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International Journal of Environmental Health Research

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A review of endosulfan, dichlorvos, diazinon, and diuron pesticides used in Jamaica

Kayon Barrett & Foday M. Jaward
a a a

Department of Environmental and Occupational Health, College of Public Health, University of South Florida, Tampa, FL, USA Version of record first published: 22 Jun 2012.

To cite this article: Kayon Barrett & Foday M. Jaward (2012): A review of endosulfan, dichlorvos, diazinon, and diuron pesticides used in Jamaica, International Journal of Environmental Health Research, 22:6, 481-499 To link to this article: http://dx.doi.org/10.1080/09603123.2012.667794

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International Journal of Environmental Health Research Vol. 22, No. 6, December 2012, 481499

A review of endosulfan, dichlorvos, diazinon, and diuron pesticides used in Jamaica

Kayon Barrett and Foday M. Jaward*
Department of Environmental and Occupational Health, College of Public Health, University of South Florida, Tampa, FL, USA (Received 25 August 2011; nal version received 14 January 2012) The global agricultural sector is the primary user of pesticides, consuming more than three billion kilograms of pesticides annually. Although pesticides are benecial in controlling the proliferation of pests, they have been associated with adverse human and ecological impacts. Approximately 87% of the annually imported pesticides in Jamaica are applied within agricultural or household settings. However, in Jamaica, the potential impact on humans, their property, and the environment is unknown, as the fate of many of the locally applied pesticides has not been established. This review discusses four pesticides extensively applied in agricultural practices in Jamaica endosulfan, diazinon, diuron, and dichlorvos. The information presented is essential for the development of fate and transport models of these chemicals. Consequently, health and ecological impact assessments may be conducted from the generated models. Keywords: pesticides; persistence; fate; standards; toxic eects

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1. Introduction Pesticides are used globally to control pests, which are organisms that negatively impact on humans or their property (Moore 2007). Negative impacts include adverse health eects, ecological injury, damaged infrastructure, as well as ill health of pets or livestock. With the worlds explosive population growth, food security is of global importance. However, since pests reduce food productions annually by about 45% (Abhilash and Singh 2009), it is critical to reduce pest infestation. One way to achieve this is the use of pesticides. Of the three billion kilograms of pesticides produced annually, more than 75% is used in agricultural practices (Moore 2007). The Pesticide Control Authority (PCA), the pesticide regulatory body in Jamaica, reports that agriculture by itself uses 54% of the islands imported pesticides while an additional 33% is used in agriculture/household settings (PCA 2010). In 2005 alone, about 2512 tons (*3 million kilograms) of pesticides were imported to Jamaica. Despite the benets of pesticides in reducing the proliferation of pests, these chemicals have also been associated with adverse health and ecological impacts. There are concerns that the misuse and overuse of pesticides in lesser developed countries have led to higher acute mortality rates despite using less than 25% of
*Corresponding author. Email: fjaward@health.usf.edu
ISSN 0960-3123 print/ISSN 1369-1619 online The work was authored as part of Kayon Barrett and Foday Jawards ocial duties as employees of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105 no copyright protection is available for such works under U.S. law http://dx.doi.org/10.1080/09603123.2012.667794 http://www.tandfonline.com

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produced pesticides (Moore 2007). During the past several decades, developed countries have donated thousands of tons of pesticides to developing countries to enhance food production and combat anticipated crop diseases (Jain 1992). In many cases, the pesticide donations exceeded the true need of the countries. These excess aging, obsolete, and dangerous after years of neglect and poor storage condition pesticides are posing serious environmental, health, and safety problems. In Jamaica, although the PCA registers and regulates the distribution of pesticides, the monitoring of pesticide residues in some food items is a joint venture between the PCA, the local Ministry of Agriculture and the Bureau of Standards. However, fate and transport models for pesticides have not been developed in Jamaica. Additionally, concentrations in the environmental media are not monitored. As a result, the potential for local impact due to the application of pesticides is not known and local standards have yet to be developed. Instead, when necessary, the PCA refers to standards and policies developed in the United States (US) and the European Union for given imported pesticides. There is clearly the need for monitoring. An independent study which collected sediment and water samples, between October 1991 and December 1992, in areas such as Portland, Jamaica, found concentrations of endosulfan and its derivatives in excess of the 0.22 mg/L limit necessary to protect aquatic life in freshwater (Robinson and Mansingh 1999). The aim of this review is to highlight four major types of pesticides: endosulfan, diazinon, diuron, and dichlorvos used in Jamaica. This examination provides the foundation and baseline data for the development of fate and transport models for these pesticides, which will ultimately allow for the development of standards and policies specic to the country. Also, this review may provide the impetus for periodic monitoring of the concentrations of these pesticides in Jamaicas environmental media, especially in agricultural communities such that continuous impact assessments may be done and appropriate interventions applied. 2. Background Once applied, pesticides may enter the atmospheric, aquatic, soil, biotic, or indoor air media by various means. For example, pesticides enter the atmospheric environment by drift spray, post-application volatilization, and wind erosion of soil. These emissions are inuenced by numerous physical and chemical factors (Bidleman 1999; Walker et al. 1999; Bailey 2001). For example, persistence of pesticides in the atmosphere is a function of their residence times which is determined by their half-lives. Also, the rate of dry deposition inuences atmospheric residence times and hence persistence (Sadiki and Poissant 2008). In this review, only water, atmospheric, and indoor air media are discussed. The pesticides predominantly enter the atmosphere as vapor, aerosols, or adsorbed onto suspended soil particles (Sadiki and Poissant 2008). During direct drift, pesticide aerosols are created while spraying occurs. Indirect drift involves the volatilization from soil or the resuspension of soil particles some time after spraying has occurred (Scheyer et al. 2007). Evaporation is highest immediately after application and is generally higher from plants than from soil (Carlsen et al. 2006); soil is generally acting as a sink or reservoir, although it can also act as a source when environmental conditions are right for the pesticide to re-evaporate into the atmosphere. Both the gasparticle coecient, which is itself determined by the octanolair partition coecient, and the vapor pressure of the given pesticide inuence the state

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in the atmosphere (Sanusi et al. 1999). However, the removal of the pesticide from the atmosphere depends on the airwater partition coecient, i.e. Henrys law constant pesticides with low Henrys law constant, such as those adsorbed onto soil particles, are more easily removed by wet deposition. Adsorbed pesticides may otherwise be removed from the atmosphere via photodegradation and reactions with radicals and oxidizing agents, such as ozone (Bossan et al. 1995). The associated Henrys law constant also explains the pesticides potential for long-range transport. Pesticides with higher Henrys law constants are less likely to be removed via wet or dry deposition and, consequently, are more likely to exhibit long-range transport deposition (Scheyer et al. 2008). Given their higher Henrys law constant, pesticides in the gaseous phase are more prone to long-range transport. Overall, gaseous phase pesticides are mainly removed by photochemical degradation and dry deposition, while particle phase (adsorbed onto soil particles) pesticides are removed via wet and dry deposition (Sanusi et al. 1999). Surface water contamination with pesticides is commonly the result of diuse sources such as agricultural run-o. Other diuse sources of contamination include wet and dry deposition, whereas potential point sources include sewage plants and manufacturing locations. The degree of contamination is not only a function of the physicochemical properties of the pesticide such as octanolwater coecient (Kow) and aqueous solubility but is also a function of local factors such as climate, topography, and the proximity of waters to the site of application (Dabrowski et al. 2002). Other factors inuencing contamination of surface waters by pesticide application rates include percentage of applied pesticide available for run-o, amount of impeding organic matter en route to the waters, land use, rainfall duration and intensity, and soil characteristics. The pesticide burden in surface waters includes the solute concentrations, concentrations adsorbed to settled and suspended particles, as well as concentrations in aquatic biota (Holvoet et al. 2007). River uxes also determine point concentrations. Groundwaters are also contaminated by agricultural application of pesticides. While the degree of groundwater contamination is determined by properties and pesticide usage as in surface water contamination, additional inuential properties include the vertical distance between surface application site and the water table as well as the recharge capabilities of the groundwater (Pionke and Glotfelty 1989). Pesticides are also used indoors to control pests associated with pets, in the homes and gardens and may also have been added to furnishings during manufacture (Rudel and Perovich 2009). In the indoor environment, the more volatile pesticides may be suspended in the vapor phase, whereas the less volatile pesticides are usually adsorbed to settled or suspended particles (Rudel and Perovich 2009). Degradation of pesticides occurs at slower rates in the indoors because of the reduced likelihood of degradative processes involving microbes, sunlight, and high temperatures. Pesticides, applied in the outdoor environment, may be atmospherically transported to indoor environments, where dust act as a reservoir, and degradation by photochemical and other reactive processes is less likely than outdoors (Tan et al. 2007). Given the nite volume of the space, indoor exposure may pose a greater risk than outdoor exposure. The above considerations are important for developing pesticide fate and transport models as well as when the researchers conduct the associated assessments.

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K. Barrett and F.M. Jaward Pesticide assessment Approach

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An assessment of pesticide usage in Jamaica between 2005 and 2006 reveals that herbicides accounted for most of the imported pesticides, approximately 40.4%. Other major imports included insecticides, 34.2%, and fungicides, 22.6%. The preparations of fungicides used in Jamaica usually contain active ingredients which are either inorganic or fall under the insecticide or herbicide classes of pesticides (PCA 2010). Pesticides were chosen for this review if they satised any of the following criteria: (1) used currently in Jamaica but banned in many/most developed countries; (2) exhibit long residence time and bioaccumulate; (3) associated with adverse health eects chronic or acute; and (4) imported in large quantities. The top four chosen were endosulfan (otherwise called Thiadon), diazinon, diuron, and dichlorvos. Endosulfan is an organochlorine insecticide, while diazinon and dichlorvos are both organophosphate insecticides and diuron is a herbicide. Table 1 provides a summary of the properties, uses and toxicities of these pesticides.

3.2.

Endosulfan

3.2.1. Overview Endosulfan (6,7,8,9,10,10-hexachloro-1,5,5a,6,9,9a-hexahydro-6,9-methano-2,3,4benzo(e)dioxathiepin-3-oxide; Awasthi et al. 2000) is an organochlorine insecticide. Organochlorines are very persistent (Dehn et al. 2005), resisting biodegradation because of their cyclic nature (Smith and Gangolli 2002). They are the rst manmade organic pesticides used in agriculture (Kalyoncu et al. 2009). Given their lipophilic nature, organochlorines are adsorbed onto sediments and enter the food chain, where they bioaccumulate. They are ubiquitous and exhibit longrange transport during atmospheric exchanges, water currents, and animal migrations (Dehn et al. 2005; Guan et al. 2009). Past uses of organochlorines include the elimination of vegetal insects as well as disease vectors (Chang and Doong 2006). Growing knowledge and research about their toxic capabilities in conjunction with their environmental persistence have generated concern (Smith and Gangolli 2002). Despite the ban of most organochlorine pesticides in many countries since the 1970s and 1980s, they have recently been found in human fat and breast milk, shes, birds, and dairy products (Harris et al. 2001; Man osa et al. 2003; Kalyoncu et al. 2009; Salem et al. 2009). They have been reported to be primarily neurotoxic but have also been associated with developmental and endocrine disruption, nervous system impairment, as well as immunological and reproductive dysfunction (Kalyoncu et al. 2009). Endosulfan is currently in use in many countries including China, Europe, Canada, and India, with common market names such as Thiodan, Thiomul, Malix, Thionex, and Tiovel (Weber et al. 2010). It was banned in the US in June 2010 (USEPA 2010). Annual global use between 1996 and 2004 exceeded 11,000 tons (Weber et al. 2010). Agricultural application includes the following crops: cotton, paddy, coee, oil seeds, as well as vegetables and fruits (Awasthi et al. 2000). Endosulfan is among the more commonly observed organochlorine pesticides in the atmosphere and surface waters in the US as well as in the arctic atmosphere (Weber et al. 2010).

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Table 1. Dichlorvos Organophosphate insecticide Diazinon Herbicide

Data summary for endosulfan, dichlorvos, diazinon, and diuron. Diuron

Chemical

Endosulfan

Type

Organochlorine insecticide

Use

Agricultural insects on cotton, paddy, coee, vegetables, and fruits; Public health disease vectors Days (ATSDR 2010a, 2010b, 2010c) Primarily neurotoxic; also associated with immunotoxicity and respiratory disorders Class 2B

Organophosphate insecticide Agricultural insects on livestock and crops

Agricultural weeds on cotton, sugar, wheat, and fruits; Industrial antifouling paints, and weeds along railways Months (Gooddy et al. 2002)

Half-lives

Agricultural insects on fruits, vegetables, ornamental plants, and pastures; Public health disease vectors; Industrial insects Sediments weeks to months; Waters hours to weeks (ATSDR 2008)

Toxicity

Tropics hours to days; Temperate zones months (Singh et al. 1991; Hii et al. 2007) Primarily neurotoxic; also associated with endocrine disruption and hepatotoxicity

Photosystem inhibition; also associated with ecological harm and neurotoxicity Class L

Carcinogenicity (USEPA*)

Class 2A

Primarily neurotoxic; also associated with immunotoxicity, genotoxicity, and reproductive toxicity Unclassied

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The high lg Kow and lg Koc of 3.55 and 3.5, respectively, are indicators of the lipophilic nature of this chemical. Endosulfan has a low aqueous solubility in the range of 60100 mg/L and a higher solubility in organic solvents in the order of g/L. The vapor form of endosulfan is stable in the atmosphere. The b-endosulfan isomer has a higher scavenging rate and aqueous solubility than a-endosulfan and is therefore more easily removed from the atmosphere and dissolved into surface waters (Weber et al. 2010). b-Endosulfan degrades irreversibly to a-endosulfan and both are eventually oxidized to endosulfan sulfate, which is the most common form in environmental media (Weber et al. 2010). Although rare, both isomers of endosulfan can also be hydrolyzed to endosulfan diol. Endosulfan exhibits aquatic half-lives in the order of hours to days in tropical regions (Singh et al. 1991). However, in temperate climates, aquatic half-lives extend to months. Aquatic half-lives vary considerably and are functions of oxygen content, pH, turbidity and the presence of other contaminants (Hii et al. 2007), among other factors. 3.2.2. Toxic eects

Endosulfan is toxic not only to insects but also to mammals. Although a-endosulfan is more toxic than b-endosulfan (Silva and Beauvais 2010), the most toxic form is the metabolite endosulfan sulfate. Endosulfan exerts its neurological eects by preventing the binding of g-amino-butyric acid (GABA) to its receptor site (GABAr). Generally, when GABA binds to GABAr, chloride channels are opened and the chloride ions migrate into neurons across a concentration gradient. When the ions migrate, neuron ring/excitation is hindered. Therefore, endosulfan results in continued, uncontrolled neuron excitation in the central nervous system (Silva and Beauvais 2010). Endosulfan is also considered to be an endocrine disrupter. Caride et al. (2010) reported that endosulfan inuences the secretion of prolactin as well as other luteinizing and thyroid-stimulating hormones. Additionally, this pesticide is genotoxic rez et al. 2008). Both developmental and to shes, bacteria, and mammals (Pe behavioral disruptions in exposed tadpoles have also been reported (Brunelli et al. 2009). Another study demonstrated that endosulfan inhibited acetylcholinesterase (AChE), an enzyme necessary to prevent extended muscle contractions, in shes (Dutta and Arends 2003). This pesticide is also hepatotoxic and has been found to cause hematological alterations in sh at concentrations as low as 5 mg/L (Hii et al. 2007). The human health impact data on endosulfan are limited. However, acute exposures have reportedly caused deaths in humans (ATSDR 2000). It is classied, respectively, by the United States Environmental Protection Agency (USEPA) and the World Health Organization (WHO), as a Class II and IB pesticide (Hii et al. 2007). Concerns regarding endosulfans environmental persistence conjunction to ndings on the carcinogenicity/mutagenicity of related organochlorines (dioxin, chlordane, dieldrin, and dichlorodiphenyltrichloroethane (DDT)) led to research on its toxic eects and the subsequent development of health and environmental standards/limits. In Jamaica, endosulfan is currently registered as Thiodan EC and used predominantly in the coee industry. It is imported from Columbia as an emulsiable concentrate and is classied as a Class 1 toxic pesticide (PCA 2010). Since Jamaica has not set standards or limits for this chemical, the US federal standards are used.

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The USEPA has developed a non-carcinogenic reference dose for oral exposure to endosulfan of 6E73 mg/kg/day (USEPA IRIS 2010). Also, the intermediate and chronic minimal risk levels (MRLs) for oral exposure set by the Agency for Toxic Substances and Disease Registry (ATSDR) are 5E73 mg/kg/day and 2E73 mg/kg/ day, respectively. To protect human health, the maximum contaminant limit for water is 240 mg/L, while limits of 0.22 mg/L and 0.034 mg/L were established to protect aquatic life in freshwater and saltwater, respectively (USEPA 2010). Also, the USEPA has established tolerances for endosulfan in foods, generally in the range of 0.12.0 ppm and specically 24 ppm in/on dried teas. In the US, there is no federal atmospheric standard for endosulfan. However, Florida has issued acceptable average concentrations in air over 8 h, 24 h, and 1 year of 1 mg/m3, 0.24 mg/m3, and 0.05 mg/m3, respectively (ATSDR 2010a, 2010b, 2010c). Endosulfan is also listed on the National Priorities List, under the Comprehensive Environmental Response and Liability Act (CERCLA). The USEPA has posted both ecological and health risk screening/benchmark levels for Superfund sites to determine the need for further investigation or remediation. The risk estimates use generic data based on reasonable maximum exposure levels. The ecological benchmark concentrations for both a- and b-endosulfan for fresh water, marine water, as well as adsorbed onto sediments in both these types of waters, respectively, are 0.02 mg/L, 0.001 mg/L, 0.00214 mg/kg, and 0.000107 mg/kg. For residential exposure, non-carcinogenic screening levels for soil and tap-water exposures are 3.67E 02 mg/kg and 2.19E 02 mg/L, respectively. 3.3. Organophosphates

Diazinon and dichlorvos are organophosphate insecticides. They were developed subsequent to World War II. Chemically derived from phosphoric acid, organophosphates are biodegradable (Moore et al. 2007) and, hence, are not persistent. They are generally applied as systemic insecticides to control insects such as eas and ticks (Lazarini et al. 2004). Exposure to these compounds occurs primarily via agricultural application and use in homes. In fact, the study by Lu et al. (2004) showed that higher organophosphate pesticide concentrations in the indoor air of homes in agricultural communities were more likely. Also, it was found that the concentrations in indoor dust were greater than those in the soils of these communities. Diet also played a major role in organophosphate pesticide exposure in children (Lu et al. 2004; Kawahara et al. 2007). The metabolism of organophosphates is commonly achieved by the enzymes cytochrome P450s and hydrolases (Fujioka and Casida 2007). The then formed oxon compounds interact with and inhibit the action of AChE. The oxidized organophosphate causes hydrolysis of the enzyme via phosphorylation. As an irreversible intermediate step, a complex is formed between the oxidized compound and the enzyme, subsequent to which the phosphorylation step is rapid (Ryu et al. 1991). AChE is required to hydrolyze acetylcholine, a neurotransmitter which, when released, modies the concurrent passages of potassium and sodium at muscle junctions thereby inciting required muscle contractions (Moore 2007). The hydrolysis by AChE is necessary to cease the time-indenite action of acetylcholine, hence preventing persistent muscle contractions. Organophosphates are degraded primarily by hydrolysis, which depends on temperature, pH, chemical structure, and the presence of catalysts. The hydrolysis is

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the result of an attack by nucleophiles on the phosphorus atom. Other degradation processes include photo-isomerization, photooxidation, and phosphorylation (Kang and Zettel 1995). There are three methods commonly used to identify exposure to organophosphates. One method assesses the products of enzyme hydrolysis, which is eective in identifying the responsible insecticide but is hindered by the rapid excretion of these products from the body. Another method, in lieu of assessing the inactivated AChE, assesses the blood enzyme butyrylcholinesterase, which also reacts with organophosphates and whose products are longer retained within the body. Yet the third method, which is the most longstanding, directly measures the AChE activity but fails to identify the causative organophosphate (Fidder et al. 2002). Acute health eects of poisoning include paralysis of respiratory muscles, stomach cramping, tremors, muscle weakness, and even death (Keifer and Firestone 2007). Early death by acute poisoning is mediated through the central nervous system (Bird et al. 2003). In a report submitted to the Intergovernmental Forum on Chemical Safety by Kishi (2002), cholinesterase-inhibiting pesticides, which include organophosphates, were identied as the major causes of acute and severe pesticide toxicity. Many organophosphate insecticides are restricted or banned in developed countries. However, the use in developing countries are less controlled and applicators often display at risk behavior for acute pesticides poisoning such as eating and drinking with contaminated hands, failure to wear personal protective equipment and using leaking or damaged equipment (Kishi 2002). Organophosphate exposure has been linked to neurological impairment. In a recent study of Hispanic immigrants, agricultural workers performed worst on neurobehavioral tests and the poor performance was found to be associated with organophosphate exposure (Rothlein et al. 2006). In general, organophosphates are considered less toxic than organochlorines. This is due to the fact they are easily biodegradable. Additionally, the high solubility prevents bioaccumulation and hence environmental persistence. 3.3.1. Dichlorvos

3.3.1.1. Overview. Dichlorvos is an organophosphate insecticide and is commonly called 2,2-dichlorovinyl dimethyl phosphate (DDVP). Registered trade names include Atgard, Dichlorman, Divipan, Herkol, Vapona, and Nuvan (ATSDR 1997). Given the low vapor pressure of 1.2E 7 2 mmHg, dichlorvos readily vaporizes. Today, organophosphates are still widely used, as is dichlorvos. At room temperature and pressure, dichlorvos is a slightly colored liquid (ATSDR 2010a, 2010b, 2010c). This chemical has a relatively short half-life. The demonstrated halflives in the respective media are: air 52 days; water days to weeks; and soil *17 days. Dichlorvos is used to control insects on both domestic and livestock animals as well as in homes. This chemical is also applied to crops. Dichlorvos has also been used to treat sea lice on aquatic creatures including Salmon (Murison et al. 1997). Hydrolysis is the main metabolic route in mammals (Booth et al. 2007). In the environment, dichlorvos degenerates rapidly by biotic and abiotic processes to metabolites including dichloroacetic acid, dimethylphosphate, and dichloroethanol (WHO 2007).

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3.3.1.2. Toxic eects. Dichlorvos is considered to be among the more toxic organophosphate pesticides. The WHO classies dichlorvos as highly hazardous (WHO 2007). The pesticide displays a high acute toxicity and the major exposure route in humans is via inhalation (Lazarini et al. 2004). In the human body, dichlorvos inhibits the AChE enzyme irreversibly (Binukumar et al. 2010). The result of such an activity is the accumulation of acetylcholine at the nerve junction. Acute health eects include paralysis of respiratory muscles, stomach cramping, tremors, muscle weakness, and even death (Keifer and Firestone 2007). The recent study by Binukumar et al. (2010) points to a possible eect of chronic exposure to dichlorvos by liver metabolic interruptions. Dichlorvos has demonstrated a slight association with diabetes (Montgomery et al. 2008) and a more pronounced association with respiratory disorders (Hoppin et al. 2006) among pesticide applicators. This pesticide also demonstrated immunotoxic eects by repressing the immune activity of cytotoxic T lymphocyte, natural killer, and lymphokine-activated killer cells (Li et al. 2005). The mechanism of eect occurred through the signicant decreases in releases of perforin, ganzyme A, and granulysin, which are proteins responsible for eliminating virus infected and tumor cells (Li et al. 2005). Although agencies such as International Agency for Research on Cancer (IARC) and USEPA classify dichlorvos as possibly carcinogenic, at least one review of 11 cancer studies of dichlorvos refutes the carcinogenicity of this chemical. The review indicated that only the two studies conducted by National Toxicological Program reported any level of carcinogenicity, which may not have been associated with dichlorvos exposure (Ishmael et al. 2006). In vitro genotoxicity of this pesticide has been demonstrated. However, it has been shown that in vivo exposure at environmental concentrations demonstrates little genotoxicity (Booth et al. 2007). In the few studies reviewed which involved in vivo genotoxicity at environmental levels, concerns were expressed regarding methodology. Dichlorvos is toxic to aquatic creatures, having been shown to reduce plankton and sh counts. Crustaceans appear to be the more sensitive of the aquatic invertebrate (Murison et al. 1997). Increasing levels of applied dichlorvos in three studied sh farms showed decreased AChE activity in the analyzed sh samples (Murison et al. 1997). The reproductive eect of dichlorvos was demonstrated in rats with the observed eect of endometrial damage via shrinkage of the epithelial cells and their nuclei of the endometrium when a sub-chronic dosage of 4 mg/kg was administered. Previous studies had proposed that organophosphate pesticides induce cell apoptosis by causing oxidative stress to the cells (Oral et al. 2006). However, the study involving Wistar rats treated with 0, 1, 2, and 4 mg/kg of dichlorvos over a period of 9 weeks demonstrated in signicant testicular eects (Okamura et al. 2005). The oxidative stress to neuronal cells was indicated in a 12-week chronic exposure of rat brain to dichlorvos. Mitochondrial calcium uptake and resultant oligonucleosomal DNA fragmentations, which are precursors to cellular apoptosis, were observed in the dichlorvos-administered rat brains (Kaur et al. 2007). This study proposes another mechanism of neurotoxicity rather than via the known AChE inhibition with a postulated route of cellular oxidative stress. Similarly, oxidative stress was proposed to cause mitochondrial calcium uptake in the liver cells causing liver dysfunction in male rats chronically exposed (6 mg/kg bw for 12 weeks) to dichlorvos (Binukumar et al. 2010).

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Dichlorvos is both manufactured and imported for use in Jamaica. This chemical is restricted and used principally in the industrial regions of Jamaica. Thus, there lies the potential for exposure due to contamination from manufacturing wastes, agricultural run-o and agricultural products. Individuals may also be exposed occupationally or during use at their respective homes. The PCA (2010) determines dichlorvos to be a Class I toxicant. Given the known adverse impacts of this chemical, it is necessary to assess the distribution of this chemical island-wide and its potential to impact on health. As mentioned earlier, the IARC and USEPA have classied dichlorvos as a Class 2B (possible) human carcinogen based on sucient animal data and no supporting human data (IARC 2010; USEPA IRIS 2011). An oral slope factor of 2.9E 7 1 kgday/kg was the attributed carcinogenic risk, while the drinking water unit risk estimate was 8.3E 7 6 L/mg. A chronic oral reference dose has been set at 5E 7 4 mg/kg/day with a medium-to-high condence rating. The chronic inhalation reference concentration, with a medium condence level, is 5E 7 4 mg/m3 (USEPA IRIS 2011). USEPA established tolerances for dichlorvos in foods range from 0.02 ppm in goat and cattle meats to 2.0 ppm in packaged, non-perishable, or bagged raw agricultural products (USEPA-OPP 2010). Dichlorvos is one of the 188 toxic air pollutants listed by the USEPA. The USEPA has no established maximum contaminant limits for dichlorvos in drinking water. In 1997, Codex adopted maximum residue levels for dichlorvos in foods such as cereal grains and wheat our ranging from 1 to 10 mg/kg (FAO/WHO 2010). 3.3.2. Diazinon

3.3.2.1. Overview. Diazinon is a widely used organophosphate insecticide. Given lg Kow and lg Koc of 3.81 and 1.6022.635, respectively, diazinon appears to readily partition to organic matter. However, the low vapor pressure of 9.01E 7 5 mmHg at 208C and Henrys law constant of 1.17E 7 7 atm-m3/mol (ATSDR 2008) are indicative that diazinon vaporizes easily. In one experiment, the Henrys law constant for diazinon was measured between 283 K and 301 K. At 293.05 K, Henrys law constants of 2.6 + 0.5 M/atm and 2.9 + 0.6 M/atm were obtained, whereas a value of 1.5 + 0.3 M/atm was obtained at 297.55 K (Feigenbrugel et al. 2004). Diazinon displays variable half-lives, which appear dependent on soil type and pH. At the neutral pH of 7 and in sandy loam soil, a maximum half-life of 209 days was observed. The lowest half-life of 14 days was observed at a pH of 4, in peated sandy loam soil (ATSDR 2008). Half-lives in water are relatively short, ranging from 70 h to 12 weeks, which depend on sunlight, microorganisms, pH, and temperature. Diazinon is otherwise marketed as Diazol, Basudin, Garden-tox, or Alfa-tox and has a chemical abstracts service registry number (CASRN) of 333-41-5. Diazinon is also otherwise called O-2,2-dichlorovinyl-O,O-dimethyl phosphate, often shortened to DDVP. Diazinon is degraded under a number of dierent processes including hydrolysis, oxidation, photolysis, and photocatalytic degradation (Kouloumbos et al. 2003). Metabolites from the hydrolysis of diazinon include diethylthiophosphate and 2-isopropyl-6-methyl-pyrimidin-4-ol, whereas photolysis produces diazoxon, isodiazinon, and hydroxydiazinon. Photocatalysis additionally produced diazinon methyl ketone and hydroxydiazoxon. The major pathways for the transformations include the cleavage of the pyrimidine (PO) group and

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oxidative desulfuration of the thiono group by OH radicals (substitution of sulfur with oxygen in the PS bond) succeeded by hydrolysis or direct oxidation of diazinon. Hydroxydiazoxon is thought to be produced through a double oxidative mechanism (Kouloumbos et al. 2003). Hydrolyses of the pyrimidine bonds of diazinon and diazoxon produce 2-isopropyl-6-methyl-pyrimidin-4-ol, whereas hydroxylation forms hydroxydiazinon and hydroxydiazoxon (Zhang et al. 2011). Dehydration succeeded by oxidation in conjunction with decarboxylation and then oxidation produces diazinon methyl ketone (Zhang et al. 2011). The metabolites are more polar than the parent chemical and are expected to exhibit greater persistence in the aquatic environment (Kouloumbos et al. 2003). Degradation of metabolites is both pH and temperature dependent. Generally, degradation of diazinon is improved in acidic environments and it has been shown that increasing solution temperatures increases degradation (Zhang et al. 2011). A photodegradation study to assess the impact of diazinon and its products on the AChEs and Na/K ATPases of human and commercial cells showed that diazoxon was more than 1000 times more potent at inhibiting AChEs than the parent compound. Also, inhibition of AChE increased as irradiation time increased, indicative of the increased potency of byproducts (Colovic et al. 2010). It is hypothesized that the in vivo metabolism of diazinon predominantly involves the hepatic enzymes CYP1A2 and CYP3A4, which are cytochrome P450 enzymes primarily located in the liver. These enzymes are thought to respond by sulfoxidation of diazinon to diazoxon (Vittozzi et al. 2001). With global sales in 2003 of approximately 40 million US dollars, this chlorinated organophosphate insecticide is widely used to control insects for industrial, agricultural, household, and public health purposes (Liu et al. 2009). Diazinon has wide-range usage as it is eective in the use on eld crops, fruits, pasturelands, n-Pe rez et al. 2007). Given the lipophilic vegetables, and ornamental plants (Giro nature of this chemical and the stability of its metabolites in aquatic media, diazinon has the potential to contaminate water and food resources, given its longevity in soils and despite the low persistence in the aquatic media. Hence, it is necessary to review its potency. 3.3.2.2. Toxic eects. Acute exposure to diazinon has been associated with muscurinic and nicotinic eects including nausea, vomiting, bronchoconstriction, weakness, and cramping. Other central nervous system eects include confusion, insomnia, coma, and seizures. However, death from high acute exposures is often the result of respiratory or cardiac failure (ATSDR 2008). In a recent study of diabetic versus non-diabetic rats, the metabolism of diazinon to diazoxon was enhanced in the diabetic rats. The AChE activities in the erythrocytes of the diabetic rats were greatly reduced early in the administration of the diazinon. This has implications for the potential for acute toxicity at low doses in diabetic individuals (Ueyama et al. 2007). The resistance to toxicity by diazinon and its metabolites may be explained by the delicate balance between the sensitivity of brain AChE and the detoxicating capacity/ability of the liver. Fishes with insensitive AChEs and limited bioactivation of diazinon were more resistant to toxicity by this chemical than shes either with high bioactivating activity in conjunction with sensitive AChEs or with limited bioactivation and sensitive AChE (Keizer et al. 1995).

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The reproductive toxicity of some organophosphates has been demonstrated via hormonal imbalances and altered sperm quality. Diazinon and the more potent diazoxon were shown to induce DNA fragmentation in mature sperm cells (SalazarArredondo et al. 2008). Diazinon toxicity is often veried by urine tests for the metabolites or other biological monitoring procedures such as peripheral esterase enzyme activities. The potential for genotoxicity of diazinon and its metabolites was demonstrated in an in vitro study involving blood cells of agricultural students. Genetic changes, such as increased sister chromatid exchanges, were observed in blood cells exposed to diazinon (Hatjian et al. 2000). High immunotoxicity was observed by reduced phagocytic index, stimulation index of lymphocytes and spleen n-Pe rez et al. 2007). Renal weights in sh acutely exposed to this pesticide (Giro toxicity was recently observed in a study of rats exposed to diazinon. The activities of the renal phase II metabolizing enzymes, glutathione-S-transferase, and quinine reductase activities decreased consistently, whereas blood urea nitrogen and serum creatinine levels increased with increasing doses of administered diazinon (Shah and Iqbal 2010). Given known environmental and human toxicity of diazinon, a number of standards exist. The maximum residue limits for diazinon designated by the United Nations through the FAO/WHO and maintained in the Codex Alimentarius range from 0.01 mg/kg, in foods such as walnuts and potatoes, to 5 mg/kg in almond hulls (FAO/WHO 2010). WHO currently has no drinking water standards for diazinon, having listed this chemical as unlikely to occur in drinking water (WHO 2008). The sale of diazinon for residential purposes has been banned in the US since 31 December 2004 (USEPA 2011). The USEPA has not established maximum contaminant levels for diazinon in drinking water. Tolerances for pesticides in the US range from 0.1 ppm, in foods such as potatoes, to 0.75 ppm in fruits and vegetables such as turnips and tomatoes (USEPA-OPP 2010). There was no toxicity information for diazinon in the Integrated Risk Information System. Respective intermediate oral and inhalational MRLs of 0.002 mg/kg/day and 0.01 mg/m3 as well as acute and chronic oral MRLs of 0.0006 mg/kg/day and 0.0007 mg/kg/day, respectively, are proposed by the ATSDR (2008). The IARC has not classied diazinon in terms of carcinogenicity. Diazinon is manufactured in Jamaica as an emulsiable concentrate. Its use is restricted to agricultural purposes on crops such as carrot, cabbage, beans, cucumber, pepper, mango, and ornamental plants. The PCA classies diazinon as a Class II toxicant. In the absence of local environmental and food standards, Jamaica uses international standards in the regulation of this chemical.

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3.4. 3.4.1.

Diuron Overview

Diuron, N-(3,4-dichlorophenyl)-N,N-dimethyl-urea, is a herbicide (Giacomazzi and Cochet 2004). Synonyms for diuron include Diurex, Duran, Drexel, Karmex, Dailon, Herbatox, Kelvar, among others. It exhibits a relatively low Henry law constant, 5E 7 5 Pa m3/mol (Giacomazzi and Cochet 2004) and is more likely to be removed by wet or dry deposition. With an aqueous solubility of 42 mg/L and a high Kow of 102.6 (Giacomazzi and Cochet 2004), diuron is moderately soluble in water and exhibits a greater anity for sediments or soil particles. Half-lives vary from 1 to

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12 months, with degradation predominantly achieved by microbes (Gooddy et al. 2002). Also, spontaneous chemical degradation may occur forming 3,4-dichloroaniline (Salvestrini et al. 2004). Common formulations of diuron include wettable powders and suspension concentrates (Gooddy et al. 2002). Diuron is among the most frequently used herbicide in agricultural practices. It is often used on cotton, sugar cane, wheat, and fruits to control a variety of broadleaf and grassy weed (Gooddy et al. 2002). However, the prevailing usage is in non-crop areas such as along railways. Current usages also include the addition to antifouling paints, enhancing their plant growth retardation properties (Lamoree et al. 2002). However, diuse contamination of water bodies by herbicides occurs from agricultural sources (Siber et al. 2009). The use of herbicides has increased since World War II and they are the most frequently applied pesticides in agriculture (Freemark and Boutin 1995). Global sales of herbicides are higher than other pesticides (Jones 2005). Classication of herbicides is a function of operation modes, chemical properties, or the resultant symptoms induced (Jones 2005). Some herbicides may interfere with the light processing of target plants, whereas others restrict metabolism, nutrient transport, or the growth of plant cells. The dierential features of plants allow for the selective nature of herbicides (Moore et al. 2007). Herbicides are broadly classied by the associated photosystem which they inhibit. There are two distinct photosystem mechanisms in plants Photosystem I and Photosystem II. These are complex chains of protein structures, within the thylakoid membrane of chloroplasts, that contain pigment and cofactor properties necessary for the ecient capture of light for photosynthesis (Borodich et al. 2003; Busch and Hippler 2011). The two photosystems occupy dierent sites in the membrane and absorb dierent light frequencies, subsequently storing the absorbed energy in dierent chemical forms (Borodich et al. 2003). Photosystem II is the more temperature sensitive (Morgan-Kiss et al. 2002). Diuron is a Photosystem II herbicide. Not only does diuron inhibit Photosystem II but it also prevents oxygen production, a product of photosynthesis. 3.4.2. Toxic eects

Given its persistence and large quantities used, concerns regarding ecological impacts exist (Salvestrini et al. 2004). In the aquatic environment, diuron does not readily biodegrade (Romero et al. 2010). Many studies have reported detectable levels of diuron in the aquatic environment (Thomas et al. 2001; Okamura et al. 2003; McMahon et al. 2005; Pesce et al. 2006; Sheikh et al. 2009). The potential impact on shes and other aquatic creatures is vast. Diuron inhibits the photosynthesis of phytoplankton by reducing the dissolved oxygen, nitrogenous waste, and diminishing zooplankton population. Fishes and other aquatic creatures consequently experience toxicity and death (Perschbacher and Ludwig 2004). There have also been concerns that levels of diuron in the waters of the Great Barrier Reef may potentially cause ecological harm to the reef (Lewis et al. 2009). Diuron inhibits the photosynthesis of coral larvae, thereby aecting the adult population. Diuron and its metabolites, 3,4-dichlorophenyl and 3,4-dichloroaniline, are potentially toxic to humans, aquatic, and other creatures (Fernandes et al. 2007; Romero et al. 2010). It has been linked to spinal deformation in pink snapper shes (Gagnon and Rawson 2009). The potential for neurotoxicity was demonstrated when

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diuron was found to inhibit AChE in exposed shes (Bretaud et al. 2000). Female rats mated with male rats exposed to 125 mg/kg/day for 30 consecutive days exhibited signicantly lower fetal counts and weights than control groups (Fernandes et al. 2007). High concentrations of diuron were also associated with cell necrosis of the urothelial cells of rats (Nascimento et al. 2006). The USEPA has developed an oral reference dose for diuron of 2E 7 3 mg/kg/day (USEPA IRIS 2010). However, the condence in the reference dose is listed as low. The USEPA has not completed evaluations into the carcinogenicity of this chemical. Inhalation reference concentrations are also unavailable. However, under the 2005 guidelines, the USEPA classied diuron as Group L likely to be carcinogenic and recommended a cancer health advisory (HA) of 0.2 mg/L (for a 1074 risk). One-day and 10-day HAs for water quality for a 10-kg child were both 1 mg/L. The USEPA does not list diuron as a hazardous air pollutant. Tolerances in foods range from 0.05 to 7.0 ppm. The ATSDR has not set MRLs for this chemical. Diuron is listed under CERCLA as well as under the European Union Water Framework Directives List as a hazardous substance. 4. Conclusion

Endosulfan, diazinon, and dichlorvos exhibit the potential for adverse human and ecological eects. The unmonitored use of these pesticides in Jamaica is cause for concern. On the other hand, the amount of diuron imported is indicative of extensive use. Given the limited ecological and health impact data, it is necessary to monitor environmental concentrations of diuron. Once adequate monitoring of these pesticides have been implemented, informative impact assessments may be performed which would guide the generation of policies and standards specic to the country. However, monitoring and assessments are achievable given appropriate tools such as fate and transport models developed specically for these chemicals in Jamaica. The accuracy of fate and transport models is greatly improved by using the appropriate physicochemical properties. However, such properties are dynamic and depend on the given climatic conditions under which the chemicals are used. The study by Singh et al. (1999) determined the half-lives during volatilization, photolysis, and hydrolysis for both a- and b-endosulfan under tropical conditions, similar to that experienced in Jamaica. However such studies have yet to be conducted for diuron, dichlorvos, and diazinon. Also, there is limited data on environmental partitioning under tropical conditions. Once such analyses have been completed and the properties under tropical conditions determined, the developed fate and transport models can be improved and will be more ecient in reducing the potential for health impacts in Jamaica. References
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