following: recycling exhausted automobile batteries (130; 47; 139), pottery production (90; 112; 83; 111; 62), operating a target range (114); cutlery production where the cutlery is quenched in a bath of molten lead (84); printing operations (84); recovery of gold and silver from jeweler's waste (136); battery repair (36); and processing gold ore rich in lead (breaking, grinding, and drying ore) inside family compounds (18; 183; 71). The highest blood lead levels were typically found in children aged 1 to 6 years old, as adults. Living in the home but not actively involved in working with lead had the lowest levels (47; 83). As in the case of environmental contamination, chronic oral ingestion and inhalation of particulate lead are the major sources of lead uptake in exposed individuals, particularly children (47; 83; 18; 183; 71).

An acute severe lead poisoning outbreak in Zamfara State, Northern Nigeria, in 2010 affected approximately 1000 children (18; 183; 71). Two thirds of households with affected children reported processing gold ore rich in lead (breaking, grinding, and drying ore) inside family compounds (18). Lead concentrations in soil and dust ranged from 45 parts per million (ppm) to over 100,000 ppm; 85% of family compounds exceeded the U.S. Environmental Protection Agency standard (400 ppm) for areas where children are present. In the 12 months beginning May 2009, 26% of 463 children aged under 5 years old in the surveyed compounds died, with 82% of the deaths within the preceding 6 months, and with 82% of children who died having had convulsions before death, a sign of severe lead poisoning (18). The response involved oral chelation therapy for affected children and environmental remediation (eg, removal of contaminated soil). Among 972 affected living children identified in 2010, with venous blood lead levels of at least 45 ug/dl and with neurologic status recorded, 4% had severe features, including witnessed convulsions, 5% reported recent seizures, and 1% had other neurologic abnormalities (71). Lead poisoning was likely a primary cause of death in five as these children had recent high venous blood lead levels (104–460 mg/dL) and symptoms consistent with lead encephalopathy, with no other obvious cause of death (71).

Transplacental exposure. Lead is readily transmitted transplacentally (03; 40; 174). Because the fetus is most susceptible to lead poisoning during the stage of most active growth early in pregnancy, the result of maternal lead poisoning is often miscarriage (03) or preterm delivery (110). The rate of spontaneous abortions is increased in women lead workers compared with rates in those women before beginning lead work and compared with rates for comparable employees not exposed to lead (03). In addition, fetal exposure can cause adverse neurologic effects in utero or during postnatal development (16; 109; 179). Available data do not support adverse effects of fetal lead exposure on birth weight, hemoglobin concentration, or packed red blood cell volumes (40).

Fomites. The final route of para-occupational exposure to lead is via fomites carried home by workers. An extensive literature review has developed on this source of exposure, including original reports (30; 31; 32; 33; 35; 14; 54; 182; 48; 140; 178; 173; 117; 141; 85; 67; 42; 104; 126; 142; 69; 180; 81; 21) and editorials and review articles (39; 61; 145; 70; 87; 104; 72). The industries involved include primary (42) and secondary lead smelting (30; 14; 54; 182; 140), battery manufacturing (31; 32; 48; 178; 129; 117; 141) and reclamation (69), electronic parts manufacturing (33; 85), radiator repair (67; 126), metal founding (35), electric cable splicing (142), construction (180), and paint remediation (21).

The Occupational Safety and Health Administration (OSHA) lead standard. To limit the transmission of lead dust to workers' homes, the Occupational Safety and Health Administration (OSHA) lead standard requires certain hygiene facilities and practices (Occupational Safety and Health Administration 1989). Employers must (1) provide protective work clothing, such as coveralls or similar full-body work clothing, gloves, hats, and shoes or disposable shoe coverlets; and (2) provide for cleaning of protective work clothing at least weekly, and daily for employees with exposures to high concentrations of airborne lead dust. In addition, for employees who work in areas where their airborne exposure to lead is above the permissible exposure level, employers must (1) provide clean change rooms and assure that all protective clothing is removed at the end of the work shift only in the change rooms provided for that purpose; (2) assure that change rooms are equipped with separate storage facilities for protective work clothing and for street clothes, which prevents cross-contamination; (3) provide shower facilities and ensure that employees shower at the end of the work shift; and (4) ensure that employees do not leave the workplace wearing any clothing worn during the work shift.

Improper work and personal hygiene practices in lead-related industries. Reports of improper work and personal hygiene practices persist in lead-related industries (31; 32; 48; 140; 178; 67; 126; 69) (Table 3). Some of these exposures occurred before the original OSHA lead standard, which was promulgated in 1978 (31; 32; 48; 178), but several occurred well after the OSHA standard (67; 126; 69). Deficiencies in proper work practices and personal hygiene in lead workers are associated with greater lead exposures in their children (117). Just changing clothes before going home is inadequate for lead containment (117), eg, lead workers frequently have high concentrations of lead dust in and on their hair (182). Even with a program that includes showering and changing clothes, lead may reach home by various routes (140; 178): (1) on contaminated work clothes that are laundered at home (178); (2) on street clothes contaminated either while left in dirty lockers, while worn under work outer garments, or while worn walking across contaminated areas of the plant on the way to and from work (140); and (3) on or in automobiles parked near the plant during the work shift (140; 67).

Table 3. Work Practices in Selected Fomite-Related Para-Occupational Lead Exposures

Authors (year)	State	Industry	No protective work clothing provided	Work clothes cleaned at home	No end-of-shift showers at work	Work clothing worn home
(178)	VT	Battery factory	?	87%	90%	0%
(31; 48)	NC	Battery factory	100%	100%	100%	86%
(140)	?	Secondary lead smelters	?	0%	Some	Some
(67)	VA	Radiator repair	?	?	Some	Some
(126)	NY	Radiator repair	?	100%	?	4%
(69)	AL	Battery reclamation	?	?	20%	33%
Abbreviations: AL, Alabama; NC, North Carolina; NY, New York; VA, Virginia; VT, Vermont

To minimize fomite-related para-occupational lead exposures, multiple steps are necessary: (1) protective work clothing should be provided by the company; (2) work clothing should not be transported home; (3) work clothing should be cleaned by an industrial laundry; (4) street clothes should not be worn under work clothes; (5) street clothes should be stored in clean lockers separate from the lockers used to store their work clothes; (6) workers should always shower and shampoo their hair before going home; and (7) vehicles driven to work should be regularly washed and vacuumed. In addition, all children of parents working in lead-related industries should have periodic blood lead screening (Centers for Disease Control 1985b). Adults should be considered a "sentinel" event for para-occupational exposures in the workers' families.

Childhood susceptibility to para-occupational lead exposures. The highest lead levels were generally seen in children aged 1 to 6 (15; 32; 48). The elevated blood lead levels were not explained by differences in the ingestion of either lead-based paint, lead-contaminated food or water, or airborne lead exposure from factory emissions or busy roadways (32; 48; 140). Blood lead levels of workers frequently (15; 31; 117), but not universally (178; 117; 85), correlated positively with blood lead levels of their children. Reasons for weak or nonsignificant correlations (31; 178; 117; 85) include the following: (1) worker blood lead levels may have been measured at different times from that of their family members; (2) lead dust carried home by workers is only a fraction of the lead that workers were exposed to in the plant; (3) exposures in the home may vary with the level of general cleanliness and the method of cleaning work clothes; and (4) individual children's behavior patterns may be strong determinants of their lead levels, even when the lead has an occupational source (85). Despite sometimes markedly elevated blood levels requiring chelation (30; 35; 67), in most studies, few para-occupationally exposed individuals had symptoms suggestive of lead poisoning (182; 129), and the vast majority had normal physical and neurologic examinations (48).

With para-occupational lead poisoning due to either environmental contamination, direct exposure to nonworking industrial bystanders at industrial sites, or exposure to fomites carried home by workers, young children are the most susceptible to overt plumbism (lead poisoning). Subclinical manifestations may include alterations in nerve conduction velocity, vitamin D metabolism, and hemoglobin synthesis (148). Clinical manifestations may include hyperactivity, cognitive deficits, antisocial behavior (121; 120), colic, or even nephropathy, encephalopathy with seizures and hydrocephalus, and death (148). Children in this age range have a greater risk than adults from the effects of lead because (1) children show a greater prevalence of iron deficiency, which is associated with greater gastrointestinal absorption of ingested lead; (2) as a result of greater hand-to-mouth activity and crawling along floors and carpets, children ingest more dust and dirt, which can be contaminated with lead, and (3) children show greater susceptibility to lead's effects (148).

Para-occupational mercury poisoning

Minamata disease (methylmercury poisoning). Minamata disease, due to methylmercury poisoning, is a disease of the central and peripheral nervous system caused by acute methylmercury poisoning. The first well-documented epidemic of methylmercury poisoning arose in 1953 in the small factory town of Minamata, Japan, on the west coast of Kyushu Island, located in Kumamoto Prefecture at the southern tip of Japan.

Minamata map illustrating Chisso factory effluent routes

(Source: User: Bobo12345 via Wikimedia Commons. Creative Commons Attribution 3.0 Unported [CC BY 3.0] license, creativecommons.org/licenses/by/3.0.)
Map of Japan with highlight on Kumamoto prefecture, which includes Minamata

(Source: User: Lincun via Wikimedia Commons. Creative Commons Attribution 3.0 Unported [CC BY 3.0] license, creativecommons.org/licenses/by/3.0.)

People were exposed by eating fish and shellfish contaminated with methylmercury from the discharge of industrial wastewater from a chemical factory owned by the Chisso Corporation. The clinical picture was officially recognized and called Minamata disease in 1956 (74; 53). Signs and symptoms included ataxia, numbness in the hands and feet, muscle weakness, loss of peripheral vision, and damage to hearing and speech. In severe cases, insanity, paralysis, coma, and death followed within weeks of symptom onset. A congenital form of the disease was also recognized in which children with transplacental fetal exposure and exposure through breastfeeding developed microcephaly, extensive cerebral damage, and symptoms resembling cerebral palsy (89).

At autopsy, the most conspicuous cerebral pathology was found in the anterior portions of the calcarine cortex, with less severe but similar lesions evident in the post-central, precentral, and temporal transverse cerebral cortices and deep in the cerebellar hemispheres (57). Secondary degeneration from primary lesions may be seen in cases with long survival. In the cerebellum, the granule cell population was more affected, compared with Purkinje cells. In the peripheral nervous system, sensory nerves were more affected than motor nerves.

The release of methylmercury in industrial wastewater continued from 1932 to 1968. In addition, some of the mercury sulfate in the wastewater was metabolized to more toxic methylmercury by bacteria in the sediment. Methylmercury subsequently bioaccumulated in shellfish and fish in Minamata Bay and the adjoining Shiranui Sea. The poisoning and resulting deaths of both humans and animals continued for 36 years, while Chisso and the Kumamoto prefectural government avoided responsibility and did little to prevent the epidemic. By 2010 more than 14,000 victims of Minamata disease had received financial compensation, but this greatly underestimates the magnitude of the problem in the city. Pre- or postnatal exposure to methylmercury is associated with psychiatric symptoms among the general population in Minamata, even after excluding officially certified patients (185).

As methylmercury dispersed from Minamata to the Shiranui Sea (also called the Yatsushiro Sea), a shallow semi-enclosed inland sea separating the island of Kyushu from the Amakusa Islands, people along the coast also had long-term dietary exposure to methylmercury and developed atypical and milder presentations of Minamata disease (123; 122; 76).

The Yatsushiro Sea (also called Shiranui Sea) and surroundings

(Source: User: Bobo12345 via Wikimedia Commons. Creative Commons Attribution 3.0 Unported [CC BY 3.0] license, creativecommons.org/licenses/by/3.0.)

By 1960, mercury concentrations in the hair of residents on the coast were 10 to 20 times higher than those of people in Kumamoto Prefecture who had not been poisoned (123). In addition, residents of the Ooura fishing village on the coast of the Shiranui Sea showed a significantly higher frequency of neurologic signs characteristic of methylmercury poisoning (eg, hypoesthesia, ataxia, impaired hearing and vision, and dysarthria) compared with people in the nonpolluted Ichiburi fishing village (123; 76). Fishermen and their families living in some mercury-polluted areas along the Shiranui Sea showed a very high rate of neurologic symptoms, particularly stocking-glove sensory disturbances (76). Even 30 years after cessation of exposure to anthropogenic methylmercury, coastal residents complained of acral and perioral paresthesia, and quantified sensory testing documented significantly elevated touch and 2-point discrimination thresholds of the proximal and distal extremities relative to nonexposed controls (122). The evenly distributed increases in sensory thresholds of both distal and proximal portions of the extremities and the lips revealed that the persistent somatosensory disturbances were not caused by injuries to their peripheral nerves. Instead, astereognosis, increased sensory thresholds, and limb apraxia all resulted from diffuse damage to the somatosensory cortex (122).

A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965.

Map of Japan with highlight on Niigata prefecture

(Source: User: Lincun via Wikimedia Commons. Creative Commons Attribution 3.0 Unported [CC BY 3.0] license, creativecommons.org/licenses/by/3.0.)

Niigata Minamata disease (also called "second Minamata disease" or "Agano River organic mercury poisoning") was due to methylmercury released in wastewater from mercury-sulfate-catalyzed acetaldehyde production at the Showa Denko Electrical Company's chemical plant in Kanose village. Methylmercury was released untreated into the Agano River where it bioaccumulated up the food chain; when local people ate contaminated fish, they developed symptoms identical with those of Minamata disease victims more than a decade earlier. A congenital form was similarly recognized (150; 151). At least 690 people from the Agano River basin have been certified as having developed Niigata Minamata disease. The Showa Denko corporation responded by trying to discredit the researchers who reported the outbreak and by launching a disinformation campaign that rejected their wastewater as the cause of the disease, suggesting the cause might have been an "agricultural chemical run-off" that entered the river after the 1964 Niigata earthquake. A lawsuit was ultimately successful, however, and in 1971 the court found Showa Denko guilty of negligence. This, in turn, forced a re-examination of the earlier Minamata victims, leading to a similar successful suit against the polluting company in Minamata.

Artisanal and small-scale gold mining (ASGM) (inorganic and organic mercury poisoning). The rapid escalation of gold prices has spurred a new gold rush in developing countries, particularly using artisanal and small-scale gold mining (ASGM), ie, mining activities that use rudimentary methods to extract and process minerals and metals on a small scale (161).

Gold price in USD per troy ounce by year, 1971-2024

(Source: Dan Polansky, 2024. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)
Gold, deforestation, and mercury import increases over time in the Peruvian Amazon

International biweekly gold prices, forest conversion to mining area, and annual mercury imports to Peru (Superintendencia Nacional de Aduanas del Peru). Mercury imports for 2009 were recorded to September and projected for the...

Although ASGM has become an important source of income for many marginalized people in underdeveloped countries, it has also had devastating social and environmental consequences, including mercury pollution and poisoning, deforestation, organized crime, human rights abuses, and displacement of indigenous communities (135; 162; 46; 50).

Land disturbances at an Artisanal and Small-Scale Gold Mining site in Tarkwa, Wassa West District, Ghana

(Source: Rajaee M, Obiri S, Green A, et al. Integrated assessment of artisanal and small-scale gold mining in Ghana-Part 2: natural sciences review. Int J Environ Res Public Health 2015;12[8]:8971-9011. Creative Commons Attribu...
Land disturbances at an Artisanal and Small-Scale Gold Mining site in Tarkwa, Wassa West District, Ghana

(Source: Rajaee M, Obiri S, Green A, et al. Integrated assessment of artisanal and small-scale gold mining in Ghana-part 2: natural sciences review. Int J Environ Res Public Health 2015;12[8]:8971-9011. Creative Commons Attribu...
Land disturbances at an Artisanal and Small-Scale Gold Mining site in Talensi District, Upper East Region, Ghana

(Source: Rajaee M, Obiri S, Green A, et al. Integrated assessment of artisanal and small-scale gold mining in Ghana-part 2: natural sciences review. Int J Environ Res Public Health 2015;12[8]:8971-9011. Creative Commons Attribu...
Mercury cycle in a typical Artisanal and Small-Scale Gold Mining process

Numbers represent key steps in the ASGM process: 1—excavation, 2—crushing and grinding, 3—sifting/shanking, 4—washing/sluicing, 5—amalgamation, and 6—burning. Letters represent key steps in the mercury cycle: A—residual mercury...
Satellite photos of Tarkwa, Western Region, Ghana, from 1986 to 2015, depicting rapid gold mining development

(A) December 1986; (B) January 2002; and (C) January 2015. (Source: Images from Google Earth [2015]. Rajaee M, Obiri S, Green A, et al. Integrated assessment of artisanal and small-scale gold mining in Ghana-part 2: natural sci...
NASA Landsat satellite images showing the change in gold mining activity in two areas of the Peruvian Amazon from 2003 to 2009

(A) Guacamayo (126519S, 706009W) along the Interoceanic Highway and (B) Colorado-Puquiri (126449S, 706329W) in the buffer zone of the Amarakaeri Communal Reserve. (Source: Swenson JJ, Carter CE, Domec JC, Delgado CI. Gold minin...

Globally, 14 to 19 million people, typically the poorest and most marginalized, work in ASGM, which produces about 20% of global gold output—the world's largest anthropogenic source of mercury emissions (158). Based on human biomonitoring data, between 25% and 33% of these miners—3.3 to 6.5 million people globally—suffer from moderate chronic metallic mercury vapor intoxication (158). Although these figures underestimate para-occupational poisoning of mining families, the resulting global burden of mercury poisoning from ASGM is estimated to range from 1.22 to 2.39 million disability-adjusted life years (158). Children of miners begin working with immediate contact to mercury from as early as 7 years old (24).

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 (162).

Most miners in the Amazon mine from alluvial gold (ie, deposits found in loose sediments deposited by running water in floodplains, alluvial fans, or related landforms). Alluvial mining typically involves some combination of (wet or dry) hand panning, sluice boxes, heavy equipment, hydraulic mining, and dredging.

Prospector "dry" panning for gold, Pinos Altos, New Mexico, 1940 (1)

In dry panning, the pan is rotated until the dirt is on one side and then with a decisive toss it is thrown into the air, the light dirt being then blown away by the wind and the heavy gold being caught again in the pan. Source...
Prospector "dry" panning for gold, Pinos Altos, New Mexico, 1940 (2)

In dry panning the pan is rotated until the dirt is on one side and then with a decisive toss it is thrown into the air, the light dirt being then blown away by the wind and the heavy gold being caught again in the pan. Source:...
"Pan" of gold from "dry" panning, Pinos Altos, New Mexico, 1940

Not all the shiny particles are gold but include mica and a few particles of quicksilver (elemental mercury). The gold usually appears in the pan as a minute shiny upper rim of the dirt in the pan. Source: Photographer Russell ...
Pattern-reversal visual evoked potential stimulus and waveform

Pattern-reversal visual evoked potential stimulus (A) and waveform (B). (Contributed by Dr. Han Cheng.)
Man "wet" panning for gold on Nome Beach, Alaska

(Source: Lomen Bros. photographer, Nome, between ca. 1900 and ca. 1930. Courtesy of the Frank and Frances Carpenter Collection, U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Three men in gulch with a sluice, placer mining for gold, c. 1872

(Source: Photographer William Henry Jackson [1843-1942]. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Gold miner at work in sluice box, Two Bit Creek, South Dakota, 1938

(Source: Photographer Russell Lee [1903-1986] for the Office of War Information. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
"Gold mining in California,” c. 1871

Gold miners shoveling sand from stream into sluice while one miner pans for gold in the same stream, small building and mountains in the background. (Published by Currier & Ives, New York. Courtesy of the U.S. Library of Co...
"The Sluice,” 1883, by Henry Sandham

Hydraulic mining for gold in California. (Source: The Century illustrated monthly magazine, January 1883:324. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)<...
Hydraulic mining near French Corral, Nevada County, California, 1866

(Half of a stereograph published by Lawrence & Houseworth. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Hydraulic mining "the big boulder," Kentucky Claim, Timbuctoo, Yuba County, California, 1866

(Half of a stereograph published by Lawrence & Houseworth. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Hydraulic mining, California gulch, Colorado, c. 1878

(Source: Photographer W.G. Chamberlain, Denver, Colorado. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain.)
Exterior of a mining dredge (1)

Gold Placers Incorporated, Coal Creek Dredge, Near Coal Creek & Yukon River, Eagle, Alaska. (Source: Jet Lowe, 1984. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain....
Exterior of a mining dredge (2)

Gold Placers Incorporated, Coal Creek Dredge, Near Coal Creek & Yukon River, Eagle, Alaska. (Source: Jet Lowe, 1984. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public domain....

In the Amazon, miners often clear forest cover and then remove topsoil using machinery and high-pressure hoses to form a mining pit. The mixture of gold-bearing soil and water (a “slurry”) is passed down a sluice system to trap the denser gold. Miners may also use hoses to suck or conveyor-belt contraptions of scoops or shovels to lift river sediments into a sluice system onboard a barge.

Detail of a mining dredge showing the bucket system

Gold Placers Incorporated, Coal Creek Dredge, Near Coal Creek & Yukon River, Eagle, Alaska. (Source: Todd A Croteau, 2014. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public d...
Detail of a mining dredge showing the bucket system and control room above

Gold Placers Incorporated, Coal Creek Dredge, Near Coal Creek & Yukon River, Eagle, Alaska. (Source: Todd A Croteau, 2014. Courtesy of the U.S. Library of Congress, Prints and Photographs Division, Washington, D.C. Public d...
Detail of the buckets of a mining dredge looking straight on

Gold Placers Incorporated, Coal Creek Dredge, Near Coal Creek & Yukon River, Eagle, Alaska. Note the suspended walkway bridge at right and the control wires and pulleys for controlling the dredge movement. (Source: Todd A C...

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.

Mercury metal in an ampoule

(Source: Wilco Oelen, 2007. Creative Commons Attribution 3.0 Unported [CC BY 3.0] license, creativecommons.org/licenses/by/3.0.)
Pouring mercury from small tube into pen which contains flour gold mixed with the natural dirt

(Source: Pinos Altos, New Mexico, 1940, by photographer Russell Lee [1903-1986]. Farm Security Administration, Office of War Information Photograph Collection, Library of Congress, Washington, D.C. Public domain.)

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 ASGM (51; 172).

Gold prospector cooking mercury with "dirty flour" gold

The "flour gold" which is in small, almost powder flakes, will attach itself to the mercury as the water boils away. (Source: Pinos Altos, New Mexico, 1940, by photographer Russell Lee [1903-1986]. Farm Security Administration,...

Mercury-contaminated slurry is also typically discarded directly into waterways (172).

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 bioaccumulated through the food chain) (172; 101; 88; 138).

Common sources of mercury, with bioaccumulation in fish

This figure shows some common sources of mercury, the conversion to toxic methylmercury, and the outline of EPA consumption recommendations for certain types of fish based on mercury levels. Mercury from coal-fired power plants...
Mercury biomagnification: conceptual illustration of mercury accumulating up the food web

Mercury levels increase exponentially up the food web as algae are eaten by small invertebrates which are eaten by larger invertebrates (such as dragonfly larvae) which are eaten by fish and other higher-order predators. (Sourc...
Physical mercury cycle

(Source: MacKenzie E. Jewell, 2020. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)

The bioaccumulation of methylmercury in fish poses an especially large risk to indigenous people as fish consumption tends to be an essential component of their diet.

ASGM-associated mercury pollution has been documented in Canada, the United States, South America, Africa, China, Indonesia, the Philippines, and Siberia. In the U.S., environmental mercury contamination is mostly from historical gold mining practices (Texas, Nevada, California, Alaska) (52; 88), but small numbers of cases of inhalational mercury toxicity from artisanal gold extraction continue to occur in the U.S. (124; 171). Since the 1990s, the most severe problems with mercury poisoning related to ASGM have been in South America's Amazon River Basin (Bolivia, Brazil, Colombia, Ecuador, Guyana, Peru, Suriname, and Venezuela) (26; 20; 100; 77; 44; 43; 86; 153; 64; 132; 17; 66; 172; 63; 02; 177; 138), Africa (75; 157; 24; 23; 156; 128; 163; 175; 149), Indonesia (24; 22; 118; 131; 79), and the Philippines (04; 51). At least 2000 tonnes of mercury have been released into the environment in the present gold rush in Brazil alone (note a tonne is a metric unit of 1000 kgs or approximately 2200 pounds) (100).

Exposure to mercury in these small-scale mining communities is a particularly serious health hazard to the children living and working there. Children working with inorganic mercury accumulate high levels in various biomonitors and show typical symptoms of mercury intoxication (eg, neurocognitive deficits, ataxia, tremor, dysdiadochokinesia, eye movement abnormalities, dysgeusia and metallic taste, excess salivation, etc.) (43; 24; 22; 23). Vaporized mercury is the main form of exposure, but children are also exposed to mercury from the contaminated soil around such operations and by eating fish (containing methylmercury) obtained from contaminated waterways. Long-term environmental methylmercury exposure is associated with peripheral neuropathy and cognitive impairment (138). Analyses of hair and blood are useful for determination of exposure to methylmercury, but urine is preferred for determination of exposure to inorganic mercury, with blood normally being of value only if exposure is ongoing (143).

Para-occupational herbicide and pesticide poisoning. Pesticides remain in the environments of farmworker families for long periods, and children in farmworker homes experience multiple sources of pesticide exposure, including para-occupational exposures and possible exposures from spray drift (59; 58; 06; 05; 19; 134; 146; 45; 28; 41; 80; 49; 133).

Organophosphate exposure in children of agricultural families is associated with deficits in learning, particularly in tests of motor function (28). Negative effects of pesticides and neurotoxic elements on children's neurodevelopment were found in multiple countries, particularly affecting less-privileged children from laboring families (49). In addition, organophosphate pesticides can act as thyroid disruptors that can adversely affect fetal neural development during the first half of pregnancy, when adequate maternal thyroxine (T4) concentrations are critical (168).

A study of preschool children of agricultural producers and farm workers in the tree fruit region of Washington state found that soil and house dust concentrations of pesticides were elevated in homes of agricultural families when compared to nonagricultural reference homes in the same community (59). Dialkyl phosphate metabolites of organophosphorus pesticides measured in children's urine were also elevated for agricultural children when compared to reference children. Proximity to farmland was associated with increased organophosphorus pesticide concentrations in house dust and organophosphorus pesticide metabolites in urine.

In a study of 60 children of Latino farmworkers, aged 1 to 6 years old from eastern North Carolina, organophosphorus pesticide urinary metabolite levels [diethylphosphate (DEP), diethylthiophosphate (DETP), and the summed diethyl metabolites] were significantly elevated compared to national reference data (06). Organophosphate pesticide metabolites were detected in a substantial proportion of these children, particularly metabolites of parathion/methyl parathion (90%), chlorpyrifos/chlorpyrifos methyl (83%), and diazinon (55%) (05). Boys, children living in rented housing, and children with mothers working part-time had more metabolites detected.

Practices related to the safe handling of pesticides and use of personal protective equipment are largely unknown among agricultural workers in developing countries (19; 133). In a study of 99 Mexican agricultural workers (35 women and 64 men), men handled pesticides more frequently than women (67% vs. 20%) (19). The workers used mostly manual application equipment, had a low rate of correct usage of personal protective equipment (2%), and had poor hygienic practices, all of which contributed to their personal exposure. Moreover, their poor hygienic practices and the high frequency of storing pesticide products and application equipment at home (42%) contributed to para-occupational exposure for their families.

Similar problems were documented in a study of workers in the South African Working for Water (WfW) program, a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species (133). Observational study of personal hygiene and practices related to the care and maintenance of personal protective equipment of WfW forestry workers documented multiple para-occupational herbicide residue exposure risks among their families.

South African Working for Water worker’s dermal exposures to herbicide formulations and working conditions

The South African Working for Water (WfW) program is a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species. (Sour...
Herbicide residues (blue) on a South African WfW worker’s hands, clothing, and boots, which are being removed at home

The South African Working for Water (WfW) program is a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species. (Sour...
South African WfW worker handwashing personal protective equipment at home

The South African Working for Water (WfW) program is a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species. (Sour...
South African WfW worker’s personal protective equipment mixed with household laundry during washing

The South African Working for Water (WfW) program is a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species. (Sour...
Child touching herbicide-contaminated water being used to clean WfW personal protective equipment

The South African Working for Water (WfW) program is a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species. (Sour...
Washed WfW personal protective equipment hung to dry with household laundry

South African Working for Water (WfW) workers were unaware that residues could remain on washed personal protective equipment and be transferred to household laundry and consequently held the view that drying personal protectiv...
South African WfW workers hung children’s laundry separate from WfW personal protective equipment

The South African Working for Water (WfW) program is a national government-wide initiative that hires unemployed members of poor, marginalized communities to use herbicides for the removal of alien invasive plant species. (Sour...
South African WfW worker personal protective equipment stored with household laundry

South African Working for Water (WfW) workers were unaware that residues could remain on washed personal protective equipment and be transferred to household laundry and consequently held the view that drying personal protectiv...
South African WfW worker's living conditions

South African Working for Water (WfW) workers predominately live in townships that are characterized by low-cost shacks. The space within their homes was limited due to the size of the dwellings and overcrowding from multiple m...
South African WfW worker's personal protective equipment remains contaminated even after handwashing

Because most South African Working for Water (WfW) workers hand-washed their personal protective equipment, they had difficulty in properly removing residues and soil from the personal protective equipment. The WfW program is a...

The absence of provisions related to para-occupational ("take-home") exposure in national legislation and workplace policies contributed to poor adherence to risk reduction practices at worksites, in addition to workers transporting herbicide residues to their homes (133).

Among school-aged children living in rice and aquacultural farming regions of Thailand, organophosphate pesticide metabolite levels were strongly influenced by farming activity, household environments, and child behaviors (146). The frequency of organophosphate pesticide application on rice farms and living in a rice farming community were significant predictors of urinary dialkyl phosphate metabolite levels. Increasing 3,5,6-trichloro-2-pyridinol metabolite levels were significantly related to proximity to a rice farm, being with a parent while working on a farm, playing on a farm, and the presence of observable dirt accumulated on the child's body.

In a cross-sectional study of 271 children aged 4 to 9 years old living in agricultural Ecuadorian communities, half (51%) cohabited with one or more flower plantation workers; erythrocyte acetylcholinesterase activity and systolic blood pressures were lower among children living with flower workers (160).

Lay health promoter–led, community-based participatory pesticide safety intervention with farmworker families can be effective in reducing para-occupational exposures (134).

Media

References

01: Abbritti G, Muzi G, Fiordi T, et al. Increased lead absorption in children living in an area with high concentration of ceramic workshops. Med Lav 1992;83(6):576-86. PMID 1296138
02: Alcala-Orozco M, Caballero-Gallardo K, Olivero-Verbel J. Mercury exposure assessment in indigenous communities from Tarapaca village, Cotuhe and Putumayo Rivers, Colombian Amazon. Environ Sci Pollut Res Int 2019;26(36):36458-67. PMID 31728948
03: Angle CR, McIntire MS. Lead poisoning during pregnancy. Fetal tolerance of calcium disodium edetate. Am J Dis Child 1964;108:436-9. PMID 14186666
04: Appleton JD, Williams TM, Breward N, Apostol A, Miguel J, Miranda C. Mercury contamination associated with artisanal gold mining on the island of Mindanao, the Philippines. Sci Total Environ 1999;228(2-3):95-109. PMID 10371050
05: Arcury TA, Grzywacz JG, Barr DB, Tapia J, Chen H, Quandt SA. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Environ Health Perspect 2007;115(8):1254-60. PMID 17687456
06: Arcury TA, Grzywacz JG, Davis SW, Barr DB, Quandt SA. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Am J Ind Med 2006;49(9):751-60. PMID 16804908
07: Baghurst PA, McMichael AJ, Tong S, Wigg NR, Vimpani GV, Robertson EF. Exposure to environmental lead and visual-motor integration at age 7 years: the Port Pirie Cohort Study. Epidemiology 1995;6(2):104-9. PMID 7742393
08: Baghurst PA, McMichael AJ, Wigg NR, et al. Environmental exposure to lead and children's intelligence at the age of seven years. The Port Pirie Cohort Study. N Engl J Med 1992a;327(18):1279-84. PMID 1383818
09: Baghurst PA, Robertson EF, McMichael AJ, Vimpani GV, Wigg NR, Roberts RR. The Port Pirie Cohort Study: lead effects on pregnancy outcome and early childhood development. Neurotoxicology 1987;8(3):395-401. PMID 2443882
10: Baghurst PA, Tong SL, McMichael AJ, Robertson EF, Wigg NR, Vimpani GV. Determinants of blood lead concentrations to age 5 years in a birth cohort study of children living in the lead smelting city of Port Pirie and surrounding areas. Arch Environ Health 1992b;47(3):203-10. PMID 1596103
11: Baghurst PA, Tong S, Sawyer MG, Burns J, McMichael AJ. Sociodemographic and behavioural determinants of blood lead concentrations in children aged 11-13 years. The Port Pirie Cohort Study. Med J Aust 1999;170(2):63-7. PMID 10026685
12: Bah HAF, Bandeira MJ, Gomes-Junior EA, et al. Environmental exposure to lead and hematological parameters in Afro-Brazilian children living near artisanal glazed pottery workshops. J Environ Sci Health A Tox Hazard Subst Environ Eng 2020;55(8):964-74. PMID 32400283
13: Baker EL, Feldman RG. Paraoccupational exposure to mixed solvents. J Toxicol Clin Toxicol 1982;19(1):27-34. PMID 7154139
14: Baker EL, Folland DS, Taylor TA, et al. Lead poisoning in children of lead workers: home contamination with industrial dust. N Engl J Med 1977a;296(5):260-1. PMID 831108
15: Baker EL Jr, Hayes CG, Landrigan PJ, et al. A nationwide survey of heavy metal absorption in children living near primary copper, lead, and zinc smelters. Am J Epidemiol 1977b;106(4):261-73. PMID 910795
16: Bellinger D, Leviton A, Waternaux C, Needleman H, Rabinowitz M. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N Engl J Med 1987;316(17):1037-43. PMID 3561456
17: Berzas Nevado JJ, Rodríguez Martín-Doimeadios RC, Guzmán Bernardo FJ, et al. Mercury in the Tapajós River basin, Brazilian Amazon: a review. Environ Int 2010;36(6):593-608. PMID 20483161
18: Biya O, Gidado S, Haladu S, et al. Outbreak of acute lead poisoning among children aged <5 years — Zamfara, Nigeria, 2010. MMWR 2010;59(27):846.
19: Blanco-Munoz J, Lacasana M. Practices in pesticide handling and the use of personal protective equipment in Mexican agricultural workers. J Agromedicine 2011;16(2):117-26. PMID 21462024
20: Boischio AA, Cernichiari E. Longitudinal hair mercury concentration in riverside mothers along the Upper Madeira river (Brazil). Environ Res 1998;77(2):79-83. PMID 9600799
21: Boraiko C, Wright EM, Ralston F. Lead contamination of paint remediation workers' vehicles. J Environ Health 2013;75(7):22-7. PMID 23505771
22: Bose-O'Reilly S, Drasch G, Beinhoff C, et al. Health assessment of artisanal gold miners in Indonesia. Sci Total Environ 2010a;408(4):713-25. PMID 19945736
23: Bose-O'Reilly S, Drasch G, Beinhoff C, et al. Health assessment of artisanal gold miners in Tanzania. Sci Total Environ 2010b;408(4):796-805. PMID 19945738
24: Bose-O'Reilly S, Lettmeier B, Gothe RM, Beinhoff C, Siebert U, Drasch G. Mercury as a serious health hazard for children in gold mining areas. Environ Res 2008;107(1):89-97. PMID 18321481
25: Bouquillon A, Castaing J, Barbe F, et al. Lead‐glazed rustiques figulines (rustic ceramics) of Bernard Palissy (1510–90) and his followers. Archaeometry 2017;59(1):69-83.
26: Branches FJ, Erickson TB, Aks SE, Hryhorczuk DO. The price of gold: mercury exposure in the Amazonian rain forest. J Toxicol Clin Toxicol 1993;31(2):295-306. PMID 8492342
27: Buchet JP, Roels H, Hubermont G, Lauwerys R. Placental transfer of lead, mercury, cadmium, and carbon monoxide in women. II. influence of some epidemiological factors on the frequency distributions of the biological indices in maternal and umbilical cord blood. Environ Res 1978;15(3):494-503. PMID 679905
28: Butler-Dawson J, Galvin K, Thorne PS, Rohlman DS. Organophosphorus pesticide exposure and neurobehavioral performance in Latino children living in an orchard community. Neurotoxicology 2016;53:165-72. PMID 26820522
29: Carrizales L, Razo I, Téllez-Hernández JI, et al. Exposure to arsenic and lead of children living near a copper-smelter in San Luis Potosi, Mexico: importance of soil contamination for exposure of children. Environ Res 2006;101(1):1-10. PMID 16171795
30: Centers for Disease Control. Lead poisoning Tennessee. MMWR Morb Mortal Wkly Rep 1976;25(11):85.
31: Centers for Disease Control. Increased lead absorption in children of lead workers -- Vermont. MMWR Morb Mortal Wkly Rep 1977a;26(8):61-2.
32: Centers for Disease Control. MMWR Morb Mortal Wkly Rep 1977b;26(39):312.
33: Centers for Disease Control. Lead poisoning in a capacitor and resistor plant--Colorado. MMWR Morb Mortal Wkly Rep 1985a;34(25):384-5. PMID 3925315
34: Centers for Disease Control. Preventing lead poisoning in young children: a statement by the Centers for Disease Control: January 1985b. Atlanta: Centers for Disease Control, 1985.
35: Centers for Disease Control. Occupational and paraoccupational exposure to lead--Colorado. MMWR Morb Mortal Wkly Rep 1989a;38(19):338-40, 345. PMID 2497329
36: Centers for Disease Control. Occupational and environmental lead poisoning associated with battery repair shops--Jamaica. MMWR Morb Mortal Wkly Rep 1989b;38(27):474, 479-81. PMID 2500588
37: Chao KY, Wang JD. Increased lead absorption caused by working next to a lead recycling factory. Am J Ind Med 1994;26(2):229-35. PMID 7977398
38: Chenard L, Turcotte F, Cordier S. Lead absorption by children living near a primary copper smelter. Can J Public Health 1987;78(5):295-8. PMID 3690445
39: Chisolm JJ Jr. Fouling one's own nest. Pediatrics 1978;62(4):614-7. PMID 714598
40: Clark AR. Placental transfer of lead and its effects on the newborn. Postgrad Med J 1977;53(625):674-8. PMID 593994
41: Connolly A, Coggins MA, Galea KS, et al. Evaluating glyphosate exposure routes and their contribution to total body burden: a study among amenity horticulturalists. Ann Work Expo Health 2019;63(2):133-47. PMID 30608574
42: Cook M, Chappell WR, Hoffman RE, Mangione EJ. Assessment of blood lead levels in children living in a historic mining and smelting community. Am J Epidemiol 1993;137(4):447-55. PMID 8460625
43: Counter SA, Buchanan LH, Ortega F. Neurocognitive screening of mercury-exposed children of Andean gold miners. Int J Occup Environ Health 2006;12(3):209-14. PMID 16967826
44: Counter SA, Buchanan LH, Ortega F, Laurell G. Elevated blood mercury and neuro-otological observations in children of the Ecuadorian gold mines. J Toxicol Environ Health A 2002;65(2):149-63. PMID 11820503
45: Deziel NC, Friesen MC, Hoppin JA, Hines CJ, Thomas K, Freeman LE. A review of nonoccupational pathways for pesticide exposure in women living in agricultural areas. Environ Health Perspect 2015;123(6):515-24. PMID 25636067
46: Diringer SE, Berky AJ, Marani M, et al. Deforestation due to artisanal and small-scale gold mining exacerbates soil and mercury mobilization in Madre de Dios, Peru. Environ Sci Technol 2020;54(1):286-96. PMID 31825606
47: Dolcourt JL, Finch C, Coleman GD, Klimas AJ, Milar CR. Hazard of lead exposure in the home from recycled automobile storage batteries. Pediatrics 1981;68(2):225-30. PMID 7267229
48: Dolcourt JL, Hamrick HJ, O'Tuama LA, Wooten J, Barker EL Jr. Increased lead burden in children of battery workers: asymptomatic exposure resulting from contaminated work clothing. Pediatrics 1978;62(4):563-6. PMID 714588
49: Dorea JG. Exposure to environmental neurotoxic substances and neurodevelopment in children from Latin America and the Caribbean. Environ Res 2021;192:110199. PMID 32941839
50: Douine M, Lambert Y, Plessis L, et al. Social determinants of health among people working on informal gold mines in French Guiana: a multicentre cross-sectional survey. BMJ Glob Health 2023;8(12):e012991. PMID 38103896
51: Drasch G, Böse-O'Reilly S, Beinhoff C, Roider G, Maydl S. The Mt. Diwata study on the Philippines 1999--assessing mercury intoxication of the population by small scale gold mining. Sci Total Environ 2001;267(1-3):151-68. PMID 11286210
52: Eisler R. Mercury hazards from gold mining to humans, plants, and animals. Rev Environ Contam Toxicol 2004;181:139-98. PMID 14738199
53: Ekino S, Susa M, Ninomiya T, Imamura K, Kitamura T. Minamata disease revisited: an update on the acute and chronic manifestations of methyl mercury poisoning. J Neurol Sci 2007;262(1-2):131-44. PMID 17681548
54: Elwood WJ, Clayton BE, Cox RA, et al. Lead in human blood and in the environment near a battery factory. Br J Prev Soc Med 1977;31(3):154-63. PMID 588854
55: Esterman AJ, Maynard EJ. Changes in airborne lead particulate in Port Pirie, South Australia, 1986-1996. Environ Res 1998;79(2):122-32. PMID 9841811
56: Estevez-Garcia JA, Farías P, Tamayo-Ortiz M. A review of studies on blood lead concentrations of traditional Mexican potters. Int J Hyg Environ Health 2022;240:113903. PMID 34954665
57: Eto K. Minamata disease. Neuropathology 2000;20 Suppl:S14-9. PMID 11037181
58: Fenske RA. State-of-the-art measurement of agricultural pesticide exposures. Scand J Work Environ Health 2005;31 Suppl 1:67-73. PMID 16190151
59: Fenske RA, Lu C, Simcox NJ, et al. Strategies for assessing children's organophosphorus pesticide exposures in agricultural communities. J Expo Anal Environ Epidemiol 2000;10(6 Pt 2):662-71. PMID 11138658
60: Filigrana PA, Mendez F. Blood lead levels in schoolchildren living near an industrial zone in Cali, Colombia: the role of socioeconomic condition. Biol Trace Elem Res 2012;149(3):299-306. PMID 22547322
61: Fischbein A, Cohn J, Ackerman G. Asbestos, lead, and the family: household risks. J Fam Pract 1980;10(6):989-92. PMID 7373267
62: Fischbein A, Sassa S, Butts G, Kaul B. Increased lead absorption in a potter and her family members. N Y State J Med 1991;91(7):317-9. PMID 1876321
63: Fraser B. Peru's gold rush prompts public-health emergency. Nature 2016;534(7606):162. PMID 27279188
64: Garcia-Sanchez A, Contreras F, Adams M, Santos F. Airborne total gaseous mercury and exposure in a Venezuelan mining area. Int J Environ Health Res 2006;16(5):361-73. PMID 16990177
65: Garcia-Vargas GG, Rothenberg SJ, Silbergeld EK, et al. Spatial clustering of toxic trace elements in adolescents around the Torreón, Mexico lead-zinc smelter. J Expo Sci Environ Epidemiol 2014;24(6):634-42. PMID 24549228
66: Gardner E. Peru battles the golden curse of Madre de Dios. Nature 2012;486(7403):306-7. PMID 22722169
67: Garrettson LK. Childhood lead poisoning in radiator mechanics' children. Vet Hum Toxicol 1988;30(2):112. PMID 3381479
68: Gharehzadehshirazi A, Kadivar M, Shariat M, Shirazi M, Zarkesh MR, Ghanavati Najed M. Comparative analyses of umbilical cord lead concentration in term and IUGR complicated neonates. J Matern Fetal Neonatal Med 2021;34(6):867-72. PMID 31096814
69: Gittleman JL, Engelgau MM, Shaw J, Wille KK, Seligman PJ. Lead poisoning among battery reclamation workers in Alabama. J Occup Med 1994;36(5):526-32. PMID 8027877
70: Grandjean P, Bach E. Indirect exposures: the significance of bystanders at work and at home. Am Ind Hyg Assoc J 1986;47(12):819-24. PMID 3799485
71: Greig J, Thurtle N, Cooney L, et al. Association of blood lead level with neurological features in 972 children affected by an acute severe lead poisoning outbreak in Zamfara State, northern Nigeria. PLoS One 2014;9(4):e93716. PMID 24740291
72: Grimsley EW, Adams-Mount L. Occupational lead intoxication: report of four cases. South Med J 1994;87(7):689-91. PMID 8023200
73: Gundacker C, Hengstschlager M. The role of the placenta in fetal exposure to heavy metals. Wien Med Wochenschr 2012;162(9-10):201-6. PMID 22717874
74: Harada M. Minamata disease: methylmercury poisoning in Japan caused by environmental pollution. Crit Rev Toxicol 1995;25(1):1-24. PMID 7734058
75: Harada M, Nakachi S, Cheu T, et al. Monitoring of mercury pollution in Tanzania: relation between head hair mercury and health. Sci Total Environ 1999;227(2-3):249-56. PMID 10231987
76: Harada M, Nakanishi J, Konuma S, et al. The present mercury contents of scalp hair and clinical symptoms in inhabitants of the Minamata area. Environ Res 1998;77(2):160-4. PMID 9600809
77: Harada M, Nakanishi J, Yasoda E, et al. Mercury pollution in the Tapajos River basin, Amazon: mercury level of head hair and health effects. Environ Int 2001;27(4):285-90. PMID 11686639
78: Hegde S, Sridhar M, Bolar DR, Bhaskar SA, Sanghavi MB. Relating tooth- and blood-lead levels in children residing near a zinc-lead smelter in India. Int J Paediatr Dent 2010;20(3):186-92. PMID 20409199
79: Junaidi M, Krisnayanti BD, Juharfa, Anderson C. Risk of mercury exposure from fish consumption at artisanal small-scale gold mining areas in West Nusa Tenggara, Indonesia. J Health Pollut 2019;9(21):190302. PMID 30931162
80: Kalweit A, Herrick RF, Flynn MA, et al. Eliminating take-home exposures: recognizing the role of occupational health and safety in broader community health. Ann Work Expo Health 2020;64(3):236-49. PMID 31993629
81: Kar-Purkayastha I, Balasegaram S, Sen D, et al. Lead: ongoing public and occupational health issues in vulnerable populations: a case study. J Public Health (Oxf) 2012;34(2):176-82. PMID 21954302
82: Karwowski MP, Just AC, Bellinger DC, et al. Maternal iron metabolism gene variants modify umbilical cord blood lead levels by gene-environment interaction: a birth cohort study. Environ Health 2014;13:77. PMID 25287020
83: Katagiri Y, Toriumi H, Kawai M. Lead exposure among 3-year-old children and their mothers living in a pottery-producing area. Int Arch Occup Environ Health 1983;52(3):223-9. PMID 6629511
84: Kawai M, Toriumi H, Katagiri Y, Maruyama Y. Home lead-work as a potential source of lead exposure for children. Int Arch Occup Environ Health 1983;53(1):37-46. PMID 6654500
85: Kaye WE, Novotny TE, Tucker M. New ceramics-related industry implicated in elevated blood lead levels in children. Arch Environ Health 1987;42(3):161-4. PMID 3606214
86: Kazantzis G. Mercury exposure and early effects: an overview. Med Lav 2002;93(3):139-47. PMID 12197264
87: Knishkowy B, Baker EL. Transmission of occupational disease to family contacts. Am J Ind Med 1986;9(6):543-50. PMID 2426943
88: Kolipinski M, Subramanian M, Kristen K, Borish S, Ditta S. Sources and toxicity of mercury in the San Francisco Bay Area, spanning California and beyond. J Environ Public Health 2020;2020:8184614. PMID 33014081
89: Kondo K. Congenital Minamata disease: warnings from Japan's experience. J Child Neurol 2000;15(7):458-64. PMID 10921517
90: Koplan JP, Wells AV, Diggory HJ, Baker EL, Liddle J. Lead absorption in a community of potters in Barbados. Int J Epidemiol 1977;6(3):225-9. PMID 591168
91: Kopp RS, Kumbartski M, Harth V, Brüning T, Käfferlein HU. Partition of metals in the maternal/fetal unit and lead-associated decreases of fetal iron and manganese: an observational biomonitoring approach. Arch Toxicol 2012;86(10):1571-81. PMID 22678741
92: Krachler M, Rossipal E, Micetic-Turk D. Trace element transfer from the mother to the newborn--investigations on triplets of colostrum, maternal and umbilical cord sera. Eur J Clin Nutr 1999;53(6):486-94. PMID 10403586
93: Kranz BD, Simon DL, Leonardi BG. The behavior and routes of lead exposure in pregrasping infants. J Expo Anal Environ Epidemiol 2004;14(4):300-11. PMID 15254477
94: Kvasnicka J, Cohen Hubal EA, Siegel JA, Scott JA, Diamond ML. Modeling clothing as a vector for transporting airborne particles and pathogens across indoor microenvironments. Environ Sci Technol 2022;56(9):5641-52. PMID 35404579
95: Landrigan PJ, Baker EL Jr, Feldman RG, et al. Increased lead absorption with anemia and slowed nerve conduction in children near a lead smelter. J Pediatr 1976;89(6):904-10. PMID 993916
96: Landrigan PJ, Gehlbach SH, Rosenblum BF, et al. Epidemic lead absorption near an ore smelter. The role of particulate lead. N Engl J Med 1975;292(3):123-9. PMID 1196336
97: Lauwerys R, Buchet JP, Roels H, Hubermont G. Placental transfer of lead, mercury, cadmium, and carbon monoxide in women. I. Comparison of the frequency distributions of the biological indices in maternal and umbilical cord blood. Environ Res 1978;15(2):278-89. PMID 668658
98: Levine RJ, Moore RM, McLaren GD, Barthel WF, Landrigan PJ. Occupational lead poisoning, animal deaths, and environmental contamination at a scrap smelter. Am J Public Health 1976;66(6):548-52. PMID 937600
99: Li A, Zhuang T, Shi J, Liang Y, Song M. Heavy metals in maternal and cord blood in Beijing and their efficiency of placental transfer. J Environ Sci (China) 2019;80:99-106. PMID 30952357
100: Malm O. Gold mining as a source of mercury exposure in the Brazilian Amazon. Environ Res 1998;77(2):73-8. PMID 9600798
101: Marinho JS, Lima MO, de Oliveira Santos EC, et al. Mercury speciation in hair of children in three communities of the Amazon, Brazil. Biomed Res Int 2014;2014:945963. PMID 24734253
102: Matte TD, Figueroa JP, Burr G, Flesch JP, Keenlyside RA, Baker EL. Lead exposure among lead-acid battery workers in Jamaica. Am J Ind Med 1989a;16(2):167-77. PMID 2773946
103: Matte TD, Figueroa JP, Ostrowski S, et al. Lead poisoning among household members exposed to lead-acid battery repair shops in Kingston, Jamaica. Int J Epidemiol 1989b;18(4):874-81. PMID 2621024
104: McDiarmid MA, Weaver V. Fouling one's own nest revisited. Am J Ind Med 1993;24(1):1-9. PMID 8352287
105: McFarlane AC, Searle AK, Van Hooff M, et al. Prospective associations between childhood low-level lead exposure and adult mental health problems: the Port Pirie cohort study. Neurotoxicology 2013;39:11-7. PMID 23958641
106: McIntire MS, Angle CR. Air lead: relation to lead in blood of black school children deficient in glucose-6-phosphate dehydrogenase. Science 1972;177(4048):520-2. PMID 5077325
107: McMichael AJ, Baghurst PA, Robertson EF, Vimpani GV, Wigg NR. The Port Pirie cohort study. Blood lead concentrations in early childhood. Med J Aust 1985;143(11):499-503. PMID 4069047
108: McMichael AJ, Baghurst PA, Vimpani GV, Wigg NR, Robertson EF, Tong S. Tooth lead levels and IQ in school-age children: the Port Pirie Cohort Study. Am J Epidemiol 1994;140(6):489-99. PMID 8067342
109: McMichael AJ, Baghurst PA, Wigg NR, Vimpani GV, Robertson EF, Roberts RJ. Port Pirie Cohort Study: environmental exposure to lead and children's abilities at the age of four years. N Engl J Med 1988;319(8):468-75. PMID 3405253
110: McMichael AJ, Vimpani GV, Robertson EF, Baghurst PA, Clark PD. The Port Pirie cohort study: maternal blood lead and pregnancy outcome. J Epidemiol Community Health 1986;40(1):18-25. PMID 3711766
111: Molina-Ballesteros G, Zúñiga-Charles MA, Cárdenas Ortega A, Solís-Cámara P, Solís-Cámara P. Lead concentrations in the blood of children from pottery-making families exposed to lead salts in a Mexican village. Bull Pan Am Health Organ 1983;17(1):35-41. PMID 6860838
112: Molina-Ballesteros G, Zuñiga-Charles MA, García-de Alba JE, Cárdenas-Ortega A, Solis-Camara P. Lead exposure in two pottery handicraft populations. Arch Invest Med (Mex) 1980;11(1):147-54. PMID 7396631
113: Moller SA, Rasmussen PU, Frederiksen MW, Madsen AM. Work clothes as a vector for microorganisms: accumulation, transport, and resuspension of microorganisms as demonstrated for waste collection workers. Environ Int 2022;161:107112. PMID 35091375
114: Moore RS, Ducatman AM, Jozwiak JA. Home on the range: childhood lead exposure due to family occupation. Arch Pediatr Adolesc Med 1995;149(11):1276-7. PMID 7581764
115: Morales Bonilla C, Mauss EA. A community-initiated study of blood lead levels of Nicaraguan children living near a battery factory. Am J Public Health 1998;88(12):1843-5. PMID 9842385
116: Moreno ME, Acosta-Saavedra LC, Meza-Figueroa D, et al. Biomonitoring of metal in children living in a mine tailings zone in Southern Mexico: a pilot study. Int J Hyg Environ Health 2010;213(4):252-8. PMID 20418157
117: Morton DE, Saah AJ, Silberg SL, Owens WL, Roberts MA, Saah MD. Lead absorption in children of employees in a lead-related industry. Am J Epidemiol 1982;115(4):549-55. PMID 7072703
118: Nakazawa K, Nagafuchi O, Kawakami T, et al. Human health risk assessment of mercury vapor around artisanal small-scale gold mining area, Palu city, Central Sulawesi, Indonesia. Ecotoxicol Environ Saf 2016;124:155-62. PMID 26513531
119: Nashashibi N, Cardamakis E, Bolbos G, Tzingounis V. Investigation of kinetic of lead during pregnancy and lactation. Gynecol Obstet Invest 1999;48(3):158-62. PMID 10545737
120: Needleman HL, McFarland C, Ness RB, Fienberg SE, Tobin MJ. Bone lead levels in adjudicated delinquents. a case control study. Neurotoxicol Teratol 2002;24(6):711-7. PMID 12460653
121: Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA 1996;275(5):363-9. PMID 8569015
122: Ninomiya T, Imamura K, Kuwahata M, Kindaichi M, Susa M, Ekino S. Reappraisal of somatosensory disorders in methylmercury poisoning. Neurotoxicol Teratol 2005;27(4):643-53. PMID 16087068
123: Ninomiya T, Ohmori H, Hashimoto K, Tsuruta K, Ekino S. Expansion of methylmercury poisoning outside of Minamata: an epidemiological study on chronic methylmercury poisoning outside of Minamata. Environ Res 1995;70(1):47-50. PMID 8603658
124: Noble MJ, Decker SL, Horowitz BZ. Inhalational mercury toxicity from artisanal gold extraction reported to the Oregon poison center, 2002-2015. Clin Toxicol (Phila) 2016;54(9):847-51. PMID 27338817
125: Norman R, Mathee A, Barnes B, et al. Estimating the burden of disease attributable to lead exposure in South Africa in 2000. S Afr Med J 2007;97(8 Pt 2):773-80. PMID 17952236
126: Nunez CM, Klitzman S, Goodman A. Lead exposure among automobile radiator repair workers and their children in New York City. Am J Ind Med 1993;23(5):763-77. PMID 8506854
127: Occupational Safety and Health Administration. Code of Federal Regulations 29 Part 1910.1025. Washington, DC: Office of the Federal Register, National Archives and Records Administration,1989:155-93.
128: Oosthuizen MA, John J, Somerset V. Mercury exposure in a low-income community in South Africa. S Afr Med J 2010;100(6):366-71. PMID 20529437
129: O'Tuama LA, Rogers JF, Rogan W. Lead absorption by children of battery workers. JAMA 1979;241(18):1893. PMID 430768
130: Oyanguren H, Perez E. Poisoning of industrial origin in a community. Arch Environ Health 1966;13(2):185-9. PMID 5968499
131: Pateda SM, Sakakibara M, Sera K. Lung function assessment as an early biomonitor of mercury-induced health disorders in artisanal and small-scale gold mining areas in Indonesia. Int J Environ Res Public Health 2018;15(11):2480. PMID 30405024
132: Peplow D, Augustine S. Community-directed risk assessment of mercury exposure from gold mining in Suriname. Rev Panam Salud Publica 2007;22(3):202-10. PMID 18062855
133: Pududu BA, Rother HA. Whose jurisdiction is home contamination? Para-occupational 'take-home' herbicide residue exposure risks among forestry workers' families in South Africa. Int J Environ Res Public Health 2021;18(19):10341. PMID 34639641
134: Quandt SA, Grzywacz JG, Talton JW, et al. Evaluating the effectiveness of a lay health promoter-led, community-based participatory pesticide safety intervention with farmworker families. Health Promot Pract 2013;14(3):425-32. PMID 23075501
135: Rajaee M, Obiri S, Green A, et al. Integrated assessment of artisanal and small-scale gold mining in Ghana-part 2: natural sciences review. Int J Environ Res Public Health 2015;12(8):8971-9011. PMID 26264012
136: Ramakrishna RS, Brooks RR, Ponnampalam M, Ryan DE. Blood lead levels in Sri Lankan families recovering gold and silver from jewellers' waste. Arch Environ Health 1982;37(2):118-20. PMID 7073325
137: Razagui IB, Ghribi I. Maternal and neonatal scalp hair concentrations of zinc, copper, cadmium, and lead: relationship to some lifestyle factors. Biol Trace Elem Res 2005;106(1):1-28. PMID 16037607
138: Reboucas BH, Kubota GT, Oliveira RAA, et al. Long-term environmental methylmercury exposure is associated with peripheral neuropathy and cognitive impairment among an Amazon indigenous population. Toxics 2024;12(3):212. PMID 38535945
139: Rees D, Schneider H. Para-occupational lead poisoning in Soweto. S Afr Med J 1993;83(6):443. PMID 8211475
140: Rice C, Fischbein A, Lilis R, Sarkozi L, Kon S, Selikoff IJ. Lead contamination in the homes of employees of secondary lead smelters. Environ Res 1978;15(3):375-80. PMID 679900
141: Richter ED, Baras M, Berant M, Tulchinsky T. Blood zinc protoporphyrin levels in the children and wives of lead battey workers: a preliminary report. Isr J Med Sci 1985;21:761-4. PMID 4055339
142: Rinehart RD, Yanagisawa Y. Paraoccupational exposures to lead and tin carried by electric-cable splicers. Am Ind Hyg Assoc J 1993;54(10):593-9. PMID 8237792
143: Risher JF, De Rosa CT. Inorganic: the other mercury. J Environ Health 2007;70(4):9-16. PMID 18044248
144: Roberts TM, Hutchinson TC, Paciga J, et al. Lead contamination around secondary smelters: estimation of dispersal and accumulation by humans. Science 1974;186(4169):1120-3. PMID 4469700
145: Rogan WJ. The sources and routes of childhood chemical exposures. J Pediatr 1980;97(5):861-5. PMID 7431184
146: Rohitrattana J, Siriwong W, Tunsaringkarn T, et al. Organophosphate pesticide exposure in school-aged children living in rice and aquacultural farming regions of Thailand. J Agromedicine 2014;19(4):406-16. PMID 25275406
147: Romero RA, Granadillo VA, Navarro JA, Rodríguez-Iturbe B, Pappaterra J, Pirela H. Placental transfer of lead in mother/newborn pairs of Maracaibo City (Venezuela). J Trace Elem Electrolytes Health Dis 1990;4(4):241-3. PMID 2136289
148: Royce SE. ATSDR case studies in environmental medicine #1: Lead toxicity. Atlanta: U.S. Department of Health and Human Services, 1992:1-28.
149: Saalidong BM, Aram SA. Mercury exposure in artisanal mining: assessing the effect of occupational activities on blood mercury levels among artisanal and small-scale goldminers in Ghana. Biol Trace Elem Res 2022;200(10):4256-66. PMID 34773577
150: Saito H. Congenital Minamata disease: a description of two cases in Niigata. Neurotoxicology 2020a;81:360-3. PMID 33741117
151: Saito H, Sekikawa T, Taguchi J, et al. Prenatal and postnatal methyl mercury exposure in Niigata, Japan: adult outcomes. Neurotoxicology 2020b;81:364-72. PMID 35587140
152: Sakamoto M, Yasutake A, Domingo JL, Chan HM, Kubota M, Murata K. Relationships between trace element concentrations in chorionic tissue of placenta and umbilical cord tissue: potential use as indicators for prenatal exposure. Environ Int 2013;60:106-11. PMID 24028800
153: Santos EC, de Jesus IM, Câmara V de M, et al. Mercury exposure in Munduruku Indians from the community of Sai Cinza, State of Pará, Brazil. Environ Res 2002;90(2):98-103. PMID 12483799
154: Sawyer MG, Mudge J, Carty V, Baghurst P, McMichael A. A prospective study of childhood emotional and behavioural problems in Port Pirie, South Australia. Aust N Z J Psychiatry 1996;30(6):781-7. PMID 9034467
155: Searle AK, Baghurst PA, van Hooff M, et al. Tracing the long-term legacy of childhood lead exposure: a review of three decades of the port Pirie cohort study. Neurotoxicology 2014;43:46-56. PMID 24785378
156: Spiegel SJ. Occupational health, mercury exposure, and environmental justice: learning from experiences in Tanzania. Am J Public Health 2009;99(Suppl 3):S550-8. PMID 19890157
157: Spiegel SJ, Savornin O, Shoko D, Veiga MM. Mercury reduction in Munhena, Mozambique: homemade solutions and the social context for change. Int J Occup Environ Health 2006;12(3):215-21. PMID 16967827
158: Steckling N, Tobollik M, Plass D, et al. Global burden of disease of mercury used in artisanal small-scale gold mining. Ann Glob Health 2017;83(2):234-47. PMID 28619398
159: Strachan DP, Leon DA, Dodgeon B. Mortality from cardiovascular disease among interregional migrants in England and Wales. BMJ 1995;310(6977):423-7. PMID 7873946
160: Suarez-Lopez JR, Jacobs DR Jr, Himes JH, Alexander BH. Acetylcholinesterase activity, cohabitation with floricultural workers, and blood pressure in Ecuadorian children. Environ Health Perspect 2013;121(5):619-24. PMID 23359481
161: Swenson JJ, Carter CE, Domec JC, Delgado CI. Gold mining in the Peruvian Amazon: global prices, deforestation, and mercury imports. PLoS One 2011;6(4):e18875. PMID 21526143
162: The Global Initiative Against Transnational Organized Crime. Organized crime and illegally mined gold in Latin America. Geneva, Switzerland: The Global Initiative Against Transnational Organized Crime, 2016.
163: Tomicic C, Vernez D, Belem T, Berode M. Human mercury exposure associated with small-scale gold mining in Burkina Faso. Int Arch Occup Environ Health 2011;84(5):539-46. PMID 21279378
164: Tong IS, Lu Y. Identification of confounders in the assessment of the relationship between lead exposure and child development. Ann Epidemiol 2001;11(1):38-45. PMID 11164118
165: Tong S, Baghurst P, McMichael A, Sawyer M, Mudge J. Lifetime exposure to environmental lead and children's intelligence at 11-13 years: the Port Pirie cohort study. BMJ 1996;312(7046):1569-75. PMID 8664666
166: Tong S, Baghurst PA, Sawyer MG, Burns J, McMichael AJ. Declining blood lead levels and changes in cognitive function during childhood: the Port Pirie Cohort Study. JAMA 1998;280(22):1915-9. PMID 9851476
167: Tong S, McMichael AJ, Baghurst PA. Interactions between environmental lead exposure and sociodemographic factors on cognitive development. Arch Environ Health 2000;55(5):330-5. PMID 11063408
168: Torres-Sanchez L, Gamboa R, Bassol-Mayagoitia S, et al. Para-occupational exposure to pesticides, PON1 polymorphisms and hypothyroxinemia during the first half of pregnancy in women living in a Mexican floricultural area. Environ Health 2019;18(1):33. PMID 30975138
169: Truska P, Rosival L, Balázová G, et al. Blood and placental concentrations of cadmium, lead, and mercury in mothers and their newborns. J Hyg Epidemiol Microbiol Immunol 1989;33(2):141-7. PMID 2768816
170: Vimpani G, McMichael A, Robertson E, Wigg N. The Port Pirie Study: a prospective study of pregnancy outcome and early childhood growth and development in a lead-exposed community--protocol and status report. Environ Res 1985;38(1):19-23. PMID 4076107
171: Waack A, Ranabothu M, Vattipally V. Mercury poisoning from artisanal gold mining equipment. Radiol Case Rep 2022;18(2):607-9. PMID 36465164
172: Wade L. Mercury pollution. Gold's dark side. Science 2013;341(6153):1448-9. PMID 24072903
173: Walter SD, Yankel AJ, von Lindern IH. Age-specific risk factors for lead absorption in children. Arch Environ Health 1980;35(1):53-8. PMID 7362271
174: Wang JD, Shy WY, Chen JS, Yang KH, Hwang YH. Parental occupational lead exposure and lead concentration of newborn cord blood. Am J Ind Med 1989;15(1):111-5. PMID 2929605
175: Wanyana MW, Agaba FE, Sekimpi DK, et al. Mercury exposure among artisanal and small-scale gold miners in four regions in Uganda. J Health Pollut 2020;10(26):200613. PMID 32509414
176: Wasserman GA, Graziano JH, Factor-Litvak P, et al. Consequences of lead exposure and iron supplementation on childhood development at age 4 years. Neurotoxicol Teratol 1994;16(3):233-40. PMID 7523846
177: Watson LC, Hurtado-Gonzales JL, Chin CJ, Persaud J. Survey of methylmercury exposures and risk factors among indigenous communities in Guyana, South America. J Health Pollut 2020;10(26):200604. PMID 32509405
178: Watson WN, Witherell LE, Giguere GC. Increased lead absorption in children of workers in a lead storage battery plant. J Occup Med 1978;20(11):759-61. PMID 712444
179: Weitzman M, Glotzer D. Lead poisoning. Pediatr Rev 1992;13(12):461-8. PMID 1293574
180: Whelan EA, Piacitelli GM, Gerwel B, et al. Elevated blood lead levels in children of construction workers. Am J Public Health 1997;87(8):1352-5. PMID 9279275
181: Wigg NR, Vimpani GV, McMichael AJ, Baghurst PA, Robertson EF, Roberts RJ. Port Pirie Cohort study: childhood blood lead and neuropsychological development at age two years. J Epidemiol Community Health 1988;42(3):213-9. PMID 3251001
182: Winegar DA, Levy BS, Andrews JS Jr, Landrigan PJ, Scruton WH, Krause MJ. Chronic occupational exposure to lead: an evaluation of the health of smelter workers. J Occup Med 1977;19(9):603-6. PMID 599390
183: World Health Organization. Nigeria: mass lead poisoning from mining activities, Zamfara State. Geneva, Switzerland: World Health Organization, 2011.
184: Ye D, Brown JS, Umbach DM, et al. Estimating the effects of soil remediation on children's blood lead near a former lead smelter in Omaha, Nebraska, USA. Environ Health Perspect 2022;130(3):37008. PMID 35319254
185: Yorifuji T, Tsuda T, Inoue S, Takao S, Harada M. Long-term exposure to methylmercury and psychiatric symptoms in residents of Minamata, Japan. Environ Int 2011;37(5):907-13. PMID 21470684
186: References especially recommended by the author or editor for general reading.

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Para-occupational poisoning

Also Relevant

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Clinical Categories

Neurotoxicology

Para-occupational poisoning …

Para-occupational poisoning

Introduction

Overview

Key points

Historical note and terminology

Description

Table 1. Routes of Para-Occupational Poisoning

Clinical applications

Table 2. Occupations and Exposure Routes in Para-occupational Lead Poisoning

Table 3. Work Practices in Selected Fomite-Related Para-Occupational Lead Exposures

Para-occupational mercury poisoning

Media

References

Contributors

Author

ICD & OMIM codes

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Also in This Category

Thallium neuropathy

Occupational neurotoxicology: metals

Occupational neurotoxicology: overview

Mass poisoning events with neurotoxic agents

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Neurologic disorders related to biological warfare agents and toxins

Carbon monoxide poisoning

Para-occupational poisoning

Introduction

Overview

Key points

Historical note and terminology

Description

Table 1. Routes of Para-Occupational Poisoning

Clinical applications

Table 2. Occupations and Exposure Routes in Para-occupational Lead Poisoning

Table 3. Work Practices in Selected Fomite-Related Para-Occupational Lead Exposures

Para-occupational mercury poisoning

Media

References

Contributors

Author

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Thallium neuropathy

Occupational neurotoxicology: metals

Occupational neurotoxicology: overview

Mass poisoning events with neurotoxic agents

Alcohol abuse and its neurologic complications

Neurologic disorders related to chemical warfare nerve agents

Neurologic disorders related to biological warfare agents and toxins

Carbon monoxide poisoning

This is an article preview.
Start a Free Account
to access the full version.