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

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

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

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).

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

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.

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).

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.

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).

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).

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.

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.

Miners use liquid mercury to separate the gold from either refined ore (concentrate amalgamation) or whole ore without concentration (whole ore amalgamation, which requires greater quantities of mercury), forming a mercury-gold amalgam.

The amalgam is then heated to burn off the mercury, leaving purified gold behind; since at least the 1990s, this is typically done in the open with a blow torch for ASGM (51; 172).

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).

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.

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).