Environmental Health Hazards in the Tropics

Environmental Health Hazards in the Tropics

26 

Ema G Rodrigues, David C Christiani

Key features Features unique to the tropics and key differences in resource-poor areas l l l l

Lack of alternative resources/options Less stringent or poorly enforced environmental and occupational regulations Burden of disease on families may be greater in developing countries Access to healthcare may be very limited

Pediatric considerations l Children may be more likely to be exposed to some contaminants and toxins due to hand-to-mouth activity l For a given exposure, children have greater exposures per unit of body weight l Children less efficiently metabolize and excrete many toxic chemicals

INTRODUCTION Diseases caused by environmental exposures are often not readily treatable, but are often preventable. Exposures to environmental hazards can be modified or controlled in many cases, thus reducing or preventing the risk of developing disease. Countries undergoing economic development may be especially vulnerable to environmental hazards since the introduction of new materials, processes, and industries into nascent or emerging economies often precedes the introduction of proper controls, regulation, and experience in those settings. The Environmental Kuznets Curve (EKC) hypothesizes that during the initial phase of a country’s economic development, environmental emissions increase as per capita income increases, but that as the economy matures, pollutant levels may subsequently decrease. This inverted U-shaped curve was initially described by Simon Kuznets to represent the relationship between income and inequality, and represents the pattern of emissions of some pollutants quite well. The eventual decrease in pollution may result from the implementation of controls and environmental policies as the negative societal impact of pollution begins to outweigh the positive societal impact of production and economic growth. The likelihood of exposure to environmental toxins is often affected by economic and regional factors. For instance, some pesticides that are banned in the USA and the EU (e.g. DDT) continue to be used in several countries worldwide, as these countries balance the low cost and high effectiveness of such agents against environmental health aspects. A more recent industry that has posed environmental health hazards to those in developing countries is the electronic waste (e-waste) recycling industry, with China being the largest importer of

e-waste from developed countries [1]. While the majority of electronics are composed of iron, aluminum, plastic and glass, they also contain copper, platinum and lead which are often recycled for profit. The exportation of e-waste from the US and EU to less developed countries is often the result of more stringent environmental and occupational regulations in industrialized nations. Access to training and healthcare are other important aspects that may affect a population’s risk of developing environmental-related disease following exposure. This chapter will discuss methods used to control personal exposures to environmental hazards, but it is crucial that those who are required to work with hazardous substances be trained on ways to avoid or minimize toxicity. Similarly, individuals exposed to toxins should have access to healthcare to monitor exposure and to minimize and treat exposure-related disease. Unfortunately, this is not often the case in developing regions. For instance, workers in the industrialized world are typically exposed to chronic low-level exposures and preclinical effects can be detected with routine monitoring, while acute poisonings are more common in developing countries where exposures are typically higher and access to healthcare is often limited.

EXPOSURE CONCEPTS Several considerations must be made when assessing the risk of exposure to environmental and occupational hazards. First, the source of the hazard must be identified. Is the source of the hazard in the workplace, home, or neighborhood? Typically, occupational exposures to substances are significantly higher than environmental exposures, but environmental contaminants usually affect a larger number of individuals. While workers are exposed to higher contaminant levels, they are typically healthier than the general population, which includes children, the elderly, and those who have chronic health conditions. In developing countries, this division between work and home may be less clear. For example, families may live on the agricultural lands where they work; all individuals may be exposed to occupational chemicals, such as pesticides and herbicides, throughout the day rather than only during certain work hours. Additionally, child labor remains common. Many children in developing countries contribute to both family and non-family work where exposures may be higher than those of the general population (Table 26-1). Second, the route of exposure must be considered. Exposure to environmental contaminants occurs mainly through ingestion of contaminated food or water, inhalation of contaminated air, or dermal absorption of chemical or biological agents. The health effects associated with a hazard may vary depending on the route of exposure, since absorption differs by organ (lung, skin, or gastrointestinal tract). The absorbed dose, described as mass of chemical per mass of the individual’s bodyweight, is an important consideration when determining how much exposure of a chemical is considered “safe”. Because children have lower bodyweights than adults, equal exposures will result in higher doses for children. In addition to dose quantities, other considerations associated with the health effects of environmental hazards include duration and timing of exposure. In some cases, chronic exposures over a lengthy period of time may have

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cumulative effects leading to disease, whereas the effects of short-term or periodic exposures may be naturally repaired. For example, exposure to heavy metals may induce DNA damage, but DNA repair mechanisms may prevent the development of disease if exposures are short-term. Timing of exposure is also important since individuals are more susceptible to the health effects of environmental exposures during certain periods of life, such as during fetal development, childhood, and advanced age.

MAJOR ENVIRONMENTAL AND OCCUPATIONAL HAZARDS AMBIENT AIR POLLUTION Air pollution is a widespread environmental health hazard with sources ranging from anthropogenic sources (e.g. combustion of fossil fuels in power plants or motor vehicles) to natural sources (e.g.

TABLE 26-1  Child Labor, 5–14 Years (%), 1999–2007 Bangladesh

13

Belize

40

Brazil

6

forest fires and dust storms). Air pollution is comprised of various contaminants, including particulate matter (PM), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3) and polycyclic aromatic hydrocarbons (PAHs), among others. Rapid industrialization in several tropical countries has led to significantly higher concentrations of air pollutants compared to those in developed countries. Increase in some air pollutants, such as NO2 and O3, is often due to an increase in the use of motor vehicles, coupled with lack of environmental regulations to enforce controls [2]. Increased air pollution levels have been associated with cardiovascular disease, upper and lower respiratory tract infections, and lung cancer [3–5]. Additionally, individuals with chronic health conditions such as asthma, emphysema and cardiovascular disorders are more susceptible to the health effects associated with air pollution. Particulate matter, typically characterized by particle size defined by the aerodynamic diameter in microns (e.g. PM10, PM2.5, PM1.0), has been shown to be especially harmful. While larger particles are typically trapped in the nose and throat, smaller particles are more likely to be inhaled into the deeper regions of the lung (i.e. alveoli), making smaller particles more likely to contribute to pulmonary and heart disease. Weather conditions in many tropical zones may exacerbate the level of pollution. For instance, high temperatures in combination with high humidity and lack of rain lead to faster rates of the formation of smog, a term used to describe the interaction of nitrogen oxides, volatile organic compounds, and other pollutants, and there is some evidence that ambient PM10 concentrations have a greater effect on mortality and hospitalizations due to cardiovascular and respiratory causes during the warm periods and summer [6].

Cambodia

45

Ghana

34

INDOOR AIR POLLUTION

India

12

Mexico

16

Nicaragua

15

The health effects associated with indoor air pollution (IAP) are of great concern in developing countries, where it has been estimated that more than 2.4 billion people use biomass fuels (BMF) such as wood, dung and coal for cooking and heating [7]. Figure 26.1 indicates that developing countries in tropical zones account for the majority of deaths attributed to exposure to indoor smoke from burning of solid fuels. BMF smoke is also associated with chronic obstructive pulmonary disease (COPD), tuberculosis, lung

Data from: The State of the World’s Children 2009, UNICEF. © 2009 the United Nations Children’s Fund.

IAP deaths/million

FIGURE 26.1 Deaths from indoor smoke from solid fuels. Redrawn from WHO World Health Report, 2002.© WHO 2005. All rights reserved.

0–10 10–50 50–100 100–200 200–300 300–400 400–610 Data not available

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cancer, and an interstitial lung disease known as “hut lung”. In developing countries, women are at highest risk of developing BMF smokerelated illness since they are exposed to the highest levels while cooking [8]. A recent study conducted in rural China reported a substantial decrease in the incidence of COPD among men and women after installation of household chimneys on previously un-vented stoves [9].

ARSENIC Arsenic (As), a naturally occurring metal embedded in the earth’s crust, is characterized as a known human carcinogen by the International Agency for Research on Cancer [10]. Exposure to arsenic occurs mainly through ingestion of contaminated water from deep wells (30–180 feet), but can also occur through food or inhalation of arsenic fumes from coal burning or smelting. Arsenic is leached into drinking water supplies from the bedrock surrounding the aquifers, and elevated arsenic levels in drinking water have been documented in several tropical countries such as India, Chile, Mexico, Bangladesh, Peru, Taiwan, Mongolia and Thailand, as well as in parts of the US. While inorganic arsenic occurs in several forms, the trivalent (AsIII) and pentavalent (AsV) species are most toxic, whereas organic forms such as arsenobetaine occur in shellfish such as shrimp and are not toxic to humans. In an effort to provide clean water free of microbial contamination, the United Nations Children’s Fund (UNICEF) began to install tube wells in Bangladesh in the 1970s. While this effort was aimed at reducing the morbidity and mortality due to gastrointestinal disease, it also caused one of the largest arsenic poisonings in history. It has been estimated that more that 35–77 million people may be exposed to arsenic-contaminated drinking water across Bangladesh [11]. Also, large numbers of people in nearby West Bengal in India have been similarly affected. The clinical manifestations of chronic arsenic exposure are numerous, and include hyperpigmentation, keratoses, and skin, bladder and lung cancers (Fig. 26.2) [12–14]. There is no ideal treatment for chronic arsenic-related health effects, but affected individuals are usually told to avoid drinking additional arseniccontaminated water and to consume a protein-rich diet. Additionally, higher selenium blood levels may reduce the risk of arsenic-related skin lesions [15]. In severe cases of arsenic poisoning, chelation with 2,3-dimercapto-1-propanesulfonate (DMPS) can increase the urinary excretion of arsenic and improve symptoms. Additionally, for arsenicrelated cancers, surgical methods can be used to remove the cancer if it is detected early [16].

LEAD POISONING Lead is a durable, malleable metal that is highly resistant to corrosion and is used worldwide for many applications. It has been used for the manufacture of water pipes, as an anti-knock agent in gasoline, as an anti-corrosive pigment in paint, additive in cosmetics, and in traditional medicines. Among the many uses, leaded gasoline is one of the major sources of airborne lead pollution and personal exposure. The phase-out of lead from gasoline has significantly reduced the air lead concentrations and blood lead levels in humans in many countries, including Austria, Brazil, Canada, Colombia, India [17], Japan, Pakistan [18], Slovakia, Sweden, Thailand and the US. Another source of lead, especially in developing countries, is lead glazes used in ceramics. When ceramic pottery is used for cooking or storing food, the lead contained in the glaze may leach into food [19]. Another source of lead exposure and poisonings in developing countries is the recycling of electronics containing lead and lead-acid batteries [20]. While lead exposures are very high in these workplaces, children and adults can also be exposed to dangerous levels of lead in air or soil while living near one of these facilities or living with an individual working with lead [21]. Cosmetics and traditional remedies containing lead are also commonly used in tropical countries. Given its many uses, lead is a very common contaminant and is a leading cause of environmental-related illness among both children and adults worldwide. Lead is mainly absorbed into the bloodstream through ingestion and inhalation. Absorbed lead is redistributed and

A

B FIGURE 26.2 Hyperkeratotic rash of arsenic intoxication. Photos courtesy of Dr Molly Kile, Harvard School of Public Health

BOX 26.1  Pediatric Considerations – Lead l

Children absorb lead more efficiently than adults Children who are malnourished are particularly susceptible to lead due to lower intakes of iron and calcium which can reduce the absorption of lead l Blood lead levels ≥10 µg/dL among children are considered elevated, but no level is considered safe l

stored in bone and soft tissues until remobilized into the bloodstream. Because lead has a relatively long half-life for excretion (T1/2 ~28 days), health effects associated with lead are chronic and longlasting. Health effects related to increased blood lead levels in children include encephalopathy, and decreases in IQ, hemoglobin synthesis, growth, nerve conduction velocity and cognitive function (Box 26.1). Abdominal symptoms (called “lead colic”) include abdominal pain, intermittent vomiting and constipation. High-level exposure can lead to interstitial nephritis. Research has shown that children in India under 3 years of age with blood lead levels ≥10 µg/ dL are more likely to have moderate or severe anemia, but no lead level is considered safe [22]. Health effects in adults include anemia,

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constipation, mental status changes, cardiovascular disease and hypertension, chronic renal dysfunction, decreased sperm count and increased abnormal sperm in men, and higher incidence of spontaneous abortions in women [23] (Table 26-2). Diagnosis usually rests on direct measurement of blood lead levels. Basophilic stippling of erythrocytes and gingival lead lines may be seen. Once internalized, lead enters bone, and boney tissues can act as long-term reservoirs. The most important feature of treatment is to minimize additional exposure. Chelation therapy can reduce immediate toxicity during acute exposures and severe intoxications, but may not appreciably alter long-term cognitive impairment.

PESTICIDES In developing countries, acute pesticide poisonings are still a major health concern. Pesticides are widely available and widely used, and include insecticides, herbicides and rodenticides (Table 26-3). To maximize crop productivity, pesticides are in wide use in many areas of emerging economies. Health outcomes associated with pesticide exposures include death, and neurologic, reproductive, developmental, ophthalmic, genotoxic and carcinogenic effects. Many insecticides are organophosphates or carbamates, and are potent cholinesterase inhibitors. Signs and symptoms of intoxication relate to level, identity

TABLE 26-2  Health Effects Associated with Fibrogenic and Metal Dusts Agent

Industry

Disease/health outcome

Clinical presentation/symptoms

Asbestos

Construction Fire proofing

Pleural plaques Malignant mesothelioma Pleural effusion

Chest pain Cough Shortness of breath Chest tightness

Silica

Ceramics Construction Cement manufacturing Glass manufacturing Semiconductors Metallurgy Sand blasting Stone cutting

Silicosis

Chronic cough Shortness of breath Fluid in lungs

Cotton dust

Textiles

Byssinosis

Chest tightness Cough Wheezing

Coal dust

Coal mining

Black lung disease

Breathlessness

Lead

Battery recycling Construction/painting Electronics

Anemia Reproductive effects (male and female) Cardiovascular disease Encephalopathy Nephropathy Death

Fatigue Nausea Headaches Hypertension Constipation Increased blood lead levels Increased erythrocyte protoporphyrin

Manganese

Manganese processing Battery manufacturing Welding Steel production Mining Glass manufacturing Fungicides

Manganism Anemia

Neurological effects Slowed hand movements Behavioral changes Tremors Hypertension

Chromium

Steel production Chrome plating Leather industry Cement

Eczema Asthmatic bronchitis

Skin rashes/dermatitis Ulcers Kidney damage

Beryllium

Ceramics Nuclear weapons

Beryllium sensitization Chronic beryllium disease (CBD)

Shortness of breath

Mercury (inorganic)

Battery manufacturing Mercury recycling Auto manufacturing Thermometers Lighting

Minamata disease

Dermatitis Mood changes Memory loss Muscle weakness Tremors Kidney effects Respiratory failure Slurring of speech

Dusts

Metals

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TABLE 26-3  Adverse Health Effects Caused by Selected Classes of Pesticides* Chemical/ chemical class

Examples of pesticides

Clinical presentation

Treatment

Route of exposure†

Arsenicals

Sodium arsenate

Abdominal pain, nausea, vomiting, garlic odor, metallic taste, bloody diarrhea, headache, dizziness, drowsiness, weakness, lethargy, delirium, shock, kidney insufficiency, neuropathy

Wash skin thoroughly and remove contaminated clothing Gastric lavage and/or activated charcoal (avoid cathartics as arsenicals can cause diarrhea) Intravenous fluid administration and monitoring of electrolytes Chelation: Agents include meso-2,3dimercapto-succinic acid (succimer) or British Anti-Lewisite (BAL or dimercaprol); DMPS (sodium salt of 2,3-dimercapto-1propane sulfonic acid) is also used but is not FDA-approved for use in the United States

O, R, D (rarely)

Borates (insecticide)

Borax

Upper airway irritation, abdominal pain, nausea, vomiting, diarrhea, headache, lethargy, tremor, kidney insufficiency

Wash skin thoroughly and remove contaminated clothing Gastric lavage (NOTE: activated charcoal has limited ability to absorb boric acid) Dialysis

O, R, D (broken skin)

Carbamates (insecticide)

Carbaryl thiram, aldicarb mecarbam

Malaise, weakness, dizziness, sweating, headache, salivation, nausea, vomiting, diarrhea, abdominal pain, confusion, dyspnea, dermatitis, pulmonary edema

Wash skin thoroughly and remove contaminated clothing Activated charcoal within first hour of ingestion Oxygen Endotracheal intubation often required for depressed mental status, bronchospasm, copious secretions, and respiratory depression Atropine Pralidoxime (must be given along with atropine)

O, D

Chloralose

Chloralose

Vomiting, vertigo, tremor, myoclonus, fasciculations, confusion, seizures, rhabdomyolysis

Gastric lavage and/or activated charcoal Benzodiazepines for seizures Intravenous fluids

O

Coumarins (rodenticide)

Brodifacoum warfarin

Ecchymoses, epistaxis, excessive bleeding, hematuria, prolonged prothrombin time, intracranial bleed, anemia, fatigue, dyspnea

Vitamin K Fresh frozen plasma +/− recombinant human factor VIIa for lifethreatening bleeding GI decontamination if large ingestion

O, D (possible)

Diethyltoluamide (insect repellent)

DEET (N,N-diethyl-metatoluamide

Dermatitis, ocular irritation, headache, restlessness, ataxia, confusion, seizures, urticaria

Gastric lavage within 1 hour and/or activated charcoal Benzodiazepines for seizures

O, D

Dipyridil (herbicide)

Paraquat, diquat

Mucous membrane and airway irritation, abdominal pain, diarrhea, vomiting, gastrointestinal bleeding, pulmonary edema, dermatitis, renal and hepatic damage, coma, seizures

Gastric lavage using diatomaceous earth clays (bentonite or Fuller’s earth) Activated charcoal if diatomaceous earth clays not available Hemodialysis

O, D (via broken skin)

Phosphonates (herbicide)

Glyphosate

Airway, skin, and mucous membrane irritation, abdominal, pain, nausea, vomiting, shock, dyspnea, respiratory failure

Rinse mouth with milk or water Activated charcoal for later ingestions Monitor for acute lung injury and hypotension

O, R

Continued

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TABLE 26-3  Adverse Health Effects Caused by Selected Classes of Pesticides—cont’d Chemical/ chemical class

Examples of pesticides

Clinical presentation

Treatment

Route of exposure†

Fluoroacetate (rodenticide)

Sodium fluoroacetate

Vomiting, paresthesias, tremors, seizures, hallucinations, coma, confusion, arrhythmias, hypertension, cardiac failure

Gastric lavage within 1 hour and/or activated charcoal Monitor for and treat hypocalcemia (Administration of Monoacetin and ethanol have been used, but safety and efficacy have not been proven in humans)

O, D (possible)

Mercury, organic (fungicide)

Methyl mercury

Metallic taste, paresthesias, tremor, headache, weakness, delirium, ataxia, visual changes, dermatitis, renal dysfunction

Removal from source and gastric lavage and activated charcoal Chelation for acute neurologic symptoms or chronic toxicity: agents include penicillamine, BAL, DMPS, and dimercaptosuccinic acid (DMSA)

O, R, D

Metal phosphides (rodenticide, fumigant)

Zinc-, aluminum-, magnesiumphosphide

Abdominal pain, diarrhea, acidosis, shock, jaundice, paresthesias, ataxia, tremors, coma, pulmonary edema, tetany, dermal irritation

Wash skin thoroughly and remove contaminated clothing Be prepared to isolate vomited material as phosphine gas produced in stomach can off-gas into environment after vomiting

O, R, D

Halocarbons (fumigant)

Cellfume, methyl bromide

Skin/airway/mucous membrane irritant, cough, renal dysfunction, confusion, seizures, coma, pulmonary edema

Wash skin thoroughly and remove contaminated clothing Gastric lavage and/or activated charcoal if ingested

O, R, D

Organochlorines (insecticide)

Lindane, DDT

Cyanosis, excitability, dizziness, headache, restlessness, tremors, convulsions, coma, paresthesias, nausea, vomiting, confusion, tremor, cardiac arrhythmias, acidosis

Wash skin thoroughly and remove contaminated clothing Diazepam for convulsions Oxygenation Cholestyramine resin to enhance elimination

O, R, D

Organophosphates (insecticides)

Malathion, parathion dichlorvos chlorpyrifos

Headache, dizziness, bradycardia, weakness, anxiety, excessive sweating, fasciculations, vomiting, diarrhea, abdominal cramps, dyspnea, miosis, paralysis, salivation, tearing, ataxia, pulmonary edema, confusion, acetylcholinesterase inhibition

Same management as for carbamates

O, D

Organotin (fungicide)

Fentin acetate

Airway, skin and mucous membrane irritation, dermatitis, salivation, delirium, headache, vomiting, dizziness

Wash skin thoroughly and remove contaminated clothing Dilution with water or milk Activated charcoal

O, R, D

Phenol derivatives (fungicide, wood preservative)

Pentachlorophenol

Skin, airway and mucous membrane irritation, contact dermatitis, dyspnea, diaphoreses, urticaria, tachycardia, headache, abdominal pain, fever, tremor, hypotension, rhabdomyolysis

Gastric lavage and/or activated charcoal Intravenous fluids (NOTE: salicylates are contraindicated for fever)

O, R, D

Pyrethrins, pyrethroids

Allethrin cyfluthrin permethrin

Allergic reactions, anaphylaxis, dermatitis, paresthesias, wheezing, seizures, coma, pulmonary edema, diarrhea, abdominal pain

GI decontamination is usually not required For allergic or hypersensitivity reactions, antihistamines, inhaled beta-agonists, corticosteroids, or epinephrine may be used

R, D

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TABLE 26-3  Adverse Health Effects Caused by Selected Classes of Pesticides—cont’d Chemical/ chemical class

Examples of pesticides

Clinical presentation

Treatment

Route of exposure†

Strychnine (rodenticide)

Strychnine

Muscle rigidity, opisthotonus, rhabdomyolysis, hyperthermia, respiratory compromise

Endotracheal intubation is generally required High-dose benzodiazepines to control muscle activity Nondepolarizing neuromuscular blockade agents (e.g. vecuronium) may also be used in intubated patients Opioids (muscle contractions are extremely painful) Aggressive intravenous fluid administration

O

Thallium (rodenticide)

Thallium sulfate

Abdominal pain, nausea, vomiting, bloody diarrhea, headache, weakness, liver injury, hair loss, paresthesias, neuropathy, encephalopathy, cardiac failure

Gastric lavage and/or activated charcoal Insoluble Prussian blue to increase elimination rate Monitor for and treat hypocalcemia

O

Triazines (herbicide)

Atrazine, prometryn

Mucous membrane, ocular and dermal irritation

Gastric lavage and/or activated charcoal

O, R, D

Modified from Thundiyil JG, Stober J, Besbelli N, Pronczuk J: Acute pesticide poisoning: a proposed classification tool. Bull World Health Organ 2008;86:205–9. *This list is an overview and is not meant to be a comprehensive list of all pesticides and pesticide classes. Gastric emptying is most effective when used within 1 hour of an acute and large dose ingestion, and should rarely be performed if more than 4 hours have elapsed since ingestion. Gastric emptying should in general not be performed following ingestion of corrosives and many hydrocarbons. Complications include aspiration and perforation. † Route of exposure key: O, oral/ingestion; R, respiratory/inhalation; D, dermal or ocular.

BOX 26.2  Pediatric Considerations – Pesticides l

Approximately 70% of working children work in agriculture and may be exposed to pesticides at occupational levels worldwide l Children are particularly vulnerable to the effects of pesticides because they have lower levels of enzymes involved in the metabolism and excretion of pesticides such as organophosphates

and fat solubility of the agent, and include: salivation, lacrimation, urination, defecation, gastric emesis, bronchorrhea, bronchospasm, bradycardia (SLUDGE/BBB), respiratory depression, cardiac arrhythmias, miosis, neuropathy and altered mental status. Death may result from respiratory and cardiovascular compromise. Diagnosis is usually one of clinical recognition. Treatment involves decontamination, supportive care, atropine, and oximes such as pralidoxime.

FIGURE 26.3 DDT spraying in Namibia. Reprinted with permission from Peter Arnold, Inc.

It has been estimated that 3 million cases of severe acute pesticide poisonings occur each year globally, resulting in 220,000 deaths annually, and that 99% of these deaths occur in the developing world. Globally, pesticides are also commonly used to commit suicide, since they are inexpensive, widely available, and effective. It is estimated that two-thirds of all pesticide-related deaths worldwide are the result of suicide [24].

many agricultural workers worldwide are illiterate, all workers should also be trained in proper handling and usage. While the use of personal protective equipment (PPE) such as respirators and impermeable gloves and clothing is effective in reducing exposures, PPE can be very costly and uncomfortable, and is less likely to be used in hot humid areas (Fig. 26.3). The lack of PPE use emphasizes the need to regulate the most toxic pesticides and replace them with less toxic alternatives. Additional interventions can include introducing crop rotation to minimize the need for pesticide use [25].

Occupational exposure to pesticides can occur through inhalation, incidental ingestion, and dermal contact during job-related tasks such as mixing and spraying (Box 26.2). Pesticide containers should be clearly labeled in the local language with ample use of illustrations in low-literacy populations to communicate proper handling. Since

While pesticide use is essential in the developing world for agricultural purposes and the reduction of vector-borne diseases, actions can be taken to minimize the hazards of pesticide use, including selfpoisonings. For the most part, highly toxic pesticides have been banned or are approved for restricted use by a certified applicator in

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developed countries (e.g. arsenic oxide, DDT, parathion), but these regulations are not normally extant or are not enforced in developing countries. In fact, DDT was banned in several African countries for several years before it was reintroduced for indoor use due to an increase in malaria deaths. Currently, a Global Environment Facility (GEF) initiative aims to phase-out the use of DDT by the early 2020s, while assuring that malaria infection rate reductions are met.

MOLD/FOOD IMPURITIES The high heat, humidity, and long rainy seasons in tropical countries make infestation of mold a likely environmental problem, especially in agricultural communities. Aflatoxins, highly toxic metabolites produced by the fungi Aspergillus flavus and Aspergillus parasiticus, are contaminants found in animal feed and some crops such as corn, peanuts and cotton. Ingestion of aflatoxins can lead to liver necrosis, failure and cirrhosis. A recent outbreak of aflatoxin poisoning in eastern and central provinces in Kenya (2004) due to contaminated maize that had been stored in damp conditions lead to 317 cases of acute poisoning and 125 deaths. Levels of aflatoxin measured in maize from the households that were affected ranged from 20 ppb to 8000 ppb, up to 400 times the WHO recommended maximum limit [26]. Aflatoxin is also a major contributor to liver cancer [27,28] and is classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC) [29]. Diagnosis usually involves clinical recognition, especially of outbreaks from common ingestion, and measuring toxin or metabolites in blood or urine. Treatment is usually supportive. Ergotism (also called St. Anthony’s Fire), a disease caused by the ingestion of ergot alkaloids produced by ergot, is manifested in two forms: the gangrenous form and the convulsive form. The causative agent, alkaloid ergotamine, and derivatives affect vascular constriction and neurotransmission. The gangrenous form of ergotism is characterized by symptoms including edema of the legs, severe pain, and gangrene at the tendons, while the convulsive form is characterized by nausea and vomiting followed by drowsiness, twitching, uterine contractions and abortion, convulsions, blindness, hallucinations and paralysis. Chronic complications include cardiac valvular fibrosis. The main source of exposure to ergot alkaloids is contaminated grains (especially rye) that are stored in humid environments susceptible to contamination of fungi of the genus Claviceps. The clinical symptoms experienced by individuals who have ingested ergot alkaloids depend on the type of alkaloids produced by the various fungi. Ergotism can be prevented by thorough cleaning practices and by destroying the alkaloids by cooking and baking the flour products [30]. Farmer’s lung disease (FLD) is a type of hypersensitivity pneumonitis resulting from an allergic reaction to inhaled microbial agents, including mold spores. Farmers may inhale fungal microorganisms typically found in hay stored in damp conditions with poor ventilation. The symptoms of this disease include shortness of breath, productive cough, bronchospasm, fever, and malaise. The chest x-ray shows bilateral, fleeting infiltrates. Additionally, patients with FLD have been shown to have higher precipitating immunoglobulin G (IgG) levels associated with various microbes, compared with farmers without the disease [31]. Chronic farmer’s lung can lead to obliterating bronchiolitis and fibrosis. Treatment usually involves minimizing additional exposure and treatment with steroids (inhaled and systemic) and bronchodilators. Melamine is another example of a toxic food impurity. Unlike mold contamination, food products containing melamine have been intentionally contaminated. Foods contaminated with melamine will appear to have higher protein content because melamine is rich in nitrogen, which is measured to determine protein levels. In an attempt to make some food items more marketable, a variety of products, such as infant formula and wheat flour used in pet food, originating in China have been contaminated with melamine. Tens of thousands of infants and young children in China have been hospitalized with kidney stones and obstructive renal failure after the consumption of melamine-contaminated formula. Some cases resulted in death [32]. Successful treatment of cases included dialysis to correct their

electrolyte levels, hydration (orally or intravenously), alkalization, or surgical removal of the stones [33].

RECOGNITION OF ENVIRONMENTAL AND OCCUPATIONAL HAZARDS Several methods can be used by physicians and public health professionals to identify diseases related to environmental conditions. Sentinel cases or unexpected cases of disease may give clues to causative agents. For example, in 1775, Percivall Pott was one of the first surgeons to observe a high incidence of scrotal cancers in young boys who worked as chimney sweeps. Pott suspected that this unexpected high incidence of cancer was a result of dermal contact with coal soot (that is now known to contain various polycyclic aromatic hydrocarbons and now known to be carcinogenic), and he noted that regular washing prevented the disease. Continuous surveillance and the maintenance of disease registries can also be valuable in the identification of an environmental or occupational health outcome. Registries allow for the methodical collection of demographic and occupational information from individuals who have developed specific illnesses (e.g. cancer, asthma, diabetes). Additionally, targeted registries can collect biological measurements on healthy people who may be at high risk for specific exposures (e.g. blood lead levels among construction workers). Physicians play a crucial role in detecting and the critical role in treating individuals with disease relating to environmental exposure or poisoning. In many cases, the best treatment for an environmental disease is removal from exposure. Information about the patient’s work environment as well as the home environment is crucial in the identification of disease. It is also important for physicians to consider previous jobs as well as current jobs. Some diseases have a long latency period and may have clinical impact years after the patient was exposed. Thorough exposure histories may identify a causative agent responsible for the patient’s symptoms, and medical screening tests (e.g. beryllium sensitization test, pulmonary function) can be used to monitor exposed patients

CONTROL AND REDUCTION   OF ENVIRONMENTAL AND OCCUPATIONAL HAZARDS While several methods can be used to reduce the levels of personal exposure to environmental hazards, each method differs in terms of feasibility, expense and efficacy. The most efficient way to reduce the health effects associated with a hazard is to eliminate it from use or substitute it with a less hazardous substance. A common successful implementation of this is the elimination and substitution of lead in gasoline in several countries. Elimination of a hazard is the most desirable option, but it may not always be feasible. It is necessary to have a suitable less hazardous substitute that can be used for the purpose. When substitution is not an option, engineering controls, such as ventilation, or a redesigning of equipment can be used to minimize personal exposures to the hazard. While engineering controls are usually effective, they can be expensive to implement and maintain over time. The implementation of cooking stoves with enclosed wood-burning chambers with chimneys as opposed to open fires is an example of a redesign that reduced personal exposure to indoor air pollution and respiratory symptoms, specifically among women [34,35]. In the absence of feasible engineering controls, the use of administrative controls can reduce workplace exposures (not necessarily environmental exposures) to individuals by rotating jobs among workers or limiting the time a worker performs a specific task, such as spraying pesticides. Finally, workers can use personal protective equipment (PPE), such as respirators, and protective clothing (e.g. gloves, overalls, boots) to minimize the absorption of environmental hazards that cannot be controlled by any other means. The use of PPE may be effective, but it also poses additional challenges to workers. PPE requires routine cleaning and maintenance for efficacy and can be very cumbersome to wear, especially in hot and humid climates.

E nv i ro n m e nt a l H e a l t h H a z a rd s i n the Tropics

Other common control measures include regular hand washing to avoid exposure through hand-to-mouth contact while eating, drinking or smoking, and changing clothes after being exposed to dusts or chemicals to minimize further absorption and exposure to others.

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