Chemical Food Contaminants (Mycotoxins) – III

Mycotoxins

Mycotoxins are a group of naturally occurring chemicals produced by certain molds/fungi. There are many such compounds, but only a few of them are regularly found in food and animal feedstuffs such as grains and seeds. They can grow on a variety of different crops and foodstuffs including cereals, nuts, spices, dried fruits, apple juice and coffee, often under warm and humid conditions, where presence of mycotoxins in grains and other staple foods and feedstuffs has serious implications for human and animal health. Since they are produced by fungi, mycotoxins are associated with diseased or moldy crops, although the visible mold contamination can be superficial. Many countries have enacted regulations stipulating maximum amounts of mycotoxins permissible in food and feedstuffs. Most developed countries will not permit the import of commodities containing amounts of mycotoxins above specified limits, where Mycotoxins have implications for trade between nations. Thus prevention of fungal invasion of commodities is by far the most effective method of avoiding mycotoxin problems, where integrated commodity management program focusing on the maintenance of commodity quality from the field to the consumer will be one of the best alternatives.

Aflatoxins

Aflatoxins were discovered over 30 years ago which have been subject to a great deal of research. They are potent human carcinogens and interfere with the functioning of the immune system. Among livestock, they are particularly toxic to chickens. In 1993, the International Agency for Research on Cancer (IARC) assessed and classified naturally occurring mixtures of aflatoxins as class 1 human carcinogens where Aflatoxins B1, B2, G1, and G2 have been found to occur in commodities and have been detected in human sera. IARC has concluded that aflatoxin B1 is a class 1 human carcinogen including residues of aflatoxin B and/or its metabolite, aflatoxin M, can occur in animal products, and milk. Aflatoxin M, is also found in human milk if the mother consumes food containing aflatoxin B1. IARC has given aflatoxin M, a lower carcinogenicity rating than aflatoxin B1.

Types of Mycotoxins

There are five groups of mycotoxins, which occur quite often in foods from both groups are: deoxynivalenol/nivalenol, zearalenone, ochratoxin, fumonisins and aflatoxins. T-2 toxin is also found in a variety of grains but its occurrence, to date, is less frequent than the preceding five mycotoxins. The fungi that produce mycotoxins in food fall broadly into two groups: those that invade before harvest, commonly called field fungi, and those that occur only after harvest, called storage fungi.

There are three types of toxicogenic field fungi:

Plant pathogens such as F. graminearum (deoxynivalenol, nivalenol);

Fungi that grow on senescent or stressed plants, such as F. moniliforme (fumonisin) and sometimes A. flavus (aflatoxin); and

Fungi that initially colonise in the plant before harvest and predispose the commodity to mycotoxin contamination after harvest, such as P. verrucosum (ochratoxin) and A. flavus (aflatoxin).

Mycotoxins in Grains and Seeds

Mycotoxin	Commodity	Fungal Source(s)	Effects of Ingestion
deoxynivalenol/ nivalenol	wheat, maize, barley reported from	Fusarium graminearum	Human toxicoses India, China, Japan, and Korea. Toxic to animals, especially pigs
		Fusarium crookwellense
		Fusarium culmorum
zearalenone	maize, wheat	F. graminearum	Identified by the International Agency for Research on Cancer (IARC) as a possible human carcinogen. Affects reproductive system in female pigs
		F. culmorum
		F. crookwellense
ochratoxin A	barley, wheat, and many other commodities	Aspergillus ochraceus	Suspected by IARC as human carcinogen. Carcinogenic in laboratory animals and pigs
		Penicillium verrucosum
fumonisin B1	maize	Fusarium moniliforme plus several less common species	Suspected by IARC as human carcinogen. Toxic to pigs and poultry. Cause of equine eucoencephalomalacia (ELEM), a fatal disease of horses
aflatoxin B1, B2	maize, peanuts, and many other commodities	Aspergillus flavus	Aflatoxin B1, and naturally occurring mixtures of aflatoxins, identified as potent human carcinogens by IARC. Adverse effects in various animals, especially chickens
aflatoxin B1, B2, G1, G2	maize, peanuts	Aspergillus parasiticus

Ecology

In the case contamination of mycotoxin contamination, there is a more or less well defined association between the fungus and its plant host. Aspergillus and Fusarium species are likely to be the most significant mycotoxin producing field fungi found in tropical developing countries, i.e., moldy, damaged peanuts. High levels of aflatoxins in this commodity have frequently been found in parts of South-East Asia due to the result of poor handling and storage practices. Fusarium kernel rot is one of the most important ear diseases of maize in hot growing areas which is associated with warm, dry years and/or insect damage. There is a strong relationship between insect damage and fusarium kernel rot. It has been found during field survey work, for example, that the incidence of the European corn borer increased F. moniliforme disease and fumonisin concentrations. Maize infected with fusarium kernel rot, one of the most important ear diseases of maize in hot growing areas because temperature stress of the growing plant is important, because studies of fumonisin occurrence in maize hybrids grown across the U.S. Corn Belt, Europe and Africa, indicate that hybrids grown outside their range of temperature adaptation have higher fumonisin concentrations.

After harvest, when grains or seeds have become moribund or dormant as a result of drying, associations between fungi and plants disappear, and physical factors dictate whether or not members of the other group - the storage fungi - will grow and/or produce mycotoxins. The primary factors influencing fungal growth in stored food products are the moisture content (more precisely, the water activity) and the temperature of the commodity. As a generally accepted fact about tropics; the temperature is almost always suitable for storage fungi, so it is the water activity that becomes the prime determinant of fungal invasion and growth in stored grains.

Food Safety and Mycotoxins

The mycotoxins of most concern from a food safety perspective include the aflatoxins (B1, B2, G1, G2 and M1), ochratoxin A, patulin and toxins produced by Fusarium moulds, including fumonisins (B1, B2 and B3), trichothecenes (principally nivalenol, deoxynivalenol, T-2 and HT-2 toxin) and zearalenone. Mycotoxins can cause a variety of adverse health effects in humans. Aflatoxins, including aflatoxin B1 are the most toxic and have been shown to be genotoxic i.e. can damage DNA and cause cancer in animal species. There is also evidence that they can cause liver cancer in humans. Other mycotoxins have a range of other health effects including kidney damage, gastrointestinal disturbances, reproductive disorders or suppression of the immune system. For most mycotoxins, a tolerable daily intake (TDI) has been established, which estimates the quantity of mycotoxin which someone can be exposed to daily over a lifetime without it posing a significant risk to health.

It is clear that exposure to aflatoxins is hazardous to human health where, most countries have regulations governing the allowable concentrations of aflatoxin in food and feed.  Aflatoxin B, the most toxic of the aflatoxins, causes a variety of adverse effects in different domestic animals. Effects on chickens include liver damage, impaired productivity and reproductive efficiency, decreased egg production in hens, inferior egg-shell quality, inferior carcass quality and, most important from a human perspective, increased susceptibility to disease.

Exposure Methods

When people are around toxic mold they are usually exposed to airborne mycotoxins by breathing them in. These mycotoxins end up in the lungs and cause breathing problems and other severe symptoms. Mycotoxins in the air can also enter through a person's eyes. Trichothecene mycotoxins can be absorbed through the skin as well. Another way mycotoxins get into a person's body is by the person eating food with mycotoxins in it. This can happen if toxic mold has been growing on crops. Many mycotoxins, for example trichothecene, remain toxic even after being cooked. This is one reason why mycotoxins are a big problem in agriculture. A binding agent is used on crops such as grain after harvesting to remove mycotoxins.

Symptoms

In 2004, there were 125 people died after eating maize contaminated with aflatoxin mycotoxins in Kenya, and there are many cases of pets dying from eating pet food with mycotoxins in it as well. The effects of some food-borne mycotoxins are acute, symptoms of severe illness appearing very quickly. Other mycotoxins occurring in food have longer term chronic or cumulative effects on health, including the induction of cancers and immune deficiency. Information about food-borne mycotoxins is far from complete, but enough is known to identify them as a serious problem in many parts of the world, causing significant economic losses.

Risks of Contamination

The food-borne mycotoxins likely to be of greatest significance for human health in tropical developing countries are the fumonisins and aflatoxins. Fumonisins were discovered as recently as 1988, thus there is little information on their toxicology. To date, there is sufficient evidence in experimental animals for the carcinogenicity of cultures of Fusarium moniliforme that contain significant amounts of fumonisins; and there is limited evidence in experimental animals for the carcinogenicity of fumonisin B1. F. moniliforme growing in maize may produce fumonisin B1, a suspected human carcinogen. Also, fumonisin B1 is toxic to pigs and poultry, and is the cause of equine leucoencephalomalacia (ELEM), a fatal disease of horses. Fumonisins have been found as a very common contaminant of maize-based food and feed in Africa, China, France, Indonesia, Italy, the Philippines, South America, Thailand, and the USA. Strains of F. moniliforme from maize from all over the world, including Africa, Argentina, Brazil, France, Indonesia, Italy, the Philippines, Poland, Thailand, and the USA, produce fumonisins. At present, strains of F. moniliforme isolated from sorghum are considered to be poor producers of fumonisins.

Prevention of Mycotoxin Contamination – Common Control Measures

Drying – Fungi cannot grow (or mycotoxins be produced) in properly dried foods, where efficient drying of commodities and maintenance of the dry state is an effective control measure against fungal growth and mycotoxin production. To reduce or prevent production of most mycotoxins, drying should take place soon after harvest and as rapidly as feasible. The critical water content for safe storage corresponds to a water activity (a_w) of about 0.7. Maintenance of foods below 0.7 a_w is an effective technique used throughout the world for controlling fungal spoilage and mycotoxin production in foods. Problems in maintaining an adequately low a_w often occur in the tropics, where high ambient humidities make control of commodity moisture difficult. Where grain is held in bags, systems that employ careful drying and subsequent storage in moisture-proof plastic sheeting may overcome this problem. 

Proper rapid drying is the best means to avoid fungal growth and mycotoxin production in grain after harvest. At times when sun drying is not possible or unreliable some form of mechanical drying may be necessary. While it is possible to control fungal growth in stored commodities by controlled atmospheres or use of preservatives or natural inhibitors, such techniques are almost always more expensive than effective drying, and are rarely feasible in developing countries.

Minimize Grain Damage – Damaged grain is more prone to fungal invasion and thereby mycotoxin contamination where it is important to avoid damage before and during drying, and storage. Drying of maize on the cob, before shelling, is a very good practice. Insects are a major cause of damage where field insect pests and some storage species damage grain on the head and promote fungal growth in the moist environment of the ripening grain. In storage, many insect species attack grain, and the moisture that can accumulate from their activities provides ideal conditions for the fungi. To avoid moisture and mold problems, it is essential that numbers of insects in stored grain be kept to a minimum. Such problems are intensified if the grain lacks adequate ventilation, particularly if metal containers are used.

Ensure Proper storage Conditions – While keeping commodities dry during storage in tropical areas can be difficult, the importance of dry storage cannot be overemphasized. On a small scale, polyethylene bags are effective; on a large scale, safe storage requires well-designed structures with floors and walls impermeable to moisture. Maintenance of the water activity of the stored commodity below 0.7 is crucial. In tropical areas, outdoor humidity is usually fall well below 70% on sunny days, where appropriately timed ventilation, fan-forced if necessary, will greatly assist the maintenance of the commodity at below 0.7 a_w. Ideally, all large-scale storage areas should be equipped with instruments for measuring humidity, so that air appropriate for ventilation can be selected. Sealed storage under modified atmospheres for insect control is also very effective for controlling fungal growth, provided the grain is adequately dried before storage, and provided diurnal temperature fluctuations within the storage are minimized. 

If commodities must be stored before adequate drying, it should be only for short periods of no more than three days. Use of sealed storage or modified atmospheres will prolong this safe period, but such procedures are relatively expensive and gaslight conditions are essential. A proven system of storage management is needed, with mycotoxin considerations an integral part of it. A range of decision-support systems is becoming available covering the varying levels of sophistication and scale involved.

Methods of Eliminating Mycotoxins

Mycotoxins aren't actually alive like mold spores, where removal or destruction is really means breaking down of mycotoxins and their toxicity which will no longer dangerous to humans. Bleach with 5% sodium hypochlorite disintegrates trichothecene mycotoxins as well as other mycotoxins including aflatoxin. It takes fire at 500⁰F (260⁰C) for half an hour or fire at 900⁰F (482⁰C) for 10 minutes to destroy trichothecene mycotoxins. In addition, ozone is supposed to oxidize most or all mycotoxins, but the level of ozone you need to oxidize mycotoxins is not safe for humans. Therefore, if you use an ozone-generator there must be no one in the building. HEPA air filters are not effective at removing mycotoxins where activated carbon filters can remove mycotoxins from the air. Mycotoxins are eventually broken down and lose their toxicity after some time, but some types of mycotoxins may take several years though, for example trichothecene mycotoxins which are among the most resilient.

Detection of mycotoxins

Mycotoxins occur, and exert their toxic effects, in extremely small quantities in foodstuffs where identification and quantitative assessment generally require sophisticated sampling, sample preparation, extraction, and analytical techniques. Under practical storage conditions, the aim should be to monitor for the occurrence of fungi and if fungi cannot be detected, then there is unlikely to be any mycotoxin contamination. The presence of fungi indicates the potential for mycotoxin production, and the need to consider the fate of the batch of commodity affected. While there are means of decontaminating affected commodities, all are relatively expensive, and their efficiency is still a matter of debate. The need for simple, rapid, and efficient mycotoxin analysis methods that can be handled by relatively unskilled operators has been recognize and some progress made towards developing them. The U.S. Federal Grain Inspection Service (FGIS) has evaluated eight commercially available, rapid tests for aflatoxin in maize. FGIS-approved kits include rapid ELISA, immune-affinity cartridge, solid-phase ELISA, and selective adsorbent mini-column procedures. There remains a need for efficient, cost-effective sampling and analysis methods that can be used in developing country laboratories. Various governments have set regulatory limits for mycotoxins in food and animal foodstuffs presented for sale or import. For aflatoxin, guidelines range from 4 to 50 µg/kg (parts per billion). Regulatory limits for fumonisin are under consideration. For all mycotoxins, it is likely that, as analytical techniques and knowledge of the toxins improve, allowable limits will fall.

Chemical Food Contaminants (Heavy Metals) – II

Heavy Metals

Although there is no clear definition of what a heavy metal is, density is in most cases taken to be the defining factor. Heavy metals are commonly defined as those having a specific density of more than 5 g/cm³. Heavy metals have been used in many different areas for thousands of years. Lead has been used for at least 5000 years, early applications including building materials, pigments for glazing ceramics, and pipes for transporting water. In ancient Rome, lead acetate was used to sweeten old wine, and some Romans might have consumed as much as a gram of lead a day. Mercury was allegedly used by the Romans as a salve to alleviate teething pain in infants, and was later (from the 1300s to the late 1800s) employed as a remedy for syphilis. Claude Monet used cadmium pigments extensively in mid 1800s, but the scarcity of the metal limited the use in artists’ materials until the early 1900s.

Although several adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues, and is even increasing in some parts of the world, in particular in less developed countries, though emissions have declined in most developed countries over the last 100 years. The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic (arsenic is a metalloid, but is usually classified as a heavy metal). Emissions of heavy metals to the environment occur via a wide range of processes and pathways, including the air (e.g. during combustion, extraction and processing), to surface waters (via runoff and releases from storage and transport) and to the soil and hence into ground waters as well as crops. Atmospheric emissions tend to be of greatest concern in terms of human health, both because of the quantities involved and the widespread dispersion and potential for exposure that often ensues.

Cadmium – Cd  

Cadmium occurs naturally in ores together with zinc, lead and copper. Cadmium compounds are used as stabilizers in PVC products, colour pigment, several alloys and, now most commonly, in re-chargeable nickel– cadmium batteries. Metallic cadmium has mostly been used as an anticorrosion agent (cadmiation). Cadmium is also present as a pollutant in phosphate fertilizers. EU cadmium usage has decreased considerably during the 1990s, mainly due to the gradual phase-out of cadmium products other than Ni-Cd batteries and the implementation of more stringent EU environmental legislation (Directive 91/338/ECC). Notwithstanding these reductions in Europe, however, cadmium production, consumption and emissions to the environment worldwide have increased dramatically during the 20th century. Cadmium containing products are rarely re-cycled, but frequently dumped together with household waste, thereby contaminating the environment, especially if the waste is incinerated. Cigarette smoking is a major source of cadmium exposure. Inhalation of cadmium fumes or particles can be life threatening, and although acute pulmonary effects and deaths are uncommon, sporadic cases still occur. Cadmium exposure may cause kidney damage. The first sign of the renal lesion is usually a tubular dysfunction, evidenced by an increased excretion of low molecular weight proteins [such as β₂-microglobulin and α₁-microglobulin (protein HC)] or enzymes [such as N-Acetyl-β-D-glucosaminidase (NAG)]. It has been suggested that the tubular damage is reversible, but there is overwhelming evidence that the cadmium induced tubular damage is indeed irreversible.

In non-smokers, food is the most important source of cadmium exposure. Natural as well as anthropogenic sources of cadmium, including industrial emissions and the application of fertilizer and sewage sludge to farm land, may lead to contamination of soils, and to increased cadmium uptake by crops and vegetables, grown for human consumption. The uptake process of soil cadmium by plants is enhanced at low pH. Recent research data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures. Cadmium is present in most foodstuffs, but concentrations vary greatly, and individual intake also varies considerably due to differences in dietary habits. Women usually have lower daily cadmium intakes, because of lower energy consumption than men. Gastrointestinal absorption of cadmium may be influenced by nutritional factors, such as iron status. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects.

Mercury – Hg

The chemical element mercury is a shiny metallic liquid which occurs in only trace amounts in igneous and sedimentary rocks. Mercury is found principally in the form of the ore cinnabar (mercury sulfide), but can also be found in the uncombined state. Mercury will dissolve numerous metals to form amalgams and is thus used to extract gold dust from rocks by dissolving the gold and then boiling off the mercury. The amalgam used in dental fillings contains tin and silver (and sometimes gold) dissolved in mercury. The mercury compound cinnabar (HgS), was used in pre-historic cave paintings for red colours, and metallic mercury was known in ancient Greece where it (as well as white lead) was used as a cosmetic to lighten the skin. In medicine, apart from the previously mentioned use of mercury as a cure for syphilis, mercury compounds have also been used as diuretics [calomel (Hg₂Cl₂)], and mercury amalgam is still used for filling teeth in many countries. Metallic mercury is used in thermometers, barometers and instruments for measuring blood pressure. A major use of mercury is in the chlor-alkali industry, in the electrochemical process of manufacturing chlorine, where mercury is used as an electrode. The largest occupational group exposed to mercury is dental care staff. During the 1970s, air concentrations in some dental surgeries reached 20 μg/m³, but since then levels have generally fallen to about one-tenth of those concentrations. Inorganic mercury is converted to organic compounds, such as methyl mercury, which is very stable and accumulates in the food chain. Until the 1970s, methyl mercury was commonly used for control of fungi on seed grain.

Some of the major sources of mercury pollution include coal-fired power plants, boilers, steel production, incinerators, and cement plants. Power plants are the largest source, emitting around 33 tons of mercury pollution in the US annually, and contributing to almost half of all mercury emissions. Large boilers and heaters, many of which are powered by coal or oil, are the next largest source of mercury emissions, followed by steel production. Incinerators are another major source.

Acute mercury exposure may give rise to lung damage. Chronic poisoning is characterized by neurological and psychological symptoms, such as tremor, changes in personality, restlessness, anxiety, sleep disturbance and depression. The symptoms are reversible after cessation of exposure. Because of the blood–brain barrier there is no central nervous involvement related to inorganic mercury exposure. Metallic mercury may cause kidney damage, which is reversible after exposure has stopped. It has also been possible to detect proteinuria at relatively low levels of occupational exposure.

Methyl mercury poisoning has a latency of 1 month or longer after acute exposure, and the main symptoms relate to nervous system damage. The earliest symptoms are parestesias and numbness in the hands and feet. Later, coordination difficulties and concentric constriction of the visual field may develop as well as auditory symptoms. High doses may lead to death, usually 2–4 weeks after onset of symptoms. The Minamata catastrophe in Japan in the 1950s was caused by methyl mercury poisoning from fish contaminated by mercury discharges to the surrounding sea. In the early 1970s, more than 10,000 persons in Iraq were poisoned by eating bread baked from mercury-polluted grain, and several thousand people died as a consequence of the poisoning.

The general population is primarily exposed to mercury via food, fish being a major source of methyl mercury exposure, and dental amalgam. Several experimental studies have shown that mercury vapour is released from amalgam fillings, and that the release rate may increase by chewing. Mercury in urine is primarily related to (relatively recent) exposure to inorganic compounds, whereas blood mercury may be used to identify exposure to methyl mercury. However, the general population does not face a significant health risk from methyl mercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna; fish (such as pike, walleye and bass) taken from polluted fresh waters should especially be avoided.

Lead – Pb

Lead is a naturally occurring metal found in rock and soil and also has many industrial applications. Due to both its natural occurrence and long history of global use, lead is ubiquitous in the environment and is present in air, water and soil as well as in food, drinking water and household dust. Levels of lead in most environmental media have declined significantly over the past few decades due to the discontinued use of lead in paint, gasoline and the solder used in food cans. Lead has no known function in the human body. Infants and children are most sensitive to the harmful effects of lead because they are undergoing a period of rapid development and they absorb lead more easily and excrete it less efficiently than adults. The most sensitive endpoint of lead toxicity in infants and children is the reduction of intelligence quotient (IQ) score. In adults, the strongest scientific evidence to date suggests low levels of lead exposure may cause a small increase in blood pressure. Since the phase-out of leaded gasoline and the subsequent reduction of airborne lead, food and drinking water are the primary sources of lead exposure to adults within the general population. In addition to food and drinking water, the ingestion of house dust and soil containing lead can also significantly contribute to the lead exposure of infants and toddlers.

The general population is exposed to lead from air and food in roughly equal proportions. Earlier, lead in foodstuff originated from pots used for cooking and storage, and lead acetate was previously used to sweeten port wine. Occupational exposure to inorganic lead occurs in mines and smelters as well as welding of lead painted metal, and in battery plants. Low or moderate exposure may take place in the glass industry. High levels of air emissions may pollute areas near lead mines and smelters. Airborne lead can be deposited on soil and water, thus reaching humans via the food chain.  Up to 50% of inhaled inorganic lead may be absorbed in the lungs. Adults take up 10–15% of lead in food, whereas children may absorb up to 50% via the gastrointestinal tract. Lead in blood is bound to erythrocytes, and elimination is slow and principally via urine. Lead is accumulated in the skeleton, and is only slowly released from this body compartment. Half-life of lead in blood is about 1 month and in the skeleton 20–30 years.

The symptoms of acute lead poisoning are headache, irritability, abdominal pain and various symptoms related to the nervous system. Lead encephalopathy is characterized by sleeplessness and restlessness. Children may be affected by behavioural disturbances, learning and concentration difficulties. In severe cases of lead encephalopathy, the affected person may suffer from acute psychosis, confusion and reduced consciousness. People who have been exposed to lead for a long time may suffer from memory deterioration, prolonged reaction time and reduced ability to understand. Individuals with average blood lead levels under 3μmol/l may show signs of peripheral nerve symptoms with reduced nerve conduction velocity and reduced dermal sensibility. If the neuropathy is severe the lesion may be permanent.

  

Arsenic – As

Arsenic is a widely distributed metalloid, occurring in rock, soil, water and air. Inorganic arsenic is present in groundwater used for drinking in several countries all over the world (e.g. Bangladesh, Chile and China), whereas organic arsenic compounds (such as arsenobetaine) are primarily found in fish, which may give rise to human exposure. Smelting of non-ferrous metals and the production of energy from fossil fuel are the two major industrial processes that lead to arsenic contamination of air, water and soil, smelting activities being the largest single anthropogenic source of atmospheric pollution. Other sources of contamination are the manufacture and use of arsenical pesticides and wood preservatives. The working group of the EU DG Environment concluded that there were large reductions in the emissions of arsenic to air in several member countries of the European Union in the 1980s. In 1990, the total emissions of arsenic to the air in the member states were estimated to be 575 tons. In 1996, the estimated total releases of arsenic to the air in the UK were 50 tons. Concentrations in air in rural areas range from <1 to 4 ng/m³, whereas concentrations in cities may be as high as 200 ng/m³. Much higher concentrations (>1000 ng/m³) have been measured near industrial sources. Water concentrations are usually <10 μg/l, although higher concentrations may occur near anthropogenic sources. Levels in soils usually range from 1 to 40 mg/kg, but pesticide application and waste disposal can result in much higher concentrations.

General population exposure to arsenic is mainly via intake of food and drinking water. Food is the most important source, but in some areas, arsenic in drinking water is a significant source of exposure to inorganic arsenic. Contaminated soils such as mine-tailings are also a potential source of arsenic exposure. Absorption of arsenic in inhaled airborne particles is highly dependent on the solubility and the size of particles. Soluble arsenic compounds are easily absorbed from the gastrointestinal tract. However, inorganic arsenic is extensively methylated in humans and the metabolites are excreted in the urine. Inorganic arsenic is acutely toxic and intake of large quantities leads to gastrointestinal symptoms, severe disturbances of the cardiovascular and central nervous systems, and eventually death. In survivors, bone marrow depression, haemolysis, hepatomegaly, melanosis, polyneuropathy and encephalopathy may be observed. Ingestion of inorganic arsenic may induce peripheral vascular disease, which in its extreme form leads to gangrenous changes.

Populations exposed to arsenic via drinking water show excess risk of mortality from lung, bladder and kidney cancer, the risk increasing with increasing exposure. There is also an increased risk of skin cancer and other skin lesions, such as hyperkeratosis and pigmentation changes. Studies on various populations exposed to arsenic by inhalation, such as smelter workers, pesticide manufacturers and miners in many different countries consistently demonstrate an excess lung cancer. Although all these groups are exposed to other chemicals in addition to arsenic, there is no other common factor that could explain the findings. The lung cancer risk increases with increasing arsenic exposure in all relevant studies, and confounding by smoking does not explain the findings. The latest WHO evaluation concludes that arsenic exposure via drinking water is causally related to cancer in the lungs, kidney, bladder and skin, the last of which is preceded by directly observable precancerous lesions. Uncertainties in the estimation of past exposures are important when assessing the exposure–response relationships, but it would seem that drinking water arsenic concentrations of approximately 100μg/l have led to cancer at these sites, and that precursors of skin cancer have been associated with levels of 50–100μg/l. 

Reference:

http://large.stanford.edu/publications/coal/references/docs/167.pdf

http://www.nrdc.org/health/effects/mercury/sources.asp

http://extoxnet.orst.edu/faqs/foodcon/mercury.htm

http://www.hc-sc.gc.ca/fn-an/securit/chem-chim/environ/lead_plomb-eng.php