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Chefbest. “The Advantages and Disadvantages of Pesticides | ChefsBest.” Food Marketing Awards | ChefsBest | Home : ChefsBest, 25 Aug. 2016, www.chefsbest.com/advantages-disadvantages-pesticides/.

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Esperanca. “Food Deserts and Their Impact on Community Health.” Esperança, 20 July 2021, esperanca.org/food-deserts-and-their-impact-on-community-health/.

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npic.orst.edu/health/food.html#:~:text=Pesticides%20allow%20growers%20to%20increase.”

It gives information on why pesticides are good and bad

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A tiered approach to prioritizing registered pesticides for potential cancer hazard evaluations: implications for decision making - PubMed

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Our scoping report provides a map of the existing literature on real-world exposures and human cancer that has accumulated on pesticides classified as potential carcinogens by USEPA and used in high volumes. We also illustrate that several pesticides which are “data-rich” may warrant updated authori…

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Section:

FEATURE SWEET CONFUSION

When chemists Richard Marshall and Earl Kooi started fiddling with -starch, the powder made from the dense insides of corn kernels, their intention was to turn glucose, which is easily produced from the starch, into fructose, which is sweeter. The idea wasn't that far-fetched. The two sugar molecules are cousins, both made from the same atomic parts slightly rearranged.

The duo's experiment, which took place at the Corn Projects Refining Company in Argo, I11., was a success. Marshall and Kooi discovered that the bacterium Aeromonas hydrophila produced an enzyme that could reconfigure the components of glucose from corn like so many Lego blocks. It was the first leap forward for a food industry dream: a mass-produced glucose- fructose-blend sweetener that would free commercial food manufacturers from the historical volatility of cane sugar crops.

The scientists announced their triumph in a short report in Science in 1957. There the discovery sat in quiet obscurity for almost two decades, until a worldwide spike in sugar prices sent manufacturers scrambling. By the end of the 1980s, high fructose corn syrup had replaced cane sugar in soft drinks, and it soon became popular among makers of baked goods, dairy products, sauces and other foods.

Few consumers seemed to care until 2004, when Barry Popkin, a nutrition scientist at the University of North Carolina at Chapel Hill, along with George Bray, at the Pennington Biomedical Research Center in Baton Rouge, La., published a commentary in the American Journal of Clinical Nutrition pointing out that the country's obesity crisis appeared to rise in tandem with the embrace of high fructose corn syrup by food producers. That shift began in the early 1970s -- just about the time Japanese researchers, who had noted Marshall and Kooi's experiment with keen interest, overcame the technical hurdles of industrial production.

What he didn't anticipate was the birth of blogging, which catapulted his theory across the digital universe.

Much of what has emerged since then has kept bloggers well supplied and turned high fructose corn syrup into a dietary boogeyman. Excessive fructose is cited as an accomplice in the twin epidemics of obesity and diabetes, and among the constellation of risk factors (including abdominal fat, high blood pressure and elevated triglycerides) that produce the dangerous condition known as metabolic syndrome. Further damaging are studies suggesting that once in the body, fructose is more likely to take up residence as fat around the belly and less likely to engage the appetite-control mechanisms that help put the brakes on eating. The story gets worse: In addition to the consequences for American waistlines, data also point to unique threats to the kidneys, liver and other organs.

Yet some caution that public opinion has gotten ahead of science and that fructose tunnel vision may distract us from the complex causes of the country's obesity crisis. Having a corn-based bad guy in the crosshairs has been an advertising boon for the sugar industry, Popkin says. The phrase on food labels that says "made with natural sugar" is popularly interpreted as "healthier," as is "no high fructose corn syrup." In truth, the consumption of high fructose corn syrup has been falling since 2004. Yet obesity rates remain high.

Perhaps chief among the concerns over fructose are its effects on the liver, which is the first stop after sugar leaves the intestine. The liver either absorbs sugar or allows it to pass into the bloodstream to be turned into energy for the brain, muscles and other organs. But it matters what kind of sugar it is. Table sugar, or sucrose, is abound dimer of glucose and fructose, which means the two sugar molecules are locked arm in arm until broken apart by the intestine. In high fructose corn syrup, fructose and glucose are not chemically bound. (The ratio of fructose to glucose depends on the type of corn syrup: the kind typically used in soda is 55 percent fructose and 42 percent glucose. Other types have more glucose and less fructose.) An enzyme called phosphorfructokinase acts as a kind of thermostat to detect whether the liver needs fuel. If it doesn't, glucose moves into the blood straightaway.

But fructose seeps into the liver whether or not the energy is needed. This is a major concern to scientists like Kimber Stanhope, a molecular biologist at the University of California, Davis. "The enzyme that controls fructose metabolism is fructose kinase," she says. "It appears to be almost always turned on." Unless you are energy depleted, really starved of calories that the rest of the body needs, "when you consume fructose, it all goes to the liver," says Robert Lustig, a pediatric endocrinologist at UC San Francisco who has become one of the most outspoken critics of added sugar, and especially of fructose. This flood of energy makes its way to the mitochondria, which are the power plants of a cell. "When your mitochondria get overloaded, the excess energy is turned into liver fat," Lustig says. In a paper this year in Advances in Nutrition, he characterized fructose as "alcohol without the buzz," because of its potential to cause liver damage.

In October 2012, writing in PLOS ONE, researchers from the University of Colorado Denver, with others, added another dimension to the story of fructose metabolism, describing evidence that in liver cells uric acid can accelerate the metabolism of fructose to fat. If the finding holds up in further work, it might help explain why some people appear more sensitive to the effects of fructose -- uric acid levels vary from person to person.

While individual studies can make a damning case against fructose, it's not so easy to reach a verdict when the evidence is considered as a whole, says John Sievenpiper, a nutrition researcher at St. Michael's Hospital in Toronto. People are not only consuming more calories from fructose, they are consuming more calories period. Weight gain alone poses serious health risks, Sievenpiper and others point out, regardless of where the extra calories come from.

Over the last few years, Sievenpiper has published several studies that compile the body of work on fructose into a sweeping analysis. This is the only way to get a true sense of the health effects, he contends, and the danger he's found so far is underwhelming. Although his recent fructose studies were funded by the Canadian government, Sievenpiper readily reveals that he has received unrestricted research grants from the beverage industry. Still, he says, "My frame of mind going in, to be honest with you, was that we were going to find a signal for harm because of the biochemistry."

That has not been the case. In February 2012, in the Annals of Internal Medicine, he and his coauthors tallied 41 human feeding studies that examine whether fructose is more likely to lead to weight gain than other forms of carbohydrates. The result: When people eat the same number of calories of any carbohydrate, "it doesn't look like the fructose is behaving differently," he says. But when volunteers consume more energy from fructose than they burn, the sugar does appear to cause weight gain. If s hard to tell, however, whether that's because of the fructose or just the overabundance of calories, Sievenpiper says.

Other researchers point out that many experiments finding reason for concern about fructose have been conducted in animals. Or studies compare intake of pure glucose and pure fructose, neither of which is what's in a soda bottle. "If fructose is really causing a problem, demonstrate it in physiological or real-world diets," says John White, a former corn industry researcher who is now a consultant. He says he would like to see a study that examines high fructose corn syrup the way most people consume it. "Do that experiment, and publish it, and prove to us that it's a problem," White says. He also points out that the graph published by Popkin and Bray, when plotted today, does not show the correlation it did in 2004. " High fructose corn syrup has been in decline now for 14 years," White says. "Whaf s happened to obesity rates? They've continued to climb."

Fructose could pose a particular harm -- but not for everyone at the same dose, says Miriam Vos, a pediatric liver specialist at Emory University School of Medicine. Just as certain people are more susceptible, probably because of genetics, to the effects of salt on blood pressure or tobacco on cancer risk, some may be more sensitive to the biochemical complications of fructose. Last year in the Journal of Clinical Endocrinology and Metabolism, Vos reported that fructose raised triglyceride levels in teenagers with fatty liver disease more than in healthy teens, even when they consumed the same number of calories. "My impression is that fructose alone would not cause fatty liver disease in someone who is not susceptible," she says.

The focus on fructose has been scientifically beneficial, but Vos worries that one unintended consequence has been to make other sweeteners look good by comparison. Sucrose and high fructose corn syrup are both made of glucose and fructose. "From a public health standpoint, it may be less important which half of the sugar is causing the problem, because first of all, maybe it's both together, and then second of all, maybe the real question is, what's a safe dose? Not which half is safer," she says. "Because no one is going to advocate for a pure glucose drink."

G. Bray and B. Popkin. Calorie-sweetened beverages and fructose: what we have learned 10 years later. Pediatric Obesity. 2013.

Brain

Unlike glucose, fructose only weakly curbs the brain's hunger signals that control appetite.

Liver

When fructose is consumed, some always ends up in the liver, where it may be packaged for short-term storage as glycogen, or for long-term storage as fat. It may promote fatty liver disease.

Kidney

Fructose that seeps into the liver may increase uric acid, a risk factor for kidney disease.

Heart

Fructose-sweetened drinks can raise triglyceride levels, a risk factor in heart disease.

Abdomen

Fructose is more likely to take up residence as fat around the abdomen.

Pancreas

Fructose can lead to insulin resistance, which taxes the pancreas to pump out more insulin and ups diabetes risk.

Bloodstream

Triglycerides circulating in the blood can harm the heart and liver.

GRAPH: Looking for a link For decades obesity in American adults over 20 was on the rise along with consumption of HFCS, high fructose corn syrup. But in the last decade, consumption has dropped while obesity has not.

DIAGRAM: Where it begins The starch component of the corn kernel yields glucose, which is processed into fructose.

DIAGRAM: Effects Of fructose

PHOTO (COLOR)

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By Laura Beil

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Sweet confusion: Does high fructose corn syrup deserve such a bad rap?

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Section: FEATURE SWEET CONFUSION When chemists Richard Marshall and Earl Kooi started fiddling with -starch, the powder made from the dense insides of corn kernels, their intention was to turn glucose, which is easily produced from the starch, into fructose, which is sweeter. The idea wasn't that far-fetched.

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What is pesticides
EPA.gov

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Gossett, D.R. “Pesticides and Herbicides (environmental impact).” Pingsso.ebscohost.com, 2023, discovery.ebsco.com/c/nkxeyc/viewer/html/cdxlmkpokb. Accessed 8 May 2023.

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Gossett, D. R. “Pesticides and herbicides (environmental impact).” 2023

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Robbins, Ocean. “Pesticides in Food: What You Should Know and Why It Matters.” Food Revolution Network, 20 Sept. 2019, foodrevolution.org/blog/pesticides-facts/.

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Food deserts are residential areas with poor access to affordable, healthy food. Most families understand the importance of eating nutritious foods like fruits and vegetables and avoiding processed foods like chips and fast food. When you live in a food desert, however, this can be hard to do.

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Robbins, Ocean. “Pesticides in Food: What You Should Know and Why It Matters.” Food Revolution Network, 20 Sept. 2019, foodrevolution.org/blog/pesticides-facts/.

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US EPA. “Food and Pesticides | US EPA.” US EPA, 7 Mar. 2018, www.epa.gov/safepestcontrol/food-and-pesticides.

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For all pesticides to be effective against the pests they are intended to control, they must be biologically active, or toxic.

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“Food Safety.” Npic.orst.edu, npic.orst.edu/health/food.html#:~:text=Pesticides%20are%20commonly%20used%20on.

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Pimentel, David, et al. “Environmental and Economic Costs of Pesticide Use.” BioScience, vol. 42, no. 10, 1992, pp. 750–760, www.jstor.org/stable/pdf/1311994.pdf?casa_token=zHt13o2GVaEAAAAA:A_dDncrfUcUKlsQf4M_odletWoLFYEgHULIFkBZuxyKCRDdBECqxgTx5WzsODv8b514PaQ3j-iW5iSniUNHnqpkRHa3CSwGEE7audTXW3g_PcpiK0Nw, https://doi.org/10.2307/1311994. Accessed 13 Nov. 2020.

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Loecher, Barbara. “Beyond 🤬.” Prevention, vol. 55, no. 3, 1 Mar. 2003, p. 126, web.p.ebscohost.com/ehost/detail/detail?vid=19&sid=4692b3ed-2d91-465e-b11e-e9202cac0b53%40redis&bdata=JkF1dGhUeXBlPWNvb2tpZSxzaGliLHNzbyx1cmwsdWlkLGNsZXZlciZhdXRodHlwZT1zaGliJnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#AN=9075928&db=hxh. Accessed 11 May 2023.

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“Why We Use Pesticides.” US EPA, 21 Feb. 2013, www.epa.gov/safepestcontrol/why-we-use-pesticides#:~:text=Pesticides%20are%20used%20to%20control.

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Introduction

The term pesticide covers a wide range of compounds including insecticides, fungicides, herbicides, rodenticides, molluscicides, nematicides, plant growth regulators and others. Among these, organochlorine (OC) insecticides, used successfully in controlling a number of diseases, such as malaria and typhus, were banned or restricted after the 1960s in most of the technologically advanced countries. The introduction of other synthetic insecticides - organophosphate (OP) insecticides in the 1960s, carbamates in 1970s and pyrethroids in 1980s and the introduction of herbicides and fungicides in the 1970s-1980s contributed greatly to pest control and agricultural output. Ideally a pesticide must be lethal to the targeted pests, but not to non-target species, including man. Unfortunately, this is not the case, so the controversy of use and abuse of pesticides has surfaced. The rampant use of these chemicals, under the adage, "if little is good, a lot more will be better" has played havoc with human and other life forms.

Production and usage of pesticides in India

The production of pesticides started in India in 1952 with the establishment of a plant for the production of BHC near Calcutta, and India is now the second largest manufacturer of pesticides in Asia after China and ranks twelfth globally (Mathur, 1999). There has been a steady growth in the production of technical grade pesticides in India, from 5,000 metric tons in 1958 to 102,240 metric tons in 1998. In 1996-97 the demand for pesticides in terms of value was estimated to be around Rs. 22 billion (USD 0.5 billion), which is about 2% of the total world market.

The pattern of pesticide usage in India is different from that for the world in general. As can be seen in , in India 76% of the pesticide used is insecticide, as against 44% globally (Mathur, 1999). The use of herbicides and fungicides is correspondingly less heavy. The main use of pesticides in India is for cotton crops (45%), followed by paddy and wheat.

Hazards of pesticides

Direct impact on humans

If the credits of pesticides include enhanced economic potential in terms of increased production of food and fibre, and amelioration of vector-borne diseases, then their debits have resulted in serious health implications to man and his environment. There is now overwhelming evidence that some of these chemicals do pose a potential risk to humans and other life forms and unwanted side effects to the environment (Forget, 1993; Igbedioh, 1991; Jeyaratnam, 1981). No segment of the population is completely protected against exposure to pesticides and the potentially serious health effects, though a disproportionate burden, is shouldered by the people of developing countries and by high risk groups in each country (WHO, 1990). The world-wide deaths and chronic diseases due to pesticide poisoning number about 1 million per year (Environews Forum, 1999).

The high risk groups exposed to pesticides include production workers, formulators, sprayers, mixers, loaders and agricultural farm workers. During manufacture and formulation, the possibility of hazards may be higher because the processes involved are not risk free. In industrial settings, workers are at increased risk since they handle various toxic chemicals including pesticides, raw materials, toxic solvents and inert carriers.

OC compounds could pollute the tissues of virtually every life form on the earth, the air, the lakes and the oceans, the fishes that live in them and the birds that feed on the fishes (Hurley et al., 1998). The US National Academy of Sciences stated that the DDT metabolite DDE causes eggshell thinning and that the bald eagle population in the United States declined primarily because of exposure to DDT and its metabolites (Liroff, 2000). Certain environmental chemicals, including pesticides termed as endocrine disruptors, are known to elicit their adverse effects by mimicking or antagonising natural hormones in the body and it has been postulated that their long-term, low-dose exposure is increasingly linked to human health effects such as immune suppression, hormone disruption, diminished intelligence, reproductive abnormalities and cancer (Brouwer et al., 1999; Crisp et al., 1998; Hurley et al., 1998)

A study on workers (N=356) in four units manufacturing HCH in India revealed neurological symptoms (21%) which were related to the intensity of exposure (Nigam et al., 1993). The magnitude of the toxicity risk involved in the spraying of methomyl, a carbamate insecticide, in field conditions was assessed by the National Institute of Occupational Health (NIOH) (Saiyed et al., 1992). Significant changes were noticed in the ECG, the serum LDH levels, and cholinesterase (ChE) activities in the spraymen, indicating cardiotoxic effects of methomyl. Observations confined to health surveillance in male formulators engaged in production of dust and liquid formulations of various pesticides (malathion, methyl parathion, DDT and lindane) in industrial settings of the unorganised sector revealed a high occurrence of generalised symptoms (headache, nausea, vomiting, fatigue, irritation of skin and eyes) besides psychological, neurological, cardiorespiratory and gastrointestinal symptoms coupled with low plasma ChE activity (Gupta et al., 1984).

Data on reproductive toxicity were collected from 1,106 couples when the males were associated with the spraying of pesticides (OC, OP and carbamates) in cotton fields (Rupa et al., 1991).A study in malaria spraymen was initiated to evaluate the effects of a short-term (16 week) exposure in workers (N=216) spraying HCH in field conditions (Gupta et al., 1982).

A study on those affected in the Seveso diaster of 1976 in Italy during the production of 2,4,5 T, a herbicide, concluded that chloracne (nearly 200 cases with a definite exposure dependence) was the only effect established with certainty as a result of dioxin formation (Pier et al., 1998). Early health investigations including liver function, immune function, neurologic impairment, and reproductive effects yielded inconclusive results. An excess mortality from cardiovascular and respiratory diseases was uncovered, possibly related to the psychosocial consequences of the accident in addition to the chemical contamination. An excess of diabetes cases was also found. Results of cancer incidence and mortality follow-up showed an increased occurrence of cancer of the gastrointestinal sites and of the lymphatic and haematopoietic tissue. Results cannot be viewed as conclusive, however, because of various limitations: few individual exposure data, short latency period, and small population size for certain cancer types. A similar study in 2001 observed no increase in all-cause and all-cancer mortality. However, the results support the notion that dioxin is carcinogenic to humans and corroborate the hypotheses of its association with cardiovascular- and endocrine-related effects (Pier et al., 2001). During the Vietnam War, United States military forces sprayed nearly 19 million gallons of herbicide on approximately 3.6 million acres of Vietnamese and Laotian land to remove forest cover, destroy crops, and clear vegetation from the perimeters of US bases. This effort, known as Operation Ranch Hand, lasted from 1962 to 1971. Various herbicide formulations were used, but most were mixtures of the phenoxy herbicides 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Approximately 3 million Americans served in the armed forces in Vietnam during the Vietnam War. Some of them (as well as some Vietnamese combatants and civilians, and members of the armed forces of other nations) were exposed to defoliant mixtures, including Agent Orange. There was evidence on cancer risk of Vietnam veterans, workers occupationally exposed to herbicides or dioxins (since dioxins contaminated the herbicide mixtures used in Vietnam), and of the Vietnamese population (Frumkin, 2003).

Impact through food commodities

For determining the extent of pesticide contamination in the food stuffs, programs entitled 'Monitoring of Pesticide Residues in Products of Plant Origin in the European Union' started to be established in the European Union since 1996. In 1996, seven pesticides (acephate, chlopyriphos, chlopyriphos-methyl, methamidophos, iprodione, procymidone and chlorothalonil) and two groups of pesticides (benomyl group and maneb group, i.e. dithiocarbamates) were analysed in apples, tomatoes, lettuce, strawberries and grapes. An average of about 9 700 samples has been analysed for each pesticide or pesticide group. For each pesticide or pesticide group, 5.2% of the samples were found to contain residues and 0.31% had residues higher than the respective MRL for that specific pesticide. Lettuce was the crop with the highest number of positive results, with residue levels exceeding the MRLs more frequently than in any of the other crops investigated. The highest value found in 1996 was for a compound of the maneb group in lettuce which corresponded to a mancozeb residue of 118 mg/kg. In 1997, 13 pesticides (acephate, carbendazin, chlorothalonil, chlopyriphos, DDT, diazinon, endosulfan, methamidophos, iprodione, metalaxyl, methidathion, thiabendazole, triazophos) were assessed in five commodities (mandarins, pears, bananas,beans, and potatoes). Some 6 000 samples were analysed. Residues of chlorpyriphos exceeded MRLs most often (0.24%), followed by methamidophos (0.18%), and iprodione (0.13%). With regard to the commodities investigated, around 34% contained pesticide residues at or below the MRL, and 1% contained residues at levels above the MRL. In mandarins, pesticide residues were most frequently found at levels at or below the MRL (69%), followed by bananas (51%), pears (28%), beans (21%) and potatoes (9%). MRLs were exceeded most often in beans (1.9%), followed by mandarins (1.8%), pears (1.3%), and bananas and potatoes (0.5%). Estimation of the dietary intake of pesticide residues (based on the 90th percentile) from the above-mentioned commodities, where the highest residue levels of the respective pesticides were found, shows that there is no exceeding of the ADI with all the pesticides and commodities studied (European Commission, 1999). In 1998, four commodities (oranges, peaches, carrots, spinach) were analysed for 20 pesticides (acephate, benomyl group, chlopyriphos, chlopyriphos-methyl, deltamethrin, maneb group, diazinon, endosulfan, methamidophos, iprodione, metalaxyl, methidathion, thiabendazole, triazophos, permethrin, vinclozolin, lambdacyalothrin, pirimiphos-methyl, mercabam). With regard to all four commodities investigated in 1998 (oranges, peaches, carrots, spinach), about 32% contained residues of pesticides at or below MRL, and 2% above the MRL (1.8% for EU-MRLs, 0.4% for national MRLs). Residues at or below the MRL were found most often in oranges (67%), followed by peaches (21%), carrots (11%) and spinach (5%). MRL values were exceeded most often in spinach (7.3%), followed by peaches (1.6%), carrots (1.2%)and oranges (0.7%). The intake of pesticide residues has not exceeded the ADI in any case. It was found to be below 10% of the ADI for all pesticides. The exposure ranges from 0.35% of the ADI for the benomyl group to 9.9% of the ADI for the methidathion group. In 1999, four commodities (cauliflower, peppers, wheat grains, and melon) were analysed for the same 20 pesticides as in the 1998 study (European Commission, 2001). Overall, around 4700 samples were analysed. Residues of methamidophos exceeded MRLs most often (8.7%), followed by the maneb group (1.1%), thiabendazole (0.57%), acephate (0.41%) and the benomyl group (0.35%). The MRL for methamidophos was exceeded most often in peppers and melons (18.7 and 3.7%, respectively). The residues of the maneb group exceeded the MRL most often in cauliflower (3.9%); residues of thiabendazole exceeded the MRL most often in melons (2.8% of the melon samples). With regard to all the commodities investigated, around 22% of samples contained residues of pesticides at or below the MRL and 8.7% above the MRL. Residues at or below MRL were found most often in melons (32%), followed by peppers (24%), wheat grains (21%) and cauliflower (17%). MRL values were exceeded most often in peppers (19%), followed by melons (6.1%), cauliflower (3%) and wheat grains (0.5%). The intake of pesticide residues did not exceed the ADI in any case. It was below 1.5% of the ADI for all pesticides. The exposure ranged between 0.43% of the ADI for methamidophos and 1.4% of the ADI for endosulfan. The intakes for the highest residue levels in a composite sample for chlorpyriphos, deltamethrin, endosulfan and methidathion were below the ARfD for adults. They range between 1.5% of the ARfD for deltamethrin and 67% of the ARfD for endosulfan (Nasreddine and Parent-Massin, 2002). In spite of food contamination, most pesticide deaths recorded in hospital surveys are the result of self-poisoning (Eddleston, 2000). The Global Burden of Disease Study 6 estimated that 798 000 people died from deliberate self-harm in 1990, over 75% of whom were from developing countries (Murray and Lopez, 1996). More recent WHO estimates showed that over 500 000 people died from self-harm in Southeast Asia and the Western Pacific during 2000 alone (WHO, 2001). Suicide is the commonest cause of death in young Chinese women and Sri Lankan men and women (Murray and Lopez, 1996; Sri Lankan Ministry of Health, 1995; WHO, 2001).

In India the first report of poisoning due to pesticides was from Kerala in 1958, where over 100 people died after consuming wheat flour contaminated with parathion (Karunakaran, 1958). This prompted the Special Committee on Harmful Effects of Pesticides constituted by the ICAR to focus attention on the problem (Report of the Special Committee of ICAR, 1972). In a multi-centric study to assess the pesticide residues in selected food commodities collected from different states of the country (Surveillance of Food Contaminants in India, 1993), DDT residues were found in about 82% of the 2205 samples of bovine milk collected from 12 states. About 37% of the samples contained DDT residues above the tolerance limit of 0.05 mg/kg (whole milk basis). The highest level of DDT residues found was 2.2 mg/kg. The proportion of the samples with residues above the tolerance limit was highest in Maharastra (74%), followed by Gujarat (70%), Andhra Pradesh (57%), Himachal Pradesh (56%), and Punjab (51%). In the remaining states, this proportion was less than 10%. Data on 186 samples of 20 commercial brands of infants formulae showed the presence of residues of DDT and HCH isomers in about 70 and 94% of the samples with their maximum level of 4.3 and 5.7 mg/kg (fat basis) respectively. Measurement of chemicals in the total diet provides the best estimates of human exposure and of the potential risk. The risk of consumers may then be evaluated by comparison with toxicologically acceptable intake levels. The average total DDT and BHC consumed by an adult were 19.24 mg/day and 77.15 mg/day respectively (Kashyap et al., 1994). Fatty food was the main source of these contaminants. In another study, the average daily intake of HCH and DDT by Indians was reported to be 115 and 48 mg per person respectively, which were higher than those observed in most of the developed countries (Kannan et al., 1992).

Impact on environment

Pesticides can contaminate soil, water, turf, and other vegetation. In addition to killing insects or weeds, pesticides can be toxic to a host of other organisms including birds, fish, beneficial insects, and non-target plants. Insecticides are generally the most acutely toxic class of pesticides, but herbicides can also pose risks to non-target organisms.

Surface water contamination

Pesticides can reach surface water through runoff from treated plants and soil. Contamination of water by pesticides is widespread. The results of a comprehensive set of studies done by the U.S. Geological Survey (USGS) on major river basins across the country in the early to mid- 90s yielded startling results. More than 90 percent of water and fish samples from all streams contained one, or more often, several pesticides (Kole et al; 2001). Pesticides were found in all samples from major rivers with mixed agricultural and urban land use influences and 99 percent of samples of urban streams (Bortleson and Davis, 1987-1995). The USGS also found that concentrations of insecticides in urban streams commonly exceeded guidelines for protection of aquatic life (U.S. Geological Survey, 1999). Twenty-three pesticides were detected in waterways in the Puget Sound Basin, including 17 herbicides. According to USGS, more pesticides were detected in urban streams than in agricultural streams (US Department of the Interior, 1995). The herbicides 2,4-D, diuron, and prometon, and the insecticides chlorpyrifos and diazinon, all commonly used by urban homeowners and school districts, were among the 21 pesticides detected most often in surface and ground water across the nation (U.S. Geological Survey, 1998). Trifluralin and 2,4-D were found in water samples collected in 19 out of the 20 river basins studied (Bevans et al., 1998; Fenelon et al., 1998; Levings et al., 1998; Wall et al., 1998). The USGS also found that concentrations of insecticides in urban streams commonly exceeded guidelines for protection of aquatic life (U.S. Geological Survey, 1999). According to USGS, "in general more pesticides were detected in urban streams than in agricultural streams", (Bortleson and Davis, 1987-1995). The herbicide 2,4-D was the most commonly found pesticide, detected in 12 out of 13 streams. The insecticide diazinon, and the weed-killers dichlobenil, diuron, triclopyr, and glyphosate were detected also in Puget Sound basin streams. Both diazinon and diuron were found at levels exceeding concentrations recommended by the National Academy of Sciences for the protection of aquatic life (Bortleson and Davis, 1987-1995).

Ground water contamination

Groundwater pollution due to pesticides is a worldwide problem. According to the USGS, at least 143 different pesticides and 21 transformation products have been found in ground water, including pesticides from every major chemical class. Over the past two decades, detections have been found in the ground water of more than 43 states (Waskom, 1994). During one survey in India, 58% of drinking water samples drawn from various hand pumps and wells around Bhopal were contaminated with Organo Chlorine pesticides above the EPA standards (Kole and Bagchi, 1995). Once ground water is polluted with toxic chemicals, it may take many years for the contamination to dissipate or be cleaned up. Cleanup may also be very costly and complex, if not impossible (Waskom 1994; O'Neil, 1998; US EPA, 2001).

Soil contamination

A large number of transformation products (TPs) from a wide range of pesticides have been documented (Barcelo' and Hennion, 1997; Roberts, 1998; Roberts and Hutson, 1999). Not many of all possible pesticide TPs have been monitored in soil, showing that there is a pressing need for more studies in this field. Persistency and movement of these pesticides and their TPs are determined by some parameters, such as water solubility, soil-sorption constant (K oc), the octanol/water partition coefficient (K ow), and half-life in soil (DT ₅₀). Pesticides and TPs could be grouped into:(a) Hydrophobic, persistent, and bioaccumulable pesticides that are strongly bound to soil. Pesticides that exhibit such behavior include the organochlorine DDT, endosulfan, endrin, heptachlor, lindane and their TPs. Most of them are now banned in agriculture but their residues are still present. (b) Polar pesticides are represented mainly by herbicides but they include also carbamates, fungicides and some organophosphorus insecticide TPs. They can be moved from soil by runoff and leaching, thereby constituting a problem for the supply of drinking water to the population. The most researched pesticide TPs in soil are undoubtedly those from herbicides. Several metabolic pathways have been suggested, involving transformation through hydrolysis, methylation, and ring cleavage that produce several toxic phenolic compounds. The pesticides and their TPs are retained by soils to different degrees, depending on the interactions between soil and pesticide properties. The most influential soil characteristic is the organic matter content. The larger the organic matter content, the greater the adsorption of pesticides and TPs. The capacity of the soil to hold positively charged ions in an exchangeable form is important with paraquat and other pesticides that are positively charged. Strong mineral acid is required for extracting these chemicals, without any analytical improvement or study reported in recent years. Soil pH is also of some importance. Adsorption increases with decreasing soil pH for ionizable pesticides (e.g. 2,4-D,2,4,5-T, picloram, and atrazine) (Andreu and Pico', 2004).

Effect on soil fertility (beneficial soil microorganisms)

Heavy treatment of soil with pesticides can cause populations of beneficial soil microorganisms to decline. According to the soil scientist Dr. Elaine Ingham, "If we lose both bacteria and fungi, then the soil degrades. Overuse of chemical fertilizers and pesticides have effects on the soil organisms that are similar to human overuse of antibiotics. Indiscriminate use of chemicals might work for a few years, but after awhile, there aren't enough beneficial soil organisms to hold onto the nutrients" (Savonen, 1997). For example, plants depend on a variety of soil microorganisms to transform atmospheric nitrogen into nitrates, which plants can use. Common landscape herbicides disrupt this process: triclopyr inhibits soil bacteria that transform ammonia into nitrite (Pell et al., 1998); glyphosate reduces the growth and activity of free-living nitrogen-fixing bacteria in soil (Santos and Flores, 1995) and 2,4-D reduces nitrogen fixation by the bacteria that live on the roots of bean plants (Arias and Fabra, 1993; Fabra et al., 1997), reduces the growth and activity of nitrogen-fixing blue-green algae (Singh and Singh, 1989; Tözüm-Çalgan and Sivaci-Güner, 1993), and inhibits the transformation of ammonia into nitrates by soil bacteria (Frankenberger et al., 1991, Martens and Bremner, 1993). Mycorrhizal fungi grow with the roots of many plants and aid in nutrient uptake. These fungi can also be damaged by herbicides in the soil. One study found that oryzalin and trifluralin both inhibited the growth of certain species of mycorrhizal fungi (Kelley and South, 1978). Roundup has been shown to be toxic to mycorrhizal fungi in laboratory studies, and some damaging effects were seen at concentrations lower than those found in soil following typical applications (Chakravarty and Sidhu, 1987; Estok et al., 1989). Triclopyr was also found to be toxic to several species of mycorrhizal fungi (Chakravarty and Sidhu, 1987) and oxadiazon reduced the number of mycorrhizal fungal spores (Moorman, 1989).

Contamination of air, soil, and non-target vegetation

Pesticide sprays can directly hit non-target vegetation, or can drift or volatilize from the treated area and contaminate air, soil, and non-target plants. Some pesticide drift occurs during every application, even from ground equipment (Glotfelty and Schomburg, 1989). Drift can account for a loss of 2 to 25% of the chemical being applied, which can spread over a distance of a few yards to several hundred miles. As much as 80-90% of an applied pesticide can be volatilised within a few days of application (Majewski, 1995). Despite the fact that only limited research has been done on the topic, studies consistently find pesticide residues in air. According to the USGS, pesticides have been detected in the atmosphere in all sampled areas of the USA (Savonen, 1997). Nearly every pesticide investigated has been detected in rain, air, fog, or snow across the nation at different times of the year (U.S. Geological Survey, 1999). Many pesticides have been detected in air at more than half the sites sampled nationwide. Herbicides are designed to kill plants, so it is not surprising that they can injure or kill desirable species if they are applied directly to such plants, or if they drift or volatilise onto them. Many ester-formulation herbicides have been shown to volatilise off treated plants with vapors sufficient to cause severe damage to other plants (Straathoff, 1986). In addition to killing non-target plants outright, pesticide exposure can cause sublethal effects on plants. Phenoxy herbicides, including 2,4-D, can injure nearby trees and shrubs if they drift or volatilise onto leaves (Dreistadt et al., 1994). Exposure to the herbicide glyphosate can severely reduce seed quality (Locke et al., 1995). It can also increase the susceptibility of certain plants to disease (Brammall and Higgins, 1998). This poses a special threat to endangered plant species. The U.S. Fish and Wildlife Service has recognized 74 endangered plants that may be threatened by glyphosate alone (U.S. EPA Office of Pesticides and Toxic Substances, 1986). Exposure to the herbicide clopyralid can reduce yields in potato plants (Lucas and Lobb, 1987). EPA calculated that volatilisation of only 1% of applied clopyralid is enough to damage non-target plants (US EPA, 1990). Some insecticides and fungicides can also damage plants (Dreistadt et al., 1994). Pesticide damage to plants is commonly reported to state agencies in the Northwest. (Oregon Dept. of Agriculture, 1999; Washington Dept. of Health, 1999). Plants can also suffer indirect consequences of pesticide applications when harm is done to soil microorganisms and beneficial insects. Pesticides including those of new the generation, e.g., dacthal, chlorothalonil, chlorpyrifos, metolachlor, terbufos and trifluralin have been detected in Arctic environmental samples (air, fog, water, snow) (Rice and Cherniak, 1997), and (Garbarino et al., 2002). Other studies have identified the ability of some of these compounds to undergo short-range atmospheric transport (Muir et al., 2004) to ecologically sensitive regions such as the Chesapeake Bay and the Sierra Nevada mountains (LeNoir et al., 1999; McConnell et al., 1997; Harman-Fetcho et al., 2000, Thurman and Cromwell , 2000). One long-term study that investigated pesticides in the atmosphere of British Columbia (BC), dating from 1996 (Belzer et al., 1998) showed that 57 chemicals were investigated at two sampling sites (Agassiz and Abbotsford) in the Fraser Valley, from February 1996 until March 1997. Atrazine, malathion, and diazinon, highly toxic chemicals identified as high-priority pesticides by Verrin et al. (2004), were detected as early as the end of February (72 pg/m ³) until mid-October (253 pg/m ³), with a peak concentration in mid-June of 42.7 ngm −3. Dichlorvos is a decomposition product of another pesticide, Naled (Dibrom) (Hall et al., 1997). Captan and 2,4-D showed the highest concentrations and deposition rates at these two sites, followed by dichlorvos and diazinon (Dosman and Cockcraft, 1989). Air concentrations of currently used pesticides in Alberta were investigated in 1999 at four sampling sites that were chosen according to geography and pesticide sales data (Kumar, 2001). Triallate and trifluralin were the two mostly detected pesticides at the four sites. Insecticides (malathion, chlorpyrifos, diazinon and endosulfan) were detected intermittently with concentrations in the range 20-780 pg/m ³. South of Regina, Saskatchewan, in 1989 and 1990, 2,4-D reached 3.9 and 3.6 ng/m ³ at the end of June (Waite et al., 2002a). Triallate, dicamba, bromoxynil concentrations were also higher in 1989 (peak concentration of 4.2 ng/m ³ in mid-June) compared with 1990 (600-700 pg/m ³ in mid-June). In a more recent study, Waite et al. (2005) studied spatial variations of selected herbicides on a threesite, 500km transect that included two agricultural sites-Bratt's Lake, located 35 km southwest of Regina and Hafford to the North-and a background site at Waskesiu. Some acid herbicides were also investigated in South Tobacco Creek, Manitoba during 1993-1996. Once again, maximum concentrations occurred during periods of local use (Rawn et al., 1999a). A neutral herbicide, atrazine, was also investigated in 1995 (Rawn et al., 1998). It was first detected in mid-April, peaked mid- June at about 300 pg/m ³, and was detected until the end of October. The insecticide dacthal was identified throughout the sampling periods in 1994, 1995 and 1996 (Rawn and Muir, 1999) even though it was not used in this area (<20-300 pg/m ³).

Non-target organisms

Pesticides are found as common contaminants in soil, air, water and on non-target organisms in our urban landscapes. Once there, they can harm plants and animals ranging from beneficial soil microorganisms and insects, non-target plants, fish, birds, and other wildlife. Chlorpyrifos, a common contaminant of urban streams (U.S. Geological Survey, 1999), is highly toxic to fish, and has caused fish, kills in waterways near treated fields or buildings (US EPA, 2000). Herbicides can also be toxic to fish. According to the EPA, studies show that trifluralin, an active ingredient in the weed-killer Snapshot, "is highly to very highly toxic to both cold and warm water fish" (U.S. EPA, 1996). In a series of different tests it was also shown to cause vertebral deformities in fish (Koyama, 1996). The weed-killers Ronstar and Roundup are also acutely toxic to fish (Folmar et al., 1979; Shafiei and Costa, 1990). The toxicity of Roundup is likely due to the high toxicity of one of the inert ingredients of the product (Folmar et al., 1979). In addition to direct acute toxicity, some herbicides may produce sublethal effects on fish that lessen their chances for survival and threaten the population as a whole. Glyphosate or glyphosate-containing products can cause sublethal effects such as erratic swimming and labored breathing, which increase the fish's chance of being eaten (Liong et al., 1988). 2,4-D herbicides caused physiological stress responses in sockeye salmon (McBride et al., 1981) and reduced the food-gathering abilities of rainbow trout (Little, 1990). Several cases of pesticide poisoning of dolphins have been reported worldwide. Because of their high trophic level in the food chain and relatively low activities of drug-metabolising enzymes, aquatic mammals such as dolphins accumulate increased concentrations of persistent organic pollutants (Tanabe et al., 1988) and are thereby vulnerable to toxic effects from contaminant exposures. Dolphins inhabiting riverine and estuarine ecosystems are particularly vulnerable to the activities of humans because of the restricted confines of their habitat, which is in close proximity to point sources of pollution. River dolphins are among the world's most seriously endangered species. Populations of river dolphins have been dwindling and face the threat of extinction; the Yangtze river dolphin (Lipotes vexillifer) in China and the Indus river dolphin (Platanista minor) in Pakistan are already close to extinction (Renjun, 1990; Perrin et al., 1989; Reeves et al., 1991; Reeves and Chaudhry, 1998). In addition to habitat degradation (such as construction of dams) (Reeves and Leatherwood, 1994), boat traffic, fishing, incidental and intentional killings, and chemical pollution have been threats to the health of river dolphins (Kannan et al., 1993b, 1994, 1997; Senthilkumar et al., 1999). Earlier studies reported concentrations of heavy metals (Kannan et al., 1993), organochlorine pesticides and polychlorinated biphenyls (PCBs) (Kannan et al., 1994), and butyltin compounds (Kannan et al., 1997) in Ganges river dolphins and their prey. The continuing use of organochlorine pesticides and PCBs in India is of concern (Kannan et al., 1992; Kannan et al., 1997a; Kannan et al., 1997b; Tanabe et al., 1998). The Ganges river basin is densely populated and heavily polluted by fertilizers, pesticides, and industrial and domestic effluents (Mohan, 1989). In addition to fish, other marine or freshwater animals are endangered by pesticide contamination. Exposure to great concentrations of persistent, bioaccumulative, and toxic contaminants such as DDT (1,1,1-trichloro-2,2-bis[ p-chlorophenyl]ethane) and PCBs has been shown to elicit adverse effects on reproductive and immunological functions in captive or wild aquatic mammals (Helle et al., 1976; Reijnders, 1986; Ross et al., 1995; Martineau et al., 1987; Kannan et al., 1993; Colborn and Smolen, 1996). Aquatic mammals inhabiting freshwater systems, such as otters and mink, have been reported to be sensitive to chemical contamination (Leonards et al., 1995; Leonards et al., 1997). 2,4-D or 2,4-D containing products have been shown to be harmful to shellfish (Cheney et al., 1997) and other aquatic species (U.S. EPA, 1989; Sanders, 1989) The weed-killer trifluralin is moderately to highly toxic to aquatic invertebrates, and highly toxic to estuarine and marine organisms like shrimp and mussels (U.S. EPA, 1996). Since herbicides are designed to kill plants, it makes sense that herbicide contamination of water could have devastating effects on aquatic plants. In one study, oxadiazon was found to severely reduce algae growth (Ambrosi et al., 1978). Algae is a staple organism in the food chain of aquatic ecosystems. Studies looking at the impacts of the herbicides atrazine and alachlor on algae and diatoms in streams showed that even at fairly low levels, the chemicals damaged cells, blocked photosynthesis, and stunted growth in varying ways (U.S. Water News Online, 2000). The herbicide oxadiazon is also toxic to bees, which are pollinators (Washington State Department of Transportation, 1993). Herbicides may hurt insects or spiders also indirectly when they destroy the foliage that these animals need for food and shelter. For example spider and carabid beetle populations declined when 2,4-D applications destroyed their natural habitat (Asteraki et al., 1992). Non-target birds may also be killed if they ingest poisoned grains set out as bait for pigeons and rodents (US EPA, 1998). Avitrol, a commonly used pigeon bait, poses a large potential for ingestion by non target grain feeding birds. It can be lethal to small seed-eating birds (Extoxnet, 1996). Brodifacoum, a common rodenticide, is highly toxic to birds. It also poses a secondary poisoning hazard to birds that may feed on poisoned rodents (US EPA, 1998). Herbicides can also be toxic to birds. Although trifluralin was considered "practically nontoxic to birds" in studies of acute toxicity, birds exposed multiple times to the herbicide experienced diminished reproductive success in the form of cracked eggs (U.S. EPA, 1996). Exposure of eggs to 2,4-D reduced successful hatching of chicken eggs (Duffard et al., 1981) and caused feminisation or sterility in pheasant chicks (Lutz et al., 1972). Herbicides can also adversely affect birds by destroying their habitat. Glyphosate treatment in clear cuts caused dramatic decreases in the populations of birds that lived there (MacKinnon et al., 1993) Effects of some organochlorines (OCs) on fish-eating water birds and marine mammals have been documented in North America and Europe (Barron et al., 1995; Cooke, 1979; Kubiak et al., 1989). Despite the continuing usage, little is known about the impacts of OCs in bird populations in developing countries. Among the countries that continue to use OCs, India has been one of the major producers and consumers in recent years. As a consequence, wild birds in India are exposed to great amounts of OC pesticides (Tanabe et al., 1998). Use of OCs in tropical countries may not only result in exposure of resident birds but also of migratory birds when they visit tropical regions in winter. The Indian sub-continent is a host to a multitude of birds from western Asia, Europe and Arctic Russia in winter(Woodcock, 1980). Hundreds of species of waterfowl, including wading birds such as plovers, terns and sandpipers, migrate each winter to India covering long distances (Grewal, 1990). While concentrations of OC pesticides in wholebody homogenates of birds have been reported elsewhere (Tanabe et al., 1998), concentrations of OCs in prey items and in eggs of Indian birds have not been reported.

A few studies related to the decline in the populations of bats in various parts of the world to OC exposure were also being conducted (Altenbach et al., 1979; Clark, 1976; Clark, 1983; Clark, 1981; Geluso et al., 1976; Jefferies, 1976; Thies and Mc Bee, 1994). The world population of bats was estimated to be 8.7 million during 1936 and it declined to approximately 200,000 in 1973 (Geluso et al., 1976) It has recovered slightly to an estimated number of 700,000 in 1991 (Geluso et al., 1976; Thies and Mc Bee, 1994). High tissue concentrations of p,p'-dichlorodiphenyldichloroethene ( p,p'-DDE) have been found in bats in Carlsbad Caverns in Mexico and in New Mexico in the USA (Geluso et al., 1976; Thies and Mc Bee, 1994). Occurrence of stillbirths in little brown bats exposed to high concentrations of PCBs, p,p'-DDE, and/or oxychlordane was documented (Clark, 1976; Jefferies, 1976). These observations indicate that bats can accumulate high concentrations of OCs and may be affected by their potential toxic effects. The flying fox or the new world fruit bat, short-nosed fruit bat and Indian pipistrelle bat are resident species and are very common in South India. Their habitat is mainly agricultural areas, rock caves, and abandoned houses in domesticated areas. Insects constitute an important diet for many bats, allowing the passage of OCs in their body (Mc Bee et al., 1992). Several studies found OC pesticides and PCBs in livers and eggs of birds in developed countries (Becker, 1989; Bernardz et al., 1990; Cade et al., 1989; Castillo et al., 1994; Mora, 1996; Mora, 1997). Similarly, several studies reported OCs in a variety of biota including humans and wildlife from India (Senthilkumar et al., 2000). However, no study has used whole body homogenates of birds, which is important to evaluate biomagnification features and body burdens of OCs (Mc Bee et al., 1992). Earlier studies used specific body tissues to estimate biomagnification of OCs. However theoretically, estimation of biomagnification factors requires whole body concentrations rather than specific tissue concentrations.

Conclusion

The data on environmental-cum-health risk assessment studies may be regarded as an aid towards a better understanding of the problem. Data on the occurrence of pesticide-related illnesses among defined populations in developing countries are scanty. Generation of base-line descriptive epidemiological data based on area profiles, development of intervention strategies designed to lower the incidence of acute poisoning and periodic surveillance studies on high risk groups are needed. Our efforts should include investigations of outbreaks and accidental exposure to pesticides, correlation studies, cohort analyses, prospective studies and randomised trials of intervention procedures. Valuable information can be collected by monitoring the end product of human exposure in the form of residue levels in body fluids and tissues of the general population. The importance of education and training of workers as a major vehicle to ensure a safe use of pesticides is being increasingly recognised.

Because of the extensive benefits which man accrues from pesticides, these chemicals provide the best opportunity to those who juggle with the risk-benefit equations. The economic impact of pesticides in non-target species (including humans) has been estimated at approximately $8 billion annually in developing countries. What is required is to weigh all the risks against the benefits to ensure a maximum margin of safety. The total cost-benefit picture from pesticide use differs appreciably between developed and developing countries. For developing countries it is imperative to use pesticides, as no one would prefer famine and communicable diseases like malaria. It may thus be expedient to accept a reasonable degree of risk. Our approach to the use of pesticides should be pragmatic. In other words, all activities concerning pesticides should be based on scientific judgement and not on commercial considerations. There are some inherent difficulties in fully evaluating the risks to human health due to pesticides. For example there is a large number of human variables such as age, sex, race, socio-economic status, diet, state of health, etc. - all of which affect human exposure to pesticides. But practically little is known about the effects of these variables. The long-term effects of low level exposure to one pesticide are greatly influenced by concomitant exposure to other pesticides as well as to pollutants present in air, water, food and drugs.

Pesticides are often considered a quick, easy, and inexpensive solution for controlling weeds and insect pests in urban landscapes. However, pesticide use comes at a significant cost. Pesticides have contaminated almost every part of our environment. Pesticide residues are found in soil and air, and in surface and ground water across the countries, and urban pesticide uses contribute to the problem. Pesticide contamination poses significant risks to the environment and non-target organisms ranging from beneficial soil microorganisms, to insects, plants, fish, and birds. Contrary to common misconceptions, even herbicides can cause harm to the environment. In fact, weed killers can be especially problematic because they are used in relatively large volumes. The best way to reduce pesticide contamination (and the harm it causes) in our environment is for all of us to do our part to use safer, non-chemical pest control (including weed control) methods.

The exercise of analysing the range and nature of benefits arising from pesticide use has been a mixture of delving, dreaming and distillation. There have been blind alleys, but also positive surprises. The general picture is as we suspected: there is publicity, ideological kudos and scientific opportunity associated with 'knocking' pesticides, while praising them brings accusations of vested interests. This is reflected in the imbalance in the number of published scientific papers, reports, newspaper articles and websites against and for pesticides. The colour coding for types of benefit, economic, social or environmental, reveals the fact that at community level, most of the benefits are social, with some compelling economic benefits. At national level, the benefits are principally economic, with some social benefits and one or two issues of environmental benefits. It is only at global level that the environmental benefits really come into play.

There is a need to convey the message that prevention of adverse health effects and promotion of health are profitable investments for employers and employees as a support to a sustainable development of economics. To sum up, based on our limited knowledge of direct and/or inferential information, the domain of pesticides illustrates a certain ambiguity in situations in which people are undergoing life-long exposure. There is thus every reason to develop health education packages based on knowledge, aptitude and practices and to disseminate them within the community in order to minimise human exposure to pesticides.

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Impact of pesticides use in agriculture: their benefits and hazards

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The term pesticide covers a wide range of compounds including insecticides, fungicides, herbicides, rodenticides, molluscicides, nematicides, plant growth regulators and others. Among these, organochlorine (OC) insecticides, used successfully in controlling a number of diseases, such as malaria and typhus, were banned or restricted after the 1960s in most of the technologically advanced countries.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7299236/

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Abstract

In this article, we discuss the most recent trends in food-retail access in low- and moderate-income communities in the United States of America. We begin with a review of the current literature on the number of people impacted by food deserts and then review several critical retail trends, including supercentres (such as Walmart), dollar stores, farmers markets and online food retail. We discuss the growing investment in incentive programmes, as well as new understandings of the impact of food deserts on health. In the United States of America, the number of communities without adequate access to healthy affordable food has declined, though more than 5.6 percent of the population still lives in low-access census tracts. At the same time, racial and economic disparities in food access remain a considerable concern, with around 30 percent more non-white residents facing limited access to food retail than white residents. We also provide recommendations for areas of future research.

INTRODUCTION

The Scottish Nutrition Task Force first coined the term "food desert" in 1995 ( Beaumont et al., 1995). Today, the term generally refers to a geographic area that lacks sufficient access to grocery stores, especially in low-income communities ( Shaw, 2006). While much of the food-desert concept remains grounded in a conceptualization of geographic proximity, whereby concern remains for those that live far from affordable access to healthy nutritious foods, recent policy efforts, changes in the retail industry and new research findings have prompted new considerations about how food deserts can or should be defined. These include a broader understanding for how food deserts impact the economic well-being of communities ( Richardson et al., 2017), how store quality influences access ( Hilmers et al., 2012), how supercentres and dollar stores influence shopping patterns, and how new technologies (including online ordering and home delivery) may help to alleviate gaps.

In 2009, the United States Department of Agriculture (USDA) began mapping food access to identify communities where there was low availability of affordable nutritious foods and found that food deserts exist in every American state, in all types of communities. It estimated that roughly 23 million people lived in 6 529 food-desert communities (USDA, 2012). The USDA's research elicited increased recognition of the vital role of people's environment in supporting health and reducing disparities ( Neff et al., 2009).

In the United States of America, national funds were allocated to address food-desert areas for the first time in 2011, following a series of city and state financing efforts, which began with the Pennsylvania Fresh Food Financing Initiative in 2004 ( Karpyn et al., 2010). To date, such public efforts have provided more than USD 220 million, which has leveraged more than USD 1 billion in private investment through public-private partnerships, to fund nearly 1 000 retailers serving areas of limited food access in 35 states ( PolicyLink, The Food Trust and The Reinvestment Fund, 2015).

HAS THE NUMBER OF RESIDENTS LIVING IN FOOD DESERTS CHANGED?

In its most recent 2017 report, the USDA's Economic Research Service determined that the number of census tracts that met the classification of "low access" had declined measurably since 2010, indicating a general improvement in the proximity of supermarkets to residents across the country ( Rhone et al., 2017). Specifically, the US saw a 15 percent decline in the number of individuals living in a limited-supermarket-access area. From 2010 to 2016, the share of the population living in limited-supermarket-access areas declined gradually, from 6.8 percent of the population to 5.6 percent ( Rhone et al., 2017).

However, because the number of low-income communities across the country had increased by more than 5 percent since 2010, the net number of low-income and low-access communities increased 0.36 percent ( Rhone et al., 2017). The overall increase in low-income areas in the United States of America - the cause of the net increase in low-income food deserts - raises concerns about the growing number of struggling households with limited access to affordable nutritious foods, and the ways in which disparities may expand in part as a result.

State by state, the greatest improvement in increasing food access, as denoted by the percentage decrease in limited-supermarket-access-area populations, was witnessed in North Dakota (41 percent), Idaho (41 percent), Iowa (40 percent), Rhode Island (38 percent), Wisconsin (36 percent), Alabama (35 percent), Kansas (35 percent), New York (34 percent), Arkansas (32 percent) and Indiana (32 percent). In contrast, several states have experienced a substantial worsening of the problem, including Maine (with an increase of 27 percent) and Nevada (with a rise of 26 percent) ( The Reinvestment Fund, 2018).

In addition to examining food access at state level, research has also considered food access at the census-tract level. Census tracts are relatively small geographical subdivisions of an area, defined for the purpose of collecting national census data. Depending on definitional parameters, estimates indicate that somewhere between 35.2 million and 83.5 million individuals (5.6 percent to 17.7 percent of the US population, respectively) reside in census tracts with limited access to a store ( Rhone, et al., 2017). Further, racial and economic disparities in food access persist across the country, with approximately 30 percent more non-white residents facing limited access to food retail than their white counterparts ( Rhone, et al., 2017). Rhode Island, for example, was home to more than 274 000 non-white residents as of 2018 (26 percent of the state's population), yet 60 percent of those living in food deserts were non-white ( The Reinvestment Fund, 2018).

NOTABLE TRENDS IN GROCERY RETAIL AND FOOD-DESERT COMMUNITIES

In 2011, as a team member of Michelle Obama's National Healthy Food Financing Initiative, Walmart announced that it would open between 275 and 300 stores to serve USDA-designated food-desert areas ( Walmart Inc., 2011). In the United States of America, USD 1 in every USD 3 grocery dollars is spent at Walmart ( Hauter, 2014), the country's largest food retailer. According to its 2019 annual report ( Walmart Inc., 2019), Walmart increased its revenue by 6.6 percent, from USD 482 billion in 2015 to USD 514 billion in 2019. It did so in part through store expansion, increasing its retail units by 5.6 percent between 2015 and 2019, including adding 4.8 percent more supercentres (to total 3 570 such stores), 27 percent more neighbourhood markets (now 813 stores) and 18 percent more discount stores (now 386 stores). While the net result has been expansion, stores have closed as well. From 2015 to 2019, Walmart closed a total of 223 stores in the United States of America, creating at least 3 new food deserts and another 31 neighbourhoods in 15 states that no longer sell fresh produce and meat ( CBS News, 2016).

Walmart entering a region can result in social concerns, including weakened union bargaining power, reduced wages and benefits, and decreased employment levels ( Neumark et al., 2008; Davis et al., 2009). Large supercentres also evoke considerable worry about the viability of local retail. For example, a report by Manhattan Borough President Scott Stringer showed that (a new) Walmart on 125th street in Harlem, New York would result in 25 percent of the nearby supermarkets and bodegas going out of business within a year ( CBS New York, 2011). Such concerns magnify the potential impact of superstore closings on communities.

At the same time, the nations' largest grocer has been a significant partner in several evidence-based health promotion and nutrition interventions. For example, in 2011, Walmart helped to lead a national effort to work with manufacturers to reformulate products to reduce sodium, added sugar and trans fats in frequently purchased and consumed foods without adding considerable cost for consumers ( Stolberg, 2011).

The dollar-store market, although a very different model from the supercentre, has also grown considerably in food-desert communities, prompting concerns. As of 2018, dollar-store chains (including Dollar Tree, Dollar General and Family Dollar, which was acquired by Dollar Tree in 2015) grew from roughly 18 000 locations in 2009 to more than 27 000, with plans to continue expanding to more than 50 000 ( Donahue, 2018). Like Walmart, dollar stores often serve food deserts, are rapidly expanding in rural and low-income communities, and have raised concerns in relation to their proclivity to decrease the profits of local grocers in the surrounding area, causing such stores to close ( Donahue, 2018).

Community advocates have noted worrying ripple effects on communities, as dollar-store chains employ fewer people on average than local grocery stores, rely more heavily on publicly subsidized health care for their employees and offer a limited selection of healthy foods ( Donahue, 2018). Dollar stores typically do not carry fresh produce and their selection of food is mostly processed ( Donahue, 2018). Furthermore, dollar-store chains often appeal to low-income customers by offering low sticker prices, though their per-unit prices are actually higher than the competition ( Hoium, 2012). Taken together, this suggests that dollar-store chains are contributing to growing economic and health disparities in rural and low-income communities across the United States of America.

Just when the physical landscape of the food desert is evolving in terms of the types of retailer sited in low-income and underserved areas, online food delivery is emerging and starting to realize its potential. While it remains unclear to what extent these types of solutions will effectively meet the needs of low-income residents, the recent merger between Amazon and Whole Foods has fuelled hope that online delivery will soon be able to reach customers whom to date have not had adequate access to healthy, affordable foods ( Karsten and West, 2017).

At the federal level, in April 2019, the USDA's Food and Nutrition Service, which administers the Supplemental Nutrition Assistance Program (SNAP), launched an online, two-year pilot programme in New York to test the use of SNAP benefits in online grocery shopping and delivery systems ( USDA, 2019). Specifically, Amazon and ShopRite (a full-service retailer) will be providing the service to the New York City area, while Walmart will provide online services in upstate New York locations ( USDA, 2019).

The novel approach responds to ongoing questions about how receptive low-income families are to online ordering, how feasible online ordering is for them (including access to technology and internet access for online orders) and the extent to which families will be able to pay for the delivery fee associated with the service using non-SNAP forms of payment. While promising, the extent to which food purchasing patterns will be altered in the New York pilot remains to be seen. It is unknown whether the programme will increase the sale of healthier foods among food-desert residents who are receiving food-assistance benefits and decrease sales of unhealthy items.

Farmers markets, defined as a location where two or more farmer-producers sell their own agricultural products (such as fruits, vegetables, meat, fish, poultry, dairy products and grains) directly to the general public at a fixed location ( USDA Agricultural Marketing Service, 2019), have also seen considerable growth in low-income areas and are proving a promising strategy for addressing food deserts. The number of US farms selling directly to consumers increased from 116 733 in 2002 to 144 530 in 2012 ( Low et al., 2015).

Farmers markets, in parallel with the number of farms selling directly to consumers, have witnessed substantial growth over the past 10 years, with more than 8 767 such markets in operation nationally as of 2018, up 200 percent from 2006 ( Low et al., 2015). Local farmers markets, in addition to providing locally grown food in low-income areas, have a positive job multiplier effect, with each full-time-equivalent job created at a farmers market supporting approximately half of another full-time-equivalent job in other sectors of the region's economy ( Low et al., 2015).

Evidence from the past 10 years shows a steady increase in SNAP-benefit use at farmers markets. In 2015, more than USD 19.4 million SNAP redemptions were honoured by farmers markets, compared with only USD 2.7 million in 2008 ( USDA Food and Nutrition Service, 2015). Despite increased farmers-market usage, however, lower-than-recommended fruit-and-vegetable consumption patterns persist among low-income residents ( Moore et al., 2015), while rates of diet-related chronic disease remain high ( National Center for Health Statistics, 2016). And while early data on the health and economic benefits of increased SNAP shopping at farmers markets suggest positive impacts on fruit and vegetable intake and body mass index, especially where additional financial incentives are available ( Dimitri et al., 2015), these studies remain limited in geography and research design (for example, no comparison group) ( Savoie-Roskos et al., 2016). Consequently, it is unclear whether the improved diet is a result of increased access alone, or whether it is mediated by the individual characteristics of the farmers-market shopper, who may be inherently more likely to purchase and consume healthier products.

HOW DO FOOD DESERTS IMPACT COMMUNITIES?

Food deserts and their consequences are far more complex than once thought ( Richardson et al., 2017). Research has evolved to support a growing understanding of the causes of food deserts and their economic impacts in terms of lost wages, reductions in the local tax base and lost potential for food retail to serve as an anchor institution for other retail development. The economic impacts of a new grocery store or retention of an existing, but struggling grocery store, reflect our growing understanding of the multi-faceted importance of employment and community on health and well-being (Horster et al., 2016; Hardcastle et al., 2015; Buro et al., 2015).

Research has further re-defined adequate store access beyond store counts to include measures of store quality, community acceptability, healthy and unhealthy food-marketing practices, product quality and affordability ( Adam and Jensen, 2016). In addition, new approaches to incentivizing healthy food have taken centre stage as a mechanism for helping low-income consumers ( Broers et al., 2017). New research has also emerged, which estimates that 9 percent of nutritional inequalities are attributable to food deserts ( Allcott et al., 2017). However, more recent conversations about the need to solve the food-desert problem emphasize the importance of both ensuring the fundamental human right to food and the economic value of community retail, and de-emphasize the role of food deserts as an obesity-prevention or obesity-reduction strategy, where connections are likely more distal ( Haspel, 2018).

Food insecurity is also closely tied to wellness, and to the availability of healthy food, disproportionately affecting those in low-income communities ( FAO, IFAD, UNICEF, WFP and WHO, 2018). Food insecurity, or a lack of secure access to sufficient amounts of safe and nutritious food for an active healthy life, and normal growth and development, is a result of limited food availability due to inadequate physical access to food (in other words, food deserts), limited economic access to food (namely, poverty, or high food costs), inadequate utilization (for example, lack of kitchen or household facilities for food preparation, or challenges in meeting the costs of living in a way that adequately addresses food needs), or a lack of stability in one's environment or income, further disrupting physical, economic or utilization capacity.

Inadequate access to affordable, nutritious food, particularly when combined with stress, anxiety or depression, disordered eating patterns and/or inadequate pre-natal and child nutrition, results in an inadequate diet and contributes to excess and/or insufficient nutritional quality. Consumption of calories, protein, vitamins or minerals and intake of sugar, salt and/or fat are often impacted, in terms of either excess consumption or inadequate consumption, or both. In turn, child stunting and wasting, micronutrient deficiencies and overweight and obesity result ( FAO, IFAD, UNICEF, WFP and WHO, 2018).

NEW UNDERSTANDINGS OF THE ECONOMIC POTENTIAL OF FOOD DESERTS

In spite of food deserts' negative attributes, there is increasing evidence that such areas offer significant economic potential. To date, food deserts have witnessed substantial grocery "leakage" due to unmet demand for food retail. For example, analysis in Newark, New Jersey showed that residents of low-income areas underserved by food retailers were travelling more than twice as far to full-service food-retail locations as residents of similar areas that were solidly middle income ( PolicyMap, 2018). Newark's low-income residents still need to purchase food - corresponding to retail demand of USD 24 million - but as these low-income families are underserved by food retail, their available food supply is only valued at about USD 6 million, meaning that almost USD 18 million of total retail food demand is leaking outside these low-income areas ( PolicyMap, 2018).

In addition to this untapped retail demand, food deserts offer potential to decrease unemployment rates among the formerly incarcerated. In the US, close to 700 000 persons are released from prison each year, many of whom are low income and in need of jobs ( SHRM, 2019). Supermarkets are one of a limited number of employers that will hire and train formerly incarcerated individuals ( Von Bergen, 2017). The US Congress and others have recognized the critical nature of such opportunities for families and recently passed the First Step Act (December 2018), which includes increased rehabilitation programming, among other things, to support former prisoners ( 115th US Congress, 2018).

PROVIDING FUNDING AND INCENTIVES FOR LOW-INCOME RESIDENTS TO PURCHASE HEALTHIER FOOD

Dating back to 1939, Congress began providing financial benefits to citizens needing assistance to purchase food to meet their nutritional needs in the form of a food-stamp programme ( USDA, 2018a). While the original programme ended in 1943, Congress restarted the provision of food assistance in 1961 and this has remained uninterrupted ( USDA, 2018a). Since 1973, food assistance has been authorized and funded by Congress as part of the Farm Bill ( Farm Policy Facts, n.d.). This legislation is typically revised and reauthorized every five to six years and is administered by USDA ( Snap to Health! 2018).

Relatively recent and noteworthy developments related to the provision of food assistance include the establishment of electronic benefits transfer (EBT) ( USDA, 2018a). Also, to reduce the stigma of receiving benefits and in recognition of those benefits as a significant source of nutrition, the programme was renamed the Supplemental Nutrition Assistance Program (SNAP) in 2008 ( USDA, 2018a). SNAP is the largest programme in the United States of America's hunger safety-net ( USDA, n.d.), providing nutrition assistance benefits to approximately 42.1 million Americans as of September 2017 ( Cronquist and Lauffer, 2019). Furthermore, the aforementioned online purchase programme for SNAP beneficiaries was launched in April 2019 ( USDA, 2019).

To help address disparities in food access and nutrition among low-income residents, a series of efforts have been made to provide financial discounts, or "bonus" dollars, for the purchase of healthy foods, often in conjunction with SNAP. Efforts to understand incentive programmes largely began in 2008 when that year's Farm Bill provisions for the SNAP programme committed USD 20 million to projects intended to incentivize recipients to increase their purchase of fruits and vegetables and other healthful foods at the point of sale ( Rosenbaum, 2008).

In 2011, a USD 4.4 million healthy-incentive pilot was the first attempt in this area of research to systematically study the impact of fruit and vegetable incentives on SNAP participants' purchase and consumption patterns ( Bartlett et al., 2014). Results showed that by instituting a 30 percent incentive within a retail setting for purchases of targeted fruits and vegetables, among a randomly selected sample of 7 500 SNAP participants, mean total fruit and vegetable intake increased by 0.32 cups per day compared with the control group ( Bartlett et al., 2014). Researchers reported an increase from 2.294 to 2.616 cups per day of all fruits and vegetables, including potatoes, legumes and 100 percent juice ( Bartlett et al., 2014). More recently, the USDA Food Insecurity Nutrition Incentive grant programme was established by the 2014 Farm Bill ( USDA, 2018b) and renewed in the 2018 Farm Bill, with more than USD 100 million to be dispensed over five years to support projects that utilize incentives (financial and non-financial) to increase the amount of fruit and vegetables purchased and consumed by SNAP participants.

CONCLUSIONS

Since the term's emergence in 1995, the nutrition field's understanding of how to address food deserts has evolved into a far more nuanced and complex web of considerations and, perhaps, we now have more questions than answers. Research to date shows that a new supermarket in a low-income neighbourhood is unlikely to have an effect on obesity reduction ( Adam and Jensen, 2016; Dubowitz et al., 2015a; Pechey and Monsivais, 2015); however that new supermarket will probably have an impact on community health and well-being, including economic benefits ( Adam and Jensen, 2016; Dubowitz et al., 2013; Dubowitz et al., 2015b; Aggarwal et al., 2014; Cannuscio et al., 2013). At the same time, online food retail is nascent and it remains unclear to what extent this new phenomenon will help food-desert residents to purchase healthy food, or perhaps perpetuate inequities by causing new store closings, reducing the number of bricks-and-mortar stores across the nation.

Choice is an important variable in the food-desert discussion and residential shopping is determined by an increasingly evolving retail landscape, driven by price, convenience, and cultural and practical considerations, which together add a significant nuance to the "if we build it, they will come" interpretation of the food-desert definition ( Dubowitz et al., 2015b).

Our next generation of efforts to make healthy foods "accessible" to residents of food deserts requires an understanding of meaning and context, as well as of place and space. Both quantitative and qualitative research are needed to understand how food retail availability and store operations - including retail jobs, community and family perceptions of the relative value of healthy and less healthy foods, food cultures and traditions, food marketing efforts and food prices - collectively impact health.

Footnotes

Authors' statement: The authors declare having no conflict of interest at the time of publishing.

¹ According to the Merriam-Webster dictionary, a supercentre is a very large discount department store that also sells a complete line of grocery merchandise.

Contributor Information

ALLISON E. KARPYN, Center for Research in Education and Social Policy (CRESP) and Department of Human Development and Family Sciences, University of Delaware.

DANIELLE RISER, Department of Human Development and Family Sciences, University of Delaware.

TARA TRACY, University of Delaware, CRESP.

RUI WANG, School of Education, University of Delaware.

YE SHEN, School of Education, University of Delaware.

References

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# data[].attributes.attachment_link.description
In this article, we discuss the most recent trends in food-retail access in low- and moderate-income communities in the United States of America. We begin with a review of the current literature on the number of people impacted by food deserts and then ...

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According to the Environmental Protection Agency (EPA), the government body that regulates pesticides in the U.S., a pesticide is any substance or mixture of substances intended for preventing, destroying, repelling or mitigating any pest. Though often misunderstood to refer only to insecticides, the term pesticide also applies to herbicides, fungicides, and various other substances used to control pests. Pesticides also include plant regulators, defoliants and desiccants.

Learn about the health and environmental effects of specific pesticides, as well as alternatives, in the Pesticide Gateway.

What's in a Pesticide Product?

We normally think of a pesticide as the product that can be purchased in the store - the insecticide, the weed killer or the fungicide. But, unfortunately, there is much more to it than that. The product that you buy or are exposed to is actually a pesticide formulation that contains a number of different materials, including active and inert ingredients, as well as contaminants and impurities. In addition, pesticides, when subject to various environmental conditions, break down to other materials known as metabolites, which are sometimes more toxic than the parent material.

Active Ingredients

The active ingredient, usually the only component of the formulation listed on the pesticide label, is by nature biologically and chemically active against a target pest, be it an insect, weed or fungus. By definition these chemicals kill living things.

Contaminants and Impurities

Contaminants and impurities are often a part of the pesticide product and responsible for product hazards. Dioxin and DDT have been identified as contaminants, which have not been purposefully added but are a function of the production process.

Metabolites

Metabolites are breakdown products that form when a pesticide is used in the environment and mixes with air, water, soil or living organisms. Often the metabolite is more hazardous than the parent pesticide.

Inert Ingredients

If you were to go to your local hardware store and take a look at the label on a can of ant and roach killer, the contents might read something like this, "5% Permethrin, 95% Inert Ingredients." After reading the label, you may wonder what makes up the other 95%. The fact is, the manufacturer doesn't have to tell you. Currently, under the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), pesticide manufacturers are only required to list the active ingredients in a pesticide, leaving consumers and applicators unaware of the possible toxics present in the inert ingredients of pesticide products they are using, unless the EPA administrator determines that the chemical poses a public health threat. Pesticide manufacturers argue they cannot release information on inert ingredients because they are trade secrets, and if released, their products could be duplicated. Quite often inert ingredients constitute over 95% of the pesticide product. Inert ingredients are mixed into pesticides products as a carrier or sticking agent, and are often as toxic as the active ingredient.

The Hazards of Inert Ingredients

Despite their name, these ingredients are neither chemically, biologically or toxicologically inert. In general, inert ingredients are minimally tested, however, many are known to state, federal and international agencies to be hazardous to human health. For example, the U.S. government lists creosols as a "Hazardous Waste" under Superfund regulations, yet allows these chemicals to be listed as inert ingredients in pesticide products. Creosols are known to produce skin and eye irritations, burns, inflammation, blindness, pneumonia, pancreatitis, central nervous system depression and kidney failure.

Some inert ingredients are even more toxic than the active ingredients. One of the most hazardous ingredients in the commonly used herbicide RoundUp is a surfactant, which is classified as an inert, and therefore not listed on the label. The pesticide naphthalene is an inert ingredient in some products and listed as an active ingredient in others. According a 2000 report produced by the New York State Attorney General, The Secret Ingredients in Pesticides: Reducing the Risk, 72 percent of pesticide products available to consumers contain over 95 percent inert ingredients; fewer than 10 percent of pesticide products list any inert ingredients on their labels; more than 200 chemicals used as inert ingredients are hazardous pollutants in federal environmental statutes governing air and water quality; and, of a 1995 list of inert ingredients, 394 chemicals were listed as active ingredients in other pesticide products.

# data[].attributes.attachment_link.description
According to the Environmental Protection Agency (EPA), the government body that regulates pesticides in the U.S., a pesticide is any substance or mixture of substances intended for preventing, destroying, repelling or mitigating any pest. Though often misunderstood to refer only to insecticides, the term pesticide also applies to herbicides, fungicides, and various other substances used to control pests.

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Food deserts: Definition, effects, and solutions

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Food deserts are areas where people have limited access to healthful and nourishing foods. Poverty and other socioeconomic factors can cause food deserts.

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US EPA. “Human Health Issues Related to Pesticides | US EPA.” US EPA, 11 Aug. 2015, www.epa.gov/pesticide-science-and-assessing-pesticide-risks/human-health-issues-related-pesticides.

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CropLife International. “Importance & Benefits of Pesticides - Pesticide Facts.” Pesticide Facts, 2018, pesticidefacts.org/topics/necessity-of-pesticides/.

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*Food Empowerment Project (F.E.P.) recognizes the problem with the term food desert, defined by the USDA as mostly being about proximity to food providers, rather than considering other factors such as racism, cost of living, people being time poor and cash poor, cultural appropriateness of available foods, the ability of people to grow their owns foods, etc. F.E.P. considers terms like food apartheid and food oppression to be more accurate, but since food desert is the term that is most commonly used, we have kept it as our title.

Food deserts can be described as geographic areas where residents' access to affordable, healthy food options (especially fresh fruits and vegetables) is restricted or nonexistent due to the absence of grocery stores within convenient traveling distance. For instance, according to a report prepared for Congress by the Economic Research Service of the US Department of Agriculture, about 2.3 million people (or 2.2 percent of all US households) live more than one mile away from a supermarket and do not own a car. [1] In urban areas, access to public transportation may help residents overcome the difficulties posed by distance, but economic forces have driven grocery stores out of many cities in recent years, making them so few and far between that an individual's food shopping trip may require taking several buses or trains. In suburban and rural areas, public transportation is either very limited or unavailable, with supermarkets often many miles away from people's homes.

The other defining characteristic of food deserts is socio-economic: that is, they are most commonly found in black and brown communities and low-income areas (where many people don't have cars). Studies have found that wealthy districts have three times as many supermarkets as poor ones do, [2] that white neighborhoods contain an average of four times as many supermarkets as predominantly black ones do, and that grocery stores in African-American communities are usually smaller with less selection. [3] People's choices about what to eat are severely limited by the options available to them and what they can afford-and many food deserts contain an overabundance of fast food chains selling cheap "meat" and dairy-based foods that are high in fat, sugar and salt. Processed foods (such as snack cakes, chips and soda) typically sold by corner delis, convenience stores and liquor stores are usually just as unhealthy.

Food Empowerment Project's report, " Shining a Light on the Valley of Heart's Delight (PDF)," shows that it is possible to overlook communities that are located in food deserts when relying on data collected by the US government. We found that, "Part of the problem is how the US government's North American Industry Classification System (NAICS is the standard used by the federal statistical agencies in classifying business establishments) categorizes retail outlets that sell food. According to the NAICS code, small corner grocery stores are statistically lumped together with supermarkets, such as Safeway, Whole Foods Market, etc. In other words, a community with no supermarket and two corner grocery stores that offer liquor and food would be counted as having two retail food outlets even though the food offered may be extremely limited and consist mainly of junk food."

In addition to this, we found that many of the convenience stores that had items such as a bunch of bananas or a few apples would sell the fruits individually. Because these items are not priced, the customers are often at the mercy of the person behind the counter who determines the cost then and there. Customers who don't have a good understanding of English might never ask the price of the item.

Those living in food deserts may also find it difficult to locate foods that are culturally appropriate for them, and dietary restrictions, such as lactose intolerance, gluten allergies, etc., also limit the food choices of those who do not have access to larger chain stores that have more selection. Additionally, studies have found that urban residents who purchase groceries at small neighborhood stores pay between 3 and 37 percent more than suburbanites buying the same products at supermarkets. [4]

Healthier foods are generally more expensive than unhealthful foods, particularly in food deserts. For instance, while the overall price of fruits and vegetables in the US increased by nearly 75 percent between 1989 and 2005, the price of fatty foods dropped by more than 26 percent during the same period. [5] While such inflation has strained the food budgets of many families regardless of their financial status, the higher cost of healthy foods often puts them entirely beyond the monetary means of many lower-income people.

While unhealthy eating may be economically cheaper in the short-term, the consequences of long-term constrained access to healthy foods is one of the main reasons that ethnic minority and low-income populations suffer from statistically higher rates of obesity, type 2 diabetes, cardiovascular disease, and other diet-related conditions than the general population. [6]

Whatever their age, obesity puts people at a greater risk for serious, even fatal health disorders (particularly coronary heart disease and diabetes, [7] the first and seventh leading causes of death in the US respectively): [8]

The incidence of diabetes among US adults doubled between 1996 and 2007, and "type 2 diabetes" (a variant of the disease that is often caused by obesity) [9] may account for 90 to 95 percent of these cases. [10] Only twenty years ago, type 2 diabetes was virtually unknown among people under 40 years old, but in the past decade it has increased tenfold among adolescents (mirroring this age group's escalating obesity rates). [11] While the incidence of type 2 diabetes has risen across demographic lines in recent years, the greatest increases have occurred among black and brown communities. The highest rates of escalation have been identified in Native American youth [12] and African-Americans and Latinos of all age groups, with these groups suffering disproportionately higher rates of type 2 diabetes compared to whites. [13]These are also the groups most likely to live in food deserts, and researchers have established a strong correlation between food insecurity and increased diabetes rates. One study of Chicago neighborhoods found the death rate from diabetes in food deserts to be twice that of areas offering access to grocery stores, [14] while another conducted in California found that adults ages 50 and over from black and brown communities had double the diabetes rate of whites from the same age demographic. Researchers explain this disparity by emphasizing that the high-calorie foods most readily available in food deserts put residents living in these areas at greater risk for diabetes in the first place, and that having restricted access to healthy foods also makes it harder for them to manage diabetes once they are diagnosed. [15]

Heart disease causes more than 2.4 million deaths in the US every year. [16] One of the main causes of cardiovascular disease is a diet high in unhealthy fats and low-density lipoprotein (LDL) cholesterol [17] -typified by the types of fare commonly available in food deserts. Just as African-Americans are statistically more likely than other populations to live in food deserts, heart disease kills more blacks every year than whites [18] (despite the fact that whites make up almost 80 percent of the total US populace, and blacks comprise slightly more than 13 percent).[19] Even children and adolescents living in food deserts are at greater risk for cardiovascular disease (both now and when they reach adulthood) due to the increased prevalence of obesity in those communities. [20]
Food for Thought
Public awareness of the formidable problems posed by food deserts is growing, thanks largely to the efforts of community activists, entrepreneurs and government officials committed to increasing people's access to healthy food options. On the national level, First Lady Michelle Obama has spearheaded the "Let's Move" campaign to combat childhood obesity, which includes a goal of eradicating food deserts by 2017 with a $400 million investment from the government focused on providing tax breaks to supermarkets that open in food deserts. [21] Many urban areas are also implementing initiatives locally to solve their food desert challenges.

- More than 500,000 residents (mostly African-American) live in food deserts, and an additional 400,000 live in neighborhoods with a preponderance of fast food restaurants and no grocery stores nearby. [22] Some food justice activists have sought to close this gap by opening food co-ops in underserved areas where supermarkets have historically been unsuccessful. In addition to selling fresh and organic fruits and vegetables, bulk whole grains and beans, and soy-based meat substitutes, some of these stores (like Fresh Family Foods on the city's South Side) also offer cooking and nutrition classes to educate the public about making healthy food choices. [23]

Los Angeles - In 2008, the Los Angeles City Council voted to enact a moratorium on new fast food outlets in a 32-square-mile zone encompassing some of South L.A.'s most arid food deserts, an area where about 97 percent of the population is either Latino, African-American, or of mixed race. [24] Having fewer fast food restaurants created greater demand for more and better food choices, so Councilmembers subsequently passed another measure offering grocery stores and sit-down restaurants serving healthier meals financial incentives to open up in underserved communities. [25] These policies have so far succeeded in bringing the first new supermarket to South L.A. in about a decade. [26]

New York City - An estimated 750,000 New York City residents live in food deserts, [27]while about three million people live in places where stores that sell fresh produce are few or far away. [28] Supermarkets throughout New York City have closed down in recent years due to increasing rents and shrinking profit margins, but the disappearance of urban grocery stores has had the most serious impact on low-income communities, especially those that are predominantly African-American (such East/Central Harlem and North/Central Brooklyn).[29] To fill this void, the city started its Green Carts program, which has been bringing affordable fresh fruits and vegetables to underserved areas while providing jobs for vendors since 2008. Hundreds of Green Carts are already on the streets in food deserts, and that number is rapidly increasing as prospective vendors obtain training, licenses and permits from the city.[30]
What can I do if I live in a food desert?
If you recognize that you are living in a food desert, you can start by helping those in your community understand what this means and talk about ways to make change. Discussing different options, such as growing your own food, working with local retailers to sell healthy, vegan foods, etc. is a good place to start. It is also important to bring your ideas and concerns to policy makers-city councilmembers, state legislators, etc.

To learn more you can also reach out to others who have worked on this issue.

If you are interested in using Food Empowerment Project's survey that was the basis for our report, " Shining a Light on the Valley of Heart's Delight (PDF)," please contact us.
References:
[1] "Access to Affordable and Nutritious Food: Measuring and Understanding Food Deserts and Their Consequences." United States Department of Agriculture Economic Research Service. 2009. Retrieved 8/25/17 from https://www.ers.usda.gov/webdocs/publications/42711/12716_ap036_1_.pdf?v=41055

[2] Walsh, Bryan. "It's Not Just Genetics." Time. June 12, 2008. http://www.time.com/time/magazine/article/0,9171,1813984,00.html (3/05/11)

[3] Morland, K., Wing, S., et al. "Neighborhood characteristics associated with the location of food stores and food service places." American Journal of Preventive Medicine. January 2002, vol. 22(1): p. 23-29. http://www.ncbi.nlm.nih.gov/pubmed/11777675 (3/05/11)

[4] Bullard, Robert D. (editor). Growing Smarter: Achieving Livable Communities, Environmental Justice, and Regional Equity. The MIT Press. 2007. p. 173. ttp://books.google.com/books?id=NAcmSchlTOYC&pg=PA173&lpg=PA173&dq=It+has+been+shown+that+... (3/05/11)

[5] Walsh, Bryan. "It's Not Just Genetics." Time. June 12, 2008. http://www.time.com/time/magazine/article/0,9171,1813984,00.html (3/05/11)

[6] Gallagher, Mari. "Examining the Impact of Food Deserts on Public Health in Chicago." Study commissioned by LaSalle Bank. 2006. http://www.marigallagher.com/2006/07/18/examining-the-impact-of-food-deserts-on-public-health-in-chicago-july-18-2006/ (8/21/17)

[7] "NHANES data on the Prevalence of Overweight Among Children and Adolescents: United States, 2003-2006." CDC National Center for Health Statistics. 2010. http://www.cdc.gov/nchs/data/hestat/obesity_child_09_10/obesity_child_09_10.htm (3/05/11)

[8] "Deaths and Mortality." Centers for Disease Control and Prevention. 2011. http://www.cdc.gov/nchs/fastats/deaths.htm (3/05/11)

[9] "Type 2 diabetes: Causes." Mayo Clinic. 2011. http://www.mayoclinic.com/health/type-2-diabetes/DS00585/DSECTION=causes (3/05/11)

[10] "National Diabetes Fact Sheet, 2011." Centers for Disease Control and Prevention. 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf (5/10/11)

[11] Rates of new diagnosed cases of type 1 and type 2 diabetes on the rise among children, teens. (2017, April 17). Retrieved December 06, 2017, from https://www.nih.gov/news-events/news-releases/rates-new-diagnosed-cases-type-1-type-2-diabetes-rise-among-children-teens

[12] Rates of new diagnosed cases of type 1 and type 2 diabetes on the rise among children, teens. (2017, April 17). Retrieved December 06, 2017, from https://www.nih.gov/news-events/news-releases/rates-new-diagnosed-cases-type-1-type-2-diabetes-rise-among-children-teens

[13] "Diabetes Basics." American Diabetes Association. http://www.diabetes.org/diabetes-basics/type-2/ (3/05/11)

[14] Curry, Andrew. "Bringing Healthy Fare to Big-City 'Food Deserts.'" Diabetes Forecast. December 2009. http://forecast.diabetes.org/magazine/your-ada/bringing-healthy-fare-big-city-food-deserts (4/17/11)

[15] "The Inextricable Connection Between Food Insecurity and Diabetes." California Pan-Ethnic Health Network. May 2010. https://cpehn.org/sites/default/files/resource_files/diabetesbrief2010.pdf (9/5/17)

[16] "Deaths and Mortality." Centers for Disease Control and Prevention. 2011. http://www.cdc.gov/nchs/fastats/deaths.htm (3/05/11)

[17] "The Truth About Fats: The Good, the Bad, and the In-Between." Harvard Health Publications. 2015. Retrieved from https://www.health.harvard.edu/staying-healthy/the-truth-about-fats-bad-and-good (9/5/17)

[18] "Heart Disease and African Americans." The Office of Minority Heatlh. 2010. https://minorityhealth.hhs.gov/omh/browse.aspx?lvl=4&lvlid=19 (3/05/11)

[19] "QuickFacts: Population Estimates." U.S. Census Bureau. July 1, 2016. https://www.census.gov/quickfacts/fact/table/US#viewtop (8/21/17)

[20] "Childhood Obesity." Centers for Disease Control and Prevention. 2008. http://www.cdc.gov/healthyyouth/obesity/ (3/05/11)

[21] "You All Took a Stand." White House Blog. February 20, 2010. http://www.whitehouse.gov/blog/2010/02/19/you-all-took-a-stand (4/02/11)

[22] Gallagher, Mari. "Examining the Impact of Food Deserts on Public Health in Chicago." Study commissioned by LaSalle Bank. 2006. http://www.marigallagher.com/2006/07/18/examining-the-impact-of-food-deserts-on-public-health-in-chicago-july-18-2006/ (8/21/17)

[23] Ogburn, Stephanie. "Would a Walmart solve West Oakland's and Nashville's food problems?" Grist. 5 Oct 2010. http://www.grist.org/article/food-2010-10-05-would-a-walmart-solve-oaklands-and-nashvilles-food-problems/PALL/print (4/02/11)

[24] "Neighborhoods of the City of Los Angeles Population & Race 2010 Census." Los Angeles Almanac. 2010. http://www.laalmanac.com/population/po24la.htm (4/17/11)

[25] Severson, Kim. "Los Angeles Stages a Fast Food Intervention." The New York Times. August 12, 2008. http://www.nytimes.com/2008/08/13/dining/13calo.html?scp=16&sq=food%20deserts&st=cse (4/02/11)

[26] Medina, Jennifer. "In South Los Angeles, New Fast-Food Spots Get a 'No, Thanks.'" The New York Times. January 15, 2011. http://www.nytimes.com/2011/01/16/us/16fastfood.html?_r=1(4/02/11)

[27] "Fresh Food for Urban Deserts." The New York Times. March 20, 2009. http://www.nytimes.com/2009/03/21/opinion/21sat4.html?scp=3&sq=food%20deserts&st=cse (4/02/11)

[28] "Going to Market: New York City's Neighborhood Grocery Store and Supermarket Shortage." New York City Department of City Planning. 2008. http://www.nyc.gov/html/misc/pdf/going_to_market.pdf (8/21/17)

[29] Gordon, C., Purciel-Hill, M., et al. "Measuring food deserts in New York City's low-income neighborhoods." Health Place. March 2011. Vol. 17(2), pages 696-700. http://www.ncbi.nlm.nih.gov/pubmed/21256070 (4/17/11)

[30] McMahon, Jeff. "New York rolls veggie carts into food deserts; can other cities follow?" The New York Times. March 11, 2010. http://jeffmcmahon.com/2010/new-york-green-cart-chicago-farm-fork-financing/ (8/21/17)

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Food deserts can be described as geographic areas where residents' access to affordable, healthy food options (especially fresh fruits and vegetables) is restricted or nonexistent.

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“Food Safety.” Npic.orst.edu, 12 Feb. 2018, npic.orst.edu/health/food.html#:~:text=Pesticides%20allow%20growers%20to%20increase.

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https://www.hartfordhospital.org/

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https://www.helpguide.org/articles/healthy-eating/organic-foods.htm#:~:text=Organic%20farming%20tends%20to%20be,who%20live%20close%20to%20farms.

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Organic Foods: What You Need to Know - HelpGuide.org

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Is organic food really healthier? Is it worth the expense? Find out what the labels mean and which foods give you the most bang for your buck.

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www.ncbi.nlm.nih.gov

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https://www.ams.usda.gov/services/organic-certification/organic-basics#

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Esperanca. “Food Deserts and Their Impact on Community Health.” Esperança, 20 July 2021, esperanca.org/food-deserts-and-their-impact-on-community-health/.

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healthy eating
Is organic food really healthier? Is it worth the expense? Find out what the labels mean and which foods give you the most bang for your buck.

What does "organic" mean?

The term "organic" refers to the way agricultural products are grown and processed. While the regulations vary from country to country, in the U.S., organic crops must be grown must be grown without the use of synthetic herbicides, pesticides, and fertilizers, or bioengineered genes (GMOs).

Organic livestock raised for meat, eggs, and dairy products must be raised in living conditions accommodating their natural behaviors (such as the ability to graze on pasture) and fed organic feed and forage. They may not be given antibiotics, growth hormones, or any animal by-products.

Organic produce:

Conventionally-grown produce:

Grown with natural fertilizers (manure, compost).

Grown with synthetic or chemical fertilizers.

Weeds are controlled naturally (crop rotation, hand weeding, mulching, and tilling) or with organic-approved herbicides.

Weeds are controlled with chemical herbicides.

Pests are controlled using natural methods (birds, insects, traps) and naturally-derived pesticides.

Pests are controlled with synthetic pesticides

Organic meat, dairy, eggs:

Conventionally-raised meat, dairy, eggs

Livestock are given all organic, hormone- and GMO-free feed.

Livestock are given growth hormones for faster growth, as well as non-organic, GMO feed.

Disease is prevented with natural methods such as clean housing, rotational grazing, and healthy diet.

Antibiotics and medications are used to prevent livestock disease.

Livestock must have access to the outdoors.

Livestock may or may not have access to the outdoors.

The benefits of organic food

How your food is grown or raised can have a major impact on your mental and emotional health as well as the environment. Organic foods often have more beneficial nutrients, such as antioxidants, than their conventionally-grown counterparts and people with allergies to foods, chemicals, or preservatives may find their symptoms lessen or go away when they eat only organic foods.

Organic produce contains fewer pesticides. Chemicals such as synthetic fungicides, herbicides, and insecticides are widely used in conventional agriculture and residues remain on (and in) the food we eat.

Organic food is often fresher because it doesn't contain preservatives that make it last longer. Organic produce is sometimes (but not always, so watch where it is from) produced on smaller farms nearer to where it is sold.

Organic farming tends to be better for the environment. Organic farming practices may reduce pollution, conserve water, reduce soil erosion, increase soil fertility, and use less energy. Farming without synthetic pesticides is also better for nearby birds and animals as well as people who live close to farms.

Organically raised animals are NOT given antibiotics, growth hormones, or fed animal byproducts. Feeding livestock animal byproducts increases the risk of mad cow disease (BSE) and the use of antibiotics can create antibiotic-resistant strains of bacteria. Organically-raised animals tend to be given more space to move around and access to the outdoors, which help to keep them healthy.

Organic meat and milk can be richer in certain nutrients. Results of a 2016 European study show that levels of certain nutrients, including omega-3 fatty acids, were up to 50 percent higher in organic meat and milk than in conventionally raised versions.

Organic food is GMO-free. Genetically Modified Organisms (GMOs) or genetically engineered (GE) foods are plants whose DNA has been altered in ways that cannot occur in nature or in traditional crossbreeding, most commonly in order to be resistant to pesticides or produce an insecticide.

Organic food vs. locally-grown food

Unlike organic standards, there is no specific definition for "local food". It could be grown in your local community, your state, your region, or your country. During large portions of the year it is usually possible to find food grown close to home at places such as a farmer's market.

The benefits of locally grown food

Financial: Money stays within the local economy. More money goes directly to the farmer, instead of to things like marketing and distribution.

Transportation: In the U.S., for example, the average distance a meal travels from the farm to the dinner plate is over 1,500 miles. Produce must be picked while still unripe and then gassed to "ripen" it after transport. Or the food is highly processed in factories using preservatives, irradiation, and other means to keep it stable for transport.

Freshness: Local food is harvested when ripe and thus fresher and full of flavor.

Some small local farmers use organic methods but may not be able to afford to become certified organic. Visit a farmer's market and talk with the farmers to find out what methods they use.

Understanding GMOs

The ongoing debate about the effects of GMOs on health and the environment is a controversial one. In most cases, GMOs are engineered to make food crops resistant to herbicides and/or to produce an insecticide. For example, much of the sweet corn consumed in the U.S. is genetically engineered to be resistant to the herbicide Roundup and to produce its own insecticide, Bt Toxin.

GMOs are also commonly found in U.S. crops such as soybeans, alfalfa, squash, zucchini, papaya, and canola, and are present in many breakfast cereals and much of the processed food that we eat. If the ingredients on a package include corn syrup or soy lecithin, chances are it contains GMOs.

GMOs and pesticides

The use of toxic herbicides like Roundup (glyphosate) has increased 15 times since GMOs were introduced. While the World Health Organization announced that glyphosate is "probably carcinogenic to humans," there is still some controversy over the level of health risks posed by the use of pesticides.

Are GMOs safe?

While the U.S. Food and Drug Administration (FDA) and the biotech companies that engineer GMOs insist they are safe, many food safety advocates point out that no long term studies have ever been conducted to confirm the safety of GMO use, while some animal studies have indicated that consuming GMOs may cause internal organ damage, slowed brain growth, and thickening of the digestive tract.

GMOs have been linked to increased food allergens and gastro-intestinal problems in humans. While many people think that altering the DNA of a plant or animal can increase the risk of cancer, the research has so far proven inconclusive.

Does organic mean pesticide-free?

As mentioned above, one of the primary benefits of eating organic is lower levels of pesticides. However, despite popular belief, organic farms do use pesticides. The difference is that they only use naturally-derived pesticides, rather than the synthetic pesticides used on conventional commercial farms. Natural pesticides are believed to be less toxic, however, some have been found to have health risks. That said, your exposure to harmful pesticides will likely be lower when eating organic.

What are the possible risks of pesticides?

Most of us have an accumulated build-up of pesticide exposure in our bodies due to numerous years of exposure. This chemical "body burden" as it is medically known could lead to health issues such as headaches, birth defects, and added strain on weakened immune systems.

Some studies have indicated that the use of pesticides even at low doses can increase the risk of certain cancers, such as leukemia, lymphoma, brain tumors, breast cancer and prostate cancer.

Children and fetuses are most vulnerable to pesticide exposure because their immune systems, bodies, and brains are still developing. Exposure at an early age may cause developmental delays, behavioral disorders, autism, immune system harm, and motor dysfunction.

Pregnant women are more vulnerable due to the added stress pesticides put on their already taxed organs. Plus, pesticides can be passed from mother to child in the womb, as well as through breast milk.

The widespread use of pesticides has also led to the emergence of "super weeds" and "super bugs," which can only be killed with extremely toxic poisons like 2,4-Dichlorophenoxyacetic acid (a major ingredient in Agent Orange).

Does washing and peeling get rid of pesticides?

Rinsing fresh produce reduces but does not eliminate pesticides. Peeling sometimes helps, but valuable nutrients often go down the drain with the skin. The best approach: eat a varied diet, wash and scrub all produce thoroughly, and buy organic when possible.

The best bang for your buck when shopping organic

Organic food is often more expensive than conventionally-grown food. But if you set some priorities, it may be possible to purchase organic food and stay within your food budget.

Know your produce pesticide levels

Some types of conventionally-grown produce are much higher in pesticides than others, and should be avoided when possible. Others are low enough that buying non-organic is relatively safe.

Fruits and vegetables where the organic label matters most

According to the Environmental Working Group, a nonprofit organization that analyzes the results of government pesticide testing in the U.S., the following fruits and vegetables have the highest pesticide levels, so are best to buy organic:

Fruits and vegetables you DON'T need to buy organic

Known as the "Clean 15", these conventionally-grown fruits and vegetables are generally low in pesticides:

Buy organic meat, eggs, and dairy if you can afford to

In the U.S., industrially-raised animals may be fed corn, grains, antibiotics, animal byproducts, growth hormones, pesticides, and sewage sludge. These practices can have health consequences for both the animals themselves and people consuming their meat, eggs, or milk.

If you can afford to pay the higher prices, look for beef and dairy products labeled "pasture raised" or "100% grass fed." For pork, chicken, or eggs, look for a "certified organic" label. You may find that buying cheaper cuts of meat from organically raised animals enables you to eat organic without breaking your food budget. Try buying organic chicken thighs instead of conventionally raised chicken breasts, for example.

Other ways to keep the cost of organic food within your budget

Shop at farmers' markets. Many cities, as well as small towns, host a weekly farmers' market, where local farmers sell their produce at an open-air street market, often at a discount to grocery stores.

Join a food co-op. A natural foods co-op, or cooperative grocery store typically offers lower prices to members, who pay an annual fee to belong

Join a Community Supported Agriculture (CSA) farm, in which individuals and families join up to purchase "shares" of produce in bulk, directly from a local farm. Local and organic!

Organic food buying tips

Buy in season. Fruits and vegetables are cheapest and freshest when they are in season. Find out when produce is delivered to your market so you're buying the freshest food possible.

Shop around. Compare the price of organic items at the grocery store, the farmers' market, online, and in other venues (even the freezer aisle).

Remember that organic doesn't always equal healthy. Making junk food sound healthy is a common marketing ploy in the food industry but organic baked goods, desserts, and snacks are usually still very high in sugar, salt, fat, or calories. It pays to read food labels carefully.

Why is organic food often more expensive?

Organic food is more labor intensive since the farmers do not use synthetic pesticides, chemical fertilizers, or drugs. Organic certification is expensive and organic feed for animals can cost twice as much. Organic farms tend to be smaller than conventional farms, which means fixed costs and overhead must be distributed across smaller produce volumes without government subsidies.

Where to shop for organic food

To find farmers' markets, organic farms, and grocery co-ops in your area, visit:

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Organic Foods: What You Need to Know - HelpGuide.org

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healthy eating The term "organic" refers to the way agricultural products are grown and processed. While the regulations vary from country to country, in the U.S., organic crops must be grown must be grown without the use of synthetic herbicides, pesticides, and fertilizers, or bioengineered genes (GMOs).

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Bradley, Jessie. “The Advantages and Disadvantages of Pesticides | ChefsBest.” Food Marketing Awards | ChefsBest | Home : ChefsBest, 25 Aug. 2016, www.chefsbest.com/advantages-disadvantages-pesticides/#:~:text=In%20the%20short%2Drange%2C%20pesticides. Accessed 11 May 2023.

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https://www.verywellhealth.com/what-are-food-deserts-4165971