The problem of Genericville City about mosquitoes does not just involve health but also economy. Since the city is highly dependent on summer tourism, mosquitoes and diseases that they carry could adversely affect their source of income. It endangers not only lives of the residents and the tourists but also non-human inhabitants of the place. A particular disease, West Nile Virus, threatens to have significant number of incidence and fatalities this year. This is why a mosquito control program using Malathion as pesticide could be useful. However, long-term effects of the chemical are of question for the opponents of the pesticide application.
The ways of controlling mosquito population is divided into two, the chemical and non-chemical ways. According to United States Environmental Protection Agency [EPA] (2007), the first step that governments usually take is surveillance of larval habitats and diseases acquired. For non-chemical approach, the goal is to prevent breeding of mosquitoes, done through eliminating small breeding sites, controlling water levels in potential breeding sites and having fishes that feed on larvae. The chemical method involves the use of pesticides. EPA (2007) elaborates that the pesticide may be larvacides like bacteria, growth inhibitor, oils and films, killing the larva before turning to adult mosquito; or an adulticide, killing mosquitoes in adult form by spraying, one of which is malathion.
Malathion is an organophosphate insecticide (EPA, 2006) that is not naturally occurring, thus, exists in the environment only when manufactured or used (Agency for Toxic Substances and Disease Registry [ATSDR], 2005). Through ultra-low volume (ULV) spray, which uses about 2.5 fluid ounces of active ingredient per acre, fine aerosol droplets get in contact with and kill adult mosquitoes with minimum exposure (St. Charles County Government, 2007).
Exposure to malathion usually occurs through oral, dermal and inhalation routes. This chemical is a cholinesterase inhibitor, at the lowest doses tested in chronic studies, that targets the nervous system (EPA, 2006, pp 8). When it is transformed through indirect photolysis (ATSDR, 2005), or chlorination in water treatment (EPA, 2006, pp 20), it could break down into a more potent cholinesterase inhibitor, malaoxon. According to Pluth et al. (1996), two studies using mammals showed results that malathion causes gene mutation, one involving rats proved it has teratogenic effects, and in humans had genotoxic effects. However, the EPA (2006, pp 8) reports that the available evidence in the literature and studies do not support the supposed mutagenic effects of malathion. Carcinogenic effect is still not certain, but several studies provide evidence that exposure to excessive doses may cause occurrence of tumors. So, the Agency classified it as a suggestive carcinogen (EPA, 2006, pp 15). Acute/short-term effects mentioned are eye and dermal irritation, but malathion still has low acute toxicity. However, ATSDR (2005) holds that overexposure to large amounts of the chemical could cause difficulty breathing, chest tightness, vomiting, cramps, diarrhea, watery eyes, blurred vision, salivation, sweating, headaches, dizziness, loss of consciousness, and death. But when provided with proper treatment immediately, no long-term negative effects could be avoided.
For non-targets, depending on species and habitat, the effect ranges from below level of concern to very high toxicity (EPA, 2007, pp 48-54). Mammals and birds have the lowest risk quotient while freshwater fishes and insects have the highest.
Since the use of malathion is for mosquito control, exposure that is more likely to occur would be non-dietary; incidental oral, dermal and inhalation. According to EPA (2006, pp 11-12), short- and intermediate-term exposure of general population to the chemical needs about 127mg/kg/day to produce more or less 20% effect level in terms of cholinesterase inhibition. Calculated and determined benchmark doses for different populations having different levels of concern, uncertainty and safety factors are presented, showing that no observed adverse effect level for inhalation in children is 25.8mg/kg/day while lowest observed adverse effect level for the same condition is 115mg/kg/day.
Residential exposure to malathion may be through residue in the food and drinking water, and post-application exposure in dry grounds where malathion is not easily broken down. Through ultra-low volume spray using non-volatile oils, spray drift and human exposure is lessened. This method uses 260g/hectare in aerial application, which causes exposure far from that causing adverse effect in the laboratory tests, and is applied either early morning or at night with the information passed to the residents (Pest Management and Regulatory Agency, 2003). But EPA still requires a certain amount of time to pass before people go out to the site of application, especially to farmers in the fields (ATSDR, 2005). When absorbed by the body, malathion exit through urine after a few days.
Non-target animals could also be exposed through their habitat and food (EPA, 2007, pp 48-54). Water-dwelling animals get exposed to malathion if they are in contaminated body of water. This makes their exposure greater because they are in contact with the chemical. Birds and mammals usually absorb malathion through ingestion of residues in plants. These could occur through spray drift or water runoff.
From the dose-response and exposure assessment, infants and children have the highest risk to be affected by malathion. Having lower weight compared to adults, they need lower exposure to be affected (EPA, 2005). But having greater exposure, the handler also has increased risk. As for the non-target animals, the greatest risk is on the freshwater fishes and invertebrates.
From the risk assessment, the pesticide application using malathion seem to have enough safeguards to minimize human exposure. However, the sacrifice would be passed to non-target animals that are at risk with malathion. In the situation of Genericville, decision on the manner of mosquito control must not only consider human residents but also other creatures that make their place attractive to tourists. It can even cause problems if surrounding cities are against the use of pesticides because there is a chance that some amount, how little it may be, could be transported to them. The fact that the known metabolite of malathion is more toxic makes the idea of pursuing pesticide use more harmful so the vote goes to the opponents of the project.
Agency for Toxic Substances and Disease Registry. (2005). Toxicologic Profile for Malathion (CAS Number 121-75-5). Retrieved May 30, 2008 from http://www.atsdr.cdc.gov/toxprofiles/phs154.html
Agency for Toxic Substances and Disease Registry. Potential for human exposure. Retrieved May 30, 2008 from http://www.atsdr.cdc.gov/toxprofiles/tp154-c6.pdf
Pest Management and Regulatory Agency (2003). Fact sheet on the use of Malathion in mosquito control programs. Retrieved May 30, 2008 from http://www.pmra-arla.gc.ca/english/pdf/fact/fs_malathion-e.pdf
Pluth, J. Nicklas, J. O’Neill, P. Albertini, R. (1996). Increased Frequency of Specific Genomic Deletions Resulting from Malathion Exposure. Cancer Research, 65:2393-2399 as cited in Malathion-what is it? Retrieved May 30, 2008 from http://www.ncchem.com/malathion.htm
St Charles County Government Department of Community Health and the Environment. (2007). Malathion and Mosquito control. Retrieved May 30, 2008 from http://www.scchealth.org/docs/ph/ph_docs/pdfs/malathion_052907.pdf
United States Environmental Protection Agency. (2007). Methods of mosquito control. Retrieved May 30, 2008 from http://www.epa.gov/opp00001/health/mosquitoes/mosquito.htm
United States Environmental Protection Agency. (2006). Reregistration Eligibility Decision (RED) for Malathion. (EPA 738-R-06-030). Retrieved May 30, 2008 from http://www.epa.gov/pesticides/reregistration/REDs/malathion_red.pdf