II. Food Hazards

Pesticide Regulation

The trace quantities of pesticides and their breakdown products that are present in food are called residues. Residue levels reflect the amount of pesticide applied to a crop, the time that has elapsed since application, and the rate of pesticide dissipation and evaporation. Most Americans consume pesticide residues regularly, so in order to protect Americans against dietary pesticides and their potentially harmful effects, the U.S. Congress has enacted legislation to regulate residue exposures. The Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) of 1996 provided federal control of pesticide distribution, sale, and use. Under FIFRA, the U.S. Environmental Protection Agency (EPA) was given authority to study the consequences of pesticide usage as well as to require pesticide users to register when purchasing pesticides. Pesticide users must take exams for certification as applicators of pesticides and all pesticides used in the U.S. must be registered by EPA. In addition to being registered, all pesticides must be granted a tolerance concentration, defined under the Federal Food, Drug, and Cosmetic Act (FFDCA) as the maximum quantity of a pesticide residue allowable on a raw agricultural commodity (RAC) (FFDCA, Section 408, http://www.fda.gov/opacom/laws/fdcact/fdcact4.htm) and in processed food when the pesticide has concentrated during processing (FFDCA, Section 409). Before a pesticide can be legally sold, EPA registration of the pesticide and approval of a label with detailed instructions for its use are required.

As mandated by the Food Quality Protection Act (FQPA), by August 3, 2006, EPA was required to review the safety of all existing tolerances that were in effect as of August 1996.

This act amended FIFRA and FFDCA by requiring EPA to consider the cumulative effects of chemicals with a common mechanism of toxicity (i.e. organophosphates) in its tolerance reassessment decisions. To meet the requirements of FQPA, EPA developed methodologies for conducting cumulative risk assessments. On July 31st, 2006, the Office of Pesticide Programs (OPP) published Organophosphate Cumulative Risk Assessment- 2006 Update. This assessment reported a reduction in the uncertainty factors for several organophosphates (OPs), stating that the “evaluation of the total risk from exposure to organophosphates (OPs) in foods indicated that the cumulative margin of exposures (MOEs) of 107 and 99 for children 1-2 years old and 3-5 years old, respectively, from exposure to OPs in foods do not raise a concern with respect to the 21 day rolling average period where the target MOE is 100” (U.S. EPA, 2006). Additionally, “for the 24-hour single MOEs, cumulative MOEs of 30 and 34 for children 1-2 years old and 3-5 years old, respectively, from exposure to OPs in foods do not raise a concern since the single day exposures assessment is compared to hazard endpoints based on steady state exposures which are 2-11-fold smaller (ie, more protective) than those for single day toxicity studies” (U.S. EPA, 2006). The Pesticide Action Network North America (PANNA), responded to the assessment, claiming that “uncertainty factors selected by EPA are not protective of the population, especially children, that important residential exposure pathways (especially inhalation) were not considered and that highly exposed farm children and farm worker children were not considered” (PANNA, 2006).

When attempting to reduce the risk of pesticide-related health issues, the fact that profound differences exist between children and adults must be taken into account. Infants and children are growing and developing and they have more rapid metabolic rates than adults. There are differences in their ability to activate, detoxify, and excrete xenobiotic compounds. Children also eat more food per body mass than adults and their diets are often rich in foods containing higher levels of pesticide residues, such as juices, fresh fruits, and fresh vegetables. All these differences can affect the toxicity of pesticides in infants and children differently than research completed solely on adults would suggest. The National Research Council’s (NRC) report Pesticides in the Diets of Infants and Children stated that dietary intake represents the major source of pesticide exposure in infants and children. The following is a compilation of some of the research on the effects of pesticide exposure in adults as well as in infants and children.

Pesticides (Organophosphates)

Pesticides are widely used in conventional agriculture in the United States in order to increase crop yields. There are more than 130 different classes of synthetic pesticides (Magkos et al., 2006). One of the most common families of pesticide is the organophosphate pesticides, including dimethyl alkyl phosphate which is an adulticide used to kill adult mosquitoes, malathion which is used as a treatment for head lice, body lice and scabies, and chlorpyrifos which is used as a termiticide; mosquitocide; a treatment for lawns, turf and ornamentals; an indoor crack and crevice and spot treatment; as a pet collar; as a treatment for pasture, woodland and lots/farmsteads; and as a cattle eartag (U.S. EPA). Their use has increased the quantity of fresh fruits and vegetables in the American diet, but not without environmental and potentially, health costs. Pesticides can enter the food chain by various paths, including consumption, agricultural application drift for those living on or near treated croplands, occupational exposure and tracking pesticide-laden dust into the home on shoes and clothes, contaminated groundwater, and household and garden use (Zahm & Ward, 1998).

Organophosphates inhibit the enzyme acetylcholinesterase, which destroys acetylcholine, a neurotransmitter that activates cholinergic neurons. Cholinergic neurons control signals in the peripheral nervous system, brain and spinal cord. When acetylcholine is not inactivated, it overstimulates the nervous system causing nausea, dizziness, confusion, and at high exposures, respiratory paralysis, and death (Colborn, 2006). Developmental neurotoxicity is also a concern, as indicated by continuously expanding literature illustrating the scope of non-cholinergic neurotoxic effects (PANNA, 2006). Dietary consumption being one of the most universal routes of organophosphate exposure is also one of the most scientifically controversial. The question still remains as to whether the level of consumption of pesticides poses a significant threat to human health. What has been shown to be true is that (1) acute, massive exposure to pesticides can cause significant adverse health effects; (2) food products have occasionally been contaminated with pesticides, which can result in toxicity; and (3) most, if not all, commercially purchased food contains trace amounts of agricultural pesticides (Magkos et al., 2006). Some scientists report that pesticide exposure is associated with increased risk for cancer, acute and chronic injury to the nervous system, lung damage, reproductive dysfunction, brain and nervous system disturbances, and possibly dysfunction of the endocrine and immune systems (NRC, 1993).

In a 2003 study, Curl et al. assessed organophosphorous pesticide exposure from diet by collecting 24-hour urine samples of preschool children (2-5 years old) who consumed conventional (n=21) or organic diets (n=18), as determined by parent-kept food diaries. Residential pesticide use was recorded for each home as well. The urine samples showed significantly lower concentrations of total dimethyl alkyl phosphate metabolites in the urine of children with organic diets than those with conventional diets. In addition, dose estimates were generated from pesticide metabolite data and suggested that organic diets can reduce children’s exposure levels from above to below the EPA’s chronic reference doses. This would shift exposures from a range of uncertain risk to a range of negligible risk.

Three years later, through urinary biomonitoring, Lu et al. (2006) measured dietary organophosphorous exposure in a group of 23 elementary school-age children. The children’s conventional diets were substituted with organic diets for 5 consecutive days during the 15-day study. For the 15 days, parents collected urine samples from their child’s first morning voids and last voids before bedtime. The urine samples showed that the median urinary concentrations of metabolites for malathion and chlorpyrifos decreased to nondetectable levels immediately after the introduction of organic diets, and remained undetectable until the conventional diets began again. The authors concluded that “an organic diet provide a dramatic and immediate protective effect against exposure to organophosphorous pesticides that are commonly used in agricultural production” (Lu, 2006).

Researchers at the Columbia Center for Children’s Environmental Health evaluated the effects of prenatal insecticide exposures among African American and Dominican women from minority communities in New York City, whose insecticide use as a population appears to be particularly high. Chlorpyrifos, diazinon, and propoxur were detected in 99.7-100% of 48-hour personal air samples collected from the mothers during pregnancy (n=394) and in 39-70% of blood samples collected from the mothers (N=326) and/or newborns (n=341) at delivery. The study also found an association between adverse growth outcomes in children exposed to organophosphate pesticides in utero before the 2000-2001 U.S. Environmental Protection Agency’s regulatory actions to phase out residential use of chlorpyrifos and diazinon (Whyatt et al., 2005). For those children born before 1/1/01, birth weight decreased by 67.3g and birth length decreased by 0.43cm for each unit increase in log-transformed cord plasma chlorpyrifos levels. Combined levels of log-transformed cord plasma chlorpyrifos and diazinon levels were also inversely associated with birth weight and length. For those with the highest exposures, birth weight averaged 215.1g less compared to those without detectable levels. These results are consistent with experimental evidence in laboratory animals, which has shown a link between chlorpyrifos and diazinon exposure during pregnancy and reduced fetal growth (U.S. EPA, 2001).

Neurodevelopmental disorders, unlike most obvious structural defects, cannot be seen at birth or sometimes even later in life. Since they are usually expressed in behavior and function, they are difficult to quantify. Therefore, there is a great deal of uncertainty about the neurodevelopmental affects of pesticides. Studies suggest a link between neurodevelopment impairment and exposure to 2 pesticides (fumigant phosphine and herbicide glyphosate) during gestation (Garry et al., 2002), between a reduction in newborn head circumference and maternal T3, 5, 6-trichloro-2-pyridinol (TCP) concentration above the detection limit (Berkowitz et al., 2004) and between increasing numbers of abnormal reflexes in infants between 3-62 days of age and total concentration of maternal urine organophosphate metabolites (Young et al., 2005).

The International Agency for Research on Cancer (IARC) considers the “spraying and application of non-arsenical insecticides” to be probably carcinogenic to humans. Residential insecticide exposure has been associated with a variety of childhood cancers, including lymphoma, brain tumors, neuroblastoma, Wilm’s tumor, Ewing’s sarcoma and acute leukemia (Menegaux et al., 2006). Menegaux et al. found that home insecticide use, garden insecticide use and insecticide use for pediculosis were associated with childhood acute leukemia.

The reproductive health of both men (Jensen et al., 2006) and women have been shown to be disrupted by pesticide exposure. In 1977 agricultural workers and workers in a dibromochloropropane (DBCP) pesticide factory in California were found to be infertile. Many of the workers who handled DBCP experienced azoospermia and oligospermia, damage of germinal epithelium, genetic alterations in the sperm, reduced fertility to increased risk of spontaneous abortions among wives (Jensen et al., 2006). These findings were duplicated in other DBCP production plants. Women also experience negative reproductive effects when exposed to pesticides, such as spontaneous abortions, congenital defects, pre-maturity, infertility and delay in conception (Figa-Talamanca, 2006).

Nitrates

One of the major differences in the production of organically produced food from conventional techniques is its reliance on natural methods of providing soil nutrients, such as nitrogen from nitrates. Organic agriculture gets the majority of its nitrates from manure and compost sources, which have a slower transfer of nitrogen to the soil than synthetic fertilizers. Since the release of nitrogen is spread out over the growing season, the leaching of nitrates into water sources where they can cause health problems is reduced (Wikipedia). Kramer et al. (2006) found that the use of organic fertilizers in Washington apple orchards significantly reduced nitrate leaching and enhanced denitrifier activity and efficiency. These results are theoretically achievable in other crops since the microbial processes in the orchards operate in other soil systems. There is also a concern about the nitrate content of the agriculture itself. The Soil Association of England reviewed 16 studies comparing the nitrate contents of organically and non-organically grown fruit and vegetables for nitrate content. Their review revealed that 14 studies demonstrated a trend toward significantly lower nitrate contents in organically grown crops, 6–19 averaging around 50 percent lower, and two studies found inconsistent or not significant differences (Heaton 2001).

Nitrate occurs naturally in soil from nitrogen-fixing bacteria, decaying plants, and animal manure and synthetically from nitrogenous fertilizers and airborne nitrogen compounds emitted by industry and automobiles. Nitrate penetrates the soil and enters groundwater, which is the source for >50% of drinking water supplies, 96% of private water supplies and an estimated 39% of public water supplies (USGS, 1996a). Nitrate toxicity is related to the in vivo conversion of nitrate to nitrite, which can directly oxidize hemoglobin to methemoglobin, a form that is unable to bind oxygen (Manassaram, 2006).

The magnitude of the risk of nitrate to human health is unclear. Until recently nitrate was perceived to be a purely harmful dietary component, linked to gastric cancer and infantile methaemoglobinaemia, also known as blue baby syndrome (Heaton 2001). However, others claim that in the quantities normally occurring in food, nitrate becomes toxic only under conditions in which it is reduced to nitrite and at reasonable concentrations nitrate is rapidly excreted in the urine (Heaton 2001). Some studies have suggested an association between exposure to nitrate in drinking water and spontaneous abortions, intrauterine growth restriction and birth defects, however Manassaram et al. concluded that “the current literature does not provide sufficient evidence of a causal relationship between exposure to nitrates in water and adverse reproductive effects” (2006).

Microbials

There are concerns that organic production may lead to higher levels of pathogens in fresh produce due to the use of manure rather than chemical fertilizers and due to reduced processing. The evidence on this is mixed. To quote a review of the evidence as of 2006, “the bulk of available evidence from comparative studies shows no significant differences in the bacterial status of organically and conventionally grown cereal (wheat, rye) and vegetable (carrots, spring mix, Swiss chard, salad vegetables) crops.” However, “although no meaningful conclusions can be drawn from just a few studies, it is clear that organic produce is not immune to contamination incidents” (Magkos et al. 2006).